Note: Page numbers of article titles are in boldface type. Abdomen ...

Index

Note: Page numbers of article titles are in boldface type.

A

Abdomen, interventional ultrasonography in. See

Interventional ultrasonography.

Abdominal aortic aneurysms, aortic endografting for,

372–373

complications of, 369–370

CT of, 373

Ehlers-Danlos syndrome and, 370

risk factors for, 368

ultrasonography of, 365–373

anatomy and histology in, 365–366

as screening tool, 370

false aneurysms, 370–371

flow characteristics in, 366

for aortic dissection, 371–372

inflammatory aneurysms, 371

limitations of, 370

mycotic aneurysms, 371

technique for, 366–368

Abdominal ectopic pregnancy, ultrasonography

of, 333

Abdominal injuries, emergency ultrasonography

of, 421

Abdominal surgery, during pregnancy,

ultrasonography in, 323

Abortion, spontaneous, and first-trimester bleeding,

301–303, 306

ultrasonography of, 322

Abruption, placental, ultrasonography of, 319

Abscesses, abdominal, interventional ultrasonogra-

phy for. See Interventional ultrasonography.

intratesticular, ultrasonography of, 353–354

liver, diagnosis of, 268–270

lung, interventional ultrasonography for, 462

tubo-ovarian, ultrasonography of, 338–339

Abscess-pleural symphysis, lung abscesses and, 462

Acalculous cholecystitis, acute, ultrasonography

of, 260

Acute painful scrotum, ultrasonography of, 349–363

anatomy in, 349–350

for appendageal torsion, 356–357for cellulitis, 353

for epididymo-orchitis, 351–353for Fournier’s gangrene, 351

for idiopathic varicocele, 357–358

for inguinal hernia, 360–361

for intratesticular abscess, 353–354

for intratesticular arteriovenous

malformation, 359

for intratesticular varicocele, 358–359

for primary orchitis, 353

for secondary varicocele, 358

for testicular torsion, 354–356

for testicular trauma, 359–360

for testicular tumor, 361


Adenomas, hepatic, ultrasonography of, 271–273

Adnexal masses, ultrasonography of, 329–348

corpus luteal cysts, 329–331

cystadenocarcinoma, 342

cystic teratomas, 341

diverticulitis, 344

ectopic pregnancy, 331–334

abdominal, 333

adnexal ring sign in, 332

cervical, 333

double decidual sac sign in, 332

b-human chorionic gonadotropin in, 334

interstitial, 333

intradecidual sign in, 331–332

management of, 333–334

endometriomas, 339–340

epiploic appendages, 345

follicular cysts, 329

leiomyomata, 340–341luteoma of pregnancy, 338

ovarian hyperstimulation syndrome, 334–336

0033-8389/04/$ – see front matter D 2004 Elsevier Inc. All rights reserved.

doi:10.1016/S0033-8389(04)00032-6

Radiol Clin N Am 42 (2004) 479–486

ovarian neoplasms, 341

ovarian torsion, 336–338

pelvic inflammatory disease and tubo-ovarian

abscess, 338–339

perforated appendicitis, 343–344

serous and mucinous cystadenomas, 341–342

theca lutein cysts, 334

Adnexal ring sign, in ectopic pregnancy, 332

Amniotic sac, ultrasonography of, 301

Androgens, and priapism, 430–431

Aneurysms, ultrasonography of, abdominal aortic.

See Abdominal aortic aneurysms.

iliac artery, 377–379

peripheral artery, 379

popliteal, 379

splanchnic artery, 377

splenic artery, 377

in pregnancy, 325

Ankle-brachial index, in arterial injuries, 383–384

Antipsychotic drugs, and priapism, 430

Aortic dissection, ultrasonography of, 371–372

Aortic endografting, for abdominal aortic aneurysms,

372–373

Appendageal torsion, scrotal, ultrasonography of,

356–357

Appendicitis, acute, in infants and children, 452–454


perforated, ultrasonography of, 343–344

Arterial embolization, for acute limb ischemia,

392–394

for priapism, 436–437

Arterial injuries, ankle-brachial index in, 383–384

pathologic validation of, 383


acute limb ischemia, 392–394

arteriovenous fistulas, 388–389

craniocervical dissections, 389–391

diabetic foot, 394

hematomas, 386–388

pseudoaneurysms, 384–386

stroke and carotid artery stenosis, 391–392

upper limb ischemia, 394–395

Arteriovenous fistulas, renal, ultrasonography of,

406–407


Arteriovenous malformations, and first-trimester

bleeding, 309–311

intratesticular, ultrasonography of, 359

B

Barium enema examination, of intussusception, in

infants and children, 449–450

Bell-clapper deformity, scrotal, ultrasonography

of, 354

Biliary duct dilatation, diagnosis of, 264–266

Biliary obstruction, diagnosis of, 266

Biopsy, renal, complications of, 406–407, 410

Bleeding, first-trimester. See First-trimester bleeding.

Bowel strangulation, inguinal hernias and, 360–361

Budd-Chiari syndrome, ultrasonography of, 275

C

Calf veins, ultrasonography of, for thromboembolic

disease, 287–288

Carotid artery dissection, ultrasonography of,

389–390

Carotid artery stenosis, and stroke, ultrasonography

of, 391–392

Cellulitis, scrotal, ultrasonography of, 353

Cervical ectopic pregnancy, ultrasonography of, 333

Chest, interventional ultrasonography in. See

Interventional ultrasonography.

Chest injuries, emergency ultrasonography of,

421–424

Chest tube insertion, ultrasonography in, 459–462

Chlorpromazine, and priapism, 430

Cholecystitis, ultrasonography of, acute, 257

acute acalculous, 260

complicated, 260–261

emphysematous, 263–264

gangrenous, 261–262

Cholecystostomy, percutaneous, ultrasonography in,

463–465

Choriocarcinoma, and first-trimester bleeding, 309

Chronic intestinal ischemia, ultrasonography of,

373–377

Cirrhotic native liver, ultrasonography of. See Liver.

Cocaine, and priapism, 430

Compression ultrasonography, of thromboembolic

disease, 281, 283, 286, 287, 291, 294

Computed tomography, in trauma patients, versus

ultrasonography, 420

Index / Radiol Clin N Am 42 (2004) 479–486480

of abdominal aortic aneurysms, 373

of acute hepatic vein thrombosis, 275

of diverticulitis, 344

of intra-abdominal abscesses, 465–466

Corpus luteal cysts, ultrasonography of, 329–331

Craniocervical dissections, ultrasonography of,

389–391

Crown-rump length, of embryo, 301, 305

Cystadenocarcinoma, ultrasonography of, 342

Cystadenomas, ultrasonography of, 341–342

Cystic teratomas, ultrasonography of, 341

Cysts, corpus luteal, ultrasonography of, 329–331

follicular, ultrasonography of, 329

theca lutein, ultrasonography of, 334

Cytotec, and spontaneous abortion, 322

D

Deep venous thrombosis, ultrasonography of,

286–294

Diabetic foot, ultrasonography of, 394

D-dimer test, for thromboembolic disease, 284, 286

Diverticulitis, CT of, 344


Double decidual sac sign, in ectopic pregnancy, 332

in transvaginal ultrasonography, 299

E

Echinococcal abscesses, interventional

ultrasonography for, 470

Ectopic pregnancy, ultrasonography of. See Adnexal

masses.

Edema, re-expansion pulmonary, thoracentesis

and, 459

Ehlers-Danlos syndrome, and abdominal aortic

aneurysms, 370

Embolization, arterial, for acute limb ischemia,

392–394

for priapism, 436–437

transcatheter, for priapism, 437–438

Embryo, ultrasonography of, 300–301, 305

Emphysematous cholecystitis, ultrasonography of,

263–264

Empyema, chest tubes for, 460–462

versus lung abscesses, 462

Endoluminal repair, of abdominal aortic aneurysms,

372–373

Endometriomas, ultrasonography of, 339–340

Endometrium, sonographic anatomy of, 297

Endovaginal ultrasonography, of ectopic

pregnancy, 331

Epididymo-orchitis, ultrasonography of, 351–353

Epiploic appendages, ultrasonography of, 345

F

Fatty infiltration of liver, and liver enlargement, 270

Fatty liver of pregnancy, and liver enlargement,

270–271

Fibroids, uterine, ultrasonography of, 322–323

First-trimester bleeding. See also Pregnancy.


anatomy in, 297–298

for absent intrauterine gestational sac,

303–304

for arteriovenous malformations, 309–311

for choriocarcinoma, 309

for gestational sac with embryo, 305

for gestational trophoblastic disease, 306–309

for hydatidiform mole, 307–309

for intrauterine growth restriction, 305

for retained products of conception, 306

for spontaneous abortion, 301–303

for subchorionic hematoma, 305–306

for trophoblastic tumors, 309

technique for, 298

versus normal ultrasonography, 298–301

amniotic sac in, 301

embryo in, 300–301

gestational sac in, 298–300

yolk sac in, 300

yolk sac criteria for, 304–305

Fistulas, abdominal, interventional ultrasonography

for, 468, 470

arteriovenous, renal, ultrasonography of,

406–407


Focal hemorrhagic lesions, hepatic, diagnosis of,

271–274

Focused abdominal sonography for trauma

technique. See Trauma patients, emergency

ultrasonography in.

Index / Radiol Clin N Am 42 (2004) 479–486 481

Follicular cysts, ultrasonography of, 329

Foot, diabetic, ultrasonography of, 394

Fournier’s gangrene, ultrasonography of, 351

Fungal abscesses, interventional ultrasonography

for, 470

G

Gallbladder disease, in pregnancy, ultrasonography

of, 324

Gallbladder perforation, ultrasonography of,

262–263

Gallbladder wall thickening, ultrasonography of, 260

Gallstones, ultrasonography of, 257–260

Gangrene, Fournier’s, ultrasonography of, 351

Gangrenous cholecystitis, ultrasonography of,

261–262

Gestational sac, ultrasonography of, 298–300,

303–305

Gestational trophoblastic disease, and first-trimester

bleeding, 306–309

H

HELLP syndrome, ultrasonography of, 316–317

Hematoceles, ultrasonography of, 359

Hematomas, infected, interventional ultrasonography

for, 470

scrotal, ultrasonography of, 359–360

subchorionic, and first-trimester bleeding,

305–306


Hemorrhage, postpartum, ultrasonography of, 321

thoracentesis and, 459

Hemorrhagic lesions, hepatic, diagnosis of, 271–274

Hepatic abscesses, interventional ultrasonography

for, 466–467

Hepatic artery stenosis, ultrasonography of, 398, 399

Hepatic artery thrombosis, ultrasonography of,

275–276, 398

Hepatic vein thrombosis, ultrasonography of, 275

Hepatic veins, ultrasonography of, 399–400

Hepatitis, diagnosis of, 266–268

Hepatobiliary ultrasonography, 257–278

Murphy’s sign in, 257

of acute acalculous cholecystitis, 260

of acute cholecystitis, 257

of acute right upper quadrant pain, 276

of biliary duct dilatation, 264–266

of biliary obstruction, 266

of complicated cholecystitis, 260–261

of emphysematous cholecystitis, 263–264

of focal hemorrhagic lesions, 271–274

of gallbladder perforation, 262–263

of gallbladder wall thickening and pericholecystic

fluid, 260

of gallstones, 257–260

of gangrenous cholecystitis, 261–262

of hepatic artery stenosis, 398, 399

of hepatic artery thrombosis, 275–276, 398

of hepatic vascular abnormalities, 274–276

of hepatic vein thrombosis, 275

of hepatitis, 266–268

of liver abscesses, 268–270

of noninfectious liver enlargement, 270–271

of portal vein thrombosis, 274–275, 399,

401–402, 405

Hepatocellular carcinoma, ultrasonography of,

273–274

Hepatofugal flow, ultrasonography of, 402

Hernias, inguinal, ultrasonography of, 360–361

b-Human chorionic gonadotropin, in ectopic

pregnancy, 334

in molar pregnancy, 308–309

in ovarian hyperstimulation syndrome, 334

in pregnancy, 299–300

Hydatidiform mole, and first-trimester bleeding,

307–309

Hydronephrosis, in pregnancy, ultrasonography

of, 325

Hydrosalpinx, ultrasonography of, 339

Hypertension, in pregnancy, ultrasonography of,

316–317

portal, ultrasonography of, 402

Hypertrophic pyloric stenosis, in infants and children,

445–449

clinical features of, 445

incidence of, 445


I

Iliac artery aneurysms, ultrasonography of, 377–379

Inferior vena cava, ultrasonography of, 399–400

Inflammatory aneurysms, ultrasonography of, 371


Inguinal hernias, ultrasonography of, 360–361

Interstitial ectopic pregnancy, ultrasonography

of, 333

Interventional ultrasonography, 457–478

abdominal, 463–474

for echinococcal abscesses, 470for fistulas, 468, 470

for fungal abscesses, 470for hepatic abscesses, 466–467

for infected hematomas, 470for pelvic abscesses, 470, 472–474

for renal and perinephric abscesses, 467for splenic abscesses, 468

in intra-abdominal abscess drainage, 465–466in paracentesis, 463

in percutaneous cholecystostomy, 463–465in percutaneous nephrostomy, 467–468

of chest, 457–462

for lung abscesses, 462

in chest tube insertion, 459–462

in thoracentesis, 457–459

Intestinal ischemia, chronic, ultrasonography of,

373–377

Intracavernosal arteries, laceration of, and

priapism, 431

Intracorporeal injection therapy, and priapism, 430

Intradecidual sign, in ectopic pregnancy, 331–332

in transvaginal ultrasonography, 299

Intratesticular abscesses, ultrasonography of,

353–354

Intratesticular arteriovenous malformations,


Intratesticular varicoceles, ultrasonography of,

358–359

Intrauterine growth restriction, ultrasonography

of, 305

Intussusception, in infants and children, 449–452

barium enema examination for, 449–450

diagnosis of, 449–450

management of, 452

plain films of, 449

J

Jugular vein, ultrasonography of, for thromboembolic

disease, 289–290

K

Kidneys, ultrasonography of, 405–412

after transplantation, 405–409

allograft dysfunction, 408–409

arteriovenous fistulas, 406–407

pseudoaneurysms, 406

renal artery stenosis, 407

renal vein thrombosis, 408

anatomy and appearance in, 405

during transplantation, 407

native kidney, 409–412

for biopsy complications, 410

for pyelonephritis, 410

for renal artery stenosis, 411–412

for renal trauma, 411

for renal vein thrombosis, 411

for urinary obstruction, 410

L

Leiomyomata, ultrasonography of, 340–341

Limb ischemia, ultrasonography of, 392–395

Liver, ultrasonography of, 397–405

after transplantation, 398–400

hepatic artery stenosis, 398, 399

hepatic artery thrombosis, 398

hepatic veins and inferior vena cava,

399–400

portal vein thrombosis, 399

pseudoaneurysms, 400

anatomy and appearance in, 397–398

native cirrhotic liver, 400–404

after transjugular intrahepatic

portosystemic shunt, 400–404

for portal hypertension, 402

for portal vein aneurysmal ectasia, 404

for portal vein thrombosis, 401–402

noncirrhotic native liver, 404–405

Liver abscesses, diagnosis of, 268–270

interventional ultrasonography for, 466–467

Liver enlargement, noninfectious, diagnosis of,

270–272

Lower extremities, thromboembolic disease in,

ultrasonography of, 286–288, 291, 293–294

Lung abscesses, interventional ultrasonography

for, 462

Luteoma of pregnancy, ultrasonography of, 338


M

Magnetic resonance imaging, of acute hepatic vein

thrombosis, 275

Mesenteric vasculature, ultrasonography of, 373–377

Metastatic disease, and liver enlargement, 270

Methotrexate, for ectopic pregnancy, 333–334

Mifepristone, and spontaneous abortion, 322

Molar pregnancy, and first-trimester bleeding,

307–309

Mucinous cystadenomas, ultrasonography of,

341–342

Murphy’s sign, in hepatobiliary ultrasonography, 257

Mycotic aneurysms, ultrasonography of, 371

Myometrium, sonographic anatomy of, 297

N

Nephrostomy, percutaneous, interventional

ultrasonography in, 467–468

Neurologic disease, and priapism, 431

O

Orchitis, ultrasonography of, 353

Ovarian hyperstimulation syndrome, ultrasonography

of, 334–336

Ovarian neoplasms, ultrasonography of, 341

Ovarian torsion, ultrasonography of, 336–338

Ovaries, sonographic anatomy of, 297

Ovulation induction therapy, and ovarian

hyperstimulation syndrome, 335

P

Paracentesis, ultrasonography in, 463

Parapneumonic effusions, chest tubes for, 459–460

Pelvic abscesses, interventional ultrasonography for,

470, 472–474

Pelvic inflammatory disease, ultrasonography of,

338–339

Pelvic pain, adnexal masses and. See

Adnexal masses.

Pelvic thrombophlebitis, in pregnancy,


Percutaneous cholecystostomy, ultrasonography in,

463–465

Percutaneous nephrostomy, interventional


Pericholecystic fluid, ultrasonography of, 260

Perinephric abscesses, interventional ultrasonography

for, 467

Peripheral artery aneurysms, ultrasonography of, 379

Placentation, abnormal, ultrasonography of, 317–319

Plain films, in trauma patients, versus

ultrasonography, 422–424

of intussusception, in infants and children, 449

Pleural effusions, chest tubes for, 459–462

emergency ultrasonography of, 421

Pleuritic pain, thoracentesis and, 459

Pneumothorax, emergency ultrasonography of,

421–423

thoracentesis and, 458–459

Popliteal aneurysms, ultrasonography of, 379

Popliteal vein, ultrasonography of, for

thromboembolic disease, 287

Portal hypertension, ultrasonography of, 402

Portal vein aneurysmal ectasia, ultrasonography

of, 404

Portal vein thrombosis, ultrasonography of,

274–275, 399, 401–402, 405

Pregnancy. See also First-trimester bleeding.

ectopic, ultrasonography of. See Adnexal masses.

molar, and first-trimester bleeding, 307–309


during abdominal surgery and trauma, 323

for abnormal placentation, 317–318

for acute renal disorders, 324–325

for gallbladder disease, 324

for pelvic thrombophlebitis, 324

for placenta previa, 318–319

for placental abruption, 319

for postpartum hemorrhage, 321

for pregnancy-induced hypertension, 316–317

for retained products of conception, 321–322

for splenic artery aneurysms, 325

for spontaneous abortion, 322

for uterine fibroids, 322–323

for uterine rupture, 317

for vasa previa, 320–321

for venous thromboembolism, 323–324



Priapism, 427–443

arterial embolization for, 436–437

definition of, 427–428

diagnosis of, 434–436

epidemiology of, 428, 430

etiology of, 430–431


complications of, 439–440

pathophysiology of, 431–434

sickle cell anemia and, 430, 433, 439

transcatheter embolization for, 437–438

ultrasonography of, 436, 438

anatomy in, 428

technique for, 428

Pseudoaneurysms, hepatic, ultrasonography of, 400

renal, ultrasonography of, 406


Pulmonary edema, re-expansion, thoracentesis

and, 459

Pulmonary embolism, ultrasonography of, 294

Pyelonephritis, ultrasonography of, 410

Pyogenic liver abscesses, interventional

ultrasonography for, 466–467

R

Raynaud’s phenomenon, ultrasonography of,

394–395

Renal abscesses, interventional ultrasonography

for, 467

Renal artery stenosis, ultrasonography of, 407,

411–412

Renal disorders, in pregnancy, ultrasonography of,

324–325

Renal trauma, ultrasonography of, 411

Renal vein thrombosis, ultrasonography of, 408, 411

Retained products of conception, and first-trimester

bleeding, 306


RU 486, and spontaneous abortion, 322

S

Scrotum, acute painful. See Acute painful scrotum.

Seldinger technique, for percutaneous

cholecystostomy, 464

Serous cystadenomas, ultrasonography of, 341–342

Shunts, for priapism, 439

Sickle cell anemia, and priapism, 430, 433, 439

Solid organ injuries, emergency ultrasonography of,

420–421

Splanchnic artery aneurysms, ultrasonography

of, 377

Splenic abscesses, interventional ultrasonography

for, 468

Splenic artery aneurysms, ultrasonography of, 377

in pregnancy, 325

Spontaneous abortion, and first-trimester bleeding,

301–303, 306


Stroke, carotid artery stenosis and, ultrasonography

of, 391–392

Subchorionic hematomas, and first-trimester

bleeding, 305–306

T

Testicular torsion, ultrasonography of, 354–356

Testicular trauma, ultrasonography of, 359–360

Testicular tumors, ultrasonography of, 361

Theca lutein cysts, ultrasonography of, 334

Thioridazine, and priapism, 430

Thoracentesis, ultrasonography in, 457–459

Thrombin injection, for pseudoaneurysms, 386

Thromboembolic disease, clinical evaluation of,

283–284

clinical features of, 279–281

D-dimer test for, 284, 286


adjuncts to, 291

deep venous thrombosis, 286–294

in lower extremities, 286–288, 293–294

in pregnancy, 323–324

in upper extremities, 288–290, 294

pitfalls of, 291

pulmonary embolism, 294

Thrombophlebitis, pelvic, in pregnancy,


Transabdominal ultrasonography, technique for, 298

Transcatheter embolization, for priapism, 437–438

Transhepatic approach, to percutaneous

cholecystostomy, 464


Transjugular intrahepatic portosystemic shunt,

ultrasonography after, 400–404

Transplantation, kidney, ultrasonography after.

See Kidneys.

liver, ultrasonography after. See Liver.

Transvaginal approach, to pelvic abscess drainage,

472–474

Transvaginal ultrasonography, of embryo, 300–301

of gestational sac, 298–300

of molar pregnancy, 308–309

of yolk sac, 300

technique for, 298

Trauma, during pregnancy, ultrasonography of, 323

renal, ultrasonography of, 411

testicular, ultrasonography of, 359–360

Trauma patients, emergency ultrasonography in,

417–425

for chest injuries, 421–424

for solid organ injuries, 420–421

free fluid in, 417–418

free fluid scoring systems in, 419–420

pitfalls in, 418–419

sensitivity of, 420

versus CT, 420

versus plain films, 422–424

Trazodone, and priapism, 430

Trophoblastic tumors, and first-trimester

bleeding, 309

Tubo-ovarian abscesses, ultrasonography of,

338–339

U

Ultrasonography, endovaginal, of ectopic

pregnancy, 331

hepatobiliary. See Hepatobiliary ultrasonography.

in trauma patients. See Trauma patients.

interventional. See Interventional ultrasonography.

of abdominal aortic aneurysms. See Abdominal

aortic aneurysms.

of adnexal masses. See Adnexal masses.

of arterial injuries. See Arterial injuries.

of first-trimester bleeding. See

First-trimester bleeding.

of hypertrophic pyloric stenosis, in infants and

children. See Hypertrophic pyloric stenosis.

of intussusception, in infants and children.

See Intussusception.

of kidneys. See Kidneys.

of liver. See Liver.

of mesenteric vasculature, 373–377

of pregnancy-related emergencies. See Pregnancy.

of priapism, 428, 436, 438

of thromboembolic disease. See

Thromboembolic disease.

transvaginal. See Transvaginal ultrasonography.

Upper extremities, thromboembolic disease in,

ultrasonography of, 288–290, 294

Urinary obstruction, ultrasonography of, 410

Urolithiasis, in pregnancy, ultrasonography of, 325

Uterine fibroids, ultrasonography of, 322–323

Uterine rupture, in pregnancy, ultrasonography

of, 317

Uterus, sonographic anatomy of, 297

V

Varicoceles, ultrasonography of. See Acute

painful scrotum.

Vasa previa, in pregnancy, ultrasonography of,

320–321

Vasovagal reactions, thoracentesis and, 459

Venous thromboembolism, in pregnancy,


Y

Yolk sac, ultrasonography of, 300, 304–305


FORTHCOMING ISSUES

May 2004

Cardiac ImagingMartin Lipton, MD, andLawrence Boxt, MD, Guest Editors

July 2004

Breast ImagingCarl D’Orsi, MD, Guest Editor

September 2004

PET Imaging IAbass Alavi, MD, Guest Editor

RECENT ISSUES

January 2004

Arthritis ImagingBarbara N. Weissman, MD, Guest Editor

November 2003

Imaging of the Acute AbdomenEmil J. Balthazar, MD, Guest Editor

September 2003

Advances in Renal ImagingPhilip J. Kenney, MD, Guest Editor

THE CLINICS ARE NOW AVAILABLE ONLINE!

Access your subscription at:http://www.TheClinics.com

Radiol Clin N Am 42 (2004) xi

Preface

Emergency ultrasound

Vikram Dogra, MD

Guest Editor

Ultrasonography has undergone many technologic tient care. Most of the articles describe sonography

changes resulting in its present state-of-the-art equip-

ment that is capable of high-resolution real-time

gray-scale imaging and tissue harmonics, including

color and power Doppler. These advances in ultra-

sound technology have resulted in improved work-up

of patients undergoing evaluation in emergency de-

partments because it is the first imaging performed on

almost all patients presenting to an emergency facil-

ity. This easily available imaging modality remains

the primary workhorse in diagnostic radiology not

only in day-to-day practice but also in emergency

situations. There has been a need for the Radiologic

Clinics of North America to dedicate an issue solely

to the practice of emergency ultrasound and I am

honored to be the guest editor of this issue. Great care

has been given to the selection of topics for this issue,

and pertinent findings have been summarized in the

form of tables for easy reference in most of the

articles where problem-solving algorithms are also

included. Relevant topics have been included that

are helpful to all clinicians involved in emergency pa-

0033-8389/04/$ – see front matter D 2004 Elsevier Inc. All right

doi:10.1016/j.rcl.2004.01.004

techniques and pertinent sonographic anatomy to help

those who are new to the field of ultrasonography.

This issue on emergency ultrasound provides the

reader with up-to-date information on what is new,

exciting, and relevant in the practice of ultrasonog-

raphy as it pertains to acutely ill patients.

I wish to express my thanks to Joseph Molter for

preparing the illustrations, to Bonnie Hami, MA, for

her editorial assistance, and to Adrienne Jones for her

secretarial assistance. In addition, my sincere thanks

go to Barton Dudlick at Elsevier Science for his

administrative and editorial assistance.

Vikram Dogra, MD

Division of Ultrasound

Department of Radiology

Case Western Reserve University

University Hospitals

11100 Euclid Avenue

Cleveland, OH 44106, USA

E-mail address: [email protected]

s reserved.

Radiol Clin N Am 42 (2004) 257–278

Hepatobiliary imaging and its pitfalls

Deborah J. Rubens, MD

Departments of Radiology and Surgery, University of Rochester Medical Center, 601 Elmwood Avenue,

Rochester, NY 14642-8648, USA

Diagnosis of acute cholecystitis Sonographic Murphy’s sign

Acute cholecystitis is the result of obstruction of

the gallbladder and accompanying inflammation of

the gallbladder wall with associated infection and

sometimes necrosis. Ninety percent to 95% of cases

of acute cholecystitis are caused by obstruction by

gallstones in either the gallbladder neck or the cystic

duct [1]. Acute cholecystitis occurs in only approxi-

mately 20% of patients who have gallstones [2]. This

means that many patients with gallstones have no

symptoms, and their right upper quadrant pain may

be caused by a different etiology [3]. Of patients who

present with right upper quadrant pain, only 20% to

35% have acute cholecystitis [1,2]. As the definition

of ‘‘right upper quadrant pain’’ becomes less specific,

especially lacking an accompanying elevated white

blood cell count and fever, the percentage of patients

who actually have acute cholecystitis given the his-

tory of right upper quadrant pain diminishes further.

Specific criteria for the diagnosis of acute cholecys-

titis are important, because many patients have gall-

stones but may not have acute cholecystitis. The

primary diagnostic criterion is a positive sonographic

Murphy’s sign in the presence of gallstones. Second-

ary signs of acute cholecystitis include gallbladder

wall thickening more than 3 mm, a distended or

hydropic gallbladder (loss of the normal tapered neck

and development of an elliptical or rounded shape),

and pericholecystic fluid.


doi:10.1016/j.rcl.2003.12.004


The sonographic Murphy’s sign is defined as

specific reproducible point tenderness over the gall-

bladder as the transducer applies pressure. In a classic

article by Dr. Phillip Ralls [4], which included only

patients with right upper quadrant pain, fever, and an

elevated white blood cell count, a sonographic Mur-

phy’s sign was 87% specific for the diagnosis of

acute cholecystitis. When a positive sonographic

Murphy’s sign is used in conjunction with the pres-

ence of gallstones, it has a positive predictive value of

92% for diagnosing acute cholecystitis. Persons in

whom a sonographic Murphy’s sign may be absent

include persons who are medicated; therefore, careful

attention to a patient’s clinical status is important.

Denervated gallbladders in patients who have diabe-

tes or gangrenous cholecystitis may result in the loss

of a sonographic Murphy’s sign.

Gallstone diagnosis and pitfalls

Gallstones are diagnosed by the presence of

gravity-dependent, mobile intraluminal echoes within

the gallbladder, which cast a posterior shadow

(Fig. 1). Although ultrasound (US) has a high accu-

racy ( > 95%) for the diagnosis of gallstones, some

stones may be missed [3]. False-negative results

occur because of stones that are too small to cast a

shadow (usually smaller than 1 mm), soft stones that

lack strong echoes [1], and gallstones that are im-

pacted in the gallbladder neck or in the cystic duct

and may not be as readily visible (see Fig. 1) [5]. If

the gallbladder is focally tender but no gallstones are

appreciated, the patient should be examined from

s reserved.

Fig. 1. Gallstones. (A, left) Gallstone in the gallbladder neck (arrow) casts no significant shadow and is nearly invisible. Gas in

the duodenum (arrowhead) obscures the fundus and casts a strong sharp shadow (asterisk). (Right) With patient in sitting

position, stone (arrow) moves out of the neck and casts a clear shadow (asterisk). Adjacent duodenum (arrowheads) is separate

from the gallbladder but still casts a strong shadow, equivalent to the gallstone. (B, left) Multiple gallstones (arrowheads), some

of which cast shadows (arrows) and some of which do not. (Right) Normal caliber common duct (6 mm at the porta) with stones

(arrows) in same patient. Choledocholithiasis may be difficult to detect, especially in the distal duct, if the stones do not shadow

or are not outlined by the distal fluid. (C, left) Longitudinal US shows a normal gallbladder. (Right) Harmonic imaging reveals

multiple small stones (arrows).

D.J. Rubens / Radiol Clin N Am 42 (2004) 257–278258

multiple positions, including prone position or up-

right position, to help stretch out the gallbladder

[3,6]. Decubitus or intercostal scanning also may

help visualize the neck, which may not be as easily

apparent from a subcostal supine approach.

Resolution of small stones in the gallbladder can

be improved with use of harmonic imaging [7,8]. This

approach uses the higher frequency of the returning

sound beam for better resolution and decreases the

scattering from superficial structures in the abdominal

wall and in the adjacent liver. Harmonic imaging

improves the echoes cast by stones and strengthens

their posterior shadows. This improved resolution

may permit visualization of stones not seen with

conventional gray scale US (see Fig. 1).

Fig. 2. Pseudo gallbladders. (A) Transverse image in the right upper

containing debris (asterisk). Note that the ‘‘gallbladder’’ does not ex

(B, left) CT image of the same area as in A shows a fluid-containin

aorta (A). This was a hematoma.(Right) The true gallbladder (GB) is

fluid- and debris-containing structure believed to represent an abnor

(Right) The true gallbladder (arrows) is compressed and displaced

pancreatic pseudocyst (P) displacing the gallbladder (arrows).

Echogenicity of stones may be decreased in soft

pigment stones. These stones are commonly associ-

ated with recurrent pyogenic cholangiohepatitis and

are more often seen in the bile ducts than in the

gallbladder. They look more like soft-tissue masses

than stones and may or may not cast acoustic shad-

ows. They may be misinterpreted as sludge or debris

and give a false-negative diagnosis for gallstones.

False-positive results may arise from side lobe

artifacts, which give rise to echoes that seem to arise

within the gallbladder lumen but are actually gener-

ated from the wall or outside the wall [1]. Similarly,

partial volume artifacts from gas in the adjacent bowel

may mimic stones with strong echoes and posterior

shadowing (see Fig. 1A). A calcium bile salt precipi-

quadrant with structure identified as the gallbladder (arrows)

tend anteriorly and that the aorta (A) is immediately adjacent.

g structure (arrows) with similar attenuation to blood in the

lateral to the aorta and extends anteriorly. (C, left) Distended

mal gallbladder in this patient with right upper quadrant pain.

by the adjacent mass, a pancreatic pseudocyst. (D) CT of the

D.J. Rubens / Radiol Clin N Am 42 (2004) 257–278 259


tate may form with the use of Ceftriaxone and mimic

gallstones on sonographic examination. These precip-

itates resolve after the patient ends therapy.

Other fluid-containing structures may mimic the

gallbladder, especially if the gallbladder is out of its

normal position or is small and contracted. These

structures include the duodenum, gastric antrum or

colon, hematomas, pancreatic pseudocysts (Fig. 2), or

even dilated vascular collaterals. Mistaking these

structures for the gallbladder may result in missed

pathology in the true gallbladder or a false-positive

diagnosis of gallbladder disease (ie, obstructed gall-

bladder or acalculous cholecystitis).

Gallbladder wall thickening and pericholecystic

fluid

Gallbladder wall thickening is defined as a wall

diameter more than 3 mm and is present in 50% of

patients with acute cholecystitis (Fig. 3) [1]. The

gallbladder wall may be thickened because of hepatic

congestion or edema from liver disease, right heart

failure, or generalized edema from hypoproteinemia,

which is often associated with renal disease or hepatic

dysfunction [3]. A thickened gallbladder wall also

can occur in association with adjacent inflammatory

conditions, including hepatitis, peptic ulcer disease

(Fig. 4), pancreatitis, perihepatitis (Fitz-Hugh-Curtis

syndrome), and pyelonephritis (Fig. 5).

A thickened, striated gallbladder wall consists of

alternating hyper- and hypoechoic layers. When seen

in the setting of acute cholecystitis, it is strongly

Fig. 3. Acute cholecystitis. This patient presented with right

upper quadrant pain and a positive sonographic Murphy’s

sign. Longitudinal US shows stones (arrows) and diffuse

gallbladder wall thickening (cursors) that measures 5 mm.

associated with complications such as gangrenous

cholecystitis [9]. A striated wall also is nonspecific,

however, and may be seen in all the other causes of

wall thickening, including hepatitis (Fig. 6) [10].

Similarly, pericholecystic fluid is a nonspecific

finding; it may occur because of ascites or localized

inflammation from other causes, such as peptic ulcer

disease (see Fig. 4) [2]. Teefey et al [10] described

two specific patterns of pericholecystic fluid. Type I,

a thin, anechoic, crescent-shaped collection adjacent

to the gallbladder wall, is nonspecific (see Fig. 4B).

Type II, a round or irregular shaped collection with

thick walls, septations, or internal debris, is associated

with gallbladder perforation and abscess formation

(Fig. 7) [10]

Acute acalculous cholecystitis

This is an acute inflammation of the gallbladder

that occurs in up to 14% of patients with acute

cholecystitis [11]. It is most frequently seen in post-

trauma and postsurgical patients and other hospital-

ized patients and occurs because of conditions that

lead to ischemia, hypotension, or sepsis [12]. These

critically ill patients are often medicated with nar-

cotics, are on ventilators, and receive hyperalimenta-

tion, which contributes to biliary stasis and functional

cystic duct obstruction [2,12]. Gallbladder gangrene

is associated in 40% to 60% of cases, with increased

risk of perforation [2]. Mortality ranges from 6% to

44% but can be reduced by early diagnosis and

therapy [12]. In the series by Cornwall et al [12],

only 50% had a sonographic Murphy’s sign. This is

a difficult clinical and ultrasonic diagnosis, because

gallstones are absent and the sonographic Murphy’s

sign may be limited because of other illnesses

and medication. The diagnosis is made by gallblad-

der tenderness (if present) and is associated with

gallbladder distension, intraluminal debris, and gall-

bladder wall thickening that is not caused by other

etiologies, such as hypoalbuminemia, congestive

heart failure, or hepatic congestion (Fig. 8). Because

gallbladder wall thickening is nonspecific, CT can be

used to visualize pericholecystic inflammation to

improve diagnostic specificity [2,13].

Complicated cholecystitis

Complications of acute cholecystitis include gan-

grenous cholecystitis, emphysematous cholecystitis,

Fig. 4. Peptic ulcer perforation and thick gallbladder wall. (A) Patient with right upper quadrant pain, fever, and elevated white

blood cell count. US shows focal gallbladder wall thickening (7-mm cursors) and gallstones (asterisks) and could be interpreted

as cholecystitis. The free air with reverberation shadows (arrows) that leads to the correct diagnosis could be overlooked easily.

(B) Transverse US shows wall thickening (cursors) and simple pericholecystic fluid (arrow). (C) CT image shows peri-

cholecystic fluid (arrows), free air (arrowheads), and extraluminal accumulated air (paired arrowheads) in perforated duo-

denal ulcer.


and gallbladder perforation. These complications oc-

cur in up to 20% of patients [3]. Complications of

acute cholecystitis are important to detect because they

are associated with increased morbidity (10%) and

mortality (15%) [14] and require emergency surgery

[2]. There is also approximately a 30% conversion

for laparoscopic cholecystectomy to an open proce-

dure in the setting of complicated cholecystitis [14].

Gangrenous cholecystitis

Gangrenous cholecystitis is defined histologically

as coagulative necrosis of the mucosa or the entire

wall associated with acute or chronic inflammation

[10]. It occurs in up to 20% of patients with acute

cholecystitis and has an increased risk of perforation

[3]. Unfortunately, US is relatively nonspecific for the

Fig. 5. Pyelonephritis with gallbladder wall thickening. (A) Gallbladder wall shows marked 1.3 cm thickening (cursors) and

hypoechoic fluid within the wall. (B) Transverse US of the lower pole of the right kidney shows a 3-cm echogenic mass

(arrows). (C) CT through the right lower pole shows the characteristic round, heterogeneous decreased attenuation area of

pyelonephritis (arrows).


diagnosis of gangrenous cholecystitis because a sono-

graphic Murphy’s sign is absent in two thirds of

patients [15]. A relatively specific finding is intra-

luminal membranes caused by a fibrous exudate or

necrosis and sloughing of the gallbladder mucosa

(Fig. 9). This finding is present, however, in only

5% of patients [10].

Gallbladder perforation

Gallbladder perforation occurs in 5% to 10% of

patients with acute cholecystitis, most often in asso-

ciation with gangrenous cholecystitis [3]. The fundus

is the most common site for perforation because it has

the least blood supply. Acute perforation with free

intraperitoneal bile results in peritonitis and is rare.

More commonly, subacute perforation occurs, which

results in pericholecystic abscess formation [2].

These abscesses may occur in or adjacent to the

gallbladder wall in the gallbladder fossa, within the

liver, or along the free margin of the gallbladder

within the peritoneal cavity [10]. They are character-

ized by complex fluid collections with inflammatory

changes in the adjacent fat on US or CT [2]. Patients

with peritoneal or liver abscesses require immediate

surgery and drainage, respectively, whereas abscesses

Fig. 6. Hepatitis, with striated gallbladder wall thickening.

Longitudinal US of contracted gallbladder with a thickened

striated wall (arrows) with alternating echogenic and hypo-

echoic layers. This patient had right upper quadrant pain,

fever, abnormal liver function tests, and a negative sono-

graphicMurphy’s sign. She tested positive for hepatitis B and

clinically had acute alcoholic hepatitis. The striated wall is

not specific for gallbladder disease.

Fig. 7. Complicated cholecystitis with gallbladder perforation. (A

irregularly marginated pericholecystic intrahepatic fluid (arrows)

surgery and was found to have acute cholecystitis with an adjacent

shows a pericholecystic collection (arrow) that contains debris. Th

contained within the gallbladder wall (double arrow). (C) CT

inflammatory edema in the adjacent fat (arrowheads).


in the gallbladder wall and fossa may respond to

conservative management [16].

Pericholecystic fluid adjacent to the gallbladder

wall may mimic perforation. Upon careful inspection,

however, the wall is intact and the fluid anechoic (see

Fig. 4B). Fluid that appears within the walls been

noted to precede perforation in one case [17]; how-

ever, no specific US features predict which gallblad-

ders will perforate.

Emphysematous cholecystitis

This is a rare complication of acute cholecystitis

(less than 1% of all complicated cases) and is

associated with gas-forming bacteria in the gallblad-

der lumen or in the gallbladder wall. As many as 40%

of patients with emphysematous cholecystitis have

diabetes [2]. The clinical course is rapidly progres-

sive, with 75% incidence of gallbladder gangrene and

20% incidence of perforation [18]. Emphysematous

cholecystitis can be recognized by the antidependent

gas echoes within the lumen (Fig. 10). Intramural gas

may be more difficult to identify because it may

mimic the calcified wall of a porcelain gallbladder.

The type of shadowing (‘‘clean’’ versus ‘‘dirty’’) does

not differentiate between calcium and air. The loca-

tion of the echoes does. If the presence of gas is

) Longitudinal US of the gallbladder (GB) with adjacent

. This patient presented with sepsis 2 weeks after prostate

liver abscess. (B) Longitudinal US of gallbladder with stones

e collection abuts the free wall of the gallbladder and is not

shows an enhancing rim around the fluid (arrows) and

Fig. 7 (continued).

Fig. 9. Gallbladder gangrene/mucosal sloughing. Longitu-

dinal US of patient with acute cholecystitis secondary to

stone (arrow) impacted in the gallbladder neck. Note the

intraluminal membranes (arrowheads), which are associ-

ated with gallbladder gangrene.


uncertain, either CT or plain film radiography can be

used to differentiate between gas and calcification.

Biliary ducts

Dilated biliary ducts in the acute patient represent

a relative emergency because sepsis in association

with dilated ducts requires rapid decompression.

Biliary duct dilatation may be the result of multiple

causes, including stones, tumor, stricture, or adjacent

Fig. 8. Acalculous cholecystitis. Longitudinal US of a debris-

filled (asterisk) gallbladder with a thick, striated wall (ar-

rows). No stones are visualized. At surgery, this was acute

acalculous cholecystitis.

extrinsic masses with biliary duct compression and

obstruction. The diagnosis is made by evaluation of

intra- and extrahepatic ducts, because one or both

may be dilated, depending on the level of obstruction.

Ultrasound diagnosis of duct dilatation

The extrahepatic common duct is measured from

outer wall to outer wall at the level of the crossing of

the right hepatic artery. The diameter at this level

should not exceed 6 mm [1]. The diameter of the

common duct is slightly greater distally as it ap-

proaches the pancreas, sometimes as much as 1 to

2 mm. There is still debate in literature as to whether

the bile duct dilates with age or after cholecystectomy

[1]. Most laboratories consider a duct smaller than

6 mm normal and a duct 8 mm or larger abnormal

[1,19]. Clinically, if a patient has dilated ducts but no

accompanying symptoms—elevated bilirubin, pain,

sepsis, or elevated liver enzymes, including alkaline

phosphatase—the dilated ducts are unlikely to be

clinically relevant. Similar to the presence of gall-

stones, when assessing the ducts for biliary disease,

the clinical scenario is of prime importance. Intra-

hepatic biliary ducts are normal if they are 2 mm or

smaller in the porta or no more than 40% of the

diameter of the accompanying portal vein [1]. With

the advent of newer equipment, however, it is possi-

ble to see intrahepatic biliary ducts in normal patients,

especially with the use of harmonic imaging, which

diminishes scatter. Clinical correlation is important,

because many young and slender patients may show

normal ducts with high-frequency transducers

(Fig. 11A). In general, intrahepatic biliary duct dila-

Fig. 10. Emphysematous cholecystitis. (A) Transverse supine view of the gallbladder reveals nondependent echoes anteriorly

(arrowheads), which cast a dense posterior shadow. (B) When viewed longitudinally from the flank, the dependent echogenic

gallstones (arrows) can be seen. Note that the shadow cast by the gas in (A) is denser and sharper than that from the stones (B).

The bowel gas does not necessarily cast a ‘‘dirty’’ or reverberant echo-filled shadow. Thus, the shadow cannot distinguish gas

from the stones.

Fig. 11. Normal ducts. (A) Normal intrahepatic ducts (cursors) in a post-cholecystectomy patient. Multicolored vessel in the

center of the color box is the hepatic artery (HA), and dark red adjacent vessel is the portal vein (PV). (B,C) Patient with

abdominal pain, nausea, and jaundice, 1 month after cholecystectomy. Note multiple anechoic irregularly branching tubes with

confluence in the porta hepatis. Color Doppler image (C) confirms that some are avascular and represent ducts (arrowheads), and

the portal veins (red), hepatic veins(blue) and hepatic arteries (HA) are correctly identified. The inferior vena cava (IVC) and

hepatic vein (HV) as shown can be recognized by its anatomic position.


Fig. 11 (continued).


tation can be diagnosed by irregular angular branch-

ing, a central stellate configuration, and acoustic

enhancement posteriorly to the ducts (Fig. 11B) [1].

The use of color and power Doppler may be valuable

to demonstrate that the dilated structures are ducts

and that the normal portal veins and hepatic arteries

course adjacent to them (Fig. 11C). Biliary duct

necrosis is a critical complication that occurs after

liver transplant. In this situation, the ducts may not be

filled with bile but may be filled with pus or necrotic

debris. They also may appear echogenic and irregular

and enlarged without any fluid component (Fig. 12).

If the diagnosis of biliary disease is in question on

US, CT scan or transhepatic cholangiography may be

helpful in posttransplant patients.

Diagnosis of biliary obstruction

Assuming a patient has a dilated duct (6 mm or

larger) associated with clinical signs of obstruction

(including elevated bilirubin or elevated alkaline

phosphatase), how well does US identify the level

and cause of obstruction?

With good technique, the level of obstruction can

be defined in up to 92% of patients and the cause in

up to 71% [1]. Important technical factors include

positioning the patient in the erect right posterior

oblique or right lateral decubitus position to minimize

overlying bowel gas from the antrum or the duode-

num and using transverse scans to follow the duct

accurately [1]. Additional technical improvements

sometimes can be achieved by having the patient

drink water to displace gas or by using large a

footprint curvilinear transducer to compress bowel

and bowel gas away from the distal duct. Ninety

percent of obstruction occurs in the distal duct be-

cause of common duct stones, pancreatic carcinoma,

or pancreatitis [1]. Obstruction also may occur at the

level of the porta hepatis, usually because of tumor

(cholangiocarcinoma) or adenopathy. Sclerosing

cholangitis gives rise to segmentally dilated ducts,

often only in one portion of the liver (Fig. 13). These

patients may develop infection and present with

sepsis. Other causes of obstruction between the

pancreas and the porta hepatis include masses of

the colon or duodenum (Fig. 14), primary biliary

malignancy, or adenopathy.

Pitfalls include patients who have obstruction

without dilatation, which can occur in ascending

cholangitis, intermittent obstruction from stones, or

sclerosing cholangitis. As many as one third of

common bile duct calculi are found in nondilated bile

ducts (see Fig. 1B) [1]. In this group of patients, US is

relatively insensitive to make the diagnosis. MR

cholangiopancreatography (MRCP) and endoscopic

retrograde cholangiopancreatography (ERCP) should

be considered the alternative diagnostic modalities,

especially for stone disease.

Acute hepatic disease processes

Multiple abnormalities of the liver may present

with right upper quadrant pain. Some of these situa-

tions involve medical emergencies, including lesions

that are hemorrhagic or patients who have infection

and sepsis. Space-occupying disorders that stress the

liver capsule also may present with right upper

quadrant pain. These disorders range from acute fatty

infiltration to hepatitis to diffuse metastatic disease.

The important clinical features to determine are

whether the patient has infection or sepsis and if

the pain is localized to the liver or is more diffuse

(peritoneal signs). Anatomically the hepatic processes

can be divided into diffuse disease, focal disease, and

diseases that involve the vasculature.

Hepatitis

Hepatitis is a viral infection of the liver. The most

common acute presentation is from hepatitis A,

which is spread via oral ingestion with a 99%

recovery rate [20]. Patients present acutely with

jaundice, fever, and hepatomegaly. Sonographically,

Fig. 12. Biliary duct necrosis. (A) Transverse US of a liver transplant patient who presented with sepsis. Amorphous echogenic

debris (arrows) is seen on gray scale. (B) Two months later, the process has progressed. The echogenic areas (arrows) are more

confluent and linear and cast acoustic shadows, which obscure the adjacent parenchyma. (C) Color Doppler image shows

echogenic debris in a ductal distribution (arrows) and a low resistive index (less then 0.5) in the hepatic artery, which signifies

hepatic arterial stenosis or thrombosis. (D) The extensive biliary duct necrosis (arrows) and the resulting liver abscess

(arrowheads) are documented by CT. The abscess was obscured on the US because of shadowing from the ducts.


most often the liver parenchyma is normal [20,21].

Rarely, the liver may have diffusely decreased echo-

genicity with relatively increased echogenicity of the

portal triads—the ‘‘starry-sky’’ appearance [21]. The

overall echogenicity of the liver is decreased relative

to the adjacent kidney (Fig. 15). Confirmation should

be obtained by checking the echogenicity of the

spleen relative to the left kidney to confirm that there

is no medical renal disease [20]. More commonly,

hepatitis has associated gallbladder findings, includ-

ing gallbladder wall thickening (see Fig. 6) and

sometimes a contracted gallbladder [20,21]. When

Fig. 13. Sclerosing cholangitis. Patient presented with sepsis and abdominal pain. (A) Longitudinal US of the right lobe is

normal, with a common duct (cursors) measuring 2 mm. (B) Longitudinal US of the left lobe shows multiple markedly enlarged

ducts (arrows). (C) CT shows the asymmetrically enlarged ducts (arrows) with enhancing walls, which indicates inflammation.

Emergent biliary drainage was performed, which alleviated the patient’s symptoms.


the patient recovers from hepatitis, the gallbladder

wall and distention return to normal. Other viral

infections that involve the liver, such as mononucleo-

sis, may cause a similar pattern, with liver swelling,

tenderness, and gallbladder wall thickening (Fig. 16).

Liver abscess

The most common liver abscesses are pyogenic,

caused by bacteria. Patients most often present with

right upper quadrant pain, fever, and malaise. The

cause may be biliary (ascending cholangitis or from

the adjacent gallbladder), portal venous (from diver-

ticulosis or Crohn’s disease), or arterial. Fifty percent

of liver abscesses do not have a clear source [20]. The

appearance of liver abscesses varies. Microabscesses,

lesions smaller than 2 cm, may be widely scattered in

the liver or may cluster in a single focus. Pyogenic

abscess cavities probably begin as a small cluster of

microabscesses, which coalesce into a larger drainable

collection [22]. Sonographically, abscess margins are

often indistinct; which make abscesses less conspicu-

ous than on contrasted CT scans. This is particularly

true in small clustered microabscesses (Fig. 17A, B).

Predominately abscesses are hypoechoic (see Fig. 7A)

but also may be isoechoic, solid appearing, or even

hyperechoic if they contain gas and debris (Fig. 17C).

Fifty percent or less have enhanced through transmis-

sion. Because of this variable appearance, the differ-

ential diagnosis is large and includes tumor, simple

cyst with hemorrhage, hematoma, or other forms of

infection, including amebic abscess or ecchinococcal

infection. The absence of flow centrally helps to

Fig. 14. Duodenal mass with biliary, pancreatic, and bowel obstruction. Patient presented to the emergency department with

nausea and rising bilirubin. (A) Transverse US of the pancreas shows a 1.8-cm common duct (CD) and a dilated pancreatic duct

(arrowheads). (B) Longitudinal US shows a distended gallbladder with a soft-tissue mass (arrows) behind it. (C) On transverse

imaging, the mass (arrows) obstructs the duodenum (Duod), which has a fluid-filled proximal lumen. GB, gallbladder. (D) CT

confirms the circumferential duodenal tumor (arrows). Note distended gallbladder (GB) and common duct (CD).


confirm that these are not solid tumors; however,

necrotic neoplasm remains in the differential diagno-

sis. The most helpful feature is a clinical scenario that

includes signs of infection. Abscesses are frequently

multiple, and US may be limited near the dome or

underneath the ribs for identifying the extent of

abscess involvement. In this case, contrast-enhanced

CT is often helpful in detecting the total abscess

burden and may identify the cause, especially if the

abscess arises from the bowel. After liver transplant,

patients are particularly prone to abscesses, especially

if biliary necrosis is present because of hepatic arterial

Fig. 15. Acute hepatitis. Transverse image shows a hypo-

echoic liver relative to the kidney (K) and bright portal triads

(arrowheads), the ‘‘Starry Sky’’ appearance. Although strik-

ing, this appearance is rare. Most often the hepatic echo-

genicity is normal.


thrombosis. If a transplant patient presents with a

hepatic abscess, the patency of the hepatic arteries

should be assessed (see Fig. 12).

Noninfectious diffuse enlargement of the liver

Patients with diffuse metastatic disease may pres-

ent with right upper quadrant pain, sometimes with

fever and jaundice. When patients are questioned

closely, their symptoms are usually not as acute as

Fig. 16. Mononucleosis. (A) Initial longitudinal US in a patient 18

vomiting. The gallbladder is thick walled (arrows) and contains deb

(B) One week later the galbladder wall (arrows) has returned to nor

for mononucleosis.

that of cholecystitis or hepatitis. On imaging, meta-

static disease may be of any type from cystic metas-

tases of carcinoid to echogenic metastases from colon

carcinoma or any other primary lesion. The liver is

enlarged and tender to palpation, usually because of

stretching of the liver capsule (Fig. 18A). Another

disease process that causes rapid hepatic enlargement

is acute fatty infiltration of the liver, which may be

diffuse and homogenous fatty infiltration (Fig. 18B)

of the liver or segmental fatty infiltration with areas

of focal sparing. The liver may enlarge rapidly and

give rise to the clinical symptoms of right upper

quadrant tenderness. Vessels are not distorted, how-

ever, and if there are areas of focal fatty infiltration,

they should have a geographic margin. If metastatic

disease is in the differential diagnosis, a sulfur colloid

nuclear medicine scan can be performed, which

should produce normal results in the setting of fatty

infiltration. An MR imaging scan with and without

fat suppression also defines the cause of the US

abnormalities. Acute fatty liver of pregnancy is a

relatively rare but serious complication that occurs in

the third trimester and peripartum. Two-thirds of

patients have associated pre-eclampsia or the hemo-

lysis, elevated liver enzymes and low platelets

(HELLP) syndrome [23]. Patients present with vari-

ous symptoms, most commonly nausea, vomiting,

abdominal pain, fever, and jaundice [23,24]. Symp-

toms commonly mimic hepatitis. Laboratory ab-

normalities include elevated liver enzymes and

coagulopathy (prolonged prothrombin time [PTT]).

Disseminated intravascular coagulation occurs in up

to 50% [23]. US and CT may have high false-

weeks pregnant with right upper quadrant pain, nausea, and

ris. A diagnosis of acute acalculous cholecystitis was offered.

mal and the sludge is diminishing. The patient tested positive

Fig. 17. Liver abscesses. (A) Transverse US of nearly invisible microabscesses (cursors) within the liver. There are no specific

US features to identify this as an abscess. The area is slightly heterogeneous and lacks a normal vessel pattern. (B) CT of the left

lobe contains a typical rosette pattern diagnostic of clustered small abscesses with enhancing rims (arrows). A right lobe abscess

(arrow) could not be seen by US. (C) Mixed abscesses and gas. Longitudinal US of a patient with multifocal abscesses. The

fluid-containing abscess (A) anteriorly contains gas (arrow) with a reverberant echo posteriorly. The isoechoic abscess more

posteriorly (arrowheads) with central gas is more difficult to detect. (D) CT scan shows both abscesses. The more central abscess

(arrowheads) is much more extensive on CT than on US.


negative rates (as high as 80%), and the diagnosis

largely depends on clinical features and biopsy, if

necessary [23,24].

Focal lesions with hemorrhage

Any focal hepatic lesion can potentially bleed,

which leads to acute right upper quadrant pain with

subsequent presentation of the patient for emergency

US. Even innocuous lesions, such as benign liver

cysts, occasionally can hemorrhage with resultant

symptoms. Hemangiomas, the most common benign

tumors of the liver, are mostly small and asympto-

matic and discovered incidentally. Lesions larger than

5 or 6 cm occasionally may present with either

hemorrhage or thrombosis [20]. Hepatic adenoma, a

benign tumor associated with estrogen or anabolic

Fig. 18. Diffuse liver enlargement. (A) Carcinoid metastases. Longitudinal US of a patient with acute right upper quadrant pain to

‘‘rule out (R/O) cholecystitis.’’ The gallbladder is normal; however, the liver was enlarged at 21 cm and riddled with cystic thick-

walled metastases (arrows) from a carcinoid primary. (B) Acute fatty infiltration. Longitudinal US in a patient with acute right

upper quadrant pain and abnormal liver function tests. The liver is enlarged at 18.4 cm with diffusely increased echogenicity, loss

of the normal vascular pattern, and increased attenuation, which causes poor delineation of the diaphragm posteriorly (arrows).


steroid therapy, does have a predisposition for bleed-

ing [25]. The rate of intratumoral or intra-abdominal

hemorrhage with adenomas is reported as high

50% to 65% [26]. Contrary to focal nodular hyper-

plasia and hemangioma, which are usually managed

conservatively, except if the patient has significant

symptoms, adenomas are usually resected, especially

Fig. 19. Hemorrhagic adenoma. (A) Transverse US in a patient

contraceptive pills shows a mixed echogenicity mass (arrows) wi

(arrowhead). The through transmission indicates fluid. (B) CT sh

enhanced, whereas the remaining hemorrhage did not.

if larger than 5 cm. On US, hepatic adenomas have a

variable appearance that ranges from hypoechoic

masses to mixed heterogeneous masses, which cor-

respond pathologically with intratumoral hemorrhage

and necrosis [25]. Masses also may be isoechoic to

the liver with a hypoechoic rim or even hyperechoic

if they contain fat. The mixed echogenic pattern is

with acute right upper quadrant pain who is taking oral

th through transmission (asterisk) displacing the gallbladder

ows a heterogenous mass (arrows). The tumor portion (A)


most likely to correspond to hemorrhagic necrosis;

however, it cannot be distinguished from other tu-

mors that can hemorrhage (Fig. 19) [25].

After adenoma, the other hepatic tumor likely to

present with hemorrhage is hepatocellular carcinoma.

Similar to adenomas, the US appearance of these

Fig. 20. Hepatocellular carcinoma with hemorrhage. (A) Trans

hypoechoic fluid (F) and an echogenic region that has a straight-line

(H). (B) Color Doppler image from the liver shows an area with hig

of 0.49) flow, which indicates tumor shunt flow. (C, D) CT confirm

image (D) shows the acute clot (H) bordering the lateral liver mar

Fig. 19A. F, fluid.

lesions varies greatly and ranges from echogenic to

hypoechoic or mixed [21]. Tumors even may be

diffuse and infiltrative and relatively invisible by

US. A clue to the presence of an underlying malig-

nancy is increased hepatic arterial flow in the lesion

compared with the remaining normal liver (Fig. 20).

verse US shows a heterogeneous liver echogenicity with

margin (arrows) with the more superficial hypoechoic tissue

h velocity (1.6 m/second) and low resistance (resistive index

s enhancing tumor at the dome (arrows), and a more caudal

gin (arrows). This accounted for the straight margin seen in


Most patients with hepatocellular carcinomas also

have predisposing risk factors, including cirrhosis or

hepatitis B or C.

The important feature to remember about acute

hemorrhage is that it may mimic the adjacent liver

parenchyma. Color Doppler imaging is useful for

showing vessels in a normal liver or in the tumor,

whereas the hemorrhage has no vascularity within the

hematoma. Straight lines and geographic margins are

also a clue to the presence of hemorrhage (Fig. 20).

Usually this indicates a subcapsular component with

compression of the adjacent liver capsule. Because

US can have difficulty differentiating between the

acute blood and the adjacent liver, CT scan is often

used to map the extent of the process and differentiate

hepatic tissue from blood and tumor.

Abnormalities of hepatic vasculature

Pathologic processes that involve the hepatic

vasculature may result in acute symptoms and emer-

gent presentations of the patient for US examination.

The liver has three vascular systems: the hepatic

arterial and portal venous for incoming blood and

the hepatic venous for outgoing blood.

Acute portal vein thrombosis

Acute portal venous thrombosis has multiple

causes, including septic thrombophlebitis [27], as-

sociated pancreatitis, and hypercoagulable states,

Fig. 21. Portal vein thrombosis. (A) Longitudinal US in a patient

portal vein (arrows) is distended and hypoechoic with no flow on c

portal vein (arrow), which fails to enhance. Thrombus also involv

including stem cell transplantation [28]. Septic throm-

bophlebitis has a mortality rate as high as 50% [27].

The most common cause is diverticulitis, with inflam-

matory bowel disease, bowel perforation, and suppu-

rative pelvic and pancreatitis infections as potential

sources. Most patients present with sepsis, fever,

chills, and upper abdominal pain because the primary

bowel source is often asymptomatic [27].

Patients without sepsis and acute portal vein

thrombosis present with nonspecific right upper

quadrant or epigastric pain. Some patients also have

abnormal liver function tests without hyperbilirubi-

nemia [29]. On US, the portal vein is dilated and may

be completely anechoic, but it is more often filled

with low-level echoes and shows no flow on color or

power Doppler (Fig. 21). The main portal vein is seen

on 97% of upper abdominal US [30]. Failure to

visualize a patent main portal vein on gray scale

and Doppler US should indicate portal vein throm-

bosis. False-positive results may occur in patients

with slow flow caused by portal hypertension. In

these cases, maximum Doppler sensitivity should be

achieved with low wall filter and lower Doppler

angles and lower Doppler frequencies to improve

penetration at depth. Spectral Doppler always should

be used to confirm absent flow on color or power

Doppler images [29]. If flow remains absent but no

thrombosis can be visualized, contrast-enhanced US,

CT, or MR imaging could be used to confirm the

presence of thrombosis [31]. In the subacute to

chronic phase, older thrombosis becomes hyper-

echoic and recanalizes, or the patient forms collater-

als. These smaller multiple portal channels are called

cavernous transformation of the portal vein. On

with right upper quadrant pain on oral contraceptives. The

olor Doppler. (B) Contrasted CT scan shows low-attenuation

es the splenic vein (paired arrows).


spectral Doppler they have the typical monophasic

spectral waveform of the portal system.

Acute hepatic venous thrombosis

Acute hepatic venous thrombosis is otherwise

known as Budd-Chiari syndrome. This rare entity

results from venous obstruction usually caused by

thrombosis of the hepatic veins, although proximal

suprahepatic webs or obstruction of the inferior vena

cava (IVC) also can cause it [30,31]. Etiologic factors

include hypercoagulable states, including pregnancy,

birth control pill use, and post–bone marrow trans-

plant status, and other malignancies, including hepa-

toma, which may directly invade the veins [30].

Patients present with abdominal pain, ascites, and liver

enlargement. US findings include abnormal flow in

one or more hepatic veins [32]. Flow may be absent or

completely monophasic on spectral Doppler, which

indicates loss of cardiac pulsatility because of inter-

ruption between the vein and the heart. Reversed or ‘‘to

and fro’’ flow also may be seen in these excluded

segments if they form collaterals with the portal veins

or the IVC [30,33]. Nonvisualization of the veins on

color or power Doppler is nonspecific because they

may be compressed in the setting of cirrhosis [32].

Portal venous flow is present, although it may be

biphasic or reversed in fairly severe cases [30]. Ob-

struction of the suprahepatic IVC also can be docu-

mented by US, visualization of the thrombus, or absent

flow in the obstructed segment. The inferior IVC and

iliacs may be patent but should have a monophasic

spectral Doppler waveform and lack the normal re-

Fig. 22. Hepatic artery thrombosis with infarction postpartum. A

failure 3 days postpartum. (A) US shows a diffusely disorgan

(arrowheads). Echogenic lines (arrows) represent gas. (B) CT scan s

ducts (arrows).

sponse to a Valsalva’s maneuver [30]. Findings may

be confirmed with either CT or MR imaging. CT in

acute cases shows global ascites and liver enlargement

with decreased attenuation in the affected areas before

contrast and heterogeneous patchy enhancement after

contrast with rim enhancement of the hepatic veins

[34]. MR imaging may show heterogeneous enhance-

ment of the hepatic parenchyma with edema and

relative caudate sparing because the caudate drains di-

rectly into the IVC and does not go through the hepa-

tic veins [35]. Severe involvement of the veins may

lead to liver failure, which requires transplantation.

Hepatic artery thrombosis

Hepatic arterial thrombosis is a major contributor

to acute hepatic dysfunction in patients after liver

transplant. In particular, the biliary ducts depend on

adequate hepatic arterial perfusion for oxygenation.

Hepatic arterial thrombosis or stenosis occurs in up to

13% of patients after liver transplant and is a major

cause of graft failure [36]. Clinically, hepatic arterial

thrombosis is suspected when liver function studies

deteriorate, fever of unknown origin occurs, or the

biliary tract is involved, with either a delayed biliary

leak secondary to ischemia or development of liver

abscesses [37]. Without treatment, mortality rate may

be as high as 70%. Graft salvage may be achieved by

arterial revision, or retransplantation may be required

[38]. The diagnosis could be made by Doppler US in

as many as 10% of patients who are clinically

asymptomatic by using aggressive US screening in

the early postoperative period (days 1–3) [37]. US

liver transplant patient presented with acute pain and liver

ized liver pattern with no discernable vessels anteriorly

hows the large infarct (arrowheads) and the gas in the biliary

Fig. 23. Hemorrhagic adrenal adenoma. Patient presented with fever and acute right upper quadrant pain. Clinically the attending

surgeon was convinced she had acute cholecystitis. (Left) Longitudinal US shows mass (M) posterior to retroperitoneal reflection

(arrows) and separate from kidney (K). The gallbladder was normal. (Right) Transverse CT shows non-enhancing adrenal mass

(M) caused by hemorrhage of an adrenal adenoma.


diagnosis consists of color Doppler and spectral

Doppler examination. Absent hepatic arteries indicate

thrombosis, although vessels may be small and diffi-

cult to visualize in the immediate postoperative

patient. This may be a situation in which US contrast

is useful. If flow is visualized in the vessels, a

resistive index is obtained (peak systolic velocity =

end diastolic velocity divided by systolic velocity). A

resistive index of less than 0.5 or acceleration from

beginning of systolic to systolic peak of more than

0.08 seconds yields 73% to 81% sensitivity for

hepatic thrombosis or stenosis [39,40]. Additional

diagnostic criteria include a resistive index of 1 in

the extrahepatic artery with no flow visualized in the

intrahepatic arteries [37]. Confirmation of US find-

ings is usually performed angiographically. Prompt

revascularization or retransplantation is desirable be-

cause asymptomatic patients may achieve up to an

80% graft salvage rate versus 43% on symptomatic

patients [37]. Massive acute hepatic arterial throm-

bosis may result in liver infarction (Fig. 22).

