Turk J Emegr Med 2014 / 3

ISSN 1304-7361

Turkish Journal of Emergency Medicine

Turkish Journal of Emergency Medicine Türkiye Acil Tıp Dergisi VOLUME 14

NUMBER 3

YEAR 2014

Citation Abbreviation: Turk J Emerg Med Visual Diagnosis A Rare Cause of Compression of the Ulnar Nerve Neuritis: Deep Vein Thrombosis Bayramoglu A, Calmasur A, Akoz A, Saritemur M Türkiye Acil Tıp Dergisi

Ultrasonographic Examination of Patella Kilic TY, Duman Atilla O ORIGINAL ARTICLES Can Intestinal Fatty Acid Binding Protein (I-FABP) Be A Marker in the Diagnosis of Abdominal Pathology?

Uzun O, Turkmen S, Eryigit U, Mentese A, Turkyilmaz S, Turedi S, Karahan SC, Gunduz A Factors Affecting Mortality and Complications in Mushroom Poisonings Over a 20 Year Period: A Report from Central Anatolia Cevik AA, Unluoglu I Rapid Intravenous Rehydration to Correct Dehydration and Resolve Vomiting in Children with Acute Gastroenteritis Azarfar A, Ravanshad Y, Keykhosravi A, Bagheri S, Gharashi Z, Esmaeeli M Sudden Suspected Death in Emergency Department: Autopsy Results Gurger M, Turkoglu A, Atescelik M, Bork T, Tokdemir M, Alatas OD, Ekingen E

VOLUME 14 NUMBER 3 YEAR 2014

The Analysis of Escherichia Coli Resistance in Urine Culture and in Antibiograms as Requested by Emergency Service Yigit Y, Yazici V, Ayhan H, Gencer EG, Halhalli HC, Karakayali O, Gunaydin YK Evaluation of Prevalence of Low Back Pain Among Residents of Tabriz University of Medical Sciences in Relation with Their Position in Work Vahdati SS, Khiavi RS, Ghafouri RR, Adimi I CASE REPORTS A Rare Cause of Chronic Headache that May Be Misdiagnosed as Migraine: Chronic Carbon Monoxide Poisoning Kanburoglu MK, Cizmeci MN, Akelma AZ Acute Coronary Syndrome During Pregnancy: A Case Report and Literature Review Yılmaz S, Sahinkus S, Kilic H, Gunduz H, Akdemir R Spontaneous Bladder Rupture and Pelvic Fracture Due To Bladder Cancer Oray D, Limon O, Ertan C, Ugurhan A A Case of Ramsay Hunt Syndrome with Atypical Presentation Kayayurt K, Yavasi O, Bilir O, Ersunan G, Giakoup B

@TrJEmergMed

Issued by The Emergency Medicine Association of Turkey This Journal is indexed in Turkish Medical Index of TUBITAK-ULAKBIM, EBSCOhost, Index Copernicus, DOAJ, Gale/Cengage Learning, SCOPUS, EMBASE and Turkiye Citation Index.

www.trjemergmed.com

ISSN 1304-7361

Turkish Journal of Emergency Medicine T羹rkiye Acil T覺p Dergisi VOLUME 14

NUMBER 3

YEAR 2014

Citation Abbreviation: Turk J Emerg Med Visual Diagnosis A Rare Cause of Compression of the Ulnar Nerve Neuritis: Deep Vein Thrombosis Bayramoglu A, Calmasur A, Akoz A, Saritemur M Ultrasonographic Examination of Patella Kilic TY, Duman Atilla O ORIGINAL ARTICLES Can Intestinal Fatty Acid Binding Protein (I-FABP) Be A Marker in the Diagnosis of Abdominal Pathology?

Uzun O, Turkmen S, Eryigit U, Mentese A, Turkyilmaz S, Turedi S, Karahan SC, Gunduz A Factors Affecting Mortality and Complications in Mushroom Poisonings Over a 20 Year Period: A Report from Central Anatolia Cevik AA, Unluoglu I Rapid Intravenous Rehydration to Correct Dehydration and Resolve Vomiting in Children with Acute Gastroenteritis Azarfar A, Ravanshad Y, Keykhosravi A, Bagheri S, Gharashi Z, Esmaeeli M Sudden Suspected Death in Emergency Department: Autopsy Results Gurger M, Turkoglu A, Atescelik M, Bork T, Tokdemir M, Alatas OD, Ekingen E The Analysis of Escherichia Coli Resistance in Urine Culture and in Antibiograms as Requested by Emergency Service Yigit Y, Yazici V, Ayhan H, Gencer EG, Halhalli HC, Karakayali O, Gunaydin YK Evaluation of Prevalence of Low Back Pain Among Residents of Tabriz University of Medical Sciences in Relation with Their Position in Work Vahdati SS, Khiavi RS, Ghafouri RR, Adimi I CASE REPORTS A Rare Cause of Chronic Headache that May Be Misdiagnosed as Migraine: Chronic Carbon Monoxide Poisoning Kanburoglu MK, Cizmeci MN, Akelma AZ Acute Coronary Syndrome During Pregnancy: A Case Report and Literature Review Y覺lmaz S, Sahinkus S, Kilic H, Gunduz H, Akdemir R Spontaneous Bladder Rupture and Pelvic Fracture Due To Bladder Cancer Oray D, Limon O, Ertan C, Ugurhan A A Case of Ramsay Hunt Syndrome with Atypical Presentation Kayayurt K, Yavasi O, Bilir O, Ersunan G, Giakoup B

@TrJEmergMed

Issued by The Emergency Medicine Association of Turkey This Journal is indexed in Turkish Medical Index of TUBITAK-ULAKBIM, EBSCOhost, Index Copernicus, DOAJ, Gale/Cengage Learning, SCOPUS, EMBASE and Turkiye Citation Index.

www.trjemergmed.com

Test early.

Treat right.

Save lives.

Her testin arkasında kurtarılacak bir yaşam vardır

Dispne ile başvuran hastalarda erken ve doğru tanı sonuçları iyileştirir ve hayat kurtarır NT-proBNP testi akut kalp yetersizliğinin tanısında/ihtimal dışı bırakılmasında ve prognozunda güçlü bir belirteçtir.1,2,3

1 Januzzi et al. (2005). Am J Cardiol. 95(8), 948-54 2 Moe et al. (2007). Circulation. 115(24), 3103-10 3 Januzzi et al. (2006). Eur Heart J. 27(22), 2619-20

Roche Diagnostics Turkey A.Ş. Esentepe Mah. Kırgülü Sok. No:4 34394 Şişli, İstanbul / Türkiye Tel 0212 306 06 06 Fax 0212 216 73 51 www.roche.com.tr

Turkish Journal of Emergency Medicine EDITORS

ASSOCIATE EDITORS

Suleyman TUREDI, M.D.

Haldun AKOGLU, M.D.

Karadeniz Technical University, Faculty of Medicine, Department of Emergency Medicine

Marmara University, Faculty of Medicine, Department of Emergency Medicine

Orhan CINAR, M.D.

Mersin University Faculty of Medicine, Department of Emergency Medicine

Gulhane Military Medical Academy (GMMA), Department of Emergency Medicine

Cem ERTAN, M.D. Izmir University Faculty of Medicine, Department of Emergency Medicine

Arzu DENIZBASI, M.D.

Nurettin Ozgur DOGAN, M.D.

Marmara University, Faculty of Medicine, Department of Emergency Medicine

Nese COLAK ORAY, M.D.

INTERNATIONAL EDITORIAL BOARD Jeffrey ARNOLD, M.D. Elizabeth DEVOS, M.D. Geijsel FEMKE, M.D. C. James HOLLIMAN, M.D. Monseireus KOEN, M.D. Mark LANGDORF, M.D. Frank LOVECCHIO, M.D. Matej MARINSEK, M.D.

Resmiye ORAL, M.D. Pini RICARDO, M.D. Petrina ROBERTA, M.D. Brown RUTH, M.D. Lemoyne SABIN, M.D. Selim SUNER, M.D. Judith E. TINTINALLI, M.D.

Seyran BOZKURT, M.D.

Kocaeli University, Faculty of Medicine, Department of Emergency Medicine Dokuz Eylul University Faculty of Medicine, Department of Emergency Medicine

Mehmet Ali KARACA, M.D.

Hacettepe University Faculty of Medicine, Department of Emergency Medicine

Ozlem KOKSAL, M.D.

Uludag University Faculty of Medicine, Department of Emergency Medicine

Serkan SENER, M.D.

Ac覺badem University, Faculty of Medicine, Department of Emergency Medicine

Ibrahim TURKCUER, M.D.

Pamukkale University, Faculty of Medicine, Department of Emergency Medicine

CONSULTING EDITORS (2014, Number 3)

RESEARCH MEDHODOLOGY EDITOR

Serhat AKAY, M.D. Okhan AKDUR, M.D. Ersin AKSAY, M.D. Can AKTAS, M.D. Basak BAYRAM, M.D. Mehtap BULUT, M.D. Tuba CIMILLI OZTURK, M.D. Serkan Emre EROGLU, M.D. Murat ERSEL, M.D.

Levent DONMEZ, M.D.

Betul GULALP, M.D. Nil HOCAOGLU AKSAY, M.D. Cemil KAVALCI, M.D. Tanzer KORKMAZ, M.D. Gul PAMUKCU GUNAYDIN, M.D. Murat OZSARAC, M.D. Serkan YILMAZ, M.D. Neslihan YUCEL, M.D.

Akdeniz University, Faculty of Medicine, Department of Public Health

FORMER EDITORS Rifat TOKYAY, M.D. (2001-2003), Hamit HANCI, M.D. (2003-2004), Oktay ERAY, M.D. (2004-2007), Sedat YANTURALI, M.D. (2006-2008), Cenker EKEN, M.D. (2007-2010, 2012), Ersin AKSAY, M.D. (2009-2011), Murat PEKDEMIR, M.D. (2010-2013)

Issued by The Emergency Medicine Association of Turkey This Journal is indexed in Turkish Medical Index of TUBITAK-ULAKBIM, EBSCOhost, Index Copernicus, DOAJ, Gale/Cengage Learning, SCOPUS, EMBASE and Turkiye Citation Index.

www.trjemergmed.com

Turkish Journal of Emergency Medicine ISSN 1304-7361

ISSUED BY THE EMERGENCY MEDICINE ASSOCIATION OF TURKEY

VOLUME 14 NUMBER 3 SEPTEMBER 2014

OWNER YILDIRAY CETE, M.D. on behalf of the Emergency Medicine Association of Turkey

CORRESPONDENCE Turkiye Acil Tip Dernegi, Cankaya Mah., Cinnah Cad., No: 51/10 Cankaya, Ankara, Turkey Tel: +90 - 312 - 438 12 66 • Fax: +90 - 312 - 438 12 68 e-mail: bilgi@tatd.org.tr, editor@trjemergmed.org Published four times a year.

PUBLISHER

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KARE YAYINCILIK | karepublishing Sogutlucesme Cad., No: 76/103, 34730 Kadikoy, İstanbul, Turkey Tel: +90 - 216 - 550 61 11 Fax: +90 - 216 - 550 61 12

Periodical

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This publication is printed on paper that meets the international standard ISO 9706: 1994.

Free full-text articles in Turkish and English are available at www.trjemergmed.com.

KARE

@TrJEmergMed

Turkish Journal of

Emergency Medicine Contents viii

Publishing with the Turk J Emerg Med

SEPTEMBER 2014

ix

Instructions for Authors

97 98

99

Visual Diagnosis A Rare Cause of Compression of the Ulnar Nerve Neuritis: Deep Vein Thrombosis Bayramoglu A, Calmasur A, Akoz A, Saritemur M Ultrasonographic Examination of Patella Kilic TY, Duman Atilla O

ORIGINAL ARTICLES Can Intestinal Fatty Acid Binding Protein (I-FABP) Be A Marker in the Diagnosis of Abdominal Pathology?

Uzun O, Turkmen S, Eryigit U, Mentese A, Turkyilmaz S, Turedi S, Karahan SC, Gunduz A

104

Factors Affecting Mortality and Complications in Mushroom Poisonings Over a 20 Year Period: A Report from Central Anatolia Cevik AA, Unluoglu I

111

Rapid Intravenous Rehydration to Correct Dehydration and Resolve Vomiting in Children with Acute Gastroenteritis Azarfar A, Ravanshad Y, Keykhosravi A, Bagheri S, Gharashi Z, Esmaeeli M

115

Sudden Suspected Death in Emergency Department: Autopsy Results Gurger M, Turkoglu A, Atescelik M, Bork T, Tokdemir M, Alatas OD, Ekingen E

121

The Analysis of Escherichia Coli Resistance in Urine Culture and in Antibiograms as Requested by Emergency Service Yigit Y, Yazici V, Ayhan H, Gencer EG, Halhalli HC, Karakayali O, Gunaydin YK

125

Evaluation of Prevalence of Low Back Pain Among Residents of Tabriz University of Medical Sciences in Relation With Their Position in Work Vahdati SS, Khiavi RS, Ghafouri RR, Adimi I

CASE REPORTS

132

A Rare Cause of Chronic Headache that May Be Misdiagnosed as Migraine: Chronic Carbon Monoxide Poisoning Kanburoglu MK, Cizmeci MN, Akelma AZ

135

Acute Coronary Syndrome During Pregnancy: A Case Report and Literature Review Y覺lmaz S, Sahinkus S, Kilic H, Gunduz H, Akdemir R

139

Spontaneous Bladder Rupture and Pelvic Fracture Due To Bladder Cancer Oray D, Limon O, Ertan C, Ugurhan A

142

A Case of Ramsay Hunt Syndrome with Atypical Presentation Kayayurt K, Yavasi O, Bilir O, Ersunan G, Giakoup B

Turkish Journal of

Emergency Medicine Publishing with the Turk J Emerg Med

1. The Turkish Journal of Emergency Medicine (Turk J Emerg Med) is published four times per year. The total number of original research articles is 15 per year and research articles (including original research, case studies, letters to the editor and reviews) constitute at least 50% of the published material. Every issue published will contain a minimum of 4 research articles. Apart from the research articles, Turk J Emerg Med also publishes articles in the categories of case studies, case series, visual diagnoses in emergency medicine, letters to the editor, brief reports, reviews and evidence based emergency medicine in consultation with the editorial board.

Reviews are presented upon invitation from the editor.

2. All reviewer comments, signed copies of manuscripts and corrections will be kept in digital format in the journal archives for a minimum period of 5 years.

3. The submitted manuscripts are first reviewed by the journal’s editor who determines whether the manuscript deserves further evaluation or not. For submissions that are granted further evaluation, the editor assigns the manuscript to one of the assistant editors.

The editor and the assistant editor then forwards the manuscript to two reviewers or one reviewer and a member of the scientific board for evaluation. If both the editor and the assistant editor determines the manuscript is not scientifically valuable or not an original work, or if it does not relate to emergency medicine or does not address the journal’s target audience, then they reject the manuscript directly without forwarding it to the reviewers.

4. The goal of the Turk J Emerg Med is to notify the authors with the acceptance of their submission for peer review within 14 days, peer review period of 21 days and final evaluation and notification of 28 days from the receipt of the manuscript. The authors are given 10 days for minor revisions and 20 days for major revisions. The final page layout is provided to the authors

within 30 days of the acceptance of the manuscript for publication, for final review and proof.

5. The assistant editor may consult the research methodology editor to clarify any problems in the statistical design and evaluation of the study during the peer review process. Even if such consultation is not sought during the review process, it can be implemented upon request of the editor in chief prior to the final acceptance of the manuscript.

6. All manuscripts containing material written in English will be evaluated by the language editor before the manuscripts are considered for publication.

7. Manuscripts submitted to the Turk J Emerg Med are expected to conform with the Helsinki Declaration and meet the common requirements of the biomedical journals.

8. Articles are listed on the content page and are published in appropriate sections (original research, case report, review, etc.).

9. The journal is printed on acid-free paper.

10. Advertisements are not allowed within articles.

11. The editor(s) of the Turk J Emerg Med are elected by the Board of the Emergency Medicine Association of Turkey once a year in January. The Turk J Emerg Med board consists of editor(s), assistant editors, a research methodology editor and a language editor.

12. All material published in the Turk J Emerg Med are the property of the Emergency Medicine Association of Turkey. This material may not be referred without citation nor may it be copied in any format. Authors are responsible for all statements made in their articles.

Editors of the Turk J Emerg Med Assoc. Prof. Dr. Suleyman TUREDI Assoc. Prof. Dr. Orhan CINAR Prof. Dr. Arzu DENIZBASI

Turkish Journal of

Emergency Medicine Instructions for Authors Turk J Emerg Med is the official publication of the Emergency Medicine Association of Turkey. It is a peer-reviewed journal that publishes national and international articles. Founded in 2000, it is the first journal of its kind in Turkey and is indexed in the Turkish Medical Index, EBSCO Host, Index Copernicus, DOAJ, Gale/Cengage Learning, SCOPUS, EMBASE and Turkiye Citation Index. Turk J Emerg Med publishes articles relevant to emergency medicine and emergency medical services such as; scientific research, case reports, case series, visual diagnoses, brief reports, evidence based emergency medicine articles, opinions and relevant scientific announcements.

The main sections of the journal include emergency medicine systems, academic emergency medicine, emergency medicine education, emergency department management, disaster medicine, environmental emergencies, trauma, resuscitation, analgesia, pediatric emergencies, medical emergencies, pre-hospital medicine, toxicology, emergency nursing, health policy, ethics, management, imaging and procedures.

The articles published in the Turk J Emerg Med are expected to conform with the Helsinki Declaration and meet the common requirements of biomedical journals. Further information can be found in the following article: “Uniform requirements for manuscripts submitted to biomedical journals and declaration of Helsinki; Recommendations guiding physicians in biomedical research involving human subjects. JAMA 1997;277:927-934” The editorial board of the Turkish Journal of Emergency Medicine is appointed by the Board of the Emergency Medicine Association of Turkey once a year in December.

CATEGORIES Research Articles: Original studies of basic or clinical investigations in emergency medicine. Turkish and English abstracts are required. Articles must include introduction, material and method, results, discussion, limitations and conclusion sections. The maximum number of words is 4,000 with a total of six tables or figures are allowed. For single centre studies the number of authors is limited to eight. The approval from the Institutional Review Board (IRB) is required prior to publication. Pharmeceutical studies require approval from the Regional Ethics Board prior to publication.

Case Reports: Brief descriptions of clinical cases or the complications that are seldom encountered in emergency medicine practice and have an educational value. Consideration will be given to articles presenting clinical conditions, clinical manifestations or complications previously undocumented in the existing literature and unreported side of adverse effects of the known treatment regimes or scientific findings that may trigger further research on the topic. Turkish and English abstracts are required. Case reports must include introduction, case presentation and discussion sections. They must be limited to 1,500 words, contain 15 references or less and two tables or figures. A maximum of five authors for a case study will be permitted.

Case Series: Brief descriptions of clinical cases or the complications that are seldom encountered in emergency medicine practice and have educational value. Case series must include introduction, case presentation and discussion sections. They must be limited to 2,500 words, contain 15 references or less and three tables or figures. A maximum of six authors for a case series will be permitted.

Brief Reports: Reports involving a small number of cases that require further investigation. Preliminary data and results are shared. Turkish and English abstracts are required. Reports must include introduction, methods, results, discussion, limitations and conclusion sections. They are limited to 4,000 words and four tables or figures. For single centre studies he number of authors are limited to six. Approval from the Institutional Review Board (IRB) is required prior to publication. Pharmeceutical studies require approval from the Regional Ethics Board approval prior to publication.

Concepts: Clinical or non-clinical articles related to the field of emergency medicine and detailing improvements to emergency medicine practice.

Turkish and English abstracts are required. The manuscripts must not exceed 4,000 words and limited three authors per article.

Review Articles: Comprehensive articles reviewing national and international literature related to current emergency medicine practice. Generally Turk J Emerg Med publishes invited review articles. Other authors should contact the editor prior to submission of review articles. Manuscripts must be limited to 4,000 words and a maximum two authors. There is no limit to the number of references.

Evidence-Based Emergency Medicine: Articles seeking to detail clinical and medical practices should present a clinical scenario followed by the research question(s), followed by a selection of the best available evidence, analysis of the evidence and the application of the evidence. Turkish and English abstracts are required. The manuscript must be limited to 4,000 words and a maximum of four authors. The authors should also submit copies of the articles proposed as supporting evidence.

Images in Emergency Medicine: Short case reviews with interesting and educative visual material. The case study is to be presented in two parts.

In the first part, the case is summarized and the image is presented. In the second part, the diagnosis is provided in the heading, followed by a discussion of the management of the case and the specifications of the images.

The review should consist of a maximum of 500 words and 5 references are allowed. The article should be prepared by no more than two authors.

There is no need for abstract.

Letter to the Editor: Opinions, comments and suggestions made concerning articles published in Turk J Emerg Med or other journals. Letters should contain a maximum of 1,000 words and 5 references are allowed for these single author submissions. No abstract is required.

SUBMITTING MANUSCRIPTS Turk J Emerg Med accepts online manuscript submission. Users should go to the journal’s web site (http://www.journalagent.com/tatd/) and create an account before submitting their manuscripts.

REQUIRED SUBMISSION DOCUMENTS Cover Letter: The author(s) should present the title, type and category of the article, and whether the submitted work had previously been presented in a scientific meeting. In addition, the full name of the corresponding author and his/her contact information including the address, phone number, fax number and email address should be provided at the bottom of the cover letter.

Title Page: On the title page, the title of the article, and the names of the authors’, including their academic titles and institutions should be listed in order. In addition, the running title and the name of the corresponding author along with his/her contact information should be provided.

For the Blind Initial Review: The names of the authors’, and any identifying information including the academic titles, institutions and addresses must be omitted. Manuscripts submitted with any information pertaining to the author(s) will be rejected.

MANUSCRIPT PREPARATION Turkish and English Abstracts: Turkish and English abstracts containing a maximum of 250 words are required for original research articles, evidence based emergency medicine and brief reports. The abstracts for original research articles and brief reports must contain four sections including the aim, material and method, results and conclusion. For a case report of medical care the Turkish and English abstracts should not exceed 150 words.

Turkish Journal of

Emergency Medicine Instructions for Authors Key Words: Key words must be chosen carefully from PubMed MeSH (www. nlm.nih.gov) websites.

Sections of Original Research Articles: Original research articles should contain the following sections: Introduction: A three-paragraph structure should be used. Background information on study subject (1st paragraph), context and the implications of the study (2nd paragraph) and the hypotheses and the goals of the study (3rd paragraph).

Material and Method: The method section, is one of the most important sections in original research articles, and should contain sufficient detail.

The investigation method, study sample, analyses performed, commercial statistical programs used, details of measurement and evaluation (e.g.: make and model of biochemical test devices and kits) should all be clearly stated. There should be a list of the inclusion exclusion criteria. In survey studies, information concerning who implemented the survey and how it was performed should be specified.

Results: The demographic properties of the study population, the main and secondary results of the hypothesis testings must be provided. Commenting on the results and discussing the literature findings should be avoided in this section. The results should be presented with graphs, mean, median and standard deviation values as well as a 95% confidence interval.

Discussion: The main and secondary results of the study should briefly presented and compared with similar findings in the literature. Providing intensive and encylopedical information should be avoided in this section.

Limitations: The limitations of the study should be mentioned in a separate paragraph subtitled as the “Limitations” in the end of the discussion.

Conclusion: A clear conclusion should be made in the light of the results of the study. The potential effects of the results of the study on the current clinical applications should be stated in a single sentence. Inferences that are not supported by the study results should be avoided.

Points to be considered for general writing Statistical Analysis: All studies should be analysed in consultation with those experienced in statistical analysis.

Units of Measure: Standard units of measure should be used when presenting the substances used, drugs and laboratory values. Normal limits should be provided for the laboratory values.

Drugs: Generic names for drugs should be used. Doses and routes for the drugs should be stated.

Use of Turkish/English: Proper use of Turkish/English terminology and grammar should be emplolyed.

References: References should be written double spaced at the end of the article. They should be numbered in the order they appear in the text, and not listed alphabetically. The references that are used in the “Abstract” section should be stated as “(abstract)”. The names of the first three authors should be included in a given reference followed by “et al”. The authors are responsible for the accuracy of the references.

Examples of Referencing Article: Raftery KA, Smith-Coggins R, Chen AHM. Gender-associated differences in emergency department pain management. Ann Emerg Med 1995;26:414-21.

Book: Callaham ML. Current Practice of Emergency Medicine. 2nd ed. St. Luis, MO: Mosby; 1991.

Book Chapter: Mengert TJ, Eisenberg MS. Prehospital and emergency medicine thrombolytic therapy. In: Tintinalli JE, Ruiz E, Krome RL, eds. Emergency Medicine: A Comprehensive Study Guide. 4th ed. New York, NY: McGrawHill;1996:337-343.

Courses and Lectures (unpublished): Sokolove PE, Needlesticks and high-risk exposure. Course lecture presented at: American College of Emergency Physicians, Scientific Assembly, October 12, 1998, San Diego, CA. Internet: Fingland MJ. ACEP opposes the House GOP managed care bill.

American College of Emergency Physicians Web site. Available at: http:// www.acep.org/press/pi980724.htm. Accessed August 26, 1999.

