Postischemic hyperthermia exacerbates neurologic injury after deep hypothermic circulatory arrest

D. Shum-Tim, M. Nagashima, T. Shinoka, J. Bucerius, G. Nollert, H. G W Lidov, A. Du-Plessis, P. C. Laussen, R. A. Jonas, J. A. Swain, D. A. Murphy, S. Sano, T. L. Spray

Research output: Contribution to journalArticle

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Abstract

Background: Aggressive surface warming is a common practice in the pediatric intensive care unit. However, recent rodent data emphasize the protective effect of mild (2°-3°C) hypothermia after cerebral ischemia. This study evaluates different temperature regulation strategies after deep hypothermic circulatory arrest with a survival piglet model. Methods: Fifteen piglets were randomly assigned to 3 groups. All groups underwent 100 minutes of deep hypothermic circulatory arrest at 15°C. Brain temperature was maintained at 34°C for 24 hours after cardiopulmonary bypass in group I, 37°C in group II, and 40°C in group III. Neurobehavioral recovery was evaluated daily for 3 days after extubation by neurologic deficit score (0, normal; 500, brain death) and overall performance category (1, normal; 5, brain death). Histologic examination was assessed for hypoxic-ischemic injury (0, normal; 5, necrosis) in a blinded fashion. Results: All results are expressed as mean ± standard deviation. Recovery of neurologic deficit score (12.0 ± 17.8, 47.0 ± 49.95, 191.0 ± 179.83; P = .05 for group I vs III), overall performance category (1.0 ± 0.0, 1.4 ± 0.6, 2.8 ± 1.3; P <.05 for group I vs III), and histologic scores (0.0 ± 0.0, 1.0 ± 1.2, 2.8 ± 1.8; P <.05 for group I vs III cortex) were significantly worse in hyperthermic group III. These findings were associated with a significantly lower cytochrome aa3 recovery determined by near-infrared spectroscopy in group III animals (P = .0041 for group I vs III). No animal recovered to baseline electroencephalographic value by 48 hours after deep hypothermic circulatory arrest. Recovery was significantly delayed in the hyperthermic group III animals, with a lower amplitude 14 hours after the operation, which gradually increased with time (P <.05 for group III vs groups I and II). Conclusions: Mild postischemic hyperthermia significantly exacerbates functional and structural neurologic injury after deep hypothermic circulatory arrest and should therefore be avoided.

Original languageEnglish
Pages (from-to)780-792
Number of pages13
JournalJournal of Thoracic and Cardiovascular Surgery
Volume116
Issue number5
DOIs
Publication statusPublished - 1998
Externally publishedYes

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Deep Hypothermia Induced Circulatory Arrest
Nervous System Trauma
Fever
Brain Death
Neurologic Manifestations
Pediatric Intensive Care Units
Temperature
Near-Infrared Spectroscopy
Electron Transport Complex IV
Hypothermia
Brain Ischemia
Cardiopulmonary Bypass
Rodentia
Necrosis
Wounds and Injuries
Brain

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Shum-Tim, D., Nagashima, M., Shinoka, T., Bucerius, J., Nollert, G., Lidov, H. G. W., ... Spray, T. L. (1998). Postischemic hyperthermia exacerbates neurologic injury after deep hypothermic circulatory arrest. Journal of Thoracic and Cardiovascular Surgery, 116(5), 780-792. https://doi.org/10.1016/S0022-5223(98)00449-8

Postischemic hyperthermia exacerbates neurologic injury after deep hypothermic circulatory arrest. / Shum-Tim, D.; Nagashima, M.; Shinoka, T.; Bucerius, J.; Nollert, G.; Lidov, H. G W; Du-Plessis, A.; Laussen, P. C.; Jonas, R. A.; Swain, J. A.; Murphy, D. A.; Sano, S.; Spray, T. L.

In: Journal of Thoracic and Cardiovascular Surgery, Vol. 116, No. 5, 1998, p. 780-792.

Research output: Contribution to journalArticle

Shum-Tim, D, Nagashima, M, Shinoka, T, Bucerius, J, Nollert, G, Lidov, HGW, Du-Plessis, A, Laussen, PC, Jonas, RA, Swain, JA, Murphy, DA, Sano, S & Spray, TL 1998, 'Postischemic hyperthermia exacerbates neurologic injury after deep hypothermic circulatory arrest', Journal of Thoracic and Cardiovascular Surgery, vol. 116, no. 5, pp. 780-792. https://doi.org/10.1016/S0022-5223(98)00449-8
Shum-Tim, D. ; Nagashima, M. ; Shinoka, T. ; Bucerius, J. ; Nollert, G. ; Lidov, H. G W ; Du-Plessis, A. ; Laussen, P. C. ; Jonas, R. A. ; Swain, J. A. ; Murphy, D. A. ; Sano, S. ; Spray, T. L. / Postischemic hyperthermia exacerbates neurologic injury after deep hypothermic circulatory arrest. In: Journal of Thoracic and Cardiovascular Surgery. 1998 ; Vol. 116, No. 5. pp. 780-792.
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abstract = "Background: Aggressive surface warming is a common practice in the pediatric intensive care unit. However, recent rodent data emphasize the protective effect of mild (2°-3°C) hypothermia after cerebral ischemia. This study evaluates different temperature regulation strategies after deep hypothermic circulatory arrest with a survival piglet model. Methods: Fifteen piglets were randomly assigned to 3 groups. All groups underwent 100 minutes of deep hypothermic circulatory arrest at 15°C. Brain temperature was maintained at 34°C for 24 hours after cardiopulmonary bypass in group I, 37°C in group II, and 40°C in group III. Neurobehavioral recovery was evaluated daily for 3 days after extubation by neurologic deficit score (0, normal; 500, brain death) and overall performance category (1, normal; 5, brain death). Histologic examination was assessed for hypoxic-ischemic injury (0, normal; 5, necrosis) in a blinded fashion. Results: All results are expressed as mean ± standard deviation. Recovery of neurologic deficit score (12.0 ± 17.8, 47.0 ± 49.95, 191.0 ± 179.83; P = .05 for group I vs III), overall performance category (1.0 ± 0.0, 1.4 ± 0.6, 2.8 ± 1.3; P <.05 for group I vs III), and histologic scores (0.0 ± 0.0, 1.0 ± 1.2, 2.8 ± 1.8; P <.05 for group I vs III cortex) were significantly worse in hyperthermic group III. These findings were associated with a significantly lower cytochrome aa3 recovery determined by near-infrared spectroscopy in group III animals (P = .0041 for group I vs III). No animal recovered to baseline electroencephalographic value by 48 hours after deep hypothermic circulatory arrest. Recovery was significantly delayed in the hyperthermic group III animals, with a lower amplitude 14 hours after the operation, which gradually increased with time (P <.05 for group III vs groups I and II). Conclusions: Mild postischemic hyperthermia significantly exacerbates functional and structural neurologic injury after deep hypothermic circulatory arrest and should therefore be avoided.",
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AU - Shum-Tim, D.

