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Cocaine

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Cocaine, Cocaine Abuse, Cocaine Intoxication, Cocaine Toxicity

  • 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
  • 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)
  • Mechanism
  1. Affects central and peripheral Neurotransmitters (blocks their reuptake)
    1. Norepinephrine
    2. Dopamine - arousal
    3. Serotonin - awakening
  • 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
  • Symptoms
  1. Increased energy and alertness
  2. Euphoria
  3. Sociability
  4. Appetite suppression
  5. Decreased need for sleep
  1. See Cocaine-Induced Coronary Vasospasm
  2. See Sympathomimetic Toxicity
  3. Hypertensive
  4. Sinus Tachycardia (significant)
  5. Diaphoresis
    1. Contrast with AmitriptylineOverdose which causes dryness (instead of diaphoresis)
  • 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
  • Labs
  1. See Urine Drug Screen
  2. Detectable in blood, urine, hair, Saliva, sweat, Breast Milk
  • Management
  • Toxicity
  1. See Sympathomimetic Toxicity
  2. Avoid Beta Blockers (risk of unopposed alpha-agonist effect)
  3. Benzodiazepines and other sedatives
  4. Treat hyperthermia with cooling
  • 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
  • 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]
  • References
  1. Moore, Behar, Claudius and Farrah in Herbert (2018) EM:Rap 18(5):11-2
  2. Klega (2018) Am Fam Physician 98(2): 85-92 [PubMed]
  3. Shih (1996) Hosp Physician p. 11-20 [PubMed]