Alcoholic hepatitis case presentation: history, findings and tests

This alcoholic hepatitis case is easy to miss because he says he stopped drinking ten days before he became ill, and the jaundice has crept in over three weeks rather than during a binge. Your next patient has turned yellow with soreness under his right ribs and a swollen belly. The history holds traps: a past withdrawal seizure, recent hallucinations, shivery and hot with no source, and no paracetamol overdose, new drugs or herbal remedies.

This page walks through how the case presents, what to pick up in the history, the tests and the teaching points. Expect the biochemical signature with modest transaminases and an AST:ALT pattern, why numbers in the thousands point elsewhere, and why symptoms often begin after drinking stops. This man scores 52.

How the case presents

Your next patient has turned yellow over 3 weeks with soreness under his right ribs and a swollen belly. In their own words: "He has turned yellow over a few weeks and is sore under his right ribs."

Observations on arrival:

What to pick up in the history

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

• Yellow for three weeks, eyes first then the skin: deep jaundice over weeks drives both the Maddrey score and the search for a hepatocellular cause.
• Right upper quadrant ache with a swollen belly.
• Nothing to drink for ten days before he became ill: alcoholic hepatitis characteristically declares itself after cessation, so abstinence is part of the story, not against it.
• Withdrawal seizure three years ago, recent hallucinations.
• Shivery and hot with no obvious source of infection.

Red flags you must not miss

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

• Nothing to drink for ten days before he became ill.
• An urgent care doctor saw him four days ago and told him it was 'probably a gallstone' and to see his GP.
• Asked about it directly, he admits he drinks first thing in the morning to stop the shakes, has tried and failed to cut down several times, gets annoyed when family mention it, and feels guilty about it.
• Withdrawal seizure three years ago, recent hallucinations.
• Shivery and hot with no obvious source of infection.
• He has not vomited blood and has not passed black tarry stools.
• He has never been offered help with the drinking, has never seen an alcohol service, and has never had a hepatitis jab.

