Journal articles: 'Childbed fever'

1

Whitfill, Kimberly. "The Tragedy of Childbed Fever." Journal of Midwifery & Women's Health 46, no. 3 (May 6, 2001): 201–2. http://dx.doi.org/10.1016/s1526-9523(01)00117-9.

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Hamlin, Christopher, and Irvine Loudon. "The Tragedy of Childbed Fever." American Historical Review 106, no. 4 (October 2001): 1325. http://dx.doi.org/10.2307/2692960.

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Graham, WJ, SJ Dancer, IM Gould, and W. Stones. "Childbed fever: history repeats itself?" BJOG: An International Journal of Obstetrics & Gynaecology 122, no. 2 (December 26, 2014): 156–59. http://dx.doi.org/10.1111/1471-0528.13189.

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Parsons, Gail Pat. "The Tragedy of Childbed Fever (review)." Bulletin of the History of Medicine 75, no. 2 (2001): 319–20. http://dx.doi.org/10.1353/bhm.2001.0089.

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Hallett, Christine. "The Attempt to Understand Puerperal Fever in the Eighteenth and Early Nineteenth Centuries: The Influence of Inflammation Theory." Medical History 49, no. 1 (January 1, 2005): 1–28. http://dx.doi.org/10.1017/s0025727300000119.

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Puerperal fever was a devastating disease. It affected women within the first three days after childbirth and progressed rapidly, causing acute symptoms of severe abdominal pain, fever and debility. Although it had been recognized from as early as the time of the Hippocratic corpus that women in childbed were prone to fevers, the distinct name, “puerperal fever” appears in the historical record only in the early eighteenth century.

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Delacy, Margaret. "The Tragedy of Childbed Fever. Irvine Loudon." Isis 92, no. 4 (December 2001): 764–65. http://dx.doi.org/10.1086/385376.

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Carter, K. Codell (Kay Codell),. "Book Review: Childbed Fever: A Documentary History." Bulletin of the History of Medicine 70, no. 3 (1996): 539–40. http://dx.doi.org/10.1353/bhm.1996.0101.

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Ács, Nándor. "The aetiology, concept and prophylaxis of childbed fever." Orvosi Hetilap 152, no. 51 (December 2011): 2036–38. http://dx.doi.org/10.1556/oh.2011.29282.

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9

Tigre, Clovis H., Ignaz Semmelweis, and K. Codell Carter. "The Etiology, Concept, and Prophylaxis of Childbed Fever." Journal of Public Health Policy 8, no. 4 (1987): 582. http://dx.doi.org/10.2307/3342284.

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RINKER, SYLVIA. "Childbed Fever: A Scientific Biography of Ignaz Semmelweis." Nursing History Review 5, no. 1 (January 1997): 222–23. http://dx.doi.org/10.1891/1062-8061.5.1.222.

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Edwards, T. Keith. "Childbed Fever: A Scientific Biography of Ignaz Semmelweis." JAMA: The Journal of the American Medical Association 272, no. 23 (December 21, 1994): 1871. http://dx.doi.org/10.1001/jama.1994.03520230081049.

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Seri, I. "Historical Perspectives: Perinatal Profiles: Childbed Fever and Ignac Fulop Semmelweis." NeoReviews 8, no. 6 (June 1, 2007): e235-e238. http://dx.doi.org/10.1542/neo.8-6-e235.

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13

Halliday, Jane, and Stephen Halliday. "Zepherina Veitch (1836–94), childbed fever and the registration of midwives." Journal of Medical Biography 15, no. 4 (November 2007): 241–45. http://dx.doi.org/10.1258/j.jmb.2007.06-56.

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14

Hallett, Christine. "The Tragedy of Childbed Fever, by Irvine LoudonThe Tragedy of Childbed Fever, by Irvine Loudon. Oxford, Oxford University Press, 2000. xiv, 236 pp. $116.00 Cdn (cloth)." Canadian Journal of History 38, no. 1 (April 2003): 172–73. http://dx.doi.org/10.3138/cjh.38.1.172.

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15

KADAR, NICHOLAS, and RUSSELL D. CROFT. "Why Semmelweis's doctrine was rejected: evidence from the first publication of his results by Friedrich Wieger, and an editorial commenting on the results." British Journal for the History of Science 53, no. 3 (July 3, 2020): 389–95. http://dx.doi.org/10.1017/s0007087420000229.

