Relevant bibliographies by topics / Control Embolism

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

Academic literature on the topic 'Control Embolism'

Author: Grafiati
Published: 30 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Control Embolism"

1

JONES, H. G., and R. A. SUTHERLAND. "Stomatal control of xylem embolism." Plant, Cell and Environment 14, no. 6 (August 1991): 607–12. http://dx.doi.org/10.1111/j.1365-3040.1991.tb01532.x.

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2

Broder, Sarah, and Peter Paré. "Diagnosis and Management of Pulmonary Embolism in Pregnancy." Canadian Respiratory Journal 3, no. 3 (1996): 187–91. http://dx.doi.org/10.1155/1996/674564.

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Pulmonary embolism in pregnancy is a significant and under-recognized problem. In British Columbia, where there are 46,000 pregnancies per year, it is estimated that there are approximately 160 pulmonary embolisms per year and one maternal death every two years secondary to pulmonary embolism. A complete assessment for suspected pulmonary embolus can be performed without putting the fetus at significant risk from radiation exposure. An algorithm is provided for the workup of pulmonary embolus during pregnancy. Heparin is the drug of choice for anticoagulating pregnant women, initially managing the situation with intravenous heparin and then switching to the subcutaneous route given in a bid or tid regimen, aiming to keep the activated partial thromboplastin time 1.5 to 2 times the control. The risks to both the fetus and the mother from anticoagulation during pregnancy are reviewed.
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3

Kalemci, Serdar, Arife Zeybek, Serap Cilaker Mıcılı, Aydın Sarıhan, Meryem Çalışır, Abdullah Şimşek, Fatih Akın, Alperen İhtiyar, and Osman Yılmaz. "The Protective Effect of The Interleukin 1 Receptor Antagonist on Chronic Thromboembolic Pulmonary Hypertension Model." Postępy Higieny i Medycyny Doświadczalnej 73 (December 31, 2019): 944–50. http://dx.doi.org/10.5604/01.3001.0013.7878.

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Chronic thromboembolic pulmonary hypertension (CTEPH) is one of the main reasons of severe pulmonary hypertension and has significantly higher morbidity and mortality rates. The pathogenesis of the disease is characterized by the incomplete resolution of acute embolisms. The elevated inflammatory conditions after the acute embolism are one of the critical factors. Therefore, we aimed to investigate whether or not anakinra is an option for treating CTEPH in an animal model. We studied twenty-one rats in this study They were randomly divided into three groups containing seven animals: the control group: saline-treated control; the embolism group: CTEPH + normal saline; the anakinra group: CTEPH + anakinra. We have observed that the layers of the segmental arteries and the alveolar were normal in the control group. In the cardiac tissue it was observed that muscular tissues and connective tissue were normal in the right ventricle. In embolism group, we detected a widening of the alveolar septum, a surrounding the alveolar infiltrates and a thickening of the segmental arteries in the muscular layer and a hypertrophy in the right ventricle tissues. We have determined that the lung and cardiac tissue specimens in the anakinra group are similar to control group. We have showed that anakinra was useful option for the CTEPH model in rats. Anakinra may be considered as protective effect and the regression of the increased inflammation in CTEPH. The effectiveness of anakinra will continue to be subject to the further experimental and clinical studies.
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Kulesh, A. A., D. A. Demin, and O. I. Vinogradov. "Cryptogenic stroke. Part 1: Aorto-arterial embolism." Meditsinskiy sovet = Medical Council, no. 4 (April 20, 2021): 78–87. http://dx.doi.org/10.21518/2079-701x-2021-4-78-87.

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The article discusses the concept of embolic stroke from an unspecified source and the role of aorto-arterial embolism in its development. Potential causes of embolic cryptogenic stroke such as aortic atheromatosis, non-stenotic atherosclerosis of the cervical arteries, carotid web and intracranial atherosclerosis are discussed in detail. The discussion of each cause covers epidemiology, pathogenesis, and current approaches to diagnosis and secondary prevention. The diagnostic search is presented in the form of an algorithm. To identify aorto-arterial sources of embolism and to determine their clinical significance, a comprehensive examination including CT angiography with targeted assessment of the aortic arch, transesophageal echocardiography, MRI of the arterial wall and transcranial Doppler is required. When mechanical thrombectomy is performed, histological examination of the thromboembolus is advisable. Given that atherosclerosis is usually systemic, the search for a possible cause of aorto-arterial embolism should be a diagnostic priority in patients with cryptogenic stroke and other arterial (coronary, lower extremity) lesions. With regard to secondary prevention of cryptogenic stroke in the presence of potential sources of aorto-arterial embolism, the principle ‘the more embologenic the source, the more aggressive the prevention’ applies. The arsenal of secondary prevention includes strategies such as strict control of vascular risk factors, achieving target blood pressure, short- and medium-term dual antiplatelet therapy, and intensive hypolipidemic therapy. Surgical prophylaxis is warranted for stroke against a carotid background, the efficacy of which in non-stenotic atherosclerosis requires early evaluation in randomised trials. Each potential cause of cryptogenic stroke considered is illustrated by a clinical example.
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5

Kamalov, I. A., I. R. Agliullin, and M. G. Tukhbatullin. "Optimization of proper diagnosis of thromboses associated with high risk of embolism in patients with neoplasms." Kazan medical journal 94, no. 2 (April 15, 2013): 202–7. http://dx.doi.org/10.17816/kmj1589.

