Relevant bibliographies by topics / Fat embolism

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Fat embolism'

Author: Grafiati
Published: 4 June 2021
Last updated: 26 January 2023

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Journal articles on the topic "Fat embolism"

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LATIF, ANSAR, ANILA BASHIR, AURANGZEB ,, and Umar Ghani. "FAT EMBOLISM AND FAT EMBOLISM SYNDROME;." Professional Medical Journal 15, no. 04 (March 10, 2008): 407–13. http://dx.doi.org/10.29309/tpmj/2008.15.04.2940.

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Fat Embolism and the associated Fat Embolism Syndrome is a serious and potentially life threatening condition. It tends tooccur usually after fractures or intramedullary instrumentation of long bones. Non-traumatic conditions such as Diabetes Mellitus severe Burns,SLE, sickle cell disease and Pancreatitis can also lead to Fat Embolic syndrome. Young adults are commonly affected. Presentation consistsof an asymptomatic interval followed by pulmonary and neurological manifestations combined with petechial haemorrhages. The diagnosislargely depends on high index of suspicion and exclusion of other conditions. Treatment of this condition remains supportive. Mortalityassociated with this condition is significant, ranging from 10-20% .
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Rothberg, David L., and Christopher A. Makarewich. "Fat Embolism and Fat Embolism Syndrome." Journal of the American Academy of Orthopaedic Surgeons 27, no. 8 (April 2019): e346-e355. http://dx.doi.org/10.5435/jaaos-d-17-00571.

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Capan, Levon M., Sanford M. Miller, and Katie P. Patel. "FAT EMBOLISM." Anesthesiology Clinics of North America 11, no. 1 (March 1993): 25–54. http://dx.doi.org/10.1016/s0889-8537(21)00766-5.

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Yakovlev, V. N., Yu V. Marchenkov, N. S. Panova, V. G. Alekseyev, and V. V. Moroz. "Fat Embolism." General Reanimatology 9, no. 4 (August 20, 2013): 50. http://dx.doi.org/10.15360/1813-9779-2013-4-50.

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Peltier, Leonard F. "Fat Embolism." Clinical Orthopaedics and Related Research 422 (May 2004): 148–53. http://dx.doi.org/10.1097/01.blo.0000131647.64240.89.

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HARRIS, HELENE. "Fat embolism." Nursing 34, no. 6 (June 2004): 96. http://dx.doi.org/10.1097/00152193-200406000-00064.

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Mellor, A., and N. Soni. "Fat embolism." Anaesthesia 56, no. 2 (February 2001): 145–54. http://dx.doi.org/10.1046/j.1365-2044.2001.01724.x.

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Prys-Roberts, C. "Fat embolism." Anaesthesia 56, no. 7 (July 2001): 692–93. http://dx.doi.org/10.1046/j.1365-2044.2001.02137-5.x.

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Horowitz, P. E., and N. Soni. "Fat embolism." Anaesthesia 57, no. 8 (July 18, 2002): 818–38. http://dx.doi.org/10.1046/j.1365-2044.2002.02752_17.x.

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Gupta, Amandeep, and Charles S. Reilly. "Fat embolism." Continuing Education in Anaesthesia Critical Care & Pain 7, no. 5 (October 2007): 148–51. http://dx.doi.org/10.1093/bjaceaccp/mkm027.

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Dissertations / Theses on the topic "Fat embolism"

1

Aebli, Nikolaus, and n/a. "Fat embolism and cardiovascular changes during vertebroplasty in an animal model." University of Otago. Dunedin School of Medicine, 2006. http://adt.otago.ac.nz./public/adt-NZDU20070205.103827.

