Travma 2014 / 3 by KAREPUBLISHING

ISSN 1306 - 696X

TURKISH JOURNAL of TRAUMA & EMERGENCY SURGERY Ulusal Travma ve Acil Cerrahi Dergisi

Volume 20 | Number 3 | May 2014

www.tjtes.org

TURKISH JOURNAL of TRAUMA & EMERGENCY SURGERY Ulusal 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

THE TURKISH ASSOCIATION OF TRAUMA AND EMERGENCY SURGERY ULUSAL TRAVMA VE ACİL CERRAHİ DERNEĞİ President (Başkan) Vice President (Başkan Yardımcısı) Secretary General (Genel Sekreter) Treasurer (Sayman) Members (Yönetim Kurulu Üyeleri)

Recep Güloğlu Kaya Sarıbeyoğlu M. Mahir Özmen Ali Fuat Kaan Gök Hakan Teoman Yanar Gürhan Çelik Osman Şimşek

CORRESPONDENCE İLETİŞİM Ulusal Travma ve Acil Cerrahi Derneği Şehremini Mah., Köprülü Mehmet Paşa Sok. Dadaşoğlu Apt., No: 25/1, 34104 Şehremini, İstanbul, Turkey

Tel: +90 212 - 588 62 46 - 588 62 46 Fax (Faks): +90 212 - 586 18 04 e-mail (e-posta): travma@travma.org.tr Web: www.travma.org.tr

ISSUED BY THE TURKISH ASSOCIATION OF TRAUMA AND EMERGENCY SURGERY ULUSAL TRAVMA VE ACİL CERRAHİ DERNEĞİ YAYIN ORGANI Owner (Ulusal Travma ve Acil Cerrahi Derneği adına Sahibi) Editorial Director (Yazı İşleri Müdürü) Managing Editor (Yayın Koordinatörü) Amblem Correspondence address (Yazışma adresi) Tel Fax (Faks)

Recep Güloğlu Recep Güloğlu M. Mahir Özmen Metin Ertem Ulusal Travma ve Acil Cerrahi Dergisi Sekreterliği Şehremini Mah., Köprülü Mehmet Paşa Sok., Dadaşoğlu Apt., No: 25/1, 34104 Şehremini, İstanbul +90 212 - 531 12 46 - 588 62 46 +90 212 - 586 18 04

Annual subscription rates: 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.)

KARE www.tjtes.org

INFORMATION FOR THE AUTHORS The Turkish Journal of Trauma and Emergency Surgery (TJTES) is an official publication of the Turkish Association of Trauma and Emergency Surgery. It is a peer-reviewed periodical that considers for publication clinical and experimental studies, case reports, technical contributions, and letters to the editor. Six issues are published annually.

tion, called “Upload Your Files”.

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 / Science 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.

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 photomicrographs 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 prepared. 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.

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 Association 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 language 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 addition 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, rejected manuscripts will not be returned to the authors, including accompanying materials. TJTES is indexed in Science Citation Index-Expanded (SCI-E), Index Medicus, Medline, EMBASE, Excerpta Medica, and the Turkish Medical Index of TUBITAK-ULAKBIM. Priority of publications is given to original studies; therefore, selection criteria are more refined for reviews 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 further information you may visit the web site (http://www.travma.org/en/ journal/). Manuscript preparation: Manuscripts should have double-line spacing, 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 institutions and correspondence address, abstract in Turkish (for Turkish authors only), and title and abstract in English are uploaded to the Journal Agent system in the relevant steps. The main text includes Introduction, 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 submitted 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-

Abstract: The abstract should be structured and serve as an informative 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.

References: All references should be numbered in the order of mention in the text. All reference figures in the text should be given in brackets without changing the font size. References should only include articles that have been published or accepted for publication. Reference format should conform to the “Uniform requirements for manuscripts submitted to biomedical journals” (http://www.icmje.org) and its updated versions (February 2006). Journal titles should be abbreviated 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: McGraw-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 articles 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 issue of the journal. The presented case(s) should be educative and of interest to the readers, and should reflect an exclusive rarity. Case reports should contain the title, summary, and the case, discussion, and references sections. These reports may consist of maximum five authors. Letters to the Editor: “Letters to the Editor” are only published electronically 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 exceed 500 words. The letter must clearly list the title, authors, publication date, issue number, and inclusive page numbers of the publication for which opinions are released. Informed consent - Ethics: Manuscripts reporting the results of experimental 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.

YAZARLARA BİLGİ Ulusal Travma ve Acil Cerrahi Dergisi, Ulusal Travma ve Acil Cerrahi Derneği’nin yayın organıdır. Travma ve acil cerrahi hastalıklar konularında 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 Medicus 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 indekslerinde ve 2008 yılından itibaren Index Copernicus indeksinde yer almaktadır. 2001-2006 yılları arasındaki 5 yıllık dönemde SCI-E kapsamındaki 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 dışında), başka bir yerde yayınlanmasının düşünülmediği ve Ulusal Travma ve Acil Cerrahi Dergisi’nde yayınlanmasının tüm yazarlar tarafından uygun bulunduğu anlamına gelmektedir. Yazar(lar), çalışmanın yayınlanmasının kabulünden başlayarak, yazıya ait her hakkı Ulusal Travma ve Acil Cerrahi Derneği’ne devretmektedir(ler). Yazar(lar), izin almaksızın 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 yazılar önce editör tarafından ön değerlendirmeye alınır; daha sonra incelenmesi için danışma kurulu üyelerine gönderilir. Tüm yazılarda editöryel değerlendirme ve düzeltmeye başvurulur; gerektiğinde, yazarlardan bazı soruları yanıtlanması ve eksikleri tamamlanması istenebilir. Dergide yayınlanmasına karar verilen yazılar “manuscript 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 zorunluluğu 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. Sayfada her iki tarafta uygun miktarda boşluk bırakılmalı ve ana metindeki sayfalar numaralandırılmalıdır. Journal Agent sisteminde, başvuru mektubu, başlık, yazarlar ve kurumları, iletişim adresi, Türkçe özet ve yazının İngilizce başlığı ve özeti ilgili aşamalarda yüklenecektir. İngilizce yazılan 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 okunduğu, 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” bölümünde, 10. aşamada yer alan dosya yükleme aşamasında yollanmalıdır. Başlık sayfası: Yazının başlığı, yazarların adı, soyadı ve ünvanları, çalışmanın yapıldığı kurumun adı ve şehri, eğer varsa çalışmayı destekleyen fon ve kuruluşların açık adları bu sayfada yer almalıdır. Bu sayfaya ayrıca “yazışmadan sorumlu” yazarın isim, açık adres, telefon, faks, mobil 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 Sözcükler başlıklarını; İngilizce özet Background, Methods, Results, Conclusion ve Key words başlıklarını içermelidir. İngilizce olarak hazırlanan çalışmalarda da Türkçe özet yer almalıdır. Özetler başlıklar hariç 190210 sözcük olmalıdır. Tablo, şekil, grafik ve resimler: Şekillere ait numara ve açıklayıcı bilgiler 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. Makale içinde geçen kaynak numaraları köşeli parantezle ve küçültülmeden belirtilmelidir. Kaynak listesinde yalnızca yayınlanmış ya da yayınlanması 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.” eklenmelidir. 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.travma.org.tr adresli web sayfamızda eski yayınlara tam metin olarak ulaşabileceğiniz bir arama motoru vardır. Derleme yazıları: Bu tür makaleler editörler kurulu tarafından gerek olduğunda, konu hakkında birikimi olan ve bu birikimi literatüre de yansımış kişilerden talep edilecek ve dergi yazım kurallarına uygunluğu saptandıktan sonra değerlendirmeye alınacaktır. Derleme makaleleri; başlık, Türkçe özet, İngilizce başlık ve özet, alt başlıklarla bölümlendirilmiş metin ile kaynakları içermelidir. Tablo, şekil, grafik veya resim varsa yukarıda belirtildiği şekilde gönderilmelidir. Olgu sunumları: Derginin her sayısında sınırlı sayıda olgu sunumuna yer verilmektedir. Olgu bildirilerinin kabulünde, az görülürlük, eğitici olma, ilginç olma önemli ölçüt değerlerdir. Ayrıca bu tür yazıların olabildiğince kısa hazırlanması gerekir. Olgu sunumları başlık, Türkçe özet, İngilizce başlık ve özet, olgu sunumu, tartışma ve kaynaklar bölümlerinden 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 mektuplar 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 olarak 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 bildiren 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 hükümlere uyulduğunu belirtmeli ve kurumdan aldıkları Etik Komitesi onayını göndermelidir. Hayvanlar üzerinde yapılan çalışmalarda ağrı, acı ve rahatsızlık verilmemesi için neler yapıldığı açık bir şekilde belirtilmelidir. Yazı gönderme - Yazıların gönderilmesi: Ulusal Travma ve Acil Cerrahi 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 “Online Makale Gönderme” ikonuna tıklandığında ulaşılan Journal Agent sisteminden yollanmaktadır. Sistem her aşamada kullanıcıyı bilgilendiren özelliktedir.

TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY ULUSAL TRAVMA VE ACİL CERRAHİ DERGİSİ Vol. - Cilt 20

Number - Sayı 3 May - Mayıs 2014

Contents - İçindekiler

Experimental Study - Deneysel Çalışma 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

Original Articles - KlinikArticles Çalışma Klinik Çalışma - Original 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

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TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY ULUSAL TRAVMA VE ACİL CERRAHİ DERGİSİ Vol. - Cilt 20

Number - Sayı 3 May - Mayıs 2014

Contents - İçindekiler

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 CaseSunumu Reports- -Case OlguReports Sunumu 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

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

EXPERIMENTAL STUDY

Captopril protects against burn-induced cardiopulmonary injury in rats Esra 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 1

Department of Laboratory of Clinical Pharmacogenetics, Uskudar University Istanbul Neuropsychiatry Hospital, Istanbul

Department of Pharmacology, Marmara University Faculty of Pharmacy, Istanbul

Department of Medical Pharmacology, Marmara University Faculty of Medicine, Istanbul

Department of Histology & Embryology, Marmara University Faculty of Medicine, Istanbul

Department of Biochemistry, Marmara University Faculty of Pharmacy, Istanbul

Department of Cardiology, Gulhane Military Medical Academy, Istanbul

ABSTRACT BACKGROUND: This study was designed to determine the possible protective effect of captopril treatment against oxidative damage 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 disturbances. It causes direct tissue damage as well as inflammatory reactions.[1] Thermal trauma causes a progressive decrease in #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: esra.k.saglam@gmail.com Qucik Response Code

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

cardiac output and cardiac stroke volume, release of vasoconstrictor 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 pulmonary 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 output and cardiac dysfunction after severe thermal trauma.[5,6] Angiotensin converting enzyme (ACE) catalyzes the conversion of angiotensin I (Ang I) to angiotensin II (Ang II). ACE also cleaves the terminal dipeptide of vasodilating hormone bradykinin 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 etiology of high blood pressure, obesity and metabolic syndrome. [7] Therefore, inhibition of ACE is generally used as one of the 151

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

methods in the treatment of hypertension and chronic inflammation.[8,9] Pharmacologically, it is known that ACE inhibitors containing a sulfhydryl or a thiol radical, such as the orally active compound captopril, have an antioxidant activity.[10,11] In the light of these findings, we hypothesized that captopril would provide protection against burn-induced cardiopulmonary 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 Animals Wistar albino rats of both sexes, weighing 200-250 g, were obtained from Marmara University School of Medicine Animal 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 experiments, but were allowed free access to water. All experimental protocols were approved by the Marmara University Animal Care and Use Committee.

Thermal Injury and Experimental Design This 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 treated 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 applied 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, intraperitoneal (i.p.); Sigma-Aldrich; St. Louis, MO, USA) or saline 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 saline 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 administration of captopril could potentially have a systemic effect.[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 echocardiography 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 determination of pro-inflammatory cytokine [tumor necrosis factor-α (TNF-α)], malondialdehyde (MDA) and glutathione (GSH) 152

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 experienced histologist who was unaware of the treatment conditions performed the histological assessments.

Echocardiography Echocardiographic imaging and calculations were done according 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 parasternal long- and short axes at the level of the papillary muscles after observation of at least six cardiac cycles. Interventricular 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 images 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 enzyme-linked immunosorbent assay (ELISA). Heart and lung tissues (100 mg) were homogenized in an ice-cold bath. After 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. Absorbance of standards and samples was determined on a plate reader at 405 nm. Results are expressed as pg/100 mg tissue.

Malondialdehyde and Glutathione Assays Tissue 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 modification 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 measured immediately after mixing. GSH levels were calculated Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

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

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

Myeloperoxidase Activity Myeloperoxidase (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 histochemically 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 present 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 enzyme required for cellular transport, is very sensitive to free radical reactions and lipid peroxidation, reductions in this activity can indicate membrane damage indirectly. Measurement of Na+, K+-ATPase activity is based on the measurement of inorganic phosphate released by ATP hydrolysis during incubation of homogenates with an appropriate medium containing 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 presence 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 addition of the homogenate (0.1 ml), and a 5-min preincubation 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 supernatant fraction was determined by the method of Fiske and Subarrow.[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 Activity Caspase-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 manufacturer. 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 (AspGlu-Val-Asp p-nitroanilide) substrate (200 µM final concentration), 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 pretreatment level (untreated samples).

Histopathological Analysis For light microscopic investigations, heart and lung specimens

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 experienced histologist who was unaware of the experimental groups.

Statistics Statistical 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 measurements of the experimental groups. In the saline-treated burn group, LVPW, LV end-diastolic and end-systolic dimensions 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

(a)

3000

Saline-treated

the other hand, in the captopril-treated burn group, echocardiographic 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-treated burn group were significantly increased, while TNF-α levels 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 levels 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 significantly 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-

(a)

Saline-treated

Captopril-treated

TNF-a (pg/100 mg tissue)

(b)

+++ 1000

***

Burn

2000

+++

++ 2

***

1000

0 Burn

Figure 1. Tumor necrosis factor-α (TNF-α) levels in the (a) heart and (b) lung tissues of control (C) and saline- or captopril-treated burn groups. Each group consists of 8 animals. ***: p<0.001: compared to saline-treated control group; +++: p<0.001: compared to saline-treated burn group.

154

Burn

(b)

3000

4000

GSH (μmol/g)

***

2000

GSH (μmol/g)

TNF-a (pg/100 mg tissue)

Captopril-treated

Burn

Figure 2. Glutathione (GSH) levels in the (a) heart and (b) lung tissues of control (C) and saline- or captopril-treated burn groups. Each group consists of 8 animals. **: p<0.01, ***: p<0.001: compared to saline-treated control group; + p<0.05, ++: p<0.01: compared to saline-treated burn group.

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

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

(a) 100

Saline-treated

MPO (U/g)

Burn

(b) 100

(b) 40

Burn

60 40

MPO (U/g)

MDA (nmol/g)

Captopril-treated

***

+++ 10

20 0

***

Saline-treated

Captopril-treated

80 MDA (nmol/g)

(a) 40

0 Burn

Burn

Figure 3. Malondialdehyde (MDA) levels in the (a) heart and (b) lung tissues of control (C) and saline- or captopril-treated burn groups. Each group consists of 8 animals. **: p<0.01, ***: p<0.001: compared to saline-treated control group; +: p<0.05: compared to saline-treated burn group.

Figure 4. Myeloperoxidase (MPO) activity in the (a) heart and (b) lung tissues of control (C) and saline- or captopril-treated burn groups. Each group consists of 8 animals. ***: p<0.001: compared to saline-treated control group; ++: p<0.01, +++: p<0.001: compared to saline-treated burn group.

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).

