Download Free Medical Acute Respiratory Distress Syndrome-Fat Embolism and Thromboembolic Disease PowerPoint Presentation

Acute Respiratory Distress Syndrome-Fat Embolism and Thromboembolic Disease PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical titled "Acute Respiratory Distress Syndrome, Fat Embolism, & Thromboembolic Disease in the Orthopaedic Trauma Patient" by Dr Christopher Domes MD, AT ret and Dr Reza Firoozabadi MD, MA.

This medical talks about Acute Respiratory Distress Syndrome, Fat Embolism, and Thromboembolic Disease in the Orthopaedic Trauma Patient.

Tags : Acute Respiratory Distress Syndrome, Fat Embolism, Thromboembolic Disease, Orthopaedic Trauma Patient, Emergency Medicine, Emergency Medicine

Published on : Apr 14, 2023 | Views : 960 | Downloads : 1

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Acute Respiratory Distress Syndrome, Fat Embolism, & Thromboembolic Disease in the Orthopaedic Trauma Patient Dr Christopher Domes MD, AT ret Dr Reza Firoozabadi MD, MA January 2016
Slide 2-

Objectives Review History Diagnosis Classification Epidemiology Pathophysiology Treatment Acute Respiratory Distress Syndrome Fat Embolism Venous Thromboembolism
Slide 3-

Acute Respiratory Distress Syndrome Relatively clear CXR Diffuse bilateral coalescent opacities
Slide 4-

ARDS- History “ The respiratory-distress syndrome in 12 patients was manifested by acute onset of tachypenia, hypoxemia and loss of compliance after a variety of stimuli; the syndrome did not respond to usual and ordinary methods of respiratory therapy”
Slide 5-

Consensus definition with empirical evaluation Timing- Within 1 week of clinical insult or new/worsening respiratory symptoms Chest Xray- Bilateral opacities- not fully explained by effusions, collapse or nodules Origin of edema- Respiratory failure not fully explained by cardiac failure, fluid overload- Needs objective assessment (echo) Oxygenation- Mild- 200mmHg < PaO2/FiO2, ≤ 300mmHg w/ PeeP or CPAP ≥ 5cm H2O Moderate- 100 mmHg < PaO2/FiO2, ≤ 200 mmHg w/ PEEP ≥ 5 cm H2O Severe- PaO2/FiO2 ≤ 100mmhg w/ PEEP ≥ 5 cm H2O
Slide 6-

Outcomes with Berlin Definition Severity of ARDS found to be associated with worse mortality and duration of requiring mechanical ventilation. Mortality increase with level of oxygenation Mild- 27% Moderate- 32% Severe- 45% Mechanical ventilation requirements Mild- 5 days Moderate- 7 days Severe- 9 days
Slide 7-

ARDS Epidemiology Incidence 78.9 per 100,000 person-years 38.5% in hospital mortality rate -190,600 cases per years in US -74,500 associated deaths per year in US =
Slide 8-

Epidimiology Age associated increase in Incidence 15-19 yo’s- 16 per 100,000 75-84 yo’s- 306 per 100,000 Age associated increase in Mortality 15-19 yo’s- 24% >85 yo’s- 60%
Slide 9-

Causes Sepsis Aspiration Trauma Transfusion Embolism Burns Systemic inflammatory process Multi-organ failure Drug overdose Stem-cell transplant Multifactorial
Slide 10-

Pathophysiology Lung Injury Decreased gas exchange Increase pulmonary arterial pressure Decreased lung compliance Fluid accumulation in lung interstitium and alveoli IL-6 IL-1 Cytokines Alveolar & Vessel damage
Slide 11-

Pathology Slide of Alveoli Hyaline membranes ARDS patient Injury to Type I (and Type II) pneumocytes Decreased surfactant production Plasma protein leak Inactivate surfactant with increase in proteinaceous material in alvioli (albumin and fibrin) Slide from personal collection of Dr Rodney A. Schmidt MD (UW Pathology)
Slide 12-

Differential Diagnosis Underlying lung disease Pulmonary fibrosis, chronic interstitial lung disease Cardiogenic pulmonary edema Diffuse alveolar hemmorage Pneumonia
Slide 13-