Investigations and what they showed

• Liver function tests: 7), ALP 178 U/L, GGT 940 U/L, albumin 24 g/L. Why it helps: this single panel is the diagnosis. The signature of alcoholic hepatitis is modestly raised transaminases, almost always under 300, with an AST:ALT ratio greater than 2, a disproportionately high bilirubin and a markedly raised GGT.
• Aspartate aminotransferase: 168 U/L, raised, but only modestly. Why it helps: AST is preferentially raised in alcohol-related liver injury because of mitochondrial damage and pyridoxine deficiency. The absolute number is unimpressive; it is the ratio to ALT that carries the information.
• Alanine aminotransferase: An AST:ALT ratio above 2 is close to specific for alcohol-related liver injury; above 3 it is almost diagnostic.
• Bilirubin: Total 312 µmol/L and rising, grossly elevated and out of all proportion to the transaminases. Why it helps: the bilirubin is both the clinical signature and one of the two variables that drive every severity score.
• Prothrombin time / INR: The prothrombin time is the best real-time measure of hepatic synthetic function and the second variable in the severity score.
• Albumin: 24 g/L, markedly low. Why it helps: reflects both impaired synthesis and profound malnutrition, and contributes to the ascites and oedema. It also feeds the Glasgow alcoholic hepatitis score alongside age, white cell count, urea, bilirubin and prothrombin time.
• Full blood count: 4 × 10⁹/L, Hb 104 g/L, MCV 104 fL (macrocytic), platelets 92 × 10⁹/L. Why it helps: A neutrophil leucocytosis in the absence of infection is characteristic of alcoholic hepatitis and is itself a marker of severity, but it is also exactly what sepsis looks like, which is why infection must be actively excluded rather than assumed away. The raised MCV reflects alcohol and folate deficiency; the low platelets reflect alcohol-induced marrow suppression, folate deficiency and hypersplenism.
• Gamma-glutamyl transferase: 940 U/L, markedly raised. Why it helps: GGT is induced by alcohol and, in a picture with modest transaminases and a huge bilirubin, a very high GGT strongly supports an alcohol-related cause. It is a supportive marker, not a proof of current drinking, it stays up for weeks after stopping, which is another reason his ten days of abstinence do not exonerate alcohol.
• Urea and electrolytes: 4 mmol/L. Why it helps: hyponatraemia is usual in decompensated liver disease; hypokalaemia is near-universal in heavy drinkers and worsens hepatic encephalopathy. Urea is also a variable in the Glasgow alcoholic hepatitis score.
• Creatinine: 118 µmol/L, up from a baseline of 74 six months ago. Why it helps: A rising creatinine in severe alcoholic hepatitis is ominous, it signals developing acute kidney injury and hepatorenal syndrome, the commonest way these patients die.
• Capillary blood glucose: 6 mmol/L, low. Why it helps: hypoglycaemia is common in alcohol-related liver disease from depleted glycogen and impaired gluconeogenesis, and must be looked for and corrected.
• Magnesium: 56 mmol/L, low. Why it helps: hypomagnesaemia is near-universal in chronic heavy drinkers, causes refractory hypokalaemia and hypocalcaemia, lowers the seizure threshold during withdrawal, and must be replaced before the potassium will correct.
• Phosphate: 58 mmol/L, low. Why it helps: A malnourished man who is about to be fed is at high risk of refeeding syndrome. Baseline phosphate, potassium and magnesium must be measured and replaced, and monitored daily as nutrition is started.
• Potassium: 1 mmol/L, low. Why it helps: hypokalaemia worsens hepatic encephalopathy by increasing renal ammonia production, and will not correct until the magnesium is replaced.
• Ultrasound abdomen: An enlarged, diffusely bright (echogenic) liver with a coarse heterogeneous texture and a slightly nodular outline, moderate ascites, a mildly enlarged spleen, and no focal liver lesion. Doppler shows a patent portal vein with normal hepatopetal flow and patent hepatic veins. no intrahepatic or extrahepatic biliary dilatation. Only limited collaterals are seen at the splenic hilum, ultrasound routinely understates the collateral network. Why it helps: ultrasound is the first-line imaging in jaundice and its job here is subtractive: it excludes biliary obstruction (which is what the urgent care doctor's 'gallstone' label predicted), excludes a liver mass, and, with Doppler, excludes portal vein thrombosis and Budd-Chiari syndrome as causes of acute decompensation with ascites. What it shows positively is a fatty, chronically injured liver with portal hypertension. Ultrasound cannot diagnose alcoholic hepatitis; it makes the diagnosis defensible by removing the alternatives. What ultrasound does poorly is map the collateral circulation and characterise a focal lesion; if either question is left open, that is when cross-sectional imaging earns its place, bearing in mind his rising creatinine when contrast is proposed.
• Inspect the sclera: Deep, unmistakable yellow discolouration of both scleras, visible from the end of the bed. Why it helps: scleral icterus is the earliest reliable place to see jaundice and appears once the bilirubin exceeds roughly 40 to 50 µmol/L.
• Inspect the patient's colour: Generalised deep jaundice of the skin, most obvious on the face, neck and upper chest, with a slightly greenish cast; there are scratch marks over the forearms. Why it helps: whole-body jaundice of this depth in a man of 49 narrows the field immediately to liver failure, severe hepatitis or biliary obstruction.