DISCUSSION

Caspase-3 activities in both the heart and lung tissues were increased significantly (p<0.001), while treatment with captopril 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 connective tissue of muscle fibers showed congestion in addition to vacuolization in the cytoplasm of most of the cardiomyocytes (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 welldesignated 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). Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

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 proinflammatory cytokines will activate non-specific host immunity, tissue injury or infection, cytokines are approached as being important components in the postburn pathophysiological process. [21-23] Accordingly, after thermal trauma, a great many cytokines are induced rapidly,[12,24-27] and ACE mediates inflammation 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 demonstrate that burn-induced cardiac and lung injury involve oxidant formation and inflammation, while captopril treatment greatly attenuated these responses. The ability of captopril to protect against thermal trauma was observed with significant decreases in tissue MDA and TNF-Îą levels and MPO and caspase-3 activities, which were found to be increased 155

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

(a)

Saline-treated

(a)

***

(b)

Caspase-3 activity (fold increase)

Na+-K+ATPase (μmol/mg protein/h)

Captopril-treated

Burn

(b)

2.5

Captopril-treated

+++

Saline-treated

Burn

2.0 1.5

Caspase-3 activity (fold increase)

Na+-K+ATPase (μmol/mg protein/h)

+++

***

1.0

***

0.5 0

0 Burn

Burn

Figure 5. Na+-K+ ATPase activity in the (a) heart and (b) lung tissues of control (C) and saline- or captopril-treated burn groups. Each group consists of 8 animals. ***: p<0.001: compared to saline-treated control group; +: p<0.05, +++: p<0.001: compared to saline-treated burn group.

Figure 6. Caspase-3 activity in the (a) heart and (b) lung tissues of control (C) and saline- or captopril-treated burn groups. Each group consists of 8 animals. ***: p<0.001: compared to saline-treated control group; ++: p<0.01, +++: p<0.001: compared to salinetreated burn group.

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.

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 expression is associated with improved cardiac function.

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 demonstrated that increased serum TNF-α, which plays an essential role in the inflammatory processes, was also decreased with captopril 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 transforming 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 156

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 cardiovascular function such as reduced cardiac output, myocardial inflammation and an intrinsic defect in myocardial performance 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 therapeutic 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 levels and MPO, Na+, K+-ATPase and caspase activities were reversed in both tissues. One of the causative agents accountable for the development of burn shock and distant organ damage in animal models of burn injury are oxygen radicals.[27] Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

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

Figure 7. (a) Control group: regular alignment of muscle cells with centrally located nuclei (**). (b) Burn group: capillary vasocongestion among the connective tissue of the muscle cells (arrow), vacuolization in the cytoplasm of the cardiac muscle cells and degeneration of some gapjunctions (arrowhead). (c) Burn and captopril treatment: the capillary vasocongestion was reduced, and vacuolization in the cytoplasm of the cells was decreased (**), H&E staining, x200, insets x400.

Figure 8. (a) Control group demonstrated a regular alveolar structure (arrow) with no distention in its walls. (b) Burn group, severe congestion (**) and interstitial edema, which led to a decrease in alveolar space (arrow) in most areas of the tissue. In some regions, the alveoli united with each other resulting in large distended alveolar spaces (arrowhead-inset). (c) Burn and captopril group: reduced interstitial congestion and edema (**) and expanded alveolar areas and no congestion present.

The distant organs involved in the thermal damage during experimental 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, accumulation and activation of neutrophils induce tissue damage and release of different cytotoxic proteins into the extracellular fluid. MPO activity, an indirect marker of neutrophil infiltration,[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 other hand, in the captopril- treated burn groups, MPO activities 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 occlusion 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 dosedependent manner. Furthermore, Li et al.[44] demonstrated Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

that pathological injury of the lung in rats with intense acute pancreatitis was decreased with captopril treatment. Malondialdehyde (MDA), an end product of lipid peroxidation, 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 antioxidant system. The GSH molecule acts as an electron acceptor 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 antioxidant. 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. 157

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

Apoptosis is an orchestrated form of cell ‘death by suicide’. It is principal in both the development and normal continuation 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 characterizing a “systemic apoptotic response”.[49] Currently, ROS may mediate apoptosis through the starting of poly (ADPribose) polymerase (PARP), advances in mitochondrial permeability 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 diffuse across cell membranes, including the lysosomal membrane. 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 lysosome 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 apoptosis. On the other hand, captopril treatment effectively lessened caspase-3 activity and protected tissues, as also confirmed histologically. Na+, K+-ATPase is a considerable membrane protein that carries 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 cellular transport, is very sensitive to free radical reactions and lipid peroxidation, decrease in this activity can show membrane 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 control 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 treatment 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 provided regular cellular morphology in lung and heart tissues, 158

which caused a concomitant decrease in lipid peroxidation and increase in tissue antioxidant defense. Therefore, these results suggest an anti-inflammatory, cardiopulmonary protective effect of captopril, with a reduction in the circulating proinflammatory markers and an increase in those antiinflammatory cytokines; these effects result in a benefit on the cardiopulmonary inflammatory process associated with burninduced thermal trauma. Thus, captopril treatment merits consideration as a potential therapeutic agent for restoring organ damage following thermal trauma. Conflict of interest: None declared.

REFERENCES 1. Chandran PK, Kuttan R. Effect of Calendula officinalis Flower Extract on Acute Phase Proteins, Antioxidant Defense Mechanism and Granuloma Formation During Thermal Burns. J Clin Biochem Nutr 2008;43:5864. 2. Parihar A, Parihar MS, Milner S, Bhat S. Oxidative stress and anti-oxidative mobilization in burn injury. Burns 2008;34:6-17. 3. Horton JW, Garcia NM, White DJ, Keffer J. Postburn cardiac contractile function and biochemical markers of postburn cardiac injury. J Am Coll Surg 1995;181:289-98. 4. Mueller M, Sartorelli K, DeMeules JE, Gamelli RL. Effects of fluid resuscitation on cardiac dysfunction following thermal injury. J Surg Res 1988;44:745-53. 5. Adams HR, Baxter CR, Izenberg SD. Decreased contractility and compliance of the left ventricle as complications of thermal trauma. Am Heart J 1984;108:1477-87. 6. Gao S, Chen ZW, Zheng H, Chen XL. Ligustrazine attenuates acute myocardium injury after thermal trauma. Burns 2007;33:321-7. 7. de Kloet AD, Krause EG, Woods SC. The renin angiotensin system and the metabolic syndrome. Physiol Behav 2010;100:525-34. 8. Bhuyan BJ, Mugesh G. Synthesis, characterization and antioxidant activity of angiotensin converting enzyme inhibitors. Org Biomol Chem 2011;9:1356-65. 9. Kubota M, Shimizu M, Sakai H, Yasuda Y, Ohno T, Kochi T, et al. Renin-angiotensin system inhibitors suppress azoxymethane-induced colonic preneoplastic lesions in C57BL/KsJ-db/db obese mice. Biochem Biophys Res Commun 2011;410:108-13. 10. Molteni A, Ward WF, Ts’ao CH, Taylor J, Small W Jr, Brizio-Molteni L, et al. Cytostatic properties of some angiotensin I converting enzyme inhibitors and of angiotensin II type I receptor antagonists. Curr Pharm Des 2003;9:751-61. 11. Bagchi D, Prasad R, Das DK. Direct scavenging of free radicals by captopril, an angiotensin converting enzyme inhibitor. Biochem Biophys Res Commun 1989;158:52-7. 12. Sener G, Sehirli AO, Satiroğlu H, Keyer-Uysal M, C Yeğen B. Melatonin improves oxidative organ damage in a rat model of thermal injury. Burns 2002;28:419-25. 13. Ripley EB, Gehr TW, Kish CW, Sica DA. Hormonal, blood pressure, and peritoneal transport response to short-term ACE inhibition. Perit Dial Int 1994;14:378-83. 14. Schiller NB, Shah PM, Crawford M, DeMaria A, Devereux R, Feigenbaum H, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-

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Saglam et al. Captopril protects against burn-induced cardiopulmonary injury in rats Dimensional Echocardiograms. J Am Soc Echocardiogr 1989;2:358-67. 15. Buege JA, Aust SD. Microsomal lipid peroxidation. Methods Enzymol 1978;52:302-10. 16. Beutler E. Glutathione in red blood cell metabolism. A manual of biochemical methods. E Beutler (editor). New York: Grune&Stratton; 1975. p. 112-4. 17. Hillegass LM, Griswold DE, Brickson B, Albrightson-Winslow C. Assessment of myeloperoxidase activity in whole rat kidney. J Pharmacol Methods 1990;24:285-95. 18. Reading HW, Isbir T. The role of cation-activated ATPases in transmitter release from the rat iris. Q J Exp Physiol Cogn Med Sci 1980;65:10516. 19. Fiske CH, Subbarow Y. The colorimetric determination of phosphorus. J Biol Chem 1925;66:375-400. 20. LOWRY OH, ROSEBROUGH NJ, FARR AL, RANDALL RJ. Protein measurement with the Folin phenol reagent. J Biol Chem 1951;193:265-75. 21. Ravage ZB, Gomez HF, Czermak BJ, Watkins SA, Till GO. Mediators of microvascular injury in dermal burn wounds. Inflammation 1998;22:61929. 22. Yeh FL, Lin WL, Shen HD. Changes in circulating levels of an anti-inflammatory cytokine interleukin 10 in burned patients. Burns 2000;26:454-9. 23. Summer GJ, Romero-Sandoval EA, Bogen O, Dina OA, Khasar SG, Levine JD. Proinflammatory cytokines mediating burn-injury pain. Pain 2008;135:98-107. 24. Sener G, Sehirli AO, Gedik N, Dülger GA. Rosiglitazone, a PPARgamma ligand, protects against burn-induced oxidative injury of remote organs. Burns 2007;33:587-93. 25. Sehirli O, Sener E, Sener G, Cetinel S, Erzik C, Yeğen BC. Ghrelin improves burn-induced multiple organ injury by depressing neutrophil infiltration and the release of pro-inflammatory cytokines. Peptides 2008;29:1231-40. 26. Wang G, Tian J, Tang H, Zhu S, Huan J, Ge S, et al. The role of Kupffer cells on the postburn production of TNFalpha, IL-1beta and IL-6 in severely scalded rats. [Article in Chinese] Zhonghua Shao Shang Za Zhi 2002;18:282-4. [Abstract] 27. Demiralay E, Saglam IY, Ozdamar EN, Sehirli AO, Sener G, Saglam E. nNOS expression in the brain of rats after burn and the effect of the ACE inhibitor captopril. Burns 2012. pii: S0305-4179(12)00328-2. 28. Constantinescu CS, Ventura E, Hilliard B, Rostami A. Effects of the angiotensin converting enzyme inhibitor captopril on experimental autoimmune encephalomyelitis. Immunopharmacol Immunotoxicol 1995;17:471-91. 29. Jerng JS, Hsu YC, Wu HD, Pan HZ, Wang HC, Shun CT, et al. Role of the renin-angiotensin system in ventilator-induced lung injury: an in vivo study in a rat model. Thorax 2007;62:527-35. 30. Dutka DP, Elborn JS, Delamere F, Shale DJ, Morris GK. Tumour necrosis factor alpha in severe congestive cardiac failure. Br Heart J 1993;70:1413. 31. Levine B, Kalman J, Mayer L, Fillit HM, Packer M. Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N Engl J Med 1990;323:236-41. 32. Miguel-Carrasco JL, Zambrano S, Blanca AJ, Mate A, Vázquez CM. Captopril reduces cardiac inflammatory markers in spontaneously hypertensive rats by inactivation of NF-kB. J Inflamm (Lond) 2010;7:21. 33. Youn TJ, Kim HS, Oh BH. Ventricular remodeling and transforming growth factor-beta 1 mRNA expression after nontransmural myocardial infarction in rats: effects of angiotensin converting enzyme inhibition and

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angiotensin II type 1 receptor blockade. Basic Res Cardiol 1999;94:24653. 34. Albuquerque D, Nihei J, Cardillo F, Singh R. The ACE inhibitors enalapril and captopril modulate cytokine responses in Balb/c and C57Bl/6 normal mice and increase CD4(+)CD103(+)CD25(negative) splenic T cell numbers. Cell Immunol 2010;260:92-7. 35. Lang CH, Frost RA, Vary TC. Thermal injury impairs cardiac protein synthesis and is associated with alterations in translation initiation. Am J Physiol Regul Integr Comp Physiol 2004;286:R740-50. 36. Lupia E, Spatola T, Cuccurullo A, Bosco O, Mariano F, Pucci A, et al. Thrombopoietin modulates cardiac contractility in vitro and contributes to myocardial depressing activity of septic shock serum. Basic Res Cardiol 2010;105:609-20. 37. Zang QS, Maass DL, Wigginton JG, Barber RC, Martinez B, Idris AH, et al. Burn serum causes a CD14-dependent mitochondrial damage in primary cardiomyocytes. Am J Physiol Heart Circ Physiol 2010;298:H1951-8. 38. Xiao R, Lei ZY, Dang YM, Huang YS. Prompt myocardial damage contributes to hepatic, renal, and intestinal injuries soon after a severe burn in rats. J Trauma 2011;71:663-72. 39. Marciniak A, Szpringer E, Lutnicki K, Beltowski J. Influence of early excission of burn wound on the lipid peroxidation in selected rat tissues. Bull Vet Pulawy 2002;46:255-65. 40. Bradley PP, Priebat DA, Christensen RD, Rothstein G. Measurement of cutaneous inflammation: estimation of neutrophil content with an enzyme marker. J Invest Dermatol 1982;78:206-9. 41. Işeri SO, Gedik IE, Erzik C, Uslu B, Arbak S, Gedik N, et al. Oxytocin ameliorates skin damage and oxidant gastric injury in rats with thermal trauma. Burns 2008;34:361-9. 42. Leor J, Varda-Bloom N, Hasdai D, Ovadia Z, Battler A. Failure of captopril to attenuate myocardial damage, neutrophil accumulation, and mortality following coronary artery occlusion and reperfusion in rat. Angiology 1994;45:717-24. 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 vitro 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 Chinese] 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. Leukotriene receptor blocker montelukast protects against burn-induced oxidative 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. 47. Ballatori N, Krance SM, Notenboom S, Shi S, Tieu K, Hammond CL. Glutathione dysregulation and the etiology and progression of human diseases. Biol Chem 2009;390:191-214. 48. Gurer H, Neal R, Yang P, Oztezcan S, Ercal N. Captopril as an antioxidant in lead-exposed Fischer 344 rats. Hum Exp Toxicol 1999;18:27-32. 49. Gravante G, Delogu D, Sconocchia G. “Systemic apoptotic response” after thermal burns. Apoptosis 2007;12:259-70. 50. Shupp JW, Nasabzadeh TJ, Rosenthal DS, Jordan MH, Fidler P, Jeng JC. A review of the local pathophysiologic bases of burn wound progression. J Burn Care Res 2010;31:849-73. 51. Gibran NS, Heimbach DM. Current status of burn wound pathophysiology. Clin Plast Surg 2000;27:11-22.

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54. Uhal BD, Gidea C, Bargout R, Bifero A, Ibarra-Sunga O, Papp M, et al. Captopril inhibits apoptosis in human lung epithelial cells: a potential antifibrotic mechanism. Am J Physiol 1998;275:L1013-7.

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

55. Ottlecz A, Bensaoula T. Captopril ameliorates the decreased Na+,K(+)ATPase activity in the retina of streptozotocin-induced diabetic rats. Invest Ophthalmol Vis Sci 1996;37:1633-41.

