Umesh Yadav presented on fat embolism syndrome. Key points include: 1) Fat embolism syndrome is a serious complication of long bone fractures that can cause multi-system organ dysfunction, most commonly involving the lungs and brain. 2) The pathophysiology involves fat globules entering the bloodstream from broken bone marrow and lodging in the pulmonary vasculature and brain. This can lead to hypoxemia, neurological changes, and petechial rashes. 3) Diagnosis is clinical based on criteria like Gurd's that require respiratory symptoms plus findings in two other organ systems. Treatment focuses on fracture stabilization, ventilation, volume resuscitation and sometimes

1. PRESENTOR-UMESH YADAV
DEPARTMENT OF ORTHOPAEDICS
PGIMS,ROHTAK
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2. HISTORY
Zenker, a pathologist,1st identified fat
embolism syndrome at autopsy 1862.
First diagnosed in 1873 by Dr Von
Bergmann
1879 Fenger and Salisbury published
description of FES
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3. Some definitions…
Fat Emboli: Fat particles or droplets
that travel through the circulation
Fat Embolism: A process by which fat
emboli passes into the bloodstream
and lodges within a blood vessel.
Fat Embolism Syndrome (FES):
serious manifestation of fat embolism
occasionally causes multi system
dysfunction, the lungs are always
involved and next is brain
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4. Causes of FES
 Blunt
Trauma
(90%)
 Long bone
(Femur,
tibia, pelvic)
factures
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5. Causes of FES(cntd.)
 More frequent in CLOSED # than OPEN #
 Younger pts > old patients d/t increased bone
marrow.
 A single bone # has 1-5% chances of developing FES,
directly correlates with the no. of long bone fractures.
 FES has been reported as high as 33% in b/l shaft
femur fractures.
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6. Causes of FES
• Non Trauma: agglutination of chylomicrons and VLDL
by high levels of plasma CRP.
– disease-related
• Diabetes, acute pancreatitis, burns, SLE, sickle cell crisis
– drug-related
• parenteral lipid infusion
– procedure-related
• Orthopedic surgery, liposuction
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7. Pathophysiology of FES
Exact mechanism unknown, but two main hypothesis
• Mechanical vs. Biochemical
• Mechanical – Fat globules from disrupted bone
marrow or adipose tissue are forced into torn venules
in areas of trauma.
• Biochemical – Hormonal changes caused by trauma
and/or sepsis induce systemic release of free fatty
acids (FFA) as chylomicrons which cause the systemic
FES.
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8. Mechanical hypothesis-
 – Fractures of marrow-containing bone (Femur,
Pelvis) have the highest incidence of FES and
cause the largest volume of fat emboli, because the
disrupted venules in the marrow remain tethered
open by their osseous attachments.
 – The marrow contents enter the venous circulation
with little difficulty.
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9. Mechanical hypothesis (cntd.)
This theory is supported by research on Orthopaedic
long bone (IM reaming) and spinal surgeries which
cause fat globules to enter the blood circulation when
vigorous reaming/fixation is done.
 Increased Pressure + Volume Extravasation
 Measuring fat globules pre and post reaming shows
significant difference in concentration.
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10. Cntd.-
Fat droplets are deposited in the pulmonary capillary
beds and travel through arteriovenous shunts to the
brain. Systems affected include LUNG, BRAIN and
CIRCULATION.
 Microvascular lodging of droplets produces local
ischemia and inflammation, with concomitant release
of inflammatory mediators, platelet aggregation, and
vasoactive amines.
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11. Biochemical Hypothesis-
 FES is dependent upon degradation of the embolized
fat into free fatty acids.
 Neutral fat does not cause an acute lung injury, it is
hydrolyzed over the course of hours to several
products, including FFA, which cause ARDS in animal
models.
 CRP (acute phase reactant), which is elevated in
trauma patients, appears to be responsible in lipid
agglutination (FES) for both traumatic and non-
traumatic FES.
