Transcript 4 GP TMF presentation

Collaborative Care Model
GP’s and Specialist Care
Introduction: Dr Jane Allan
MOSS MHSOP 0.3FTE Liaison/clinical advisor at primary/secondary interface
TDHB as a “demonstration site” in the management of “Uncomplicated
Dementia” (no BPSD) using a Collaborative Care Model-GP’s ands Specialist Care
Part of the “Better, Sooner, More Convenient Strategy” MOH
• All referrals in category “uncomplicated dementia”
MHSOP • Collated by MHSOP, discussed at MDT
MOSS
GP
• Allocated to MOSS to liaise with primary referrer
• Provide education, guidance, treatment direction
• Liaison support and education from “Older Peoples Health”
• Managing uncomplicated dementia in primary care.
Scope of the problem
 Growing aged population
 Dementia affects 5% of people over 65
 20% of people over 80
 In 2002 12% of NZ pop > 65
 In 2051 25 % of NZ pop > 65
 NZ over 40,000 people have dementia
 Local demographic information?
Types of Dementia
Alzheimer’s Disease: 50 to 60 %
Vascular Dementia: 10 to 20 %
Mixed: 10 %
Lewy Body Dementia: 10 to 20 %
Fronto-temporal Dementia: <10 %
Develop best practice standards
Audit aim
Guidelines
Standard
Improve the dementia
care pathway for
“uncomplicated
dementia”
“Use of a clinical
pathway benefits both
health professionals
and service users” (1)
All primary care
providers in Taranaki
aware of, & using the
“dementia care pathway”
Improve the liaison
between primary and
specialist services and
provide education to
the primary care sector
Primary/specialist
integrated approach
(collaborative care) is
effective in managing
uncomplicated
dementia in primary
care setting (2)
All GP’s will be
confident and have the
knowledge and skills to
manage uncomplicated
dementia in a primary
care setting with
accessible liaison
support from specialists
Develop best practice standards
Audit aim
Guidelines
Standard
Reduce the referral rate
and number of cases
actively managed by
MHSOP for those with
“uncomplicated
dementia”
“Uncomplicated
dementia” can be
managed effectively in a
primary care setting (2)
MHSOP actively
manage
dementia cases with
BPSD and provide
liaison for those with
“uncomplicated
dementia”.
Research
 Need for early diagnosis due to availability of CEM
 GP’s good opportunity for early detection-diagnosis
 Central role in continuing medical care
 Australian GP study 1993 :better cognitive check-ups
needed & better coordination between specialist & GP
 Swedish study: Why GP dementia detection rate low?
 GP survey: good knowledge but asked for more
education, clear assessment procedures & easy to use
screening tool.
Research Results
 40-50% tell patients dementia diagnosis; 95%





terminal cancer diagnosis (T: 60% confidence)
Only 12% discussed driving licence (T:70%)
Most reported difficulty (76%) in assessment of social
circumstances and organising social support
43% GP’s satisfied with specialist clinic (T:79% )
High correlation between making a diagnosis and
prescribing a drug.
Sceptical about CEM; underestimated occurrence
dementia (T 80% lack confidence in prescribing)
Survey Results: 44% Response
 60% GP’s confident diagnosing , informing & referring
 Less confident in providing treatment, resources & advice,
follow up and management in a primary care setting.
 80% low confidence re CEM & CT scan interpretation.
GP’s are keen to have support from specialists:
 96% would use E-mail consultation with specialist
 >80% guidelines, and further resources
 71% a phone/e-mail liaison with a specialist MHSOP nurse
 >50% attend workshop or refer patients/caregiver to group
Is this memory loss normal?
 A 65 year old male
presents complaining
of increased
forgetfulness. He is
worried that he is
developing dementia.
 What would you do?
Uncomplicated or Complicated?
 Assessment
Rule out other causes: depression, delirium, red flags
Consider performing a memory test
 A provisional diagnosis
Age-related cognitive decline or early stage dementia
 Make a plan
Follow-up, investigations, advice, review, referral
Rule out other causes for memory loss
Depression/Delirium/Drugs
Depression “Pseudo dementia”
 Commonly causes memory impairment
 Often co-exists with dementia.
 Memory selective or patchy, rather than generally impaired.
 Duration weeks or months rather than gradual decline
 Screening tool e.g. Geriatric Depression Scale
 Past History
 Low energy, anxiety, sleep, appetite, suicidal ideas
Other Mental Health Problems
 Anxiety
 Stress
 Substance misuse/dependence
(alcohol, BZD, opiates)
 Sleep Disorder
Medications
 Sedatives: BZD, zopiclone
 Analgesics: Opiates, NSAID
 Anticholinergics: Antihistamines, antiparkinsons;
antispasmodics, TCA’s, neuroleptics
 Cardiac: antiarryhthmics, antihypertensives, digoxin
 Gastro-intestinal: H2 agonists, prochlorperazine,
metoclopramide
 Others: Anticonvulsants, corticosteroids, lithium,
antibiotics, SSRI’s (serotonergic syndrome)
Medical Conditions
 Cerebrovascular disease
 Neurodegenerative disease
 Brain tumour and infections
 Head injury
 Epilepsy
 Thyroid disease
 Malnutrition, vitamin deficiencies
 Chronic pain
Consider neurological /medical/surgical referral
Patient
 Less than 60 years
History
 Rapid decline (1-2mths) in cognition or function
 Unexplained neurological symptoms (severe headache, seizures)
 Anticoagulants/bleeding disorder
 History of cancer
 Family history of neurodegenerative disease e.g. Huntington’s
Examination
 New localising signs
 Atypical cognitive symptoms or presentation
 Gait disturbance
Investigations






