Your next patient felt sick and off his food for 2 weeks, and now he’s looking yellow with dark urine. Here's how the hepatitis A case unfolds and what to pick up on the way.

This hepatitis a case is easy to misread because the prodrome is vague and the patient often feels better once jaundice appears. Two weeks of exhaustion, nausea and being off all food, even off cigarettes, then dark tea coloured urine and yellow eyes can be written off as a viral upset just as he starts to perk up.

Backpacking in South Asia with street food and tap water sits neatly within the 2 to 6 week incubation. This page walks through the presentation, the history to pick up, the tests and the teaching points. We focus on the biphasic course, how to separate hepatocellular from obstructive patterns on bloods and ultrasound, why to check the clotting with INR as the earliest sign of synthetic failure, and how Anti-HAV IgM confirms acute infection while IgG alone means past infection or vaccination.

How the case presents

Your next patient felt sick and off his food for 2 weeks, and now he’s looking yellow with dark urine. In their own words: "Two weeks of feeling sick and off his food, and now he has turned yellow."

Observations on arrival:

Observation	On arrival
Heart rate	74 beats per minute
Blood pressure	116/72 mmHg
Respiratory rate	14 breaths per minute
Oxygen saturation	99%
Temperature	37.3 °C

What to pick up in the history

These are the findings the case is built around. Each one moves you towards or away from hepatitis A, and the scorecard checks whether you found it.

Two weeks of exhaustion, nausea and malaise: A subacute prodrome fits viral hepatitis rather than biliary colic or a sudden toxic insult.
Off all food and off cigarettes, very unlike him: profound anorexia with distaste for cigarettes is a classic viral hepatitis prodrome.
Dark tea-coloured urine for three to four days: conjugated bilirubinuria localises the jaundice to hepatic or post-hepatic causes, not haemolysis.
Yellow eyes and skin noticed two days ago: confirms jaundice and dates the icteric phase, which drives infectivity and work exclusion advice.
He feels better since the jaundice appeared: the biphasic course is typical of acute viral hepatitis and argues against obstruction or sepsis.
Backpacking in South Asia, street food and tap water: faecal-oral exposure five weeks ago fits the hepatitis A incubation period exactly.
No confusion, drowsiness or altered sleep pattern.

Red flags you must not miss

The case marks these as must-elicit. They only come out if you ask.

He drinks about six to eight units of alcohol a week and has not been binge drinking. He has not touched alcohol for two weeks because it makes him feel sick.
No confusion, drowsiness or altered sleep pattern.
He has had no unusual bruising, nosebleeds or bleeding gums, and no black or bloody stools.

