Substance Use Disorder

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Continuing Education Activity

Substance use disorders result from long-term exposure to substances and subsequent mental and physical dependence. This can lead to social, academic, and occupational impairment, along with negative health effects. To treat these disorders, a combination of pharmacological and non-pharmacological therapies is used to help individuals appropriately. This activity describes the evaluation, the mechanism of substance use disorders, and the treatments of substance use disorders and highlights the role of the interprofessional team in managing patients with these conditions.

Objectives:

  • Outline the various presentations of substance use disorders.
  • Identify etiologies and pathophysiology of substance use disorders
  • Describe various treatment options for several types of substance use.
  • Identify how interprofessional team strategies can improve patient outcomes in substance use disorders.

Introduction

Substance use disorders involve excessive use of nicotine, alcohol, and other illicit substances that leads to social, academic, and occupational impairment. The most common illicit substances seen include cannabis, sedatives, hypnotics, anxiolytics, inhalants, opioids, hallucinogens, and stimulants. The specific factors of substance use disorder consist of abuse, intoxication, and physical/psychological dependence. 

Different substances can be classified based on their effects on the central nervous system. These effects vary depending on the substance and can produce everything from increased energy and euphoria to profound sedation. In general, while the effects vary significantly, the initial stages of substance use disorders are characterized by positive reinforcement, where individuals experience a sense of well-being or euphoria with use. As physiological and psychological dependence progresses, an individual experiences negative reinforcement where substances primarily relieve dysphoria and unpleasant withdrawal symptoms.

Etiology

The cause of substance use disorders is multifactorial and includes psychological, biological, socio-cultural, and environmental factors. Co-morbid psychiatric disorders have been associated with an increased risk of illicit substance use. For example, those with attention deficit hyperactivity disorder (ADHD) and bipolar affective disorders have an increased risk of developing a substance use disorder in adulthood compared to the general population.  

Environmental and genetic factors also play a strong role in substance use disorder. An individual's genetic make-up for stress-response predisposes the risk of dependence on substances. Individual variations in genetics have been demonstrated to influence stress response and predispose some individuals to develop a substance use disorder.[1] 

The Adverse Childhood Experience Study (ACES) demonstrated that exposure to a range of traumatic events during childhood is associated with an increased risk of substance use later in life. This risk association was demonstrated to follow a dose-response-like pattern where increased trauma exposure was directly correlated with increased risk of developing a substance use disorder.

Epidemiology

The cause of substance use is multifactorial. It includes psychological, biological, socio-cultural, and environmental factors. Some mental health disorders predispose individuals to abuse illicit substances; for example, those with ADHD have a high chance of abusing illicit substances in their adulthood.[1]

Cannabis is the most common abused drug in the United States.[2]

The Services Administration for Mental Health and Substance Abuse (SAHMSA), the National Institute on Alcohol Abuse and Alcoholism (NIAAA), and the National Institute of Drug Abuse (NIDA) have accumulated data on substance use and its consequences over the years. Studies show individuals who abuse one substance are more like to abuse other substances as well. In 2012, studies showed that the lifetime prevalence of alcohol use disorder was 8%, and illicit substance use was 2-3%.[3]

A cross-sectional study was conducted in the US with 36,309 adults, and the data was obtained from April 2012 to June 2013. The study showed a 12-month prevalence of substance use disorder was 3.9% and lifetime substance use disorder was 9.9%. Substance use disorder was more prominent among certain population groups. They were men, Caucasian, Native Americans, young single or previously married adults, lower educated individuals, lower-income individuals, and those residing on the Western side of the country. There was a significant association with individuals with disabilities, with a 12-month prevalence of 13.5% and a lifetime prevalence of 24.6%.[4]

Pathophysiology

Substance use disorders involve both psychological and physical dependence on the substance(s) of use. Severe dependence is characterized by an inability to regulate use. Substance use disorders and addiction stem in part from adaptive changes in the brain as it seeks to regain homeostasis.[5] Chronic and/or prolonged stress plays a strong role in developing drug-seeking behavior; it alters the corticotropin-releasing factor and hypothalamic-pituitary-adrenal axis (CRF/HPA)". In animal model studies, it demonstrated CRF circuitry could increase "dopamine activity in the mesolimbic reward circuit."[6] 

