1. Dr. Faran Mahmood
FCPS Orthop.

2.  First diagnosed in 1873 by Dr Von Bergmann
 Published in 1879 Fenger and Salisbury.

3.  Fat Embolism:
Traumatic fat embolism occurs in up to 90% of
individuals with severe skeletal injuries, but <
10% of such patients have any clinical symptoms /
signs
 Fat Embolism Syndrome:
FE with clinical manifestation .

4.  Incidence: 1-3% femur #, 5-10% if bilateral or
multiple.
 Mortality: 5-15%
 Clinical diagnosis, No specific laboratory test is
diagnostic
 Mostly associated with long bone/pelvic #s, and
more frequent in closed fractures.
 Onset is 24-72 hours from initial insult

6.  A high index of suspicion is needed for diagnosis is
to be made.
 An asymptomatic latent period - 12-48 hours.
 The fulminant form presents as acute cor pulmonale,
respiratory failure, - death within a few hours of
injury.

7. Mechanical Theory
 Physical obstruction of the pulmonary & 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,
& vasoactive amines.

8. The biochemical theory
 Circulating FFAs -directly toxic to Pneumocytes /
capillary Endothelium in the lung - interstitial
hemorrhage, edema & chemical pneumonitis.
 Coexisting shock, hypovolemia and sepsis - reduce liver
flow exacerbate the toxic effects of FFAs.

9. H/E stain lung –
- blood vessel with
fibrinoid material and
-optical empty space
-lipid dissolved during
the staining process.

10. TRAUMA

11. Hypoxemia
Neurological Petechial
abnormalities rash

12.  Dyspnea,
 Tachypnea
 Hypoxemia PaO2 < 60 mm Hg

13.  Clinically Tachpnea, Dyspnea, Hypoxia, rales, pleural
friction rub & ARDS.
 High spiking temperatures.
 Hypoxemia - ventilation-perfusion mismatch &
intrapulmonary shunting. Acute cor pulmonale
-respiratory distress, hypoxemia, hypotension and
elevated CVP.
 ½ of pts require mechanical ventilation
 CXR normal early on - later may show ‘snowstorm’
pattern- diffuse bilateral infiltrates
 CT chest: ground glass opacification with interlobular
septal thickening

14.  CNS signs usually occur after respiratory symptoms
- nonspecific - features of diffuse encephalopathy
 Acute confusion, stupor, coma, rigidity, or
convulsions - Transient and reversible in most cases
 CT Head: general edema – nonspecific
 MRI brain: Low density on T1 & High intensity T2
signal - correlates to degree of impairment

15.  Reddish-brown non-palpable Petechial rash - upper
anterior body, chest, neck, upper arm, axilla,
shoulder, oral mucous membranes and conjunctivae
in 20 - 50% patients.
 Pathognomonic, however, it appears late and
disappears within hours.
 Results from occlusion of dermal capillaries by fat
globules - extravasations of RBC

16.  Retinopathy (exudates, cotton wool spots,
hemorrhage)
 Lipiduria
 Fever
 DIC
 Myocardial depression (R heart strain)
 Thrombocytopenia
 Anemia, Decreased Hematocrit
 Hypocalcemia

17. Gurd’s criteria
 Most commonly used
 1 major, plus 4 minor

19.  Continuous pulse oximetry monitoring - at-risk
patients ( those patients with long bone fractures) -
detecting desaturations early.
 Consultations recommended include orthopedists,
neurologists/ neurosurgeons, trauma care specialists,
critical care specialists, pulmonologists,
hematologists, and nutritionists.

20.  The most effective prophylactic measure - operative
reduction/rigid fixation of long bone fractures as
soon as possible. Higher incidence (5 fold) when
fixation delayed greater than 24 hours.
 Supportive care includes maintenance of adequate
oxygenation and ventilation, stable hemodynamics,
blood products as clinically indicated, hydration,
prophylaxis of DVT and stress-related GI bleeding.

21.  Albumin has been recommended - not only restores
blood volume / binds fatty acids - may decrease the
extent of lung injury.
 High dose corticosteroids have been effective in
preventing development of FES in several trials, but
controversy on this issue still persists.

22.  Heparin has also been proposed as it activates
lipase, but no evidence exists for its use in FES.

23.  Difficult to predict –FES is frequently subclinical or
overshadowed by other illnesses or injuries.
 Increased alveolar-to-arterial oxygen gradient and
neurologic deficits, including coma, may last days
or weeks.

24.  As in ARDS, pulmonary sequelae usually resolve
almost completely within 1 year.
 Residual subclinical diffusion capacity deficits may
exist.
 Residual neurologic deficits may range from
nonexistent to subtle personality changes to memory
and cognitive dysfunction to long-term focal
deficits.

25.  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.