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Cocaine Toxicity Medication

  • Author: Lynn Barkley Burnett, MD, EdD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Jun 30, 2016
 

Medication Summary

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.

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Benzodiazepines

Class Summary

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.

Lorazepam (Ativan)

 

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.

Midazolam (Versed)

 

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.

Diazepam (Valium)

 

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.

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Cardiovascular agents

Class Summary

Alkalinization may benefit cardiac conduction if a wide QRS is noted. Other treatment for cardiac arrest, dysrhythmias, or acute hypertension may also be required.

Sodium bicarbonate (Neut)

 

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).

Lidocaine (Anestacon, Dilocaine, Xylocaine, Zilactin-L, Dermaflex)

 

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.

Bretylium

 

Class III antiarrhythmic agent for treatment of PVCs. Has catecholamine-releasing properties and adverse effects. Should not be used as initial treatment.

Esmolol (Brevibloc)

 

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.

NTG (Deponit, Nitrostat)

 

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.

Phentolamine (Regitine)

 

Alpha1- and alpha2-adrenergic blocking agent that blocks circulating epinephrine and norepinephrine action, reducing hypertension due to catecholamine effects on alpha-receptors.

Nitroprusside (Nitropress)

 

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.

Norepinephrine (Levophed)

 

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.

Epinephrine

 

Considered the single most useful drug in cardiac arrest. Increases coronary perfusion pressure.

Vasopressin

 

May improve vital organ blood flow, cerebral oxygen delivery, ability to be resuscitated, and neurologic recovery.

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GI agents

Class Summary

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.

Polyethylene glycol (Colovage, CoLyte, GoLYTELY, NuLytely)

 

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.

Activated charcoal (Liqui-Char)

 

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.

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Nutrients

Class Summary

Thiamine should be administered before glucose to prevent Wernicke encephalopathy.

Thiamine (Vitamin B1)

 

Administered before glucose to prevent Wernicke encephalopathy.

Dextrose (D-glucose)

 

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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Contributor Information and Disclosures
Author

Lynn Barkley Burnett, MD, EdD LLB(c), Medical Advisor, Fresno County Sheriff's Office; Attending Consultant-in-Chief and Chairman, Medical Ethics, Community Medical Centers; Adjunct Assistant Clinical Professor of Emergency Medicine and Forensic Pathology, Touro University College of Osteopathic Medicine, California; Core Graduate Adjunct Professor of Forensic Pathology, National University Master of Forensic Science Program; Core Graduate Adjunct Professor of Leadership in Healthcare, Health Law and Healthcare Ethics, Kaplan University Graduate School of Healthcare Administration

Lynn Barkley Burnett, MD, EdD is a member of the following medical societies: American Academy of Hospice and Palliative Medicine, American Association for the Advancement of Science, American Association of Suicidology, American Cancer Society, American College of Sports Medicine, American Heart Association, American Public Health Association, American Society for Bioethics and Humanities, American Society of Law, Medicine & Ethics, Association of Military Surgeons of the US, Christian Medical and Dental Associations, European Society of Cardiology, New York Academy of Sciences, Royal Society of Medicine, Society for Academic Emergency Medicine, Society of Critical Care Medicine, American Professional Society on the Abuse of Children, American Stroke Association, Royal College of Surgeons of Edinburgh, World Association for Disaster and Emergency Medicine, European Society of Intensive Care Medicine, European Society of Paediatric and Neonatal Intensive Care, European Society for Trauma and Emergency Surgery, International Homicide Investigators Association

Disclosure: Nothing to disclose.

Coauthor(s)

Jonathan Adler, MD, MS Instructor, Department of Emergency Medicine, Harvard Medical School, Massachusetts General Hospital

Jonathan Adler, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Carlos J Roldan, MD, FAAEM, FACEP Associate Professor, Department of Emergency Medicine, University of Texas Health Science Center at Houston Medical School; Consulting Staff, Department of Emergency Medicine, Memorial Hermann Hospital Lyndon Baines General Hospital and MD Anderson Cancer Center

Carlos J Roldan, MD, FAAEM, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Pain Society, American Society of Regional Anesthesia and Pain Medicine, International Association for the Study of Pain, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Undersea and Hyperbaric Medical Society, Wilderness Medical Society, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT Associate Clinical Professor, Department of Surgery/Emergency Medicine and Toxicology, University of Texas School of Medicine at San Antonio; Medical and Managing Director, South Texas Poison Center

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, Texas Medical Association, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

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Patient transporting cocaine packets seen on KUB and lateral radiographs (mostly on left side). The patient was admitted, and a large number of packets was later obtained without procedural intervention or complication.
Patient transporting cocaine packets seen on KUB and lateral radiographs (mostly on left side). The patient was admitted, and a large number of packets was later obtained without procedural intervention or complication.
CT scan of patient transporting cocaine packets.
Schematics show the 3 types of action potentials in the right ventricle: endocardial (End), mid myocardial (M), and epicardial (Epi). A, Normal situation on V2 ECG generated by transmural voltage gradients during the depolarization and repolarization phases of the action potentials. B-E, Different alterations of the epicardial action potential that produce the ECGs changes observed in patients with Brugada syndrome. Adapted from Antzelevitch, 2005.
Three types of ST-segment elevation in Brugada syndrome, as shown in the precordial leads on ECG in the same patient at different times. Left panel shows a type 1 ECG pattern with pronounced elevation of the J point (arrow), a coved-type ST segment, and an inverted T wave in V1 and V2. The middle panel illustrates a type 2 pattern with a saddleback ST-segment elevated by >1 mm. The right panel shows a type 3 pattern in which the ST segment is elevated < 1 mm. According to a consensus report (Antzelevitch, 2005), the type 1 ECG pattern is diagnostic of Brugada syndrome. Modified from Wilde, 2002.
Table 1. Onset of Effects, Peak Effects, Duration of Euphoria, and Plasma Half-Life by Routes of Administration
Route Onset Peak Effect (min) Duration (min) Half-Life (min)
Inhalation 7 s 1-5 20 40-60
Intravenous 15 s 3-5 20-30 40-60
Nasal 3 min 15 45-90 60-90
Oral 10 min 60 60 60-90
Table 2. DAWN Data, 2011
Total ED Visits for Cocaine in US 505,224
White 185,748
Black 236,089
Hispanic 49,810
Other/2+ Race/Ethnicities 5086
Unknown 28,490
Table 3. Current Cocaine Use by Age: 2011
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%)
Table 4. 2011 DAWN Data on Emergency Department Visits for Cocaine, by Age
Age, y Number of Visits
0-11 ...
12-17 5904
18-20 15,198
21-24 37,643
25-29 57,398
30-34 55,247
35-44 127,405
45-54 154,101
55-64 47,064
≥65 4887
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