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.