Maintaining MAP ≥65 mmHg During Cataract Surgery Does Not Cause Stroke—The Infarct Likely Results from Thromboembolism or Patient-Specific Vascular Risk
The right MCA infarct after cataract surgery is almost certainly not caused by the anesthesia or the maintenance of MAP above 65 mmHg, because this blood pressure target is protective against perioperative stroke rather than causative. The most probable mechanisms are thromboembolism (70-80% of perioperative strokes) or underlying patient-specific cerebrovascular disease, not hemodynamic hypoperfusion. 1
Why MAP ≥65 mmHg Is Protective, Not Harmful
Maintaining MAP ≥65 mmHg throughout the procedure represents optimal hemodynamic management and reduces—rather than increases—the risk of perioperative stroke. 1
MAP ≥65 mmHg is the universally recommended minimum threshold for organ perfusion during noncardiac surgery, because values below this mark the failure of cerebral autoregulation and the onset of pressure-dependent blood flow. 1, 2
Intraoperative hypotension (MAP <65 mmHg for even 10 minutes) is strongly associated with postoperative myocardial infarction and death, with each 10-minute episode on postoperative day 0 increasing risk by 3%. 1
Hypoperfusion-related strokes (watershed or border-zone infarcts) account for only 20-30% of perioperative strokes and occur when MAP falls below the autoregulatory threshold, not when it is maintained above it. 1
In this case, MAP was maintained above 65 mmHg throughout the procedure, making hemodynamic hypoperfusion an extremely unlikely mechanism. 1, 2
The Actual Mechanism: Thromboembolism Is the Dominant Cause
Thromboembolism accounts for 70-80% of perioperative strokes and is the most likely explanation for a focal MCA territory infarct after any surgical procedure. 1
Postoperative thrombosis and embolism are the leading causes of perioperative stroke after vascular and non-vascular surgery alike, occurring in approximately 40% of cases during surgery and 60% in the early postoperative period (peak at 40 hours). 3, 4, 5
Early postoperative stroke (within 7 days) is primarily attributable to postoperative arrhythmias—especially new-onset atrial fibrillation—and thromboembolism from cardiac or arterial sources. 1, 5
Cataract surgery, though low-risk for cardiac events, does not eliminate the patient's baseline thromboembolic risk, particularly in elderly patients with pre-existing cardiovascular disease, atrial fibrillation, or carotid stenosis. 1
The imaging pattern of a focal MCA territory infarct strongly suggests an embolic mechanism rather than hypoperfusion, because watershed strokes present as border-zone infarcts between vascular territories, not as focal cortical or subcortical lesions. 1, 5
Patient-Specific Risk Factors Likely Explain the Stroke
Elderly patients undergoing even low-risk surgery carry baseline cerebrovascular risk that is independent of the anesthetic technique or blood pressure management. 1
Age ≥65 years is an independent risk factor for perioperative stroke, and the incidence of stroke increases with advanced age regardless of the surgical procedure. 1, 5
Underlying cardiovascular disease—coronary artery disease, congestive heart failure, cerebrovascular disease, diabetes, or chronic hypertension—substantially increases the risk of perioperative thromboembolism. 1
Postoperative atrial fibrillation is the most common cause of early postoperative stroke (within 7 days) and should be actively sought with ECG and telemetry monitoring. 1, 5
Pre-existing carotid stenosis or intracranial atherosclerosis can serve as embolic sources, and these conditions are common in elderly patients even in the absence of prior neurological symptoms. 1, 3, 4
Diagnostic Approach to Determine the Actual Cause
Immediate evaluation should focus on identifying the embolic source and ruling out cardiac arrhythmia, not on blaming the anesthetic management. 5
Obtain an ECG and initiate continuous telemetry to detect new-onset atrial fibrillation, which is the leading cause of early postoperative stroke. 1, 5
Perform echocardiography (transthoracic or transesophageal) to identify cardiac thrombus, valvular disease, or patent foramen ovale as potential embolic sources. 5
Image the carotid arteries and intracranial vessels with CT angiography or MR angiography to assess for atherosclerotic stenosis or acute thrombosis. 5
Review the imaging pattern of the infarct: focal cortical or large subcortical infarctions indicate embolism, whereas border-zone or watershed infarcts suggest hypoperfusion. 1, 5
Multiple territorial infarcts or an embolic shower pattern on imaging strongly support a cardioembolic or artery-to-artery embolic mechanism. 5
Common Pitfalls to Avoid
Do not attribute the stroke to "anesthesia" or "sedation" without evidence of intraoperative hypotension (MAP <65 mmHg for prolonged periods), because this misattributes causation and delays appropriate workup. 1, 2
Cataract surgery under IV sedation is classified as low-risk for cardiac complications, with perioperative MI rates of 0.03% and no expected increase in stroke risk from the procedure itself. 1
The use of IV sedation (monitored anesthesia care) is not associated with increased stroke risk compared to general anesthesia, and in fact may reduce the incidence of hypotension if managed appropriately. 1
Blaming the anesthetic technique distracts from the true cause—thromboembolism or underlying cerebrovascular disease—and prevents appropriate secondary stroke prevention measures such as anticoagulation for atrial fibrillation or antiplatelet therapy for atherosclerotic disease. 1, 5
Conclusion: The Stroke Is Not Due to Anesthesia
The right MCA infarct is almost certainly caused by thromboembolism (70-80% probability) or patient-specific vascular risk factors, not by the anesthetic management or the maintenance of MAP ≥65 mmHg. 1, 5, 3, 4 The appropriate response is to complete a full stroke workup—including cardiac rhythm monitoring, echocardiography, and vascular imaging—to identify the embolic source and guide secondary prevention, rather than attributing the event to optimal hemodynamic management during a low-risk procedure. 1, 5