DENEYSEL ÇALIŞMA - ÖZET OLGU SUNUMU

Sıçanlarda yanıkla uyarılan kardiyopulmoner hasara karşı kaptoprilin koruyucu etkisi Dr. 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 Üsküdar Üniversitesi, İstanbul Nöropsikiyatri Hastanesi, Klinik Farmakogenetik Laboratuvarı, İstanbul Marmara Üniversitesi Eczacılık Fakültesi, Farmakoloji Anabilim Dalı, İstanbul 3 Marmara Üniversitesi Tıp Fakültesi, Tıbbi Farmakoloji Anabilim Dalı, İstanbul 4 Marmara Üniversitesi Tıp Fakültesi, Histoloji ve Embriyoloji Anabilim Dalı, İstanbul 5 Marmara Üniversitesi Eczacılık Fakültesi, Biokimya Anabilim Dalı, İstanbul 6 Gülhane Askeri Tıp Akademisi, Kardiyoloji Anabilim Dalı, İstanbul 1 2

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 hasarından 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 bulundu. 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

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doi: 10.5505/tjtes.2014.96493

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EXPERIMENTAL STUDY

The effect of hyperbaric oxygen therapy on fracture healing in nicotinized rats Abdullah 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 1

Department of Orthopaedics and Traumatology, Dicle University Faculty of Medicine, Diyarbakir

Department of Pathology, Dicle University Faculty of Medicine, Diyarbakir

Department of Biophysics, Dicle University Faculty of Medicine, Diyarbakir

Department of Biostatistics and Medical Informatics, Dicle University Faculty of Medicine, Diyarbakir

Department of Undersea and Hyperbaric Medicine, Anadolu Hyperbaric Oxygen Centre, 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]

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: abdullah_demirtas@yahoo.com Qucik Response Code

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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 method 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 fracture 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 161

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

radiological, histopathological and dual-energy X-ray absorptiometry (DXA) findings. In this study, we investigated the effects of nicotine and HBO together in fracture healing in terms of radiological, histopathological 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): nicotinized (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, unlimited 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 atmospheric pressure 100% oxygen as a single session, 2 hours/ day) was applied in Groups 2 and 3 starting immediately after 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 anesthesia. 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 histopathological evaluations. One rat in Group 1 was excluded due to infection at the fracture site.

Surgical Procedure Preoperatively, anesthetic ketamine (Ketalar®, Pfizer, Istanbul, Turkey) 50 mg/kg and xylazine (Rompun®, Bayer, Istanbul, Turkey) 10 mg/kg combination was administered subcutaneously. 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). Under sterile conditions, a 2-2.5 cm incision was made starting anterolateral of the left knee, extending to the lateral femur distally. Proximally, the joint was reached via the lateral parapatellar approach. The femoral condyles were ex162

Figure 1. The images of the rats during HBO application.

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 stabilized with absorbable sutures. Following the closure of the skin with non-absorbable sutures, the wound was cleaned with povidone iodine. Table 1. The histopathological scoring for the evaluation of fracture healing Score

Histopathological findings

Fibrous tissue

Predominantly fibrous tissue with little cartilage tissue

Equal amounts of fibrous and cartilage tissue

Only cartilage tissue

Predominantly cartilage tissue with little immature

(woven) bone

Equal amounts of cartilage and immature bone tissue

Predominantly immature bone with little cartilage

tissue 8

Healing with immature (woven) bone

Immature bone with little mature bone

Healing with mature (lamellar) bone

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

Radiological Evaluation For 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=onset 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 positive effect.

(a)

(b)

(c)

(d)

(e)

(f)

(g)

(h)

Histopathological Evaluation For 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 embedded 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 scoring 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.

Figure 2. The anteroposterior [(a) Group 1; (b) Group 2; (c) Group 3; (d) Group 4] and the lateral [(e) Group 1; (f) Group 2; (g) Group 3; (h) Group 4] X-ray images of the samples of the groups at the end of the experiment.

DXA Assessment The 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 (Hologic, Discovery QDR 4500A, WA, USA). Before each procedure, calibration of the instrument was done in accordance with the manufacturer’s standard “small step phantom”, including 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 Evaluation All the data were recorded and analyzed using the SPSS (Statistical Package for the Social Sciences) 18.0. The Kolmogorov-Smirnov and Shapiro-Wilk tests were performed to determine if the data were normally distributed. Nonparametric 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 radiological, histopathological and DXA evaluations. The data were summarized as median (minimum-maximum). A p value <0.05 was considered statistically significant. Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

Figure 3. The histopathological images of the samples of the groups at the end of the experiment: (a) In a rat in Group 1, a field containing a small amount of cartilage, with mostly fibrous tissue [hematoxylin & eosin (H&E, 100x)]; (b) In a rat in Group 2, a field full of immature bone tissue (H&E, 100x); (c) In a rat in Group 3, a field containing mostly cartilage and a small amount of immature bone tissue (H&E, 100x); and (d) In a rat in Group 4, a field containing equal amounts of cartilage and immature bone tissue (H&E, 100x).

RESULTS Radiological Findings The radiological scores for all groups are given in Table 2. The radiological score of Group 1 was significantly lower as compared to Groups 2, 3 and 4 (p=0.009, p=0.027, p=0.016, respectively). There was no statistically significant difference be163

164

Group 1: Nicotine group; Group 2: HBO group; Group 3: Nicotine+HBO group; Group 4: Control group; BMD R1: Bone mineral density of the total left femur; BMC R1: Bone mineral content of the total left femur; BMD R2: Bone mineral density of the left femur fracture site; BMC R2: Bone mineral content of the left femur fracture site; BMD total: Whole body bone mineral density; BMC total: Whole body bone mineral content.

0.865 0.736

0.626 0.602

0.821 0.005

0.006

0.027

7 (6-8)

0.005

3 (2-3)

7 (5-8)

3 (2-3)

7.5 (6-8) 4 (2-7) Histopathological score

Radiological score

1 (1-3)

2.5 (2-3)

0.009

0.016

0.317

0.748

1.000

0.712

0.834

0.874

0.916

0.163

0.105

0.238

0.355

0.323

0.132

0.168 (0.160-0.180)

13.47 (11.84-14.79)

0.169 (0.160-0.180) 0.168 (0.160-0.190)

13.23 (11.73-14.89)

0.170 (0.160-0.180)

13.80 (13.58-14.60)

BMD total (g/cm )

BMC total (g)

13.22 (12.20-14.11)

0.915 0.493

0.600 0.372

0.562 0.221

0.115

0.269

0.862 0.255 (0.200-0.500)

0.203 0.135 (0.116-0.348)

0.230 (0.130-0.610) 0.210 (0.170-0.260) BMC R2 (g)

0.235 (0.200-0.580)

0.129 (0.109-0.296) 0.134 (0.129-0.121) BMD R2 (g/cm )

0.131 (0.117-0.272)

0.222

0.954

0.563

0.674 0.832 0.635

0.674 0.268 0.400 0.728 0.487

0.325 (0.280-0.720)

0.446

0.129 (0.111-0.325)

0.320 (0.220-0.740) 0.250 (0.240-0.370) BMC R1 (g)

0.335 (0.210-0.990)

0.119 (0.107-0.282) 0.128 (0.121-0.164) BMD R1 (g/cm2)

0.126 (0.110-0.215)

0.165

0.200

p Group 2-4 p Group 2-3 p Group 1-4 p Group 1-3 p Group 1-2 Group 4 median (min-max) Group 3 median (min-max) Group 2 median (min-max) Group 1 median (min-max)

Table 2. Bone mineral content, bone mineral density values, radiological and histopathological scores of the groups

p Group 3-4

DemirtaĹ&#x; 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 Findings The histopathological scores of all tissue samples taken from all groups at the end of the 21st day are given in Table 2. The histopathological 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 Findings Table 2 shows the fracture site, whole left femur and whole body BMC and BMD values measured in all groups, before the experiment was terminated, 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 literature, 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 regenerate 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)-Îą 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 ended 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 immediately after cessation of smoking. In our study, a significant negative effect 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 corUlus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

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 accelerates 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 reduces the deleterious effects of smoking. In our study, there was a statistically significant difference in radiological and histopathological scores in the nicotinized+HBO group compared to the nicotinized group, whereas no statistically 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 histopathologically. 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 scintigraphically, 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 significantly 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 Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

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 findings in bone healing. Different results have been reported in studies in the literature concerning the timing of DXA findings related to nicotine. Ueng et al.[2] reported that nicotine begins to change BMD values after 3 weeks and reduces progressively in the 4th, 5th and 6th weeks in proportion to application time. Fung et al.[28] reported that a 2-month period of nicotine application does not change BMC and BMD values. Gao et al.[29] reported that 2- or 3- month periods of nicotine 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 association between different types of nicotinization procedures and HBO therapy might be performed. In conclusion, in the short-term follow-up, the negative effects of nicotine on fracture healing were relieved with HBO therapy; however, HBO alone did not cause significant changes 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.

REFERENCES 1. Buckwalter JA, Einhorn TA, Marsh JL. Bone and joint healing. In: Rockwood CA, Green DP, Bucholz RW, Heckman JD, editors. Rockwood and Green’s Fractures in Adults. Vol 1. 5th ed. Philadelphia: Lippincott Williams 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. Nicotinic 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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Demirtaş et al. The effect of hyperbaric oxygen therapy on fracture healing in nicotinized rats 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 hyperbaric 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 musculocutaneous 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 proliferation 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 healing 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 prostaglandin 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 pattern 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 grafting. 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, biochemical, 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 Gynaecol 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 ischemia 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 smoking 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 posterolateral intertransverse fusion in rabbits. J Trauma 2002;52:333-8. 27. Eralp L, Kocaoğlu M, Ozkan K, Türker M. A comparison of two osteotomy techniques for tibial lengthening. Arch Orthop Trauma Surg 2004;124:298-300. 28. Fung YK, Mendlik MG, Haven MC, Akhter MP, Kimmel DB. Shortterm effects of nicotine on bone and calciotropic hormones in adult female 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.

DENEYSEL ÇALIŞMA - ÖZET OLGU SUNUMU

Nikotinize sıçanlarda hiperbarik oksijen tedavisinin kırık iyileşmesi üzerine etkisi Dr. 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 Dicle Üniversitesi Tıp Fakültesi, Ortopedi ve Travmatoloji Anabilim Dalı, Diyarbakır Dicle Üniversitesi Tıp Fakültesi, Patoloji Anabilim Dalı, Diyarbakır 3 Dicle Üniversitesi Tıp Fakültesi, Biyofizik Anabilim Dalı, Diyarbakır 4 Dicle Üniversitesi Tıp Fakültesi, Tıbbi Biyoistatistik Anabilim Dalı, Diyarbakır 5 Anadolu Hiberbarik Oksijen Merkezi, Sualtı Hekimliği ve Hiperbarik Tıp Anabilim Dalı, İstanbul 1 2

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

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doi: 10.5505/tjtes.2014.52323

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

EXPERIMENTAL STUDY

Effectiveness of hyperbaric oxygen and ozone applications in tissue healing in generated soft tissue trauma model in rats: an experimental study Ali 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 1

Department of Emergency Medicine, GMMA, Haydarpasa Military Hosital, Istanbul

Department of Emergency Medicine, GMMA School of Medicine, Ankara

Department of Emergency Medicine, Hakkari Military Hospital, Hakkari

Department of Physiology, GMMA School of Medicine, Ankara

Department of Pathology, GMMA School of Medicine, Ankara

Department of Emergency Medicine, Elazig Military Hospital, Elazig

Department of Orthopaedics and Traumatology, GMMA, Haydarpasa Military Hosital, Istanbul

Department of Biochemistry, Gmma School of Medicine, Ankara

ABSTRACT BACKGROUND: Soft tissue trauma is a type of acute traumatic ischemia. We investigated in this study whether the edema, inflammation 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 antiinflammatory 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. Related clinical trials will be helpful in clarifying the effects. Key words: Experimental; hyperbaric oxygen; ozone; soft tissue trauma.

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: draliosmanyildirim@gmail.com Qucik Response Code

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

INTRODUCTION Soft tissue trauma (STT) is commonly encountered in emergency departments. STT defines lesions of the musculoskeletal system tissues other than bone. Lesions of these tissues represent the most commonly seen group of all sports injuries.[1] Crush injuries or acute soft tissue injuries are an important health problem that can threaten the viability and function of 167

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 microcirculation 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 requirement is increased 20-fold or more to provide good wound healing and control of infection. These metabolic needs cannot be provided without increased blood flow. When ischemia increases, the tissues cannot maintain the intracellular fluid content, because oxygen is required for active transport. Therefore, this process is accompanied by edema and inflammation.[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 increasing 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 plasma 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 antioxidant 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 increased tissue partial oxygen pressure is provided biochemically with ozone. Patients with STT admit with complaints such as swelling, limitation of movement and pain. There are various approaches to the treatment of these patients, who are diagnosed 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, elevation, cold application, topical non-steroidal inflammationsuppressing 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 therapy in STT may provide new perspectives on this issue. Thus, the effectiveness of HBO and ozone in STT was investigated in this study. 168

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 - Research and Development Center - Department of Experimental Animals, and were kept in the same laboratory conditions 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 intraperitoneal (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 Therapy For the application of HBO, a specially designed and manufactured cylindrical hyperbaric chamber, with a diameter of 40 cm and length 60 cm, maintained at T.S.K. 800 Main Warehouse 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 provided 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 presTable 1. Working groups Groups Days

1st day

3rd day

7th day

Ozone + STT

7 rats

HBO + STT

7 rats

STT (Control)

7 rats

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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

(a)

(b)

(c)

Figure 1. (a, b) Procedures for soft tissue trauma and (c) tissue sampling.

sure and with fixed oxygen amount. At the end of the session, 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 Application

An 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 control real-time gas flow rate and ozone concentration. The ozone flow rate was kept constant at 60 mg/ml concentration, 97% oxygen + 3% ozone gas mixture at 3 L/min.

Sampling After 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 Analysis Routine 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 dismutase (SOD) and glutathione peroxidase (GSH-Px) enzyme levels to detect antioxidant system functioning were measured. In addition, hypoxia-inducible factor (HIF-1) and heme oxygenase (HO-1) levels were measured to determine the recovery of hypoxic tissues, and inducible nitric oxide synthase (iNOS) levels were measured to determine wound healing.

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

LPO SOD HO-1a 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

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

<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

<0.001 <0.001 0.109 0.105 <0.001 0.001

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Histopathological Evaluation After trauma and administration of HBO and ozone treatment for 7 days, edema, inflammation and necrosis in tissue were evaluated and scored by an experienced pathologist. Injured skeletal muscle and adipose tissue were extracted from the rear thigh. Tissues were fixed in 4% buffered formaldehyde. 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), moderate: 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 Analysis The 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 comparisons, 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 coefficient. p<0.05 values were considered significant.

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

Figure 2. Intense edema and inflammation between muscle fibers and a few necrotic muscle fibers (Control group, 1st day) (a). Moderate edema and inflammation in adipose tissue (HBO group, 1st day) (b). Moderate edema and inflammation in adipose tissue (Ozone group, 1st day) (c). Intense edema and inflammation (Control, 3rd day) (d). Moderate edema and inflammation in muscle tissue (HBO, 3rd day) (e). Mild inflammation in muscle tissue (f). Mild inflammation in muscle tissue (Ozone 3rd day) (g). Moderate edema and inflammation in adipose tissue (Control, 7th day) (h). Mild inflammation and edema (HBO, 7th day) (I).

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

LPO SOD HO-1a 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

0.175 0.017 <0.001 <0.001 0.004 0.307

the Control group on days 1, 3 and 7. There was a significant decrease in SOD, GSH-Px and iNOS levels only in the treatment 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 between the Control and HBO groups for tissue on the 1st day, SOD, iNOS and GSH-Px levels of the HBO group were sig-

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

Days 1st 3rd 7th

HBO

Days p

1st 3rd 7th

Ozone

Days p

1st 3rd 7th

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

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 <0.001 0 0 7 <0.001

(+)

0 0 0

0 0 7

Inflammation 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.

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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 difference 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 between 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, respectively). 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 significantly 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 Findings In 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 intense, moderate and mild on the 1st, 3rd and 7th days, respectively. 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 moderate, mild and absent on the 1st, 3rd and 7th days, respectively. This decrease in the Ozone group was statistically significant (p<0.001). Necrosis was not seen in this group (Table 4). 172

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 create an inflammation model using antigenic substances such as Freud adjuvant, carrageenan or zymosan. However, soft tissue 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 traumatic 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 treatment. 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 orthopedic disorders including arthritis and rheumatic diseases.[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 effective 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 response to oxygen.[14] Soolsma[20] could find no evidence of a benefit of HBO treatment on delayed muscle pain treatment process in his grade 2 medial collateral ligament injuries study in 1996. Four studies 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 regard 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 infectious 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] Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

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The therapeutic effect of ozone, especially in pathophysiological situations due to an intense inflammatory process in which the immune system is forefront, is surprising. MartinezSanchez 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 useful 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 colleagues[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 results. Although an increase in antioxidant enzyme activities indicates 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 levels was statistically significant in the HBO group compared to the Control group on the 1st, 3rd and 7th days, and the decrease 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, vasodilation, angiogenesis, increase in glucose transport, increase in glucolysis, and apoptosis are activated. In the treatment of tumors, antiangiogenesis reduces the tumor blood flow, causing 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 Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

genes and vascular endothelial growth factor (VEGF).[26,27] Reduction 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 vasculature 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 insignificant. 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 demolition 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, antiinflammatory and antiapoptotic properties.[29-31] However, in one study it was demonstrated that induction of hem oxygenase 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 according to time points. The protection of HO-1 levels is considered 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 detrimental 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 histopathological findings support the biochemical findings. 173

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

In conclusion, as a result of the study findings and the literature 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 results are supported by the significant reduction in inflammation and edema on the histopathological examination in the treatment groups.

