Understanding Acute and Chronic Hepatic Encephalopathy
Acute and chronic hepatic encephalopathy are two forms of a complex neuropsychiatric syndrome caused by liver dysfunction. While acute hepatic encephalopathy is a sudden and severe condition that can occur in people with acute liver failure, chronic hepatic encephalopathy is a long-term condition that can happen to individuals with chronic liver disease. The symptoms and treatment options for these two types can vary significantly.
What Is Hepatic Encepalopathy?
Hepatic encephalopathy is a brain dysfunction, which occurs due to liver insufficiency and/or portal-systemic shunting (a condition where blood bypasses the liver).
Usually, this dysfunction is potentially reversible and can manifest as a wide spectrum of neurological or psychiatric abnormalities. It ranges from subtle cognitive changes to coma [1, 2, 3, 4, 5, 6]
Hepatic encephalopathy is a common complication, typically accompanying a chronic liver disease. In fact, around 60% to 80% of patients with liver cirrhosis develop hepatic encephalopathy [6, 7, 8, 9].
The symptoms of hepatic encephalopathy can vary widely, We can observe minor personality changes, and intellectual impairment but also depressed levels of consciousness and coma. Patients may experience an inverted sleep-wake pattern, where they sleep during the day and stay awake at night. Unfortunately, as the condition progresses it leads to confusion, lethargy, and personality changes that may worsen an overall brain dysfunction may lead to coma and death [7, 8, 9, 10].
Unfortunately, the exact cause of hepatic encephalopathy is not understood properly. It may be related to the accumulation of toxins, such as ammonia, due to liver dysfunction.
These toxins can reach the brain and cause neurological symptoms. The condition is often associated with other complications of liver disease, such as portal hypertension and liver cirrhosis [11, 12, 13].
What Is The Difference Between Acute and Chronic Hepatic Encephalopathy?
Acute hepatic encephalopathy typically occurs in the case of fulminant liver failure or in chronic liver disease that is decompensated by external or internal factors.
Although the encephalopathy is acute, acute hepatic encephalopathy can also be a sign of terminal liver failure. The symptoms of acute hepatic encephalopathy can range from mild cognitive impairment to severe disorientation, confusion, and coma [14, 15, 16].
One the other hand, chronic hepatic encephalopathy is associated with long-term liver disease such as cirrhosis. It can be permanent or recurrent. It is in fact the individuals with recurrent versions, that have multiple episodes of hepatic encephalopathy throughout their lives.
Chronic hepatic encephalopathy can lead to psychomotor dysfunction, impaired memory, increased reaction time and even sensory abnormalities, and poor concentration. In severe forms, it can lead to coma [14, 16, 17].
What Is The Pathogenesis of Hepatic Encephalopathy?
The pathogenesis of hepatic encephalopathy is multifaceted and complex, it involves several disruptions in homeostasis following a reduction in liver function [18].
One contributor to the development of hepatic encephalopathy is the elevation of ammonia levels in the body. For instance, this can happen due to a disruption in the urea cycle following liver dysfunction. The elevated levels of circulating ammonia can then enter the brain and disrupt the functioning of astrocytes and leading to dysregulation of metabolic pathways, oxidative stress and cerebral edema [18].
In addition, it can also be the circulating chemokines and cytokines that are increased due to liver injury. In turn, it can lead to the activation of microglia (a type of immune cell in the brain) and result in neuroinflammatory response. The combination of astrocyte dysfunction and microglia activation contributes to the pathogenesis of hepatic encephalopathy [18].
Some other theories of the pathogenesis are altered ammonia metabolism, glutamine and glutamate transmission, an increase in gamma-aminobutyric acid agonists and benzodiazepine-like substances or the alternations of the serotonergic system and inflammatory mediators [19].
Recently, studies have also shown that aberrant bile acid signalling in the development of key features of hepatic encephalopathies, such as neuronal dysfunction, neuroinflammation and increased blood-brain barrier permeability [20].