ARDS Treatment Supportive care Nutritional support GI prophylaxis Glucose control Sedation/paralysis VTE prophylaxis Hemodynamic monitoring Control causes of sepsis Prevent aspiration/pneumonia Treat underlying injuries/organ dysfunction Prone positioning Respiratory specific Ventilator support Fully supported ventilator mode Low tidal volume ventilation High PEEP Intermittent recruitment measure High % inspired O2 All carry their own potential associated complications Ongoing area of research
Slide 14-

Complications of ARDS Delirium VTE Stress ulcers Pressure ulcers Catheter associated infections UTI’s Ventilator associated Pneumonia ~2x incidence as compared to pts without ARDS on ventilator Mechanical trauma from ventilator settings (barotrauma)
Slide 15-

Key Clinical Factors Early identification and initiation of supportive care are essential. Remember VTE prophylaxis and nutritional support Patients with ARDS have high mortality rates as well as extended period of ventilator support Pulmonary status may limit ability for positioning patient for procedures
Slide 16-

68 year old F involved in MVC with bilateral femur fractures and traumatic head injury. Portable X-ray in Trauma bay after ET tube placed
Slide 17-

Worsening respiratory status and vent settings in ICU waiting for operative stabilization of bilateral femurs and clearance by neurosurgery.
Slide 18-

Fat Emboli Syndrome(FES)
Slide 19-

FES- History First described in 1861 by Zenker, F. A. Fat desposits in the lungs of postmortum accident patients Clinical description by Bergmann, E. B. 1873 Confusion, dyspnea, and petechiae Classic Triad
Slide 20-

Definition Syndrome 1) hypoxemia 2) respiratory insufficiency 3) neurologic impairment 4) +/- petechial rash Usually within the first 24-72 hours In the setting of Long bone or pelvic fracture No other etiology- PE, ARDS Diagnosis of Exclusion
Slide 21-

FES Epidemiology Incidence 0.5% to 8.5% of all fracture patients Possibly up to 35% in patients with long bone fracture Uncommon in young patients and isolated upper extremity injuries Mortality 2.5% to 8.5%
Slide 22-

Incidence- 27 patients identified 0.9% of patients with long bone fractures Mean Injury Severity score of 9.5 52% single long-bone fracture 48% multiple long-bone fractures Sign or Symptom associated with diagnosis of FES Hypoxia (96%) Tachycardia (heart rate > 120 beats per minute (93%) Temperature higher than 39 degrees C (70%) Unexplained anemia (67%) Mental status changes (59%) Petechiae (33%) Fat Embolism Syndrome: A 10-Year Review Eileen M. Bulger, MD; Douglas G. Smith, MD; Ronald V. Maier, MD; Gregory J. Jurkovich, MD Arch Surg. 1997;132(4):435-439.
Slide 23-

Overall mortality rate of 7%. Author conclusions FES is a diagnosis of exclusion FES is rare and may be masked by associated injuries No association between FES and fracture pattern or location was found Early intramedullary fixation did not increase the incidence or severity of FES FES management remains primarily supportive Fat Embolism Syndrome: A 10-Year Review Eileen M. Bulger, MD; Douglas G. Smith, MD; Ronald V. Maier, MD; Gregory J. Jurkovich, MD Arch Surg. 1997;132(4):435-439.
Slide 24-

Pathophysiology Two major theories on how injury occurs with FES Mechanical Gauss, H. 1924. The pathology of fat embolism. Arch. Surg. 9:593-605 Physiochemical Lehman, E. P., Moore, R. M. 1927. Fat embolism including experimental production without trauma. Arch. Surg. 14:621-62
Slide 25-

Mechanical Fracture Fat uptake by venous system Fat causes obstruction Fat liberated from bone Skin/eyes Brain Lungs Patent Foramen Ovale Hypoxia Petechiae Confusion
Slide 26-

Physiochemical High amounts of unbound fatty acids (as occurs with a fracture) in the blood stream leads to toxic metabolites that effects pulmonary, cerebral and coetaneous tissue. Experimentally seen w/ injection of fatty acids into dogs resulting in pulmonary failure (Cahill, J. M. 1974) Amount of fatty acids released is the blood stream appears proportional to the magnitude of injury. (McNamara, J. D. 1972)
Slide 27-

Prevention of FES Early immobilization With both operative fixation or temporary stabilization (Riska EB et al. 1982) Corticosteroids Controversial- unknown dose or duration Meta-analysis by Bederman et al. 2009 shows may prevent hypoxia and FES but NO mortality benefit
Slide 28-

