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FAT EMBOLISM SYNDROME (FES)_Dr. Mousa.ppt
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- 4. •Fat embolism syndromeis a well-known cause of pulmonary and neurologic dysfunction secondary to a variety of injuries. •Its presentation vary from a sub clinical state to fulminant respiratory failure.
- 5. •The amount ofmanipulation of injured tissue and degree of hypovolemia or hypoperfusion are thought to be factors that predispose the patient to fat embolism syndrome. •Overall mortality range from 5 to 15 %.
- 7. Pathophysiology •FES most commonlyassociated with long bone and pelvic fractures, and most common in closed rather than open fracture. •Patients with a single long bone fracture have 1-3 % chance of developing the syndrome .
- 11. Pathophysiology (Cont’d.) •The incidenceincrease to 33 % with bilateral femoral fractures. •Other less common causes include liposuction thrombolytic therapy and orthopedic reconstructive surgery. •
- 12. Pathophysiology Cont’d. •Theories aboutthe origin of fat deposition in the pulmonary vasculature include venous fat embolization originating from traumatized bone marrow or excessive mobilization of free fatty acid from peripheral tissue secondary to stress hormones.
- 13. Pathophysiology Cont’d. •Those acidscoalesce in the blood and form fat aggregates. •Regardless of the site of origin of fat emboli the pulmonary capillaries act as filters and the emboli are carried to the lung where they lodge in pulmonary capillaries and increase resistance to blood flow.
- 14. Pathophysiology Cont’d. •The lungparenchymal produce lipase to remove emboli. •Hydrolysis of the triglycerides to glycerol and fatty acid occur and chemical pneumonitis results.
- 15. Pathophysiology Cont’d. •This inflammatoryresponse is mediated by complement activation platelet aggregation and leukocyt enzymatic action.
- 16. Pathophysiology Cont’d. •Morphologically thereis increase in the permeability of the capillaries and alveolar cell With leakage of fluid and protein into the alveolar wall and into alveolar space.
- 17. Pathophysiology Cont’d. •Lung surfactantactivity is decreased, functional residual capacity is reduced and there is diffusion barrier. •This cascade of events is seen clinically as decreased pulmonary compliance, increase a work of breathing and hypoxia.
- 18. Pathophysiology Cont’d. •Other studiesdemonstrate presents of echogenic material passing into right heart during orthopedic and spinal surgery, with continued emoblization ,pulmonary artery and right pressure rise and material can pass through patent foramen ovale into systemic circulation resulating in paradoxical embolism.
- 19. Pathophysiology Cont’d. •Serum fromacutely ill patients has the capacity to agglutinate chylomicrons, low density lipoprotein and liposomes of nutritional fat emulsions.
- 20. Pathophysiology Cont’d. •C reactiveprotein which appear to be elevated in these patient appear to be responsible for the lipid agglutination and may also participate in the mechanism for non traumatic fat embolism .
- 22. Clinical Manifestation •FES typicallymanifest 24 to 72 hours after the initial insult rarely occur as early as 12 hours or as later 2 weeks after the inciting events.
- 23. Clinical Manifestation (Cont’d.) 1.Pulmonary abnormalities - Tachypnea - Dyspnea - Hypoxemia
- 24. Clinical Manifestation (Cont’d.) 1.Pulmonary abnormalities - Diffuse bilateral inspiratory crepitation - Approximately one half of the patients with FES develop severe hypoxemia and require mechanical ventilation
- 25. Clinical Manifestation (Cont’d.) 2.Neurological abnormalities • Neurological abnormalities occur in majority of patient with FES and often occur after development of respiratory distress.
- 26. Clinical Manifestation (Cont’d.) 2.Neurological abnormalities • Affected patients usually develop a confusional state followed by an altered level of consciousness. • Seizures and focal deficits also have been described.
- 27. Clinical Manifestation (Cont’d.) 2.Neurological abnormalities • In severe injured patients it may difficult to separate changes caused by fat embolism from these caused by head injury.
- 28. Clinical Manifestation (Cont’d.) 2.Neurological abnormalities In general changes caused by fat embolism are diffuse without localization and may change quickly.