Acute right upper quadrant pain, outside the

hepatobiliary system

The differential diagnosis for patients with right

upper quadrant pain is extensive and includes pneu-

monia, appendicitis, peritoneal tumor, primary bowel

disease, pancreatitis, and peritonitis caused by either

bowel or pelvic pathology, such as hemorrhagic

adnexal masses. Retroperitoneal processes, such as

renal infarction, renal obstruction, and renal or adre-

nal hemorrhage (Fig. 23), also can present occasion-

ally with right upper quadrant pain, which mimics

acute cholecystitis.

Summary

In summary, US is the initial imaging modality for

the evaluation of acute right upper quadrant pain. It

permits accurate diagnosis of acute cholecystitis and

successfully identifies multiple other causes of patient

symptomatology. Some of these processes lie outside

the hepatobiliary system and include renal infection

and obstruction, pancreatitis and its sequelae, duode-

nal or colonic perforation or mass lesions, peritoneal

tumor spread, adrenal hemorrhage, and even remote

problems, such as pneumonia. The limitations on US

include incomplete imaging of the liver, most often at

the dome or beneath ribs on the surface, and incom-

plete visualization of lesion boundaries, particularly

with some infections and tumors. For these clinical

scenarios, contrast-enhanced CT is complementary to

US and should be encouraged. In the biliary tree, US

has limitations in situations in which the ducts are not

dilated and sometimes with imaging the extrahepatic

ducts, especially distally. For these patients, CT or

MR imaging (MRCP) is especially useful. If one

keeps the clinical scenario in mind and always images

a patient where he or she hurts, US is a powerful and

effective diagnostic method for evaluating acute right

upper quadrant pain.


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Radiol Clin N Am 42 (2004) 279–296

Venous protocols, techniques, and interpretations of the

upper and lower extremities

James D. Fraser, MDa,*, David R. Anderson, MDb

aDepartment of Diagnostic Radiology, Dalhousie University, Queen Elizabeth II Health Sciences Centre, 3rd Floor,

Victoria Building, 1278 Tower Road, Halifax, Nova Scotia, Canada B3H 2Y9bDivision of Hematology, Department of Medicine, Dalhousie University, Queen Elizabeth II Health Sciences Centre,

Victoria General Site, 4th Floor, Bethune Building, 1278 Tower Road, Halifax, Nova Scotia, Canada B3H 2Y9

Deep venous thrombosis (DVT) and pulmonary Clinical presentations

embolism (PE), collectively known as venous throm-

boembolism, are common problems and are frequent-

ly in the differential diagnosis of patients presenting

to the emergency department and in the acute care

setting. In the United States, the annual combined in-

cidence of DVT and PE is at least 70 per 100,000 in-

dividuals [1,2]. Clinical signs and symptoms of both

of these entities are nonspecific and it is important

to perform objective testing to confirm the diagnosis

and initiate appropriate therapy. This approach leads

to a demand for emergent diagnostic studies. Com-

pression ultrasonography (CUS) is the diagnostic pro-

cedure of choice for the assessment of patients with

suspected DVT. It has been shown to be highly sen-

sitive and specific for the diagnosis of DVT, particu-

larly in the lower extremities in symptomatic patients.

Bilateral leg CUS combined with assessment of the

clinical pretest probability and D-dimer testing has

also been shown safely to reduce the need for pul-

monary angiography in patients with suspected PE.

This article reviews the clinical indications, diag-

nostic techniques, and interpretation of CUS for the

assessment of DVT in the upper and lower extrem-

ities and evaluates the role of CUS in the assessment

of patients with suspected PE.


doi:10.1016/j.rcl.2004.01.001

* Corresponding author.

E-mail address: [email protected] (J.D. Fraser).

Patients who eventually require assessment for

potential venous thromboembolic disease may pres-

ent with symptoms suggestive of DVT of the upper or

lower extremity, PE, or both. Most commonly, DVT

begins in the veins of the calf and moves proximally

with time. Patients who present with acute calf-

popliteal vein thrombosis experience pain and swell-

ing in the calf of one leg, which is exacerbated with

ambulation and improved with rest. There may be

associated warmth, redness, and tenderness in the calf

area [3]. Over time, these symptoms tend to become

more severe and may progress proximally to the

popliteal fossa and into the medial thigh area. On

average, these patients’ symptoms persist for about

7 days before presenting for medical assessment

[4,5]. Less than 20% of patients who are confirmed

to have lower-extremity DVT have thrombi isolated

to the calf veins.

In approximately 10% of patients with lower-

extremity DVT, the thrombus is isolated in the

iliofemoral region (Fig. 1) [6]. These patients initially

present with symptoms of pain in the buttock or

groin region, which over time extend to the medial

thigh and cause swelling and dusky discoloration of

the proximal leg. Superficial veins in the groin and

proximal thigh become prominent because of venous

engorgement [7]. Iliofemoral disease is a common

presentation of DVT during pregnancy with over

90% occurring on the left side usually caused by

extrinsic compression of the left iliac vein. Iliofe-

s reserved.

Fig. 1. Iliofemoral DVT. A 35-year-old pregnant woman with isolated iliofemoral DVT, who presented with left buttock pain.

(A) Longitudinal image with color flow Doppler shows a small amount of spontaneous venous flow around the thrombus (T).

(B) A transverse image of the iliac with compression was obtained with the maximum compressed anteroposterior diameter

measured. Normal compressibility of the (C) superficial femoral vein and (D) popliteal veins (arrowheads), which are free of

thrombus. Arrowheads in (A) and (B) delineate the left iliac vein. The arrows in (C) and (D) designate the accompanying artery.

The asterisk in (C) denotes the deep femoral artery branch. Note the superficial position of the vein relative to the artery in the

popliteal fossa.

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279–296280

Fig. 1 (continued).

J.D. Fraser, D.R. Anderson / Radiol Clin N Am 42 (2004) 279–296 281

moral DVT is associated with pelvic masses, recent

pelvic surgery, oral contraceptive use, and the anti-

phospholipid antibody syndrome.

In contrast, patients presenting with upper-extrem-

ity DVT (Fig. 2) usually have thrombosis initiating in

the proximal veins (subclavian and brachiocephalic).

Pain and swelling of the proximal arm and superficial

vein distention in the upper chest and proximal arm

are commonly seen. Functional impairment also may

be present. Upper-extremity DVT most commonly

occurs in patients with malignancy and incidence is

much higher when they have indwelling central ve-

nous catheters. It occasionally occurs in otherwise

healthy individuals or following strenuous upper-

extremity exercise, such as weight lifting [8].

Patients with acute PE may present with dyspnea,

pleuritic chest pain, dizziness, and loss of conscious-

ness with or without symptoms of DVT. Tachypnea,

tachycardia, and hypotension may be noted on phys-

ical examination. The range of presentation of PE is

great, from minimal chest symptoms to life-threaten-

ing shock.

The role of ultrasound in the evaluation of

thromboembolic disease

Because of the nonspecific nature of the presen-

tation of venous thromboembolic disease, clinical

assessment is certainly not sufficient to make a

diagnosis. Given the possible serious consequences

of a misdiagnosis, objective testing for DVT and PE

is crucial.

In the lower extremities, CUS is the method of

choice to evaluate patients with symptoms suspected

to be DVT. The sensitivity and specificity exceeds

97% for the diagnosis of DVT involving the proximal

leg veins. Accuracy studies using CUS for evaluation

of the calf veins have been relatively few and have

demonstrated much greater variation. The range of

sensitivities varies between 11% and 100%, whereas

the specificity ranges between 90% and 100% [9–12].

A meta-analysis of methodologically high-quality

studies reported the sensitivity of CUS for the diag-

nosis of DVT isolated to the calf to be 73% [11]. The

rate of technically inadequate studies has been re-

ported to be much higher than those for the evaluation

of proximal DVT (ie, in the range of 20%–40%)

[12,13].

In contrast to patients with suspected DVT of the

lower extremities, the validity of ultrasound for the

evaluation of upper-extremity DVT is less well estab-

lished. In a recent systematic review of the sensitivity

and specificity of ultrasonography in the diagnosis of

upper-extremity DVT, Mustafa et al [14] found only

six original prospective studies, only one of which

met their predefined criteria for adequately determin-

ing sensitivity and specificity and included a total of

58 patients [8]. The sensitivity of duplex ultrasound

from this review ranged from 56% to 100% with a

specificity ranging from 94% to 100%. None of

these studies evaluated the safety of withholding

anticoagulation therapy in a patient with a negative

result on ultrasound evaluation who did not undergo

further testing and concluded that the safety of this

approach is uncertain [14]. More recently in a pro-

spective study published in 2002 comparing color

Doppler with contrast venography in 126 patients,

Baarslag et al [15] reported a sensitivity and speci-

ficity of 82%. He also noted that incompressibility of

the vein during ultrasound correlated well with

thrombus, whereas only 50% of isolated flow-related

abnormalities proved to be thrombus-related. He

concluded that patients with isolated flow abnormal-

Fig. 2. Upper-extremity DVT. Cancer patient who developed a painful swollen right arm secondary to extensive DVT of the

upper extremity. (A) Longitudinal color flow image of the internal jugular vein with spontaneous flow above the thrombus.

(B) Thrombus (arrow) can be seen within the distal jugular vein (arrowheads). (C) Clot is seen (arrowheads) extending down to

the confluence with the subclavian vein (arrows). (D) Color flow Doppler demonstrates complete occlusion of the subclavian

vein (arrowheads). The presence of clot in the axillary (arrowhead) vein (E) and basilic vein (arrowhead) (F) is confirmed

because of the inability to compress the vein in the transverse plane. The arrows denote the associated arteries.


ities on duplex color ultrasound should have contrast

venography performed for further evaluation.

The optimal strategy to diagnose PE remains

controversial. Spiral CT and ventilation-perfusion

scanning are used routinely for the evaluation of

patients with suspected PE, but neither test is partic-

ularly sensitive. Ultrasonography may be added to

diagnostic algorithms for suspected PE to increase

the sensitivity of noninvasive testing because most

PEs are believed to originate in the veins of the legs.

Patients with nondiagnostic pulmonary investigation

may be confirmed to have venous thromboembolism

by leg ultrasonography and thereby avoid the need

for angiography [16]. A definitive diagnosis or ex-

clusion of PE may not be possible at the initial

presentation using noninvasive testing. Most cases

of DVT (approximately 90%) start in the calf and

rarely cause clinically important PE unless they

Fig. 2 (continued).


extend into the proximal deep venous system. Eighty

percent of clots isolated to the calf are asympto-

matic; however, if left untreated approximately 25%

extend to involve the proximal veins. This usually

occurs within the first week or so after presentation.

Seventy-five percent of patients diagnosed with PE

have DVT, two thirds of which are located in the

proximal veins (Fig. 3). Up to one-quarter of patients

with symptomatic PE have clinical evidence of DVT

[17]. Given this information, various algorithms have

been developed that incorporate the use of CUS in the

work-up of patients with suspected PE (Fig. 4).

Clinical assessment and the use of D-dimer

Clinical assessment

Although the clinical presentation of DVT is

nonspecific and clinical assessment alone is unreli-

able, recent studies have shown that with explicit

clinical criteria, patients can be categorized accurately

into high, moderate, or low pretest probability groups

based solely on a clinical evaluation [18]. These

criteria combine the signs and risk factors for DVT

and take into consideration the likelihood of an

Fig. 2 (continued).


alternate diagnosis as the cause for the patient’s

presentation. A simple, nine-point clinical criteria

scoring system has been developed to determine the

pretest probability for DVT (Table 1) [19]. Using

such criteria, patients with a high pretest probability

have a greater than 75% prevalence of DVT con-

firmed by objective testing. Patients in whom the

diagnosis of DVT cannot be excluded on clinical

grounds but who have a low pretest probability have

less than a 5% prevalence of DVT. The use of this

clinical categorization tool has proved to be a valu-

able adjunct to noninvasive testing for the evaluation

of patients with suspected DVT and PE [16,20,21].

D-dimer

Several serologic markers of thrombosis have

been investigated for their predictive value in the

diagnosis of DVT. The test that has emerged as the

most useful is the D-dimer test. D-dimer represents a

breakdown product of the cross-linked fibrin clot.

Several D-dimer assays have been validated to be

sensitive but nonspecific markers of DVT and PE,

indicating that a positive test has a low predictive

value but a negative test has a reported negative

predictive value of more than 97% [16,22–29].

Combinations of clinical assessment and D-dimer

Fig. 3. Lower-extremity DVT with PE. Patient presenting with shortness of breath and chest pain who underwent chest CT as

per PE protocol. (A) It revealed bilateral pulmonary emboli (arrowheads). CUS of the legs confirmed DVT involving the

popliteal and superficial femoral veins (arrowheads) to the mid thigh (B,C) with normal venous flow and no clot present within

the superficial femoral veins (arrowheads) above the mid thigh (D). Arrows in (B) and (C) designate the accompanying arteries.


Fig. 3 (continued).

Table 1

Clinical evaluation table for predicting pretest probability of

deep vein thrombosis

Clinical characteristics Score

Active cancer (treatment ongoing, within

previous 6 mo or palliative)

1


results have been shown safely to reduce or eliminate

the need for noninvasive testing in certain patient

groups [30,31]. For example, patients with a low

suspicion of DVT or PE but in whom a diagnosis

cannot be excluded on clinical assessment alone may

safely avoid the need for radiographic imaging on the

basis of a negative D-dimer study (see Figs. 4–6). D-

dimer is less useful for excluding venous throm-

boembolism in hospital patients, particularly those

having had major surgery or trauma in whom the test

is highly likely to be positive [32].

A variety of D-dimer assays have been validated

for diagnostic testing for venous thromboembolism.

The accuracy parameters of these assays (sensitivity,

specificity) vary and physicians need to be aware of

these and of the validated laboratory cut-off points

for defining a positive and negative test.

Non-diagnostic Ventilation Perfusion (VQ)/Computerized axial Tomography (CT) Scan

Bilateral Compression Ultrasound (CUS)

Pretest Probability (PTP) + D-dimer (DD)

Low PTPor - DD

Mod/High PTPand + DD

PE excluded Pulmonary angiogram or 1 wk CUS

Treat for PE

+

+ -

Fig. 4. Algorithm for investigation of patients with sus-

pected PE. CUS, compression ultrasound; DD, D-dimer; PE,

pulmonary embolism; PTP, pretest probability.

Ultrasound technique for the evaluation of deep

venous thrombosis of the extremities

Lower extremities

The venous anatomy of the lower extremity is

shown in Fig. 7. CUS of the deep venous system of

the lower extremities is performed with the patient

in the supine position ideally with the head elevated

Paralysis, paresis, or recent plaster

immobilization of the lower extremities

1

Recently bedridden > 3 d or major surgery

within 12 wk requiring general or regional

anesthesia

1

Localized tenderness along the distribution

of the deep venous system

1

Entire leg swollen 1

Calf swelling 3 cm larger than asymptomatic

side (measured 10 cm below tibial tuberosity)

1

Pitting edema confined to the symptomatic leg 1

Collateral superficial veins (nonvaricose) 1

Alternative diagnosis at least as likely as deep

vein thrombosis

�2

A score of 3 or higher indicates a high probability of deep

vein thrombosis; 1 or 2, a moderate probability: and 0 or

lower, a low probability. In patients with symptoms in both

legs, the more symptomatic leg is used.

Clinically Suspected DVT

Pretest Probability (PTP)

Low

D-dimer (DD) Compression Ultrasound (CUS)

DD/PTP

DVT Excluded

Low PTPor - DD


Venogram Treat for DVT

- +

+ -

-

+

Moderate/High

Fig. 6. Algorithm for suspected DVT in the upper extremity.

CUS, compression ultrasound; DD, D-dimer; DVT, deep

vein thrombosis; PTP, pretest probability.

Clinically Suspected Deep Vein Thrombosis (DVT)

Pretest Probability (PTP)

Low

D-dimer (DD) Compression Ultrasound (CUS)

DD/PTP

DVT Excluded

Low PTPor - DD


1 wk CUS Treat for DVT

-

+

+

+-

-

Moderate/High

Fig. 5. Algorithm for clinically suspected DVT. CUS,

compression ultrasound; DD, D-dimer; DVT, deep vein

thrombosis; PTP, pretest probability.


20 to 30 degrees to promote venous pooling and

distention of the veins. A linear transducer with a

frequency in the 5- to 10-MHz range is used, ideally

with duplex and color Doppler capability, although

these are not required but can be helpful in localizing

the vessels and characterizing their flow. The leg is

rotated externally and flexed slightly at the knee. The

transducer is placed transversely in the groin area to

identify the common femoral vein just medial to the

common femoral artery. Gentle pressure is applied to

the vessels with the transducer and in the absence of

DVT, the lumen of the vein should collapse with

complete apposition of the anterior and posterior walls

(see Fig. 1C, D). In the presence of DVT, the lumen

does not collapse completely even with enough pres-

sure to occlude the adjacent artery (Fig. 8). This

compression is performed at 1-cm intervals moving

down the leg following the common femoral vein,

superficial femoral vein, and popliteal vein until it

divides into the three calf branches at the popliteal

trifurcation. Compression of the veins within the

muscular adductor (Hunter’s) canal is often difficult

and visualization limited because of the depth of the

vein. This can usually be overcome by placing one

hand underneath the medial aspect of the distal thigh

and compressing the vein between the fingers and the

transducer. This not only aids in compressing the

vein but also brings the vein closer to the transducer

head, allowing better visualization.

Scanning along the axis of the vein is often ad-

vantageous for following the course of the vein and

for assessing flow (see Figs. 2A, 3D). It is important,

however, to confirm compressibility in the transverse

plane; compression in the longitudinal plane is unre-

liable because the transducer may slide off the vessel,

possibly resulting in a false-negative interpretation.

In a mobile patient, the popliteal vein is assessed

most easily with the patient in the lateral decubitus or

prone position with the knee passively flexed to

approximately 10 to 15 degrees to avoid collapse of

the vein. Very often the patient is not able to move

from the supine position but the popliteal vein can

usually be assessed adequately by lifting the affected

leg with a hand sufficiently under the distal thigh to

place the transducer behind the knee. The popliteal

vein is superficial to the popliteal artery (see Fig. 1D)

in the popliteal fossa and can be compressed easily by

the extended knee. It is important to keep the knee

slightly flexed while interrogating the popliteal vein.

There remains controversy over the value of

performing CUS of the calf veins if the more proximal

veins are normal. Approximately 10% to 20% of

patients with symptomatic DVT have thrombus iso-

lated to the calf veins of, which 20% to 30% eventu-

ally extend into the proximal venous system [33,34].

The positive predictive value of CUS for detecting

DVT in the calf is significantly lower than it is for

proximal DVT, and there are a relatively large number

of cases in which the studies are considered non-

diagnostic or inadequate. Reported rates of nondiag-

nostic studies vary in the literature from 9.3% to

82.7%. Gottlieb et al [35] had a nondiagnostic rate

of 41% for the evaluation of calf veins. The same

study found no significant difference in adverse out-

comes in patients undergoing a protocol in which the

deep calf veins were routinely evaluated or a protocol

in which the calf was evaluated only if physical signs

or symptoms were present.

Inferior vena cava

Common iliac vein

External iliac vein

Common femoral vein

Superficial femoralvein

Great saphenous vein(superficial)

Poplitealvein

Anteriortibial vein

PeronealveinSmallSaphenous(superficial)

Posteriortibial vein

Poplitealvein

Peronealvein

Anterior tibialvein

Fig. 7. Diagrammatic representation of the veins of the lower extremity.


The authors have previously described the tech-

nique for the evaluation of the calf veins [1]; however,

their present protocols for the evaluation of patients

with suspected thromboembolic disease do not in-

clude evaluation of the calf and the technique is not

discussed in this article. It should be stressed, how-

ever, that when assessing the proximal venous system,

one should ensure that the examination includes the

distal popliteal vein all the way down to its trifurca-

tion point to have the highest possible sensitivity for

DVT. In addition, if there is focal tenderness or

swelling within the calf region, it is useful to scan

this area to evaluate for nonvenous focal pathology,

such as a hematoma, which might explain the pa-

tient’s symptoms.

Upper extremities

The venous anatomy of the upper extremity is

shown in (Fig. 9). The technique for evaluating the

upper extremities for DVT is similar to that for the

lower extremities; however, compression of the deep

venous system is more limited particularly in the area

where the subclavian vein passes beneath the clavi-

cle. Because of this limitation, technical modifications

are required, such as the use of adjunctive procedures


and the findings of Doppler and color flow Doppler

analysis (see Fig. 2). Once again, a linear transducer

with a frequency in the 5- to 10-MHz range with

Doppler or color flow Doppler is preferable. With the

patient in the supine position, the head is tilted slightly

away from the side of interrogation. It is often easiest

to begin by evaluating the internal jugular vein,

following this down to the confluence with the sub-

clavian vein (see Fig. 2C), which is located under the

proximal third of the clavicle, and is best visualized

by placing the transducer longitudinally along the

Fig. 8. Extensive lower-extremity DVT involving the iliac vein.

involving the popliteal vein (A) and extending up to involve the supe

(C) (arrowheads), all of which are not compressible despite sufficie

course of the vessel just below the clavicle and

angling it slightly cephalad. The vein can be differen-

tiated from the adjacent artery by its generally larger

size, lack of internal pulsations, and its vascular flow

pattern as assessed by Doppler. Attempts to compress

the vein with the transducer in the transverse plain

often fail because of the presence of the clavicle. At-

tempts should then be made to compress the vein with

the transducer along the length of the vessel. If

compression is not possible, one must evaluate with

spectral or color flow Doppler to determine if the lack

Patient with painful swollen left leg with extensive DVT

rficial femoral veins (not shown), CFV (B), and the iliac vein

nt pressure to partially compress the adjacent artery (arrows).

Fig. 8 (continued).


of compressibility is caused by thrombus or by over-

lying structures preventing adequate force to be trans-

mitted to the vein. The subclavian vein is followed

distally to the axillary, cephalic, brachial, and basilic

veins, which are assessed with transverse compression

similar to the evaluation of the lower-extremity veins

(see Fig. 2E, F). Assessment of the axillary, brachial,

and basilic veins is performed using an axillary ap-

proach by raising the arm. High in the axilla, the vein is

superficial to the artery [36]. In such areas as the sub-

clavian where the vein may not be accessible to com-

Internal jugular veinExternal jugular vein

Subclavian vein

Axillary vein

Cephalic vein

Brachial vein

Basalic vein

Median cubital vein

Fig. 9. Diagrammatic representation of the veins of the upper lim

superior vena cava.

pression and color Doppler is used for assessment of

patency, it is important to pay close attention to the

color flow gain settings to avoid oversaturation,

which may obscure small intraluminal clots or areas

of incomplete thrombosis [37]. Similar to assessment

of the leg, if thrombosis is discovered it is important to

document the full extent of the disease including

evaluation of the contralateral neck and proximal

arm because this information may be important for

subsequent evaluation for progression or recurrence of

disease or for the effectiveness of treatment.

BCP veinSVC

b and thoracic inlet. BCP vein, brachiocephalic vein; SVC,


Diagnostic criteria for the diagnosis of deep

venous thrombosis of the extremity

In the absence of DVT, the vein being evaluated

should collapse and the walls of the vein should

be completely apposed with less pressure than re-

quired to occlude the adjacent artery. The inability

completely to compress the vein lumen is the prin-

cipal criterion for the diagnosis of DVT [6,7,38–40].

Other adjunctive findings are often observed in the

presence of DVT but have much poorer sensitivi-

ties and specificities. These include distention of

the involved vein in acute DVT and the absence of

or reduced spontaneous blood flow on Doppler

evaluation (see Fig. 8). In patients with incomp-

lete obstruction, there is usually loss of the normal

phasic respiratory venous flow pattern, often giving

a reduced continuous flow pattern (monophasic

flow), which is minimally affected by the Valsalva’s

maneuver or attempts to augment flow, such as

gently squeezing the calf. The monophasic pattern

indicates some degree of obstruction to venous flow

returning to the right side of the heart and should

increase one’s suspicion for the presence of DVT.

This pattern can also be seen, however, in the ab-

sence of thrombosis when sufficient external com-

pression on the deep venous system exists. The

appearance of the vein alone is unreliable because

acute thrombus is often anechoic mimicking a patent

vein and internal echoes are not infrequently seen

within a patent vein lumen in the presence of slow-

flowing blood.

The ultrasound appearance of DVT changes over

time with the clot retracting and becoming more

echogenic. The vein wall in the area of previous

thrombus may become thickened, echogenic, and

resistant to compression [41]. Over a 12- to 24-month

period, only about 50% of patients have complete

resolution of thrombus and normal compressibility of

the proximal leg veins [41–43]. Although the ultra-

sound appearance in patients with previous DVT may

be suggestive of chronic disease, it is usually difficult

to rule out acute or chronic disease unless the patient

has a posttreatment baseline study available for com-

parison. In the latter setting, unequivocal evidence of

thrombosis in a venous segment previously demon-

strated to be free of disease or increase in compressed

venous diameter greater than 4 mm from a baseline

study may be considered diagnostic of recurrent DVT

in the appropriate clinical setting.

Compression ultrasound occasionally diagnoses

an alternative cause for pain and swelling of the

lower extremity in the absence of DVT, such as a

ruptured Baker’s cyst or a calf hematoma (Fig. 10).

Adjunctive procedures, pitfalls, and limitations

There are a number of procedures that may be

helpful when examining a patient whose deep venous

system is difficult to localize. Placing the patient in a

position that promotes venous pooling in the extrem-

ity of interest distends the veins, making them easier

to localize and assess. Similarly, having the patient

perform a Valsalva’s maneuver also results in venous

distention [7]. When duplex or color flow Doppler is

available, it can be used to localize the venous system

based on its flow characteristics. The presence of

spontaneous flow, normal respiratory phasic flow

variation, and flow augmentation with manual com-

pression of the limb suggests patency. It is, however,

important to remember that spontaneous flow and

flow augmentation can occur in the presence of

incomplete thrombosis (see Fig. 1A), adequate collat-

eralization, and in patients with duplication of the

deep venous system. Augmentation may even force

blood around an area of complete thrombosis and

should probably be used only to aid in the localization

of venous segments that are difficult to visualize.

Patients in whom adequate compression studies of

the proximal deep venous system may be difficult to

perform include obese patients, patients with tense

swollen extremities, burn patients, and patients with

recent surgery in the area of interest. These limitations

seldom preclude evaluation of the areas where DVT

most commonly occurs (ie, the common femoral and

popliteal veins).

Pitfalls occasionally encountered include missing

a thrombosed vein segment when a nonthrombosed

duplicated vein segment is present (Fig. 11) and

occasionally mistaking a large collateral for a patent

venous segment when thrombosis is present in the

underlying vein. The latter can usually be avoided by

confirming the normal course of the vein in relation-

ship to the adjacent artery.

Suggested protocols

Diagnosis of acute deep venous thrombosis of the

lower extremities

To maximize patient safety and the efficiency of

resources, clinicians should be encouraged to follow

validated nomograms that encompass consideration

of clinical probability, D-dimer testing, and venous

ultrasound imaging. The algorithm outlined in Fig. 5

has been demonstrated to be safe for patients with

low pretest probability for DVT because only less

than 1% of these patients, if left untreated, develop

Fig. 11. Duplicated superficial femoral and popliteal veins. Patient with symptomatic DVT who has duplication of the poplit-

eal veins (A) and the superficial femoral veins (B) of the leg. Noncompressible clot is seen within the more superficial of the two

deep veins at both levels (2), with the deeper vein (1) demonstrating normal compressibility (A,B). Duplication of the artery

within the popliteal fossa is appreciated only on the color Doppler images with a more superficial artery (A) and a deeper


objective evidence of DVT or PE in follow-up over

a 3-month period.

The ultrasound examination in this algorithm is

restricted to the proximal venous system. Pretest

probability should be judged either by experienced

clinicians or by using a validated clinical model.

D-dimer testing should be done using a validated as-

say for the diagnosis of venous thromboembolism.

Fig. 10. Calf hematoma. Patient who presented to the emergency

DVT. The deep venous system (arrowheads) within the common

with normal compressibility. A hematoma was discovered (arrow

muscles (C), explaining the patient’s calf pain and tenderness.

Using this approach, most patients can have a diag-

nosis of DVT confirmed or excluded on initial

testing. Recognizing that a small proportion of

patients may have DVT isolated to the calf veins, it

is advisable that these higher-risk patients as defined

by moderate or high pretest probability and positive

D-dimer should have the ultrasound repeated ap-

proximately 1 week following their initial evaluation.

department with a painful swollen calf area suspicious for

femoral (A) and popliteal regions (B) demonstrates patency

s) between the heads of the gastrocnemius and the soleus


This is to detect patients whose calf DVT may have

extended to the proximal venous system, which has

thereby increased the risk of PE.

Diagnosis of deep venous thrombosis of the upper

extremities

Unfortunately, validated diagnostic algorithms

are not available for patients presenting with DVT

of the upper extremity. There also are no models to

assist clinicians in determining pretest probability.

Fig. 6 contains an algorithm based on one of the

principles of DVT investigation of the lower extrem-

ities with the recognition that CUS is less sensitive in

the evaluation of the upper extremities. This algo-

rithm is based on the opinion and clinical experience

of the authors. It is their opinion that venography

should be performed in patients in whom the clin-

ical suspicion of upper extremity DVT is moderate or

high, D-dimer is positive, and the ultrasound is neg-

ative. As a second option, a repeat ultrasound may

be performed 1 week later; however, the safety of

this approach has not been demonstrated in con-

trolled trials.

Diagnosis of pulmonary embolism

Ultrasonography is particularly valuable in the

investigation of patients in whom PE is not conclu-

sively confirmed or refuted by other radiographic

imaging techniques. Patients with high-probability

ventilation-perfusion lung scans or positive spiral

CT may be treated for PE. Those with normal venti-

lation-perfusion scans may be considered to have PE

excluded. For patients with abnormal ventilation-per-

fusion scans that are not high probability or with

normal spiral CT scans, however, a significant pro-

portion may have underlying PE. It is recommended

that these patients undergo bilateral ultrasound imag-

ing of the proximal venous system of the lower ex-

tremities. Those with positive studies may be treated

for venous thromboembolism. Those patients with

negative ultrasound investigations have a much lower

likelihood of having PE responsible for their symp-

toms. Clinical trials have demonstrated that patients

with suspected PEs who have the combination of

negative spiral CT and bilateral CUS may safely have

the diagnosis of PE excluded [44–46]. Patients with

non–high-probability ventilation-perfusion scans

with normal spiral CT may have the diagnosis of

PE excluded if clinical pretest probability is low or the

D-dimer is negative. Other patients should be consid-

ered for 1-week follow-up CUS or pulmonary angi-

ography, particularly if the clinical pretest probability

is high.

Other considerations

Frequently, patients with suspected venous throm-

boembolism present at inopportune times when im-

mediate access to diagnostic testing may not be

available. With the advent of low-molecular-weight

heparin, diagnostic testing can be scheduled safely

within 24 hours of presentation. Such patients may

receive a single dose of subcutaneous low-molecular-

weight heparin designed to treat DVT or PE while

awaiting diagnostic testing [16,30]. The only restric-

tion to this regimen is that patients are at increased risk

of major bleeding.

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Radiol Clin N Am 42 (2004) 297–314

Sonographic evaluation of first-trimester bleeding

Raj Mohan Paspulati, MD*, Shweta Bhatt, DMRD, DMRE, Sherif Nour, MD

Department of Radiology, University Hospitals of Cleveland, Case Western Reserve University, 11100 Euclid Avenue,


Vaginal bleeding in the first trimester of preg- and external cervical os. The internal os is the

nancy is a common presentation in emergency care

facilities. About 25% of all gestations present with

vaginal spotting or frank bleeding in the first few

weeks of pregnancy; half of these progress into

miscarriage or abortion [1]. The acuity of these

symptoms may vary from occasional spotting to se-

vere hemorrhage, associated with cramping and ab-

dominal pain. The bleeding often is self-limited and

is most likely caused by implantation of the concep-

tus into the endometrium. The important causes of

first-trimester bleeding are spontaneous abortion, ec-

topic pregnancy, and gestational trophoblastic dis-

ease. The clinical assessment of pregnancy outcome

is unreliable and ultrasound (US) evaluation com-

bined with quantitative beta human chorionic gonado-

tropin (b-hCG) is an established diagnostic tool in

these patients. This article reviews the role of ultra-

sonography in the evaluation of patients presenting

with first-trimester bleeding.

Sonographic anatomy

The uterus is a pear-shaped, muscular organ that

varies greatly in size and shape depending on age and

prior pregnancies. The normal postpuberty uterus in

an adult measures approximately 7.5 to 8 cm in

length, 4 to 5 cm in width, and about 2 cm in an-

teroposterior dimension. The normal cervix is 3.5 to

4 cm in length. The cervix is comprised of internal


doi:10.1016/j.rcl.2004.01.005


E-mail address: [email protected] (R.M. Paspulati).

junction of the uterine cavity and the cervical canal

and the external os is the junction of the cervical

canal and the vagina. Transvaginal US (TVUS) of the

normal myometrium reveals three distinct layers.

Arcuate vessels separate the thin outer layer from

the thick middle layer, and both layers are homoge-

neous with the outer layer more hypoechoic relative

to the middle layer [2]. The inner layer consists of a

thin hypoechoic halo that surrounds the endometrium

and corresponds to the junctional zone seen on MR

imaging. The endometrial thickness measurements

are optimally made on sagittal (long-axis) images of

the uterus; this measurement should be performed

on the thickest portion of the endometrium excluding

the hypoechoic inner myometrium (Fig. 1). The en-

dometrial thickness should be reported as the ‘‘dou-

ble thickness’’ measurement [3]. If endometrial fluid

is present, its diameter should be omitted; in such

cases the endometrial thickness should be reported

as the sum of the measurements obtained from the

anterior and posterior endometrial walls. An endo-

metrial thickness of 4 to 14 mm is normal in an adult

premenopausal woman. Endometrial thickness and

appearance vary with the phase of the menstrual

cycle [4].

The position of the ovaries is variable but they are

usually found in the posterior fold of the broad

ligament, posterior and distal to the fallopian tubes.

On sonography the ovaries can be localized anterior

to the internal iliac vessels. The postpubertal ovary

measures approximately 3 cm in length, 2 cm in

width, and 1 cm in anteroposterior dimension. The

upper limit for normal ovarian volume is highest in

young adult women measuring approximately 9.8 to

14 mL and declines with increasing age [5]. Normal

s reserved.

Fig. 1. Sagittal TVUS of the uterus demonstrates a normal

endometrial lining (arrowheads).

R.M. Paspulati et al / Radiol Clin N Am 42 (2004) 297–314298

fallopian tubes cannot be visualized with current US

imaging equipment

Table 1

First-trimester scanning milestones

Parameter Transabdominal US Transvaginal US

Gestational sac — Present at 5 wk

(5 mm)

Yolk sac Always present

if GS > 20 mm

Always present

when GS > 10 mm

Cardiac activity GS > 2.5 cm GS > 18 mm

Abbreviations: GS, gestational sac; US, ultrasound.

Scanning technique

Ultrasound evaluation of the female pelvis is

conducted with a real-time scanner, preferably using

a sector or curvilinear transducer. The scanner is

adjusted to operate at the highest clinically appropri-

ate frequency, realizing that there is a trade-off

between the resolution and beam penetration.

Transabdominal pelvic US is performed with a

full bladder using transducer frequencies of 3.5 MHz

and above. Adequate distention of the bladder dis-

places the bowel from the field of view. Transab-

dominal US gives an initial overview of the uterus,

adnexa, and any intra-abdominal free fluid. TVUS is

performed with the patient’s bladder being empty,

using a transducer frequency of 5 to 7.5 MHz. TVUS

gives detailed information about the uterus and the

adnexa. Higher-frequency transvaginal probes can be

positioned closer to the pelvic organs resulting in

improved spatial resolution and diagnostic accuracy.

Currently available transducers of 10 MHz and above

can identify the finer details of intrauterine gestation

and have greatly contributed to the early diagnosis of

abnormal gestation and to the management of first-

trimester bleeding. Color flow Doppler and pulsed

Doppler may be added to the examination, as indi-

cated by the gray-scale US findings. It is important to

bear in mind that the energy output of Doppler US is

substantially higher than that used for imaging and it

may have potentially harmful effects on the concep-

tus [6]. Because of this risk, caution has been

expressed over the routine use of Doppler US in

early pregnancy evaluation. While performing Dopp-

ler US in early pregnancy, the concept of ‘‘as low as

reasonably achievable’’ is important [7] and the

advantages of the Doppler US should outweigh the

potentially harmful effects on the conceptus.

Normal first-trimester sonography

Scanning in the first trimester may be performed

either transabdominally or transvaginally. TVUS is

preferred and is the community standard. The first-

trimester milestones are given in Tables 1 and 2.

A gestational sac can be identified with TVUS at

5 weeks of gestational age, when it measures 5 mm.

The yolk sac should always be seen by TVUS when

a gestational sac measures greater than 10 mm and

by transabdominal US when the mean sac diameter

is greater than 20 mm [8,9]. An embryo with car-

diac activity should be seen transvaginally when the

gestational sac measures greater than 18 mm, and

transabdominally when the gestational sac measures

2.5 cm. These discriminatory criteria should be used

as guidelines. If the findings of the US examination

are equivocal and the examination is technically

difficult, a follow-up examination should be obtained.

Gestational sac

The blastocyst implants into the endometrium by

approximately 23 days of menstrual age [10]. It mea-

sures 0.1 mm and is too small to be visualized on

TVUS. Demonstration of peritrophoblastic flow by

transvaginal color flow Doppler at this focal decidual

thickening has improved the diagnostic sensitivity of

intrauterine pregnancy (IUP) from 90% with TVUS

alone to 99% using transvaginal color flow Dopp-

ler [11,12]. The peritrophoblastic flow has a charac-

teristic high-velocity and low-impedance flow caused

by shunting of blood from the spiral arteries into the

intervillous spaces. According to Emerson et al [11],

the peak systolic velocity of peritrophoblastic flow

in a normal IUP ranges from 8 to 30 cm/second, be-

fore the visualization of the gestational sac. Yeh et al

Table 2

Land marks of normal first-trimester pregnancy

Gestational age Embryologic change Sonographic appearance

23 d Blastocyst implantation Blastocyst measures 0.1 mm and is too small to visualize

3.5–4 wk Decidual changes at

implantation site

Focal echogenic decidual thickening at implantation site

4–4.5 wk Trophoblastic tissue High-velocity and low-impedance trophoblastic flow at the implantation site

on TVCFD

4.5–5 wk Exocoelomic cavity of

the blastocyst

Gestational sac (a sonographic term) is always seen when it measures > 5 mm

and the serum b-hCG is between 1000 and 2000 mIU/mL (IRP)

5–5.5 wk Secondary yolk sac Yolk sac is seen as a thin-walled cystic structure within the gestational sac and

should always be seen when the GS is > 10 mm; it is the first sign of a true

gestational sac before the visualization of embryo

5–6 wk Embryo Seen as a focal echogenic area adjacent to the yolk sac; should always be seen

when the GS is > 18 mm

5–6 wk Embryonic cardiac

activity

Embryonic cardiac activity should always be seen when the embryo is > 5 mm;

normal heart rate ranges from 100–115 beats/min between 5–6 wk of gestation

Abbreviations: CG, human chorionic goradotropin; GS, gestational sac; IRP, international reference preparation; TVCFD,

transvaginal color flow Doppler.

Fig. 2. Coronal TVUS of the uterus shows a gestational sac

with hyperechoic margins (arrow) and endometrial cavity

(curved arrow).

R.M. Paspulati et al / Radiol Clin N Am 42 (2004) 297–314 299

[13] described a focal, eccentric, anechoic area in the

endometrium caused by the embedded blastocyst as

the ‘‘intradecidual sign.’’ They described this sign as

early as 3.5 weeks of menstrual age on transabdomi-

nal US and reported a sensitivity rate of 92%, a

specificity rate of 100%, and an accuracy rate of

93%. Laing et al [14] used TVUS to demonstrate this

sign and found that the overall sensitivity, specificity,

and accuracy for the intradecidual sign were only

48%, 66%, and 45%, respectively. With currently

available high-frequency transvaginal probes, a ges-

tational sac as small as 2 to 3 mm can be demon-

strated at 4 weeks of gestational age [15–17]. On

TVUS, the gestational sac is seen as a well-defined

fluid-filled cavity with a surrounding hyperechoic

rim, embedded eccentrically in the endometrial lining

of the fundus or midbody of the uterus (Fig. 2). The

sonographic term ‘‘gestational sac’’ represents the

exocoelomic cavity of the blastocyst and the sur-

rounding echogenic rim is caused by the developing

chorionic villi and decidual tissue. The echogenic rim

should have a minimum thickness of 2 mm and its

echogenicity should exceed that of myometrium [1].

The double decidual sac sign of intrauterine

gestation was first described in 1982 [18]. The double

decidual sac sign consists of two concentric echo-

genic rings encasing a central anechoic focus that im-

press on the endometrial stripe. The inner echogenic

rim represents the decidua capsularis and chorion

laeve, whereas the outer echogenic rim represents

the decidua parietalis; these echogenic rims are sepa-

rated by a thin rim of fluid in the endometrial cavity

(Fig. 3). This is a useful sign of IUP between 4 and

6 weeks of gestation. The crown-rump length (CRL)

of the embryo is a more accurate indicator of gesta-

tional age than the mean gestational sac diameter. The

mean gestational sac diameter should be recorded,

however, when an embryo is not identified.

Because hCG production and gestational sac

growth are related to trophoblastic function, there is

excellent correlation of the serum hCG level, sac size,

and the stage of pregnancy [19]. Kadar et al [20] first

introduced the concept of a discriminatory level of

the b subunit of hCG. The range of the serum b-hCGlevel at which an intrauterine gestational sac is

visualized is the discriminatory zone. Although the

discriminatory range of b-hCG varies from one labo-

ratory to another, the widely accepted range is from

Fig. 3. Double decidual sac sign. (A) Coronal TVUS of the uterus reveals an intrauterine gestational sac (straight arrow),

decidua capsularis (curved arrow), decidua parietalis (arrowhead), and effaced endometrial cavity (asterisks). (B) Corresponding

line diagram.

Fig. 4. TVUS of the uterus demonstrates a yolk sac (thin

arrow) outside the amniotic membrane (arrowhead), which

has not yet fused with the chorion (curved arrow). Embryo

(thick arrow) is seen within the amniotic sac.


1000 to 2000 mIU/mL international reference prepa-

ration (IRP) for TVUS and 2400 to 3600 mIU/mL

(IRP) for transabdominal US [10]. In normal preg-

nancy serum b-hCG should double or increase by at

least 66% in 48 hours.

Yolk sac

The first structure to be seen within the gestational

sac is the secondary yolk sac, which is a reliable

indicator of a true IUP with a positive predictive

value of 100%. The primary yolk sac is not seen by

US because it shrinks at 4 weeks menstrual age and

gradually disappears with the formation of the sec-

ondary yolk sac [21]. The secondary yolk sac is first

seen on TVUS as a thin-walled cystic structure by the

fifth gestational week and is virtually always seen by

5.5 weeks gestational age (Fig. 4) [22]. The yolk sac

is round, measures less than 6 mm, and should be

visualized by TVUS when a gestational sac measures

more than 10 mm [10]. The yolk sac is involved in

nutritive, metabolic, hemopoietic, and secretive func-

tions during early embryonic development and or-

ganogenesis [23,24]. Abnormalities in its size and

appearance are predictors of abnormal gestation [25].

Embryo

The embryo should always be visualized by

TVUS when the gestational sac measures greater than

18 mm, and transabdominally when the gestational

sac measures 2.5 cm (Fig. 5). With the currently

available high-frequency transvaginal transducers,

the embryonic disk is initially seen as a focal echo-

genic area of 1- to 2-mm thickness adjacent to the

yolk sac between 5 and 6 weeks of gestational age

[26–29]. Embryonic cardiac activity should always

be seen when an embryo measures greater than 5 mm.

Occasionally the heartbeat may be seen adjacent to

the yolk sac even before the embryo is clearly visible.

Fig. 5. TVUS of the uterus shows a normal embryo and

separate amniotic membrane (arrow) in close relation to the

embryo. This should not be mistaken for nuchal translucency.


Levi et al [3] suggested a 4-mm CRL cutoff because

their study demonstrated cardiac activity in all em-

bryos with a CRL of 4 mm [30]. Other studies

demonstrated 5 mm as the discriminatory CRL for

detecting cardiac activity [31,32]. Although visual-

ization of a living embryo does not ensure a viable

pregnancy, the abortion rate decreases for living em-

bryos as the gestational age increases, with a 0.5%

demise rate for living embryos between 6 and 10 mm

[33]. If the length of the embryo is less than 5 mm,

follow-up US should be performed until the expected

CRL exceeds the discriminatory value. Most of the

studies reported a heart rate of 100 to 115 beats per

minute between 5 and 6 weeks [34–36]. By 9 weeks

of gestational age, the mean heart rate increases to

about 140 beats per minute. The cardiac activity

should be documented by M-mode.

Amniotic sac

The amniotic sac is formed in the fourth week

of gestation between the ectoderm layer and the adja-

cent trophoblast. Before 6.5 weeks the amniotic

membrane is so close to the embryo that the amniotic

cavity around the embryo is not easily seen. The di-

ameter of the amniotic cavity is nearly equal to the

CRL. Between 5 and 7 weeks of gestational age the

embryo is located between the amniotic and yolk

sacs. On US, this amniotic sac–embryo–yolk sac

complex appears as two small sacs and is called the

double bleb sign [9]. The embryo and the inner

amnion grow at a faster rate than the outer chorionic

cavity with eventual fusion of the amniotic and

chorionic membranes by 16 weeks of gestation

[37]. Separation of the amniotic and chorionic mem-

branes before 14 weeks of gestation is considered

normal (see Figs. 4 and 5).

Spontaneous abortion

Spontaneous abortion is defined as pregnancy

terminating before the 20th completed week of ges-

tation. Approximately 80% of spontaneous abortions

occur in the first trimester. The causes of spontaneous

abortions fall into two categories: genetic and envi-

ronmental (maternal) as listed next:

Genetic or fetal causes

Trisomy

Polyploidy or aneuploidy

Translocations

Environmental or maternal causes

Uterine

Congenital uterine anomalies

Leiomyoma

Intrauterine adhesions or synechiae (Asherman’s

syndrome)

Endocrine

Progesterone deficiency (luteal phase defect)

Hypothyroidism

Diabetes mellitus (poorly controlled)

Luteinizing hormone hypersecretion

Immunologic

Autoimmunity: antiphospholipid syndrome, sys-

temic lupus erythematosus

Infections

Toxoplasma gondii, Listeria monocytogenes,

Chlamydia trachomatis, Ureaplasma urea-

lyticum, Mycoplasma hominis, herpes simplex,

Treponema pallidum, Borrelia burgdorferi,

Neisseria gonorrhoeae

Genetic abnormalities are the most common cause

of spontaneous abortions accounting for almost 50%

to 60% of cases. Autosomal trisomy is the most

frequently identified chromosomal abnormality re-

sulting in first-trimester abortions. The incidence of

abortions secondary to chromosomal abnormalities

markedly increases after the maternal age of 35 years.

The environmental or maternal causes account for

a small percentage of spontaneous abortions. These in-

clude infection; anatomic defects (maternal mullerian

defects); endocrine factors (failure of corpus luteum);

immunologic factors (antiphospholipid antibody syn-

drome); and maternal systemic disease (diabetes mel-

litus, hypothyroidism). The algorithmic approach to

first-trimester bleeding is summarized in Fig. 6.

First Trimester Ultrasound

MSD > 18MM

ED

YS present

F/U re: sacgrowth andembryo

1

MSD < 10MM

ED

MSD > 10MM

YS absent

MSD < 18MM

Embryo not visualized

A

F/Ure: growth andcardiac activity

1

EDF/U2wksre: growthand cardiacactivity

1

F/U2

? F/U18 wks

1

HR N HR AbN

MSD-CRL> 5MM

MSD-CRL< 5MM

YS normal YS abnormal

YS present YS absent

CRL > 5MM CRL < 5MM

Cardiac activitypresent

CRL > 5MM CRL < 5MM

Cardiac activityabsent

Embryo visualizedB

Fig. 6. (A, B) Proposed algorithms for evaluating women with first trimester bleeding. ED, embryonal demise; F/U, follow-up;

HR ABN, heart rate abnormal; HR N, heart rate normal; YS, yolk sac. (From McGahan J, Goldberg B. Diagnostic ultrasound:

a logical approach. Philadelphia: Lippincott, Williams & Wilkins; 1998; p. 142–3; with permission.)


The most common morphologic finding in early

spontaneous abortions is an abnormality of devel-

opment of the zygote, embryo, early fetus, or the

placenta. Spontaneous abortion is clinically classified

into threatened, inevitable, missed, incomplete, and

complete abortions (Table 3).

Ultrasound findings in abortion

The US findings depend on the developmental

stage of the pregnancy at which the patient presents

with symptoms. Familiarity with normal sonographic

landmarks of first-trimester pregnancy is essential

Table 3

Classification of spontaneous abortion

Types Clinical features US findings

Threatened abortion Vaginal bleeding before 20 wk gestation

without cervical dilatation

Depending on the stage of pregnancy, US may show an

empty uterus, intrauterine gestational sac with or without

an embryo

Incomplete abortion Vaginal bleeding with partial expulsion

of products of conception before 20 wk

gestation and cervical dilatation

Thick, irregular endometrial lining caused by residual

trophoblastic tissue and fluid

Missed abortion Embryonic demise before 20 wk of

gestation without expulsion of products

of conception; may or may not have

vaginal bleeding

Embryo without cardiac activity; small size of the embryo

for the gestational age (see Fig. 10)

Complete abortion Vaginal bleeding and expulsion of all

products of conception before 20 wk

gestation

Empty uterus

Inevitable abortion Vaginal bleeding before 20 wk gestation

with cervical dilatation

Variable depending on the degree of bleeding and expulsion

of the products of conception

Abbreviations: US, ultrasound.

Table 4

TVUS features of pregnancy failure

Ultrasound findings Comments

Absence of IUGS with serum

b-hCG above the

discriminatory level

(1000 mIU/mL)

Ectopic pregnancy

has to be excluded

IUGS > 10 mm without

a yolk sac

Follow-up with serum

b-hCG and TVUS

IUGS of >18 mm without

an embryo

Anembryonic pregnancy

Embryo of 5 mm and above

without cardiac activity

Embryonic demise

Embryo with bradycardia

(< 100 beats/min)

Poor prognosis and

needs close follow-up

with TVUS

Subchorionic hematoma Correlation of pregnancy

outcome with the size

of hematoma is not well

established and needs

TVUS follow-up

Abbreviations: hCG, human chorionic gonadotropin; IUGS,

intrauterine gestational sac; TVUS, transvaginal ultrasound.


to diagnose a failing pregnancy. TVUS features of

failing pregnancy are summarized in Table 4. The

sonographic findings are to be correlated with serum

b-hCG and menstrual age. In the pre-embryonic stage,

the pregnancy outcome depends on the presence of

the gestational sac and yolk sac and their morpho-

logic features.

Absent intrauterine gestational sac

Failure to demonstrate intrauterine gestational sac

by TVUS may be secondary to early IUP (b-hCG <

1000 mIU/mL) or secondary to ectopic pregnancy.

When the serum b-hCG is more than 1000 mIU/mL

(IRP) and there is no IUP, an ectopic pregnancy

[19,20] must be excluded by careful evaluation of

the adnexa. If there is no identifiable ectopic gesta-

tional sac, adnexal mass, or a large amount of adnexal

fluid in the cul-de-sac, follow-up with b-hCG and

TVUS is necessary until a definite diagnosis is made.

When the endometrial lining is thick with echoes in

the endometrial cavity and no intrauterine gestational

sacs, an incomplete abortion with retained products

of conception must be distinguished from decidual

reaction of ectopic gestation. Transvaginal color flow

Doppler of the endometrial contents is useful in dif-

ferentiating trophoblastic tissue from blood clots and

pseudogestational sac. Sparse flow on color Doppler

with low peak systolic velocities (< 6 cm/second) and

low to absent end diastolic flow suggests decidual re-

action of an ectopic pregnancy (Fig. 7) [38,39]. With

early IUP (< 5 weeks) multiple flashes of color with a

peak systolic velocity of greater than 8 cm/second

and high diastolic component caused by trophoblastic

arterial flow are noted [40].

Intrauterine gestational sac without an embryo

A common and difficult problem arises when the

gestational sac in the uterus lacks an embryo or yolk

sac [41–43]. This can be caused by early normal IUP,

Fig. 7. Decidual reaction. (A) Sagittal TVUS shows thick echogenic endometrial lining without a gestational sac (arrowheads).

This sonographic appearance can be seen in molar pregnancy; correlation with beta hCG is very important. (B) Sagittal TVUS

with color Doppler did not demonstrate trophoblastic flow, confirming it to be decidual reaction (arrowheads). Patient’s beta

hCG was 650 IU. On follow-up, the patient was shown to have a normal intrauterine pregnancy.


anembryonic gestation, or a pseudogestational sac of

ectopic pregnancy. Anembryonic gestation is a form

of failed pregnancy defined as a gestational sac in

which the embryo failed to develop (Fig. 8A). A

mean gestational sac diameter greater than 18 mm

(TVUS) without a visualized embryo is unequivocal

evidence of a failed, anembryonic pregnancy [44].

This also is referred to as an ‘‘empty amnion’’ sign

(Fig. 8B) because of its sonographic appearance of a

large well-defined amniotic sac without an embryo

[45]. The growth rate of an anembryonic gestational

sac is slower than that of a normal gestational sac,

which increases by 1.13 mm/day. An abnormal ges-

tational sac can be identified confidently when the

rate of increase of the mean sac diameter is less than

Fig. 8. Anembryonic pregnancy. (A) TVUS of uterus shows a large (

‘‘empty amnion sign’’ of anembryonic gestation (arrow).

0.6 mm/d on follow-up US [46]. Other minor crite-

ria of an abnormal gestational sac include distorted

sac shape and weakly echogenic or irregular chorio-

decidual reaction (Fig. 9). The presence of gestational

sac in the lower uterine segment or cervix is usually

seen in patients with abortion in progress (Fig. 10),

but can also be seen secondary to low implantation.

Demonstration of trophoblastic vascular flow on

color Doppler is useful in differentiating low implan-

tation from abortion.

Yolk sac criteria of an abnormal gestation

The absence of a yolk sac when the mean sac

diameter of the gestational sac is more than 10 mm is

> 18 mm) gestational sac (arrow) without an embryo. (B) An

Fig. 9. Abnormal shape of the gestational sac. A 30-year-old

woman with 5 week’s of amenorrhea presents with vaginal

spotting. A TVUS of the uterus shows an intrauterine gest-

ational sac of abnormal shape and lobulated contour. On fol-

low-up patient had a spontaneous complete abortion.

Fig. 10. Abortion in progress. ATVUS of the uterus shows a

low-lying gestational sac (arrow). Mixed hyperechoic and

hypoechoic contents in the endometrial cavity of the fundus

(arrowheads) represent decidual reaction and hemorrhage.

The patient had a complete spontaneous abortion a few

hours after the scan.


indicative of an abnormal gestation and is associated

with spontaneous abortion [47–49]. A failing or

failed pregnancy is also suggested when the yolk

sac is abnormal in size and shape. Large (> 6 mm)

irregular and calcified yolk sacs have been found to

correlate with early pregnancy failure [50–52]. A

large yolk sac is considered to be caused by an

alteration of the metabolic functions of the yolk sac

membrane with accumulation of secretions following

embryonic death [53]. The association of a large yolk

sac with aneuploidy has also been reported [50].

Although abnormal large yolk sac size is reported

to be associated with subsequent pregnancy failure,

another study with yolk sac diameter greater than the

95th percentile for gestational age reported normal

pregnancy outcomes [54]. Because of this controver-

sial issue, any patient with a large yolk sac should

have a follow-up US because there is increased risk

of spontaneous abortion. Apart from size, irregular,

echogenic, calcified, or double yolk sacs (vitelline

duct cyst) also are associated with early pregnancy

failure [55,56].

Gestational sac with an embryo

Although visualization of a living embryo does

not ensure a viable pregnancy, the abortion rate

decreases for living embryos as the gestational age

increases, with a 0.5% demise rate for living embryos

between 6 and 10 mm [29]. Because cardiac activity

may not be demonstrated [57] in early normal em-

bryos (CRL < 4 mm), follow-up US and correlation

with the serum b-hCG level is useful in determining

the viability of the gestation. The most convincing

evidence that a pregnancy has failed is to document

absence of cardiac activity when CRL length is

greater than 5 mm. In a missed abortion, the embryo

may be small for the gestational age with a discrep-

ancy between the mean sac diameter and the CRL

(Fig. 11). Embryonic bradycardia is a poor prognos-

ticator of pregnancy viability and requires follow-up

[58]. Embryonic bradycardia is defined as a heart rate

of less than 100 beats per minute before 6.2 weeks

gestational age and less than 120 beats per minute

between 6.3 and 7 weeks [59].

Intrauterine growth restriction

First-trimester growth restriction is a sign of a

failing pregnancy. Growth restriction is detected by

comparing the mean sac diameter with the CRL or

by serial follow-up of these growth parameters. The

average gestational sac diameters should be at least

5 mm larger than the CRL. A difference in size be-

tween mean sac diameter and CRL of less than 5 mm

caries a high risk of subsequent embryonic demise

[60]. When there is sac size and CRL discrepancy, a

follow-up US examination is recommended because

these fetuses have higher incidence of low birth

weight and premature delivery [61,62].

Subchorionic hematoma

Up to 20% of women with a threatened abortion

have a subchorionic hematoma [44]. Perigestational

Fig. 11. Missed abortion. A 35-year-old woman with

10 weeks of amenorrhea presents with intermittent vaginal

bleeding. TVUS shows a relatively small-sized embryo (ar-

row) compared with the gestational sac. No cardiac activity

was demonstrated on pulsed Doppler.

Fig. 12. Subchorionic hemorrhage. TVUS shows a gesta-

tional sac (curved arrow), chorion (straight thick arrow),

and a subchorionic hemorrhage (straight thin arrow).


hemorrhage from chorionic frondosum is the most

common source of vaginal bleeding in the first

trimester of pregnancy. Subchorionic hemorrhage is

secondary to abruption of the edge of the chorion

frondosum–decidua basalis complex or may be

caused by marginal sinus rupture [63,64]. Although

the hemorrhage usually abuts or elevates the edge of

the chorion frondosum–decidua basalis complex, the

bulk of the hemorrhage is usually situated between

the decidua capsularis, chorion laeve, and the decidua

vera. Acute hemorrhage may be hyperechoic or

isoechoic relative to the chorion, and it becomes

isoechoic with the chorionic fluid in 1 to 2 weeks

(Fig. 12). Several studies have correlated the preg-

nancy outcome in these patients with the size of the

subchorionic hematoma, gestational age, and the

maternal age. One of the largest studies [65] showed

that the rate of pregnancy loss increases with hema-

toma size, advancing maternal age, and earlier gesta-

tional age. In this study, the size of the hematoma was

graded according to the percentage of the chorionic

sac circumference elevated by the hematoma. It was

graded as small when it involved less than one third

of the chorionic sac circumference, moderate when it

involved one-third to one-half of the chorionic sac

circumference, and large when two-thirds or greater

of the chorionic sac circumference was involved.

There was little difference in the rates of spontaneous

abortion between pregnancies with small- and mod-

erate-size hematomas (7.7% and 9.2%, respectively),

but the rate doubled with large hematomas (18.8%).

The spontaneous abortion rate was also twice as

high in women 35 years of age or older compared

with that in younger women (13.8% versus 7.3%, re-

spectively), and was 2.3 times higher in women who

presented with vaginal bleeding at 8 weeks gesta-

tional age or less compared with that in women who

presented with bleeding at more than 8 weeks gesta-

tional age (13.7% versus 5.9%, respectively). Some

investigators have calculated the volume of a sub-

chorionic hematoma as a percentage of the gesta-

tional sac volume. When the volume of a hematoma

is less than 40% of the gestational sac volume, the

pregnancy outcome is favorable [64,66].

Retained products of conception

Retained products of conception typically consist

of retained placental tissue. An echogenic mass in the

uterine cavity is the most suggestive US finding. A

heterogeneous mass or collection in the central cavity

may represent a blood clot, or some combination of

retained placenta, necrotic debris, and clot (Fig. 13).

Color Doppler may help to differentiate vascularized

trophoblastic tissue from nonvascularized blood clots.

A normal-appearing endometrial stripe or punctate

echogenic foci not associated with a discrete mass

makes retained products of conception unlikely.

Gestational trophoblastic disease

Gestational trophoblastic disease is a spectrum of

pregnancy-related trophoblastic proliferative abnor-

malities that can present with first-trimester bleeding.

Fig. 13. Retained products of conception with variable appearance. Sagittal (A) and coronal (B) TVUS in two different patients

with persistent vaginal bleeding after spontaneous abortion show retained products of conception with increased echogenicity

(arrowheads) in (A) and heterogeneous appearance in (B). This appearance is secondary to necrosis and blood clots. (C) Increased

vascularity on color flow Doppler evaluation in a patient with retained products of conception.


Classification of gestational trophoblastic disease is

as follows:

Hydatidiform mole

Complete mole

Partial mole

Gestational trophoblastic tumors

Choriocarcinoma

Invasive mole

Placental site trophoblastic tumor

Hydatidiform mole (molar pregnancy)

Molar pregnancy is a noninvasive process charac-

terized by varying degrees of trophoblastic prolif-

eration and edema of villous stroma. Its incidence is

1 in every 1000 to 2000 pregnancies [67] and is

estimated to be as high as 1 in 41 in patients with

miscarriages [68]. Hydatidiform mole constitutes

80% of the cases of gestational trophoblastic disease

with relatively high frequency of molar pregnancy at

the beginning and end of the childbearing period.

Mole recurrence is seen in about 1% to 2% of cases

[69]. The absence or presence of fetus or embryonic

elements is used to classify a molar pregnancy into

complete or partial moles. Complete molar pregnan-

cies are most often 46 XX, with the chromosomes

completely of paternal origin and are referred to as

‘‘androgenesis.’’ The karyotype in partial mole is usu-

ally triploid (69 XXY) or even tetraploid (92 XXXY)

with one maternal and two paternal haploid compo-


nents. The fetus in partial mole is usually nonviable

and exhibits features of triploidy, which include

multiple congenital anomalies and growth restriction

[70]. Histologically, the molar tissue has prominent

villi with central acellular space corresponding to the

macroscopic appearance of vesicles. In partial mole

these changes are focal and less advanced.

The clinical presentation of molar pregnancy,

listed below, has changed appreciably over the last

decades because of early diagnosis with TVUS and

quantitative b-hCG estimation.

� Uterine bleeding, which may vary from spotting

to profuse hemorrhage� Uterine enlargement out of proportion to the

duration of pregnancy in 50% of cases� Absence of fetal parts or fetal heart sounds

despite an enlarged uterus� Pregnancy-induced hypertension before

24 weeks gestation� Hyperemesis� Thyrotoxicosis, which is usually subclinical� History of passage of grape-like vesicles trans-

vaginally

Uterine bleeding is the most common presentation

and it may vary from spotting to profuse bleeding.

Occasionally patients may pass grape-like vesicles

transvaginally. Clinically the uterine fundal height is

more than is expected for the gestational period. Di-

Fig. 14. Complete hydatidiform mole. (A) Transabdominal sonogr

defined anechoic cystic areas (arrows) corresponding to the vesic

(B) Corresponding T1-weighted postgadolinium image of the uteru

multiple well-defined hypointense lesions that are not enhancing a

agnosis is made by markedly elevated serum b-hCGlevels expected for the stage of gestation and by the

characteristic sonographic appearance.

Sonographic features of molar pregnancy

Molar changes can be detected from 8 weeks of

pregnancy by US. The uterine cavity is filled with

multiple sonolucent areas of varying size and shape.

This has been described as a ‘‘snow storm’’ appear-

ance with low-frequency transabdominal scanning.

With high-frequency transvaginal transducers, nu-

merous discrete, anechoic (cystic) spaces are visual-

ized corresponding to the hydropic villi (Fig. 14).

These cystic spaces range from 1 to 30 mm in size

and increase in size with gestational age. Large sono-

lucent areas or maternal lakes resulting from the stasis

of maternal blood are seen between the vesicles. In

partial mole, an intrauterine embryo is noted along

with molar changes [71,72]. Because the trophoblas-

tic changes develop at a slower rate in partial mole,

it may present as enlarged placenta without macro-

scopic vesicular changes [73]. Women with a high

b-hCG level for the gestational age without sono-

graphic molar changes should have follow-up US to

exclude partial mole. In missed abortion, impaired

trophoblastic vascularity leads to hydropic degenera-

tion of villi and can resemble a partial hydatidiform

mole on US. The serum b-hCG is not elevated, how-

ever, and may be normal or at a lower level than for

am of the uterus shows a complex mass with multiple well-

les of hydatidiform mole. There was no associated embryo.

s demonstrates intrauterine complex mass (arrowheads) with

nd represent vesicles of hydatidiform mole (arrow).


the expected gestational age. Rarely, a viable fetus

may be associated with complete molar pregnancy

[74] and is caused by the coexistence of a true mole

and a normal fetus in dizygotic twin gestation. Dem-

onstration of the typical trophoblastic flow is useful

in differentiating the trophoblastic tissue of molar

pregnancy from intrauterine blood clots in a patient

with abortion. Theca-leutin ovarian cysts are seen in

up to 25% to 60% of cases because of hyperstimu-

lation of the ovaries by chorionic gonadotrophin

secreted by the trophoblastic tissue [75]. In this con-

dition, the ovaries are enlarged with multiple cysts

having a soap bubble or spoke-wheel appearance.

Treatment of hydatidiform mole consists of im-

mediate evacuation of the mole and subsequent fol-

low-up with serial measurement of serum b-hCG for

detection of persistent trophoblastic proliferation

or malignant change. TVUS is useful in monitor-

ing patients following evacuation and chemotherapy

[76–79]. If the b-hCG levels plateau or continue to

rise, persistent trophoblastic tissue is diagnosed. Fol-

lowing evacuation of a hydatidiform mole, 18% to

29% with complete hydatidiform mole and 1% to

11% with partial mole develop a persistent tropho-

blastic tumor [80–83]. TVUS reveals nodules of

residual echogenic trophoblastic tissue and central

hypoechoic blood spaces. Doppler interrogation

reveals typical low-resistance and high-peak systolic

velocity vascular flow of trophoblastic tissue.

Gestational trophoblastic tumors

Gestational trophoblastic tumor refers to chorio-

carcinoma, invasive mole, and placental site tropho-

blastic tumor. It may follow a normal or a molar

pregnancy, abortion, or ectopic pregnancy. Diagnosis

is made primarily by persistent elevation of the serum

b-hCG. Fifty percent of these tumors arise following

hydatidiform mole, 25% following abortion, and 25%

following normal or ectopic pregnancy [84].

