updated in some dr.faran sir's .ppt

1. Dr. Ankit Desai
Dr.B.L.Chandrakar

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. Fat Emboli: Fat particles or droplets that
travel through the circulation
Fat Embolism: A process by which fat
emboli passes into the bloodstream and
lodges within a blood vessel.
Fat Embolism Syndrome (FES):
serious manifestation of fat embolism
occasionally causes multi system
dysfunction, the lungs are always
involved and next is brain

5.  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. commanly with
lower limb injury
 Onset is 24-72 hours from initial insult

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,veno arterial shunting,hypoxemia
leeds to alveolar hypoperfusion leading to PD
 Size of fat globules 2 to 200 micron
 Blood vessele <75 micron

8. The biochemical theory
Free fatty acid is culprit
 Circulating FFAs -directly toxic to Pneumocytes /
capillary Endothelium in the lung – decrease surfactant
,nterstitial hemorrhage, edema & chemical pneumonitis.
 Local hydrolysis of Triglycerides and fat emboli by
pneumocyte lipase -- Increase fatty acid .
 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. Pulmonary
dysfunction
Neurological
abnormalities
Petechial
rash

11.  Dyspnea,
 Tachypnea
 Hypoxemia PaO2 < 60 mm Hg
 confusion

12.  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

13. • Chest x-ray
– shows multiple flocculent shadows (snow storm appearance). picture
may be complicated by infection or pulmonary edema.
– CT chest: ground glass opacification with interlobular septal
thickening
• CT Scan brain
– may be normal or may reveal diffuse white-matter petechial
haemorrhages
• Helical CT Scan chest
– may be normal as the fat droplets are lodged in capillary beds. Can
detect lung contusion, acute lung injury, or ARDS may be evident.

14. ER admit
AP & expiratory film so we cannot comment
on cardiac shadow. However, there is no
evidence of lung contusion, pneumo, haemo
or pneumohaemothorax.
SICU admit (12 hours later)
upper lobe diversion and
bilateral pulmonary
infiltrates
Altaf Hussain: “A Fatal Fat Embolism.” The Internet Journal of Anesthesiology, 2004. Volume 8 Number 2.

15.  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

16. post operative day 14 and
shows evolving cortical
infarctions
post operative day 2
showing multiple
hyperintense areas
consistent with multiple
emboli
Source:http://www.ispub.com/journal/the_internet_journal_of_anesthesiology/volume_19_number_2/article/acute_fatal_fat_embolism_syndrome_in_bilateral_total_knee_arthroplasty_a_review_of_the_fat_embolism_syndrome.html

17.  Reddish-brown non-palpable Petechial rash - upper
anterior body, chest, neck, upper arm, axilla,
shoulder, oral mucous membranes and conjunctivae
in 20 - 50% patients.2 to 3re day
 Resolvs in 7 day
 Pathognomonic, however, it appears late and
disappears within hours.
 Results from occlusion of dermal capillaries by fat
globules - extravasations of RBC

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

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

21.  Clinical examination preferred over diagnostic

22.  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.

23.  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.

24.  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.

25.  Heparin has also been proposed as it activates
lipase, but no evidence exists for its use in FES.
 Ethanol/alcohol in bolus dose iv :as lipase inhibitor

26.  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.

27.  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.

29.  THANK U