Fat Embolism Syndrome (FES) is a Syndrome characterized by: Hypoxia, Confusion and Petechiae. Presenting soon after long bone fracture and soft tissue injury. Diagnosed by exclusion of other causes 0f (Hypoxia & Confusion). It occurs in 0.9 – 8.5% of all fracture patients. Up to 35% of the multiply injured. Mortality 2.5 – 15 - 20%. Rare in upper limb injury and children. Treatment includes prompt stabilization of long bone fractures and supportive measures which includes: 1- Oxygen Therapy to maintain PaO2. 2- Mechanical Ventilation. 3- Adequate Hydration.

1. Dr. Fathi Neana, MD
Chief of Orthopaedics
Dr. Fakhry & Dr. A. Al-Garzaie Hospital
January, 15 - 2019
Polytrauma
Part 3
(FES)
Fat Embolism Syndrome

4. Trauma
Tissue injury
Infection
Inflammatory
Mediators
Release
Organ
Injury
Acute respiratory distress syndrome ARDS
ARDS related to MODS & MOF
Common Pathological Pathways
1- Inflammatory mediators ->> Systemic inflammatory response syndrome (SIRS )
2- Anti-inflammatory mediators ->> Compensatory anti-inflammatory response syndrome (CARS)
3- The conflict between these two immune responses (SIRS) vs. (CARS) will end up with:
A- Cure
B- Death (Parenchymal cell Necrosis and Apoptosis )
C- Long standing inflammation ->> Multi organ Dysfunction Syndrome (MODS ) or Failure (MOF)

5. Inflammatory Mediators Release
(SIRS vs CARS)
A Host defence immune response Release of
1- Inflammatory mediators Local and systemic
(pro-inflammatory cytokines, arachidonic acid metabolites,
proteins of the contact phase and coagulation systems,
complement factors and acute phase proteins, as well as
hormonal mediators)
Clinically : Systemic inflammatory response syndrome (SIRS)
2- Anti-inflammatory mediators
are produced (compensatory anti-inflammatory response
syndrome) (CARS)
Imbalance of these Two immune responses (SIRS & CARS) is
responsible for organ dysfunction & increased susceptibility to
infections
Endothelial cell damage, Accumulation of leukocytes,
Disseminated intravascular coagulation (DIC) and
Microcirculatory disturbances
Finally lead to Apoptosis and Necrosis of Parenchymal cells
& Development of multiple organ dysfunction syndrome
(MODS) or multiple organ failure (MOF)

7. MODS - MOF (Multi Organ Dysfunction or Failure Syndrome)

8. Fat Embolism
Syndrome
(FES)

9. What is Fat Embolism Syndrome
(FES)
A Syndrome characterized by
Hypoxia,
Confusion
and Petechiae
presenting soon after long bone
fracture and soft tissue injury
Diagnosis of Exclusion of other
causes 0f (Hypoxia & Confusion)
Occurs in 0.9 – 8.5% of all fracture
patients
Up to 35% of the multiply injured
Mortality 2.5 – 15 - 20%
Rare in upper limb injury and
children

10. Incidence ranges from <1% to 29% in different studies
Fat globules detected in blood of 67% of orthopaedic trauma
patients. Increased to 95% in blood samples near to the fracture
site
The presence of fat globules in the blood does not automatically
lead to FES
Men are more likely than women
Rare in children aged 0-9 years
Age group commonly affected 10-39 years
Fat Embolism Syndrome (FES)
Epidemiology

12. Fat macro-globules embolic pass into
small vessels (lung and other sites)
Producing Endothelial Damage
Leading to
Respiratory failure (ARDS-like picture)
Cerebral Dysfunction
Petechial Rash
Fat embolism syndrome
(FES)

13. Can be difficult to diagnose
Diagnosis by exclusion of other
Causes of dyspnoea, hypoxia ,
confusion and abnormal CXR. (Ex.
Thromboembolism and
pneumonia)
Index Patient
Young adult with Long Bone injury
seen after long transfer without
supporting therapy or splintage
Fat embolism syndrome (FES)
Historically
Fat embolism was first
described as an Autopsy
finding by Zenker
in 1862
Described as a Clinical
syndrome for the first time by
Von Bergmann in 1873

