Fat embolism syndrome is a serious consequence of fat emboli producing a distinct pattern of clinical symptoms and signs. It is most commonly associated with fractures of long bones and the pelvis, and is more frequent in closed, rather than open, fractures. The incidence increases with the number of fractures involved. Thus, patients with a single long bone fracture have a 1–3% chance of developing the syndrome, but it has been reported in up to 33% of patients with bilateral femoral fractures.
fat embolism causes
Fat embolism syndrome can also occur in relation to other trauma, for example, soft tissue injury, liposuction, bone marrow harvest. Non-trauma-related causes (e.g. acute pancreatitis, sickling crisis) are less likely to lead to fat embolism syndrome compared with those associated with trauma.
fat embolism signs and symptoms
Fat embolism syndrome typically presents 24–72 h after the initial injury. Rarely, cases occur as early as 12 h or as much as 2 weeks later. Patients present with a classic triad:
- respiratory changes
Dyspnoea, tachypnoea, and hypoxaemia are the most frequent early findings. The severity of these symptoms varies but a number of cases may progress to respiratory failure and a syndrome indistinguishable from acute respiratory distress syndrome (ARDS) may develop. Approximately one-half of thepatients with fat embolism syndrome caused bylong bone fractures develop severe hypoxaemiaand respiratory insufficiency and require mechanicalventilation. - neurological abnormalities
Neurological features resulting from cerebral embolism frequently present in the early stages. Cerebral emboli produce neurological signs in up to 86% of cases and often occur after the development of respiratory distress. The changes range across a wide spectrum from mild confusion and drowsiness through to severe seizures. The more common presentation is with an acute confusional state but focal neurological signs, including hemiplegia, aphasia, apraxia, visual field disturbances, and anisocoria, have been described. Seizures and decorticate posturing have also been seen. Fortunately, almost all neurological deficits are transient and fully reversible. - petechial rash
The characteristic petechial rash may be the last component of the triad to develop. It occurs in up to 60% of cases and is due to embolization of small dermal capillaries leading to extravasation of erythrocytes. This produces a petechial rash in the conjunctiva, oral mucous membrane, and skin folds of the upper body, especially the neck and axilla.6 It does not appear to be associated with any abnormalities in platelet function. The rash appears within the first 36 h and is self-limiting, disappearing completely within 7 days.
fat embolism treatment
There is no specific therapy for fat embolism syndrome; prevention, early diagnosis, and adequate symptomatic treatment are of paramount importance. Supportive care includes maintenance of adequate oxygenation and ventilation, stable haemodynamics, blood products as clinically indicated, hydration, prophylaxis of deep venous thrombosis and stress-related gastrointestinal bleeding, and nutrition. The goals of pharmacotherapy are to reduce morbidity and prevent complications. Supportive care is the mainstay of therapy for clinically apparent fat embolism syndrome. Mortality is estimated to be 5–15% overall, but most patients will recover fully.
Conservative approach would be to give prophylactic steroid therapy only to those patients at high risk for fat embolism syndrome, for example, those with long bone or pelvic fractures, especially closed fractures. Methylprednisolone 1.5 mg kg21 i.v. can be administered every 8 h for six doses.
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