Fat Emboli Syndrome

History
• First diagnosed in 1873 by Dr Von
Bergmann
• 1879 Fenger and Salisbury published
description of FES.
Fat Emboli
• FE: fat in the vascular circulation, can
cause embolic phenomenon, more
common 90% pts with traumatic injury
(ECHO and BAL have shown high
incidence of FE after fractures and
orthopedic surgery)
• FE: Incidence 1-3% femur fx, 5-10% if
bilateral or multiple.
Fat Emboli Syndrome
• Mortality: 5-15%
• Clinical diagnosis, No specific
laboratory test is diagnostic
• Mostly associated with long bone and
pelvic fxs, and more frequent in closed
fractures
• Single long bone fracture 1-3% chance
of developing FES, and increases with
number of fxs
• Onset is 24-72 hours from initial insult
Diagnostic Criteria
• Gurd criteria most
commonly used
• 1 major, plus 4 minor
Gurd Criteria
Pathophysiology
• Two theories exist about FES:
– Mechanical theory states that large fat
droplets are released into venous
system, deposit into pulmonary
capillary beds, and through a-v shunts
to the brain; microvascular lodging of
droplets causes local ischemia and
inflammation
– Biochemical theory states that hormonal
changes caused by trauma and/or sepsis
induce systemic release of free fatty
acids and chylomicrons; acute phase
reactants cause chylomicrons to
coalesce and create ischemia
Pathogenesis of ARDS in FE
• fat emboli obstructs
lung vessel
(20microns) platelets
and fibrin adhere
• Lipase creases FFA
• Inflammatory
changes->endothelial
damage->ARDS
Triad of FES
• Hypoxemia
• Neurological
abnormalities
• Petechial rash
Early Signs
• Dyspnea,
• Tachypnea
• hypoxemia
Pulmonary
• Hypoxia, rales, pleural friction rub
• ARDS may develop
• ½ of pts with FES require mechanical
ventilation (Bulger, Archives of Surgery
1997; 132: 435-9)
• CXR usually normal early on, later may
show ‘snowstorm’ pattern- diffuse
bilateral infiltrates
• CT chest: ground glass opacification
with interlobular septal thickening
Neurological findings
• Usually occur after respiratory symptoms (not
in this case with PFO)
• Incidence 80% patients with FES
• Minor global dysfunction most common, but
ranges from mild delirium to coma.
• Seizures/focal deficits not common but can
occur
• Transient and reversible in most cases
• CT Head: general edema
• MRI brain: Low density on T1, and high
intensity T2 signal, correlates to degree of
impairment
Rash
• Petechial
• Usually on conjuntiva, MM, neck,
axillae
• Results from occlusion of dermal
capillaries by fat globules and then
extravasations of RBC
• Resolves in 5-7 days
• Pathognomonic, but only present in 20-
50% of patients
Other findings
• Retinopathy (exudates, cotton wool
spots, hemorrhage)
• Lipiduria
• Fever
• DIC
• Myocardial depression (R heart strain)
• Thrombocytopenia/Anemia
• Hypocalcemia
Treatment
• Early Medical care
– Supportive in nature
– Maintain oxygenation and ventilation
– Stabilize hemodynamics
– Blood products as needed
– Hydration
– stress related GI bleed prophylaxis
– Nutrition
• Surgical care
– Early stabilization of long bone
fractures to minimize bone marrow
embolization into venous system
– ORIF over conservative tx also
reduces risk.
– Higher incidence when fixation
delayed greater than 24 hours.
Steroids
• Steroid prophylaxis is controversial to prevent
FES
• Theorized blunting of inflammatory response
and complement activation
• Prospective studies suggests prophylactic
steroids benefit high risk patients
• Few studies and small study size, so remains
controversial.
• Once FES established, steroids have not
shown improved outcomes.
• Heparin and ASA have also been
proposed for tx as they active lipase and
block thromboxane respectively, but no
evidence exists for either use in FES.