Acute Liver Failure (ALF) is a disease that develops seemingly overnight, often catching patients and their families by surprise. When liver function declines to the point where only 80-90% of its function is lost, the dangers of the disease will become apparent. This phenomenon not only causes serious problems in the liver itself, but may also cause brain edema, which can lead to a series of more serious complications. All of this happens so quickly that the medical community needs to pay more attention to the early warning of this symptom.
The main characteristics of patients with acute liver failure include the rapid onset of jaundice, physical weakness and eventual confusion, all of which are closely related to brain health. In particular, the occurrence of hepatic encephalopathy (Hepatic Encephalopathy) may lead to neurological dysfunction and even coma, all of which originate from liver failure.
Hepatic encephalopathy may begin with mild mood and attention deficits, but can eventually progress to a deep coma, worsening so rapidly that the patient's prognosis is greatly reduced.
In the context of acute liver failure, the formation of cerebral edema is caused by a combination of several factors. First, toxic substances in the body (such as ammonia, thiols, serotonin, and tryptophan) accumulate in the brain. The accumulation of these toxins causes damage to the levels of neurotransmitters and the activation of their receptors. Secondly, there are also cases of dysfunction of autonomic regulation of blood flow, thus exacerbating the brain's anaerobic glycolysis and oxidative stress responses. In this case, the brain neurons of astrocytes are highly susceptible to edema, which ultimately leads to an increase in intracranial pressure.
The increase in intracranial pressure will cause symptoms such as papilledema and loss of pupillary reflex, but these signs are mostly late in the course of the disease and may not be noticed by patients in the early stages.
The first step in diagnosing acute liver failure is measurement of the prothrombin time. If a prolonged prothrombin time is found accompanied by a change in consciousness, medical personnel should strongly suspect the disease. A comprehensive laboratory examination of the patient is essential at this time, including assessment of liver function indices such as AST, ALT, and bilirubin. At the same time, special attention is paid to watching for signs of cerebral edema, and patients should be admitted to the intensive care unit as early as possible so that they can be closely monitored.
Patients with acute liver failure are often at risk of multiple organ failure, among which renal failure is particularly common. This is not only due to primary liver damage, but also to the emergence of hepatorenal syndrome, a type of functional renal failure, due to the body's highly dynamic circulation. Infection is also a common complication in patients with acute liver failure, because 61% of ALF patients have systemic inflammatory response syndrome, which increases the risk of multi-organ failure.
Regarding infections in ALF patients, data from several medical studies show that up to 80% of patients will encounter bacterial infections, while 30% of patients may develop fungal infections, which aggravates the patient's condition.
The treatment effectiveness of acute liver failure has improved with the promotion of liver transplantation technology. However, many patients still unfortunately die while waiting for liver transplantation. Early intervention and timely therapy are crucial to improving patient prognosis. Therefore, how to effectively identify high-risk patients and conduct early referral is still a challenge facing today's medical workers.
Under the threat of cerebral edema, the future of patients with acute liver failure is still full of uncertainty. People can't help but think, in the face of such complex diseases and the ever-changing medical environment, how can we better deal with acute liver failure and the brain edema caused by it?