14. Initial presentation :
by mechanical occlusion of multiple
blood vessels with fat globules (too
large to pass in the capillaries)
Lungs Paradoxical systemic embolism
can occur from shunting
Vascular occlusion is temporary &
incomplete (fat globules fluidity and
deformability)
Late presentation :
from hydrolysis of the fat to the irritating
free fatty acids which migrate to other
organs via the systemic circulation
Fat embolism syndrome (FES)
Pathological Pathways
In the lungs
Direct toxicity of free fatty acids
on lung tissue or capillary
endothelium
+
The pathogenetic reaction of
lung tissue to Shock and
Hyper coagulability

15. Fat embolism syndrome (FES)
Pathological Pathways
Mechanical Theory
Fracture Liberates Fat Intravasation
->> Fat Enters Venous System
Mechanical Obstruction (Lung)
Patent Foramen Ovale or Pulmonary
Pre-Capillary Shunts
->> Systemic Fat Embolization - (Skin
petechiae, CNS signs)
Seen here with Oil red O stain in a peripheral
cerebral artery branch are globules of lipid.
This is fat embolism syndrome. Treatment
is supportive.
An Oil Red O stain demonstrates the fat
globules within the pulmonary arterioles. The
globules stain reddish-orange. The cumulative
effect of many of these globules throughout
the lungs is similar to a large pulmonary
embolus, but the onset of dyspnea is usually 2
to 3 days following the initiating event, such as
blunt trauma with bone fractures.

16. The rounded clear holes seen in the small
pulmonary arterial branch in this section of
lung are characteristic for fat embolism.
Fat embolism syndrome is most often a
consequence of trauma with long bone
fractures.
It can also be seen with extensive soft tissue
trauma, burn injuries, severe fatty liver, and
very rarely with orthopedic procedures
The capillary loops of this glomerulus
contain fat globules in a patient with fat
embolism syndrome.

17. Fat embolism syndrome (FES)
Pathological Pathways
Bio - chemical Theory
•Neutral Fat and Chemical Mediators
Released at Time of Fracture
•Neutral Fat Metabolized by Lipases
releasing Free Fatty Acids
•Free Fatty Acids Result in Endothelial
Lung Damage
+ Other Organs via Systemic circulation
Oleic acid (OA) can induce acute
lung injury in experimental models,
we proved that increased
inflammatory parameters after OA
challenges were not due to the
activation of the TLR4 receptor. With
OA being a Na/K-ATPase inhibitor,
we suggest the possible involvement
of this enzyme as an OA target
triggering lung inflammation.

18. FES To Brain On MRI
From several days to a week following the event initiating
fat embolism syndrome, there may be loss of
consciousness from lesions evidenced by the "brain
purpura" as shown here. Numerous petechial
hemorrhages are produced by fat emboli to the brain,
particularly in the white matter. Subsequent to this there
can be brain edema with herniation.
With cerebral fat embolism syndrome, there is loss of consciousness. Note the multitude of petechial hemorrhages
here, mostly within white matter. Cerebral edema and herniation may follow. Overall, few persons with a history of
trauma will develop fat embolism, but it is difficult to predict which patients will. Protean manifestations include:
hypoxemia, mental status changes, petechiae, fever, tachycardia, and thrombocytopenia

19. . ↑ in intra medullary pressure → fat droplets → get filtered in the pulmonary
circulation
• minute droplets go through pulmonary circulation & get trapped in
cerebral circulation
• alveolar lipase → hydrolysis of fat → release of fatty acids (palmitic,
stearic, oleic acids)
• Neutralisation by albumin
• failure of neutralistion by albumin
• fatty acids + calcium → intercellular septa rupture → diffuse areas of
haemorrhage & oedema in pulmonary interstitium & alveolar space
• Integrins CD11b & CD18 cause adherence of neutrophils & endothelium
• Injured pneumocytes stop surfactant production → collapse of alveoli
• ↑ shunt and dead space
Fat embolism syndrome (FES)
Pathological Pathways - Summary

