OLD AGE PSYCHIATRY - PowerPoint Presentation

Download presentation
OLD AGE PSYCHIATRY
OLD AGE PSYCHIATRY

OLD AGE PSYCHIATRY - Description


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 Download Presentation

Tags

drugs dementia symptoms brain dementia drugs brain symptoms cognitive problems depression people behaviour risk care disease agitation treat assessment

Embed / Share - OLD AGE PSYCHIATRY


Presentation on theme: "OLD AGE PSYCHIATRY"— Presentation transcript


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???

Shom More....
By: alida-meadow
Views: 87
Type: Public

Download Section

Please download the presentation after appearing the download area.


Download Presentation - The PPT/PDF document "OLD AGE PSYCHIATRY" is the property of its rightful owner. Permission is granted to download and print the materials on this web site for personal, non-commercial use only, and to display it on your personal computer provided you do not modify the materials and that you retain all copyright notices contained in the materials. By downloading content from our website, you accept the terms of this agreement.

Try DocSlides online tool for compressing your PDF Files Try Now

Related Documents