• neurological complications of cardiac surgery are serious, increasing mortality, length of hospital stay, and costs
  • fatal cerebral infarction and severe diffuse encephalopathy with dementia represent the extremes in the spectrum of disabilities that can result from extracorporeal circulation surgery
  • MRI studies demonstrated recent ischemic lesions even in asymptomatic patients!
    • “asymptomatic” lesions are not harmless; they increase the risk of delayed cognitive impairment (especially in the case of another ischemic stroke)
  • based on detailed knowledge of the etiopathogenesis and risk factors (see below), the high-risk patients can be identified, and surgical methods and procedures can be modified
    • for example, early detection of severe localized aortic atherosclerosis  (TEE, CTA, perioperative palpation, or sonography) may reduce the risk of cerebral embolization by changing the clamp position or cannulation site  Different types of atherosclerotic lesions on TEE
    • lower risk of embolization was reported in procedures without extracorporeal circulation (off-pump bypass), especially if contact with the ascending aorta is minimized


  • based on the clinical symptoms, 2 types of complications can be distinguished (they may coincide):
    • type 1 – cerebral infarction – focal motor deficit, oculomotor and speech disorders, etc.
    • type 2 – diffuse/multifocal encephalopathy – symptoms range from discrete neuropsychiatric changes (memory disorders, personality changes, attention deficit disorder) to severe disorders of consciousness – both qualitative (delirium) and quantitative (sopor, coma)
  • incidence of perioperative stroke ~ 1-6.1%
  • neuropsychiatric changes are observed in 7-76% (!!) of patients in the early postoperative period [Roach, 1996]  [Vingerhoets, 1997]

Ischemic stroke

  • typically territorial ischemic lesion due to large vessel occlusion of embolic origin
  • no difference in the incidence of neurological complications was found for valve surgery or revascularization procedures, but combined procedures (intracardiac surgery + revascularization) are associated with a 2.5-5 times higher risk of cerebral involvement than revascularization alone  [Almassi, 1999]
  • see risk factors below


  • a wide range of neurological deficits occurs:
    • subtle attentional deficits
    • delirium (acute phase) / cognitive impairment (impaired memory, concentration, attention, etc.)
    • vegetative state or brain death
  • severe global hypoxic encephalopathy with a persistent altered level of consciousness is often a consequence of hypovolemic or cardiogenic shock in the preoperative period, while qualitative disturbances are more consistent with multifocal involvement (embolization)
  • risk factors for encephalopathy
    • older age, history of stroke, arterial hypertension, diabetes mellitus, and presence of carotid stenosis  [Guy, 2002]
    • perioperative risks: hypotension with hypoperfusion and also the duration of extracorporeal circulation (a 30-50% increase in relative risk for every 30 minutes was reported) [Rolfson, 1999]
  • etiopathogenesis of encephalopathy is multifactorial
    • most usually due to hypoperfusion and/or microembolization  [Murkin, 2001]
      • probably, there is an interaction between hypoperfusion and embolization – reduced perfusion at the time of microembolization limits the ability of the bloodstream to “washout” the embolus (especially in the so-called “border zones”)   Border zone infarcts (BZI)
      • during connection to the extracorporeal circulation, small fat particles can be torn from the aortic wall, causing “mini-infarcts” in the brain tissue; bubbles released from the device can also pose a problem
    • confounding factors:
      • quality of collateral circulation
      • the preoperative condition of the brain tissue and the quality of perfusion during surgery determine whether the lesion will be symptomatic (in addition to its location and extent)

Diagnostic evaluation

Neurological examination

  • a more detailed examination, including assessment of cognitive function, speech, and accurate quantification of paresis, is possible only after the patient is awake and weaned from the ventilator
  • assess the level of consciousness after sedation was stopped (appropriate timing is essential)
  • look for asymmetric tone and response to pain stimuli in the limbs
  • describe the oculomotor disorders and facial palsy (assess grimacing in response to a painful stimulus)

Brain imaging

  • acute stroke protocol
  • brain CT + CT angiography  (+CT perfusion)
    • look for early signs of ischemia and potential thrombosis (dense artery sign) on NCCT 
    • assess core and penumbra if CTP is available
    • detect occlusion and its extent on CTA and decide whether mechanical recanalization is feasible  (IV thrombolysis is usually contraindicated)
  • brain MRI, incl. FLAIR, GRE and DWI  + MRA (+PWI) Multiple emboli on DWI after surgery in ECC Diffuse edema due to hypoperfusion during surgery in ECC
    • in the acute phase, MR DWI is ideal for the early detection of even subtle ischemic changes and subtle hemorrhages
    • in the subacute phase, MRI is best suited to assess the extent of WML

Neuropsychological evaluation

  • discrete neuropsychiatric impairments may go unnoticed; their detection depends on the type of tests used during the examination
  • a complete assessment of the neuropsychiatric status is very lengthy and difficult
  • there is no consensus on the optimal number and type of tests, timing, and optimal method of data analysis
  • the situation is further complicated by the fact that the initial postoperative cognitive deficit may improve initially and then progress over months to years [Guy, 2002]   [Selnes, 2001]

