Fat embolism syndrome is a clinical diagnosis characterized by a triad of hypoxemia, neurological abnormalities, and petechial rash that develops within 24-72 hours of long bone fractures or other trauma. Fat particles released from the bone marrow can cause pulmonary and systemic complications by lodging in the lungs and other organs. While supportive care focuses on oxygenation, ventilation, and hemodynamic stability, the most effective prevention method is early surgical fixation of fractures within 24 hours to reduce risk. Outcomes range from full recovery to respiratory failure and death, depending on severity.

1. FAT EMBOLISM
BY,
DR VARUN KUMAR A

2. HISTORY
Zenker, a Pathologist, first identified Fat
embolism syndrome at an autopsy in 1862
1862
First diagnosed in 1873 byDr Von Bergmann
1873
FengerandSalisburypublished description of
FES in 1879
1879

3. • It is a Clinical diagnosis, No specific laboratory test is diagnostic
• Mostly associated with long bone/pelvic #s
• Onset is within 24-72 hours from initial insult
• Mortality: 5-15%

4. DEFINITIONS
• Fat Emboli: Fat particles or droplets that
travel through the circulation
• Fat Embolism: A process by which fat
emboli passes into the blood stream and
lodges within a blood vessel
• Fat Embolism Syndrome: Serious
manifestation of fat embolism occasionally
causing multi system dysfunction, the lungs
are always involved and next is the brain

5. CAUSES OF FES:
• Blunt Trauma (90%) –
- Long bone # (Femur, tibia, pelvic fractures)
- More frequent in Closed # than Open #
- Younger patients > Older patients
- A single bone # has 1-5% chances of
developing FES
- FES has been reported as high as 33% in
B/L shaft of femur fractures

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: Orthopaedic surgeries, liposuction

7. RISK FACTORS:

8. PATHOGENESIS:
Mechanical Theory:
Physical obstruction
of the pulmonary and
systemic vasculature
with embolized fat
Temporary rise in I/M
pressure - forces
marrow into injured
venous sinusoids
Cor pulmonale –
Inadequate
compensatory
pulmonary
vasodilatation
Microvascular
lodging – local
ischemia and
inflammation
Release of
inflammatory
mediators, platelet
aggregation and
vasoactive amines

9. Biochemical Theory:
Circulating FFAs – Directly
toxic to pneumocytes /
capillary endothelium in the
lung causing
interstitialhaemorrhage,
edema and chemical
pneumonitis
Coexisting shock,
hypovolemia and sepsis –
reduce liver flow, exacerbate
the toxic effects of FFAs

10. H/E STAIN OF
LUNG:
• Blood vessel with fibrinoid material
• Optical empty space - Lipid dissolved
during the staining process

11. CLINICAL
PRESENTATION:
• FES typically manifests 24 to 72 hours after
the initial insult, rarely <12 hours or >72
hours
• Classic triad – Hypoxemia, Neurologic
abnormalities and a Petechial rash
• Early signs – Dyspnea, Tachypnea and
Hypoxemia

12. PULMONARY:
• Hypoxia, rales, pleural friction rub
• ARDS may develop
• 50% of patients with FES require mechanical ventilation
• CXR is usually normal early on, later may show ‘snowstorm’ pattern – diffuse
bilateral infiltrates
• CT chest – Ground glass opacification with interlobular septal thickening

13. NEUROLOGICAL FINDINGS:
• Usually occur after respiratory symptoms
• Incidence – 80% of FES patients
• Minor global dysfunction most common but ranges from
mild delirium to coma
• Seizures / Focal deficits are rare,
• Transient and reversible in most cases
• CT head – general edema, usually non-specific
• MRI Brain – Low intensity on T1 and high intensity on T2
signal, correlates to degree of impairment

14. MRI:
• Foci of ischemia S/O FES
• Post-op day 2 showing multiple hyperintense areas consistent
with multiple emboli
• Post-op day 14 shows evolving cortical infarctions

15. DERMATOLOGICAL
FINDINGS:
• Petechial
• Usually on conjunctiva, 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

16. OTHER FINDINGS:
• Retinopathy (exudates, cotton wool spots, haemorrhage)
• Lipiduria
• Fever
• DIC
• Myocardial depression
• Thrombocytopenia/Anemia
• Hypocalcemia