• Inspect the abdomen: The abdomen is distended with a full, tense contour and flanks that bulge when he lies flat; the skin is stretched and shiny. There is visible fullness in the right upper quadrant and he flinches when the area below the right costal margin is touched, a tender, enlarged liver. Why it helps: ascites with a tender hepatomegaly is the combination that should push you past 'decompensated cirrhosis' towards an acute inflammatory hepatitis on top of it. A cirrhotic liver alone is usually small, shrunken and painless; a large, sore liver means something acute is happening inside it.
• Inspect the umbilicus: Caput medusae is portosystemic collateral flow through recanalised umbilical veins and is direct visual proof of portal hypertension. It establishes that the liver disease is chronic and established, which reframes today's jaundice as an acute event superimposed on cirrhosis, and it predicts the oesophageal varices that will need surveillance once he is stable.
• Inspect the palms: Both palms are diffusely RED over the thenar and hypothenar eminences, sparing the central palm, palmar erythema. The nails are pale and whitened. Why it helps: palmar erythema reflects the hyperdynamic circulation and altered oestrogen handling of chronic liver disease. On its own it is soft, it occurs in pregnancy, thyrotoxicosis and rheumatoid arthritis, but as one of a cluster with spider naevi, gynaecomastia and Dupuytren's it builds an unmistakable chronic liver picture at the bedside, before a single blood test returns.
• Inspect the hands: A firm nodule in the palmar fascia at the base of the ring finger with a puckered cord running distally and fixed flexion of the ring and little fingers, dupuytren's contracture. The fingertips show no clubbing. Why it helps: dupuytren's contracture has a well-recognised association with alcohol and alcohol-related liver disease, and its presence quietly corroborates a drinking history the patient is minimising. The absence of clubbing is worth noting too: clubbing occurs in chronic liver disease but is not required, and its absence must not be used to argue against the diagnosis.
• Inspect the upper limbs: With the arms outstretched, wrists dorsiflexed and fingers spread, there is a coarse, irregular flapping tremor, the hands drop and are jerked back every few seconds. asterixis is present but mild, and there is no resting tremor. Why it helps: asterixis is a negative myoclonus, a momentary loss of postural tone, and is the bedside sign of early hepatic encephalopathy.
• Inspect the chest wall: Multiple spider naevi over the upper chest, shoulders and neck, central arterioles a few millimetres across with radiating legs, each blanching from the centre outwards on pressure and refilling from the centre. There are more than a dozen. Why it helps: more than five spider naevi in the superior vena caval distribution is significant and correlates with the severity of liver disease. The refill-from-the-centre test distinguishes them from telangiectasia and from Campbell de Morgan spots. Alongside the caput medusae, they date the liver disease as chronic.
• Inspect the chest: Bilateral gynaecomastia with palpable glandular tissue behind both nipples, and marked loss of body hair over the chest and axillae. Why it helps: gynaecomastia, testicular atrophy and loss of body hair reflect the feminisation of chronic liver disease, impaired hepatic oestrogen metabolism, made worse by alcohol's direct gonadal toxicity and by spironolactone if he is already taking it. It is another chronic-disease marker in a man whose acute problem is the hepatitis on top.
• Inspect the ankles: Bilateral pitting oedema to mid-shin, leaving deep thumbprints that are slow to refill; the skin is shiny and taut. Why it helps: oedema here is the peripheral counterpart of the ascites, a low albumin of 24 g/L plus portal hypertension and secondary hyperaldosteronism. It matters practically because it tempts the reflex of diuresis, which in a man with a creatinine already climbing from 74 to 118 risks tipping him into hepatorenal syndrome.
• Inspect the tongue: The tongue is smooth, red and depapillated with a glazed dorsum, glossitis, and there are cracked, sore fissures at both angles of the mouth. Why it helps: atrophic glossitis and angular cheilitis are the visible face of the B-vitamin and folate deficiency that is universal in men who obtain most of their calories from alcohol.
• Inspect the patient's body habitus: Striking sarcopenia, hollowed temples, wasted shoulder girdle and deltoids, prominent clavicles and ribs, and thin limbs, carried above a grossly distended abdomen. He looks, as his family put it, 'like a spider'. Why it helps: this mismatch, a swollen belly on a wasted frame, is the physical definition of the malnutrition that dominates outcome in alcoholic hepatitis. Weight and BMI are useless here because the ascites conceals the wasting.
• Inspect the patient's level of alertness and demeanour: He is drowsy but rousable and fully orientated in time, place and person, with a slightly slowed response and a reversed sleep pattern reported by his brother. He is quiet, avoids eye contact, and becomes guarded when alcohol is mentioned, but answers honestly if asked directly and without judgement. Why it helps: two things are being read at once. Clinically, this is grade 1 hepatic encephalopathy, day-night reversal and slowed cognition with preserved orientation, which is enough to change the choice of benzodiazepine and to prompt a hunt for precipitants, but is not the florid confusion of case 10.
• Inspect the mucous membranes: The conjunctival membranes and oral mucosa are pale, consistent with a haemoglobin of 104 g/L, and the mucosa is dry. There are no petechiae, no gum bleeding and no bruising over the pressure points. Why it helps: the pallor reflects the macrocytic anaemia of alcohol and folate deficiency. 9 and a platelet count of 92, you are actively looking for mucosal bleeding, purpura and bruising, their absence is what makes an ascitic tap safe to perform, and their appearance would change the whole risk calculation.

