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Fat embolism syndrome (FES) is a rare but potentially fatal complication of trauma or orthopaedic surgery, which presents predominantly with pulmonary symptoms. The rapid worsening respiratory failure in a previously normal orthopaedic surgery or trauma patients usually get evaluated for pulmonary embolism, fat‐embolism‐related acute respiratory distress or transfusion related acute lung injury. Orthopaedic surgeons and clinicians need to be aware of related entity termed 'Fat Embolism related Diffuse Alveolar Haemorrhage' (FEDAH). The clinical presentation in an orthopaedic surgery of trauma patient with FEDAH are haemoptysis, worsening type 1 respiratory failure and oxygen requirement, drop in haemoglobin levels with chest x‐ray/computed tomography suggestive of Diffuse alveolar haemorrhage (DAH). Early bronchoscopy and bronchoalveolar lavage (BAL) confirmation of DAH, presence of BAL haemosiderophages and lipid‐laden macrophages are the pointers in the early diagnosis of FEDAH. It needs a high clinical suspicion and interdepartmental collaborative measures. Timely referral from orthopaedic surgeons, early bronchoscopy and treatment with steroids is key in diagnosis and management. [ABSTRACT FROM AUTHOR]

Abstract Fat embolism syndrome (FES) is a rare but potentially fatal complication of trauma or orthopaedic surgery, which presents predominantly with pulmonary symptoms. The rapid worsening respiratory failure in a previously normal orthopaedic surgery or trauma patients usually get evaluated for pulmonary embolism, fat‐embolism‐related acute respiratory distress or transfusion related acute lung injury. Orthopaedic surgeons and clinicians need to be aware of related entity termed ‘Fat Embolism related Diffuse Alveolar Haemorrhage’ (FEDAH). The clinical presentation in an orthopaedic surgery of trauma patient with FEDAH are haemoptysis, worsening type 1 respiratory failure and oxygen requirement, drop in haemoglobin levels with chest x‐ray/computed tomography suggestive of Diffuse alveolar haemorrhage (DAH). Early bronchoscopy and bronchoalveolar lavage (BAL) confirmation of DAH, presence of BAL haemosiderophages and lipid‐laden macrophages are the pointers in the early diagnosis of FEDAH. It needs a high clinical suspicion and interdepartmental collaborative measures. Timely referral from orthopaedic surgeons, early bronchoscopy and treatment with steroids is key in diagnosis and management.

Fat embolism syndrome (FES) is a rare condition that can occur as a complication of sickle cell disease. We describe a case of a patient with sickle cell disease (homozygous Hb S or HBB: c.20A>T) presenting with initial signs and symptoms consistent with a vaso-occlusive crisis (VOC). Within 24 hours, the patient developed evidence of coagulopathy, multi organ failure and a reduced level of consciousness (LOC) prompting intubation. A diagnosis of FES was made on the basis of the patient's clinical presentation, in conjunction with magnetic resonance imaging (MRI) of the brain revealing innumerable tiny foci of restricted diffusion, intracytoplasmic microvesicular fat on Sudan Red staining of bronchoalveolar lavage samples and evidence of a pulmonary shunt on echocardiogram bubble study. Red blood cell (RBC) exchange transfusion was initiated 3 days following initial presentation and no further exchange transfusions were needed on the basis of subsequent Hb S (HBB: c.20A>T) levels. The LOC gradually improved and the patient was extubated 12 days following presentation. Neurological improvement was slow, with mild cognitive impairment initially evident at 3 months and no cognitive or neurological deficits remaining within 6 months of admission. This case highlights the importance of understanding the pathophysiology and clinical presentation of FES, as early exchange transfusion may improve survival in patients with sickle cell disease and FES. [ABSTRACT FROM AUTHOR]

Objective · To investigate the effect of Toll-like receptor 4 (TLR4) in the pathological injury in fat embolism mice model. Methods · One hundred and twenty male C57BL/6 mice were randomly divided into 10 groups. One group was set as blank control group, and others were injected separately with 1, 2…9 μL/g of allogeneic perirenal fat via tail vein, respectively. The mortality of each group was counted, median lethal dose (LD50) of fat injection in mice was calculated by Bliss method, and the fat embolism LD50 mice model was established. The TLR4 protein expression in the pulmonary tissue of surviving mice was detected by Western blotting. Sixty male C57BL/6 mice were randomly divided into the control group (the same dose of saline was given via tail vein) and the experimental groups (group 2 h, group 8 h, group 24 h and group 48 h, the LD50 fat was given via tail vein) .The TLR4 protein expression at different time after fat injection was detected by Western blotting. The mortality of 20 TLR4 gene-knockout mice (TLR4-/-mice) was recorded and compared with 60 wild-type mice after LD50 fat injection. Results · The LD50 of fat embolism mice model was (3.93±0.78) μL/g.After the injection of 1-7 μL/g fat, the expressions of TLR4 protein in the pulmonary tissue of all seven groups were significantly increased, compared with the control group (all P=0.000) . In the fat embolism LD50 mice model, compared with the control group, the expressions of TLR4 protein in group2 h were significantly increased (P=0.005) . Then, expression level of TLR4 protein was gradually reduced after 2 h, and there was no significant difference between the control group and group 48 h. The mortality of TLR4-/- mice injected with LD50 fat was lower than that of wild-type mice (P=0.043) .Conclusion · TLR4 protein involves in the pathologic process of fat embolism syndrome. The knockout of TLR4 gene can reduce the mortality of fat embolism mice. TLR4 and its correlated non-infectious inflammatory response may be an important molecular mechanism of biochemical injury in fat embolism syndrome. Blocking the activation of TLR4-mediated signaling pathway can significantly improve the prognosis, which provides new basis for the prevention, evaluation and treatment of fat embolism syndrome. [ABSTRACT FROM AUTHOR]

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A 25-year-old man was admitted to our hospital because of pulmonary embolism and suspected fat embolism after sustaining bilateral femoral shaft fracture. A left arm weakness, tachycardia and sudden hemoglobin drop delayed his definitive fixation with intramedullary nailing. His clinical course was further complicated by bleeding from the pin sites of the external fixators which had initially been used to temporarily stabilize his femoral fractures (clotting disturbances). A lower leg Doppler ultrasound and a new pelvic-chest CT angiography excluded any remaining thrombus, meanwhile the embolus had broken in smaller pieces, more distally. His unfractionated heparin was revised to a Low Molecular Weight Heparin at prophylactic dose. After a 10 day period and when his condition had been improved bilateral reamed nailing was performed. Although bilateral closed femoral shaft fractures should be stabilized early, fat embolism syndrome (FES) and thromboembolic events (TEV) should always be kept in mind in these patients. [ABSTRACT FROM AUTHOR]