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8. Psychopharmacology > Neuroleptic Malignant Syndrome > Flashcards

Neuroleptic Malignant Syndrome Flashcards

1
Q

what is NMS

A

life threatening idiosyncratic reaction to DOPAMINE ANTAGONISTS (most commonly antipsychotics but not always just antipsychotics)

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2
Q

what are the characteristic features of NMS

A

fever

altered mental status

muscle rigidity

autonomic dysfunction

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3
Q

what is the hypothesized underlying mechanism of NMS

A

excessive dopamine receptor blockade

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4
Q

what is the incidence of NMS

A

0.01-0.02% among those treated with antipsychotics

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5
Q

how soon does NMS develop after drug initiation

A

most develop within first 24 hours of drug initiation

may be within first week

virtually all cases are within first 30 days

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6
Q

what is the fatality rate of NMS

A

10-20% when UNrecognized

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7
Q

what is the mean recovery time after drug discontinuation

A

7-10 days

most people recover within 1 week and nearly all within 30 days

residual neurological signs may persist for weeks after the acute hyper metabolic symptoms resolve

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8
Q

do people tend to have recurrences of NMS?

A

people generally do NOT experience a recurrence of NMS when re-challenged with an antipsychotic

but theoretically there is a risk

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9
Q

list risk factors for NMS

A

agitation

exhaustion

dehydration

iron deficiency

parenteral administration of drug

rapid titration

higher total drug doses (though most cases occur within the dose range)

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10
Q

what types of antipsychotics present greater risk of NMS

A

higher potency are higher risk

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11
Q

what other types of drugs, other than antipsychotics, could cause NMS

A

ANY dopamine antagonist–> i.e metoclopramide or prochloperazine

can also see it in those with parkinsons disease if there is withdrawal of L-dopa or dopamine agonist therapy, dose reductions or a switch from one dopamine agonist to another

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12
Q

how are NMS and catatonia related

A

NMS related to malignant catatonia–> NMS being iatrogenic form of malignant catatonia

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13
Q

is there consensus or diagnostic criteria for NMS

A

no–> there was proposed criteria by a “2011 international consensus study of NMS diagnostic criteria”

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14
Q

what is a mnemonic to remember the clinical and lab findings of NMS

A

FEVERR

Fever

Encephalopathy (confusion, mental status changes)

Vital sign instability (tachycardia, tachypnea, and/or labile BP)

Enzyme elevation (creatinine phosphokinase increase due to rhabdo)

Rhabdomyolysis (caused by muscle rigidity)

Rigidity (generalized lead pipe muscle rigidity)

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15
Q

what feature distinguishes NMS from other toxidromes like serotonin syndrome and anticholinergic toxicity

A

muscle rigidity often leading to rhabdo

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16
Q

what are the 8 proposed diagnostic criteria mentioned previously

A
  1. recent dopamine agonist withdrawal or dopamine antagonist exposure (within last 72 hours)
  2. hyperthermia (above 38 on at least two oral measurements)
  3. rigidity (lead pipe)
  4. mental status alteration (reduced or fluctuating LOC)
  5. CK elevation
  6. sympathetic nervous system lability (defined by at least two of: BP elevation 25% or more above baseline; BP fluctuation of 20mmHg systolic change within 24 hours; diaphoresis; urinary incontinence)
  7. hypermetabolism (HR increase 25% or more above baseline AND respiratory rate increase of 50% or more above baseline)
  8. negative workup for infectious, toxic, metabolic or neurologic causes
17
Q

what amount of CK elevation is expected in NMS

A

at least 4x upper limit of normal

18
Q

what features do you look for in terms of assessing sympathetic nervous system instability when assessing for NMS

A

defined by at least two of:

BP ELEVATION 25% or more above baseline

BP FLUCTUATION of 20mmHg systolic change within 24 hours

diaphoresis (often profuse)

urinary incontinence

19
Q

what features do you look for in terms of assessing hypermetabolism when assessing for NMS

A

HR increase of 25% or more above baseline

RR increase of 50% or more above baseline

20
Q

what other neuro signs can be present with NMS

A

tremors

trismus

dysarthria

dysphagia

akinesia

sialorrhea

myoclonus

21
Q

what might you see on EEG for NMS

A

generalized slowing

22
Q

what might you see on blood work for someone with NMS

A

leukocytosis

metabolic acidosis

hypoxia

decreased serum iron concentrations

elevations in serum muscle enzymes and catecholamines

23
Q

does NMS show up on CSF analysis or neuroimaging studies

A

no–> these are generally unremarkable in NMS

24
Q

how do you make the diagnosis of NMS

A

diagnosis of exclusion

must exclude other infectious, toxic, metabolic and neuropsychiatric conditions i.e status epilepticus

25
Q

ddx of NMS

A

serotonin syndrome

parkinsonian hyperthermia syndrome (usually following ubrupt discontinuation of dopamine agonists)

alcohol or sedative withdrawal

malignant hyperthermia (during anesthesia)

hyperthermia associated with abuse of stimulants and hallucinogens

atropine poisoning

malignant catatonia

CNS infection

inflammatory or autoimmine conditions

status epilepticus

structural cortical lesions

systemic conditions i.e pheo, thyrotoxicosis, tetanus, heat stroke

26
Q

what is the first think you should do once you suspect NMS

A

stop all dopamine antagonists

27
Q

what is the treatment of NMS

A

supportive care

includes:
fluid replacement
–> aggressive hydration often required especially if highly elevated CPK levels threaten to damage kidneys

supporting cardiac, lung and renal function
–>consider bicarbonate loading to prevent renal failure

temperature reduction

trend and monitor WBC, CK, temp, serum iron, liver transaminases

28
Q

what pharmacologic options are there to treat NMS

A

bromocriptine–> pro dopaminergic and pro-serotonergic agent

amantadine

dantrolene –> muscle relaxant that inhibits calcium release from the sarcoplasmic reticulum

(bromocriptine and dantrolene are most common)

*for more severe cases

29
Q

what is the classic triad of NMS

A

fever
muscle rigidity
altered mental status

*there is a lot of heterogeneity in presentation

30
Q

does the muscle rigidity seen in NMS tend to respond to antiparkinsonian agents

A

no

31
Q

how serious is NMS

A

considered neurological emergency

32
Q

why might you consider empiric pharmacotherapy for NMS with bromocriptine and/or dantrolene

A

may SHORTEN the course of the syndrome and possibly REDUCE MORTALITY when used alone or in combo

33
Q

why is bromocriptine given in NMS

A

to reverse the hypodopaminergic state

admin orally or by NG

34
Q

what is the dosing of bromocriptine for NMS

A

2.5 mg 2-3x daily

increasing doses by 2.5 mg every 24 hours until response or until max dose of 45mg/day reached

generally continued for at least 10 days for NMS related to oral neuroleptics and 2-3 weeks for depot neuroleptics

35
Q

dosing of dantrolene

A

can be admin IV statting with 1-2.5mg/kg bolus followed by 1mg/kg every 6 hours up to max dose of 10mg/kg/day

36
Q

what risks are there with dantrolene

A

hepatotoxicity (so stop once patient is improving)

37
Q

what is dantrolene

A

muscle relaxant (blocks calcium release from sarcoplasmic reticulum)

38
Q

what other pharmacologic agents other than bromocriptine/amantadine and dantrolene can be used to manage NMS

A

benzos

carbamazepine

clonidine

39
Q

if standard care is not helping, what other treatment can u use for NMS

A

ECT

8. Psychopharmacology (21 decks)

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