David Anthony, Jose Diaz-Gomez, C. Allen Bashour and Robert Johnson

Chapter Outline

Neurologic Care

Despite improvements in cardiac surgery techniques and perioperative critical care, postcardiotomy neurologic complications remain a major cause of morbidity and death following cardiac surgery. A spectrum of neurologic complications is seen in the postoperative period. Complications can be classified as generalized (global deficit) or focal. Generalized deficits can be manifested as delayed awakening from general anesthesia, coma, or new onset of seizure. Focal deficits may be transient or permanent. Except in their most severe form, neurologic complications cannot be completely assessed until the patient returns to consciousness and is weaned from the ventilator. Focal abnormalities are usually evaluated by a computed tomography (CT) scan. A CT for nonfocal, cognitive dysfunction rarely yields new information that is helpful for patient management, and imaging studies most often show old, chronic changes such as atrophy or lacunar infarcts. The patient must be stable enough to withstand transport to the CT (if the institution does not have a portable scanner), which is usually not the case in the early postoperative period.

The risk factors for neurologic injury after cardiac surgery have been well elucidated, but effective risk modification to reliably prevent neurologic complications has been elusive. In certain operations, measures to reduce risk have been implemented and have become incorporated in perioperative management.1,2 For example, patients with descending thoracic aortic operations are at significant intraoperative risk for spinal cord ischemia, as well as delayed injury (days postoperatively). These patients usually have a spinal drain placed preoperatively to reduce the risk of spinal cord injury. Spinal cord perfusion pressure (SCPP) is the difference between mean arterial pressure (MAP) and cerebrospinal fluid pressure (CSFP) (SCPP = MAP − CSFP); thus, lowering of CSFP will increase SCPP and potentially improve neurologic function as long as an adequate MAP is maintained.³

Neurologic complications are still considered one of the major risks associated with coronary artery grafting. The advanced age of bypass patients, high incidence of associated carotid occlusive disease, and increased aortic atheroembolic burden place older coronary artery bypass graft (CABG) patients at increased risk of central neurologic complications in the postoperative period.⁴

Other strategies for preoperative and intraoperative risk modification are becoming routine. They include selective use of preoperative carotid imaging, routine use of intraoperative transesophageal echocardiography (TEE) and epiaortic echocardiography, descending aortic cannulation with TEE guidance, aortic-no-touch technique, high-flow/high-pressure cardiopulmonary bypass (CPB), retrograde cerebral perfusion during circulatory arrest, carbon dioxide insufflation, intraoperative cerebral oxygen saturation monitoring, echocardiography de-airing, and maintenance of baseline perioperative blood pressure.5,6 Early neurologic complications vary in clinical presentation from focal to global neurologic deficit such as seizures, ischemic encephalopathy, and coma. Several authors have classified these complications as type I (focal injury, stupor, and coma) and type II (seizures, neurocognitive dysfunction, and delirium).⁷ This classification does not emphasize pathophysiologic mechanisms that could better inform preventive measures.^5,7 Regardless of the classification system used, overlap often exists.

In comparison to the other complications, focal neurologic deficits from stroke carry a mortality rate of up to 20% in the first postoperative month and prolong ICU and hospital lengths of stay.8–10 In a mixed cardiac surgery patient population, the incidence of stroke varied among those patients having CABG, combined CABG and heart valve surgery, and ascending aorta repair.^11–13 The incidence of stroke depends on the surgical procedure (isolated CABG, 1.4-3.8%; combined CABG and valve, 7.4%; isolated valve, 4.8-8.8%; multiple valve, 9.7%; and aorta, 8.7%).¹²

Unfortunately, most of the known baseline patient variables associated with perioperative stroke are not modifiable. Despite the identification of many intraoperative variables that cause intraoperative stroke (macroembolism of debris, air embolism, hypoperfusion, hypoxemia, coagulation status), risk remains significant and continues in the early postoperative period. Although there was early enthusiasm for off-pump CABG as an operative technique to reduce stroke, in the most recent multicenter clinical trial the 30-day incidence of stroke was not significantly decreased compared with on-pump CABG.¹⁴

The majority of strokes are ischemic (62%); fewer are due to hypoperfusion (9%) or hemorrhage (<1%).¹² Hemorrhagic strokes are rare after cardiac surgery and the clinical presentation is notable for delayed awakening and coma despite discontinuing sedation or progressive clinical deterioration as intracranial pressure (ICP) increases. Hemorrhagic transformation is recognized in 20% of ischemic strokes.¹⁰ Embolic strokes tend to present with acute hemiparesis and represent a compromise of specific cerebral artery area. Thrombotic or ischemic strokes are related to diminished blood flow with the most vulnerable areas being those between major cerebral artery perfusion territories (watershed areas).

