Neurologic Changes Following Profound Hypothermia

Egerton, Nancy; Egerton, William S.; Kay, Jerome Harold

doi:10.1097/00000658-196303000-00007

Cited by 78 publications

(13 citation statements)

References 15 publications

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“…Our study supports the clinical findings of Egerton and colleagues [10] that significant brain injury will occur at very low temperature (8-12°C) using cardiopulmonary bypass without circulatory arrest. In their report, moderate to severe injury occurred when the mean cardiopulmonary bypass time at or below 12°C was more than 2 hours compared to slight injury when it was approximately 1 hour.…”

Section: Commentssupporting

confidence: 91%

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Experimental Evidence of Cerebral Injury from Profound Hypothermia During Cardiopulmonary Bypass

et al. 1998

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Choreoathetosis, seizures, and impaired mental development continue to occur in children undergoing cardiopulmonary bypass (CPB) and profound hypothermia with or without circulatory arrest. Although there is some evidence that the hypothermia itself may be causing these neurologic problems, skepticism remains because of lack of evidence from experimental studies simulating the clinical setting. In this experimental study, we examined the effect of profound and moderate hypothermia on the brain while maintaining normal flow rates during CPB. Ten adult mongrel dogs equally divided into two groups were anesthetized and subjected to CPB and varying levels of hypothermia (group 1, < or = 15 degreesC; group 2, < or = 2 degreesC). Both groups were kept at the desired temperature for 1 hour prior to rewarming and discontinuation of CPB. The dogs were euthanized 4-6 weeks later and neuropathologic studies were performed. The mean CPB flow rates during cooling and at the desired rectal temperature were comparable in both groups: group 1, 108 +/- 10 ml/kg/min versus 106 +/- 7 ml/kg/min in group 2 (p = NS) and 95 +/- 12 ml/kg/min in group 1 versus 101 +/- 5 ml/kg/min in group 2 (p = NS). Because of the difference in temperature between the two groups, the mean cooling time (onset of CPB to desired rectal temperature) was longer in group 1 (70 +/- 14 minutes) than in group 2 (28 +/- 11 minutes, p = 0.007). Hence, the total mean CPB time was also longer in group 1 (198 +/- 25 minutes) than in group 2 (143 +/- 13 minutes, p = 0.002). The lowest mean blood and rectal temperature achieved in group 1 were 11 +/- .9 degreesC and 12 +/- 1 degreesC versus 29 +/- .4 degreesC (p < 0.001) and 30 +/- .6 degreesC (p = 0.001), respectively, in group 2 (p = 0.001). Neuronal loss and degeneration was noted in all dogs in group 1 ranging from 2 to 8 cells per 1000 cells counted compared to none in group 2 (p = 0.05). These lesions occurred in both the basal ganglia and the cortex, although they were more marked in the caudate when compared to the cortex and cerebellum. Both in the cortex and in the caudate, neuronal loss was more marked around the capillaries. We conclude that the use of profound hypothermia of < or =15 degreesC and maintenance of normal flow rates during cooling at this temperature for 1 hour produces neuronal loss and degeneration in the brain. These lesions being more marked around capillaries points to the vulnerability of the neurons, probably because of their high lipid content to injury from the cold perfusate.

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Section: Commentssupporting

confidence: 91%

“…Egerton and colleagues [10] reported 15 of 16 adult patients sustaining varying degrees of brain dam- age at 8-12°C. Transient disorientation, retrograde amnesia, facial and supranuclear palsies, generalized hypotonia, and loss of reflexes and irreversible coma were found.…”

Section: Commentsmentioning

confidence: 99%

Experimental Evidence of Cerebral Injury from Profound Hypothermia During Cardiopulmonary Bypass

et al. 1998

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“…Thus deep hypothermia may not be necessary during ASCP and cerebral oxygen demands should be met at moderate hypothermia. Furthermore, there is increasing evidence that deep hypothermia is associated with direct negative effects on cerebral neuronal integrity [13,14].…”

Section: Discussionmentioning

confidence: 99%

Antegrade selective cerebral perfusion in thoracic aorta surgery: safety of moderate hypothermia

Pacini

Leone

Marco

et al. 2007

European Journal of Cardio-Thoracic Surgery

128

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In our experience, ASCP was a safe technique for thoracic aorta surgery allowing complex aortic repairs to be performed with good results in terms of hospital mortality and neurologic outcomes. The fact that there was no difference between the two groups suggests that moderate systemic hypothermia (26 degrees C) appears to be a safe and sufficient tool for brain protection. Moreover, the well known hypothermia-related side effects may be avoided.

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“…However, profound hypothermia (PH), defined here as temperatures less than 18°C, is associated with neurologic injury. Concerns about the deleterious effects of hypothermia date from the early days of cardiac surgery 4–6 , with deeper levels of profound hypothermia (<18 °C) associated with frequent neurologic complications 7,8 . The causes of neurologic injuries caused by hypothermia have been little studied compared to hypoxic or ischemic injury.…”

Section: Introductionmentioning

confidence: 99%

Anesthetic Protection of Neurons Injured by Hypothermia and Rewarming

Bickler¹,

Warren

Clark

et al. 2012

Anesthesiology

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Background Mild hypothermia is neuroprotective following cerebral ischemia but surgery involving profound hypothermia (PH, temperature <18 °C) is associated with neurological complications. Rewarming (RW) from PH injures hippocampal neurons by glutamate excitotoxicity, N-methyl-D-aspartate receptors and intracellular calcium. Because neurons are protected from hypoxia-ischemia by anesthetics that inhibit N-methyl-D-aspartic acid receptors, we tested whether anesthetics protect neurons from damage caused by PH/RW. Methods Organotypic cultures of rat hippocampus were used to model PH/RW injury, with hypothermia at 4°C followed by RW to 37°C and assessment of cell death 1 or 24 h later. Cell death and intracellular Ca2+ were assessed with fluorescent dye imaging and histology. Anesthetics were present in the culture media during PH and RW or only RW. Results Injury to hippocampal CA1, CA3, and dentate neurons following PH and RW involved cell swelling, cell rupture, and adenosine triphosphate loss; this injury was similar for 4 through 10 h of PH. Isoflurane (1 and 2%), sevoflurane (3%) and xenon (60%) reduced cell loss but propofol (3 μM) and pentobarbital (100 μM) did not. Isoflurane protection involved reduction in N-methyl-D-aspartate receptor-mediated Ca2+ influx during RW but did not involve γ-amino butyric acid receptors or KATP channels. However, cell death increased over the next day. Conclusions Anesthetic protection of neurons rewarmed from 4°C involves suppression of N-methyl-D-aspartate receptor-mediated Ca2+ overload in neurons undergoing adenosine triphosphate loss and excitotoxicity. Unlike during hypoxia/ischemia, anesthetics acting predominately on γ-amino butyric acid receptors do not protect against PH/RW. The durability of anesthetic protection against cold injury may be limited.

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Neurologic Changes Following Profound Hypothermia

Cited by 78 publications

References 15 publications

Experimental Evidence of Cerebral Injury from Profound Hypothermia During Cardiopulmonary Bypass

Experimental Evidence of Cerebral Injury from Profound Hypothermia During Cardiopulmonary Bypass

Antegrade selective cerebral perfusion in thoracic aorta surgery: safety of moderate hypothermia

Anesthetic Protection of Neurons Injured by Hypothermia and Rewarming

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