Hepatitis A

Hepatitis A virus (HAV) is a non-enveloped RNA picornavirus transmitted via the fecal-oral route (contaminated food/water, or close personal contact), causing acute, self-limiting hepatitis without progression to chronic infection, in contrast to hepatitis B and C.

Severity and likelihood of symptomatic disease increase with age at infection, most childhood infections are asymptomatic or mild, while adult infection is more often symptomatic and occasionally severe.

A prodrome of fever, malaise, anorexia, nausea, and right upper quadrant discomfort precedes jaundice by several days to a week, followed by dark urine, pale stools, and pruritus as cholestatic features develop.

The illness is typically self-limiting over several weeks, though a prolonged cholestatic phase (weeks to months of persistent jaundice and itching) and, rarely, a relapsing course occur in a minority.

Fulminant hepatic failure is rare (under 1%) but carries significant mortality, more common in older patients or those with underlying chronic liver disease.

Anti-HAV IgM confirms acute infection (positive from symptom onset, persisting for several months); anti-HAV IgG indicates past infection or vaccination and confers lifelong immunity.

LFTs show markedly elevated transaminases (often in the thousands), with bilirubin elevation reflecting the degree of cholestasis.

Coagulation profile (INR) is essential in any significant hepatitis presentation to screen for evolving liver failure.

Supportive care only: rest, hydration, avoidance of hepatotoxic substances (alcohol, unnecessary hepatotoxic medications including, where possible, paracetamol at reduced doses given already-stressed hepatic metabolism), and symptomatic treatment of nausea and pruritus
No specific antiviral treatment exists
Monitor for fulminant hepatitis (worsening jaundice, coagulopathy, encephalopathy) requiring urgent liver unit referral (see Acute Liver Failure entry) if it develops
Prevention: hepatitis A vaccine (inactivated, 2-dose schedule) for travelers to endemic areas, close contacts of a case, and at-risk groups; post-exposure prophylaxis with vaccine (preferred if within 2 weeks of exposure and age 1 to 40 without contraindication) or human normal immunoglobulin (for those outside this range or with contraindications to vaccine) for close contacts
Public health notification (notifiable disease in most jurisdictions) and food handler exclusion until no longer infectious, per local protocol

Referral: hepatology urgently for any evidence of fulminant hepatitis (coagulopathy, encephalopathy).

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Bacterial Overgrowth Syndrome

Small intestinal bacterial overgrowth (SIBO) is excessive proliferation of colonic-type bacteria within the small intestine, normally kept low by gastric acid, intestinal motility, and the ileocecal valve.

Predisposing factors include anatomical abnormalities (surgical blind loops, strictures, diverticula), motility disorders (diabetic autonomic neuropathy, scleroderma, opioid use), achlorhydria (PPI use, atrophic gastritis, prior gastric surgery), and immunodeficiency.

Bloating, abdominal distension and discomfort (often worse after meals), flatulence, diarrhea (from bacterial deconjugation of bile acids impairing fat absorption, causing steatorrhea in more significant cases), and, with chronic disease, malabsorption leading to weight loss and micronutrient deficiency, particularly vitamin B12 deficiency (paradoxically, folate can be normal or elevated, since colonic-type bacteria synthesize folate while consuming B12, a useful distinguishing biochemical pattern from simple dietary B12 deficiency).

Hydrogen/methane breath testing (glucose or lactulose substrate) is the standard non-invasive test, an early rise in breath hydrogen or methane after substrate ingestion supports the diagnosis, though sensitivity and specificity are imperfect
Small bowel aspirate and culture (quantitative bacterial count) is more invasive but more specific where available
B12, folate, and fat-soluble vitamin levels assess for malabsorptive consequences
Investigation for and correction of the underlying predisposing anatomical or motility abnormality

Antibiotic treatment: rifaximin 550 mg PO tds for 14 days is preferred given minimal systemic absorption and good efficacy against the typically anaerobic/coliform overgrowth flora; alternatives include a 10 to 14 day course of a combination or single systemic agent (e.g. ciprofloxacin, co-amoxiclav, or metronidazole) per local practice, particularly if methane-predominant (associated with Methanobrevibacter, sometimes treated with rifaximin plus neomycin)
Recurrence is common, particularly where the underlying predisposing factor (motility disorder, anatomical abnormality) cannot be corrected, and cyclical or recurrent antibiotic courses are often needed
Address the underlying cause where feasible (surgical correction of a blind loop, optimizing diabetic control, reviewing chronic PPI use)
Nutritional support and replacement of deficiencies (B12 IM as per standard protocol, fat-soluble vitamins as needed)
Dietary modification (low FODMAP approaches) may reduce symptom burden as an adjunct, though does not treat the underlying overgrowth itself

Referral: gastroenterology for breath testing, recurrent disease, or where an underlying anatomical/motility cause requires further workup.

Hepatitis A

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management