Palaces liver hijacker
Known liver failure as a hijacker of hepatic failure combined Phase III or IV encephalopathy (Alausen deep Somnolence or hibernate mode), which occurs after less than eight weeks when the patient does not have a hepatic lesion precedent. And the resulting limitations hijacker usually severe hepatic necrosis and subsequent destruction of the acute febrile infection Balhamat b, a, d or A - B. May also result from fatty liver, gestational, or ischemic necrosis, or exposure to liver toxins such as acetaminophen and isoniazid, Alhalotan, Valbreuek Valproic acid and tetracycline, and fungal toxins such as toxin Valeods Amanita mushroom Amanita Phalloides and carbon tetrachloride.
RI-like syndrome Reye's Syndrome, a hijacker liver failure disease tends to affect children and is characterized by infiltration greasy small vesicles in cells with hepatic necrosis where mild.
Diagnosis:
Diagnosis depends on meeting the following elements: encephalopathy, acute liver disease (high blood bilirubin and enzymes Turansamnz), and hepatic failure, which usually refers to low blood Albrocrumbin.
Treatment: The treatment of liver failure hijacker is usually supportive treatment are rarely to be the causative agent of liver failure may be treated. However, most of the events that cause tooth decay and a broad defect in the liver and lightning are the cases where short-lived. It often happens liver regeneration and healing functions in patients who survive the death resulting from complications of liver failure. The treatment proved to be spoken in support provided in the scope of the intensive care unit increases the survival rate. And must be treated at liver failure hijacker centers have the expertise in dealing with this disease. The diagnosis and treatment of the many complications that accompany liver failure hijacker is essential in the management of this disease ..
The hepatic encephalopathy is often the first sign of liver failure and the most exciting. His presence is a necessary condition for the diagnosis of liver failure hijacker.
The mechanism of pathogenicity of hepatic encephalopathy mysterious and unknown reason, however, most clinical Views refers to the role played by proteins and toxins in the intestinal origin, and they have the same stop the liver in normal cases and remove toxicity. May play a neurotransmitter irregularities that artificially from the surplus of aromatic amino acids play a role in hepatic encephalopathy diseases.
Different from hepatic encephalopathy accompanying liver failure hijacker on morbidity accompanying chronic liver disease Nahitn important:
1 - rarely be caused by one of the factors accelerated therapy, does not respond to treatment only when improved and liver function.
2 - often accompanied by two more grounds for sleep susceptible to treatment and the reduced blood sugar and edema of the brain and because of the severity of the lesion in these patients to stop giving the protein completely given intravenous glucose and 1500-1000 calories a day and Allaktuluz given by oral, nasal gastric tube or by enemas to clean the colon.
The lack of blood sugar are common to double in the palaces of the liver that all patients should be given glucose solution by almost 10% in intravenous with frequent monitoring blood sugar levels have. There are other metabolic abnormalities are common also in the palaces of the liver, such as hyponatraemia and the lack of Albotasmip Alkaline and respiratory and metabolic acidosis, so it had to be repeated monitoring of blood and Khrlja Bahaih PH may occur gastrointestinal bleeding from stress ulcers, especially with an imbalance in the establishment of blood clotting factors. And must be given to all patients and prevention of vitamin K digestive mucosa giving antacids by mouth or by intravenous Alsimtidin of the county on the PH stomach above the fifth degree. Must not be given fresh frozen plasma only if there is clinically significant bleeding. The total failure is common in patients with liver failure.
Very important to deny the presence of hypovolemia as a cause of Hypovolemia Azotmip the mediation of central venous pressure measurement if necessary. It seems that the rate of survival among patients with hepatic renal syndrome or acute tubular Balennkr not improving the use of dialysis. The cerebral edema that do not know pathogenicity mechanism, it is common for double hijacker liver failure in children and young people. May cause cerebral edema, intracranial ruptured, signaling the end of fatal general. Not helpful in addressing Alstroieidat cortical cerebral edema, but reports indicate that the improved survival in selected cases using Mannitol intravenously with intracranial pressure monitoring. Have experimented with many forms of liver failure treatment in a snap, and to give a Alstroieidat corticosteroids, and replacement of blood, plasmapharesis, and hemodialysis, and hemodialysis Bimrarh a layer of coal, and the liquidation of blood outside the body Bimrarh in the human body or in the liver of the pig, but that none of the These methods did not give better results than conventional treatment supporting planting liver ..
Hepatic Transp; antation tried to address a small number of patients with liver failure hijacker by planting the liver and the results were encouraging. Since the implantation of the liver is required urgently, it was the transfer of patients to be candidates for such an operation to one of the centers of membership before planting appears to have important implications (such as Hibernate or cerebral edema, bleeding or infections.
Warning: The warning in the long Algosairse very survival as the rate of twenty percent on average. The warning in the long run for those who remained alive, he is very good. The follow-up of these patients showed that the liver function and histological structure of the liver were together when all patients who remained alive, for whatever reason which led to additional limitations.
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