Non-invasive Doppler ultrasonographic study of cerebral arteries [transcranial Doppler (TCD)] has been extensively applied on both outpatient and inpatient settings. It is performed placing a low-frequency (≤ 2 MHz) transducer on the scalp of the patient over specific acoustic windows, in order to visualize the intracranial arterial vessels and to evaluate the cerebral blood flow velocity and its alteration in many different conditions. Nowadays the most widespread indication for TCD in outpatient setting is the research of right to left shunting, responsable of so called "paradoxical embolism", most often due to patency of foramen ovale which is responsable of the majority of cryptogenic strokes occuring in patients younger than 55 years old. TCD also allows to classify the grade of severity of such shunts using the so called "microembolic signal grading score". In addition TCD has found many useful applications in neurocritical care practice. It is useful on both adults and children for day-to-day bedside assessment of critical conditions including vasospasm in subarachnoidal haemorrhage (caused by aneurysm rupture or traumatic injury), traumatic brain injury, brain stem death. It is used also to evaluate cerebral hemodynamic changes after stroke. It also allows to investigate cerebral pressure autoregulation and for the clinical evaluation of cerebral autoregulatory reserve.

Posttraumatic vasospasm (PTV) is a relatively common event following traumatic brain injury (TBI) that has been strongly correlated with worse neurological outcome in many studies. However, vasospasm continues to be an under-recognized source of secondary injury following TBI, and currently published guidelines do not address screening or management strategies for PTV. Brain tissue oxygen (P(bt)O(2)) monitoring probes allow for continuous screening for cerebral hypoxia following TBI, but their use as a monitor for PTV has not been previously described.

Case report and literature review.

We present a case of PTV identified by persistent low P(bt)O(2) despite aggressive medical therapy. Computed tomography and digital subtraction angiography confirmed severe cerebral arterial vasospasm involving both anterior and posterior circulations. The patient was successfully treated with serial intraarterial therapy including balloon angioplasty and verapamil infusion.

Posttraumatic vasospasm should be included in the differential diagnosis of cerebral hypoxia (e.g., low P(bt)O(2)) following TBI. Management strategies for PTV may include early, aggressive intraarterial therapies including drug infusion and balloon angioplasty.

The purpose of this prospective study was to evaluate the cumulative incidence, duration, and time course of cerebral vasospasm after traumatic brain injury (TBI) in a cohort of 299 patients.

Transcranial Doppler (TCD) ultrasonography studies of blood flow velocity in the middle cerebral and basilar arteries (VMCA and VBA, respectively) were performed at regular intervals during the first 2 weeks posttrauma in association with 133Xe cerebral blood flow (CBF) measurements. According to current definitions of vasospasm, five different criteria were used to classify the patients: A (VMCA > 120 cm/second); B (VMCA > 120 cm/second and a Lindegaard ratio [LR] > 3); C (spasm index [SI] in the anterior circulation > 3.4); D (VBA > 90 cm/second); and E (SI in the posterior circulation > 2.5). Criteria C and E were considered to represent hemodynamically significant vasospasm. Mixed-effects spline models were used to analyze the data of multiple measurements with an inconsistent sampling rate. Overall 45.2% of the patients demonstrated at least one criterion for vasospasm. The patients in whom vasospasm developed were significantly younger and had lower Glasgow Coma Scale scores on admission. The normalized cumulative incidences were 36.9 and 36.2% for patients with Criteria A and B, respectively. Hemodynamically significant vasospasm in the anterior circulation (Criterion C) was found in 44.6% of the patients, whereas vasospasm in the BA-Criterion D or E-was found in only 19 and 22.5% of the patients, respectively. The most common day of onset for Criteria A, B, D, and E was postinjury Day 2. The highest risk of developing hemodynamically significant vasospasm in the anterior circulation was found on Day 3. The daily prevalence of vasospasm in patients in the intensive care unit was 30% from postinjury Day 2 to Day 13. Vasospasm resolved after a duration of 5 days in 50% of the patients with Criterion A or B and after a period of 3.5 days in 50% of those patients with Criterion D or E. Hemodynamically significant vasospasm in the anterior circulation resolved after 2.5 days in 50% of the patients. The time course of that vasospasm was primarily determined by a decrease in CBF.