Choriocarcinoma

Choriocarcinoma is a malignant form of tropho-

blastic tumor that invades uterine myometrium and

blood vessels resulting in distant metastasis. The ab-

sence of villous pattern is characteristic of chorio-

carcinoma, in contrast to hydatidiform mole and

invasive mole. The most common sites of metastases

are the lungs (over 75%) and the vagina (50%). Other

sites of metastases include the vulva, liver, kidneys,

brain, ovaries, and bowel [85]. The US appearance

is indistinguishable from a complete mole, except

in cases with myometrial and parametrial extension.

TVUS reveals a heterogeneous intrauterine mass with

or without myometrial invasion. Doppler interroga-

tion reveals typical trophoblastic flow and differen-

tiates trophoblastic tissue from areas of hemorrhage

and necrosis. Ovarian theca-leutin cysts are identified

in more than a third of such cases. Cross-sectional

imaging with CT and MR imaging is more accurate in

demonstrating invasion of the myometrium and para-

metrium. Radiologic evaluation for distant metastases

is mandatory in all cases of choriocarcinoma.

Invasive mole

This is defined as excessive trophoblastic over-

growth with invasion of the myometrium and oc-

casional extension to the peritoneum or adjacent

parametrium. Unlike choriocarcinoma there are no

distant metastases. Invasive mole presents clinically

as heavy vaginal bleeding after the evacuation of the

molar pregnancy with persistent elevation of serum

b-hCG. On TVUS it appears as focal areas of in-

creased echogenicity within the myometrium [86].

Doppler color flow mapping of this area can evaluate

the extent of this lesion and its subsequent response

to chemotherapy (Fig. 15) [87–89].

Placental site trophoblastic tumor

This is a very rare trophoblastic tumor, which arises

from the placental implantation site following either a

normal term pregnancy or abortion. These patients

present with either abnormal bleeding or amenorrhea

and might be presumed to be pregnant. Moreover, the

b-hCG levels are not as high as in other forms of

gestational trophoblastic disease [90,91]. They may

invade the myometrium and in 15% to 20% cases

behave in a malignant fashion with distant metastases.

US features are indistinguishable from those of other

gestational trophoblastic tumors [92,93].

Arteriovenous malformation of the uterus

It is important to consider arteriovenous malfor-

mations in the differential diagnosis of first-trimester

bleeding because of their sonographic resemblance

to retained products of conception and gestational

trophoblastic disease. Vascular malformations of the

uterus are rare and potentially life-threatening le-

sions. They can be congenital or acquired following

uterine trauma (surgery or curettage); use of intra-

uterine contraceptive devices; endometrial or cervi-

cal carcinoma; and previous treatment of gestational

trophoblastic tumors [94]. Congenital arteriovenous

malformations have multiple arteriovenous commu-

nications and may extend through the myometrium

into the parametrium. Acquired lesions are arterio-

Fig. 15. Invasive mole. (A) TVUS showing molar tissue invading the myometrial wall (arrowheads) of the fundus and

endometrial cavity (arrow). (B) Color flow Doppler evaluation shows vascularity of the invaded myometrium. Endometrial

cavity is shown by arrow. (C) Corresponding T2-weighted, sagittal image of the uterus demonstrates hyperintense myometrium

(arrow) representing invasive molar tissue. Uninvolved endometrial lining is shown (arrowheads).


venous fistulas between a single artery and a vein.

Vascular malformations persist following treatment

in 10% to 15% of patients with gestational trophoblas-

tic tumors. Gray-scale US shows multiple anechoic

spaces with mosaic pattern of color signals within the

cystic spaces on color Doppler US. Spectral analysis

of the vessels shows high-velocity blood flow with a

low resistive index [95,96], indistinguishable from a

gestational trophoblastic disease (Fig. 16). These

vessels can be distinguished from gestational tropho-

blastic disease because the serum b-hCG is normal.

Uterine arteriovenous malformations are one of the

common causes of spontaneous abortions. Contrast-

enhanced CT, MR imaging, and angiography are other

imaging modalities used to diagnose uterine arterio-

venous malformations. The diagnosis of uterine arte-

riovenous malformations as the cause of vaginal

bleeding is crucial because treatment is entirely dif-

ferent from that for retained products of conception or

gestational trophoblastic disease, which can mimic

arteriovenous malformations. The treatment of arte-

riovenous malformations is by embolization if the

Fig. 16. Uterine arteriovenous malformation in a 35-year-old woman with history of spontaneous abortion presenting with

vaginal bleeding. She was referred to exclude retained products of conception. (A) TVUS shows complex endometrial mass

(arrowheads) with anechoic spaces (arrow). (B) Corresponding color flow Doppler demonstrates the mosaic pattern of flow

within the mass (arrowheads). Arrow points to endometrial cavity. Pulsed Doppler (C) shows arterialized venous flow,

diagnostic of arteriovenous malformation.


patient desires fertility and by hysterectomy if fertility

is not an issue.

Summary

Vaginal bleeding is a leading cause of presentation

for emergency care during the first trimester of the

pregnancy. Clinical assessment of the pregnancy

outcome at this stage is less reliable. US examination

is crucial in establishing IUP and early pregnancy

failure and to exclude other causes of bleeding, such

as ectopic pregnancy and molar pregnancy. Diagnosis

of a normal IUP at this stage not only assists the

physician in an expectant management, but also gives

a psychologic boost to the patient. With recent ad-

vances in US technology and the availability of high-

frequency transvaginal transducers, reliable diagnosis

of early pregnancy failure can be made even before

the embryo is visible.

Acknowledgment

The authors thank Bonnie Hami, MA, Department

of Radiology, University Hospitals of Cleveland,

Ohio, for her editorial assistance in the preparation of

this article.

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Radiol Clin N Am 42 (2004) 315–327

The role of ultrasound in pregnancy-related emergencies

Noam Lazebnik, MD*, Roee S. Lazebnik, PhD

Department of Obstetrics and Gynecology, MacDonald Women’s Hospital, University Hospitals of Cleveland,

Case Western Reserve University School of Medicine, 11100 Euclid Avenue, Cleveland, OH 44106, USA

Although most births are uneventful, about 15% Ultrasound examinations in emergency situations

of all birthing women experience potentially life-

threatening complications, and at least 1% to 2%

require major surgery. Although some complications

can be prevented, and some predicted preemptively,

most of the severe complications cannot be antici-

pated. To reduce mortality, a key component of ma-

ternal health care is the ability to diagnose, confirm,

and treat women whose medical status is unstable

in the antenatal, delivery, and postpartum periods.

Sonography is the imaging modality of choice for

diagnosing maternal-related abnormalities both dur-

ing and following pregnancy and delivery. Pelvic

ultrasound has long been the mainstay for evaluation

of the female pelvis. It is widely used during preg-

nancy in countries where antenatal care is available.

Most pregnant women are referred for ultrasound

study to confirm gestational age and to rule out fetal

malformations, abnormal placentation, and uterine

and cervical abnormalities. At University Hospitals

of Cleveland, Case Western Reserve University, a

tertiary care medical facility, more than 12,000 ob-

stetric ultrasound studies are performed yearly. About

13% of the total studies are performed in an emer-

gency obstetric setup. This article describes the

emergency conditions during pregnancy and the

immediate postpartum period that might lead to a

life-threatening situation for the pregnant patient or

her fetus, and the spectrum of imaging findings

associated with these conditions.


doi:10.1016/j.rcl.2004.01.006


E-mail address: [email protected] (N. Lazebnik).

are ordered to obtain specific, limited information

when it is necessary or impossible to perform a

complete fetal, placental, or pelvic organ survey.

Limited examinations in antepartum and intrapartum

emergency settings may include identification of

fetal number, fetal presentation, presence or absence

of fetal cardiac activity, localization of the placenta,

assessment of amniotic fluid volume, and a biophysi-

cal profile. The relevant clinical information can be

obtained by performing transabdominal study, trans-

vaginal study, or combination of the two modalities.

Occasionally, additional ultrasound studies are needed

in cases of medical or surgical complications of the

pregnant patient. Examples of such disorders include

renal and gastrointestinal abnormalities and maternal

vascular abnormalities.

Sonographic technique

Modern ultrasound devices have variable-focus

depths that allow the examiner to study structures

in the near or far field as needed without changing

transducers. A 2- to 5-MHz and 4- to 9-MHz trans-

ducer for transabdominal and transvaginal study,

respectively, is very well suited. For a pelvic sono-

gram, performed transabdominally, the patient’s uri-

nary bladder should be distended. A full bladder

usually is unnecessary. The more advanced the preg-

nancy, the lesser the need for a full bladder. When-

ever cervical and lower uterine segment or pelvic

organs images are needed, endovaginal scanning is

superior to transabdominal scanning. Improved visu-

alization may be achieved using the vaginal ap-

proach, because the transducer is brought closer to

s reserved.

N. Lazebnik, R.S. Lazebnik / Radiol Clin N Am 42 (2004) 315–327316

the area being examined. It can be very helpful in

studying the lower uterine segment and its relation

to the placenta, evaluating the uterus, or measuring a

cyst in an ovary in the early stage of pregnancy. The

sonologist performing the study decides whether

one or a combination of approaches is best for the

particular case.

There are no known contraindications to abdomi-

nal ultrasound study. Transvaginal studies are not

recommended in case of premature rupture of the

membranes. The use of this modality is controversial

in cases of placenta previa, as discussed later. Careful

judgment should always be applied in choosing to

perform a transvaginal study because it might be

contraindicated for maternal or fetal reasons. Further-

more, regardless of the indication for the study, one

should always perform a transabdominal evaluation

before considering vaginal scanning. The added

views obtained by combining the two scanning

modalities might be of significant help in establish-

ing a correct diagnosis.

It is highly advisable to follow a strict routine

when one performs ultrasound study for an obstetric

emergency. The first priority in a true obstetric

emergency is to document a live in utero gestation,

with a stable and normal heartbeat. Once this has

been achieved one should document that there is no

suspicion for a significant volume of free fluid or

blood clots inside the gestational sac, the abdominal

cavity, or the posterior cul-de-sac. The bladder and

uterus should appear normal and intact, and no

adnexal mass should be present.

Second- and third-trimester obstetric emergencies

Pregnancy-induced hypertension

Pregnancy-induced hypertension complicates 6%

to 8% of pregnancies in the United States and ac-

counts for 15% of maternal deaths. It ranks second

only to embolic events as a cause of maternal mor-

tality. It also is an important cause of perinatal mor-

bidity and mortality. In pregnant women, two distinct

hypertensive disorders are common: chronic hyper-

tension and pregnancy-induced hypertension. Women

with chronic underlying hypertension are at risk for

pregnancy-induced hypertension, a multiorgan patho-

logic state with various subsets. One of the more

severe forms of hypertensive disorder during preg-

nancy is HELLP syndrome.

The HELLP syndrome in a pregnant woman is

characterized by hemolytic anemia, elevated liver

enzymes, and a low platelet count. Progressive nau-

sea and vomiting, upper right quadrant abdominal

pain, and headache are usually the most common

symptoms. During the physical examination, the

physician notes impressive abdominal tenderness,

especially in the right upper quadrant. The liver

may be enlarged and liver function tests are abnor-

mally elevated with evidence of hemolysis on a

peripheral blood smear and the red blood cell and

platelet counts may be low. When the disease is not

treated early, up to 25% of affected women develop

serious complications. Without treatment, approxi-

mately 1.1% to 3.5% of patients die from HELLP

syndrome, usually because of liver rupture or other

related maternal complications [1]. The pathophysio-

logic process of this condition begins with arteriolar

vasospasm, which causes endothelial damage and

fibrin deposition in the vessel lumen. This leads to

the following events: (1) platelet deposition on the

fibrin aggregates, reducing the number of circulat-

ing platelets (unlike disseminated intravascular co-

agulation, coagulation factors are not involved);

(2) erythrocyte destruction by the fibrin aggregates

(a microangiopathic hemolytic anemia), leading to

abnormal cells in the peripheral smear (burr cells and

schistocytes), an elevated indirect bilirubin level, and

anemia; and (3) hepatocyte destruction caused by

hepatic microemboli [2]. HELLP syndrome occurs

in approximately 10% of pregnant women with

preeclampsia or eclampsia. Preeclampsia may be mild

or severe. Severe cases with high blood pressure and

protein in the urine can progress to seizures (eclamp-

sia). Severe cases are life-threatening to both the

mother and fetus. Many women have a high blood

pressure and are diagnosed with preeclampsia before

they develop the HELLP syndrome. In some cases,

however, HELLP symptoms are the first warning of

preeclampsia and the condition is misdiagnosed as

hepatitis, gallbladder disease, idiopathic thrombocy-

topenic purpura, hemolytic uremic syndrome, or

thrombotic thrombocytopenic purpura.

The fatality rate among neonates born to mothers

with HELLP syndrome varies, depending on such

factors as birth weight. The main treatment is delivery

of the baby as soon as possible, because liver func-

tion in the mother rapidly deteriorates with this con-

dition, a harmful state for both the mother and fetus.

Sonographic findings

Unlike the traditional role of sonography during

pregnancy where the fetus, placenta, or the pelvic

organs are the targets of the study, sonography plays a

different role in HELLP syndrome; it can exclude

biliary tract disease and identify altered hepatic

and renal echo textures. Possible findings include

N. Lazebnik, R.S. Lazebnik / Radiol Clin N Am 42 (2004) 315–327 317

patchy areas of increased echogenicity in the liver,

diffusely increased renal echo texture and size, peri-

renal fluid, and hepatic subcapsular hematoma [3,4].

Uterine rupture

One of the major causes of maternal and perinatal

mortalities is rupture of the uterus. This obstetric

hazard is also associated with short-term maternal

morbidities, such as vesicovaginal fistula, rectovagi-

nal fistula, bladder rupture, foot drop, psychologic

trauma, and anemia [5]. In the long-term, because of

the surgical intervention, the woman may become

infertile as a result of indicated hysterectomy.

Uterine rupture is defined as separation that

requires operative intervention or is symptomatic. It

involves the full thickness of the uterine wall. Uterine

rupture may occur spontaneously but is more com-

monly associated with history of uterine surgery,

such as dilation and curretage, classical cesarean or

low transverse cesarean section, and myomectomy.

Induction of labor using low- and high-dose regi-

mens of prostaglandin E2 or with misoprostol might

also result in uterine rupture. Prolonged deceleration

(alone or proceeded by either severe late or variable

decelerations) is the most reliable clinical finding

occurring in 100% of cases when total fetal extrusion

occurred [6]. The incidence of uterine rupture is

0.05% of all pregnancies [7], occurring between 1 in

140 and 1 in 300 of women with a pre-existing scar

[8]. The risk of uterine rupture increases with the

number of caesarean sections [9]. The perinatal mor-

tality is 10 times that of the maternal mortality [7].

Leung et al [6] evaluated 78 cases of uterine rupture

in a large tertiary care medical center and reported

significant neonatal morbidity when 18 minutes or

more elapsed between the onset of prolonged decel-

eration and birth. When the prolonged deceleration

was preceded by severe late or variable decelera-

tions, fetal asphyxia occurred as early as 10 minutes

from the onset of prolonged deceleration.


The sonographic findings of uterine rupture dur-

ing pregnancy include extrauterine blood collection,

fetal parts outside the uterine cavity, intra-amniotic

hemorrhage, and focal bulging of membranes through

the site of dehiscence [10]. In a recently published

study the authors raised numerous questions regard-

ing the significance of cesarean scar defects and the

ability of transvaginal ultrasound to predict the risk

of uterine rupture in women choosing trial labor after

cesarean section [11]. Transvaginal ultrasound dem-

onstrated a cesarean scar as an echogenic line through

the myometrium near the level of the internal os, and

a cesarean scar defect was present when there was

an anechoic area (fluid) within the scar. Women who

had prolonged labor before cesarean section were

more likely to show a cesarean scar defect, and so

were women who had multiple cesarean deliveries.

The researcher reported that real-time transvaginal

ultrasound was 87% sensitive and 100% specific

for detecting cesarean scars [11].

Abnormal placentation

Abnormal placentation in the form of placenta

accreta, percreta, or increta is a rare but potentially

life-threatening complication of pregnancy that is

an increasingly frequent cause of maternal morbidity

and mortality. The term refers to any placental im-

plantation resulting in abnormal adherence to the

uterine wall. Life-threatening hemorrhage can occur

at delivery because of failure of placental separation

from the uterine wall and occurs in about 40% of

cases. It is associated with significant maternal mor-

bidity and in rare cases maternal mortality [12].

Pathologically it occurs when the decidua basalis is

partially or totally absent in conjunction with an

imperfect development of Nitabuch’s membrane, a

fibrinoid layer that separates the decidua basalis

from the placental villi [13]. The placental villi are

in direct contact with the myometrium without in-

tervening endometrial decidua. Clark et al [14] dem-

onstrated the effect of previous cesarean section

deliveries on the incidence of placenta accreta. They

showed that the risk of placenta previa increases

proportionately with the number of previous cesarean

section deliveries (0.26% in an unscarred uterus, and

up to 10% in women with four or more previous

cesarean sections). Surgical intervention in the form

of total abdominal hysterectomy is often indicated

because of life-threatening hemorrhage at delivery,

secondary to failure of placental separation from

the uterine wall.


Placenta accreta can be diagnosed using gray-

scale and color Doppler sonography. Gray-scale

findings include loss of the normally visible retropla-

cental hypoechoic rim corresponding to the decidua

basalis and dilated venous vessels [12]. Progressive

thinning of the retroplacental hypoechoic zone on

serial examinations is an important clue (Fig. 1).

Multiple placental lakes that may represent dilated

vessels extending from the placenta through the myo-

metrium form the so-called ‘‘Swiss cheese’’ appear-

Fig. 1. Placenta accreta. Longitudinal color Doppler image

of placenta demonstrates thinning of the retroplacental

hypoechoic zone (arrowheads). Color flow Doppler ultra-

sound highlights areas of increased turbulent flow that

extend from the placenta into the surrounding uterine wall

and cervix (arrows).


ance of the placenta [15]. Depending on the location

of the implantation, the condition is referred to as

‘‘placenta accreta,’’ ‘‘placenta increta,’’ or ‘‘placenta

percreta.’’ If the placental villi extend beyond the

confines of the endometrium and attach to the super-

ficial aspect of the myometrium, the term ‘‘placenta

accreta’’ is used. Placenta increta refers to a situation

in which the villi invade the myometrium, whereas

the term ‘‘placenta percreta’’ is used if the villi ad-

vance into the serosa or parametria. Although this

classification scheme is widely accepted, most pub-

lished literature discusses these abnormalities collec-

tively as placenta accreta [16]. Doppler ultrasound

highlights areas of increased turbulent flow that

may extend from the placenta into the surrounding

uterine wall and cervix (see Fig. 1). Lerner et al [17]

reported a sensitivity of 100% and a specificity of

94% for the prenatal detection of placenta accreta

using color Doppler.

This technique also allows turbulent flow to be

visualized in cases of placenta percreta where placen-

tal vessels extend beyond the uterine serosa and may

involve other pelvic organs, such as the bladder.

Chou et al [18] have described the following findings

associated with placenta accreta: dilated vascular

channels with diffuse lacunar flow, irregular vascular

lakes with focal lacunar flow, hypervascularity linking

the placenta to the bladder, dilated vascular channels

with pulsatile venous flow over cervix, and poor

vascularity at sites of loss of hypoechoic zone.

Placenta previa

Placenta previa occurs in approximately 1 in

200 to 250 pregnancies and is associated with po-

tentially serious consequences from hemorrhage,

abruption of the placenta, or emergency cesarean

delivery. Abruption of the placenta occurs 14 times

more frequently in pregnancies with placenta previa

than in normal pregnancies, and cesarean delivery

occurs four times more frequently because of the

potentially serious consequences of persistent pla-

centa previa at delivery. There are three types of

placenta previa: (1) marginal previa where the edge

of the placenta is less than 2 cm from the opening

of the cervix, (2) partial placenta previa where the

placenta partly covers the cervical opening, and

(3) total previa where the placenta completely covers

the cervical os (Fig. 2A).

Marginal placenta previa is also known as ‘‘low-

lying’’ placenta. The natural history of marginal

placenta previa was studied by Rizos et al [19].

Placental localization by diagnostic ultrasound was

performed at 16 to 18 weeks’ gestation in 1098 pa-

tients before amniocentesis for genetic indications.

Marginal placenta previa was diagnosed in 58 pa-

tients, 47 of whom went on to delivery uncompli-

cated by placenta previa. There were five patients

with placenta previa at delivery, four of whom had

third-trimester bleeding. One patient was diagnosed

as having a normal placental implantation at mid-

trimester but placenta previa was demonstrated at

delivery. The incidence of placenta previa at 16 to

18 weeks’ was 5.3% and fell to 0.58% at delivery,

indicating a 90% conversion rate. This conversion

occurs secondary to rapid growth of lower uterine

segment in the third trimester resulting in superior

migration of placenta relative to the internal cervical

os. Most cases of asymptomatic low-lying placenta

convert to normal location of the placenta before

delivery. The authors concluded that these patients

should be observed with serial ultrasound studies at

6- to 8-week intervals until delivery or unequivocal

conversion. They also recommended no restriction

in activity unless the placenta previa persists beyond

30 weeks or becomes clinically manifest [19].

Traditionally, transabdominal study is used to

document sagittal midline images of the lower uter-

ine segment and cervix, preferably with a full bladder

to document the presence of placental tissue extend-

Fig. 2. Placenta previa. (A) Transvaginal sonographic view at 10 weeks gestation reveals the placenta completely covering the

internal cervical os. (B) Transabdominal view of the same case at 34 weeks gestation. The placenta covers the entire internal

cervical os. The retroplacental hypoechoic zone is invisible in the lower uterine segment adjacent to the cervix also suggesting

placenta accrete (arrows).


ing down to the region of the cervix (Fig. 2B). Be-

cause of concerns regarding the use of transvaginal

study in patients with vaginal bleeding, possibly as a

result of placenta previa, translabial (transperineal)

study has been suggested as an alternative to trans-

abdominal study [20].

Farine et al [21] compared the accuracy of the

diagnosis of placenta previa using transvaginal so-

nography with that of the traditional transabdominal

sonography. They concluded that transvaginal sonog-

raphy was superior to transabdominal sonography in

diagnosing placenta previa and invariably correct in

ruling it out. Timor-Tritsch and Yunis [22] confirmed

the safety of transvaginal sonography in patients

suspected of placenta previa. They concluded that

the angle between the cervix and vaginal probe is

sufficient to prevent the probe from inadvertently

slipping into the cervix and initiating or further

aggravating vaginal bleeding.

Placental abruption

Third-trimester placental abruption complicates

less than 1% of pregnancies but is associated with

increased risk of preterm delivery and fetal death

when it does occur [23]. The clinical diagnosis is

usually based on bleeding, abdominal pain, and con-

tractions, but sonography is often performed to visu-

alize the extent of subchorionic or retroplacental

hematoma (Fig. 3). The diagnostic sensitivity for

abruption has not improved despite significant

improvements in ultrasound technology. Only one of

every nine sonograms obtained to rule out placental

abruption revealed evidence of a subchorionic or

retroplacental hematoma [23]. Ultrasound study

performed specifically to document placental abrup-

tion is usually unremarkable and is positive in only

25% of cases of placental abruption that are con-

firmed at delivery [24]. These researchers noted that

there were no significant differences in clinical char-

acteristics between women with positive or negative

sonographic findings. They concluded that sonogra-

phy is not sensitive for detecting abruption, but

when a clot is visualized on sonography, the positive

predictive value for abruption at delivery is high.

They also noted that the shorter the scan-to-delivery

interval, the greater the positive predictive value.

When delivery occurred within 2 weeks of a positive

sonographic finding, the diagnosis of placental abrup-

tion was confirmed in 100% of cases. Given that

sonography is not a sensitive tool to diagnose pla-

cental abruption, sound clinical judgment suggests

that even if the placenta appears grossly normal, a

diagnosis of abruption should be considered when

vaginal bleeding, abdominal pain, and uterine hyper-

tonicity are present.

Fig. 3. Placental abruption. (A) Retroplacental blood clot (arrows). (B) Large blood clot resulting from placental abruption

occupying most of the fundal region of the uterus. Hyperechoic and hypoechoic irregular areas are seen within the clot (arrows).

segment (arrows).


Vasa previa

Despite dramatic improvements in diagnosis of

maternal, fetal, and placental abnormalities vasa

previa remains a true diagnostic challenge and con-

tinues to be a fatal condition for the fetus. For many

years even following the introduction of ultrasound

technology the diagnosis was made only after the

membranes were ruptured and fetal exsanguina-

tion occurred.

Vasa previa is a condition in which vessels run

through the membranes below the presenting part,

running over, or in close proximity to, the internal

cervical os, unsupported by placenta or cord (Fig. 4)

[25]. Spontaneous or artificial rupture of the mem-

branes in labor often leads to fetal exsanguination,

with mortality approaching 100%. With a high index

(C) A second blood clot is seen in the anterior lower uterine

of suspicion, however, vasa previa can be diagnosed

prenatally using ultrasound and color Doppler, allow-

ing for elective delivery by cesarean section before

membrane rupture with almost universal fetal sur-

vival [25]. Fung and Lau [26], Oyelese et al [27], and

Lee et al [28] showed that a good outcome in vasa

previa depended entirely on antenatal diagnosis

of the condition by ultrasound. Screening all patients

for vasa previa is time consuming and unnecessary

because of low incidence. Documentation of placen-

tal cord insertion, however, should be part of any

detailed obstetric sonographic examination. Recently

Fung and Lau [26] and Oyelese et al [27] indepen-

dently concluded that a low-lying placenta in the

second trimester was the most important risk factor

for vasa previa at term, whether or not the placenta

subsequently remained low-lying at term. Other risk

Fig. 4. Vasa previa. The placenta is posterior in location

with marginal previa. The vessels (red and blue) commu-

nicate with an accessory placental lobe implanted on the left

anterior lower uterine segment. Arrow points to the cervix.

Fig. 5. Retained products of conception. An echogenic area

(calipers) representing placental tissue, debris, and blood is

present in the endometrial cavity following manual removal

of the placenta. Patient underwent dilation and curettage for

continued uterine bleeding. The arrows point to retained

products of conception still present subsequent to the

dilation and curettage.


factors for vasa previa include multiple pregnancies,

pregnancies resulting from in vitro fertilization, and

those with succenturiate lobe and bilobed placen-

tae [25]. In all such pregnancies it is prudent to

examine the region overlying the internal cervical

os for evidence of vessels running over it.

Postpartum hemorrhage

Obstetric delivery has been associated with the

potential for acute, massive blood loss to a degree

unparalleled by other surgical procedures. Data from

the Maternal Mortality Collaborative in 1988 indicate

that hemorrhage was responsible for 11% of direct

maternal deaths occurring in 1980 through 1985 [29].

No other condition in obstetrics, except perhaps

shoulder dystocia, requires such rapid recognition

and skillful response by the clinician to prevent

loss of life.


The sonographic findings of retained placental

tissue are often nonspecific because blood clots and

retained products feature considerable overlap in

sonographic appearance. In the first and early second

trimester on transabdominal or transvaginal views

of the endometrial cavity, thickened hyperechoic

endometrial stripe greater than 5 mm, gestational

sac (with or without a nonliving embryo), and round

to ovoid fluid sac are suggestive of retained prod-

ucts. If the endometrial stripe is less than 5 mm,

especially if it is less than 2 mm, retained blood in

the endometrial cavity is more likely than retained

products of conception.

Hertzberg and Bowie [30] reviewed the ultra-

sound images of 53 postpartum patients referred for

possible retained products of conception and corre-

lated specific ultrasound patterns with clinical and

pathologic follow-up. The most common finding in

patients with retained placental tissue was an echo-

genic mass in the uterine cavity, seen in 9 of

11 patients with pathologically proved retained pla-

cental tissue. In the remaining two patients with

pathologically confirmed retained placenta, a hetero-

geneous mass was seen in the uterine cavity some-

time during the course of serial sonography. Retained

placental tissue was found unlikely when ultrasound

demonstrated a normal uterine stripe endometrial

fluid, or hyperechoic foci in the uterine cavity with-

out an associated mass. The latter finding often was

associated with recent uterine instrumentation. The

sonographic appearance of retained placental tissue

was shown to be variable, but detection of an echo-

genic mass in the uterus strongly supported the

diagnosis. The authors concluded that solid echogenic

masses in the lumen or uterine wall are the most

specific findings for a retained placenta, whereas

heterogeneous mass could be caused by retained pla-

centa or from blood clots or infected or necrotic ma-

terial in the absence of placental tissue [30]. The


authors suggested that sonographic evaluation for

retained products of conception is best performed

before uterine instrumentation to avoid confusion

with iatrogenically introduced air. An example of

retained products following term vaginal delivery is

illustrated in Fig. 5.

Di Salvo [10] noted anecdotally that low-resist-

ance Doppler signals in these masses also can be

predictive. When using Doppler sonography in this

setting, however, it is important not to confuse low-

resistance arterial signals that arise within the myo-

metrium, which represent the placental implantation

site, with similarly appearing Doppler signals arising

from tissue within the endometrial cavity, which

represent retained products [10].

Retained products of conception

A spontaneous abortion is the loss of a fetus dur-

ing pregnancy because of natural causes. The term

‘‘miscarriage’’ is the spontaneous termination of a

pregnancy before fetal development has reached

20 weeks. The term ‘‘spontaneous abortion’’ refers

to these naturally occurring events, not elective or

therapeutic abortion procedures. More specific terms

include missed abortion (a pregnancy demise where

nothing is expelled); incomplete abortion (not all of

the products of conception are expelled); complete

abortion (all of the products of conception are ex-

pelled); threatened abortion (symptoms indicate a

miscarriage is possible); inevitable abortion (the

symptoms cannot be stopped and a miscarriage will

happen); and infected abortion. Any one of these

conditions might be associated with some degree of

vaginal bleeding. The bleeding in incomplete abor-

tion in which parts of the fetus or placental material

are retained within the uterus might be associated

with significant blood loss, however, and mandate

surgical intervention in the form of uterine curettage

to remove the remaining material from the uterus [31].

In the last decade with the introduction of mife-

pristone (RU 486) and oral or vaginal misoprostol to

induce abortion in the first trimester, vaginal bleeding

secondary to retained products of conception became

more common [32]. Studies clearly establish miso-

prostol as an effective agent to ‘‘empty’’ the pregnant

uterus in the first trimester [33]. Chia and Ogbo [32]

showed medical evacuation of missed abortion with

misoprostol to be an effective, safe, and cost-effective

alternative to surgical evacuation of the uterus, and

particularly suited for women not desiring hospital

admission or a surgical procedure under general

anesthesia [32]. Misoprostol is a synthetic prostaglan-

din E1 analogue. It was developed and marketed for

prevention of peptic ulcer disease caused by prosta-

glandin synthetase inhibitors, but with its potent

uterotonic and cervical ripening activity has found

applications in the management of gynecologic and

obstetric problems. In the United States it has been

marketed as Cytotec, in 100- and 200-mg tablets. Simi-

lar effectiveness has been shown when it is given

for a ‘‘failed’’ pregnancy or missed abortion [34,35].

Potential hypertonus as a result of drug accumu-

lation has been associated with uterine rupture in the

second or third trimester, and retained products of

conception with significant bleeding [36]. Transvagi-

nal sonography is a useful supplement to the clinical

assessment in women who experience a spontaneous

first-trimester abortion. Its use results in reduction

of unnecessary general anesthesia and uterine curet-

tage. Wong et al [37] showed that a first-trimester

vaginal ultrasound study has a sensitivity and speci-

ficity of 100% and 80%, respectively, using a bilayer

endometrial thickness of 8 mm or less. The ultra-

sound findings suggesting retained products of con-

ception are a thickened endometrium of greater than

8 mm; complex hyperechogenic (blood and tissue

debris) and hypoechogenic fluid material inside the

endometrial cavity; a gestational saclike structure; or

a space-occupying collection.

Uterine fibroids

Fibroid tumors are benign growths that develop

in the muscular wall of the uterus. Although fibroids

do not always cause symptoms, their size and loca-

tion could lead to complications during pregnancy for

some women including recurrent miscarriage, infer-

tility, premature labor, fetal malpresentations, and

complications of labor [38]. Lev-Toaff et al [39]

reported their ultrasound findings of uterine fibroids

during pregnancy. Fibroid size changes were ana-

lyzed on the basis of trimesters. In the second tri-

mester, smaller fibroids increased in size, whereas

larger fibroids decreased in size. In the third trimester,

a decrease in size was documented regardless of

initial size.

The most common patterns of echotexture were

hypoechoic, heterogeneous, and echogenic rim. The

development of a heterogeneous pattern or anechoic-

cystic spaces on a follow-up study was accompa-

nied by severe abdominal pain. The development

of these patterns apparently indicates significant

degeneration of the fibroid (Fig. 6). Fibroids located

in the lower uterine segment were accompanied by

a higher frequency of cesarean section and retained

placenta. Fibroids located in the uterine corpus were

Fig. 6. Color flow Doppler of uterus demonstrates a poste-

rior lower uterine segment degenerating fibroid. The

heterogeneous pattern with anechoic-cystic spaces suggests

degeneration process within the fibroid. A ‘‘feeding’’ ves-

sel can be seen between the myometrium and the fi-

broid (arrow).

Fig. 7. Gray-scale ultrasound longitudinal view shows a

posterior lower uterine segment fibroid undergoing degen-

eration. The patient experienced premature uterine con-

tractions starting at 29 weeks and delivered prematurely at

31 weeks by cesarean section secondary to lower uterine

segment obstruction from the fibroid. Arrowhead points to

the internal cervical os and calipers depict the whole length

of the cervix.


more frequently associated with early abortions.

Multiple fibroids were accompanied by a higher

frequency of malpresentation and premature con-

tractions compared with cases with one or two

fibroids (Fig. 7) [39].

Abdominal surgery and trauma during pregnancy

Emergency surgery is indicated during pregnancy

for the management of trauma, malignancy, or acute

medical illness. Women in the childbearing years

are among the population at greatest risk for trauma.

Trauma occurs in 5% to 10% of pregnancies and is

responsible for 36 maternal deaths per 100,000

pregnancies, which is considerably higher than preg-

nancy-related mortality [40]. Penetrating abdominal

injury from gunshot and knife wounds or associated

with motor vehicle accidents results in 5% maternal

mortality. A much higher perinatal death rate in the

range of 41% to 71% is reported [41]. Fetal death

can be the result of maternal instability, placental

abruption, direct fetal injury and hemorrhage, or as a

consequence of premature delivery. The fetal status

must be assessed carefully for evidence of develop-

ing compromise. Monitoring fetal heart rate is an

important aspect of these procedures, and is techni-

cally feasible after the 16th week for nonabdominal

surgery. The surgeon and obstetrician alike must be

aware that fetal heart rate monitoring helps guide the

management of maternal cardiorespiratory parame-

ters, and is useful even if it does not influence a

decision to deliver the fetus [42]. Anesthetic drugs

create loss of heart rate variability, presumably by

anesthetizing the brainstem center that modulates

intrinsic cardiac automaticity. In addition, vasoactive

agents cross the placenta and produce predictable

changes to fetal heart rate and further influence the

interpretation of the fetal tracing, rendering fetal

heart rate monitoring through the use of standard

external Doppler probes useless. In many similar

challenging cases, the use of real-time ultrasound

and color Doppler adds valuable data to assess the

fetal status. Intermittent abdominal real-time ultra-

sound assessment of the fetus and placenta can be

used for abdominal procedures that do not permit

the use of standard external Doppler probes by

covering the ultrasound transducer with a sterile

sleeve. Abrupt changes in heart rate, baseline rates

outside the acceptable range of 120 to 160 beats per

minutes, and abnormal Doppler readings of the fetus

or the placental vasculature should prompt the

anesthesiologist to look for obvious causes of ute-

roplacental insufficiency.

Maternal nonobstetric emergencies during

pregnancy

Venous thromboembolism

Venous thromboembolism occurs infrequently

during pregnancy. It is a leading cause of illness

and death during pregnancy and the puerperium and


remains a diagnostic and therapeutic challenge [43].

In the general population the incidence of pregnancy-

associated venous thromboembolism has been esti-

mated to vary from 1 in 1000 to 1 in 2000 deliveries

[43]. The risk of venous thromboembolism is five

times higher in a pregnant woman than in a nonpreg-

nant woman of similar age. Postpartum venous

thromboembolism is more common than antepartum

venous thromboembolism [43]. Women with congen-

ital thrombophilic abnormalities, such as mutations

within factor II or V of the coagulation factors,

mutations leading to deficiency of protein S, or

protein Cor persistent presence of antiphospholipid

antibodies have an increased risk of venous throm-

boembolism during pregnancy and the puerperium. In

individuals with well-defined hereditary thrombosis

risk factors, such as the factor V:R506Q mutation, the

factor II:G20210A mutation, antithrombin deficiency,

or protein C deficiency, a relative risk of pregnancy-

associated venous thromboembolism between 3.4 and

15.2 has been found [43]. Women with previous

venous thromboembolism have an approximately

3.5-fold increased risk of recurrent venous thrombo-

embolism during pregnancy compared with nonpreg-

nant periods [43].

Pelvic thrombophlebitis

Pelvic thrombophlebitis is considered to be a rare

disorder of the puerperium with an incidence of

0.05% to 0.18% [44]. The ovarian veins are the most

frequently involved veins in puerperal pelvic venous

thrombosis. The clinical manifestations of the condi-

tion range from asymptomatic or dull abdominal pain

to sepsis, pulmonary embolism, and even death.

Unremitting fever and lower-quadrant or flank pain

usually occurs within the first 1 to 2 days after

delivery [45]. An abdominal mass is palpable in

about half of the patients, which may lead to the

suspicion of acute appendicitis. Torsion of the ovar-

ian pedicle, broad ligament hematoma, and pelvic

abscess may also occur. This condition is usually

managed conservatively, with intravenous heparin

and antibiotics, and rarely surgically. Imaging mo-

dalities used in the diagnosis include sonography, CT,

and MR imaging [44].

Gallbladder disease

Gallbladder disease is four times as common in

women as in men, and pregnancy seems to contribute

to the development of gallstones [46]. The symptoms

of gallbladder disease during pregnancy do not differ

from those reported for the nonpregnant population

and include steady, severe pain in the upper abdomen

that increases rapidly and lasts from 30 minutes to

several hours, pain in the back between the shoulder

blades, pain under the right shoulder, nausea or

vomiting, abdominal bloating, recurring intolerance

of fatty foods, belching, and indigestion. Ultrasound

scans are highly sensitive to the detection of gall-

stones. Sonographic findings with biliary disease

include gallstones, sludge, wall thickening, the sono-

graphic Murphy’s sign, biliary dilatation, and ductal

stones [47]. In a study done in Dublin, Ireland, real-

time ultrasound scanning was used to examine the

pelvic area and the upper part of the abdomen in a

prospective study of 512 healthy, pregnant women to

determine the prevalence of gallstones [47]. Twenty-

three women (4.5%) had gallstones. Fourteen

(60.9%) of the pregnant women were unaware of

the presence of gallstones. Ultrasound technique was

shown as the modality of choice to diagnose gall-

bladder disease in the parous and nonparous state

including acute gallbladder disease [46]

Acute renal disorders

Acute renal failure has become a rare complica-

tion of pregnancy [48]. This is the result of the

significant decline of septic abortion and its related

complications; the improvement of prenatal care; the

prevention of volume contraction, which is mainly

caused by uterine hemorrhage; early diagnosis; and

the treatment of other classic maternal complications,

such as preeclampsia and acute pyelonephritis [48].

The incidence of bilateral renal cortical necrosis has

also been declining during the last decade. Acute

fatty liver, a potentially fatal disease, often is com-

plicated by acute renal failure [48].

Ultrasound often is the first imaging technique

to be used in patients with renal failure, hematuria,

or proteinuria. Gray-scale ultrasound evaluation,

color flow Doppler, and resistive indices provide

adequate renal evaluation. In the initial clinical stages

of renal parenchymal diseases, the kidneys may

present normal ultrasound appearance and normal

resistive indices values. Different renal parenchymal

diseases may reveal similar appearance on ultrasound

and Doppler ultrasound evaluation [48]. Percutane-

ous renal biopsy is often necessary to reach definite

diagnosis. Renal vasculitides and tubular-interstitial

nephropathies are identified more frequently by

gray-scale ultrasound and Doppler ultrasound than

glomerular nephropathies, because glomerular com-

ponent accounts only for 8% of the renal paren-

chyma, whereas the highest percentage is occupied

by vascular and tubulointerstitial component [48].


Follow-up of acute renal failure, during and after

medical treatment, is the most useful field of use of

gray-scale ultrasound and Doppler ultrasound techni-

ques, because a progressive lowering of resistive

indices is correlated to a progressive recovery of

renal function [48].

Hydronephrosis in pregnancy occurs in more than

80% of pregnancies and begins as early as 11 to

15 weeks [49]. The dilatation of the ureters in the

early months of pregnancy is probably caused by

atony of the neuromuscular apparatus, but what un-

derlies this is not clear. The cause of the later dilata-

tion of the abdominal segment of the right ureter

and renal pelvis is a somewhat controversial sub-

ject. It is believed to be caused by pressure on the

right ureter at the pelvic brim by the natural inclina-

tion to the right of the enlarged uterus, whereas the

left ureter is protected by the rectosigmoid.

Urolithiasis during pregnancy is a difficult clinical

problem in which carefully selected radiologic stud-

ies play an essential role. It has been shown that

sonography, particularly Doppler sonography, plays

a major role in the diagnosis of urolithiasis in preg-

nancy [49]. Studies evaluating the intrarenal resistive

index in asymptomatic pregnant patients have shown

that both right and left kidneys have similar resistive

indices, and there is no change in resistive indices

during pregnancy [50]. In the absence of underlying

renal disease, however, a difference of greater than

0.1 in resistive indices should prompt further sono-

graphic confirmation of mechanical ureteral obstruc-

tion. This includes unilateral absence of a distal

ureteral jet or direct visualization of a stone either

at the ureterovesical or ureteropelvic junction [10].

Unilateral absence of a ureteral jet with the patient

supine should always be confirmed by re-evaluation

with the patient in the contralateral decubitus posi-

tion, because the cause of the absent jet may merely

be compression of the ureter by the uterus rather than

an obstructing calculus [51].

Splenic artery aneurysm

Splenic artery aneurysm occurs predominantly in

women and most of the aneurysms are asymptomatic

until rupture [52]. Over half of those that rupture

occur during pregnancy or in women who have had

children. Rupture during pregnancy is associated

with a very high maternal and fetal mortality rate

[52]. Although this condition is uncommon, good

maternal-fetal outcome can only be achieved by early

diagnosis and prompt treatment. Ordinarily, in sus-

pected unruptured splenic artery aneurysm the gold

standard for diagnosis is arteriography [53]. Ultraso-

nography and pulsed Doppler, however, are prefera-

ble in pregnancy [54]. Gray-scale sonography might

fail to detect the unruptured splenic artery aneurysm

if marked calcification of the aneurysmal wall is

present [54]. Pulsed Doppler sonography has been

used to document turbulent pulsatile flow along the

aneurysmal wall. When patients with ruptured splenic

artery aneurysm present with acute abdominal pain,

an emergency ultrasound scan may reveal free fluid

in the upper abdomen and the diagnosis is subse-

quently confirmed at laparotomy [54].

Summary

Most complications of pregnancy allow time for

transfer to specialized obstetric ultrasound units, but

many women present to the emergency room or the

labor and delivery unit with signs and symptoms

suggesting genuine acute medical emergencies,

where successful outcome depends on prompt diag-

nosis of the disorder and rapid appropriate medical

management. The use of ultrasound technology in

obstetric emergencies is well established. Ultrasonog-

raphy plays a major role in such cases as the most

important tool clinicians are using to identify the

correct etiology and diagnosis, whereas in other cases

it helps limit the differential diagnosis. One of the

goals of any advanced training program in obstetrics

and gynecology and radiology is to allow the skilled

physician to perform the proper ultrasound study in

case of an obstetric emergency to facilitate the proper

diagnosis, enabling the medical team to provide the

best possible care.

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Radiol Clin N Am 42 (2004) 329–348

Adnexal mass with pelvic pain

Emily M. Webb, MD, Gretchen E. Green, MD, Leslie M. Scoutt, MD*

Department of Diagnostic Radiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA

The routine use of ultrasound (US) in the evalua- and unnecessary surgery can be avoided, to the

tion of pregnant patients has resulted in more fre-

quent detection of adnexal masses, which occur in

approximately 2% of pregnancies. This estimation in-

cludes masses with a wide variety of appearances

and etiologies that range from asymptomatic ovarian

cysts to surgical emergencies, including ovarian tor-

sion, ectopic pregnancy, and tubo-ovarian abscess [1].

Although many adnexal masses are detected inciden-

tally, this article focuses on the evaluation of preg-

nant women who present with an adnexal mass in

the setting of acute pelvic pain. Clinical diagnosis in

pregnancy is a challenge because the differential di-

agnosis for an adnexal mass that presents with pelvic

pain is broad and includes pregnancy-related and

unrelated causes. The clinical presentation and natu-

ral history of abdominal and pelvic disease may be

altered in pregnancy. US is an ideal tool for evaluating

a pregnant patient. It is excellent in defining pelvic

anatomy and pathology without the risks of ionizing

radiation inherent to many imaging techniques.

Pregnancy-related disease

Several disease processes, either specific to preg-

nancy or with an increased incidence in pregnant

patients, can cause acute pelvic pain and an associ-

ated adnexal mass. These disease processes vary

from benign, often asymptomatic entities to diseases

that require emergent treatment. Differentiation is

critical so that appropriate treatment can be provided


doi:10.1016/j.rcl.2003.12.006



(L.M. Scoutt).

benefit of mother and fetus.

Follicular cysts and corpus luteal cysts

Most adnexal masses identified during pregnancy

are non-neoplastic, physiologic cysts, including cor-

pus luteal cysts and follicular cysts. These cysts can

be seen in early pregnancy but usually involute by

midterm [1]. Follicular cysts vary in size from 3 to

8 cm in diameter. They result from failure in ovu-

lation, most likely secondary to changes in the re-

lease of pituitary gonadotropins. The fluid contained

within the immature follicle is not completely re-

absorbed, which produces an enlarged follicular cyst

[2]. On US examination, a follicular cyst should ap-

pear as a thin-walled, anechoic, round, or oval struc-

ture that demonstrates increased through transmission

(Fig. 1). After ovulation has occurred from a mature

follicle, the granulosa cells, which line the follicle,

become luteinized. Blood accumulates in the central

cavity during vascularization and then resorbs to form

the corpus luteum [2]. The corpus luteum is described

as a cyst when it reaches more than 2.5 to 3 cm [2].

Corpus luteal cysts are typically thin-walled, uni-

locular cysts that can range in diameter from approxi-

mately 3 to 11 cm [2]. The corpus luteum can have

a wide range of appearances on US in the first tri-

mester of pregnancy, however. The most common ap-

pearance is that of a round, thin-walled hypoechoic

structure that demonstrates diffuse, homogenous, low-

level echoes (Fig. 2) [3]. Other reported gray scale

appearances in order of decreasing frequency include

a cyst with a thick wall and anechoic center (Fig. 3), a

cyst that contains scattered internal echoes, or a thin-

walled simple cyst that is similar in appearance to

a follicular cyst [3]. In most cases, color Doppler

s reserved.

Fig. 1. Simple ovarian or follicular cysts. These two ovarian

cysts are completely anechoic, with thin, nearly impercep-

tible walls (arrow), and they demonstrate increased through

transmission (arrowheads).

Fig. 3. Atypical corpus luteal cyst. This exophytic cyst has

an anechoic center with a thick, relatively hypoechoic wall

(arrow) with a thin rim of vascularity. Although it may be

difficult to differentiate such a structure from an ectopic

pregnancy, in general the wall of an ectopic pregnancy is

more echogenic and usually not so thick.

E.M. Webb et al / Radiol Clin N Am 42 (2004) 329–348330

evaluation of the corpus luteum demonstrates a cir-

cumferential ‘‘ring of fire’’ of vascularity with a low

resistance waveform pattern. In a study by Durfee

and Frates [3], 92% of corpus luteal cysts demon-

strated this pattern of blood flow with a mean resist-

ance index of 0.49 and mean peak systolic velocity of

17 cm/second.

Acute pelvic pain in pregnancy is commonly

caused by hemorrhage into a follicular or corpus

luteal cyst. Cyst rupture or leakage also may cause

severe pelvic pain and hemorrhage, sometimes re-

quiring laparoscopy or laparotomy [2,4]. The US

appearance of hemorrhagic ovarian cysts varies be-

cause the US characteristics of hemorrhage change

over time [4–7]. Initially a hemorrhagic cyst dem-

onstrates a diffuse, homogeneous pattern of low-

Fig. 2. Corpus luteal cyst. This exophytic corpus luteal cyst

contains low-level internal echoes. The cyst wall is mark-

edly vascular on color Doppler evaluation, which dem-

onstrates ring of fire (arrows).

level echoes. The wall may be vascular but should

be thin and regular. In a study by Baltarowich et al

[6], most hemorrhagic cysts (92%) demonstrated

increased through transmission. Over time as the clot

forms, a lace-like, reticular pattern of internal echoes

develops because of the presence of fine fibrous

Fig. 4. Hemorrhagic cyst. Note lace-like or spider web

pattern of internal echoes. The cyst wall is smooth and

regular. Increased through transmission is present. Doppler

interrogation reveals no evidence of internal blood flow,

and the appearance changes over time as the blood clot

continues to resorb.

Fig. 5. Hemorrhagic cyst. Clot within a hemorrhagic cyst

often adheres to the cyst wall and is lenticular in shape

(arrow). Doppler examination does not demonstrate internal

vascularity within adherent clot but may do so in a neo-

plastic mural nodule. Despite the absence of vascularity on

this color Doppler image, follow-up imaging in 6 weeks is

recommended to ensure that the clot continues to resolve.

Occasionally Doppler interrogation does not demonstrate

vascularity in tumor nodules because of low velocity, low

volume flow, or sampling error.

E.M. Webb et al / Radiol Clin N Am 42 (2004) 329–348 331

septae (‘‘fish net’’) (Fig. 4). The clot may appear as

an echogenic mass either mobile or adherent to the

cyst wall but without evidence of vascularity. Typi-

cally, the clot retracts over time and adheres to the

cyst wall in a lenticular shape (Fig. 5). Lysis of red

blood cells may result in layering fluid or debris.

Follow-up examination at a 6- to 8-week interval

should demonstrate that a hemorrhagic cyst changes

in appearance and decreases in size [7]. In patients

with rupture or leakage of fluid from the corpus luteal

cyst, the cyst may have an angular or crenated

appearance, and free fluid that contains low-level

echoes or frank clots may be observed in the cul-

de-sac or surrounding the ovary [2,7].

Box 1. Conditions that predispose toectopic pregnancy

� Prior pelvic inflammatory disease� Presence of an intrauterine device� Treatment of infertility� Tubal surgery� Previous ectopic pregnancy� Diethylstillbestrol exposure

Ectopic pregnancy

The incidence of ectopic pregnancy has increased

over the past three decades, and it recently reached a

plateau at a reported rate of 19.7 per 1000 pregnan-

cies [8]. Ectopic pregnancy remains the leading cause

of maternal death in the first trimester and the second

leading cause of maternal mortality overall [8]. Im-

proved treatments for infertility and pelvic inflam-

matory disease and an increase in the size of the

patient population at risk for ectopic pregnancy in

large part account for the increased incidence. Other

risk factors include presence of an intrauterine device,

exposure to diethylstilbestrol, adhesions from prior

surgery, and previous ectopic pregnancy (Box 1).

The reported increased incidence of ectopic preg-

nancy is also likely in part accounted for by an

‘‘apparent’’ increase because of early US evaluation

of symptomatic pregnant patients. Endovaginal US

almost certainly documents some early ectopic preg-

nancies that otherwise would have resolved without

coming to medical attention. Endovaginal US, com-

bined with quantitative b-human chorionic gonado-

tropin (b-HCG) analysis, is an excellent tool for

identifying ectopic pregnancy and differentiating

from other causes of adnexal mass in the pregnant

patient with pelvic pain. The first goal of endovaginal

US in the patient suspected of harboring an ectopic

pregnancy is to assess for an intrauterine pregnancy

because ectopic pregnancy can be reasonably ex-

cluded when an intrauterine pregnancy is identified

[9]. Only rarely does an ectopic pregnancy occur

synchronously with an intrauterine gestation. Hetero-

topic pregnancy is estimated to occur in only 1 in

2600 to 1 in 30,000 pregnancies in the general

population [10], but it likely occurs in up to 1 in

100 in patients with multiple risk factors who are

undergoing infertility treatment [11].

An intrauterine gestational sac should be seen

on endovaginal US when the b-HCG is more than

2000 mIU/mL (approximately 4–6 weeks’ gestation).

The earliest positive sign of an intrauterine pregnancy

is the intradecidual sign, which is defined as a fluid

collection with an echogenic rim located eccentrically

within either the anterior or posterior layer of the

endometrium adjacent to the echogenic line that

represents the endometrium [12,13]. The intradecid-

ual sign should be visible at 4.5 weeks’ gestation, but

it can be confused with a pseudosac or decidual cyst.

A study reported by Laing et al [12] demonstrated a

low enough sensitivity and specificity to warrant a

recommendation to document the development of

a yolk sac or fetal pole on follow-up examination to

Fig. 7. Ectopic pregnancy. Note echogenic tubal ring

(arrow) medial to the right ovary (cursors). Amorphous

hypoechoic material between ovary and ectopic pregnancy

likely represents hemorrhage.


confirm an intrauterine pregnancy. The double decid-

ual sac sign is formed when the gestational sac is

surrounded, at least in part, by two echogenic

layers—decidual capsulans (inner) and decidual parie-

talis (outer)—and is separated by the hypoechoic

endometrial cavity [9]. It should be seen when the

mean sac diameter is more than 10 mm. Because

endovaginal US (when using a high-frequency trans-

ducer) typically demonstrates a yolk sac with an

intrauterine pregnancy by the time the mean sac

diameter (MSD) is more than 8 mm, the double

decidual sign is of limited use in the evaluation of

patients with suspected ectopic pregnancy. The pres-

ence of trophoblastic flow (high velocity, low imped-

ance) around an endometrial fluid collection further

supports the diagnosis of an intrauterine pregnancy,

although pulsed Doppler should be used with caution

because of concerns regarding heat deposition in the

developing fetus.

A pseudosac, an intrauterine fluid collection

formed in response to hormonal influences on the

endometrium as the result of the presence of an

ectopic pregnancy, can be distinguished from an

intrauterine pregnancy by its central location in the

endometrial cavity, oval shape, poorly defined mar-

gins, absence of decidual reaction, single decidual

layer, and absence of trophoblastic flow.

Ectopic pregnancy most commonly (95%) occurs

in the ampullary or isthmic portions of the fallopian

tube. An ectopic pregnancy can be diagnosed with

confidence when an adnexal mass that contains a

yolk sac or viable embryo is identified (Fig. 6) [14].

In the absence of a visualized yolk sac or fetal pole,

the so-called echogenic adnexal (or tubal) ring sign

Fig. 6. Ectopic pregnancy. A yolk sac (arrow) and fetal pole

(arrowhead) are present within this echogenic tubal ring

(curved arrow) located in the cul de sac. U, uterus. Note that

the wall or ring of this ectopic pregnancy is much more

echogenic than the wall of the corpus luteal cyst in Fig. 3.

is the next most specific US finding for ectopic

pregnancy (Fig. 7) [15]. Adnexal rings are usually

located between the ovary and uterus. In 14% to 33%

of cases, the adnexal ring is contralateral to the cor-

pus luteum [16]. The echogenic adnexal ring typi-

cally has a relatively anechoic center and vascular

wall (sometimes only focally). It may be difficult to

differentiate the tubal ring of an ectopic pregnancy

from an exophytic corpus luteal cyst. An anechoic

structure with an echogenic, vascular rim truly lo-

cated within the ovary is statistically much more

likely to be a corpus luteal cyst, because true intra-

ovarian ectopic pregnancies are rare.

Frates et al [17] reported that the wall of the

adnexal ring is more echogenic compared with the

ovarian stroma in 88% of ectopic pregnancies, where-

as the wall of the corpus luteal cyst was usually

relatively hypoechoic. Corpus luteal cysts and ectopic

pregnancy demonstrate low-resistance arterial flow

on Doppler examination [18]. Color Doppler is

helpful primarily for increasing conspicuity. Differ-

entiation between an ectopic pregnancy and an

exophtic corpus luteal cyst can be aided by gently

tapping on the ovary with the transducer. Independent

movement of the ovary indicates an extraovarian

location of the adnexal ring, which confirms ectopic

pregnancy. A hemorrhagic ovarian cyst occasionally

can produce an adnexal ring sign, and when associ-

ated with significant hemoperitoneum, it may mimic

ectopic pregnancy [19].

Evaluation of the cul-de-sac and Morrison’s pouch

is important to detect echogenic fluid that could

represent blood (Fig. 8) [20]. Transabdominal US is

particularly helpful for evaluation of these areas and

visualization of the patient’s point of maximal ten-

derness if not imaged on endovaginal US. Blood need

Fig. 8. Hemoperitoneum from a ruptured ectopic pregnancy.

Note echogenic free fluid (arrow) outlining loops of bowel.


neither be echogenic nor the consequence of tubal

rupture, however; hemoperitoneum may be anechoic

(albeit rarely) and can occur secondary to leakage

from the fimbriated end of the fallopian tube or even

from a ruptured hemorrhagic corpus luteal cyst.

Endovaginal US has replaced culdocentesis as the

method of choice for detecting hemoperitoneum

[21]. Brown and Doubilet [14] reported that demon-

stration on US of an extrauterine gestational sac that

contains a yolk sac or embryo or a tubal ring has high

specificity rate (99.5%–100%) and high positive

predictive value (97.8%–100%) for the diagnosis

of ectopic pregnancy. Sensitivity rate was, however,

found to be low (20.1%–64.6%). When the most non-

specific finding that suggests ectopic pregnancy—

the presence of any adnexal mass other than a simple

cyst—was used as the sole diagnostic criterion, sen-

sitivity rate was improved (84.4%) with only slightly

diminished specificity rate (98.9%) and positive pre-

dictive value (96.3%) [14]. The sonographer should

remember that in up to 26% of ectopic pregnancies,

no intrauterine pregnancy or adnexal abnormality

may be detectable by endovaginal sonography [22].

Clinical correlation and close follow-up are of para-

mount importance.

Although the terms are occasionally used inter-

changeably, the term ‘‘cornual pregnancy’’ should be

reserved for an intrauterine pregnancy implanted in

one horn of a bicornuate or septate uterus, whereas an

interstitial ectopic pregnancy (approximately 2%–4%

of all ectopic pregnancies) occurs in the interstitial

(or intramyometrial) portion of the fallopian tube. An

interstitial ectopic pregnancy typically develops much

longer before becoming symptomatic, and it often

presents late in the first trimester or early in the

second trimester. A ruptured interstitial pregnancy

poses a significantly increased risk of severe, life-

threatening hemorrhage. On US examination, the sac

is eccentrically located within the uterine wall, and

the surrounding myometrium is thinned (<5 mm) or

even absent laterally. The ‘‘interstitial line sign’’

describes an echogenic line that reflects the two

opposing layers of endometrium seen adjacent to

the gestational sac but not surrounding it. This sign

has been reported to be 80% sensitive and 99%

specific for diagnosing interstitial ectopic pregnancy,

compared with 40% sensitive and 62% specific for

eccentric location or 40% sensitive and 74% specific

for myometrial thinning [23]. Even more convinc-

ing is visualization of myometrial tissue interposed

between the gestational sac and echogenic line (en-

dometrial cavity). It may be difficult to distinguish

interstitial and cornual pregnancies. Braxton Hicks

contractions or fibroids occasionally can cause a nor-

mal intrauterine pregnancy to be eccentrically placed.

If there is doubt about the diagnosis, follow-up may

be helpful.

Cervical pregnancies are rare but are important

to diagnose accurately because routine dilation and

curettage may cause life-threatening hemorrhage.

Cervical ectopic pregnancies may be difficult to

differentiate from pregnancies implanted in the lower

uterine segment or miscarriages. An hourglass ap-

pearance of the uterus, a gestational sac seen within

the cervical canal or in an eccentric location, invasion

of the cervical stroma or the presence of trophoblastic

flow, and visualization between the external and

internal cervical os may be helpful in differentiating

a cervical pregnancy from an impending miscarriage,

although trophoblastic flow occasionally can be noted

during miscarriage.

Abdominal pregnancy, defined as an ectopic preg-

nancy located in the peritoneal cavity, occurs in 1 in

10,000 pregnancies. It is a medical emergency be-

cause of high associated maternal and fetal morbidity

and mortality. Surgery is indicated as soon as the

diagnosis is made. In rare cases of undetected ad-

vanced abdominal pregnancy with fetal demise, litho-

pedion formation (fetal calcification) can occur.

This is usually found incidentally and can appear

on US as a large echogenic mass.

Treatment for ectopic pregnancy increasingly in-

cludes medical and even expectant management,

in addition to laparoscopic surgery. Close interval

follow-up with endovaginal US, monitoring serial

b-HCG levels, and reassessment of the patient’s clini-

cal stability are crucial elements of expectant therapy

[24]. Methotrexate is a folic acid antagonist that in-

hibits the synthesis of purines and pyrimidines, which

Box 3. Medical contraindications tomethotrexate therapy

� Abnormal liver function tests (LFTs)(elevated transaminases)

� Immunodeficiency� Any type of blood dyscrasia� Leukocyte count of <2000� Platelet count of >100,000� Peptic ulcer disease� Active pulmonary disease� Renal disease� Known sensitivity to methotrexate


prevents DNA synthesis and cell multiplication. It

acts primarily on the rapidly dividing trophoblastic

cells of the embryo [87]. Although exact eligibility

criteria continue to change with increasing experience

and vary somewhat among institutions, medical man-

agement with methotrexate is most effective when an

ectopic pregnancy is small (<3–4 cm), b-HCG is

low (<15,000–20,000 IU/mL International Reference

Preparation [IRP]), and cardiac activity is absent.

Medical management of ectopic pregnancy may,

however, be attempted despite one or more of these

criteria not being met. These patients have a higher

incidence of failure of treatment and may require

multiple doses of methotrexate [88]. Absolute

contraindications to medical therapy include pain,

hemodynamic instability, or evidence of large hemo-

peritoneum. Eligibility criteria and absolute contra-

indications of methotrexate treatment are further

discussed in Boxes 2 and 3 [87,88].

In the 2 to 4 weeks after methotrexate adminis-

tration, an ectopic pregnancy can demonstrate persist-

ent vascularity and can increase in size secondary to

infarction and hemorrhage. These findings are nor-

mal, and, in an asymptomatic patient, do not represent

failure of treatment. To avoid confusion, sonographic

follow-up is sometimes avoided during this time as

long as the patient remains asymptomatic. If a patient

develops pain, US follow-up is necessary to evaluate

for signs of tubal rupture, such as a dramatic increase

in the size of the ectopic pregnancy or large hemoperi-

toneum. Pain can develop during the normal course

of methotrexate therapy, 4 to 5 days after adminis-

tration, because of the infarction of trophoblastic

tissue. The development of pain does not necessarily

indicate failure of treatment or tubal rupture. Pain

secondary to trophoblastic tissue infarction should

resolve within 12 to 24 hours. Baseline b-HCG levels

are recorded before methotrexate administration. The

b-HCG begins to fall gradually after 4 days. If there is

Box 2. Eligibility criteria for methotrexatetherapy

� Hemodynamically stable� Absence of large hemoperitoneum� Absence of pain� Ectopic size <3.5–4 cm� C-HCG levels with peak values>15,000–20,000 mIU/mL (IRP)

� F Cardiac activity in gestational sac� Absence of any contraindications

more than a 15% fall in b-HCG from the baseline, a

second injection of methotrexate is not required [88].

Theca lutein cysts

Theca lutein cysts are caused by elevated levels

of chorionic gonadotropin and are seen in patients

with hydatidiform mole or choriocarcinoma and in

the setting of exogenous chorionic gonadotropin ad-

ministration for treatment of infertility [2]. The cysts

are lined by theca cells, which may or may not be

luteinized [2]. Cysts are usually multiple and bilateral

and typically range in diameter from 3 to 20 cm [25].

Symptoms are usually mild, including pelvic fullness

and dull pelvic pain. Acute pain can occur in the

setting of cyst rupture or hemorrhage [2]. The cysts

resolve spontaneously after treatment of gestational

trophoblastic disease or cessation of fertility therapy.

Theca lutein cysts may persist for long periods,

however, despite relatively low levels of b-HCG[25]. US examination demonstrates multiple simple

cysts in both ovaries (Fig. 9).

Ovarian hyperstimulation syndrome

Ovarian hyperstimulation syndrome (OHSS) is a

potentially dangerous iatrogenic complication of

pharmacologic ovulation induction for the treatment

of infertility [26]. It occurs in the setting of abnor-

mally high levels of b-HCG and less frequently has

been reported in spontaneous singleton and multi-

ple pregnancies, sex hormone–producing tumors,

and choriocarcinoma [26–28]. Although the precise

pathophysiology remains unknown, b-HCG seems to

trigger an increase in vascular permeability that

Fig. 9. Theca lutein cysts. Note multiple simple bilateral

ovarian cysts in this patient with a hydatidiform mole.

A pocket of free fluid is present between the two ova-

ries (arrow).


results in ovarian enlargement, cyst formation, and

third spacing of fluid. The renin-angiotensin system,

vascular endothelial growth factor, and cytokines are

believed to be chemical mediators in this process

[29,30]. Whelan and Vlahos [31] emphasize risk

stratification as the key to preventing OHSS or

minimizing its severity. Generally accepted risk fac-

tors include young age, presence of theca lutein

cysts, and elevated estradiol levels. Known polycys-

tic ovarian syndrome or the presence of multiple pe-

ripheral ovarian follicles (the ‘‘necklace sign’’) on US

in a patient with a clinical presentation that suggests

polycystic ovarian syndrome is also a risk factor for

OHSS [32].

Women who undergo ovulation induction ther-

apy whose ovaries contain several small or interme-

diate-sized follicles are at greater risk for developing

OHSS than women with large (>15 mm) follicles,

especially when seen in conjunction with high levels

of estradiol (>3000 pg/mL) [33]. Higher baseline

ovarian volume of more than 10 mL also has been

shown by Danninger et al [34] to predict subsequent

development of OHSS and may become a more

important predictor with the widespread availability

of US units capable of providing three-dimensional

images with highly accurate, reproducible measure-

ments of ovarian volume. A patient at higher risk for

OHSS may require more intensive monitoring (in-

cluding US) or undergo an alternative pharmacologic

ovulation induction technique. It is estimated that

mild OHSS may occur in as many as 65% of women

who undergo ovulation induction. The incidence of

clinically important (moderate to severe) OHSS

ranges from 1% to 10% of exogenously induced

ovulation cycles, but only a small percentage of these

cases are severe (0.5% to 5%) [35,36].

