Case Presentation: A 57-year-old man with sickle cell disease complicated by post-transfusion hyper-hemolysis, bilateral avascular necrosis, prior acute chest syndrome, and pulmonary fibrosis on home oxygen presented with a vaso-occlusive pain crisis in the setting of rhinovirus infection. His course was notable for severe hemolytic anemia (Hb 3.8 g/dL) and acute hypoxic respiratory failure requiring high-flow nasal cannula. After transfusions with steroid and IVIG pre-medication, he demonstrated prompt hematologic recovery and was weaned to baseline oxygen needs.Despite these improvements, he developed persistent and escalating focal left anterior chest pain that differed from his typical pain. Pulmonary embolism was ruled out by CT angiogram, serial high sensitivity troponins were normal, and EKGs remained unchanged. The discordance between his objective recovery and worsening pain was initially attributed by some to behavioral or psychosocial factors, a common bias in the care of patients with sickle cell disease. On re-examination, the localized and severe nature of the pain prompted reconsideration of the differential, and chest wall bony infarction was suspected. In consultation with radiology, his CT was re-reviewed and revealed subtle features consistent with an acute anterior chest wall osseous infarct. The patient’s symptoms were validated, targeted analgesic strategies were continued, and his pain improved gradually with supportive care.
Discussion: Rib and chest wall infarction are under-recognized causes of acute pain in adults with sickle cell disease. Infarction may present with focal, severe, reproducible chest wall tenderness that can be mistaken for musculoskeletal strain, pneumonia, acute chest syndrome, or opioid-related behavior, particularly when no new infiltrate is visible on initial imaging. Reported incidence varies, but rib infarcts are thought to occur in a substantial minority of vaso-occlusive crises and may contribute to the development of acute chest syndrome through splinting, hypoventilation, and atelectasis.Diagnosis is challenging as chest radiography is often normal early in the course, and CT findings may be subtle and easily overlooked without directed review. MRI is more sensitive for marrow changes but not always readily performed. Management is supportive and includes aggressive analgesia, hydration, incentive spirometry, and close monitoring for respiratory compromise. While symptoms generally improve with time, recognition is important to avoid unnecessary diagnostic delays, inappropriate judgments about patient behavior, and inadvertent undertreatment of pain.
Conclusions: Chest wall bony infarction should be included in the differential for focal chest pain in patients with sickle cell disease, even when initial imaging is unrevealing. Early recognition prevents misattribution of symptoms and supports timely, appropriate management.