Geriatric Case Conferenc - PowerPoint Presentation

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Geriatric Case Conference

Bow&Tum22/6/55

Presentation…

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Patient profileผู้ป่วยหญิงไทยโสด อายุ 60 ปี

อาชีพ รับราชการครู ปัจจุบันเกษียณแล้ว (สอนสังคมศาสตร์ ม.ต้น รร.ปทุมคงคา)การศึกษา ปริญญาตรีภูมิลำเนา จ.นนทบุรีศาสนา พุทธ

สิทธิการรักษา ข้าราชการ

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Chief complaintหลงลืม 5 ปี

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Present illness 5 ปีก่อน เริ่มมีอาการหลงลืมเรื่องทีเพิ่งทำไป อารมณ์ฉุนเฉียว โกรธง่าย หวาดระแวง มีปัญหาในการทำงานที่โรงเรียน อาศัยอยู่คอนโดคนเดียว

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Present illness

ปี 2550 ผู้ปกครองมาแจ้งทางโรงเรียนว่า อ.อิ่มให้การบ้านนักเรียนวาดแผนที่ทุกวันซ้ำๆ เริ่มมีปัญหาเรื่องการสอนที่โรงเรียน จัดแผนการสอนผิด เขียนใบเสร็จไม่ถูกต้อง ทางโรงเรียนจึงพิจารณาย้ายจากอาจารย์สอนวิชาสังคมมาเป็นอาจารย์ฝ่ายแนะแนว

เริ่มมีพฤติกรรมก้าวร้าว ด่าว่าเพื่อนครูในโรงเรียน เพื่อนครูจึงแนะนำให้เกษียณก่อนกำหนด และแจ้งให้ญาติทราบ เนื่องจากผู้ป่วยอาศัยอยู่คนเดียวที่คอนโดมาตลอด ญาติไปพบที่คอนโดว่าปล่อยให้รกรุงรัง เดินแก้ผ้าในห้อง รื้อเสื้อผ้า ลืมรับประทานอาหาร

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ญาติพาผู้ป่วยเข้ารับการรักษาที่รพ.พระมงกุฎฯ ได้รับยาและติดตามอาการ แต่ยังมีอาการสับสน เห็นภาพหลอน เช่น พูดคนเดียวกับกระจก พูดไม่เป็นคำ เรียงประโยคผิด อารมณ์เสียง่าย ชอบด่าว่าญาติและพูดเหตุการณ์เก่าๆ ญาติเป็นกังวลมากและคิดว่าผู้ป่วยแกล้ง และคิดว่าผู้ป่วยเป็นโรคทางจิต ต่อมาอาการสับสนเพิ่มมากขึ้น ญาติจึงพามารักษาที่รพ.รามาธิบดี

Present illness

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Genogram

CA Colon

72

ปี

1

st

2

nd

AD

Dx

40+ yrs

คุณ

หล่าน

62

ปี

คุณเปี๊ยก

คุณ

ธาริณี

60 ปี

คุณดารีรัตน์

58 ปี

คุณ

โด้ง

CA liver

56 ปี

คุณต๋ง

CA liver

47 ปี

ตู่

41

ปี

ตรอง

21 ปี

ตั๊ก

20 ปี

โอม

25 ปี

ไอซ์

21 ปี

ดิว

23 ปี

แอ๊น

20 ปี

แตม

17 ปี

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Timeline

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Timeline

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Timeline

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Problems list

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Differential diagnosis

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Interfere with work or usual activitiesDecline from prior level of functioningNew Dementia Criteria

Loss cognitive or neuropsychiatric symptom

Not explained by delirium or other psychiatric disorder

เสีย

ADLs

R/O other cause

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Loss cognitive or neuropsychiatric symptom

Impairment ≥ 2

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Physical ExaminationGA : หญิงไทยแต่งตัวดี สะอาด ไม่ค่อยแสดงสีหน้า

BP 120/80 mmHg PR 70/minHEENT : not pale, anicteric

sclera, normal tooth & gum, no oral lesion

LN :

no cervical LN enlargement

Heart :

regular, normal s1,s2, no murmur

Lung :

clear, equal both, no adventitious sound

Abd

:

soft, no mass, not tender ,no

hepatosplenomegaly

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Physicial ExaminationExt :

No edema, no cogwheel rigidity, no spastic, no resting tremorN/S : pupil 3 mm. RTLBE, full EOM, motor power gr. V all, BBK – plantar flextion both

Gait :

normal

Speech :

normal

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Test/Date28/6/54

24/1/5528/2/55

ครั้งที่ 1

ครั้งที่

2

ครั้งที่ 3

Orientation for time

0

0

0

Orientation

for place

1

2

3

Registration

32

2Attention/Calculation0

00Recall0

00Naming

222Repetition

001Verbal command

110

Writing command011

Wristing00

0Visuo-contruction00

0คะแนนรวม7

89

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Test/Date

28/6/54

24/4/55

ครั้งที่ 1

ครั้งที่ 2

CDT

2/10

1/10

Test/Date

28/6/54

24/4/55

ครั้งที่ 1

ครั้งที่ 2

Cube

incorrect

Incorrect

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Dementia?Severity?

