Travma 2014 / 3

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www.tjtes.org Volume 20 | Number 3 | May 2014 ISSN 1306 - 696X TURKISH JOURNAL of TRAUMA & EMERGENCY SURGERY Ulusal Travma ve Acil Cerrahi Dergisi

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Transcript of Travma 2014 / 3

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www.tjtes.orgVolume 20 | Number 3 | May 2014

ISSN 1306 - 696X

TURKISH JOURNAL of TRAUMA& EMERGENCY SURGERYUlusal Travma ve Acil Cerrahi Dergisi

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TURKISH JOURNAL of TRAUMA& EMERGENCY SURGERYUlusal Travma ve Acil Cerrahi Dergisi

Editor-in-Chief Recep Güloğlu

Editors Kaya Sarıbeyoğlu (Managing Editor) Hakan Yanar M. Mahir Özmen

Former Editors Ömer Türel, Cemalettin Ertekin, Korhan Taviloğlu

Section Editors Anaesthesiology & ICU Güniz Meyancı Köksal, Mert Şentürk Cardiac Surgery Münacettin Ceviz, Murat Güvener Neurosurgery Ahmet Deniz Belen, Mehmet Yaşar Kaynar Ophtalmology Cem Mocan, Halil Ateş Ortopedics and Traumatology Mahmut Nedim Doral, Mehmet Can Ünlü Plastic and Reconstructive Surgery Ufuk Emekli, Figen Özgür Pediatric Surgery Aydın Yagmurlu, Ebru Yeşildağ Thoracic Surgery Alper Toker, Akif Turna Urology Ali Atan, Öner Şanlı Vascular Surgery Cüneyt Köksoy, Mehmet Kurtoğlu

www.tjtes.org

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THE TURKISH ASSOCIATION OF TRAUMA AND EMERGENCY SURGERYULUSAL TRAVMA VE ACİL CERRAHİ DERNEĞİ

President (Başkan) Recep Güloğlu Vice President (Başkan Yardımcısı) Kaya Sarıbeyoğlu Secretary General (Genel Sekreter) M. Mahir Özmen Treasurer (Sayman) Ali Fuat Kaan Gök Members (Yönetim Kurulu Üyeleri) Hakan Teoman Yanar Gürhan Çelik Osman Şimşek

CORRESPONDENCEİLETİŞİM

ISSUED BY THE TURKISH ASSOCIATION OF TRAUMA AND EMERGENCY SURGERYULUSAL TRAVMA VE ACİL CERRAHİ DERNEĞİ YAYIN ORGANI

UlusalTravmaveAcilCerrahiDerneği Tel: +90 212 - 588 62 46 - 588 62 46ŞehreminiMah.,KöprülüMehmetPaşaSok. Fax (Faks): +90 212 - 586 18 04DadaşoğluApt.,No:25/1, e-mail (e-posta):[email protected]Şehremini,İstanbul,Turkey Web:www.travma.org.tr

Owner (Ulusal Travma ve Acil Cerrahi Derneği adına Sahibi) RecepGüloğluEditorialDirector (Yazı İşleri Müdürü) RecepGüloğluManagingEditor (Yayın Koordinatörü) M.MahirÖzmenAmblem MetinErtemCorrespondenceaddress (Yazışma adresi) UlusalTravmaveAcilCerrahiDergisiSekreterliği ŞehreminiMah.,KöprülüMehmetPaşaSok., DadaşoğluApt.,No:25/1,34104Şehremini,İstanbul Tel +90 212 - 531 12 46 - 588 62 46 Fax (Faks) +90 212 - 586 18 04

Annualsubscriptionrates:75.-(USD)Abonelik: 2013 yılı abone bedeli (Ulusal Travma ve Acil Cerrahi Derneği’ne bağış olarak) 75.- YTL’dir. Hesap No: Türkiye İş Bankası, İstanbul Tıp Fakültesi Şubesi 1200 - 3141069 no’lu hesabına yatırılıp makbuz dernek adresine posta veya faks yolu ile iletilmelidir.

p-ISSN 1306-696x • e-ISSN 1307-7945 • Included in Index Medicus, Medline; EMBASE, Excerpta Medica; Science Citation Index-Expanded (SCI-E), Index Copernicus, DOAJ, and Turkish Medical Index (Index Medicus, Medline; EMBASE, Excerpta Medica; Science Citation Index-Expanded (SCI-E), Index Copernicus, DOAJ ve TÜBİTAK ULAKBİM Türk Tıp Dizini’nde yer almaktadır.)

Publisher (Yayımcı): KARE Yayıncılık (KARE Publishing) • Design (Tasarım): Ali Cangül • Graphics (Grafikler): Edibe Çomaktekin • Linguistic Editor (İngilizce Editörü): Corinne Can • Redaction (Redaksiyon): Erman Aytaç • Online Manuscript & Web Management (Online Dergi & Web): LookUs • Press (Baskı): Yıldırım Matbaacılık • Press date (Basım tarihi): May (Mayıs) 2014 • This publication is printed on paper that meets the international standard ISO 9706: 1994 (Bu dergide kullanılan kağıt ISO 9706: 1994 standardına uygundur.)

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KARE

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The Turkish Journal of Trauma and Emergency Surgery (TJTES) is an official publication of the Turkish Association of Trauma and Emer-gency Surgery. It is a peer-reviewed periodical that considers for pub-lication clinical and experimental studies, case reports, technical con-tributions, and letters to the editor. Six issues are published annually.As from 2001, the journal is indexed in Index Medicus and Medline, as from 2005 in Excerpta Medica and EMBASE, as from 2007 in Science Citation Index Expanded (SCI-E) and Journal Citation Reports / Sci-ence Edition, and as from 2008 in Index Copernicus. For the five-year term of 2001-2006, our impact factor in SCI-E indexed journals is 0.5. It is cited as ‘Ulus Travma Acil Cerrahi Derg’ in PUBMED. Submission of a manuscript by electronic means implies: that the work has not been published before (except in the form of an abstract or as part of a published lecture, review, or thesis); that it is not under consideration for publication elsewhere; and that its publication in the Turkish Journal of Trauma and Emergency Surgery is approved by all co-authors. The author(s) transfer(s) the copyright to the Turkish Asso-ciation of Trauma and Emergency Surgery to be effective if and when the manuscript is accepted for publication. The author(s) guarantee(s) that the manuscript will not be published elsewhere in any other lan-guage without the consent of the Association. If the manuscript has been presented at a meeting, this should be stated together with the name of the meeting, date, and the place.Manuscripts may be submitted in Turkish or in English. All submissions are initially reviewed by the editor, and then are sent to reviewers. All manuscripts are subject to editing and, if necessary, will be returned to the authors for answered responses to outstanding questions or for ad-dition of any missing information to be added. For accuracy and clarity, a detailed manuscript editing is undertaken for all manuscripts accepted for publication. Final galley proofs are sent to the authors for approval.Unless specifically indicated otherwise at the time of submission, re-jected manuscripts will not be returned to the authors, including ac-companying materials.TJTES is indexed in Science Citation Index-Expanded (SCI-E), Index Medicus, Medline, EMBASE, Excerpta Medica, and the Turkish Medi-cal Index of TUBITAK-ULAKBIM. Priority of publications is given to original studies; therefore, selection criteria are more refined for re-views and case reports.Open Access Policy: Full text access is free. There is no charge for publication or downloading the full text of printed material.Manuscript submission: TJTES accepts only on-line submission via the official web site (please click, www.travma.org.tr/en) and refuses printed manuscript submissions by mail. All submissions are made by the on-line submission system called Journal Agent, by clicking the icon “Online manuscript submission” at the above mentioned web site homepage. The system includes directions at each step but for fur-ther information you may visit the web site (http://www.travma.org/en/journal/).Manuscript preparation: Manuscripts should have double-line spac-ing, leaving sufficient margin on both sides. The font size (12 points) and style (Times New Roman) of the main text should be uniformly taken into account. All pages of the main text should be numbered consecutively. Cover letter, manuscript title, author names and institu-tions and correspondence address, abstract in Turkish (for Turkish au-thors only), and title and abstract in English are uploaded to the Journal Agent system in the relevant steps. The main text includes Introduc-tion, Materials and Methods, Results, Discussion, Acknowledgments, References, Tables and Figure Legends.The cover letter must contain a brief statement that the manuscript has been read and approved by all authors, that it has not been submit-ted to, or is not under consideration for publication in, another journal. It should contain the names and signatures of all authors. The cover letter is uploaded at the 10th step of the “Submit New Manuscript” sec-

tion, called “Upload Your Files”.Abstract: The abstract should be structured and serve as an informa-tive guide for the methods and results sections of the study. It must be prepared with the following subtitles: Background, Methods, Results and Conclusions. Abstracts should not exceed 200 words.Figures, illustrations and tables: All figures and tables should be numbered in the order of appearance in the text. The desired position of figures and tables should be indicated in the text. Legends should be included in the relevant part of the main text and those for photo-micrographs and slide preparations should indicate the magnification and the stain used. Color pictures and figures will be published if they are definitely required and with the understanding that the authors are prepared to bear the costs. Line drawings should be professionally pre-pared. For recognizable photographs, signed releases of the patient or of his/her legal representatives should be enclosed; otherwise, patient names or eyes must be blocked out to prevent identification.References: All references should be numbered in the order of men-tion in the text. All reference figures in the text should be given in brack-ets without changing the font size. References should only include articles that have been published or accepted for publication. Refer-ence format should conform to the “Uniform requirements for manu-scripts submitted to biomedical journals” (http://www.icmje.org) and its updated versions (February 2006). Journal titles should be abbrevi-ated according to Index Medicus. Journal references should provide inclusive page numbers. All authors, if six or fewer, should be listed; otherwise the first six should be listed, followed by “et al.” should be written. The style and punctuation of the references should follow the formats below:Journal article: Velmahos GC, Kamel E, Chan LS, Hanpeter D, Asensio JA, Murray JA, et al. Complex repair for the management of duodenal injuries. Am Surg 1999;65:972-5.Chapter in book: Jurkovich GJ. Duodenum and pancreas. In: Mattox KL, Feliciano DV, Moore EE, editors. Trauma. 4th ed. New York: Mc-Graw-Hill; 2000. p. 735-62.Our journal has succeeded in being included in several indexes, in this context, we have included a search engine in our web site (www.travma.org.tr) so that you can access full-text articles of the previous issues and cite the published articles in your studies.Review articles: Only reviews written by distinguished authors based on the editor’s invitation will be considered and evaluated. Review ar-ticles must include the title, summary, text, and references sections. Any accompanying tables, graphics, and figures should be prepared as mentioned above.Case reports: A limited number of case reports are published in each is-sue of the journal. The presented case(s) should be educative and of in-terest to the readers, and should reflect an exclusive rarity. Case reports should contain the title, summary, and the case, discussion, and refer-ences sections. These reports may consist of maximum five authors.Letters to the Editor: “Letters to the Editor” are only published elec-tronically and they do not appear in the printed version of TJTES and PUBMED. The editors do not issue an acceptance document as an original article for the ‘’letters to the editor. The letters should not ex-ceed 500 words. The letter must clearly list the title, authors, publica-tion date, issue number, and inclusive page numbers of the publication for which opinions are released.Informed consent - Ethics: Manuscripts reporting the results of ex-perimental studies on human subjects must include a statement that informed consent was obtained after the nature of the procedure(s) had been fully explained. Manuscripts describing investigations in animals must clearly indicate the steps taken to eliminate pain and suffering. Authors are advised to comply with internationally accepted guidelines, stating such compliance in their manuscripts and to include the approval by the local institutional human research committee.

INFORMATION FOR THE AUTHORS

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Ulusal Travma ve Acil Cerrahi Dergisi, Ulusal Travma ve Acil Cerrahi Derneği’nin yayın organıdır. Travma ve acil cerrahi hastalıklar konuların-da bilimsel birikime katkısı olan klinik ve deneysel çalışmaları, editöryel yazıları, klinik olgu sunumlarını ve bu konulardaki teknik katkılar ile son gelişmeleri yayınlar. Dergi iki ayda bir yayınlanır.Ulusal Travma ve Acil Cerrahi Dergisi, 2001 yılından itibaren Index Me-dicus ve Medline’da, 2005 yılından itibaren Excerpta Medica / EMBASE indekslerinde, 2007 yılından itibaren Science Citation Index-Expanded (SCI-E) ile Journal Citation Reports / Science Edition uluslararası in-dekslerinde ve 2008 yılından itibaren Index Copernicus indeksinde yer almaktadır. 2001-2006 yılları arasındaki 5 yıllık dönemde SCI-E kapsa-mındaki dergilerdeki İmpakt faktörümüz 0,5 olmuştur. Dergide araştırma yazılarına öncelik verilmekte, bu nedenle derleme veya olgu sunumu türündeki yazılarda seçim ölçütleri daha dar tutulmaktadır. PUBMED’de dergi “Ulus Travma Acil Cerrahi Derg” kısaltması ile yer almaktadır. Dergiye yazı teslimi, çalışmanın daha önce yayınlanmadığı (özet ya da bir sunu, inceleme, ya da tezin bir parçası şeklinde yayınlanması dışın-da), başka bir yerde yayınlanmasının düşünülmediği ve Ulusal Travma ve Acil Cerrahi Dergisi’nde yayınlanmasının tüm yazarlar tarafından uygun bulunduğu anlamına gelmektedir. Yazar(lar), çalışmanın yayın-lanmasının kabulünden başlayarak, yazıya ait her hakkı Ulusal Travma ve Acil Cerrahi Derneği’ne devretmektedir(ler). Yazar(lar), izin almaksı-zın çalışmayı başka bir dilde ya da yerde yayınlamayacaklarını kabul eder(ler). Gönderilen yazı daha önce herhangi bir toplantıda sunulmuş ise, toplantı adı, tarihi ve düzenlendiği şehir belirtilmelidir.Dergide Türkçe ve İngilizce yazılmış makaleler yayınlanabilir. Tüm yazı-lar önce editör tarafından ön değerlendirmeye alınır; daha sonra incelen-mesi için danışma kurulu üyelerine gönderilir.Tüm yazılarda editöryel değerlendirme ve düzeltmeye başvurulur; ge-rektiğinde, yazarlardan bazı soruları yanıtlanması ve eksikleri tamam-lanması istenebilir. Dergide yayınlanmasına karar verilen yazılar “ma-nuscript editing” sürecine alınır; bu aşamada tüm bilgilerin doğruluğu için ayrıntılı kontrol ve denetimden geçirilir; yayın öncesi şekline getirilerek yazarların kontrolüne ve onayına sunulur. Editörün, kabul edilmeyen yazıların bütününü ya da bir bölümünü (tablo, resim, vs.) iade etme zo-runluluğu yoktur.Açık Erişim İlkesi: Tam metinlere erişim ücretsizdir. Yayınlanan basılı materyali tam metni indirmek için herhangi bir ücret alınmaz.Yazıların hazırlanması: Tüm yazılı metinler 12 punto büyüklükte “Times New Roman” yazı karakterinde iki satır aralıklı olarak yazılmalıdır. Say-fada her iki tarafta uygun miktarda boşluk bırakılmalı ve ana metindeki sayfalar numaralandırılmalıdır. Journal Agent sisteminde, başvuru mek-tubu, başlık, yazarlar ve kurumları, iletişim adresi, Türkçe özet ve yazının İngilizce başlığı ve özeti ilgili aşamalarda yüklenecektir. İngilizce yazı-lan çalışmalara da Türkçe özet eklenmesi gerekmektedir. Yazının ana metnindeyse şu sıra kullanılacaktır: Giriş, Gereç ve Yöntem, Bulgular, Tartışma, Teşekkür, Kaynaklar, Tablolar ve Şekiller.Başvuru mektubu: Bu mektupta yazının tüm yazarlar tarafından okun-duğu, onaylandığı ve orijinal bir çalışma ürünü olduğu ifade edilmeli ve yazar isimlerinin yanında imzaları bulunmalıdır. Başvuru mektubu ayrı bir dosya olarak, Journal Agent sisteminin “Yeni Makale Gönder” bölü-münde, 10. aşamada yer alan dosya yükleme aşamasında yollanmalıdır.Başlık sayfası: Yazının başlığı, yazarların adı, soyadı ve ünvanları, ça-lışmanın yapıldığı kurumun adı ve şehri, eğer varsa çalışmayı destekle-yen fon ve kuruluşların açık adları bu sayfada yer almalıdır. Bu sayfaya ayrıca “yazışmadan sorumlu” yazarın isim, açık adres, telefon, faks, mo-bil telefon ve e-posta bilgileri eklenmelidir. Özet: Çalışmanın gereç ve yöntemini ve bulgularını tanıtıcı olmalıdır. Türkçe özet, Amaç, Gereç ve Yöntem, Bulgular, Sonuç ve Anahtar Söz-cükler başlıklarını; İngilizce özet Background, Methods, Results, Conc-lusion ve Key words başlıklarını içermelidir. İngilizce olarak hazırlanan çalışmalarda da Türkçe özet yer almalıdır. Özetler başlıklar hariç 190-210 sözcük olmalıdır. Tablo, şekil, grafik ve resimler: Şekillere ait numara ve açıklayıcı bil-giler ana metinde ilgili bölüme yazılmalıdır. Mikroskobik şekillerde resmi açıklayıcı bilgilere ek olarak, büyütme oranı ve kullanılan boyama tekniği de belirtilmelidir. Yazarlara ait olmayan, başka kaynaklarca daha önce yayınlanmış tüm resim, şekil ve tablolar için yayın hakkına sahip kişiler-

den izin alınmalı ve izin belgesi dergi editörlüğüne ayrıca açıklamasıyla birlikte gönderilmelidir. Hastaların görüntülendiği fotoğraflara, hastanın ve/veya velisinin imzaladığı bir izin belgesi eşlik etmeli veya fotoğrafta hastanın yüzü tanınmayacak şekilde kapatılmış olmalıdır. Renkli resim ve şekillerin basımı için karar hakemler ve editöre aittir. Yazarlar renkli baskının hazırlık aşamasındaki tutarını ödemeyi kabul etmelidirler. Kaynaklar: Metin içindeki kullanım sırasına göre düzenlenmelidir. Ma-kale içinde geçen kaynak numaraları köşeli parantezle ve küçültülmeden belirtilmelidir. Kaynak listesinde yalnızca yayınlanmış ya da yayınlan-ması kabul edilmiş çalışmalar yer almalıdır. Kaynak bildirme “Uniform Requirements for Manuscripts Submitted to Biomedical Journals” (http://www.icmje.org) adlı kılavuzun en son güncellenmiş şekline (Şubat 2006) uymalıdır. Dergi adları Index Medicus’a uygun şekilde kısaltılmalıdır. Altı ya da daha az sayıda olduğunda tüm yazar adları verilmeli, daha çok yazar durumunda altıncı yazarın arkasından “et al.” ya da “ve ark.” ek-lenmelidir. Kaynakların dizilme şekli ve noktalamalar aşağıdaki örneklere uygun olmalıdır:Dergi metni için örnek: Velmahos GC, Kamel E, Chan LS, Hanpeter D, Asensio JA, Murray JA, et al. Complex repair for the management of duodenal injuries. Am Surg 1999;65:972-5.Kitaptan bölüm için örnek: Jurkovich GJ. Duodenum and pancreas. In: Mattox KL, Feliciano DV, Moore EE, editors. Trauma. 4th ed. New York: McGraw-Hill; 2000. p. 735-62.Sizlerin çalışmalarınızda kaynak olarak yararlanabilmeniz için www.trav-ma.org.tr adresli web sayfamızda eski yayınlara tam metin olarak ulaşa-bileceğiniz bir arama motoru vardır.Derleme yazıları: Bu tür makaleler editörler kurulu tarafından gerek ol-duğunda, konu hakkında birikimi olan ve bu birikimi literatüre de yan-sımış kişilerden talep edilecek ve dergi yazım kurallarına uygunluğu saptandıktan sonra değerlendirmeye alınacaktır. Derleme makaleleri; başlık, Türkçe özet, İngilizce başlık ve özet, alt başlıklarla bölümlendiril-miş metin ile kaynakları içermelidir. Tablo, şekil, grafik veya resim varsa yukarıda belirtildiği şekilde gönderilmelidir.Olgu sunumları: Derginin her sayısında sınırlı sayıda olgu sunumu-na yer verilmektedir. Olgu bildirilerinin kabulünde, az görülürlük, eğitici olma, ilginç olma önemli ölçüt değerlerdir. Ayrıca bu tür yazıların olabil-diğince kısa hazırlanması gerekir. Olgu sunumları başlık, Türkçe özet, İngilizce başlık ve özet, olgu sunumu, tartışma ve kaynaklar bölümlerin-den oluşmalıdır. Bu tür çalışmalarda en fazla 5 yazara yer verilmesine özen gösterilmelidir.Editöre mektuplar: Editöre mektuplar basılı dergide ve PUBMED’de yer almamakta, ancak derginin web sitesinde yayınlanmaktadır. Bu mektup-lar için dergi yönetimi tarafından yayın belgesi verilmemektedir.Daha önce basılmış yazılarla ilgili görüş, katkı, eleştiriler ya da farklı bir konu üzerindeki deneyim ve düşünceler için editöre mektup yazılabilir. Bu tür yazılar 500 sözcüğü geçmemeli ve tıbbi etik kurallara uygun ola-rak kaleme alınmış olmalıdır. Mektup basılmış bir yazı hakkında ise, söz konusu yayına ait yıl, sayı, sayfa numaraları, yazı başlığı ve yazarların adları belirtilmelidir. Mektup bir konuda deneyim, düşünce hakkında ise verilen bilgiler doğrultusunda dergi kurallarına uyumlu olarak kaynaklar da belirtilmelidir. Bilgilendirerek onay alma - Etik: Deneysel çalışmaların sonuçlarını bil-diren yazılarda, çalışmanın yapıldığı gönüllü ya da hastalara uygulanacak prosedür(lerin) özelliği tümüyle anlatıldıktan sonra, onaylarının alındığını gösterir bir cümle bulunmalıdır. Yazarlar, bu tür bir çalışma söz konusu olduğunda, uluslararası alanda kabul edilen kılavuzlara ve T.C. Sağlık Bakanlığı tarafından getirilen yönetmelik ve yazılarda belirtilen hüküm-lere uyulduğunu belirtmeli ve kurumdan aldıkları Etik Komitesi onayını göndermelidir. Hayvanlar üzerinde yapılan çalışmalarda ağrı, acı ve ra-hatsızlık verilmemesi için neler yapıldığı açık bir şekilde belirtilmelidir.Yazı gönderme - Yazıların gönderilmesi: Ulusal Travma ve Acil Cer-rahi Dergisi yalnızca www.travma.org.tr adresindeki internet sitesinden on-line olarak gönderilen yazıları kabul etmekte, posta yoluyla yollanan yazıları değerlendirmeye almamaktadır. Tüm yazılar ilgili adresteki “Onli-ne Makale Gönderme” ikonuna tıklandığında ulaşılan Journal Agent sis-teminden yollanmaktadır. Sistem her aşamada kullanıcıyı bilgilendiren özelliktedir.

YAZARLARA BİLGİ

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ULUSAL TRAVMA VE ACİL CERRAHİ DERGİSİVol. - Cilt 20 Number - Sayı 3 May - Mayıs 2014

Deneysel Çalışma - Experimental Study

151-160 Captopril protects against burn-induced cardiopulmonary injury in rats Sıçanlarda yanıkla uyarılan kardiyopulmoner hasara karşı kaptoprilin koruyucu etkisi Sağlam E, Şehirli AÖ, Özdamar EN, Contuk G, Çetinel Ş, Özsavcı D, Süleymanoğlu S, Şener G

161-166 The effect of hyperbaric oxygen therapy on fracture healing in nicotinized rats Nikotinize sıçanlarda hiperbarik oksijen tedavisinin kırık iyileşmesi üzerine etkisi Demirtaş A, Azboy İ, Bulut M, Uçar BY, Alemdar C, Alabalık U, Akpolat V, Yıldız İ, İlgezdi S

167-175 Effectiveness of hyperbaric oxygen and ozone applications in tissue healing in generated soft tissue trauma model in rats: an experimental study Sıçanlarda oluşturulan yumuşak doku travma modelinde, hiperbarik oksijen ve ozon uygulamalarının doku iyileşmesi üzerine etkinliği: Deneysel çalışma Yıldırım AO, Eryılmaz M, Kaldırım Ü, Eyi YE, Tuncer SK, Eroğlu M, Durusu M, Topal T, Kurt B, Dilmen S, Bilgiç S, Serdar M

Klinik Çalışma - Original Articles

176-180 Psychiatric disorders and their association with burn-related factors in children with burn injury Yanık yaralanması olan çocuklarda görülen psikiyatrik bozukluklar ve yanık-ilişkili faktörlerle olan bağlantısı Karaçetin G, Demir T, Baghaki S, Çetinkale O, Yüksel ME

181-188 Traumatic wound dehiscence after penetrating keratoplasty: case series and literature review Penetran keratoplasti sonrası travmatik yara ayrışması, olgu serisi ve literatüre genel bakış Kartal B, Kandemir B, Set T, Kuğu S, Keleş S, Ceylan E, Akmaz B, Apil A, Özertürk Y

189-193 Comparison of intramedullary nail and plate fixation in distal tibia diaphyseal fractures close to the mortise Mortise yakın distal tibia diafiz kırıklarının tedavisinde intramedüller çivi ve plak tedavisinin karşılaştırılması Yavuz U, Sökücü S, Demir B, Yıldırım T, Özcan Ç, Kabukçuoğlu YS

194-198 A new, simple technique for gradual primary closure of fasciotomy wounds Fasyotomi defektlerinin aşamalı primer kapatılmasında yeni ve basit bir yöntem Özyurtlu M, Altınkaya S, Baltu Y, Özgenel GY

199-204 Skafoid psödoartroz tedavisinde otolog kemik grefti ve titanyum başsız kanüllü kompresyon vidası kombinasyonu uygulama sonuçları The results of autologous bone graft and titanium headless cannulated compression screw for treatment of scaphoid nonunion Özdemir G, Çiçekli Ö, Akgül T, Zehir S, Yücel F, Eşkin D

Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3 vii

Contents - İçindekiler

TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY

Original Articles - Klinik Çalışma

Experimental Study - Deneysel Çalışma

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205-210 Triangular fibrokartilaj kompleks periferik (Palmer tip 1B) yırtıklarında artroskopik tamir sonuçları Results of arthroscopic repair of triangular fibrocartilage complex peripheral tears (Palmer type 1B) Kabakaş F, Özçelik İB, Uğurlar M, Mersa B, Yazar M, Uzun M

Olgu Sunumu - Case Reports

211-213 Supraventricular tachycardia due to blunt chest trauma in an adolescent Bir adolösanda künt göğüs travmasına bağlı supraventriküler taşikardi Alp H, Baysal T, Karaarslan S

214-216 Are blank cartridge guns really harmless? Kurusıkı silahlar gerçekten zararsız mı? Gülşen İ, Ak H, Sosuncu E, Bulut MD

217-220 Successful emergency department thoracotomy for traumatic cardiac rupture: effective utilization of a fret sternum saw Travmatik kardiyak rüptür için başarılı acil servis torakotomisi: Fret sternum testeresinin efektif kullanımı Nakamura T, Masuda K, Hitomi E, Osaka Y, Nakao T, Yoshimura N

221-223 An unusual entry site for a nasal foreign body: a neglected trauma patient Burunda yabancı cisimde sıradışı bir giriş yolu: İhmal edilmiş bir travma olgusu Mülazımoğlu S, Ocak E, Beton S, Özgürsoy OB

224-226 Oksipital kondil kırıkları: Bir olgu sunumu Occipital condyle fractures: A case report Dinç C, Türkoğlu ME, Tuncer C, Aykanat Ö, Özçelik D, Özkan G

Ulus Travma Acil Cerrahi Derg, Mayıs 2014, Cilt. 20, No. 3viii

Contents - İçindekiler

Case Reports - Olgu Sunumu

ULUSAL TRAVMA VE ACİL CERRAHİ DERGİSİVol. - Cilt 20 Number - Sayı 3 May - Mayıs 2014

TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY

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Captopril protects against burn-inducedcardiopulmonary injury in ratsEsra Sağlam, M.D.,1# Ahmet Özer Şehirli, PhD.,2 Emine Nur Özdamar, M.D.,3 Gazi Contuk, PhD.,4

Şule Çetinel, M.D.,4 Derya Özsavcı, PhD.,5 Selami Süleymanoğlu, M.D.,6 Göksel Şener, PhD.2

1DepartmentofLaboratoryofClinicalPharmacogenetics,UskudarUniversityIstanbulNeuropsychiatryHospital,Istanbul2DepartmentofPharmacology,MarmaraUniversityFacultyofPharmacy,Istanbul3DepartmentofMedicalPharmacology,MarmaraUniversityFacultyofMedicine,Istanbul4DepartmentofHistology&Embryology,MarmaraUniversityFacultyofMedicine,Istanbul5DepartmentofBiochemistry,MarmaraUniversityFacultyofPharmacy,Istanbul6DepartmentofCardiology,GulhaneMilitaryMedicalAcademy,Istanbul

ABSTRACT

BACKGROUND: This study was designed to determine the possible protective effect of captopril treatment against oxidative dam-age in heart and lung tissues induced by burn injury.

METHODS: Under ether anesthesia, the shaved dorsum of Wistar albino rats was exposed to 90°C water bath for 10 seconds. Captopril was administered intraperitoneally (10 mg/kg) after the burn injury and repeated twice daily. In the sham group, the dorsum was dipped in a 25°C water bath for 10 seconds. At the end of the 24 hours, echocardiographic recordings were performed, then animals were decapitated and heart and lung tissue samples were taken for the determination of tumor necrosis factor-α (TNF-α) as a pro-inflammatory cytokine, malondialdehyde and glutathione levels and myeloperoxidase, caspase-3, and Na+,K+-ATPase activity in addition to the histological analysis.

RESULTS: Burn injury caused significant alterations in left ventricular function. In heart and lung tissues, TNF-α and malondialdehyde levels and myeloperoxidase and caspase-3 activities were found to be increased, while glutathione levels and Na+, K+-ATPase activity were decreased due to burn injury. Captopril treatment significantly elevated the reduced glutathione level and Na+, K+-ATPase activity, and decreased cytokine and malondialdehyde levels and myeloperoxidase and caspase-3 activities.

CONCLUSION: Captopril prevents burn-induced damage in heart and lung tissues and protects against oxidative organ damage.

Key words: Captopril; cytokine; lipid peroxidation; myeloperoxidase; thermal trauma.

INTRODUCTION

Thermal trauma produces profound systemic changes such as oligemic shock, anemia, renal failure, and metabolic distur-bances. It causes direct tissue damage as well as inflammatory reactions.[1] Thermal trauma causes a progressive decrease in

cardiac output and cardiac stroke volume, release of vasocon-strictor mediators such as vasopressin, altered baroreceptor and chemoreceptor reflexes, and reabsorption of fluid.[2] A number of experimental and clinical studies have shown that, despite aggressive fluid resuscitation and maintenance of pul-monary capillary wedge pressure, stroke work and ejection fraction (EF) often decrease after thermal trauma.[3,4] Several studies have indicated that decreased cardiac contractility is one of the important mechanisms for decreased cardiac out-put and cardiac dysfunction after severe thermal trauma.[5,6]

Angiotensin converting enzyme (ACE) catalyzes the conver-sion of angiotensin I (Ang I) to angiotensin II (Ang II). ACE also cleaves the terminal dipeptide of vasodilating hormone brady-kinin to inactivate this hormone. Hyperactivity of the renin–angiotensin system (RAS), an endocrine system with critical roles in cardiovascular function, has been implicated in the eti-ology of high blood pressure, obesity and metabolic syndrome.[7] Therefore, inhibition of ACE is generally used as one of the

EXPERIMENTAL STUDY

Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3 151

#Current affiliation: Maltepe University, School of Medicine,

Department of Pharmacology and Clinical Pharmacology, Istanbul

Address for correspondence: Esra Saglam, M.D.

Alemdağ Cad., Site Yolu, No: 27, Ümraniye, İstanbul, Turkey

Tel: +90 216 - 633 06 33 E-mail: [email protected]

Qucik Response Code Ulus Travma Acil Cerrahi Derg2014;20(3):151-160doi: 10.5505/tjtes.2014.96493

Copyright 2014TJTES

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Saglam et al. Captopril protects against burn-induced cardiopulmonary injury in rats

methods in the treatment of hypertension and chronic inflam-mation.[8,9] Pharmacologically, it is known that ACE inhibitors containing a sulfhydryl or a thiol radical, such as the orally ac-tive compound captopril, have an antioxidant activity.[10,11]

In the light of these findings, we hypothesized that captopril would provide protection against burn-induced cardiopul-monary damage. We aimed to investigate whether and to what extent captopril reduces this damage, by determining the presence of oxidative tissue injury using biochemical and histological parameters.

MATERIALS AND METHODS

AnimalsWistar albino rats of both sexes, weighing 200-250 g, were obtained from Marmara University School of Medicine Ani-mal House. The rats were kept at a constant temperature (22±1ºC) with 12-hour (h) light and dark cycles, fed with standard rat chow, and fasted for 12 h before the experi-ments, but were allowed free access to water. All experimen-tal protocols were approved by the Marmara University Ani-mal Care and Use Committee.

Thermal Injury and Experimental DesignThis is a randomized controlled trial. All groups were elected in exactly the same way. Twenty-four animals were divided into three groups of eight rats each: One group served as controls. Two groups underwent burn injury and were treat-ed with saline or captopril. Under brief ether anesthesia, the dorsum of the rats was shaved and exposed to 90° water bath for 10 seconds (s), which resulted in a second-degree burn involving 30% of the total body surface area.[12] To rule out the effects of the anesthesia, the same protocol was ap-plied in the control group, except that the dorsa were dipped in a 25°C water bath for 10 s. After sham or burn injury, rats were resuscitated with physiological saline solution (10 ml/kg subcutaneous). ACE inhibitor captopril (10 mg/kg, intra-peritoneal (i.p.); Sigma-Aldrich; St. Louis, MO, USA) or sa-line was given intraperitoneally to rats immediately after the burn injury, and the injections were repeated twice a day. Two groups (controls and the first burn group) received sa-line and the second burn group received i.p. captopril (10 mg/kg in saline) administered immediately after the burn, and the injections were repeated twice a day. Intraperitoneal ad-ministration of captopril could potentially have a systemic ef-fect.[13] In both the saline- and captopril-treated burn groups, rats were decapitated at 24 h following burn injury. At the end of the experimental period, transthoracic echocardiog-raphy was performed to assess the cardiac function of the rats. Then, the animals were decapitated in order to evaluate the presence of oxidant injury in the heart, and lung tissue samples were taken and stored at -80°C for the determina-tion of pro-inflammatory cytokine [tumor necrosis factor-α (TNF-α)], malondialdehyde (MDA) and glutathione (GSH)

levels and myeloperoxidase (MPO) and Na+, K+-ATPase and caspase-3 activities. For histological analysis, samples of the tissues were fixed in 10% (vol/vol) buffered p-formaldehyde and prepared for routine paraffin embedding. Tissue sections (6 µm) were stained with hematoxylin and eosin (H&E) and examined under a light microscope (Olympus-BH-2). An ex-perienced histologist who was unaware of the treatment con-ditions performed the histological assessments.

EchocardiographyEchocardiographic imaging and calculations were done ac-cording to the guidelines published by the American Society of Echocardiography[14] using a 12 MHz linear transducer and 5-8 MHz sector transducer (Vivid 3, General Electric Medical Systems Ultrasound, Tirat Carmel, Israel). Under ketamine (50 mg/kg, i.p.) anesthesia, measurements were made from M-mode and two-dimensional images obtained in the para-sternal long- and short axes at the level of the papillary mus-cles after observation of at least six cardiac cycles. Interven-tricular septal thickness (IVS), left ventricular diameter (LVD) and left ventricular posterior wall thickness (LVPW) were measured during systole (s) and diastole (d). EF, fractional shortening (FS) and left ventricular mass (LVM) and relative wall thickness (RWT) were calculated from the M-mode im-ages using the following formulas: % EF = [(LVDd)3 - (LVDs)3/(LVDd)3 x 100], % FS = [LVDd-LVDs/LVDd x 100], LVM= [1.04 x ((LVDd+LVPWd+IVSd)3 - (LVDd)3) x 0.8 + 0.14], and RWT = [2 x (LVPWd/LVDd)].

Determination of Tissue TNF-α Levels: The levels of TNF-α in the tissues were measured by en-zyme-linked immunosorbent assay (ELISA). Heart and lung tissues (100 mg) were homogenized in an ice-cold bath. Af-ter centrifugation, the supernatant was collected and total protein content was determined. Tissue TNF-α levels were measured with rat TNF-α ELISA kits (Invitrogen; Taastrup, Denmark) according to the manufacturer’s instructions. Ab-sorbance of standards and samples was determined on a plate reader at 405 nm. Results are expressed as pg/100 mg tissue.

Malondialdehyde and Glutathione AssaysTissue samples were homogenized with ice-cold 150 mM KCl for the determination of MDA and GSH levels. The MDA levels were assayed for products of lipid peroxidation by monitoring thiobarbituric acid reactive substance formation as described previously.[15] Lipid peroxidation was expressed in terms of MDA equivalents using an extinction coefficient of 1.56x105 M-1 cm-1, and results are expressed as nmol MDA/g tissue. GSH measurements were performed using a modifica-tion of the Ellman procedure.[16] Briefly, after centrifugation at 3000 rev/minute (min) for 10 min, 0.5 ml of supernatant was added to 2 ml of 0.3 mol/L Na2HPO4.2H2O solution. A 0.2 ml solution of dithiobisnitrobenzoate (0.4 mg/ml 1% sodium citrate) was added, and the absorbance at 412 nm was mea-sured immediately after mixing. GSH levels were calculated

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using an extinction coefficient of 1.36x104 M-1 cm-1. Results are expressed in µmol GSH/g tissue.

Myeloperoxidase ActivityMyeloperoxidase (MPO) is an enzyme found predominantly in the azurophilic granules of polymorphonuclear leukocytes (PMN). Tissue MPO activity is frequently utilized to estimate tissue PMN accumulation in inflamed tissues, and correlates significantly with the number of PMN determined histo-chemically in tissues. MPO activity was measured in tissues in a procedure similar to that documented by Hillegass et al.[17] Tissue samples were homogenized in 50 mM potassium phosphate buffer (PB, pH 6.0), and centrifuged at 41,400 g (10 min); pellets were suspended in 50 mM PB containing 0.5% hexadecyltrimethylammonium bromide (HETAB). After three freeze and thaw cycles, with sonication between cycles, the samples were centrifuged at 41,400 g for 10 min. Aliquots (0.3 ml) were added to 2.3 ml of reaction mixture containing 50 mM PB, o-dianisidine, and 20 mM H2O2 solution. One unit of enzyme activity was defined as the amount of MPO pres-ent that caused a change in absorbance measured at 460 nm for 3 min. MPO activity was expressed as U/g tissue.

Na+, K+-ATPase Activity Since the activity of Na+, K+-ATPase, a membrane-bound en-zyme required for cellular transport, is very sensitive to free radical reactions and lipid peroxidation, reductions in this ac-tivity can indicate membrane damage indirectly. Measurement of Na+, K+-ATPase activity is based on the measurement of inorganic phosphate released by ATP hydrolysis during incu-bation of homogenates with an appropriate medium contain-ing 3 mM ATP as a substrate. The total ATPase activity was determined in the presence of 100 mM NaCl, 5 mM KCl, 6 mM MgCl2, 0.1 mM EDTA, and 30 mM Tris HCl (pH 7.4), while the Mg2+-ATPase activity was determined in the pres-ence of 1mM ouabain. The difference between the total and the Mg2+-ATPase activities was taken as a measure of the Na+,

K+-ATPase activity.[18] The reaction was initiated with the ad-dition of the homogenate (0.1 ml), and a 5-min preincuba-tion period at 37ºC was allowed. Following the addition of Na2ATP and a 10-min re-incubation period, the reaction was terminated by the addition of ice-cold 6% perchloric acid. The mixture was then centrifuged at 3500 g, and Pi in the superna-tant fraction was determined by the method of Fiske and Sub-arrow.[19] The specific activity of the enzyme was expressed as µmol Pi mg-1 protein h-1. The protein concentration of the supernatant was measured by the Lowry method.[20]

Caspase-3 ActivityCaspase-3 activity was measured using ApoTargetCaspase-3/CPP32 Colorimetric Protease Assay (Invitrogen; Taastrup, Denmark) kit according to the manufacturer’s instructions. Briefly, brain and lung tissue samples were homogenized and treated for 10 min with iced lysis buffer supplied by the manu-facturer. The cell lysates were subjected to three freeze and thaw cycles and 2x10 s sonication to fully disrupt the cells and disperse cell debris. The cell lysate was then centrifuged at 20,000 g for 5 min and the supernatant transferred to new Eppendorf tubes. Following protein determination, cytosol extracts were diluted in 50µL lysis buffer and 50 µL reaction buffer (10mM dithiothreitol). Samples were added to wells and the microplate was equilibrated at 37°C for 10 min. The reaction was initiated by adding 5 µl of DEVD-pNA (Asp-Glu-Val-Asp p-nitroanilide) substrate (200 µM final concen-tration), and the reaction was carried out at 37°C for 2 h in the dark. The colorimetric release of p-nitroaniline (pNA) from the Ac-DEVD-pNA substrate was recorded at 405 nm using a microplate reader. Experiments were performed in triplicate. Results are presented as mean±SD of six separate experiments and expressed as fold-increase over pretreat-ment level (untreated samples).

Histopathological AnalysisFor light microscopic investigations, heart and lung specimens

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Table 1. Transthoracic echocardiography measurements in the experimental groups

Parameter Control group Burn group

Saline-treated Saline-treated Captopril-treated

Interventricular septal thickness (mm) 2.36±0.18 3.01±0.11** 2.45±0.08+

Left ventricular posterior wall thickness (mm) 1.73±0.12 2.55±0.11* 1.77±0.11+

Relative wall thickness 0.66±0.03 0.98±0.10* 0.71±0.08+

Left ventricular diameter in systole (mm) 2.63±0.27 3.96±0.15** 2.98±0.21+

Left ventricular diameter in diastole (mm) 4.09±0.16 5.18±0.14** 4.32±0.24+

Ejection fraction (%) 79.03±3.67 63.60±2.73* 77.78±3.44+

Fractional shortening (%) 42.27±3.54 26.61±2.24** 39.71±3.21+

Heart/body weight ratio (mg/g) 2.21±0.12 2.73±0.08** 2.29±0.09+

Data are the mean±SEM of six animals. *p<0.05, **p<0.01 compared to saline-treated control group; +p<0.05 compared with the saline-treated burn group.