14. Harrison BC, Robinson D, Davison BJ, Foley B, Seda E, Byrnes WC. Treatment of exercise-induced muscle injury via hyperbaric oxygen therapy. Med Sci Sports Exerc 2001;33:36-42.

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 determine any clear result that revealed the superiority of either HBO or ozone. Further studies on this subject, which is a popular topic in the treatment of soft tissue injuries, will provide new insights.

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

Conflict of interest: None declared.

REFERENCES 1. Yucesir I, Bayraktar B. Soft tissue injuries and ;rinciples of healing. Türkiye Klinikleri J Orthop & Traumatol-Special Topics 2010;3:24-8. 2. Bywaters EG, Beall D. Crush injuries with impairment of renal function. 1941. J Am Soc Nephrol 1998;9:322-32. 3. Mabvuure NT, Malahias M, Hindocha S, Khan W, Juma A. Acute compartment syndrome of the limbs: current concepts and management. Open Orthop J 2012;6:535-43. 4. Feldmeier JJ. Hyperbaric oxygen 2003: Indications and results: The Hyperbaric Oxygen Therapy Committee Report. Undersea and Hyperbaric Medical Society, Inc., Kensington, MD, 2003. 5. Bocci V. How does ozone act? How and why can we avoid ozone toxicity? In: Bocci V, editor. Ozone; A new medical drug. Dordrecht: Springer; 2005. p. 19-28. 6. Davies SL, Siau C, Bennett GJ. Characterization of a model of cutaneous inflammatory pain produced by an ultraviolet irradiation-evoked sterile injury in the rat. J Neurosci Methods 2005;148:161-6. 7. Dixon CE, Clifton GL, Lighthall JW, Yaghmai AA, Hayes RL. A controlled cortical impact model of traumatic brain injury in the rat. J Neurosci Methods 1991;39:253-62. 8. Tavazzi B, Signoretti S, Lazzarino G, Amorini AM, Delfini R, Cimatti M, et al. Cerebral oxidative stress and depression of energy metabolism correlate with severity of diffuse brain injury in rats. Neurosurgery 2005;56:582-9. 9. Kranke P, Bennett MH, Martyn-St James M, Schnabel A, Debus SE. Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev 2012;4:CD004123. 10. Babul S, Rhodes EC, Taunton JE, Lepawsky M. Effects of intermittent exposure to hyperbaric oxygen for the treatment of an acute soft tissue injury. Clin J Sport Med 2003;13:138-47. 11. Staples JR, Clement DB, Taunton JE, McKenzie DC. Effects of hyperbaric oxygen on a human model of injury. Am J Sports Med 1999;27:6005. 12. Germain G, Delaney J, Moore G, Lee P, Lacroix V, Montgomery D. Effect of hyperbaric oxygen therapy on exercise-induced muscle soreness. Undersea Hyperb Med 2003;30:135-45. 13. Bennett MH, Feldmeier J, Hampson N, Smee R, Milross C. Hyperbaric oxygen therapy for late radiation tissue injury. Cochrane Database of Systematic Reviews 2009, Issue 3. Art. No: CD005005.

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15. Bocci V. The case for oxygen-ozonetherapy. Br J Biomed Sci 2007;64:449. 16. Martínez-Sánchez G, Al-Dalain SM, Menéndez S, Re L, Giuliani A, Candelario-Jalil E, et al. Therapeutic efficacy of ozone in patients with diabetic foot. Eur J Pharmacol 2005;523:151-61.

18. Kim HS, Noh SU, Han YW, Kim KM, Kang H, Kim HO, et al. Therapeutic 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 maxillofacial 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. Correlation between hyperbaric oxygen exposure pressures and oxidative parameters in rat lung, brain, and erythrocytes. Clin Biochem 2005;38:706-11. 26. Carmeliet P, Dor Y, Herbert JM, Fukumura D, Brusselmans K, Dewerchin 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 human 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 oxygenase-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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DENEYSEL ÇALIŞMA - ÖZET OLGU SUNUMU

Sıçanlarda oluşturulan yumuşak doku travma modelinde, hiperbarik oksijen ve ozon uygulamalarının doku iyileşmesi üzerine etkinliği: Deneysel çalışma Dr. 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 GATA Haydarpaşa Asker Hastanesi, Acil Tıp Anabilim Dalı, İstanbul GATA, Askeri Tıp Fakültesi, Acil Tıp Anabilim Dalı, Ankara 3 Hakkari Asker Hastanesi, Acil Servis, Hakkari 4 GATA, Askeri Tıp Fakültesi, Fizyoloji Anabilim Dalı, Ankara 5 GATA, Askeri Tıp Fakültesi, Patoloji Anabilim Dalı, Ankara 6 Elazığ Asker Hastanesi, Acil Servis, Elazığ 7 GATA Haydarpaşa Asker Hastanesi, Ortopedi ve Travmatoloji Anabilim Dalı, İstanbul 8 GATA, Askeri Tıp Fakültesi, Biyokimya Anabilim Dalı, Ankara 1 2

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 enflamasyonda 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 değerlendirilmektedir. 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

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ORIGIN A L A R T IC L E

Psychiatric disorders and their association with burn-related factors in children with burn injury Gül 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 Department of Child and Adolescent Psychiatry, Bakirkoy Training and Research Hospital For Psychiatry, Neurology and Neurosurgery, Istanbul

1 2

Department of Child and Adolescent Psychiatry, Istanbul University Cerrahpasa Faculty of Medicine, Istanbul

Department of Plastic, Reconstructive and Aesthetic Surgery, Istanbul University Cerrahpasa Faculty of Medicine, 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 patients (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 presence 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.

INTRODUCTION Having a severe burn injury is one of the most traumatic accidents 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 number of ways. Firstly, a burn injury is an unexpected, painful, and

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: drgul21@yahoo.com Qucik Response Code

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life-changing injury, which can cause pain and feelings of uncertainty and fear in the child.[4] Secondly, the burn injury threatens 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 intensive 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 research 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 psychopathology that persists after one month.[6,7] Children with burn injury were reported to have ASD,[8-10] PTSD,[11-15] separation 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 satisfying quality of life[17] and were not different from their healthy peers in terms of depression scores[18] in the long-term. In Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

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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 psychiatric 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 systematic diagnostic assessment. The second aim of the study was to assess the association of psychiatric disorders with burnrelated factors.

MATERIALS AND METHODS Children admitted to the Cerrahpasa Medical Faculty Burn Unit between January 2013 and August 2013 were first assessed by the plastic surgeon (SB), and those with psychological 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 excluded from this study. As a result, the psychiatric and burnrelated records of 31 children were assessed. The psychiatric diagnoses were assessed by means of the Diagnostic 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 Analyses Chi-square or Fisher’s exact test was used to compare categorical 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 Statistical Package for the Social Sciences (SPSS) 16-pocket program. 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 Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

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 Surface 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 associated 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. Psychological symptoms that prompted referral to the child psychiatrist 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 sleeping (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 diagnostic 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 factors 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 (MannWhitney test, p=0.022). The duration between burn and psychiatric 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 assessment.

DISCUSSION To 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 177

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finding was in line with previous studies reporting that ASD is a core feature of a childâ&#x20AC;&#x2122;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 sample, 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 studies. Our sample consisted of children who were referred for psychiatric assessment because of their psychological symptoms, 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 consistent 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 neurobiological abnormalities, such as reduced hippocampal size due to autonomic arousal and the acquisition of conditioned fear with chronic re-experiencing of traumatic events.[24] Recognizing 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 development 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 previous studies reporting the prevalence of PTSD as 10%,[11,12] 13.2%,[13] 25%, and 33%.[15] As PTSD describes the psychopathology 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 pediatric 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] 178

The second most common psychiatric diagnosis in our sample was depression, with a rate of 9.7%, which was higher than the rate of depression in Turkish children.[26] This finding 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 lifetime,[16] indicating that the risk of depression in pediatric burn patients continues for oneâ&#x20AC;&#x2122;s lifetime. On the other hand, our findings were inconsistent with some of the studies reporting 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 differences 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 describing cases of delirium in children with burn injury.[29-31] The precipitating factor for delirium in our study was hyponatremia, which is one of the risk factors reported in the etiology 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 presentation 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, irritability, 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 injuries known; both the injury itself and the treatment procedures can be frightening and difficult to cope with for children. Intensive medical treatments, painful dressings often 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 findings suggest that psychiatric interventions may help children to cope with the painful treatment and their emotional effects and may reduce the psychiatric sequelae of burn injury. [32] As psychiatric disorders may have a negative impact on the Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

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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 referring children to a child psychiatrist for evaluation. Conflict of interest: None declared.

REFERENCES 1. Landolt MA, Grubenmann S, Meuli M. Family impact greatest: predictors of quality of life and psychological adjustment in pediatric burn survivors. J Trauma 2002;53:1146-51. 2. Blakeney PE, Rosenberg L, Rosenberg M, Faber AW. Psychosocial care of persons with severe burns. Burns 2008;34:433-40. 3. Moi AL, Vindenes HA, Gjengedal E. The experience of life after burn injury: a new bodily awareness. J Adv Nurs 2008;64:278-86. 4. Maskell J, Newcombe P, Martin G, Kimble R. Psychosocial functioning differences in pediatric burn survivors compared with healthy norms. J Burn Care Res 2013;34:465-76. 5. Bakker A, Maertens KJ, Van Son MJ, Van Loey NE. Psychological consequences of pediatric burns from a child and family perspective: a review of the empirical literature. Clin Psychol Rev 2013;33:361-71. 6. Stoddard FJ. Care of infants, children and adolescents with burn injuries. In: Lewis M, editor. Child and adolescent psychiatry, a comprehensive textbook. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2002. p. 1188-208. 7. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Text Revision, 4th ed. American Psychiatric Press, Washington, DC; 2000. 8. Stoddard FJ, Saxe G, Ronfeldt H, Drake JE, Burns J, Edgren C, et al. Acute stress symptoms in young children with burns. J Am Acad Child Adolesc Psychiatry 2006;45:87-93. 9. Miller A, Enlow MB, Reich W, Saxe G. A diagnostic interview for acute stress disorder for children and adolescents. J Trauma Stress 2009;22:549-56. 10. Saxe G, Stoddard F, Chawla N, Lopez CG, Hall E, Sheridan R, et al. Risk factors for acute stress disorder in children with burns. J Trauma Dissociation 2005;6:37-49. 11. De Young AC, Kenardy JA, Cobham VE. Diagnosis of posttraumatic stress disorder in preschool children. J Clin Child Adolesc Psychol 2011;40:375-84. 12. De Young AC, Kenardy JA, Cobham VE, Kimble R. Prevalence, comorbidity and course of trauma reactions in young burn-injured children. J Child Psychol Psychiatry 2012;53:56-63. 13. Graf A, Schiestl C, Landolt MA. Posttraumatic stress and behavior problems in infants and toddlers with burns. J Pediatr Psychol 2011;36:92331. 14. Saxe GN, Stoddard F, Hall E, Chawla N, Lopez C, Sheridan R, et al. Pathways to PTSD, part I: Children with burns. Am J Psychiatry 2005;162:1299-304. 15. Stoddard FJ, Norman DK, Murphy JM. A diagnostic outcome study of

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children and adolescents with severe burns. J Trauma 1989;29:471-7. 16. Stoddard FJ, Stroud L, Murphy JM. Depression in children after recovery from severe burns. J Burn Care Rehabil 1992;13:340-7. 17. Sheridan RL, Hinson MI, Liang MH, Nackel AF, Schoenfeld DA, Ryan CM, et al. Long-term outcome of children surviving massive burns. JAMA 2000;283:69-73. 18. Liber JM, Faber AW, Treffers PD, Van Loey NE. Coping style, personality and adolescent adjustment 10 years post-burn. Burns 2008;34:77582. 19. Zero to three. Diagnostic classification of mental health and developmental disorders of infancy and childhood: Revised edition (DC: 0-3R). Washington, DC: Zero to Three Press; 2005. 20. Daviss WB, Racusin R, Fleischer A, Mooney D, Ford JD, McHugo GJ. Acute stress disorder symptomatology during hospitalization for pediatric injury. J Am Acad Child Adolesc Psychiatry 2000;39:569-75. 21. Winston FK, Kassam-Adams N, Vivarelli-O’Neill C, Ford J, Newman E, Baxt C, et al. Acute stress disorder symptoms in children and their parents after pediatric traffic injury. Pediatrics 2002;109:90. 22. Drake JE, Stoddard FJ Jr, Murphy JM, Ronfeldt H, Snidman N, Kagan J, et al. Trauma severity influences acute stress in young burned children. J Burn Care Res 2006;27:174-82. 23. Difede J, Ptacek JT, Roberts J, Barocas D, Rives W, Apfeldorf W, et al. Acute stress disorder after burn injury: a predictor of posttraumatic stress disorder? Psychosom Med 2002;64:826-34. 24. Shucard JL, Cox J, Shucard DW, Fetter H, Chung C, Ramasamy D, et al. Symptoms of posttraumatic stress disorder and exposure to traumatic stressors are related to brain structural volumes and behavioral measures of affective stimulus processing in police officers. Psychiatry Res 2012;204:25-31. 25. Yabanoğlu H, Yağmurdur MC, Taşkıntuna N, Karakayalı H. Early period psychiatric disorders following burn trauma and the importance of surgical factors in the etiology. Ulus Travma Acil Cerrahi Derg 2012;18:43640. 26. Demir T, Karacetin G, Demir DE, Uysal O. Epidemiology of depression in an urban population of Turkish children and adolescents. J Affect Disord 2011;134:168-76. 27. Fukunishi I. Posttraumatic stress symptoms and depression in mothers of children with severe burn injuries. Psychol Rep 1998;83:331-5. 28. Pope SJ, Solomons WR, Done DJ, Cohn N, Possamai AM. Body image, mood and quality of life in young burn survivors. Burns 2007;33:747-55. 29. Ratcliff SL, Meyer WJ 3rd, Cuervo LJ, Villarreal C, Thomas CR, Herndon DN. The use of haloperidol and associated complications in the agitated, acutely ill pediatric burn patient. J Burn Care Rehabil 2004;25:4728. 30. Brown RL, Henke A, Greenhalgh DG, Warden GD. The use of haloperidol in the agitated, critically ill pediatric patient with burns. J Burn Care Rehabil 1996;17:34-8. 31. Turkel SB, Tavaré CJ. Delirium in children and adolescents. J Neuropsychiatry Clin Neurosci 2003;15:431-5. 32. Langeland W, Olff M. Psychobiology of posttraumatic stress disorder in pediatric injury patients: a review of the literature. Neurosci Biobehav Rev 2008;32:161-74.

