Central Nervous System

Stroke is the commonest neurological complication after cardiac surgery, occurring through embolism or hypoperfusion. The incidence of clinically relevant stroke has decreased to under 2% after CABG and under 4% after single valve replacement, despite the demographic increase in the proportion of elderly at-risk patients. Postoperative diffusion-weighted MRI scans demonstrate clinically silent new lesions in up to 18%. Valve replacement and combined CABG and valvular surgery procedures carry a higher risk of causing embolic territorial and branch infarcts, whereas prolonged cardiopulmonary bypass increases the risk of watershed infarcts related to hypoperfusion. In most cases currently, there is no acute active treatment as major surgery is a contraindication for thrombolysis, but the increasing availability of emergency clot retrieval may change the situation. Stroke associated with left ventricular assist devices has recently been shown to benefit from endovascular treatment, if recognised early. One likely consequence will be that rapid diagnosis in patients evidencing a neurological focal deficit on awakening becomes necessary more often in the near future, increasing the need for imaging. Ischaemic and haemorrhagic stroke cannot be differentiated clinically, so the different management mandates CT scanning of the brain, if emergency MRI is not feasible. Specific locations of ischaemic stroke are associated with particular risks, such as ‘malignant’ complete MCA territory stroke with the risk of life-threatening hemispheric swelling, or cerebellar stroke with the risk of hydrocephalus and brain stem compression; both these forms of stroke have high fatality if diagnosed late, but often have good outcomes if treated with prompt surgical decompression.

Intracranial haemorrhage is infrequent in cardiac surgery, and is related to a combination of intentional treatment and effects of bypass on platelet function and clotting factors, especially in patients with previously unrecognised predisposing conditions (Figure 46.1). The location of haemorrhage can be intraparenchymal, subdural, epidural and subarachnoid, and is often atypical. Intracranial haemorrhage warrants neurosurgical consultation and some cases may need decompression.

Figure 46.1 A 39 year old female admitted for redo pulmonary endarterectomy. Postoperatively she was heparinised, but also had low platelets (66 × 10⁹). Failure to awaken, and right sided weakness prompted imaging. CT showed subdural haemorrhage and bleeding into two pre-existing, unrecognised arachnoid cysts. (a)–(e) Initial CT scans; (d) tonsillar herniation into the foramen magnum; (e) upward transtentorial herniation; (f), (g) CT post hemicraniectomy and cyst decompression shows improvement of midline shift.

Encephalopathy is an umbrella term for diffuse brain dysfunction that can be due to multiple different aetiologies. In the acute phase after surgery, encephalopathy manifests as failure to awaken, and global hypoxia or ischaemia of the brain needs to be differentiated from sedative overhang. Elderly patients or those with cerebrovascular disease are at greater risk of encephalopathy. Patients scheduled for CABG are a population with risk factors for cerebrovascular disease, with a high prevalence of silent infarcts on preoperative MRI of the brain. A clinical diagnosis of global encephalopathy demands the absence of a focal neurological deficit, which makes a careful examination of oculomotor and other cranial nerve functions important. Dysconjugate eye movements imply the presence of a focal brain stem lesion, for instance stroke in the basilar distribution, which may go undetected in routine CT of the brain. Multiple simultaneous emboli can simulate global brain dysfunction, making imaging of the brain mandatory as well as extensive metabolic and infectious screening in prolonged encephalopathy. Negative CT but persistent failure to awaken will mean an indication for MRI of the brain and/or electrophysiological studies. Lumbar puncture may be needed after imaging, in the early postoperative period, to exclude subarachnoid haemorrhage, and in the later postoperative period to exclude infection.

Encephalopathic patients, when they awaken, may have persistent confusion or delirium, a fluctuating conscious state, or recurrent agitation and hallucinations. Repetitive movements such as tremor, asterixis, choreoathetosis or myoclonus are frequent, and are often suspected to be epileptic seizures. The clinical diagnosis or exclusion of epileptic seizures versus movement disorders, stereotypies or paroxysmal dysautonomia is notoriously unreliable. EEG is mostly needed to confirm the suspicion and make the indication for anticonvulsant drugs. Even in the absence of abnormal movements or stereotypes, a prolonged EEG may be necessary to exclude non-convulsive status epilepticus (NCSE). This condition has only recently been recognised and its incidence in cardiosurgical patients is unclear, but it has been shown to be prevalent in neurotrauma and in sepsis patients. A fluctuating dyscognitive state may be the only clinical sign of NCSE, and the features may be so unspecific that only EEG may differentiate it from other causes of delirium.

Posterior reversible encephalopathy is a syndrome of vasogenic oedema affecting predominantly white matter, more often the posterior region of the brain, and is diagnosed by MRI. It is occasionally seen in the immediate postoperative phase where it can occur as a form of ‘reperfusion syndrome’, for example after repair of aortic stenosis, after carotid endarterectomy or after transplantation when there is a rapid shift of arterial pressures. More often, in patients who have undergone transplantation, PRES is related to toxicity of calcineurin inhibitors, in particular tacrolimus, where a pronounced tremor is often a feature, or to many other drugs (Figure 46.2).

Figure 46.2 A 29 year old patient post double lung transplant. Agitation and visual hallucinations developed shortly after initialising the full dose of tacrolimus. CT scan was unremarkable. MRI shows PRES with symmetric high posterior white matter signal in FLAIR image sequence.