Personal Communication: Use of personal communications should be avoided. If necessary, the person’s name, academic title, and the month and year of the communication should be included in the reference. A letter of permission from the person refered to should accompany the manuscript.

Tables: Tables summarizing the data should be clearly formatted. Data presented in the tables should not be included in its entireity in the text. Tables must be numbered consecutively. Each table must be referred to in the text.

Figures / Pictures: The information contained in the figure/image should not be repeated in its entirety, however reference to the figure/image must be referred in the text. Pictures should be saved in JPEG, EPS or TIF format.

Color and gray scaled pictures should have a minimum resolution of 300 dpi and the line art should be at least 1200 dpi.

JOURNAL POLICY Original Content: The Turk J Emerg Med prefers publishing randomized controlled trials (RCTs) as they provide higher level of evidence. All articles containing original information and data must not have been published or simultaneously submitted for publication in another scientific journal. This restriction does not apply to an abstract presented in scientific meetings and congresses.

Multiple Authors: All authors share the responsibilities of the content and duties in the preparation of the submitted material.

Statistical Consultant: All articles containing statistical analysis must be prepared in consultation with an individual experienced in statistical analysis in the given subject. One of the authors or a person other than the author(s) who experienced in statistical analysis should claim responsibility for the correctness of the statistical information.

Randomized Controlled Trials (RCTs): The journal prefers to publish RCTs. Permissions: Written consent for reproduction should accompany any submitted material, such as the tables and figures that have appeared in another journal or a book . Approval from the appropriate ethics board should be obtained for original research and written consent should be obtained from the patients refered to in case reports, images and case series.

REVIEW AND PUBLICATION PROCESS Initial Review: A blind initial review is performed for all submitted material. The editor will review all the manuscripts for completeness and content. Then the material will be assigned to one of the assisstant editors for further evaluation. If required, requests for revisions are sent to the authors by the editors. The editor of the Turk J Emerg Med can on occasion accept or reject submitted material without sending it for further review.

Responsibility for Published Information: The authors are responsible for all the information contained in the text. Turk J Emerg Med is not responsible for statements made by the author(s).

Copyright: All or part of the published articles, including the tables and figures contained in them, may not be published elsewhere without the approval and written consent of the editor of the Turk J Emerg Med and the board members of the Emergency Medicine Association of Turkey.

Access to Data: Editors of the Turk J Emerg Med may request the author(s) to submit the original data during the peer-review process in order to better assess the manuscripts. It is, therefore, vital to submit a full address and other contact information on the title page of the manuscript.

VISUAL DIAGNOSIS

A Rare Cause of Compression of the Ulnar Nerve Neuritis: Deep Vein Thrombosis Atif BAYRAMOGLU,1 Altan CALMASUR,2 Ayhan AKOZ,1 Murat SARITEMUR1 Deparment of Emergency, Ataturk University Faculty of Medicine, Erzurum;

1

Department of Radiology, Regional Training and Research Hospital, Erzurum

2

A 21-year-old woman presented to the emergency department with complaint of pain in the right elbow, and ring and pinky finger numbness. The patient had no prior history of systemic disease.

The patient reported similar symptoms had occurred intermittently after physical exertion during the previous three months. However, the patient presented at the hospital after experiencing the symptoms while at rest. Physical examination identified a palpable soft mass at the beginning of the third distal humerus and extending to the cubital region on the inner side of the right elbow with the consistency of the dough. The Tinel test was positive. Other system examination findings were normal. The patient’s laboratory findings, complete blood count and blood chemistry tests were normal. Magnetic resonance imaging of the patient is shown in Figure 1 and Figure 2a, b. [see page 130 for diagnosis]

Figure 1. An increase in brachial diameter and thrombus in fat-suppressed proton density T1-weighted MR images sequences at the same level (*).

(a)

(b)

Figure 2. (a) An increase in brachial diameter and thrombus in axial T1-weighted MR images. Thin white arrows: brachial vein filled within thrombus. *: m. pronator teres, **: m. brakialis, black triangles: a. brachialis, curved white arrow: v. basilica, thick white arrow: v. cephalica. (b) An increase in brachial diameter and thrombus in fat-suppressed proton density in the axial image at the same level with figure 2a.

Submitted: August 21, 2013 Accepted: October 31, 2013 Published online: January 20, 2014 Correspondence: Dr. Atıf Bayramoğlu. Ataturk Universitesi Tıp Fakultesi Kampus, 25240 Erzurum, Turkey. e-mail: atifbay@gmail.com

Turk J Emerg Med 2014;14(3):97 [130]

doi: 10.5505/1304.7361.2014.59319

97

VISUAL DIAGNOSIS

98

Ultrasonographic Examination of Patella Turgay Y覺lmaz KILIC, Ozge DUMAN ATILLA Department of Emergency Medicine, Tepecik Training and Research Hospital, Izmir

A 52-year-old female patient presented to the emergency department (ED) complaining of knee pain after falling. Upon admission to the ED, vital signs of the patient were normal. Physical examination revealed mild swelling and tenderness on the right patella, limitation of motion of the knee, and difficulty walking.

Neurovascular examination was within normal limits. Bedside ultrasonographic examination (Mindray簧 M5, Color Diagnostic Ultrasound System, China) was performed before X-rays (Figure 1). [see page 131 for diagnosis]

Figure 1. Cortical disruption (arrow) and hematoma (asterisk) of patella with longitudinal ultrasonography view.

Submitted: April 18, 2014 Accepted: April 30, 2014 Published online: June 24, 2014 Correspondence: Dr. Turgay Yilmaz Kilic. Izmir Tepecik Egitim ve Arastirma Hastanesi, Acil Tip Klinigi, Izmir, Turkey. e-mail: turgayyilmaz.kilic@gmail.com

Turk J Emerg Med 2014;14(3):98 [131]

doi: 10.5505/1304.7361.2014.39260

ORIGINAL ARTICLE

Can Intestinal Fatty Acid Binding Protein (I-FABP) Be A Marker in the Diagnosis of Abdominal Pathology?

FABP’nin İntestinal Tipi (I-FABP) Abdominal Patolojilerin Tanısında Belirteç Olabilir mi?

Ozlem UZUN,1 Suha TURKMEN,2 Umut ERYIGIT,2 Ahmet MENTESE,3 Serdar TURKYILMAZ,4 Suleyman TUREDI,2 Suleyman Caner KARAHAN,5 Abdulkadir GUNDUZ2 Department of Emergency Medicine, Bagcilar Training and Research Hospital, İstanbul; Department of Emergency Medicine, Karadeniz Technical University Faculty of Medicine, Trabzon; 3 Department of Biochemistry, Karadeniz Technical University Faculty of Medicine, Trabzon; 4 Department of General Surgery, Karadeniz Technical University Faculty of Medicine, Trabzon; 5 Department of Biochemistry, Ozel Yildizli Guven Hospital, Trabzon 1

2

SUMMARY

ÖZET

Objectives Biochemical markers play an important role in the early diagnosis of abdominal pain. This study aimed to investigate the diagnostic value of intestinal type fatty acid binding protein (I-FABP) in patients with abdominal pathology.

Amaç Biyokimyasal belirteçler karın ağrısının sebebinin erken tanısında oldukça önemlidir. Bu çalışmada FABP’nin intestinal tipinin (I-FABP) abdominal patolojisi olan hastaların ayırıcı tanısındaki değeri araştırıldı.

Methods This prospective and descriptive study was performed at the University Hospital Emergency Department. Serum I-FABP levels of patients presenting with acute abdominal pain were measured at time of admission and were compared with those of healthy individuals.

Gereç ve Yöntem Mevcut çalışma üniversite hastanesi acil servisinde ileriye yönelik tanımlayıcı olarak çalışma gerçekleştirildi. Karın ağrısı şikayeti ile acil servise başvuran hastalarda başvuru anında alınan serum örneklerinden I-FABP değerlerine bakıldı. Bulgular sağlıklı gönüllülerdeki düzeyler ile karşılaştırıldı.

Results The mean I-FABP level of the 171 patients enrolled in this study was 170.1±543.4 pg/ml, while that of a healthy control group was 61.4±47.4 pg/ml. Although I-FABP levels were higher in the patient group, this difference was not statistically significant (p>0.05).

However, I-FABP levels of patients with mesenteric ischemia and intra-abdominal mass were significantly higher than those of healthy individuals (p<0.05).

Bulgular Kayıtlı 171 hastada ölçülen ortalama I-FABP seviyesi 170.1±543.4 pg/ ml olarak belirlendi. Sağlıklı gönüllülerde I-FABP seviyesi 61.4±47.4 pg/ ml olarak bulundu. Hasta grubunun I-FABP seviyeleri sağlıklı gönüllülere göre yüksek olarak bulunmuşsa da, aradaki fark istatistiksel olarak anlamlı değildi (p>0.05). Başvuru anında ölçülen I-FABP seviyeleri sağlıklı gönüllülerle kıyaslandığında akut mezenter iskemide (AMI) ve karıniçi kitle tespit edilen hastalarda istatistiksel olarak anlamlı yüksekti (p<0.05).

Conclusions I-FABP levels that are evaluated at time of admission in patients presenting with abdominal pain to the emergency department are significantly higher in patients with mesenteric ischemia and intraabdominal mass than are those of healthy individuals.

Sonuç Acil servise karın ağrısı şikayeti ile başvuran hastalardan mezenter iskemi ve karıniçi kitle tanısı alan hastalarda başvuru anında ölçülen serum I-FABP değerleri sağlıklı gönüllülere kıyaslandığında anlamlı olarak yüksek bulunmuştur.

Key words: Abdominal mass; abdominal pain; I-FABP; mesenteric ischemia.

Anahtar sözcükler: Karın ağrısı; batında kitle; I-FABP; mezenter iskemisi.

Submitted: July 23, 2013 Accepted: May 06, 2014 Published online: June 24, 2014 Correspondence: Dr. Umut Eryigit. Karadeniz Teknik Universitesi Tip Fakultesi, Acil Tıp Anabilim Dali, 61080 Trabzon, Turkey. e-mail: umuteryigitacil@gmail.com

Turk J Emerg Med 2014;14(3):99-103

doi: 10.5505/1304.7361.2014.15679

99

Turk J Emerg Med 2014;14(3):99-103

100

Introduction Biochemical markers can be easily obtained, are widely used, and are becoming very important in the early diagnosis of abdominal pathology. Specific biochemical markers have been reported for several pathologies, including alanine aminotransferase for hepatic injury and amylase for pancreatitis.[1] Although several studies have been published regarding this issue, several abdominal pathologies have no specific biochemical markers. These previously published studies include investigations regarding the diagnostic and prognostic values of D-dimer, MMP-9, IMA, I-FABP, alpha glutathione S transferase, D-lactate and S100 A8/A9 levels in patients with abdominal pain.[2-8] Fatty acid binding protein (FABP) is a small (12-15 kDa) intracellular protein that increases in conditions such as inflammation and ischemia. It plays a role in protecting cells from the side effects of fatty acids and increases in association with various pharmacological and pathophysiological effects, such as ischemia.[9] Several types of FABP have been described immunologically, including heart, intestinal, liver, epidermal, muscle and adipocyte. Intestinal FABP (I-FABP) is located exclusively in gastric epithelial cells and intestinal mucosa.[10] Recently, Vermeulen et al. reported that I-FABP levels increase significantly due to intestinal ischemia after aortic surgery.[11] Another study

by Relja et al. showed that I-FABP and liver FABP (L-FABP) levels increase after abdominal trauma and are correlated with the severity of abdominal tissue injury in patients with polytrauma.[12] The purpose of this study was to compare I-FABP levels in patients admitted to the emergency department with abdominal pain and who were preliminarily diagnosed with abdominal pathology with I-FABP levels in a healthy control group. This study was based on the hypothesis that I-FABP may be a useful diagnostic marker in the differential diagnosis of abdominal pathology.

Materials and Methods This prospective and descriptive study was performed with patients who presented to our University Hospital Emergency Department between June 2009 and June 2010 with abdominal pain and who were diagnosed with abdominal pathology by emergency physicians and general surgeons. Patients were diagnosed on the basis of physical examination, ultrasonography and computerized tomography. Patients with trauma (n=80), pain lasting longer than 48 hours (n=24), those who were younger than 18 years (n=46), those who were unavailable for monitoring (n=13) and those who declined to participate (n=23) were excluded from the study. The control group consisted of age and

gender matched healthy hospital employees with no history of abdominal pathology. Approval for this study was obtained from the Ethics Committee of Karadeniz Technical University, Turkey (2009-21). Patients enrolled in the study were registered using a form that included demographic data, written permission, and routine patient evaluation data such as histories, physical examination results, biochemical values and radiological results. Venous blood specimens (10 cc) were taken from patients who presented to the emergency department with abdominal pain in order to measure serum I-FABP levels. Serum specimens obtained by centrifugation at 3000 x g for 10 min were kept at -20ºC for a maximum of 6 months. Serum I-FABP levels were measured simultaneously at the end of the collection process.

Human serum I-FABP levels from patients and healthy individuals were measured using a commercial ELISA (EnzymeLinked Immunosorbent Assay kit; Hycult Biotech, the Netherlands) kit according to the manufacturer’s instructions.

Absorbance values were measured using a VERSA max tunable microplate reader (designed by Molecular Devices in California, USA) at a wavelength of 450 nm. Results were expressed as picograms/mL. Data were analyzed using SPSS version 10.0. Standard deviations of means and percentage frequency distributions were used as descriptive statistics. Normal distributions were calculated using the Kolmogorov-Smirnov test for numeric data. Nonparametric data were analyzed using the MannWhitney U test. The chi-square test was used for analyzing nominal parameters.

The sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and optimal cut-off value of I-FABP in patients presenting with abdominal pain were calculated using a receiver operating curve (ROC) analysis. The ROC analysis was used to determine the causes of abdominal pain for which the mean I-FABP levels were higher than those in healthy individuals.

Results Three hundred and one cases were enrolled in this study, with 130 in the control group and 171 in the patient group.

The mean age of the patient group was 52±21 years (range: 18-92 years) and was 56±8 years for healthy individuals.

The mean I-FABP level in the 171 patients was 170.1±543.4 pg/ml and was 61.4±47.4 pg/ml in the 130 healthy volunteers. Although the I-FABP levels in the patient group were higher than those in the healthy individuals, this difference was not statistically significant (p>0.05).

Uzun O et al.

Intestinal Fatty Acid Binding Protein and Diagnosis of Abdominal Pathology

Table 1. I-FABP values of patients admitted to the emergency department with abdominal pain at the time of presentation Definitive Diagnosis (n)

I-FABP levels pg/ml

(Mean±SD) Nonspecific abdominal pain (n=51)

53.5±55.7

Appendicitis (n=11)

73.9±131.4

Gall bladder diseases (n=30)

290.8±708.5

Ileus-volvulus (n=17)

130.8±221.9

Pancreatitis (n=14)

112.1±167.1

Mesenteric ischemia (n=7)

708.6±669.1*

Ovarian diseases (n=6)

Our results show that the mesenteric ischemia and intra-abdominal mass patients were the only patients whose I-FABP levels were significantly higher than those of the healthy individuals. In addition, the I-FABP levels of the mesenteric ischemia patients were significantly higher than those of the mass patients. I-FABP sensitivity, specificity and ROC curves for NPV and PPV values were determined for these 2 diseases, and these data are shown in Figures 1 and 2.

387.4±1380.2*

Gastritis–peptic ulcer (n=2)

65.1±34.1

Urolithiasis nephrolithiasis (n=11)

40.7±32.1

Hernia (n=4)

76.6±97.3

Perforation (n=1)

438.1

Total Patient (n=171)

ovarian diseases, 15 (8.8%) with intra-abdominal mass, 2 (1.2%) with gastritis-peptic ulcer, 11 (6.4%) with nephrolithiasis-urolithiasis, 4 (2.3%) with herniation, 1 (0.6%) with perforation and 51 (29.8%) with non-specific abdominal pain.

The patients’ I-FABP levels were expressed as groups and subgroups (Table 1). The average values for the acute mesenteric ischemia group and the intra-abdominal mass group were 708.6±669.1 pg/ml and 387.4±1380.2 pg/ml, respectively.

129.3±261.2

Mass (n=15)

101

170.1±543.3

*p<0.05 for mean I-FABP levels between the patient and control groups.

The optimum cut-off I-FABP levels for the mesenteric ischemia and intra-abdominal mass patients according to ROC analysis as well as the sensitivity, specificity, NPV and PPV values for these levels are shown in Table 2.

The patients were definitively diagnosed as follows: 11 (6.4%) with appendicitis, 30 (17.5%) with gall bladder diseases, 17 (9.9%) with ileus-volvulus, 14 (8.2%) with pancreatitis, 7 (4.1%) with mesenteric ischemia, 6 (3.5%) with

The mean I-FABP level of the 49 patients who underwent surgery was 173.54387 pg/ml, and that of the 122 patients who did not undergo surgery was 168.6516 pg/ml. The difference between these values was not statistically significant (p>0.05).

Control (n=130)

61.4±47.4

100

80

80

Sensitivity: 71.4 Specificity: 94.6 Criterion: >144.9131

60

Sensitivity

Sensitivity

100

40

20

60

Sensitivity: 60.0 Specificity: 83.8 Criterion: <=14.6797

40

20

0

0 0

20

40 60 100-Specificity

80

100

Figure 1. ROC curve of I-FABP values showing cut-off value, sensitivity, and specificity for mesenteric ischemia patients.

0

20

40 60 100-Specificity

80

100

Figure 2. ROC curve of I-FABP values showing cut-off value, sensitivity, and specificity for mass patients.

Turk J Emerg Med 2014;14(3):99-103

102

Table 2. Sensitivity, specificity, PPV and NPV values for patients with mesenteric ischemia and mass

AUC Cut-off Sensitivity Specificity PPV NPV

For mesenteric ischemia

0.755

144.9

71.4

94.6

41.7

98.4

For mass

0.695

14.7

60.0

83.8

30.0

94.8

Discussion Abdominal pain can be simple, but it may also be associated with life-threatening pathology. The early diagnosis of acute abdominal pain in the emergency department is highly important, especially for pathologies that may require surgical intervention. The most common etiological causes of abdominal pain are appendicitis, cholecystitis, small bowel obstruction, urinary colic, peptic ulcer perforation, pancreatitis and diverticulitis.[13] In their review of abdominal pain, Grundmann et al.[14] reported that the most frequent cause of acute abdominal pain was nonspecific abdominal pathology (24%-44.3%), followed by appendicitis (15.9%-28.1%) and biliary disease (2.9%-9.7%). Similarly, the most common cause of acute abdominal pain in our study was nonspecific abdominal pathology (29.8%), followed by gall bladder diseases (17.5%), ileus-volvulus (9.9%), intra-abdominal mass (8.8%), acute pancreatitis (8.2%), acute appendicitis (6.4%) and mesenteric ischemia (4.1%). The breakdown of patient groups in our study may be different from those previously published because our study was performed in a tertiary teaching and research hospital that works in co-ordination with other institutions.

Both clinical findings and laboratory tests are often used for diagnosing acute abdomen. White blood cell (WBC) count is an important and oft-used laboratory parameter,[15] and Ddimer is frequently used in the evaluation of patients with acute abdominal pain.[1,16] Studies have reported that MMP-9 levels are increased in patients with ureteral stones, acute cholecystitis and intestinal obstructions.[4] Significantly elevated ischemia modified albumin (IMA) levels have also been reported in mesenteric ischemia models.[5] Several recent reviews have indicated that the most optimistic plasma biomarkers are I-FABP, alpha-glutathione S-transferase and D-lactate. I-FABP and alpha-glutathione S-transferase are localized in the mucosa of the small intestine. Since intestinal injury during acute mesenteric ischemia begins at the intestinal mucosa, these markers can potentially be used in the early phase.[17] In addition, I-FABP, alpha-glutathione S-transferase and CK-MB levels differed significantly from the control group in a suspected acute mesentery ischemia population. Serum phosphate level has also been investigated for the diagnosis of acute mesentery ischemia. Clinical and experimental studies have shown that the increase in serum

phosphate levels in acute mesentery ischemia develops following ischemia-related intestinal necrosis and widespread cell death. Therefore, elevated serum phosphate is not a suitable marker for the early diagnosis of acute mesentery ischemia. However, it can be used as a prognostic indicator as well as an indicator of irreversible intestinal necrosis.[18,19] Evennett et al.[1] reported that the most reliable plasma markers for intestinal ischemia are I-FABP, which is present in the mucosa of the small intestine, alpha-glutathione Stransferase, and D-lactate, which is released from bacteria in the intestinal lumen as a product of bacterial fermentation.

Another study showed that an alpha-glutathione S-transferase level <4 ng/ml has a 100% negative predictive value in eliminating ischemic intestinal disease. The same study also showed that the increase in alpha GST levels had a negative predictive value of 92% in patients with suspected acute mesentery ischemia.[6] Bealer et al.[7] determined a diagnostic value of S100A8/A9 (calgranulin A/B) with 93% sensitivity and 54% specificity in patients with suspected acute appendicitis.

In a clinical study investigating the use of I-FABP as a marker in acute abdomen cases, Kanda et al.[20-22] enrolled a total of 96 individuals. Of these, 13 were diagnosed pre-surgically with ischemic intestinal disease (5 cases of mesenteric ischemia and 8 of strangulated hernia), 48 had a diagnosis of acute abdomen, and 35 served as healthy controls. This study also reported significantly high I-FABP values (>100 ng/mL) in 5 cases with mesenteric ischemia.

Tรถlle et al.[23] reported elevated B-FABP in renal cell carcinoma patients and recommended that wider series be investigated to determine whether B-FABP could act as a tumor marker. Abdominal mass may cause ischemia, inflammation and intestinal membrane cell destruction, which do not typically lead to elevated FABP. These secondary causes may be assistant factors in these proteins being released into serum.

In our study with 171 patients and 130 healthy controls, the mean I-FABP levels were 170 pg/ml in the patient group and 61 pg/ml in the control group. Although there was a considerable numerical difference between these two means, this difference was not significant. Among the abdominal pathologies included in our study, I-FABP levels were only sig-

Uzun O et al.

Intestinal Fatty Acid Binding Protein and Diagnosis of Abdominal Pathology

nificantly higher in patients with acute mesenteric ischemia and intra-abdominal mass when compared with the control group. However, there were no significant differences between I-FABP values among subgroups (p>0.05).

Conclusions Although average I-FABP levels of patients presenting to the emergency department with abdominal pain at the time of admission were higher than those of the healthy individuals, this difference was not statistically significant. Serum I-FABP levels of patients presenting with abdominal pain and diagnosed with mesenteric ischemia and intra-abdominal mass were significantly higher when compared to those of the healthy volunteers. Therefore, I-FABP levels may be used to diagnose such fatal pathologies. Further studies with wider series are needed in order to investigate the diagnostic value of I-FABP in patients with abdominal pain.

Limitation The very low patient numbers in some of the subgroups made it impossible to obtain reliable statistical data. Therefore, I-FABP should be investigated in wider study groups.

Conflict of Interest The authors declare that there is no potential conflicts of interest.

References 1. Evennett NJ, Petrov MS, Mittal A, Windsor JA. Systematic review and pooled estimates for the diagnostic accuracy of serological markers for intestinal ischemia. World J Surg 2009;33:1374-83.

2. Acosta S, Nilsson TK, Björck M. D-dimer testing in patients with suspected acute thromboembolic occlusion of the superior mesenteric artery. Br J Surg 2004;91:991-4.

3. Acosta S, Nilsson TK, Björck M. Preliminary study of D-dimer as a possible marker of acute bowel ischaemia. Br J Surg 2001;88:385-8.

4. Solberg A, Holmdahl L, Falk P, Palmgren I, Ivarsson ML. A local imbalance between MMP and TIMP may have an implication on the severity and course of appendicitis. Int J Colorectal Dis 2008;23:611-8.

5. Gunduz A, Turkmen S, Turedi S, Mentese A, Yulug E, Ulusoy H, et al. Time-dependent variations in ischemia-modified albumin levels in mesenteric ischemia. Acad Emerg Med 2009;16:539-43.

6. Delaney CP, O’Neill S, Manning F, Fitzpatrick JM, Gorey TF. Plasma concentrations of glutathione S-transferase isoenzyme are raised in patients with intestinal ischaemia. Br J Surg 1999;86:1349-53.

7. Bealer JF, Colgin M. S100A8/A9: a potential new diagnostic

aid for acute appendicitis. Acad Emerg Med 2010;17:333-6.

8. Acosta S, Nilsson T. Current status on plasma biomarkers for acute mesenteric ischemia. J Thromb Thrombolysis 2012;33:355-61.

9. Niewold TA, Meinen M, van der Meulen J. Plasma intestinal fatty acid binding protein (I-FABP) concentrations increase following intestinal ischemia in pigs. Res Vet Sci 2004;77:89-91.

10. Glatz JF, van der Vusse GJ. Cellular fatty acid-binding proteins: their function and physiological significance. Prog Lipid Res 1996;35:243-82.

11. Vermeulen Windsant IC, Hellenthal FA, Derikx JP, Prins MH, Buurman WA, et al. Circulating intestinal fatty acid-binding protein as an early marker of intestinal necrosis after aortic surgery: a prospective observational cohort study. Ann Surg 2012;255:796-803.

