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 Liver abscesses 

Bacterial abscesses may arise from systemic infection or local portal phlebitis. Common associations include obstructive biliary tree disease (30–40%, often causing multiple abscesses), intra-abdominal infection (15–25%, particularly diverticular disease, appendicitis, inflammatory bowel disease, and colonic malignancy), systemic infection (15–20%, especially infective endocarditis), and direct trauma. Pre-existing liver lesions constitute a significant risk, especially with prior instrumentation or tumour necrosis, e.g. following chemoembolization or radiofrequency ablation of hepatocellular carcinoma.

     Infections are often polymicrobial, with gut-derived Gram-negative bacteria (Escherichia coli, Klebsiella), Grampositive organisms (enterococci, Streptococcus milleri), and anaerobes (Bacteroides). Staphylococcus aureus is common in children. 

Presentation of  Liver abscesses 

• Liver abscesses commonly present with fever and night sweats, weight loss, or right upper quadrant (RUQ) or intercostal pain.

• The underlying cause (e.g. appendicitis) may be silent or barely noticed. Ask about recent abdominal pain, altered bowel habit, diarrhoea, biliary colic, rectal bleeding, or inflammatory bowel disease.

• The travel history, occupation (farming is a risk factor for amoebiasis), or contact with infected persons (TB) may help.

• Examine for jaundice, hepatomegaly, pleural effusions (commonly right-sided), intercostal tenderness (characteristic of amoebic abscesses), abdominal masses (tumour or inflammatory mass), and lymphadenopathy. Perform a rectal examination for pelvic tumour.

•  Severe infection may be associated with septic shock. 

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Causes of  Liver abscesses 

•  Pyogenic organisms (appendicitis, diverticulitis, carcinoma, biliary).

•  Amoebic abscess (Entamoeba histolytica).

•  Hydatid cyst (Echinococcus granulosus).

•  Tuberculosis (TB, very rare).

Investigations of  Liver abscesses 

Biochemistry including U&Es detects renal impairment due to sepsis. LFTs typically show an elevated ALP and reduced albumin. Non-specific LFTs are usually due to cholestasis and may be normal with amoebic abscess. Inflammatory markers (WCC, CRP, and ESR) are often raised. Blood cultures are positive in 50–80%.

• Prothrombin time may be prolonged with multiple abscesses.

• FBC (leucocytosis, eosinophilia, non-specific anaemia).

• Blood cultures, CRP, ESR.

• Amoebic and hydatid serology. ELISA for E. histolytica should be performed in travellers from endemic regions.

• Stool may contain amoebic cysts or vegetative forms.

• CXR (looking for effusion or pulmonary TB). CXR may demonstrate a raised right hemidiaphragm, pleural effusion, or right lower lobe consolidation.

• USS of liver, biliary tree, and abdomen (iliac fossae, in particular). Ultrasound has a sensitivity of 80–90%. The main differential is a simple cyst; abscesses appear as hypoechoic masses with irregular borders. Ultrasound also allows close evaluation of the rest of the biliary tree.

• CT scan with contrast, looking for masses, and sensitivity is almost 100%. Both pyogenic and amoebic abscesses tend to be thick-walled; hydatid cysts are thin-walled, and there may be daughter cysts. Solid tumours are echodense but may have necrotic hypodense centres.

• Gallium scans (or indium-111 labelled WBC scans) will show up pyogenic foci in the liver and elsewhere (e.g. terminal ileitis); amoebic abscesses do not take up the label.

• Aspirate large abscesses, and send the aspirate/pus for Gram stain and culture. If there is a suspicion of hydatid disease, aspiration is contraindicated.

• The primary site of infection should be carefully sought, with a low threshold for echocardiogram and colonoscopy.

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Management of  Liver abscesses 

•  Antibiotics should initially be given empirically to cover the broad spectrum of organisms above (e.g. cefuroxime and metronidazole, or piperacillin-tazobactam), then adjusted, according to sensitivities. Treatment should be continued for 2 weeks intravenously, then 6 weeks orally.

• Aspirate any large abscesses under USS. It is pointless to try and drain multiple abscesses. If there is a continuing intra-abdominal source, it is virtually impossible to eradicate liver abscesses without removing or dealing with the source (e.g. appendix).

• Pyogenic abscess: perform percutaneous aspiration of any large abscesses. Commence broad-spectrum antibiotics (e.g. cefotaxime and metronidazole).

• Amoebic abscess: treat with metronidazole (or tinidazole), followed by diloxanide furoate. USS-guided aspiration may help to improve penetration of the drugs and shorten illness (see Chapter 6). Secondary bacterial infection occurs in up to 20%.

•  Hydatid disease: open surgical drainage is the treatment of choice. Albendazole may help to reduce the risk of recurrence post-surgery or be used in inoperable cases.

• Anti-tuberculous therapy for tuberculous abscesses.

• Surgery is rarely required but may be indicated for abscesses that are >5 cm, multiloculated, or ruptured.

Complications of  Liver abscesses 

• Sepsis.

•  Empyema.

• Peritonitis.

• Endophthalmitis (particularly with Klebsiella bacteraemia).

Prognosis

Treatment is successful in 80–90%, although abscesses may take weeks to months to resolve. Be guided clinically, rather than radiologically. Nonetheless, mortality is high in children and the elderly, as well as those with severe comorbidity or delayed diagnosis.