Cardiac transplantation has a higher associated occurrence of neurologic complications than CABG.15,16 Symptom onset for focal motor deficits in these patients usually occur after the second postoperative day, especially in patients receiving mechanical circulatory support or experiencing major postsurgical complications such as tamponade, severe cardiac dysfunction, prolonged CPB, or postoperative hepatic failure.

Predictive models may enable implementation of earlier interventions.¹⁴ More than half of strokes are identified within the first day after CABG.¹⁰ Because of associated morbidity and death, an objective neurologic evaluation by minimizing sedation in the first 2 postoperative hours is desirable. Weaning sedation should be initiated only when the risk of doing so is minimal (i.e., a normothermic, nonacidemic, nonagitated patient with minimal chest tube output).

Once a new focal neurologic deficit, seizure, or delayed awakening is documented, a noncontrast brain CT scan should be obtained immediately. The most important tomographic findings include loss of insular ribbon, loss of gray-white interface, loss of sulci, acute hypodensity, mass effect, and dense mean cerebral artery sign. Owing to the relative insensitivity of CT scans for diagnosing ischemia, early CT scans may be normal, despite areas of brain infarction.¹⁷ Magnetic resonance imaging (MRI) may help identify these lesions.¹⁷ MRI usually cannot be obtained safely in the early postoperative period because of the need to move the patient off the unit to a usually remote location and because non-MRI compatible pericardial pacing wires are routinely placed in cardiac surgery patients. MRI will document a new lesion in 26% to 50% of cases, but there is often lack of correlation with the neurocognitive deficit.^18,19 Brain CT scans are more sensitive in diagnosing large air embolism, which is often the cause of abnormal postoperative neurologic findings in these patients. In the patient with a focal deficit or persistent embolic events, transcranial Doppler, transthoracic echocardiography (TTE), or TEE can be used to help identify sources of recurrent cardiac or aortic embolization.

Stabilization of the patient who develops stroke after cardiac surgery is the most important initial intervention and includes continuation of cardiopulmonary support and tracheal intubation if the patient cannot protect the airway or has a Glasgow Coma Scale score less than 9. Secondary brain injury, which is additional brain injury due to the factors that initially caused an imbalance between oxygen supply and demand, should be prevented. The most important measures are prevention of hypoxemia, hypotension, hypercarbia, and hyperthermia.

From a ventilator standpoint, higher levels of positive end-expiratory pressure (PEEP) to maintain optimal oxygenation might be required. If the patient has documented intracranial hypertension and requires PEEP 10 cm H₂O or higher, ICP monitoring should be considered as high levels of PEEP and lung recruitment maneuvers may decrease cerebral perfusion. Increased PEEP may decrease cerebral perfusion pressure (CPP) by elevating ICP because CPP is the difference between MAP and ICP.

Although acute treatment of ischemic stroke is imperative, the traditional 3-hour time window for active stroke intervention and institution of thrombolytic therapy is often lost because the time of the last known normal is usually just before induction of anesthesia and duration of surgery usually exceeds 3 hours. Furthermore, intravenous administration of tissue plasminogen activator (tPA) is contraindicated in the immediate postoperative period because of the associated postoperative bleeding risk.

Intra-arterial administration of tPA is an alternative for acute treatment of ischemic stroke within 6 hours of clinical presentation. The safety and efficacy of intra-arterial urokinase and tPA in selected patients who presented ischemic stroke within 12 days after cardiac surgery have been demonstrated.²⁰ The mean time from operation to stroke was 4.3 days. Thrombolytic therapy was commenced within 3.6 hours. No operative intervention for bleeding was necessary and 38% of the patients had neurologic improvement. Mechanical clot retrieval is another acute stroke therapy in the first 8 hours since neurologic deficit. Patients who will likely benefit from this therapy include those with significant neurologic deficit and large vessel occlusion with core ischemia approximately less than 30% of the middle cerebral artery territory.

