الفهرس 
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Abstract
Traumatic brain injuries (TBI) are common and have continued to be increasingly diagnosed over the last several years. TBIs vary in range, anatomical location, and severity and can result in significant short-term and long-term disability. Cerebral vasospasm is a common complication of SAH that develops as a sequel to the hemorrhage and is one of the major contributors to mortality [3]. Traumatic SAH is common in 41%–55% of patients after moderate or severe traumatic brain injury.
Calcium antagonists such as nimodipine is a dihydropyridine agent that blocks voltage-gated calcium channels and has a dilatory effect on arterial smooth muscle. It is the only FDA-approved agent for vasospasm, with a half-life of about nine hours [7]. Its beneficial effect on CVS derives most likely from its neuroprotective properties compared to arterial smooth muscle cell relaxation[8]. Nimodipine may achieve favorable results in angiographic response, clinical outcomes, and low complication rates. In addition, nimodipine may reduce the risk of secondary cerebral ischemia after an aneurysmal hemorrhage[9].
The stellate ganglion (SG) belongs to the sympathetic ganglion, formed by a fusion of the inferior cervical and first thoracic sympathetic ganglia. It can modulate the immune response, diminish inflammation, and improve cerebral perfusion [10]. Many studies have tried stellate ganglion block (SGB) in SAH patients with diagnosed CVS and observed beneficial outcomes [11, 12].
It was suggested that cervical sympathetic block might benefit patients with subarachnoid hemorrhage and that SGB may have therapeutic value in relieving cerebral vasospasm in certain neurological conditions.
Patient and method:
This prospective, randomized, double-blind comparative study. This study was conducted in the Assiut University Trauma Center according to following inclusion criteria: Age: 16-70 y, ASA: I, II, hemodynamically stable patient, SAH diagnosed by CT brain. Excluded from the study patients with: Penetrating head trauma ,any coagulation disorder.
A computer-generated randomization technique was used to randomly allocate 40 patients into two groups: group (1): 20 patients had taken stellate ganglion block 10 ml bupivacaine 0.5% and nimodipine 60 mg every four hours; group (2): 20 had taken nimodipine 60 mg every four hour.
All patients treated in the ICU with a standard protocol that included intensive care monitoring, normotension, fluid therapy to maintain normovolemia (positive fluid balance >500 ml/day), and spontaneous hemodilution to maintain a hematocrit of 30 ± 5%. Normothermia (35.5°C-36.5°C) maintained during the study period, and a Five-lead electrocardiogram, non-invasive arterial blood pressure, and arterial oxygen saturation monitored continuously for 24 hours. The severity of the trauma evaluated by determining the GCS score on admission, after resuscitation measures, and then was categorized as mild (13 to 15), moderate (9 to 12), and severe (less than 9)
We gave stellate ganglion block 4 hours after giving nimodipine by Ultrasound-guided C6 transverse approach. The patient was supine with the neck slightly extended and the head slightly rotated contralaterally to the approached side. The site was cleaned and draped, and the transducer was placed perpendicular to the tracheal axis at the cricoid cartilage and was moved inferiorly until the superior aspect of the thyroid gland was visualized. Later, the transducer should be relocated laterally to visualize the anterior aspect of the Chassaignac’s tubercle on the C6 transverse process
After giving block or giving nimodipine orally or by ryle. We isonated middle cerebral artery (MCA) on both sides through the temporal acoustic window using two 2 MHz transcranial Doppler ultrasound probes with separate TCD machines. The TCD probes fixed at a constant angle using a headband, and a stable continuous tracing of waveform of blood flow velocities in vessels would established. Vessels identified and confirmed using standard criteria.
We gave stellate block day by day and assess GCS day by day. Baseline observations including hemodynamic parameters (heart rate, mean blood pressure), and TCD values [peak, mean, diastolic blood flow velocity, pulsatility index (PI)] in MCA both sides recorded. Vasospasm in the MCA was defined by mean flow velocity (FV) of more than 120 cm/sec.
Baseline hemodynamic assessed at admission 12h and 24 h and TCD parameters assessed at admission 10 min, 30 min, 2h, 12h and 24 hours. Simultaneously neurological status assessed. Sedative medications avoided during the study period. A hematocrit of 30 ± 5% and temperature (35.5°C–36.5°C) maintained throughout the study period.