Effect of Mild Hypothermia on Uncontrollable Intracranial Hypertension after Severe Head Injury

Shiozaki, Tadahiko; Sugimoto, Hisashi; Taneda, Mamoru; Yoshida, Hiroyoshi; Iwai, Atsushi; Yoshioka, Toshiharu; Sugimoto, Tsuneaki

doi:10.1097/00132586-199408000-00021

Cited by 82 publications

(132 citation statements)

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“…Although the occurrence of cerebral vasospasm very likely influenced the absolute MFVMCA values, relative changes in MFVMCA after both induction of hypothermia (on average 5 days after SAH) and rewarming to normothermia (on average 13 days after SAH) were opposite to the time course of pathological changes in arteries after SAH. Finally, the study confirms previous reports on ICP reductions during hypothermia in patients with acute brain injury [16][17][18]33]. In order to avoid rebound of ICP, rewarming should be performed ICP-controlled and no faster than 0.5-1 °C per 24 h. Furthermore, an abnormal increase in Doppler blood flow velocities during rewarming may serve as an index in the prediction of acute brain swelling, undermining the use of TCD as a rapid and noninvasive method to monitor cerebral hemodynamics during hypothermia [34].…”

Section: Discussionsupporting

confidence: 90%

“…As a consequence, hypothermia has consistently been associated with reduced cerebral blood flow (CBF) under physiological conditions [14,15]. However, CBF measurements during hypothermia in patients with acute brain injury are conflicting and the existing data are mainly limited to patients with traumatic brain injury [16][17][18]. The aim of this study was to evaluate changes in blood flow velocities via transcranial Doppler (TCD) sonography in patients with severe SAH who were treated with prolonged hypothermia due to refractory high ICP or DCI.…”

Section: Introductionmentioning

confidence: 99%

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Therapeutic Hypothermia Reduces Middle Cerebral Artery Flow Velocity in Patients with Severe Aneurysmal Subarachnoid Hemorrhage

et al. 2013

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Background: Transcranial Doppler (TCD) is widely used to detect and follow up cerebral vasospasm after sub-arachnoid hemorrhage (SAH). Therapeutic hypothermia might influence blood flow velocities assessed by TCD. The aim of the study was to evaluate the effect of hypo-thermia on Doppler blood flow velocity after SAH. Methods: In 20 patients treated with hypothermia (33°) due to refractory intracranial hypertension or delayed cerebral ischemia (DCI), mean flow velocity of the middle cerebral artery (MFVMCA) was assessed by TCD. Thirteen patients were treated with combined hypothermia and barbiturate coma and seven with hypothermia alone. MFVMCA was obtained within 24 h before and after induction of hypothermia as well as before and after rewarming. Results: Hypothermia was induced on average 5 days after SAH (range 1-12) and maintained for 144 h (range 29-270). After hypothermia induction, MFVMCA decreased from 113.7 ± 49.0 to 93.8 ± 44.7 cm/s (p = 0.001). The decrease was independent of SAH-related complications and barbiturate coma. MFVMCA further decreased by 28.2 cm/s between early and late hypothermia (p < 0.001). This second decrease was observed in patients with DCI (p < 0.001), but not in patients with intracranial hypertension (p = 0.715). Compared to late hypothermia, MFVMCA remained unchanged after rewarming (65.6 ± 32.1 vs 70.3 ± 36.8 cm/s; p = 0.219). However, patients treated with hypothermia alone showed an increase in MFVMCA after rewarming (p = 0.016). Conclusion: Therapeutic hypothermia after SAH decrea-ses Doppler blood flow velocity in both intracranial hypertension and DCI cases. The results can be the effect of hypothermiarelated mechanisms or resolving cerebral vasospasm during prolonged hypothermia. AbstractBackground: Transcranial Doppler (TCD) is widely used to detect and follow up cerebral vasospasm after sub-arachnoid hemorrhage (SAH). Therapeutic hypothermia might influence blood flow velocities assessed by TCD. The aim of the study was to evaluate the effect of hypo-thermia on Doppler blood flow velocity after SAH. Methods: In 20 patients treated with hypothermia (33°) due to refractory intracranial hypertension or delayed cerebral ischemia (DCI), mean flow velocity of the middle cerebral artery (MFVMCA) was assessed by TCD. Thirteen patients were treated with combined hypothermia and barbiturate coma and seven with hypothermia alone. MFVMCA was obtained within 24 h before and after induction of hypothermia as well as before and after rewarming. Results: Hypothermia was induced on average 5 days after SAH (range 1-12) and maintained for 144 h (range 29-270). After hypothermia induction, MFVMCA decreased from 113.7 ± 49.0 to 93.8 ± 44.7 cm/s (p = 0.001). The decrease was independent of SAH-related complications and barbiturate coma. MFVMCA further decreased by 28.2 cm/s between early and late hypothermia (p < 0.001). This second decrease was observed in patients with DCI (p < 0.001), but not in patients with intracranial hypertension (p = 0.715). Compared to late hypotherm...

