Prevalence: cocaine is the most common etiology acute drug-related emergency department visits in the US
Routes of Cocaine Exposure
Gastrointestinal
Onset: 30-60 min
Peak Effect: 60-90 min
Duration of Action: unknown
Types of Exposure
Body Packing: swallowing large quantities of prepackaged drugs with the intent to smuggle them
Body Stuffing: swallowing small quantities of drugs to evade prosecution from law enforcement
Inhalation/Smoking
Onset: <1 min
Peak Effect: 3-5 min
Duration: 30-60 min
Available Preparations
Crack Cocaine: smoking or inhalation of solid form of cocaine
Free-Basing: smoking or inhalation of cocaine in organic phase of liquid
Intravenous Cocaine Injection
Onset: <1 min
Peak Effect: 3-5 min
Duration of Action: 30-60 min
Nasal Snorting of Cocaine
Onset: 1-5 min
Peak Effect: 20-30 min
Duration of Action: 60-120 min
Pharmacology
History
Cocaine is Isolated from the Coca Plant (Erythroxylum Coca)
Erythroxylum Coca is Indigenous to the Andean Highlands in South America
Andean Natives Chew or Brew Coca Leaves into a Tea: used for refreshment or to relieve fatigue
Purified Cocaine was First Isolated in the 1880’s: first used as a local anesthetic in ocular surgery
Utility in Upper Airway and Ocular Surgery is Related to the Anesthetic and Vasoconstrictor Properties of Cocaine
Absorption
Cocaine is Rapidly Absorbed from Oral/Nasal/Gastrointestinal/Rectal/Vaginal Mucosa and Pulmonary Alveoli (Via Inhalation)
Bioavailability When Smoked: 90%
Bioavailability When Used Intranasally: 80%
Mechanisms of Action
Cocaine Inhibits the Presynaptic Neuronal Reuptake of Biogenic Amines (Serotonin and Dopamine/Norepinephrine/Epinephrine)
Cocaine Functions as an Indirect Sympathomimetic Agent
Norepinephrine (and to a Lesser Extent, Epinephrine) Stimulation of α1-Adrenergic Receptors (see α1-Adrenergic Receptor Agonists, [[α1-Adrenergic Receptor Agonists]])
Cardiac Vasoconstriction
Peripheral Vasoconstriction
Norepinephrine (and to a Lesser Extent, Epinephrine) Stimulation of α2-Adrenergic Receptors (see α2-Adrenergic Receptor Agonists, [[α2-Adrenergic Receptor Agonists]])
Norepinephrine (and to a Lesser Extent, Epinephrine) Stimulation of β1-Adrenergic Receptors (see β1-Adrenergic Receptor Agonists, [[β1-Adrenergic Receptor Agonists]])
Norepinephrine (and to a Lesser Extent, Epinephrine) Stimulation of β2-Adrenergic Receptors (see β2-Adrenergic Receptor Agonists, [[β2-Adrenergic Receptor Agonists]])
Cocaine Inhibition of Neuronal Serotonin Reuptake Mediates Euphoric Effects
Cocaine Inhibition of Neuronal Dopamine Reuptake Mediates Addictive Effects
Cocaine Inhibits the Neuronal Sodium Channel
Effect of Neuronal Sodium Channels Mediates Anesthetic Effects
Effect on Cardiac Sodium Channels Mediates QRS Prolongation and Negative Inotropy
Cocaine Increases the Concentration of Excitatory Amino Acids, Glutamate and Aspartate, in the Brain: especially in the nucleus accumbens
Increased Risk of Human Immunodeficiency Virus (HIV) (see Human Immunodeficiency Virus, [[Human Immunodeficiency Virus]]): regardless of the route of cocaine use
May Be Related to Increased High-Risk Sexual Behaviors
Increased Risk of Viral Hepatitis: regardless of the route of cocaine use
May Be Related to Increased High-Risk Sexual Behaviors
Neurologic Manifestations
Cognitive Impairment
Impaired Attention
Impaired Risk-Reward Decision Making
Impaired Verbal Memory
Impaired Visual-Motor Performance
Suicidal Ideation/Attempts: risk factors include depression, severe cocaine withdrawal, coexistent ethanol dependence, coexistent opiate dependence, history of childhood trauma, and family history of suicidality
Otolaryngologic Manifestations
