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Intensive Care Management of Major Trauma
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
Fat embolism can occur when fat leaks into the systemic circulation. It results in embolic symptoms and most commonly occurs after long-bone or pelvic trauma but has been described in other situations. Fat embolism occurs after all major long bone fractures but usually goes unnoticed. Some patients will develop fat embolism syndrome (FES), which is a more serious condition affecting multiple organ systems, usually developing 24–72 hours after long-bone or pelvic trauma. Fat can be detected in the lungs after even minor trauma and may pass into the systemic circulation via pulmonary capillaries or shunts or a patent foramen ovale. Fat embolus can be found in 90% of patients with long-bone fractures and invariably in all patients after reaming for intramedullary nail fixation, but FES occurs in only 1–5%. The biochemical theory provides an explanation alternative for fat embolization. This theory proposes that the inflammatory response to trauma causes the release of free fatty acids from the bone marrow into the venous system. The elevated free fatty acids as well as the inflammatory mediators cause damage to capillary beds. Elevated free fatty acid levels have been associated with hypoxaemia. Free fatty acids have also been shown to induce inflammation within the lungs.35 A retrospective study of patients with pelvic fractures requiring intensive care showed an incidence of 67% of ALI/ARDS and that this worsened around the time of the procedure. This implies that orthopaedic injuries generally and interventions in particular are associated with ALI.36
Paper 4
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
Fat embolism can be encountered following trauma or other significant insults such as pancreatitis, burns, liposuction and severe sepsis. In the setting of trauma, long bone fractures are often the underlying cause due to fat from bone marrow entering the circulation. Initial imaging is normal, followed by delayed development at around 24–48 hours of consolidation, and ground glass opacity within the lungs, with fat density pulmonary artery filling defects also possible.
Hemoglobinopathies and Thalassemias
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Chest pain must be treated with aggressive analgesia combined with use of the incentive spirometer to prevent development of pulmonary infiltrates. Adult respiratory distress syndrome may develop if arterial oxygenation cannot be maintained with nasal oxygen; red cell pheresis and intubation may be necessary. Acute, unexpected circulatory collapse may indicate fat embolism syndrome. Emergency red cell pheresis, intubation, intravenous corticosteroids, and systemic support are indicated.
Doxorubicin concentration in brain remains high for one day after triolein emulsion infusion induced BBB opening
Published in International Journal of Neuroscience, 2020
In Sook Lee, Hak Jin Kim, Seon Hee Choi, Yong-woo Kim, Ki Joo Choi
Fat embolism syndrome usually occurs one day after a long bone fracture, and in most cases the syndrome is self-limited and reversible. Triolein is a major constituent of bone marrow fat and a causative agent of fat embolism syndrome in the clinical setting, and in an experimental study, triolein infusion into a carotid artery caused infarction and the early appearance of vasogenic edema [2]. Fat emboli differ from most emboli in that they are fluid and can penetrate capillaries, and hence, vascular occlusion is often temporary and/or incomplete [3]. Furthermore, if triolein is infused in an emulsion state into a carotid artery, transient, reversible opening of the BBB occurs without infarction or serious brain injury [4–8]. Vascular permeability increases immediately after triolein emulsion infusion into a carotid artery, peaks at 2–6 h, and then decreases to baseline in 1–4 days, which is reminiscent of the clinical manifestations of fat embolism syndrome. Thus, triolein emulsion is viewed as a potential chemotherapy adjuvant for the treatment of brain tumours.
Asthma and the outcome of sickle cell disease
Published in Expert Opinion on Orphan Drugs, 2018
Alan Lunt, Sarah S. Sturrock, Anne Greenough
Fat emboli may also play a significant role in the pathogenesis of ACS. Severe vaso-occlusive pain crises, typically involving the proximal skeleton, result in bone marrow infarction and necrosis resulting in the release of fatty contents into the bloodstream. In the pulmonary vasculature severe lung inflammation, acute pulmonary hypertension and hypoxemia are triggered by means of direct mechanical occlusion and inflammation [33–36]. Fat-laden alveolar macrophages obtained during bronchoscopy are diagnostic of pulmonary fat embolism. In the national ACS study cohort, fat embolism was diagnosed in 16% of ACS cases in adults and children [15]. Another study found that patients with ACS in whom lipid-laden macrophages were identified in induced sputum followed a more severe clinical course, with more severe extra-thoracic pain and a greater incidence of neurological symptoms compared to patients without evidence of fat embolus [35].
Evidence for angiotensin mediation of the late histopathological effects of pulmonary fat embolism: Protection by losartan in a rat model
Published in Experimental Lung Research, 2018
Alan Poisner, Devin Bass, Amanda Fletcher, Ashwin Jain, Janessa Pennington England, Mariah Gawlik Davis, Dauod Arif, Agostino Molteni
Fat embolism (FE) secondary to long bone fracture or related bone trauma may lead to acute respiratory insufficiency1 but there are few or any reports on the long term effects of FE in experimental models or on humans with documented FE. In a model of fat embolism using triolein-treated rats, we have reported that the acute pulmonary histopathological changes (rapid initial inflammatory and fibrotic responses that peaked at 48 hrs),2 were ameliorated by the ACE1 inhibitor captopril, the angiotensin ATI receptor blocker, losartan (Los),3 and the renin inhibitor aliskiren.4 The acute changes diminished thereafter but persisted at 6 weeks5 and were exacerbated by a “second hit” at that time using LPS.6 The purpose of the present study was to ascertain whether FE causes persistent and progressive effects over a longer period (approaching 3 months) and whether Los would also to be protective at this late time in this chronic model. If in fact the AT1 blocker is protective at this late stage, this would be a strong indicator that pathophysiological processes involving the renin-angiotensin system continue to occur long after the initial insult and have important clinical implications.