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Relevant bibliographies by topics / Inflammatory response syndrome

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Academic literature on the topic 'Inflammatory response syndrome'

Author: Grafiati

Published: 15 February 2025

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Journal articles on the topic "Inflammatory response syndrome"

1

Williams, John G., and Ronald V. Maier. "The Inflammatory Response." Journal of Intensive Care Medicine 7, no. 2 (March 1992): 53–66. http://dx.doi.org/10.1177/088506669200700203.

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Inflammation is a critical component of the normal healing process. In the patient with extensive injury or infection, however, this same process may lead to organ dysfunction and failure as seen in adult respiratory distress syndrome and multiple organ failure syndrome. In this article we review: (1) the evolution of current concepts of inflammation; (2) individual elements of the host response to inflammatory stimuli; and (3) current strategies for the prevention and treatment of adult respiratory distress syndrome and multiple organ failure syndrome. From the Department of Surgery, University of Washington School of Medicine, Harborview Medical Center, Seattle, WA.

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Botwinski, Carol. "Systemic Inflammatory Response Syndrome." Neonatal Network 20, no. 5 (August 2001): 21–28. http://dx.doi.org/10.1891/0730-0832.20.5.21.

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Despite advances in perinatal care in the past decade, sepsis and its complications continue to present problems for the neonate, remaining a major cause of neonatal morbidity and mortality. Sepsis research is focusing on how the neonate (host) responds to bacteria. The newborn may develop a systemic reaction to bacteria that induces the release of substances known as inflammatory mediators. Termed the systemic inflammatory response syndrome (SIRS), this reaction is believed to be responsible for the signs and symptoms of sepsis. This article introduces the neonatal nurse to SIRS, providing an overview of various inflammatory mediators and cytokines, their clinical consequences, and potential new therapies in the management of SIRS.

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Ahmed, Najma, and Nicolas Christou. "SYSTEMIC INFLAMMATORY RESPONSE SYNDROME." Shock 5 (June 1996): S39–42. http://dx.doi.org/10.1097/00024382-199606001-00008.

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Ahmed, Najma, and Nicolas Christou. "SYSTEMIC INFLAMMATORY RESPONSE SYNDROME." Shock 6, Supplement (October 1996): S39—S42. http://dx.doi.org/10.1097/00024382-199610001-00008.

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Adams-Chapman, Ira, and Barbara J. Stoll. "Systemic inflammatory response syndrome." Seminars in Pediatric Infectious Diseases 12, no. 1 (January 2001): 5–16. http://dx.doi.org/10.1053/spid.2001.19230.

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Davies, M. G., and P. O. Hagen. "Systemic inflammatory response syndrome." British Journal of Surgery 84, no. 7 (July 1997): 920–35. http://dx.doi.org/10.1002/bjs.1800840707.

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Angood, Peter B. "Pancreatitis inflammatory response syndrome (PIRS)? Can there be another inflammatory response syndrome?" Critical Care Medicine 27, no. 12 (December 1999): 2832–33. http://dx.doi.org/10.1097/00003246-199912000-00041.

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van der Poll, Tom, and Joost C. M. Meijers. "Systemic Inflammatory Response Syndrome and Compensatory Anti-Inflammatory Response Syndrome in Sepsis." Journal of Innate Immunity 2, no. 5 (2010): 379–80. http://dx.doi.org/10.1159/000318190.

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Vanourny, Jaime, and Brian L. Swick. "Sweet Syndrome With Systemic Inflammatory Response Syndrome." Archives of Dermatology 148, no. 8 (August 1, 2012): 969. http://dx.doi.org/10.1001/archdermatol.2012.766.

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Ansari, Shuaib, Irfan Murtaza Shahwani, Zeeshan Ali, Syed Zulfiquar Ali Shah, and Faisal Shahab. "SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS)." Professional Medical Journal 22, no. 03 (March 10, 2015): 293–98. http://dx.doi.org/10.29309/tpmj/2015.22.03.1343.

