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Life-threatening presentation of mediastinal neoplasms: report on 7 consecutive pediatric patients
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Transcript of Life-threatening presentation of mediastinal neoplasms: report on 7 consecutive pediatric patients
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Brief Reports
Life-threatening presentation of mediastinal neoplasms:report on 7 consecutive pediatric patients
Marco Piastra MDa,*, Antonio Ruggiero MDb, Elena Caresta MDa, Antonio Chiaretti MDa,Silvia Pulitano MDa, Giancarlo Polidori MDa, Riccardo Riccardi MDb
aPediatric Intensive Care Unit, Catholic University Medical School, 00168 Rome, ItalybPediatric Oncology, Catholic University Medical School, 00168 Rome, Italy
Received 20 December 2003; accepted 21 December 2003
AbstractBackground: Cases of respiratory failure at presentation in children with anterior mediastinal
malignancies can be very challenging for clinicians. Seven consecutive children presenting with
superior mediastinal syndrome are reported needing urgent critical care approach.
Patients and Methods: Seven children (age range from 0.8 to 14 years; mean, 4.5 years) suffered from
critical mediastinal neoplasms. Clinical presentation, laboratory findings, treatment, and outcome are
discussed. Setting: a tertiary-care 6-bed medical and surgical pediatric intensive care in a university
hospital. Interventions included emergency management, resuscitation and intensive care admission,
and diagnostic and therapeutic procedures.
Results: All cases showed a respiratory compromise and underwent ventilatory and/or cardiovascular
support. Two patients needed renal replacement therapy. Pediatric Intensive Care Unit discharge was
achieved in all patients.
Conclusions: Critical or extreme presentation of mediastinal neoplasms does not preclude a good
clinical outcome: an intensive care approach is essential to allow patient recovery and effective
antineoplastic therapy administration.
D 2005 Elsevier Inc. All rights reserved.
1. Introduction
Superior mediastinal syndrome and superior vena cava
syndrome (SVCS) are almost synonymous terms to indicate
the compression of vital structures of superior mediastinum:
namely, SVCS means a predominant venous compression.
0735-6757/$ – see front matter D 2005 Elsevier Inc. All rights reserved.
doi:10.1016/j.ajem.2003.12.025
* Corresponding author. Tel.: +39 06 30155203; fax: +39 06
35402286.
E-mail address: [email protected] (M. Piastra).
This is a rare but serious condition, sometimes manifesting
bde novo,Q requiring prompt treatment. In children, malig-
nant lymphomas are the second most common cause [1] of
SVCS after surgery for congenital heart diseases. The
clinical picture at onset may be critical—as in presented
cases—and upper airway obstruction, superior vena cava
(SVC), cardiac or pulmonary artery compression, and acute
pulmonary edema can represent the initial clinical signs in
previously apparently healthy children. Up to now, cases of
mediastinal neoplasm emergencies have been reported only
American Journal of Emergency Medicine (2005) 23, 76–82
Life-threatening presentation of mediastinal neoplasms: report on 7 consecutive pediatric patients 77
rarely as single-case reports or among general series [1-3];
on the contrary, perioperative morbidity and mortality of
patients with superior mediastinal syndrome/SVCS under-
going surgical procedures have been previously analyzed by
several authors, and therapeutic approach discussed. All
authors agree in defining these children as extremely
unstable and challenging for the caregivers.
2. Illustrative cases
From 1994 to 2002, 7 patients suffering from severe
cardiorespiratory compromise because of the newly diag-
nosed anterior mediastinal mass were admitted to the
Pediatric Intensive Care Unit (PICU) at Catholic University
of Rome (Table 1). Their ages ranged from 0.8 to 14 years
(mean, 4.5 years). The clinical manifestations of SVC
compression included variable degrees of face, neck, and
upper thorax swelling; external jugular and superficial chest
vein distension was present in all patients, sometimes
associated with cyanosis or plethora. Stridor, dyspnea, and
cough were almost always apparent at presentation, together
with increased oxygen need.