12. Relja B, Szermutzky M, Henrich D, Maier M, de Haan JJ, Lubbers T, et al. Intestinal-FABP and liver-FABP: Novel markers for severe abdominal injury. Acad Emerg Med 2010;17:729-35.

13. Parker LJ, Vukov LF, Wollan PC. Emergency department evaluation of geriatric patients with acute cholecystitis. Acad Emerg Med 1997;4:51-5.

14. Grundmann RT, Petersen M, Lippert H, Meyer F. The acute (surgical) abdomen - epidemiology, diagnosis and general principles of management. [Article in German] Z Gastroenterol 2010;48:696-706. [Abstract] 15. Silen W. Abdominal pain. Harrison’s principles of internal medicine. 15th ed. Vol. I. 1998.

16. Akyildiz HY, Sözüer E, Akcan A, Küçük C, Artis T, Biri I, et al.

The value of D-dimer test in the diagnosis of patients with nontraumatic acute abdomen. Ulus Travma Acil Cerrahi Derg 2010;16:22-6.

17. Ockner RK, Manning JA. Fatty acid-binding protein in small intestine. Identification, isolation, and evidence for its role in cellular fatty acid transport. J Clin Invest 1974;54:326-38.

18. Lores ME, Cañizares O, Rosselló PJ. The significance of elevation of serum phosphate levels in experimental intestinal ischemia. Surg Gynecol Obstet 1981;152:593-6.

19. Chen Y, Milles AM, Grisham BM. Pathophysiology and reactive oxygen metabolites. Oxidative stress and antioxidant defenses in biology. 1st ed. New York: Chapman and Hall Co; 1995. p. 62-95.

20. Kanda T, Fujii H, Tani T, Murakami H, Suda T, Sakai Y, et al.

Intestinal fatty acid-binding protein is a useful diagnostic marker for mesenteric infarction in humans. Gastroenterology 1996;110:339-43.

21. Kanda T, Nakatomi Y, Ishikawa H, Hitomi M, Matsubara Y, Ono T, et al. Intestinal fatty acid-binding protein as a sensitive marker of intestinal ischemia. Dig Dis Sci 1992;37:1362-7.

22. Kanda T, Fujii H, Fujita M, Sakai Y, Ono T, Hatakeyama K. Intestinal fatty acid binding protein is available for diagnosis of intestinal ischaemia: immunochemical analysis of two patients with ischaemic intestinal diseases. Gut 1995;36:788-91.

23. Tölle A, Jung M, Lein M, Johannsen M, Miller K, Moch H, et al. Brain-type and liver-type fatty acid-binding proteins: new tumor markers for renal cancer? BMC Cancer 2009;9:248.

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ORIGINAL ARTICLE

104

Factors Affecting Mortality and Complications in Mushroom Poisonings Over a 20 Year Period: A Report from Central Anatolia Yirmi Yılda Mantar Zehirlenmelerinde Mortalite ve Komplikasyonu Etkileyen Faktörler: Anadolu’dan Bir Rapor Arif Alper CEVIK,1,2 Ilhami UNLUOGLU3 Department of Emergency Medicine, Eskisehir Osmangazi University Faculty of Medicine, Eskisehir 2 United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, UAE 3 Department of Family Medicine, Eskisehir Osmangazi University Faculty of Medicine, Eskisehir

1

SUMMARY

ÖZET

Objectives Mushroom poisoning (MP) is one of the world’s leading seasonal and regional health problems. The aim of this study was to analyze the relationship between clinical factors and outcomes of mushroom poisoning.

Amaç Mantar zehirlenmeleri (MZ) dünyanın önde gelen mevsimsel ve bölgesel sağlık problemidir. Bu araştırmanın amacı MZ’de klinik faktörlerle sonuçlar arasındaki ilişkiyi incelemektir.

Methods The study was conducted in the emergency department. The patients who presented between January 1st, 1991 and December 31, 2010 were retrospectively reviewed.

Gereç ve Yöntem Araştırma Acil Tıp departmanında gerçekleştirilmiştir. 1 Ocak 1991 ve 31 Aralık 2010 tarihlerinde başvuran hastalar geriye dönük olarak incelenmiştir.

Results 599 MP cases were enrolled into the statistical analysis. The elderly group had a higher rate of mortality (8.8%) and complications (12.3%) (p=0.005) (OR 3.98, 95% CI: 1.9291 to 8.2290; p=0.0002). The patients who presented in summer had a higher rate of mortality (9.5%) and complications (11.9%) (p<0.001). (OR: 3.83, 95% CI 1.7068 to 8.6074, p=0.0011). The rate of mortality and complications in patients who had eaten self-harvested wild mushrooms (WM) was 6.8%, while those who purchased WM had a mortality and complication rate of 15.2% (p=0.016), (Purchased WM OR 2.46, 95% CI 1.1609 to 5.2353, p=0.0189).

The rate of mortality and complications in the patients who presented with gastrointestinal symptoms was 9.9% (OR: 3.98, 95% CI 1.5503 to 10.2679; p=0.0041).

Bulgular 599 MZ olgusu araştırmaya dahil edildi. Yaşlı hastalar daha yüksek mortalite (%8.8) ve komplikasyon (%12.3) oranına sahiptiler (p=0.005). (Odd oranı [OO]: 3.98, %95 [Güven Aralığı] GA 1.9291 - 8.2290, p=0.0002). Yaz aylarında başvuran hastalar daha yüksek mortalite (%9.5) ve komplikasyona (%11.9) sahiptiler (OO: 3.83, %95 GA 1.7068 to 8.6074, p=0.0011).

Mantarları kendi toplayıp yemiş olan hastalarda mortalite ve komplikasyon oranı %6.8 iken bu oran satın alınmış vahşi mantarlarda %15.2 idi (p=0.016), (satın alınan mantarlar için OO: 2.46, 95% GA 1.1609 - 5.2353, p=0.0189). Gastrointestinal semptomları olan hastaların mortalite ve komplikasyon oranı %9.9 olarak saptandı (OO: 3.98, %95 GA 1.5503 10.2679, p=0.0041).

Conclusions Factors such as being elderly, summer season, purchased WM, and gastrointestinal symptoms were significantly associated with mortality and complications in our study.

Sonuç Yaşlılık, yaz mevsimi, satın alınmış vahşi mantarlar ve gastrointestinal semptomlar mortalite ve komplikasyonlar ile anlamlı ilişki göstermiştir.

Key words: Elderly; emergency department; mushroom; poisoning; summer season.

Anahtar sözcükler: Yaşlılık; acil servis; mantar; zehirlenme; yaz mevsimi.

Submitted: March 16, 2014 Accepted: April 22, 2014 Published online: Agusut 30, 2014 Correspondence: Arif Alper Cevik, MD, FEMAT. United Arab Emirates University, College of Medicine and Health Sciences, Al Ain, UAE. e-mail: aacevik@uaeu.ac.ae

Turk J Emerg Med 2014;14(3):104-110

doi: 10.5505/1304.7361.2014.36024

Ă&#x2021;evik AA et al.

Factors Affecting Mortality and Complications in Mushroom Poisonings Over A 20 Year Period

Introduction Mushroom poisoning (MP) is one of the worldâ&#x20AC;&#x2122;s leading seasonal and regional health problems. Eating poisonous wild mushrooms (WM) can lead to unwanted reactions such as gastroenteritis or more severe pathologies including fatal liver failure. Fatal MP is very well described in the literature.

[1] Fortunately, though, the majority of MP cases have a good prognosis.

The Central Anatolian region of Turkey has considerable reputation in terms of MP. MP can be commonly observed in Europe, Anatolia and the Middle East, and the reports from these regions, including incidence and prognosis, have significant differences.[2-5]

Basic descriptive data of cases including age (age groups [017: child and adolescent, 18-39: young adults, 40-64: middle age, 65 and older: elderly), gender, presenting months and seasons, presenting symptoms (neurological, gastrointestinal, and other), how WM were obtained (self harvest from nature, purchased from public market), the means of admission (direct presentation or transferred), laboratory results (Blood Urea Nitrogen (BUN, mg/dL), Creatinine (Cr, mg/dL), alanine aminotranferase (ALT, U/L), aspartate aminotransferase (AST, U/L), clinical care area (emergency department, ward, or intensive care unit [ICU]), length of stay in the hospital, and outcome (mortality, complication (end stage renal failure, seizure disorder, etc.), full recovery) were collected.

In our previous studies, we tried to call attention to different aspects of MP.[6-8] These studies consisted of short-term data and had no detailed evaluation of the relationship between clinical data and outcome measures (mortality and/or complications). As far as we are aware, in the English literature, the number of studies evaluating this relationship and prognostic criteria is limited. Additionally, other studies have concentrated on different variables.[9-11]

Inclusion and Exclusion Criteria

The aim of our study was to analyze the relationship between clinical factors and outcomes of MP. In this study, we report MP cases admitted to our hospital serving four Anatolian cities with a total population of approximately two and a half million people over the last 20 years.

Patient data were evaluated for their relationships with mortality, complications (end stage renal failure, seizure disorder, etc.), and full recovery.

The patients who had the above clinical/laboratory details in their files were included into the study. The patients who had co-ingestion of drugs in overdose, drugs of abuse, missing clinical follow-up or did not have the above clinical/laboratory details in their files were excluded from the study.

Outcome Measures

Data Analysis

The patients who presented or transferred to the emergency department and were diagnosed as MP between January 1st, 1991 and December 31, 2010 were included in the study group. The patients included into the study group were selected according to the inclusion criteria.

Statistical Package for the Social Sciences (SPSS, version 18) and Statistical Analysis and Graphics Software (NCSS 2007) were used for statistical analyses. Chi-Square and the Fisher Exact test were used for descriptive analyses. KolmogorovSmirnov test was used to show the distribution of the data.

Mann-Whitney U-test in binary groups and Kruskal-Wallis One Way Analyses of Variance test for three or more groups of data were used, as the data did not show a normal distribution in the Kolmogorov-Smirnov test. Median values were given for the results of variables that did not show normal distribution. Odds ratio (OR) was calculated for variables that may affect the outcome, such as age, presenting symptoms, the way of obtaining WM, and admission. A p-value less than 0.05 was accepted as significant. SD: standard deviation, SE: standard error.

Data acquisition

Results

ICD-10 and 9 codes of MP were entered into the hospital information system. The list of cases was obtained by use of these codes. The detailed information of cases was found retrospectively in electronic health records as well as in archived patient files for cases admitted before 2007.

721 MP cases were admitted to the hospital within a period of 20 years. 117 cases who did not have clinical/laboratory information in their files and five patients who had been transferred to different cities were removed from the study.

599 cases were enrolled into the statistical analyses.

Materials and Methods Hospital The study was conducted in the emergency department of the university hospital, which is a tertiary care center for all medical and trauma patients, as well as for toxicology and environmental cases.

Patients

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Gender and Age Groups

cal care area. The child and adolescent group was mainly treated in the ward area (128 cases, 79.0%) while 43 cases (75.4%) from the elderly group received medical care in the ICU (χ2=325,932, p<0.001). The elderly group had a higher rate of mortality (8.8%) and complications (12.3%) than the other age groups (χ2=18.664, p=0.005). The odds ratio (OR) was 3.98 (95% CI: 1.9291 to 8.2290, Z = 3.736, p=0.0002).

There were 319 females (53.3%) and 280 males in the study.

The mean age of males and females were similar. According to age groups, there were 162 (27.0%) cases in children and adolescents, 187 (31.2%) cases in young adults, 193 (32.2%) cases were in middle-aged adults, and 57 (9.5%) in the elderly. Comparison data on gender and age groups are presented in Table 1. Although distributions of genders were similar in three age groups, the number of female patients in the young adult group was significantly higher (120, 64.2%) (χ2=13.56, p=0.004).

The mean ages of the patients in mortality, complication and full recovery groups were significantly different (41.50 [SE: 4.45], 44.91 [SE: 4.26], 33.98 [SE: 0.88] respectively, χ2=6.429904, p=0.0401).

Presenting Season

There were no significant differences between genders and among the age groups for patients’ presenting season, the means of obtaining WM, and symptoms. There were no differences between genders for distribution of clinical care area and outcome. However, there was a significant difference among the age groups for distribution in the clini-

The seasonal distribution of MP showed a binary peak.

Spring (April, May, June) had the highest number of patients (367 cases, 61.3%). Autumn (October, November, December) was the second highest season with 166 cases (27.7%). The highest number of patients was seen in June (237, 39.5%).

Table 1. Comparison data on gender and age groups

Gender

Age Group (years)

Female Male 0-17 18-39 40-64 ≥65

n % n % n % n % n % n %

N

319 53.3 280 46.7 162 27 187 31.2 193 32.2 57 9.5

Mean age (SD)

32.25 (19.85) 35.19 (22.26) 9.29 (4.31) 28.63 (6.28) 50.76 (6.70) 72.79 (4.71)

Presenting season

Winter

12 3.8 12 4.3 4 2.5 9 4.8 8 4.1 3 5.3

Spring

198 62.1 169 60.4 96 59.3 123 65.8 113 58.5 35 61.4

Summer

20 6.3 22 7.9 11 6.8 13 7.0 13 6.7 5 8.8

Autumn

89 27.9 77 27.5 51 31.5 42 22.5 59 30.6 14 24.6

Obtaining WM Self harvest

281 88.1 252 90 149 92.0 167 89.3 170 88.1 47 82.5

38

Purchased from public market

11.9

28

10

13

8.0

20

10.7

23

11.9

10

17.5

Presenting symptoms Neurologic

72 22.6 61 21.8 32 19.8 41 21.9 50 25.9 10 17.5

Gastrointestinal

221 69.3 192 68.6 124 76.5 124 66.3 122 63.2 43 75.4

Other

26 8.2 27 9.6 6 3.7 22 11.8 21 10.9 4 7.0

Clinical care area Emergency department

70 21.9 53 18.9 11 6.8 50 26.7 50 25.9 12 21.1

Ward

73 22.9 83 29.6 128 79.0 16 8.6 10 5.2 2 3.5

ICU

176 55.2 144 51.4 23 14.2 121 64.7 133 68.9 43 75.4

Outcome Full recovery

295 92.5 258 92.1 151 93.2 179 95.7 178 92.2 45 78.9

Mortality

11 3.4 11 3.9 6 6.3 3 1.6 8 4.1 5 8.8

Complications*

13 4.1 11 3.9 5 3.1 5 2.7 7 3.6 7 12.3

*End stage renal failure in 23 patients and permanent seizure in one patient were complications in our study.

Çevik AA et al.

Factors Affecting Mortality and Complications in Mushroom Poisonings Over A 20 Year Period

Neurologic symptoms were higher in autumn (109 of 133 cases, 82.0%). Gastrointestinal symptoms were common in spring (218 of 413 cases, 52.8%) and autumn (143 of 413 cases, 34.6%). Presenting symptoms differed significantly among seasons (χ2=43.578, p<0.001).

primary or secondary health care centers (478 cases, 79.8%), and then were transferred to our emergency department.

Forty-seven of the 121 (38.8%) directly presented cases were admitted to the ICU, while the ICU admission rate was 57.1% in transferred cases (χ2=16.620, p<0.001).

In winter, complications were seen in only two cases, while there were no fatal cases. The patients who presented in summer had a higher rate of mortality (9.5%) and complications (11.9%) than other seasons (χ2=28.108, p<0.001). The OR was found to be 3.83 (95% CI: 1.7068 to 8.6074, Z=3.255, p=0.0011).

The patients who were admitted had clinical care in three different locations: 320 cases (53.4%) in the ICU, 156 cases (26.0%) in the ward, and 123 cases (20.5%) in the emergency department.

The means of obtaining mushrooms The majority of cases (foragers) had obtained and eaten selfharvested WM (533 cases, 89.0%), while 66 patients (11.0%) had eaten WM purchased from a public market.

282 patients who had eaten self-harvested WM were treated in the ICU (52.9%). The ICU admission rate was higher in patients (38 cases, 57.6%) who had eaten purchased WM (χ2=7.084, p=0.029).

The outcome was also significantly different between these two groups. The rate of mortality and complications in the patients who had eaten self-harvested WM was 6.8% (36 of 533 cases, 19 mortality, 17 complications), while the group that purchased WM had a 15.2% rate of mortality and complications (10 of 66 cases, 3 mortality, 7 complications (χ2=5.841, p=0.016). The OR of purchased WM was found to be 2.46 (95% CI: 1.1609 to 5.2353, Z=2.348, p=0.0189).

Presenting symptoms Patients described gastrointestinal (413 cases, 68.9%), neurologic (133 cases, 22.2%) or other symptoms (53 cases, 8.8%) as their first presenting symptom. Among all symptoms, nausea was the most common (322 cases, 53.8%), followed by light-headedness and vomiting (13.4% and 8.3%, respectively).

The rate of mortality and complications in the patients who presented with gastrointestinal symptoms was 9.9% (41 of 413 cases, 20 mortality, 21 complications). The OR of gastrointestinal symptoms for mortality and complications was 3.98 (95% CI: 1.5503 to 10.2679, Z=2.869, p=0.0041). The rate of mortality and complications was lower in patients with neurological symptoms (3.0%) and the other symptoms (1.9%). There was a significant difference for mortality and complications among the groups (χ2=9.547, p=0.008).

Admission to the hospital and length of stay 121 (20.2%) patients directly presented to our emergency department. The majority of cases had first been admitted to

The hospital length of stay of transferred cases (mean: 3.24 (CI: 2.86-3.61); median: 2.0) was significantly higher than in the directly presented group (mean: 2.42 (CI: 2.02-2.83); median: 2.0) (p<0.001).

The elderly group had 5.80 (SE: 0.50) days of hospital stay.

Child and adolescent, young adult, and middle age groups had 2.90 (SE: 0.29), 2.51 (SE: 0.27), and 2.95 (SE: 0.27) days, respectively. There was a significant difference among the age groups for length of hospital stay (χ2=18.36774, p<0.001).

The mean length of stay of fully recovered patients was 2.76 (SE: 0.15) days, while the mean lengths of stay were 7.31 (SE: 0.79) days in fatal cases and 6.37 (SE: 0.76) days in complicated cases (χ2=5.908688, p=0.043).

Mortality and complications in directly presented cases were 0.8% (one case) and 3.3% (four cases) respectively. Transferred cases had higher rates of mortality (21 cases, 4.4%) and complications (20 cases, 4.2%). Although there was a difference between the two groups, it was not significant. The OR for transferred cases was found to be 2.17, but it was also not significant (95% CI: 0.8412 to 5.6324, Z=1.603, p=0.1088).

Laboratory Results BUN, Cr, AST and ALT levels of all cases were evaluated. All laboratory levels showed differences between outcome groups. The levels evaluated were the first laboratory levels obtained in the emergency department.

Mean BUN levels by outcome were found as follows: 16.14 (SE: 0.58) in the full-recovery group, 35.09 (SE: 2.93) in the mortality group, and 61.54 (SE: 2.80) in the complication group (χ2=59.43019, p<0.001). Creatinine levels were 1.10 (SE: 8.20) in the full-recovery group, 3.19 (SE: 0.41) in the mortality group, and 4.27 (SE: 0.39) in the complication group (χ2=58.21726, p<0.001). AST levels were 63.79 (SE: 28.66) in the full-recovery group, 2983.09 (SE: 143.73) in the mortality group, and 313.58 (SE: 137.61) in the complication group (χ2=83.94112, p<0.001). ALT levels were 62.83 (SE: 31.01) in the full-recovery group, 3056.95 (SE: 155.48) in the mortality group, and 480.20 (SE: 148.86) in the complication group (χ2=74.45051, p<0.001).

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Discussion Most articles on MP are case reports or series. The effects of demographic data and other key information on outcomes are not well studied or published in the literature. There are many factors that affect the outcome of MP, including type of ingested mushroom, location, the amount of toxin delivered, laboratory results, clinical findings, medical treatment given, hemodialysis, or liver transplantation. In addition to many known details of this toxicity, MP still has some diagnostic and treatment dilemmas for medical professionals.

Although MP has a complex and challenging clinical progress, mortality is seen very rarely. In 2010, 6,275 MP cases were reported to the American Association of Poison Control Centers (AAPCC). Only one death was reported.[12] Unfortunately, there is no center collecting poisoning reports in Europe and in the Middle East. There are also no annually published poisoning reports in these regions. Therefore, it is difficult to estimate the true incidence of MP in this part of the world. According to the report of one of the regional poison information centers in our country, MP accounted for 1.2% (799 cases) of the 65,176 poisoning cases in the last 14 years. Only one death was reported in this report, and the source was an unknown type of WM4. Although public awareness about WM and a more skeptical approach by physicians to MP has decreased mortality, some unpublished reports of deaths have been declared to be fatal MP cases in the Assam area of India in 2008.[13] There are different reasons for exposure to WM in different age groups. Children may be unintentionally poisoned by eating WM found in outdoor areas.[2] However, adults are more prone to collect and eat WM intentionally. Schenk-Jaeger et al. reported that 86.4% of their cases were accidental exposure to mushrooms.[2] They also report abuse and suicide cases (12.8% and 6.3%, respectively). We did not determine abuse or suicidal ingestion in our cases. Hocaogluâ&#x20AC;&#x2122;s study also had the same finding.[4] The number of female patients was found to be higher in our study as in some other reported studies.[3,4,14] Hocaoglu reported a female/male ratio of 1.24. Another report from northeast part of Turkey found 67.5% female patients.[3] In the present study, we have no strong data showing a relationship between gender and outcome.

We can estimate risk groups for poisoning because of their physiologic and metabolic factors or comorbidities. Children and elderly are at the greatest risk for toxicity and the worst outcomes for all types of poisoning. Therefore, evaluation of the outcome among the age groups was one of the main focuses of our study. In 2010, AAPCC reported that 70.1% of all MP cases were in patients with an age of 19 years or less.

Although our study did not use the same age ranges as the AAPCC report, we found 27.0% of cases in those patients less than 18 years old. This demonstrated a difference in the age distribution of MP cases between countries. Mortality and complication rate (21.3%) in the elderly group (65 and older) in our study was higher than the other age groups, with an OR of 3.98. In patients under 19 years old, we found a 9.4% rate of mortality and complications. The mean age of full-recovery cases was also significantly lower than the mortality and complication groups. According to this finding, we may suggest that MP does not have the worst outcomes in children and adolescents. However, mortality and complication rates rise with increasing age according to our results and our previous report.[8] Because our study showed that elderly patients have the worst outcomes, emergency physicians and ICU physicians should pay special attention in taking care of this age group.

[12]

MP has some seasonal variations in literature. Schenk-Jaeger et al. reported that there is one peak in their study, occurring in late summer.[2] In Ishiharaâ&#x20AC;&#x2122;s report, summer and early autumn were the most common seasons for MP.[15] MP in our region has a binary peak, in spring and autumn. However, mortality and complication rates were highest in summer (total 21.4%). Most WM poisoning affects the gastrointestinal system, and patients present with nausea, vomiting or diarrhea. The most serious effect of MP is on the kidneys and liver. Deterioration of these two important organ functions and failure to recover lead to mortality or irreversible complications such as permanent renal failure. Dehydration is one of the main problems, and it worsens renal function.

Inadequate supportive treatment may lead to renal failure.

This may affect the outcome, especially in elderly patients.

Cases of acute prerenal failure following dehydration are observed not only in elderly patients, but also in young and previously healthy patients.[2] Eating WM in our country is still a quite common habit. WMs are also commonly sold in public markets, and there are no regional or national regulations to control it. Yardan et al. showed that 87.7% of patients had collected and ate WM, while only 12.3% had purchased WM from a local bazaar.[3] These findings are quite similar to our results. Foragers usually pick WM from open rural fields, woodlands, gardens, or roadsides, then cook and eat.[7] This habit is also widespread in European and Middle Eastern countries.[2,5] Unfortunately, we found higher mortality and complications in patients who purchased WM from public markets. This is one of the main issues of public health in many countries. Emergency physicians may play a more active role in educating the public on MP. MP may present varying grades of gastrointestinal and

Ă&#x2021;evik AA et al.

Factors Affecting Mortality and Complications in Mushroom Poisonings Over A 20 Year Period

neurologic symptoms and hepatic/renal involvement depending on the type and amount of mushroom consumed.

Gastrointestinal symptoms were the most prominent complaints in our patients. We found that gastrointestinal symptoms have higher mortality and complication rates. Most reports indicate that gastrointestinal symptoms, especially nausea, vomiting and diarrhea, are prominent symptoms.

Nausea and vomiting were found in 86.8% and 79.8% of cases in the middle Black Sea region of Turkey.[3] Nausea and vomiting were determined in 93.8% of cases in another report.[16] A. phalloides is one of the well-known toxic mushrooms which cause these symptoms. It is also considered the sole cause of liver damage.[17] Differentiating benign gastroenteritis from potentially life-threatening A. phalloides (amatoxin) poisoning is critical for health care professionals. A. phalloides causes these symptoms, as do other types of mushrooms, and inadequate treatment or delayed diagnosis can increase the chance of mortality and complications.

