Abstract
Biomarkers for the prediction of vasospasm and delayed cerebral ischemia in patients with a ruptured cerebral aneurysm could be helpful.In this prospective clinical study, endothelin-1, lactate, pCO2, and pO2 were measured in arterial and internal jugular vein blood before, during and after surgical treatment of a cerebral aneurysm, and were tested as potential predictors of neurologic outcome in patients.Forty-one patients were enrolled in the study, 23 of them were operated on after aneurismal rupture with development of subarachnoid hemorrhage (SAH) and 18 patients were operated on for a nonruptured aneurysm.All of the involved patients survived. There was no difference in neurologic outcome between those operated on with a ruptured or nonruptured aneurysm.Endothelin-1 and lactate concentrations as well as pO2 and pCO2 from arterial and venous blood samples and their venoarterial difference did not differ between groups with and without an aneurismal rupture. Venoarterial difference of endothelin-1 concentrations on the day after surgery significantly differed between the groups with favorable and nonfavorable neurologic outcome. Other variables did not show a statistically significant difference.Significant correlation was found between endothelin-1 and lactate concentrations, suggesting involvement of the same pathophysiological process.Another interesting finding was lower arterial and venous pCO2 in patients with lower initial Glasgow Coma Scale (GCS) score and higher Hunt Hess score in the phase after extubation.We can conclude that the measured biochemical parameters did not show sufficient predictive power to be useful for prediction of cerebral vasospasm and neurologic outcome in everyday clinical practice. However, some correlations that do exist between them suggest involvement of the same pathophysiological process.
Highlights
Subarachnoid hemorrhage (SAH) is a dramatic event with a rapid rise in intracranial pressure
Incidence of SAH is 7-13/100000 of population per year. [1,2,3,4,5] Incidence of cerebral aneurysm is around 1.8 to 2 %. [6,7,8] Mortality from a ruptured cerebral aneurysm and development of SAH is rather high, around 50%. [9] Approximately 10% of patients die before reaching hospital, 25 % die in the first 24 hours, and another 25% die in the first month after rupture, usually due to recurrent bleeding
It is difficult to estimate the real incidence of cerebral vasospasm due to lack of a uniform definition, adequate diagnostic method and clear understanding of the pathophysiologic mechanism of spasm of cerebral arteries and changes in the microcirculation
Summary
Subarachnoid hemorrhage (SAH) is a dramatic event with a rapid rise in intracranial pressure. [6,7,8] Mortality from a ruptured cerebral aneurysm and development of SAH is rather high, around 50%. [9] Approximately 10% of patients die before reaching hospital, 25 % die in the first 24 hours, and another 25% die in the first month after rupture, usually due to recurrent bleeding. [11,12] The majority (73%) of recurrent bleeding occurs in the first 3 days after rupture. Patients with SAH can develop delayed cerebral ischemia. It is explained mainly by the development of cerebral vasospasm. Clinical manifestations of these events are impaired consciousness and focal neurologic deficits
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