AU - Nagashima, M.

AU - Shinoka, T.

AU - Bucerius, J.

AU - Nollert, G.

AU - Lidov, H. G W

AU - Du-Plessis, A.

AU - Laussen, P. C.

AU - Jonas, R. A.

AU - Swain, J. A.

AU - Murphy, D. A.

AU - Sano, S.

AU - Spray, T. L.

PY - 1998

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N2 - Background: Aggressive surface warming is a common practice in the pediatric intensive care unit. However, recent rodent data emphasize the protective effect of mild (2°-3°C) hypothermia after cerebral ischemia. This study evaluates different temperature regulation strategies after deep hypothermic circulatory arrest with a survival piglet model. Methods: Fifteen piglets were randomly assigned to 3 groups. All groups underwent 100 minutes of deep hypothermic circulatory arrest at 15°C. Brain temperature was maintained at 34°C for 24 hours after cardiopulmonary bypass in group I, 37°C in group II, and 40°C in group III. Neurobehavioral recovery was evaluated daily for 3 days after extubation by neurologic deficit score (0, normal; 500, brain death) and overall performance category (1, normal; 5, brain death). Histologic examination was assessed for hypoxic-ischemic injury (0, normal; 5, necrosis) in a blinded fashion. Results: All results are expressed as mean ± standard deviation. Recovery of neurologic deficit score (12.0 ± 17.8, 47.0 ± 49.95, 191.0 ± 179.83; P = .05 for group I vs III), overall performance category (1.0 ± 0.0, 1.4 ± 0.6, 2.8 ± 1.3; P <.05 for group I vs III), and histologic scores (0.0 ± 0.0, 1.0 ± 1.2, 2.8 ± 1.8; P <.05 for group I vs III cortex) were significantly worse in hyperthermic group III. These findings were associated with a significantly lower cytochrome aa3 recovery determined by near-infrared spectroscopy in group III animals (P = .0041 for group I vs III). No animal recovered to baseline electroencephalographic value by 48 hours after deep hypothermic circulatory arrest. Recovery was significantly delayed in the hyperthermic group III animals, with a lower amplitude 14 hours after the operation, which gradually increased with time (P <.05 for group III vs groups I and II). Conclusions: Mild postischemic hyperthermia significantly exacerbates functional and structural neurologic injury after deep hypothermic circulatory arrest and should therefore be avoided.

AB - Background: Aggressive surface warming is a common practice in the pediatric intensive care unit. However, recent rodent data emphasize the protective effect of mild (2°-3°C) hypothermia after cerebral ischemia. This study evaluates different temperature regulation strategies after deep hypothermic circulatory arrest with a survival piglet model. Methods: Fifteen piglets were randomly assigned to 3 groups. All groups underwent 100 minutes of deep hypothermic circulatory arrest at 15°C. Brain temperature was maintained at 34°C for 24 hours after cardiopulmonary bypass in group I, 37°C in group II, and 40°C in group III. Neurobehavioral recovery was evaluated daily for 3 days after extubation by neurologic deficit score (0, normal; 500, brain death) and overall performance category (1, normal; 5, brain death). Histologic examination was assessed for hypoxic-ischemic injury (0, normal; 5, necrosis) in a blinded fashion. Results: All results are expressed as mean ± standard deviation. Recovery of neurologic deficit score (12.0 ± 17.8, 47.0 ± 49.95, 191.0 ± 179.83; P = .05 for group I vs III), overall performance category (1.0 ± 0.0, 1.4 ± 0.6, 2.8 ± 1.3; P <.05 for group I vs III), and histologic scores (0.0 ± 0.0, 1.0 ± 1.2, 2.8 ± 1.8; P <.05 for group I vs III cortex) were significantly worse in hyperthermic group III. These findings were associated with a significantly lower cytochrome aa3 recovery determined by near-infrared spectroscopy in group III animals (P = .0041 for group I vs III). No animal recovered to baseline electroencephalographic value by 48 hours after deep hypothermic circulatory arrest. Recovery was significantly delayed in the hyperthermic group III animals, with a lower amplitude 14 hours after the operation, which gradually increased with time (P <.05 for group III vs groups I and II). Conclusions: Mild postischemic hyperthermia significantly exacerbates functional and structural neurologic injury after deep hypothermic circulatory arrest and should therefore be avoided.

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