Regional cerebral blood flow during mechanical hyperventilation in patients with fulminant hepatic failure

Strauss, Gitte; Høgh, Peter; Møller, Kirsten; Knudsen, Gitte M.; Hansen, Bent Adel; Larsen, Fin Stolze

doi:10.1002/hep.510300608

Cited by 42 publications

(20 citation statements)

References 26 publications

(46 reference statements)

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“…4,22 Variation in regional cerebral blood flow, however, has been reported in patients with ALF; this finding suggests that some areas of the brain may be more prone to ischemia. 23 Increased cerebral lactate efflux shortly after episodes of IH in patients with severe ALF also has been reported. 24 Whether hypertonic saline has any effect on cerebral blood flow and metabolism in patients with ALF currently is unknown and requires further investigation.…”

Section: Discussionmentioning

confidence: 89%

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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Section: Discussionmentioning

confidence: 89%

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

et al. 2004

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“…The reason for the increased vascular resistance in the frontal region is probably multifactorial, as discussed previously. 10 In the present study, patients were administered midazolam for sedation. Only a few studies have evaluated the effect of midazolam and benzodiazepines on regional cerebral perfusion.…”

Section: Discussionmentioning

confidence: 99%

Regional cerebral blood flow autoregulation in patients with fulminant hepatic failure

et al. 2000

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The absence of cerebral blood flow autoregulation in patients with fulminant hepatic failure (FHF) implies that changes in arterial pressure directly influence cerebral perfusion. It is assumed that dilatation of cerebral arterioles is responsible for the impaired autoregulation. Recently, frontal blood flow was reported to be lower compared with other brain regions, indicating greater arteriolar tone and perhaps preserved regional cerebral autoregulation. In patients with severe FHF (6 women, 1 man; median age, 46 years; range, 18 to 55 years), we tested the hypothesis that perfusion in the anterior cerebral artery would be less affected by an increase in mean arterial pressure compared with the brain area supplied by the middle cerebral artery. Relative changes in cerebral perfusion were determined by transcranial Doppler-measured mean flow velocity (V mean ), and resistance was determined by pulsatility index in the anterior and middle cerebral arteries. Cerebral autoregulation was evaluated by concomitant measurements of mean arterial pressure and V mean in the anterior and middle cerebral arteries during norepinephrine infusion. Baseline V mean was lower in the brain area supplied by the anterior cerebral artery compared with the middle cerebral artery (median, 47 cm/s; range, 21 to 62 cm/s v 70 cm/s; range 43 to 119 cm/s, respectively; P < .05). Also, vascular resistance determined by pulsatility index was greater in the anterior than middle cerebral artery (median, 1.02; range 1.00 to 1.37 v 0.87; range 0.75 to 1.48; P < .01). When arterial pressure was increased from 84 mm Hg (range 57 to 95 mm Hg) to 115 mm Hg (range, 73 to 130 mm Hg) during norepinephrine infusion, V mean remained unchanged in 2 patients in the anterior cerebral artery, whereas it increased in the middle cerebral artery in all 7 patients. In the remaining patients, V mean increased approximately 25% in both the anterior and middle cerebral arteries. Thus, this study could only partially confirm the hypothesis that autoregulation is preserved in the brain regions supplied by the anterior cerebral artery in patients with FHF. Although the findings of this small study need to be further evaluated, one should consider that autoregulation may be impaired not only in the brain region supplied by the middle cerebral artery, but also in the area corresponding to the anterior cerebral artery. (Liver Transpl 2000;6:795-800.)

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“…This delicate balance of regional CBF and the metabolic requirement is lost in patient and animal models of ALF. 26,27 This may cause increase in CBF, cerebral congestion which aggravates cerebral edema. CBF correlates very closely with the brain water and ICP in experimental ammonia induced brain edema.…”

Section: Loss Of Cerebral Auto Regulationmentioning

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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Regional cerebral blood flow during mechanical hyperventilation in patients with fulminant hepatic failure

Cited by 42 publications

References 26 publications

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

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

Regional cerebral blood flow autoregulation in patients with fulminant hepatic failure

Management in Acute Liver Failure

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