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The studies documented here have demonstrated that similar to joint arthroplasty, VP causes FE with cardiovascular changes. Following the augmentation of each VB there is a transient acute response affecting the homeostasis of the cardiovascular system. This response is biphasic. Phase 1 was seen within 3 s after the beginning of bone cement injection and is likely to be due to a autonomous nerve reflex. Phase 2 was observed within ~16 s, reaching a peak response after ~30 s returning to a steady state between I and 5 minutes (approximately 10 % below pre-injection baseline). Consequently multiple VP caused baseline cardiovascular variables to progressively deteriorate. This fundamental response occurred whether bone cement or bone wax was used. A vent-hole did not prevent the peak response but attenuated the progressive deterioration of the baseline. Pathomechanism of Fat Embolism: The exact mechanism(s) responsible for the cardiovascular responses to FE are still not entirely clear. However several theories have been put forward in the literature (see Chapter 1). The present studies have eluciated the role of some of these variables. The primary mechanism responsible for FE has been attributed to an increase in IMP (Breed, 1974; Engesaeter et al., 1984; Orsini et al., 1987, Hofmann et al., 1999). The present investigation measured the IMP during VP and found that the peak increase in IMP (>500mmHg) was similar to that reported for arthroplasty. The consequences of an increase in IMP are 1) a release of bone marrow content into the venous system and 2) a likely stimulation of nerve endings within the bone marrow cavity. By using transoesophageal echocardiography, this thesis provides evidence that the emboli originate from the bone marrow cavity and not from the agglutination of plasma fat. Because the cardiovascular response was seen in the first seconds after the pressurisation (phase 1) and before the bone marrow content had reached the lung, it is most likely that this reaction was triggered by a nerve reflex. On the basis of either an up regulation of the vagus or a down regulation of the sympathetic tone. Pressurisation with bone cement and bone wax caused similar cardiovascular deterioration, which clearly gives evidence that bone cement monomer is not the only factor in this process. In the vent-hole group there was also a similar phase 1. Although the IMP was not measured in this group it is likely that the peak IMP was less in the vent hole group but still exceeding the threshold for nerve reflex stimulation. After the initial cardiovascular response (fall in HR and MABP) a secondary cardiovascular response occurred (phase 2). Two possible mechanisms responsible for phase 2 are: 1) the effect of the released bone marrow content and its mediators on the pulmonary and systemic vascular system and 2) continuous stimulation of nerve endings within the VB caused by the pressure of the injected material. Phase 2 was characterised by an increase in PAP and CVP and a decrease in MABP starting ~16 seconds after the beginning of the bone cement / bone wax injection. The time and response pattern for phase 2 was similar for each augmentation (VP1-VP2) and similar between the groups. This similarity gives evidence that the peak responses were a result of a reflex vasoconstriction of the lung vessels to the microembolisation of bone marrow particles (Byrick et al., 1989; Woo et al., 1995). Other authors also have reported that an increase in PVR was observed during FE (Wheelwright et al., 1993; Byrick et al., 1994), but this work is the first to suggest that a pulmonary vasoconstriction reflex may be involved. This is the first study which measured the cardiovascular responses during FE continuously, unlike other studies which measured responses after 3 to 5 minutes (Wheelwright et al., 1993; Byrick et al., 1994). In the vent-hole group, Q was also measured during the transient response and therefore it was possible to calculate the PVR. The results showed that PVR was increased 3 to 5 times the pre-injection value at the peak response proving evidence that an increase in PVR is likely to be responsible for the increase in PAP and CVP and the decrease in MBP Based on the observation that the wax and non-vent hole groups had similar peak responses to the vent hole group for PAP, CVP and MBP it can be concluded that PVR responses are also similar for all the groups. The bone cement and the bone wax group had similar peak responses, therefore bone cement monomer can not solely be responsible for the vasoconstriction of the lung vessels. Although the amount of the fat was likely to be reduced by using a vent-hole the peak responses were similar. This suggests that even a reduced amount of bone marrow content released in the vent-hole group exceeded the 'threshold' for initiating a reflex response. The fact that a certain threshold has to be reached to initiate a reflex response may explain why only a small percentage of patients develop FE during arthroplasty. Small amounts of bone marrow may not trigger the reflex. This finding is of significant clinical relevance as far as VP is concerned. To prevent the initiation of the reflex during injection of bone cement for VP or implantation of a prosthesis has to be performed as slowly as possible to reduce the amount of bone marrow content released into the circulation which reduces the risk of triggering reflex pulmonary vasoconstriction. The problem with medium viscosity bone cement used in this study is