Optic neuropathies are uncommon but well-recognised complications of cardiac surgery. Infarction of the optic nerve results in permanent monocular loss of visual acuity and visual field defects, with optic disc swelling (anterior optic neuropathy) or without (posterior optic neuropathy). A monocular disturbance of vision needs to be differentiated from incongruous hemianopia due to infarction affecting the optic tracts, which does not affect the pupillary reaction and where the visual field defect in each eye differs in size. Infarction of the visual cortex causes homonymous hemianopia with an identical visual field defect in both eyes.

Peripheral Nervous System

Brachial plexus injury causes denervation in the distribution of multiple peripheral nerves, and after median sternotomy with sternal retraction a lower brachial plexus injury of varying severity occurs in up to 5% of patients. The majority are mild and transient, with sensory and motor symptoms resembling ulnar nerve injury, although findings on careful examination may show a Horner’s syndrome, or sensory deficits and reflex abnormalities exceeding the distribution of a single peripheral nerve. Persistent and severe deficits warrant neurophysiological examination, which may help prognostication by estimating the degree of axonal injury versus demyelination. Intraoperative monitoring of sensory nerve conduction may help to avoid brachial plexus injury, and identify factors which make brachial plexus injury less likely, such as minimising the opening of the sternal retractor, caudal positioning of the retractor and reducing asymmetric traction. Transient injury to sympathetic fibres through ipsilateral jugular venous cannulation causing Horner’s sign, but with no abnormalities in the arm, is a differential diagnosis to partial lower brachial plexopathy.

The phrenic nerve passes through the mediastinum adjacent to the pericardium and is therefore vulnerable to injury during surgery. The frequency of unilateral diaphragmatic weakness due to phrenic nerve injury may reach 10% after cardiac surgery. Diaphragmatic weakness causes weakness of inspiration and atelectasis, and predisposes to postoperative respiratory complications, especially in the presence of pre-existing pulmonary disease. Most cases recover within months, but weakness may persist if there is significant axonal degeneration, as with nerve transection. Rare bilateral phrenic nerve palsy causes failure to wean from the ventilator.

Unilateral recurrent laryngeal nerve injury causes dysphonia; the left side is more often affected due to its longer intrathoracic course. Bilateral laryngeal palsy leads to severe stridor and aspiration. Several mechanisms can be suspected, from central venous catheterisation to traction along the nerve’s intrathoracic course, for instance traction on the oesophagus, subclavian arteries, or on the heart. Other mono‑ neuropathies have been described related to nerve compression or trauma during prolonged surgery, including ulnar, radial, long thoracic, spinal accessory, peroneal, lateral femoral cutaneous, and facial nerves. Most of these are related to typical nerve compression sites, and are seldom persistent.

Intensive care unit acquired weakness (ICU-AW) is a complication which was originally named critical illness polyneuropathy, but is now recognised to affect primarily muscle at least as often, causing an acute or subacute myopathy. The exact causation remains unclear, but ICU-AW is most often associated with prolonged ventilation, sepsis and use of steroids and muscle relaxants. Muscle biopsy findings are variable, with some cases showing only Type 2 fibre atrophy, which is an unspecific abnormality, others showing necrotising myopathy or acute myosin loss. The clue to diagnosis is a patient who after prolonged ventilation is tetraplegic, fails to wean, but has relatively preserved eye and often facial movements. Nerve conduction studies are often normal, electromyography may be myopathic but is often unspecific, and muscle biopsy may be needed for confirmation. Crucially, CNS pathology, including spinal cord damage, has to be conclusively excluded.

Guillain–Barré syndrome (GBS), an autoimmune acquired demyelinating neuropathy, may rarely occur after cardiac or other surgery. In the chronic postoperative phase GBS has been described as a consequence of CMV reactivation after cardiac transplantation or as a symptom of graft-versus-host disease. Neuropathy after transplantation can be caused by tacrolimus toxicity, or by other commonly used neurotoxic medications such as amiodarone.

Cognitive Decline after Cardiac Surgery

Immediate postoperative neuropsychological impairment in the absence of a structural defect is common but reversible over the course of the days following surgery. A more persistent cognitive impairment, however, wears off over weeks or months; it is considered comparable to cognitive problems after non-cardiac surgery, possibly due to brain injury at a cellular level. Better cognitive performance is seen at 3 months after CABG surgery performed off pump compared with patients undergoing bypass, with a risk of cognitive decline reduced from 29% to 21%, but the difference becomes insignificant after 12 months (30.8% versus 33.6%) and currently no surgical technique has been shown to be protective.

Delayed cognitive decline occurring over the 5 years after CABG surgery has been described by various authors. However, comparative studies have demonstrated a similar change in patients treated with angioplasty and no difference between neuropsychological performance in patients treated with bypass CABG and with off-pump CABG. Therefore, the theory that the delayed decline is causally linked to CABG surgery remains unproven, although it seems that cognitive decline may be linked to an accumulation of vascular risk factors, and to the patients’ preoperative conditions. The best preventative measure is therefore meticulous attention to the control of vascular risk factors postoperatively, and no decline has been demonstrated where this was the case. Microembolic brain injuries have been implicated in the genesis of delayed Alzheimer dementia after cardiac surgery, but there is currently no evidence that patients who undergo cardiac surgery are really at increased risk for dementia or Alzheimer’s disease, and the significance of microemboli is not yet established.