SudaMediCa, The Sudanese Medical Community

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.[4] Patients present with a classic triad: respiratory changes;neurological abnormalities;petechial rash.Respiratory changes are often the first clinical feature to present. 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 the patients with fat embolism syndrome caused by long bone fractures develop severe hypoxaemia andrespiratory insufficiency and require mechanical ventilation.[5]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 transientand fully reversible.The characteristic petechial rash may be the last component of the triad to develop. It occurs in up to 60% of cases andis due to embolization of small dermal capillaries leading to extravasation of erythrocytes. This produces a petechial rashin the conjunctiva, oral mucous membrane, and skin folds ofthe 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.A number of minor features of fat embolism syndrome may be present and these appear to result from the release of toxic mediators secondary either to the initial injury or to dysfunctional lipid metabolism. These include pyrexia, tachycardia, myocardial depression,ECG changes indicative of right heart strain, soft fluffy retinalexudates with macular oedema scotomata (Purtscher's retinopathy),coagulation abnormalities (which mimic disseminated intravascularcoagulation),[7] and renal changes presenting as oliguria, lipiduria,proteinuria, or haematuria. The presence of any these features may be of help in diagnosis