Fat embolism

Fat embolism seminar

1. Fat embolism MODERATOR: DR. SAGAR ASSOCIATE PROFESSOR DEPT OF ORTHOPAEDICS RLJALAPPA HOSPITAL KOLAR PRESENTED BY: DR. ABHI SHARMA JUNIOR RESIDENT

2. History First case : 1861 by Zenker , who reported the presence of fat droplets in lung capillaries. In 1865 Wagner described the correlation of fat embolism(FE) with fractures and attributed the origin of fat in the lungs to bone marrow.

3. Von Bergmann was the first to describe the symptoms of FES in 1873 , in a patient with comminuted distal femur fracture. Sixty hours after the injury, he developed confusion, dyspnea , and petechiae and died after 19 hours. A massive pulmonary FE was found at autopsy.

4. Introduction 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.

5. Fat Embolism Syndrome (FES): serious manifestation of fat embolism. occasionally causes multi system dysfunction. The lungs are almost always involved followed by brain manifestations.

6. Epidemiology Fat embolization and FES are not synonymus . pulmonary FE has been found in 68% to 82% of blunt trauma patients. The clinical entity of FES is much less common. Among all patients with fractures, the incidence of FES is 0.17%.

7. Of isolated fractures, femur fractures were the most common with a rate of 0.54%. Multiple fractures that included the femur had the highest incidence of 1.29% .

8. The incidence is more common in male patients. Patients with Duchenne muscular dystrophy develops FES at a relatively high rate of 1%to 20% after minor trauma and fractures.

9. Pathophysiology Two pathophysiologic mechanisms were proposed for the clinical manifestations of FES: The mechanical theory: by Gauss in 1924. Biochemical theory: by Lehman and Moore in 1927 .

10. The mechanical theory Trauma and fractures of long bones disrupts fat in the marrow and also tears intraosseous blood vessels.

11. arthroplasty and intramedullary instrumentation increases intramedullary pressure forcing fat into the veins. These droplets then enter into the pulmonary capillary beds and travel to the brain through arterio -venous shunts .

12. concomitant release of inflammatory mediators as a reaction to both ischemia and ongoing inflammation platelet aggregation Ischemia(facilitated by release of vasoactive amines)

13. Biochemical theory After an insult or trauma, fat was mobilized from body stores and embolized into the tissues, initiating an inflammatory response . Bone marrow fat embolized to the lungs causes the local releases of lipase which breaks fat down into free fatty acids and glycerol. Free fatty acids are toxic to endothelial cells and cause vasogenic edema and hemorrhage

14. These conditions release proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin (IL)-1 and IL-6 , which can cause acute respiratory distress syndrome (ARDS). Elevated acute phase reactants, such as C-reactive protein cause lipids in the blood to agglutinate into larger molecules, which occludes vessels.

15. Bone marrow fat is prothrombotic . In the circulation, it is quickly covered in platelets and fibrin setting off the coagulation cascade, leading to thrombocytopenia. In extreme cases, it will lead to disseminated intravascular coagulation .

16. Risk factors

17. Causes Traumatic causes: Fractures of long bones. Major orthopedic surgery Extensive soft tissue injury Higher degree burns injury Bone marrow biopsy

18. Non-traumatic causes: Removal of large volume of adipose tissue in liposuction Hemo-globinopathy Collagen vascular disease Diabetes mellitus Severe infection Neoplasm Blood transfusion

19. Cardiopulmonary bypass Hepatic steatosis (fatty liver) Long duration corticosteroid therapy Acute pancreatitis Osteomyelitis Medical conditions causing bone infarcts, especially sickle cell disease

20. Clinical features The classic triad of symptoms of FES: generally develops 24–72 hours after trauma.

21. Respiratory distress Seen in 75% of patients. tachypnea , dyspnea and hypoxemia are the earliest to manifest. Early persistent tachycardia . Progress to respiratory failure in 10% of the cases. Patients have high grade fever.

22. Dermatologic petechial rash develops in about 20–60% of cases. Mostly seen in mucous membrane (oral), the conjunctiva, and skin folds of the neck and axilla . Resolves in 5-7 days .

