Cocaine

Aka: Cocaine, Cocaine Abuse, Cocaine Intoxication, Cocaine Toxicity

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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

  1. QRS Widening
  2. Sinus Tachycardia
  3. Paroxysmal Supraventricular Tachycardia and other tachyarrhythmias

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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