Artikel
Continuous intravenous cooling – an additional treatment option for patients with severe cerebral vasospasm after subarachnoid haemorrhage
Kontinuierliche intravenöse Kühlung- eine zusätzliche Behandlungsoption für Patienten mit schwerem zerebralen Vasospasmus nach Subarachnoidalblutung
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Autoren
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Sylvia Bele
- Universitätsklinikum Regensburg, Klinik und Poliklinik für Neurochirurgie, Regensburg, Deutschland
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Elisabeth Bründl
- Universitätsklinikum Regensburg, Klinik und Poliklinik für Neurochirurgie, Regensburg, Deutschland
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Karl-Michael Schebesch
- Universitätsklinikum Regensburg, Klinik und Poliklinik für Neurochirurgie, Regensburg, Deutschland
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Nils-Ole Schmidt
- Universitätsklinikum Regensburg, Klinik und Poliklinik für Neurochirurgie, Regensburg, Deutschland
| Veröffentlicht: | 25. Mai 2022 |
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Gliederung
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Objective: Cerebral vasospasm (CV) remains one of the leading causes for mortality and morbidity in patients suffering from subarachnoid hemorrhage (SAH). We established a treatment protocol for patients with severe refractory CV using multimodal neuromonitoring and continuous intra-arterialnimodipine infusion (CIAN)1,2 in addition to hypertensive therapy (HT). But even with this invasive treatment some patients still show ischemic PbtO2 values in multimodal neuromonitoring. We believe that those patients might benefit from moderate hypothermia. The presentstudy was designed to find out if continuous intravenous cooling is an additional treatment option for patients with severe CV.
Methods: When neuromonitoring controlled HHT was not sufficient to keep PbtO2 levels > 15 mmHg in patients suffering from severe CV, CIAN was initiated.If PbtO2 values continued to stay < 15 mmHg despite this treatment we additionally induced a mild hypothermia (35°C) using an intravenouscooling system via the subclavian vein. Outcome was evaluated 6 months after dischargeusing the Glasgow Outcome Scale (GOS).
Results: Eight of 21 patients showed PbtO2 <15 mmHg despite maximum nimodipine dosage of 1.2 mg/h. In those patients we induced hypothermia (35°C). All patients reached target temperature within 65 min and median cooling time was 94 h. PbtO2levels stabilized in all patients within 60 min after start of hypothermia. The mean PbtO2 before hypothermia start was 11,2 +/-3 mmHg andincreased to 20,9 +/-2,8 mmHg. After PbtO2 levels were stable, rewarming was done in a controlled manner with 0.2°C/h. At 6 months after discharge 6 patients were GOS 4 and 2 patients GOS 5.
Conclusion: This small group study showed that continuous intravenous cooling using the ThermoagardXP® is a feasible technique to induce mild hypothermiain neurointensive care patients with a low complication rate. This method allows rapid and precise cool-down and the temperature can be keptstable within a small range (+/-0.2°C) of the predefined temperature. Mild hypothermia led to a significant improvement of PbtO2 levels in all treatedpatients and the outcome was good. This might be also due to the fact that hypothermia leads to a lower oxygen consumption of the brain and otherpositive effects, e.g. decreased endotoxicity3 or prevention of ATP depletion3 that might protect against hypoxic brain damage.
We believe that mild hypothermia is a valuable treatment addition for patients suffering from severe CV.
