Epidemiology
- 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
Chronic Cocaine Abuse
Epidemiology
Clinical Manifestations
Cardiovascular Manifestations
- Congestive Heart Failure (CHF) (see Congestive Heart Failure, [[Congestive Heart Failure]])
- Physiology: dilated cardiomyopathy
- Coronary Artery Disease (CAD)
- Epidemiology: associated with chronic cocaine use
- Physiology: accelerated atherogenesis
- Left Ventricular Hypertrophy (LVH)
- Myocarditis (see Myocarditis, [[Myocarditis]])
Infectious Manifestations
- 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
- Increased Alveolar Epithelial Permeability
- Pulmonary Hypertension (see Pulmonary Hypertension, [[Pulmonary Hypertension]])
- Epidemiology: possibly associated with pulmonary hypertension
- Talc/Foreign Body Granulomatosis (see Foreign Body Granulomatosis, [[Foreign Body Granulomatosis]])
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
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
Clinical Manifestations
Cardiovascular Manifestations
- Acute Myocardial Infarction/Myocardial Ischemia (see Coronary Artery Disease, [[Coronary Artery Disease]])
- Epidemiology: associated with crack cocaine use
- Physiology: coronary vasoconstriction
- Clinical
- Diaphoresis (see Diaphoresis, [[Diaphoresis]])
- Dyspnea (see Dyspnea, [[Dyspnea]])
- Substernal Chest Pain (see Chest Pain, [[Chest Pain]]): occurs in 76% of cases
- Aortic Dissection (see Aortic Dissection, [[Aortic Dissection]])
- Physiology:
- Clinical: aortic rupture can occur
- Arrhythmias
- Epidemiology: associated with crack cocaine use
- Physiology: due either to myocardial ischemia or catecholaminergic effects
- Clinical
- Supraventricular Arrhythmias
- Ventricular Arrhythmias
- Congestive Heart Failure (CHF) (see Congestive Heart Failure, [[Congestive Heart Failure]])
- Physiology: at high cocaine concentrations, negative inotropy can occur
- Endocarditis (see Endocarditis, [[Endocarditis]])
- Epidemiology: associated with crack cocaine use
- Hypertension (see Hypertension, [[Hypertension]])
- Epidemiology: typical hemodynamic manifestation
- Physiology: due to vasoconstriction (with increased systemic vascular resistance)
- Hypotension (see Hypotension, [[Hypotension]])
- Epidemiology: may occur in the setting of massive cocaine intoxication
- Physiology: due to sodium channel blockade, arrhythmias, or myocardial ischemia
- Myocarditis (see Myocarditis, [[Myocarditis]])
- Epidemiology: associated with crack cocaine use
- QT Prolongation without Definite Association with Torsade (see Torsade, [[Torsade]])
- Sinus Tachycardia (see Sinus Tachycardia, [[Sinus Tachycardia]])
Dermatologic Manifestations
Gastrointestinal Manifestations
- Acute Mesenteric Ischemia (see Acute Mesenteric Ischemia, [[Acute Mesenteric Ischemia]])
- Anorexia (see Anorexia, [[Anorexia]])
- Colonic Ischemia (Ischemic Colitis) (see Colonic Ischemia, [[Colonic Ischemia]])
- Elevated Liver Function Tests (LFT’s) (see xxxx, [[xxxx]])
- Perforated Peptic Ulcer Disease (PUD) (see Peptic Ulcer Disease, [[Peptic Ulcer Disease]])
- Physiology: due to increased sympathetic tone with increased gastric acid production and/or local gastro-intestinal ischemia
- Subfulminant Hepatic Failure (see Fulminant Hepatic Failure, [[Fulminant Hepatic Failure]])
- Weight Loss (see Weight Loss, [[Weight Loss]])
Hematologic Manifestations
