P2.A012: Diffuse alveolar hemorrhage in the setting of chronic opioid inhalation

Introduction: Hospitalization for medical misuse of opioids in the pediatric population continues to rise. This case presentation highlights the life-threatening cardiopulmonary complication of opioid misuse in an adolescent, presenting as diffuse alveolar hemorrhage (DAH). Although it has been established that acute lung injury and ARDS is a potential consequence of opioid inhalation, DAH is a lesser-known complication that requires prompt recognition and emergent treatment and management.

Case Description: 16-year-old male previously healthy presenting with acute onset hemoptysis and chest pain from diffuse alveolar hemorrhage. Patient endorsed inhaling oxycodone prior to symptom onset. At an outside hospital, the patient was hypoxemic to 70% on room air and placed on BiPAP (IPAP 12, EPAP 5), FiO2 60%. Narcan was not given due to GCS 14 and stable vital signs. Chest CT scan showed diffuse alveolar hemorrhage.

Upon arrival at the pediatric intensive care unit, patient was intubated given impending respiratory failure despite escalation of respiratory support. The pediatric pulmonologist recommended a 7-day steroid course. Urine gas chromatography/mass spectroscopy collected on hospital day 2 (about 24 hours after last use) was negative for opioid metabolites. A bronchoscopy showed inflammation in the left and right main-stem bronchi. Cytology of BAL fluid showed scattered neutrophils with abundant red blood cells. Rare alveolar macrophages were noted.

Substance use history was obtained: patient endorsed recreational opioid use for 1 year with daily use in the months leading up to hospitalization.

Discussion: Current literature shows scant documentation of opioid-related DAH and is an under-recognized complication of opioid abuse. This specific case differed from previous case reports due to the absence of the classic signs and symptoms of opioid overdose [5,6,7].

While the etiology of opioid-induced DAH is likely a combination of cardiovascular and pulmonary dysfunction, this case highlights a primary pulmonary etiology and secondary cardiac abnormalities due to acute lung injury. Negative pressure pulmonary hemorrhage was described by Schwartz et al, in which negative intrathoracic pressure causes increase in pulmonary vascular volume and increase in capillary transmural pressures. Ultimately this damages the alveolar-capillary membranes, eliciting an inflammatory response and recruitment of neutrophils. Patient demonstrated a good response to systemic steroids, suggesting there is an inflammatory process in the pathogenesis of opioid-induced DAH. Damage to surrounding microvasculature leads to diffuse hemorrhage, leading to decrease in preload, coronary perfusion, and ultimately myocardial ischemia.

Conclusion: Our case suggests classic symptoms of opioid overdose are not evident in opioid-induced DAH. Clinicians must maintain constant clinical vigilance when assessing acute-onset hemoptysis. Other differential diagnoses for hemoptysis were considered but given the sequence of events and the lack of other clinical and laboratory evidence of infectious, autoimmune, or malignancy causes, inhalation of opioids was the most likely cause of DAH.