This presentation is about Fat Embolism Syndrome in orthopedics. I would like to thank Dr hemanth sir and Dr Prateek sir who guided me.

1. Fat Embolism Syndrome
PRESENTER: Dr. RAJESH MEENA
MODERATOR : Dr. HAMENTH RAJ
FACULTY : Dr. PRATEEK BEHERA

2. Outline for discussion
1. HISTORY
2. DEFINITIONS
3. EPIDEMIOLOGY
4. ETIOLOGY
5. PATHOPHYSIOLOGY
6. CLINICAL FEATURES
7. DIAGNOSIS
8. TREATMENT AND PREVENTION
9. PROGNOSIS

3. HISTORY
 1861: Zenker first reported on the autopsy findings
of fat droplets found in the lungs of a railway worker
who died due to severe thoraco-abdominal crush
injury.
 1873: Bergmann diagnosed fat embolism clinically
in a patient with fractured femur.
 1970: Gurd defined the characteristics of this
phenomenon. He later defined the fat embolism
criteria together with Wilson, thus created Gurd and
Wilson’s criteria for fat embolism syndrome in 1974.

4.  1983: Schonfeld suggested a scoring system for
diagnosis of fat embolism syndrome.
 1987: Lindeque proposed another scoring system
that diagnosed fat embolism syndrome by using
respiratory changes alone.

5. DEFINITIONS
 Embolus: A unattached mass that travels in blood
circulation.
 Fat Emboli: Fat particles that travel through the
blood circulation.
 Fat Embolism: A process in which fat emboli passes
into bloodstream and lodges within a blood vessel.
 Fat Embolism Syndrome (FES): Term used to
describe clinical manifestations due to fat
embolism.

6. EPIDEMIOLOGY
 Most common cause : long bone fracture & pelvic
fracture
 ↑ no. of fracture = ↑ incidence
 Incidence: ranges from < 1 to 29% in different studies.
 Non-traumatic causes: rare
 Mortality 5-15%

7. ETIOLOGY

8. RISK FACTORS

9. PATHOPHYSIOLOGY
1. Gauss mechanical theory
2. Lehman’s biochemical theory

10. 1. Gauss mechanical theory
Trauma
Elevated intramedullary
pressure
Release of fat globules
in venous circulation
Right side of heart
Obstruction of pulmonary
capillaries

11. Small diameter of
Lung cap.
Fat emboli fail to pass
Into systemic circulation
20-30% population
Have patent foramen ovale
Fat emboli pas into systemic
circulation

12.  Limitation of mechanical theory:
1.It doesn’t explain development of nontraumatic FES.
2.It doesn’t explain 24-72 h delay for FES development
following the acute insult.

13. 2. Lehman’s biochemical theory
Trauma
Inflammation
Increased activity of
lipoprotein lipase
Breakdown of triglyceride
into free fatty acids
FFA in venous
circulation
Damage to cap. beds
of lungs and other organs

14. CLINICAL FEATURES
 Symptoms onset : after 12 hours to 3 days
 The three most characteristic features are:
(i). Pulmonary Dysfunction
(ii). Neurological Dysfunction
(iii). Dermatological Signs

15. (i). Pulmonary Dysfunction: (75% cases)
occlusion of pulmonary capillaries by fat globules and damage to capillaries
by circulating FFA
Exudation
Diffuse B/L infiltrate
(crackle, pleural frictional rubs)
V/Q mismatch
Hypoxia
ARDS
Ground glass app.
On CT chest
Snowstorm app.
on chest x ray

16. (ii). Neurologic dysfunction: (86% cases)
• Lethargy, restlessness, drop in Glasgow coma
scale (GCS)
Due to cerebral oedema rather than cerebral ischemia.
Neurological signs are not lateralised to one side of the body.
 Transient and reversible
 CT head: generalised cerebral oedema; non
specific.

17. MRI Brain:
 More sensitive then CT scan
 Demonstrate earlier and specific changes
 Typical findings: low intensity signs on T1 and high
intensity signs on T2.
 Multiple hyper intense punctate lesion disseminated in
white matter on diffusion weighted MRI.

