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
pulmonary
GIT
hepatitis, nausea, vomiting, diarrhoea, GIT ischaemia
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
2nd line
seizures
1st line
2nd line
decreased conscious state
hyponatraemia
may occur due to either:
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
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:
VT/VF
standard protocols
VT and
VF
ischaemic chest pain
cerebrovascular emergencies
References