Controlled hyperventilation in the prevention of cerebral oedema in fulminant hepatic failure

Ede, R J; Gimson, Alexander; Bihari, David; Williams, Roger

doi:10.1016/s0168-8278(86)80007-1

Cited by 168 publications

(72 citation statements)

References 14 publications

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“…Prophylactic hyperventilation does not reduce the frequency of intracranial hypertension in ALF, but a moderate reduction in pCO 2 to 25-30 mmHg is helpful in decreasing the ICP once cerebral edema has begun to develop. 45 Excessive hyperventilation may lead to cerebral vasoconstriction.…”

Section: Hyperventilationmentioning

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: Hyperventilationmentioning

confidence: 99%

Management in Acute Liver Failure

Shalimar

Acharya

2015

Journal of Clinical and Experimental Hepatology

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“…Although a direct correlation between HE and intracranial pressure (ICp) remains unproven, 80% of ALF patients with grade 4 HE have significant cerebral oedema (28). Sudden increases in ICp may cause brain herniation during dissection of the native liver and especially during reperfusion phase.…”

Section: Quality Of the Graftmentioning

confidence: 99%

Bridging Therapies and Liver Transplantation in Acute Liver Failure; 10 Years of MARS Experience from Finland

Kantola¹,

Ilmakunnas²,

Koivusalo³

et al. 2011

Scand J Surg

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acute liver failure is a life-threatening condition in the absence of liver transplantation option. the aetiology of liver failure is the most important factor determining the probability of native liver recovery and prognosis of the patient. extracorporeal liver assist devices like Mars (Molecular adsorbent recirculating system) may buy time for native liver recovery or serve as bridging therapy to liver transplantation, with reduced risk of cerebral complications. Mars treatment may alleviate hepatic encephalopathy even in patients with a completely necrotic liver. taking this into account, better prognostic markers than hepatic encephalopathy should be used to assess the need for liver transplantation in acute liver failure.

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“…However, it should be pointed out that hyperventilation (high V T and frequency) could prevent cerebral edema during AHF. 47 Overall, our study is a novel approach to investigate the pathophysiologic process of lung injury in an experimental model of liver devascularization. Obviously, such studies cannot be performed in a clinical setting because of the inability to control a great variety of confounding factors that could play a role in the development and evolution of lung injury, including (1) presence of different causes of liver failure (viral, toxic, ischemic, and others), (2) application of different treatment strategies (ventilation, use of N-acetylcysteine, vasoconstrictors and mannitol), and (3) availability of the patient for study at different time points of the disease process.…”

Section: Discussionmentioning

confidence: 99%

Alterations in Bronchoalveolar Lavage Fluid During Ischemia–Induced Acute Hepatic Failure in the Pig

et al. 2003

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The objective of this controlled experimental animal study was to evaluate whether acute hepatic failure (AHF) can cause acute lung injury (ALI) and to investigate possible pathophysiologic mechanisms. Seventeen domestic pigs were randomly assigned to AHF and sham groups. AHF was induced by surgical devascularization of liver in 10 animals. Seven animals were sham operated. Hemodynamics, lung mechanics, extravascular lung water (EVLW), and intracranial pressure, blood gas, liver function tests, and serum endotoxin levels were measured. Cells count, total protein, and phospholipids and phospholipases A 2 were determined in the bronchoalveolar lavage (BAL) fluid. Measurements were obtained after the insertion of central lines and 4 hours and 7 hours after the completion of the surgical procedure. Hemodynamic, biochemical, neuromonitoring, and histologic data confirmed the development of liver failure. Seven hours after devascularization, EVLW was higher in AHF (13.7 ؎ 1.8 mL/kg) compared with the sham group (5.9 ؎ 0.7 mL/kg) (P < .05); in AHF, increase of neutrophils (5% ؎ 8% to 25% ؎ 8%, P < .001), total protein (6.2 ؎ 3.7 to 11.2 ؎ 6.5 g/mL, P < .048), and phospholipase A 2 (1.43 ؎ 0.56 to 2.38 ؎ 1.38 nmoL/mL/h, P < .03) and decrease in PAF-acetylhydrolase (0.114 ؎ 0.128 to 0.039 ؎ 0.038 nmol/mL/h, P < .01) compared with baseline were observed; total phospholipids decreased in AHF and increased in the sham model. Histologic examination confirmed lesions compatible with acute lung injury. In conclusion, AHF due to hepatic devascularization induced acute lung injury, confirmed by the increase of inflammatory cells in the alveoli as well as by histologic findings. The decreased PAF-AcH and the increased phospholipase A 2 may play a significant role in the perpetuation of inflammation accompanied by surfactant disorders. (HEPATOLOGY 2003;37:1130-1138

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Controlled hyperventilation in the prevention of cerebral oedema in fulminant hepatic failure

Cited by 168 publications

References 14 publications

Management in Acute Liver Failure

Management in Acute Liver Failure

Bridging Therapies and Liver Transplantation in Acute Liver Failure; 10 Years of MARS Experience from Finland

Alterations in Bronchoalveolar Lavage Fluid During Ischemia–Induced Acute Hepatic Failure in the Pig

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