Fat Embolism Syndrome (Fes)_dr. Mousa

8/3/2019 Fat Embolism Syndrome (Fes)_dr. Mousa

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BYBY

DR. MOUSA ELDR. MOUSA EL--SHAMLYSHAMLY

Consultant, PulmonologyConsultant, Pulmonology

King Saud HospitalKing Saud Hospital


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Fat embolism syndrome is aFat embolism syndrome is awellwell--known cause of pulmonaryknown cause of pulmonaryand neurologic dysfunctionand neurologic dysfunction

secondary to a variety ofsecondary to a variety ofinjuries.injuries.

Its presentation vary from a subIts presentation vary from a subclinical state to fulminantclinical state to fulminant

respiratory failure.respiratory failure.


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The amount of manipulation ofThe amount of manipulation ofinjured tissue and degree ofinjured tissue and degree ofhypovolemiahypovolemia ororhypoperfusionhypoperfusionare thought to be factors thatare thought to be factors that

predispose the patient to fatpredispose the patient to fat

embolism syndrome.embolism syndrome.Overall mortality range from 5 toOverall mortality range from 5 to15 %.15 %.


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PathophysiologyPathophysiologyFES most commonly associatedFES most commonly associatedwith long bone and pelvicwith long bone and pelvicfractures, and most common infractures, and most common inclosed rather than open fracture.closed rather than open fracture.

Patients with a single long bonePatients with a single long bone

fracture havefracture have 11--33 % chance of% chance ofdeveloping the syndrome .developing the syndrome .


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Pathophysiology (Contd.)Pathophysiology (Contd.)The incidence increase to 33 %The incidence increase to 33 %with bilateral femoral fractures.with bilateral femoral fractures.

Other less common causes includeOther less common causes includeliposuction thrombolytic therapyliposuction thrombolytic therapy

and orthopedic reconstructiveand orthopedic reconstructivesurgery.surgery.


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Pathophysiology Contd.Pathophysiology Contd.Theories about the origin of fatTheories about the origin of fatdeposition in the pulmonarydeposition in the pulmonary

vasculature include venous fatvasculature include venous fatembolization originating fromembolization originating fromtraumatized bone marrow ortraumatized bone marrow or

excessive mobilization of free fattyexcessive mobilization of free fattyacid from peripheral tissue secondaryacid from peripheral tissue secondaryto stress hormones.to stress hormones.


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Pathophysiology Contd.Pathophysiology Contd.Those acids coalesce in the bloodThose acids coalesce in the bloodand form fat aggregates.and form fat aggregates.

Regardless of the site of origin of fatRegardless of the site of origin of fatemboli the pulmonary capillaries actemboli the pulmonary capillaries actas filters and the emboli are carriedas filters and the emboli are carriedto the lung where they lodge into the lung where they lodge in

pulmonary capillaries and increasepulmonary capillaries and increaseresistance to blood flow.resistance to blood flow.


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PathophysiologyPathophysiology Contd.Contd.

The lungThe lung parenchymalparenchymal produceproduce

lipase to remove emboli.lipase to remove emboli.Hydrolysis of the triglycerides toHydrolysis of the triglycerides to

glycerol and fatty acid occurglycerol and fatty acid occurand chemicaland chemical pneumonitispneumonitis

results.results.


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Pathophysiology Contd.Pathophysiology Contd.This inflammatory response isThis inflammatory response ismediated by complementmediated by complementactivation platelet aggregationactivation platelet aggregationand leukocyt enzymatic action.and leukocyt enzymatic action.


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PathophysiologyPathophysiology Contd.Contd.Morphologically there is increaseMorphologically there is increase

in th

e permeability of th

ein th

e permeability of th

ecapillaries and alveolar cellcapillaries and alveolar cellWith leakage of fluid and proteinWith leakage of fluid and protein

into the alveolar wall and intointo the alveolar wall and intoalveolar space.alveolar space.


