Hip fractures occur most commonly in the femoral neck or intertrochanteric region. The femoral neck is particularly vulnerable because it is composed largely of cancellous bone with limited periosteal blood supply from the medial and lateral circumflex arteries. Fracture disrupts the retinacular blood vessels that supply the femoral head, creating a high risk of avascular necrosis (AVN), especially with displaced intracapsular fractures. The fracture hematoma triggers an inflammatory cascade with release of cytokines (IL-1, IL-6, TNF-alpha) and prostaglandins that initiate bone healing through callus formation. In elderly patients, osteoporosis causes decreased bone mineral density through osteoclast-mediated resorption exceeding osteoblast bone formation, making fractures possible with minimal trauma (fragility fractures). Fat embolism syndrome can occur 24-72 hours post-fracture when marrow fat enters the bloodstream through disrupted intramedullary sinusoids, lodging in pulmonary and cerebral microvasculature.