BUKU PEGANGAN TUTOR

Modul SAKIT PERUT KANAN

Diberikan pada mahasiswasemester IV FK UNHAS

SISTEM UROGENITALIAFAKULTAS KEDOKTERAN

UNIVERSITAS HASANUDDINMAKASSAR

2006

PENDAHULUAN

Modul sakit perut kanan ini diberikan pada mahasiswa yang mengambil mata

kuliah sistim Urogenitalia di semester IV. TIU dan TIK pada sistim ini disajikan pada

permulaan buku modul agar dapat dimengerti secara menyeluruh tentang konsep dasar

penyakit-penyakit Sistem Urogenitalia yang memberikan gejala sakit perut kanan.

Mahasiswa diharapkan mampu menjelaskan semua aspek tentang system Urogenitalia

dan patomekanisme terjadinya penyakit, kelainan jaringan, dan pemeriksaan lain yang

dibutuhkan pada penyakit yang memberikan gejala sakit perut kanan.

Sebelum menggunakan modul ini, mahasiswa diharapkan membaca TIU dan TIK

sehingga tidak terjadi penyimpangan pada diskusi dan tujuan serta dapat dicapai

kompetensi minimal yang diharapkan. Bahan untuk diskusi dapat diperoleh dari bacaan

yang tercatum di akhir modul. Kuliah pakar akan diberikan atas permintaan mahasiswa

yang berkaitan dengan penyakit ataupun penjelasan dalam pertemuan konsultasi antara

peserta kelompok diskusi mahasiswa dengan tutor atau ahli yang bersangkutan.

Penyusun mengharapkan modul ini dapat membantu mahasiwa dalam

memecahkan masalah penyakit Urogenitalia yang disajikan.

Makassar, 2 Desember 2005

Penyusun

TUJUAN INSTRUKSIONAL UMUM

Setelah mempelajari modul ini mahasiswa diharapkan dapat menjelaskan tentang penyakit-penyakit yang menyebabkan gejala sakit perut kanan, penyebab dan patomekanisme, gambaran klinik, cara diagnosis, penanganan dan pencegahan penyakit-penyakit yang menyebabkan sakit perut kanan.

TUJUAN INSTRUKSIONAL KHUSUS

Setelah pembelajaran dengan modul ini mahasiswa diharapkan dapat:

1. Menguraikan struktur anatomi, histologi dan histofisologi dari sistem uropoetika.

2. Menyebutkan fungsi masing-masing bagian dari nefron, fungsi sel-sel JGA dalam

renin angiotensin system.

3. Menjelaskan faktor-faktor yang mempengaruhi GFR, prinsip hukum Starling pada

filtrasi ginjal, proses reabsorbsi dan sekresi di ginjal.

4. Menjelaskan perubahan biokimia urine dan kompensasi ginjal dalam

keseimbangan asam basa.

5. Menjelaskan penyakit-penyakit yang dapat memberikan gejala sakit perut kanan.

6. Menjelaskan patomekanisme timbulnya gejala sakit perut kanan.

7. Menjelaskan cara anamnesis, pemeriksaan fisis, dan pemeriksaan penunjang yang

dibutuhkan untuk mendiagnosis banding beberapa penyakit yang mempunyai

gejala sakit perut kanan.

8. Mampu melakukan pemeriksaan laboratorium sederhana untuk pemeriksaan

penyakit-penyakit sistem Urogenitalia, terutama yang memberikan gejala sakit

perut kanan.

9. Mampu menganalisis hasil laboratorium dan pemeriksaan radiologik (BNO dan

IVP) pada penderita penyakit sistim Urogenitalia, terutama yang memberikan

gejala sakit perut kanan.

10. Menjelaskan penatalaksanaan penderita-penderita sistem Urogenitalia, terutama

yang memberikan gejala sakit perut kanan.

11. Menjelaskan asuhan nutrisi yang sesuai untuk penyakit-penyakit sistem

Urogenitalia, terutama yang memberikan gejala sakit perut kanan.

12. Menjelaskan epidemiologi dan tindakan-tindakan pencegahan penyakit-penyakit

sistem urogenitalia terutama yang memberi gejala sakit perut kanan

PROBLEM TREE

Lab : Urine Kimia darah UrinalisisPemeriksaan lain :BNOCT Scan, USGPA

Diagnosis Banding AppendicitisNefropathyTumor UGISKLowBack Pain

Anamnesis :Sakit perut menjalar ke paha, nyeri datang-datang. Mual

Fisik Diagnostik :Suhu tubuh normalTampak amat nyeri (kolik)

SAKIT PERUTKANAN

AnatomiHistologiFisiologiBiokimiaPatologi Anatomi FarmakologiMikrobiologi

Bedah

Medikamentosa Non MedikamentosaNutrisi

PenatalaksanaanPengendalian

Preventif Promotif Non Bedah

Prognosis Komplikasi

Skenario 1. Sakit perut kanan

1. Setelah membaca dengan teliti skenario di atas anda harus mendiskusikan kasus

tersebut pada satu kelompok diskusi terdiri dari 12 – 15 orang, dipimpin oleh seorang

ketua dan seorang penulis yang dipilih oleh anda sendiri. Ketua dan sekretaris ini

sebaiknya berganti-ganti pada setiap kali diskusi. Diskusi kelompok ini bisa dipimpin

oleh seorang tutor atau dilakukan secara mandiri oleh kelompok.

2. Melakukan aktivitas pembelajaran individual di perpustakaan dengan menggunakan

buku ajar, majalah, slide, tape atau video, dan internet, untuk mencari informasi

tambahan.

3. Melakukan diskusi kelompok mandiri (tanpa tutor) , melakukan curah pendapat bebas

antar anggota kelompok untuk menganalisa dan atau mensintese informasi dalam

menyelesaikan masalah.

4. Berkonsultasi pada nara sumber yang ahli pada permasalahan dimaksud untuk

memperoleh pengertian yang lebih mendalam (tanpa pakar).

5. Mengikut kuliah khusus (kuliah pakar) dalam kelas untuk masalah yang belum jelas

atau tidak ditemukan jawabannya.

6. Melakukan latihan dilaboratorium keterampilan klinik dan praktikum di laboratorium.

Seorang ibu, 35 thn, datang ke RS dengan keluhan sakit di daerah perut kanan dan menjalar sampai ke bawah 5 jam yang lalu. Sakitnya bersifat datang-datang. Penderita merasa mual tapi tidak sampai muntah, tidak ada demam.

