5- Psychiatric emergencies Flashcards
name the key psychiatric emergencies
- Neuroleptic malignant syndrome
- Delirium tremens
- Wernicke’s
- Acute dystonia
- Lithium toxicity
- Clozapine induced agranulocytosis
antipsychotics are broadly divided into 2 categories
first generation
second generation
first generation antipsychotics
‘Typicals’
- Dopamine (D2) receptor antagonists.
- Developed in the 1950s.
- Examples include haloperidol, chlorprothixene
- Also exert antagonism on noradrenergic, cholinergic, and histaminergic neurones
second generation
‘atypicals’
- serotonin-dopamine receptor antagonists.
- Examples include aripiprazole, risperidone, olanzapine.
why are first gen antipsychotics associated with more side effects
Also exert antagonism on noradrenergic, cholinergic, and histaminergic neurons
First-generation antipsychotics are associated with more side-effects that include:
- Extrapyramidal: movement disorders like parkinsonism and dystonia
- Anti-cholinergic: dry mouth, dry eyes, constipation, urinary retention
- Anti-histamine: sedating
- Cardiovascular: prolonged QT interval, arrhythmias
- Neuroleptic malignant syndrome
second-gen antipsychotics side effects
- have a lower side-effect profile
However, there is still a risk of
- extrapyramidal side-effects,
- cardiovascular side-effects (e.g. prolonged QT interval, arrhythmias), and
- neuroleptic malignant syndrome.
- Weight gain and metabolic syndrome long-term
neuroleptic malignant syndrome (NMS)
is a rare, life-threatening disorder that is associated with the use of antipsychotic drugs (previously known as neuroleptic
medications).
- High mortality
prevalence of NMS
- Up to 3% of those taking antipsychotics
- Can occur at any age- predominant in young males
aetiology of NMS
The exact cause is unknown.
- Seen most commonly with potent first generation antipsychotic (typical antipsychotics)
o Haloperidol
o Fluphenazine
- Can also be precipitated by a sudden dose reduction or withdrawal of antiparkinsonian agents in patients with Parkinson’s disease
pathophysiology of NMS
- Central blockade of dopamine in they hypothalamus leads to hyperthermic and dysautonomia. Blockage of other central pathways give rise to movement disorders
RF for NMS
- High antipsychotic dose/ high potency antipsychotics
- Concomitant drug use e.g. lithium
- Depot
- Medical illness
- Previous NMS
presentation of NMS
Occurs within 2 weeks of starting
- Altered mental state (confusion)
- Fever >38 degrees
- Muscular rigidity
- Dysautonomia (autonomic instability)
o Tachycardia,
o Labile blood pressure
o Profuse sweating
o Arrhythmias
Investigations for NMS
Requires a low index of suspicion whilst taking antipsychotics
- Clinical diagnosis
- Raised creatine kinase (CK) due to muscle rigidity (may be normal if rigidity is not profound
o Can lead to rhabdomyolysis
complications of NMS
cardiac arrest and arrhythmias, AKI, rhabdomyolysis, DIC, VTE
DD for NMS
- Serotonin syndrome: similar presentation to NMS in association with selective serotonin reuptake inhibitor (SSRI) drug use. Characterised by nausea, vomiting, diarrhoea, shivering, hyperreflexia, myoclonus, and ataxia.
- Malignant hyperthermia: a rare genetic disorder characterised by hyperthermia, muscle rigidity, and dysautonomia in the setting of exposure to certain anaesthetic agents (e.g. succinylcholine) or vigorous exercise.
- Recreational drug use: both use of MDMA (i.e. ecstasy) and cocaine have been associated with an NMS-like syndrome.
management of NMS
Largely supportive. Most episodes resolve within two weeks of removing offending drug
1) Stop causative agent
2) Determine if mild or severe case
Mild cases- supportive care
1) Cardiac monitoring
2) CK and U&Es monitoring
3) IV fluids
4) Antipyretics
5) Cooling blankets for hyperthermia
6) Antihypertensive agents
7) Benzos for agitation
Severe cases- medical therapy
1) Supportive care
2) Dantrolene: ryanodine receptor antagonist (causes skeletal muscle relaxation). Helps treat hyperthermia and rigidity.
