The portosystemic encephalopathy is a neuropsychiatric syndrome. It is usually the result of a high oral protein intake or acute metabolic stress (eg., Gastrointestinal bleeding, infection, electrolyte imbalance) in patients with portosystemic shunts. The symptoms are neuropsychiatric (eg. As drowsiness, asterixis, coma). Diagnosis is based on clinical criteria. The treatment is usually correct the acute cause, a diet that includes vegetable protein as the primary protein source, oral lactulose and non-absorbable antibiotics like rifaximin.

The portosystemic encephalopathy is a neuropsychiatric syndrome. It is usually the result of a high oral protein intake or acute metabolic stress (eg., Gastrointestinal bleeding, infection, electrolyte imbalance) in patients with portosystemic shunts. The symptoms are neuropsychiatric (eg. As drowsiness, asterixis, coma). Diagnosis is based on clinical criteria. The treatment is usually correct the acute cause, a diet that includes vegetable protein as the primary protein source, oral lactulose and non-absorbable antibiotics like rifaximin.

See also liver structure and function and assessment of patients with liver disease.) The portosystemic encephalopathy is a neuropsychiatric syndrome. It is usually the result of a high oral protein intake or acute metabolic stress (eg., Gastrointestinal bleeding, infection, electrolyte imbalance) in patients with portosystemic shunts. The symptoms are neuropsychiatric (eg. As drowsiness, asterixis, coma). Diagnosis is based on clinical criteria. The treatment is usually correct the acute cause, a diet that includes vegetable protein as the primary protein source, oral lactulose and non-absorbable antibiotics like rifaximin. (See also the American College of Gastroenterology practice guidelines Hepatic Encephalopathy.) The term “portosystemic encephalopathy” describes the pathophysiology better than “hepatic encephalopathy” or “hepatic coma,” but all three terms are equivalent needed. Etiology A portosystemic encephalopathy may in fulminant hepatitis caused by viruses, drugs or toxins occur, but is more common in cirrhosis and other chronic diseases in which there is a pronounced portosystemic collateral circulation has formed as a result of portal hypertension. Encephalopathy may also be the result of portosystemic anastomoses such. B. surgically created anastomoses connecting the portal circulation to the vena cava (portocaval shunts or transjugular intrahepatic portosystemic shunt [TIPS]). Triggering causes in patients with chronic liver disease are episodes of encephalopathy usually caused by reversible causes. The most common are the following: Metaboliischer stress (eg, infections, electrolyte imbalance, particularly hypokalemia, dehydration, use of diuretics.) diseases that cause an increase in proteins in the gut (eg gastrointestinal bleeding, high protein diet. ) Non-specific cerebral sedative (e.g., for example, alcohol, sedatives, analgesics) Due to the pathophysiology portosystemic shunt pass agents, which are normally detoxified in the liver, into the systemic circulation and may therefore toxic effects in the brain, v. a. unfold in the cerebral cortex. The substances that have a toxic effect on the brain, are not precisely known. Ammonia as a breakdown product of protein metabolism plays an important role, but other factors (eg. As changes in the cerebral benzodiazepine receptors and neurotransmitters such as gamma-aminobutyric acid [GABA]) also contribute to encephalopathy. The concentration of the aromatic amino acids in serum is usually high, the branched-chain low; but probably this combination does not cause encephalopathy. Symptoms and discomfort symptoms and clinical findings of encephalopathy develop progressively in stages (see Table: Clinical stages of portosystemic encephalopathy). Clinical stages of portosystemic encephalopathy stage cognition and behavior Neuromuscular Function 0 (subclinical) Asymptomatic loss of cognitive skills No one sleep difficulty concentrating depression, anxiety or irritability Monotone voice tremor Poor handwriting Constructive apraxia 2 drowsiness Disorientation Inadequate short-term memory uninhibited behavior ataxia dysarthria asterixis automation (eg. B. yawning, blinking, sucking) 3 drowsiness confusion memory loss anger, paranoia or other bizarre behavior nystagmus muscle rigidity hyperreflexia or hyporeflexia 4 coma Dilated pupils Oculo | cerebral syndromes or oculovestibul√§re reflexes neuromuscular dysfunction The symptoms are first noticeable as a rule, when the brain function as standard is limited. Apraxia, in which the patient is not able to reproduce simple drawings (eg. As a star), early developed. Excitement and mania can occur, but are rare. A characteristic flapping tremor (asterixis) is triggered when the patient dorsiflexion wrists with outstretched