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Home , Cocaine intoxication, Stimulant use disorder, Substance use disorder

USE DISORDER

ABSTRACT

Cocaine is a serious public health problem. Millions of Americans regularly use cocaine, and some develop a . Cocaine is generally not ingested, but 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 , bupropion, , 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. 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 . 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. 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 , 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, , 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 (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 .8

Relatively benign arrhythmias like supraventricular are common while serious arrhythmias like ventricular tachycardia are not. Aortic aneurysm and dissection and rupture and 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 are common, and patients can be confused and delirious, as well.10 Coma, intracranial hemorrhage, seizures, and can occur but seldom do.3,10 Elevation of body temperature and (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, 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), ,22 chronic kidney disease,23 structural brain damage and cognitive impairment,24 stroke, impaired sexual function in men,24 and .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 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 over time form the same amount

• Withdrawal symptoms after stopping use

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A substance use disorder is “substance use that is unregulated and destructive ... and progressively uncontrollable drug use in the face of negative consequences.”27

Incidence of Cocaine Use

Approximately 1.6 million Americans in 2016 were considered to be current users of cocaine,28 and since 2009 the incidence of cocaine use appears to have been stable and not increasing.29 Most users are adults age 26 and older, usually male, and the majority use powder cocaine; crack cocaine use is far less common.29

The National Survey on Drug Use and Heath estimated that in 2014, 913,000 Americans would meet the DSM-5 diagnostic criteria for cocaine use disorder,28 people who use cocaine have a high risk of developing cocaine use disorder,24 particularly if they are intravenous (IV) users or smoke cocaine.

The Effects of Maternal Cocaine Use

Most women who are addicted to cocaine are of childbearing age. Estimates suggest that about 5 percent of pregnant women use one or more addictive substances,50 and there are around 750,000 cocaine-exposed pregnancies every year.51 Although women may be reluctant to report substance use patterns because of social stigma and fear of losing custody of their children, they should be aware that drug use while pregnant is associated with specific risks that may be reduced with appropriate care.

7 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com Cocaine use during pregnancy is associated with maternal migraines and seizures, premature membrane rupture, and separation of the placental lining from the uterus prior to delivery.50 Pregnancy is accompanied by normal cardiovascular changes, and cocaine use exacerbates these— sometimes leading to serious problems with high blood pressure (hypertensive crises), spontaneous , preterm labor, and difficult delivery.51 Cocaine-using pregnant women must receive appropriate medical and psychological care—including addiction treatment—to reduce these risks.50

Sex-specific addiction treatment and comprehensive services—including prenatal care, counseling, vocational/employment assistance, and parenting skills training—can promote drug abstinence and other positive health behaviors.52 Motivational incentives/ (see "Behavioral Interventions") as an adjunct to other addiction treatment is a particularly promising strategy to engage women in prenatal care and counseling for substance use.53

It is difficult to estimate the full extent of the consequences of maternal drug use and to determine the specific hazard of a particular drug to the unborn child. This is because multiple factors—such as the amount and number of all drugs used, including or alcohol; extent of prenatal care; exposure to violence in the environment; socioeconomic conditions; maternal nutrition; other health conditions; and exposure to sexually transmitted diseases—can all interact to influence maternal and child outcomes.51,54,55 Similarly, parenting styles, quality of care during early childhood, exposure to violence, and continued parental drug use are strong environmental factors influencing outcomes.56,57

8 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com Babies born to mothers who use cocaine during pregnancy are often prematurely delivered, have low birth weights and smaller head circumferences, and are shorter in length than babies born to mothers who do not use cocaine. 51,54,55 Dire predictions of reduced intelligence and in babies born to mothers who used crack cocaine while pregnant during the 1980s—so-called "crack babies"—were grossly exaggerated. However, the fact that most of these children do not show serious overt deficits should not be overinterpreted to indicate that there is no cause for concern.

Using sophisticated technologies, scientists are now finding that exposure to cocaine during fetal development may lead to subtle, yet significant, later deficits in some children.56,57 These include behavior problems (e.g., difficulties with self-regulation) and deficits in some aspects of cognitive performance, information processing, and sustained attention to tasks— abilities that are important for the realization of a child’s full potential.57,58 Some deficits persist into the later years, with prenatally exposed adolescents showing increased risk for subtle problems with language and memory.59 Brain scans in teens suggests that at-rest functioning of some brain regions—including areas involved in attention, planning, and language—may differ from that of non-exposed peers.60 More research is needed on the long-term effects of prenatal cocaine exposure.

