Recently, the PeriOperative Ischemic Evaluation (POISE)-2 trial demonstrated that perioperative aspirin did not reduce the incidence of death or nonfatal myocardial infarction after noncardiac surgery, but did increase the risk of major bleeding.36 Of note, patients who had aspirin therapy that was initiated in the course of the study had a reduced incidence of stroke compared to placebo; patients who were continuing aspirin therapy showed no reduction in stroke incidence. Stroke was not a primary outcome of the study and the authors acknowledged that the findings in the initiation group could be spurious. However, the results suggest that some patients at risk of stroke may benefit from preoperative initiation of aspirin therapy, but this must be balanced against the now well-documented risk of significant increases in bleeding and must be demonstrated in a larger trial.
The original POISE trial, which evaluated the cardioprotective effects of metoprolol in 8351 noncardiac surgery patients, demonstrated that patients receiving metoprolol had a significantly higher risk of stroke (hazard ratio 2.17, p=0.005) and death (hazard ratio 1.33, p=0.032).37 Data from the POISE trial and other investigations contributed to a meta-analysis suggesting that beta blockers increase risk of nonfatal stroke after noncardiac surgery38; patients from the POISE trial constituted the majority in this study. A retrospective case-control study subsequent to the POISE trial suggested no increased risk of perioperative stroke with clinically routine doses of beta blockers39; a study of low-dose bisoprolol also concluded that there was no increased risk of perioperative stroke.40 Based on these studies it is unclear if there is a drug-specific effect of metoprolol that increases risk of stroke or whether increased risk in the POISE trial was due to bradycardia and hypotension in the treatment group. Based on retrospective data from a single-center observational study, Mashour et al8 demonstrated that routinely prescribed p.o. metoprolol conferred a higher risk of postoperative stroke compared to a matched cohort taking atenolol. These data are consistent with the results of a U.S.-wide Veterans Administration hospital study by London et al showing a higher risk of stroke after noncardiac surgery in patients taking metoprolol compared to atenolol.41 In a single-center observational study, Ashes et al demonstrated that bisoprolol is associated with a lower stroke risk than either metoprolol or atenolol.42 Current guidelines endorse the perioperative continuation of beta blockers in surgical patients who are already taking this class of drug. Large prospective studies are required to confirm that surgical patients who continue perioperative beta blockers are at increased risk of stroke if metoprolol is administered vs. another beta blocker. In surgical patients who are beta-blocker-naïve, high-dose beta blockers should not be administered without dose titration.43
As with beta blockers, discontinuation of statins in the perioperative period may have adverse consequences. With respect to nonoperative stroke, discontinuation of statins in individuals with acute ischemic stroke was associated with a high risk of early neurologic deterioration.44 A recent, preliminary, retrospective study of asymptomatic surgical patients presenting for carotid endarterectomy suggested that statins could reduce neurologic injury, as defined by both stroke and cognitive dysfunction.45 Statins have also been shown to reduce the incidence of atrial fibrillation and other adverse outcomes that may be associated with postoperative stroke.46,47 However, there are no data to suggest that starting statins in the preoperative period can prevent stroke around the time of noncardiac, nonneurologic and noncarotid surgery.
There has been extensive interest in the possible neuroprotective effects of anesthetic agents. Most studies have been in patients for whom cerebral ischemia is predictable; examples of predictable cerebral ischemia include carotid endarterectomy, cerebral aneurysm surgery and procedures requiring deep hypothermic circulatory arrest. For these procedures, anesthetic technique may be adjusted prospectively in an attempt to minimize neurologic injury. However, data supporting anesthetic neuroprotection even for these procedures is limited or absent. Given the low incidence of perioperative stroke in noncardiac and nonvascular surgical patients (making RCT difficult), investigators have studied neurologic outcome after cardiac surgery, in which the stroke risk is higher. Bilotta et al performed an extensive literature review of randomized trials but could not make definitive conclusions due to the small number and heterogeneity of studies.48
In a retrospective study of 651,775 patients undergoing noncardiac, noncarotid and nonneurologic surgery, patients receiving more than four units of packed red blood cells (as a surrogate for major hemorrhage) had an approximately 2.5 fold increased risk for stroke or Q-wave myocardial infarction.64 The POISE trial also found “significant bleeding” to be an independent predictor of postoperative stroke (adjusted OR 2.18, 95% CI 1.45-8.52) in the population of high risk patients undergoing noncardiac surgery.37 The authors commented on a dose-response relationship between the volume transfused and stroke but did not examine the interaction between hypotension and anemia. There is evidence in nonoperative stroke that anemia is associated with stroke in the absence of hypotension,65,66 and thus it seems reasonable to assume that this association exists in surgical patients as well.67,68 Furthermore, recent observational data suggest that intraoperative anemia (hemoglobin <9 gm/dl) in the setting of beta blockade increases risk of stroke, but the study was not able to distinguish acute from chronic use.42
Hyperglycemia has long been recognized to have a negative influence on neurologic outcomes following cerebral ischemia.69 This is true for both global and focal ischemia as well as specific surgical populations for which focal ischemia is predictable, including cardiothoracic surgery,70 carotid endarterectomy71 and open cerebral aneurysm ligation.72 It should also be noted that in a relatively small randomized trial of cardiac patients, intensive intraoperative insulin therapy (glucose goal of 80-100 mg/dL) was associated with an increased risk of stroke and death, despite no increases in hypoglycemic events.73 A recent meta-analysis concluded that intravenous insulin for tight glycemic control within 24 hours after nonoperative stroke may not be beneficial and may increase the risk of hypoglycemia.74 This is clearly a complex issue and most authors recommend an intervention with serum glucose exceeding 150 mg/dL, with an absolute upper limit of 180 mg/dL, in hyperglycemic patients undergoing major surgery.75,76
In sum, it seems that there is an association between intraoperative hypotension and perioperative stroke, but the clinical significance of this association is poorly defined. Further prospective research is clearly necessary to make strong evidence-based recommendations regarding intraoperative blood pressure management. It is probable that there are subsets of patients at increased risk for stroke who clearly are harmed by hypotension or low flow states. Some of these populations may include patients with unrecognized critical stenosis of carotid or intracranial arteries or congenital anomalies of the cerebral circulation.91
Various physiologic, pharmacologic and pathologic factors in the postanesthetic period can mask symptoms of intraoperative or postoperative stroke. Careful evaluation and resolution of pharmacologic contributions to a neurologic deficit is paramount to reduce delay in stroke diagnosis.98 Certain drugs that are commonly used during the intraoperative period can be reversed, including narcotics (with naloxone), benzodiazepines (with flumazenil), and neuromuscular blockers (with a cholinesterase inhibitor or sugammadex, where available). Although the presence of residual inhaled anesthetics can be quantified routinely in the operating room at the end of a surgical case, the effect of drugs such as propofol and dexmedetomidine cannot be conveniently measured in real time.