1. A 4-year-old boy with signs of impending cardiore-
spiratory failure was referred to our PICU in November
1994 from another hospital. He was diagnosed having a
mediastinal mass 7 days before: the onset of clinical history
was characterized by signs of worsening respiratory
compromise. Physical examination revealed hepatospleno-
megaly and lymph node enlargement. After a peripheral
node biopsy, chemotherapy was initially performed using
cyclophosphamide, vincristine, and methylprednisolone. On
arrival, the child appeared extremely distressed, gasping,
and cyanotic, and then was immediately intubated and bag
ventilated; a chest x-ray showed a large anterior mediastinal
mass that impaired pulmonary ventilation, mostly on the
right lung (Fig. 1). Pressure-regulated volume-controlled
ventilation was set (tidal volume, 6 mL/kg; rate, 20/min).
Table 1 Clinical presentation and complications during the PICU stay
Case no./year Age Sex Pathological
diagnosis
Cardi
comp
1/1994 4 M T-cell lymphoma Sever
2/1995 14 F T-cell lymphoma Extre
3/1995 1.6 M T-cell lymphoma Mode
4/1998 4 M Pleuropulmonary
blastoma
Sever
5/1999 7 F T-cell lymphoma Extre
6/2002 0.8 M Teratoma Mode
7/2003 1.4 F Anaplastic lymphoma Mode
Abbreviations: PD, peritoneal dialysis; CVVH, continuous veno-venous hemofilt
Given are the arterial blood gas analysis results: pH 7.3;
Pao2, 87; Paco2, 51.5; Sao2, 95; Fio2, 0.7). Instead of a
previously suggested irradiation treatment, a further che-
motherapy approach using daunomycin (60 mg/m2) was
used. On day 2, a clear picture of SVC obstruction appeared,
with a swelling of the upper torso/facial tissues; liver margin
was appreciable at 4 cm. At the echocardiographic examina-
tion, suprahepatic dilated veins and pericardial effusion
were detected; because of the initial heart pump failure, an
inotropic support was added (dopamine, 5 lg/kg per
minute; dobutamine, 7 lg/kg per min). From day 4, the
child progressively improved spontaneous breathing capac-
ity—as revealed by a spirometer—and could be weaned and
extubated uneventfully. Subsequently, he was discharged
from the PICU to the Oncologic Department. After
prolonged chemotherapy treatment, he is at present free
from disease and off-therapy from 1996.
2. A 14-year-old girl was admitted to the PICU on June
1995 because of acute respiratory distress. She complained
respiratory difficulties, progressive fatigue, and weight loss
for 15 days, together with slight elevated body temperature.
A huge mediastinal mass was diagnosed in the emergency
department by a chest x-ray (Fig. 2). On physical examina-
tion, the child had polypnea/orthopnea and labial cyanosis;
because of rapid worsening of patient’s spontaneous
breathing after an initial trial of mask ventilation, endotra-
cheal intubation and positive pressure ventilation were
necessary. A pericardial effusion with signs of cardiac
tamponade needed pericardial drainage. During the clinical
course in PICU, she developed severe hypotension, and
inotropic support was added using a dopamine/dobutamine
association. After a bone marrow aspirate, chemotherapeutic
treatment with cyclophosphamide, vincristine, and methyl-
prednisolone was given. Oliguria (b0.3 mL/kg per hour)
and increasing blood urine nitrogen, creatinine, and uric
acid occurred, necessitating peritoneal dialysis. Fluid
retention and systemic hypertension were controlled,
whereas a moderate reduction in tumor size permitted
of patients described in cases 1 to 7
orespiratory
romise
Mechanical
ventilation (d)
Complications
in the PICU
e 3 Right/left ventricular
pump deficit,
left ventricular diastolic
dysfunction
me 8 Acute renal failure (PD),
cerebral hemorrhage, coma
rate-severe – No complications in PICU
e 5 Respiratory failure,
heart diastolic dysfunction
me 15 Acute renal failure (CVVH),
coma, septic shock
rate-severe 4 Respiratory failure
rate-severe – No complications in PICU
ration.
Fig. 3 Radiological appearance of mediastinal mass on PICU
admission in patient 3. Of interest, the tracheal displacement on the
anteroposterior film is well appreciable.