that it cures too rapidly. Therefore it is essential to find a bone cement material which can be injected much slower to reduce the amount of bone marrow content released and, consequently, the chance of triggering a nerve reflex. These findings are also relevant for joint arthroplasty. By reducing the injection pressure less bone marrow content is released into the circulation and the chances of initiating this reflex mechanism are minimised. Future studies are required to measure the cardiovascular changes by injecting bone cement at low speed. Because such bone cement is not yet available, it would be possible to use calcium phosphate cements instead. A similar amount of fat would be released but whether the magnitude of the cardiovascular effect is altered would be interesting to explore. The recovery of PVR was responsible for the recovery of MABP. This was quicker in the bone wax group compared to the group where bone cement was used. It is therefore likely that the bone cement monomer has a vasoconstrictor effect on the vascular system of the lung. Alternatively bone cement has been implicated in the increase of circulation levels of coagulating substances such as thrombin or fibrinopeptides (Dahl et al., 1988; Sharrock et al., 1995). However we could not demonstrate that bone cement monomer altered the peak reflex response. Several authors have implicated bone cement monomer as having an effect on the cardiovascular system (Berman et al., 1974). This is the first study which provides compelling evidence that bone cement plays a role during FE. The peak response for HR was different in the bone wax group compared to the cement groups. With bone wax HR decreased during phase 2 whereas with bone cement HR gradually increased. From the previous study we know that the fall in MABP and HR in phase 1 is caused by a nerve reflex (Chapter 3). This would normally result in an increase in sympathetic activity. In the bone cement group the primary peripheral vasoconstriction response was attenuated resulting in a secondary increase in HR in order to restore MABP. This dulled response may be attributed to the bone cement monomer. However in the bone wax group the sympathetic response caused a severe and rapid vasoconstriction to restore MABP. Therefore an increase in HR did not happen and HR dropped further in phase 2. This result may have a major impact on the clinical use of bone cement in the future, especially when treating patients with cardiovascular risk factors. Baseline Changes: The injection of five consecutive VB in the same animal caused a progressive decrease in MABP in all groups. The fall in MABP was primarily correlated to SVR. The fall in SVR is mostly likely caused either by: 1) vasoactive substances, or 2) a decrease in sympathetic tone. A vent hole was able to attenuate the progressive decrease in MABP. Because the quantity of bone marrow content released into the circulation was lower in the vent-hole group, compared to the bone cement group, the amount of vasoactive substances would also be lower in this group. This suggests that vasoactive substances are responsible for the decrease in SVR. The quantity of injected PMMA was not different between the vent hole and bone cement group. Therefore, the methylmethacrylate monomer does not seem to play a major role in the development of the fall in baseline MABP during multiple VP. The fact that the decrease in MABP was similar in the bone cement and bone wax group supports this theory as well, since a similar amount of bone marrow is released. Blood Gas Changes: In the present study, multiple VP induced prolonged hypoxaemia, hypercapnia and acidosis. According to the literature, the likely cause for these changes in arterial blood gases is ventilation-perfusion (V/Q) mismatch and pulmonary shunting, which is a consequence of the fat and marrow particles causing microembolisation of the pulmonary vessels (Modig et al., 1974; Pitto et al., 1998). The V/Q mismatching may also be accentuated by mediators causing pulmonary vasoconstriction (Woo et al., 1995). The severity of V/Q mismatch is likely to be correlated to the amount of bone marrow reaching the lung which was similar in the bone wax and bone cement group. A vent hole reduced the amount of fat released and therefore the mismatch. Consequently, PaCO2 and pHa did not significantly change and the fall in PaO2 in the vent hole group was less than the bone cement group. Similarly, Pitto et al. (1999) reported that the hypoxaemia that normally develops during hip arthroplasty, can be prevented if a vent hole is drilled into the distal femur and a vacuum applied. Clinical Implications: Surgeons have to be aware that FE occurs during VP and is similar to what happens during arthroplasty. Therefore VP can potentially cause hypotension, cardiac arrest and even death (personal communication with Prof. Jens R. Chapman). The potential risk increases with the number of augmented VBs. As a result of the current work it has been shown that a maximum of 3 - 4 VBs can be augmented safely in one operation and that cardiovascular monitoring is mandatory. A vent hole is also recommended to attenuate the adverse cardiovascular response. The use of bone substitute material does not reduce or prevent the risk of FE and consequently similar precautions are recommended.
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Nussbaum, Clive Joel. "Fat embolism syndrome : a study of its clinical manifestations and long term outcome." Master's thesis, University of Cape Town, 1987. http://hdl.handle.net/11427/26362.

