Fat embolism syndrome is a rare but potentially fatal problem. The syndrome involves pulmonary, cerebral, and cutaneous manifestations and occurs 24 to 48 hours postinjury.
Young men with fractures are at an increased risk for developing fat embolism syndrome.
· Fractures of the pelvis, femur, tibia, or ribs
· Orthopedic surgery
Bone marrow from a fractured bone or other injured adipose tissue releases fatty globules that enter the systemic circulation through torn veins at the injury site. These fatty globules travel to the lungs, where they form an embolus that blocks pulmonary circulation. Lipase breaks down the trapped fat emboli into free fatty acids.
This process causes a local toxic effect that damages the epithelium, increases capillary permeability, and inactivates lung surfactant. The increased capillary permeability allows protein-rich fluid to leak into the interstitial space and alveoli, increasing the workload of the right side of the heart and causing pulmonary edema. The decreased surfactant causes alveolar collapse, a decrease in functional reserve capacity, and ventilation-perfusion mismatch, leading to hypoxemia. Platelet aggregation on fat, normal injury-related platelet consumption, and platelet dilution through I.V. crystalloid administration all contribute to thrombocytopenia, petechiae and, possibly, disseminated intravascular coagulation.
Signs and symptoms
· Increased respiratory rate
· Accessory muscle use
· Mental status changes
Diagnostic test results
Gurd's criteria are used to diagnose fat embolism syndrome. At least one major and three minor criteria are required for diagnosis. Major criteria include:
· petechiae in a “vest” distribution
· hypoxia, with a partial pressure of arterial oxygen (PaO2) less than 60 mm Hg
· pulmonary edema
· change in level of consciousness.
Minor criteria include:
· tachycardia, with a heart rate greater than 110 beats/minute
· pyrexia, with a temperature higher than 103 F (39.4 C)
· retinal changes
· fat in urine or sputum
· unexplained drop in hematocrit or platelet count
· increasing erythrocyte sedimentation rate
· renal changes.
· Arterial blood gas analysis reveals PaO2 less than 60 mm Hg; partial pressure of arterial carbon dioxide initially decreases and later increases.
· Chest X-ray is normal initially but later shows patchy areas of consolidation to complete “white out,” if the condition progresses.
· Complete blood count shows decreased platelets and decreased hemoglobin levels.
· Supplemental oxygen
· Endotracheal intubation and mechanical ventilation
· I.V. fluids such as crystalloids (avoid colloids)
· Coughing and deep breathing
HOW FAT EMBOLISM THREATENS PULMONARY CIRCULATION