Fat Embolism Syndrome and Leukocytosis
Yes, fat embolism syndrome (FES) can cause leukocytosis as part of the systemic inflammatory response that occurs following fat embolization. 1
Pathophysiology and Inflammatory Response
Fat embolism syndrome occurs when fat globules enter the circulatory system, typically following:
- Long bone fractures (especially femur and tibia)
- Pelvic fractures
- Orthopedic procedures involving intramedullary manipulation
- Multiple trauma
The pathophysiological mechanism involves a biphasic process:
- Initial mechanical phase: Fat globules directly obstruct blood vessels
- Biochemical phase: Fat breaks down into free fatty acids, triggering an inflammatory cascade 2
This inflammatory response includes:
- Release of inflammatory mediators
- Activation of the complement system
- Recruitment of white blood cells to affected tissues
- Systemic inflammatory response syndrome (SIRS)
Clinical Manifestations and Diagnosis
FES typically presents 12-36 hours after injury with the characteristic triad:
- Respiratory distress (most common)
- Neurological symptoms
- Petechial rash 1
Laboratory findings that support FES diagnosis include:
- Leukocytosis (elevated white blood cell count)
- Anemia
- Thrombocytopenia
- Elevated inflammatory markers 3
Prevention and Management
Early fracture fixation (within 24 hours) is the primary preventive measure for FES, as delayed stabilization (>5 days) is associated with a higher incidence of fat embolism (18%) 1.
Management is primarily supportive:
- Oxygen supplementation to maintain SpO2 > 92%
- Ventilatory support for severe hypoxemia
- IV fluid management to maintain euvolemia
- Vasopressor support if needed
- Pain control with multimodal analgesia
- Maintaining urine pH at 6.5 1
Monitoring
For patients at risk of FES, continuous monitoring should include:
- Respiratory status
- Neurological status
- Skin examination for petechiae
- Arterial blood gases
- Complete blood count (to track leukocytosis and other hematological changes) 1
Important Clinical Considerations
- FES can occur in non-orthopedic trauma patients, making diagnosis challenging 4
- The condition is self-limiting in most cases but can lead to significant respiratory failure, neurological damage, and mortality in severe cases 5
- No specific pharmacological intervention has been proven to alter the course of FES, and treatment remains primarily supportive 1
- High-dose corticosteroids have shown detrimental effects in patients with traumatic brain injury and spinal cord injury 1
Clinicians should maintain a high index of suspicion for FES in trauma patients, particularly those with long bone fractures, who develop unexplained respiratory distress, neurological symptoms, or petechial rash, especially when accompanied by leukocytosis and other laboratory abnormalities.