II. Background

  1. Naturally derived from Coca plant
    1. South American shrub
    2. Not the same as the cocoa plant
  2. Class
    1. Stimulant
    2. Local Anesthetic
    3. Schedule I

III. Preparations

  1. Formulations (same Cocaine molecule and CNS, cardiovascular effects despite different delivery methods)
    1. Salt: Fine white powder (blow, coke, snow)
      1. Snorted or mixed with water and injected
    2. Base: Crystalline or Rock Crystal (Crack Cocaine)
      1. Appears similar to soap pieces caked together
      2. Smoked (vaporizes when heated)
      3. Second-hand inhalation can effect infants and children
  2. Street Names
    1. Coke
    2. Snow Flake
    3. Toot
    4. Star Dust
    5. Happy Dust
    6. Bernice
  3. Methods of abuse
    1. Swallowed
    2. Snorted
    3. Intravenous
    4. Freebase residue
    5. Smoked (solid crack)

IV. Mechanism

  1. Affects central and peripheral Neurotransmitters (blocks their reuptake)
    1. Norepinephrine
    2. Dopamine - arousal
    3. Serotonin - awakening
  2. Class Ib Antiarrhythmic Drug
    1. Sodium Channel Blocker that shortens Action Potential duration

V. Pharmacokinetics

  1. Metabolized by serum and hepatic Cholinesterases
  2. Excreted by Kidneys
  3. Crosses the placenta by simple diffusion
  4. Crosses into Breast Milk
  5. Prolonged Duration and toxicity
    1. Excessive intake
      1. "Body Packers" with ruptured bag
    2. Concurrent Alcohol ingestion
  6. Cocaine (20-300 mg)
    1. Onset intranasal effects in 1 hour
      1. Onset faster with intravenous or smoked forms
    2. Duration: 2-4 hours
    3. Half life: 90 minutes
  7. Peak Toxicity
    1. Swallowing: 60-90 minutes
    2. Snorting: 30-60 minutes
    3. Intravenous or Smoked: Minutes

VI. Symptoms

  1. Increased energy and alertness
  2. Euphoria
  3. Sociability
  4. Appetite suppression
  5. Decreased need for sleep
  6. Restlessness
  7. Excitement

VII. Signs: Toxicity (Systemic Sympathomimetic Effect)

  1. See Cocaine-Induced Coronary Vasospasm
  2. See Sympathomimetic Toxicity
  3. Hypertensive
  4. Sinus Tachycardia (significant)
  5. Tremors
  6. Agitation
  7. Generalized Tonic Clonic Seizures
  8. Pressured speech
  9. Diaphoresis
    1. Contrast with AmitriptylineOverdose which causes dryness (instead of diaphoresis)

VIII. Diagnostics: Electrocardiogram

IX. Adverse Effects (increased with duration and dose)

  1. Acute effects
    1. See Cocaine-Induced Coronary Vasospasm
    2. See Sympathomimetic Toxicity
    3. Psychosis (e.g. Hallucinations, paranoia) in 80% of patients
    4. Aortic Dissection
    5. Cerebrovascular Accident (both ischemic and Hemorrhagic CVA)
    6. Hypertension
    7. Crack Lung (diffuse alveolar injury)
    8. Tactile Hallucinations (crawling bugs)
  2. Chronic effects
    1. Cardiomyopathy
    2. Perforated nasal septum
    3. Memory Loss
    4. Movement Disorders
    5. Psychiatric disorders

X. Labs

  1. See Urine Drug Screen
  2. Detectable in blood, urine, hair, Saliva, sweat, Breast Milk

XI. Management: Toxicity

  1. See Sympathomimetic Toxicity
  2. See Cocaine-Induced Coronary Vasospasm
  3. Avoid Beta Blockers (risk of unopposed alpha-Agonist effect)
  4. Administer Benzodiazepines
    1. Preferred agents in Seizures
    2. Preferred agents in Sympathomimetic Toxicity (Agitation, Hypertension, Tachycardia)
  5. Treat hyperthermia with cooling
  6. Evaluate for Dysrhythmia
  7. Treat Seizures (starting with Benzodiazepines)
    1. See Status Epilepticus

XII. Management: Withdrawal

  1. Ativan until adequate sedation
    1. May require significant dosages
  2. Propranolol 20 mg qid (indicated for chills)
    1. Beta Blockers are typically avoided in Cocaine use - theoretical risk of coronary vasospasm

XIII. Management: Abstinence

  1. Combined group and individual counseling most effective
    1. Minozzi (2016) Cochrane Database Syst Rev (9):CD011866 [PubMed]
  2. Study of effective options for therapy
    1. Cognitive behavior therapy
    2. Disulfiram (effective even if no Alcohol Abuse)
    3. Caroll (2004) Arch Gen Psychiatry 61:264-72 [PubMed]
  3. Medication therapy
    1. No medications have been found significantly helpful
    2. Disulfiram use supported by only low level evidence
    3. Substitution Therapy (e.g. Ritalin replaces Cocaine) may have benefit (experimental)
      1. Castelis (2016) (9):CD007380 [PubMed]

XIV. References

  1. Moore, Behar, Claudius and Farrah in Herbert (2018) EM:Rap 18(5):11-2
  2. Tagliaferro (2023) Crit Dec Emerg Med 37(1): 21-9
  3. Klega (2018) Am Fam Physician 98(2): 85-92 [PubMed]
  4. Shih (1996) Hosp Physician p. 11-20 [PubMed]

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Related Studies

Ontology: Cocaine (C0009170)

Definition (MEDLINEPLUS)

Cocaine is a white powder. It can be snorted up the nose or mixed with water and injected with a needle. Cocaine can also be made into small white rocks, called crack. Crack is smoked in a small glass pipe.

