Abstract
Acute neurological morbidity following repair of congenital heart disease (CHD) in infancy is well recognized, particularly with the modalities of hypothermic cardiopulmonary bypass (CPB) and profound hypothermic circulatory arrest (PHCA). Reduced O2 delivery (perfusion defect) during rewarming following PHCA has been shown in the operating room. This reduction in cerebral blood flow coincides with disordered cerebral metabolism and oxygen utilisation after PHCA. The objective of this study was to extend the period of investigation of cerebral blood flow velocity (CBFV) behaviour in infants following PHCA to determine if hypoperfusion persisted in the paediatric intensive care unit (PICU). Ten patients undergoing CHD surgery were divided, based on the pump modality employed, into either mild hypothermic CPB or profound hypothermic CPB with circulatory arrest. Following admission to the PICU, sequential recordings of the mean CBFV in the middle cerebral artery, anterior fontanelle pressure, haemodynamic variables, tympanic membrane temperature, haematocrit and PaCO2 were performed. The PHCA group had a consistently reduced CBFV compared with the control group (P < 0.05). The CBFV values at one, two and four hours were 60 ± 11, 51.8 ± 11.4 and 52.6 ± 11.9 respectively in the mild hypothermic CPB group. The CBFV values at one, two and four hours were 26.6 ± 6.8, 32.6 ± 10 and 34 ± 8 respectively in the PHCA group. There was no difference in cerebral perfusion pressure between both groups. Tympanic temperature, haematocrit and PaCO2 did not vary between groups at any interval. This study demonstrates a sustained reduction in the CBFV pattern following PHCA into the postoperative period despite adequate cerebral perfusion pressures. This abnormality correlates with electroencephalographic aberrations documented after PHCA. It supports the concept of a prolonged unreactive cerebrovascular bed which could potentially contribute to the acute neurological morbidity following PHCA in neonates.
Résumé
La morbidité neurologique infantile attribuable aux malformations cardiaques congénitales (MCG) opérées sous circulation extracorporelle (CEC) en hypothermie et sous arrêt circulatoire en hypothermie profonde (ACHP) est bien connue. En salle d’opération, on a déjà démontré une diminution de l’apport en oxygène (insuffisance de perfusion) au cours du réchauffement pendant l’ACHP. Cette réduction de la perfusion cérébrate coïncide avec un bouleversement du métabolisme cérébral et de l’utilisation de l’oxygène après l’ACHP. L’objectif de ce travail était d’étendre la durée de l’examen du comportement de la vélocite du débit sanguin cérébral (VDSC) après un ACHP chez les enfants pour déterminer si l’hypoperfusion persistait à l’unité des soins intensifs pédiatriques (UPSI). Après l’admission à l’UPSI, des enregistrements séquentiels de la VDSC moyenne de l’artère cérébrale moyenne, de la pression de la fontanelle antérieure, de l’hématocrite et de la PaCO2 ont été effectués. Le groupe ACHP avait une VDSC diminuée comparativement au groupe contrôle (P < 0,05). Les valeurs de la VDSC à la premiére, deuxième et quatrième heure étaient de 60 ± 11, 51,8 ± 11,4 et 52,6 ± 11,9 respectivement dans le groupe de la CEC légèrement hypothermique. On n’a pas trouvé de différence pour la pression cérébrate de perfusion entre les deux groupes. La température tympanique, l’hématocrite et la PaCO2 n’ont varié en aucun moment entre les groupes. Cette étude montre une réduction soutenue dans l’évolution de la VDSC aprés une ACHP pendant la période postopératoire malgré des pressions de perfusion adéquates. Cette anomalie concorde avec les changements électroencéphaliques trouvés aprèsc l’ACHP. Elle confirme le concept de non réactivité du lit cérébrovasculaire qui pourrait contribuer à la morbidité neurologique après l’ACHP chez le nouveau-né.
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O’Hare, B., Bissonnette, B., Bohn, D. et al. Persistent low cerebral blood flow velocity following profound hypothermic circulatory arrest in infants. Can J Anaesth 42, 964–971 (1995). https://doi.org/10.1007/BF03011066
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DOI: https://doi.org/10.1007/BF03011066