OHSS is more severe in patients who become

pregnant after ovulation induction. The spectrum of

clinical presentation ranges from nausea, vomiting,

and abdominal pain to massive ascites, acute respi-

ratory distress syndrome, and hypotension, classified

according to severity by Golan et al [30]. Pain may be

caused by rupture of or hemorrhage into the enlarged

cysts or ovarian torsion. Approximately 20% of

patients who receive gonadotropin therapy develop

mild to moderate ovarian enlargement [37]. Ovarian

diameter more than 5 cm is a criterion for diagnosis

of mild OHSS, although the ovaries are frequently

more than 10 cm in diameter. US is the most exact

method of detecting ovarian enlargement. It is also

preferable to bimanual examination because of the

risk of ovarian rupture [30]. On US, multiple large,

thin-walled cysts are identified. Pulsed Doppler may

demonstrate increased intra-ovarian arterial diastolic

flow or nonphasic venous flow, which indicates de-

creased venous return [38]. Acute pain may be caused

by hemorrhage into a cyst, cyst rupture, or ovarian

torsion. Debris or low-level echoes within the cysts

may be seen when hemorrhage occurs. Cyst rupture

can result in an irregularly shaped cyst with adjacent

free fluid or fluid in the cul-de-sac (Fig. 10).

Because ovarian enlargement predisposes to ovar-

ian torsion, documentation of ovarian blood flow is

important in patients who present with acute pain (see

next section). In severe cases of OHSS, US can be

used to detect and monitor complications. US exami-

nation may demonstrate ascites or pleural fluid,

criteria used in determining whether hospitalization

is necessary [31]. Oliguria may prompt a request for

renal US evaluation, although in the setting of OHSS

this is usually secondary to impaired venous return

from the kidneys secondary to extrinsic compression

by ascites. Patients with OHSS are at increased risk

of thromboembolism caused by hemoconcentration

and may benefit further from US examination for

various complications, such as deep venous throm-

bosis. Thoracic complications, such as pulmonary em-

bolism (1.9%), acute respiratory distress syndrome

(2.4%), infection (3.8%), atelectasis (20%), and pleu-

ral effusion (29%; usually right-sided), may occur

[39]. Unilateral pleural effusion has been reported

as an isolated finding in OHSS [40,41]. A large pleu-

ral effusion often predicts hemodynamic instability.

Treatment is supportive: hemodynamics, hemato-

crit, electrolytes, liver and kidney function (includ-

ing urine output), and coagulation parameters are

monitored. Some authors have advocated an out-

patient treatment approach, facilitated in part by

Fig. 10. Ovarian hyperstimulation syndrome. (A) Note marked enlargement of the right ovary within calipers. Numerous cysts

are seen, several of which contain internal echoes. There is a small amount of free fluid adjacent to the enlarged ovary. (B) Pulse

Doppler interrogation reveals high-velocity systolic and diastolic flow, which excludes the diagnosis of ovarian torsion. The

patient’s pain is likely caused by hemorrhage into these cysts or rupture of these hemorrhagic cysts.


US-guided follicular aspiration [42]. Navot et al [32]

reported US-guided paracentesis as the treatment of

choice when medical therapy is insufficient; alter-

natives include transvaginal aspiration of ascites or

follicular cysts. OHSS typically resolves in 7 to

10 days unless pregnancy ensues, in which case

recovery is more prolonged.

Ovarian torsion

Ovarian or adnexal (ovary and fallopian tube)

torsion is a surgical emergency that requires prompt

diagnosis and treatment. There is increased risk

during pregnancy, and ovarian torsion occurs in ap-

proximately 1 in 1800 pregnancies [1,43]. Approxi-

mately 25% of adnexal torsions occur in pregnant

patients [1]. Adnexal torsion most commonly occurs

between 6 and 14 weeks’ gestation and in the

immediate puerperium [1,44]. Ovarian torsion is the

result of partial or complete rotation of the ovarian

pedicle on its axis, which results initially in impaired

lymphatic and venous drainage and eventual loss of

arterial perfusion [43,45]. It occurs more commonly

on the right side [44]. Torsion can be difficult to

diagnose clinically because the presenting symptoms,

including pain, nausea, and vomiting, are nonspecific

and similar to many causes of acute abdomen [43,45].


Because ovarian enlargement of more than 6 cm

predisposes to ovarian torsion [46,47], women who

undergo ovulation induction have the highest inci-

dence because of the development of numerous theca

lutein cysts, which can massively enlarge the ova-

ries [2,30]. Mashiach et al [47] reported that tor-

sion was more common in women with OHSS

who subsequently became pregnant, compared with

women with OHSS alone. Enlargement of the ovary

secondary to a corpus luteal cyst or incidental benign

ovarian neoplasm, most commonly a mature mature

cystic teratomas or cystademoma, also can predispose

to ovarian torsion [44]. Ovarian torsion rarely occurs

in the presence of ovarian carcinoma or endometri-

osis because of fixation of the ovaries to adjacent

structures by adhesions.

The US appearance of ovarian torsion varies de-

pending on the degree of ischemia and infarction

and the time course [44]. The ovary is typically

enlarged. Numerous small follicles are often seen at

the periphery of the ovary [43,45,48]. The central

ovarian stroma becomes heterogeneous with areas of

increased echogenicity, which represent hemorrhage,

and more hypoechoic areas, which represent edema

Fig. 11. Ovarian torsion. (A) The ovary is enlarged with several sm

stroma is heterogeneous, with echogenic areas representing hemor

detected with color Doppler. (B) Because pulse Doppler is more sen

with pulse Doppler should be performed. No flow could be demo

(Fig. 11A) [44]. With frank infarction, cystic, clotted

areas may be observed. Free fluid within the pelvis

or adjacent to the ovary also can be seen [44,50].

Although the range of gray scale features varies, the

ovary rarely has a completely normal appearance.

Classically, Doppler interrogation demonstrates ab-

sence of arterial flow (Fig. 11B). It is important,

however, to remember that early in the process there

may be obstruction of lymphatic and venous flow with

preservation of arterial perfusion [49–51]. Occasion-

ally only diastolic or venous flow is lost early on.

Because the ovary has dual arterial supply, in

early torsion only one may be occluded [51]. In a

patient who presents with acute pain and an ovary

that demonstrates real-time findings consistent with

ovarian torsion, the diagnosis should be suggested

even in the presence of documented arterial blood

flow (Fig. 12) [48–51]. When color Doppler imaging

and pulsed Doppler sampling do not demonstrate

arterial flow within the ovarian parenchyma, the

diagnosis is more easily made. All Doppler parame-

ters must be set carefully to maximize detection of

slow flow to avoid a false-positive diagnosis caused

by technical factors. Sampling error also may cause

all peripherally located cysts (arrows). The central ovarian

rhage and hypoechoic areas representing edema. No flow is

sitive to low-velocity, low-volume flow, meticulous sampling

nstrated in this case.

Fig. 12. Early ovarian torsion. Note classic gray scale

features of torsion: ovarian enlargement, central amorphous,

heterogeneous stroma, and small peripheral cysts. Pulse

Doppler interrogation revealed some arterial flow in this

woman, who presented less than 2 hours after the acute

onset of severe pelvic pain.

Box 4. Sonographic findings of ovariantorsion


false-positive diagnoses. Fleischer et al [52] reported

that the preservation of parenchymal venous flow

is a useful indicator of ovarian viability. The twisted

vascular pedicle also can be seen on color Doppler

sonography. Demonstration of flow within the

twisted vascular pedicle may be a useful marker of

ovarian viability (Box 4).

Adnexal torsion that is diagnosed before tissue

infarction is managed with laparoscopic ‘‘detorsion’’

surgery followed by progesterone replacement if

the corpus luteum is removed. If tissue infarction

and necrosis have occurred, then laparotomy with

salpingo-oophorectomy is usually required to pre-

vent peritonitis.

Gray scale findings

Ovarian enlargementPeripherally located folliclesHeterogeneous central ovarian stroma

� Internal hemorrhage (echogenic)� Internal edema (hypoechoic)

Cystic necrosis of the ovaryFree fluidF Underlying precipitating mass

Range of color/pulsed Doppler findings

NormalLoss of venous flowLoss of diastolic flowAbsence of flowTwisted vascular pedicle

Luteoma of pregnancy

Luteoma of pregnancy is a rare entity, with fewer

than 200 cases reported in the literature [53]. Luteo-

mas consist of non-neoplastic tumor-like masses of

lutein cells and are often multifocal and bilateral

[2,53]. The luteoma range up to 20 cm in diameter,

but most are in the 5- to 10-cm range [2]. Luteomas

are usually clinically occult, only coming to attention

when visualized during cesarean section or postpar-

tum tubal ligation [2]. Occasionally, luteomas can

have androgenic effects that result in fetal hirsutism

and virilization. As is the case with any large adnexal

mass, however, luteomas may precipitate ovarian

torsion that results in acute pelvic pain. Although

their morphologic appearance can be ominous and

suggest malignancy, biopsy is adequate for diagnosis,

and masses spontaneously resolve several months

after delivery [53]. The diagnosis should be enter-

tained to avoid unnecessary oophorectomy. In case

reports, the lesions have been described on US as

solid ovarian masses. Cystic components may be

present secondary to necrosis [53].

Disease unrelated to pregnancy

Diagnoses such as ectopic pregnancy and ovarian

torsion are likely to be at the top of the differential

list in a pregnant patient who presents with acute

pelvic pain and an adnexal mass. There are, however,

many gynecologic and nongynecologic causes of

acute pelvic pain and pelvic mass that are unrelated

to pregnancy and may still occur in this population.

Pelvic inflammatory disease and tubo-ovarian

abscess

Pelvic inflammatory disease (PID) is most com-

monly caused by sexually transmitted infection by

Chlamydia species or Neisseria gonorrhea. Uterine

instrumentation and the placement of intrauterine

contraceptive devices also are risk factors [44]. Less

frequently, PID may be caused by direct extension

Fig. 14. Tubovarian abscess. Note complex fluid collection

engulfing right ovary (arrow).


of infection from appendicular or diverticular ab-

scesses, and in these instances disease tends to be

unilateral [44,46]. Fortunately, acute PID is a rare

entity in the pregnant patient. The cause of PID in

pregnancy is uncertain, but recurrence of old in-

flammatory disease is considered the most common

cause [54]. PID is typically an ascending infection

that begins as a cervicitis, progresses to endometritis,

and ultimately involves fallopian tubes or ovaries

(tubo-ovarian complex). Only approximately 5% of

patients with PID progress to abscess formation.

PID can be difficult to diagnosis secondary to vague

or confusing symptoms. It should be suspected in

the setting of fever, pelvic discomfort, and purulent

vaginal discharge. Many patients do not demonstrate

these classic symptoms, however, and US imaging

often plays a crucial role in diagnosis and patient

management [4].

Pelvic US is frequently normal in the early stages

of PID [44,46]. As disease worsens or becomes

more chronic, several appearances can be identified

on US imaging. US may reveal dilatation of one or

both fallopian tubes. Hydrosalpinx is characterized

by its tubular shape or folded configuration [55]. A

well-defined echogenic wall and linear echoes that

protrude into the anechoic tubal lumen are also

characteristic [55]. Hydrosalpinx can be differentiated

from fluid-filled bowel loops by the absence of

peristalsis [55]. Dilated fallopian tubes also may

contain diffuse, low-level echoes that represent debris

or hemorrhage (Fig. 13) or appear as a complex cys-

tic adnexal mass that demonstrates multiple fluid

levels and septations [4,44]. Once the disease has

progressed to abscess formation (Fig. 14), a complex

adnexal mass is observed on US examination. The

ovary may not be identifiable separate from the

mass but actually may be engulfed by the infection,

Fig. 13. Pyosalpinx. Note layering debris or pus (curved

arrow) in the dilated fallopian tube.

although relative sparing of the ovary has been re-

ported. The ovary is sometimes enlarged with indis-

tinct margins secondary to peri-ovarian inflammation,

termed the tubo-ovarian complex [4].

Pressure from the transducer often causes pain

during the examination, and the pelvic organs may

appear fixed to the surrounding tissues. The serosal

contour of the uterus may be indistinct because of

surrounding inflammatory exudate. Pus may be seen

within the cul-de-sac or around the liver with an

appearance of free fluid–containing low-level echoes

[4,44,46]. A US that demonstrates findings that sug-

gest PID (ie, a thick-walled, fluid-filled tubular ad-

nexal mass with or without free intrapelvic fluid) has

been reported to have a sensitivity rate of 85% and a

specificity rate of 100% for the diagnosis [56]. Any

complex multilocular adnexal mass in an appropriate

clinical setting can represent PID, however. Hydro-

salpinx is not always present. Abscess drainage or

conservative surgical procedures with antibiotic

therapy are often recommended in managing PID

complicated by tubo-ovarian abscess during preg-

nancy. There is no true consensus on management

in this population, however [54].

Endometrioma

Endometriosis is a common cause of abdominal

pain. In younger women, endometriosis is defined

as the presence of functional endometrial tissue out-

side of the uterus [43]. The classic triad of clinical

symptoms includes pelvic pain, dysmenorrhea, and

infertility [43,57]. Endometriosis has an estimated

prevalence of 1% in reproductive age women [57];

however, the incidence of endometriosis in women

with infertility is closer to 40% [43]. Overall, endo-

Fig. 15. Endometrioma. The cystic lesion medial to the right

ovary contains diffuse low-level echoes (arrow) and demon-

strates increased through transmission. The wall is thin

and regular.


metriomas account for approximately 4% of adnexal

masses diagnosed during pregnancy [1]. Endometrio-

mas can have a diverse range of appearances on US,

from anechoic cysts to complex cystic masses that

contain multiple septations to heterogeneous echo-

genicity. Classically endometriomas appear on US as

thin-walled unilocular cystic masses that contain

diffuse, low-level echoes (Fig. 15) [43,57–59]. Patel

et al [59] reported that hyperechoic wall foci and

multilocularity, in the absence of malignant features,

highly suggest endometrioma. Layering or anechoic

foci within a background of homogeneous low-level

echoes also have been described. Margins may be

indistinct and angulated secondary to associated

adhesions. The appearance on US may be similar to

Fig. 16. Acute hemorrhagic infarction of a fibroid in a patient

(A) Sagittal US image of the uterus (U) reveals an echogenic subs

fluid. (B) Follow-up CT scan demonstrates lack of enhancement

hemorrhagic infarction.

that of a hemorrhagic cyst [60]. The pattern of in-

ternal echoes within a hemorrhagic cyst is more

often lace-like, however, as opposed to the homoge-

neous hypoechoic internal echoes characteristic of

endometrioma, and hemorrhagic cysts more often

present with acute pain [43].

Endometriomas are more frequently multiple,

and their appearance is more stable over time when

compared with hemorrhagic cysts. Hemorrhagic cysts

and endometriomas may have vascular walls on color

Doppler interrogation [61]. An increased likelihood

of mural vascularity in endometriomas has been re-

ported in patients with acute pelvic pain and may

serve as a relative marker of disease activity, although

this is somewhat controversial [62]. Endometriomas

can be bizarre looking and cannot always be distin-

guished readily from malignancy. The presence of

irregular walls or vascular nodularity should raise

concern, because clear cell or endometroid carcino-

mas rarely may develop within endometriomas (<1%).

MR imaging may be useful to document the presence

of hemorrhage within an ovarian mass when US

examination is equivocal.

Leiomyomata

Leiomyomata are the most common benign uter-

ine neoplasms and are composed of smooth muscle

cells with varying amounts of fibrous connective

tissue and collagen. Leiomyomata are most com-

monly diagnosed in premenopausal women, with an

incidence of 20% to 30% in women over the age

of 30 [43]. Some studies have indicated that careful

who presented with acute pelvic pain 4 days postpartum.

erosal fibroid (arrow) with a small amount of adjacent free

of the uterine mass (arrow), which is consistent with acute

Fig. 17. Pedunculated leiomyoma. Note large left leiomyoma

connected to the uterus by a thin pedicle (arrowhead).


pathologic evaluation can demonstrate leiomyomas

in up to 80% of women of reproductive age [1].

Uterine leiomyomata are diagnosed in 0.3% to 4% of

pregnancies, usually because a pedunculated subse-

rosal leiomyoma simulates an ovarian neoplasm

[1,45]. Pedunculated leiomyomata may undergo tor-

sion and necrosis, which results in acute pelvic pain

[45]. Fibroids are hormonally dependent and can

rapidly increase in size during pregnancy, which

results in hemorrhagic infarction, which may cause

acute, severe pelvic pain (Fig. 16). Leiomyomata

have variable appearance on US. They most fre-

quently appear as round, homogeneous solid, well-

circumscribed masses that are usually hypoechoic or

isoehoic to the myometrium and more rarely rela-

tively echogenic. Areas of decreased echogenicity

secondary to degeneration and necrosis may be seen,

especially in lesions larger than 5 cm. Distal acoustic

shadowing, often in a striated pattern, is commonly

noted. Calcification is most common in older women

[63]. It may be difficult to identify the site of myo-

metrial attachment of a pedunculated leiomyoma on

gray scale imaging. Both ovaries should be identifi-

able separate from the mass, however (Fig. 17), and

color Doppler imaging may help to identify a vascu-

lar pedicle. When sonographic evaluation of an

adnexal lesion is indeterminate in differentiating a

pedunculated leiomyoma from a solid ovarian neo-

plasm, MR imaging can be useful in further charac-

terization [64].

Fig. 18. Mature cystic teratoma of the ovary. Note large

echogenic mass on the left (arrowheads).

Benign and malignant neoplasms

Ovarian neoplasms are most often asymptomatic

unless they precipitate ovarian torsion, although such

lesions may present with vague abdominal or pelvic

pain and urinary frequency. Most ovarian neoplasms

detected during pregnancy are benign. The most

common of these are mature cystic teratomas and

cystadenomas [1]. Mature cystic teratomas are benign

neoplasms that usually contain tissue derived from

all three germ cell layers [2,43]. Occurring most

commonly in the active reproductive years [43],

dermoids account for 40% to 50% of benign ovarian

neoplasms and are bilateral in 10% to 15% of cases

[43]. Malignant transformation is rare (<2% of

cases) and is most common in older women [47].

Dermoids are usually asymptomatic unless torsion

or rupture occurs [43]. US appearance of mature

cystic teratomas ranges from that of a solid homo-

geneously echogenic mass with posterior attenuation

(Fig. 18) to a completely anechoic structure that

mimics an ovarian cyst.

Several US features, however, have been described

as specific to mature cystic teratomas. A predomi-

nately cystic mass with an echogenic mural nodule

is a characteristic appearance. The mural nodule, or

dermoid plug, may contain hair, teeth, or fat [65]. If

calcium is present, distal acoustic shadowing is ob-

served. [43,66]. Linear echogenic foci that represent

hair fibers, an echogenic hair ball floating at a fluid-

fluid interface (Fig. 19), and fat-fluid levels are also

specific features [43,67,68]. A study by Patel et al

[66] found that the positive predictive value was

100% when an ovarian mass had two or more US

features considered specific for mature cystic terato-

mas. In this study, the sensitivity of US for detection

of dermoids was reported as 85% [66]. Diffusely

echogenic mature cystic teratomas can escape detec-

tion by US because they appear similar to bowel [43].

When a palpable adnexal mass can be diagnosed

confidently as a mature cystic teratoma, surgery can

be delayed safely until after delivery. If US is non-

diagnostic but suspicious, CT or MR imaging may

Fig. 19. Mature cystic teratoma of the ovary. Note echogenic

hairball ‘‘floating’’ (arrow) at the fat/fluid interface. The

liquid fatty layer contains low-level echoes. Becuase the fat

is lighter than the serous fluid, the more echogenic layer is

more anterior in this supine patient.

Fig. 20. Serous cystadenoma. Note thin, regular septations

(arrow) in this cystic adnexal mass.


document the presence of fat within dermoids, thereby

confirming the diagnosis.

Serous and mucinous cystadenomas are benign

neoplasms that most commonly occur in reproductive

age women [43]. They can be difficult to differentiate

sonographically from malignant cystadenocarci-

nomas because of the wide spectrum of appearances

on US. Serous cystadenomas typically are large,

unilocular, thin-walled cystic lesions that may demon-

strate thin septations or papillary projections (Fig. 20).

They are bilateral in 20% of cases [43]. Mucinous

cystadenomas are typically larger, measure up to

30 cm, and may contain internal low-level echoes

secondary to mucin content. Septations are common.

Papillary projections are less common and the mass

usually unilateral [43]. Malignant neoplasms com-

prise approximately 3% of adnexal masses diagnosed

in pregnancy [1]. The most common malignant neo-

plasms that come to attention during pregnancy in-

clude germ cell tumors, low-grade ovarian cancers,

and invasive epithelial ovarian cancers. Most women

diagnosed with ovarian cancer during pregnancy

present with stage 1 disease [1].

In many cases the US appearance of complex

cystic adnexal masses is indeterminate and the differ-

ential diagnosis of cystadenoma or cystadenocarci-

noma must be considered. The presence of thick

vascular septations (>3 mm), mural nodularity, papil-

lary processes, thick, irregular walls, solid areas,

invasion or fixation of adjacent structures, and asso-

ciated findings, such as ascites or serosal implants,

increase the likelihood of malignancy (Figs. 21, 22)

[68,69]. The likelihood of malignancy also increases

with age, elevation of serum CA-125 level, and

positive family history [70]. It is not possible to dif-

ferentiate benign solid lesions (eg, fibromas or theco-

mas) from malignant germ cell or stromal tumors [69].

The presence of a purely solid tumor indicates a

higher probability of metastatic carcinoma than pri-

mary ovarian cancer (Fig. 23) [71]. Numerous authors

have reported that ovarian malignancies tend to have

increased peak systolic flow (peak systolic velocity

>35 cm/second) and low resistance perfusion (resis-

tive index <0.4 or perfusion index <1) [68,70,72,73].

There is significant overlap in the distribution

of peak systolic velocity, resistive index, and perfu-

sion index values between benign and malignant

lesions, however, and no discriminatory value is

accepted [68,70,72,73]. Lack of detectable flow by

means of color Doppler US does not exclude ovarian

malignancy [72]. The management of an ovarian

mass during pregnancy is controversial. Surgery in

the first trimester is associated with pregnancy loss,

and surgery in the third trimester can result in

premature labor [1]. Although US is excellent at

detecting adnexal masses, it is not always accurate

in differentiating benign from malignant lesions.

Although the previously described morphologic char-

acteristics and internal vascularity with high peak

systolic velocity and low resistive index suggest

malignancy, these features are nonspecific, with a

positive predictive value of approximately 50% [73].

The real value of US lies in the high negative

predictive value (nearly 99%) of US features con-

sidered to be benign [73]. In a pregnant patient with a

palpable adnexal mass and US features diagnostic of

a benign entity, such as a serous or hemorrhagic cyst,

dermoid or pedunculated fibroid, surgery may be

postponed safely until after delivery or avoided

Fig. 21. Stage 1 serous cystadenocarcinoma. This 28-year-old patient presented at 12 weeks’ gestation with a palpable right

adnexal mass. (A) US reveals mural irregularity (arrow), which represents small papillary projections. (B) These papillary

projections (arrow) are seen on corresponding MR image. Gravid uterus (U) is anterior.


altogether. Masses with multiple malignant features

require prompt surgery. Masses that appear more

benign are often followed by serial examinations

until the second trimester, which is the optimal time

for surgery in terms of maternal and fetal safety. In

equivocal cases, MR imaging may be useful in

further characterizing an adnexal mass.

Perforated appendicitis

Appendicitis is the most common cause of non-

gynecologic acute pelvic pain in women and the most

common diagnosis that requires emergent surgical

intervention during pregnancy [4,74]. The inci-

Fig. 22. Serous cystadenocarcinoma. Note large complex

adnexal mass on color Doppler with a vascular solid com-

ponent (arrow).

dence of gestational appendicitis has been reported

as 0.05% to 0.14% [45,74]. Although the incidence

of acute appendicitis is not increased in pregnancy,

appendiceal rupture occurs two to three times more

frequently and occurs in up to 25% of cases, second-

ary to delay in diagnosis and surgery [1,45]. Patients

with appendicitis typically present with fever, leuko-

cytosis, nausea, vomiting, and peri-umbilical pain,

which gradually moves to the right lower quadrant.

These symptoms may be altered, muted, or absent in

pregnancy, however, which contributes to delays in

Fig. 23. Krukenberg tumor (metastasis from gastric carci-

noma). This 27-year-old woman presented at 32 weeks’

gestation with acute abdominal pain, bilateral solid ovarian

masses, and ascites (only one mass is shown here). Although

the differential diagnosis would include benign lesions, such

as fibroma and fibrothecoma, the pronounced vascularity

and ascites are worrisome for malignancy.


diagnosis and the increased incidence of perforation

and associated morbidity and mortality in this popu-

lation [1,45,74–76].

In pregnancy, the most common presenting symp-

tom is right-sided abdominal pain, regardless of the

gestational age [76]. The position of the appendix is

elevated above McBurney’s point after the first tri-

mester, however, and pain may be more localized to

the right upper quadrant than the right lower quad-

rant and is often confused with cholecystitis [45].

Although CT is the imaging modality of choice in

evaluating patients with suspected appendicitis, it is

to be avoided in pregnant patients because of the

risks of ionizing radiation to the fetus. US examina-

tion is often the first-line imaging modality in this

patient population. US is a specific, although rela-

tively insensitive, test for the diagnosis of acute

appendicitis. Prospective studies have reported US

specificity rates of 86% to 100% and sensitivity rates

as high as 75% to 90% in patients with clinically

suspected appendicitis [4]. In most clinical practices,

however, the appendix is infrequently visualized,

which limits the sensitivity and negative predictive

value of the examination. In one study, on-call

residents were only able to detect the appendix by

US in 13% of cases in which appendicitis was

clinically suspected [77]. Sensitivity for detection

of appendicitis was 50% on US compared with

100% on CT [77].

Fig. 24. Acute appendicitis. Transverse view demonstrates a

thick-walled (arrow), noncompressible appendix with a

surrounding fluid collection (F).

The examination is performed with a linear array

transducer. The cecum and psoas muscle can be used

as landmarks to help localize the appendix. Graded

compression is used to displace overlying bowel at

the point of maximum tenderness [4,78]. An abnor-

mal appendix appears as a blind-ending, aperistaltic

loop of bowel that does not compress [4,79]. Trans-

versely, the loop should be more than 6 mm in

diameter (outer wall to outer wall) (Fig. 24) [4,

80–82]. This measurement criterion provides high

sensitivity but limited specificity, because the normal

appendix has been reported to have a diameter of up

to 13 mm secondary to intraluminal contents [81,82].

The combined wall thickness should not exceed 6 mm

in a normal appendix [4,82]. Increased vascularity

may be noted on Doppler interrogation. In some

cases, a shadowing appendicolith is seen [4]. The

surrounding area also should be evaluated carefully to

exclude loculated periappendiceal fluid or gas, which

suggests abscess formation [4,78]. Recent reports

suggest that MR imaging may be beneficial in eval-

uating patients for suspected appendicitis when US is

nondiagnostic [83,84]. Appendicitis in pregnancy

requires prompt surgery. Maternal mortality from

appendicitis has diminished to approximately 0.1%

but still exceeds 4% when perforation occurs [1].

Fetal mortality is less than 2% but is more than 30%

in the case of perforation [1].

Diverticulitis

Diverticulitis is uncommon in pregnant women.

Patients present with lower quadrant (usually left)

pain, fever, and leukocytosis [4]. Whereas CT is the

gold standard in evaluation of suspected diverticu-

litis, US is a preferred modality in the pregnant

patient, and a small body of literature has indicated

that US can be used to make this diagnosis accu-

rately. Pradel et al [85] reported that CT and US

had an accuracy rate of 84% in diagnosing diverticu-

litis. US and CT findings were not statistically

significantly different in terms of sensitivity rates

(85% and 91%, respectively) and specificity rates

(84% and 77%, respectively) [85]. Although trans-

abdominal US scanning seems less sensitive in iden-

tifying diverticular abscess compared with CT,

endovaginal US scanning is just as sensitive if the

area is within reach of the vaginal probe [4]. US

may identify an abnormal loop of bowel in the re-

gion of the patient’s pain with an irregular lumen

and outpouchings beyond the bowel wall. The co-

lonic wall may appear thickened but less concentri-

cally so than in primary colitis. An adjacent walled


off fluid collection or extraluminal shadowing air

suggests perforation and abscess formation [4]. These

results are operator dependent; however, US should

not be overlooked as a viable alternative imaging

modality for diagnosing diverticulitis in the preg-

nant patient.

Epiploic appendigitis

Epiploic appendigitis is an uncommon entity. It

is caused by torsion or ischemic infarction of one of

the epiploic appendages of the colon, which incites a

subsequent inflammatory reaction [4,86]. Epiploic

appendages are rudimentary in children and reach

their full size in adulthood. Most of them measure

2 to 5 cm in length and are 1 to 2 cm thick [4,86]. The

largest appendages are found in the descending colon

and cecum, which are the most common locations

for torsion to occur [86]. Epiploic appendages are

enlarged in obese patients, which increases their risk

for torsion [86]. Patients most commonly present

with acute or subacute left lower quadrant pain and

leukocytosis. When cecal epiploic appendages are

involved, the clinical picture may mimic appendicitis.

Fever is usually absent [4,86]. Normal epiploic appen-

dages are not visible on US unless the colon is

surrounded by extraluminal fluid. In epiploic ap-

pendigitis, US demonstrates an ovoid, hyperechoic,

solid, noncompressible mass at the point of maxi-

mum tenderness. The mass is often surrounded by a

thin hypoechoic rim, believed to represent thicken-

ing of the serosa of the appendage and the adjacent

parietal peritoneum [4,86]. The lesions are typically

located between the anterior abdominal wall and the

colon, from which they arise. The mass often adheres

to the adjacent peritoneum, which can be observed

on real-time sonography during inspiration and expi-

ration [86]. Color Doppler signal is typically absent

within the echogenic mass. Minimal blood flow is

sometimes identified immediately external to the

hypoechoic rim, however. This lack of vascularity is

in contrast to the prominent color flow that is seen

in secondary inflammation of the epiploic append-

ages in persons with diverticulitis [86].

Summary

In a pregnant woman who presents with acute

pelvic pain and an adnexal mass, pregnancy-related

etiologies, such as ectopic pregnancy or ovarian tor-

sion, are typically the first diagnoses to be consid-

ered. Many other causes of pelvic pain associated

with an adnexal mass can occur in pregnant patients,

however. Some causes are benign and others require

urgent management and treatment. Clinical presenta-

tion and physical examination can be misleading

in pregnancy. The location of pain may be atypical

for the pathologic entity, the pain may be muted, and

in the case of infection, fever and leukocytosis can

be absent. US examination is a safe and effective

method for evaluating these patients. Sonographic

characterization of adnexal masses may make a de-

finitive diagnosis or focus the differential, which al-

lows for prompt and appropriate treatment of patients.

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Radiol Clin N Am 42 (2004) 349–363

Acute painful scrotum

Vikram Dogra, MD*, Shweta Bhatt, DMRD, DMRE

Department of Radiology, Case Western Reserve University, University Hospitals, 11100 Euclid Avenue,


High-frequency transducer sonography using across the testis in the craniocaudal direction. If

gray scale along with pulsed and color Doppler is

the imaging modality of choice for evaluating pa-

tients who present with acute scrotal pain. Disease

processes such as testicular torsion, epididymo-orchi-

tis, and intratesticular tumors have the common

symptom of pain at presentation, and sonographic

evaluation helps in differentiating patients who re-

quire surgical from patients for whom conservative

management is sufficient. Sonography with a high-

frequency transducer helps to characterize better the

testicular flow and, in many instances, suggests more

specific diagnoses. This article is organized on the

basis of the pathophysiology of the disease process

with emphasis on color Doppler when applicable.

This article is intended to familiarize the reader with

new technology and provide new insights into the

sonographic diagnosis of painful scrotum.

Imaging anatomy

A normal adult testis has medium-level echoes

and measures 5�3�2 cm [1]. The tunica albuginea is

the fibrous sheath that covers the testicle. The tunica

albuginea is covered by the tunica vaginalis. Septae

extend from the tunica albuginea into the testicle and

divide the testes into lobules (Fig. 1). The posterior

surface of the tunica albuginea is reflected into the

interior of the gland, which forms the incomplete

septum known as the mediastinum of the testis. Sono-

graphically, the mediastinum of the testis is an echo-

genic band (Fig. 2) of variable thickness that extends


doi:10.1016/j.rcl.2003.12.002


E-mail address: [email protected] (V. Dogra).

imaged at an angle, it may resemble a testicular tumor.

Each lobule is composed of many seminiferous tu-

bules that open via tubuli recti into dilated spaces

called the rete testes within the mediastinum. The

normal rete testis can be identified at high-frequency

ultrasound (US) in 18% of patients as a hypoechoic

area with a striated configuration adjacent to the

mediastinum testis [1]. These in turn communicate

via efferent ductules with the epididymal head. The

epididymis is composed of a head, body, and tail,

the ducts of which continue as the vas deferens in

the spermatic cord. The epididymis is seen as a 5- to

12-mm pyramidal structure lying atop the superior

pole of the testes. The head of the epididymis is usu-

ally isoechoic to the testis, and its echotexture may be

coarser than that of the testicle [2,3]. High-frequency

transducer sonography permits visualization of the

body of epididymis, which measures 2 to 4 mm.

The right and left testicular arteries—branches of

the abdominal aorta—provide the vascular supply to

the testis. A transmediastinal artery branch of the

testicular artery occurs in approximately one half of

normal testes (Fig. 3) [4]. It courses through the

mediastinum to supply the capsular arteries and is

usually accompanied by a large vein. The deferential

artery, a branch of the superior vesicle artery, and the

cremasteric artery, a branch of the inferior epigastric

artery, supply the epididymis, vas deferens, and

peritesticular tissue [5]. Branches of the pudendal ar-

tery supply the scrotal wall [6]. Venous drainage is

via the pampiniform plexus.

Four testicular appendages have been described:

the appendix testis, the appendix epididymis, the vas

aberrans, and the paradidymis. They are remnants of

embryologic ducts [7]. The appendix testis and the

appendix epididymis are usually seen on scrotal so-

s reserved.

Fig. 1. Diagrammatic transverse representation of the anatomy of the testis illustrates the relationships of the tunica albuginea

to the mediastinum testis and the mediastinum testis to the rete testis. (Courtesy of Vikram Dogra, MD.)

V. Dogra, S. Bhatt / Radiol Clin N Am 42 (2004) 349–363350

nography. The appendix testis is attached to the upper

pole of the testis in the groove between the testis and

the epididymis (Fig. 4A). The appendix epididymis,

another appendage (Fig. 4B), is attached to the head

of the epididymis and is encountered unilaterally in

34% and bilaterally in 12% of postmortem series.

Presence of minimal fluid facilitates their visualiza-

tion on sonography.

Scanning technique

Scrotal sonography is performed with the patient

lying in a supine position and the scrotum supported

by a towel placed between the thighs. Optimal results

Fig. 2. Longitudinal view of a normal testis demonstrates

the mediastinum testis (arrow) as an echogenic band.

are obtained with 7- to 14-MHz high-frequency

linear-array transducers.

The testes are studied in two planes (ie, along the

long and transverse axes). The size and echogenicity

of each testicle and the epididymis are compared with

those on the opposite side. In patients being evaluated

for an acute scrotum, the asymptomatic side should

be scanned initially to set the gray scale and color

Doppler gains to allow comparison with the affected

side. Color Doppler and pulsed Doppler are opti-

mized to display low-flow velocities, and blood flow

in the testis and surrounding scrotal structures is

documented, including the spectral Doppler recording

of the intratesticular arterial flow in both testes.

Transverse images with portions of each testis on

the same image should be recorded in gray scale and

color Doppler. Power Doppler also may be used to

Fig. 3. Transverse oblique view of the testis demonstrates the

transmediastinal artery as a linear hypo-echoic band (arrow).

Fig. 4. (A) Appendix testis (arrow) directly attached to the testis (T). Presence of fluid (asterisk) facilitates its visualization.

(B) The appendix of the epididymis (cystic appearance) (arrow) is seen attached to the head of the epididymis (E).

V. Dogra, S. Bhatt / Radiol Clin N Am 42 (2004) 349–363 351

visualize intratesticular flow in patients with an acute

scrotum. Additional techniques, such as the Valsal-

va’s maneuver or upright positioning, can be used as

needed for venous evaluation.

Inflammatory causes

Fournier’s gangrene

Fournier’s gangrene constitutes a urologic emer-

gency that demands early recognition because of its

high mortality rate, which is reportedly as great as

75% [8]. The diagnosis of Fournier’s gangrene is

based primarily on clinical examination rather than

on imaging studies. When clinical findings are am-

biguous, however, diagnostic imaging is useful [1].

Fournier’s gangrene is a synergistic polymicrobial

necrotizing fasciitis of the perineum or perirectal or

genital area that predominantly affects the scrotum in

men and frequently extends to involve the lower

abdominal wall. Predisposing conditions include di-

abetes mellitus, alcoholism, advanced age, and im-

munodeficiency syndrome [9]. Fournier’s gangrene

is characterized by obliterative endarteritis, which re-

sults in a cutaneous and subcutaneous vascular necro-

sis. The most common pathogens isolated in patients

with this syndrome are Klebsiella, Proteus, Strepto-

coccus, Staphylococcus, Peptostreptococcus, Esche-

richia coli, and Clostridium perfringens [8,10,11]. It

was first described in 1883 as an idiopathic condition

of the scrotum. The disease currently differs from

the original description in that it includes women and

is known to be secondary to a defined source of in-

fection in 95% of the cases.

Conventional radiography, CT, and sonography

can aid in determining the location and cause of gas

in the scrotum. Crepitus (gas in the tissue) has been

reported in 18% to 62% of cases and can be detected

by US, CT, and conventional radiography. Subcuta-

neous gas within the scrotal wall is the sonographic

hallmark of Fournier’s gangrene [12]. Sonographi-

cally, the gas appears as numerous discrete hyper-

echoic foci with reverberation artifacts (Fig. 5A, B)

[12,13]. Other sonographic findings include scrotal

wall thickening while the echotexture of the testis

and epididymis remains normal. Inguinoscrotal her-

nia can present with gas on sonographic examination

and can be differentiated from Fournier’s gangrene

by the presence of gas within the protruding bowel

lumen and away from the scrotal wall [1].

Epididymo-orchitis

Acute epididymo-orchitis or epididymitis is the

most common cause of acute scrotum in adolescent

boys and adults. Sexually transmitted Chlamydia

trachomatis and Neisseria gonorrhea are common

pathogens in men younger than 35 years. In prepu-

bertal boys and men over 35 years of age, the dis-

Fig. 5. (A) Surgically confirmed case of Fournier gangrene. Longitudinal US of the testis (T) shows sparing of the testis. Both

sonograms show air (arrowhead) parallel to the transducer face with reverberation artifact (arrow). (B) Axial CT in another

patient with proven Fournier gangrene, which shows subcutaneous air (arrowhead) dissecting the fascial planes.


ease is most frequently caused by E coli and Proteus

mirabilis [14]. Prehn [15] described the clinical dif-

ferentiation of scrotal pain associated with epididy-

mitis and acute torsion. Pain associated with acute

epididymo-orchitis is usually relieved when the tes-

ticles are elevated over the symphysis pubis; how-

ever, the scrotal pain associated with testicular torsion

is not lessened with this maneuver (Prehn’s sign).

Other causes, such as sarcoidosis, brucellosis, tuber-

culosis, cryptococcus, and mumps, also may cause

epididymitis and orchitis. Drugs, such as amiodarone,

also may cause epididymitis (chemical epididymitis)

[16]. Complications of acute epididymitis include

chronic pain, infarction, abscess, gangrene, infertility,

atrophy, and pyocele.

Epididymitis first affects the tail of the epididymis

and then spreads to involve the body and head of the

Fig. 6. Clinically proven epididymo-orchitis. Transverse

US of the testis (T) shows a markedly enlarged epididymis

(arrows) with variable echotexture.

epididymis. Orchitis develops in 20% to 40% of cases

of epididymo-orchitis by direct spread of infection.

On gray scale, the epididymis is enlarged and

usually appears hypoechoic or hyperechoic (second-

ary to hemorrhage) (Fig. 6) [17]. Other signs of in-

flammation, such as reactive hydrocele or pyocele

with scrotal wall thickening, are present in most cases.

Diffuse testicular involvement is confirmed by testicu-

lar enlargement and an inhomogeneous testicular

echotexture. Gray scale sonographic findings are non-

specific, but acute epididymo-orchitis is the most

common disorder with this combination of findings.

In one study that involved 20 cases of epididymo-

orchitis, 11 of 20 cases had enlarged and heteroge-

neous appearance of the epididymis or testis [18].

In orchitis there is edema of the testis contained within

an unyielding tunica albuginea, which results in var-

ious scales of reflectivity, seen as heterogeneity on

sonography [16,19]. This variable reflectivity may be

seen as a diffuse process or focal involvement, the

latter manifested as multiple hypoechoic lesions

within the testicular parenchyma. It is difficult to

differentiate focal areas of heterogeneity from neo-

plastic lesions. A heterogeneous echo pattern does not

always signify orchitis.

The increased blood flow to the epididymis and

testis on color Doppler examination is a well-estab-

lished criterion for the diagnosis of epididymo-orchi-

tis (Fig. 7) [20]. Normally, epididymal arterial flow is

of a low-resistance, high-flow state. With the US

machines currently in use, blood flow can be seen in

a normal epididymis on color Doppler sonography. In

one study it was seen in 100% of the cases [21]. The

mere presence of color flow in epididymis is not

equivalent to epididymitis; therefore, it is important

to compare the vascularity in both epididymii.

Fig. 7. Clinically proven epididymo-orchitis. Color Dopp-

ler of the testis (T) shows marked hyperemia of the epi-

didymis (arrow).


Increase of vascularity in acute epididymitis is

secondary to the increased number and concentration

of identifiable vessels with hyperemia, which results

in a high-flow/low-resistance pattern [22–24]. Analy-

sis of the spectral waveform also can provide use-

ful information, because inflammation of epididymis

and testis is associated with decreased vascular resist-

ance to that seen in normal individuals. In the testes

of a normal healthy volunteer, the resistive index (RI)

is rarely less than 0.5, but more than half the patients

with epididymo-orchitis have an RI of less than 0.5

(Fig. 8) [22,24,25]. In normal testes, intratesticular

venous flow is difficult to detect. Easy detectability

and increased venous flow in the testes greatly

suggest orchitis. The absence of venous flow in the

presence of arterial signal in orchitis is abnormal

and suggests venous occlusion, which may be sec-

ondary to impending infarction or underlying coagu-

lopathic disorder. Reversal of the spectral Doppler

diastolic plateau in acute epididymo-orchitis suggests

venous infarction. In all cases of testicular inhomo-

geneity diagnosed as epididymo-orchitis, if there is

no demonstrable improvement with antibiotic treat-

ment, the diagnosis should be reconsidered. Tumor

markers, a hypercoagulation profile, or repeat US

may reveal a different diagnosis, such as testicular

tumor or thrombosis.

Fig. 8. Duplex Doppler evaluation of the testis demonstrates

an RI of 0.44 and increased vascularity of the testis in a

patient with epididymo-orchitis.

Primary orchitis

Mumps is the commonest cause of orchitis without

accompanying epididymitis and is bilateral in 14% to

35% of cases [1]. Sonographically, the testes appear

enlarged with decreased echogenicity. In one study of

mumps-related epididymo-orchitis, 9 of 11 cases were

unilateral, and all 11 cases had an enlarged testis and

increased testicular vascularity. Testicular echogeni-

city was uniformly decreased in all 11 cases [26].

Hyperemia and heterogeneity isolated to the testis can

be seen in cases of orchitis, tumor, infarction, and

especially transient torsion of the testis. Because

intratesticular venous flow is difficult to detect in

normal testes, increased and easily detected venous

flow in the testes greatly suggests orchitis [20].

Cellulitis

Scrotal wall cellulitis is common in patients who

are obese or immunocompromised or have diabetes.

The sonographic signs are an increase in scrotal wall

thickness and the presence of hypoechoic areas with

increased blood flow shown on color Doppler. Scrotal

wall cellulitis may lead to scrotal abscess. Such ab-

scesses are usually well loculated, with irregular

walls and low-level internal echoes [1].

Intratesticular abscess

This condition is usually secondary to epididymo-

orchitis, but other causes include mumps, trauma, and

testicular infarction (Fig. 9). The sonographic features

include shaggy irregular walls, an intratesticular lo-

Fig. 9. Surgically confirmed testicular abscess. Transverse

US of the testis (T) shows fluid-debris level (arrow) con-

sistent with intratesticular abscess that developed secondary

to epididymo-orchitis.


cation, low-level internal echoes, and occasional

hypervascular margins [27].

Fig. 10. Diagram represents abnormal (Bell-Clapper defor-

mity) and normal insertion of the tunica vaginalis. (From

Dogra V, Ledwidge ME, Winter III TC, et al. Bell-Clap-

per deformity. AJR Am J Roentgenol 2003;180:1176–7;

with permission.)

Vascular

Testicular torsion

Testicular torsion and epididymo-orchitis com-

monly present with pain. The main role of US is to

differentiate acute testicular torsion, which is a sur-

gical emergency, from epididymo-orchitis. Clinical

differentiation of these conditions is difficult, with

a nearly 50% false-positive rate for diagnoses of

testicular torsion based solely on clinical findings,

which often results in unnecessary surgical explora-

tion [28]. Hunter described the first case of testicular

torsion [15]. Torsion of the spermatic cord occurs

most commonly from 12 to 18 years of age but can

occur at any age. The chance of torsion of the testis or

its appendage developing by age 25 is approximately

1 in 160 [29], with 2% of testicular torsions being

bilateral [30].

Patients with acute torsion present after a sudden

onset of pain followed by nausea, vomiting, and a

low-grade fever. Physical examination reveals a swol-

len, tender, and inflamed hemiscrotum. The cremas-

teric reflex is usually absent [31], and the pain cannot

be relieved by elevation of the scrotum [15].

Testicular torsion causes venous engorgement that

results in edema, hemorrhage, and subsequent arterial

compromise, which results in testicular ischemia. The

extent of testicular ischemia depends on the degree of

torsion, which ranges from 180� to 720� or more.

Experimental studies indicate that 720� torsion is

required to occlude the testicular artery [32]. When

torsion is 180� or less, diminished flow is seen. The

testicular salvage rate depends on the degree of tor-

sion and the duration of ischemia. A nearly 100%

salvage rate exists within the first 6 hours after the

onset of symptoms, a 70% rate in 6 to 12 hours, and a

20% rate in 12 to 24 hours [33].

Intravaginal torsion occurs within the tunica va-

ginalis. In patients with ‘‘Bell-Clapper deformity’’

(Fig. 10), tunica vaginalis completely encircles the

epididymis, distal spermatic cord, and the testis

rather than attaches to the posterolateral aspect of the

testis [1,34]. This leaves the testis free to swing and

rotate within the tunica vaginalis, much like a clapper

inside a bell. Bell-Clapper deformity is bilateral in

80% of patients.

Testicular perfusion can be evaluated by color

Doppler, power Doppler, or spectral Doppler sonog-

raphy. Color Doppler sonography can demonstrate

intratesticular flow reliably [17,24,35]. Power Dopp-

ler sonography uses the integrated power of the

Doppler signal to depict the presence of blood flow.

Higher power gains are more likely with power

Doppler sonography than with standard color Dopp-

ler sonography, which results in increased sensitivity

for detecting blood flow. Power Doppler sonography

is valuable in scrotal sonography because of its

increased sensitivity to low-flow states and its inde-

pendence from the Doppler angle correction [36,37].

Pulsed Doppler sonography is a useful method to

identify flow in the testis using the time-velocity

spectrum to quantify blood flow [38]. The spectral

waveform of the intratesticular arteries characteristi-

cally has a low-resistance pattern [35], with a mean

RI of 0.62 (range, 0.48–0.75) [17]. This is not true for

testicular volumes less than 4 cm3, however, which

Fig. 11. Surgically confirmed testicular torsion. (A) Color Doppler US of the testis (T) demonstrates the absence of intrates-

ticular blood flow with peripheral hyperemia (arrows). (B) Involvement of the epididymis in testicular torsion. There is no blood

flow within the testis (T) or epididymis (E). Peripheral hyperemia is seen (arrow).


are often found in prepubertal boys, in whom dia-

stolic arterial flow may not be detectable [39].

The role of color Doppler and power Doppler

sonography in the diagnosis of acute testicular torsion

is well established [24,40]. Using the presence or ab-

sence of identifiable intratesticular flow as the only

criterion for detecting testicular torsion, color Dopp-

ler was 86% sensitive, 100% specific, and 97% ac-

curate in the diagnosis of torsion and ischemia in

painful scrotum (Fig. 11A, B) [23]. The high degree

of accuracy is attributable to the improved depiction

of power Doppler sonography over color Doppler

sonography in normal prepubertal and postpubertal

testes [41]. Sonographic findings vary with the dura-

tion and degree of rotation of the spermatic cord.

Fig. 12. Surgically confirmed testicular torsion. Gray scale US o

appearance. (B) Epididymal involvement in testicular torsion in a

hypoechoic. There was no blood flow in the testis or epididymis o

Gray scale images are nonspecific for detecting

testicular torsion [22] and often appear normal if the

torsion has just occurred. Testicular swelling and

decreased echogenicity are the most commonly en-

countered findings 4 to 6 hours after the onset of

torsion. Twenty-four hours after the onset, the testis

has a heterogeneous echotexture secondary to vascu-

lar congestion, hemorrhage, and infarction, which is

referred to as late or missed torsion. An enlarged and

hypoechoic epididymal head may be visible because

the deferential artery that supplies the epididymis is

often involved in the torsion (Fig. 12A, B). In the

setting of testicular torsion, normal testicular echo-

genicity is a strong predictor of the testicular viability

[42]. Gray scale findings of testicular torsion are sum-

f the testis (A) shows an enlarged testis with a hypoechoic

nother patient. The epididymis (E) is enlarged and appears

n color Doppler examination (not shown).

Table 1

Gray scale findings of testicular torsion

Testicular torsion Gray scale patterns

Acute torsion with

viable testis

Normal

Acute torsion

with infarction

Hypoechoic pattern that may be

total or partial in case of a

partial infarct

Acute torsion with

hemorrhagic infarction

Hyperechoic and heterogeneous

echo patterns

Chronic torsion Hypoechoic with small testis

Box 1. Testicular torsion: color flowDoppler patterns

1. Absent arterial and venous flow2. Increased RI on affected side (dimin-

ished or reversed diastolic flow)3. Decreased flow velocity difficult to

measure because of small vessels/angle correction but may be subjec-tively inferred by relative difficulty infinding small, low-amplitude flow onsymptomatic side


marized in (Table 1). Other indicators include the pres-

ence of scrotal wall thickening and reactive hydrocele.

Because gray scale findings are often normal in the

early phases of torsion, the Doppler component of the

examination is essential. The absence of testicular

flow on color and power Doppler sonography is con-

sidered diagnostic of ischemia provided that the US

scanner is optimized to detect slow flow, is limited to

the use of a small color-sampling box, and is adjusted

for the lowest repetition frequency and the lowest

possible threshold setting [43]. The threshold should

be set just above the detection of color noise. The

absence of color flow Doppler on US examination is

not synonymous with testicular torsion, because other

conditions, such as testicular polyarteritis nodosa,

can mimic torsion [44]. The color flow Doppler and

spectral Doppler waveform findings in testicular tor-

sion are summarized in Box 1.

Torsion may be complete, incomplete, or transient.

Cases that show partial or transient torsion present a

diagnostic challenge. The ability of color Doppler

imaging to diagnose incomplete torsion accurately

remains undetermined. The role of spectral Doppler

analysis is not well established for diagnosing partial

torsion, but the findings may be useful (Fig. 13A, B)

[45]. No studies are available to validate the role of

spectral Doppler in partial torsion; however, sporadic

case reports exist to suggest its usefulness [46,47].

Asymmetry in the testicular RIs with decreased dia-

stolic flow or diastolic flow reversal may be seen. The

presence of a color or power Doppler signal in a

patient with the clinical presentation of torsion does

not exclude torsion [47].

Extravaginal testicular torsion occurs exclusively

in newborns. Torsion occurs outside the tunica vagi-

nalis when the testis and gubernaculums are not fixed

and are free to rotate [48]. The affected neonate

presents with swelling, discoloration of the scrotum

on the affected side, and a firm painless mass in the

scrotum [49,50]. The testis is typically infarcted and

necrotic at birth. Sonographic findings include an

enlarged, heterogeneous testis, ipsilateral hydrocele,

skin thickening, and no color flow Doppler signal

in the testis or the spermatic cord [51]. In children,

power Doppler US is more sensitive than color Dopp-

ler US for detection of intratesticular blood flow. In

one study, power Doppler US demonstrated intra-

testicular blood flow in 66 (97%) testes, whereas

color Doppler US demonstrated intratesticular blood

flow in 60 (88%) testes. Combined techniques de-

picted blood flow in all 68 (100%) testes [52].

Appendiceal torsion

The normal appendix testis appears as an ovoid

structure 5 mm in length in the groove between the

testis and the epididymis. The appendix testis is iso-

echoic to the testis and occasionally may be cystic.

The appendix epididymis is of the same approximate

dimensions as the appendix testis but is more often

pedunculated [53]. These appendages may become

twisted. Torsion of either appendage produces pain

similar to that experienced with testicular torsion, but

the onset is more gradual. The classic finding on

physical examination is a small, firm nodule that is

palpable on the superior aspect of the testis and

exhibits a bluish discoloration through the overlying

skin; this is called the ‘‘blue dot’’ sign [54]. The cre-

masteric reflex still can be elicited, although it is usu-

ally absent in testicular torsion. Approximately 91%

to 95% of twisted testicular appendices involve the

appendix testis and occur most often in boys aged 7 to

14 years.

Sonographic evaluation of torsion of the append-

ages of the testes usually reveals a circular mass with

variable echogenicity adjacent to the testis or epididy-

mis (Fig. 14) [55,56]. Reactive hydrocele and skin

thickening are common in these cases. Increased

peripheral flow may be seen around the torsed testicu-

Fig. 13. Surgically confirmed partial torsion. (A) The left testis shows normal intratesticular arterial spectral waveform. (B) In

the same patient, the right testis demonstrates diastolic flow below the baseline, which indicates loss of tissue perfusion. This

waveform pattern is abnormal and suggests partial testicular torsion. (From Dogra VS, Sessions A, Mevorach A, et al. Reversal

of diastolic plateau in partial testicular torsion. J Clin Ultrasound 2001;29:105–8; with permission.)


lar appendage on color Doppler US [14,23,24]. These

cases are managed conservatively with attention given

to pain management. The pain usually resolves in 2 to

3 days with atrophy of the appendix that may calcify.

The role of sonographic examination in torsion of the

testicular appendages is to exclude testicular torsion

and acute epididymo-orchitis.

Varicocele

Idiopathic varicocele

Venous drainage of the scrotum is via the pam-

piniform plexus of draining veins; it is formed around

the upper half of the epididymis in a variable fashion

and continues as the testicular vein through the deep

inguinal ring. The right testicular vein empties into

Fig. 14. Clinically proven case of appendiceal torsion. Lon-

gitudinal view of the testis (T) shows a predominantly

hypoechoic area (arrow) adjacent to the epididymis (E).

the inferior vena cava and the left testicular vein

into the left renal vein. Abnormal dilatation of the

veins of the pampiniform plexus results in varicocele,

which is usually caused by incompetent valves in the

internal spermatic vein. This results in impaired

drainage of blood into the spermatic cord veins when

the patient assumes an upright position or during a

Valsalva’s maneuver. Varicoceles have been noted in

approximately 15% of the general population and in

up to 40% of men with infertility [57]. Patients with

idiopathic varicoceles usually present between the

ages of 15 and 25 years. The veins of the pampini-

form plexus normally range from 0.5 to 1.5 mm in

diameter, with the main draining vein as large as

2 mm in diameter. Varicoceles are more common

on the left side for the following reasons: (1) the left

testicular vein is longer, (2) the left testicular vein

enters the left renal vein at a right angle, (3) in some

men, the left testicular artery arches over the left renal

vein, thereby compressing it, (4) the descending

colon distended with feces may compress the left

testicular vein [58], and (5) a ‘‘nutcracker’’ effect of

compression of the left renal vein may occur be-

tween the superior mesenteric artery and the abdomi-

nal aorta [59].

Varicocele is a clinical diagnosis, and palpation

reveals a scrotal mass that may feel like a bag of

worms with or without a palpable thrill. In one study,

all patients with palpable varicoceles had a spermatic

vein diameter of 5 to 6 mm [60]. The clinical gra-

dation of varicoceles is given in Table 2.

Sonography should be performed in supine and

upright positions. The sonographic appearance of

Table 2

Grade I Not visible but palpable on

Valsalva’s maneuver.

Grade II Less visible but palpable

without Valsalva’s maneuver

Grade III Always visually identifiable

and palpable without

Valsalva’s maneuver.


varicocele consists of multiple, serpigenous, tubular

structures of varying sizes larger than 2 mm in diam-

eter, which are usually best visualized superior or

lateral to the testis. When large, they can extend

posterior and inferior to the testis. Occasionally, low-

level internal echoes can be detected in these dilated

veins secondary to slow flow. Color flow and duplex

Doppler sonography optimized for low-flow velocities

confirms the venous flow pattern with phasic variation

and retrograde filling with Valsalva’s maneuver. The

sensitivity and specificity rates of varicocele detec-

tion approach 100% with color Doppler sonography.

The relationship between nonpalpable (subclini-

cal) varicocele and infertility remains controversial.

After treatment, however, these patients’ partners

have a 40% pregnancy rate [61]. Approximately one

third of men who undergo evaluation for infertility

present with varicocele; however, not all patients with

infertility have a palpable varicocele. In a study of

1372 infertile men, varicocele was found in 29% by

sonography; however, only 60% had a palpable vari-

cocele [62]. Diagnosis of subclinical varicocele is

important because treatment improves sperm quality

in as much as 53% of these cases.

Fig. 15. Intratesticular varicocele. (A) Longitudinal view of the

within the testis. (B) Corresponding spectral Doppler waveform d

va’s maneuver.

Secondary varicoceles

Secondary varicoceles result from increased

pressure on the spermatic vein produced by disease

processes, such as hydronephrosis, cirrhosis, or ab-

dominal neoplasm. Neoplasm is the most likely

cause of nondecompressible varicocele in men over

40 years of age. It is classically from a left renal

malignancy invading the renal vein [3]. Nondecom-

pressible varicoceles on the left or right should

prompt evaluation of the retroperitoneum to exclude

retroperitoneal masses and thrombus or tumor exten-

sion to the left renal vein. An abdominal mass always

should be suspected when an older man presents with

a new varicocele.

Intratesticular varicocele

An intratesticular varicocele can occur in associa-

tion with an extratesticular varicocele, but intrates-

ticular varicoceles are more commonly found alone

[63]. Clinical implications and the pathogenesis of

the newly defined condition, intratesticular varico-

cele, are not yet well established. Patients with intra-

testicular varicocele may have pain related to passive

congestion of the testis, which eventually stretches

the tunica albuginea. The sonographic findings of

intratesticular varicocele are similar to those of pam-

piniform plexus varicocele [58].

Sonographic features include multiple anechoic,

serpigenous, tubular structures of varying sizes within

the testis. Color flow and duplex Doppler sonography

demonstrate the venous flow pattern with a charac-

teristic venous spectral wave form, which increases

testis (T) shows tortuous anechoic, tubular areas (arrow)

emonstrates characteristic venous flow with positive Valsal-


with Valsalva’s maneuver (Fig. 15A, B) [58]. The

main differential considerations are cyst, hematoma,

epidermoid cyst (echogenic rim), and tubular ectasia.

Use of color flow and duplex Doppler affords easy

differentiation. In every longstanding case of varico-

cele that presents with pain, this entity should be

considered and sought [58].

Fig. 17. Surgically confirmed testicular fracture secondary

Intratesticular arteriovenous malformation

Intratesticular arteriovenous malformation is a

rare, benign entity. Its pathogenesis may be congeni-

tal or posttraumatic. The characteristic arterialized

venous spectral waveform is universal to all arterio-

venous malformations [64], and the main differential

consideration is intratesticular hemangioma [65].
to trauma. Color Doppler US of the testis demonstrates a
linear hypoechoic area (arrow) that runs obliquely across the

testis and represents the testicular fracture line.
Testicular trauma
Testicular trauma typically results from athletic

injury, a motor vehicle accident, a direct blow, straddle

injury, or penetrating gunshot trauma. Blunt trauma

accounts for approximately 85% of these cases, and

penetrating trauma comprises the remaining 15%. A

direct blow to the testis with impingement against the

symphysis pubis or ischial ramus is the most common

mechanism of injury from blunt trauma. Approxi-

mately 50 kg of pressure is necessary to rupture the

tunica albuginea during blunt trauma. Testicular rup-

ture is a surgical emergency, and more than 80% of

Fig. 16. Surgically confirmed tunica albuginea rupture. In

this case of testicular trauma, color Doppler US shows a

contour abnormality (arrow) that represents extruded tes-

ticular contents through the ruptured tunica albuginea. The

asterisk represents accompanying hematocele.

ruptured testes can be saved if surgery is performed

within 72 hours after injury [66,67].

Trauma can result in contusion, hematoma, frac-

ture, or rupture of the testis [1]. Scrotal US with color

flow Doppler is helpful in determining the nature and

extent of the injury. The scrotal sonography has 100%

sensitivity for testicular injuries and 80% specificity

for tunica albuginea fractures [68]. Approximately

20% of patients who seek medical attention after

testicular trauma have testicular rupture [69]. Sono-

graphic findings in testicular rupture include inter-

ruption of the tunica albuginea, contour abnormality

(Fig. 16), a heterogeneous testis with irregular, poorly

defined borders, scrotal wall thickening, and a large

hematocele [70,71]. Color and power Doppler sonog-

raphy are helpful because either can detect disruption

of the normal capsular blood flow of the tunica

vasculosa. Heterogeneous intratesticular lesions are

caused by hemorrhage or infarction. Direct visual-

ization of a fracture line is rare and is seen only in

17% of cases (Fig. 17) [71]. Sonographic findings in

testicular trauma are summarized in Box 2.

Hematocele is a blood collection within the tu-

nica vaginalis. On sonography, acute hematoceles

are echogenic, whereas older hematoceles appear as

fluid collections with low-level echogenicity, fluid-

fluid levels, or septations. Hematoceles may be

caused by extratesticular or intratesticular bleeding,

although there is no definite US evidence of testicular

rupture. The presence of associated hyperechoic or

hypoechoic changes in the testicular parenchyma

suggests testicular rupture.

Box 2. Sonographic findings in testiculartrauma

1. Contour abnormality of the testis2. Disruption of the tunica albuginea

(evidenced by interruption of tunicavasculosa)

3. Direct visualization of a fracture line4. Presence of hematocele5. Intra- or extratesticular hematoma6. Heterogeneous appearance of the

testis7. Hyperemia of the epididymis

Note that any of the above mentionedfindings may be seen in isolation or inany combination.


Hematomas can involve the testis, epididymis, or

scrotal wall. Their sonographic appearance varies

with time. Acute hematomas appear hyperechoic

and subsequently become complex with cystic com-

ponents. Hematoma appears avascular on color

Doppler sonography [14,40]. Color Doppler sonog-

raphy in posttrauma patients may reveal focal or

diffuse hyperemia of epididymis, which is called

traumatic epididymitis [72].

Patients with intratesticular hematomas fare

poorly without exploration, and 40% of the hema-

tomas result in testicular infection or necrosis, which

often requires orchiectomy. Scrotal exploration is

warranted if there is compelling evidence of testicular

fracture or rupture on scrotal sonography or physical

examination. The presence of a large hematocele is

another indication for exploration. Small hematoceles,

epididymal hematomas, or contusions of the testis

generally pose little risk to the patient and do not

require surgical exploration [73]. In posttrauma

patients with sonographic testicular abnormality, if

surgical exploration is not immediate, their progress

should be followed to demonstrate sonographic reso-

lution of the lesion, because 10% to 15% of testicular

tumors first present after an episode of scrotal trauma

[6]. Complications of testicular trauma include testic-

ular atrophy, infection, infarction, and infertility.

Fig. 18. Surgically confirmed case of inguinal hernia. Gray

scale US of the testis (T) shows the presence of air (arrow-

head) in a loop of bowel away from the skin surface with

reverberation artifact (arrow). (Compare with Fig. 5A.)

Miscellaneous conditions

Inguinal hernia

A hernia may present acutely as a nonpainful

mass or as a painful swelling with incarcerated bowel.

Hernias occur because of persistent patency of the

process vaginalis with protrusion of the peritoneal

contents, such as omentum or bowel, through it into

the tunica vaginalis [32].

US is helpful for patients with equivocal physical

findings and patients who present with acute inguino-

scrotal swelling. Herniation of the abdominal or

pelvic contents in the groin region may be divided

into two main categories: inguinal and femoral. In-

guinal hernias are the most common and can be sub-

divided into direct and indirect types. Direct inguinal

hernias travel through the Hassalbach’s triangle, a

weakness in the anterior abdominal wall. The borders

of this triangle are formed by the lateral border of

the rectus sheath medially, the inferior epigastric

artery laterally, and the inguinal ligament inferiorly

[74]. Indirect hernias travel lateral to the inferior

epigastric artery and through the inguinal canal; they

constitute 80% of all hernias. A femoral hernia occurs

within the femoral canal that lies medial to the femo-

ral vein. Because of the narrowness of the femoral

ring (the opening that forms the neck of a femoral her-

nia), it is more likely than an inguinal hernia to be-

come incarcerated [75]. Femoral hernia is common in

women, with the right side more frequently affected.


Sonographic appearance depends on the hernial

sac contents. Most commonly it contains bowel; the

next most common content is omentum. Other rare

contents include Meckel’s diverticulum and urinary

bladder. Gray scale findings are a fluid- or air-filled

loop of bowel in the scrotum (Fig. 18). Finding real-

time peristalsis indicates the presence of bowel. Oc-

casionally, because contraction of the dartos also can

mimic peristalsis on real-time sonography; the exam-

iner should be aware of this possibility to avoid

misdiagnosis [1]. If the omentum has herniated, areas

of high echogenicity are present, which correspond to

omental fat.

Bowel strangulation is more common with indi-

rect than direct inguinal hernia. An akinetic dilated

loop of bowel observed sonographically in the hernial

sac is reported to have high sensitivity (90%) and

specificity (93%) rates for the recognition of bowel

strangulation [76]. Hyperemia of the scrotal soft tis-

sue and bowel wall suggests strangulation [17].

