Fat Embolism Syndrome

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Fat Embolism Syndrome

• Ri
• P. Vs.

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Fat embolism syndrome

• First described by Zenker in 1861.
• Persistent debate has remained as to the
  specifics of the diagnosis and management of this
  clinical syndrome.

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• Current concepts of respiratory insufficiency
  syndromes after fracture. Journal of Bone
  Joint Surgery - British Volume. 83(6)781-91
  2001 Aug.
• Fat embolism syndrome. A 10-year review.
  Archives of Surgery. 132(4)435-9 1997 Apr

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Fat Embolism

• Term fat embolismrefer to the presence of fat
  globules in the lung parenchyma and peripheral
  circulation
• Fat embolism occurs in over 90 of patients after
  fracture

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Fat Embolism syndrome

• Fat embolism syndrome(FES) is a serious
  manifestation of respiratory dermatological and
  neurological symptoms.
• FES is quite unusual about incidence 1-5 after
  long bone fracture.

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Pathophysiological mechanism
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Pathophysiological mechanism

• FE can produce tissue damage by direct vascular
  occlusion breakdown to toxic free-fatty acids
  activation of platelets and coagulative and
  fibrinolytic cascades.
• FES may occur either from massive FE paticular
  in a patent foramen ovale or abnormal response
  of the individual to intravascular fat.

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Pathophysiological mechanism

• Histological finding include microvascular
  occlusion from fibrin and platelet aggregate
  interstitial leakage of protein and neutrophil
  rich fluid lead to diffuse alveolar damage.
• Detectable change include decrease functional
  residual capacity decrease compliance and
  increase pulmonary vascular resistance.

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Diagnosis

• FES remains a diagnosis of exclusion and is based
  on clinical criteria

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Gurd Criteria

• 3 major signs of hypoxia (PaO2lt60mmHg and
  FiO2gt0.4) CNS depression petechiae
• minor signs of tachycardia(HRgt120)
  pyrexia(Tgt39) thrombocytopenia (pltlt150K/uL)
  fat globules in urine or sputum retinal emboli
  decline in hematocrit cant be accounted for
  blood loss or fluid dilution
• 1 major and 3 minor or 2 major and 2 minor

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Incidence

• 27 cases of FES was identified from 3026 pt with
  long bone fracture incidence 0.9
• the mean ISS was 9.5
• 4 pt have all 3 major signs 16 pt had 2 major
  signs 7 pt had 1 major sign. 6 pt demonstrated
  hypoxia as their only major sign.

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Incidence
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Fat embolism vs. thromboembolism

• Fat embolism syndrome often occurred within 24-48
  hrs after trauma but thromboembolism is uncommon
  sooner than 5 days after immobilization.
• Contrast venography is diagnostic gold standard
  of thromboembolism.

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Suggested framework

• Fat embolism is often occurred within 24-48 hr
  after injury but thromboembolism is uncommon
  sooner than 5 days after immobilization
• To diagnosis thromboembolism contrast venography
  is the gold standard

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Ventilation-perfusion scans

• It were helpful for excluding pulmonary
  embolus(10 of 27 Pt one was read as multiple
  small peripheral defects others interpreted
  negative )
• Emboli tend to be too small to be detected. The
  cause of pulmonary damage is direct toxic effect
  of free fatty acids rather than to obstruction of
  the vascular.

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Labratory test

• ABG thrombocytopenia anemia were all
  non-specific
• Fat globules in urine(6 of 11) other research
  suggested an poor specificity

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Bronchoalveolar Lavage

• Bronchoalveolar lavage in trauma patients for
  diagnosis of fat embolism syndrome. Chest.
  19921021323-1327.
• It divide three groups (1)26 pt without
  trauma.(2)22 pt with trauma and without FES.(3)9
  pt with trauma and FES
• It exam total cells neutrophils macrophages
  fat droplets in macrophages(6/269/226/9)
• presence of fat droplets in alveolar macrophage
  is not reliable method for diagnosis of FES after
  trauma many conditions are associated with fat
  droplets in alveolar macrophages.

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Chest X-ray
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Risk factors of fracture pattern

• The literature suggest a higher incidence of FES
  in patient with more than one long bone fracture.
• Location clearly favors the lower extremities
  but no greater risk of total fracture population
• The paper documented a highter proportion of open
  fracture in the group with FES(26) than total
  fracture population

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Management strategies

• Support care
• 12 pt intubation for hypoxia or altered mental
  status.
• Mean stay in ICU is 6 days hospital stay is 15
  days of intubation pt.

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Ventilatory strategies

• Lung protective stratery Low tidal volumes
  adequate PEEP.
• Pressure-control mood(PCV) and inverse IE ratio
  can increase mean distending pressure without
  increasing peak pressure.
• To achieves SaO2gt90 with FiO2lt0.6 and no
  significant cardiac output compromise
• prone position

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Medication

• Heparin albumin hypertonic glucose with insulin
  all failed to show benefit by studies
• corticosteroids human trial have poor control and
  showed increasing infection rate. One study
  suggests a potential benefit for prophylactic
  treatment.

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Early fracture fixation

• One paper suggest early fracture stabilization
  decreases the incidence of FES. The other paper
  showed no notable difference but it dose not
  seem to increase incidence of FES.

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Prognosis

• Pt with FES may have persistent neurological
  deficits.
• Severe trauma mortality from FES is usually
  between 5-15 other are due to other injury or
  secondary infection.

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THE END