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Cilt - Volume 19

Sayı - Number 6

Kasım - November 2013

TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY

www.tjtes.org Index Medicus, Medline, EMBASE/Excerpta Medica, Science Citation Index-Expanded (SCI-E), Index Copernicus, DOAJ ve TÜBİTAK-ULAKBİM Türk Tıp Dizini’nde yer almaktadır. Indexed in Index Medicus, Medline, EMBASE/Excerpta Medica and Science Citation Index-Expanded (SCI-E), Index Copernicus, DOAJ, and the Turkish Medical Index of TÜB‹TAK-ULAKB‹M.

ISSN 1306 - 696x


TURKISH JOURNAL OF TRAUMA AND EMERGENCY SURGERY ULUSAL TRAVMA VE ACİL CERRAHİ DERGİSİ Editor (Editör) Recep Güloğlu Associate Editors (Yardımcı Editörler) Kaya Sarıbeyoğlu Hakan Yanar M. Mahir Özmen Former Editors (Geçmiş Dönem Editörleri) Ömer Türel Cemalettin Ertekin Korhan Taviloğlu

NATIONAL EDITORIAL BOARD (ULUSAL BİLİMSEL DANIŞMA KURULU) Fatih Ağalar Yılmaz Akgün Levhi Akın Alper Akınoğlu Murat Aksoy Şeref Aktaş Ali Akyüz Ömer Alabaz Orhan Alimoğlu Nevzat Alkan Edit Altınlı Acar Aren Gamze Aren Cumhur Arıcı Oktar Asoğlu Ali Atan Bülent Atilla Levent Avtan Yunus Aydın Önder Aydıngöz Erşan Aygün Mois Bahar Akın Eraslan Balcı Emre Balık Umut Barbaros Semih Baskan M Murad Başar Mehmet Bayramiçli Ahmet Bekar Orhan Bilge Mustafa Bozbuğa Mehmet Can Başar Cander Nuh Zafer Cantürk Münacettin Ceviz Banu Coşar Figen Coşkun İrfan Coşkun Nahit Çakar Adnan Çalık Fehmi Çelebi Gürhan Çelik Oğuz Çetinkale M. Ercan Çetinus Sebahattin Çobanoğlu Ahmet Çoker Cemil Dalay Fatih Dikici Yalım Dikmen Osman Nuri Dilek Kemal Dolay Levent Döşemeci Murat Servan Döşoğlu Kemal Durak Engin Dursun

İstanbul Çanakkale İstanbul Adana İstanbul İstanbul İstanbul Adana İstanbul İstanbul İstanbul İstanbul İstanbul Antalya İstanbul Ankara Ankara İstanbul İstanbul İstanbul İstanbul İstanbul Elazığ İstanbul İstanbul Ankara Kırıkkale İstanbul Bursa İstanbul Edirne İstanbul Konya Kocaeli Erzurum İstanbul Ankara Edirne İstanbul Trabzon Sakarya İstanbul İstanbul İstanbul Edirne İzmir Adana İstanbul İstanbul Sakarya Antalya Antalya Düzce Bursa Ankara

Atilla Elhan Mehmet Eliçevik İmdat Elmas Ufuk Emekli Haluk Emir Yeşim Erbil Şevval Eren Hayri Erkol Metin Ertem Mehmet Eryılmaz Figen Esen Tarık Esen İrfan Esenkaya Ozlem Evren Kemer Nurperi Gazioğlu Fatih Ata Genç Alper Gökçe Niyazi Görmüş Feryal Gün Ömer Günal Nurullah Günay Haldun Gündoğdu Mahir Günşen Emin Gürleyik Hakan Güven İbrahim İkizceli Haluk İnce Fuat İpekçi Ferda Şöhret Kahveci Selin Kapan Murat Kara Hasan Eşref Karabulut Ekrem Kaya Mehmet Yaşar Kaynar Mete Nur Kesim Yusuf Alper Kılıç Haluk Kiper Hikmet Koçak M Hakan Korkmaz Güniz Meyancı Köksal Cüneyt Köksoy İsmail Kuran Necmi Kurt Mehmet Kurtoğlu Nezihi Küçükarslan İsmail Mihmanlı Mehmet Mihmanlı Köksal Öner Durkaya Ören Hüseyin Öz Hüseyin Özbey Faruk Özcan Cemal Özçelik İlgin Özden Mehmet Özdoğan

Ankara İstanbul İstanbul İstanbul İstanbul İstanbul Diyarbakır Bolu İstanbul Ankara İstanbul İstanbul İstanbul Ankara İstanbul İstanbul Tekirdağ Konya İstanbul Düzce Kayseri Ankara Adana Bolu İstanbul İstanbul İstanbul İzmir Bursa İstanbul Ankara İstanbul Bursa İstanbul Samsun Ankara Eskişehir Erzurum Ankara İstanbul Ankara İstanbul İstanbul İstanbul Ankara İstanbul İstanbul İstanbul Erzurum İstanbul İstanbul İstanbul Diyarbakır İstanbul Ankara

Şükrü Özer Halil Özgüç Ahmet Özkara Mahir Özmen Vahit Özmen Niyazi Özüçelik Süleyman Özyalçın Emine Özyuvacı Salih Pekmezci İzzet Rozanes Kazım Sarı Esra Can Say Ali Savaş İskender Sayek Tülay Özkan Seyhan Gürsel Remzi Soybir Yunus Söylet Erdoğan Sözüer Mustafa Şahin Cüneyt Şar Mert Şentürk Feridun Şirin İbrahim Taçyıldız Gül Köknel Talu Ertan Tatlıcıoğlu Gonca Tekant Cihangir Tetik Mustafa Tireli Alper Toker Rıfat Tokyay Salih Topçu Turgut Tufan Fatih Tunca Akif Turna Zafer Nahit Utkan Ali Uzunköy Erol Erden Ünlüer Özgür Yağmur Müslime Yalaz Serhat Yalçın Sümer Yamaner Mustafa Yandı Nihat Yavuz Cumhur Yeğen Ebru Yeşildağ Hüseyin Yetik Cuma Yıldırım Bedrettin Yıldızeli Sezai Yılmaz Kaya Yorgancı Coşkun Yorulmaz Tayfun Yücel

Konya Bursa İstanbul Ankara İstanbul İstanbul İstanbul İstanbul İstanbul İstanbul İstanbul İstanbul Ankara Ankara İstanbul Tekirdağ İstanbul Kayseri Tokat İstanbul İstanbul İstanbul Diyarbakır İstanbul Ankara İstanbul İstanbul Manisa İstanbul İstanbul Kocaeli Ankara İstanbul İstanbul Kocaeli Urfa İzmir Adana İstanbul İstanbul İstanbul Trabzon İstanbul İstanbul Tekirdağ İstanbul Gaziantep İstanbul Malatya Ankara İstanbul İstanbul


INTERNATIONAL EDITORIAL BOARD

ULUSLARARASI BİLİMSEL DANIŞMA KURULU

Juan Asensio Zsolt Balogh Ken Boffard Fausto Catena Howard Champion Elias Degiannis Demetrios Demetriades Timothy Fabian Rafi Gürünlüoğlu Clem W. Imrie Kenji Inaba Rao Ivatury Yoram Kluger Rifat Latifi Sten Lennquist Ari Leppaniemi Valerie Malka Ingo Marzi Kenneth L. Mattox Carlos Mesquita

Miami, USA New Castle, Australia Johannesburg, S. Africa Bologna, Italy Washington DC, USA Johannesburg, S. Africa Los Angeles, USA Memphis, USA Denver, USA Glasgow, Scotland Los Angeles, USA Richmond, USA Haifa, Israel Tucson, USA Malmö, Sweden Helsinki, Finland Sydney, Australia Frankfurt, Germany Houston, USA Coimbra, Portugal

Ernest E Moore Pradeep Navsaria Andrew Nicol Hans J Oestern Andrew Peitzman Basil A Pruitt Peter Rhee Pol Rommens William Schwabb Michael Stein Spiros Stergiopoulos Michael Sugrue Otmar Trentz Donald Trunkey Fernando Turegano Selman Uranues Vilmos Vecsei George Velmahos Eric J Voiglio Mauro Zago

Denver, USA Cape Town, S. Africa Cape Town, S. Africa Celle, Germany Pittsburgh, USA San Antonio, USA Tucson, USA Mainz, Germany Philadelphia, USA Petach-Tikva, Israel Athens, Greece Liverpool, Australia Zurich, Switzerland Oregon, USA Madrid, Spain Graz, Austria Vienna, Austria Boston, USA Lyon, France Milan, Italy

REDACTION (REDAKSİYON) Erman Aytaç

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

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. Annual subscription rates: 75.- (USD) 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 (Yayıncı): KARE Yayıncılık (KARE Publishing) • Design (Tasarım): Ali Cangül • Linguistic Editor (İngilizce Editörü): Corinne Can • Online Manuscript & Web Management (Online Dergi & Web): LookUs • Press (Baskı): Yıldırım Matbaacılık • Press date (Basım tarihi): November (Kasım) 2013 • This publication is printed on paper that meets the international standard ISO 9706: 1994 (Bu dergide kullanılan kağıt ISO 9706: 1994 standardına uygundur.)


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.


