Early transcranial Doppler after subarachnoid hemorrhage: clinical and radiological correlations

The initial decrease in the level of consciousness after subarachnoid hemorrhage (SAH) is commonly considered secondary to cerebral hypoperfusion and metabolic depression. Age, intracranial pressure, and the amount of cisternal blood are closely related to the clinical grade on admission after SAH. Transcranial Doppler (TCD) may partially and indirectly estimate cerebral blood flow through analysis of flow velocity in the middle cerebral artery (MCA). Besides, pulsatility index (PI) can also be considered an indirect estimator of cerebrovascular resistance. The objective of this study was to determine the TCD parameters in the early stage after SAH and to analyze their correlation with the main clinical and radiological variables on admission.

A series of 52 consecutive patients diagnosed with SAH, with an abnormal computed tomography (CT) scan on admission and a TCD performed in the first 24 hours from the onset of the hemorrhage, were retrospectively reviewed. Age, sex, clinical grade, presence of cisternal blood or hydrocephalus on initial CT scan, and parameters of TCD examination were recorded for every patient. The relationship between sonographic and clinical and radiological variables was evaluated by partial correlation test, Kruskal-Wallis, and Student t test for paired samples.

There were no significant differences in blood flow velocities or PIs between the left and right sides. Lower velocities and higher PIs correlated with a worse clinical condition at admission. Lower velocities also correlated with larger amounts of cisternal blood on the initial CT scan. No significant correlation was observed between PI and the amount of blood in the initial CT scan.

A global decrease in blood velocity in the MCA along with a rise in PI is present in the first 24 hours after SAH. These changes correlate with the clinical deterioration and partially with the amount of blood in the initial CT scan. These findings support the hypothesis that low cerebral perfusion caused by high intracranial pressure leads to diffuse ischemic changes in the early phase of SAH.