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Chapter 6. Substance Use Disorder
145
of binge- drinking episodes, emergency room visits, motor
vehicle accidents, and arrests [24–27]. Brief interventions may
consist of the following [7, 26–28]:
• Motivational interviewing.
• Targeted patient education.
• Providing concrete services (such as linking to assistance
with housing, food, employment and education).
• Linking to care or therapy (including psychiatric care,
group support, and psychotherapy).
Moderate to Severe Risk Patients with AUDIT scores of 16
or higher should be assessed for alcohol use disorder. They
often need to be referred to behavioral therapy or a
treatment program [7, 16].
Alcohol Use Disorder Management All substance use
disorders are stratified by severity based on the DSMV
criteria [11]:
• 2–3: mild
• 4–5: moderate
• 6+: severe.
The goal of alcohol use disorder treatment is to decrease
relapses and mortality related to alcohol use. Patients with
moderate to severe alcohol disorder who are interested in
reducing alcohol intake should be offered medication-assisted
treatment (MAT) [16]. This consists of medication with
behavioral therapy. Behavioral therapy may consist of the
following [28]:
• Individualized therapy, including cognitive behavioral
therapy (CBT) or motivational therapy (MET).
• Twelve-step facilitation (such as group therapy, alcoholic
anonyms, or smart recovery).
146
K. Cartmill
The primary care provider may refer these patients to psychotherapy with an experienced social worker, psychologist,
psychiatrist, or addiction specialist. In addition to supplying
the referral, the clinician has the important role of ensuring
the patient was able to follow through with the recommendation and of troubleshooting potential barriers.
Behavioral treatment should be combined with medication to decrease relapse rates [27]. There are three FDAapproved medications for alcohol use disorder [29]:
naltrexone, acamprosate, and disulfiram.
Disulfiram is rarely used due to poor compliance, adverse
reactions, and drug interactions. It requires the patient be
highly motivated and has better success with supervised
administration. The patient must have no alcohol use 12hours
prior and 14 days after taking the tablet. The medication
causes build-up of aldehyde leading to tachycardia, flushing,
headache, nausea, and vomiting. There are several concerns
with disulfiram, including increased risks of seizures, cardiac
events, and liver toxicity [29].
Naltrexone and acamprosate are two medications that
should be prescribed by primary care providers for the treatment of alcohol use disorder [26, 27, 29]. These medications
should not be started if the patient is unstable or in acute
alcohol withdrawal. Such patients should first complete
detoxication, which should be in an inpatient setting or supervised by an experienced clinician. Outpatient detoxification
in the primary care clinic is not recommended for any patient
with a history of complicated alcohol withdrawal, including
delirium tremens and seizures.
A patient should be started on naltrexone or acamprosate
once treatment for acute alcohol withdrawal is completed.
Some patients may not want to go through detoxification,
opting to cut down on their alcohol use instead. If the patient
is stable, the clinician could initiate naltrexone or acamprosate to help the patient reduce his or her intake.
The following is a brief description of each medication [29]:
Naltrexone: This is preferred over acamprosate due to less
frequent dosing.
Chapter 6. Substance Use Disorder
147
Mechanism: opioid receptor antagonist
Administration: either a daily oral tablet or monthly intramuscular injection
• Oral: may take with or without food. Administration after
food recommended to reduce gastrointestinal side effects.
To minimize side effects, can be started at 25 mg (cut
50 mg tablet in ½) for 1 week and then increase to the
recommended dose of 50mg daily.
• Intramuscular injection: 380 mg in gluteal muscle every
28days.
Contraindications:
• Acute hepatitis or liver failure.
– Liver enzymes (AST or ALT) over three times the
upper limit of normal.
– Decompensated cirrhosis.
– Please note, It CAN be given with stable Child’s Class
A cirrhosis.
• Opioid use.
– Naltrexone is an opioid blocker, so it can cause acute
opioid withdrawal.
Common side effects: nausea, diarrhea; for injection: can
cause injection site reactions
Acamprosate:
Mechanism: modulates glutamate receptors
Administration:
• Oral: may take with or without food. Recommended with
food to increase compliance. Can start with 333 mg (one
tablet) three times daily and titrate up to goal 666mg (two
tablets) three times daily.
Concerns:
• Renally dosed. A dose reduction is needed if creatitine
clearance is 30–50.
• Contraindicated with creatitine clearance under 30.
148
K. Cartmill
Common side effects: nausea, abdominal discomfort, and
dizziness
These two medications can be given together. Liver and
renal function should be monitored at least every 6–12months.
Risky Opioid Use or OUD
Harm Reduction In addition to the harm reduction
counselling referenced above, there are specific strategies
related to risky opioid use. Each patient should receive a
naloxone kit. If none is available, assist the patient in obtaining
one. Naloxone has been shown to reduce overdose death [30].
In addition, the clinician can inform patients of circumstances
that put them at higher risk of overdose, such as using opioids
after a period of abstinence [31].
Medication-Assisted Treatment Similar to AUD, patients
with opioid use disorder (OUD) should be offered medicationassisted treatment (MAT). The behavioral interventions are
similar to those used for alcohol use disorder. However, the
emphasis on treatment with medication is even greater for
OUD as robust evidence demonstrates significant decreases
in morbidity and mortality [2].