20. Pathological Pathways
(FES) Often Placed in the Category of (ARDS)
May share common pathological pathways
Fat Embolism Syndrome
(FES)
Fat globules - Free fatty acids
(phagocytosis) - Inflammatory Mediators
+ enzymatic
Acute respiratory distress syndrome
(ARDS)
Trauma – tissue damage - cell
necrosis – infection
(Phagocytosis) - Inflammatory
mediators

21. Fat Embolism Syndrome
(FES)
Acute respiratory distress syndrome
(ARDS)
Pathological Pathways
ARDS VS. FES

22. Non-traumatic settings occasionally
lead to fat embolism
Liposuction
Fatty liver
Prolonged corticosteroid
therapy
Acute pancreatitis
Osteomyelitis
Conditions causing bone
infarcts, especially sickle cell
disease
Fat Embolism Syndrome(FES)
Etiology
Fractures
Closed fractures of a long bone >
Open fractures
>Long bones, pelvis and ribs
>Multiple fractures
<Sternum and clavicle
Other causes
Orthopaedic procedures,
intramedullary nailing, hip, knee
replacements
Massive soft tissue injury
Severe burns
Bone marrow biopsy

23. Closed fractures of a long
bone > Open fractures

25. Minimal invasive plate osteosynthesis (MIPO)
Fat embolism

27. Sudden onset 24-72 hours after injury
(Second Peak)
Breathlessness (dyspnoea) ± vague chest
pains. can progress to respiratory failure
with tachypnoea, and hypoxia
Fever - 38.3°C with a disproportionately
high pulse rate
Petechial rash upper anterior trunk, arm
and neck, buccal mucosa & conjunctivae
, may be transient
CNS symptoms, from mild headache to
significant cerebral dysfunction
(restlessness, disorientation, confusion,
seizures, stupor or coma)
Renal - oliguria, haematuria, anuria
Fat Embolism Syndrome(FES)
Presentation
Drowsiness with oliguria is almost
pathognomonic
98% of the patients presented with mental
status changes, only 22% had focal signs
and / or seizures
There is a fulminant form presents as
acute cor pulmonale, respiratory failure
and /or embolic phenomena leading to
death within a few hours of injury

28. Minor criteria
1- Tachycardia
2- Pyrexia (usually >39°C)
3- Confusion
4- Sustained pO2 <8 kPa
5- Sustained respiratory rate >35/minute, in
spite of sedation
6- Retinal changes - cotton wool exudates and
small hemorrhages, occasionally fat globules
seen in retinal vessels
7- Jaundice
8- Renal signs
9- Thrombocytopenia
10- Anemia
11- High ESR
12- Fat macroglobulinemia
13- Diffuse alveolar infiltrates 'snow storm
appearance' on CXR
Major criteria
1- Respiratory insufficiency
2- Cerebral involvement
3- Petechial rash
Fat Embolism Syndrome(FES)
Diagnostic criteria
(combined from various sources)
Diagnostic criteria first by Gurd have been updated

29. Major criteria
Respiratory insufficiency
Cerebral involvement
Petechial rash
Fat Embolism Syndrome(FES)
Diagnostic criteria
(combined from various sources)
Diagnostic criteria first by Gurd have been updated

30. At least Two symptoms for the Major criteria
or
One symptom for the Major criteria and
Four symptoms for the Minor criteria
Must be present to diagnose the syndrome
Fat Embolism Syndrome(FES)
Diagnosis

31. 1- Cytological examination
of urine, blood and sputum may detect fat globules either free or in macrophages.
This test has low sensitivity and a negative result does not exclude fat embolism
2- The CXR
show evenly distributed, fleck-like pulmonary shadows (snow storm appearance),
increased pulmonary markings and dilatation of the right side of the heart
3- Blood gases
hypoxia, pO2 usually less than 8 kPa (60 mm Hg) and hypocapnia.
4- Continuous pulse oximeter
monitoring detect hypoxia before it is clinically apparent (suggested by recurrent
desaturations below 90%)
Fat Embolism Syndrome(FES)
Investigations