Stimulants, specifically cocaine and amphetamines, exert their effect by preventing the recycling of dopamine, norepinephrine, and serotonin.  This results in increased concentrations of these neurotransmitters within the synaptic cleft. The influx of these neurotransmitters gives the user a euphoric effect.[7]

Worldwide and in the United States, tobacco use disorder is the most prevalent addiction.  Most commonly, nicotine is absorbed through the lungs when individuals burn and inhale tobacco products. It is absorbed through the pulmonary circulation, crosses the blood-brain barrier in less than 10 seconds, and attaches to the nicotinic cholinergic receptors in the central nervous system (CNS). The metabolite of nicotine is cotinine, which can be detected as a urinary marker of the substance.[8] Nicotine influx in the CNS leads to neurotransmitters' release, especially dopamine, which stimulates the brain’s reward area. Chronic nicotine use results in tolerance, when excessive stimulation of nicotine acetylcholine receptors results in desensitization of the receptors; these neuroadaptations produce a state where the brain requires nicotine to function in homeostasis. This is referred to as physiological dependence.[9] CYP2D6 metabolizes nicotine. Therefore, it can alter the metabolism of other medications, such as antipsychotics.  

Alcohol produces euphoric effects through the dopamine neurons of the mesolimbic system. Alcohol inhibits NMDA receptors and results in the upregulation of GABA receptors. Chronic consumption of alcohol leads to GABA receptor desensitization and tolerance, potentiating the loss of drinking control.[10] Alcohol is mostly absorbed in the digestive tract's mucosal lining, specifically at the proximal small intestine, where B vitamins are absorbed. Individuals who drink excessively may have a deficiency of B vitamins.[11] Vitamin B1 (Thiamine) and vitamin B9 (Folic Acid) are the two most common B-vitamins deficiencies. Deficiency of thiamine can lead to neurological findings such as hyporeflexia and sensory and motor deficiency. More profound deficiencies over time can lead to Wernicke's Encephalopathy and Korsakoff syndrome [12]. Chronic alcohol consumption can also result in Vitamin B9 (Folic acid) deficiency; after 8-16 weeks of deficient stores of folic acid in the body, individuals may develop "glossitis, angular stomatitis, and oral ulcers," along with "depression, irritability, insomnia, cognitive decline, fatigue, and psychosis."[13]

Opioids include codeine, heroin, hydrocodone, hydromorphone, methadone, meperidine, morphine, and oxycodone. Opioids bind to delta, kappa, and mu receptors, which provide analgesia for severe pain and produce euphoria feelings. Higher doses carry a risk of respiratory suppression and death. Individuals with chronic exposure to opioids can experience profound withdrawal symptoms if opioid use is stopped abruptly. The withdrawal symptoms include but are not limited to diarrhea, excess sweating, excess lacrimation, nausea, vomiting, and insomnia.[14]

Sedative, Hypnotic, Anxiolytics are a class of medications that can cause CNS depression, and if taken inappropriately, the effects can be fatal. They include benzodiazepines: alprazolam, clonazepam, lorazepam, diazepam, chlordiazepoxide; Barbiturates:  phenobarbital, pentobarbital, butabarbital; it also includes other sedative medications. Other classes of drugs have properties that share a similar mechanism of action with benzodiazepine and barbiturates. These agents mediate gamma-aminobutyric acid (GABA) effects, producing inhibitory effects within the central nervous system. Alcohol can be classified in this group, but alcohol is more commonly used and is not utilized therapeutically, so healthcare experts have classified it separately.[15] The euphoric and sedative effects of these agents precipitate and perpetuate a cycle of overuse and dependence. 

