fat embolism syndrome orthopaedics slides

fes

1. FAT EMBOLISM SYNDROME Presenter : Dr Seetha Govindaraju Supervisor : Dr Sallehudin

2. 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.

3. ETIOLOGY TRAUMATIC ATRAUMATIC Long bone ( Femur, Tibia ) fracture Diabetes Pelvic fractures Pancreatitis, Orthopaedic procedures (intramedullary reaming, hip and knee arthroplasty) Osteomyelitis Soft tissue injuries ( eg chest compression with or without rib fractures) Sickle cell haemoglobinopathies Burns SLE, Liposuction panniculitis Bone marrow harvesting and transplant Steroid therapy, Lipid infusion, Cyclosporine A solvent Bone Marrow biopsy

4. 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. PATHOPHYSIOLOGY

5. 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.

6. CLINICAL FEATURES Diagnosis is made CLINICALLY NOT CHEMICALLY. It does not matter how much fat globules are in the circulation, it just matters if you have their side effects. FES typically manifests 24 to 72 hours after the initial insult. Rarely <12 hrs or >72 hrs. History The history of a patient with fat embolism may include the following: Major blunt trauma, usually resulting in long-bone fractures, pelvic fractures, or both Elective long-bone orthopedic procedures or cardiothoracic procedures Parenteral lipid infusion Recent corticosteroid administration

7. CLINICAL MANIFESTATION TRIAD OF FES RESPIRATORY ABNORMALITIES CNS MANIFESTATION DERMATOLOGY CHANGES Dyspnea Tachypnea Hypoxemia

8. CNS Manifestations: from mild headache to significant cerebral dysfunction (restlessness, disorientation, confusion, seizures, stupor or coma) Fortunately, almost all neurological deficits are transient and fully reversible.

9. Rash Petechial rash on upper anterior trunk, arm and neck, buccal mucosa & conjunctivae , may be transient Results from occlusion of dermal capillaries by fat globules and then extravasations of RBC PATHOGNOMONIC, but only present in 20-50% of patients.

10. Ocular Manifestations On fundoscopy, Purtscher’s retinopathy may be seen Cotton wool exudates, macular oedema and macular haemorrhage can also be found.

11. CVS Involvement Early persistent tachycardia, though nonspecific, is almost invariably present in all patients with fat embolism Renal Manifestations Oliguria haematuria anuria

12. DIAGNOSTIC 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

13. GURD AND WILSON’S CRITERIA 1 MAJOR CRITERIA + 4 MINOR CRITERIA

14. LINEQUES CRITERIA

15. SCHONFELD’S CRITERIA

16. Investigations Hematology and Biochemistry Urine and Sputum Radiological

17. Hematological Investigations An unexplained anemia (70% of patients) and thrombocytopenia (platelet count <1,50,000 /mm3 in up to 50% of patients) are often found. Hypocalcemia (due to binding of free fatty acids to calcium) and elevated serum lipase have also been reported. Hypofibrinogenemia, raised ESR and prolongation of prothrombin time may be seen ABG reveals a low partial pressure of O 2 and low partial pressure of CO 2 with respiratory Alkalosis

18. Urine and sputum Analysis of the sputum or urine for fat has not proved to be accurate. Bronchoalveolar lavage and staining with Oil Red O can demonstrate neutral fat. Microscopic examination of the blood for fat globules when it is collected from pulmonary circulation through Swan-Ganz catheter is the diagnostic test.

19. Radiological CXR usually normal early on, later may show ‘snowstorm’ pattern- diffuse bilateral infiltrates , enlargement of right side of the heart. CT chest: ground glass opacification with interlobular septal thickening CT Head: general edema, usually nonspecific MRI brain: Low density on T1, and high intensity T2 signal, correlates to degree of impairment Diffusion weighted-MRI (DW-MRI) of the brain showing a “Star Field” pattern of multiple small high-intensity lesions with diffusion restriction supports the diagnosis.

20. Management There is no specific therapy for the fat embolism syndrome, so prevention, early diagnosis, and adequate symptomatic treatment are of paramount importance Adequate oxygenation and ventilation Stable hemodynamics Blood products as clinically indicated Hydration / i.v. fluids Prophylaxis of deep venous thrombosis and stress related gastrointestinal bleeding

21. Management 1) Early fracture stabilization Early fracture stabilization (within 24 hours) of long bone fracture 2) 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. 3) Adequate fluid resuscitation and maintenance of hydration Maintenance + deficit

22. PULMONARY EMBOLISM 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

23. EVALUATION There are scoring systems to assist in the determination of likelihood of PE and thromboembolic events. 1. Modified Wells Criteria

24. 2. Revised Geneva Score

25. 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

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

27. I M A G I N G Chest x-ray is usually normal Findings, such as Focal oligaemia ( westermark sign ), A peripheral wedge-shaped opacity, usually in the lower half of the lung field ( hampton’s hump ), or An enlarged right descending pulmonary artery ( Pallas’s sign ) are rare

28. I M A G I N G

29. 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

30. T R E A TME N T 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)

31. REFERENCE Essential Orthopaedics Principles and Practice, Manish Kumar Varshney , Jaypee Publishers Apley’s and Solomon’s System of Orthopaedics and Trauma, 10 th Edition, CRC Press, Taylor and Francis Group Textbook of Orthopaedics and Trauma, Second Edition, GS Kulkarni, Jaypee Publishers Concomitant fat embolism syndrome and pulmonary embolism in a patient with a femoral shaft fracture. Masatomo Ebina , Akira, Takahiro 2015 Jul 3.  doi :  10.1002/ams2.127