In the literature, A. phalloides toxicity is responsible for 90% of fatal MP.[18,19] Liver failure because of toxic mushrooms may be fatal if the organ transplantation cannot be arranged.[19] We have Amanita, Gyromitra, Inocybe and Omphalatus species in our region.[8] The majority of deaths are thought to be due to Amanita. However, diagnostic typing of consumed mushrooms was unavailable in our cases, and this is a wellknown problem in MP in all countries. The AAPCC reported an unknown mushroom type in 79.3% of cases in 2010.[12] Patients who were transferred from other health care centers were a significant majority of our cases (79.8%). In our previous studies, we have found and published higher mortality and complication rates in patients admitted to and cared for in another hospital for couple days before being transferred to our emergency department.[6-8] Unfortunately, we have no data on the previous treatments used in such cases, and we cannot perform a detailed discussion on the treatments of transferred patients that may affect outcome.

However, transferred patients had higher ICU admissions, longer lengths of stay, and higher mortality and complication rates in our study, and these results suggest that they may not receive enough supportive treatment in previous facilities and/or delayed transfer8. Our mortality (3.7%) and complication (4.0%) rate is higher than some other reports.

[3,12] This might be due to medical treatment initiated relatively late in previous health care centers. Yardan et al. reported three deaths in their hospital (0.9%) in six years.[3] In a regional poison center report,[4] 91.2% of cases were observed and had medical care in emergency departments.

In our study, this percentage was 20.5%. They also reported that 3.3% of cases had ward and ICU admission, but this rate

was 79.4% in our study. We transferred five cases (0.8%) to different hospitals that had facilities for liver transplantation.

The transfer rate was reported as 5.4% in Hocaogluâ&#x20AC;&#x2122;s report.

[4] We believe that this report reflects the regional fact more rationally. Regional and institutional differences for health care facilities affect patient care and outcomes in MP. Unfortunately, there is no current MP guideline in the English literature, so each institution and region must create its own specific approach to these cases.

Laboratory results (BUN, Cr, ALT, AST) were higher in fatal and complicated cases in our study. Trabulus et al. described the factors associated with greater likelihood of death[10] such as low sodium values and high urea, AST, ALT, total bilirubin, lactate dehydrogenase, prothrombin time, international normalized ratio (INR), and activated partial thromboplastin time values. Some laboratory (INR, etc.) and clinical (encephalopathy, etc.) parameters have also been reported as factors associated with outcome of the patients who needed liver transplantation.[11] Limitations Our study has several limitations. This is a retrospective analysis of cases despite the organized prospective data compilation. Because there are no particular descriptions of mushroom type by patients or relatives, and we did not determine the type of mushroom in our laboratory, this uncertain information make some biases in admitted cases. When symptoms happened after consumption of mushrooms, foodborne illnesses caused by other ingredients of the meal could not be eliminated. We did not include treatment parameters into the study that may play an important role in outcomes. Because we have no data on previous treatment of transferred patients (the majority of our cases), we could not include these data in our analyses. We did not evaluate the relationship of vital signs to outcome because we previously showed that vitals signs are not a parameter for outcome in MP.[7] Unfortunately, we could not process the data concerning symptom time after ingestion, which is a parameter related to outcome.[11] Finally, we could not use 16% of the data, which may affect the results. We also applied logistic regression analysis for age, presenting season, the means of obtaining mushrooms, and presenting symptoms. However, the group of variables that we chose here were not able to predict mortality and complication rate in high percentage of patients. The retrospective data collection and institution specific decisions on admissions and other critical factors related to patient management might have affected these results. Prospective data collection and choosing the variables after correlation with outcome measures will give a more accurate analysis on logistic regression.

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Conclusion We retrospectively analyzed demographic and clinical factors to evaluate their importance on outcome. Some factors, such as being elderly, summer season, purchased WM, and gastrointestinal symptoms, were significantly associated with mortality and complications in our study. Since our study showed that elderly patients have the highest mortality and complication rates, we suggest that emergency physicians and ICU physicians should pay special attention in taking care of this age group. Local or national laws should ban selling of WMs in public markets. Emergency physicians may also play a more active role in educating the public on MP. Since the mortality and complication rates of patients who directly presented to our tertiary care center was lower, we may suggest that MP cases should be transferred as soon as possible to experienced centers in high-risk regions.

These variables and outcome measures should be evaluated and analyzed with logistic regression in prospective studies.

Acknowledgement We are pleased to have Dr. Setenay Oner’s help with statistical analyses and Dr. Baran Tokar’s help with general evaluation of the manuscript.

Conflict of Interest The authors declare that there is no potential conflicts of interest.

Financial Disclosure This research received no specific grants from any funding agency in the public, commercial, or not-for-profit sectors.

References 1. Sanz P, Reig R, Piqueras J, Marti G, Corbella J. Fatal mushroom poisoning in Barcelona, 1986-1988. Mycopathologia 1989;108:207-9.

2. Schenk-Jaeger KM, Rauber-Lüthy C, Bodmer M, Kupferschmidt H, Kullak-Ublick GA, Ceschi A. Mushroom poisoning: a study on circumstances of exposure and patterns of toxicity. Eur J Intern Med 2012;23:85-91.

3. Yardan T, Baydin A, Eden AO, Akdemir HU, Aygun D, Acar E, et al. Wild mushroom poisonings in the Middle Black Sea region in Turkey: analyses of 6 years. Hum Exp Toxicol 2010;29:76771.

4. Hocaoglu N, Kalkan S, Tuncok Y. Mushroom poisonings reported to the Dokuz Eylul University drug and poison

information center. [Article in Turkish] Turk J Emerg Med 2010;10:119-25.

5. Pajoumand A, Shadnia S, Efricheh H, Mandegary A, Hassanian-Moghadam H, Abdollahi M. A retrospective study of mushroom poisoning in Iran. Hum Exp Toxicol 2005;24:60913.

6. Unluoglu I, Tayfur M. Mushroom poisoning: an analysis of the data between 1996 and 2000. Eur J Emerg Med 2003;10:23-6.

7. Unluoglu I, Alper Cevik A, Bor O, Tayfur M, Sahin A. Mushroom poisonings in children in Central Anatolia. Vet Hum Toxicol 2004;46:134-7.

8. Cevik AA, Unluoglu I, Ergun N, Sahin A. Poisoning severity scores of cases with mushroom poisoning presenting to the emergency department. Turk J Emerg Med 2007;7:102-8.

9. Ozçay F, Baskin E, Ozdemir N, Karakayali H, Emiroglu R, Haberal M. Fulminant liver failure secondary to mushroom poisoning in children: importance of early referral to a liver transplantation unit. Pediatr Transplant 2006;10:259-65.

10. Trabulus S, Altiparmak MR. Clinical features and outcome of patients with amatoxin-containing mushroom poisoning.

Clin Toxicol (Phila) 2011;49:303-10.

11. Escudié L, Francoz C, Vinel JP, Moucari R, Cournot M, Paradis V, et al. Amanita phalloides poisoning: reassessment of prognostic factors and indications for emergency liver transplantation. J Hepatol 2007;46:466-73.

12. Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Dart RC. 2010 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 28th Annual Report. Clin Toxicol (Phila) 2011;49:910-41.

13. http://www.indianexpress.com/news/assam-poisonousmushrooms-kill-17/292815. Accessed: December 02, 2012.

14. Nordt SP, Manoguerra A, Clark RF. 5-Year analysis of mushroom exposures in California. West J Med 2000;173:314-7.

15. Ishihara Y, Yamaura Y. Descriptive epidemiology of mushroom poisoning in Japan. [Article in Japanese] Nihon Eiseigaku Zasshi 1992;46:1071-8. [Abstract] 16. Durukan P, Yildiz M, Cevik Y, Ikizceli I, Kavalci C, Celebi S. Poisoning from wild mushrooms in Eastern Anatolia region: analyses of 5 years. Hum Exp Toxicol 2007;26:579-82.

17. Wieland T. Poisonous principles of mushrooms of the genus Amanita. Four-carbon amines acting on the central nervous system and cell-destroying cyclic peptides are produced. Science 1968;159:946-52.

18. Mullins ME, Horowitz BZ. The futility of hemoperfusion and hemodialysis in Amanita phalloides poisoning. Vet Hum Toxicol 2000;42:90-1.

19. Enjalbert F, Rapior S, Nouguier-Soulé J, Guillon S, Amouroux N, Cabot C. Treatment of amatoxin poisoning: 20-year retrospective analysis. J Toxicol Clin Toxicol 2002;40:715-57.

ORIGINAL ARTICLE

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Rapid Intravenous Rehydration to Correct Dehydration and Resolve Vomiting in Children with Acute Gastroenteritis Akut Gastroenteritli Çocuklarda Dehidratasyonu Düzeltmek ve Kusmayı Geçirmek için Hızlı intravenöz Rehidrasyon Anoush AZARFAR,1 Yalda RAVANSHAD,1 Aghillolah KEYKHOSRAVI,1 Sepideh BAGHERI,1 Ziaoddin GHARASHI,2 Mohammad ESMAEELI1 Mashhad University of Medical Sciences, Mashhad, Iran; 2 Tabriz University of Medical Sciences, Tabriz, Iran

1

SUMMARY

ÖZET

Objectives The objective of this study is to evaluate the effect of rapid intravenous rehydration to resolve vomiting in children with acute gastroenteritis.

Amaç Bu çalışmanın amacı, akut gastroenteritli çocuklarda, hızlı intravenöz rehidratasyon tedavisinin kusma üzerine etkisini değerlendirmektir.

Methods This randomized control trial was conducted in the pediatric emergency department in a tertiary care center in Tabriz, North-West of Iran. The study participants’ were 150 children with acute gastroenteritis and vomiting who were moderately dehydrated, had not responded to oral rehydration therapy and without any electrolyte abnormalities. 20-30 cc/kg of a crystalloid solution was given intravenously over 2 hours and the control group was admitted in the emergency department (ED) for a standard 24 hour hydration.

Effectiveness of rapid intravenous rehydration in the resolution of vomiting in children with acute gastroenteritis was evaluated.

Gereç ve Yöntem Bu randomize kontrollü çalışma İran’ın Kuzeybatısındaki Tebriz ilinde üçüncü basamak çocuk acil servisinde gerçekleştirildi. Çalışmaya orta derecede dehidrate, elektrolit anormalliği olmayan ve oral rehidrasyon tedavisine yanıt vermemiş akut gastroenteritli 150 çocuk katıldı. İki saat içinde intravenöz yolla 20-30 cc/kg kristaloid çözelti verildi ve kontrol grubu standart 24 saatlik hidrasyon için acil servise alındı.

Akut gastroenteritli çocuklarda, hızlı intravenöz rehidratasyon tedavisinin kusma üzerine etkisi değerlendirildi.

Results In 63 children of the intervention group (out of 75) vomiting was resolved after rapid IV rehydration and they were discharged.

Among them, 12 that did not tolerate oral fluids were admitted. In the control group, 62 patients’ vomiting was resolved in the first 4 hours after admission, and there was no significant difference between the two groups regarding resolution of vomiting.

Bulgular Müdahale grubundaki 75 çocuğun 63’ünde hızlı IV rehidrasyondan sonra kusma geçti ve hastalar taburcu edildi. Bu çocukların 12’si oral sıvıları tolere edemedikleri için hastaneye kabul edildi. Kontrol grubunda 62 hastanın kusması hastaneye kabulden sonraki ilk 4 saat içinde geçmiş olup, iki grup arasında kusmanın geçmiş olması açısından herhangi bir anlamlı farklılık yoktu.

Conclusions Rapid intravenous rehydration in children with moderate dehydration and vomiting due to gastroenteritis is effective in reducing admission rates in the ED.

Sonuç Gastroenterite bağlı orta derecede dehidratasyon ve kusması olan çocuklarda hızlı intravenöz rehidrasyon acil servisten yatış oranlarını azaltmada etkilidir.

Key words: Emergency department; gastroenteritis; rehydration; vomiting.

Anahtar sözcükler: Acil servis; gastroenterit; rehidrasyon; kusma.

Submitted: February 15, 2014 Accepted: April 07, 2014 Published online: June 09, 2014 Correspondence: Dr. Sepideh Bagheri. Dr. Sheikh Childrens Hospital, Mashhad, Iran. e-mail: bagheris@mums.ac.ir

Turk J Emerg Med 2014;14(3):111-114

doi: 10.5505/1304.7361.2014.66049

Turk J Emerg Med 2014;14(3):111-114

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Introduction

Participants

Acute gastroenteritis is the most common cause of dehydration in children and represents one of the most common conditions in pediatric emergency departments.[1,2] Oral rehydration is appropriate for most children, but intravenous rehydration is the treatment of choice for severe dehydration and in cases of failure of oral rehydration therapy.[3] Given the high incidence of acute gastroenteritis in children, this can lead to overcrowding in emergency departments.[4] The most appropriate method of intravenous rehydration is still under investigation. The volume and rate of administration of intravenous fluids are the focal point of many discussions.

Slow restoration regimens and rapid rehydration regimens have both been used by clinicians treating dehydrated children.[5,6] Rapid rehydration regimens might have the potential benefits of achieving earlier rehydration and reduction in length of hospital stay and costs.[7]

The study population consisted of 150 children with moderate dehydration or vomiting due to gastroenteritis who had not responded to oral rehydration therapy. 565 children were referred to the hospital with the diagnosis of acute gastroenteritis during the study period. We excluded children with severe dehydration, shock and hypotension, electrolyte abnormalities, those who were not dehydrated or were mildly dehydrated. Parents signed informed consent before entry into the study and the study was approved by the medical ethics committee of the Tabriz University of Medical Sciences prior to entrance into the study.

Considering the large incidence of acute gastroenteritis in our country, we carried out this study to evaluate the effectiveness of the rapid intravenous rehydration on the resolution of vomiting and correction of dehydration in moderately dehydrated children with acute gastroenteritis in whom oral rehydration therapy had failed and were therefore candidates for intravenous rehydration therapy.

Materials and Methods Settings A randomized control trial was conducted in the emergency department of Tabriz children's hospital, North-West of Iran.

Enrollment and Intervention Eligible patients were children with moderate dehydration or vomiting due to gastroenteritis who had not responded to an oral rehydration therapy. They were randomly assigned to each of the study groups: rapid intravenous rehydration or standard 24 hour intravenous therapy. They were allocated in a 1:1 ratio for each group. Nine patients in the intervention group were excluded from the study due to electrolyte abnormalities. In the intervention group, 54 patients received metoclopramide prior to admission and 49 patients in the control group received metoclopramide as well; this was not significantly different between two groups (p=0.7).

The intervention group received 20-30 cc/kg of a crystalloid solution over 2 hours. Four hours after the initiation of IV therapy, the patients were visited by the attending physician at which time they were discharged or admitted.

Table 1. Patients’ characteristics in intervention and control groups

Intervention group

Control group

Population 75 Age (year)

2.73±2.53

p

75 – 2.1±1.74

0.07

Sex (female)

27 F

31 F

0.33

Weight (kg)

12.27±5.6

11.48±4.22

0.11

Table 2. Patients’ outcomes in intervention and control groups Outcomes

Intervention group

Control group

n %

n %

Stop vomiting after 4 hours

63

84

62

Persistent vomiting

2

3

82

p >0.05 >0.05

Azarfar A et al.

Rapid Intravenous Rehydration to Correct Dehydration and Resolve Vomiting

Follow up information was collected on day 3 following admission. Patients in the control group were also visited at this time to control their vomiting.

Randomization The randomization sequence was generated by the statistical adviser of the research program. A computerized randomizer was used for this purpose.

Outcome Measure The primary outcome measure was resolution of vomiting in children with gastroenteritis receiving rapid intravenous rehydration.

Statistical Analysis Statistical analysis was performed using SPSS software.

Studentâ&#x20AC;&#x2122;s T-test and chi square tests were used for quantitative and qualitative data. P-values less than 0.05 were considered to be significant.

Results During the study period, 150 patients met the enrollment criteria and were enrolled in the study (75 to rapid rehydration and 75 to standard rehydration). The two groups were similar regarding sex, age and weight (Table 1). At two hours, 84% (63) of children given rapid IV rehydration had rehydrated or experienced resolution of vomiting and were discharged.

16% (12) were admitted to the ED (Table 2). Patients in the rapid rehydration group received 20-30 cc/kg of isotonic solution over 2 hours and patients in the standard 24 hours rehydration group had received about 30-35 cc/kg of intravenous solution over four hours according to their degree of dehydration which is not significantly different between two groups. This demonstrates that rapid intravenous rehydration can result in a substantial reduction of ED admissions.

Among 63 patients who were discharged, 2 cases had recurrence of vomiting and were readmitted.

where oral rehydration therapy fails, intravenous rehydration is a necessary alternative for dehydrated babies. A few studies have also reported an effective rehydration with administration of fluids in amounts of 20-40 cc/kg over varying periods.[8] Considering its benefits, this method of treatment is being adopted into clinical practice.[9-11] Almost all children in our study recovered without complications and only 2 cases had recurrence of vomiting and were admitted.

Some pediatric nephrologists believe that the prolonged deficit therapy is outdated, and they believe in the implementation of high volume fluid resuscitation.[5] Although multiple studies have shown usefulness and effectiveness of rapid IV rehydration,[13,14] the amounts and rates of fluid administration have not been defined. In our study, we administered 20-30 ml/kg of fluids over two hours; this was well tolerated by patients and no significant complications were observed. In the study by Phin et al. on moderately dehydrated children, significant reductions were observed in the admission rates and number of discharges in a period of eight hours or less in the intervention group compared with the control group; no significant differences in the rates of re-presentation or rate of procedures were observed.[12] Freedman et al.[9] have compared rapid versus standard IV rehydration and concluded that resolution of dehydration after two hours was the same in both groups and they suggested avoidance of using rapid rehydration due to possible complications. We did not encounter any significant complications during our investigation. However, this needs to be investigated further in larger multicenter trials.

Conclusion Rapid rehydration in children dehydrated from gastroenteritis is effective in reducing admission rates and lengths of stay in emergency departments. According to the results of this study this method can be used safely in pediatric patients with dehydration due to acute gastroenteritis.

Limitations

In 62 patients of the control group, vomiting resolved after 4 hours and only 3 had persistent vomiting for more than 12 hours. Comparing the two groups regarding the resolution of vomiting, chi square test did not indicate a significant difference between the two groups (p>0.05) (Table 2).

Our study was performed to show the preliminary advantages of rapid intravenous rehydration regimens. The analysis of serious complications and its safety and the rate and volume of fluids administered requires further investigation.

Discussion

This article is extracted from the MD Thesis of Atefe Ahmadzade.

The results of this study show that rapid intravenous rehydration is as effective as standard rehydration regimens in the treatment of dehydration and vomiting in children with gastroenteritis, and it can thus prevent unnecessary admissions to EDs and reduce unnecessary expenses. In cases

Acknowledgements

Conflict of Interest The authors declare that there is no potential conflicts of interest.

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References 1. Bonadio WA. Acute infectious enteritis in children. Emergency department diagnosis and management. Emerg Med Clin North Am 1995;13:457-72.

2. Wathen JE, MacKenzie T, Bothner JP. Usefulness of the serum electrolyte panel in the management of pediatric dehydration treated with intravenously administered fluids. Pediatrics 2004;114:1227-34.

3. King CK, Glass R, Bresee JS, Duggan C; Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep 2003;52:1-16.

4. Bender BJ, Ozuah PO. Intravenous rehydration for gastroenteritis: how long does it really take? Pediatr Emerg Care 2004;20:215-8.

5. Holliday MA, Friedman AL, Wassner SJ. Extracellular fluid restoration in dehydration: a critique of rapid versus slow. Pediatr Nephrol 1999;13:292-7.

6. Nager AL. Intravenous rehydration in paediatric gastroenteritis. BMJ 2011;343:d7083.

7. Nager AL, Wang VJ. Comparison of ultrarapid and rapid intravenous hydration in pediatric patients with dehydration. Am J Emerg Med 2010;28:123-9.

8. Moineau G, Newman J. Rapid intravenous rehydration in the pediatric emergency department. Pediatr Emerg Care 1990;6:186-8.

9. Freedman SB, Sivabalasundaram V, Bohn V, Powell EC, Johnson DW, Boutis K. The treatment of pediatric gastroenteritis: a comparative analysis of pediatric emergency physiciansâ&#x20AC;&#x2122; practice patterns. Acad Emerg Med 2011;18:38-45.

10. Nager AL. Fluid and electrolyte therapy in infants and children.

In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, editors. Tintinalliâ&#x20AC;&#x2122;s emergency medicine: a comprehensive study guide. 7th ed. McGraw-Hill; 2010. p. 971-5.

11. Shaw KN, Spandorfer PR. Dehydration. In: Fleisher GR, Ludwig S, editors. Textbook of pediatric emergency medicine. 6th ed.

Lippincott Williams & Wilkins; 2010. p. 206-11.

12. Phin SJ, McCaskill ME, Browne GJ, Lam LT. Clinical pathway using rapid rehydration for children with gastroenteritis. J Paediatr Child Health 2003;39:343-8.

13. Pizarro D, Posada G, Mohos E. Rapid rehydration by intravenous route in dehydrated children by diarrhea. [Article in Spanish] Bol Med Hosp Infant Mex 1980;37:365-74. [Abstract] 14. Vesikari T, Isolauri E, Baer M. A comparative trial of rapid oral and intravenous rehydration in acute diarrhoea. Acta Paediatr Scand 1987;76:300-5.

ORIGINAL ARTICLE

Sudden Suspected Death in Emergency Department: Autopsy Results Acil Servisteki Ani, Şüpheli Ölümler: Otopsi Sonuçları Mehtap GURGER,1 Abdurrahim TURKOGLU,2 Metin ATESCELIK,1 Turgay BORK,2 Mehmet TOKDEMIR,2 Omer Dogan ALATAS,3 Evren EKINGEN3 Department of Emergency, Fırat University Faculty of Medicine, Elazig; Department of Forensic Medicine, Fırat University Faculty of Medicine, Elazig; 3 Department of Emergency Service, Elazıg Training and Research Hospital, Elazig 1

2

SUMMARY

ÖZET

Objectives Sudden deaths occur within 24 hours after symptoms’ onset and are caused by cardiac, neurological and pulmonary diseases. Autopsy is the gold standard in determining cause of death. In this study, death’s etiology was evaluated in cases applied to our department that underwent autopsy with sudden death indication.

Amaç Ani ölümler semptomlar başladıktan sonra 24 saat içerisinde oluşur. En yaygın nedenleri kardiyak, nörolojik ve pulmoner hastalıkları içerir. Otopsi bu ölümlerin nedenini tespit etmede altın standarttır. Bu çalışmada acil servisimize başvuran ani ölüm olgularının otopsi bulgularına göre ölüm nedenlerini değerlendirdik.

Methods This study included cases aged 18 or older with sudden, suspected, non-traumatic death applying to our department between 2008 and 2012. Patients’ age, sex, death time, co-morbid diseases, initial signs, cardiac rhythm, and autopsy findings were recorded after reviewing patient charts.

Gereç ve Yöntem Bu retrospektif çalışmaya 2008-2012 yılları arasında acil servisimize başvuran, yaşları 18 ve üzeri olan, nontravmatik, ani, şüpheli ölüm vakaları alındı. Hastaların dosyaları incelenerek yaşları, cinsiyetleri, ölüm zamanı, bilinen hastalıkları, semptomlar başladıktan sonra geçen zaman, başvuru anındaki şikayeti, vital bulguları ve otopsi sonucu kaydedildi.

Results The study included 46 patients. Mean age was 45.73±19.6. Of the cases, 84.78% applied to emergency with cardiopulmonary arrest. Thirty-two cases (69.6%) were male. The most frequent cause of death was cardiovascular diseases (52.2%), followed by central nervous system disorders (21.7%), intoxications (15.2%), and respiratory diseases (10.9%).

The most common diseases were myocardial infarction (45.7%), subarachnoid hemorrhage (8.7%), and chronic obstructive pulmonary disease. There were three drug ingestions, three carbon monoxide intoxications, and one corrosive material ingestion among the intoxication cases.

Bulgular Çalışmaya 46 hasta alındı. Ortalama yaş 45.73±19.6 idi. Vakaların % 84.78’ i acil servise geldiğinde kardiyopulmoner arestti. 32 vaka (%69.6) erkekti. Ölümün en yaygın nedeni kardiyovasküler hastalıklardı (%52.2).

Bunu nörolojik hastalıklar (%21.7), intoksikasyonlar (%15.2) ve solunum sistemi ile ilgili hastalıklar (%10.9) izledi. En sık gözlenen hastalıklar myokard infarktüsü (%45.7), subaraknoid kanama (%8.7) ve kronik obstriktif akciğer hastalığı (%6.6) idi. İntoksikasyon vakalarının üçü ilaç alımı, üçü karbonmonoksit zehirlenmesi, biri koraziv madde içimiydi.

Conclusions Sudden deaths are rarely encountered. Emergency clinicians should consider cause in differential diagnosis and provide appropriate approaches at first evaluation.

Sonuç Bu kritik hastaları ilk değerlendiren hekim olan acil servis doktorları, ölümlerin altında yatan nedenlerin ayırıcı tanısını yapmalı ve uygun tedavi yaklaşımını uygulamalıdır. Ani ölümlerin en sık nedeni kardiyovasküler hastalıklar olmakla birlikte acil serviste diğer nedenler de göz önünde tutulmalıdır.

Key words: Autopsy; emergency service; sudden death.

Anahtar sözcükler: Otopsi; acil servis; ani ölümler.