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Systemic inflammatory response syndrome (SIRS) is a generalized disorder,immune response to infection which results in disturbed microcirculation, visceral perfusion andultimately visceral failure. Objectives: To determine the frequency of systemic inflammatoryresponse syndrome in patients with liver cirrhosis. Design: Cross sectional descriptive.Period: Six months study. Setting: At Liaquat University Hospital Hyderabad. Patients andmethods: All the patients with liver cirrhosis for 06 months duration admitted in the ward werefurther evaluated for systemic inflammatory response syndrome. The data was analyzed inSPSS 16 and the frequency and percentage was calculated. Results: During six months studyperiod, total 100 cirrhotic subjects were studied for SIRS. The mean ± SD for age in all (100)cirrhotic patients was 45.74 ± 7.537. The mean temperatures was 40.42±0.32 where as it was39.72±0.43 and 38.92±0.11 in male and female population respectively. The mean heart beatwas 128.42±6.74 where as it was 115.83±8.93 and 120.62±5.53 in male and female populationrespectively. The mean respiratory rate was 25.31±3.52 where as it was 23.52±2.31 and26.63±3.21 in male and female population respectively. The mean white blood cell count was28.81±4.51 where as it was 23.74±4.73 and 30.83±5.73 respectively. The SIRS was observedin 70% subjects of which 47(67.1%) were males and 23(32.9%) were females (p=0.04). Majorityof SIRS subjects were 30-39 years of age and male population was predominant (p=0.03). Thegender distribution in relation to severity of liver disease was statistically significant (p=0.05)while the SIRS in relation statical analysis. Conclusions: The systemic inflammatory responsesyndrome occurs in patients with liver cirrhosis.

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Dissertations / Theses on the topic "Inflammatory response syndrome"

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Slyvka, N. O. "Systemic inflammatory response as a part of hepatorenal syndrome." Thesis, БДМУ, 2020. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18059.

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Chen, Xu-wu. "Neutrophil-endothelium interactions in patients with systemic inflammatory response syndrome." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ29673.pdf.

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Chen, Xu-wu 1955. "Neutrophil-endothelium interactions in patients with systemic inflammatory response syndrome." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=27298.

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Multiple Organ Dysfunction Syndrome (MODS) is associated with high mortality in patients admitted to the surgical intensive care unit (SICU). MODS begins with a systemic response described as Systemic Inflammatory Response Syndrome (SIRS). Studies on SIRS patients may provide an insight into the mechanisms by which SIRS progresses to MODS. In this thesis, the interactions between circulating polymorphonuclear neutrophils (PMNs) from patients with SIRS and endothelial cells (ECs) from human umbilical veins were measured in order to elucidate the mechanism for PMN adhesion and subsequent cytotoxicity of the ECs. PMNs from patients with SIRS were compared to PMNs from pre-operative surgical patients without SIRS and with healthy control subjects, in vitro. The results showed that PMNs adherence to ECs increased progressively from healthy controls to patients with SIRS. PMN-HUVE cytotoxicity, however, did not show this trend. PMNs from SIRS patients treated with lipopolysaccharide, unlike PMNs from patients without SIRS or healthy controls, showed no increase in PMN-EC adhesion. The results also showed that EC activation with TNF-$ alpha$ and Il-1$ beta$ led to high levels of PMN-EC adhesion and cytotoxicity, whereas PMN treatment with lipopolysaccharide played a lesser role. Autologous plasma provided significant protection from PMN mediated EC damage. From this data I conclude that activation of the EC by cytokines associated with SIRS is far more important in promoting PMN-EC adhesion and subsequent cytotoxicity than PMN stimulation with lipopolysaccharide and that there are host factors in plasma that modulate this response.

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Sydorchuk, Ryslan Ihorovuch, Oleg Yosypovych Khomko, Ruslan Ihorovych Polyanskyi, and Oleksandr Matviyovych Plegutsa. "Systemic inflammatory response syndrome associated with pancreatitis: efficacy of passive immunotherapy." Thesis, Вінницький національний медичний університет ім. М.І.Пирогова, 2015. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/10764.