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Aim. To optimize a proper diagnosis of thromboses associated with high risk of embolism and pulmonary embolism prevention in patients with neoplasms. Methods. Ultrasonography of veins of lower extremities, iliac veins and the distal part of inferior vena cava was performed in patients with and without neoplasms in a prospective study to detect thromboses associated with high risk of embolism and thrombophlebitis. Ultrasonography was performed once in control group subjects, and before and during specialized antineoplastic treatment (surgical, chemotherapy, radiotherapy) in patients of the main group, the results were compared. A detection of a new thrombus in previously intact venous segment of inferior vena cava system was assessed as a high risk for pulmonary embolism. Results. Thromboses associated with high risk of embolism and thrombophlebitis were found in 6 patients of control group, in 5 patients of the main group before and in 27 patients of the main group while at specialized antineoplastic treatment. Specific measures for pulmonary embolism prevention were taken immediately in all of the cases according to ultrasonography results after the detection of thromboses associated with high risk of embolism. No fatal cases of pulmonary embolism were registered both in main (before and while at treatment) and control groups. Conclusion. Ultrasonography of veins of lower extremities, iliac veins and the distal part of inferior vena cava in patients with neoplasms before the start of specialized antineoplastic treatment allows to optimize the choice of prevention measures for pulmonary embolism and thus significantly decreases mortality from pulmonary embolism.
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6

Qiao, Zhihong, Ningyang Jia, and Qian He. "Does preoperative transarterial embolization decrease blood loss during spine tumor surgery?" Interventional Neuroradiology 21, no. 1 (February 2015): 129–35. http://dx.doi.org/10.15274/inr-2014-10091.

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This paper aimed to evaluate the effect of preoperative transarterial embolization (TAE) on estimated blood loss (EBL) during surgical excision of the vertebral tumors. Three hundred and forty-eight patients with spinal tumors were retrospectively analyzed. The preoperative TAE group consisted of 190 patients and the control group consisted of 158 patients. Gelatin sponge particles mixed withy contrast agent were used in the TAE group to embolize the tumor-feeding artery. The factors evaluated included: the time interval between embolism and surgery; the number of vertebrae involved by the tumor; pathological type of tumor; surgical approach; extent of excision and instrumental fixation. The time interval (P = 0.4669)between embolism and surgery had no significant correlation with EBL during surgery. The pathological diagnosis of vertebral tumor such as plasma cell myeloma, giant cell tumor, chondrosarcoma, hemangioma and metastasis had no significant correlation with EBL between the TAE group and control group during surgery, while the EBL of chordoma in the TAE group was significantly higher than that in the control group (p = 0.0254). The number of vertebrae involved (p = 0.4669, 0.6804, 0.6677), posterior approach (p = 0.3015), anterior approach (p = 0.2446), partial excision (p = 0.1911) and instrumental fixation (p = 0.1789) had no significant correlation with EBL during surgery between the TAE group and the control group. This study showed that preoperative TAE of the spinal tumor had no significant effect on intra-operative blood loss during surgical excision of the spinal tumor. In view of the risk of embolism, this method should be carefully considered.
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7

García Suquia, Angela, Alberto Alonso-Fernández, Mónica de la Peña, David Romero, Javier Piérola, Miguel Carrera, Antonia Barceló, et al. "High D-dimer levels after stopping anticoagulants in pulmonary embolism with sleep apnoea." European Respiratory Journal 46, no. 6 (July 23, 2015): 1691–700. http://dx.doi.org/10.1183/13993003.02041-2014.

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Obstructive sleep apnoea is a risk factor for pulmonary embolism. Elevated D-dimer levels and other biomarkers are associated with recurrent pulmonary embolism. The objectives were to compare the frequency of elevated D-dimer levels (>500 ng·mL−1) and further coagulation biomarkers after oral anticoagulation withdrawal in pulmonary embolism patients, with and without obstructive sleep apnoea, including two control groups without pulmonary embolism.We performed home respiratory polygraphy. We also measured basic biochemical profile and haemogram, and coagulation biomarkers (D-dimer, prothrombin fragment 1+2, thrombin-antithrombin complex, plasminogen activator inhibitor 1, and soluble P-selectin).64 (74.4%) of the pulmonary embolism cases and 41 (46.11%) of the controls without pulmonary embolism had obstructive sleep apnoea. Plasmatic D-dimer was higher in PE patients with OSA than in those without obstructive sleep apnoea. D-dimer levels were significantly correlated with apnoea–hypopnoea index, and nocturnal hypoxia. There were more patients with high D-dimer after stopping anticoagulants in those with pulmonary embolism and obstructive sleep apnoea compared with PE without obstructive sleep apnoea (35.4% versus 19.0%, p=0.003). Apnoea–hypopnoea index was independently associated with high D-dimer.Pulmonary embolism patients with obstructive sleep apnoea had higher rates of elevated D-dimer levels after anticoagulation discontinuation for pulmonary embolism than in patients without obstructive sleep apnoea and, therefore, higher procoagulant state that might increase the risk of pulmonary embolism recurrence.
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Koć, Marcin, Maciej Kostrubiec, Waldemar Elikowski, Nicolas Meneveau, Mareike Lankeit, Stefano Grifoni, Agnieszka Kuch-Wocial, et al. "Outcome of patients with right heart thrombi: the Right Heart Thrombi European Registry." European Respiratory Journal 47, no. 3 (January 21, 2016): 869–75. http://dx.doi.org/10.1183/13993003.00819-2015.