18. Hyper intense punctate lesion disseminated
in white matter on DWI.(source: www.radiopaedia.org)

19. (iii). Dermatological signs: (60% cases)
 Petechial rash
 Usually on conjunctiva, neck, axilla, upper limbs.
occlusion of dermal capillaries by fat globules and damage to
capillaries by circulating FFA.
extravasation of RBC
petechial rash
• Such skin manifestation is temporary and can
disappear within 5-7 days.

21. OTHER FINDINGS:
 Retinopathy:
-cotton wool spots
-retinal haemorrhages.
 Lipduria: turbid white urine.
 Fever
 DIC: excessive bleed
Cont.

22.  Myocardial depression: SOB, cyanosis
 Thrombocytopenia/Anaemia: excessive bleed and
pallor
 Hypo-calcemia: muscle weakness and tetany
 Hypo-albuminemia

23. DIAGNOSIS
-young male
-closed multiple fractures
-disorientation / lethargy
-difficulty in breathing
-raised RR / spO2 < 92%
-petechial rash.
Suspect FES
Monitor with pulse oximeter
And GCS charting
ABG and routine
investigations

24. • In fat embolism:
1. ABG: pO2<8 kpa(60mmHg), pCO2>
7.3kpa(54.75mmHg)
2. LFT: raised AST/ALT, hypoalbuminemia
3. RFT: raised urea and creatinine
4. CBC: thrombocytopenia and anemia
5. S. Electrolyte: hypocalcemia
Cont.

25. 6. Raised S.lipase, S.FFA, S.phospholipase A2
7. ECG: ST depression and T wave inversion in lead V1-
V4, III, aVF
8. Chest X- ray : Diffuse bilateral infiltrate
9. Blood/urine/sputum microscopy: fat globules

26. • Following criteria’s have been developed to aid in
clinical diagnosis of FES:
(i). Gurd’s and Wilson’s criteria
(ii). Schonfeld scoring system
(iii). Lindeque criteria

27. Major criteria
A least two positive major criteria plus one minor criteria or
four positive minor criteria are suggestive of fat embolism syndrome.
(source: The fat embolism syndrome. Gurd AR, Wilson RI J Bone Joint Surg Br. 1974 Aug; 56B(3):408-16.

28. (source: Fat embolism prophylaxis with corticosteroids. A prospective study in high-risk patients.Schonfeld SA,
Ploysongsang Y, DiLisio R, Crissman JD, Miller E, Hammerschmidt DE, Jacob HS Ann Intern Med. 1983 Oct; 99(4):438-43.)

29. (source: Fat embolism and the fat embolism syndrome. A double-blind therapeutic study. Lindeque BG,
Schoeman HS, Dommisse GF, Boeyens MC, Vlok AL J Bone Joint Surg Br. 1987 Jan; 69(1):128-31.)

30. Additional laboratory and imaging test :
Done when routine investigations are not conclusive
• Bronchoalveolar Lavage:
-Lipid inclusions within macrophages
-It is invasive test so can not be done routinely.
 MRI Brain:
-Low intensity signs on T1 and high intensity signs on T2.
-Multiple hyper intense punctate lesion disseminated in white
matter

31.  CT chest: Diffuse areas of vascular congestion and pulmonary
oedema.
 Transcranial Doppler USG: periventricular oedema.
 Intraoperative TEE: Fat emboli in cardiac chambers.

32. TREATMENT AND PREVENTION
 No specific therapy
 Prevention, early diagnosis and adequate
symptomatic treatment are important.
 Mainstay of treatment: supportive
 If respiratory compromise is moderate to severe
(PaO2/FiO2: 200 to 100mmHg), patient should be
shifted to ICU where respiratory supports are
available.

33. SUPPORTIVE MEDICAL CARE
 Maintenance of adequate oxygenation and ventilation.
 Maintenance of hemodynamic stability
 Administration of blood products as clinically indicated.
 Adequate hydration
 Nutrition
 Adequate analgesia

34. Oxygenation and ventilation
• Oxygen supplementation could be done by nasal
prongs, face masks, CPAP, BiPAP with high flow
oxygen to maintain SpO2 >90% and PaO2 b/w 60-
90mmHg on ABG.
• In cases of severe respiratory compromise,
intubation and mechanical ventilation is required.