Delayed emergence, altered mental status and/or the presence of new focal neurologic deficit in the absence of convincing confounders should raise suspicion for stroke.99 A detailed neurologic examination should include the use of the National Institutes of Health Stroke Scale (NIHSS) (Table 5; see also: http://www.ninds.nih.gov/doctors/NIH_Stroke_Scale.pdf or http://www.ninds.nih.gov/doctors/NIH_Stroke_Scale_Booklet.pdf). Clinical evaluation also includes measurement of blood pressure, oxygen saturation, temperature, blood glucose, serum electrolytes, complete blood count and coagulation status. Immediate diagnostic studies of all patients with suspected stroke should include noncontrast computed tomography (CT) or magnetic resonance imaging (MRI) of the brain to determine whether the stroke is ischemic or hemorrhagic in origin and to correlate neurologic deficit with radiologic findings.100 The role of CT angiography and CT perfusion imaging is to provide supplementary information, especially in determining the need for urgent endovascular intervention. The presence of a large ischemic penumbra or thrombus in a major vessel (e.g., middle cerebral artery) would prompt consideration of endovascular therapy. One of the limitations of conventional MRI is the duration of the scan; however, diffusion-perfusion MRI enables the identification of an ischemic penumbra and identification of patients who may benefit from late thrombolysis.101
Interventions such as recombinant tissue plasminogen activator (rtPA) should be considered with a multidisciplinary team that includes stroke neurology, interventional neuroradiology and the primary surgical service. The risk/benefit balance will vary depending on the patient, severity and location of the stroke, and type of surgical intervention.
Intravenous rtPA is the drug of choice for thrombotic strokes, but it is contraindicated in a number of situations (Table 6). Importantly, major surgery—with the exception of intracranial or spinal surgery—is a relative rather than absolute contraindication, but there is a paucity of literature regarding the management of stroke after a noncardiac, nonvascular or nonneurologic procedure. Oral administration of aspirin (initial dose is 325 mg) within 24 to 48 hours after stroke onset is recommended but is not a substitute for other acute interventions such as rtPA.92 Furthermore, the administration of aspirin (or other antiplatelet agents) as an adjunctive therapy within 24 hours of intravenous fibrinolysis is not recommended.92 Urgent anticoagulation with the goal of preventing early recurrent stroke, halting neurological deterioration or improving outcomes after ischemic stroke is not recommended,92 nor is the initiation of anticoagulation therapy within 24 hours of treatment with intravenous rtPA. In addition to intravenous rtPA, intra-arterial thrombolysis has American Heart Association Class IIa, Level C evidence of safety and efficacy.100,104 Although endovascular mechanical thrombolysis has recently been shown not to be superior to intravenous rtPA,105 it may be an attractive alternative in the postoperative patient. Again, all interventions should be discussed with a multidisciplinary team including neurologists, neuroradiologists, and the primary surgical service, while keeping in mind that “time is brain.”
Patients with acute cerebral ischemia should have cardiac monitoring for at least the first 24 hours, and any serious arrhythmia should be treated.92 Myocardial ischemia and cardiac arrhythmias are potential sequelae of acute cerebrovascular disease and systemic hypertension is common after stroke. Common postoperative conditions that may contribute to hypertension include stress response to surgery, pain, nausea, hypervolemia, full bladder, or physiological response to hypoxia. Every effort should be made to preserve cerebral perfusion pressure during the first 24 hours. Unless the patient is eligible for acute reperfusion intervention, systolic blood pressure is usually treated only if it is greater than 220 mm Hg, and diastolic pressure is treated only if it is greater than 120 mm Hg.92 In patients who receive rtPA (intravenous or intra-arterial) or undergo mechanical clot retrieval, systolic blood pressure above 180 mm Hg and diastolic pressure above 105 mm Hg should be treated with anti-hypertensive drugs such as labetolol or nicardipine.92 However, no data are available to guide selection of medications for the lowering (or raising) of blood pressure in the setting of acute ischemic stroke. Both hypovolemia and unstable cardiac arrhythmias may result in arterial hypotension, which is detrimental in the setting of stroke. As such, correction of hypovolemia with normal saline and restoration of normal sinus rhythm is beneficial.92
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