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Pathophysiology Contd.Pathophysiology Contd.Lung surfactant activity is decreased,Lung surfactant activity is decreased,functional residual capacity isfunctional residual capacity is

reduced and there is diffusion barrier.reduced and there is diffusion barrier.This cascade of events is seenThis cascade of events is seenclinically as decreased pulmonaryclinically as decreased pulmonarycompliance, increase a work ofcompliance, increase a work ofbreathing andhypoxia.breathing andhypoxia.


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Pathophysiology Contd.Pathophysiology Contd.Other studies demonstrate presents ofOther studies demonstrate presents ofechogenic material passing into rightechogenic material passing into right

heart during orthopedic and spinalheart during orthopedic and spinalsurgery, with continued emoblizationsurgery, with continued emoblization,pulmonary artery and right pressure,pulmonary artery and right pressure

rise and material can pass throughrise and material can pass throughpatent foramen ovale into systemicpatent foramen ovale into systemiccirculation resulating in paradoxicalcirculation resulating in paradoxical

embolism.embolism.


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Pathophysiology Contd.Pathophysiology Contd.Serum from acutely ill patientsSerum from acutely ill patientsh

as th

e capacity to agglutinateh

as th

e capacity to agglutinatechylomicrons, low densitychylomicrons, low densitylipoprotein and liposomes oflipoprotein and liposomes of

nutritional fat emulsions.nutritional fat emulsions.


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Pathophysiology Contd.Pathophysiology Contd.C reactive protein which appearC reactive protein which appear

to be elevated in th

ese patientto be elevated in th

ese patientappear to be responsible for theappear to be responsible for thelipid agglutination and may alsolipid agglutination and may also

participate in the mechanism forparticipate in the mechanism fornon traumatic fat embolism .non traumatic fat embolism .


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Clinical ManifestationClinical ManifestationFES typically manifest 24 to 72FES typically manifest 24 to 72h

ours after th

e initial insulth

ours after th

e initial insultrarely occur as early as 12 hoursrarely occur as early as 12 hoursor as later 2 weeks after theor as later 2 weeks after the

inciting events.inciting events.


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Clinical Manifestation (Contd.)Clinical Manifestation (Contd.)1.1. Pulmonary abnormalitiesPulmonary abnormalities

-- TachypneaTachypnea-- DyspneaDyspnea

-- HypoxemiaHypoxemia


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Clinical Manifestation (Contd.)Clinical Manifestation (Contd.)1.1. Pulmonary abnormalitiesPulmonary abnormalities

-- Diffuse bilateral inspiratoryDiffuse bilateral inspiratorycrepitationcrepitation

-- Approximately one half of theApproximately one half of the

patients with FES developpatients with FES developsevere hypoxemia and requiresevere hypoxemia and requiremechanical ventilationmechanical ventilation


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Clinical Manifestation (Contd.)Clinical Manifestation (Contd.)22. Neurological abnormalities. Neurological abnormalities

Neurological abnormalitiesNeurological abnormalitiesoccur in majority of patient withoccur in majority of patient withFES and often occur afterFES and often occur after

development of respiratorydevelopment of respiratorydistress.distress.


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Clinical Manifestation (Contd.)Clinical Manifestation (Contd.)2. Neurological abnormalities2. Neurological abnormalities

Affected patients usuallyAffected patients usuallydevelop a confusional statedevelop a confusional statefollowed by an altered level offollowed by an altered level of

consciousness.consciousness. Seizures and focal deficits alsoSeizures and focal deficits also

have been described.have been described.


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In severe injured patients itIn severe injured patients itmay difficult to separatemay difficult to separatechanges caused by fatchanges caused by fat

embolism from these causedembolism from these causedby head injury.by head injury.


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Clinical Manifestation (Contd.)Clinical Manifestation (Contd.)

2. Neurological abnormalities2. Neurological abnormalities

In general changes causedIn general changes causedby fat embolism are diffuseby fat embolism are diffuse

without localization and maywithout localization and maychange quickly.change quickly.


