How common are neuropsychological complications after cardiopulmonary bypass (CPB)? How predictable and severe are they?

Neuropsychological complications have been found to occur in a proportion of patients following CPB. These problems reveal themselves as impaired cognitive function, i.e. difficulties with memory, attention, concentration, and speed of motor and mental response. However, the reported frequency with which these problems occur varies considerably. Studies assessing patients 5–10 days postoperatively have suggested an incidence of neuropsychological deficits ranging from 12.5 to 90%. Later assessments, at about 2 to 6 months after surgery, have indicated deficits in 12 to 37% of patients studied.

How predictable are they?
The variation in reported incidence has been ascribed to several factors such as number, type, sensitivity, and timing of neuropsychological tests used, as well as the definition of neuropsychological deficit and the method of statistical analysis employed. These methodological issues have been addressed at international consensus conferences in 1994 and 1997. Patient related variables such as age and disease severity have also been associated with cognitive decline post-cardiac surgery. Therefore centres employing different criteria for surgery may report differing rates of deficit.

Deficits detected within a few days of surgery are also problematic in that they are often transient in nature. These assessments appear to be contaminated by postoperative readjustment and anaesthetic residue as well as genuine neuropsychological difficulties. Long term deficits (over 6 weeks) are considered to be more stable and to reflect a more persistent neuropsychological problem.

How severe are they?
Given that these problems reflect a decline in performance of approximately 20–25% from that prior to surgery, they can be considered severe. What is more difficult is how they translate into the patient’s everyday life. This is dependent upon the nature of their activities. A cardiac surgeon who suffered a 20% decline in their fine motor movements would undoubtedly have a severe disability. In contrast a road sweeper would not suffer unduly, at least in their work. The tests customarily performed in this area are most useful as a window onto surgery rather than showing an impact on quality of life.

Can they be prevented?
The mechanisms for neuropsychological decline are considered to be multifactorial. The most popular explanation for cognitive dysfunction is microemboli delivered to the brain during surgery. These can be either air or particulate (atheromatous matter, fat, platelet aggregates, etc.) in nature. In an attempt to reduce the incidence of neuropsychological decline various interventional studies have been designed. Much of this work has centred on the impact of different equipment and techniques used in surgery on neuropsychological outcome. Early studies comparing bubble and membrane oxygenators indicated a higher frequency of microemboli detected when using bubble oxygenators with decreased neuropsychological deficits occurring in the membrane group. Studies have also found that the introduction of an arterial line filter into the CPB circuit significantly reduces the number of microemboli detected at the middle cerebral artery during CABG.

A significant reduction in neuropsychological deficits in the filter group has also been reported. In contrast a study comparing pulsatile and non-pulsatile flow found no difference in neuropsychological outcome between the two techniques. As the use of hypothermic perfusion during CPB has been based on the protective effects of low temperature in limiting the effects of cerebral ischaemia it is surprising that studies so far have failed to find any advantage for hypothermic bypass on neuropsychological outcome. Two studies have examined the impact of pH management on cognitive performance and both have reported benefit from using the alpha stat technique. Less disruption to autoregulation has also been reported in the alpha stat group.

More recently pharmacological neuroprotection has been attempted in these patients with a variety of compounds. Most of these studies have been underpowered and only one appears to have produced some suggestion of neuroprotection.