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Our aim was the assessment of the prognostic significance of right heart thrombi (RiHT) and their characteristics in pulmonary embolism in relation to established prognostic factors.138 patients (69 females) aged (mean±sd) 62±19 years with RiHT were included into a multicenter registry. A control group of 276 patients without RiHT was created by propensity scoring from a cohort of 963 contemporary patients. The primary end-point was 30-day pulmonary embolism-related mortality; the secondary end-point included 30-day all-cause mortality. In RiHT patients, pulmonary embolism mortality was higher in 31 patients with systolic blood pressure <90 mmHg than in 107 normotensives (42% versus 12%, p=0.0002) and was higher in the 83 normotensives with right ventricular dysfunction (RVD) than in the 24 normotensives without RVD (16% versus 0%, p=0.038). In multivariable analysis the simplified Pulmonary Embolism Severity Index predicted mortality (hazard ratio 2.43, 95% CI 1.58–3.73; p<0.0001), while RiHT characteristics did not. Patients with RiHT had higher pulmonary embolism mortality than controls (19% versus 8%, p=0.003), especially normotensive patients with RVD (16% versus 7%, p=0.02).30-day mortality in patients with RiHT is related to haemodynamic consequences of pulmonary embolism and not to RiHT characteristics. However, patients with RiHT and pulmonary embolism resulting in RVD seem to have worse prognosis than propensity score-matched controls.
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Branger, Annette B., and David M. Eckmann. "Accelerated Arteriolar Gas Embolism Reabsorption by an Exogenous Surfactant." Anesthesiology 96, no. 4 (April 1, 2002): 971–79. http://dx.doi.org/10.1097/00000542-200204000-00027.

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Background Cerebrovascular gas embolism can cause profound neurologic dysfunction, and there are few treatments. The authors tested the hypothesis that an exogenous surfactant can be delivered into the bloodstream to alter the air-blood interfacial mechanics of an intravascular gas embolism and produce bubble conformations, which favor more rapid bubble absorption. Methods Microbubbles of air were injected into the rat cremaster microcirculation after intravascular administration of either saline (control, n = 5) or Dow Corning Antifoam 1510US (surfactant, n = 5). Embolism dimensions and dynamics were directly observed after entrapment using intravital microscopy. Results To achieve embolization, the surfactant group required twice as many injections as did controls (3.2 +/- 1.3 vs. 1.6 +/- 0.9; P &lt; 0.05). There was no difference in the initial lodging configuration between groups. After bubble entrapment, there was significantly more local vasoconstriction in the surfactant group (24.2% average decrease in diameter) than in controls (3.4%; P &lt; 0.05). This was accompanied by a 92.7% bubble elongation in the surfactant group versus 8.2% in controls (P &lt; 0.05). Embolism shape change was coupled with surfactant-enhanced breakup into multiple smaller bubbles, which reabsorbed nearly 30% more rapidly than did parent bubbles in the control group (P &lt; 0.05). Conclusions Intravascular exogenous surfactant did not affect initial bubble conformation but dramatically increased bubble breakup and rate of reabsorption. This was evidenced by both the large shape change after entrapment and enhancement of bubble breakup in the surfactant group. These dynamic surfactant-induced changes increase the total embolism surface area and markedly accelerate bubble reabsorption.
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Martinelli, Ida, Marco Cattaneo, Daniela Panzeri, and Pier Mannuccio Mannucci. "Low Prevalence of Factor V:Q506 in 41 Patients with Isolated Pulmonary Embolism." Thrombosis and Haemostasis 77, no. 03 (1997): 440–43. http://dx.doi.org/10.1055/s-0038-1655985.

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SummaryIn 70-80% of cases, pulmonary embolism is the consequence of lower extremity deep vein thrombosis. It has been demonstrated that the most common coagulation defect predisposing to venous thrombosis, resistance to activated protein C (APC), is not associated with an increased risk for pulmonary embolism, but the evidence was based on a functional assay to diagnose APC resistance and no information about concomitant deep vein thrombosis was provided. The aim of our study was to evaluate the prevalence of factor V:Q506, the gene mutation responsible for APC resistance, in patients with symptomatic non-fatal pulmonary embolism, whether or not associated with deep vein thrombosis. Patients with uncomplicated deep vein thrombosis and healthy controls were investigated as comparison groups. The overall prevalence of factor V:Q506 in 106 patients with pulmonary embolism was 12.3%, lower than that found in 106 patients with deep vein thrombosis (22.6%, OR 0.5, 95% Cl 0.2-1.0) but significantly higher than that found in 212 healthy subjects taken as controls (2.8%, OR 4.8,95% Cl 1.8-13.0). In the 41 patients with isolated pulmonary embolism, i.e., without the presence of deep vein thrombosis, the prevalence was 4.9%, similar to that in controls (OR 1.8,95% Cl 0.3-9.6), while in the remaining 65 patients with pulmonary embolism associated with deep vein thrombosis the prevalence was significantly higher (16.9%, OR 5.5, 95% Cl 2.0-15.8). In conclusion, the prevalence of factor V:Q506 is high in patients with pulmonary embolism associated with deep vein thrombosis, whereas in patients with isolated pulmonary embolism it is similar to that found in control subjects. This intriguing finding is of difficult interpretation and needs confirmation by further studies.
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Dissertations / Theses on the topic "Control Embolism"

1

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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2

"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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3

Moodley, Pramodhini. "Descriptive study of Venous Thromboembolic Disease in the adult population admitted to Tshepong Hospital comparing the proportion of HIV and non-HIV infected patients." Thesis, 2019. https://hdl.handle.net/10539/28163.