Investigations and what they showed

Liver function tests: ALT 2,180 U/L and AST 1,540 U/L (both in the thousands), bilirubin 168 µmol/L, ALP only 145 U/L, albumin 41 g/L (normal). Why it helps: this is the pattern that makes the diagnosis a category rather than a guess: transaminases in the thousands with a comparatively modest ALP is a hepatocellular injury, viral, drug/toxin or ischaemic, whereas an obstructed biliary tree raises the ALP disproportionately. A normal albumin says the liver's synthetic function is intact and that this is an acute insult, not chronic disease.
Prothrombin time / INR: 0, entirely normal. Why it helps: the single most important prognostic test in acute hepatitis. Clotting factors have a short half-life, so the INR is the earliest marker of failing synthetic function.
Hepatitis A serology: Anti-HAV IgM positive (IgG not yet detectable), confirms acute hepatitis A infection. Why it helps: the decisive test. IgM anti-HAV indicates acute infection, whereas IgG alone would indicate past infection or vaccination. It fits the incubation period (roughly 2 to 6 weeks after faecal-oral exposure), the street food and unvaccinated travel, and the unwell travelling companions.
Split bilirubin: Total 168 µmol/L with conjugated 122 µmol/L (about 73%), a predominantly conjugated hyperbilirubinaemia. Why it helps: conjugated bilirubin is water-soluble, so it spills into the urine (dark urine), this is what separates hepatic/post-hepatic jaundice from an unconjugated picture such as haemolysis or Gilbert's syndrome, where the urine stays normal in colour.
Hepatitis B serology: HBsAg negative, anti-HBc negative, anti-HBs negative, no current or past infection, and no immunity. Why it helps: hepatitis B causes an identical clinical picture but can become chronic, so it must be excluded rather than assumed away. The negative anti-HBs is also actionable: he is not immune and should be offered hepatitis B vaccination.
Urine dipstick / urinalysis: Bilirubin ++ and raised urobilinogen; no blood, no protein, no nitrites or leucocytes. Why it helps: A thirty-second bedside test that explains the dark urine: conjugated bilirubin is water-soluble and appears in the urine. The absence of blood also excludes haemoglobinuria/myoglobinuria as a cause of dark urine, which is the common trap when a patient says 'my wee has gone brown'.
Ultrasound abdomen: 4 cm craniocaudal in the mid-clavicular line, smooth outline, with a diffusely darker (hypoechoic) parenchyma against which the walls of the portal vein branches stand out as bright white specks scattered through the liver, the 'starry SKY' appearance. The gallbladder is collapsed and its wall is thickened and layered at 6 mm, with no stones, no sludge and a negative sonographic Murphy's sign. Common bile duct 3 mm (not dilated); portal vein patent with normal hepatopetal flow; spleen normal; no ascites; no focal liver lesion. Why it helps: it answers two separate questions. The structural one first, because it must be answered in every jaundiced patient: the ducts are not dilated and there are no stones, so this is not mechanical obstruction, which matches the nearly spared ALP and leaves ERCP with no role. It also excludes a liver abscess, a mass and the nodular shrunken outline of established cirrhosis. The second is that the liver itself looks acutely inflamed. Oedematous hepatocytes lower the background echogenicity, so the portal triad walls that are normally lost in it become visible as bright dots, that is all the starry sky is, and it is suggestive rather than specific, being seen in any acute hepatitis and in acute right heart failure.
Inspect the sclera: Both scleras are unmistakably yellow against otherwise healthy-looking eyes, icterus visible in ordinary daylight, with clear corneas and normal pupils. Why it helps: the sclera is where jaundice shows first and most reliably, because scleral collagen binds bilirubin avidly, it is detectable there from roughly 40 to 50 µmol/L, well before the skin looks yellow. Look in natural light and look at the sclera, not the skin, in patients with darker skin tones.
Inspect the patient's colour: Generalised yellow discolouration of the skin as well as the sclerae, a deep golden-yellow across the face and neck. He is otherwise well perfused, not pale, not grey and not cyanosed. Why it helps: generalised jaundice confirms a substantial bilirubin and, with dark urine and pale stools, places the problem in the liver or the bile ducts. Note what is not there: no bronze or slate-grey pigmentation of haemochromatosis, no pallor to suggest a haemolytic cause.
Inspect the urine: A specimen pot of dark, deep amber-brown urine, the colour of strong tea or cola, clear rather than cloudy, with no visible blood. Why it helps: dark urine in jaundice means conjugated (water-soluble) bilirubin is being excreted by the kidneys, so the jaundice is hepatic or post-hepatic. Unconjugated jaundice, haemolysis, Gilbert's, leaves the urine a normal colour. The dipstick then makes it objective: bilirubin positive.
Inspect the stool: Pale, putty or light clay-coloured stool with a bulky, greasy appearance, much lighter than his normal. Why it helps: pale stools mean less bilirubin is reaching the gut to be converted to stercobilin, which is what normally colours the stool. Paired with dark urine this is the classic couplet of cholestasis, but note that it occurs in hepatitic as well as obstructive disease, so it does not by itself mean a blocked duct.
Inspect the abdomen: A flat, non-distended abdomen with a yellow tinge to the skin. There is fullness under the right costal margin on deep inspiration, where a smooth liver edge is palpable about 3 cm below the ribs and is tender. No visible distension, no shifting dullness, no dilated periumbilical veins. Why it helps: A smooth, tender, mildly enlarged liver is the expected finding in acute hepatitis, the capsule is stretched by an inflamed liver, which is what produces his right upper quadrant ache. A hard, knobbly or grossly enlarged liver would point elsewhere entirely.
Inspect the patient's level of alertness and demeanour: This is the safety assessment, and it is done by watching and talking rather than by testing. Encephalopathy, even subtle inattention, reversed sleep pattern or asterixis, combined with a rising INR defines acute liver failure and mandates urgent transfer to a liver unit.

Imaging findings

CT abdomen and pelvis: Not needed here, and if it has already been done for the abdominal pain it shows: a mildly enlarged liver whose parenchyma is diffusely lower in attenuation than normal, it loses its crisp uniform density and looks flat and muddy, so that the hepatic vessels appear relatively bright against it, with periportal oedema, a low-attenuation cuff of fluid tracking along the portal vein branches out from the hilum. The gallbladder wall is thickened, there are a few mildly prominent portacaval nodes, and the biliary tree, pancreas, bowel and appendix are all normal, with no ascites and no focal lesion.
MRCP: Normal biliary tree, no duct dilatation, no filling defects, no strictures; pancreatic duct normal.

Why the diagnosis is hepatitis A

The decisive diagnosis is hepatitis A, a faecal-orally acquired acute viral hepatitis in an unvaccinated traveller who ate street food in an endemic area. The story is the classic biphasic one: a one-to-two-week prodrome of nausea, profound anorexia (classically including a distaste for cigarettes), malaise, low-grade fever and right upper quadrant ache, followed by dark urine, pale stools and jaundice, at which point the patient starts to feel better. Examination shows a smooth, tender, mildly enlarged liver with no stigmata of chronic disease. The biochemistry seals the category: ALT and AST in the thousands with a relatively spared ALP is hepatocellular injury, not obstruction, and the ultrasound confirms non-dilated ducts. Anti-HAV IgM is positive.

