Dr.E.

Kaizar Ennis
Definition
The term “fat embolism” denotes the presence of
globules of fat (20 microns) in the lung parenchyma
and peripheral circulation after a fracture of a long
bone or other major trauma.
The term “fat embolism syndrome” (FES)
denotes a more serious manifestation of the same
phenomenon.
Introduction
Fat emboli were first noted by F.A. Zenker in 1861 in a
railroad worker with a thoraco-lumbar crush injury at
autopsy.
Clinical diagnosis of Fat Embolism Syndrome (FES) was
first described by Von Bergman in 1873 .
Fat embolism develops in nearly all pts (90%) with
fractured bones or during ortho procedures and is
asymptomatic.
In minority of pts SIGNS & SYM. develop as a result of
organ dysfunction, notably lungs, brain, and skin.
i.e FES
FES
Mortality: 10-20%
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.
Cont…
The fat embolism syndrome denotes clinical or subclinical
respiratory insufficiency developing in patients with long-
bone fractures. It usually runs a mild course and responds
well to measures for respiratory support. The subclinical
form is detected by blood gas analysis and is associated
with a PaO2 value of less than 60 mmHg. The overt clinical
form, which usually appears within 24 to 72 hours and
presents the classic picture, is easy to diagnose. The severe,
fulminant form, which develops within hours, deteriorates
rapidly despite respiratory support and other resuscitative
measures, and is frequently fatal. This form is caused by
a massive embolism followed by a succession of further
massive embolisms.
Causes
Pathophysiology
Common after skeletal injury, and is most likely to
occur in patients with multiple long bone and pelvic
fractures, orthopedic procedures like reaming for
intramedullary nailing, hip and knee replacements when
cement is injected, resulting in increased pressure in the
marrow canal. In Patients undergoing nailing for
fractures of long bone, Unreamed nailing and reamed
nailing of the medullary cavity stand equal chances of
developing pulmonary fat embolism.
Young men with fractures are at increased risk.
Cont…
The mechanical theory
The initial symptoms are probably caused by
mechanical occlusion of multiple blood vessels with
fat globules that are too large to pass through the
capillaries.
The biochemical theory
Degradation of fat to Free fatty acids are toxic to
pneumocytes and capillary endothelium in the lung,
causing interstitial hemorrhage, edema and chemical
pneumonitis.
Triad of FES
Hypoxemia
Neurological abnormalities
Petechial rash
Diagnostic Criteria - Gurd Criteria
JBJS VOL. 69-B, No. 1, JANUARY
1987
 A DOUBLE-BLIND THERAPEUTIC STUDY
Proposed criteria for a positive diagnosis of FES comprise
the following factors.
1. A sustained PaO2 of less than 60 mmHg.
2. A sustained PaCO2 of more than 55 mmHg or a pH of
less than 7.3.
3. A sustained respiratory rate of more than 35 breaths
per minute even after adequate sedation.
4. Increased work of breathing - dyspnoea, the use of
accessory respiratory muscles, and tachycardia - combined
with anxiety. A patient showing at least one of the
above criteria was judged to have developed FES.
 (Pa02 reflects oxygen diffusion from the alveoli to the lung
capillaries which is essential for tissue oxygenation)
Pulmonary findings
Hypoxia, rales, pleural friction rub.
ARDS may develop.
½ of pts with FES require mechanical ventilation.
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.
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, usu nonspecific.
Rash
Petechial
Usually on conjuntiva, oral mucous membrane, 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.
Petechial Rash
Laboratory Studies
Laboratory tests are mostly nonspecific and there is no
pathognomonic test during the course of a FES.
1. Urinary fat stains are not sensitive or specific enough
for diagnosing fat embolism or for detecting a risk of it.
Fat globules in the urine are common after trauma.
2. Serum lipase level increases after bone injuries and
is often misleading.
3. During the acute phase of Fat Embolic Syndrome,
there may be positive D Dimer test, thrombocytopenia
and other coagulation abnormalities
Cytologic examination of urine, blood, CSF and sputum
may detect fat globules.
Arterial blood gas
Depending on the condition of patient, serial ABG’s are
carried to monitor treatment including fluids and
oxygen therapy as well as ventilatory support.
Imaging Studies
Chest X-ray -multiple flocculent shadows
(snow storm appearance).
CT Scan brain (plain)-may be normal or may reveal
diffuse white-matter petechial haemorrhages consistent
with microvascular injury.
CT chest- ground glass opacification with interlobular
septal thickening.
High-resolution CT (HRCT) -Lungs
Bilateral ground-glass opacities and thickening of
the interlobular septa, whereas in some cases
centrilobular nodular opacities were present. HRCT was
performed in patients in whom a clinical diagnosis of FES
had been made.
Other investigations
ECG - usually normal but may show right
heart strain or ischemia.
Nuclear medicine ventilation/perfusion imaging
of the lungs, are essential to look for pulmonary
embolism.
TREATMENT
PREVENTION
The basic principles in the management of long-bone
fractures -early aggressive resuscitation, adequate splinting
of fractures, administration of intravenous analgesics,
administration of blood and prevention of sepsis in
compound fractures.

