A middle-aged  man underwent an elective re-do aortic arch replacement for a 6.1cm ascending aortic aneurysm distal to a pre-existing composite graft. Past medical history included a Bentall procedure (metallic aortic valve replacement, aortic root and ascending aorta replacement with coronary re-implantation into the composite graft) 20 years ago. Preoperative echocardiogram showed a well seated AVR and good biventricular function. Drug history included Warfarin (target INR 2-3) and Atenolol.

Anaesthetic induction and re-sternotomy were uneventful. Cerebral oximetry (rSO₂) monitoring was utilized in this case. Cardiopulmonary bypass (CPB) was achieved uneventfully and deep hypothermic circulatory arrest (DHCA) was instituted. The patient was cooled to 18°C using CPB and icepacks. Prior to CPB and DHCA being commenced, intravenous thiopentone and methylprednisolone were administered for neuroprotection. Total DHCA time was 40 minutes and selective anterograde perfusion via the right axillary artery (chosen as it is relatively free of atheroma) was employed when rSO₂ dropped to <40% and they remained >40% for the remainder of DHCA. Total CPB time was 105 minutes.

Following successful insertion of a new graft, the patient was carefully rewarmed to normothermia and weaned off CPB uneventfully, only requiring minimal vasopressor support. The patient was transferred to the cardiothoracic critical care unit.

After optimization of cardiorespiratory physiology, correcting coagulopathy and maintaining normothermia, with strict avoidance of hyperthermia, the patient was extubated the following day. For the first 48-72 hours postoperatively, delirium was the most active medical issues and this was managed according to conventional treatment. There was no focal upper or lower limb neurology. The patient did not require any other organ system support.

Following resolution of his delirium the patient was discharged to the ward to continue his rehabilitation. Prior to discharge, at approximately postoperative days 7-10, he was complaining of loss of short-term memory, reduced attention span and difficulty with finding words. A neurology review attributed this to cognitive dysfunction but no formal tests were carried out. A neurology clinic follow-up and an outpatient MRI scan were arranged.

What are the neurological complications after cardiac surgery?

Akshay Shah

What is deep hypothermic circulatory arrest (DHCA)?

DHCA is a technique that utilizes profound systemic hypothermia (15 – 20°C) during cessation of systemic circulation to provide optimal operating conditions whilst providing cerebral protection. Indications include aortic arch surgery, complex neonatal cardiac surgery, pulmonary thromboendarterectomy, complex intracranial aneurysm surgery and surgical resection of tumours with caval infiltration.

Deep hypothermia reduces cerebral metabolic rate and oxygen consumption by 6-7% for every 1°C drop in temperature. Majority of patients will tolerate DHCA for 30 minutes without significant neurological impairment. The incidence of stroke following DHCA is reported to be 5-10%.

Classification of neurological injury

Neurological injury following cardiac surgery can broadly classified into Types 1 (focal) and 2 (non-focal).¹ Type 1 injuries consist of non-fatal stroke, new transient ischaemic attack (TIA) and brain death whereas delirium and postoperative cognitive dysfunction (POCD) are classified as Type 2 injuries.

The incidence of neurological injury depends of the type of surgery being performed and the clinical endpoint being measured. The overall incidence of stroke following coronary artery bypass graft (CABG) surgery is 1.6% and is thought to rise to 8.7% for aortic repair surgery.^{2, 3} The incidence of POCD, now the most significant frequent neurological injury following cardiac surgery, varies greatly from 10-50%. This variation in reported rates is because there is no uniform diagnosis or gold standard test battery for POCD.⁴

Pathophysiology and risk factors

The primary mechanism traditionally thought to contribute to neurological injury post-cardiac surgery was embolization – both macro and micro, during CPB. However, the Randomised On/Off Bypass trial showed no clear advantage of off-pump compared to on-pump surgery in reducing the rates of POCD.⁵

More recent work has suggested that hypoperfusion and systemic inflammatory response may also play an important role by reducing the washout of emboli.^{6, 10} The likely aetiology is multifactorial and related to various perioperative factors (Table 1). Majority of the preoperative risk factors are related to the architecture of the cerebral blood vessels.

Preoperative	Atheroma of ascending aorta Previous cardiac surgery Older age Patient co-morbidities: Previous stroke Carotid stenosis History of peripheral vascular disease History of diabetes mellitus History of hypertension Smoking history
Intraoperative	Severe hypotension Manipulation of atherosclelrotic ascending aorta CPB time >2 hours DHCA time >30 minutes Extreme haemodilution (>12% drop in haematocrit from baseline)
Postoperative	Atrial fibrillation Postoperative infection Hypoxia Delirium

Table 1. Risk factors for perioperative neurological injury following cardiac surgery.

What is Postoperative Cognitive Dysfunction (POCD)?

POCD is a decline in cognitive function following surgery and anaesthesia from the preoperative baseline level and patients often complain for deterioration in memory and attention, poor ability to carry out complex tasks and impairment in language skills.

Diagnosing POCD

At present, diagnosing POCD is difficult as there is no international consensus on diagnostic criteria and testing often involves a battery of tests to test multiple mental processes. Hence its current use is mainly limited to the research setting.

