Fat embolism syndrome

FES & PE

1. FAT EMBOLISM SYNDROME & PULMONARY EMBOLISM FARAH AZUREEN ABD ZAIM

2. FAT EMBOLISM SYNDROME BACKGROUND EPIDEMIOLOGY CAUSES PATHOPHYSIOLOGY CLINICAL FEATURES DIAGNOSTIC CRITERIA INVESTIGATIONS TREATMENT REFERENCES

3. BACKGROUND First diagnosed in 1873 by Ernt Von Bergmann A systemic inflammatory cascade affecting multiple organ systems, particularly involving the triad of lungs, brain, and skin . ___ Key points Fat embolism syndrome is a clinical diagnosis with non-specific/insensitive diagnostic tests;  A high index of suspicion is important to ensure diagnosis;  The classic triad of respiratory changes, neurological abnormalities, and petechial rash is not always present;  Treatment is supportive;  Prophylactic steroid therapy may be considered for patients at a high risk

4. definition 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) : A physiological response to fat within the systemic circulation. It occasionally causes multisystem dysfunction, the lungs are always involved and next is brain.

5. epidemiology Most commonly associated with long bones fractures and the pelvis and more frequent in closed rather than open fractures. Incidence increases with number of fractures involved. 3-4% with isolated long bone trauma 10-15 % with polytrauma Some cases are associated with trauma in the absence of fractures and rare cases. Mortality is estimated to be 5–15% overall, but most patients will recover fully. Orthobullet

6. Causes TRAUMA RELATED NON TRAUMA RELATED Long bone fractures (e.g. femur, tibia) Acute p ancreatitis Pelvic fractures Diabetes mellitus Fractures of other marrow-containing bones Osteomyelitis Orthopaedic procedures (e.g. intramedullary nailing, pelvic and knee arthroplasty) Bone tumor lyses Soft tissue injuries (e.g. chest compression with or without rib fractures) Steroid therapy Liposuction Sickle cell hemoglobinopathies Bone marrow harvesting and transplant Alcoholic (fatty) liver disease Burns Lipid fusion

7. pathophysiology Exact pathophysiology of FES remains unclear. Two theories have been proposed regarding causes of FES : Mechanical theory embolism is caused by droplets of bone marrow fat released into venous system Biochemical theory stress from trauma causes changes in chylomicrons which result in formation of fat emboli

8. Mechanical Theory Fat droplets, released by marrow of adipose tissue following injury, embolise throughout circulation causing microvascular occlusion. As they travel through the venous system, they trigger rapid aggregation of platelets and accelerated fibrin generation, eventually lodging in the pulmonary arterial circulation. Pulmonary capillary obstruction leads to interstitial hemorrhage and edema, alveolar collapse, and reactive hypoxemic vasoconstriction. Massive fat emboli may also lead to macrovascular obstruction and shock . Fat cells may also enter the arterial circulation via a patent foramen ovale or directly through the pulmonary capillary bed, causing the characteristic neurological and dermatologic findings FES.

9. 2. Biochemical theory Toxicity of Free Fatty Acid (FFA) Circulating FFA directly affect pneumocytes , producing abnormalities in gas exchange. Co-existing shock, hypovolemia and sepsis impair liver function and augment effect of FFA Hormonal changes caused by trauma or sepsis induce systemic release of FFA as chylomicrons. Acute-phase reactants (CRP) cause chylomicrons to coalesce. It explains non traumatic form of FES and why symptoms take 12 hours to develop.

10. Clinical features May develop 24-72h after trauma or surgery Characterized by classic triad of FES: Respiratory failure Neurological abnormalities Dermatological changes

11. Respiratory changes 1 st clinical feature to present (earliest) Dyspnea, tachypnea, hypoxemia May progress to respiratory failure and acute respiratory distress syndrome (ARDS)

12. Neurological abnormalities Typically manifest after the respiratory changes.  Resulted from cerebral embolism which produce neurological signs in up to 86% of cases. Leads to wide spectrum of changes: mild confusion and drowsiness to severe seizures. More common presentation : acute confusional state. Focal neurological signs may also present including hemiplegia, aphasia, apraxia, visual field disturbances, anisocoria and decorticate posturing. Almost all neurological deficits are transient and fully reversible.

13. Dermatological changes Petechial rash (non palpable). It occurs in up to 60% of cases. Last component of the triad to develop. Appears within first 36h and is self-limiting and disappear within 7 days. Due to embolization of small dermal capillaries leading to extravasation of erythrocytes. Location : conjunctiva, oral mucous membrane, skin fold of the upper body especially neck and axilla.

14. Other changes.. Pyrexia Cardiovascular changes include tachycardia, myocardial depression, ECG changes indicative of right heart strain Retina shows soft fluffy retinal exudates with macular oedema scotomata ( Purtscher's retinopathy ) Renal changes such as oliguria, lipiduria , proteinuria, or haematuria . Hepatic damage may manifest as jaundice.