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Price, Susanna. "Role of vasoactive mediators in the modulation of cardiac function in sepsis." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271284.

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Pevec, Till. "Dexamethason-21-isonicotinat als Begleittherapie bei Kühen mit Systemic Inflammatory Response Syndrome." Doctoral thesis, Universitätsbibliothek Leipzig, 2007. http://nbn-resolving.de/urn:nbn:de:bsz:15-20071210-143013-1.

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Dexamethason-21-isonicotinat als Begleittherapie bei Kühen mit Systemic Inflammatory Response Syndrome Schlüsselwörter: Dexamethason, SIRS, Phagozytoseaktivität/Burstaktivität von Monozyten und neutrophilen Granulozyten, Tumornekrose Faktor alpha

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Keyser, Eric J. "Exhaled nitric oxide and the Systemic Inflammatory Response Syndrome (SIRS) after cardiac surgery." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31247.

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Background. Septic patients produce increased nitric oxide (NO). We postulated increased exhaled nitric oxide (exNO) in SIRS after cardiopulmonary bypass surgery (CPB).
Methods. Forty-two intubated patients were studied postoperatively and at two-hour intervals for eight hours or until extubated. Hemodynamic indices, including indexed systemic vascular resistance (SVRi) and cardiac index (CI) were measured. ExNO was analyzed by ozone chemiluminescence.
Results. Six patients (14%) Manifested SIRS, defined as SVRI <1800 dynes·sec/cm5/m2. ExNO indexed by expired volume of minute ventilation and body surface area (exNO· V˙Ei) was less in SIRS patients at each interval. Overall, normal exNO·V˙Ei was 4.3 +/- 0.4 nL/min/m2 with a Cl of 2.56 +/- 0.05 L/min/m 2 and an SVRI of 2488 +/- 62 dynes·sec/cm5/m 2, whereas in SIRS exNO·V˙Ei was 0.7 +/- 0.3 (p < 0.001) with a Cl of 2.97 +/- 0.09 (p < 0.001) and an SVRi of 1826 +/- 86 (p < 0.001).
Conclusions. Pulmonary production of NO in post-CPB SIRS differs from sepsis and may not be reflective of systemic levels. Increased pulmonary blood flow may scavenge lung production of NO thereby decreasing exhaled levels.

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Lewis, A. "Modulation of the systemic inflammatory response syndrome in lower limb ischaemia-reperfusion injury." Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421004.

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Harkin, Denis William. "Modulation of the systemic inflammatory response syndrome in lower limb ischaemia-reperfusion injury." Thesis, Queen's University Belfast, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326388.

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Hoffman, Crystal Joyce. "Glucocorticoid Receptor Density and Binding Affinity in Horses with Systemic Inflammatory Response Syndrome." Thesis, Virginia Tech, 2014. http://hdl.handle.net/10919/48423.