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12. Biochemical theroy (cntd.)
 The process of Neutral fat cells -> FFA ->
Agglutination with CRP may explain the time
sequence of clinical findings in FES.
 Onset of symptoms may coincide with Agglutination.
 This theory is animal model based and circumstantial
at best.
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13. CLINICAL PRESENTATION-
 Diagnosis is made clinically NOT chemically. It does
not matter how much fat globules are in your
circulation, it just matters if you have their side
effects.
 FES typically manifests 24 to 72 hours after the initial
insult. Rarely <12 hrs or >72 hrs.
 Classic triad: Hypoxemia; Neurologic abnormalities;
and a Petechial Rash
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14. Early Signs
 Dyspnea,
 Tachypnea
 hypoxemia
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15. Pulmonary
 Hypoxia, rales, pleural friction rub
 ARDS may develop
 ½ of pts with FES require mechanical ventilation
(Bulger, Archives of Surgery 1997; 132: 435-9)
 CXR usually normal early on, later may show
‘snowstorm’ pattern- diffuse bilateral infiltrates
 CT chest: ground glass opacification with interlobular
septal thickening
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17. Neurological findings
 Usually occur after respiratory symptoms.
 Incidence 80% patients with FES
 Minor global dysfunction most common, but
ranges from mild delirium to coma.
 Seizures/focal deficits not common but can occur
 Transient and reversible in most cases
 CT Head: general edema, usu nonspecific
 MRI brain: Low density on T1, and high intensity
T2 signal, correlates to degree of impairment
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18. MRI showing foci of ischemia
suggestive of fat embolism
syndrome
post operative day 14 and
shows evolving cortical
infarctions
post operative day 2
showing multiple
hyperintense areas
consistent with multiple
emboli
Source:http://www.ispub.com/journal/the_internet_journal_of_anesthesiology/volume_19_number_2/article/acute_fatal_fat_embolism_syndrome_in_bilateral_total_knee_arthroplasty_a_review_of_the_fat_embolism_syndrome.html
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19. Rash
 Petechial
 Usually on conjuntiva,neck, axillae
 Results from occlusion of dermal capillaries by fat
globules and then extravasations of RBC
 Resolves in 5-7 days
 Pathognomonic, but only present in 20-50% of
patients
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22. Other findings
 Retinopathy (exudates, cotton wool spots,
hemorrhage)
 Lipiduria
 Fever
 DIC
 Myocardial depression
 Thrombocytopenia/Anemia
 Hypocalcemia
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23. DIAGNOSIS-
 FES is CLINICAL diagnosis, not biochemical.
 A high degree of suspicion is needed to make diagnosis .
-Common misconception that the presence of fat globules, either
in sputum, urine, or a wedged PA catheter, is necessary to
confirm the diagnosis of FES
In 50% of fracture patients, fat globules was demonstrated in
the serum, without symptoms of FES.
 HOWEVER
 Growing literature on the use of bronchoscopy with
bronchoalveolar lavage to detect fat droplets in alveolar
macrophages as a means to diagnose fat embolism. Sensitivity
and specificity are unknown, being studied in Trauma patients. .