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Krebs, Jörg. "Pathophysiology of cardiovascular changes after cement and fat embolism during vertebroplasty in an animal model /." Bern : [s.n.], 2007. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Appelblad, Micael. "Fat contamination of pericardial suction blood in cardiac surgery : clinical and experimental studies in perspectives of transfusion logistics." Doctoral thesis, Umeå : Kirurgisk och perioperativ vetenskap Surgical and Perioperative Sciences, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-754.

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Hermann, Bertrand. "Nouvelles approches diagnostiques et thérapeutiques pour les patients souffrant de troubles de la conscience Wisdom of the caregivers: pooling individual subjective reports to diagnose states of consciousness in brain-injured patients, a monocentric prospective study Unexpected good outcome in severe cerebral fat embolism syndrome." Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS638.

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Le diagnostic et le traitement des troubles de conscience est complexe. Dans ce travail, nous avons i) introduit une nouvelle échelle comportementale pour mesurer l’état de conscience, fondée sur l’intelligence collective, ii) validé la mesure de l’indice métabolique du PET au fluorodeoxyglucose comme étant l’une des meilleures techniques de neuroimagerie pour le diagnostic de l’état de conscience minimale (ECM), et iii) mis au point un signe clinique d’ECM nouveau et fiable, l’habituation du réflexe de sursaut au bruit. Ces résultats sont en faveur de la réinterprétation de l’ECM comme étant un état médié par le cortex. Par ailleurs, l’investigation des effets comportementaux et électrophysiologiques de la stimulation électrique transcrânienne en courant continu (tDCS) préfrontale chez les patients souffrant de troubles de la conscience nous a permis de mettre en évidence un effet authentique et direct de la stimulation sur la conscience, agissant via la modulation de l’activité corticale et de la connectivité cortico-corticale résiduelle. Enfin, dans le but de développer de nouveaux paradigmes de stimulation, influencés par la théorie, nous avons utilisé la tDCS et la stimulation électrique transcranienne en courant alternatif (tACS) chez des sujets sains pour tester des prédictions de la théorie de l’espace de travail neuronal global lors d’une tâche visuelle d’accès conscient, avec des effets hétérogènes. Au total, nos résultats plaident pour l’investigation systématique des effets de la stimulation sur l’activité cérébrale et pour le développement de procédures de stimulation plus efficaces et ciblées
Accurate diagnosis and treatment of consciousness disorders (DoC) remains a challenging issue. In this work, we introduced a new behavioral scale for DoC capitalizing on the wisdom of the crowd phenomenon, we validated the FDG-PET metabolic index of the best preserved hemisphere as one of the best neuro-imaging technique for minimally conscious state (MCS) diagnosis and proposed a new and reliable clinical sign of MCS, the habituation of auditory startle reflex. In addition to enriching and refining our repertoire of diagnostic procedures available for DoC diagnosis, our results support the interpretation of the generic and elusive MCS as a cortically-mediated state, which reflects the preservation of activity within specialized cortical networks and could include both conscious and non-conscious states. On the therapeutic side, by investigating the effects of prefrontal transcranial direct current stimulation (tDCS) on behavior and brain activity of patients suffering from DoC, we provided evidence for a genuine and direct cortical effect of the stimulation on consciousness through the modulation of residual cortical activity and cortico-cortical connectivity. Finally, in an attempt to develop theory-driven stimulation paradigms, we used tDCS and transcranial alternative stimulation to test predictions of the global neuronal workspace theory on conscious access in healthy subjects, with heterogeneous stimulation responses. Taken together, our results advocate for the systematic investigation of stimulation effect on brain activity and for the future development of more powerful and targeted stimulation procedures
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Gray, Andrew Colin. "Damage control orthopaedics and the cognitive effects of cerebral fat embolus." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/24640.

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This thesis consists of two clinical projects and a large animal (ovine) model of severe musculoskeletal trauma under terminal anaesthesia. It involved the analysis of haemodynamic, pulmonary embolic, coagulative and inflammatory response to bilateral femoral fractures and hypovolaemic shock comparing two different surgical strategies of fracture fixation (damage control versus early total care). This study aimed to better quantify the relative consequences of initial surgical management (external fixation versus intramedullary stabilisation) against a background of relative severe injury. Both clinical projects involved the use of Transcranial Doppler ultrasound monitoring of the cerebral circulation to quantify the cerebral embolic load, with detailed clinical cognitive testing and the measurement of a serum marker (S100B protein) of neuronal injury. One study involved trauma patients requiring intramedullary stabilisation of femoral and tibial diaphyseal fractures and the other examined patients undergoing primary lower limb arthroplasty. The primary aim of both studies was to accurately quantify cognitive change following surgery and to assess whether these measurements correlated with intraoperative cerebral embolic load and serum S100B protein concentrations following surgery. The animal study demonstrated a higher pulmonary embolic load with early intramedullary femoral fracture fixation compared to external fixation. However the initial fracture fixation method did not affect animal mortality or changes seen in the measured coagulation and inflammatory markers. Specific and quantifiable defects in cognitive function occurred following surgery in both clinical studies. However, no direct correlation was found between cognitive change and cerebral emboli detection. Altering surgical technique can reduce the embolic load. However a linear correlation between embolic load and clinical outcome was not established.
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"The study of pathogenesis of pulmonary fat embolization after intramedullary reaming and possible improvement in reaming technique." 2000. http://library.cuhk.edu.hk/record=b6073246.

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Cheung Ngai man Edmund.
"August 2000."
Thesis (Ph.D.)--Chinese University of Hong Kong, 2000.
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Mode of access: World Wide Web.
Abstracts in English and Chinese.
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"The effect of reaming on intramedullary pressure and marrow fat embolisation." 1997. http://library.cuhk.edu.hk/record=b5889301.

