The Poison Control Center

Cocaine Toxicity

Forms of cocaine


A 31-year-old male reportedly swallowed 1/2 gram of cocaine while being chased by police. He stated that he swallowed the powder, not the packets, and was brought to an emergency room (E.R.) by the police. The E.R. contacted the poison control center and reported the patient to be asymptomatic with initial B.P. of 148/110 with a pulse of 130-140. Ipecac had been given to the patient prior to calling. Recommendations were to begin an I.V., follow vital signs closely and to protect the patient's airway if his gag reflex was absent. Activated charcoal/cathartic was to be administered once the airway was secure.

One and a half hours after the presentation, the patient remained hypertensive with B.P. of 180/110 and a pulse of 110. A second dose of Ipecac had been administered without result and the patient had been lavaged. Activated charcoal/cathartic was administered. Further physical exam reported that he was sloughing of mucous membranes of the soft palate and buccal mucosa. Labetalol was administered and resulting B.P. was 148/80 with a pulse in the 90's four hours after E.R. presentation. The patient was subsequently released to the police.



Use of cocaine, which now crosses all segments of society, has risen due to its increased availability, decreased cost, and more advantageous routes of administration through the use of freebase cocaine. The introduction of "body stuffers" and "body packers" of cocaine has provided new toxic means for systemic delivery of the drug. These factors, coupled with the greater reported side effects both in the medical literature and in the lay press, has caused greater public awareness of the problem of cocaine abuse. This is reflected by the increase in the number of patient visits to Emergency Rooms with cocaine-related complaints. An increase in the number of cocaine-related phone calls received by the Poison Control Center at The Children's Hospital of Philadelphia has also occurred. This report is Part I of a review of cocaine toxicity and will present historical aspects of cocaine use, forms of the drug, its pharmacokinetics, and pharmacology.

Cocaine is an alkaloid which is contained in the Erythroxylon coca which grows in the Andes mountains of Peru and Bolivia 1000 to 3000 m. above sea level.1 The first use of cocaine in history was by the Peruvian Indians in the 6th century who chewed on the coca leaves for the sense of wellness and endurance which it produced and who believed it to be a part of the Inca religion.2

Cocaine was introduced to Europe by the Spanish explorers, first used by a Spanish physician in 1596, and the alkaloid was first isolated from plant leaves in 1860.3 The leaves contain approximately two percent cocaine and are processed to yield the cocaine HCI salt.4 A suggestion for its use as a local anesthetic was made in 1880 by Von Anrep.1 In 1884, Freud began personal experimentation to relieve depression and subsequently produced the first major report on the drug, recommending its use as a stimulant for digestive disorders of the stomach, in the treatment of alcohol and morphine addiction, in treatment of asthma, as an aphrodisiac, and as a local anesthetic.2 His friend Karl Koller, also in 1884, was the first to introduce its legal use in medicine as a local anesthetic in ophthalmic surgery.2


Forms of Cocaine

Coca plants today are grown mainly in Peru and Bolivia where coca paste is converted from the leaves. The coca paste is then refined primarily in Columbia into cocaine HCI salt and it predominantly enters the U.S. in this form. Coca paste is also entering the U.S. now. Ecuador and Brazil are also producing more cocaine and new refineries are opening in Panama, Venezuela, Argentina and Miami.

Cocaine HCI in the U.S. is a Schedule 11 drug, is water soluble, and has been used medically for many years in topical form. When it is used illegally, its purity may range as low as 10-50 percent.5 Dilutents such as mannitol, lactose, talc or sucrose are first added to the pure cocaine HCI, followed by adulterants such as caffeine, quinidine, procainamide, ephedrine, phencyclidine, tetracaine, nicotine or amphetamine. Any of these listed may be substituted partially, or totally for cocaine and sold as such.5,6 From 1970 to 1978, cocaine HCI was primarily used intranasally but could also be used I.V. or S.C.3 The HCI form cannot be smoked as heat causes it to decompose.3

