result of liver failure as well as from infection. Clinical bleeding should be treated with
factor replacement rather than treating laboratory abnormalities. Infusion of factor concentrates or platelets may be necessary. Plasmapheresis may be useful for
temporary correction of coagulopathy without resulting in volume overload. Administration of fresh frozen plasma should not be routinely practiced due to its volume overload.
Infection Infection and uncontrolled bleeding remain the main two causes of demise in patients with FHF. A high index of suspicion and frequent bacteriological investigation are necessary for early investigation. Over 50% of patients experience serious infection including septicemia, pneumonia, peritonitis, and urinary tract infections. Infections with gram positive and gram-negative organisms, as well as fungal infections can occur.
Hepatic Encephalopath Hepatic encephalopathy may become a medical emergency. Hospitalization is required. The first step is to identify and treat any factors that may have caused hepatic encephalopathy. Table 4 lists the triggering factors for hepatic encephalopathy. Table 5 shows the factors that mimic hepatic encephalopathy. Sedation should be avoided as much as possible to allow close monitoring if the patient’s mental status. . The key factors in the management of hepatic encephalopathy are:
«Autoimmune hepatitis can present as FHF with most of the affected patients having liver/ kidney microsomal antibodies»
A. Osmotic diuresis, which is believed to maintain cerebral perfusion pressure B. Hyperventilation may worsen oxygen availability to the brain.
Lactulose is a non-absorbable disaccharide, is metabolized to organic acids by the colonic flora decreasing microbial ammonia synthesis and works by trapping of ammonia in the acidic colonic contents. It is administered by either oral rout or retention enema. Neomycin, a non-absorbable antibiotic
may be given to suppress enteric bacteria, which produce ammonia. While some practitioners prefer to hold on daily protein intake others restrict protein intake to an amount enough to avoid metabolic catabolism at a half gram per kg per day. Several approaches have been used
to remove toxins contributing to the encephalopathy. Plasma perfusion such as plasmapheresis may result in some clinical improvement but these treatments, when analyzed in controlled trials, did not improve survival. Recently, liver-assist devices (liver dialysis) such as Molecular Absorbant Recycling System (MARS), Prometheus, Single Pass Albumin Dialysis
(SPAD) (perfusion of the patient’s plasma through an anion exchange resin, albumin and charcoal columns). The is the first human liver-based cells(C3A) cell biologic, ELAD depends on perfusion of patient’s plasma through columns of neuoblastoma cells that are found to duplicate the function of hepatocytes is under evaluation. These devices are being used to support patients until regeneration of the patient’s liver occurs, or bridging the liver for transplant. Corticosteroid administration is of no
real value. Placement of an intracranial pressure
monitor may be useful in guiding treatment but rarely used in infants and children. Orthotopic liver transplantation is
life-saving in patients who reach advanced stages of coma. Reduced-sized allograft and living related donor transplantation have been additional advances in the treatment of infants with hepatic failure.
Prognosis The prognosis varies and depends on the etiology of the hepatic injury and stage of encephalopathy. Mortality rate approaches 75% by
some reviewers. With intensive medical therapy, rates of survival of over 50 % can be achieved in liver failure complicating acetaminophen overdose and some patients with fulminant hepatitis A or B infection. In contrast, children with non-A, non-B, non-C hepatitis or the acute form of Wilson’s disease rarely recover without liver transplantation. In patients who progress to stage IV coma, the prognosis is extremely poor.
Complications of liver failure including
sepsis, haemorrhage, or renal failure increase the mortality. Patients who are fortunate enough to recover with only supportive care do not usually develop cirrhosis or chronic liver disease. ■
AH
AUTHOR INFO 1
Section of Paediatric Gastroenterology and Hepatology, Department of Paediatrics
Section of Paediatric Gastroenterology and Hepatology, Department of Paediatrics, King Faisal Specialist Hospital and Research Center, Riyadh, Saudi Arabia.
Sheikh Khalifa Medical City, Abu Dhabi, UAE. 2
REFERENCES References available on request (
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