Screening for Cocaine Use

If it is known or suspected that the patient uses cocaine, he or she should be examined for current intoxication and, if not intoxicated, appropriate testing should be performed to check for possible physical consequences of use. A urine drug screen can be done, but a positive result only indicates prior use, not current intoxication or impairment, or the patient’s pattern of use or

9 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com consumption. The patient should be asked about the use of cocaine and, when it is appropriate, collateral family reporting on the issue can be sought.

The U.S., Preventive Services Task Force’s Guide to Clinical Preventive Services states that “... the evidence is insufficient to determine the harms of screening for illicit drug use.”30 The Guidelines also state that there are valid, reliable screening tests for drug use/misuse but there is not enough evidence to evaluate their usefulness in a primary care setting.30 However, recent research (2015, 2016) has found that short self-administered and clinician-administered screening tools can reliably detect if a patient has been using illicit drugs or has a substance use disorder, including cocaine.24,31-34

McNeely, et al., used an adaption of the , Alcohol, Prescription Medications, and Other Substance screening tool to evaluate its performance for detecting clinically relevant substance use, asking the participants the following questions.34

• In the past three months, did you use cocaine or crack? • If you did use cocaine or crack did you use either one more than once a week? • Has anyone told you they are worried about your use of cocaine?

DSM-5 Criteria

The DSM-5 criteria for cocaine use disorder are the same criteria stated above for substance use disorder. In this case, however, the criteria are evaluated specifically for cocaine use. The DSM-5 states that for the diagnosis to be made for cocaine use disorder, a patient must have a

10 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com problematic pattern of cocaine use that causes significant distress, and a problematic pattern of use and significant distress are considered present if within the prior 12 months the patient has had two or more of the following:

• Cocaine is often taken in larger amounts or over a longer period than was intended • There is a persistent desire or unsuccessful efforts to cut down or control cocaine use • A great deal of time is spent in activities necessary to obtain cocaine, use cocaine, or recover from its effects • Craving, or a strong desire or urge to use cocaine • Recurrent cocaine use resulting in a failure to fulfill major role obligations at work, school, or home • Continued cocaine use, despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of cocaine • Important social, occupational, or recreational activities are given up or reduced because of cocaine use • Recurrent cocaine use in situations in which its use is physically dangerous • Continued cocaine use despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by cocaine • Tolerance • Withdrawal

The severity can be categorized as mild, with two-three symptoms, moderate, with four to five symptoms, or severe with six or more symptoms. The diagnosis can be further defined by: 1) In sustained remission - after full criteria for cocaine use disorder were previously met- none of the criteria for cocaine use disorder have been met (with the exception of craving)

11 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com during a period of 12 months or longer; and 2) In a controlled environment - if the individual is in an environment where access to cocaine is restricted.

Treatment of Cocaine Use Disorder

Treatment of a cocaine use disorder consists of psycho-social interventions, pharmacotherapy, or both. A wide variety of therapies and drugs have been used. The evidence at this time suggest that psycho-social interventions have been more successful and are more likely to be successful than pharmacotherapy.35 Pharmacological interventions can be effective, but according to a recent (2018) review of pharmacological intervention for , at this time there is no evidence of consistent efficacy for medications as a treatment option.35

Pharmacotherapy

Pharmacotherapy as a treatment for cocaine addiction has focused on the use of drugs that affect dopamine. Dopamine is a monoamine neurotransmitter (epinephrine, histamine, norepinephrine, and serotonin are the others) and it is an integral part of areas of the brain that are called the . Activities like eating and sex, and the use of psychoactive drugs like cocaine, stimulate the reward system, and increase the level of dopamine in the brain. This produces a physical sensation of pleasure and the incentive to repeat the behavior.

As with all neurotransmitters, dopamine is released into the synapse, it binds to post-synaptic receptors, and then by way of dopamine transporters it is returned to the pre-synaptic storage sites. Cocaine blocks dopamine re- uptake, primarily by interfering with the activity of dopamine transporters,

12 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com and increases the activity and level of dopamine in the brain;35 the reinforcing properties of cocaine use, i.e., the pleasurable physical and psychological effects of cocaine intoxication, are thought to be due to blockade of dopamine re-uptake.

