A known complication of cirrhosis of the liver is newly altered level of awareness (LOA). Although several entities can cause altered LOA, hepatic encephalopathy (HE) must be near the top of your differential because it is associated with poor survival and a high risk of recurrence when left untreated.1
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Unfortunately, the definition of HE is rather nebulous: “a brain dysfunction caused by liver insufﬁciency and/or porto-systemic shunting; it manifests as a wide spectrum of neurological or psychiatric abnormalities ranging from subclinical alterations to coma.” HE is graded in four stages accordingly. The characteristic asterixis may be absent in stage 1 and missed in stage 4. (While present in stage 4, it is often overlooked because patients are too obtunded to follow commands; however, asterixis can still be elicited by the clinician passively). As a result, HE can be difficult to diagnose in the emergency department.1
Below, I outline a simple seven-step approach to diagnosis and treatment of HE.
Step 1: Rule Out Other Causes
Rule out alternative or concurrent causes of altered LOA, including sepsis, renal failure, alcohol withdrawal, intracranial hemorrhage, or trauma.
Step 2: Assess/Address Precipitants
Assess for and address common precipitants of HE, which include medications (ie, nonadherence or overdosed diuretics, or benzodiazepines), gastrointestinal bleeding, hypokalemia, alkalosis, volume depletion, and sepsis. Addressing and treating precipitating factors in HE management is important because almost 90 percent of patients with HE can be effectively treated by correcting the precipitating factor alone. If your HE treatment does not produce the expected effect, you must reconsider the diagnosis or search for unrecognized precipitating factors and correct them.
Step 3: Make the Diagnosis
After excluding other altered LOA causes, consider HE. Look for the constellation of symptoms that includes personality changes as reported by the patient’s family (eg, apathy, irritability, or disinhibition), disturbances of the sleep-wake cycle (ie, excessive daytime sleepiness or complete reversal of the sleep-wake cycle), and extrapyramidal dysfunction (eg, muscular rigidity, bradykinesia, monotony, slowness of speech, parkinsonian-like tremor, dyskinesia).2 The physical examination plays a major role. The onset of asterixis or disorientation heralds onset. Asterixis can be easily elicited by actions that require postural tone (eg, hyperextension of the wrists with separated ﬁngers or rhythmic squeezing of the examiner’s ﬁngers). If the patient cannot follow commands due to LOA, one trick to elicit asterixes is to place the patient’s forearm on the stretcher railing and forcibly extend the wrist. However, remember that asterixes are not specific for HE and are also seen in patients with renal insufficiency. A reversal of HE manifestations with treatment clinches the diagnosis.