TUGAS MAHASISWA

PROSES PEMECAHAN MASALAH

Dalam diskusi kelompok dengan menggunakan metode curah pendapat, mahasiswa

diharapkan memecahkan problem yang terdapat dalam skenario ini, yaitu dengan

mengikuti 7 langkah penyelesaian masalah di bawah ini:

1. Klarifikasi istilah yang tidak jelas dalam scenario di atas, dan tentukan kata/ kalimat

kunci skenario diatas.

2. Identifikasi problem dasar scenario diatas dengan, dengan membuat beberapa

pertanyaan penting.

3. Analisa problem-problem tersebut dengan menjawab pertanyaan-pertanyaan diatas.

4. Klasifikasikan jawaban atas pertanyaan-pertanyaan tersebut di atas.

5. Tentukan tujuan pembelajaran yang ingindi capai oleh mahasiswa atas kasus

tersebut diatas.

6. Cari informasi tambahan tentang kasus diatas dari luar kelompok tatap muka.

Langkah 6 dilakukan dengan belajar mandiri.

7. Laporkan hasil diskusi dan sistesis informasi-informasi yang baru ditemukan.

Langkah 7 dilakukan dalm kelompok diskusi dengan tutor.

Penjelasan :

Bila dari hasil evaluasi laporan kelompok ternyata masih ada informasi yang

diperlukan untuk sampai pada kesimpulan akhir, maka proses 6 bisa diulangi, dan

selanjutnya dilakukan lagi langkah 7.

Kedua langkah diatas bisa diulang-ulang di luar tutorial, dan setelah informasi

dirasa cukup maka pelaporan dilakukan dalam diskusi akhir, yang biasanya dilakukan

dalam bentuk diskusi panel dimana semua pakar duduk bersama untuk memberikan

penjelasan atas hal-hal yang belum jelas.

1. Pertemuan pertama dalam kelas besar dengan tatap muka satu arah dan tanya jawab.

Tujuan : menjelaskan tentang modul dan cara menyelesaikan modul, dan membagi

kelompok diskusi. Pada pertemuan pertama buku modul dibagikan.

2. Pertemuan kedua : diskusi mandiri. Tujuan :

* Memilih ketua dan sekretaris kelompok,

* Brain-storming untuk proses 1 – 3,

* Membagi tugas

3. Pertemuan ketiga: diskusi tutorial dipimpin oleh mahasiswa yang terpilih menjadi

ketua dan penulis kelompok, serta difasilitasi oleh tutor. Tujuan: untuk melaporkan

hasil diskusi mandiri dan menyelesaikan proses sampai langkah 5.

4. Anda belajar mandiri baik sendiri-sendiri. Tujuan: untuk mencari informasi baru yang

diperlukan,

5. Pertemuan keempat: adalah diskusi tutorial. Tujuan: untuk melaporkan hasil diskusi

lalu dan mensintese informasi yang baru ditemukan. Bila masih diperlukan informasi

baru dilanjutkan lagi seperti No. 2 dan 3.

6. Pertemuan terakhir: dilakukan dalam kelas besar dengan bentuk diskusi panel untuk

melaporkan hasil diskusi masing-masing kelompok dan menanyakan hal-hal yang

belum terjawab pada ahlinya (temu pakar).

TIME TABLE

PERTEMUANI II III IV V VI VII

Pertemuan I(Penjelasan)

Pertemuan Mandiri(Brain

Stroming)

Tutorial I Pengum-

pulan informasiAnalisa &

sintese

Mandiri

PraktikumCSL

Kuliah kosultasi

Tutorial II(Laporan &

Diskusi)

Pertemuan Terakhir (Laporan)

JADWAL KEGIATAN

STRATEGI PEMBELAJARAN

1. Diskusi kelompok difasilitasi oleh tutor

2. Diskusi kelompok tanpa tutor

3. CSL : Pemeriksaan benjolan pada leher

4. Praktikum PA

5. Konsultasi pada pakar

6. Kuliah khusus dalam kelas

7. Aktivitas pembelajaran individual diperpustakaan dengan menggunakan buku ajar

Majalah,slide,tape atau video dan internet

A. Buku Ajar dan Jurnal

1 Urology : R.W. Barnes, R.T.Bergman, H.Hodley, Toppan Co.(S) PTE-LTD,Singapore2 Davitson VL and Sittman DB : Biochemistry3 Kumar, Contran, Robbins: Pathology Basis of Diseases, 20034 Chandrasoma- Taylor: Concise Pathology, 19995 Kenneth J Rothman, 1986, Modern Epidemiology, Little Brownc and Company, Bon 6 World Health Organization, 1992, International statistical Classification of Diseases

an and related Health Problems, 10th revision, volume 1, WHO, Geneva

7 Goodharmt R : Modern nutrition in health and disease, Lee Ferbeger, 20028 Robinson : Normal and Therapeutic Nutrition, Mac Millian Co., New York9 Lenne EH et al ; Manual of Clinical Microbiology , 4th edition, 1985

10 Prescott LM et al : Microbiology, 2nd edition, Wm.c Brown Publisher, Melbourne, 1993

11 WF. Ganong : Review of Medical Physiology, edisi 20, 200312 Synopsis of analysis of Roentgen sign in general Radiology, Isadore Meschan, 197613 Junguiera LC, Carneiro J : Basic Histology 3th edition, Los Altos California USA,

Lange Medical Publication, 198014 Stites DP, Stobo JD, Fudenberg HH : basic and Clinical Immunology, 4th edition, Los

Altos California, Lange Medical Publication, 1982

15 Schlesinger ER, Sultz HA, Mosher WE, et al. The Nephrotic Syndrome. Its incidence and implications for the community. Am J Dis Child 1968, 116; 623

16 International Study of Kidney Disease in Children. Nephrotic Syndrom in Children. Prediction of histopathology from clinical and laboratory characteristics at time of diagnosis. Kidney Int. 1978, 13: 159.

17 Kher KK. Obstructive uropathy. Dalam : Kher KK, Marker SP, penyunting. Clinical Pediatric Nephrology. New York: Mc Graw – Hill 1992: 447-65.

18 Behrman RE. Nelson textbook of pediatrics; edisi ke 14. Philadelphia: WB Saunders,

BAHAN BACAAN & SUMBER INFORMASI LAIN

1992; 1344-50.19 Homes HD, Weinberg JM. Toxic nephropathies. Dalam: Brenner Rector FC,

penyunting, The Kidney, II; edisi ke-Philadelphia: WB Saunders Co, 1986; 1491-532.20 Barrat TM. Acute renal failure. Dalam: Holliday MA, Barrat TM, Vernier RL,

penyunting. Pediatric nephrology, edisi ke-2. Baltimore: Williams & Wilkins 1987; 766-72.

