Transcript Delirium
Disordered minds and
brains?
Dr Lesley Young
Sunderland Royal Hospital
A condition affecting….
20% all hospital in-patients (40% >80yr
olds O`Regan et al 2010)
60-80% ICCU patients (50% will develop longterm cognitive deficits) Ely EDA 2008
And has……..
20-30% in-patient mortality
(10-14% for acute GI bleed, 4-5% for ACS)
30% institutionalized
Increased complication rate
Increased length of stay
3x increased risk developing dementia
Delirium
What I am going to tell you
Definitions
Why does delirium happen?
– What we can learn from mice
Recognising it
Risks and precipitants
Prevention is better than cure
Drug treatment
Prognosis and outcomes
Delirium – DSM IV
Disturbance of consciousness
reduced ability to focus, sustain or shift attention
A change in cognition or the development of a
perceptual disturbance that is not due to a preexisting dementia
Develops over a short period of time and tends to
fluctuate
Evidence that disturbance is caused by the
direct physiological consequences of a general
medical condition, substance intoxication or
withdrawal.
The get out clause……
Why do old people get
delirium with a UTI?
Aberrant stress response?
Inflammatory theory?
– Systemic infection
– Injury
– surgery
Cholinergic theory? (↓ Ach →delirium)
– Severe illness / trauma →↓ Ach
– Hypoxia/hypoglycaemia →↓ Ach
– ↑SAA →delirium
Predisposing factors
Precipitating factors
High vulnerability
Noxious insult
Low vulnerability
Mild insult
After Inouye
What we can learn from
mice (Cunningham)
Mice with neurodegenerative
dementia-type disease (ME7)
–
–
–
–
Affective (11-13 weeks)
Coginitve (12-16 weeks)
Motor (16-19 weeks)
Death (24 weeks)
Effect of inflammatory insult
on cognitive function
controls
normal+LCP
prion+LCP
Long term follow up:
accelerated decline in LCP
group
controls
prion+saline
prion+LCP
ME7 mouse studies have shown
a cognitive deficit that:
Is induced by systemic infection
Is acute onset and transient
Occurs in “demented” but not normal
mice
Affects working memory > reference
memory
Is dependent on prior microglial cell
activation
(After Cunningham EDA 2008-10)
Aging
Dementia
Prion disease
Primed microglial
cells
Location of
activated
microglial
cells
determines
dysfunction
Infection
Injury
Surgery
Other insult
Activation of
microglial
cells
DELIRIUM
Neuronal death
Disease
progression
In clinical practice.....
Identify those at risk
Prevent incident delirium
Recognise prevalent delirium
Identify and treat precipitants
Manage behaviour well for better
outcomes
But…..
Delirium is under-recognised:
– In published studies only 20-50% of
cases recorded as delirium in records
(Collins Age and ageing 2010 28% prevalent delirium detected)
Failure to recognize associated with
poor management (Young Age&Ageing 2003)
Use of cognitive screening tests can
improve recognition (Jitapunkul 1991, Anthony
Psychol Med 1982, O`Keeffe JAGS 2005, Young Age &Ageing 2003)
72.6% cases identified when cognitive screening attempted v
42.9% when not p<0.0001 (Young 2003)
Barriers to recognition
(Davies et al to
EDA 2007)
*p<0.001
Geriatrics
experience
(n=399)
No geriatrics
experience
(n=351)
28%
14%
Acute onset
89%
88%
Inattention
32%
31%
Visual hallucinations
35%
38%
Agitation
52%
49%
Aware of poor prognosis
57%
52%
Aware under-recognised
80%
80%
Adequate training *
24%
9%
Confident of diagnostic
criteria*
Aids to recognition
Cognitive screening
tests:
–
–
–
–
– CAM
– CAM-ICU
– Delirium Observation
Scale
– Neecham
– DSI
AMTS
MMSE
6-CIT
Sweet 16
Measures of attention
– Serial 7`s
– Months backwards
– Digit span
(forwards/backwards)
– Trail making
– Letter cancellation tests
Delirium screening
tools
Delirium +/- dementia?
–
–
–
–
Cognitive history
IQCODE
AD8
Visual perceptual deficits
Risk factors
Age > 75
Dementia (2/3 cases)
Severe illness
Physical frailty
Dehydration
Infection
Visual impairment
Drugs (opiates, anticholinergics)
Surgery
Alcohol excess
Renal impairment
Precipitants
Infection
Drugs
– opiods OR 2.5, benzodiazepines OR 3, dihydropyridines OR2.4,
antihistimines OR 1.8, Clegg and Young Age and Aging 2010
– Anticholinergic drugs (Tune REF, Pitkala 2007)
Dehydration or electrolyte disturbance
Immobility
Malnutrition
Intercurrent illness e.g.
