Hepatic encephalopathy acute liver failure

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. 

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]. 

There can be a pronounced increase in methionine and its derivatives in acute liver failure or in serious cases of cirrhosis. From these substances, mercaptans are formed in the colon (e. g. methandiol, ethandiol, dimethyldisul-phide). The cause of the sweetish aromatic smell of the expiratory air ( fresh-raw liver ) known as hepatic foetor (F. Umber, 1926 L. Schiff, 1946) is deemed to be volatile dimethylsulphide. (38) Its concentration does not correlate with the degree of encephalopathy or hepatic insufficiency, but with the intensity of the portosystemic shunts. Trimethylamine is also suspected of being a causative factor. (22) (s.pp 267, 379)... 

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. 

The decompensated stage, i.e. manifest liver insufficiency, can present as cellular decompensation (e. g. in the case of acute liver failure due to toxic or inflammatory mass necrosis) or be expressed only in the form of portal decompensation (e.g. in cases of postsinusoidal intra-hepatic portal hypertension). As a rule, chronic liver insufficiency is accompanied by a combined decompensation with a loss in function of the liver cells and, at the same time, the sequelae of portal decompensation (collateral varicosis, encephalopathy, ascites, hepatorenal syndrome, variceal bleeding), (see chapters 15 19 and 35)... 

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)... 

Also in contrast to cirrhotics and patients with porto-systemic bypass without hepato-cellular disease, altered mental status in patients with acute liver failure may be due to the presence of seizure activity or hypoglycemia. A status of complex partial seizures may be misinterpreted as bizarre behaviour in the course of acute hepatic encephalopathy. Seizures may even continue under neuroleptanalgesia, and then cannot be detected by clinical observation. 

Unfortunately, the development of brain edema can hardly be monitored in patients with acute liver failure. Brain edema mostly occurs when hepatic encephalopathy has progressed to grades III to IV. In grades I-II encephalopathy, it has rarely been observed. With progression to grade III HE cerebral edema occurs in up to 35% and with grade IV HE in 65 to 75% of the patients (Munoz, 1993). 

As in acute liver failure, the main symptoms of HE are alterations in consciousness, cognitive dysfunction and motor disturbances. While patients with ALE often appear irritable and restless in the very beginning, psychomotor slowing is characteristic for type C HE. The alteration of consciousness is the basis for the 4-stage grading system of hepatic encephalopathy used world wide (West Haven classification) (Atterbury et al., 1978). 

Yurdaydin, C., Herneth, A.M., Puspok, A., Steindl, R, Singer, E., and Ferenci, P. 1996. Modulation of hepatic encephalopathy in rats with thioacetamide-induced acute liver failure by serotonin antagonists. Eur. J. Gastroenterol. Hepatol. 8 667-671. 

A 48-year-old woman with normal liver function took venlafaxine 75 mg/day and trazodone 200 mg/day for depression and 4 months later developed increasing jaundice and encephalopathy. She had markedly raised transaminases and bilimbin. There were no other explanations for her hepatic failure, and she received an urgent liver transplantation. The pathology showed severe acute hepatitis compatible with toxic acute liver failure. She recovered fully, and had normal liver function tests 1 year later. 

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>. 

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. 

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 precise pathogenesis of the central nervous system (CNS) signs and symptoms that accompany liver failure (hepatic encephalopathy) in patients such as Percy Veere is not completely understood. These changes are, however, attributable in part to toxic materials that are derived from the metabolism of nitrogenous substrates by bacteria in the gut that circulate to the liver in the portal vein. These materials "bypass" their normal metabolism by the liver cells, however, because the acute inflammatory process of viral hepatitis severely limits the ability of liver cells to degrade these compounds to harmless metabolites. As a result, these toxins are "shunted" into the hepatic veins unaltered and eventually reach the brain through the systemic circulation ("portal-systemic encephalopathy"). 

The two most serious complications of acute viral hepatitis found in J patients such as Percy Veere are massive hepatic necrosis leading to ful- minant liver failure and the eventual development of chronic hepatitis. Both complications are rare in acute viral hepatitis type A, however, suggesting that acetaminophen toxicity may have contributed to Percy s otherwise unexpectedly severe hepatocellular dysfunction and early hepatic encephalopathy. 

B. After 24-48 hours, when transaminase levels (AST and ALT) begin to rise, hepatic necrosis becomes evident. If acute fulminant hepatic failure occurs, death may ensue. Encephalopathy, metabolic acidosis, and a continuing rise in the prothrombin time (PT) indicate a poor prognosis. Acute renal failure occasionally occurs, with or without concomitant liver failure. 

Hepatic Encephalopathy (HE) is a serious neuropsychiatric complication of both acute and chronic liver failure. A study group concluded in 2002 that HE is a spectrum of neuropsychiatric abnormalities seen in patients with liver dysfunction after exclusion of other known brain diseases (Ferenci et al., 2002). A multiaxial definition of HE was proposed that defines both the type of hepatic abnormality and the characteristics of the neurological manifestations. Three types of hepatic abnormalities were defined, namely ... 

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome associated with severe, acute and chronic liver failure. According to the recommendations of a working party (Ferenci et al 2002) held at the d"" World Congress of Gastroenterology in Vienna in 1998, 3 types of HE should be differentiated, on principle ... 

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