Buprenorphine-naloxone is used to treat chronic pain and opioid use disorder. Each medication in this combination has been associated with noncardiogenic pulmonary edema. Here we report the case of a 56-year-old woman treated for chronic pain with buprenorphine-naloxone, and a history of multiple hospitalizations for pulmonary edema. Her buprenorphine-naloxone was held on admission and her symptoms improved gradually with supportive care. CASE PRESENTATION:A 56-year-old woman with past history significant for congestive heart failure, chronic obstructive pulmonary disease, and chronic pain treated with buprenorphine-naloxone presented to the emergency department via ambulance for altered mental status and worsening dyspnea for 3 days. Upon arrival to the ED she was tachypneic with a SpO2 of 50% on room air and required non-invasive ventilation. Physical exam revealed diminished breath sounds bilaterally and no peripheral edema. Laboratory data was significant for an elevated D-dimer and BNP. Covid-19 screening was negative. Chest xray showed diffuse hazy opacities. CTA chest was negative for pulmonary embolism, but did show extensive parenchymal opacities and diffuse ground glass densities bilaterally. Steroids and antibiotics were initiated, and buprenorphine-naloxone was discontinued.She described several similar prior hospitalizations, but denied ever receiving a diagnosis. Echocardiogram showed a normal ejection fraction and grade II diastolic dysfunction. Infectious and vasculitis etiologies were ruled out. The patient declined bronchoscopy. Records from prior hospitalizations revealed non-diagnostic bronchoalveolar lavage and wedge biopsies. Environmental exposure was ruled out via a peer reviewed questionnaire and negative allergen testing. With no clear etiology, the patient's hypoxia improved. We propose that the patient's presentation was secondary to noncardiogenic pulmonary edema induced by buprenorphine-naloxone.DISCUSSION: Non-cardiogenic pulmonary edema is an acute process resulting in hypoxia secondary to an increase in capillary permeability. Major causes include ARDS, pulmonary embolism, TRALI, and opioid overdose, but many other etiologies have been implicated. Buprenorphine, like other opioids, is a known cause of pulmonary edema (1). Naloxone induced pulmonary edema, while rare, has also been described (2). A review of the literature was not able to find buprenorphine-naloxone combination as a cause of non-cardiogenic pulmonary edema. We believe this patient's pulmonary edema may have been secondary to this medication's opioid effects, naloxone effects, or possibly an allergic reaction. Given the wide use of this medication physicians should be made aware of this possible complication.
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