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Therapeutic Hypothermia Reduces Middle Cerebral Artery Flow Velocity in Patients with Severe Aneurysmal Subarachnoid Hemorrhage

et al. 2013

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“…11,12 Among the therapeutic strategies, clinical and experimental effectiveness of mild-to-moderate systemic hypothermia for the treatment of central nervous system (CNS) injury due to brain injury or ischemia has been reported. [13][14][15][16][17] However, a great deal remains unknown as to how hypothermia protects neuronal and supporting cells following injury. Our recent studies have also shown that hypothermia protects against neuronal cell death in experimental brain injury and ischemia models.…”

Section: Introductionmentioning

confidence: 99%

Post-traumatic moderate systemic hypothermia reduces TUNEL positive cells following spinal cord injury in rat

et al. 2004

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Study design: A standardized animal model of contusive spinal cord injury (SCI) with incomplete paraplegia was used to test the hypothesis that moderate systemic hypothermia reduces neural cell death. Terminal deoxynucleotidyl transferase [TdT]-mediated deoxyuridine triphosphate [dUTP] nick-end labeling (TUNEL) staining was used as a marker of apoptosis or cell damage. Objective: To determine whether or not moderate hypothermia could have a neuroprotective effect in neural cell death following spinal cord injury in rats. Setting: Kagawa Medical University, Japan. Methods: Male Sprague-Dawley (SD) rats (n ¼ 39) weighing on average 300 g (280-320 g) were used to prepare SCI models. After receiving contusive injury at T11/12, rats were killed at 24 h, 72 h, or 7 days after injury. The spinal cord was removed en bloc and of examined at five segments: 5 and 10 mm rostral to the center of injury, center of injury, and 5 and 10 mm caudal to the center of injury. Rats that received hypothermia (321C/4 h) were killed at the same time points as those that received normothermia (371C/3 h). The specimens were stained with hematoxylin and eosin, and subjected to in situ nick-end labeling (TUNEL), a specific method for visualizing cell death in the spinal cord. Results: At 24 h postinjury, TUNEL positive cells (TPC) decreased significantly 10 mm rostral to center of injury in hypothermic animals compared to the normothermia group. At 72 h post-SCI, TPC also decreased significantly at 5 mm rostral, and 5 and 10 mm caudal to the lesion center compared to normothermic animals. At 7 days postinjury, a significant decrease of TPC was observed at the 5 mm rostral and 5 mm caudal sites compared to normothermic animals. Conclusion: These results indicate that systemic hypothermia has a neuroprotective effect following SCI by attenuating post-traumatic TPC.

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“…Brain swelling is an important problem in pediatric TBI, and hypothermia has been shown to reduce intracranial pressure in adult and pediatric patients and to reduce cerebral swelling in animal models [81,82]. Induced hypothermia has also been shown to decrease mortality and improve outcome in neonates with hypoxic-ischemic injury [83].…”

Section: Hypothermiamentioning

confidence: 99%

Pediatric Neurocritical Care

Murphy

2012

Neurotherapeutics

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Pediatric neurocritical care is an emerging multidisciplinary field of medicine and a new frontier in pediatric critical care and pediatric neurology. Central to pediatric neurocritical care is the goal of improving outcomes in critically ill pediatric patients with neurological illness or injury and limiting secondary brain injury through optimal critical care delivery and the support of brain function. There is a pressing need for evidence based guidelines in pediatric neurocritical care, notably in pediatric traumatic brain injury and pediatric stroke. These diseases have distinct clinical and pathophysiological features that distinguish them from their adult counterparts and prevent the direct translation of the adult experience to pediatric patients. Increased attention is also being paid to the broader application of neuromonitoring and neuroprotective strategies in the pediatric intensive care unit, in both primary neurological and primary non-neurological disease states. Although much can be learned from the adult experience, there are important differences in the critically ill pediatric population and in the circumstances that surround the emergence of neurocritical care in pediatrics.

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Effect of Mild Hypothermia on Uncontrollable Intracranial Hypertension after Severe Head Injury

Cited by 82 publications

References 0 publications

Therapeutic Hypothermia Reduces Middle Cerebral Artery Flow Velocity in Patients with Severe Aneurysmal Subarachnoid Hemorrhage

Therapeutic Hypothermia Reduces Middle Cerebral Artery Flow Velocity in Patients with Severe Aneurysmal Subarachnoid Hemorrhage

Post-traumatic moderate systemic hypothermia reduces TUNEL positive cells following spinal cord injury in rat

Pediatric Neurocritical Care

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