23. Neurologic They result from cerebral embolism and seen in up to 86% of cases. Common presentation:- acute confusional state . Transient and reversible in most cases. Fundoscopic examination reveals retinal hemorrhages with intra-arterial fat globules .

24. Focal neurological signs, such as aphasia, apraxia , hemiplegia , visual field disturbances, anisocoria , seizures and decorticate posturing, are also sometimes seen.

25. Other miscellaneous findings Right heart failure pattern is common on an ECG. Macular edema causing scotomata associated with soft fluffy retinal exudates ( Purtscher’s retinopathy )

26. Coagulation abnormalities similar to disseminated intravascular coagulation Renal symptom presenting as oliguria , lipiduria , proteinuria or hematuria .

27. Diagnosis It is mainly a clinical diagnosis whereby other causes are systematically excluded Gurd’s and Wilson’s criteria Schonfeld’s criteria Lindeque’s criteria

28. Gurd’s and Wilson’s criteria One major, four minor criteria, and the presence of macroglobulinemia are required for the diagnosis Major: Symptoms and radiologic evidence of respiratory insufficiency Cerebral sequelae unrelated to head injury or other conditions Petechial rash

29. Minor criteria Clinical findings: Tachycardia (heart rate > 110 beats/min) Pyrexia (temperature > 38.5°C) Retinal changes of fat or petechiae Renal dysfunction( anuria , oliguria ) Jaundice

30. Laboratory features: Acute drop in hemoglobin level(>20%) Sudden thrombocytopenia(> 50%) Elevated erythrocyte sedimentation rate(> 71mm/hr.) Fat microglobulinemia .

31. Schonfeld’s criteria Cumulative score more than five required for diagnosis symptoms Score Petechiae 5 Chest X-ray changes (diffuse alveolar infiltrates 4 Hypoxemia (PaO2 < 9.3 kPa ) 3 Fever (> 38°C) 1 Tachycardia (> 120 bpm ) 1 Tachypnea (> 30 bpm ) 1

32. Lindeque’s criteria FES can be diagnosed on the basis of respiratory system involvement alone . Sustained pO2 < 8 kpa Sustained pCO2 > 7.3 kpa Sustained respiratory rate > 35/min, in spite of sedation Increased work of breathing, dyspnea , tachycardia, anxiety

33. LABORATORY STUDIES Arterial blood gas: Reveal hypoxia , with a PaO2 of less than 60 mm Hg along with hypocapnia (paCO2) less than 30 mm Hg. Unexplained increase in pulmonary shunt fraction difference is strongly suggestive of the syndrome.

34. Urine and sputum examination: staining of urine, blood and sputum with Sudan or Oil Red O may show fat globules. May be free or located within macrophage. Sensitivity and negative predictive value of this test is very low

35. Bronchoalveolar lavage : In FES, it has been shown that bronchial lavages had 30% of alveolar macrophages filled with lipid inclusions as compared with 13% to 15% in ARDS.

36. Hematocrit , platelet count, and fibrinogen : Fall in hematocrit occurs within 24–48 hours It is due to intra-alveolar hemorrhage . Coagulation abnormalities, thrombocytopenia and hypofibrogenemia are often seen.

37. Imaging studies Plain chest radiographs: findings appear within 24–48 hours of onset of clinical findings- Diffusely distributed bilateral pulmonary infiltrates Snow storm appearance Prominent pulmonary bronchiolar markings Enlargement of the right side of the heart

38. High-resolution CT thorax: Shows patchy ground glass opacities and consolidation with interlobular thickening called the “crazy paving ” pattern. The extent of these findings has correlated with disease severity.

39. Noncontrast head CT:- Usually it is normal. show diffuse edema with scattered hemorrhage .

40. MRI brain: More sensitive T2-weighted images typically demonstrate a “ starfield pattern ” with multiple, small, nonconfluent , hyperintense lesions. The lesions occur in the periventricular , subcortical , and deep white matter.