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AbstractWe present English translations of two French documents to show that the main reason for the rejection of Semmelweis's theory of the cause of childbed (puerperal) fever was because his proof relied on the post hoc ergo propter hoc fallacy, and not because Joseph Skoda referred only to cadaveric particles as the cause in his lecture to the Academy of Science on Semmelweis's discovery. Friedrich Wieger (1821–1890), an obstetrician from Strasbourg, published an accurate account of Semmelweis's theory six months before Skoda's lecture, and reported a case in which the causative agent originated from a source other than cadavers. Wieger also presented data showing that chlorine hand disinfection reduced the annual maternal mortality rate from childbed fever (MMR) from more than 7 per cent for the years 1840–1846 to 1.27 per cent in 1848, the first full year in which chlorine hand disinfection was practised. But an editorial in the Gazette médicale de Paris rejected the data as proof of the effectiveness of chlorine hand disinfection, stating that the fact that the MMR fell after chlorine hand disinfection was implemented did not mean that this innovation had caused the MMR to fall. This previously unrecognized objection to Semmelweis's proof was also the reason why Semmelweis's chief rejected Semmelweis's evidence.

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Kadar, Nicholas. "A Note on Semmelweis’s Animal Experiments and Their Historical Significance." Journal of the History of Medicine and Allied Sciences 75, no. 4 (October 1, 2020): 383–407. http://dx.doi.org/10.1093/jhmas/jraa039.

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Abstract This article seeks to establish what animal experiments Semmelweis conducted, and when and why he conducted them, because the Semmelweis literature contains conflicting claims about these topics or has ignored them altogether. Semmelweis first conducted animal experiments between 22 March and 20 August 1849 with Rokitansky’s assistant, Georg Maria Lautner, because his chief, Johann Klein, did not accept that by merely reducing the mortality rate from childbed fever with chlorine hand-disinfection, Semmelweis had proved his theory of the cause of childbed fever. However, Skoda concluded that the Lautner experiments did not resolve the doubts about Semmelweis’s theory they were intended to resolve, and, therefore, asked the Academy of Sciences to award Semmelweis a grant to conduct further and more varied experiments with the physiologist, Ernst Ritter von Brücke. These additional experiments were conducted in the spring and summer of 1850, but yielded only ambiguous results, and led Brücke to conclude that questions about Semmelweis’s theory could only be resolved by clinical observations, not animal experiments. This article discusses the reasoning behind these animal experiments, and Skoda’s and Brücke’s responses to them, and argues that their responses to the experiments caused Semmelweis to delay publishing his research until he had collected sufficient clinical evidence to prove his theory.

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De Costa, Caroline M. "“The contagiousness of childbed fever”: a short history of puerperal sepsis and its treatment." Medical Journal of Australia 177, no. 11 (December 2002): 668–71. http://dx.doi.org/10.5694/j.1326-5377.2002.tb05004.x.

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18

Lee, R. C. (Raphael Carl), and Anna Chien. "The Doctor's Plague: Germs, Childbed Fever, and the Strange Story of Ignac Semmelweis (review)." Perspectives in Biology and Medicine 48, no. 4 (2005): 616–18. http://dx.doi.org/10.1353/pbm.2005.0095.

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19

Smith, R. B. "Review: The Doctors' Plague: Germs, Childbed Fever, and the Strange Story of Ignac Semmelweis." Journal of the History of Medicine and Allied Sciences 60, no. 2 (April 1, 2005): 232–34. http://dx.doi.org/10.1093/jhmas/jri028.

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20

Carter, K. Codell (Kay Codell). "The Doctors' Plague: Germs, Childbed Fever, and the Strange Story of Ignac Semmelweis (review)." Bulletin of the History of Medicine 78, no. 4 (2004): 898–99. http://dx.doi.org/10.1353/bhm.2004.0159.

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DeLacy, Margaret. "Childbed Fever: A Scientific Biography of Ignaz Semmelweis. K. Codell Carter , Barbara R. Carter." Isis 86, no. 3 (September 1995): 506–7. http://dx.doi.org/10.1086/357291.

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22

Putnam, Constance. "Irvine Loudon, The tragedy of childbed fever, Oxford University Press, 2000, pp. ix, 236, £40.00 (0-19-820499-X)." Medical History 45, no. 1 (January 2001): 127–28. http://dx.doi.org/10.1017/s002572730006748x.

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23

Raju, Tonse. "Ignac Semmelweis, the Epidemiologist: His Insights into Fetal and Neonatal Sepsis and the Eventual Discovery of the Etiology of Childbed Fever." Pediatric Research 45, no. 4, Part 2 of 2 (April 1999): 273A. http://dx.doi.org/10.1203/00006450-199904020-01622.

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Aragón-Méndez, María del Mar, José Antonio Acevedo-Díaz, and Antonio García-Carmona. "Prospective biology teachers’ understanding of the nature of science through an analysis of the historical case of Semmelweis and childbed fever." Cultural Studies of Science Education 14, no. 3 (June 16, 2018): 525–55. http://dx.doi.org/10.1007/s11422-018-9868-y.