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by Cheung Ngai Man, Edmund.
Thesis (M.Phil.)--Chinese University of Hong Kong, 1997.
Includes bibliographical references (leaves 73-83).
Acknowledgments --- p.i
Abstract --- p.iii
List of Figures --- p.viii
List of Tables --- p.xi
Chapters
Chapter 1 --- Introduction --- p.1
Chapter 1.1 --- Intramedullary nailing --- p.1
Chapter 1.2 --- Reaming technique for intramedullary nailing --- p.3
Chapter 1.3 --- The relationship between pulmonary fat embolism and reaming technique --- p.7
Chapter 1.4 --- Objectives --- p.10
Chapter 2 --- Methodology --- p.12
Chapter 2.1 --- The measurement of the intramedullary pressure --- p.12
Chapter 2.1.1 --- Animal model --- p.12
Chapter 2.1.2 --- Intramedullary pressure measurement device --- p.12
Chapter 2.1.3 --- Operative procedure --- p.14
Chapter 2.1.4 --- Intramedullary pressure measurement --- p.16
Chapter 2.2 --- The measurement of the plasma lipids and marrow lipids --- p.19
Chapter 2.2.1 --- Samples collection --- p.19
Chapter 2.2.2 --- Lipid extraction --- p.19
Chapter 2.2.3 --- Thin layer chromatography --- p.20
Chapter 2.2.4 --- Methylation --- p.24
Chapter 2.2.5 --- Gas chromatographic analysis --- p.24
Chapter 2.3 --- The measurement of the pulmonary lipids and fat emboli --- p.27
Chapter 2.3.1 --- Pulmonary tissue collection --- p.27
Chapter 2.3.2 --- Preparation for measurement of pulmonary lipids --- p.27
Chapter 2.3.3 --- Fat emboli staining --- p.27
Chapter 2.3.4 --- Image analysis --- p.28
Chapter 2.4 --- Statistical analysis --- p.31
Chapter 3 --- Results --- p.32
Chapter 3.1 --- Intramedullary pressure measurement --- p.32
Chapter 3.2 --- The analysis of bone marrow lipids --- p.34
Chapter 3.3 --- The changes of the plasma lipids during reaming --- p.39
Chapter 3.4 --- The measurement of the pulmonary fat emboli --- p.44
Chapter 3.5 --- The relationship between the intramedullary pressure and plasma lipids and pulmonary fat intravasation --- p.52
Chapter 4 --- Discuss --- p.55
Chapter 4.1 --- The experimental design --- p.55
Chapter 4.2 --- The change of the intramedullary pressures --- p.57
Chapter 4.3 --- The application of the gas chromatography --- p.59
Chapter 4.4 --- The composition of bone marrow lipids --- p.62
Chapter 4.5 --- The changes of plasma lipids --- p.63
Chapter 4.6 --- The pulmonary fat embolisation --- p.65
Chapter 5 --- Conclusion --- p.69
Chapter 6 --- Future direction on this study --- p.71
References --- p.73
Appendix --- p.84
Chapter 1 --- The operation of the IM Press device --- p.84
Chapter 2 --- The calibration of the IM Press --- p.85
Chapter 3 --- The preparation of the internal standards for the lipid analysis --- p.89
Chapter 4 --- The composition of the bone marrow lipids --- p.91
Chapter 5 --- The composition of plasma lipids --- p.95
Chapter 6 --- The composition of pulmonary lipids --- p.101
Chapter 7 --- The measurement of the pulmonary fat emboli --- p.105
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Ayach, Bilal M. "Modulation of the endothelin system in acute pulmonary air embolism in rats /." 2005. http://proquest.umi.com/pqdweb?did=974392721&sid=53&Fmt=2&clientId=9268&RQT=309&VName=PQD.

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Books on the topic "Fat embolism"

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Soni, Neil. Assessment and management of fat embolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0337.

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Fat embolism syndrome is a complication of a range of conditions. It is hard to prevent, difficult to diagnose, and there is no specific effective treatment. The syndrome is composed of respiratory, haematological, neurological, and cutaneous symptoms and signs associated with trauma, in particular long bone fractures, and other disparate surgical and medical conditions. It most commonly follows orthopaedic surgery, but can also follow liposuction and medical conditions, as disparate as cardiopulmonary resuscitation and sickle cell disease are possible precipitants. The pathogenesis is still debated. It is clear that while fat emboli occur quite commonly, the clinical syndrome with respiratory, neurological, and other sequelae is rare. Diagnosis is by pattern recognition, but recently characteristic features seen on cerebral magnetic resonance imaging can be used to increase the probability of the diagnosis. Various therapeutic options have been tried and failed and treatment is currently supportive.
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The pathophysiologic effects of fat embolism: A new animal model. Ottawa: National Library of Canada, 2002.

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Singer, Mervyn. Pathophysiology and causes of pulmonary embolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0170.

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Pulmonary embolus is predominantly due to thrombus breaking off from deep veins or from within the right heart, lodging within large or small vessels within the pulmonary vasculature, causing a variable degree of clinical features ranging from asymptomatic through to shock and cardiac arrest. Non-thrombotic causes include air or fat embolism. Outcome is predicated by the degree of right ventricular dysfunction. There are multiple risk factors including surgery, arrhythmias, prolonged immobility, venous stasis, pregnancy and an underlying pro-thrombotic tendency, either congenital or acquired. Numerous risk stratification scores have been developed derived from clinical features, imaging findings and biochemical markers of right ventricular strain and myocardial damage.
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Wilson-MacDonald, James, and Andrew James. Complications of fractures. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.012002.