Regarding cannabis, it contains multiple types of terpenophenolic compounds, called cannabinoids, that cross the blood-brain barrier; the most studied cannabinoids are cannabidiol (CBD) and tetrahydrocannabinol (THC). Cannabinoids act on the cannabinoid receptors, which are located in the central and peripheral nervous system. CBD and THC both come from the hemp plant, also known as marijuana; legal rules and regulations differentiate the definitions. There are many types of hemp plants that produce various percentages of THC and CBD. Hemp has less than or equal to 0.3% of THC by dry weight, while marijuana has more than 0.3 % of THC by dry weight. CBD is a non-psychotropic cannabinoid that does not exert euphoric properties like THC.[16] THC, the psychoactive cannabinoid, exerts its effects in the brain’s reward center in increasing dopamine levels in the prefrontal cortex, providing the euphoric effect.[2] THC activates the CB1 and CB2 receptors of the endocannabinoid system, which gives its psychoactive properties and regulating eating, learning, memory, growth, development, and anxiety.[17] CBD does not activate CB1 or CB2 receptors, but limited studies show it has neuroprotective and anti-inflammatory effects.[18]

There are various hallucinogens; the most common one presented in the hospitals is phencyclidine or phenylcyclohexyl piperidine (PCP), or also known by its street name "angel dust," is not only a hallucinogen but also acts as a stimulant. Its mechanism of action is characterized by NMDA receptor antagonism impairing the feeling of pain and other various neurological functions and psychosis. It can also facilitate the increase of dopamine and norepinephrine and provide a sympathomimetic effect.[19] Another common hallucinogen is Lysergic acid diethylamide (LSD), or known by its street name as "acid"; it has a mechanism of action that is not fully understood, but from studies so far, it facilitates serotonin receptors 5HT2A, 5HTAR, 5HT2C, and 5HT1A. LSD exerts receptor modulation leading to cognitive impairment and hallucinations. Other hallucinogens include MDMA with street names of “Molly, Ecstasy, X,” another hallucinogen is Ketamine with a street name of “K-Hole.”

History and Physical

In addition to the physical exam, assessment of substance use should include a thorough history that screens several psychiatric symptoms to diagnose and rule out disorders. The patient should be asked about any current life stressors, and the patient should be screened for current depression, mania, trauma, anxiety, and psychosis.  

Current substance use screening questions include: 

  • Which substance(s) are used? Certain substances can cause more negatives effects than others, so it is important to determine which ones were used, which may help in the recovery process. 
  • When was the last time the substance was used, and how much and how often was it used? The negative consequences of withdrawal symptoms may be fatal, such as from benzodiazepines or alcohol. If the provider was notified of the last use, then appropriate treatment can be administered on time. Also, recent substance use can influence an individual’s behavior and cognitive processes, such as being agitated from Methamphetamine or Cocaine. This would help in the treatment process. For example, a patient may not need inpatient admission if the exhibited psychotic symptoms were substance-induced instead of a psychotic episode of Schizophrenia. The frequency of substance use helps determine the severity of the dependency. 
  • Any experience of withdrawal symptoms? Some substance use can lead to severe withdrawal symptoms. Alcohol and Benzodiazepine withdrawal can lead to seizures and have the potential to be fatal.  
  • What is the user’s perception of using the substance(s)? How an individual perceives illicit substances will vary from person to person. Some individuals use substances to cope with life stressors, while others may use it as an alternative to medications such as cannabis for treating their anxiety.  
  • Any feelings or readiness to change, such as cutting back use or quitting? Does the patient have any cravings for the substance?  

Past Psychiatric History: if the patient has any psychiatric history, detailed information regarding mental health history should be obtained. When asking about a period in the past, it is easier to have the patient recall an event by age than recall the year. The questions to ask include: 