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25

Lawrence, Christopher. "Irvine Loudon. The Tragedy of Childbed Fever. New York: Oxford University Press. 2000 Pp. xiv, 236. $65.00. ISBN 0-19-820499-X." Albion 33, no. 3 (2001): 494–95. http://dx.doi.org/10.2307/4053244.

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26

Leavitt, Judith Walzer. "Book Review The Tragedy of Childbed Fever By Irvine Loudon. 249 pp. New York, Oxford University Press, 2000. $65. 0-19-820499-X." New England Journal of Medicine 343, no. 8 (August 24, 2000): 587. http://dx.doi.org/10.1056/nejm200008243430819.

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27

Bonnett, Penny. "The 1997 Bishop and LeFanu Memorial Lecture. ‘The tragedy of childbed fever’ given by Dr Irvine Loudon. Institute of Child Health, 3 November 1997." Health Libraries Review 15, no. 3 (September 1998): 209. http://dx.doi.org/10.1046/j.1365-2532.1998.15302091.x.

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Nikolic, Branka, Ana Mitrovic, Svetlana Dragojevic-Dikic, Snezana Rakic, Zlatica Cakic, Milena Saranovic, and Milan Sikimic. "Group a streptococcal cellulitis in the early puerperium." Vojnosanitetski pregled 68, no. 7 (2011): 607–10. http://dx.doi.org/10.2298/vsp1107607n.

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Introduction. Infectious diseases caused by Streptococcus pyogenes, a member of the group A Streptococci (GAS) are among the most common life threatening ones. Patients with GAS infections have a poor survival rate. Cellulitis is a severe invasive GAS infection and the most common clinical presentation of the disease associated with more deaths than it can be seen in other GAS infections. According to the literature data, most cases of GAS toxic shock syndrome are developed in the puerperium. However, there are two main problems with GAS infection in early puerperium and this case report is aimed at reminding on them. The first problem is an absence of awareness that it can be postpartal invasive GAS infection before the microbiology laboratory confirms it, and the second one is that we have little knowledge about GAS infection, in general. Case report. A 32- year-old healthy woman, gravida 1, para 1, was hospitalized three days after vaginal delivery with a 38-hour history of fever, pain in the left leg (under the knee), and head injury after short period of conscious lost. Clinical picture of GAS infection was cellulites. Group A Streptoccocus pyogenes was isolated in vaginal culture. Rapid antibiotic and supportive treatment stopped development of streptococcal toxic shock syndrome (STSS) and potential multiorganic failure. Signs and symptoms of the infection lasted 25 days, and complete recovery of the patient almost 50 days. Conclusion. In all women in childbed with a history of fever early after delivery, vaginal and cervical culture specimens should be taken as soon as possible. Early recognition of GAS infection in early puerperium and prompt initiation of antimicrobial drug and supportive therapy can prevent development of STSS and lethal outcome.

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29

Worboys, Michael. "Irving Loudon (ed.), Childbed fever: a documentary history, Diseases, Epidemics, and Medicine series, New York and London, Garland Publishing, 1995, pp. xvii, 224, $43.00 (0-8153-1079-X)." Medical History 41, no. 2 (April 1997): 230–31. http://dx.doi.org/10.1017/s0025727300062438.

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30

Loudon, Irvine. "Book Review The Doctors' Plague: Germs, Childbed Fever, and the Strange Story of Ignác Semmelweis (Great Discoveries.) By Sherwin B. Nuland. 191 pp., illustrated. New York, Norton, 2003. $21.95. 0-393-05299-0." New England Journal of Medicine 350, no. 13 (March 25, 2004): 1368–70. http://dx.doi.org/10.1056/nejmbkrev35977.

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31

Gazda, István. "Semmelweis – egy gondolkodó ember. Tudománytörténeti tanulságok." Orvosi Hetilap 159, no. 26 (July 2018): 1055–64. http://dx.doi.org/10.1556/650.2018.31174.