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were fixed in 10% buffered formalin for 48 h, dehydrated in an ascending alcohol series, and embedded in paraffin wax. Approximately 5-μm-thick sections were stained with H&E for general morphology. Histological assessments were made with a photomicroscope (Olympus BX 51; Tokyo) by an ex-perienced histologist who was unaware of the experimental groups.

StatisticsStatistical analysis was carried out using GraphPad Prism 3.0 (GraphPad Software; San Diego, CA, USA). All data were expressed as means±SEM. Groups of data were compared with an analysis of variance (ANOVA) followed by Tukey’s multiple comparison tests. Values of p<0.05 were regarded as significant.

RESULTS

Table 1 summarizes the transthoracic echocardiography mea-surements of the experimental groups. In the saline-treated burn group, LVPW, LV end-diastolic and end-systolic dimen-sions and RWT, and heart/body weight ratio were increased significantly compared to the control group (p<0.05-0.01), while percent FS and EF were decreased significantly. On

the other hand, in the captopril-treated burn group, echo-cardiographic measurements were significantly different than those of the saline-treated burn group (p<0.05), but similar to those of the control group.

TNF-α levels in the heart and lung tissues of the saline-treat-ed burn group were significantly increased, while TNF-α lev-els were found to be decreased in the captopril- treated burn group (p<0.001; Figs. 1a, b).

Burn injury caused significant decreases in the GSH lev-els of the heart and lung tissues of the saline-treated burn group (p<0.01-0.001), but this antioxidant was restored in the captopril-treated burn group (p<0.05-0.01; Figs. 2a, b). On the other hand, MDA levels in both tissues were signifi-cantly increased following burn injury (p<0.01-0.001), while treatment with captopril reversed burn-induced elevations in MDA back to the control levels (p<0.05-0.01; Figs. 3a, b). In the saline-treated burn group, MPO activities in both the heart and lung tissues were increased significantly (p<0.001), and treatment with captopril prevented these alterations (p<0.01-0.001; Figs. 4a, b).

Na+, K+-ATPase activities measured in the cardiac and pulmo-

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Figure 1. Tumornecrosisfactor-α(TNF-α)levelsinthe(a)heartand (b)lungtissuesofcontrol(C)andsaline-orcaptopril-treatedburngroups.Eachgroupconsistsof8animals.***:p<0.001:com-paredtosaline-treatedcontrolgroup;+++:p<0.001:comparedtosaline-treatedburngroup.

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Figure 2. Glutathione (GSH) levels in the (a)heartand (b) lungtissuesofcontrol(C)andsaline-orcaptopril-treatedburngroups.Eachgroupconsistsof8animals.**:p<0.01,***:p<0.001:com-paredtosaline-treatedcontrolgroup;+p<0.05,++:p<0.01:com-paredtosaline-treatedburngroup.

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nary tissues were reduced in the saline-treated burn group (p<0.001, Figs. 5a, b). In the captopril-treated burned rats, the measured Na+, K+-ATPase activities in the studied tissues were increased (p<0.05-0.001).

Caspase-3 activities in both the heart and lung tissues were increased significantly (p<0.001), while treatment with capto-pril reduced these increases (p<0.01-0.001; Figs. 6a, b).

Light microscopic evaluation of the cardiac muscle cells in the control group revealed regular nuclei with central alignment (Fig. 7a). In the burn group, the capillaries present in the con-nective tissue of muscle fibers showed congestion in addition to vacuolization in the cytoplasm of most of the cardiomyo-cytes (Fig. 7b). On the other hand, in the captopril-treated burn group, vasocongestion was reduced and regular cellular morphology was settled (Fig. 7c).

In lung tissues, the control group demonstrated a well-designated morphology (Fig. 8a), whereas severe interstitial edema with bronchiolar hemorrhage and stretched alveolar walls were observed in the burn group (Fig. 8b), which was ameliorated by captopril treatment, revealing the reversal of degeneration in the interstitium (Fig. 8c).

DISCUSSION

The aim of the present work was to explore the effect of captopril, a known ACE inhibitor, on the cardiopulmonary inflammatory process associated with burn in rats.

Thermal trauma is a stressful condition challenging whole body homeostatic mechanisms, accompanied by both local and distant effects leading to intense inflammation, tissue damage and infection. As local production of proinflamma-tory cytokines will activate non-specific host immunity, tissue injury or infection, cytokines are approached as being impor-tant components in the postburn pathophysiological process.[21-23] Accordingly, after thermal trauma, a great many cyto-kines are induced rapidly,[12,24-27] and ACE mediates inflam-mation to elicit T cell stimulation. On the other hand, the ACE inhibitor captopril inhibits conclusive immune functions and attenuates inflammation.[28,29] Our data above demon-strate that burn-induced cardiac and lung injury involve oxi-dant formation and inflammation, while captopril treatment greatly attenuated these responses. The ability of captopril to protect against thermal trauma was observed with sig-nificant decreases in tissue MDA and TNF-α levels and MPO and caspase-3 activities, which were found to be increased

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Figure 3. Malondialdehyde(MDA) levels inthe(a)heartand(b) lung tissues of control (C) and saline- or captopril-treated burngroups.Eachgroupconsistsof8animals.**:p<0.01,***:p<0.001:comparedtosaline-treatedcontrolgroup;+:p<0.05:comparedtosaline-treatedburngroup.

Figure 4. Myeloperoxidase(MPO)activityinthe(a)heartand(b) lung tissues of control (C) and saline- or captopril-treated burngroups.Eachgroupconsistsof8animals.***:p<0.001:comparedto saline-treated control group; ++: p<0.01, +++: p<0.001: com-paredtosaline-treatedburngroup.

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following thermal trauma. Furthermore, captopril treatment in the burned rats caused significant increases in both GSH levels and Na+, K+-ATPase activities, which were found to be depleted in the burn group.

TNF-α is a cytokine excreted by macrophages and monocytes in response to different stimuli, and concentrations were found to be high in patients with heart disease, in association with noticeable activation of the RAS. Levine et al.[30-32] found increased concentrations of TNF-α in heart disease patients with high renin concentrations. In addition, they demonstrat-ed that increased serum TNF-α, which plays an essential role in the inflammatory processes, was also decreased with cap-topril treatment. In our study, following burn injury, increased cytokine TNF-α was associated with impaired cardiac function since in the saline treated-burn group, LVPW, LV end-diastolic and end-systolic dimensions and RWT, and IVS thickness were significantly higher as compared to control rats (p<0.05-0.01), while FS and EF were found to be significantly decreased. Youn et al.[33] studied both ACE inhibition and angiotensin receptor antagonism in a rat model of acute infarction in which trans-forming growth factor (TGF) beta-1 mRNA expression was also increased. Their results demonstrated that both captopril and losartan suppressing the acute induction of TGF-beta1

mRNA expressions attenuated LV remodeling. Captopril has been shown to express immune-regulating, antioxidant and anti-inflammatory properties.[34] In agreement with these studies, our results showed that depressing cytokine expres-sion is associated with improved cardiac function.

Major burn injuries can lead to life-threatening end-organ dysfunction including cardiac dysfunction, which is a major contributor to mortality.[35,36] Despite prompt and adequate fluid replacement following burn injury, alterations in cardio-vascular function such as reduced cardiac output, myocar-dial inflammation and an intrinsic defect in myocardial per-formance can cause multiple organ dysfunction syndrome. Numerous experimental studies have been performed to identify the molecular mechanisms involved in burn-related cardiac dysfunction with the end goal of creating novel thera-peutic interventions and agents to reduce the incidence of life-threatening complications.[37,38] In our study, by improving cardiac function, captopril protected cardiac and lung tissues since oxidative injury observed through MDA and GSH lev-els and MPO, Na+, K+-ATPase and caspase activities were re-versed in both tissues. One of the causative agents account-able for the development of burn shock and distant organ damage in animal models of burn injury are oxygen radicals.[27]

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Figure 5. Na+-K+ATPaseactivityinthe(a)heartand(b)lungtis-sues of control (C) and saline- or captopril-treated burn groups.Eachgroupconsistsof8animals.***:p<0.001:comparedtosa-line-treatedcontrolgroup;+:p<0.05,+++:p<0.001:comparedtosaline-treatedburngroup.

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Figure 6. Caspase-3activityinthe(a)heartand(b)lungtissuesof control (C)andsaline-or captopril-treatedburngroups.Eachgroupconsistsof8animals.***:p<0.001:comparedtosaline-treat-edcontrolgroup;++:p<0.01,+++:p<0.001:comparedtosaline-treatedburngroup.

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The distant organs involved in the thermal damage during ex-perimental skin burn are thought to be the lungs, heart, liver, kidney, and gastrointestinal mucosa. In all cases of thermal trauma, neutrophils diffuse these organs, being the potent source of reactive oxygen metabolites.[39] As is known, accu-mulation and activation of neutrophils induce tissue damage and release of different cytotoxic proteins into the extracel-lular fluid. MPO activity, an indirect marker of neutrophil in-filtration,[40] has been shown to be significantly increased in various tissues of burned rats.[12,41] Similarly, in the present study, increased MPO activity in both heart and lung tissues suggests that neutrophil accumulation in these tissues assist in organ injury distant from the original wound. On the oth-er hand, in the captopril- treated burn groups, MPO activi-ties were reduced. The effects of captopril on MPO activity were studied previously in different experimental models of inflammation. Leor et al.[42] studied the effects of captopril experimentally, and proposed that captopril did not decrease neutrophil-induced myocardial injury following coronary oc-clusion and reperfusion. Nonetheless, Van Antwerpen et al.[43] in their in vitro study showed that captopril, by inhibiting the MPO/HOCl system, was able to significantly reduce the oxidative modification of low-density lipoprotein in a dose-dependent manner. Furthermore, Li et al.[44] demonstrated

that pathological injury of the lung in rats with intense acute pancreatitis was decreased with captopril treatment.

Malondialdehyde (MDA), an end product of lipid peroxida-tion, is major evidence of lipid peroxidation, and in this study, its levels were found to be significantly advanced due to burn in both heart and lung tissues. Results from animal and human studies suggested that there is a relationship between tissue MDA levels and the degree of burn complications, including shock and remote organ damage.[25,41,45,46] Our results showed that captopril treatment in the burned rats caused significant reduction in MDA.

Esterified GSH is a significant component of the cellular anti-oxidant system. The GSH molecule acts as an electron accep-tor for hydrogen peroxide by forming an oxidized thiol and then undergoing degradation by glutathione reductase.[47] In a previous study, GSH levels have been reported to be decreased in the lung, liver and kidney of rats after burn.[12,25,26,28,45] In this study, lessening effects of captopril on MDA concurred with preservation of tissue GSH level, which is an important anti-oxidant. Moreover, Gurer et al.,[48] studying GSH, suggested that captopril has a promising beneficial role in augmenting the reducing capacity of the cells by increasing GSH.

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Figure 7. (a)Controlgroup:regularalignmentofmusclecellswithcentrallylocatednuclei(**).(b)Burngroup:capillaryvasocongestionamongtheconnectivetissueofthemusclecells(arrow),vacuolizationinthecytoplasmofthecardiacmusclecellsanddegenerationofsomegap-junctions(arrowhead).(c)Burnandcaptopriltreatment:thecapillaryvasocongestionwasreduced,andvacuolizationinthecytoplasmofthecellswasdecreased(**),H&Estaining,x200,insetsx400.

Figure 8. (a)Controlgroupdemonstratedaregularalveolarstructure(arrow)withnodistentioninitswalls.(b)Burngroup,severecongestion(**)andinterstitialedema,whichledtoadecreaseinalveolarspace(arrow)inmostareasofthetissue.Insomeregions,thealveoliunitedwitheachotherresultinginlargedistendedalveolarspaces(arrowhead-inset).(c) Burnandcaptoprilgroup:reducedinterstitialcongestionandedema(**)andexpandedalveolarareasandnocongestionpresent.

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Apoptosis is an orchestrated form of cell ‘death by suicide’. It is principal in both the development and normal continua-tion of tissue function. Apoptotic nerve cell death is related to the pathogenesis of several devastating neurodegenerative diseases. Recently, apoptosis was found to be important in the pathophysiological changes occurring after major burns. After thermal injuries, nearly every organ or tissue seems affected and manifests this peculiar cellular mechanism char-acterizing a “systemic apoptotic response”.[49] Currently, ROS may mediate apoptosis through the starting of poly (ADP-ribose) polymerase (PARP), advances in mitochondrial per-meability with the release of cytochrome C, and activation of caspases.[50,51] ROS-triggered release of lysosomal ingredients can also lead to apoptosis. Hydrogen peroxide can freely dif-fuse across cell membranes, including the lysosomal mem-brane. Inside the lysosome, hydrogen peroxide can react with iron to form the potent hydroxide radical, at least causing damage to the lysosomal membrane and leakage of contents. The translocation of the protease cathepsin D from the lyso-some to the cytosol yields to the induction of apoptosis.[52] Since captopril has recently been found to inhibit Fas-induced apoptosis in human-activated T cells[53] and lung epithelial cells,[54] we hypothesized that suppression of apoptosis could be one of the mechanisms bringing about the efficacy of ACE inhibitors. In the present study, we examined the apoptosis measuring caspase-3 activity in the heart and lung tissues, and found that thermal trauma increased heart and lung apopto-sis. On the other hand, captopril treatment effectively less-ened caspase-3 activity and protected tissues, as also con-firmed histologically.

Na+, K+-ATPase is a considerable membrane protein that car-ries out the coupled extrusion and uptake of Na+ and K+ ions across the plasma membranes. As the activity of Na+, K+-ATPase, a membrane-bound enzyme required for cellu-lar transport, is very sensitive to free radical reactions and lipid peroxidation, decrease in this activity can show mem-brane damage indirectly. Na+, K+-ATPase activities measured in the cardiac and pulmonary tissues were reduced in the saline-treated rats (p<0.001), indicating damaged transport function in these tissues (Fig. 5a, 5b). In the captopril-treated burned rats, the measured Na+, K+-ATPase activities in the studied tissues were increased compared to those of the con-trol rats (p<0.05-0.001). Ottlecz et al.[55] demonstrated that stimulation of retinal Na+, K+-ATPase activity in diabetes is most likely one of the mechanisms through which captopril can improve retinal complications. Our study has shown that Na+, K+-ATPase activities were significantly reduced in both cardiac and lung tissues of burned rats, while captopril treat-ment significantly protected the enzyme activity.

In conclusion, the findings of the present study demonstrated that captopril treatment protected multiorgan damage in thermal trauma through inhibition of pro-inflammatory and oxidative pathways. Furthermore, captopril treatment pro-vided regular cellular morphology in lung and heart tissues,

which caused a concomitant decrease in lipid peroxidation and increase in tissue antioxidant defense. Therefore, these results suggest an anti-inflammatory, cardiopulmonary pro-tective effect of captopril, with a reduction in the circulating proinflammatory markers and an increase in those antiinflam-matory cytokines; these effects result in a benefit on the cardiopulmonary inflammatory process associated with burn-induced thermal trauma. Thus, captopril treatment merits consideration as a potential therapeutic agent for restoring organ damage following thermal trauma.

Conflict of interest: None declared.

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43. Van Antwerpen P, Legssyer I, Zouaoui Boudjeltia K, Babar S, Moreau P, Moguilevsky N, et al. Captopril inhibits the oxidative modification of apolipoprotein B-100 caused by myeloperoxydase in a comparative in vi-tro assay of angiotensin converting enzyme inhibitors. Eur J Pharmacol 2006;537:31-6.

44. Li SL, Chen X, Zhang XW, Wu T, Ji ZZ. Protective effects of captopril against lung injury in rats with severe acute pancreatitis. [Article in Chi-nese] Nan Fang Yi Ke Da Xue Xue Bao 2010;30:2742-5. [Abstract]

45. Sener G, Kabasakal L, Cetinel S, Contuk G, Gedik N, Yeğen BC. Leukot-riene receptor blocker montelukast protects against burn-induced oxida-tive injury of the skin and remote organs. Burns 2005;31:587-96.

46. Sabry A, Wafa I, El-Din AB, El-Hadidy AM, Hassan M. Early markers of renal injury in predicting outcome in thermal burn patients. Saudi J Kidney Dis Transpl 2009;20:632-8.

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48. Gurer H, Neal R, Yang P, Oztezcan S, Ercal N. Captopril as an antioxi-dant in lead-exposed Fischer 344 rats. Hum Exp Toxicol 1999;18:27-32.

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53. Déas O, Dumont C, Mollereau B, Métivier D, Pasquier C, Bernard-Pom-ier G, et al. Thiol-mediated inhibition of FAS and CD2 apoptotic signal-ing in activated human peripheral T cells. Int Immunol 1997;9:117-25.

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OLGU SUNUMU

Sıçanlarda yanıkla uyarılan kardiyopulmoner hasara karşı kaptoprilin koruyucu etkisiDr. Esra Sağlam,1# Ahmet Özer Şehirli,2 Emine Nur Özdamar,3 Gazi Contuk,4 Şule Çetinel,4

Derya Özsavcı,5 Selami Süleymanoğlu,6 Göksel Şener2

1ÜsküdarÜniversitesi,İstanbulNöropsikiyatriHastanesi,KlinikFarmakogenetikLaboratuvarı,İstanbul2MarmaraÜniversitesiEczacılıkFakültesi,FarmakolojiAnabilimDalı,İstanbul3MarmaraÜniversitesiTıpFakültesi,TıbbiFarmakolojiAnabilimDalı,İstanbul4MarmaraÜniversitesiTıpFakültesi,HistolojiveEmbriyolojiAnabilimDalı,İstanbul5MarmaraÜniversitesiEczacılıkFakültesi,BiokimyaAnabilimDalı,İstanbul6GülhaneAskeriTıpAkademisi,KardiyolojiAnabilimDalı,İstanbul

AMAÇ: Bu çalışma, kalp ve akciğer dokularında yanıkla uyarılan oksidatif hasara karşı kaptopril tedavisinin olası koruyucu etkisini saptamak için tasarlandı.GEREÇ VE YÖNTEM: Eter anestezisi altında sırt derileri traş edilen Wistar albino türü sıçanlar 10 saniye süreyle 90°C suya tutuldu. Yanık hasarın-dan sonra ve 12 saat sonra olmak üzere 10 mg/kg intraperitoneal kaptopril uygulandı. Kontrol grubunda ise sıçanların sırtı 10 saniye süreyle 25°C suya tutuldu. Yanık hasarından 24 saat sonra ekokardiyografik kayıtları alınan sıçanlar dekapite edildi ve kalp ve akciğer doku örnekleri çıkartılarak tümör nekroz faktör-α (TNF-α), malondialdehit ve glutatyon düzeyleri, miyeloperoksidaz, kaspaz-3 ve Na+, K+-ATPaz aktiviteleri tayini ile histolojik analizler yapıldı.BULGULAR: Yanık sol ventrikül fonksiyonlarında önemli değişikliklere neden oldu. Kalp ve akciğer dokularında yanık hasarına bağlı olarak glutatyon düzeyleri ve Na+, K+-ATPaz aktivitelerinin azaldığı ve TNF-α ve malondialdehit düzeyleri ile miyeloperoksidaz ve kaspaz-3 aktivitelerinin arttığı bu-lundu. Kaptopril tedavisinin, azalmış glutatyon düzeyi ve Na+, K+-ATPaz aktivitesini anlamlı düzeyde yükselttiği ve sitokin ve malondialdehit düzeyleri ve miyeloperoksidaz ve kaspaz-3 aktivitelerini ise anlamlı düzeyde azalttığı bulundu.TARTIŞMA: Kaptopril kalp ve akciğer dokularında yanıkla uyarılan hasarı önler ve oksidatif organ hasarına karşı korur.

Anahtar sözcükler: Kaptopril; lipid peroksidasyonu; miyeloperoksidaz; sitokin; yanık.#Şimdiki kurumu: Maltepe Üniversitesi Tıp Fakültesi, Farmakoloji ve Klinik Farmakoloji Anabilim Dalı, İstanbul

Ulus Travma Acil Cerrahi Derg 2014;20(3):151-160 doi: 10.5505/tjtes.2014.96493

DENEYSEL ÇALIŞMA - ÖZET

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The effect of hyperbaric oxygen therapyon fracture healing in nicotinized ratsAbdullah Demirtaş, M.D.,1 İbrahim Azboy, M.D.,1 Mehmet Bulut, M.D.,1

Bekir Yavuz Uçar, M.D.,1 Celil Alemdar, M.D.,1 Ulaş Alabalık, M.D.,2

Veysi Akpolat, M.D.,3 İsmail Yıldız, M.D.,4 Savaş İlgezdi, M.D.5

1DepartmentofOrthopaedicsandTraumatology,DicleUniversityFacultyofMedicine,Diyarbakir2DepartmentofPathology,DicleUniversityFacultyofMedicine,Diyarbakir3DepartmentofBiophysics,DicleUniversityFacultyofMedicine,Diyarbakir4DepartmentofBiostatisticsandMedicalInformatics,DicleUniversityFacultyofMedicine,Diyarbakir5DepartmentofUnderseaandHyperbaricMedicine,AnadoluHyperbaricOxygenCentre,Istanbul

ABSTRACT

BACKGROUND: The aim of the present study was to investigate the effect of hyperbaric oxygen therapy on fracture healing in nicotinized rats.

METHODS: Thirty-two rats were divided as follows: nicotinized group (1), hyperbaric oxygen group (2), nicotinized + hyperbaric oxygen group (3), and control group (4). For 28 days, nicotine was administered in Groups 1 and 3. Then, a standard shaft fracture was induced in the left femur of rats. Groups 2 and 3 underwent hyperbaric oxygen therapy for 21 days. At the end of the experiment, fracture site, left femur and whole body bone mineral content and density were measured.

RESULTS: The radiological and histopathological scores of Group 1 were statistically significantly lower compared to Groups 2, 3 and 4, and there was no statistically significant difference between the Groups 2, 3 and 4. In a comparison between the groups, no statistically significant difference was found in terms of bone mineral content and density values measured at the fracture site, left femur and whole body.

CONCLUSION: The negative effects of nicotine on fracture healing are eliminated with hyperbaric oxygen therapy, but hyperbaric oxygen alone does not cause significant changes in healing (radiologically and histopathologically).

Key words: Fracture healing; hyperbaric oxygen; nicotine.

INTRODUCTION

Fracture healing is a dynamic process governed by cellular and biochemical agents. Despite the investigation of many factors that may affect this process and the achieved progress on this issue, there are still problems in fracture healing.[1]

Common cigarette use in society represents a significant health problem. In the literature, it has been reported in many studies that cigarettes and their major component nicotine delay bone healing because of their negative effects on osteoblasts and tissue oxygenation.[2-7] Hyperbaric oxygen (HBO), on the other hand, increases tolerance to ischemia by increasing tissue oxygenation[8-10] and is used as a meth-od of therapy in diabetic wounds, compartment syndrome, crush injuries, anaerobic infections, and irradiated wounds.[11] In studies carried out recently, it has been stated that HBO treatment has positive effects on osteoblasts in addition to tissue oxygenation and increases bone healing.[12-15]

We postulated that the negative effects of nicotine on frac-ture healing could be eliminated by the positive effects of HBO on bone metabolism. To the best of our knowledge, there are no experimental studies evaluating the effects of nicotine and HBO together in a fracture healing model using

EXPERIMENTAL STUDY

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Address for correspondence: Abdullah Demirtaş, M.D.

Dicle Üniversitesi Tıp Fakültesi, Ortopedi ve Travmatoloji

Anabilim Dalı, Diyarbakır, Turkey

Tel: +90 412 - 248 80 01 E-mail: [email protected]

Qucik Response Code Ulus Travma Acil Cerrahi Derg2014;20(3):161-166doi: 10.5505/tjtes.2014.52323

Copyright 2014TJTES

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Demirtaş et al. The effect of hyperbaric oxygen therapy on fracture healing in nicotinized rats

radiological, histopathological and dual-energy X-ray absorp-tiometry (DXA) findings.

In this study, we investigated the effects of nicotine and HBO together in fracture healing in terms of radiological, histo-pathological and DXA findings.

MATERIALS AND METHODS

In this study, 32 male Sprague-Dawley rats (weight: 230-262 g; age: 3 months) were used. The experiments were conducted after approval was obtained from the Institutional Review Board, and animal care complied with the guidelines of the authors’ institution or any national law on the care and use of laboratory animals (reference number: 2011/62). The included rats were randomly divided into four groups (n=8): nicotin-ized (Group 1), HBO (Group 2), nicotinized+HBO (Group 3), and control (Group 4). The rats were followed for a period of 48 hours in the lab and kept at 22°C during the study, with a 12-hour light and dark rhythm. For the feeding of rats, unlim-ited tap water and standard rodent feed were used.

Prior to the surgical procedure, for 28 days, in Groups 1 and 3, nicotine (Sigma CAS No. 22083-74-5) (2 mg/kg, twice a day subcutaneously)[16,17] and in Groups 2 and 4, saline solution (1 ml, twice a day subcutaneously) were administered.

After the surgical procedure, for 21 days, HBO (2.5 atmo-spheric pressure 100% oxygen as a single session, 2 hours/day) was applied in Groups 2 and 3 starting immediately af-ter the surgery[2,14] (Fig. 1), whereas Groups 1 and 4 did not receive any therapy. At the end of the 21st day, in all rats, the Kirschner wire was reached via an anterolateral incision between the femoral condyles in the left knee, under anes-thesia. The Kirschner wires were removed retrogradely (in order to avoid affecting DXA measurements). After the DXA measurements, all rats were sacrificed by cervical dislocation. The left femurs of rats were disarticulated at the hip and knee joints, and the callus tissue was dissected, without damaging the soft tissues, to perform the radiological and histopatho-logical evaluations. One rat in Group 1 was excluded due to infection at the fracture site.

Surgical ProcedurePreoperatively, anesthetic ketamine (Ketalar®, Pfizer, Istan-bul, Turkey) 50 mg/kg and xylazine (Rompun®, Bayer, Istanbul, Turkey) 10 mg/kg combination was administered subcutane-ously. The open osteotomy method used by Doyon et al.[18] in their studies was applied with modification in the surgical technique. Accordingly, the left knee and femurs of the rats were shaved. The local field was cleaned with a solution of povidone iodine (Batticon®, ADEKA, Istanbul, Turkey). Un-der sterile conditions, a 2-2.5 cm incision was made start-ing anterolateral of the left knee, extending to the lateral femur distally. Proximally, the joint was reached via the lat-eral parapatellar approach. The femoral condyles were ex-

posed by dislocating the patella medially. The distal femur was reached with blunt dissection along the vastus lateralis and hamstring muscles. The standard fracture was induced with a Gigli wire, at the middle 1/3 of the femur shaft. Kirschner wire (Hippocrates®, Izmir, Turkey) of 1 mm diameter was placed retrogradely in the intramedullary canal, towards the greater trochanter from the distal femoral condyles. After the fixation of the fracture, the patella was reduced and sta-bilized with absorbable sutures. Following the closure of the skin with non-absorbable sutures, the wound was cleaned with povidone iodine.

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Table 1. The histopathological scoring for the evaluation of fracture healing

Score Histopathological findings

1 Fibrous tissue

2 Predominantly fibrous tissue with little cartilage tissue

3 Equal amounts of fibrous and cartilage tissue

4 Only cartilage tissue

5 Predominantly cartilage tissue with little immature

(woven) bone

6 Equal amounts of cartilage and immature bone tissue

7 Predominantly immature bone with little cartilage

tissue

8 Healing with immature (woven) bone

9 Immature bone with little mature bone

10 Healing with mature (lamellar) bone

Figure 1. TheimagesoftheratsduringHBOapplication.

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Demirtaş et al. The effect of hyperbaric oxygen therapy on fracture healing in nicotinized rats

Radiological EvaluationFor the radiological evaluation, anteroposterior and lateral radiographs of the left femurs of the rats were taken. The healing was evaluated by an independent orthopedic surgeon, using the radiological scoring system described by Lane et al.,[19] over 4 points (0=no healing, 1=callus formation, 2=on-set of bony union, 3=beginning of disappearance of fracture line, 4=complete bony union). In bilateral group comparisons, a decrease in the score was assigned as a negative effect on fracture healing, whereas an increase was evaluated as a posi-tive effect.

Histopathological EvaluationFor the histopathological assessment, all femurs were fixed in 10% buffered formalin solution for a period of two weeks, and then in Bouin’s solution for two days. After the fixation, the femurs were decalcified in 10% acetic acid, 0.85% NaCl and 10% formalin solutions. The samples were then embed-ded in paraffin blocks and after the 3-4 micron thick sections were taken, they were stained with hematoxylin and eosin. For the evaluation of fracture healing, the histopathological improvement scale, as defined by Huo et al.,[20] in which scor-ing is done over 10 points, was used (Table 1). The slides were evaluated by the same pathologist to ensure standardization. In bilateral group comparisons, a decrease in the score was assigned as a negative effect on fracture healing, whereas an increase was evaluated as a positive effect.

DXA AssessmentThe left femur fracture site (the fracture center plus an area of 0.3 cm proximally and distally), whole left femur and whole body bone mineral density (BMD) and bone mineral content (BMC) measurements of the rats were done using DXA (Ho-logic, Discovery QDR 4500A, WA, USA). Before each pro-cedure, calibration of the instrument was done in accordance with the manufacturer’s standard “small step phantom”, in-cluding the two measurements and the recordings before and after the application of the “small animal” mode. The measurements were assessed by the same person to ensure standardization.

Statistical EvaluationAll the data were recorded and analyzed using the SPSS (Statistical Package for the Social Sciences) 18.0. The Kol-mogorov-Smirnov and Shapiro-Wilk tests were performed to determine if the data were normally distributed. Nonpara-metric tests were performed for the parameters without a normal distribution. The Kruskal-Wallis test was used for comparison between the groups. The Mann-Whitney U test was used for comparison between two groups in radiologi-cal, histopathological and DXA evaluations. The data were summarized as median (minimum-maximum). A p value <0.05 was considered statistically significant.

RESULTS

Radiological FindingsThe radiological scores for all groups are given in Table 2. The radiological score of Group 1 was significantly lower as com-pared to Groups 2, 3 and 4 (p=0.009, p=0.027, p=0.016, re-spectively). There was no statistically significant difference be-

Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3 163

Figure 2. Theanteroposterior[(a)Group1;(b)Group2;(c)Group3;(d)Group4]andthelateral[(e)Group1;(f)Group2;(g)Group3;(h)Group4]X-rayimagesofthesamplesofthegroupsattheendoftheexperiment.

(a)

(e)

(b)

(f)

(c)

(g)

(d)

(h)

Figure 3. Thehistopathologicalimagesofthesamplesofthegro-upsattheendoftheexperiment:(a)InaratinGroup1,afieldcon-tainingasmallamountofcartilage,withmostlyfibroustissue[he-matoxylin&eosin(H&E,100x)];(b)InaratinGroup2,afieldfullofimmaturebonetissue(H&E,100x);(c)InaratinGroup3,afieldcontainingmostlycartilageandasmallamountofimmaturebonetissue(H&E,100x);and(d)InaratinGroup4,afieldcontainingequalamountsofcartilageandimmaturebonetissue(H&E,100x).

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Demirtaş et al. The effect of hyperbaric oxygen therapy on fracture healing in nicotinized rats

tween Groups 2, 3 and 4 in terms of radiological scores (p>0.05) (Fig. 2).

Histopathological FindingsThe histopathological scores of all tissue samples taken from all groups at the end of the 21st day are given in Table 2. The histopathologi-cal score of Group 1 was statistically significantly lower compared to Groups 2, 3 and 4 (p=0.005, p=0.005, p=0.006, respectively). There was no statistically significant difference between Groups 2, 3 and 4 in terms of histopathological scores (p>0.05) (Fig. 3).

DXA FindingsTable 2 shows the fracture site, whole left femur and whole body BMC and BMD values measured in all groups, before the experiment was ter-minated, at the end of the 21st day. There was no statistically significant difference between groups in terms of BMC and BMD values (p>0.05).

DISCUSSION

Many factors having an effect on fracture healing have been analyzed, and nicotine is among the most well known. In many studies in the lit-erature, nicotine has been reported to reduce BMD and to delay healing due to its negative effects on bone metabolism.[2-7,21,22]

Nicotine delays fracture healing through different mechanisms of action. In a rabbit model of mandibular lengthening, Zheng et al.[3] studied the effects of nicotine on bone healing, and reported that nicotine reduces bone formation by their inhibitory effect on osteoblasts. In the same study, they also demonstrated that nicotine reduces blood flow due to the lack of compensation for vasoconstriction in the distraction re-generate and decreases bone formation due to the decreased oxygen tension. Theiss et al.[4] reported that nicotine reduces the expression of genes related to cytokines, which affect osteoblast differentiation and neoangiogenesis. Chen et al.[21] reported that nicotine delays fracture healing by inhibiting the secretion of tumor necrosis factor (TNF)-α through the activation of the cholinergic anti-inflammatory pathway.

In our study, a fixed dose of subcutaneous nicotine was given for the nicotinization of the rats. The exposure of the rats to nicotine was end-ed preoperatively because we believe that patients subject to a fracture would stop smoking for at least the duration of healing. However, we believe that the negative effects of smoking would not disappear imme-diately after cessation of smoking. In our study, a significant negative ef-fect on fracture healing was observed in the nicotinized compared with the control group, in terms of the radiological and histopathological findings (p=0.016, p=0.006, respectively). This demonstrates that the negative effects of nicotine continue despite the preoperative cessation of nicotine administration.

The HBO therapy is a method of 100% oxygen inhalation, in a closed pressure chamber, at high pressure of more than 1 atmosphere. In many studies, HBO therapy has been reported to have positive effects on bone healing.[12-15] Wu[12] and Hsieh et al.,[13] in their studies investigating the effectiveness of HBO on human osteoblasts in vitro, reported that HBO increases the proliferation and differentiation of osteoblasts. Muhonen et al.[15] reported in a mandibular distraction osteogenesis model they created in rabbits, that preoperative HBO application increases the cor-

Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3164

Tabl

e 2.

Bo

ne m

iner

al c

onte

nt, b

one

min

eral

den

sity

val

ues,

rad

iolo

gica

l and

his

topa

thol

ogic

al s

core

s of

the

gro

ups

Gro

up 1

Gro

up 2

Gro

up 3

Gro

up 4

p

p p

p p

p

med

ian

(min

-max

) m

edia

n (m

in-m

ax)

med

ian

(min

-max

) m

edia

n (m

in-m

ax)

Gro

up 1

-2

Gro

up 1

-3

Gro

up 1

-4

Gro

up 2

-3

Gro

up 2

-4

Gro

up 3

-4

BMD

R1

(g/c

m2 )

0.

128

(0.1

21-0

.164

) 0.

119

(0.1

07-0

.282

) 0.

126

(0.1

10-0

.215

) 0.

129

(0.1

11-0

.325

) 0.

165

0.48

7 0.

728

0.40

0 0.

268

0.67

4

BMC

R1

(g)

0.25

0 (0

.240

-0.3

70)

0.32

0 (0

.220

-0.7

40)

0.33

5 (0

.210

-0.9

90)

0.32

5 (0

.280

-0.7

20)

0.44

6 0.

222

0.20

0 0.

635

0.83

2 0.

674

BMD

R2

(g/c

m2 )

0.

134

(0.1

29-0

.121

) 0.

129

(0.1

09-0

.296

) 0.

131

(0.1

17-0

.272

) 0.

135

(0.1

16-0

.348

) 0.

203

0.26

9 0.

954

0.56

3 0.

372

0.60

0

BMC

R2

(g)

0.21

0 (0

.170

-0.2

60)

0.23

0 (0

.130

-0.6

10)

0.23

5 (0

.200

-0.5

80)

0.25

5 (0

.200

-0.5

00)

0.86

2 0.

221

0.11

5 0.

562

0.49

3 0.

915

BMD

tot

al (

g/cm

2 )

0.17

0 (0

.160

-0.1

80)

0.16

8 (0

.160

-0.1

90)

0.16

9 (0

.160

-0.1

80)

0.16

8 (0

.160

-0.1

80)

0.32

3 0.

238

0.16

3 0.

874

0.71

2 0.

748

BMC

tot

al (

g)

13.8

0 (1

3.58

-14.

60)

13.2

3 (1

1.73

-14.

89)

13.2

2 (1

2.20

-14.

11)

13.4

7 (1

1.84

-14.

79)

0.13

2 0.

355

0.10

5 0.

916

0.83

4 1.

000

Rad

iolo

gica

l sco

re

1 (1

-3)

3 (2

-3)

2.5

(2-3

) 3

(2-3

) 0.

009

0.02

7 0.

016

0.31

7 0.

602

0.62

6

Hist

opat

holo

gica

l sco

re

4 (2

-7)

7.5

(6-8

) 7

(5-8

) 7

(6-8

) 0.

005

0.00

5 0.

006

0.82

1 0.

736

0.86

5

Gro

up 1

: Nic

otin

e gr

oup;

Gro

up 2

: HBO

gro

up; G

roup

3: N

icot

ine+

HBO

gro

up; G

roup

4: C

ontr

ol g

roup

; BM

D R

1: B

one

min

eral

den

sity

of t

he t

otal

left

fem

ur; B

MC

R1:

Bon

e m

iner

al c

onte

nt o

f the

tot

al le

ft fe

mur

; BM

D R

2: B

one

min

eral

den

sity

of t

he le

ft fe

mur

frac

ture

site

; BM

C R

2: B

one

min

eral

con

tent

of t

he le

ft fe

mur

frac

ture

site

; BM

D t

otal

: Who

le b

ody

bone

min

eral

den

sity

; BM

C t

otal

: Who

le b

ody

bone

min

eral

con

tent

.

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Demirtaş et al. The effect of hyperbaric oxygen therapy on fracture healing in nicotinized rats

rupted osteoblastic activity in bones that previously received radiation, but it could not be taken to the level of the control group not receiving radiation. In the same study, it was stated that HBO has apparent effects on neovascularization.

In the literature, there are studies conducted with different agents, which eliminate the negative effects of nicotine on wound healing.[23] As far as we know, only two studies have been conducted on the effectiveness of HBO to resolve the negative effects of nicotine on bone healing. In a model of tibial lengthening in rabbits, using BMD measurements and biomechanical testing, Ueng et al.[2] reported that inhalation of cigarettes delays bone healing, and HBO therapy acceler-ates the healing by reducing the effect of the cigarettes. In their study in rabbits, Yen et al.[24] reported that by inhalation of cigarettes, bone healing was delayed as a result of impaired function of the tibial vascular endothelial cells and decreased blood flow. The same study also emphasized that HBO re-duces the deleterious effects of smoking.

In our study, there was a statistically significant difference in ra-diological and histopathological scores in the nicotinized+HBO group compared to the nicotinized group, whereas no sta-tistically significant difference was found between the HBO, nicotinized+HBO and control groups (Table 2). This suggested that the negative effects of nicotine on fracture healing are eliminated with HBO therapy, but HBO alone did not cause significant changes in healing radiologically or histopathologi-cally. This condition may have been caused by the fact that HBO can manifest its positive effects on fracture healing more apparently in the presence of the negative effects of nicotine (probably due to the interaction of reverse mechanisms), while its positive effects are not sufficiently manifested in the absence of nicotine (probably due to the other more effective factors on the process). In some studies in the literature, it has been shown that positive effects of HBO treatment on bone metabolism occur in longer terms than the length of our follow-up. Kürklü et al.[25] reported in a nonunion model they created in rabbit tibia that applying HBO therapy 2 hours per day over a 20-day period under 2.5 atmospheric pressure did not affect healing on the 30th day radiologically or scintigraphi-cally, while healing increased to a significant level on the 90th day. Chen et al.[26] reported in a lumbar intertransverse fusion model in rabbits that application of HBO therapy 2 hours per day under 2.5 atmospheric pressure had accelerated healing significantly in the 4th and 8th weeks in terms of radiologic, manual assessment and torsional overload findings. Eralp et al.[27] reported in a bone defect model they created in rat tibia that 6-week HBO application increased the healing significant-ly radiologically and histologically. In light of the literature, in a longer-term follow-up model of femur fracture, we think that HBO can have an effect on fracture healing.

In our study, in the comparison of groups, no statistically significant difference was found in terms of the BMC and BMD values measured in the left femur fracture site, total

left femur and whole body (p>0.05). Although these findings support the radiological and histopathological aspects in the HBO, nicotinized+HBO and the control groups, they do not support the findings in the nicotinized group. This condition may be due to the fact that DXA findings related to nicotine are revealed later than radiologic and histopathological find-ings in bone healing. Different results have been reported in studies in the literature concerning the timing of DXA find-ings related to nicotine. Ueng et al.[2] reported that nicotine begins to change BMD values after 3 weeks and reduces pro-gressively in the 4th, 5th and 6th weeks in proportion to ap-plication time. Fung et al.[28] reported that a 2-month period of nicotine application does not change BMC and BMD val-ues. Gao et al.[29] reported that 2- or 3- month periods of nic-otine application did not change BMD values, but a 4-month period of application reduced BMD values. The controversial results were likely due to the variable dosages and methods of nicotine administration and the different healing models used to study the influence of nicotine.[3] We think that, in the case of a longer follow-up, there would be a significant correlation between the DXA findings and the radiological and histopathological findings in all groups.

The limitations of our study are the short follow-up and the lack of different dosages and durations of the nicotinization procedure and HBO therapy. New studies evaluating the as-sociation between different types of nicotinization proce-dures and HBO therapy might be performed.

In conclusion, in the short-term follow-up, the negative ef-fects of nicotine on fracture healing were relieved with HBO therapy; however, HBO alone did not cause significant chang-es in healing, radiologically or histopathologically. We suggest that patients who undergo surgery for fracture should cease smoking and receive HBO therapy.

Conflict of interest: None declared.

REFERENCES1. Buckwalter JA, Einhorn TA, Marsh JL. Bone and joint healing. In: Rock-

wood CA, Green DP, Bucholz RW, Heckman JD, editors. Rockwood and Green’s Fractures in Adults. Vol 1. 5th ed. Philadelphia: Lippincott Wil-liams and Wilkins; 2001. p. 245-71.