Submitted: February 17, 2014 Accepted: May 09, 2014 Published online: August 30, 2014 Correspondence: Dr. Mehtap Gurger. Firat Universitesi Tip Fakultesi Hastanesi, Acil Servis, 23100 Elazig, Turkey. e-mail: drmhtp@yahoo.com

Turk J Emerg Med 2014;14(3):115-120

doi: 10.5505/1304.7361.2014.47560

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Introduction

Statistical Analysis

The World Health Organization (WHO) definition of sudden death, a significant health problem is “death, occurring less than 24 hours from the onset of sudden changes in previous clinical condition”.[1,2] Sudden deaths are non-traumatic deaths.[1] Autopsy should be performed in order to understand the cause of death in patients who die suspiciously and unexpectedly.[2-4] Emergency rooms (ER), a significant entry to hospitals for the critically ill patients, play a crucial role in the treatment and health care of these patients.

Management of these patients, who are brought to hospital with a life-threatening condition or with cardiopulmonary arrest, is difficult, and finding the underlying cause and treatment for that cause is challenging. Previous medical history of the patient could be unknown by the health team and family members of the patient who brought him/ her to emergency room, or patient may not have a relative with him/her and this could be his/her first admittance to a hospital. In this circumstance, preexisting diseases of the patient are not disclosed. Most of these patients suffer cardiopulmonary arrest when they are brought to emergency room and a detailed medical history cannot be obtained because the event occurs suddenly and because of absence of eyewitness or family members witnessing the event.[5] We therefore believe that determining the cause of sudden, unexpected deaths in emergency rooms is important in management of the critically ill patients admitted to emergency department.

Data obtained were transferred to SPSS 17.0 (Statistical Package for Social Science) program. Chi Square Test was used for statistical analysis of the data and they were evaluated in 95% confidence interval. A p value < 0.05 was considered statistically significant, and the average of data complying with normal distribution was given as arithmetic mean ± standard deviation.

Results During the five-year-period, 231 patients died in the ER. Among these cases, 46 (19.91%) were considered as sudden and suspicious death. The average age of the cases was 45.73±19.68 (min:18-max:92) and 69.6% were male. Thirtynine cases (84.78%) were brought to emergency department as cardiopulmonary arrest. The average time of stay in the emergency department was 41.95±23.65 minutes (min:10-max:120 min.). According to autopsy reports, most common cause of death was cardiovascular disease (52.2%), followed by central nervous system diseases (21.7%), intoxications (15.2%), and respiratory diseases (10.9%) (Figure 1).

The most common disease was acute myocardial infarction (AMI) (n=20) among the cardiovascular diseases (n=24). This was followed by valve diseases (n=2), aortic dissection (n=1) and pulmonary emboli (n=1). One of the cases with valve disease was pregnant and had aortic stenosis, the other had mitral valve insufficiency.

The purpose of this study was to determine cause of death according to autopsy findings in patients who were brought to our emergency department and who died suddenly, unexpectedly, and non-traumatically.

Among central nervous system diseases (n=10), most common was subarachnoid hemorrhage (SAH) (n=4), followed by intracranial bleeding (n=2), asphyxia due to epileptic seizure (n=2), ischemic stroke (n=1), and meningitis (n=1).

Materials and Methods

Seven of the cases were intoxication patients. One of these cases took tricyclic antidepressant drug, one case took narcotic substance, one case took benzodiazepine, beta block-

Patients who died within 24 hours, were brought to our emergency department with cardiopulmonary arrest, did not have trauma marks in the body, and whose cause of death cannot be determined during the intervention in ER, as well as non-traumatic cases who died a short time after being admitted to the ER before a diagnoses could be made, were determined to have suffered from sudden, suspicious death. All patients in the study were 18 and over at the time of death. Medical records of the cases who were diagnosed as sudden suspicious death between 2008 and 2012 were analyzed retrospectively. Cause of death in these cases were recorded according to autopsy results. Prior to study, approval was obtained from Fırat University ethical committee. Traumatic deaths and cases who were diagnosed during emergency intervention were excluded.

Percentage of cases Central nervous system (21.7%) Cardiovascular system (52.2%)

Respiratory system (10.9%) Intoxication (15.2%)

Figure 1. Distribution of cases according to causes of death.

Gürger M et al.

Sudden Suspected Death in Emergency Department

oxide poisoning; one of them was affected from stove, one from water heater, and one from commercial liquefied petroleum gas.

Table 1. Causes of death in sudden death cases

according to autopsy results

n

%

Among respiratory diseases, three cases had respiratory failure due to chronic obstructive lung disease (COLD). One case had respiratory failure due to Behçet’s disease, and one case had respiratory failure due to Wegener granulomatosis.

Distribution of death causes of the cases according to autopsy results is shown in Table 1.

Cardiovascular system

Myocardial infarction

20

45.7

Heart valve disease

2

4.3

Aortic dissection

1

2.2

Pulmonary embolism

1

2.2

Central nervous system Subarachnoid hemorrhage 4 8.7 Epilepsy

2

4.3

Intracranial hemorrhage

2

4.3

Meningitis

1

2.2

1

2.2

Ischemic cerebrovascular disease

A statistically significant difference was detected in analysis done between gender of the cases and cause of death in autopsy reports (χ2 4.493 p=0.035) (Table 2). Advanced analysis revealed that this significance originated from deaths due to cardiovascular causes and genders.

Respiratory system Chronic obstructive lung disease 3 6.6

Pulmonary failure

2

117

When causes of death and age groups were investigated, it was seen that central nervous system related deaths were higher among age groups between 18-29 and 40-49, while cardiovascular system related deaths were higher among other age groups (Table 3).

4.3

Intoxication

7 15.2

Total

46 100

Discussion

er and selective serotonin reuptake inhibitor, and one case took corrosive substance. Three cases were carbon mon-

Sudden death is a very important public health problem

Table 2. Distribution of causes of death according to gender

Gender

Causes of death Cardiovascular system

Central nervous system

Respiratory system

Intoxication

Total

n

%

n

%

n

%

n

%

n

%

Male

20

83.3

7

70.0

2

40.0

3

42.9

32

69.6

Female

4

16.7

3

30.0

3

60.0

4

57.1

14

30.4

Total

24

100

10

100

5

100

7

100

46

100.0

(χ²=4.493, p=0.035).

Table 3. Distribution of causes of death according to age groups Causes of death

Age groups

18-29

30-39

40-49

n

n

n

50-59

60 and above

n

n

Total n

%

Cardiovascular system

3

7

1

4

9

24

52.2

Central nervous system

4

1

3

–

2

10

21.7

1

5 10.9

Respiratory system 2 – 1 1 Intoxication

2 1 1 2

1

7 15.2

Total

11

13

46 100.0

9

6

7

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worldwide, and time interval between onset of symptoms and mortality is less than 24 hours.[1] Autopsy is required to explain cause of death in these cases.[2] Although it differs from one country to another, the most common cause of natural sudden deaths is cardiovascular disease, while central nervous system disease is second. We found that the most common non-traumatic sudden deaths in our emergency department occurred due to cardiovascular diseases (52.2%), followed by central nervous system disease (21.7%), intoxications (15.2%), and respiratory system diseases (10.9%).

It is reported that 78.4% of the suspected deaths occur at the scene.[7] In our cases, 84.7% were brought to emergency room as cardiopulmonary arrest. However, since our study was a retrospective one, no information during file analysis could be achieved whether arrest was at the scene or on the way to ER. Most common cardiovascular diseases that cause death include coronary heart disease, hypertrophic cardiomyopathy, aortic diseases, and pulmonary emboli.[8] Cause of death in youngsters is different from adults. Congenital heart diseases, myocarditis, hypertrophic cardiomyopathy, and conduction system anomaly are the most common underlying causes below 20 years of age.[9,10] Incidence of coronary artery disease increase with age and is most common above 30 years of age.[10] Manfredini et al.[11] found in a study in Italy that AMI was responsible for 55% of 732 sudden death cases, pulmonary emboli in 7.5%, aortic aneurism rupture in 3.8% and stroke in 2.3%. Thomas et al.[12] reported 322 sudden death cases aged between 18-69 as a result of three-year-analysis. They detected ischemic heart disease in 58.7% of these cases, non-ischemic heart disease in 7.5%, respiratory disease in 17.7%, central nervous system disease in 4.3%, aortic aneurism in 3.4% and gastrointestinal bleeding in 2.2%. In our study, consistent with the literature, we found that non-traumatic suspicious deaths occurring in our emergency department were most commonly due to cardiovascular system diseases. AMI was present in 45.7% of the cardiovascular diseases and it constituted the most common disease group that caused death. Valve disease was the cause in 4.3% of the cases. In autopsy of one of these cases, aortic stenosis and pregnancy was detected, while mitral insufficiency was found in the other. Case with mitral stenosis had been brought to emergency department in arrest, following a severe exercise. Sudden death in aortic stenosis is well defined and can be precipitated by exercise. Increased cardiac demand associated with physical effort in presence of a fixed left ventricular outlet obstruction can lead to fatal ventricular arrhythmias.[13] Sudden deaths due to intracranial causes in the adults are

not uncommon among adults and can occur due to trauma, tumor, hemorrhage, ischemic stroke, and epilepsy. Lynch et al.[14] examined 499 non-traumatic sudden death cases without known central nervous system abnormality according to autopsy and radiologic findings for 10 years. They found that 48 of these cases occurred due to central nervous system disease. Aneurism rupture was found in 11 of these 48 cases, hemorrhage in 9, tumor-cyst in 8, subdural hematoma in 5, sinus vein thrombosis in 4, meningitis in 3, infarction in 3, arteriovenous malformation in 2, cerebral abscess in 1, brain metastasis in 1, arterial dissection in one case. In our study, 10 cases died due to causes related with central nervous system. In four of these SAH was present, two had intraparenchymal bleeding, two had epilepsy, one had meningitis and one had ischemic stroke.

About 15% of the patients with subarachnoid hemorrhage died before being admitted to the hospital, and more than 20% died within 48 hours after onset of symptoms. Sudden deaths related to central nervous system can occur as a result of acute damage or suppression of vital centers.

Central nervous system dysfunction or sudden increase in intracranial pressure can result in life-threatening arrhythmias. ECG alterations such as prolongation in QT interval, sharp or reverse T wave, depression or elevation in ST segment, non-sustained ventricular tachycardia, and R on T phenomenon can occur in SAH or other intracranial events.

[15,16] These alterations are associated with incompatibility of heart in autonomous control; the heart was found to be normal in autopsies of most of the patients who died because of central nervous system lesion. On the other hand, focal myocytolysis, myofibrillar degeneration, lipofuscin pigment accumulation in myocardium, and histiocyte accumulation in necrosis region were shown in various brain diseases. Autonomous nervous system and several chemical mediators are involved in pathogenesis.[18] In autopsies of three cases, we did not find any other pathology that explains cause of death besides SAH in our study. SAH and aspiration were present in one case. No information on ECG alteration could be reached because cases suffered arrest when they were brought to emergency department.

Epilepsy is one of the most common serious neurologic disorders worldwide and risk of early death is 2-3 times greater compared to general population.[17,18] Onset of epilepsy at early age, long and frequent seizures, generalized tonic clonic seizure, nocturnal seizures, dementia, presence of cerebrovascular disease, asthma, male gender, low antiepileptic drug compliance, low antiepileptic drug levels in postmortem studies, and alcohol use are risk factors. Although the mechanism of death is not well known, cardiac arrhythmia, apnea, neurogenic pulmonary edema, obstructive respiratory failure, and positional asphyxia due to seizure were

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Sudden Suspected Death in Emergency Department

suggested. In our study, three of 46 cases had history of epilepsy and it was found that one died because of AMI while two died asphyxia due to epileptic seizure.

Seven of the suspected, sudden death cases were diagnosed as intoxication at the end of autopsy. One of these cases took tricyclic antidepressant drug, one case took benzodiazepine, beta blocker and selective serotonin reuptake inhibitor, and one case took narcotic substance. These cases were brought to emergency department in arrest and diagnosis was made as a result of toxicologic investigation at the forensic medicine department. One of the three study subjects died due to carbon monoxide poisoning was affected from stove, one from water heater, and one from commercial liquefied petroleum gas. All these three cases were found in cardiopulmonary arrest in a closed environment. Autopsies of these cases revealed that cause ıf death was asphyxia due to carbon monoxide, while one case also had aspiration. Carbon monoxide poisoning should be taken into account in deaths occurring, particularly in closed areas.[19] There were five death cases associated with respiratory disease in our study. Among these, three cases had respiratory failure due to chronic obstructive lung disease (COLD), one case had respiratory failure due to Behçet’s disease, and one case had respiratory failure due to Wegener granulomatosis.

Intermittent hypoxia, Theophylline and cathecolamines can cause ventricular arrhythmias in COLD patients, particularly in those with subclinical myocardial ischemia and sedative tranquilizers, which can lead to death by suppressing respiration.[12] Two COLD cases in our study had been brought to emergency department in arrest and no explanation other than COLD could be found in their autopsies. In one case, the patient suffered cardiopulmonary arrest shortly after being brought to emergency department. Arrhythmia and ischemia sign was not found in ECG of that patient and it was seen in autopsy that no pathology was detected beside COLD. Limitations Since this study is retrospective, detailed information on complaints of the patients prior to arrest, time interval between onset of complaints and arrest, and risk factors for sudden death could not be attained.

Conclusion Patients who are brought to the emergency department with cardiopulmonary arrest and no witness and die unexpectedly, or whose cause of death cannot be explained with existing disease and die shortly after being brought to the emergency department without diagnosis should be defined as sudden, suspected death and autopsy should

be performed in order to detect certain cause of death in these forensic cases. Cardiovascular disease is the most common cause underlying the on-traumatic, sudden, suspicious deaths, followed by central nervous system diseases. Acute myocardial infarction is the most important disease among these. We should keep in mind aortic dissection, pulmonary emboli, intoxications, and diseases involving central nervous system and respiratory system beside myocardial infarction in differential diagnosis of sudden death cases brought to emergency department. We believe that underlying causes of sudden and unexpected deaths are crucial in the management of emergency patients.

Conflict of Interest The authors declare that there is no potential conflicts of interest.

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2. Gülmen MK, Meral D. Ani kardiyak ölümler. Klinik Gelişim 2009;22:56-9.

3. Ersoy G, Toprak S. Güncel durumu ile hukuki ve tıbbi açıdan otopsi süreci. Klinik Gelişim 2009;22:64-75.

4. Yaniv G, Guranda L, Or J, Zaitsev K, Konen E, Hiss J. Correlation between radiological and pathological findings for a sudden death incident in the emergency department. Isr Med Assoc J 2011;13:707-8.

5. Mushtaq F, Ritchie D. Do we know what people die of in the emergency department? Emerg Med J 2005;22:718-21.

6. Yağmur F, Din H, Özbek A, Kaya M. Dissekan aort anevrizmasına bağlı ani ölüm: Üç olgu. Düzce Tıp Dergisi 2010;12:68-71.

7. Yağmur F, Din H. Kayseri ilinde 2007 yılında adli ölü muayenesi ve otopsileri yapılan olguların değerlendirilmesi. Adli Tıp Dergisi 2009;23:18-24.

8. Tian ZX, Lü YY, Nugessur CR, Yan W, Zhao WK, Kong LL, et al.

Common underlying diseases do not contribute in determining the causes of sudden unexplained death. Chin Med J (Engl) 2013;126:870-4.

9. Meyer L, Stubbs B, Fahrenbruch C, Maeda C, Harmon K, Eisenberg M, et al. Incidence, causes, and survival trends from cardiovascular-related sudden cardiac arrest in children and young adults 0 to 35 years of age: a 30-year review. Circulation 2012;126:1363-72.

10. Jouven X, Desnos M, Guerot C, Ducimetière P. Predicting sudden death in the population: the Paris Prospective Study I. Circulation 1999;99:1978-83.

11. Manfredini R, Portaluppi F, Grandi E, Fersini C, Gallerani M. Out-of-hospital sudden death referring to an emergency department. J Clin Epidemiol 1996;49:865-8.

12. Thomas AC, Knapman PA, Krikler DM, Davies MJ. Commu-

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nity study of the causes of “natural” sudden death. BMJ 1988;297:1453-6.

13. Killip T. Time, place, event of sudden death. Circulation 1975;52(6 Suppl):III160-3.

14. Lynch KM, Brett F. Headaches that kill: a retrospective study of incidence, etiology and clinical features in cases of sudden death. Cephalalgia 2012;32:972-8.

15. Estanol BV, Marin OS. Cardiac arrhythmias and sudden death in subarachnoid hemorrhage. Stroke 1975;6:382-6.

16. Baranchuk A, Nault MA, Morillo CA. The central nervous system and sudden cardiac death: what should we know? Car-

diol J 2009;16:105-12.

17. Zhuo L, Zhang Y, Zielke HR, Levine B, Zhang X, Chang L, et al.

Sudden unexpected death in epilepsy: Evaluation of forensic autopsy cases. Forensic Sci Int 2012;223:171-5.

18. Hesdorffer DC, Tomson T. Sudden unexpected death in epilepsy. Potential role of antiepileptic drugs. CNS Drugs 2013;27:113-9.

19. Cantürk N, Başbulut AZ, Cantürk G, Dağalp R. Ankara’da 20042008 yılları arasında karbonmonoksit zehirlenmeleri otopsi bulgularının değerlendirilmesi. Adli Tıp Dergisi 2008;22:2530.

ORIGINAL ARTICLE

The Analysis of Escherichia Coli Resistance in Urine Culture and in Antibiograms as Requested by Emergency Service Acil Servisten İstenen İdrar Kültür ve Antibiogramlarında Escherichia Coli Direncinin Analizi Yavuz YIGIT,1 Vesile YAZICI,2 Harun AYHAN,3 Emin Gokhan GENCER,4 Huseyin Cahit HALHALLI,1 Onur KARAKAYALI,1 Yahya Kemal GUNAYDIN5 Department of Emergency, Derince Training and Research Hospital, Kocaeli; Department of Microbiology, Derince Training and Research Hospital, Kocaeli; 3 Department of Emergency, Haydarpasa Training and Research Hospital, Istanbul; 4 Department of Emergency, Dr. Lutfi Kirdar Kartal Training and Research Hospital, Istanbul; 5 Department of Emergency, Konya Training and Research Hospital, Konya 1

2

SUMMARY

ÖZET

Objectives The aim of this study was to determine the antibiotic resistance of infectious and non-infectious E. coli species in order to increase the success of empirical antibiotic treatment in urinary system infections.

Amaç Bu çalışmada üriner sistem enfeksiyonlarında ampirik antibiyotik tedavi başarısını artırmak için enfeksiyon etkeni olan veya olmayan E.coli suşlarının çeşitli antibiyotik türlerine direnci araştırıldı.

Methods The antibiotic susceptibility of 464 E. coli strains that were isolated from urine samples of patients who visited Derince Training and Research Hospital Emergency Department between January 1 and December 31, 2012 were retrospectively evaluated from records. The antibiogram results were classified as susceptible, moderately susceptible or resistant. Moderately susceptible strains were assumed to be resistant.

Gereç ve Yöntem 1 Ocak-31 Aralık 2012 tarihleri arasında Derince Eğitim ve Araştırma Hastanesi acil servisine başvuran hastaların mikrobiyoloji laboratuvarına gönderilmiş idrar örneklerinden izole edilen 464 E.coli suşunun antibiyotik duyarlılıkları bilgisayar kayıtları üzerinden retrospektif olarak değerlendirildi. Antibiyogram sonuçları duyarlı, orta duyarlı ve dirençli olarak sınıflandırıldı. Orta duyarlı suşlar dirençli kabul edildi.

Results Bacterial proliferation was seen in 563 (28.1%) of the 1998 urine cultures tested. One hundred and twelve cultures could not be evaluated due to contamination, and there was no proliferation in 1323 cultures.

E. coli strains were isolated in 464 (82.4%) of the cultures in which proliferation was seen. Three hundred and sixty seven (79%) of the patients were female, 97 (21%) were male, and the mean age of all of the patients was 41.1±24.1 years (min: 1, max: 90). The antibiograms of the E. coli strains revealed that meropenem had the lowest resistance (0%), while ampicillin-sulbactam had the highest resistance (36.8%).

Bulgular 1998 idrar kültüründen 563’ünde (%28.1) üreme oldu. Kültürlerin 112’si kontaminasyon nedeniyle değerlendirilemedi, 1323 kültürde ise üreme olmadı. Üreme olan kültürlerden 464’ünde (%82.4) E.coli suşları izole edildi. Hastaların 367’si (%79) kadın 97’si (%21) erkek, tüm hastaların yaş ortalaması 41.1±24.1 (min: 1, maks: 90) idi. E.coli suşlarına karşı antibiyogramlar incelendiğinde, direncin en düşük görüldüğü antibiyotik meropenem (%0), en yüksek görüldüğü antibiyotik ise ampisilinsulbaktam olarak saptandı (%36.8).

Conclusions In this study, we investigated the antibiotic resistance of E. coli strains isolated from urine cultures in our region. Future studies, perhaps similar to this one, can be performed in the future to increase the success of treatments.

Sonuç Bölgemizde idrar kültürlerinden izole edilen E.coli suşlarına karşı antibiyotik dirençlerini incelediğimiz çalışmamızın benzerlerinin ilerleyen dönemde yapılmasının tedavi başarısına yardımcı olacağını düşünmekteyiz.

Key words: Culture; E. coli; emergency; urine.

Anahtar sözcükler: Kültür; E.coli; acil; idrar.

Submitted: March 10, 2014 Accepted: May 28, 2014 Published online: August 30, 2014 Correspondence: Dr. Yavuz Yigit. Derince Egitim ve Arastirma Hastanesi, Derince, Kocaeli, Turkey. e-mail: dryavuzyigit@gmail.com

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Introduction Urinary system infection is defined by the existence of bacteria in the kidneys, collecting duct system, and/or urinary bladder, as well as pyuria and clinical symptoms. Its severity ranges from asymptomatical bacteriuria to pyelonephritis.

[1] Urinary system infection is the most common type of infection in adults.[2] 25-35% of women between the ages of 20-40 years have urinary system infection,[3] and there are 5 million attacks of cystitis in our country every year.[4] E. coli is present in 50-90% of these infections. Antibiotics are commonly used to treat urinary system infections, although they should be used with caution. The most important issues to monitor during antibiotic treatment are duration of treatment, toxicity of the medication, and cost. Antibiotics used should not spoil the intestinal, perineal and vaginal flora, but should be effective against E. coli colonization.[5] Local antibiotic resistance should be followed up regularly in order to successfully treat urinary system infections.[6] Several studies have shown that antibiotic resistance is increased in E. coli strains that cause urinary system infections. Antibiotic resistance is particularly common with cotrimoxazole and betalactams, which are relatively old molecules.[7] However, more recent research has indicated that resistance is increasing in fluoroquinolones as well.[8] In this study, the antibiotic resistance of infectious and non-infectious E. coli species was investigated to increase the success of empirical antibiotic treatment in urinary system infections.

Materials and Methods Patients with symptoms of urinary tract infection who presented at Derince Training and Research Hospital Emergency Department, Turkey, between January and December 2012 were included in this study. Clinical evidence for urinary tract infection included dysuria, fever, urgency, frequency, suprapubic or flank pain, or other clinical presentations consistent with a urinary tract infection. For patients with more than one sample, we included only the first positive sample.

The antibiotic susceptibility of 464 E. coli strains was retrospectively evaluated from hospital records. The ethics committee approved this study. The urine samples were isolated in a sterile way, inoculated in 5% sheep blood agar (RTA) and EMB (RTA) via a quantitative method, and were placed in an incubator (37°C) for 24-48 hours. Bacteria were detected by gram staining, evaluating colony morphology, and by traditional biochemical tests (TSI agar, Simmon’s citrate agar, movement medium, Christensen urea agar, reactions in indol medium, catalase, oxidase, coagulase, esculin hydrolysis). Bacteria were identified by an automated Phoenix system (BBL Becton Dickinson). Antibiotic susceptibility in proliferating bacteria was evaluated by the Kirby-Bauer disc diffusion method in accordance with the CLSI (Clinical Labo-

ratory Standards Institute) criteria using Müler-Hinton agar (RTA) for automated systems. Escherichia coli (ATCC 25922), Staphylococcus aureus (ATCC 29213), Staphylococcus aureus (ATCC 25923) and Pseudomonas aeruginosa (ATCC 27853) were used as quality controls. The antibiogram results were classified as susceptible, moderately susceptible or resistant.

Moderately susceptible strains were assumed to be resistant.

Statistical Analysis Data from this study were recorded and evaluated using SPSS version 13.0 for Windows. The Chi-square test was used to evaluate categorical variables. Continuous variables were expressed as mean±standard deviation, minimum and maximum values were expressed as parenthetical values, and qualitative variables were expressed as number and percentage (%). P<0.05 was regarded as statistically significant.

Results Bacterial proliferation was detected in 563 (28.1%) of the 1998 urine cultures. One hundred and twelve cultures could not be evaluated due to contamination and there was no proliferation in 1323 cultures. E. coli strains were isolated in 464 (82.4%) of the cultures in which there was proliferation.