Imaging findings

• CT abdomen and pelvis with contrast (staging): Performed only after the renal risk is weighed. The liver is diffusely low in attenuation, darker than the spleen on the same slice, from macrovesicular fat and hepatocyte swelling, with a coarse, mildly nodular contour and a hypertrophied caudate lobe. Bands of low attenuation track along the central hepatic veins (pericentral oedema). There is moderate ascites, a mildly enlarged spleen, and an extensive network of tortuous, serpiginous collateral varices, para-oesophageal, gastric fundal and a recanalised paraumbilical vein, mapping severe portal hypertension. no arterially enhancing focal lesion with washout, no portal or hepatic vein thrombus, no biliary dilatation.
• MRI abdomen / liver: The alternative when iodinated contrast is unwise. Chemical-shift imaging shows a marked drop in liver signal on opposed-phase compared with in-phase sequences, confirming diffuse fat; T2-weighted images show high signal in the pericentral zones (oedema). The liver outline is nodular with caudate hypertrophy, and there is ascites, splenomegaly and a mass of flow voids from para-oesophageal and gastric collaterals. no focal lesion showing the arterial hyperenhancement with portal-venous washout of hepatocellular carcinoma. MRCP sequences show a normal-calibre, non-dilated biliary tree with no stone and no stricture.
• X-ray chest: Clear lung fields, no consolidation, no effusion, normal heart size.
• Histology / biopsy: If performed (transjugular route, because the prothrombin time is prolonged and there is ascites): macrovesicular steatosis, hepatocyte ballooning, a neutrophil infiltrate and eosinophilic mallory-denk bodies within ballooned hepatocytes, on a background of pericellular 'chicken-wire' fibrosis and established cirrhosis.
• OGD / gastroscopy: Small grade 1 oesophageal varices with no red signs; no ulcer and no bleeding stigmata.

Why the diagnosis is alcoholic hepatitis

7), GGT 940, albumin 24, a prolonged prothrombin time and a neutrophil leucocytosis. The trap this case is built around is the ten days of abstinence: alcoholic hepatitis characteristically declares itself after drinking stops or is reduced, not in the middle of a binge, and learners who accept 'but I've stopped' as exculpatory go looking for a gallstone or a virus instead. 'alcohol-related liver disease' earns real partial credit, it correctly identifies the aetiology and the organ, and it will not lead to any actively harmful decision. e.

Alcoholic hepatitis at a glance

What it is

Alcoholic hepatitis is acute inflammation of the liver caused by heavy alcohol use, ranging from mild derangement of liver biochemistry to florid jaundice, coagulopathy and death. It characteristically presents after drinking has stopped or been reduced, often days to weeks after the last drink, because the patient felt too unwell to continue or was told to stop, "I haven't touched a drop in ten days" is part of the typical story, not evidence against the diagnosis.