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Abstract: In this article we examine why Semmelweis’s seemingly simple, logical and practical discovery was categorically dismissed by the majority of his contemporaries, and why even many years after his death it was accepted with such reservation. We invoke wherever possible Semmelweis’s own words citing from the series of articles appearing in the ‘Orvosi Hetilap’ [Hungarian Medical Weekly Journal] published in 1858 in Hungary, and also from the German language summary of the Journal published in 1860. We came to the conclusion that although Semmelweis did everything in his power to show the causal relationship between the development of puerperal fever (childbed fever) and some infectious substance on the hands of examining doctors and medical students, this was not convincing enough. The predominant theory at the time held that infection was caused by miasma transmitted in the air and therefore stubbornly precluded any notion of infectious matter physically transmitted on unclean hands. We also concluded that the causal sequence observed by Semmelweis was missing an essential empirical element: visual proof of the infectious agent he correctly postulated as physically transmitted. Visually demonstrating the presence of the infectious agent by means of a microscope would have made his case. This finally did occur but only two years after Semmelweis’s death. Had the renowned Hungarian obstetrician realized the significance of taking advantage of the opportunity afforded by Dávid Gruby who was conducting experiments in the same town, a more convincing argument could have been made for his theory. In the 1840s and 1850s, Dávid Gruby was experimenting with various microscopic techniques and their application with success in Vienna before continuing his work in France. Gruby’s work, especially that of microscopic observations of tissues, received international acceptance. Therefore, the involvement of Gruby and his work with microscopes to support Semmelweis’s observations would most probably have forestalled much of the criticism and rejection his theory was initially awarded (among which perhaps Virchow’s rejection proved the most damaging). Had Semmelweis utilized microscopic techniques, he would have been celebrated among the first to discover bacterial pathogens, contributing to the development of the currently predominant germ theory. Failure to utilize the microscope was the root cause leading to the tragedy of Semmelweis’s rejection by the medical establishment of the time. Despite the increasing numbers of scientists utilizing the microscope at the University of Pest, offered to corroborate his daims with microscopic observations. Efforts have been made have since been to rehabilitate him as the key figure who not only discovered the method of transmission of infectious disease, but also implemented measures of prevention. Elevating him among the ranks of the ten greatest doctors who ever lived is certainly recognition due, but sadly denied to him in his lifetime. Orv Hetil. 2018; 159(26): 1055–1064.

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Kankante, Santoshi, Sunil Natha Mhaske, and Sharada Aher. "Study of Hepatic Dysfunction of Dengue Fever in Children." Pediatric Education and Research 7, no. 1 (2019): 3–6. http://dx.doi.org/10.21088/per.2321.1644.7119.1.

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Prasanna, Lakshmi, and Gadham Jayaram. "PATHO CLINICAL PROFILE OF DENGUE FEVER IN HOSPITALISED CHILDREN." International Journal of Integrative Medical Sciences 5, no. 7 (August 20, 2018): 700–704. http://dx.doi.org/10.16965/ijims.2018.126.

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34

Weindling, Paul. "Ignaz Semmelweis, The Etiology, Concept, and Prophylaxis of Childbed Fever. Translated and Edited with an Introduction by K. Codell Carter. Madison and London: The University of Wisconsin Press, 1983. Pp. xii + 262. $35 cloth, $10.95 paper." British Journal for the History of Science 18, no. 1 (March 1985): 120. http://dx.doi.org/10.1017/s0007087400022032.

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Ahn, Sang Hyun, Jooho Zhiang, Hyery Kim, Seyun Chang, Jaewon Shin, Myeongchan Kim, Yura Lee, Jae-Ho Lee, and Yu Rang Park. "Postvaccination Fever Response Rates in Children Derived Using the Fever Coach Mobile App: A Retrospective Observational Study." JMIR mHealth and uHealth 7, no. 4 (April 22, 2019): e12223. http://dx.doi.org/10.2196/12223.

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Background Postvaccination fever is a mild adverse event that naturally improves without complications, but is highly prevalent and can be accompanied by febrile convulsions in some cases. These adverse effects may cause parents to delay or avoid vaccinating their children. Objective This study aimed to identify postvaccination fever patterns and the ability of antipyretics to affect changes in these patterns from data collected from a mobile app named Fever Coach. Methods Data provided by parents of feverish children derived from a mobile app, Fever Coach, were used to identify postvaccination fever patterns according to vaccinations and the use of antipyretic drugs. We selected single vaccination records that contained five or more body temperature readings performed within 48 hours of vaccination, and we analyzed postvaccination fever onset, offset, duration, and maximum body temperature. Through observing the postvaccination fever response to vaccination, we identified the effects of antipyretic drugs on postvaccination fever onset, offset, and duration times; the extent of fever; and the rate of decline. We also performed logistic regression analysis to determine demographic variables (age, weight, and sex) involved in relatively high fevers (body temperature ≥39°C). Results The total number of Fever Coach users was 25,037, with 3834 users having entered single vaccination records, including 4448 vaccinations and 55,783 body temperature records. Most records were obtained from children receiving the following vaccinations: pneumococcus (n=2069); Japanese encephalitis (n=911); influenza (n=669); diphtheria, tetanus, and pertussis (n=403); and hepatitis A (n=252). According to the 4448 vaccination records, 3427 (77.05%) children had taken antipyretic drugs, and 3238 (89.15%) children took antibiotics at body temperatures above 38°C. The number of children taking antipyretics at a body temperature of 38°C was more than four times that of those taking antipyretics at 37.9°C (307 vs 67 cases). The number of instances in which this temperature threshold was reached was more than four times greater than the number when the temperature was 37.9°C. A comparative analysis of antipyretic and nonantipyretic cases showed there was no difference in onset time; however, offset and duration times were significantly shorter in nonantipyretic cases than in antipyretic cases (P<.001). In nonantipyretic cases, offset times and duration times were 9.9 and 10.1 hours shorter, respectively, than in antipyretic cases. Body temperatures also decreased faster in nonantipyretic cases. Influenza vaccine-associated fevers lasted relatively longer, whereas pneumococcus vaccine-associated fevers were relatively short-lived. Conclusions These findings suggest that postvaccination fever has its own fever pattern, which is dependent on vaccine type and the presence of antipyretic drugs, and that postvaccination temperature monitoring may ease fever phobia and reduce the unnecessary use of antipyretics in medical care.

