Download Dementia & Delirium

Dementia & Delirium
Dr Sue Hazel
Consultant Geriatrician
RBCH Trust
Scope of the Talk
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What is dementia?
The different forms of dementia
Symptoms & diagnosis of dementia
Causes of memory problems other than
dementia
What is delirium?
Model of the Memory system
Sensory Input
Working Store
Seeing
Short-term memory
Hearing
(working memory)
Long-term Store
Long-term memory
Feeling
Implicit memory
Explicit memory
Skills
Habits
Priming
Episodic Memory
Classical conditioning
Events
Facts and source
Semantic Memory
General knowledge
Memory Line
DEATH
Having to
move
home
Death of spouse
MEMORIES
Retirement
Grandchildren
Loss of a parent
Having children
Getting Married
Leaving school
1st day at
school
BIRTH
Starting work
MEMORIES
Changing
school
Dementia
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Diagnosis ICD-10 & DSM-IV:
Multiple cognitive defects which must include:
Amnesia
Functional impairment
Clear consciousness
Clear change from previous level
Long duration (>6 months)
Who gets Dementia?
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There are about 820,000 people in the UK with
dementia
Dementia mainly effects people over 65 years of age
There are about 18,500 people in the UK under 65
who have dementia
It effects men & women equally
In a few cases the diseases that cause dementia are
inherited
Prevalence of Alzheimer’s Disease
Prevalence of Alzheimer’s
disease in an aging
population.
Prevalence increases
dramatically with age and
approaches 50% of those
over 85 years old.
(Adapted from Evans et al.,
1989.)
Forms of Dementia
Alzheimer’s disease
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Vascular Dementia
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Dementia in Parkinson’s & Lewy Body Dementia
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Frontotemporal Dementia
Neurological dementias:
Normal Pressure hydrocephalus
Cerebral Vasculitis
Corticobasal Degeneration
Dementia in MS
HIV/AIDS Dementia
Huntington’s Dementia
Prion Diseases - CJD
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Prevalence of the forms of dementia
Cause
Percentage
Alzheimer’s disease
55%
Vascular dementia
20%
Dementia with Lewy Bodies
15%
Frontotemporal dementia
5%
Rarer causes (all)
5%
‘Ich habe mich
verloren’
Auguste Deter
Alzheimer’s Disease –
Diagnosis
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Fulfil criteria for dementia syndrome
Insidious onset
Gradual progression
No focal neurological signs
No evidence for a systemic or brain disease
sufficient to cause dementia
Alzheimer’s Disease - features
Cognitive symptoms:
Amnesia – early features are impaired new learning & recall,
disorientation in time & place, late features include impaired
semantic memory & visuospatial memory
Aphasia (dysphasia) – deficits in cortical language function –
early features are nominal aphasia, verbal perseveration, late
features include mutism & echolalia
Apraxia (dyspraxia) – common forms are: ideomotor
dyspraxia (cannot carry out motor function to command),
dressing dyspraxia, constructional dyspraxia (inability to
copy intersecting pentagons or draw a clockface)
Cognitive Features
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Agnosia especially visual agnosia (inability to recognise
objects) & prosopagnosia (inability to recognise faces)
Frontal-executive function – inflexible (concrete thinking).
Difficulties with problem solving or planning, difficulty
correctly sequencing behaviour.
Dyslexia
Dysgraphia
Acalculia
R/L disorientation
Non-cognitive symptoms
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Psychotic:
Delusions often paranoid
Misidentification
Hallucinations commonly visual
Mood:
Depression
Anxiety
Euphoria
Behavioural:
Apathy
Over activity
Aggression
Non-cognitive symptoms
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Neurovegetative Symptoms:
Sleep disturbance, day-night reversal in about 30% patients
Eating: poor oral intake or binge eating
Sexual disinhibition
Personality change
Physical Symptoms:
Primitive reflexes (grasp & palmomental reflexes)
Incontinence (often a late feature in AD)
Weight loss
Deterioration in gait
Falls
Dementia with Lewy Bodies (DLB)
Lewy bodies: neuronal inclusion bodies found in:
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The substantia nigra, locus coerulus, amygdala &
olfactory bulb in PD & in:
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Cortical areas especially the frontal & temporal
neocortex in DLB
Dementia with Lewy Bodies (DLB)
Evidence of dementia with:
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Two of the following core features are essential in order
to diagnose possible DLB:
Fluctuations: with marked variation in cognition, attention,
conscious level, mobility & coherence probably due to
cholinergic mechanisms
Spontaneous features of parkinsonism: rigidity,
bradykinesia & tremor with adverse reactions to dopamine
antagonists
Visual hallucinations: usually well formed & detailed:
people & animals. Vivid dreams which may involve REM
sleep behaviour disorder where people enact their dreams.
