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?