Pathogenesis

Alcohol metabolites directly injure hepatocytes and trigger a neutrophilic inflammatory response, producing hepatocyte ballooning, steatosis and, in established disease, Mallory-Denk bodies. The biochemical signature is distinctive: transaminases are usually only modestly raised (AST and ALT typically under 300), with an AST:ALT ratio above 2, alongside a very high bilirubin, a raised GGT and a low albumin.

Who it affects

People with a history of heavy, sustained alcohol intake, typically presenting in middle age. It sits on a spectrum with fatty liver and cirrhosis, and can occur with or without established cirrhosis underneath it.

How serious it is

Severe alcoholic hepatitis kills roughly 30 to 40% of patients within 28 days, which is why the acute event must be named specifically rather than folded into a vaguer label like "alcohol-related liver disease".

Causes and risk factors

Sustained heavy alcohol intake is the cause. There is no safe threshold that guarantees protection, though risk rises with the quantity and duration of drinking.

Investigations and lab tests

Send bilirubin, transaminases, GGT, albumin and clotting to calculate the severity score. In anyone with ascites, a diagnostic ascitic tap with a neutrophil count is mandatory: 250/mm³ or more is spontaneous bacterial peritonitis whatever the culture grows. A non-invasive liver screen and an ultrasound with Doppler exclude the structural mimics, alcohol is a diagnosis you demonstrate.

Teaching points

• The biochemical signature: alcoholic hepatitis gives only modestly raised transaminases, AST and ALT are usually under 300, with an AST:ALT ratio above 2, alongside a very high bilirubin, a raised GGT, a low albumin and a neutrophil leucocytosis. 4.
• Transaminases in the thousands are not alcohol. If the numbers are that high, stop and rethink.
• Alcoholic hepatitis characteristically presents after drinking stops or is reduced, not during a binge, often days to weeks after the last drink, because the patient felt too ill to drink or was told to stop. 'I haven't touched a drop in ten days' is part of the typical story, not evidence against the diagnosis.
• This man scores 52.
• Severe alcoholic hepatitis kills roughly 30 to 40% of patients within 28 days. That is why the acute event has to be named, not folded into 'alcohol-related liver disease' or 'decompensated cirrhosis'.
• Blood cultures, chest X-ray, urinalysis and, in anyone with ascites, a diagnostic ascitic TAP with a neutrophil count. An ascitic neutrophil count of 250/mm³ or more is spontaneous bacterial peritonitis whatever the culture grows.
• A previous withdrawal seizure means withdrawal must be anticipated, not observed.
• Do not restrict protein. Inadequate calorie intake independently predicts death.
• Start it in hospital: alcohol liaison referral while he is an inpatient, motivational rather than moralising, with community follow-up and peer support arranged before discharge.
• Alcohol is a diagnosis you demonstrate, not one you assume, and a raised ferritin in an acute hepatitis is an acute-phase reactant, not haemochromatosis.
• Request the ultrasound with doppler. It excludes biliary obstruction, a liver mass, portal vein thrombosis and Budd-Chiari, the structural mimics, and demonstrates the fatty, chronically injured liver underneath. It cannot make the diagnosis; it makes it defensible.
• Watch the creatinine. A rising creatinine signals acute kidney injury and hepatorenal syndrome, the commonest cause of death here; avoid nephrotoxics and NSAIDs, use albumin, and escalate early.
• Biopsy is the reference standard but is rarely needed when the picture is typical, and if it is needed with a prolonged prothrombin time and ascites, it must be transjugular. The histology shows steatosis, ballooned hepatocytes, a neutrophil infiltrate and mallory-denk bodies.

Practise a similar case

Reading a case is very different from being the one who has to ask, in order, and catch a line like, “I haven’t touched a drop for ten days.” Under a little time pressure, you decide what to chase and what to park. Try taking a history from another gastro patient and put that into practice.

Here's one from the same specialty, with the diagnosis left for you to find. Your next patient’s wife says he has become confused and very sleepy over 3 days. Take this patient's history in Diagnosica. It's free to start, no card needed.

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