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T., Karthikraj, Jenish Rajma J., Jeyabalaji R. V., and Shivani Kuttuva. "Spectrum of febrile thrombocytopenia among children in a tropical country-a hospital based observational study in South India." International Journal of Contemporary Pediatrics 8, no. 2 (January 22, 2021): 354. http://dx.doi.org/10.18203/2349-3291.ijcp20210128.

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Background: Febrile thrombocytopenia is a common reason for pediatric admission. Though infections are the major cause, noninfectious causes are not uncommon. This study was done to estimate the prevalence of thrombocytopenia as a presentation in pediatric fever cases, to analyze the various etiologies, presentations and relationship between platelet count and the severity of disease and prognosis.Methods: Retrospective observational study done by collecting data from hospital records of children admitted in Velammal Medical college hospital from January 2016 to December 2017. Children in the age group of 6 months to 15 years with fever and thrombocytopenia at admission were included in the study. Children on treatment with anti-platelet drugs, other chronic diseases and infants less than 6 months were excluded.Results: Out of 2523 fever cases admitted, 372 children fulfilled this criterion. 70% had positive dengue serology, other infectious causes were other viral hemorrhagic fevers, complicated enteric fever, scrub typhus and sepsis. The predominant non-infectious causes were hematological malignancies, Idiopathic thrombocytopenic purpura and Hemolytic uremia syndrome.Conclusions: Febrile thrombocytopenia is a common clinical presentation in children in dengue endemic areas. Most viral fevers have leukopenia but presence of thrombocytopenia with warning signs like pain abdomen, vomiting or oliguria should prompt suspicion of dengue. Infections like enteric fever, scrub typhus or chikungunya may also mimic similar findings. Rarely diseases like leukemia, Idiopathic thrombocytopenic purpura, Hemolytic uremic syndrome or Sepsis may also present as febrile thrombocytopenia. The need for antibiotics or blood products is very minimal.

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Qadr H. Khurshid, Bakhtyar, Jamal Ahmed Rashid, and Khalid Hama Salih. "FAMILIAL MEDITERRANEAN FEVER AMONG KURDISH CHILDREN; A SINGLE CENTER STUDY." Journal of Sulaimani Medical College 9, no. 1 (March 21, 2019): 37–43. http://dx.doi.org/10.17656/jsmc.10188.

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Shihabuddin, B., I. Stehmeier, W. El-Halabi, and C. Scarfi. "Fever in Children With Sickle Cell Disease: Are All “Fevers” Equal?" Annals of Emergency Medicine 62, no. 4 (October 2013): S153. http://dx.doi.org/10.1016/j.annemergmed.2013.07.250.

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Shihabuddin, Bashar Sami, and Catherine Ann Scarfi. "Fever in Children With Sickle Cell Disease: Are All Fevers Equal?" Journal of Emergency Medicine 47, no. 4 (October 2014): 395–400. http://dx.doi.org/10.1016/j.jemermed.2014.06.025.

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Kumar, Radha, Ganthimathi Sekhar, Ananthi N, and Kalyani M. "Clinical profile, laboratory investigations and outcome in dengue positive children in south India." International Journal of Research in Pharmaceutical Sciences 11, SPL2 (April 30, 2020): 175–80. http://dx.doi.org/10.26452/ijrps.v11ispl2.2197.

