Downloaded 25 times
Uploaded byfathi neana
Polytrauma part 3 (FES)
The document discusses Fat Embolism Syndrome (FES), a post-traumatic complication characterized by symptoms like hypoxia and confusion following long bone fractures. It details the pathological mechanisms, diagnostic criteria, and management strategies for FES, including the roles of inflammatory mediators and supportive treatments. Prevention primarily involves early immobilization and fracture stabilization to reduce the incidence of the syndrome.
More Related Content
Similar to Polytrauma part 3 (FES)
Polytrauma part 3 (FES)
- 1. Dr. Fathi Neana,MD Chief of Orthopaedics Dr. Fakhry & Dr. A. Al-Garzaie Hospital January, 15 - 2019 Polytrauma Part 3 (FES) Fat Embolism Syndrome
- 4. Trauma Tissue injury Infection Inflammatory Mediators Release Organ Injury Acute respiratorydistress syndrome ARDS ARDS related to MODS & MOF Common Pathological Pathways 1- Inflammatory mediators ->> Systemic inflammatory response syndrome (SIRS ) 2- Anti-inflammatory mediators ->> Compensatory anti-inflammatory response syndrome (CARS) 3- The conflict between these two immune responses (SIRS) vs. (CARS) will end up with: A- Cure B- Death (Parenchymal cell Necrosis and Apoptosis ) C- Long standing inflammation ->> Multi organ Dysfunction Syndrome (MODS ) or Failure (MOF)
- 5. Inflammatory Mediators Release (SIRSvs CARS) A Host defence immune response Release of 1- Inflammatory mediators Local and systemic (pro-inflammatory cytokines, arachidonic acid metabolites, proteins of the contact phase and coagulation systems, complement factors and acute phase proteins, as well as hormonal mediators) Clinically : Systemic inflammatory response syndrome (SIRS) 2- Anti-inflammatory mediators are produced (compensatory anti-inflammatory response syndrome) (CARS) Imbalance of these Two immune responses (SIRS & CARS) is responsible for organ dysfunction & increased susceptibility to infections Endothelial cell damage, Accumulation of leukocytes, Disseminated intravascular coagulation (DIC) and Microcirculatory disturbances Finally lead to Apoptosis and Necrosis of Parenchymal cells & Development of multiple organ dysfunction syndrome (MODS) or multiple organ failure (MOF)
- 7. MODS - MOF(Multi Organ Dysfunction or Failure Syndrome)
- 8.
- 9. What is FatEmbolism Syndrome (FES) A Syndrome characterized by Hypoxia, Confusion and Petechiae presenting soon after long bone fracture and soft tissue injury Diagnosis of Exclusion of other causes 0f (Hypoxia & Confusion) Occurs in 0.9 – 8.5% of all fracture patients Up to 35% of the multiply injured Mortality 2.5 – 15 - 20% Rare in upper limb injury and children
- 10. Incidence ranges from<1% to 29% in different studies Fat globules detected in blood of 67% of orthopaedic trauma patients. Increased to 95% in blood samples near to the fracture site The presence of fat globules in the blood does not automatically lead to FES Men are more likely than women Rare in children aged 0-9 years Age group commonly affected 10-39 years Fat Embolism Syndrome (FES) Epidemiology
- 12. Fat macro-globules embolicpass into small vessels (lung and other sites) Producing Endothelial Damage Leading to Respiratory failure (ARDS-like picture) Cerebral Dysfunction Petechial Rash Fat embolism syndrome (FES)
- 13. Can be difficultto diagnose Diagnosis by exclusion of other Causes of dyspnoea, hypoxia , confusion and abnormal CXR. (Ex. Thromboembolism and pneumonia) Index Patient Young adult with Long Bone injury seen after long transfer without supporting therapy or splintage Fat embolism syndrome (FES) Historically Fat embolism was first described as an Autopsy finding by Zenker in 1862 Described as a Clinical syndrome for the first time by Von Bergmann in 1873