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There were three objectives of this study. The first was to determine if commercially available fluorochromes could be used to determine the glucocorticoid receptor (GR) density and binding affinity (BA) in equine peripheral blood mononuclear cells. The second was to determine if there was a correlation between elevated plasma cortisol and GR density or binding affinity in healthy adult horses. The third objective was to evaluate the HPA axis in adult horses presenting with systemic inflammatory response syndrome (SIRS), and to determine where any alterations in HPA axis function occur in these patients compared to healthy adults. For the first part of the study, peripheral venous blood was collected from 3 healthy research horses on 3 days. Peripheral blood mononuclear cells were isolated using Ficoll gradient centrifugation. Phycoerythrin (PE)-CD44 was then used to extracellularly label leukocytes, and then an intracellular GR antibody was used to determine a baseline measurement of GR density and fluorescein isothiocyanate (FITC)-dexamethasone was used to determine binding affinity via flow cytometric analysis. Comparison of control samples to those for CD44, GR density, and GR binding affinity showed a statistically significant difference for all samples (P<0.0001, P<0.0001, and P<0.0001 respectively). This showed that the CD44, GR antibody, and FITC-dexamethasone could successfully be used to analyze equine peripheral blood mononuclear cells for GR activity. For the second part of the study, an ACTH stimulation test was performed on 8 healthy horses in order to induce an increase in endogenous cortisol production. Plasma cortisol levels, GR density, and GR binding affinity were measured at baseline, 4, 8, and 24 hours after treatment. Median basal cortisol concentration was 4.9, range 3.2-6.1 μg/dl. This initially increased following ACTH stimulation to 5.6, range 4.8-7.4 μg/dl, then showed a significant decrease by 8 hours post ACTH administration to 1.4, range 1.1-2.7 μg/dl (P=0.0221). No correlation was observed between plasma cortisol concentration in healthy horses and GR density or binding affinity (r=-0.145, P=0.428 and r=0.046, P=0.802, respectively). For the third phase of the study, horses (N=10) with systemic inflammatory response syndrome (SIRS) were compared to healthy, age and sex matched controls (N=10) presenting for lameness evaluation or ophthalmologic examination. Blood was collected from SIRS cases and controls on presentation to the Equine Medical Center. A CBC, serum biochemistry, and serum ACTH and cortisol measurements were performed. GR density and binding affinity were also determined. Nonsurvivors had a significantly decreased GR binding affinity (P=0.008) and demonstrated a trend towards an increase in the ACTH:cortisol ratio. ROC analysis was performed for serum ACTH and cortisol concentrations, the ACTH:cortisol ratio, GR density and GR binding affinity, and triglycerides to determine cut-off values associated with nonsurvival. These were then used to analyze this population using Fischer's exact test to determine the odds ratio (OR) associated with nonsurvival for each variable. This revealed that a serum triglyceride concentration greater than 28.5 mg/dl was associated with nonsurvival (OR=117, 95% CI, 1.94-7060). The other variables were not found to be significantly associated with nonsurvival, although a Delta BA% of less than 35.79% was found to be closely associated with nonsurvival (OR=30.33, 95% CI, 0.96-960.5). Additionally, a significant negative correlation was detected between the plasma ACTH concentration and Delta BA% (r=-0.685, P=0.029) and the ACTH:cortisol ratio and the Delta BA% (r=-0.697, P=0.025). This study showed that nonsurviving horses with SIRS had a significantly decreased GR binding affinity compared to survivors, and a tendency toward an increase in their ACTH:cortisol ratios. This confirms that HPA axis dysfunction occurs in adult horses with SIRS as tissue resistance to glucocorticoids, and potentially relative adrenal insufficiency as well. These results suggest that there are horses with SIRS that might benefit from "physiologic" doses of synthetic glucocorticoids to complement their relative adrenal insufficiency in addition to their poor tissue sensitivity. Further research should focus on methods to more rapidly determine which horses might benefit from treatment with glucocorticoids on presentation, as well as to more accurately determine prognosis for survival.
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Books on the topic "Inflammatory response syndrome"

1

Dorinsky, Paul M. The Sepsis syndrome. Philadelphia: W.B. Saunders, 1996.

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Barra, Pedro Miguel Craveiro. RNA turnover and energy metabolism of children with systemic inflammatory response syndrome and sepsis. London: University of Surrey Roehampton, 2001.

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K, Choi Augustine M., ed. Acute respiratory distress syndrome. 2nd ed. New York: Informa Healthcare USA, 2009.

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Cavaillon, Jean-Marc, and Christophe Adrie. Sepsis and non-infectious systemic inflammation: From biology to critical care. Weinheim: Wiley-VCH, 2009.

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Moaveni, Daria M. Systemic Inflammatory Response Syndrome and Sepsis in the Pregnant Patient. Edited by Matthew D. McEvoy and Cory M. Furse. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190226459.003.0047.