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Clinical Manifestation (Contd.)Clinical Manifestation (Contd.)22. Neurological abnormalities. Neurological abnormalities

The etiology of these mentalThe etiology of these mentalchanges may related tochanges may related tohypoxia or direct fat embolismhypoxia or direct fat embolism

to the brain.to the brain.


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The duration and severity ofThe duration and severity ofthe neurological disturbancesthe neurological disturbancesare directly related to theare directly related to the

degree ofhypoxemia.degree ofhypoxemia.


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There is no relation betweenThere is no relation betweenthe severity of neurologicalthe severity of neurologicalsigns and the prognosis forsigns and the prognosis for

recovery.recovery.

The neurological finding areThe neurological finding are

reversible in most cases.reversible in most cases.


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Clinical Manifestation (Contd.)Clinical Manifestation (Contd.)3. Petechialhaemorrhage3. Petechialhaemorrhage

The classic clinical finding in patientsThe classic clinical finding in patients

with fat emnbolism is petechialwith fat emnbolism is petechialhaemorrhage which may appear ashaemorrhage which may appear asearly as 12 hours after injury or lateearly as 12 hours after injury or late

as 3 to 4 days.as 3 to 4 days. The petechiae occur in 40 % ofThe petechiae occur in 40 % of

patient with FES.patient with FES.


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Clinical Manifestation (Contd.)Clinical Manifestation (Contd.)33. Petechialhaemorrhage. Petechialhaemorrhage

They can be seen most easily in

They can be seen most easily inthe head, neck, anterior thorax,the head, neck, anterior thorax,

axilla and subconjunctiva, overaxilla and subconjunctiva, over

the sclera and may accompaniedthe sclera and may accompaniedby haemorrhages in the eyeby haemorrhages in the eye

ground.ground.


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The petec

hiae come in crops

The petec

hiae come in cropsand feed over 48 hours.and feed over 48 hours.

The presence of 6 to 12 classicThe presence of 6 to 12 classic

petechiae firmly establishes thepetechiae firmly establishes theclinical diagnosis of fatclinical diagnosis of fatembolism.embolism.


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The petechial rash result fromThe petechial rash result from

occlusion of dermal capillaries byocclusion of dermal capillaries byfat globules loading tofat globules loading toextravasation of erythrocyte or mayextravasation of erythrocyte or may

due to increase capillary fragility.due to increase capillary fragility.

The rash usually resolve in 5 to 7The rash usually resolve in 5 to 7

days.days.


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DiagnosisDiagnosis FES clinical diagnosisFES clinical diagnosis

usually ch

aracterized byusually ch

aracterized bypresence of respiratorypresence of respiratoryinsufficiency, neurologicalinsufficiency, neurological

impairment and petechialimpairment and petechialrash.rash.


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Diagnosis (Contd.)Diagnosis (Contd.) Chest XChest X--Ray normal in majorityRay normal in majority

of patientsof patients

Minority have diffuse or patchyMinority have diffuse or patchyair space consolidation, theseair space consolidation, these

ch

anges are due to oedema orch

anges are due to oedema oralveolarhaemorrhage and arealveolarhaemorrhage and aremost prominent in the peripherymost prominent in the periphery

and bases.and bases.


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Diagnosis (Contd.)Diagnosis (Contd.) Ventilation/perfusion scansVentilation/perfusion scans

may demonstrate mottledmay demonstrate mottledpattern of subsegmentalpattern of subsegmentalperfusion defects with normalperfusion defects with normal

ventilatory pattern.ventilatory pattern.


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Diagnosis (Contd.)Diagnosis (Contd.) Focal areas of ground glassFocal areas of ground glass

opacification with interlobaropacification with interlobarseptal thickening areseptal thickening aregenerally seen on chest CT.generally seen on chest CT.


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Diagnosis (Contd.)Diagnosis (Contd.) MRI of the brain may revealMRI of the brain may reveal

high

intensityT

2 signal wh

ich

h

igh

intensityT

2 signal wh

ich

correlate with the degree ofcorrelate with the degree ofclinical neurologicalclinical neurological

impairment.impairment.


