Psychiatric Emergencies (NMS, Delirium Tremons, SS) Flashcards
What is a pyschiatric emergency? [1]
When a pysc. conditions becomes life-threatening and requires prompt treatment.
E.g.:
- suicidical patient
- Neuroleptic malignant sydnrome
- Serotonin syndrome
When does alcohol withdrawal typically start after last drink [1] & when is the peak? [1]
Typically:
* 3-12 hrs after last drink
Peak:
- 24-48hrs after last drink
NB: blood alcohol does not need to be zero for withdrawal to start
Withdrawal symptoms occur at different times after alcohol consumption ceases> What are these with for:
6-12 hours: [4]
12-24 hours: [1]
24-48 hours: [1]
24-72 hours: [1]
6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: delirium tremens
HSD !
Which assessment tool is used to assess for alcohol withdrawal? [1]
Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar)
Which CIWA-Ar scores would indicate:
- Absent or minimal withdrawal
- Moderate withdrawal
- Severe withdrawal
Absent or minimal withdrawal
- 10 or less
Moderate withdrawal
- 15 or less
Severe withdrawal
- Over 15
Describe the basic pathophysiology alcohol withdrawal [2]
chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors
- alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission)
Describe the treatment of alcohol withdrawal [3]
Chlordiazepoxide (benzodiazepine)
- Fixed dose is straightforward, but symptom based has been shown to reduce overall drug amount
If a patient has liver failue - choose oxazepam or lorazepam as has shorter half life
High-dose B vitamins (Pabrinex) are given intramuscularly or intravenously, followed by long-term oral thiamine.
- This is used to prevent Wernicke-Korsakoff syndrome.
GO OVEr
You have treated a person for acute alcohol withdrawal.
What advice might you give with regards to the long term mangement of their alcohol dependence? [6]
Interventions in the long-term management of alcohol dependence include:
Specialist alcohol service involvement
Alcohol detoxification programme
Oral thiamine to prevent Wernicke-Korsakoff syndrome
Psychological therapy (e.g., cognitive behavioural therapy)
Acamprosate, naltrexone or disulfiram are medications used to help maintain abstinence
Informing the DVLA (their driving licence will be revoked until an extended period of abstinence)
TOM TIP: Calculating alcohol units is a very common exam question.
How do you do this? [1]
Volume (ml) x Alcohol Content (%) ÷ 1000 = Units of Alcohol
For 750 mls of 12% wine: 0.75 x 12 = 9 units
For a 25 ml shot of 40% vodka: 0.025 x 40 = 1 unit
For 500 mls of 5.2% lager: 0.5 x 5.2 = 2.6 units
CAGE Questions
The CAGE questions can be used to screen for harmful alcohol use quickly:
What are they? [4]
C – CUT DOWN? Do you ever think you should cut down?
A – ANNOYED? Do you get annoyed at others commenting on your drinking?
G – GUILTY? Do you ever feel guilty about drinking?
E – EYE OPENER? Do you ever drink in the morning to help your hangover or nerves?
Why do people with alcohol have thiamine deficiency? [3]
Nutritional intake depleted
Alcohol disrupts absorption in gut
Thiamine stored in liver = damaged :(
Describe what is meant by delirium tremens [1] and the characteristics of this [+]
When alcohol is removed, the GABA system under-functions and the glutamate system over-functions, causing extreme excitability and excessive adrenergic (adrenaline-related) activity.
Presentation:
* Disorientation
* Acute confusion
* Severe agitation
* Delusions and hallucinations
* Tremor
* Tachycardia
* Hypertension
* Hyperthermia
* Ataxia (difficulties with coordinated movements)
* Arrhythmias
Describe the hallucinations seen in delirium tremens [1]
Hallucinations are often visual and Lilliputian in nature (small little people)
How do you treat delirium tremens? [4]
Sedation (diazepam or lorazepam)
Fluids
Electrolyte replacements
High potency vitamins
Describe the pathophysiology of WE [2]
Thiamine is an essential cofactor for several metabolic reactions in the body.
- storage occurs for a maximum of 18 days meaning a moderate consumption of thiamine is needed to maintain stores.
