Hepatic encephalopathy acute

Add protein back in 20 g increments every 3-5 d once acute hepatic encephalopathy improves and until protein caloric goal is achieved (usually 0.8-1 g/kg/d)... 

In acute hepatic encephalopathy, temporary protein restriction to decrease the rate of ammonia production can... 

Rifaximin Rifamycin Antibiotic Gut bacteria Enteric infection Diarrhea, infectious Hepatic encephalopathy Small intestine bacterial overgrowth Inflammatory bowel disease Colonic diverticular disease Irritable bowel syndrome Constipation Clostridium difficile infection Helicobacter pylori infection Colorectal surgery Bowel decontamination, selective Pancreatitis, acute Bacterial peritonitis, spontaneous Nonsteroidal anti-inflammatory drug enteropathy... 

Rifaximin is available in Europe for the treatment of acute intestinal bacterial infections, hepatic encephalopathy, bacterial overgrowth syndrome, diverticular disease of the colon, and for the prevention of infections after colorectal surgery [3, 4]. Rifaximin is also licensed in Mexico, Asia and Northern Africa and has recently been approved in USA for the treatment of traveler s diarrhea. 

Mas A, Rodes J, Sunyer L, Rodrigo L, Planas R, Vargas V, Castells L, Rodriguez-Martinez D, Fernandez-Rodriguez C, Coll I, Pardo A Comparison of rifaximin and lactitol in the treatment of acute hepatic encephalopathy Results of a randomized, double-blind, doubledummy, controlled clinical trial. J Hepatol 2003 38 51-58. 

Treatment Goals Acute and Chronic Hepatic Encephalopathy... 

Lactulose (Constulose, Generlac, Enulose, Others) [Laxative/ Osmotic] Uses Hepatic encephalopathy constipation Action Acidifies the colon, allows ammonia to diffuse into colon Dose Acute hepatic encephalopathy. 30-45 mLPO qlh until soft stools, then tid-qid Chronic laxative therapy 30-45 mL... 

Six unselected patients (four women), mean age 27 years, with acute liver failure and grade IV hepatic encephalopathy received terlipressin 0.005 mg/kg as a single intravenous bolus (16). There was an increase in cerebral blood flow 1 hour after the bolus, which returned to baseline at 5 hours, and an increase in intracranial pressure at 1 hour, which returned to baseline at 2 hours. The authors speculated that terlipressin could have a deleterious effect on cerebral hemodynamics in patients with severe hepatic encephalopathy. 

Lactitol 40 is a disaccharide that has been used in the management of hepatic encephalopathy, a major neuropsychiatric complication of both acute and chronic liver failure. It has mild laxative properties and is used to reduce the production and absorption of gut-derived neurotoxic substances symptomatic of hepatic encephalopathy. Although long considered a first-line pharmacological treatment, there is a lack of sufficient evidence to support lactitol s efficacy and continued use when weighed against other suitable therapeutic alternatives such as oral antibiotics <2006MI94>. 

Hepatic encephalopathy is a neuropsychiatric syndrome which may complicate almost all types of liver disease. It may occur intermittently and be reversible or may occur acutely, with rapid progression to coma and death. Mrs MW presented with signs of hepatic encephalopathy including flapping tremor of the hands, intellectual deterioration, slurred speech, confusion, drowsiness and irritability. 

Drugs that can disturb fluid-electrolyte balance must be used with caution in patients with certain types of liver impairment. Diuretics, for example, are often required to treat ascites but can cause hypo-natraemia, hypo- or hyperkalaemia. A disturbance in electrolyte balance can lead to encephalopathy in susceptible patients such as cirrhotics or those with acute liver failure. Dehydration induced by diuretics is a common precipitant of hepatic encephalopathy. The mechanism is not fully understood, but could possibly be due to the reduced metabolism of hepatic toxins because of hepatic hypoxia [5]. 

Suppression of bowel flora is thought by some to be useful in hepatic encephalopathy. Here, absorption of products of bacterial breakdown of protein (ammonium, amines) in the intestine lead to cerebral symptoms and even to coma. In acute coma, neomycin 6 g/d should be given by gastric tube as prophylaxis, 1-4 g/d may be given to patients with protein intolerance who fail to respond to dietary protein restriction (see also lactulose, p. 640). 