Neurologic/Psychiatric Manifestations
- Akathisia (see Akathisia, [[Akathisia]])
- Buccolingual Dyskinesia (“Twisted Mouth”)
- Choreoathetosis (“Crack Dancers”) (see Chorea, [[Chorea]])
- Dystonia (see Dystonia, [[Dystonia]])
- Epidemiology: neuroleptic medications may compound the risk of dystonia
- Euphoria
- Exacerbation of Tardive Dyskinesia (see Tardive Dyskinesia, [[Tardive Dyskinesia]])
- Exacerbation of Tourette’s Syndrome
- Headache (see Headache, [[Headache]])
- Epidemiology: common
- Physiology: due to neurotransmitter dysregulation and hemodynamic effects
- Improved Performance on Tasks of Vigilance
- Increased Alertness
- Intracerebral Hemorrhage (Hemorrhagic Cerebrovascular Accident) (see Intracerebral Hemorrhage, [[Intracerebral Hemorrhage]])
- Ischemic Cerebrovascular Accident (CVA) (see Ischemic Cerebrovascular Accident, [[Ischemic Cerebrovascular Accident]])
- Physiology: due to cerebral vasoconstriction, hypertension, vasospasm, and Intravascular thrombosis (due to platelet aggregation)
- Obtundation-Coma (see Obtundation-Coma, [[Obtundation-Coma]])
- Psychomotor Agitation (see Agitation, [[Agitation]])
- Physiology: due to central nervous system excitatory amino acids (glutamate, aspartate) and release of excitatory neurotransmitters (norepinephrine, serotonin, dopamine)
- Psychotic Symptoms (see Psychosis, [[Psychosis]])
- Delusions
- Hallucination (see Hallucination, [[Hallucination]]): visual and/or tactile hallucinations are typical of stimulant-associated psychosis
- Formication (“Cocaine Bugs”): sensation of insects crawling under the skin
- Paranoia
- Repetitive Behaviors
- Foraging for Drugs
- Picking at the Skin
- Seizures (see Seizures, [[Seizures]])
- Epidemiology: occur in 3-4% of cocaine-related emergency department visits associated with acute/chronic abuse
- May occur even with first-time cocaine use
- Clinical: usually tonic-clonic and occurring within 90 min of cocaine use
- Sense of Self-Confidence
- Sleep Disturbance
- Decreased Need for Sleep
- Insomnia (see Insomnia, [[Insomnia]])
- Subarachnoid Hemorrhage (SAH) (see Subarachnoid Hemorrhage, [[Subarachnoid Hemorrhage]])
- Epidemiology: cocaine is associated with both aneurysmal and non-aneurysmal subarachnoid hemorrhage
- Transient Ischemic Attack (TIA) (see Transient Ischemic Attack, [[Transient Ischemic Attack]])
- Tremor (see Tremor, [[Tremor]])
- Vasospasm-Induced Anterior Spinal Cord Syndrome (see Spinal Cord Infarction, [[Spinal Cord Infarction]])
Ophthalmologic Manifestations
- Acute Angle-Closure Glaucoma (see Glaucoma, [[Glaucoma]])
- Corneal Epithelial Injury
- Physiology: due to crack cocaine use -> thermal injury to cornea
- Mydriasis (see Mydriasis, [[Mydriasis]]): pupil remains reactive to light
- Vision Loss (Unilateral or Bilateral)
- Physiology: due to retinal vasoconstriction
Pulmonary Manifestations
Acute Respiratory Distress Syndrome (ARDS) (see Acute Respiratory Distress Syndrome, [[Acute Respiratory Distress Syndrome]])
- Epidemiology: associated with inhalational crack cocaine use
- Diagnosis
- Open Lung Biopsy: diffuse alveolar damage, organizing pneumonia
- Clinical: dyspnea
- Treatment: supportive
Angioedema (see Angioedema, [[Angioedema]])
- Epidemiology: associated with crack cocaine use
- Physiology: due to crack cocaine being heated to the high temperatures required for vaporization
