Inhalatorial Sedation in Patient With Subarachnoid Hemorrhage (SAH) Versus Conventional Intravenous Sedation

Stroke Clinical Trial

— GAS-SAH  

Official title:

Inhalatorial Sedation in Patient With SAH Versus Conventional Intravenous Sedation (GAS-SAH)

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT00830843
• Other study ID #: 1-citerio
• Status: Completed
• Phase: Phase 4
• First received: January 27, 2009
• Last updated: August 19, 2016
• Start date: January 2009
• Est. completion date: July 2011

Study information

• Verified date: November 2011
• Source: Azienda Ospedaliera San Gerardo di Monza
• Contact: n/a
• Is FDA regulated: No
• Health authority: Italy: The Italian Medicines Agency
• Study type: Interventional

Clinical Trial Summary

Recent study has shown that inhalatory sedation is a practicable, effective and not risky method in Intensive Care Unit. Sevoflurane effect on cerebral system have been described in previous studies: it causes an increasing of cerebral blood flow and a decrease of oxygen cerebral consumption. Clinical strategy for Subarachnoid Hemorrhage is orientated to increase cerebral blood flow to limit vasospasm phenomena after SAH. Scope of this study is to evaluate the Cerebral Blood Flow variation associated to Isoflurane sedation versus conventional sedation with propofol .

Recruitment information / eligibility

• Status: Completed
• Enrollment: 13
• Est. completion date: July 2011
• Est. primary completion date: July 2011
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 18 Years and older

Eligibility

Inclusion Criteria:

• diagnosis of aSAH

• indication to DVE positioning

• clinical indication to sedation and assisted ventilation

• indication to ICP and CBF monitoring

• age > 18

Exclusion Criteria:

• documented cranial hypertension (ICP>18) not controller by liquor drainage

• age < 18.

Study Design

Allocation: Non-Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Crossover Assignment, Masking: Open Label, Primary Purpose: Treatment

Related Conditions & MeSH terms

• Hemorrhage
• Stroke
• Subarachnoid Hemorrhage

Intervention

Drug:
• Propofol
Propofol(3-4 mg/kg/ora)administrated for 2 hours.
• Isoflurane
Isoflurane inhalatorial administration for 2 hours at 0.8-1.0% Minimum Alveolar Concentration

Locations

Country	Name	City	State
Italy	Azienda Ospedaliera San Gerardo	Monza

Sponsors (1)

Lead Sponsor	Collaborator
Azienda Ospedaliera San Gerardo di Monza

Country where clinical trial is conducted

Italy, 

References & Publications (13)

Berton J, Sargentini C, Nguyen JL, Belii A, Beydon L. AnaConDa reflection filter: bench and patient evaluation of safety and volatile anesthetic conservation. Anesth Analg. 2007 Jan;104(1):130-4. — View Citation

Kapinya KJ, Löwl D, Fütterer C, Maurer M, Waschke KF, Isaev NK, Dirnagl U. Tolerance against ischemic neuronal injury can be induced by volatile anesthetics and is inducible NO synthase dependent. Stroke. 2002 Jul;33(7):1889-98. — View Citation

L'her E, Dy L, Pili R, Prat G, Tonnelier JM, Lefevre M, Renault A, Boles JM. Feasibility and potential cost/benefit of routine isoflurane sedation using an anesthetic-conserving device: a prospective observational study. Respir Care. 2008 Oct;53(10):1295-303. — View Citation

Lee JJ, Li L, Jung HH, Zuo Z. Postconditioning with isoflurane reduced ischemia-induced brain injury in rats. Anesthesiology. 2008 Jun;108(6):1055-62. doi: 10.1097/ALN.0b013e3181730257. — View Citation

Maekawa T, Tommasino C, Shapiro HM, Keifer-Goodman J, Kohlenberger RW. Local cerebral blood flow and glucose utilization during isoflurane anesthesia in the rat. Anesthesiology. 1986 Aug;65(2):144-51. — View Citation

McAuliffe JJ, Joseph B, Vorhees CV. Isoflurane-delayed preconditioning reduces immediate mortality and improves striatal function in adult mice after neonatal hypoxia-ischemia. Anesth Analg. 2007 May;104(5):1066-77, tables of contents. — View Citation

Newberg LA, Milde JH, Michenfelder JD. The cerebral metabolic effects of isoflurane at and above concentrations that suppress cortical electrical activity. Anesthesiology. 1983 Jul;59(1):23-8. — View Citation

Reinstrup P, Ryding E, Algotsson L, Messeter K, Asgeirsson B, Uski T. Distribution of cerebral blood flow during anesthesia with isoflurane or halothane in humans. Anesthesiology. 1995 Feb;82(2):359-66. — View Citation

Sackey PV, Martling CR, Granath F, Radell PJ. Prolonged isoflurane sedation of intensive care unit patients with the Anesthetic Conserving Device. Crit Care Med. 2004 Nov;32(11):2241-6. — View Citation

Sackey PV, Martling CR, Nise G, Radell PJ. Ambient isoflurane pollution and isoflurane consumption during intensive care unit sedation with the Anesthetic Conserving Device. Crit Care Med. 2005 Mar;33(3):585-90. — View Citation

Zhao P, Peng L, Li L, Xu X, Zuo Z. Isoflurane preconditioning improves long-term neurologic outcome after hypoxic-ischemic brain injury in neonatal rats. Anesthesiology. 2007 Dec;107(6):963-70. — View Citation

Zhao P, Zuo Z. Isoflurane preconditioning induces neuroprotection that is inducible nitric oxide synthase-dependent in neonatal rats. Anesthesiology. 2004 Sep;101(3):695-703. — View Citation

Zheng S, Zuo Z. Isoflurane preconditioning induces neuroprotection against ischemia via activation of P38 mitogen-activated protein kinases. Mol Pharmacol. 2004 May;65(5):1172-80. — View Citation

* Note: There are 13 references in all — Click here to view all references

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Cerebral Blood Flow		after 2 hours of drug administration	No