Neurologic Complications of Cardiac Surgery

Stroke After Coronary Artery Bypass Grafting

The rate of stroke in patients undergoing CABG has decreased over the past few decades, with most series reporting a rate of less than 2 percent. Clinically silent stroke detected by magnetic resonance imaging (MRI) may occur at a higher rate, and often these strokes are multifocal. A large single-center review of more than 40,000 patients found that the rate of stroke decreased over a 30-year span despite increasing patient risk profile. When stroke does occur, it leads to a significant increase in hospital mortality, prolongs length of stay in the intensive care unit and the hospital, results in significant disability, and typically requires inpatient rehabilitation or nursing home placement at the time of hospital discharge.

In patients with acute neurologic symptoms concerning for stroke, brain imaging is important to rule out alternative etiologies and to help elucidate the etiology of stroke and overall burden to inform prognosis for neurologic recovery. Ischemic stroke following cardiac surgery is usually the result of either emboli or hypoperfusion. Watershed infarction occurs at the border zone between major cerebral arteries and often involves the subcortical white matter on MRI scans; it is suggestive of stroke due to hypoperfusion and is a common pattern of ischemia in patients who were exposed to decreased cerebral perfusion. Embolic stroke is often related to emboli from the heart or proximal aorta and is typically multifocal on imaging, involving all vascular territories. Although patients in the postoperative period following CABG are not candidates for systemic intravenous thrombolysis therapy, given the advent of extended windows for endovascular therapy it is important to pursue computed tomography (CT) angiography to identify large-vessel occlusions and facilitate thrombectomy discussions with a local stroke center.

Intracerebral hemorrhage is rare after CABG but may necessitate urgent medical and surgical treatment and decompression. It can occur during cardiopulmonary bypass due to effects on platelet adhesion and coagulation factors, but it most commonly occurs due to hemorrhagic conversion of an area of cerebral infarction. Rarely, cardiopulmonary bypass is complicated by pituitary apoplexy resulting from acute hemorrhage or infarction of an unrecognized pituitary adenoma during surgery; patients awaken with headache, ptosis, visual impairment, and ophthalmoplegia and may require transsphenoidal surgical decompression.

Intraoperative stroke represents between 30 and 50 percent of all strokes associated with CABG, and about half of these events are felt to be due to hypoperfusion. A decrease of mean arterial pressure of more than 10 mmHg is an important predictor of watershed strokes, and a prolonged cardiopulmonary bypass time exceeding 2 hours is associated with a higher rate of stroke.

Thromboembolic stroke also occurs intraoperatively and is related to specific surgical factors. For example, manipulation of the aorta during cannulation and cross-clamping can lead to dislodgement of atheroma or calcium. Studies using ultrasound to detect cerebral emboli have noted increased frequency of emboli during these moments of aortic manipulation. Stroke also occurs at higher frequency when valvular heart surgery is combined with CABG due to the additional risk of cerebral macroemboli associated with removal or repair of diseased heart valves. There have been multiple studies comparing the risk of stroke between “off pump” CABG techniques, wherein cardiopulmonary bypass machines were not used, compared to “on pump” CABG, and the overall results are conflicting, with rates likely varying due to differences in patient selection and preoperative risk factors. Less common causes of embolic stroke include surgical complications such as air emboli, which can propagate into the cerebral vasculature and often present with focal stroke symptoms, encephalopathy, or seizures.

The majority of postoperative strokes following CABG occurs during the first 7 days after surgery. New-onset postoperative atrial fibrillation occurs in up to 30 percent of patients following CABG, especially within the first 3 days, and is associated with a higher risk of stroke. Low cardiac output after CABG is also associated with stroke due to hypoperfusion. After the first week, patients post-CABG remain at higher risk for stroke although this is largely related to a greater risk for thromboembolic events due to comorbidities such as older age, hypertension, diabetes mellitus, dyslipidemia, peripheral vascular disease, higher rates of chronic atrial fibrillation, and the need for further revascularization procedures.

