Neurological Injury in Cardiac Surgery

The aetiology of the neurological injury seen is multifactorial and due to cerebral microemboli  and  hypoperfusion,  exacerbated  by  ischaemia  and  reperfusion  injury.

The  injury may vary from cognitive dysfunction to stroke and depends on the duration of ischaemia and whether it was regional or global.  Strategies to reduce the risk include haemodynamic management, i.e. maintaining an adequate cerebral perfusion pressure (CPP) by avoiding low mean arterial pressures (MAP) and high central venous pressures (CVP) and aiming for a higher MAP in high-risk or chronic hypertensive patients who may have altered cerebral autoregulation. 

Mild to moderate hypothermia reduces the cerebral metabolic rate and excitatory neurotransmitter release. To date pharmacological neuroprotection has had disappointing clinical results. There are a variety of monitors that have been used in the effort to identify and quantify neurological injury during cardiac surgery, such as transcranial Doppler, single- or multi-channel electroencephalography (EEG) and cerebral oximetry. Cerebral oximetry determines the saturation of blood in cerebral tissue (rSO2 ) using near-infrared spectroscopy (NIRS).  It is non-invasive, has a fast signal–response time, and has been subject to a number of randomized controlled studies. Patients that had higher morbidity had more desaturations and lower mean rSO2  levels and there was a significant inverse correlation between intra-operative rSO2  and duration of postoperative hospitalization. 

The interventions and class of evidence used to reduce the risk of neurological injury in cardiac surgery are:

• heparin-bonded cardiopulmonary bypass circuit
• epi-aortic ultrasound (Class IIb)
• modified aortic cannula
• leukocyte-depleting filter
• cell-saver processing of pericardial aspirate
• CO2  wound insufflation
• maintaining ‘higher’ MAP targets (>50 mm Hg) (Class IIb)
• non-pulsatile (versus pulsatile) perfusion (Class IIb)
• alpha-stat versus pH-stat acid–base management (Class IIb)
• minimal haematocrit target during CPB of 27% 
• thiopental, propofol, nimodipine, prostacylin, GM1 ganglioside, pegorgotein, clomethiazole (Class III)
• remacemide, lidocaine, aprotinin, pexelizumab
• ‘tight’ glucose intra-operative control
• hypothermia.