Fat Embolism Workup

  • Author: Lisa Kirkland, MD, FACP, CNSP, MSHA; Chief Editor: Vincent Lopez Rowe, MD   more...
 
Updated: Sep 8, 2011
 

Laboratory Studies

  • Arterial blood gas: An otherwise unexplained increase in pulmonary shunt fraction alveolar-to-arterial oxygen tension difference, especially if it occurs within 24-48 hours of a sentinel event associated with fat embolism syndrome, is strongly suggestive of the syndrome.
  • Hematocrit, platelet count, fibrinogen: Thrombocytopenia, anemia, and hypofibrinogenemia are indicative of fat embolism syndrome; however, they are nonspecific.
  • Urine studies: Urinary fat stains are not felt to be sensitive or specific enough for diagnosing fat embolism or for detecting a risk of it.
    • Fat globules in the urine are common after trauma.
    • Preliminary investigations of the cytology of pulmonary capillary blood obtained from a wedged pulmonary artery catheter revealed fat globules in patients with FES and showed that this method may be beneficial in early detection of patients at risk.
    • In the future, genotyping for polymorphisms associated with increased susceptibility to inflammatory stimuli may help identify those at risk of fat embolism syndrome.
  • Specific antibody therapy targeting inflammatory molecules has not been useful.
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Imaging Studies

  • Chest radiography: Serial radiographs reveal increasing diffuse bilateral pulmonary infiltrates within 24-48 hours of onset of clinical findings.
  • Noncontrast head CT: Findings from head CT performed because of alterations in mental status may be normal or may reveal diffuse white-matter petechial hemorrhages consistent with microvascular injury.
  • 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.
  • Helical chest CT for pulmonary embolism: As the embolic particles are lodged in the capillary beds, helical CT findings may be normal. Parenchymal changes consistent with lung contusion, acute lung injury, or adult respiratory distress syndrome may be evident. Nodular or ground glass opacities in the setting of trauma suggest fat 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.[7] Cerebral microembolic signals were detected as long as 4 days after injury.
  • 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.
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Procedures

  • Bronchoalveolar lavage (BAL) with staining of alveolar macrophages for fat
    • BAL specimens have been evaluated in trauma patients and sickle cell patients with acute chest syndrome, and the results have been mixed.[8, 9]
    • 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.
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Contributor Information and Disclosures
Author

Lisa Kirkland, MD, FACP, CNSP, MSHA  Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo Clinic; ANW Intensivists, Abbott Northwestern Hospital

Lisa Kirkland, MD, FACP, CNSP, MSHA is a member of the following medical societies: American College of Physicians, Society of Critical Care Medicine, and Society of Hospital Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard M Stillman†, MD, FACS  Honorary Medical Staff, Northwest Medical Center; Former Chief of Staff and Medical Director, Wound Healing Center, Department of Surgery, Northwest Medical Center

Richard M Stillman†, MD, FACS is a member of the following medical societies: American College of Angiology, American College of Surgeons, Association for Academic Surgery, and Society of University Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Travis J Phifer, MD  Chief, Division of Vascular Surgery, Professor, Department of Surgery and Radiology, Louisiana State University Health Sciences Center in Shreveport

Travis J Phifer, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Society for Academic Emergency Medicine, Society for Vascular Surgery, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Paolo Zamboni, MD  Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy

Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences

Disclosure: Nothing to disclose.

Chief Editor

Vincent Lopez Rowe, MD  Associate Professor of Surgery, Department of Surgery, Division of Vascular Surgery, University of Southern California Medical Center

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, Pacific Coast Surgical Association, Peripheral Vascular Surgery Society, Society for Clinical Vascular Surgery, Society for Vascular Surgery, and Western Vascular Surgical Society

Disclosure: Nothing to disclose.

References

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  9. Mimoz O, Edouard A, Beydon L, Quillard J, Verra F, Fleury J. Contribution of bronchoalveolar lavage to the diagnosis of posttraumatic pulmonary fat embolism. Intensive Care Med. Dec 1995;21(12):973-80. [Medline].

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  18. Hofmann S, Hopf R, Huemer G, Kratochwill C, Koller-Strametz J, Schlag G. [Modified surgical technique for reduction of bone marrow spilling in cement-free hip endoprosthesis]. Orthopade. Apr 1995;24(2):130-7. [Medline].

  19. Kallenbach J, Lewis M, Zaltzman M, Feldman C, Orford A, Zwi S. 'Low-dose' corticosteroid prophylaxis against fat embolism. J Trauma. Oct 1987;27(10):1173-6. [Medline].

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  23. Scully RE, Mark EJ, McNeely WF. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 23-1998. Tachypnea, changed mental status, and pancytopenia in an elderly man with treated lymphoma. N Engl J Med. Jul 23 1998;339(4):254-61. [Medline].

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Haematoxylin and eosin stain of a section of the lungs showing a blood vessel with fibrinoid material and an optical empty space indicative of the presence of lipid dissolved during the staining process. This 55-year-old woman died of massive fat embolism after developing pancreatitis due to endoscopic retrograde cholangiopancreaticography. Image source: Pancreatitis with an unusual fatal complication following endoscopic retrograde cholangiopancreaticography: a case report. Journal of Medical Case Reports. 2008;2:215.
Table 1
DoseModelTimingDuration of StudyEffect on Disease Incidence
30 mg/kgDogPre-event60 minNone
10 mg/kg q8h for 24 hHuman traumaAt admissionNo dataDeclining
7.5 mg/kg q6h for 12 h or placeboHuman traumaWithin 12 h2 dDeclining
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