Acute Confusion Flashcards
(21 cards)
Acute confusional state
Delirium or acute organic brain syndrome
Predisposing factors of acute confusional state
Over 65
Dementia history
Significant injury
Frailty or multimorbidity
Polypharmacy
Precipitating events - multifactorial of ACC
infection: particularly urinary tract infections
metabolic: e.g. hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration
change of environment
any significant cardiovascular, respiratory, neurological or endocrine condition
severe pain
alcohol withdrawal
constipation
Features of ACC
memory disturbances (loss of short term > long term)
may be very agitated or withdrawn
disorientation
mood change
visual hallucinations
disturbed sleep cycle
poor attention
Management of ACC
Treat underlying cause
Modification of environment
No Parkinson’s disease - haloperidol 0.5mg
With PD use lorazepam
Urgent treatment - quetiapine and clozapine
Subdural haemorrhage
Haematoma - collection of blood deep to the dural layer of meninges
Classification of subdural haemorrhage
Acute - within 48 hours of injury, rapid neurological deterioration
Subacute - days to weeks post injury, gradual progression
Chronic - elderly, develops over weeks to months (no injury?)
Neurological symptoms of SH
Fluctuations in levels of consciousness
Weakness on one side of body
Aphasia
Visual field defects
One sided headache worse over time
Seizures - acute or expanding haematoma
Physical examination findings of SDH
Papilloedema - raised ICP
Pupil changes
Gait - ataxia or weakness in one leg
Hemiparesis or hemiplegia - reflecting mass effect and midline shift
Behavioural and cognitive changes of SDH
Memory loss - chronic SDH
Personality changes - irritability, apathy or depression
Cognitive impairment - difficulty attention, problem solving
SDH associated features
Nausea and vomiting - due to ICP raised
Drowsiness - stupor and coma severe case
Other signs of high ICP - bradycardia, hypertension and Cushing’s triad
Acute subdural haematoma
Collection of fresh blood in subdural space
Caused by high-impact trauma
CT - first line
Large ones push on brain causing midline shift or herniation
Monitor intracranial pressure
Decompressive craniectomy
Chronic subdural haematoma
Collection of blood in subdural space present for weeks-months
Rupture of small bridging veins causes slow bleeding
Elderly and alcoholic patients due to brain atrophy
History of confusion, reduced consciousness or neurological deficit
Fragile bridging veins rupture in shaken baby syndrome
CT imaging findings for SDH
Crescentic in shape
Chronic subdural dark
Treatment for SDH
Small with no associated neurological deficit - manage conservatively with hope it will dissolve
Patient confused, neurological deficit or severe imaging findings - surgical decompression with burr holes required
What is Wernicke’s encephalopathy?
Neuropsychiatric disorder
Caused by thiamine deficiency
Alcoholics
Rare causes - persistent vomiting, anorexia nervosa, stomach cancer and dietary deficiency
Classic triad Wernicke’s encephalopathy
Ophthalmoplegia/nystagmus
Ataxia
Encephalopathy
Features of WE
oculomotor dysfunction
nystagmus (the most common ocular sign)
ophthalmoplegia: lateral rectus palsy, conjugate gaze palsy
gait ataxia
encephalopathy: confusion, disorientation, indifference, and inattentiveness
peripheral sensory neuropathy
Investigations in WE
Decreased red cell transketolase
MRI
Treatment of WE
Urgent replacement of thiamine
Wernicke-Korsakoff syndrome
If WE left untreated / not treated with thiamine
Korsakoff’s syndrome - amnesia and confabulation
