What would be the most appropriate treatment for symptom reversal in patient with suspected opiate overdose?
ExplanationD. Opiate use and intoxication classically are associated with miosis, or pinpoint pupils, not mydriasis. Of note, this must be differentiated from pontine lesions, which can also cause pinpoint pupils. All of the other options can be seen with opiate intoxication, including decreased body temperature and coma. In addition to these findings, common side effects include euphoria, drowsiness, analgesia, and constipation (hence the use of opiates and opiate derivatives as antidiarrheals). Opiate toxicity/overdose creates a “silent gut”, which can help in the diagnosis. Because of its cough suppressant effects, codeine is sometimes used in cough medicines. Treatment of suspected opiate overdose includes the opioid antagonist naloxone at 0.4 to 2 mg intravenously every 2 to 3 minutes. The diagnosis should be questioned if there is no response even after administration of 10 mg. Naltrexone is also an opioid antagonist, but used in longer-term treatment of opioid and alcohol dependence as opposed to naloxone, which is used in emergency settings. Flumazenil is given for benzodiazepine overdose. The dose of flumazenil is 0.2 to 0.5 mg intravenously every minute to a maximum total dose of 5 mg. Thiamine and glucose are not used for opiate overdose. Opiate withdrawal occurs within hours to several days of cessation. Withdrawal symptoms are often quite severe and cause significant functional impairment. They include dysphoria, myalgias, nausea, vomiting, rhinorrhea, lacrimation, piloerection, diaphoresis, diarrhea, mydriasis, fever, and insomnia. Difficulty often exists in differentiating opiate from sedative (e.g., alcohol, benzodiazepines) withdrawal. Hyperactive deep tendon reflexes (DTRs) can help in this differentiation because increased DTRs are typical in alcohol or sedative withdrawal but not opioid withdrawal. Therefore, if you see increased DTRs and give more opioids for suspected opioid withdrawal in the setting of actual sedative withdrawal, benzodiazepine or alcohol withdrawal seizures will be a likely complication. Opiates are one of multiple euphoria-producing drugs. All euphoria-producing drugs cause release of dopamine from the midbrain to the forebrain in the reward circuit (ventral tegmental area and the nucleus accumbens). The caudate nucleus is included in this pathway. These areas contain especially high concentrations of dopaminergic synapses. The opiates also interact with other structures modulated by endorphins, including the amygdala, locus coeruleus, arcuate nucleus, thalamus, and the periaqueductal gray matter, which influence dopaminergic pathways indirectly. There are natural and synthetic forms of opiates. Opioid receptors are a group of G-protein coupled receptors, with opioids acting as ligands. The endogenous opioids are dynorphins, enkephalins, endorphins, and endomorphins. There are four major subtypes of opioid receptors. The first is δ, including subtypes δ1 and δ2. They are involved with analgesia, antidepressant effects, and physical dependence. The second is κ and includes κ1, κ2, and κ3. These are involved in spinal analgesia, sedation, miosis, and inhibition of antidiuretic hormone release. The third is μ and includes μ1, μ2, and μ3. The subtype μ1 is involved in supraspinal analgesia and physical dependence; μ2 is involved in respiratory depression, miosis, euphoria, reduced gastrointestinal motility, and physical dependence. The actions of μ3 are not clear. The fourth is ORL1/orphanin (or nociceptin receptor), which is involved in anxiety, depression, appetite, and development of tolerance to μ agonists