Freebase cocaine is essentially pure cocaine that is made today by preparing an aqueous solution of cocaine HCI and adding ammonia or bicarbonate to alkalinize the solution and precipitate alkaloidal cocaine.6 The "freebase" formed is nonwater-soluble, does not decompose. with heat and can be crushed, and mixed with tobacco and smoked. It can also be melted, vaporized, and inhaled intranasally, or smoked in a "base pipe," a process called "freebasing."6 Alkaloidal cocaine can be bought as "crack" or "rock" on the street. It has become more profitable to make freebase cocaine at home using kits sold for this purpose as the cost of cocaine HCI has dropped.5

Coca paste is another form of cocaine that is 60-80 percent cocaine sulfate and can also be smoked.7 The cocaine sulfate is a byproduct of the purification process of cocaine HCI and the paste may contain such impurities as lead, sulfuric acid, kerosene, and methanol.5 In past years it had been used mainly by inhabitants of coca plant producing countries such as Peru7 but since 1982 has also become popular in the United States.3 However, alkaloidal cocaine remains the predominant new form in use today.

Another route for systemic delivery has resulted when accidental rupture of cocaine HCI or paste-filled balloons or condoms occurs within the gastrointestinal tract of individuals functioning as "body packers" or "mules."4 They may ingest from 50-100 packages, take constipating agents, enter the United States, then take laxatives upon arrival to facilitate transit of the packages. Potential exists for abdominal obstruction and, depending on the type, spontaneous rupture of the packets.4 Female body packers may transport the packets vaginally.4 The syndrome of "bodystuffing" has arisen when individuals secretly ingest the illegal drugs they are carrying in an effort to escape police detection.8 These are loosely wrapped packages such as cellophane, glassine, paper or foil, and usually release their contents into the GI tract.8

The more widespread use and popularity of cocaine today as well as its use in larger quantities can be due to the decrease in the cost, the increased purity and the more intense "high" experienced with the use of "crack."



Cocaine is absorbed from all sites of application including mucous membranes and the gastrointestinal mucosa. The amount and rate of absorption is limited by the amount of local vasoconstriction it produces.1

The blood levels achieved will vary depending on the rate and route of absorption. Significant blood levels are achieved by nasal application, peaking within 15 minutes to one hour with a duration of 1 to 1.5 hours.2 With oral dosing, peak effects may be delayed to 45 to 90 minutes after administration, subjective effects may be higher, and duration last up to 4 hours.9 The highest blood levels of cocaine occur in a few minutes when used intravenously and last for approximately 30-45 minutes. When cocaine is smoked as freebase and inhaled, delivering the cocaine rapidly to the pulmonary vascular bed, a rapid increase in blood concentration occurs with intense euphoric effects similar to that of rapid I.V. injection but lasting only 20 minutes.6 In one study comparing smoking of freebase with I.V. cocaine HCI use, smoking 50 mg. of freebase (inhaling 16 mg. cocaine) caused a more pleasurable euphoria than 20 mg. I.V. of cocaine HCI.10

Once cocaine enters the blood it is inactivated by plasma and liver cholinesterases and its inactive metabolites are excreted in the urine1. Only a small amount is excreted unchanged in the urine. Cocaine and/or its inactive metabolites may be present in the urine for 24 to 36 hours after administration.3,11 In individuals with a congenital cholinesterase deficiency, a small dose of cocaine will produce high and prolonged blood levels.3

As cocaine is a powerful stimulant it is often abused for this effect1. The phenomenon of acute tolerance to cocaine has been linked with the fact that the euphoric effects of cocaine after I.V. or intranasal administration decrease faster than the corresponding cocaine blood level.7,12 An often dysphoric "crash" may occur after the intense euphoria of I.V. or inhalation use leading to frequent repeated doses in an effort to prevent the "crash."6 A second dose administered within an hour will also cause less of an intense response.12 For these reasons cocaine users will take the drug repeatedly every 30 to 40 minutes if available.7 It has been reported that the craving for another dose after smoking freebase is more intense than after I.V. cocaine HCI and explains the high addiction potential of freebasing.10



