Dr Suhana Ahmed ST5 to Dr Debbie Stinson Sutton Older Peoples Community Mental Health Team Agenda What is it What did we do What do we do The team Referrals Memory assessment amp fu Dementia ID: 551564
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Slide1
OLD AGE PSYCHIATRY
Dr Suhana Ahmed
ST5 to Dr Debbie Stinson
Sutton Older People’s Community Mental Health TeamSlide2
Agenda
What is it
What did we do
What do we do
The team
Referrals
Memory assessment & f/u
Dementia
DrugsSlide3
Old Age Psychiatry
general psychiatry in the elderly population
?definition of elderly
Service to all elderly people suffering from organic illness, i.e. dementias of various types or functional illness, i.e. depression, schizophrenia, etc.
complexity of cases, i.e. psychiatric conditions modified by physical illness and organic mental changes and the coexistence of organic and functional illness.
close working relationship with primary care and other agencies such as social servicesSlide4
What we do now
Multidisciplinary team
3 beds for Sutton out of borough (
Tolworth
)
Intensive Home Treatment
Challenging behaviour service
SS separate service
Change in referrals over years – younger age, more complex, interface with other specialties. Slide5
Intensive Home Treatment Team
Inpatient ward staff
Community Psychiatric nurses
Recovery Support workers
Reduction in beds
Help treat people in their own homes and keep them out of hospital
Can see people up to twice a day
Roles:
- supervise meds
- monitor risk
- monitor mental state
- support family and client
Access only via CMHTSlide6
Challenging Behaviour Service
Psychologists
CPNs
Challenging behaviour in context of dementia
e.g
agitation, violence, not eating and drinking, under or over stimulation
Holistic assessment – staff, environment, observation
Only in care homes at present
Work with staff and clients to help manage behaviour
Use of psychological measures rather than medication
Direct referrals from GPsSlide7
Old Age Liaison Team
Based at St Helier’s
OT and CPN
Small amount of medical input
Due to increase resources in next few months.
Assessments for those picked up on screening. Slide8
Sutton Older People’s Community Mental Health Team
Old Age Psychiatry Consultants
Specialty doctor
Core Trainee (1)
Specialist Trainee (1)
Community Practice Nurses (4)
Occupational Therapists
Recovery Support worker
Clinical PsychologistsSlide9
Referrals
What?
Memory problems
Clarify diagnosis
Functional e.g. moderate/severe depression
Agitated behaviour
Capacity
MCI/ Worried well
Early diagnosis
CQUIN in acute setting - confusion
QOF in GP – dementia diagnosis
Early diagnosis
Who?
GPs
Adult Psychiatry
Other services
e.g
social services
Other specialties – neurology, old age
A&ESlide10
Referrals
Appropriate referrals
Chronic cognitive impairment
Severe mental illness – psychosis, depression
‘Inappropriate’ referrals
Acute confusion
Previous mental illness, nil current
Multiple simultaneous referrals
Purely social care
Timely diagnosis
Our criteria - ageSlide11
OPC – Memory assessment.
Dear colleague,
I would be grateful for your review of this 84 year old man.
Mr X and her son came to see me at the surgery. His son reports problems with his short term memory. He forgets where he puts keys and cannot recall recent conversations.
AMT was 7.
Many thanks,
GPSlide12
OPC – Memory assessment
Prior to appointment: (GPs to provide)
GP summary – med list, medical history
Dementia blood screen
Screen out physical causes
e.g
delirium or neuro problems
Ideally some cognitive testing
History
Collateral history
Mental State Examination
Formal cognitive assessment – SMMSE, ACE III
RiskSlide13
OPC – management plan
Consider any physical causes – and treat
Consider effects of physical meds
Neuroimaging (if appropriate)
?Further cognitive testing if required
F/u apt in 8-10/52
Social input
CCA
OT
Any other servicesSlide14
F/U appointment
Further cognitive assessment (if required)
Review scan with clinical history (do they correlate?)
MCI
Discuss diagnosis
Treatment – medication, cognitive stimulation.
Alzheimer’s society
?further f/u (mandatory if started on meds)Slide15
Have you thought about these services……
Admiral nurses
specialist dementia
nurses
practical
and emotional support to family
carers
tailored to their individual needs and challenges
.