- 29. Clinical Manifestation (Cont’d.) 2.Neurological abnormalities • The etiology of these mental changes may related to hypoxia or direct fat embolism to the brain.
- 30. Clinical Manifestation (Cont’d.) 2.Neurological abnormalities • The duration and severity of the neurological disturbances are directly related to the degree of hypoxemia.
- 31. Clinical Manifestation (Cont’d.) 2.Neurological abnormalities • There is no relation between the severity of neurological signs and the prognosis for recovery. • The neurological finding are reversible in most cases.
- 32. Clinical Manifestation (Cont’d.) 3.Petechial haemorrhage • The classic clinical finding in patients with fat emnbolism is petechial haemorrhage which may appear as early as 12 hours after injury or late as 3 to 4 days. • The petechiae occur in 40 % of patient with FES.
- 33. Clinical Manifestation (Cont’d.) 3.Petechial haemorrhage • They can be seen most easily in the head, neck, anterior thorax, axilla and subconjunctiva, over the sclera and may accompanied by haemorrhages in the eye ground.
- 34. Clinical Manifestation (Cont’d.) 3.Petechial haemorrhage • The petechiae come in crops and feed over 48 hours. • The presence of 6 to 12 classic petechiae firmly establishes the clinical diagnosis of fat embolism.
- 35. Clinical Manifestation (Cont’d.) 3.Petechial haemorrhage • The petechial rash result from occlusion of dermal capillaries by fat globules loading to extravasation of erythrocyte or may due to increase capillary fragility. • The rash usually resolve in 5 to 7 days.
- 37. Diagnosis • FES clinicaldiagnosis usually characterized by presence of respiratory insufficiency, neurological impairment and petechial rash.
- 38. Diagnosis (Cont’d.) • ChestX-Ray normal in majority of patients • Minority have diffuse or patchy air space consolidation, these changes are due to oedema or alveolar haemorrhage and are most prominent in the periphery and bases.
- 41. Diagnosis (Cont’d.) • Ventilation/perfusionscans may demonstrate mottled pattern of subsegmental perfusion defects with normal ventilatory pattern.
- 42. Diagnosis (Cont’d.) • Focalareas of ground glass opacification with interlobar septal thickening are generally seen on chest CT.
- 46. Diagnosis (Cont’d.) • MRIof the brain may reveal high intensity T2 signal which correlate with the degree of clinical neurological impairment.
- 47. Diagnosis (Cont’d.) • Thereis growing literature on the use of bronchoscopy with BAL to detect fat globules in the alveolar macrophage as mean to diagnose fat embolism.
- 48. Gurd’s criteria Mostcommonly used 1 major, plus 4 minor
- 51. Treatment and Prevention 1.Early immoblization of the fractures reduce the incidence of FES. The risk further reduce by operative correction rather than conservative management (i.e. traction alone).
- 54. Treatment and Prevention 2.Supportive care is the mainstay of therapy for FES. 3. Mortality is estimated to be between 5 and 15 %.
- 55. Treatment and Prevention •Use of corticosteroid prophylaxis. There is number of study report decrease incidence of FES by use of prophylactic steroid.
- 56. Treatment and Prevention •Methyl Prednisolone 7.5 mg/kg every 6 hours for 12 doses. No complication related to steroid treatment was observed.
- 60. Treatment and Prevention •One rational, conservative approach would be to give prophylactic steroid therapy only to those patient at high risk for FES as those with long bone or pelvic fractures especially closed fractures. Give methyl Prednisolone 1.5 mg/kg every 8 hours for six doses.
- 62. Treatment and Prevention •Because hypoxemia is the fundamental physiological defect, its prevention by early administration of oxygen is reasonable.
- 63. Treatment and Prevention •If it becomes impossible to maintain Pa02 above 60 mmHg with 40 % oxygen inhalation, intubation and use of mechanical ventilation must be considered.
- 64. Treatment and Prevention •The use of positive end expiratory pressure is helpful to maintaining adequate oxygenation with lower concentration of oxygen. • There is no benefit to raising Pa02 above 100 mmHg.