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-

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TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY ULUSAL TRAVMA VE ACİL CERRAHİ DERGİSİ Vol. - Cilt 19

Number - Sayı 6 November - Kasım 2013

Contents - İçindekiler ix

Editörden

Experimental Study - Deneysel Çalışma Deneysel Çalışma - Experimental Study 491-499 The role of thoracic trauma in inflammatory responses, apoptosis and bacterial translocation following multiple traumas Multipl travmayı takiben enflamatuvar yanıt, apopitozis ve bakteriyel translokasyonda torasik travmanın rolü Ayan E, Koksel O, Polat A, Tamer L, Ersöz G, Demir M, Yıldırım Yaroğlu H, Akdağ A, Özdülger A, Erden S 500-506 Hypertonic saline, normal saline or neither: which is best for uncontrolled hemorrhagic shock? An experimental study in goats Hipertonik salin, normal salin veya hiçbiri: Kontrol altına alınamayan hemorajik şok için en iyisi hangisi? Keçilerde deneysel çalışma Saeedi M, HajiseyedJavadi H, Shams Vahdati S, Eslami V, Mokhtarpour M, Momeni M, Farnia MR, Hafezi Nejad N 507-515 Antioxidant and anti-inflammatory effects of curcumin against hepatorenal oxidative injury in an experimental sepsis model in rats Sıçanlarda deneysel sepsis modelinde oluşan hepatorenal oksidatif hasara karşı curcuminin antioksidan ve antienflamatuvar etkisi Yılmaz Savcun G, Özkan E, Dulundu E, Topaloğlu Ü, Şehirli AÖ, Tok OE, Ercan F, Şener G

Original Articles - KlinikArticles Çalışma Klinik Çalışma - Original 516-520 Management of soft tissue extremity degloving injuries with full-thickness grafts obtained from the avulsed flap Yumuşak doku ekstremite avülzyon (degloving) yaralanmalarının avülze flepten elde edilmiş tam kalınlıklı deri grefti ile onarımı Pilancı Ö, Aköz Saydam F, Başaran K, Datlı A, Güven E 521-528 Functional outcomes after treatment of traumatic brachial plexus injuries: clinical study Travmatik brakiyal plesus yaralanmaları cerrahisi sonrası fonksiyonel sonuçlar: Klinik çalışma Aras Y, Aydoseli A, Sabancı PA, Akçakaya MO, Alkır G, İmer M 529-535 Factors affecting mortality caused by falls from height Yüksekten düşmelerde mortaliteyi etkileyen faktörler İçer M, Güloğlu C, Orak M, Üstündağ M 536-542 An analysis of firearms-related deaths between 1993-2010: a retrospective study 1993-2010 yılları arasında gerçekleşmiş ateşli silah yaralanmasına bağlı ölümler: Geriye dönük çalışma Toygar M, Türker T, Eroğlu M, Kaldırım Ü, Poyrazoğlu Y, Eyi YE, Durusu M, Eryılmaz M 543-547 A new application technique of circular fixator for the treatment of open tibial fractures: circular fixator-hinge technique Açık tibia kırıklarının sirküler fiksatörler ile tedavisinde yeni bir uygulama tekniği: Fiksatör-menteşe yöntemi Demir B, Sökücü S, Özden E, Yavuz U, Duman S, Kabukçuoğlu YS

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TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY ULUSAL TRAVMA VE ACİL CERRAHİ DERGİSİ Vol. - Cilt 19

Number - Sayı 6 November - Kasım 2013

Contents - İçindekiler 548-553 Cemented calcar replacement versus cementless hemiarthroplasty for unstable intertrochanteric femur fractures in the elderly Yaşlı hastalarda görülen dengesiz intertrokanterik kırıkların tedavisinde, çimentosuz ve çimentolu kalkar replasmanlı hemiartroplastinin karşılaştırılması Çankaya D, Özkurt B, Tabak AY 554-558 Çocuk apandisitlerinde risk faktörlerinin analizi Analysis of risk factors for the development of pediatric appendicitis Yıldız T, Bozdağ Z, Erkorkmaz Ü, Emre A, Turgut T, İlçe Z 559-563 Karıniçi basınç artışına yol açabilen hastalıkların tedavisi intravezikal basınç ölçümü kontrolü altında daha güvenle yapılabilir mi? Can increased intra-abdominal pressure (IAP) be treated more effectively with intravesical pressure measurement in high-risk patients? Divarcı E, Ergün O, Karapınar B, Yalaz M, Çelik A

Olgu CaseSunumu Reports- -Case OlguReports Sunumu 564-566 Iliopsoas hematoma due to muscular rupture following defibrillation Defibrilasyon sonrası gelişen kas yırtığına bağlı iliopsoas hematomu Jahollari A, Cavolli R, Tavlasoglu M, Sallahu F, Muriqi S 567-569 Trauma-associated bleeding from the bilateral internal iliac arteries resolved using angiographic embolization Travma sonucu oluşmuş bilateral internal iliyak arter kanamasının anjiyografik embolizasyon ile sonlandırılması Aygün A, Karaca Y, Ayan E, Suha T, Dinç H 570-572 A rare cause of acute appendicitis: an ingested foreign body Akut apandisitin nadir bir nedeni: Yabancı cisim yutulması Hazer B, Dandin Ö, Karakaş DÖ 573-575 Acute intestinal obstruction secondary to left paraduodenal hernia: a case report Sol paraduodenal fıtığa bağlı akut intestinal tıkanıklık: Olgu sunumu Busra Cengiz M, Hasbahçeci M, Cipe G, Karatepe O, Müslümanoğlu M 576-580 Travma sonrası geç prezente olmuş pulmoner arteriyovenöz fistülün septal tıkayıcı cihaz ile kapatılması Late presentation of posttraumatic pulmonary arteriovenous fistulea occlusion with septal occluder device Güçyetmez B, Salihoğlu E, Ayyıldız A, Saltık L, Telci L 581-584 Mediastinoskopi ile çıkarılan mediastinal yabancı cisim (saçma çekirdeği): Olgu sunumu Removal of mediastinal foreign body (steel shot) using mediastinoscopy: case report Metin B, Tözüm H, Kaya S 585-592 Ulusal Travma ve Acil Cerrahi Dergisi 2013 yılı 19. cilt konu ve yazar dizini Index of volume 19

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Değerli Okurlarımız, Ulusal Travma ve Acil Cerrahi Dergisi’nin bir yılını daha bu sayıyla geride bırakıyoruz. Dergimiz PubMed ve SCI-expanded başta olmak üzere birçok prestijli dizinde yer almakta ve bu niteliğiyle ülkemizin öncü bilimsel süreli yayını özelliğini korumaktadır. Özellikle son yıllarda dergimize gösterilen yoğun ilgi kaliteden ödün vermemek adına bir dizi değişikliğin hayata geçirilmesine öncülük etti. İlk olarak kapak tasarımında önemli değişiklikler yapıldı. Yazı özetlerinin yerleşimi, dizgi, punto seçimi vs. gibi birçok biçimsel konuda değişiklikler yapıldı. Başlangıç sayfasına kare okuyucu konuldu ve atıf yapacak yazarların işini kolaylaştırmak amacıyla her yazının ilk sayfasına yazının künyesi ilave edildi. Dergimizde basılan yazıların bu son haliyle daha kolay okunacağı kanısındayız. 2014 yılı ilk sayısıyla beraber hayata geçecek olan bu yeni şeklimizi beğeneceğinizi umuyoruz. Bu fırsatla çok nitelikli iş çıkaran Kare Yayıncılık ekibine ve özverili çalışmaları nedeniyle Sayın Ali Cangül’e çok teşekkür ediyoruz. Dergimizin işleyişiyle ilgili de bazı yenilikler 2014 itibariyle devreye girecek. SCI-expanded dizininde yer alan dergimizi bir üst dizin olan SCI’ye ve Current Contents-Clinical Medicine’a dahil edebilmek için büyük çaba sarf etmekteyiz. Bunu başarabilmenin yolu dergimizin impact factor’ünü yükseltmekten geçmektedir. Artık uluslararası dergi niteliği kazanmış olan Ulusal Travma ve Acil Cerrahi Dergisi’ne büyük çoğunlukla dili İngilizce olan yazılar gönderilmektedir. Dergimize ulaşan yazıların yaklaşık dörtte biri Türkiye dışı ülkelerden gönderilmektedir ki bu bizleri ülkemiz adına gururlandırmaktadır. Bildiğiniz gibi dergimizde yer alan makaleleri resmi internet sitemizde tam metin ve bedelsiz olarak pdf formatında yayımlamaktayız. Dergimizin impact factor’ünün yükseltilebilmesinin tek yolu, yayımlanan makalelere başka dergilerde yapılacak olan atıfların sayısının artmasıdır. Birçok yazı Türkçe basıldığı ve sadece özeti İngilizce olduğu için beklenenden daha az ilgi uyandırmakta. Bu sorunu aşabilmek için Türkçe basılan makaleleri internet sitemizde İngilizce olarak yayımlama kararı aldık. Yazarlarımızdan 2014 itibariyle dergimizde yayınlanmak üzere kabul edilen Türkçe makalelerini İngilizceye çevirmelerini talep edeceğimizi şimdiden bildirmek istiyoruz. Dergimizin dilinin İngilizce ve Türkçe oluşu özelliğini değiştirmeden, impact factor puanımızı ancak bu şekilde yükseltebileceğimizi düşünmekteyiz. Yazarlarımız makalelerinde bilimsel dil tercihlerini belirlemede özgür olmaya devam edeceklerdir. Ancak yazım dili İngilizce olan makalelerin atıf alma şansları çok daha yüksek olacağından, böyle bir tercihin hem yazarların hem de derginin lehine olacağı da unutulmamalıdır. Dergimizin diğer bir önemli özelliği travma alanında çok değişik cerrahi branşların yazılarını değerlendirip yayımlamasıdır. Son yıllarda birçok branşta 600’ün üzerinde yıllık başvuru alan dergimiz, konulara göre bölüm editörlüğü ve dolayısıyla konuya özel hakem seçim sistemine yine 2014 yılında geçecektir. Bu yeni değerlendirme sisteminin hem yazıların değerlendirme süreçlerini kısaltacağından, hem de kalitesini yükselteceğinden eminiz. Ulusal Travma ve Acil Cerrahi Dergisi artık sadece derneğimizin bir yayın organı olmanın ötesine geçerek, ülkemizi yurtdışında temsil eden bir dergi olma misyonunu üstlenmiştir. Bu zor görevi birlikte başaracağımızdan eminiz. Amacımız her geçen yıl dergimizi daha ileri götürmektir. Tüm editörler kurulu adına dergimize olan ilgi ve katkılarınızın devamı dileğiyle, sizlere çalışmalarınızda sonsuz başarılar diliyorum. Saygılarımla, Dr. Recep Güloğlu