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The chapter “Systemic Inflammatory Response Syndrome and Sepsis in the Pregnant Patient” reviews diagnostic criteria for sepsis in pregnant women, as well as the etiology, risk factors, workup, and treatment of this preventable and treatable cause of maternal morbidity and mortality. It also briefly reviews the history and epidemiology of sepsis. It compares the original diagnostic criteria for systemic inflammatory response syndrome established in 1992, the sepsis diagnostic criteria from the Surviving Sepsis Campaign, and the Sepsis in Obstetrics Score. It discusses the initial workup and resuscitation, fluid management, vasopressor choice and dosing, and antimicrobial treatment for pregnant women with sepsis. It also reviews the obstetric implications of septic parturients.

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Choi, Augustine M. K. Acute Respiratory Distress Syndrome. Taylor & Francis Group, 2016.

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Acute respiratory distress syndrome. 2nd ed. New York: Informa Healthcare USA, 2010.

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Choi, Augustine M. K. Acute Respiratory Distress Syndrome. Taylor & Francis Group, 2016.

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(Editor), Arthur E. Baue, Eugen Faist (Editor), and Donald Fry (Editor), eds. Multiple Organ Failure: Pathophysiology, Prevention, and Therapy. Springer, 2000.

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Yurdakul, Sebahattin, Emire Seyahi, and Hasan Yazici. Behçet’s syndrome. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0135.

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Behçet's syndrome is a systemic inflammatory panvasculitis (affecting all sizes of vessels) of unknown aetiology. It is in vogue to include it among the systemic autoinflammatory conditions. Behçet's syndrome is more frequent along the ancient 'Silk Route' across Asia than it is in Western countries. The usual onset is the second or third decade, equally affecting either gender. However, young patients and male patients have more severe disease. Almost all patients have recurrent oral ulceration. Scar-forming genital ulcers, a variety of skin lesions including acneiform, erythema nodosum-like lesions, arthritis, potentially blinding panuveitis, thrombophlebitis, gastrointestinal disease, central nervous system (CNS) involvement, and life-threatening bleeding pulmonary artery aneurysms are seen. The pathergy phenomenon is a heightened tissue inflammatory response. The strongest genetic association is with HLA B51. There are immunological aberrations but not prominent enough to call it an autoimmune disease. Similarly, Behçet's syndrome does not fit easily into the broad concept of autoinflammatory diseases. The histopathology is also non-specific and the diagnosis is mainly clinical. Differentiation from Crohn's disease is very difficult. In more than one-half of the patients the disease burns out in time, thus only symptomatic therapy is indicated in some patients. However, eye involvement, pulmonary vascular disease, thrombophilic complications, CNS involvement, and gastrointestinal disease need prompt recognition and treatment. Brief courses of glucocorticosteroids along with immunosuppressives including the newer biologicals, interferon, and colchicine are commonly used. However, controlled clinical trials are not available for some of these medications especially when thrombophilia, CNS, and gastrointestinal disease are present.

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Book chapters on the topic "Inflammatory response syndrome"

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Zomaya, Martin P., and Khanjan H. Nagarsheth. "Systemic Inflammatory Response Syndrome." In Encyclopedia of Trauma Care, 1543–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-29613-0_155.

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Kashani, John, Richard D. Shih, Thomas H. Cogbill, David H. Jang, Lewis S. Nelson, Mitchell M. Levy, Margaret M. Parker, et al. "Systemic Inflammatory Response Syndrome (SIRS)." In Encyclopedia of Intensive Care Medicine, 2192. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_3329.

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McMahon, Scott W. "Pediatric Chronic Inflammatory Response Syndrome." In Nutrition and Integrative Medicine for Clinicians, 49–70. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/b23304-5.

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Mestres, Carlos A., Cecilia Marcacci, Gerard Espinosa, Jose L. Pomar, Andrea Colli, and Ricard Cervera. "Heart Valve Surgery and the Antiphospholipid Syndrome." In Inflammatory Response in Cardiovascular Surgery, 321–29. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4429-8_38.

