odamphetamines

Mx of psychostimulant toxicity from amphetamines and related substances

see also:

do not use beta blockers (may result in uncontrolled hypertension) or phenytoin (potential cardiac adverse effects)

Clinical manifestations of psychostimulant toxicity

acute toxicity

cardiovascular
CNS
  • agitation, panic states, paranoia, euphoria, hallucinations and psychosis, bruxism, hyper-reflexia, intracrebral haemorrhage, choreoathetoid movements, anorexia, delirium, seizures, coma
other sympathetic
  • mydriasis, diaphoresis, tremor, tachypnoea
pulmonary
  • non-cardiogenic pulmonary oedema / ARDS
GIT
  • hepatitis, nausea, vomiting, diarrhoea, GIT ischaemia
metabolic
other

chronic toxicity

  • behavioural/psychiatric illness, cardiomyopathy, cardiac valve disease, pulm. hypertension, vasculitis

Clinical signs indicating significant amphetamine toxicity

  • seizure, focal neurologic deficit, reduced level of consciousness, abnormal motor movements, hyperthermia, arrhythmias, hypotension, hypertension, coronary artery spasm, autonomic instability or other major disturbance of homeostasis.

DDx of amphetamine toxicity

other drug toxicity

systemic conditions

Specific Mx interventions in toxicity

agitation

  • treat aggressively aiming for a state of rousable drowsiness without causing respiratory depression
  • no sedation protocol is 100% safe, and thus these are only indicated when all other simpler, safer measures fail or are inappropriate, and the patient is deemed a significant risk to self or others. It is a crisis management tool.
  • it is critical in the initial period of physical restraint and parenteral sedation for direct visual observation of the patient's cardio-respiratory status to be maintained, and once the patient has settled sufficiently, electronic monitoring should be initiated as soon as reasonably possible to ensure patient safety.
  • a medical officer with advanced airway skills should remain with the patient whilst aggressive sedative Rx occurs
  • observations of vital signs and patient status should occur continuously in 1st 10min after parenteral sedation and every 10min for 1st 30min, then every 15min for 60min, then hourly for 4 hours after last dose or until awake
  • if resp. depression does occur following benzodiazepine sedation, only consider using flumazenil to reverse it if there is no evidence of concomitant pro-arrhythmic or pro-convulsant drug taken such as tricyclic antidepressants, or they are a regular benzodiazepine user, otherwise there is risk of seizures or cardiac arrest - usually safer to intubate than give flumazenil as inaccuracy of drug use history and polypharmacy tend to be issues.

1st line
  • Aust. Govt guidelines to Emerg. Depts 2005 for Mx of psychostimulant toxicity advise either:
    • protocol 1 using oral diazepam:
      • 10-20mg o diazepam initial dose
      • if behavioural control or a state of rousable drowsiness is achieved within 30min of 1st dose, no more sedation needed.
      • insufficient clinical response by 30min, a further dose of 10mg o diazepam should be given
        • repeat this regime until a state of rousable drowsiness or a total of 60mg o diazepam (only exceed 60mg if no obvious resp. depression evident. Do not exceed 120mg in a 24 hour period).
    • protocol 2 using iv diazepam:
      • diazepam is the preferred agent iv over midazolam but diazepam is not suitable for im use
      • 2.5-5mg iv diazepam initial dose
      • if behavioural control or a state of rousable drowsiness is achieved within 10min of 1st dose, no more sedation needed.
      • insufficient clinical response by 10min, a further dose of 5-10mg iv diazepam should be given
        • repeat this regime until a state of rousable drowsiness or a total of 60mg diazepam (only exceed 60mg if no obvious resp. depression evident. Do not exceed 120mg in a 24 hour period).
    • protocol 3 using im midazolam when iv access not available:
      • 5mg im midazolam initial dose
      • if behavioural control or a state of rousable drowsiness is achieved within 10min of 1st dose, no more sedation needed.
      • insufficient clinical response by 10min, a further dose of 10mg im midazolam or 2.5-5mg iv midazolam should be given
        • repeat this 2nd dose for a 3rd dose if needed and if still inadequate response, resort to 2nd line.
        • NB. absorption of im doses is unreliable and may be delayed response - iv is preferable if iv access is possible.
2nd line
  • consider use of these earlier if paranoia or hallucinations are prominent
  • Aust. Govt guidelines to Emerg. Depts 2005 for Mx of psychostimulant toxicity advise either:
    • droperidol 2.5mg-5mg iv every 20min as needed to max. dose 20mg in 24hr period
      • preferably after checking QTc is not prolonged, and beware seizures, sudden hypotension and laryngeal dystonia
      • do not give to antipsychotic naive patients unless an adequate benzodiazepine regime has been exhausted
    • olanzapine 10mg IM or oral wafer

seizures

1st line
2nd line

decreased conscious state

hyponatraemia

  • may occur due to either:
    • water intoxication from excess water intake at rave parties
    • drug effects of MDMA or PMA
      • the combination of hyponatraemia + hypoglycaemia or hyperkalaemia suggests PMA toxicity
  • beware central pontine myelinolysis
  • avoid hypotonic fluid administration
  • fluid restrict in non-dehydrated patients
  • hyponatraemia should be corrected over a similar time frame to it occurring but not at a rate > 0.5mM/hr during a 24hr period.
  • cautious administration of 3% saline if Na < 115mM and only to Na of 120mM - seek advice
    • sodium required to obtain 120mM = (120-sodium concentration) x 0.6 x weight in kg, or,
    • X ml/kg of 3% saline will raise the serum sodium by X mM
  • monitor U&E at least 4hrly initially

hyperthermia

rhabdomyolysis

  • maintain urine output > 1.5-2ml/kg/hr
  • urinary alkalinisation but beware this will increase amphetamine half life

hypertension

  • hypertension is often transient and does not usually require Rx unless severe.
  • avoid beta blockers as blockade of beta 2 receptor which mediates skeletal vasodilatation may result in uncontrolled hypertension in a setting of unopposed alpha stimulation.
  • vasodilators eg. GTN infusion (5mcg/min then titrate) or nitroprusside infusion (0.25-10mcg/kg/min)
  • rarely, may need to resort to alpha-adrenergic blockers - prazosin 2-5mg o or phentolamine 5mg slow iv

SVT

VT/VF

  • standard protocols VT and VF

ischaemic chest pain

  • usually more of an issue with cocaine but may occur with amphetamines
  • avoid aspirin as risk of subarachnoid haemorrhage (SAH) if uncontrolled hypertension
  • avoid beta adrenergic blockers as risk of uncontrolled hypertension
  • sublingual GTN reverses cocaine-induce coronary vasospasm
  • consider benzodiazepines if anxiety, tachycardia or hypertensive as they reduce BP and HR, and thus reduce myocardial oxygen demand in addition to their anxiolytic effects.

cerebrovascular emergencies

References

odamphetamines.txt · Last modified: 2019/06/27 07:38 by wh