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Confusion in the Elderly. M Ward Horton January 2011. Outline. Personal Case Histories Group Case Histories Review of Delirium & Dementia Literature review. Case A. Mrs FG 92 yr old retired school cook widow Living alone, malnourished Tripped over her enormous dog - # NOF

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confusion in the elderly

Confusion in the Elderly

M Ward

Horton

January 2011

outline
Outline
  • Personal Case Histories
  • Group Case Histories
  • Review of Delirium & Dementia
  • Literature review
case a
Case A
  • Mrs FG
  • 92 yr old retired school cook widow
  • Living alone, malnourished
  • Tripped over her enormous dog - # NOF
  • Admitted for DHS
  • 6 hours post op - agitated, confused
  • Bloods normal
  • CT Brain normal
case a1
Case A
  • Altered level of consciousness
  • No focal or lateralizing signs
  • MRI Brain - DWI - acute infarct right & left parietal lobes
  • Started aspirin 300mg
  • 48 hrs later - complete resolution of confusional state - Good recovery
case b
Case B
  • Mr JH
  • 74 yr old male retired Professor of Hebrew studies
  • Increasingly vague and distant for 3 months
  • Increased apathy
  • Withdrawn
  • Stopped initiating activities - Passive
case b1
Case B
  • Previously fit & well
  • Prior to the change in character had visited Avignon with wife - caught a nasty viral infection and had been unwell - sore throat,runny nose, myalgia, lethargy for 2-3 weeks
  • Since then - never returned to previous level of function
case b2
Case B
  • Referred by GP - ?memory loss, personality change
  • Wife very concerned …..
  • Clinic - Very mild asymmetric cogwheel rigidity left arm, possible loss of facial expression , normal eye movements
  • MMSE 30/30 BP 130/70 No drop
case b3
Case B
  • CT Brain
  • CXR
  • Bloods
  • 1 monthly review
  • Trial of Sinemet
  • Gastritis - referred for OGD
  • ∆ Gastritis - started on PPI
case b4
Case B
  • Small vessel disease
case b5
Case B
  • Further review - no significant benefit from sinemet
  • Current working ∆ Possible vascular parkinsonism
  • Prior to next monthly review --admitted to HGH with increased tiredness
  • GP had checked bloods - creat 590
  • Renal biopsy - Tubulointerstitial nephritis 2° to PPI
case b6
Case B
  • Steroids started - good renal recovery and mentally started to recover
  • Asymmetric cogwheel rigidity had disappeared
  • Sinemet withdrawn - no deterioration
  • Conclusion: Significant Delirium illness
case c
Case C
  • Mrs BT
  • 86 yr old former ballerina
  • 6 month history of increasingly mild forgetfulness , decreased mobility, ?incontinence
  • Lives alone with informal support network
  • Admitted at the weekend after calling Police 5 times and next of kin
case c1
Case C
  • Agitated and confused
  • Rambling conversation
  • No focal neurological deficit
  • No neck stiffness
  • Bloods normal, urine dip -ve
  • CT Brain
case c2
Case C
  • ∆ Normal Pressure Hydrocephalus
  • LP - 40 mls withdrawn
  • CSF normal
  • No symptomatic improvement
  • Good nursing care
  • Less agitated - MMSE 17/30
case d
Case D
  • Mrs EB found wandering by husband
  • Acutely confused
  • Brought to ED
  • 2 seizures in ED
  • CT Brain - Small vessel disease, old lacunar infarct
  • Bloods -
case d1
Case D
  • Confusion persisted for 24 hrs
  • Then resolved
  • TROP 3.4
acute confusional state
Acute Confusional State
  • This state is at one end of the spectrum of disordered levels of consciousness
  • The other end - coma
  • Disordered LOC reflects either a bilateral cortical insult or focal brainstem insult
plum posner 1980
Plum & Posner (1980)
  • Assessment of patient with stupor or coma:
  • Stupor/coma with focal/lateralizing signs above or below tentorium
  • Stupor/coma with signs of meningeal irritation
  • Stupor/coma related to toxic/metabolic insults
slide21
P & P
  • Allows rapid determination of which path to follow in the acute presentation of illness
  • Toxic/metabolic causes most common
  • Followed by focal/lateralizing signs
stupor coma
Stupor/Coma
  • This approach helps you to rule out catastrophic, potentially treatable illness
  • Helps you determine whether patient needs urgent neuroimaging and LP
delirium
Delirium
  • Can occur in the setting of a specific neurological insult - stroke, psychotropic medication, SAH, encephalitis
  • Can occur in anyone ill enough
  • Historically, delirium noted to be a non-specfic marker of illness - a geriatric giant
  • Theoretically any illness could give rise to delirium
  • Hence books contain long lists of causes of delirium
delirium1
Delirium
  • Reality - common illnesses make up the vast majority of cause of delirium
  • Previously delirium was felt to be short lived - however, the current literature suggests some patients experience persistence of problems for some time
delirium dsm iv
Delirium DSM-IV
  • Disturbance of consciousness ie reduced clarity of awareness of the environment , with reduced ability to focus,sustain or shift attention
  • A change in cognition ie memory deficit, disorientation, language disturbance
  • Disturbance tends to develop over short period of time and tends to fluctuate during the day
  • Medical examination, lab findings linked to direct physiological consequence of a gen med condition
pathophysiology
Pathophysiology
  • Delirium essentially a disorder of arousal and attention - involving RAS and nucleus basalis of Meynert
  • Cholinergic deficiency demonstrated
  • CRP link
delirium2
Delirium
  • Prevalence - gen int med 15-25%
  • Amongst older pts in surgery - ≥66%
  • Highest rates are those who are frail and those with dementia
delirium3
Predisposing