Increased levels of dopamine reinforce drug use behaviors and affect brain chemistry in many complicated and inter-related ways, and cocaine’s psychoactive and addictive properties are mediated through dopamine. Blocking the effects of dopamine via dopamine antagonists such as use of medications (which act as dopamine receptor antagonists) prevent the psychoactive effects of cocaine from occurring, and has seemed a logically intuitive way of treating cocaine use disorder. However, the little research done in this area has produced disappointing and unsuccessful results.36-38

Drugs that affect dopamine release and re-uptake and that can affect dopamine transporters however have shown more promise. The basic premise of using these drugs to treat cocaine use disorder has been termed substitution therapy, and it is a well-established approach to treating substance use disorders. Substitution therapy uses a drug that binds to and activates the same receptors that are involved in substance use disorder. The drug binding to the receptor prevents withdrawal from happening, the prescription medications do not produce the same level of impairment as the illicit substance, the reinforcing effect of cocaine is removed, the dose and the dosing interval is controlled, and their duration of effect is significantly longer than that of cocaine. In addition, these drugs are legal, and the procurement and use is not associated with risk-taking behavior and with situations and behaviors that reinforce the use of cocaine.

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Medications that have been used as substitution therapy for treatment of cocaine use disorder include amphetamine, bupropion, methylphenidate, and modafinil.

Amphetamine

Amphetamine acts primarily to stimulate the release of dopamine and other catecholamines from pre-synaptic storage areas. It also (to a lesser degree) blocks the re-uptake of dopamine, and these similarities to cocaine make amphetamine a logical choice for substitution therapy. In addition, amphetamine has a slower onset of action and a longer duration of action than cocaine, properties that make it useful for substitution therapy.

There is little research and current research on the use of amphetamine for the treatment of cocaine use disorder. The available data does suggest amphetamine can be an effective treatment for cocaine use disorder. However, the studies are small (i.e., 7-8 subjects) and they have different methodological approaches and designs, and these factors limit the practical application of the findings. Four controlled trials and two literature reviews published between 2013-2016 will be discussed here. Research done before 2013 is not included.

Research on Amphetamine Treatment for Cocaine Addiction

Nuijten, et al., (2016) performed a randomized, double-blind placebo- controlled trial with subjects who had a cocaine substance use disorder, who were evaluated to be treatment-resistant, and who had regularly used crack cocaine. The subjects were also receiving either methadone or diacetyl as treatment for use disorder. The study lasted 12 weeks, and the subjects were given either a placebo35 or 60 mg a day or sustained-

14 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com release .38 Subjects who were given dextroamphetamine had significantly fewer days of self-reported cocaine use, mean of 44.9 days versus a mean of 60.6 days for the placebo group.39

Reed, et al., (2016) measured the effectiveness of placebo and different doses of amphetamine for decreasing , risk-taking, and subjective measures of drug use liability. There were 34 subjects, regular cocaine users, and in five sessions each subject was given a placebo or a drug, and before the session and at 0.25 hours, 1, 2, 3, 4 and 5 hours after administration of the placebo or the amphetamine; the subjects completed questionnaires that measured impulsivity, risk-taking, and drug use liability. For drug use liability, the subjects completed the Drug Effects Questionnaire, which asks “... participants to rate “good effects,” “bad effects,” “strength of the drug effect,” and the degree they would be “willing to take the drug again” on a 5-point scale and rate how much they liked the drug effect on a 9-point scale from −4 (“dislike very much”) to 4 (“like very much”).” The group that received amphetamine had a minimal improvement on drug use liability but no improvement on impulsivity or risk-taking as per the results of the questionnaires.40 Mooney, et al., (2015) performed a randomized, double-blind, placebo- controlled trial in which 43 cocaine-use subjects were given placebo (21) or 70 mg (22) for 14 weeks.41 A urine drug screen was done twice a week during the study period. Compared to placebo lisdexamfetmine did not significantly reduce cocaine use. However, the subjects receiving lisdexamfetamine did report much less craving for cocaine than the placebo group.

Levin, et al., (2015) administered 60 mg or 80 mg of extended release amphetamine or placebo to 126 adults who had been diagnosed as having

15 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com Attention Deficit Hyperactivity Disorder (ADHD) and cocaine use disorder. The study was randomized and double blinded, the duration was 13 weeks, and the subjects participated in a weekly session of cognitive behavioral therapy. The rate of abstinence in the last three weeks of the study was 7.0% for the placebo group, 17.5% for the 60 mg group, and 30.2% for the 80 mg group. The odds of a cocaine negative week were higher for the groups given amphetamine than placebo.42

Kampman (2018) reviewed pharmacotherapy for stimulant use disorder.43 The author examined four controlled studies (including the one by Nuijten that was previously discussed). These involved 403 patients who had been diagnosed with cocaine use disorder, and amphetamine was used as substitution therapy. The author concluded that the Nuijten’s work was promising but that the three earlier studies had a high dropout rate and the results were mixed.

