Complications of hepatic encephalopathy

Hepatic encephalopathy is not as simple as its literal meaning suggests. It is a type of brain damage, coma or even death caused by severe liver disease. The most common complication of this disease is cerebral edema, but this is more common in acute liver disease, and the incidence of chronic liver disease is relatively low. In addition to this, it may also cause renal insufficiency or gastrointestinal bleeding. The following article introduces in detail the clinical manifestations and complications of this disease. Let’s take a look.

Complications of hepatic encephalopathy:

1. Cerebral edema: Cerebral edema has been confirmed to be a complication of fulminant hepatic failure, with an incidence rate of over 80%. There is no consensus on whether chronic liver disease causes cerebral edema, but most scholars believe that chronic hepatic encephalopathy may be complicated by cerebral edema. The incidence rate reported by various sources is also inconsistent, with most believing it to be 21% to 58%. However, recent autopsy results have found that the detection rate of cerebral edema in patients with cirrhosis is as high as 89.5%, of which 23.7% have mild edema, 65.8% have severe edema, and 21% have clear encephalopathy. This indicates that the incidence of cerebral edema in chronic liver failure is also very high and is one of the main causes of death.

2. Gastrointestinal bleeding.

3. Renal insufficiency.

4. Water, electrolyte, acid and alkali imbalance.

5. Infection.

Hepatic encephalopathy in the elderly

Clinical manifestations

Acute hepatic encephalopathy is common in acute severe hepatitis, with massive hepatocyte necrosis and acute liver failure. The cause is not obvious. The patient falls into a coma within a few days of onset and eventually dies. There may be no prodromal symptoms before the coma. Chronic hepatic encephalopathy is more common in patients with cirrhosis and/or after portal-caval shunt surgery, with chronic recurrent stupor and coma as prominent manifestations. It is often induced by ingesting large amounts of protein, upper gastrointestinal bleeding, infection, paracentesis, and large amounts of potassium-excreting diuretics. Clinically, hepatic encephalopathy is divided into four stages based on the degree of consciousness disorder, neurological manifestations and electroencephalogram changes.

1. In the first stage (prodromal stage), patients only have mild personality changes and behavioral abnormalities, such as euphoria or indifference, untidy clothing or urinating and defecating anywhere, anxiety, and lack of concentration. They respond accurately but their speech is unclear and slow. There may be a flapping tremor. EEG is usually normal. This period lasts for several days or weeks, and sometimes the symptoms are not obvious and can be easily ignored.

2. The second stage (pre-coma) is characterized by confusion, sleep disorders, and abnormal behavior. Symptoms from the previous period worsen. There is a decrease in orientation and comprehension, confusion about time, place, and people, slurred speech, dysgraphia, and abnormal behavior. Most of them have irregular sleep schedules, sleeping during the day and waking at night, and even hallucinations, fear, and mania, and are therefore considered to be common mental illnesses. Patients at this stage have obvious neurological signs, such as hyperreflexia of tendon, increased muscle tension, ankle spasm and positive Babinski sign. During this period, flapping tremors are present and the electroencephalogram has characteristic abnormalities.

3. The third stage (comatose stage) is characterized by lethargy and mental confusion, and various neurological signs worsen. When awake, they can still answer questions, but they often feel confused and have hallucinations. Asterixis can still be elicited. Muscle tone increases, and passive movement of the limbs is often resisted. Pyramidal tract signs are often positive and the EEG has abnormal waveforms.

4. Stage 4 (coma): complete loss of consciousness and inability to be awakened. In light coma, there is still response to painful stimuli and uncomfortable positions, tendon reflexes and muscle tone are still hyperactive; flapping tremors cannot be induced. In deep coma, various reflexes disappear, muscle tone decreases, pupils are often dilated, and paroxysmal convulsions, ankle clonus and hyperventilation may occur. The EEG was obviously abnormal.

There is no clear boundary between the above stages, and the clinical manifestations of the early and late stages may overlap. Recently, subclinical hepatic encephalopathy or latent hepatic encephalopathy has gradually received more attention. Some scholars have suggested that it is necessary to classify subclinical hepatic encephalopathy as stage 0 in clinical staging.