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24. Gurd’s Criteria
 FES = 1 major + 4 minor + fat microglobulinemia
 Still widely used today
Major features Minor features
Petechial rash Tachycardia> 120 /min
Respiratory symptoms
plus bilateral signs with
positive radiographic
changes
Pyrexia > 39.4 ℃
Retinal fat or petechiae
Urinary fat globules or oligoanuria
Sudden drop in Hb level > 20%
Cerebral signs
unrelated to head injury
Sudden thrombocytopenia > 50%
High ESR > 71 mm/h
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25. Lindeque’s Criteria
 FES = femur fracture ± tibia fracture + 1 feature
 Based on respiratory parameters
A sustained PaO2 < 8 kPa (60 mmHg)
A sustained PaCO2 > 7.3 kPa (55 mmHg) or pH <
7.3
A sustained respiratory rate > 35 /min even after
adequate sedation
Increased work of breathing judged by dyspnea,
use of accessory muscles, tachycardia and anxiety
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26. Schonfeld: Fat Embolism Index
 FES = 5 or more points
Points
Diffuse petechiae 5
Alveolar infiltrates 4
Hypoxemia (< 70 mmHg) 3
Confusion 1
Fever > 38 ℃ 1
Heart rate > 120 /min 1
Respiratory rate > 30 /min 1
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27. SEVITT’S CLASSIFICATION-
 3 TYPES- In 1962
 SUBCLINICAL FES
 NON FULMINANT FES
 FULMINANT FES
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28. SUB CLINICAL FES
 Around 3 days post trauma
 Probably occurs in almost all long bone
fractures of the lower extremity and fractures of the
pelvis
 Characterised by decreased PaO2, decreased Hb% and
decreased platelets. No clinical signs and symptoms of
respiratory insufficiency.
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29. NON FULMINANT FES
- Any time ,upto 6 days post trauma
-Clinical signs and symptoms are clearly
evident.
 Petechiae, tachycardia, respiratory failure, and signs of
CNS embolism.
 Thrombocytopaenia, anaemia, and coagulation
abnormalities can be found, as can pulmonary alveolar
and interstitial opacities on chest x ray
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30.  There is no definitive test for this version of the
syndrome, as most of the changes described can occur
as a result of trauma as well as a result of fat
embolism, the diagnosis remains a clinical one, and
the significance is uncertain.
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31. FULMINANT FES
 Occurs very suddenly and rapidly after injury, and
progresses very quickly, often resulting in death
within a few hours of the initial trauma.
 Clinical features are acute respiratory failure, acute
cor pulmonale and embolic neurological changes.
 These occur shortly after injury and often result in the
death of the patient.
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32.  Pats. with multiple fractures are particularly
susceptible to this form of the syndrome, which,
although it is relatively rare, is of immense clinical
significance because of its high mortality.
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33. TREATMENT-
 ATLS protocol
 1. Early immobilization of fracture and early
definitive reduction (open or closed).
 2. Maintain intravascular volume to maintain
cardiovascular stability (hypovolemic shock
resuscitation), may use colloids (albumin) as it can
expand fluid and bind FFA.
 3. Mechanical ventilation with PEEP
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34. Rx (cntd.)
 4. IV Ethanol has been used in Russia, Europe and some
American centres to decrease rate of FES.
J Bone Joint Surg Am. 1977 Oct;59(7):878-80
 “A raised level of alcohol in the blood was associated with a
lower incidence of fat embolism” all other variables controlled.
- Other studies
- Can J Surg. 1970 Jan;13(1):41-9
- Br Med J. 1978 May 13;1(6122):1232-4
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35. Rx- STEROIDS
 Steroid prophylaxis is controversial to prevent FES
 Theorized blunting of inflammatory response and
complement activation
 Prospective studies suggests prophylactic steroids
benefit high risk patients
 Few studies and small study size, so remains
controversial.
 Once FES established, steroids have not shown
improved outcomes.
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36. Rx-HEPARIN
 Like steroids, controversial role in management.
 Stimulates lipase to reduce lipemia.
 Reverses the DIC picture.
 S/E- Inc in circulating free fatty acids,
 -bleeding risks
 Routine use not recommended.
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37. Rx-SUMMARY
 Treatment
 The overall outcomes of FES with respect to isolated long
bone, pelvis and spine fractures is good with standard
immobilization and reduction of fracture, fluid
resuscitation and ventilator y support as needed.
 Steroids and Ethanol treatments can be adjuncts to
treatment, but most be started early.
 Recommended to start with low dose and for a
period of 24-48 hours.
 No evidence on Steroids or Ethanol Tx once FES is
diagnosed. This is only for Prophylaxis
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38. Risk Factors
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39. UMY