Aspiration Pneumonia (see Aspiration Pneumonia, [[Aspiration Pneumonia]])
Asthma Exacerbation (see Asthma, [[Asthma]])
- Epidemiology: associated with crack cocaine use
Barotrauma
- Epidemiology: associated with crack cocaine use
- Physiology: associated with intranasal and inhalational cocaine abuse -> forceful inhalation with Valsalva maneuver
- Clinical
Cough (see Cough, [[Cough]])
- Clinical: sometimes with black sputum production
“Crack Lung” (Hemorrhagic Alveolitis)
- Epidemiology: associated with inhalational crack cocaine use
- Usually Occurs Minutes-Hours After Crack Use
- Diagnosis
- Clinical
- Treatment: corticosteroids have been used (although there are no trials to support this) (see Corticosteroids, [[Corticosteroids]])
Cryptogenic Organizing Pneumonia (COP) (see Cryptogenic Organizing Pneumonia, [[Cryptogenic Organizing Pneumonia]])
- Epidemiology: associated with crack cocaine use
Diffuse Alveolar Hemorrhage (DAH) (see Diffuse Alveolar Hemorrhage, [[Diffuse Alveolar Hemorrhage]])
- Epidemiology: associated with inhalational crack cocaine use
- Usually Occurs Minutes-Hours After Crack Use
- Physiology: may involve damage due to pulmonary vasoconstriction or due to direct alveolar injury
- Clinical
- Autopsy studies demonstrate pulmonary hemorrhage in >50% of cases
- May coexist with peripheral eosinophilia
Dyspnea (see Dyspnea, [[Dyspnea]])
- Epidemiology: associated with crack cocaine use
Lung Mass with/without Cavitation (see Lung Nodule or Mass, [[Lung Nodule or Mass]])
Pharyngeal Burns
- Epidemiology: associated with inhalational crack cocaine use
- Physiology: due to crack cocaine being heated to the high temperatures required for vaporization
Pulmonary Infarction (Am J Med, 1991) [MEDLINE]
- Epidemiology
- In Contrast, There is No Known Association Between Cocaine Abuse and the Risk of Acute Pulmonary Embolism (PE)
- Physiology: due to vasoconstriction, vasospasm, and increased thrombus formation
- Clinical
- Dyspnea
- Pleuritic Chest Pain
Thermal Airway Injury
- Epidemiology: associated with crack cocaine abuse
- Physiology: due to crack cocaine being heated to the high temperatures required for vaporization
Renal Manifestations
- Lactic Acidosis (see Lactic Acidosis, [[Lactic Acidosis]])
- Physiology: decreased oxygen delivery to tissues + epinephrine-induced β2-adrenergic receptor stimulation
- In Addition, Clenbuterol (Found as an Adulterant in Cocaine) Can Cause Lactic Acidosis (see Clenbuterol, [[Clenbuterol]]))
- Clinical: marked hyperlactatemia may be seen in in patients having seizures or who are restrained
- Renal Infarction (see Renal Infarction, [[Renal Infarction]])
Rheumatologic Manifestations
Toxicologic Manifestations
- Hyperthermia (see Fever, [[Fever]])
- Physiology: peripheral vasoconstriction prevents heat dissipation
- Prognosis: mortality can be as high as 33% in the presence of cocaine-induced hyperthermia
- Methemoglobinemia (see Methemoglobinemia, [[Methemoglobinemia]])
- Epidemiology: case reports (Acute Med, 2013) [MEDLINE]
- Serotonin Syndrome (see Serotonin Syndrome, [[Serotonin Syndrome]])
- Epidemiology: case reports (Case Rep Med, 2015) [MEDLINE]
Manifestations Associated with Cocaine Use During Pregnancy
Manifestations Related to Cocaine Adulterants
Levamisole (see Levamisole, [[Levamisole]])
- Epidemiology: common adulterant