2. Ueng SW, Lee SS, Lin SS, Wang CR, Liu SJ, Tai CL, et al. Hyperbaric oxygen therapy mitigates the adverse effect of cigarette smoking on the bone healing of tibial lengthening: an experimental study on rabbits. J Trauma 1999;47:752-9.

3. Zheng LW, Ma L, Cheung LK. Changes in blood perfusion and bone healing induced by nicotine during distraction osteogenesis. Bone 2008;43:355-61.

4. Theiss SM, Boden SD, Hair G, Titus L, Morone MA, Ugbo J. The effect of nicotine on gene expression during spine fusion. Spine (Phila Pa 1976) 2000;25:2588-94.

5. Walker LM, Preston MR, Magnay JL, Thomas PB, El Haj AJ. Nico-tinic regulation of c-fos and osteopontin expression in human-derived osteoblast-like cells and human trabecular bone organ culture. Bone 2001;28:603-8.

6. Yuhara S, Kasagi S, Inoue A, Otsuka E, Hirose S, Hagiwara H. Effects of

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nicotine on cultured cells suggest that it can influence the formation and resorption of bone. Eur J Pharmacol 1999;383:387-93.

7. Kucukdeveci O, Sarisozen B, Atici T, Ozcan R. The effect of nicotine on distraction osteogenesis: an experimental study on rabbits. J Trauma 2009;67:1376-83.

8. Zhang Q, Chang Q, Cox RA, Gong X, Gould LJ. Hyperbaric oxygen attenuates apoptosis and decreases inflammation in an ischemic wound model. J Invest Dermatol 2008;128:2102-12.

9. Richards L, Lineaweaver WC, Stile F, Zhang J, Zhang F. Effect of hy-perbaric oxygen therapy on the tubed pedicle flap survival in a rat model. Ann Plast Surg 2003;50:51-6.

10. Hong JP, Kwon H, Chung YK, Jung SH. The effect of hyperbaric oxygen on ischemia-reperfusion injury: an experimental study in a rat musculo-cutaneous flap. Ann Plast Surg 2003;51:478-87.

11. Gill AL, Bell CN. Hyperbaric oxygen: its uses, mechanisms of action and outcomes. QJM 2004;97:385-95.

12. Wu D, Malda J, Crawford R, Xiao Y. Effects of hyperbaric oxygen on proliferation and differentiation of osteoblasts from human alveolar bone. Connect Tissue Res 2007;48:206-13.

13. Hsieh CP, Chiou YL, Lin CY. Hyperbaric oxygen-stimulated prolifera-tion and growth of osteoblasts may be mediated through the FGF-2/MEK/ERK 1/2/NF-κB and PKC/JNK pathways. Connect Tissue Res 2010;51:497-509.

14. Ueng SW, Lee SS, Lin SS, Wang CR, Liu SJ, Yang HF, et al. Bone heal-ing of tibial lengthening is enhanced by hyperbaric oxygen therapy: a study of bone mineral density and torsional strength on rabbits. J Trauma 1998;44:676-81.

15. Muhonen A, Haaparanta M, Grönroos T, Bergman J, Knuuti J, Hinkka S, et al. Osteoblastic activity and neoangiogenesis in distracted bone of irradiated rabbit mandible with or without hyperbaric oxygen treatment. Int J Oral Maxillofac Surg 2004;33:173-8.

16. Eskitascioglu T, Gunay GK. The effects of topical prostacyclin and pros-taglandin E1 on flap survival after nicotine application in rats. Ann Plast Surg 2005;55:202-6.

17. Selçuk CT, Kuvat SV, Bozkurt M, Yaşar Z, Gülsün N, Ilgezdi S, et al. The effect of hyperbaric oxygen therapy on the survival of random pat-tern skin flaps in nicotine-treated rats. J Plast Reconstr Aesthet Surg

2012;65:489-93. 18. Doyon AR, Ferries IK, Li J. Glucocorticoid attenuates the anabolic effects of

parathyroid hormone on fracture repair. Calcif Tissue Int 2010;87:68-76.19. Lane JM, Sandhu HS. Current approaches to experimental bone graft-

ing. Orthop Clin North Am 1987;18:213-25.20. Huo MH, Troiano NW, Pelker RR, Gundberg CM, Friedlaender GE.

The influence of ibuprofen on fracture repair: biomechanical, biochemi-cal, histologic, and histomorphometric parameters in rats. J Orthop Res 1991;9:383-90.

21. Chen Y, Guo Q, Pan X, Qin L, Zhang P. Smoking and impaired bone healing: will activation of cholinergic anti-inflammatory pathway be the bridge? Int Orthop 2011;35:1267-70.

22. Kyrö A, Usenius JP, Aarnio M, Kunnamo I, Avikainen V. Are smokers a risk group for delayed healing of tibial shaft fractures? Ann Chir Gynae-col 1993;82:254-62.

23. Baykan H, Günay GK, Ozyazgan I, Soyuer I. The effect of angiotensin (1-7) on survival of random pattern skin flaps with nicotine-induced isch-emia in rats. Ann Plast Surg 2012;68:88-93.

24. Yen CY, Tu YK, Ma CH, Yeh JH, Kao FC, Yu SW, et al. Measurement of tibial endothelial cell function after cigarette smoking, cessation of smok-ing and hyperbaric oxygen therapy. Injury 2008;39 Suppl 4:40-6.

25. Kürklü M, Yurttaş Y, Köse O, Demiralp B, Yüksel HY, Kömürcü M. Adjunctive hyperbaric oxygen therapy in the treatment of atrophic tibial nonunion with Ilizarov external fixator: a radiographic and scintigraphic study in rabbits. Acta Orthop Traumatol Turc 2012;46:126-31.

26. Chen WJ, Lai PL, Chang CH, Lee MS, Chen CH, Tai CL. The effect of hyperbaric oxygen therapy on spinal fusion: using the model of postero-lateral intertransverse fusion in rabbits. J Trauma 2002;52:333-8.

27. Eralp L, Kocaoğlu M, Ozkan K, Türker M. A comparison of two os-teotomy techniques for tibial lengthening. Arch Orthop Trauma Surg 2004;124:298-300.

28. Fung YK, Mendlik MG, Haven MC, Akhter MP, Kimmel DB. Short-term effects of nicotine on bone and calciotropic hormones in adult fe-male rats. Pharmacol Toxicol 1998;82:243-9.

29. Gao SG, Li KH, Xu M, Jiang W, Shen H, Luo W, et al. Bone turnover in passive smoking female rat: relationships to change in bone mineral density. BMC Musculoskelet Disord 2011;12:131.

Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3166

OLGU SUNUMU

Nikotinize sıçanlarda hiperbarik oksijen tedavisinin kırık iyileşmesi üzerine etkisiDr. Abdullah Demirtaş,1 Dr. İbrahim Azboy,1 Dr. Mehmet Bulut,1 Dr. Bekir Yavuz Uçar,1

Dr. Celil Alemdar,1 Dr. Ulaş Alabalık,2 Dr. Veysi Akpolat,3 Dr. İsmail Yıldız,4 Dr. Savaş İlgezdi5

1DicleÜniversitesiTıpFakültesi,OrtopediveTravmatolojiAnabilimDalı,Diyarbakır2DicleÜniversitesiTıpFakültesi,PatolojiAnabilimDalı,Diyarbakır3DicleÜniversitesiTıpFakültesi,BiyofizikAnabilimDalı,Diyarbakır4DicleÜniversitesiTıpFakültesi,TıbbiBiyoistatistikAnabilimDalı,Diyarbakır5AnadoluHiberbarikOksijenMerkezi,SualtıHekimliğiveHiperbarikTıpAnabilimDalı,İstanbul

AMAÇ: Bu çalışmanın amacı, nikotinize sıçanlarda hiperbarik oksijen tedavisinin kırık iyileşmesi üzerine etkisini incelemektir.GEREÇ VE YÖNTEM: Otuz iki adet sıçan dört gruba ayrıldı: nikotinize grup (1), hiperbarik oksijen grubu (2), nikotinize + hiperbarik oksijen grubu (3) ve kontrol grubu (4). Yirmi sekiz gün boyunca grup 1 ve grup 3’e nikotin uygulandı. Daha sonra, sıçanların sol femurlarında standart cisim kırığı oluşturuldu. Yirmi bir gün boyunca grup 2 ve grup 3’e hiperbarik oksijen tedavisi uygulandı. Deneyin sonunda kırık alanı, sol femur ve tüm vücut kemik mineral içeriği ve dansitesi ölçüldü.BULGULAR: Radyolojik ve histopatolojik skorlar grup 1’de, grup 2, 3 ve 4’e göre anlamlı düzeyde düşük bulundu. Grup 2, 3 ve 4 arasında radyolojik ve histopatolojik skorlar açısından istatistiksel olarak anlamlı fark saptanmadı. Gruplar arası karşılaştırmada kırık alanı, total sol femur ve tüm vücutta ölçülen kemik mineral içeriği ve dansitesi değerleri bakımından istatistiksel olarak anlamlı fark bulunmadı.TARTIŞMA: Nikotinin kırık iyileşmesi üzerindeki olumsuz etkileri hiperbarik oksijen tedavisi ile giderilmekte, ancak hiperbarik oksijen tek başına iyileşme üzerinde anlamlı değişikliğe sebep olmamaktadır (radyolojik ve histopatolojik olarak).

Anahtar sözcükler: Hiperbarik oksijen; kırık iyileşmesi; nikotin.

Ulus Travma Acil Cerrahi Derg 2014;20(3):161-166 doi: 10.5505/tjtes.2014.52323

DENEYSEL ÇALIŞMA - ÖZET

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Effectiveness of hyperbaric oxygen and ozoneapplications in tissue healing in generated soft tissuetrauma model in rats: an experimental studyAli Osman Yıldırım, M.D.,1 Mehmet Eryılmaz, M.D.,2 Ümit Kaldırım, M.D.,2

Yusuf Emrah Eyi, M.D.,3 Salim Kemal Tuncer, M.D.,2 Murat Eroğlu, M.D.,1

Murat Durusu, M.D.,2 Turgut Topal, M.D.,4 Bülent Kurt, M.D.,5

Serkan Dilmen, M.D.,6 Serkan Bilgiç, M.D.,7 Muhittin Serdar, M.D.8

1DepartmentofEmergencyMedicine,GMMA,HaydarpasaMilitaryHosital,Istanbul2DepartmentofEmergencyMedicine,GMMASchoolofMedicine,Ankara3DepartmentofEmergencyMedicine,HakkariMilitaryHospital,Hakkari4DepartmentofPhysiology,GMMASchoolofMedicine,Ankara5DepartmentofPathology,GMMASchoolofMedicine,Ankara6DepartmentofEmergencyMedicine,ElazigMilitaryHospital,Elazig7DepartmentofOrthopaedicsandTraumatology,GMMA,HaydarpasaMilitaryHosital,Istanbul8DepartmentofBiochemistry,GmmaSchoolofMedicine,Ankara

ABSTRACT

BACKGROUND: Soft tissue trauma is a type of acute traumatic ischemia. We investigated in this study whether the edema, inflam-mation and ischemia caused by the trauma could be affected positively by hyperbaric oxygen (HBO) and ozone therapy.

METHODS: Soft tissue trauma was generated in a total of 63 adult male Sprague-Dawley rats. Subsequently, rats were divided into three groups. The first group was treated with ozone, the second group with HBO, and the third group served as controls. Tissue and blood samples were taken at the end of the procedures. Tissue lipid peroxidation (LPO), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), inducible nitric oxide synthase (iNOS), heme oxygenase (HO)-1, and hypoxia-inducible factor (HIF)-1 levels were detected. Hematoxylin-eosin staining was used to determine the inflammation and edema histopathologically.

RESULTS: We also detected HIF-1 activity, which decreases when the oxygen concentration increases, HO-1 activity, which has anti-inflammatory effects, and iNOS activity, which releases in any type of acute case. We determined a statistically significant reduction in iNOS and LPO levels in both the HBO and Ozone groups. A significant decrease in inflammation was detected in both the Ozone and HBO groups compared with the Control group, and a significant decrease in edema was detected in all three groups.

CONCLUSION: We think that HBO and Ozone therapy have beneficial effects on biochemical and histopathological findings. Re-lated clinical trials will be helpful in clarifying the effects.

Key words: Experimental; hyperbaric oxygen; ozone; soft tissue trauma.

INTRODUCTION

Soft tissue trauma (STT) is commonly encountered in emer-gency departments. STT defines lesions of the musculoskel-etal system tissues other than bone. Lesions of these tissues represent the most commonly seen group of all sports inju-ries.[1]

Crush injuries or acute soft tissue injuries are an important health problem that can threaten the viability and function of

EXPERIMENTAL STUDY

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Address for correspondence: Ali Osman Yıldırım, M.D.

GATA Haydarpaşa Hastanesi, Acil Tıp Anabilim Dalı, İstanbul, Turkey

Tel: +90 216 - 542 20 20 E-mail: [email protected]

Qucik Response Code Ulus Travma Acil Cerrahi Derg2014;20(3):167-175doi: 10.5505/tjtes.2014.09465

Copyright 2014TJTES

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Yıldırım et al. Effectiveness of hyperbaric oxygen and ozone applications in tissue healing in generated soft tissue trauma model in rats

the tissues.[2] Crush injuries may also be defined as a kind of acute traumatic ischemia. The cause of ischemia is cutting or crushing of large vessels and stasis or reduction in microcir-culation secondary to occlusion. As a result, adequate tissue perfusion to provide the metabolic needs of the tissue is not achieved. In the early phase of crush, tissue oxygen require-ment is increased 20-fold or more to provide good wound healing and control of infection. These metabolic needs can-not be provided without increased blood flow. When isch-emia increases, the tissues cannot maintain the intracellular fluid content, because oxygen is required for active transport. Therefore, this process is accompanied by edema and inflam-mation.[3]

Hyperbaric oxygen (HBO) therapy is based on ventilating the patient with 100% oxygen over atmospheric pressure in a pressure-resistant room. HBO improves perfusion by in-creasing the level of free oxygen in the blood. Cell viability, energy production, and the production of collagen, which is important in wound healing, is thereby maintained.[4]

Ozone is a molecule consisting of three oxygen atoms. Ozone therapy is administration of a certain amount of oxygen/ozone mixture into body cavities or the circulatory system. Ozone reduces the amounts of antioxidants in plas-ma by activating them. The hydrogen peroxide that occurs is responsible for the biological and therapeutic effects of ozone. The decrease in the antioxidant level and stimulating effect of hydrogen peroxide generate a shock effect on the body in the ozone contacting process. As a result of this effect, a variety of defense systems, including primarily anti-oxidant enzyme expression, are stimulated. Thus, resistance to the oxidative processes increases. One of the first effects of hydrogen peroxide, which is thought to be one of the molecules responsible for the therapeutic activity of ozone, is slipping the hemoglobin-oxygen dissociation curve to the right and releasing oxygen to the tissues easily by increasing 2,3-diphosphoglycerate levels in red blood.[5] The situation emerging during ozone therapy may be interpreted as in-creased tissue partial oxygen pressure is provided biochemi-cally with ozone.

Patients with STT admit with complaints such as swelling, limitation of movement and pain. There are various ap-proaches to the treatment of these patients, who are diag-nosed after excluding bone and other pathologies based on physical examination and imaging. Support of the foot and ankle with materials such as plaster, splints and bandages, el-evation, cold application, topical non-steroidal inflammation-suppressing drugs, vascular dilators, blood clot-dissolving drugs, and antioxidants are the commonly used treatment methods for soft tissue edema, ischemia and inflammation. Demonstration of the effectiveness of HBO and ozone ther-apy in STT may provide new perspectives on this issue. Thus, the effectiveness of HBO and ozone in STT was investigated in this study.

MATERIALS AND METHODS

The study was approved by the decision of GATA Command Ethics Committee for Animal Experiments on 3 March 2011 (decision 2011/11). Animals were supplied by GATA - Re-search and Development Center - Department of Experi-mental Animals, and were kept in the same laboratory condi-tions during the study. The animals were fed with commercial rat chow and tap water.

In this study, a total of 63 adult male Sprague-Dawley rats weighing 230±20 g were used. The rats were divided into a total of three groups of 21 rats each using ‘simple random sampling’ method. Initially, experimental STT was performed in each group. The ozone procedure was performed in one group (Ozone+STT group), the HBO procedure in another (HBO+STT group), and the third group served as controls (Table 1). On the 1st, 3rd and 7th days, the samples were taken from seven rats randomly in each group, and results were compared at the different time points.

Experimental Acute Soft Tissue Injury Model The animals were anesthetized with a combination of in-traperitoneal (IP) ketamine (20-40 mg/kg) and xylazine (4-8 mg/kg). The subjects were fixed in the prone position, the rear leg was shaved, and the trauma application location was marked with a tissue pen (Fig. 1a). The STT was created using a 0.5 kg weight released for free fall movement from a 45 cm height, in a 3 cm diameter plastic tube, at a 90° angle, on to the left rear leg of the rat (Fig. 1b).

Hyperbaric Oxygen TherapyFor the application of HBO, a specially designed and manufac-tured cylindrical hyperbaric chamber, with a diameter of 40 cm and length 60 cm, maintained at T.S.K. 800 Main Ware-house and Factory Command (Etimesgut, Ankara), was used. The chamber had a chromium, nickel and steel mixture body and had been tested for resistance to 10 ATA pressure. 1.5-2 L/min flow rate of oxygen input into the chamber was pro-vided using tubes containing pure oxygen under high pressure and obtained from GATA - Biomedical Clinical Engineering Center - Medical Gases Department. After the animals in the HBO+STT group were placed in the chamber, HBO therapy was applied for 2 hours/day under 2.5 ATA application pres-

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Table 1. Working groups

Groups Days

1st day 3rd day 7th day

Ozone + STT 7 rats 7 rats 7 rats

HBO + STT 7 rats 7 rats 7 rats

STT (Control) 7 rats 7 rats 7 rats

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sure and with fixed oxygen amount. At the end of the ses-sion, the chamber was returned to environment pressure at a slower rate. This procedure was repeated on days 3 and 7. After HBO therapy, a subgroup of animals (on days 1, 3 and 7) were sacrificed.

Ozone ApplicationAn ozone/oxygen mixture of 0.7 g/kg was administered IP to the rats in the ozone group on days 1, 3 and 7. Ozone is created by an ozone generator (OZONOSAN Photonic 1014, Hans GmbH Nordring & Iffezheim, Germany), in which a spectrometer was placed that allowed the operator to con-trol real-time gas flow rate and ozone concentration. The ozone flow rate was kept constant at 60 mg/ml concentra-tion, 97% oxygen + 3% ozone gas mixture at 3 L/min.

SamplingAfter creating an experimental model of STT, tissue and

blood samples were taken from each subgroup of 7 rats on the 1st, 3rd and 7th days. After anesthesia, required blood samples were taken from the inferior vena cava. Traumatic tissue samples were excised and placed in 10% formalin for histopathological analysis. A portion of traumatic tissue was frozen with liquid nitrogen and stored at -80°C deep freeze for subsequent biochemical assessments (Fig. 1c).

Biochemical AnalysisRoutine biochemistry levels to follow the general condition of the animal, tissue lipid peroxidation (LPO) levels to detect the level of tissue oxidative stress, and tissue superoxide dis-mutase (SOD) and glutathione peroxidase (GSH-Px) enzyme levels to detect antioxidant system functioning were mea-sured. In addition, hypoxia-inducible factor (HIF-1) and heme oxygenase (HO-1) levels were measured to determine the re-covery of hypoxic tissues, and inducible nitric oxide synthase (iNOS) levels were measured to determine wound healing.

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Table 2. Comparison of tissue enzyme levels of all groups according to time points

LPO SOD HO-1α HIF-1 iNOS GSH-PX nmol/g U/mg nmol/g pg/mg IU/mg nmol/min/mg Mean.±SD Mean.±SD Mean.±SD Mean.±SD Mean.±SD Mean.±SD

1st day 69.54±14.5 7.55±3.2 1169.8±251.2 73.34±22.15 38.70±16.6 10.73±2.31

3rd day 53.60±12.6 6.15±2.48 1091.71±243.8 37.92±15.53 31.73±9.15 9.20±3.05

7th day 43.98±20.54 5.37±2.29 838.85±348.44 22.74±8.87 24.42±6.35 9.80±3.50

p 0.028 0.337 0.104 <0.001 0.097 0.639

1st day 52.97±16.13 23.44±9.77 1191±322.90 50.35±17.35 70.39±23.31 27.50±9.94

3rd day 15.29±5.11 18.65±7.40 1105.71±262.7 40.61±13.92 46.73±17.27 6.86±3.05

7th day 17.46±8.92 11.7±1.91 866.71±290.01 28.52±10.51 27.4±9.91 7.11±2.87

P <0.001 0.023 0.128 0.033 0.001 <0.001

1st day 62.54±14.74 18.36±6.53 1067.57±291.92 56.48±32.01 79.25±23.96 12.25±3.19

3rd day 33.61±9.84 10.92±4.36 715.50±178.61 35.15±12.09 43.08±23.21 9.49±2.48

7th day 24.29±7.57 4.05±1.87 969.33±356.1 31.58±10.14 16.38±3.9 4.92±2.25

P <0.001 <0.001 0.109 0.105 <0.001 0.001

Figure 1. (a, b) Proceduresforsofttissuetraumaand(c) tissuesampling.

(a) (b) (c)

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Histopathological EvaluationAfter trauma and administration of HBO and ozone treat-ment for 7 days, edema, inflammation and necrosis in tissue were evaluated and scored by an experienced pathologist. In-jured skeletal muscle and adipose tissue were extracted from the rear thigh. Tissues were fixed in 4% buffered formalde-hyde. Tissues were sampled completely, paraffin blocks were obtained, and 5 micron thickness slides were prepared. Slides were stained with hematoxylin-eosin. Evaluation and scoring were performed by light microscope (Nikon, E600, Tokyo, Japan).

Histological scoring was as follows:1. Edema: absent: 0, mild: 1+, moderate: 2+, intense: 3+2. Inflammation: absent: 0, mild: 1+, moderate: 2+, intense:

3+3. Necrosis: absent: 0, mild: 1+ (a few muscle fibers), moder-

ate: 2+ (between score 1 and 3), intense: 3+ (many muscle fibers)

As shown in Table 4, the minimum score was 0 and maximum score was 9.

Statistical AnalysisThe numbers (%) for defining the discrete data points and median (25%-75%) values for defining continuous data were used. The Kruskal-Wallis test was used in all group compari-sons, and then Mann-Whitney U-test was used to compare the groups in pairs that showed significant results. Chi-square or Fisher’s exact test was used in comparison of the discrete data between the two groups. The simultaneous changes in continuous variables were assessed by Spearman relevant co-efficient. p<0.05 values were considered significant.

RESULTS

Biochemical ResultsIn tissue samples analysis, a significant decrease in LPO levels was observed in the HBO and Ozone groups compared to

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Figure 2. Intenseedemaandinflammationbetweenmusclefibersandafewnecroticmusclefibers(Controlgroup,1stday)(a).Moderateedemaandinflammationinadiposetissue(HBOgroup,1stday)(b).Moderateedemaandinflammationinadiposetissue(Ozonegroup,1stday)(c).Intenseedemaandinflammation(Control,3rdday) (d).Moderateedemaandinflammationinmuscletissue(HBO,3rdday)(e).Mildinflammationinmuscletissue(f).Mildinflammationinmuscletissue(Ozone3rdday)(g).Moderateedemaandinflammationinadiposetissue(Control,7thday)(h).Mildinflammationandedema(HBO,7thday)(I).

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the Control group on days 1, 3 and 7. There was a significant decrease in SOD, GSH-Px and iNOS levels only in the treat-ment groups (Table 2). The values of all parameters in serum samples were measured as significantly lower on the 7th day compared to the 1st day except in SOD/GSH-Px in the HBO group and in SOD/iNOS in the Ozone group (Table 3). The values of LPO, HIF-1, HO-1α, GSH-Px, SOD, and iNOS from

tissue samples are presented in Table 2, and the values of LPO, HIF-1, HO-1α, GSH-Px, SOD, and iNOS from serum samples are presented in Table 3.

With regard to binary comparisons of the parameters be-tween the Control and HBO groups for tissue on the 1st day, SOD, iNOS and GSH-Px levels of the HBO group were sig-

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Table 4. Comparison of edema, necrosis and inflammation in the Control, HBO and Ozone groups according to days 1, 3 and 7

Control HBO Ozone

Days Days Days

1st 3rd 7th p 1st 3rd 7th p 1st 3rd 7th p

Edema

0 0 0 0 <0.001 0 0 0 <0.001 0 7 7 <0.001

(+) 0 0 0 0 0 7 0 0 0

(++) 0 0 7 7 7 0 7 0 0

(+++) 7 7 0 0 0 0 0 0 0

Necrosis

0 0 7 7 <0.001 7 7 7 (*) 7 7 7 (*)

(+) 7 0 0 0 0 0 0 0 0

(++) 0 0 0 0 0 0 0 0 0

(+++) 0 0 0 0 0 0 0 0 0

Inflammation

0 0 0 0 (*) 0 0 0 <0.001 0 0 7 <0.001

(+) 0 0 0 0 0 7 0 7 0

(++) 7 7 7 0 7 0 7 0 0

(+++) 0 0 0 7 0 0 0 0 0

(*) Chi-square test could not be applied.

Table 3. Comparison of serum enzyme level of Control, HBO and Ozone groups according to the 1st and 7th days

LPO SOD HO-1α HIF-1 iNOS GSH-PX nmol/L U/ml ng/ml pg/ml IU/ml nmol/min/ml Mean.±SD Mean.±SD Mean.±SD Mean.±SD Mean.±SD Mean.±SD

Control

1st day 4.99±1.03 0.96±0.40 280.10±69.81 15.73±2.90 3.80±0.91 1.67±0.34

7th day 2.85±0.91 0.24±0.16 201.33±20.64 13.15±3.64 3.32±0.94 0.80±0.28

P 0.001 0.001 0.014 0.168 0.354 <0.001

HBO

1st day 3.07±0.72 1.90±0.38 410.94±97.27 25.14±9.19 4.31±0.62 1.56±0.49

7th day 1.37±0.40 2.66±1.06 268.86±80.24 22.28±3.25 4.02±0.92 1.81±0.28

P <0.001 0.102 0.011 0.453 0.499 0.270

OZONE

1st day 1.66±0.47 1.74±0.63 439.15±58.12 34.65±7.45 2.46±0.68 1.52±0.30

7th day 1.35±0.25 2.70±0.58 143.45±41.94 7.89±3.67 4.79±1.57 1.20±0.71

P 0.175 0.017 <0.001 <0.001 0.004 0.307

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nificantly higher than in the Control group (p<0.001, p=0.001 and p<0.001, respectively). LPO and HIF-1 levels of the HBO group were significantly lower than in the Control group (p=0.023 and p=0.017, respectively). On the 3rd and 7th days, LPO levels in the HBO group were significantly lower than in the Control group (p<0.001 and p<0.001, respectively), and SOD levels of the HBO group were significantly higher than in the Control group (p<0.001 and p=0.027, respectively). Differences in HIF-1, iNOS and GSH-Px levels between the HBO and Control groups were not statistically significant on the 3rd and 7th days. There was no statistically significant dif-ference in HO-1α levels on the 1st, 3rd and 7th days between the Control and HBO groups.

With regard to binary comparisons of the parameters be-tween the Control and Ozone groups for tissue, SOD and iNOS levels were significantly higher in the Ozone group than Control group on the 1st day (p<0.001 and p<0.001, respec-tively). LPO and HO-1α levels were significantly lower in the Ozone group than Control group on the 3rd day (p=0.009 and p=0.023, respectively). LPO and GSH-Px levels were sig-nificantly lower in the Ozone group than Control group on the 7th day (p=0.010 and p=0.048, respectively). Differences in other parameters were not statistically significant between the Ozone and Control groups.

Histopathological FindingsIn all groups, the total score was less on the 3rd and 7th days than on the 1st day. The 1st day score of the Ozone group was lower than the 1st day score of the Control and HBO groups. 7th day score of the Ozone group was lower than of the HBO group.

In the Control group, edema was intense on the 1st and 3rd days, but was moderate on the 7th day. The difference between 1st or 3rd vs. 7th day was statistically significant (p<0.001). Inflammation was moderate on all days; therefore, chi-square test could not be applied. While necrosis was mild on the 1st day, it was absent on the 3rd and 7th days in the Control group, and this was also statistically significant (p<0.001) (Table 4).

In the HBO group, edema was moderate on the 1st and 3rd days, but on the 7th day it was mild. Inflammation was in-tense, moderate and mild on the 1st, 3rd and 7th days, re-spectively. This decrease in the HBO group was statistically significant. However, necrosis was not seen in the HBO group on any day (Table 4).

In the Ozone group, edema was moderate on the 1st day, but absent on the 3rd and 7th days. Inflammation was mod-erate, mild and absent on the 1st, 3rd and 7th days, respec-tively. This decrease in the Ozone group was statistically significant (p<0.001). Necrosis was not seen in this group (Table 4).

Examples of histopathological images of the Control and treatment groups are presented in Figure 2. DISCUSSION

In the review of the literature about models of STT, there are methods created chemically (such as zymosan), by ultraviolet radiation and mechanically (or physically). The components of the immune system are also activated when trying to cre-ate an inflammation model using antigenic substances such as Freud adjuvant, carrageenan or zymosan. However, soft tis-sue injuries that occur in reality are usually sterile. There are also sterilized injury models created by ultraviolet exposure.[6] This injury model was developed on the model of trau-matic brain injury studies in rats.[7,8]

There are various clinical studies in the literature about HBO effectiveness in STT treatment. The common view in these studies is that HBO is not effective in STT treat-ment. However, a review of the Cochrane Collaboration, published in 2009, expressed the limitations of the studies and the necessity for further, more comprehensive studies. Although the efficacy of ozone in the inflammatory process is known, we could not find any study in the literature on ozone use in STT except in lumbar disc herniation and or-thopedic disorders including arthritis and rheumatic diseas-es.[14-19] In their study, Brooke et al. performed HBO therapy in 21 collegiate volunteers who had exercise-induced muscle injury, and they concluded that HBO therapy is not an ef-fective treatment in muscle injury. It was thought that this result could be attributed to the fact that it is not possible to standardize STT severity. One of the other factors that possibly contributes to unsuccessful HBO treatment is that structures such as muscle ligaments, tendons and fascia are also affected, and these structures have a much lower re-sponse to oxygen.[14]

Soolsma[20] could find no evidence of a benefit of HBO treat-ment on delayed muscle pain treatment process in his grade 2 medial collateral ligament injuries study in 1996. Four stud-ies published results showing that HBO had decreased pain significantly in patients at the end of 48 hours, but there was no evidence of improvement in muscle tension or decrease in edema. There was no difference between groups with re-gard to signs of edema and muscle tension. There was also no significant difference in clinical outcomes after 24 hours delayed HBO treatment in the study of Harrison and Staples.[11,14,21] The apparent incompatibility of these results with ours is thought to be due to use of ligament injury as a model and the limited response of ligaments to oxygen.

Ozone therapy has shown positive effects on wound healing, age-related macular degeneration, and ischemic and infec-tious diseases in case-analysis studies. In addition, it has been effectively applied in a variety of infectious diseases ranging from simple dental or mouth infections to hepatitis.[22,23]

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The therapeutic effect of ozone, especially in pathophysi-ological situations due to an intense inflammatory process in which the immune system is forefront, is surprising. Martinez-Sanchez and colleagues[16] applied HBO treatment to patients with diabetic foot, and they reported that wound healing was accelerated, length of hospital stay was shortened, control of blood sugar levels was better, and antioxidant enzyme levels were increased in the HBO treatment group when compared to the antibiotic treatment group. It has also been reported that injection of an oxygen/ozone mixture into the disc is use-ful in lumbar disc herniations.[17] The studies have shown that ozone applications increase the secretion of platelet-derived growth factor (PDGF), transforming growth factor (TGF)-ß1, and cytokines such as interleukin (IL)-8 from platelets. Kim et al.[18] also showed the same results in their wound healing study. In that study, topically applied ozone increased PDGF, TGF and VEGF expression and accelerated wound healing in scar tissue. Koca et al.[19] recently showed that inflammatory cytokines and oxidative stress decreased in both the ozone and HBO groups.

There are important studies in the literature about how the HBO application affects the antioxidant enzymes in various tissues in the organism. In one of them, Harabin and col-leagues[24] reported an increase in SOD activity in the lung and decrease in GSH-Px activity in brain and lung tissues in HBO-applied rats and guinea pigs. There are other researches as well that report that HBO may lead to an increase in SOD activity. These results seem compatible with our study re-sults.

Although an increase in antioxidant enzyme activities indi-cates an increase in free radical production, this increase has importance especially when these enzymes exceed the capacity. The lipid peroxidation, which is one of the most important harmful effects of free radicals, must be evaluated to assess the effect of increased free radical level. The best indicator of this is LPO. In our study, the decrease in LPO lev-els was statistically significant in the HBO group compared to the Control group on the 1st, 3rd and 7th days, and the de-crease in LPO levels was insignificant on the 1st day and was statistically significant on the 3rd and 7th days. These values show that the decrease in LPO level was less in the Control group than in the Ozone and HBO groups. This situation may show that there is an intense oxidative stress that exceeds the capacity of antioxidant enzymes in the created trauma.

Organisms needing oxygen for life must have a physiological adaptation to hypoxia. In mammals, including humans, vaso-dilation, angiogenesis, increase in glucose transport, increase in glucolysis, and apoptosis are activated. In the treatment of tumors, antiangiogenesis reduces the tumor blood flow, caus-ing the tumor cells to become resistant to chronic hypoxia. It has been found that the signaling pathway stimulated by hypoxia improves the acquired tolerance to chronic hypoxia. HIF-1α controls this by influencing apoptosis and regulating

genes and vascular endothelial growth factor (VEGF).[26,27] Re-duction in oxygen in a region increases the production of the gene regulatory protein HIF-1. This protein increases VEGF production particularly affecting the VEGF gene promoter. The VEGF secreted by surrounding tissue increases vascu-lature by activating endothelial cells in this region. When the formation of new blood vessels occurs and the oxygen concentration increases, HIF-1 activity and VEGF production decrease.[28] In our study, there was a statistically significant decrease in the Control and HBO groups at the different time points. In the Ozone group, it was statistically insignifi-cant. Decrease in the level of HIF-1 between the Control and HBO groups was statistically significant on day 1 and was statistically insignificant on day 3 and day 7. Based on these findings, it is known that HBO therapy has a more active role than Ozone treatment in tissue oxygenation, especially in the early days of the trauma.

It has been reported that with application of ozone, the HO-1 enzyme is also stimulated. The reason for the increase in this enzyme may be due to red blood cell hemolysis or ROT. HO-1 is a microsomal enzyme involved in the demoli-tion of heme ring, and the production is stimulated by an increase in oxidative stress, inflammatory cytokines and NO. This enzyme smashes the heme molecule in biliverdin and carbon monoxide (CO). Several studies performed in recent years showed that the HO-1 enzyme had antioxidant, anti-inflammatory and antiapoptotic properties.[29-31] However, in one study it was demonstrated that induction of hem oxy-genase is one of the protective mechanisms against oxidative stress in the pathogenesis of pulmonary disease. HO-1, the inducible form of HO, catalyzes heme to bilirubin, and this causes free iron and CO production.[32] In our study, change in HO-1 activity between groups was not significant accord-ing to time points. The protection of HO-1 levels is consid-ered to be significant in our study, in which the enzyme levels were generally decreased.

iNOS that is released in any acute event (trauma, stress, acute inflammation, etc.) may have either a protective or detrimen-tal effect on tissue. NO is important in wound healing. NO synthesis by macrophages continues for a long time in vitro. NO produced by structural NOS is necessary to maintain the normal physiological events. High NO concentrations produced by iNOS increase the damage.[33] In short, the NO molecule may show either protective or damaging effects in acute inflammatory events. In burning wounds as well, the level of iNOS increases immediately after the trauma. Koca et al.[19] created skeletal muscle ischemia-reperfusion injury in rats, and reported that HBO treatment decreased MDA and NOS levels, and significantly increased GSH-Px enzyme activity. These findings seem to be compatible with our study. On histopathologic examination of the tissues exposed to trauma, the inflammation was more significantly decreased in the treatment groups than the Control group. The histo-pathological findings support the biochemical findings.

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In conclusion, as a result of the study findings and the litera-ture review, we find that there are laboratory results showing that ozone and HBO reduce oxidative stress, improve tissue healing and increase tissue partial oxygen pressure. These re-sults are supported by the significant reduction in inflamma-tion and edema on the histopathological examination in the treatment groups.

In this study, the ozone and HBO treatments in STT were considered to be of benefit based on the biochemical and histopathological findings. However, we were unable to de-termine any clear result that revealed the superiority of ei-ther HBO or ozone. Further studies on this subject, which is a popular topic in the treatment of soft tissue injuries, will provide new insights.

Conflict of interest: None declared.

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17. Muto M, Ambrosanio G, Guarnieri G, Capobianco E, Piccolo G, An-nunziata G, et al. Low back pain and sciatica: treatment with intradiscal-intraforaminal O(2)-O (3) injection. Our experience. [Article in English, Italian] Radiol Med 2008;113:695-706. [Abstract]

18. Kim HS, Noh SU, Han YW, Kim KM, Kang H, Kim HO, et al. Thera-peutic effects of topical application of ozone on acute cutaneous wound healing. J Korean Med Sci 2009;24:368-74.

19. Koca K, Yurttas Y, Bilgic S, Cayci T, Topal T, Durusu M, et al. Effect of preconditioned hyperbaric oxygen and ozone on ischemia-reperfusion induced tourniquet in skeletal bone of rats. J Surg Res 2010;164:83-9.

20. Soolsma SJ. The effect of intermittent hyperbaric oxygen on short term recovery from grade II medial collateral ligament injuries. Thesis (1996), University of British Columbia, Vancouver.

21. Mekjavic IB, Exner JA, Tesch PA, Eiken O. Hyperbaric oxygen therapy does not affect recovery from delayed onset muscle soreness. Med Sci Sports Exerc 2000;32:558-63.

22. Stübinger S, Sader R, Filippi A. The use of ozone in dentistry and maxil-lofacial surgery: a review. Quintessence Int 2006;37:353-9.

23. Nogales CG, Ferrari PH, Kantorovich EO, Lage-Marques JL. Ozone therapy in medicine and dentistry. J Contemp Dent Pract 2008;9:75-84.

24. Harabin AL, Braisted JC, Flynn ET. Response of antioxidant enzymes to intermittent and continuous hyperbaric oxygen. J Appl Physiol (1985) 1990;69:328-35.

25. Oter S, Korkmaz A, Topal T, Ozcan O, Sadir S, Ozler M, et al. Cor-relation between hyperbaric oxygen exposure pressures and oxida-tive parameters in rat lung, brain, and erythrocytes. Clin Biochem 2005;38:706-11.

26. Carmeliet P, Dor Y, Herbert JM, Fukumura D, Brusselmans K, Dew-erchin M, et al. Role of HIF-1alpha in hypoxia-mediated apoptosis, cell proliferation and tumour angiogenesis. Nature 1998;394:485-90.

27. Communal C, Sumandea M, de Tombe P, Narula J, Solaro RJ, Hajjar RJ. Functional consequences of caspase activation in cardiac myocytes. Proc Natl Acad Sci U S A 2002;99:6252-6.

28. Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P. Histology: The lives and deaths of cells in tissues. In: Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P, editors. Molecular biology of the cell. 4th ed. New York: Garland Science; 2002, p. 1259-312.

29. Bocci V, Aldinucci C, Mosci F, Carraro F, Valacchi G. Ozonation of hu-man blood induces a remarkable upregulation of heme oxygenase-1 and heat stress protein-70. Mediators Inflamm 2007;2007:26785.

30. Bach FH. Heme oxygenase-1: a therapeutic amplification funnel. FASEB J 2005;19:1216-9.

31. Otterbein LE, Soares MP, Yamashita K, Bach FH. Heme oxygen-ase-1: unleashing the protective properties of heme. Trends Immunol 2003;24:449-55.

32. Horvath I, Loukides S, Wodehouse T, Kharitonov SA, Cole PJ, Barnes PJ. Increased levels of exhaled carbon monoxide in bronchiectasis: a new marker of oxidative stress. Thorax 1998;53:867-70.

33. Kubes P, McCafferty DM. Nitric oxide and intestinal inflammation. Am J Med 2000;109:150-8.

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Yıldırım et al. Effectiveness of hyperbaric oxygen and ozone applications in tissue healing in generated soft tissue trauma model in rats

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OLGU SUNUMU

Sıçanlarda oluşturulan yumuşak doku travma modelinde, hiperbarik oksijen ve ozonuygulamalarının doku iyileşmesi üzerine etkinliği: Deneysel çalışmaDr. Ali Osman Yıldırım,1 Dr. Mehmet Eryılmaz,2 Dr. Ümit Kaldırım,2 Dr. Yusuf Emrah Eyi,3

Dr. Salim Kemal Tuncer,2 Dr. Murat Eroğlu,1 Dr. Murat Durusu,2 Dr. Turgut Topal,4

Dr. Bülent Kurt,5 Dr. Serkan Dilmen,6 Dr. Serkan Bilgiç,7 Dr. Muhittin Serdar8

1GATAHaydarpaşaAskerHastanesi,AcilTıpAnabilimDalı,İstanbul2GATA,AskeriTıpFakültesi,AcilTıpAnabilimDalı,Ankara3HakkariAskerHastanesi,AcilServis,Hakkari4GATA,AskeriTıpFakültesi,FizyolojiAnabilimDalı,Ankara5GATA,AskeriTıpFakültesi,PatolojiAnabilimDalı,Ankara6ElazığAskerHastanesi,AcilServis,Elazığ7GATAHaydarpaşaAskerHastanesi,OrtopediveTravmatolojiAnabilimDalı,İstanbul8GATA,AskeriTıpFakültesi,BiyokimyaAnabilimDalı,Ankara

AMAÇ: Yumuşak doku travmaları bir çeşit akut travmatik iskemidir. Travmayla ortaya çıkan ödem, enflamasyon ve iskemiye, HBO ve ozonun olumlu etkileri olacağı düşünüldü. GEREÇ VE YÖNTEM: Toplam 63 yetişkin erkek Sprague-Dawley türü sıçanın her birine başlangıçta yumuşak doku travması (YDT) uygulanmış sonrasında bir kısmına ozon, bir kısmına HBO tedavi prosedürü uygulandı. Prosedürler bitiminde doku ve kan örnekleri alınan hayvanlarda, doku oksidatif stres düzeyini tespitte doku LPO düzeyleri, antioksidan sistemin işlerliğini tespitte doku SOD ve GSH-Px enzim düzeyleri, histopatolojik olarak, enflamasyon ve ödemin tespitinde rutin hematoksilen-eozin boyaması kullanıldı. BULGULAR: Oksijen konsantrasyonu arttığında azalan HIF1 aktivitesine, antienflamatuvar etkilerinin olduğu gösterilen HO-1 aktivitesine, her türlü akut olayda salınan iNOS aktiviteleri de çalışmamızda tespit edildi. Sonuç olarak, HBO ve ozon gruplarında LPO, iNOS düzeylerinde istatiksel olarak anlamlı azalma tespit ettik. Bu sonuçlarla uyumlu olarak histopatolojik incelemede de kontrol grubuna kıyasla HBO ve ozon gruplarında enflamas-yonda anlamlı bir azalma ve her üç grupta ödemde anlamlı düşme mevcuttu. TARTIŞMA: YDT’lerinde, HBO ve ozon tedavisinin çalışmamızdaki biyokimyasal ve histopatolojik bulgulara göre faydalı etkilerinin olduğu değerlen-dirilmektedir. Konuyla ilgili klinik çalışmaların yapılması etkilerinin daha iyi irdelenmesi adına faydalı olacağı söylenebilir.