Fig. 1 Radiological appearance of mediastinal mass on PICU
admission in patient 1.
M. Piastra et al.78
tracheal extubation on day 8. Chemotherapeutic toxicity
occurred (thrombocytopenia; nadir value, 18000/lL on
day 14). The patient was discharged from the PICU on day
10 and readmitted on day 13 because of sudden onset of
deep coma. Right anisocoria was present, and a cerebral
computed tomography (CT) scan showed a subdural
hemorrhage in the posterior cranial fossa and a triventricular
hydrocephalus. A surgical drainage was performed and
antiedema therapy was started. Hypercellularity in cerebro-
spinal fluid examination was found (955 cells/lL, primarily
blasts) and intrathecal methothrexate was given. No further
improvement of the clinical status was obtained: the
patient’s condition gradually deteriorated and she died
7 days later.
3. A 20-month-old boy with signs of SVCS and
respiratory compromise was admitted on November 1995.
The clinical history began 2 weeks before having signs of
intermittent wheezing and deteriorated after 48 hours from
admission, showing the picture of SVCS. On chest x-rays,
an anterior mediastinal mass was diagnosed, causing
compression and right displacement of the trachea (Fig. 3).
The child appeared polypneic (respiratory rate N45/min) and
tachycardic; labial cyanosis was present on room air; Sao2
more than 88% to 89% could only be achieved by mask
Fig. 2 Radiological appearance of mediastinal mass on PICU
admission in patient 2.
oxygen therapy (Fio2 60%) and subsequent continuous
positive airway pressure +4 to 6 cm H2O administration via
a tight-fitting face mask. Spontaneous breathing improved
by turning the child in a semiprone position. A chest CT scan
showed an infiltrating mass constricting the pulmonary
artery trunk and posteriorly displacing the trachea and
mainstem bronchi. A bone marrow tap showed lymphoma-
tous infiltration (immature T-cell lymphoma). Before
definitive histology, a chemotherapeutic treatment was
started using cyclophosphamide (300 mg/m2) and methyl-
prednisolone (60 mg/m2). In the following 24 to 36 hours, a
dramatic improvement of spontaneous breathing capacity
was obtained, and the child was discharged to the oncologic
ward to continue chemotherapy in an aseptic environment.
Control chest x-rays showed a visible mass reduction and
pulmonary ventilation improvement. The child is now
disease free and off-therapy from August 1998.
4. A 3-year-old child came to our PICU in June 1998
because of impending respiratory failure, with a 1-month
history of cough, dyspnea, andwheezing that is misdiagnosed
as asthma. On admission, chest radiograms and CT scan
showed an enormous mass that caused an extreme tracheal
Fig. 4 Radiological appearance of mediastinal mass on PICU
admission in patient 4. Of interest, the tracheal displacement on the
anteroposterior film is well appreciable.
Fig. 5 a, Radiological appearance of mediastinal mass on PICU
admission in patient 5. b, The postintensive chest film has been
added, showing a remarkable narrowing of the tracheal lumen.
Life-threatening presentation of mediastinal neoplasms: report on 7 consecutive pediatric patients 79
distortion, and a right shift was evidenced (Fig. 4). Due to the
severity of clinical presentation and the poor general status,
chemotherapy was immediately started using cyclophospha-
mide 1 g/m2 intravenously, even in the absence of a
histological confirmation. In the following hours, the child
developed acidosis and hypercapnia as respiratory muscles
became seriously fatigued. Arterial blood gas analysis
worsened further (pH 7.04; Pao2, 62 mm Hg; Paco2, 73.5
mm Hg, HCO3, 19.2 mEq/L; base excess (BE), �13; Sao2,
89%-90%; Fio2, 1) and the child needed tracheal intubation
and mechanical ventilation. Initial parameters were peak
inspiratory pressure (PIP), 35 mm Hg; positive end-
expiratory pressure, 5; risk ratio, 24; inspiratory time, 35%;
Fio2, 1. A pulmonary biopsy was performed and histology
showed a mesenchymal neoplasm with ovoid cells.