To rule out potentially reversible factors
FBC, LFT’s
Serum electrolytes, calcium & glucose
TSH
Vitamin B12 & folate
CRP
?Referral for CT/MRI- white matter changes associated
with worsening cognitive function (Survey showed
18% GP’s are confident in interpreting scan results)
Memory and Ageing: What’s Normal?
 Harder to pay attention “ distractions”, hearing, vision
 Slower at processing information ( new learning,




retrieval e.g. of names)
85% forget names
60% lose keys
50% cant remember what has just
been said
40% forget faces or directions
Normal age-related memory decline
 Subjective memory concern
 Mild episodic memory
impairment
 Preserved procedural
& semantic memory
 Possible mild non memory
cognitive dysfunction
(e.g. attention)
 No functional impairment
or behavioural abnormalities
Symptoms










Changes in memory
Reasoning
Judgement
Recognition
Language
Orientation
Mood
Motivation
Personality
Ability to perform ADL’s
Normal age-related
“forgetfulness”
Mild Cognitive
Impairment
Dementia
Sometimes misplaces items Frequently misplaces items
Forgets what an item is
used for. Puts it in an
inappropriate place
Momentarily forgets a
person’s name
Frequently forgets names &
slow to recall
May not remember
knowing a person
Occasionally has to search
for a “word”
Finding words becomes
more difficult
Starts to lose language
skills. Withdraws socially
Occas. forgets an errand
Begins to forget events
Loses sense of day & time
May forget event from
distant past
May forget more recent
events or new info
Working memory
impaired. Difficulty
learning or remembering
new info
Driving-may forget to
turn, quickly re-orients
Temporarily lost.
Trouble with maps
Easily lost in familiar
places-st for hours
Jokes about memory
loss
Worries about memory
loss. Family & friends
notice lapses.
May have little or no
awareness of cognitive
problems
Mild Cognitive Impairment
 Most maintain cognitive