Hepatic encephalopathy (HE) is defined as a functional, potentially reversible disorder of the brain in the wake of severe (either acute or chronic) liver disease. The term comprises all neurological and mental symptoms. 

Levy, L.J., Bolton, R.R, Losowsky, M.S. The visual evoked potential in clinical hepatic encephalopathy in acute and chronic liver disease. Hepato-Gastroenterol. 1990 (Suppl. II) 37 66-73... 

The occurrence of hepatic encephalopathy (HE) is only possible under the following conditions (1.) a serious (acute or chronic) liver disease, in which the detoxification function is significantly restricted, has to be present, and/or (2.) a functional or anatomic portosystemic collateral circulation must exist — this can be placed surgically or in the form of a TIPS (72, 90) -through which the nondetoxified portal blood bypasses the liver, so that toxic substances can reach the brain. 

While hepatic encephalopathy is nearly always found in acute liver failure, it can only be expected in some 25-40% of patients with a portosystemic shunt. When these two preconditions coincide, as in the case of liver cirrhosis, manifest hepatic encephalopathy is witnessed in 30-50% of patients and a subclinical course of disease in 50-70%. In other words, the frequency, the degree of severity and the course taken by HE depend on the underlying conditions. 

Laccetti, M., Manes, G., Uomo, G., Lioniello, M., Rabitti, P.G., Balz-ano. A. Flumazenil in the treatment of acute hepatic encephalopathy... 

Sushma, S., Dasarathy, S., Tandon, R.K., Jain, S., Gupta,S., Bhist, M.S. Sodium benzoate in the treatment of acute hepatic encephalopathy a double-blind randomized trail Hepatology 1992 16 138—144... 

Complications The possible outcome of oesophageal haemorrhage can take the following forms (7.) haemorrhagic shock, (2.) acute liver or kidney failure, (S.) hepatic encephalopathy (culminating in hepatic coma), (4.) consumptive coagulopathy, and (5.) aspiration pneumonia. 

Clinically, there are three different courses of disease following the onset of jaundice .) fulminant or hyperacute liver failure (= occurrence of hepatic encephalopathy in the 1 week), (2.) acute liver failure (= occurrence of hepatic encephalopathy between the and 4 week), and (5.) subacute liver failure (= occurrence of hepatic encephalopathy between the 5 and 8 week). Surprisingly, however, it could be shown that 30-40% of the hyperacute forms survived in spite of the development of hepatic coma and cerebral oedema. As opposed to this, the subacute forms displayed a survival rate of only 10-20%, despite a lower frequency of cerebral oedema and better liver function, (s. tab. 20.1)... 

In the course of acute or chronic liver disease, the biochemical functions of the liver may be compromised indefinitely the outcome is decompensated liver insufficiency. (s. pp 277, 381) (s. tab. 20.4) The stage of decompensation is synonymous with the onset of life-threatening complications. These mainly take the form of hepatic encephalopathy with transition to hepatic coma (see chapter 15), oedema and ascites with imbalance of the electrolytes and the acid-base equilibrium (see chapter 16) through to the hepatorenal syndrome (see chapter... 

Hepatic encephalopathy is a metabolic disorder characterized by a wide spectrum of neuropsychiatric dysfunction. It may occur as an acute syndrome in patients with acute hepatic failure from viral or drug-induced hepatitis or as a chronic syndrome associated with liver failure and cirrhosis. 

The pathophysiology of hepatic encephalopathy is not completely understood but includes an increased sensitivity to dietary proteins. Ammonia concentrations are always increased with acute encephalopathy and usually increased with chronic encephalopathy. A reduction of plasma ammonia is often associated with symptomatic improvement. However, since plasma ammonia concentrations do not correlate with the severity of the encephalopathy, it has been suggested that other factors are involved. It is now recognized that a variety of neurotransmitter systems are dysfunctional in hepatic encephalopathy, but the exact cause for the changes is not known. One important contributor is the endogenous benzodiazepine agonist system, but other abnormalities must be invoked to explain all the findings. ... 

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