DISCUSSION
The clinical course of this patient with major trauma was characterised by two episodes of dramatic circulatory compromise that occurred after changing his body position. Although our snap diagnosis was pulmonary thromboembolism, the contrast-enhanced CT scan showed no signs of thrombus in the pulmonary artery. The patient developed delirium, acute kidney injury, skin petechiae, thrombocytopenia, anaemia and coagulopathy, all of which were supportive of the final diagnosis of FES2.
Bajuri et al. 4 proposed two variants of FES; an acute fulminant type and a classic type. The former type of FES develops in a short period through an obstructive mechanism often accompanied by severe hypotension and hypoxemia, whereas the latter typically has a latency period of 24–36 h through subsequent biochemical reactions presenting with various organ symptoms, including the brain, skin, kidney, blood cell and coagulation. In our patient, both variants were therefore overlapped during the 9-day hospital course.
Importantly, according to our investigation, massive fat globules appeared in the blood samples collected immediately after the two episodes of circulatory collapse.
Significance of detecting fat globules in blood remains controversial; in fact, some diagnostic criteria includes it2, while others not5. One possible explanation is the lack of specificity. Fat globules in blood could be observed in trauma patients without the development of FES and even in non-trauma patients6. In patients with traumatic long bone fractures, fat embolism itself in the pathology was observed in >90% of cases, whereas the incidence of FES, which was diagnosed based on Gurd’s criteria, was 0.9%5.
However, in acute fulminant FES occurring through the mechanism of massive embolism of pulmonary microcirculation7, the amount of fat globules in blood may correspond to the clinical symptoms, which was observed in our case. A previous report indicated that fat globules can pass through pulmonary microcirculation because of their deformability and enter systemic circulation within 3 h after bone surgery8. Moreover, fat globules can pass through patent foramen ovale and other arteriovenous shunts in the subpleural parts of the lungs or anastomoses between bronchial or pulmonary arteries and capillary net in the peribronchial tissues9. Our case indicates that serial changes in a quantity of fat globules may have great significance in some cases of FES, and should be evaluated in the future.
Our patient developed FES almost a week after the trauma. It is possible that fat globules could have entered into systemic circulation intermittently from unstable fractured bones that had not been surgically fixed. A previous study reported that the period of fat globulemia was longer in patients with long bone fractures treated conservatively than in patients with fractures surgically fixed early10. If this were the case, stabilising the fractured bones as early as possible may prevent the risk of FES11.