Serial arterial blood-gas analyses showed a phase of primary hypoxaemia in thirty-two out of fifty fracture patients (64 per cent) without head, chest or abdominal injury. The incidence was greater in those with shaft fractures of the femur or tibia or both, than in those with fractured hips, and was related to the severity of injury and the nature of the accident. Most affected subjects were already hypoxaemic on admission to hospital: the arterial PO2 commonly fell to between 60 and 70 millimetres of mercury, and the episode generally lasted a few days. The hypoxaemia was generally subclinical but four patients developed mild clinical fat embolism. Early hypoxaemia was not found in six patients admitted with only soft-tissue injuries. One or more subsequent attacks of subclinical hypoxaemia, each lasting a few days, occurred in half of those previously affected. Most episodes followed fracture operation or manipulation. Pulmonary thromboembolism seemed responsible in two patients, but it could be excluded in others given oral anticoagulant prophylaxis from soon after admission. Pulmonary fat embolism is the most likely explanation of the primary episodes and could account for most of the subsequent periods of hypoxaemia.