Despite the advances in neurosurgical and -radiological techniques and intensive care, the mortality and morbidity rates in SAH have not changed in recent years. There is still only a limited understanding of the mechanisms of secondary insults causing brain injury after SAH, also called delayed cerebral ischemia (DCI). In this study, the investigators are exploring the use of quantifiable biomarkers from blood and continuous EEG monitoring as tools for the diagnostics of DCI. Additionally, the investigators are looking into other clinical variables (eg. pain, heart function) as factors of DCI.
Subarachnoidal hemorrhage (SAH) is a cause of long-term disability and death. Annually about 1000 people in Finland suffer from SAH, their average age being under 50 years. SAH has a mortality rate of 12 % acutely and 40 % of patients die within a month from admission to hospital. In addition, 30 % of the surviving patients remain with neurological deficits. Most survivors of the primary insult suffer from a secondary injury during the first 2-3 weeks from the insult. Despite the advances in neurosurgical and -radiological techniques and intensive care, the mortality and morbidity rates in SAH have not changed in recent years. There is still only a limited understanding of the mechanisms of secondary insults causing brain injury after SAH, also called delayed cerebral ischemia (DCI). In this study, the investigators are exploring the use of quantifiable biomarkers from blood and continuous EEG monitoring as tools for the diagnostics of DCI. Additionally, the investigators are looking into other clinical variables (eg. pain, heart function) as factors of DCI.
Study Type
OBSERVATIONAL
Enrollment
62
ROTEM measurements 24,48, 72, 120, 192 and 288 hours from aneurysmal SAH
Continuous EEG-monitoring after aneurysm treatment until patient transferred to ward or up to 14 days after aneurysmal SAH
to exclude asymptomatic deep venous thrombosis once over days 3 to 7
Tampere University Hospital
Tampere, Finland
Incidence of delayed cerebral ischemia
Incidence of DCI (delayed cerebral ischemia)
Time frame: 14 days
Maximal clot firmness of FIBTEM (FIBTEM-MCF) analysis
Maximal clot firmness of FIBTEM analysis (FIBTEM-MCF) using rotational thromboelastometry (ROTEM) assay
Time frame: at 72 hours
Incidence of deep venous thrombosis
Incidence of deep venous thrombosis
Time frame: Within 3-7 days
Other rotational thromboelastometry analysis
Maximal clot firmness of extrinsic (EXTEM) analysis (EXTEM-MCF) using rotational thromboelastometry
Time frame: from 24 to 288 hours
Assessment of neurological outcome
Description of the neurological outcome by using extended Glasgow Outcome Score 1. Death 2. Vegetative sate 3. Lower severe disability 4. Upper severe disability 5. Lower moderate disability 6. Upper moderate disability 7. Lower good recovery 8. Upper good recovery
Time frame: 90 days
Assessment of pain
Critical Care Pain Observation Tool values, from 0: no pain to 8: maximum pain
Time frame: Up to 14 days
Assessment of cardiopulmonary function by transthoracic echocardiography
Function of the left and right ventricle using scale 1. hyperkinetic,2. normal, 3. moderately impaired, 4. severely impaired
Time frame: At admission and at at 24±4 hours
Continuous electroencephalography
Continuous electroencephalography will be evaluated for signs that are potential surrogates of developing delayed cerebral ischemia (such as alpha-delta-ratio, focal slowing, epileptiform abnormalities, relative alpha variability)
Time frame: From 48 hours to 14 days
Neuroglial brain injury biomarkers
Peripheral blood biomarkers potentially reflecting neuroglial injury will be analysed with enzyme-linked immunosorbent assays
Time frame: From 24 to 288 hours
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