Cerebral hemodynamic and metabolic profiles in fulminant hepatic failure: Relationship to outcome

Aggarwal, Shushma; Obrist, Walter D.; Yonas, Howard; Kramer, David J.; Kang, Yoogoo; Scott, Victor L.; Planinsic, Raymond M.

doi:10.1002/lt.20479

Cited by 82 publications

(38 citation statements)

References 34 publications

(50 reference statements)

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“…Aggarwal et al have described several stages in the evolution of the clinical picture of ALF with severe encephalopathy (9). Their observations note the importance of an increased cerebral blood flow (CBF) preceding the rise in ICP.…”

Section: B) Monitoring Cerebral Blood Flowmentioning

confidence: 99%

Brain edema in acute liver failure: Can it be prevented? Can it be treated?

Blei

2007

Journal of Hepatology

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Acute liver failure; Brain edema; intracranial pressure; Cerebral blood flowThe management of cerebral edema in Acute Liver Failure (ALF) is still imperfect, reflecting the limited tools to control brain swelling in this disease as well as in other neurological conditions (1). A better understanding of the unique mechanisms responsible for brain edema in ALF has emerged over the last years (2). Data arising from studies in experimental animals and in humans allow a more rational approach to the prevention and treatment of this serious complication of ALF. A. THE PATHOGENESIS OF BRAIN EDEMA IN ALFA net increase in water content defines the presence of brain edema. In the setting of an intact blood-brain barrier, water moves into brain via 3 possible routes: Via diffusion through the lipid bilayer of plasma membranes, via co-transport with organic and inorganic ions and through specialized water channels, aquaporins (2). Of special interest is aquaporin 4, the predominant aquaporin in brain. Mainly localized to cerebral endothelial cells and astrocyte foot processes that surround them, aquaporin-4 may play an important role in the pathogenesis of cytotoxic brain edema. Brain edema as a result of water intoxication is markedly reduced in aquaporin-4-deficient mice (reviewed in 3).For many years, an accepted tenet has been the presence of an intact blood-brain barrier and a cytotoxic etiology to explain brain edema in ALF. This concept has been recently challenged (4) with the possibility of a "leaky" rather than a bona fide rupture of the barrier. Effects on endothelial tight-junction proteins could be present, a change potentially explained by the action of endotoxin and/or pro-inflammatory cytokines on cellular permeability (5). Still, cytotoxic mechanisms need to be considered as a major pathogenic factor. In a recent study, all 7 patients with ALF and deep encephalopathy showed evidence of cytotoxic edema using diffusion-weighted MRI of the brain (6).Figure 1 depicts current views of the complex pathogenesis of brain edema in ALF. Astrocyte swelling is initiated by the accumulation of glutamine, the result of the detoxification of ammonia. As a result of swelling, ions (such as K + ) and other osmolytes Correspondence: Andres T Blei, MD, Northwestern University Feinberg School of Medicine, Division of Hepatology, 303 E Chicago Avenue -Searle 10-574, Chicago, IL 60611, e-mail: a-blei@northwestern.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (including myo-inositol, glutamate and taurine) are released. Ammonia-induced effects in vitro include an increase in aquapor...

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Section: B) Monitoring Cerebral Blood Flowmentioning

confidence: 99%

Brain edema in acute liver failure: Can it be prevented? Can it be treated?

Blei

2007

Journal of Hepatology

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“…In the study, it was concluded that hyperemia alone was not related to the outcome, despite having occurred more frequently during elevated ICP. All patients with malignant intra cranial hypertension previously had hyperemia [62,63] . Nielsen et al [36] reported that both pressure and arterial oxygen saturation were maintained during infusion with norepinephrine.…”

Section: Near Infrared Spectroscopymentioning

confidence: 99%

“…Glucose is most frequently determined as the cellular energy substrate. In conditions where there is a decrease in both cerebral tissue glucose and PtiO2, a reduction of capillary blood flow may be inferred [63,64] . Lactate studies can indicate the intensity of anaerobic metabolism, while glycerol studies can evaluate tissue damage since glycerol is one of the structural components in the tissue lipid layer of cell membranes [66] .…”

Section: Metabolic 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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“…Loss of auto-regulation [20] and cerebral hyperemia [21] are two common manifestations of ALF and encephalopathy. Systemic inflammatory response syndrome, particularly tumor necrosis factor has been shown to correlate with development of encephalopathy and raised intracranial pressure [22].…”

Section: Cerebral Blood Flowmentioning

confidence: 99%

“…Younger age, development of renal failure, hyponatremia, inflammatory response and the need for hemodynamic support for cardiovascular collapse are additional risk factors associated with the development of intracranial hypertension [24]. Similarly higher cerebral blood flow rates are seen in patients with cerebral edema and intracranial hypertension and are associated with higher mortality [21].…”

Section: Clinical Correlatesmentioning

confidence: 99%