Signs of hepatic coma may include a bright white tinged tongue, a pale and puffy complexion, and a rapid heart rate. Decreased liver function tests, jaundice, and a rapid, deep breathing can all be signs of hepatic coma. However, these signs are not specific to hepatic coma.
There is no evidence that hepatic coma can be cured. The main challenge will continue in improving the management and improving the outcome with these complex problems.
The authors conclude that the average yearly incidence rate of hepatic coma in the United States is 2.1 per 100,000 person-years (1.2 per 100,000 person-years in the United States population). This rate is higher than that reported by most other authors and warrants further investigation for reasons ranging from the definition of hepatic coma to its occurrence.
The most common treatment for hepatic coma is hepatic artery infusion for the treatment of blood loss. Additional treatments include a hypertonic saline solution and the placement of an arterial drip for the prevention of hepatic encephalopathy.
A significant number of patients who develop hepatic coma do not meet the criteria for severe sepsis or disseminated intravascular coagulation. The authors hypothesize that a combination of hepatic venous occlusion (leading to hepatic hypoperfusion and hypoxia) combined with a high level of cellular stress (due to ischemia induced mitochondrial dysfunction or increased neutrophil sequestration in injured tissue) is required to produce hepatic coma.
This article examines the hepatic coma as the state of being severely ill from the hepatic point of view. It can be found that a lot of the time patients with hepatic coma are at risk of dying from a variety of factors. It can not be denied that even patients with very mild degree of hepatic coma may still have a chance to live and the possibility of recovery from the comatose cases may also occur.
All cases of hepatic coma are still fatal. The cause of liver failure is not known, but several treatment options have been assessed and no consensus has emerged. At our centre, the mainstay of care is palliative treatment as it continues to improve. It appears that a greater understanding of the precise pathophysiology is needed for progress.
The causes of hepatic coma can be divided into primary and secondary. Most often, the causes are traumatic and may include liver injury, gastrointestinal bleeding, hypovolemia, electrolyte disturbances, and hypothermia. There is, however, no absolute evidence as to the exact cause of hepatic coma. Although it may be difficult to define an exact cause, early recognition and care might result in a better outcome and lessen the need for invasive medical measures. Liver failure, which is a major cause of hepatic coma, is uncommon, because patients usually experience either significant trauma to the liver or significant blood loss due to gastrointestinal bleeding. Hepatic coma has been considered an emergency, needing resuscitation, as soon as possible.
Familial hepatic coma is characterized by mild to moderate forms of familial hypertriglyceridemia type 1 but other lipid disorders such as dyslipidemias, lipodystrophy, and familial hypercholesterolemia are not likely to play a major role.
The new oral capsule systems are more consistent in their performance compared with preloaded fmt oral capsules (FCR-3, FCR-5) and show similar efficacy and safety profiles for treating a very specific set of patients and indications. Moreover, they provide a simplified therapeutic pathway for the intestinal microbiota by providing an alternative to the older FC-suppository in terms of safety and convenience. This novel oral capsule version has the potential to simplify therapy for very specific indications and patients.
The study concluded that the main primary hepatic causes of hepatic coma were bleeding from portal hypertension and alcoholic liver disease. This has not changed in recent years, but the causes in the other group have changed. The leading cause of severe hepatic coma has also changed: it is now hemorrhagic shock from traumatic shock. The other subgroup of traumatic shock now leads to serious liver dysfunction. The most common causes of acute liver dysfunction are infections and drug-related liver dysfunction. These data contribute to the theory of a nonspecific liver injury as the main underlying pathologic condition, and emphasize that liver injury from hemorrhaging or traumatic shock is usually reversible.
Hepatic coma is rare before age 50 and much less common after age 50. The average age of an individual at the time of presentation was 60.2 years for males and 55.5 years for females with HCC. These data support the hypothesis that hepatic coma develops as a result of chronic liver disease.