Treatment of FES Supportive therapy Oxygen Maintain a high PaO2 level May require mechanical ventilation Hydration Corticosteroids?
Slide 29-

FES with Facture Care Overall remains controversial Definitive Care vs Damage Control Early immobilization is preventative
Slide 30-

Three principle factors that control clinical course 1. Initial degree of injury (1st hit) 2. Individual biological response 3. Type of Treatment (2nd hit) DCO intervenes here to provide- Temporary stability , decrease blood loss, help with pain control, and allow for the 1st hit and initial biological response to occur with a reduced 2nd hit as compared to definitive fixation. Definitive fixation occurs at a delayed date.
Slide 31-

Reaming and FES Any intramedullary pressure increase of more that 40mmHG is associated with fat emboli. Includes guide wire insertion Highest pressure at initial insertion Solid fat have been seen w/ pressures > 200mmHg Pressure while reaming depends on Compressive force while reaming Sharpness of reamer Drill speed Reamer head shape Conical w/ large flutes is better – Muller CA et al. 2000
Slide 32-

No difference in pulmonary complications or mortality in patients with femur fractures treated with reamed nails vs plate fixation No difference in reamed vs. unreamed nailing
Slide 33-

Case Examples 57 yo male involved in forklift accident with R open GA III-B tibia-fibula fracture.
Slide 34-

Initially taken for I&D, spanning external fixation and antibiotic bead placement on injury day 1 and transferred to the floor post-op.
Slide 35-

POD #2 developed mental status changes, desaturation to 89% on 4L NC and transferred to ICU. CT done which showed filling voids concerning for FES. Found to have patechial rash diffusely over body. No other clear etiology.
Slide 36-

Patient was treated with supportive oxygen with recovery of his mental status and pulmonary status over next 4 days. Discharged from ICU to floor on HD #6. Underwent staged management of his fracture with antibiotic spacer placement and eventual bone transport. Full mental status and pulmonary recovery.
Slide 37-

HPI: 20 y/o female, suicide attempt by trying to walk into traffic: Open L femoral shaft fracture Closed L tibial shaft fracture Closed R femoral shaft fracture Pulmonary contusion 12cm R scapular laceration/degloving Head lacerations PMHx: Asperger’s, depression, gender dysphoria Clinical Case
Slide 38-

Patient received appropriate chemoprophylaxis with enoxaparin 30mg SC. No missed doses. On hospital day 2, patient taken for I&D L femur, IMN of all three fractures. Open L femoral shaft fracture Closed L tibial shaft fracture Closed R femoral shaft fracture
Slide 39-

ppt slide no 39 content not found
Slide 40-

ppt slide no 40 content not found
Slide 41-

Post-operatively, patient was extubated but found to have decreased mental status and hypoxemia requiring re-intubation. CT –PE protocol showed a small apical segmental pulmonary embolus MRI brain obtained showing diffuse punctate foci of restricted diffusion in "star field" pattern consistent with Fat Emboli Syndrome Echo demonstrated patent foramen ovale
Slide 42-

Patient treated with heparin drip, high dose statin, supportive care in ICU Patient failed extubation attempts required tracheostomy Remaining Hospitalization: Mental status slowly improved Hospital Acquired PNA Dischargd to inpatient Rehab
Slide 43-

Long bone fractures with Classic Triad: Respiratory Changes (dyspnea, tachypnea, hypoxemia) Neurological Abnormalities (range from confusion to seizures) focal neurological signs, hemiplegia, aphasia, apraxia, visual field disturbances, and anisocoria Petechial Rash (conjuctiva, oral mucous, neck & axilla) appears within the first 36 h and is self-limiting Generally disappearing completely within 7 days Treatment- Supportive care Case- Learning Points
Slide 44-

Venous Thromboembolism(VTE) Deep Vein Thrombosis (DVT) & Pulmonary embolism (PE)
Slide 45-

DVT Clotting of blood that obstruct a deep vein in an extremity. Most commonly seen in the lower extremities Can be obstructive or non-obstructive
Slide 46-

PE Clotting of blood that obstructs a veins of any degree in the lungs. Ranges from blockage of small sub-segmental pulmonary arteries to segmental and massive emboli blocking an entire pulmonary artery.
Slide 47-