  • Have you been diagnosed with any psychiatric diagnosis in the past by a physician? This question should be asked, and it should be verified if the diagnosis was made by a medical professional or if someone else told them the diagnosis. 
  • Any history of medication trials for substance use or other mental health disorder? This open-ended question may not have a complete answer because the patient may have difficulty recalling the complicated names of medications from the past. If the patient affirms taking medications but cannot recall the name, an effective way to get the information is to call the pharmacy to get the list or get the medical records from their last prescriber. 
  • Any history of self-harm or attempted suicide? Perceptual disturbance during an intoxicated state may lead to hallucinations, such as having bugs or snakes on their skin. The visual hallucinations may lead to self-harm to rid self of the hallucinations. Also, auditory hallucinations of commanding nature may result in a suicide attempt. If past suicide attempts are identified, then it is recommended to ask when the first attempt was, how many were attempted, and what lead to the suicide attempts, 
  • Any history of violence towards others? A study regarding ED visits due to Cocaine-induced chest pain found 40% of the patients were involved in violence a year after discharge from the ED.[20] Substance abuse can cause loss of impulse control and agitation, in which the user will have mood dysregulation leading to violent behavior. Obtaining history about the patient’s history of violence enables the provider to assess for any future risks. 
  • At what age were the first and last psychiatric hospitalization? How many hospitalizations regarding substance use or other mental health illness can you recall? These questions should be asked in more detail and asked about the differences of being treated in the ED, such as for psychiatric stability or due to intoxication, and if the patient was admitted to inpatient for stabilization. Those who are treated in the ED due to intoxication usually are stabilized and discharged after a day. But those admitted to the inpatient for psychiatric care are admitted for at least 5 days or so until they are psychiatrically stabilized.  

Substance Use History Questions: 

  • At what age did the individual initiate use of the substance? This question is asked because substance use affects brain development and can influence impulsive/risky behaviors from an early age. Substance use at an early age can predispose people to be cardiac and neurological disorders in adulthood. 
  • What benefit is sought out from substance use? Those who use substances may not always use them for recreational use. Some may use it for self-treatment of their co-morbid psychiatric or medical illnesses or dealing with stress. For example, those who are diagnosed with ADHD may use Cocaine or Methamphetamine as an aid to focus. Some may use Cannabis to treat their anxiety, insomnia, or neuropathic pain. Therefore, it is important to be aware of what is the motivation behind substance use. 
  • Has the individual ever attempted to cut back or stop using? This question helps to determine the motivation for change.  It should be followed up by questions assessing periods of success and potential barriers to implementing strategies to reduce or eliminate use.  
  • Has the patient previously received treatment for a substance use disorder? Treatment options can include community self-help groups, outpatient treatment clinics, intensive outpatient programs, medical detoxification, or residential treatment facilities (Rehab)
  • Is there a family history of drug use? If so, have there been any fatalities from substance use? It is important to be aware of any substance use by other family members because family influences the individual’s risk of substance use.

Evaluation

Evaluation of the patient initially involves approaching the patient in a non-judgmental manner. The provider's diction should concentrate on recovery and goal setting. How well the first interview is conducted sets the tone for establishing a good rapport between the provider and patient. The provider should always complete the history and physical for assessment. Additionally, the healthcare provider should obtain a full set of labs to help the health provider assess the patient’s health. The lab tests that are recommended include:

  • Blood Alcohol Level and Urine Drug Screen to screen for acute substance use. It is usually done in the Emergency Room if the patient exhibits agitation, sedation, or cognitive impairment. Urine pregnancy tests should also be obtained when appropriate.
  • Complete Blood Count (CBC) may show anemia and infection, while Basic Metabolic Panel (BMP) will show any abnormal electrolyte imbalance regarding substance use and any other co-morbidity.
  • Liver Function Test and Hepatitis Panel can help show any negative effects on the liver from chronic alcohol use or other substances; it can also show any hepatitis B & C infections from IV drug use. HIV antibody test should also be added to rule out any infection from IV drug use.
  • Pancreatic Enzyme's serum level can show any issues with the pancreas from alcohol binge drinking or heavy nicotine use.

For establishing a diagnosis based on substance use, the DSM-5 is used. Per DSM-5, the individual must meet at least two criteria out of 11 criteria, over a 12-month period, to have substance use disorder established for that substance. Overall, the criteria are similar among the substances. PCP Use Disorder does not have a withdrawal criterion established, so there are only 10 criteria for that disorder. Some stimulants, opioids, sedatives, anxiolytics, and hypnotics can be used under a physician’s supervision, so tolerance is omitted for individuals taking them for treatment purposes. The 11 problems include: 