ability at a functioning level
throughout life.
20% of 65 yr olds have MCI;
5 % have dementia
MCI may be a precursor to
dementia.
Meta-analysis study reported
annual conversion from MCI
to dementia is 5-10% per yr
Many people with MCI did
NOT progress to dementia
with 10 years follow-up.
Objectively impaired
memory testing
(MMSE >=26 BUT
ADL’s INTACT)
Criteria for Diagnosing Dementia
Impairment of memory and one or more of
 Aphasia: production/understanding language disturbed
 Apraxia: trouble carrying out motor activities
 Agnosia: failure to recognise, identify objects, people,
places
 Executive functioning: sequencing, planning, organising,
judgements & abstracting
 Must interfere with work, social activities or
relationships and represent a significant decline in
the persons functioning (ask about managing money,
using the phone, transport, taking medications )
 Gradual onset and continuing decline.
 Other physical or mental conditions that can look like
dementia have to be excluded
*Person may not be aware of changes may have to ask
permission to speak to someone who knows them well
Describing Dementia-DSM 1V
Early Onset: Before 65 years
Late onset: After 65 years
Uncomplicated: Alzheimers or vascular dementia with
no BPSD or complex co-morbidities
Complicated: with delusions, depressed mood or
behavioural disturbance/or have signs of another
neurodegenerative disorder e.g. gait disturbance,
extra-pyramidal symptoms, focal or lateralising
neurological signs (e.g. Parkinson’s, Huntington’s)
Mild
(MMSE >20)
2-7yrs
Moderate
Severe
(MMSE 10-20)
MMSE <10
2-3 yrs
4-7 yrs
Activities
of daily
living
(ADLs)
Problems with
routine tasks
Needs help with
basic ADLs
(eg, feeding,
dressing, bathing)
Behavior
Changes in
personality
Anxiety,
suspicion, pacing,
insomnia
Cognition
Place of Care
Difficulty
Confusion and
recognizing family
memory loss, ie
and friends
– Misplacing
objects
Chronic loss of
– Forgetting names
recent memory
– Disorientation
Home
Home with Support
Progresses to
total dependence
on caregiver
(eg, feeding, toileting)
Agitation,
wandering
Loss of speech
Misidentifies or is
unable to recognize
familiar people
Rest Home/Hospital
Vascular Dementia
 Gradual or sudden episodes of ischaemia
 Several small CVA, TIA’s
 Course variable: sudden then leveling period
 More likely gait , urinary problems
 Predisposed: High blood pressure, diabetes, elevated lipids,
smoking, family history of vascular disease.
 CT scan: indications of ischaemia
Barriers to Early Detection
 Misidentification by the family of early
signs as normal aging process
 Social skills often maintained
 Denial and lack of insight by patient
 Reluctance to report symptoms (patient
and caregiver)—stigma
 Lack of definitive screening tools
Early Diagnosis and Discussion
Benefits
 Baseline & monitoring allows





earlier intervention with
support, reduces risks of
accidents, driving, abuse
and hospital admission
People can prepare
Enduring Power of Attorney,
wills
Move homes, visit family
overseas
Better understanding of changes
No cure but treatment can alter
the course of the illness
Risks
 Impact person’s self-esteem
 Threaten their independence
 Affect relationships
 Employment
 Future Plans change
 Clinical judgement as to
timing of discussion
 62% reasonably/very
confident
Is a memory test needed?
 Diagnosis is mainly from the history provided by
patient and informant
 Memory tests help confirm and quantify impairment
Conversation Clues
 How did they answer questions?
 Hesitation to find words, recall facts, sequence events?
 Anomalies in language use?
 Is reported impairment beyond what you classify as
“normal”.
Which Memory Test?
 Brief, standardised screening appropriate in primary care setting
Survey results showed
 75% used MMSE (30) and 40% MMSE (12)
 18% use mini-cog -repeat 3 words; draw clock, no.’s & time; recall
words
 80% used a memory test if cognitive problems were suspected
 13% cognitive screen patients over 74 for DRIVING medical
 0% follow-up those with dementia 6 monthly with screening
 60% perform cognitive screen themselves
 17% have nursing staff perform memory screening (driving test)
Which memory test?
Test
% GP’s
Time
taken
Interpreting Scores
Sensitivity &
specificity
MMSE
8-10mins
Age, education,
language & cultural bias, used for 30
years
Insensitive to mild
alzheimers (<=23
detected 52% with
dementia, missed
the “mild”)
Mini-Cog
<=5mins
Result of “probably” or “probably not”
demented
High sensitivity
High specificity
>80%. Validated in
GP studies
Missclassification
rate <=MMSE 15%
Brief test
GPcog
Pt /inf
5-10mins
Has a scoring system, so severity can
be monitored over time. Informant
interview required.
TYM
Self
administered
2 mins to
mark
Self-administered -saves GP time.
Similar to ACE-R 45/50 MCI; 4244/50 mild dementia
Double score= comparable with ACER
93% sensitive (<=
42/50 for
dementia) 86%
specific
ACE-R
20 mins
<=80/100 MCI progress to dementia
Sensitive to mild
alzheimers
Make a plan
 Some score well on test but still have cognitive impairment
 Some score low function well due to anxiety or mild dysphasia
From Assessment Classify:
 No Cognitive Impairment
 Mild Cognitive Impairment
 Uncomplicated Dementia
 Complicated Dementia
No signs of Cognitive Impairment
Reassurance and Lifestyle Advice
To protect against cognitive decline e.g. reduce risk CVD
Hypertension, stroke & small vessel disease, diabetes, hyperlipidaemia,
obesity have all been associated with an increased risk of age-related
cognitive decline.
 Exercise: increased fitness improves
memory & learning
 Diet rich in antioxidants and omega-3
 Alcohol (one unit/day)
 Stop Smoking
Use it-don’t lose it!
 Higher education/ occupation is protective
 Reading, puzzles, computer activities, crafts
 Social interaction: clubs & groups
 Use memory recall strategies
A place for everything
Lists, diary, alarms, wristwatch
Repeat out loud
Mneumonics, acronyms, rhymes & stories
Concentrate, relax……Sleep on it!
Supplements?
 Ginko Biloba reported as safe but no reliable
evidence of clinically significant benefit.
 Antioxidant supplements e.g. Vitamins A, E &
carotene may increase mortality & no significant
improvement in longevity
 No evidence to support oestrogen or HRT some
studies report increased mortality
Mild Cognitive Impairment