15. Diagnosis criteria Diagnosis of FES is usually made from clinical findings. The most commonly used criteria is Gurd’s and Wilson’s Criteria. Other indexes: Lineques’s criteria Schonfeld’s criteria

16. Gurds’s diagnosticcriteria MAJOR Hypoxemia (Pao2 < 60mmHg) CNS depression (changes in mental status) Petechial rash Pulmonary edema MINOR Tachycardia Pyrexia Retinal emboli Fat in urine or sputum Jaundice Renal changes Laboratory features: Thrombocytopenia Elevated ESR Anemia Microglobulinemia at least 1 major + 4 minor criteria

17. Lindeque’s criteria

18. Schonfeld’s criteria -a quantitative measure to diagnose FES -it ranks signs and symptomsof fes in relation to their incidence of presentation

19. Laboratory studies ARTERIAL BLOOD GAS Hypoxemia (PaO2<60mmHg) HEMATOLOGICAL TESTS Thrombocytopenia Anemia High ESR

20. BIOCHEMICAL TESTS Liver function test Renal profile Serum electrolytes, e.g hypocalcemia URINE & SPUTUM EXAMINATION May detect fat globules Non specific Blood lipid concentration is not helpful for diagnosis because circulating fat concentrations do not correlate with the severity of the syndrome.

21. imaging CHEST X-RAY May be normal initially Shows multiple flocculent shadows (snow storm appearance) Serial radiographs reveal increasing diffuse bilateral pulmonary infiltrates ECG Evidence of right heart strain / ischemic patterns and tacycardia .

22. Treatment & prevention There are no specific therapy for FES. Prevention, early diagnosis, and adequate symptomatic treatment are important. Mainstay of treatment : supportive

23. Supportive medical care Maintenance of adequate oxygenation and ventilation Maintenance of hemodynamic stability Administration of blood products as clinically indicated Adequate hydration Prophylaxis of deep venous thrombosis Nutrition Adequate analgesia

24. Maintenance of adequate oxygenation and ventilation High flow rate oxygen is given to maintain the arterial oxygen tension in the normal range. Mechanical ventilation and PEEP may be required to maintain arterial oxygenation. Hemodynamic stability Maintenance of intravascular volume is important, because shock can exacerbate the lung injury causes by FES. Albumin has been recommended for volume resuscitation in addition to balanced electrolyte solution. It restores blood volume and also binds with fatty acid and thus decrease of lung injury.

25. prophylaxis Early fracture stabilization Early fracture stabilization (within 24 hours) of long bone fracture Reduce risk of fat emboli Limit the elevation in intraosseous pressure during orthopaedic procedures It reduces the intravasation of intramedullary fat E.g : use of external fixation for definitive fixation of long bone fractures . Adequate fluid resuscitation and maintenance of hydration Maintenance + deficit

26. Example of calculation: A 70 kg man sustained closed fracture of left tibia. Eg : Hip : 2L Femur : 1.5L Tibia : 1L 70kg Maintenance =1000mL+500mL+ 1000mL =2500mL (5pints) Deficit (tibia) =1000 (2pints) Total =7 pints/24 hours

27. Venous thromboembolism (VTE) Encompasses two interrelated conditions Pulmonary embolism (PE) Deep vein thrombosis (DVT) They share common risk factors, pathophysiologies and management

28. Risk factors 3 main factors contribute to the development of VTE:

29. Cont’d

30. Pulmonary embolism (PE) PE is the obstruction of blood flow to one or more arteries of the lung by a thrombus lodged in a pulmonary vessel. Occur when deep venous thrombi detach and embolize to the pulmonary circulation. Pulmonary vascular occlusion occurs and impairs gas exchange and circulation. 90% of PE results from DVT occurring in the deep veins of lower extremities. Procedures associated with PE: Hip fracture Elective total hip arthroplasty (activation of the clotting cascade) Elective total knee arthroplasty Spine fracture with paralysis

31. evaluation There are scoring systems to assist in the determination of likelihood of PE and thromboembolic events.  Modified Wells Criteria

32. Revised Geneva Score

33. investigations FBC : abnormalities in HB, WCC, Platelet Coagulation Profile : prolongation of PT and APTT Arterial blood gas : hypoxaemia , hypocapnea and respiratory alkalosis Plasma D-Dimer : >500ng/ mL. If less than 500ng/mL, PE is excluded. ECG : sinus tachycardia is often present. S1Q3T3 pattern

34. Chest xray : nuclear medicine ventilation-perfusion scan (V/Q) pulmonary angiography ( gold standard) helical chest CT (widely considered first line imaging modality)

35. prophylaxis Prophylaxis treatment should be determined by weighing risk of bleeding vs risk of pulmonary embolus Prophylaxis in hip & knee replacement mechanical prophylaxis -compressive stockings recommended -pneumatic compression devices (increase venous return and decrease stasis) medical treatment -anticoagulation

36. treatment Continuous IV heparin infusion followed by warfarin -as first line treatment technique continuous IV heparin infusion typically given for 7-10 days monitor heparin therapy with PTT (partial thromboplastin time) warfarin therapy typically given for 3 months monitor warfarin therapy with INR (international normalized ratio)

37. Thank you..