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EXPERIMENTAL STUDY

The role of thoracic trauma in inflammatory responses, apoptosis and bacterial translocation following multiple traumas Erhan Ayan, M.D.,1 Oğuz Koksel, M.D.,1 Ayşe Polat, M.D.,2 Lülüfer Tamer, M.D.,3 Gülden Ersöz, M.D.,4 Murat Demir, M.D.,1 Hatice Yıldırım Yaroğlu, M.D.,3 Alper Akdağ, M.D.,4 Ali Özdülger, M.D.,1 Sema Erden, M.D.5 1

Department of Thoracic Surgery, Mersin University Faculty of Medicine, Training and Research Hospital, Mersin

2

Department of Pathology, Mersin University Faculty of Medicine, Training and Research Hospital, Mersin

3

Department of Biochemistry, Mersin University Faculty of Medicine, Training and Research Hospital, Mersin

4

Department of Infectious Disease, Mersin University Faculty of Medicine, Training and Research Hospital, Mersin

5

Health Occupation High School, Biostatistics, Mersin

ABSTRACT BACKGROUND: Blunt chest trauma and its complications are commonly encountered in emergency medicine. Herein, we used a rat model to investigate the role of thoracic trauma in inflammation, apoptosis and bacterial translocation following multiple traumas. METHODS: Ninety Wistar rats were divided equally into nine groups. Rats underwent a standardized blunt thoracic and/or head trauma and were sacrificed 24 or 48 hours after the trauma. Specimens from various organs and blood samples were collected and quantitatively cultured for aerobic organisms. Interleukins, TNF-α, and MCP-1 levels were assessed in the sera and markers of apoptosis were detected in the lungs. RESULTS: Levels of interleukins, TNF-α and MCP-1 in all of the groups undergoing trauma were significantly higher than those of the control group (p=0.001). Levels of apoptotic cells in the groups undergoing head and thoracic trauma (HTT) were significantly higher than those of the control group (p=0.009). Light microscopic evaluation indicated that damage in the HTT groups was significantly higher than that in the control group. The incidence of bacterial translocation was also significantly higher in the HTT groups (p=0.003). CONCLUSION: Multiple inflammatory mediators are activated in multiple traumas (including blunt thoracic trauma), which allow bacterial translocation and apoptotic processes to occur. Our results indicate that thoracic trauma plays a major role in post-traumatic bacterial translocation, inflammation, and apoptosis following multiple traumas. Key words: Head trauma; interleukin; lung injury; systemic inflammatory response syndrome; thoracic trauma.

INTRODUCTION Blunt traumas and their associated complications are major causes of death in young and middle-aged people. Previous Address for correspondence: Erhan Ayan, M.D. Mersin Üniversitesi Tıp Fakültesi Araştırma ve Uygulama Hastanesi, 33100 Mersin, Turkey Tel: +90 324 - 337 43 00 E-mail: erhanayan10@hotmail.com Qucik Response Code

Ulus Travma Acil Cerr Derg 2013;19(6):491-499 doi: 10.5505/tjtes.2013.29660 Copyright 2013 TJTES

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studies have reported that acute lung injury (ALI) associated with pulmonary contusion, sepsis and multiple organ failure (MOF) are major complications of blunt trauma that can lead to morbidity and mortality. Approximately one-third of trauma cases presenting at hospitals present with thoracic trauma. Lung contusion resulting from thoracic injury plays an important role in the development of ALI and Acute Respiratory Distress Syndrome (ARDS). It has been reported that ALI can lead to the development of MOF, and that morbidity and mortality are significantly higher in blunt trauma cases with lung injury than those in traumas without.[1,2] Studies using an experimental thoracic trauma model have shown that an acute inflammatory response develops shortly after the trauma, but this response subsides with time, returning to normal levels within approximately 7 days. Because of these 491


Ayan et al., The role of thoracic trauma in inflammatory responses, apoptosis and bacterial translocation following multiple traumas

results, it has been hypothesized that the change in inflammatory response alone is not sufficient to explain the etiology of complications like ALI and ARDS, and that additional processes that might trigger the development of these pathologies should be investigated. Furthermore, it was noted that apoptosis following thoracic traumas may be associated with the inflammatory response.[3-6] Bacterial translocation refers to the spread of bacteria and their products in the intestinal flora to solid organs, which can be due to intestinal hypoperfusion, burns and stress. Bacterial translocation has been cited as one of the leading factors in the development of acute lung injury, MOF and sepsis. [7-10] We undertook the current study to determine whether there was a correlation between the cellular and humoral inflammatory responses, apoptosis and bacterial translocation in a model of lung contusion developed after blunt thoracic trauma and/or multiple traumas accompanied by blunt thoracic trauma. We also aimed to determine the effects of blunt thoracic trauma in the development of the aforementioned processes.

MATERIALS AND METHODS All experiments were performed in accordance with the National Institutes of Health Guidelines on the Care and Use of Laboratory Animals. The approval of the Ethics Committee was obtained before the onset of the study. This study was approved by the Mersin University Institutional Ethics Committee for Animal Studies with document number 26.12.2007/13 and was funded by the Mersin University Scientific Research Projects unit. In this study, 90 Wistar rats were equally divided into nine groups as follows: (C; control, C24; control sacrificed 24 hours after first anesthesia, C48; control sacrificed 48 hours after first anesthesia, TT24; thoracic trauma and sacrificed 24 hours after trauma, TT48; thoracic trauma and sacrificed 48 hours after trauma, HT24; head trauma and sacrificed 24 hours after trauma, HT48; head trauma and sacrificed 48 hours after trauma, HTT24; thoracic and head trauma and sacrificed 24 hours after trauma, HTT48; thoracic and head trauma and sacrificed 48 hours after trauma. For twenty-four hours prior to trauma, the animals were given standard rat chow as well as water containing 80,000 cfu/mL E.coli. In all of the groups, anesthesia was given as 25 mg/kg-1 thiopental sodium (Pental Sodyum, İ.E. Ulugay, Turkey) before trauma. Only the control group (Group C) received anesthesia without any trauma. The thoracic trauma groups (Group TT) were exposed to thoracic trauma using the mechanism published by Raghavendran et al. with a force of 2.7 J followed by anesthesia.[4] In the head trauma groups (Group HT), severe head trauma was created according to the method described by Foda et al.[11] Sequential thoracic and head traumas were created in the same manner as 492

mentioned above in the groups receiving thoracic and head traumas (Group HTT). Twenty four or 48 hours after the trauma, the rats were anesthetized and the chest cavities were opened. The animals were euthanized by cardiac blood aspiration. Following sacrifice at 24 and 48 hours, multiple specimens were taken from the rats’ mesenteric lymph nodes, spleen, liver, lungs and ileum, and blood samples were collected and evaluated for bacterial growth in corresponding 5% blood agar. In the blood, interleukin - 1 beta (IL-1β), interleukin-10 (IL-10), interleukin-4 (IL-4), tumor necrosis factor alpha (TNF α), and monocyte chemoattractant protein-1 (MCP-1) were evaluated, while apoptosis was assessed in the lung. In the first 30 minutes after trauma, we noted a reduction in the rats’ movements and food intake. After two hours, the rats regained normal movements. The food and liquid consumption of the rats that underwent trauma was 50% less than that of the control groups.