Dementia with Lewy Bodies (DLB)
Other supportive features:
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Falls
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Syncope
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Systematised delusions
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Hallucinations in modalities other than vision
DLB vs. PD & dementia
‘Rule of thumb’ if the symptoms of dementia
precede or present within one year of the diagnosis
of PD then the diagnosis is likely to be DLB
Vascular Dementia
I. Criteria for the clinical diagnosis of probable
vascular dementia:
1. Dementia
2. Cerebrovascular disease: focal signs on neurological examination
+/- evidence of cerebrovascular disease on CT or MRI
3. A relationship between the above 2 disorders:
(a) Onset of dementia within 3 months of a stroke
(b) Abrupt deterioration in cognitive functions or fluctuating stepwise
progression of cognitive deficits
Other features:
Gait disturbance
Falls
Urinary symptoms
Vascular Dementia
Periventricular
small vessel
disease
(Ischaemia)
Frontotemporal dementia - Features
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Usual age of onset - < 65 years, often a family history
Behavioural disorder – insidious onset, early loss of insight, early signs
of disinhibition & lack of judgement, mental rigidity, stereotypical
behaviour, hyperorality
Affective Symptoms – depression, anxiety, apathy, hypochondriasis &
somatisation
Speech Disorder – reduction in speech, perseveration, echolalia, mutism
Physical signs – early primitive reflexes, early incontinence, low & labile
blood pressure
Investigations – normal EEG, abnormalities of frontal & anterior
temporal lobe on imaging
Diagnosing Dementia
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Differential diagnosis:
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Delirium
Learning disability
Depression – ‘pseudo-dementia’
Previous brain injury e.g. trauma, stroke
Aging
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Memory Complaints in Aging, Depression
& Dementia
Aging
Depression
Dementia
Complaint
May report a mild or
subtle memory
problem
More likely to complain
about their memory
Expresses variable, nonspecific memory
problems or may be
unaware
Functional
Interference
No interference with
daily functioning
Minimal interferencefunctional problems
more likely due to mood
disorder
Clearly interferes with
daily functioning:
missing appointments,
unpaid bills, medication
compliance
Cognitive
Status
Onset of problem
unclear. Cognition is
normal on testing
Onset may be reported
Gradual onset &
as sudden, subtle deficits progression
on testing only
Cognition impaired on
testing
Mood
Not associated with
depression or anxiety
Associated with a
depressed or anxious
mood
May be associated with
fluctuating or blunted
affect
Diagnosing Dementia –The History
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Duration, fluctuation, progression of problems
Forgetfulness / repetitiveness
Misplacing or losing things
Reasoning & judgement e.g. finances / Insight
Safety concerns
Change in personality or behaviour
Night time disturbance
Loss of hygiene
Falls
PMH & medication compliance
Diagnosing dementia –
mental state examination
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Appearance & behaviour
Speech
Mood
Abnormal beliefs (delusions)
Abnormal perceptions (hallucinations)
Personality – present & previous
Insight
Cognition: MMSE, Frontal Lobe Score, ADAS-Cog,
ACE-R
Diagnosing dementia –
Physical Examination
A full physical examination should be carried out
looking for:
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Focal neurological weakness
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Evidence of parkinsonism
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Evidence of dyspraxia
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Evidence of anaemia or hypothyroidism
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Evidence of intercurrent illness causing a delirium
Diagnosing Dementia- Investigations
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Bloods: FBC, U&Es, LFTs, Calcium, Glucose,
TFTs, B12, Folate
CT or MRI brain if you suspect: cerebral tumour,
normal pressure hydrocephalus, subdural
haematoma, & to assess degree of vascular change
DaTSCAN (ioflupane SPECT) if suspect DLB but
clinical uncertainty
EEG: generally not helpful but is abnormal in
classical sporadic Creutzfeldt-Jacob Disease
(triphasic waves)
DaTSCAN in DLB
Normal DaTSCAN
DaTSCAN in PD & DLB –
Decreased dopaminergic
neurones in the striatal area
Management of Dementia
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Assess for physical illness & depression
Establish functional abilities & any risks
Carer assessment
Education of carers
Planning for future care
Cholinesterase inhibitors
Management of behavioural problems
Terminal care
Anti-dementia drugs
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Cholinesterase inhibitors:
Donepezil:
A reversible inhibitor of acetyl cholinesterase
Galantamine: As for Donepezil + nicotinic receptor agonist
Rivastigmine: Non-competitive inhibitor of acetyl cholinesterase,
Licensed for dementia in PD
N-methyl-D- aspartate (NMDA) receptor antagonist:
Memantine: Some evidence it is effective in more advanced
dementia, & beneficial in behaviourally disturbed AD in
conjunction with a cholinesterase inhibitor