Patients with Richter’s hernia, a strangulated hernia

in which only a portion of the circumference of the

bowel is obstructed [77], usually present with gastro-

enteritis. Such cases can present a diagnostic chal-

lenge because of the hernia’s small size and the

eccentric bowel wall involvement with limited lumi-

nal compromise. This hernia commonly occurs at a

femoral site. It is important to recognize this condi-

tion because preoperative delays in diagnosis and

high postoperative morbidity are common compared

with other types of strangulated hernias [78].

Testicular tumors

Testicular tumors sometimes can present with

acute pain. This presentation is usually secondary

to epididymo-orchitis or hemorrhage within the tu-

mor. Ten percent of testicular tumors are brought to

attention secondary to epididymo-orchitis [1]. Semi-

noma is the most common tumor to masquerade

as acute orchitis. It is presumed to infiltrate and

obstruct the seminiferous tubules, and it results in

orchitis [1]. Leukemia and lymphoma can have a

similar presentation.

Gray scale findings of intratesticular tumors are

nonspecific and usually hypoechoic in appearance.

Hyperemia also can be seen in testicular tumors.

Acute epididymo-orchitis and intratesticular tumors

larger than 1.5 cm may have increased blood flow on

color Doppler examination. Hypervascularity seen

with tumors is sonographically indistinguishable

from inflammatory hypervascularity [2]. There are

no reliable sonographic criteria to distinguish malig-

nant from focal benign intratesticular lesions, such as

infarction, hemorrhage, infection, or non–germ-cell

tumor [79]. The presence of epididymal involvement

strongly suggests a nonneoplastic process.

All patients with a heterogeneous echo pattern of

testis should be followed to demonstrate their sono-

graphic resolution so that tumors with epididymo-

orchitis presentation are not missed.

Summary

The ability of US to diagnose the pathogenesis of

the acute scrotum is unsurpassed by any other imaging

modality. It is the first imaging performed in patients

with acute scrotum. Knowledge of the normal and

pathologic sonographic appearance of the scrotum and

proper sonographic technique is essential for accurate

diagnosis of acute scrotum. High-frequency trans-

ducer sonography combined with color flow Doppler

sonography provides the information essential to

reach a specific diagnosis in patients with testicular

torsion, epididymo-orchitis, and testicular trauma.

Acknowledgments

The authors would like to acknowledge Bonnie

Hami, MA, for her assistance in the preparation of the

manuscript and Joseph Molter for his assistance in

preparation of photographs.

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Radiol Clin N Am 42 (2004) 365–381

Ultrasound evaluation of abdominal aortic and iliac

aneurysms and mesenteric ischemia

Kathryn Hermsen, MD*, Wui K. Chong, MB, FRCR

Department of Radiology, CB #7510, University of North Carolina, 101 Manning Drive, Chapel Hill, NC 27599, USA

Ultrasound (US) has been used routinely since of an endothelial lining, a connective tissue layer, and

the mid 1980s to evaluate the abdominal aorta. Color

Doppler imaging allows characterization of flow pat-

terns [1]. It is the preferred method for diagnosis and

surveillance of abdominal aortic aneurysms (AAAs)

because of its accuracy, ease of use, and cost effec-

tiveness [1,2]. US has been used to characterize aor-

tic diseases, such as mycotic aneurysm, posttraumatic

pseudoaneurysm, dissection, and detection of mural

thrombus and AAA rupture [3,4]. Other applications

of sonography include characterization of iliac arterial

disease and postoperative evaluation of endovascular

AAA repair. US plays a role in noninvasive diagnosis

of mesenteric vascular occlusive disease in patients

with suspected chronic intestinal ischemia.

Anatomy and histology

The aorta enters the abdomen at the aortic hiatus

at the T12 level. It descends anterior to the lumbar

vertebrae immediately left of midline and tapers dis-

tally [5]. The normal luminal diameter of the in-

frarenal abdominal aorta varies according to age and

gender. In young patients without vascular disease, it

measures 2.3 cm in men and 1.9 cm in women [6].

It increases in size with age. In one study, average

luminal diameter in men without aneurysm with a

mean age 70.4 years was 2.8 cm [2].

The aorta is an elastic artery composed of three

layers: the tunica intima, tunica media, and tunica ad-

ventitia. The aortic intima is thick and is composed


doi:10.1016/j.rcl.2003.12.003


E-mail address: [email protected] (K. Hermsen).

an internal elastic membrane. The endothelium con-

sists of squamous cells oriented parallel to the direc-

tion of blood flow and connected by tight junctions.

The tunica media is composed of smooth muscle

and connective tissue. The tunica adventitia of the

aorta is thin and consists of connective tissue fibers,

fibroblasts, and macrophages. It also contains the in-

nervation of the aorta and its blood supply (vasa va-

sorum) [7].

The aorta bifurcates to form the common iliac ar-

teries near the level of the umbilicus (approximately

L4). The common iliac arteries proceed anterolaterally

in association with the common iliac veins and bifur-

cate into the internal and external iliac arteries [5].

Major branches of the abdominal aorta routinely

visualized by US include the celiac axis, superior

mesenteric artery (SMA), and renal arteries. The ce-

liac axis is the first major division of the abdominal

aorta. It generally gives rise to the left gastric, hepatic,

and splenic arteries, although anatomic variants are

frequent [3]. The left gastric artery is seldom visual-

ized by US [8]. The SMA arises anterior to the L1

vertebra and posterior to the body of the pancreas [9].

It travels with the superior mesenteric vein anterior to

the duodenum and inferiorly to divide within the

mesentery 5 to 6 cm from its origin. The normal

inferior mesenteric artery is infrequently visualized by

US. In disease states it may hypertrophy and become

visible [8]. The renal arteries arise from the lateral

wall of the aorta within 1.5 cm of the SMA [3].

Supernumerary renal arteries are frequent [3].

Branches of the aorta and the iliac arteries are

classified as muscular arteries. When compared with

the elastic arteries, such as the aorta, their intima

are thinner and have less subendothelial connective

s reserved.

K. Hermsen, W.K. Chong / Radiol Clin N Am 42 (2004) 365–381366

tissue. Likewise, the tunica media contains less elas-

tic material. The tunica adventitia is thicker and has

greater collagen content [7].

Flow characteristics

As characterized by color Doppler, the aorta is

a high-resistance vessel. Velocity climbs rapidly in

early systole and falls rapidly in early diastole [3].

The proximal aorta demonstrates biphasic waveforms

with reversal of flow in early diastole. The distal aorta

demonstrates triphasic waveforms (small component

of forward flow in late diastole). Normal blood flow

is laminar (Fig. 1) [1].

The celiac axis demonstrates high-resistance flow

at its origin with rapid systolic upstroke and rapid de-

cline (Fig. 2). Hepatic and splenic arteries are low-

resistance vessels with substantial forward flow

throughout diastole [3].

The SMA is a high-resistance vessel in the fasting

state. In the fasting patient, flow is triphasic, with

rapid systolic upstroke and reversal of flow in early

diastole. In the postprandial state, spectral Doppler

waveform of the SMA changes to a low-resistance,

high-flow pattern secondary to decrease in splanchnic

vascular resistance. Peak systolic velocity (PSV)

increases and forward flow is seen throughout dias-

tole (Fig. 3) [8]. Moneta et al [10] described the

effects of meal content on mesenteric vascular resist-

ance. Test subjects were imaged after ingesting vary-

ing amounts of fat, proteins, and carbohydrates.

Control meals consisted of water or mannitol. In the

Fig. 1. (A) Normal aorta with normal triphasic waveform. Note rapid

flow characteristic of a high resistance vessel. (B) Normal aortic t

SMA, PSV, end diastolic velocity (EDV), and mean

velocity increased with all except water. The great-

est changes were demonstrated in end diastolic flow

[10]. The neurohumoral mechanisms behind this

response are incompletely understood. Hormones re-

leased in the presence of fat, carbohydrates, and pro-

teins, including cholecystekinin, vasoactive intestinal

peptide, gastrin, secretin, and kinins, are released into

the bowel wall and act as vasodilators. Decreased

oxygen concentration that results from increased con-

sumption associated with active transport of nutrients

may act as a vasodilatory stimulus [11]. Postpran-

dial changes in vascular resistance are considerably

less pronounced in the celiac axis (CA), which indi-

cates that this is a low-resistance circuit regardless of

feeding [8]. In the study by Moneta et al, minimal

changes were observed in the CA with feeding [10].

Imaging techniques

The primary limitations in imaging the abdominal

aorta are patient body habitus and the presence of

bowel gas. Thinner patients are more easily imaged.

No bowel preparations have proved effective in lim-

iting the effect of interposed bowel gas. In imaging of

the abdominal aorta, patients are usually scanned after

an 8- to 10-hour fast. The presence of barium within

the bowel attenuates US transmission, and imaging

should be postponed after gastrointestinal procedures.

The patient is initially scanned in the supine position

using linear 4-, 3.5-, or 2.5-MHz transducers; curved

5- or 3.5-MHz transducers are also used, depending

systolic peak followed by rapid decline and brief reversal of

ransverse diameter measurement.

Fig. 2. Normal celiac axis origin and bifurcation. The left

gastric artery is seldom seen.

Fig. 4. (A, B) Importance of obtaining measurement per-

pendicular to plane of vessel. Oblique measurements may

overestimate lumen diameter.

K. Hermsen, W.K. Chong / Radiol Clin N Am 42 (2004) 365–381 367

on patient body habitus [1]. The aorta is imaged in

sagittal and transverse planes at its proximal, mid, and

distal portions. In the presence of a tortuous aorta, it is

important to obtain measurements perpendicular to

the long axis of the vessel. Oblique measurements

Fig. 3. (A) Fasting SMA. Note rapid systolic upstroke and

low diastolic flow. (B) Postprandial SMA. Note increased

diastolic forward flow.

may overestimate the lumen diameter (Fig. 4) [12].

The anteroposterior and transverse diameters are mea-

sured from outer wall to outer wall. The common iliac

arteries are imaged at the level of the bifurcation in

anteroposterior and transverse diameter. In the upper

abdomen, a good acoustic window is often found in

the midline between the rectus abdominus muscles.

The lateral aspect of the rectus muscles also may

provide a good window, especially for visualizing

the iliac vessels [3]. A left lateral decubitus or oblique

approach is often helpful in patients with excessive

bowel gas and for visualizing the mid and lower ab-

dominal aorta. Use of slow graded compression with

the transducer may displace bowel loops. Color

Doppler may aid in identifying the aorta [1]. Flow

characteristics (laminar versus turbulent) and mea-

surements, including PSV and EDV, are documented.

Flow within the renal arteries is demonstrated, and

each kidney is observed in long axis.

The aorta is visualized similarly after endovascu-

lar stenting using 2.5- and 3.75-MHz curved trans-

ducers. Duplex and color flow Doppler analysis is

obtained at the level superior to the stent, at its

proximal attachment, including right and left iliac

attachments. Flow within the SMA and renal arteries

is documented. The maximum transverse diameters

of the graft lumen and aneurysm sac are measured in

the anteroposterior and transverse planes. The clot

within the aneurysm sac is observed with color

Doppler in the transverse and longitudinal planes to

evaluate for leak around the stent or flow within the

sac. Detectable flow is considered an indication of

leak [13]. Another indicator of graft compromise is

enlargement of the aneurysm sac or failure of the

aneurysm sac to regress. Multiple types of endoleaks

have been described. In 1997, White first described

endoleaks (Box 1) [14,15].

Cursory evaluation of the mesenteric arterial vas-

culature is undertaken in routine imaging of the

Box 1. White classification ofendoleaks[15]

Type I: Direct communication betweenthe graft and aneurysm sac via anineffective seal at the graft ends orattachment sites.

Type II: Retrograde flow through lum-bar arterials, the inferior mesentericartery (IMA), or accessory renal ar-teries feeds into the aneurysm sac.

Type III: Seen in modular, multisegmen-tal grafts. Leak occurs through defi-ciency in graft fabric and may be aresult of altered hemodynamics sec-ondary to aneurysm sac shrinkage.

Type IV: On contrast, CT appears as ablush of contrast outside the graftfrom contrast diffusion through thenaturally porous graft fabric orthrough small defects in the fabricat the site of sutures or struts. Mayrequire angiography to distinguishfrom Type III graft.


abdominal aorta. More detailed examination to assess

for mesenteric occlusive disease faces several techni-

cal challenges. Bowel gas, respiratory motion, and

vessel depth confound identification of the mesen-

teric vessels [8]. Various methods have been used to

reduce interference by gas, including cathartic bowel

preparation the night before, oral simethicone 15 min-

utes before examination, liquid diet the evening be-

fore followed by 8- to 12-hour fast, and fasting alone

[16,17].

The CA is scanned from its origin to its bifurca-

tion. The SMA is examined from its origin and

followed 5 to 6 cm distally. In the fasting state, the

normal SMAwaveform is triphasic. Should a biphasic

waveform be observed, the sonographer searches for a

replaced hepatic artery. This anatomic variant occurs

in approximately 20% of the population. It arises from

the lateral SMA and travels cephalad and right to

supply the liver. The presence of a replaced hepatic

artery results in biphasic SMA flow [16,17]. The

position of the CA and SMA in the upper abdomen

often requires high Doppler angles of insonation.

Unfortunately, this introduces error in determining

flow velocities, which usually results in falsely ele-

vated values [8]. Care must be taken to maintain a

Doppler angle of 60� or less while obtaining velocity

measurements [8,18–20].

Abdominal aortic pathology

Aneurysm

An aneurysm is an abnormal expansion of a vessel.

Aneurysms are classified as false or true. True aneu-

rysms include all three layers of the vessel wall. Mul-

tiple configurations of true aneurysms are described.

Most AAAs are true aneurysms and are fusiform; 97%

are infrarenal. Only 2% to 7% extend to the juxtarenal

or suprarenal aorta [21]. Aneurysms that occur proxi-

mal to the renal arteries are more likely to be mycotic

or posttraumatic. AAA is a common condition, with

a prevalence of 1% to 4% in people aged 50 or older

[1]. Most of these aneurysms are idiopathic. The

strongest association with AAA is atherosclerotic

disease. Other risk factors for development of AAAs

include male gender, smoking, chronic obstructive

pulmonary disease, age, and family history. Most pa-

tients with AAA are asymptomatic. Some patients

may present with abdominal or lower extremity pain

[3]. The most common physical examination finding

is a pulsatile abdominal mass. The physical examina-

tion, however, has poor predictive value in the detec-

tion of AAA [22].

Sonography is the primary imaging study for

detection of aortic aneurysms. The accuracy of US

in the diagnosis of AAA approaches 100% [3,27]. The

typical US appearance of AAA is of a dilated vessel

with an irregular lumen. Ulceration or cystic changes

may be seen as focal hypoechoic regions within

the vessel wall [3]. Echogenic mural thrombus is

present in most large lesions and may be circumfer-

ential or eccentric (Figs. 5, 6). Juxtarenal AAAs may

appear to involve the renal arteries at US because

of apparent overlap of the aneurysm wall with the

renal ostia. Careful evaluation of the course of the

renal arteries and aorta in multiple planes may clarify

the relationship of the aneurysm to the renal arteries.

Multidetector CT with coronal reconstruction or aor-

tography is usually required to evaluate renal artery

involvement in juxtarenal aneurysms, however [1].

Flow within AAAs may be laminar or turbulent.

Turbulent flow is associated with formation of mural

thrombus (Fig. 7). It has been proposed that thrombus

imparts tensile strength to the aneurysm wall by

absorbing forces generated by flow. Mower used

computer-generated models of AAA that ranged in

size from 2 to 4 cm to study the effects of thrombus

size and composition on wall stress [23]. In this

Fig. 5. (A) Transverse view of AAA with mural thrombus

(arrow). (B) Color Doppler demonstrates turbulent flow

within lumen outlining thrombus.

Fig. 6. Pitfalls in measuring AAA. (A) This echogenic line

(solid arrow) is easily mistaken for the aortic wall. It ac-

tually represents the surface of the thrombus that lines the

wall of a large AAA. Open arrow demarcates the true aortic

wall. (B) On the transverse view, the large mural thrombus is

better seen. (Open arrows mark the true vessel wall.)

Fig. 7. Turbulent flow within AAA. Note the hypoechoic

thrombus (arrow).


study, the larger the mural thrombus, the greater the re-

duction in wall stress. Organized mural thrombi im-

parted greater tensile strength than more pliant ones.

The authors speculated that the tendency of eccen-

tric mural thrombi to collect along the ventral wall

may explain the rarity of ventral rupture [23]. The

presence of mural thrombus also may help to restore

laminar flow.

The most catastrophic complication of abdominal

aortic aneurysm is rupture. Rupture carries a high

mortality rate. Fifty percent of patients do not reach

the hospital alive. The overall mortality rate is 80% to

94% [1]. Signs and symptoms associated with rupture

include severe abdominal and back pain, nausea and

vomiting, and hypotension [1]. Aneurysm size and

rate of enlargement are the most important factors in

predicting potential rupture. In a 15-year study,

Brown et al [24] followed 476 patients with AAA

larger than 5 cm who were deemed unfit surgical

candidates. The risk of rupture in male patients with

AAA of 5 to 5.9 cm was 1% per year; in male patients

with AAA 6 cm or larger, the risk was 14.1%. Gender

differences also were noted in this study. Women with

aneurysms of similar size were at fourfold higher risk

for rupture [24]. Aneurysms are generally expected to

enlarge 2 to 4 mm per year. Aneurysms that enlarge by

5.5 to 6 mm per year are regarded as high risk for

rupture [12]. Sharp et al [25] identified 32 patients

with aneurysms less than 5.5 cm per year that had

enlarged 5 mm or more in the past 6 months. Over a

period of 50 patient years, none ruptured. Thus,

the risk of rupture was calculated to be 0 to 6 per

100 patient years [25]. CT is the imaging modality of

choice in the setting of rupture because it is not subject

to technical factors, such as interposed bowel gas, and

grants a greater perspective on the extent of bleeding


[3]. The US appearance of rupture is that of a large,

usually hypoechoic retroperitoneal fluid collection.

Other complications of AAA include embolization

of mural thrombus, occlusion of the renal and splanch-

nic arteries, obstructive uropathy (usually on the left),

and arteriovenous fistula (usually with the inferior

vena cava [IVC], or left renal vein) (Fig. 8) [2,3]. A

less common complication is duodenal obstruction,

which results from compression of the duodenum

(SMA syndrome) between an enlarging AAA and

the SMA [26].

US is ideal for monitoring AAAs because it is

inexpensive, does not require the use of contrast

material or radiation, and is highly accurate. CT is

often used in AAA evaluation, but it faces some

technical limitations. Because the aneurysmal aorta is

frequently ectatic, slices obtained in the axial plane

only may be obtained with a degree of obliquity,

which potentially overestimates the size of the aneu-

rysm. Because changes in measurements of only a

few millimeters may influence management greatly,

potential effects of measurement variability be-

tween CT and US are an important consideration.

Fig. 8. Left ureteral obstruction by AAA. (A) Distal AAA.

Lumen diameter is normal proximally and expands distally.

(B) Mild left hydronephrosis secondary to compression

by AAA.

Wanhainen et al [2] evaluated differences in observer

measurements between CT and US in 475 patients.

Thirty-three were found to have AAAs (defined as

diameter larger than 3 cm). In patients with normal

aortas (<3 cm), US overestimated the diameter by

2.8 mm in anteroposterior diameter and 3.8 in trans-

verse diameter. The difference in aneurysmal aortas

was greater, with a variability of 8 mm or less in

anteroposterior and 10.6 mm in transverse measure-

ments. The authors found the variability in transverse

measurements to be unacceptably high and preferred

using anteroposterior diameters in assessing aneurysm

size [2]. There is no true ‘‘gold standard’’ modality in

the measurement of AAA. Lanne et al [12] reported

greater reliability for US using an automated echo

tracking device for measurement of the aortic lumen.

Frequent indications for aortic US are the finding

of a pulsatile abdominal mass on physical exami-

nation and evaluation of an AAA incidentally dis-

covered on a CT performed for another purpose.

Unfortunately, however, many AAAs are not discov-

ered until rupture. Given the dismal prognosis of

rupture and the relatively low mortality rate for repair

(2%–5%), is screening for AAA in high-risk patients

a viable option? Lee et al [27] examined the cost

effectiveness of conducting a ‘‘quick screen’’ (ie, ab-

breviated US) evaluation of the abdominal aorta in at-

risk populations. The examination was limited to less

than 5 minutes and was performed at reduced cost.

The sensitivities and specificities for the quick screen

and standard duplex US were 100%. The emphasis

was on screening patients with known risk factors,

such as male gender, smoking, hypertension, hyper-

lipidemia, other peripheral vascular disease, and coro-

nary artery disease. They found screening in at-risk

populations to be cost effective and recommend

screening in men over age 60 [27].

Although most AAAs are idiopathic, certain con-

nective tissue disorders carry an increased risk of

AAA. Ehler-Danlos syndrome is a group of disorders

associated with abnormal collagen synthesis. Type IV

Ehler-Danlos syndrome is associated with vascular

abnormalities, including aneurysms of the elastic ar-

teries and their major branches. Catastrophic com-

plications have been reported with angiography in

patients with Type IV Ehlers-Danlos syndrome, and it

is generally avoided [28].

Pseudo or false aneurysms are generally the result

of a defect in the intima through which blood flows.

Blood escapes through a defect in the arterial wall

and is contained by the surrounding soft tissue. Blood

flows into the aneurysm during systole and out during

diastole, which produces a characteristic appearance

on color Doppler imaging that has been likened to the

Fig. 9. Classic color Doppler ‘‘Yin-Yang’’ appearance of

pseudoaneurysm. Blood enters the false aneurysm (red),

strikes the back wall, and reverses direction (blue).


Yin-Yang sign (Fig. 9). False aneurysms caused

by penetrating trauma show ‘‘to and fro’’ flow in the

neck, with blood leaving the artery during systole and

re-entering during diastole. Aortic pseudoaneurysms

are most frequently posttraumatic or mycotic [3,28].

Mycotic aneurysms refer to aneurysms of any type

that have become infected. They are more frequent in

patients younger than 50 years, unlike idiopathic

AAAs, which are more frequent in patients over age

60. Two broad categories of mycotic aneurysms have

been described: those that form secondary to aortic

wall factors (atherosclerosis or stents) and those that

are seeded from a distant source. The second group is

divided according to source of infection: intravascular

(frequently in the form a septic emboli) and extravas-

cular (usually formed by contiguous spread from a

nearby infected site). The most frequent causative

organisms are staphylococci and salmonella. An im-

portant feature of mycotic aneurysms is their tendency

to enlarge rapidly and their propensity for rupture

[4,29]. Few specific US findings are reported. Naga-

numa et al [4] described the presence of gas echoes in

the wall of a mycotic aneurysm with sonography.

Inflammatory aneurysms are a relatively uncom-

mon type of true aneurysm that constitutes approxi-

mately 4% of AAA. They are characterized by fibrotic

thickening of the adventitia and chronic inflammatory

changes [30]. They most frequently occur in the iliacs,

followed by the aorta. On sonography, the aneurysm

wall is thickened with surrounding hypoechoic fi-

brotic tissue. US and CT have proved the most useful

modalities in diagnosing inflammatory aneurysms

[31]. Inflammatory AAAs may be seen in the setting

of retroperitoneal fibrosis. In this setting, the fibrotic

tissue may extend laterally into the retroperitoneum,

and the ureters may become obstructed [32]. Inflam-

matory aneurysms carry a higher rate of morbidity and

mortality than idiopathic AAAs and are more likely to

present with pain in the absence of rupture [30].

Erythrocyte sedimentation rate is usually elevated.

Pennell et al [33] described a triad of chronic abdom-

inal pain, weight loss, and elevated erythrocyte sedi-

mentation rate in a patient with AAA as highly

suggesting inflammatory AAA.

Dissection

Aortic dissection occurs when a defect in the

aortic wall allows the entry of blood, which separates

the intima from the media [34]. Two lumens are

created: a false lumen, which consists of blood within

the vessel wall, and the true vessel lumen. Although

the vessel does enlarge, dilatation is considerably less

pronounced than with true aneurysms. Most often,

dissection occurs along a segment of varying length

and ends with re-entry of the blood column into the

true lumen via a second intimal defect. This serves to

decompress the hematoma and delay rupture [35].

Isolated abdominal aortic dissection is exceedingly

rare in the absence of blunt abdominal trauma [36].

Most aortic dissections originate in the thoracic aorta,

usually the ascending aorta. Several classifications

exist; the most commonly used are the DeBakey and

Stanford classifications. Two thirds of dissections

involve the ascending aorta, usually within a few

centimeters of the aortic valve. In DeBakey types 1

and 3, the dissection plane may extend into the

abdominal aorta [37].

The pathogenesis behind dissection remains con-

troversial. Dissection in the absence of a clear intimal

tear has been documented, which suggests that dis-

section occurs through a defect in the media created

by intramural hemorrhage. The importance of abnor-

malities of the media has been a topic of interest in

the pathogenesis of dissection. Increased incidence of

dissection in patients with Turner’s, Ehlers-Danlos, or

Marfan syndrome, all of which have underlying ab-

normalities of the media, suggests that a primary

defect of the media underlies dissection. To date, no

specific histologic abnormalities have been demon-

strated [38]. Sonesson et al [39] used US to show that


patients with Marfan syndrome had abnormal com-

pliance of the aorta. Most dissections occur in pa-

tients without connective tissue disorders, however.

In these cases, by far the strongest association with

dissection is the presence of hypertension [37].

CT and MR imaging are the imaging modalities of

choice in dissection that involves the abdominal

aorta. Dissection may be an incidental finding in

US evaluation of the aorta, however. The intimal flap

created between the true and false lumen is best

visualized with US in the transverse plane [38]. The

flap moves with arterial pulsation if flow through the

false lumen is preserved. (This may not be seen if

the flap is thickened.) Doppler waveforms in both lu-

mens may appear bizarre, with spectral broadening

and reversed flow. Velocity tends to be slower in the

false lumen (Fig. 10).

A true AAA with organizing thrombus may look

like a dissection on sonography. The outer layer of

thrombus can appear echogenic and be mistaken for

an intimal flap, whereas deeper thrombus appears

anechoic and can mimic the false lumen [40]. Color

Doppler increases the specificity of US in evaluating

dissection. Flow in the false lumen may be too slow

for detection with Doppler. Thrombosis within the

false lumen frequently occurs and is a significant

Fig. 10. (A, B) Abdominal aortic dissection with intimal

pitfall in the use of US for characterization of dis-

section. Nguyen [41] described a case of ‘‘pseudo-

dissection’’ in which an intimal flap with flow on

either side was described with sonography. This was

shown on CT to be an AAA with mural thrombus.

The perception of flow within the ‘‘false lumen’’ was

attributed to mirror image artifact caused by a calci-

fied thrombus surface layer or incorrect color flow

assignment in the anechoic portion of the throm-

bus [41].

US is not the primary imaging modality for aortic

dissection because most dissections involve the tho-

racic aorta.

Ultrasound and aortic endografting

In the early 1990s, Parodi [42] first reported the

endoluminal repair of abdominal aortic aneurysm.

Given the relatively high operative morbidity and

mortality rates associated with open repair (3% –

10% mortality and 15%–40% perioperative morbid-

ity) [43], AAA repair using stent grafts offers a less

invasive alternative to open repair, with reduced

morbidity and mortality rates. The most frequent com-

plication of endografting is the development of leak-

flap (arrow). (C) Turbulent flow within dissection.


age into the aneurysm sac excluded by the graft. This

may occur via direct communication with the graft

lumen at its attachment site or back flow from

collateral arteries communicating with the aneurysm

sac. Leaks are frequent, with cited incidences as high

as 40% [13]. Lifelong monitoring is required. Al-

though the gold standard for postoperative monitor-

ing is CT, US has been used with varying success. It

offers several potential advantages, including avoid-

ance of potentially nephrotoxic contrast agents and

radiation exposure [3,44,45]. Initial studies that

compared CT and US demonstrated promising results

for US. In 1998, Kronzon et al [43] studied 17 pa-

tients after stent repair of AAA with color Doppler

imaging (CDI) and CT. US was successful in dem-

onstrating flow within the excluded aneurysm lumen

using color Doppler and in measuring aneurysm size

(Figs. 11, 12).

Sato et al [44] reported a sensitivity rate of 97%,

specificity rate of 74%, and accuracy rate of 82% for

US in detecting endoleak. With the advent of im-

proved helical scanning techniques, including thinner

collimation and delayed imaging, Golzarian et al [45]

demonstrated improved reliability of CT compared

with US. US detected clinically significant leaks

within the stent graft and iliac limbs; however, it

frequently missed small perigraft leaks. Using CT as

the standard for evaluating US performance, US

detected endoleak with a sensitivity rate of 77% and

specificity rate of 90% [45]. After this, Pages et al [13]

demonstrated a poorer sensitivity and specificity in

endoleak detection of 48% and 93%, respectively.

Although CDI did detect some endoleaks not detected

on CT, the use of delayed postcontrast CT imaging

could detect these leaks. CDI performed better in

monitoring aneurysm size, with a sensitivity rate of

88% and specificity rate of 76% in demonstrating no

change in AAA size. As with unrepaired AAA, US

Fig. 11. (A) Longitudinal image of AAA shows stent (arrow) an

Doppler demonstrates flow within the graft lumen and hypoechoic

and CT demonstrated some discrepancy in measure-

ments. If a preoperative US is available as a baseline,

however, US can be effective in monitoring aneurysm

size [13]. Some authors suggest using both CTand US

when following endografts [13,45].

In a recent study, Greenfield et al [46] found that

US was more accurate than CT for characterizing

endoleaks. In a study of seven endoleaks classified as

type II by CT, US demonstrated two of these to be

type I leaks. Type I leaks generally require immediate

repair, whereas type II are often managed conserva-

tively because they tend to resolve without treatment.

These findings dramatically altered care. US findings

in proximal limb type I leaks were high velocity flow

at the site of the proximal attachment. Distal limb

attachment site leaks demonstrated flow in the sac

opposite the direction of that in the lumen. IMA flow

was antegrade in type I leaks. Type II leaks were

characterized by slower flow within the aneurysm sac

and retrograde flow in the IMA. These finding sug-

gest an adjunct role for US in characterizing endo-

leaks detected by CT [46].

Mesenteric vascular ultrasound

Chronic intestinal ischemia

Chronic intestinal ischemia (CII) is caused by

inadequate blood supply to meet the metabolic de-

mands of the enteric tract after feeding. In the post-

prandial state, intestinal motility increases, as does

oxygen demand from active transport of nutrients.

Clinically, this presents as postprandial pain.

The clinical diagnosis is one of exclusion. It is a

relatively rare entity with no pathognomonic find-

ings. CII occurs most commonly in elderly women

(75%) [8,20]. Patients typically present with colicky

d wall of aneurysm (thick arrow). (B) Application of color

clot (arrow) in the excluded aneurysm sac.

Fig. 12. Type 2 endoleak. (A, B) Color Doppler demonstrates flow outside the graft lumen (arrow). (C) CT correlate: blush of

contrast outside the limbs of the stent (arrow).


postprandial epigastric pain, occasionally with radia-

tion to the back. Symptoms begin 15 to 30 minutes

after eating and persist 1 to 3 hours. Patients associate

feeding with pain and frequently develop ‘‘food

phobia,’’ with anorexia and marked weight loss.

Changes in bowel habits are also frequent [16]. The

abdominal examination is usually nonspecific, with

no localizing or peritoneal signs. An abdominal bruit

is often present, but this finding is too nonspecific to

make the diagnosis of CII to make the diagnosis of

CII. Laboratory data are neither sensitive nor specific.

Malabsorption of various nutrients has been de-

scribed in the setting of CII. Villous atrophy and

epithelial flattening has been shown in biopsy series.

These findings are unreliable and nonspecific, how-

ever [8,16,20,47].

Atherosclerotic narrowing at the origin of the mes-

enteric vessels is the most common factor that pre-

disposes to CII. Other processes, such as vasculitis,

extrinsic or intrinsic compression, and drug reactions,

also may produce symptoms (Box 2). Although CII

is relatively rare, atherosclerotic narrowing of the

mesenteric vasculature is common. In one autopsy

series, 6% to 10% of patients had stenosis of 50% or

more. High-grade CA stenosis is also frequently well

tolerated. In high-grade CA stenosis or occlusion, the

Box 2. Associations with chronicintestinal ischemia

Atherosclerotic diseaseInflammatory vasculitis

RadiationPolyarteritis nodosa (PAN)

Connective tissue disease

1. Berger’s2. Systemic lupus erythematosus

(SLE)3. Rheumatoid arthritis (RA)

Extrinsic compression

1. Neurofibromatosis2. Median arcuate ligament

syndrome

Drug reactions

Cocaine


gastro- and pancreaticoduodenal arteries form an

important collateral pathway. In SMA stenosis or

occlusion, flow may be reconstituted via the hepatic

artery and pancreaticoduodenal arteries. In high-

grade stenosis or occlusion of the SMA and CA,

the IMA may form sufficient collaterals via the

middle colic artery and pancreaticoduodenals (the

arch of Riolan) to supply the foregut. IMA stenosis

is most frequently asymptomatic [8]. Because the

splanchnic vessels are able to form extensive collat-

eral pathways, significant stenosis or occlusion of

two of the three mesenteric vessels is generally

required to produce symptomatic ischemia, although

high-grade stenosis of the SMA alone may produce

symptoms. Collateralization also makes prediction of

CII difficult. The presence of two-vessel disease or

complete SMA occlusion does not imply the presence

of CII in the absence of symptoms [8].

The diagnosis of CII frequently is delayed because

of its tendency to mimic more common disorders,

such as symptomatic gallstones, cholecystitis, pancre-

atic cancer, and peptic ulcer disease. The average time

from onset of symptoms to diagnosis is 18 months

[16]. Traditionally, CII has been diagnosed via an-

giography. There is reluctance to perform angio-

grams for nonspecific clinical findings because of

its invasiveness, cost, and potential complications in

elderly patients. Noninvasive screening tests in

symptomatic patients are needed to evaluate the mes-

enteric vasculature.

The successful application of Doppler sonography

for diagnosis of mesenteric ischemia was first de-

scribed by Jager in 1984 [47]. High PSVs were found

at the origins of the SMA and celiac arteries. PSV in

the SMA was more than 300 cm/second. Spectral

broadening and monophasic waveforms with loss of

reversed diastolic flow also were noted [47].

In a subsequent validation study, Moneta [19]

sought to establish specific US criteria for high-grade

SMA and CA stenosis. One hundred patients under-

went mesenteric duplex scanning followed by arteri-

ography. In this study, a PSV of 275 cm/second or

more predicted 70% stenosis, with a sensitivity rate of

92% and specificity rate of 96%. In CA stenosis, a

PSVof 200 cm/second or more predicted stenosis with

87% sensitivity rate and 80% specificity rate (Fig. 13).

Although elevations in EDVwere observed in stenotic

vessels, use of EDV did not improve the sensitivity or

specificity of results. In a different study, Moneta [18]

found that the ratios of PSV to EDV were not pre-

dictive. These studies addressed one important tech-

nical factor in acquiring PSV data. In patients with

peripheral atherosclerotic disease but no mesenteric

occlusive disease, PSVs were elevated over control

subjects. This result suggests that tortuousity of the

mesenteric vessels in patients with atherosclerosis

may limit the sonographer’s ability to maintain Dopp-

ler angles less than 60� [18]. This inability could resultin falsely elevated PSVs.

Bowersox [20] found that EDV and PSV were

elevated in confirmed SMA stenosis . The study

accepted 50% or more stenosis as being significant.

In normal control subjects, SMA flow was triphasic

with a normal PSV of 134 (F 18) cm/second and

EDV of 24 (F 4) cm/second. (except in replaced

hepatic artery, in which flow was biphasic). PSVs

increased with increasing SMA stenosis. PSV of 300

cm/second diagnosed 50% or more stenosis with a

sensitivity rate of 63% and specificity rate of 100%.

Unlike Moneta, however, Bowersox [20] found that

EDV was more sensitive and specific than PSV. An

EDV of more than 45 cm/second was found to be

100% sensitive and 92% specific in detecting severe

stenosis. Significant CA values could not be estab-

lished in this study. One proposed reason is that col-

laterals through the gastroduodenal arcade can restore

CA flow in the presence of severe stenosis [20].

Two more recent publications favor the use of

EDVs in predicting significant stenosis. Perko et al

[44] evaluated 39 patients with suspected intestinal

Fig. 13. Celiac stenosis. (A) Color Doppler with narrowing at the celiac origin and turbulent flow. (B) Doppler spectrum with

elevated PSV (>300 cm/second) and spectral broadening. (C) Angiogram demonstrates narrowing of the CA (arrow) and SMA.


ischemia using Moneta’s criteria in addition to the

following other parameters: EDV, early diastolic ve-

locity (EaDV), and PDV. A control group of hyper-

thyroid patients was included in this study. They

found that the Moneta criteria (PSV >275 cm/second)

were 90% accurate for stenoses more than 50%. Ac-

curacy improved dramatically, however, when EDV,

EaDV, and PDV were considered. EDVof more than

50cm/second, EaDV of more than 50cm/second, and

PDV of more than 70 cm/second predicted signifi-

cant stenosis with a sensitivity and specificity rate of

100%. PSV in the CA also was examined according

to Moneta’s criteria. An accuracy rate of 94% was

demonstrated using a PSV of more than 200 cm/sec-

ond to predict more than 50% stenosis. As with SMA

disease, evaluation of EDV, EaDV, and PDV pre-

dicted significant CA stenosis with 100% sensitivity

and specificity. In this study, two false-positive results

were noted using PSV as a criteria, one in a hyper-

thyroid patient and the other in a hypertensive patient

with extensive atherosclerotic calcification. Elevated

PSVs occurred in the thyrotoxic group, likely related

to increased stroke volume. EDVand EaDV were un-

affected. High output states may elevate PSV artifi-

cially [48].

Zwolack et al [17] found similar results to the

Perko study. In a retrospective study of 243 patients

with suspected mesenteric ischemia, an EDVof more


than 45 cm/second predicted more than 50% stenosis

with an accuracy rate of 91% (sensitivity 90%, speci-

ficity 91%). Their results for using PSV to predict

SMA stenosis were similar to the Bowersox study,

with a low sensitivity rate (60%) but high specificity

rate (100%) for PSVs of more than 300 cm/second.

Similar to the Perko study, a PSVof more than 200 cm/

second and an EDVof more than 55 cm/sec predicted

CA stenosis with good accuracy, although EDV

demonstrated the greatest accuracy (95% for EDV

versus 93% for PSV). This study also demonstrated

high-grade CA stenosis or occlusion in 100% of

patients with reversed hepatic flow. Because the CA

is frequently difficult to visualize, this finding may be

particularly helpful in inferring CA stenosis [17].

Several factors may account for disagreement

regarding the accuracy in PSV in SMA stenosis.

Zwolack et al [17] described several potential explan-

ations for the discrepancies in results. First, in the

Moneta study [18], 88% of subjects were men. In the

Zwolack study, 70% percent were women. Gender

differences in flow characteristics in the mesenteric

vasculature may be present, although to date these

have not been explored fully. Second, aliasing is more

frequent at PSVs more than 200 cm/second and vary

according to the type of equipment used. This occur-

rence may account for the low sensitivity encountered

using the Moneta criteria for SMA stenosis of 300 cm/

second, whereas PSVs of 200 cm/second predicted

CA stenosis in both studies [17]. Another potential

pitfall in the use of PSV, as described by Moneta et al

[19], is the difficulty encountered in acquiring veloc-

ities at the level of stenosis. Stenoses usually arise at

the origin of the vessel. Distal to this, the PSV is

expected to fall. The reduced sensitivity in PSV

described in some studies may be the result of

sampling of the SMA distal to the stenosis.

The studies described have used different percent

stenoses as significant values. The Moneta criteria

use 70% as a critical value, whereas the remaining

studies use 50%. Using different percentages to

define significant stenoses did not significantly alter

the findings between the studies. In the study by

Zwolack et al [17], the diagnosis of CII was sus-

pected in all patients. Approximately half were found

to have occlusive disease; symptoms in the remaining

patients were attributed to other causes. In the CII

group, most had stenoses of 70% or more at arteri-

ography. In the group without CII, most had stenosis

less than 50%. This finding created a bimodal distri-

bution of vascular lesions. Only 12% of patients fell

between these two groups. This result suggests that

either value is acceptable and may explain the accu-

racy the Perko group demonstrated using the Moneta

criteria of PSV 275 cm/second to predict lesions of

50% or more [17].

In conclusion, duplex US scanning of the mesen-

teric vasculature has been demonstrated to be an

effective screening test in patients with suspected

CII. An adequate examination of the splanchnic ves-

sels can be achieved in only 60% of the general

population. The remaining 40% are limited by body

habitus and interposed bowel gas. Patients with CII

tend to be thinner than the general population and

are easier to scan. Although controversy still exists in

the literature as to the sensitivity and specificity of

using PSV to predict SMA stenosis, PSV is a reliable

parameter for diagnosing CA stenosis. Reversal of

hepatic flow also has been shown to predict CA oc-

clusion [17,19]. EDV reliably predicted significant

SMA and CA stenosis in several studies. In clinical

practice, the US finding of normal vasculature or

subcritical stenoses in patients with abdominal pain

and weight loss can exclude CII. Most patients

with positive duplex US proceed to CT or conven-

tional angiography. Mesenteric US may be a valuable

screening tool.

Splanchnic artery aneurysms

Historically, splenic artery aneurysms have been

the most common visceral artery aneurysms. In recent

years, hepatic artery aneurysms have surpassed splen-

ic aneurysms in incidence with increasing use of

percutaneous biliary procedures [49]. Posttraumatic

pseudoaneurysms in the splanchnic vasculature, most

commonly the hepatic artery, have been reported after

trauma in children (Fig. 14). Blunt trauma is most

frequently implicated, although it has been described

in penetrating trauma. Embolization is the treatment

of choice, although spontaneous thrombosis has been

reported [50,51]. Splenic artery aneurysms are asso-

ciated with acute pancreatitis. They occur in 10% of

elderly patients [52]. In women of childbearing age,

more than half of ruptured splenic artery aneurysms

are related to pregnancy, and survival is uncommon

[53]. Hepatic and splenic artery aneurysms appear as

cystic structures in communication with the parent

artery, which demonstrates arterial flow within the

cystic portion on color Doppler (Fig. 15).

Iliac artery aneurysm

Seventy-five percent of iliac artery aneurysms

(IAAs) occur in association with AAA either as a

Fig. 14. Traumatic hepatic artery aneurysm. (A) Cystic central area surrounded by thrombus (arrow). (B) Color Doppler

shows turbulent flow within cystic portion of aneurysm.


direct extension of AAA or coincident with AAA

[54,55]. The common iliac artery is the most com-

monly involved (99%), followed by the internal then

external iliac [54]. According to standards created by

the Subcommittee on Reporting Standards for Arterial

Aneurysms, Ad Hoc Committee on Reporting Stan-

dards, Society for Vascular Surgery and the North

American Chapter of the International Society for

Cardiovascular surgery, IAA is defined by a lumi-

nal diameter that exceeds 1.5 cm [55]. They may be

Fig. 15. Splenic artery aneurysm. (A) Cystic structure communicate

ler shows turbulent flow.

fusiform, saccular, or bilobed. Atherosclerotic disease

is the most common predisposing factor [54,55].

Pseudoaneurysms are less frequent and may be asso-

ciated with trauma (accidental or iatrogenic), preg-

nancy, infection, or collagen vascular disease (Fig. 16)

[54]. Several hypotheses have been proposed to

explain the association with pregnancy, including

trauma and instrumentation associated with delivery,

infection, and increased vascular demand associated

with pregnancy [56].

s with vessel lumen. Note disordered flow. (B) Color Dopp-

Fig. 16. Right internal iliac artery with surrounding hypo-

echoic fluid collection represents hematoma after stent pro-

cedure (arrow).


IAAs are frequently asymptomatic but may cause

pelvic, flank, or groin pain [54,55]. Ureteral obstruc-

tion may complicate IAA because of the close prox-

imity to the genitourinary tract. Sciatic and femoral

root compression may result in symptoms. Arteriove-

nous fistula with resulting lower extremity ischemia is

a less frequent manifestation [54,56,57]. Santilli et al

[55] found that rate of expansion depended on aneu-

rysm size. Common IAAs smaller than 3 cm expand-

ed approximately 1 mm per year; IAAs larger than

3 cm expanded 2.6 mm per year. In that study,

approximately 50% of the patient population with

IAA was symptomatic. All symptomatic patients had

aneurysms larger than 4 cm. The risk of rupture

increased with increasing aneurysm size. For common

IAAs, the risk of rupture for aneurysms smaller than

5 cm in diameter was 0%; for aneurysms larger than

5 cm, it was 33% [55]. Richardson and Greenfield

[58] found that internal IAAs tended to be larger at

detection and carried a 33% incidence of rupture.

Santilli et al [55] found that B-mode US and CT

had similar accuracy in measuring iliac aneurysms.

US is most effective in diagnosing IAA when it is

large enough to cause a palpable mass. Under these

circumstances, IAAs are more likely to displace bowel

loops, which aids visualization. Gentle graded com-

pression is also helpful in displacing bowel loops [54].

Color Doppler shows a characteristic swirling pattern

along with intraluminal thrombus, if present [54].

Santilli et al [55] recommended annual screening

with B-mode US of IAAs smaller than 3 cm and

biannually for those larger than 3 cm. Repair is

frequently undertaken in association with AAA repair.

Elective IAA repair is indicated in symptomatic IAA

and IAA larger than 4 cm. More urgent repair is

performed in IAA larger than 5 cm given their higher

risk of rupture [55].

IAAs, although uncommon, carry a risk of rupture

with high associated mortality. As in AAA, US is a

modality well suited to surveillance of IAA. Because

75% of IAAs occur in association with AAA [55], the

routing screening for AAA as proposed by Lee [27]

could potentially unmask most IAAs.

Other peripheral arterial aneurysms

The most common lower extremity aneurysms are

popliteal, which comprise 80% of all peripheral

arterial aneurysms. They tend to be bilateral (50%).

Patients often present with acute limb ischemia sec-

ondary to embolization or thrombosis. This carries

a poor prognosis, with 15% requiring amputation

[59]. Forty percent of patients with popliteal aneu-

rysms have coincident AAA [56]. In a prospective

study of patients with AAA, Diwan et al [60] found

popliteal or femoral artery aneurysms in 51 of 313

patients. The association of femoral and popliteal

aneurysms with AAA suggests a common pathogen-

esis. Jacob et al [61] found reduced vascular smooth

muscle, increased inflammatory infiltrate, and in-

creased expression of signaling molecules involved

in cell death in surgical specimens obtained from

AAA, iliac, popliteal, femoral, and carotid artery

repairs. US is the imaging modality of choice in

diagnosing popliteal aneurysm. In a series of 21

patients, MacGowan et al [62] found that sonography

was superior to angiography in detecting surgically

confirmed popliteal aneurysm. Popliteal aneurysm is

diagnosed by focal dilatation of more than 20% of the

vessel diameter. As with AAA, popliteal aneurysm

can be followed sonographically. Popliteal aneurysm

larger than 2 cm generally require surgical interven-

tion regardless of the presence or absence of symp-

toms although much controversy regarding this still

exists [63,64].

Summary

The role of US in imaging of the abdominal

vasculature has broadened over recent years. Long


considered the modality of choice in the detection of

AAA, its use has expanded to diagnosing and moni-

toring IAAs and PAAs, screening for mesenteric

ischemia, and posttreatment monitoring of endovas-

cular stents.

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Radiol Clin N Am 42 (2004) 383–396

Arterial injuries: a sonographic approach

Brian D. Davison, MDa,*, Joseph F. Polak, MD, MPHb

aDepartment of Radiology, Harvard Medical School, Brigham and Women’s Hospital, 75 Francis Street, Boston, MA 02115, USAbDepartment of Radiology, Tufts Medical School, New England Medical Center, Box 299, 750 Washington Street, Boston,

MA 02111, USA

Acute arterial emergencies can arise from direct setting of proximity injuries or where a mechanism of

traumatic injury to the artery or be spontaneous. In the

case of spontaneous injuries, the likelihood of a spe-

cific arterial event increases in the presence of certain

risk factors or medical conditions. For example, the

incidence of acute arterial occlusions is increased in

the presence of popliteal artery aneurysms or atrial

fibrillation. This article emphasizes the various pre-

sentations of arterial emergencies. These include acute

arterial occlusions; excessive bleeding; and hematoma

formation caused by penetrating arterial wall injuries,

pseudoaneurysms, and arteriovenous fistulas. The

broad category of arterial occlusions includes trau-

matic lacerations, embolizations, and arterial dissec-

tions. The caliber of the artery can also, on occasion,

be significantly narrowed because of spasm. This of-

ten exacerbates the clinical impact of the injury.

Modern ultrasound equipment is a rapid and con-

venient imaging approach in many of these clinical

scenarios. In combination with MR angiography and

CT angiography, these noninvasive tests can diagnose

the presence of most arterial injuries, and be used to

measure their impact. Conventional angiography is

reserved for problem solving or directed therapy.

Validation studies: pathologic validation

In the emergency setting color Doppler imaging

and duplex ultrasound have shown use in the evalua-

tion of potential vascular injuries, especially in the


doi:10.1016/j.rcl.2004.01.007



(B.D. Davison).

injury is not in accordance with other physical find-

ings. Since the late 1980s studies have been conducted

to screen patients with vascular injuries that need

possible surgical management. Ultrasound can be up

to 95% to 100% sensitive for diagnosing vascular

injuries in the hands of highly qualified personnel

with a high index of suspicion [1]. This high diag-

nostic accuracy has actually been validated with

animal studies. Panetta et al [2] created different types

of arterial injuries in the femoral and carotid arteries of

dogs. These injuries including intimal flaps, crush

injuries, and lacerations, and were compared with

control limbs. The studies were performed by a

sonographer blinded to the type and location of the

injury. Results were correlated against operative ob-

servation and pathologic study of the injured artery

1 month after the injury. The sensitivity and specific-

ity of ultrasound were 96.5% and 86.4%, respectively,

with an accuracy of 95%. The ultrasound findings

correlated well with the histopathologic examination.

All arteries subjected to crush injury in these studies

showed abnormal duplex findings with measurable

changes in the arterial wall thickness. The site of the

crush injury showed intramural hemorrhage or mural

thrombus at the site of injury. Most intimal flaps had

healed at the time of pathologic examination, 1 month

after the injury. Overall, the findings of Doppler

ultrasound suggested that it has clinical use in the

evaluation of acute arterial trauma.

Nonimaging Doppler techniques

The ankle-brachial index is a quick comparison of

blood pressure readings. Doppler is used instead of a

stethoscope. Systolic pressures are obtained in both

s reserved.

B.D. Davison, J.F. Polak / Radiol Clin N Am 42 (2004) 383–396384

brachial arteries. Pressures are obtained in the poste-

rior tibial artery, or the dorsalis pedis in both legs. By

dividing the highest left and right ankle values by the

highest brachial value an ankle-brachial index is

calculated. Someone with no disease should have a

ratio of greater than 0.96. For evaluation of periph-

eral vascular disease a value of 0.81 to 0.95 suggests

mild disease, 0.51 to 0.80 suggests moderate disease,

0.31 to 0.50 suggests moderate to severe disease, and

0.30 or below suggests severe disease. Simple mea-

surement of the ankle-brachial index can be used to

screen for lower-extremity arterial injuries. This adds

value to the clinical finding of depressed pulses or

pulses that change strength, waxing and waning over

a few minutes. More direct comparisons of pressure

in one limb with the other can also be done. Johansen

et al [3] used the Doppler arterial-pressure index to

compare the systolic arterial pressure in the injured

extremity to the arterial pressure in the uninvolved

side. A ratio of 0.9 or less was indicative of major

arterial injury with a sensitivity and specificity of

95% and 90%, respectively. The negative predictive

value was high. Most physicians, however, consider

a negative arterial-pressure index as a poor indica-

tor of potentially unstable injuries, such as arterial

dissections, disruptions, and pseudoaneurysms. These

findings were confirmed in a study by Lynch and Jo-

hansen [4] where the arterial-pressure index calculated

in 100 consecutive injured limbs in 93 trauma vic-

tims. All of these patients subsequently had angiog-

raphy. An arterial-pressure index of less than 0.9 had

a sensitivity of 80% and specificity of 97% for the

presence of arterial disruption.

Overall, the sensitivity of the pressure index for

detecting injuries requiring intervention ranges from

44% to 95%, depending on clinical circumstances and

extent of the injury. Angiography remains the gold

standard for the evaluation of traumatic arterial inju-

ries. There are several disadvantages include cost,

time delay, and a 0.6% major complication rate.

Vascular injuries requiring intervention are present

on only 1% to 1.5% of angiograms in patients missing

true signs of vascular injury. Impaired renal function

and the amount of iodinated contrast already given

should be weighed before an angiographic procedure.

Pseudoaneurysm

Pseudoaneurysm or false aneurysm is defined by

the loss of integrity of the three layers of the arterial

wall. This results in a contained rupture of the blood

vessel. The most common origin of pseudoaneurysms

is traumatic, secondary to a penetrating injury. Of

these, iatrogenic compromise of the arterial wall

following medical interventions is most common.

Diagnostic and interventional arterial catheterizations

are the most common sources of iatrogenic pseudo-

aneurysms. Other common sources are postsurgical,

typically at the site of an arterial anastomosis or

following an arterial repair.

Pseudoaneurysms following femoral artery cathe-

terization have a reported incidence of 7% to 8% [5].

The likelihood of an iatrogenic pseudoaneurysm fol-

lowing arterial catheterization increases with the size

of the catheter, the length of the procedure, and the

concurrent use of anticoagulants. Additional factors

include poor puncture [6] and compression techniques

[5]. Antegrade punctures and use of compression

devices increase the likelihood of pseudoaneurysm

formation. Other factors include poor coagulation

factors caused by liver failure and thrombocytopenia,

and other patient factors, such as obesity, hyperten-

sion, and stresses to the catheter entry site [5,7].

The patient who presents acutely to the emergency

room typically has suspicious physical signs, such as

swelling in the injured region, a pulsatile mass, or the

presence of a thrill. This occurs in the case of

postcatheterization pseudoaneurysm 1 to 10 days

after the actual catheterization. Ecchymotic skin

changes are often present starting 1 to 2 days post-

injury. If the mass of the pseudoaneurysm presses

sufficiently on the native arteries, then blood flow can

be decreased despite intact or even increased pulses.

A bruit may be heard on auscultation.

Gray-scale ultrasound analysis reveals anechoic

or hypoechoic areas resembling fluid collections

(Fig. 1A). These are located adjacent to or can abut

the arterial wall. Color Doppler ultrasound, however,

is most useful in identifying the nature of the lesion.

Classically, the description of the blood flow pattern

as seen on color Doppler ultrasound has been de-

scribed as the yin and yang sign (Fig. 1B). These

signals are caused by swirling motion of blood within

the pseudoaneurysm cavity. The inflow jet of blood is

directed along one wall causing a positive frequency

shift (red color), and the outflow is along the opposite

wall causing a negative frequency shift (blue color).

The presence of a communicating channel or neck

between the artery and the collection is needed,

however, to confirm the diagnosis. Blood flow in this

communicating channel has a very typical pattern.

Inflow of blood causes the pseudoaneurysm collection

to expand during systole. Sampling of the Doppler

waveform in the neck of the pseudoaneurysm shows a

positive inflow into the channel. During diastole,

blood flows out of the collection into the artery. This

is caused by the release of elastic energy stored by the

Fig. 1. (A) Color Doppler image in a patient with a knife wound shows a superficial hematoma (arrow) and a collection

containing flow signals. (B) The presence of a pseudoaneurysm is confirmed by the alternating to-and-fro signals at the neck

of the pseudoaneurysm.

B.D. Davison, J.F. Polak / Radiol Clin N Am 42 (2004) 383–396 385

soft tissues surrounding the pseudoaneurysm cavity.

Blood flow is directed out of the collection into the

artery. This biphasic to-and-fro blood flow pattern

with pandiastolic reversal of flow is characteristic of

a pseudoaneurysm.

Once diagnosed, gray-scale ultrasound can be

used to estimate the size of the neck of the pseudo-

aneurysm. Smaller diameter and long necks are more

suitable for percutaneous interventions than pseudo-

aneurysms with short (less than 1 cm) and wide necks

(larger than 2–3 cm), and location must be consid-

ered. The natural history is varied. Most pseudo-

aneurysms spontaneously thrombose [8]. Over time

pseudoaneurysms can mature and a fibrous capsule

may form. The dreaded complication of a pseudo-

aneurysm is continued expansion and bleeding into

the thigh or retrograde bleeding into the pelvis. With

rapid enough expansion, the dissecting blood can

cause a compartment syndrome, compromise blood

flow to the distal limb, and lead to ischemia and

irreversible tissue loss. Many pseudoaneurysms at

presentation contain varying degrees of clotted blood.

Pseudoaneurysms can have multiple separate com-

partments or collections connected by thin tracts or

canals. Expanding pseudoaneurysms can cause limb

ischemia through compression. The thrombus form-

ing within them theoretically can escape and cause

distal emboli [9].

Pseudoaneurysms involving surgical sites, most

often the anastomosis of bypass grafts, typically have

very wide necks. They tend to be large and have well-

formed capsules. They often contain mural thrombus.

Pseudoaneurysms caused by gunshot wounds or

penetrating knife wounds should be considered as

potentially being infected. This type of pseudoaneu-

rysm seldom resolves spontaneously, and often re-

quires direct surgical intervention.

Historically, treatment of pseudoaneurysms has

been by open surgical repair, but evolution in endo-

vascular devices has allowed multiple options for

treating these lesions. Ultrasonography should be

used to assess the neck of the pseudoaneurysm. If it

is wide or in a position not directly accessible for

compression, other therapies should be considered.

Ultrasound-guided manual compression of the pseu-

doaneurysm has been used for over 15 to 20 years as

a treatment for pseudoaneurysms. The procedure

allows natural thrombosis of the pseudoaneurysm

cavity. Using gray-scale imaging as a guide, force

can be applied directly to the skin overlying the neck.

With enough pressure, blood flow stops and the con-

tents of the pseudoaneurysm thrombose. Success rates

are reported in the range of 51% to 73% [10–13].

The procedure is noninvasive, but can be time con-

suming and painful for both the patient and operator.

Unfortunately, this technique may require several


attempts before complete obliteration of the pseudo-

aneurysm. Patients treated with anticoagulants can be

refractory to this form of therapy. The recurrence rate

of pseudoaneurysms after ultrasound-guided com-

pression may be as high as 20% [5].

Direct thrombin injection using a sterile technique

and real-time Doppler ultrasound guidance into a

pseudoaneurysm causes thrombosis of the pseudo-

aneurysmwithin seconds. The procedure usually takes

less than 15 minutes. This procedure is safe and can be

performed on outpatients. A 20-gauge can be used and

the tip should be directed away from the neck.

Percutaneous thrombin injection for the treatment of

pseudoaneurysm has been described in the subclavian,

brachial, radial, and tibial arteries and carotid and

temporal arteries [14–16]. The proximity to these key

arteries requires that the operator have great technical

skills to prevent excess injection of thrombin and

thrombosis of the native artery. Success rates for

thrombin injection vary between 93% and 100% in

the literature [12,14–19]. Patients on antiplatelet

therapy or heparin can have thrombin injection with-

out decreasing success rates [14,19].

Pseudoaneurysms that have very short and wide

necks or that are located posterior to the artery are at

higher risk for failure or complications than those

with long necks and located near the skin. Compli-

cations include inadvertent direct injection of throm-

bin into the artery, or subsequent emboli emission

through a large neck. Sensitivity or allergy to throm-

bin has been reported [20]. The long-term effects of

bovine thrombin injection are not known.

Percutaneous transcatheter embolization and other

endovascular techniques, such as exclusion of the

pseudoaneurysm with covered stent placement, are

Fig. 2. (A) Transverse scan of the right groin in a patient with acut

dial to the vein. (B) The CT of the pelvis shows a right pubic ram

successful but invasive. Covered wall grafts have

been percutaneously placed to treat internal carotid

artery aneurysms [21]. In a small series, 16-month

follow-up did not show evidence of occlusion or

stenosis or reperfusion to the pseudoaneurysm. In-

dications included penetrating trauma and compli-

cations of percutaneous interventions [5,7,22].

Temporary balloon occlusion has been tried and can

be successful in properly selected patients. Repair of

large neck aneurysm with balloon occlusion and

thrombin injection has not been shown to be an

acceptably safe procedure.

In the event that the previously described proce-

dures fail or rupture is threatened by the rapid

expansion of the pseudoaneurysm, surgery should

be performed. Other surgical indications include

infection, distal ischemia, an embolic event, or ex-

tensive tissue damage. There is significant morbidity

associated with emergently performed surgery [12].

Hematoma

A hematoma is the natural outcome of a vascular

disruption. This can occur spontaneously in smaller

arteries especially in the setting of anticoagulation

[2,23,24]. The hematoma can be the result of blunt or

penetrating trauma or represent a thrombosed pseu-

doaneurysm (Figs. 2–4). The hematoma may remain

restricted to the surrounding soft tissue especially if it

occurs in a muscle, or it can tract through fascial

planes when caused by a larger arterial disruption.

Hematomas commonly occur in the retroperitoneum

[23,25], the rectus sheath [26], and in the extremities

around joints associated with muscle tears [24].

e pain following a fall shows an avascular mass (arrow) me-

us fracture (arrow) and the hematoma lying superior to it.

Fig. 3. (A) Arteriogram of the upper limb shows an intact duplicated brachial artery (arrows) and a distal humeral fracture.

(B) The corresponding color Doppler image shows a hematoma (within calipers) and no evidence of a pseudoaneurysm.

A, duplicated brachial artery.


Physical finding include swelling in the injured

region, which is most often nonpulsatile, and silent on

auscultation. Ecchymotic skin changes are almost al-

ways present. If causing compression and narrowing,

hematomas can present with diminished blood flow

and pulses to the affected limb. If bleeding is severe

and within a fascial compartment, then a compartment

syndrome can ensue, causing severe pain, markedly

diminished pulses, pallor, and paresthesias. Hemato-

mas should be delineated with a marking pen on the

skin and measured carefully on ultrasound to rule out a

rapidly evolving hematoma. Although not a common

site of arterial puncture, a high brachial puncture used

for catheterization is difficult to compress following

catheter removal. This can result in an extensive

hematoma. Extension into the axilla is of great con-

cern because the resulting hematoma can compress

and injure the brachial plexus [27,28]. The common

femoral artery remains the preferred site for arterial

access for catheterization procedures. Hematomas

here usually result in local groin swelling adjacent to

the puncture site. Rarely, they can expand to pelvis,

leg, or retroperitoneum. Vigorously compressed to

break apart, the hematoma ultimately decreases pa-

tient discomfort. Careful fluoroscopic checking of the

anatomic landmark of the femoral head ensures proper

needle placement, and is paramount in minimizing the

risk of postprocedure hematoma.

Gray-scale ultrasound analysis shows variable

findings dependent on the time interval since the

original hemorrhage and possibly intermittent nature

of bleeding episodes. In the acute period (hours)

hematoma may present as solid or mixed echogenic

structures because of mixing of liquid with clotting

blood [11,26]. It can be well or ill defined, and should

be imaged carefully to document its extent, location,

and dimensions. The size seen on ultrasound should

be compared with the physical effect on the extrem-

ity. Hematomas can often dissect in a diffuse fashion

and not form a well-circumscribed mass. A baseline

Fig. 4. (A) Color flow Doppler image shows a large hematoma in a patient following penetrating trauma. (B) Doppler signals

confirm the presence of an additional arteriovenous fistula.


measurement of size should be done because this can

help document possible rebleeding and expansion of

the hematoma. Over the course of days the clotted

blood breaks down to fluid in areas, giving a complex

cystic and solid appearance. At this point, without

proper history, the collection can be misdiagnosed an

abscess cavity or perhaps a pseudoaneurysm. Cystic,

necrotic, or hemorrhagic neoplasms may also have

similar imaging findings, and should be excluded

with follow-up. As discussed previously, however,

color flow Doppler is most useful in identifying and

differentiating these lesions from pseudoaneurysms

(see Fig. 1). Over weeks liquefactive necrosis of the

entire hematoma usually occurs [11,26]. Ultrasound

at this point shows all fluid signals, but a hematocrit

level may be seen within. A 2- to 3-month follow-up

scan is recommended to assess for decreasing size or

resolution to differentiate the hematoma from a mass.

Secondary infections are relatively rare. Their

likelihood increases if there is a persistent foreign

body in the case of penetrating trauma. Other exam-

ples where foreign material remains in the soft tissues

include after the use of closure devices used to seal

the needle access site following catheterization, or

post–synthetic graft placement.

Arteriovenous fistulas

Arteriovenous fistulas represent a direct connec-

tion between a vein and an artery. Like hematomas

and pseudoaneurysms, arteriovenous fistulas can be

spontaneous, but are often the result of penetrating

trauma. Arteriovenous fistulas are often asympto-

matic, but when significant can cause rapid shunting

with return of oxygenated blood to the right heart.

Rarely, they can contribute to high-output cardiac

failure [29]. They can also shunt away blood from the

extremity and cause symptoms of distal ischemia.

Arteriovenous fistulas are often caused by

low-arterial punctures, large-diameter catheters, anti-

coagulant use, and they are associated with pseudo-

aneurysms [2,30–32]. The femoral artery and vein

are parallel and side-by-side in the region of the

groin. Variant anatomy or punctures in the lower thigh

(where the femoral vein travels behind superficial

femoral and profunda arteries) are risk factors for

the formation of iatrogenic arteriovenous fistulas. Iat-

rogenic arteriovenous fistulas are not uncommon

elsewhere in the body, and not infrequently seen as

a consequence of a biopsy, such as in the kidney.

Physical examination can reveal little to no swelling

or ecchymosis, but a palpable thrill is often present.

Patients may present with pain but are most often

asymptomatic, but have a bruit on local auscultation.

Gray-scale ultrasound imaging is not helpful in

the evaluation of arteriovenous fistulas unless the

arteriovenous fistula is chronic and the high flow

state has caused dilatation of the vein and artery.

Color Doppler imaging and pulsed wave Doppler are

usually diagnostic. Tissue vibrations caused by tur-

bulent flow are the most notable color Doppler

finding (see Fig. 4). Also, the track between artery

and vein can sometimes be directly visualized. The

Doppler waveform in the feeding artery shows a low

resistance pattern with increased diastolic flow. The


jet of arterial flow entering the vein can cause a

marked flow disturbance and chaotic waveform or in

more severe case an arterial waveform is present.

Compression repair is usually not successful for

closing arteriovenous fistulas. Small arteriovenous

fistulas can spontaneously remit [8]. Percutaneous

placement of a covered stent or surgical repair is

often indicated.

