of subcutaneous veins. Examination of nasal tissue can uncover signs of intranasal insufflation of opioids such as septum perforation. Infectious signs such as lymphadenopathy, cellulitis, abscesses, and new heart murmur may also be observed. Patients who are acutely intoxicated with opioids may present with drowsiness, pinpoint pupils, slurred speech, respiratory depression, or impaired cognition. Urine drug screens can be utilized to determine the current presence of opioids or their metabolites. Opioid use disorder is diagnosed based on the criteria for substance use disorder, discussed earlier in this course. 182,184 Treatment of Opioid Use Disorder Treatment for opioid use disorder is evolving. Previously, treatment involved stopping opioids, managing withdrawal, and then focusing on avoiding relapse using psychosocial therapy. Psychosocial therapy was thought to help patients develop healthy habits for non-drug lifestyles. Medications were only prescribed for short-term use to ease the transition and were then discontinued. However, research has shown that short-term medication treatment is not effective; many patients will require long-term therapy. 185 Treatment of opioid use disorder may be best conducted by specialists in addiction medicine due to the complexity of this condition. Treatment often starts with the treatment of opioid withdrawal. Patients who are physiologically dependent on opioids can experience opioid withdrawal syndrome after abruptly discontinuing or reducing the dose of opioids used. Symptoms of opioid withdrawal syndrome include tachycardia, hypertension, piloerection, mydriasis, rhinorrhea, lacrimation, insomnia, and gastrointestinal distress. This clinical syndrome is informally considered to be non-life threatening; however, opioid withdrawal can cause severe fluid loss and resultant electrolyte abnormalities that can lead to hemodynamic instability and death. 186 The clinical time course of opioid withdrawal syndrome is typically dependent on the half-life of the opioid used. Opioids with a short half-life have a more rapid onset of withdrawal symptoms; for example, heroin has a half-life of 3 to 5 hours, and is associated with an onset of withdrawal within 12 hours of the last use. Opioids with a longer half-life, such as methadone with a half-life of up to 96 hours, can lead to withdrawal symptoms 1 to 3 days after the last use. The duration of withdrawal is also dependent on the half-life of the opioid used; heroin withdrawal typically lasts 4 to 5 days, and methadone withdrawal can last 7 to 14 days or longer. 186 Medically Supervised Withdrawal Medically supervised withdrawal, or detoxification, can be used on an inpatient or outpatient basis to help reduce withdrawal symptoms and safely transition the patient to a medication-assisted treatment program. This typically involves patients visiting a treatment center on an inpatient or outpatient basis for counseling, medications, and medical treatment. Medically supervised withdrawal should be incorporated as part of a comprehensive treatment program, and should not be used as a standalone
treatment. People who complete detoxification and do not move on to further treatment are at a high risk of relapse, and after completing withdrawal from opioids, they often experience a lower physiological tolerance to opioids. This creates a high risk of overdose if the patient returns to using the same dosages of opioids that they were using prior to medically supervised withdrawal. 186 Medications used in the treatment of opioid withdrawal syndrome focus on targeting the underlying pathophysiology of the condition. The euphoria produced by opioids is primarily a result of the opioid binding to the μ-opioid receptor. This binding results in a suppression of the release of norepinephrine in the locus coeruleus, causing the characteristic symptoms of sedation, decreased respiration rate, and hypotension associated with opioid intoxication. When opioids are discontinued or abruptly tapered, an increase of norepinephrine release from the locus coeruleus leads to the characteristic withdrawal symptoms of diaphoresis, lacrimation, mydriasis and tachycardia. Treatment of withdrawal focuses on these mechanisms, with μ-opioid receptor agonists and partial agonists, as well as α 2 agonists, being critical elements of opioid withdrawal therapy. 186 Buprenorphine Buprenorphine is a partial agonist with a high affinity for the μ-opioid receptor that is used alone or in combination with naloxone for the treatment of both opioid withdrawal and opioid use disorder. Since buprenorphine partially activates the opioid receptor, it provides effective treatment for opioid withdrawal symptoms. Naloxone, an opioid antagonist, has little effect when taken orally but is often included in combination products with buprenorphine to prevent intravenous abuse of buprenorphine – if buprenorphine/naloxone is liquefied and injected, naloxone will take effect and prevent buprenorphine from activating the μ-opioid receptor. This effect is generally avoided when buprenorphine/naloxone is taken as prescribed, though a small amount of naloxone can be absorbed sublingually and displace other opioids from the opioid receptor, resulting in precipitated withdrawal in patients who have not had a sufficient amount of time pass since their last opioid dose. Patients taking methadone or other long- acting opioids may be at a higher risk of developing precipitated withdrawal. The use of buprenorphine monotherapy may be considered initially in patients taking long-acting opioids to minimize this effect, though buprenorphine monotherapy can also precipitate withdrawal due to its high affinity for the opioid receptor. 187 Buprenorphine has a higher affinity for the μ-opioid receptor when compared to most full opioid agonists. Because of this, buprenorphine is able to displace full opioid agonists from the receptor, precipitating withdrawal on its own if insufficient time has passed since the patient’s last dose of opioids. Patients with current opioid dependence should wait until mild to moderate opioid withdrawal sets in before initiating buprenorphine treatment in order to reduce the risk of precipitated withdrawal.
Book Code: CA23CME
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