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Investigation

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InvestigationCBC

WBC 5200 N 60 L 31 M 6 E 2 B 1 Hb 12.7 Hct 40.9 MCV 89 MCH 27.2

RBC

morpho

normochromia

Cr 0.77

TSH 1.646 (0.35-4.94)

Vitamin B12 338.5 (243.0-894.0)

VDRL NR

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MRI brainMild volume loss of hippocampi

and parahippocampal gyri with thining

of

entorhinal

cortex, bilaterally which may be represent Alzheimer disease.

The bilateral pars

compacta

of the

substantia

nigra

of the midbrain are well identified.

The rest of brain parenchyma shows normal signal intensity

without space occupying lesion. Brainstem and the cerebellum are unremarkable. The

calvarium and the skull base have normal marrow signal intensity. No midline shifting, hydrocephalus or extraaxial collection is detected.Impression

Mild volume loss of hippocampi and parahippocampal gyri with thining of entorhinal cortex, bilaterally which may be represent Alzheimer disease.

Generalized mild cerebral volume loss.

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FDG PETThe study reveals severely decreased FDG activity in bilateral

parietotemporal cortices which is relative symmetric. There is also mildly to moderately decreased FDG activity in the frontal cortices, right slightly involved more than left. The tracer distribution in the rest of the scanned regions appears within normal limits. Limited low dose,

noncontrast

CT images show no corresponding abnormality.

Impression

Severe

hypometabolism

of bilateral

parietotemporal

cortices with less involvement of frontal cortices favor Alzheimer’s disease, less likely Pick’s disease.

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Diagnosis

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Clinical Features Distinguishing AD and Other DementiasAD:

Memory, language, visual-spatial disturbances, indifference, delusions, agitationFrontotemporal dementia:

Relative

preservation of memory and visual-spatial, skills, personality change, executive dysfunction, excessive eating and drinking

Lewy

body dementia:

visual

hallucinations, delusions, extrapyramidal,

symptoms,fuctuating

mental status, sensitivity to antipsychotic medications

Vascular dementia:

abrupt

onset, stepwise deterioration, executive dysfunction, gait changes

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Cognitive domain

ADDLBbvFTD

VaD

Depres-sion

Free recall

+++

++

+/-

+

+

Recognition

+++

-

-

--

Prompting X√

√√

√Intrusions +++

++++++++

Semantic memory (naming)+++++

+/-Procedural memory-

+-++

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Cognitive domain

AD

DLB

bvFTD

VaD

Depression

Working memory

++

+++

+++

++

+/-

Insight

+++

+

+++-

-Attention+++++

++

+++++Executive functions

++ typical AD+++ frontal variant++++++

+++++Visuospatial skills++ typical AD

+++ PCA+++-++

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Memory impairment in AD

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Memory impairment in AD

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Memory impairment in AD

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Memory impairment in AD

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Memory impairment in AD

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Alzheimer’s dementiacriteriaProbable ADPossible ADProbable or possible AD with

evidence of the AD pathophysiological processBiomarkers of brain amyloid-beta (Ab) protein depositionBiomarkers of downstream neuronal degeneration or injury

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Atypical ADLogopenic progressive aphasiaLanguageFrontal variant ADBehavior, Executive

Posterior cortical atrophyVisuospatial

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Frontotemporal dementia

FTD

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FTDDementia in persons younger than 65 yearsA neurodegenerative disease of unknown

etiologyBehavioral and language Relatively preserved memory

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Neuroimaging (MRI) usually demonstrates frontotemporal atrophy

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Types of FTDBehavioral variant frontotemporal dementiaSemantic dementia

Progressive nonfluent aphasia

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Diagnostic Behavioral and Language Features of Frontotemporal Dementia Variants