Hepatitis A at a glance

What it is

Hepatitis A is an acute liver infection caused by the hepatitis A virus (HAV), spread by the faecal-oral route through contaminated food or water. It runs a characteristic biphasic course: a one-to-two-week prodrome of nausea, profound anorexia (classically a distaste for cigarettes in a smoker), malaise, low-grade fever and right-upper-quadrant ache, followed by dark urine, pale stools and jaundice, and patients typically feel better once the jaundice appears.

Pathogenesis

After faecal-oral exposure, HAV replicates in the gut before reaching the liver, where it infects hepatocytes. Liver injury is caused mainly by the immune response to infected cells rather than direct viral cytotoxicity, producing widespread hepatocyte inflammation and death. This.

Hepatocellular disruption releases transaminases in large amounts and impairs bilirubin conjugation and excretion, producing conjugated.

Hyperbilirubinaemia: dark urine, pale stools and jaundice.

Who it affects

Linked to travel to areas with poor sanitation, contaminated water, street food and shellfish, and to close contact with an infected person; incubation is roughly two to six weeks after exposure. It affects all ages but is often more symptomatic in adults than young children, who are more often subclinical.

How serious it is

The great majority make a full recovery and the infection never becomes chronic. A normal INR in an alert patient is the reassuring finding.

Causes and risk factors

Faecal-oral transmission from contaminated water, food (especially shellfish and produce washed in unclean water) and close contact with an infected person are the main routes; travel to endemic regions without prior vaccination is the classic setting.

Investigations and lab tests

ALT and AST in the thousands indicate a hepatocellular pattern of injury (viral, drug/toxin, or ischaemic); a disproportionately raised ALP with dilated ducts on ultrasound points to an obstructive picture instead. Anti- HAV IgM confirms acute hepatitis A, while IgG alone reflects past infection or vaccination. Ultrasound in acute hepatitis classically shows a "starry sky" liver, hypoechoic, oedematous parenchyma against bright portal triads.

At a glance: Confirms the diagnosis: anti-HAV IgM. Full hepatitis screen: A, B, C and E (B and C can become chronic; E is clinically identical to A). Vaccinate if anti-HBs is negative.

Teaching points

Acute viral hepatitis runs a characteristic biphasic course: a one-to-two-week prodrome of nausea, profound anorexia (classically a distaste for cigarettes), malaise, low-grade fever and right upper quadrant ache, then dark urine, pale stools and jaundice, and the patient typically feels better once the jaundice appears.
An obstructive picture raises the ALP disproportionately and dilates the bile ducts on ultrasound. Deciding which pattern you are looking at is the core skill in any jaundiced patient.
Check the clotting. The INR is the earliest and most important marker of hepatic synthetic failure.
Anti-HAV IgM confirms acute hepatitis A; IgG alone indicates past infection or vaccination. Incubation is roughly 2 to 6 weeks after faecal-oral exposure, which fits travel, street food, contaminated water and shellfish.
Hepatitis A is self-limiting and never becomes chronic.
Send the whole acute hepatitis screen, A, B, C and E, because B and C can become chronic and E is clinically identical to A. A negative anti-HBs is also an opportunity: vaccinate.
Acute hepatitis A is a notifiable disease.
Food handlers, healthcare workers and childcare staff must be excluded from work until at least 7 days after the onset of jaundice, ask what the patient does for a living.
In any febrile returning traveller, exclude malaria with thick and thin films before settling on a benign diagnosis; jaundice with fever after travel is falciparum malaria until proven otherwise.
Dark urine plus pale stools means conjugated bilirubin is spilling into the urine and not reaching the gut, it points to hepatic or post-hepatic jaundice and away from haemolysis or Gilbert's syndrome.
Prevention is the real lesson: pre-travel hepatitis A vaccination is highly effective and this illness was entirely avoidable, counsel him and his contacts about vaccination and food and water precautions before the next trip.

Practise a similar case

Reading a case is one thing, asking the right questions under a bit of pressure is another. When the clock is ticking, remember to ask about travel exposures like street food and tap water, and to confirm dark tea-coloured urine and that he felt better once the jaundice appeared. Now try a fresh gastro history.

Here's one from the same specialty, with the diagnosis left for you to find. Your next patient is a 24-year-old man with vomiting and diarrhoea for 2 days and wants to know why. Take this patient's history in Diagnosica. It's free to start, no card needed.

Hepatitis A case presentation: history, findings and tests