Advanced age

Frailty

Dementia

Psychiatric illness

Malnutrition

Chronic anticholinergic drug use

Precipitating

Any acute illness

Any medication

Withdrawal of meds

Any trauma

Any anaesthetic

Environmental change

Delirium
management
Management
  • Identify & treat underlying cause
  • No RCTs for pharm Mx of delirium
  • Supportive care - skilled calm care appreciated by delirious patients
prognosis
Prognosis
  • Difficult to give accurate figures due to wide variety of methods that delirium has been diagnosed the literature- hence some patients with delirium have dementia
  • However, patients tend to be frail, have underlying cognitive impairment
  • Studies suggest increased LOS
  • Increased rate of discharge to NH
  • Increased mortality
dementia
Dementia
  • Acquired impairment of intellectual and memory function caused by disease of the brain
  • Not associated with disordered LOC
case history july 2008
Case HistoryJuly 2008

63, vehicle welder, lives Swindon

Referred to OXMAC Jul 2008

5 year history memory problems

Simple memory lapses

Conversations

Appointments

Daily

Continuous

case history
Case History

Had been seen in another memory clinic over period of few years

Diagnosis = mild cognitive impairment

GP wished second opinion

‘Long term implications of this diagnosis, could any improvement be foreseen’

case history1
Case History

Working as welder, no problems with work

Driving, often on own, probably ok

Anxiety, shaking and hyperventilation episodes

Low mood

Worse mornings, improves thro’ day

Abnormal sleep

Treatment Fluoxetine

examination
Examination

Mild evidence of parkinsonism

Immobile face, difficulty turning, reduced arm swing particularly on left

MMSE 26/30

Hopkins Verbal Learning Test 26/36

Clox 11 and 14/15

case history2
Case History

Seemed depressed

Increase Fluoxetine

Parkinsonism mild, but may be relevant

case history october 2008
Case HistoryOctober 2008

Reviewed clinic Oct 08

More marked parkinsonism

Cog-wheeling right arm

Driving worse according to wife (roundabouts / too slow)

Probably worsening cognition despite increased Fluoxetine

Still working

case history3
Case History

MMSE 25/30

No clear fluctuation

No clear history hallucinations

Considering diagnosis early dementia

DaT scan

case history january 2009
Case HistoryJanuary 2009

Seen clinic Jan 09

Worsening Parkinsonism

Balance and gait deteriorating and affecting work

Prominent dreams, no hallucinations

MMSE 22/30

CLOX 8+14

HVLT 25/36

case history4
Case History

Diagnosis likely Dementia with Lewy Bodies

case history april 2009
Case HistoryApril 2009

Seen in PD clinic April 09

Started L-Dopa

dementia with lewy bodies
Dementia with Lewy Bodies

Increasingly recognised

Possibly second most prevalent behind AD

10-22% dementias

Severe nigrostriatal dopaminergic degeneration

This is not present in AD

neuropathology
Neuropathology

Round, eosonophilic, intracytoplasmic inclusions in nuclei of neurons

Immunohistochemical stain for ubiquitin and alpha-synuclein facilitated identification outside substantia nigra

slide54
Lewy

Alzheimer

Lewy

Anatomical Lab Munich 1906

  • Frederich Lewy, 1923, neuropathology PD
    • Half cases had dementia
is making a clinical diagnosis of dlb important
Is making a clinical diagnosis of DLB important?

