PubMed · 14530772
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Mark Shaffrey, Elana Farace. 2003. Decompressive craniectomy.. https://doi.org/10.1097/01.ccm.0000089636.73484.bf
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Acute liver failure is a rare and life-threatening clinical syndrome following severe hepatic injury. Depending on the rapidity of its development, two distinct complications contribute to a high mortality: in hyperacute liver failure, rapid development of massive hepatic necrosis and apoptosis gives rise to severe hyperammonemia, hepatic encephalopathy and life-threatening cerebral edema. The high risk of cerebral herniation requires early listing for emergency liver transplantation. Patients with hyperacute liver failure surviving the initial episode of cerebral edema have a substantial potential for hepatic recovery. If progressive hepatic failure develops more slowly, astrocytic osmoregulation prevents cerebral herniation in most instances. Unfortunately, these patients have a small potential of hepatic regeneration and transplantation should be performed before renal failure, sepsis or multiorgan failure emerge. Experimental treatment methods including detoxification by artificial or bioartificial liver support or by stimulating hepatic regeneration are currently evaluated. Recognition of ammonia toxicity has stimulated the search for early ammonia-lowering strategies and strongly renewed the interest in dialytic therapies. Anti-apoptotic interventions are among the most promising pharmacological options for the near future.
INTRODUCTION: A case of accumulation of CSF into the brain parenchyma simulating a brain tumor, secondary to an obstructed ventriculoperitoneal shunt, is presented. Until now, only seven cases of this rare complication have been described. CASE REPORT: Magnetic resonance showed an expansive, low-density intracranial lesion on the right frontal and parietal lobe. This mass was biopsied, but no tumor was found and the diagnosis was brain edema. CONCLUSION: The mistake in the diagnosis was due to the clinical symptoms and to the MR images.
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