In research articles, the term, postoperative cognitive dysfunction, or POCD, denotes postoperative memory and/or thinking problems that have been corroborated by neuropsychological testing. Although not yet a recognized diagnostic code in the International Classification of Diseases (ICD), clinicians are beginning to use the term POCD as a general description of postoperative patients who complain of memory and thinking problems. Typically,
these complaints include difficulty staying focused on a task, difficulty completing more than one task at the same time, problems finding words, and difficulty recalling information recently heard or read. Postoperative cognitive dysfunction should not be confused with delirium, which, in contrast to POCD, involves fluctuating orientation and confusion.

When POCD needs to be listed as a diagnosis, the Diagnostic and Statistical Manual‘s (DSM-IV)² definition of “Cognitive Disorder Not Otherwise Specified” (ICD Code Number: 296.5) may be appropriate. This requires the clinician to document cognitive changes that cannot be attributed to another etiology such as delirium, dementia, or cognitive dysfunction due to a specific cause.

As demonstrated by the examples in the preceding text, an individual of almost any age or education level can experience POCD. The symptoms also vary. Clinicians, therefore, need to remain attentive to all patients and listen carefully to their postoperative complaints.

A number of studies demonstrate that, at least during the first 3 postoperative months, elderly patients have higher rates of POCD than young and middle-aged adults. In large studies of patients undergoing noncardiac surgery, the prevalence of POCD among adults 60 years of age and older was between 20% and 30% at 1 week and 10% to 15% at 3 months.³,⁴ We know little about POCD occurring beyond 1 year. One study reports that only 1% of elderly adults experience the persistent effects of cognitive decline after surgery,⁵ which may indicate that POCD is reversible even among the elderly.

Apart from age, another strong risk factor for POCD appears to be years of formal education. A low educational level has been shown to predict cognitive decline, whereas high educational levels seem to protect against cognitive decline following surgical procedures involving cardiopulmonary bypass.⁶ One proposed rationale for this relationship involves the concept of cerebral cognitive reserve: Extensive education or high occupational attainment has been associated with the ability to recruit neuronal structures to replace damaged processing pathways.⁷ Other explanations for the relationship between POCD and educational level include test-taking skills, enhanced social support, and excellent postoperative medical care. Of course, there are always exceptions to these findings, as shown from the case descriptions at the beginning of this chapter, and therefore predicting who is at great risk for POCD will be at best tentative.

Surprisingly, as compared to age and level of education, comorbidity has been largely ignored in research. Intuitively, we would expect increased susceptibility to POCD in patients suffering debilitating conditions known to affect postoperative morbidity, such as high blood pressure, congestive heart failure, repeat coronary artery bypass grafting, anemia, carotid arteriosclerosis, diabetes, left ventricular ejection fraction lower than 45%, chronic pulmonary disease, and unstable angina—all conditions that have been shown to affect postoperative morbidity.

Importantly, both clinicians and researchers have a tendency to ignore the role of mental comorbidities (e.g., depression, presurgical cognitive impairment) as possible risk factors for postoperative complications. The importance of mental health influences is alluded to by a retrospective study by Berstein and Offenbartl.⁸ These authors report that out of 975 general surgery patients, 57 had postoperative fatal and nonfatal complications; most of those who had a fatal complication had symptoms of dementia before surgery (25 of 32 who died had dementia). These findings suggest that a patient with a presurgical mental disorder, specifically a dementia, may be particularly sensitive to surgical events.

As discussed in the preceding text, despite evidence pointing to population risk factors, predicting who is at risk for POCD remains problematic. Therefore, direct observations and documentation of patients’ cognitive abilities before surgery and again after surgery may be helpful.

To date, no research has directly examined which brain regions are most often associated with the primary symptoms of POCD (e.g., mild to moderate attention disturbance, word finding problems, difficulty learning new information). We can speculate, however, which anatomic zones may be most susceptible. We base this speculation not only on a general understanding of neuropsychology but also on recent research suggesting that there may be subtypes of POCD.¹⁸ Some patients experience primary disturbances in attention, whereas others experience only learning and memory difficulties.

Attention is an extremely complex function that is regulated by cortical gray matter regions, subcortical nuclei, and white matter tracts. The most vulnerable regions to surgical factors, however, are likely the subcortical gray matter nuclei (e.g., caudate, putamen, nucleus accumbens, globus pallidus, substantia nigra, subthalamic nucleus, thalamus) and white matter tracts (e.g., the internal and external capsules) because they are highly susceptible to numerous neurotransmitter and small vessel changes. The importance of the basal ganglia, in particular, on one’s ability to attend and inhibit distracting information has been demonstrated mostly by elegant animal studies¹⁹ and also by studies on neurodegenerative illnesses such as Parkinson disease.²⁰ Additionally, the thalamus is a primary subcortical structure necessary for both attention and memory. It is, unfortunately, also the most common site for ischemic changes and dysfunction, particularly among older adults.

The subcortical nuclei are in very close proximity to the intricate vessels of the Circle of Willis and smaller intracranial arterioles, such as the lenticulostriate arteries (see Fig. 27.4), which nourish important subcortical nuclei (e.g., caudate) and associated white matter tracts. Intracranial arterioles such as the lenticulostriate arteries are particularly vulnerable to hemodynamic changes.²¹ These changes may result in reduced arteriole wall integrity thereby leading to reduced nourishment or possible protein leakage into the white matter or gray nuclei. This would lead to the development of white matter changes (Fig. 27.2) and lacunae within the thalamus and basal ganglia.²¹ Such damage is hypothesized to result in a disconnection to the frontal lobe thereby leading to attention disturbances. This disconnection can be at least partially explained by neurotransmitter disruption, for the interplay between subcortical nuclei and white matter is largely regulated by inhibitory (GABAergic [γ-aminobutyric acid]) and excitatory (glutaminergic) neurotransmitters.¹⁹