![]() In daily practice, we perform serial TCD examinations (one to two/day) in all SAH patients, together with close neurological clinical monitoring we use TCD for the assessment of all main intracranial vessels and, using TCCD, investigate different segments of such vessels, as vasospasm could be extremely localized. Indeed, we evaluate the constriction of the cerebral vessels that is associated with a progressive increase of mean FV. ![]() Although angiography remains the gold standard, we use TCD daily to assess vasospasm, to guide additional investigations, and to monitor the clinical treatment. However, this method requires a specific software and a higher competency to interpret the data to improve patients’ management.ĭetection of cerebral vasospasm following aneurysmal subarachnoid hemorrhage (SAH) is crucial as this is one of the main determinants of delayed cerebral ischemia and poor neurological outcome in this setting. Clinicians have to consider that the monitoring of dynamic autoregulation, using the mean flow index (Mx), which is calculated as the correlation coefficient indices between FV and CPP during spontaneous fluctuations in blood pressure, would be more accurate to assess CA. The most simple methods to assess CA at the bedside are (a) the static autoregulatory index, which is obtained by calculating the percentage of changes in cerebrovascular resistance (CVR = mean arterial pressure/mean FV) after changes in arterial blood pressure, or (b) the transient hyperemic response test (if there are no risks of embolism or hemodynamic instability), which is obtained by compressing the carotid artery and calculating the percentage of change in systolic FV from the baseline (an increase ≥ 10% is considered as intact CA). In case of impaired CA, we use TCD to target blood pressure to a level corresponding to the patient’s individual optimal autoregulatory status. We assess cerebral autoregulation (CA) at the bedside as altered CA is related with a poor outcome in many diseases and may increase the risk of cerebral damage. ![]() Finally, we perform repeated TCD assessment rather than a single examination (i.e., every 1–2 h) to better understand the changes in the brain hemodynamics following an increase in ICP or after specific ICP-directed therapies. ![]() Moreover, we also estimate ICP using formulas combining FV and blood pressure, but only as “confirmatory” findings before additional validation of their accuracy will be available. As such, after having considered these conditions, we use the combination of elevated PI and low diastolic FV (< 20 cm/s) to suggest elevated ICP at the bedside. We do not rely on only PI (i.e., PI > 1.4), because other conditions (Additional file 1: Table S1) could affect this parameter. However, when indications are unclear or invasive methods are not available (i.e., low-income countries) or contraindicated (i.e., severe coagulopathy), we use TCD as a “triage” tool to non-invasively discriminate patients who are at risk of developing intracranial hypertension. When the indications for invasive intracranial pressure (ICP) monitoring are met, we recommend intraparenchymal or intraventricular probes, as TCD cannot substitute invasive ICP measurement.
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