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Fat Embolism Syndrome Ri 周周周 周周周 :P 周周周 . Vs 周周周 .
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May 31, 2015

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Fat Embolism Syndrome

Ri 周兆亮指導者 :P 柯文哲 . Vs 徐紹勛 .

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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 embolism”refer 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 vas

cular 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 o

cclusion 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 (PaO2<60mmHg a

nd FiO2>0.4), CNS depression, petechiae minor signs of tachycardia(HR>120), pyrexi

a(T>39), thrombocytopenia (plt<150K/uL), fat globules in urine or sputum, retinal emboli, decline in hematocrit can’t 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 p

’t with long bone fracture, incidence 0.9% the mean ISS was 9.5 4 p’t have all 3 major signs, 16 p’t had 2

major signs, 7 p’t had 1 major sign. 6 p’t 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 wit

hin 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 P’t, 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 re

search suggested an poor specificity

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Bronchoalveolar Lavage Bronchoalveolar lavage in trauma patients for diagnosis of fat e

mbolism syndrome. Chest. 1992;102:1323-1327. It divide three groups: (1)26 p’t without trauma.(2)2

2 p’t with trauma and without FES.(3)9 p’t with trauma and FES

It exam total cells, neutrophils, macrophages, fat droplets in macrophages(6/26,9/22,6/9)

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 p’t intubation for hypoxia or alter

ed mental status. Mean stay in ICU is 6 days, hospital sta

y is 15 days of intubation p’t.

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Ventilatory strategies Lung protective stratery: Low tidal volumes,

adequate PEEP. Pressure-control mood(PCV) and inverse I:E

ratio can increase mean distending pressure without increasing peak pressure.

To achieves SaO2>90% with FiO2<0.6 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 P’t 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