Craniocervical dissections

There are two types of dissections likely to affect

the carotid and vertebral arteries. The first is a

primary dissection of the artery, sometimes associated

with a vague history of trauma or rapid movement of

the head. This is seen more often in young patents

less than 50 years of age. Secondary dissections occur

as an extension of a ‘‘type A’’ dissection of the aortic

arch into the origins of the brachycephalic, carotid,

and subclavian arteries. This is typically seen in older

patients or patients with a weakness of the media in

the aortic wall, typically with cystic medial necrosis.

Primary dissections

Although any of the arteries in the neck may be

affected, primary dissections of the internal carotid

Fig. 5. (A) Spectral Doppler waveform demonstrates a high resis

25-year-old patient. (B) The corresponding arteriogram shows abru

of an internal carotid artery dissection.

artery are the most common. Internal carotid artery

dissections typically occur in the proximal internal

carotid artery, just beyond the carotid bulb. Primary

dissections of the intracranial portion of the internal

carotid artery can occur but they are much less

common than the classic primary dissection of the

internal carotid artery (Fig. 5). Dissections of the

vertebral arteries are also seen but a careful investi-

gation is rarely done because symptoms, if present,

tend to be minimal. Patients with an internal carotid

artery dissection have nonspecific presenting symp-

toms, such as a sensory or motor deficit. The classic

presentation is that of a headache. The dissection

often happens in a previously healthy individual and

develops either spontaneously or following various

degrees of trauma. As medical imaging equipment

has evolved, better visualization of this area is pos-

sible. This fact coupled with more awareness has

made this diagnosis less difficult.

A dissection is the disruption of the media or

second layer of the artery. Once the dissection starts,

the intima along with a portion of the media is lifted

from the artery wall. Collagen is exposed to blood

and this usually starts a clotting cascade. The pathol-

ogy of the primary dissection of the internal carotid

artery is one of an intramural blood clot. If the size

and volume of the blood clot is large enough, the

artery occludes. If the size of the clot is intermediate,

tance and low amplitude in the internal carotid artery of a

pt termination of the internal carotid artery (arrow) at the site

Fig. 6. This patient was found to have an acute traumatic

intimal tear of the internal carotid artery on the carotid

arteriogram (not shown). The internal carotid artery color

Doppler image demonstrates evidence of a periarterial soft

tissue mass consistent with a hematoma (arrow). The inti-

mal tear seen in arteriogram could not be seen on color

flow Doppler.

Fig. 7. Gray-scale ultrasound image shows the leading edge

of an aortic dissection extending from the arch into the

common carotid artery. The leading edge of the dissection

has re-entered the lumen of the artery.


then the lesion causes a stenosis or even occlusion of

the proximal internal carotid artery (see Fig. 5). If

relatively small, the patient can present with acute

symptoms and no neurologic deficit because the

lesion does not compromise blood flow in the internal

carotid artery. This can occur in spontaneous and

posttraumatic dissections (Fig. 6). The latter scenario

is typical of up to 40% of patients with primary

internal carotid artery dissections. Physical examina-

tion can reveal motor weakness or a sensory deficit.

Rarely, the patient can present clinically with cranial

nerve palsy, such as Horner’s syndrome [33–35].

A double lumen with a separating intimal flap can

be seen on gray-scale imaging in cases of primary

internal carotid artery dissections, but is less common

than an intramural hematoma. Typically, the dissec-

tion consists of an intramural hematoma or thrombus

that is hypoechoic and hard to perceive. The Doppler

findings are variable. In the absence of a significant

obstruction, the signals can be normal. A more

significant dissection with large intramural hematoma

shows direct evidence of a stenosis with a zone of

elevated blood flow velocities. Very severe dissec-

tions can occlude or subtotally occlude the internal

carotid artery. Doppler ultrasound is quite specific for

the detection of significant vessel obstruction when

the Doppler waveform is altered and shows a high-

resistance pattern (see Fig. 5). This pattern, however,

is the least common of the patterns seen in patients

with proved dissections. Internal carotid artery dis-

sections may or may not cause symptoms depending

on the integrity of the circle of Willis. Atherosclerotic

disease may be present in the adjacent arterial seg-

ment. Spectrum analysis may demonstrate two sepa-

rate frequency curves when the dissected lumen is

still open. Doppler ultrasound has been used to

monitor and follow patients with internal carotid

artery dissection.

Secondary dissections

These dissections extend into the neck arteries

from a primary dissection arising from the ascending

aorta (Fig. 7). The patients present with the symptoms

of acute chest pain, radiating to the back. Because

these ‘‘type A’’ dissections are, a priori, triaged to

surgical intervention, it is very likely that the aorta

will be repaired. The extension of the dissection into

the neck arteries is rarely symptomatic, probably be-

cause the dissecting lumen re-enters the lumen at varia-

ble locations in the common or, less often, the internal

carotid arteries. Neurologic symptoms are rare.

Gray-scale imaging shows the typical luminal

flap. Doppler waveforms are altered. If there is a site

of re-entry, forward blood flow is mainly seen. If one

of the lumens (the false lumen) does not re-enter the


carotid lumen, then an alternating systolic-diastolic

waveform is seen in that lumen.

Stroke and carotid artery stenosis

The patient who presents with a stroke (or sig-

nificant transient ischemic attack) likely has an arte-

rial embolus in the intracranial circulation or primary

disease of the intracranial branches. Other and more

common sources of stroke include emboli from the

heart and from the aorta. In the aggregate, most

Fig. 8. (A) Color Doppler image shows an abrupt termination of

the proximal internal carotid artery. This corresponds to an embol

sound image shows the filling defect. (C) The spectral Doppler w

presence of the obstructing embolus.

patients with strokes have nonsignificant lesions in

the carotid arteries. If a significant lesion is detected,

then the focus shifts to this lesion. It is then consid-

ered to be a ‘‘culprit’’ lesion. Significance is defined

in one of three ways. A 50% or greater narrowing of

the internal carotid artery is considered a hemo-

dynamic significant stenosis. In asymptomatic pa-

tients, a 60% or greater narrowing of the lumen

diameter of the internal carotid artery is considered

significant. In symptomatic patients, the definition

varies. The North American Symptomatic Carotid

Endarterectomy Trial (NASCET) study showed that

color Doppler signals before an echogenic filling defect in

us in a 35-year-old patient. (B) Transverse gray-scale ultra-

aveform shows a high resistance pattern consistent with the

Fig. 9. Triphasic spectral Doppler waveform. The systolic

peak is marked (arrowhead) followed by an area of flow

reversal (short arrow). This is followed by a small area of

antegrade flow (long arrow).


a 70% diameter stenosis was a threshold above which

there was a high-risk for a permanent stroke in the

next few months or years [36]. A second NASCET

report indicated that a 50% or greater stenosis should

be considered to be significant [37]. Rarely, an acute

embolus can occlude the carotid artery proper; the

source of the embolus is then the heart or even the

aortic arch (Fig. 8).

Physical examination shows diminished pulses

only for the most severe stenoses. Presence of a carotid

bruit can be heard on auscultation. A carotid bruit

is, however, an unreliable sign of significant stenosis.

Gray-scale imaging can show the fibrofatty

changes (hypoechoic) of carotid artery plaque. The

most common finding, however, is the presence of a

heterogeneous plaque with mixed dense and hypo-

echoic elements. Calcium deposits cause acoustic

shadowing. Pulsed wave Doppler is the most impor-

tant ultrasound approach to evaluating the degree of

carotid stenosis. The degree of carotid stenosis is

graded by the blood flow velocity elevation caused at

the site of stenotic narrowing. The peak systolic and

end-diastolic velocity is correlated to the degree of

internal carotid artery stenosis. The ratio of the inter-

nal carotid artery to common carotid artery peak

systolic velocities is considered a sturdy diagnostic

criterion that accounts for changes in blood flow ve-

locities caused by altered (either lowered or increased)

cardiac output. When a stenosis in the internal carotid

arteries lumen is reduced by 50%, a noticeable change

in blood flow velocity can be measured. This corre-

sponds to a 50% diameter stenosis. When flow values

approach and exceed 230 cm/second, then the pres-

ence of a 70% or greater stenosis is very likely. Rarely,

a critical stenosis is so severe as to decrease blood

flow volume and blood flow velocity to the point that

the Doppler signal is no longer detectable. This

remains a limitation of Doppler ultrasound: mistaking

a subtotal occlusion to be a total occlusion is still a

diagnostic limitation of ultrasound imaging. Patients

with a subtotal occlusion could still benefit from an

intervention, whereas there is no lasting benefit to

opening a previously occluded internal carotid artery.

In the setting of recurrent transient ischemic at-

tacks in a patient with an ipsilateral high-grade carotid

lesion, carotid endarterectomy should be considered.

Currently, appropriate therapy in an acute setting is

not necessarily surgical endarterectomy. Percutaneous

stenting of the carotid is a viable option in the

emergent setting, especially if the patient is evolving

toward a major stroke. There is increasing controversy

as to how and when to treat the culprit lesion in the

neck, especially if an acute revascularization of the

intracranial arteries is being attempted. In this context,

a fully percutaneous approach with stenting of the

carotid and lysis of the embolus offers a reasonable

therapeutic option.

Acute limb ischemia: arterial embolization

The normal appearance of an extremity artery is

triphasic (Fig. 9). Pulse Doppler waveform shows an

initial narrow antegrade systolic peak, followed by an

early diastolic retrograde peak or notch. Finally, a

variable antegrade diastolic peak is seen. Under the

arterial envelope a clear area is seen. Extremity arte-

rial waveforms convert to a lower resistance pattern

during exercise, with a broadened spectral peak, and

pandiastolic antegrade flow.

Acute limb ischemia is usually caused by a sudden

arterial obstruction. There are two main causes: acute

thrombosis of an existing arterial lesion; and embo-

lism from the heart or from a more central arterial

lesion, such as an aneurysm or an ulcerated plaque.

Emboli usually lodge at major branch points in the

arteries. Symptom onset is rapid. Depending on the

physiologic impact of the occlusion, the patient may

have severe claudication, rest pain, or sensory loss.

Emergent intervention by surgical embolectomy,

surgical bypass, or percutaneous thrombolysis is re-

quired to save the limb from necrosis of the muscles.

In severe cases, amputation may be needed because

further myonecrosis causes release of myoglobin and

can trigger further metabolic pathways that lead to

organ failure and finally death. The impact of the

arterial occlusion depends on the extent of arterial

disease and the presence of arterial collaterals. For

example, acute occlusion of an artery in a young,

relatively healthy patient can be devastating, because

there are almost no collateral branches to feed the

more distal leg arteries. A patent with claudication

and slowly progressing arterial disease likely has

Fig. 10. (A) This patient with acute onset of calf pain had evidence of a Baker cyst (within calipers) on ultrasound examina-

tion. (B) Imaging lower in the calf shows a hypoechoic mass extending along the fascia. This is consistent with an acute dis-

secting Baker cyst.


well-developed collateral branches. An acute occlu-

sion in this patient may only cause an abrupt increase

in the severity of claudication.

Gray-scale imaging from the groin to the calf

arteries is relatively easy, as is the upper arm. Diffi-

culty can be experienced, especially in diabetic pa-

tients, when calcium deposits in the arterial walls

impair ultrasound beam penetration. Sometimes an

alternative diagnosis for acute pain can be made with

gray-scale imaging (Fig. 10). Long-standing occlu-

sion can result in contraction of the artery to a small

scarred cord that runs parallel to the deep vein. New

thrombus in the vessel lumen can appear hyper-

Fig. 11. (A) Transverse color flow Doppler image shows low-amp

spectral Doppler waveform shows low-amplitude signals in the art

echoic, especially if it originates from the heart.

Thrombus is most often anechoic with echogenicity

similar to that of blood. Dilation of the artery proxi-

mal to an occlusion is rarely seen.

Acute occlusions are most likely diagnosed by

combining color flow Doppler with pulsed wave

Doppler waveform analysis. Absence of flow or

low amplitude signal in the affected vessel is diag-

nostic of occlusion (Fig. 11), whereas high-grade

stenosis is associated with increased blood flow

velocities. Care should be taken to reduce the pulse

repetition frequency and to scan in orthogonal planes

to assess for the presence of very slow blood flow.

litude signals in the brachial artery. (B) The corresponding

ery just proximal to an acute embolus to the brachial artery.

Fig. 12. (A) Spectral Doppler waveform from the superficial femoral artery shows a reversing component to blood flow during

diastole. This is caused by high peripheral resistance from a distal (calf) compartment syndrome following trauma. (B) The

contralateral normal superficial femoral artery spectral Doppler waveform is shown for comparison.


This helps distinguish an occlusion from a stenosis.

In transverse plane, tortuous small collaterals may be

seen in both cases. One should look for reconstitution

of the occluded vessel, distal to the occlusion.

Extensive thrombosis extending over long seg-

ments is more difficult to treat using endovascular

approaches than shorter occlusions. Thrombolysis

can be used alone or in combination with a surgical

bypass operation. Surgical thrombectomy alone or in

combination with surgical bypass operations is a very

common therapeutic option. Uncommonly, a compart-

ment syndrome can occur where tissue pressures in

the compartment exceed systolic pressure (Fig. 12).

Diabetic foot

Vascular disease in the diabetic patient is usually

insidious in its presentation and slowly progressive.

Close control of the diabetic status and medical

examination of known diabetics is the best way to

avoid an emergency. Careful routine clinical exami-

nation and self-inspection of the diabetic foot on a

regular basis is the most effective preventive mea-

sure. Peripheral neuropathy is a risk factor associated

with poor outcome. Loss of sensory feedback adds to

the effects of arterial obstruction because symptoms

are ignored and the extent of tissue loss can increase

without the patient noticing. The prevalence of lower-

extremity occlusive arterial disease in diabetics is four

times more prevalent than in nondiabetics of a similar

age [38]. Calcification of the arterial wall is generally

widespread, and the larger vessels of the pelvis are

less affected than the small vessels of the calf and foot.

Falsely elevated pressures that are measured with

external pressure cuffs, typically greater than 30 mm

Hg above the brachial pressure, suggest the presence

of noncompliant arteries. Of the run-off vessels, the

dorsalis pedis artery is often spared [39]. The calcifi-

cation of the peripheral vasculature generally affects

the more distal vessels to a lesser degree. Distal pedal

pulses can be intact and the vessels remain compress-

ible. This allows pressures measured at the toe to be

used as an alternative noninvasive approach to assess

lower-extremity arterial disease. A toe-to-brachial

index of greater than 0.6 is considered normal. A

vascular work-up including transcutaneous oxygen

measurement [40], the ankle-brachial index, and the

absolute toe systolic pressure [41] is appropriate. In

the acute setting, where lower-extremity ischemia is

strongly suspected, arteriography or MR imaging

should be performed to confirm or rule out ischemia.

Ischemia of the upper limbs

Acute ischemia in the upper extremity can be

caused by other etiologies than arterial embolization

from central arteries, heart, and aorta. An accurate

diagnosis can sometimes be difficult in the presence of

an underlying vascular disease. The most noticeable

signs and symptoms are changes in color and sensa-

tion in the hand caused by Raynaud’s phenomenon.

This can be seen in as much as a fifth of the


population, and is four times more likely to occur in

women. The disorder affects the smallest blood ves-

sels in the hand with exposure to stress, vibration, or

cold triggering arterial-arteriole contraction and vaso-

spasm. This contraction results in blanching or bluing

of the skin of the digits from diminished blood supply.

There is marked rubor and paresthesias as hyperemia

results on rewarming.

Raynaud’s phenomenon is a manifestation of many

diseases, most often collagen vascular processes,

whereas primary or idiopathic Raynaud’s phenome-

non is called Raynaud’s disease. The etiology of these

changes is thought to be multifactorial and variable.

Noninvasive vascular testing is occasionally used

to evaluate patients with Raynaud’s disease and

includes digital pulse volume recordings and mea-

surement of digital systolic blood pressure and digital

blood flow. Stress testing for cold sensitivity should

be considered. Past medical history is most important

diagnosing the etiology of Raynaud’s. Laboratory

testing for antinuclear antibody, cryoglobulins, rheu-

matoid factor, sedimentation rate, and others may

suggest a specific secondary cause of Raynaud’s

phenomenon. Atherosclerosis, thromboembolism,

acrocyanosis, reflex sympathetic dystrophy, throm-

boangiitis obliterans, and hypothenar hammer syn-

drome are in the differential diagnosis. These entities

may all result in macrothrombus or microthrombus in

the circulatory system and can all present acutely.

Noninvasive diagnosis is limited in the acute,

limb-threatening situation. Arteriography and possi-

bly MR angiography are more useful for confirming

the diagnosis on morphologic basis. Doppler ultra-

sound is useful when it confirms patency of the large

conduit arteries to the hand. It can also be used to

confirm the presence of arterial aneurysms as are seen

in cases of hypothenar hammer syndrome.

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Radiol Clin N Am 42 (2004) 397–415

Emergency Doppler evaluation of the liver and kidneys

Michelle M. McNamara, MD*, Mark E. Lockhart, MD, MPH,Michelle L. Robbin, MD

Abdominal Imaging Section, Department of Radiology, University of Alabama at Birmingham, 619 19th Street South, JTN 353,

Birmingham, AL 35249-6830, USA

Vascular complications of hepatic and renal trans- orly. The left intersegmental fissure separates the left

plants are potentially catastrophic. They may result

in loss of the allograft with significant morbidity for

the recipient. Doppler evaluation of renal and he-

patic transplants may provide data that are essential

for preserving allograft function. Timely recogni-

tion of these problems improves the likelihood that

intervention to correct vascular abnormalities will

be successful.

Emergent applications of Doppler in the native

liver and kidneys are more limited. Sonographic

evaluation of patients with cirrhosis, with or without a

transjugular intrahepatic portosystemic shunt (TIPS),

may elucidate a cause for acute clinical decompen-

sation. Ultrasound is a readily available means of

assessing patients with acute renal dysfunction. Im-

portantly, ultrasound can be used to determine if

active hemorrhage is present at liver or renal biopsy

sites in the postbiopsy patient with a decreasing he-

matocrit level.

Hepatic ultrasound

Anatomy and appearance

The liver is divided into lobes and segments by

three fissures. The main lobar fissure divides the right

and left lobes. The boundaries of this fissure are the

middle hepatic vein superiorly, the gallbladder neck

in the midportion, and the inferior vena cava inferi-


doi:10.1016/j.rcl.2003.12.001



(M.M. McNamara).

lobe into the lateral and medial segments. The ana-

tomic boundaries of this fissure are the left hepatic

vein superiorly and the falciform ligament inferiorly.

The ascending portion of the left portal vein is at the

midportion of this fissure. The right intersegmental

fissure separates the right lobe into anterior and

posterior segments. The right hepatic vein defines

this fissure superiorly.

The main portal vein divides into right and left

branches in the liver hilum. The left portal vein

courses horizontally (horizontal segment) and then

changes to a more vertical orientation in the left

intersegmental fissure, termed the ‘‘ascending por-

tion,’’ or umbilical segment of the left portal vein.

The right portal vein divides into anterior and poste-

rior divisions. The anterior and posterior divisions

of the right portal vein course centrally in the ante-

rior and posterior right hepatic lobe segments, respec-

tively, and are equidistant from the middle and right

hepatic veins.

The hepatic veins, surrounded by liver paren-

chyma, drain into the inferior vena cava. They are

in open communication with the right heart. Cardiac

physiology and hepatic parenchymal compliance in-

fluence the hepatic vein waveform. The normal

hepatic vein waveform is phasic, similar to the in-

ferior vena cava (Fig. 1A). Two large antegrade

waves reflect atrial diastole and ventricular systole.

A small reversal in flow is seen between the larger

antegrade waves at atrial systole.

The main portal vein provides 70% to 80% of

hepatic blood flow. Normal portal venous waveforms

reflect minimal undulations from respiratory and

cardiac activity, because they are normally isolated

from the central venous system (Fig. 1B). The hepatic

s reserved.

Fig. 1. Spectral Doppler of normal hepatic waveforms. (A) Right hepatic vein shows triphasic flow. (B) Portal vein waveform

demonstrates monophasic flow. (C) Hepatic artery with sharp systolic upstroke.

M.M. McNamara et al / Radiol Clin N Am 42 (2004) 397–415398

artery, which provides 20% to 30% of hepatic blood

flow, originates from the celiac trunk. The common

hepatic artery (Fig. 1C) becomes the proper hepatic

artery after it gives rise to the gastroduodenal artery.

The proper hepatic artery bifurcates into the right and

left hepatic arteries. Variations in hepatic anatomy are

common, however, and may not be sonographically

apparent [1].

Transplant liver

Clinical

Hepatic artery thrombosis is the most common

vascular complication of orthotopic liver transplant,

and it occurs in 3% to 10% of all recipients [2,3]. The

incidence is at the higher end of the spectrum in

pediatric recipients, and it occurs in up to 12% of

transplant recipients [3,4]. If this complication oc-

curs, it is most often seen in the first 2 weeks after

transplant [4]. Clinical manifestations include biliary

dysfunction and sepsis [4]. Hepatic artery anasto-

motic stenosis usually precedes thrombosis [5]. He-

patic artery stenosis and thrombosis can be detected

with Doppler ultrasound.

Early arterial occlusion is associated with liver

failure and may require retransplantation. Alterna-

tively, if significant hepatic artery stenosis can be

detected before life-threatening ischemia occurs, an-

gioplasty or surgical revascularization may salvage

the liver transplant [4–6]. Doppler spectral analysis

is an effective tool for evaluating a patient for hepatic

artery thrombosis or stenosis, and it has sensitiv-

ity and specificity rates of 97% and 64%, respec-

tively [6].

Other vascular complications include portal vein,

hepatic vein, and inferior vena cava (IVC) stenosis

and thrombosis, and pseudoaneurysm formation at the

arterial anastomosis [7]. The narrowing that results

from nonocclusive thrombus cannot always be differ-

entiated sonographically from stenosis secondary to

other causes [6]. These less frequent complications

Fig. 1 (continued).

Fig. 2. Immediate post – liver transplant hepatic artery

Doppler. Color and spectral Doppler documents antegrade

flow with RI of 1. In the perioperative period, a high re-

sistance waveform does not necessarily indicate a patho-

logic condition.

M.M. McNamara et al / Radiol Cl

may develop independently or concomitantly. Prompt

diagnosis and treatment of vascular complications are

crucial to graft and patient survival [8].


For most adult patients, a 3.5-MHz or lower

frequency transducer is preferred, especially in the

immediate posttransplant period, when available

sonographic imaging windows may be limited. Lower

frequency transducers facilitate adequate tissue pene-

tration without compromising resolution for Doppler

evaluation. Optimum Doppler angle is less than 60�.Low wall filter settings increase sensitivity for detec-

tion of low flow [9]. Direct gray scale inspection of

the vessels is performed, as is color and spectral

Doppler analysis of the main, right, and left hepatic

arteries, the main, right, and left hepatic veins, the

main, right, and left portal veins, IVC, and splenic

vein. Patency, flow direction, velocities, resistive

indices (RIs), and waveforms are assessed. Anasto-

motic sites are interrogated for narrowing [7].

Sonographic criteria

Hepatic artery stenosis

Hepatic artery stenosis is suspected if RIs are less

than 0.5 [5] or if there is a focal peak systolic velocity

(PSV) more than 200 to 300 cm/second [2]. Other

indicators of significant hepatic arterial narrowing

include a systolic acceleration time (end diastole to

first systolic peak) more than 0.08 seconds [5]. In the

first 48 hours after transplant, RIs may be low or high

(Fig. 2) [10]. Essentially, the presence of an arterial

signal in the immediate postoperative period is satis-

factory, as long as a focal gradient is not found [6]. In

the authors’ experience, a PSV ratio at the anastomo-

sis of more than approximately 3:1 correlates with a

hemodynamically significant stenosis. A low resis-

tance arterial waveform may be seen downstream

from the stenosis (Fig. 3).

Portal vein thrombus

The portal vein is evaluated for presence or ab-

sence of flow, nonocclusive filling defects, and flow

direction. In the authors’ experience, a PSV gradient

equal to or more than approximately 3:1 at the anas-

tomosis is consistent with a hemodynamically signifi-

cant stenosis, a finding rarely encountered.

Hepatic veins and inferior vena cava

Flow direction and pulsatility are evaluated in the

hepatic veins with spectral Doppler. Monophasic

flow in the hepatic veins after transplant is a rela-

in N Am 42 (2004) 397–415 399

Fig. 3. Hepatic artery stenosis in a transplant liver. Color and

spectral Doppler of the right hepatic artery (Doppler gate)

shows abnormal waveform with RI of 0.37. RIs in the left

and main hepatic arteries (not shown) were 0.32 and 0.44,

respectively. Angiography documented 80% stenosis at the

hepatic artery surgical anastomosis.


tively common finding. Although it is not always

clinically significant, monophasic flow in the hepatic

veins can be a result of outflow stenosis or obstruc-

tion at the cranial IVC anastomosis. In the authors’

experience, a distended IVC with a peak systolic ratio

of more than approximately 3:1 can be seen in cases

with IVC anastomotic stenosis (Fig. 4A–C). An IVC

venogram with measurement of pressures across the

stenosis can be a useful confirmation of clinically

significant abnormality. Hepatic vein thrombosis is

uncommonly seen on Doppler (Fig. 5).

Pseudoaneurysm

Pseudoaneurysms appear as a simple or complex

hypoechoic lesion on grayscale ultrasound. Unless a

pseudoaneurysm is completely thrombosed, typical

‘‘to-and-fro’’ color and spectral Doppler findings

should be elicited (Fig. 6) [9].

Cirrhotic native liver

Clinical

Cirrhosis is a diffuse process characterized by

fibrosis and alteration of normal liver architecture.

Pathologic mechanisms include cell death, fibrosis,

and regeneration, which result in the formation of

nodules. In the micronodular type of cirrhosis, nod-

ules measure less than 1 cm, whereas in the macro-

nodular type, nodules of varying size may measure up

to 5 cm. Alcoholism and viral hepatitis are common

causes. Other causes include biliary cirrhosis, scle-

rosing cholangitis, Wilson’s disease, and hemochro-

matosis. Cirrhosis is a common cause of intrahepatic

portal hypertension, with resultant ascites, portosys-

temic collateral formation, and gastrointestinal bleed-

ing. Doppler ultrasound is a useful noninvasive

means of assessing the status of a TIPS and portal

vein flow in patients with cirrhosis who present with

acute decompensation [11]. Depending on criteria

selected to define abnormal, Doppler ultrasound

sensitivity rate for detection of TIPS malfunction

ranges from 92% to 94% [12], with a specificity rate

of 72% to 100% [12].


Comprehensive evaluation of the hepatic vessels

includes acquiring angle-corrected color and spectral

Doppler to determine flow direction, pulsatility, PSV,

and patency. As with transplant liver Doppler evalua-

tion, a lower frequency transducer may facilitate

penetration [13]. Low pulse repetition frequency

settings increase color Doppler sensitivity but may

result in aliasing, which can mimic flow reversal

[11,14]. Direction of flow should be confirmed by

modifying pulse repetition settings or with spectral

Doppler [14]. High wall filter settings should be

avoided because they may decrease the ability to

detect low velocity flow [2].

The main, right, and left portal veins, middle left

and right hepatic veins, hepatic artery, splenic vein,

and IVC are evaluated with gray scale followed by

assessment with color and spectral Doppler. Varices

are sought in the coronary, periumbilical, peripancre-

atic, and splenic regions, typically the most fruitful

locations for sonographic variceal detection. Vessels

are sampled proximal to (upstream) and at any abnor-

mality. Parenchymal abnormalities are imaged in

transverse and longitudinal planes. Doppler interro-

gation of any thrombus seen is performed to aid in

determining if it is bland or tumor thrombus, particu-

larly in the presence of a liver mass. Tumor thrombus

may demonstrate flow on color or spectral Doppler.

Sonographic evaluation of TIPS is complex. Ve-

locities in as much of the shunt as is acoustically

visible should be evaluated. A complete assessment

Fig. 4. IVC stenosis after liver transplant. (A) Narrowing is visually apparent on gray scale images (arrows). (B) Spectral Doppler

demonstrates PSV of 24 cm/second 2 cm caudal to the infrahepatic anastomosis. (C) PSV at the anastomosis is 115 cm/second,

which results in a PSV ratio of 115/24, or 4.8. IVC venogram (not shown) showed stenosis without significant pressure gradient

at this level.

M.M. McNamara et al / Radiol Clin N Am 42 (2004) 397–415 401

may require changes in patient position during the

examination—including the left lateral decubitus and

prone positions—to get the best angle and shunt

visualization. Main portal vein velocity and flow

direction should be assessed. Values for the hepatic

venous end within the stent, mid-shunt and portal

venous end within the stent, and highest and lowest

intrashunt velocities (if at a different location) are

recorded [2,13,15]. Flow direction and PSV in the

intrahepatic right and left portal veins and in the right,

middle, and left hepatic veins are also evaluated [2].

Stent diameter is measured.


Portal vein thrombosis

The presence of occlusive low-level echoes, or a

nonocclusive filling defect, may be observed at gray

scale imaging. Color Doppler may be useful in

finding hypoechoic thrombus not apparent on gray

scale imaging (Fig. 7). Normal portal vein caliber

ranges from 9 to 13 mm [16]. A small vessel in the

region of the portal vein is suspicious for prior

portal vein thrombus, with subsequent vein sclero-

sis or collateral formation. Cavernous transformation,

Fig. 5. Hepatic vein thrombosis after liver transplant. Color

Doppler shows a hypoechoic linear structure (arrows) in the

region of the right hepatic vein without Doppler flow.

Fig. 7. Cirrhotic liver with nonocclusive portal vein throm-

bus. Color Doppler demonstrates linear hypoechoic throm-

bus (asterisks) within the portal vein (arrows). Spectral

Doppler (not shown) also documented vessel patency.


which represents multiple small periportal venous

collaterals, suggests chronic portal vein thrombosis.

Portal hypertension

Portal venous hypertension may manifest sono-

graphically as slow antegrade, stagnant, or hepatofu-

gal flow in the main portal vein, intrahepatic branches

only, or extrahepatic collaterals only [11]. The portal

vein may be enlarged and measure more than 1.3 cm,

a sensitive but not specific sign of portal venous

Fig. 6. A 6.2-cm hepatic artery pseudoaneurysm at the ar-

terial anastomosis. Liver transplant was performed at an

outside institution. Color and spectral Doppler show typical

biphasic ‘‘to and fro’’ pattern.

hypertension [17]. Bi-directional flow may precede

reversal of flow [11].

Although cirrhosis is the most common cause of

hepatofugal flow, there are exceptions. Large porto-

systemic collaterals may persist after transplantation

and result in reversed flow in the absence of recurrent

portal hypertension. Liver function and portal vein

patency may be compromised as a result. Hepatofu-

gal flow in one or more intrahepatic portal veins may

occur with a focal arterioportal shunt from a biopsy or

tumor and is not specific for portal hypertension [11].

Transjugular intrahepatic portosystemic shunt

malfunction

TIPS is an effective and widely used means of

treating symptomatic portal hypertension. Timely

identification of TIPS malfunction increases the

probability of successful shunt revision with a conse-

quent decrease in recurrence of complications of portal

hypertension. Sensitivity and specificity rates for de-

tection of TIPS dysfunction range from 92% to 94%

and 72% to 100%, respectively, depending on the

number of abnormal criteria present [12,18]. Clinical

manifestations of TIPS dysfunction may include as-

cites recurrence, variceal bleeding, and splenomegaly.

A wide range of velocities is seen in patent shunts

[13,15], which necessitates determination of baseline

velocities in individual patients for long-term follow-

up [13]. Integration of data from several parameters is

needed to suggest TIPS malfunction. If multiple

abnormalities are identified, the likelihood of TIPS

dysfunction increases [12,18,19]. Stenosis most com-

monly involves the draining hepatic vein.


Direct signs of TIPS malfunction include lack of

flow with color and spectral Doppler, consistent with

shunt occlusion. Stenosis is suggested by a velocity

within the shunt that is less than 90 cm/second or

exceeds 189 cm/second. Velocity gradient across the

shunt also correlates with stenosis. Similar sensitivity

and specificity for detection of stenosis has been

shown when either 50 cm/second or 100 cm/second

is selected as the upper limit of normal for velocity

Fig. 8. Stenotic TIPS. (A) Main portal vein velocity is abnormally

gradient within the TIPS. Velocity at the hepatic vein side is 135

(not shown) were 60 and 50 cm/second, respectively. (C) The steno

is 206 cm/second.

gradient [12,20]. Normal main portal vein velocity

when a TIPS is present is approximately 43 cm/

second. Velocities in the main portal vein less than

30 to 33 cm/second correlate with TIPS malfunction

(Fig. 8A–C) [12,18,20].

Comparison with prior studies is helpful for

evaluating for TIPS malfunction. Decrease in main

portal vein velocity of 20% from baseline or peak

shunt velocity decrease of more than 40 cm/second

low, 28 cm/second. (B) Spectral Doppler shows a velocity

cm/second. Velocities mid-shunt and at the portal vein side

sis is located in the draining hepatic vein, where the velocity

Table 1

Indicators of transjugular intrahepatic portosystemic shunt stenosis [12]

Criteria Diagnostic threshold Sensitivity/specificity

Main portal vein velocity Less than 30 cm/sec Sensitivity 82%, specificity 77%

Decrease of 20% from baseline Sensitivity 78%, specificity 75%

Velocity within the TIPS <90 or >189 cm/sec Sensitivity 84%, specificity 70%

Decrease of >40 cm/sec or increase of

>60 cm/sec from baseline

Sensitivity 71%, specificity 88%

Gradient across the TIPS More than 100 cm/sec Sensitivity 56%, specificity 78%


or increase more than 60 cm/second correlates with

stenosis [12]. A change from retrograde to antegrade

flow in a portal vein not drained by the TIPS and

reappearance of varices or patent periumbilical col-

lateral strongly suggests shunt malfunction [13] but

may be a relatively late sign (Table 1).

Main portal vein velocity after TIPS placement

may be influenced by the size of the stent. Higher

flow velocities may be observed with 12-mm versus

10-mm shunts. A higher main portal vein velocity

threshold for shunt malfunction may be necessary;

however, significant differences in maximum and

minimum intrashunt velocities are not likely [19].

Portal vein aneurysmal ectasia

Aneurysmal ectasia of the portal vein is uncom-

monly seen and may be congenital or secondary to

portal venous hypertension or vessel wall weakening

related to inflammatory processes, such as acute

pancreatitis. There is considerable variation in the

size of the portal vein. The measurement at which

dilatation is called aneurysmal is somewhat arbitrary.

Aneurysmal ectasia is present if there is significant

focal portal vein diameter enlargement compared

with the rest of the vessel, especially if a saccular

or fusiform appearance is identified [21,22]. It gen-

erally appears as a cystic structure. Turbulent or ‘‘to

and fro’’ flow is identified with Doppler interrogation

[23], unless the vein is thrombosed.

Fig. 9. Postbiopsy hemorrhage. Color Doppler of native

liver after biopsy shows active hemorrhage demonstrated

by a jet from the biopsy tract to the liver surface (arrow).

Noncirrhotic native liver

Clinical

Applications of urgent Doppler ultrasound in

patients without cirrhosis include evaluation for

post– liver biopsy complications, sequela of inflam-

matory processes, and determination of the cause of

acutely elevated liver function tests. An acute drop in

hematocrit or unusual pain after biopsy may warrant

sonographic evaluation for active hemorrhage or

pseudoaneurysm. Portal vein thrombus and pseudo-

aneurysm are rare, usually sequelae to inflammatory

processes such as pancreatitis or septicemia. Portal

vein thrombus also may be seen with hypercoagula-

ble states and malignancy.


Comprehensive sonographic evaluation is similar

to evaluation of the cirrhotic native liver. All anechoic

structures are evaluated for flow. If the evaluation is

for a postbiopsy complication, evidence of active

hemorrhage also is sought.


Postbiopsy complications

Active hemorrhage may be observed as a jet on

color Doppler (Fig. 9) and demonstrate an arterial

spectral waveform. Additional findings consistent

with hemorrhage include the presence of hematoma

or fluid adjacent to the liver or in the pelvis. A non-


thrombosed pseudoaneurysm demonstrates the typi-

cal ‘‘to and fro’’ color and spectral pattern.

Portal vein thrombosis

Evaluation is the same as for a cirrhotic liver.

Portal vein thrombosis is rare in the native noncir-

rhotic liver and may not be detected on a routine

abdominal ultrasound. The authors have found that a

brief look at the main portal vein with gray scale and

color Doppler on routine abdominal ultrasound ex-

amination occasionally has been useful in detecting

clinically unsuspected portal vein thrombus.

Renal ultrasound

Anatomy and appearance

The kidney has several distinct anatomic features

that may be differentiated by ultrasound. The renal

cortex and medullary pyramids are similar in echo-

texture in the normal kidney. Each pyramid and sur-

rounding cortex converges into a renal papilla and

collecting system infundibulum. In echogenic kid-

neys, the pyramids of the renal medullary region are

hypoechoic to the renal cortex. Each of these struc-

tures may be distinguished easily from the echogenic

fat of the central sinus. The anechoic renal calyces

course into the renal pelvis and proximal ureter, struc-

tures that may be visualized if distended with urine.

Normal cortical thickness averages 10 mm, but

differentiation of medulla and cortex may be difficult.

Instead, the combined thickness of the capsule to the

renal sinus may be better depicted and normally mea-

sures approximately 15 to 16 mm [24]. The length of

kidneys varies with patient height, but their median

length is 11 cm; most kidneys measure 9.8 to 12.3 cm

long and are symmetric in length [24].

A single renal artery arises from each side of the

abdominal aorta caudal to the superior mesenteric

artery to supply each kidney. In up to 30% of

kidneys, however, accessory renal arteries may be

present [25]. Accessory arteries may arise near the

main renal artery, distal aorta, or common iliac

arteries. The main renal artery bifurcates or trifurcates

into branches that supply the dorsal and ventral

portions of the kidney. Segmental renal arteries

course within the renal parenchyma near the pyra-

mids. Multiple renal vein branches join to form the

main renal veins, which drain directly into the inferior

vena cava.

The normal spectral waveform in the native renal

artery is a rapid systolic upstroke with a small early

systolic peak followed by smooth tapering to the end

diastolic velocity. Flow should be laminar without

aliasing. In the normal kidney, diastolic flow should

be present in the artery, and the upper limit of RI

has been described as 0.7 in adults [26,27]. Flow in

the main renal vein should have normal mild respi-

ratory phasicity.

Transplant kidney

Clinical

Ultrasound is the best initial imaging modality in

the renal transplant patient with elevated creatinine

level. Using ultrasound as the initial screening test

avoids the use of radiation, increased cost, and the

potential nephrotoxic effects of iodinated contrast

associated with CT. Common allograft abnormalities

include hydronephrosis with ureteral obstruction,

renovascular disease, acute tubular necrosis, and

rejection. Peritransplant seromas or lymphoceles

may cause hydronephrosis or compress the renal

vessels. Rarely, a mass from posttransplant lympho-

proliferative disorder may cause renal artery stenosis

or hydronephrosis [28]. Many of these etiologies

overlap in their clinical symptomatology, and the

underlying problem must be diagnosed accurately to

guide therapy.

Doppler ultrasound can document patency of a

transplant renal artery and vein and may aid in the

detection of renal artery stenosis or an arteriovenous

fistula. Decreased or absent perfusion in the post-

operative allograft is rare but requires immediate

intervention [29]. Gray scale ultrasound is sensitive

and specific for hydronephrosis, which is caused by

obstruction in up to 8% of transplanted kidneys [30].

Ultrasound may evaluate delayed function of the

kidney or a sudden functional decline after good

initial results.


Sonographic characteristics of the renal transplant

are similar to native kidneys with a few significant

differences. Renal transplants are most commonly

placed within the right or left pelvis. The superficial

location may allow easier visualization of the trans-

plant vessels and anastomoses compared with the

vessels of the native kidneys. A higher frequency

transducer—3.5 mHz or higher (usually a curved

transducer, which allows good visualization of the

near and far portions of the kidney)—is used. The

entire course of the renal artery and vein should be


visualized, with special attention paid to the anasto-

moses, usually at the external iliac artery and vein.

Rarely, a transplant may be placed in the midabdo-

men with anastomoses to visceral vessels. The kidney

is often best visualized from an anterolateral approach

with displacement of any overlying bowel loops with

gentle graded compression by the ultrasound trans-

ducer. Adynamic ileus in the perioperative period

may hinder the sonographic examination, however.

Once the allograft is localized, the renal vessels

can be traced to the areas of anastomosis. Angle-

corrected flow evaluation should maintain an angle

less than 60� from the sonographic beam. An initial

scan with power or color Doppler to demonstrate

areas of decreased flow is useful. Regional decreased

flow may be the only suggestion of a segmental

stenosis or infarction. Subsequently, a representative

segmental renal artery waveform in the upper pole,

midportion, and lower pole is evaluated with spectral

Doppler, and an RI is calculated. The detection of an

abnormal acceleration time or absence of the early

systolic peak may suggest transplant renal artery

stenosis [31].

Color Doppler is used to identify turbulent vessel

flow by the depiction of aliasing. Spectral Doppler is

obtained in the areas of aliasing to evaluate for

potential stenosis. PSV measurements are obtained

at and approximately 2 cm proximal to the area of

aliasing or visual narrowing, which allows the calcu-

lation of a PSV ratio. The main renal artery anasto-

mosis is specifically evaluated with color and spectral

Fig. 10. Postrenal biopsy hemorrhage. (A) Color Doppler of kidne

capsule (arrow) into a perinephric hematoma. Renal parenchym

demonstrates arterial waveform.

Doppler at each examination, because it is a relatively

common site of abnormality. If a stenosis at the renal

artery anastomosis is suspected, a PSV is obtained in

the proximal iliac artery approximately 2 cm from the

anastomosis, which allows for the calculation of a

renal artery anastomosis to proximal iliac artery PSV

ratio. The main renal vein is also evaluated with color

and spectral Doppler, which usually demonstrates a

normal antegrade venous waveform.



Interrogating the transplant kidney after instru-

mentation or biopsy is important to assess for com-

plications that could result in loss of life or loss of the

allograft. Color Doppler can detect active extravasa-

tion (Fig. 10A, B) of blood from the margin of the

kidney at the point of biopsy. The biopsy tract is often

visible, and active hemorrhage presents as a jet of

color that projects from this region into the perineph-

ric fat.

Pseudoaneurysm is a documented complication of

renal biopsy [32]. In a kidney with history of instru-

mentation, any anechoic structure should be evalu-

ated with Doppler to exclude a vascular structure

[33]. Flow that fills a cavity that does not conform to

the renal vessels confirms a pseudoaneurysm. Spec-

tral Doppler may detect the ‘‘to and fro’’ waveform

that diagnoses pseudoaneurysm in other sites.

y after biopsy shows jet of active extravasation through the

al denoted by asterisk. (B) Spectral Doppler of the jet

Fig. 11. Postbiopsy 0.6-cm arteriovenous fistula (cursors)

in a transplant kidney. Spectral Doppler (not shown) dem-

onstrated bidirectional flow in the renal parenchyma de-

noted by asterisks. Also, a needle track pseudoaneurysm is

seen (arrows).


Arteriovenous fistula is a common complication

of renal biopsy (Fig. 11), and it is detected on follow-

up imaging in 10% to 15% of biopsies [34,35]. It is

important to find a fistula if present, because it can

cause a significant steal from normal parenchyma,

which causes transplant dysfunction. A fistula may be

suspected based on low resistance main renal artery

flow in the absence of a vascularized collection.

There may be aliasing of signal on color Doppler

[35]. On color Doppler, tissue reverberation may

cause color artifact in the renal parenchyma [35,36].

High volume of flow may be present on spectral

Doppler in the renal artery and vein [37]. Close to the

arteriovenous fistula (AVF), the draining vein typi-

cally has an arterialized waveform [35,38].

Intraoperative renal ultrasound

Although intraoperatively the surgeon may note

by visual inspection that kidney perfusion is failing,

the cause of the abnormal perfusion may not be clear.

The sonologist can be helpful to the surgeon during a

difficult surgical procedure by documenting renal

flow characteristics. Doppler ultrasound can docu-

ment patency of the main renal artery and main renal

vein. It can detect an arterial dissection and may be

able to differentiate it from renal artery thrombosis.

Intraoperative Doppler may assist the surgeon in

differentiating an inflow problem with low renal

artery resistance downstream in the segmental arter-

ies, from an inflow, or intrinsic transplant abnormality

with high-resistance arterial waveforms.

Transplant vascular compromise

Severe vascular complications can result in rapid

loss of the transplant allograft. In this setting, emer-

gent Doppler may identify the cause of the dysfunc-

tion and allow intervention in a timely manner. In one

series, emergent ultrasound and intervention in pa-

tients decreased loss of the organ from 4.7% to

1.05%. In that series, the most common cause of

severe perfusional failure of the transplant was renal

artery stenosis [29], which may occur in as many as

8% to 16% of renal transplant allografts [39,40].

In the authors’ experience, there is an increased

incidence of transplant renal artery stenosis in living

related donor allografts compared with cadaveric

kidneys. This is likely because of different surgical

techniques in the cadaveric renal transplant versus

living related donor. In the cadaveric transplant, a

patch of the aorta is taken around the main renal artery

aorta takeoff. The anastomosis in the cadaveric trans-

plant is actually a larger anastomosis than just that of

the main renal artery, from the aortic patch to the iliac

artery, with resultant decrease in technical complica-

tions. Taking an aortic patch would not be desirable in

the living related transplant. The main renal artery

anastomosis with the iliac artery is generally a much

smaller diameter anastomosis, with increased poten-

tial for technical problems that cause stenosis.

Critical vascular compromise of a transplant kid-

ney may be demonstrated with abnormal color Dopp-

ler perfusion. In the setting of rapid allograft failure,

reduced or absent flow in the kidney and main renal

artery suggests renal artery thrombosis [29]. This is a

rare occurrence but may have severe impact on the

allograft. Occasionally, only segmental arteries are

thrombosed. In these cases, segmental infarctions

may be detected on color Doppler [41]. Power

Doppler may increase confidence for detection of

perfusional defects associated with areas of allograft

infarction, however [42]. Renal artery stenosis also

may cause allograft dysfunction.

In transplant renal artery stenosis, high PSVs of

more than 200 cm/second have been described at the

site of a significant renal artery stenosis (Fig. 12A)

[43]. The accuracy is improved if a PSVof more than

350 cm/second criterion is used in combination with

acceleration time and evaluation for dampened intra-

renal waveforms [31]. Measurement of a tardus-par-

vus waveform (slow systolic acceleration with low

peak flow velocity) of poststenotic flow in the allo-

graft also may suggest main renal artery stenosis

Fig. 12. Renal artery stenosis in a transplant kidney. Spectral Doppler shows an elevated velocity of 469 cm/second at the

arterial anastomosis (A) and parvus-tardus waveform (B) in an intrarenal segmental artery.

Fig. 13. Spectral Doppler shows reversal of diastolic flow in

the main renal artery. The renal vein was not definitely iden-

tified (not shown). At surgery, a large peritransplant hema-

toma was evacuated, which restored flow in the renal vein.


(Fig. 12B) [31,44]. Iliac artery stenosis proximal to

the transplant artery may affect a renal transplant

adversely in much the same way as renal artery

stenosis [45,46].

Renal vein thrombosis is rare, but it may cause

allograft loss if the diagnosis remains unrecognized.

Diastolic reversal of flow (Fig. 13) or absent flow in

the main renal artery has been documented in renal

transplant allografts with renal vein thrombosis

[43,47,48]. Both findings are nonspecific and may

occur with severe rejection [49], acute tubular necro-

sis, or acute interstitial nephritis [47]. Recognition of

the arterial waveform abnormality is useful to prompt

directed main renal vein evaluation for thrombus,

however. The normal main renal vein flow should

be antegrade with minimal variability, unlike the

rapid pulsatile waveforms of the renal artery.

Posttransplant allograft dysfunction

In a functioning, normal renal transplant, an RI of

0.5 to 0.7 has been generally reported [29]. Elevation

of the RI in a transplant has been described as an

indicator of allograft dysfunction (Fig. 14A) [50–52],

but it is not specific in determining the cause of the

allograft failure [52,53]. Elevated RIs may be associ-

ated with hydronephrosis (Fig. 14B). More worrisome

is a change in RIs over time without a morphologic

cause, such as hydronephrosis [54]. Interval increases

in RI are also nonspecific, however, and may be

caused by acute rejection, chronic rejection, acute

Fig. 14. Elevated RIs in two separate renal allografts. Spectral Doppler demonstrates increased RIs in segmental arterial

branches. (A) The RI of 0.91 was secondary to acute rejection 3 days after transplant, documented by Tc 99m MAG 3 study and

clinical findings. (B) The cause of the RI of 1 was severe hydronephrosis.


tubular necrosis, or cyclosporine toxicity. The RI in a

transplant kidney may be elevated in the perioperative

period because of acute tubular necrosis [55].

Native kidney

Clinical

Sonography is commonly used in the evaluation

of abnormal renal function or evidence of urinary

pathology. In the emergency setting, ultrasound is

often the first imaging test to evaluate acute renal

failure, flank pain, hematuria, or a postbiopsy drop in

hematocrit because it is rapid and inexpensive and

does not use ionizing radiation or potentially neph-

rotoxic contrast agents. Ultrasound may help differ-

entiate between various causes of renal dysfunction

that may be clinically similar in physical examination

and laboratory tests.

For most chronic renal pathologic conditions, gray

scale ultrasound is adequate to differentiate medical

renal disease from hydronephrosis or renovascular

abnormality. Renal vascular abnormality and hydro-

nephrosis must be discerned from medical renal

disease, because the therapies differ. Renal artery

stenosis may be suggested by hypertension and renal

atrophy on gray scale images. Renal artery occlusion

may occur secondary to embolus or thrombus and

may affect the main renal artery or branches. Renal

vein thrombosis is another cause of renal failure.

Renal vein thrombosis may occur acutely and is

usually secondary to an underlying abnormality of

the kidney, abnormal hydration, or coagulation status.

The cause may be suggested in the presence of the

nonspecific finding of an enlarged kidney [56].

There are several situations in which the use of

Doppler ultrasound is more controversial. Doppler

ultrasound is not considered adequate for exclusion of

acute renal trauma [57]. Although gray scale ultra-

sound may grade the severity of hydronephrosis

caused by acute obstruction by a renal stone, Doppler

assessment of RIs in this clinical setting is no longer

generally performed. If hydronephrosis is detected

and there is clinical concern for ureteral calculus, a

noncontrast CT for urinary calculi is obtained.

Fig. 15. Pyelonephritis in a native kidney. Interval delay

transverse image using ultrasound contrast with agent detec-

tion imaging shows focal area of decreased perfusion (arrow)

in the mid-kidney. Ps, psoas; SP, spleen.

iol Clin N Am 42 (2004) 397–415


Sonographic settings and imaging technique for

evaluation of the kidneys must be optimized individ-

ually because the patient and scanning situation are

often suboptimal in the emergent setting. Flow de-

tection by color Doppler should be maximized with-

out introducing too much color artifact in the adjacent

tissues. The gain should be increased until artifact

occurs and then slightly reduced below the level

where artifacts are noted. Spectral Doppler should

use a gate that overlies most of the vessel diameter

and is angled with the direction of flow.

If evaluating for renal artery stenosis, complete

color and spectral Doppler of renal artery always

should be attempted. Any areas of turbulent flow or

aliasing on color Doppler should be evaluated closely

with gray scale and spectral Doppler for stenosis. The

arterial waveform of the aorta at the level of the renal

arteries should be obtained if renal artery stenosis is

suspected. If there is a focal site of injury, such as in a

renal biopsy, the biopsy site should be investigated

carefully with gray scale for adjacent hematoma and

Doppler for active hemorrhage. In this setting, any

intrarenal anechoic structure should be checked with

Doppler for the possibility of pseudoaneurysm.



Immediately after renal biopsy, color Doppler is

useful for evaluating active bleeding from the site

of biopsy. The authors generally wait approximately

2 minutes after the biopsy before looking for sig-

nificant bleeding, however, because brief bleeding

is common with the large 14- to 16-gauge biopsy

needles used. Hemorrhage and urinoma are the most

common complications after renal biopsy [32]. Ac-

tive hemorrhage is detected as a fountain of color

that originates from the edge of the renal parenchyma

on color Doppler. The scale and filters must be ad-

justed to optimize for detection of flow. Typically

there is no sonographic evidence of arteriovenous

fistula in the immediate postprocedural setting. Arte-

riovenous fistulas and pseudoaneurysms from renal

biopsies occasionally can be seen on subsequent ul-

trasound evaluations, however.

Severe acute urinary obstruction

Severe acute urinary obstruction may be associ-

ated with Doppler abnormalities. The RI may be ele-

vated in a severely hydronephrotic kidney [58–60].

Comparison of RIs with the contralateral normal

kidney also may be helpful [26]. The usefulness of

M.M. McNamara et al / Rad410

RI criteria is limited because of the lack of sensitivity

of Doppler for partial obstruction or moderate hydro-

nephrosis [61]. In pregnant patients with clinical

concern for ureteral obstruction and additional con-

cern about exposure to ionizing radiation, an RI more

than 0.7 or more than the contralateral kidney may be

accurate and useful for detecting obstruction [62].

Current clinical practice includes evaluating most

patients with suspected renal colic with noncontrast

CT rather than ultrasound.

Pyelonephritis

Pyelonephritis is a common clinical diagnosis in

the emergent setting that is often referred to a

radiologist for imaging. The differentiation between

pyelonephritis and cystitis may be difficult in a

patient with leukocytes in the urine. Ultrasound

may be requested to evaluate for renal abscess or

perinephric abscess. Color and power Doppler have

been documented to show focal peripheral areas of

decreased perfusion in an infected kidney [63]. Al-

though not approved in the United States for clinical

use within the urinary system, microbubble contrast

agents may demonstrate focal areas of infarction

associated with pyelonephritis with good detail and

may obviate the need for CT (Fig. 15) [64].

iol Clin N Am 42 (2004) 397–415 411

Renal vein thrombosis

Renal vein thrombosis is associated with dehy-

dration, hypercoagulability, renal disease, tumor, sur-

gery, extension of existing venous thrombus, and

trauma [65]. Color or power Doppler may detect ab-

sent renal vein flow or thrombus as a filling defect

within the detected flow [66,67] or demonstrate ab-

sent or slow flow. It is important to realize that

venous collaterals develop quickly after native renal

vein thrombosis, in contradistinction to the renal

transplant. It is important to evaluate the entire

renal vein—and not just the renal vein at the hi-

lum—if this diagnosis is a clinical consideration.

Monophasic venous flow is also abnormal and may

indicate collateral flow or incomplete thrombosis

[65]. Absent diastolic flow may be noted in the native

renal artery. Absent or reversed diastolic flow is

neither sensitive nor specific for renal vein thrombo-

sis in the native kidney, however [68].

Renal trauma

Gray scale ultrasound may detect a renal lacera-

tion or contusion in the emergency setting; however,

there is little use of color or spectral Doppler evalua-

tion of the kidneys in the setting of acute abdominal

trauma. The ability of ultrasound to visualize a renal

M.M. McNamara et al / Rad

Fig. 16. Renal artery stenosis in a native kidney. (A) Spectral Do

with a PSV of 57 cm/second. (B) Elevated PSV of 610 cm/second

which resulted in a renal artery to aorta PSV ratio of 10.7.

injury is low [57]. Although demonstration of active

hemorrhage may direct a surgeon to the appropriate

area of the body, absence of visualization does not

exclude a significant renal injury. Patients with active

extravasation of urine or blood are often treated with

conservative management [69] or angiographically

directed embolization.

Renal artery stenosis

Many sonographic criteria are reported for the

evaluation of renal artery stenosis in the native

kidneys with variable degrees of success [70]. The

most widely accepted criteria are based on direct

visualization of the main renal artery with elevated

PSV of more than 180 to 200 cm/second [70–72].

Stenosis may be detected as a focal area of turbulence

or an area aliasing on color Doppler, confirmed by

spectral Doppler [67,73]. Other direct criteria include

a ratio of the PSV within the renal artery divided by

the PSV of the aorta of at least 3.5:1 (Fig. 16A, B)

[74–76].

Several indirect criteria also have been suggested

and are sometimes reported in conjunction with direct

criteria to increase detection of renal artery stenosis.

The loss of the normal early systolic peak was the

most sensitive of the indirect criteria in one series

ppler demonstrates normal aorta (Doppler gate) waveform

is detected in the proximal main renal artery (Doppler gate),


[77]. Other criteria include the tardus-parvus wave-

form in the segmental renal arteries [67,78]. Delayed

acceleration time of the systolic upstroke has been

useful in some studies [79]. A difference in the RI

between the kidneys may suggest renal artery stenosis

[80]. A low RI can be seen downstream from an area

of focal narrowing in renal artery stenosis [81,82].

Poor detection of stenosis of accessory renal

arteries has been a limitation of ultrasound. In one

sonographic study of renal artery stenosis, nearly half

of the false-negative results were caused by stenosis

of an accessory renal artery [82]. A recent article

suggested that significant stenosis isolated to an

accessory renal artery occurs in only 1.5% of patients

with clinically significant renal artery stenosis [83].

Another important consideration in the assessment of

renal artery stenosis deals with the potential to correct

hypertension by angioplasty or surgery. In patients

with renal artery stenosis and RI more than 0.8, there

may be little improvement in a patient’s hypertension,

kidney survival, or renal function after repair of the

focal stenosis [84].

Renal artery occlusion is less common than renal

vein thrombosis, but it is also devastating to the

kidney. No flow is documented in the renal artery if

complete occlusion is present. Partial arterial throm-

bosis may be more difficult to detect, however, and

careful insonation of the entirety of the renal artery is

necessary. Segmental arterial occlusion is sonograph-

ically indistinguishable from decreased perfusion

secondary to pyelonephritis, which presents as a

focal area of decreased or absent flow on color or

power Doppler.

Summary

Doppler ultrasound is useful in the emergent

evaluation of the liver and kidney transplant patient.

Arterial stenosis, pseudoaneurysm, and venous throm-

bosis are treatable causes of allograft failure that can

be detected easily with color and spectral Doppler.

Doppler has a limited but important role in the

emergent evaluation of the native liver and kidneys,

usually involving prior biopsy or instrumentation.

Acknowledgments

The authors would like to thank Trish Thurman

for her assistance in manuscript preparation and

Anthony Zagar for photographic assistance.

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Radiol Clin N Am 42 (2004) 417–425

Emergency ultrasound in trauma patients

John P. McGahan, MDa,*, John Richards, MDb, Maria Luisa C. Fogata, MDa

aDivision of Diagnostic Radiology, University of California, Davis, School of Medicine, 4860 Y Street, Suite 3100,

Sacramento, CA 95817, USAbDivision of Emergency Medicine, University of California, Davis, School of Medicine, 2315 Stockton Boulevard,

PSSB 2100, Sacramento, CA 95817, USA

Although ultrasound (US) was first described in documented that sonographic sensitivity for the de-

the detection of blunt traumatic splenic injuries more

than 30 years ago [1], it was never widely advocated

until approximately 10 years ago [2–4]. There are

probably two reasons for the initial limited use of

sonography in blunt traumatized patients. The first is

that the use of CT evolved at approximately the

same time and was shown to be highly sensitive for

evaluation of blunt abdominal trauma [5]. CT not

only detected free fluid but also directly demonstrated

the organ injury. Sonography also was used initially

to detect specific organ injury rather than the free

fluid associated with the injury. There were limita-

tions in the ability and sensitivity of sonography in

directly demonstrating the injured organ. It was not

until the 1990s that the focused abdominal sonogra-

phy for trauma (FAST) was developed for the main

objective of detecting free fluid in patients with blunt

abdominal trauma [2–4].

Sonographic examination

The initial focus of sonographic examination was

a single view of the hepatorenal fossa (Morison’s

pouch) [2]. It was soon realized that a more compre-

hensive examination of the abdomen improved de-

tection of free fluid, however [4]. This included

examinations of both upper quadrants, the paracolic

gutters, and pelvis. In 1997, McGahan et al [4]


doi:10.1016/j.rcl.2003.12.005



(J.P. McGahan).

tection of free fluid could be improved by having a

full bladder. Often in traumatized patients a Foley

catheter is placed and the bladder is decompressed,

which eliminates the acoustic window in the pelvis

needed to detect small or moderate amounts of free

fluid. More recently, in an article by Hahn et al [6],

patients with proven intra-abdominal injuries after

blunt abdominal trauma were evaluated and it was

demonstrated that the finding of free fluid with

sonography was important. Seventy-eight percent of

patients with free fluid on sonography required lapa-

rotomy, whereas only 27% without free fluid needed

laparotomy. They also showed that examination of

Morison’s pouch had the highest detection rate of

free fluid in these patients (66%), whereas free fluid

was detected 56% of the time in the upper quadrants,

48% of the time in the paracolic gutters, and 36% of

the time in the pelvis. Examination of all areas was

important, however, because 3 of the 604 patients

with intra-abdominal injuries had free fluid only in

paracolic gutters [6]. At our institution we always

include an examination of the heart for pericardial

fluid as a part of the FAST scan. US is also useful in

examinations of the chest for pneumothorax or pleu-

ral effusion, which are discussed later in this article.


Free fluid

Free fluid typically appears as a hypoechoic

region within the peritoneal cavity or pelvis and is

usually linear or triangular in shape (Fig. 1). The

s reserved.

Fig. 1. Patterns of free fluid. (A) Real-time US examination of the right upper quadrant demonstrates small triangular-shaped

hypoechoic region (arrow) that corresponds to free fluid. (B) Real-time US of the right upper quadrant demonstrates larger

hypoechoic region, with acute angles (arrow), noted just inferior to the liver and the right kidney that corresponds to free fluid.

(C) In the same patient as B, linear hypoechoic region in the hepatorenal fossa (Morison’s pouch) corresponds to free

fluid (arrow).

J.P. McGahan et al / Radiol Clin N Am 42 (2004) 417–425418

shape of the fluid depends on its compression by the

surrounding structures. For instance, in Morison’s

pouch, the fluid between the kidney and liver usually

has a linear shape (see Fig. 1). Fluid that surrounds

bowel often appears triangular. Fluid often accumu-

lates at the site of injury but then flows throughout

the abdomen and into the pelvis. At the site of in-

jury, the blood may appear echogenic as it forms a

clot adjacent to the injured organ (Figs. 2, 3). There

maybe several pitfalls in recognition of free fluid

within the abdomen (Box 1).

Pitfalls

Patients with pre-existing ascites or iatrogenic

free fluid (eg, dialysis patients) may have false-

positive sonogram results. It is impossible in these

patients to know if the free fluid is caused by pre-

existing ascites, traumatic injury, or a combination of

the two. In women of childbearing age, a small

amount of ‘‘physiologic’’ free fluid may be noted in

the pelvis. It is important to recognize that although

this free fluid is most likely pre-existing and probably

physiologic, it may be secondary to an injury. In

this situation, searching for free fluid in other sites

is important.

Loops of fluid-filled bowel should not be con-

fused with free intraperitoneal fluid. Bowel loops

can be distinguished from free fluid because they

are round and have peristalsis. This should cause little

confusion. In almost all recent studies of the use

of sonography for detection of free fluid in patients

with blunt abdominal trauma, the specificity of so-

nography is high [4]. In some cases sonography may

detect small amounts of free fluid that are not vi-

sualized with CT [4].

Sonographic sensitivity in detecting injuries in

patients with blunt abdominal trauma may be de-

creased for several reasons. The sensitivity of sonog-

raphy for detection of free fluid in the pelvis may be

decreased if a full bladder is not used. With the

bladder decompressed after placement of a Foley

catheter, free fluid in the dependant portion of the

pelvis can be missed. Another potential pitfall of US

detection of free fluid is that hematomas may appear

echogenic. With severe injury, clotted blood at the

Fig. 2. Echogenic clot/liver laceration. (A) Real-time US examination of the right upper quadrant of the abdomen shows right

kidney (RTK) and echogenic clot anterior to the liver (RT LOBE). (B) Real-time examination of the liver demonstrates fairly well

marginated echogenic region in the liver (arrows) that corresponds to liver laceration.

J.P. McGahan et al / Radiol Clin N Am 42 (2004) 417–425 419

site of the injury may be echogenic and should not be

overlooked (see Figs. 2, 3). Finally, there is often no

free fluid associated with contained injuries of solid

organs, such as the liver, spleen, or kidney. In the

article by Hahn et al [6], in several patients no free

fluid was detected, yet 27% of these patients required

laparotomy. This may be the greatest pitfall of the

FAST scan and is discussed later in this article.

Finally, sonography is limited and unable to show

some types of injuries, including spinal and pelvic

fractures, bowel and mesentery injuries, pancreatic

injuries, vascular injuries, diaphragmatic ruptures,

and adrenal injuries [4].

Fig. 3. Subcapsular hematoma of the spleen. Longitudinal

real-time US of the spleen demonstrates well-demarcated,

slightly hyperechoic region along the anterior aspect of the

spleen (arrow) that corresponds to subcapsular hematoma.

(From McGahan JP, Wang L, Richards JR. From the RSNA

refresher courses: focused abdominal US for trauma. Ra-

diographics 2001;21(Spec No):S191–9; with permission.)

Free fluid scoring systems

Scoring systems have been developed to help

stratify patients into groups who may or may not

require laparotomy. Others have stratified patients

based on either the amount of free fluid in one

location or the number of locations in which free

fluid was detected. For instance, Sirlin et al [7,8]

described a scoring system based on the location of

the fluid. For each anatomic region in which fluid

was detected, one point was given. The percentage of

patients with a score of 0 who had intra-abdominal

injury or required surgical intervention (based on this

scoring system) was 1.4% and 0.4%, respectively.

For the score of 1, the rate of intra-abdominal injury

was 59%, and the rate of surgical intervention was

13%. The rate of intra-abdominal injury increased to

85% and rate of surgical intervention was 36%, for

a score of 2. For a score of 3, the percentage of pa-

Box 1. Pitfalls in examination of theabdomen for free fluid

� Pre-existing fluid (ascites)� Iatrogenic free fluid as in dialysis ordirect peritoneal lavage

� Pelvic fluid (female)� Loops of fluid filled bowel� Incomplete or empty bladder� Echogenic clot� Contained injury

Fig. 4. Splenic laceration. US examination of the left up-

per quadrant demonstrates poorly marginated spleen with

mixed echo pattern (arrows), which corresponds to severe

splenic laceration.


tients with intra-abdominal injury remained static at

83%, but rate of surgical intervention was 63%. The

higher the score, the higher the injury rate and the

greater the need for laparotomy. Others have advo-

cated scoring systems based on the number of free

fluid sites or the vertical height of free fluid [9,10]. A

common theme would be the more the amount of

free fluid, the greater the likelihood of injury or the

need for surgical intervention.

