Hemodynamic management and outcome of patients treated for cerebral vasospasm with intraarterial nicardipine and/or milrinone.
BACKGROUND
Vasospasm is a potentially devastating complication after aneurysmal subarachnoid hemorrhage. Although endovascular treatment with intraarterial nicardipine and milrinone is an accepted clinical treatment strategy, there is little information either on hemodynamic management during treatment or on outcome and consequences of the hemodynamic management. We tested 2 hypotheses: (1) intraarterial administration of nicardipine and milrinone to treat cerebral vasospasm would require increased administration of vasoconstrictor to support arterial blood pressure at target levels; and (2) high-dose vasopressors administered to increase blood pressure in these patients would lead to systemic acidosis and end-organ ischemic damage.


METHODS
We conducted a single-center, retrospective review of consecutive patients with clinically symptomatic vasospasm after aneurysmal subarachnoid hemorrhage that failed medical management with "triple H therapy" and subsequently received intraarterial nicardipine and/or milrinone between March 2005 and July 2007.


RESULTS
Of 160 endovascular interventions in 73 patients (aged 52 +/- 10 years; 50 women), 96 received only nicardipine, 5 only milrinone, and 59 both drugs. General anesthesia with muscle relaxation was performed for 93% of procedures. During treatment, both the number and dose of vasopressors required to maintain arterial blood pressure at target levels increased; the median dose of phenylephrine increased from 200 (n = 121) to 325 microg/min (n = 122), norepinephrine increased from 12 (n = 60) to 24.5 microg/min (n = 87), and vasopressin infusions increased from 7 to 24. Nonetheless, arterial blood pressure decreased 13% during treatment. In >90% of procedures, the postprocedure angiogram showed improved vessel caliber. A single patient demonstrated troponin T increase; no patients had a decrease in renal function, bowel or peripheral ischemia, systemic acidosis, or acute stroke. Overall mortality was 11%.


CONCLUSIONS
Intraarterial administration of nicardipine and/or milrinone requires use of vasopressors to maintain arterial blood pressure. Despite high doses of vasoconstrictors, treatment has low mortality, minimal end-organ ischemic damage or systemic acidosis, and results in improved caliber of cerebral vessels affected by vasospasm.
Schmidt
Ulrich
U
Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, MA 02114, USA.
Bittner
Edward
E
Pivi
Silvia
S
Marota
John J A
JJ
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001794:Blood Pressure / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000008:administration & dosage* / Q000009:adverse effects; D004359:Drug Therapy, Combination; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007261:Infusions, Intra-Arterial; D002532:Intracranial Aneurysm / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D020105:Milrinone / Q000008:administration & dosage* / Q000009:adverse effects; D009529:Nicardipine / Q000008:administration & dosage* / Q000009:adverse effects; D010726:Phosphodiesterase Inhibitors / Q000008:administration & dosage* / Q000009:adverse effects; D012189:Retrospective Studies; D013345:Subarachnoid Hemorrhage / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D013997:Time Factors; D016896:Treatment Outcome; D014662:Vasoconstrictor Agents / Q000627:therapeutic use; D014665:Vasodilator Agents / Q000008:administration & dosage* / Q000009:adverse effects; D020301:Vasospasm, Intracranial / Q000188:drug therapy* / Q000503:physiopathology
D002121:Calcium Channel Blockers; D010726:Phosphodiesterase Inhibitors; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009529:Nicardipine; D020105:Milrinone