3) Bromocriptine: dopamine agonist. Prescribed to restore ‘dopaminergic tone’.
delirium tremens
- Withdrawal delirium due to alcohol withdrawal
- Only occurs in people with a high alcohol intake for more than a month
aetiology of delirium tremens
- Due to long periods of drinking being stopped abruptly
- When alcohol use ceases, the unregulated mechanisms result in hyperexcitability of neurons as natural GABAergic systems are down-regulated and excitatory glutamatergic systems are unregulated. This combined with increased noradrenergic activity results in the symptoms of delirium tremens
BASICALLY NOT ENOUGH GABA WHICH IS INHIBITORY
RF for delirium tremens
- Physical illness
presentation of delirium tremens
- cognitive impairment
- vivid perceptual abnormalities
- formication – tactile hallucinations e.g. bugs crawling on skin
- paranoid delusions
- marked tremor
- autonomic arousal (e.g. tachy, fever, pupillary dilatation, increased sweating)
Signs- dehydration and electorlytre disturbance
complication of delirium tremens
death
investigations ofr DT
- U&Es (electrolyte abnormalities), LFT (liver function tests) and alcoholic hepatitis
management of DT
- large dose of benzodiazepine e.g. lorazepam, chlordiazepoxide until sleeping
- haloperidol for any psychotic features
- intravenous pabrinex
o Contains thiamine (B1), riboflavin (B2), pyridoxine (B6) and nicotinamide, and also benzyl alcohol as a local anaesthetic.
Management
summarise the course of Wernicke-korsakoff syndrome
Wernicke-Korsakoff syndrome
refers to two distinct neurological syndromes resulting from thiamine (Vitamin B1) deficiency
- Wernicke’s encephalopathy
- Korsakoff syndrome
prevalence of WE
Lesions associated with WE are found in up to 2.5% of autopsy- majority of which had been alcohol dependent
- Vascular congestion, microglial proliferation and petechial haemorrhage
aetiology of WE
- In presence of chronic alcoholism
- Can also be caused by anorexia nervosa and hyperemesis gravidarum and GI disease
Due to thiamine (B1) deficiency
- Thiamine def leads to neuronal injury
causes of thiamine deficiency
o Dietary def
o Reduce GI absorption e.g. gastric bypass
o Reduced hepatic uptake
o Impaired utilisation
presentation of WE
triad of
o Confusion
o Ataxia
o Oculomotor dysfunction (Nystagmus)
presentation of korsakoff syndrome
- Chronic amnesic syndrome: Defects in Anterograde and retrograde memory
- Confabulation: stories made up to fill gaps in memory
- Poor insight: unaware of heir illness
investigations for WE
- Clinical diagnosis normally
- Cane criteria
o Dietary def
o Oculomotor dysfunction
o Altered mentals status or mild memory impairment - Neuroimaging e.g. CT to exclude alternative cause of confusion
management of Wernickes
Intravenous thiamine e.g. Pabrinex
- Should be give 2-3 pairs up to three times a day for 3-5 days
- Should be administered before or alongside any glucose infusion
- After initial treatment, patients should be given orqal thiamine replacement and continued until patient not at risk
At risk patients
- Pabrinex prophylactically
Management of Korsakoff syndrome
- Patients rarely recover
- no specific treatment
- May need help with ADL e.g. carers
acute dystonia background
- Extrapyramidal side effect
- An acute medication-induced dystonia- movement disorders characterised by involuntary contractions of muscles, and typically develop within minutes or hours following a trigger such as a medication.