Evaluation of the Bacterial Translocation Blood samples (1 mL each) were incubated aerobically for 48 hours at 37oC in 5 mL of triptych soy broth and plated on triptych soy agar with 5% blood plates. Liver, spleen, mesenteric lymph nodes and lung were extracted, weighed separately, and placed in sterile grinding tubes. The samples were homogenized with 1 ml of triptych soy broth using sterile ground glass stoppers. After grinding (Pottere S, Biolab, Melcungen-Germany), 500 μL of homogenate was transferred into a tube containing 4.5 mL of 0.9% NaCl and was used to perform four serial dilutions. The final dilution was 10-4. From this dilution, 100-μL aliquots were plated onto tyriptic soy agar plates with 5% blood and EMB agar plates. Quantitative culture results were determined with the following formula [(number of colony-forming units (CFU) x reciprocal of dilution x 10)/ weight of tissue].[12] Finally, the terminal ileal loop was excised and placed in a tube of thioglycollate broth to determine indigenous bacteria. To prevent contamination of the environment, these cultures were prepared as indicated in the previous procedure. All agar plates and thioglycollate broth tubes were incubated aerobically in 5% CO2 for 24 hours at 37 °C. We did not study obligate anaerobes, because these organisms are rare causes of translocation.[13] The gram negative enteric organisms were identified by biochemical profiles, staphylococcus was identified by the catalase test and the tube coagulase test, and Enterococcus was identified by esculin hydrolysis in the presence of bile and was grown in broth containing 6.5% NaCl.

Histopathological Evaluation Tissue samples were taken from the most traumatized part of the left lung, immersed in 10% buffered formalin and embedded in paraffin using a standard procedure. Serial sections from paraffin-embedded tissues were deparaffinized in xyUlus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Ayan et al., The role of thoracic trauma in inflammatory responses, apoptosis and bacterial translocation following multiple traumas

lene, dehydrated through graded concentrations of ethanol, and evaluated following haematoxylin and eosin staining. Microscopic evaluations were performed by a single pathologist who was unaware of the characteristics or treatment of the animals.

TUNNEL (Terminal Deoxynucleotidyl Transferase Mediated dUTP Nick-End Labeling) Method The TUNNEL method (in situ Apoptosis Detection Kit, Biogen, USA) was used to investigate apoptosis in lung tissue. After being deparaffinized and rehydrated, sections were pretreated with proteinase K for 15 minutes at room temperature, and then endogenous peroxidase activity was quenched with 2% H2O2. Slices were then incubated at 37 °C for 60 min with 50 μl of TdT buffer. Finally, the reaction was visualized colorimetrically with a streptavidin-biotin- peroxidase complex and diaminobenzidine. TUNNEL labeled slides were counterstained with 1% methyl green.

Morphological Analysis Light microscopic analyses of hematoxylin and eosin stained slides of lung specimens were evaluated with regards to pulmonary architecture, tissue edema formation, polymorphonuclear leukocyte infiltration and alveolar hemorrhage using a modified method by Koksel et al.[14] Lung injury was scored 0 to 3 as follows: 0 = normal histology; 1 = a few inflammatory cells in alveolar spaces; 2 = perivascular mild edema formation, moderate inflammatory cell infiltration, focal hemorrhage and partial destruction of pulmonary architecture, 3 = severe edema and dense inflammatory cell infiltration, marked hemorrhage and complete destruction of pulmonary architecture.

antibody on a second site. After removal of excess secondary antibody, Streptavidin-Peroxidase is added, which binds to the biotinylated antibody to complete the four member sandwich. After a second incubation and washing to remove the unbound enzyme, a substrate solution is added, which reacts with the bound enzyme to produce color. The intensity of this colored product is read at 450 nm, and the intensity of the color is directly proportional to the concentration of sample present in the original specimen (as compared to a standard).

Statistical Analyses A one-sample Kolmogorov-Smirnov test was used to determine whether serum cytokine levels were normally distributed. All of the variables were normally distributed. A one-way ANOVA was used to detect variations in variables among the groups. Tukey Post Hoc Tests were used for pair wise comparisons. The relationships between categorical variables were determined by chi-square analyses using the SPSS 11.5 software program. Correlation coefficients were determined with Microsoft Excel.

RESULTS Survival and Gross Morphology of Lung Contusion Injury Marked hemorrhage and pulmonary contusion were observed ventrally and dorsally in both lungs in all of the rats exposed to thoracic trauma (Figure 1). Within the first 30 minutes following trauma, 3 rats in the head trauma (HT) group and 4 rats in the thoracic trauma (TT) group died and

To numerically evaluate the density of apoptotic cells in the lung sections, the total number of dark brown stained (TUNNEL positive) nuclei (alveolar epithelium and endothelial) were counted in 10 randomly selected high power fields (10x400) with light microscopy.

Biochemical Evaluation MCP-1, TNF-α, IL-1β, IL-4 and IL-10 levels were detected using BioSource Immunoassay kits (Rat MCP-1 catalog no:KRC1012, Rat TNF-α catalog no: KRC3011, Rat IL-1β catalog no:KRC0011, Rat IL-4 catalog no:KRC0042, Rat IL-10 catalog no:KRC0101; Biosource International, Camarillo, CA). The BioSource kit is a solid phase sandwich Enzyme LinkedImmuno-Sorbent Assay (ELISA). A specific antibody coats the wells of the provided microtiter strips. Samples, standards, and control specimens are pipetted into these wells, followed by the addition of a biotinylated secondary antibody. During the first incubation, the specific antigen (MCP-1, TNF-α, IL-1β, IL-4, IL-10) binds simultaneously to the immobilized antibody on one site, and to the solution phase biotinylated Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

Figure 1. Macroscopic appearance. The bilateral upper lobes present significant contusion.

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were excluded from the study. Rats were added to both of these groups to replace those that died and corresponding traumas were repeated. Of the three rats that died in the HT group, 2 had epistaxis, while the other had no marked macroscopic signs. An evaluation of the 4 rats that died in the TT group showed that 3 of them had massive hemothorax while other rat was observed to have cardiac tamponade.

HT groups (p=0.000). No significant difference was found between the C and HT groups. IL-10 values in the HTT group at 48 hours were significantly higher than those in the TT group at that time point (p<0.05). There was a significant increase in the values of the HTT group at 48 hours relative to the values at 24 hours. This difference was not significant in any of the other groups.

Serious dyspnea developed in all of the groups that were subjected to trauma, and the rats remained motionless for an hour following the trauma. Dyspnea regressed after the first six hours, while motor movements remained mostly unchanged. At 12 hours, the rats were motile in their cages, and at 24 hours they showed a marked increase in motility and a decrease in dyspnea. No treatment or oxygen support was given to the rats during this observation process. All of the rats that were exposed to thoracic trauma had macroscopic contusion.

Interleukin-4

Serum Cytokine Levels Biochemical data pertinent to all groups are presented in Table 1.

Interleukin-1ß At 24 and 48 hours after the trauma, IL-1β was significantly higher in all of the trauma groups than in the control group (p=0.000). There were no significant differences between the trauma groups. At 48 hours, values in the head and thoracic trauma (HTT) group were significantly higher than those in the HT and TT groups. When values in the trauma groups at 24 and 48 hours were compared with one another, only the HTT group showed an increase in the values at 48 hours, relative to those at 24 hours (p<0.05); there was no significant difference in the values of the other groups.

Interleukin-10 Values of IL-10 in the TT and HTT groups at 24 and 48 hours after trauma were significantly higher than those of the C and

IL-4 values in the HT and HTT groups at 24 hours following trauma were higher than those in the C group (p=0.000). The IL-4 values of the TT group were not significantly different from those of the C group. IL-4 values in the TT and HTT groups at 48 hours were significantly higher than those of the C group. IL-4 values in the HTT group were significantly higher than those in the HT group (p<0.01). There was no significant difference between the HT and C groups at 48 hours.

TNF-α Although TNF-α levels in the TT and HTT groups were higher than those of the C group at 24 hours (p=0.000), this difference was not significant. TNF-α values in the TT and HTT groups at 24 hours were significantly higher than those of the HT group at 24 hours. The TNF-α levels of all of the trauma groups were significantly higher at 48 hours relative to the control values (p=0.000-0.003), although there were no differences between the trauma groups.

MCP-1 MCP-1 was significantly higher in all of the trauma groups in comparison to the C group at 24 and 48 hours (p=0.000), although there were no differences in these values between the trauma groups.

Bacterial Translocation (BT) Any bacterial growth in the solid organs (i.e., liver, spleen,

Table 1. Serum cytokine levels of all groups Groups IL-1β Statistical IL-4 Statistical IL-10 Statistical TNF-α Statistical MCP-1 Statistical (pg/ml) Significance (pg/ml) Significance (pg/ml) Significance (pg/ml) Significance (pg/ml) Significance C-0 108.59±5.06 22.47±4.50 26.15±2.89 59.35±7.70 192.31±25.08 C - 24 105.78±5.26 * 23.45±5.17 * 21.32±4.01 * 50.97±5.04 * 203.58±27.02 * HT - 24 170.88±27.39 *p<0.001 31.80±7.09 *p<0.01 16.43±3.37 n.s. 96.45±14.80 *p<0.001 283.08±46.60 *p<0.001 TT - 24 192.94±50.36 *p<0.001 28.18±2.20 n.s. 33.76±6.81 *p<0.001 249.48±37.25 *p<0.001 293.32±18.38 *p<0.001 HTT - 24 189.33±28.84 *p<0.001 33.70±5.44 *p<0.001 37.39±8.05 *p<0.001 237.61±62.18 *p<0.001 289.16±17.16 *p<0.001 C - 48 114.78±8.05 ** 22.47±4.50 ** 26.15±2.89 ** 59.35±7.70 ** 192.31±25.08 ** HT - 48 171.45±32.94 **p<0.001 31.11±5.82 **p<0.01 26.67±4.95 n.s. 213.54±68.03 **p<0.05 307.90±41.45 **p<0.001 TT - 48 182.18±29.65 **p<0.001 35.76±5.79 n.s. 42.38±6.58 **p<0.001 231.66±5.79 **p<0.001 293.76±28.18 **p<0.001 HTT - 48 239.03±48.10 **p<0.001 39.82±6.09 **p<0.001 50.59±7.14 **p<0.001 237.20±77.04 **p<0.001 312.16±27.17 **p<0.001 (C-0: Control Group time 0, C-24: Control Group 24th hour, C-48: Control Group 48th hour, HT-24: Head Trauma Group 24th hour, HT-48: Head Trauma Group 48th hour, TT-24: Thoracic Trauma Group 24th hour, TT-48: Thoracic Trauma Group 48th hour, HTT-24: Head and Thoracic Trauma Group 24th hour, HTT-48: Head and Thoracic Trauma 48th hour.) Cytokine levels were compared using a pair-wise comparison. For each cytokine, the results of the 24th hour trauma group were compared with the result of C - 24. Similarly, for each cytokine, the results of the 48th hour trauma group were compared with the result of C - 48. Statistical significance levels (p values) are given in the column next to each cytokine. (n.s.: not statistically significant according to pair-wise comparison).

