Fat embolism syndrome is a serious complication of long bone fractures and other trauma involving bone marrow. Fat droplets released from the bone marrow can cause pulmonary and neurological dysfunction. While diagnosis is clinical, imaging may show a "snowstorm" pattern on chest x-ray or fat globules in blood viewed through a Swan-Ganz catheter. Treatment is supportive, focusing on oxygenation, ventilation, and prevention of deep vein thrombosis. Outcomes are often good if respiratory failure can be managed, though fulminant cases can be fatal. Prevention prioritizes early fracture stabilization to reduce intramedullary pressure.

1. FAT EMBOLISM
SYNDROME
DR. VASKAR HUMAGAIN
RESIDENT, ORTHOPAEDICS AND TRAUMA SURGERY
2076/01/03

2. INTRODUCTION
• Major cause of morbidity and mortality after fractures in the patient with
multiple injuries.
• It is a type of embolism in which the embolus consists of fatty material.
• Embolus (Greek: plug) : detached intravascular solid, liquid, or gaseous
mass that is carried by the blood to a site distant from its point of origin.
• Fat embolism may be defined as a blockage of blood vessels by
intravascular fat globules ranging from 10-40 µm in diameter
• Fat embolism syndrome: It is a serious manifestation of fat embolism
characterized by multisystem involvement (lungs are almost always
involved)
• Diagnosis of exclusion of other causes of dyspnea, hypoxia or confusion.

3. HISTORY
• Zenker, a pathologist, 1st identified Fat Embolism syndrome at
autopsy in 1862.
• First diagnosed in 1873 by Dr. Von Bergmann
• Fenger and Salisbury, In 1879 , first described this syndrome in
American Literature.

4. ETIOLOGY
Related to Trauma
• Long bone ( Femur, Tibia ) fracture
• Pelvic fractures
• Orthopaedic procedures (intramedullary reaming, hip and knee
arthroplasty)
• Soft tissue injuries (eg chest compression with or without rib fractures)
• Burns
• Liposuction
• Bone marrow harvesting and transplant
• Bone Marrow biopsy

5. ETIOLOGY - ATRAUMATIC
A. Disease related:
• Diabetes, Pancreatitis, Osteomyelitis, Sickle cell
haemoglobinopathies , burns, SLE, panniculitis
B. Drug related:
• Steroid therapy, Lipid infusion, Cyclosporine A
solvent

6. EPIDEMIOLOGY
• 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

7. PATHOPHYSIOLOGY
• The pathophysiology of the fat embolism is not clearly established
• Mechanical Hypothesis (Obstruction of Vessels and Capillaries)
• Biochemical Hypothesis (Toxicity of Free Fatty Acids)
• Coagulation Theory

8. Mechanical Hypothesis (Gauss,1924)
• mechanical obstruction of the systemic vasculature by fat droplets
released from the bone marrow of damaged bone due to high
intramedullary pressure during elective orthopedic surgery or
trauma, travels through torn veins and lodges in distal capillaries
causing mechanical obstruction.
• Smaller fat droplets travel through the pulmonary capillaries into the
systemic circulation: Embolization to cerebral vessels or renal
vessels also leads to central nervous system and renal dysfunction

9. 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.
Lehmann and Moore, 1927

10. Coagulation Theory
• This states that tissue thromboplastin is released
with marrow elements following long bone
fractures .
• This activates the complement system and
extrinsic coagulation cascade via direct activation
of factor VII .
• These lead to increase pulmonary vascular
permeability, both by their direct actions on the
endothelial lining and through the release of
numerous vasoactive substances.

12. An Oil Red O stain demonstrates the fat globules within the pulmonary arterioles. The
globules stain reddish-orange.

13.  ↑ 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 neutralisation 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

14. Clinical Features
• Diagnosis is made CLINICALLY NOT CHEMICALLY.
• It does not matter how much fat globules are in the 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.

15. Early Signs
• Dyspnea
• Tachypnea
• Hypoxemia
Respiratory manifestations in 95% of the cases
Drowsiness with oliguria is almost pathognomonic

16. CNS Manifestations:
• from mild headache to significant cerebral dysfunction
(restlessness, disorientation, confusion, seizures, stupor or coma)
• Fortunately, almost all neurological deficits are transient and fully
reversible.

17. Rash
• Petechial rash on upper anterior trunk, arm and neck, buccal
mucosa & conjunctivae , may be transient
• Results from occlusion of dermal capillaries by fat globules and
then extravasations of RBC
• PATHOGNOMONIC, but only present in 20-50% of patients.

19. Renal Manifestations
• Oliguria
• haematuria
• anuria

20. Ocular Manifestations
• On fundoscopy, Purtscher’s
retinopathy may be seen
• Cotton wool exudates, macular
oedema and macular
haemorrhage can also be found.