21 Kher KK. Chronic renal failure. Dalam Kher KK, Marker SP, penyunting, clinical pediatric nephrology. New York: MC Graw-Hill Inc, 1992, 501-41.

22 Karjomanggolo WT, Alatas H. Kelainan congenital ginjal dan saluran kemih. Dalam: Naskah lengkap PKB. IKA XXVI : Penelitian tractor urinarius pada anak. Jakarta 11 – 12 September 1992: 1176-84.

23 Londe S causes of hypertension in the young. Pediatric Clin North Am 1978; 25-55.24 Henry JB : Clinical Diagnosis and Manage,ent by laboratory Methods, 19th ed, 199625 H. Beers and R. Berkow editor : The Merck Manual 17th ed, 199926 Harrison : Disorders of the kidney and Urinary tractus, 15th edition, Volume I, Mc

Graw Hill, 2002, pp : 1535-163027 Ginjal Hipertensi dalam Buku Ajar Ilmu Penyakit Dalam jilid II, edisi III, Balai Penerbit

FKUI Jakarta, 2001

B. Diktat dan hand-out

1. Diktat Anatomi1. Diktat Histologi2. Buku Ajar Fisiologi Ginjal3. Diktat Kuliah Radiologi

C. Sumber lain : VCD, Film, Internet, Slide, Tape

D. Nara sumber (Dosen Pengampu)

DAFTAR NAMA NARA SUMBER

No. NAMA DOSEN BAGIAN TLP. KANTOR

HP/FLEXI

1. Prof.Dr. dr. Syarifuddin Rauf Sp.PA

Anak 0811411109

2. Prof.Dr.dr. Syakib Bakri, Sp.PD

Penyakit Dalam 0816250620

3. Prof.dr. Ahmad M Palinrungi Sp.B, Sp.U

Bedah Urologi 08164384040

4. Prof.Dr.dr. M.Dali Amiruddin, Sp.KK

Kulit Kelamin 08194229858

5. Dr. Irfan Idris, MS Fisiologi 584730 0813426953486. Dr. Theopilus Buranda, MS Anatomi 0813424364447. Dr. Robby Lianury Histologi 08114117238. Dr. Agnes Kwenang, MS Biokimia9. Dr. dr. Gatot Lawrence Patologi 0816255306

Anatomi10. Dr. dr. Nurpudji Astuti,

SpGKGizi 0811443856

11. Dr. dr. Fatmawati Farmakologi 08152412036812. Dr. Randana Bandaso, MS Patologi

Anatomi13. Dr. Nurlaily Idris, Sp.R Radiologi 081144106414. Dr. H, Ibrahim Samad, SpPK Patologi Klinik15. Dr. Baedah Madjid, SpMK Mikrobiologi 081144432616. Dr. Sastri, SpKK Kulit Kelamin 08124217393

Apa yang dimaksud dan mekanisme ‘kata kunci’ berikut ini :

o Sakit perut yang menjalar (kolik) : nyeri pada daerah perut dan menjalar

ke arah perut kanan bawah. Nyeri ini umumnya amat hebat dan menjalar

sesuai dengan perjalanan batu dalam ureter

o Sakit perut yang datang-datang : nyeri yang hilang dan timbul kembali

akibat perjalanan batu di ureter.

o Mual : nyeri yang terjadi pada batu ureter sering disertai mual dan muntah

Apa penyebab dan bagaimana pato-mekanisme gejala-gejala yang menjadi kata

kunci tersebut

o Sakit perut yang menjalar : Nyeri akibat spasme ureter oleh karena perjalanan batu, penjalaran ini biasanya sampai ke arah kemaluan.

o Sakit yang datang-datang karena spasme terjadi tidak kontinue, bila ada spasme akan terasa nyeri dan bila tidak nyeri akan hilang

o Mual : Nyeri yang mengenai organ visceral disertai mual dan muntah, sebab nyeri visceral dihantar via saraf simpatis dan juga merangsang terjadinya mual dan muntah

Sebutkan beberapa penyakit yang dapat di differential diagnosis

dengan tanda dan gejala pada skenario :

Appendicitis Biliary Colic Cholecystitis Constipation Diverticulitis Duodenal Ulcers Gastritis, Acute Gastroenteritis, Viral Glomerulonephritis, Acute Ileus Inflammatory Bowel Disease Liver Abscess Lumbar Disc Disease Lumbar Spondylosis Nephrolithiasis Nephrolithiasis: Acute Renal Colic

PETUNJUK UNTUK TUTOR

Splenic Abscess Urinary Tract Infection, Females Urinary Tract Obstruction

Pemeriksaan penunjang yang dibutuhkan untuk menegakkan diagnosis penyakit

yang termasuk dalam DD penyakit tersebut

1. Urinalysis dan Urinalysisi 24 jam

2. Darah lengkap dan kimia darah

3. Elektrolit

4. Radiologi : BNO, USG, IVP, CT Scan

Bagaimana cara penatalaksanaan dari penyakit-penyakit yang termasuk dalam

DD penyakit tersebut

1. Medikamentosa

2. Bedah

3. ESWL

4. Diet

Epidemiologi penyakit tersebut

1. Masih banyak terjadi di Negara-negara berkembang, di USA 2-3% dalam

populasi pertahun.

2. Pada usia di atas 70 thn, kejadiannya 1 diantara 8 orang

3. Pria : wanita = 3 : 1, umunya pada umur 29-40 thn

Komplikasi penyakit-penyakit yang termasuk DD pada skenario

o Abscess formation

o Serious infection of the kidney that diminishes renal function

o Urinary fistula formation

o Ureteral scarring and stenosis

o Ureteral perforation

o Extravasation

o Urosepsis

o Renal loss due to long-standing obstruction Prognosis penyakit-penyakit tersebut

1. Recurence rate 50% dalam 5 thn, dan 70% dalam 10 tahun atau lebih2. Tindakan medis secara efektif memperlambat proses pembentukan batu

Nephrolithiasis

Background: Nephrolithiasis is a common disease estimated to produce medical costs of $1.83 billion a year in the United States. Nephrolithiasis specifically refers to calculi in the kidneys, but this article discusses both renal calculi (Image 1) and ureteral calculi (ureterolithiasis). Ureteral calculi almost always originate in the kidneys, although they may continue to grow once lodged in the ureter.

Urinary tract stone disease has been a part of the human condition for millennia; in fact, bladder and kidney stones have even been found in Egyptian mummies. Some of the earliest recorded medical texts and figures depict the treatment of urinary tract stone disease.

Pathophysiology: Urinary tract stone disease (Image 3) is likely caused by 2 basic phenomena.