What do NICE say? (March 2011)
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The cholinesterase inhibitors can be prescribed for clinically
mild or moderate AD or those with an MMSE 10-24
Memantine is recommended as an option for managing
people with moderate AD who are intolerant / have a
contraindication to cholinesterase inhibitors or for severe AD
Only specialists in Old Age Psychiatry or those geriatricians
with specific expertise may start therapy
Patients need to be reviewed at 3/12 & then 6/12 intervals to
assess response with an MMSE score, a global functional &
behavioural assessment & carer views to be considered
If benefit noted they may continue on therapy until the
MMSE<10
Management of Aggression
Environmental
Interventions
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Create a calm
environment
Turn off TV / radio
Take person to a
quiet area
Remove objects
that can be used as
weapons
Dim lighting if
possible
Behavioural
Interventions
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Talk slowly & softly
Never turn your back on
the patient
Place yourself between
the exit & the patient
Innocuous questions e.g.
what did you have for
lunch can be a
distraction
Convey concern
Allow patient to
verbalise feelings
Use restraint if
necessary
Medical interventions
•Consider a physical cause
for agitation e.g.
constipation, pain, urinary
retention
•Consider issues relating
to the patient’s mental
capacity / DOLS
•Review medications as
appropriate
Pharmacological interventions
Indications for sedation:
 In order to carry out essential investigations or
treatment
 To prevent a patient endangering themselves or
others
 To relieve distress in a highly agitated or
hallucinating patient, after assessing whether there is
a physical cause for that distress
Pharmacological intervention
Acutely:
Haloperidol, Olanzapine and Lorazepam
are the drugs of choice
Do not use Haloperidol in patients with
Parkinson’s disease or Dementia with Lewy
Bodies
Medium term : Haloperidol or atypical antipsychotics:
(up to 6 weeks) Amisulpiride, Quetiapine, Olanzapine,
Risperidone (caution in cerebrovascular disease)
Longer term:
Cholinesterase inhibitors, NMDA Receptor
antagonists
Organising your affairs & making your wishes known
Lasting Power of Attorney
Finance & Property
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Health & Welfare
Advance Care Planning – how do you wish to be cared for in the future?
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Talk to your nearest & dearest about what your wishes are whilst
you still can – it will help them & you in the future
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The Alzheimer’s Society is an excellent source of information &
support
Delirium
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Accounts for 30% of all elderly medical in-patients
Can occur in up to 50% of older patients
postoperatively
Occurs in about 80% people at the end of life
In studies, patients with delirium have a high
mortality rate (22-76%), they have a high rate of
discharge to residential care & have longer length of
stay than non-delirious patients
Diagnosis of delirium
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For a diagnosis a person must show each of the following
features:
1. Disturbance of consciousness with reduced ability to focus,
sustain or shift attention
2. A change in cognition (memory deficit, disorientation,
language disturbance) or the development of perceptual
disturbance which was not present with a pre-existing
dementia
3. The disturbance occurs over a short time (usually hours or
days) & fluctuates during the day
4. There is evidence that it has been caused by general medical
condition, substance intoxication or withdrawal
Psychomotor Forms of Delirium
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Hyperactive:
Marked by increased motor activity,
agitation, hallucinations, inappropriate
behaviour & vigilance
Hypoactive:
Marked by lethargy with a decrease in
motor activity, has a poorer prognosis. It is
often missed (up to 2/3rds cases)
Mixed
Pathogenesis
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EEG can show diffuse slowing of cortical background
activity
Neuropsychological & neuro-imaging studies show
generalised disruption in higher cortical function
Cholinergic deficiency – anti- cholinergic drugs can
precipitate delirium & physostigmine & cholinesterase
inhibitors can reverse delirium
Dopaminergic excess – levodopa can precipitate delirium &
dopamine antagonists can reverse it
Evidence also exists for the role of other neurotransmitters
but less strong
Risk factors for delirium developing as
an inpatient
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Old age
Severe illness
Pre-existing dementia, depression or previous delirium
Physical frailty – functional dependence, falls
Infection
Dehydration or malnutrition
Sensory impairment
Polypharmacy especially with psychoactive drugs
Surgery especially #NOF
Previous alcohol excess
Renal or hepatic impairment
Metabolic derangement e.g. hyponatraemia
Terminal illness
Precipitating factors for delirium as an
inpatient
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Immobility
Use of physical restraint
Urinary catheter
Malnutrition
Dehydration
Intercurrent illness
Psychoactive medications
Inadvertent withdrawal of psychoactive medications e.g.