Ischemic complications following CABG can lead to visual disorders and symptoms. Retinal abnormalities on examination are common after CABG, including multifocal areas of retinal nonperfusion and cotton wool spots or retinal emboli; these findings are usually not associated with diminished visual acuity. Much less common, but more likely to cause visual impairment, is ischemic optic neuropathy. Anterior ischemic optic neuropathy due to infarction of the optic nerve head is associated with monocular, painless, and often permanent visual impairment along with optic disc swelling on examination. Visual testing may reveal central scotoma or altitudinal deficits. Retrobulbar or posterior ischemic optic neuropathy is rare and is often seen after a period of hypoperfusion; it is due to infarction of the intraorbital nerve and presents with acute blindness, which can be bilateral, without optic disc swelling on fundoscopic examination. The presence of a homonymous visual field deficit or cortical blindness (associated with normal pupillary and retinal examination) should prompt urgent imaging to evaluate for occipital lobe injury. Similarly, gaze deviation or gaze paralysis in the postoperative setting may suggest brainstem or hemispheric stroke.

Nonstroke Neurologic Complications After Coronary Artery Bypass Grafting

Encephalopathy is common after CABG surgery, occurring in between 10 and 30 percent of patients, and has a variety of etiologies. Delirium, an acute disorder of fluctuating attention and confusion, is more common in patients older than 65 years, and is associated with prolonged hospital length of stay and complications following surgery. Patients may present with hyperactive agitation, visual hallucinations, confusion, or hypoactive states. Aside from older age, preoperative risk factors for the development of delirium after cardiac surgery include baseline neurocognitive dysfunction, a history of prior stroke, a history of depression, baseline renal dysfunction, and a low serum albumin level. Postoperative associations with delirium include the need for mechanical ventilation for more than 24 hours, prolonged operating time, postoperative stroke, worsening renal function, and the use of benzodiazepines. Onset of encephalopathy should also prompt an appropriate diagnostic work-up to rule out and correct inciting factors such as multifocal stroke, metabolic disorders including sodium disturbances and hypoglycemia due to excess insulin and decreased nutritional states around the time of surgery, and systemic infection including pneumonia and urinary tract infection.

Encephalopathy presenting as persistent coma is rare but usually suggests severe neurologic dysfunction with a poor neurologic prognosis. The most common causes include a large burden of stroke (usually involving the brainstem or bilateral cerebral hemispheres) or global hypoxic ischemic injury. The latter is often due to dysrhythmia, mechanical injury to the heart, or frank cardiac arrest.

Seizures occur in up to 1 percent of patients after cardiac surgery including CABG and may be due to acute or recent stroke, metabolic derangements, hypoxic ischemic brain injury, or exposure to medications including high-dose tranexamic acid, procainamide, and lidocaine. Unrecognized alcohol dependence or inadvertent cessation of chronic medications such as benzodiazepines or anticonvulsants in the perioperative period may also cause seizures due to withdrawal. Seizures without clear tonic-clonic or focal motor manifestations may be difficult to recognize and patients may present with prolonged alteration in mental status or subtle findings such as intermittent gaze deviation or nystagmoid movements. As such, evaluation with electroencephalography can be valuable in the encephalopathic postoperative patient.

Peripheral nervous system complications after CABG are often related to mechanical factors leading to compression or stretch injury of nerves adjacent to the surgical field or those that are susceptible due to patient positioning factors. Brachial plexopathy has been reported to occur after cardiac surgery in 1 to 5 percent of patients who undergo median sternotomy. The lower trunk is the most commonly involved and clinically may mimic an ulnar neuropathy; the loss of the triceps reflex on the affected side helps distinguish plexopathy from a more peripheral lesion. There is usually weakness of intrinsic hand muscles, sensory loss or pain over the medial hand, and rarely, Horner syndrome. Risk factors include sternal retraction, direct trauma due to first rib fracture, and adducted arm position. Deficits usually reverse within 1 to 3 months, but may lead to more prolonged and permanent disability in some patients. Intraoperative electrophysiologic monitoring of sensory nerve conduction may help to detect and predict postoperative nerve injury and potentially allow for adjustment of intraoperative factors to decrease the incidence and severity of injury. Prevention strategies including more precise midline sternotomy, more caudal placement of retractors, avoiding asymmetric retraction, and maintaining neutral head and arm abduction positioning with appropriate cushioning, may help reduce the frequency of brachial plexopathy.

