Artikel
Intraarterial nimodipine versus induced hypertension for delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage – a prospective study of a modified treatment protocol
Intraarterielles Nimodipin versus induzierte Hypertonie bei verzögerter zerebraler Ischämie nach aneurysmatischer Subarachnoidalblutung – eine prospektive Studie über ein modifiziertes Behandlungsprotokoll
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Autoren
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Miriam Weiss
- Uniklinik RWTH Aachen, Klinik für Neurochirurgie, Aachen, Deutschland
| Veröffentlicht: | 25. Mai 2022 |
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Gliederung
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Objective: Rescue treatment for delayed cerebral ischemia (DCI) after subarachnoid hemorrhage may include induced hypertension (iHTN) (first-line treatment) and, in refractory cases, the addition of continuous intraarterial vasodilation with nimodipine (IAN) (second-line treatment). The combination of iHTN and IAN can dramatically increase vasopressor demand. In case of unsustainable doses, iHTN is often prioritized over IAN. However, evidence in this regard is largely lacking. We investigated the effects of a classical and modified treatment protocol.
Methods: Rescue treatment for DCI was initiated with iHTN (target >180mmHg systolic) and escalated to IAN in refractory cases. Until 07/2018, concurrent treatment with iHTN >180mmHg and IAN was offered in refractory cases according to local protocol (iHTN+IAN), with reduction of IAN dose in case of unsustainable vasopressor demand. After protocol modification in 08/2018, treatment escalation in refractory cases included initiation of IAN with preemptive reduction of iHTN to >120mmHg (IAN only). Primary outcome was noradrenaline demand during rescue treatment. Secondary outcomes were minor and major noradrenaline-associated complications, mean intraparenchymal brain tissue oxygen during treatment, DCI related infarction and favorable 3-month outcome (Glasgow Outcome Scale 4-5).
Results: A total of n=29 and n=18 patients were treated according to the classical and modified protocol, respectively. Protocol modification resulted in a significant reduction of mean noradrenaline demand (iHTN+IAN 0.70±0.54µg/kg/min, IAN only 0.28±0.21µg/kg/min, p<0.0001) and minor complications (48.3%, 11.1%, p<0.05) with a comparable incidence of major complications (20.7%, 22.2%, p=1.0). Brain tissue oxygen was significantly higher with IAN only (iHTN+IAN 26.6±12.8mmHg, IAN only 39.8±9.4mmHg, p<0.05). Incidence of DCI related infarction (37.9%, 44.4%, p=0.76) and favorable clinical outcome (30.4%, 36.4%, p=0.57) were comparable.
Conclusion: Assuming the potential of iHTN to be exhausted out at time of secondary deterioration, additional IAN may serve as a last-resort measure to bridge hypoperfusion in the DCI phase. With close monitoring, preemptive lowering of pressure target after induction of IAN may be a safe alternative to alleviate total noradrenaline load and potentially reduce complication rate.
