Abstract Introduction Diffuse alveolar hemorrhage (DAH), a potentially life-threatening condition, is characterized by bleeding into the alveoli due to disruption of the alveolar-capillary basement membranes. The etiology is usually inflammation or injury from vasculitis, infection, or certain drugs. More recently, inhalation injury from crack cocaine, tobacco, or marijuana is increasingly being noted as a potential cause. We present a case of DAH associated with smoked marijuana. Case Description A 34-year-old female with a history of seizures, migraines, and occasional cannabis use presented with an unwitnessed tonic clonic seizure and hemoptysis. She had non-compliance with levetiracetam for two days and reported recent smoked cannabis use. CT of the chest showed diffuse infiltrates, mainly on the left side. Four months prior, she had a similar presentation with similar CT findings. A bronchoscopy showed hyperemic mucosa with bloody secretions on the left and right upper lobes. Serial bronchoalveolar lavage of both lobes showed increasingly bloody secretions, which was confirmed by cell counts. Hence, the diagnosis of DAH was established. On both occasions, extensive autoimmune workup, including anti-neutrophil cytoplasmic antibodies (ANCA), anti-glomerular basement membrane (GBM), and anti-cyclic citrullinated peptide (CCP), was negative. Symptoms resolved rapidly after a 3-day course of high dose methylprednisolone. She briefly required high flow oxygen support, which was weaned off soon. Considering the negative autoimmune workup, rapid response to steroids, and temporal correlation with marijuana use, inhalant injury was deemed the most likely etiology. Outpatient thoracoscopic lung biopsy is planned to exclude pauci-immune capillaritis. Discussion Inhalation-induced DAH is being increasingly recognized as an entity due to studies on smoking or vaping marijuana, cocaine, or other substances. It should be suspected in cases of substance use within 90 days of presentation, in whom other causes like infection or rheumatological conditions are ruled out. Various acute lung injuries from smoked marijuana have been reported, including hypersensitivity pneumonitis, diffuse alveolar damage, and organizing pneumonia. The pathophysiology is believed to involve direct mucosal toxicity from cannabis and its combustion products, Δ;-9 THC induced activation of oxidative stress pathways and lipid peroxidation, as well as immune modulation via the aryl hydrocarbon receptor. Further studies are needed to establish optimum diagnostic and therapeutic modalities. Current mainstay of treatment involves respiratory supportive measures and high dose glucocorticoids to suppress inflammation. This abstract is funded by: None
Chatterjee et al. (Fri,) studied this question.