Avascular necrosis (AVN) is a rare but important complication after supracondylar humerus fractures. Posttraumatic humerus deformity was first reported in 1948 and sporadically thereafter. AVN deformity has been classified as type A (AVN of the lateral ossification center) and type B (AVN of the entire medial crista and a metaphyseal portion). In this article, we present 5 cases of AVN after supracondylar humerus fracture, discuss the importance of late clinical findings, and postulate a mechanism of AVN in nondisplaced fractures. Five cases of AVN after supracondylar humerus fracture were reviewed from the Children's of Alabama database. Four of the 5 patients were female. Four patients sustained a Gartland type III fracture, and 1 patient sustained a nondisplaced Gartland type I fracture. Age at time of injury ranged from 5 years to 10 years. All patients had an asymptomatic clinical period after treatment and re-presented 6 months to 7 years later with elbow pain or loss of motion. All patients were treated symptomatically. AVN of the trochlea has a late clinical presentation. The cause of this complication is interruption of the trochlea blood supply. In displaced fractures, the medial and/or lateral vessels are injured, leading to type A or type B deformity. In nondisplaced fractures, the lateral vessels are interrupted by tamponade because of encased fracture hematoma; this presents as a type A deformity. Both type A and type B deformities can be clinically significant. AVN of the trochlea should be considered in patients with late presentation of pain or loss of motion after treatment of supracondylar humerus fractures.