History DVT Described as far back as 1271 Guillaume de Saint Pathus- described a case of calf swelling that extended up the leg of a 20 year old cobbler. 1676: Wiseman- DVT is a consequence of an alteration of blood. 1793: Hunter - occlusion of the vein by blood clots Galanaud, JP et al. 2013
Slide 48-

History PE Discovery largely credited to Rudolph Virchow in 1858 He described two types of PE occurrence DVT that embolizes to the lung Blockage in a pulmonary artery distal as a result of stagnant blood flow Virchow R. Die Cellularpathologic in Ihrer Begrudung auf Physiologische und Pathologische Gewebelehre. Berlin: A. Hirschwald, 1858
Slide 49-

Etiology Virchow Triad – 1858 Hemostasis Immobilization, occlusion, tournaquet use Endothial injury Direct trauma or pressure from injury Hypercoagulable state Genetic, activation of clotting cascade, depression of thrombolytic enzymes Virchow‘s overarching hypothesis of VTE has remained largly unchanged in 150+ years, with expansions of the definitions of each contributing factor
Slide 50-

Epidemiology Occurrence of non fatal, symptomatic VTE rates after major orthopaedic surgery 4.3% (1.5% PE, 2.8% DVT) – No prophylaxis 1.8% (0.55% PE, 1.25% DVT)- LMWH In cumulative postoperative period of 0-35 days
Slide 51-

Different orthopedic injuries carry different rates of VTE PE- as high as 61% in pelvic ring injuries Ankle fractures VTE rate from 0.26-40 % Lapidus et al 2013 reported 514 VTE events (1.1%) in 36,388 patients who underwent 45,968 orthopaedic procedures DVT rate increase associated with increased ISS Epidemiology
Slide 52-

Wells Score- DVT assessment Paralysis, paresis or recent orthopedic casting of lower extremity (1 point) Recently bedridden (more than 3 days) or major surgery within past 4 weeks (1 point) Localized tenderness in deep vein system (1 point) Swelling of entire leg (1 point) Calf swelling 3 cm greater than other leg (measured 10 cm below the tibial tuberosity) (1 point) Pitting edema greater in the symptomatic leg (1 point) Collateral non varicose superficial veins (1 point) Active cancer or cancer treated within 6 months (1 point) Alternative diagnosis more likely than DVT (Baker's cyst, cellulitis, muscle damage, superficial venous thrombosis, post phlebitic syndrome, inguinal lymphadenopathy, external venous compression) (-2 points) DVT Diagnosis 3-8 Points: High probability 1-2 Points: Moderate probability -2-0 Points: Low Probability Wells PS et al. 1997
Slide 53-

PE Diagnosis Well’s score for PE Symptoms of DVT (3 points) No alternative diagnosis better explains the illness (3 points) Tachycardia with pulse > 100 (1.5 points) Immobilization (>= 3 days) or surgery in the previous four weeks (1.5 points) Prior history of DVT or pulmonary embolism (1.5 points) Presence of hemoptysis (1 point) Presence of malignancy (1 point) Score > 6 High probability Score > 2 Moderate probability Score < 2 Low Probability Wells PS et al. 2000
Slide 54-

Diagnostic Studies DVT- Venous Ultrasound- non-invasive D-dimer- limitations due to elevation w/ many factors- rule out test. PE CT (PE protocol)- contrast study VQ scan pregnant patients or pts allergic to contrast Venography- uncommon
Slide 55-

Prevention of VTE Mechanical and/or Chemical
Slide 56-

Mechanical Prophylaxis Mobilization, Mobilization, Mobilization Increase venous flow Sequential compressive devices (SCD’s) Increase venous return and fibrinolysis Vena Cava Filters- for PE Block emboli Compression Stockings Reduce stasis
Slide 57-

Mechanical All have varying levels of efficacy in orthopaedic patients and limitations to use Ability to apply therapy in setting of injury Mobilization, SCD’s and stockings Patient adherence- mobilzation, SCD’s and stockings Invasiveness of the intervention IVC filter Availability & Cost All
Slide 58-

Chemical Prophylaxis Aspirin Heparin (unfractonated) Low Molecular Weight Heparin (LMWH) Coumadin (warfarin) Fondaparinux Rivaroxaban Argatroban
Slide 59-

