Fat embolism syndrome
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This slide show gives a brief overview about the causes, theories, clinical featuers and managment of Fat embolism syndrome.
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Fat embolism syndrome
- 1. FAT EMBOLISM SYNDROME Dr Siddhartha Sinha Assistant Professor, Department of Orthopaedics HIMSR, New Delhi
- 2. Fat Emboli: Fat particles or droplets that travel through the circulation Fat Embolism: A process by which fat emboli passes into the bloodstream and lodges within a blood vessel. Fat Embolism Syndrome (FES): serious manifestation of fat embolism occasionally causes multi system dysfunction, the lungs are always involved and next is brain
- 3. • First described in mid 1800s • Mortality 5-15% • Associated with long bone/pelvic fractures, • Closed fractures • Orthopedics surgeries • Liposuction • Burns • Soft tissue injuries • Non-traumatic: • Pancreatitis • DM • Osteomyelitis • Bone tumor lysis • Steroids • Fatty liver • Cyclosporin • Lipid infusion
- 4. • FES typically manifests 12 to 72 hours after the initial insult or as late as two weeks • MCC- blunt trauma
- 5. FES Etiology Mechanical Hypothesis Obstruction of vessels and capillaries • Increase in intermedullary pressure forces fat and marrow into bloodstream • Bone marrow contents enter the venous system and lodge in the lungs as emboli • Smaller fat droplets may travel through the pulmonary capillaries into the systemic circulation: Embolization to cerebral vessels or renal vessels also leads to central nervous system and renal dysfunction
- 6. • Biochemical theory • Biochemical basis of disease • Fat broken down to FFA which hydrolyses causing ARDS • Coagulation theory • Thromboplastin released after trauma which activates complement system and causes coagulation
- 7. • Classic triad: • Hypoxemia • Neurologic abnormalities • Petechial rash (pathognomonic) • Early findings: • Dyspnea • Tachypnea • Hypoxemia (PaO2<60 mm Hg) • Neurological : • Confusion, • Seizures • Focal deficits • Coma. • Late: • possible petechial rash of head, neck, anterior thorax, subconjunctiva, and axillae – resolved in 5-7 days • Minor: • Lipiduria, • Scotomata (Purtscher's retinopathy), • Fever • Coagulation abnormality • Myocardial depression:
- 8. Petechiae • 50-60% of patients with FES • Characteristic distribution secondary to embolization within dermal fat –chest, neck, axillae, oral mucous membrane, conjunctiva • Emboli “floating” like oil on water to non-dependant vasculature
- 9. Diagnosis • Clinical presentation • Gurd’s Criteria
- 10. • Radiologic: • CXR: normal in most, minority with evenly distributed, fleck-like pulmonary shadows (Snow Storm appearance), increased pulmonary markings and Rt heart dilatation • V/Q: mottled pattern of subsegmental perfusion defects with a normal ventilatory pattern • Chest CT: Focal areas of ground glass opacification with interloblar septal thickening • Brain MRI: may reveal high intensity T2 signal. • PET scanning: cerebral blood flow alterations & correction
- 11. FES Prevention • Appropriate Splinting • Early Fracture Stabilization • Oxygen Therapy
- 12. Treatment • ABC and electrolytes. • Oxygen to correct hypoxemia (O2 conc b/w 75 & 90 mm Hg) • Mechanical ventilatory assistance - endotracheal intubation • Fluid restriction , diuretics • N- acetyl cysteine (may be given). • IV Methylprednisolone (Solu-Medrol) 10 mg/Kg/day in 3 divided doses(8 hourly)iv for 2 days.
- 13. Timing of Fracture Fixation • Early Fracture Fixation Optimal • Decreases Pulmonary Complications • Decompresses fracture hematoma • Eliminates pain & physiological stress • Delayed Fracture Fixation • Increased Pulmonary Dysfunction • WAIT FOR PATIENT TO STABILIZE BEFORE SURGERY
- 14. Type of Fracture Fixation -Controversial- • IM Nail - Reamed vs Un-Reamed • Increased Pulmonary Dysfunction With Reamed technique • Decreased with Unreamed Technique • Pape et al • IM Nail Reamed vs Plate Osteosynthesis • No Difference In Pulmonary Dysfunction • Bosse et al
- 15. PROGNOSIS • Clinically most patients improve spontaneously & return to normal after 5 days. • Mortality rate10 to 20%. Long term morbidity is associated with cerebral complications.
- 16. REFERENCES 1. Rockwood & Greens – fractures in adults (7th edition) 2. Rockwood & Greens – fractures in children (7th edition) 3. Textbook of orthopedics & trauma – G.S.Kulkarni (3rd edition) 4. Essential Orthopaedics Maheshwari and Mhaskar (5th edition) 5. www.google.com
- 17. THANK YOU
Notes de l'éditeur
- Fat embolism is very common. Fat embolism is often temporary or incomplete since fat globules do not completely obstruct capillary blood flow because of their fluidity and deformability. But count be fatal if it develops into FES
- Increase in intermedullary pressure forces fat and marrow into bloodstream Bone marrow contents enter the venous system and lodge in the lungs as emboli Smaller fat droplets may travel through the pulmonary capillaries into the systemic circulation and hence to the brain and other organs. Embolization to cerebral vessels or renal vessels also leads to central nervous system and renal dysfunction First, the mechanical theory states that large fat droplets are released into the venous system. These droplets are deposited in the pulmonary capillary beds and travel through arteriovenous shunts to the brain. Microvascular lodging of droplets produces local ischemia and inflammation, with concomitant release of inflammatory mediators, platelet aggregation, and vasoactive amines. http://www.urmc.rochester.edu/neuroslides/slide147.html Petechial hemorrhages in fat embolism: This section of temporal lobe shows the typical, multiple petechial hemorrhages that may occur in fat embolism. Hemorrhage is a consequence of occlusion of vessels, predominantly of capillary size, by fat emboli.