17. DIAGNOSIS:
FES is a CLINICAL diagnpsis, not
biochemical
High degree of suspicion is needed to
make diagnosis
In 50% of fracture patients, fat globules
was demonstrated in the serum, without
other symptoms of FES
Growing literature on the use of
bronchoscopy with bronchoalveolar
lavage to detect fat drplets in alveolar
macrophages as a means to diagnose
fat embolism (sensitivity and specifity
are unknown, being studied in Trauma
patients)

18. GURD’S CRITERIA:

19. LINDEQUE’S
CRITERIA:
FES = Femur fracture +/- tibia fracture + 1
feature
Based on respiratory parameters

20. SCHONFELD:
FAT
EMBOLISM
INDEX
FES = 5 or more points

21. SEVITT’S CLASSIFICATION:
SUBCLINICAL
FES
NON-
FULMINANT
FES
FULMINANT
FES

22. SUB CLINICAL
FES:
Around 3 days post trauma
Probably occurs in almost all long
bone fractures of the lowrer
extremity and fractures of the pelvis
Characterised by decreased PaO2,
decreased Hb% and decreased
platelets.
No clinical signs and symptoms of
respiratory insufficiency

23. 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
Thrombocytopenia, anaemia and
coagulation abnormalities can be found
Pulmonary alveolar and interstitial
opacities on CXR

24. FULMINANT FES:
Occurs very suddenly and rapidly
after injury and progresses
quickly, often resulting in death
within few hours of initial trauma
Clinical features are acute
respiratory failure, acute cor-
pulmonale and embolic
neurological changes
Patients with multiple fractures are
particularly susceptible to this
form of FES, relatively rare but
significant because of its mortality

25. TREATMENT:
• Prophylaxis:
- Immobilisation and early internal fixation of fracture
- Fixation within 24 hours has been shown to yield 5 fold reduction in the
incidence of ARDS
- Continuous saturation monitoring in high-risk patients may help in detecting
desaturation early, allowing early institution of O2 and possible steroid
therapy

26. SUPPORTIVE
MEDICAL CARE:
Maintenance of
adequate
oxygenation and
ventilation
Maintenance of
haemodynamic
stability
Administration of
blood products
as indicated
Hydration
Prophylaxis
ofDVT
Nutrition

27. OXYGENATION AND
VENTILATION:
High flow rate
Oxygen is given to
maintain the arterial
oxygen tension in
the normal range
Mechanical
ventilation and
PEEP may be
required to maintain
arterial oxygenation

28. HAEMODYNAMIC STABILITY:
Maintenance ofintravascular
volumeis important as shock
can exacerbate the lung injury
caused by FES
Albuminhas been
recommended for volume
resuscitation in addition to
balanced electrolyte solution
as it restores blood volume
andbinds with FAand
maydecrease extent of lung
injury

29. STEROIDS:
• Steroid prophylaxis is controversial to prevent FES
• Blunting of inflammatory response and complement activation
• Prospective studies suggest prophylactic steroids benefit high
risk patients
• Once FES is established, steroids have not shown improved
outcomes

30. HEPARIN:
• Like steroids, controversial role in management
• Stimulates lipase to reduce lipemia
• Reverses the DIC picture
• S/E – increase in circulating FFAs, bleeding risks
• Routine use is not recommended

31. PROGNOSIS:
• Most deaths are contributed to pulmonary dysfunction
• Hard to determine exact mortality rate
• Difficult to predict duration of FES – As it is frequently
subclinical or overshadowed by other illness or injuries
• Increased alveolar-to-arterial oxygen gradient and neurologic
deficits, including coma may last for few days to weeks

32. SEQUELAE:
As in ARDS, pulmonary
sequelae usually
resolve almost
completely within 1 year
Residual subclinical
diffusion capacity
deficits may exist
Resisual neurologic
deficits may range from
non-existent to subtle
personality changes,
memory and cognitive
dysfunction

33. SUMMARY:
Clinical diagnosis, so high index of
suspicion
Most effective management is prevention
with rigid fixation of fractures within 24
hours
When developed management is
supportive

34. THANK YOU