Anahtar sözcükler: Deneysel; hiperbarik oksijen; ozon; yumuşak doku travması.

Ulus Travma Acil Cerr Derg 2014;20(3):167-175 doi: 10.5505/tjtes.2014.09465

DENEYSEL ÇALIŞMA - ÖZET

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Psychiatric disorders and their association withburn-related factors in children with burn injuryGül Karaçetin, M.D.,1 Türkay Demir, M.D.,2 Semih Baghaki, M.D.,3

Oğuz Çetinkale, M.D.,3 Mine Elagöz Yüksel, M.D.1

1DepartmentofChildandAdolescentPsychiatry,BakirkoyTrainingandResearchHospitalForPsychiatry,NeurologyandNeurosurgery,Istanbul2DepartmentofChildandAdolescentPsychiatry,IstanbulUniversityCerrahpasaFacultyofMedicine,Istanbul3DepartmentofPlastic,ReconstructiveandAestheticSurgery,IstanbulUniversityCerrahpasaFacultyofMedicine,Istanbul

ABSTRACT

BACKGROUND: The aim of this study was to assess psychiatric disorders and their association with burn-related factors in a population of Turkish children with burns.

METHODS: Thirty-one children admitted to the Cerrahpasa Medical Faculty Burn Unit between January 2013 and August 2013 were first assessed by the plastic surgeon, and then those with psychological symptoms were referred to a child psychiatrist, and the records were analyzed retrospectively.

RESULTS: The percentage of burned area to Total Body Surface Area (TBSA) ranged between 2-60% (mean, 17.3%). Nineteen pa-tients (61.3%) had a psychiatric diagnosis, which included acute stress disorder (ASD) (n=15), depression (n=3), posttraumatic stress disorder (n=2, comorbid with depression), and delirium (n=1). The percentage of burned area to TBSA was associated with the pres-ence of psychopathology and ASD. Further, psychopathology was associated with the number of burned major body regions.

CONCLUSION: Pediatric burn patients are at risk of developing psychopathology. The children with a greater percentage of burned area to TBSA and more burned body regions have the greatest risk of psychopathology. Surgeons have an important role in patient referral for psychiatric interventions, so that psychiatric disorders can be prevented as early as possible.

Key words: Burn; children; major body regions; percentage of burned area; psychopathology.

life-changing injury, which can cause pain and feelings of uncer-tainty and fear in the child.[4] Secondly, the burn injury threat-ens the child’s health and bodily integrity,[5] which may result in psychological trauma in the child.[4] Further, burn injury may result in permanent scarring, limited functionality, and inten-sive and long-lasting physical treatment,[5] all of which may place the affected children at risk of psychiatric disorders.[6]

The above risk factors and the psychological impact of burn injury on children have long been the subject of many re-search efforts. Most of the research has been focused on stress disorders, namely, acute stress disorder (ASD) and posttraumatic stress disorder (PTSD).[6] ASD describes the psychopathologic response in the intermediate aftermath and up to one month after trauma, whereas PTSD describes psy-chopathology that persists after one month.[6,7] Children with burn injury were reported to have ASD,[8-10] PTSD,[11-15] sepa-ration anxiety disorder,[12] depression,[16] and lower quality of life.[4] On the other hand, some of the studies have reported that children and adolescents with burn injury had a satisfy-ing quality of life[17] and were not different from their healthy peers in terms of depression scores[18] in the long-term. In

O R I G I N A L A R T I C L E

Address for correspondence: Gül Karaçetin, M.D.

Bakırköy Prof. Dr. Mazhar Osman Ruh Sağlığı ve Sinir Hastalıkları

Hastanesi, Çocuk ve Ergen Psikiyatri Kliniği, İstanbul, Turkey

Tel: +90 212 - 409 15 15 / 2829 E-mail: [email protected]

Qucik Response Code Ulus Travma Acil Cerrahi Derg2014;20(3):176-180doi: 10.5505/tjtes.2014.49033

Copyright 2014TJTES

INTRODUCTION

Having a severe burn injury is one of the most traumatic ac-cidents a child or adolescent can experience.[1] Advances in burn care and treatment have increased survival in patients with burns, which in turn has resulted in progression of the focus of burns research to include the psychological impacts of burn injury.[2,3] Pediatric burn injuries can place the affected children at risk of suffering from psychiatric diseases in a num-ber of ways. Firstly, a burn injury is an unexpected, painful, and

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one of these studies, it was stated that methodologically strong systematic research could overcome the discrepancies between studies and improve understanding of psychosocial functioning in children with burn injury.[4] Although there are many studies in the international literature about the psychi-atric aspects of burn in children,[4,5,8-18] there are no published studies about this topic in Turkey.

The aim of this study was to assess the psychiatric disorders in a population of Turkish children with burns with a system-atic diagnostic assessment. The second aim of the study was to assess the association of psychiatric disorders with burn-related factors.

MATERIALS AND METHODS

Children admitted to the Cerrahpasa Medical Faculty Burn Unit between January 2013 and August 2013 were first as-sessed by the plastic surgeon (SB), and those with psychologi-cal symptoms were referred to the child psychiatrist (GK), who performed the psychiatric assessments. Records of the psychiatric diagnosis and burn-related factors were analyzed retrospectively. Children with mental retardation were ex-cluded from this study. As a result, the psychiatric and burn-related records of 31 children were assessed.

The psychiatric diagnoses were assessed by means of the Di-agnostic and Statistical Manual of Mental Disorders Fourth Edition, Text Revised (DSM-IV, TR).[7] In addition, Diagnostic Classification of Mental Health and Developmental Disorders of Infancy and Early Childhood: Revised Edition (DC: 0-3R)[19] was used for children below 4 years of age. Two diagnostic systems were used in the study because previous studies have pointed out the importance of systematic diagnostic tools[4] and developmental stage of the child.[5] Further, as the DC: 0-3R does not cover the whole range of possible disorders in the preschool age, the authors of the DC: 0-3R recommend that clinicians use DSM-IV-TR or International Classification of Diseases (ICD-10) diagnoses, if they better describe the symptoms.[19] We used DSM-IV-TR as an additional diagnostic tool. Age, sex, cause and etiology of the burn, duration after the burn, reason for consultation, psychiatric symptoms and signs, psychiatric diagnosis, and treatment were recorded.

Statistical AnalysesChi-square or Fisher’s exact test was used to compare cat-egorical variables. Quantitative variables were compared by Student’s t-tests. Mann-Whitney U-test was used to assess nonparametric scales. The data were analyzed using the Sta-tistical Package for the Social Sciences (SPSS) 16-pocket pro-gram. The significance level was set as p<0.05.

RESULTS

Of the 31 children, 23 were male and 8 were female. The age of the patients ranged from 15 months to 15 years, with

a mean of 6.18 (±4.09) years. The most common cause of burns was negligence (59.8%), and the remaining consisted of burns due to accident. The most common mechanism of burn was scald, with a ratio of 74.2% (n=23), followed by flame (12.9%, n=4), contact (9.7%, n=3) and electrical burns (3.2%, n=1). The percentage of burned area to Total Body Sur-face Area (TBSA) ranged from 2-60%, with a mean of 17.32 (±13.59)%. Four (12.9%) patients had only 2nd-degree deep burn, 6 (19.4%) had only 3rd- degree burn, and 21 (67.7%) had 2nd- and 3rd-degree burn. With respect to the affected major body region, 8 patients had injury involving one major region of the body, as trunk (n=2), upper extremity (n=3) and lower extremity (n=3). Head and neck injury was associ-ated with trunk injury in 9 patients, who also had additional injury to the lower extremity (n=3), upper extremity (n=2) and both extremities (n=1). In addition, trunk injuries were associated with injury of the lower extremity (n=4), upper extremity (n=1) and both extremities (n=3).

The duration between burn and psychiatric assessment ranged from 4-190 days, with a mean of 21.1 days. Psycho-logical symptoms that prompted referral to the child psychia-trist were multiple in 83.9% (n=26) of the patients, and 16.1% (n=5) of the patients were mono-symptomatic. The most common psychiatric symptom was agitation (n=24), followed by difficulty falling asleep (n=9), startle response while sleep-ing (n=11), reluctance to speak (n=2), and frequent crying (n=6). As a result of the psychiatric assessment of children, 61.3% (n=19) had a psychiatric diagnosis satisfying the diag-nostic criteria for DC: 0-3R or DSM-IV. ASD was the most common diagnosis, found in 48.4% (n=15) of the children, followed by depression, which was diagnosed in 9.7% (n=3) of the patients. Of these depressive children, 2 had comorbid PTSD, which was found in 6.5% of the whole sample. One of the patients had delirium, with loss of orientation and visual hallucinations, which was associated with hyponatremia.

Assessment of the association between burn-related fac-tors and psychiatric diagnosis revealed that the percentage of burned area to TBSA was associated with the presence of psychopathology (Mann-Whitney test, p=0.001) and ASD (Mann-Whitney test, p=0.036). Further, psychopathology was associated with the number of major body regions (Mann-Whitney test, p=0.022). The duration between burn and psy-chiatric assessment was positively associated with depression (Mann-Whitney test, p=0.005) and PTSD (Mann-Whitney test, p=0.019); that is, children with depression and PTSD had a longer duration between burn and psychiatric assess-ment.

DISCUSSIONTo the best of our knowledge, the present study is the first to assess psychiatric diagnoses and their association with burn-related factors in Turkish children with burn injury. ASD was the most common diagnosis in the study group, and this

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finding was in line with previous studies reporting that ASD is a core feature of a child’s initial psychiatric reaction to a traumatic event.[8,9,20,21] This finding was also consistent with previous studies reporting ASD in children with burn injury.[8-10] The prevalence of ASD diagnosis was 48.4% in our sam-ple, which was higher than in previous studies reporting an ASD prevalence of 40%,[6] 39.4%,[9] 31%,[10] and 29%.[8] The higher prevalence of ASD in our study may be attributable to the differences in the sampling procedure between stud-ies. Our sample consisted of children who were referred for psychiatric assessment because of their psychological symp-toms, whereas the studies reporting lower prevalence rates for ASD included children with burns without regard for the presentation of symptoms. The percentage of burned area to TBSA was associated with ASD, and this finding was consis-tent with previous studies reporting an association between the size of the burn and ASD.[8,22] In addition, the burn size was associated with the presence of psychopathology in our study, a finding consistent with studies reporting that the burn size might be related to psychological reactions.[5]

Acute stress disorder (ASD) was reported to predict PTSD,[6,23] which is associated with long-lasting neurobiologi-cal abnormalities, such as reduced hippocampal size due to autonomic arousal and the acquisition of conditioned fear with chronic re-experiencing of traumatic events.[24] Recog-nizing acute stress symptoms in children is reported to be a critical first step in the path toward developing interventions to ameliorate traumatic stress responses and prevent the de-velopment of PTSD.[9]

Children with major burn injury form a particular high-risk group for developing PTSD, which was found in 6.5% of the patients in our study. This ratio was lower than in the previ-ous studies reporting the prevalence of PTSD as 10%,[11,12] 13.2%,[13] 25%, and 33%.[15] As PTSD describes the psycho-pathology that persists after one month, this difference may be attributable to the relatively short interval between burn injury and psychiatric assessment in our sample, with a mean of 21.1 days, which was shorter than in the previous studies, in which this interval was 6 months[11-12] and 15 months.[13] One of the prevalence rates (25%-33%) that was higher than in our study was reported by Stoddard et al.[15] in children with severe burns. Severe burns (>20% TBSA) constituted 29% of our sample, which may be the factor impacting on the lower prevalence rate of PTSD than in the study of Stoddard et al.,[15] which included severe burns. In a study including Turkish adult patients with burns, patients with PTSD were reported to have high burn rates and excessive burn-related pain symptoms.[25] This was also found in studies of pediat-ric burn patients reporting PTSD symptoms to be correlated with trauma severity.[13] In our study, PTSD was associated with the duration between burn and psychiatric assessment, and this is in line with the finding that PTSD was higher in studies with longer post-burn duration[13] than in those with shorter post-burn duration.[12]

The second most common psychiatric diagnosis in our sam-ple was depression, with a rate of 9.7%, which was higher than the rate of depression in Turkish children.[26] This find-ing was consistent with a previous study reporting lifetime rates for depression in children with burn injury to be higher than in the general population.[16] In this previous study, the rate of depression was lower than in our sample (3%) for the present time and higher than our sample (27%) for the life-time,[16] indicating that the risk of depression in pediatric burn patients continues for one’s lifetime. On the other hand, our findings were inconsistent with some of the studies report-ing that children with burns were not at risk of developing symptoms of depression.[18,27,28] As pointed out by previous authors,[5] the divergent results may be attributed to the dif-ferences in burn severity across the samples, with the more positive studies comprising less severely injured children.[18,27,28] For example, our sample consisted of children with a mean burn size of 17.3% (corresponding to moderate burn), whereas one of the conflicting results belonged to a sample of children with mild to moderate burns,[18] while another had a mean burn size of 22.5%, showing that there may be factors other than burn size impacting the rate of depression in pediatric burn patients.[28]

One of the patients in our sample had delirium, which was associated with hyponatremia. This is in line with studies de-scribing cases of delirium in children with burn injury.[29-31] The precipitating factor for delirium in our study was hypona-tremia, which is one of the risk factors reported in the etiol-ogy of delirium in previous studies.[29] Other risk factors that were reported to have a role in the pathogenesis of delirium in pediatric burn patients are hypertension, hypoglycemia, electrolyte imbalance, and sepsis.[29] The case with delirium in our study had loss of orientation and visual hallucinations, which were among the symptoms reported in the presenta-tion of delirium in previous studies.[31] Other symptoms that were reported in the presentation of delirium in previous studies were impaired attention, sleep disturbance, confusion, impaired responsiveness, impaired level of consciousness, ir-ritability, affective lability, agitation, apathy, and auditory and tactile hallucinations.[31] The surgeons should be alert to the risk factors and symptoms of delirium, because delirium can complicate patient care and be life-threatening.[6,29]

In conclusion, severe burn injuries are the most painful in-juries known; both the injury itself and the treatment pro-cedures can be frightening and difficult to cope with for children. Intensive medical treatments, painful dressings of-ten necessitating sedation and massive surgical treatments are too difficult for children and adolescents to handle. The traumatic nature of the burn and the painful treatment may induce ASD, PTSD, depression, and delirium. Research find-ings suggest that psychiatric interventions may help children to cope with the painful treatment and their emotional ef-fects and may reduce the psychiatric sequelae of burn injury.[32] As psychiatric disorders may have a negative impact on the

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prognosis and treatment of children with burns, the diagnosis and treatment of psychiatric disorders are very important. Surgeons who lead the burn team have a critical role in refer-ring children to a child psychiatrist for evaluation.

Conflict of interest: None declared.

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Karaçetin et al. Psychiatric disorders and their association with burn-related factors in children with burn injury

OLGU SUNUMU

Yanık yaralanması olan çocuklarda görülen psikiyatrik bozukluklar veyanık-ilişkili faktörlerle olan bağlantısıDr. Gül Karaçetin,1 Dr. Türkay Demir,2 Dr. Semih Baghaki,3 Dr. Oğuz Çetinkale,3 Dr. Mine Elagöz Yüksel1

1BakırkoyProf.Dr.MazharOsmanRuhSağlığıveSinirHastalıklarıHastanesi,ÇocukveErgenPsikiyatriKliniği,İstanbul2İstanbulÜniversitesiCerrahpaşaTıpFakültesi,ÇocukveErgenPsikiyatriAnabilimDalı,İstanbul3İstanbulÜniversitesiCerrahpaşaTıpFakültesi,Plastik,RekonstrüktifveEstetikCerrahiAnabilimDalı,İstanbul

AMAÇ: Bu çalışmada, yanık yaralanması olan Türk çocuklarda psikiyatrik bozuklukların ve bu bozuklukların yanık-ilişkili faktörlerle bağlantısı değer-lendirildi. GEREÇ VE YÖNTEM: Ocak 2013 ile Ağustos 2013 tarihleri arasında Cerrahpaşa Tıp Fakültesi Yanık Ünitesi’nde yatmakta olan 31 hasta öncelikle plastik cerrah tarafından değerlendirildi, psikolojik semptomları olan hastalar çocuk psikiyatristine yönlendirildi, daha sonra veriler geriye dönük olarak analiz edildi.BULGULAR: Hastaların yanık yüzdesi %2 ile %60 arasında değişmekteydi (ortalama yanık yüzdesi= %17.32). On dokuz hastada (%61.3) psikiyatrik bozukluk saptandı. Psikiyatrik bozukluklar arasında, akut stres bozukluğu (ASB) (n=15), depresyon (n=3), travma sonrası stres bozukluğu (n=2, depresyona eşlik etmektedir) ve delirium (n=1) bulundu. Yanık yüzdesi psikopatoloji varlığıyla ve ASB ile ilişkili bulundu. Ayrıca, psikopatoloji yanan vücut bölgesi sayısıyla ilişkili bulundu.TARTIŞMA: Pediatrik yanık hastaları psikopatoloji açısından risk altındadırlar. Yanık yüzdesi ve yanan vücut bölgesi fazla olan çocuklar psikopatoloji açısından en fazla risk taşıyan gruptur. Hastaların psikiyatrik değerlendirilme için yönlendirilmesi ve böylece psikiyatrik bozuklukların gelişmesini önlemek açısından cerrahlar önemli role sahiptir.Anahtar sözcükler: Çocuklar; psikopatoloji; vücut bölgeleri; yanık; yanık yüzdesi.

Ulus Travma Acil Cerrahi Derg 2014;20(3):176-180 doi: 10.5505/tjtes.2014.49033

KLİNİK ÇALIŞMA - ÖZET

Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3180

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Traumatic wound dehiscence after penetrating keratoplasty: case series and literature reviewBaki Kartal, M.D.,1 Baran Kandemir, M.D.,2 Turan Set, M.D.,3 Süleyman Kuğu, M.D.,2

Sadullah Keleş, M.D.,4 Erdinç Ceylan, M.D.,1 Berkay Akmaz, M.D.,2

Aytekin Apil, M.D.,5 Yusuf Özertürk, M.D.2

1DepartmentofOphthalmolgy,RegionalTrainingandResearchHospital,Erzurum2DepartmentofOphthalmology,Dr.LutfiKirdarKartalTrainingandResearchHospital,Istanbul3DepartmentofFamilyMedicine,AtatürkUniversityFacultyofMedicine,Erzurum4DepartmentofOphthalmology,AtatürkUniversityFacultyofMedicine,Erzurum5DepartmentofOphthalmolgy,BakirköySadiKonukTrainingandResearchHospital,Istanbul

ABSTRACT

BACKGROUND: We aimed to evaluate the risk factors, clinical features and outcomes of surgery for traumatic wound dehiscence (TWD) following penetrating keratoplasty (PK).

METHODS: Twenty-six patients with TWD following PK were evaluated retrospectively in terms of factors related to the trauma, types of reconstructive surgery, final graft clarity, and visual acuity.

RESULTS: There were 26 patients with a mean age of 40.7±19.6 years. In 12 (46.1%) patients, the better eye was affected by the trauma. The most frequent type of trauma was blunt trauma by various objects (9). In all cases, the dehiscence was at the graft host junction. The mean extent of detachment was 135.4°±57.6°. Crystalline or intraocular lens damage was present in 42.3% of cases. Median follow-up time after the reconstructive surgery was 36 months. The graft remained clear in 13 (50%) patients, whereas graft insufficiency/graft rejection developed in 13 (50%) patients. Final visual acuity was over 20/200 in 13 (50%) patients.

CONCLUSION: TWD may occur at any time after PK, most frequently within the first postoperative year. Low visual acuity in the other eye seems to be a major risk factor. In patients without major complications such as posterior segment damage, visual outcomes and graft survival can be favorable.

Key words: Graft survival; penetrating keratoplasty; traumatic wound dehiscence; visual prognosis.

The incidence of traumatic globe rupture after penetrating keratoplasty (PK) and after planned extracapsular cataract extraction (ECCE) was reported as 0.6-5.8%[3-4] and 0.4-1.4%,[5-6] respectively. Therefore, PK is more prone to trau-matic globe rupture than the other types of ocular surgery. The World Health Organization (WHO) reported that al-most 120,000 PKs were performed worldwide in 2000,[7] and the donor supply increased 21% between 1990 and 2000 in the United States.[8,9] Considering this increase in the num-ber of PKs (which is currently the most common homolo-gous organ transplantation), an increase in cases of traumatic wound dehiscence (TWD) is also expected. Despite the low incidence of TWD following PK, the potentially serious com-plications with poor outcomes make the growing number of such cases a concern.

MATERIALS AND METHODS

This study was performed by retrospectively reviewing the

O R I G I N A L A R T I C L E

Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3 181

Address for correspondence: Baki Kartal, M.D.

Dr. Refik Saydam Caddes, Yıldızkent, Palandöken, Erzurum, Turkey

Tel: +90 442 - 232 52 94 E-mail: [email protected]

Qucik Response Code Ulus Travma Acil Cerrahi Derg2014;20(3):181-188doi: 10.5505/tjtes.2014.36589

Copyright 2014TJTES

INTRODUCTION

Although the eyes comprise only 0.27% of our total body surface and 4% of the face, they are the third most frequently affected organ by trauma, after the hands and feet.[1] World-wide, there are currently 1.6 million blind and 19 million mon-ocular individuals as a result of ocular trauma, which makes it one of the most significant causes of ocular morbidity.[2]

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Kartal et al. Traumatic wound dehiscence after penetrating keratoplasty

records of 26 patients who were diagnosed with and under-went reconstructive surgery to correct traumatic graft rup-ture in the Eye Clinic of Kartal Dr. Lütfi Kirdar Training and Research Hospital between 2003 and 2012. Patients’ records were evaluated with respect to age, gender, indication of PK, suturing technique, time interval between PK and the trauma, type of trauma, presence of sutures, steroid usage at the time of trauma, accompanying anterior and posterior segment damage, wound specifications, type of reconstructive surgical procedures, and final visual acuity and graft clarity.

The Statistical Package for the Social Sciences (SPSS) 18.0 package program were used and statistical analyses were done by frequency tables, Mann-Whitney U, Kruskal-Wallis, chi-square, and Wilcoxon tests. A value of p<0.05 was ac-cepted as statistically significant.

RESULTS

There were 14 (54%) males and 12 (46%) females, with a mean age of 40.7±19.6 years (range, 4-71). There was no sig-

Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3182

Table 1. General demographic and medical data

PatientNo

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

16

17

18

19

20

21

22

23

24

25

26

AGV: Ahmed glaucoma valve implant present; ICS: Interrupted combined with continuous sutures; IS: Interrupted sutures; PBK: Pseudophakic bullous keratopathy.

56

28

11

23

24

45

47

15

60

71

25

37

50

30

45

30

47

66

48

44

8

4

61

49

71

64

Female

Female

Male

Male

Male

Male

Male

Male

Male

Male

Female

Female

Female

Female

Female

Male

Female

Female

Male

Male

Male

Female

Male

Female

Male

Female

2

0.6

2

6

12

9

3

1

6.5

56

59

16

18

1

72

1

7

1

30

44

2

18

30

4

35

26

112

105

93

68

58

52

40

22

24

31

26

26

25

21

20

19

12

12

6

43

117

65

84

64

27

16

IS

ICS

IS

IS

IS

IS

IS

ICS

IS

IS

IS

IS

IS

IS

IS

ICS

IS

IS

ICS

IS

IS

IS

IS

IS

IS

IS

+

+

+

+

+

+

+

+

+

Removed

Removed

+

Removed

+

Removed

+

+

+

Removed

Removed

+

Removed

Removed

+

Removed

Removed

+

+

+

+

+

+

+

+

+

Stopped

Stopped

Stopped

Stopped

+

Stopped

+

+

+

Stopped

Stopped

+

Stopped

Stopped

+

Stopped

Stopped

Glaucoma

Low vision in

other eye

Glaucoma

Glaucoma

Glaucoma

Glaucoma

+Deafness

Glaucoma

+Single Eye

Glaucoma

(AGV)

Single Eye

Single Eye

Single Eye

Single Eye

Single Eye

Single Eye

Corneal Scar

Keratoconus

Leukoma Adherence

Granular Dystrophy

Corneal Scar

Keratoconus

Macular Dystrophy

Keratoconus

Fuchs

PBK

Corneal Scar

PBK

Corneal Scar

Keratoconus

Herpetic Keratitis

Keratoconus

Corneal Scar

PBK

Corneal Scar

Corneal Scar

Graft Rejection

Corneal Scar

Leukoma Adherence

Graft Rejection

Leukoma Adherence

Corneal Scar

Age Gender Indication of PK

Between PK-trauma

Follow-up (month) Suture

Aftertrauma

Suturingtechnique

Presence of sutures

during trauma

Steroid usage during trauma

Pretraumaticother risk factors

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Kartal et al. Traumatic wound dehiscence after penetrating keratoplasty

nificant difference in the average age by gender (Z=-0.386, p=0.699). Among the 1,625 PKs performed during the study period, the incidence of TWD was 1.6%. The most frequent primary PK indication was corneal scar (8). In 30.8% (8/26) of these cases, PK was combined with cataract extraction and intraocular lens (IOL) implantation; 69.2% (18/26) underwent PK alone. Twenty-two (84.6%) patients had been operated with 16 single sutures. The most frequent risk factor was low vision in the other eye (8), and the better eyes were affected by the trauma in 12 (46.1%) cases. Sutures were present in 16 (61.6%) patients, and 15 (57.7%) patients were using steroids at the time of the trauma (Table 1). Visual acu-ity was 0.26±0.21 (5 mps-20/25) in the traumatized eye and

0.47±0.40 (P[-] - 20/20) in the other eye prior to trauma.

The median time interval between the PK and trauma was 8.0 months (range, 0.6-72 months). All of the traumas were blunt and found to be caused by various objects (9), by falls (6), and by hand (6) or finger slap (5). The average age of the fall-re-lated injuries was found to be significantly higher (χ2=12.540; p=0.006), but there was no significant relationship between etiology of the trauma and gender (χ2=0.829; p=0.843).

The median time between the trauma and reconstructive surgery was 6 hours (range, 1-120 hours) in 21 cases, and the time was not recorded in the remaining 5. No statistically

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Table 2. Data about dehiscence, final graft status and vision

Patient Quadrant of Extent of Final graft Pretraumatic Final visual Final low visual No dehiscence dehiscence status visual acuity acuity acuity reasons

1 Superior 120 Clear 1mFC 2mFC Pretraumatic PDRP

2 Superior 45 Clear 0.1 1.0 –

3 Nasal 180 Clear 2mFC 2mFC Amblyopia/Exotropia

4 Superior 90 Clear 0.7 0.7 –

5 Except Nasal 270 Insufficiency 0.4 HM Graft Insufficiency

6 Inferior 120 Insufficiency 0.3 0.15 Graft Insufficiency

7 Inferior 120 Clear 0.2 0.6 Macular Pucker

8 Temporal 30 Clear 0.5 0.5 –

9 Inferior 180 Clear 0.2 HM Epithelial

Ingrowth+PVR

10 Superior 180 Insufficiency 0.15 HM Graft

Insufficiency+Secondary

Glaucoma

11 Superior 180 Rejected 50 cmFC 50 cmFC Pretraumatic Graft Rejection

12 Superior 120 Clear 0.4 0.7 –

13 Inferior 90 Clear 0.4 P(+) Suprachoroidal Hemorrhage

14 Nasal 45 Rejected 0.15 0.15 –

15 Superior 180 Insufficiency 0.2 10cmFC Graft Rejection

16 Nasal 140 Clear 0.4 0.4 –

17 Temporal 60 Rejected 0.8 0.2 Graft Rejection

18 Nasal 180 Insufficiency 2mFC 10cmFC Graft

Insufficiency+Fibrous Ingrowth

19 Inferior 180 Clear 0.05 30cmFC Geographic Atrophy

20 Inferior 180 Rejected 0.5 0.1 Graft Rejection

21 Inferior 150 Rejected 1 mFC P (+) Graft Rejection

22 Nasal 90 Insufficiency 0.2 HM Graft Insufficiency

23 Inferior 180 Clear 0.4 0.15 Retinal Vein Branch Occlusion

24 Inferior 200 Rejected 0.05 P(+) Graft Rejection

25 Temporal 120 Clear 0.3 0.1 Geographic Atrophy

26 Inferior 90 Clear 0.4 0.5 –

FC: Finger count; HM: Hand motion; PDRP: Proliferative diabetic retinopathy; PVR: Proliferative vitreoretinopathy.

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significant relationship was found between the time elapsed from trauma to reconstructive surgery and the final graft clar-ity (p>0.05) (Table 2). Each dehiscence was on the host-graft junction and was observed to be between 30° and 270° (mean, 135.38±57.61°) (Table 2). The degree of the host-graft dehis-cence was not found to be statistically related to primary sur-gical indication, pretraumatic risk factors, suturing techniques, presence of the sutures, steroid use, etiology of the trauma, place of the dehiscence, or final graft status (p>0.05) (Table 3). The most frequent site of dehiscence was in the inferior quadrant (10 patients). There was no significant relation-ship between the affected quadrant and the etiology of the trauma (χ2=9.908; p=0.820) or degree of the graft dehiscence (χ2=9.054; p=0.06). The ratio of patients with crystalline lens/IOL damage was 42.3%, and traumatic damage to these struc-tures was found to be significantly related to final graft clarity (p<0.05), but not related to the degree of the host-graft de-hiscence (p>0.05) (Table 3). Eight of the corneas (30.8%) were clear, and the remaining 18 (69.2%) were affected in varying degrees from mild corneal edema to totally opaque cornea at presentation after the trauma. Posttraumatic graft edema was not related to crystalline lens/IOL damage (χ2=1.418; p=0.234), degree of dehiscence (Z=-0.459; p=0.646) or final graft status (χ2=0.680; p=0.409). Other common anterior

segment complications were vitreous (10) and iris prolapse (7). Posterior segment damage was noted as suprachoroidal hemorrhage (1), macular pucker (1), or retinal detachment with proliferative vitreoretinopathy (PVR) (1), and all of these patients had crystalline lens/IOL damage (Table 4).

Reconstructive surgical procedures were done under local anesthesia (retrobulbar and periocular) in 20 (76.9%) patients and under general anesthesia in the remaining 6 (23.1%) pa-tients. Primary suture (PS) alone was employed in 13 patients, and PS combined with other interventions was performed in the remaining cases (Table 4).

Median follow-up time was 36 months (range, 6–117 months) after the reconstructive surgery. The rates of clear graft and graft insufficiency/graft rejection were 13 (50%) and 13 (50%), respectively. There was no significant relationship between the final graft status and age, gender, primary surgical indica-tion, median time interval between PK and trauma, degree of dehiscence, affected quadrant, etiology of the trauma, or reconstructive surgery type (p>0.05) (Table 3). Visual acuity was 0.05±0.1 (hand motions - 20/40) after the trauma, and it was 0.20±0.28 (P(+) - 20/20) at the final follow-up. There was no significant difference between pre-traumatic and final visual acuity (Z=-1.736; p=0.083), but a statistically significant difference was found between posttraumatic and final visual acuity (Z=-3.081; p=0.002). Visual acuity was decreased in 14 (53.8%) cases, remained the same in 7 (26.9%) cases, and in-creased in 5 (19.2%) cases. At the final follow-up, visual acuity was better than 20/200 in 13 (50%) eyes (Table 2). Epithelial ingrowth (1), fibrous ingrowth (1) and secondary glaucoma (1) were noted as anterior segment complications in addition to posterior segment-related complications (Table 2).

DISCUSSIONAny trauma to the globe with proper mechanism and suf-ficient force would cause rupture of the globe at the weak-est region.[4] In virgin eyes, these regions are insertions of extraocular muscles or the corneoscleral limbus,[10] whereas in wounded eyes with previous surgery or penetrating trau-ma, the rupture site will be the previous corneal scar.[11] PK comprises a full thickness 360° surgical wound and creates permanent weakness in the eyeball throughout patients’ lives.[12-14] Calkins et al.[15] demonstrated that in human corneas, weakness at the host-graft junction persists even a year after PK, despite the appearance of having healed.

Mental retardation, low vision in both eyes, deafness, and al-cohol consumption are accepted risk factors for traumatic rupture following PK.[3,11,16,17] Older age, obesity, use of non-irritating nylon sutures, improper suturing, early suture re-moval, and glaucoma have been reported to delay corneal wound healing.[18] In our study group, at least one of these risk factors was present in 53.8% (14) of cases: low vision in the other eye (8), glaucoma (7) and deafness (1). Addition-

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Kartal et al. Traumatic wound dehiscence after penetrating keratoplasty

Table 3. Factors associated with degree of the host-graft dehiscence and final graft status

Degree of the host-graft dehiscence

Primary surgical indication* χ2=8.156 p=0.319

Pretraumatic risk factors* χ2=2.651 p=0.449

Suturing techniques¶ Z=-0.656 p=0.512

Presence of sutures¶ Z=-1.189 p=0.234

Steroid use¶ Z=-0.931 p=0.352

Etiology of the trauma* χ2=1.502 p=0.682

Place of the dehiscence* χ2=9.054 p=0.060

Final graft status* χ2=1.141 p=0.565

Crystalline lens/IOL damage¶ Z=-1.170 p=0.116

Final graft status

Age* χ2=1.099 p=0.577

Gender€ χ2=1.666 p=0.435

Primary surgical indication€ χ2=9.547 p=0.216

Median time between PK and trauma Z=-0.668 p=0.504

Degree of dehiscence Z=-0.657 p=0.511

Affected quadrant χ2=2.076 p=0.722

Etiology of the trauma χ2=1.867 p=0.631

The median time between trauma Z=-0.179 p=0.858

and reconstructive surgery

Reconstructive surgery type χ2=1.385 p=0.239

Crystalline lens/IOL damage¶ χ2=7.369 p=0.025

*: Kruskal-Wallis test; ¶: Mann-Whitney U test; €: Chi-square test.

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ally, prolonged use of topical steroids against graft rejection has been shown to delay the wound healing process in many studies.[11,16,18-20] In our study group, 57.7% (15) of the patients were using topical steroids at the time of injury.

Traumatic graft dehiscence can occur at any time after PK.[13,18] In the literature, occurrences of traumatic graft rupture have been reported from 3 days to 33 years after PK.[18,21,22] Thirty-three years is the longest reported time interval after PK, indicating a lifetime risk of traumatic dehiscence. The mean

time interval between PK and TWD was 17.7 months in our study group, and in 15 (57.7%) cases, trauma had occurred within the first postoperative year. Various types of injury resulting in graft dehiscence have been reported (following removal of rigid gas permeable lens, during self-installation of topical drugs, following impact by champagne cork, and bilat-eral graft rupture due to airbag deployment during a car ac-cident).[11,16,20,23,24] However, many graft ruptures occur during daily activities that are considered ‘low-risk activities’.[22] Pre-vious reports have noted that traumatic graft dehiscence was

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Kartal et al. Traumatic wound dehiscence after penetrating keratoplasty

Table 4. Surgical procedures, traumatic crystalline lens/IOL and posterior segment damage

Patient Surgical Secondary surgery Status of lens Posterior segment No procedure damage

Pre-trauma Post-trauma

1 PS – Pseudophakic Pseudophakic –

Decentralized

2 PS + AV + LA Secondary Sulcus PC Phakic Traumatic cataract –

IOL Implantation

3 PS L Phakic Lens Subluxation –

4 PS + IR – Phakic Phakic –

5 PS + AV – Phakic Aphakia –

6 PS + AV + IE – Pseudophakic Pseudophakic –

7 PS + IR PPV / Scleral Fixation IOL Phakic Aphakia Macular Pucker

8 PS – Phakic Phakic –

9 PS + AV + IR Re-PK + Retroiridal Phakic Aphakia PVR + Retinal

Membrane Excision + L Detachment

10 PS – Pseudophakic Pseudophakic –

11 PS – Pseudophakic Pseudophakic –

12 PS – Pseudophakic Pseudophakic –

13 PS + AV + IOL E – Pseudophakic Aphakia Suprachoroidal

Hemorrhage

14 PS – Phakic Phakic –

15 PS + AV + IE – Phakic Aphakia –

16 PS + AV + L AV + Scleral Fixation IOL Phakic Traumatic cataract –

17 PS – Pseudophakic Pseudophakic –

18 PS – Pseudophakic Pseudophakic –

19 PS + AV – Phakic Aphakia –

20 PS + IE+AV – Aphakia Aphakia –

21 PS – Phakic Phakic –

22 PS+IR – Phakic Phakic –

23 PS – Phakic Phakic –

24 PS Re-PK Pseudophakic Pseudophakic –

25 PS+AV – Pseudophakic Aphakia –

26 PS – Phakic Phakic –

AV: Anterior vitrectomy; IE: Iris excision; IOL E: IOL extraction; IR: Iris repositioning; L: Lensectomy; LA: Lens aspiration; PC: Posterior chamber; PPV: Pars plana vitrec-tomy; PS: Primary suture; PVR: Proliferative vitreoretinopathy; Re-PK: re-Penetrating keratoplasty.

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most often due to sports- or accident-related injuries and intentional assaults in the younger age group,[25,26] whereas falls or self-inflicted poking were found to be more frequent in the older age group.[17,25,27] In the current study, fall-related injuries were significantly more frequent compared to other causes in the older age group. Although Nagra et al.[20] re-ported a predominance of women in their study, men were found to be at higher risk for TWD in other studies.[4,11,14,16-

19,22,28,29] Williams[25] noted that younger men are subjected to sport injuries and intentional assaults, whereas the older age group is exposed to fall-related injuries without any gender predominance. In our study group, neither gender was pre-dominant, and no relationship was found between gender and age or trauma etiology.

There are various reports concerning the relation between primary PK indication and TWD.[14,19,28-31] It has been noted that the most frequent indications in TWD are keratoco-nus, corneal scars, bullous keratopathy, herpetic keratitis, and Fuchs endothelial dystrophy.[4,11,14,16-20,22,23,25-32] In the present study, the most frequent PK indications were consistent with the general literature: corneal scar, keratoconus, leukoma, and bullous keratopathy. As these are most common indi-cations for PK,[33] there are no definite data concerning the relationship between TWD and PK indications.

In all of our patients, the wound dehiscence was at the host-graft junction. Likewise, other studies have also reported this region to be the most frequent site of wound separa-tion.[16-20,25-32] The presence of sutures does not seem to protect against wound dehiscence, and there are differing reports about the effect of suturing techniques.[11,18,19,20,25,27] In our study group, interrupted suture was the most com-monly used suturing technique, and in 16 (61.7%) eyes, all or some of the sutures were in place at the time of injury. We observed no significant relationship between the extent of wound dehiscence and the suturing techniques or the pres-ence or absence of sutures at the time of trauma. Referring to special anatomical position and the protective effects of bony structures, certain quadrants of the globe have been proposed to be more vulnerable by some researchers, while others found no quadrant predominance.[11,17,27] In our series, the inferior quadrant was affected most frequently, followed by superior, nasal and temporal.

Kawashima et al.[27] asserted that the extent of dehiscence is not related to etiology of the trauma. In our study, we observed no significant relationship between etiological fac-tors and extent of dehiscence, consistent with the literature. Lam et al.[22] apprised that grafts with larger dehiscence were more likely to fail and more likely to have loss of clarity at presentation, but we observed no significant relation be-tween degree of dehiscence and final graft status. In the pres-ent study, damage to the crystalline lens or IOL was present in 11 (42.3%) cases. In the literature, crystalline lens or IOL damage is reported to be range from 37%[28] - 100%,[29] and is

accepted as a bad prognostic sign. In a study by Tran et al.[31]

, extensive dehiscence was more frequent in cases with lens and posterior segment damage. Other studies also support this finding, and damage to crystalline lens or IOL at presen-tation (commonly accompanied by posterior segment injury) has been proposed as a bad prognostic sign for final visual acuity in such eyes.[26,27] Likewise, three of our patients with posterior segment damage also had concomitant crystalline lens or IOL damage.

Surgical intervention was resuturing of the original graft in all cases, and the time interval between the causative trauma and first presentation was a mean 23.76 hours (1-120 hours). Unless the graft is lost, resuturing of the original graft is rec-ommended, especially in older patients, to avoid risk of ex-plosive hemorrhage, even if the graft seems opaque.[17,20,23,25] There is insufficient data in the literature regarding the effect of time interval from trauma to resuturing on final graft sta-tus. Topping et al.[16] reported a case with 20/20 visual acuity and clear graft who had resuturing two days after the trauma. Similarly, one of our patients who admitted three days after trauma had maintained graft clarity, whereas another who was admitted five days after the injury developed graft rejec-tion. Nevertheless, we found no significant relation between final graft status and the time interval between injury and resuturing.