- 14. Initial presentation : bymechanical occlusion of multiple blood vessels with fat globules (too large to pass in the capillaries) Lungs Paradoxical systemic embolism can occur from shunting Vascular occlusion is temporary & incomplete (fat globules fluidity and deformability) Late presentation : from hydrolysis of the fat to the irritating free fatty acids which migrate to other organs via the systemic circulation Fat embolism syndrome (FES) Pathological Pathways In the lungs Direct toxicity of free fatty acids on lung tissue or capillary endothelium + The pathogenetic reaction of lung tissue to Shock and Hyper coagulability
- 15. Fat embolism syndrome(FES) Pathological Pathways Mechanical Theory Fracture Liberates Fat Intravasation ->> Fat Enters Venous System Mechanical Obstruction (Lung) Patent Foramen Ovale or Pulmonary Pre-Capillary Shunts ->> Systemic Fat Embolization - (Skin petechiae, CNS signs) Seen here with Oil red O stain in a peripheral cerebral artery branch are globules of lipid. This is fat embolism syndrome. Treatment is supportive. An Oil Red O stain demonstrates the fat globules within the pulmonary arterioles. The globules stain reddish-orange. The cumulative effect of many of these globules throughout the lungs is similar to a large pulmonary embolus, but the onset of dyspnea is usually 2 to 3 days following the initiating event, such as blunt trauma with bone fractures.
- 16. The rounded clearholes seen in the small pulmonary arterial branch in this section of lung are characteristic for fat embolism. Fat embolism syndrome is most often a consequence of trauma with long bone fractures. It can also be seen with extensive soft tissue trauma, burn injuries, severe fatty liver, and very rarely with orthopedic procedures The capillary loops of this glomerulus contain fat globules in a patient with fat embolism syndrome.
- 17. Fat embolism syndrome(FES) Pathological Pathways Bio - chemical Theory •Neutral Fat and Chemical Mediators Released at Time of Fracture •Neutral Fat Metabolized by Lipases releasing Free Fatty Acids •Free Fatty Acids Result in Endothelial Lung Damage + Other Organs via Systemic circulation Oleic acid (OA) can induce acute lung injury in experimental models, we proved that increased inflammatory parameters after OA challenges were not due to the activation of the TLR4 receptor. With OA being a Na/K-ATPase inhibitor, we suggest the possible involvement of this enzyme as an OA target triggering lung inflammation.
- 18. FES To BrainOn MRI From several days to a week following the event initiating fat embolism syndrome, there may be loss of consciousness from lesions evidenced by the "brain purpura" as shown here. Numerous petechial hemorrhages are produced by fat emboli to the brain, particularly in the white matter. Subsequent to this there can be brain edema with herniation. With cerebral fat embolism syndrome, there is loss of consciousness. Note the multitude of petechial hemorrhages here, mostly within white matter. Cerebral edema and herniation may follow. Overall, few persons with a history of trauma will develop fat embolism, but it is difficult to predict which patients will. Protean manifestations include: hypoxemia, mental status changes, petechiae, fever, tachycardia, and thrombocytopenia
- 19. . ↑ inintra medullary pressure → fat droplets → get filtered in the pulmonary circulation • minute droplets go through pulmonary circulation & get trapped in cerebral circulation • alveolar lipase → hydrolysis of fat → release of fatty acids (palmitic, stearic, oleic acids) • Neutralisation by albumin • failure of neutralistion by albumin • fatty acids + calcium → intercellular septa rupture → diffuse areas of haemorrhage & oedema in pulmonary interstitium & alveolar space • Integrins CD11b & CD18 cause adherence of neutrophils & endothelium • Injured pneumocytes stop surfactant production → collapse of alveoli • ↑ shunt and dead space Fat embolism syndrome (FES) Pathological Pathways - Summary
- 20. Pathological Pathways (FES) OftenPlaced in the Category of (ARDS) May share common pathological pathways Fat Embolism Syndrome (FES) Fat globules - Free fatty acids (phagocytosis) - Inflammatory Mediators + enzymatic Acute respiratory distress syndrome (ARDS) Trauma – tissue damage - cell necrosis – infection (Phagocytosis) - Inflammatory mediators
