Liver function, cerebral blood flow autoregulation, and hepatic encephalopathy in fulminant hepatic failure

Strauss, Gitte; Hansen, Bent Adel; Kirkegaard, Preben; Rasmussen, Allan; Hjortrup, A; Larsen, Fin Stolze

doi:10.1002/hep.510250409

Cited by 101 publications

(64 citation statements)

References 9 publications

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“…This loss of autoregulation is restored within 1 day of liver transplant and within 4 days of spontaneous recovery. 32 Even hypothermia restored cerebral autoregulation in a series of 14 patients with ALF. 33 …”

Section: Loss Of Cerebral Auto Regulationmentioning

confidence: 95%

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: Loss Of Cerebral Auto Regulationmentioning

confidence: 95%

Management in Acute Liver Failure

Shalimar

Acharya

2015

Journal of Clinical and Experimental Hepatology

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“…CBF could be a differentiating factor involved in the development of intracranial hypertension in ALF vs. CLD. A decrease in CBF has been documented in patients with CLD (Almdal et al, 1989, Burra et al, 2004, Dam et al, 1998, Iversen et al, 2009, Iwasa et al, 2000and Trzepacz et al, 1994, whereas an increase in CBF commonly occurs during ALF (Jalan et al, 2004a, Larsen et al, 1996, Strauss et al, 1997and Wendon et al, 1994. Given that blood accounts for 10% of brain volume, a rise in CBF could contribute to intracranial hypertension, as observed in ALF.…”

Section: Relationship Between Intracranial Pressure and Brain Edemamentioning

confidence: 97%

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Bosoi

Rose

2013

Neurochemistry International

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Hepatic encephalopathy (HE) is a complex neuropsychiatric syndrome that typically develops as a result of acute liver failure or chronic liver disease. Brain edema is a common feature associated with HE. In acute liver failure, brain edema contributes to an increase in intracranial pressure, which can fatally lead to brain stem herniation. In chronic liver disease, intracranial hypertension is rarely observed, even though brain edema may be present. This discrepancy in the development of intracranial hypertension in acute liver failure versus chronic liver disease suggests that brain edema plays a different role in relation to the onset of HE. Furthermore, the pathophysiological mechanisms involved in the development of brain edema in acute liver failure and chronic liver disease are dissimilar. This review explores the types of brain edema, the cells, and pathogenic factors involved in its development, while emphasizing the differences in acute liver failure versus chronic liver disease. The implications of brain edema developing as a neuropathological consequence of HE, or as a cause of HE, are also discussed. HighlightsBrain edema is a common feature in ALF and CLD. HE is inconsistently associated with the presence of brain edema. Fibrous and protoplasmic astrocytes are differentially implicated in the pathogenesis of HE. The pathogenesis of HE is multifactorial causing an array of neurological symptoms.

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“…10,29,40,42 However, at least two distinct mechanisms may be of importance for development of high CBF. One is that CBF autoregulation is impaired in ALF, [43][44][45] which implies that normal or even mildly elevated cerebral perfusion pressure will increase CBF (Fig. 1).…”

Section: Hydrostatic Pressurementioning

confidence: 99%

Brain edema in liver failure: Basic physiologic principles and management

Larsen

Wendon

2002

Liver Transpl

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In patients with severe liver failure, brain edema is a frequent and serious complication that may result in high intracranial pressure and brain damage. This short article focuses on basic physiologic principles that determine water flux across the blood-brain barrier. Using the Starling equation, it is evident that both the osmotic and hydrostatic pressure gradients are imbalanced across the blood-brain barrier in patients with acute liver failure. This combination will tend to favor cerebral capillary water influx to the brain. In contrast, the disequilibration of the Starling forces seems to be less pronounced in patients with cirrhosis because the regulation of cerebral blood flow is preserved and the arterial ammonia concentration is lower compared with that of patients with acute liver failure. Treatments that are known to reverse high intracranial pressure tend to decrease the osmotic pressure gradients across the blood-brain barrier. Recent studies indicate that interventions that restrict cerebral blood flow, such as hyperventilation, hypothermia, and indomethacin, are also efficient in preventing edema and high intracranial pressure, probably by decreasing the transcapillary hydrostatic pressure gradient. In our opinion, it is important to recall that rational fluid therapy, adequate ventilation, and temperature control are of direct importance to controlling cerebral capillary water flux in patients with acute liver failure. These simple interventions should be secured before more advanced experimental technologies are instituted to treat these patients.

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Liver function, cerebral blood flow autoregulation, and hepatic encephalopathy in fulminant hepatic failure

Cited by 101 publications

References 9 publications

Management in Acute Liver Failure

Management in Acute Liver Failure

Brain edema in acute liver failure and chronic liver disease: Similarities and differences

Brain edema in liver failure: Basic physiologic principles and management

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