Stoops and Rush (2013) reviewed three clinical trials and two small (17 total subjects) self-administration studies.36 In all five the use of amphetamine was effective as a substitution therapy, i.e., reducing an individual’s preference for cocaine and decreasing cocaine use. The authors concluded that the literature clearly supported “… the continued development of amphetamine isomers” for cocaine drug use.

Castells, et al., (2016) reviewed the literature on psychostimulant drugs (including amphetamine) as a treatment for cocaine use, examining essentially the same published information as Stoops, et al., and Kampman, and the authors wrote that the quality of the research was low; they indicated that psychostimulants improved abstinence rates but not treatment retention, the dropout rate in the studies was high and this could

16 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com have influenced the findings, and substitution therapy with psychostimulants “... appears promising and deserves further investigation.”44

Methylphenidate

Methylphenidate is a central nervous system stimulant, and its primary mechanism of action is blocking the re-uptake of catecholamines. As with amphetamine, the pharmacologic similarity of methylphenidate to cocaine and the similarity of cocaine intoxication to the physical and psychological effects of methylphenidate made methylphenidate a logical choice for substitution therapy.

Research in the area, however, is limited. The most recent article was a review of the literature by Dürsteler, et al., that examined five case reports three open label trials, and five double blinded, randomized, placebo- controlled trials.45 The authors’ literature search was from 1965 to September 2014, and the total number of subjects in the 13 articles was 384. The authors concluded there was no definitive evidence for the effectiveness of methylphenidate as a treatment for cocaine use disorder; the findings were inconsistent, but the negative findings may have been due in part to the study designs. (See the pervious section on and 2016 work by Castells, et al.)

Bupropion

Bupropion inhibits the re-uptake of dopamine and norepinephrine. A literature search found four articles on the use of bupropion as a treatment of cocaine use disorder;46-49 the publication dates were 1995, 2002, 2006, and 2008, and the total number of subjects was 336. The results were mixed and a review of three of these four studies were by Castells, et al.

17 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com Bupropion (300 mg/day) was not found to be efficacious compared with placebo for DSM-IV cocaine use in a 12-week clinical trial of 149 patients with co-occurring cocaine and opioid use receiving .27

Bupropion acts primarily as a reuptake inhibitor of dopamine and norepinephrine. It has shown to be efficacious in treating major depression and nicotine use. Bupropion’s mechanism of action in the treatment of tobacco and use may be related to its effects on dopamine reuptake. It is thought to potentially alleviate stimulant withdrawal symptoms by facilitating dopamine neurotransmission.

Case Study: Charlie’s Story

Charlie is a 20-year old male residing in a small rural community in Alaska who was admitted to a regional hospital acute care unit for localized mandibular (jawbone) osteomyelitis that recurred following a remote self- inflicted gunshot wound to the jaw at age five. He was admitted for symptoms of acute inflammation, swelling and pain to his right jaw (and there had been multiple prior episodes that resolved with antibiotic use), and was prescribed an intravenous broad-spectrum antibiotic and pain medication to resolve the infection and discomfort.

The small remote and rural community where Charlie lived had a significant social problem of alcohol and drug use, and cocaine had been easy to obtain. Charlie attended school until age 14 and then dropped out. Employment for him was sporadic and he primarily relied on social assistance and unemployment income. He lived in a small family home with his mother, siblings, an aunt and cousins. Charlie’s individual strength was that he had an outgoing and friendly personality, and he had a strong family and

18 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com community support network. He had committed to sobriety at age 19 years after a cousin completed suicide while high on cocaine, and he had been regularly attending sobriety support groups.

On this hospital admission, Charlie admitted to feeling unable to endure the jaw pain and feared that if pain persisted that he may to cocaine use, which remained widespread and available in his community. Also, Charlie expressed that he profoundly missed his family while hospitalized and that he felt deeply saddened and isolated because of yet another discouraging hospital stay related to this recurring jaw infection and pain. He also expressed feeling agitated and self-reproachful for having caused the initial jaw injury.

