FRCA Notes

Neurological Complications of Cardiac Surgery

Resources

  • Neurological complications following cardiac surgery are an important cause of post-operative morbidity and mortality
  • Classified by the ACC/AHA as either Type 1 or Type 2
  • The incidence of Type 1 complications has stabilised, with an increasing focus on Type 2 injury
Type 1 Type 2
Death (up to 3%) Post-operative cognitive impairment
Stroke (1.2%) or TIA Delirium / agitation
Focal neurological deficits e.g. visual field defects
Coma
Seizures (especially in children)
Emergency of primitive reflexes

Post-operative cognitive dysfunction (POCD)

  • Post-operative cognitive dysfunction includes decreased intellect, impaired memory
  • It is the most common neurological sequela post-cardiac surgery
  • 20 - 50% will experience short-term POCD, 10 - 30% will experience long-term POCD

  • Hard to diagnose
  • Typically requires a decline from baseline of >20% (or >1 standard deviation) on two or more neuropsychological tests
  • May be a short-term phenomenon lasting <6 weeks, or longer-term with changes still present at 6 months

Peripheral nerve injuries

Nerve injury Cause
Paraplegia Spinal cord ischaemia
Brachial plexopathy Excessive sternal retraction
Ulnar neuropathy Improper positioning
Phrenic nerve injury Cold cardioplegia | IMA harvesting
Intercostal nerve injury If intercostal incision made
Saphenous nerve injury During vein harvesting


Type 1 injury

  • Type 1 complications are embolic-ischaemic in nature
  • It is caused by micro-emboli; small gas emboli, platelet fragments, cholesterol particles or fragments of atheroma
    • These particles are typically <200μm in diameter and aren't filtered out by in-line filters
    • Typically dislodged from the aorta during cannulation
  • The presence of pre-existing cognitive or neurological disease as risk factors suggests already-diseased cerebral circulation is further compromised by micro-emboli

Type 2 injury

  • Type 2 complications relate more to damage from microvascular insufficiency and impaired cerebral metabolism
  • The risk factors for type 2 injury include low-flow states, so limiting the periods of intra-operative hypotension may help reduce risk of Type 2 injury


Patient factors Surgical factors
Advanced age >70yrs Use of CPB
Male gender Use of IABP
Previous CVA/TIA/cognitive impairment Long duration of surgery / prolonged deep hypnotic time
Arterial hypertension CPB micro-emboli (dose-response relationship)
Proximal aortic atherosclerosis Rapid rewarming (impairs cerebral autoregulation)
Diabetes mellitus Failure to maintain CPP intra-operatively
Alcohol excess
Cardiac comorbidities e.g. HF, AF, previous CABG
  • One can identify some of those at risk of neurological injury with pre-operative CT head, MRI brain or carotid Doppler testing

Surgical

  • Identification and avoidance of aortic atheroma by pre-operative imaging
  • Avoiding multiple aortic cross-clamping

CPB-related

  • Avoid CPB
  • Minimise exposure/duration of CPB
  • Avoid air entrainment by use of bubble traps and embolus filters
  • Maintain adequate CPP and flow
  • Use of arterial line filter
  • Avoid hyperthermia during re-warming

Physiological

  • Maintain adequate MAP
  • Maintaining normoglycaemia

Monitoring

  • Cerebral oximetry using near-infrared spectroscopy (NIRS) to monitor regional tissue oxygenation (rSO2)
  • Processed EEG e.g. BIS, which allows reduction in cumulative deep hypnotic time and better titration of anaesthetic agents with respect to haemodynamics
  • Transcranial Doppler

Pharmacological methods

  • Propofol or barbiturate induction
  • Volatile agents may play a role through pre-conditioning effect
  • NMDA antagonists i.e. ketamine, magnesium
  • Steroids

  • Although opioids contribute to delirium they do not increase risk of POCD
  • Although lidocaine was historically thought to be neuroprotective, it is not evidence-based and may increase cognitive decline in diabetic patients