Your next patient’s wife says he has become confused and very sleepy over 3 days. Here's how the hepatic encephalopathy case unfolds and what to pick up on the way.

This hepatic encephalopathy case is easy to get wrong because the history can sound like simple tiredness or a sleep problem. A carer reports three days of confusion with daytime drowsiness and wakefulness at night, while the patient oddly refers to himself as my husband, looks more jaundiced and has a sweet, musty breath. In a hurried clerking you might miss the flapping hands, the week without lactulose and five days without opening bowels, and overvalue the absence of melaena or haematemesis.

This page walks through how it presents, what to pick up in the history, the bedside and laboratory tests to request, and the teaching points that matter for diagnosis and reasoning.

How the case presents

Your next patient’s wife says he has become confused and very sleepy over 3 days. In their own words: "My husband has become confused and drowsy over the past few days."

Observations on arrival:

Observation	On arrival
Heart rate	92 beats per minute
Blood pressure	116/70 mmHg
Respiratory rate	16 breaths per minute
Oxygen saturation	97%
Temperature	37.2 °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 hepatic encephalopathy, and the scorecard checks whether you found it.

Three days of confusion with reversed sleep pattern: day-night reversal with fluctuating confusion is the signature early picture of hepatic encephalopathy.
Hands flap when held outstretched: asterixis places the confusion in a metabolic encephalopathy rather than a structural stroke.
No bowels opened for five days: constipation is a common precipitant; clearing it is central to reversing the encephalopathy.
More jaundiced with sweet, musty breath: deepening jaundice and fetor hepaticus confirm decompensated liver failure.
No melaena and no haematemesis: excludes gastrointestinal bleeding, the other major precipitant needing urgent endoscopy.
Becoming harder to rouse through the day: A falling conscious level grades severity and flags the need for airway protection.

Red flags you must not miss

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

No melaena and no haematemesis.
He has not had any fall or bang to the head, and has not been on blood thinners.
There has been no sudden weakness or drooping of the face, arm or leg on one side and no sudden loss of speech.
Becoming harder to rouse through the day.

Investigations and what they showed

Ammonia: Raised venous ammonia at 118 µmol/L. Why it helps: supports the diagnosis in the right clinical picture, but a raised ammonia is neither necessary nor sufficient, levels correlate poorly with severity and a normal value would not exclude hepatic encephalopathy, which stays a clinical diagnosis.
Liver function tests: Bilirubin 62 µmol/L (raised), albumin 27 g/L (low), mildly raised transaminases, raised ALP/GGT, a chronic, decompensated picture. Why it helps: confirms established liver disease and impaired synthetic function (low albumin), consistent with decompensated cirrhosis.
Urea and electrolytes: 4 mmol/L (low-normal), urea and creatinine at the upper end, watch for hepatorenal syndrome.
Ultrasound abdomen: Coarse, nodular, shrunken liver with a recanalised/patent portal vein, splenomegaly and moderate ascites, the picture of cirrhosis with portal hypertension. Why it helps: confirms the underlying chronic liver disease and portal hypertension that make encephalopathy possible, and localises ascites for a diagnostic tap.
MRI brain: Symmetrical high T1 signal in both globus pallidi (manganese deposition of chronic liver disease); no acute infarct, mass or haemorrhage. Why it helps: A supportive, characteristic (though non-specific) sign of chronic liver disease and it helps exclude a structural intracranial cause, but it does not by itself grade or clinch the encephalopathy.
EEG: Generalised slowing with triphasic waves, a metabolic encephalopathy pattern. Why it helps: supports a metabolic encephalopathy and helps exclude non-convulsive seizures, but the findings are non-specific and the diagnosis remains clinical; rarely needed routinely.
CT abdomen and pelvis: A shrunken, nodular cirrhotic liver with splenomegaly, ascites and varices (portal hypertension). Why it helps: confirms cirrhosis and portal hypertension in more detail than ultrasound and screens for hepatocellular carcinoma.
MRI abdomen / liver: A nodular cirrhotic liver with regenerative nodules, splenomegaly and ascites; characterises any focal lesion. Why it helps: characterises the cirrhotic liver and any suspicious nodule (HCC) without ionising radiation.
Inspect the sclera: Both sclerae are deeply yellow, scleral icterus, easily seen against the white of the eye. Why it helps: the sclerae yellow before the skin does, so this is the earliest visible confirmation that he is jaundiced from decompensated liver disease rather than simply confused.
Inspect the patient's colour: The whole face and skin are yellow-orange with markedly icteric sclerae, generalised jaundice. Why it helps: jaundice deep enough to colour the skin puts him firmly in decompensated cirrhosis, which is the background against which the confusion must be read.
Inspect the abdomen: A grossly distended, tense abdomen with fullness in the flanks, a flattened/everted umbilicus and dilated veins tracking over the abdominal wall, gross ascites. Why it helps: ascites confirms portal hypertension and, critically, means he must have a diagnostic ascitic tap, spontaneous bacterial peritonitis is the commonest occult precipitant of encephalopathy.
Inspect the chest: Several spider naevi over the upper trunk, small red central arterioles with radiating legs. Why it helps: more than about five spider naevi in the SVC distribution is a signature of chronic liver disease and anchors the diagnosis as a decompensation of cirrhosis rather than a primary neurological event.
Inspect the palms: Bright red mottled erythema over the thenar and hypothenar eminences, sparing the centre of the palm, palmar erythema. Why it helps: A classic peripheral stigma of chronic liver disease that costs nothing to look for and reinforces the hepatic origin of the confusion.
Inspect the ankles: Swollen ankle and foot with loss of the malleolar contours and a pit that persists after pressure is released.
Inspect the hands: With the arms held out, wrists dorsiflexed and fingers spread, the hands drop and jerk back up in a coarse, irregular flapping tremor, asterixis (the hepatic flap). Why it helps: asterixis is the cardinal bedside sign of hepatic encephalopathy and is what separates it from alcohol withdrawal (a fine, regular tremor); it is also a negative myoclonus, so it only appears on sustained posture.
Inspect the patient's level of alertness and demeanour: Grading the conscious level (West Haven) is how encephalopathy is staged and monitored, a falling level means airway risk and escalation, and day-night reversal is highly characteristic.
Inspect the skin: Scattered bruises and purpura over the arms and shins from minor knocks, with no petechial rash. Why it helps: 6) and thrombocytopenia (platelets 92) of cirrhosis, the same coagulopathy that makes a subdural haematoma a real possibility in a confused cirrhotic and mandates the CT head.
Inspect the fingernails: White, opaque nail beds (leuconychia) with loss of the normal pink lunulae. Why it helps: leuconychia is the nail sign of hypoalbuminaemia (albumin 27 g/L) and, like the spider naevi, points to chronic rather than acute liver disease.

