Hypothermia

Therapeutic Hypothermia With the Use of Intracranial Pressure Monitoring for Acute Disseminated Encephalomyelitis With Brainstem Lesion: A Case Report

Authors: Miyamoto K, Kozu S, Arakawa A, Tsuboi T, Hirao JI, Ono K, Arisaka O.

Acute disseminated encephalomyelitis confined to the brainstem is associated with poor prognosis. We describe a case of a 10-year-old boy with acute disseminated encephalomyelitis in the brainstem that developed after influenza A infection. A 10-year-old boy presented with fever and prolonged disturbance of consciousness and was admitted to our hospital. Magnetic resonance imaging (MRI) of the midbrain, with T2-weighted and fluid-attenuated inversion recovery images, suggested acute disseminated encephalomyelitis accompanied by a brainstem lesion. Lumbar puncture showed pleocytosis and increased protein content, including myelin basic protein, interleukin-6, and immunoglobulin G, all suggestive of acute disseminated encephalomyelitis. Treatments such as methylprednisolone pulse therapy, intravenous immunoglobulin, and therapeutic hypothermia were performed. Although the patient presented with anisocoria with increased intracranial pressure monitoring during hypothermia, prompt therapy with d-mannitol and dopamine was effective. Our case results suggest that hypothermia could be included in the choice of therapy for acute disseminated encephalomyelitis with brainstem lesions.

Short-duration hypothermia after ischemic stroke prevents delayed intracranial pressure rise

Authors: Murtha LA, McLeod DD, McCann SK, Pepperall D, Chung S, Levi CR, Calford MB, Spratt NJ.

BACKGROUND: Intracranial pressure elevation, peaking three to seven post-stroke is well recognized following large strokes. Data following small-moderate stroke are limited. Therapeutic hypothermia improves outcome after cardiac arrest, is strongly neuroprotective in experimental stroke, and is under clinical trial in stroke. Hypothermia lowers elevated intracranial pressure; however, rebound intracranial pressure elevation and neurological deterioration may occur during rewarming.
HYPOTHESES: (1) Intracranial pressure increases 24 h after moderate and small strokes. (2) Short-duration hypothermia-rewarming, instituted before intracranial pressure elevation, prevents this 24 h intracranial pressure elevation.

Effects of xenon and hypothermia on cerebrovascular pressure reactivity in newborn global hypoxic-ischemic pig model

Authors: Chakkarapani E, Dingley J, Aquilina K, Osredkar D, Liu X, Thoresen M.

Autoregulation of cerebral perfusion is impaired in hypoxic-ischemic encephalopathy. We investigated whether cerebrovascular pressure reactivity (PRx), an element of cerebral autoregulation that is calculated as a moving correlation coefficient between averages of intracranial and mean arterial blood pressure (MABP) with values between -1 and +1, is impaired during and after a hypoxic-ischemic insult (HI) in newborn pigs. Associations between end-tidal CO2, seizures, neuropathology, and PRx were investigated. The effect of hypothermia (HT) and Xenon (Xe) on PRx was studied. Pigs were randomized to Sham, and after HI to normothermia (NT), HT, Xe or xenon hypothermia (XeHT). We defined PRx >0.2 as peak and negative PRx as preserved. Neuropathology scores after 72 hours of survival was grouped as 'severe' or 'mild.' Secondary PRx peak during recovery, predictive of severe neuropathology and associated with insult severity (P=0.05), was delayed in HT (11.5 hours) than in NT (6.5 hours) groups. Seizures were associated with impaired PRx in NT pigs (P=0.0002), but not in the HT/XeHT pigs. PRx was preserved during normocapnia and impaired during hypocapnia. Xenon abolished the secondary PRx peak, increased (mean (95% confidence interval (CI)) MABP (6.5 (3.8, 9.4) mm Hg) and cerebral perfusion pressure (5.9 (2.9, 8.9) mm Hg) and preserved the PRx (regression coefficient, -0.098 (95% CI (-0.18, -0.01)), independent of the insult severity.Journal of Cerebral Blood Flow & Metabolism advance online publication, 31 July 2013; doi:10.1038/jcbfm.2013.123.

Hypothermia Decreases Cerebrospinal Fluid Asymmetric Dimethylarginine Levels in Traumatic Brain Injury Children

Authors: Thampatty BP, Klamerus MM, Oberly PJ, Feldman KL, Bell MJ, Tyler-Kabara EC, Adelson PD, Clark RS, Kochanek PM, Poloyac SM.

OBJECTIVES:: Pathological increases in asymmetric dimethylarginine, an endogenous nitric oxide synthase inhibitor, have been implicated in endothelial dysfunction and vascular diseases. Reduced nitric oxide early after traumatic brain injury may contribute to hypoperfusion. Currently, methods to quantify asymmetric dimethylarginine in the cerebrospinal fluid have not been fully explored. We aimed to develop and validate a method to determine asymmetric dimethylarginine in the cerebrospinal fluid of a pediatric traumatic brain injury population and to use this method to assess the effects of 1) traumatic brain injury and 2) therapeutic hypothermia on this mediator. 

Moderate hypothermia with intracranial pressure monitoring as a therapeutic paradigm for the management of acute liver failure: a systematic review

Authors: Dmello D, Cruz-Flores S, Matuschak GM.

OBJECTIVE: To systematically review the literature and present data on the safety and efficacy of induced moderate hypothermia combined with ICP monitoring in critically ill patients with acute liver failure.

DESIGN: We conducted a retrospective observational search of MEDLINE database using both OVID and PubMed with the following MeSH terms, "Hypothermia, Induced," "Brain Edema," "Intracranial Hypertension" (ICH), "Liver failure, Acute" and "Liver Failure, Fulminant." We limited our search to case series involving at least three human subjects and all other clinical trials. Baseline ICP, cerebral perfusion pressure (CPP) and cerebral blood flow (CBF) as well as the response of these variables to hypothermia were recorded when available. Additional clinical and demographic data were also recorded.

RESULTS: Five case series were identified. Pre-existing coagulopathy from liver failure was reversed by various modalities in all studies prior to insertion of ICP monitors. Induction of moderate hypothermia combined with ICP monitoring consistently improved ICP, CPP and CBF in four trials; one trial demonstrated the feasibility and effectiveness of moderate induced hypothermia as part of a protocolized strategy for the management of ICH.

CONCLUSIONS: Limited data exist concerning the safety and efficacy of moderate hypothermia and ICP monitoring for the treatment of ICH in acute liver failure. The available evidence shows that induction of moderate hypothermia in this clinical setting is feasible and possibly efficacious. Well-designed prospective clinical trials are warranted in this challenging context, given the potential of providing a bridge to liver transplantation or even clinical recovery.

Hypothermia for intracranial hypertension

Authors: Bruder N, Velly L, Codaccioni JL.

There is a large body of experimental evidence showing benefits of deliberate mild hypothermia (33-35 degrees C) on the injured brain as well as an improvement of neurological outcome after cardiac arrest in humans. However, the clinical evidence of any benefit of hypothermia following stroke, brain trauma and neonatal asphyxia is still lacking. Controversial results have been published in patients with brain trauma or neonatal asphyxia. Hypothermia can reduce the elevation of intracranial pressure, through mechanisms not completely understood. Hypothermia-induced hypocapnia should have a role on the reduction of intracranial pressure. The temperature target is unknown but no additional benefit was found below 34 degrees C. The duration of deliberate hypothermia for the treatment of elevated intracranial pressure might be at least 48 hours, and the subsequent rewarming period must be very slow to prevent adverse effects.

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