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The Journal of Thoracic and Cardiovascular Surgery, Vol 116, 780-792, Copyright © 1998 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
NOTE: Fulltext is available only in pdf format
D Shum-Tim, M Nagashima, T Shinoka, J Bucerius, G Nollert, HG Lidov, A du Plessis, PC Laussen and RA Jonas
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 degrees - 3 degrees 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
degrees C. Brain temperature was maintained at 34 degrees C for 24 hours
after cardiopulmonary bypass in group I, 37 degrees C in group II, and 40
degrees 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.
ARTICLES
Postischemic hyperthermia exacerbates neurologic injury after deep hypothermic circulatory arrest
Department of Cardiovascular Surgery, Children's Hospital, Harvard Medical School, Boston, Mass 02115, USA.
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