  1. The substance use amount is taken more than what was intended and taken longer than what was intended. 
  2. There is the intention and failed attempts to decrease use. 
  3. Extra time and effort are used to obtain and use the substance or recover after taking them. 
  4. Having a strong craving for the substance. 
  5. The use of the substance leads to the individual unable to fulfill his or her responsibility. 
  6. Continued use of the substance despite having social and occupational impairment due to the substance use. 
  7. Other activities are reduced or given up due to continued substance use. 
  8. Using the substance in a high-risk setting, such as when operating a motor vehicle or operating heavy machinery 
  9. Continued use of the substance with the knowledge of the psychological and physical harmful effects caused by the substance. 
  10. Tolerance development either from taking more amount of the substance to reach the same effect from last time or from having decreased effect from using the same amount of the substance. 
  11. Withdrawal symptoms are manifested after the substance use is discontinued, and the withdrawal symptoms are relieved with the continuation of substance use. 

The number of criteria the patient meets determines the severity level of the disorder; 2-3 sets the severity level as mild, 4-5 sets the severity level as moderate, and 6 or more sets the severity level as severe. A patient can relapse after reaching remission. For the patient to be in remission, the patient must meet at least 2 criteria, which are listed above, over a 12-months period, and be abstinent from substance use for at least 3 months. The period of time from 3-12 months where symptoms are in remission is referred to as early full remission; after 12 months, the condition is classified as sustained remission.

Treatment / Management

Currently, nicotine, alcohol, and opioids are the only substances with FDA-approved medication treatments. Individuals with severe addiction may require assistance in a structured environment for the recovery process. The American Society of Addiction Medicine (ASAM) provides a set of criteria for individualized treatment planning and placement of individuals with addiction. The ASAM criteria involve six dimensions: intoxication/withdrawal potential, medical condition and history, mental health, individual's willingness to change, relapse/continue use potential, and recovery/living situation.[21] Patients who require further assistance after being discharged from 24-hour inpatient care or do not qualify for inpatient care may receive treatment from intensive outpatient programs (IOPs). IOPs do not require patients to be admitted. Instead, the patients can stay in their homes while they are treated in an outpatient clinic for substance use during the day. IOPs comprise psychosocial support, developing coping skills, and any other needed services individually.[22]

To treat nicotine use disorder, bupropion, varenicline, and nicotine replacement therapy are available. 

Bupropion is a dual reuptake inhibitor of dopamine and norepinephrine, which helps with nicotine cravings and withdrawal symptoms.[23] Varenicline has a strong affinity to nicotinic acetylcholine receptors and acts as a partial agonist, reducing withdrawal symptoms and blocking nicotine binding. It provides the same stimulation as nicotine and decreases the urge to use nicotine. Also, varenicline does not interact with CYP450 enzymes, which can be beneficial when treating patients with other medications metabolized through the CYP450 pathway.[24] Nicotine replacement therapy (NRT) with patches and nicotine gum help with cravings and withdrawal symptoms. Some studies show a combination of the gum and the patch improves smoking cessation rates.[25] In any clinical setting, healthcare providers should provide education and resources for smoking cessation, as the health benefits of smoking cessation are significant. 

For stimulant use disorder, such as with cocaine and amphetamine drugs, there are no approved pharmacological treatments.[26] However, non-pharmacological therapy, such as contingency management, is available; it involves operant conditioning reinforcement. The goal of the treatment is to influence a certain type of behavior via behavioral rewards. In substance use, behavior is modified by providing a reward in exchange for the desired behavior, such as decrease substance use or abstinence.[27]

The FDA approves acamprosate, naltrexone, and disulfiram to treat alcohol use disorder.[28] Disulfiram, an aldehyde dehydrogenase inhibitor, produces an unpleasant set of symptoms such as headache, nausea, vomiting, flushing, dizziness, and weakness when alcohol is consumed to prevent further alcohol consumption.[29] Naltrexone blocks the central mu-receptor, reducing cravings, and aids in preventing relapse to alcohol use.[30] Acamprosate aids in reducing withdrawal symptoms by countering excessive NMDA receptor activation from alcohol withdrawal. In the clinical setting, it is important to include vitamin B1 and vitamin B9, along with multivitamins supplements, to address any nutritional deficiencies.  

