The relation between tissue injury and the manifestations of pulmonary fat embolism

The syndrome of fat embolism and its origin.

“…Forty-one of the injured patients with fractures died within a week of the accident: fat emboli were found in the lungs in every case, the average number of emboli being 1,017 ± 259 per mm3 (Table I). After trauma fat droplets are reported to disappear fairly quickly from the lungs (Vance, 1931;Whiteley, 1954;Sevitt, 1960), and this was confirmed in the 33 patients with fractures who died one week or later after injury: in them the lung emboli count was only 89 ± 24 per mm3. In those without bone injury who succumbed to trauma within one week the lung embolus count was surprisingly high, 213 ± 117 Emboli per.…”

Postoperative pulmonary perfusion defects: their natural history, origin and significance

“…A further possible cause of unmatched perfusion defects is fat embolism. This was found in 100 per cent of post-mortems following routine operations (Whiteley, 1954). However, fat embolism is attended by fissure silhouetting on the chest X-ray, and the obstruction of pulmonary capillaries produces a perilobar pruning of perfusion and not a segmental defect of perfusion; as a result it would not be recorded as an unmatched perfusion defect.…”

Genesis of fat emboli.

“…Only 0.3 ml per kilogram body weight was found lethal for some rabbits (Kronke, 1957) and the proportional amount for a man would be about 20 ml. Traumatic or posthaemorrhagic shock appears to increase the sensitivity of animals to intravenously injected fat (Harman and Ragaz, 1950;Moser and Wurnig, 1954;Whiteley, 1954); the emboli in the lungs are fewer but larger, lying within arterioles rather than capillaries. Experimentally the minimum lethal dose may be reduced by a factor of 3 (Moser and Wurnig, 1954) and there is circumstantial evidence that a similar state of affairs obtains in man (Fig.…”

“…However, it is rarely important (Robb-Smith, 1945;Palmovic and Mc-Carroll, 1965) and the few fat emboliwhichappear are more likely to originate from fat liberated from adipose tissue than from chylomicrons (Frazer, Elkes, Sammons, Govan, and Cooke, 1945). Rats subjected to hind limb ischaemia showed no evidence of chylomicron flocculation, and experiments in vitro with extracts of ischaemic muscle also gave negative results (Whiteley, 1954). Increased secretion of adrenocortical hormones due to the stress of injury was put forward as a cause of chylomicron flocculation (Glas, Grekin, and Musselman, 1953) but this could not be confirmed experimentally (Glas, Grekin, Davies, and Musselman, 1956).…”