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Füssle, Roswitha, Andreas Sziegoleit, and Jürgen Biscoping. "Sepsis/Systemic Inflammatory Response Syndrome (SIRS)." In 1×1 der Infektiologie auf Intensivstationen, 49–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-97657-5_7.

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Bryant, Clare E., and James N. Moore. "Pathophysiology of Systemic Inflammatory Response Syndrome." In The Equine Acute Abdomen, 183–92. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781119063254.ch16.

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Bone, R. C. "The Systemic Inflammatory Response Syndrome (SIRS)." In Update in Intensive Care and Emergency Medicine, 3–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79224-3_1.

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Lindberg, Harald L., and Tom N. Hoel. "The Systemic Inflammatory Response Syndrome Following Cardiopulmonary Bypass in Children." In Inflammatory Response in Cardiovascular Surgery, 245–53. London: Springer London, 2013. http://dx.doi.org/10.1007/978-1-4471-4429-8_28.

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Kashani, John, Richard D. Shih, Thomas H. Cogbill, David H. Jang, Lewis S. Nelson, Mitchell M. Levy, Margaret M. Parker, et al. "Systemic Inflammatory Response Syndrome (SIRS) with Infection." In Encyclopedia of Intensive Care Medicine, 2192. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_2264.

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Rinewalt, Daniel, and José M. Velasco. "Systemic Inflammatory Response Syndrome (SIRS) and Sepsis." In Common Surgical Diseases, 361–62. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1565-1_91.

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Conference papers on the topic "Inflammatory response syndrome"

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Greulich, T., W. Groenewold, R. Koczulla, C. Herr, C. Vogelmeier, and R. Bals. "Vitamin D Is Suppressed in Systemic Inflammatory Response Syndrome." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4706.

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Knopf, M., C. Weingart, M. Fulde, A. Lübke-Becker, R. Merle, C. Robé, U. Rösler, et al. "Systemic Inflammatory Response Syndrome (SIRS) bei 149 Hunden – Ursachen und Outcome." In DVG. Georg Thieme Verlag, 2024. http://dx.doi.org/10.1055/s-0044-1779643.

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Martin, JB, LM Weavind, DJ Maron, EW Ely, and TW Rice. "Electronic Identification of Septic Patients Using Modified Systemic Inflammatory Response Syndrome Criteria." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4720.

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Greulich, Timm, Wiebke Groenewold, Christian Herr, Andreas R. Koczulla, Claus F. Vogelmeier, and Robert Bals. "Alpha-1-Antitrypsin Is Elevated In Patients With Systemic Inflammatory Response Syndrome." 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.a6156.

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Kirupaharan, P., C. Blazoski, and M. Baram. "Systemic Inflammatory Response Syndrome After Extracorporeal Membrane Oxygenation Decannulation in COVID-19 Patients." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1510.

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Honorato, Pedro Fechine, Dhiego Alves de Lacerda, Anaylle Vieira Lacerda de Oliveira, Maria Eduarda Borges e. Cunha, Yasmin Teixeira Santana, Brendha Vitória Pereira da Silva, Gabrielly Celestino de Maria, et al. "Post-myocardial infarction pericarditis: Dressler syndrome and its clinical implications." In III Seven International Medical and Nursing Congress. Seven Congress, 2024. http://dx.doi.org/10.56238/iiicongressmedicalnursing-016.

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Dressler syndrome, a rare complication following myocardial infarction or cardiac surgery, is characterized by a triad of fever, chest pain, and pericardial effusion. Caused by an autoimmune response to cardiac damage, the syndrome can lead to serious complications such as cardiac tamponade and constrictive pericarditis. Diagnosis is made through clinical findings, laboratory tests, and imaging, and treatment involves anti-inflammatory drugs, corticosteroids, and, when necessary, pericardial drainage. Early detection and appropriate management are crucial to prevent complications and improve patient prognosis.