Three hundred and sixty seven (79%) of the patients were female, 97 (21%) were male, and the mean age of all of the patients was 41.1±24.1 years (min:1, max:90). Antibiograms of the E. coli strains revealed that the lowest resistance was found in cultures treated with meropenem (0%), nitrofurantoin (3.9%), ceftazidime (8.2%), gentamicin (8.3%), and cefepime (9.5%). Those with the highest resistance included amoxicillin-clavulanic acid (23.4%), ampicillin-sulbactam (36.8%), norfloxacin (14.9%), cefazoline (15.1%), ceftriaxone Table 1. Resistance rates of antibiotics Antibiotic

Resistance (%)

Meropenem 0 Nitrofurantoin 3.9 Ceftazidime 8.2 Gentamicin 8.3 Cefepime 9.5 Amoxicillin- Clavulanic Acid

23.4

Ampicillin-Sulbactam 36.8 Norfloxacin 14.9 Cefazoline 15.1 Ceftriaxone 11.1 Cefuroxime 12.9 Ciprofloxacin 17.7 Cotrimoxazole 28

Yiğit Y et al.

The Analysis of Escherichia Coli Resistance in Urine Culture

(11.1%), cefuroxime (12.9%), ciprofloxacin (17.7%) and cotrimoxazole (28%) (Table 1).

Discussion The culture positivity ratio in our study was 28.1%, while those in previously published studies were 51.2% (in Ertuğrul et al.’s study),[4] 35% (in Gupta et al.’s study),[9] and 57.8% (in Pekdemir’s study).[11] We hypothesize that the difference between the results of our study and others is that we included patients younger than 18 years, while the other studies did not. Urine culture is frequently used in female children younger than 10 years presenting to emergency service.

E. coli is the pathogen frequently responsible for urinary tract infection. Worldwide, the proliferation ratio of E. coli in urine cultures is 75-90%.[9] In our country, various studies have reported this ratio to be 65-80%.[10] E. coli was the most common pathogen (82.3%) in the current study, which is similar to previously reported results.

Ciprofloxacin and cotrimoxazole are antibiotics that are often used for the treatment of simple urinary tract infection.

In our study, resistance to ciprofloxacin was 17.7%, which is similar to other studies, in which it was reported to be between 5-46%.[4,12,13] When compared with other antibiotics included in our study, ciprofloxacin is the 4th most resistant molecule.

Resistance to cotrimoxazole was 28% in our study, which was lower than that found in Güneysel’s study (34%)[14] and Pekdemir’s study (40.4%).[11] Cotrimoxazole was the 2nd most resistant antibiotic used in our study. The results of our study and others suggest that cotrimoxazole is very resistant in empirical treatment.

In our study, the resistance ratios of ampicillin-sulbactam (36.8%), amoxicillin-clavulonic acid (23.4%) and ciprofloxacin (17.7%) were significantly higher than that of nitrofurantoin (3.9%) (p<0.05). On average, nitrofurantoin is used at 400 mg/day in 4 equal doses to treat urinary tract infections in adults. At this concentration, it is only effective in the urine and kidneys, and is not effective in other tissues.[15] Cotrimoxazole and ciprofloxacin are most often used in the empirical treatment of simple urinary tract infections, and because they are used only twice a day, patient compliance is higher. These antibiotics are effective in tissues other than the urine and kidneys. In our study and others, nitrofurantion was more successful in treating urinary tract infections, but the guidelines of the Infectious Diseases Society of America (IDSA) indicate that there is no difference between nitrofurantoin and cotrimoxazole in seven day-treatment, and that more comparative studies are necessary.[16] Since susceptibility to nitrofurantoin is significantly high, we be-

lieve that future studies should compare its treatment with that of other oral antibiotics.

Limitations One limitation of this study is its retrospective methodology, as the urine culture indications could not be determined clearly from the records. In addition, because not all of the medical records were clear, there is a possibility that we misclassified some of the patients. The external validity of this study is also limited because it was performed in a single center. Centers with different demographic characteristics and those in different geographic regions might have different resistance patterns.

Conclusion It is important to evaluate local antibiotic resistance to ensure the successful treatment of urinary system infections. In this study, we investigated the antibiotic resistance among E. coli strains isolated from urine cultures in our region. Future studies similar to this can be performed in order to help increase the success of treatment.

Conflict of Interest The authors declare that there is no potential conflicts of interest.

References 1. Özsüt H. İdrar yolu infeksiyonları. In: Topçu AW, Söyletir G, Doğanay M, editors. İnfeksiyon hastalıkları ve mikrobiyolojisi. İstanbul: Nobel Tıp Kitabevleri; 2002. p. 1059-6.

2. Kunin CM. Urinary tract infections: detection, prevention, and management. 5th ed. Baltimore: Williams&Wilkins; 1997. p.

1-21, 128-64, 363-96.

3. Hooton TM, Stamm WE. Diagnosis and treatment of uncomplicated urinary tract infection. Infect Dis Clin North Am 1997;11:551-81.

4. Ertuğrul MB, Atilla-Güleç L, Akal D, Çağatay AA, Özsüt H, Eraksoy H, et al. Üropatojen Escherichia coli suşlarının tedavide sık kullanılan antibiyotiklere duyarlılıkları. Klinik Dergisi 2004;17:132-6.

5. Eraksoy H, Özsüt H. Hastane dışı üriner sistem infeksiyonlarında ampirik antibiyotik tedavisi. In: Kanra G, Akalın HE eds. Empirik Antibiyotik Tedavisi. Ankara: Enfeksiyon Hastalıkları Derneği Yayınları 1994;2:241-52.

6. Norrby SR, Cheng AFB. Treatment regimens for urinary tract infections. Curr Opin Infect Dis 1996;9:31-3.

7. Akata F. Üriner sistem infeksiyonlarında uygun antibiyotik kullanımı. Klimik Derg 2001; 14:114-23.

8. Pérez-Trallero E, Urbieta M, Jimenez D, García-Arenzana JM, Cilla G. Ten-year survey of quinolone resistance in Escherichia coli causing urinary tract infections. Eur J Clin Microbiol Infect Dis 1993;12:349-51.

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9. Gupta K, Hooton TM, Naber KG, Wullt B, Colgan R, Miller LG, et al. International clinical practice guidelines for the treatment of acute uncomplicated cystitis and pyelonephritis in women: A 2010 update by the Infectious Diseases Society of America and the European Society for Microbiology and Infectious Diseases. Clin Infect Dis 2011;52:e103-20.

10. Arslan H, Azap OK, Ergönül O, Timurkaynak F; Urinary Tract Infection Study Group. Risk factors for ciprofloxacin resistance among Escherichia coli strains isolated from communityacquired urinary tract infections in Turkey. J Antimicrob Chemother 2005;56:914-8.

11. Pekdemir M, Yılmaz S, Dündar DÖ, Uygun M. Analyzes of urine cultures and antibiograms ordered from emergency department. [Article in Turkish] Turk J Emerg Med 2006;6:154-7.

12. Sucu N, Aktoz-Boz G, Bayraktar Ö, Çaylan R, Aydın K. Üropa-

tojen Escherichia coli suşlarının antibiyotik duyarlılıklarının yıllar içerisindeki değişimi. Klimik Dergisi 2004;17:128-31.

13. Şencan İ, Sevinç ME. Toplum kökenli üropatojen Escherichia coli izolatlarında antimikrobiyal direncin izlemi. Klimik Dergisi 2002;15:85-88.

14. Güneysel Ö, Erdede M, Denizbaşı A. Trimethoprim sulfamethoxazole resistance in urinary tract infections: which is next? Eur J Emerg Med 2006;13:48.

15. Kayaalp O. Rasyonel tedavi yönünden tıbbi farmakoloji. 7. baskı. Ankara: Güneş Kitabevi; 1994. p. 894-9.

16. Warren JW, Abrutyn E, Hebel JR, Johnson JR, Schaeffer AJ, Stamm WE. Guidelines for antimicrobial treatment of uncomplicated acute bacterial cystitis and acute pyelonephritis in women. Infectious Diseases Society of America (IDSA). Clin Infect Dis 1999;29:745-58.

ORIGINAL ARTICLE

Evaluation of Prevalence of Low Back Pain Among Residents of Tabriz University of Medical Sciences in Relation with Their Position in Work Tebriz Üniversitesi Tıp Bilimlerinde Görevli Asistan Doktorlar Arasında İş Yeri Pozisyonlarına Bağlı Olarak Yaygın Görülen Bel Ağrısının Değerlendirilmesi Samad SHAMS VAHDATI,1 Reza SARKHOSH KHIAVI,2 Rouzbeh RAJAEI GHAFOURI,1 Ida ADIMI3 Assistant Professor of Emergency Medicine, Tabriz University of Medical Sciences, Tabriz, Iran; 2 Medical Student (internship), Tabriz, Iran; 3 Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran

1

SUMMARY

ÖZET

Objectives Lower back pain is one of the most common complaints among the general population and among health professionals. Multiple workplace-related risk factors may contribute to back pain among physicians. The aim of this study was to assess the prevalence of lower back pain among medical residents of different medical specialties and to evaluate the relevant risk factors.

Amaç Genel popülasyon ve sağlık çalışanları arasında bel ağrısı en yaygın şikayetlerden biridir. İş yerindeki çeşitli risk faktörleri doktorlar arasında görülen bel ağrısına sebep olabilir. Bu çalışmanın amacı, farklı tıbbi uzmanlık alanlarında görevli asistan doktorlar arasında bel ağrısı şikâyet sıklığını ve ilgili risk faktörlerini değerlendirmekti.

Methods A Dutch Musculoskeletal Questionnaire (DMQ) was completed by 125 medical residents. Part I concerned general demographic information, part II evaluated workplace-specific factors, and part III assessed the individual characteristics of lower back pain.

Gereç ve Yöntem Alman Kas-İskelet Sistemi Rahatsızlık Anketi 125 asistan doktor tarafından dolduruldu. Anketin 1. bölümü genel demografik bilgiler ile ilgili olup 2. bölüm iş yerine özel risk faktörlerini, 3. bölüm ise bel ağrısının özel niteliklerini değerlendiriyordu.

Results The overall prevalence of lower back pain among residents was 56.8%, with 45.1% of men and 76.5% of women reporting lower back pain.

A total of 94.4% of affected individuals believed that their lower back pain was related to their current job, and 72.6% claimed that the onset of lower back pain occurred after beginning medical work. Statistical analysis revealed a significant correlation between lower back pain and certain risk factors, such as working in the same position for long periods, repetitive movement (bending, twisting) of the lumbar region, working in uncomfortable postures, stress, walking, and standing for long periods. However, no significant relationship was found between lower back pain and heavy lifting, smoking, or prolonged sitting. The role of exercise as a protective factor in reducing the incidence of lower back pain was supported by the statistical analysis.

Bulgular Asistan doktorlar arasında görülen bel ağrısının genel sıklık derecesi %56,8’ken bel ağrısından şikâyetçi olan kadınlar %76,5’lik ve erkekler %45,1’lik bir dilimi oluşturdu. Bel ağrısı şikâyeti olan bireylerin %94,4’ü, bel ağrılarının mevcut işleri dolayısıyla ortaya çıktığına inanırken %72,6’sı bel ağrısının sağlık sektöründe çalışmaya başladıktan sonra başladığını iddia etti. İstatiksel analiz, uzun süre aynı pozisyonda çalışmak, bel bölgesinin yinelenen hareketleri (eğilme, bükülme), rahatsızlık verici postür ile çalışmak, stres, yürümek ve uzun süre ayakta kalmak gibi çeşitli risk faktörleri ile bel ağrısı arasında bir bağlantı olduğunu ortaya koydu.

Ancak, ağır kaldırmak, sigara içmek ve uzun süre oturmak ile bel ağrısı arasında önemli bir ilişki saptanmadı. Bel ağrısı şikâyetini azaltmak için uygulanan belirli egzersizlerin koruyucu özelliği bu istatiksel analizle de desteklenmiştir.

Conclusions The prevalence of lower back pain among residents is high and is associated with a number of workplace-related risk factors.

Sonuç Asistan doktorlar arasında bel ağrısı şikâyeti yüksek olmakla birlikte iş yerine özel birçok risk faktörüyle de bağlantılıdır.

Key words: Low back pain; resident; position.

Anahtar sözcükler: Bel ağrısı; ikamet; pozisyon.

Submitted: February 19, 2014 Accepted: June 03, 2014 Published online: August 30, 2014 Correspondence: Dr. Ida Adimi. Gholghasht Street, Imam Reza Hospital, Emergency Department Tabriz, Iran. e-mail: ida.adimi@gmail.com

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Introduction Lower back pain is one of the most common complaints among the general population[1] as well as among healthcare professionals. In the general population, point prevalence of 12-33%, annual incidence of 22-65%, and lifetime prevalence of 11-48% have been reported.[2] The annual prevalence of lower back pain among healthcare professionals is approximately 77%.[3] The working conditions for physicians have been considered as a major risk for the development of musculoskeletal disorders (MSD).[4] Important risk factors for MSD include prolonged standing and sitting, poor posture, heavy lifting, pushing or pulling of objects, bending and twisting, or heavy physical work. Nevertheless, these factors differ according to each physician specialty.

Unfortunately, most epidemiological studies on this topic have been conducted in developed countries and do not necessarily reflect the specific risks associated with healthcare work. The occupational hazards associated with lower back pain have not been examined thoroughly within the medical community, particularly in developing regions.

The aim of this study was to investigate the prevalence of lower back pain and the associated risk factor among residents within the emergency medicine, surgery, internal medicine, radiology, dermatology and neurosurgery departments relative to the general population.

Materials and Methods This cross-sectional study included 125 residents (emergency medicine, surgery, internal medicine, radiology, dermatology, and neurosurgery) out of the total population of 194 residents at the Imam Reza Hospital of Tabriz University of Medical Sciences in the northwest health center of Iran. The study was approved by the Ethics Committee of the Tabriz University of Medical Sciences, Tabriz, Iran. All subjects participated voluntarily and the exclusion criteria consisted of trauma to the lumbar area or vertebral fractures. Finally, senior residents of all specialties were excluded due to a study break coinciding with the period in which the questionnaire was distributed.

In order to standardize the study methods, the Dutch Musculoskeletal Questionnaire (DMQ) was translated into Persian. After the verification of the translation by the Research Committee Experts of Tabriz University of Medical Sciences, the DMQ was distributed to residents. Because of the comprehensive nature of the questionnaire, only the part of the questionnaire specifically relating to the study topic of our study was selected and modified. The resulting question-

naire was composed of three parts. The first part concerned demographics (28 questions about age, sex, weight, height, etc.). Part II concerned workplace-specific factors (eight questions) while part III consisted of questions assessed the characteristics of the subjectâ&#x20AC;&#x2122;s lower back pain (11 questions). Instructions on completion of the questionnaire and the purpose of the study were provided to the participants.

Following completion of the questionnaires the data were divided into two categories. The term positive group was used for subjects who had experienced lower back pain during the past 12 months, whereas subjects who did not have lower back pain during the past 12 months were designated as the negative group. Univariate analysis with the t-test and chi-square test (SPSS 14 software) were used for comparing occupational risk factors between the positive and negative groups. The overall prevalence of lower back pain and prevalence among each specialty field was calculated. A P-value less than 0.05 was considered statistically significant.

Results In this study, 150 medical residents (emergency medicine, surgery, internal medicine, dermatology, radiology and neurosurgery) from Tabriz University of Medical Sciences, Tabriz, Iran, completed a questionnaire regarding lower back pain between 1 June 2013 and 31 August 2013. A total of 25 cases were excluded from the initial sample for the following reasons: 23 were senior residents, one had a history of major trauma to the lumbar area, and one had a history of vertebral fracture. Of the 125 participants included in the final study population, 73 (58.4%) were male while 52 (41.6 %) were female.

The prevalence of lower back pain during the previous 12 months was 56.8% among all residents (prevalence of lower back pain according to specialty is summarized in Table 1).

Among residents, 48.1% of the emergency medicine residents, 75% of the dermatology residents, 90.9% of the internal medicine residents, 100% of the surgery residents, and 80% of the neurosurgery residents believed that lower back pain was attributable to their current work.

Gender was a significant risk factor for lower back pain, with 76.9% of women and 45.2% of men reporting lower back pain in the previous year (p=0.004). The mean age among individuals reporting lower back pain was 33.44 years, while the negative group had a mean age of 33.81 years. The mean BMI (body mass index) among individuals with lower back pain was 24.61 compared to 24.87 among individuals who did not report lower back pain (Table 3).

No significant relationship was found between incidence of lower back pain and heavy lifting (p=0.54), smoking

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Table 1. Prevalence of low back pain among specialties Specialty (n)

Emergency medicine Radiology Internal medicine General Surgery Dermatology Neurosurgery (n=31) (n=23) (n=38) (n=38) (n=9) (n=8)

Prevalence (%)

83.9

43.5

57.9

43.7

33.3

37.5

Table 2. Calculated significances of risk factors among residents of different specialities Specialty Surgery Radiology Neurosurgery Dermatology Internal Emergency Total

medicine medicine Risk factor (p-value) (p-value) (p-value) (p-value) (p-value) (p-value) (p-value) Working in the same

*

0.012

*

0.974

0.464

0.113

0.043

position for long periods Repetitive movement

0.362 0.370

0.408

0.453 0.031 0.746 0.030

0.028

0.018

(bending, twisting) of lumbar region Working in uncomfortable

*

0.008

0.080

0.424

≤0.0001

posture Stress

0.086 0.092

*

*

0.023 0.038 ≤0.0001

Standing for long periods

*

0.005

*

0.343

*

*

≤0.0001

Walking for long periods

*

*

0.168

*

*

0.521

0.016

Movement of heavy loads

0.362

0.002

*

*

0.215

0.371

0.054

Smoking

0.881 0.265

Prolonged sitting

0.949

*

0.766

0.942 0.652 0.591 0.372

*

*

0.503 0.429 0.245

*Relations could not be compared due to similarity of data.

Table 3. Distribution analysis of individual factors

Total (n=125)

With low back pain (n=71)

Without low back pain (n=54)

33.6 (4.81)

33.33 (5.27)

33.81 (4.16)

0.6

52 (41.6)

40 (76.9)

12 (23.07)

0.004

Age

Mean (SD)

Sex

Female, n (%)

Male, n (%)

73 (58.4)

33 (45.2)

40 (54.7)

BMI

Mean (SD)

24.72 (2.67)

24.61 (2.5)

24.87 (2.7)

p

0.5

(p=0.372), or prolonged sitting (p=0.245).

Discussion

There was a statistically significant correlation between lower back pain and workplace risk factors including holding the same position for long periods (p=0.043), repetitive movement (bending, twisting) involving the lumbar region (p=0.03), working in uncomfortable postures (p≤0.0001), stress (p≤0.0001), walking (p<0.01), prolonged standing (p≤0.0001) and exercise (p=0.021).There was a significant relationship between exercise and the frequency of lower back pain (p= 0.021). The results of the statistical analysis are presented in Table 2.

Among participants in the present study, 56.8%had experienced lower back pain within the previous 12 months. These data are consistent with a systematic review by Aireksinen et al., in which the prevalence of lower back pain in the general population was estimated at 22- 65%.[2] The present study results are also consistent with a report by Omokhodion et al., which examined the prevalence of lower back pain among workers at a hospital in Nigeria. In that study, 46% of healthcare workers, including 69% of nurses,

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reported lower back pain.[5] In a Malaysian study performed

by Wong et al., the prevalence of lower back pain was 56.9% among hospital staff.[6] Mehrdad et al. conducted a study of lower back pain among general practitioners and specialists in a hospital in Tehran, Iran, and reported an overall prevalence of 15.1%.[4] This lower prevalence may be due to the greater workload places on medical residents relative to other doctors.

Two studies, one by Walsh et al. in Britain and another by Rotgoltz et al., in Israel, showed no difference in the prevalence of lower back pain between males and females.[7,8] However, the systematic review by Omokhodian et al. in Australia revealed an increased prevalence of lower back pain among women relative to men,[5] similar to the present study.

In 2010, a Malaysian orthopedics journal published a study

by Wong et al. regarding the prevalence of lower back pain and associated risk factors among hospital staff. In that study, 84.1% of individuals who reported lower back pain believed that their pain was related to their current job.[6] The results of this research were similar to our results, in which 94.4% participants believed that their pain was related to their current job and 72.6% believed that their pain began during their current job.

A study performed by Frank et al. in 1993 reported a strong correlation between smoking and lower back pain.[9] This result contrasts with the present study as well as the report by Wong et al.[6] In the present report, the relatively low number of smokers among participants (11% of the total study group) May account for the difference between the various reports.

Concerning the role of exercise as a risk factor for lower back pain, the available studies have yielded a variety of results.

For example, in the study conducted by Wong et al. there was no relationship between exercise and lower back pain.

[6] The study by Demblans-Dechans et al. suggested that exercise was associated with more severe lower back pain,[10] while a study by Henchoz et al. demonstrated that exercise had a protective role in lower back pain.[11] The results of the present study are consistent with the report by Henchoz et al.. The apparent discrepancies in the published literature may be attributable to variation in exercise type and intensity.

Psychological stress can influence the development and severity of multiple disorders. Systematic reviews by Hoogendoorn et al.[12] and Linton et al.,[13] have supported the important role of stress as a risk factor for lower back pain and the present study is in agreement with these data.

Barrero et al.,[14] and Smedley et al.[15] raised questions regard-

ing the relationship between heavy lifting and the development of lower back pain. However, the present study did not reveal evidence of any association between lower back pain heavy lifting. The subjects participating in the study reported relatively infrequent heavy lifting during normal working conditions. Studies by Mehrdad et al.[4] and Wong et al.[6] have reported an association between prolonged standing and lower back pain, an association that was also demonstrated in the present study. The present study also revealed a significant correlation between repetitive bending and twisting with lower back pain, as had been previously suggested in studies by Kwon et al.[16] and the study of Wong et al.[6] Prolonged standing was a risk factor for the development of lower back pain among radiology residents in the present study. While relative to other specialties, some radiologists spend a larger portion of time in a seated position, long periods standing next to the attending radiologist during training may contribute to lower back pain among residents. The low sample size may also introduce bias in the evaluation of lower back pain among radiologists.

The present study provides evidence of several important occupational risk factors for the development of lower back pain in medical professionals. However, when specialties were evaluated individually, not all specialties were affected by the same occupational risk factors. Sub-division of the dataset according to specialty results in a loss of statistical power and may account for this apparent discrepancy. In addition, not all workplaces involve the same exposure to occupational hazards. For example, in emergency medicine prolonged standing is widely prevalent due to the nature of the work and therefore does not correlated with the presence or absence of lower back pain.

Mean BMI was normal in both positive and negative subjects included in this study and could not be adequately evaluated as a risk factor for the development of lower back pain.

Limitations Several limitations apply to the interpretation of the study results. Sub-division of the dataset according to medical specialty reduced statistical power for the identification of risk factors for lower back pain. Consequently, a larger sample size would facilitate a more statistically robust analysis of lower back pain risk factors within medical specialties.

Finally, due to the self-report design of the study, recall bias is likely to be a significant factor.

Conclusion Lower back pain is prevalent among medical residents, with an overall incidence that is comparable to the general population. Further studies are required to develop an effective

Vahdati SS et al.

Low Back Pain and Position in Work

preventive method for this relatively common problem.

Conflict of Interest The authors declare that there is no potential conflicts of interest.

References 1. Khruakhorn S, Sritipsukho P, Siripakarn Y, Vachalathiti R. Prevalence and risk factors of low back pain among the university staff. J Med Assoc Thai 2010;93 Suppl 7:142-8.

2. Airaksinen O, Brox JI, Cedraschi C, Hildebrandt J, Klaber-Moffett J, Kovacs F, et al. Chapter 4. European guidelines for the management of chronic nonspecific low back pain. Eur Spine J 2006 Mar;15 Suppl 2:192-300.

3. Jensen JN, Holtermann A, Clausen T, Mortensen OS, Carneiro IG, Andersen LL. The greatest risk for low-back pain among newly educated female health care workers; body weight or physical work load? BMC Musculoskelet Disord 2012;13:87.

4. Mehrdad R, Dennerlein JT, Morshedizadeh M. Musculoskeletal disorders and ergonomic hazards among Iranian physicians. Arch Iran Med 2012;15:370-4.

5. Omokhodion FO, Umar US, Ogunnowo BE. Prevalence of low back pain among staff in a rural hospital in Nigeria. Occup Med (Lond) 2000;50:107-10.

6. Wong TS, Teo N, Kyaw MO. Prevalence and risk factors associated with low back pain among health care providers in a district hospital. Malays Orthop J 2010;4:23-8.

7. Walsh K, Cruddas M, Coggon D. Low back pain in eight areas

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of Britain. J Epidemiol Community Health 1992;46:227-30.

8. Rotgoltz J, Derazne E, Froom P, Grushecky E, Ribak J. Prevalence of low back pain in employees of a pharmaceutical company. Isr J Med Sci 1992;28:615-8.

9. Frank A, Townsend J. Low back pain. Smoking linked to back pain. BMJ 1993;306:1268.

10. Demblans-Dechans B, Ayrolles C, Clément JL, Lassoued S, Fournié B, Fournié A. Lumbar biomechanics and sports.

Spondylolysis of L5. [Article in French] Rev Rhum Mal Osteoartic 1988;55:405-10. [Abstract] 11. Henchoz Y, Kai-Lik So A. Exercise and nonspecific low back pain: a literature review. Joint Bone Spine 2008;75:533-9.

