Neurological complications rank as the second cause of morbidity and mortality post-cardiac surgery, after heart failure. These complications can be classified into three categories: cerebrovascular complications, encephalopathy, and peripheral nervous system disorders. Encephalopathy includes conditions such as coma, delirium, seizures, and neuro-cognitive decline (NCD).
Today’s article provides an updated review on the prevalence of NCD, its pathophysiological mechanisms, and potential treatment strategies. This topic is particularly relevant as the persistence of these neurological sequelae causes a significant impact on both the quantity and quality of life.
COMMENTARY:
NCD following cardiac surgery encompasses impairments in memory, executive, motor, and attentional functions, among others. Depending on the adopted definition and diagnostic measures used, this complication can be detected in 3% to 79% of patients in the immediate postoperative period. Given the highly variable nature of this complication, which has proven to be significantly prevalent in various studies, it is essential to explore the potential long-term implications on the quality of life for our patients.
One of the primary limitations in diagnosing NCD lies within its own definition. Broadly, it is the loss of neurocognitive function when comparing a patient’s preoperative to postoperative state. But what specific metrics should be assessed to determine this decline? Should we evaluate discrete neurocognitive items or take a global approach? It is important to differentiate NCD from conditions like stroke, as it does not involve focal deficits. To ascertain this type of deficit, preoperative and postoperative assessments are fundamental. The timing of assessment is also critical; some studies consider the diagnosis of NCD beyond 30 days post-surgery to differentiate it from alterations characteristic of an acute postoperative phase. These deficits can be detected through a range of methods, from simple questionnaires or complex scoring systems to imaging tests like MRI. However, imaging lacks a clinico-radiologic correlation and thus does not contribute to diagnosis. In many cases, these deficits are not apparent to the patient or their treating physicians. Therefore, is it even worth detecting it? Despite the limitations of a homogeneous diagnostic definition, it is evident that a patient with NCD has an elevated risk of adverse events, including prolonged hospitalization, mortality, hospital costs, and reduced quality of life.
What Causes It?
The etiology of NCD is multifactorial, starting with microemboli of air, fat, or other particles entering the cerebral circulation. However, this factor alone does not appear decisive, given that valvular surgery has a sevenfold higher frequency of microemboli compared to coronary surgery, yet the incidence of NCD does not vary significantly between the two. Other potential causes range from cerebral ischemia due to low cardiac output, intraoperative malperfusion, and anemia. Additionally, there is increasing evidence linking inflammation to NCD. Inflammatory “triggers” are equally varied: pre-existing inflammation exacerbated by diabetes, whether due to poor control or long disease duration, impacts neurological function during surgery. Moreover, cytokine release and complement activation secondary to surgical trauma, extracorporeal circulation, and ischemia-reperfusion injury may cross the blood-brain barrier both directly and indirectly, often via vagal nerve stimulation.
Who Is Affected?
The article highlights risk factors such as cardiovascular disease, advanced age, diabetes mellitus, depression, heart failure, prior stroke, carotid stenosis, and baseline cognitive impairment. Although up to 98% of patients recover by the third month post-surgery, in some, the effects persist up to six years after the intervention. It is likely that these individuals already had subclinical cognitive impairment or dementia, which worsened following surgery.
What Can Be Done?
The article suggests various recommendations: avoid prolonged intubation, use heparin-coated extracorporeal circuits, ensure adequate individualized cerebral blood flow, maintain strict glycemic control, rewarm slowly without reaching hyperthermia, manipulate the aorta carefully, minimize renal damage and anemia, and identify at-risk patients for early rehabilitation.
In Conclusion Today’s article is an expert review on a topic that is seldom discussed in daily practice. It addresses an issue of significant relevance that warrants our attention, yet it is essential to maintain a clear focus. The lack of a consensus definition within the scientific community regarding NCD prevents uniform comparisons across studies, limiting our understanding of the magnitude of this problem. Meanwhile, it is important to remember that despite the risk factors predisposing our patients to NCD, cardiac interventions can provide them with years of high-quality life. Cardiac surgery is sometimes a “necessary evil” that has a positive impact on our patients’ lives.
REFERENCE:
Stanley ME, Sellke FW. Neurocognitive decline in cardiac surgery patients: What do we know? J Thorac Cardiovasc Surg. 2023 Aug;166(2):543-552. doi: 10.1016/j.jtcvs.2022.07.028.
