Downloaded 170 times
More Related Content
Similar to Fat embolism syndrome
Fat embolism syndrome
- 1.
- 2. First diagnosedin 1873 by Dr Von Bergmann Published in 1879 Fenger and Salisbury.
- 3. Fat Embolism: Traumaticfat embolism occurs in up to 90% of individuals with severe skeletal injuries, but < 10% of such patients have any clinical symptoms / signs Fat Embolism Syndrome: FE with clinical manifestation .
- 4. Fat Emboli: Fatparticles 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
- 5. Incidence: 1-3%femur #, 5-10% if bilateral or multiple. Mortality: 5-15% Clinical diagnosis, No specific laboratory test is diagnostic Mostly associated with long bone/pelvic #s, and more frequent in closed fractures. commanly with lower limb injury Onset is 24-72 hours from initial insult
- 7. Mechanical Theory Physicalobstruction of the pulmonary & systemic vasculature with embolized fat. Temporary rise in I/M pressure - forces marrow into injured venous sinusoids. Cor pulmonale - inadequate compensatory pulmonary vasodilatation. Microvascular lodging - local ischemia and inflammation. Release of inflammatory mediators, platelet aggregation, & vasoactive amines,veno arterial shunting,hypoxemia leeds to alveolar hypoperfusion leading to PD Size of fat globules 2 to 200 micron Blood vessele <75 micron
- 8. The biochemical theory Freefatty acid is culprit Circulating FFAs -directly toxic to Pneumocytes / capillary Endothelium in the lung – decrease surfactant ,nterstitial hemorrhage, edema & chemical pneumonitis. Local hydrolysis of Triglycerides and fat emboli by pneumocyte lipase -- Increase fatty acid . Coexisting shock, hypovolemia and sepsis - reduce liver flow exacerbate the toxic effects of FFAs.
- 9. H/E stain lung– - blood vessel with fibrinoid material and -optical empty space - lipid dissolved during the staining process.
- 10.
- 11. Dyspnea, Tachypnea Hypoxemia PaO2 < 60 mm Hg confusion
- 12. Clinically Tachpnea,Dyspnea, Hypoxia, rales, pleural friction rub & ARDS. High spiking temperatures. Hypoxemia - ventilation-perfusion mismatch & intrapulmonary shunting. Acute cor pulmonale - respiratory distress, hypoxemia, hypotension and elevated CVP. ½ of pts require mechanical ventilation
- 13. • Chest x-ray –shows multiple flocculent shadows (snow storm appearance). picture may be complicated by infection or pulmonary edema. – CT chest: ground glass opacification with interlobular septal thickening • CT Scan brain – may be normal or may reveal diffuse white-matter petechial haemorrhages • Helical CT Scan chest – may be normal as the fat droplets are lodged in capillary beds. Can detect lung contusion, acute lung injury, or ARDS may be evident.
- 14. ER admit AP &expiratory film so we cannot comment on cardiac shadow. However, there is no evidence of lung contusion, pneumo, haemo or pneumohaemothorax. SICU admit (12 hours later) upper lobe diversion and bilateral pulmonary infiltrates Altaf Hussain: “A Fatal Fat Embolism.” The Internet Journal of Anesthesiology, 2004. Volume 8 Number 2.
- 15. CNS signsusually occur after respiratory symptoms - nonspecific - features of diffuse encephalopathy Acute confusion, stupor, coma, rigidity, or convulsions - Transient and reversible in most cases CT Head: general edema – nonspecific MRI brain: Low density on T1 & High intensity T2 signal - correlates to degree of impairment
- 16. post operative day14 and shows evolving cortical infarctions post operative day 2 showing multiple hyperintense areas consistent with multiple emboli Source:http://www.ispub.com/journal/the_internet_journal_of_anesthesiology/volume_19_number_2/article/acute_fatal_fat_embolism_syndrome_in_bilateral_total_knee_arthroplasty_a_review_of_the_fat_embolism_syndrome.html
- 17. Reddish-brown non-palpablePetechial rash - upper anterior body, chest, neck, upper arm, axilla, shoulder, oral mucous membranes and conjunctivae in 20 - 50% patients.2 to 3re day Resolvs in 7 day Pathognomonic, however, it appears late and disappears within hours. Results from occlusion of dermal capillaries by fat globules - extravasations of RBC
- 18. Retinopathy (exudates,cotton wool spots, hemorrhage) Lipiduria Fever DIC Myocardial depression (R heart strain) Thrombocytopenia Anemia, Decreased Hematocrit Hypocalcemia
- 19. Gurd’s criteria Mostcommonly used 1 major, plus 4 minor
- 21. Clinical examinationpreferred over diagnostic
- 22. Continuous pulseoximetry monitoring - at-risk patients ( those patients with long bone fractures) - detecting desaturations early. Consultations recommended include orthopedists, neurologists/ neurosurgeons, trauma care specialists, critical care specialists, pulmonologists, hematologists, and nutritionists.
- 23. The mosteffective prophylactic measure - operative reduction/rigid fixation of long bone fractures as soon as possible. Higher incidence (5 fold) when fixation delayed greater than 24 hours. Supportive care includes maintenance of adequate oxygenation and ventilation, stable hemodynamics, blood products as clinically indicated, hydration, prophylaxis of DVT and stress-related GI bleeding.
- 24. Albumin hasbeen recommended - not only restores blood volume / binds fatty acids - may decrease the extent of lung injury. High dose corticosteroids have been effective in preventing development of FES in several trials, but controversy on this issue still persists.
- 25. Heparin hasalso been proposed as it activates lipase, but no evidence exists for its use in FES. Ethanol/alcohol in bolus dose iv :as lipase inhibitor
- 26. Difficult topredict –FES is frequently subclinical or overshadowed by other illnesses or injuries. Increased alveolar-to-arterial oxygen gradient and neurologic deficits, including coma, may last days or weeks.
- 27. As inARDS, pulmonary sequelae usually resolve almost completely within 1 year. Residual subclinical diffusion capacity deficits may exist. Residual neurologic deficits may range from nonexistent to subtle personality changes to memory and cognitive dysfunction to long-term focal deficits.
- 29.
Editor's Notes
- #5 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
- #15 21 year old involved in a MVC. Femur and tibia fractures lacerations on head. Stable in ER for 12 hours Then his heart and respiratory rates then increased gradually and oxygen saturation decreased. Serial arterial blood gases (ABGs) were done showing progressive acidosis, hypercapnia and severe hypoxemia. Bradycardia and hypotension – died 26 hours after admission.
- #17 75 yr-old Male with knee arthroplasty (reconstructive ortho surgery) Had diabetes. Developed encepholopathy Source:http://www.ispub.com/journal/the_internet_journal_of_anesthesiology/volume_19_number_2/article/acute_fatal_fat_embolism_syndrome_in_bilateral_total_knee_arthroplasty_a_review_of_the_fat_embolism_syndrome.html
- #22 Clinical examination is still the preferable diagnostic method in fat embolic syndrome as there is no universal criteria used for diagnosis; which is always made on clinical grounds.