Article
Delayed cerebral ischemia after aneurysmal subarachnoid haemorrhage is preceded by failure to meet optimal cerebral perfusion pressure (CPPopt)
Verzögerte Ischämien nach aneurysmatischer Subarachnoidalblutung sind assoziiert mit Unterschreitung des optimalen zerebralen Perfusionsdrucks (CPPopt)
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Published: | June 4, 2021 |
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Objective: Delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH) has frequently been associated with poor cerebral autoregulation and outcome. However, means to improve autoregulation have been lacking so far. A new concept has been introduced where an “optimal” cerebral perfusion pressure (CPPopt) can be identified at which autoregulation may function best. The relationship between CPP, CPPopt and the incidence of DCI is yet unclear.
Methods: We prospectively recruited patients with aSAH treated at a single tertiary center between 04/2014 and 09/2020. The well-known pressure reactivity index (PRx) and associated CPPopt were retrospectively calculated for patients with available high frequency ICP/CPP data in the early phase after aSAH. Daily means were calculated during the first seven days after hemorrhage and for 6-hour intervals prior to the occurrence of DCI (neurological deterioration, territorial or watershed hypoperfusion on CT perfusion imaging). Blood pressure management was liberal with a lower CPP limit > 60 mmHg. Deviation of CPP from CPPopt (ΔCPP, defined as actual CPP-CPPopt) was recorded.
Results: Data of n=45 patients (DCI n=24, no DCI n=21) were analyzed and a large variability of individual CPPopt was observed for the first seven days (range 65.9-115.7mmHg). CPPopt increased continuously from day 0-1 to day 2-4 to day 5-7 (77.3±11.8 to 84.4±9.5 to 87.2±7.5mmHg, repeated measures ANOVA p<0.05). This dynamic was matched by spontaneously higher levels of CPP (75.7±9.9 to 81.3±11.9 to 84.7±9.4mmHg, p<0.01), observed both in patients with and without DCI (all intervals DCI vs. no DCI p>0.05). In the two days before DCI, CPPopt was relatively stable (85.7±8.9mmHg). However, in the 6 hours preceding DCI diagnosis, actual CPP decreased significantly (CPP 48-6h before DCI: 85.4±10.1mmHg, 6-0h: 79.5±8.5mmHg, p<0.05), which was associated with negative ΔCPP (48-6h: -0.5±4.3mmHg, 6-0h: -4.8±8.3mmHg, p<0.01) and worsening of autoregulation status (PRx 48-6h: 0.10±0.21, 6-0h: 0.18±0.29, p<0.01).
Conclusion: Patients with aSAH may upregulate their individual CPP in the early post-bleeding phase to compensate for the increasing cerebral demand. Spontaneous decreases below calculated CPPopt may be associated with development of DCI. Bedside calculation of CPPopt and fine-tuning CPP accordingly could assist in avoiding such episodes, and the effect on DCI and outcome should be investigated in prospective trials.