The first is supersaturation of the urine by stone-forming constituents, including calcium, oxalate, and uric acid. Crystals or foreign bodies can act as nidi, upon which ions from the supersaturated urine form microscopic crystalline structures. The overwhelming majority of renal calculi contain calcium. Uric acid calculi and crystals of uric acid, with or without other contaminating ions, comprise the bulk of the remaining minority. Other, less frequent stone types include cystine, ammonium acid urate, xanthine, dihydroxyadenine, and a variety of rare stones related to precipitation of medications in the urinary tract.

Other current theories also include renal tubular damage or dysfunction as an important component of the initiation of stone formation. The initial crystal agglomerations likely form in distal collecting tubules that drain into the renal papilla. As these masses grow, they gradually extrude into the collecting system through the papilla and eventually drop off to become free urinary calculi.

Frequency:

In the US: The overall incidence of urinary tract stone disease is 2-3% of the population per year. The likelihood that a white male will develop stone disease by the age of 70 years is 1 in 8. Stones of the upper urinary tract are more common in the United States than in the rest of the world. Roughly 1.2 million patients present with stone disease each year in the United States.

Internationally: Urinary tract stone disease incidence in developed countries is similar to that observed in the United States. In developing countries, bladder calculi are more common than upper urinary tract calculi, which is the reverse of the situation in developed countries. These differences are believed to be diet related.

Mortality/Morbidity:

The morbidity of urinary tract calculi is primarily due to obstruction with its associated pain, although it is well recognized that nonobstructing calculi can still produce considerable discomfort.

Conversely, patients with obstructing calculi can be asymptomatic, which is the usual scenario in the atypical patient who experiences loss of renal function from chronic, untreated obstruction.

Stone-induced hematuria is frightening to the patient but rarely dangerous by itself.

The most morbid and potentially dangerous aspect of stone disease is the combination of obstruction and infection of the upper urinary tract. Pyelonephritis, pyonephrosis, and urosepsis can ensue.

Race: Compared to the prevalence in Asians and whites, urinary tract calculi are far less common in Native Americans, Africans, African Americans, and some natives of the Mediterranean region. Although some differences may be attributable to geography (stones are more common in hot and dry areas) and diet, heredity appears to be a factor as well.

Sex:

In general, urolithiasis occurs more often in males (male-to-female ratio, 3:1).

Stones due to discrete metabolic/hormonal defects (eg, cystinuria, hyperparathyroidism) and stone disease in children are equally prevalent between the sexes.

Stones due to infection (struvite calculi) are more common in women than in men.

Age:

Most urinary calculi occur in patients aged 20-49 years.

Patients in whom multiple, recurrent stones form usually experience their first stones while in their teens or twenties.

It is relatively uncommon for patients to experience their first stone attacks after age 50 years.

CLINICAL

History:

Patients with urinary calculi may report pain, infection, or hematuria. Small, nonobstructing stones in the kidneys cause symptoms only occasionally. If present, symptoms are usually moderate and easily controlled.

The passage of stones into the ureter with subsequent acute obstruction, proximal urinary tract dilation, and spasm is associated with classic renal colic.

o Renal colic is characterized by undulating cramps and severe pain and is often associated with nausea and vomiting.

o As the stone travels through the ureter, the pain moves from the flank to the upper abdomen, then to the lower abdomen, down to the groin, and eventually to the scrotal or labial areas.

o Associated bladder irritative symptoms are common when the stone is located in the distal or intramural ureter.

Patients with large renal stones known as staghorn calculi (Image 2) are often relatively asymptomatic.

o Staghorn refers to the presence of a branched kidney stone occupying the renal pelvis and at least one calyceal system. Such calculi usually manifest with infection and hematuria rather than with acute pain.

o In uncommon cases in which asymptomatic bilateral obstruction has occurred, the patient presents with symptoms of renal failure.

Important historical features are as follows:

o Duration, characteristics, and location of pain

o History of urinary calculi

o Prior complications related to stone manipulation

o Urinary tract infections

o Loss of renal function

o Family history of calculi

o Solitary or transplanted kidney

Physical:

Often, dramatic costovertebral angle tenderness occurs, which can move to the upper or lower abdominal quadrant as a ureteral stone migrates distally.

Peritoneal signs are usually lacking—an important consideration in distinguishing renal colic from other sources of flank or abdominal pain.

Findings should correlate with the reports of pain, so that complicating factors (eg, urinary extravasation, abscess formation) can be detected.

Beyond this, the specific location of tenderness often does not indicate the exact location of the stone, although the calculus is often in the general area of maximum discomfort.

Causes:

Most research on the etiology and prevention of urinary tract stone disease has been directed toward the role of elevated urinary levels of calcium, oxalate, and uric acid in stone formation.

Hypercalciuria is the most commonly noted metabolic abnormality.

Magnesium and especially citrate are important inhibitors of stone formation in the urinary tract. Decreased levels of these in the urine cause a predisposition for stone formation.

A low fluid intake, with consequent high concentrations of stone-forming solutes in the urine, is another significant factor in stone formation.

The exact nature of the tubular damage or dysfunction that leads to stone formation has not been characterized.

The most common findings on 24-hour urine studies are hypercalciuria, hyperoxaluria, hyperuricosuria, hypocitraturia, and low urinary volume. Other factors, such as high urinary sodium and low urinary magnesium concentrations, may also play a role. To identify these risk factors, a 24-hour urine profile, including appropriate serum tests of renal function, uric acid, and calcium, is needed. Such testing is available from a variety of commercial laboratories.

DIFFERENTIAL

Abdominal Abscess Aortic Dissection Appendicitis Biliary Colic Cholecystitis Constipation Diverticulitis Duodenal Ulcers Gastritis, Acute Gastroenteritis, Viral Glomerulonephritis, Acute Ileus Inflammatory Bowel Disease Liver Abscess Lumbar Disc Disease Lumbar Spondylosis Nephrolithiasis Nephrolithiasis: Acute Renal Colic Pancreatitis, Acute Pyonephrosis Renal Arteriovenous Malformation Renal Vein Thrombosis Splenic Abscess Splenic Infarct Thoracic Aortic Aneurysm Urinary Tract Infection, Females Urinary Tract Infection, Males Urinary Tract Obstruction

Lab Studies:

Urinalysis

o Evaluate the urine for evidence of hematuria and infection. Approximately 85% of patients with urinary calculi exhibit hematuria.

o Absence of hematuria does not preclude presence of urinary calculi; in fact, approximately 15% of patients with urinary stones do not exhibit hematuria.

o Offer strongly motivated patients a metabolic 24-hour urinalysis.