Thiamine deficiency leads to neuronal injury
- In chronic disease, there is evidence of neuronal loss, most notably in the medial thalamus
Wernicke’s encephalopathy presents with which triad? [3]
- What are other presenting features [+]
Triad of:
- opthalmoplegia / nystagmus (especially lateral rectus palsy, conjugate gaze palsies: inability to move both eyes in a single horizontal & nystagmus
- ataxia
- confusion
Confusion:
- This is often one of the first noticeable symptoms. Patients may appear disoriented, unable to concentrate, or have difficulty following conversations.
Memory Deficits:
- Both anterograde and retrograde amnesia may be present, and in severe cases, this could progress to Korsakoff’s syndrome.
Apathy or Agitation:
- Emotional changes including apathy, indifference, or even agitation and combativeness can occur.
Other Clinical Features
Hypothermia:
- Although not commonly discussed, hypothermia is a known complication and can be severe in some cases.
Altered Consciousness:
- Severe deficiency can lead to coma, and potentially death, if not treated promptly.
Gastrointestinal Symptoms:
- These are not specific but can include nausea, vomiting, and abdominal pain, often preceding the neurological symptoms.
Tachycardia
NB: This triad of features is only seen in up to one-third of patients.
How would you differentiate DT with WE? [2]
DT is associated with hyperthermia rather than hypothermia in WE.
- DT iss usually associated with a history of having significantly reduced alcohol intake in the prior 5 days.
Cane criteria is the diagnostic criteria proposed for WE. Based on the presence of ≥2 of the following criteria in patients with chronic alcoholism [4]
- Dietary deficiency
- Oculomotor abnormalities
- Cerebellar dysfunction
- Altered mental status or mild memory impairment
How do you tx WE? [2]
WE is managed through urgent administration of parenteral (not oral) thiamine for a minimum of 5 days.
- Oral treatment should follow parenteral treatment.
Care must be taken when administering glucose to those suspected of exhibiting WE as glucose metabolism requires thiamine and such metabolisis will further reduce thiamine levels.
- Thiamine must be administered before or concurrently with any glucose administration.
Describe the features of KS [4]
Korsakoff syndrome
- KS is characterised by profound memory defects. Interestingly, long-term memory is relatively preserved in the condition.
Memory deficit:
- anterograde and retrograde
Confabulation:
- stories made up to fill gaps in memory
Poor insight:
- unaware of their illness
Global cognitive dysfunction:
- seen in some patients. Significant impairment in mental function with the development of dementia
Describe the relationship between Korsakoffs and Wernicke’s encephalopathy [1]
Korsakoffs is a consequence of Wernicke’s encephalopathy
Describe what is meant by neuroleptic malignant syndrome [1]
Describe the presentation [+]
Rare, life threatening, idiosyncratic reaction to anti-pyschotic use
Presentation:
- Muscular rigidity
- Hyperthermia
- Altered mental state
- Autonomic dysfunction
- Tachycardia
- Labile BP
- Sweating
The majority of patients with NMS will develop altered mental status followed by rigidity, fever, and finally dysautonomia.
Altered mental status:
- often presents with agitation and delirium.
- Catatonia can be present.
- May progress to severe encephalopathy and coma.
Rigidity:
- felt as a generalised increase in tone and may be severe. Other motor abnormalities can be present.
Fever (>38º):
- less pronounced with second-generation antipsychotics. May be >40º.
Dysautonomia:
- describes abnormalities in the autonomic nervous system. Thus, often termed ‘autonomic instability’.
- Leads to tachycardia, labile blood pressure, profuse sweating (i.e. diaphoresis) and/or arrhythmias.
NB: mayb present over days!
Describe the typical natural history of NMS [1]
NMS will typically occur within the first two weeks of starting an antipsychotic. However, it can occur after a single dose or after many years of using the medication.
Which clinical investigations would suggest NMS [3]
Increased CK (due to muscle rigidity), WCC and abnormal LFTS
- If severe, muscle necrosis and rhabdomyolysis may develop so AKI may occur
What impact may NMS have on Na levels? [1]
Why? [1]
Hyponatremia may occur secondary to inappropriate secretion of antidiuretic hormone or dehydration.
