Amphetamine Toxicity Medication
- Author: Neal Handly, MD, MS, MSc; Chief Editor: Asim Tarabar, MD more...
Medications available for amphetamine toxicity include gastric decontaminants (charcoal with or without sorbitol), sedatives to control CNS stimulation caused by amphetamines (benzodiazepines, antipsychotics), muscle relaxants (benzodiazepines, dantrolene), and several drugs to control possible hemodynamic cardiovascular disturbances (alpha-adrenergic blockers, nitrates, diuretics).
These agents are used to adsorb amphetamine after acute ingestion and to limit absorption into systemic circulation. Limited utility beyond 4 h of ingestion, unless the patient ingested sustained-release formulation or is suspected of being a body packer (ie, ingestion of a large amount of drug in a plastic bag or condom to smuggle or avoid arrest). Charcoal is not beneficial for other routes of exposure (eg, IV, inhalation or injection). Clinician should be aware of potential risk of charcoal aspiration and death due to aspiration pneumonia, especially in patients with altered mental status and/or having seizures. Prudent airway control is recommended in such population.
Network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water.
For maximum effect, administer within 30 min of ingestion of poison. May administer as aqueous suspension or combine with cathartic (usually sorbitol 70%) in the presence of active bowel sounds.
Repeat dose, if necessary (without cathartic), to adsorb large pill masses or drug packages.
With superactivated forms, use of doses of 0.5 g/kg PO may be possible.
These agents are important for sedation counteracting the CNS and PNS excitation of amphetamines. A benzodiazepine is generally considered as the first agent of choice for hypertension and agitation, in addition to their utility for treating seizures.
Beneficial for sedative and anticonvulsant effects. In addition, the calming effects may prove beneficial for the adverse cardiovascular effects (eg, hypertension, tachycardia) of amphetamines.
Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Third-line agent for agitation or seizures because of shorter duration of anticonvulsive effects and accumulation of active metabolites that may prolong sedation.
Used as alternative in termination of refractory status epilepticus. Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects. Thus, clinician must wait 2-3 min to evaluate sedative effects fully before initiating procedure or repeating dose. Has twice the affinity for benzodiazepine receptors than diazepam. May be administered IM if unable to obtain vascular access.
Antipsychotics are used to manage psychosis, agitation, and hyperthermia that may result from amphetamine use.
DOC for patients with acute psychosis when no contraindications exist. Noted for high potency and low potential for causing orthostasis. Downside is the high potential for EPS (dystonia) and lowering the seizure threshold.
Use in acute amphetamine toxicity is controversial. If haloperidol is being considered, administer a benzodiazepine first. May then be used as adjunctive therapy to control agitation in afebrile patients with normal vital signs.
Parenteral dosage form may be admixed in syringe with 2 mg lorazepam for better anxiolytic effects.
Skeletal muscle relaxants
These agents are used to control or reverse hyperthermic effects. Most hyperthermia is mediated by neuromuscular agitation.
Has been used successfully in isolated case reports to control hyperthermia; however, efficacy has not been established for amphetamine-associated hyperthermia. Reverse of hyperthermic effects may take several hours. Because morbidity and mortality from hyperthermia is closely correlated with severity and duration of hyperthermia, aggressive cooling (eg, ice bath) and agents that work more readily to reverse hyperthermia are preferred over dantrolene.
Alpha- and beta-adrenergic antagonists control peripheral vasoconstriction that results from sympathetic stimulation due to amphetamines. Treating with a beta-blocker to control the heart rate will leave unopposed alpha activity that can cause vasoconstriction. Combination alpha- and beta-adrenergic antagonists, such as labetalol, may have therapeutic value. Alpha-adrenergic antagonists specifically may be used to treat severe headache, SAH, cardiac ischemia, and hypertension associated with amphetamines. Use nitrates to control vasoconstriction and hypertensive emergency.
Blocks beta1-, alpha-, and beta2-adrenergic receptor sites decreasing blood pressure.
Alpha1- and alpha2-adrenergic blocking agent that blocks circulating epinephrine and norepinephrine action, reducing hypertension that results from catecholamine effects on the alpha-adrenergic receptors.
Produces vasodilation and increases inotropic activity of the heart. May exacerbate myocardial ischemia at higher doses by increasing heart rate.
Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. The result is a decrease in blood pressure. Valuable for controlling cardiac pain and pulmonary edema.
May administer bolus of 12.5-25 mcg or give a 400-mcg tab SL as a bolus before continuous infusion.
Initial infusion rate of 10-20 mcg/min may be increased 5-10 mcg/min q5-10min until desired clinical or hemodynamic response is achieved. Infusion rates of 500 mcg/min occasionally have been required.
These agents are used to control and treat pulmonary edema and could be beneficial in a hypertensive crisis.
Increases excretion of water by interfering with chloride-binding cotransport system that, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.
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