Increase in number
Alzheimer’s society
Dementia advisors
Carer support
Activity groupsSlide16
Carers centre
Carers assessment/support
Counselling and wellbeing
Benefits and advice
Support groups/training
Age UK
Home and care including equipment
Money matters
Advice and support
Social services
Community care assessment
Safeguarding
Have you thought about these services……Slide17
Summary
Various changes to service including new sub teams – IHTT, CBS
Reduction in beds
Multidisciplinary team
Functional and organic
Various modes of referral
Memory assessment – various parts
Consider other servicesSlide18
DEMENTIA Slide19
Types
DEMENTIA
Alzheimer’s
62%
Vascular
17%
Mixed
10%
Lewy
body dementia
4%
Fronto
-
temporal
2%
Parkinson’s Dementia
2%
Other:
3%Slide20
Alzheimer’s
extracellular deposition of beta amyloid-Aβ and intracellular accumulation of tau protein.
Proteins
build up in the brain to form structures called 'plaques' and 'tangles'.
loss
of connections between nerve
cells
death
of nerve cells and loss of brain tissue.
Shortage of acetylcholineSlide21
Alzheimer’sSlide22
Alzheimer’s - symptoms
Short term memory
Recall
Learning new info
language
visuospatial
skills
–
concentrating
, planning or
organising
Orientation
Anxiety, irritability, depression
Communication
Psychotic symptoms
Unusual/out of character
behaviour
– agitation, calling out, sleep, aggression
Awareness, frailty, eating. Slide23
Atypical
Alzheimer’s
earliest symptoms are not memory loss.
underlying damage (plaques and tangles) is the
same
first part of the brain to be affected is not the hippocampus
.
Posterior cortical atrophy (PCA)
atrophy of the back (posterior) part of the cerebral cortex
Visual info/ spatial awareness
e.g
identify objects/ reading, uncoordinated, judge distances
Logopenic
aphasia
left posterior temporal
cortex
and inferior parietal
lobule
primary progressive aphasia
language
speech labored
with long pauses.
Frontal variant Alzheimer's disease frontal lobesplanning
and decision-making.socially inappropriate, lack of empathySlide24
Vascular Dementia
reduced blood supply to the brain due to diseased blood vessels
.
Death of brain cells
Stroke –related
Post stroke dementia
20% within 6 months
Single-infarct
Small
Temporary
asymptomatic
Multi-infarct
Sub cortical
Most common
diseases of the very small blood vessels that lie deep in the
brain
thick walls and become stiff and twisted, meaning that blood flow through them is reduced
.
‘small vessel disease’Slide25
Vascular
dementiaSlide26
Vascular dementia
most common cognitive symptoms in the early
stages
problems with
planning or
organising
, making decisions or solving problems
difficulties following a series of steps (
eg
cooking a meal)
slower speed of thought
problems concentrating
, including short periods of sudden confusion
.
memory-
problems recalling recent events (often mild)
language
- eg speech may become less fluent
visuospatial skills - problems perceiving objects in three dimensions.Mood – apathy, lability, depressionSlide27
Vascular dementia
subcortical vascular
dementia
Early
loss of bladder control
common
.
mild
weakness on one side of their body,
or
less
steady walking and more prone to falls.
clumsiness
, lack of facial expression and problems pronouncing words. Slide28
Vascular dementia
Stroke-related dementia
progresses
in a 'stepped'
way
long
periods when symptoms are stable and periods when symptoms rapidly get
worse
Subcortical dementia
more often symptoms get worse
gradually (similar to Alzheimer’s course)Slide29
Fronto-
temporal dementia
Frontal
– behaviour and emotions
Temporal
– understanding of words
nerve
cells in the frontal and/or temporal lobes of the brain
pathways that connect them change
the
brain tissue in the frontal and temporal lobes shrinks
.
Younger age group
behavioural variant frontotemporal dementia
progressive non-fluent aphasia
semantic dementia.Slide30
Fronto-temporal dementia
Behavioural
variant
frontotemporal
dementia
two
thirds
Personality
and
behaviour
lose their inhibitions
lose
interest in people and things - lose motivation
lose
sympathy or empathy
show
repetitive, compulsive or
ritualised
crave sweet or fatty foods, lose table etiquette, or binge on 'junk' foods, alcohol or cigarettes.Slide31
Fronto-temporal dementia
Language variants of frontotemporal
dementia
early
symptoms- progressive
difficulties with
language
apparent
slowly, often over two or more years.
progressive non-fluent
aphasia
initial
problems
- speech.
slow, hesitant speech
–
errors
in
grammar
semantic
dementia,
speech is fluent lose their vocabulary and understanding of what objects are
asking the meaning of familiar words trouble finding the right word, difficulty recognising
familiar people or common objects.Slide32
Fronto-temporal dementia
Progression - differences
between the three
types
become much less obvious.
later
stages,
damage to the brain becomes more widespread.