41. Treatment Prevention Immobilization and early internal fixation of fracture. Fixation within 24 hours has been shown to yield a 5 fold reduction in the incidence of ARDS.

42. Continuous pulse oximeter monitoring in high risk patients It will help in detecting desaturation early, allowing early oxygen and possibly steroid therapy

43. No specific treatment is available for FES. Supportive treatment goals: Maintenance of adequate tissue oxygenation and pulmonary ventilation Adequate fluid balance prophylaxis for DVT Maintain nutrition Fracture stabilization

44. Maintenance of adequate tissue oxygenation and pulmonary 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.

45. Adequate fluid balance: Restrict only excess fluid. Maintenance of intravascular volume is necessary as shock can further exacerbate lung injury caused by FES. Blood products should be only instituted as clinically indicated and not irrationally.

46. Medication Role of albumin: Recommended for volume resuscitation in addition to balanced electrolyte solution Because it not only restores blood volume but also binds with the fatty acids and decrease extent of lung injury

47. Role of steroids: Steroid prophylaxis is controversial to prevent FES . Decrease inflammatory reaction in lungs caused by free fatty acids Decrease capillary leakage by stabilizing lysosomal and capillary membrane Prophylactic dose of methyl prednisolone : 1.5 mg/kg IV can be administered every 8 hours for six doses.

48. Prognosis Mortality from FES is uncommon (< 5–15%). Most cases that fail to recoup result from associated damage to other organs. Neurological complications like deficit and coma are often transient and may last for days or sometimes up to weeks. Pulmonary complications usually resolve completely within a year and are clinically inconsequential despite deficits persistence in residual diffusion capacity.

49. Applications In trauma: Timing to Surgery : Studies conducted by Riska et al concluded that the number of fractures treated with early surgical intervention decreased the number of cases of FES. FES rates are higher in the nonsurgical group versus in the surgical group. Riska EB, von Bonsdorff H, Hakkinen S, Jaroma H, Kiviluoto O, Paavilainen T: Prevention of fat embolism by early internal fixation of fractures in patients with multiple injuries. Injury 1976;8:110-116.

50. Further studies during 1989 concluded that more pulmonary complications were found with late stabilization, both in the cases with isolated femur fractures and the multiply injured group. Bone LB, Johnson KD, Weigelt J Scheinberg R: Early versus delaye stabilization of femoral fractures: prospective randomized study. J Bone Join Surg Am 1989;71:336-340.

51. However, FES and pulmonary complications are just one of a multitude of factors to consider in the optimal timing of fracture stabilizationin polytrauma patients there is a subset of patients for whom damage control orthopaedics followed by definitive treatment at a later date may increase the chance of survival

52. Fixation Method: Intramedullary reaming increases canal pressures and stimulates an inflammatory response this situation leads to an increased the incidence of FES compared with other fixation methods

53. Bosse et al compared reamed intramedullary nails with plating in 453 patients. No significant differences in pulmonary complications or mortality were observed Bosse MJ, MacKenzie EJ, Riemer BL, 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. J Bone Joint Surg Am 1997;79:799-809.

54. Study conducted by Pape et al in multiply injured patients in the borderline stable group to intramedullary nail versus external fixation concluded Six times greater incidence in acute lung injury with the intramedullary nail group, but no difference was found in ARDS or mortality. Pape HC, Rixen D, Morley J, et al: Impact of the method of initial stabilization for femoral shaft fractures in patients with multiple injuries at risk for complications (borderline patients). Ann Surg 2007;246: 491-501

55. The amount of embolized fat and intramedullary pressure was significantly lower with slower advancement and faster revolutions .

56. Bilateral Femur Fractures: Bilateral femur fractures treated with intramedullary nail have up to a 7.5% incidence of FES. mortality rates of 5% to6% which is about 5 to 6 times higher than isolated femoral shaft fractures.

57. Applications in Arthroplasty : Cause intramedullary pressurization, particularly with cementing. The use of an intramedullary bone vacuum during cementation significantly decrease embolization of marrow contents.

58. THANK YOU