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♦ Fat embolism syndrome is defined as the presence of globules of fat in the lungs and in other tissues and occurs occasionally in long bone fractures♦ Reflex sympathetic dystrophy is characterized by intense prolonged pain, vasomotor disturbance, delayed functional recovery, and trophic changes♦ Avascular necrosis typically affects intra-articular bone after fracture and can occur in up to 70% of displaced talar neck fractures♦ Immobility associated with recovery from fracture is associated with deep vein thrombosis, which carries a risk of pulmonary embolism, and should be treated with anti-coagulants♦ Gas gangrene is a rapidly-spreading infection of devitalized tissue, removal of the affected area and treatment with penicillin is required♦ Compartment syndrome within a closed compartment can result in tissue ischaemia and necrosis followed by fibrosis and muscle contracture
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Beed, Martin, Richard Sherman, and Ravi Mahajan. Breathing. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199696277.003.0003.

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Respiratory failureSevere hypercapniaComplications of mechanical ventilationSevere pneumoniaAspirationInhalational injuryAsthma/severe bronchospasmExacerbation of COPDAir trappingTension pneumothoraxMassive haemothoraxPulmonary haemorrhagePulmonary oedemaAcute respiratory distress syndromePulmonary embolism/fat embolismRespiratory failure occurs when air transfer in and out of the lungs is reduced, or when gas exchange within the lungs fails (due to shunt, VQ mismatch, or poor gas diffusion), resulting in either: ...
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Griffiths, Richard, and Ralph Leighton. Orthopaedic surgery. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198719410.003.0018.

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This chapter discusses the anaesthetic management of orthopaedic surgery. It begins with general principles of the anaesthetic management of orthopaedic surgical patients, including the management of fat embolism syndrome, bone cement implantation syndrome, compartment syndrome, and the use of tourniquets. Surgical procedures covered include total hip joint replacement (including revision total hip joint replacement), femoral neck fracture surgery, total knee joint replacement, arthroscopy, cruciate ligament repair, ankle surgery, foot surgery, spinal surgery (including the cervical spine), shoulder surgery (including total shoulder joint replacement), elbow replacement surgery, hand surgery, and trauma, including fractures of limbs or spine.
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Griffiths, Richard, and Ralph Leighton. Orthopaedic surgery. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198719410.003.0018_update_001.

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This chapter discusses the anaesthetic management of orthopaedic surgery. It begins with general principles of the anaesthetic management of orthopaedic surgical patients, including the management of fat embolism syndrome, bone cement implantation syndrome, compartment syndrome, and the use of tourniquets. Surgical procedures covered include total hip joint replacement (including revision total hip joint replacement), femoral neck fracture surgery, total knee joint replacement, arthroscopy, cruciate ligament repair, ankle surgery, foot surgery, spinal surgery (including the cervical spine), shoulder surgery (including total shoulder joint replacement), elbow replacement surgery, hand surgery, and trauma, including fractures of limbs or spine.
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Adam, Sheila, Sue Osborne, and John Welch. Trauma and major haemorrhage. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199696260.003.0011.

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This chapter discusses the medical and nursing management of trauma patients from their initial assessment in the emergency department to their subsequent management in the critical care unit. Each section of the chapter covers a specific area of trauma and describes its underlying physiology, management, and associated complications. Injuries discussed include spinal, head, chest, cardiovascular, genitourinary, renal, abdominal, pelvic, musculoskeletal, burn injury, hypothermia, and drowning. Major complications, such as fat embolism syndrome, compartment syndrome, and rhabdomyolysis, are described in detail. The chapter also discusses the management of major haemorrhage and the complications of massive blood replacement therapy.
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Sell, Alex, Paul Bhalla, and Sanjay Bajaj. Anaesthesia for orthopaedic and trauma surgery. Edited by Philip M. Hopkins. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0063.

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This chapter is divided into three main sections. The first section concerns the patient population that presents for orthopaedic surgery, specifically examining chronic diseases of the musculoskeletal system and the medications commonly used for their management, and the impact this has when these patients present for surgery. Included in this section are the surgical considerations and the anaesthetic implications of orthopaedic surgery, ranging from patient positioning to bone cement implant syndrome. The last part of this first section looks at specific orthopaedic operations, starting with the most commonly performed, hip and knee arthroplasties, and moving onto the specialist areas of spinal deformity, paediatric, and bone tumour surgery that are not usually found outside of specialist centres. The middle section gives a brief overview on analgesia concentrating on pharmacological methods as, although orthopaedic surgery lends itself well to regional anaesthesia, this is covered elsewhere in its own dedicated chapters. No section on analgesia would be complete without mentioning enhanced recovery: the coordinated, multidisciplinary approach that improves the patient experience, increases early mobilization, and reduces length of stay, which should be the standard obtained for every patient. The final section covers the anaesthetic management of in-hospital trauma, giving an overview on initial assessment, timing of surgery, and management of haemorrhage and coagulopathy. This section finishes by covering the orthopaedic-specific topics of compartment syndrome, fat embolism syndrome, and the management of fractured neck of femur and spinal injury.
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Gray, Andrew C. Orthopaedic approach to the multiply injured patient. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.012003.