CBC count

o In the context of nephrolithiasis, an elevated white blood cell count suggests renal or systemic infection.

o A depressed red blood cell count suggests a chronic disease state or severe ongoing hematuria.

Serum electrolytes, creatinine, calcium, uric acid, and phosphorus studies o These are needed to assess a patient's current renal-function status and to begin

the assessment of metabolic risk for future stone formation. o A high serum uric acid finding may indicate gouty diathesis or hyperuricosuria,

while hypercalcemia suggests either renal-leak hypercalciuria or hyperparathyroidism.

Calcium, oxalate, and uric acid

o Elevation of the 24-hour excretion rate of any of these 3 components indicates a predisposition to form calculi.

o Hypercalciuria can be subdivided into absorptive, resorptive, and renal-leak categories by the results of blood tests and 24-hour urinalysis on both regular and calcium-restricted diets.

Depending on the specific subtype, the treatment of absorptive hypercalciuria may include dietary calcium restriction, thiazide diuretics, oral calcium binders, or phosphate supplementation.

Resorptive hypercalciuria is primary hyperparathyroidism and requires parathyroidectomy.

Renal-leak hypercalciuria, which is relatively uncommon, is usually associated with secondary hyperparathyroidism and is best managed with thiazide diuretics.

o Another clinical approach to hypercalciuria, once hyperparathyroidism has been excluded by appropriate blood tests, is to avoid excessive dietary calcium (usual recommendation, 600-800 mg/d) and to use thiazides. If thiazide therapy fails, additional workup (eg, calcium-loading test, more thorough evaluation) may be needed.

o Hyperoxaluria may be primary (a rare genetic disease), enteric (owing to malabsorption and associated with chronic diarrhea or short-bowel syndrome), or idiopathic. Oxalate restriction and vitamin B-6 supplementation are somewhat helpful for patients with idiopathic hyperoxaluria but can be extremely helpful for those with enteric hyperoxaluria, who often respond dramatically to dietary calcium supplementation.

o Calcium citrate is the recommended supplement because the citrate tends to further reduce stone formation. Supplementation with calcium carbonate is less expensive but does not provide citrate's added benefit. Calcium therapy works by acting as an oxalate binder, reducing oxalate absorption from the intestinal tract. Calcium should be administered with meals, especially meals containing high oxalate levels. The supplement should not contain added vitamin D because vitamin D increases calcium absorption, leaving less in the intestinal tract to work on oxalate binding.

o Hyperuricosuria causes a predisposition to formation of calcium-containing calculi because sodium urate can produce malabsorption of macromolecular inhibitors or can serve as a nidus for the heterogeneous growth of calcium oxalate crystals. Gouty diathesis, a condition of increased stone production associated with high serum uric acid levels, is also possible. Therapy involves potassium citrate supplementation and/or allopurinol. In general, allopurinol is the treatment for patients with pure uric acid stones and hyperuricemia, and citrate supplementation is the treatment for those with hyperuricosuric calcium stones.

Sodium, phosphorus

o Excess sodium excretion can contribute to hypercalciuria by a phenomenon known as solute drag.

o An elevated phosphorus level is useful as a marker for a subtype of absorptive hypercalciuria known as renal phosphate leak (absorptive hypercalciuria type III).

o Renal phosphate leak is identified by high urinary phosphate levels, low serum phosphate levels, high serum 1,25 vitamin D-3 (calcitriol) levels, and hypercalciuria. This type of hypercalciuria is uncommon and does not respond well to standard therapies. The above laboratory tests are confirmatory, but they are performed only if the index of clinical suspicion is high. Any hypercalciuric patient with a low serum phosphorus level and a high-normal or high urinary phosphorus level may have this condition.

o Phosphate supplements are used to correct the low serum phosphate level, which then decreases the inappropriate activation of vitamin D originally caused by the hypophosphatemia.

Citrate, magnesium

o Magnesium and especially citrate are important chemical inhibitors of stone formation. Hypocitraturia is one of the most common metabolic defects causing a predisposition to stone formation, and some authorities have recommended citrate therapy as primary or adjunctive therapy to almost all patients who have formed recurrent calcium-containing stones.

o Liquid pharmacologic citrate preparations are recommended when absorption is a problem or in cases of chronic diarrhea. Sustained-release tablets are available and may be more convenient for some patients. Concentrates of lemon juice, such as lemonade, can also provide citrate.

o Potassium citrate is the preferred type of pharmacologic citrate supplement, although a potassium/magnesium preparation is under investigation.

o Magnesium is a more recently recognized inhibitor of stone formation, and the clinical role of magnesium replacement therapy is less well defined than for citrate.

Creatinine

o Creatinine is the control that allows verification of a true 24-hour sample. Most individuals excrete 1-1.5 g of creatinine daily.

o Values at either extreme that are not explained by estimates of lean body weight should prompt consideration that the sample is inaccurate.

o Consider the sample inaccurate if values at either extreme are not explained by estimates of lean body weight.

Total volume

o Patients in whom stones form should strive to achieve a urine output of more than 2 L daily in order to reduce the risk of stone formation.

o Patients with cystine stones or those with resistant cases may need a daily urinary output of 3 L for adequate prophylaxis.

Twenty-four–hour urinalysis (calcium, oxalate, uric acid, sodium, phosphorus, citrate, magnesium, creatinine, total volume)

o This study is designed to provide more information about the exact nature of the chemical problem that caused the stone. This information is useful not only to allow more specific and effective therapy for stone prevention but also to identify patients with renal calculi who might have other significant health problems.

o The following are indications for a metabolic evaluation with a 24-hour urinalysis: Residual calculi after surgical treatment Initial presentation with multiple calculi Renal failure Renal transplantation Solitary kidney Family history of calculi More than 1 stone in the past year

o Metabolic studies are recommended for patients younger than 25 years. Studies are also recommended for patients with multiple stone surgeries or recurrences and for those with renal failure or only a single working kidney (eg, renal transplant recipients).

o Whether or not to perform a 24-hour urine study depends on the patient. If a patient is strongly motivated to follow a protracted stone-prevention treatment plan (involving diet, supplements, and/or medications), order the study. If a patient is unlikely or unwilling to follow a long-term treatment plan, there is little point in performing such a tedious and inconvenient study.