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A research report submitted to the University of Witwatersrand, Johannesburg in fulfilment for the requirements of the degree of Master of Medicine 4 June 2019 Descriptive study of Venous Thromboembolic Disease in the adult population admitted to Tshepong Hospital comparing the proportion of HIV and non-HIV infected patients
Background HIV and TB independently incur increased risk for venous thromboembolic disease (VTE): deep vein thrombosis (DVT) and/or pulmonary embolism (PE). Data from high HIV and TB burden settings describing VTE is scarce. The Wells’ DVT and PE scores are widely used but their utility in these settings has not been reported on extensively. We therefore report clinical and treatment aspects of in-patients with newly diagnosed VTE to assess HIV and TB prevalence, and their Wells’ score. Setting Tshepong Hospital in the North West Province of South Africa. Methods A prospective cohort of adult in-patients with radiologically confirmed VTE were recruited. Demographics, presence of TB, HIV status, duration of treatment, CD4 count, viral load, VTE risk factors, and parameters to calculate the Wells’ score were collected. Results One hundred patients were recruited, of whom 59 were HIV-infected; 39 had TB disease and 32 were HIV/TB co-infected. Eighty -three patients had a DVT only; 11 patients had a PE, and six had both a DVT and PE. Eighteen of 42 patients on antiretroviral treatment (ART) were on treatment for less than six months. Twenty patients of 39 were on TB treatment for less than one month. The median DVT and PE Wells’ score in all sub-groups was 3.0 (IQR: 1.0-4.0) and 3.0 (IQR: 2.5-4.5), respectively. There were nine deaths. Conclusion HIV /TB co-infection appear to confer a risk for VTE, especially early after ART and/or TB treatment, and therefore require careful monitoring for VTE and early initiation of thrombo-prophylaxis.
E.K. 2019
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4

Liu, Da-Wei, and 劉大衛. "The motion control of Fe3O4 nanomaterial and Its application on vessel embolism cleaning in vitro." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/18302770386725217762.

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碩士
中原大學
機械工程研究所
102
High cholesterol will cause cardiovascular disease, which is the second leading cause of death in Taiwan. High level of low-density lipoprotein (LDL) in blood will deposit in the inner vascular wall. If the LDL deposit continually the blood vessel will become narrow and the vascular wall can be damaged because of the formation of thrombus. This study will develop a magnetic manipulation system (MMS) to control the Fe3O4 nanomaterial for removal of thrombus. 　 The MMS is composed of permanent magnets and an electromagnetic coil. The static magnetic field generated by the permanent magnets will magnetize the nanoparticles to form microwires, which move in a liquid suspension through the gradient field. The electromagnetic coil connects to an alternating current source thereby producing an oscillating field to rotate the microwires. A high speed camera attached to a microscope tracks the motion of the microwires. Video recordings are captured and loaded to a computer. The control parameters of the motion and size of the Fe3O4 in the MMS are identified. By suspending the nanoparticles in water, the experiment show that aspect ratio of the length and width of the microwire is proportional to the square of the magnitude of the static magnetic field. Meanwhile, the translation speed of the microwires is found to be linearly dependent on the product of the static field strength and gradient magnetic field. Moreover, the rotation speed of the microwires is proportional to the square of the oscillating field strength. The results are in good agreement with the theoretical model of the MMS. The model system for thrombus removal application uses a 0.8mm diameter microchannel fabricated by photolithography to simulate a blood vessel. Blood droplets are allowed to dry in the microchannel to clog fluid flow and simulate a thrombus. By injecting the nanoparticles on one side of the microchannel and controlling the motion towards the thrombus, microwires rotating on their long axis are able to remove 0.055mm2 thrombus in 5 seconds with an alternating field strength of 624 A/m and gradient field strength of 3.2T/m. Similarly, microwires rotating on their short axis are able to remove 0.047 mm2 thrombus demonstrating the potential of Fe3O4 nanomaterial for thrombus removal using the proposed MMS.
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5

"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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Books on the topic "Control Embolism"

1

National Library of Medicine (U.S.), ed. Prevention of venous thrombosis and pulmonary embolism: January 1984 through January 1986, 250 citations in English. [Bethesda, Md: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health], 1986.

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2

Medicine, Consortium for Spinal Cord. Prevention of thromboembolism in spinal cord injury. 2nd ed. Washington, DC: Paralyzed Veterans of America, 1999.

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3

T, Stober, ed. Central nervous system control of the heart: Proceedings of the IIIrd International Brain Heart Conference, Trier, Federal Republic of Germany. Boston: Nijhoff, 1986.

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Sharnoff, J. G. Prevention of Venous Thrombosis and Pulmonary Embolism. Springer, 2011.

