Pulmonary fat embolism
Pulmonary fat embolism is a specific subtype of pulmonary embolism where the embolic particles are composed of fat.
It usually occurs in the context of a long bone fracture and may occur in 1-3% of patients with simple tibial or femoral fractures and up to 20-33% of individuals with more severe trauma.
Other less common causes include:
- soft tissue trauma
- major burns
- overwhelming infection
- blood transfusion
The exact pathophysiology is not entirely clear but presumably occurs by one of two mechanisms or a combination thereof:
- production of free fatty acids, which initiates a toxic reaction in the endothelium. This process is further complicated by the accumulation of neutrophils and other inflammatory cells, which cause damage to the vasculature.
- mechanical obstruction of the pulmonary vasculature by fat globules, aggregates of red blood cells, and platelets.
Urinalysis for fat globules may be useful in the setting of large a pulmonary fat embolism.
Imaging findings typically become evident ar around 24-48 hours after the traumatic insult.
Non-specific but can resemble those in acute respiratory distress syndrome from any cause, and shows widespread homogeneous and heterogeneous areas of increased opacity. A normal heart size and the absence of other features of cardiogenic edema (septal lines, pleural effusion, and pulmonary venous hypertension) may aid in the differentiation from noncardiogenic pulmonary edema.
Commonly reported findings include:
- may show areas of consolidation
- ground-glass opacities: can occur with a geographic distribution and or in association with interlobular septal thickening 7
- small (<1 cm) nodules (can sometimes be ground glass like) of various sizes: presumed to represent alveolar edema ,inflamed intrapulmonary lymph nodes or hemorrhage secondary to the fat embolism syndrome 5,6,12
- fat attenuating filling defects in pulmonary arteries: rarely described in non-fulminant fat embolism syndrome
Treatment and prognosis
Prophylactic treatment consists of prompt treatment of the causative factor, e.g. fracture fixation. Treatment is largely supportive and involves fluid resuscitation, maintaining good arterial oxygenation and sufficient intravascular volume. Adding albumin to the electrolyte solution used for volume resuscitation can help bind the free fatty acids 8. Mechanical ventilation and PEEP may be required in certain cases. Symptoms are often transient with good prognosis.
- some imaging features can resemble those of acute respiratory distress syndrome 11
- other considerations for multifocal ground glass changes include
- multifocal infective inflammatory changes
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