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Dengue fever is one of the most commonly occurring mosquito borne-viral illnesses that has a wide range of presentation in children and is common during the monsoon season. The severity of illness ranges from mild undifferentiated fever, dengue with warning signs, severe dengue fever and dengue fever with organ dysfunction. The symptoms of dengue may be easily mistaken for those of flu or other viral infections. Contrary to other fevers, complications in dengue occur during the phase of defervescence and can be life threatening in children due to shock or profuse hemorrhage. 55 dengue positive children who were diagnosed by dengue antigen detection or dengue antibody positive were included in the study. Most of children were above 10 years and the commonest presenting symptoms were fever, headache, body pain, nausea, anorexia, abdominal pain and vomiting. Most of the children presented with two or more warning signs like persistent vomiting, thrombocytopenia, increasing hematocrit and hepatomegaly. Few children developed features of early shock, which was diagnosed early and treated effectively. All the children responded well to treatment measures and recovered well during hospital stay. Having a high of suspicion and careful monitoring of children is crucial for reducing occurrence of complications and death due to this severe infection.

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Bhaskaran, Jyothy Kothanath, and Srihari Sheshagiri. "Early Clinical Diagnosis of Fever (Jwara) in Children - A Case Study." Journal of Research in Traditional Medicine 2, no. 6 (March 26, 2017): 170–72. http://dx.doi.org/10.21276/jrtm.2016/433.

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Jeyakumar, Deepa, Matthew Zibelman, Ryan Hurth, Lani Krauz, Santosh Saraf, Robert Molokie, and Joseph DeSimone. "Fever In Hospitalized Adult Patients with Sickle Cell Disease." Blood 116, no. 21 (November 19, 2010): 2652. http://dx.doi.org/10.1182/blood.v116.21.2652.2652.

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Abstract Abstract 2652 Background: Sickle cell disease is complicated by veno-occlusive crises leading to pain crises, chronic end-organ damage and early mortality. With recent advances in the management of sickle cell disease in childhood, sickle cell patients are living longer. However, our understanding of the clinical course of adult sickle cell disease remains limited and is based largely on extrapolation of knowledge from children with sickle cell disease. Unfortunately, adult patients remain at an elevated risk of infections due to encapsulated organisms in the setting of functional asplenia. This risk is exacerbated by possible indwelling catheters and exposure to the health care environment. Fever in these patients can herald a serious infection. Alternatively, brisk hemolysis can be associated with fever. Wierenga, et. al. (2001) described that fevers to 39F in children were associated with acute chest syndrome (21%), painful vaso-occlusive crisis (27%), and bacteremia in 6%. To our knowledge, no such review of fever in hospitalized adult sickle cell patients has been published in the medical literature. Therefore, the clinician is placed in a diagnostic dilemma regarding the management of fever in adult patients with sickle cell disease. Objective: To determine the etiologies of fevers in hospitalized adult patients with sickle cell disease in an urban tertiary hospital setting. Methods: We performed an IRB-approved retrospective analysis of 143 admissions between 1995–2008 with sickle cell pain crisis and had a fever greater than 38.5C during the admission. The aim was to determine the prevalence of fevers due to infectious versus hemolysis-related causes in the population of interest. Elevated white blood cell count (defined as greater than 1.5x upper limit of normal), radiologic and/or culture data were used to classify a fever as due to infection. Elevated LDH and total bilirubin (defined as greater than 2x upper limit of normal) were used to classify a fever as due to hemolysis. The risks of infection in patients on hydroxyurea as well as indwelling catheters (including central lines and foley catheters) were assessed. We also evaluated the risk of hemolysis in patients on hydroxyurea. Finally, the use of antibiotics and duration of the fever in patients with hemolysis and infection were also evaluated. Results: Among patients admitted with sickle cell pain crisis and had a fever during their hospitalization, we found evidence of infection in 65% and hemolysis in 58%. Interestingly, 35% had evidence of both infection and hemolysis. Approximately, 11.8% had no significant evidence of infection or hemolysis. Antibiotics were used in 66% of all patients with pain crisis and fever. Among the patients who received antibiotics, 81% had evidence of infection and 19% had no evidence of infection. Approximately 1/5 patients with fevers received antibiotics despite the absence of evidence of infection. Infections were not increased among hydroxyurea users (61.5% with fever) over non-hydroxyurea users (67.9% with fever), p = 0.4. Fevers due to documented infections were found in 78% of patients with indwelling catheters compared with 62% of patients without catheters, p≤0.05. The risk of fever due to hemolysis was not significantly different between hydroxyurea and non-hydroxyurea users at 58% versus 57% respectively, p=0.9. Of patients with fevers for more than one day, infection was found in 69% of patients compared with 31% of patients who had no evidence of infection p=0.5. Whereas, of patients with fevers for more than one day, hemolysis was found in 57% of patients compared with 42% of patients who did not have evidence of hemolysis with p=0.9. Conclusions: Among adult sickle cell patients hospitalized with pain crisis and fever, hemolysis accounted for 58% of cases while infections accounted for 65% with 35% evidence of both. Infections were not increased among hydroxyurea users. Indwelling catheters did increase the risk of fevers due to infection. The risk of fever due to hemolysis was not significantly increased among patients on hydroxyurea. Finally, in patients with fevers for more than one day, hemolysis accounted for 57% of cases and infection accounted for 45%. These findings provide initial investigation of the etiologies of fevers in adult hospitalized sickle cell patients and further studies are necessary to confirm these findings. Disclosures: No relevant conflicts of interest to declare. Disclosures: No relevant conflicts of interest to declare.

