Clinical monitoring of intracranial pressure in fulminant hepatic failure.

Hanid, M A; Davies, Melanie J.; Mellon, P. J.; Silk, D. B. A.; Strunin, L.; McCabe, Jennifer; Williams, Roger

doi:10.1136/gut.21.10.866

Cited by 99 publications

(36 citation statements)

References 9 publications

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“…In about 20% of patients a paradoxical increase in ICP occurs after mannitol infusion. 38 High doses can result in acute renal failure and damage to the BBB. Mannitol works best in mild to moderate intracranial hypertension and is less effective when the ICP is greater than 60 mmHg.…”

Section: Osmotherapymentioning

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: Osmotherapymentioning

confidence: 99%

Management in Acute Liver Failure

Shalimar

Acharya

2015

Journal of Clinical and Experimental Hepatology

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“…2,7 Dialysis in the Pre-OLT Candidate Acute Dialysis: FHF Increased intracranial pressures (Ͼ10 mm Hg) and cerebral edema are not uncommon in patients with hepatic failure, especially those with FHF. 27 Elevated intracerebral pressures are associated with marginal cerebral perfusion and elevated brain lactate levels. 28 Histologically, cerebral vessels in FHF show endothelial cell swelling, with increased numbers of vesicles and vacuoles, enlarged and vacuolized basement membranes, vacuolated pericytes, and swollen astroglial foot processes.…”

Section: Pre-olt Renal Failurementioning

confidence: 99%

Identification of patients best suited for combined liver[ndash ]kidney transplantation: Part II

Davis

Gonwa

Wilkinson

2002

Liver Transplantation

117

105

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Liver-kidney transplantation (LKT) should be reserved for those recipients with primary disease affecting both organs. However, increasing transplant list waiting times have increased the development and duration of acute renal failure before liver transplantation. Furthermore, the need for posttransplant calcineurin inhibitors can render healing from acute renal failure difficult. Because of the increasing requests for and controversy over the topic of a kidney with a liver transplant (OLT) when complete failure of the kidney is not known, the following article will review the impact of renal failure on liver transplant outcome, treatment of peri-OLT renal failure, rejection rates after LKT, survival after LKT, and information on renal histology and progression of disease into the beginnings of an algorithm for making a decision about combined LKT. (Liver Transpl 2002;8:193-211.)

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“…The objective of ICP monitoring is to maintain ICP below 20 mmHg and have adequate cerebral perfusion pressure (CPP) = arterial blood pressure (ABP) ICP. The ideal management of CPP should take cerebral metabolic and hemodynamic data into account in order to avoid excessive cerebral hyperemia, as well as uncoupling of cerebral blood flow and metabolism [6,7] . Despite a lack of evidence that treatment of elevated ICP can improve survival rates of patients with FHF, it is generally accepted that Grade 34 HE patients, especially those awaiting liver transplantation, should undergo ICP monitoring [6,7] .…”

Section: Invasive Icp Monitoringmentioning

confidence: 99%

“…The ideal management of CPP should take cerebral metabolic and hemodynamic data into account in order to avoid excessive cerebral hyperemia, as well as uncoupling of cerebral blood flow and metabolism [6,7] . Despite a lack of evidence that treatment of elevated ICP can improve survival rates of patients with FHF, it is generally accepted that Grade 34 HE patients, especially those awaiting liver transplantation, should undergo ICP monitoring [6,7] . ICP higher than 40 mmHg and prolonged low CPP < 50 mmHg are strongly associated with poor neurological recovery in FHF patients who are traditionally bad candidates for liver transplantation [8] .…”

Section: Invasive Icp Monitoringmentioning

confidence: 99%

Multimodal brain monitoring in fulminant hepatic failure

Paschoal¹,

Nogueira²,

Ronconi³

et al. 2016

WJH

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Acute liver failure, also known as fulminant hepatic failure (FHF), embraces a spectrum of clinical entities characterized by acute liver injury, severe hepatocellular dysfunction, and hepatic encephalopathy. Cerebral edema and intracranial hypertension are common causes of mortality in patients with FHF. The management of patients who present acute liver failure starts with determining the cause and an initial evaluation of prognosis. Regardless of whether or not patients are listed for liver transplantation, they should still be monitored for recovery, death, or transplantation. In the past, neuromonitoring was restricted to serial clinical neurologic examination and, in some cases, intracranial pressure monitoring. Over the years, this monitoring has proven insufficient, as brain abnormalities were detected at late and irreversible stages. The need for real-time monitoring of brain functions to favor prompt treatment and avert irreversible brain injuries led to the concepts of multimodal monitoring and neurophysiological decision support. New monitoring techniques, such as brain tissue oxygen tension, continuous electroencephalogram, transcranial Doppler, and cerebral microdialysis, have been developed. These techniques enable early diagnosis of brain hemodynamic, electrical, and biochemical changes, allow brain anatomical and physiological monitoring-guided therapy, and have improved patient survival rates. The purpose of this review is to discuss the multimodality methods available for monitoring patients with FHF in the neurocritical care setting.

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Clinical monitoring of intracranial pressure in fulminant hepatic failure.

Cited by 99 publications

References 9 publications

Management in Acute Liver Failure

Management in Acute Liver Failure

Identification of patients best suited for combined liver[ndash ]kidney transplantation: Part II

Multimodal brain monitoring in fulminant hepatic failure

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