Neurological complications during extracorporeal circulation

David Goldemund M.D.
Updated on 11/01/2024, published on 14/04/2023
  • 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 (ECC) 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 a detailed understanding of the etiopathogenesis and risk factors (see below), 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 when minimizing contact with the ascending aorta


  • based on the clinical symptoms, two types of complications can be distinguished (and they may coincide):
    • type 1 – cerebral infarction (stroke) – characterized by 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

  • ischemic stroke typically results in territorial ischemic lesion due to embolic arterial occlusion
  • 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 may occur:
    • subtle attentional deficits
    • delirium (acute phase) / cognitive impairment (impaired memory, concentration, attention, etc.)
    • vegetative state or even 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 (microembolization)
  • 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]
      • there is likely an interaction between hypoperfusion and embolization, where 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 → Basic neurological examination
  • 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, involving 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; intravenous thrombolysis (IVT) is usually contraindicated
  • brain MRI, incl. FLAIR, GRE and DWI  + MRA (+PWI) Multiple emboli on DWI after 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 white matter lesions (WML)  → FAZEKAS

Neuropsychological evaluation

  • discrete neuropsychiatric impairments may go unnoticed; their detection depends on the types of tests used during the examination
  • a complete assessment of the neuropsychiatric status is time-consuming and challenging
  • 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 initially improve and then progress over months to years [Guy, 2002]   [Selnes, 2001]

Risk factors

Carotid artery stenosis

  • traditionally, stroke occurring during cardiac surgery in patients with carotid stenosis has been attributed to hypoperfusion secondary to the stenosis ⇒ prophylactic carotid endarterectomy (CEA) was considered to prevent such hypoperfusion
  • but:
    • 2/3 of strokes occur within 24 hours after the procedure
    • 50% of patients experiencing stroked have no significant carotid stenosis
    • CT and autopsy studies showed that up to 60% of stroke lesions do not correlate with the side of the carotid stenosis
  • the current consensus suggests that microembolization, mainly from the aortic arch, is the predominant 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 more a predictor rather than a direct cause of perioperative stroke
  • therefore, the general indication for CEA before ECC-related procedures has been abandoned

Symptomatic stenosis

  • symptomatic stenosis of 50-99% is indicated for CEA
    • risk of stroke is high (up to 18%)
  • prefer CEA to CABG when possible (in cardiac stable patients)
    • CEA, followed by 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 (with probably increased perioperative risk)

Asymptomatic stenosis

  • there is currently no consensus on how to proceed with asymptomatic stenosis; the usefulness of CEA/CAS before open heart surgery (OHS) remains controversial
  • it is recommended not to perform revascularization in asymptomatic stenosis < 70%
  • for unilateral asymptomatic stenosis >70-80%, CAS followed by OHS (staged CAS-OHS) seems to be the safest option rather than staged CEA-OHS
    • cardiac disease must be stable enough to allow the delay of cardiac surgery for at least 4 weeks (minimum required duration of DAPT after CAS)
    • staged CEA-OHS is associated with the highest risk in the early phase due to the MI rate
  • combined procedure (CEA+OHS) may be considered
  • in patients with bilateral stenosis > 75%, staged 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 OHS
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 postpone surgery by at least 4 weeks after a 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 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 aortic atherosclerotic lesions Different types of aortic atherosclerotic lesions on TEE  Aortic atherosclerosis on CTA
    • the stroke 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)
  • a 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]
  • besides hypoperfusion injury, the main cause 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 originating  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 ~ 25-40% of patients, most often in the first 4 postoperative days
    • most cardioembolic events occur between days 2-4 after surgery
  • a history of diabetes generally increases the risk of complications
  • multiple mechanisms are involved:
    • 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 maintaining a  higher perioperative MAP (> 80 mmHg) in reducing the incidence of neurological complications [Plestis, 2001]
  • interaction between hypoperfusion and embolization was discussed earlier

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Neurological complications during extracorporeal circulation