Cocaine Toxicity Medication
- Author: Lynn Barkley Burnett, MD, EdD; Chief Editor: Asim Tarabar, MD more...
The general objectives of pharmacotherapeutic intervention in cocaine toxicity are to reduce the CNS and cardiovascular effects of the drug by using benzodiazepines initially and then control clinically significant tachycardia and hypertension while simultaneously attempting to limit deleterious drug interactions.
In a cardiac arrest, vasopressin may offer considerable advantage over epinephrine.
Some patients who abuse cocaine have enhanced sensitivity to benzodiazepines despite a significantly decreased plasma concentration. Be alert to the extreme sedative effects that have been noted after the administration of lorazepam to some patients who used cocaine.
NTG or nitroprusside may be needed to treat severe hypertension. For both of these drugs, an infusion system that ensures a precise rate of flow is needed. Closely monitor the patient's vital signs when vasoactive and antihypertensive medications are used. When vasoactive agents are discontinued, taper them slowly.
Hypotension may compound the patient's status; if present, norepinephrine may be required.
Hypoglycemia is always a possibility in patients presenting with neuropsychiatric syndromes. If bedside glucose results confirm the need, administer thiamine and glucose. Thiamine should be administered before dextrose. Before the intravenous administration of thiamine, administer an intradermal test dose to patients in whom thiamine sensitivity is suspected.
By increasing the action of GABA, a major inhibitory neurotransmitter in the brain, these drugs may depress all levels of the CNS, including the limbic system and reticular formation.
DOC for status epilepticus because it persists in CNS longer than diazepam. Rate of injection should not exceed 2 mg/min. May be administered IM if unable to obtain vascular access.
Alternative for termination of refractory status epilepticus. Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects; therefore, clinician must wait 2-3 min to fully evaluate sedative effects before initiating procedure or repeating dose. Has twice the affinity for benzodiazepine receptors as diazepam. May be administered IM if unable to obtain vascular access.
Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing GABA activity. Third-line agent for agitation or seizures because of shortened duration of anticonvulsive effects and accumulation of active metabolites that may prolong sedation.
Alkalinization may benefit cardiac conduction if a wide QRS is noted. Other treatment for cardiac arrest, dysrhythmias, or acute hypertension may also be required.
Useful for alkalization of urine in patients with rhabdomyolysis. Appropriate for dysrhythmias from direct toxic effects of cocaine (ie, QRS greater than 100 ms due to sodium channel blockade).
Class IB antiarrhythmic that increases electrical stimulation threshold of ventricle, suppresses automaticity, and slows conduction velocity through ischemic tissue. Indicated for cocaine-induced VF and VT.
Class III antiarrhythmic agent for treatment of PVCs. Has catecholamine-releasing properties and adverse effects. Should not be used as initial treatment.
Beta-blockers are generally contraindicated in cocaine toxicity. Some recommend to "save use" together with a vasodilator, only to manage life-threatening hypertension, tachycardia, and aortic dissection unresponsive to other therapeutic interventions. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.
Used to treat acute hypertension and cardiac chest pain. Relaxes vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production, decreasing BP. Selection of NTG or sodium nitroprusside based on clinician's preference.
Alpha1- and alpha2-adrenergic blocking agent that blocks circulating epinephrine and norepinephrine action, reducing hypertension due to catecholamine effects on alpha-receptors.
Used to treat acute hypertension. Produces vasodilation and increases cardiac inotropic activity. At high dosages, may exacerbate myocardial ischemia by increasing heart rate. Selection of NTG or sodium nitroprusside based on clinician's preference.
Stimulates alpha and beta1-adrenergic receptors with alpha-adrenergic predominance which increases cardiac muscle contractility, heart rate, and vasoconstriction; results are increased systemic BP and coronary blood flow. As a vasopressor, useful in hypotension not responsive to IV fluids alone.
Considered the single most useful drug in cardiac arrest. Increases coronary perfusion pressure.
May improve vital organ blood flow, cerebral oxygen delivery, ability to be resuscitated, and neurologic recovery.
Whole-bowel irrigation with polyethylene glycol promotes the passage of cocaine packets through the GI tract. Activated charcoal may be empirically used to minimize systemic absorption of the toxin.
Laxative with strong electrolyte and osmotic effects. Cathartic actions in GI tract. May be indicated in treatment of cocaine ingestion in people who carry cocaine packages in their body. Must administer after activated charcoal. Liquid reconstituted per package instructions.
Emergency treatment for absorption of drugs or chemicals. Network of pores adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water. Some formulations also contain a cathartic.
For maximum effect, administer within 30 min of poison ingestion. Although value of multiple doses to treat acute drug ingestion not established, in some carefully considered situations, dose may be repeated at half original dose q2-6h until symptoms of toxicity subside, serum drug concentrations return to reference range (if initially elevated) or drug packets eliminated. Repeat doses should not contain cathartic.
Thiamine should be administered before glucose to prevent Wernicke encephalopathy.
Administered before glucose to prevent Wernicke encephalopathy.
Monosaccharide absorbed from intestine and distributed, stored, and used by tissues. Parenteral injection used in patients unable to sustain adequate oral intake. Direct oral absorption rapidly increases blood glucose concentrations. Effective in small doses and no evidence suggests toxicity. Concentrated infusions provide increased amounts of glucose and increased caloric intake in small volume of fluid.
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|Route||Onset||Peak Effect (min)||Duration (min)||Half-Life (min)|
|Total ED Visits for Cocaine in US||505,224|
|Age Range (y)||Cocaine Use, Any Form, Past Month (Percentage of Same-age Population)||Crack Cocaine Use, Past Month (Percentage of Same-age Population)|
|Total||1.5 million (0.6%)||354,000 (0.1%)|
|12-17||39,000 (0.2%)||8000 (<0.1%)|
|18-25||473,000 (1.4%)||29,000 (0.1%)|
|≥26||1.0 million (0.5%)||317,000 (0.2%)|
|Age, y||Number of Visits|