Cast bronchitis has been associated1–3 with multiple and varied causes, mainly with cardiac, respiratory, and hematologic conditions. Cyanotic heart disease remains the most common associated condition,4 particularly in patients post-Fontan. Cast formation as part of the acute chest syndrome in sickle cell anemia has been described5 and rarely has been associated6 with α-thalassemia. Historically, various classification systems have been developed in an attempt to better understand the pathophysiology. Seear et al7 originally proposed a pathologic classification system that divided casts into one of two types. Type I, or inflammatory, casts comprise fibrin, eosinophils, and Charcot-Leyden crystals associated with allergic and inflammatory conditions. Type II, or noninflammatory, casts comprise mucin and are associated with changes in vessel hydrostatics (eg, cyanotic heart disease). Subsequent identification8 of inflammatory-type casts associated with cyanotic heart disease, however, proved this classification system to be inadequate. Brogan et al3 suggested a classification system based on clinical presentation, dividing casts into allergic and asthmatic, cardiac, or idiopathic etiologies. Most recently, Madsen et al2 attempted to combine both classification systems, focusing initially on clinical presentation and further categorizing the casts based on pathology if the etiology is unclear. Regardless of classification, inflammation appears to be an important driving force in the production of casts. Further studies aimed at identifying inflammatory markers involved in the process may increase our understanding of the pathophysiology and advance therapeutic options.