Memory loss with no other cognitive domains
involved and no loss of function, change in
behaviour.
Lifestyle Advice
Follow up 6 monthly to watch for deterioration
Consider serial observations with mental state testing
Recruit family to observe for worsening cognition or
impact on ADL’s
Ask about EPOA & Driving
Management of Uncomplicated Dementia
Focuses on slowing the progression through lifestyle,
behavioural and sometimes pharmacological methods.
 Refer Alzheimers Society, education & support groups
 Driving Assessment (ruler test & AA)
 3-6 monthly follow-up :cognition, functioning & ADL’s
 Assess caregiver situation & their stress
 Refer NASC if needed
 Competency (activate EPOA if necessary)
 Psychosocial treatments e.g. behaviour, emotion,
cognition & stimulation oriented.
CEM’s available in NZ
There is no evidence to suggest that they prevent the onset
or ultimate progression of dementia
 Donepezil (Donepezil-Rex) only funded CEM
(Doesn’t require special authority)
 Rivastigmine (Excelon)
 Galantamine (Reminyl)
 Memantine ( Ebixa)
*Patients with community cards can claim disability
allowance which can cover payment for unfunded CEMs.
Aims of treatment with CEM’s
 Small improvement, stabilisation or less than expected
decline
 Positively affect the patients quality of life
reduce cognitive deterioration
maintain functional ability
reduce behavioural problems
prolong time to nursing home placement
 Reduce caregiver burden
What are the indications for CEM’s
 NICE guidelines UK -moderate dementia (MMSE 10-




20) “cost effective due to reduced costs of care”.
Now studies support use in mild and severe dementia
on both clinical & economic grounds for use
GP’s recommended to discuss treatment with a
specialist & become familiar with local protocols
GP’s and care team can assess response to therapy.
GP familiar with patient over a longer time period.
Effect of Alzheimer’s Disease on
the Cholinergic System
 Major changes occur in the cholinergic system
including
 Loss of cholinergic neurons
 Depletion of acetylcholine (ACh)
 Decline in choline acetyltransferase (ChAT) activity
  Acetylcholinesterase (AChE)
  Butyrylcholinesterase (BuChE)
 Loss of muscarinic receptors
What to tell patients:
How do CEM’s work?
 In dementia there is a shortage of Acetyl Choline
(ACh) , a brain chemical important for memory.
 ACh is broken down in the brain by an enzyme called
acetylcholinesterase.
 The CEM-AchI prevents this enzyme from working.
 The less ACh that’s destroyed the more there is to
transmit messages around the brain to form memories
 ACh is associated with sleep cycles, mood, attention,
memory, and cognition.
Are CEM’s Effective?
 Results are variable.
 On average 6 months preserved cognitive function.