Pettinelli et al.[23] alleged retrobulbar anesthesia to be con-traindicated in cases with opened and distorted globe. We encountered no complications in the five patients underwent surgery under retrobulbar anesthesia. Rehany et al.[14] report-ed a case of sulcus-fixated IOL during primary surgical repair, and they also noted that this process may pose a risk to the eye and corneal graft. None of our patients had IOL implan-tation during the primary surgical repair. Six of our patients required various secondary surgical procedures including PK. Especially in eyes with posterior segment damage, need for secondary surgical procedures has also been emphasized by other researchers.[20,31]

The reported percentage of grafts remaining clear after TWD varies in a wide range between 20%[3] and 100%.[16,29] Although more endothelial cell loss is expected following trauma that is severe enough to cause lens/vitreous loss, due to some physi-ological transformation of endothelial cells following trans-plantation, long-term results following resuturing are usually satisfactory.[3] Lam et al.[22] analyzed various factors affecting graft survival following rupture. They found no statistically significant difference when comparing sex, age, original indi-cation for grafting, or time interval between primary surgery and trauma. However, in patients in whom sutures were re-moved, grafts had a more extensive dehiscence; additionally, grafts with 180° or more of dehiscence were more prone to clarity loss. Likewise in our study, regarding graft clarity, we observed no statistically significant differences in age, gender, primary surgical indication, median time interval between PK

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and trauma, degree of dehiscence, affected quadrant, etiol-ogy of the trauma, median time interval between trauma and surgery, or reconstructive procedure. Among the published studies, the highest number of regrafts was reported by Tseng et al.[17] In their series, 71.4% of grafts remained clear. Raber et al.[19] also found that regrafting affords good prognosis. In our study group, one patient had been regrafted, and the graft remained clear during the 18-month follow-up.

Other complications apart from early damage to anterior and posterior segment structures are reported as vitreous hemorrhage, suprachoroidal hemorrhage, retinal detach-ment, macular pucker, glaucoma, epithelial ingrowth, hypo-tonia, phthisis bulbi, and need of evisceration due to com-plete disturbance of intraocular structures.[4,11,14,18,20,22,23,25,27,31,

34] Among our study population, we encountered secondary glaucoma, macular pucker, epithelial ingrowth with retinal de-tachment, fibrous ingrowth, and suprachoroidal hemorrhage.

Many researchers have determined severity of the trauma and posterior segment complications to be the major de-terminants of final visual acuity.[11,14,16-19,22,25,26,31] In our series, when pretraumatic and final visual acuities were compared, visual acuity was improved in 5 eyes, unchanged in 7, and worse in 14 cases. In patients whose final visual acuity was worse, the trauma was severe enough to cause ≥120° graft dehiscence (with the exception of patients 13 and 22) and/or crystalline lens/IOL damage (patients 5, 9, 13, 15, 19 and 25); posterior segment complications were also noted (patients 9, 13, 19, 23) (Table 2).

In conclusion, as a part of their treatment, patients should be well informed about the risk of TWD and its possible seri-ous complications.[31] In patients without major complications such as posterior segment damage, visual results and graft survival following TWD can be favorable.

Conflict of interest: None declared.

REFERENCES

1. Nordberg E. Injuries as a public health problem in sub-Saharan Africa: epidemiology and prospects for control. East Afr Med J 2000;77(12 Sup-pl):1-43.

2. Négrel AD, Thylefors B. The global impact of eye injuries. Ophthalmic Epidemiol 1998;5:143-69.

3. Rohrbach JM, Weidle EG, Steuhl KP, Meilinger S, Pleyer U. Traumatic wound dehiscence after penetrating keratoplasty. Acta Ophthalmol Scand 1996;74:501-5.

4. Elder MJ, Stack RR. Globe rupture following penetrating keratoplasty: how often, why, and what can we do to prevent it? Cornea 2004;23:776-80.

5. Ball JL, McLeod BK. Traumatic wound dehiscence following cataract surgery: a thing of the past? Eye (Lond) 2001;15:42-4.

6. Lambrou FH, Kozarsky A. Wound dehiscence following cataract surgery. Ophthalmic Surg 1987;18:738-40.

7. Human organ and tissue transplantation. Report by the Secretariat. Executive Board, EB112/5, 112th session, Provisional agenda item 4.3. World Health Organization. May 2003. Available: http://apps.who.int/gb/archive/pdf_files/EB112/eeb1125.pdf.

8. Kang PC, Klintworth GK, Kim T, Carlson AN, Adelman R, Stinnett S, et al. Trends in the indications for penetrating keratoplasty, 1980-2001. Cornea 2005;24:801-3.

9. Aiken-O’Neill P, Mannis MJ. Summary of comeal transplant activity Eye Bank Association of America. Cornea 2002;21:1-3.

10. Cherry PM. Rupture of the globe. Arch Ophthalmol 1972;88:498-507.

11. Agrawal V, Wagh M, Krishnamachary M, Rao GN, Gupta S. Traumatic wound dehiscence after penetrating keratoplasty. Cornea 1995;14:601-3.

12. Jeganathan SV, Ghosh S, Jhanji V, Lamoureux E, Taylor HR, Vajpayee RB. Resuturing following penetrating keratoplasty: a retrospective analy-sis. Br J Ophthalmol 2008;92:893-5.

13. Renucci AM, Marangon FB, Culbertson WW. Wound dehiscence after penetrating keratoplasty: clinical characteristics of 51 cases treated at Bascom Palmer Eye Institute. Cornea 2006;25:524-9.

14. Rehany U, Rumelt S. Ocular trauma following penetrating keratoplasty: incidence, outcome, and postoperative recommendations. Arch Ophthal-mol 1998;116:1282-6.

15. Calkins JL, Hochheimer BF, Stark WJ. Corneal wound healing: holo-graphic stress-test analysis. Invest Ophthalmol Vis Sci 1981;21:322-34.

16. Topping TM, Stark WJ, Maumenee E, Kenyon KR. Traumatic wound dehiscence following penetrating keratoplasty. Br J Ophthalmol 1982;66:174-8.

17. Tseng SH, Lin SC, Chen FK. Traumatic wound dehiscence after pen-etrating keratoplasty: clinical features and outcome in 21 cases. Cornea 1999;18:553-8.

18. Das S, Whiting M, Taylor HR. Corneal wound dehiscence after pen-etrating keratoplasty. Cornea 2007;26:526-9.

19. Raber IM, Arentsen JJ, Laibson PR. Traumatic wound dehiscence after penetrating keratoplasty. Arch Ophthalmol 1980;98:1407-9.

20. Nagra PK, Hammersmith KM, Rapuano CJ, Laibson PR, Cohen EJ. Wound dehiscence after penetrating keratoplasty. Cornea 2006;25:132-5.

21. Farley MK, Pettit TH. Traumatic wound dehiscence after penetrating keratoplasty. Am J Ophthalmol 1987;104:44-9.

22. Lam FC, Rahman MQ, Ramaesh K. Traumatic wound dehiscence after penetrating keratoplasty-a cause for concern. Eye (Lond) 2007;21:1146-50.

23. Pettinelli DJ, Starr CE, Stark WJ. Late traumatic corneal wound dehis-cence after penetrating keratoplasty. Arch Ophthalmol 2005;123:853-6.

24. Maharshak I, Bourla D, Grinbaum A, Weinberger D, Axer-Siegel R. Air-bag-induced bilateral corneal graft dehiscence. Cornea 2005;24:110-1.

25. Williams MA, Gawley SD, Jackson AJ, Frazer DG. Traumatic graft de-hiscence after penetrating keratoplasty. Ophthalmology 2008;115:276-8.

26. Steinberg J, Eddy MT, Katz T, Fricke OH, Richard G, Linke SJ. Trau-matic wound dehiscence after penetrating keratoplasty: case series and literature review. Eur J Ophthalmol 2012;22:335-41.

27. Kawashima M, Kawakita T, Shimmura S, Tsubota K, Shimazaki J. Char-acteristics of traumatic globe rupture after keratoplasty. Ophthalmology 2009;116:2072-6.

28. Bowman RJ, Yorston D, Aitchison TC, McIntyre B, Kirkness CM. Trau-matic wound rupture after penetrating keratoplasty in Africa. Br J Oph-thalmol 1999;83:530-4.

29. Foroutan AR, Gheibi GH, Joshaghani M, Ahadian A, Foroutan P. Trau-matic wound dehiscence and lens extrusion after penetrating keratoplas-

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ty. Cornea 2009;28:1097-9.

30. Hiratsuka Y, Sasaki S, Nakatani S, Murakami A. Traumatic wound de-hiscence after penetrating keratoplasty. Jpn J Ophthalmol 2007;51:146-7.

31. Tran TH, Ellies P, Azan F, Assaraf E, Renard G. Traumatic globe rupture following penetrating keratoplasty. Graefes Arch Clin Exp Ophthalmol 2005;243:525-30.

32. Egrilmez S, Uzunel UD, Yagcı A. Ocular trauma following penetrating keratoplasty. MN Oftalmoloji 2004;11:200-4.

33. Garg P, Krishna PV, Stratis AK, Gopinathan U. The value of corneal transplantation in reducing blindness. Eye (Lond) 2005;19:1106-14.

34. Nagra PK, Raber IM. Epithelial ingrowth in a phakic corneal transplant patient after traumatic wound dehiscence. Cornea 2003;22:184-6.

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OLGU SUNUMU

Penetran keratoplasti sonrası travmatik yara ayrışması, olgu serisi ve literatüre genel bakışDr. Baki Kartal,1 Dr. Baran Kandemir,2 Dr. Turan Set,3 Dr. Süleyman Kuğu,2 Dr. Sadullah Keleş,4

Dr. Erdinç Ceylan,1 Dr. Berkay Akmaz,2 Dr. Aytekin Apil,5 Dr. Yusuf Özertürk2

1BölgeEğitimveAraştırmaHastanesi,GözHastalıklarıKliniği,Erzurum2Dr.LütfiKırdarKartalEğitimveAraştırmaHastanesi,GözHastalıklarıKliniği,İstanbul3AtatürkÜniversitesiTıpFakültesi,AileHekimliğiAnabilimDalı,Erzurum4AtatürkÜniversitesiTıpFakültesi,GözHastalıklarıAnabilimDalı,Erzurum5BakırköySadiKonukEğitimveAraştırmaHastanesi,GözHastalıklarıKliniği,İstanbul

AMAÇ: Penetran keratoplasti (PK) sonrası travmatik yara ayrışması için risk faktörleri, klinik özellikler ve cerrahi sonuçları değerlendirmek.GEREÇ VE YÖNTEM: Penetran keratoplasti sonrası travmatik yara ayrışması gelişen 26 hasta travma ile ilişki faktörler, rekonstriktif cerrahi işlemler ile sonuç greft sağkalımı ve görme keskinliği açısından geriye dönük olarak değerlendirildi.BULGULAR: Yaş ortalaması 40.7±19.6 yaş olan 26 hastanın 12’sinde (%46.1) travmadan daha iyi gören göz etkilenmişti. En sık travma tipinin dokuz olguda (%34.6) olmak üzere çeşitli objelerle gelişen künt travma olduğu görüldü. Ayrışma bütün olgularda greft ile alıcı bileşkesinde gelişmişti. Ay-rışma genişliği ortalama 135.4°±57.6° idi. Kristalin lens veya göz içi lens hasar oranı %42.3 olarak bulundu. Cerrahi sonrası medyan takip süresi 36 aydı. On üç (%50) hastada greft saydam kalırken, 13 hastada (%50) greft yetmezliği/greft reddi gelişmişti. Sonuç görme keskinliği 20/200 üzerinde olan hasta sayısı 13 (%50) idi.TARTIŞMA: Travmatik yara ayrışması PK sonrası en sık birinci yılda olmak üzere herhangi bir zamanda gelişebilir. Diğer gözde görme azlığı önemli bir risk faktörü olarak gözükmektedir. Arka segmenti hasarı gibi önemli komplikasyonu olmayan hastalarda görsel sonuçlar ve greft sağkalımı olumludur.

Anahtar sözcükler: Görsel prognoz; greft sağkalımı; penetran keratoplasti; travmatik yara ayrışması.

Ulus Travma Acil Cerrahi Derg 2014;20(3):181-188 doi: 10.5505/tjtes.2014.36589

KLİNİK ÇALIŞMA - ÖZET

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Comparison of intramedullary nail and plate fixation in distal tibia diaphyseal fractures close to the mortiseUmut Yavuz, M.D., Sami Sökücü, M.D., Bilal Demir, M.D., Timur Yıldırım, M.D., Çağrı Özcan, M.D., Yavuz Selim Kabukçuoğlu, M.D.

DepartmentofOrthopaedicsandTraumatology,MSBaltalimaniBoneDiseasesTrainingandResearchHospital,Istanbul

ABSTRACTBACKGROUND: In this study, we aimed to compare the functional and radiological results of intramedullary nailing and plate fixa-tion techniques in the surgical treatment of distal tibia diaphyseal fractures close to the ankle joint.

METHODS: Between 2005 and 2011, 55 patients (32 males, 23 females; mean age 42 years; range 15 to 72 years) who were treated with intramedullary nailing (21 patients) or plate fixation (34 patients) due to distal tibia diaphyseal fracture were included in the study. The average follow-up period was 27.6 months (range, 12-82 months). The patients were evaluated with regard to nonunion, malunion, infection, and implant irritation. The AOFAS (American Orthopaedic Foot and Ankle Society) scale was used for the clinical evaluation.

RESULTS: No statistically significant difference was found between the two surgical methods with respect to unification time, AO-FAS score, accompanying fibula fracture, material irritation, and malunion. Nine patients had open fractures, and these patients were treated with plate fixation (p=0.100). Nonunion developed in three patients who were treated with plates. Infection occurred in one patient. Anterior knee pain was significantly higher in patients who were treated with intramedullary nails. There was no malunion in any patient.

CONCLUSION: As the distal fragment is not long enough, plate fixation technique is usually preferred in the treatment of distal tibia diaphyseal fractures. In this study, we observed that if the surgical guidelines are followed carefully, intramedullary nailing is an ap-propriate technique in this kind of fracture. The malunion rates are not significantly increased, and it also has the advantages of being a minimally invasive surgery with fewer wound problems.

Key words: AOFAS; distal tibia fracture; intramedullary nail; plate.

cations reporting higher rates of anterior knee pain occur-ring after nailing.[4-6] Although plate fixation is preferred more in distal tibia fractures close to the joint, infection, wound problems and implant-related problems are more common in patients treated with plate.[1,2,7,8]

In this study, we aimed to compare the functional and radio-graphic results of distal tibia shaft fractures treated with plate fixation or intramedullary nail.

MATERIALS AND METHODS

Fifty-five patients (32 males, 23 females) who presented to our hospital with distal tibia shaft fractures and underwent surgical treatment were evaluated retrospectively between 2005 and 2011. The mean follow-up period was 27.6 months (range, 12-82 months). The mean age of the patients was 42 years (range, 15-72 years). Twenty-one (38%) patients were treated with intramedullary nailing technique and 34 (62%) were treated with plate fixation. Orthopaedic Trauma As-sociation (OTA) staging was performed before the surgery in all patients. Patients were evaluated with respect to age, time to surgery, fracture type, sagittal and coronal alignment, AO-

O R I G I N A L A R T I C L E

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Address for correspondence: Umut Yavuz, M.D.

Baltalimanı Kemik Hastalıkları Eğitim ve Araştırma Hastanesi, Rumelihisarı Caddesi, No: 62, Sarıyer, İstanbul, Turkey

Tel: +90 212 - 323 70 75 E-mail: [email protected]

Qucik Response Code Ulus Travma Acil Cerrahi Derg2014;20(3):189-193doi: 10.5505/tjtes.2014.92972

Copyright 2014TJTES

INTRODUCTION

Surgical treatment of displaced distal tibia fractures provides appropriate alignment and stability as well as protection of bone and surrounding soft tissues. It also allows early mo-bilization of nearby joints. Intramedullary nailing and plate fixation have been accepted as two effective options in the surgical treatment. Intramedullary nailing has been accepted as the standard treatment in displaced tibia shaft fractures. However, it is difficult to achieve alignment with intramedul-lary fixation in proximal and distal shaft fractures, which leads to increasing rates of malalignment.[1-3] There are also publi-

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Yavuz et al. Comparison of intramedullary nail and plate fixation in distal tibia diaphyseal fractures close to the mortise

FAS hindfoot-ankle score, infection, anterior knee pain, and implant problems. Patients with fractures in the proximal me-taphyseal tibia, distal tibia fractures extending into the joint line, knee ligament injury, fractures with soft tissue coverage, fractures with vascular injury, and pathological fractures were excluded from the study.

A transpatellar approach was preferred for intramedullary nailing. After intramedullary reaming, a nail of appropriate diameter was used. Open reduction was not applied in any of the patients. As the fracture was too distal, two parallel locking screws were inserted in the distal side of the nail. A medial longitudinal approach was used on the medial mal-leolus for plate fixation. Stainless steel or titanium plates were implanted. Intravenous antibiotic prophylaxis was used pre- and postoperatively for three days, and first-generation cephalosporin was preferred.

The measurements were taken from radiographs obtained in the pre-operative, early postoperative and the last follow-up periods. The distance from the distal-most point of the frac-ture line to the ankle joint was measured in millimeters. The fracture was accepted as unified if unification was observed in at least three planes. If unification was not observed at the end of the sixth month, it was accepted as non-union. The criteria for malunion were angulation of more than 5° and translation of more than 5 millimeters.

The American Orthopedic Foot and Ankle Society (AOFAS) foot and ankle scoring system was used to evaluate the clini-cal results related with the ankle joint.

Statistical analysis was made using a computer software pro-gram, the Statistical Package for the Social Sciences (SPSS) ver. 13. For parametric measurements, Mann-Whitney U test was used, and for non-parametric measurements, chi-square test was used. A value of p<0.05 was accepted to indicate statistical significance.

RESULTS

Fifty-five patients with distal tibia fractures who were treated with intramedullary nailing or plate fixation were evaluated. The mean age was 42 years (range, 15-72 years). According to the OTA classification, 33 (60%) patients were classified as 42-A1, 11 (20%) as 42-A2 and 11 (20%) as 42-A3. The patient groups were homogeneous with regard to age, gender and fracture classification.

Nine of the patients had an open fracture. According to Gustilo-Anderson classification, 7 patients were type 1 and 2 patients were type 2; none of the patients was type 3. Six of the patients were treated by plate fixation and three by intramedullary nailing.

The mean distance between the joint and fracture line was 72.9 mm (range, 42-89 mm) in the patients treated by in-tramedullary nailing and 56.5 mm (range 33-90 mm) in the patients treated by plate fixation. The two groups were con-sidered statistically homogeneous (p=0.188).

The mean time to surgery was 4.5 days (range, 1-15 days) in the patients treated by intramedullary nailing and 4.8 days

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Table 1. Demographic data of the patients

Nail Plate Total

N % N % N %

Male 13 23.6 19 34.6 32 58.2

Female 8 14.5 15 27.3 23 41.8

Age (range) 38 17-67 44 15-72 42 15-72

Follow-up (months) 27 12-82 27.9 12-78 27.6 12-82

OTA classification

42-A 18 32.8 29 52.8 47 85.6

42-B 2 3.6 3 5.4 5 9

42-C 1 1.8 2 3.6 3 5.4

Mean distance to 72.9 42-89 56.5 33-90 62.7 33-90

mortise (mm) (range)

Open fracture 3 5.4 6 10.8 9 16.2

Fibula fracture 14 25.4 26 47.3 40 72.7

Fibula fixation 3 5.4 12 21.8 15 27.2

Time to operation (day) 4.5 1-15 4.8 1-17 4.7 1-17

OTA: Orthopaedic Trauma Association.

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(range, 1-17 days) in those treated by plate fixation, and there was no significant difference between the groups (p=0.760). The mean union time was 5.3 months (2-12 months) for all patients, 4.9 months for the intramedullary nailing group, and 5.5 months for the plate fixation group, and there was no significant difference between the groups (p=0.894).

The AOFAS scoring system was used to evaluate ankle ar-thritis. The mean AOFAS score was 87.8 (range, 55-100). It was 88.3 (range, 71-96) in patients treated by intramedullary nailing and 87.5 (range, 59-100) in patients treated by plate fixation, and there was no significant difference between the groups (p=0.794). Forty of the patients had an accompanying fibula fracture. In 15 of them, the fibular fracture was fixed surgically. Three of them were in the intramedullary nailing group and 12 were in the plate fixation group. There was no significant difference between the patients who did or did not undergo fibular fixation with regard to AOFAS scores (p=0.800). Fibular fixation was applied more often in the

plate fixation group. In one patient, deep venous thromboem-bolism developed three months after the treatment. In four patients, unification delay occurred, and they were treated with open reduction and plate fixation (p=0.010). In one, au-tografting derived from the iliac crest was performed, and unification was observed one year later.

Closed reduction was performed in all patients treated by intramedullary nailing, and open reduction was required in nine of the patients treated by plate fixation. In three of them, there was a delay in unification. One developed infec-tion, considered to be nosocomial. As debridement was per-formed but deemed insufficient, the implants were extracted, and external fixation was performed. At the end of the 20th postoperative month, the infection persisted. Two other pa-tients had an AOFAS score of 76.5 and are able to walk with support. Although nonunion was observed radiologically, the patients refused surgery.

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Table 2. Findings at the final follow-up and the statistical comparison

Nail Plate Total p

Union time (months) 4.9 5.5 5.3 0.894

AOFAS 88.3 (71-96) 88.1 (55-100) 88.2 (55-100) 0.794

Infection 0 3 (%5.4) 3 (%5.4) 0.100

Nonunion 0 3 (%5.4) 3 (%5.4) 0.100

Malunion (Degree)

Valgus 0.84 (0-3.8) 1.67 (0-8.3) 1.36 (0-8.3) 0.484

Varus 1 (0-4.2) 1.31 (0-8) 1.19 (0-8) 0.977

Recurvatum 0.7 (0-6.7) 1.13 (0-10) 0.97 (0-10) 0.450

Procurvatum 0.71 (0-5) 0.84 (0-5.6) 0.79 (0-5.6) 0.846

Material irritation 7 (%12.7) 14 (%25.4) 21 (%38.1) 0.211

Anterior knee pain 14 (%25.4) 0 14 (%25.4) 0.001

Figure 1. (a)Preoperativeradiographsofa35-year-oldmalepatientwithrightdistaldi-aphysealtibiafractureextendingtothemetaphysis,resultingfromafall.(b)Radiographsofthepatientinthefirstyearoffollow-up,afterintramedullarynailing.

(a) (b)

Malunion was determined in 13 patients. Two of them were treated by intramedul-lary nailing and 11 by plate fixation. None of the patients demonstrated malunion with more than 10° angulation. Four pa-tients had valgus and three patients varus deformity, and all of them were in the plate fixation group (p=0.484; p=0.977). Four patients had recurvatum deformity. One of them was treated by intramed-ullary nailing and three by plate fixation (p=0.450). Three patients had procur-vatum deformity. One of these patients was treated by intramedullary nailing and two by plate fixation (0.846). One pa-tient had multiplanar deformity and was treated by plate fixation because it was an isolated tibia fracture.

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In 21 patients, the implants were extracted. Seven of these were intramedullary nails and 14 were plates and screws. One of the extractions was performed due to infection. Ten of the patients who were treated by intramedullary nailing had anterior knee pain. Implant irritation occurred in three of the patients treated by plate fixation.

DISCUSSIONTibial fractures are seen often, and successful results may be achieved with various surgical techniques.[1-3,9] Distal tibia fractures are much more problematic because of the surrounding soft tissues being thinner than the proximal tis-sues and the poor vascularization.[9-13] Furthermore, in these patients, knee and ankle pain is observed more.[4,5] Our aim was to compare the results of intramedullary nailing and plate fixation techniques in the treatment of distal tibia fractures close to the joint.

In the previous studies, it was reported that 47.4% of the pa-tients treated by intramedullary nailing had anterior knee pain.[4,5,14,15] As the etiology is not obviously clear, it is suggested that anterior knee pain may be due to patellar tendon and ret-ropatellar fat pad damage. On the contrary, in another study comparing the parapatellar approach and the transtendinous approach, no difference with regard to anterior knee pain was reported.[18] We used a transpatellar approach in all our pa-tients. In our study, anterior knee pain was in acceptable limits according to the literature, and pain did not affect life or work-ing quality in any of our patients. We suggest that protection of the patellar tendon, appropriate nail length, and correct nail entry point were essential for decreasing the complaints.

Three patients who were treated by plate fixation had AO-FAS scores of ≤70. In the literature, the requirement for secondary surgery in patients treated by plate fixation was reported as 20%, whereas this ratio was reported as 42% in patients treated by intramedullary nailing. In our study, three of our patients required secondary surgery. All of them were in the plate fixation group and had been treated with open reduction. When the results were evaluated, our study also verifies that protecting surrounding soft tissues and ensuring vascularization of the fracture site decrease both the infec-tion risk and the need for secondary surgery.[27,29]

Malalignment, which may occur after the treatment of frac-tures in close proximity to joints, may present with pain in the early postoperative period, and then as arthritis in the late phase because it disrupts the weight distribution of the joint. In patients with more than 5° of malalignment, it is observed that the complaints and degeneration in the ankle are increased,[30] and this is suggested to be the result of in-creased contact at any point of the ankle joint.[30-33] We used the AOFAS scale in order to clinically evaluate the consistent ankle pain and early osteoarthritis in our cases. When the scores of the intramedullary nailing and plate fixation groups

were compared, a statistical significance was found, and the results were good or perfect. When the above-mentioned results were evaluated, it was determined that malalignment up to 10° may be tolerated by the patients, and there was no significant radiological difference between the groups.

Surgical reduction of a fibular fracture accompanying a dis-tal tibia fracture is a related subject. Fibular fixation must be done if syndesmosis tear is present,[1,34] and it is suggested that it may facilitate indirect reduction of the tibia fracture. However, in some studies,[3,34,35] fibular fixation is said to de-lay bone healing. We did not use fibular fixation except for displaced distal fibular fractures, which may cause valgus de-formity. Whether fibular fixation was done or not, no signifi-cant difference was found with regard to bone healing, valgus deformity and AOFAS scores.

When the radiological and functional results were compared in the intramedullary nailing and plate fixation groups, both groups were found to have satisfying results. Evaluation of cost efficiency showed us that, as costs may differ between countries, intramedullary nailing was approximately 30% (range, 0-80%) less expensive. We think that intramedullary nailing instead of minimally invasive plate fixation, in some patients and with proper indication, may be useful in reducing health expenses.

Our study shows that intramedullary nailing in distal tibia di-aphyseal fractures close to the ankle joint has no negative effect on malalignment and stability, and it also ensures more minimally invasive surgery, results in fewer wound problems, aids in earlier mobilization, and is more economical. We thus believe that intramedullary nailing should be considered in the treatment of this kind of fracture.

Conflict of interest: None declared.

REFERENCES1. Im GI, Tae SK. Distal metaphyseal fractures of tibia: a prospective ran-

domized trial of closed reduction and intramedullary nail versus open reduction and plate and screws fixation. J Trauma 2005;59:1219-23; dis-cussion 1223.

2. Janssen KW, Biert J, van Kampen A. Treatment of distal tibial fractures: plate versus nail: a retrospective outcome analysis of matched pairs of pa-tients. Int Orthop 2007;31:709-14.

3. Vallier HA, Le TT, Bedi A. Radiographic and clinical comparisons of distal tibia shaft fractures (4 to 11 cm proximal to the plafond): plating versus intramedullary nailing. J Orthop Trauma 2008;22:307-11.

4. Court-Brown CM, Gustilo T, Shaw AD. Knee pain after intramedul-lary tibial nailing: its incidence, etiology, and outcome. J Orthop Trauma 1997;11:103-5.

5. Larsen LB, Madsen JE, Høiness PR, Øvre S. Should insertion of intra-medullary nails for tibial fractures be with or without reaming? A pro-spective, randomized study with 3.8 years’ follow-up. J Orthop Trauma 2004;18:144-9.

6. Lefaivre KA, Guy P, Chan H, Blachut PA. Long-term follow-up of tib-ial shaft fractures treated with intramedullary nailing. J Orthop Trauma 2008;22:525-9.

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7. Borg T, Larsson S, Lindsjö U. Percutaneous plating of distal tibial frac-tures. Preliminary results in 21 patients. Injury 2004;35:608-14.

8. Joveniaux P, Ohl X, Harisboure A, Berrichi A, Labatut L, Simon P, et al. Distal tibia fractures: management and complications of 101 cases. Int Orthop 2010;34:583-8.

9. Yang SW, Tzeng HM, Chou YJ, Teng HP, Liu HH, Wong CY. Treatment of distal tibial metaphyseal fractures: Plating versus shortened intramed-ullary nailing. Injury 2006;37:531-5.

10. Schmidt AH, Finkemeier CG, Tornetta P III. Treatment of closed tibial fractures. J Bone Joint Surg 2003;85:352-68.

11. Batten RL, Donaldson LJ, Aldridge MJ. Experience with the AO method in the treatment of 142 cases of fresh fracture of the tibial shaft treated in the UK. Injury 1978;10:108-14.

12. Orthopedic Trauma Association. Fracture and dislocation compendium. J Orthop Trauma 1996;10:66-70.

13. Baker SP, O’Neill B, Haddon W Jr, Long WB. The injury severity score: a method for describing patients with multiple injuries and evaluating emergency care. J Trauma 1974;14:187-96.

14. Keating JF, Orfaly R, O’Brien PJ. Knee pain after tibial nailing. J Orthop Trauma 1997;11:10-3.

15. Katsoulis E, Court-Brown C, Giannoudis PV. Incidence and aetiology of anterior knee pain after intramedullary nailing of the femur and tibia. J Bone Joint Surg Br 2006;88:576-80.

16. Gustafsson J, Toksvig-Larsen S, Jonsson K. MRI of the knee after locked unreamed intramedullary nailing of tibia. Chir Organi Mov 2008;91:45-50.

17. Weil YA, Gardner MJ, Boraiah S, Helfet DL, Lorich DG. Anterior knee pain following the lateral parapatellar approach for tibial nailing. Arch Orthop Trauma Surg 2009;129:773-7.

18. Väistö O, Toivanen J, Kannus P, Järvinen M. Anterior knee pain after intramedullary nailing of fractures of the tibial shaft: an eight-year fol-low-up of a prospective, randomized study comparing two different nail-insertion techniques. J Trauma 2008;64:1511-6.

19. Collinge C, Sanders R, DiPasquale T. Treatment of complex tibial peri-articular fractures using percutaneous techniques. Clin Orthop Relat Res 2000;375:69-77.

20. Francois J, Vandeputte G, Verheyden F, Nelen G. Percutaneous plate fixa-tion of fractures of the distal tibia. Acta Orthop Belg 2004;70:148-54.

21. Helfet DL, Shonnard PY, Levine D, Borrelli J Jr. Minimally invasive plate osteosynthesis of distal fractures of the tibia. Injury 1997;28 Suppl 1:A42-8.

22. Mosheiff R, Safran O, Segal D, Liebergall M. The unreamed tibial nail in

the treatment of distal metaphyseal fractures. Injury 1999;30:83-90.23. Dogra AS, Ruiz AL, Thompson NS, Nolan PC. Dia-metaphyseal distal

tibial fractures-treatment with a shortened intramedullary nail: a review of 15 cases. Injury 2000;31:799-804.

24. Freedman EL, Johnson EE. Radiographic analysis of tibial fracture malalignment following intramedullary nailing. Clin Orthop Relat Res 1995;315:25-33.

25. Konrath G, Moed BR, Watson JT, Kaneshiro S, Karges DE, Cramer KE. Intramedullary nailing of unstable diaphyseal fractures of the tibia with distal intraarticular involvement. J Orthop Trauma 1997;11:200-5.

26. Nork SE, Schwartz AK, Agel J, Holt SK, Schrick JL, Winquist RA. In-tramedullary nailing of distal metaphyseal tibial fractures. J Bone Joint Surg Am 2005;87:1213-21.

27. Bhandari M, Guyatt GH, Swiontkowski MF, Schemitsch EH. Treat-ment of open fractures of the shaft of the tibia. J Bone Joint Surg Br 2001;83:62-8.

28. Stegemann P, Lorio M, Soriano R, Bone L. Management protocol for un-reamed interlocking tibial nails for open tibial fractures. J Orthop Trauma 1995;9:117-20.

29. Whorton AM, Henley MB. The role of fixation of the fibula in open frac-tures of the tibial shaft with fractures of the ipsilateral fibula: indications and outcomes. Orthopedics 1998;21:1101-5.

30. Puno RM, Vaughan JJ, Stetten ML, Johnson JR. Long-term effects of tibial angular malunion on the knee and ankle joints. J Orthop Trauma 1991;5:247-54.

31. Milner SA, Davis TR, Muir KR, Greenwood DC, Doherty M. Long-term outcome after tibial shaft fracture: is malunion important? J Bone Joint Surg Am 2002;84-A:971-80.

32. Tarr RR, Resnick CT, Wagner KS, Sarmiento A. Changes in tibiotalar joint contact areas following experimentally induced tibial angular defor-mities. Clin Orthop Relat Res 1985;199:72-80.

33. van der Schoot DK, Den Outer AJ, Bode PJ, Obermann WR, van Vugt AB. Degenerative changes at the knee and ankle related to malunion of tibial fractures. 15-year follow-up of 88 patients. J Bone Joint Surg Br 1996;78:722-5.

34. Vallier HA, Cureton BA, Patterson BM. Randomized, prospective com-parison of plate versus intramedullary nail fixation for distal tibia shaft fractures. J Orthop Trauma 2011;25:736-41.

35. Casstevens C, Le T, Archdeacon MT, Wyrick JD. Management of extra-articular fractures of the distal tibia: intramedullary nailing versus plate fixation. J Am Acad Orthop Surg 2012;20:675-83.

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Mortise yakın distal tibia diafiz kırıklarının tedavisindeintramedüller çivi ve plak tedavisinin karşılaştırılmasıDr. Umut Yavuz, Dr. Sami Sökücü, Dr. Bilal Demir, Dr. Timur Yıldırım, Dr. Çağrı Özcan, Dr. Yavuz Selim KabukçuoğluBaltalimanıKemikHastalıklarıEğitimveAraştırmaHastanesi,OrtopediveTravmatolojiKliniği,İstanbul

AMAÇ: Bu çalışmada ayak bileği eklemine (mortis) yakın distal tibia diafiz kırıklarının tedavisinde intramedüller çivi veya plak tedavisinin fonksiyonel ve radyolojik sonuçlarını karşılaştırmayı amaçladık. GEREÇ VE YÖNTEM: 2005-2011 yılları arasında intramedüller çivi (21 hasta) veya plak (34 hasta) ile tedavi edilen 55 hasta (32 erkek, 23 kadın; orta-lama yaş 42; dağılım 15-72 yıl) çalışmaya alındı. Ortalama takip süresi 27.6 ay (dağılım 12-82 ay) idi. Hastalar kaynamama (nonunion), yanlış kaynama (malunion), enfeksiyon, implant irrtasyonu ve klinik açıdan AOFAS (American Orthopaedic Foot and Ankle Society) skoru ile değerlendirildi.BULGULAR: Kırığın ekleme uzaklığı, kaynama zamanı, AOFAS skoru, ilave fibula kırığı, malunion, materyal irritasyonu açısından istatistiksel fark göz-lenmedi. Hastaların dokuz tanesinde açık kırık mevcuttu ve bu hastalar plak ile tedavi edilmişti (p=0.100). Plak ile tedavi edilen üç hastada kaynamama gelişti. Bir hastada enfeksiyon gelişti. Diz önü ağrısı çivi yapılan hastalarda istatistiksel olarak fazla idi. <10° malunion gelişen hastamız yoktu. Çivi veya plak uygulanan hastalar arasında minimal malunion (13 hasta) açısından karşılaştırıldığında fark yoktu.TARTIŞMA: Distal tibia diafiz kırıklarının tedavisinde distal parça kısa olduğu için genellikle plak tercih edilmektedir. Çalışmamızda cerrahi kurallara dikkat edildiğinde çivi tedavisinin malunionu artırmadığı bununla birlikte kapalı cerrahi ve daha az yara yeri problemi nedeniyle avantajları olduğunu gördük.Anahtar sözcükler: AOFAS; çivi; distal tibia kırığı; plak; sonuçlar.

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A new, simple technique for gradualprimary closure of fasciotomy woundsMustafa Özyurtlu, M.D.,1 Süleyman Altınkaya, M.D.,2

Yahya Baltu, M.D.,2 Güzin Yeşim Özgenel, M.D.2

1DepartmentofPlasticSurgery,BursaSevketYilmazTrainingandResearchHospital,Bursa2DepartmentofPlastic,ReconstructiveandAestheticSurgery,UludagUniversityFacultyofMedicine,Bursa

ABSTRACT

BACKGROUND: The aim of this study was to demonstrate a new, easy and safe technique, which has not been defined in the lit-erature previously, that enables the gradual primary closure of fasciotomy wounds using barbed sutures.

METHODS: The technique was performed on five patients who presented with fasciotomy wounds on both upper and lower ex-tremities, varying in size, observed after compartment syndrome due to different causes. The average width of the defects for which primary closure was planned was 8.8 cm. Following the fasciotomy incision, absorbable barbed sutures were inserted through the dermal tissue around the wound similar to that of a subcuticular closure, but left loose, after which closed dressing was applied. During the clinical follow-up, with the decrease in tissue edema and tightness around the wound, the barbed suture was tightened at bedside every 48-72 hours.

RESULTS: At the end of this gradual closure, all the fasciotomy defects were primarily closed within an average of 8.6 days. All the patients had complete and uncomplicated primary closure with the exception of one with high-voltage electrical burn injury, who developed necrosis in the distal part of the defect, and was treated by secondary healing.

CONCLUSION: The gradual fasciotomy closure technique with barbed suture seems to be an easy, rapid and effective method.

Key words: Barbed sutures; compartment syndrome; fasciotomy wounds; gradual primary closure.

skin thickness, skin graft donor site problems, and possible complications that may be observed in the grafted area in the long-term as a result of unwanted adherences and the need for a secondary operation to fix these problems.[1-4] The impossibility of primary closure in the early period following fasciotomy due to edema or wound tightness and possible long-term complications of skin grafting have led investiga-tors to search for new methods with better outcomes both cosmetically and functionally.

There are various techniques in the literature describing the gradual primary closure of fasciotomy wounds by utilizing the elastic properties of the skin. In almost all of these tech-niques, with the regression of the edema after compartment syndrome, the margins of the wound are brought closer to-gether gradually via a special device until the wound is com-pletely closed. Some of the described methods are techni-cally easy, whereas others are expensive and require special equipment.

In this study, we present a five-case pilot study demonstrating the feasibility of the V-Loc wound closure device (Covidien, Mansfield, MA), which is a barbed suture used routinely for

O R I G I N A L A R T I C L E

Address for correspondence: Mustafa Özyurtlu, M.D.

Mimar Sinan Mahallesi, 16350 Yıldırım, Bursa, Turkey

Tel: +90 224 - 483 67 42 E-mail: [email protected]

Qucik Response Code Ulus Travma Acil Cerrahi Derg2014;20(3):194-198doi: 10.5505/tjtes.2014.54077

Copyright 2014TJTES

INTRODUCTION

Various reconstructive strategies may be performed for the closure of fasciotomy wounds that are secondary to com-partment syndrome. Of these, closure via skin grafts and delayed gradual primary closure are the most commonly em-ployed methods. In the early period, fasciotomy wounds can be closed easily with partial or full-thickness skin grafts. With this method, the risk of wound infection is avoided; how-ever, the long-term outcome may carry some disadvantages. These disadvantages include both cosmetic and functional problems, such as sensory loss in the grafted area, decreased

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surgical closures, as a gradual delayed closure technique for fasciotomy wounds.

MATERIALS AND METHODS

The V-Loc wound closure device was used as the barbed su-ture in this study. This device includes a combination of loop, unidirectional barbed suture and a needle, and is used for the closure of surgical incisions. This product has been designed in order to provide rapid closure and to shorten the opera-tion time by eliminating the need for knot tying during tissue closure through its barbed design. Furthermore, it eliminates the need to knot for anchoring due to the loop design on the back end of the suture. In this study, two absorbable trans-parent 3/0 V-Locs with cutting needles were used in each patient (Fig. 1).

Between December 2011 and May 2013, the V-Loc wound closure device was used in five different fasciotomy wounds, of varying size, occurring after compartment syndrome due to different causes. Demographic characteristics of the pa-tients such as age, gender, affected extremity, and compart-

ment syndrome etiology are shown in Table 1. Placement of the barbed sutures was performed immediately after the fasciotomy in three cases and during the clinical follow-up in two cases. The placement of the device was performed under general anesthesia in all cases.

The first step of placement was the fixation of the barbed suture to the corner of the fasciotomy wound (anchoring). The needle of the suture was first passed through the der-mis, and then through the loop at the back of the suture, and the fixation was completed. Subsequently, the suture was ad-vanced along the opposing wound edges in a horizontal mat-tress fashion (Fig. 2). Again, all needles were passed through the dermis layer. Special attention was taken in the anchoring phase to ensure that healthy parts of the dermal sites were sutured. Passage of the suture through a subcutaneous plane rather than the dermis can lead to the rupture of these tis-sues by the suture since it is softer than the dermis. The suture was advanced, and the needle was finally inserted into the dermis and extracted from the skin. The needle was then passed through the rubber part of the injector piston. This maneuver was done to prevent the barbed part of the su-ture from catching on the rubber part and pulling back. After placement of the V-Loc on the edges of the wound, it was left loose, and an antibacterial closing dressing was applied to the fasciotomy wound. A bedside tightening procedure of the

Table 1. Demographic characteristics of patients and causes of compartment syndrome

Patients Age Gender Extremity with fasciotomy Cause of the compartment syndrome

Case 1 35 Male Upper extremity Electrical burn injury

Case 2 37 Male Lower extremity Blunt trauma

Case 3 30 Female Lower extremity Gunshot trauma

Case 4 39 Male Upper extremity Snake bite injury

Case 5 38 Male Upper extremity Penetrating injury

Figure 1. 3/0cuttingneedleabsorbableV-Locwoundclosurede-vice.Itconsistsofunidirectionalbarbsandloopcombinationthatareplacedbehindthesuture.

Figure 2. Perioperativeviewof theV-LocwoundclosuredeviceadvancementinCase4.Afteranchoring,thesuturewasadvancedalongtheopposingwoundedgesinahorizontalmattressfashion.

