Acute Liver Failure

(Fulminant hepatic failure)

Acute liver failure is most commonly caused by drugs and hepatitis viruses. Main manifestations are jaundice, coagulopathy and encephalopathy. The diagnosis is made clinically. The treatment is mainly supportive, sometimes with liver transplantation and / or specific therapies (eg. B. N -Acetylcystein at paracetamol toxicity).

Acute liver failure is most commonly caused by drugs and hepatitis viruses. Main manifestations are jaundice, coagulopathy and encephalopathy. The diagnosis is made clinically. The treatment is mainly supportive, sometimes with liver transplantation and / or specific therapies (eg. B. N -Acetylcystein at paracetamol toxicity).

See also liver structure and function and assessment of patients with liver disease.) Acute liver failure is most commonly caused by drugs and hepatitis viruses. Main manifestations are jaundice, coagulopathy and encephalopathy. The diagnosis is made clinically. The treatment is mainly supportive, sometimes with liver transplantation and / or specific therapies (eg. B. N -Acetylcystein at paracetamol toxicity). Liver failure can be classified in various ways, but no system is universally accepted (see Table: Classification of liver failure *). Classification of liver failure * Severity Common findings Acute (fulminant) Portosystemic encephalopathy eight weeks develops within 2 weeks of jaundice in a patient without previous liver disease often cerebral edema Subacute (subfulminante) A encephalopathy develops within six months, but later than in acute liver failure , Kidney failure, portal hypertension (frequently than in acute liver failure) Chronic encephalopathy develops after 6 months. often caused by cirrhosis of the liver * No classification is universally accepted. Generally etiology are the most common causes of acute liver failure drug viruses and toxins In developing countries, viral hepatitis is usually considered a leading cause in developed countries usually toxins. In summary, hepatitis B is the most common viral cause; Hepatitis C is not a common cause. Other viral causes include cytomegalovirus, Epstein-Barr virus, herpes simplex virus, human herpesvirus 6, parvovirus B19, varicella-zoster virus, hepatitis A virus (rare), hepatitis E virus (especially if it was acquired during pregnancy), and viruses that cause hemorrhagic fever (overview of infections by arbovirus, Arena virus and filovirus). The most common toxin is paracetamol; Toxicity is dose dependent. Predisposing factors for paracetamol-induced liver failure are pre-existing liver disease, chronic alcohol consumption and the use of drugs that stimulate the cytochrome P-450 enzyme system (z. B. antiepileptics). Other toxins are amoxicillin / clavulanate halothane, iron compounds, isoniazid, NSAIDs, some components phalloides in plant products and Amanita mushrooms (liver damage caused by medications). Some drug reactions are idiosyncratic. Less common causes include vascular metabolic disorders Vascular causes are hepatic vein thrombosis (Budd-Chiari syndrome), ischemic hepatitis, portal vein thrombosis and venous occlusive liver disease, sometimes induced by drugs or toxins. Metabolic causes include acute fatty liver of pregnancy, HELLP syndrome (hemolysis, elevated liver enzymes and low platelets), Reye’s syndrome and Wilson’s disease. Other causes include autoimmune hepatitis, Lebermetastasierte infiltration, heat stroke and sepsis. In up to 20% of cases the cause can not be identified. Pathophysiology In the context of acute liver failure is a multi-organ failure may develop that lead the reasons and mechanisms to do so are not clear. Affected systems are liver: hyperbilirubinemia is almost always detectable. The degree of hyperbilirubinemia is an indicator of the severity of liver failure. Coagulopathy due to hepatic synthesis of clotting factors is frequent. Hepatocellular necrosis, by elevated aminotransferase is present. Cardiovascular: reduce the peripheral vascular resistance and blood pressure and lead to a hyperdynamic circulatory situation with increased heart rate and increased cardiac output. Cerebral: Portosystemic encephalopathy occurs, possibly secondary to increased ammonia production by nitrogenous substances in the intestine. Secondary to acute liver failure is a cerebral edema common in patients with severe encephalopathy; Entrapment is possible and usually fatal. Renal: For unknown reasons, occurs acute renal failure in up to 50% of patients. As the urea concentration is dependent on the liver synthesis, the mirror can be misleading low; Therefore creatinine indicates kidney damage to better. As with hepatorenal syndrome, decrease the sodium in the urine and the excretion of fractionated sodium, even if no diuretics are used and no tubular injury is present (as may occur due to acetaminophen toxicity). Immunologically: arise defects of the immune system; they also include a defective opsonization, a lack of complement and dysfunctional leukocytes and lymphocytes. Bacterial translocation from the gastrointestinal tract strengthened. Respiratory and urinary tract infections and sepsis are common; Pathogens can be bacteria, viruses or fungi. Metabolism: Metabolic and respiratory alkalosis may occur early. When a shock developed metabolic acidosis can be added. Hypokalemia is common, in part because of the sympathetic tone decreases, but also because diuretics are used. Hypophosphatemia and hypomagnesemia may develop. Hypoglycemia can occur because the liver glycogen is depleted and the gluconeogenesis and insulin degradation are impaired. Pulmonary Pulmonary edema nichtkardiogenen origin can develop. Symptoms and complaints Characteristic symptoms are an altered mental state (usually due to the portosystemic