Fat Embolism: Diagnosis and Treatment
Kirsten Odegard, MD
Department of Anesthesiology
New York University Medical Center
Fat embolism syndrome follows long bone fractures. Its classic
presentation consists of an asymptomatic interval followed by
pulmonary and neurologic manifestations combined with petechial
hemorrhages. The syndrome follows a biphasic clinical course. 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. Unlike other embolic events, the vascular
occlusion in fat embolism is often temporary or incomplete since
fat globules do not completely obstruct capillary blood flow because
of their fluidity and deformability. The late presentation is
thought to be a result of hydrolysis of the fat to more irritating
free fatty acids which then migrate to other organs via the systemic
Many aspects of the fat embolism syndrome remain poorly understood,
and disagreement about its etiology, pathophysiology, diagnosis and
treatment persists. It is therefore difficult to determine the
incidence of this complication. It ranges from less than 2% to 22%
in different studies. Fat embolism has been associated with many
nontraumatic disorders. It is most common after skeletal injury,
and is most likely to occur in patients with multiple long bone and
pelvic fractures. Patients with fractures involving the middle and
proximal parts of the femoral shaft are more likely to experience
fat embolism. Age also seems to be a factor in the development of
FES: young men with fractures are at increased risk.
Fat embolism and FES are also more likely to occur after closed,
rather than open, fractures. Two events promote entrance of marrow
contents into the circulation following a fracture: movement of
unstable bone fragments and reaming of the medullary cavity during
placement of an internal fixation device. Both of these cause
distortion of and increased pressure within the medullary cavity,
permitting entry of marrow fat into torn venous channels that remain
open even in shock because they are attached to the surrounding bone.
Multiple fractures release a greater amount of fat into the marrow
vessels than do single fractures, increasing the liklihood of FES.
There are two theories which have gained acceptance:
It is also possible that coexisting shock, hypovolemia and
sepsis, all of which reduce liver flow, facilitate the
development of FES by exacerbating the toxic effects of free
- The mechanical theory: FES results from physical obstruction of
the pulmonary and systemic vasculature with embolized fat.
Increased intramedullary pressure after injury forces marrow
into injured venous sinusoids, from which the fat travels to
the lung and occludes pulmonary capillaries. Fat emboli can
cause cor pulmonale if adequate compensatory pulmonary
vasodilation does not occur.
- The biochemical theory: Circulating free fatty acids are
directly toxic to pneumocytes and capillary endothelium in the
lung, causing interstitial hemorrhage, edema and chemical
A thorough knowledge of the signs and symptoms of the syndrome and a
high index of suspicion are needed if the diagnosis is to be made.
An asymptomatic latent period of about 12-48 hours precedes the
clinical manifestations. The fulminant form presents as acute cor
pulmonale, respiratory failure, and/or embolic phenomena leading to
death within a few hours of injury.
Clinical fat embolism syndrome presents with tachycardia, tachypnea,
elevated temperature, hypoxemia, hypocapnia, thrombocytopenia, and
occasionally mild neurological symptoms.
A petechial rash that appears on the upper anterior portion of the
body, including the chest, neck, upper arm, axilla, shoulder, oral
mucous membranes and conjunctivae is considered to be a
pathognomonic sign of FES, however, it appears late and often
disappears within hours. It results from occlusion of dermal
capillaries by fat, and increased capillary fragility.
CNS signs, including a change in level of consciousness, are not
uncommon. They are usually nonspecific and have the features of diffuse
encephalopathy: acute confusion, stupor, coma, rigidity, or convulsions.
Cerebral edema contributes to the neurologic deterioration. Hypoxemia
is present in nearly all patients with FES, often to a Pa02 of well below
60 mmHg. Arterial hypoxemia in these patients has been attributed to
ventilation-perfusion inequality and intrapulmonary shunting. Acute cor
pulmonale is manifested by respiratory distress, hypoxemia, hypotension
and elevated central venous pressure.
The chest X-ray may show evenly distributed, fleck-like pulmonary
shadows (Snow Storm appearance), increased pulmonary markings and
dilatation of the right side of the heart.
Laboratory tests are mostly nonspecific:
In summary, the diagnosis of FES may be difficult because, except for
the petechiae, there are are no pathognomonic signs.
- Serum lipase level increases in bone trauma - often misleading.
- Cytologic examination of urine, blood and sputum with Sudan or
oil red O staining may detect fat globules that are either free or in
macrophages. This test is not sensitive, however, and does not rule
out fat embolism.
- Blood lipid level is not helpful for diagnosis because
circulating fat levels do not correlate with the severity of
- Decreased hematocrit occurs within 24-48 hours and is attributed
to intra-alveolar hemorrhage.
- Alteration in coagulation and thrombocytopenia.
The most effective prophylactic measure is to reduce long bone
fractures as soon as possible after the injury.
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 fatty acids,
and may decrease the extent of lung injury.
Mechanical ventilation and PEEP may be required to maintain arterial
High dose corticosteroids have been effective in preventing development
of FES in several trials, but controversy on this issue still persists.
A high index of suspicion is needed to make the diagnosis of the
often fatal fat embolism syndrome.
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