| Summary: | The occurrence o f fat embolisation following trauma is a well
recognised clinical entity and may occur in up to 90% of patients with
long bone fractures. However, the fat embolism syndrome (FES) which
consists of hypoxia, acute lung injury, central nervous system
depression, and axillary or subconjunctival petechiae is only noted in
0.5-3% of these patients. Various theories have been put forward to
explain the syndrome but none have thus far been able to explain this
discrepancy.
OBJECTIVES
Our aim was to show that there is stimulation of the inflammatory
system in patients with long bone fractures resulting in the production
of lipid peroxides, and that an imbalance between the pro and antiinflammatory
mediators may be responsible for the hypoxia observed
in most patients.
METHODS
Nineteen people with long bone fractures of the lower limbs were
followed for 48 hours. Blood specimens were taken for arterial blood
gas (ABG), lipid peroxides (LPO), vitamin C, glutathione, C-reactive
protein (CRP), full blood count (FBC) at time of admission and 12, 24
and 48 hours after admission.
RESULTS
There was evidence of lung involvement with an increase in the
alveolar/arterial difference (A-aD02) from a mean of 13.8 mmHg to
23.3mmHg. Thirteen out of 16 patients (who had accurate ABG’s)
showed an increased A-aD02. The white cell count (WCC) was raised
initially with a mean of 13.8 x 109A. Within 48 hours, there had been a
decrease to 8.9 x 109/1 (p=0.003). In keeping with an inflammatory
response, there was a significant rise in the CRP in the 48 hours period
from a mean of 9.7pg/l to 127.3pg/l (pO.OOOl) and a decrease in the
platelet count from a mean of 256 x 109/1 to 193 x 109/1 (p=O.OOOJ}
Furthermore, there was an increase in the lipid peroxides from
3.79nmol/ml to 5.81nmol/ml (p=0.03) over the first 24 hours ami to
6.42nmol/ml (p=0.20) over the 48 hour period. The anti-oxidants
vitamin C and glutathione showed a decrease, vitamin C from
8.26jjg/ml to 7.45p,g/ml (p=0.05) and glutathione from 5.96pmol/ml to
3.84jimol/ml (p=0.22). Only one of the patients developed the fat
embolism syndrome suggested by contusion, hypoxia, and upper body
petechiae.
CONCLUSION
Patients with fractured long bones appear to have stimulation of their
inflammatory system. There is evidence of activation of the
coagulation system in keeping with this process. Serum antioxidants
maintain homeostasis and may be responsible for the prevention of the
FES in most patients. However, even in asymptomatic individuals,
there is evidence of pulmonary involvement. One explanation for the
development of FES in patients with long bone fractures is an
imbalance between the pro and anti-inflammatory mediators with the
production of lipid peroxides leading to organ dysfunction such as
ARDS.
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