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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.