Elderly

Question 1

Delirium
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

Answer 1

Syndrome of acute confusion characterised by fluctuations in awareness, cognition and awareness

Most susceptible groups:
- Elderly patients >65 years
- Hospitalised patients

Secondary to;
- Metabolic causes (hypercalcaemia, hypoglycaemia, hyponatraemia, dehydration)
- Infections (UTIs, pneumonia)
- Trauma (hip fractures)
- Drugs
- Change in environment
- Constipation
- Urinary retention (may be due to BPH- may present with suprapubic distension and weakness)

CLINICAL FEATURES
- Acute alteration in level of awareness and attention (decreased consciousness)- this distinguishes delirium and dementia
- Hallucinations
- Cognitive deficits e.g. memory problems
- Agitation
- Severity of symptoms fluctuates throughout day and worsens in evening

Two types:
- Hypoactive (25%)- decreased psychomotor activity- withdrawn, lethargic, slow to respond
- Hyperactive (75%)- increased psychomotor activity

INVESTIGATIONS
Confusion screen:
- TFTs (hypothyroidism)
- B12
- Folate
- Glucose (hypoglycaemia)
- Bone profile (hypercalcaemia)

Look into underlying cause:
- Urinalysis (UTI)
- Chest x ray (infection)
- CRP/WCC
- Serum glucose (hypoglycaemia)
- Bladder scan (urinary retention)
- Electrolytes

Cognitive impairment screening: AMTS (6 or less suggests delirium or dementia)

MANAGEMENT
- Treat underlying condition e.g. acute urinary retention → catheterise
- Patient comfort and symptoms: fever control, pain management, hydration
- Treat agitation: 1st line antipsychotics e.g. haloperidol/respiradone (in Parkinsons this will worsen symptoms so use lorazepam a benzodiazepine instead).
Offer meds orally, if refuses and poses immediate physical risk to another patient then IM

PREVENT
- early identification of patients at risk
- avoid drugs that worsen delirium (benzodiazepines, anticholinergics, opioids)
- reorient patient regularly

Question 2

What is delerium tremens

Answer 2

Extreme form of acute alcohol withdrawal developing around 72 hours after ceasing alcohol intake

Hallucinations and fluctuating consciousness levels

Chlordiazepoxide and Pabrinex

Question 3

compare and contrast delirium and dementia

Answer 3

Delirium: SUDDEN, rapid and fluctuant, decreased consciousness, impaired attention, recent memory loss, disorganised thought process, hallucinations (VISUAL or tactile), abnormal EEG

Dementia: insidious, slowly progressive deterioration, consciousness INTACT, usually alert unless in advanced phase, recent then REMOTE MEMORY LOSS, hallucinations only in advanced, normal EEG,

Question 4

Dementia
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

Answer 4

Acquired disorder of cognitive function

Most common to least
Alzheimers> Vascular <Lewy Body dementia< Frontotemporal

Alzheimers:
Degeneration of the cerebral cortex, with cortical atrophy and reduction in acetylcholine production
Build up of APP (amyloid precursor proteins) → due to beta and gamma secretase

Vascular dementia:
Brain damage due to several incidents of cerebrovascular disease e.g. strokes/TIAs

Lewy Body Dementia:
Deposition of abnormal proteins (Lewy bodies) within the brain stem and neocortex

Frontotemporal Dementia:
Specific degeneration of the frontal and temporal lobes. Thought to be caused by pick bodies

CLINICAL FEATURES
- Memory impairment
- Cognitive impairment

Alzheimers: Slowly progressive, episodic impairment of memory

Vascular demential: Abrupt cognitive decline and stepwise deterioration

Lewy Body Dementia: steady decline, fluctuating consciousness levels, visual hallucinations, parkinsonian motor disorders

Frontotemporal motor disorders: early changed in personality (impulsiveness and aggressive), family history, 50-60yrs old so earlier than others

Depression can mimic dementia in elderly. But if its depression will have a shorter history with a rapid onset and biological symptoms like sleep disturbances

INVESTIGATIONS
MMSE:
0-17 severe cognitive impairment
18-23 mild cognitive impairment
24-30 no cognitive impairment

In primary care: Blood screen in primary care to exclude reversible causes i.e. FBC, U&E, LFTs, calcium, glucose, TFTs (hypothyroidism), vit B12 and folate levels

In secondary care: Neuroimaging CT/MRI/PET
- Cortical atrophy and hippocampal atrophy in Alzheimer’s
- Lacunar infarcts (white areas on MRI) in Vascular
- Metabolic disorders and atrophy in frontal and temporal lobes in Frontotemporal
- Also look for reversible causes such as subdural haematoma

Lewy body dementia: SPECT (DATscan)

MANAGEMENT
- Cognitive stimulation therapy to improve memory and problem solving skills
- Cognitive rehabilitation

1st (mild mod alzheimers: acetylcholinesterase inhibitors (donepezil, rivastigmine (if hallucinations one of main symptoms), galantamine) can cause prolonged QT

2nd (severe) memantine (NMDA receptor antagonist, leading to decreased glutamate induced excitotoxicity)

Avoid antipsychotics in Lewy Body Dementia → may cause irreversible parkinsonism

Question 5

Multi organ dysfunction syndrome
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication

Answer 5

A clinical syndrome characterised by the development of progressive and potentially reversible physiologic dysfunction of 2 or more organs or organ systems that is induced by a variety of insults, including sepsis

Causes:
- Infection
- Injury
- Hypoperfusion
- Hypermetabolism

These causes then trigger a systemic inflammatory response (sepsis or SIRS)

Finally leads to MODS

SIRS + infection → sepsis → severe sepsis → MODS

DIAGNOSIS
MODS score:
- Stage 1 - increased volume requirements, mild respiratory alkalosis, oliguria, hyperglycaemia, increased insulin requirements
- Stage 2 - tachypnoea, hypocapnia, hypoxaemia, moderate liver dysfunction and haematologic abnormalities
- Stage 3 - shock, azotaemia (high nitrogen in the blood), acid-base disturbance, significant coagulation abnormalities
- Stage 4 - vasopressor dependent, oliguria or anuria, development of ischaemic colitis and lactic acidosis

INVESTIGATIONS
- monitor vitals
- ABG for hypoxaemia, lactic acidosis