When temporary arterial occlusion of the parent artery is difficult for anatomical reasons, or when inadvertent aneurysmal rupture occurs during surgical dissection, adenosine administration can be used to produce flow arrest and brief, profound systemic hypotension that can facilitate intracranial aneurysm clip ligation. There is a concern, however, that the flow arrest and profound hypotension produced by adenosine, although brief, may cause cerebral ischemia and therefore worsen neurologic outcome compared with other techniques to facilitate aneurysm clip ligation. Therefore, we performed a retrospective, case-control study to determine whether adenosine-induced flow arrest had negative effects on the neurologic outcome of our patients.
We reviewed the perioperative records of all patients in our intracranial aneurysm surgery outcomes database between August 1, 2006, and June 15, 2012. The primary outcome was the presence or absence of a poor neurologic outcome 48 hours after surgery, with a modified Rankin scale score >2 being defined as a poor neurologic outcome. The neurologic outcome at the time of hospital discharge was a secondary outcome. Secondary outcomes related to cardiac morbidity included atrial or ventricular arrhythmia requiring treatment and elevated cardiac biomarkers consistent with ischemia (i.e., Troponin-I).
During the study period, adenosine-induced flow arrest was used in 72 of the 413 patients (17.4%) who underwent intracranial aneurysm clip ligation. The difference in the incidence of poor neurological outcome, with or without the use of adenosine, was no larger than 15.7% at 48 hours after surgery (P =0.524) or −12.7% at discharge (P = 0.741). In addition, the difference in the incidence of cardiac morbidity was no larger than −16.0% for persistent arrhythmia (P = 0.155) or −9.4% for biomarkers of myocardial ischemia (P = 0.898) in the initial 48 hours after surgery.
When used to facilitate intracranial aneurysm clip ligation, adenosine-induced flow arrest was associated with no more than a 15.7% increase or a 12.7% decrease in the incidence of a poor neurologic outcome at either 48 hours or at the time of hospital discharge. In addition, adenosine use was not associated with cardiac morbidity in the perioperative period (i.e., persistent arrhythmia or biomarkers of cardiac ischemia).
From the Department of Anesthesiology and Neurological Surgery, Northwestern University Feinberg School of Medicine, Chicago, Illinois.
Accepted for publication June 25, 2013.
Carine Zeeni, MD, is currently affiliated with Department of Anesthesiology, American University of Beirut, Beirut, Lebanon; Mark S. DeWood, BS, is currently affiliated with Department of Anesthesiology, University of Cincinnati College of Medicine, Cincinnati, Ohio; and Vijay K. Ramaiah, MBBS, MD, is currently affiliated with Department of Anesthesia, Stanford University School of Medicine, California.
Funding: Departmental support (Anesthesiology & Neurologic Surgery).
Edina S. Kim, MD, is currently affiliated with the University of Illinois, Chicago, IL.
The authors declare no conflicts of interest.
This report was previously presented, in part, at the SNACC & ASA 2012.
Reprints will not be available from the authors.
Address correspondence to Dhanesh K. Gupta, MD, Department of Anesthesiology and Neurological Surgery, Northwestern University Feinberg School of Medicine, Ward Memorial Building #13-179 303 East Chicago Ave., Chicago, IL 60611. Address e-mail to email@example.com.