Most frequent diagnostic confusion between DLB and AD

Lack of viable clinical methods to assess fluctuating attention and cognition

is making a clinical diagnosis of dlb important1
Is making a clinical diagnosis of DLB important?

Modify pharmacotherapy

Assess patient for additional DLB specific symptoms

Avoidance of typical and atypical antipsychotics

Some patients may respond well to cholinesterase therapy

consensus criteria for diagnosis central core suggestive features
Consensus criteria for diagnosisCentral / Core / Suggestive Features

Progressive cognitive decline

Fluctuating cognition

Recurrent well formed detailed hallucinations

Spontaneous features of Parkinsonism

REM sleep disorder

Severe neuroleptic sensitivity

Low Dopamine transport uptake on DaT scan

consensus criteria for diagnosis supportive features
Consensus criteria for diagnosisSupportive Features

Repeated falls

Syncope

Severe autonomic dysfunction

Hallucinations in other modalities

Systematized delusions

Depression

Relative preservation of medial temporal lobe on MRI / CT

Generalised reduced uptake on SPECT or PET perfusion imaging

consensus criteria for diagnosis
Consensus Criteria for Diagnosis

Conflicting Features

Evidence in imaging or clinically of cerebrovascular disease

First appearance of Parkinsonism at late (severe) dementia stage

consensus criteria for diagnosis1
Consensus Criteria for Diagnosis
  • Temporal sequence of symptoms
    • DLB when dementia before or with parkinsonism
    • PDD, dementia in context of well established Parkinson’s disease

Consensus criteria of the 3rd report of DLB consortium, McKeith et al,

Neurology 2005;65:1863

dat scan dopaminetransporter imaging with i 123 spect
DaT ScanDopamineTransporter Imaging with I123 SPECT

Demonstration of low Dopaminergic activity in Striatum in DLB

Also seen in PD, multi- system atrophy, progressive supranuclear palsy

Not seen in AD

slide62
Sensitivity and specificity of dopamine transporter imaging with I 123 SPECT in dementiaMcKeith et al Lancet Neurol 2007;6:305-13

326 patients

Probable, possible, non-DLB dementia

Clinical diagnosis established by consensus panel

slide63
Sensitivity and specificity of dopamine transporter imaging with I 123 SPECT in dementia McKeith et al Lancet Neurol 2007;6:305-13

Abnormal scans 77.7% sensitivity for detecting clinical probable DLB

Specificity 90.4% for excluding non DLB dementia

summary
Summary

DaT scan can make contribution increasing diagnostic accuracy in DLB

Abnormal scan in dementia without history of PD is suggestive DLB

Use in ‘possible’ DLB to increase diagnostic confidence

Confirm in ‘probable’ if remain uncertain

Acceptable to patients

summary1
Summary

Significant advance in distinguishing DLB from AD

james parkinson
James Parkinson

‘The senses and intellect are uninjured’

  • Frederich Lewy, 1923, neuropathology PD
    • Half cases had dementia
slide71

Anatomical Lab Munich c. 1906

Alzheimer

LEWY

Cerletti

slide72

Visual assessment of DATscan (FP-CIT)

Normal

Abnormal type1

Abnormal type 2

Abnormal type 3

differential diagnosis
Differential Diagnosis

Delirium superimposed on AD and other dementias may mimic DLB (fluctuations and hallucinations)

NPH

CJD

neuropathology1
In DLB; LB’s found in deep cortical layers throughout the brain esp ant frontal and temporal lobes

In PD LB’s in substantia nigra and brainstem nuclei

Pathology of DLB and PD similar, in PD LB’s in cortex as age and develop cognitive problems

Neuropathology
neuropathology2
Alpha-synuclein (ASN) aggregates in insoluble form as filaments and is a major component of LB

Amyloid plaques also seen but less frequent than AD

Neurofibrillary tangles much less common than AD

ASN as LB’s also seen in MND and multi system atrophy (the alpha synucleopathies)

Neuropathology
slide83

Caudate

Putamen

Globus pallidus

dat scan
DaT Scan

Ioflupane

Phenyltropane compound

I 123

Visible to Gamma camera

½ life 13 hours

High binding affinity for dopamine transporters in the brain, particularly the striatal regions

Shows a quantitative measure and spatial distribution of the transporters

dat scan1
DaT Scan

Oral potassium iodide to block thyroid uptake

Injection 3-6 hours pre scan

differential diagnosis1
Differential Diagnosis

Parkinson’s disease dementia

Arbitrary, setting of established PD

One year rule does not correlate well to pathology

Older age onset

Faster decline

Decreased L-dopa responsivity

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