Coma endogenous

Eulminant liver failure (ELF) is caused by an extensive lost of the liver parenchyma, which results in a severe deterioration of liver function. This clinical picture, which in most cases ends fatally, is also known as liver cell degeneration coma , endogenous liver coma , acute liver insufficiency or acute liver failure . Its causes are multiple and its pathogenesis is complex, see chapter 20)... 

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). 

Naloxone is approved for use in neonates to reverse respiratory depression induced by maternal opioid use. In addition, naloxone has been used to improve circulation in patients in shock, an effect related to blockade of endogenous opioids. Other experimental and less well documented uses for naloxone include reversal of coma in alcohol overdose, appetite suppression, and alleviation of dementia from schizophrenia. Side effects of naloxone are minor. 

The introduction of insulin coma treatment by Sakel was from a historical point of view the decisive step from a purely symptomatic to a curative therapy of the endogenous psychoses. 

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)... 

Exogenous hepatic coma has a better prognosis than endogenous hepatic coma. 

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)... 

Colourless oily liquid chloroform-like odour. Sweet taste. Vapour can be ignited. Irritant to eyes and gut. CNS depressant. Sensitizes myocardium to endogenous catecholamines. Headache, ataxia, dizziness, dilated pupils, convulsions, coma, renal failure (tubular necrosis), liver damage (jaundice), extrapyramidal effects can occur. Death arrhythmia. 

Seiler N, Sarhan S, Knoedgen B, et al. 1993. Enhanced endogenous ornithine concentrations protect against tonic seizures and coma in acute ammona intoxication. Pharmacol Toxicol 72(2) 116-123. 

Naloxone blocks receptor binding of endogenous opioids, called endorphins or enkephalins, produced by the pituitary, as well as blocking the effects of administered narcotics, such as morphine. These blocking drugs are used to awaken patients operated on under opiate anesthesia. Persons in coma from ingesting illegal narcotics, such as morphine or heroin, wake up within seconds after administration of naloxone. 

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