Biliary tract infections and liver abscesses. Cholecystitis Cholangitis Liver abscesses - pyogenic liver abscess - amoebic liver abscess Hydatid cyst.

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Presentation transcript:

Biliary tract infections and liver abscesses

Cholecystitis Cholangitis Liver abscesses - pyogenic liver abscess - amoebic liver abscess Hydatid cyst

Acute cholecystitis Acute inflammation of the gallbladder wall Female > male Other risk factors: increasing age, obesity, pregnancy, certain ethnic groups etc.

Pathogenesis Impaction of gallstones in the cystic duct (>90% cases)  Obstruction and dilatation of gallbladder  Vascular congestion and oedema  Necrosis of wall, bacterial proliferation  Complications eg. gangrene, perforation, liver abscess, cholangitis, bacteraemia etc.

Clinical features Epigastric or RUQ pain Nausea, vomitting Fever, anorexia, chills, sweats Moderate pyrexia Local peritonitis, RUQ tenderness (Murphy’s sign) Palpable gallbladder (30-40%) Jaundice unusual

Diagnosis Moderate leukocytosis LFT:  bilirubin (50%), transaminases (40%) & alk phos (25%) Cultures of aspirate/biopsy specimens: - not usually available - enteric organisms: Gram-neg bacilli, anaerobes, enterococci etc. Imaging studies: ultrasound, CT scan

Complications Infection – develops in >50% cases Gangrene/empyema Perforation (10-15%) Obstruction of bile duct; cholangitis; pancreatitis Liver abscess Peritonitis Bacteraemia

Treatment Medical Rx: IV fluids; IV antibiotics; analgesia; anti-emetics; bowel rest (NPO) Surgical Rx: usually cholecystectomy (laparoscopic or open)

Cholangitis Inflammation involving the hepatic and common bile ducts Pathogenesis similar to that of cholecystitis: obstruction of common bile duct  oedema, congestion, necrosis of walls  bacterial proliferation within biliary tree. Causes of obstruction: - gallstones - biliary tract surgery, tumour, parasitic infection, calcific pancreatitis etc.

Clinical features High fever RUQ pain Jaundice (usually prominent) (Charcot’s triad: present in 85% cases) Chills, rigors RUQ tenderness, pale stools Sepsis, septic shock

Complications Bacteraemia (about 50% cases) Liver abscesses Septic shock

Diagnosis Marked leukocytosis Marked  bilirubin, alk phosphatase; moderate  transaminases Blood cultures: - enteric GNB and anaerobes most frequently isolated. Imaging studies: - ultrasound; CT scan - ERCP (endoscopic retrograde cholangio- pancreatography), PTC (percutaneous transhepatic cholangiography)

Treatment Prompt institution of appropriate antimicrobial therapy essential: - initial choice usually empirical - eg. 3 rd gen cephalosporin/quinolones/co- amoxiclav + metronidazole. Surgery: - usually necessary in most patients - decompression & exploration of cbd, T- tube drainage, +/- cholecystectomy.

Liver abscess Relatively rare Described since the time of Hippocrates (400 BC) Remains uniformly fatal if untreated Improvements in radiological, microbiological & drainage techniques have decreased mortality rates to 5-30%.

Epidemiology Incidence (US): 8-16 cases / 100,000 hosp patients Current mortality 5-30% Most commonly in the 6 th /7 th decades of life Right lobe > left lobe (2:1)

Pathophysiology Biliary tract disease (60%) Portal venous system (25%) Haematogenous dissemination Contiguous spread eg. gallbladder Others: trauma-related, post-surgical, secondary infection of tumour/cyst Cryptogenic

Microbiology Pathogens vary according to underlying pathology. GI conditions (via biliary tract or portal vein): - frequently polymicrobial - enteric Gram-negative bacilli eg. E. coli, Klebsiella, Enterobacter spp etc. - Anaerobes eg. Bacteroides & Fusobacterium spp - Others: Strep milleri, Enterococcus, Candida etc. - Entamoeba histolytica (see later)

Haematogenous dissemination: - S. aureus - Streptococci eg. Group A Strep, viridans Strep. - Rarer: GNB; Candida spp.

Clinical features Fever, chills, malaise, anorexia, weight loss Dull RUQ pain at times Diaphragmatic irritation: referred pain (Rt shoulder), cough, pleurisy, hiccups. Solitary lesions tend to have a more insidious course than multiple abscesses Indolent cases can present as PUO (pyrexia of unknown origin)

Pyrexia Tender hepatomegaly Mid-epigastric tenderness (left lobe involvement) Pleural rub, pleural effusion, decreased basal breath sounds Jaundice not often present (25%) – obstructive cholangitis or extensive hepatic involvement

Differential diagnoses Cholecystitis; biliary tract disease Acute gastritis Hepatitis (viral/non-viral) Hepatocellular carcinoma; liver metastases Rt basal pneumonia / empyema Hydatid cyst (see later)

Diagnosis Lab markers: - anaemia +/- leukocytosis -  alkaline phosphatase;  albumin - variable elevations in transaminases & bilirubin - Blood cultures (positive in 50% cases) - Culture of abscess fluid - Anti-amoebic serology

Radiological studies: - Ultrasound, CT scan, radionuclide scan - Chest x-ray Percutaneous needle aspiration (under CT or ultrasound guidance)

Treatment Antibiotics and drainage Antimicrobial therapy: - empirical (based on expected pathogens) - specific (based on culture results) Percutaneous catheter drainage: - ultrasound or CT guidance Open surgery: may be required in difficult cases

Amoebic liver abscess Caused by Entamoeba histolytica Humans acquire organism via ingestion of cysts in faecally contaminated food/fluid. Infection may be asymptomatic; 2 forms of symptomatic disease: - intestinal amoebiasis- amoebic dysentery  colonic mucosal ulcers; bloody diarrhoea - extraintestinal disease- liver abscess; occ. other sites.

Intestinal complications: perforation; toxic megacolon. Liver abscess complications: direct extension, rupture. Diagnosis: - stool examination for cysts/trophozoites. - examination of ‘anchovy paste’ aspirate for trophozoites - serum anti-amoebic antibodies - radiological studies

Rx: metronidazole + lumenal agent (diloxanide) Prevention/control - individual measures - public health measures

Hydatid disease Infestation caused by tapeworm Echinococcus spp, most commonly E. granulosus Endemic areas: Mediterranean countries, Middle East, northern Europe/Asia, southern areas of South America/Africa, Australia/NZ. Canines are definitive hosts for Echinococcus, humans acquire infection via ingestion of food or water contaminated with tapeworm eggs

Adult Echinococcus in canine host  Production and shedding of eggs into environment  Ingestion of eggs via contaminated food/water  Hatching into metacestodes in the GIT  Entry into portal circulation and subsequent infestation of viscera (eg. liver)

Many cysts remain asymptomatic Pressure effects; secondary pyogenic infection Rupture/leakage: risk of anaphylactic reaction and seeding of daughter cysts Diagnosis: imaging + serology Rx: Surgical resection + cysticidal agent; If inoperable  chemotherapy with albendazole or mebendazole