Artikel
Inhalative nitric oxide treatment for patients with severe cerebral vasospasm after aneurysmal subarachnoid hemorrhage
Inhalative Stickstoffmonoxid (iNO) Behandlung bei Patienten mit schwerem, therapierefraktärem zerebralen Vasospasmus nach Subarachnoidalblutung
Suche in Medline nach
Autoren
-
Christian Fung
- Universitätsklinik Freiburg, Neurochirurgie, Freiburg, Deutschland
-
Werner Z’Graggen
- Universitätsklinik Bern, Neurochirurgie, Bern, Switzerland
-
Andreas Raabe
- Universitätsklinik Bern, Neurochirurgie, Bern, Switzerland
-
Stephan Jakob
- Universitätsklinik Bern, Intensivmedizin, Bern, Switzerland
-
Matthias Hänggi
- Universitätsklinik Bern, Intensivmedizin, Bern, Switzerland
-
Jan Gralla
- Universitätsklinik Bern, Institut für Diagnostische und Interventionelle Neuroradiologie, Bern, Switzerland
-
Jürgen Beck
- Universitätsklinik Freiburg, Neurochirurgie, Freiburg, Deutschland
| Veröffentlicht: | 8. Mai 2019 |
|---|
Gliederung
Text
Objective: To assess the safety and feasibility of inhalative nitric oxide (iNO) treatment for patients with severe cerebral vasospasm after aneurysmal subarachnoid hemorrhage.
Methods: Eligible patients had severe symptomatic cerebral vasospasm despite hyperdynamic treatment. Vasospasm was diagnosed either by digital subtraction angiography (DSA), CT angiography or transcranial doppler (TCD) and cerebral hypoperfusion by persisting neurologic deficit, decrease in focal intraparenchymal tissue oxygen tension (ptiO2) or impaired perfusion in CT perfusion imaging. Inalativ NO was started at a dose of 1ppm and increased to 40ppm. The primary endpoint was a combined endpoint of improvement of severe vasospasm in DSA or an improvement of the cerebral perfusion measured by (ptiO2) or improvement of the vasospasm induced neurologic deficit. A follow up assessment was performed 6 months after ictus.
Results: Between February 2013 and September 2016 we included 7 patients with a median age of 51.7 years, four good grade and three poor grade SAH patients. All 7 patients presented severe symptomatic cerebral vasospasm despite maximal hyperdynamic treatment. Mean duration of iNO application was 32.9 hours. 2 patients showed an improvement of TCD values and 3 patients an improvement of vasospasm assessed by DSA. In 5 patients an improvement of ptiO2 values at predefined timepoints was noticed. PtiO2 values (maximum) increased between 15.8 and 301.3% (median 64, IQR 55–114.6) compared to baseline. Due to continued sedation an assessment of clinical improvement during application of iNO was not possible. In 4 patients a new ischemia was diagnosed. 7 patients had a good outcome, 2 patients died. We did not observe any relevant side effect related to the application of iNO.
Conclusion: Application of iNO in the setting of severe cerebral vasospasm after aneurysmal SAH is feasible and does not expose the patients to an increased risk. Inhalative NO seems to have a greater effect on intraparenchymal oxygen tension than on large vessels. Although outcome was good in 5 out of 7 patients the small patient number allows no conclusion with respect to efficacy.
