Uncomplicated Rapid Posthypothermic Rewarming Alters Cerebrovascular Responsiveness

Ueda, Y.; Suehiro, Eiichi; Wei, Enoch P.; Kontos, Hermes A.; Povlishock, John T.

doi:10.1161/01.str.0000113693.56783.73

Cited by 41 publications

(21 citation statements)

References 23 publications

(22 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In adult rats, although rapid rewarming over 30 min from moderate hypothermia was not associated with persistent biochemical or (21), there were greater early changes in cardiac output and heart rate, in a similar pattern to the present study, compared with slower rewarming over 2 h. Similarly, others have reported that rapid rewarming over 30 min can cause transient uncoupling of cerebral circulation and metabolism, with a transient increase in extracellular glutamate and lactate (22). Of greater concern, very rapid rewarming over 15 min after 1 h of hypothermia in adult rats can exacerbate traumatic axonal injury and impair cerebrovascular responsiveness, compared with slow rewarming over 90 min (23,24). Although these studies used very short periods of hypothermia combined with faster rewarming than the mean of 47 min in our experimental study, they support the concept that very rapid rewarming can have undesirable physiologic and neural effects.…”

Section: Discussionsupporting

confidence: 84%

Epileptiform Activity During Rewarming from Moderate Cerebral Hypothermia in the Near-Term Fetal Sheep

et al. 2005

View full text Add to dashboard Cite

Moderate hypothermia is consistently neuroprotective after hypoxic-ischemic insults and is the subject of ongoing clinical trials. In pilot studies, we observed rebound seizure activity in one infant during rewarming from a 72-h period of hypothermia. We therefore quantified the development of EEG-defined seizures during rewarming in an experimental paradigm of delayed cooling for cerebral ischemia. Moderate cerebral hypothermia (n ϭ 9) or sham cooling (n ϭ 13) was initiated 5.5 h after reperfusion from a 30-min period of bilateral carotid occlusion in near-term fetal sheep and continued for 72 h after the insult. During spontaneous rewarming, fetal extradural temperature rose from 32.5 Ϯ 0.6°C to control levels (39.4 Ϯ 0.1°C) in 47 Ϯ 6 min. Carotid blood flow and mean arterial blood pressure increased transiently during rewarming. The cooling group showed a significant increase in electrical seizure events 2, 3, and 5 h after rewarming, maximal at 2 h (2.9 Ϯ 1.2 versus 0.5 Ϯ 0.5 events/h; p Ͻ 0.05). From 6 h after rewarming, there was no significant difference between the groups. Individual seizures were typically short (28.8 Ϯ 5.8 s versus 29.0 Ϯ 6.8 s in sham cooled; NS), and of modest amplitude (35.9 Ϯ 2.8 versus 38.8 Ϯ 3.4 V; NS). Neuronal loss in the parasagittal cortex was significantly reduced in the cooled group (51 Ϯ 9% versus 91 Ϯ 5%; p Ͻ 0.002) and was not correlated with rebound epileptiform activity. In conclusion, rapid rewarming after a prolonged interval of therapeutic hypothermia can be associated with a transient increase in epileptiform events but does not seem to have significant adverse implications for neural outcome. There is now consistent experimental evidence that a sufficient interval of moderate cerebral hypothermia started shortly after severe perinatal hypoxia-ischemia can reduce secondary neuronal injury and improve functional outcomes (1). Although only pilot data are available in newborn infants (2), early induction of moderate hypothermia in adult patients after cardiac arrest improves neurologic recovery (3,4). Rewarming after cooling treatment for severe hypoxic-ischemic encephalopathy (HIE), however, is potentially a more complex process than the original induction of cooling: first because it might lead to destabilizing cardiovascular changes such as a loss of peripheral tone with an increased requirement for cardiac work (5) and second because damaging processes such as release of excitatory amino acid neurotransmitters that have been suppressed by hypothermia could become active again (6,7).In view of such considerations, clinical studies of therapeutic hypothermia typically have rewarmed infants at no more than 0.5°C/h (8 -10); however, there are few systematic data. During our early pilot studies of head-cooling with mild systemic hypothermia for neonatal HIE, we observed a case of an infant who exhibited transient clinical seizures during rewarming. To examine the hypothesis that rewarming from prolonged moderate hypothermia may be associated with rebound seizure activ...

show abstract

Section: Discussionsupporting

confidence: 84%

Epileptiform Activity During Rewarming from Moderate Cerebral Hypothermia in the Near-Term Fetal Sheep

et al. 2005

View full text Add to dashboard Cite

show abstract

“…Another cause may be the less pronounced rebound effect in the rewarming period after hemicraniectomy. Animal experimental studies have shown an exacerbation of axonal injury after uncontrolled, rapid rewarming of cerebral tissue [26, 27], which is followed by disturbances of cerebral microcirculation, further vessel dilatation, an increase in the cerebral metabolic rate for oxygen, temporarily unmatched by cerebral blood flow [28], and impairment of the vascular smooth muscle as well as the endothelium [29], whereas a slow rewarming showed no rebound effect [29]. Therefore, we applied a slow, feedback-controlled rewarming protocol.…”