For opioid use disorder, several treatment options are available. They include methadone, naltrexone, and buprenorphine, which are frequently combined with naloxone to reduce the risk of misuse. Methadone (full mu agonist) can only be used to treat opioid use disorder by specific treatment facilities designated as Opioid Treatment Programs (OTPs). Methadone has decades of research demonstrated reduced illegal drug use, criminal activity, mortality, and morbidity, buprenorphine-naloxone (partial agonist at the mu-opioid receptor). As a partial agonist, this agent has less potential for overdose.[14] During opioid withdrawal, the patient can experience dysregulated mood, dyssomnia, pupillary dilation, muscle pain, nausea, vomiting, excessive lacrimation, and other symptoms. The (Clinical Opiate Withdrawal Scale) COWS scale is an 11-item rating system used to measure the severity of opioid withdrawal; a score of 5 or above indicates active withdrawal. Clonidine, an alpha-2 receptor agonist, may help reduce the severity of withdrawal symptoms and stabilize blood pressure. Loperamide may also be needed to aid the patient's GI effect in the setting of repeated diarrhea during withdrawal.[31]

Mainstreaming Addiction Treatment (MAT) Act

The Mainstreaming Addiction Treatment (MAT) Act provision updates federal guidelines to expand the availability of evidence-based treatment to address the opioid epidemic. The MAT Act empowers all health care providers with a standard controlled substance license to p escribe buprenorphine for opioid use disorder (OUD), just as they prescribe other essential medications. The MAT Act is intended to help destigmatize a standard of care for OUD and will integrate substance use disorder treatment across healthcare settings. 

As of December 2022, the MAT Act has eliminated the DATA-Waiver (X-Waiver) program. All DEA-registered practitioners with Schedule III authority may now prescribe buprenorphine for OUD in their practice if permitted by applicable state law, and SAMHSA encourages them to do so. Prescribers who were registered as DATA-Waiver prescribers will receive a new DEA registration certificate reflecting this change; no action is needed on the part of registrants.

There are no longer any limits on the number of patients with OUD that a practitioner may treat with buprenorphine. Separate tracking of patients treated with buprenorphine or prescriptions written is no longer required. 

Pharmacy staff can now fill buprenorphine prescriptions using the prescribing authority's DEA number and does not need a DATA 2000 waiver from the prescriber. However, depending on the pharmacy, the dispensing software may still require the X-Waiver information in order to proceed. Practitioners are still required to comply with any applicable state limits regarding the treatment of patients with OUD. Contact information for State Opioid Treatment Authorities can be found here: https://www.samhsa.gov/medicationassisted-treatment/sota.

Differential Diagnosis

  • Depression can be exhibited from opioids, alcohol, sedative, anxiolytic, hypnotic, and cannabis use. It is also associated with withdrawal from stimulants. 
  • Mania and anxiety can be exhibited from stimulants (cocaine and amphetamine). 
  • Psychosis can be associated with substances but varies from individual to individual and with time.

Toxicity and Adverse Effect Management

Patients who are physically dependent on sedative effects often require medication during the detoxification process to minimize the risks associated with complicated withdrawal. Acute intoxication can present with slurred speech, cognitive impairment, poor coordination, and unsteady gait. For alcohol and benzodiazepine withdrawal, the Clinical Institute Withdrawal Assessment (CIWA) scale helps determine the frequency of medication dosing to prevent withdrawal complications. In an emergency setting, treatment for alcohol and benzodiazepine intoxication is primarily supportive, with close monitoring of vitals. Benzodiazepines are considered a first-line treatment to prevent worsening withdrawal symptoms.[32] In cases of severe benzodiazepine intoxication, particularly if the patient is becoming hypoxic, flumazenil may be indicated. Flumazenil reduces the expression of GABA subunit receptors, reversing the effect of benzodiazepines.[33]

For opioid intoxication, naloxone is used to reverse respiratory depression caused by opioid overdose. Naloxone is a competitive mu-opioid receptor antagonist, which reverses the effects of opioids. It can be administered intramuscularly, intravenously, or nasally; the fastest route of administration is intravenous.[34]

For PCP intoxication, the focus is stabilizing the patient with supportive care. The patient may exhibit ataxia, nystagmus, increase cardiac workload, muscle rigidity, and seizures. Hyperacusis is another side-effect of PCP use, which is why it may be necessary to place the patient in a low stimulus environment. A high stimulus environment may trigger agitation and increase the likelihood that restraints are required. In some cases, gastric suction or the use of activated charcoal may be indicated. Benzodiazepines may help to control agitation and reduce the risk of seizures.[19]

Staging

During the recovery process of substance use, the individual transitions through various stages of change, demonstrated as the stages of change model. 