The incidence of vasospasm after TBI is similar to that following aneurysmal subarachnoid hemorrhage. Because vasospasm is a significant event in a high proportion of patients after severe head injury, close TCD and CBF monitoring is recommended for the treatment of such patients.

1) To know the transcranial Doppler (TCD) patterns in the early phase of the severe and moderate head injury and its prognostic implications. 2) To ascertain the TCD measurements concordance among different operators.

A prospective observational study in 275 consecutive intensive care unit patients with severe or moderate head injury was designed. Within 12 hrs. of the traumatic event a TCD study was done and a second one within the first 24 hrs. All patients were managed following a protocol made with the aim of promoting the early evacuation of the intracranial space occupying mass, preventing delayed brain damage and keeping the intracranial pressure (ICP) < 20 mm Hg and the cerebral perfusion pressure (CPP) > 60 mm Hg. The patient outcome was categorized with the Glasgow Outcome Score (GOS) at the discharge of the ICU. The mean velocity (MV) and the pulsatily index (PI) were measured in both middle cerebral arteries (MCA) and in the intracranial part of the internal carotid arteries in order to calculate the Lindegaard index. The presence of hypoperfusion, hyperaemia, vasospasm and cerebral circulatory arrest was registered. The presence of high intracranial pressure (HICP), the ICP peak and mode, the lowest CPP, the CPP mode, the minor medium arterial pressure (MAP) and the MAP mode were also recorded. A concordance analysis was made to ascertain the validity of the TCD data obtained by different operators.

The concordance analysis among observers showed a kappa index of 0.7863 (p < 0.0001). The median stay in ICU was 7 days (Q1-Q3 of 3-15 days). The intra-ICU mortality was 20.72% (57/275) and the 53.44% of patients (147/275) showed favourable outcome (GOS 4-5) at the discharge of the ICU. The initial TCD showed a MV decreased and a PI increased in the MCA. Eighty of the e 275 patients showed a normal haemodynamic pattern whereas the pattern was abnormal in the remaining 195, degrees the hypoperfusion pattern predominated overall (181/275, 61.87%). HIPO was registered in 123 patients (58.01) an not in 89 (41.99%). A statistic significant correlation was found between the HICP and the DTC data. The early hypoperfusion pattern was related with a higher incidence of HICP (p > 0.05). The decrease in the MV and the increase in the PI were significantly associated with a higher mortality and a worse functional outcome (except for the MV within the first day). The PI was high within the first 24 h in the group of patients who died but was normalised among the survivals group.

Early TCD detects a cerebral hypoperfusion status in the severe and moderate head injury that may imply therapeutic considerations. This hypoperfusion strongly correlates with the severity of the injury, the incidence of HICP and the functional outcome at the ICU discharge. In experienced hands, TCD measurements are reliable when done by different operators.

Cerebral blood flow velocities were measured in 50 severely head injured (Glasgow Coma Scale (GCS) 8 or less) patients using transcranial Doppler ultrasonography (TCD). Abnormally high TCD velocities were recorded in 35 patients; in 20 this was deemed to be due to vasospasm and in the other 15 to hyperemia. Patients who developed hyperemia also had the highest intracranial pressure (ICP) and the lowest cerebral perfusion pressure (CPP) of the three groups. Outcome was assessed at six months after injury using the Glasgow outcome scale and the disability rating scale. In the normal velocity group 87% of patients had a good outcome, compared with 47% of those with hyperemia and 40% of those with vasospasm. The highest velocity (HVEL), GCS, age, ICP and CPP were entered into a logistic regression analysis. HVEL, age and CPP were found to be the most significant predictors of outcome (chi 2 = 29.5; p < 0.0001). These factors predicted outcome with 82% accuracy, 86% sensitivity and 76% specificity. Routine monitoring of TCD velocity may be useful in detecting hyperemia and vasospasm after severe head injury, allowing appropriate treatment to be started as early as possible.