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Diagnosis (Contd.)Diagnosis (Contd.) It is a comoon misconceptionIt is a comoon misconception

th

at th

e presence of fatth

at th

e presence of fatglobule either in sputumglobule either in sputum,urine or a wedgedPA,urine or a wedgedPA

catheter is necessary tocatheter is necessary toconfirm the diagnosis of FES.confirm the diagnosis of FES.


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Diagnosis (Contd.)Diagnosis (Contd.) In one study presence of fatIn one study presence of fat

was demonstrated in th

ewas demonstrated in th

eserum of more thanserum of more than 5050 % of% offracture patients withoutfracture patients without

symptom suggestive of FES.symptom suggestive of FES.


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Diagnosis (Contd.)Diagnosis (Contd.) There is growing literature onThere is growing literature on

th

e use of bronch

oscopy with

th

e use of bronch

oscopy with

BAL to detect fat globules inBAL to detect fat globules inthe alveolar macrophage asthe alveolar macrophage as

mean to diagnose fatmean to diagnose fatembolism.embolism.


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Treatment andPreventionTreatment andPrevention1. Early immoblization of the1. Early immoblization of the

fractures reduce th

e incidencefractures reduce th

e incidenceof FES. The risk furtherof FES. The risk furtherreduce by operative correctionreduce by operative correction

rather than conservativerather than conservativemanagement (i.e. tractionmanagement (i.e. tractionalone).alone).


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Treatment andPreventionTreatment andPrevention2. Supportive care is the2. Supportive care is the

mainstay of th

erapy for FES.mainstay of th

erapy for FES.3. Mortality is estimated to be3. Mortality is estimated to be

between 5 and 15 %.between 5 and 15 %.


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Treatment andPreventionTreatment andPrevention Use of corticosteroidUse of corticosteroid

proph

ylaxis.Th

ere is numberproph

ylaxis.Th

ere is numberof study report decreaseof study report decreaseincidence of FES by use ofincidence of FES by use of

prophylactic steroid.prophylactic steroid.


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Treatment andPreventionTreatment andPrevention MethylPrednisolone 7.5MethylPrednisolone 7.5

mg/kg every 6h

ours for 12mg/kg every 6h

ours for 12doses. No complicationdoses. No complicationrelated to steroid treatmentrelated to steroid treatment

was observed.was observed.


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Treatment andPreventionTreatment andPrevention One rational, conservative approachOne rational, conservative approach

would be to give prophylactic steroidwould be to give prophylactic steroid

therapy only to those patient athigh risktherapy only to those patient athigh riskfor FES as those with long bone orfor FES as those with long bone or

pelvic fractures especially closed pelvic fractures especially closed

fractures. Give methylPrednisolone 1.5 fractures. Give methylPrednisolone 1.5mg/kg every 8 hours for six doses.mg/kg every 8 hours for six doses.


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Treatment andPreventionTreatment andPrevention Because hypoxemia is theBecause hypoxemia is the

fundamental ph

ysiologicalfundamental ph

ysiologicaldefect, its prevention by earlydefect, its prevention by earlyadministration of oxygen isadministration of oxygen is

reasonable.reasonable.


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Treatment andPreventionTreatment andPrevention If it becomes impossible toIf it becomes impossible to

maintainP

a02 above 60maintainP

a02 above 60mmHg with 40 % oxygenmmHg with 40 % oxygeninhalation, intubation and useinhalation, intubation and use

of mechanical ventilationof mechanical ventilationmust be considered.must be considered.


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Treatment andPreventionTreatment andPrevention The use of positive endThe use of positive end

expiratory pressure is helpful toexpiratory pressure is helpful to

maintaining adequatemaintaining adequateoxygenation with loweroxygenation with lowerconcentration of oxygen.concentration of oxygen.

There is no benefit to raisingThere is no benefit to raisingPa02 above 100 mmHg.Pa02 above 100 mmHg.


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Fat Embolism Syndrome (Fes)_dr. Mousa

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