Postperfusion syndrome

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Overview
Postperfusion syndrome, also known as pump head, is a constellation of neurocognitive impairments attributed to cardiopulmonary bypass (CPB) during cardiac surgery. Symptoms of postperfusion syndrome are subtle and include defects associated with attention, concentration, short term memory, fine motor function, and speed of mental and motor responses. Studies have shown a high incidence of neurocognitive deficit soon after surgery, but the deficits are transient with no permanent neurological impairment.

Evidence for postperfusion syndrome
A study by Newman et al. at Duke University Medical Center published in the New England Journal of Medicine (NEJM), showed an increased incidence of cognitive decline after coronary artery bypass surgery (CABG); both immediately (53 percent at discharge from hospital) and over time (36 percent six weeks, 24 percent at six months, and 42 percent at five years). This study shows an association of neurocognitive decline with CABG, but does not show causation; the study lacks a control group and is considered level II-3 evidence.

Subsequent studies have compared "on-pump" CABG with off-pump coronary artery bypass (OPCAB) - essentially establishing controls to compare of the incidence of neurocognitive decline in CABG with and without the use of CPB. A small study (60 patients total, 30 in each treatment arm) by Zamvar et al. demonstrated neurocognitive impairment at both 1 week and 10 weeks postoperatively. A larger study (281 patients total) by Van Dijk et al. showed CABG surgery without cardiopulmonary bypass improved cognitive outcomes 3 months after the procedure, but the effects were limited and became negligible at 12 months. Furthermore, the Van Dijk study showed no difference between the on-pump and off-pump groups in quality of life, stroke rate, or all-cause mortality at 3 and 12 months. More recently OPCAB has been proposed to be beneficial in patients at high-risk of neurological injury; a study by Jenson et. al published in Circulation found no significant difference in the incidence of cognitive dysfunction 3 months after either OPCAB or conventional on-pump CABG.

Given the above evidence, there is high incidence of neurocognitive deficit post bypass surgery, but the deficits are transient with no permanent neurological impairment. Controlled "on-pump" versus "off-pump" cardiac surgery has only been studied in the setting of CABG and is not necessarily generalizable to other types of cardiac surgery. Recent advancements in transcatheter and percutaneous valve replacement may soon allow comparison of other types of cardiac surgery with and without CPB.

Neurocognitive deficit as a consequence of vascular disease
A study by McKhann et al. compared the neurocognitive outcome of people with coronary artery disease (CAD) to heart-healthy controls (people with no cardiac risk factors). People with CAD were subdivided into treatment with CABG, OPCAB and non-surgical medical management. The three groups with CAD all performed significantly lower at baseline than the heart-healthy controls. All groups improved by 3 months, and there were minimal intrasubject changes from 3 to 12 months. No consistent difference between the CABG and off-pump patients was observed. The authors concluded patients with long-standing coronary artery disease have some degree of cognitive dysfunction secondary to cerebrovascular disease before surgery; there is no evidence the cognitive test performance of bypass surgery patients differed from similar control groups with coronary artery disease over a 12 month follow-up period. A related study by Selnes et al. concluded patients with coronary artery bypass grafting did not differ from a comparable nonsurgical control group with coronary artery disease 1 or 3 years after baseline examination. This finding suggests that late cognitive decline after coronary artery bypass grafting previously reported by Newman et al. may not be specific to the use of cardiopulmonary bypass, but may also occur in patients with similar risk factors for cardiovascular and cerebrovascular disease.

Proposed mechanism of injury
Physicians have theorized that the syndrome is caused by tiny debris and air bubbles (microemboli) that enter the brain via cardiopulmonary bypass. Surgeons attempt to minimize time spent on bypass to decrease postoperative deficits; studies have shown increased bypass time is associated with increased incidence and severity of postperfusion syndrome and mortality.