Cocaine speeds up your whole body. You may feel full of energy, happy, and excited. But then your mood can change. You can become angry, nervous, and afraid that someone's out to get you. You might do things that make no sense. After the "high" of the cocaine wears off, you can "crash" and feel tired and sad for days. You also get a strong craving to take the drug again to try to feel better.

No matter how cocaine is taken, it is dangerous. Some of the most common serious problems include heart attack and stroke. You are also at risk for HIV/AIDS and hepatitis, from sharing needles or having unsafe sex. Cocaine is more dangerous when combined with other drugs or alcohol.

It is easy to lose control over cocaine use and become addicted. Then, even if you get treatment, it can be hard to stay off the drug. People who stopped using cocaine can still feel strong cravings for the drug, sometimes even years later.

NIH: National Institute on Drug Abuse

Definition (NCI) A tropane alkaloid with central nervous systems (CNS) stimulating and local anesthetic activity. Cocaine binds to the dopamine, serotonin, and norepinephrine transport proteins and inhibits the re-uptake of dopamine, serotonin, and norepinephrine into pre-synaptic neurons. This leads to an accumulation of the respective neurotransmitters in the synaptic cleft and may result in increased postsynaptic receptor activation. The mechanism of action through which cocaine exerts its local anesthetic effects is by binding to and blocking the voltage-gated sodium channels in the neuronal cell membrane. By stabilizing neuronal membranes, cocaine inhibits the initiation and conduction of nerve impulses and produces a reversible loss of sensation.
Definition (MSH) An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake.
Definition (CSP) alkaloid ester extracted from the leaves of plants including coca; has powerful central nervous system effects similar to the amphetamines and is a drug of abuse; acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake; it is also a local anesthetic and vasoconstrictor and is clinically used for that purpose.
Concepts Hazardous or Poisonous Substance (T131) , Organic Chemical (T109)
MSH D003042
SnomedCT 14816004, 387085005
LNC LP16048-8, MTHU006815
English Cocaine, 8-Azabicyclo(3.2.1)octane-2-carboxylic acid, 3-(benzoyloxy)-8-methyl-, methyl ester, (1R-(exo,exo))-, cocaine in any form, cocaine product, (1R,2R,3S,5S)-2-Methoxycarbonyltropan-3-yl Benzoate, Cocaine [Chemical/Ingredient], cocaine substance, cocaine (Schedule I substance), Blow, C, Snow, Coke, cocaine, Coca, COCAINE, Cocaine product, Cocaine (product), Cocaine (substance)
Swedish Kokain
Czech kokain
Finnish Kokaiini
Russian KOKAIN, КОКАИН
Japanese コカイン塩基, ベンゾイルメチルエクゴニン, コカイン, エリスロキシリン
Croatian KOKAIN
Polish Kokaina
Norwegian Not Translated[Cocaine]
Spanish cocaína (producto), cocaína (sustancia), cocaína, Cocaína
French Cocaïne
German Cocain, Kokain
Italian Cocaina
Portuguese Cocaína

Ontology: Cocaine Abuse (C0009171)

Concepts Mental or Behavioral Dysfunction (T048)
MSH D019970
ICD9 305.60, 305.6
ICD10 F14.1
SnomedCT 78267003
DSM4 305.60
English Cocaine abuse, unspecified use, Abuse, Cocaine, cocaine abuse (diagnosis), cocaine abuse, Cocaine abuse-unspec, Abuse;drug(s);cocaine, abuse cocaine, abuse cocaine disorders, Cocaine abuse, unspecified, Cocaine abuse, Cocaine abuse (disorder), cocaine; abuse, abuse; cocaine, Cocaine Abuse
Portuguese Abuso de Cocaína, Abuso de cocaína, Abuso de cocaína, uso NE
Spanish Abuso de cocaína, uso no especificado, Abuso de cocaína, Abuso de Cocaína, abuso de cocaína (trastorno), abuso de cocaína
French Abus de cocaïne, usage non précisé, Abus de cocaïne
Dutch cocaïnemisbruik, cocaïnemisbruik, niet-gespecificeerd gebruik, cocaïne; misbruik, misbruik; cocaïne, Cocaïnemisbruik
German Kokainmissbrauch, Kokainmissbrauch, unspezifische Verwendung, Kokain-Mißbrauch
Italian Abuso di cocaina, non specificato, Abuso di cocaina
Japanese コカイン乱用, コカインランヨウ, コカイン乱用、使用の詳細不明, コカインランヨウシヨウノショウサイフメイ
Czech Abúzus kokainu, Abúzus kokainu, blíže neurčené užívání
Hungarian Kokain abúzus, Kokain abúzus, nem meghatározott használat
Norwegian Kokainmisbruk

Ontology: Cocaine intoxication (C0009176)

Concepts Mental or Behavioral Dysfunction (T048)
SnomedCT 27956007
DSM4 292.89
English Cocaine Intoxication, cocaine intoxication, cocaine intoxication (diagnosis), Cocaine intoxication, Cocaine intoxication (disorder), cocaine; intoxication, intoxication; cocaine
Dutch cocaïne; intoxicatie, intoxicatie; cocaïne
Spanish intoxicación por cocaína (trastorno), intoxicación por cocaína