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Özyurtlu et al. A new, simple technique for gradual primary closure of fasciotomy wounds

suture was performed at 48-72-hour intervals for as far as the edema would allow. In order to minimize the pain during this tightening procedure, intramuscular analgesia was achieved by

administering Pethidine (Aldolan, Liba, Istanbul, Turkey) to all the cases one-half hour before the tightening. The tightening procedure was continued until the edges met, and when a

Figure 3. (a)ViewofCase1.Fromtoptobottom:Largeopenfasciotomywoundthatoccurredafterhigh-voltageelectricalinjury(day0).Approximatedwoundmargins:notethetissuelossatthelevelofthewrist,whichhealedsecondarilyafterdebridementanddressings.Finalresultinthepostoperativesixthmonth.(b)ViewofCase2.Fromtoptobottom:openfasciotomywoundatthelowerextremity.Two3/0cuttingneedleV-Locwoundclosuredeviceswereappliedtothewoundmargins.Approximatedwoundedgesaftertwotightenings(middlepicture).Notethesyringepistolrubberthatwasplacedtopreventthesuturefrompullingback(Case2,day4).Finalresult(day6).(c) The gradualclosurestagesofCase4.Fromtoptobottom:largefasciotomywoundaftersnakebiteinjury,approximatedwoundmarginsonday4,andendresult(15daysafteropeningfasciotomy).

(a) (b) (c)

Table 2. Size and location of fasciotomy wounds, widths of the wounds to be primarily closed, number of barbed sutures used for each case, total duration of wound closure with V-Loc, total duration of hospitalization, and complications

Patient Wound size Width Number of barbed Time to primary Total duration Complications and location of wound sutures used closure of the of hospital (cm) (cm)* wound **(days) stay (days)

Case 1 15x9 9 2 14 82 3x2 skin necrosis

Case 2 15x10 10 2 10 10 No

Case 3 18x8 8 2 6 33 No

Case 4 21x9 9 2 7 7 No

Case 5 16x8 8 2 6 15 No

Mean 8.8 cm 8.6 days

*: The widest part of the wound planned to be brought together. **: Duration between the placement time of the barbed suture into the wound and the time of complete primary closure.

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total closure was achieved, skin staples were placed on the scar line to support the barbed sutures. Any excess barbed suture protruding from the skin was cut, and the remainder was left in since it was absorbable.

RESULTS

In one case, skin necrosis measuring 3x2 cm was observed in the distal part of the fasciotomy line. The necrosis was removed following total closure and left for secondary heal-ing (Fig. 3a). Complication-free total closure was obtained in all the remaining cases (Figs. 3b, c). Table 2 shows the wound sizes and locations, primary width of the wound to be closed, number of barbed sutures used, total duration required for closure in the V-Loc-applied wounds, and duration of hospital stay for each patient.

The mean duration between the day of suturing on the fas-ciotomy line and the day of complete primary closure was 8.6 days (8-14 days). The duration of hospital stay, on the other hand, differed according to the presence of additional trauma (7-82 days). The mean duration of perioperative V-Loc placement into the fasciotomy wound was approximately 3 minutes. The duration for bringing the wound edges closer in each session was approximately 2 minutes for each patient. No suture-related complication was observed in any of the patients (e.g., suture rupture, suture lock–up, or rupture of tissues by the suture).

DISCUSSIONBarbed suture V-Loc provided complete primary wound clo-sure in the targeted regions of all patients. Only in Case 1, who had fasciotomies in both upper and one lower extremity due to high-voltage electrical burn injury (Fig. 3), in whom barbed sutures were placed only on the upper right extremity, necro-sis was observed in the distal part of the fasciotomy wound following complete closure. Debridement and dressings were performed on the necrotic area, and the wound healed sec-ondarily within 22 days. The long hospitalization of this patient was due to the time needed for the reconstruction of the fasciotomy wounds and burn defects occurring in the remain-ing extremities. The duration of hospitalization for Case 3 was also long due to additional trauma (femur fracture).

There are various studies in the literature describing the gradual primary closure of fasciotomy wounds.[1-12] Some of them included methods that were produced as a result of revising the equipment used in routine surgical practice, while others included techniques using specifically designed devices for dermotraction. The described methods were reported to yield successful outcomes.

With regards to the duration of gradual primary closure of fasciotomy wounds, our results were found to be similar to those of other studies.[1-4] In the series by Taylor et al., Zor-

rilla et al., Medina et al., and Govaert et al., mean delayed closure time was reported as 6.3 - 9.8 days. In our study, the mean duration of closure was found to be 8.6 days.

Our technique was most similar to the ‘approximation with a prepositioned suture’ technique previously described in the literature.[5,11] In that technique, the monofilament su-tures are placed on the edges of the wound, and tightening is performed at intervals in order to bring the edges of the wound together. The technical difference from our technique was that following each tightening procedure, the suture was knotted in order to prevent its pulling back. Rupture or lock-ups of the sutures may be observed during tightening.[4] The presence of this possibility necessitates increased effort and time for each procedure. During the bringing together of the tissues by barbed sutures, the barbs are caught by tissues, thus preventing the sutures from pulling back. This non-pull-ing back property eliminates the need for fixation of the su-ture by knot- tying; therefore, the tightening procedures can be performed faster. A shorter tightening period will be less painful for the patient. There is no need for the suture to be removed after complete closure since it is absorbable, which is another advantage.

In Turkey, the cost of fasciotomy wound closure by STSG (split-thickness skin grafting) surgery is approximately 800 dollars. The cost of gradual wound closure by V-Loc, on the other hand, is approximately 80 dollars for each suture, and depends on the number of sutures used. Assuming that two sutures are used for a patient, gradual primary closure with barbed suture seems more economical than STSG. However, further comparative cost-effective studies with larger sample sizes should be carried out.

In conclusion, the gradual fasciotomy closure technique with barbed suture seems to be an easy, rapid and effective method. It may be applied to fasciotomy defects observed following compartment syndrome due to different causes. However, more attention should be paid in cases with dermal tissue damage, such as that due to burn injuries. Although our results demonstrate that this technique is reliable, fur-ther controlled studies are needed in order to demonstrate its efficacy.

Conflict of interest: None declared.

REFERENCES

1. Medina C, Spears J, Mitra A. The use of an innovative device for wound closure after upper extremity fasciotomy. Hand (N Y) 2008;3:146-51.

2. Taylor RC, Reitsma BJ, Sarazin S, Bell MG. Early results using a dynamic method for delayed primary closure of fasciotomy wounds. J Am Coll Surg 2003;197:872-8.

3. Zorrilla P, Marín A, Gómez LA, Salido JA. Shoelace technique for grad-ual closure of fasciotomy wounds. J Trauma 2005;59:1515-7.

4. Govaert GA, van Helden S. Ty-raps in trauma: a novel closing technique

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of extremity fasciotomy wounds. J Trauma 2010;69:972-5.

5. Chiverton N, Redden JF. A new technique for delayed primary closure of fasciotomy wounds. Injury 2000;31:21-4.

6. Harris I. Gradual closure of fasciotomy wounds using a vessel loop shoe-lace. Injury 1993;24:565-6.

7. Asgari MM, Spinelli HM. The vessel loop shoelace technique for closure of fasciotomy wounds. Ann Plast Surg 2000;44:225-9.

8. Walker T, Gruler M, Ziemer G, Bail DH. The use of a silicon sheet for gradual wound closure after fasciotomy. J Vasc Surg 2012;55:1826-8.

9. Caruso DM, King TJ, Tsujimura RB, Weiland DE, Schiller WR. Prima-ry closure of fasciotomy incisions with a skin-stretching device in patients with burn and trauma. J Burn Care Rehabil 1997;18:125-32.

10. McKenney MG, Nir I, Fee T, Martin L, Lentz K. A simple device for closure of fasciotomy wounds. Am J Surg 1996;172:275-7.

11. Almekinders LC. Tips of the trade #32. Gradual closure of fasciotomy wounds. Orthop Rev 1991;20:82, 84.

12. Harrah J, Gates R, Carl J, Harrah JD. A simpler, less expensive technique for delayed primary closure of fasciotomies. Am J Surg 2000;180:55-7.

Özyurtlu et al. A new, simple technique for gradual primary closure of fasciotomy wounds

OLGU SUNUMU

Fasyotomi defektlerinin aşamalı primer kapatılmasında yeni ve basit bir yöntemDr. Mustafa Özyurtlu,1 Dr. Süleyman Altınkaya,2 Dr. Yahya Baltu,2 Dr. Güzin Yeşim Özgenel2

1BursaŞevketYılmazEğitimveAraştırmaHastanesi,PlastikCerrahiKliniği,Bursa2UludağÜniversitesiTıpFakültesi,PlastikveRekonstrüktifCerrahiAnabilimDalı,Bursa

AMAÇ: Bu çalışmanın amacı, kancalı (barbed) dikişler kullanılarak fasyotomi defektlerinin aşamalı olarak primer kapatılmasına olanak sağlayan ve literatürde daha önce tanımlanmayan, yeni, basit ve güvenli bir tekniğin gösterilmesidir.GEREÇ VE YÖNTEM: Teknik beş farklı hastada, çeşitli etiyolojik nedenlere bağlı olarak gelişen kompartman sendromu sonrası açılan hem üst, hem de alt ekstremitelerdeki değişik boyutlardaki fasyotomi defektlerine uygulandı. Hastalarda yaklaştırılarak primer kapatılması planlanan ortalama defekt genişliği 8.8 cm idi. Fasyotomi açılmasını takiben, eriyebilir kancalı dikiş yara kenarlarındaki dermal dokudan subkutiküler kapatmaya benzer şekilde geçirildi ancak gevşek bırakıldı ve kapalı pansumana alındı.BULGULAR: Klinik takipler sırasında doku ödemi ve yara kenarlarındaki gerginliğin azalmaya başlamasıyla birlikte, kancalı dikiş her 48-72 saatte bir yatakbaşı gerim yapıldı ve tüm olgularda aşamalı olarak ortalama 8.6 günde fasyotomi defektlerinin tamamı primer olarak kapatıldı. Yüksek gerilim elektrik yanığı nedeniyle fasyotomi açılan bir hastada defektin distal kısmında meydana gelen ve sekonder iyileşmeyle tedavi edilen nekroz dışında, tüm hastalarda komplikasyonsuz tam primer kapatım sağlandı.TARTIŞMA: Sonuç olarak kancalı dikiş ile aşamalı fasyotomi kapatma yöntemi teknik olarak oldukça basit, hızlı ve etkili bir yöntem gibi görünmek-tedir. Çeşitli etiyolojilere bağlı olarak gelişen kompartman sendromu sonrası açılan fasyotomi defektlerine uygulanabilir.Anahtar sözcükler: Aşamalı primer kapatım; fasyotomi yarası; kancalı dikişler; kompartman sendromu.

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Skafoid psödoartroz tedavisinde otolog kemik grefti vetitanyum başsız kanüllü kompresyon vidasıkombinasyonu uygulama sonuçlarıDr. Güzelali Özdemir,1 Dr. Özgür Çiçekli,2 Dr. Turgut Akgül,3

Dr. Sinan Zehir,4 Dr. Ferit Yücel,5 Dr. Deniz Eşkin2

1KanuniSultanSüleymanEğitimveAraştırmaHastanesi,OrtopediveTravmatolojiKliniği,İstanbul2ŞanlıurfaEğitimveAraştırmaHastanesi,OrtopediveTravmatolojiKliniği,Şanlıurfa3İstanbulÜniversitesiİstanbulTıpFakültesi,OrtopediveTravmatolojiAnabilimDalı,İstanbul4HititÜniversitesiTıpFakültesi,OrtopediveTravmatolojiAnabilimDalı,Çorum5ŞanlıurfaEdessaÖzelHastanesi,Şanlıurfa

ÖZET

AMAÇ: Bu çalışmada skafoid psödoartroz tedavisinde uyguladığımız debridman, otolog iliak kanat kemik grefti ile titanyum başsız kanüle kompresyon vidası kombinasyonunun radyolojik ve klinik sonuçlarını sunmaktır.

GEREÇ VE YÖNTEM: 2009-2012 tarihleri arasında skafoid psödoartroz tanısı ile iliak kanat kemik grefti ve başsız kanüle vida ile ameliyat edilen ve en az 12 aylık takibi olan 24 hastanın 24 el bileği geriye dönük olarak incelendi. Psödoartroz standart çekilen grafiler-de kırık zamanından sekiz hafta geçmesine rağmen kaynama bulgusu olmaması olarak belirlendi. Skafoid kırıkları Herbert sınıflamasına ve anatomik yerleşime göre sınıflandı. Hastalarının klinik değerlendirilmesinde Mayo el bilek skorlaması kullanıldı.

BULGULAR: Herbert sınıflamasına göre 20 hasta D1 ve dört hasta D2, anatomik sınıflamaya göre bir hasta distal, altı hasta proksimal ve 17 hasta gövde kırığı olarak belirlendi. İki hasta haricinde tüm hastalarda tam kaynama ortalama 9.5 (6 ila 15 hafta) haftada sağlandı. Son kontrollerde skafolunat ve radiolunat açıları sırası ile ortalama 32° (39° ile 50°) ve 7° (4° ile 10°) idi. İstatistiksel olarak kaynama ve psödoartroz süreleri arasında bağlantı tespit edildi (p=0.003). Kırık hattı proksimal bölgeye yaklaştıkça kaynama süresi uzamakta idi (p=0.004). Mayo el bilek skoru ortalama 86 (80-95) olarak belirlendi.

SONUÇ: Skafoid psödoartroz tedavisinde volar yaklaşımla iliak kanattan alınan trikortikal otogreft ve başsız kanüle kompresyon vidası kombinasyonu, başarılı kaynama ve fonksiyonel sonuç veren bir yöntemdir.

Anahtar sözcükler: Başsız kompresyon vidası; el bileği volar yaklaşım; otolog iliak kemik grefti; skafoid kaynamama; skafoid psödoartroz.

GİRİŞ

Skafoid kırıkları karpal kemik kırıkları içinde en sık rastlanan kırıklardır ve ortalama görülme sıklığı 23-43/100000 olarak bildirilmektedir.[1] Skafoid kırıkları, sıklıkla el bileğinin hipe-rekstansiyon ve radial deviasyonda iken aksiyel sonrasında

meydana gelmektedir.[2] Tanıda kullanılan standart radyografi incelemelerinde skafoid kırık hattının net olarak belirlene-memesi nedeni ile sıklıkla geç tanı konulmakta veya gözden kaçırılmaktadır. Kırık tanısı konulduktan sonraki ilk tedavi yöntemi, deplase olmamış ve stabil kırıklarda konservatif te-davi yöntemi olan alçı uygulamasıdır.[3,4] Skafoid psödoartrozu; tedavi edilmeyen olgularda, tanısı konulamayan ve konservatif tedaviye rağmen iyileşme meydana gelmeyen hastalarda gelişir.

Literatürde kırık oluşumundan altı hafta sonra tanı konulan ve sekiz haftalık konservatif tedaviye rağmen radyolojik olarak kaynama bulgusu görülmeyen skafoid kırıklarında psödoart-roz gelişme riski bildirilmektedir.[5-7] Psödoartroz veya yanlış kaynama olgularını en aza indirmek için cerrahi endikasyonlar; deplase kırıklar, parçalı kırıklar, proksimal kutup yerleşimli kı-rıklar, tedavisi gecikmiş kırıklar, hasta uyumsuzluğu ve açısal sorunlar olarak bildirilmiştir.[6-8] Psödoartroz gelişme insidan-

K L İ N İ K Ç A L I Ş M A

Sorumlu yazar: Dr. Turgut Akgül,

İstanbul Üniversitesi İstanbul Tıp Fakültesi, Ortopedi ve Travmatoloji

Anabilim Dalı, İstanbul

Tel: +90 212 - 414 20 00 E-posta: [email protected]

Ulus Travma Acil Cerrahi Derg2014;20(3):199-204doi: 10.5505/tjtes.2014.92255

Telif hakkı 2014 TJTES

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Özdemir ve ark. Skafoid psödoartroz tedavisinde otolog kemik grefti ve titanyum başsız kanüllü kompresyon vidası kombinasyonu

sı, hastalarının bir kısmının semptomsuz olarak devam etme-leri nedeni ile tam olarak bilinememektedir. Psödoartroz ge-lişen semptomlu olgularda kronik el bileği ağrıları ve ilerleyici artroz gelişebileceği bildirilmiştir.[5] Psödoartrozın tedavisinde cerrahi gereklilik üzerinde fikir birliği olmakla beraber cerrahi seçenekler açısından fikir birliği bulunmamaktadır. Literatürde vasküler pediküllü greft, otolog kemik greftleri ve çeşitli fik-sasyon yöntemleri ile başarılı sonuçlar bildirilmiştir.[9-16]

Çalışmamızda skafoid psödoartroz olgularında uyguladığımız otolog iliak trikortikal kemik grefti ve başsız tam yivli kompre-sif kanüle vida kombinasyonu cerrahi tedavisinin radyolojik ve klinik sonuçları ile kaynamaya etki eden faktörleri araştırdık.

GEREÇ VE YÖNTEM

Kliniğimizde 2009-2012 tarihleri arasında 35 skafoid psödo-artrozlu hasta ameliyat edildi. Cerrahi tedavisi sırasında tespit materyali olarak K-teli, Herbert vidası kullanılan olgular, iliak kemik grefti haricinde greft kullanılan olgular ile eksizyon veya artrodez uygulanan olgular çalışmaya alınmadı. Çalışmada, ta-kiplerde konservatif tedavi ile kaynama gerçekleşmeyen veya tanısı geç konulduğu için skafoid psödoartroz tanısı konulan ve ameliyat sonrası en az 12 ay takibi olan 24 hasta geriye dönük olarak değerlendirildi.

Çalışmaya alınan hastaların ortalama yaşı 25 (18-36) yıl ve hastaların 23’ü erkek ve biri kadın idi. Travmaya maruz kalan ekstremite, dokuz hastada sağ ve 15 hastada sol taraf idi ve hastaların %50’sinde dominant taraf etkilenmişti. Skafoid kırı-ğına neden olan travmalar 15 hastada basit düşme, altı hastada spor yaralanması ve üç hastada trafik kazası olarak saptandı.

Hastalar ameliyat öncesi standart olarak çekilen el bileği ön-arka, yan ve ulnar deviasyonda ön-arka grafileri ile değerlendi-

rildi. Hastalara ameliyat öncesi bilgisayarlı tomografi (BT) in-celemesi rutin olarak yapıldı. Standart olarak uygulanmamakla beraber çalışmada kemik kollapsının değerlendirilmesi için bazı hastalara manyetik rezonans görüntüleme (MRG) incele-mesi yapıldı. Skafoid kırıkları, Herbert tarafından tarif edilen sınıflamaya ve anatomik yerleşimlerine göre sınıflandırıldı[17] (Şekil 1). Ameliyat sonrası takipler standart radyografiler ile yapıldı. Hastaların radyolojik kaynama kriterleri kırık hattında radyolüsensi görülmemesi, psödoartroz hattının kaybolması, kırık hattını geçen trabekülasyonun varlığı ve implant yetmez-liği olmaması olarak belirlendi.[18,19]

Bütün hastalar aynı standart cerrahi prosedür ile tedavi edildi. Russe tarafından tarif edilen volar yaklaşım ile skafoid psö-doartroz bölgesine ulaşıldı.[20] Psödoartroz hattında küret ve yüksek devirli burr yardımı ile debridman uygulandı (Şekil 2a). Debridman sonrası kalan boşluğa iliak kanattan alınan tri-kortikal greft kambur deformitesini engelleyecek ve skafoid uzunluğunu sağlayacak şekilde yerleştirildi. Takiben floroskopi kontrolünde başsız tam yivli kompresif kanüle vida [Acutrak, Acumed, USA] için K-teli yerleştirildi. Bir adet K-teli daha yerleştirilerek oluşabilecek rotasyon deformitesi engellendi (Şekil 2b). Ardından k-teli üzerinden drilleme yapılarak komp-resyon yapacak şekilde vida yerleştirildi.

Ameliyattan sonra hastalara başparmağı içine alan kısa kol alçı yapıldı. Üç hafta sonra alçı çıkarıldı ve splint uygulaması ile el bileği egzersizleri başlandı. Klinik değerlendirme Mayo el bilek skorlaması ile yapıldı.[21]

İstatistiksel değerlendirmede “SPSS for Windows 15.0” is-tatistik paket programı kullanıldı. Verilerin değerlendirilmesi ise Ki-kare ve Kaplan-Meier testleri ile yapıldı. P<0.05 değeri istatistiksel olarak anlamlı kabul edildi.

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Şekil 1. SkafoidkırıklarınınHerbertsınıflaması.

TipA

A2

A1

TipB4

TipB1

TipC TipD1 TipD2

TipB2 TipB3

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Şekil 2. (a)Elbileğivolaryaklaşımileberaberskafoidpsödoartrozsahasıvedebridmansonrasıskafoidinklinikgörünümü.(b)CerrahitedavisırasındatrikortikalgreftkullanılmasınınardındanantirotasyonK-telivebaşsıztamyivlikompresifkanülevidasınınfloroskopidegörünümü.

(a) (b)

Şekil 3. Yirmibiryaşındaerkekhastabirsenedirelbileğindeağrışikayetiiletarafımızabaşvurdu.Skafoidpsödoartroztanısıileiliakkanattrikortikalotogrefonajvetamyivlibaşsızkompresyonvidasıkombinasyonuyöntemiyleameliyatedildi.Ameliyatöncesiçekilenelbileğiön-arka(a),elbileğilateral(b)grafileriilebera-beroperasyonöncesiçekilenmanyetikrezonansgörüntülemekesitleri(c)kaynamasonrasındaikincisenekontrolündeçekilenelbileğiulnardeviasyondaön-arka(d)lateral(e)grafielbileğibilgisayarlıtomografi(f) görüntüleribulunmaktadır.

(a)

(c)

(e) (f)

(d)

(b)

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BULGULAR

Hastaların kırık oluşumundan ameliyat olmalarına kadar geçen süre ortalama 10 ay (3 ay ile 24 ay) olarak bulundu. Ameliyat sonrası ortalama takip süresi 13 ay (12 ay ile 38 ay) olarak saptandı.

Skafoid kırıklarının anatomik bölgelerine göre sınıflamasında bir distal, altı proksimal ve on yedi orta skafoid kırığı saptandı. Herbert sınıflamasına göre ise kırıkların yerleşimi 20 hastada D1 ve dört hastada D2 olarak belirlendi.

Ameliyat edilen 24 skafoid psödoartoz kırığının 22’sinde tam kaynama belirlendi. Kırık kaynama süresi ortalama 9.5 hafta (6 hafta ile 15 hafta) olarak tespit edildi. İki hastada kaynama tespit edilmedi, bu hastalarda kırığın yerleşim bölgesi skafoid proksimal kutup idi. Bu hastalarda ağrı şikayetlerinin devam etmesi üzerine skafoid eksizyonu yapıldı.

İstatistiksel olarak ameliyat öncesi geçen psödoartroz süresi ile kırık kaynama süreleri arasında uyumlu bir ilişki saptadık.

İstatistiksel olarak kırık oluşma zamanı ile psödoartroz cerra-hisi arasındaki zamanda 12 aydan fazla uzama ile kaynama za-manının artışı arasında paralellik saptandı (p=0.003) (Şekil 4). Bununla beraber proksimal yerleşimli kırıklarda istatistiksel anlamlı olarak kaynama süresi daha uzun bulundu (p=0.004). Yaş ile kaynama zamanı arasında anlamlı istatistiksel bağlantı saptanmadı (Şekil 5).

Hastaların kaynama sonrası son kontrollerinde çekilen grafile-rinde skafolunat açı ortalaması 42° (39°-50°) olarak ölçüldü. Aynı radyografilerde radiolunat açı ortalaması ise 7° (4°-10°) olarak belirlendi.

Hastaların fonksiyonel ve klinik ölçümleri Mayo klinik skorla-masına göre ortalama 86 (80-95) olarak saptandı. Bu sonuca göre 6 hastada mükemmel ve 18 hastada iyi sonuç saptandı. Bütün hastalar kırık kaynaması sonrası aktif hayatlarına geri döndü.

Hastaların hiç birinde ameliyat sonrası enfeksiyon görülmedi. Üç hastada fizik tedavi uygulamaları ve medikal terapi ile teda-vi edilebilen Sudeck atrofisi görüldü.

TARTIŞMA

Skafoid psödoartroz olgularının prognozu, semptomsuz has-taların varlığı nedeni ile kesin olarak bilinememektedir. Semp-tomlu olan skafoid psödoartrozlarının skafoid kollapsına ve el bilek artrozuna neden olabileceği bildirilmiştir.[6-22] Bununla beraber birçok çalışma skafoid psödoartrozu sonrasında el bileği artrozuna neden olacak prognostik faktörleri belirle-yememiştir.[5,7,10] Semptomlu skafoid psödoartoz olgularında, kalıcı sakatlıkları engellemek için tedavi büyük önem kazan-maktadır. Skafoid psödoartroz cerrahi tedavisinde, avasküler dokuların uzaklaştırılması ve greftleme tedavinin esasını oluş-turmaktadır.

Literatürde birçok çalışmada skafoid psödoartroz tedavisinde uygulanan greftleme yöntemleri bildirilmiştir. Fisk, radial kama greft kullanarak interkarpal K-teli uyguladıkları transfiksasyon tekniği ile kaynama sağlandığını göstermiştir.[11] Stark ve ark. iliak kanattan alınan kemik grefti ve K-teli fiksasyonu ile %97 kaynama bildirmiştir.[12] Fernandez literatürde daha önceden Fisk tarafından tarif edilen yöntemi revize ederek iliak kanat-tan alınan greft ile skafoid uzunluğunu sağlamıştır. Bu çalışma-da k-teli ile fiksasyon kullanılmasına rağmen %100 kaynama ile başarılı sonuç bildirmiştir.[9]

Zaidemberg ve ark. skafoid psödoartroz olgularında radial bi-rinci ve ikinci dorsal kompartman arterini kullanarak aldıkları vaskülarize kemik greftini kullandıkları 22 skafoid psödoart-rozlu olgu çalışmasında tam kaynama bildirmişlerdir.[13] Vaskü-larize kemik grefti kullanımı skafoid psödoartroz hastalarında uygulanan ve başarılı sonuçlar alınabilen bir yöntemdir ancak cerrahinin güçlüğü ve sık kullanılmaması nedeniyle diğer tek-niklere üstünlüğü kanıtlanamamıştır. Son yıllarda vaskülarize

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Şekil 4. Ameliyatöncesigeçensüreilekırıkkaynamasıarasındakiilişkidiyagramı.

45

35

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15

5

10

01 3 5 7 9 11 13 15 17 19 21 23

Kaynamasüresi(hafta)

Şekil 5. Hastayaşıilekaynamasüresinikarşılaştırandiyagram.

45

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Yaş Kaynamasüresi

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kemik grefti kullanılarak farklı cerrahi yaklaşımlar tarif edil-mekle beraber standart uygulama halini alamamıştır.[10,14-16]

Hastalarımızın tamamında iliak kanattan alınan trikortikal kama kortikospongioz greft kullandık. Hastalarımızın %90’dan fazlasında kırık kaynaması tam olarak gerçekleştiği ve hörgüç deformitesinin düzelmiş olduğunu gördük. Skafoid kırıkla-rının cerrahisinde günümüzde kabul edilen görüş kompres-yon yapan vidalarının kullanımıdır. Literatürde, Stark ve ark. ile Fernandez skafoid psödoartroz tedavisinde fiksasyon için kullandıkları K-teli ile yetersiz fiksasyon ve redüksiyon kaybı sorunları ile karşılaştıklarını bildirmişlerdir.[9,12] Herbert 1984 yılında kendisi tarafından tarif edilen iki ucu yivli kompres-yon vidası ile başarılı sonuçlar bildirmiştir.[17] Whipple, Her-bert tarafından tarif edilen vidanın kanüllü hale getirilmesini sağlamış ve Herbert ile benzer yüksek başarılı klinik sonuçlar yayınlamıştır.[23] Literatürde Herbert vidası ile başarılı sonuç-lar bildiren klinik çalışmalar bulunmakla beraber biyomekanik çalışmalar standart kanüllü vidaların biyomekanik olarak daha üstün olduğu bildirilmiştir.[16,18,23-28] Son çalışmalarda, başsız tam yivli kompresif vidaların Herbert vidasına göre biyomeka-nik olarak daha stabil ve kırık hattına daha fazla kompresyon yapabildiği gösterilmiştir.[27,28] Bununla beraber biyomekanik çalışmalarda ortaya konulan bu fark klinik çalışmalar ile korele edilememiştir ve iki tür vidayı karşılaştıran çalışmalarda kay-nama ve fonksiyonel sonuçlar arasında fark bulunamamıştır.[29-31] Psödoartroz olgularında başsız tam yivli kanüle vida hem stabilite hem de kompresyon açısından başarılı bir seçenek olarak bildirilmektedir. Çalışmamızda greftleme yaptığımız skafoid psödoartroz olgularında fiksasyon için Acutrak tam yivli başsız kompresif vida kullandık. Yeterli stabilizasyon ve kompresyonun sağlandığını ve kontrol radyografilerinde vida etrafında radyolüsen görüntü olmadığını, gevşeme olmadığını saptadık. Uygun vida uzunluğu ve başsız vida kullanımının olası komplikasyonları da azalttığını düşünmekteyiz.

Skafoid psödoartozu beş yıldan uzun olan olgularda kaynama oranın düşük olduğu ve artritik değişikliklerin varlığının kay-namayı olumsuz yönde etkilediği çalışmalar da gösterilmiştir.[5,32] Trumble ve ark. yaptıkları çalışmada ileri derecede ska-foid kollaps görülmesi halinde greftleme ile başarılı sonuçlar alınamayacağını, eksizyon veya artrodez seçeneklerinin daha uygun olacağını bildirmişlerdir.[24] Bizim olgularımızda, has-talarda artritik değişiklikler standart el bileği grafileri ve BT kullanılarak değerlendirildi. Çalışmaya aldığımız hastaların hiç birinde artroz bulguları yoktu ve psödoartroz süresinin uzaması ile kaynama süresinin uzaması arasında istatistiksel olarak anlamlı paralellik saptadık. Kırık oluşumu ile cerrahi uygulama arasındaki zaman uzadıkça kaynama süresinin uza-dığını belirledik.

Literatürde yapılan birçok çalışmada skafoid psödoartroz cer-rahisi sonrasında kaynama sağlanması ile beraber fonksiyonel sonuçlarda belirgin iyileşme bildirilmiştir.[18,24,31,33-35] Çalışma-mızda, kaynama gerçekleşen 22/24 hastanın klinik değerlen-

dirilmesinde kullanılan Mayo el bilek skorlamasına göre hasta-larda iyi ve mükemmel sonuçlar alındı.

Çalışmamızda proksimal kutup yerleşimli skafoid psödoart-rozlarında kaynama elde edemedik. Robbins ve ark., bu kırık-larda volar yaklaşımın yetersiz kalacağını, yeterli debridmanın yapılamayacağını ve dorsal yaklaşımın bu bölge kırıklarında daha uygun olduğunu bildirmiştir.[36] Zaidemberg ve ark. ile Yuceturk ve ark., proksimal kutup kırıklarında dorsalden yer-leştirilecek vasküler pediküllü greftler ile başarılı sonuçların elde edilebileceğini bildirmişlerdir.[13,14] Çalışmamızda yapılan istatistiksel değerlendirme sonucunda proksimal yerleşimli kırıklarda kaynama süresinin anlamlı olarak daha uzun olduğu tespit edilmiştir.

Skafoid psödoartrozu tedavisinde volar yaklaşımla iliak kanat-tan alınan trikortikal otogreft ve başsız tam yivli kanüle komp-resif vida kombinasyonu, yüksek oranda kaynama ve başarılı fonksiyonel sonuçlar veren bir yöntemdir.

Çıkar örtüşmesi: Çıkar örtüşmesi bulunmadığı belirtilmiştir.

KAYNAKLAR

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2. Weber ER. Biomechanical implications of scaphoid waist fractures. Clin Orthop Relat Res 1980;149:83-9.

3. Terkelsen CJ, Jepsen JM. Treatment of scaphoid fractures with a remov-able cast. Acta Orthop Scand 1988;59:452-3.

4. Gellman H, Caputo RJ, Carter V, Aboulafia A, McKay M. Comparison of short and long thumb-spica casts for non-displaced fractures of the carpal scaphoid. J Bone Joint Surg Am 1989;71:354-7.

5. Gelberman RH, Wolock BS, Siegel DB. Fractures and non-unions of the carpal scaphoid. J Bone Joint Surg Am 1989;71:1560-5.

6. Amadio PC, Berquist TH, Smith DK, Ilstrup DM, Cooney WP 3rd, Linscheid RL. Scaphoid malunion. J Hand Surg Am 1989;14:679-87.

7. Trumble TE, Salas P, Barthel T, Robert KQ 3rd. Management of scaph-oid nonunions. J Am Acad Orthop Surg 2003;11:380-91.

8. Bain GI, Bennett JD, Richards RS, Slethaug GP, Roth JH. Longitudinal computed tomography of the scaphoid: a new technique. Skeletal Radiol 1995;24:271-3.

9. Fernandez DL. A technique for anterior wedge-shaped grafts for scaph-oid nonunions with carpal instability. J Hand Surg Am 1984;9:733-7.

10. Buijze GA, Ochtman L, Ring D. Management of scaphoid nonunion. J Hand Surg Am 2012;37:1095-100; quiz 1101.

11. Fisk GR. An overview of injuries of the wrist. Clin Orthop Relat Res 1980;149:137-44.

12. Stark HH, Rickard TA, Zemel NP, Ashworth CR. Treatment of un-united fractures of the scaphoid by iliac bone grafts and Kirschner-wire fixation. J Bone Joint Surg Am 1988;70:982-91.

13. Zaidemberg C, Siebert JW, Angrigiani C. A new vascularized bone graft for scaphoid nonunion. J Hand Surg Am 1991;16:474-8.

14. Yuceturk A, Isiklar ZU, Tuncay C, Tandogan R. Treatment of scaphoid nonunions with a vascularized bone graft based on the first dorsal meta-carpal artery. J Hand Surg Br 1997;22:425-7.

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15. Hamdi MF, Amara K, Tarhouni L, Baccari S. Nonunion of the scaphoid treated by anterior vascularized bone graft: a review of 26 cases. Chin J Traumatol 2011;14:205-8.

16. Jones DB Jr, Bürger H, Bishop AT, Shin AY. Treatment of scaphoid waist nonunions with an avascular proximal pole and carpal collapse. Surgical technique. J Bone Joint Surg Am 2009;91 Suppl 2:169-83.

17. Herbert TJ, Fisher WE. Management of the fractured scaphoid using a new bone screw. J Bone Joint Surg Br 1984;66:114-23.

18. Rajagopalan BM, Squire DS, Samuels LO. Results of Herbert-screw fix-ation with bone-grafting for the treatment of nonunion of the scaphoid. J Bone Joint Surg Am 1999;81:48-52.

19. Dias JJ. Definition of union after acute fracture and surgery for fracture nonunion of the scaphoid. J Hand Surg Br 2001;26:321-5.

20. RUSSE O. Fracture of the carpal navicular. Diagnosis, non-operative treat-ment, and operative treatment. J Bone Joint Surg Am 1960;42:759-68.

21. MacDermid JC, Turgeon T, Richards RS, Beadle M, Roth JH. Patient rating of wrist pain and disability: a reliable and valid measurement tool. J Orthop Trauma 1998;12:577-86.

22. Düppe H, Johnell O, Lundborg G, Karlsson M, Redlund-Johnell I. Long-term results of fracture of the scaphoid. A follow-up study of more than thirty years. J Bone Joint Surg Am 1994;76:249-52.

23. Whipple TL. Stabilization of the fractured scaphoid under arthroscopic control. Orthop Clin North Am 1995;26:749-54.

24. Trumble TE, Clarke T, Kreder HJ. Non-union of the scaphoid. Treat-ment with cannulated screws compared with treatment with Herbert screws. J Bone Joint Surg Am 1996;78:1829-37.

25. Daly K, Gill P, Magnussen PA, Simonis RB. Established nonunion of the scaphoid treated by volar wedge grafting and Herbert screw fixation. J Bone Joint Surg Br 1996;78:530-4.

26. Shaw JA. A biomechanical comparison of scaphoid screws. J Hand Surg

Am 1987;12:347-53.27. Baran O, Sagol E, OXaz H, Sarikanat M, Havitcioglu H. A biomechani-

cal study on preloaded compression eVect on headless screws. Arch Or-thop Trauma Surg 2009;129:1601-5.

28. Wheeler DL, McLoughlin SW. Biomechanical assessment of compres-sion screws. Clin Orthop Relat Res 1998;350:237-45.

29. Trumble TE, Gilbert M, Murray LW, Smith J, Rafijah G, McCallister WV. Displaced scaphoid fractures treated with open reduction and inter-nal fixation with a cannulated screw. J Bone Joint Surg Am 2000;82:633-41.

30. Gregory JJ, Mohil RS, Ng AB, Warner JG, Hodgson SP. Comparison of Herbert and Acutrak screws in the treatment of scaphoid non-union and delayed union. Acta Orthop Belg 2008;74:761-5.

31. Gereli A, Nalbantoglu U, Sener IU, Kocaoglu B, Turkmen M. Compari-son of headless screws used in the treatment of proximal nonunion of scaphoid bone. Int Orthop 2011;35:1031-5.

32. Inaparthy PK, Nicholl JE. Treatment of delayed/nonunion of scaphoid waist with Synthes cannulated scaphoid screw and bone graft. Hand (N Y) 2008;3:292-6.

33. Kömürcü M, Basbozkurt M, Gur E. Surgical treatment results in scaph-oid nonunion. J South Orthop Assoc 2001;10:215-20.

34. Akmaz I, Kiral A, Pehlivan O, Mahirogullari M, Solakoglu C, Rodop O. Biodegradable implants in the treatment of scaphoid nonunions. Int Orthop 2004;28:261-6.

35. Matsuki H, Ishikawa J, Iwasaki N, Uchiyama S, Minami A, Kato H. Non-vascularized bone graft with Herbert-type screw fixation for proxi-mal pole scaphoid nonunion. J Orthop Sci 2011;16:749-55.

36. Robbins RR, Ridge O, Carter PR. Iliac crest bone grafting and Herbert screw fixation of nonunions of the scaphoid with avascular proximal poles. J Hand Surg Am 1995;20:818-31.

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OLGU SUNUMU

The results of autologous bone graft and titanium headless cannulated compressionscrew for treatment of scaphoid nonunionGüzelali Özdemir, M.D.,1 Özgür Çiçekli, M.D.,2 Turgut Akgül, M.D.,3Sinan Zehir, M.D.,4 Ferit Yücel, M.D.,5 Deniz Eşkin, M.D.2

1DepartmentofOrthopaedicsandTraumatology,KanuniSultanSüleymanTrainingandResearchHospital,Istanbul2DepartmentofOrthopaedicsandTraumatology,ŞanlıurfaTrainingandResearchHospital,Sanliurfa3DepartmentofOrthopaedicsandTraumatology,İstanbulUniversityİstanbulFacultyofMedicine,Istanbul4DepartmentofOrthopaedicsandTraumatology,HititUniversityFacultyofMedicine,Corum5ŞanlıurfaEdessaHospital,Sanliurfa

BACKGROUND: We aimed to present the clinical and radiological results of patients treated with debridement, iliac bone graft and titanium headless compression screw for scaphoid nonunion.METHODS: We retrospectively evaluated 24 patients (23 males, 1 female) who underwent this technique between 2009 and 2012, with a mini-mum of 12 months’ follow-up. Nonunion was determined as no union evidence within eight weeks on radiological view. Scaphoid fracture was classified according to Herbert classification and anatomical location. Functional evaluation was performed using the Mayo wrist scoring system. RESULTS: According to the Herbert classification system, there were 20 D1 and 4 D2 fractures. Anatomical location included 1 distal, 6 proximal and 17 corpus. Fracture union was achieved in all but 2 patients, with a mean union time of 9.5 weeks (6-15). Scapholunate angle and radiolunate angle were measured as a mean 32° (39°-50°) and 7° (4°-10°) at the latest follow-up radiographic examination. There was a statistically significant correlation between the length of the pseudoarthrosis period and union time (p=0.003). Union time of proximal fractures was longer than of the others (p=0.004). Mayo wrist score was 86 (80-95). DISCUSSION: Autologous iliac bone graft and titanium headless cannulated compression screw combination via volar approach is safe and effec-tive for scaphoid nonunion.Key words: Autologous iliac bone graft; headless compression screw; scaphoid nonunion; scaphoid pseudoarthrosis; wrist volar approach.

Ulus Travma Acil Cerrahi Derg 2014;20(3):199-204 doi: 10.5505/tjtes.2014.92255

ORIGINAL ARTICLE - ABSTRACT

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Triangular fibrokartilaj kompleks periferik (Palmer tip 1B) yırtıklarında artroskopik tamir sonuçlarıDr. Fatih Kabakaş,1 Dr. İsmail Bülent Özçelik,1 Dr. Meriç Uğurlar,2

Dr. Berkan Mersa,1 Dr. Memet Yazar,3 Dr. Metin Uzun4

1İst-elElCerrahiMikrocerrahiveRehabilitasyonGrubu,İstanbul2KartalYavuzSelimDevletHastanesi,OrtopediveTravmatolojiKliniği,İstanbul3ŞişliEtfalEğitimveAraştırmaHastanesi,PlastikveRekonstruktifCerrahiKliniği,İstanbul4MaslakAcıbademHastanesi,OrtopediveTravmatolojiKliniği,İstanbul

ÖZET

AMAÇ: Triangular fibrokartilaj kompleks (TFKK) hasarlanması el bileğinin ulnar taraf ağrılarının başlıca nedenidir. Bu çalışmada, artros-kopik olarak onarılan TFKK periferik (Palmer tip 1B) yırtıklarının tedavi sonuçları geriye dönük olarak değerlendirildi.

GEREÇ VE YÖNTEM: TFKK periferik (Palmer tip 1B) yırtığı nedeniyle Şubat 2007-Temmuz 2012 arasında artroskopik tamir uygula-nan 38 hasta (30 erkek, 8 kadın; ortalama yaş 27.6; dağılım: 19-42) değerlendirildi. Değerlendirme Mayo el bileği değerlendirme formu ve ameliyat öncesi, ameliyat sonrası VAS (Görsel analog skala) ile yapıldı.