12. Hoogendoorn WE, van Poppel MN, Bongers PM, Koes BW, Bouter LM. Systematic review of psychosocial factors at work and private life as risk factors for back pain. Spine 2000;25:2114-25.

13. Linton SJ. Occupational psychological factors increase the risk for back pain: a systematic review. J Occup Rehabil 2001;11:53-66.

14. Barrero LH, Hsu YH, Terwedow H, Perry MJ, Dennerlein JT, Brain JD, et al. Prevalence and physical determinants of low back pain in a rural Chinese population. Spine 2006;31:272834.

15. Smedley J, Trevelyan F, Inskip H, Buckle P, Cooper C, Coggon D. Impact of ergonomic intervention on back pain among nurses. Scand J Work Environ Health 2003;29:117-23.

16. Kwon BK, Roffey DM, Bishop PB, Dagenais S, Wai EK. Systematic review: occupational physical activity and low back pain.

Occup Med (Lond) 2011;61:541-8.

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VISUAL DIAGNOSIS [see page 97]

DIAGNOSIS: Cubital Tunnel Syndrome Cubital tunnel syndrome (CuTS) is the most common form of entrapment of the ulnar nerve and the second most common nerve compression syndrome of the upper extremities, the most common being carpal tunnel syndrome. The incidence is 24.7 cases per 100,000 person-years; men are affected twice as often as women. Clinical findings include paraesthesia and tingling in the lateral 2 fingers, pain related to the elbow joint, and in severe cases, weakness or atrophy of the intrinsic muscles of the hand.[1-3] Soft tissue masses such as ganglia, lipomas, fibrolipomas, and epidermoid cysts can compress the ulnar nerve as it lies in the condylar groove or within the cubital tunnel.

However, it was not reported that the ulnar nerve was wrapped and compressed by the DVT mass. In this respect, the present case has the distinction of being unique. We present the first case of CuTS due to DVT. Magnetic resonance imaging of the patient detect-

Turk J Emerg Med 2014;14(3):97 [130]

ed an acute phase deep vein thrombosis (DVT) that could not be compressed, causing an increase in the lumen diameter in the brachial vein and in the right elbow (Figure 1, 2). After cardiovascular surgery, consulting physicians initiated medical treatment with enoxaparine (150 anti-Xa IU/kg, once-daily).

Control returned to the patient and the patient was discharged. The patientâ&#x20AC;&#x2122;s symptoms completely resolved three months later.

References 1. Assmus H, Antoniadis G, Bischoff C, Hoffmann R, Martini AK, Preissler P, et al. Cubital tunnel syndrome - a review and management guidelines. Cent Eur Neurosurg 2011;72:90-8.

2. Fullbier L, Renz B. Operative treatment of cubital tunnel syndrome. Aktuel Neurol 2011;38:298-302.

3. McPherson SA, Meals RA. Cubital tunnel syndrome.

Orthop Clin North Am 1992;23:111-23.

doi: 10.5505/1304.7361.2014.59319

VISUAL DIAGNOSIS [see page 98]

DIAGNOSIS: Fracture of Patella Patellar fractures account for 1% of all skeletal fractures and is most common between the ages of 2050.[1] The most observed fracture pattern is transverse.

It generally occurs as a result of the implementation of direct force, fall on a flexed knee, or strong contraction of the quadriceps.

patients with a suspected fracture. To our knowledge, there has been no clinical study that has diagnosed patella fractures with a bedside ultrasound. The case report presented here underscores the impact of ultrasonography on the diagnosis of patella fractures as well as bone injuries.

The anteroposterior x-ray helps assess the fracture pattern and the direction of displacement, while the lateral and Merchant views assist in understanding the amount and location of comminution. In case of failure of direct radiography, other techniques can be used including computed tomography, magnetic resonance imaging or scintigraphy.

In our case, standard anteroposterior and lateral knee radiographs were obtained after ultrasonographic examination (Figure 2). The patient who underwent consultation at the orthopedic clinic was prescribed a conservative treatment consisting of rest, ice, immobilization with a cylinder cast from the groin to the ankle, keeping the knee in extension, and non-steroidal anti-inflammatory drugs.

Bedside ultrasonography in the diagnosis of fractures is frequently used by emergency medicine physicians.

[2,3] It may be guiding in the diagnosis of fractures especially in unstable patients. In addition, it has a major advantage in that it can be used if radiation exposure is a concern in certain situations such as children and pregnancy. Also, it can be applied in a short time and at bedside. Therefore, ultrasonography can provide rapid diagnosis in busy emergency departments.

Interestingly, there was a case report demonstrating the use of ultrasonography to identify the transverse fracture of the patella.[4] Currently, standard radiographs are being used as a first imaging modality in

References 1. Sahin MS, Sarı AS, Canbeyli ID, Cakmak G. Erişkinlerde patella kırıkları. TOTBİD Dergisi 2012;11:357-61.

2. Aksay E, Yesilaras M, Kilic TY, Tur FC, Sever M, Kaya A. Sensitivity and specificity of bedside ultrasonography in the diagnosis of fractures of the fifth metacarpal.

Emerg Med J 2013 Oct 23.

3. Yesilaras M, Aksay E, Atilla OD, Sever M, Kalenderer O. The accuracy of bedside ultrasonography as a diagnostic tool for the fifth metatarsal fractures. Am J Emerg Med 2014;32:171-4.

4. Wilkerson RG, Stone MB. Ultrasound identification of patella fracture. Wilderness Environ Med 2009;20:92-3.

Figure 2. (a) Anteroposterior knee radiography. (b) Lateral knee radiograph shows transverse fracture of the patella.

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CASE REPORT

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A Rare Cause of Chronic Headache that May Be Misdiagnosed as Migraine: Chronic Carbon Monoxide Poisoning Migren ile Karışabilen Nadir bir Kronik Baş Ağrısı Nedeni: Kronik Karbon Monoksit Zehirlenmesi Mehmet Kenan KANBUROGLU, Mehmet Nevzat CIZMECI, Ahmet Zulfikar AKELMA Department of Pediatrics, Turgut Ozal University Faculty of Medicine, Ankara

SUMMARY

ÖZET

Differential diagnosis of primary headache disorders can be challenging for physicians. Although the association of headache with acute carbon monoxide intoxication is very well-defined, in refractory nonspecific headaches associated with chronic low dose exposure to carbon monoxide, CO intoxication is usually overlooked, mostly due to vague symptoms. Herein we present a 15-year-old female patient with chronic carbon monoxide poisoning who was undergoing two years of follow-up care for migraines. Chronic carbon monoxide intoxication may mimic the episodic nature and familial predisposition of migraine attacks. Normal carboxyhemoglobin levels do not exclude the diagnosis, and smoking is a confounding factor. In emergency rooms, patients presenting with headaches had higher levels of carboxyhemoglobin, but, as far as we know, there have been no studies investigating carboxyhemoglobin levels in migraine patients. Chronic carbon monoxide poisoning should be suspected in migraine patients, especially if the attacks occur during winter months.

Primer baş ağrısında ayırıcı tanının yapılması bazen doktorlar açısından zor olabilmektedir. Literatürde karbon monoksit ile baş ağrısı arasındaki ilişki çok iyi ortaya konulmuş olmasına karşın, dirençli ve nonspesifik başağrısı nedenlerinden biri olan kronik düşük doz karbon monoksit maruziyeti kendine özgü bulgusu olmadığından sıklıkla atlanmaktadır.

Bu yazıda, iki yıl migren tanısı ile takip ve tedavi edilen kronik karbon monoksit zehirlenmesi olan bir olgu sunuldu. Kronik karbon monoksit zehirlenmesi epizodik paterni ve aile fertlerinde benzer şikayetlerin olması nedeniyle migren ataklarını andırabilmektedir. Karboksihemoglobin konsantrasyonlarının normal saptanması tanıyı ekarte ettirmemekte, ayrıca sigara kullanımı da karıştırıcı bir faktör olabilmektedir.

Acil servislerine baş ağrısı ile başvuran hastaların karboksihemoglobin seviyeleri başağrısı olmadan acile başvuran hastalardan daha yüksek saptanmaktadır; fakat bildiğimiz kadarı ile karboksihemoglobin seviyesi ile migren arasındaki ilişkinin araştırıldığı bir çalışma literatürde bulunmamaktadır. Migren atakları özellikle kış aylarında tekrarlayan hastalarda kronik karbon monoksit zehirlenmesi akılda tutulmalıdır.

Key words: Carbon monoxide; emergency; headache; migraine; pediatric.

Anahtar sözcükler: Karbon monoksit; acil; baş ağrısı; migren; çocuk.

Introduction Acute carbon monoxide (CO) poisoning is the cause of most CO-related admissions to the emergency department and is the source of most scientific knowledge about CO intoxication.[1] Chronic low-dose CO intoxication is usually overlooked, mainly due to moderately low carboxyhemoglobin

(COHb) levels and to the lack of the specific symptoms of acute intoxication. A wide range of symptoms, including dizziness, paresthesia, chest pain, palpitations, abdominal pain, diarrhea and visual disturbances may be associated with chronic CO poisoning; however, most patients only have flu-like symptoms and headache.[2] Herein, we present

Submitted: March 05, 2013 Accepted: April 01, 2014 Published online: June 24, 2014 Correspondence: Dr. Mehmet Kenan Kanburoglu. Turgut Ozal Universitesi Tip Fakultesi, Pediatri Anabilim Dali, Emek, 06510 Ankara, Turkey. e-mail: madduckk@gmail.com

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Kanburoglu MK et al.

Chronic Carbon Monoxide Poisoning

a patient with chronic carbon monoxide poisoning who was undergoing follow-up care for two years for the diagnosis of migraines.

Case Report A 15-year-old girl was admitted to the pediatric emergency room after suffering from a headache that did not respond to analgesics. The headache was described as a diffuse pain, which was worse in the evenings but gradually disappeared at school. She was admitted to the hospital three times in the previous week and her condition improved after injection of an analgesic on all occasions. Her headaches were not waking her from sleep and were not related to meals.

Her medical history revealed that she had been in the followup care of a pediatric neurologist for migraine over the last two years, and she had nine migraine attacks since then.

These headaches met the diagnostic criteria for migraine without aura.[3] Her mother and father also had headaches, and her mother had been diagnosed with migraines as well.

Both her migraine attacks and those of her mother usually appeared on similar occasions and mostly in winter. She was the only child in her family, and there was no history of smoking or second-hand smoke exposure.

On examination, her vital signs showed a blood pressure of 106/61 mmHg, a heart rate of 106 beats/min, a respiratory rate of 30 breaths/min and a temperature of 36.8 °C. The patient had normal neurologic, respiratory, cardiovascular, musculoskeletal and abdominal examinations, although she had a borderline tachycardia and tachypnea, which were attributed to the headache.

Carbon monoxide poisoning was suspected because the headaches only occurred at home and usually at the same time as other family members. A venous blood gas sample was taken an hour after she left the house, and it revealed a COHb level of 11.9%. Two hours after oxygen treatment, her symptoms were relieved. Blood samples were also taken from the mother and father, which revealed COHb levels of 11.1% and 7.9%, respectively.

Investigation at home revealed a leaking domestic gas burner in the kitchen. Direct measurement showed 78 parts per million (ppm) of carbon monoxide throughout the kitchen.

The patient was followed for one year after identification and repair of the cause, during which time only one episode of headache occurred. An MRI scan of the patient taken three months after the diagnosis was unremarkable. The final diagnosis of the patient was confirmed to be chronic CO poisoning due to prolonged exposure to non-lethal concentrations of CO.

Discussion CO is a colorless, odorless and nonirritant gas, so patients do not realize they are being exposed to poison. The classic symptoms of acute CO intoxication, such as syncope, palpitations, chest pain, and seizures, are unexpected in patients with chronic CO poisoning and migraine. Patients with chronic CO poisoning may be diagnosed with chronic fatigue syndrome, depression, and influenza in the emergency room.[4] Although migraine may have a familial predisposition, similar symptoms may also occur in the family members of a patient with CO exposure. Moreover, occasional increases in carbon monoxide exposure may mimic the episodic nature of migraine attacks. Normal COHb levels do not exclude the diagnosis of CO poisoning because COHb levels may decrease before the patient’s admission to the hospital, as its elimination half-life in room air is about five hours.[5] Furthermore, smoking is a confounding factor in the differential diagnosis of chronic CO poisoning; smokers’ COHb levels may range from 1-14%.[6] A biochemical marker for chronic CO poisoning has yet to be found. Occasionally, household pets that were found dead or behaving strangely may provide an important clue to the diagnosis.[2] In the present case, low levels of serum COHb and indoor CO, and the absence of the classical findings of acute CO intoxication led us to the diagnosis of chronic carbon monoxide poisoning. However, some of her previous migraine attacks may have been acute CO intoxication.

The association between unsuspected CO poisoning and headache has been investigated in several studies. Heckerling et al.[4] investigated the frequency of occult CO poisoning in patients presenting with headache and dizziness.

Of 48 patients presenting with headache, they found increased levels of COHb (greater than 10%) in seven patients, giving a prevalence of 14.6% for CO intoxication. Clarke et al.[7] measured COHb levels of 1758 patients using a pulse CO-oximeter and venous samples. They found that patients presenting with headaches, flu-like symptoms, chest pains, or seizures had higher levels of COHb. Ambient levels of carbon monoxide, such as long-term exposure to traffic-related air pollution, may also increase daily emergency department visits for headache.[8] To the best of our knowledge, there has been no study investigating migraine cases to determine if they are the result of chronic CO poisoning.

In conclusion, in patients who have the diagnosis of migraine or present with non-specific refractory headaches, chronic carbon monoxide poisoning should be suspected, especially if the attacks occur during the winter months.

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Conflict of Interest The authors declare that there is no potential conflicts of interest.

References 1. Wright J. Chronic and occult carbon monoxide poisoning: we donâ&#x20AC;&#x2122;t know what weâ&#x20AC;&#x2122;re missing. Emerg Med J 2002;19:386-90.

2. Kirkpatrick JN. Occult carbon monoxide poisoning. West J Med 1987;146:52-6.

3. Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders: 2nd edition. Cephalalgia 2004;24 Suppl 1:9160.

4. Heckerling PS. Occult carbon monoxide poisoning: a cause of winter headache. Am J Emerg Med 1987;5:201-4.

5. Myers RA, Linberg SE, Cowley RA. Carbon monoxide poisoning: the injury and its treatment. JACEP 1979;8:479-84.

6. Light A, Grass C, Pursley D, Krause J. Carboxyhemoglobin levels in smokers vs. non-smokers in a smoking environment.

Respir Care 2007;52:1576.

7. Clarke S, Keshishian C, Murray V, Kafatos G, Ruggles R, Coultrip E, et al. Screening for carbon monoxide exposure in selected patient groups attending rural and urban emergency departments in England: a prospective observational study.

BMJ Open 2012;2.

8. Szyszkowicz M. Ambient air pollution and daily emergency department visits for headache in Ottawa, Canada. Headache 2008;48:1076-81.

CASE REPORT

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Acute Coronary Syndrome During Pregnancy: A Case Report and Literature Review Gebelik Sırasında Akut Koroner Sendrom: Olgu Sunumu ve Literatür Taraması Sabiye YILMAZ, Salih SAHINKUS, Harun KILIC, Huseyin GUNDUZ, Ramazan AKDEMIR Department of Cardiology, Sakarya University Training and Research Hospital, Sakarya

SUMMARY

ÖZET

A 32-year-old multiparous woman who presented with chest pain at seven weeks gestation was admitted to our hospital 35 minutes after the onset of symptoms. Sudden cardiac arrest developed while the patient was waiting in the triage room. Cardiopulmonary resuscitation was performed, and the patient was immediately intubated. Electrocardiography revealed an inferior myocardial infarction. The patient underwent coronary angiography, which revealed slow coronary flow of the circumflex and left anterior descending coronary arteries. For treatment, the combination of aspirin with clopidogrel and unfractionated heparin was initiated. She had previously had three healthy children and hadn’t had any problems during her previous pregnancies. She had a history of family and smoking, but no history of other coronary risk factors such as diabetes mellitus, hypertension, or dyslipidemia. She was discharged home on day five after admission with clopidogrel, aspirin and a beta-blocker with close outpatient follow-up. Elective abortion was planned for two weeks after the myocardial infarction.

Otuz iki yaşında yedi haftalık multipar gebe bir kadın, acil servisimize 35 dakika önce başlayan göğüs ağrısı şikayeti ile başvurdu. Hasta bekleme odasında beklerken ani kardiyak arrest gelişti.

Kardiopulmoner resüsitasyon yapılıp hasta hemen entübe edildi.

Elektrokardiyografide inferior miyokart enfaktüsü saptandı. Hastaya koroner anjiyografi yapıldı ve sirkumfleks arter ile sol ön inen arterde yavaş akım izlendi. Medikal tedavide asetilsalisilik asit ve klopidogrel kombinasyonu ile unfraksiyone heparin başlandı. Hastamız üç tane sağlıklı çocuğa sahipti ve önceki gebeliklerinde herhangi bir problem yaşamamıştı. Risk faktörlerinden aile öyküsü ve sigara içiciliği mevcuttu ancak diyabetes mellitus, hipertansiyon, dislipidemi yoktu. Çıkış tedavisi asetilsalisilik asit, klopidogrel ve beta bloker olarak düzenlendi ve yatışının beşinci gününde sıkı takip önerildi. Miyakart enfaktüsündan iki hafta sonra elektif abortus planlandı.

Key words: Coronary thrombosis; myocardial infarction; pregnancy.

Anahtar sözcükler: Koroner trombüs; miyokart enfaktüsü; gebelik.

Introduction Acute myocardial infarction (AMI) during pregnancy is rare but serious condition that it is a cause of maternal mortality and fetal loss. Pregnancy has been shown to increase the risk of AMI, which has been reported to occur in 3-10 cases per 100,000 deliveries.[1-4] With the rise in maternal age and the increasing number of high-risk women who become pregnant, the prevalence of pregnancy-related acute coronary syndrome (ACS) is expected to increase. Pregnancy leads to

excessive hypercoagulability by increasing platelet adhesion and decreasing fibrinolysis; these hemostatic changes lead to an increased risk of thromboembolic events.[3-5] It is strongly related to the traditional risk factors of coronary heart disease, including diabetes mellitus, hypertension, dyslipidemia, family history of coronary artery disease and smoking. Additionally, other conditions that contribute to ACS are preeclampsia, eclampsia, thrombophilia, postpartum infections, severe postpartum hemorrhage, and spontaneous

Submitted: February 09, 2014 Accepted: April 04, 2014 Published online: June 24, 2014 Correspondence: Dr. Sabiye Yilmaz. Korucuk Baytur Sitesi, Orkide 1, Daire 6, Sakarya, Turkey. e-mail: ssevincdr@gmail.com

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coronary artery dissections.[4] Maternal mortality after ACS is estimated to be 5-10% and is highest during the peripartum period. Survival has improved with primary percutaneous coronary intervention (PCI).[2-4] This article accompanies pregnancy in patients with ST elevation myocardial infarction (STEMI), and we consider a general approach to treatment.

Case Report A 32-year-old multiparous woman at seven weeks gestation presented to the Emergency Department (ED) with a sudden onset of chest pain within the previous 35 minutes. She had three healthy children and had no problems during previous pregnancies. She had a family history of coronary artery disease but no history of other coronary risk factors such as diabetes mellitus, hypertension, dyslipidemia or smoking.

Sudden cardiac arrest developed while she was waiting in the triage room. Cardiopulmonary resuscitation (CPR) was performed and patient was immediately intubated. Ventricular fibrillation developed during CPR and defibrillation was performed. Clinical examination showed she had flexor response to painful stimuli and her pupillary light reflex was present. Her blood pressure was 90/55 mmHg with a pulse of 102 beats per minute, oxygen saturation of 96%, and normal heart sounds. There were ST elevations in leads DII, DIII, and aVF; conversely ST depression in leads V1-V4; and atrial fibrillation (AF) on electrocardiography (ECG) following CPR (Figure 1a, b). Portabilizer echocardiography was performed in the emergency department by cardiologists. The echocardi-

ogram demonstrated that the wall motions were severely reduced in the inferior and lateral regions, consistent with AMI, and the estimated ejection fraction of the left ventricle was 40%. With the diagnosis of an inferior STEMI, aspirin (300 mg) and clopidogrel (600 mg) were given in the ED. The patient was then referred for primary angioplasty, which was performed within 45 minutes. Catheterization was performed after shielding the patientâ&#x20AC;&#x2122;s back and abdomen with lead aprons.

Coronary angiography showed slow coronary flow of the circumflex (CX) and left anterior descending (LAD) coronary arteries. Right coronary artery was normal (Figure 2). The combination of aspirin (100 mg/day) with clopidogrel (75 mg/day for 2 weeks) and unfractionated heparin was initiated for medical treatment. Biochemistry tests [urea, creatinine, glucose, aspartate aminotransferase (AST), alanine aminotransferase (ALT)] were normal, except for mild leukocytosis. The serum levels of troponin peaked at 13 ng/ml.

We consulted an obstetrician regarding the safety of administering clopidogrel and the use of radiation after angiography. and both were consequently considered to be unsafe because organogenesis was not complete. She was discharged home on day five after admission with clopidogrel, aspirin and a beta-blocker with close outpatient follow-up.

Elective abortion was planned for two weeks after the MI. There was no prior history of connective tissue disease, vasculitis, impaired anticoagulant mechanism (protein C deficiency, protein S deficiency), or antiphospholipid antibody syndrome, which are associated with a thrombotic tendency. Birth control pills had never been used. Immunologic

(a)

(b)

Figure 1. (a, b) Atrial fibrillation (AF) and ST elevations in leads DII, DIII, and aVF; conversely ST depression in leads V1-V4 on electrocardiography (ECG) following CPR.

Yilmaz S et al.

Acute Coronary Syndrome During Pregnancy

Figure 2. Coronary angiography showed slow coronary flow of the circumflex (Cx) and left anterior descending (LAD) coronary arteries.

tests performed prior to admission, which included antiphospholipid antibodies, were negative.

Discussion There are few published statistics concerning acute myocardial infarction (AMI) in pregnant women. The incidence of AMI in pregnancy ranges from 3-6 cases per 100,000 deliveries.[1-4] A previous review demonstrated that pregnancyassociated AMI occurs at all stages of pregnancy. It is more common late in pregnancy, with a peak incidence during the peripartum or postpartum period. This may be due to the fact that, during this period, there is also a higher occurrence of hypertension and preeclampsia, which are the most important risk factors for AMI in these patients.[4] In our patient, however, the event was occurred relatively early, in the first trimester of pregnancy.

The physiopathology of ACS in pregnant women is quite different from the normal population. Pregnancy-associated AMI has been thought to be related to both an excess procoagulant state and increased stress on the cardiovascular system, leading to coronary thrombosis or spontaneous coronary dissection.[3-5] A study by Roth et al. reviewed coronary lesions in pregnant patients with ACS. The following results were revealed: 39% of arteries had atherosclerotic lesions, 19% were found to have an intracoronary thrombus without any other lesion, 15% had a coronary dissection, and 27% of the arteries were apparently normal.[4] As can be seen, contrary to the rest of the population, a much higher proportion of normal coronary arteries and intracoronary dissections are the cause of the coronary syndrome.[4] Paradoxical coronary embolism through a patent foramen ovale is an additional potential mechanism of myocardial infarcti-

on during pregnancy, although this case showed clear-cut coronary artery disease. Ladner et al. identified hypertension, diabetes, advanced maternal age, preeclampsia and eclampsia as independent risk factors for pregnancy-associated AMI, and James et al. also found that thrombophilia, transfusion, and postpartum infections were significant risk predictors for AMI.[2,3] Spontaneous coronary artery dissections are more prevalent among pregnant than non-pregnant women, and are mostly reported around delivery or in the early postpartum period.[4] They may be related to high progesterone levels with subsequent structural changes in the collagen of the vessel wall. Ergometrine given for bleeding postpartum may lead to coronary vasospasm and ischemia.

Thrombi and dissections occur more frequently in the peripartum period than in delivery.[4] Although our patient was young and did not have any risk factors for pregnancy-associated AMI, percutaneous coronary angiogram demonstrated normal coronary arteries with slow flow in circumflex, the ECG was STEMI. Maternal mortality after ACS is estimated at 5-10% and is highest during the peripartum period. Survival has improved with PCI.[2-4] Long-term maternal prognosis mainly depends on the severity of maternal heart disease and the cardiovascular risk profile. Before delivery, ACS may result in fetal mortality or prematurity.

The first step during pregnancy in ST-elevation ACS is a primary PCI, which is preferred to thrombolysis as it will also diagnose coronary artery dissection. Although recombinant tissue plasminogen activator does not cross the placenta, it may induce bleeding complications such as subplacental bleeding; therefore, thrombolytic therapy should be reserved for life-threatening ACS when there is no access to PCI.[6] The risk of potential damage to the fetus should be kept in mind, especially in the first trimester. However, this can be overcome with the use of appropriate radiological protection. In our case, a decision was taken to use lead apron protection. The patientâ&#x20AC;&#x2122;s abdomen was covered and, to protect the fetus from excessive radiation, additional protection was also placed between the patientâ&#x20AC;&#x2122;s back and the table. β-Blockers and low dose acetylsalicylic acid are considered to be relatively safe during both the second and third trimesters, while the safety profile is unknown for thienopyridines.