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80.0

Percent (%)

60.0

40.0

20.0

0.0

C 0

C2 4

C4 8

HT2 4

TT2 HTT2 HT4 4 4 8 Group

TT4 HTT4 8 8

Figure 2. Bacterial growth in solid organs. (C-0: Control Group time

Figure 3. Light microscopy of lung tissue (HEx100). (a) Normal lung parenchyma in the control group. (b) Diffuse inflammatory cell infiltration (double arrows) and alveolar hemorrhage (arrows) are seen in lung parenchyma in the HTT group.

0, C-24: Control Group 24th hour, C-48: Control Group 48th hour, HT-24: Head Trauma Group 24th hour, HT-48: Head Trauma Group 48th hour, TT24: Thoracic Trauma Group 24th hour, TT-48: Thoracic Trauma Group 48th

higher than that of the C and HT groups, this difference was not statistically significant.

hour, HTT-24: Head and Thoracic Trauma Group 24th hour, HTT-48: Head and Thoracic Trauma 48th hour.) The incidence of bacterial translocation in the 24th HTT group was significantly higher than that of all other groups (p<0.05). Although the rate of bacterial translocation in the 24th TT group was higher than that of the C and HT groups, this difference was not statistically significant.

lymph nodes) without any growth in the lungs was accepted as a positive sign of BT. BT was found in 7 rats in the 24th hour HTT group (70%), in 4 rats of the 24th hour TT group (40%) and in 2 rats in each the 24th hour C and 24th hour HT groups (17% each). All of the blood cultures remained sterile. No significant difference was found in the cultures of the control group and trauma groups at 48 hours (Figure 2). The isolated bacteria were E. coli (90%), Enterococci (7%) and Staphylococci (3%). As the indigenous flora of the intestines includes enterococci and staphylococci as well as E. coli, their growth in harvested tissue cultures was accepted as a sign of BT as well. The incidence of BT in the 24th hour HTT group was significantly higher than that of all other groups (p<0.05). Although the rate of bacterial translocation in 24th hour TT group was

Light Microscopy Light microscopic evaluation of hematoxylin and eosin stained slides revealed almost normal morphology in the C group. In contrast, the HT group had mild to moderate lung injury at both 24 and 48 hours. In the TT and HTT groups, moderate to severe injury was recorded at both 24 and 48 hours (Figure 3a, b). The light microscopy score of the HTT group was significantly different than those of the C and HT groups at 24 and 48 hours (p<0.05). The other groups were not significantly different (Table 2).

Apoptosis (TUNNEL) The number of TUNNEL positive stained nuclei in the lung tissue for each group is presented in Figure 4. The control group had only a few TUNNEL positive stained nuclei (alveolar epithelial, endothelial). The number of TUNNEL positive stained nuclei was increased in the TT, HT, and HTT groups at 24 and 48 hours (Figure 5a, b). There was a significantly higher number of TUNNEL stained nuclei in the HTT group than in the C group 24 hours follow-

Table 2. Correlations of the serum cytokine levels, bacterial growth and apoptosis

Control groups (n)

Injury level 0th hour 24th hour 48th hour

TT groups (n)

HT groups (n)

24th hour 48th hour

24th hour 48th hour

HTT groups (n) 24th hour

Severe 0 0 0 4 6 0 0 Moderate 0 0 0 3 3 5 0 Minimaly 0 0 0 3 1 3 5 No injury 10 10 10 0 0 2 5 Total 10 10 10 10 10 10 10

Total (n)

48th hour

5 9 24 4 1 16 1 0 13 0 0 37 10 10 90

C: Control; HT: Head trauma; TT: Thoracic trauma; HTT: Head and thoracic trauma.

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80

+

95% CI TUNEL 24 and TUNNEL 48

70

Table 3. Correlations of the serum cytokine levels, bacterial growth and apoptosis

60

*

50

b

40 30 20 10

+b

* 0 -10

HTT-48

HT-48

TT-48

C-48

HTT-24

HT-24

TT-24

C-24

-20

Groups

Figure 4. Lung tissue apoptotic cell numbers. Error bars represent 95% confidence intervals of the means (95% CI). In the HTT-24 group, lung tissue apoptotic cell numbers were elevated when compared with the C-24 group (*p<0.05). In the HTT-48 group, lung tissue apoptotic cell numbers were elevated when compared with the C-48 group (+p<0.001). In the TT-48 group, lung tissue apoptotic cell numbers were elevated when compared with the C-48 group (β p<0.01). (C-24: Control Group 24th hour, C-48: Control Group 48th hour, HT-24: Head Trauma Group 24th hour, HT-48: Head Trauma Group 48th hour, TT-24: Thoracic Trauma Group 24hth hour, TT48: Thoracic Trauma Group 48th hour, HTT-24: Head and Thoracic Trauma Group 24th hour, HTT-48: Head and Thoracic Trauma 48th hour.)

Parameters

R

Statistical significance

MCP-1 IL-1β 0.924 MCP-1 IL-4 0.924 IL-1β IL-4 0.923 IL-4 Tunnel 0.914 MCP-1 TNF-α 0.889 IL-1β TNF-α 0.878 IL-1β Tunnel 0.863 IL-10 Tunnel 0.836 IL-4 TNF-α 0.781 IL-10 TNF-α 0.749 IL-1β IL-10 0.730 IL-4 IL-10 0.714 TNF-α Tunnel 0.691 MCP-1 Tunnel 0.687 TNF-α Growth 0.592 Growth Tunnel 0.533 MCP-1 IL-10 0.529 IL-1β Growth 0.511 IL-10 Growth 0.459 MCP-1 Growth 0.401 IL-4 Growth 0.363

p<0.001 p<0.001 p<0.001 p<0.001 p<0.001 p<0.001 p<0.01 p<0.01 p<0.01 p<0.05 p<0.05 p<0.05 p<0.05 p<0.05 n.s. n.s. n.s. n.s. n.s. n.s. n.s.

R: Correlation coefficient; n.s.: Not statistically significant; MCP-I: Monocyte chemoattractant protein-1; IL-1β: Interleukin-1; IL-4: Interleukin-4; IL10: Interleukin-10; TNF-α: Tumor necrosis factor alpha.

between IL-1β and MCP-1, IL-1β and IL-4, IL-1β and TNF-α, IL-4 and MCP-1, IL-4 and TUNNEL, and TNF-α and MCP-1 (p<0.001). Significant correlations were observed between IL-4 and TNF-α, IL-1β and TUNNEL, and IL-10 and TUNNEL (p<0.01). The correlations between IL-10 and IL-1β, IL-10 and TNF-α, IL-10 and IL-4, TNF-α and TUNNEL, and MCP-1 and TUNNEL were also significant, but not as significant as the aforementioned correlations (p<0.05).

DISCUSSION

Figure 5. TUNNEL staining of lung tissue (X200). (a) Very rare TUNNEL positive cells in the control group. (b) Widespread TUNNEL positive alveolar epithelium and stromal cells (arrows) are seen in the HTT group.

ing trauma (p<0.05). The TT and HTT groups were significantly higher than the C and HT groups at 48 hours (p<0.05). (Figure 5a, b).

