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Steve Morgan, MD & Scott Adams, MD Original Authors: Steve Morgan, MD; March 2004;

Acute Respiratory Distress Syndrome, Fat Embolism, & Thromboembolic Disease in the Orthopaedic Trauma Patient. Steve Morgan, MD & Scott Adams, MD Original Authors: Steve Morgan, MD; March 2004; New Authors: Steve Morgan, MD & Scott Adams, MD; Revised January 2007 and November 2011. Define

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Steve Morgan, MD & Scott Adams, MD Original Authors: Steve Morgan, MD; March 2004;

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  1. Acute Respiratory Distress Syndrome, Fat Embolism, & Thromboembolic Disease in the Orthopaedic Trauma Patient Steve Morgan, MD & Scott Adams, MD Original Authors: Steve Morgan, MD; March 2004; New Authors: Steve Morgan, MD & Scott Adams, MD; Revised January 2007 and November 2011

  2. Define ARDS FES Thromboembolic Disease Understand Etiology & Physiology of each Condition Understand Prevention Diagnosis Treatment Outcomes Objectives

  3. ARDSAcute Respiratory Distress Syndrome • Acute respiratory failure in the post traumatic period characterized by a decreased PaO2 and a diffuse and often massive extravasations of fluid from the pulmonary vasculature to the interstitial space of the lungs.

  4. ARDS Clinical Definition • Acute onset of symptoms • Ratio of PaO2 to FIO2 of 200 mm Hg or less • Bilateral infiltrates on CXRs • Pulmonary arterial wedge pressure of 18 mm Hg or less or no clinical signs of left atrial hypertension • American-European Consensus Conference (AECC) on ARDS, 94

  5. ARDS • Incidence 5% – 8% after polytrauma • Much lower in isolated fracture • Mortality up to 40% • Uncommon in Children and the Elderly

  6. Trauma Massive Transfusion Embolism Sepsis Aspiration Abdominal Distension Pulmonary Edema Prolonged LOC Cardiopulmonary Bypass Pancreatitis Major Burns ARDSCommon Causes MULTIFACTORAL

  7. ARDS Etiology • ARDS related to MODS • Release of inflammatory mediators results in organ dysfunction Inflammatory Mediators Organ Injury Trauma

  8. Systemic Inflammatory Mediators Damage to Endothelial Lining Increased Capillary Permeability Fluid Extravasation Alveolar Collapse Decreased Pulmonary Compliance Ventilation Perfusion Abnormalities Arteriolar Hypoxemia ARDS PATHOPHYSIOLOGY

  9. ARDS Chest Radiograph AutopsySpecimen

  10. ARDS Chest CT Scan

  11. Limiting Blood Loss Decreasing Transfusion Requirements Early Stabilization Of Unstable Fractures Early Prophylactic Mechanical Ventilation ARDSPrevention Temporary Ex-Fix For Stabilization

  12. ARDS Treatment • Ventilator Support • Acceptable ABG’s • Avoid further alveolar damage • Toxic FIO2 • Barotrauma • General Organ Support • Research • Optimal ventilator settings • Pharmalogical agents

  13. ARDSOutcome • Significant Cause of Mortality • Major Cause of Death in Patients with the Lowest ISS scores • 30% - 40% Mortality Rate • Mortality Rate Slowly Decreasing with Changing & Improving Therapy

  14. Fat Embolism Syndrome(FES) • A condition characterized by hypoxia, confusion and petechiae presenting soon after long bone fracture and soft tissue injury. • Diagnosis of Exclusion

  15. FES • Often Placed in the Category of ARDS • May share common pathological pathways • R/O other Causes of Hypoxia & Confusion • Index Patient • young adult with isolated LE injury seen after long transfer with no supporting therapy or splintage.

  16. FES • Occurs in 0.9 – 8.5% of all fracture patients • Up to 35% of the multiply injured • Mortality 2.5% • Rare in upper limb injury and children

  17. Etiology • The likely pathogenetic reaction of lung tissue to shock, hypercoagulability and lipid metabolism • Mechanical Theory • Biochemical Theory

  18. Mechanical Theory • Fracture Liberates Fat • Intravasation - Fat Enters Venous System • Fat Causes Mechanical Obstruction

  19. Mechanical Theory FES To Brain On MRI • Systemic Fat Embolization • Patent Foramen Ovale • Pulmonary Pre-Capillary Shunts • Skin petechiae, CNS signs

  20. Biochemical Theory • Neutral Fat and Chemical Mediators Released at Time of Fracture • Neutral Fat Metabolized by Lipases releases Free Fatty Acids • Free Fatty Acids Result in Endothelial Lung Damage

  21. Major Criteria Hypoxemia CNS Depression Petechial Rash Pulmonary Edema Minor Criteria Tachycardia Pyrexia Retinal Emboli Fat in Urine Fat in Sputum Thrombocytopenia Decreased Hematocrit FES Diagnosis Gurd et al

  22. FES Diagnosis • Gurd & Wilson Criteria • At least 1 Major Sign • 4 Minor Signs Gurd et al

  23. FES Prevention • Appropriate Splinting • Early Fracture Stabilization • Oxygen Therapy

  24. FES Prevention • Therapies • Fluid Loading • Hypertonic Fluid • Alcohol • Heparin • Dextran • Aspirin • None Shown to be Effective