The most commonly used test statistic is the z-score – a dimensionless unit that indicates how far a subject’s performance deviates from the average performance of a control group. This score was used in the landmark International Study in Postoperative Cognitive Dysfunction (ISPOD1)⁷. In clinical practice, preoperative baseline scores are needed, with the patient acting as their own control, and POCD is defined as a score of 2 or more. Commonly used tests include:

• Visual verbal learning test – immediate recall and short-term working memory
• Concept shifting task – visual concept and visuomotor skills
• Stroop colour word test
• Letter digit coding test

POCD can be further subclassified into short-term – cognitive decline lasting up to 6 weeks post-surgery, and long term – subtle deterioration in cognitive function 6 months after surgery. Short-term POCD is more common than long-term POCD – 20-50% vs. 10-30%.⁴

POCD should also be differentiated from the other two cognitive conditions – delirium, more common in the intensive care setting, and dementia, which are distinguished by the timings of their presentation and duration of their symptoms and shown in Table 2.¹⁰

	Delirium	POCD
Onset Characteristic of onset Duration Consciousness Concentration and attention Reversibility	Hours to days Acute Days to weeks Altered but with lucid intervals Impaired Yes	Weeks to months Subtle Weeks to months Normal Impaired Yes, but can be prolonged

Table 2. Differences between delirium and POCD.

Why is POCD important?

Multiple observational studies have shown that patients who suffer from POCD have longer hospital stays and are five times more likely to be dead 1 year after surgery.⁷

In addition, patients’ perception of their health correlates directly with their neurocognitive function and POCD manifests as poor quality of life, loss of independence, and withdrawal from society. POCD even 1 week after surgery increases the risk of leaving the labour market early and if present at 3 months – increases the risk of dependency on social welfare payments and increased mortality at a median of 8.5 years.^8,9

Intensive care management for POCD

Management in intensive care involves prevention and/or attenuation of any pre-existing cognitive dysfunction. Although there are no high quality evidence interventions, pragmatic goals to optimize oxygen delivery include:

• Maintaining haemodynamic stability
• Preserving cerebral blood flow and perfusion pressure by maintaining normoxia, normocarbia and normothermia

Postoperative hypoxia of any aetiology and complications such as infection, especially chest, have been associated with higher levels of POCD. Weak evidence suggests that strictly controlling cerebrovascular and cardiovascular risk factors, for example by using lipid-lowering agents and beta-blockers, may reduce POCD.¹⁰ These can be instituted in the intensive care setting.

Other strategies to reduce iatrogenic POCD include avoiding or using minimal sedation, promoting good sleep hygiene and early physical rehabilitation.

Pre and intra-operative management strategies include identification of high-risk patients, pharmacological protection for example using agents such as volatiles, local anaesthetics, and methylprednisolone, avoiding hypergylcaemia, anterograde/retrograde perfusion during prolonged DHCA and using various monitors such as cerebral oximetry and bi-spectral index to guide haemodynamic management. The evidence for all these interventions is experimental and/or weak at best and a detailed review can be found elsewhere.¹¹

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Lessons learnt

• Neurological complications, in particular POCD, are common after cardiac surgery and the incidence may continue to rise with an increasing ageing and high-risk population.
• The pathophysiology is multi-factorial and the association with CPB appears to be overstated. Perioperative management strategies should perhaps be targeted towards identifying high-risk patients, avoiding hypoperfusion and attenuating the inflammatory response.
• There, as yet, appears to be no clear consensus on the diagnostic criteria for POCD.
• The long-term implications of POCD are significant to both patients and healthcare services.
• Strategies such as optimizing cerebral oxygen delivery, and aggressively treating postoperative complications such as atrial fibrillation and infection may be effective in reducing POCD.

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References

1. Eagle KA, Guyton RA, Davidoff R et al. ACC/AHA guidelines for coronary artery bypass graft surgery: executive summary and recommendations. Circulation 1999; 100: 1464–80.
2. Tarakji JG, Sabik JF, Bhudia SK et al. Temporal onset, risk factors, and outcomes associated with stroke after coronary artery bypass graft surgery. JAMA 2011; 305: 381-90.
3. McKhann GM, Grega MA, Borowicz LM et al. Stroke and encephalopathy after cardiac surgery: An update. Stroke 2006; 37: 562-71.
4. Newman MF, Kirchner JL, Phillips-Bute B et al. Longitudinal assessment of neurocognitive function after coronary artery bypass surgery. NEJM 2001; 344: 395-402.
5. Shroyer AL, Grover FL, Hattler B et al. On-pump versus off-pump coronary artery bypass surgery. NEJM 2009; 361: 1827-37.
6. Caplan LR, Henericci M. Impaired clearance of emboli is an important link between hypoperfusion, embolism and ischaemic stroke. Arch Neurol 1998; 55: 1475-82.
7. Moller JT, Cluitmans P, Rasmussen LS et al. Long-term postoperative cognitive dysfunction in the elderly: ISPOCD1 study. Lancet 1998; 351: 857-61.
8. Newman MF, Grocott HP, Mathew JP et al. Report of the substudy assessing the impact of neurocognitive function on quality of life 5 years after cardiac surgery. Stroke 2001; 32: 2874-81.
9. Steinmetz J, Christensen KB, Lund T et al. Long-term consequences of postoperative cognitive dysfunction. Anesthesiology 2009; 110: 548-55.
10. Van Harten AE, Scheeren TWL, Absalom AR. A review of postoperative cognitive dysfunction and neuroinflammation associated with cardiac surgery and anaesthesia. Anaesthesia 2012; 66: 280-93.
11. Tan AMY, Amoako D. Postoperative cognitive dysfunction after cardiac surgery. CEACCP 2013; doi:10.1093/bjaceaccp/mkt022