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Jafari, Mostafa, Kalman Katlowitz, Carlos De la Garza, Alexander Sellers, Shawn Moore, Hayden Hall, Aaron Desai, Vikramjeet Singh, and Rahul Damani. "Systemic inflammatory response syndrome deteriorates the outcomes of mechanical thrombectomy in acute stroke (P14-5.031)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000201731.

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Yetti, Husna, Herlina Herlina, Mayetti Mayetti, Abdiana Abdiana, and Indra Ihsan. "CD64 Index as a Predictor of Outcome for Children with Systemic Inflammatory Response Syndrome (SIRS)." In Proceedings of the 1st EAI International Conference on Medical And Health Research, ICoMHER November 13-14th 2018, Padang, West Sumatera, Indonesia. EAI, 2019. http://dx.doi.org/10.4108/eai.13-11-2018.2283708.

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Stritt, Matthew, William D. Freeman, Ognjen Gajic, and Emir Festic. "Can Serum Procalcitonin Levels Distinguish Between Systemic Inflammatory Response Syndrome And Systemic Infection In Aneurysmal Subarachnoid Hemorrhage Patients?" In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5850.

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Jenke, A., M. Yazdanyar, M. Immohr, S. Miyahara, A. Chekhoeva, J. Kistner, U. Boeken, A. Lichtenberg, and P. Akhyari. "The Synthetic Adiponectin Receptor Agonist AdipoRon Attenuates Impairment of Cardiac Function Associated with Cardiopulmonary Bypass-Induced Systemic Inflammatory Response Syndrome." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678921.

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Reports on the topic "Inflammatory response syndrome"

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Fan, Yihua, Xiaoyin Zhao, Xiaoxu He, and Huixin Chen. Efficacy and safety of Chinese herbal compound in the treatment of acute gouty arthritis: A protocol of a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0153.

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Abstract:

Review question / Objective: To evaluate the efficacy and safety of Chinese herbal compound in the treatment of acute gouty arthritis. Eligibility criteria: 1.1.1 Literature type Randomized controlled trials of treating AGA with Chinese herbal compound alone, whether blind or not, was limited to Chinese literature and English literature.1.1.2 SubjectsThe time of onset, gender, and age of patients diagnosed with acute gouty arthritis were not restricted.1.1.3 Intervention measures The treatment group was treated with traditional Chinese medicine compound, which could be proprietary Chinese medicine, self-made prescription or classic prescription, and the dosage form could be traditional decoction, granule or pill, while the control group was treated with non-steroidal anti-inflammatory painkillers, and the frequency, dosage and course of use were not limited.1.1.4 Outcome indicators(1) Main outcome measures: total response rate; (2) Secondary outcome indicators: visual analog scale (VAS), TCM syndrome score, blood uric acid, ESR, CRP, and incidence of adverse reactions.

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Fan, Yihua, Xiaoyin Zhao, Xiaoxu He, and Huixin Chen. Efficacy and safety of Chinese herbal compound in the treatment of acute gouty arthritis: A protocol of a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0153.

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Abstract:

Review question / Objective: To evaluate the efficacy and safety of Chinese herbal compound in the treatment of acute gouty arthritis. Eligibility criteria: 1.1.1 Literature type Randomized controlled trials of treating AGA with Chinese herbal compound alone, whether blind or not, was limited to Chinese literature and English literature.1.1.2 SubjectsThe time of onset, gender, and age of patients diagnosed with acute gouty arthritis were not restricted.1.1.3 Intervention measures The treatment group was treated with traditional Chinese medicine compound, which could be proprietary Chinese medicine, self-made prescription or classic prescription, and the dosage form could be traditional decoction, granule or pill, while the control group was treated with non-steroidal anti-inflammatory painkillers, and the frequency, dosage and course of use were not limited.1.1.4 Outcome indicators(1) Main outcome measures: total response rate; (2) Secondary outcome indicators: visual analog scale (VAS), TCM syndrome score, blood uric acid, ESR, CRP, and incidence of adverse reactions.

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