There are three FDA-approved treatments for opioid use
disorder maintenance: methadone, buprenorphine, and naltrexone. Only methadone and buprenorphine can be used to
treat acute opioid withdrawal. After the patient is stabilized,
these medications should be continued at a maintenance
dose for at least 6–12months. Failure to continue methadone
or buprenorphine results in high relapse rates, poor retention
in care, and increased use of illicit drugs [32, 33].
As discussed in the section on alcohol use disorder, pri-
mary care doctors can prescribe naltrexone. However, many
patients with opioid use disorder have difficulty starting naltrexone because they must stop using opioids for 10–14days
prior to initiation [34]. Thus, methadone and buprenorphine
are the most commonly used medications for OUD.
Chapter 6. Substance Use Disorder
149
There are restrictions on prescribing buprenorphine and
methadone for OUD. Methadone must be provided in a certified program; this cannot be prescribed by the primary care
provider. Buprenorphine is often prescribed by a certified
primary care provider, psychiatrist, or addiction medicine
specialist. Primary care providers gain certification by completing a brief training and obtaining a X-waiver from the
DEA.Even if the clinician is not prescribing the medications,
it is important to have basic knowledge of methadone and
buprenorphine to better engage, counsel, and refer patients
seeking treatment.
Buprenorphine is usually prescribed as a film or tablet;
however, it is also available as a monthly subcutaneous injection or subdermal implant every 6months. The sublingual or
buccal film and sublingual tablet is usually prescribed at least
daily. The films and tablets may be available at 2mg, 4mg,
and 8mg doses. They can be prescribed alone or as a combination with naloxone. The naloxone component is added to
buprenorphine as a deterrent. Naloxone is poorly absorbed
when the buprenorphine-naloxone film or tablet is taken as
prescribed. If the medication is manipulated for intravenous
or intranasal use, naloxone’s opioid antagonist activity takes
effect and could cause an acute opioid withdrawal [34].
Buprenorphine is a partial opioid agonist with a high affin-
ity for the mu opioid receptor. It has a long half-life of at least
24 h [34]. Because it is a partial agonist, there is a “ceiling
effect.” This means once the opioid receptors are saturated,
higher doses would be unlikely to cause respiratory depression. This makes the risk of overdose lower compared to
methadone.
Methadone is a full-opioid agonist usually taken daily by
mouth. Like buprenorphine, it has a long half-life. It reaches
its peak effect after about 3–5days of continuous use [34].
Thus, caution with dose escalation is recommended to prevent overdose.
Both methadone and buprenorphine show equivalent effi-
cacy for opioid withdrawal and maintenance when dosed
appropriately [35, 36]. However, there are several major dif-
150
K. Cartmill
ferences between buprenorphine and methadone. First,
methadone requires more frequent visits compared to
buprenorphine. Methadone programs usually require daily
attendance for supervised administration while buprenorphine can be given as a monthly prescription. Stable patients
may be seen every 3months based on the prescribing clinician’s discretion.
Another major difference is how the medications are
started. Buprenorphine is usually initiated once the patient is
in opioid withdrawal. This is done to prevent an acute, or
precipitated, withdrawal. Rapid-onset, severe opioid withdrawal can occur if buprenorphine is taken when there are
already full agonists attached to opioid receptors. Since
buprenorphine has stronger receptor binding affinity but
weaker effect, withdrawal can occur when it rapidly displaces
the other opioids from the receptor.
Buprenorphine is usually initiated at a low dose once the
patient is in opioid withdrawal [34]. However, patients who
are unable to tolerate withdrawal symptoms can be induced
with a different technique in which buprenorphine can be
started at extremely low doses while the patient is weaning
off another opioid [37]. Methadone does not carry the same
risk of induced opioid withdrawal.
The last major difference to highlight is the different risk
profiles of these two medications. As referenced above,
methadone has a higher risk of overdose. In addition, it is
more likely to have drug-drug interactions and QT interval
prolongation compared to buprenorphine [34, 38, 39].
Given the differences in visit frequency, induction proto-
cols, and risks, the clinician and patient should engage in
shared decision-making when choosing a medication for
OUD.This discussion should begin by assessing the patient’s
preference. There are websites with excellent materials for
both clinicians and patients to assist in shared decisionmaking for opioid use disorder treatment, including the California Health Care Foundation Project SHOUT website:
https://www.chcf.org/collection/webinar-series-supporthospital-opioid-use-treatment- project- shout/ [40].
Chapter 6. Substance Use Disorder
151
Clinical Pearls
• Primary care providers play an important role in screening,
preventing, and treating patients with risky substance use
and substance use disorder.
• Screening starts with a question screener. Positive alcohol
screens should have a follow-up with the AUDIT.For positive drug screens, follow up with the DAST-10.
• Management depends the patient’s risk:
– No or low risk: brief intervention via counselling.
– Moderate, high, or severe risky use: referral to therapy
or a treatment program.
– Moderate to severe substance use disorder: medication-
assisted treatment, ideally via referral to a treatment
program.
Don’t Miss This!
• Engage all patients with risky substance use in harm
reduction strategies. Give naloxone kits to patients with
risky opioid use.
• Substance use care should be patient-centered and nonjudgmental. Help patients reach their individual goals
instead of focusing solely on abstinence.
• Offer medication for moderate to severe opioid and alcohol use disorder treatment.
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