Behavioral variant frontotemporal dementia

Semantic dementia

Progressive

nonfluent

aphasia

Core features

Insidious onset and gradual progression

Insidious onset and gradual progression

Insidious onset and gradual progression

Early decline in social and interpersonal conduct

Language disorder characterized by progressive, fluent, empty, spontaneous speech; loss of word meaning; impaired naming and comprehension; semantic

paraphasia

Nonfluent

, spontaneous speech with at least one of the following:

agrammatism

, phonemic paraphasia*, anomia

Early impairment in regulation of personal conductPerceptual disorder characterized by impaired recognition of familiar faces and/or objects—

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Diagnostic Behavioral and Language Features of Frontotemporal Dementia Variants

Behavioral variant frontotemporal dementia

Semantic dementia

Progressive

nonfluent

aphasia

Core features

Early emotional blunting

Preserved perceptual matching and drawing reproduction

—

Early loss of insight

Preserved single-word repetition and ability to read aloud

—

Supportive features

Behavioral disorder, with decline in personal hygiene; distractibility and

impersistence

;

hyperorality; dietary changes; repetitive stereotypic behavior; utilization behaviorBehavioral changes with loss of sympathy and empathy; narrowed preoccupations; parsimonyBehavioral changes with early preservation of social skills; late behavioral changes similar to behavioral variant

frontotemporal dementia

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Diagnostic Behavioral and Language Features of Frontotemporal Dementia Variants

Behavioral variant frontotemporal dementia

Semantic dementia

Progressive

nonfluent

aphasia

Supportive features

Speech and language changes with altered speech output; echolalia†; perseveration‡;

mutism

Speech and language changes with press of speech; idiosyncratic word usage; absence of phonemic

paraphasia

*;

dysgraphia

§; preserved calculation

Speech and language changes with stuttering; impaired repetition; alexia∥;

dysgraphia§; early preservation of word meaning; late mutism

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AD Criteria, con’tPathophysiologically proved AD dementiaMeets clinical criteria +

neuropathological examDementia unlikely to be due to ADDoes NOT meet clinical criteria ORMeets

criteria but there is evidence for alternative diagnosis, such as HIV dementia or HD that rarely overlap with AD

Meets

criteria but both

Aβ

and neuronal injury biomarkers are negative

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MCI due to AD CriteriaEstablish clinical and cognitive criteriaCognitive concern reflecting a change in

cognitionreported by patient or informant or clinician (i.e., historical or observed evidence of decline over time)Objective evidence of Impairmentin one or more cognitive domains, typically including memory (i.e, formal or bedside testing to establish level of cognitive function in multiple domains)

Preservationof

independence in functional abilities

Not

demented

Examine

etiology of MCI consistent with AD

pathophysiological

process

Rule

out vascular, traumatic, medical causes of cognitive decline, where possible

Provide

evidence of longitudinal decline in cognition, when feasibleReport history consistent with AD genetic factors, where relevant

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New Dementia CriteriaCognitive or neuropsychiatric symptoms:Interfere with work or usual activities

Decline from prior level of functioningNot explained by delirium or other psychiatric disorderImpairment involves 2 or more of the following:Inability to acquire and remember new information

Impaired

reasoning and handling of complex task; poor judgment

Impaired

visuospatial

abilities

Impaired

language

Change

in personality behavior, or comportment

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Treatment

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MedicationRivastigmine patch(10) 1 patch แปะ q 24 hr

Memantine (10) 1 x 1 oral pcSertraline(50) 1 x 1 oral pcNa valproate chrono(500) 1 x 1 oral pcQuetiapine (25) 1 x 1 oral

hs

Amlodipine (5) 1 x 1 oral pc

Folic (5) 1 x 1 oral pc

Vitamin B1612 1 x 2 oral pc

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Therapeutic strategiesSymptomatic treatmentDisease-modifying therapy Lifestyle

DietPhysical ExerciseMental Exercise

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Cholinesterase InhibitorsDonepezil, Rivastigmine, Galantamine

Mild to moderate dementiaBenefit in severe dementia not as clear

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MemantineMechanism of action: partial NMDA-receptor antagonistMay block glutamate excitotoxicity

May provide symptomatic benefit via effects on hippocampal neuronsModerate to severeAlzheimer’s dementia

