B50-07 Traumatic Left Diaphragmatic Hernia Unmasked by “stemi” Alert

Abstract Traumatic diaphragmatic injury after blunt force is uncommon and can be radiographically occult on initial assessment. Early contrast CT may miss small tears that later widen as intra-abdominal pressure rises. Subsequent herniation can mimic primary cardiopulmonary disease. We report a restrained driver whose delayed shoulder and chest pain triggered a STEMI activation, with the ultimate diagnosis established only after repeat imaging, illustrating how routine post-injury complaints can conceal a surgically correctable condition. A 64-year-old Spanish-speaking man presented after a T-bone collision. On arrival: Glasgow coma scale was 15, BP 145/96, HR 93, SpO2 95%. Exam revealed deformity of the left femur, an open left tibia/fibula fracture with non-pulsatile bleeding, a posterior scalp laceration, and minor left-hand abrasion. Initial trauma imaging showed no thoracic or abdominal injury. He underwent orthopedic fixation of the femur and tibia/fibula. On post-operative day (POD) 3 he developed 10/10 left chest and shoulder pain with tachycardia, diaphoresis, troponin elevation, and minimal ST-segment elevation. STEMI protocol was activated; emergent coronary angiography demonstrated non-obstructive coronary disease with preserved LV function. Ongoing left shoulder pain prompted radiography showing an elevated left hemidiaphragm and air-filled viscus in the lower hemithorax. Repeat contrast CT revealed a 4.8 × 4 cm left diaphragmatic defect with intrathoracic herniation of the stomach, small left pleural effusion, basilar atelectasis, and grade-1 splenic subcapsular hematoma not seen on admission imaging. The patient underwent laparoscopic reduction and primary suture repair with concurrent left chest tube placement. He improved rapidly; the chest tube was removed on day 2 after repair, oxygen weaned, and he was discharged to a skilled nursing facility on day 11. Several features complicated timely recognition. First, comprehensive early imaging was negative, underscoring that small tears may be missed and only declare themselves after physiologic stress, coughing, or mobilization. Second, symptom overlap with acute coronary syndrome led appropriately to a cardiac pathway; only after angiography excluded culprit coronary disease did attention return to the diaphragm. Third, referred left shoulder pain, often attributed to musculoskeletal injury, was the pivotal clue; a simple shoulder radiograph suggested intrathoracic stomach and redirected evaluation. Finally, despite multiple concomitant orthopedic injuries and transient oxygen needs, a minimally invasive approach achieved definitive repair with low blood loss and quick recovery. For trauma patients with new chest/shoulder pain, rising biomarkers, or evolving basilar atelectasis/effusion after initially negative studies, a low threshold for repeat cross-sectional imaging can prevent missed gastrothoracic herniation and avoid cardiorespiratory compromise. This abstract is funded by: None