Liver hepatic coma

Kanamycin, neomycin, and paromomycin are used orally in the management of hepatic coma. In this disorder, liver failure results in an elevation of blood ammonia levels. By reducing tire number of ammoniaforming bacteria in the intestines, blood ammonia levels may be lowered, thereby temporarily reducing some of the symptoms associated with this disorder. 

Liver and kidney disease Use with extreme caution in patients with advanced hepatorenal disease and in all patients with abnormal liver function tests because hepatic coma may be precipitated. 

The first human experiments which suggested a toxic effect of ammonia in disease were done by Van Caulaert. The revival and extension of this work by the group led by Davidson (G2) in the Boston City Hospital has stimulated widespread interest in ammonia as a factor in the production of mental symptoms in liver disease. The ability of various factors, such as urea feedings, high-protein diet, cation resins in the ammonia cycle, and amino acids, to induce symptoms of coma in patients with liver disease (G2, M3, M4, P7, S8) made it quite clear that ammonia was associated with the symptom complex called hepatic coma. The severe toxicity of ammonia in animals and the ability of intravenous or oral ammonium salts to provoke episodes of impending liver coma tended to substantiate the clinical impressions. Rapid confirmation of these observations was furnished by the experiments of other groups (Bll, C2, E2, FI). 

It must not be assumed from the foregoing that ammonia is the only cause of hepatic coma, however. Recently evidence has been presented that hepatic failure can be due to a deficiency of certain trace amino acids, precursors of neurohumors normally synthesized in the liver and... 

B8. Bessman, S. P., and Bessman, A. N., The cerebral and peripheral uptake of ammonia in liver disease with an hypothesis for the mechanism of hepatic coma. J. Clin. Invest. 32, 622 (1955). 

A3. Amatuzio, D. S., Weber, L. J., and Nesbitt, S., Bilirubin and protein in the cerebrospinal fluid of jaundiced patients with severe liver disease with and without hepatic coma. /. Lab. Clin. Med. 41, 615-618 (1953). 

Since the disaccharide lactulose cannot be hydrolyzed by digestive enzymes, it also acts as an osmotic laxative. Fermentation of lactulose by colon bacteria leads to acidification of bowel contents and a reduced number of bacteria. Lactulose is used in liver failure to forestall hepatic coma by preventing bacterial production of ammonia and its subsequent absorption (absorbable NH3 —< nonabsorbable NH4 ). Another disaccharide, lac-titol, produces a similar effect. 

A 43-year-old man was admitted to hospital suffering halluoinations. He had fallen off his bike, fraotured a bone in his shoulder, and was presoribed one to two tablets of Tylenol (paracetamol plus codeine) every four to six hours for two days. He oontinued to suffer occasional hallucinations and vomiting and from jaundice. Once in hospital liver function tests on his blood indioated that he had liver damage. He died in a hepatic coma thirty hours after being admitted to hospital. It was later revealed by relatives that the patient had also treated himself with nine Tylenol tablets plus ten tablets of another preparation after the bicycle accident. Another important factor was that he regularly drank half a case (twelve bottles) of beer each day. ... 

In endogenous hepatic coma (= due to loss of liver parenchyma), which in most cases develops from an existing chronic liver disease ( acute on chronic ), the prognosis is better than for acute liver failure, but nevertheless remains extremely poor. According to the information available in the relevant literature, 10-20% of patients die in stage I and 40-50% in stage II in stages III and IV, lethality is 80-90%, the same rate as in acute liver failure, (see chapter 20)... 

Phillips, G.B., Schwartz, R., Gabuzda, G.X, Dabidson, C.S. The syndrome of impending hepatic coma in patients with cirrhosis of the liver given certain nitrogenous substances. New Engl. J. Med. 1952 247 239 - 246... 

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 coma can be subdivided according to its aetiology as follows (7.) hepatocyte disintegration coma (= endogenous coma as a result of the loss of parenchyma), (2.) liver cell failure coma (= exogenous coma as a result of metabolic disorders, almost always in the presence of cirrhosis), (3.) electrolyte coma (= so-called false coma due to dyselectrolytaemia, almost always iatrogenic), and (4.) mixed forms of coma. (s. pp 214, 276, 381) (s. tab. 15.5)... 

Acute liver failure (ALF) is defined as an acute clinical picture with jaundice due to a most severe disorder in the liver function and/or massive liver cell necrosis which, without any pre-existing liver disease, culminates in hepatic coma (= endogenous coma) within 8 weeks. Potentially, the condition is fully reversible (C. Trey et al., 1970). In addition, coagulopathy must also be present (D.F. Schafer et al., 1989). 

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... 

Fulminant or protracted liver failure is caused by medicaments in 10-15% of cases. A reduction in the functional liver mass to < 20-35% is deemed to be a critical stage. However, the death of the patient may already occur due to secondary metabolic disorders (so-called exogenous hepatic coma) before the extent of the parenchymal loss has fallen below the critical threshold (so-called endogenous hepatocellular disintegration coma), (s. tab. 29.10)... 

Complications such as variceal bleeding, hepatic encephalopathy, ascites and infections as well as reduced renal function also influence the mortality rate of liver cirrhosis (in Germany some 25,000/year). The main causes of death are hepatic coma or liver failure (25-40%), bleeding (20-30%), infections (about 10%) and HCC (about 5%). Spontaneous bacterial peritonitis is fatal in 50-70%, and with liver dysfunction even in 90% of cases. Occurrence of the hepatorenal syndrome is almost invariably fatal. 

Occlusion of the hepatic artery is responsible for a 50% reduction in oxygen supply. Even if an unimpaired oxygen supply via the portal vein is guaranteed, arterial occlusion usually causes ischaemic infarction. The clinical and morphological pictures are characterized (1.) by the speed with which an occlusion develops and (2.) by the presence of variants that can be used as a bypass or of collaterals that have already been established in gradual vascular occlusion. This results in a broad clinical spectrum, which may range from a symptom-free condition to liver hypoxia, including infarction up to hepatic coma. 

Increased sensitivity to drugs is also encountered in liver disease. The use of anticoagulants increases the risk of bleeding due to the reduced absorption of vitamin K or decreased production of vitamin K-dependent clotting factors. There is an enhanced risk for respiratory depression and hepatic encephalopathy due to morphine or barbiturates in patients with severe liver disease. Vigorous use of diuretics can precipitate hepatic coma due to potassium loss in liver disease. There is an increased risk of hypoglycemia with... 

Summary 21-year-old female at 35-week gestation with malaise, nausea and vomiting, jaundice, elevated blood pressures, elevated Uver function tests, coagulopathy, hypoglycemia, and subsequently hepatic coma and renal failure. She has been diagnosed with acute fatty liver of pregnancy. 

Chapter 6 reviewed tryptophan and toxic liver disease. This section deals with the effects or influences of tryptophan on chronic liver disease in association with hepatic coma. Chronic liver disease in humans is often associ-... 

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