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KLİNİK ÇALIŞMA - ÖZET OLGU SUNUMU

Yanık yaralanması olan çocuklarda görülen psikiyatrik bozukluklar ve yanık-ilişkili faktörlerle olan bağlantısı Dr. Gül Karaçetin,1 Dr. Türkay Demir,2 Dr. Semih Baghaki,3 Dr. Oğuz Çetinkale,3 Dr. Mine Elagöz Yüksel1 Bakırkoy Prof. Dr. Mazhar Osman Ruh Sağlığı ve Sinir Hastalıkları Hastanesi, Çocuk ve Ergen Psikiyatri Kliniği, İstanbul İstanbul Üniversitesi Cerrahpaşa Tıp Fakültesi, Çocuk ve Ergen Psikiyatri Anabilim Dalı, İstanbul 3 İstanbul Üniversitesi Cerrahpaşa Tıp Fakültesi, Plastik, Rekonstrüktif ve Estetik Cerrahi Anabilim Dalı, İstanbul 1 2

AMAÇ: Bu çalışmada, yanık yaralanması olan Türk çocuklarda psikiyatrik bozuklukların ve bu bozuklukların yanık-ilişkili faktörlerle bağlantısı değerlendirildi. 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

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doi: 10.5505/tjtes.2014.49033

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ORIGIN A L A R T IC L E

Traumatic wound dehiscence after penetrating keratoplasty: case series and literature review Baki 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 1

Department of Ophthalmolgy, Regional Training and Research Hospital, Erzurum

Department of Ophthalmology, Dr. Lutfi Kirdar Kartal Training and Research Hospital, Istanbul

Department of Family Medicine, Atatürk University Faculty of Medicine, Erzurum

Department of Ophthalmology, Atatürk University Faculty of Medicine, Erzurum

Department of Ophthalmolgy, Bakirköy Sadi Konuk Training and Research Hospital, 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.

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] Worldwide, there are currently 1.6 million blind and 19 million monocular individuals as a result of ocular trauma, which makes it one of the most significant causes of ocular morbidity.[2] Address for correspondence: Baki Kartal, M.D. Dr. Refik Saydam Caddes, Yıldızkent, Palandöken, Erzurum, Turkey Tel: +90 442 - 232 52 94 E-mail: baki_kartal@yahoo.com Qucik Response Code

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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 0.41.4%,[5-6] respectively. Therefore, PK is more prone to traumatic globe rupture than the other types of ocular surgery. The World Health Organization (WHO) reported that almost 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 number of PKs (which is currently the most common homologous 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 complications with poor outcomes make the growing number of such cases a concern.

MATERIALS AND METHODS This study was performed by retrospectively reviewing the 181

Kartal et al. Traumatic wound dehiscence after penetrating keratoplasty

records of 26 patients who were diagnosed with and underwent reconstructive surgery to correct traumatic graft rupture 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 accepted 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-

Table 1. General demographic and medical data Patient No

Age

Gender

Indication of PK

Follow-up (month) Between PK-trauma

After trauma

Suture Suturing technique

Presence of sutures during trauma

Steroid usage during trauma

Pretraumatic other risk factors

Female

Corneal Scar

112

Glaucoma

Keratoconus

0.6

105

ICS

–

Female

Male

Leukoma Adherence

–

Male

Granular Dystrophy

Male

Corneal Scar

–

Male

Keratoconus

Low vision in

other eye 7

Male

Macular Dystrophy

Male

Keratoconus

ICS

–

6.5

Glaucoma

–

Male

Fuchs

Male

PBK

Removed

Stopped

–

Removed

Stopped

Glaucoma

Female

Corneal Scar

Female

PBK

Stopped

Glaucoma

Removed

Stopped

–

Female

Corneal Scar

Female

Keratoconus

Glaucoma +Deafness

Female

Herpetic Keratitis

Removed

Stopped

Glaucoma +Single Eye

Male

Keratoconus

ICS

Glaucoma (AGV)

Female

Corneal Scar

–

PBK

–

Female

Male

Corneal Scar

ICS

Removed

Stopped

Single Eye

Male

Corneal Scar

Removed

Stopped

–

Graft Rejection

117

Single Eye

Corneal Scar

Removed

Stopped

Single Eye

Leukoma Adherence

Removed

Stopped

Single Eye

Graft Rejection

Single Eye

Leukoma Adherence

Removed

Stopped

Single Eye

Corneal Scar

Removed

Stopped

–

Male

Female

Male

Female

Male

Female

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

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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 acuity 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-related 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

Table 2. Data about dehiscence, final graft status and vision Patient No

Quadrant of dehiscence

Extent of dehiscence

Final graft status

Pretraumatic visual acuity

Final visual acuity

Superior

120

Clear

1mFC

2mFC

Superior

Clear

0.1

1.0

Final low visual acuity reasons Pretraumatic PDRP –

Nasal

180

Clear

2mFC

Superior

Clear

0.7

Amblyopia/Exotropia

Except Nasal

270

Insufficiency

0.4

Graft Insufficiency

Inferior

120

Insufficiency

0.3

0.15

Graft Insufficiency

–

Inferior

120

Clear

0.2

0.6

Macular Pucker

Temporal

Clear

0.5

–

Inferior

180

Clear

0.2

Epithelial

Ingrowth+PVR

Graft

Superior

180

Insufficiency

0.15

Insufficiency+Secondary

Glaucoma

Superior

180

Pretraumatic Graft Rejection

Superior

120

Clear

0.4

0.7

–

Inferior

Clear

0.4

P(+)

Suprachoroidal Hemorrhage

Rejected

50 cmFC

Nasal

Rejected

0.15

Superior

180

Insufficiency

0.2

10cmFC

– Graft Rejection

Nasal

140

Clear

0.4

–

Temporal

Rejected

0.8

0.2

Graft Rejection

Nasal

180

Insufficiency

2mFC

10cmFC

Graft Insufficiency+Fibrous Ingrowth

Inferior

180

Clear

0.05

30cmFC

Inferior

180

Rejected

0.5

0.1

Graft Rejection

Geographic Atrophy

Inferior

150

Rejected

1 mFC

P (+)

Graft Rejection

Nasal

Insufficiency

0.2

Graft Insufficiency

Inferior

180

Clear

0.4

0.15

Retinal Vein Branch Occlusion

Inferior

200

Rejected

0.05

P(+)

Graft Rejection

Temporal

120

Clear

0.3

0.1

Geographic Atrophy

Clear

0.4

0.5

–

Inferior

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

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Kartal et al. Traumatic wound dehiscence after penetrating keratoplasty

significant relationship was found between the time elapsed from trauma to reconstructive surgery and the final graft clarity (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 dehiscence was not found to be statistically related to primary surgical 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 relationship 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 structures was found to be significantly related to final graft clarity (p<0.05), but not related to the degree of the host-graft dehiscence (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 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

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%) patients. 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 indication, 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 increased 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).

Presence of sutures

Z=-1.189 p=0.234

Steroid use¶

Z=-0.931 p=0.352

DISCUSSION

Etiology of the trauma*

χ2=1.502 p=0.682

Place of the dehiscence*

χ2=9.054 p=0.060

Final graft status*

Crystalline lens/IOL damage

Any trauma to the globe with proper mechanism and sufficient force would cause rupture of the globe at the weakest 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 trauma, 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.

χ2=1.141 p=0.565 ¶

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.

184

Mental retardation, low vision in both eyes, deafness, and alcohol consumption are accepted risk factors for traumatic rupture following PK.[3,11,16,17] Older age, obesity, use of nonirritating nylon sutures, improper suturing, early suture removal, 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). AdditionUlus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

Kartal et al. Traumatic wound dehiscence after penetrating keratoplasty

Table 4. Surgical procedures, traumatic crystalline lens/IOL and posterior segment damage Patient No

Surgical Secondary surgery Status of lens procedure

Pre-trauma

Pseudophakic

–

Post-trauma Pseudophakic

Decentralized

Traumatic cataract

PS + AV + LA

Secondary Sulcus PC

Phakic

Posterior segment damage

– –

IOL Implantation

Phakic

Lens Subluxation

–

PS + IR

–

Phakic

–

PS + AV

–

Phakic

Aphakia

–

PS + AV + IE

–

Pseudophakic

–

PS + IR

PPV / Scleral Fixation IOL

Phakic

Aphakia

Macular Pucker

–

Phakic

–

PS + AV + IR

Re-PK + Retroiridal

Phakic

Aphakia

Membrane Excision + L

PVR + Retinal Detachment

–

Pseudophakic

–

Pseudophakic

–

Pseudophakic

–

PS + AV + IOL E

–

Pseudophakic

Aphakia

Suprachoroidal

Hemorrhage

–

Phakic

PS + AV + IE

–

Phakic

Aphakia

–

PS + AV + L

AV + Scleral Fixation IOL

Phakic

Traumatic cataract

–

Pseudophakic

–

Pseudophakic

–

PS + AV

–

Phakic

Aphakia

–

PS + IE+AV

–

Aphakia

–

Phakic

–

PS+IR

–

Phakic

–

Phakic

–

Re-PK

Pseudophakic

–

PS+AV

–

Pseudophakic

Aphakia

–

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 vitrectomy; PS: Primary suture; PVR: Proliferative vitreoretinopathy; Re-PK: re-Penetrating keratoplasty.

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] Thirtythree years is the longest reported time interval after PK, indicating a lifetime risk of traumatic dehiscence. The mean Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

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 bilateral graft rupture due to airbag deployment during a car accident).[11,16,20,23,24] However, many graft ruptures occur during daily activities that are considered ‘low-risk activities’.[22] Previous reports have noted that traumatic graft dehiscence was 185

Kartal et al. Traumatic wound dehiscence after penetrating keratoplasty

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] reported a predominance of women in their study, men were found to be at higher risk for TWD in other studies.[4,11,14,1619,22,28,29] 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 predominant, 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 keratoconus, 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 indications 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 hostgraft junction. Likewise, other studies have also reported this region to be the most frequent site of wound separation.[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 commonly 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 presence 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 factors 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 between degree of dehiscence and final graft status. In the present 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 186

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 presentation (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 recommended, especially in older patients, to avoid risk of explosive 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 status. 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 rejection. 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 contraindicated in cases with opened and distorted globe. We encountered no complications in the five patients underwent surgery under retrobulbar anesthesia. Rehany et al.[14] reported 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 implantation 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 physiological transformation of endothelial cells following transplantation, 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 indication for grafting, or time interval between primary surgery and trauma. However, in patients in whom sutures were removed, grafts had a more extensive dehiscence; additionally, grafts with 180째 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 Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

Kartal et al. Traumatic wound dehiscence after penetrating keratoplasty

and trauma, degree of dehiscence, affected quadrant, etiology 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 detachment, macular pucker, glaucoma, epithelial ingrowth, hypotonia, phthisis bulbi, and need of evisceration due to complete 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 detachment, fibrous ingrowth, and suprachoroidal hemorrhage. Many researchers have determined severity of the trauma and posterior segment complications to be the major determinants 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 serious 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.

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 analysis. 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 Ophthalmol 1998;116:1282-6. 15. Calkins JL, Hochheimer BF, Stark WJ. Corneal wound healing: holographic 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 penetrating keratoplasty: clinical features and outcome in 21 cases. Cornea 1999;18:553-8. 18. Das S, Whiting M, Taylor HR. Corneal wound dehiscence after penetrating 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;25:1325. 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;21:114650.

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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 Suppl):1-43.

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

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;23:77680.

25. Williams MA, Gawley SD, Jackson AJ, Frazer DG. Traumatic graft dehiscence after penetrating keratoplasty. Ophthalmology 2008;115:276-8. 26. Steinberg J, Eddy MT, Katz T, Fricke OH, Richard G, Linke SJ. Traumatic 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. Characteristics of traumatic globe rupture after keratoplasty. Ophthalmology 2009;116:2072-6.

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

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

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

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

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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.

KLİNİK ÇALIŞMA - ÖZET OLGU SUNUMU

Penetran keratoplasti sonrası travmatik yara ayrışması, olgu serisi ve literatüre genel bakış Dr. 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 Bölge Eğitim ve Araştırma Hastanesi, Göz Hastalıkları Kliniği, Erzurum Dr. Lütfi Kırdar Kartal Eğitim ve Araştırma Hastanesi, Göz Hastalıkları Kliniği, İstanbul Atatürk Üniversitesi Tıp Fakültesi, Aile Hekimliği Anabilim Dalı, Erzurum 4 Atatürk Üniversitesi Tıp Fakültesi, Göz Hastalıkları Anabilim Dalı, Erzurum 5 Bakırköy Sadi Konuk Eğitim ve Araştırma Hastanesi, Göz Hastalıkları Kliniği, İstanbul 1 2 3

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. Ayrışma 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

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doi: 10.5505/tjtes.2014.36589

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

ORIGIN A L A R T IC L E

Comparison of intramedullary nail and plate fixation in distal tibia diaphyseal fractures close to the mortise Umut Yavuz, M.D., Sami Sökücü, M.D., Bilal Demir, M.D., Timur Yıldırım, M.D., Çağrı Özcan, M.D., Yavuz Selim Kabukçuoğlu, M.D. Department of Orthopaedics and Traumatology, MS Baltalimani Bone Diseases Training and Research Hospital, Istanbul

ABSTRACT BACKGROUND: In this study, we aimed to compare the functional and radiological results of intramedullary nailing and plate fixation 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, AOFAS 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 appropriate 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.

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 mobilization 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 intramedullary fixation in proximal and distal shaft fractures, which leads to increasing rates of malalignment.[1-3] There are also publiAddress 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: umut78@yahoo.com Qucik Response Code

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cations reporting higher rates of anterior knee pain occurring 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 radiographic 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 Association (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, AO189

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 metaphyseal 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.

Statistical analysis was made using a computer software program, 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.

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 malleolus 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.

RESULTS

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 fracture 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 5째 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 clinical results related with the ankle joint. Table 1.

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 intramedullary nailing and 56.5 mm (range 33-90 mm) in the patients treated by plate fixation. The two groups were considered 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

Demographic data of the patients

Nail Plate Total

Male

23.6

% 34.6

58.2

Female

14.5

27.3

41.8

Age (range)

17-67

15-72

Follow-up (months)

12-82

27.9

12-78

27.6

12-82

85.6

OTA classification

42-A

32.8

52.8

42-B

3.6

5.4

42-C

1.8

3.6

5.4

72.9

42-89

56.5

33-90

62.7

33-90

Open fracture

5.4

10.8

16.2

Fibula fracture

25.4

47.3

72.7

Fibula fixation

5.4

21.8

27.2

4.5

1-15

4.8

1-17

4.7

1-17

Mean distance to mortise (mm) (range)

Time to operation (day)

OTA: Orthopaedic Trauma Association.

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

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

Nail

Union time (months) AOFAS

Plate

Total

4.9

5.5

5.3

0.894

88.3 (71-96)

88.1 (55-100)

88.2 (55-100)

0.794

Infection

3 (%5.4)

0.100

Nonunion

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)

0.001

(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).

plate fixation group. In one patient, deep venous thromboembolism 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, autografting derived from the iliac crest was performed, and unification was observed one year later.

The AOFAS scoring system was used to evaluate ankle arthritis. 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

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 infection, considered to be nosocomial. As debridement was performed 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 patients had an AOFAS score of 76.5 and are able to walk with support. Although nonunion was observed radiologically, the patients refused surgery.

(a)

(b)

Figure 1. (a) Preoperative radiographs of a 35-year-old male patient with right distal diaphyseal tibia fracture extending to the metaphysis, resulting from a fall. (b) Radiographs of the patient in the first year of follow-up, after intramedullary nailing.

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Malunion was determined in 13 patients. Two of them were treated by intramedullary nailing and 11 by plate fixation. None of the patients demonstrated malunion with more than 10째 angulation. Four patients 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 intramedullary nailing and three by plate fixation (p=0.450). Three patients had procurvatum deformity. One of these patients was treated by intramedullary nailing and two by plate fixation (0.846). One patient had multiplanar deformity and was treated by plate fixation because it was an isolated tibia fracture. 191

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

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.

DISCUSSION Tibial 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 tissues 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 patients 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 retropatellar 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 patients. In our study, anterior knee pain was in acceptable limits according to the literature, and pain did not affect life or working 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 AOFAS 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 infection risk and the need for secondary surgery.[27,29] Malalignment, which may occur after the treatment of fractures 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 increased 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 192

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 distal 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 delay bone healing. We did not use fibular fixation except for displaced distal fibular fractures, which may cause valgus deformity. Whether fibular fixation was done or not, no significant 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 diaphyseal 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.

