Studies on the genesis of traumatic fat embolism in man.

Two mAnq viEws are held with regard to the pathogenesis of traumatic fat embolism. The classic view is that such embolism follows the intravenous incursion of fat droplets liberated from traumatized adipose tise and bone marrow. The mode of entrance of embolic fat globules into the bloodstream from a fracture site can be satisfactorily explained by analogy with the hydrodynamic model of Young and Griffith' This view is also supported by the observation that pulmonary fat emboli are sometimes accompanied by embolic fragments of bone marrow 2 or even by spicules of bone.3 Nevertheless, it is diflicult to conceive that in all cases sufficient fat can be liberated from localized areas of trauma to account for the severity of the subsequent fat embolism.4A Again, fat embolism has been reported in circumstances in which there is no overt tissue damage-for example, following decompression in low pressure chambers or in flying accidents.8'7 These considerations and others of a more positive nature have prompted an alternative view that the embolic fat globules are derived mainly or entirely from the lipids normally present in the plasma.8'9 This view has been the subject of much controversy and we are inclined to agree with Sevitt 10 that it remains unproven. A relatively neglected approach, the investigation of the physical properties and chemical composition of the embolic fat, might be expected to provide some clues as to its origin The intense sudanophilia of the emboli and their stainability with osmium tetroxide are in keeping with the reactions given by the triglycerides in adipose tissue cells. Evidence for the presence of free fatty acids is inconclusive, owing to the unreliability of the available techniques." Beyond this, little attention seems to have been given to the nature of the embolic fat until the important observations of LeQuire et aL'I These workers reported that the emboli in 9 cases of human pulmonary fat embolism often included masses of birefringent acicular

[1]  S. Sevitt The boundaries between physiology, pathology, and irreversibility after injury. , 1966, Lancet.

[2]  H. A. Ellis EFFECTS OF THE LONG-TERM ADMINSTRATION TO ANIMALS OF DEXTRAN SULPHATE. , 1965, The Journal of pathology and bacteriology.

[3]  D. I. Fryer Pathological Findings in Fatal Sub-Atmospheric Decompression Sickness , 1962 .

[4]  W. Fleet,et al.  A study of the pathogenesis of fat embolism based on human necropsy material and animal experiments. , 1959, The American journal of pathology.

[5]  Peltier Lf Fat embolism. I. The amount of fat in human long bones. , 1956 .

[6]  J. T. Bell,et al.  AN IMPROVED METHOD FOR THE SCHULTZ CHOLESTEROL TEST , 1956, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.

[7]  W. Haymaker,et al.  Pathology of decompression sickness; a comparison of the lesions in airmen with those in caisson workers and divers. , 1955, Military medicine.

[8]  C. Reiner The Schultz histochemical reaction for cholesterol; observations on specificity and sensitivity. , 1953, Laboratory investigation; a journal of technical methods and pathology.

[9]  H. Rappaport,et al.  Bone Marrow Embolism. , 1951, The American journal of pathology.

[10]  H. Griffith,et al.  The dynamics of parenchymatous embolism in relation to the dissemination of malignant tumours. , 1950, The Journal of pathology and bacteriology.

[11]  Robert M. Moore,et al.  FAT EMBOLISM: INCLUDING EXPERIMENTAL PRODUCTION WITHOUT TRAUMA , 1927 .