Safe

in combination

with

ChEI

Slide53

Pharmacologic Treatment of Agitation

Symptoms

Medication

Agitation in context of

nonacute

psychosis

Olanzapine

2.5–10 mg/d

Quetiapine

12.5–100 mg/d

Risperidone

0.25–3 mg/d

Agitation in context of depression

SSRI, eg, citalopram 10–30 mg/d

Anxiety, mild to moderate irritability

Trazodone

50–100 mg/d

Agitation or aggression unresponsive to first-line treatment

Carbamazepine

300–600 mg/d

Olanzapine

(intramuscular) 2.5–5 mg IM

Sexual aggression, impulse-control symptoms in men

Second-generation antipsychotic

If no response, conjugated equine estrogens 0.625–1.25 mg/d

Slide54

DietMediterranean diet (Scarmeas N. JAMA. 2009)High in vegetables, legumes, fruits, nuts, cereal, fish, olive oil

Low in saturated fatsUp to 40% reduction in risk for developing dementia

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Non pharmacological treatment in dementiaCognitive focus interventionCognitive stimulation Cognitive training

Cognitive rehabilitationOtherMusic therapy Aromatherapy Massage and touchExercise

Cognitive stimulation is engagement in a range of activities and

discussions (usually in a group) aimed at general enhancement of

cognitive and social functioning.

Cognitive training is guided practice on a set of standard tasks

designed to reflect particular cognitive functions; a range of difficulty

levelsmay

be available within the standard set of tasks to suit

the individual’s level of ability. It may be offered in individual or

group sessions, with pencil and paper or

computerised

exercises.

Cognitive rehabilitation is an

individualised

approach where personally

relevant goals are identified and the therapist works with

the person and his or her family to devise strategies to addressthese. The emphasis is on improving performance in everyday liferather than on cognitive tests, building on the person’s strengthsand developing ways of compensating for impairments

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Cognitive stimulation

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Control group : usual activityDoing nothingGame : bingo, singing, art and crafts

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Intervention : programme14-session programme , twice a week, 45min per session over 7 weeks

Reality orientation and cognitive stimulationTopic : using money, word games, the present day and famous facesReality orientation board

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Cognition

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Follow up

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Communication and social interaction

QoL

GDS

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ADL, Behavior, caregiver  non significant

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Cognitive training and cognitive rehabilitation

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Cognitive training : 9 studies Cognitive rehabilitation : none

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Change in MMSE

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CHANGE in…Immediate verbal memory scoresDelayed verbal memory scoresVerbal letter fluency scoresVerbal category fluency scores

Executive function scoresSelf-report of memory functioningParticipant self-report of mood (depression)Informant report of participant

memory functioning

Non significant

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CHANGE in…Informant report of participant mood (depression)Informant report of participant functional ability (ADLs)Informant report of informant reaction to participant memory and

behaviour problems(Follow up) immediate verbal memory scores(Follow up) executive function (sequencing) scores(Follow up) informant report of participant memory functioning(Follow up) informant report of participant functional ability (activities of daily living)

Non significant

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Music therapy

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Type of music therapyReceptive music therapyActive music therapy

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Total minute spent not wandering during all sessions of main therapy

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Mean change in MMSE

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Number of agitated behavior

2 week

4

week

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Massage and touch

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The use of hand massage for an immediate and short-term reduction of agitated behaviourThe addition

of touch to verbal encouragement to eat for the normalization of nutritional intake

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Mean agitate score

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Aroma therapy

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Only 2 RCT, other not good study designStatistical significant in decreased agitated

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Evaluation of Response to Any Cognitive EnhancerElicit caregiver observations of patient’s cognitive function and behavior (alertness, initiative) and follow functional status (ADLs and instrumental ADLs).Follow cognitive status (eg

, improved or stabilized) by caregiver’s report or serial ratings of cognition (eg, Mini-Cog, MMSE)

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Test/Date28/6/54

24/1/5528/2/55

ครั้งที่ 1

ครั้งที่

2

ครั้งที่ 3

Orientation for time

0

0

0

Orientation

for place

1

2

3

Registration

32

2Attention/Calculation0

00Recall0

00Naming

222Repetition

001Verbal command

110

Writing command011

Wristing00

0Visuo-contruction00

0คะแนนรวม7

89

Slide84

Test/Date

28/6/5424/4/55ครั้งที่ 1

ครั้งที่ 2

CDT

2/10

1/10

Test/Date

28/6/54

24/4/55

ครั้งที่ 1

ครั้งที่ 2

Cube

incorrect

Incorrect

Slide85

Follow up

Typical AD  MMSE drop ≥ 3/yr

MMSE drop ≤ 2/yr

 work

Advance directive !!!

MMSE

Hallu

/

Delu

Apathy

Depression

Agitation

Manic-like/attention

ADLs/

iADLs

REM

Insomnia

Increase day sleep

Driving, falling, financial

GI, GU,

cardio,temp

,

dysphagia

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THANK YOU