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TOMMASINI, ALBERTO, and LOREDANA LEPORE. "Le sindromi autoinfiammatorie: quando non è solo PFAPA." Medico e Bambino 40, no. 4 (April 23, 2021): 221–25. http://dx.doi.org/10.53126/meb40221.

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PFAPA (Periodic Fever, Aphthous Stomatitis, Pharyngitis and Adenitis) is the most common self-inflammatory disorder in children. The diagnosis of PFAPA is easy, based on Thomas criteria, and the prognosis is good. Differential diagnosis with hereditary periodic fever syndromes (Familial Mediterranean Fever, Mevalonate Kinase Deficiency, TRAPS and CAPS) should be considered only in the presence of red flags such as early onset, severe abdominal complaints, arthritis and severe rashes. Some patients may present distinct clinical entities with periodic fevers that neither meet PFAPA criteria nor hereditary periodic fever syndromes genotypes. Subjects with these “Undifferentiated Periodic Fever” may respond to glucocorticoids or colchicines or to anakinra in the most severe cases and still have an undetermined prognosis.

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Matlani, Monika, Pramod Kumar, Shyam S. Meena, Mohan Vashistha, and Vinita Dogra. "Etiological Trends and Epidemiological Profile of Tropical Fever in Children Presenting with Acute Undifferentiated Fever at a Tertiary Care Centre in North India." Journal of Nepal Paediatric Society 41, no. 1 (April 24, 2021): 54–60. http://dx.doi.org/10.3126/jnps.v41i1.29595.

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Introduction: The objective of this study was to determine the etiology of acute undifferentiated fevers (AUF) in hospitalised children with in a tertiary care centre in North India. The various causes of acute undifferentiated fevers included dengue, malaria, scrub typhus, enteric fever, leptospirosis and Chikungunya. The clinical spectrum and therapeutic outcome of these cases was also studied. Methods: This retrospective study was conducted over a period of 6 months from June 2019 to December 2019. The clinical information of 126 children who tested positive for any of the causes of AUF namely dengue, malaria, scrub typhus, enteric fever, chikungunya and leptospirosis was obtained from the Paediatrics Department. The information was recorded in a predesigned proforma. Various tests performed for the diagnosis of these illnesses were noted. They included dengue NS1 antigen ELISA and IgM ELISA, peripheral blood smear (PBS) for malarial parasite and rapid malarial antigen detection test (RMAT), scrub typhus IgM ELISA, leptospira IgM ELISA, and Chikungunya IgM ELISA. Results: The diagnosis of AUF were dengue (55.5%; 70/126), malaria (19%; 24/126) and scrub typhus (19%; 24/126), enteric fever (4.7%;6/126) and Chikungunya (1.5%; 2/126). The most common presenting symptom was fever or pyrexia followed by myalgia, generalised aches and pains in the body and vomiting. Commonly observed complications included thrombocytopenia, hepatitis and shock. Conclusions: Dengue, malaria and scrub typhus are the major causes of AUF in the hospitalised children with dengue being the most prevalent infection. The study further emphasises the need to develop a systematic approach to the diagnosis of AUFs. This should be using a combination of clinical, epidemiological and laboratory parameters, which will be very useful for developing a relevant action plan for treatment and prevention of such fevers in any hospital setup.

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Radović, Jelena, Jelena Vojinović, Vladmila Bojanić, Tatjana Jevtović-Stoimenov, Gordana Kocićs, Maja Milojković, Andrej Veljković, Ivana Marković, Svetlana Stojanovic, and Dušica Pavlović. "LIPID PEROXIDATION AND OXIDATIVE PROTEIN PRODUCTS IN CHILDREN WITH EPISODIC FEVER OF UNKNOWN ORIGIN / LIPIDNA PEROKSIDACIJA I OKSIDATIVNI PROTEINSKI PRODUKTI KOD DECE SA EPIZODINOM GROZNICOM NEPOZNATOG UZROKA." Journal of Medical Biochemistry 33, no. 2 (April 1, 2013): 197–202. http://dx.doi.org/10.2478/jomb-2013-0023.

