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FAT EMBOLISMSYNDROME

(FES)

Harun Rosidi


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FES-Introduction

FES may be defined as a complexalteration of haemostasis which occurs asan infrequent complication of fractures ofthe pelvis and/or long bones andmanifests clinically as acute respiratoryinsufficiency.

First described in 1862 by Von Bergmannas a triad of confusion, dyspneu andpetechiae following fracture of long bones


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Introduction-FES

FES commonly follows long bone fracturesalthough it is also associated with othernontraumatic causes such as fatty liver,

prolonged corticosteroids use, acute pancreatitisand osteomyelitisClassic presentation consists of asymptomaticinterval (12-48 hours ) followed by pulmonaryand neurologic manifestations combined withpetechial hemorrhage.


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Introduction-FES

Biphasic clinical course-Initial symptoms probably caused bymechanical occlusion of multiple bloodvessels with fat globules which is oftentemporary and incompleteLate presentation thought to be caused by

hydrolysis of fat globules to more irritant freefatty acids which migrate to other organs


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Incidence

Exact incidence and mortality not knownHoyt et al studied the incidence ofpulmonary complications in trauma victimsduring a three year study period and foundthat 11.2 % trauma patients develop fatembolism


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FES-Risk factors

Most common after skeletal injury andmore likely in long bone and pelvicfractures

More likely in closed rather than openfracturesMore common when there is movement of

unstable bone fragments and reaming ofmedullary cavity during internal fixation


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FES-Risk factors

Multiple fracture more at risk than singlefractureYoung men with fractures are more at riskthan older men and children


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FES-Pathophysiology

Two theories-

Mechanical theory

Biochemical theory


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Pathophysiology

Mechanical theoryPhysical obstruction of pulmonary andsystemic vasculature with embolized fat .

Increased intramedullary pressure forcesmarrow into injured venous sinusoids, fromwhich fat travels to lung and occludes

pulmonary capillaries.Fat emboli can cause cor-pulmonale if noadequate pulmonary vasodilatation occur


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Pathophysiology

Biochemical theory -proposed byBaker et al

Circulating free fatty acids are directly toxic topneumocytes and capillary endothelium,causing interstitial hemorrhage , edema andchemical pneumonitis

It is also possible that shock, hypovolemiaand sepsis can exacerbate the toxic effects offree fatty acids


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Clinical Presentation

Must have high index of suspicion andthorough knowledge of FES for diagnosisto be made.

An asymptomatic period of about 12-48hours precedes clinical manifestationsFulminant form presents as acute cor-pulmonale, respiratory failure and laterdeath within few hours of injury


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TachycardiaTachypneu

Elevated temperatureHypoxemiaHypocapnia

Thrombocytopenia


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HypoxaemiaOccuring in nearly all patients with FES

PaO2 below 60 mmHg Attributed to ventilation-perfusion inequalityand intrapulmonary shunting


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Acute cor-pulmonaleManifested by respiratory distress,hypoxemia, hypotension and elevated centralvenous pressure.Pulmonary insufficiency occurs in 75% and10% progress to respiratory failure

Chest X-ray may show Snow stormappearance, increased pulmonary markingsand dilated right side of the heart


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CNS signs-occur in up to 86% patients Acute confusionStuporComaRigidityconvulsions


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Petechial rash that appears on upperanterior portion of body-occur in 50-60%pts

NeckChestUpper arm

AxillaShouldersOral mucous membrane and conjunctivae


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Diagnosis

Gurds Criteria for diagnosis Major Features(at least one)

1. Respiratory Insufficiency2. Cerebral Involvement

3. Petechial RashMinor Features(at least four)

1. Pyrexia2. Tachycardia3. Jaundice4. Retinal Changes5. Renal Changes

Laboratory Features(at least #1)

1. Fat Macroglobulinemia2. Anemia3. Thrombocytopenia4. High ESR


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Diagnosis

Schonfelds Fat Embolism Index

Symptom Score Petechiae

Diffuse Alveolar infiltrates

Hypoxemia ( PaO2 38 oC Heart Rate > 120 beats/min

Respiratory Rate > 30/min

5

4

3

1

11

1

A score > 5 is con s idered d iagnos t ic


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Laboratory Tests

Non-specificSerum lipase level-which can be misleading inbone traumaCytologic examination of urine, blood andsputum with Sudan or oil red O staining todetect fat globules-not sensitive

Haematocrit-decreased within 24-48 hoursdue to intra alveolar haemorrhage


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Laboratory tests

Blood lipid level-not helpful becausecirculating fat levels does not correlatewith severity of syndromeDeranged coagulation andthrombocytopaenia


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Management

Prophylactic measure-Early immobilization and reduction of longbone fracture


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Management

Supportive measures-Maintenance of adequate intravascular

volume as shock can exacerbate lung injurycaused by FES

Albumin has been recommended for volume

resuscitation. It balances electrolyte solutionand also binds to the toxic fatty acids


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Management

Supportive measures-

Mechanical ventilation and PEEP to maintain

arterial oxygenationHigh dose corticosteroids still controversial

Maintain perfusion by optimizing cardiac

output through use of inotropes

Haematocrit to be kept above 30% w/p RBC


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Morbidity and mortality

Most commonly self-limiting andpulmonary function returns to normal if

adequate supportive care givenMortality is about 5-15% and is closelycorrelated to respiratory complications

Most long term morbidity is secondary tofocal cerebral neurologic deficits


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Conclusion

FE usually sub clinical, occurring mostly inlong bone fracture particularly tibia and

femurClinical diagnosis is still the cornerstone ofdiagnosing FE

Respiratory insufficiency, petechiae andCNS changes still pathognomic of FES


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Conclusion

Management consists of prophylacticmeasures and aggressive supportive carewhich includes early immobilization andreduction of fracture, possible mechanicalventilation, volume replacement andanalgesia.

Fortunately, most patients survive FESwithout sequelae today


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