Controlled trial of dexamethasone and mannitol for the cerebral oedema of fulminant hepatic failure.

Canalese, J.; Gimson, Alexander; Davis, Chester; Mellon, P. J.; Davis, Michael; Williams, Roger

doi:10.1136/gut.23.7.625

Cited by 290 publications

(121 citation statements)

References 9 publications

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“…65 In a controlled trial of 44 patients it was found that the use of dexamethasone could not prevent the development of cerebral edema or improve survival. 66 In a recent prospective randomized trial involving 30 patients with ALF, it was found that use of hypertonic (30%) sodium chloride infusion to maintain serum sodium levels between 145 and 155 mmol/L led to a significant decrease in ICP. 35 …”

Section: Ammonia Lowering Strategiesmentioning

confidence: 99%

Management in Acute Liver Failure

Shalimar

Acharya

2015

Journal of Clinical and Experimental Hepatology

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Acute liver failure (ALF) is a rare, potentially fatal complication of severe hepatic illness resulting from various causes. In a clinical setting, severe hepatic injury is usually recognised by the appearance of jaundice, encephalopathy and coagulopathy. The central and most important clinical event in ALF is occurrence of hepatic encephalopathy (HE) and cerebral edema which is responsible for most of the fatalities in this serious clinical syndrome. The pathogenesis of encephalopathy and cerebral edema in ALF is unique and multifactorial. Ammonia plays a central role in the pathogenesis. The role of newer ammonia lowering agents is still evolving. Liver transplant is the only effective therapy that has been identified to be of promise in those with poor prognostic factors, whereas in the others, aggressive intensive medical management has been documented to salvage a substantial proportion of patients. A small fraction of patients undergo liver transplant and the remaining are usually treated with medical therapy. Therefore, identification of the complications and causes of death in such patients, and use of appropriate prognostic models to identify those who need liver transplant and those who can be managed with medical treatment is a vital component of therapeutic strategy. In this review, we discuss the various pathogenetic mechanisms and treatment options available. ( J CLIN EXP HEPATOL 2015;5:S104-S115)A cute liver failure (ALF) can be a fatal complication of acute hepatic injury and occurs unpredictably. It is a rare clinical entity marked by the sudden loss of hepatic function and a severe life-threatening course in a person with no prior history of liver disease. ALF represents a syndrome rather than a specific disease, having multiple causes that vary in course and outcome. ALF is difficult to identify in its early stages, resulting in frequent delays in initiation of treatment. The causes of ALF include viral hepatitis, drug induced and toxin-induced liver damage, metabolic errors, ischemia, and miscellaneous rare causes.ALF is defined by three criteria: (1) rapid development of hepatocellular dysfunction (jaundice, coagulopathy), (2) encephalopathy, and (3) absence of a prior history of liver disease. 1 However, the interval between onset of acute hepatic injury (jaundice) and onset of liver failure (encephalopathy with or without coagulopathy) in such patients (icterus-encephalopathy interval; IEI) has been described to be between 4 weeks (Indian definition) 2-4 to 24 weeks (AASLD-ALF study group). 5 Further, due to the diverse natural course, ALF has been sub-classified as hyperacute (IEI # 7 day), acute (IEI # 4 weeks) and sub-acute ALF (IEI $ 5 week to #12 weeks) by British authors. 6 Despite these differences in definitions, the central and most important clinical event in ALF is occurrence of hepatic encephalopathy (HE) and cerebral edema which is responsible for most of the fatalities in this serious clinical syndrome. The pathogenesis of encephalopathy and cerebral edema in ALF is unique an...

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Section: Ammonia Lowering Strategiesmentioning

confidence: 99%

Management in Acute Liver Failure

Shalimar

Acharya

2015

Journal of Clinical and Experimental Hepatology

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“…3 The glutamine hypothesis 7 suggests that water diffuses across the blood-brain barrier and into astrocytes, resulting in cerebral edema and IH. Thus, it can be expected that agents that increase extracellular osmolality, such as mannitol, will reduce IH 8 and that in contrast, a decrease in extracellular fluid osmolality will be associated with an increase in brain swelling. 3 In the current prospective randomized controlled clinical trial, we investigated the effects of systemic hypernatremia (via hypertonic saline infusion) on the incidence of IH in patients with ALF and Grade III or IV encephalopathy.…”

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confidence: 99%

The effect of hypertonic sodium chloride on intracranial pressure in patients with acute liver failure

et al. 2004

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Acute liver failure (ALF) is a rare condition characterized by the development of encephalopathy in the absence of chronic liver disease. Cerebral edema occurs in up to 80% of patients with Grade IV encephalopathy. In the current prospective randomized controlled clinical trial, we examined the effect of induced hypernatremia on the incidence of intracranial hypertension (IH) in patients with ALF. Thirty patients with ALF and Grade III or IV encephalopathy were randomized. Patients in Group 1 (n ‫؍‬ 15) received the normal standard of care. Patients in Group 2 (n ‫؍‬ 15) received standard care and hypertonic saline (30%) via infusion to maintain serum sodium levels of 145-155 mmol/L. Intracranial pressure (ICP) was monitored in all patients with a subdural catheter (Camino Systems, San Diego, CA) for up to 72 hours after inclusion. Serum sodium levels became significantly different from the levels observed in the control group at 6 hours (P < .01). Over the first 24 hours, norepinephrine dose increased relative to baseline in the control group (P < .001; 13 patients) but not in the treatment group. ICP decreased significantly relative to baseline over the first 24 hours in the treatment group (P ‫؍‬ .003; 13 patients) but not in the control group. The incidence of IH, defined as a sustained increase in ICP to a level of 25 mm Hg or greater, was significantly higher in the control group (P ‫؍‬ .04). In conclusion, induction and maintenance of hypernatremia can reduce the incidence and severity of IH in patients presenting with ALF. (HEPATOLOGY 2004;39:464 -470.)

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“…2 For many years, the treatment of brain edema in FHF has been symptomatic. The use of mannitol to remove intracerebral water, 3 mild elevation of the head of the bed to favor venous drainage, 4 or continuous renal replacement methods to lessen the impact of rapid fluid shifts with intermittent dialysis 5 are useful approaches but are inherently limited. They do not address the mechanisms that lead to the development of brain edema.…”

mentioning

confidence: 99%

Medical Therapy of Brain Edema in Fulminant Hepatic Failure

Blei

2000

Hepatology

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Controlled trial of dexamethasone and mannitol for the cerebral oedema of fulminant hepatic failure.

Cited by 290 publications

References 9 publications

Management in Acute Liver Failure

Management in Acute Liver Failure

The effect of hypertonic sodium chloride on intracranial pressure in patients with acute liver failure

Medical Therapy of Brain Edema in Fulminant Hepatic Failure

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