Chronic Rhinitis: due to intranasal cocaine abuse
Nasal Septal Perforation: due to intranasal cocaine abuse
Oropharyngeal Ulcers: due to intranasal cocaine abuse
Osteolytic Sinusitis: due to intranasal cocaine abuse
Pulmonary Manifestations
Moderately Decreased DLCO (see Pulmonary Function Tests, [[Pulmonary Function Tests]]): even when asymptomatic
Manifestations Associated with Cocaine Use During Pregnancy (see Pregnancy, [[Pregnancy]])
Abnormal Fetal Development
Other Manifestations
Risk of General Anesthesia: cocaine abuse does not increase the risk of general anesthesia (assuming that the patient has normal hemodynamic parameters at the time of surgery)
Treatment
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Cocaine Intoxication
Diagnosis
Urine Testing for Benzoylecgonine (Main Urinary Metabolite of Cocaine)
Benzoylecgonine Can Be Detected in the Urine for Several Days (for Intermittent Use) or Up to 10 days (for Heavy Use): in contrast, cocaine is rapidly metabolized and detectable only hours after use
Can Also Test Blood/Saliva/Hair/Meconium Samples
Gas Chromatography-Mass Spectrometry: gold standard for testing for cocaine and its metabolites
Psychomotor Agitation (see Agitation, [[Agitation]])
Physiology: due to central nervous system excitatory amino acids (glutamate, aspartate) and release of excitatory neurotransmitters (norepinephrine, serotonin, dopamine)
Avoid Succinylcholine (see Succinylcholine, [[Succinylcholine]])
Plasma cholinesterases metabolize succinylcholine and cocaine -> succinylcholine use can prolong the effects of both agents
Succinylcholine may worsen hyperkalemia
Treatment of Cocaine Intoxication Associated with Body Packing/Body Stuffing
General Comments: most patients who will have adverse clinical outcomes have symptoms at presentation or within the first few hours
Gastrointestinal Decontamination: for cocaine intoxication associated with body packing/body stuffing
Activated Charcoal (see Activated Charcoal, [[Activated Charcoal]]): useful for orally ingested cocaine
Administration: 1 g/kg (up to max: 50 g) q4hrs PO x several doses
Surgery: may be required for intestinal obstruction or symptoms due to large quantities of packets in GI tract
Treatment of Chest Pain/Acute Myocardial Ischemia or Infarction (see Coronary Artery Disease, [[Coronary Artery Disease]])
Aspirin (see Acetylsalicylic Acid, [[Acetylsalicylic Acid]]): as used standard lay (when aortic dissection is not present)
Avoid Beta Blockers in Cocaine Intoxication see β-Adrenergic Receptor Antagonists, [[β-Adrenergic Receptor Antagonists]]): due to fact that they may allow unopposed α1-adrenergic receptor stimulation, resulting in coronary vasoconstriction and end-organ ischemia
Paradoxical Hypertension and Clinical Deterioration Have Been Demonstrated to Occur in Cocaine Intoxication with the Administration of Esmolol and Metoprolol: these agents are selective β1-adrenergic receptor antagonists
In Rare Cases Where Beta Blockers May Be Necessary, Phentolamine Should Be Given First
Avoid Labetalol (Trandate) in Cocaine Intoxication (see Labetalol, [[Labetalol]]): due to its alpha/beta antagonism ratio or 1:7, labetalol use has not been demonstrated to reverse cocaine-induced coronary artery vasospasm (and may result in unopposed α1-adrenergic receptor stimulation)
Lorazepam (Ativan) (see Lorazepam, [[Lorazepam]]): has been demonstrated to add benefit over nitroglycerin alone (Am J Emerg Med, 2003) [MEDLINE]
Nitroglycerin (see Nitroglycerin, [[Nitroglycerin]]): useful
Surface Cooling: ice packs or ice water are rapidly effective
Treatment of Hypertension (see Hypertension, [[Hypertension]])
