3. Postoperative Cognitive Dysfunction and Delirium

The three commonest disorders of mental function in the surgical and critical care patient are postoperative cognitive dysfunction (POCD), delirium and dementia. exist. Dementia is a state of chronic and progressive brain failure which is a significant risk factor for delirium and may well be exacerbated by the factors responsible for the other two conditions, but otherwise it is unlikely to feature in the oral the underlying causes of POCD remain speculative, and the numerous confounding variables mean overall that the data are not robust. The oral may therefore feel rather superficial, but the information in the following account should be sufficient.

this can most simply be defined as any acute disturbance of cognitive function. The most familiar postoperative presentation is the typical hyperactive psychomotor state with restlessness, irritability, inability to respond to requests or commands, and disconnection from the environment. Delirium, however, can also be hypoactive and may present in a patient who superficially is calm but who also has inattention and disconnection

metabolic derangements, acute febrile and critical illness, hypothermia, prescribed and illicit drugs, and by other factors such as sleep deprivation. associated with a threefold increase in postoperative mortality, increased infection rates and lengthened hospital stay.

Delirium in critical care: this is believed to affect up to 60–80% of ventilated patients in intensive care. Hypoactive delirium is much more common than hyperactive, and is probably undiagnosed. (There are detailed diagnostic and assessment criteria that have been described, such as CAM-ICU, but any proper consideration of these would take up too much time in the oral.)

• Acute change / Fluctuating mental status • Inattention Squeeze my hand on • Altered LOC RASS • Disorganised thinking

include increasing age, pre-morbid abuse of alcohol or other substances, a history of depression or cognitive impairment, smoking (which may relate to nicotine withdrawal) hearing or visual deficits which increase the probability of disorientation.. In addition, there are the effects of the critical illness itself, such as sepsis, multi-organ dysfunction and metabolic derangement, on top of which are superimposed immobilization, prolonged sedation and sleep deprivation.

It is estimated that patients in critical care ‘sleep’ for only 2 hours in 24, with about 5% rather than the usual 25% being rapid eye movement (REM) sleep.

Critical care delirium can be reduced by substituting sedation with benzodiazepines such as dexmedetomidine, by instituting sedation breaks, by reinforcing orientation and by endeavouring to reinstitute a more normal sleepwake cycle. None of this is easy.

Postoperative cognitive dysfunction (POCD): this can also be defined as a disturbance of cognition, but it is one that is temporally related to surgery and anaesthesia. Moreover, a proper diagnosis of POCD can be made only if there has been a baseline pre-operative neuropsychiatric evaluation with which postoperative cognition can be compared. Technically this is important because POCD can be very subtle and it may affect only one or two domains of cognition, which include memory, perception, attention span, information processing, language understanding abstract thinking.

: the difficulty in accurate diagnosis means that the true incidence of POCD is hard to determine. Although postoperative mental deterioration has been recognized anecdotally for decades, it was not until the late 1990s that the phenomenon was investigated in detail. This came in the form of the International Study of Post-Operative Cognitive Dysfunction (ISPOCD-1) that was published in 1998 and which evaluated more than 1,200 patients aged over 60 years undergoing major noncardiac surgery and, crucially, who had completed baseline pre-operative psychometric tests (Lancet 1998, 351: 857–61). Cognitive dysfunction was present in 25% of the patients at discharge and in 10% at 3 months. A later study using a similar trial design found an incidence of 30–40% (in 1,064 adults of all ages), which reduced to 13% at 3 months in the over-60 age group

Association of lower educational attainment with POCD. Others include increasing age studies tend to concentrate on patients >60 years major and prolonged surgery, high alcohol intake and/ or other substance abuse pre-existing degrees of mild cognitive impairment and co-morbidity

? underlying cause neuronal pathology of some kind, and intuitively it would seem logical that hypotension and/or hypoxaemia could compromise cerebral perfusion and oxygen delivery - ISPOCD-1 study amongst others concluded that there was no correlation between episodes of perioperative hypotension or hypoxia and POCD. concern about the effects of general anaesthetics on both the developing and the ageing brain In cardiac surgery it has been suggested that the high incidence of POCD (which is quoted in some studies as being as high as 30–80% immediately post-surgery and 10–60% at 3 months) may be due to microemboli generated during cardiopulmonary bypass. that an inflammatory response may underlie the development of POCD.

inflammatory mediators, starting with the release of tumour necrosis factor (TNF-α) and the production of cytokines, particularly interleukin-1β (IL-1β), which breach the blood–brain barrier and allow leucocyte migration into the hippocampus consensus that an inflammatory response probably does underlie some of these postoperative neurological manifestations.