encephalopathy), bleeding, purpura, jaundice and ascites. Other symptoms may be non-specific (eg. As malaise, anorexia) or develop from the causative disorder out. Fetor hepaticus (a musty smell or sweet breath) and motor disturbances are common. Tachycardia, tachypnea and hypotension may occur with or without sepsis. Signs of cerebral edema may be impaired consciousness, coma, bradycardia and hypertension. Patients with infection sometimes localized symptoms (eg. As cough, dysuria), but these symptoms may be absent. Diagnostic extension of the PT and / or clinical manifestations of encephalopathy in patients with hyperbilirubinemia and elevated aminotransferases. In order to determine the cause: a history of drug use, exposure to toxins, serological tests for hepatitis viruses, autoimmune markers and other tests in case of suspected A suspected acute liver failure occurs when patients (acute jaundice, unexplained bleeding or changes in mental status may evidence of encephalopathy) have, or if the condition of patients with known liver disease deteriorates rapidly in some way. The laboratory testing of liver enzymes, bilirubin and prothrombin confirm liver failure and indicate the severity. In patients with clinically suspected and / or on the basis of reasonable of laboratory parameters indicate acute liver damage acute liver failure is confirmed, as a rule, if impaired consciousness or thromboplastin time at> 4 prolonged s or if the INR> 1.5 , The detection of cirrhosis suggesting a chronic liver failure. Patients with acute liver failure should be tested for complications. Tests in the initial phase of the diagnosis usually include blood count, serum electrolytes (including calcium, phosphate and magnesium), renal function tests and urinalysis. If acute liver failure was confirmed, arterial blood gases, amylase and lipase, and blood group should be investigated and antibody screening are performed. Ammonia in plasma is sometimes recommended for the diagnosis of encephalopathy or for the control of severity. In case of a hyperdynamic circulatory disorder and tachypnea infection should be excluded by cultures (e.g., blood, urine, or ascites) removed and the chest cavity is x-rayed. When the mental state of patients affected or deterioration has occurred, should be performed in patients with coagulopathy a CT scan of the head, in particular, to exclude intracranial bleeding. To find the cause of acute liver failure, doctors should perform a complete medical history from ingested drugs and toxins, including prescription and rezeptfreine medications, herbal products and dietary supplements. Routine tests to determine the cause are serological tests (to viral hepatitis z. B. IgM antibodies against hepatitis A virus [IgM anti-HAV], hepatitis B surface antigen [HBsAg], IgM antibody to hepatitis B core antigen [IgM anti-HBcAg], antibodies to the hepatitis C virus [anti-HCV]) autoimmune markers (z. B. antinuclear antibodies [ANA], antibodies to the smooth muscle, immunoglobulin levels) Other tests are the basis of reports and conducted clinical suspicion, as for the following: travel to developing countries lately: tests for hepatitis a, B and D, and e women of childbearing age: pregnancy test Age <40 and relatively normal aminotransferase levels: determine Ceruloplasminspiegel and verify a Wilson's disease suspected changes due to structural abnormalities (eg. as Budd-Chiari syndrome, portal vein thrombosis, hepatic metastases): ultrasonography and, if necessary, other imaging methods Patients should be closely (on complications such. As subtle changes in vital signs with infection) are monitored and the threshold for the tests should be low. Doctors should not assume that the deterioration of the mental state is due to encephalopathy, for example; In such cases, a CT scan of the head and usually a blood glucose test should be performed at the bedside. Routine laboratory tests (eg. As daily prothrombin time, serum electrolytes, renal function tests, blood glucose and arterial blood gases) should be repeated regularly in most cases. However, it may be that certain tests have to be done more frequently (eg., Blood sugar every 2 hours in patients with severe encephalopathy). Prognosis A prediction of the development can be difficult. Important predictive variables are degree of encephalopathy: Worse, if the encephalopathy is difficult age of the patient: Worse, when age <10 or> 40 years prothrombin time: Worse, if the prothrombin time is prolonged cause of acute liver failure: Better with paracetamol toxicity, hepatitis A, hepatitis B than with hypersensitivity to drug or Wilson’s disease Various scores ([II APACHE] typically Kings College criteria or Acute Physiologic Assessment and Chronic Health evaluation II credit score) can be prognostic factors in patient populations, but in individual patients not accurate enough. Therapy Supportive N -Acetylcystein in acetaminophen poisoning Sometimes liver transplantation (See also the American Association for Study of Liver Disease’s practice guideline Management of Acute Liver Failure: Update 2011.) Whenever possible, patients should be treated in an intensive care unit of a center is able to perform liver transplants. Patients should be laid as soon as possible because deterioration can occur rapidly and complications (eg. As bleeding, aspiration, at worst shock) are more likely when the liver failure progresses. Intensive supportive measures are the mainstay of treatment. Drugs, the manifestations of acute liver failure (z. B. hypotension, sedation) could worsen, should be avoided or used in the lowest possible doses. When low blood pressure and acute kidney injury, maximizing tissue perfusion is the goal of treatment. Treatment includes the administration of intravenous fluids and, to