Risk factors

Carotid artery stenosis

  • traditionally, stroke during cardiac surgery in patients with carotid stenosis has been attributed to hypoperfusion behind the stenosis ⇒ prophylactic CEA was justified by the prospect of preventing this hypoperfusion
  • but:
    • 2/3 of strokes occur within 24 hours of the procedure
    • 50% of patients who experience a stroke have no significant carotid stenosis
    • according to CT and autopsy studies, up to 60% of stroke lesions do not correlate with the side of carotid stenosis
  • the prevailing opinion is that microembolization, mainly from the aortic arch, is the main etiopathogenetic mechanism of perioperative stroke during ECC
  • stenoses in the extracranial ICA segments are usually associated with generalized atherosclerosis, including the aorta and coronary arteries
    • aortic plaques pose a greater risk than carotid stenosis (see below)
    • carotid stenosis is a predictor rather than a cause of perioperative stroke
  • therefore, a general indication for CEA before ECC-related procedures was abandoned

Symptomatic stenosis

  • symptomatic stenosis  50-99% is indicated for CEA
    • the risk of stroke is high (up to 18%)
  • prefer CEA to CABG if possible (in cardiac stable patients)
    • CEA→CABG is associated with the lowest risk of stroke but with the highest risk of myocardial infarction   [Naylor, 2003]
  • in patients at high cardiac risk, perform CAS followed by CABG or combined CEA+CABG (probably with increased perioperative risk)

Asymptomatic stenosis

  • no consensus on how to proceed in asymptomatic stenosis; the efficacy of CEA before CABG or combined procedure remains controversial
  • it is recommended not to perform CEA in asymptomatic stenosis < 70%
  • for unilateral asymptomatic stenosis >70-80%, CAS followed by CABG seems to be the safest option rather than CEA followed by CABG
    • cardiac disease must be stable enough to allow the delay of cardiac surgery for at least 4 weeks (minimal required duration of DAPT after CAS)
  • combined procedure (CEA+CABG) may be considered, but the effectiveness of this procedure is not proven; there is a higher risk of complications
  • in patients with bilateral stenosis > 75%, sequential or combined procedures may be considered, but their efficacy has not been proven
  • in patients with asymptomatic stenosis >60% and contralateral occlusion, available data do not support CEA before CABG
Overall risk
  • history of stroke is an independent predictor of perioperative stroke  [Roach, 1996]
    • it is probably related to impaired vascular autoregulation and inadequate collateral circulation around the infarct site
  • it is recommended to operate at least 4 weeks after the recent stroke
  • incidence of aortic atherosclerosis increases with age
    • it occurs in 9% of patients aged 50-59 years and in up to 33% of patients aged > 80 years
  • it is considered to be the most important risk factor for perioperative stroke [Roach, 1996]
    • the risk of perioperative stroke in patients with aortic atherosclerosis is 5-19% compared to 0-2% in the absence of atherosclerosis
    • TCD trials have shown that maximum embolization to the MCA occurs at the time of manipulation with the ascending aorta (especially during the release of  the aortic clamp)
  • TEE or CTA offers a new way of imaging and quantifying atherosclerotic lesions, mainly in the aortic arch and descending aorta   Aortic atherosclerosis on CTA
    • risk increases with the degree of atherosclerosis; severe involvement is defined as:
      • wall enlargement > 5mm
      • significant calcification
      • protruding or mobile plaques (considered particularly risky)
    • TEE has limited visibility of the ascending aorta
  • epiaortic perioperative sonography with a probe placed directly over the ascending aorta allows modification of the procedure based on local findings of advanced atheromatosis (cannulation site and clamp position, identification of the optimal site for proximal graft anastomosis)
  • longer duration of extracorporeal circulation is associated with a higher risk of perioperative stroke and encephalopathy  [John, 2000]    [Almassi, 1999]
    • the risk increases for procedures lasting longer than 2 hours  [Odell, 2001]
  • the main cause, besides hypoperfusion injury, is  cerebral embolization
  • it is controversial whether extracorporeal circulation per se can lead to brain damage due to non-pulsatile perfusion, complement activation, systemic inflammatory response, or the increased tendency of platelets to aggregate and form microemboli
  • chronic Afib increases the risk of cardioembolism (most commonly from the LAA); preoperative TEE is suggested
    • in the absence of a thrombus, the risk of stroke is acceptable
    • if thrombi are found in the left atrium, anticoagulation for 3-4 weeks is indicated, followed by TEE
  • postoperative Afib
    • occurs in approx. 25-40% of patients, most often in the first 4 postoperative days
    • most cardioembolic events occur on days 2-4 after surgery
  • history of diabetes generally increases the risk of complications
  • multiple mechanisms:
    • accelerated atherosclerosis (including aortic arch)
    • impaired autoregulation due to diabetic arteriolopathy
    • renal impairment and higher incidence of arterial hypertension in diabetics
  • chronic hypertension increases the cerebral autoregulatory threshold
  • some authors have reported a beneficial effect of higher perioperative MAP (> 80 mmHg) in reducing the incidence of neurological complications [Plestis, 2001]
  • interaction between hypoperfusion and embolization was discussed above

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Neurological complications during extracorporeal circulation
link: https://www.stroke-manual.com/neurological-complications-during-extracorporeal-circulation/