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
6.
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.
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
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.
Fat embolism is very common. Fat embolism is often temporary or incomplete since fat globules do not completely obstruct capillary blood flow because of their fluidity and deformability. But count be fatal if it develops into FES
21 year old involved in a MVC. Femur and tibia fractures lacerations on head.
Stable in ER for 12 hours
Then his heart and respiratory rates then increased gradually and oxygen saturation decreased. Serial arterial blood gases (ABGs) were done showing progressive acidosis, hypercapnia and severe hypoxemia. Bradycardia and hypotension – died 26 hours after admission.
75 yr-old Male with knee arthroplasty (reconstructive ortho surgery)
Had diabetes. Developed encepholopathy
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
Clinical examination is still the preferable diagnostic method in fat embolic syndrome as there is no universal
criteria used for diagnosis; which is always made on clinical grounds.