Symptoms
are often then similar to those of the later stages of Alzheimer's disease
.
10-20
per cent of people with frontotemporal dementia also develop a motor disorder, before or after the start of dementia.
motor
neurone disease
progressive
supranuclear
palsy
corticobasal
degeneration.a person with both conditions will live for two or three years after diagnosis.Slide33
Lewy Body dementia
symptoms with both
Alzheimer's disease
and Parkinson's
disease
under-diagnosed
tiny deposits of protein in nerve
cells
low levels
acetylcholine
and
dopamine
loss
of connections between nerve cells
.
progressive death of nerve cells and loss of brain tissue
.
brain and nervous systemSlide34
Lewy Body dementia Slide35
Lewy Body dementia
often
subtle
, but gradually worsen to cause problems with daily living
attention
and
alertness
-
fluctuate
widely over the course of the day, by the hour or even a few minutes
.
judging distances
and
perceiving
objects
planning and
organising
Visual hallucinations
-
people or animals, and are experienced as detailed and convincing.Delusions
movement problems – rigidity, tremor, bradykinesiaSleep
disordersSlide36
Lewy Body dementia
Worsening movement problems mean that walking gets slower and less
steady
speech and swallowing, leading to chest infections or risk of choking.
Eventually, someone with DLB is likely to need extensive nursing
care
Diagnostic difficultySlide37
MedicationsSlide38
Dementia and Drugs
Drugs to treat Alzheimer’s disease
Drugs to treat symptoms associated with dementia
Drugs to treat physical disorders in people with dementiaSlide39
Drugs to treat Alzheimer’s diseaseSlide40
Anti Dementia Drugs
Acetylcholinesterase inhibitors
Donepezil
Galantamine
Rivastigmine
MemantineSlide41
Anti Dementia Drugs
Initiation of anti-Alzheimer drugs is usually by a specialist.
More follow up in primary care (SLAM).
Little to choose between
AChEIs
.
Main side effects are syncope & GI
Contraindicated in cardiac conduction problems or if pulse rate <60.
Continue even in more severe stages, if tolerated.
May cause agitation in advanced dementia.Slide42
Monitoring
Regularly check by specialist team
check-up - assessment of the patient's cognition,
behaviour
and ability to cope with daily life
views of
carers
discussed at start of drug treatment and at check-ups
treatment is continued as long as it is judged to be having a worthwhile effect
cholinesterase inhibitor - least expensive of the three drugs is prescribed first.
However, if not suitable - another cholinesterase inhibitor could be chosen. Slide43
Acetylcholinesterase inhibitors
Mechanism of action:
P
revent enzyme acetylcholinesterase from breaking down acetylcholine in the brain.
Increased concentrations of acetylcholine - increased communication between the nerve cells that use acetylcholine
Indications:
mild-to-moderate
Alzheimer's disease
dementia with
Lewy
bodies and dementia related to Parkinson's disease -
rivastigmine
(most evidence)
Not started in acute setting
Effectiveness
40-70 per cent with Alzheimer's disease benefit from cholinesterase inhibitor treatment
N
ot effective for everyone and
M
ay improve
symptoms
only temporarily, between six and 12 months in most casesSlide44
Acetylcholinesterase inhibitors
Donepezil
(Aricept)
Rivastigmine
(Exelon)
Galantamine
(
Reminyl
)
Tends to be first line
ON.
Starting dose 5mg ON
,
increased to 10mg OD after 1/12 if necessary.
maximum licensed total 10mg OD
capsules or oral solution
BD
Starting dose 3mg a day in 2 doses, usually increase to 6mg - 12mg a day
Patch-two versions.
D
aily dosages of 4.6mg or 9.5mg. Fewer side-effects than the capsules
starting dose 8mg OD 4/52, increased to 16mg OD for another 4/52. Maintenance dose of 16-24mg daily
Slow-release capsules (
Reminyl
XL) are available (once a day).
maximum licensed total daily dose is 24mg.Slide45
Memantine (
Ebixa
)
Mechanism of action:
NMDA receptor antagonist
B
locks glutamate.
Glutamate released in excessive amounts when brain cells are damaged by Alzheimer's disease - brain cells damaged further.
