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Indian Pediatr 2013;50: 701-703 |
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Inferior Vena Caval and Right Atrial
Thrombosis: Complicating Pyogenic Liver Abscess
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Narendra Bagri, Dinesh Yadav and Alok Hemal
From the Department of Pediatrics, PGIMER and
associated Dr RML Hospital, New Delhi, India.
Correspondence to: Dr Narendra Bagri, Deptt. of
Pediatrics, PGIMER and associated Dr RML Hospital, New Delhi, India.
Email:
[email protected]
Received: February 14, 2013;
Initial review: March 05, 2013;
Accepted: March 26, 2013.
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Vascular complication of liver
abscess are rare but life-threatening. We herein report a 2 year 9 month
boy with pyogenic hepatic abscess complicated by inferior vena cava
thrombus extending to right atrium. Early clinical suspicion aided by
ultrasonography and echocardiography confirmed the diagnosis. The child
was treated successfully with timely medical and surgical intervention.
Key words: Complication, Liver abcess,
Pyogenic.
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The common complications of liver
abscess include rupture into pleural, peritoneal cavity and
pericardial spaces. Unusual vascular complication like
inferior vena cava (IVC) thrombosis has been reported only
in adult patients of amebic liver abscess but has never been
reported in cases of pyogenic liver abscess [1,2]. We herein
report a child with pyogenic (Staphylococcal aureus)
hepatic abscess complicated with inferior vena cava thrombus
extending to right atrium.
Case Report
A 2-year-9 months-old boy presented with
high grade fever, abdominal distension and cough for 4 days.
On examination, child was febrile, had pallor, with blood
pressure of 108/66 mmHg, heart rate of 118/min, respiratory
rate of 32/min, and was malnourished (weight <3rd percentile
on WHO standards). Abdominal examination revealed tender
hepatomegaly (6 cm below right costal margin) while rest of
the systemic examination was unremarkable. Hematological
investigations showed a hemoglobin of 6.9 g/dL and white
blood cell count of 32,700/mm 3
with 87% polymorphs. Peripheral smear showed toxic granules.
Liver function test showed bilirubin of 0.8 mg/dL (direct-
0.3mg/dL), aspartate aminotransferase 65 IU/L (normal range,
<50 IU/L), alanine aminotransferase 31 IU/L (normal range,
<50 IU/L) and alkaline phosphatase of 630 U/L. Renal
function tests and chest X-ray were normal.
Ultrasonography (USG) abdomen at admission showed a large
(5×4.8×5.8 cm; 120 mL), heterogeneously hypoechoic lesion
with internal echoes in the segment IV and VIII of liver,
suggestive of liver abscess. 25 mL of thick yellowish pus
was aspirated on US guided tap. Routine microscopy of this
pus revealed protein of 2.9 gm % with many polymorphonuclear
cells. The child was started on intravenous antibiotics
ceftriaxone, vancomycin and metronidazole. On day 2 of
admission child continued to have fever, developed pedal
edema and a repeat USG showed a thrombus in IVC;
echocardiography demonstrated a thrombus measuring 2.25 ×
1.31 cm in right atrium at the junction of IVC and right
atrium with normal cardiac anatomy and function without any
evidence of pericardial effusion. As the child’s clinical
condition deteriorated the child was taken for surgical
management. Surgery was performed by cardiothoracic and
pediatric surgeons. Peroperative findings were suggestive of
around 100 mm3
partially liquified liver abcess in 4th segment and a
organized thrombus adherent to inflamed ostia of left
superior hepatic vein extending to IVC and right atrium.
Peroperative culture sent from abscess cavity grew Staphylococcus
aureus that was sensitive to vancomycin, cloxacillin and
ciprofloxacin.
Postoperatively child was managed with
intravenous fluids and appropriate antibiotics for 4 weeks.
Gradually child improved, fever subsided and repeat USG and
echocardiography demonstrated resolution of abscess and
thrombus, respectively and child was discharged on oral
antibiotics for another 2 weeks.
Discussion
IVC and/or hepatic vein thrombosis are
infrequent but life-threatening complications of liver
abscess. Budd-Chiari syndrome or pulmonary
embolism could cause rapid deterioration of these patients.
These vascular complications have been previously described
mostly in autopsy studies. In a series of 95 autopsies of
amebic liver abscess subjects, thrombosis of hepatic vein
and IVC obstruction was observed in 8% of the cases [3].
Apart from this study, there have been anecdotal case
reports of IVC obstruction in adult patients with amebic
liver abscess [2,4,5]. Hodkinson, et al. [1] reported
a 50-year-old man with amebic liver abcess where the patient
developed IVC obstruction due to a thrombus which extended
up to the right atrium [1]. Gupta, et al. [6]
recently reported ALA complicated by IVC thrombus in a
6-year child. The pathophysiology of vascular thrombosis is
uncertain. The proposed mechanisms are external compression
coupled with contiguous spread of inflammation over the
vessel wall resulting in endotheliitis, which predisposes to
stasis and thrombosis [5].This endothelial damage is further
accentuated by respiratory movements of the diaphragm and
coughing and can contribute to thrombus formation in IVC
[7].
While evaluating a child with thrombosis
it must be assumed that interplay of multiple factors play a
role in evolution of thrombus; in most cases, some insult to
endothelium (e.g. indwelling vascular catheter,
infectious vasculitis) as well as some dysregulation of
coagulation (e.g. sepsis, congenital or acquired
coagulation protein abnormalities) will be present [8].
Therefore most pediatric thrombotic patients should be
investigated for congenital or acquired coagulation protein
abnormalities (e.g. Protein C and S, lupus
anticoagulant, total cholesterol, antiphospholipid
antibodies). It is also essential to remember that many
abnormal results in acute phase (e.g. consumption of
Protein C and S secodary to thrombotic event) need to be
confirmed by repeating atleast 3-6 months after acute
thrombotic event [8]. In our case, sepsis-induced
endothelitis seems to be the most important factor for
thrombosis; it is likely that the inflammatory process in
the wall of the abscess spread directly to the adjacent wall
of the right hepatic vein which later propagated into the
IVC and right atrium. Work-up for procoagulant states has
been planned at follow up.
Contributors: All the authors have
contributed, designed and approved the study.
Funding: None; Competing interests:
None stated.
References
1. Hodkinson J, Couper-Smith J, Kew MC.
Inferior vena caval and right atrial thrombosis complicating
an amebic hepatic abscess. Am J Gastroenterol. 1988;
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2. Huddle KR. Amoebic liver abscess,
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SR. Vascular complications of hepatic amoebiasis–a
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4. Sharma MP, Sarin SK. Inferior vena
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5. Sodhi KS, Ojili V, Sakhuja
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al. Inferior vena cava thrombosis in a pediatric patient
of amebic liver abscess. J Indian Assoc Pediatr Surg.
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vena cava thrombosis at its hepatic portion. Hepatobiliary
Pancreat Dis Int. 2002;1:499-509.
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