Correlations Correlations were calculated between inflammatory responses and bacterial translocation, and these results are presented in Table 3. There were highly significant correlations 496

Two-thirds of the patients who die of complications that develop following a major trauma have single or multiple organ failure, of which the most commonly encountered is pulmonary dysfunction.[1,3,15] Previous studies have reported that the first organ to fail after trauma is the respiratory system, which serves as a pacemaker in the development of MOF.[1] It has been noted in a clinical study that if patients with head trauma also had lung injury, a significant increase was seen in their morbidity, length of hospital stay and mortality.[16] Recent studies have focused on systemic inflammatory processes, immunologic mechanisms, controlling inflammatory responses and improving immunomodulator procedures that reinforce the body’s defense. Our objective in this study is to contribute to research on systemic inflammatory responses that arise in traumas, histopathologic changes that occur in pulmonary tissue, apoptosis and bacterial translocation, and the correlations between these processes. In general, our results showed that IL-1ß and MCP-1 increased significantly Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Ayan et al., The role of thoracic trauma in inflammatory responses, apoptosis and bacterial translocation following multiple traumas

in all trauma groups (HTT, TT and HT groups) in comparison to the control group. Additionally, IL-10, IL-4 and TNF-α were significantly elevated in all HTT groups. IL-10, IL-4 and TNF-α levels were higher in some HT groups and lower in TT groups at different time points, while they were higher in TT groups and lower in HT groups at other times. However, in general, the values in the HT and TT groups were significantly higher than those of the C group. Since IL-10 was significantly higher in the TT and HTT groups at both 24 and 48 hours and since there was not any significant difference in IL-10 between these groups, we can hypothesize that there is a correlation between thoracic trauma and IL-10 levels. Similarly, since there was a significant difference in TNF-α levels in the TT and HTT groups and the HT group, we hypothesize that there is a correlation between thoracic trauma and TNF-α. There were significant correlations between all of the measured cytokine levels; in particular, the correlations between MCP-1 and IL-1ß with other cytokines were the strongest. The correlations of MCP-1 with other cytokines were also significant, but the correlation coefficients were lower. TNF-α was correlated with all cytokines, but levels of significance were variable. TUNNEL is an indication of apoptosis that was significantly correlated with cytokines. On the other hand, bacterial growth, which is an indicator of bacterial translocation, was not significantly correlated with cytokine levels and TUNNEL results. Experimental models of blunt thoracic trauma have shown that a severe inflammatory response develops during the first 24-48 hours, but normal levels are restored at 72 hours. This data suggests that additional processes should be investigated in order to clarify lung injury and causes of morbidity. [3-5] These studies also reported that TNF-α and IL-1ß were primary mediators in the activation of other cytokines, and ensured prostaglandin release, synthesis of pro-coagulant factors and activation of leukocyte chemotaxis with adhesion molecules like ICAM and E-selectin. Accumulation of neutrophils increases the production and release of vasoactive substances (leukotrienes, eicosanoids, platelet-activating factor) and proteolytic enzymes (elastase, cathepsin G). All of these substances have been reported to cause injury to the endothelial layer and neighboring tissues.[16] Previous studies have reported a correlation between TNF-α and apoptosis. Furthermore, in the early post-traumatic period, TNF-α, IL1ß and MCP-1 values showed an increase parallel to the increase in local and systemic neutrophil accumulation, and that the former peaked especially in the first 24 hours.[17-19] Sato et al.[17] reported that there were significantly lower TNF-α and IL-1ß levels in a trauma group treated with a potent inhibitor of TNF-α and IL-1ß production, FR167653, relative to the untreated trauma group. The correlation between these values and blood gas values may indicate that TNF-α and IL-1ß play a role in post-traumatic acute lung injury. In the current study, we found that although IL-1ß and MCP-1 values increased in all trauma groups at 24 and 48 hours, IL-1ß values in the HTT Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

group at 48 hours were significantly higher than those in the HT and TT groups. We established that TNF-α values in the HTT and TT groups at 24 and 48 hours were significantly higher than those of the control group. However, the 24 hour TNF-α values in the HT group were the same as those of the C group, which peaked at 48 hours. Even though our results are consistent with those of the literature, the significantly higher levels of IL-1ß in the HTT group relative to the other trauma groups may be interpreted in relation with the cumulative effect of multiple traumas. Many studies have been conducted regarding the relationship between trauma and IL-10, but the results differ widely, especially in evaluations of the lung.[20] Turina et al.[15] stressed that IL-10 levels in BALF increased in the early post-traumatic period of patients with severe trauma, and that this increase resulted in alveolar neutrophil apoptosis. It has also been reported that anti-IL-10 treatment reduced apoptosis in patients with post-traumatic pulmonary dysfunction.[15] On the contrary, Raghavedran et al.[3] showed in their experimental thoracic trauma model that levels of IL-10 in BALF did not significantly increase. Murphy et al.[21] on the other hand, reported a significant increase in IL-10 levels in the blood of trauma patients. Previous in vitro studies reported that there might be differences in the cytokine production of immune system cells stimulated by nitrogen. Likewise, conservative mutations in the areas where cytokines are coded, as well as nucleotide changes in the regulatory area might cause the differences in cytokine production. These genetic polymorphisms have been shown to affect cytokine release in both in vivo and in vitro media.[22,23] Contradictory results have been obtained in similar trauma groups, and therefore, results of further studies aiming to clarify the relationships and correlations between thoracic trauma, multiple trauma and IL-10 will be important.[24] In the present study, we found that serum IL-10 values in the HTT and TT groups were significantly higher than those in the C and HT groups at 24 and 48 hours. However, there was no significant increase in the HT group relative to the C group. In addition, the development of apoptosis, which has been reported to peak at 48 hours, was significantly higher in the HTT and TT groups at 48 hours than in the C and HT groups. Our current results indicate that there is a direct relationship between IL-10 increase, apoptosis and acute lung injury. Clinical and experimental studies have shown that apoptosis develops within 48 hours following trauma. Post-traumatic systemic inflammatory responses and toxic metabolites released from the neutrophils due to increased neutrophil accumulation is the first step of apoptosis formation.[5,15] Ward et al.[25] reported that IL-10 inhibited the activation of the extracellular signal-related kinase (ERK) pathway in purified human neutrophils, and that the inhibition of ERK eliminated the inhibitor effect on Caspase 8, thereby enabling more apoptosis, which was influenced by PMN. In our study, we established that significantly more apoptosis developed in the HTT and TT groups than in the HT and C groups at 48 hours. 497


Ayan et al., The role of thoracic trauma in inflammatory responses, apoptosis and bacterial translocation following multiple traumas

It has been reported that the respiratory system (28%) was among the leading infection foci in patients with multiple traumas, and that the most commonly reproduced microorganisms were bacteria of the gastrointestinal flora like S. aureus (19-20%), E. coli (18%), Pseudomonas (10%) and Enterococci (9%).[2,26] In our study, we determined that the reproduced bacteria were E. coli (90%), Enterococci (7%) and Staphylococci (3%). The major cause of the death of patients undergoing multiple traumas has been shown to be MOF, the pathogenesis of which sepsis and pulmonary dysfunction are the most commonly blamed factors. Previous studies have shown that bacterial translocation developed in patients who had abdominal trauma, hemorrhage and burn.[7-9] In one of our previous studies, we reported the development of bacterial translocation in multiple traumas, including thoracic trauma.[27] In the same study, our results indicated that bacterial translocation developed in some cases of isolated thoracic trauma, although it was not statistically significant. In the present study, we found that bacterial translocation did not occur in the HT group, was extremely high in the TT group, but was only significantly higher in the HTT group, relative to other groups. In consideration of the quantitative measure of bacterial translocation in the TT group, we believe that thoracic trauma may significantly affect the development of bacterial translocation. In our examination of the literature, we found that research generally included patients with severe multiple traumas, and that the number of studies aimed at patients with isolated thoracic trauma was insufficient. As a result of our study, we found that multiple and/or thoracic trauma can trigger inflammatory and anti-inflammatory cascades. Based on our results, we believe that inflammatory mediators stemming from the lungs are the major cause of these triggers. In conclusion, thoracic trauma plays a major role in critical inflammation, bacterial translocation and tissue damage following multiple traumas. Conflict of interest: None declared.

REFERENCES 1. Laudi S, Donaubauer B, Busch T, Kerner T, Bercker S, Bail H, et al. Low incidence of multiple organ failure after major trauma. Injury 2007;38:1052-8. 2. Lazarus HM, Fox J, Burke JP, Lloyd JF, Snow GL, Mehta RR, et al. Trauma patient hospital-associated infections: risks and outcomes. J Trauma 2005;59:188-94. 3. Raghavendran K, Davidson BA, Woytash JA, Helinski JD, Marschke CJ, Manderscheid PA, et al. The evolution of isolated bilateral lung contusion from blunt chest trauma in rats: cellular and cytokine responses. Shock 2005;24:132-8. 4. Raghavendran K, Davidson BA, Helinski JD, Marschke CJ, Manderscheid P, Woytash JA, et al. A rat model for isolated bilateral lung contusion from blunt chest trauma. Anesth Analg 2005;101:1482-9. 5. Liener UC, Knöferl MW, Sträter J, Barth TF, Pauser EM, Nüssler

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DENEYSEL ÇALIŞMA - ÖZET OLGU SUNUMU

Multipl travmayı takiben enflamatuvar yanıt, apopitozis ve bakteriyel translokasyonda torasik travmanın rolü Dr. Erhan Ayan,1 Dr. Oğuz Köksel,1 Dr. Ayşe Polat,2 Dr. Lülüfer Tamer,3 Dr. Gülden Ersöz,4 Dr. Murat Demir,1 Dr. Hatice Yıldırım Yaroğlu,3 Dr. Alper Akdağ,4 Dr. Ali Özdülger,1 Dr. Sema Erden5 Mersin Üniversitesi Tıp Fakültesi Araştırma ve Uygulama Hastanesi, Göğüs Cerrahisi Anabilim Dalı, Mersin Mersin Üniversitesi Tıp Fakültesi Araştırma ve Uygulama Hastanesi, Patoloji Anabilim Dalı, Mersin 3 Mersin Üniversitesi Tıp Fakültesi Araştırma ve Uygulama Hastanesi, Biokimya Anabilim Dalı, Mersin 4 Mersin Üniversitesi Tıp Fakültesi Araştırma ve Uygulama Hastanesi, Engeksiyon Hastalıkları Anabilim Dalı, Mersin 5 Sağlık Meslek Lisesi, Biyoistatistik, Mersin 1 2

