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Analysis of Pulmonary Fat Embolism in Blunt Force Fatalities

Mudd, Kenneth L. MS; Hunt, Allison BA; Matherly, Renee C.; Goldsmith, L. Jane PhD; Campbell, Ferrell R. PhD; Nichols, George R. II MD; Rink, Richard D. PhD

Journal of Trauma-Injury Infection & Critical Care: April 2000 - Volume 48 - Issue 4 - pp 711-715
Article Titles

Objective: To investigate the incidence, severity, and origin of pulmonary fat embolism (PFE) in persons dying from blunt force trauma within 24 hours of injury.

Methods: The study population consisted of blunt force fatalities. Controls were subjects dying from natural causes or nonblunt force injury. Tissue was removed from lung lobes and prepared for histologic examination using osmium tetroxide to stain for fat. Lung sections were graded for PFE on a scale of 0 (no emboli) to 4 (five or more emboli in a majority of fields).

Results: The blunt force group consisted of 56 decedents. Mortality was 93% within 4 hours. Fractures were present in 54 (96%) of decedents, and soft tissue injury was universal. Thirty eight (68%) of decedents were positive for PFE vs. 3 of 20 (15%) in controls. Mean score for PFE was 2.94 ± 1.15 and 1.01 ± 0.94, respectively (p < 0.005). Bone marrow emboli were not observed in any of the sections. Severity of PFE was positively associated with survival time. Analysis of PFE against sex, age, height, weight, number of injuries, and number of fractures showed no significant correlations.

Conclusions: A significant degree of PFE develops rapidly in a majority of persons dying of blunt force trauma. Although the source of fat for embolization has been suggested to be bone marrow, no evidence of myeloid tissue was found in any of the lung sections. Nor was there a correlation of PFE and number of fractures. Soft tissue injury is considered the primary cause of PFE.

Pulmonary fat embolism (PFE) is often associated with blunt force trauma, with incidences ranging from 47 to 100% in decedents. 1–5 Release of fat from fractured bone has been indicated as a significant source of PFE. 6–8 Armin and Grant cite several cases of bone marrow emboli, as well as fat emboli, in fatalities with fractures. 9 However, most reports fail to clarify whether PFE in fracture cases is accompanied by bone marrow emboli, i.e., fat droplets associated with myeloid cells. This condition remains a rarely described phenomenon, despite the notion that PFE is attributable to release of fat from perturbed bone marrow.

PFE also occurs in association with soft-tissue injury unaccompanied by fracture. 5–7,10–14 The significance of adipose soft-tissue injury as a source of PFE is disputed. Palmovic and McCarroll reported that massive fat embolism was never found in cases of soft-tissue injury only but was frequent in the presence of multiple fractures. 7 By contrast, other studies have found marked fat embolism in decedents with extensive contusions only. 5,6,14,15

The association of PFE with morbidity and death within a few hours of blunt force trauma remains unclear because of a relative lack of basic knowledge about the frequency and severity of PFE in decedents. The present study undertook to examine prospectively the occurrence of PFE in deaths occurring within 24 hours of blunt force trauma. A grading system was applied to the examination of lung tissue to determine the association, if any, between parameters such as duration of survival and locations and forms of traumatic injury.

From the Marshall University School of Medicine (A.H.), Huntington, West Virginia; Kentucky State Medical Examiner’s Office (R.C.M., G.R.N.), Louisville, Kentucky; Department of Family and Community Medicine (L.J.G.), Department of Anatomical Sciences and Neurobiology (F.R.C., R.D.R.), and Department of Pathology (G.R.N.), University of Louisville School of Medicine (K.L.M.), Louisville, Kentucky.

Address for reprints: Richard D. Rink, PhD, Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Health Sciences Center, 500 South Preston, 915A, Louisville, KY 40202.

Submitted September 20, 1999. Accepted January 12, 2000.

© 2000 Lippincott Williams & Wilkins, Inc.