[7] Heparin does not cross the placenta, and several reports have demonstrated that heparin is safe to use during pregnancy.[8] In conclusion, AMI in pregnancy is a rare event with specific features that are related to both an excess procoagulant state and increased stress on the cardiovascular system, leading to coronary thrombosis or spontaneous coronary dissecti-

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on. Understanding the causes of pregnancy-related acute myocardial infarction and identification of women at risk are the first steps for prevention. Screening and preventive measures should focus on women with advanced maternal age, known coronary risk factors, thrombophilia, postpartum complications, and being a smoker. Family history and smoking are the most important risk factors, and these have a higher-than-normal rate for non-atherosclerotic coronary disease in these groups. Management of these patients should include the use of bare-metal stents, precaution with the use of antiplatelet therapy, and appropriate protection during radiological procedures.

Our patient had normal coronary artery with slow coronary flow and drug treatment was administered. Elective abortion was planned for two weeks after the MI. This article suggests that acute coronary syndrome should be considered in pregnant women who have chest pain. In these patients, the ECG should be performed immediately.

Conflict of Interest The authors declare that there is no potential conflicts of interest.

References 1. Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy. Ann Intern Med 1996;125:751-62.

2. Ladner HE, Danielsen B, Gilbert WM. Acute myocardial infarction in pregnancy and the puerperium: a population-based study. Obstet Gynecol 2005;105:480-4.

3. James AH, Jamison MG, Biswas MS, Brancazio LR, Swamy GK, Myers ER. Acute myocardial infarction in pregnancy: a United States population-based study. Circulation 2006;113:156471.

4. Roth A, Elkayam U. Acute myocardial infarction associated with pregnancy. J Am Coll Cardiol 2008;52:171-80.

5. Joyal D, Leya F, Koh M, Besinger R, Ramana R, Kahn S, et al.

Troponin I levels in patients with preeclampsia. Am J Med 2007;120:819.e13-4.

6. Leonhardt G, Gaul C, Nietsch HH, Buerke M, Schleussner E. Thrombolytic therapy in pregnancy. J Thromb Thrombolysis 2006;21:271-6.

7. Imperiale TF, Petrulis AS. A meta-analysis of low-dose aspirin for the prevention of pregnancy-induced hypertensive disease. JAMA 1991;266:260-4.

8. Bates SM, Greer IA, Hirsh J, Ginsberg JS. Use of antithrombotic agents during pregnancy: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest 2004;126(3 Suppl):627-44.

CASE REPORT

Spontaneous Bladder Rupture and Pelvic Fracture Due To Bladder Cancer Mesane Kanserine Bağlı Gelişen Pelvis Kırığı ve Mesane Rüptürü Deniz ORAY, Onder LIMON, Cem ERTAN, Asli UGURHAN Department of Emergency Medicine, Izmir University Faculty of Medicine, Izmir

SUMMARY

ÖZET

Bladder rupture is a rare complication following bladder cancer, but has a high mortality rate. Since bladder rupture is an emergency, the diagnosis and treatment of the cancer is usually delayed. Here we report a 56-year-old male patient who presented to our emergency department with severe abdominal pain, abdominal distension, left leg pain and difficulty in walking without history of significant trauma and ended up with diagnoses of spontaneous bladder rupture and non-traumatic pelvic fracture caused by bladder carcinoma.

Mesane rüptürü, mesane kanserinin nadir bir komplikasyonu olsa da, gerçekleştiğinde mortalite hızı yüksek seyretmektedir. Mesane rüptürü acil bir durum olduğundan, altta yatan neden olarak kanserin tanınması ve etiyolojiye yönelik tedavi gecikebilmektedir. Bu yazıda, acil servise travma öyküsü olmaksızın şiddetli karın ağrısı, batında şişkinlik, sol bacakta ağrı ve yürüme güçlüğü ile başvuran ve mesane kanserine bağlı spontan mesane rüptürü ve pelvis kırığı tanısı alan 56 yaşında bir erkek hasta sunuldu.

Key words: Bladder cancer; bladder rupture; emergency department; pelvic fracture.

Anahtar sözcükler: Mesane kanseri; mesane rüptürü; acil servis; pelvis kırığı.

Introduction

Case Report

Spontaneous bladder rupture is typically described in association with recent trauma, malignant diseases, anatomical outflow obstructions, indwelling catheters, instrumentation or a combination of these.[1,2] Bladder rupture is a rare complication following bladder cancer, but carries a high mortality rate. This condition is an emergency; therefore the diagnosis and treatment of the underlying disease is usually delayed.[3] Pelvic fracture co-exists with 83% of bladder ruptures.[4]

A 56-year-old male presented to our emergency department (ED) with severe abdominal pain, abdominal distension, left leg pain and difficulty walking without any history of trauma that started about 24 hours prior. He was discharged in good condition from another university hospital three days earlier following a pelvic radiotherapy session for his bladder carcinoma. At presentation, his pulse rate was 110 beats per minute, his blood pressure was 90/50 mmHg and pulse oximeter value was 93% on room air. He was oriented and cooperative. The abdomen was distended and there was guarding with rebound tenderness. There was tenderness at the left iliac bone with application of direct pressure. An 18

Here we report a patient with bladder carcinoma with a pathologic fracture of the pelvic bone and spontaneous extraperitoneal bladder rupture in combination with intra-peritoneal rupture.

Submitted: February 18, 2014 Accepted: March 21, 2014 Published online: June 24, 2014 Correspondence: Dr. Cem Ertan. Medical Park Izmir Hastanesi, Acil Servisi, Yeni Girne Blv., Karşiyaka, Izmir, Turkey. e-mail: cem_ertan@hotmail.com

Turk J Emerg Med 2014;14(3):139-141

doi: 10.5505/1304.7361.2014.55707

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confirmed the presence of extensive free fluid both in the peritoneal space and extra-peritoneal area (Figure 1). The CT cystogram revealed the extravasation of the contrast medium from the left side of the bladder, thru the mass defined by the CT, surrounding the iliopsoas muscle (Figure 2).

A Foley catheter was inserted and there was 100 mL of urine drainage. Emergent antibiotic therapies consisting of ampicillin, cefotaxime and metronidazole, along with ongoing fluid therapy was started in the ED. The patient was assessed by a medical oncologist, an urologist and an orthopedic surgeon, and was hospitalized for medical treatment and possible surgical repair. Unfortunately, the patient died before surgery.

Discussion Figure 1. Contrast enhanced abdominal CT showing the iliac bone fracture.

gauge IV line was inserted and a 2000 mL normal saline infusion was started. The abdominal ultrasound scan revealed that there was only a small amount of urine in the bladder.

It also showed free fluid in the peritoneal cavity. A contrast enhanced computed tomography (CT) scan of the abdomen and retrograde CT cystogram were ordered. The CT scan showed a 10 cm x 9 cm mass with soft tissue components at the left iliac bone along with a pathological fracture and

Bladder rupture is an alarmingly mortal pathology (12-22%) which usually occurs in association with blunt or penetrating lower abdominal injuries.[3] It is commonly classified as extraperitoneal or intra-peritoneal. Extra-peritoneal ruptures are found alone in 62% of cases, while intra-peritoneal ruptures alone constitute 25% of all bladder injuries and they are combined in 12% of cases.[3] It is reported that 83% of all bladder ruptures are accompanied by a pelvic fracture.[4] Spontaneous rupture of the urinary bladder is a rare occurrence; in the available literature it is predominantly associated with risk factors such as radiotherapy for pelvic malignancies.[2,5-7] According to a recent article by Baxter et

Figure 2. CT cystogram showing contrast extravasation from the left side of the bladder and iliac bone fracture.

Oray D et al.

Spontaneous Bladder Rupture and Pelvic Fracture Due To Bladder Cancer

al., women who undergo radiation therapy to the pelvis for cancers of the cervix, rectum, or anus are at an increased risk for pelvic fractures.[8] In other cases, substance abuse with alcohol, cocaine and amphetamines have all been associated with bladder rupture.[9,10] Our case, in concordance with the literature, had metastatic malignancy under treatment with radiotherapy which was anticipated to be the possible cause of the pathological pelvic fracture.

The presentation of spontaneous bladder rupture typically presents with acute abdominal pain. Urine may continue to drain after bladder catheterization. The injury, if unsuspected, may go undiagnosed for a period ranging from days to weeks.[2,11] The combination of CT and cystography is an accurate method for assessing bladder pathology.[12] Clinical suspicion is the key to early diagnosis. Our patient presented with acute abdominal pain and left leg pain without any trauma. Urine was drained from the bladder following urinary catheterization. He was completely symptom free at discharge three days before re-admission. Another possible cause of bladder rupture that must be considered in this patient was pelvic bone metastasis due to bladder cancer. A CT cystogram was diagnostic for both the rupture and the fracture in our case.

Operative treatment includes drainage of urine from the peritoneal cavity, closing the rupture and instituting good vesicle drainage. Early diagnosis and prompt surgical treatment decreases the morbidity and mortality associated with this condition.[1,11] In our present case the patient never had the chance to make it to surgery despite his early admission to the hospital, timely diagnosis and treatment efforts in the ED. But on the other hand, the fact that the patient was under heavy pain medication with fentanyl patches and getting used to living with pelvic discomfort may have delayed his presentation to the hospital.

In the presented case we suggest that the cause of the rupture in this patient was a combination of pelvic fracture caused by metastatic bladder carcinoma and radiotherapy for pelvic malignancy. Appropriate management of high risk group patients during follow up and at presentation to ED may decrease the morbidity and mortality associated with this condition.

Conflict of Interest The authors declare that there is no potential conflicts of interest.

References 1. Haddad FS, Wachtel TL. Spontaneous intraperitoneal rupture of the bladder. Urol Int 1987;42:467-9.

2. Engin O, Yakan S, Yıldırım M, Kozacıoğlu Z. A rare cause of acute abdomen: bladder rupture due to catheterization. J Clin Anal Med 2013;4:327-8.

3. Santucci RA, Mcaninch JW. Bladder injuries: evaluation and management. Int Braz J Urol 2000;26:408-14.

4. Chan DP, Abujudeh HH, Cushing GL Jr, Novelline RA. CT cystography with multiplanar reformation for suspected bladder rupture: experience in 234 cases. AJR Am J Roentgenol 2006;187:1296-302.

5. Schein M, Weinstein S, Rosen A, Decker GA. Spontaneous rupture of the urinary bladder-delayed sequel of pelvic irradiation. A case report. S Afr Med J 1986;70:841-2.

6. Fujikawa K, Yamamichi F, Nonomura M, Soeda A, Takeuchi H. Spontaneous rupture of the urinary bladder is not a rare complication of radiotherapy for cervical cancer: report of six cases. Gynecol Oncol 1999;73:439-42.

7. Addar MH, Stuart GC, Nation JG, Shumsky AG. Spontaneous rupture of the urinary bladder: a late complication of radiotherapy-case report and review of the literature. Gynecol Oncol 1996;62:314-6.

8. Baxter NN, Habermann EB, Tepper JE, Durham SB, Virnig BA. Risk of pelvic fractures in older women following pelvic irradiation. JAMA 2005;294:2587-93.

9. Lynn SJ, Mark SD, Searle M. Idiopathic spontaneous bladder rupture in an intoxicated patient. Clin Nephrol 2003;60:430-2.

10. Pradhan AA. Spontaneous rupture of bladder: a rare clinical entity. MJAFI 2007;63:92-3.

11. Heyns CF, Rimington PD. Intraperitoneal rupture of the bladder causing the biochemical features of renal failure. Br J Urol 1987;60:217-22.

12. Limon O, Unluer EE, Unay FC, Oyar O, Sener A. An unusual cause of death: spontaneous urinary bladder perforation. Am J Emerg Med 2012;30:2081.e3-5.

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CASE REPORT

142

A Case of Ramsay Hunt Syndrome with Atypical Presentation Atipik Prezentasyonlu Bir Ramsay Hunt Sendromu Olgusu Kamil KAYAYURT, Ozcan YAVASI, Ozlem BILIR, Gokhan ERSUNAN, Baris GIAKOUP Department of Emergency, Recep Tayyip Erdogan University Faculty of Medicine, Rize

SUMMARY

ÖZET

Ramsay Hunt syndrome is a rare complication of herpes zoster which results from the reactivation of the latent varicella-zoster virus in the geniculate ganglion. Although facial nerve is the most common affected nerve in Ramsay Hunt syndrome, other cranial and cervical nerves can also be affected. We present an atypical case of Ramsay Hunt syndrome in a 42-year-old male, with cervical nerve involvement. As spontaneous recovery rate in Ramsay Hunt syndrome is low, early diagnosis and treatment plays a key role in full recovery of paralysis.

Ramsay Hunt sendromu, varisella-zoster virüsün latent olarak kaldığı genikulat ganglionda aktifleşmesiyle oluşan herpes zosterin nadir bir komplikasyonudur. Ramsay Hunt sendromunda fasiyal sinir en sık etkilenen sinir olmasına rağmen diğer kraniyal sinirler ve servikal sinirler de tutulabilir. Bu yazıda, 42 yaşındaki erkek hastada servikal tutulumun da eşlik ettiği atipik bir Ramsay Hunt sedromu olgusu sunuldu. Ramsay Hunt sedromunda spontan iyileşme oranları düşük olduğundan bu hastaların tanılarının erken dönemde konması ve tedavilerinin hemen başlanması paralizinin tam olarak iyileşmesinde kilit role sahiptir.

Key words: Facial palsy; Ramsay Hunt syndrome; varicella-zoster virus.

Anahtar sözcükler: Fasiyal paralizi; Ramsay Hunt sendromu; varisella-zoster virüs.

Introduction

Here, we report a case of RHS, in which C2-C4 cervical nerves are affected together with the facial nerve.

Ramsay Hunt Syndrome (RHS), also known as Herpes Zoster Oticus, was first defined by James Ramsay Hunt in 1907.

[1] The disease is a rare complication of the primary varicella zoster virus infection (VZV). Activated many years after inoculation, VZV is followed by a latency period in the geniculate ganglion and spreads along the sensory tract of the facial nerve. Ipsilateral facial paralysis, otalgia, and vesicular rash of the skin of external auditory canal compose the classical triad of the disease. In contrary to Bell’s palsy, the patients who are untreated or delayed in their treatment have poor prognosis and the full recovery rate is as low as 10-30% in these patients.[2,3] RHS is also known as cranial polyneuropathy and besides facial nerve, cranial nerves 5, 8, 9, 10, 11, 12, and C2-C4 cervical nerves may also be affected. The eighth cranial nerve is the most common involved nerve together with facial nerve, while the others are rarely involved.[4]

Case Report A 42-year-old man presented to our emergency department with the complaints of redness, numbness, and pain around left eye and face following an episode of otalgia, otorrhea, decreased hearing, and swelling of the left ear lasting three days. He did not have any chronic disease and medication history. His vital signs were as follows: blood pressure, 140/90 mmHg; heart rate, 76 bpm; respiratory rate, 16/minute; and temperature, 36.7 ºC. Physical examination revealed edema of the external auditory canal and auricula of the left ear with a vesicular rash and serous discharge, periorbital and facial erythema and edema, stage 2 peripheric facial paralysis on the left side and vesicular rash of the left anterior cervical region (Figure 1a-c). Ophtalmic examination revealed no

Submitted: March 14, 2014 Accepted: April 29, 2014 Published online: June 24, 2014 Correspondence: Dr. Kamil Kayayurt. Recep Tayyip Erdogan Universitesi Tip Fakultesi, Acil Tip Anabilim Dalı, Rize, Turkey. e-mail: kamilkayayurt@yahoo.com

Turk J Emerg Med 2014;14(3):142-145

doi: 10.5505/1304.7361.2014.82788

Kayayurt K et al.

(a)

A Case of Ramsay Hunt Syndrome with Atypical Presentation

(b)

(c)

Figure 1. (a) Left facial palsy and periorbital edema. (b) Vesicular rash on the left face and periauricular region with serous auricular discharge. (c) Vesicular rash on the left anterior cervical region.

pathological findings. Hematological or biochemical findings were not substantial except a white blood cell count of 14.6 K/mL. The patient was hospitalized with the diagnosis of RHS and acyclovir 10 mg/kg/day and prednisolone 1 mg/ kg/day were initiated. Following the regression of his clinical symptoms and physical findings, he was discharged at the third day of his admittance for ambulatory treatment and follow-up.

Discussion In United States of America, it is estimated that one out of every three people are infected by VZV.[5] However, clinical findings of herpes zoster do not develop in all infected subjects. The population based herpes zoster incidence was reported as 22.4 / 10,000 in a prospective study conducted

by Paul and Thiel.[6] RHS develops in 0.2% of primary herpes zoster infections.[5] The incidence of the disease demonstrated an increase after fifth decade and peaked at eighth decade, parallel to the decreasing cellular immunity with the aging process. It is 20% more common in females compared to males.[7] The present case developed facial paralysis and vesicles around the left ear and neck following an episode of otalgia, otorrhea, decreased hearing, and swelling of the left ear, which lasted three days. Vesicular rash may manifest prior to or following facial paralysis or may not be observed at any time. When present, these vesicles may be observed at the external auditory canal, auricule, skin of the cheeks, the anterior two thirds of the tongue, hard palate, or cervical region.[4] Our patient had vesicles at the external auditory

canal, auricule, and anterior cervical region with no presentation in other regions. The key clinical finding is facial paralysis and RHS, which covers 12% of cases with non-traumatic facial paralysis.[7] Otalgia is the second most common symptom and 73% of the patients manifest otalgia as a complaint.

[2] Involvement of the vestibulocochlear nerve together with facial nerve is observed in 50% of the cases, causing hearing loss, vertigo, nausea, vomiting and nystagmus.[4] Dysphagia, disturbances of gaze and taste, double vision suggest involvement of other cranial nerves. Furthermore, cardiac arrhythmias may develop when vagal nerve is involved.[2,4] Our patient did not have any cranial nerve involvement other than facial nerve.

The cervical involvement observed in our case is not a typical finding in RHS.[5] Three different theories are proposed for this clinical situation. The first theory is spreading of VZV through cerebrospinal fluid (CSF) or by hematogenous way.

In 38% of the cases with cutaneous herpes zoster, pleocytosis is detected in CSF.[8] Another study reported presence of 21% of the VZV in CSF of the patients manifesting cutaneous lesions.[9] The second proposed theory is the presence of anastomoses between cervical nerves and branches of the facial nerve as an anatomical variation, leading to the spread of inflammation to more than one dermatome along these anastomoses.[5,10] The last theory is the simultaneous activation of the virus in more than one ganglion, causing clinical symptoms.[5] The case presented here was diagnosed clinically. There was no need for ancillary laboratory or imaging studies. RHS is a clinical diagnosis with the unilateral facial paresis, otalgia

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Turk J Emerg Med 2014;14(3):142-145

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and vesicular rash in ipsilateral ear, hard palate, and the anterior two third of the tongue being sufficient for diagnosis.

It is hard to differentiate between RHS and Bellâ&#x20AC;&#x2122;s palsy when vesicles are not present in patients. Complement fixation tests and increased antibody levels may support the diagnosis. The detection of the virus by polymerase chain reaction in mononuclear cells of external auditory canal fluid, tear, CSF, and blood is accepted as the gold-standard in diagnosis of VZV.[11] Jonsson et al. evaluated the cases with facial paralysis and reported that there were no extra benefits of contrast enhanced magnetic resonance imaging for either diagnosis or prognosis of the patients.[12] There are not so many randomized, prospective controlled studies for RHS in the medical literature. The data is mostly based on the case reports and retrospective case series.

The actual management is starting with a combination of an antiviral agent and steroids.[13] The most commonly used antiviral agent is acyclovir, however; a new generation antiviral drugs such as valacyclovir, famciclovir, penciclovir, and brivudine are being preferred due to increasing resistance.

[14] Prednisolone is suggested as the drug of choice for steroid therapy. In a retrospective study, Murakami et al. compared the effectiveness of the combination therapy of acyclovir and prednisolone with prednisolone therapy alone.

They concluded that the full neurological recovery rate of the combination therapy group was significantly higher than the group treated merely with prednisolone. Moreover, when patients were grouped according to the time of initiation of drug therapy, the group in which therapy was initiated in the first three days showed a full neurological recovery rate of 75%. The rate decreased to 48% in the second group in which therapy was initiated in 4 to 7 days similar to the decrease of 30% in the third group in which therapy was initiated in later than 7 days. There was no clinically significant difference between therapeutic effects of parenteral and oral administration of acyclovir.[3] Kinishi et al. compared the groups of patients who started acyclovir alone and prednisolene alone therapy in the first seven days. They reported significantly better nerve stimulation test results in the acyclovir alone group.[15] Since patients suffer from severe pain, pain management must also be taken into consideration in addition to the treatments mentioned above. Cellulitis may develop following infection of the vesicles, necessitating antibiotic therapy.

Following discharge from the hospital, most of the patients need rehabilitation and long term follow-up.[5] Our patient was administered a combination therapy of acyclovir and prednisolone after the clinical diagnosis was made. He was discharged at the third day for ambulatory treatment and follow-up.

The most important aspect of RHS when compared to Bellâ&#x20AC;&#x2122;s palsy is the significantly worse prognosis when left untreated. In non-treated patients or patients in whom treatment was started later than seven days, the full neurological recovery rate is significantly as low as 10 to 30%. Advanced age, involvement of more than one cranial nerve, and a higher stage of facial paralysis during first admittance are well-defined prognostic indicators of RHS.[2,3] The absence of the prognostic factors as well as the early initiation of therapy yielded full neurological recovery in the present case, consistent with the literature. The most common complication of RHS is postherpetic neuralgia that increases with age.

Meningoencephalitis, myelitis, cerebrovascular problems associated with vasculitis, ventriculitis, and cerebral venous thrombosis may also develop.[4] Examination of our patient during follow-up visits indicated no development of any of these listed complications.

Conclusion RHS is a medical emergent condition necessitating early diagnosis and treatment in order to have a good prognosis. In patients with facial paralysis but no external vesicular findings, otoscopic and audiometric examinations must be performed. The combination therapy with antivirals and steroids must be initiated as soon as possible in order to minimize the risk of permanent neuronal damage.

Conflict of Interest The authors declare that there is no potential conflicts of interest.

References 1. Hunt JR. On herpetic inflammation of the geniculate ganglion. A new syndrome and its complications. J Nerv Ment Dis 1907;34:73-96.

2. Ko JY, Sheen TS, Hsu MM. Herpes zoster oticus treated with acyclovir and prednisolone: clinical manifestations and analysis of prognostic factors. Clin Otolaryngol Allied Sci 2000;25:139-42.

3. Murakami S, Hato N, Horiuchi J, Honda N, Gyo K, Yanagihara N. Treatment of Ramsay Hunt syndrome with acyclovir-prednisone: significance of early diagnosis and treatment. Ann Neurol 1997;41:353-7.

4. Wagner G, Klinge H, Sachse MM. Ramsay Hunt syndrome. [Article in English, German] J Dtsch Dermatol Ges 2012;10:23844. [Abstract] 5. Worme M, Chada R, Lavallee L. An unexpected case of Ramsay Hunt syndrome: case report and literature review. BMC Res Notes 2013;6:337.

6. Paul E, Thiel T. Epidemiology of varicella zoster infection. Results of a prospective study in the Ansbach area. [Article in German] Hautarzt 1996;47:604-9. [Abstract]

Kayayurt K et al.

A Case of Ramsay Hunt Syndrome with Atypical Presentation

7. Robillard RB, Hilsinger RL Jr, Adour KK. Ramsay Hunt facial paralysis: clinical analyses of 185 patients. Otolaryngol Head Neck Surg 1986;95:292-7.

8. Gold E. Serologic and virus-isolation studies of patients with varicella or herpes-zoster infection. N Engl J Med 1966;274:181-5.

9. Haanpää M, Dastidar P, Weinberg A, Levin M, Miettinen A, Lapinlampi A, et al. CSF and MRI findings in patients with acute herpes zoster. Neurology 1998;51:1405-11.

10. Brown H, Burns S, Kaiser CW. The spinal accessory nerve plexus, the trapezius muscle, and shoulder stabilization after radical neck cancer surgery. Ann Surg 1988;208:654-61.

11. Sweeney CJ, Gilden DH. Ramsay Hunt syndrome. J Neurol

Neurosurg Psychiatry 2001;71:149-54.

12. Jonsson L, Tien R, Engström M, Thuomas KA. Gd-DPTA enhanced MRI in Bell’s palsy and herpes zoster oticus: an overview and implications for future studies. Acta Otolaryngol 1995;115:577-84.

13. Hato N, Murakami S, Gyo K. Steroid and antiviral treatment for Bell’s palsy. Lancet 2008;371:1818-20.

14. Dworkin RH, Johnson RW, Breuer J, Gnann JW, Levin MJ, Backonja M, et al. Recommendations for the management of herpes zoster. Clin Infect Dis 2007;44 Suppl 1:S1-26.

15. Kinishi M, Amatsu M, Mohri M, Saito M, Hasegawa T, Hasegawa S. Acyclovir improves recovery rate of facial nerve palsy in Ramsay Hunt syndrome. Auris Nasus Larynx 2001;28:223-6.

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