Imaging Studies:

Plain abdominal radiograph

o A plain abdominal radiograph (also known as a flat plate or kidney, ureter, and bladder [KUB] radiograph) may suffice for assessing total stone burden as well as the size, shape, and location of urinary calculi in some patients.

o Calcium-containing stones (~85% of all upper urinary tract calculi) are radiopaque, but pure uric acid, indinavir-induced, and cystine calculi are relatively radiolucent on plain radiography.

o When used with other imaging studies, such as a renal sonogram or, particularly, a CT scan, the plain film helps provide a better understanding of the size, shape, location, orientation, and composition of urinary stones identified by these other imaging studies. (This may be helpful in planning surgical therapy.)

Renal sonogram

o A renal sonogram by itself is frequently adequate to determine the presence of a renal stone. The study is mainly used, in combination with a plain abdominal radiograph, to determine hydronephrosis or ureteral dilation associated with an abnormal radiographic density believed to be a urinary tract calculus.

o A stone easily identified on the renal sonogram but not visible on the plain radiograph may be a uric acid or cystine stone, which is potentially dissolvable with urinary alkalinization therapy.

o Ureteral calculi, especially in the distal ureter, and stones smaller than 5 mm are not easily observed on sonography.

Intravenous urogram

o An intravenous urogram (IVU) test, also known as an intravenous pyelogram (IVP), is the standard for determining size and location of urinary calculi. IVU provides anatomical and functional information.

o There has been great interest in finding a replacement imaging examination because the IVU is labor intensive.

It may take up to 6 hours to complete in the presence of severe obstruction.

For optimal results, it requires a bowel preparation. It involves intravenous injection of potentially allergic and mildly

nephrotoxic contrast material.

o Although some authorities have advocated substituting a plain abdominal radiograph plus a renal sonogram for IVU, a helical CT scan without contrast material is currently believed to be the best radiographic examination for acute renal colic.

o The so-called delayed nephrogram on the IVU is one of the hallmark signs for acute urinary obstruction. The relative delay in penetration of intravenous contrast passing through an obstructed kidney elicits this sign. The kidney appears to develop a whitish color, and contrast appearance within the collecting system of the affected renal unit is significantly delayed.

o The IVU is helpful in identifying the specific problematic stone among numerous pelvic calcifications and for establishing that the other kidney is functional. These determinations are particularly helpful if the degree of hydronephrosis is mild and the CT scan is not definitive.

Helical CT scan without contrast material

o Technological advances in CT scanning allow imaging of the entire abdomen in a single breath hold.

o When performed with thin cuts and without intravenous contrast material, a CT scan is the most sensitive clinical imaging modality for calcifications. Even calculi that are radiolucent on a plain radiograph (except for indinavir-induced stones) are clear and distinct on a CT scan.

o Contrast is not used because it makes the entire urinary collecting system appear white on the study, thus masking the stones.

o At most institutions offering this examination, CT scanning has replaced or is replacing the IVU for the assessment of urinary tract stone disease, especially for acute renal colic.

o Adding a plain radiograph to the noncontrast CT scan increases the value of the study by allowing visualization of the size, shape, and relative position of the stone.

Visualization is especially useful if surgery is being considered. It is extremely helpful in observing the patient because only the KUB

radiograph may be needed later to determine if the stone has moved or passed.

A lucent stone on the KUB radiograph that is clearly visible on the CT scan may indicate a uric acid calculus. This suggests a different diagnosis and therapy (allopurinol and/or urinary alkalinization) than for a calcium stone. For these reasons, many institutions routinely perform a KUB radiograph whenever a renal colic noncontrast CT scan is performed.

o Advantages of a CT scan include the following: It can identify other pathology (eg, abdominal aneurysms, appendicitis,

cholecystis). It can be performed quickly. It avoids the use of intravenous contrast materials.

o Disadvantages of CT scan include the following: It cannot assess individual renal function. It can miss some unusual radiolucent stones, such as those caused by

indinavir, which are invisible on CT scan. Because of this possibility, IVUs with contrast should be used for patients taking indinavir.

At most institutions, a CT scan is still more expensive than an IVU.

Plain renal tomograms

o Although largely replaced by helical CT scans without contrast (when available), plain renal tomograms are often helpful in finding small stones in the kidneys, especially in large or obese patients whose bowel contents make it difficult to observe any renal calcifications.

o These tomograms do not require extensive preparation and can be performed quickly.

o Plain renal tomograms are most useful when monitoring a difficult-to-observe stone after therapy or for clarification of stones not clearly detected or identified by other studies.

o They are also useful in ascertaining the number of stones present in the kidneys before instituting a stone-prevention program. This information is used to better differentiate stones formed before therapy began from those formed later.

TREATMENT

Medical Care: The first part of this section discusses emergency management of renal (ureteral) colic. The second part addresses the issues of medical therapy for stone disease. Medical therapy for stone disease takes both short- and long-term forms (the former to dissolve the stone and the latter to prevent further stone formation). Additionally, it is advisable to aggressively treat patients who initially formed stones in their teens or twenties and all patients younger than 16 years as they are more likely to have recurrent stone formation.

General guidelines for emergency management are as follows: o After diagnosing renal (ureteral) colic, determine the presence or absence of

obstruction or infection. o Obstruction in the absence of infection can be initially managed with analgesics

and by other medical measures to facilitate passage of the stone. Infection in the absence of obstruction can be initially managed with antimicrobial therapy. In either case, promptly refer the patient to a urologist.

o If neither obstruction nor infection is present, then analgesics and other medical measures to facilitate passage of the stone can be initiated with the expectation

that the stone will likely pass from the upper urinary tract if its diameter is smaller than 5-6 mm (larger stones are more likely to require surgical measures).

o If both obstruction and infection are present, then emergent decompression of the upper urinary collecting system is required (see Surgical Care). Immediately consult with a urologist for patients whose pain fails to respond to ED management.

Specific guidelines for emergency management are as follows:

o Although the role of supranormal hydration in the management of renal (ureteral) colic is controversial, dehydrated or ill patients need adequate restoration of circulating volume.

o The cornerstone of management of ureteral colic is analgesia. Analgesia can be attained most expediently with parenteral narcotics or nonsteroidal anti-inflammatory drugs (NSAIDs).

Morphine sulfate is the narcotic analgesic drug of choice for parenteral use.

Ketorolac tromethamine is the only NSAID approved for parenteral use in the United States, and it is often effective when used for renal colic. Even in very difficult cases, the combination of these medications usually provides excellent relief of renal (ureteral) colic.

Antiemetic agents such as metoclopramide HCl and prochlorperazine may also be added as needed.

o Traditional outpatient treatment has included combinations of narcotics (eg, codeine, oxycodone, hydrocodone) plus acetaminophen. To provide more effective pain relief and to facilitate stone passage, additional therapy with NSAIDs, nifedipine, and prednisone may be added.