(Minor improvements in cognitive & ADL testing)
Clinical improvement noted in 39% on donepezil V
22% placebo
Increased dose may lead to greater improvement but
adverse effects may be intolerable.
All CEM’s in NZ similarly effective & similar adverse
effects in large studies but note local study results!
Lack of response to one doesn’t exclude a response to
one of the others
DEMOGRAPHICS
Sample
detail
Baseline
6 months
12 months
24 months
36+ months
Total sample
166
138
112
63
39
Ages - < 69
- 70 - 79
- 80 - 89
30
80
56
28
66
44
26
58
28
16
34
13
15
18
06
Medication
Exelon tab
- patch
Reminyl
Aricept
Ebixa
48
15
26
65
12
46
09
22
52
09
35
03
22
44
08
23
11
24
05
18
08
11
02
Diagnosis
DAT
MID/MIX
107
59
91
47
79
33
44
19
29
10
Exelon patch vz other CEM's
50
48
46
44
Exelon Patch
Exelon tab
Aricept
Reminyl
42
40
38
36
34
32
30
TRS baseline
TRS 3m
TRS 6m
TRS 12m
Maintenance
More sociable
Less repetitive
Short term memory improved
More conversational
More alert
Reduced aggressive behaviours
More confident
More interested
Doing odd jobs
Using telephone more
Reading newspaper
Outcomes
Reported
from
Caregiver
Followup
More settled at night
Resumed a hobby
Cooking again
Longer-term memory improved
More interest in finances
Reduced wandering
Handcrafts
Learned new skill
0
5
10
15
20
25
30
35
Conclusions
 Women presented later and were more impaired.
 Serial cognitive testing assists with decision-making
for patients & clinicians.
 Most people achieve some benefit from AcChEI’s, even
short term.
 The attrition rate before 6/12 is 15% due mainly to
inability to tolerate the drug (nausea, headaches.)
 Deterioration, confounding medical conditions,
death, and entry to Rest Home, are main reasons for
attrition over longer term.
 Exelon appeared to be the more effective of the
available medications.
‘The person most likely to respond to ChEI’s’
 Generally fit, active and medically well
 Age 72 years (range 65 -79) when starting CEM’s
 History of gradual memory loss and minimal speech
involvement
 CT scan reported as ‘normal’ or ‘age-related atrophy’
 Alzheimers rather than a Vascular (Mixed) profile
 Baseline MMSE (short form) of at least 9/12
Starting Donepezil
 Trial donepezil first because it is funded!
 Individual response unpredictable
 Clear diagnosis of Alzheimers or Vascular dementia
 Consult with specialist (E-mail ok)
 Start 5mg at night for one month. Monitor for AE
 Assess clinical response and tolerability at one month
 Increase to 10mg & reassess at 3 & 6 months
 Consider cognitive screen at 6mths on full dose
 Reduce to 5mg if AE, or no clinical benefit
Informed Decision
 Explain symptomatic treatment, temporary gains
 Discuss treatment goals
 Discuss adverse effects before starting as this can
effect treatment goals
 Involve family & carers in observing for treatment
response and adverse effects.
 Supervision of compliance with medication
 Competency?
Precautions
 Risk of bradycardia: caution sick sinus syndrome , SA
or AV block
 Asthma and COPD
 Epilepsy or seizure disorder
 Urinary retention
 History GI ulcers, NSAID’s
Contra-indications:
 Hypersensitivity to piperidine derivatives e.g.
antiangina; antidepressants; antipsychotics; urological
Adverse Effects
Very Common
 Nausea , dyspepsia, diarrhoea & vomiting 20% people
Common
 Headache, dizziness, fatigue
 Syncope, bradycardia
 Agitation, confusion
 Sweating, tremor
AE are dose dependent, short duration & resolve
spontaneously or after dose reduction.
START LOW-GO SLOW!
Drug Interactions
 Risk bradycardia: B- blockers, digoxin, amiodarone
and calcium channel blockers
 Other anticholinergic drugs: oxybutinin &
benztropine
Metabolised in liver but few interactions of cytochrome
p450 system clinically significant
 Donepezil increased by fluoxetine, paroxetine,
erythromycin, azole antifungals
 Donepezil decreased by phenytoin, carbamazapine,
dexamethasone, alcohol.
Assessing response to treatment
Cognitive testing can help monitor
 Progression dementia
 Response to CEM
Assess cognitive function & ADL prior to treatment
(self –reported or family observation of behaviour)
 Assess initial treatment response at one month
 After 6 months at highest dose assess cognition and
function with testing.
Baseline assessment cognition/function
Start Donepezil 5mg
One month assess
Initial treatment response/AE
Increase Donepezil 10mg
AE
Assess cognition/function at
6 months on highest dose tolerated
Cognitive/functional
improvement or stability
Deterioration or Adverse effects
Poor compliance/monitoring
Continue & monitor 6 mthly
Consider discontinuing
Persist with therapy 1-2 years
Re-evaluate response
global function, cognition, ADL. behaviour
Improvement or
stabilisation
Continue for
1-2 years
Clinical
response
uncertain
Drug holiday 3-4 weeks
then re-assess
Rapid decline
No change
Re-instate
Discontinue
Discontinuation Effects?
 Always reduce dose gradually before stopping.
 No research evidence to suggest rebound effect after




sudden stop
BUT may be observed in clinical practice
Usually followed by gradual deterioration
Sudden loss of cognitive function is possible
Support and monitor patients during discontinuation
Robertson Davies
How long is a goldfish’s memory?
Questions?