14.5.6 Cerebral protection and neurological sequelae

Postoperative neurological complications are common in neonates and children: 6-25% [7], including 2.3% acute complications [16]. While these tend to be embolic in adults, most neurological sequelae are ischaemic in children, due largely to frequent episodes of low flow or deep hypothermic circulatory arrest [1]. Moreover, some congenital malformations are combined with cerebral conditions that adversely affect prognosis.

Neurological sequelae manifest in several forms.
 
  • Convulsions: 20% of neonates; EEG signs are more common than clinical convulsions. Although these convulsions resolve spontaneously, they adversely affect long-term neurological prognosis [18].
  • Choreoathetosis: 1-20% of circulatory arrest cases. Hyperkinetic movements are caused by lesions of the basal ganglia – they occur most commonly in children with aortopulmonary collaterals that divert blood flow from the systemic circulation. Children are most vulnerable between the ages of 6 months and 6 years [22].
  • Delayed psychomotor and cognitive development: circulatory arrest of up to 30 min at 18°C only has minimal effects [17]. Cyanotic children with aortopulmonary collaterals are most at risk [14].
Many observational and prospective studies demonstrate a link between postoperative neurological complications and various aspects of perioperative management: the duration of circulatory support (CPB, ECMO), the duration of cerebral ischaemia, the quality of cooling and rewarming, haematocrit, acid-base regulation, and blood glucose management. A cooling period of less than 20 minutes and α-stat-type regulation are statistically linked to diminished cognitive development in young children [2]. Rapid rewarming leads to a cerebral hyperthermic rebound effect (mean brain T° 39.6°C) [3] – this temperature rise is directly related to postoperative neurological deficiencies [10,20]. Although hyperglycaemia is linked to an exacerbation of neurological sequelae in cases of cerebral ischaemia in adults, it does not appear to be a critical factor in post-CPB neuronal function in children. Hypoglycaemia is a greater cause of concern in infants [5]. However, comprehensive studies demonstrate that preoperative neurobehavioural status and postoperative non-hospital circumstances have a considerable influence and surpass the impact of perioperative events, which only account for 5% of status decline [9]. Despite progress made in terms of perioperative management, the psychomotor development of children aged < 1 year operated for congenital heart diseases has scarcely improved over time, largely because it is mainly linked to weight at birth, genetic abnormalities, associated malformations, the child's specific neurological status, and the family’s sociocultural background [8].

Cerebral protection

Due to the complexity of surgical reconstructions and the small operating field in infants, CPB often needs to be suspended briefly. A systematic review of the means used to protect young children’s delicate brains during this critical period reveals that no clinical data demonstrate the superiority of any one technique over the others, or prove its positive impact on children’s neurological outcomes [11]. According to the standard classification of recommendations, all cerebral protection techniques are class IIB (the procedure may be considered) or III (the procedure is not beneficial). The level of evidence is category B (observational studies) or C (registries, expert consensus) [11]. Only a few measures appear to offer benefits in terms of neurological sequelae (class IIA: the procedure is reasonable).
 
  • Avoiding excessive haemodilution and maintaining Ht > 24% [23];
  • Avoiding hypoglycaemia – strict control of blood glucose levels is not indicated [5].
  • Cooling the brain [13];
  • Limiting the duration of circulatory arrest [21].
A thorough analysis of the abundant literature on the topic demonstrates that none of the numerous clinical approaches taken is identified as having a clearly significant impact on cerebral protection: alpha-stat or pH-stat management of acid-base balance, neurological monitoring methods, cooling procedures, surgical techniques (deep hypothermic circulatory arrest, continuous low-flow CPB, or isolated cerebral perfusion) [11]. However, such are the stakes that we cannot settle for cold minimalism. A whole set of measures exists that, when combined, tend to limit risk factors and increase the safety margin. Even though protocols differ from one centre to another, results can be gradually improved by ensuring that they are rigorously applied by a team that has routine experience of them. A bundle of techniques is available to minimise neurological sequelae [4].
 
  • Maintaining haematocrit at > 24%, including during deep hypothermia [23].
  • Maintaining sufficient blood glucose levels to prevent any hypoglycaemia [5].
  • Ensuring that circulatory arrest is performed for durations that are conducive to likely neurological recovery: 3-5 minutes at 37°, 12 minutes at 28°, 35 minutes at 18° [13].
  • Continuous or intermittent hypothermic cerebral perfusion (22-28°) by CPB [6].
  • Regional hypothermic cerebral perfusion (22-28°) by carotid artery cannulation [21].
  • pH-stat-type strategy during cooling and rewarming [2].
  • Sufficient duration of cooling and rewarming periods (≥ 20 minutes) [2,24].
  • Limitation of tissue oedema: restrictive fluid regimen, modified ultrafiltration at the end of CPB [19].
  • Maintaining adequate O2 supply, perfusion pressure, and cardiac output once CPB is ended.
  • Treatment of any postoperative hyperthermia [3].
  • Neuroprotective drugs: steroids, mannitol, allopurinol, calcium channel blockers, magnesium. None of these offers guaranteed efficacy [15].
  • Deep anaesthesia and curarisation [12].
 
 Neurological sequelae
Neurological sequelae (6-25% of cases) are mainly ischaemic rather than embolic in children (hypothermia-rewarming, circulatory arrest, hypoxia, hypoperfusion, hypoglycaemia).
    - Delirium, agitation
    - Convulsions
    - Choreoathetosis
    - Psychomotor retardation

Cerebral protection measures:
    - Maintain Ht ≥ 24%
    - Avoid hypoglycaemia
    - Limit the duration of arrest (5 minutes at 37°, 12 minutes at 28°, 35 minutes at 18°)
    - Slow cooling and rewarming (> 20 minutes or 0.5°/min)
    - Avoid cerebral hyperthermia (max blood T° 37°)
 
 
 © BETTEX D, BOEGLI Y, CHASSOT PG, June 2008, last update May 2018
 
 
References
 
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