- 21. Fat Embolism Syndrome (FES) Acuterespiratory distress syndrome (ARDS) Pathological Pathways ARDS VS. FES
- 22. Non-traumatic settings occasionally leadto fat embolism Liposuction Fatty liver Prolonged corticosteroid therapy Acute pancreatitis Osteomyelitis Conditions causing bone infarcts, especially sickle cell disease Fat Embolism Syndrome(FES) Etiology Fractures Closed fractures of a long bone > Open fractures >Long bones, pelvis and ribs >Multiple fractures <Sternum and clavicle Other causes Orthopaedic procedures, intramedullary nailing, hip, knee replacements Massive soft tissue injury Severe burns Bone marrow biopsy
- 23. Closed fractures ofa long bone > Open fractures
- 25. Minimal invasive plateosteosynthesis (MIPO) Fat embolism
- 27. Sudden onset 24-72hours after injury (Second Peak) Breathlessness (dyspnoea) ± vague chest pains. can progress to respiratory failure with tachypnoea, and hypoxia Fever - 38.3°C with a disproportionately high pulse rate Petechial rash upper anterior trunk, arm and neck, buccal mucosa & conjunctivae , may be transient CNS symptoms, from mild headache to significant cerebral dysfunction (restlessness, disorientation, confusion, seizures, stupor or coma) Renal - oliguria, haematuria, anuria Fat Embolism Syndrome(FES) Presentation Drowsiness with oliguria is almost pathognomonic 98% of the patients presented with mental status changes, only 22% had focal signs and / or seizures There is a fulminant form presents as acute cor pulmonale, respiratory failure and /or embolic phenomena leading to death within a few hours of injury
- 28. Minor criteria 1- Tachycardia 2-Pyrexia (usually >39°C) 3- Confusion 4- Sustained pO2 <8 kPa 5- Sustained respiratory rate >35/minute, in spite of sedation 6- Retinal changes - cotton wool exudates and small hemorrhages, occasionally fat globules seen in retinal vessels 7- Jaundice 8- Renal signs 9- Thrombocytopenia 10- Anemia 11- High ESR 12- Fat macroglobulinemia 13- Diffuse alveolar infiltrates 'snow storm appearance' on CXR Major criteria 1- Respiratory insufficiency 2- Cerebral involvement 3- Petechial rash Fat Embolism Syndrome(FES) Diagnostic criteria (combined from various sources) Diagnostic criteria first by Gurd have been updated
- 29. Major criteria Respiratory insufficiency Cerebralinvolvement Petechial rash Fat Embolism Syndrome(FES) Diagnostic criteria (combined from various sources) Diagnostic criteria first by Gurd have been updated
- 30. At least Twosymptoms for the Major criteria or One symptom for the Major criteria and Four symptoms for the Minor criteria Must be present to diagnose the syndrome Fat Embolism Syndrome(FES) Diagnosis
- 31. 1- Cytological examination ofurine, blood and sputum may detect fat globules either free or in macrophages. This test has low sensitivity and a negative result does not exclude fat embolism 2- The CXR show evenly distributed, fleck-like pulmonary shadows (snow storm appearance), increased pulmonary markings and dilatation of the right side of the heart 3- Blood gases hypoxia, pO2 usually less than 8 kPa (60 mm Hg) and hypocapnia. 4- Continuous pulse oximeter monitoring detect hypoxia before it is clinically apparent (suggested by recurrent desaturations below 90%) Fat Embolism Syndrome(FES) Investigations
- 32. 1- Platelets arereduced. 2- Decreased haematocrit occurs within 24-48 hours and is attributed to intra-alveolar hemorrhage. 3- Lipase is elevated but this is not pathognomonic, as it occurs in any bone trauma. 4- Calcium is reduced 5- Brain MRI scan help in the diagnosis of cerebral fat embolism - hypointense areas consistent with fat globules at the grey-white matter junction 6- Transoesophageal echocardiography (TEE) of value in detecting intra-operative release of marrow contents into the bloodstream during intramedullary reaming and nailing Fat Embolism Syndrome(FES) Investigations
- 33.
