Inferior vena cava thrombosis in a pediatric patient of amebic liver abscess.

Amebic liver abscess (ALA) in pediatric age group is rare. We describe a successful thrombectomy and open drainage of a large left lobe ALA associated with thrombus in the hepatic veins and inferior vena cava extending into the right atrium in a 6-year-old boy.

INTRODUCTION

Amebic liver abscess (ALA) is a common entity especially in an endemic region. It can present in a myriad fashion with various complications with significant morbidity and mortality.[1] or may remain asymptomatic. ALA as a cause of inferior vena cava (IVC) thrombosis is exceedingly rare.[2] Herein, we describe a successful management of a 6-year-old child with ALA and IVC thrombosis with an aggressive surgical approach.

CASE REPORT

A 6-year-old malnourished boy was referred with a history of fever of 1-month duration, pain in right upper abdomen, loose motions, and vomitings for 14 days. The prior medical history was unremarkable. The physical examination revealed tachycardia and tachypnea. There was hepatomegaly with tenderness and guarding in the upper abdomen with ascites. On chest auscultation, the air entry was diminished on left side. Blood investigations are tabulated in Table 1. The chest radiograph showed left pleural effusion. An ultrasound showed a large single abscess of 94 ml in the left lobe of liver closely abutting the intra-hepatic vena cava. An echogenic lesion of 27 mm length extended from abscess to the IVC. Ascites was also noted. Contrast-enhanced computed tomography of abdomen revealed left lobe liver abscess in segments II and III. The thrombus was visible in the middle and left hepatic veins together with a thrombus in the IVC which extended up to the right atrium [Figure 1].

Table 1

Laboratory investigations of patient

Figure 1

Contrast-enhanced computed tomography (CECT) scan images showing (a) thrombus in inferior vena cava (IVC), (b) thrombus in right atrium, (c) abscess in left liver lobe in reconstructed coronal section, and (d) abscess in left liver lobe in axial section

Two-dimensional-echocardiography confirmed the above findings. The patient tested positive for amebic antibody by Enzyme-linked immunosorbent assay (ELISA) test. Broad spectrum antibiotics including metronidazole had been started by the referring institute. The patient was taken up for surgical intervention on an emergency basis. Median sternotomy and vertical pericardiotomy were performed. Cardiopulmonary bypass was established with aortocaval cannulation. After cooling to 20°C, cardioplegic arrest was achieved with root cold blood cardioplegia. Total circulatory arrest was established. Right atrium was opened parallel to the atrio-ventricular groove. Piecemeal extraction of the thrombus was done [Figure 2].

Figure 2

Thrombus extracted from inferior vena cava (IVC) and atrium

The IVC was thoroughly irrigated with normal saline. The circulation was temporarily restarted to flush any small remnant thrombus in the IVC. The right atrium was closed and circulation was restarted. Trans-esophageal echocardiography confirmed complete removal of thrombus. Cardiopulmonary bypass was weaned off after re-warming. Left pleural cavity was drained with a tube. After reversal of systemic heparinization, the abdomen was opened by a roof top incision and the falciform ligament was divided. The left triangular ligament was divided to mobilize the left lobe. The abscess was palpable in the postero-superior aspect of segment II lying just left of the divided falciform ligament. It was adhered to the diaphragm which was dissected free and then the abscess was de-roofed. About 100 ml of anchovy sauce pus was drained from the abscess cavity. Lavage was performed followed by placement of tube drain in left sub-diaphragmatic space. Pus was sent for examination which failed to reveal any trophozoites on microscopic examination and was negative for pyogenic organisms. The patient was discharged on 10th post-operative day. The patient is on regular follow-up and he is in good health at 6 months from the date of operation.

DISCUSSION

ALA occurs because of hematogenous spread of the trophozoites of Entameba histolytica from the intestinal mucosa to the liver through the portal vein. ALA is most common in the tropical and sub-tropical regions.[3] In the pediatric age group, the incidence of ALA is relatively rare and only 21-30% of liver abscesses are of amebic type.[45]

ALA afflicts commonly the right lobe. Left lobe lesions are less common, accounting for only 10-35% of all ALAs.[67] This skewed distribution is thought to be due to the greater width and the more linear course of the right branch of the portal vein.[8] ALA is usually clinically suspected in any patient with characteristic features of pain in right upper abdomen, fever, and tender hepatomegaly. Diagnosis is confirmed radiologically by demonstrating a space occupying lesion in the liver supported by a positive amebic serological test.[3] The usual course of an ALA is favorable and predictable if early diagnosis and management are initiated. There are infrequent complications of ALA which could be potentially life-threatening. IVC and/or hepatic vein thrombosis are among them which are very rare and reported scarcely in the literature.[92] Budd-Chiari syndrome or pulmonary embolism could cause rapid deterioration of the patient. These vascular complications have been previously described mostly in autopsy studies.[1011] The pathophysiology of vascular thrombosis is uncertain. The proposed mechanisms are external compression together with a contiguous spread of inflammation over the vessel wall.[2] The resultant endotheliitis predisposes to stasis and thrombosis and this ongoing process is the cause of extension of thrombosis into the vascular system. On this backdrop, respiratory movements of the diaphragm and coughing can cause further damage to the endothelial lining of the IVC, and this may predispose to thrombus formation in this part of the IVC.[12]

ALA causing IVC thrombosis and extending into the atrium has been reported in adults by a few authors. Hodkinson et al.[9] reported IVC thrombosis with atrial extension as a complication of ALA in a 50-year-old patient. Barcat et al.,[13] Sodhi et al.,[14] Khan et al.,[15] and Zia-ur-Rehman et al.[16] have described cases with similar presentation as ours in adults. Barcat et al. managed it with thrombolysis alone, whereas a percutaneous drainage with pig tail was required by Sodhi et al. Surgical removal was resorted to by the last two authors. In our case, the distinctive points were (I) involvement of the left lobe, (II) a prolonged trial of conservative management could not have been given,and (III) precarious and close relation to the pericardium and IVC precluded us to try percutaneous drainage. Hence, a laparotomy was done after thrombus extraction which resulted in a thorough and controlled drainage.

To conclude, our case is the first pediatric case of ALA reported in English literature, to be managed in this manner. This report highlights the importance of promptly diagnosing these exceptional cases and also emphasizes individualizing the management based on patient's clinical profile and available multimodality expertise for optimum outcome. An early aggressive surgical approach may prove life saving and crucial in preventing pulmonary embolism or Budd–Chiari syndrome which may have an overall poor outcome.