Liver Abscess — Amoebic vs Pyogenic: Causes, Diagnosis, Drainage and Drugs

A liver abscess is a pus-filled mass in the liver arising from liver injury or from an intra-abdominal infection that reaches the liver through the portal circulation or the biliary tree. Most are pyogenic (bacterial) or amoebic; a minority are parasitic (hydatid cyst, Echinococcus granulosus) or fungal (Candida, usually in immunosuppressed patients).

The liver is vulnerable because it receives blood from both the systemic and portal circulations and lies next to the gall bladder. Even so, an abscess is uncommon, partly because the Kupffer cells protect the parenchyma. Untreated, liver abscess carries a high mortality.

Infection begins when quadrinucleate cysts are swallowed in contaminated food or water. Excystation in the small intestine releases motile trophozoites, which usually stay in the gut lumen and encyst again. Occasionally trophozoites adhere to the colonic epithelium through a galactose/N-acetylgalactosamine-specific lectin, lyse the cells and invade the mucosa, provoking a neutrophilic response. From there they enter the portal circulation and reach the liver, where they cause inflammation and necrosis. Hepatocyte death by apoptosis and necrosis contributes to abscess formation.

• Only E. histolytica is pathogenic; E. dispar and E. moshkovskii are non-pathogenic colonisers. Humans and non-human primates are the only natural hosts.
• Risk factors: travel to or residence in endemic regions (India is among the highest-rate regions), poor sanitation and unsafe water, malnutrition, immunosuppression, alcohol misuse.
• The abscess contains liquefied necrotic hepatocytes with a rim of connective tissue; the trophozoites sit at the periphery, which explains the relatively few organisms in large abscesses and the value of serology rather than aspirate microscopy.
• The hepatocyte injury can occur without direct cell contact — the organism mediates destruction at a distance.

Both types present with fever and right upper quadrant or epigastric pain, with tender hepatomegaly (point tenderness in the right upper quadrant or intercostal spaces). About 80% of amoebic cases become symptomatic within 2 to 4 weeks of exposure, with fever, dull RUQ pain and cough. In pyogenic abscess fever is present in about 90% and abdominal pain in 50–75%; other features include chills, night sweats, anorexia, weight loss, dark urine, jaundice and right shoulder pain from phrenic nerve irritation. A chest X-ray may show a raised right hemidiaphragm or a right pleural effusion.

Appendicitis once was the main cause but now accounts for under 10%. Today biliary tract disease — stones, strictures, malignancy, congenital anomalies — is the major cause, and about half of bacterial cases follow cholangitis. Other sources are portal vein bacteraemia (diverticulitis, bowel leak), hepatic artery bacteraemia, cholecystitis, penetrating trauma and cryptogenic cases. Organisms are mostly polymicrobial (E. coli, Klebsiella, streptococci, staphylococci, anaerobes). If Streptococcus or Staphylococcus grows alone, search for another source such as endocarditis.

*Klebsiella pneumoniae* liver abscess is prominent in Southeast Asia, is typically monomicrobial, occurs on a background of diabetes without underlying hepatobiliary disease, and is associated with colorectal cancer. It can send septic emboli to the eye, meninges and brain, and these problems may persist after the abscess is drained.

• Drainage plus antibiotics are the cornerstones.
• Under 5 cm: needle aspiration (repeated if needed) may be sufficient. Over 5 cm: percutaneous catheter drainage is the most successful approach.
• Empiric antibiotics must cover Enterobacteriaceae, anaerobes, streptococci, enterococci and E. histolytica: a cephalosporin or beta-lactam/beta-lactamase inhibitor plus metronidazole (fluoroquinolone or carbapenem as alternatives). Duration is usually 2 to 6 weeks, switching to oral when stable. Add antifungal cover in immunosuppressed patients at risk of fungaemia.
• Surgery (transperitoneal or posterior transpleural approach) for peritonitis, thick-walled abscess, ruptured abscess, multiple large abscesses or failed drainage; laparoscopic drainage is also used.
• ERCP drainage when there has been previous biliary intervention or a biliary source.

In-hospital mortality is estimated at 2.5% to 19%, higher in elderly patients, those in ICU or in shock, malignancy, fungal infection, cirrhosis, renal failure and a biliary origin. Recurrence is frequent when biliary disease is present.

About 15% of patients do not respond to medical treatment and need aspiration or surgery. Percutaneous drainage (needle aspiration or catheter; catheter drainage gives higher success and faster resolution) is indicated when:

• there is no improvement after 5–7 days of antiamoebic therapy;
• the abscess is at high risk of rupture — larger than 5 cm or in the left lobe;
• there is bacterial co-infection of the amoebic abscess.

Surgery is reserved for multiple loculated or inaccessible abscesses, failure of percutaneous drainage, bacterial superinfection, and rupture into the peritoneum or pericardium, which is a surgical emergency (laparoscopic drainage is preferred when feasible).

An amoebic abscess can rupture into the lung, pleural cavity, pericardium or peritoneum. Abdominal rupture causes peritonitis, shock and death. Cardiac involvement, usually via rupture into the pericardium, can lead to pericarditis, pericardial abscess, tamponade, constrictive pericarditis and heart failure — it carries a high mortality. Rare complications are inferior vena cava or hepatic vein thrombosis and spread to the brain.

More surgery and medicine questions on the liver and biliary tract are collected in NEET PG Surgery PYQs and NEET PG Medicine PYQs; the highest-yield patterns across subjects are on most repeated topics.