Psychiatric emergencies✅ Flashcards
(26 cards)
Neuroleptic malignant syndrome
- cause
- timing
- Antipsychotic medications (especially typical, e.g. haloperidol)
- Within hours to days of starting med
What is the suspected mechanism of NMS?
Dopamine blockade may trigger massive glutamate release, causing neurotoxicity and muscle damage.
rigid muscles generate heat causing hyperthermia
What are the key clinical features of NMS?
- Pyrexia
- muscle rigidity
- autonomic instability (hypertension, tachycardia, tachypnoea)
- agitated delirium with confusion.
Blood marker of NMS
raised CK
NMS - complications
Rhabdomyolysis: release of CK and myoglobin:
- myoglobin is nephrotoxic -> cause AKI
- break down of muscle cells releases potassium -> causes hyperkalaemia, can lead to arrhythmias and death
other:
- hyperthermia
NMS
- Mx
initial:
- immediate cessation of the antipsychotic
- IV fluids to prevent renal failure
- transfer to a medical ward
medications:
- dantrolene -> decreasing excitation-contraction coupling in skeletal muscle
- bromocriptine -> dopamine agonist
Describe the neurochemical mechanism of alcohol withdrawal
Chronic alcohol use enhances GABA (inhibitory) and suppresses NMDA (excitatory) glutamate activity. Withdrawal reverses this balance, causing CNS hyperexcitability.
alcohol withdrawal timeline
6–12 hrs: tremor, sweating, anxiety, tachycardia
12–24 hrs: hallucinations
24–48 hrs: seizures
24–72 hrs: delirium tremens
delirium tremens
- Sx
alcohol withdrawal
- tool
- Mx
- CIWA-Ar tool to assess severity
- First-line treatment is a reducing regimen of long-acting benzodiazepines (e.g., chlordiazepoxide or diazepam).
(Lorazepam in liver failure) - High-dose B vitamins (Pabrinex) given parenterally, followed by oral thiamine to prevent Wernicke-Korsakoff syndrome.
Wernicke-Korsakoff syndrome
- cause
- alcohol excess leads to thiamine (B1 deficiency)
- poorly absorbed in presence of alcohol
- alcoholics have poor diets
- get many calories from alcohol
Wernicke’s encephalopathy
- patho
- triad
- petechial haemorrhages occur in the brain
1. confusion
2. oculomotor disturbances (nystagmus, ophthalmoplegia
3. ataxia
Wernicke’s encephalopathy
- Ix
decreased red cell transketolase, MRI
Wernicke’s encephalopathy
- Mx
→ medical emergency, high mortality rate
→ Mx - urgent replacement of thiamine
korsakoff syndrome
- memory impairment (retrograde and anterograde)
- behavioural changes
→ often irreversible - patients often require full-time institutional care
acute dystonias
- cause
- definition
- due to antiphsychotics - more common in typical
- abnormal muscle tone leading to abnormal postures
acute dystonias
- examples
- torticollis → involuntary contractions of neck muscles leading to abnormal head positioning
- oculogyric crisis → sustained involuntary upward eye movement
acute dystonias
- Mx
management - procyclidine (anticholinergic)
lithium toxicity
- why is it common?
- lithium has very narrow therapeutic range (0.4-1.0mmol/L) and long half-life
- excreted by kidneys
- lithium toxicity usually if >1.5mmol/L
lithium toxicity
- precipitating factors
- dehydration
- renal failure
- drugs: diuretic (thiazides), ACE inhibitors/ARBs, NSAIDs and metronidazole
lithium toxicity
- features
- coarse tremor
- hyperreflexia
- acute concfusion
- polyuria
- seizure
- coma
lithium toxicity
- Mx
- mild-moderate - volume resuscitations with saline
- IV fluids with isotonic saline, until euvolemic, then twice maintenance rate
- monitory sodium closely if there is concern about lithium-induced nephrogenic DI
- haemodyalsis may be needed in severe toxicity
- sodium bicarbonate sometimes used by limited evidence
clozapine-induced agranulocytosis
- RFs
- previous history of agranulocytosis
- concurrent use of other drugs that affect blood counts
