Hepatic encephalopathy (portal-systemic encephalopathy)

Hepatic encephalopathy (portal-systemic encephalopathy)

    * Introduction
    * Causes
    * Signs and symptoms
    * Diagnosis
    * Treatment
Hepatic encephalopathy is a brain suffering acute or chronic, potentially reversible and repetitive injuries resulting from central nervous system or neuro-muscular system given by shunting blood around the liver and decreased hepatocyte function, determining abnormal metabolites that produce cerebral edema and retraction of astrocytes. Hepatic encephalopathy is a reversible cerebral metabolic disorder with a multifactorial pathogenesis. The most accepted theory on the cause of liver failure and it is increasing in the blood of toxins resulting from metabolism. Ammonia is the main toxin involved. The condition can occur in a fulminating viral hepatitis, toxic or most commonly pathogenic in the cirrhosis or other chronic disorders, in which developed a network of porto-systemic collaterals of portal hypertension as a result. In patients with chronic liver disease, acute episodes of encephalopathy are precipitated by reversible causes. The metabolic dysfunctions encountered are: infection, electrolyte imbalance, hypokalemia, dehydration use of diuretics, disorders that increase the production of essential proteins: gastrointestinal bleeding, high protein diet, depression and unspecific brain: alcohol, sedatives, analgesics. Signs and symptoms are evident only when brain function is severely impaired. These include: asterisk, agitation, anger, apraxia, symmetrical neurological deficits, coma and death. Development encephalopathy indicate decompensated liver disease and other disorders associated with decompensation of course such as: impaired coagulation, the formation of esophageal varices, ascites and portal hypertension. Complications that can occur are severe and life threatening: spontaneous bacterial peritonitis, gastrointestinal bleeding. Because of the potential for rapid evolution to coma, and predicting clinical monitoring is required endotracheal intubation for ventilatory support. Altered consciousness puts the patient at risk and should be clinically evaluated and treated quickly. In chronic liver disease, cause regression correction causal encephalopathy without permanent neurological sequelae. Some patients, especially those with porto-cava shunts or TIPS, require continuous therapy and extrapyramidal signs or irreversible spastic paraparesis develops slowly. Coma-stage IV of encephalopathy associated with fulminant hepatitis is fatal to 80% of patients, despite intensive therapy.
Pathogenesis
The porto-systemic shunting toxic byproducts of metabolism are not sent through the portal circulation to the liver to be detoxified, but go through the systemic circulation to the brain, particularly the cortex. Home toxin is ammonia, it is extremely toxic to the brain, affecting neurons and astrocytes. Normal blood ammonia is removed from the liver through a series of chemical reactions-urea cycle. In this reaction ammonia is converted into urea and excreted in urine. The brain has the urea cycle and has a limited ability to remove ammonia from the blood because of pressure to get high. The only way to remove ammonia is through a reaction mediated by an enzyme glutamine synthetase, a molecule that combines the amino acid glutamate with a molecule of ammonia to form amino acid glutamine. The enzyme is present only in astrocytes and not neurons and can not remove all the ammonia. Other brain toxins are short-chain fatty acids, phenols and thiols. Pathological changes caused by toxic products ammonia and the rest consist of abnormalities in gene expression of astrocytes leading to their swelling. A role-plays and fake neurotransmitters: octopamina, diazepam, benzodiazepines, endogenous depression they cause central nervous system by binding to GABA receptors. He also suggested the involvement of opioid receptor ligands, such as beta-endorphin in the pathogenesis of encephalopathy. Cytokines are intercellular substances conumicare: IL-1, IL-6 and TNF-alpha, are examples of cytokines that are elevated in the systemic circulation and possibly contributing to the pathogenesis encephalopathy. Endotoxemia due in part to intestinal mucosal permeability is demonstrated in cirrhosis with portal hypertension. NO metabolites are also reported to be present, suggesting the contribution suntarii proinflammatory substances absorbed from the intestine into the blood, initiates a cascade of events that culminates in a typical traffic hiperdinamica advanced liver disease. Cerebral ischemia is another mechanism that contributes to porto-systemic encephalopathy but may be a consequence of ammonia toxicity.