A fat embolism is a type of embolism that is often caused by physical trauma such as
fracture of long bones, soft tissue trauma, and burns.
Presentation Unlike emboli that arise from thrombi, fat
emboli are small and multiple, and thus have widespread effects.
Fat embolism syndrome is distinct from the presence of fat emboli.
Symptoms usually occur 1–3 days after a traumatic injury and are predominantly pulmonary,
neurological, dermatological, and haematological.
The syndrome manifests more frequently in closed fractures of the pelvis or long bones.
The petechial rash, which usually resolves in 5–7 days, is said to be pathognomonic
for the syndrome, but only occurs in 20–50% of cases.
Fat emboli occur in almost 90% of all patients with severe injuries to bones, although only
10% of these are symptomatic.
The risk of fat embolism syndrome is thought to be reduced by early immobilization of fractures
and especially by early operative correction.
There is also some evidence that steroid prophylaxis of high-risk patients reduces the incidence.
The mortality rate of fat-embolism syndrome is approximately 10–20%.
Fat emboli can be either traumatic or non-traumatic.
Pathogenesis The pathogenesis occurs due to both mechanical
obstruction and biochemical injury.
It is aggravated by local platelet and erythrocyte aggregation.
The release of fatty acids from the fat globules also causes local toxic injury to endothelium.
The vascular damage is aggravated by platelet activation and recruitment of granulocytes.
Several mechanisms have been proposed to explain the pathogenesis of fat embolism.
They may be acting together or singly.
Mechanical.
Mobilisation of fluid fat following trauma to bone and soft tissue.
Emulsion instability.
Explains the pathogenesis of fat embolism in non-traumatic cases.
Fat embolus formed by aggregation of plasma lipids due to disturbances in emulsification
of fat.
Symptoms include fatty liver.
Intravascular coagulation.
May result from disseminated intravascular coagulation.
Toxic injury.
Blood vessels injured by high plasma levels of free fatty acid, results in increased vascular
permeability and consequently pulmonary edema.
Complications Complications from a fat embolism tend to
be serious: Pulmonary fat embolism.
Widespread obstruction causes sudden death.
Systemic fat embolism.
These may get lodged in capillaries of organs like brain, kidney, skin etc., causing minute
hemorrhage and microinfarcts.
Embolized fat travels through the venous system to the lungs and can occlude pulmonary capillaries.
Fat emboli may cause cor pulmonale if adequate compensatory pulmonary vasodilation does not
occur.
Circulating free fatty acids are directly toxic to pneumocytes and capillary endothelium
in the lung, causing interstitial hemorrhage, edema and chemical pneumonitis.
Signs and symptoms 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 mucosa 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.
Central nervous system 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 PaO2 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, increased pulmonary
markings and dilatation of the right side of the heart.
Diagnosis Diagnosis of FES may be difficult because,
except for the petechiae, there are no pathognomonic signs.
Laboratory tests are mostly nonspecific: 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 the syndrome.
Decreased hematocrit occurs within 24–48 hours and is attributed to intra-alveolar
hemorrhage.
Alteration in coagulation and thrombocytopenia.
Treatment 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.
See also Air embolism
Cholesterol embolism Pulmonary embolism
CT pulmonary angiogram References
External links 973471750 at GPnotebook
Fat_embolism_syndrome at the Duke University Health System's Orthopedics program
Fat Embolism MRI Brain Injury from Fat Embolism