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(Editor), T. Stober, K. Schimrigk (Editor), D. Ganten (Editor), and D. G. Sherman (Editor), eds. Central Nervous System Control of the Heart (Topics in the Neurosciences). Springer, 1986.

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6

Waldo, Albert L. Rate versus rhythm control therapy for atrial fibrillation. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0511.

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Based on data from several clinical trials, either rate control or rhythm control is an acceptable primary therapeutic strategy for patients with atrial fibrillation. However, since atrial fibrillation tends to recur no matter the therapy, rate control should almost always be a part of the treatment. If a rhythm control strategy is selected, it is important to recognize that recurrence of atrial fibrillation is common, but not clinical failure per se. Rather, the frequency and duration of episodes, as well as severity of symptoms during atrial fibrillation episodes should guide treatment decisions. Thus, occasional recurrence of atrial fibrillation despite therapy may well be clinically acceptable. However, for some patients, rhythm control may be the only strategy that is acceptable. In short, for most patients, either a rate or rhythm control strategy should be considered. However, for all patients, there are two main goals of therapy. One is to avoid stroke and/or systemic embolism, and the other is to avoid a tachycardia-induced cardiomyopathy. Also, because of the frequency of atrial fibrillation recurrence despite the treatment strategy selected, patients with stroke risks should receive anticoagulation therapy despite seemingly having achieved stable sinus rhythm. For patients in whom a rate control strategy is selected, a lenient approach to the acceptable ventricular response rate is a resting heart rate of 110 bpm, and probably 90 bpm. The importance of achieving and maintaining sinus rhythm in patients with atrial fibrillation and heart failure remains to be clearly established.
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7

F, Pérez-Gómez, Prentice C. R. M, and Meyer Jürgen MD, eds. Coronary thrombosis: Intracardiac thrombosis. New York, NY: Raven Health Care Communications, 1994.

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Perez-Gomez, F., C. R. M. Prentice, and Jurgen Meyer. Coronary Thrombosis: Intracardiac Thrombosis. Raven Health Care Communications, 2001.

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Khouri, George, Shelly Ozark, and Bruce Ovbiagele. Common Risk factors for Stroke and Medical Prevention Therapies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0103.

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Stroke from thrombosis or emboli in cerebral vessels or hemorrhage is one of the most commonly encountered and most devastating neurological diseases. Rapid loss of function occurs due to an interruption of blood supply to the brain, leading to tissue ischemia and cell death. The risk of both ischemic and hemorrhagic stroke doubles for each successive decade after age 55, which is likely independent of other risk factors such as diabetes, hypertension, and hyperlipidemia. Lifestyle modifications, antiplatelet therapy and control of hyperlipidemia and hypertension are the mainstays of prevention.
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Jain, Shilpa, and Mark T. Gladwin. Sickle crisis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0275.

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Sickle cell disease crises are precipitated by an acute occlusion of microvessels, which can lead to end organ ischaemia reperfusion injury and acute haemolysis. Acute fat emboli syndrome, acute lung injury (the acute chest syndrome), acute pulmonary hypertension, and cor pulmonale, haemorrhagic and occlusive stroke, and systemic infection represent the most common life-threatening complications observed in current ICU practice. General principles of management in all patients admitted to the critical care unit are hydration, antibiotics, pain control, and maintenance of oxygenation and ventilation. Red blood cell transfusion therapy is the treatment of choice for most complications of sickle cell disease requiring intensive care management. Transfusion of sickle negative, leukoreduced red blood cells, phenotypically matched for Rhesus and Kell antigens is the minimum standard of care in sickle cell disease patients as they have a high incidence of red blood cell alloimmunization.
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Book chapters on the topic "Control Embolism"

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Jerjes-Sánchez, Carlos, and Alicia Ramirez-Rivera. "Thrombolytic Therapy: Evidence-Based Results from Multicenter Control Trials." In Thrombolysis in Pulmonary Embolism, 41–105. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19707-4_3.

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Kuramoto, K., S. Matsushita, and H. Yamanouchi. "Cerebral Embolism in Atrial Fibrillation and Nonbacterial Thrombotic Endocarditis." In Central Nervous System Control of the Heart, 255–59. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2327-3_25.

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Hart, R. G. "Timing of Hemorrhagic Transformation of Cardioembolic Stroke Cerebral Embolism Study Group." In Central Nervous System Control of the Heart, 229–32. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2327-3_20.

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Yamaguchi, T., K. Minematsu, J. Choki, T. Miyashita, and T. Omae. "Recurrent Cerebral Embolism and Factors Related to Early Recurrence - Analysis of 186 Consecutive Cases." In Central Nervous System Control of the Heart, 237–43. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2327-3_22.

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Sherman, D. G., and R. G. Hart. "Brain Hemorrhage in Embolic Stroke." In Central Nervous System Control of the Heart, 249–53. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2327-3_24.

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Lodder, J. "A Prospective Study on the Risk of Immediate Anticoagulation in Cardiac Embolic Stroke." In Central Nervous System Control of the Heart, 245–48. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2327-3_23.

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Minematsu, K., T. Yamaguchi, J. Choki, and M. Tashiro. "Sequential Changes of Regional Cerebral Blood Flow in Embolic and Thrombotic Cerebral Artery Occlusion." In Central Nervous System Control of the Heart, 221–27. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2327-3_19.