Adriamycin, 20-mg intravenous bolus as a single dose,
was added to his therapy. Bone marrow aspirate resulted
negative. The child was then paralyzed and underwent
controlled one-lung ventilation with permissive hypercap-
nia. After 5 days, the functional obstruction was gradually
removed, thus, allowing spontaneous breathing restoration
and tracheal extubation. A control CT scan confirmed a mass
volume reduction; day 9 from admission, the child could be
discharged to the pediatric oncology division. Definitive
histological diagnosis revealed a rare pleuropulmonary
blastoma. On October 1998, the child underwent left lower
lobectomy; off-therapy from May 1999, he had no evidence
of disease.
5. A 7-year-old girl was admitted to the PICU of Catholic
University in September 1999 on emergency basis because
of sudden onset of cardiorespiratory failure. Previous
clinical history was unremarkable, except for the presence
of cervical vein engorgement 48 hours before the admission.
The patient suddenly awoke from night sleep having severe
asphyxia and hypotension, and then precipitated into a deep
coma. After initial resuscitation, arterial blood gases showed
severe mixed acidosis (pH 6.7; Pco2, 158 mm Hg; BE,
�15; HCO3, 20). On arrival to the PICU, an extreme picture
of cardiac tamponade and respiratory failure was diagnosed.
A very high resistance to pulmonary inflation was encoun-
tered, due in part to the presence of cardiogenic pulmonary
edema: hand ventilation was performed intermittently to
supply inflation pressures in excess of 60 to 70 cm H2O: the
patient tolerated the highest airway pressures poorly and
became hypotensive, needing intravenous colloid intake and
elevated dopamine/dobutamine inotropic support. Maximal
steroid therapy was started on admission to the PICU. A CT
scan confirmed the chest x-ray findings, showing an
enormous mediastinal mass inglobating the heart and the
great vessels, and no pericardial fluid was detected (Fig. 5a).
In spite of the maximal inotropic support, the patient
remained severely hypotensive (arterial pressure, 60/40 mm
Hg) and a further epinephrine infusion needed to be titrated
up to 0.4 lg/kg per minute. At 10 to 12 hours from the
admission, hemodynamic status progressively improved, and
blood pressure was stabilized (N90/50 mm Hg). Chemother-
apy was started on presumptive basis (suspected diagnosis of
lymphoblastic lymphoma) after a percutaneous biopsy was
performed. In the following days, oliguria/anuria with
hyperuricemia (uric acid level, 12 mg/dL before chemother-
apy) developed, and continuous venovenous hemodiafiltra-
tion via an indwelling femoral double-lumen catheter was
started to replace renal function and to control fluid/
electrolyte balance. In spite of the aggressive chemotherapy,
the mass showed minimal or absent volume reduction, and
the patient still needed high inflation pressures (in excess of
40 cm H2O) to obtain a satisfying pulmonary ventilation.
Hematologic toxicity also developed. Moderate improve-
ment of airway patency was achieved by a radiotherapeutic
treatment on the mediastinum in a divided dose of 150 cGy
for 4 days, and the trachea could be extubated on day 18
from admission. Previously, attempts to withdraw endo-
tracheal (ET) tube were unsuccessful, and a tracheal tube was
still necessary to maintain airway patency. On control chest
radiogram in absence of endotracheal tube, narrowing and
displacement of the trachea resulted well appreciable
(Fig. 5b). Humidified and heated oxygen and aerosolized
epinephrine and steroids were given to minimize mucosal
edema and made spontaneous breathing easier. The girl was
transferred to the oncologic ward 3 weeks after PICU
admission. One week later, she was readmitted to the PICU
Fig. 7 Radiological appearance of mediastinal mass on PICU
admission in patient 7.
M. Piastra et al.80
after a trial of chemotherapy because of respiratory failure,
then she died on the 30th hospital day in septic shock.
Postmortem examination confirmed a T-cell lineage lym-
phoblastic lymphoma.