  25. FES Treatment • Supportive • Oxygen Therapy to maintain PaO2 • Mechanical Ventilation • Adequate Hydration

  26. FES Treatment Steroids • Steroids • Decrease endothelial damage • 30mg/kg initial dose repeated @ 4 Hours, 1gm dose repeated @ 8 Hours: Total 3 Doses • Complications - Frequent • Infection • GI • Steroid Therapy Avoided Secondary To Poor Risk Benefit Ratio

  27. ARDS MODS Threshold Post Injury Inflammatory Response in 2 Patients Systemic Effects of Trauma Second Hit in susceptible patients 24 hours 48 hours Injury (First Hit) IM Nailing as a Cause of Secondary Systemic Injury

  28. Early Total Care Definitive Early Fixation Nail or Plate Damage Control Temporary Stability External Fixator Limit Further Blood Loss Limit Anesthetic Time Delay Definitive Fracture fixation Fracture Fixation Technique-Controversial-

  29. Effect of IM Nailing • Increased IM Pressure • Embolic Showers On Echocardiograms • Caused by • Canal Opening • Reaming • Nail Insertion (both reamed & unreamed)

  30. Fracture Fixation Technique-Controversial- • IM Nail - Reamed vs Un-Reamed • Decreased with Unreamed Technique • Pape et al • No Difference • Keating et al • Canadian OTS • IM Nail Reamed vs Plate Osteosynthesis • No Difference In Pulmonary Dysfunction • Bosse et al

  31. DVT Incidence • DVT occurrence 60% if ISS >9. • 35%-60% DVT in pelvic fracture • PE-Most common preventable cause of death in trauma.

  32. Virchow Triad

  33. Hypercoaguability • Tissue Thromboplastin • Activated Procoagulants • Decreased Fibrinolytic Activity • Ineffective Heparin Clearance of Activated Clotting Factors • Catecholamine Release

  34. Endothelial Injury • Direct Trauma to Vein at time of Injury • Compression of the Vein Secondary to Fracture Position • Vein Manipulation at Time of Fracture Fixation

  35. Venous Stasis • Immobilization • Hypotension • Venous Occlusion • Edema • Fracture Position • Tourniquet

  36. DVT Prevention Goals • Clinically significant events • PE • Post Thrombotic syndrome • Low Complication Rate • High Compliance Rate • Cost Effective

  37. DVT Prevention Mechanical Non Pharamcologic Pneumatic Compression Elastic Stockings Vena Cava Filter

  38. DVT Prevention Pharamcologic Pentasacharides Unfractionated Heparin Elastic Stockings LMWH Heparin Warfarin Oral Anticoagulants

  39. Elastic Stockings Mechanical Compression Devices Early Mobilization IVC Filter (PE Prophylaxis) Pentasaccharide Low Molecular Weight Heparin Heparin Aspirin Warfarin Prophylaxis

  40. Mechanical Methods • Activity • Compression Stockings • Sequential Compression Device • Pedal Pumps Mechanism of Action • Decrease Stasis •  Fibrinolytic Activity

  41. IVC Filter Indications • Anticoagulation Prohibited • High Risk Patients • DVT Prior to Necessary Surgery • PE Despite Anticoagulation

  42. Prevents Major PE Low Morbidity 96% Patent 8% Migration 4% PE Filter insertion in the ICU Expensive Invasive Does not treat DVT Venous Insufficiency Filter Occlusion IVC Filter Advantages Disadvantage

  43. No Recommendation for Vena Caval Filter ACCP Recommendation on Vena Cava Filter

  44. Pentsaccharide • Selective Inhibitor of Activated Xa • Decreased DVT rate with no change in major bleeding rate compared to LMWH • Eriksson B I et al N Engl J Med 2001 • Increased risk of minor bleeding • Delay administration for several hours after surgery and removal of epidural catheter

  45. Low Molecular Weight Heparin(LMWH) • Potentiates Antithrombin III • Inhibits Factor Xa & II • Minimal effects on other Factors

  46. No Monitoring Increased Efficacy Longer 1/2 life Predictable Response Lower risk of thrombocytopenia Parenteral Administration Cost LMWH Advantages Disadvantage

  47. Heparin • Heparin Potentiates Anti-Thrombin III Activity • Complex Inhibits • Thrombin (IIa), IXa, Xa • Heparin effect relative short duration • Reversed with Protamine Sulfate • Significant hemorrhage risk

  48. Low Cost No Monitoring Convenient Relatively Low Incidence of Bleeding Insufficient Efficacy in High Risk Patients Unpredictable Responses Heparin Induced Thrombocytopenia SQ Heparin Advantages Disadvantage

  49. Oral Administration Tolerated well In-expensive No Monitoring ? Efficacy when used alone GI Intolerance Prolonged anti-platelet effect Aspirin Advantages Disadvantage

  50. Aspirin • Inhibits cyclooxygenase • Decreases Platelet Adherence • ? Effectiveness in Musculoskeletal Trauma • Venous clots not typically found to have Platelet aggregates

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