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Cenzato, Marco, Davide Boeris, Maurizio Piparo, Alessia Fratianni, Maria Angela Piano, Flavia Dones, Francesco M. Crisà, and Giuseppe D’Aliberti. "Complications in AVM Surgery." In Acta Neurochirurgica Supplement, 77–81. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63453-7_11.

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AbstractIn AVM surgery perioperative complications can arise and can have serious perioperative consequences. Surgically related complications in AVM treatment, in many cases, can be avoided by paying attention to details:1. Careful selection of the patient: - addressing a patient with eloquent AVM to Gamma Knife treatment - preoperative treatment with selective embolization of the accessible deep feeders - preoperative gamma knife or embolize those patient with an over-expressed venous pattern2. Meticulous coagulation of deep medullary feeders: - Using dirty coagulation - Using dry non-stick coagulation - Using micro clips - Using laser - Reaching the choroidal vessel in the ventricle when possible - Avoiding occlusive coagulation with hemostatic agents3. Check and avoiding any residual of the AVM4. Keep the patient under pressure control during postoperative periodFulfilling these steps contributes to reduce complications in this difficult surgery, leading to a safer treatment that compares favorably with natural history of brain arteriovenous malformations.
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Haynes, Gary R., and Brian P. McClure. "Pulmonary Pathophysiology in Anesthesia Practice." In Thoracic Anesthesia Procedures, 251–72. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197506127.003.0019.

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This chapter compares normal and abnormal pulmonary function and discusses clinical considerations when evaluating patients for surgery and anesthesia. Basic pulmonary physiology and the effect that positive pressure ventilation has on lung function are reviewed. The action of anesthetic drugs on the control of ventilation, and the pathophysiologic effect of the common pathophysiologic conditions of pulmonary hypertension and pulmonary embolism are discussed.
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Becker, Richard C., and Frederick A. Spencer. "Cardiac Chamber, Aortic, and Valvular Thromboembolism." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0009.

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The left-sided cardiac chambers (left atrium, left ventricle) and heart valves (mitral valve, aortic valve) (native, prosthetic) serve as potential niduses for systemic thromboembolism, including fatal or debilitating stroke. The ascending aortic is also recognized as a source for embolism (aortoembolism) and should be considered when a comprehensive patient evaluation is being undertaken. The pathogenesis of intracavitary mural thrombosis, much like venous thromboembolism, follows the construct of Virchow’s triad. The area of stasis is often provoked by chamber dilation, reduced performance, or impaired flow across an existing heart valve (e.g., left atrial dilation from mitral stenosis). Endothelial injury may follow either an acute (e.g., myocardial infarction) or chronic (e.g., dilated cardiomyopathy) cardiac process. In the case of aortoembolism, plaque rupture in areas of advanced atherosclerosis serves as the primary site for thrombus development. The third component, prothrombotic state, may be focal (areas of inflammation and necrosis) and/or systemic. Left ventricular mural thrombosis is diagnosed either echocardiographically or at the time of autopsy among patients with myocardial infarction (MI), especially in those with anterior infarction involving the ventricular apex. In large, nonrandomized clinical trials of anticoagulant therapy, researchers have reported an incidence of cerebral embolism of 2% to 4% among nontreated patients, frequently causing either severe neurologic deficits or death. Of these trials, two showed a statistically significant reduction in stroke with early anticoagulation, whereas the third trial demonstrated a positive trend (Davis and Irelant, 1986). A meta-analysis performed by Vaitkus and Barnathan (1993) supports the findings of three previous studies published in the early 1980s. The odds ratio for systemic embolism in the presence of echocardiographically demonstrated mural thrombus was 5.45 (95% confidence interval [CI] 3.02–9.83). The odds ratio of anticoagulation versus no anticoagulation in preventing embolism was 0.14 (95% CI 0.04–0.52) with an event rate difference of –0.33 (95% CI –0.50 to –0.16). The odds ratio of anticoagulation versus control in preventing mural thrombus formation was 0.32 (95% CI 0.20–0.52) and the event difference was –0.19 (95% CI 0.09–0.28).
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Conference papers on the topic "Control Embolism"

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Un, Haluk. "A New Device Preventing Air Embolism During the Angiography, Air Trap Device: An In-Vitro Experimental Air Emboli Study." In 2019 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/dmd2019-3247.

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Air embolism occurs when an air bubble enters the arterial system through the catheters. This can happen due to different reasons such as lack of attention, connection failure, or inexperience. This situation results in tissue damage in vital organs such as the heart and brain which may lead to death. To our knowledge, there is no technology preventing an air embolus from happening. Doctors try to prevent this complication with their attention and catheter control. In this project, a new air-trap device that prevents air embolus was tested in-vitro in air embolism model. Experimental results with a prototype showed that the new design was successful. Air embolism was blocked at various pressure-speed ranges. Air Trap device can be used to prevent air embolism by cardiologists, interventional radiologists and cardiovascular surgeons that perform a percutaneous intervention.
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Huisman, M. V., H. R. Buller, J. W. ten Cate, E. A. van Royen, and J. Vreeken. "SILENT PULMONARY EMBOLISM IN PATIENTS WITH DEEP VEIN THROMBOSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642890.