AMAÇ: Künt göğüs travması ve komplikasyonları acil servislerde karşılaşılan en yaygın klinik problemlerden biridir. Postkontüzyon pnömoninin patogenezi, akut akciğer hasarı, akut solunum yetersizliği sendromu ve diğer etkili faktörler ile enflamatuvar yanıt arasındaki ilişkisi konusunda araştırmalara ihtiyaç duyulmaktadır. Bu çalışmamızda çoklu travma modelinde enflamasyon, apopitozis ve bakteriyel translokasyonun gelişimini araştırdık. GEREÇ VE YÖNTEM: Doksan adet Wistar cinsi sıçanı dokuz gruba ayırdık; 24 ve 48. saat torasik travma (TT), 24 ve 48. saat kafa travması (HT), 24 ve 48. saat kafa ve toraks travması (HTT), 0.24 ve 48 saat kontrol grupları. Sıçanlara standart künt toraks ve/veya kafa travması uygulandı ve travma sonrası 24. ve 48. saatte sakrifiye edildi. Farklı organlardan alınan çoklu örnekler ve kan örnekleri toplandı ve aerobik organizmalar için kantitatif kültür yapıldı. Serumda interlökinler, MCP-1 seviyeleri ve akciğerde apopitozis değerlendirildi. BULGULAR: Kontrol grubu ile karşılaştırıldığında tüm travma gruplarında interlökin, TNF-α, MCP-1 sevileri anlamlı olarak yüksekti (p=0.001). Kontrol grubu ile karşılaştırıldığında HTT grubunda apopitotik hücreler anlamlı olarak fazlaydı (p=0.009). Tüm grupların ışık mikroskopik değerlendirmesinde kontrol grubuna göre HTT grubunda belirgin artış vardı. Bakteriyel translokasyon HTT grubunda anlamlı biçimde yüksekti (p=0.003). TARTIŞMA: Künt toraks travmasının olduğu çoklu travmalarda çok sayıda enflamauvar mediatör artmakta ve bakteriyel translokasyon ve apopitotik proçesi etkilemektedirler. Travma ile ilişkili enflamasyon ve enfeksiyonlar arasındaki ilişkinin anlaşılmasının komplike hastaları tedavi yaklaşımlarında etkili olacağına inanıyoruz. Anahtar sözcükler: Apopitozis; bakteriyel translokasyon; göğüs travması; interlökin; sistemik enflamatuvar yanıt sendromu; çoklu travma. Ulus Travma Acil Cerr Derg 2013;19(6):491-499

doi: 10.5505/tjtes.2013.29660

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EXPERIMENTAL STUDY

Hypertonic saline, normal saline or neither: which is best for uncontrolled hemorrhagic shock? An experimental study in goats Morteza Saeedi, M.D.,1 Houman HajiseyedJavadi, M.D.,2 Samad Shams Vahdati, M.D.,2 Vahid Eslami, M.D.,1 Mohamad Mokhtarpour, M.D.,3 Mehdi Momeni, M.D.,1 Mohammad Reza Farnia, M.D.,1 Nima Hafezi Nejad, M.D.1 1

Department of Emergency Medicine, Tehran University of Medical Sciences, Tehran, Iran

2

Department of Emergency Medicine, Tabriz University of Medical Sciences, Tabriz, Iran

3

Department of Emergency Medicine, Aja University of Medical Sciences, Tehran, Iran

ABSTRACT BACKGROUND: To evaluate the effects of various fluids on uncontrolled hemorrhagic shock (UHS). Controversy exists over the appropriate doses and types of fluids for best treating UHS. This study evaluated the effects of hypertonic saline (HTS), normal saline (NS), and no fluid resuscitation (NFR) on UHS. METHODS: Thirty goats were anesthetized and underwent right leg ablation. The animals were randomly assigned to equal NFR, HTS, and NS groups. The following features of UHS were analyzed: hemoglobin, heart rate, blood loss, mean arterial pressure, bleeding time, and pH. Animals were sacrificed two hours after ablation. RESULTS: All of the goats who received HTS died within 60 minutes. Four goats in the NS group and one goat in the NFR group died within 120 minutes. The NFR group had significantly higher hemoglobin values than the NS and HTS groups at the end of the trial. Blood loss in the HTS group was greater than in the other two groups (p<0.05). The NS group had higher blood loss than the NFR group (p<0.05). Mean arterial pressure in the HTS group decreased sharply toward zero within the first 60 minutes. In the NFR and NS groups, mean arterial pressure was higher than in the HTS group (p<0.05), and remained constant at 60mmHg after 35 minutes. The NFR group had higher pH values compared to the other two groups (p<0.05). CONCLUSION: Our study demonstrated that HTS is not suitable for treating UHS when compared to NFR and NS. Goats treated with NFR had superior values for all UHS features, including hemoglobin, pH, blood pressure, and bleeding time, compared to those treated with HTS and NS. Pre-hospital field treatment with NS or HTS may worsen the condition until surgical repair is accomplished. Key words: Fluid; goat; hypertonic saline; resuscitation; uncontrolled hemorrhagic shock.

INTRODUCTION The rate of death from injury, for which hemorrhagic shock is a major contributing factor, is estimated to reach more than 8 million per year globally by 2020.[1,2] Fluid therapy is Address for correspondence: Morteza Saeedi, M.D. Tehran University of Medical Sciences, North Amirabad Street Tehran, Iran Tel: 00982144263995 E-mail: m_saeedi@tums.ac.ir Qucik Response Code

Ulus Travma Acil Cerr Derg 2013;19(6):500-506 doi: 10.5505/tjtes.2013.31799 Copyright 2013 TJTES

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a commonly accepted treatment for resuscitating trauma patients. However, controversy exists over the choice of fluid therapy, (such as colloids or crystalloids) to manage uncontrolled hemorrhagic shock (UHS) in a pre-hospital setting. [3] Although fluid resuscitation is often the main treatment for UHS, the benefits are doubtful, as demonstrated in both animal and human studies.[4,5] The rationale for upholding blood pressure in trauma patients is to maintain tissue oxygenation; however, more bleeding may result due to impairing the coagulation process.[6] Excessive fluid administration may cause brain edema, abdominal compartment syndrome, and acute respiratory distress syndrome.[7] Studies have shown that hypertonic saline (HTS) is useful for treating UHS patients.[8,9] Moreover, HTS is thought to decrease lung tissue damage and pulmonary inflammation, Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Saeedi et al., Hypertonic saline, normal saline or neither

and increase cellular protection in animal models of UHS.[10,11] Studies of rats, dogs, swine, and pigs showed the relative efficacy of HTS fluid compared to normal saline (NS) for treating UHS.[12-17] Studies in the literature have proven the benefits of HTS in cases of brain and cord trauma.[18-20] Modeling UHS in animals can lead us to a definite decision on the optimal fluid therapy for UHS in humans. Therefore, studies demonstrating the benefits of using hypertonic fluid in cases of human UHS[21,22] led us to design a goat study to compare hypertonic and isotonic fluid, as well as no fluid treatment, in a clinically relevant model.

MATERIALS AND METHODS a. Animal Care Committee Approval The study was approved by the Animal Care Committee of Tabriz University of Medical Sciences and reviewed by a group other than the authors according to procedures approved by the Report Review Committee.

b. Study Design The study was a randomized trial conducted in a goat model. The model was based on a pre-hospital setting in which there is no access to packed red blood cells or other resuscitation options except fluids. After the insertion of a 20G venous cannula in the vein of the goat’s right ear, blood was obtained for primary and homogeneity comparison. All goats were anesthetized completely before the intervention with 5 mg/kg intravenous ketamine and 0.2 mg/kg diazepam, which was repeatedly administered every 10 minutes, as necessary. Following anesthesia, tracheostomy was performed on the goats.[23] Ventilators designed for humans were used. Ventilator settings were as follows: respiratory rate, 8; FiO2, 50%; positive end-expiratory pressure, 3; and tidal volume, 15 cc/kg. The goats were monitored intensively using heart rate and invasive continuous blood pressure monitoring.[24]

c. Materials The administered fluids included 20 cc/kg of normal saline (NS)[25] for the NS group, and 8 cc/kg of 3% saline for the HTS group.