Aspirin Irreversibly inhibits platelets Blocks cyclo-oxygenase-1activity Reduced thromboxane A-2 which allows platelets to aggregate Platelet turnover is ~10%/day So return of normal platelet activity in 7-10 days Advantages Inexpensive, oral, no monitoring Disadvantages Irreversible, GI intolerance, unclear efficacy w/ VTE
Slide 60-

Heparin Increases Anti-Thrombin III Activity Inbibits factors IIa, III, Xa Overall decreases clotting cascade response Advantages Reversible w protamine sulfate Disadvantages Variable half-life, injectable, Heparin-induced thrombocytopenia (HIT), bleeding
Slide 61-

Low Molecular Weight Heparin Derivative of Heparin molecule Inhibits factor Xa Advantages No monitoring, reversible with protamine, longer half-life than heparin, less risk of HIT Disadvantages Cost, injectable, requires wt based/creatinine clearance based dosing, bleeding
Slide 62-

Coumadin (Warfarin) Blocks Vit K dependant enzymes in clotting cascade. Factors II, VII, IX, X, Protein C &S Advantages Oral, inexpensive, reversible by Vit K or FFP Disadvantages Requires close monitoring, effected by Vit K intake, bleeding, medication interactions
Slide 63-

Others Fondaparinux - Indirect factor Xa inhibitor High bleeding complication rate, Cost No monitoring required Rivaroxaban - Direct Xa inhibitor Bleeding complications rate, Cost No monitoring required Continued difficulty with reversibility, cost, availability Ongoing research into their role in VTE prophylaxis in orthopaedics
Slide 64-

Others Argatroban - direct thrombin inhibitor Used in patients with HIT Dabigatran- oral direct thrombin inhibitor Issues with use Continuous infusion requiring monitoring Reversible Cost Bleeding
Slide 65-

Other Factors Potential contraindication to chemical VTE prophylaxis Spinal cord injury Solid organ injury Uncontrolled bleeding Medication allergy Upcoming operation Platelet count < 50,000 Previous head bleed
Slide 66-

Ideal Agent! Want a VTE prophylaxis agent that is: Inexpensive Oral Reversible Doesn't require monitoring No medication interactions Low bleeding risk Doesn’t yet Exist
Slide 67-

VTE Treatment DVT Anticoagulation- prevent further DVT/PE LMWH, Warfarin (INR 2-3), Maybe factor Xa inhibitor or direct thrombin inhibitor Duration of therapy is dependent on If first DVT Provoked vs unprovoked Associated w/ Malignancy Associated w/ genetic disorder Remains unknown but ranges from 30 days to indefinite. Requires a discussion about risks.
Slide 68-

VTE Treatment PE Depends on hemodynamic stability Stable patient- Treat very similar to DVT + supplemental Oxygen. Unstable patient- treat like a patient in shock Anticoagulation Supportive care with Repiratory support- Fluids Vasopressors Invasive interventions- Thrombolytic therapy, Embolectomy, Surgical or catheter based IVC filter
Slide 69-

Outcomes Mortality rate ratio (MRR) at 30 years DVT – 1.55 (CI 1.53 - 1.57) PE – 2.77 (CI 2.74 – 2.81 People with VTE have a higher 30 year mortality PE reoccurrence rate 8 % six months, 13 % one year, 23 % five years, 30 % 10 years den Exter, PL et al. 2013
Slide 70-

Recommendations The next section will go over recommendations from major groups regarding orthopedic patients and specific procedure. This is a resource for you to review.
Slide 71-

OTA Recommendations Most recent guidelines put out by the OTA specific to Orthopedic Trauma patients Based on 185 OTA members who responded to a survey of their clinical practices regarding VTE prophylaxis and in conjunction with an expert panel they put forth 13 recommendations
Slide 72-

http://www.orthoguidelines.org/topic?id=1006 September 24, 2011 Useful VTE Prophylaxis Guideline Websites http://www.orthoguidelines.org/topic?id=1000 http://www.orthoguidelines.org/topic?id=1017
Slide 73-

2.2.1. In patients with a high clinical suspicion of acute VTE, we suggest treatment with parenteral anticoagulants compared with no treatment while awaiting the results of diagnostic tests (Grade 2C). 2.5.1. In patients with acute DVT of the leg, we suggest LMWH or fondaparinux over IV UFH (Grade 2C) and over SC UFH (Grade 2B for LMWH; Grade 2C for fondaparinux). 2.13.1. In patients with acute DVT of the leg, we recommend against the use of an inferior vena cava (IVC) filter in addition to anticoagulants (Grade 1B). 2.13.2. In patients with acute proximal DVT of the leg and contraindication to anticoagulation, we recommend the use of an IVC filter (Grade 1B). 2.14. In patients with acute DVT of the leg, we suggest early ambulation over initial bed rest (Grade 2C). Highlighted Chest Guidelines
Slide 74-