Continuous pulse oximetry monitoring in at-risk

patients(i.e, those with long-bone fractures), may help in
detecting the syndrome early, allowing early oxygen
therapy and possibly steroids, decreasing the chances of
hypoxic insult and possible systemic complications of FES.
Cont…
Maintenance of intravascular volume is important
because shock can exacerbate the lung injury caused
by FES. Albumin has been recommended for volume
resuscitation because it not only restores blood
volume but also binds free fatty acids, and may
decrease the extent of lung injury. Adequate analgesia
is important to limit the sympathomimetic response
to injury.
Medical care
– Supportive in nature
– Maintain oxygenation and ventilation
– Stabilize hemodynamics
– Blood products as needed
– Hydration
– DVT & stress related GI bleed prophylaxis
– Nutrition.
Steroid Therapy.
High dose corticosteroids have been effective in
preventing development of FES and is currently
recommended.
Steroid prophylaxis is controversial to prevent FES.
Theorized blunting of inflammatory response and
complement activation.
Prospective studies suggests prophylactic steroids benefit
high risk patients.
Once FES established, steroids have not shown improved
outcomes.
Low-dose corticosteroid
prophylaxis against fat embolism
 J Trauma. 1987 Oct;27(10):1173-6.
(Kallenbach J, Lewis M, Zaltzman M, Feldman C, Orford A, Zwi S.)
 82 skeletal trauma pts. Identified as high risk for FES
 42 control subjects given placebo and 40 steroid-treated subjects
(9 mg/kg methylprednisolone)
 Fat embolism occurred in ten controls (23.8%) and
one steroidtreated subject (2.5%)
 Hypoxemia was severe (PaO2 less than 50 mm Hg) in 12 controls
(28.6%) and two (5%) of the steroid-treated subjects
 Although methylprednisolone in a relatively low dose provides
protection against fat embolism and pulmonary dysfunction after
skeletal trauma, the safety of this therapy requires further
evaluation.
Other measures
Dextrans and hypertonic dextrose , Aspirin,
intravenous alcohol and Heparin: These agents may
exacerbate bleeding. No clinical benefit has been
conclusively demonstrated with any of these agents.
Surgical Treatment
Early stabilization of long bone fractures is
recommended to minimize bone marrow embolization
into the venous system.
Conclusion
Fat Embolism Syndrome is a significant cause of morbidity
and mortality in trauma patients and elective orthopedic
surgery. Despite certain laboratory and radiologic aids,
clinical suspicion is still the mainstay in diagnosis of fat
embolism syndrome. All possible laboratory and imaging
aids must be used to rule out other treatable conditions.
Treatment is essentially supportive, consisting of
cardiovascular and respiratory resuscitation and
stabilization. Maintenance of intravascular volume is
important because shock can exacerbate the lung injury
caused by FES. Intravenous albumin and steroids remains
the mainstay of therapy while ventilatory support, oxygen
and heparin can improve the prognosis in many patients.
Cont…
JBJS VOL. 69-B, No. 1, JANUARY 1987
The routine early administration of intravenous
methylprednisolone to patients admitted with long-
bone fractures offers advantages in the maintenance
of PaO2 levels and a reduction in the incidence of the
fat embolism syndrome.
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