BACKGROUND AND PURPOSE: Papaverine is the primary intra-arterial (IA) treatment for vasospasm after aneurysmal subarachnoid hemorrhage (SAH); however, is it limited in effect and by adverse effects. We prospectively studied the use of IA nicardipine as a treatment for vasospasm. METHODS: Over 12 months, all patients with SAH who required interventional treatment for vasospasm were given IA nicardipine with or without angioplasty. Vasospasm was determined by serial clinical assessments and/or daily transcranial Doppler (TCD) imaging and confirmed by angiography. Doses of IA nicardipine per vessel were 0.5-6 mg. All patients were monitored for increased intracranial pressure (ICP) and change in cardiovascular or neurologic status. RESULTS: Forty-four vessels in 18 patients with vasospasm were treated with IA nicardipine alone. TCD data for 38 vessels (15 cases) were available. All vessels demonstrated immediate angiographic dilatation after IA nicardipine. No sustained cardiovascular changes were after treatment. ICP was transiently elevated in five patients and persistently elevated in one. Mean peak systolic velocities at TCD imaging were significantly reduced from pretreatment values in all treated vessels for 4 days after infusion (268.9 +/- 77.8 vs 197.6 +/- 74.1 cm/s, P <.001). Neurologic improvement after IA nicardipine occurred in eight (42.1%) patients. No clinical deterioration was noted. CONCLUSION: As shown by TCD imaging, IA nicardipine has an immediate and sustained effect on vasospasm. It does not appear to have sustained effect on ICP or cardiovascular status. This treatment warrants further study to determine its safety and efficacy.
BACKGROUND AND PURPOSE:Papaverine is the primary intra-arterial (IA) treatment for vasospasm after aneurysmal subarachnoid hemorrhage (SAH); however, is it limited in effect and by adverse effects. We prospectively studied the use of IA nicardipine as a treatment for vasospasm. METHODS: Over 12 months, all patients with SAH who required interventional treatment for vasospasm were given IA nicardipine with or without angioplasty. Vasospasm was determined by serial clinical assessments and/or daily transcranial Doppler (TCD) imaging and confirmed by angiography. Doses of IA nicardipine per vessel were 0.5-6 mg. All patients were monitored for increased intracranial pressure (ICP) and change in cardiovascular or neurologic status. RESULTS: Forty-four vessels in 18 patients with vasospasm were treated with IA nicardipine alone. TCD data for 38 vessels (15 cases) were available. All vessels demonstrated immediate angiographic dilatation after IA nicardipine. No sustained cardiovascular changes were after treatment. ICP was transiently elevated in five patients and persistently elevated in one. Mean peak systolic velocities at TCD imaging were significantly reduced from pretreatment values in all treated vessels for 4 days after infusion (268.9 +/- 77.8 vs 197.6 +/- 74.1 cm/s, P <.001). Neurologic improvement after IA nicardipine occurred in eight (42.1%) patients. No clinical deterioration was noted. CONCLUSION: As shown by TCD imaging, IA nicardipine has an immediate and sustained effect on vasospasm. It does not appear to have sustained effect on ICP or cardiovascular status. This treatment warrants further study to determine its safety and efficacy.
Authors: E S Flamm; H P Adams; D W Beck; R S Pinto; J R Marler; M D Walker; J C Godersky; C M Loftus; J Biller; D J Boarini Journal: J Neurosurg Date: 1988-03 Impact factor: 5.115
Authors: Michael F Stiefel; Alejandro M Spiotta; Joshua D Udoetuk; Eileen Maloney-Wilensky; John B Weigele; Robert W Hurst; Peter D LeRoux Journal: Neurocrit Care Date: 2006 Impact factor: 3.210
Authors: Khalid A Hanafy; R Morgan Stuart; Alexander G Khandji; E Sander Connolly; Neeraj Badjatia; Stephan A Mayer; Christian Schindler Journal: J Clin Neurosci Date: 2010-05-14 Impact factor: 1.961