P
rotect brain cells by blocking effects of excess glutamate.
Indications
severe Alzheimer's disease
moderate disease who cannot take the cholinesterase inhibitor drugs
.
Administration
Tablets or oral drops
recommended starting dose 5mg OD, increasing after 4/52 to up to 20mg OD
maximum licensed total daily dose is 20mgSlide46
Summary
Anticholinesterase inhibitors – Donepezil,
rivastigmine
,
galantamine
NMDA antagonist –
Memantine
Not indicated for all dementias
e.g
not indicated for vascular dementia
Compliance – supervision, prompt
Risks: syncope, GI and bradycardia
Not tolerated – change to another
AChEI
Regular monitor including cognitive assessment. Slide47
Drugs to treat symptoms associated with dementiaSlide48
Depression and Dementia
common psychological conditions that are frequently experienced by people with dementia and their
carers
particularly common in people who have vascular dementia
or Parkinson's dementia
Diagnostic difficulty – overlap in symptoms between dementia and depression
Depression may worsen
behavioural
symptoms
dementia = aggression
,
problems sleeping or refusal to eat.
later stages of dementia, depression tends to show in the form of depressive 'signs‘ - tearfulness and weight lossSlide49
Depression and Dementia
early stages
of dementia- may be linked to a person's worries about their memory
and about the future.
Chemical changes in the brain, caused by the dementia, may also lead to depression or anxiety.
People living in care homes
seem to be particularly at risk of depression. Slide50
Treatment of depression in dementia
Psychological
Cognitive
Behavioural
Therapy
helpful for people in the early stages of dementia
Less appropriate in the later stages of dementia, communication problems are common.
Medications
Selective serotonin reuptake inhibitors (first line)
Sertraline or citalopram (max 20mg)
Mirtazapine (Atypical) – sedation and appetite
Trazodone (tricyclic antidepressant) – sedating
S/e – mild, GI
Caution:
HyponatraemiaSlide51
Psychosis in Dementia
Paranoia, hallucinations, delusions
Difficult to treat and can be resistant to drug treatment
Risperidone
, quetiapine, olanzapine – low doses
Caution with
lewy
body dementia and Parkinson's Dementia – worsening of physical symptoms
Side effects: sedation (and falls), worsening confusion, parkinsonism,
risk of stroke.
Regular review, reduce and discontinue if no effect. Slide52
Agitation in Dementia
any possible underlying factors
& treat
Physical
Comorbid mental health – depression, anxiety
Medications
e.g
codeine, tramadol
comfortable and well cared
for
(abuse, neglect)
Recent changes
e.g
move to home, staff
Over and under stimulation
Non- medical
non-drug treatments
used
before medication reminiscence therapy and social
interactionAnimal therapyMusic and dance therapySlide53
Agitation in Dementia
Antipsychotics
risperidone
– license (6 weeks). Other prescribed '
off-licence
‘
NICE
- antipsychotic
drugs
not first line
Exception: severe
behavioural
and psychological symptoms
- certain
, clearly defined circumstances
.
full discussion with the
person
and carers benefits and risks of treatment (e.gs increased risk of stroke vs improvement in agitation)
all prescriptions monitored and stopped after 12
weeks, except in extreme circumstancesSlide54
Agitation in Dementia
E
vidence
that people with dementia are being inappropriately prescribed antipsychotic drugs.
prescribed
for long periods of time
prescribed
to treat mild
behavioural
and psychological
symptoms
A
round
two-thirds of antipsychotic prescriptions are inappropriate
.
National drive to decrease the use of antipsychotics
Challenging
behaviour
teamSlide55
Mrs X
84 year old
In a well known care home
Dx
: Mixed Dementia – vascular and Alzheimer’s
Referral:
- Poor self care – aggressive when being bathed
- Hiding in cupboards
- Disinhibition – exposing herself
Request for review and medication Slide56
Challenging Behaviour Team
D/w staff
Observation
Poor self care
Hiding in cupboard
‘Disinhibition’ – exposing herself
Behaviour is a form of communicationSlide57
Agitation in Dementia
Benzodiazepines
Lorazepam, diazepam, clonazepam
Not first line – non medical measures tried
If used
- time limited
- target behaviour
- frequency
- clear monitoring – to observe whether this has decreased.
Minimum effective dose
Risks: sedation (falls), worsening agitation, worsening confusion, respiratory depression
Request by care homes to manage clientsSlide58
Summary
Depression and anxiety common
Diagnostic clarity
Similar treatment pathway to depression and anxiety in younger population
Antipsychotic use for psychosis – limited benefit and risks
Agitation – non medical treatment first line. Meds to be used cautiously, time limited and stopped as soon as able to due to risks.