REFERENCES 1. Im GI, Tae SK. Distal metaphyseal fractures of tibia: a prospective randomized trial of closed reduction and intramedullary nail versus open reduction and plate and screws fixation. J Trauma 2005;59:1219-23; discussion 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 patients. 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 intramedullary 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 intramedullary nails for tibial fractures be with or without reaming? A prospective, 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 tibial shaft fractures treated with intramedullary nailing. J Orthop Trauma 2008;22:525-9.

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Yavuz et al. Comparison of intramedullary nail and plate fixation in distal tibia diaphyseal fractures close to the mortise 7. Borg T, Larsson S, Lindsjö U. Percutaneous plating of distal tibial fractures. 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 intramedullary 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 follow-up of a prospective, randomized study comparing two different nailinsertion techniques. J Trauma 2008;64:1511-6. 19. Collinge C, Sanders R, DiPasquale T. Treatment of complex tibial periarticular fractures using percutaneous techniques. Clin Orthop Relat Res 2000;375:69-77. 20. Francois J, Vandeputte G, Verheyden F, Nelen G. Percutaneous plate fixation 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. Intramedullary nailing of distal metaphyseal tibial fractures. J Bone Joint Surg Am 2005;87:1213-21. 27. Bhandari M, Guyatt GH, Swiontkowski MF, Schemitsch EH. Treatment 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 unreamed 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 fractures 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. Longterm 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 deformities. 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 comparison 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 extraarticular fractures of the distal tibia: intramedullary nailing versus plate fixation. J Am Acad Orthop Surg 2012;20:675-83.

KLİNİK ÇALIŞMA - ÖZET OLGU SUNUMU

Mortise yakın distal tibia diafiz kırıklarının tedavisinde intramedüller çivi ve plak tedavisinin karşılaştırılması Dr. Umut Yavuz, Dr. Sami Sökücü, Dr. Bilal Demir, Dr. Timur Yıldırım, Dr. Çağrı Özcan, Dr. Yavuz Selim Kabukçuoğlu Baltalimanı Kemik Hastalıkları Eğitim ve Araştırma Hastanesi, Ortopedi ve Travmatoloji Kliniği, 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; ortalama 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 gözlenmedi. 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. Ulus Travma Acil Cerrahi Derg 2014;20(3):189-193

doi: 10.5505/tjtes.2014.92972

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ORIGIN A L A R T IC L E

A new, simple technique for gradual primary closure of fasciotomy wounds Mustafa Özyurtlu, M.D.,1 Süleyman Altınkaya, M.D.,2 Yahya Baltu, M.D.,2 Güzin Yeşim Özgenel, M.D.2 1

Department of Plastic Surgery, Bursa Sevket Yilmaz Training and Research Hospital, Bursa

Department of Plastic, Reconstructive and Aesthetic Surgery, Uludag University Faculty of Medicine, Bursa

ABSTRACT BACKGROUND: The aim of this study was to demonstrate a new, easy and safe technique, which has not been defined in the literature 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 extremities, 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.

INTRODUCTION Various reconstructive strategies may be performed for the closure of fasciotomy wounds that are secondary to compartment syndrome. Of these, closure via skin grafts and delayed gradual primary closure are the most commonly employed 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; however, 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

Address for correspondence: Mustafa Özyurtlu, M.D. Mimar Sinan Mahallesi, 16350 Yıldırım, Bursa, Turkey Tel: +90 224 - 483 67 42 E-mail: mustafaozyurtlu@yahoo.com Qucik Response Code

194

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 investigators 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 techniques, with the regression of the edema after compartment syndrome, the margins of the wound are brought closer together gradually via a special device until the wound is completely closed. Some of the described methods are technically 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 Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

Ă&#x2013;zyurtlu et al. A new, simple technique for gradual primary closure of fasciotomy wounds

Figure 2. Perioperative view of the V-Loc wound closure device advancement in Case 4. After anchoring, the suture was advanced along the opposing wound edges in a horizontal mattress fashion. Figure 1. 3/0 cutting needle absorbable V-Loc wound closure device. It consists of unidirectional barbs and loop combination that are placed behind the suture.

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 suture 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 operation 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 transparent 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 patients 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 dermis, and then through the loop at the back of the suture, and the fixation was completed. Subsequently, the suture was advanced along the opposing wound edges in a horizontal mattress 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 tissues 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 suture 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

Male

Upper extremity

Electrical burn injury

Case 2

Male

Lower extremity

Blunt trauma

Case 3

Female

Lower extremity

Gunshot trauma

Case 4

Male

Upper extremity

Snake bite injury

Case 5

Male

Upper extremity

Penetrating injury

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Ă&#x2013;zyurtlu et al. A new, simple technique for gradual primary closure of fasciotomy wounds

(a)

(b)

(c)

Figure 3. (a) View of Case 1. From top to bottom: Large open fasciotomy wound that occurred after high-voltage electrical injury (day 0). Approximated wound margins: note the tissue loss at the level of the wrist, which healed secondarily after debridement and dressings. Final result in the postoperative sixth month. (b) View of Case 2. From top to bottom: open fasciotomy wound at the lower extremity. Two 3/0 cutting needle V-Loc wound closure devices were applied to the wound margins. Approximated wound edges after two tightenings (middle picture). Note the syringe pistol rubber that was placed to prevent the suture from pulling back (Case 2, day 4). Final result (day 6). (c) The gradual closure stages of Case 4. From top to bottom: large fasciotomy wound after snakebite injury, approximated wound margins on day 4, and end result (15 days after opening fasciotomy).

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

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 and location of wound sutures used closure of the (cm) (cm)* wound **(days)

Total duration of hospital stay (days)

Complications

Case 1

15x9

3x2 skin necrosis

Case 2

15x10

Case 3

18x8

Case 4

21x9

Case 5

16x8

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 healing (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 fasciotomy 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 VLoc 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).

DISCUSSION Barbed suture V-Loc provided complete primary wound closure 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, necrosis 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 secondarily 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 remaining 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., ZorUlus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

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 sutures 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 lockups 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-pulling back property eliminates the need for fixation of the suture 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, further 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 gradual 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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5. Chiverton N, Redden JF. A new technique for delayed primary closure of fasciotomy wounds. Injury 2000;31:21-4.

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

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

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.

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

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

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.

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.

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

KLİNİK ÇALIŞMA - ÖZET OLGU SUNUMU

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

Bursa Şevket Yılmaz Eğitim ve Araştırma Hastanesi, Plastik Cerrahi Kliniği, Bursa Uludağ Üniversitesi Tıp Fakültesi, Plastik ve Rekonstrüktif Cerrahi Anabilim Dalı, 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 görünmektedir. Çeşitli etiyolojilere bağlı olarak gelişen kompartman sendromu sonrası açılan fasyotomi defektlerine uygulanabilir. Anahtar sözcükler: Aşamalı primer kapatım; fasyotomi yarası; kancalı dikişler; kompartman sendromu. Ulus Travma Acil Cerrahi Derg 2014;20(3):194-198

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

K Lİ NİK Ç A LI ŞM A

Skafoid psödoartroz tedavisinde otolog kemik grefti ve titanyum başsız kanüllü kompresyon vidası kombinasyonu uygulama sonuçları Dr. Güzelali Özdemir,1 Dr. Özgür Çiçekli,2 Dr. Turgut Akgül,3 Dr. Sinan Zehir,4 Dr. Ferit Yücel,5 Dr. Deniz Eşkin2 1

Kanuni Sultan Süleyman Eğitim ve Araştırma Hastanesi, Ortopedi ve Travmatoloji Kliniği, İstanbul

Şanlıurfa Eğitim ve Araştırma Hastanesi, Ortopedi ve Travmatoloji Kliniği, Şanlıurfa

İstanbul Üniversitesi İstanbul Tıp Fakültesi, Ortopedi ve Travmatoloji Anabilim Dalı, İstanbul

Hitit Üniversitesi Tıp Fakültesi, Ortopedi ve Travmatoloji Anabilim Dalı, Çorum

Şanlıurfa Edessa Özel Hastanesi, 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 grafilerde 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 hiperekstansiyon ve radial deviasyonda iken aksiyel sonrasında

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

Sorumlu yazar: Dr. Turgut Akgül, İstanbul Üniversitesi İstanbul Tıp Fakültesi, Ortopedi ve Travmatoloji Anabilim Dalı, İstanbul Tel: +90 212 - 414 20 00 E-posta: doktorturgut@yahoo.com Ulus Travma Acil Cerrahi Derg 2014;20(3):199-204 doi: 10.5505/tjtes.2014.92255 Telif hakkı 2014 TJTES

Ulus Travma Acil Cerrahi Derg, Mayıs 2014, Cilt. 20, Sayı. 3

Literatürde kırık oluşumundan altı hafta sonra tanı konulan ve sekiz haftalık konservatif tedaviye rağmen radyolojik olarak kaynama bulgusu görülmeyen skafoid kırıklarında psödoartroz gelişme riski bildirilmektedir.[5-7] Psödoartroz veya yanlış kaynama olgularını en aza indirmek için cerrahi endikasyonlar; deplase kırıklar, parçalı kırıklar, proksimal kutup yerleşimli kırıklar, tedavisi gecikmiş kırıklar, hasta uyumsuzluğu ve açısal sorunlar olarak bildirilmiştir.[6-8] Psödoartroz gelişme insidan199

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

sı, hastalarının bir kısmının semptomsuz olarak devam etmeleri nedeni ile tam olarak bilinememektedir. Psödoartroz gelişen 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 fiksasyon yöntemleri ile başarılı sonuçlar bildirilmiştir.[9-16] Çalışmamızda skafoid psödoartroz olgularında uyguladığımız otolog iliak trikortikal kemik grefti ve başsız tam yivli kompresif 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 psödoartrozlu 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, takiplerde 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 kırığına 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 önarka, yan ve ulnar deviasyonda ön-arka grafileri ile değerlendi-

rildi. Hastalara ameliyat öncesi bilgisayarlı tomografi (BT) incelemesi rutin olarak yapıldı. Standart olarak uygulanmamakla beraber çalışmada kemik kollapsının değerlendirilmesi için bazı hastalara manyetik rezonans görüntüleme (MRG) incelemesi 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 yetmezliği olmaması olarak belirlendi.[18,19] Bütün hastalar aynı standart cerrahi prosedür ile tedavi edildi. Russe tarafından tarif edilen volar yaklaşım ile skafoid psödoartroz bölgesine ulaşıldı.[20] Psödoartroz hattında küret ve yüksek devirli burr yardımı ile debridman uygulandı (Şekil 2a). Debridman sonrası kalan boşluğa iliak kanattan alınan trikortikal 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 kompresyon 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” istatistik paket programı kullanıldı. Verilerin değerlendirilmesi ise Ki-kare ve Kaplan-Meier testleri ile yapıldı. P<0.05 değeri istatistiksel olarak anlamlı kabul edildi.

A1 A2

Tip A

Tip B4

Tip B1

Tip C

Tip B2

Tip D1

Tip B3

Tip D2

Şekil 1. Skafoid kırıklarının Herbert sınıflaması.

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

(a)

(b)

Şekil 2. (a) El bileği volar yaklaşım ile beraber skafoid psödoartroz sahası ve debridman sonrası skafoidin klinik görünümü. (b) Cerrahi tedavi sırasında trikortikal greft kullanılmasının ardından antirotasyon K-teli ve başsız tam yivli kompresif kanüle vidasının floroskopide görünümü.

(a)

(b)

(c)

(e)

(d)

(f)

Şekil 3. Yirmi bir yaşında erkek hasta bir senedir el bileğinde ağrı şikayeti ile tarafımıza başvurdu. Skafoid psödoartroz tanısı ile iliak kanat trikortikal otogrefonaj ve tam yivli başsız kompresyon vidası kombinasyonu yöntemiyle ameliyat edildi. Ameliyat öncesi çekilen el bileği ön-arka (a), el bileği lateral (b) grafileri ile beraber operasyon öncesi çekilen manyetik rezonans görüntüleme kesitleri (c) kaynama sonrasında ikinci sene kontrolünde çekilen el bileği ulnar deviasyonda ön-arka (d) lateral (e) grafi el bileği bilgisayarlı tomografi (f) görüntüleri bulunmaktadır.

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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.

Kaynama süresi (hafta)

40 35 30 25 20 15 10 5 0

Şekil 4. Ameliyat öncesi geçen süre ile kırık kaynaması arasındaki ilişki diyagramı.

Yaş

Kaynama süresi

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İstatistiksel olarak kırık oluşma zamanı ile psödoartroz cerrahisi arasındaki zamanda 12 aydan fazla uzama ile kaynama zamanının 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 grafilerinde 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 skorlamasına 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 tedavi edilebilen Sudeck atrofisi görüldü.

TARTIŞMA Skafoid psödoartroz olgularının prognozu, semptomsuz hastaların varlığı nedeni ile kesin olarak bilinememektedir. Semptomlu 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 belirleyememiştir.[5,7,10] Semptomlu skafoid psödoartoz olgularında, kalıcı sakatlıkları engellemek için tedavi büyük önem kazanmaktadır. Skafoid psödoartroz cerrahi tedavisinde, avasküler dokuların uzaklaştırılması ve greftleme tedavinin esasını oluşturmaktadır. 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 kanattan alınan greft ile skafoid uzunluğunu sağlamıştır. Bu çalışmada k-teli ile fiksasyon kullanılmasına rağmen %100 kaynama ile başarılı sonuç bildirmiştir.[9]

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Şekil 5. Hasta yaşı ile kaynama süresini karşılaştıran diyagram.

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Zaidemberg ve ark. skafoid psödoartroz olgularında radial birinci ve ikinci dorsal kompartman arterini kullanarak aldıkları vaskülarize kemik greftini kullandıkları 22 skafoid psödoartrozlu olgu çalışmasında tam kaynama bildirmişlerdir.[13] Vaskülarize kemik grefti kullanımı skafoid psödoartroz hastalarında uygulanan ve başarılı sonuçlar alınabilen bir yöntemdir ancak cerrahinin güçlüğü ve sık kullanılmaması nedeniyle diğer tekniklere üstünlüğü kanıtlanamamıştır. Son yıllarda vaskülarize Ulus Travma Acil Cerrahi Derg, Mayıs 2014, Cilt. 20, Sayı. 3

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

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

dirilmesinde kullanılan Mayo el bilek skorlamasına göre hastalarda iyi ve mükemmel sonuçlar alındı.

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 kırıklarının cerrahisinde günümüzde kabul edilen görüş kompresyon 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 kompresyon vidası ile başarılı sonuçlar bildirmiştir.[17] Whipple, Herbert tarafından tarif edilen vidanın kanüllü hale getirilmesini sağlamış ve Herbert ile benzer yüksek başarılı klinik sonuçlar yayınlamıştır.[23] Literatürde Herbert vidası ile başarılı sonuçlar 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 biyomekanik 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 kaynama 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.

Çalışmamızda proksimal kutup yerleşimli skafoid psödoartrozlarında kaynama elde edemedik. Robbins ve ark., bu kırıklarda 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 yerleştirilecek 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 psödoartozu beş yıldan uzun olan olgularda kaynama oranın düşük olduğu ve artritik değişikliklerin varlığının kaynamayı olumsuz yönde etkilediği çalışmalar da gösterilmiştir. [5,32] Trumble ve ark. yaptıkları çalışmada ileri derecede skafoid kollaps görülmesi halinde greftleme ile başarılı sonuçlar alınamayacağını, eksizyon veya artrodez seçeneklerinin daha uygun olacağını bildirmişlerdir.[24] Bizim olgularımızda, hastalarda 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 uzadığını belirledik. Literatürde yapılan birçok çalışmada skafoid psödoartroz cerrahisi sonrasında kaynama sağlanması ile beraber fonksiyonel sonuçlarda belirgin iyileşme bildirilmiştir.[18,24,31,33-35] Çalışmamızda, kaynama gerçekleşen 22/24 hastanın klinik değerlenUlus Travma Acil Cerrahi Derg, Mayıs 2014, Cilt. 20, Sayı. 3

Skafoid psödoartrozu tedavisinde volar yaklaşımla iliak kanattan alınan trikortikal otogreft ve başsız tam yivli kanüle kompresif vida kombinasyonu, yüksek oranda kaynama ve başarılı fonksiyonel sonuçlar veren bir yöntemdir. Çıkar örtüşmesi: Çıkar örtüşmesi bulunmadığı belirtilmiştir.

