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Listen "Managing Opioid Use Disorder (OUD) and Withdrawal in the Fentanyl-Era: Fast, Compassionate Inpatient Management That Keeps Patients Safe"
Episode Synopsis
In this episode of Hospital Medicine Unplugged, we tackle opioid withdrawal on the inpatient ward—a syndrome that’s not usually lethal, but absolutely destabilizing, deeply uncomfortable, and a leading driver of patient-directed discharge.
We open with why this matters now: fentanyl has changed everything. Its high potency and lipophilicity make withdrawal more severe, more unpredictable, and often prolonged, leaving standard opioid agonist approaches underpowered. Add in common polysubstance use—stimulants, benzodiazepines, xylazine—and clinicians must often manage multiple withdrawal syndromes in parallel.
Diagnosis starts with timing: 8–12 hours after short-acting opioids, 8–24 hours after fentanyl, up to 30 hours after methadone. Patients present with the classic multisystem storm—autonomic activation (sweating, tachycardia, piloerection, dilated pupils), GI distress, myalgias, and intense craving. We rely on COWS and SOWS for objective tracking; SOWS often detects symptoms earlier, COWS guides treatment thresholds.
But step one is simple: ask about withdrawal and treat it aggressively. Untreated withdrawal drives AMA discharges, worsens medical illness, and erodes trust. Starting MOUD early lowers AMA discharge risk by ~27%.
Treatment goals are clear: rapid symptom relief, stabilize with opioid agonists, prevent complications, and set up continuity of care.
Our backbone: opioid agonist therapy.
• Methadone shines here—no need to wait for withdrawal, no risk of precipitated withdrawal, and a full agonist profile that suits high-tolerance fentanyl users. Standard starts (20–30 mg/day) often fall short in the fentanyl era; rapid inpatient titration is increasingly used safely under monitoring. Watch QTc and delayed respiratory depression.
• Buprenorphine brings a stellar safety profile and easy outpatient continuation. But it demands mild–moderate withdrawal (COWS >10) to avoid precipitated withdrawal—still a real fear among fentanyl-exposed patients. Enter microdosing/low-dose induction, now routinely used to bridge patients onto buprenorphine without requiring abstinence.
• Some centers use slow-release oral morphine for patients with QTc issues or previous induction failures, and emerging inpatient data support short-acting full-agonist opioids as adjuncts for severe fentanyl withdrawal when standard regimens aren’t enough.
If patients decline opioid agonists, we move to symptom-targeted therapy:
• Alpha-2 agonists (clonidine, lofexidine) reduce autonomic symptoms; lofexidine offers less hypotension.
• GI agents (loperamide, ondansetron, dicyclomine) smooth out the abdominal churn.
• NSAIDs/acetaminophen ease myalgias; trazodone or cautious benzodiazepine use can support sleep and anxiety.
But remember—non-opioid therapy alone is inferior and reserved for patients who decline MOUD.
The differential stays broad: alcohol or benzodiazepine withdrawal, stimulant intoxication, viral GI illness, thyroid storm, adrenal crisis, and sepsis, especially in people who inject drugs. Missing these can be disastrous, so vitals, exam, and targeted labs remain central.
We close with the systems moves that make withdrawal care consistent and safe: normalize withdrawal screening, default to MOUD first, incorporate COWS/SOWS into nursing workflows, build fentanyl-aware induction pathways, manage concurrent withdrawals, and hard-wire outpatient linkage—OTP confirmation lines, buprenorphine follow-up, and harm-reduction resources.
Fast, compassionate, and evidence-driven—treat withdrawal early, stabilize with MOUD, support symptoms, and never miss a life-threatening mimic.
We open with why this matters now: fentanyl has changed everything. Its high potency and lipophilicity make withdrawal more severe, more unpredictable, and often prolonged, leaving standard opioid agonist approaches underpowered. Add in common polysubstance use—stimulants, benzodiazepines, xylazine—and clinicians must often manage multiple withdrawal syndromes in parallel.
Diagnosis starts with timing: 8–12 hours after short-acting opioids, 8–24 hours after fentanyl, up to 30 hours after methadone. Patients present with the classic multisystem storm—autonomic activation (sweating, tachycardia, piloerection, dilated pupils), GI distress, myalgias, and intense craving. We rely on COWS and SOWS for objective tracking; SOWS often detects symptoms earlier, COWS guides treatment thresholds.
But step one is simple: ask about withdrawal and treat it aggressively. Untreated withdrawal drives AMA discharges, worsens medical illness, and erodes trust. Starting MOUD early lowers AMA discharge risk by ~27%.
Treatment goals are clear: rapid symptom relief, stabilize with opioid agonists, prevent complications, and set up continuity of care.
Our backbone: opioid agonist therapy.
• Methadone shines here—no need to wait for withdrawal, no risk of precipitated withdrawal, and a full agonist profile that suits high-tolerance fentanyl users. Standard starts (20–30 mg/day) often fall short in the fentanyl era; rapid inpatient titration is increasingly used safely under monitoring. Watch QTc and delayed respiratory depression.
• Buprenorphine brings a stellar safety profile and easy outpatient continuation. But it demands mild–moderate withdrawal (COWS >10) to avoid precipitated withdrawal—still a real fear among fentanyl-exposed patients. Enter microdosing/low-dose induction, now routinely used to bridge patients onto buprenorphine without requiring abstinence.
• Some centers use slow-release oral morphine for patients with QTc issues or previous induction failures, and emerging inpatient data support short-acting full-agonist opioids as adjuncts for severe fentanyl withdrawal when standard regimens aren’t enough.
If patients decline opioid agonists, we move to symptom-targeted therapy:
• Alpha-2 agonists (clonidine, lofexidine) reduce autonomic symptoms; lofexidine offers less hypotension.
• GI agents (loperamide, ondansetron, dicyclomine) smooth out the abdominal churn.
• NSAIDs/acetaminophen ease myalgias; trazodone or cautious benzodiazepine use can support sleep and anxiety.
But remember—non-opioid therapy alone is inferior and reserved for patients who decline MOUD.
The differential stays broad: alcohol or benzodiazepine withdrawal, stimulant intoxication, viral GI illness, thyroid storm, adrenal crisis, and sepsis, especially in people who inject drugs. Missing these can be disastrous, so vitals, exam, and targeted labs remain central.
We close with the systems moves that make withdrawal care consistent and safe: normalize withdrawal screening, default to MOUD first, incorporate COWS/SOWS into nursing workflows, build fentanyl-aware induction pathways, manage concurrent withdrawals, and hard-wire outpatient linkage—OTP confirmation lines, buprenorphine follow-up, and harm-reduction resources.
Fast, compassionate, and evidence-driven—treat withdrawal early, stabilize with MOUD, support symptoms, and never miss a life-threatening mimic.
In God we trust