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In patients presenting with clinically suspected deep vein thrombosis symptomatic pulmonary embolism is rarely apparent. To assess the prevalence of asymptomatic pulmonary embolism in outpatients with proven deep vein thrombosis, perfusion ventilation lungscans were performed in 101 consecutive patients at the first day of treatment and after one week of therapy. Fifty-one percent of these patients had a high probability lung-scan at the start of treatment. In control patients (n=44) without deep venous thrombosis but referred through the same filter, the prevalence of high-proba-bility scans was only 5%. After one week of anticoagulant treatment complete to partial improvement was observed in 55% of the patients while in another 24% of the patients the scan remained normal.It is concluded that lungscan detected asymptomatic pulmonary embolism occurs frequently in patients presenting with symptomatic deep venous thrombosis and that the majority of these emboli resolve within one week of anticoagulant treatment.
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Routley, Ben, Ferdinand Miteff, and Andrew J. Fleming. "Modelling and control of nitrogen partial pressure for prophylaxis and treatment of air embolism." In 2017 American Control Conference (ACC). IEEE, 2017. http://dx.doi.org/10.23919/acc.2017.7963049.

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Pretice, C. R. M., and H. A. Townsend. "ANCROD PROPHYLAXIS AFTER SURGERY FOR FRACTURED NECK OF FEMUR: A STUDYOF FATAL PULMONARY EMBOLISM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643685.

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A pilot multi-centre randomized controlledtrial was carried out to compare ancrod (Arvin, Knoll) versus no medical treatment in 453 patients having surgery for fractured neck of femur to assess prevention of fatal post-operative pulmonary embolism (PE).Ancrod was given subcutaneously by 5 daily injections starting immediately post-operatively; initially 4u/kg bw were given followed by 4 injections of 1u/kg bw, to reduce fibrinogen levels to 80mg/dl. The primary objective of the study was to record mortality due to PE, as shown by the DeathCertificate, within 3 months after surgery.Death Certificates were analysed by 2 medical assessors, unaware of the patient treatment group. Of 239 control patients, not given ancrod, there were 5 deaths due to PE and 2 deaths where PE may have been contributory. Total deaths were 30 (12.5%). In 214 ancrod treated patients there were 2 deaths due to PE and a further 3 where it may have been contributory. Total deaths were 31 (14.5%), not significantly different from the control group. Deaths from PE occurred between16 and 66 days after surgery. Although in this study there was abeneficial tendency for ancrod to reduce fatal PE it is likely that at least 6,000 patients would be needed to demonstrate that any drug significantly reduces by 50% the incidence of fatal PE compared to the control group. Wound infection was recorded in 16 patients in both groups. Wound haematomas were seen in 26 ancrod patients compared to 6 controls (p<0.02) but were not sufficiently serious to warrant re-exploration or prolonged hospital stay. The low mortality due to PE in our patients with fractured neck of femur (2%) is contrasted with the figures of Sevitt & Gallagher, 1959(8%). The low incidence of fatal PE in thehigh risk group studied here should be taken into account when assessing future antithrombotic prophylaxis after surgery. Advances in anaesthetics, surgery and rehabilitation may have contributed to the decline in fatal post-operative PE. Effective assessment of drugs for prophylaxis against post-operative venous thrombosis is best carried out by large scale simple controlled trials using fatal PE a the primary end point. Collaborative Centres were located in Portsmouth, Cape Town, Glasgow, Belfast and Leeds.
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Arzt, Michael, Ruth Luigart, Carola Schum, Lars Luthje, Iris Koper, Cornelia Hecker, Rio Dumitrascu, and Richard Schulz. "Sleep-Disordered Breathing In Deep Vein Thrombosis And Acute Pulmonary Embolism - A Prospective Nested Case-Control Study." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5014.

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Kahloul, Mohamed, Chawki Jebali, Marwa Chaabani, Syrine Chouchane, Sana Aissa, Mohamed Aymen Jaouadi, Habiba Ben Hamada, Mohamed Said Nakhli, and Walid Naija. "High « red cell distribution width » levels can predict pulmonary embolism risk in multiple trauma patients: a case control study." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa3119.

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DELAHOUSSE, B., Y. GRUEL, P. MOALIC, L. QUILLIET, F. TOULEMONDE, and J. LEROY. "MODIFICATIONS OF BIOLOGICAL PARAMETERS DURING TREATMENT OF PULMONARY EMBOLISM BY A VERY LOW MOLECULAR HEPARIN FRAGMENT (CY 222)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643230.

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45 patients with pulmonary embolism (PE) were treated by a very low molecular weight heparin fragment (CY 222, Institut CHOAY - France) in an open range dose study. Patients were included into three groups (I, II and III) and received respectively 500, 750 or 1000 IC (Institut Choay) antiXa units/ kg/day by continuous intravenous infusion for ten days. The laboratory screen carried out at Day 0 and at 2 - 8 - 12 - 24 - 36, 48 hours and then every day until Day 10, included : Platelet count, Thromboelastography (TEG) on platelet rich plasma (PRP), Amidolytic assays for anti Xa (CBS 3139 STAGO) and anti Ila (S2238 KABI) activities (Calibration with Hepanorm STAGO), Heptest (Diamed, France), Amidolytic assay for tissue plasminogen activator (t-PA) and its inhibitor (PAI, Verheijen's method). Results showed no modification of platelet count and t-PA or PAI levels; An hypocoagulabi 1 ity was demonstrated with TEG on PRP (r+k > 35 mm) in 20 cases (3 patients from group III with haemorrhagic manifestations and 17 cases from groups II and III without complication). Anti-IIa activities were always lower than 0.15 U/ml. Anti-Xa activities and Heptest (Control adult values = 12.75 sec + 1.15) were (Mean + SD):Any significant biological difference between patients who have good or poor clinical results was observed, excepted for 1 patient who had a high level of PAI at Day 0 and recurrence of PE.
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Felez, J., R. Rodriguez-Pinto, A. Oliver, F. Velasco, I. de Diego, L. J. Steegmann, and S. Martin. "MULTICENTRIC SPANISH STUDY OF BIOLOGICAL CAUSES OF DEEP VEIN THROMBOSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643044.

