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Fat Embolism


Estimated to occur in 3-10% of orthopedic trauma patients. Mortality is 10-20%


Theory #1 (mechanical): large fat droplets are released into the venous system. These droplets are deposited in the pulmonary capillary beds and travel through arteriovenous shunts to the brain. Microvascular lodging of droplets produces local ischemia and inflammation, with concomitant release of inflammatory mediators, platelet aggregation, and vasoactive amines.

Theory #2 (biochemical): hormonal changes caused by trauma and/or sepsis induce systemic release of free fatty acids as chylomicrons. Acute-phase reactants, such as C-reactive proteins, cause chylomicrons to coalesce and create the physiologic reactions described above. The biochemical theory helps explain nontraumatic forms of fat embolism syndrome.



Trauma to long bone/pelvis, recent orthopedic procedure, recent lipid infusion

Signs Under General Anesthesia

Clinical signs may include hypoxia/increased A-a gradient, tachycardia, and a petechial rash on the upper portions of the body (petechiae occur in only 20-50% of patients but are virtually diagnostic). Pulmonary compliance will likely decrease. PA pressures will rise and cardiac output will fall (although normally this information is not available). Delayed wake up may manifest. Mental status changes occur in awake patient, but are missed in patients under general anesthesia

There are two classification schemes for diagnosis – Gurd and Schonfeld’s

Gurd’s Diagnostic Criteria

Gurd’s Diagnostic Criteria

Major Criteria

  • Respiratory insufficiency
  • Cerebral involvement
  • Petechial rash

Minor Criteria

  • Tachycardia
  • Fever
  • Jaundice
  • Retinal changes
  • Renal changes

Laboratory Features

  • Microglobulinemia (required)
  • Thrombocytopenia
  • Elevated ESR
  • Anemia

One major and 4 minor criteria, plus fat microglobulinemia, must be present to formally diagnose fat embolism syndrome

Schonfeld Fat Embolism Syndrome Index

Schonfeld Fat Embolism Syndrome Index

  • 5 points: petechial rash
  • 4 points: diffuse alveolar infiltrates
  • 3 points: hypoxemia (Pao2<70 mm Hg with an Fio2 100%)
  • 1 point: confusion, fever, tachycardia, tachypnea

Note: 5 or more points are needed to make a diagnosis



  1. ABG: increase in pulmonary shunt fraction alveolar-to-arterial oxygen tension difference, especially if it occurs within 24-48 hours of a sentinel event;
  2. Hematocrit, platelet count, fibrinogen: thrombocytopenia, anemia, and hypofibrinogenemia are indicative of fat embolism syndrome;
  3. Microglobulinemia is a required diagnostic test based on Gurd’s criteria. Note that urinary fat stains are not felt to be sensitive or specific enough for diagnosing fat embolism or for detecting a risk of it, and are thus not indicated.


  1. Chest radiography: increasing diffuse bilateral pulmonary infiltrates within 24-48 hours of onset of clinical findings.
  2. Noncontrast head CT: diffuse white-matter petechial hemorrhages consistent with microvascular injury.
  3. Nuclear medicine ventilation/perfusion imaging of the lungs: Performed for suspicion of pulmonary embolus, the findings from this scan may be normal or may demonstrate subsegmental perfusion defects.
  4. Helical chest CT to rule out pulmonary embolism
  5. MRI: Scant data exist regarding MRI findings in patients with this syndrome; however, in one small patient group, multiple, nonconfluent, hyperintense lesions were seen on proton-density– and T2-weighted images.
  6. Transcranial Doppler sonography: In a small case study, 5 patients with trauma were monitored with intracranial Doppler sonography, 2 during intraoperative nailing of long bone fractures. Cerebral microembolic signals were detected as long as 4 days after injury.
  7. Transesophageal echocardiography (TEE): TEE may be of use in evaluating intraoperative release of marrow contents into the bloodstream during intramedullary reaming and nailing. The density of the echogenic material passing through the right side of the heart correlates with the degree of reduction in arterial oxygen saturation. Repeated showers of emboli have been noted to increase right heart and pulmonary artery pressures. Embolization of marrow contents through patent foramen ovale also has been noted. However, evidence of embolization by means of TEE is not correlated with the actual development of FES.


Bronchoalveolar lavage (BAL) with staining of alveolar macrophages for fat (controversial)

BAL specimens have been evaluated in trauma patients and sickle cell patients with acute chest syndrome, and the results have been mixed. Lipid inclusions commonly appear in patients with traumatic and nontraumatic respiratory failure; the standard cut-off of 5% fat-containing macrophages in the BAL studies results in a low specificity for the test. Some authors suggest increasing the cut-off to 30% to improve specificity. Presently, using BAL to aid in the diagnosis or to predict the likelihood of fat embolism syndrome is controversial.


“Supportive,” steroids don’t currently have a role in treatment (conflicting data).

Other References

  1. Keys to the Cart: June 12, 2017; A 5-minute video review of ABA Keywords Link