Hepatic encephalopathy stages

Chronic hepatitis (disease lasting longer than 6 months) is usually associated with hepatitis B, C, and D. Chronic viral hepatitis may lead to the development of cirrhosis, which may induce end-stage liver disease (ESLD). Complications of ESLD include ascites, edema, jaundice, hepatic encephalopathy, infections, and bleeding esophageal varices. Therefore, prevention and treatment of viral hepatitis may prevent ESLD. 

End-stage liver disease Liver failure that is usually accompanied by complications such as ascites or hepatic encephalopathy. 

Owing to the multitude of factors interfering with the ammonia concentration as well as to the multifactorial pathogenesis of hepatic encephalopathy (HE), it is understandable that there is no correlation between the levels of ammonia and the prevailing HE stage. Nevertheless, a hyperammonia syndrome is generally presumed if concentrations in the venous or arterial plasma reach 135-170 4g/dl. A value of > 150 gg/dl can be attributed to coma stage I. Here, the arterial ammonia level correlates better with HE than do the values found in venous blood, (s. pp 56, 266)... 

With regard to an altered state of consciousness, the subclinical form of PSE ranges between stages 0 (= normal) and I (= manifestation). (s. pp 270, 276) It is to be expected, as is the case with the majority of diseases, that the manifestation of hepatic encephalopathy will be preceded by a stage of latency. 

Tab. 15.5 Diagram of the stages of hepatic encephalopathy (subclinical and latent forms and manifestation I-IV) as well as their respective symptomatology...

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... 

Fortunately, bed rest, rehydration, parenteral nutrition, and therapy directed at decreasing the production of toxins that result from bacterial degradation of nitrogenous substrates in the gut lumen (e.g., administration of lactulose, which reduces gut ammonia levels by a variety of mechanisms, the use of enemas and antibiotics to decrease the intestinal flora, a low-protein diet) prevented Percy Veere from progressing to the later stages of hepatic encephalopathy. As with most patients who survive an episode of fulminant hepatic failure, recovery to his previous state of health occurred over the next 3 months. Percy s liver function studies returned to normal, and a follow-up liver biopsy showed no histologic abnormalities. 

The client in end-stage liver failure would have hepatic encephalopathy, which affects the cKent s neurological status. Therefore, sedatives, tranquilizers, and analgesic medications are not administered to the cKent. The nurse would question this order. 

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). 

Absolute contraindications include pregnancy, breast feeding, life expectancy less than 1 month, hepatic encephalopathy, tumour stage greater Okuda II and allergy to iodine-containing contrast media. 

Lactulose (certain brands) Prevention and treatment of portal-systemic encephalopathy, including the stages of hepatic precoma and coma. 

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)... 

Lactulose is a hyperosmotic agent, which produces increased osmotic pressure within colon and acidifies its contents, resulting in increased stool water content and stool softening. It causes migration of ammonia from blood into colon, where it is converted to ammonium ion and expelled through laxative action. It is indicated in the treatment of constipation and prevention and treatment of portal-systemic encephalopathy, including stages of hepatic precoma and coma. 

If the patient with kidney failure also has cirrhosis or some other form of hver failure, this additional ammonia load may present a stress that cannot be adequately handled by the diseased liver. The result may be increased blood and central nervous system ammonia levels with development of encephalopathy (Fraser Arieff, 1985). Thus, patients with cirrhosis and end-stage kidney disease are at particular risk for developing encephalopathy since both conditions act synergistically to increase both blood and central nervous system ammonia. It should also be noted that plasma urea and serum creatinine do not always adequately reflect renal function in patients with severe liver disease. Recent studies suggest that many patients who have cirrhosis, ascites, and normal plasma urea and creatinine may in fact have severe renal functional impairment (Gines et al., 1988 Papadakis Arieff, 1987 Takabatake et al., 1988). In such individuals, differentiation of hepatic from uremic encephalopathy on clinical grounds may be difficult. 

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