Anticoagulation therapy has not proved beneficial in the cardiac surgery patient with ischemic stroke. However, it should be considered in cases of basilar stenosis, internal carotid dissection, and suspected cardiac embolism and specifically with concurrent atrial fibrillation and stroke. In this circumstance, the risk of ongoing embolism to cerebral circulation may be considered higher than active bleeding after cardiac surgery. A hematology consult is recommended in cases of suspected hypercoagulable state as the cause of this disorder demands a more comprehensive workup and potentially may require lifelong anticoagulation therapy. Antiplatelet therapy should be initiated in all cardiac surgery patients with acute stroke, especially if thrombolytic therapy is contraindicated. Aspirin is usually prescribed. The dose ranges between 160 mg and 1300 mg per day. Combined antiplatelet therapy with clopidogrel is not recommended because of the significant risk of bleeding.

In cases of suspected perioperative air embolism (i.e., opening of heart chambers for valve repair or replacement), the patient should remain in the supine position to avoid further embolic phenomena. If tolerable, the patient should be maintained in Trendelenburg position and mechanical ventilator support with FIO₂ of 1.0 should be instituted. Measures to control intracranial hypertension (more common in intracranial hemorrhage) should be individualized after reassessment of brain CT imaging. Hyperventilation, as well as diuresis with mannitol or furosemide is recommended in the patient with intracranial hypertension.

In the cardiac surgery patient, coma is defined as prolonged unconsciousness after discontinuation of anesthetics, sedatives, and opioids and inability to show response to motor/verbal commands. A recent retrospective investigation found an incidence of delayed awakening in approximately 0.5% of all cardiac surgery patients.²¹ However, the period of time in the immediate postoperative phase can be challenging as the necessity of adequate neurologic examination must be weighed against the patient’s hemodynamic stability. If a specific diagnosis is not found, and there is concomitant severe heart failure, it portends a worse outcome.²¹ Moreover, up to 20% of patients with postcardiotomy stroke present with delayed awakening and coma-like symptoms.²¹

Evaluation with brain CT is mandatory in these cases and it should occur as soon as the coma state has been recognized and reversible metabolic causes have been treated. The identified risk factors for delayed awakening after cardiac surgery in the aforementioned investigation included urgent cardiac surgery, elevated serum creatinine (Cr), and lower postoperative hemoglobin level.²¹ Most of these patients had normal brain CT scan imaging and ultimately recovered consciousness after being comatose during the first 24 hours.²¹ Although some investigators have proposed a role for altered renal excretion of sedatives in patients with postoperative renal failure or decreased oxygen delivery to the brain with anemia, the specific underlying mechanisms in these cases remain unclear.

Postoperative seizure is an independent predictor of permanent neurologic deficit and increased mortality risk.22,23 A recent study showed seizures were a strong predictor of permanent neurologic deficit and increased mortality risk. It is important to remember that any neurologic injury can present initially as a seizure. The independent risk factors for postoperative seizures included deep hypothermic circulatory arrest, aortic calcification or atheroma, and critical preoperative state. Other specific risk factors for early seizures include perioperative administration of the antifibrinolytic tranexamic acid administration and preexisting renal insufficiency.

Tranexamic acid has proconvulsant properties and it is reasonable to hold the infusion of this agent in the early postoperative period if the patient presents with seizures. The most common proposed mechanism of seizures after cardiac surgery is focal or global ischemia from hypoperfusion (air or atheroembolism) or metabolic disorders. Early brain CT scan is essential because it may detect potential reversible causes of neurologic injury such as cerebral edema, intracranial bleeding, or emboli in a major cerebral artery.¹⁰

Delirium is considered a subtle category of brain injury in the postcardiotomy patient. The intensivist should include perioperative stroke in the differential diagnosis of perioperative psychomotor agitation or delirium in the ICU. A common missed diagnosis is drug and alcohol withdrawal in patients with acute delirium in the ICU.

Cardiovascular Care