Anesth Analg 2006;103:1618-1620
© 2006 International Anesthesia Research Society
doi: 10.1213/01.ane.0000246399.10396.15
LETTER TO THE EDITOR
Editor-in-Chief Steven L. Shafer
Using Dexmedetomidine to Manage Patients with Cocaine and Opioid Withdrawal, Who Are Undergoing Cerebral Angioplasty for Cerebral Vasospasm
Ehab Farag, MD, FRCA,
Ali Chahlavi, MD,
Maged Argalious, MD,
Zeyd Ebrahim, MD,
Robert Hill, MD,
Demetrios Bourdakos, MD, and
Henry Woo, MD
Departments of General Anesthesiology and Outcomes Research; Cleveland Clinic Lerner College of Medicine of Case Western Reserve University; farage{at}ccf.org (Farag)
Department of Neurological Surgery (Chahlavi)
Department of General Anesthesiology; Cleveland Clinic Lerner College of Medicine of Case Western Reserve University (Argalious)
Department of General Anesthesiology (Ebrahim)
Division of Anesthesiology, Critical Care Medicine and Comprehensive Pain Management (Hill)
Department of General Anesthesiology (Bourdakos)
Sections of Endovascular and Cerebrovascular Neurosurgery; Cleveland Clinic; Cleveland, Ohio (Woo)
To the Editor:
A 45-yr-old woman with a history of hypertension and addiction to alcohol, heroin, and cocaine presented with severe headache. Using a computed tomography scan, we diagnosed subarachnoid hemorrhage (Fig. 1), which was emergently treated with coiling of a 4-mm aneurysm of the anterior communicating artery. Postoperatively the patient received hypervolemic therapy and nimodipine 60 mg every 6 h to prevent cerebral vasospasm.

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Figure 1. Preangioplasty. (A) Right AP internal carotid infection and (B) right vertebral artery injection demonstrating vasospasm in multiple vessels of anterior and posterior circulations.
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On the 10th day after coiling, the patients neurologic status abruptly deteriorated. Using transcranial Doppler, we diagnosed her with severe vasospasm in multiple cerebral vessels. She concurrently developed pulmonary edema with increasing pulmonary artery occlusion pressure to 29 mm Hg. Her heart rate increased to 130 bpm, and her arterial blood pressure increased to 230/120 mm Hg. We diagnosed the patient as having withdrawal syndrome from her multiple addictions. However, her declining neurological status required emergent cerebral angioplasty.
Before the procedure we tried to stabilize her condition with diuretics and vasodilators, with no response. We then used a remifentanil infusion to offset possible opioid withdrawal, again with no response. We started a dexmedetomidine infusion by giving 1 µg/kg over 10 min, followed by an infusion titrated dose to maintain systolic blood pressure <160 mm Hg. Her heart rate decreased to 6070 bpm, and her pulmonary arterial pressure decreased from 60/45 to 42/30 mm Hg. The patient tolerated the emergent cerebral angioplasty well (Fig. 2). Postoperative echocardiogram showed an ejection fraction of 70% and normal ventricular function.

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Figure 2. Postangioplasty. (A) Right AP internal carotid injection and (B) right vertebral artery injection demonstrating patent vessels and no evidence of vasospasm.
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The hypertension and cardiac failure in our patient likely resulted from a complex interplay of her substance addiction, subarachnoid hemorrhage, and hypervolemic therapy. Dexmedetomidine is a selective 2 agonist that has been used to manage withdrawal symptoms in the intensive care unit (1). Dexmedetomidine has unique neuroprotective and cardioprotective effects (2,3). It also decreases platelet aggregation by stimulating its 2 receptors to release nitric oxide, a potent inhibitor of platelet aggregation, an effect that may be beneficial for improving cerebral perfusion in the presence of cerebral vasospasm (4). Dexmedetomidine appears to have utility for managing withdrawal symptoms in patients with subarachnoid hemorrhage and cerebral vasospasm.
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