Cerebral Edema: A Major Complication of Massive Hepatic Necrosis

Ware, A. A.; D'Agostino, A; Combes, Burton

doi:10.1016/s0016-5085(19)33402-x

Cited by 246 publications

(68 citation statements)

References 15 publications

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“…The patients with acute liver failure experience asterexis, hyperflexia, cortical blindness, retarded speech, seizures, brain edema and coma. The death in these cases is more often due to cerebral edema as a result of increased intracranial pressure and brain herniation [9,10]. In hepatic failure surveillance study, a very poor survival rate was observed in these patients.…”

Section: Introductionmentioning

confidence: 99%

Thioacetamide-Induced Fulminant Hepatic Failure Induces Cerebral Mitochondrial Dysfunction by Altering the Electron Transport Chain Complexes

et al. 2011

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Fulminant hepatic failure (FHF) is an acute form of hepatic encephalopathy resulting from severe inflammatory or necrotic liver damage without any previously established liver damage. This develops as a complication due to viral infections, and drug abuse. FHF also occurs in acute disorders like Reye's syndrome. Although the exact mechanisms in the etiology of FHF are not understood, elevated levels of brain ammonia have been consistently reported. Such increased ammonia levels are suggested to alter neurotransmission signals and impair cerebral energy metabolism due to mitochondrial dysfunctions. In the present study we have examined the role of cerebral electron transport chain complexes, including complex I, II, III IV, and pyruvate dehydrogenase in the non-synaptic mitochondria isolated from the cortex of the thioacetamide-induced FHF rats. Further, we have examined if the structure of mitochondria is altered. The results of the current study demonstrated a decrease in the activity of the complex I by 31 and 48% at 18 and 24 h respectively after the thioacetamide injection. Similarly, the activity of electron transport chain complex III was inhibited by 35 and 52% respectively, at 18 and 24 h, respectively. The complex II and complex IV, on the other hand, revealed unaltered activity. Further the activity of pyruvate dehydrogenase at 18 and 24 h after the induction of FHF was inhibited by 29 and 43%, respectively. Our results also suggest mitochondrial swelling in FHF induced rats. The inhibition of the respiratory complexes III and I and pyruvate dehydrogenase might lead to the increased production of free radical resulting in oxidative stress and cerebral energy disturbances thereby leading to mitochondrial swelling and further contributing to the pathogenesis of FHF.

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Section: Introductionmentioning

confidence: 99%

Thioacetamide-Induced Fulminant Hepatic Failure Induces Cerebral Mitochondrial Dysfunction by Altering the Electron Transport Chain Complexes

et al. 2011

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“…Mortality is variably estimated to be between 50 and 90% [2]. The usual cause of neurologic morbidity and mortality is cerebral edema [3], thought to originate from astrocytic swelling [4]. Astrocytic edema is caused largely by elevated ammonia, which can only be metabolized by astrocytic glutamine synthetase, leading to glutamine accumulation and osmotic swelling [5].…”

Section: Introductionmentioning

confidence: 99%

Recovery of Awareness after Hyperacute Hepatic Encephalopathy with “Flat” EEG, Severe Brain Edema and Deep Coma

Hunter

Young

2010

Neurocrit Care

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“…Age as a significant risk factor was first reported by Ware et al in 1971 with a risk cut off at approximately 30-35 years-similar observations have been made by Bernal et al [3,16]. It may well be that the protective effect of aging in regard of cerebral edema and its associated complications are merely that extra space is afforded by a shrinking aged brain in a fixed cranium.…”

Section: Mechanisms Of Cerebral Edemamentioning

confidence: 60%

Encephalopathy and Cerebral Edema in the Setting of Acute Liver Failure: Pathogenesis and Management

Wendon

Lee

2008

Neurocrit Care

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Cerebral edema is a potential life-threatening complication in patients with acute liver failure who progress to grade III/IV encephalopathy. The incidence is variably reported but appears to be most prevalent in those patients with hyperacute liver failure as opposed to subacute forms of liver failure. In those patients who are deemed at risk of cerebral edema and raised intracranial pressure, insertion of an intra-cranial pressure monitoring device may be considered to optimize treatment and interventions. The pathogenesis of cerebral edema in this setting remains controversial, although recent work suggests a pivotal role for arterial ammonia, whose effects appear to be potentiated by the presence of systemic inflammation. Recent work has also suggested the import of free radical formation occurring at a mitochondrial level as being the potential mediator of cellular dysfunction as opposed to ammonia per se. Treatment of such patients requires a multi-disciplinary approach incorporating both hepatology and critical care. In a significant proportion of such cases, consideration of liver transplantation may be required. Treatment should be focused at optimizing liver function and regenerative capacity and minimizing the inflammatory milieu. Controlled studies are lacking and much of the management has been extrapolated from neurocritical care. Sustained elevation of intracranial pressure may be responsive to mannitol or hypertonic saline bolus, and in those with hyperemia indomethacin has been reported as beneficial in case series. Recently, interest has developed into the use of cooling in the management of patients with acute liver failure and raised intracranial pressure. Animal studies support this treatment option as do case series, although randomized trials are still awaited.

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Cerebral Edema: A Major Complication of Massive Hepatic Necrosis

Cited by 246 publications

References 15 publications

Thioacetamide-Induced Fulminant Hepatic Failure Induces Cerebral Mitochondrial Dysfunction by Altering the Electron Transport Chain Complexes

Thioacetamide-Induced Fulminant Hepatic Failure Induces Cerebral Mitochondrial Dysfunction by Altering the Electron Transport Chain Complexes

Recovery of Awareness after Hyperacute Hepatic Encephalopathy with “Flat” EEG, Severe Brain Edema and Deep Coma

Encephalopathy and Cerebral Edema in the Setting of Acute Liver Failure: Pathogenesis and Management

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