Fat emboli syndrome was first diagnosed in 1873 and involves the blockage of small blood vessels by fat globules, typically occurring 1-3 days after long bone fractures or pelvic fractures. It is characterized by a triad of hypoxemia, neurological abnormalities, and petechial rash. Treatment is supportive, with mechanical ventilation sometimes needed for respiratory failure and steroids proposed but controversial to prevent the inflammatory response. Prognosis is generally good with most neurological deficits being transient or reversible.

1. Fat EmboliFat Emboli
SyndromeSyndrome
Samir el ansarySamir el ansary

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

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.

7. Diagnostic CriteriaDiagnostic Criteria
Gurd criteria most commonlyGurd criteria most commonly
usedused
1 major, plus 4 minor1 major, plus 4 minor

8. Gurd CriteriaGurd Criteria

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

14. Triad of FESTriad of FES
HypoxemiaHypoxemia
Neurological abnormalitiesNeurological abnormalities
Petechial rashPetechial rash

15. Early SignsEarly Signs
Dyspnea,Dyspnea,
TachypneaTachypnea
HypoxemiaHypoxemia

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

19. Other findingsOther findings
 Retinopathy (exudates, cotton woolRetinopathy (exudates, cotton wool
spots, hemorrhage)spots, hemorrhage)
 LipiduriaLipiduria
 FeverFever
 DICDIC
 Myocardial depression (R heart strain)Myocardial depression (R heart strain)
 Thrombocytopenia/AnemiaThrombocytopenia/Anemia
 HypocalcemiaHypocalcemia

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%

25. Good luckGood luck
Samir elSamir el