Introduction

Neurological complications have been a major concern throughout the history of cardiac surgery. Advances in technology and technique have led to open, less invasive or minimally invasive, and endovascular interventions to repair cardiac valvular, and vascular pathology. Coronary artery bypass grafting (CABG), surgical interventions for valve disease, thoracic aortic aneurysm, and surgical procedures for heart failure are now completed more safely than ever. Despite these advances, neurological complications, including ischemic stroke, delirium, and cognitive decline still occur frequently.

Neurologic complications are second only to heart failure as a cause of morbidity and mortality following cardiac surgery, and the presence of neurologic morbidity significantly increases the likelihood of requiring long-term care with a significant impact on the overall cost of medical care and decreased quality of life.[1],[2] These implications are expected to remain substantial, despite improving surgical and anesthetic techniques, because of the increasing risk profile of patients undergoing cardiac operations.

Most neurologic problems following cardiac surgery can be divided into 3 categories (Table1):

• Stroke
• Neuropsychiatric abnormalities, including postoperative cognitive dysfunction
• Peripheral neuropathies

In this chapter we will review the cerebral injury after cardiac surgery, including risk factors, mechanism of injury, clinical and radiological manifestations, and different neuroprotective strategies. Spinal cord ischemia and infarction associated with descending thoracic aorta and thoracoabdominal aorta aneurysm repair will be discussed in the chapters dedicated to the management of this complex aortic pathology.

There are a variety of manifestations of perioperative cerebral injury, including ischemic (or, less commonly, hemorrhagic) stroke that occurs in 1.5% to 5.2% of patients, encephalopathy affecting 8.4% to 32% of patients, and neurocognitive dysfunction affecting 20% to 30% of patients 1 month after their operation.[2],[3],[4],[5] There are variations among reported incidences, likely due to different patient populations (eg, patient age and risk status, types of procedures), diagnostic definitions, and the intensity of clinical surveillance. After a systematic neurological examination, stroke is defined as a motor-sensory deficit localized to a focal region of the brain, with or without decreased levels of consciousness, and encephalopathy as a decrease or fluctuation in the level of consciousness with cognitive deterioration, in the absence of focal motor deficits, after recovery from anesthesia. These definitions are adaptations of those accepted by The Society of Thoracic Surgeons.

Contemporary studies, using sensitive brain MRI with diffusion-weighted imaging, report that as many as 45% of patients who have undergone cardiac surgery have new silent ischemic brain lesions.[3],[6] Epidemiologic, clinical, and neuroimaging investigations continue to refine the understanding of postcardiac surgery cerebral injury. Historically, the use of cardiopulmonary bypass (CPB) has made cardiac surgery unique, and the working assumption has been that many of the adverse cognitive outcomes were simply related to its complex physiologic experience. However, multiple studies did not show significantly different cognitive outcomes for patients undergoing off-pump CABG compared with on-pump CABG.[7]

Although off-pump CABG removes the CPB-associated variables like extensive manipulation of the aorta with cannulation and clamping, as well as the inflammatory response, it introduces other factors that may be associated with neurologic injury, including the extensive cardiac manipulation required for coronary exposure with associated hemodynamic instability and hypoperfusion as well as the manipulation of the aorta for construction of proximal anastomosis.