3. Postoperative Cognitive Dysfunction and Delirium Flashcards
Intro
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.
Delirium:
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
Causes
Sequealae
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:
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.)
CAM-ICU
- Acute change / Fluctuating mental status
- Inattention
Squeeze my hand on - Altered LOC
RASS - Disorganised thinking
risk factors for Delerium
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.
Sleep in ICU
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:
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):
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.
Incidence
: 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
Risk factors for POCD
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
Aetiology of POCD
? 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.
Immunity and the role of inflammatory mediators
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
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.
Management of POCD:
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).