6. A 10-month-old child was referred to the ED from a
peripheral hospital with a 7-month history of recurrent upper
respiratory infections. Wheezing signs were reported inter-
mittently. Two weeks before the admission, the patient had a
high fever and productive coughing. An antibiotic treatment
(10 days intramuscular ceftazidime) obtained only a brief
interval of apyrexia. Chest x-ray revealed a massive
opacification of the right lung; the midline resulted shifted
to the left. A right posterior basal indistinct image was
present. The chest CT scan showed a 10-cm-diameter mass,
arising from the anterior mediastinum. Solid, liquid, and fat
areas were present, together with calcifications. A mediasti-
nal teratoma was hypothesized, extending mostly on the right
hemithorax and causing compression of the homolateral
parenchyma and right mainstem bronchus. Signs of air
trapping were well appreciable peripherally. The echocardio-
gram demonstrated a compression on the right atrial wall. On
admission to PICU, the child was distressed, polypneic, and
peripheral oxygen saturation on Fio2 70% was 89% to 90%.
Metallic, repetitive coughing attacks were present. An
emergency surgical removal of the mass was undertaken.
After surgery, the child was paralyzed and mechanically
ventilated for 72 hours. Aspiration chest drainages promoted
right lung reexpansion. The child was extubated and could
resume spontaneous breathing. Histology confirmed amature
teratoma (Fig. 6).
7. A 17-month-old child came to the ED for cough and
increasing dyspnea with a 2-week history of upper airway
infections. A chest x-ray documented a mediastinal enlarge-
ment and right pleural effusion (Fig. 7). A bidimensional
echocardiography revealed a moderate cardiac effusion and
a 6-cm diameter mass anterior to the pulmonary artery,
expanding to the right with a moderate infundibulum
compression. On physical examination, enlarged supra-
Fig. 6 Radiological appearance of mediastinal mass on PICU
admission in patient 6.
clavicular nodes and a reduced air entry mostly in the right
hemithorax were evidenced. The child’s clinical conditions
suddenly deteriorated, dyspnea worsened, and high oxygen
support (Fio2, 0.70) was necessary to achieve an 88% to
90% peripheral oxygen saturation. Node biopsy, bone
marrow aspiration, and biopsy were performed in emergen-
cy; sedation/analgesia was provided by propofol/fentanyl
intravenous administration, avoiding muscle relaxants and
tracheal intubation. On these bases, steroids were started
without a definitive diagnosis. Oxygen supplementation
through Venturi mask and intermittent continuous positive
airway pressure were adopted to allow an acceptable arterial
gas analysis; circulatory status was stabilized with colloid
supplementation and low-dose dopamine infusion. Clinical
conditions improved in the following 24 to 48 hours,
permitting oxygen support decrease. A total body CT scan
was performed, revealing a jugular and supraclavear node
enlargement (2-cm diameter). An anterior mediastinal mass
with a dysomogeneous enhancement (5 cm diameter) was
evidenced, compressing the vena cava and the right atrium
and ventricle, and inglobating the epiaortic vessels and
trachea. Pulmonary parenchyma resulted uninjured. No
abdominal anomalies were recorded. Node histology
revealed an anaplastic non-Hodgkin’s lymphoma (CD30+)
and a chemotherapeutic treatment was started.
3. Discussion
Rapidly evolving symptoms of respiratory compromise
from an anterior mediastinal neoplasm represent true
emergencies that mandate prompt treatment in an ICU
setting. Large mediastinal masses may result in life-
threatening events such as upper airway obstruction, cardiac
or pulmonary artery compression, and acute pulmonary
edema. Airway obstruction can arise unexpectedly at any
time, even after the trachea has been secured through
intubation. In addition, circulatory compromise becomes
clinically apparent when compression of the great vessels
Life-threatening presentation of mediastinal neoplasms: report on 7 consecutive pediatric patients 81
occurs despite airway patency. Airway obstruction and
cardiovascular compression are the cornerstone of the
clinical picture of these patients: as tumors increase in size,
the trachea and the mainstem bronchi as well as the major
vessels may be exposed to an increasingly positive pressure.
When the transmural pressure of the airway/SVC exceeds
the elastic recoil of the wall of these structures, extrinsic
compression develops. Once these complications occur, the
death rate appears to be high.
