Pyogenic liver abscess presenting as fatal fulminant acute liver failure – a case report

Case report

A 3-year-old malnourished girl presented on the 8^th day of illness with fever, abdominal pain and distension, with poor oral intake. Acute liver failure (ALF) was diagnosed. ^a On ultrasound scan, two large liver abscesses were detected (one in segment VII and another in segment IVA & IVB), the largest measuring 6.4 × 6.0 cm. Investigations showed a leucocytosis (51.3 × 10⁹/L with neutrophils 75%, and lymphocytes 20%), but normal platelet count, and raised inflammatory markers (Procalcitonin: 8.8 ng/mL, and C-reactive protein at 188 mg/L). Intravenous ceftriaxone, cloxacillin and metronidazole were started. Two pigtail catheters, inserted into each abscess, drained thick pus but despite this, she deteriorated rapidly with vasoplegic shock, encephalopathy, respiratory failure and acute kidney injury (AKI) stage-3 (urea-32 mmol/L (1.7–8.3), creatinine-0.15 mmol/L (0.04–0.10) and fluid overload-13.5%) in the first 24 h of admission, i.e the 9^th day of illness. Vancomycin was added, considering the possibility of methicillin resistant staphylococcal aureus (MRSA).

On the 11^th day of illness, mechanical ventilation was introduced in view of respiratory failure and renal replacement therapy was started in view of AKI stage-3 (anuria). On the 16^th day of illness, renal function improved but encephalopathy, and hepatic function (bilirubin (0.14 mmol/L) and INR (5.8) did not. Rupture of a liver abscess was suspected on ultrasound and two abdominal drains were thus inserted. Her ammonia levels rose to 200 µmol/L and platelets fell to 19 × 10⁹/L; despite all our efforts, the child did not improve and succumbed to ALF and multi organ dysfunction syndrome (MODS) on the 21^st day of illness. Her blood culture had grown a MRSA and the pus from the liver showed gram positive cocci, but was negative for an amoebic polymerase chain reaction test. The abdominal drain culture did not grow any organism, and the baby's immune deficiency work up was negative.

Discussion

Around 30% of childhood ALF is caused by infection ¹ ; liver abscess, as aetiology, is rare. ¹ An Indian study found amoebic liver abscess causing ALF in 4/28 children. ² It also showed that non-viral aetiology had lower mortality rate (25%) as compared to viral (50%) in ALF.

Usually, a liver abscess does not cause hepatic derangement, as it defines a focal hepatic necrosis. Recent data, however, demonstrate that a complicated liver abscess could have raised transaminases as compared to uncomplicated. ³ Also, most children (77%) have a deranged coagulogram at admission. ³ The mechanism for this is considered to be a mass effect of multiple abscesses. A second observation in our case is that the child had MRSA septicaemia and Gram positive cocci were detected in the abscess. The most common organisms worldwide are Klebsiella pneumonae followed by E.coli, but in India it is staphylococcus,^3,4 though the overall yield of culture is very low (3–12%).^3,4 Multiple abscesses were seen in 25% of children, and abscesses >5 cm in diameter were noted in 68%. ⁴ Survival is the rule even in multiple, large volume abscess, even with complications.

Septicaemia, per se, is the most likely cause of ALF; thus when a child presents with such, primary liver abscesses should be searched for as an underlying aetiology. The signs of ALF were apparent in our case de novo, prior to the discovery of liver abscesses and prior to abscess drainage.

Conclusion

Pyogenic liver abscess is rarely associated with ALF. Nevertheless, when a child presents with signs of ALF, evaluating for possible liver abscess and secondary sepsis is important.