Tara Wofford
CA-1
4/28/10
Case: 75 yo M with PMH of DM2, OA, and hypothyroidism having bilateral TKA. Pt had unremarkable preop eval and negative stress test. Anesthetic for case was spinal with light IV sedation and 2L 02 via NC. After the tourniquet was released on knee #1 pt had drop in O2 sat to 92%, placed on facemask at 8L, sat improved to 98%. Sat dropped again after tourniquet release on knee #2 to 91%. Pt arrived in PACU on 15L NRB and
O2 sat 93%, pt was alert and oriented and VSS.
3 hours later pt still in PACU pt developed respiratory distress and noted to have acute deterioration of MS. He now has 02 sat 75%, tachypneic, bilateral rales, and barely arousable and not oriented to person.
He is intubated in PACU for respiratory distress, EKG and ECHO undiagnostic, CXR shows new bilateral opacities. Prior to transfer to ICU pt becomes hypotensive and pressors are initiated.
Fat Emboli : fat droplets in systemic circulation, occurs commonly in trauma patients and after ortho surgery involving long bone instrumentation. (Studies using ECHO and BAL show up to 90% incidence after multiple traumatic fracture and femoral reaming)
Fat Embolism Syndrome : FE with systemic inflammatory response that manifests as pulmonary, neuro, hemodynamic, and cutaneous symptoms.
Epidemiology:
-Can be immediate but onset usually 12-72 hours after initial insult
-1-3% with femur fx, 5-10% with multiple or bilateral
-More common in long bone and pelvic fractures or orthopedic procedures. More associated with closed fxs and cemented prosthesis.
-Clinical diagnosis, no specific test
-Mortality 5-15%
Pathophysiology :
Mechanical Phase:
- Fat emboli enter venous system via sinusoids in medulla
-Temporary occlusion of pulmonary capillary meshwork, the amount is variable depending on intramedullary pressure
-fat emboli can cross pulm capillary bed and effect end organs without presence of PFO or other cardiac septal defect
-HD changes: HTN,

PaO2,

PVR/PAP,

shunt
Biochemical Phase:
Alveolar cells secrete lipase and attempt to hydrolyze fat emboli
-In FES fatty acids initiate ARDS type rxn in lungs

-Fatty acids thought to activate alveolar macrophages
-DIC effect can be seen as well
Common clinical findings :
Pulm- dyspnea, tachypnea, rales, diffuse patch bilateral opacities on CXR, fat stain on
BAL
Neuro- ranges from delirium to coma, usually occurs after onset of pulm symptoms, transient and reversible in most cases
Hemodynamic- right heart strain, hypotension, tachycardia
Cutaneus- petechial rash on neck, chest, mucus membranes axillae, found in 20-50% of cases but is pathognomonic for FES
Workup:
Labs :
CBC/fibrinogen (anemia and thrombocytopenia, hypofibrinogenemia common)
ABG (increased A-a gradient)
BAL- fat globules commonly seen
Imaging:
CXR (new diffuse bilateral opacities)
Chest CT (Ground glass or ARDS type appearance)
Head CT (can be normal at first but may show embolic foci for diffuse hemorrhages)
Treatment:
Steroid therapy is first line although still debated
Supportive Care: about half will require intubation, may need pressors
Early stabilization of fractures
Use on non-cemented prosthesis or femoral venting by surgeon
SCHONFELD FAT EMBOLISM SYNDROME INDEX (score > 5 is predictive)
Petchial Rash 5
Diffuse Alveolar Infiltrates 4
Hypoxemia PaO2<70mmHG, FiO2 100% 3
Confusion
Fever >38

C
1
1
Heart Rate >120 bpm
Respiratory Rate >30
1
1