Imaging findings

CT head: No intracranial haemorrhage, no mass, no established infarct. Normal.
X-ray chest: Clear lung fields, no consolidation. Normal.
X-ray abdomen: Non-specific, a plain abdominal film cannot show cirrhosis; at most a gasless/hazy abdomen from ascites. Non-diagnostic here.

Hepatic encephalopathy at a glance

What it is

Hepatic encephalopathy is a reversible decline in brain function that occurs when a failing liver, usually already cirrhotic, can no longer clear toxins that the gut normally produces. It ranges from subtle confusion and day-night reversal of sleep to drowsiness, agitation and, in severe cases, coma.

Pathogenesis

A cirrhotic liver loses much of its capacity to convert ammonia, a byproduct of protein breakdown in the gut, into urea for safe excretion by the kidneys. Portal hypertension also diverts blood around the liver through collateral vessels, bypassing what detoxifying capacity remains. Ammonia and other gut-derived substances accumulate in the blood, cross into the brain and disturb neurotransmission, producing the confusion, drowsiness and characteristic flapping tremor (asterixis) of the syndrome. The process is usually triggered by an identifiable precipitant that adds to the toxin load or worsens liver function acutely.

Who it affects

Hepatic encephalopathy occurs in patients with significant liver disease, most often decompensated cirrhosis, and can also follow acute liver failure. Over time, a large proportion of people with cirrhosis will develop at least one episode.

Causes and risk factors

The underlying substrate is significant liver disease, usually cirrhosis.

Investigations and lab tests

Hepatic encephalopathy is a clinical diagnosis: fluctuating confusion, day-night reversal, drowsiness and asterixis on a background of liver disease. Every decompensated cirrhotic with ascites needs a diagnostic ascitic tap to exclude spontaneous bacterial peritonitis, and new confusion in a coagulopathic cirrhotic warrants a CT head to exclude a subdural haematoma. Ammonia may be raised but a normal level does not exclude the diagnosis.

At a glance: Clinical diagnosis, no single confirmatory test. Always check: bedside glucose, ascitic tap (exclude SBP), CT head if coagulopathic. Ammonia is supportive, not definitive.

Teaching points

Hepatic encephalopathy is a clinical diagnosis: fluctuating confusion, day-night reversal, drowsiness progressing to coma, with asterixis and fetor hepaticus on a background of liver disease.
Ammonia may be raised but a normal level does not exclude the diagnosis and values correlate poorly with grade, do not rely on ammonia to rule it in or out.
In any confused patient, check a bedside glucose first, hypoglycaemia is the fastest reversible mimic and cirrhotics are prone to it.
Every decompensated cirrhotic with ascites needs a diagnostic ascitic tap to exclude spontaneous bacterial peritonitis.
New confusion in a coagulopathic cirrhotic warrants a CT head to exclude a subdural haematoma or other structural cause.

Practise a similar case

Reading a tidy case is not the same as steering the questions yourself when the clock is ticking. It feels different to spot asterixis only if you decide to ask the patient to hold their hands out. Now try taking a history from a different simulated gastroenterology patient.

Here's one from the same specialty, with the diagnosis left for you to find. Your next patient has turned yellow over 3 weeks with soreness under his right ribs and a swollen belly. Take this patient's history in Diagnosica. It's free to start, no card needed.

Hepatic encephalopathy case presentation: history, findings and tests