Oral NSAIDs such as ibuprofen further mitigate pain (thus diminishing the need for narcotics) and reduce ureteral inflammation, in addition to having some ureteral relaxant properties.

The calcium channel blocker nifedipine also relaxes ureteral smooth muscle, and the corticosteroid prednisone reduces ureteral inflammation.

o Amelioration of both ureteral inflammation and ureteral muscle tone appears to facilitate stone passage. A typical regimen for this aggressive management is 1-2 oral narcotic/acetaminophen tablets every 4 hours as needed for pain, 600-800 mg ibuprofen every 8 hours, 30 mg nifedipine extended-release tablet once daily, and 10 mg prednisone twice daily. Limit administration of nifedipine and prednisone to 5-10 days. If outpatient treatment fails, promptly consult a urologist.

Calcium-containing urinary calculi o Urinary calculi composed predominantly of calcium cannot be dissolved with

current medical therapy; however, medical therapy is important in the chronic chemoprophylaxis of further calculus growth or formation.

o Prophylactic therapy might include limitation of dietary components, addition of stone-formation inhibitors or intestinal calcium binders, and, most importantly, augmentation of fluid intake.

o Besides advising patients to avoid excessive salt and protein intake and to increase fluid intake, base medical therapy for the chronic chemoprophylaxis of urinary calculi upon the results of a 24-hour urinalysis for chemical constituents.

Uric acid and cystine calculi

o Uric acid and cystine calculi can be dissolved with medical therapy. Patients with uric acid stones who do not require urgent surgical intervention for reasons of

pain, obstruction, or infection can often have their stones dissolved with alkalinization of the urine.

o Sodium bicarbonate can be used as the alkalinizing agent, but potassium citrate is usually preferred because of the availability of slow-release tablets and the avoidance of a high sodium load.

o The dosage of the alkalinizing agent should be adjusted to maintain urinary pH between 6.5-7.0. Urinary pH of more than 7.5 should be avoided because of the potential deposition of calcium phosphate around the uric acid calculus, which would make it undissolvable. Both uric acid and cystine calculi form in acidic environments.

o Even very large uric acid calculi can be dissolved in patients who comply with therapy.

o Practical ability to alkalinize the urine significantly limits the ability to dissolve cystine calculi. Chemoprophylaxis of uric acid and cystine calculi consists primarily of long-term alkalinization of urine.

o If hyperuricosuria or hyperuricemia is documented in patients with pure uric acid stones (present in only a relative minority), allopurinol (300 mg qd) is recommended because it reduces uric acid excretion.

o Pharmaceuticals that can bind free cystine in the urine (eg, penicillamine, 2alpha-mercaptopropionyl-glycine) help reduce stone formation in cystinuria. Therapy should also include long-term urinary alkalinization and aggressive fluid intake.

Surgical Care:

The primary indications for surgical treatment include pain, infection, and obstruction. Additionally, certain occupational and health-related reasons exist.

General contraindications to definitive stone manipulation include the following:

o Active, untreated urinary tract infection o Uncorrected bleeding diathesis o Pregnancy (a relative, but not absolute, contraindication)

Specific contraindications may apply to a given treatment modality. For example, do not perform extracorporeal shock-wave lithotripsy (ESWL) if there is ureteral obstruction distal to the calculus or in pregnancy.

For an obstructed and infected collecting system secondary to stone disease, virtually no contraindications exist for emergency surgical relief by either ureteral stent placement (a small tube placed endoscopically into the entire length of the ureter from the kidney to the bladder) or by percutaneous nephrostomy (a small tube placed through the skin of the flank directly into the kidney). Urologists place ureteral stents in the operating room while patients are under anesthesia; interventional radiologists perform percutaneous nephrostomies in the radiology suite while patients are under local anesthesia.

o Many urologists have a preference for one or the other, but, in general, patients who are acutely ill, who have significant medical comorbidities, or who harbor stones that probably cannot be bypassed with ureteral stents undergo percutaneous nephrostomy, while others receive ureteral stent placement.

o Infection combined with obstruction in the urinary tract is an extremely dangerous situation, with significant risk of urosepsis and death, and must be treated emergently in virtually all cases.

The vast majority of symptomatic urinary tract calculi are now treated with noninvasive or minimally invasive techniques, while open surgical excision of a stone from the urinary tract is now limited to isolated, atypical cases.

In general, stones that are 4 mm in diameter or smaller probably pass spontaneously, and stones that are 7 mm or larger are unlikely to pass without surgical intervention. The larger the stone, the lower the possibility of spontaneous passage, although many other factors determine what happens with a particular stone.

Extracorporeal shock-wave lithotripsy

o Approximately 85% of urinary tract calculi requiring treatment are currently managed with this modality. ESWL is the least invasive of the surgical methods of stone removal.

o The patient, under varying degrees of anesthesia depending on the type of lithotriptor, is placed on a table or in a gantry that is then brought into contact with the shock head.

o The shock head delivers shock waves developed from an electrohydraulic, electromagnetic, or piezoelectric source. The shock waves are focused on the calculus, and the energy released as the shock wave impacts the stone produces fragmentation. The resulting small fragments pass in the urine.

o ESWL is limited somewhat by the size and location of the calculus. A stone more than 2 cm in diameter or one located in the lower section of the kidney is treated less successfully. Fragmentation still occurs, but the large volume of fragments or their location in a dependent section of the kidney precludes complete passage.

Ureteroscopy

o Ureteroscopic manipulation of a stone is the next most commonly applied modality (see Image 4). A small endoscope, which may be rigid, semirigid, or flexible, is passed into the bladder and up the ureter to directly visualize the stone.

o The typical patient has acute symptoms caused by a distal ureteral stone, usually measuring 5-8 mm. This calculus can be rapidly addressed with miniaturized instruments. A stone can either be directly extracted using a basket or grasper or be broken into small pieces using a variety of lithotrites (eg, laser, ultrasonic, electrohydraulic, ballistic).

o Often, a ureteral stent must be placed following this procedure in order to prevent obstruction from ureteral spasm and edema. A ureteral stent is often uncomfortable; consequently, many urologists eschew stent placement following ureteroscopy in selected patients.

Percutaneous nephrostolithotomy

o Percutaneous nephrostolithotomy allows fragmentation and removal of very large calculi from the kidney and ureter. A needle, and then a wire, over which is passed a hollow sheath, are inserted directly in the kidney through the skin of the flank.

o Percutaneous access to the kidney typically uses a sheath with a 1-cm lumen. Relatively large endoscopes with powerful and effective lithotrites can be used to rapidly fragment and remove large stone volumes.

o Because of their increased morbidity compared with ESWL and ureteroscopy, percutaneous procedures are generally reserved for large and/or complex renal stones.

o In some cases, a combination of ESWL and a percutaneous technique is necessary to completely remove all stone material from a kidney. This technique,

called sandwich therapy, is reserved for staghorn or other complicated stone cases.