32. 1- Platelets are reduced.
2- Decreased haematocrit
occurs within 24-48 hours and is attributed to intra-alveolar hemorrhage.
3- Lipase is elevated
but this is not pathognomonic, as it occurs in any bone trauma.
4- Calcium is reduced
5- Brain MRI scan
help in the diagnosis of cerebral fat embolism - hypointense areas consistent with
fat globules at the grey-white matter junction
6- Transoesophageal echocardiography (TEE)
of value in detecting intra-operative release of marrow contents into the
bloodstream during intramedullary reaming and nailing
Fat Embolism Syndrome(FES)
Investigations

33. Fat Embolism Syndrome
(FES)
Prevention

34. • Early immobilization of fractures
The most effective way of
reducing the incidence of this
condition
• Appropriate Splinting
• Early Fracture Stabilization
• Oxygen Therapy
• Corticosteroids
are occasionally used prior to long-
bone intramedullary nailing but
the evidence for their
effectiveness in preventing FES is
Fat Embolism Syndrome FES
Prevention
Therapies
• Fluid Loading
• Hypertonic Fluid
• Alcohol
• Heparin
• Dextran
• Aspirin
None Shown to be
Effective

35. Minimize the Second Hit (Surgical
trauma)
Be a Biological Orthopedic Surgeon
Surgical Technique
Implant Contact
What is the Second Hit ?
Early Fracture Stabilization

36. 1st hit
Trauma
Release of inflammatory
mediators (cytokines,
chemokines) ->> central
nervous system and systemic
Hypoxia
Acidosis
Coagulopathy
Systemic inflammation
2nd hit
Surgery
1st
hit: Head
Mechanical insult to
brain tissue blunt or
penetrating
breakdown of the blood
brain barrier
1st
hit: body
Mechanical insult
Chest, Abdomen,
extremities

37. Systemic Effects of Trauma
Injury (First Hit)
24 hours 48 hours
Post Injury
Inflammatory
Response in
2 Patients
Second Hit in susceptible patients
ARDS
MODS
Threshold
IM Nailing as a Cause of Secondary Systemic Injury

38. Injury (First Hit) Surgery (Second Hit)
Surgical Technique & Implant contact
Systemic Effects of Trauma

39. Early Total Care (ETC)
Definitive Early Fixation
By Nail or Plate
Damage Control (DCO)
Temporary Stability
By External Fixator
– Limit Further Blood Loss
– Limit Anesthetic Time
– Delay Definitive Fracture
fixation
Fracture Fixation Controversy

41. Effect of IM Nailing
• Increased IM Pressure
• Embolic Showers On
Echocardiograms
Caused by:
– Canal Opening
– Reaming
– Nail Insertion (both reamed
& unreamed)
Fracture Fixation Controversy
• IM Nail - Reamed vs. Un-
Reamed
– Decreased with Unreamed
Technique
Pape et al
– No Difference
Keating et al
Canadian OTS
• IM Nail Reamed vs. Plate
Osteosynthesis
– No Difference In Pulmonary
Dysfunction
Bosse et al

42. Fracture Fixation Controversy
Current Recommendations
Classify the patients
according to their
physical status
1- stable grade I
2- borderline grade II
3- unstable grade III
4- In extremis grade IV
The Criteria used in the physical status
classification
 Shock – B.P, No of blood units, lactate levels, B.D
(Base deficit), ATLS (Advanced Trauma Life Support)
Coagulation status
Temperature
Soft tissue injuries