Cerebral oxygen desaturation: near infrared spectroscopy has demonstrated that ‘silent’ episodes of cortical oxygen desaturation can occur even while haemodynamic indices show little alteration and peripheral oxygen saturation remains unchanged. Should cerebral oxygen monitoring become routine then any causal link between silent hypoxia and POCD may become much clearer, but in the meantime it must remain speculative.

it may be that in due course pro-inflammatory modulators could have a role in attenuating POCD, assuming that the condition is dynamic and not due to a single temporal event. Until the aetiology of the condition has been better elaborated, its management is supportive, with the treatment of any obvious acute medical precipitants, including uncontrolled pain, and the avoidance of any interventions which might make it worse. This would usually include sedative or neuroleptic drugs. If a patient is acutely agitated (which makes delirium a more likely diagnosis), then haloperidol is the most commonly used agent. (It is a dopamine D2-receptor antagonist with a prolonged half-life of 20–36 hours. The intravenous dose is 0.5–1.0 mg repeated every 15 minutes and titrated against response).

• Physiological effects of anaesthesia and surgery 2.Pharmacological effects Drugs Withdrawal • Specific patient events

ABC – exclude emergency causes, e.g. airway obstruction/respiratory distress Physiological effects of anaesthesia and surgery
Hypoxaemia
Hypotension
Hypercapnia/Hypocapnia
Metabolic -Hypoglycaemia -Hyponatraemia -Hypercalcaemia
Pain or discomfort (including bladder distension)
Sepsis
Hypothermia/Hyperthermia _______________________________________ Pharmacological effects Drugs -Anticholinergics -Opioids -Ketamine/propofol -Benzodiazepines -Volatiles Withdrawal -Delirium tremens -Benzodiazepines Specific patient events
Pre-existing cognitive dysfunction
CVA (emboli – especially with by-pass)
Hepatic failure
Renal failure

Post-operative confusion may be multi-factorial. Many studies are conflicting over causation. There are changes in neurotransmitter levels (catecholamines and the cholinergic system). Increased cortisol levels post-operatively may play a role in post-operative delirium in the elderly. The incidence reported varies considerably between studies. ∼25% of patients over 60 years of age will have evidence of cognitive dysfunction at 1 week. Emergency surgery and increased blood loss are implicated

• Hypoxic • Anaemic • Ischaemic • Histotoxic

Hypoventilation is the most common cause and can itself result from a number of peri-operative situations:
Residual effects of anaesthetics, benzodiazepines and/or opioids
Incomplete reversal of neuromuscular blockade
Airway obstruction laryngospasm, laryngeal oedema, reduced conscious level, retained airway packs, etc.)
Pain, particularly from thoraco-abdominal procedures can also lead to hypoventilation. Atelectasis and lobar collapse Pulmonary oedema Pneumonia (and aspiration pneumonitis) Bronchospasm (and anaphylaxis) Pneumothorax Pulmonary embolism Shock Pre-existing lung disease It is important to note that there is a significant alteration in normal respiratory physiology with advancing age, e.g. closing capacity encroaches on FRC, reduced elastic recoil, increased V/Q mismatch, all of which result in much less respiratory reserve and faster onset hypoxia.

After giving supplementary oxygen, perform an examination of the patient following an ABC approach. Review the patient’s medical and operative history. Pay particular attention to what drugs had been given and intra-operative haemodynamic and respiratory stability. Urinary retention should be remembered as a frequently encountered and easily remedied cause of confusion. Arterial blood gases, FBC, U & Es, chest X-ray, and ECG may form part of the assessment. Lateralising neurological deficits will require further investigation with CT scan if persistent.

should be reserved for patients with profound delirium and for those with withdrawal Haloperidol 0.5–5 mg i.v. (low dose in elderly patients) Benzodiazepines may be necessary but current evidence suggests that these drugs are more of a cause of the problem than a solution Chlordiazepoxide 10–20 mg p.o. for alcohol withdrawal. Thiamine may be added if there are concerns regarding Korsakoff’s psychosis