Sensitivity of sonography

The sensitivity of sonography depends on what is

used as the ‘‘gold’’ standard to which US is com-

pared. When sonographic results are compared with

clinical outcome, the sensitivity rates of sonography

are high, usually more than 95% [11–13]. McGahan

et al [4] calculated a sensitivity rate of only 63%

when sonography was compared with CT or laparot-

omy and not using clinical observation as a gold

standard. The probable reason for this discrepancy

in sensitivities is that McGahan et al [4] showed that

several minor lacerations of the liver or spleen were

detected on CT but not detected by FAST. These

patients did not require surgical intervention, and all

improved clinically. If clinical improvement had

been used as the ‘‘gold’’ standard, these patients

would have been deemed as having true negative

results. When using CT as the ‘‘gold’’ standard,

however, they were deemed as having false-negative

results. This is the main reason for discrepancies in

the sensitivities of FAST scan.

Numerous other studies have been published on

the topic of the sensitivity of FAST. For instance, in

744 pediatric patients with blunt abdominal trauma,

Richards et al [14] demonstrated a sonographic sen-

sitivity rate of 68% for detecting free fluid or solid

organ injuries. In a large review of 3264 patients, this

same study group showed that sonography had a sen-

sitivity rate of 67% in detection of intra-abdominal

injury [15]. Other results from recent literature vary.

Miller et al [16] reported a sensitivity rate of 42%

for the FAST scan when compared with CT. Polletti

et al [17] demonstrated a sensitivity rate of 93% for

sonography, however. Other studies have shown that

sonography may miss injuries that may require sur-

gery. Dolich et al [18] reported on 43 patients with

false-negative sonography results, 10 of whom (33%)

required surgery. Shanmuganathan et al [19] studied

the use of sonography in more than 11,000 patients

with blunt abdominal trauma: 467 patients had intra-

abdominal injury, 310 (66%) of whom had free fluid

detected by sonography. This detection rate is simi-

lar to past studies. In this larger study by Shanmuga-

nathan et al, 157 patients (34%) with intra-abdominal

injury had no free fluid, and 26 of these patients

required surgery or further intervention. Sonography

can be used to triage patients, but one must remember

that it may miss significant injuries that require

further intervention. CT should be used for patients

with a negative sonography result in whom there is a

suggestion of intra-abdominal injury [20,21].

Solid organ injury

After the initial studies on the use of sonography

in detecting organ injuries in the 1970s [1], more

recent studies focused on the detection of free fluid

[11–13]. A few recent studies have demonstrated the

ability of sonography to detect parenchymal organ

abnormalities directly. Rothhin et al [12] reported a

sensitivity rate of 41.4% for the direct detection of

solid organ injuries by sonography. McGahan et al [4]

also reported a sensitivity rate of 41% detection in

solid organ injuries. More recently, Polletti et al [17]

showed a sensitivity rate of 41% for direct demon-

stration of organ injury. Stengel et al [22] showed

that a 7.5-MHz linear ray probe detected solid or-

gan injuries much more readily than a 3.5-MHz

convex probe.

Sonographic appearance of solid organ injuries

Much of the work on sonographic classification

and appearance of solid organ injuries has been

performed by McGahan et al [23,24] and Richards

et al [25,26]. When identified, acute solid organ

injuries are often echogenic on sonography. A diffuse

heterogeneous echogenic pattern is the predominant


pattern identified with splenic injuries (Fig. 4). A dis-

crete hyperechoic or diffuse hyperechoic pattern is

seen with hepatic injuries (see Fig. 2). Renal injuries

are echogenic, with a disorganized appearance that

occurs with severe renal lacerations (Fig. 5).

More recently, contrast-enhanced abdominal US

has been used in the evaluation of solid organ inju-

ries in trauma patients (Fig. 6). For instance, Marte-

gani et al [27] presented the preliminary evaluation

of micro-bubble–enhanced US of abdominal organs

in blunt and penetrating trauma. They evaluated

14 patients with abdominal trauma who were scanned

with unenhanced US and contrast-enhanced sonogra-

phy. These authors use SonoVue (Bracco/ ALTANA

Pharm, Konstanz, Germany), a phospholipid coated

micro-bubble, at the dose of 1.2 to 2.4 mL scanned

with a low mechanical index. The liver, spleen, and

kidneys were studied over a 3- to 5-minute interval.

They demonstrated that on the unenhanced scan, no

lesions were confidently visualized. Excellent en-

hancement of the parenchymal organs was obtained

in all cases using contrast-enhanced sonography,

however. They detected injuries in the liver in 5 pa-

tients, the spleen in 5 patients, and the kidney in

4 patients. In 7 patients there was confirmation with

CT, and there was good correlation between contrast-

enhanced sonography and contrast-enhanced CT in

terms of the position and size of the abnormality.

The authors believed that the contrast-enhanced so-

nography might expedite management of trauma

patients [27].

The chest

Sonography has been shown to detect pleural

effusions [28]. In traumatized patients, sonography

Fig. 5. Renal laceration. (A) Longitudinal scan of the right uppe

without reniform shape, which corresponds to severe renal lacer

performed immediately after the US examination. (B) Real-time

an echogenic region inferior to the kidney in the right paracolic g

can be used to diagnose pneumothorax or free fluid

within the thorax. More recently, sonography also

has been shown to be helpful in diagnosing peri-

cardial effusions [29,30] in traumatized patients. The

main reason for diagnosing pericardial effusions is to

prevent patients from having a traumatically induced

pericardial tamponade. We incorporate the subcostal

view of the heart as a portion of the FAST scan in all

patients with blunt abdominal trauma. This is helpful

in diagnosing pericardial effusions (Fig. 7). It must

be emphasized that inexperienced examiners often

have problems diagnosing pericardial effusions. For

instance, Blavias et al [30] set up a study with

emergency medicine residents and fellows trained in

sonography. They had trouble discerning the epicar-

dial fat, which appeared hypoechoic on US, from a

true pericardial effusion. Sonography had a sensitiv-

ity rate of 73% and a specificity rate of only 44%

in this study [30]. With more experienced examiners,

sonography may be useful in detecting moderate

pericardial effusions.

More recently, sonography also has been proved

to be useful in diagnosing pneumothorax [31,32]. The

parietal pleura adheres to the inner muscle of the tho-

rax, whereas the visceral pleura adheres to the lung.

During inspiration and expiration the visceral pleura

‘‘slides’’ back and forth adjacent to the parietal

pleura. The bright echogenic line of the visceral

pleura, which adheres to the lung as it moves and

slides during normal inspiration and expiration, may

be observed on real-time sonography and is a normal

finding (Fig. 8). Absence of the sliding lung is a

direct sign of pneumothorax (Fig. 9). Remembering

that the free air within the thorax rises to the most

nondependent portion of the thoracic cavity, the US

probe is placed in this area to check for pneumotho-

r quadrant of the abdomen demonstrates ill-defined region

ation (shattered kidney) (arrows). Right nephrectomy was

US examination of the right paracolic gutter demonstrates

utter that corresponds to hematoma (arrow).

Fig. 6. Contrast-enhanced US of splenic laceration. (A) Noncontrast US of the spleen appears normal. (B) Contrast-enhanced US

with SonoVue demonstrates a large, wedge-shaped defect in the central portion of the spleen. (C) Correlative CT demonstrates

splenic laceration. (Courtesy of Thomas Albrecht, MD, FRCR, Berlin, Germany.)


rax. Either a curved array probe or, better yet, a linear

array probe may be used to detect pneumothorax. The

US probe is placed in the intercostal space. The

normal ‘‘to and fro’’ motion of the visceral pleura

against the parietal pleura is observed in a normal

Fig. 7. Pericardial effusion. Subcostal real-time US of the

heart demonstrates anechoic region (long arrow) anterior

to the heart, which corresponds to pericardial effusion.

patient. The normal motion of the visceral pleura

against the parietal pleura is absent with pneumotho-

rax, however. In a normal patient, a ‘‘reverberation

artifact’’ usually is noted posterior to the parietal

visceral pleura interface in a normal patient (see

Fig. 8). This is observed as lines that are equally

spaced from one another and gradually decrease in

echogenicity. This is the reverberation of the US

beam as it strikes the interface between the parietal

and visceral pleura and the air in the lung and is

reflected back to the transducer. This reverberation

produces multiple equally spaced echoes. The rever-

beration artifact is not identified when there is a

pneumothorax. A pneumothorax may produce acous-

tic shadowing. Absence or decrease of the reverber-

ation artifact also may occur in a normal patient if

the gain settings are set too low.

An article by Rowan et al [33] compared the

accuracy of sonography with that of the supine

chest radiograph in detecting traumatic pneumotho-

rax, with CT serving as the reference or ‘‘gold’’

standard. They studied 27 patients who sustained

Fig. 8. Normal lung. (A) Real-time US examination using linear array probe demonstrates the appearance of the normal lung on

US. Note that the first echogenic line (open arrow) corresponds to the interface between the parietal and the visceral pleura.

Parallel equally spaced lines of decreasing echogenicity are observed posterior to this, which corresponds to reverberation

artifacts (arrows). (B) Drawing of reverberation artifact. The US probe is placed on the skin surface (S). R refers to the interface

between the parietal and visceral pleura. Lines labeled as numbers 1 and 2, which are of decreasing echogenicity posterior to this,

correspond to reverberation artifacts caused by the US beam ‘‘reverberating’’ or ‘‘bouncing’’ between the pleura and transducer.

(C) Similar pattern is seen with sector scan of the lung in another patient.


blunt thoracic trauma and had US. The radiographic

and US findings were compared with CT findings.

Eleven of 27 patients had pneumothoraces as seen

with CT. All of the pneumothoraces were detected

by sonography, for a sensitivity rate of 100%. The

specificity rate of sonography was 94%, and 1 of

16 patients had a false-positive diagnosis of pneu-

mothorax. Supine chest radiography had a sensitivity

rate of only 36% (4 of 11 patients), with a specificity

rate of 100%. In their study, US was more sensitive

Fig. 9. Small pneumothorax. Real-time US examination of

thorax in this patient with a small pneumothorax demon-

strates the echogenic line that corresponds to the parietal

and visceral pleura, which is noted to the left side of image.

Note more distal reverberation artifacts. To the right side

of the image there is loss of this pattern because of a

small pneumothorax.


than chest radiography in the detection of trauma-

tic pneumothoraces.

Summary

US will be used more frequently in the future for

the evaluation of traumatized patients. Previously,

the main focus of the sonographic examination was

for the detection of free fluid. Unstable patients with

free fluid often can be triaged to the operation room

without further imaging tests. In patients who are

more stable or in whom US results are negative, CT

is required. Based on recent studies, sonography has

a sensitivity rate of approximately 40% in direct

detection of solid organ injuries. In the future, how-

ever, with the use of contrast-enhanced agents, so-

nography may more reliably detect solid organ

injuries. Within the chest, US has been shown to be

helpful in detecting pleural effusions and may be

useful in detecting pericardial effusions. US has been

shown to be sensitive in detecting pneumothoraces in

traumatized patients.

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Radiol Clin N Am 42 (2004) 427–443

Priapism

Hossein Sadeghi-Nejad, MDa,b,*, Vikram Dogra, MDc, Allen D. Seftel, MDd,Mamdouh A. Mohamed, MDd,e

aDivision of Urology, University of Medicine and Dentistry of New Jersey, Medical School, 185 South Orange Avenue,

MSB G536, Newark, NJ 07103-2714, USAbCenter for Human Sexuality and Male Reproductive Medicine, Hackensack University Medical Center, 20 Prospect Avenue,

#711, Hackensack, NJ 07601, USAcDivision of Ultrasound, Department of Radiology, Case Western Reserve University, University Hospitals, 11100 Euclid Avenue,

Cleveland, OH 44106, USAdDepartment of Urology, Case Western Reserve University, University Hospitals of Cleveland,

Cleveland Veterans Affairs Medical Center, 11100 Euclid Avenue, Cleveland, OH 44106–5046, USAeDepartment of Urology, El-Mina University Hospital, El-Mina, Egypt

Priapism is a relatively uncommon medical con- Definition

dition that is defined as a pathologic prolonged en-

gorgement or erection of the penis or clitoris that is

unrelated to sexual arousal. Recent advances in the

study of erectile physiology and the pathophysiology

of erectile dysfunction have resulted in better under-

standing of the processes leading to various subtypes

of priapism and the factors implicated in its resolu-

tion or recurrence. Despite these advances, there is a

paucity of randomized studies and basic science

investigations pertaining to priapism. The recently

published American Urological Association (AUA)

Guideline on the management of priapism sheds

further light on the management of this potentially

emergent condition, but the guideline ‘‘does not es-

tablish a fixed set of rules or define the legal standard

of care for the treatment of priapism’’ [1].


doi:10.1016/j.rcl.2004.01.008

* Corresponding author. Division of Urology, Univer-

sity of Medicine and Dentistry of New Jersey, Medical

School, 185 South Orange Avenue, MSB G536, Newark,

NJ 07103-2714.

E-mail addresses: [email protected],

www.hsadeghi.com (H. Sadeghi-Nejad).

The term ‘‘priapism’’ is derived from Priapus, a

minor god of fertility, luck, and the deity of gardens

and fields in Greek mythology [2]. A famous painting

in the entrance to the House of Vettii in Pompeii

depicts Priapus with a disproportionately large phal-

lus, leaning against a pillar and weighing his massive

penis. Conditions related to the prolonged engorge-

ment of the penis were associated with Priapus in

the Greek language and were later assimilated into

Latin and modern languages [2]. In the early twenti-

eth century, Hinman [3] classified priapism as either

mechanical or nervous in etiology and suggested

corporal vein thrombosis as the cause of mechanical

priapism. The condition is more common in men and

typically involves the paired corpora cavernosa, al-

though rare exceptions with involvement of the

corpus spongiosum and sparing of the cavernosal

spaces have been reported [4].

Priapism is broadly classified as low-flow (ische-

mic) or high-flow (arterial and nonischemic). Low-

flow priapism and the associated severe decrease in

venous drainage from the corpora cavernosa is a

potential medical emergency and may lead to irre-

versible ischemic tissue changes. High-flow priapism

is less commonly encountered and involves unregu-

s reserved.

H. Sadeghi-Nejad et al / Radiol Clin N Am 42 (2004) 427–443428

lated inflow that is typically secondary to some form

of arterial trauma. One of the earliest reports of

arterial priapism was published in 1960 following a

case of traumatic coitus that was surgically managed

by ligation of the internal pudendal artery [5]. Unlike

the ischemic subtype, arterial priapism is not consid-

ered an emergency: the patient does not have pain

and spontaneous resolution is the likely outcome in

more than half the cases. Hauri et al [6] elaborated on

the different management approaches to arterial ver-

sus veno-occlusive priapism and was one of the first

to suggest that the prognosis of the latter is far less

favorable than arterial priapism. Nonetheless, the

long-term outcome of nonischemic priapism has not

been thoroughly investigated and it is clear that

completely normal erectile function after these epi-

sodes cannot be guaranteed in all cases. Stuttering

priapism refers to a condition of recurrent, intermit-

tent, painful erections. These episodes are more

common in patients with various hemoglobinopa-

thies. Stuttering priapism is especially troublesome

for both the affected patient, facing repeated painful

episodes and potential emergency room visits, and

the physician challenged to arrive at a practical and

efficacious management plan for the patient. Malig-

nant priapism is a rare clinical entity that is caused

by metastasis of solid tumors to the penis.

Sonographic anatomy of the penis

The penis is composed of two dorsal corpora

cavernosa and one ventral corpus spongiosum. The

two corpora cavernosa are enclosed in a fibrous

sheath, the tunica albuginea, which partially covers

the corpus spongiosum. The tunica albuginea is com-

posed of elastic fibers that form an irregular, latticed

network on which collagen fibers rest. The septum

between the two corpora cavernosa is complete proxi-

mally and is incomplete in its distal two thirds. The

corpora cavernosa join beneath the pubis (penile

hilum) to form the major portion of the body of the

penis. The corpora cavernosa are composed of si-

nusoidal spaces lined by smooth muscles (erectile

tissue) and endothelium. The glans penis is formed

by the expansion of the corpus spongiosum.

The corpus spongiosum is traversed throughout

its length by the anterior urethra, which begins at the

perineal membrane. The corpus spongiosum provides

support to the urethra and helps with the expulsion

of semen from the urethra. Buck’s fascia surrounds

both cavernosal bodies dorsally and splits to sur-

round the spongiosum ventrally (Fig. 1).

The penile blood vessels arise from the internal

pudendal artery. The common penile artery continues

in the Alcock’s canal above the perineal membrane

and terminates in three branches to supply the erectile

bodies. The bulbourethral artery supplies the urethra,

spongiosum, and the glans. The cavernosal artery

enters the corpora cavernosa on the superomedial

surface of the penis. The cavernosal artery travels in

the center of each corporal body and gives off straight

and helicine arteries. Helicine arteries form a bridge

between the cavernosal artery and the lacunar spaces

in the corpora cavernosa [7]. It is the cavernosal artery

and its branches that dilate and bring extra blood to the

erectile tissue during penile erection. The dorsal artery

of the penis passes between the crus penis and the

pubis to reach the dorsal surface of the corporal

bodies. The dorsal artery mainly supplies blood to

the glans and runs between the dorsal vein and the

dorsal penile nerve. The venous blood is returned by

the venous plexus beneath the tunica albuginea. The

emissary veins perforate the tunica albuginea, and

the blood is drained by the venae circumflexae into

the deep dorsal veins.


A penile sonographic examination is performed

with the patient supine with the penis lying on the

anterior abdominal wall or supported with towels

between the thighs. High frequency (7.5–12 MHz)

linear array ultrasound transducers provide high-reso-

lution images of the penis [7]. Copious amounts of

acoustic gel should be used on the surface of the

penis to optimize visualization and avoid excessive

compression by the transducer.

Transverse images of the penis are recorded start-

ing at the level of the glans and moving down to the

base of the penis. The two corpora cavernosa are iden-

tified as two adjacent circular hypoechoic structures.

The tunica albuginea is identified as a hyperechoic

linear structure covering the corpora. The cavernosal

artery is visualized on the medial portion of each

corpora cavernosa. The corpus spongiosum is often

compressed and is difficult to visualize from the ven-

tral aspect (see Fig. 1). Longitudinal evaluation of the

corporal bodies should also be obtained and recorded.

During the transverse and longitudinal scanning, close

attention should be given to any plaques, calcific foci,

or arteriovenous fistulas. In the case of veno-occlu-

sive priapism, the sonographer should be extremely

gentle while performing the sonographic examination

because this is an exceedingly painful condition.

Dorsal Artery

CavernosalArtery

CorpusCavernosum

Corpus Spongiosum

Dorsal Veins

Tunica Albuginea

Buck's Fascia

Urethra

A

Internal Pudendal Artery

Dorsal Artery

Cavernosal Artery

Helicine Arteries

Bulbar ArterySpongiosal Artery

C

Fig. 1. (A) Diagrammatic representation of penile anatomy in cross-section. (B) Corresponding gray-scale ultrasound image.

(C) Diagrammatic representation of penile anatomy in longitudinal view. (From Fitzgerald SW, Erickson SJ, Foley WD, et al.

Color Doppler sonography in the evaluation of erectile dysfunction. Radiographics 1992;12(1):3–17; with permission.)

H. Sadeghi-Nejad et al / Radiol Clin N Am 42 (2004) 427–443 429


The presence of the cavernosal artery in each

corpora cavernosa along with a spectral Doppler

waveform of each should be obtained and recorded.

Color Doppler images in both transverse and longi-

tudinal views should also be obtained.

Epidemiology and etiology

Eland et al [8] have evaluated the incidence of

priapism in the general population. These investiga-

tors conducted a population-based retrospective co-

hort study using a longitudinal observational database

from the patient records of a group of general practi-

tioners in The Netherlands. They found an overall

incidence rate of 1.5 per 100,000 person-years. The

incidence rate in men 40 years old and older was

2.9 per 100,000 person-years. The authors acknowl-

edged that not all patients with priapism seek medical

care and the reported data may be an underestimation

of the actual rate in the general population. The

incidence of priapism in special at-risk subpopula-

tions is much higher. At-risk populations include men

with cocaine drug use, advanced pelvic or hemato-

logic malignancy, and those on antipsychotic medi-

cations [9–12]. Pohl et al [13] evaluated various

etiologies for priapism in a study of 230 single case

reports in the literature: idiopathic causes comprised

one-third of the cases, whereas 21% were attributed

to alcohol abuse or medications, 12% to perineal

trauma, and 11% to sickle cell anemia (SCA) [13].

For individuals on intracorporal injection ther-

apy for erectile dysfunction, the incidence range of

priapism episodes is from 1% for those on prostaglan-

din E1 and as high as 17% for patients who receive

intracorporeal injections of papaverine [14]. The most

likely cause of prolonged erection as a result of

intracavernous injection therapy is overdosage. Proper

injection technique and gradual upward titration of the

dose by the patient helps decrease this adverse event.

Priapism associated with sickle cell disease is

classically described as ischemic, although rare ex-

ceptions of high-flow priapism in association with

sickle cell disease have been reported. The pathophys-

iology of high-flow priapism in patients with sickle

cell disease is not known [15]. Fowler et al [16]

evaluated the incidence and prevalence of priapism

in sickle cell conditions. The authors reported fre-

quent self-limited priapistic episodes, mostly occur-

ring during sleep, which last less than 3 hours.

Priapism associated with SCA was unusual before

puberty and in keeping with the previously reported

6% prevalence of priapism in children with SCA

[16,17]. No correlations are observed between the

average number of priapism episodes per year and

the duration of a typical episode. A similar study from

Jamaica documented a 42% prevalence of priapism in

SCA patients [18]. Priapism was significantly associ-

ated with low hemoglobin F levels and high platelet

counts and over one fourth of those who had suffered

priapism had some degree of impotence. A more

recent survey of patients with homozygous SCA

(hemoglobin SS) and sickle cell b(0) thalassemia

(hemoglobin S-b[0]) between 5 and 20 years of age

found an 89% actuarial probability of experiencing

priapism by 20 years of age. The mean duration of an

episode in this study was 125 minutes. Episodes

typically occurred around 4:00 AM, and 75% of the

patients surveyed had at least one episode starting

during sleep or on awakening from sleep [19].

Drug-induced priapism has been reported with a

variety of medications, most commonly related to

the antihypertensive drugs guanethidine, prazosin,

and hydralazine and psychotropic medications [20].

Antipsychotics are associated with a small, but defi-

nite risk of priapism and the most commonly cited

agents are trazodone (Desyrel), thioridazine, and

chlorpromazine [21]. Abber et al [22] investigated

the mechanism of drug-induced priapism in dogs by

intravenous and intracorporeal injection of the anti-

psychotic agent chlorpromazine and the antidepres-

sant trazodone. The authors demonstrated that both

drugs induced erection in a manner similar to that of

intracorporeal injection of papaverine and showed

venous restriction and slight increases in internal

pudendal arterial flow at the beginning of tumescence.

The authors stated that the a-adrenergic antagonist

properties of chlorpromazine and trazodone probably

cause priapism by local action. Psychotropic-induced

priapism is almost always associated with low-flow

pathology and is currently believed to be caused by

the a1-adrenergic antagonism of these medications.

Chlorpromazine and thioridazine are conventional

antipsychotics with the greatest a1-adrenergic affin-

ity and have been most frequently reported to be

associated with priapism [9]. The exact pathophysiol-

ogy has not been elucidated, but is likely multifacto-

rial and may be related to the ratio of a-adrenergicblockade to anticholinergic activity. Risperidone,

olanzapine, and clozapine are the atypical antipsy-

chotics that have been reported to cause priapism on

rare occasions [9].

It has been reported that trazodone and cocaine

may have synergistic effects in promoting priapism

and their combination may pose an additional risk of

priapism. Clinicians should be aware of the possible

additive risk of priapism in this patient population,

Box 1. Etiology (AFUD classification)

� Drug induced� Hematologic� Sickle cell disease and other hemo-globinopathies

� Thrombophilia states (protein C andother thrombophilias, lupus)

� Hyperviscosity states (hyperleukocy-tosis, polycythemia)

� Idiopathic� Central nervous system mediated� Other


because trazodone is commonly used as a hypnotic

and is often chosen for polysubstance abusers because

of its low abuse potential [23]. Cocaine-induced

priapism has been reported in association with topical

application to enhance sexual performance, and intra-

nasal and intracavernous injections [24–26]. Priapism

has also been reported in association with the recrea-

tional drug ecstasy [27].

Androgens have been implicated as an important

etiologic factor with reports of priapism in hypogo-

nadal men receiving gonadotropin-releasing hormone

or high-dose testosterone, testosterone-induced pria-

pism in adolescents with SCA, and priapism after

androstenedione intake for athletic performance en-

hancement [28–31].

Examples of neurologic etiologic factors include

priapism in patients with degenerative stenosis of

the lumbar canal, where symptoms may be fully re-

lieved by surgical decompression, and priapism

secondary to cauda equina syndrome (following de-

generative stenosis of the lumbar canal and lumbar

arachnoiditis), herniated disk, or blockage of the

central inhibitory influences as seen during general

or regional anesthesia.

Noteworthy reports of systemic illnesses impli-

cated as etiologic factors include reports of priapism

occurring in widespread amyloidosis [32]. Other un-

common etiologies include glucose phosphate isom-

erase deficiency (third most commonly occurring

erythroenzymopathy), which can cause priapism

through increased rigidity of red blood cell membrane

and resultant increased blood viscosity, cell sludging

in the corpora, and increased acidity; Fabry’s disease

(glycosphingolipid lipidosis) presenting with a com-

bination of renal insufficiency and priapism; high

concentration (ie, 20% rather than 10%) fat emulsion

in total parenteral nutrition; and paradoxical throm-

boembolic events in heparin- or warfarin-induced

priapism [33–37]. Possible etiologies for increased

thromboembolic events in total parenteral nutrition–

induced priapism include increased blood coagulabil-

ity and fat emboli and direct cellular effects by high fat

content. Increased platelet function assessed by the

levels of antiheparin platelet factor 4 and b-thrombo-

globulin has been documented in priapism following

20% fat emulsion total parenteral nutrition [35].

The mechanism of malignant priapism has not

been definitively elucidated, but may be caused by

extensive organ replacement by carcinoma, venous

obstruction by the tumor, or continual stimulus to the

erectile afferent or efferent neural pathways [38].

Tumor infiltration is most frequently from the bladder

and prostate (32% and 28%, respectively) followed by

kidney (17%), gastrointestinal tract (8%), and rarely

from testis, lung, liver, bone, and sarcomas as the

primary source [39]. It has been reported that 20% to

53% of cases of penile metastasis from other primary

tumors initially present with priapism [40].

When Witt et al [41] published their paper on

traumatic laceration of intracavernosal arteries and

the pathophysiology of nonischemic high-flow pria-

pism in 1990, only five additional cases of priapism

with similar features to the reported case were cited.

Although more attention has been focused on this

subtype of priapism and numerous related papers have

been published since the early 1990s, there is general

agreement that arterial priapism is far less common

than the ischemic variant. It is estimated that the

condition is rare enough that few urologists treat more

than two cases in their lifetime [42]. Nonetheless,

because the presentation of arterial priapism is pain-

less and far less distressful to the patient, it is entirely

possible that many more cases of arterial priapism

are unreported. Nonischemic priapism has been de-

scribed in a variety of conditions causing perineal

trauma including bicycling and other straddle injuries

[43–47]. The resultant injury to the arterial system

and formation of an arteriolacunar fistula is most often

implicated as the causative factor in nonischemic

high-flow priapism. The venous outflow system is

typically unaffected in these conditions and the blood

in the corpora remains well oxygenated. The condi-

tion may also be iatrogenic following deep dorsal

vein arterialization for vasculogenic impotence [48].

This etiology is exceedingly unlikely to be reported in

the future, however, because deep dorsal vein arteri-

alization is rarely performed anymore. The most

common etiology for high-flow priapism in children

is traumatic arterial laceration, but cases associated

Box 2. Etiologic factors in priapism

Low-flow states (veno-occlusive orischemic type)

� Hemoglobinopathies and sickle celldisease

� Thrombophilia states (lupus,protein C)

� Warfarin or heparin induced� Fabry’s disease� Dialysis� Total parenteral nutrition (high fatcontent)

� Vasculitis� Hematologic malignancies� Pelvic or lower genitourinary tract(bladder and prostate) cancer andmetastatic (ie, renal) malignancies

� Psychotropics and antidepressants(chlorpromazine, trazodone,risperidol)

� Antihypertensives (guanethidine,hydralazine, prazosin)

� Erectogenic agents (intracavernosalvasoactives; sildenafil; intraurethralprostaglandin E1)

� Spinal cord stenosis� Amyloidosis� Glucose phosphate isomerasedeficiency

� Alcohol� Androgens or testosterone

High-flow states (arterial or nonischemictype)

� Penile or perineal trauma� Straddle injury� Cavernosal artery injury� Arteriosinusoidal fistula� Cocaine� Metastatic malignancy� Fabry’s disease� Iatrogenic (following deep dorsal veinarterialization)


with inherited metabolic disorders (ie, Fabry’s dis-

ease) or hematologic diseases, such as SCA, also have

been described [49–51].

Box 1 is a classification of priapism by etiology

as agreed on by the American Foundation for Uro-

logic Disease (AFUD) Thought Leader Panel on Pria-

pism [43,52]. A more detailed list of etiologic factors

based on low-flow versus high-flow subtypes of

priapism is shown in Box 2.

Pathophysiology

In broad terms, priapism may be regarded as an

imbalance between arterial inflow and outflow. Bur-

nett [53] has recently reviewed the pathophysiology

of priapism and suggested derangements in the di-

verse systems of regulatory control in erectile func-

tion. These dysregulatory functions include possible

overactivity of the veno-occlusive mechanism, arte-

rial inflow, or neurogenic processes that can affect

inflow or outflow. Conversely, the problem may be

secondary to malfunction of the normal contractile

activities of cavernosal smooth muscle cells.

Low flow

Ischemic or veno-occlusive priapism is a medical

emergency and the most common form of priapism.

It is characterized by a painful, rigid erection; absent

cavernosal blood flow; and severely acidotic corpora

(Fig. 2). The spectrum of clinical symptoms and signs

is analogous to those found in other compartment

syndromes and mandates immediate decompression

to minimize the chances of long-term sequelae. The

combination of venous outflow obstruction, high-

pressure chambers, and poor-to-absent inflow can

lead to trabecular interstitial edema and ultrastruc-

tural changes in trabecular smooth muscle cells and

functional transformation to fibroblast-like cells. In

priapism lasting more than 24 hours, severe cellular

damage and widespread necrosis may occur [54].

Destruction of the endothelial lining, formation of

blood clots within the corpora, and widespread trans-

formation of the smooth muscle cells to fibroblast-like

cells or necrosis occurs in cases lasting beyond

48 hours and eventually results in irreversible erectile

dysfunction [54]. Lack of these changes in priapism

lasting less than 12 hours emphasizes the importance

of patient education and early intervention.

In an animal model, anoxia has been shown to

eliminate spontaneous and drug-induced contractile

activity, suggesting a likely explanation for the failure

of penile injection of a-adrenergic agonists to reverse

prolonged ischemic priapism when the penis is in its

maximal rigid state [55]. The failure of detumescence

seen in low-flow priapism may be secondary to failed

a-adrenergic neurotransmission, endothelin deficit, or

Fig. 2. Low-flow priapism in a patient with sickle cell

disease. Longitudinal sonogram of the corpora cavernosa

demonstrates high-resistance flow in the cavernosal artery

suggestive of priapism. Cavernosal arterial flow is usually

absent in patients with low-flow priapism; however, high-

resistance flow may be observed.


inactivation of intracellular cofactors of smooth mus-

cle contraction caused by hypoxia or hypercarbia [55].

Recurrent episodes of veno-occlusive priapism,

occurring anywhere from a few times monthly to

recurrent daily episodes, are quite disabling and often

have an idiopathic etiology. Levine et al [56] evalu-

ated six patients with recurrent veno-occlusive pria-

pism and ruled out mechanical occlusion of corporeal

venous drainage by demonstrating elevated flows to

maintain intracavernosal pressures following smooth

muscle contraction and markedly decreased flow rates

following smooth muscle relaxation. The authors

proposed that a functional alteration of the adrenergic

or endothelial-mediated mechanisms that control pe-

nile tumescence and maintain penile flaccidity may

develop secondary to the initial ischemic episode and

reported that the use of oral phenylpropanolamine

reduced the frequency and duration of the recurrences,

and markedly reduced the need for adrenergic self-

injection. Treatment of the recurrent episodes with

intracavernous self-injection of phenylephrine re-

sulted in successful detumescence in that series and

the authors’ experience with similar cases. The pa-

tients must be instructed on the proper and early

use of phenylephrine self-injections. Most recently,

Lin et al [57] have postulated that the mechanism

of stuttering priapism in patients with sickle cell

hemoglobinopathies may involve abnormally low

expression of phosphodiesterase type 5 secondary to

hypoxia. In the human corpus cavernosum, phos-

phodiesterase type 5 is responsible for degradation

of cGMP and phosphodiesterase type 5 inhibitors,

such as sildenafil and vardenafil, have become the

mainstay of oral pharmacotherapy in the treatment of

erectile dysfunction.

Seftel et al [58] have reported on two cases of

veno-occlusive priapism refractory to conventional

therapy that later converted to high-flow priapism.

The authors suggested that the high-flow state ob-

served after treatment of veno-occlusive priapism may

represent a variant of nonischemic priapism or, alter-

natively, may be the pathophysiology of recurrent

idiopathic priapism.

Neurologic control of the efferent erectile pathway

is by the pelvic nerves that are joined by the pregan-

glionic parasympathetic nerves. The pelvic nerves

join the pelvic plexus that gives rise to the cavernous

nerve of the penis. Normally, penile stimulation

causes reflexogenic erections that are primarily con-

trolled by the sacral parasympathetic nerves originat-

ing from the S2-4 segment located at the T11-L1

vertebral levels. The afferent limb of the erection

response is mediated by the dorsal penile nerve

(a branch of the pudendal nerve), which transmits

sensory impulses to the spinal cord. The role of the

sympathetic nervous system in penile erection is not

entirely clear, but its activation is generally associated

with contraction of corpus cavernosal smooth muscle

and penile detumescence. The neuropathophysiology

of priapism in patients with lumbar stenosis has not

been fully elucidated, but it is postulated that it may

be caused by parasympathetic efferent hyperactivity

in the S2-4 cauda equina nerve roots within the

narrowed thecal sac. The parasympathetic hyperactiv-

ity may be secondary to increased intrathecal pressure

at the stenotic level and altered circulation within the

cauda equina during walking [59].

Sickle cell hemoglobinopathy results from the

inheritance of one or two genes coding for an abnor-

mal S hemoglobin and manifests in 0.15% of black

Americans in the form of sickle cell disease (homo-

zygous for hemoglobin S) and in 8% as sickle cell trait

(heterozygous for hemoglobin S). Inheritance of a

combination of a hemoglobin S gene and a second

gene coding for abnormal hemoglobin (ie, B + thal-

assemia or C hemoglobin) is possible and, as in the

homozygous type, may result in ischemic complica-


tions [16]. The pathophysiology of SCA-induced

priapism is thought to result from decreased oxygen

tension and pH developing in stagnant blood within

the corporal sinusoids, which in turn leads to a cycle

of erythrocyte sickling and sludging followed by even

more hypoxemia and acidosis [60]. Although most

cases are of the low-flow ischemic type, high-flow

priapism may be observed in patients with sickle cell

hemoglobinopathy in rare instances [15].

High flow

Nonischemic or arterial priapism is a less common

form of priapism that presents clinically as a painless

erection that typically follows some type of penile or

perineal trauma leading to unregulated arterial inflow

into the sinusoidal space. Unlike the veno-occlusive

variant, high-flow priapism is not an emergency: the

outflow mechanism is intact and the cavernosal milieu

is not anoxic. The penis is often not maximally rigid

in these cases, but intercourse may be possible. Other

clinical observations include delayed onset of pria-

pism after perineal trauma and a state of constant

suboptimal rigidity that may become more rigid with

arousal [61]. Diagnosis is typically based on the

aforementioned clinical history and physical exami-

nation, and demonstration of arterial blood on aspi-

rated cavernosal blood gas studies. A number of

recent studies have pointed to cycling trauma as the

cause of both transient neurogenic impotence and

vasculogenic pathologies in the form of arterial pria-

pism or permanent erectile dysfunction [43,46,62].

Spycher and Hauri [54] have shown that at the level of

trabecular smooth muscle cells, the ultrastructural

changes and fibroblast-like cellular transformation

seen in low-flow states do not occur with arteriogenic

priapism, even when the latter has been present for

prolonged (as late as 5 months) periods. A mechanism

for the pathophysiology of high-flow priapism is

described by Goldstein’s group in Boston: unlike a

traditional arteriovenous fistula, the condition is de-

scribed as an arterial-lacunar fistula where the helicine

arteries are bypassed and the blood passes directly into

the lacunar spaces. In turn, the high flow in the lacunar

space creates shear stress in adjacent areas, leading

to increased nitric oxide release, activation of the

cGMP pathway, and smooth muscle relaxation and

trabecular dilatation [61]. The authors also postulate

that the delay in onset of high-flow priapism may be

secondary to a delay in the complete necrosis of the

arterial wall after the initial penile or perineal trauma.

Alternatively, the delay may be secondary to clot

formation at the site of injury followed by the normal

lytic pathways, which follow in a few days.

Diagnosis

Physicians caring for patients with priapism should

remember at all times the significant anxiety and fear

experienced by most patients with this condition and

make a genuine effort to alleviate their apprehension.

A thorough history and physical examination are

prerequisites to diagnostic accuracy. The sexual and

medical history should especially focus on medica-

tions, trauma, and predisposing comorbidities. Pres-

ence or absence of pain is a fairly reliable predictor of

low-flow versus high-flow priapism, respectively. The

latter diagnosis is further suggested by a history

of penile or perineal trauma. Absence of pain in arte-

rial priapism frequently results in less patient anxiety

and discomfort as compared with veno-occlusive

priapism. Consequently, those with arterial priapism

may present days or even weeks after the original

injury. The fundamental aim of the initial phase of

assessment is to distinguish arterial from ischemic

priapism. The AFUD panel recommendations for the

management of priapism are illustrated in Fig. 3 and

follow a step-care model that has been modified and

refined over the years [43,52,63].

Physical examination of the penis is critical and

typically reveals firm corpora cavernosa and a soft

glans, indicating sparing of the corpus spongiosum in

low-flow priapism. Findings in high-flow states usu-

ally reveal a partial to full erection and sparing of the

corpus spongiosum in most cases (as in low-flow

states). General diagnostic tests include urine toxicol-

ogy screening for psychoactive drugs and metabolites

of cocaine [10,43]. These tests are particularly helpful

if the diagnosis is unclear. The AFUD panel has

additionally suggested reticulocyte count (if indi-

cated); urinalysis (if indicated); complete blood count;

platelets, and differential white blood cell count; and

urologic consultation. The reticulocyte count is often

elevated in men with SCA. The most important

warning with regard to hematologic testing is to

remember that hemoglobinopathies are not restricted

to African American men and other groups, especially

those of Mediterranean descent, may be affected

(ie, thalassemia or sickle-thalassemia). The sickledex

test and examination of the peripheral smear are less

time consuming than hemoglobin electrophoresis and

may be more appropriate for the emergency room

setting. These recommendations are similarly empha-

sized in the more recent AUA guideline on pria-

pism [1].

Urologic management of priapism includes his-

tory and physical (including penile) examination, and

assessment of corporal blood flow status (corporal

aspirate and visual inspection by color and consist-

Fig. 3. Step-care treatment model for the management of priapism recommended by the AFUD thought leader panel. CA,

cavernosal artery; CBC, complete blood count; DDU, duplex Doppler ultrasonography; HB, hemoglobin; NB, nerve block; PE,

physical examination; PSA, prostate-specific antigen; UA, urinalysis; VS, vital signs. (Data from references [43] and [52].)


ency or corporal blood gas including pH, PO2, and

PCO2, or penile duplex Doppler ultrasound) [43].

Low-flow priapism is suggested by finding low

oxygen, high carbon dioxide, and low pH in the

blood gas analysis of the aspirate. When a high-flow

state is suspected based on the bright red appearance

or blood gas analysis of the corporal aspirate, duplex

Doppler sonography may identify a dilated caver-

nosal artery or pseudocapsule formation at the site of

arterial sinusoidal fistula. These findings are helpful

if superselective arterial embolization is performed

[64]. The AUA Guideline states that the use of penile

arteriography for the identification of the site of a

cavernous artery fistula may be warranted in some

cases, but that arteriography has been largely replaced

by color duplex sonography and the former is only


used as part of an embolization procedure [1]. Fur-

thermore, penile aspiration has mainly a diagnostic

role in the management of arterial priapism (not

therapeutic). Although the data reviewed by the

AUA guideline panel did not reveal any instances

of arterial priapism resolution after aspiration or

irrigation, two separate case reports in the literature

have documented the rare resolution of arterial pria-

pism after aspiration or irrigation in cases of adult

and pediatric posttraumatic priapism [65,66].

Patients presenting with refractory low-flow

priapism who later convert to a high-flow state

represent a less common cohort of priapism patients.

Because the management of the low-flow and high-

flow states is radically different, sonography should

be considered if conventional corporal irrigation and

intracavernosal sympathomimetics (ie, phenyleph-

rine) fail to resolve the initial veno-occlusive pria-

pism [58]. When a hemoglobinopathy is suspected,

hemoglobin electrophoresis may be performed. The

AFUD panel has also recommended testing for pros-

tate-specific antigen when indicated.

Role of radiology in the diagnosis and treatment of

priapism

Most of the reports on the use of sonographic

imaging in the diagnostic and therapeutic algorithms

of priapism are focused on the high-flow variant,

although sonography may be used instead of blood

gas sampling to differentiate ischemic (low-flow

priapism) from high-flow priapism. Color duplex

Doppler sonography has replaced arteriography as

the imaging modality of choice for the diagnosis of

priapism. Penile color duplex Doppler sonography is

noninvasive, does not expose the patient to ionizing

radiation, and can reveal important information re-

garding the location of arterial injury in high-flow

priapism. Most published studies on the subject indi-

cate that in experienced hands, differentiation of the

increased color flow on the affected side from the

normal flow on the contralateral side is not problem-

atic. Two important papers from Goldstein’s group

at Boston University have shown color Doppler

ultrasound to be as sensitive as angiography for the

diagnosis of high-flow priapism [61,67]. More spe-

cifically, penile duplex Doppler sonography had a

sensitivity of 100% and a specificity of 73% with a

predictive value of 81% for a positive test and 100%

for a negative test [67]. Mabjeesh et al [68] have

reported therapeutic use of color duplex Doppler

ultrasound in one patient in whom sonography was

used to localize the fistula and subsequently apply

external compression to achieve permanent fistula

occlusion and resolution of priapism.

In a posttraumatic case of priapism with an arterial

tear, gray-scale ultrasound reveals an irregular hypo-

echoic region secondary to tissue injury or distended

lacunar spaces in the corpus cavernosum. This irregu-

lar area appears with well-circumscribed margins

analogous to a capsule formation if the injury has

been long-standing [69]. The arteries exhibit normal

or increased flows within the cavernosal arteries and

an irregular flow from the artery to the cavernosal

body at the site of injury. Arterial signs may be seen

in the pseudoaneurysm and, unlike veno-occlusive

priapism, increased venous flow may be observed in

high-flow priapism [42]. The arterial lacunar fistula

seen in high-flow priapism essentially bypasses the

helicine arteries and appears as a characteristic color

blush extending into the cavernosal tissue on color

duplex sonography. It is reported that 90% of fistulas

in adults appear as unilateral, whereas at least 50% of

arterial priapism in children is associated with bilat-

eral or multiple arterial lacerations [42,51]. Bertolotto

et al [69] recommend increasing the color Doppler

velocity scale for better detection of the cavernosal

artery tear region as a focal area with very high flow.

Because aspiration is only used for diagnostic pur-

poses in cases of arterial priapism, if the history is

suggestive of high-flow pathology and color duplex

sonography is conclusive, the patient may be spared

the discomfort of needle aspiration. Kang et al [70]

warn about the potential difficulty of accurate lesion

localization caused by pubic bone sonic attenuation

when the injury is in the region of the proximal

cavernosal artery or the distal common penile artery.

They further reiterate the importance of accurate

sonographic localization in cases where embolization

may be anticipated because internal iliac artery or

internal pudendal artery cannulization is easier from

the contralateral femoral artery.

The use of selective arterial embolization for the

management of arterial priapism is somewhat contro-

versial. The embolization of an arteriolacunar fistula

in nonischemic priapism with an autologous clot was

first reported by Wear et al [71] in 1977. Numerous

reports in the literature have since documented use

of this approach in high-flow priapism with variable

success [72–82]. The recently published AUA guide-

line recommends that the initial management of

nonischemic priapism should be observation [1]. This

approach is based on the finding that expectant

management results in spontaneous resolution in

62% of the reported cases (with erectile dysfunction

in one third of cases) reviewed by the AUA Guideline


panel. Many investigators have shown complete reso-

lution of posttraumatic high-flow priapism without

any invasive measures and the historical trend on the

management of high-flow priapism gradually seems

to be moving from surgery to embolization to expect-

ant management [1,67,83]. Selective arterial emboli-

zation with autologous clot and absorbable gels are

recommended for ‘‘patients who request treatment’’

[1]. The AUA guideline further states that any dis-

cussion of invasive treatment modalities including

Fig. 4. A 40-year-old man with cocaine-induced priapism. He

examination. After failure of urologic treatment, he was referre

angiography (A, B) demonstrates the internal pudendal artery (strai

the dorsal artery of the penis (arrowhead). (C) Complete occlusio

absorbable gelatin sponge using coaxial microcatheter. Arrow ind

(Courtesy of A. Blum, MD, and P. Kang, MD, Cleveland, OH.)

surgery or embolization must be preceded by a thor-

ough discussion of the various aspects of expectant

management and the chances of spontaneous reso-

lution. It should be noted that autologous clot is

reported to be unstable by some investigators and is

not widely used [80].

Superselective transcatheter embolization (Fig. 4)

has been performed to occlude the source of arterial

inflow with potential preservation of potency in up to

80% of patients in one recent report [84]. In rare

was confirmed to have low-flow priapism on ultrasound

d to radiology for embolization of the penile artery. The

ght arrow), the artery to the scrotal wall (curved arrow), and

n of the penile artery (arrowhead) after embolization with

icates the artery to the scrotal wall. B, bladder; P, priapism.


instances, this treatment has been associated with

perineal abscess formation [85]. When embolization

is used, serial penile duplex studies should be per-

formed in follow-up to ‘‘assure complete resolution of

the arterial lacunar fistula and ultimate restoration

of normal cavernosal blood flow’’ [67]. Based on

the AUA Guideline recommendations and earlier

work by the Boston University group, a course of

watchful waiting with regular follow-up examinations

should be discussed with the patient as a reasonable

(if not preferred) alternative to maximize the chances

of preserving potency and avoiding nonessential in-

tervention in high-flow priapism [67]. When avail-

able, arterial embolization of arteriocavernous fistulas

has been advocated by Volkmer et al [51] as the first

line of therapy in prepubertal boys with traumatic

high-flow priapism when hematologic or metabolic

causes have been eliminated [51]. The authors report

26-month mean follow-up in three cases of high-flow

priapism diagnosed by color Doppler ultrasound that

presented 4 to 7 days after the injury. After diagnosis

of the fistula location by angiography (branches of the

internal pudendal artery in two and the bulbourethral

artery in one patient), gelatin sponge (bulbourethral

artery) or microcoil (internal pudendal artery) were

used to occlude the fistula and achieve detumescence

with preservation of erectile function in all three cases

[51]. Traditionally, when embolization is performed, a

unilateral approach has been recommended to avoid

the dreaded complications of penile gangrene, gluteal

ischemia, or erectile dysfunction [61,86]. Langenhuij-

sen et al [80], however, have described highly selec-

tive embolization of bilateral cavernous arteries in a

case where unilateral embolization was unsuccessful.

The authors advocate the use of the highly selective

technique (cannulization of the cavernosal arteries) to

minimize the risk of distal embolization of embolic

material and use of resorbable materials (gelatin

sponge) to allow for later recanalization and potential

preservation of potency. The disadvantage of the

absorbable materials is that they are not radiopaque

and accurate placement can only be accomplished by

frequent control arteriography during the procedure

[80,87,88]. Callewaert et al [89] were the first to

report superselective embolization in children using

microcoils. Again, the advantage of the microcoils is

that they allow precise placement into the branch

supplying the fistula and may be performed bilaterally

and yet maintain adequate penile blood flow to

potentially preserve erectile function. Volkmer et al

[42] advocate a combined interventional approach

with intraoperative penile color Doppler ultrasound

while performing arterial embolization to minimize

iodinated contrast use and radiation exposure. This

approach allows precise angiographic catheter place-

ment and is especially useful for reducing radiation

exposure in children because of the higher likelihood

of multiple arterial lacerations.

For patients requesting treatment in areas with no

access to tertiary care centers and angiographic ex-

pertise, a trial of cavernosal aspiration and corporal

irrigation with a-adrenergic agents may be tried early

in the course of priapism and has been associated

with a positive outcome (resolution of priapism and

ability to achieve normal erections with follow-up) in

at least one case report [66].

Treatment

The duration of the veno-occlusive period in pri-

apism has a significant impact on the potential for

recovery of spontaneous erections. Conservative mea-

sures and a trial of medical therapy should always be

attempted before surgical therapy. Immediate reduc-

tion of intracorporeal pressure in low-flow states is

of paramount importance. Treatment options are fur-

ther separated based on the etiology. For patients with

non–sickle cell priapism, initial comfort measures

include local penile or systemic anesthesia in the form

of dorsal nerve block, circumferential penile block,

subcutaneous local penile shaft block, and oral con-

scious sedation for the pediatric patient [43]. The

initial diagnostic penile aspiration is also used as a

therapeutic measure and, except where contraindi-

cated, should be combined with intracavernosal instil-

lation of a sympathomimetic agent (ie, phenylephrine

injection after aspiration) to induce detumescence.

This combination addresses the two important goals

of therapy in low-flow states: decreased inflow

(phenylephrine), and increased outflow and reduced

pressures (aspiration). Transient increases in systemic

blood pressure are possible and monitoring of vital

signs is indicated when using sympathomimetic

agents. Because of its potent and selective a1-adre-

nergic stimulatory properties and lack of b1-stimula-

tory effect, which could cause arrhythmias and angina

in susceptible patients, phenylephrine is a preferred

agent for achieving detumescence by intracavernosal

injection and has been extensively reviewed by Lee

et al [90]. These authors also have prepared a useful

chart for preparation of dilutions of a-adrenergicagonists for intermittent injection or irrigation. Fail-

ing this approach, the next step in the process is

irrigation with saline with or without pharmacologic

agent except when contraindicated. The authors have

successfully used a closed system for corporeal aspi-

ration and irrigation as described by Futral and Witt


[91] that has the advantages of reduced risk of body

fluid exposure and corporeal contamination and the

capacity for extended irrigation without repeated

corporeal puncture.

The authors agree with observations by Pautler

and Brock [64] indicating that most cases of veno-

occlusive priapism treated without excessive delay

(< 12 hours) respond to a-agonist therapy and that

failure of resolution after 20 minutes of injection

(0.1 mL/minute of a 500–1000 mg/mL phenylephrine

solution for a total infused dose of 1 mg) calls for

alternative strategies for management because these

patients are unlikely to respond. The AFUD panel

highly recommended first-line treatments (aspiration

and irrigation) for low-flow priapism of more than

4-hours duration before undertaking more invasive

surgical shunts and further suggested that these ther-

apies have not shown a benefit in preserving potency

when priapism has persisted beyond 72 hours [43].

Failure of resolution after conservative measures as

described moves the step-care process to the surgical

level. A number of different surgical shunts for

diversion of blood away from the corpus cavernosum

have been described. The consensus among authori-

ties is that, in general, distal corporospongiosal shunts

should be undertaken before proximal shunts; how-

ever, there is no consensus regarding the choice of

percutaneous versus open surgical shunts. The

authors prefer to start with a transglandular Winter

shunt (corporoglandular) using a biopty gun biopsy

device to create multiple channels between the corpus

spongiosum and the corpora cavernosa [92]. If this

technique is not successful, a larger communication

between the corpora cavernosa and the corpus spon-

giosum may be created by a modified Al-Ghorab

shunt in which the distal tunica albuginea of the

corpora cavernosa is removed through a transglan-

dular incision. Proximal shunts have been described

by a number of authors and are recommended if these

shunts fail and absent cavernosal artery flow is

assessed by Doppler sonography [43,93]. A few

authors have advocated early use of penile prostheses

in cases of refractory or recurrent priapism associated

with corporal fibrosis and erectile dysfunction [94].

The AFUD panel recommendations for manage-

ment of priapism in patients with SCA include intra-

venous hydration and parenteral narcotic analgesia

while preparing for aspiration and irrigation, supple-

mental oxygen, and exchange transfusion [43]. Initial

efforts are directed at relief of pain and anxiety, and

hydration with hypotonic fluids at 1.5 times mainte-

nance. Powars and Johnson [95] state that in the static,

hypoxic, and acidotic corporal environment, it is

unlikely that red cells can reach the area of involve-

ment and question the use of red cell transfusion.

Furthermore, they emphasize that blood volume and

viscosity must be monitored closely in patients un-

dergoing exchange transfusion or rapid single-unit

transfusion, because there is an increased risk of

cerebrovascular accident, coma, and intracranial

hemorrhage. Low-flow infarctive priapism is uncom-

mon. Nonetheless, adolescent patients are more likely

to develop this condition compared with younger

children who are more likely to respond to hydration,

rest, analgesia, and warmth [95]. Failing conservative

measures as described, the rest of the management

algorithm for SCA patients with low-flow priapism is

very similar to that described for non-SCA priapism.

Stuttering or recurrent painful priapism episodes in

this population have been managed successfully with

instruction on sympathomimetic self-injection and

gonadotropin-releasing hormone analogue injection

in refractory cases [96,97]. This experience has been

corroborated by the authors. Rutchik et al [98] have

reported on a single case of refractory veno-occlusive

priapism (failure of response to intracavernosal

a-adrenergic injection or irrigation and recurrence

after an Al Ghorab surgical shunt) that responded to

intracavernosal injection of 15-mg tissue plasminogen

activator [98]. The authors resorted to this therapy

because of severe penile congestion and risk of penile

necrosis with further shunting. It must be emphasized,

however, that experience with this approach is very

limited. A novel approach for treatment of priapism

was suggested by deHoll et al [99] who described the

use of methylene blue, a guanylate cyclase inhibitor,

in 11 patients with priapism and reported immediate

detumescence in 67%. A possible explanation for the

success of this therapy is blockage of cyclic GMP-

induced muscle relaxation following the initial aspi-

ration attempts. Recently, successful treatment of

recurrent idiopathic priapism with oral baclofen has

been reported in two patients [100]. The treatment

options for high-flow arteriogenic priapism mainly

consist of conservative measures aimed at preserva-

tion of sexual function. Mechanical measures include

external compression with occlusion of arterial inflow

and topical application of ice. If these approaches fail,

surgical, pharmacologic, or radiologic approaches

may be used. Surgical and pharmacologic interven-

tions have not had great success in resolution of high-

flow priapism and restoration of potency [67]. A

detailed discussion of embolization therapy was pre-

sented in the previous section. There are very limited

data on the safety and efficacy of surgical procedures

for management of high-flow priapism and surgery

was recommended as the ‘‘option of last resort’’ by the

AUA Guideline panel [1].


Complications

Early complications typically result from injection

of a-adrenergic agents and include headaches, palpi-

tation, hypertension, and cardiac arrhythmias. Vital

signs should bemonitored during this phase of therapy.

Additional adverse events include urethral injury and

urethrocutaneous or urethrocavernosal fistula from

aggressive needle decompression, bleeding, and infec-

tion [101]. Rare cases of gangrene of the penis after

corporospongiosal shunt have been reported [102].

Complications in high-flow states are usually second-

ary to the angiographic embolization used in the

therapeutic stage of management. Use of angiography

for diagnostic purposes is seldom necessary. Color

duplex Doppler ultrasound evaluation and a thorough

history and physical examination readily delineate the

diagnosis in nearly all cases. Late complications are

usually the sequelae of ischemic damage to cavernosal

tissue and commonly manifest as corporal fibrosis and

erectile dysfunction. Early decompression of the penis

in the low-flow state is the most important preventive

measure against these adverse events.

Summary

Priapism is a relatively uncommon condition that

may present as a medical emergency associated with

significant pain and anxiety in the veno-occlusive or

low-flow variant. Pharmacologic advances and, spe-

cifically, the availability of intracavernosal a-agonisttherapy have dramatically improved the prospects

of resolution for patients with low-flow priapism

presenting within the first few hours of the acute

episode. High-flow priapism is not considered an

emergency and treatment measures are typically con-

servative aimed at preservation of potency. Urolo-

gists, radiologists, and other health care personnel

caring for the patient with priapism must be familiar

with various etiologic factors implicated in low-flow

and high-flow priapism to formulate a logical step-

care approach. Differentiation of the low-flow from

the high-flow state is perhaps the most critical initial

diagnostic challenge that determines the sequence of

further interventions including surgical shunts in low-

flow priapism refractory to medical therapy.

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Radiol Clin N Am 42 (2004) 445–456

Ultrasound evaluation of acute abdominal emergencies in

infants and children

Pauravi Vasavada, MD

Department of Pediatric Radiology, University Hospitals of Cleveland, 11100 Euclid Avenue, Cleveland, OH 44106, USA

Ultrasonography is an essential component in the position. Close to 7% of children with HPS have pa-

evaluation of acute abdominal pain and vomiting in

children. Radiation exposure is a prime consideration

in the pediatric population. Ultrasonography, unlike

CT or fluoroscopy, allows the radiologist to acquire

diagnostic information without the use of ionizing

radiation. Ultrasound (US) can be performed in any

imaging plane, which is advantageous when evaluat-

ing such structures as the pylorus and appendix,

which may not be fixed in their orientation. Small

children with abdominal pain often are not able to lie

down quietly for a CT or MR image without the

use of sedation. US, however, is able to obtain diag-

nostic images in nonsedated children. It is also cost

effective, being far less expensive than CT or MR

imaging. Real-time ultrasonography can be per-

formed in the radiology department or at bedside in

the emergency department [1,2].

Hypertrophic pyloric stenosis

Hypertrophic pyloric stenosis (HPS) is the most

common surgical disorder producing emesis in in-

fancy [1,3]. The incidence of HPS is approximately

2 to 5 per 1000 births per year and it varies with the

geographic area. HPS is less common in India, and

among black and Asian population, with a frequency

that is one third to one fifth compared with that in the

white population [3]. Boys are four times more likely

to be affected than girls, with the incidence signifi-

cantly higher in first-born boys [2–4]. Although it’s

etiology remains unknown, there is a familial predis-


doi:10.1016/j.rcl.2004.01.003


rents with the same condition [2,4].

Hypertrophic pyloric stenosis is characterized by

a defect in contractility or relaxation of the circular

muscle of the pylorus that results in hypertrophy of

the pyloric circular muscle and narrowing of the

pyloric channel [3,4]. This leads to stomach dilation

and gastric outlet obstruction of variable severity.

Pyloric stenosis should be suspected in neonates 3 to

6 weeks old with postprandial nonbilious vomiting.

Symptoms, however, can be present in the first week

of life or as late as 5 months of age. The patient

classically presents with nonbilious vomiting that is

projectile secondary to the pressures generated by the

hypertrophied gastric muscles [5]. Persistent vomiting

results in large losses of gastric secretions. Because

only gastric secretions are lost, prolonged vomiting

leads to hypokalemic, hypochloremic metabolic alka-

losis. If uncorrected the condition can lead to malnu-

trition, weight loss, dehydration, and death. More

recent evidence suggests, however, that more than

90% of infants with HPS present without any meta-

bolic disorders. This lower incidence has been linked

to proper diagnosis before protracted vomiting is

allowed to occur, and it has been suggested that easy

access to ultrasonography may be contributing to

earlier diagnosis [6]. Nonbilious vomiting can present

in several other conditions including gastroesophageal

reflux disease and pylorospasm [4].

The clinical diagnosis of HPS has traditionally

been made by palpation of an olive-shaped mass in

the epigastrium representing the hypertrophic pyloric

muscle. Palpation of a tumor-like mass in the right

upper quadrant by an experienced examiner is usually

considered specific and diagnostic without further

testing [3,4,7]. In those infants in whom a mass is

s reserved.

Fig. 1. Fluoroscopic image from an upper gastrointestinal

study in a patient with HPS. The double track sign (arrows)

is formed by contrast material coming through the mucosal

interstices of the canal.

P. Vasavada / Radiol Clin N Am 42 (2004) 445–456446

not palpated unequivocally, an imaging examination

is required. The diagnosis of HPS can be established

by imaging upper gastrointestinal tract with the help

of a radiographic contrast, such as barium, or by

sonography. An upper gastrointestinal tract reveals a

beak or a ‘‘string‘‘ sign because of the narrow open-

ing of the pylorus or the double tract sign (Fig. 1) [2].

In patients with pyloric stenosis the muscle is hyper-

trophied and the intervening mucosa is crowded and

Fig. 2. (A,B) Sonograms in a patient with a normal pylorus. Longitu

muscle. The pyloric channel is not elongated measuring 1.1 cm, a

thickened and protrudes into the distended portion

of the antrum resulting in the nipple sign. The upper

gastrointestinal tract provides indirect information

about the status of the pyloric channel based on the

morphology of the canal lumen as outlined by contrast

material. Secondary to this fact, failure of relaxation

of the pyloric channel, known as ‘‘pylorospasm,’’ may

be confused with pyloric stenosis. Upper gastro-

intestinal tract can be time consuming, because the ra-

diologist has to wait for contrast to pass through the

high-grade obstruction. Fluoroscopy time and radia-

tion exposure may be prolonged. Upper gastrointes-

tinal tract sensitivity rate has been reported to be

approximately 95% but error rate as high as 11%

has also been reported [3,7].

Sonography has become the modality of choice

for the diagnosis of HPS. Sonography is documented

to be a highly sensitive (90%–96%) and specific

modality for the diagnosis of HPS [4]. US avoids

radiation and allows direct visualization of the py-

loric muscle as opposed to the upper gastrointestinal

tract where the morphology of the muscle is inferred

by the thinness and length of the barium through the

area [1–3]. The sonographic examination is typically

performed with a 5- to 7.5-MHz linear array trans-

ducer. A transducer up to 10 MHz can be used

adjusted to the size of the infant and the depth of

the pylorus [3,4]. The patient is placed in the right

posterior oblique position, which allows fluid in the

stomach to distend the antrum and pyloric region.

dinal views demonstrate normal measurement of the pyloric

nd the muscle wall is not thickened measuring 2.6 mm.

P. Vasavada / Radiol Clin N Am 42 (2004) 445–456 447

Because the stomach in infants with pyloric stenosis is

normally distended it is usually not necessary to

introduce more fluid. If the antrum does not contain

adequate fluid, a glucose solution or water can be

given orally or through a nasogastric tube [3,4,7].

Occasionally, the stomach may become so distended

and displace the duodenal cap caudally and medially

rendering the pylorus difficult to visualize. In these

cases, if the patient is placed in the supine or left pos-

terior oblique (LPO) position, the pylorus is able to

rise anteriorly for more optimal evaluation.

Fig. 3. Hypertrophic pyloric stenosis. (A,B) Longitudinal sonogr

measuring 5.8 mm. The pyloric channel is elongated measurin

hypoechoic muscle surrounding the echogenic mucosa.

The pylorus is viewed in longitudinal and trans-

verse planes. The examination begins by placing the

transducer in the transverse plane, beginning at the

gastroesophageal junction and following the contour

of the stomach to its antrum. The duodenal cap is

recognized by its arrowhead shape. By positively

identifying the gastric antrum and the duodenal cap,

the interposed pyloric channel can be imaged [7]. A

negative study hinges on the diagnosis of a normal

pyloric ring and a distensible pyloric portion of the

stomach (Fig. 2) [3,7].

aphic views demonstrate the hypertrophied pyloric muscle

g 23 mm. (C) Cross-sectional view shows the thickened


On longitudinal views the muscle has a uniformly

hypoechoic appearance. In the short axis view, the

hypertrophic pyloric muscle has a target or bull’s eye

appearance reflecting the thickened hypoechoic mus-

cle surrounding the echogenic mucosa. The sono-

graphic hallmark of HPS is the thickened pyloric

muscle (Fig. 3). The numeric value for the diagnostic

muscle thickness has varied greatly. The exact recom-

mended measurement includes a range of numbers

with a broad range of sensitivities and specifications

[8]. Controversy persists regarding the significance

of muscle thickness between 3 and 4 mm. Some au-

thors consider 3 mm as diagnostic, whereas others

believe that this diagnosis cannot be made reliably

until a muscle thickness of 3.5 to 4 mm has been

attained [3,8]. The length of the hypertrophic canal is

variable and may range from as little as 14 mm to

more than 20 mm. Despite this variability in numbers

in the literature, a patient with HPS has an examina-

tion and overall morphology of the pylorus that is

characteristic of pyloric stenosis. The muscle thick-

ness is at least 3 mm or more during the examination

and the intervening lumen is filled with crowded or

redundant mucosa through the center of the canal.

Additionally, gastric peristaltic activity fails to distend

the preduodenal portion of the stomach [3].

In patients without HPS the muscle does not

measure more than 3 mm at any given time. Thick-

Fig. 4. (A, B) Sonographic images of the pylorus after the infant

within the antrum passing through a normal pylorus (P, arrow) int

ening of the pyloric channel may be a transient

phenomenon because of peristaltic activity or pylo-

rospasm. During a normal examination, one can

document the pyloric canal changing from a rigid

linear morphology to a relaxed canal that permits

pockets of fluid within the lumen. If the stomach is

empty and the antrum is collapsed a small amount of

fluid may be fed to the infant to document a normal

fluid-filled antrum (Fig. 4). Patients in whom the

pyloric canal relaxes to a normal morphology do not

have pyloric stenosis. Patients in whom the muscle is

2 to 3 mm thick during the examination and does not

relax warrant monitoring and follow-up examination.

Because the cause and evolution of HPS are unknown,

it is uncertain whether a young infant in whom the

canal fails to relax completely will go on to develop

HPS requiring surgery or whether the changes will be

arrested and resolve with sequelae [3].

Potential causes of errors in the diagnosis of

HPS are overdistention of the stomach, which may

lead to displacement of the pylorus posteriorly

making identification and measurement of the py-

loric thickness more difficult. Additionally, off-

midline or tangential images can lead to erroneous

diagnosis of a thickened muscle [3,4].

The treatment of HPS is pyloromyotomy in which

the hypertrophic muscle is split longitudinally. A

study by Yoshizawa et al [9] showed that although

was given a small amount of fluid. Both images show fluid

o the duodenum (D, arrow).


the pyloric muscle thickness remains abnormal after

surgery, by 5 months the dimensions gradually return

to less than or equal to normal values.

Fig. 5. Intussusception. Plain radiograph demonstrates a

round soft tissue density mass (arrows) in the right upper

quadrant protruding into the gas-filled transverse colon.