  1. Precontemplation, when the individual does not recognize the negative effects of substance use. 
  2. Contemplation, when the issues of substance use are recognized, yet no action is taken. 
  3. Preparation, when the individual has considered making a change regarding substance use and begins to make minor changes. 
  4. Action is the stage when the individual makes significant changes to prevent substance use, such as avoiding triggers or reaching out for help. 
  5. Maintenance, the stage when the action stage is maintained to prevent substance use. 
  6. Relapse, the stage when the substance use is restarted.[35]

Prognosis

Individuals who abuse substances for a chronic period develop extreme dependence on them. If the individual attempts to stop using it, their withdrawal symptoms become severe enough for the individual to restart the abuse cycle. There are predicting factors that influence the outcome for the individual; the degree of relationship between the predictor factor and the outcome varies from person to person. Some of the predicting factors include but not limited to are the degree of dependence and withdrawal, the motivation to be committed to abstinence, treatment timeframe, genetics, the severity of cravings, and how the individual copes during stressful situations.[36]

Complications

The complications of substance use are broad. 

Substance use will impact multiple systems of the body, including but not limited to neurologic, endocrine, psychiatric, cardiopulmonary, hepatic, hematologic, and immunologic. These problems include but not limited to are: 

  • Stroke and seizures 
  • Loss of nerve functions leading to muscle weakness and loss of sensation. 
  • Memory loss and overall cognitive deficits.  
  • Various forms of psychosis, loss of impulse control, personality change, and mood dysregulation. 
  • Coma and death 
  • Increased cardiac workload and with chronic use cardiac failure. 
  • Nasal Septal Perforation  
  • Respiratory depression 
  • Muscle breakdown from overuse, leading to rhabdomyolysis. 
  • Liver failure and hepatocellular carcinoma 
  • Hepatitis B & C infections, HIV, sepsis, and gangrene

Deterrence and Patient Education

Substance use frequently starts at an early age, so education of the general population starting in school can reduce the prevalence of substance use disorders.  Identifying high-risk patient populations and reducing care barriers can help limit the negative impact of substance use disorders.

Enhancing Healthcare Team Outcomes

Effective education on the treatment of substance use disorders among healthcare providers can help to improve outcomes. Unfortunately, training in substance-related/addictive disorders is frequently limited, leaving providers ill-equipped to meet the demand after training. Additionally, a lack of adequate curriculum for healthcare provider training and a negative view of patients with substance use disorders plays a role in poor healthcare outcomes.[37]

Unless emergency treatment requires it, prescribing potentially addictive medications should be limited to healthcare providers specifically trained in substance-related/addictive disorders. When utilizing medications in the treatment of substance use disorders, healthcare providers should not place arbitrary limits on treatment duration. All treatment decisions should be patient-centered and based on the unique risk/benefit analysis.  The American Academy of Addiction Psychiatry (AAAP), along with the Substance Abuse and Mental Health Services Administration (SAMHSA), sponsors Providers Clinical Support System (PCSS), a training program for physicians and other healthcare providers. This program offers training, mentorship, and other support for individuals interested in preventing, identifying, and treating opioid use disorders. 

Dealing with substance use disorder requires the efforts of all members of the interprofessional healthcare team, including clinicians, mid-level practitioners, nursing staff, and pharmacists, who can coordinate their activities and engage in open communication to help identify substance use disorder, streamline treatment, and watch for signs of relapse once therapy has been initiated. This interprofessional approach stands the best chance of patient success in recovering from substance use disorder. [Level 5]

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Azmi R. Jahan

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Doug M. Burgess

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