3.1.4. In patients with an unprovoked DVT of the leg (isolated distal [see remark] or proximal), we recommend treatment with anticoagulation for at least 3 months over treatment of a shorter duration (Grade 1B) . After 3 months of treatment, patients with unprovoked DVT of the leg should be evaluated for the risk-benefit ratio of extended therapy. In all patients who receive extended anticoagulant therapy, the continuing use of treatment should be reassessed at periodic intervals (eg, annually). 3.5. In patients who are incidentally found to have asymptomatic DVT of the leg, we suggest the same initial and long-term anticoagulation as for comparable patients with symptomatic DVT (Grade 2B). 4.1. In patients with acute symptomatic DVT of the leg, we suggest the use of compression stockings (Grade 2B). 5.1. In patients with acute PE, we recommend initial treatment with parenteral anticoagulation (LMWH, fondaparinux, IV UFH, or SC UFH) over no such initial treatment (Grade 1B). 5.2.3. In patients with a low clinical suspicion of acute PE, we suggest not treating with parenteral anticoagulants while awaiting the results of diagnostic tests, provided test results are expected within 24 h (Grade 2C). 5.9.1. In patients with acute PE who are treated with anticoagulants, we recommend against the use of an IVC filter (Grade 1B). 5.9.2. In patients with acute PE and contraindication to anticoagulation, we recommend the use of an IVC filter (Grade 1B). 9.1.1. In patients with acute upper-extremity DVT (UEDVT) that involves the axillary or more proximal veins, we recommend acute treatment with parenteral anticoagulation (LMWH, fondaparinux, IV UFH, or SC UFH) over no such acute treatment (Grade 1B) .
Slide 75-

Thank You! Special thanks to Dr Rodney A. Schmidt MD- Pathology University of Washington Medical Center Dr Stephanie Cheng MD- Chest Radiology University of Washington Medical Center
Slide 76-

Zenker, F. A. 1861. Beitrage zur Anatomie und Physiologie der Lunge. Dresden: Braunsdorf. 20 pp. Gauss, H. 1924. The pathology of fat embolism. Arch. Surg. 9:593-605 Lehman, E. P., Moore, R. M. 1927. Fat embolism including experimental production without trauma. Arch. Surg. 14:621-62 Bergmann, E. B. 1873. Ein Fall todlicher fetlenbolic. Berl. Klin. Wochenschr. 10:385-87 Cahill, J. M., Daly, B. F. T., Byrne, J. J. 1974. Ventilatory and circulatory response to oleic acid embolus. J. Trauma 14:73-76 McNamara, J. D., Molat, M., Dunn, R., Burran, E. L., Stremple, J. F. 1972. Lipid metabolism after trauma. J. Thorac. Cardiovasc. Surg. 66:968-72 Sagi HC, Ahn J, Ciesla D, Collinge C, Molina C, Obremskey WT, et al. Venous Thromboembolism Prophylaxis in Orthopaedic Trauma Patients: A Survey of OTA Member Practice Patterns and OTA Expert Panel Recommendations. Journal of orthopaedic trauma. 2015 Oct;29(10):e355-62. Epub 2015/09/25. Falck-Ytter Y, Francis CW, Johanson NA, Curley C, Dahl OE, Schulman S, et al. Prevention of VTE in orthopedic surgery patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb;141(2 Suppl):e278S-325S. Epub 2012/02/15. Virchow R. Die Cellularpathologic in Ihrer Begrudung auf Physiologische und Pathologische Gewebelehre. Berlin: A. Hirschwald, 1858 Wells PS, Anderson DR, Bormanis J, et. al. Value of assessment of pretest probability of deep-vein thrombosis in clinical management. Lancet. 1997 Dec 20-27;350(9094):1795-8. Wells PS, Anderson DR, Rodger M, et. al. Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED D-dimer. Thromb Haemost. 2000 Mar;83(3):416-20. References
Slide 77-