- In 2010 in Colorado, 78% of Patients with Positive Urine Drug Screens for Cocaine were Also Positive Also for Levamisole (JAMA, 2011) [MEDLINE]
- Pharmacology: immunomodulator
- Clinical (Acad Emerg Med, 2011) [MEDLINE]
- Agranulocytosis
- Neutropenia (see Neutropenia, [[Neutropenia]])
- Oropharyngeal Complaints: common in this setting
- Soft Tissue Infection: common in this setting
- Cutaneous Vasculitis
- Purpura (see Purpura, [[Purpura]])
- May lead to cutaneous necrosis
- Leukoencephalopathy
Clenbuterol (see Clenbuterol, [[Clenbuterol]])
- Epidemiology: has been found as an adulterant in both cocaine and heroin (see Heroin, [[Heroin]])
- Physiology: β2 agonist (see β2-Adrenergic Receptor Agonists, [[β2-Adrenergic Receptor Agonists]])
- Clinical
- Agitation (see Agitation, [[Agitation]])
- Anxiety (see Anxiety, [[Anxiety]])
- Chest Pain (see Chest Pain, [[Chest Pain]])
- Hyperglycemia (see Hyperglycemia, [[Hyperglycemia]]): occurs in 78% of cases
- Hypokalemia (see Hypokalemia, [[Hypokalemia]]): occurs in 78% of cases
- Hypotension (see Hypotension, [[Hypotension]])
- Lactic Acidosis (see Lactic Acidosis, [[Lactic Acidosis]])
- Nausea (see Nausea and Vomiting, [[Nausea and Vomiting]])
- Palpitations (see Palpitations, [[Palpitations]]): occurs in 78% of cases
- Sinus Tachycardia (see Sinus Tachycardia, [[Sinus Tachycardia]]): occurs in 89% of cases
Treatment
Supportive Care
- Mechanical Ventilation (see General Ventilator Management, [[General Ventilator Management]]): as required
- Sedation: including induction agents for intubation
- Paralysis
- 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
- Oxygen (see Oxygen, [[Oxygen]]): useful
- 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
Treatment of Ventricular Arrhythmias
Treatment of Agitation (see Agitation, [[Agitation]])
- Avoid Restraints: as these may contribute to the development of hyperthermia
- Benzodiazepines (see Benzodiazepines, [[Benzodiazepines]])
- Diazepam (Valium) (see Diazepam, [[Diazepam]]): IV
- Lorazepam (Ativan) (see Lorazepam, [[Lorazepam]]): IM or IV
Treatment of Hyperthermia (see Fever, [[Fever]])
- 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
- Vasopressors
- Norepinephrine (Levophed) (see Norepinephrine, [[Norepinephrine]])
- Phenylephrine (Neosynephrine) (see Phenylephrine, [[Phenylephrine]])
Treatment of QRS Prolongation
Cocaine Withdrawal
Clinical Manifestations
General Comments
- 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)
Neurologic/Psychiatric Manifestations
- Anhedonia (see Anhedonia, [[Anhedonia]])
- Anxiety (see Anxiety, [[Anxiety]])
- Chills (see Chills, [[Chills]])
- Cocaine Craving
- Depression (see Depression, [[Depression]])
- Difficulty Concentrating
- Fatigue (see Fatigue, [[Fatigue]])
- Involuntary Motor Movements
- Psychomotor Retardation with Depression and Suicidal Ideation (“Crash”)
- Sleep Disturbance
- Increased REM Sleep: with increased dreaming
- Increased Sleep
- Tremor (see Tremor, [[Tremor]])
Gastrointestinal Manifestations
Treatment
References
- Crack lung: an acute pulmonary syndrome with a spectrum of clinical and histopathologic findings. Am Rev Respir Dis. 1990;142(2):462 [MEDLINE]
- Pulmonary infarction associated with crack cocaine use in a previously healthy 23-year-old woman. Am J Med. 1991;91(1):92 [MEDLINE]
- Cocaine-induced eosinophilic lung disease. Thorax 1992; 47:478-479 [MEDLINE]
- 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]