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305 unselected patients under long-term oral anticoagulation treatment for having presented one o more ep^L sodes of deep vein thrombosis and/or pulmonary embolism, have been studied for the following anomalies: Dysfibrinogenemia, Lupus anticoagulant, Antithrombin-III deficiency, Protein C, Protein S, Heparin Cofactor II, and anomalies in the fibrinolytic components t-PA PAI and Plasminogen. Protein C antigen and activity as well as free Protein S antigen levels have been related to those found in a control group at different intensities of oral anticoagulantAs shown in the table this study, performed on unselected patients from the clinical point of view, has not only confirmed the presence of a previously known congenital defect in 16 patients (5%) but also has per miteed the identification of a previously unkown de- -feet in 45 patients (15%)Since the identification of a congenital abnormality permits to prevention of new thrombotic episodes and the identification of the afected members, these re- -suits support the convenience of performing such syste matic biological studies in patients suffering from thrombosis
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Breyer, H. G., R. Rahmanzadeh, P. Bacher, and B. Werner. "LMW-HEPARIN VERSUS HEPARIN-DHE IN ORTHOPAEDIC SURGERY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643689.

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The efficiancy and the side effects of a LMW heparin (FRAGMINR, KabiVitrum) and Heparin-DHE (Sandoz) have been compared in a randomized open prospective study of 120 patients (60/60) undergoing elective surgery on the lower limbs (total hip and knee replacement, corrective osteotomies). A radiofibrinogen uptake test (RFUT) was regularly done on all patients. Positive tests were controlled by ascending phlebography. The parameters, clinically obtained, included the intra-and postoperative blood loss, wound closure, and the incidence of haematoma. Hb, Hk, red and white blood cells, thrombocytes, total protein, aPTT, AT III, TT, and anti-Xy-activity were analyzed at the day before operation, the 2nd, 4th, and 6th day after operation.There were three positive RFUT in the group of LMW heparin (5 per cent), and there were six (10 per cent) in the control group. No pulmonary embolism occurred. In no case an operative treatment of deep vein thrombosis was done. There were no statistically significant differences in intra- and postoperative blood loss, and in the laboratory data, except the anti-Xa-activity, which was significantly higher in the LMW heparin group.The comparative study has shown, that a single daily injection of LMW heparin (FRAGMINR) is more effective than the two daily injections of the combination of UF heparin and DHE in order to prevent postoperative thromboembolism
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oude Egbrink, Mirjam G. A., Geert Jan Tangelder, Dick W. Slaaf, and Robert S. Reneman. "IN VIVO CHANGES IN SYSTEMIC PCO2 AND PO2 INFLUENCE THE THROMBOEMBOLIC REACTION FOLLOWING WALL PUNCTURE IN VENULES BUT NOT IN ARTERIOLES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643180.

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Changes in pH and PCO2 influence the aggregation of blood platelets in response to various agents in vitro. In the present study intravital video-microscopy was used to investigate whether changes in systemic blood gas values influence the thromboembolic reaction in vivo as induced by vessel wall injury.The microtrauma was induced by puncturing the walls of microvessels in the rabbit mesentery (diameter range: 20-40 μm) with glass micropipets (tip diameters: 6-8 μm). The thromboembolic reactions were compared in two groups of anesthetized rabbits. The control group was ventilated to keep the blood gas values within normal ranges (means: pH=7.40, pCO2=32.9 mmHg, pO2=104.7 mmHg). The experimental group breathed spontaneously (mean blood gas values: pH=7.34, pCO2=50.5 mmHg, pO2=48.1 mmHg). The pCO2 and pO2 values were significantly different between both groups.In arterioles and venules of both groups bleeding and thrombus formation started immediately following wall puncture. Bleeding times were short (medians between 1.0 and 2.6 s). Parts of the thrombi started to embolize between 11.4 and 18.2 s following wall puncture (medians). In the control group embolization continued for 101 s in the arterioles and 17 s in the venules; during these periods 6 and 1 emboli were produced, respectively (all median values). In the experimental group the duration of embolization in the arterioles was 143 s in which period 7.5 emboli were produced, values not significantly different from control. In the venules of the experimental group embolization and hence platelet reaction went on uninhibited during the whole observation period of 600 s and 30 emboli were produced. Fluid dynamic factors cannot explain the differences in thromboembolic reaction between the control and experimental venules; vessel diameters and red blood cell velocities were not significantly different between both groups. Therefore, it is likely that the change in thromboembolic reaction in the venules results from the changes in systemic PCO2 and/or pO2. The different reactions in arterioles and venules in response to the altered systemic blood gas values might arise from different reactions in the vessel walls.
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