An extensive social history had already been obtained during prior hospital admissions, and Charlie was well known and even endeared to the inpatient hospital team who knew his story well. Charlie was born and raised in his small Alaskan community (approximately 550 residents) and belonged to a large family. His father had left the family when he was an infant and had a reported heavy alcohol use disorder. His mother was a recovered alcoholic with comorbid health concerns, which included fibromyalgia and .

As a child and adolescent, Charlie was able to find cocaine most everywhere such as at school and in the home of family members. The unfortunate day that Charlie shot himself in the jaw, his mother reported that he was high on a drug that a family member had supplied. During adolescence, Charlie began to use cocaine daily and his mother noticed that he would miss school, family functions and social gatherings. Between ages 16-18, Charlie had 2 suicide attempts involving cocaine and alcohol use. An accidental

19 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com overdose occurred at age 19 that resulted in an emergency med-flight where he was admitted to an Intensive Care Unit due to respiratory distress and severe electrolyte disturbances. He was intubated during his first week of hospitalization and then recovered enough to be moved to acute care for another week of observation as the treatment team waited for a bed to open up in a chemical dependency program. Coming so close to death on that occasion, Charlie made a commitment to follow treatment to remain sober. Concurrently, he had become a new father to a son now 2 months old, and expressed a desire to be around for his son.

Cocaine use had become a daily part of Charlie’s life. By age 12 he found it being passed around school in the restrooms. By age 14, his grades and interest in school suffered to the point he stopped attending. Attempts by his mother and the school to encourage him to seek therapy failed because Charlie had lost any motivation to succeed in school and the daily use of cocaine disrupted his family and other close relationships. He had multiple breakups with girlfriends, had limited employment options, and developed feelings of failure, unworthiness, and hopelessness. He began to experience suicidal thoughts because of his addiction. Following the cocaine overdose and close brush with death at age 19, Charlie admitted to others during inpatient therapy sessions that cocaine use “took over my life and became oppressive” and that he could not say “no” to daily snorting of cocaine. He denied intravenous drug use because of a fear of needles. While using substances, Charlie explained that his monthly social assistance check was always spent by mid-month on cocaine and alcohol.

During Charlie’s therapy sessions, he expressed a realization of all that he had lost because of cocaine use. A peer support team in the drug rehab program arranged for his individualized therapy plan to include Alaskan

20 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com healing gatherings where he engaged in familiar cultural rituals such as prayer, song, drumming and smudging. He also attended (AA) and Narcotics Anonymous (NA) meetings as part of his recovery program, and had continued in those programs after hospital discharge to his community. He had progressed from inpatient treatment to a day rehab center for drug and alcohol addiction, and began to successfully transition to community activities without relapsing over a 6-month period.

Charlie had been sober for one year prior to this recent hospital admission for recurring jawbone infection, and he was acutely anxious and depressed over how the current pain was adversely affecting his thoughts and increasing cravings to use cocaine again. His childhood memories and early life exposure to daily drug use had been an ongoing struggle, yet he had stayed sober. He expressed feeling perplexed, fearful and hopeless that he had the inner strength to endure this physical set back and to remain sober.

After two weeks of broad spectrum antibiotic use, Charlie approached the nursing station in much pain and stated that he wanted to leave the hospital to get high on cocaine and that he could not take the pain any longer. A rehab specialist in the hospital connected him with an Alaskan elder who agreed to mentor Charlie during his hospital stay and to take him to a healing gathering that included prayer and the laying on of hands. Staff allowed him to leave the hospital for 4 hours to attend this planned healing event, and he joined with the group along with another male age 58 who had struggled with alcohol use.

When Charlie returned to the hospital he submitted to a urine drug screen to reassure staff he had not used drugs while away from the hospital; at the same time, he showed sadness that “you don’t trust me?” He continued to

21 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com complain of jawbone pain and paced the hospital unit throughout the evening and night, and eventually found another female elder patient who willingly visited with him during the night and offered him comfort and encouragement.

By the third week of Charlie’s hospital stay the jawbone infection started to remit and the inflamed swollen facial area began to quickly shrink in size. Charlie recovered his cheerful nature at baseline, and the craving to use cocaine and his persistent thought that it would help drive away physical pain also remitted. He was discharged on week four of his hospital stay and the clinical team notified his community health center addiction counselor and medical clinician of his health progress and provided their recommendations for follow-up. Discussion

The DSM-5 establishes criteria to diagnose a cocaine use disorder and Charlie had been previously diagnosed with a cocaine use disorder based on the fact that he showed a “problematic pattern of cocaine use that causes significant distress”, was evaluated to have a severe pattern of use leading to overdose and near death, and he had used extensively for the preceding 12 months to the hospital admission at age 19 in critical condition. He eventually had completed a successful recovery program for cocaine addiction with 1-year remission.