Consultations:

Immediate consultation with a urologist is recommended in cases of both infection and obstruction associated with urinary calculi.

Consultation with a urologist is required when immediate ED management of renal (ureteral) colic fails.

Referral to a urologist is necessary for all stones that prove refractory to outpatient management or that fail to pass spontaneously.

Diet:

For almost all patients in whom stones form, an increase in fluid intake and, therefore, an increase in urine output is recommended. This is likely the single most important aspect of stone prophylaxis.

The only other general dietary guidelines are to avoid excessive salt and protein intake.

Dietary calcium should not be altered unless specifically indicated by 24-hour urinalysis findings. Urinary calcium levels are normal in many patients with calcium stones. Reducing dietary calcium in these patients may actually worsen their stone disease, because more oxalate is absorbed from the gastrointestinal tract in the absence of sufficient intestinal calcium to bind with it. This results in a net increase in oxalate absorption and hyperoxaluria, which tends to increase new kidney stone formation in patients with calcium oxalate calculi.

As a general rule, dietary calcium should be restricted to 600-800 mg per day in patients with diet-responsive hypercalciuria who form calcium stones. This is roughly equivalent to a single high-calcium or dairy meal per day.

Drug Category: Opioid analgesics -- Used for pain reliefDrug Category: Nonsteroidal anti-inflammatory drugs -- Inhibit pain and inflammatory reactions by decreasing activity of cyclooxygenase, which is responsible for prostaglandin synthesis. Both properties are beneficial in the management of renal (ureteral) colic.Drug Category: Corticosteroids -- Strong anti-inflammatory agents that reduce ureteral inflammation. Also have profound metabolic and immunosuppressive effectsDrug Category: Calcium channel blockers -- Smooth-muscle relaxants that can facilitate ureteral stone passageDrug Category: Uricosuric agents -- Help prevent nephropathy and recurrent calcium oxalate calculiDrug Category: Alkalinizing agents, oral -- Used for treatment of metabolic acidosis and when long-term maintenance of an alkaline urine is desirable

Further Outpatient Care:

Postsurgical issues

o Following surgical treatment of urinary tract calculi, the major issues are infection, ureteral obstruction, and hemorrhage.

o The postoperative course of minimally invasive stone-removal modalities is generally characterized by short-lived discomfort easily managed with oral medications.

Continued or severe pain should prompt evaluation for complications. Repeat urine cultures and imaging studies should be performed to

assess for ureteral obstruction and perforation, and the degree of circulating blood volume should be evaluated for ongoing hemorrhage.

Postsurgical follow-up care

o A follow-up examination including an abdominal radiograph is often adequate after an uncomplicated stone removal procedure.

o Further imaging is often not necessary if a patient with a previous radiopaque stone has no further symptoms.

o In the following cases, imaging that includes assessment of renal drainage (eg, IVU, ultrasonogram, CT scan) is usually indicated:

Stones with unusual characteristics Difficult or complicated procedures Patients with unusual symptoms

o Once postoperative complications have been excluded and the patient is clinically healthy, standard radiographic follow-up care includes abdominal radiographs every 6-12 months. Radiographs are often ordered in conjunction with metabolic chemoprophylaxis.

Ongoing medical therapy

o If a patient older than 40 years has formed a single stone that passed spontaneously or was easily treated, follow-up care for recurrent stones may not be necessary. This patient is at a reasonably low risk for recurrence if adequate fluid intake is maintained.

o In other patients, whether or not they have elected directed metabolic therapy, routine follow-up care consists of plain abdominal radiographs (or renal sonograms in the case of radiolucent stones) every 6-12 months.

o If medical therapy is instituted, a 24-hour urinalysis 3 months after starting any new therapy should be performed to assess the degree of patient compliance and the adequacy of the metabolic response. Checking all possible metabolic parameters—not just the previously abnormal ones—is necessary because of the possibility of new problems arising as a result of the new therapy.

o Once a stable regimen has been established, annual 24-hour urinalyses are adequate.

Complications:

Serious complications of urinary tract stone disease

o Abscess formation

o Serious infection of the kidney that diminishes renal function

o Urinary fistula formation

o Ureteral scarring and stenosis

o Ureteral perforation

o Extravasation

o Urosepsis

o Renal loss due to long-standing obstruction

Prognosis:

As the minimally invasive modalities for stone removal are generally successful in removing calculi, the primary consideration in managing stones is not whether the stone can be removed but whether it can be removed in an uncomplicated manner with minimum morbidity.

The usually quoted recurrence rate for urinary calculi is 50% within 5 years and 70% or higher within 10 years, although a large, prospective study published in 1999 suggested that the recurrence rate may be somewhat lower at 25-30% over a 7.5-year period. Metabolic evaluation and treatment are indicated for patients at greater risk for recurrence, including those who present with multiple stones, those who have a history of previous stone formation, and those who present with stones at a younger age.

Medical therapy is generally effective at delaying (but perhaps not completely stopping) the tendency for stone formation. The most important aspect of medical therapy is maintaining an increased fluid intake and high urinary volume. Without an adequate urinary volume, no amount of medical or dietary therapy is likely to be successful in preventing stone formation.

o According to estimates, merely increasing fluid intake and regularly visiting a physician who advises increased fluids and dietary moderation can cut the stone recurrence rate by 60%. This phenomenon is known as the stone clinic effect.

o In contrast, optimal use of metabolic testing with proper evaluation and compliance with therapy can eliminate new stones completely in at least 75% of patients and significantly reduces new stone formation in up to 98% of patients.

Patient Education:

A patient who tends to develop stones should be counseled to seek immediate medical attention if he or she experiences flank or abdominal pain or notes visible blood in the urine.

A number of Internet sites offer kidney stone information, including the National Institutes of Health (NIH) and the American Foundation for Urologic Disease (AFUD).

An excellent source of detailed patient information is The Kidney Stones Handbook by Gail Savitz and Stephen W. Leslie. It is available at a reasonable cost from online booksellers such as Amazon.com and directly from the publisher, Four Geez Press, at 1-800-2KIDNEYS. A patient newsletter for patients who form kidney stones is available from the same publisher.

For excellent patient education resources, visit eMedicine's Kidneys and Urinary System Center. Also, see eMedicine's patient education articles Kidney Stones, Blood in the Urine, and Intravenous Pyelogram.

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