Therapeutic Hypercapnia After Aneurysmal Subarachnoid Hemorrhage - Optimum Duration of Hypercapnia
- Conditions
- Vasospasm Intracranial
- Interventions
- Procedure: Temporary hypercapnia
- Registration Number
- NCT04687605
- Lead Sponsor
- University of Wuerzburg
- Brief Summary
Temporary hypercapnia leads to a reproducible increase of cerebral blood flow (CBF) and brain tissue oxygenation (StiO2) as shown in a previous study (Trial-Identification: NCT01799525). The aim of this study now was to measure the course of carbon dioxide partial pressure (pCO2) reactivity after prolonged hypercapnia, and to evaluate the therapeutic effect of graded hypercapnia.
- Detailed Description
Cerebral vasospasm still is the leading cause of delayed cerebral ischemia (DCI) and secondary ischemic deficits after aneurysmal subarachnoid hemorrhage (SAH). Hypercapnia leads to a reproducible increase of cerebral blood flow (CBF) and brain tissue oxygenation (StiO2) as shown in a previous study (Trial-Identification: NCT01799525). Furthermore, the increase of CBF and StiO2 sustained after normalization of ventilation and no rebound effect was found. So, a possible optimization of the hypercapnic period may lead to prolonged effects of increased CBF and StiO2. Aim of this stuy is to find the ideal duration of hypercapnia and to evaluate the therapeutic effect of graded hypercapnia. For this, intubated and mechanically ventilated patients with an aneurysmal SAH Hunt/Hess 3-5, Fisher grade 2-4 on the initial CT scan and supplied with an external ventricular drainage will be included within the first 96 hours after ictus. Between day 4 and 14 they undergo a trial intervention in which the respiratory minute volume will be reduced in order to maintain a target PaCO2 of 50 - 55 mmHg for 2 hours. Arterial blood gas analysis (ABG) and transcranial Doppler sonography (TCD) is performed in 15-minute intervals. Intracranial pressure (ICP), cerebral perfusion pressure (CPP), and cardiovascular parameters are monitored continuously, serial measurement of CBF and StiO2 under continous hypercapnia is performed. Primary endpoint of this trial is change of CBF under hypercapnia, secondary endpoints are StiO2, measures non-invasively with near-infrared spectroscopy, mean flow velocity of intracranial vessels in TCD, delayed cerebral infarction in cranial CT and Glasgow Outcome Score (GOS) after 6 months.
Recruitment & Eligibility
- Status
- COMPLETED
- Sex
- All
- Target Recruitment
- 12
- Aneurysmal SAH
- Aneurysm occluded by clipping/coiling within 96 hours
- Hunt/Hess 3-5
- Fisher 2-4 on initial CT scan
- Intubated, sedated and mechanically ventilated patient
- Continous drainage of cerebrospinal fluid (CSF)
- Age under 18 years
- Pregnancy
- Common obstructive lung disease (COLD)
- potential of hydrogen (pH) in ABG < 7,25
- ICP > 20 mmHg
Study & Design
- Study Type
- INTERVENTIONAL
- Study Design
- SINGLE_GROUP
- Arm && Interventions
Group Intervention Description Optimum duration of hypercapnia Temporary hypercapnia Daily serial measurement of 2 hours under target hypercapnia of pCO2 50 - 55 mmHg by changes of respirator settings once per day
- Primary Outcome Measures
Name Time Method Cerebral blood flow (CBF) 2-4 hours, day 4-14 after SAH Changes of CBF (absolute, ml/100g tissue/min) under changes of arterial pCO2
- Secondary Outcome Measures
Name Time Method Cerebral tissue oxygen saturation 2-4 hours, day 4-14 after SAH Changes of tissue oxygen saturation measured by near-infrared spectroscopy (NIRS)
Glasgow Outcome Score (GOS) up to 6 months Glasgow Outcome Score (GOS 1 - 5, GOS 1 = Death, GOS 5 = none or low disability) after 14 days, after discharge and 6 months