BULGULAR: Hastaların Mayo el bileği değerlendirme formu ile yapılan değerlendirme sonuçlarına göre 30 hasta mükemmel, sekiz hasta iyi olarak değerlendirildi. Ameliyat öncesi VAS 6.53 (dağılım: 4.5-8.2) ameliyat sonrası VAS 1.48 (dağılım: 0.3-3.1) olarak saptandı.

SONUÇ: Artroskopik teknikle minimal hasarlanma ile TFKK tamiri yapılabilmekte, eklemin tüm yapılarının daha iyi görüntülenmesi ve değerlendirilmesi sağlanabilmektedir. 6R portalin 1 cm altından açılan portalden uygulanan dışarıdan içeriye dikiş tekniği ulnar sinir yüzeyel dalının etkilenme olasılığının olmadığı minimal travmatik yöntemdir. Bu yöntem ile ameliyat öncesi ağrı şikayetlerinin anlamlı olarak giderilmesi mümkündür.

Anahtar sözcükler: Artroskopi; el bileği eklemi; el bileği yaralanmaları; triangular fibrokartilaj kompleks.

GİRİŞ

Triangular fibrokartilaj kompleks (TFKK) distal radioulnar eklem stabilizasyonunda ve el bileği yük aktarımında önemli rol oynar. TFKK hasarlanması el bileği ulnar taraf ağrıları ve distal radioulnar eklem (DRUE) instabilitesinin başlıca neden-lerindendir.[1] Palmer, sınıflamasında tip 1 yırtıkların travma-tik nedenlere bağlı geliştiğini ve tip 1B yırtıkların ulnar taraflı periferal yırtıklar olduğunu tariflenmişdir.[2,3] TFKK’nin peri-ferik kısmının iyi kanlanması nedeni ile TFKK Palmer tip 1B yırtıklarının tamiri iyi sonuçlar vermektedir.[4] Geçmiş yıllarda

TFKK yırtıkları açık teknikler ile tedavi edilirken günümüz-de artroskopik teknikler ile de bu yırtıkların etkin bir şekilde tedavisi yapılabilmektedir. Artroskopik tamirin açık teknikle-re olan üstünlükleri daha iyi bir görüntü elde edilmesi, daha az diseksiyon ile daha az yumuşak dokuya hasar verilmesi ve cerrahi sonrası eklem hareket kısıtlılığının daha az meydana gelmesidir.[5]

Bu çalışmada 6R portalin 1 cm altından açılan ayrı bir portal-den dışarıdan içeriye teknik ile artroskopik tamir yaptığımız TFKK periferik (Palmer tip 1B) yırtıklarında tedavi sonuçları geriye dönük olarak değerlendirildi.

GEREÇ VE YÖNTEM

Triangular fibrokartilaj kompleks periferik (Palmer tip 1B) yırtığı nedeniyle Şubat 2007-Temmuz 2012 arasında dışarıdan içeriye teknik ile artroskopik tamir uygulanan ve ortalama yaşı 27.6 olan 38 hasta (30 erkek, 8 kadın) (dağılım:19-42) değer-lendirildi.

Bütün hastalarda çalışma ve yaşam aktiviteleri sırasında kapa-

K L İ N İ K Ç A L I Ş M A

Sorumlu yazar: Dr. İsmail Bülent Ozcelik,

Turgut Özal Cad. (Millet Cad.), Börekçi Veli Sokak,

No: 6, Kat: 1 Daire: 2, Çapa, Fatih, İstanbul

Tel: +90 212 - 632 81 44 E-posta: [email protected]

Ulus Travma Acil Cerrahi Derg2014;20(3):205-210doi: 10.5505/tjtes.2014.63933

Telif hakkı 2014 TJTES

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Kabakas ve ark. Triangular fibrokartilaj kompleks periferik (Palmer tip 1B) yırtıklarında artroskopik tamir sonuçları

sitelerini etkileyen el bileği ulnar taraf ağrı şikayeti mevcuttu. Fiziksel incelemede hastaların hepsinde el bileği ulnar taraf-ta bası ile ağrı oluşumu ve maksimum ulnar deviasyonda ağrı hissi mevcuttu. Hastaların hiçbirinde eklem hareket kısıtlılığı saptanmadı. Beş hastanın supinasyon ve pronasyon hareket-leri ağrılı idi. Ameliyat öncesinde hastaların hepsine iki yönlü direkt grafi ve manyetik rezonans görüntüleme (MRG) incele-mesi yapılmıştır. MRG incelemesinde hastaların tümünde peri-ferik TFKK yırtığı saptandı. Tüm hastalarda konservatif tedavi ile sonuç alınamayan el bileği kronik ağrısı mevcuttu. Şikayet başlama zamanları ile ameliyat arasında geçen süre ortalama 16.6 (dağılım: 4-52) ay idi. Hastalar poliklinikte görülüp tanı konduktan sonra en az üç hafta fonksiyonel el bileği ateli ile takip edilmiş ve ağrıları devam eden hastalara ameliyat öne-rilmiştir.

Triangular fibrokartilaj kompleks yırtıkları Palmer tarafından tariflenen sınıflama ile sınıflandırıldı.[2,6,7] Palmer tarafından tip 1B olarak tanımlanan periferik meniskal yırtıklar çalışmaya da-hil edildi.

Ameliyat TekniğiHastaların el bileğine 5-8 kg ağırlık ile distraksiyon uygulan-dı. Standart olarak 3-4 ve 6R portaller kullanıldı. Radiokarpal eklemin değerlendirilmesini takiben saptanan yırtık kenarları shaver yardımı ile debride edildi (Şekil 1). Yeşil iğnenin (21G) içine 4/0 prolen sütür halka şeklinde yerleştirildi (Şekil 2). 6R portalin 1 cm altından açılan insizyondan TFKK periferik yırtık kenarına gönderilen bu yeşil iğne ucundaki halka eklem için-de görüntülendi ve 6R portalden sokulan klemp yardımı ile portal dışına alındı (Şekil 3a, b). İçine 4/0 prolen’in tek bir ucu sokulmuş diğer yeşil iğne, aynı şekilde TFKK periferik yırtığına gönderilerek, yine 6R portalden klemp ile portal dışına alındı. Eklem dışına alınan ikinci ip, daha önce dışarı alınan halkanın ortasından geçirildi (Şekil 4a, b). Halka halindeki ip uçlarından çekilerek ikinci ipin ucunun 6R portal altından açılan insizyon-dan dışarı alınması sağlandı (Şekil 5a, b). Gerekli durumlarda aynı teknik ile ikinci sütür konuldu. Bu hazırlıklar tamamlan-dıktan sonra sütürlerin yırtık hattını yeterince stabilize edip etmediği ve trambolin efekti artroskopik olarak kontrol edildi (Şekil 5c). Traksiyon sonlandırılarak el bileği ekstansiyonda ip-

Ulus Travma Acil Cerrahi Derg, Mayıs 2014, Cilt. 20, Sayı. 3206

Şekil 1. Artroskopikyırtıkgörüntülenmesiveshaveriledebridman.

Şekil 2. Yeşil iğnenin(21G) içine4/0prolensütürhalkaşeklindeyerleştirilmesi.

Şekil 3. (a, b) 6Rportalin1cmaltındanaçılaninsiyondanTFKKperiferik yırtık kenarına yeşil iğne gönderilmesi ve 6R portaldensokulanklempyardımıileprolenhalkanındışarıalınması.

(a)

(b)

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Kabakas ve ark. Triangular fibrokartilaj kompleks periferik (Palmer tip 1B) yırtıklarında artroskopik tamir sonuçları

ler düğümlendi (Şekil 6a, b). El bileği 30 derece ekstansiyonda kısa kol alçı atel yapıldı. Altı hafta sonra alçı çıkarılarak fizik tedavi programına başlandı. Ameliyat sonrası ortalama takip süresi ise 11.8 (dağılım: 6-24) aydı. Değerlendirme Mayo el bileği değerlendirme formu ve ameliyat öncesi ile ameliyat sonrası VAS (Görsel Analog Skala) skorlaması ile yapıldı.

BULGULAR Hastaların Mayo el bileği değerlendirme formu ile yapılan de-ğerlendirme sonuçlarına göre 30 hasta mükemmel, sekiz hasta iyi olarak değerlendirildi. Ameliyat öncesi VAS 6.53 (dağılım: 4.5-8.2) ameliyat sonrası VAS 1.48 (dağılım: 0.3-3.1) olarak saptandı. Hastaların hiçbirinde ameliyat öncesi ve sonrası ha-reket kısıtlılığı saptanmamıştır.

TARTIŞMA

Triangular fibrokartilaj kompleks artikuler disk (meniküs), dorsal ve volar radioulnar ligamanlar, ulnar kollateral ligaman ve ekstansör karpi ulnaris (EKU) tendon kılıfından oluşur.[8] TFKK, ulnar arterin dorsal ve palmar radiokarpal arterleri ile anterior interossöz arter yoluyla kanlanır. Menisküs kanlan-ması periferden santrale doğru difüzyon yoluyla sağlanır. Peri-ferik kanlanmanın iyi olması nedeni ile bu bölgedeki yırtıkların tamir sonrası iyileşme şansı yüksektir.[1,9-11]

Triangular fibrokartilaj kompleks; ulnar stiloid, fleksör karpi ulnaris, ulnar baş volar yüzü ve pisiform arasındaki alandan palpe edilebilir. Bu bölgede palpasyon ile ağrı oluşumu “ulnar oluk belirtisi” olarak adlandırılır.[12] Zorlayıcı manevralar yo-luyla el bileği ulnar tarafının daraltılması sonrası ağrı oluşumu da lezyonun tespitinde yararlıdır. Muayenede lunotriquetral ligaman ve DRUE instabilitesinin değerlendirmesi gereklidir.[1] Çalışmamızdaki tüm hastalarda ulnar oluk belirtisi pozitifti ve zorlayıcı manevralarla el bileği ulnar tarafının daraltılması ile ağrı oluşumu mevcuttu.

Manyetik rezonans görüntüleme TFKK değerlendirmesinde önemli bir incelemedir.[13-15] MRG incelemesinde DRUE’de artmış sıvı ile birlikte volar veya dorsal ligaman hasarlanmaları tespiti DRUE instabilite tanısında faydalıdır.

Triangular fibrokartilaj kompleks yırtıklarının cerrahi tedavisi açık ve artroskopik yöntemlerle yapılabilmektedir. Her ne ka-dar açık yöntemlerde[16-18] olduğu kadar artroskopik yöntem-lerde de[10,19-24] iyi sonuçlar bildirilmesine rağmen artroskopik yöntemlerle açık yöntemlere göre eklem hareket açıklığı ile yakalama kuvvetinin artmasının[22] yanı sıra ulnar sinire bağlı oluşan komplikasyonlarında azaldığı bildirilmektedir.[18,19,21] Ay-rıca artroskopi ile yapılan ameliyat sırasında TFKK yırtıklarına eşlik eden diğer eklem içi patolojilerin değerlendirilmesi yapı-labilmektedir.[25]

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Şekil 4. (a, b) İkinciipin6Rportaldenklempiledışarıalınması.

(a) (b)

Şekil 5. (a-c) Halkanınortasındangeçirilenikinciipindiğerucununhalkayardımıile6Raltındanaçılaninsizyondançıkarılmasıvesütüröncesiartroskopikgörünüm.

(a) (b) (c)

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Triangular fibrokartilaj kompleks yırtıklarının artroskopik ta-mirinde içeriden dışarıya, dışarıdan içeriye ve hepsi içeride ol-mak üzere birçok teknik tariflenmiştir.[5,26-31] Bunların arasında dışarıdan içeriye tekniği en sık olarak kullanılan yöntem olup ilk olarak Zachee tarafından tariflenmiştir.[32]

Hermansdorfer ve Kleinman kronik yırtıklar için 11 hastada yaptıkları açık tamir sonuçlarında yakalama kuvvetinin karşı ekstremiteye göre %87 iyileştiğini, %96 oranında fleksiyon ekstansiyon arkının düzeldiğini bildirmiştir.[16] Cooney ve ark. açık tamir yaptıkları 33 hastanın modifiye Mayo el bileği skoru ile değerlendirmesinde 11 mükemmel, 15 iyi, 6 zayıf ve 1 kötü sonuç bildirmiştir.[17] Anderson ve ark. travmatik TFKK yırtı-ğı saptadıkları 38 hastaya artroskopik, 39 hastaya açık tamir ameliyatı uyguladıklarını ve istatistiksel olarak sonuçlarda fark bulmadıklarını bildirmiştir. Açık grupta ulnar sinir duyu dalın-da hasarlanma ve EKU tendinitine bağlı ameliyat sonrası ağrı şikayeti olsa bile bunun istatistiksel olarak belirgin değişiklik yaratmadığını bildirilmiştir.[18] Bu sonuçlar açık teknik ile TFKK tamir sonuçları konusunda iyimser sonuçlar vermekle birlikte

artroskopik teknikle çok önemli stabilizatör role sahip olan EKU tendonunda hasarlanma yaratmadan TFKK tamiri yapıla-bilmekte, eklemin tüm yapılarının daha iyi görüntülenmesi ve değerlendirilmesi sağlanabilmektedir. 6R portalin 1 cm altın-dan açılan portalden uygulanan dışarıdan içeriye dikiş tekniği, ulnar sinir yüzeyel dalının etkilenme olasılığının olmadığı mini-mal travmatik yöntemdir. Hastalarımızın hiçbirinde ulnar sinir duyusal dal hasarlanmasına bağlı duyusal kayıp veya hiperestezi şikayeti saptanmamıştır.

Corso ve ark.nın yaptığı çok merkezli araştırmada periferik TFKK yırtıkları nedeni ile artroskopik tamir yapılan 45 hasta-nın 37 aylık takipleri sonucunda %91 iyi ve mükemmel sonuç aldıklarını bildirilmiştir. Uyguladıkları dışarıdan içeriye tekni-ği ile hastaların tümünün el bileği eklem hareket açıklığının normal aralıklara geldiğini ve hastaların kavrama kuvvetinin karşı tarafa göre %75 olduğunu belirtmişlerdir.[19] Estrella ve ark. TFKK Palmer tip 1B, 1C ve 1D yırtıklarda 35 hastaya uyguladıkları artroskopik tamir sonuçlarının değerlendirilmesi sonucu %74 başarılı sonuç aldıklarını bildirmiştir ve karşı tara-fa göre cerrahi uygulanan tarafın kavrama gücünü %82 olarak bildirmişlerdir.[20] Haugstvedt ve ark. periferik yırtığı nedeni ile artroskopik olarak tedavi edilen 22 hastada %70 iyi ve mü-kemmel sonuç bildirmişlerdir.[23]

Pederzini ve ark. düğümün eklem içine koyulduğu bir dışarı-dan içeriye tekniği tariflemiş. Fakat bu teknikte ulnar duyu si-nirin dorsal dalının hasarlanmasından kaçınmak için 6U porta-lini ortalama 1.5 cm genişletmiş. Bu tekniğin avantajı düğümün eklem içine koyularak EKU tendon kılıfının irritasyonunun en-gellenmesidir.[33] Bizim dört hastamızda rahatsız edici düğüm granülomları meydana geldi ve bu hastalara ameliyatın altı ay veya daha sonrası lokal anestezi altında yapılan eksizyondan sonra şikayetlerinin kalmadığı görüldü.

Yapılan bir kadavra çalışmasına göre FasT-Fix kullanılarak uygulanan hepsi içeride tekniğinde sütürün dışarıdan içeri-ye tekniğine göre daha güçlü olduğu belirtilmiştir.[34] Ayrıca hepsi içeride tekniği ile ilgili ulnar duyu sinirin dorsal dalının veya diğer ulnar taraflı yapıların hasarlanması gibi bildirilmiş komplikasyonlar yoktur.[34-36] Lee hepsi içeride tekniğinde az komplikasyon görülmesinin nedenini bildirimlerin az sayıda-ki olgular ile yapıldığını ve bu tekniğin güvenilirliği için olgu sayılarının artması gerektiğini bildirmiştir.[35,36] Waterman ve ark.nın yaptıkları kadavra çalışmasında hepsi içeride tekniğin-de ankorun bir tanesinin EKU tendonu ile diğerinin ise ulnar duyu sinirin dorsal dalına temas ettiğini göstermişler ve bu tekniğin belirtildiği gibi hiç de masum bir yöntem olmadığını bildirmişlerdir.[27] Bizim hepsi içeride tekniği ile deneyimimiz olmamakla birlikte dışarıdan içeriye tekniğinde de EKU tendo-nuna ve ulnar duyu sinirinin dorsal dalına hasar vermeden iyi sonuçlar alınabildiğini tespit ettik. Hastalarımızın Mayo el bi-leği değerlendirme formu ile yapılan değerlendirme sonuçları-nın tatminkar olduğu saptadık. Ayrıca hepsi içeride tekniğinin diğer tekniklere göre daha maliyetli olduğunu düşünmekteyiz.

Kabakas ve ark. Triangular fibrokartilaj kompleks periferik (Palmer tip 1B) yırtıklarında artroskopik tamir sonuçları

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Şekil 6. (a, b) Traksiyonunsonlandırılarakelbileğiekstansiyondaikeniplerindüğümlenmesi.

(a)

(b)

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Bugüne kadar yapılan birçok çalışmada distal radioulnar eklem (DRUE) instabilitesi olan hastalar çalışmaya alınmıştır.[19,23,37] Fakat Reiter ve ark. DRUE instabilitesi olmayan ve artros-kopik olarak tedavi edilen tip 1B yırtıkları çalışmalarına dahil etmişler ve bizim çalışmamıza benzer olarak distal radius ve ulnar stiloid kırıkları ile eklem içi herhangi bir el bileği pato-lojisi bulunan hastaları çalışmalarına dahil etmemişlerdir.[38] Bu çalışmanın sonucunda karşı tarafa göre kavrama kuvvetinde, eklem hareket açıklığında ve VAS skorlarında %90 oranında iyileşme saptamışlar, %84 mükemmel ve %12 iyi sonuç bildir-mişlerdir. Fakat DASH skorlarında anlamlı bir düzelme olma-dığını bildirmişlerdir.[38] Wysocki ve ark. Palmer tip 1B akut periferik süperfisiyal yırtığı olan 28 hastanın 29 el bileğine art-roskopik tamir uygulamışlar; hastaların ortalama 31 aylık takip sonucunda VAS skorlarınun 5.4’den 0.9’a gerilediğini, preope-ratif 38 olan DASH skorunun ise ameliyat sonrası dönemde 9’a gerilediğini bildirmişlerdir.[39] Bizim çalışmamızda hastaların hiçbirinde distal radius ve ulna kırığı ile TFKK yırtığına eşlik eden el bileği patolojisi bulunmamaktadır. Bizim hastalarımıza uyguladığımız artroskopik tamir ile amacımız hastaların ağrı şikayetini geçirmektir. Hastalarda muayene sırasında el bileği instabilitesi saptanır ise TFKK foveal bağlanma yerinden ay-rışma veya diğer instabilite nedenleri araştırılarak farklı tedavi metoduna karar verilmiştir.

Triangular fibrokartilaj kompleks yırtıkları, hastaların günlük çalışma ve yaşam fonksiyonlarını kısıtlayan bir patolojidir. Çoğunlukla akut travma sonrası gözden kaçabilen bu duru-mun tanısının konulması ve artroskopik olarak onarılması ile tatminkar sonuçlar alınarak hastaların eski işlerine eksiksiz olarak dönmeleri mümkündür. TFKK periferik yırtıklarının artroskopik tamiri, açık cerrahiye göre komplikasyon riski daha az olan, erken ameliyat sonrası dönemi daha konforlu bir girişimdir.

Çıkar örtüşmesi: Çıkar örtüşmesi bulunmadığı belirtilmiştir.

KAYNAKLAR

1. Sachar K. Ulnar-sided wrist pain: evaluation and treatment of triangular fibrocartilage complex tears, ulnocarpal impaction syndrome, and lunotri-quetral ligament tears. J Hand Surg Am 2008;33:1669-79.

2. Palmer AK. Triangular fibrocartilage complex lesions: a classification. J Hand Surg Am 1989;14:594-606.

3. Tang CY, Fung B, Rebecca C, Lung CP. Another light in the dark: review of a new method for the arthroscopic repair of triangular fibrocartilage complex. J Hand Surg Am 2012;37:1263-8.

4. Bednar MS, Arnoczky SP, Weiland AJ. The microvasculature of the tri-angular fibrocartilage complex: its clinical significance. J Hand Surg Am 1991;16:1101-5.

5. Yao J, Lee AT. All-arthroscopic repair of Palmer 1B triangular fibro-cartilage complex tears using the FasT-Fix device. J Hand Surg Am 2011;36:836-42.

6. Kalainov DM, Culp RW. Arthroscopic treatment of TFCC tears. Tech Hand Up Extrem Surg 1997;1:175-82.

7. Palmer AK. Triangular fibrocartilage disorders: injury patterns and treat-ment. Arthroscopy 1990;6:125-32.

8. Palmer AK, Werner FW. The triangular fibrocartilage complex of the wrist--anatomy and function. J Hand Surg Am 1981;6:153-62.

9. Lee AT, Yao J. An update on the triangular fibrocartilage complex. Cur-rent Orthopaedic Practice 2008;19:509-14.

10. Shih JT, Lee HM, Tan CM. Early isolated triangular fibrocartilage com-plex tears: management by arthroscopic repair. J Trauma 2002;53:922-7.

11. Melone CP Jr, Nathan R. Traumatic disruption of the triangular fibrocar-tilage complex. Pathoanatomy. Clin Orthop Relat Res 1992;275:65-73.

12. Tay SC, Tomita K, Berger RA. The “ulnar fovea sign” for defining ulnar wrist pain: an analysis of sensitivity and specificity. J Hand Surg Am 2007;32:438-44.

13. Lawler E, Adams BD. Reconstruction for DRUJ instability. Hand (N Y) 2007;2:123-6.

14. Braun RM. The distal joint of the radius and ulna. Diagnostic studies and treatment rationale. Clin Orthop Relat Res 1992;275:74-8.

15. Albastaki U, Sophocleous D, Göthlin J, Pierre-Jerome C. Magnetic reso-nance imaging of the triangular fibrocartilage complex lesions: a compre-hensive clinicoradiologic approach and review of the literature. J Manipu-lative Physiol Ther 2007;30:522-6.

16. Hermansdorfer JD, Kleinman WB. Management of chronic periph-eral tears of the triangular fibrocartilage complex. J Hand Surg Am 1991;16:340-6.

17. Cooney WP, Linscheid RL, Dobyns JH. Triangular fibrocartilage tears. J Hand Surg Am 1994;19:143-54.

18. Anderson ML, Larson AN, Moran SL, Cooney WP, Amrami KK, Berger RA. Clinical comparison of arthroscopic versus open repair of triangular fibrocartilage complex tears. J Hand Surg Am 2008;33:675-82.

19. Corso SJ, Savoie FH, Geissler WB, Whipple TL, Jiminez W, Jenkins N. Arthroscopic repair of peripheral avulsions of the triangular fibrocarti-lage complex of the wrist: a multicenter study. Arthroscopy 1997;13:78-84.

20. Estrella EP, Hung LK, Ho PC, Tse WL. Arthroscopic repair of triangular fibrocartilage complex tears. Arthroscopy 2007;23:729-37.

21. Trumble TE, Gilbert M, Vedder N. Arthroscopic repair of the triangular fibrocartilage complex. Arthroscopy 1996;12:588-97.

22. Jantea CL, Baltzer A, Rüther W. Arthroscopic repair of radial-sided le-sions of the triangular fibrocartilage complex. Hand Clin 1995;11:31-6.

23. Haugstvedt JR, Husby T. Results of repair of peripheral tears in the tri-angular fibrocartilage complex using an arthroscopic suture technique. Scand J Plast Reconstr Surg Hand Surg 1999;33:439-47.

24. Ruch DS, Anderson SR, Ritter MR. Biomechanical comparison of tran-sosseous and capsular repair of peripheral triangular fibrocartilage tears. Arthroscopy 2003;19:391-6.

25. Pederzini L, Luchetti R, Soragni O, Alfarano M, Montagna G, Cerofo-lini E, et al. Evaluation of the triangular fibrocartilage complex tears by arthroscopy, arthrography, and magnetic resonance imaging. Arthroscopy 1992;8:191-7.

26. Chloros GD, Wiesler ER, Poehling GG. Current concepts in wrist ar-throscopy. Arthroscopy 2008;24:343-54.

27. Waterman SM, Slade D, Masini BD, Owens BD. Safety analysis of all-inside arthroscopic repair of peripheral triangular fibrocartilage complex. Arthroscopy 2010;26:1474-7.

28. Tang C, Fung B, Chan R, Fok M. The beauty of stability: distal radioul-nar joint stability in arthroscopic triangular fibrocartilage complex repair. Hand Surg 2013;18:21-6.

29. Cho CH, Lee YK, Sin HK. Arthroscopic direct repair for radial tear of the triangular fibrocartilage complex. Hand Surg 2012;17:429-32.

30. Geissler WB. Arthroscopic knotless peripheral ulnar-sided TFCC repair. Hand Clin 2011;27:273-9.

31. Yao J. All-arthroscopic repair of peripheral triangular fibrocartilage com-

Kabakas ve ark. Triangular fibrokartilaj kompleks periferik (Palmer tip 1B) yırtıklarında artroskopik tamir sonuçları

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plex tears using FasT-Fix. Hand Clin 2011;27:237-42. 32. Zachee B, De Smet L, Fabry G. Arthroscopic suturing of TFCC lesions.

Arthroscopy 1993;9:242-3.33. Pederzini LA, Tosi M, Prandini M, Botticella C. All-inside suture tech-

nique for Palmer class 1B triangular fibrocartilage repair. Arthroscopy 2007;23:1130.

34. Yao J. All-arthroscopic triangular fibrocartilage complex repair: safety and biomechanical comparison with a traditional outside-in technique in ca-davers. J Hand Surg Am 2009;34:671-6.

35. Yao J, Dantuluri P, Osterman AL. A novel technique of all-inside ar-throscopic triangular fibrocartilage complex repair. Arthroscopy 2007;23:1357.

36. Lee CK, Cho HL, Jung KA, Jo JY, Ku JH. Arthroscopic all-inside re-pair of Palmer type 1B triangular fibrocartilage complex tears: a technical note. Knee Surg Sports Traumatol Arthrosc 2008;16:94-7.

37. Tünnerhoff HG, Haussmann P. What are the indications for arthroscop-ic repair of ulnar tears of the TFCC?. [Article in German] Handchir Mi-krochir Plast Chir 2001;33:239-44. [Abstract]

38. Reiter A, Wolf MB, Schmid U, Frigge A, Dreyhaupt J, Hahn P, et al. Ar-throscopic repair of Palmer 1B triangular fibrocartilage complex tears. Arthroscopy 2008;24:1244-50.

39. Wysocki RW, Richard MJ, Crowe MM, Leversedge FJ, Ruch DS. Ar-throscopic treatment of peripheral triangular fibrocartilage complex tears with the deep fibers intact. J Hand Surg Am 2012;37:509-16.

OLGU SUNUMU

Results of arthroscopic repair of triangular fibrocartilagecomplex peripheral tears (Palmer type 1B) Fatih Kabakaş, M.D.,1 İsmail Bülent Özçelik, M.D.,1 Meriç Uğurlar, M.D.,2Berkan Mersa, M.D.,1 Memet Yazar, M.D.,3 Metin Uzun, M.D.4

1İst-elHandSurgeryMicrosurgeryandRehabilitationGroup,Istanbul2DepartmentofOrthopedicsandTraumatology,KartalYavuzSelimGovermentHospital,Istanbul3DepartmentofPlasticAndReconstructive,ŞişliEtfalTrainingandResearchHospital,Istanbul4DepartmentofOrthopedicsandTraumatology,MaslakAcıbademHospital,Istanbul

BACKGROUND: Triangular fibrocartilage complex (TFCC) injury is the major cause of wrist pain on the ulnar side. In this study, treatment out-comes of arthroscopically repaired peripheral TFCC tears (Palmer type 1B) were evaluated retrospectively.METHODS: Thirty-eight patients (30 males, 8 females; mean age 27.6; range 19 to 42 years) with TFCC tears (Palmer type 1B) who were treated arthroscopically between February 2007-July 2012 were evaluated retrospectively. The data were collected by Mayo wrist evaluation form and by preoperative and postoperative visual analogue scale (VAS).RESULTS: The results of the data collected by the Mayo wrist evaluation forms were perfect in 30 patients and good in 8 patients. Preoperative VAS was 6.53 (range: 4.5-8.2) and postoperative VAS was 1.48 (range: 0.3-3.1).DISCUSSION: With the arthroscopic technique, TFCC tears can be repaired with minimal harm and better visualization, and evaluation of all the structures of the wrist can be done. Outside-to-inside suturing technique, which is performed through the portal opened 1 cm inferior to the 6R portal, is the least traumatic technique and does not carry the risk of injury to the superficial branch of the ulnar nerve. With this technique, the complaints of preoperative pain can be eliminated significantly.Key words: Arthroscopy; wrist injury; wrist joint; triangular fibrocartilage.

Ulus Travma Acil Cerrahi Derg 2014;20(3):205-210 doi: 10.5505/tjtes.2014.63933

ORIGINAL ARTICLE - ABSTRACT

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Supraventricular tachycardia due toblunt chest trauma in an adolescent

C A S E R E P O R T

Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3 211

Hayrullah Alp, M.D., Tamer Baysal, M.D., Sevim Karaarslan, M.D.

DepartmentofPediatricCardiology,NecmettinErbakanUniversityMeramFacultyofMedicine,Konya

ABSTRACT

Blunt chest trauma and its associated complications represent a rare cause of cardiac arrest in a healthy child, although an increasing number of these events have been reported. Victims are most often diagnosed in ventricular fibrillation or tachycardia. However, cardiac conduction abnormalities are also reported. In this report, a healthy adolescent with supraventricular tachycardia associated with blunt chest trauma due to a football is presented. This is the first report in the literature of atrial arrhythmia in these cases with chest trauma.

Key words: Arrhythmia; blunt chest trauma; children; commotio cordis; supraventricular tachycardia.

INTRODUCTION

Blunt cardiac injury is more prevalent in children,[1] and this may cause commotio cordis or ventricular arrhythmias.[2] Commotio cordis is the devastating consequence of oth-erwise innocent-appearing chest-wall blows, with sudden cardiac death often resulting from projectiles striking the precordium.[3] This predominantly affects young male indi-viduals, and the mean age is 14 years, with 78% under 18 years of age.[4] Among children, the impact object is an imple-ment of the game, a relatively hard object such as a baseball, hockey puck or lacrosse ball.[4] The spectrum of injuries to the heart includes damage to the great vessels, myocardial rupture or contusion, and valvular disruption.[5] Pericardial ef-fusions, conduction abnormalities[6] and ventricular arrhyth-mias[7-9] may also occur. However, to our knowledge, atrial arrhythmia has not been reported in the literature until now. A recent report demonstrated that blunt chest trauma due to a football caused supraventricular tachycardia in a healthy adolescent.

CASE REPORT

A 12-year-old school girl, previously well, was referred to our pediatric emergency department due to chest pain and tachycardia. On her initial history, it was revealed that while playing football in the school courtyard, the football hit her upper anterior chest directly, throwing her to the ground and rendering her unresponsive. After this projectile hit, she ex-perienced tachycardia and chest pain.

She was born at term from a nonconsanguineous marriage and had had no chronic illness since birth. Her fetal and peri-natal history was unremarkable. On the initial physical exami-nation, vital signs showed a heart rate of 250 bpm and blood pressure of 115/75 mmHg. The patient was awake and crying intermittently with no significant increase in blood pressure. She had no hematoma on her sternum or rib fracture. The other examination findings were all normal. Laboratory find-ings included creatine phosphokinase-MB 0.3 ng/ml (normal: 0-3 ng/ml) and troponin 0.1 ng/ml (normal: 0-0.4 ng/ml). An electrocardiogram demonstrated a normal QRS axis and supraventricular tachycardia with a heart rate of 250 bpm (Fig. 1). Transthoracic echocardiography and telecardiography were all normal. She was given intravenous adenosine initially at a dose of 100 µg/kg. The sinus rhythm restored after the adenosine administration (Fig. 2). During the hospitalization, Holter monitoring did not reveal any arrhythmias besides the rare premature atrial beats. Over the next few months of the follow-up period, the electrocardiograms were normal.

DISCUSSION

Commotio cordis (disturbance of the heart) is a descriptive

Address for correspondence: Hayrullah Alp, M.D.

Necmettin Erbakan Üniversitesi Meram Tıp Fakültesi,

Çocuk Kardiyoloji Bilim Dalı, Meram, 43430 Konya, Turkey

Tel: +90 332 - 223 64 29 E-mail: [email protected]

Qucik Response Code Ulus Travma Acil Cerrahi Derg2014;20(3):211-213doi: 10.5505/tjtes.2014.90337

Copyright 2014TJTES

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Alp et al. SVT associated with blunt chest trauma

term meaning cardiac arrest associated with low-impact blunt trauma to the anterior chest, usually by a relatively low-ve-locity missile, such as a baseball, cricket ball or hockey puck, or by a blow delivered by a fist, foot, elbow, or knee dur-ing sporting activities. It is not associated with any structural damage to the ribs, sternum or heart, which is otherwise known as contusio cordis. It is usually associated with sud-den death in children.[10] However, arrhythmias may also be observed in these patients instead of commotio cordis.[6,7,10] Conduction abnormalities[6] and ventricular arrhythmias[7-9] such as ventricular tachycardia and fibrillation have been re-ported due to chest traumas. For an arrhythmia otherwise considered idiopathic, it is also novel in its clear association with a triggering factor, that is, blunt thoracic trauma. In these arrhythmias, the mechanism of onset of ventricular fibrilla-tion from a blow to the chest is well known. In an animal model, a blow falling during the vulnerable period before the T-wave peak results in a rapid rise in left ventricular pres-

sure with likely activation of ion channels via mechanoelectric coupling, leading to premature ventricular depolarization and ventricular fibrillation.[3] Similarly, we can suggest as a mecha-nism that after the direct blow to the upper anterior region of the chest, a rapid rise in atrial pressure may have activated the ion channels via mechanoelectric coupling, leading to pre-mature atrial depolarization and supraventricular tachycardia.

In commotio cordis victims, the chest blows usually strike the left chest. Most of these blows reportedly occur directly over the cardiac silhouette; however, the exact location of the chest wall strike cannot always be determined with preci-sion.[10] The spectrum of injuries to the heart includes dam-age to the great vessels, myocardial rupture or contusion, he-mopericardium, poor contractility, and valvular disruption.[5] Today, chest barriers are commonly used to protect children from the chest blows. However, in a study of Maron et al.,[4] commercially available chest wall protection was worn by

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Figure 1. Theelectrocardiogramshowingsupraventriculartachycardiawithaheartrateof250/bpm.

Figure 2. The12-leadelectrocardiogramshowingnormalaxisandsinusrhythmafteradenosineadministration.

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Alp et al. SVT associated with blunt chest trauma

22 of 79 (28%) of the commotio cordis victims in organized sports, and in 13 of these individuals, the chest wall barriers did not adequately cover the left chest wall and precordium. Further, these protectors are usually used for the sports such as hockey and baseball, but not for daily sports such as foot-ball and basketball. Thus, it can be suggested that commer-cially available chest barriers are not sufficiently effective in preventing chest-blow–induced sudden cardiac death and, in fact, probably offer only a false sense of security to athletes, families and the general public.[8]

The treatment of supraventricular tachycardia consists of short-term or as-needed pharmacotherapy using calcium channel or beta blockers when adenosine and vagal maneu-vers fail to halt or slow the rhythm. In those who require long-term pharmacotherapy, atrioventricular nodal blocking agents or class IC or III antiarrhythmics can be used. Catheter ablation is an option in patients with persistent or recurrent supraventricular tachycardia who are unable to tolerate long-term pharmacologic management.

In conclusion, blunt chest trauma and its associated complica-tions such as arrhythmias and commotio cordis are among the current problems in sportive activities. Chest protectors are not sufficiently effective in organized sports. Associated ven-tricular arrhythmias may be fatal, but atrial arrhythmias may not be life–threatening, as described in the current patient.

Conflict of interest: None declared.

REFERENCES

1. Farin M, Moskowitz WB. Traumatic heart block as a presentation of myo-cardial injury in two young children. Clin Pediatr (Phila) 1996;35:47-50.

2. Tibballs J, Thiruchelvam T. A case of Commotio cordis in a young child caused by a fall. Resuscitation 2008;77:139-41.

3. Madias C, Maron BJ, Weinstock J, Estes NA 3rd, Link MS. Commotio cordis--sudden cardiac death with chest wall impact. J Cardiovasc Elec-trophysiol 2007;18:115-22.

4. Maron BJ, Gohman TE, Kyle SB, Estes NA 3rd, Link MS. Clinical pro-file and spectrum of commotio cordis. JAMA 2002;287:1142-6.

5. El-Chami MF, Nicholson W, Helmy T. Blunt cardiac trauma. J Emerg Med 2008;35:127-33.

6. Hebson C, Mahle W, Mao C, Drossner D. Complete heart block and echocardiographic abnormalities caused by pyrotechnic chest trauma. Pe-diatr Cardiol 2010;31:572-3.

7. Horduna I, Dubuc M, Rochon AG, Khairy P. Posttraumatic left ventricu-lar tachycardia arising from the anterior papillary muscle in an otherwise healthy child. J Cardiovasc Electrophysiol 2011;22:714-6.

8. Link MS, Bir C, Dau N, Madias C, Estes NA 3rd, Maron BJ. Protecting our children from the consequences of chest blows on the playing field: a time for science over marketing. Pediatrics 2008;122:437-9.

9. Geddes LA, Roeder RA. Evolution of our knowledge of sudden death due to commotio cordis. Am J Emerg Med 2005;23:67-75.

10. Link MS. Mechanically induced sudden death in chest wall impact (com-motio cordis). Prog Biophys Mol Biol 2003;82:175-86.

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OLGU SUNUMU - ÖZET

Bir adolösanda künt göğüs travmasına bağlı supraventriküler taşikardiDr. Hayrullah Alp, Dr. Tamer Baysal, Dr. Sevim KaraarslanNecmettinErbakanÜniversitesiMeramTıpFakültesi,ÇocukKardiyolojiBilimDalı,Konya

Künt göğüs travması ve bununla ilişkili komplikasyonlar çocukluk çağında görülen kardiyak arrestin nadir nedenleridir. Ayrıca, bu olgular da giderek artan sayıda bildirilmektedir. Kurbanlar sıklıkla ventriküler fibrilasyon veya taşikardi ile teşhis edilmektedir. Bununla birlikte kardiyak ileti bozuklukları da bildirilmektedir. Bu yazıda, futbol topu ile künt göğüs travmasına bağlı supraventriküler taşikardi gelişen sağlıklı bir adolösan olgu sunuldu. Bu olgular içerisinde göğüs travmasına bağlı atrial aritmi olması nedeniyle literatürdeki ilk bildiridir.Anahtar sözcükler: Aritmi; çocuklar; kalp yaralanması; künt göğüs travması; supraventriküler taşikardi.

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Are blank cartridge guns really harmless?

C A S E R E P O R T

İsmail Gülşen, M.D.,1 Hakan Ak, M.D.,2 Enver Sosuncu, M.D.,1 Mehmet Deniz Bulut, M.D.3

1DepartmentofNeurosurgery,YuzuncuYılUniversityFacultyofMedicine,Van2DepartmentofNeurosurgery,BozokUniversityFacultyofMedicine,Yozgat3DepartmentofRadiology,YuzuncuYılUniversityFacultyofMedicine,Van

ABSTRACT

Blank cartridge guns are devices that discharge sound and gas, but no bullet or shot. These devices are very similar to real guns in the form of their external design and the sound generated during their firing. Although it is widely held in society that these devices are harmless, reports from Turkey and the world have shown that these guns are not entirely innocent. Herein, we present a 26-year-old male with a head injury due to gunshot from a blank cartridge. The purpose of this presentation is to emphasize that these devices are not harmless, contrary to common public opinion.

Key words: Blank cartridge gun; decompressive craniectomy; epidural hematoma; pneumatic effect; subdural hematoma.

INTRODUCTION

Blank cartridge guns are devices that discharge sound and gas flares, but no bullet or shot. Contrary to the widely accepted opinion, these guns are not harmless. Morbidity and mortality cases caused by these guns are increasing daily. Various types of injuries have been reported in the literature.[1-7] In particu-lar, head trauma due to these guns is an important cause of morbidity and mortality.[1,5-7]

Herein, we present a new case of head injury due to the firing of a gun with a blank cartridge, with suicidal intent. CASE REPORT

A 26-year-old male admitted to the emergency room with head injury by gunshot from a blank cartridge. He was intu-bated upon admittance to the emergency room. The physical examination revealed skin defect and burn measuring 2x3 cm

on the right temporal region. Glasgow coma scale (GCS) was 6 (E1V1M4). Light reflex was positive bilaterally; however, the right pupil was dilated slightly. Brain computed tomography (CT) revealed a fragmented displaced fracture of the right temporal bone, epidural and subdural hematoma 5 mm in thickness and intracerebral hematoma measuring 4x5 cm on the same side, and 11 mm midline shift from right to left (Fig. 1a). The patient underwent immediate surgery. During the operation, bone fragments, some of which showed pa-renchymal invasion, were cleaned. Irregular tears on the dura were observed at multiple sites. The bone defect was ex-tended with minimal craniectomy. The epidural and subdural hematoma was drained. Dura was repaired with galea graft. The patient was followed in the intensive care unit postop-eratively. GCS was 7 (E2V1M4). Anisocoria improved in the early period. Thirty-six hours postoperatively, anisocoria re-curred, and brain CT was taken, which revealed very dense edema on the right frontotemporal region and midline shift (Fig. 1b). The patient was re-operated, and decompressive craniectomy was performed. The dura was re-opened and duraplasty was extended. Bone flap was embedded in the abdomen. The patient showed an uneventful recovery after the re-operation. He was discharged without any neurologic deficit 10 days after the re-operation (Fig. 1c).

DISCUSSION

Blank cartridge guns were first used in the Prussian army for educational purposes.[5] These guns fire sound and gas flares, but no bullet or shot. They have a metal hoop that prevents ejection of the contents of the hive from the barrel. These

Address for correspondence: İsmail Gülşen, M.D.