benzodiazepines
Iatrogenic events
Common intercurrent illnesses in
delirium
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Infection
Cardiac – MI, heart failure
Respiratory – PE, hypoxia
Electrolyte imbalance – dehydration, renal failure,
hyponatraemia, hypercalcaemia
Endocrine & metabolic – cachexia, thiamine deficiency,
thyroid dysfunction
Drugs especially those with anti-cholinergic side effect
Urinary retention
Faecal impaction
Neurological – stroke, SDH, epilepsy, encephalitis
Differential Diagnosis of delirium
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Dementia
Depression
Hysteria
Mania
Schizophrenia
Dysphasia
Non convulsive epilepsy / temporal lobe epilepsy
Assessment of delirium
Confusion Assessment Method (CAM)
To have a positive CAM the patient must have:
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Presence of an acute confusion, a fluctuating course AND
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Inattention (e.g. impaired 20-1 counting on AMTS or the
inability to spell WORLD backwards on MMSE)
AND EITHER
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Disorientated thinking (disorganised or incoherent speech)
OR
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Altered level of consciousness ( usually lethargic or
stuporose)
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Assessment of delirium
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Collateral history from a carer or the NOK is
essential to establish the onset & course of confusion
to distinguish between dementia & delirium
Assess for cause of delirium
Assess cognitive function if possible on admission
(AMTS or MMSE) & subsequent serial
measurements can track patients’ progress
Assessment in delirium – the history
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Previous intellectual function & functional status
Full drug history including recent cessations
History of fluid & food intake, alcohol history
History of bladder & bowel voiding
Sensory deficits & aids used
Previous episodes of acute or chronic confusion
Co morbidities
Symptoms suggestive of underlying cause
Pre-admission social circumstances & care package
Investigations in delirium
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Routine bloods, ECG, CXR, urinalysis, pulse oximetry, blood
cultures, TFTs, B12 , Folate
CT head if:
Focal neurological signs
Confusion after fall or head injury
EEG if :
Suspect non-convulsive status or temporal lobe epilepsy
LP if:
Meningism, headache & fever
Management of Delirium Treatment of Underlying Cause
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Incriminating drugs should be withdrawn where
possible
Biochemical derangements corrected
Treatment of infection
Parenteral thiamine should be administered if
malnutrition or alcohol excess is suspected
Management of Confusion Environment
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Lighting levels appropriate for the time of day
Regular (at least 3xday) cues to orientate
Use of clocks & calendars
Hearing aids & glasses available & functioning
Continuity of care from nursing staff
Encouragement of mobility & engagement in
activities
Approach & handle gently, explain who you are,
what you are going to do & why
Environment Contd.
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Elimination of unexpected & irritating noise
Good pain control- use of Abbey Pain Scale
Encourage visits from family & friends especially at meal
times
Explain to family what delirium is & how they can help
Ensure adequate fluid & dietary intake
Adequate CNS oxygen delivery
Monitor bowels – avoid constipation
Encourage a good sleep pattern
Avoid inter & intra ward transfers
Avoid catheters where possible
Wandering
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Close observation in a safe & reasonably secure
environment
Supervise them walking rather than trying to stop
them
Identify the cause of agitation – pain, thirst, looking
for the toilet
Distraction – involve family members if possible
Rambling speech
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Do not agree with rambling speech as my re- enforce
any paranoid component
Tactfully disagree
Change the subject
Acknowledge the feelings expressed but not the
content
Prevention of Complications
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Falls
Pressure sores
Nosocomial infections
Functional impairment
Continence problems
Over sedation
Malnutrition
Thanks for Listening