arms. Neurological deficits usually occur symmetrically. Neurological signs in a coma show bilateral diffuse hemispheric dysfunction usually. Signs of disorders of brain stem function only arise in advanced coma, usually only in the hours or days before death. Musty sweet breath odor (fetor hepaticus) occurs regardless of the stage of encephalopathy. Diagnosis Clinical evaluation Often additional tests with psychometric evaluation, ammonia content, EEG, or a combination exclude other treatable diseases The diagnosis is ultimately clinically, but test methods may be helpful. Psychometric tests reveal subtle neuropsychiatric deficits, confirming an early stage of encephalopathy. Ammonia values ??are generally determined. An EEG usually shows diffuse slow wave activity, even in less severe cases, so it is sensitive but not specific for early encephalopathy. Cerebrospinal fluid are routinely not indicated, the actual pathological deviation consists in a slight increase of protein concentration. Other potentially reversible disease states which may lead to a similar clinical picture (eg. As infection, subdural hematoma, hypoglycemia and intoxications) must be excluded. If portosystemic encephalopathy is secured, must be sought after the triggering cause. Forecast In chronic liver disease causes the elimination of the triggering causes the regression of encephalopathy without permanent neurological consequences. Some patients v. a. those with portocaval shunts or TIPS require long-term therapy, irreversible extrapyramidal symptoms or spastic paraparesis rarely develops. The combination of advanced liver failure and portosystemic encephalopathy is also usually fatal. The state of coma (stage 4 encephalopathy) associated with fulminant hepatitis, resulting in> 80% of patients despite intensive therapy death. Therapy treating the cause colon cleansing with oral lactulose or enemas diet of vegetables absorbable as the primary protein source Oral antibiotics like rifaximin and neomycin Treatment of the causes leading to less severe cases usually for regression. An elimination of the toxic intestinal products is the other goal of treatment and is achieved by different methods. The intestines should be cleaned with enemas, even better should orally lactulose, z. B. are in comatose patients over a probe fed. This synthetic disaccharide has an osmotic effect. It also lowers the pH in the colon, thereby resulting in decreased fecal ammonia production. The initial dose of 30-45 ml p.o. should be set to 3 times a day, two or three loose stools are sold per day. The protein diet should be about 1.0 mg / kg / day, mainly originating from plant sources. Oral absorbable antibiotics like rifaximin and neomycin are effective in hepatic encephalopathy. Rifaximin is generally preferred, as neomycin is an aminoglycoside, or may fail the cause ototoxicity and nephrotoxicity. Sedation deepens encephalopathy and should, whenever possible, avoided. The coma in fulminant hepatitis requires very careful treatment and care, which increases along with the prevention and treatment of complications, the chances of survival. High-dose corticosteroids, exchange transfusions and other complex procedures for removing circulating toxins do not generally lead to an improvement of the course. For patients whose condition deteriorated in the course of fulminant hepatitis, remains the only treatment option liver transplantation. Other potential therapeutic approaches, incl. Levodopa, bromocriptine, flumazenil, sodium benzoate, infusions of branched chain amino acids, amino acids and prostaglandins Ketonanalogen essential have not proved effective. Complex plasma filter systems (so-called. Artificial livers) give hope, but still require intensive investigations. Conclusion Portosystemic encephalopathy is a neuropsychiatric syndrome, which occurs when portosystemic shunts absorbed products that are normally detoxified in the liver by leave, in the brain. Symptoms include cognitive behavioral disorders (eg. As confusion, impaired consciousness, coma) and neuromuscular dysfunction (eg. As flutter tremor, ataxia, hyperreflexia or hyporeflexia). The diagnosis of portosystemic encephalopathy is mainly based on clinical findings, but usually Blutammoniakspiege be measured, and if the signs are subtle or absent, conducted neuropsychological tests. Other treatable diseases (eg. As subdural hematoma, hypoglycemia, intoxication) must be excluded and after the triggers of encephalopathy (eg. As infections, intestinal bleeding, electrolyte abnormality) are sought. Treat the cause of encephalopathy and treat the encephalopathy itself with colon cleansing (with oral lactulose or enemas), restriction of protein intake on vegetable sources, and oral administration of rifaximin or neomycin.

Health Life Media Team

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