Neurological complication post cardiac surgery

CNS deficits:

• • 3% of cardiac surgery complications are neurological

  • Higher in valve surgery

  • Risk factors:

    • Preop factors:

      • prior stroke (44% develop focal neuro deficits post surgery). Of these 8.5% were new deficits, 27% represented reappearance of an old deficit, and 8.5% were worsening of the old deficit.

      • Carotid a disease

      • Increasing age ( risk of up to 10% in patients > age 75)

      • DM, smoking, HTN, PVD, renal dysfunction

      • Poor LV function

      • Reoperative surgery

      • Urgent/emergent surgery

    • Intraoperative/postoperative findings/events:

      • Ascending aortic arch atherosclerosis and calcification

      • LV mural thrombus

      • Opening of a cardiac chamber during surgery

      • Long duration of CPB

      • Perioperative hypotension or cardiac arrest

      • Postoperative AF

  • Mechanism:

    • Particulate embolism from aorta is the most common cause of stroke. TCD (transcranial doppler) studies have demonstrated an association between cerebral complications and the number of microemboli detected during surgery. Sources are as follows:

      • Atherosclerotic aorta (during cannulation or clamping and especially unclamping)

      • Solid or gaseous microembolism from the extracorporeal circuit

      • Air embolism

      • Left atrial or LV thrombus

      • Platelet-fibrin debris from carotid ulceration

    • Cerebral hypoperfusion

      • Systemic hypotension - common during CBP, although cerebral autoregulation can maintain cerebral blood flow down to a mean pressure of 40 mm Hg. However, this compensatory mechanism may not be optimum in diabetics, hypertensive patients.

      • Impaired cerebral flow from intra- or extracranial carotid disease

      • The BP may be compromised during manipulation of heart, pharmacologically, side clamp placed on the ascending aorta especially during construction of the proximal anastomosis.

      • Postop hypotension may lead to a watershed infarct, especially in patients with uncorrected carotid disease.

  • Presentation: depends primarily on the site and extent of the cerebral insult. Majority occur during surgery and will be evident withing the first 24 - 48 hours. Few Pts. awaken without neurological deficits and develop one later during the hospital stay, usually due to postop hemodynamic instability or AF.

    • Intraoperative embolization is the most common cause of stroke, multiple infarcts are a common finding on brain CT or MRI.

    • FND - hemiparesis/hemiplegia, aphasia, or dysarthria. Visual deficits may occur as the result of retinal embolization, occipital lobe infarction, or anterior ischemic optic neuropathy.

    • Posterior strokes involving the PCA and cerebellum are very common, as are MCA area strokes.

    • TIA and RINDs are common

    • Severe confusion or delirium

    • Coma

  • Prevention:

    • Preoperative evaluation for extracranial carotid disease is essential. Carotid doppler U/S, MRA. If Carotid a disease. Do a preliminary CEA or CABG-CEA procedure.

    • Intraoperative epiaortic echocardiography can be used to identify aortic atherosclerosis that might alter cannulation and clamping techniques to prevent manipulation of the diseased ascending aorta.

    • Use of OBCAB using LIMA and RIMA to LAD and RCA only.

    • Hypothermic fibrillatory circulatory arrest may be indicated to avoid aortic cross-clamping of the disease ascending aorta.

    • Careful, meticulous valve debridement, irrigation, and suction (use CUSA), and complete removal of air bubbles from the left heart after intracardiac procedures.

    • Use of a single aortic cross-clamp technique to avoid application of partial-exclusion clamp is also beneficial.

    • Particulate emboli can be captured by use of the Embol-X intra-aortic filter (Edwards Lifesciences) at the time of unclamping.

    • Use of higher mean arterial pressures during CPB

    • TCD may identify cerebral emboli during surgery

    • Cerebral oximetery (Bis monitor) may be used to assess the adequacy of cerebral oxygenation.

  • Evaluation:

    • H&P

    • CT, MRI, Carotid doppler, 2-D echo, EEG

  • Tx:

    • Heparinization recommended for an embolic stroke once the CT has demonstrated no ICH. Possible H'ge into an infarct zone is possible.

    • Reduced ICP in cerebral infarction - mannitol, diuresis, steroids

    • CEA

    • PT/OT

  • Prognosis:

    • Mortality is 25% for those who suffer a permanent stroke.

    • Comatose patient die 50% of time in 5 years or remain in a vegetative state.