43. American Society of Anesthesiologists Classification (ASA Class)
Daniel John Doyle; Emily H. Garmon.
Last Update: October 27, 2018.
ASA 1: A normal healthy patient. Example: Fit, nonobese (BMI under 30), a nonsmoking patient
with good exercise tolerance.
ASA 2: A patient with a mild systemic disease. Example: Patient with no functional limitations and
a well-controlled disease (e.g., treated hypertension, obesity with BMI under 35, frequent social
drinker or is a cigarette smoker).
ASA 3: A patient with a severe systemic disease that is not life-threatening. Example: Patient with
some functional limitation as a result of disease (e.g., poorly treated hypertension or diabetes,
morbid obesity, chronic renal failure, a bronchospastic disease with intermittent exacerbation,
stable angina, implanted pacemaker).
ASA 4: A patient with a severe systemic disease that is a constant threat to life. Example: Patient
with functional limitation from severe, life-threatening disease (e.g., unstable angina, poorly
controlled COPD, symptomatic CHF, recent (less than three months ago) myocardial infarction or
stroke.
ASA 5: A moribund patient who is not expected to survive without the operation. The patient is
not expected to survive beyond the next 24 hours without surgery. Examples: ruptured abdominal
aortic aneurysm, massive trauma, and extensive intracranial hemorrhage with mass effect.
ASA 6: A brain-dead patient whose organs are being removed with the intention of transplanting
them into another patient.
The addition of “E” to the ASAPS (e.g., ASA 2E) denotes an emergency surgical procedure. The
ASA defines an emergency as existing “when the delay in treatment of the patient would lead to
a significant increase in the threat to life or body part.”
Abbreviations used: ASA: American Society of Anesthesiologists, BMI: body mass Index, CHF: congestive heart failure,
COPD: chronic obstructive pulmonary disease.

44. Fracture Fixation Controversy
Current Recommendations
Stable patients:
- Do whatever you want
Borderline patients:
Borderline patients: Continuous reassessment
 Pao2/F102 should not drop below 200mm of Hg
 Temperature should not drop below 32C
 Requirement of fluids should not exceed 3L or 5units of blood
 Absence of significant coagulopathy
who respond to resuscitation
proceed with definitive fixation
limit the surgical duration within 2 hours
 If not → DCO
Remember: A bad surgeon can shift the ASA Grade II to IV easily
Unstable and patients in extremis:
- Life saving surgeries
- External fixation
- Resuscitation and stabilization simultaneously

45. Uncertain
Stable Grade 1 Unstable Grade IIIBorderline Grade II
Resuscitate
Reevaluate
Damage Control (DCO)Early Total Care (ETC)
Fracture Fixation Controversy
Current Recommendations
Stabilized

46. Fat Embolism Syndrome
(FES)
Treatment

47. Fat Embolism Syndrome (FES)
Treatment
A- Surgical Prompt surgical stabilization of long bone
fractures reduces the risk of the syndrome
B- Usually supportive
1- Oxygen Therapy to maintain PaO2
Ensuring good arterial oxygenation. High flow rate of O2
2- Mechanical Ventilation
Mechanical ventilation and positive end-expiratory
pressure (PEEP) may be required
3- Adequate Hydration
Restriction of fluid intake and diuretics can minimize fluid
accumulation in the lungs On the other hand,
maintenance of intravascular volume is important
because Shock can exacerbate the lung injury
caused by FES

48. Fat Embolism Syndrome (FES)
Treatment
Albumin
Recommended for volume resuscitation , balanced electrolyte solution, it
not only restores blood volume but also binds fatty acids and decrease the
extent of lung injury
Drugs
Using dextrose to decrease fatty acid mobilization, ethanol to reduce
lipolysis and heparin anticoagulation have been largely shown to be of
unproven benefit
Steroids
– Decrease endothelial damage
– 30mg/kg initial dose repeated @ 4 Hours, 1gm dose repeated @ 8
Hours: Total 3 Doses
•Complications – Frequent, Infection, GIT
•Steroid Therapy Avoided Secondary To Poor Risk Benefit Ratio

49. Fat Embolism Syndrome
(FES)
Prognosis

50. The mortality rate is <5 - >15%. Even severe respiratory failure
seldom leads to death
Neurological deficit and coma may last for days or weeks Residual
deficits include personality changes, memory loss and cognitive
dysfunction
Pulmonary sequelae usually resolve completely within a year,
although residual diffusion capacity deficits may exist
Patients presenting with mild mental status changes, focal deficits,
or seizure had a better outcome than those presenting with coma
or abnormal posturing
Fat Embolism Syndrome (FES)
Prognosis