Neuro15 - Confusion in the Elderly Patient (Delirium & Dementia) Flashcards
3 main groups of causes of confusion in elderly patients (3Ds)
- ) Delirium - acute change in consciousness/cognition
- ) Depression - change in mood/feeling of self-worth
- ) Dementia - cognitive decline due to brain disease
Delirium
Definition
Investigations
Management
Complications
- ) Definition - acute onset (1-2 days) of confusional state w/ altered level of consciousness
- hyperactive (more common): agitation, confusion, hallucinations, wandering, aggression
- hypoactive: lethargy, withdrawn, drowsy, inattention - ) Investigations
- basic obs/EWS, GCS/AVPU
- bloods - FBC, U+Es, LFTs, TFTs, clotting, bone profile, haematinics, glucose, blood cultures
- urinalysis, CXR, CT Head
- AMTS or MMSE - ) Management
- treat the underlying cause
- environment orientation: clocks, familiar objects, control noise, adequate lighting, ambient temperature
- pharmacological (last-line): haloperidol or lorezapam - ) Complications
- increased mortality, prolonged admission, increased risk of developing dementia
- can take up to 3 months to return to baseline whilst some never get back to their baseline
Causes of Delirium (CHIMPS PHONED)
C H I M P S P H O N E D
- ) Constipation - often causes hypoactive delirium
- ) Hypoxia
- ) Infection/Intracranial
- UTI, sepsis, meningitis, pneumonia
- stroke, haemorrhage, epilepsy, abscess
3.) Metabolic Disturbance - dehydration, electrolyte imbalance, normal pressure hydrocephalus
- ) Pain - esp if uncontrolled
- ) Sleeplessness
- ) Prescriptions
- anticholinergics, anti-depressants, anti-histamines
- opiates, beta-blockers, corticosteroids, benzos
- dopamine agonists, lithium, calcineurin inhibitors
7.) Hypothermia/Pyrexia
- ) Organ Dysfunction
- hepatic or renal failure
- endo: hyper/hypothyroidism, Cushing’s, Addison’s - ) Nutrition - malnutrition
- ) Environmental Changes - disorientation
- ) Drugs
- OTC, illicit drugs, smoking
- withdrawal: alcohol, benzos, cocaine, coffee
4 general features of dementia
Definition
Onset
Investigations x4
Pharmacological Treatment x4
1.) Definition - set of diseases characterised by a progressive decline in higher cortical function
- ) Onset - can be early or late
- early onset is <65, late-onset is 65+
- prion diseases and aggressive brain tumours are the most common cause of rapid-onset dementia in young people - ) Investigations
- general blood tests, random BM, vit B12/folate
- syphilis testing if risk is identified in the history - ) Pharmacological Treatment - AChEi or memantine
- AChEi: donepezil, galantamine, rivastigmine
- NMDA antagonist: memantine
Delirium vs Dementia
Onset and Progression
Hallucinations
Speech
Consciousness and GCS
- ) Onset and Progression
- delirium: rapid onset with fluctuating course
- dementia: slow onset and steady decline - ) Hallucinations - present in delirium, rare in dementia
- ) Speech - can both be slow but delirium can be fast
- ) Consciousness and GCS - reduced in delirium
5 features of Alzheimer’s dementia
Pathophysiology x2 Macroscopic Changes x3 Genetics x3 Symptoms x4 Treatment x2
- ) Pathophysiology - abnormal proteins kills neurones
- ß-amyloid plaques: accumulate and clump together between neurones due to abnormal breakdown
- neurofibrillary tau tangles: tau protein is abnormal and the microtubule structures collapse inside the neurone - ) Macroscopic Changes
- global atrophy: frontal, parietal, temporal lobes
- sulcus widening
- enlarged 3rd and 4th interventricular spaces - ) Genetics - defects in these proteins:
- early onset: ß-amyloid precursor protein, presenilin 1/2
- late-onset: apolipoprotein E gene - ) Symptoms - insidious onset with slow progression
- ↓memory, ↓spatial navigation
- ↓executive functions: language, calculation - ) Treatment - AChE inhibitors or memantine
- monotherapy: AChEi or memantine (if severe)
- memantine if AChEi are contraindicated/intolerant or are already on an AChEi for other reasons
3 features of Lewy body dementia
Pathophysiology (+4 locations)
Symptoms x3
Treatment x3
- ) Pathophysiology - presence of Lewy bodies
- aggregation of alpha-synuclein protein in cytoplasm
- fronto-temporal lobe, substantia nigra, cingulate gyrus - ) Symptoms - gradually progressive, clinical triad
- fluctuating cognition, attention and alertness
- visual hallucinations
- parkinsonian features: shuffling gait, flexed posture - ) Treatment - AChE inhibitors or memantine
- donepezil or rivastigmine (both if severe)
- galantamine if others not tolerated
- memantine if AChE inhibitors contraindicated
3 features of fronto-temporal dementia
Pathophysiology
Frontal Lobe Symptoms x4
Temporal Lobe Symptoms x2
- ) Pathophysiology - atrophy of frontal/temporal lobe
- 2nd most common cause of early onset (peak: 55-65) - ) Frontal Lobe Symptoms
- altered behaviour, personality, social conduct
- appears disinhibited and apathetic
- expressive dysphasia (Broca’s area)
- primitive reflexes (PMC): grasp and palmomental reflex - ) Temporal Lobe Symptoms
- short/long-term memory impairment
- receptive dysphasia (Wernicke’s area)
3 features of vascular dementia
Pathophysiology
Symptoms
Treatment
- ) Pathophysiology - cerebrovascular disease (i.e stroke)
- risk factors: hypertension, diabetes, smoking etc. - ) Symptoms - step-wise deterioration of cognitive function with focal neurological symptoms
- ) Treatment - treated pharmacologically if they also have Alzheimer’s, Parkinson’s or Lewy body dementia
3 features of AIDS-Dementia complex (ADC)
Pathophysiology
Symptoms x6
Treatment
- ) Pathophysiology - HIV-infected macrophages enter the brain and cause indirect damage to neurones
- gradual onset but rapid progression - ) Symptoms
- cognitive impairment, dysarthria, incontinence
- psychomotor retardation, tremor, ataxia
3.) Treatment - treat HIV (anti-virals)