Yüzüncü Yıl Üniversitesi, Dursun Odabaş Tıp Merkezi,

Beyin ve Sinir Cerrahisi Anabilim Dalı, Van, Turkey

Tel: +90 432 - 216 83 52 E-mail: [email protected]

Qucik Response Code Ulus Travma Acil Cerrahi Derg2014;20(3):214-216doi: 10.5505/tjtes.2014.90868

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Gülşen et al. Are blank cartridge guns really harmless?

guns are used worldwide as a weapon of defense with the intent of threat. They produce a significant noise with a small amount of gunpowder or nitrocellulose.[4] These guns cannot be used in sportive activities or hunting and do not provide security. These properties may lead us to consider that the aims of obtaining and carrying them might be due to passion

or malice. These guns are used in various crimes, such as kidnapping, and for the purposes of threats, forced bondage securities, murder, exposure, and firing in residential areas. They are often fired at weddings and football games, and can lead to panic and fear among those in the immediate sur-roundings due to the noise generated.[8]

(a)

(b)

(c)

Figure 1. (a)AxialCTimageofthebrainatadmissionshowingfragmentedfracturesintherighttemporalregion,intracerebralhematoma,andmidlineshift.(b)AxialCTimageofthebrainshow-ingcraniectomydefects,intracerebraledemaandmidlineshift.(c)AxialCTimageofthebrainbeforethepatient’sdischarge.

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Gülşen et al. Are blank cartridge guns really harmless?

In Turkey, the legal transactions regarding blank cartridges are done in accordance with the law legislated in 2008, according to which, these guns may be owned by individuals who have not been convicted on firearms and knives (related with law 6136), who have no history of imprisonment for more than one year for a deliberately committed crime, and who are older than 18 years of age. Thus, it is very easy to supply these guns compared with firearms.[1]

Conducted criminological studies have shown that the pres-sure at the tip of the barrel can reach up to 100-200 bars during discharge. This pressure may provide the energy nec-essary for penetrating the skin, and thus may lead to life-threatening injuries, especially when fired at close range.[6] Various organ injuries due to these guns have been reported, and include head trauma and jugular venous, abdominal, and intra-oral injuries.[1-5] Among these injuries, head injuries in particular have been reported to be mortal.[7] Fortunately, mortal head injuries due to the pneumatic effect of these guns are rare. Bone fractures have also been reported in the literature.[5] In our case, the patient shot himself using his right hand, with the gun aimed at his right temporal region, with the intent of suicide, and he thus was found to have frag-mented bone fractures at the same localization. Giese et al.[5] reported the occurrence of intracerebral hematoma in their case series. Our case also had an intracerebral hematoma of 4x5 cm in diameter. Buyuk et al.[7] reported two mortal cases. In a recent report, Çelik et al.[1] reported a lethal brain in-jury caused by a blank cartridge pistol. They discharged the patient with intact neurological status. Our patient was also discharged with intact neurological examination.

In conclusion, as is shown in the literature and in our case, blank cartridge guns are not harmless and may lead to seri-ous injuries, even death. Morbidity and mortality from such trauma may be seen with increased frequency in the future due to the ease with which these guns can be acquired. We believe that the current laws related to these guns should be revised.

Conflict of interest: None declared.

REFERENCES

1. Çelik Ö, Ekşi MŞ, Dağçınar A, Bayri Y, Konya D, Ziyal Mİ. Lethal brain injury caused by a blank cartridge pistol. [Article in Turkish] Journal of Neurological Sciences 2013:30;451-4.

2. İynen İ, Söğüt Ö, Şan İ, Kaya H, Bozkuş F. Suicidal injury caused by blank-firing gun. JAEMCR 2011:2;39-41.

3. Korkmaz Ö, Yılmaz HG, Taçyılmaz İ. Abdominal trauma due to blank cartridge guns. [Article in Turkish] Turk J Emerg Med 2006;6:66-8.

4. İkizceli İ, Avşaroğlulları L, Sözüer EM, Özdemir Ç, Tuğcu H, Sever H, et al. Juguler vein gunshot injury from blank cartridges. [Article in Turkish] Ulus Travma Acil Cerrahi Derg 2005;11:254-8.

5. Giese A, Koops E, Lohmann F, Westphal M, Püschel K. Head injury by gunshots from blank cartridges. Surg Neurol 2002;57:268-77.

6. Clarot F, Vaz E, Papin F, Clin B, Vicomte C, Proust B. Lethal head injury due to tear-gas cartridge gunshots. Forensic Sci Int 2003;137:45-51.

7. Buyuk Y, Cagdir S, Avsar A, Duman GU, Melez DO, Sahin F. Fatal cra-nial shot by blank cartridge gun: two suicide cases. J Forensic Leg Med 2009;16:354-6.

8. Bozdemir A. Kuru sıkı ve gaz tabancaları serüveni. Çağın Polisi Dergisi, Vol.19, 2002. http://www.caginpolisi.com.tr/kuru-siki-ve-gaz-tabanca-lari-seruveni/. 05.01.2014.

OLGU SUNUMU - ÖZET

Kurusıkı silahlar gerçekten zararsız mı?Dr. İsmail Gülşen,1 Dr. Hakan Ak,2 Dr. Enver Sosuncu,1 Dr. Mehmet Deniz Bulut3

1YüzüncüYılÜniversitesiTıpFakültesi,BeyinveSinirCerrahisiAnabilimDalı,Van2BozokÜniversitesiTıpFakültesi,BeyinveSinirCerrahisiAnabilimDalı,Yozgat3YüzüncüYılÜniversitesiTıpFakültesi,RadyolojiAnabilimDalı,Van

Kuru sıkı silahlar mermi çekirdeği fırlatmaksızın ses ve gaz fişekleri ateşleyen silahlardır. Bu silahların ateşleme sırasında, dış görünümü ve sesi ger-çeklerinden farksızdır. Toplulumuzda bu silahların, zarasız olduğuna dair inanış hakimken, literatürlerde bildirilen olgulara baktığımızda sanıldığı kadar masum olmadıklarını görmekteyiz. Bu yazıda kuru sıkı silah ile kafa travması geçiren 26 yaşındaki hastayı sunarak kuru sıkı silahların zararlı silahlar olduklarını göstermeyi amaçladık.Anahtar sözcükler: Dekompresif kraniotomi; epidural hematom; kuru sıkı silah; pnomotik etki; subdural hematom.

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Successful emergency department thoracotomy for traumatic cardiac rupture: effective utilization of a fret sternum sawTsukasa Nakamura, M.D.,1,2 Koji Masuda, M.D.,2 Eiji Hitomi, M.D.,3

Yoshio Osaka, M.D.,2 Toshimasa Nakao, M.D.,1 Norio Yoshimura, M.D.1

1DepartmentofOrganTransplantationandGeneralSurgery,KyotoPrefecturalUniversityofMedicine,Japan

Departmentsof2Surgery,and3Anesthegiology,OmihachimanCommunityMedicalCenter,Japan

ABSTRACT

Mortality following blunt chest injury and cardiac rupture remains high despite advances in the care of traumatic injuries. Indeed, most patients succumb to these injuries even prior to reaching a hospital. However, timely recognition and surgical intervention can save lives. We present the case of a 40-year-old woman who presented to our emergency department in cardiac arrest due to rupture of her left atrium following a major motor vehicle collision. The patient underwent emergency department thoracotomy with successful repair of the cardiac rupture. Emergency department thoracotomy, when indicated and performed by trained surgeons, can be the only life-saving procedure available. Rapid median sternotomy using a cost-effective fret sternum saw does not require significantly more time than a left lateral thoracotomy or clamshell incision in an emergency situation. It can be an effective and alternative method of thoracic entry in the emergency department. Prognosis of cardiac rupture depends largely on the mechanism of injury, location of injury, signs of life: vital signs, and availability of timely intervention. When indicated, hesitation should be avoided. Expedient cardiac exposure is essential and leads to better results with improved survival rates in patients with blunt cardiac rupture.

Key words: Blunt trauma; cardiac rupture; cardiac tamponade; emergency department thoracotomy; fret sternum saw.

INTRODUCTION

Cardiac rupture following blunt chest trauma is associated with a critically high mortality rate. It is true, however, that quick diagnosis and appropriate management can save lives. Among them, emergency department thoracotomy (EDT) remains the most challenging procedure.[1-3] The application of, indications for, and advantages and disadvantages of EDT are often debated. This case highlights the importance of and complications seen with EDT in a typical medical center.

CASE REPORT

A previously healthy 40-year-old Japanese female involved in a motorcycle collision sustained a handle bar injury to her

chest and a complex right talus fracture. Upon presentation to the ED, she was disoriented, with a heart rate (HR) of 140 beats per minutes (bpm); her blood pressure was un-measurable. Immediately, a primary survey and a focused assessment with sonography for trauma (FAST) were per-formed simultaneously. The FAST revealed significant peri-cardial fluid and cardiac tamponade. Within seconds, she decompensated into a brady-arrhythmia, followed by cardiac arrest. Pericardiocentesis was subsequently performed using a 12Fr drainage tube, and she was intubated. Blood spouted from the drainage tube, and her HR immediately rose to 140 bpm; however, her blood pressure remained significantly low. Her Glasgow Coma Scale (GCS), Injury Severity Score (ISS), Revised Trauma Score (RTS), and her probability of survival from the Trauma and Injury Severity Score (TRISS) were 3, 45, 0.733, and 2.6%, respectively.

After the patient had been in the ED for 20 minutes (min), the decision was made to perform surgical closure of the cardiac rupture in the ED, because she had lost her vital signs due to hemorrhagic shock following the pericardial drain-age. A crash midline sternotomy was performed, followed by opening her pericardium, and O, Rh(D) positive red cell con-centrate (RCC) transfusion was begun simultaneously ( Japa-nese Rh(D) positive accounts for 99.5% of the population).

C A S E R E P O R T

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Address for correspondence: Tsukasa Nakamura, M.D.

Kajii-cho 465, Kamigyo-ku Kyoto, Japan

Tel: 81752515532 E-mail: [email protected]

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A large amount of bleeding ensued and direct cardiac mas-sage was initiated. Although the massive hemorrhage made detection of the perforation difficult, a left atrium rupture, measuring approximately 2-3 cm, was identified by palpation (Fig. 1).

The rupture was side-clamped with a Satinsky clamp. The perforation was closed with running 3-0 Prolene, and hemo-stasis was obtained. Disseminated intravascular coagulation (DIC) due to the massive hemorrhage manifested as bleeding from the endotracheal tube. Immediate simple wound clo-sure and insertion of bilateral chest tubes were performed. Subsequently, the patient was transferred to the intensive care unit (ICU). Within 4 hours following the EDT, the pa-tient’s vital signs normalized and she recovered conscious-

ness. A total of 8400 ml of RCC, 748 ml of cell saver fluid, 6720 ml of fresh frozen plasma (FFP), and 60 international units of platelets were transfused within the initial 24 hours, primarily based on the massive transfusion protocol.[4] On postoperative day 8, after recovering from DIC, she under-went right talus fixation. Magnetic resonance imaging (MRI) of her brain revealed a left occipital lobe infarction primarily due to the period of low blood pressure. Her clinical symp-toms included visual impairment and a slight dysmnesia that improved after intensive rehabilitation. She was able to suc-cessfully perform her activities of daily living and thus reenter society.

DISCUSSION

Cardiac rupture due to blunt chest trauma is seen rarely in the ED, as it is often fatal at the scene. Cardiac arrest prior to hospital presentation portends an extremely poor prog-nosis. Although survival rates of EDT in blunt chest trauma are very low, only 1.4%,[3] EDT can serve as the only life-saving procedure available. Survival rates following EDT for blunt chest trauma strongly correlate with the mechanism of injury (MOI), location of major injury (LOMI), and signs of life (SOL). A more favorable prognosis is associated with isolated cardiac injury and the presence of SOL on arrival.[5] Therefore, it is of vital importance to work quickly in order to decrease the mortality of cardiac rupture.

Initially, cardiac rupture following blunt chest trauma should be diagnosed by FAST, not computed tomography (CT) scan, as ultrasound is much faster and safer.[6] Clinicians should be well aware that cardiac rupture can present with tamponade with or without intact pericardium or massive hemothorax.[7] Once the diagnosis is made, transfusion must begin as soon as possible. Due to the immediacy of the situation, type spe-cific blood is not practical; thus, O Rh(D) negative packed red blood cells and AB FFP should be ready for immediate transfusion.[8,9] However, given the limited availability of this

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Figure 2. Thisfigureillustratestheoperationofafretsternumsaw.1)Alongforcepsisinsertedbeneaththesternum.2)Thefretster-numsaw isguided.3)Thesternum isdivided.4)Assistant sur-geonsplacescissorsonthesternum.

Figure 1. (a, b)Theperforatedsiteisindicatedbytheblackandwhitearrows:theleftatrium.(b)3DcardiacCTwastakenpostoperatively.

Aorta

RCALCx

LAD

RV LV

LASiteofPerforation

(b)(a)

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Nakamura et al. Successful emergency department thoracotomy for traumatic cardiac rupture

type of blood, an immediate call to the blood bank is crucial. Auto-transfusion should be considered early and set up prior to EDT. Physicians must consider autologous blood collection from a thoracostomy drainage tube or a pericardial window by means of a cell saver or blood preservation bag. This can compensate for a shortage in stored blood.

In this case, as our patient had lost vital signs, there was no time to transfer her to the operating theater. EDT was the only option. Generally, given adequate staff and equipment, EDT is recommended in cases where cardiac tamponade due to trauma is present and in which there is no adequate sustained response to pericardial drainage,[5,10] mainly due to subsequent hemorrhagic shock. Median sternotomy, clam-shell incision and left lateral thoracotomy are all techniques employed for cardiac exposure. However, a midline sternoto-my can provide the best exposure of the heart, especially the superior mediastinal structures. Median sternotomy using a fret sternum saw, described below, does not require signifi-cantly more time than a left lateral thoracotomy or clamshell incision in an emergency situation. Needless to say, it is of vital importance to protect cerebral perfusion and prevent hypoxic damage in cases of cardiac arrest. Accordingly, the quickest approach to the heart is paramount in order to mini-mize hypoxic brain injury.

In cases of atrial cardiac rupture, it should be managed by application of a vascular clamp and oversewing the perfora-tion. On the other hand, ventricular rupture can be man-aged with mattress suture technique by means of pledget reinforcements.[11] In certain situations, it may prove difficult to identify the site of perforation or control bleeding by a direct clamping. In these situations, a short period of inflow interception accomplished by clamping of the superior (SVC) and inferior vena cava (IVC) may be effective. Furthermore, surgeons should not hesitate to set up cardiopulmonary by-pass, if necessary and readily available.

Cardiopulmonary bypass and clamping of the SVC, IVC and aorta in order to maintain cerebral perfusion might also pre-vent huge air embolism in cases of large left atrium or ven-tricle rupture while suturing. Given this additional advantage, a median sternotomy is the recommended approach as it al-lows easy access to the great vessels.

It has been argued that an electric sternum saw is too ex-pensive to be equipped in the ED. Our questionnaire survey of Japanese tertiary emergency medical centers revealed that less than 5% of the emergency centers were equipped with an electric sternum saw. The main reason was its high cost, which far outdistanced the other reasons cited, such as “un-necessary” or “non-frequent usage”. This problem due to the price can be addressed with the application of the inexpen-sive and disposable fret sternum saw. This simple and quick method is often used in multiple organ procurement in the United Kingdom and other countries after donor brain or

donor cardiac death (DBD or DCD). Application of this saw is described in Figure 2.

Instruments required for rapid thoracic entry and cardiac ex-posure are the fret sternum saw, a forceps longer than the sternum and two Kocher clamps. An assistant surgeon should be attentive to keeping the saw from leaping up, by means of holding copper scissors on the sternum (Fig. 2). Clearly, it is not difficult to install these instruments in a typical medical center in terms of the cost. We thus feel it is important for ED staff to be familiar with this method.

In conclusion, in cases of severe cardiac tamponade, EDT is the only life-saving option. The ED staff must be prop-erly trained in order for EDT to be successful. As EDT is a struggle against time, decisions must be made quickly and without hesitation based upon the proper indications. We propose our sternotomy methods to make possible a swift thoracic entry. When managed appropriately, this will lead to improved outcomes in patients with cardiac rupture.

Ethical approval: Written informed consent was obtained from the patient for publication of this case report and the accompanying images. A copy of the written consent is avail-able for review by the Editor-in-Chief of this journal upon request.

Conflict of interest: None declared.

REFERENCES1. Baker CC, Thomas AN, Trunkey DD. The role of emergency room tho-

racotomy in trauma. J Trauma 1980;20:848-55.2. Moreno C, Moore EE, Majure JA, Hopeman AR. Pericardial tamponade:

a critical determinant for survival following penetrating cardiac wounds. J Trauma 1986;26:821-5.

3. Cothren CC, Moore EE. Emergency department thoracotomy for the critically injured patient: Objectives, indications, and outcomes. World J Emerg Surg 2006;1:4.

4. Elmer J, Wilcox SR, Raja AS. Massive transfusion in traumatic shock. J Emerg Med 2013;44:829-38.

5. Rhee PM, Acosta J, Bridgeman A, Wang D, Jordan M, Rich N. Survival after emergency department thoracotomy: review of published data from the past 25 years. J Am Coll Surg 2000;190:288-98.

6. Plummer D. Principles of emergency ultrasound and echocardiography. Ann Emerg Med 1989;18:1291-7.

7. Powell MA, Lucente FC. Diagnosis and treatment of blunt cardiac rup-ture. W V Med J.1997;93:64-7.

8. Berséus O, Boman K, Nessen SC, Westerberg LA. Risks of hemolysis due to anti-A and anti-B caused by the transfusion of blood or blood components containing ABO-incompatible plasma. Transfusion 2013;53 Suppl 1:114-23.

9. Khan S, Allard S, Weaver A, Barber C, Davenport R, Brohi K. A major haemorrhage protocol improves the delivery of blood component therapy and reduces waste in trauma massive transfusion. Injury 2013;44:587-92.

10. Nan YY, Lu MS, Liu KS, Huang YK, Tsai FC, Chu JJ, et at. Blunt traumatic cardiac rupture: therapeutic options and outcomes. Injury 2009;40:938-45.

11. Williams JB, Silver DG, Laws HL. Successful management of heart rup-ture from blunt trauma. J Trauma 1981;21:534-7.

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OLGU SUNUMU - ÖZET

Travmatik kardiyak rüptür için başarılı acil servis torakotomisi:Fret sternum testeresinin efektif kullanımı Dr. Tsukasa Nakamura,1,2 Dr. Koji Masuda,2 Dr. Eiji Hitomi,3

Dr. Yoshio Osaka,2 Dr. Toshimasa Nakao,1 Dr. Norio Yoshimura1

1KyotoİdariÜniversitesiTıpFakültesi,TransplantasyonveRejeneratifCerrahiAnabilimDalı,Kyoto,Japonya;OmihachimanToplumSağlığıMerkezi,2Cerrahi ve 2AnesteziyolojiBölümü,Kyoto,Japonya

Travmatik yaralanmaların bakımında ilerlemelere rağmen künt göğüs travması ve kardiyak rüptür sonrası mortalite oranları yüksek düzeydedir. Gerçekten, hastaların çoğu hatta bir hastaneye varmadan önce ölmektedir. Ancak zamanında farkına varma ve cerrahi girişim yaşamları kurtarabil-mektedir. Büyük bir motorlu taşıt çarpmasıyla oluşan sol atriyum rüptürü sonucu acil servisimize kardiyak arrest ile getirilen 40 yaşındaki bir kadın olgu sunuldu. Hasta acil serviste torakotomi ve başarılı bir kardiyak rüptür onarımı geçirdi. Gerekli olduğunda ve eğitimli cerrahlar tarafından ger-çekleştirildiğinde acil serviste yapılan torakotomi mevcut tek yaşam kurtarıcı işlem olabilir. Maliyet-etkinlikli Fret sternum testeresi kullanılarak hızlı bir median sternotomi için acil durumda yapılan sol lateral torakotomi veya istiridye kabuğu tarzında kesiye göre anlamlı derecede daha fazla zamana gerek duyulmamaktadır. Acil serviste toraksa girişin etkili alternatif bir yöntemidir. Kardiyak rüptürün prognozu geniş ölçüde travmanın mekaniz-ması, yeri, yaşam belirtileri, yaşamsal bulgular ve zamanında müdahale olanaklarının varlığına bağlıdır. Gerekli olduğunda bir an duraklanmamalıdır. Kalbin hızlı açınımı esastır. Hızlı girişim, künt kardiyak rüptürü olan hastalarda iyileşmiş sağkalım oranlarıyla daha iyi sonuçların alınmasına yol açar.Anahtar sözcükler: Acil servis; Fret sternum testeresi; kardiyak rüptür; kardiyak tamponat; künt travma.

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An unusual entry site for a nasal foreign body: a neglected trauma patientSelçuk Mülazımoğlu, M.D., Emre Ocak, M.D., Süha Beton, M.D., Ozan Bağış Özgürsoy, M.D.

DepartmentofOtorinolaryngologyHeadandNeckSurgery,AnkaraUniversityFacultyofMedicine,Ankara

ABSTRACT

Foreign body (FB) in the nose is a frequent situation seen generally among children. A variety of objects left in different sites of the nose has been reported in the literature. Insertion of a FB to the nose is generally via the anterior nares. In this report, an unusual entry site for a nasal FB in a neglected trauma patient is presented. FB should be suspected and investigated in children after penetrat-ing facial injury.

Key words: Maxillofacial trauma; nose; penetrating injury.

INTRODUCTION

Most otorhinolaryngologists do not give careful attention in the follow-up of foreign bodies (FBs) in the nose. FB in the nose is generally seen among young children. Many fac-tors lead children to insert FBs into the upper aerodigestive system, including curiosity, frivolity, nasal itching or irritation caused by rhinitis or otalgia, and attraction to small, round objects, as shown in the literature.[1] Studies show that the younger the child, the more frequent the insertion of FBs.[2] The most common FBs are toys, nuts, beans, rubber eras-ers, grapes, and paper. Some typical anatomical sites of FBs include nasal entrance anterior to the middle turbinate and floor of the nasal cavity just below the inferior turbinate.[3] However, one must visualize every anatomical location in the nasal cavity to avoid overlooking FBs.

We present a neglected case of FB in which the FB entered the nasal cavity after external trauma to the face and went unnoticed for four years.

CASE REPORTAn 11-year-old female patient complaining of a foul nasal odor for about six months admitted to our outpatient clinic. She had a trauma history in which she fell onto a plastic pen four years ago, and as the patient described, the pen lodged in her right nasolabial skin and was removed immediately. After being taken to an emergency department, the skin laceration at the nasolabial sulcus was sutured. She complained about odorous nasal discharge and admitted to an otorhinolaryngol-ogist four years after the trauma. A paranasal computerized tomography showed a FB in the right nasal cavity penetrating through the middle concha and septum (Fig. 1). Afterwards, the patient was referred to our clinic for the removal of the FB. The physical examination revealed a 2 cm scar on the right nasolabial sulcus (Fig. 2). Nasal endoscopy under topical anesthesia showed a cylindrical FB in the right nasal cavity lateral to the middle concha (Fig. 3). The middle concha was retracted medially and the FB, a plastic pen cap, was removed using a Blakesley nasal forceps (Fig. 4). Nasal irrigation and antibiotics were given, and no infection or purulent discharge was seen in the follow-up.

DISCUSSION

Nasal FB in children is a frequent situation in otorhinolar-yngology practice. It can be presented with odorous nasal discharge, foul nasal odor, and pain or discomfort in the nose. However, some authors have reported that 63% of the cases may be asymptomatic.[4] When a patient complains of long-standing, unilateral mucopurulent nasal discharge, one should suspect FB in the nasal cavity. The most common entry site for FBs is via the anterior nares, especially in young children.[5]

C A S E R E P O R T

Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3 221

Presented at the 9th Turkish Rhinology Congress (23-26 May 2013, Antalya, Turkey).

Address for correspondence: Selçuk Mülazımoğlu, M.D.

Ankara Üniversitesi Tıp Fakültesi, Kulak Burun Boğaz Hastalıkları

Anabilim Dalı, Sıhhiye, 06100 Ankara, Turkey

Tel: +90 312 - 508 20 30 E-mail: [email protected]

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In this case, the FB had entered the nasal cavity transcutane-ously, which is very unusual. Although there have been some cases with unusual sites of penetration, such as craniofacial trauma resulting from orbital foreign body,[6] the entrance of the nasal FB described above remains unique.

Foltran et al.[7] reviewed 1475 articles regarding FB in the air-ways over a period of 30 years, and noted that pen cap is not a common FB in the nose. Patients with nasal FBs usually ad-mit to emergency departments for removal of their FBs. FBs can be removed either in the emergency service or otorhino-laryngology department. Although emergency practitioners

are familiar with the removal techniques, multiple attempts may be required for removal,[8] and their failure rate can be as high as 35%.[9] Some FBs are inert and may remain in the nose for years, but others can harm the nasal mucosa, leading to mucosal ulcerations, epistaxis and toxemia in some cases. Longstanding FBs in the nose also tend to become encrusted with calcified material and become a rhinolith.[3] There are some cases in which the FB remained in the nasal cavity up to 40 years.[10] These can cause nasomaxillary abnormalities in the growing child.

Nasal FBs should not be neglected and must be removed as soon as possible, preferably by an otorhinolaryngologist. After removal, one must visualize the entire nasal cavity, endoscopi-cally if possible, to ensure no other pieces are left in the cavity. In a child with a penetrating injury to the face, one should sus-pect and investigate any hidden FB embedded in deep tissues, even in the nasal cavity. If the penetrating object is available, it should be examined to ascertain if any part is missing.

Conflict of interest: None declared.

Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3222

Figure 1. Paranasalcomputerizedtomographyshowingtherightnasalforeignbody(arrow)penetratingthroughthemiddleconchaandseptum. Figure 2. Traumaticscarontherightnasolabialsulcus(asterisk).

Figure 3. Endoscopicviewoftherightnasalforeignbody(aster-isk)penetratingthroughthemiddleconcha(S:Septum,M:Middleconcha,I:Inferiorconcha). Figure 4. Nasalforeignbodyafterremoval(plasticpencap).

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Mülazımoğlu et al. An unusual entry site for a nasal foreign body

REFERENCES

1. Balbani AP, Sanchez TG, Butugan O, Kii MA, Angélico FV Jr, Ikino CM, et al. Ear and nose foreign body removal in children. Int J Pediatr Otorhinolaryngol 1998;46:37-42.

2. Das SK. Aetiological evaluation of foreign bodies in the ear and nose. J Laryngol Otol 1984;98:989-91.

3. Kalan A, Tariq M. Foreign bodies in the nasal cavities: a comprehensive review of the aetiology, diagnostic pointers, and therapeutic measures. Postgrad Med J 2000;76:484-7.

4. Kadish HA, Corneli HM. Removal of nasal foreign bodies in the pediat-ric population. Am J Emerg Med 1997;15:54-6.

5. Tay AB. Long-standing intranasal foreign body: an incidental finding on dental radiograph: a case report and literature review. Oral Surg Oral

Med Oral Pathol Oral Radiol Endod 2000;90:546-9.6. LaFrentz JR, Mair EA, Casler JD. Craniofacial ballpoint pen injury: en-

doscopic management. Ann Otol Rhinol Laryngol 2000;109:119-22.7. Foltran F, Ballali S, Passali FM, Kern E, Morra B, Passali GC, et al. For-

eign bodies in the airways: a meta-analysis of published papers. Int J Pe-diatr Otorhinolaryngol 2012;76 Suppl 1:12-9.

8. Chan TC, Ufberg J, Harrigan RA, Vilke GM. Nasal foreign body remov-al. J Emerg Med 2004;26:441-5.

9. Mackle T, Conlon B. Foreign bodies of the nose and ears in children. Should these be managed in the accident and emergency setting? Int J Pediatr Otorhinolaryngol 2006;70:425-8.

10. Uğur MB, Evren C, Corakçi S, Taş E, Cinar F. Foreign body which re-sembles concha bulloza in the middle meatus: a case report. Kulak Burun Bogaz Ihtis Derg 2009;19:307-10.

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OLGU SUNUMU - ÖZET

Burunda yabancı cisimde sıradışı bir giriş yolu: İhmal edilmiş bir travma olgusuDr. Selçuk Mülazımoğlu, Dr. Emre Ocak, Dr. Süha Beton, Dr. Ozan Bağış ÖzgürsoyAnkaraÜniversitesiTıpFakültesi,KulakBurunBoğazHastalıklarıAnabilimDalı,Ankara

Burunda yabancı cisim özellikle çocuklarda sıkça karşılaşılan bir durumdur. Literatürde burunun değişik bölgelerinde çok çeşitli yabancı cisim bildiril-miştir. Yabancı cisimin giriş yolu sıklıkla burun delikleridir. Bu yazıda, ihmal edilmiş bir travma hastasında, burunda yabancı cisim için sıradışı bir giriş yolu sunuldu. Çocuklarda penetran yüz yaralanması sonrasında yabancı cisimden şüphelenilmeli ve detaylı aranmalıdır.

Anahtar sözcükler: Burun; maksillofasiyal travma; penetran yaralanma.

IX. Türk Rinoloji Kongresi ’nde sunulmuştur (23-26 Mayıs, Antalya, Türkiye).

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Oksipital kondil kırıkları: Bir olgu sunumuDr. Cem Dinç,1 Dr. Mehmet Erhan Türkoğlu,2 Dr. Cengiz Tuncer,1

Dr. Ömer Aykanat,1 Dr. Derya Özçelik,3 Dr. Gamze Özkan3

1DüzceÜniversitesiTıpFakültesi,BeyinveSinirCerrahisiAnabilimDalı,Düzce2AnkaraDışkapıEğitimveAraştırmaHastanesi,BeyinveSinirCerrahisiKliniği,Ankara3DüzceÜniversitesiTıpFakültesi,PlastikveRekonstrüktifCerrahiAnabilimDalı,Düzce

ÖZET

Oksipital kondil kırıkları nadir olup, konservatif tedavi genellikle yeterlidir. Nadiren atlantooksipital dislokasyonun eşlik ettiği olgularda cerrahi tedavi gerekebilir. Acil servise travma nedeniyle başvuran olgularda direkt grafilerde sıklıkla tanı konulamayan kondil kırıklarına, son yıllarda bilgisayarlı tomografinin sık olarak kullanılması ile artan oranda tanı konulabilmektedir. Bu çalışmada, acil servisimize travma nedeniyle kabul edilen hastanın, maksillofasiyal travması ön planda olup, boyun ağrısından şikayet etmekteydi. Servikal direkt grafileri normal olan hastanın, servikal bilgisayarlı tomografisinde tek taraflı oksipital kondil kırığı saptandı.

Anahtar sözcükler: Cerrahi; konservatif tedavi; oksipital kondil kırığı; oksipitoservikal dislokasyon.

GİRİŞ

Oksipital kondil kırıkları (OKK) nadir olarak görülür.[1,2] An-cak tanısal alandaki teknolojik gelişmeler ile artan sayıda olgu-ların literatürde yer alması ve olgu çalışmalarının yayınlanması, OKK’nın klasik bilgilerimizden daha sık olduğunu göstermek-tedir. Direkt grafilerle bu kırıklara tanı konulamamakta ve bilgisayarlı tomografi (BT) taramasına ihtiyaç duyulmaktadır.[3] Günümüzde oldukça hızlı tüm spinal travma taraması yapa-bilen BT cihazlarının yaygınlaşması ile OKK daha sıklıkla sap-tanmaktadır. Mueller ve ark.[4] kendi çalışmalarında OKK insi-dansını %1.19/5 yıl olarak bildirmişlerdir. Çoğu zaman OKK’da konservatif tedavi yeterli olmaktadır. Ancak atlantooksipital instabilitenin (AOİ) eşlik ettiği olgularda oksipitoservikal füz-yon gerekebilmektedir. Morbidite ve mortalitesi yüksek sey-redebilen ve cerrahi girişim gerektiren bu tür olguları gözden kaçırmamak için, semptomsuz ya da hafif semptomlu travma hastalarında oksipitoservikal bileşke BT ile mutlaka detaylı in-celenmelidir.

OLGU SUNUMU

OLGU SUNUMU

Yirmi sekiz yaşında kadın hasta, acil servisimize araç içi trafik kazası sonrası kabul edildi. Hastanın acil servisteki fiziksel in-celemesinde, konuşma güçlüğüne yol açan iki taraflı temporo-mandibuler eklem bölgesinde ve üst servikal bölgede palpas-yonla hassasiyeti mevcuttu. Vital bulguları stabil olan hastanın fiziksel incelemesinde yaygın maksillofasyal ödem ve ekimoz-lar gözlendi. Nörolojik incelemesi tamamen normaldi. Servi-kal hassasiyet nedeniyle rijit boyunluk takıldı. Beyin ve servikal BT’lerde; iki taraflı zygoma ve maksiller kemikte LeFort 1 ile uyumlu minimal deplase kırık ve atlantooksipital dislokasyo-nun eşlik etmediği sol oksipital kondil kırığı saptandı (Şekil 1, 2). İki taraflı zygoma ark kırığı için ameliyat edilen hastanın en-tübasyonu fleksibil entübasyon ile sağlandı. Kondil kırığı nede-niyle rijit boyunluk ve yatak istirahati önerildi. Ek bir problemi olmayan hasta taburcu edildi. Üç ay sonraki kontrol servikal BT de füzyon saptanan hastanın boyunluğu çıkartılarak, boyun hareketleri için rehabilitasyon programına alındı.

TARTIŞMA

Oksipital kondil kırıklarının nadir görülen kırıklar olarak bi-linmesine karşın, son yıllarda yapılan çalışmalar acil servise travma ile başvuran her yüz hastadan birinde OKK olabile-ceğini göstermektedir.[4] Büyük bölümünün yüksek enerjili travmalardan sonra ortaya çıkmasına karşın, minör travmalar-dan sonra da OKK oluşabilir.[4] Özellikle üst servikal bölgede hassasiyeti bulunan semptomsuz, minör travmatize hastalarda OKK ihtimali mutlaka düşünülmelidir. Çocuk hastalarda ve

İletişim adresi: Dr. Ömer Aykanat,

Metek Toki Konutları, K1-46, Daire: 12, Düzce

Tel: +90 380 - 542 14 16 E-mail: [email protected]

Qucik Response Code Ulus Travma Acil Cerrahi Derg2014;20(3):224-226doi: 10.5505/tjtes.2014.22747

Telif hakkı 2014 TJTES

Ulus Travma Acil Cerrahi Derg, Mayıs 2014, Vol. 20, No. 3224

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Dinç ve ark. Oksipital kondil kırıkları

BT’nin yeterli görüntüleme sağlayamadığı olgularda manyetik rezonans görüntüleme (MRG) kullanılabilir.[5]

Literatürde OKK ile ilgili çalışma oldukça nadirdir ve çoğun-lukla olgu sunumu ya da geriye dönük çalışmalara dayanmak-tadır.[1,6,7] Tanısal alandaki gelişmeler ile artan sayıda olgu da literatürde yerini almıştır. 1988 yılına kadar literatürde yayınla-nan 20 olguya,[8] 1978-2002 yılları arasında 116 olgu eklenmiş-tir.[1] Günümüzde en çok kabul gören OKK sınıflandırmasını yapan Anderson ve Montesano,[8] bu sınıflamayı altı olguluk geriye dönük bir çalışma ile yapmışlardır. OKK’yı üç tip olarak tariflemişlerdir; tip 1, kondilin foramen magnuma deplasma-nı olmadan kompresyon kırığı. Tip 2, kaide kırığının oksipital kondile uzanımı. Bu iki tip stabil kırıklar olarak kabul edilmiş-tir. Tip 3, instabil olarak tariflenen avulsiyon kırığıdır. Mueller ve ark.[4] kendi çalışmalarında, bu üç kırık tipinin de servikal boyunluk ile altı hafta süreyle konservatif olarak tedavi edi-

lebildiğini; travmanın şiddeti, radyolojik ve klinik sonuçlar ve mortalite göz önüne alındığında istatistiksel olarak anlamlı bir fark olmadığını saptamışlardır. Anderson ve Montesano’nun[8] yaptığı sınıflamanın ihmal edilebilir olduğunu savunarak yeni bir fonksiyonel sınıflama önermişlerdir. Bu yeni sınıflama; Tip 1: tek taraflı, Tip 2: iki taraflı AOİ’nin eşlik etmediği; Tip 3 ise AOİ bulunan tek ya da iki taraflı OKK’yı tarif etmektedir.[4]

Atlantooksipital instabilitenin eşlik etmediği OKK’nın te-davisinde 6-12 hafta servikal boyunluk ya da Halo fiksatör ile immobilizasyon yeterli olmaktadır. Çoklutravmalı hasta-larda, özellikle maksillofasiyal travma ya da toraks travması nedeniyle solunum desteği gerekli olan olgularda, uygulama güçlüğü ve komplikasyonları açısından Halo fiksatör kullanı-mı önerilmemektedir.[1,4,6] AOİ bulunmayan iki taraflı OKK olguları benzer şekilde stabil olarak kabul edilerek servikal eksternal immobolizasyon tedavi edilebilir.[2,9] Bununla bir-likte, Dashti ve ark.,[10] inferior klivus kırığının eşlik ettiği iki taraflı OKK olan çoklutravmalı bir olguda Halo yelek kullanı-mı ile kemik iyileşmenin sağlandığını bildirmişlerdir. OKK’ya AOİ’nin eşlik etme riski %9.7’dir (Mueller ve ark.). Yüksek mortalite ve morbiditenin eşlik ettiği bu tür olguların tedavi-si cerrahi olup, oksipitoservikal füzyon gerektirmektedirler. Bunlara ek olarak; beyin sapı ya da spinal kord basısına neden olan, disloke kemik fragmanın izlendiği olgulara kırık tipine bakmaksızın acil olarak dekompresyon yapılarak sabitleme yapılmalıdır.

Sonuç olarak, OKK minör travmalardan sonra oluşabilir, has-talar semptomsuz olabilir ve direkt grafiler ile tanı konama-yabilir. Detaylı olarak BT görüntüleme ile bu kırıklara artan oranda tanı konabilmektedir. Oksipitoservikal bileşke şüpheli olgularda mutlaka BT ile taranmalıdır. Çoğunlukla konservatif olarak tedavi edilebilen bu kırıklara nadiren atlantooksipital instabilite eşlik edebilir ve oksiptoservikal stabilizasyon gerek-tirir.

(a) (b)

Şekil 1. (a)AksiyelkesitlikraniyalBT’deposterioradeplasesoloksipitalkondilkırığıizlenmekte.(b)KoronerkesitlikraniyalBT’deposteri-oradeplasesoloksipitalkondilkırığıizlenmekte.

Şekil 2. Aksiyelkesitlikraniyalbilgisayarlıtomografideposterioradeplasesoloksipitalkondilkırığındakifüzyonizlenmekte.

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Dinç ve ark. Oksipital kondil kırıkları

Çıkar örtüşmesi: Çıkar örtüşmesi bulunmadığı belirtilmiştir.

KAYNAKLAR

1. Caroli E, Rocchi G, Orlando ER, Delfini R. Occipital condyle fractures: report of five cases and literature review. Eur Spine J 2005;14:487-92.

2. Maserati MB, Stephens B, Zohny Z, Lee JY, Kanter AS, Spiro RM, et al. Occipital condyle fractures: clinical decision rule and surgical manage-ment. J Neurosurg Spine 2009;11:388-95.

3. Hanson JA, Deliganis AV, Baxter AB, Cohen WA, Linnau KF, Wilson AJ, et al. Radiologic and clinical spectrum of occipital condyle fractures: retrospective review of 107 consecutive fractures in 95 patients. AJR Am J Roentgenol 2002;178:1261-8.

4. Mueller FJ, Fuechtmeier B, Kinner B, Rosskopf M, Neumann C, Nerlich M, et al. Occipital condyle fractures. Prospective follow-up of 31 cases within 5 years at a level 1 trauma centre. Eur Spine J 2012;21:289-94.

5. Kapapa T, Tschan CA, König K, Schlesinger A, Haubitz B, Becker H, et al. Fracture of the occipital condyle caused by minor trauma in child. J Pediatr Surg 2006;41:1774-6.

6. Malham GM, Ackland HM, Jones R, Williamson OD, Varma DK. Occipital condyle fractures: incidence and clinical follow-up at a level 1 trauma centre. Emerg Radiol 2009;16:291-7.

7. Leone A, Cerase A, Colosimo C, Lauro L, Puca A, Marano P. Occipital condylar fractures: a review. Radiology 2000;216:635-44.

8. Anderson PA, Montesano PX. Morphology and treatment of occipital condyle fractures. Spine 1988;13:731-6.

9. Schrödel MH, Kestlmeier R, Trappe AE. Bilateral occipital condyle frac-ture: report of two cases. Skull Base 2002;12:93-6.

10. Dashti R, Ulu MO, Albayram S, Aydin S, Ulusoy L, Hanci M. Concomi-tant fracture of bilateral occipital condyle and inferior clivus: what is the mechanism of injury? Eur Spine J 2007;16 Suppl 3:261-4.

C A S E R E P O R T - ABSTRACT

Occipital condyle fractures: A case reportCem Dinç, M.D.,1 Mehmet Erhan Türkoğlu, M.D.,2 Cengiz Tuncer, M.D.,1

Ömer Aykanat, M.D.,1 Derya Özçelik, M.D.,3 Gamze Özkan, M.D.3

1DepartmentofBrainandNeurosurgery,DüzceUniversityFacultyofMedicine,Düzce2DepartmentofBrainandNeurosurgery,DışkapıTrainingandResearchHospital,Ankara3DepartmentofPlasticandReconstructiveSurgery,DüzceUniversityFacultyofMedicine,Düzce

Occipital condyle fractures are rare, and conservative treatment is sufficient for many cases. Surgical treatment may be required if the condyle fracture is accompanied by atlantooccipital dislocation. Unfortunately, condyle fracture generally cannot be diagnosed with X-ray in the emergency department. Recently, computed tomography scans have been used more frequently, and enable easier diagnosis of these types of fractures. In this report, we describe a patient who admitted to our emergency department after a major trauma. She complained of neck pain, and maxillofacial trauma was more evident. Her cervical X-rays were normal, but cervical computed tomography revealed unilateral occipital condyle fracture.Key words: Atlantooccipital dislocation; conservative treatment; occipital condyle fracture; surgery.

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