KAYNAKLAR 1. Gaebler C, McQueen MM. Carpus fractures and dislocations. In: Bucholz RW, Heckman JD, Court-Brown CM, Tornetta P, editors. Fractures in adults. 3rd ed. Philadelphia: Lippincott Williams and Wilkins; 2009. p. 782-828. 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 removable 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 scaphoid 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 scaphoid 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 ununited 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 metacarpal artery. J Hand Surg Br 1997;22:425-7.

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Özdemir ve ark. Skafoid psödoartroz tedavisinde otolog kemik grefti ve titanyum başsız kanüllü kompresyon vidası kombinasyonu 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 fixation 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 treatment, 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. Longterm 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. Treatment 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 biomechanical study on preloaded compression eVect on headless screws. Arch Orthop Trauma Surg 2009;129:1601-5. 28. Wheeler DL, McLoughlin SW. Biomechanical assessment of compression 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 internal fixation with a cannulated screw. J Bone Joint Surg Am 2000;82:63341. 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. Comparison 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 scaphoid 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 proximal 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.

ORIGINAL ARTICLE - ABSTRACT OLGU SUNUMU

The results of autologous bone graft and titanium headless cannulated compression screw for treatment of scaphoid nonunion Güzelali Özdemir, M.D.,1 Özgür Çiçekli, M.D.,2 Turgut Akgül, M.D.,3 Sinan Zehir, M.D.,4 Ferit Yücel, M.D.,5 Deniz Eşkin, M.D.2 Department of Orthopaedics and Traumatology, Kanuni Sultan Süleyman Training and Research Hospital, Istanbul Department of Orthopaedics and Traumatology, Şanlıurfa Training and Research Hospital, Sanliurfa Department of Orthopaedics and Traumatology, İstanbul University İstanbul Faculty of Medicine, Istanbul 4 Department of Orthopaedics and Traumatology, Hitit University Faculty of Medicine, Corum 5 Şanlıurfa Edessa Hospital, Sanliurfa 1 2 3

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 minimum 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 effective 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

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doi: 10.5505/tjtes.2014.92255

Ulus Travma Acil Cerrahi Derg, Mayıs 2014, Cilt. 20, Sayı. 3

K Lİ NİK Ç A LI ŞM A

Triangular fibrokartilaj kompleks periferik (Palmer tip 1B) yırtıklarında artroskopik tamir sonuçları Dr. Fatih Kabakaş,1 Dr. İsmail Bülent Özçelik,1 Dr. Meriç Uğurlar,2 Dr. Berkan Mersa,1 Dr. Memet Yazar,3 Dr. Metin Uzun4 1

İst-el El Cerrahi Mikrocerrahi ve Rehabilitasyon Grubu, İstanbul

Kartal Yavuz Selim Devlet Hastanesi, Ortopedi ve Travmatoloji Kliniği, İstanbul

Şişli Etfal Eğitim ve Araştırma Hastanesi, Plastik ve Rekonstruktif Cerrahi Kliniği, İstanbul

Maslak Acıbadem Hastanesi, Ortopedi ve Travmatoloji Kliniği, İstanbul

ÖZET AMAÇ: Triangular fibrokartilaj kompleks (TFKK) hasarlanması el bileğinin ulnar taraf ağrılarının başlıca nedenidir. Bu çalışmada, artroskopik 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 uygulanan 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 nedenlerindendir.[1] Palmer, sınıflamasında tip 1 yırtıkların travmatik nedenlere bağlı geliştiğini ve tip 1B yırtıkların ulnar taraflı periferal yırtıklar olduğunu tariflenmişdir.[2,3] TFKK’nin periferik kısmının iyi kanlanması nedeni ile TFKK Palmer tip 1B yırtıklarının tamiri iyi sonuçlar vermektedir.[4] Geçmiş yıllarda 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: bulent-ozcelik@hotmail.com Ulus Travma Acil Cerrahi Derg 2014;20(3):205-210 doi: 10.5505/tjtes.2014.63933 Telif hakkı 2014 TJTES

Ulus Travma Acil Cerrahi Derg, Mayıs 2014, Cilt. 20, Sayı. 3

TFKK yırtıkları açık teknikler ile tedavi edilirken günümüzde artroskopik teknikler ile de bu yırtıkların etkin bir şekilde tedavisi yapılabilmektedir. Artroskopik tamirin açık tekniklere 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 portalden 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) değerlendirildi. Bütün hastalarda çalışma ve yaşam aktiviteleri sırasında kapa205

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

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

Ameliyat Tekniği

Şekil 1. Artroskopik yırtık görüntülenmesi ve shaver ile debridman.

sitelerini etkileyen el bileği ulnar taraf ağrı şikayeti mevcuttu. Fiziksel incelemede hastaların hepsinde el bileği ulnar tarafta bası ile ağrı oluşumu ve maksimum ulnar deviasyonda ağrı hissi mevcuttu. Hastaların hiçbirinde eklem hareket kısıtlılığı saptanmadı. Beş hastanın supinasyon ve pronasyon hareketleri ağrılı idi. Ameliyat öncesinde hastaların hepsine iki yönlü direkt grafi ve manyetik rezonans görüntüleme (MRG) incelemesi yapılmıştır. MRG incelemesinde hastaların tümünde periferik 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 önerilmiştir.

Hastaların el bileğine 5-8 kg ağırlık ile distraksiyon uygulandı. 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 içinde 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 insizyondan dışarı alınması sağlandı (Şekil 5a, b). Gerekli durumlarda aynı teknik ile ikinci sütür konuldu. Bu hazırlıklar tamamlandıktan sonra sütürlerin yırtık hattını yeterince stabilize edip etmediği ve trambolin efekti artroskopik olarak kontrol edildi (Şekil 5c). Traksiyon sonlandırılarak el bileği ekstansiyonda ip-

(a)

(b)

Şekil 2. Yeşil iğnenin (21G) içine 4/0 prolen sütür halka şeklinde yerleştirilmesi.

206

Şekil 3. (a, b) 6R portalin 1 cm altından açılan insiyondan TFKK periferik yırtık kenarına yeşil iğne gönderilmesi ve 6R portalden sokulan klemp yardımı ile prolen halkanın dışarı alınması.

Ulus Travma Acil Cerrahi Derg, Mayıs 2014, Cilt. 20, Sayı. 3

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

(a)

(b)

Şekil 4. (a, b) İkinci ipin 6R portalden klemp ile dışarı alınması.

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 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. Hastaların hiçbirinde ameliyat öncesi ve sonrası hareket 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 kanlanması periferden santrale doğru difüzyon yoluyla sağlanır. Periferik kanlanmanın iyi olması nedeni ile bu bölgedeki yırtıkların tamir sonrası iyileşme şansı yüksektir.[1,9-11]

(a)

(b)

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 yoluyla 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 kadar açık yöntemlerde[16-18] olduğu kadar artroskopik yöntemlerde 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] Ayrıca artroskopi ile yapılan ameliyat sırasında TFKK yırtıklarına eşlik eden diğer eklem içi patolojilerin değerlendirilmesi yapılabilmektedir.[25]

(c)

Şekil 5. (a-c) Halkanın ortasından geçirilen ikinci ipin diğer ucunun halka yardımı ile 6R altından açılan insizyondan çıkarılması ve sütür öncesi artroskopik görünüm.

Ulus Travma Acil Cerrahi Derg, Mayıs 2014, Cilt. 20, Sayı. 3

207

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

(a)

(b)

Şekil 6. (a, b) Traksiyonun sonlandırılarak el bileği ekstansiyonda iken iplerin düğümlenmesi.

Triangular fibrokartilaj kompleks yırtıklarının artroskopik tamirinde içeriden dışarıya, dışarıdan içeriye ve hepsi içeride olmak 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 yırtığı saptadıkları 38 hastaya artroskopik, 39 hastaya açık tamir ameliyatı uyguladıklarını ve istatistiksel olarak sonuçlarda fark bulmadıklarını bildirmiştir. Açık grupta ulnar sinir duyu dalında 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 208

artroskopik teknikle çok önemli stabilizatör role sahip olan EKU tendonunda hasarlanma yaratmadan 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. 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 hastanın 37 aylık takipleri sonucunda %91 iyi ve mükemmel sonuç aldıklarını bildirilmiştir. Uyguladıkları dışarıdan içeriye tekniği 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 tarafa 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 mükemmel sonuç bildirmişlerdir.[23] Pederzini ve ark. düğümün eklem içine koyulduğu bir dışarıdan içeriye tekniği tariflemiş. Fakat bu teknikte ulnar duyu sinirin dorsal dalının hasarlanmasından kaçınmak için 6U portalini ortalama 1.5 cm genişletmiş. Bu tekniğin avantajı düğümün eklem içine koyularak EKU tendon kılıfının irritasyonunun engellenmesidir.[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 içeriye 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 sayıdaki olgular ile yapıldığını ve bu tekniğin güvenilirliği için olgu sayılarının artması gerektiğini bildirmiştir.[35,36] Waterman ve ark.nın yaptıkları kadavra çalışmasında hepsi içeride tekniğinde 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 tendonuna ve ulnar duyu sinirinin dorsal dalına hasar vermeden iyi sonuçlar alınabildiğini tespit ettik. Hastalarımızın Mayo el bileği değerlendirme formu ile yapılan değerlendirme sonuçlarının tatminkar olduğu saptadık. Ayrıca hepsi içeride tekniğinin diğer tekniklere göre daha maliyetli olduğunu düşünmekteyiz. Ulus Travma Acil Cerrahi Derg, Mayıs 2014, Cilt. 20, Sayı. 3

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

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 artroskopik 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 patolojisi 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 bildirmişlerdir. Fakat DASH skorlarında anlamlı bir düzelme olmadığını bildirmişlerdir.[38] Wysocki ve ark. Palmer tip 1B akut periferik süperfisiyal yırtığı olan 28 hastanın 29 el bileğine artroskopik tamir uygulamışlar; hastaların ortalama 31 aylık takip sonucunda VAS skorlarınun 5.4’den 0.9’a gerilediğini, preoperatif 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 ayrışma 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 durumun 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 lunotriquetral 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 triangular 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 fibrocartilage 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 treatment. Arthroscopy 1990;6:125-32.

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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. Current Orthopaedic Practice 2008;19:509-14. 10. Shih JT, Lee HM, Tan CM. Early isolated triangular fibrocartilage complex tears: management by arthroscopic repair. J Trauma 2002;53:922-7. 11. Melone CP Jr, Nathan R. Traumatic disruption of the triangular fibrocartilage 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 resonance imaging of the triangular fibrocartilage complex lesions: a comprehensive clinicoradiologic approach and review of the literature. J Manipulative Physiol Ther 2007;30:522-6. 16. Hermansdorfer JD, Kleinman WB. Management of chronic peripheral 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 fibrocartilage complex of the wrist: a multicenter study. Arthroscopy 1997;13:7884. 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 lesions of the triangular fibrocartilage complex. Hand Clin 1995;11:31-6. 23. Haugstvedt JR, Husby T. Results of repair of peripheral tears in the triangular 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 transosseous and capsular repair of peripheral triangular fibrocartilage tears. Arthroscopy 2003;19:391-6. 25. Pederzini L, Luchetti R, Soragni O, Alfarano M, Montagna G, Cerofolini 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 arthroscopy. Arthroscopy 2008;24:343-54. 27. Waterman SM, Slade D, Masini BD, Owens BD. Safety analysis of allinside 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 radioulnar 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-

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36. Lee CK, Cho HL, Jung KA, Jo JY, Ku JH. Arthroscopic all-inside repair 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 arthroscopic repair of ulnar tears of the TFCC?. [Article in German] Handchir Mikrochir Plast Chir 2001;33:239-44. [Abstract] 38. Reiter A, Wolf MB, Schmid U, Frigge A, Dreyhaupt J, Hahn P, et al. Arthroscopic repair of Palmer 1B triangular fibrocartilage complex tears. Arthroscopy 2008;24:1244-50. 39. Wysocki RW, Richard MJ, Crowe MM, Leversedge FJ, Ruch DS. Arthroscopic treatment of peripheral triangular fibrocartilage complex tears with the deep fibers intact. J Hand Surg Am 2012;37:509-16.

ORIGINAL ARTICLE - ABSTRACT OLGU SUNUMU

Results of arthroscopic repair of triangular fibrocartilage complex peripheral tears (Palmer type 1B) Fatih Kabakaş, M.D.,1 İsmail Bülent Özçelik, M.D.,1 Meriç Uğurlar, M.D.,2 Berkan Mersa, M.D.,1 Memet Yazar, M.D.,3 Metin Uzun, M.D.4 İst-el Hand Surgery Microsurgery and Rehabilitation Group, Istanbul Department of Orthopedics and Traumatology, Kartal Yavuz Selim Goverment Hospital, Istanbul Department of Plastic And Reconstructive, Şişli Etfal Training and Research Hospital, Istanbul 4 Department of Orthopedics and Traumatology, Maslak Acıbadem Hospital, Istanbul 1 2 3

BACKGROUND: Triangular fibrocartilage complex (TFCC) injury is the major cause of wrist pain on the ulnar side. In this study, treatment outcomes 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

210

doi: 10.5505/tjtes.2014.63933

Ulus Travma Acil Cerrahi Derg, Mayıs 2014, Cilt. 20, Sayı. 3

CA S E R EP O RT

Supraventricular tachycardia due to blunt chest trauma in an adolescent Hayrullah Alp, M.D., Tamer Baysal, M.D., Sevim Karaarslan, M.D. Department of Pediatric Cardiology, Necmettin Erbakan University Meram Faculty of Medicine, 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

CASE REPORT

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 otherwise innocent-appearing chest-wall blows, with sudden cardiac death often resulting from projectiles striking the precordium.[3] This predominantly affects young male individuals, and the mean age is 14 years, with 78% under 18 years of age.[4] Among children, the impact object is an implement 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 effusions, conduction abnormalities[6] and ventricular arrhythmias[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.

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 experienced tachycardia and chest pain.

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: drhayrullahalp@hotmail.com Qucik Response Code

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She was born at term from a nonconsanguineous marriage and had had no chronic illness since birth. Her fetal and perinatal history was unremarkable. On the initial physical examination, 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 findings 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 211

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Figure 1. The electrocardiogram showing supraventricular tachycardia with a heart rate of 250/bpm.

term meaning cardiac arrest associated with low-impact blunt trauma to the anterior chest, usually by a relatively low-velocity missile, such as a baseball, cricket ball or hockey puck, or by a blow delivered by a fist, foot, elbow, or knee during 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 sudden 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 reported 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 fibrillation 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 mechanism 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 premature 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 precision.[10] The spectrum of injuries to the heart includes damage to the great vessels, myocardial rupture or contusion, hemopericardium, 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

Figure 2. The 12-lead electrocardiogram showing normal axis and sinus rhythm after adenosine administration.

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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 football and basketball. Thus, it can be suggested that commercially 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 maneuvers 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 longterm pharmacologic management. In conclusion, blunt chest trauma and its associated complications such as arrhythmias and commotio cordis are among the current problems in sportive activities. Chest protectors are not sufficiently effective in organized sports. Associated ventricular 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 myocardial 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 Electrophysiol 2007;18:115-22. 4. Maron BJ, Gohman TE, Kyle SB, Estes NA 3rd, Link MS. Clinical profile 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. Pediatr Cardiol 2010;31:572-3. 7. Horduna I, Dubuc M, Rochon AG, Khairy P. Posttraumatic left ventricular 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 (commotio cordis). Prog Biophys Mol Biol 2003;82:175-86.