In children, most anterior mediastinal tumors are
malignant (mostly lymphomas) [4]. Their clinical presenta-
tion may be critical and the additive effects of general
anesthetics or positioning during diagnostic procedures may
contribute to worsen the airway obstruction leading to fatal
cardiorespiratory failure. Even in large malignant lympho-
mas, a prompt chemotherapy and/or radiotherapy may lead
to effective compression relief [5]. On the other hand, an
early treatment—designed to cause a rapid shrinking of the
tumor—can make definitive diagnosis impossible: if the
patient is in critical condition, however, the treatment should
not be delayed until definitive histological diagnosis is
achieved [5-7].
In literature, few cases have been described of really
critical presentation, that is, children that needed immediate
resuscitation, airway patency restoration, and intensive care
approach. Regarding this presentation, 2 children have been
reported to be admitted in near asphyxiation; they were
resuscitated with endobronchial intubation, but both patients
eventually died in the ICU from sepsis and massive
hemorrhage, respectively [8,9]. Jeng et al [10] reported 7
pediatric SVCS over a 12-year period, of whom 2 cases
received immediate resuscitation upon arrival and died
within 2 hours. Freud et al [2] recently reported 5 children
among a mixed series requiring emergency respiratory
support on admission to PICU; all were affected by a
malignant lymphoma. On the other hand, several case reports
exist of patients who developed airway and/or circulatory
complications when an elective anesthesiologic procedure
was performed. A review of 163 consecutive patients
younger than 18 years at Memorial Sloan Kettering Cancer
Center has been published in 1990 [11]. An anterior
mediastinal mass was a component of their disease; only 9/
44 patients that required anesthesia (20%) were symptomatic
preoperatively: SVCS was present in 5/44 (about 1l%).
Admission plain chest radiographs may not reveal the
presence of airway compromise; all the authors underline
the risks of managing such patients, also in elective
procedures [12], because cardiorespiratory complications
may occur abruptly, often not related to mild preoperative
respiratory symptoms and roentgenographic evidence [13].
The severity of pulmonary symptoms—although sugges-
tive—is not a reliable indicator of the degree of tracheo-
bronchial compromise [14]. Also, after a successful
resuscitative approach, the clinical picture may worsen
because of nonrespiratory complications: tumor lysis syn-
drome may be expected as a direct consequence of the
chemotherapy-induced tumor shrinking, necessitating emer-
gency extrarenal depuration, mostly by continuous venove-
nous hemofiltration or hemodiafiltration [15]. Preventive
hemofiltration/hemodiafiltration is rarely applicable to
patients with sudden onset of neoplastic SVCS.
Overall, some specific points are to be emphasized:
1. All efforts should be directed toward patient stabilization
in the emergency department and intensive care setting.
The best available cardiovascular monitoring should be
placed as soon as possible. Spontaneous breathing
should be maintained—if clinically acceptable—to
avoid the negative effects of deep sedation and muscle
paralysis [16]. Anxiety treatment with midazolam is
always desirable. Pressure support ventilation—even
noninvasively—may result more tolerated.
2. Therapeutic approach would be best guided by tissue
diagnosis, revealing the tumor nature, but diagnostic
procedures are often poorly tolerated, time-consuming,
and may lead to clinical deterioration. The least invasive
bedside procedures should be performed under local
anesthesia, avoiding the additive risks of general
anesthesia. Recently, criteria on the basis of peak
expiratory flow rate and tracheal cross-sectional area
have been proposed to identify high-risk patients
[17,18].
3. Severely symptomatic patients, with unsatisfying hemo-
dynamic and/or ventilatory stabilization, will require
empiric pretreatment of the mass before definitive
diagnosis. Therapeutic strategy will be guided by the
clinical/radiological findings.
Cases of emergency onset represent a serious challenge
for both intensivists and pediatric oncologists, and an
aggressive therapeutic approach is necessary to achieve the
best clinical result: give the patient a chance to benefit from
specific therapy, once the diagnosis has been fully estab-
lished. The initial presence of a threatening SVCS associated
with a critical clinical picture does not preclude both PICU
discharge and long-term survival in this patient group.
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