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Summary Background: Episodic fever syndromes are commonly seen in pediatric practice. Episodic fever of unknown origin (FUO) lasts for a few days or weeks and is followed by a fever-free period with a sense of well-being. In this condition, activated neutrophils and monocytes intensively generate reactive oxidative species that may further damage various mole- cules. The aim of the study was to evaluate oxidative stress biomarkers, lipid peroxidation in erythrocytes and plasma, and advanced oxidation protein products (AOPP) in children with episodic FUO. Methods: The study enrolled 25 children with episodic FUO in afebrile phase and 25 healthy children as controls. Lipid peroxidation was evaluated by measuring malondialdehyde (MDA) production with the thiobarbituric-acid-reactive sub- stances (TBARS) assay in erythrocytes and plasma. Oxidative modification of proteins was measured spectrophotometri- cally by the determination of AOPP in plasma. Results: Mean duration of episodic fevers was 3.96±2.8 years. Erythrocyte MDA levels were higher in children with FUO than in controls (86.26± 10.75 vs. 78.0±3.21 nmol/g hemoglobin), although not significantly (p=0.202). The MDA plasma concentrations were similar (2.42±0.35 vs. 2.41 ±0.39 (xmol/L) between the groups (p=0.732). Unexpectedly, levels of AOPP were significantly lower in chil- dren with FUO than in healthy controls (18.8±5.04 vs. 25.1 ±3.35 nmol/L, p=0.047). Conclusions: Episodic fevers of unknown origin with an aver- age duration of 3.96±2.8 years do not cause significant oxidative modifications of lipids and proteins in children.

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Ahirrao, Varsha Suresh, and Mohd Irfan Inamdar. "Correlation of Muco-Cutaneous Lesions with Severity of Dengue Fever in Children." Asian Journal of Clinical Pediatrics and Neonatology 7, no. 3 (September 2019): 45–48. http://dx.doi.org/10.21276/ajcpn.2019.7.3.12.

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Barik, Dr Kanai Lal. "Clinically detected Enteric Fever in Children – Blood Culture as a Diagnostic Aid." Journal of Medical Science And clinical Research 05, no. 04 (April 30, 2017): 21004–8. http://dx.doi.org/10.18535/jmscr/v5i4.199.

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K. R., Ravichandra, Bikash Ranjan Praharaj, and Sunil Agarwalla. "Opportunistic infections in HIV infected children and its correlation with CD4 count." International Journal of Contemporary Pediatrics 4, no. 5 (August 23, 2017): 1743. http://dx.doi.org/10.18203/2349-3291.ijcp20173777.

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Background: HIV infected children usually have higher viral load, weaker immune system, variable latency period, fewer opportunistic infections and fewer medicines approved for management. Knowledge of the clinical profile in HIV infected children will help in better understanding of the disease and management. The present study was aimed to study the clinical presentation, opportunistic infections, WHO clinical stage, nutritional status and its correlation with CD4 count.Methods: 50 children below 14 years of age and seropositive for HIV were included in this study and were categorized into WHO clinical stages. They were further classified based on CD4 count values in accordance with WHO classification of immunodeficiency.Results: In the study 30% of children were in the age group of 4 to 7 years. The mean age of presentation was 7.12 years. 56% of children presented with WHO clinical stage III and 30% with stage IV at first visit. Vertical transmission was the predominant mode of transmission. Anaemia (48%), fever (42%) and cough (34%) were common symptoms. Pulmonary tuberculosis (28%) was the most common opportunistic infection seen at mean CD4 count of 267±5.37.Conclusions: The manifestations of HIV infection in children mimic a number of other illnesses. Anaemia, fever and cough were the common presenting clinical features. Tuberculosis is the most common opportunistic infection in HIV infected children. As WHO clinical stage and grade of PEM increases CD4 count decreases. CD4 count is a reliable marker of disease progression in HIV infected children.

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Vangizon, Petr. "Fever in children." Spravočnik vrača obŝej praktiki (Journal of Family Medicine), no. 2 (February 1, 2020): 9–22. http://dx.doi.org/10.33920/med-10-2002-02.

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Every child has a fever — high temperature — at least once a year. There is still an opinion among parents about the extreme danger of fever, so they immediately try to bring it down, even if it is under 38 °C. Fever firmly holds the primacy in the list of symptoms when pharmacological treatment is prescribed. And doctors, wanting to alleviate condition of the child, and most importantly, trying to prescribe treatment the effect of which will be immediately visible, also often resort to the prescription of antipyretic drugs that is not always justified.

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Nizet, V., R. J. Vinci, and F. H. Lovejoy. "Fever in Children." Pediatrics in Review 15, no. 4 (April 1, 1994): 127–35. http://dx.doi.org/10.1542/pir.15-4-127.

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Journal articles on the topic 'Childbed fever'

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