21. CVS Involvement
• Early persistent tachycardia, though nonspecific, is almost
invariably present in all patients with fat embolism

22. Systemic Fever
• Moderate fever with a disproportionately high pulse rate is a very
common early sign

23. Gurd’s and Wilson’s criteria
Major Criteria
• Petechial rash
• Respiratory insufficiency
• Cerebral involvement
Minor Criteria
• Tachycardia
• Fever
• Retinal changes
• Jaundice
• Renal signs
• Thrombocytopenia
• Anaemia
• High Erythrocyte Sedimentation Rate
• Fat macroglobulinemia

24. Lindeque’s criteria
(FES = femur fracture +/- tibia fracture + 1 feature)
Based on respiratory parameters
1. Sustained PaO2 of < 8 kPa (60mm Hg)
2. Sustained PaCO2 of >7.3 kPa (55mm Hg) or a pH <7.3
3. Sustained respiratory rate >35 breaths/min, despite sedation
4. Increased work of breathing: dyspnoea, accessory muscle use,
tachycardia, and anxiety

25. Schonfield’s criteria

26. Sevitt’s Classification (1962)
• Subclinical
• Non-fulminant
• Fulminant

27. 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.

28. Non-fulminant FES
• Any time ,up to 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

29. 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.

30. Investigations
• Hematology and Biochemistry
• Urine and Sputum
• Radiological

31. Hematological Investigations
• An unexplained anemia (70% of patients) and thrombocytopenia
(platelet count <1,50,000 /mm3 in up to 50% of patients) are often
found.
• Hypocalcemia (due to binding of free fatty acids to calcium) and
elevated serum lipase have also been reported.
• Hypofibrinogenemia, raised ESR and prolongation of prothrombin
time may be seen
• ABG reveals a low partial pressure of O2 and low partial pressure of
CO2 with respiratory Alkalosis

32. Urine and sputum
• Analysis of the sputum or urine for fat has not proved to be
accurate.
• Bronchoalveolar lavage and staining with Oil Red O can
demonstrate neutral fat. Microscopic examination of the blood for
fat globules when it is collected from pulmonary circulation through
Swan-Ganz catheter is the diagnostic test.

33. Radiological
• CXR usually normal early on, later may show ‘snowstorm’ pattern- diffuse
bilateral infiltrates , enlargement of right side of the heart.
• CT chest: ground glass opacification with interlobular septal thickening
• CT Head: general edema, usually nonspecific
• MRI brain: Low density on T1, and high intensity T2 signal, correlates to
degree of impairment
• Diffusion weighted-MRI (DW-MRI) of the brain showing a “Star Field”
pattern of multiple small high-intensity lesions with diffusion restriction
supports the diagnosis.

34. Differential Diagnosis
• Pulmonary Embolism
• Thrombotic thrombocytopenic purpura

36. Management
• There is no specific therapy for the fat embolism syndrome, so prevention,
early diagnosis, and adequate symptomatic treatment are of paramount
importance
• Adequate oxygenation and ventilation
• Stable hemodynamics
• Blood products as clinically indicated
• Hydration / i.v. fluids
• Prophylaxis of deep venous thrombosis and stress related gastrointestinal
bleeding

37. Management
• Nutritional support
• Corticosteroids
• Heparin
• Antibiotics
• Early immobilisation of the fracture decreases the incidence of
FES

38. Prevention
• Because treatment is primarily supportive, our focus must be on
prevention.
• In trauma, early fracture stabilization decreases the rate of FE
syndrome.
• Use of RIA
• In arthroplasty, computer navigation and alternative cementation
techniques decrease fat embolization,

39. Measures to decrease the chances of fat
embolism while reaming
• Use of sharp reamer
• Decreasing RPM while reaming
• Gradually increasing the size of reamer by 0.5 mm
• RIA technique
• Use of flexible reamer
• Not fixing B/L femur fracture at the same setting

40. Summary
• Fat embolism occurs in many traumatic and atraumatic conditions
and is largely asymptomatic. Preventative measures include early
immobilization of fractures and methods to reduce intramedullary
pressure during surgical manoeuvres. Treatment is largely
symptomatic with therapy for respiratory failure similar to that used
in management of acute respiratory distress syndrome

41. References
1. Apley’s and Solomon’s System of Orthopaedics and Trauma, 10th Edition, CRC Press, Taylor
and Francis Group
2. Essential Orthopaedics Principles and Practice, Manish Kumar Varshney, Jaypee Publishers
3. Textbook of Orthopaedics and Trauma, Second Edition, GS Kulkarni, Jaypee Publishers
4. Fat emboli syndrome and the orthopaedic trauma surgeon: lessons learned and clinical
recommendations. Dunn, R.H., Jackson, T., Burlew, C.C. et al. International Orthopaedics
(SICOT) (2017) 41: 1729. https://doi.org/10.1007/s00264-017-3507-1
5. Rothberg DL, Makarewich CA. Fat Embolism and Fat Embolism Syndrome. J Am Acad
Orthop Surg. 2019 Apr 15;27(8):e346-e355. doi: 10.5435/JAAOS-D-17-00571.
6. Bollineni VR, Gelin G, Van Cauter S. Cerebral Fat Embolism Syndrome. J Belg Soc Radiol.
2019 Apr 2;103(1):20. doi: 10.5334/jbsr.1781.

42. THANK
YOU