Challenging behaviour team.Slide59
Drugs to treat physical disorders in people with dementiaSlide60
Background
Drugs can have adverse cognitive effects
May be a
cause
of cognitive problems (
Tannenbaum
et al
2012)
Exacerbate
impairments in dementia
Polypharmacy
is frequent - average of 8 drugs per resident in UK care homes (Shah
et al
2012)
is dangerous -the more drugs people with dementia take the higher their mortality SHELTER study (2013)
Is not necessary -20% of drugs “potentially inappropriate” in care home residents (Shah
et al
2012)Slide61
Anticholinergics
Reducing brain cholinergic activity would be expected to have an effect on brain function
But many drugs have some degree of action on anti-cholinergic activity
Two key questions
Do “anti-cholinergic” drugs affect brain function in a clinically important way?
Do drugs with anti- cholinergic activity affect adversely the benefits of cholinesterase inhibitor drugs?Slide62
Anticholinergics
While some drugs are used for anticholinergic effects
eg
oxybutynin or hyoscine
Others are not known for this function
eg
ranitidine or
CBZ
Cumulative effect
Anticholinergic risk scales of drugs vary considerably
Recent systematic review of anticholinergic risk scales
Uniform list of drugs
(Duran et al 2013)Slide63
Anticholinergic Cognitive Burden Scale
Score 3 – clinically relevant
Tricyclics
Phenothiazines
,
olanzapine,quetiapine
, clozapine
The older antihistamines-
chlorpheniramine
,
hydoxyzine
,
clemastine
Hyoscine (scopolamine)
Anitcholinergics
for movement disorders-
orphenadrine
,
procyclidine
,
trihexyphenidyl
Anticholinergics used for bladder problems- oxybutynin, tolterodine, propantheline Slide64
Anticholinergic Cognitive Burden Scale
Score 1 or 2- mild anticholinergic activity
Amantadine
Benzodiazepines
Opiates
Atenolol
Cimetidine and ranitidine
Furosemide
Digoxin
NifedipineSlide65
Does all this matter?
Study of relationship of
patients’
“Anticholinergic Cognitive Burden (ACB)” with mortality and cognitive impairment
For each 1 point increase in the ACB
a decline in MMSE of 0.33 points over 2 years
26% increase in the risk of deathSlide66
AChEIs and Anti-cholinergic drugs
Up to 50% of patients on concomitant
use
Anti-
cholinergics
interact negatively with
AChEIs
Also cause confusion, sedation, cognitive impairment, delirium and
falls
Some suggestion they can increase the risk of dementia and affect the clinical course of AD
(
Carriere
et al 2009;
Jessen
et al 2010; Lu & tune 2003
)
Risk factor for onset of psychosis in AD
(
Cancelli
et al 2009)Slide67
Anticholinergic drugs
Whether a drug worsens cognition does not just depend on its “anticholinergic activity”- other factors are:
Which receptors it acts on- M1 and M2 receptors (brain)or M3 receptors (bladder)-
Darifenacin
is selective to M3 bladder receptors
How well it
crosses
the blood brain barrier – small, lipid soluble,
unpolarized
molecules cross better-
Trospium
- poor penetration through BBB
How well it is recognised by the Permeability-glycoprotein (P-
gp
),
(
an active CNS efflux transporter which actively pumps agents back into circulation
)
Only
darifenacin
,
trospium
and fesoterodine
are reported to be P-gp substrates
oxybutynin and tolterodine are non specific and cross the BBB easilySlide68
The blood-brain barrierSlide69
Respiratory disorders
No evidence that
inhaled
anticholinergics affect cognitive
function
I
n theory
AChEIs
can exacerbate asthma/
COPD
2
studies- no ↑ risk of adverse pulmonary outcomes
(Stephenson et al 2012; Thacker &
Schneeweiss
2006)
1 study- significant association with
risk
of pneumonia, persistent cough, asthma and bronchitis
(
Helou
& Rhalimi 2010
)Caution in COPD and Asthma and close monitoring recommendedSlide70
Pain in dementia
Common and under-treated
(McLachlan et al 2011)
Pain itself can worsen cognition
(Clegg and Yong, 2011) Slide71
Pain in dementia
NSAIDs cause GI side effects and exacerbate heart
failure
Codeine associated with
falls
Tramodol
associated with
seizures
Opiates increase delirium risk
(Clegg and Young 2011) Slide72
How to treat pain in dementia
Define your target symptom
Use outcome measures – for pain (e.g. PAIN-AD) and distress (e.g. NPI or CBS)
Have a stepped protocol – for example
(
Husebo
et al 2011):
1.
paracetamol
(up to 3g per day)
2. Morphine (up to 20mg per day)
3. Buprenorphine patch (max 10mcg per hour)
4.