Over the period of Charlie’s later childhood and early adolescence he had taken larger amounts of cocaine over prolonged periods of time, showed a persistent desire to use and was unable to control his use. He was unable to continue in high school and spent most of his time obtaining and using cocaine, family relationships suffered, more time was spent finding opportunities to be high on cocaine rather than joining in community

22 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com gatherings, and despite the urgings of his mother and other family to stop using, Charlie’s cocaine use increased to the level that he missed out on meaningful social encounters and early life experiences. Charlie’s cocaine use reached dangerous levels, and nearly ended his life multiple times as a youth.

As noted already, treatment of a cocaine use disorder consists of psycho- social interventions, pharmacotherapy, or both. The current evidence suggests that psycho-social interventions are more likely to show success. Charlie’s history did not indicate that he had long-term medication replacement for his cocaine use disorder. Instead, psycho-social treatment for Charlie included a recovery program, Alcoholics Anonymous and Narcotics Anonymous in addition to outpatient therapy, and he remained sober.

Charlie’s discharge diagnosis on this hospital admission included: 1) Chronic mandibular osteomyelitis secondary to remote gunshot wound (age 5), current episode healing with antibiotic use, and 2) Cocaine use, in sustained remission. Based on DSM-5 criteria, sustained remission was met in Charlie’s case despite reported cravings to use cocaine, triggered by the intense jawbone pain and emotional suffering while in hospital; he remained in sustained remission - full criteria for cocaine use disorder were previously met, and he did not relapse (i.e., he did not meet the “criteria for cocaine use disorder,” with the exception of craving during a “12 months or longer”). Charlie’s UDS tested negative for drug use for the duration of his hospital stay.

Charlie’s prognosis remained guarded given existing risk factors of being a young male and with a history of cocaine use, severe, and history of

23 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com suicidality and multiple suicide attempts. Nonetheless, the combined efforts of the hospital health team to support Charlie through continuing psycho- social interventions, including meaningful community peer support for drug and alcohol recovery and Alaskan cultural healing gatherings, with medical treatment to control the current jawbone infection and pain helped to bring the situation under control. Charlie’s story raises the benefit of combined interdisciplinary team efforts to support sobriety in the context of a young Alaskan male.

Summary

Cocaine has become a serious and growing public health problem. Current data indicates that millions of Americans are regularly using cocaine. Cocaine intoxication commonly results in emergency admissions and is most often involved in fatal overdoses. People who use cocaine have a high risk of developing cocaine use disorder, especially if smoking or intravenously injecting cocaine. The treatment of a cocaine use disorder consists of psycho-social interventions, pharmacotherapy, or both. While a wide variety of therapies and drugs exist, the current evidence suggests that psycho- social interventions are more likely to succeed. The above case study illustrated the level of devastation that cocaine drug use can cause, as well as the ongoing challenges for individuals diagnosed to be in remission.

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29 ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com ce4less.com 56. Tiet QQ, Leyva YE, Moos RH, et al. (2015). Screen of drug use: Diagnostic accuracy of a new brief tool for primary care. JAMA Intern Med. 2015; 175(8):1371-1377. 57. McNeely J, Strauss SM, Saitz R, et al. (2015). A brief patient self- administered substance use screening tool for primary care: Two-site validation study of the Substance Use Brief Screen (SUBS). Am J Med. 2015;128(7):784.e9-e19. 58. McNeely J, Wu LT, Subramaniam G, et al. Performance of the Tobacco, Alcohol, Prescription Medication, and other Substance use (TAPS) tool for substance use screening in primary care patients. Ann Intern Med. 2016; 165(10):690-699. 59. Ashok AH, Mizuno Y, Volkow ND, Howes OD. (2017). Association of stimulant use with dopaminergic alterations in users of cocaine, amphetamine, or methamphetamine: A systematic review and meta- analysis. JAMA Psychiatry. 2017;74(5):511-519. 60. Stoops WW, Rush CR. (2013). Agonist replacement for stimulant dependence: a review of clinical research. Curr Pharm Des. 2013;19(40):7026-7035.

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