Unilateral phrenic nerve injury, leading to hemidiaphragmatic paralysis, occurs in over 10 percent of patients after open-heart surgery. The left phrenic nerve lies along the pericardium between the lung and the mediastinal aspect of the pleura, making it particularly vulnerable to injury from manipulation and the effects of topical hypothermia related to cold cardioplegia. Although unilateral phrenic nerve injury may increase the risk of respiratory complications and atelectasis, the overall morbidity is generally low, and patients often experience recovery by around 6 months. Bilateral phrenic nerve injury is a much more rare complication and leads to prolonged mechanical ventilation.

Less common mononeuropathies relate to injury of the recurrent laryngeal nerve and saphenous nerve. Similar to phrenic nerve injury, complications of internal thoracic artery dissection in combination with topical hypothermia can be associated with recurrent laryngeal nerve injury; patients present with hoarseness, ineffective cough, and aspiration when severe. Harvesting of the saphenous vein for CABG can lead to saphenous nerve injury, leading to decreased sensation, hyperesthesia, and pain along the medial lower leg.

Although not unique to cardiac surgery, there is also growing recognition of surgery as a risk factor for development of acute inflammatory demyelinating polyradiculoneuropathy as a cause of postoperative quadriparesis and respiratory failure. Critical illness polyneuropathy and myopathy may develop in patients whose postoperative course has been complicated by sepsis, multi-organ failure, and prolonged use of paralytic medications or steroids. It can lead to difficulty weaning from mechanical ventilation and a higher risk of complications related to immobility in the hospital.

Neuropsychologic studies of cognitive function before and after CABG have identified both a short-term early cognitive decline immediately after surgery and a later-onset decline about 3 to 5 years after surgery. The early decline is usually reversible on the order of weeks or a few months, and is often associated with delirium during hospitalization. Similar short-term declines have also been reported in patients who underwent noncardiac surgery, suggesting that exposure to anesthesia may contribute to symptoms in vulnerable patients, and formal studies with serial neuropsychologic testing up to 1 year after CABG have showed that cognitive changes over this time are similar compared to patients who received percutaneous coronary intervention; therefore, common pretreatment cardiac and cerebrovascular disease and vascular risk factors likely also contribute to development of symptoms.

Later-onset cognitive decline was found in up to 40 percent of patients after CABG at long-term follow-up 5 years after surgery when performance on cognitive testing was compared to baseline testing. At that time, it was assumed not only that late cognitive decline was common, but also that it was due to “on pump” cardiopulmonary bypass time in particular and the delayed effect of diffuse microemboli exposure during CABG. However, these initial studies lacked both unoperated patients with coronary artery disease and healthy patient control comparison groups. Subsequent studies shows that this delayed cognitive decline is not specific to patients who had “on pump” CABG. There are no significant differences in cognitive function 3 years after surgery in patients who had CABG with and without cardiopulmonary bypass, patients with nonsurgically treated coronary artery disease, and healthy controls; at 6 years, all three groups with coronary artery disease showed a similar degree of cognitive decline that was greater than the healthy control group. Studies of patients treated “on pump” and “off pump” during CABG showed no difference in cognitive performance 5 years after surgery. Taken together, there is no clear evidence that cardiopulmonary bypass is the major contributor to this observed late cognitive decline.

It therefore seems that preoperative cerebrovascular disease is more closely associated with the risk of delayed onset cognitive decline, due to a slow accumulation of ischemic brain injury related to ongoing vascular risk factors. Patients who had brain MRI scans showing evidence of prior cerebral ischemia before CABG have been found to have higher risk of subsequent cognitive decline. These findings highlight the importance of medical control of vascular risk factors to potentially reduce the risk of slow cognitive decline in this patient population.