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♦ Major trauma results in a systemic stress response proportional to both the degree of initial injury (1st hit) and the subsequent surgical treatment (2nd hit).♦ The key physiological processes of hypoxia, hypovolaemia, metabolic acidosis, fat embolism, coagulation and inflammation operate in synergy during the days after injury/surgery and their effective management determines prognosis.♦ The optimal timing and method of long bone fracture fixation after major trauma remains controversial. Two divergent views exist between definitive early intramedullary fixation and initial external fixation with delayed conversion to an intramedullary nail once the patient’s condition has been better stabilised.♦ There is agreement that the initial skeletal stabilisation should not be delayed and that the degree of initial injury has a more direct correlation with outcome and the development of subsequent systemic complications rather than the method of long bone fracture stabilisation.♦ Trauma patients can be screened to identify those more ‘at risk’ of developing systemic complications such as respiratory insufficiency. Specific risk factors include: A high injury severity score; the presence of a femoral fracture; the combination of blunt abdominal or thoracic injury combined with an extremity fracture; physiological compromise on admission and uncorrected metabolic acidosis prior to surgery.♦ The serum concentration of pro-inflammatory cytokine interleukin (IL) 6 may offer an accurate method of quantifying the degree of initial injury and the response to surgery.♦ The effective management of the polytraumatised patient involves a team approach and effective communication with allied specialties and theatre staff. A proper hierarchy of the injuries sustained can then be compiled and an effective surgical strategy made.
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Book chapters on the topic "Fat embolism"

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O’Donnell, John M. "Fat Embolism Syndrome." In Surgical Intensive Care Medicine, 385–95. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4757-6645-5_23.

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O’Donnell, John M. "Fat Embolism Syndrome." In Surgical Intensive Care Medicine, 277–84. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-0-387-77893-8_25.

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Nagarsheth, Khanjan H. "Fat Embolism Syndrome." In Encyclopedia of Trauma Care, 604–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-29613-0_129.

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Groskin, Stuart A. "Fat Embolism Syndrome." In Radiological, Clinical and Biomechanical Aspects of Chest Trauma, 156–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76457-8_9.

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O’Donnell, John M. "Fat Embolism Syndrome." In Surgical Intensive Care Medicine, 349–56. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-19668-8_26.

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Davies, Eryl. "Fat Embolism Syndrome." In The Final FFICM Structured Oral Examination Study Guide, 188–89. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003243694-63.

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Cárdenas-Camarena, Lázaro, Héctor César Durán-Vega, Guillermo Ramos-Gallardo, and Jorge Enrique Bayter-Marin. "Mortality Following Gluteal Fat Augmentation: Physiopathology of Fat Embolism." In Gluteal Fat Augmentation, 145–49. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-58945-5_21.

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Bulger, Eileen M. "Fat Embolism Syndrome in the Trauma Patient." In Thoracic Trauma and Critical Care, 519–21. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-1127-4_66.

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Andjelkov, Katarina, and Nikola Music. "Fat Grafting and Fat Embolism. How to Prevent, Diagnose, and Treat." In Plastic and Aesthetic Regenerative Surgery and Fat Grafting, 277–84. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-77455-4_22.

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Doumit, Gaby, and Mihiran Karunanayake. "Fat Embolism After Liposuction in Klippel-Trenaunay Syndrome." In Liposuction, 867–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-48903-1_91.

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Conference papers on the topic "Fat embolism"

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Casas, D., J. P. Sambataro, P. Kishankumar, F. Khan, and J. L. Perez. "Fat Embolism Syndrome: Elucidating a Diagnosis of Exclusion." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7019.

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Urrutia Argueta, S., A. Ositelu, and R. Kapoor. "Remarkable Recovery After Fat Embolism Syndrome in Hemoglobin SC Disease." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7206.

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Priyanka, G., Anand Bangera, Avanish Bhandary, Govind Raj Bhat, and Naresh Rai. "Recurrent Fat Embolism Syndrome in a Patient with Long Bone Fracture." In ISACON KARNATAKA 2017 33rd Annual Conference of Indian Society of Anaesthesiologists (ISA), Karnataka State Chapter. Indian Society of Anaesthesiologists (ISA), 2017. http://dx.doi.org/10.18311/isacon-karnataka/2017/ep079.

