odamphetamines
Table of Contents
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
- tachycardia, hypertension, arrhythmias, vasospasm, aortic dissection, acute coronary syndrome, hypotension (late), acute cardiomyopathy
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
- hyponatraemia - dilutional or syndrome of inappropriate ADH secretion (SIADH); acidosis
- hyperkalaemia (suggests PMA)
- hypoglycaemia
other
- hyperthermia, muscle rigidity, rhabdomyolysis, serotonin syndrome (clonus with hyper-reflexia) may occur especially if on SSRI's, tramadol, metoclopramide, etc.
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
- cocaine, anticholinergics, tricyclic antidepressants, theophylline, SSRI, serotonin syndrome, MAOI, caffeine, salicylates, LSD
systemic conditions
- thyrotoxicosis, delirium, sepsis, phaeochromocytoma, heat stroke, meningitis, encephalitis, temporal lobe epilepsy, intracranial haemorrhage
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
- exclude hyponatraemia
- see seizures and anticonvulsants
- avoid phenytoin as it may have cardiac effects from its own properties as well as its diluent (propylene glycol).
1st line
- benzodiazepines as per usual
2nd line
- phenobarbitone 20mg/kg iv
- sedation with airway control - thiopentone or propofol
decreased conscious state
- exclude hyponatraemia, hypoglycaemia
- protect airways and support respiration as per usual
- CT brain
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
- Rx aggressively if temp > 39.5degC
- active cooling measures - ice packs or baths
- NM blockade
- 5HT2 antagonists if possible serotonin syndrome and no co-ingestion of anti-muscarinic anticholinergic agents, eg:
- cyproheptadine 12mg o or via NGT although limited evidence
- chlorpromazine (Largactil) can be tried but risk of hypotension
- olanzapine
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
- usual Mx of SVT but avoid beta blockers - if must use them, try iv esmolol
- Mx options:
- verapamil (Isoptin) - 5mg iv beware of hypotension
- flecainide - 2mg/kg iv over 30min
- DC reversion
VT/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
- use of cocaine or amphetamines are considered a strong risk factor for stroke (CVA) or subarachnoid haemorrhage (SAH)
- avoid aspirin as risk of subarachnoid haemorrhage (SAH)
- avoid corticosteroids as may be harmful
- Mx complications on their merits otherwise
References
- Greene et al. Review article: Amphetamines and related drugs of abuse. EMA 2008 20:391-402
- Qld health dept - Mx of psychostimulant toxicity March 2008 (pdf) - essentially the same as Aust. Govt guidelines in 2005.
- Mx of patients with psychostimulant toxicity - Aust. Govt guidelines to Emerg. Depts 2005
odamphetamines.txt · Last modified: 2019/06/27 07:38 by 127.0.0.1