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Radiological Case of the Month
Derek S. Wheeler, MD;
W. Bradley Poss, MD;
Alton L. Stocks, MD
From the Departments of Pediatrics and Clinical Investigation, Navel
Medical Center San Diego, San Diego, Calif.
Arch Pediatr Adolesc Med. 2001;155:415-416.
A 5-DAY-OLD boy was seen for poor feeding, nonbilious vomiting, lethargy,
and decreased urine output. The history was notable for an unremarkable pregnancy
with normal findings from 16-week fetal ultrasound. Findings from initial
physical examination revealed a large, nontender right flank mass. Results
of subsequent laboratory analysis revealed acute renal failure, metabolic
acidosis, hyperkalemia, azotemia, and hematuria. Anemia and thrombocytopenia
were also present. Renal ultrasonography was performed, and results of a subsequent
computed tomographic scan of the abdomen are shown in
Figure 1 and
Figure 2.
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Figure 1.
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Figure 2.
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Denouement and Discussion: Inferior Vena Cava and Renal Vein Thrombosis in a Neonate
Figure 1. Computed tomographic scan of the abdomen demonstrating a markedly
enlarged right kidney (thick arrow), calcification of the inferior vena cava
(arrowhead), and a small, calcified left kidney (thin arrow).
Figure 2. Computed tomographic scan of the abdomen demonstrating calcifications
in the left renal vein extending into the inferior vena cava (arrowhead).
All abdominal masses detected in the neonatal period require further
investigation with ultrasonography.1 Most
of these masses originate in the genitourinary tract,1, 2
and ultrasonography should be performed to localize and differentiate between
cystic and solid structures. The differential diagnosis of cystic abdominal
masses includes hydronephrosis; multicystic-dysplastic kidney disease; intestinal
duplication; hydrometrocolpos; and choledochal, ovarian, renal, and pancreatic
cysts. The differential diagnosis of solid abdominal masses includes neuroblastoma,
teratoma, and Wilms tumor. A solid flank mass of a neonate in the presence
of hematuria, hypertension, renal failure, and thrombocytopenia suggests a
diagnosis of renal vein thrombosis.
Two types of renal vein thrombosis are recognized. In the first, the
thrombus begins intrarenally at the level of the arcuate and interlobular
veins, successively extending into the larger renal veins and to the inferior
vena cava.3 It is thought that this type
is more frequent during infancy.4, 5
However, Demirci et al6 presented a case
of bilateral renal vein thrombosis in which the inferior vena cava was completely
filled with thrombus, suggesting that the thrombus arose initially in the
inferior vena cava with subsequent retrograde extension into the renal veins.
Clinically, renal vein thrombosis is characterized by the presence of
a palpable flank mass associated with acute renal failure. Hematuria, proteinuria,
and oliguria are usually present. Predisposing factors are dehydration, asphyxia,
polycythemia, sepsis, shock, coagulopathies, and maternal diabetes.7 Ultrasound examination will show perivascular streaking
with increased echogenicity of the renal parenchyma.8
Computed tomography will demonstrate persistent parenchymal opacification
and enlargement of the affected kidney, dilation of the renal vein, and renal
vein and/or inferior vena caval thrombus.9
Surgical management with removal of the affected kidney has historically
been the treatment of choice,10 but it has
been recognized more recently that with supportive therapy alone, the short-term
prognosis of renal vein thrombosis occurring during infancy is good. However,
the involved kidney progressively becomes atrophic resulting in a small, scarred
kidney.11, 12 Treatment with
systemic anticoagulation agents may result in a better long-term prognosis.13, 14 In our patient, treatment with
low-molecular-weight heparin resulted in a return of normal renal function
by age 4 months.
AUTHOR INFORMATION
Accepted for publication February 12, 1999.
This report was sponsored by the Chief Bureau of Medicine and Surgery,
Navy Department, Washington, DC, Clinical Investigation Program, report 84-16-1968-665,
as required by NSHSBETHINST 6000.41A.
The views expressed in this article are those of the authors and do
not reflect the official policy or position of the Department of the Navy,
Department of Defense, or the US Government.
Reprints: Clinical Research Department, Medical Editing Division,
Naval Medical Center San Diego, 34800 Bob Wilson Dr, Suite 5, San Diego, CA
92134-1005 (e-mail: wmacal{at}snd10.med.navy.mil).
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SECTION EDITOR: BEVERLY P. WOOD, MD
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