sepsis can be excluded, usually empirical antibiotic therapy. If hypotension after administration of about 20 ml / kg / body weight crystalloid solution is more refractory, the doctor should measure the pulmonary capillary wedge pressure, to control the infusion therapy. If hypotension persists despite adequate filling pressure, administration of positive inotropic agents (eg. As dopamine, epinephrine, norepinephrine) should be considered. In an encephalopathy, the head of the bed should be increased to 30 °, in order to reduce the risk of aspiration; to intubation should be considered early. In the selection of drugs and dosages, the goal should be to minimize the sedation so that they can be monitored, the severity of encephalopathy. Propofol is the drug of first choice for intubation because it protects against intracranial hypertension and has a short duration of action which allows a quick recovery from the sedation. Lactulose can be helpful in encephalopathy, but it must not be given by mouth or nasogastric tube to patients whose mental status is altered until they have been intubated; the dose is 50 ml every 1-2 h p.o. until the patients have a bowel movement at least twice per day, or 300 mL to 1 L of brine, can be added dierektal. are stimuli that trigger a Valsalva maneuver, must be avoided (for example, the administration of lidocaine prior to endotracheal aspiration: the measures are taken to prevent a rise in intracranial pressure and a decreasing cerebral perfusion pressure: To avoid a sudden increase in intracranial pressure in the brain. to avoid the gag reflex). For the temporary reduction of cerebral blood flow: mannitol (0.5 to 1 g / kg, repeated once or twice as required) may, for inducing osmotic diuresis and optionally a hyperventilation be carried out, in particular when a strangulation is suspected. To monitor the intracranial pressure in the brain: It is not clear if and when the risks of intracranial pressure monitoring (eg, infection, bleeding.) To recognize outweigh the benefits, cerebral edema early and to be controlled by fluid and blood pressure attitude; some experts recommend such monitoring if encephalopathy is difficult. Goals of treatment are an intracranial pressure of <20 mmHg and a cerebral perfusion pressure of> 50 mmHg. Epileptic seizures are treatable with phenytoin; Benzodiazepines should be avoided or used only in small doses, because they cause sedation. Infections are treated with antibiotics and / or antifungal drugs: treatment begins as soon as the patient any signs of infection show (eg, fever, localized symptoms, deterioration of blood tests, mental status or renal function.). As signs of infection and acute liver failure may be similar, over-treatment of the infection is better, as long as you wait for the results of the culture. Electrolyte disturbances may require supplementation with sodium, potassium, phosphorus and magnesium. Hypoglycemia is treated continuously with a glucose infusion (eg., 10% dextrose), and the blood glucose should be monitored frequently, because the encephalopathy may mask symptoms of hypoglycemia. Coagulopathy is treated with fresh frozen plasma, if bleeding occurs, when an invasive procedure is planned, or when the coagulopathy is heavy (z. B. INR> 7). Fresh frozen plasma is otherwise avoided because it may increase the volume and to the deterioration of cerebral edema lead. In addition, the changes in prothrombin time can not be observed, but this is necessary because the prothrombin is an index of severity of acute liver failure and thus sometimes a criterion for a transplant. Recombinant Factor VII is sometimes used instead of or with fresh frozen plasma in patients with volume overload. Its importance is further developed. H2 blockers can prevent gastrointestinal bleeding. Nutritional support may be necessary if patients can not eat. Strong protein restriction is unnecessary, 60 g / day are recommended. Acute paracetamol overdose is treated with N-acetylcysteine. As a chronic acetaminophen toxicity is difficult to diagnose, the use of N-acetylcysteine ??should be considered when no cause can be found for acute liver failure. Whether N -Acetylcystein has a slightly positive effect on patients with acute liver failure due to other conditions, is currently being investigated in studies. Liver transplantation leads an average to a one-year survival rate of about 80%. Transplantation is recommended if the prognosis without transplantation is worse. However, the prediction is difficult and scores, as the Kings College criteria and APACHE II scores are not sufficiently sensitive and specific to be used as the sole criteria for transplantation; they are supportive used for clinical assessment (eg. as based on risk factors). Summary The most common causes of acute liver failure are viral hepatitis (in developing countries), drugs and toxins (in developed countries). Acute liver failure is characterized by jaundice, coagulopathy and encephalopathy. The diagnosis is confirmed by a prolonged prothrombin time or clinical manifestations of encephalopathy in patients with hyperbilirubinemia and elevated aminotransferase levels. The cause of finding the drug history and exposure to toxins is collected and conducted a hepatitis virus serology, autoimmune markers and other laboratory tests on the basis of clinical suspicion. Complications must be treated intensively, usually in an intensive care unit. N-acetylcysteine ??can with paracetamol-induced liver failure and be considered a liver transplant in patients with poor prognostic factors (eg., Age <10 or> 40, severe encephalopathy, strong increase in prothrombin time, unerwartetete drug effect, Wilson’s disease).

Health Life Media Team

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