Fever is associated with third ventricular shift after intracerebral hemorrhage: pathophysiologic implications.

BACKGROUND: Studies have shown the detrimental effect of increased temperature on brain injury. Fever is common after intracerebral hemorrhage (ICH). The term 'central fever' is often used when no cause is identified. AIM: The aim of the study was to determine the correlation of fever with third ventricular shift in 61 patients with ICH and hypothesize about the mechanism of fever. SETTING: Neurointensive Care Unit. DESIGN: Prospective observational study. MATERIALS AND METHODS: From August 1999 to April 2000, data from 61 patients with ICH were prospectively collected including maximum temperature (Tmax) and fever (T> 37.5 degrees C) at 24, 48, 72 and 96 hours, ICH volume, and third ventricular shift. Outcome measures included discharge mortality, 3-month National Institute of Health Stroke Scale (NIHSS), modified Rankin Scale (mRS), and Barthel Index (BI). STATISTICAL ANALYSIS: Spearman correlation coefficient, Mann-Whitney test, and logistic regression were used to assess relationships. RESULTS: Fifty-six per cent of patients had fever in the first 24 hours and 53% for at least two consecutive days. There was a correlation between ICH volume and Tmax at 24 hours (P =0.04) and 72 hours (P =0.03) and fever at 24 hours (P =0.039) and 72 hours (P =0.036). Tmax at 72 hours correlated with third ventricular shift (P =0.01). Those with shift were more likely to have fever within the first 72 hours (P =0.049) and worse outcome. Fever at 72 hours was associated with a higher discharge mortality (P =0.046) and trend of a worse 3-month NIHSS score (P =0.06). CONCLUSION: Fever is common after ICH and correlates with ICH volume and third ventricular shift suggesting a role of hypothalamic compression in "central fever." There was a trend towards a worse outcome with fever.

Technical refinements and drawbacks of a surface cooling technique for the treatment of severe acute ischemic stroke.

PURPOSE: To describe a technique for the induction of hypothermia and its complications for the treatment of acute ischemic stroke. METHODS: Adults with acute (<8 hours), severe (National Institutes of Health Stroke Scale>14) ischemic stroke of the anterior circulation were enrolled. Patients were intubated, sedated, and paralyzed. Surface cooling to 32 degrees+/-1 degrees C was performed with a cooling blanket and an alcohol/ice bath. Hypothermia was maintained for 12-72 hours. Physiological parameters were measured continuously. A computed tomography scan of the brain was obtained at 24 hours. Rewarming was initiated 12 hours after middle cerebral artery recanalization at a rate of 0.25 degrees C/hour. All complications and adverse outcomes were documented from initiation of hypothermia until hospital discharge. RESULTS: Eighteen patients with a mean National Institutes of Health Stroke Scale=21.4+/-5.6 were treated. The goal temperature was reached within 3.2+/-1.5 hours. Cooling time was proportional to body weight (p=0.009) and decreased with immediate paralysis to prevent shivering (p=0.033). Maintenance and rewarming were characterized by fluctuations in core temperature. All patients developed a decrease in blood pressure, heart rate, and potassium values that were proportional to temperature (p<0.05). Complications were generally mild, but pneumonia and myocardial infarction or both occurred in five patients. There were trends for increased risk of complications with longer duration of hypothermia (p=0.08) and increasing age (p=0.0504). Rewarming was well-tolerated with rebound cerebral edema occurring in only one patient. CONCLUSION: Surface cooling for the treatment of acute ischemic stroke can be performed rapidly with early neuromuscular paralysis. Advanced age and prolonged hypothermia may be associated with an increased risk of complications.

Spontaneous intracerebral hemorrhage: epidemiology, pathophysiology, and medical management.

This article introduces the basic epidemiology of intracerebral hemorrhage (ICH) and discusses the current available literature on the pathophysiology of primary ICH, hematoma enlargement, and cerebral edema. The article also includes a brief presentation of the basic steps regarding initial ICH management is presented as a framework for patient care.