2. HistoryHistory
First diagnosed in 1873 by Dr VonFirst diagnosed in 1873 by Dr Von
BergmannBergmann
1879 Fenger and Salisbury1879 Fenger and Salisbury
published description of FES.published description of FES.
3. FE vs. FESFE vs. FES
Fat emboli vs Fat emboli syndromeFat emboli vs Fat emboli syndrome
FE:FE: fat in the vascular circulation, can causefat in the vascular circulation, can cause
embolic phenomenon, more common 90% ptsembolic phenomenon, more common 90% pts
with traumatic injury (ECHO and BAL havewith traumatic injury (ECHO and BAL have
shown high incidence of FE after fractures andshown high incidence of FE after fractures and
orthopedic surgery)orthopedic surgery)
FES:FES: FE with pattern of sxs. Incidence 1-3%FE with pattern of sxs. Incidence 1-3%
femur fx, 5-10% if bilateral or multiple.femur fx, 5-10% if bilateral or multiple.
4. Fat Emboli SyndromeFat Emboli Syndrome
Mortality: 5-15%Mortality: 5-15%
Clinical diagnosis, No specific laboratory test isClinical diagnosis, No specific laboratory test is
diagnosticdiagnostic
Mostly associated with long bone and pelvic fxs,Mostly associated with long bone and pelvic fxs,
and more frequent in closed fracturesand more frequent in closed fractures
Single long bone fracture 1-3% chance ofSingle long bone fracture 1-3% chance of
developing FES, and increases with number ofdeveloping FES, and increases with number of
fxsfxs
Onset is 24-72 hours from initial insultOnset is 24-72 hours from initial insult
5.
6. Sickle Cell DiseaseSickle Cell Disease
FES can occur in SCFES can occur in SC
crisiscrisis
Bone marrow necrosis asBone marrow necrosis as
a result of hypoxia maya result of hypoxia may
release fatrelease fat
PLA2 has been seen toPLA2 has been seen to
increase 100x normal inincrease 100x normal in
SC crisis.SC crisis.
9. Pathogenesis- FEPathogenesis- FE
Direct entry of fat globules (fat entersDirect entry of fat globules (fat enters
torn venules)torn venules)
1.1. torn vesselstorn vessels
2.2. free fat presentfree fat present
3.3. temporary rise in marrow pressuretemporary rise in marrow pressure
above venous pressure.above venous pressure.
10. Pathogenesis- FEPathogenesis- FE
In orthopedic surgery echogenicIn orthopedic surgery echogenic
material can be seen inmaterial can be seen in R heartR heart
circulation.circulation.
Paradoxical embolism: fatParadoxical embolism: fat
embolism in arterial system, egembolism in arterial system, eg
PFOPFO
11. Pathogenesis- FESPathogenesis- FES
Production of toxic byproducts fromProduction of toxic byproducts from
TG/chylomicrons (lipase)TG/chylomicrons (lipase)
FES theorized to result fromFES theorized to result from degradation ofdegradation of
fat from FE to free fatty acidsfat from FE to free fatty acids causecause
vasculitis/ARDS). (inflammatory mediated).vasculitis/ARDS). (inflammatory mediated).
CRP also shown to be elevated in FE and causesCRP also shown to be elevated in FE and causes
fat agglutination.fat agglutination.
12. Pathogenesis of ARDS in FEPathogenesis of ARDS in FE
fat emboli obstructs lung vesselfat emboli obstructs lung vessel
(20 microns) platelets and fibrin(20 microns) platelets and fibrin
adhereadhere
Lipase creases FFALipase creases FFA
Inflammatory changesInflammatory changes
endothelial damage ARDSendothelial damage ARDS
13.
14. Triad of FESTriad of FES
HypoxemiaHypoxemia
Neurological abnormalitiesNeurological abnormalities
Petechial rashPetechial rash
16. PulmonaryPulmonary
Hypoxia, rales, pleural friction rubHypoxia, rales, pleural friction rub
ARDS may developARDS may develop
½ of pts with FES require mechanical½ of pts with FES require mechanical
ventilationventilation
CXR usually normal early on, later may showCXR usually normal early on, later may show
‘snowstorm’‘snowstorm’ pattern-pattern- diffuse bilateral infiltratesdiffuse bilateral infiltrates
CT chest:CT chest: ground glass opacification withground glass opacification with
interlobular septal thickeninginterlobular septal thickening
17. Neurological findingsNeurological findings
Usually occur after respiratory symptomsUsually occur after respiratory symptoms
Incidence 80% patients with FESIncidence 80% patients with FES
Minor global dysfunction most common, but rangesMinor global dysfunction most common, but ranges
from mild delirium to coma.from mild delirium to coma.
Seizures/focal deficits not common but can occurSeizures/focal deficits not common but can occur
Transient and reversible in most casesTransient and reversible in most cases
CT Head:CT Head: general edemageneral edema
MRI brain:MRI brain: Low density on T1, and high intensity T2Low density on T1, and high intensity T2
signal, correlates to degree of impairmentsignal, correlates to degree of impairment
18. RashRash
PetechialPetechial
Usually on conjuntiva, MM, neck, axillaeUsually on conjuntiva, MM, neck, axillae
Results from occlusion of dermal capillariesResults from occlusion of dermal capillaries
by fat globules and then extravasations ofby fat globules and then extravasations of
RBCRBC
Resolves in 5-7 daysResolves in 5-7 days
Pathognomonic, but only present inPathognomonic, but only present in 20-50%20-50% ofof
patientspatients
20. TreatmentTreatment
Supportive careSupportive care
Early immobilization of fx reducesEarly immobilization of fx reduces
incident of FESincident of FES
Conservative tx also reduces risk.Conservative tx also reduces risk.
Higher incidence when fixationHigher incidence when fixation
delayed greater than 24 hours.delayed greater than 24 hours.
21. SteroidsSteroids
Steroid prophylaxis is controversialSteroid prophylaxis is controversial
to prevent FESto prevent FES
Theorized blunting of inflammatoryTheorized blunting of inflammatory
response and complementresponse and complement
activationactivation
22. SteroidsSteroids
Few studies and small study size, soFew studies and small study size, so
remains controversial.remains controversial.
Prospective studies suggests prophylacticProspective studies suggests prophylactic
steroids benefit high risk patientssteroids benefit high risk patients
Once FES established, steroids have notOnce FES established, steroids have not
shown improved outcomes.shown improved outcomes.
23. Heparin and ASAHeparin and ASA
Have also been proposed for tx asHave also been proposed for tx as
they activate lipase and blockthey activate lipase and block
thromboxane respectively, but nothromboxane respectively, but no
evidence exists for either use inevidence exists for either use in
FES.FES.
24. Prevalence of PFO in the generalPrevalence of PFO in the general
population = 25%population = 25%