Fat embolism

Prepared byPrepared by
Dr Rajesh T EapenDr Rajesh T Eapen
Atlas HospitalAtlas Hospital
Ruwi MuscatRuwi Muscat

 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

 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 .

 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

 FES can occur in
Sickle Cell crisis.
 Bone marrow necrosis
as a result of hypoxia
may release fat.

 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.

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.

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.

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

Asymptomatic for the first 12-48 hours
Pulmonary Dysfunction
Neurological (nonspecific)
Dermatological Signs

 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 septal thickening.

 Usually occur after respiratory symptoms
 Incidence- 80% patients with FES
 Minor global dysfunction is most common-ranges
from mild delirium to coma.
 Seizures/focal deficits
 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.

 Petechie
 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.

Hypoxemia
Neurological
abnormalities
Petechial
rash

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

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

Gurd’s criteria
 Most commonly used
 1 major, plus 4 minor
Other indexes are
 Schonfeld Index
 Lindeque Index

 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.

 Arterial Blood Gases (ABGs)
 Urine and sputum examination
 Haemotological Tests
 Biochemical tests

• Chest x-ray
– shows multiple flocculent shadows (snow storm
appearance). picture may be complicated by infection or
pulmonary edema.

 MRI Brain
- Image showing minimal hypodense
changes in periventricular region, which are more
evident in DWI and T2WI as areas of high signals.

Prophylaxis
 Immobilization and early internal fixation of
fracture.
 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
indicated.
 Hydration
 Prophylaxis of deep venous thrombosis .
 Nutrition.

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.

Hemodynamic stability
 Maintenance of intravascular volume is important,
because shock can exacerbate the lung injury caused
by FES.
 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
complement activation
 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
improved outcomes.

 Heparin has also been proposed as it activates
lipase, 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%

 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.

Desired Outcome
The client will not experience fat embolism syndrome as
evidenced by:
1.usual mental status
2.unlabored respirations at 12-20/minute
3.absence of petechiae
4.PaO2 within normal limits.

1. Assess for and report signs and symptoms of fat
embolism syndrome (usually occurs within 72 hours after the
injury):
A. restlessness, apprehension, confusion
B. sudden onset of dyspnea
C. tachypnea
D. elevated pulse and temperature
E. petechiae on the chest, neck, or axilla
F. low PaO2 level.
2. Minimize movement of the fractured extremity during the
first few days after the injury to reduce the risk for fat emboli.

3. If signs and symptoms of fat embolism syndrome occur:
A. maintain client on bed rest and move fractured extremity
as little as possible to prevent further emboli
B. administer oxygen and assist with positive airway
pressure techniques (e.g. positive end expiratory pressure) if
ordered
C. prepare client for chest x-ray or lung scan
D. administer intravenous fluids as ordered to help maintain
adequate perfusion to vital organs and prevent shock
E. administer corticosteriods if ordered to reduce cerebral
edema and pulmonary inflammation

 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.

 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.

Fat embolism

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Fat embolism