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Cocaine Use Disorder COCAINE USE DISORDER ABSTRACT Cocaine addiction is a serious public health problem. Millions of Americans regularly use cocaine, and some develop a substance use disorder. Cocaine is generally not ingested, but toxicity and death from gastrointestinal absorption has been known to occur. Medications that have been used as substitution therapy for the treatment of a cocaine use disorder include amphetamine, bupropion, methylphenidate, and modafinil. While pharmacological interventions can be effective, a recent review of pharmacological therapy for cocaine use indicates that psycho-social efforts are more consistent over medication as a treatment option. Introduction Cocaine is an illicit, addictive drug that is widely used. Cocaine addiction is a serious public health problem that burdens the healthcare system and that can be destructive to individual lives. It is impossible to know with certainty the extent of use but data from public health surveys, morbidity and mortality reports, and healthcare facilities show that there are millions of Americans who regularly take cocaine. Cocaine intoxication is a common cause for emergency room visits, and it is one drug that is most often involved in fatal overdoses. Some cocaine users take the drug occasionally and sporadically but as with every illicit drug there is a percentage of people who develop a substance use disorder. Treatment of a cocaine use disorder involves psycho-social interventions, pharmacotherapy, or a combination of the two. 1 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com Pharmacology of Cocaine Cocaine is an alkaloid derived from the Erthroxylum coca plant, a plant that is indigenous to South America and several other parts of the world, and is cultivated elsewhere. Chemical processing of the plant yields the alkaloid in the form of a cocaine powder that can be injected, insufflated (snorted), applied to mucous membranes, or smoked. Cocaine is well-absorbed by all these routes but absorption through the mucous membranes of the oral and nasal cavities may be delayed due to local vasoconstriction. Cocaine is generally not ingested, but toxicity and death from gastrointestinal (GI) absorption can occur when people try to smuggle packages of cocaine (body packers or body pushers) or swallow cocaine packages while attempting to avoid arrest (body stuffers).1,2 Crack cocaine is powdered cocaine that is mixed with baking soda or ammonia and water and then heated. Heat separates out the cocaine and the result is small, solid nuggets (often called rocks) of cocaine that unlike powdered cocaine is not destroyed by heat. Crack cocaine rocks are put into a pipe, heat is applied to the bowl with a cigarette lighter, and the cocaine fumes/vapors are inhaled. The term crack is used because the cocaine rocks make a crackling sound when they are heated.3 Cocaine is essentially a stimulant, and there are three primary mechanisms of action that underlie cocaine intoxication and toxicity: 1) Neurotransmitter blockade and release, 2) Ion channel blockade, and 3) Excitatory neurotransmitter release.3 Neurotransmitter Blockade and Release Cocaine blocks the pre-synaptic re-uptake of the neurotransmitters dopamine, epinephrine, norepinephrine, and serotonin in the central and 2 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com peripheral nervous systems. This results in a hyper-adrenergic state and stimulation of alpha1, and alpha2, beta1, and beta2 adrenoreceptors, and it explains many of the acute and chronic effects of cocaine intoxication. Cocaine may also cause the release of catecholamines from storage sites. Ion Channel Blockade Cocaine also blocks the sodium ion channels in the myocardium and peripheral nerves, and blocks potassium in channels in the myocardium. Sodium ion channel blockade in the myocardium produces a membrane depressant effect and may cause a prolonged QRS, arrhythmias, and hypotension, sodium ion channel blockade in peripheral nerves prevents transmission of pain impulses, a local anesthetic effect, and potassium ion channel blockade in the myocardium produces QTc prolongation and can cause torsades de pointes.1,4 Excitatory Neurotransmitter Release There is some evidence that cocaine causes an increase in brain levels of the excitatory neurotransmitters glutamate and aspartate. The onset of action of cocaine is very rapid and the duration of action is short; the effects typically begin within 1-5 minutes and the duration of action is usually 30-60 minutes. Cocaine is metabolized by serum cholinesterase, and a considerable amount of the metabolites are excreted in the urine, primarily in the form of benzoylecogonine and ecgonine methyl ester. Benzoylecgonine is the metabolite that is