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Special review
Treatment of hypoxic-ischaemic brain damage by moderate hypothermia
  1. A D Edwardsa,
  2. J S Wyattb,
  3. M Thoresenc
  1. aSection of Paediatrics Imperial College School of Medicine Hammersmith Hospital London, bDepartment of Paediatrics University College London School of Medicine London, cDepartment of Child Health University of Bristol St Michael’s Hospital Bristol
  1. Professor A D Edwards Section of Paediatrics Imperial College School of Medicine Hammersmith Hospital London W12 ONN. email dedwards{at}rpms.ac.uk

https://doi.org/10.1136/fn.78.2.F85

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    To many people, especially writers of science fiction interested in preserving brains for narrative purposes, it seems self evident that cooling the brain protects it against hypoxic–ischaemic damage. Indeed, every day, cardiac surgeons and anaesthetists cool the brains of children during surgery to protect them against the effects of cardiac arrest or cardiopulmonary bypass.

    However there has long been a hope that cooling the brainafter hypoxia–ischaemia might lessen cerebral injury. Observational data in support of this were collected by Westin and colleagues 40 years ago,1 but experimental studies in animal models at that time failed to support the hypothesis and it fell from favour.2 Now the belief is gaining ground again among basic researchers that moderate brain cooling to around 32oC is one of several interventions which can be applied after hypoxia–ischaemia to modify the process of brain cell death and so lessen cerebral damage.

    Delayed cerebral damage after hypoxia–ischaemia

    A cornerstone of this growing consensus was the realisation that not only do some cells die during hypoxia–ischaemia, but many more may die hours or days later.3 In the 1980s this delayed cerebral injury was shown in infants with birth asphyxia using31P magnetic resonance spectroscopy (MRS): asphyxiated infants were usually found to have normal cerebral energy metabolism soon after resuscitation, but oxidative phosphorylation became impaired 9 to 24 hours later and remained low for many days.4 The delayed impairment of energy metabolism was not contingent on continued hypoxia–ischaemia, nor was it associated with intracellular acidosis,5 but its magnitude was linearly related to the severity of later neurodevelopmental impairment and reduced brain growth.6

    This was clear evidence that the effects of birth asphyxia might become manifest only some days after resuscitation, and indeed more recent data suggest that abnormal cerebral energy metabolism and cell death …

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