Metabolic/endocrine disturbances
Organ failure (liver, renal, cardiac etc)
Neurological problems (e.g. CVA, epilepsy)
Precipitants of delirium –
prospective study General Medical in-patients
>70yrs n=87 J Laurila EDA 2009
Infections
Drugs
Metabolic disturbance
Circulatory conditions
Neurological
Other post-op
(84%)
(46%)
(47%)
(26%)
(24%)
(18%)
Delirium is multi-factorial
Prevention
Up to 40% cases may be preventable
– Early attention to or avoidance of
precipitants in those at risk
– Adopting “HELP” approach in those at
risk (Inouye NEJM 1999; 340:669-676)
Hospital Elder Life
Program (Inouye NEJM 1999)
Complications of hospitalisation:
– Delirium
– Functional decline
– Adverse drug events
25-60%
34-50%
54%
–
–
–
–
17%
15%
10%
3%
*HAI
*Falls
*Pressure sores
*VTE
Targeted, multi-component intervention
program
Help interventions
Cognitive impairment
Reality orientation
Therapeutic activities
Vision/hearing impairment
Vision/hearing aids
Adaptive equipment
Immobilisation
Early mobilisation
Minimising immobilising
equipment
Psychoactive medication use Non-pharmacological approaches
to sleep/anxiety
Restricted use of sleeping tablets
Dehydration
Early recognition
Volume repletion
Sleep deprivation
Noise reduction strategies
Sleep enhancement program
How HELP is delivered “High touch/low tech”
Inclusion criteria:
– Aged 70+
– At least one of:
Screen (by Elder
life specialist/nurse)
– MMSE
– ADL
– Test vision and
hearing
– Usual activities
MMSE<24
Mobility or ADL
impairment
Dehydration
Vision impairment
Hearing impairment
Program delivered
by volunteers
– (16 hours training, 1x4hr
shift/week for 6/12+)
Intervention
Control p
Cognitive
decline
8%
26%
<0.05 Inouye JAGS 2000
Physical
decline
14%
45%
33%
56%
<0.05 Inouye JAGS 2000
0.03 Vidan JAGS 2009
Reduced
incident
delirium
OR=0.60
RR↓ 35%
6%
OR= 0.4
Costs
↓$831
↓$1.25 million/yr
↓$121,425
Rizzo Med care 2001
Rubin JAGS 2006
Caplan Int Med J 2007
LOS
↓0.3 d/pt
Rubin JAGS 2006
Falls /1000 3.8
pt days
1.2
38%
11.4
4.7
0.02
0.002
0.03
0.005
Reference
Inouye NEJM 1999
Rubin JAGS 2006
Caplan Int Med J 2007
Vidan JAGS 2009
Inouye NEJM 2009
However….
Prevention is better than cure
– HELP (targeted multi-component
intervention) can prevent up to 40%
incident delirium
– Little evidence for improved outcomes in
prevalent delirium (Laurila, Helsinki study J Geront
2006) at 6/12:
MMSE Sl better in intervention group
QoL Sl better in intervention group
Costs of care – no different
How should we treat
prevalent delirium?
Identify and treat underlying cause
Drugs?
– Neuroleptics??
– Benzodiazepines??
– Cholinesterase inhibitors??
Investigating the cause
Infections:
– Cultures
–
–
–
–
MSU, sputum,
swabs etc
FBC
CRP
CXR
LP (only if clinical picture
points to CNS cause)
Drug review
– Stop what you can
Metabolic upsets
– U&E, LFT, Ca, TFT,
Glucose
Circulatory
– ECG
Neurological
– CT (often abnormal,
rarely diagnostic –
consider if likely acute
CNS cause)
– EEG (? Non-convulsive
status, HSE, dementia v
delirium)
Drugs
Cochrane database 2009
Benzos – not recommended
Cholinesterase inhibitors – no evidence
Antipsychotics – effective over placebo
Haloperidol effective over lorazepam
Treatment trials are rare and difficult
RCTs antipsychotics
RCTs antipsychotics
Risperidone = olanzepine
Risperidone = haloperidol
Quetiapine > placebo
Dexmetomedine > haloperidol (ICU)
Olanzepine = haloperidol (ICCU)
Olanzepine > haloperidol (chinese dementia)
Amisulpiride = quetipine
Haloperidol/chlorpromazine > lorazepam
RCP/BGS guidelines - haloperidol
EDA 2009 consensus - haloperidol
NICE 2010– haloperidol or olanzepine
Low dose, minimum duration, to alleviate distress
Cholinesterase inhibitors
Theoretical basis why Cholinestersae
inhibitors might be helpful......BUT
Several small studies – results inconclusive
Rivastigmine does not decrease duration of
delirium and may increase mortality (Eijk 2010)
– Multicentre, double-blind placebo-controlled RCT
in ICU patients with delirium
– Trial stopped after 104 patients included
because increased mortality and trend to
increased duration of delirium in treatment group
Prognosis
Traditional view:
– Short, transient, full recovery
Delirium research shows:
– Poor outcomes even with full recovery
– Independent predictor of poor outcome
Recovery from delirium (cole
EDA 2008)
55% improved at 1 month
70% improved at 6 months (i.e. 30%
not)
A substantial minority of patients don`t
recover (~10%)
Full recovery associated with good
outcomes (= no delirium)
Incomplete recovery may impair self
management
worse outcomes
20-30% in-patient mortality
30% institutionalized
Increased complication rate
Increased length of stay
3x increased risk developing dementia
Adjusted Total 1-Year Health Care Costsa
Leslie, D. L. et al. Arch Intern Med 2008;168:27-32.
Copyright restrictions may apply.
Relation between delirium
and dementia
1.Delirium
Dementia (causal)
Delirium (marker)
2. Subclinical dementia
Dementia
3. Insult
Delirium
Dementia
Probably 1+2
Conclusion
Delirium is common
Under-recognised and low priority
Associated with poor outcomes
Prevention is possible and cost
effective in those at risk
Prevention is better than cure
Infection control
Confusion control
Thank you