Neurologic injuries are frequent and devastating complications following cardiac surgery. Previous work conducted by our research group and others has identified the principal mechanisms creating both overt and subtle neurologic injuries after cardiac surgery. Current work by our group has identified that the causes (thrombotic/lipid emboli, cerebral hypoperfusion \& hypotension, and gaseous emboli) of these injuries are byproducts of processes of surgical and perfusion care. This insight suggests that the redesign of clinical strategies and techniques to prevent the occurrence of these intraoperative sources of damage may provide an opportunity to reduce the risk of neurologic injury after cardiac surgery. The goal of this research is to identify modifiable clinical strategies and techniques of surgical and perfusion care associated with the causes (thrombotic/lipid emboli, cerebral hypoperfusion \& hypotension, and gaseous emboli) of neurologic injury secondary to coronary artery bypass graft (CABG) surgery, and subsequently to redesign these processes to reduce a patient's risk of a neurologic injury.
The goal of this research is to identify modifiable clinical strategies and techniques of surgical and perfusion care associated with the causes (thrombotic/lipid emboli, cerebral hypoperfusion \& hypotension, and gaseous emboli) of neurologic injury secondary to coronary artery bypass graft (CABG) surgery, and subsequently to redesign these processes to reduce a patient's risk of a neurologic injury. The following hypotheses will be addressed. Hypothesis #1a. Identifying alternative strategies for conducting processes of surgical and perfusion care will reveal opportunities to reduce the occurrence of causes of neurologic injury. The most common mechanisms creating neurologic injury, whether focal or global, after CABG surgery are thrombotic/lipid emboli, cerebral hypoperfusion \& hypotension, and gaseous emboli. Processes of surgical and perfusion care are associated with the creation of each of these causes of neurologic injury. Hypothesis #1b. Redesigning processes of surgical and perfusion care to reduce thrombotic/lipid emboli, cerebral hypoperfusion \& hypotension, and gaseous emboli during CABG surgery will result in reductions of tissue-level and neurologic injury. We will analyze sera for tissue-level brain injury as well as identify any new neurologic injuries present among patients undergoing CABG surgery. Redesigning CABG surgery to reduce thrombotic/lipid emboli, cerebral hypoperfusion \& hypotension, and gaseous emboli will result in decreases in tissue-level and neurologic injury. Hypothesis #2. A regional quality improvement intervention will result in changes to surgical and perfusion techniques. Regional dissemination of the findings from Hypotheses #1a,b may be realized through focused quality improvement initiatives utilizing multidisciplinary clinical teams.
Study Type
OBSERVATIONAL
Enrollment
469
determine the effectiveness of adopting quality improvement strategies to reduce embolization, hypotension and cerebral desaturation
Maine Medical Center
Portland, Maine, United States
Dartmouth-Hitchcock Medical Center
Lebanon, New Hampshire, United States
Catholic Medical Center
Manchester, New Hampshire, United States
Emboli and Hypoperfusion Counts
We will count the number of thrombotic/lipid emboli and number of gaseous emboli. Along with the number of hypotensive events. We will link counts to surgical and perfusion techniques.
Time frame: within the operative time period
Type I and II neurologic injuries
We will measure a patient's neurologic status Using a Telephone Interview for Cognitive Status tool at 3 time periods (prior to surgery, prior to discharge and at 3 months)
Time frame: within 3 months after surgery
Tissue-level neurologic injury
Blood for serum markers will be collected after surgery. We will assess plasma levels of biochemical markers of neurology injury.
Time frame: within 48 hrs of surgery
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