Avoid Beta Blockers in Cocaine Intoxication (see β-Adrenergic Receptor Antagonists, [[β-Adrenergic Receptor Antagonists]]): due to fact that they may allow unopposed α1-adrenergic receptor stimulation, resulting in coronary vasoconstriction and end-organ ischemia
Paradoxical Hypertension and Clinical Deterioration Have Been Demonstrated to Occur in Cocaine Intoxication with the Administration of Esmolol and Metoprolol: these agents are selective β1-adrenergic receptor antagonists
In Rare Cases Where Beta Blockers May Be Necessary, Phentolamine Should Be Given First
Avoid Labetalol (Trandate) in Cocaine Intoxication (see Labetalol, [[Labetalol]]): due to its alpha/beta antagonism ratio or 1:7, labetalol use has not been demonstrated to reverse cocaine-induced coronary artery vasospasm (and may result in unopposed α1-adrenergic receptor stimulation)
Nitroprusside (Nipride) (see Nitroprusside, [[Nitroprusside]]): may be used in cases with severe hypertension
Phentolamine (Regitine, OraVerse) (see Phentolamine, [[Phentolamine]])
Pharmacology: inhibits the norepinephrine-related, α1-adrenergic-mediated effects of cocaine -> decreases cocaine-induced coronary artery vasoconstriction and hypertension
Administration: 5 mg IV bolus q5-15 min PRN
Blood Pressure Target: aim to decrease diastolic blood pressure to 100-105 mm Hg within 2-6 hrs (with decrease not to exceed 25% below the presenting diastolic blood pressure value)
Treatment of Hypotension (see Hypotension, [[Hypotension]])
Intravenous Fluid Resuscitation
Normal Saline (see Normal Saline, [[Normal Saline]])
Vasopressors
Norepinephrine (Levophed) (see Norepinephrine, [[Norepinephrine]])
Phenylephrine (Neosynephrine) (see Phenylephrine, [[Phenylephrine]])
Duration of Symptoms: generally mild symptoms lasting 1-2 wks
Cardiovascular Manifestations
Myocardial Ischemia (see Coronary Artery Disease, [[Coronary Artery Disease]]): observed during the first week of withdrawal (possibly due to coronary vasospasm)
The pulmonary complications of crack cocaine, a comprehensive review. Chest 1995; 107:233-240 [MEDLINE]
NIDA conference report on cardiopulmonary complications of crack cocaine use: clinical manifestations and pathophysiology. Chest 1996; 110:1072-1076 [MEDLINE]
Cocaine-induced pneumopericardium. Circulation. 2000 Nov 28;102(22):2792-4 [MEDLINE]
Cardiovascular complications of cocaine use. N Engl J Med. 2001;345(5):351 [MEDLINE]
A prospective, randomized, controlled trial of benzodiazepines and nitroglycerine or nitroglycerine alone in the treatment of cocaine-associated acute coronary syndromes. Am J Emerg Med. 2003;21(1):39 [MEDLINE]
Management of cocaine-associated chest pain and myocardial infarction: a scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology. Circulation. 2008;117(14):1897 [MEDLINE]
Cocaine-induced spinal cord infarction. Postgrad Med J. 2008 Jul;84(993):391. doi: 10.1136/pgmj.2007.062224 [MEDLINE]
Levamisole exposure and hematologic indices in cocaine users. Acad Emerg Med. 2011 Nov;18(11):1141-7 [MEDLINE]
Prevalence of levamisole in urine toxicology screens positive for cocaine in an inner-city hospital. JAMA. 2011;305(16):1657 [MEDLINE]
An unusual complication of cocaine toxicity. Acute Med. 2013;12(2):96-7 [MEDLINE]
Stimulants and the lung : review of literature. Clin Rev Allergy Immunol. 2014 Feb;46(1):82-100 [MEDLINE]
High-resolution computed tomographic findings of cocaine-induced pulmonary disease: a state of the art review. Lung. 2014 Apr;192(2):225-33. Epub 2014 Jan 16 [MEDLINE]
Serotonin Syndrome in the Setting of Lamotrigine, Aripiprazole, and Cocaine Use. Case Rep Med. 2015;2015:769531. doi: 10.1155/2015/769531. Epub 2015 Aug 2 [MEDLINE]