Cocaine acts both locally as an anesthetic and centrally as a stimulant via its effects on neurotransmitters. Locally it blocks the initiation and propagation of nerve impulses along an axon by interference with sodium permeability during depolarization.3,11 Centrally it blocks the presynaptic reuptake of norepinephrine and dopamine. Accumulation of the neurotransmitters in the synaptic cleft occurs provoking an increase in the stimulation of postsynaptic receptors.3

Tolerance occurs when continued use requires higher doses to produce the same effects. The postsynaptic receptors become supersensitive to neurotransmitter effects and may be related to an increase in the number of alpha and beta receptors.4 This may occur in compensation for chronic cocaine use when norepinephrine becomes depleted.4

In general, the pharmacological effects of cocaine, the "cocaine reaction," can be divided into 3 phases with the degree of effects seen dependent on the amount on the amount of cocaine used.11 "Early stimulation" deals with initial adrenergic stimulation form the increase of norepinephrine and is the "fight or flight" reaction. This progresses into "advanced stimulation" in which unresponsiveness, hyperreflexia, status epilepticus, irregular respirations (Cheynes-Stokes), malignant arrhythmias, and hypotension occurs. The final "depressive stage" then enter, dealing with coma, flaccid paralysis, loss of reflexes, agonal gasps, apnea, loss of vital signs, and death.11 This depressive stage occurs due to central medullary depression and may be related to the acute depletion of neurotransmitters.



  1. Ritchie JM, Greene NM. Local anesthetics, In Gilman AG, Goodman LS, Rall TW, Murad F, (Eds). The Pharmacological Basis of Therapeutics, 7th ed. New York: Macmillan, 1985:309-10.
  2. Haddad LM. Clinical Management of Poisoning and Drug Overdose. Philadelphia, WB Saunders Co, 1983:443-7.
  3. Cregler LL, Mark H. Medical complications of cocaine abuse. N Engl J Med. 1986 Dec 4;315(23):1495-1500.
  4. Brody SL, Slovis CM. Recognition and management of complications related to cocaine abuse." Emerg Med Reports 1988;9:41-8.
  5. Becker, CE (Ed.). Poisindex® Toxicologic Managements, Vol. 56. Denver:Micromedex, Inc., 1988.
  6. Abramowicz M (Ed.) Crack. The Medical Letter 1986; 28: 69-70.
  7. Jaff JH. Drug addiction and drug abuse," In Gilman AG, Goodman LS, Rall TW, Murad F, (Eds.). The Pharmacological Basis of Therapeutics, 7th ed. New York: Macmillan, 1985:550-4.
  8. Roberts JR, Price D, Goldfrank L, Harnett L. The bodystuffer syndrome: a clandestine form of drug overdose. Am J Emerg Med 1986 Jan;4(1):24-7.
  9. Van Dyke C, Jatlow P, Ungerer J, Barash PG, Byck R. Oral cocaine: plasma concentration and central effects. Science 1978 Apr 14;200(4338):211-3.
  10. Perez-Reyes M, DiGuiseppi S, Ondrusek G, Jeffcoat AR. Free-base cocaine smoking. Clin Pharmacol Ther 1982 Oct;32(4):459-65.
  11. Gay GR. Clinical management of acute and chronic cocaine poisoning. Ann Emerg Med 1982 Oct;11(10):562-72.
  12. Chow MJ, Ambre JJ, Ruo TI, Atkinson AJ Jr, Bowsher DJ, Fischman MW. Kinetics of cocaine distribution, elimination, and chronotropic effects. Clin Pharmacol Ther 1985 Sep;38:318-24.


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