Delirium and sedation in the ICU.
Neurocrit Care. 2011 Jun;14(3):463-74
Authors: Frontera JA
Abstract
Delirium is defined by a fluctuating level of attentiveness and has been associated with increased ICU morta…

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Packed red blood cell transfusion causes greater hemoglobin rise at a lower starting hemoglobin in patients with subarachnoid hemorrhage.

Neurocrit Care. 2008;9(2):198-203

Authors: Naidech AM, Kahn MJ, Soong W, Green D, Batjer HH, Bleck TP

INTRODUCTION: Each unit of packed red blood cells (PRBCs) is expected to raise circulating hemoglobin (HGB) by approximately 1 g/dL. There are few data on modifiers of this relationship other than gender and body mass index (BMI). METHODS: We recorded HGB before and after PRBC transfusion in a retrospective cohort of 103 patients and a prospective cohort of 93 patients with subarachnoid hemorrhage (SAH). RESULTS: In the retrospective cohort, 48 of 103 patients were transfused, and in the prospective cohort, 56 of 93 patients were transfused. In both groups, lower pre-transfusion HGB was associated with a larger increase in HGB (P < 0.001) after correction for the number of units of PRBCs given. In the prospective cohort, lower pre-transfusion HGB was associated with a greater rise in HGB (P < 0.001) after correction for number of units of PRBCs given, gender, and BMI in repeated measures analysis. Pre-transfusion HGB explained an additional 12% of variance in the data (P < 0.001). In both cohorts, the magnitude of the effect was similar. CONCLUSION: In patients with SAH, transfusion at lower HGB leads to a greater increase in HGB. Transfusion at lower HGB may be relatively more cost-effective, and this should be balanced against any potential benefit from higher HGB in SAH. One rather than 2 units of PRBCs are likely to be sufficient for most HGB targets after SAH, especially in patients with more severe anemia.

PMID: 18542851 [PubMed - indexed for MEDLINE]

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Encephalopathy and cerebral edema in the setting of acute liver failure: pathogenesis and management.

Neurocrit Care. 2008;9(1):97-102

Authors: Wendon J, Lee W

Cerebral edema is a potential life-threatening complication in patients with acute liver failure who progress to grade III/IV encephalopathy. The incidence is variably reported but appears to be most prevalent in those patients with hyperacute liver failure as opposed to subacute forms of liver failure. In those patients who are deemed at risk of cerebral edema and raised intracranial pressure, insertion of an intra-cranial pressure monitoring device may be considered to optimize treatment and interventions. The pathogenesis of cerebral edema in this setting remains controversial, although recent work suggests a pivotal role for arterial ammonia, whose effects appear to be potentiated by the presence of systemic inflammation. Recent work has also suggested the import of free radical formation occurring at a mitochondrial level as being the potential mediator of cellular dysfunction as opposed to ammonia per se. Treatment of such patients requires a multi-disciplinary approach incorporating both hepatology and critical care. In a significant proportion of such cases, consideration of liver transplantation may be required. Treatment should be focused at optimizing liver function and regenerative capacity and minimizing the inflammatory milieu. Controlled studies are lacking and much of the management has been extrapolated from neurocritical care. Sustained elevation of intracranial pressure may be responsive to mannitol or hypertonic saline bolus, and in those with hyperemia indomethacin has been reported as beneficial in case series. Recently, interest has developed into the use of cooling in the management of patients with acute liver failure and raised intracranial pressure. Animal studies support this treatment option as do case series, although randomized trials are still awaited.

PMID: 18688582 [PubMed - indexed for MEDLINE]

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Effectiveness of Factor IX complex concentrate in reversing warfarin associated coagulopathy for intracerebral hemorrhage.

Neurocrit Care. 2008;8(1):36-41

Authors: Siddiq F, Jalil A, McDaniel C, Brock DG, Pineda CC, Bell RD, Lee K

INTRODUCTION: The objective of this study is to show the effectiveness of Factor IX complex concentrate (FIXCC) for rapid reversal of an elevated International Normalized Ratio (INR) in patients with anticoagulation-associated intracerebral hemorrhage (AAICH). METHODS: We, retrospectively, analyzed the clinical data of 19 patients with the diagnosis of AAICH from January 2005 to May 2006. A comparison was made among patients treated with FFP and Vit.K [FFP-group (n = 9)] and patients treated with FIXCC in addition to FFP and Vit.K [FIXCC-group (n = 10)]. INR of 1.4 or less was taken as target. RESULTS: Mean INR on admission for FFP and FIXCC group was 1.84 +/- 0.31 and 2.44 +/- 1.48, respectively (P = 0.315). After administration of therapy, the INR was reduced from 1.84 +/- 0.31 to 1.34 +/- 0.08 (P < 0.05) in FFP group and 2.44 +/- 1.48 to 1.34 +/- 0.07 (P < 0.005) in FIXCC group. Three patients in FFP group (33%) and 8 patients in FIXCC group (80%) reached their target INR in 3-4 h after initiation of therapy (P = 0.012). Mean time taken by both FFP and FIXCC groups to reach the target INR was 8.52 +/- 5.60 h and 4.25 +/- 2.12 h, respectively (P < 0.05). The mean rate of INR correction was 0.06 +/- 0.03 and 0.27 +/- 0.25 per hour for the FFP and FIXCC group, respectively (P < 0.005). There was one death in FIX group and two in FFP group and no thrombotic complications. CONCLUSION: Our data suggests that FIXCC in combination with FFP and Vit.K may result in decreased time required when compared to FFP and Vit.K alone for correction of warfarin associated coagulopathy in neurosurgical emergencies.

PMID: 17898941 [PubMed - indexed for MEDLINE]

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