OLGU SUNUMU - ÖZET

Bir adolösanda künt göğüs travmasına bağlı supraventriküler taşikardi Dr. Hayrullah Alp, Dr. Tamer Baysal, Dr. Sevim Karaarslan Necmettin Erbakan Üniversitesi Meram Tıp Fakültesi, Çocuk Kardiyoloji Bilim Dalı, 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. Ulus Travma Acil Cerrahi Derg 2014;20(3):211-213

doi: 10.5505/tjtes.2014.90337

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CA S E R EP O RT

Are blank cartridge guns really harmless? İsmail Gülşen, M.D.,1 Hakan Ak, M.D.,2 Enver Sosuncu, M.D.,1 Mehmet Deniz Bulut, M.D.3 1

Department of Neurosurgery, Yuzuncu Yıl University Faculty of Medicine, Van

Department of Neurosurgery, Bozok University Faculty of Medicine, Yozgat

Department of Radiology, Yuzuncu Yıl University Faculty of Medicine, 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 particular, 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 intubated upon admittance to the emergency room. The physical examination revealed skin defect and burn measuring 2x3 cm

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: dr-ismailgulsen@hotmail.com Qucik Response Code

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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 parenchymal invasion, were cleaned. Irregular tears on the dura were observed at multiple sites. The bone defect was extended 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 postoperatively. GCS was 7 (E2V1M4). Anisocoria improved in the early period. Thirty-six hours postoperatively, anisocoria recurred, 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 Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

GĂźlĹ&#x;en 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 surroundings due to the noise generated.[8]

(a)

(b)

(c)

Figure 1. (a) Axial CT image of the brain at admission showing fragmented fractures in the right temporal region, intracerebral hematoma, and midline shift. (b) Axial CT image of the brain showing craniectomy defects, intracerebral edema and midline shift. (c) Axial CT image of the brain before the patientâ&#x20AC;&#x2122;s discharge.

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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 pressure at the tip of the barrel can reach up to 100-200 bars during discharge. This pressure may provide the energy necessary for penetrating the skin, and thus may lead to lifethreatening 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 fragmented 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 injury 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 serious 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 cranial 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-tabancalari-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 Yüzüncü Yıl Üniversitesi Tıp Fakültesi, Beyin ve Sinir Cerrahisi Anabilim Dalı, Van Bozok Üniversitesi Tıp Fakültesi, Beyin ve Sinir Cerrahisi Anabilim Dalı, Yozgat 3 Yüzüncü Yıl Üniversitesi Tıp Fakültesi, Radyoloji Anabilim Dalı, Van 1 2

Kuru sıkı silahlar mermi çekirdeği fırlatmaksızın ses ve gaz fişekleri ateşleyen silahlardır. Bu silahların ateşleme sırasında, dış görünümü ve sesi gerçeklerinden 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. Ulus Travma Acil Cerrahi Derg 2014;20(3):214-216

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Successful emergency department thoracotomy for traumatic cardiac rupture: effective utilization of a fret sternum saw Tsukasa 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 1

Department of Organ Transplantation and General Surgery, Kyoto Prefectural University of Medicine, Japan

Departments of 2Surgery, and 3Anesthegiology, Omihachiman Community Medical Center, 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 lifesaving 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 Address for correspondence: Tsukasa Nakamura, M.D. Kajii-cho 465, Kamigyo-ku Kyoto, Japan Tel: 81752515532 E-mail: tsukasa@koto.kpu-m.ac.jp Qucik Response Code

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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 unmeasurable. Immediately, a primary survey and a focused assessment with sonography for trauma (FAST) were performed simultaneously. The FAST revealed significant pericardial 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 drainage. A crash midline sternotomy was performed, followed by opening her pericardium, and O, Rh(D) positive red cell concentrate (RCC) transfusion was begun simultaneously ( Japanese Rh(D) positive accounts for 99.5% of the population). 217

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(a)

(b)

Aorta

Site of Perforation

LCx RCA RV

LAD Figure 1. (a, b) The perforated site is indicated by the black and white arrows: the left atrium. (b) 3D cardiac CT was taken postoperatively.

A large amount of bleeding ensued and direct cardiac massage 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 hemostasis was obtained. Disseminated intravascular coagulation (DIC) due to the massive hemorrhage manifested as bleeding from the endotracheal tube. Immediate simple wound closure 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 patientâ&#x20AC;&#x2122;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 underwent 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 symptoms included visual impairment and a slight dysmnesia that improved after intensive rehabilitation. She was able to successfully 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 prognosis. Although survival rates of EDT in blunt chest trauma are very low, only 1.4%,[3] EDT can serve as the only lifesaving 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.

Figure 2. This figure illustrates the operation of a fret sternum saw. 1) A long forceps is inserted beneath the sternum. 2) The fret sternum saw is guided. 3) The sternum is divided. 4) Assistant surgeons place scissors on the sternum.

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

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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, clamshell incision and left lateral thoracotomy are all techniques employed for cardiac exposure. However, a midline sternotomy 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 significantly 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 minimize hypoxic brain injury. In cases of atrial cardiac rupture, it should be managed by application of a vascular clamp and oversewing the perforation. On the other hand, ventricular rupture can be managed 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 bypass, if necessary and readily available. Cardiopulmonary bypass and clamping of the SVC, IVC and aorta in order to maintain cerebral perfusion might also prevent huge air embolism in cases of large left atrium or ventricle rupture while suturing. Given this additional advantage, a median sternotomy is the recommended approach as it allows easy access to the great vessels. It has been argued that an electric sternum saw is too expensive 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 “unnecessary” or “non-frequent usage”. This problem due to the price can be addressed with the application of the inexpensive 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 Ulus Travma Acil Cerrahi Derg, May 2014, Vol. 20, No. 3

donor cardiac death (DBD or DCD). Application of this saw is described in Figure 2. Instruments required for rapid thoracic entry and cardiac exposure 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 properly 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 available for review by the Editor-in-Chief of this journal upon request. Conflict of interest: None declared.

REFERENCES 1. Baker CC, Thomas AN, Trunkey DD. The role of emergency room thoracotomy 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 rupture. 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 rupture from blunt trauma. J Trauma 1981;21:534-7.

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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 Kyoto İdari Üniversitesi Tıp Fakültesi, Transplantasyon ve Rejeneratif Cerrahi Anabilim Dalı, Kyoto, Japonya; Omihachiman Toplum Sağlığı Merkezi, 2Cerrahi ve 2Anesteziyoloji Bölümü, 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 kurtarabilmektedir. 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 gerçekleştirildiğinde 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 mekanizması, 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. Ulus Travma Acil Cerrahi Derg 2014;20(3):217-220

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CA S E R EP O RT

An unusual entry site for a nasal foreign body: a neglected trauma patient Selçuk Mülazımoğlu, M.D., Emre Ocak, M.D., Süha Beton, M.D., Ozan Bağış Özgürsoy, M.D. Department of Otorinolaryngology Head and Neck Surgery, Ankara University Faculty of Medicine, 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 penetrating facial injury. Key words: Maxillofacial trauma; nose; penetrating injury.

INTRODUCTION

CASE REPORT

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 factors 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 erasers, 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.

An 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 otorhinolaryngologist 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.

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. 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: selcukmulazim@gmail.com Qucik Response Code

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

DISCUSSION Nasal FB in children is a frequent situation in otorhinolaryngology 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 longstanding, 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] 221

MĂźlazÄąmoÄ&#x;lu et al. An unusual entry site for a nasal foreign body

Figure 1. Paranasal computerized tomography showing the right nasal foreign body (arrow) penetrating through the middle concha and septum.

In this case, the FB had entered the nasal cavity transcutaneously, 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 airways over a period of 30 years, and noted that pen cap is not a common FB in the nose. Patients with nasal FBs usually admit to emergency departments for removal of their FBs. FBs can be removed either in the emergency service or otorhinolaryngology department. Although emergency practitioners

Figure 2. Traumatic scar on the right nasolabial sulcus (asterisk).

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, endoscopically if possible, to ensure no other pieces are left in the cavity. In a child with a penetrating injury to the face, one should suspect 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.

Figure 3. Endoscopic view of the right nasal foreign body (asterisk) penetrating through the middle concha (S: Septum, M: Middle concha, I: Inferior concha).

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Figure 4. Nasal foreign body after removal (plastic pen cap).

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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 pediatric 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: endoscopic management. Ann Otol Rhinol Laryngol 2000;109:119-22. 7. Foltran F, Ballali S, Passali FM, Kern E, Morra B, Passali GC, et al. Foreign bodies in the airways: a meta-analysis of published papers. Int J Pediatr Otorhinolaryngol 2012;76 Suppl 1:12-9. 8. Chan TC, Ufberg J, Harrigan RA, Vilke GM. Nasal foreign body removal. 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 resembles concha bulloza in the middle meatus: a case report. Kulak Burun Bogaz Ihtis Derg 2009;19:307-10.

OLGU SUNUMU - ÖZET

Burunda yabancı cisimde sıradışı bir giriş yolu: İhmal edilmiş bir travma olgusu Dr. Selçuk Mülazımoğlu, Dr. Emre Ocak, Dr. Süha Beton, Dr. Ozan Bağış Özgürsoy Ankara Üniversitesi Tıp Fakültesi, Kulak Burun Boğaz Hastalıkları Anabilim Dalı, Ankara

Burunda yabancı cisim özellikle çocuklarda sıkça karşılaşılan bir durumdur. Literatürde burunun değişik bölgelerinde çok çeşitli yabancı cisim bildirilmiştir. 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). Ulus Travma Acil Cerrahi Derg 2014;20(3):221-223

doi: 10.5505/tjtes.2014.56805

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Oksipital kondil kırıkları: Bir olgu sunumu Dr. Cem Dinç,1 Dr. Mehmet Erhan Türkoğlu,2 Dr. Cengiz Tuncer,1 Dr. Ömer Aykanat,1 Dr. Derya Özçelik,3 Dr. Gamze Özkan3 1

Düzce Üniversitesi Tıp Fakültesi, Beyin ve Sinir Cerrahisi Anabilim Dalı, Düzce

Ankara Dışkapı Eğitim ve Araştırma Hastanesi, Beyin ve Sinir Cerrahisi Kliniği, Ankara

Düzce Üniversitesi Tıp Fakültesi, Plastik ve Rekonstrüktif Cerrahi Anabilim Dalı, 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

OLGU SUNUMU

Oksipital kondil kırıkları (OKK) nadir olarak görülür.[1,2] Ancak tanısal alandaki teknolojik gelişmeler ile artan sayıda olguların literatürde yer alması ve olgu çalışmalarının yayınlanması, OKK’nın klasik bilgilerimizden daha sık olduğunu göstermektedir. Direkt grafilerle bu kırıklara tanı konulamamakta ve bilgisayarlı tomografi (BT) taramasına ihtiyaç duyulmaktadır. [3] Günümüzde oldukça hızlı tüm spinal travma taraması yapabilen BT cihazlarının yaygınlaşması ile OKK daha sıklıkla saptanmaktadır. Mueller ve ark.[4] kendi çalışmalarında OKK insidansını %1.19/5 yıl olarak bildirmişlerdir. Çoğu zaman OKK’da konservatif tedavi yeterli olmaktadır. Ancak atlantooksipital instabilitenin (AOİ) eşlik ettiği olgularda oksipitoservikal füzyon gerekebilmektedir. Morbidite ve mortalitesi yüksek seyredebilen ve cerrahi girişim gerektiren bu tür olguları gözden kaçırmamak için, semptomsuz ya da hafif semptomlu travma hastalarında oksipitoservikal bileşke BT ile mutlaka detaylı incelenmelidir.

Yirmi sekiz yaşında kadın hasta, acil servisimize araç içi trafik kazası sonrası kabul edildi. Hastanın acil servisteki fiziksel incelemesinde, konuşma güçlüğüne yol açan iki taraflı temporomandibuler eklem bölgesinde ve üst servikal bölgede palpasyonla hassasiyeti mevcuttu. Vital bulguları stabil olan hastanın fiziksel incelemesinde yaygın maksillofasyal ödem ve ekimozlar gözlendi. Nörolojik incelemesi tamamen normaldi. Servikal 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 dislokasyonun eşlik etmediği sol oksipital kondil kırığı saptandı (Şekil 1, 2). İki taraflı zygoma ark kırığı için ameliyat edilen hastanın entübasyonu fleksibil entübasyon ile sağlandı. Kondil kırığı nedeniyle 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.

İletişim adresi: Dr. Ömer Aykanat, Metek Toki Konutları, K1-46, Daire: 12, Düzce Tel: +90 380 - 542 14 16 E-mail: yomeycik@hotmail.com Qucik Response Code

Ulus Travma Acil Cerrahi Derg 2014;20(3):224-226 doi: 10.5505/tjtes.2014.22747 Telif hakkı 2014 TJTES

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TARTIŞMA Oksipital kondil kırıklarının nadir görülen kırıklar olarak bilinmesine karşın, son yıllarda yapılan çalışmalar acil servise travma ile başvuran her yüz hastadan birinde OKK olabileceğini göstermektedir.[4] Büyük bölümünün yüksek enerjili travmalardan sonra ortaya çıkmasına karşın, minör travmalardan sonra da OKK oluşabilir.[4] Özellikle üst servikal bölgede hassasiyeti bulunan semptomsuz, minör travmatize hastalarda OKK ihtimali mutlaka düşünülmelidir. Çocuk hastalarda ve Ulus Travma Acil Cerrahi Derg, Mayıs 2014, Vol. 20, No. 3

Dinç ve ark. Oksipital kondil kırıkları

(a)

(b)

Şekil 1. (a) Aksiyel kesitli kraniyal BT’de posteriora deplase sol oksipital kondil kırığı izlenmekte. (b) Koroner kesitli kraniyal BT’de posteriora deplase sol oksipital kondil kırığı izlenmekte.

BT’nin yeterli görüntüleme sağlayamadığı olgularda manyetik rezonans görüntüleme (MRG) kullanılabilir.[5] Literatürde OKK ile ilgili çalışma oldukça nadirdir ve çoğunlukla olgu sunumu ya da geriye dönük çalışmalara dayanmaktadır.[1,6,7] Tanısal alandaki gelişmeler ile artan sayıda olgu da literatürde yerini almıştır. 1988 yılına kadar literatürde yayınlanan 20 olguya,[8] 1978-2002 yılları arasında 116 olgu eklenmiştir.[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 deplasmanı olmadan kompresyon kırığı. Tip 2, kaide kırığının oksipital kondile uzanımı. Bu iki tip stabil kırıklar olarak kabul edilmiştir. 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-

Şekil 2. Aksiyel kesitli kraniyal bilgisayarlı tomografide posteriora deplase sol oksipital kondil kırığındaki füzyon izlenmekte.

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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 tedavisinde 6-12 hafta servikal boyunluk ya da Halo fiksatör ile immobilizasyon yeterli olmaktadır. Çoklutravmalı hastalarda, özellikle maksillofasiyal travma ya da toraks travması nedeniyle solunum desteği gerekli olan olgularda, uygulama güçlüğü ve komplikasyonları açısından Halo fiksatör kullanımı önerilmemektedir.[1,4,6] AOİ bulunmayan iki taraflı OKK olguları benzer şekilde stabil olarak kabul edilerek servikal eksternal immobolizasyon tedavi edilebilir.[2,9] Bununla birlikte, Dashti ve ark.,[10] inferior klivus kırığının eşlik ettiği iki taraflı OKK olan çoklutravmalı bir olguda Halo yelek kullanımı 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 tedavisi 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, hastalar semptomsuz olabilir ve direkt grafiler ile tanı konamayabilir. 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 gerektirir. 225

Dinç ve ark. Oksipital kondil kırıkları

Çıkar örtüşmesi: Çıkar örtüşmesi bulunmadığı belirtilmiştir.

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CASE R E P O R T - ABSTRACT

Occipital condyle fractures: A case report Cem 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 Department of Brain and Neurosurgery, Düzce University Faculty of Medicine, Düzce Department of Brain and Neurosurgery, Dışkapı Training and Research Hospital, Ankara 3 Department of Plastic and Reconstructive Surgery, Düzce University Faculty of Medicine, Düzce 1 2

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. Ulus Travma Acil Cerrahi Derg 2014;20(3):224-226

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doi: 10.5505/tjtes.2014.22747

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