Intussusception

Intussusception is one of the most common causes

of acute abdomen in infancy. The condition occurs

when a segment of intestine (the intussusceptum) pro-

lapses into a more caudal segment of intestine (the

intussuscipiens). This condition usually occurs in chil-

dren between 5 months to 2 years of age. In this age

group most intussusceptions are idiopathic with no

pathologic lead point demonstrated. More than 90%

of intussusceptions are believed to be secondary to

enlarged lymphoid follicles in the terminal ileum.

Intussusception is more common in boys and the

condition is rare in children younger than 3 months.

The peak incidence is between 5 and 9 months of age.

Lead points are noted in children younger than

3 months of age or greater than 2 years of age. Lead

points include such entities as Meckel’s diverticulum,

duplication cysts, intestinal polyps, lymphoma, and

intramural hematomas [4]. Transient intussusception

is seen in patients with celiac disease (sprue).

Most intussusceptions involve the ileocolic region

(75%), where the ileum becomes telescoped into the

colon. This is followed in decreasing frequency by

ileoileocolic, ileoileal, and colocolic intussusceptions.

The classic clinical triad of acute abdominal pain

(colic), currant jelly stools or hematochezia, and a

palpable abdominal mass is present in less than 50%

of children with intussusception [10,11]. Up to 20%

of patients may be pain free at presentation. Addi-

tionally, in some instances lethargy or convulsion is

the predominant sign or symptom. This situation

results in consideration of a neurologic disorder rather

than intussusception. Given the uncertainty of achiev-

ing an accurate clinical diagnosis, imaging is required

in most cases to achieve an early and quick diagnosis

to reduce morbidity and mortality. Delay may be life-

threatening because of the development of bowel

necrosis and its complications [12].

Much controversy exists in the literature related to

the diagnosis and management of intussusception.

Realistically speaking children with intussusception

can be managed successfully in a number of different

ways. It is best to use diagnostic tools that are as

benign as possible, however, to avoid potential harm

to these children and to lessen the discomfort to the

children who are not shown to have intussusception.

Conventional radiography and the contrast enema

examination have been the principal methods used for

the diagnosis and treatment of intussusception.

Radiographs of the abdomen are useful and can

suggest the diagnosis by showing a mass usually

located in the right upper quadrant effacing the

adjacent hepatic contour (Fig. 5). Other signs include

reduced air in the small intestine, gasless abdomen, or

obstruction of the small intestine [13–15]. Identifi-

cation of a cecum filled with gas or feces in the

normal location is the finding that allows exclusion

of intussusception with most confidence [10,13]. In

the presence of intussusception, plain radiography

allows exclusion of bowel perforation, a major com-

plication of intussusception. The accuracy of plain

radiography in diagnosis on exclusion of intussuscep-

tion ranges from 40% to 90% [13,16,17].

Barium enema examination has been the standard

of reference for the diagnosis of intussusception for

many years. At many institutions liquid enema or air

enema examination is the principal diagnostic tool.

Fig. 6. Meniscus sign. Image from barium enema reduction

shows the rounded apex of the intussusception protruding

into the column of contrast material.

Fig. 7. Intestinal intussusception. Transverse sonographic

image demonstrates a soft tissue mass in the right upper

quadrant adjacent to the gallbladder (GB).


The classic signs of intussusception at enema exami-

nation are the meniscus sign and the coiled spring

sign. The meniscus sign is produced by the rounded

apex of the intussusception (the intussusceptum) pro-

truding into the column of contrast material (Fig. 6).

The coiled spring sign is produced when the edema-

tous mucosal folds of the returning limb of the in-

tussusception are outlined by contrast material in the

lumen of the colon. The enema examination, however,

can be a very unpleasant experience for both the

parent and child and is also associated with radiation.

The role of sonography in the diagnosis of intus-

susception is well established with a sensitivity of

98% to 100% and a specificity of 88% to 100% [18].

It has been suggested that sonography should be the

initial imaging modality and that the enema exami-

nation should only be performed for therapeutic

reasons [11,18,19]. Sonography not only aids in the

diagnosis of intussusception but it also allows the

identification of patients who are candidates for

therapeutic reduction. Sonography may also detect

other abnormalities that are overlooked by the enema

examination [4]. In addition, there is a high level of

patient comfort and safety with US.

A technique of graded compression is used for

the sonographic evaluation of suspected intussuscep-

tion. Because deep penetration of the US beam is not

necessary in small children, a linear high-resolution

transducer, 5 to 10 MHz, can be used to improve the

definition of the image. The abdomen and the pelvis

should be scanned in both longitudinal and transverse

planes [1]. The intussusception mass is a large struc-

ture, usually greater than 5 cm. Most intussusception

occurs in the subhepatic region often displacing adja-

cent bowel loops (Fig. 7). Even inexperienced opera-

tors can readily identify the intussusception on

sonography. An intussusception is a complex struc-

ture. The intussuscipiens (the receiving loop) contains

the folded intussusceptum (the donor loop), which has

two components: the entering limb and the returning

limb. The attached mesentery is dragged between the

entering and returning limbs. Sonographically, the

intussusception may demonstrate an outer hypoechoic

region surrounding an echogenic center, referred to as

a ‘‘target’’ or ‘‘doughnut’’ appearance (Fig. 8) [20].

The hypoechoic outer ring seen on axial scans is

formed by the everted returning limb, which is the

thickest component of the intussusception and the thin

intussuscipiens. The echogenic center of intussuscep-

tion contains the central or entering limb, which is of

normal thickness and is eccentrically surrounded by

hyperechoic mesentery [20]. Another pattern of imag-

ing that has been described is that of multiple con-

Fig. 8. Target appearance. Transverse sonographic view de-

monstrates the intussusception. The hypoechoic outer layer

represents the intussuscipiens and the central echogenic layer

represents the intussusceptum (arrow).


centric rings. Within the bowel wall the mucosa and

submucosa are echogenic, whereas the muscularis

layer is hypoechoic. Multiple hypoechoic and hyper-

echoic layers are identified when there is little bowel

edema present. This represents the mucosa, submu-

cosa, and muscularis layers of the intussusceptum and

intussuscipiens. With increasing degrees of bowel

edema, the hyperechoic mucosal and submucosal

echoes are obliterated in the intussusceptum resulting

in fewer layers. On long axis scans the hypoechoic

layers on each side of the echogenic center may result

in a reniform or pseudokidney appearance (Fig. 9).

Fig. 9. Long-axis sonographic view shows an elongated

appearance resulting in a pseudokidney appearance (arrow).

The pseudokidney sign is seen if the intussusception

is curved or imaged obliquely [1].

Although the target and pseudokidney signs are

the most common ultrasonographic signs used, they

are not pathognomic because they have also been

seen in normal or pathologic intestinal loops. Differ-

ential consideration for the US findings includes

other causes of bowel wall thickening, such as

neoplasm, edema, and hematomas. An inexperienced

operator may mistake stool or psoas muscle for

an intussusception.

In addition to diagnosing the intussusception US

has other advantages. US may detect the presence

of a lead point, which is present in approximately 5%

of intussusception. Various sonographic findings

have been reported to be predictive of success of hy-

drostatic reduction. A study by Koumanidou et al [18]

shows that the sonographic presence of enlarged

mesenteric lymph node in the intussusception is a

prediction of hydrostatic irreducibility. Small amounts

of free peritoneal fluid are seen in up to 50% of cases.

The presence of trapped peritoneal fluid within an

intussusception correlates significantly with ischemia

and irreducibility, however, because it reflects vascu-

lar compromise of the everted limb.

Fig. 10. Use of Doppler ultrasound to evaluate intussuscep-

tion. Doppler ultrasound shows blood flow within the

intussusception, suggesting its reducibility.


Additionally, the absence of flow within the intus-

susception on color Doppler sonography correlates

with a decreased success of reduction and a higher

likelihood of bowel ischemia [21–23], and presence

of color flow within the intussusception correlates

with higher success rate of its reduction (Fig. 10).

There are many different techniques used to reduce

intussusception described in the literature. Water-sol-

uble contrast material, barium, air enema guided by

fluoroscopy, and physiologic saline solution com-

bined with US have all been used [24,25]. The use

of sonography to guide hydrostatic reduction has

been predominately performed in the eastern hemi-

sphere and is increasingly being used in Europe. The

reduction rate is high (76%–95%), with only 1

perforation in 825 cases reported [25,26]. The proce-

dure may be performed with water, saline solution, or

Hartmann solution. The instilled fluid is followed as it

courses through the large bowel until the intussuscep-

tion is no longer visualized and the terminal ileum and

distal small bowel are filled with fluid or air. There has

been little experience with US-guided air enema

therapy. Because air prevents the passage of the US

beam, it may be difficult to visualize the ileocecal

valve; therefore, small residual ileoileal intussuscep-

tion can be observed. Additionally, it is difficult to de-

tect perforation resulting in pneumoperitoneum [24].

Sonography has been shown to be highly success-

ful in the diagnoses and reduction of intussusception.

The appropriate use of US in children with suspected

intussusception obviates the necessity for diagnostic

enema, and the use of enema should be limited to

therapeutic purposes [27].

Acute appendicitis

Acute appendicitis is one of the major causes of

hospitalization in children and it is the most common

condition requiring emergency abdominal surgery in

the pediatric population. The condition typically

develops in older children and young adults with the

diagnosis being rare under the age of 2. Clinical signs

and symptoms associated with acute appendicitis

include crampy, periumbilical, or right lower quad-

rant pain; nausea; vomiting; point tenderness in the

right lower quadrant; rebound tenderness; and leuko-

cytosis with a left shift [28]. When the history and

clinical findings are classic, the diagnosis of acute

appendicitis is often straightforward [29]. Not only do

one-third of children with acute appendicitis have

atypical findings, however, but also the presenting

signs and symptoms of many nonsurgical conditions

may mimic those of acute appendicitis. Most children

with acute abdominal pain have self-limited non-

surgical disease. Upper respiratory tract infections,

pharyngitis, viral syndrome, gastroenteritis, and con-

stipation are the most common associated conditions

noted in these children. The actual prevalence of acute

appendicitis in children presenting in the outpatient

setting with acute abdominal pain ranges from 1% to

4% [28,30].

The delayed diagnosis of acute appendicitis can

carry serious consequences. Perforation, abscess for-

mation, peritonitis, wound infection, sepsis, infertil-

ity, adhesions, bowel obstruction, and death have

been reported. Morbidity and mortality in acute

appendicitis are related almost entirely to appendiceal

perforation. The prevalence of appendiceal perfora-

tion in various pediatric series has ranged from 23% to

73%, with the perforation rate even higher in young

children [28,31–33]. Up to half of children with

perforated appendicitis may experience a complica-

tion, with nearly all deaths associated with perforated

appendix [28]. For fear of missing the diagnosis and

allowing the development of perforation, peritonitis,

and sepsis, a low index of suspicion and early opera-

tive intervention have been recommended. As a result,

negative laboratory rates as high as 20% have been

reported with rates of 10% to 15% widely accepted

[29,34,35]. Unnecessary appendectomy carries po-

tentially major risks and substantial costs, however,

prompting many to advocate increased efforts to avoid

unnecessary appendectomy [36]. The goal of imaging

in a child with suspected appendicitis should be to

identify the presence of disease in patients with

equivocal clinical findings. Used correctly, imaging

should reduce the negative laparotomy and perfora-

tion rates and reduce the intensity and cost of care.

The ideal diagnostic test should be fast, noninvasive,

highly accurate, and readily available [37]. The pri-

mary imaging technique over the past decade for

evaluating children with suspected appendicitis has

been graded-compression US because it is widely

available, noninvasive, and does not involve radiation

[28,38–40].

The reported diagnostic accuracy of US in the

diagnosis of acute appendicitis has varied greatly. The

sensitivity of US has ranged from 44% to 94% and

the specificity has ranged from 47% to 95% [28]. The

clinical use of US lies primarily in the subgroup of

children in whom the clinical findings are equivocal.

Not only can it establish the diagnosis of appendicitis

but also it can identify other abdominal and pelvic

conditions, especially gynecologic, that present as

right lower quadrant pain [28,41].

The graded-compression technique of US is per-

formed with a high-resolution, linear-array transducer


of 5 to 10 MHz. Graded-compression sonography

primarily consists of anterior forced compression to

reduce the distance between the pathologic process

and the transducer and to displace or compress bowel

structures to eliminate gas artifacts. Reducing the

abdominal cavity by compression enables clear visu-

alization of the retroperitoneal structures [42]. Ante-

rior compression is considered adequate when the

iliac vessels and psoas muscles are visualized because

the appendix is anterior to these structures.

Scanning is performed in both longitudinal and

transverse planes. The examination begins with the

identification of the cecum and the terminal ileum.

The ascending colon is a nonperistaltic structure

containing gas and fluid. The terminal ileum is com-

pressible easily and displays active peristalsis. The

cecal tip where the appendix arises is approximately

1 to 2 cm below the terminal ileum. The examination

can be expedited by asking the patient to point to the

area of maximal tenderness. This can also aid in

locating a retrocecal appendix [28].

In early nonperforated appendicitis, an inner

echogenic lining representing submucosa can be

identified. The inflamed, nonperforated appendix ap-

pears as a fluid-filled, noncompressible, blind-ending

Fig. 11. Acute appendicitis. Longitudinal (A) and transverse (B) u

calipers), which is enlarged.

tubular structure on longitudinal US image. The

maximal appendiceal diameter from outside wall to

outside wall is greater than 6 mm in an inflamed

appendix. A noncompressible enlarged appendix

measuring greater than 6 mm in maximal diameter

is the only US sign that is specific for appendicitis

(Fig. 11). Other findings of appendicitis include an

appendicolith, which appears as an echogenic focus

with acoustic shadowing; pericecal or periappendi-

ceal fluid; and enlarged mesenteric lymph nodes. On

transverse imaging a target appearance is delineated.

This is characterized by a fluid-filled appendiceal

lumen, which is surrounded by the echogenic mucosa

and submucosa and hypoechoic muscularis layer.

The US features of perforation include loss of the

echogenic submucosal layer and presence of a locu-

lated periappendiceal or pelvic fluid collection or

abscess (Fig. 12) [43,44]. The appendix is visible

in 50% to 70% of patients with perforated appendi-

citis [44].

The use of color Doppler has also been described

in the evaluation of appendicitis. Color Doppler US

of nonperforated appendicitis demonstrates periph-

eral wall hyperemia reflecting inflammatory hyper-

perfusion. Color flow may be absent in gangrenous

ltrasound images show an inflamed appendix (between the

Fig. 12. Right lower quadrant abscess. Two-year-old girl

presented with abdominal pain. A complex mass in the right

lower quadrant consistent with an appendiceal abscess was

demonstrated on ultrasound.


appendicitis or early inflammation [45]. Color Dopp-

ler findings of appendiceal perforation include hyper-

emia in the periappendiceal soft tissue or within a

well-defined abscess [46]. Color Doppler US does not

increase the sensitivity of the examination but it does

make interpretation of the gray-scale US findings

easier and can increase observer confidence in the

diagnosis of acute appendicitis.

Most false-negative diagnosis results from failure

to visualize the appendix. This may be secondary to

operator dependency, inability to compress the right

lower quadrant adequately, a retrocecal position of

the appendix, or appendiceal perforation [37,42]. In

patients with obesity the high-frequency transducer

may fail to reach the necessary depth, which makes

accurate diagnosis difficult because of decreased spa-

tial resolution. Another pitfall is early inflammation

limited to the appendiceal tip, which can be missed

if only the proximal appendix is imaged [47,48].

False-positive diagnosis has also been reported.

The normal appendix, which may be visible in 10%

to 50% of children and adolescents, may be mistaken

for appendicitis. The normal appendix measures 6 mm

or less, is compressible, and lacks adjacent inflamma-

tory changes. Periappendiceal changes may also be

secondary to causes other than appendicitis, such as

Crohn’s disease or pelvic inflammatory disease. The

use of US in patients with acute appendicitis is a

subject of controversy in the literature [42]. Many

studies have been performed to evaluate the use of

US in the ultimate outcome of children with suspected

appendicitis. Some studies have suggested that the

use of US has not improved outcome in children with

suspected appendicitis. A study by Roosevelt and

Reynolds [49] showed no significant differences in

the perforation rate or cost of care in children who

underwent US compared with those who did not. A

study by Lessin et al [29], however, suggests that the

early and selective US in clinically equivocal cases

could rapidly allow an accurate diagnosis, without the

need for prolonged observation or hospitalization.

There are several other tests that have been used to

facilitate the diagnosis of acute appendicitis but the

advantage of ultrasonography is its low cost, lack of

radiation exposure, easy availability, and noninvasive

nature [38].

Summary

Ultrasound is extremely beneficial in the evalua-

tion of acute pediatric abdominal disease, such

as HPS, intussusception, and acute appendicitis. As

techniques and equipment improve, its role in the eval-

uation of infants and children continues to increase.

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Radiol Clin N Am 42 (2004) 457–478

Emergent ultrasound interventions

Dean A. Nakamoto, MD*, John R. Haaga, MD

Department of Radiology, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, OH 44106, USA

Interventional radiologists are frequently asked to effusion. Ultrasound evaluation before the procedure

perform emergent diagnostic and therapeutic proce-

dures. The choice of image guidance depends on

user preference; availability of CT, ultrasound, and

MR imaging; and the ability of the modality to

visualize the target. Ultrasound is the most preferred

modality and has many advantages including real-time

imaging of the needle tip during the procedure; multi-

planar imaging capabilities; its relatively low cost; and

the equipment is mobile, so procedures can be per-

formed at the bedside of critically ill patients in the

intensive care unit. Ultrasound-guided interventions

have become very common in many institutions [1,2].

Emergent procedures frequently performed with ultra-

sound guidance include thoracentesis, paracentesis,

percutaneous nephrostomy, and percutaneous chole-

cystostomy. The role of ultrasound guidance has also

expanded to include abscess drainage, particularly in

the pelvis, and chest tube placement. This article

discusses various emergent interventions performed

with ultrasound imaging guidance.

Ultrasound-guided chest interventions

Thoracentesis

Ultrasound-guided thoracentesis is usually per-

formed easily because most pleural fluid collections

are accessible using percutaneous methods. In the

septic patient, a diagnostic thoracentesis is usually

performed to evaluate for empyema. Other indications

include evaluation for chylous, bloody, or malignant


doi:10.1016/j.rcl.2004.01.002



(D.A. Nakamoto).

confirms the presence of fluid and distinguishes

pleural fluid from atelectasis, mass, or elevated dia-

phragm. Typically, the patient is seated upright. Pleu-

ral fluid is generally anechoic, although debris or

septations may be present. The diaphragm must be

identified, and the underlying liver or spleen. A 3- to

4-MHz sector or vector probe is usually sufficient to

survey the hemithorax quickly.

Technique

Most diagnostic and therapeutic thoracenteses are

performed with ultrasound guidance. Typically, the

patient is seated upright with his or her back to the

interventionalist. To perform the procedure safely,

there should be at least one rib interspace of fluid

above and below the puncture site. If there is less

fluid, the procedure may be deferred depending on the

clinical urgency and the ability of the patient to

cooperate. Very small pleural fluid collections can

be aspirated safely, however, if the patient can coop-

erate with breath-holding. Patients who cannot sit

upright are placed either supine or in a lateral decu-

bitus position. In either of the latter two positions,

there must be a larger amount of fluid to attempt

thoracentesis. Because ultrasound can be performed

portably, ultrasound-guided thoracenteses can be per-

formed in an ICU, even on mechanically ventilated

patients [3]. If visualization is difficult because of

patient body habitus, air in the pleural fluid, or the

patient’s inability to be positioned adequately, CT

guidance may be helpful.

Initial scanning should be performed with a sector,

vector, or curvilinear probe. This is to document the

amount of fluid and quickly to find the largest pocket

of fluid. At this time, it is important to verify the

location of the diaphragm. Scanning can then be

performed with a linear probe of 6 MHz. This enables

s reserved.

Fig. 1. Aberrant intercostal artery. This sagittal color Doppler

scan performed with a 6-MHz linear probe demonstrates an

aberrant, tortuous course of the intercostal artery (arrow).

Here the artery is situated close to the midpoint of the rib

interspace. In this location, the artery is more susceptible to

injury from a needle.

D.A. Nakamoto, J.R. Haaga / Radiol Clin N Am 42 (2004) 457–478458

accurate localization of the rib interspace, particularly

in obese patients. The location of the intercostal artery

(Fig. 1) also is verified at this time. Although the

artery is usually directly adjacent to the inferior aspect

of the rib, it can be located more inferiorly and in the

rib interspace. If the patient has a malignancy, pleural-

based metastases can also be visualized at this time

and avoided (Fig. 2). It is important to be able to

recognize hypoechoic, consolidated lung and not

mistake it for pleural fluid. Sometimes consolidated

Fig. 2. Pleural-based metastases. This patient with metastatic lung c

based mass was noted (cursors); a different location was used.

lung may mimic complex fluid (Fig. 3) and color

Doppler may be helpful to verify the presence of

pulmonary vessels in consolidated lung. Following

sterile preparation of the skin, local anesthesia should

be administered from the skin surface to the pleural

surface. Although one could use ultrasound to visual-

ize needle insertion directly, typically a site is marked

on the skin surface and the needle is advanced until

fluid is obtained.

A variety of needles and catheters are available for

thoracenteses. The simplest method is to use an 18- or

20-gauge angiocatheter. The angiocatheter with punc-

ture needle is advanced into the pleural space until

fluid is aspirated, and then the angiocatheter is ad-

vanced into the pleural space over the puncture

needle. Single-step 6F trocar-based catheters (Skater,

Medical Device Technologies, Gainesville, Florida)

are also available, particularly if the procedure is

both diagnostic and therapeutic. These are used in a

similar fashion.

After a thoracentesis, the authors obtain a chest

radiograph in posteroanterior view to evaluate for

pneumothorax. The chance of pneumothorax is small

and generally ranges from 2.5% to 7.5% [4–7],

although rates up to 13.9% have been reported [8].

Symptoms caused by pneumothorax include shortness

of breath and shoulder pain on the affected side. Some

investigators do not advocate routine postprocedure

chest radiograph for the asymptomatic patient, be-

cause of the low complication rate [4,9,10]; however,

because sizable pneumothoraces may be asymptom-

atic, the authors routinely obtain a chest radiograph.

The mechanisms of postthoracentesis pneumothorax

ancer was referred for therapeutic thoracentesis. The pleural-

Fig. 3. Consolidated lung mimicking complex pleural fluid. This patient was referred for possible thoracenteses. Longitudinal

vector scan of the left hemithorax demonstrates complex-appearing mixed solid and cystic foci in the hemithorax (arrowheads)

consistent with consolidation of the lung.

D.A. Nakamoto, J.R. Haaga / Radiol Clin N Am 42 (2004) 457–478 459

include (1) inadvertent introduction of air into the

pleural space, usually by leaving the needle or catheter

open to the air after the tip is in the pleural space;

(2) puncture of the lung; and (3) rupture of the vis-

ceral pleura because of a decrease in pleural pressure

[4,11]. If the pneumothorax is large, is symptomatic,

or increases with time, the patient may require a chest

tube placement.

Other significant complications of thoracentesis

include pain, vasovagal reaction, bleeding, and re-

expansion pulmonary edema. Pleuritic pain may be

caused by the rubbing of the visceral and parietal

pleural surfaces after the fluid has been removed. Pain

during the procedure may also be caused by the

inability of the patient’s collapsed lung to re-expand

as the fluid is removed. This may be an indication to

stop the procedure [4,7].

Vasovagal reactions may occur during any inter-

ventional procedure. The patient may become tran-

siently bradycardic, hypotensive, and may then lose

consciousness. Predisposing factors include volume

depletion. A quick physical examination of these pa-

tients shows bradycardia, diaphoresis, dilated pupils,

and hypotension. These vasovagal reactions are usu-

ally minor and temporary. Placing the patient in the

Trendelenburg position to improve venous return to

the heart usually resolves the problem. If the patient

improves within a few minutes, no other action is

needed. If significant, the patient may require atro-

pine. Typical atropine doses are as follows: adult—

1 mg intravenously; children—0.02 mg/kg to 0.60 mg

(maximum) intravenously. The treatment interval is

every 3 to 5 minutes to a total of 3 mg for adults or

2 mg for children. If the atropine does not improve the

situation, then urgent consultation with the resuscita-

tion team is appropriate.

Re-expansion pulmonary edema is an uncommon

complication of uncertain etiology. It may be asymp-

tomatic; however, it can cause various degrees of

hypoxia and can even be life-threatening [12,13]. It

presents as unilateral pulmonary edema, which may

progress to bilateral edema [4,12]. Re-expansion pul-

monary edema is believed to be more likely if a large

volume (ie, greater than 1 L) of pleural fluid is as-

pirated at one time. Some investigators have removed

up to 2 L at one time, however, without adverse con-

sequences [4,7].

Bleeding is an uncommon complication. The risk

is higher in patients with coagulopathies. It also may

occur with inadvertent laceration of the intercostal

artery [14]. The authors typically check platelets,

prothrombin time and partial thromboplastin time,

and International Normalized Ratio (INR) before

any procedure and adjust accordingly. They prefer

platelet counts over 50,000, and the prothrombin time

to be within 2 seconds of normal, or INR less than

1.5. Fine-needle aspirations may be performed out-

side of these ranges. Every case, however, should be

individually tailored.

Ultrasound-guided chest tube insertion

Pleural effusions can occur in a variety of settings,

including pneumonia (parapneumonic effusion); ma-

lignancy; bleeding; and fluid overload. The pleural

fluid can be classified as transudative or exudative,

depending on the laboratory analysis as described

in Box 1. Parapneumonic effusions are generally

Box 1. Light’s criteria for diagnosis ofexudative effusions

� Pleural fluid protein to serum proteinratio > 0.5

� Pleural fluid to serum L-lactatedehydrogenase ratio > 0.6

� Pleural L-lactate dehydrogenase con-centration more than two thirds ofthe normal upper limit for serumL-lactate dehydrogenase

*satisfying any one of these criteriasuggests exudative natureData from reference [16].


divided into complicated and uncomplicated effu-

sions. The uncomplicated effusions are transudative

effusions and small free-flowing exudative effusions.

These effusions can resolve spontaneously with anti-

biotic treatment.

The complicated effusions are exudative effusions

that do not respond to medical treatment and require

drainage. Empyema, hemothorax, and malignant effu-

sions are all complicated effusions. Indications for

drainage of pleural fluid are given in Box 2.

Regarding parapneumonic effusions, there are

three stages in the evolution of empyema [15,16].

The first stage is a free-flowing exudative effusion.

The second stage is the fibrinopurulent stage during

which the cellularity and protein content of the effu-

sion increase. Fibrin is deposited on the visceral and

parietal surfaces. The third stage is the organization

stage; fibroblasts and capillaries grow into exudates

and form a pleural peel. If untreated, this stage can

result in lung entrapment and subsequent fluid drain-

age into the chest wall or into the lung. Empyema

requires emergent drainage to control sepsis. The first

two stages should be drained by closed-tube drainage,

Box 2. Indications for drainage of pleuralfluid

� A very large pleural effusion causingcardiorespiratory embarrassment

� Grossly purulent or hemorrhagicpleural fluid

� Positive Gram stain� pH > 7.2� Glucose < 40 mg/dL� L-lactate dehydrogenase > 1000 U/L

either radiologic or surgical. The third stage usually

requires surgical decortication, although there are

some data suggesting that the pleural peels may re-

solve with closed-tube drainage [17].

Anechoic pleural collections or collections with

fine linear septations on ultrasound respond best to

catheter drainage, whereas those with a complex

honeycomb pattern usually fail catheter drainage and

require decortication. Patients showing parietal pleu-

ral thickness greater than 5 mm are unlikely to re-

spond to catheter drainage.

Indications for chest tubes and technique

The primary indication for chest tube placement is

to drain an empyema and prevent progression to the

organized stage. This can be accomplished with

surgical drainage or closed-tube drainage. Closed-

tube drainage can be performed with blind insertion

of a large-bore (22–34F catheter) chest tube placed by

a surgeon or with image-guided chest tube placement

using CT or ultrasound. Typically, smaller-bore, 8 to

14F catheters are used with the image-guided meth-

ods. The smaller tubes placed by imaging methods are

usually better tolerated by the patients than the larger,

surgically placed tubes. Therapeutic options for in-

fected pleural collections are summarized in Box 3.

Large pleural fluid collections are amenable to

single-step trocar catheters. The patient can be posi-

tioned either upright or in a lateral decubitus position

with the affected side up. As with a thoracentesis,

initial scanning should confirm the location of the

diaphragm and the overall size of the effusion. Once a

site is marked and the skin is sterilely prepared,

adequate local anesthesia should be used from the

skin surface to the pleural surface. A small incision

should be made with a scalpel, and the tract should be

dilated with a small hemostat. An initial aspiration

can be performed with a 19-gauge sheath needle with

a disposable 5F tetra-fluoro-ethylene (TFE) catheter

(Yueh centesis disposable catheter needle, Cook,

Box 3. Therapeutic options for infectedpleural collections

� Antibiotics� Tube thoracotomy� Intrapleural fibrinolytics (urokinase)� Thoracoscopy with lysisof adhesions

� Decortication� Open surgical drainage


Bloomington, Indiana) to determine the viscosity of

the fluid. A trocar–based, self-retaining catheter can

then be inserted blindly or under ultrasound visuali-

zation, depending on the size of the effusion. If the

effusion is thin, a single-step, 6 to 8F catheter (Skater,

Medical Technologies, Gainesville, Florida) can be

placed. Although 10F and larger catheters are avail-

Fig. 4. Complex left pleural effusion in heart transplant patien

demonstrates a large loculated left pleural effusion, which inve

illustrating the procedure. Under ultrasound guidance, a 19-gauge d

the effusion at the level of the midaxillary line. The needle is with

7.5-mm J 0.035-inch angiographic guidewire is placed. (C) The tra

self-retaining nephrostomy-type tube is placed. Arrows point to ne

able on single-step trocars, the authors have found

that these larger catheters can be difficult to insert in a

single-step procedure. If a 10F or larger catheter is

needed, the Seldinger technique can make catheter

insertion easier (Fig. 4). A standard 0.035-inch

angiographic guidewire can be placed through the

5F Yueh catheter and the tract can then be dilated.

t, left chest tube placement. (A) Longitudinal vector scan

rts the left hemidiaphragm. (B) Schematic representation

isposable sheath needle (Yueh centesis needle) is placed into

drawn, a small amount of fluid is aspirated, and a standard

ct is sequentially dilated to 10F catheter, and a 10F catheter

phrostomy tube.

Box 4. Indications for external drainage oflung abscess

� Persistent sepsis after 5 to 7 days ofantibiotic therapy

� Abscesses 4 cm or more in diameterthat are under tension

� Abscesses 4 cm or more in diameterthat are enlarging

� Failure to wean from a ventilatorbecause of a large abscess

Box 5. Relative contraindications forexternal drainage of lung abscess

� Noncompliant patient� Lack of an abscess-pleuralsymphysis

� Coagulopathy


CT is the preferred method for smaller effusions or

effusions close to vital structures, such as the heart or

major vessels. When placing the chest tube, a lateral

approach is preferred rather than a direct posterior

approach, if possible. The ideal site for catheter

placement is usually at the level of the midaxillary

line; the authors try to avoid a direct posterior

approach so that the patient does not lay on the tube.

Once the tube is placed, some of the fluid should

be withdrawn to confirm the location of the tube.

Direct visualization with ultrasound should also doc-

ument the location. The tube should be secured to the

skin and placed to a water-seal pleural drainage

system (Pleur-Evac, Deknatel, Fall River, Massachu-

setts) with suction at �20 cm H2O. Patients are

monitored daily to ensure proper tube functioning

and to record the amount of drained fluid. Once the

fluid becomes serous, the tube output has decreased to

20 mL or less per 24 hours, and the patient has

defervesced, the tube may be removed. A CT scan

should be performed before tube removal to ensure

that there are no undrained collections. Additional

drainage tubes may be placed for any separate collec-

tions not being drained.

Many empyemas are loculated, which can make

chest tube drainage difficult. Fibrinolytic agents, such

as streptokinase and urokinase, have been used suc-

cessfully to lyse septations [18–20]. Because uro-

kinase is not always available, the authors have been

using streptokinase, 125,000 IU every 12 hours for up

to 2 days.

Success rates range from 70% to 94%, with a

cumulative success rate of approximately 85% in

various radiologic studies [19–27]. Not all empyema

are amenable to percutaneous drainage. Patients who

develop a pleural peel or who have persistent fevers

and elevated white blood cell counts despite adequate

drainage and appropriate antibiotics may require sur-

gical drainage and decortication. Surgical treatment

for such patients should not be delayed. Complica-

tions from chest tube insertion include sepsis, inap-

propriate pathway of chest tube, bleeding, and injury

to adjacent organs.

Lung abscesses

Most lung abscesses are caused by oropharyngeal

aspiration of bacteria as can occur with alcoholic

stupor, general anesthesia, seizures, or cerebral vas-

cular accidents [28,29]. Other causes include malig-

nancy, septic emboli, foreign bodies, and lung cysts

[28,29]. It is important to distinguish between lung

abscess and empyema because empyema requires

external drainage, whereas most lung abscesses re-

solve with medical management [30]. The distinction

between lung abscess and empyema is best made with

contrast-enhanced CT. A lung abscess appears round

and if it contacts the pleural surface, it forms an acute

angle with the pleura. Empyema is more biconvex in

shape and forms obtuse angles with the pleura. The

wall of an abscess may have thick and irregular en-

hancement, whereas the enhancing pleura with empy-

ema has a smooth curvilinear appearance (ie, the split

pleura sign) [31].

Indications for external drainage of lung abscess

[32] are summarized in Box 4.

Relative contraindications for external drainage of

lung abscess are given in Box 5.

The abscess-pleural symphysis occurs when a lung

abscess is continuous with the pleura. It is important to

have a needle traverse the abscess-pleural symphy-

sis to decrease the chances of complications, such as

leak of abscess fluid into the pleural space and bron-

chopleural fistula. Catheter drainage is usually per-

formed by CT; however, ultrasound can be used in

selected cases. If the abscess-pleural symphysis is

small, CT is the modality of choice because it is easier

to place the needle accurately under CT guidance.

Because lung abscesses may have fine strands of

residual normal parenchyma, which can bleed, one

should not be too aggressive with catheter insertions or

guidewire manipulations [32].


Ultrasound-guided abdominal interventions

Paracentesis

Ultrasound-guided paracentesis is a commonly

performed procedure. Typically, the procedure is per-

formed emergently in a septic patient as a diagnostic

procedure to evaluate for spontaneous bacterial peri-

tonitis [33] or for hemoperitoneum in the setting of

trauma [34]. More commonly, this procedure is per-

formed urgently as a therapeutic measure for symp-

tomatic relief of tense ascites.

Initial scanning is performed with a sector or cur-

vilinear probe to find the largest pocket. Attention is

then made to the abdominal wall to ensure that there

are no vessels at the site of subsequent needle punc-

ture, such as the epigastric artery or collateral vessels

in a patient with cirrhosis. In patients with malignan-

cy, one should ensure that there are no peritoneal

metastases at the needle insertion site. This can be

performed with a linear transducer, usually of 6 MHz

or greater. The preferred site for large-volume para-

centesis is chosen in the dependent position, such as

right or left lower quadrants. The site of puncture is

chosen usually lateral to the rectus muscle to avoid the

accidental puncture of the inferior epigastric artery.

The inferior epigastric artery normally travels at the

junction of the medial two thirds and lateral one third

of the rectus or approximately 5 cm laterally from the

midline (Fig. 5). After standard sterile skin prepara-

tion, 1% lidocaine is injected into the abdominal wall

for local anesthesia. The authors anesthetize all the

Fig. 5. Paracentesis, epigastric artery. (A) Color Doppler transvers

transducer was used to localize the location of the inferior epiga

location along the lateral aspect of the rectus abdominis muscle. (B

the epigastric arteries (arrowheads).

way to the parietal peritoneum. Then they perform the

aspiration with a standard 18-gauge angiocatheter. If

the patient is obese, the authors use a 15- or 20-cm-

long, 19-gauge sheath needle (Yueh centesis dispos-

able catheter needle; Cook, Bloomington, Indiana).

For smaller collections or collections adjacent to ma-

jor vessels or to the spleen, the authors use direct

ultrasound guidance with either the freehand tech-

nique or the needle guide.

Large-volume paracentesis provides rapid resolu-

tion of symptoms with minimal complications and is

well tolerated by most patients. Complications from

paracentesis have rarely been reported, and include

inferior epigastric artery pseudoaneurysm [35], hem-

orrhage after large-volume paracentesis [36–38],

bowel perforation [38], hypotension [39], and a frag-

ment of the catheter left in the abdominal wall or

peritoneum [38]. Postparacentesis circulatory dys-

function has been reported and is characterized by

hyponatremia, azotemia, and an increase in plasma

renin activity. Postparacentesis circulatory dysfunc-

tion is associated with an increased mortality and may

be prevented by administration of albumin intrave-

nously (6 to 8 g/L of ascites removed) along with large

volume parasynthesis (LVP).

Percutaneous cholecystostomy

Acute cholecystitis in high-risk patients in the

ICU is difficult to manage. In critically ill, oftentimes

septic patients with possible acalculous or gangrenous

cholecystitis, percutaneous cholecystostomy may be

e image of the anterior abdominal wall with a 6-MHz linear

stric artery (arrow) before paracentesis. This is the typical

) CT scan on a different patient demonstrates the location of


both diagnostic and therapeutic. These patients are not

suitable candidates for surgery. Percutaneous chole-

cystostomy is used as a diagnostic and therapeutic

procedure in these critically ill and difficult to manage

patients [26,40–43]. In unstable patients with calcu-

lous cholecystitis, percutaneous cholecystostomy per-

mits stabilization so that cholecystectomy can be

performed electively.

Indications

Percutaneous cholecystostomy may be performed

in critically ill septic patients to exclude acute cho-

lecystitis, because of the difficulties of establishing

the diagnosis of acute cholecystitis in these patients

[26,44,45]. The findings on the various diagnostic

tests can be nonspecific. A sonographically normal

gallbladder virtually excludes cholecystitis in an ICU

patient, and a positive sonographic Murphy’s sign

may be the most specific finding of acute cholecystitis

in these patients [46]. Other findings, such as sludge,

distention, pericholecystic fluid, wall thickening, and

striations, are nonspecific in this setting [46,47]. The

presence of gallstones, distention, and pericholecystic

fluid, however, have been described as findings that

may predict a more favorable response to percutane-

ous cholecystostomy [41,47]

Technique

Two access routes are used. The transhepatic route

approaches from the right midaxillary line and aims

for the ‘‘bare’’ area of the gallbladder. This route is

preferred by most investigators and theoretically

reduces the risk of bile peritonitis [26,41,42,48]. The

transperitoneal approach is from the anterior abdomen

and is aimed at the gallbladder fundus [41,49–51].

Because of the risks of bile peritonitis and inadvertent

perforation of the colon, the transperitoneal approach

is probably best reserved for patients with very dis-

tended gallbladder in which the gallbladder fundus

abuts the anterior abdominal wall. This approach is

also useful in patients with coagulopathy or underly-

ing liver disease [41,43,49–51]. The transhepatic

route for percutaneous cholecystostomy does not al-

ways result in a puncture of the ‘‘bare area’’ of the

gallbladder and the ‘‘free’’ peritoneal surface of the

gallbladder may still be punctured [52]. Some inves-

tigators have also used simple aspiration of the gall-

bladder contents without placement of a drainage tube

[45,53]. The authors typically use the transhepatic

approach and ultrasound guidance. Sometimes CT

guidance may be necessary, however, particularly

for a liver in a high subcostal location. Typically, a

small 6F single-step trocar catheter (Skater, Medical

Device Technologies, Gainesville, Florida) is used. If

the trocar-based catheter buckles against the liver or

gallbladder wall, the Seldinger technique can be used

(Fig. 6). The acutely inflamed gallbladder wall can be

friable and catheter and wire manipulations should not

be too aggressive. If the Seldinger technique is used,

the authors use a 5F catheter on a 19-gauge needle

(Yueh centesis disposable catheter needle, Cook,

Bloomington, Indiana) to puncture the gallbladder

lumen. They then use a standard 0.035-inch guide-

wire; carefully dilate the tract to 8F catheter; and then

place an 8F catheter, self-retaining nephrostomy tube.

The authors recommend not using a super-stiff guide-

wire, such as an Amplatz, because it may perforate the

gallbladder wall. If the transperitoneal approach is

used, a small 8F catheter or less, single-step trocar

catheter is recommended. The gallbladder lumen

should be punctured with a sharp jab, and the gall-

bladder should be emptied once the catheter is within

[49]. The Seldinger technique is not favored with this

technique, because there is a theoretical risk of bile

leakage into the peritoneum.

Once the self-retaining tube is within the gallblad-

der, it is recommended that it remain there for at least

2 to 3 weeks to allow formation of a mature tract along

the catheter; otherwise, there may be bile leakage once

the catheter is removed [42,48]. It also is recom-

mended that a cholangiogram be performed before

catheter removal to ensure patency of the cystic duct

and common bile duct [26,48,54]. Some investigators

also advise imaging the tract at the time of tube

removal [26,43,44], although other investigators dis-

agree [41,49] even if the transperitoneal approach is

used [49].

Complication rates generally range from 5% to

13.8% [41,43,45,49,51,55]. Complications include

bleeding, bile leakage, catheter dislodgement, and

vasovagal events. Bile leakage has been reported with

both the transhepatic and transperitoneal approaches.

Technical success rates (ie, adequate placement of a

drain in the gallbladder) are high (ie, as great as 97%–

100%) [26,41–43,45,47–49,56]. Overall patient re-

sponse is lower, however, because of the relatively

low threshold of clinicians to request the procedure

and the nonspecificity of the diagnostic tests; no

clinical response to the procedure can be found in up

to 42% of the patients [26,42]. Placement of a chole-

cystostomy tube is still helpful in these circumstances,

however, because it does reassure the clinicians that

cholecystitis is not a cause of a patient’s sepsis.

Some investigators have used simple gallbladder

aspiration in patients with suspected acute cholecys-

titis [45,53]. Simple percutaneous gallbladder aspira-

tion does seem to be beneficial in patients with acute

cholecystitis and comorbid conditions. Chopra’s et al

Fig. 6. Ultrasound-guided percutaneous cholecystostomy in a patient status-post recent myocardial infarction. (A) Longitudinal

vector scan demonstrates distended gallbladder with sludge and a thick wall. Initial attempts with a 6F catheter one-step trocar-

based catheter were not successful, because of the thickened gallbladder wall. The catheter buckled on the trocar. The Seldinger

technique was used. A 19-gauge disposable sheath needle (Yueh centesis needle) was used to enter the gallbladder lumen. A

standard 0.035-inch angiographic guidewire was placed, the tract was carefully dilated to 8F catheter, and a self-retaining 8F

catheter nephrostomy-type tube (arrowhead) was placed. (B) Schematic representation of the procedure described in Fig. 6A.


[45] patient population, although at high surgical risk,

consisted of noncritically ill patients. As stated in their

article, they excluded patients who had had prolonged

admission to the ICU.

Intra-abdominal abscess drainage

Image-guided percutaneous abscess drainage is a

well-established technique, which has become the

primary method of treatment for many patients with

intra-abdominal abscess [18,57–60]. In many hospi-

tals in the United States, CT is the imaging modality of

choice to detect abscesses. Once detected, an abscess

can be drained using either CT or ultrasound guidance

depending on which modality best delineates the

abscess and its surrounding structures. In general,

CT is used for abscesses inaccessible to ultrasound,

such as abscesses in deep locations adjacent to vital


structures (eg, major vessels or those adjacent to

bone), which may block the ultrasound beam. These

abscesses include pancreatic, interloop, and deep

retroperitoneal abscesses. Abscesses in more superfi-

cial locations of the peritoneum or visceral organs are

usually amenable to ultrasound guidance. Ultrasound

has many advantages, including its lower cost, its

ability to be performed portably at the patient’s bed-

side, and its multiplanar imaging capabilities.

Indications

In general, intraperitoneal abscesses adjacent to the

abdominal wall and abscesses in the periphery of

visceral organs, such as the liver or kidney, are

amenable to ultrasound-guided aspiration and drain-

age. The authors always avoid traversing uninvolved

spaces or organs, such as the liver or bowel, when

performing any interventional procedure. The excep-

tions are traversing the stomach for pancreatic proce-

dures and traversing the rectum or vagina for pelvic

abscess drainages. Other investigators have reported

success without significant complications from tra-

versing uninvolved spaces or organs while performing

interventional procedures [61–63]. If a loop of bowel

is inadvertently traversed with a catheter, the catheter

should be left in place for 2 to 3 weeks so a tract can

form. After this period the catheter can usually be

removed safely without spillage of bowel contents

into the peritoneum [64,65]. This assumes that the

underlying bowel is otherwise normal and that there is

no distal bowel obstruction. Relative contraindica-

tions common to all percutaneous procedures include

coagulopathy, the patient’s inability to cooperate, and

lack of safe access to the abscess.

Technique

Simple, uncomplicated abscess drainage is de-

scribed next.Management of more complex abscesses,

such as infected hematomas, abscesses associated

with fistulae, and fungal abscesses, is also discussed.

Pelvic abscesses, particularly those caused by gyne-

cologic sources, are discussed separately.

Preprocedure imaging is best performed with CT

because the size of the fluid collection, its location,

and extent can be well-delineated. The authors typi-

cally review the patient’s CT before the procedure and

if possible have a copy of the CT in the ultrasound

suite when performing the procedure. The CT pro-

vides an excellent roadmap to help plan the needle

trajectory. The authors frequently use a commercially

available needle guide, although for superficial ab-

scesses they use the freehand technique. For most

abscesses, the Seldinger technique is favored unless

the abscess is very large and superficial.

After obtaining informed consent, the fluid is

localized and the needle trajectory planned. The site

for needle insertion is marked, and the skin is prepared

and draped in a sterile manner. The ultrasound probe

is then covered with a sterile cover, and the needle

guide is attached unless the procedure is performed

freehand. A skin wheal is raised with local 1% lido-

caine, and a skin nick is made with a scalpel. Using a

19-gauge sheath needle (Yueh centesis disposable

catheter needle; Cook, Bloomington, Indiana), the

projected needle tract is anesthetized to the fluid

collection. The fluid collection is then punctured with

the 19-gauge sheath needle, the 5F disposable sheath

catheter is advanced over the needle, the sharp needle

is then removed, and the fluid is aspirated through the

5F disposable catheter sheath. If the fluid is purulent, a

standard 0.035-inch angiographic guidewire can be

advanced into the abscess. After confirming the loca-

tion of the guidewire, the tract can be dilated and an

appropriate-sized, self-retaining nephrostomy tube

can be placed. For thin pus, 8 to 10F catheters are

usually sufficient. Catheters up to 14F can be used for

more viscous pus. The tube position should then be

verified so that additional purulent fluid can be

aspirated. The catheter is then secured to the skin

either with sutures or adhesive fixation devices

(Percu-Stay Percutaneous Catheter Fastener, Derma

Sciences, Princeton, New Jersey).

Routine catheter care is then performed. The

authors place catheters to gravity drainage. Daily tube

rounds are made to evaluate the drainage progress.

Once the fluid becomes serous, the tube output has

decreased to less than 20 mL per 24 hours, the patient

has defervesced, and the white blood cell count is

normal, the tube may be removed. The authors typi-

cally repeat a CT scan before tube removal to ensure

that there are no residual fluid collections.

Liver abscess

Pyogenic liver abscesses located in the periphery

are amenable to ultrasound aspiration and drainage.

Those located more centrally are better approached

with CT guidance. Typically, a cuff of normal paren-

chyma should be included within the needle trajec-

tory to prevent spillage of the abscess contents into

the peritoneum (Fig. 7). The pleural space, loops

of bowel, and large intrahepatic vessels should be

avoided. Multilocular abscesses may be drained;

however, close follow-up and additional catheters

may be necessary [62]. The cure rate for liver abscess

Fig. 7. Ultrasound-guided liver abscess drainage in a septic patient whose previous catheter was inadvertently pulled out. (A) CT

scan demonstrates residual abscess in the dome of the right lobe of the liver (arrows). (B) Transverse ultrasound of the liver

demonstrates the 8F pigtail catheter (arrowhead) placed by the Seldinger technique into the abscess by a subphrenic approach.


is about 80% to 90%. Causes of failures of percuta-

neous drainage of liver abscess are given in Box 6.

Renal and perinephric abscess

Renal and perirenal abscesses may be drained

using ultrasound guidance; however, such abscesses

are usually better detected and delineated by CT [66].

This is particularly important for abscesses in the

pararenal space because they can extend from the

pelvis to the diaphragm. A posterolateral approach is

preferred because it avoids the erector spinal muscles,

colon, liver, and spleen.

Percutaneous nephrostomy

The main emergent indication for percutaneous

nephrostomy is pyohydronephrosis, which can occur

in native or a transplant kidney. Other urgent indica-

tions include a rapidly rising creatinine level or recent

endourologic complication. Indications of percutane-

ous nephrostomy are summarized in Box 7. Ultra-

sound is an excellent method to guide the initial

needle placement for percutaneous nephrostomy.

These procedures are typically performed in the

angiography suite using a portable ultrasound unit.

Although the entire procedure can be performed

with fluoroscopic guidance only, ultrasound is very

Box 6. Causes of failures of percutaneousdrainage of liver abscess

Preprocedure

Unable to access the abscess safelyImproper pathway to abscessInability to place the catheter appropri-

ately within the abscess

Postprocedure

Premature withdrawal of catheterDislodged catheterCatheter kinked or occludedHigh-output fistula to gastrointesti-

nal tractFungal abscessInfected necrotic tumorViscous pus or multiple septations,

resistant to fibrinolytic therapySepsis or death

Box 7. Indications for percutaneousnephrostomy

1. Relief of urinary obstructionImprove renal functionEvacuate pyonephrosisAssess recoverable renal function in

chronic obstruction2. Diversion of urine in case of urinary

leakageTraumatic or iatrogenic urinary

tract injuryInflammatory or malignant

urinary fistula3. Provide access for urinary

manipulationPerform dynamic flow-pressure

studies (Whitaker test)BiopsyStone therapyBenign stricture dilatationUreteral stent placementForeign body retrievalNephroscopic surgery

(eg, endopyelotomy)Administration of antifungal agents


useful for obtaining initial access to the renal collect-

ing system [20,67], particularly in cases where the

hydronephrosis is mild, or for renal transplants where

the renal axis can vary. For a native kidney, the

authors target a posterior calyx using a posterolateral

approach to avoid most of the erector spinus muscles.

For transplant kidneys, the authors target an anterior

calyx. Typically, they use a 20-gauge Chiba needle for

initial access, followed by instillation of contrast and a

small amount of air (3–5 mL) to confirm the needle

position (Fig. 8). The air rises to the nondependent

calices. If the needle position is satisfactory, the tract

can be dilated with a micropuncture set through the

20-gauge Chiba needle. If there is a better site to

access the collecting system, a second needle can then

be placed under fluoroscopic guidance using either a

20-gauge Chiba needle or 19-gauge sheath needle

(Yueh centesis needle). The tract is dilated using the

Seldinger technique, and an 8 to 14F catheter self-

retaining nephrostomy tube can be placed.

Splenic abscess

Splenic abscess if untreated have a mortality rate

of 80% to 100% and mortality rate of 14% to 30%

with surgical drainage. Experience with percutaneous

drainage is limited [59,68–70]. Although no major

complications were reported in these series [59,70],

their numbers were small. Green [68] described suc-

cessful percutaneous drainage in only one of four

patients. Lucey et al [67] successfully drained five

of six splenic abscesses; the one failure required a

splenectomy. The authors believe that splenic abscess

drainage should only be performed in rare circum-

stances and should generally be reserved for select

patients. Close consultation with the surgical service

is recommended so that an emergent splenectomy can

be performed if needed. If percutaneous drainage of a

splenic abscess is to be attempted, the abscess ideally

should be peripheral so that the least amount of nor-

mal splenic parenchyma is traversed. Thanos et al

[69], however, have performed drainages in two pa-

tients where the needle and catheter traversed 2.3 cm

of normal splenic parenchyma.

Fistulae

Uncomplicated abscesses have gradually decreas-

ing output following percutaneous drainage. In those

abscesses with persistently elevated output (ie, greater

than 100 mL per 24 hours) more than 3 to 4 days after

Fig. 8. Ultrasound-guided percutaneous nephrostomy in a renal transplant with pyohydronephrosis caused by ureteral calculus.

(A) Initial ultrasound demonstrates complex-appearing urine within the hydronephrotic transplant, which is consistent with

pyohydronephrosis. The indwelling stent is noted (arrows). (B) Longitudinal ultrasound of the dilated distal transplant ureter

demonstrates an obstructing calculus in the cursors. Note the ‘‘twinkle’’ artifact from the calculus with the color Doppler.

(C) Longitudinal image during placement of a nephrostomy tube (arrowhead). (D) Schematic representation of the kidney and

positioning of the catheter.


Fig. 8 (continued ).


initial catheter placement, especially drainage consist-

ing of bilious or enteric material, a gastrointestinal

fistula is likely [71,72]. At this point a sinogram con-

firms the communication to the gastrointestinal tract.

The cause of the fistula should then be determined so

that appropriate treatment may be initiated. Fistulae

caused by distal obstruction, neoplastic involvement,

or ongoing infection must have these underlying

conditions corrected or the abscess does not heal.

Low-output fistulae (ie, less than 320 mL per day)

usually close spontaneously without additional thera-

py [18]. High-output fistulae may require additional

treatment, including suction on the abscess catheter,

and bowel rest often with nasogastric tube placement.

Hyperalimentation may be necessary, and surgical

intervention may be required [18].

Infected hematomas

Most infected hematomas do not drain with simple

catheter placement because of their extensive amount

of fibrin and the protective effects of fibrin on bacteria

[18]. For patients with a suspected infected hema-

toma, the authors perform an initial aspiration. If

the fluid is bloody but not grossly infected, they only

take a sample for laboratory analysis and do not place

a catheter for the fear of secondary infection. If

the fluid is grossly purulent or if the cultures subse-

quently come back positive for infection, a drainage

catheter is placed. Sometimes local instillation of fi-

brinolytic agents, such as streptokinase, 125,000 IU

twice a day-for 2 days, may improve drainage from

such hematomas.

Fungal abscess

Fungal abscesses are difficult to treat with percu-

taneous drainage and may require surgical drainage

and debridement [18,73]. This is probably caused by

the extensive tissue invasion, necrosis, and mycotic

plaque formation in the wall of the cavity [18].

Echinococcal abscess

A number of investigators have described success-

ful treatment of hydatid cysts using percutaneous

aspiration and drainage [74–79]. The technique is

similar to routine abscess aspiration and drainage.

Various catheter irrigants are used, such as hyperto-

nic saline [74,79], scolicidal agent [75], or alcohol

[76,77,79]. Anaphylaxis is a potential complication,

which can be severe or even fatal [78]. Many of the

patients were given prophylaxis with albendazole.

Some investigators perform single-step aspiration

[74,77], whereas others aspirate the smaller cysts

and leave catheters in larger (> 6 cm) cysts [75,78,79].

Pelvic abscesses

Image-guided percutaneous drainage (Fig. 9) is

commonly performed for pelvic abscesses. Typically,

pelvic abscesses arise from gastrointestinal sources,

such as diverticulitis, ruptured appendicitis, and

Crohn’s disease, and from postoperative fluid collec-

tions. In female patients, pelvic abscesses may also

arise from gynecologic sources, such as tubo-ovarian

abscess from pelvic inflammatory disease. Such pel-

vic abscesses are traditionally treated with medical

therapy and if drainage of abscess is required many

investigators prefer image-guided interventional tech-

niques [80–87]. Pelvic abscesses in a female second-

ary to gynecologic causes are a special category and

usually have acute presentation.

Imaging-guided pelvic abscess drainage offers

several advantages to traditional surgical drainage.

The imaging-directed methods are less invasive and

do not require general anesthesia. The indications for

surgical drainage include ruptured tubo-ovarian ab-

scess, when diagnosis is uncertain; pelvic abscess

secondary to appendicitis or ruptured viscus [88];

and failed percutaneous drainage. The imaging-guid-

ed methods include transabdominal, transgluteal,

transrectal, and transvaginal approaches. The trans-

perineal approach has also been described [89]. In

general, the transabdominal approach is preferred,

Fig. 9. Ultrasound-guided pelvic abscess drainage, transabdominal, in a postsurgical patient. (A) Initial CT scan demonstrates

abscesses in the right and left lower quadrants of the pelvis (arrows). (B) Under ultrasound guidance the abscess in the right

lower quadrant was localized and punctured with a 19-gauge sheath needle. After confirming pus, a standard 0.035-inch

angiographic guidewire (Rosen) was advanced into the abscess. The tract was dilated to 10F catheter, and a self-retaining 10F

catheter nephrostomy tube (arrowhead) was placed. (C) The left lower quadrant abscess was then localized. Initial attempts were

made with a 12F one-step catheter; however, the patient complained of too much discomfort. This abscess was also punctured

with a 19-gauge sheath needle. After confirming pus, the tract was dilated and a 12F catheter nephrostomy tube was placed

(arrowhead). (D) Schematic representation of the procedure.


Fig. 9 (continued ).


using CT or ultrasound, because it is very well-

tolerated by patients. Pelvic abscesses may not be

accessible using the transabdominal approach, how-

ever, because of the presence of intervening loops of

bowel, urinary bladder, major blood vessels, or the

uterus. The transgluteal approach has several disad-

vantages, including patient discomfort, injury to the

sciatic nerve, and an increased chance of catheter

kinking and subsequent malfunction [84,90]. Al-

though initially underused, some investigators have

recently been successful using the transgluteal ap-

proach [90–93]. The transrectal [94–97] and trans-

vaginal approaches are well established [60,80–

84,88,98]. The transrectal approach can be guided

using CT [94], ultrasound [95–97,99], or ultrasound

combined with fluoroscopy [100]. The transvaginal

approach is usually guided with ultrasound.

Most patients with tubo-ovarian abscesses respond

to intravenous antibiotic therapy. As expected, the

response to antibiotics is inversely related to the size

of the abscess [82]. In unruptured tubo-ovarian ab-

scesses not responding to antibiotics, image-guided

drainage is indicated. The decision to proceed with

drainage is usually made in conjunction with the

gynecologic service. The authors prefer the trans-

abdominal approach, if possible, followed by the

transrectal approach with CT guidance, and finally

the transvaginal approach with ultrasound. Female

patients tolerate transrectal catheter placement better

as compared with transvaginal placement [99]. The

authors use the transgluteal approach only when

necessary (ie, a deep pelvic abscess in a patient with

underlying rectal mucosal disease or in premenarchal

or sexually inactive females). The transperineal ap-

proach provides an additional option for deep pelvic

abscess drainage and may be a viable alternative for

patients who have undergone abdominoperineal re-

section [89].

Technique

The transvaginal approach is best performed with

ultrasound guidance (Fig. 10). First, the abscess

should be localized by endovaginal ultrasound. The

abscess should be directly adjacent to the vaginal

vault with no intervening structures. The ultrasound

probe then is removed and the perineum and vagina

are prepared with a standard povidone-iodine solu-

tion. A vaginal speculum is then inserted and the

vaginal vault is prepared using sponges soaked in io-

dine-iodine solution. The speculum is then removed.

Despite the iodine-iodine preparation, the vagina is

still semi-sterile. If the patient is not already receiving

intravenous antibiotics, she should be given an appro-

priate antibiotic before beginning the procedure. Be-

cause it can be difficult to hold the ultrasound probe

while doing the various catheter manipulations, the

procedure generally requires two people.

The endovaginal ultrasound probe is then fitted

with a modified guide to allow catheter insertion. The

commercially available needle guides typically do not

allow placement of trocar-based catheters. Various

methods can be used [80,88], although the authors

prefer using the plastic sheath that comes with the

catheter, as described by O’Neill et al [79]. The

endovaginal probe is initially placed in a sterile probe

cover with coupling gel. A modified guide then is

made from the plastic catheter protector. The plastic

protector is cut so that approximately 5 cm of the

catheter protrudes beyond the end of the guide; a slit is

then made along the length of the guide, which

facilitates subsequent removal of the guide from the

catheter. This modified guide is then attached to the

sterilely prepared endovaginal probe with sterile rub-

ber bands along the groove intended for the metal

probe guide. The 6 to 8F trocar-based catheter (Skater,

Medical Device Technologies, Gainesville, Florida) is

then placed into the modified guide and a second

sterile probe cover is placed over the catheter and

guide. The catheter punctures the outer sterile probe

cover before puncturing the vaginal wall. One can

attempt to use local lidocaine at the vaginal wall but

this can be difficult because there are no landmarks to

ensure that the same area is traversed with the catheter.

Before placing a catheter, an initial aspiration should

be performed using an 18- to 20-gauge needle to

document infection. Initial scanning should be done

to place the abscess centrally within the scan plane

and to visualize where the catheter enters the abscess.

The tip of the trocar-based catheter should indent the

Fig. 10. Ultrasound-guided transvaginal pelvic abscess drainage. (A) Photograph shows the trocar catheter advanced through the

guide and projecting approximately 5 cm past the end of the probe (arrow). Note that the guide (plastic sheath) needs to be cut to

a length such that it allows at least 5 cm of catheter advancement so that the catheter can be advanced through the vaginal vault.

(B) Photograph shows the catheter has been fed off and the pigtail has been formed. The inner needle has been removed, but the

outer metal cannula stiffener is left in the straight portion of the catheter to stiffen it and ease the peeling away of the guide from

the catheter. (C) CT scan shows a complex right adnexal fluid collection (straight arrow). An incidentally noted right-sided

fundal fibroid is noted (curved arrow). (D) Transvaginal ultrasound scan shows trocar-catheter assembly (arrow) in the right

adnexal collection along the guide. (From O’Neill MJ, Rafferty EA, Lee SI, et al. Transvaginal interventional procedures:

aspiration, biopsy, and catheter drainage. Radiographics 2001;21:657–72; with permission.)


wall of the abscess during light palpation. Assuming

there are no intervening structures and the trajectory is

appropriate, the abscess wall is punctured using a

sharp thrust of 1 to 2 cm. This is the most difficult part

of the procedure. It is helpful to apply enough pressure

with the endovaginal ultrasound probe so that the

vaginal wall is taut before being punctured with the

trocar. The sharp needle of the trocar is removed and a

diagnostic aspiration is performed. Once pus is aspi-

rated, the catheter is advanced over the metal stiffener

of the trocar until the self-retaining loop is formed and

locked. The endovaginal probe is then removed care-

fully and the rubber bands and outer sterile cover

gradually are cut. The modified guide is then removed

from the catheter. This is easier to perform if the metal

stiffener is placed partially within the catheter. The

stiffener is then removed and more pus is aspirated.

Because of difficulties in penetrating the vaginal wall,

the authors have found that 10F or smaller catheters

are easier to insert.

Although the single-step trocar-based catheter is in

general easier to perform, the authors find the Sel-

dinger technique useful for inserting larger catheters

into abscesses with thick pus [84,101,102]. For expe-

rienced operators, ultrasound alone can be used.

Alternatively, a combination of ultrasound and fluo-

roscopy can be performed. With the Seldinger tech-

nique, the abscess is punctured with a 19-gauge sheath


needle with a disposable 5F TFE catheter (Yueh

centesis disposable catheter needle; Cook, Blooming-

ton, Inidana). After aspirating pus to confirm its

location, the 19-gauge needle is removed, leaving

the 5F catheter in the abscess, and a standard 0.035-

inch angiographic guidewire is advanced into the

abscess. The 5F TFE catheter is then removed and a

standard 5F pigtail catheter is placed over the guide-

wire and coiled into the abscess. Placement should be

confirmed with ultrasound. The disposable 5F TFE

catheter is not long enough to allow a guidewire to

coil within the abscess. The 0.035-inch guidewire is

removed, and a 0.035-inch Amplatz wire (Amplatz

Super Stiff, Boston Scientific, Medi-Tech, Miami,

Florida) is advanced into the 5F pigtail catheter. The

5F pigtail catheter is then removed, the tract can be

dilated up to 14F catheter, and an appropriate size of

self-retaining nephrostomy-type tube can be placed. If

the abscess is large enough, an Amplatz wire can be

introduced initially; however, this must be done care-

fully to avoid perforating the wall of the abscess with

the super-stiff wire. The stiffness of the Amplatz wire

(Amplatz Super Stiff, Boston Scientific, Medi-Tech,

Miami, Florida) allows the tract to be dilated despite

the distance between the operator’s hands and the

point of wire insertion in the vaginal wall. Less stiff

guidewires may kink. All of the dilatations can be

performed through the modified guide on the endo-

vaginal probe.

Some investigators perform simple needle aspi-

ration of an abscess without catheter placement

[81,103–106]. Although large, multiloculated collec-

tions can be treated this way, this method may be most

useful for small, unilocular collections. Nelson et al

[80] found no correlation between the size of an

abscess and the success rates for simple aspiration.

The advantages of this method are that it is safe, easier

to perform than catheter drainage, and there is no

problem with catheter misplacement or dislodging.

The disadvantages include multiple punctures for

multiloculated abscesses, an extended period of anti-

biotic coverage to control residual infection, and re-

peat aspiration for recurrent abscess [81,88]. For this

method, a standard needle guide attached to an endo-

vaginal probe can be used with an 18- to 20-gauge

needle. The needle must be at least 18 to 20 cm long to

fit through the needle guide. Contraindications in-

clude diffuse multifocal abscesses or abscess with

peritonitis, abscesses associated with fistulas, foreign

bodies, or abscesses caused by pancreatitis.

After the catheter is placed in the abscess and

locked in position, the authors tape the catheter to the

patient’s leg. Routine catheter care is then used. The

catheters are left to gravity drainage. The authors do

not routinely flush the catheters unless they are using

fibrinolytic agents, such as streptokinase.

Success rates for transvaginal drainage range from

78% to 100% [60,81,82,84,98,106]. Similar success

rates are noted for the other methods (ie, transabdomi-

nal, transrectal, and transgluteal) of pelvic abscess

drainage, ranging from 94% to 100% [83,91,94,96].

Complications from transvaginal drainage are infre-

quent and include bleeding, infection, underlying

organ damage, and vaginal fistula formation. Catheter

dislodgement may occur following any drainage pro-

cedure; however, this did not adversely affect patient

outcome in three of four patients in the study of Ryan

et al [94].

Summary

The interventionist can perform many emergent

procedures with ultrasound guidance, because of its

real-time, multiplanar imaging capability and porta-

bility. With the use of color Doppler, additional im-

portant information, such as aberrant vessels, can be

ascertained to help plan needle trajectory. Ultrasound

is also useful for nonemergent procedures, such as

biopsies. All interventionists are encouraged to be

facile with the use of ultrasound.

Acknowledgment

The authors thank Elena DuPont of the radiology

department at University Hospitals of Cleveland for

the line drawings and Joe Molter for assisting in the

preparation of images.

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