Reamed versus unreamed intramedullary nailing of the femur: comparison of the rate of ARDS in multiple injured patients. Journal of orthopaedic trauma. 2006 Jul;20(6):384-7. Epub 2006/07/11. Ashbaugh DG, Bigelow DB, Petty TL, Levine BE. Acute respiratory distress in adults. Lancet (London, England). 1967 Aug 12;2(7511):319-23. Epub 1967/08/12. Bederman SS, Bhandari M, McKee MD, Schemitsch EH. Do corticosteroids reduce the risk of fat embolism syndrome in patients with long-bone fractures? A meta-analysis. Canadian journal of surgery Journal canadien de chirurgie. 2009 Oct;52(5):386-93. Epub 2009/10/30. Bosse MJ, MacKenzie EJ, Riemer BL, Brumback RJ, McCarthy ML, Burgess AR, et al. Adult respiratory distress syndrome, pneumonia, and mortality following thoracic injury and a femoral fracture treated either with intramedullary nailing with reaming or with a plate. A comparative study. The Journal of bone and joint surgery American volume. 1997 Jun;79(6):799-809. Epub 1997/06/01. Bulger EM, Smith DG, Maier RV, Jurkovich GJ. Fat embolism syndrome. A 10-year review. Archives of surgery (Chicago, Ill : 1960). 1997 Apr;132(4):435-9. Epub 1997/04/01. Chastre J, Trouillet JL, Vuagnat A, Joly-Guillou ML, Clavier H, Dombret MC, et al. Nosocomial pneumonia in patients with acute respiratory distress syndrome. American journal of respiratory and critical care medicine. 1998 Apr;157(4 Pt 1):1165-72. Epub 1998/05/01. den Exter PL, van Es J, Klok FA, Kroft LJ, Kruip MJ, Kamphuisen PW, et al. Risk profile and clinical outcome of symptomatic subsegmental acute pulmonary embolism. Blood. 2013 Aug 15;122(7):1144-9; quiz 329. Epub 2013/06/06. Galanaud JP, Laroche JP, Righini M. The history and historical treatments of deep vein thrombosis. Journal of thrombosis and haemostasis : JTH. 2013 Mar;11(3):402-11. Epub 2013/01/10. Gurd AR, Wilson RI. The fat embolism syndrome. The Journal of bone and joint surgery British volume. 1974 Aug;56b(3):408-16. Epub 1974/08/01. McFadden PM, Ochsner JL. A history of the diagnosis and treatment of venous thrombosis and pulmonary embolism. The Ochsner journal. 2002 Winter;4(1):9-13. Epub 2002/01/01. Moylan JA, Evenson MA. Diagnosis and treatment of fat embolism. Annual review of medicine. 1977;28:85-90. Epub 1977/01/01. References
Slide 78-

Muller CA, Baumgart F, Wahl D, Perren SM, Pfister U. Technical innovations in medullary reaming: reamer design and intramedullary pressure increase. The Journal of trauma. 2000 Sep;49(3):440-5. Epub 2000/09/26. Pape HC, Giannoudis P, Krettek C. The timing of fracture treatment in polytrauma patients: relevance of damage control orthopedic surgery. American journal of surgery. 2002 Jun;183(6):622-9. Epub 2002/07/04. Pfeifer R, Sellei R, Pape HC. The biology of intramedullary reaming. Injury. 2010 Nov;41 Suppl 2:S4-8. Epub 2010/12/15. Ranieri VM, Rubenfeld GD, Thompson BT, Ferguson ND, Caldwell E, Fan E, et al. Acute respiratory distress syndrome: the Berlin Definition. Jama. 2012 Jun 20;307(23):2526-33. Epub 2012/07/17. Riska EB, Myllynen P. Fat embolism in patients with multiple injuries. The Journal of trauma. 1982 Nov;22(11):891-4. Epub 1982/11/01. Rubenfeld GD, Caldwell E, Peabody E, Weaver J, Martin DP, Neff M, et al. Incidence and outcomes of acute lung injury. The New England journal of medicine. 2005 Oct 20;353(16):1685-93. Epub 2005/10/21. Sogaard KK, Schmidt M, Pedersen L, Horvath-Puho E, Sorensen HT. 30-year mortality after venous thromboembolism: a population-based cohort study. Circulation. 2014 Sep 2;130(10):829-36. Epub 2014/06/28. References
Slide 79-

For questions or comments, please send to ota@ota.org