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First diagnosed in 1873 by Dr Von Bergmann
In 1879 Fenger and Salisbury published description of
Fat embolism syndrome
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
FE vs. FES
Fat embolization is a well-known complication of
skeletal trauma and surgery involving
instrumentation of the femoral medullary canal.
Fat embolism syndrome (FES) is a physiological
response to fat within the systemic circulation.
Fat embolization and FES are not synonymus.
The embolization of fat can be detected in almost all
patients who sustain a pelvic or femoral fracture, but
the incidence of FES is less than 1%.
Fat Embolism Syndrome
Clinical diagnosis, No specific laboratory test is
Mostly associated with long bone and pelvic
fractures, and more frequent in closed fractures.
Single long bone fracture has 1-3% chance of
developing FES, and increases with number of
Onset is 24-72 hours from initial insult.
Causes of fat embolism
Blunt trauma: Long bone (Femur, tibia, pelvic) factures
Soft tissue injury(chest compression with or without rib
Bone marrow harvesting and transplant.
NON TRAUMA RELATED
Osteomyelitis and panniculitis
Bone tumor lysis
Sickle cell hemoglobinopathy
Alcoholic liver disease
Most common cause of FES is blunt trauma.
90 % occursafter blunt trauma complicated by long-
Closed fractures had higher incidence compared to
open fractures. The intramedullary bone pressure is
lower in case of open fractures, which reduces the
bulk of fat emboli propelled into the blood stream.
Non-traumatic fat embolism
It occurs due to the process of fat or marrow necrosis
or by the increased concentration of lipids in the
It may be caused by agglutination of chylomicrons
and VLDL by high levels of plasma CRP.
As in Acute pancreatitis in patients with types I, IV,
and V hyperlipidaemia and avascular necrosis of bone
in patients with corticosteroid-induced
Drug-related causes of FES
Infusion of lipids at rates greater than the normal
clearance capacity of lipids.
Agglutination of lipid emulsion particles with fibrin.
Agglutination of endogenous or infused exogenous
fat such as Intra lipid.
FES can occur in SC
Bone marrow necrosis
as a result of hypoxia
may release fat.
Pathophysiology of FES
Exact mechanism unknown, but two main hypothesis
1. Mechanical Hypothesis
Obstruction of vessels and capillaries
Increase in inter medullary pressure forces fat and
marrow into bloodstream.
Bone marrow contents enter the venous system
and lodge in thelungs as emboli.
Smaller fat droplets travel through the pulmonary
capillaries into the systemiccirculation: Embolization to
cerebral vessels or renal vessels also leads to central
nervous system and renal dysfunction
Toxicity of free fatty acids
Circulating free fatty acids directly affectthe
pneumocytes, producing abnormalities in gas
Coexisting shock, hypovolemia and sepsis impair liver
function and augment toxic effects of free fatty acids.
Hormonal changes caused by trauma or sepsis
induce systemic release of free fatty acids as
Acute-phase reactants( C-reactive proteins) cause
chylomicrons to coalesce.
It explains non traumatic forms of fat embolism
syndrome and why symptoms take 12 hours to
FE in ARDS
Fat emboli obstructs
lung vessel (20microns),
platelets and fibrin
adhere to it
Lipase increases FFA
Asymptomatic for the first 12-48 hours
Hypoxia, rales, pleural friction rub
ARDS may develop.
CXR usually normal early on, later may show
‘snowstorm’ pattern- diffuse bilateral infiltrates
CT chest: ground glass opacification with interlobular
Usually occur after respiratory symptoms
Incidence- 80% patients with FES
Minor global dysfunction is most common-ranges
from mild delirium to coma.
Transient and reversible in most cases.
CT Head: general edema, usually nonspecific
MRI brain: Low density on T1, and high intensity T2
signal, correlates to degree of impairment.
Usually on conjunctiva, neck, axilla, upper limbs.
Results from occlusion of dermal capillaries by fat
globules and then extravasations of RBC.
Resolves in 5-7 days. Usually fast resolving.
Pathognomic, but only present in 20-50% of patients.
• Chest x-ray
– shows multiple flocculent shadows (snow storm
appearance). picture may be complicated by infection
or pulmonary edema.
- Image showing minimal hypodense changes
in periventricular region, which are more evident in
DWI and T2WI as areas of high signals.
Treatment and management
Immobilization and early internal fixation of
Fixation within 24 hours has been shown to yield
a 5 fold reduction in the incidence of ARDS.
Continuous pulse oximeter monitoring in high-
risk patients may help in detecting desaturation
early, allowing early institution of oxygen and
possibly steroid therapy.
High doses of corticosteroids.
Supportive Medical Care
Maintenance of adequate oxygenation and ventilation
Maintenance of hemodynamic stability.
Administration of blood products as clinically
Prophylaxis of deep venous thrombosis .
Treatment and management contd.
Treatment and management contd.
Oxygenation and ventilation
High flow rate oxygen is given to maintain the
arterial oxygen tension in the normal range.
Mechanical ventilation and PEEP may be required to
maintain arterial oxygenation.
Treatment and management contd.
Maintenance of intravascular volume is important,
because shock can exacerbate the lung injury caused
Albumin has been recommended for volume
resuscitation in addition to balanced electrolyte
solution, because it not only restores blood volume
but also binds with the fatty acids and may decrease
extent of lung injury
Steroid prophylaxis is controversial to prevent FES.
It causes blunting of inflammatory response and
Prospective studies suggests prophylactic steroids
benefit in high risk patients.
Preoperative use of methylprednisolone may prevent
the occurrence of FES
Once FES established, steroids have not shown
Results of Randomized, Controlled Trials of Corticosteroids for Prevention of Fat
Dose Model Timing Duration of
30mg/kg Dog Before event 60min None
for 24 hrs
At admission No data Declining
for 12hrs or
Within 12hrs 2 days Declining
Heparin has also been proposed for treatment as it
"clears" lipemic plasma in vivo by causing the release
of lipoprotein lipase into the circulation, but no
evidence exists for its use in FES.
The fulminant form presents as acute cor pulmonale,
respiratory failure or embolic phenomena, leading to
death within a few hours of injury.
Most death contributed to pulmonary dysfunction
Hard to determine exact mortality rate
Estimated less than 10%
The incidence of FES ranges from < 1 to 29% in
Actual incidence of FES is not known, as mild cases
often go unnoticed.
A high index of suspicion is needed to diagnose FES.
A combination of clinical criteria and MRI brain will
enable early and accurate diagnosis of FES.
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Bilateral Total Knee Arthroplasty – A Review Of The Fat Embolism
Syndrome”. The Internet Journal of Anesthesiology. 2009 Volume 19 Number
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