- 34. • Early immobilizationof fractures The most effective way of reducing the incidence of this condition • Appropriate Splinting • Early Fracture Stabilization • Oxygen Therapy • Corticosteroids are occasionally used prior to long- bone intramedullary nailing but the evidence for their effectiveness in preventing FES is Fat Embolism Syndrome FES Prevention Therapies • Fluid Loading • Hypertonic Fluid • Alcohol • Heparin • Dextran • Aspirin None Shown to be Effective
- 35. Minimize the SecondHit (Surgical trauma) Be a Biological Orthopedic Surgeon Surgical Technique Implant Contact What is the Second Hit ? Early Fracture Stabilization
- 36. 1st hit Trauma Release ofinflammatory mediators (cytokines, chemokines) ->> central nervous system and systemic Hypoxia Acidosis Coagulopathy Systemic inflammation 2nd hit Surgery 1st hit: Head Mechanical insult to brain tissue blunt or penetrating breakdown of the blood brain barrier 1st hit: body Mechanical insult Chest, Abdomen, extremities
- 37. Systemic Effects ofTrauma Injury (First Hit) 24 hours 48 hours Post Injury Inflammatory Response in 2 Patients Second Hit in susceptible patients ARDS MODS Threshold IM Nailing as a Cause of Secondary Systemic Injury
- 38. Injury (First Hit)Surgery (Second Hit) Surgical Technique & Implant contact Systemic Effects of Trauma
- 39. Early Total Care(ETC) Definitive Early Fixation By Nail or Plate Damage Control (DCO) Temporary Stability By External Fixator – Limit Further Blood Loss – Limit Anesthetic Time – Delay Definitive Fracture fixation Fracture Fixation Controversy
- 41. Effect of IMNailing • Increased IM Pressure • Embolic Showers On Echocardiograms Caused by: – Canal Opening – Reaming – Nail Insertion (both reamed & unreamed) Fracture Fixation Controversy • 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
- 42. Fracture Fixation Controversy CurrentRecommendations Classify the patients according to their physical status 1- stable grade I 2- borderline grade II 3- unstable grade III 4- In extremis grade IV The Criteria used in the physical status classification Shock – B.P, No of blood units, lactate levels, B.D (Base deficit), ATLS (Advanced Trauma Life Support) Coagulation status Temperature Soft tissue injuries
- 43. American Society ofAnesthesiologists Classification (ASA Class) Daniel John Doyle; Emily H. Garmon. Last Update: October 27, 2018. ASA 1: A normal healthy patient. Example: Fit, nonobese (BMI under 30), a nonsmoking patient with good exercise tolerance. ASA 2: A patient with a mild systemic disease. Example: Patient with no functional limitations and a well-controlled disease (e.g., treated hypertension, obesity with BMI under 35, frequent social drinker or is a cigarette smoker). ASA 3: A patient with a severe systemic disease that is not life-threatening. Example: Patient with some functional limitation as a result of disease (e.g., poorly treated hypertension or diabetes, morbid obesity, chronic renal failure, a bronchospastic disease with intermittent exacerbation, stable angina, implanted pacemaker). ASA 4: A patient with a severe systemic disease that is a constant threat to life. Example: Patient with functional limitation from severe, life-threatening disease (e.g., unstable angina, poorly controlled COPD, symptomatic CHF, recent (less than three months ago) myocardial infarction or stroke. ASA 5: A moribund patient who is not expected to survive without the operation. The patient is not expected to survive beyond the next 24 hours without surgery. Examples: ruptured abdominal aortic aneurysm, massive trauma, and extensive intracranial hemorrhage with mass effect. ASA 6: A brain-dead patient whose organs are being removed with the intention of transplanting them into another patient. The addition of “E” to the ASAPS (e.g., ASA 2E) denotes an emergency surgical procedure. The ASA defines an emergency as existing “when the delay in treatment of the patient would lead to a significant increase in the threat to life or body part.” Abbreviations used: ASA: American Society of Anesthesiologists, BMI: body mass Index, CHF: congestive heart failure, COPD: chronic obstructive pulmonary disease.