What are risk factors for NMS? [5]
Dehydration
Rapid antipysc initiation/dose escalation
Use of high-potency agents / depot IM preps
Confusion / agitation
Previous NMS
Describe how you treat NMS [+]
Medical emergency - immediately transfer to acute hosptial
Immediately stop medication that caused
Supportive therapy:
- IV fluids to correct rhabdomyolysis
- antihypertensive agents (e.g. clonidine) for profound hypertension
- Paracetamol for fever
- Cooling for hyperthermia
- Treat electrolyte imbalance, acute kidney injury, rhabdomyolysis
- Cardiac monitoring is usually required due to dysautonomia
- Benzodiazepines can help with acute behavioural disturbance and rigidity
- Severe cases: dantrolene and bromocriptine (to reverse NMS)
- Monitor for 2 weeks+
NB:
- Dantrolene: ryanodine receptor antagonist (causes skeletal muscle relaxation). Helps treat hyperthermia and rigidity.
- Bromocriptine: dopamine agonist. Prescribed to restore ‘dopaminergic tone’.
Which electrolyte changes may seen and need to be corrected for in NMS? [2]
Low levels of potassium and phosphate levels, are also important.
Which drug should you make sure to avoid if have NMS? [1]
Lithium - due to impact on kidneys
Describe the aetiology and pathophysiology of serotonin syndrome [+]
Overstimulation of serotonergic receptors
- SSRIs are the most commonly implicated medications (e.g. citalopram, fluoxetine)
- Also due to increased release of serotonin: amphetamines, MDMA (ecstasy), cocaine
- Impaired serotonin reuptake: SSRIs, SNRIs, MDMA, tricycle antidepressants
- Inhibit serotonin metabolism: Monoamine oxidase inhibitors
- Serotonin receptor agonists: Buspirone, Triptans
NOTE: SS secondary to the use of [drug class] is usually more severe and can be fatal.
NOTE: SS secondary to the use of monoamine oxidase inhibitors is usually more severe and can be fatal.
What is the triad of symptoms seen in serotonin syndrome? [3+]
Triad of:
- autonomic, cognitive / behavioural and neurological symptoms
Autonomic:
- Blood pressure liability
- Diaphoresis
- Dyspnoea
- Fever
- Tachycardia
Cognitive:
- Changes in mental state (confusion, sometimes hypomania) agitation and insomnia
Neurological
- akathisia
- hyperflexia
- impaired coordination
- myoclonus
- tremor
Hunter criteria - SS can be diagnosed in a patient taking a serotonergic agent (e.g. SSRI) and presents with one of the following features [5]
SSRI +
* Spontaneous clonus
* Inducible/ocular clonus and agitation or diaphoresis
* Tremor and hyperreflexia
* Hyperthermia, hypertonia, and ocular/inducible clonus
Describe how you treat SS
Medical emergency
Attention needs to be given to airway, breathing and circulation
Stop offending medications
Cardiac monitoring is usually required due to dysautonomia.
Patients should be monitored and specific complications treated (e.g. electrolyte imbalance, acute kidney injury, rhabdomyolysis).
Benzodiazepines if needing admission
- to help with agitation, seizures, hypertonia and myoclonus
Patients can be considered for serotonin antagonists (e.g. Cyproheptadine).
- Cyproheptadine is a histamine receptor antagonist with action against serotonin receptors.
In severe cases, patients may require organ support (e.g. intubation & ventilation, haemofiltration) and admission to intensive care.
How do you differentiate between NMS and SS with regards to
- Onset
- Neuromuscular findings
- Causative agents
- Treatment agents
- Resolution
Define acute dystonia [1]
Syndrome of sustained, often painful muscular spasms, producing repetitive, twisting movements or abnormal posture, followed by exposure to AP medication
Describe the treatment regime for acute dystonia
Procyclidine 5-10mg
- anticholinergic agent
- should work within minutes
Benzodiazepines should manage distress
- may need regular dose of this (5-7 days)
Consider switching or stopping AP if need
Antipyschotics
dantrolene
- dantrolene may be useful in selected cases
- thought to work by decreasing excitation-contraction coupling in skeletal muscle by binding to the ryanodine receptor, and decreasing the release of calcium from the sarcoplasmic reticulum
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