35. (source: Davidsons Principles and Practice of medicine 22ed)

36. • Ventilator parameter settings
a. FiO2: set to maintain SpO2>92% and PaO2 60-
90mmHg
b. PEEP: ~5cmH20
c. Tidal volume: keep low (4-6mL/Kg body weight) to
prevent barotrauma and volutrauma.
d. RR: 12-15 breaths/min then adjust to PaCO2 on ABG
to achieve adequate CO2 clearance.
e. I-E ratio: 1:2 to 1:3

37. Hemodynamic stability:
 shock can exacerbate lung injury  maintain
intravascular volume
 Albumin for volume resuscitation is recommended
because it helps in restoring euvolumia and also
binds to free fatty acids and reduces further injury of
lungs.(Abbott MG. Fat embolism syndrome: An in – depth review. Asian J Crit Care. 2005;1:19–24)
 In case of right ventricular failure ionotropic support
with dobutamine may be necessary.

38. (source: Davidsons Principles and Practice of medicine 22ed)

39. Treatment options with unclear benefit in FES:
a) Heparin: Clear lipaemic serum by stimulating lipase
activity but also increase risk of bleeding so it should
be avoided.(Mellor A, Soni N. Fat embolism Anaesthesia 2001; 56:145–154.)
b) Hypertonic glucose was also tried as 50 g oral or
intravenous (IV) infusion as it reduces the
concentration of FFAs within 30 min but results were
still disputable.
c) Dextran-40: Promote hemodilution, therefore reduce
the aggregation of platelets and erythrocytes.

40. PREVENTIVE MEASURES
 Continuous pulse oximeter monitoring in high risk patients
 Corticosteroids (controversial)
-Prospective studies suggests prophylactic steroids benefit in
high risk patients. (Stoltenberg JJ, Gustilo RB)
-It causes blunting of inflammatory response and
complement activation.
-Once FES established: not shown improved outcome.

41.  ORTHOPEDIC RELETED PREVENTIVE
MEASURES:
Definitive Care vs Damage Control
Three principle factors that control clinical course
1. Initial degree of injury (1st hit)
2. Individual biological response
3. Type of Treatment (2nd hit)

42. • Damage control orthopedic intervenes at 2nd hit to
provide:
1. Temporary stability (early immobilization)
2. Decrease blood loss
3. Help with pain control
4. Allow for the 1st hit and initial biological response to
settle.

43. • Early immobilization can be achieved with
-External fixation.
-IM nail (controversial)
Pape et al. : increased incidence of ARDS and mortality
Charash et al and Bosse et al. : no increased risk

44. • Principles of nailing in long bone fracture:
-No increased risk in reamed vs. unreamed nailing ( The
Canadian orthopedic trauma society, vol 20)
-Narrow reamer with sharp , conical head
-High rotation speed around 1350rpm, slow advance,
incremental increase in reamer diameter.
-Use of reamer irrigator aspirator device
-Distal venting 4-6mm hole in diaphysis during nailing.

45. Aspiration and venting of
distal femur with Frazier
suction tip during reaming
reamer irrigator
aspirator device

46. During hip arthroplasty
-Use low viscosity cement
-Retrograde filling of
cement in medullary cavity
-Use of cementless
prosthesis

47. PROGNOSIS
 With supportive care and early fixation FES has a
favourable outcome.
 Most patients can expect a complete recovery of
pulmonary, neurologic, and retinal abnormalities.
 Mortality rates from FES in modern studies utilizing
supportive measures and early operative fixation
report the mortality from FES between 7% and
10%.

48. BIBLIOGRAPHY
 Kwiatt, Michael E, and Mark J Seamon. “Fat embolism syndrome.”
International journal of critical illness and injury science vol. 3,1 (2013):
64-8. doi:10.4103/2229-5151.109426
 “Fat embolism syndrome: A comprehensive review and update.”Singh
Shailendra, Goyal Rahul, Baghel Purushottam Kumar, Sharma Vineet.
 Tharmviboonsri, Theerawoot & Riansuwan, Kongkhet & Phimolsarnti,
Rapin & Mahaisavariya, Banchong. (2011). Venting in Closed Femoral
Nailing: A Simple Technique Using a Frazier Suction Tip. Siriraj Medical
journal. 63. 92-93.
 Davidsons Principles and Practice of medicine 22ed
 Rockwood and Green's Fractures in Adults 8th ed

49. THANK-YOU