Cerebral fat embolism after bone fractures

Abstract

After a forklift accident, a 44-year-old man was admitted to our hospital in July, 2014, with fractures of the right fi bula and tibia, the left femur, and the pelvis. A proximal femoral nail antirotation was done to stabilise the left femur. 1 h after the operation, he developed acute respiratory failure, requiring reintubation and admission to the intensive care unit. CT angiography of the thorax showed bilateral ground-glass opacities and distinct nodular opacities (fi gure), without pulmonary embolism or aspiration. Despite intensive mechanical ventilation, severe hypoxaemia persisted (partial pressure of blood oxygen 6·7 kPa; normal range 11–13 kPa). We started antibiotic therapy because he had fever and tachycardia. 4 days later, we stopped sedative medication to allow neurological assessment, which showed he had a Glasgow Coma Scale score of 3. He developed axillar and inguinal petechiae, so 10 days after surgery we did MRI of the brain, which showed bilateral confl uent white matter abnormalities with diff usion restriction (fi gure). This pattern of cytotoxic cerebral oedema, with lesions in the white matter rather than the grey matter, is indicative of the subacute stage of fat embolism (5–14 days after an embolic event). Electro encepha lography showed diff use encephalopathy. On the basis of acute respiratory failure, petechiae in non-dependent areas, and typical fi ndings on MRI, we diagnosed cerebral fat embolism syndrome. Cardiographic imaging showed no evidence of a patent foramen ovale or rightto-left shunt. We continued supportive care, and 16 days after surgery the patient was extubated following respiratory and neurological recovery. At the end of August, 2014, our patient was transferred to a neurorehabilitation centre. The clinical triad of respiratory failure, unconsciousness, and petechiae observed in cerebral fat embolism syndrome is a direct consequence of mobilisation of bone marrow. The syndrome typically results from fractures of the pelvis and long bones, or fracture stabilisation with intramedullary devices. After trauma, medullary fat enters the circulation and can embolise to the lung. Altered pulmonary haemodynamics and the systemic infl ammatory reaction to trauma are thought to contribute to acute respiratory failure. The pliable nature of the fat emboli allows subsequent passage through the pulmonary capillaries with systemic embolisation to the skin and brain, causing petechiae and cerebral ischaemia with neurological symptoms. Although cerebral fat embolism is a clinical diagnosis, MRI showing a starfi eld pattern of scattered spot lesions with diff usion restriction in the acute phase (1–4 days) or confl uent cytotoxic cerebral oedema in periventricular and subcortical white matter in the subacute phase (5–14 days), supports the diagnosis.