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Brandorff, M., E. Jirru, and L. Lief. "Refractory Hypoxemia Secondary to Fat Embolism Syndrome Requiring Venovenous Extracorporeal Membrane Oxygenation." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5188.

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Hyder, S., B. T. Nyatanga, K. D. Stettmeier, and P. Grover. "A Big Fat Crisis: Cerebral Fat Embolism Syndrome in a Patient with Sickle Cell Trait/Beta Thalassemia Trait." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3305.

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Viseroi, M., A. Ismail, N. Patel, F. Youssef, T. R. Chandak, and J. Patel. "Altered Mental Status as Initial Presentation of Fat Embolism Syndrome in Sickle Cell Crisis." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6665.

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Junqueira, Marcel, Agostino Molteni, Frederico Adler, Alan Poisner, Terence Mciff, and Betty L. Herndon. "Clara Cell Response To Pulmonary Fat Embolism In A FES-ARDS Rat Model And Its Modification By Captopril And Losartan." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2162.

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Raza, D. "E-045 A case of left internal carotid artery stroke due to fat embolism from novel cosmetic procedure: a case report." In SNIS 19th Annual Meeting Abstracts. BMA House, Tavistock Square, London, WC1H 9JR: BMJ Publishing Group Ltd., 2022. http://dx.doi.org/10.1136/neurintsurg-2022-snis.156.

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Fabbri, Dario, Quan Long, Saroj Das, and Michele Pinelli. "Study of Embolic Particle Migration in Cerebral Arteries by Computational Modelling." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80314.

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As known, embolism is one of the major causes of stroke, which represents the rapid loss of brain functions. Two major sources of emboli which may cause ischemic attack were emboli formed in heart and from a ruptured arterial plaque in carotid arties. Due to the different characteristics of emboli formed from different mechanisms, the migration route of specific emboli in cerebral arteries may be different, so does the territory of the ischemic attack caused by them. Therefore, a good understanding of emboli migration in the complex cerebral arterial network may provide a good guidance for the diagnosis and treatment of stroke. Studies on the emboli motion in cerebral arteries so far were based on phantom models [1]. Although CFD simulation has been used on prediction of cerebral blood perfusion for many years, CFD particle tracking technique is rarely applied on study emboli migration in cerebral arteries. The present study aims to demonstrate the feasibility of using CFD particle tracking on emboli migration study with emphasis on the discussions of the particle tracking result by different coupling algorithms between blood flow and embolic particles.
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Andrade, Danúbia Ariana de, Filomena Marino Carvalho, Fernando Nalesso Aguiar, Alfredo Luiz Jacomo, and Alfredo Carlos Simões Dornellas de Barros. "SIZE OF METASTATIC INFILTRATION IN THE SENTINEL NODE AS A PREDICTOR OF NON‑SENTINEL NODES INVOLVEMENT." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1065.

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Introduction: The broad acceptance of sentinel lymph node biopsy (SLNB) led to an analysis for finding out the anatomopathological characteristics that can help predict the involvement of other axillary lymph nodes (LN) in positive sentinel lymph node (SLN) cases. Currently, it is very appropriate to investigate the cases that enable the omission of complete axillary dissection (CAD), even considering the involvement of the SLN. Some important studies on this theme were published, e.g., ACOSOG Z0011, and AMAROS. However, their results were not accepted uniformly enough because of methodological inconsistencies. Objectives: We aimed at providing a complementary basis for a pragmatic analysis of CAD after a positive SLNB in breast cancer. Methods: This is a cross-sectional study. Clinical and anatomopathological data were collected in patients with early-infiltrating breast cancer that were treated with SLNB, followed by CAD. Statistical analyses were performed using binary logistic regression and multiple logistic regression. Results: Out of 129 patients evaluated, compromise of non-sentinel additional lymph nodes was observed in 47 (36.4%) patients. According to an univariate analysis, the parameters related to non-SLN compromise were the tumor size in anatomopathological exam, histological grade III, the presence of peritumoral vascular embolism in focal area, compromise of more than one SLN, LN compromise rate of 100%, the presence of extracapsular neoplastic extension, perilymphnodal vascular involvement, perilymphatic fat compromise, and twenty or more dissected non-SNLs. The variables that increased the chance of compromise of non-SNL in the multivariate analysis were presented in following table with an accuracy of 81% (Figure). Conclusions: The tumor size on a clinical examination of the T2 category, the presence of two or more neoplastic foci in the SNL, and the size of the metastasis > 4.0 mm are the parameters that favor complete axillary lymphadenectomy.
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Reports on the topic "Fat embolism"

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He, Zuo wen, Zeqi Shi, Chenze Li, Li Ni, Yang Sun, Yan Wang, and Dao Wen Wang. Fat embolism syndrome: a case report, literature review and pooled analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2020. http://dx.doi.org/10.37766/inplasy2020.10.0039.

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