aetiology of acute dystonia
Adverse effect of antidopaminergic agents - EXTRAPYRAMIDAL
o Antiemetics e.g. metoclopramide
o Antipsychotics e.g. haloperidol and chlorpromazine
presentation of acute dystonia
Extrapyramidal side effect within a few days of taking medication
o Onset of atypical posture or position of muscles within minutes or hours of taking medications
o Ocular muscles, jaw, tongue, face, neck and trunk of the body
investigayions for acute dystonia
- Medication history
-
Neuromuscular testing to examine
o Range of motion
o Breathing ability
o Swallowing
o Speech -
Vaccine history
o Tetanus -
Bloods
o ABG (rule out hyperventilation)
o U&Es
Hypomagnesemia
Calcium
Ceruloplasmin
Wilsons disease
management of acute dystonia
- Procyclidine hydrochloride can be given parenterally and is effective emergency treatment for acute drug-induced dystonic reactions.
- If treatment with an antimuscarinic is ineffective, intravenous diazepam can be given for life-threatening acute drug-induced dystonic reactions.
lithium toxicity background
Lithium is the standard long-term therapy in bipolar affective disorder. It minimizes the risk of relapse and improves quality of life.
however can cause toxicity if used improperly
how is lithium toxicity prevented
- Contraindicated in:
o Arrythmia
o Renal impairment
o Hypothyroidism (untreated)
o Low sodium
o Diabetes insipidus
o Addison’s - Regular testing of lithium levels
aetiology of lithium toxicity
- Due to excessive intake (suicidal or accidental) or decreased excretion (dehydration- vomiting and diarrhoea, low sodium diet or kidney problems
adverse reactions to lithium
- initial: nausea, diarrhoea, vertigo, muscle weakness and dazed feeling
- polydipsia/ polyuria
- oedema
- teratogenicity
- hypothyroidisms
- hyperthyroidism
- hyperparathyroidism
o high calcium - nephrotoxicity
how is lithium prescribed to prevent toxicity
- Before lithium is started: UEs, TFTs, pregnancy status, ECG
- Due to its side effect profile and risk of toxicity lithium is strictly regulated:
describe the measuring of lithium levles
o Lithium levels – 12 hours following first dose, then weekly until therapeutic level (0.5–1.0 mmol/L) has been stable for 4 weeks. Once stable check every 3 months.
o U&Es – every 6 months; TFTs – every 12 months.
investigations/presentation of sign of toxicity
1.5–2.0 mmol/L: N+V, coarse tremor, ataxia, muscle weakness, apathy.
investigations/presentation of severe toxicity
> 2.0 mmol/L : nystagmus, dysarthria, hyperreflexia, oliguria, hypotension, convulsions and coma
management of lithium toxicity
Supportive treatment should be initiated, which includes correction of fluid and electrolyte balance.**
Clozapine induced agranulocytosis
- Antipsychotic used to treatment resistant Schizophrenia.
- Decreases neutrophil count and susceptibility to infection.
- Very effective antipsychotic but huge potential for side effects.
- Doesn’t cause extrapyramidal side effects
prevalence of clozapine induced agranulocytosis
- 0.8% of patients on clozapine
prevention and investgiations for agranuloytosis
presentation of agranulocytosis
Occurs most frequently in the first 18 weeks of treatment
- Fever
- Sore mouth
- Sore throat
- infection
management of Clozapine induced agranulocytosis
BEWARE if a patient stops smoking then amount of clozapine will need decreasing
manageging neutropenia
give granulocyte colony-stimulating factor (G-CSF)
which drug causes neuroleptic malignnat sydnrome
antipsychotivc drugs
which drug causes delirium tremens
alcohol withdrawal
what causes Wernicke-Korsakoff syndrome
B1 deficiency- thiamine def
- give pabrinex- mix of B vitamins including B1
which drugs cause acute dystonia
antidopaminergic agents e.g. metoclopramide and haloperidol
whicch drug can induce agranulocytosis
clozapine
which drug is associated with toxicity
lithium
which drugs can cause seratonin sydnrome
SSRIs