Section: Discussionmentioning

confidence: 99%

Safety and Therapeutical Benefit of Hemicraniectomy Combined with Mild Hypothermia in Comparison with Hemicraniectomy Alone in Patients with Malignant Ischemic Stroke

Els¹,

Oehm²,

Voigt³

et al. 2006

Cerebrovasc Dis

136

View full text Add to dashboard Cite

Introduction: Both for hemicraniectomy and for hypothermia, several reports describe a beneficial effect in patients with malignant supratentorial cerebral ischemia. We compared the safety and the clinical outcome in patients with a malignant supratentorial infarction who were treated with hemicraniectomy alone (HA) or received a combination therapy with hemicraniectomy and hypothermia of 35°C (HH), respectively. Methods: In a prospective and randomized study, 25 consecutive patients were treated after an ischemic infarction of more than two thirds of one hemisphere by HA (n = 13 patients) or the HH combination therapy (n = 12 patients). Safety parameters were compared between both treatment groups, the clinical outcome was assessed during treatment and after 6 months. Results: Age, cranial CT or MRI findings, initial National institutes of Health Stroke Scale Score (NIHSSS) and level of consciousness were not significantly different between both groups. Hemicraniectomy was performed within 15 ± 6 h after the ischemic event. Hypothermia was induced immediately after surgery. Overall mortality was 12% (2/13 vs. 1/12 in the two groups), but none of these 3 patients died due to treatment-related complications. There were no severe side effects of hypothermia. Duration of need for intensive care or for mechanical ventilation and infectious status did not differ significantly between both groups, but the need for catecholamine application was increased in the HH group. The clinical outcome showed a tendency for a better outcome in the HH compared with the HA group with respect to status after 6 months, as assessed by the NIHSSS (10 ± 1 vs. 11 ± 3, p < 0.08). Discussion: The present study suggests that a combined therapy of mild hypothermia and hemicraniectomy in malignant brain infarction does not imply additional risks by side effects and improves functional outcome as compared with hemicraniectomy alone.

show abstract

“…157,158 There are no systematic data from large animals. The clinical studies of therapeutic hypothermia have empirically chosen to rewarm infants at no more than 0.5°C per h, 128,130,132 however, it remains possible that rewarming still more slowly might be beneficial.…”

Section: How Long Should Cooling Be Continued?mentioning

confidence: 99%

Hypothermic neuroprotection

Gunn

Thoresen

2006

NeuroRX

212

128

View full text Add to dashboard Cite

Summary:The possibility that hypothermia during or after resuscitation from asphyxia at birth, or cardiac arrest in adults, might reduce evolving damage has tantalized clinicians for a very long time. It is now known that severe hypoxia-ischemia may not necessarily cause immediate cell death, but can precipitate a complex biochemical cascade leading to the delayed neuronal loss. Clinically and experimentally, the key phases of injury include a latent phase after reperfusion, with initial recovery of cerebral energy metabolism but EEG suppression, followed by a secondary phase characterized by accumulation of cytotoxins, seizures, cytotoxic edema, and failure of cerebral oxidative metabolism starting 6 to 15 h post insult. Although many of the secondary processes can be injurious, they appear to be primarily epiphenomena of the 'execution' phase of cell death. Studies designed around this conceptual framework have shown that moderate cerebral hypothermia initiated as early as possible before the onset of secondary deterioration, and continued for a sufficient duration in relation to the severity of the cerebral injury, has been associated with potent, long-lasting neuroprotection in both adult and perinatal species. Two large controlled trials, one of head cooling with mild hypothermia, and one of moderate whole body cooling have demonstrated that post resuscitation cooling is generally safe in intensive care, and reduces death or disability at 18 months of age after neonatal encephalopathy. These studies, however, show that only a subset of babies seemed to benefit. The challenge for the future is to find ways of improving the effectiveness of treatment.

show abstract

Uncomplicated Rapid Posthypothermic Rewarming Alters Cerebrovascular Responsiveness

Cited by 41 publications

References 23 publications

Epileptiform Activity During Rewarming from Moderate Cerebral Hypothermia in the Near-Term Fetal Sheep

Epileptiform Activity During Rewarming from Moderate Cerebral Hypothermia in the Near-Term Fetal Sheep

Safety and Therapeutical Benefit of Hemicraniectomy Combined with Mild Hypothermia in Comparison with Hemicraniectomy Alone in Patients with Malignant Ischemic Stroke

Hypothermic neuroprotection

Contact Info

Product

Resources

About