Effect of hyperventilation on regional cerebral blood flow in head-injured children

Skippen, Peter; Seear, Michael; Poskitt, Ken; Kestle, John R. W.; Cochrane, D. Douglas; Annich, Gail M.; Handel, Jeffrey

doi:10.1097/00003246-199708000-00031

Cited by 261 publications

(94 citation statements)

References 30 publications

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“…Moderate hypocapnia (PaCO 2 : 30-35 mmHg) can efficiently reduce raised ICP, but the risks of dramatically reducing the cerebral blood flow in ischemic areas with more profound hyperventilation has to be kept in mind. 15 In the presence of life-threatening brain herniation, rapid infusion of mannitol 20% is effective in lowering raised ICP. 1 6 The risk of increasing the volume of the intracranial hematoma, by decreasing the volume of the surrounding undamaged brain, is more theoretical than clinically relevant.…”

Section: Discussionmentioning

confidence: 99%

Emergency management of deeply comatose children with acute rupture of cerebral arteriovenous malformations

Meyer

Orliaguet

Zérah

et al. 2000

Can J Anesth/J Can Anesth

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REPORTS O F INVESTIGATIONCAN J ANESTH 2000 / 47: 8 / pp [758][759][760][761][762][763][764][765][766] Purpose: To assess the impact of emergency management on mortality and morbidity of acute rupture of cerebral arteriovenous malformations resulting in deep coma in children, and the factors predicting outcome. Methods: Retrospective chart review of 20 children with a Glasgow Coma Scale # 8 with acute hemorrhagic stroke from a cerebral arteriovenous malformation rupture was conducted. Protocol included: early resuscitation with tracheal intubation and ventilation after induction of anesthesia with sufentanil, and benzodiazepine, and mannitol 20% or hypertonic saline 7.5% infusion for life-threatening brain herniation. Radiological exploration was limited to contrast-enhanced CT scan preceding immediate surgical decompression. Postoperatively, children were deeply sedated and intracranial pressure monitoring allowed titration with osmotherapy , vasopressors, hyperventilation or barbiturate coma to control cerebral perfusion pressure. Analysis used stratification of the type of hemorrhage (supra or infra tentorial), location (intraparenchymal and subarachnoid, intraparenchymal and intraventricular or intraventricular alone) and relationship between presentation, evolution with resuscitation, type of cerebral lesion, and outcome. Results: Patients had a severe initial presentation (median Glasgow Coma Scale five), eight had unilateral and eight bilateral third nerve palsy. Compressive hematoma in supratentorial localisation represented 75% of the cases. Global mortality was 40%. Persistence of mydriasis after resuscitation increased mortality to 75%. Massive intraventricular flooding was associated with increased mortality. Good functional outcome was achieved in survivors. Conclusion: Acute rupture of an AVM can result in rapidly progressing coma. Emergency management with early resuscitation, minimal radiological exploration before rapid surgical decompression results in a mortality rate of 40%, but a good functional outcome can be expected in the survivors.Objectif : Évaluer l'effet et le pronostic d'une intervention d'urgence sur la mortalité et la morbidité d'une rupture imprévisible de malformations artérioveineuses cérébrales qui ont conduit à un coma profond chez des enfants. Méthode : Un examen rétrospectif des dossiers de 20 enfants, cotés # 8 à l'échelle de Glasgow, qui ont subi un accident hémorragique aigu causé par la rupture de malformations artérioveineuses cérébrales, a été réalisé. Le protocole comportait : une réanimation précoce, une intubation endotrachéale et une ventilation après l'induction de l'anesthésie avec du sufentanil, du mannitol à 20 % ou une perfusion salée hypertonique à 7,5 % pour traiter l'hernie cérébrale grave. L'exploration radiologique s'est limitée à la scanographie de prise de contraste juste avant la décompression chirurgicale. Après l'opération, les enfants ont reçu une forte sédation. Le monitorage de la pression intracrânienne a permis le titrage de l'osmothérapie, des ...

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Section: Discussionmentioning

confidence: 99%

Emergency management of deeply comatose children with acute rupture of cerebral arteriovenous malformations

Meyer

Orliaguet

Zérah

et al. 2000

Can J Anesth/J Can Anesth

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“…This is important because cerebral hypoperfusion has been associated with cerebral ischemia and poor outcome [76][77][78]. However after severe pediatric TBI, CBF may also be normal or high [79] and may result in cerebral hyperemia and cerebral hemorrhage.…”

Section: Cerebrovascular Physiology After Tbi Altered Cerebral Blood mentioning

confidence: 99%

“…Secondary insults, representing discrete events that may be monitored for and intervened upon, are predictable, potentially avoidable, and include systemic causes such as hypotension [93,94], hypocarbia, hypercarbia [78,79,95], hypoxia [11,96], hyperthermia [97], and hyperglycemia [98,99]. These insults result in secondary injuries which signify underlying neurological processes related to cellular and molecular mechanisms of injury/ death, including inflammatory responses, impairment of cerebral autoregulation, excitotoxicity, delayed cell death, and BBB breakdown [92].…”

Section: Secondary Insults and Injuriesmentioning

confidence: 99%

Cerebral Blood Flow and Autoregulation After Pediatric Traumatic Brain Injury

Udomphorn

Armstead

Vavilala

2008

Pediatric Neurology

132

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Traumatic brain injury is a global health concern and is the leading cause of traumatic morbidity and mortality in children. Despite a lower overall mortality than in adult traumatic brain injury, the cost to society from the sequelae of pediatric traumatic brain injury is very high. Predictors of poor outcome after traumatic brain injury include altered systemic and cerebral physiology, including altered cerebral hemodynamics. Cerebral autoregulation is often impaired following traumatic brain injury and may adversely impact poor outcome. Although altered cerebrovascular hemodynamics early after traumatic brain injury may contribute to disability in children, there is a paucity of information regarding changes in cerebral blood flow and cerebral autoregulation after pediatric traumatic brain injury. In this article, we discuss normal pediatric cerebral physiology and cerebrovascular pathophysiology following pediatric traumatic brain injury.

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“…Maintenance of adequate CPP (84,86,89,90) is accomplished by reducing the ICP and ensuring adequate MAP. Adequate CPP and reducing ICP Interventions are used step by step.…”

Section: Management and Treatment Of Intracranial Hypertensionmentioning

confidence: 99%

“…The first step typically includes the use of analgesia and sedation, elevation of head, airway and ventilatory management and preferably with concomitant monitoring of jugular venous saturation (86,(88)(89)(90) Obtunded patients, especially those with a GCS ≤ 8 require intubation for airway protection. Mechanical ventilation will also facilitate deep sedation and hyperventilation.…”

Section: Management and Treatment Of Intracranial Hypertensionmentioning

confidence: 99%