Successful Management Of Refractory Precipitated Opioid Withdrawal Syndrome Following Buprenorphine Intake Using Ketamine: A Case Report
Iman Attackpour Torik, Mohammad Moeini, Shahram Moghaddam, Seyede Almas Fahim Yegane
preprint DOI: 10.21203/rs.3.rs-10429635/v1 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Case study Case report |
|---|---|
| Sample size | 1 |
| Population | A 50-year-old man with a 10-year history of opioid use who developed precipitated withdrawal after buprenorphine following methadone |
| Interventions | Ketamine Buprenorphine Methadone Clonidine Midazolam Fentanyl Propofol Morphine Ibuprofen Haloperidol |
| Dose | Ketamine 30 mg (0.5 mg/kg) followed by 30 mg/hour infusion for 24 hours, then intermittent 30 mg as needed; buprenorphine three 8-mg tablets; methadone 30 mg syrup; midazolam 10 mg; fentanyl 250 µg; propofol 80 mg; morphine 5 mg; ibuprofen 400 mg; haloperidol 0.5 mg intramuscular |
| Duration | Ketamine infusion for 24 hours; discharged after 48 hours |
| Measures | Glasgow Coma Scale (GCS), blood pressure, heart rate |
| Topics | Esketamine Ketamine |
| Key findings | In this case, severe precipitated withdrawal that did not respond to multiple standard therapies—including clonidine, midazolam, fentanyl, propofol, morphine, ibuprofen, and haloperidol—was controlled with ketamine at 30 mg (0.5 mg/kg) followed by a 30 mg/hour infusion for 24 hours. The authors argue that sedative doses of ketamine may offer a rapid, effective, and safe option for withdrawal resistant to first-line treatments, possibly by acting on NMDA receptors. |
Abstract
Abstract
Introduction: Precipitated withdrawal syndrome (POW) occurs when agonist-antagonist opioids are administered to individuals dependent on full agonist opioids. This class of drugs exerts strong antagonistic effects, is associated with mu-opioid receptor depletion, and induces severe withdrawal symptoms in affected patients. Standard management typically involves supportive care and high-dose buprenorphine. This report describes a complex case of refractory case to multiple lines of therapy, and withdrawal symptoms were ultimately controlled with sedative doses of ketamine. Case Presentation : A 50-year-old man with a 10-year history of opioid use presented to the emergency department in severe distress. He had angiography and stenting, hypertension, and sleep disturbances. The patient ingested three 8-mg buprenorphine tablets following 30 mg of methadone syrup, resulting in severe withdrawal symptoms, body aches, and agitation. On admission, his Glasgow Coma Scale (GCS) was 15/15, but he was extremely agitated and unresponsive to questions. Blood pressure was 163/105 mmHg, and heart rate was 112 beats per minute. Initial management included 500 mL of normal saline, clonidine tablets, 10 mg of midazolam, and 250 µg of fentanyl. Due to persistent pain and agitation, 80 mg of propofol was administered. A single dose of 5 mg morphine and 400 mg ibuprofen was also given, but severe pain persisted. After no improvement with 0.5 mg intramuscular haloperidol, ketamine therapy was initiated at 30 mg (0.5 mg/kg), followed by an infusion at 30 mg/hour for 24 hours. After 24 hours, the infusion was discontinued, and intermittent 30 mg doses were administered as needed. The patient was sedated at the initiation of ketamine, and his vital signs stabilized and normalized. He remained calm and alert during hospitalization and was discharged after 48 hours without pain or new drug dependence.
Conclusion: This case demonstrates that sedative doses of ketamine may serve as a rapid, effective, and safe therapeutic intervention for patients with withdrawal syndrome resistant to first-line therapies. By targeting alternative pain neurotransmitter pathways, such as NMDA receptors, ketamine offers a potential option when standard therapies and mu-opioid receptor agonists are ineffective.
Comparable studies
Other case reports and case series on ketamine, most cited first.