measured in a urine drug screen (UDS); it can be detected several hours after cocaine use and if someone is using large amounts of cocaine on a regular basis, the UDS may be positive for up to 10 days after use.3 A false positive UDS for cocaine is possible but rare3 but as with any 3 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com UDS result the metabolites of cocaine can be detected long after intoxication and impairment occurred.5 Ingestion of drinking alcohol (ethanol) and the use of cocaine, which is a very common situation,6 produces a metabolite called cocaethylene.3,6 Cocaethylene is more toxic than cocaine alone,7 it has a long duration of action (up to 13 hours), and it also prolongs the duration of action of cocaine.6 Acute Cocaine Intoxication Acute cocaine intoxication affects essentially every organ system, and it can cause serious morbidity and death. Cardiovascular Elevations of blood pressure and heart rate are common.3,8,9 Cocaine increases myocardial oxygen demand but because of coronary artery vasoconstriction it reduces oxygen delivery to the myocardium. Chest pain is a common occurrence as is myocardial ischemia but fortunately only approximately 6% of patients with cocaine intoxication will have a myocardial infarction.8 Relatively benign arrhythmias like supraventricular tachycardia are common while serious arrhythmias like ventricular tachycardia are not. Aortic aneurysm and dissection and rupture and heart failure can occur but they are rare.9 Central Nervous System 4 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com Agitation, anxiety, headache and tremor are common, and patients can be confused and delirious, as well.10 Coma, intracranial hemorrhage, seizures, and stroke can occur but seldom do.3,10 Elevation of body temperature and hyperthermia (body temperature up to 40° C/104° F) can occur.1 Pulmonary Cocaine that is smoked can cause thermal injury to the upper airway, shortness of breath, and exacerbation of reversible airway disease. Less common but more dangerous effects of smoking cocaine include pneumothorax, pneumomediastinum, and pneumopericardium.3,12-14 Other Organ System Toxicity Acidosis, perforated gastric ulcer, intestinal infarction, renal infarction, rhabdomyolysis can occur as consequences of cocaine intoxication.3,15,16 Cocaine Use Disorder Diagnosis Chronic cocaine use causes inflammation and damage to the vascular system by way of inflammation, increased shear stress, stress on the myocardium, increased platelet aggregation, and thrombus formation.3,8,17,18 Atherosclerosis, bradycardia, coronary artery thrombosis, dilated cardiomyopathy, left ventricular hypertrophy, and myocarditis are all possible consequences of long-term cocaine use.3,8,19-21 Chronic cocaine users are at risk for infection with hepatitis and human immunodeficiency virus (HIV), psychosis,22 chronic kidney disease,23 structural brain damage and cognitive impairment,24 stroke, impaired sexual function in men,24 and suicide.24 Cocaine use disorder is a substance use disorder. A substance use disorder is defined by specific diagnostic criteria and categorized as mild, moderate, 5 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com or severe, and characterized by recurrent use of alcohol or a drug, use that results in impaired functioning, health problems, and adverse personal, occupational, and social consequences.25 The Diagnostic And Statistical Manual of Mental Disorders, 5th edition (DSM- 5) diagnosis for a substance use disorder are that 2 of these 11 symptoms must be present within the prior 12 months.26 • Consuming more alcohol or other substance than originally planned • Concern about stopping or having consistently failed efforts to control or stop use • Spending a large amount of time using drugs/alcohol, or in activities needed to obtain them • Substance use causes failure to meet significant obligations at home, school, and/or work • The person with a substance use disorder has craving for alcohol or the drug. (Craving in the context of substance use disorder is complex, but it is essentially a strong desire to use alcohol and/or a drug and often the inability to resist the desire.) • Continuing to use a substance despite mental or physical health problems caused or worsened by it substance use • Continuing the use of a substance despite its having negative effects on relationships with others • Repeated use of the substance in dangerous situation, i.e., driving a car) • Giving preference to alcohol or substance use over other life activities • Developing to a tolerance to the alcohol or drug. Tolerance is defined by the DSM-5 as needing to use noticeably larger amounts over time to get the desired effect or experienced a diminished effect
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