Pregabalin
(max 300mg per day)Slide73
Summary – Physical meds
Avoid
polypharmacy
Stop anything
unnecessary
If you are starting a drug monitor response and stop if no
use
Avoid anti-cholinergic and sedative
drugs
Chose drugs with least central effects where possibleSlide74
HD
83 year old
Jan 2015
Aortic valve replacement
Triple bypass
confusion
post-operatively - ??
Post-operative complications
pulmonary
oedema
AKI
2 episodes of
malaena
– subsequent OGD normal.
Confusion returnsSlide75
HD
Neurology
review on the
ward
confusion
visual
and tactile hallucinations – seeing animals and feeling things crawling on his skin.
mild
bilateral
cogwheeling
.
CT
scan
- no
acute pathology.
C
ommenced
on a
rivastigmine patch due to concern that this might be the start of lewy
body disease.
Discharge from St George’s – discharge letter to GP Slide76
HD
March 2015
rapidly improved when he was discharged home (around 4 weeks ago
now)
no
confusion and no
hallucinations recently.
some
initial perceptual abnormalities that seemed illusory in character (
eg
“seeing” people in the curtains)
- now
settled.
B
ack
to his normal self, though his daughter remains concerned that he has said some odd statements at
times/ odd
behaviour
slight tremor, essential tremor
Premorbid – ?cognition, ?hallucinationsACE 86/100 Slide77
HD
Impression:
I think it is clear that his confusion and hallucinations on the ward were the result of delirium. The underlying
aetiology
might well relate to the operation/
anaesthesia
itself, particularly as he has a known history of hallucinations caused by medication, or subsequent complications
.
Prior to the procedure there was no clear evidence of cognitive impairment, and his symptoms have largely resolved since returning home. (This marked improvement is unlikely to be the
rivastigmine
, where the positive effects are generally more subtle).
The
odd comments or
behaviour
reported by his
Mr
Daines
' daughter might relate to slow-resolving delirium (which can take months to fully resolve) or suggest a more persistent organic change. Delirium can cause a step down in functioning and 'unmask' an underlying problem. Slide78
HD
MRI head
There is evidence of significant small vessel
ischaemic
disease with confluent bilateral parietal white matter
hyperintensities
, scattered foci of white matter lesions and a small right lacunar infarct. This is associated with mild to moderate global cerebral atrophy. There are no specific features to suggest
Lewy
body dementia, but if this is considered in the differential diagnosis then further imaging with DATSCAN would be of benefit.
Impression
no evidence of
lewy
body
disease
Likely previous delirium - ?still resolving
Plan
Rivastigmine
stopped
DischargeSlide79
HD
Re-referral (Jul 2015)
disturbed by auditory hallucinations,
cameras
in his house and that his computer is being
monitored.
not confused
Chest Infection and recent (unsure of exact date) admission to Hospital for suspected UTI
.
Request from GP for review and case to be reopened to OPCMHT
.
Positive for urine dip
Similar presentation to previous infections
Abx
Not accepted. But re-refer if persistsSlide80
HD
Re-referral (Aug 2015)
Course of
antibiotics
completed, urine sample clear, further sample sent for testing.
'Profound auditory hallucinations remain'
present
- continues
to hear voices, that he is monitored by cameras and now believes that a bug has been implanted in his ear
.
Plan
Psychiatrist to review within a weekSlide81
HD
2-3
months
- new
onset auditory hallucinations. This began as only occasional
but has
rapidly progressed
2
nd
and 3
rd
person
Delusional significance, preoccupied
Not distressed
Differential diagnosis
Plan
Physical investigations
RisperidoneSlide82
HD
Worsening symptoms – visual and auditory
Falls
Driving
Agitation
Confusion
Family struggling
RisksSlide83
HD
Cellulitis - treated
Worsening psychotic symptoms
Falls
Variable in agitation and aggression
Olanzapine
Rivastigmine
Section 3Slide84
Thank you.
Questions???