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A6929 - Agitated Delirium in an Intravenous Drug User: Don’t Jump to Conclusions
Author Block: A. Abdelrahman, M. Borden, M. A. Ghamloush; Tufts Med Ctr, Boston, MA, United States.
Introduction: The most common etiology of agitated delirium in patients presenting to the emergency department (ED) include psychiatric illness, recreational drug ingestions or alcohol use. We present a case of agitated delirium in a patient with a history of active substance abuse where the underlying etiology of delirium was overlooked. Case: A 54-year-old woman with a history of depression and heroin dependence presented to the ED with confusion and agitation. Prior to presentation, she was seen at an outpatient opiate addiction center where she was directly observed and given four mg of sublingual buprenorphine-naloxone. A few minutes later she developed worsening tremors and confusion. In the ED she was febrile, tachycardic, tachypneic and severely hypertensive. She had pressured incomprehensible speech and was extremely combative with myoclonus involving her whole body requiring four-point restraints. Workup revealed a negative drug and alcohol screen. Given her history and presentation, she was assumed to have ingested a synthetic cathinone, a synthetic cannabinoid, or to be having a very severe case of narcotic withdrawal. She did not respond to large doses of lorazepam, diazepam, haloperidol and hydromorphone. She was intubated and required midazolam, propofol, and dexmedetomidine infusions. She was extubated 24 hours later after delirium resolution. Patient denied any recent ingestions and this was corroborated by patient’s family and the drug treatment facility where she was being continuously observed. On review, her long-term medications included citalopram and nortriptyline both of which inhibit serotonin reuptake. In retrospect, the temporal association between ingestion of buprenorphine and symptom onset all strongly indicate that serotonin syndrome (SS) precipitated by buprenorphine was the underlying cause of the patient’s presentation. Discussion: To our knowledge, this is only the second reported case of SS determined to be precipitated by buprenorphine. SS is a potentially fatal condition with a cluster of symptoms associated with increased serotonergic activity in the central nervous system (CNS). While meperidine, methadone and fentanyl have been known to precipitate serotonin syndrome due to weak serotonin reuptake inhibition, buprenorphine has not been shown to inhibit serotonin reuptake. Buprenorphine is now thought to inhibit GABAergic neurons thereby disinhibiting serotonin release. While our patient had a favorable clinical outcome, an earlier suspicion for serotonin syndrome may have led to targeted treatment with a serotonin antagonist such as cyproheptadine. This case sheds light on the underlying implicit bias health care providers must overcome to adequately treat patients with substance use disorders.