- 44. Fracture Fixation Controversy CurrentRecommendations Stable patients: - Do whatever you want Borderline patients: Borderline patients: Continuous reassessment Pao2/F102 should not drop below 200mm of Hg Temperature should not drop below 32C Requirement of fluids should not exceed 3L or 5units of blood Absence of significant coagulopathy who respond to resuscitation proceed with definitive fixation limit the surgical duration within 2 hours If not → DCO Remember: A bad surgeon can shift the ASA Grade II to IV easily Unstable and patients in extremis: - Life saving surgeries - External fixation - Resuscitation and stabilization simultaneously
- 45. Uncertain Stable Grade 1Unstable Grade IIIBorderline Grade II Resuscitate Reevaluate Damage Control (DCO)Early Total Care (ETC) Fracture Fixation Controversy Current Recommendations Stabilized
- 46.
- 47. Fat Embolism Syndrome(FES) Treatment A- Surgical Prompt surgical stabilization of long bone fractures reduces the risk of the syndrome B- Usually supportive 1- Oxygen Therapy to maintain PaO2 Ensuring good arterial oxygenation. High flow rate of O2 2- Mechanical Ventilation Mechanical ventilation and positive end-expiratory pressure (PEEP) may be required 3- Adequate Hydration Restriction of fluid intake and diuretics can minimize fluid accumulation in the lungs On the other hand, maintenance of intravascular volume is important because Shock can exacerbate the lung injury caused by FES
- 48. Fat Embolism Syndrome(FES) Treatment Albumin Recommended for volume resuscitation , balanced electrolyte solution, it not only restores blood volume but also binds fatty acids and decrease the extent of lung injury Drugs Using dextrose to decrease fatty acid mobilization, ethanol to reduce lipolysis and heparin anticoagulation have been largely shown to be of unproven benefit Steroids – Decrease endothelial damage – 30mg/kg initial dose repeated @ 4 Hours, 1gm dose repeated @ 8 Hours: Total 3 Doses •Complications – Frequent, Infection, GIT •Steroid Therapy Avoided Secondary To Poor Risk Benefit Ratio
- 49.
- 50. The mortality rateis <5 - >15%. Even severe respiratory failure seldom leads to death Neurological deficit and coma may last for days or weeks Residual deficits include personality changes, memory loss and cognitive dysfunction Pulmonary sequelae usually resolve completely within a year, although residual diffusion capacity deficits may exist Patients presenting with mild mental status changes, focal deficits, or seizure had a better outcome than those presenting with coma or abnormal posturing Fat Embolism Syndrome (FES) Prognosis
Editor's Notes
- #7 FIGURE 1–1 Stages of the cellular response to stress and injurious stimuli.
- #37 There is a complex interplay between brain injury and systemic insults. The imflammatory cytokines, chemokines, work in the central nervous system as well as systemically. There is also a breakdown of the usual blood brain barrier magnifying the ill effects of systemic injury on the brain. Flierl et al Femur Shaft Fixation in Head –Injured Patients: when is the right time? J Orthop Trauma, 24, 2010.