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Intraarterial nimodipine versus induced hypertension in refractory DCI after aneurysmal subarachnoid haemorrhage – investigation of a modified treatment protocol
Intraarterielles Nimodipin versus induzierte Hypertension beiverzögerter Ischämie nach aneurysmatischer Subarachnoidalblutung – Untersuchung eines modifizierten Behandlungsprotokolls
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Veröffentlicht: | 26. Juni 2020 |
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Objective: Rescue treatment for delayed cerebral ischemia (DCI) after subarachnoid hemorrhage may include induced hypertension (iHTN) >180mmHg (first-line) and the addition of continuous intraarterial nimodipine (IAN) in refractory cases (second-line). The combination of iHTN and IAN may lead to a critical exacerbation of vasopressor demand with considerable complications. In case of unsustainable doses, iHTN is often prioritized over IAN. However, evidence in this regard is largely lacking. For this purpose, we investigated the effects of a classical and modified treatment protocol.
Methods: Until 07/2018, iHTN at our institution was maintained at >180mmHg with initiation of IAN if patients showed refractory hypoperfusion. Escalated noradrenaline demand or display of complications typically triggered a secondary reduction or termination of IAN (group I). After 07/2018, we preemptively lowered pressure target to >140mmHg with initiation of IAN (group II), adequacy of treatment effect ensured by CT perfusion. We assessed noradrenaline dose for 24hours after treatment escalation and compared the need for retreatment, the rate of DCI related infarction and clinical outcome.
Results: In the n=25 and n=8 patients treated according to the original or modified protocol, respectively, mean IAN dose was comparable (I: 18.5±7.5 vs II: 17.7±9.6µg/kg/min, ns), while duration of IAN was longer in the cohort with modified protocol (I: 7.3±4.6 vs II: 12.7±6.6days, p<0.05), but MAP was lower (I: 113.9±8.4 vs II: 94.9±12.0mmHg, p<0.001). Vasopressor support was lower with the modified protocol, though the difference in noradrenaline requirements was initially not significant (I: 0.60±0.48 vs II: 0.16±0.24µg/kg/min, p=0.08). There were no differences in need for retreatment (I: 48.1% vs II: 37.5%, ns), DCI related infarction (I: 24.2% vs II: 12.5%, ns) or clinical outcome (GOS 4-5 I: 35.5% vs II: 37.5%, ns).
Conclusion: Assuming the potential of iHTN to be maxed out at time of secondary deterioration, continuous IAN may serve as a last-resort measure to bridge hypoperfusion in the DCI phase. However, combination of iHTN and IAN may carry a considerable risk profile, and microcirculatory organ perfusion may become severely impaired. With close monitoring, preemptive lowering of pressure target in favor of IAN may then be a safe option to alleviate total noradrenaline load without critically jeopardizing brain supply.