d. Uncontrolled Hemorrhagic Shock Model Thirty healthy male Mako goats with a mean weight of 28 kg (range: 15-40 kg) were included in the study. To decrease the incidence of regurgitation, goats underwent 12-hour preoperative fasting (except for water) before surgery.[24] After weighing the goats and obtaining the blood samples, ketamine and diazepam were administered. The goats underwent tracheostomy, and ventilation was performed using portable ventilators. Goats were randomly chosen to receive a specific resuscitation fluid. The 30 goats were assigned into three Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

groups (10 in each group). The first group had no fluid resuscitation (NFR); the second group received NS; and the third group received HTS resuscitation. After the insertion of an arterial line in the left carotid artery, mean arterial pressure was monitored continuously. Heart rate was monitored by ECG monitoring and recorded every five minutes. The right leg was ablated beneath the knee, so it caused bleeding from arteries, veins, muscles, and skin. No attempt was undertaken to mitigate the bleeding in order to simulate a real pre-hospital setting. Blood was collected and measured in a graded suction bottle. Blood samples were obtained from the arterial line every 15 minutes to measure hemoglobin and pH. Goats have a blood volume of approximately 70 to 72 ml/kg blood.[26] To simulate the UHS setting, researchers waited for a blood loss equal to one-third of the goat’s expected blood volume in all three groups (24 ml/kg).[27] Then, 20 ml/kg NS, 8 ml/kg HTS fluid (3%), or no fluids (for the NFR group) were administered rapidly. The starting point for the study was after saline infusion completion and was similar in all groups. The total infusion time was about 10 minutes in the NS group and less than 5 minutes in the HTS group. When their heart rates fell below 40 beats/min, the goats were announced dead and data collection was stopped. If a goat stayed alive for more than two hours, the resuscitation was deemed successful, and data collection for that goat was terminated. Throughout the whole procedure, bleeding was not controlled by the researcher in order to simulate UHS.

e. Statistical Analysis All gathered information (i.e., the duration of the goat’s life, tissue pH range, mean arterial pressure, and heart rate) was analyzed using the Statistical Package for the Social Sciences (SPSS, Windows version 15.0, SPSS, Inc., Chicago, IL). Of the non-parametric statistical tests, repeated measure analysis was used to evaluate the comparability of HTS, NS, and NFR groups and to compare the duration of life, amount of bleeding, blood pressure, and acidosis level. Survival analysis was performed by deriving Kaplan-Meier statistics and plots. The differences in survival of the three groups were investigated using log-rank (Mantel-Cox) testing, pooled over the strata. Analysis of variance was used to compare the groups. Significance was defined as p < 0.05.

RESULTS The main features of UHS, including hemoglobin, heart rate, blood loss, mean arterial pressure, and pH were analyzed at 0, 15, 30, 45, 60, 75, 90, 105, and 120 minutes. Baseline characteristics and laboratory values were similar for all groups.

a. Bleeding Time Because of massive bleeding, all the goats in the HTS group 501


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Hemoglobin level during the trial

12

No fluid Normal saline Hyper-tonic saline

10

d. Blood Loss

6 4 2 0 0

15

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Time (min)

Figure 1. Comparison of hemoglobin levels during the trial between groups. The arrow shows when differences started to become statistically meaningful.

died in under one hour and the test was terminated for the HTS group. The bleeding time for the HTS group was 53±2.4 minutes. The bleeding stopped in the NS and NFR groups after 37±4.8 and 18.4±3.9 minutes, respectively, but the trial continued for both groups until the 120th minute. There was no significant difference between the NS and NFR groups (p>0.05). There was a significant difference between the NS and HTS groups, as well as between the NFR and HTS groups, at 60 minutes (p=0.015 and p<0.001, respectively).

The blood loss gathered in the suction bottle was measured from minutes 15 to 120. Blood loss in the HTS group reached a mean of 1600 ml at the 30th minute. The HTS group had more than twice the blood loss of the other two groups, and blood loss in the NS group was higher than in the NFR group (minutes 15 to 30, p=0.021; minute 30 to end, p<0.001). The mean blood loss in the NS group was 1220 ml at the 35th minute. The mean blood loss in the NFR group was 610 ml at the 25th minute and did not increase considerably. Blood loss data are presented in Figure 3.

160 140 120

Heart rate in the NFR and HTS groups increased at first, but heart rates were lower in the NFR group. Heart rate trends were irregular during the 120 minutes. In the HTS group, from the beginning until the 45th minute, heart rate increased rapidly and then fell rapidly toward zero until the 60th minute. At the 60th minute, heart rate fell below 40 beats/min, and the goats were excluded from the rest of the study. In the NS group, heart rate decreased during the first 502

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Figure 2. Comparison of heart rates during the trial between groups. Blood loss during the trial

1800 1600 1400 1200

Blood loss (cc)

c. Heart Rate

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60

b. Hemoglobin There was no initial significant difference between the hemoglobin values of the groups. However, between 15 and 60 minutes, during which the HTS goats died, a significant difference appeared between the groups (p<0.001). The NFR group had much higher hemoglobin levels than the NS group, and the lowest hemoglobin values occurred in the HTS group. From the 60th minute to the 120th minute, the NFR group continued to have higher hemoglobin values than the NS group (p<0.001). Although decreasing hemoglobin levels were observed in all three groups, a rapid and severe decline occurred in the HTS group. Hemoglobin values for the NFR and NS groups remained parallel during the 120 minutes, but NFR group levels were statistically higher during the trial, except for during the first 15 minutes (Figure 1).

Heart rate level during the trial

180

Hg beats/min

Hg mg/dl

8

35 minutes. In general, heart rates in both the NS and NFR groups increased gradually. Heart rate differences were not statistically significant between the three groups, and no welldefined pattern was observed (Figure 2).

1000 800 600 400

No fluid Normal saline Hyper-tonic saline

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Figure 3. Comparison of blood loss during the trial between groups.

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e. Mean Arterial Pressure

f. pH

Mean arterial pressure

120

No fluid Normal saline Hyper-tonic saline

100 MAP (mmHg)

0.8

0.6

0.4 Hypersaline Normal saline No serum Normal saline-censored No serum-censored

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No statistical difference between the pH values of the groups was observed in the beginning (p=0.21). Statistically significant differences occurred at the 15th minute (p=0.020) and were present during the rest of the study period (p<0.001). The NFR group had the least acidity compared to the other two groups. The pH values in the HTS group were lower than in the NS group until the 60th minute. Data for pH are presented in Figure 5.

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0.0

20.00

40.00

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Time

Figure 6. Kaplan-Meier analysis revealing cumulative survival plotted against time and differentiated by study groups. * indicates a significant difference (p<0.05) between the NFR and NS groups. + indicates a significant difference (p<0.05) between the NS and HTS groups. # indicates a significant different (p<0.05) between the NFR and HTS groups.

In this trial, all the goats in the HTS group died before the 60th minute. In the NS and NFR groups, four goats and one goat died, respectively, during the 120 minutes of evaluation.

g. Survival Analysis

60 40 20

0

0 12

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i pr

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Figure 4. Comparison of mean arterial pressure levels during the trial between groups. â&#x20AC;&#x153;Priâ&#x20AC;? stands for primary and denotes the starting point of the study.

7.45

PN level during the trial

7.4 7.35

Figure 6 shows the cumulative survival time for each treatment group. Kaplan-Meier analysis of survival until the 120th minute revealed an overall mean survival time of 87.4 minutes (S.E = 6.9). Mean survival times for the three groups were as follows: 119.0 (S.E = 0.95) for the NFR group, 105.2 (S.E = 5.83) for the NS group, and 38.0 (S.E = 4.38) for the HTS treatment group. Overall, 50% of all the goats survived. None of the goats that received HTS treatment survived; 60% of the NS group goats survived; and 90% of the untreated group survived the full 120 minutes. Log-rank (Mantel-Cox) statistics were significant when comparing the three groups pooled over the strata (chi-square = 41.72, p<0.001).

DISCUSSION

7.3 7.25 PH

1.0

Cumulative survival

In all groups, mean arterial pressure decreased in the first approximately 10 minutes. However, after receiving fluid therapy, mean arterial pressure in the NS group continued to fall until the 35th minute, after which, values in the NS group were continuously around 60 mmHg. Similarly, the NFR group experienced a drop in BP until the 28th minute. Mean arterial pressure in the HTS group decreased sharply toward zero in the first 60 minutes, and HTS goats were excluded since all died. All of these results were statistically significant (p<0.05), and mean arterial pressure values are presented in Figure 4.

7.2 7.15 7.1

No fluid Normal saline Hyper-tonic saline

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Figure 5. Comparison of pH levels during the trial between groups.

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Previous protocols and advanced trauma life support teachings[28] have recommended that the primary treatment of UHS include controlling the source of external bleeding, and intravenous administration of crystalloids followed by packed blood cells through a catheter.[29] This approach has been challenged, and researchers have focused on different doses and types of fluids for treating UHS patients. Goats are an appropriate mammal for modeling biomedical studies. Goats have relatively low fat proportions, so goats have similar weights to humans with low body mass. Their 503


Saeedi et al., Hypertonic saline, normal saline or neither

anatomy is the most similar to humans after monkeys and dogs. Therefore, tracheostomy and other procedures are easier to perform. Surgeries and ablations on dogs are difficult, and few monkeys are available. Goats are mammals and respond to shock more similarly to humans compared to rats. As a result, we chose to use a goat model. As far as we know, no previous studies have been performed of fluid therapy for UHS cases using a goat model. Few studies have shown that resuscitation without fluid provides superior results in the treatment of UHS. In their rat study, Krausz et al.[30] showed that infusion of HTS and NS leads to more bleeding and hemodynamic instability. Studies of humans have shown that patients should not receive fluids at the accident scene in a UHS setting, and excessive fluid therapy leads to coagulopathy, increased acidosis, hypothermia, abdominal compartment syndrome, elevated intracranial pressure, and immunologic disorders.[17,31-33] Fluid therapy increases the mortality rate in such conditions.[34] In our study, blood loss in the NFR group was lower than in the NS and HTS groups. Furthermore, the administration of fluid raised blood pressure levels, which interfered with the coagulation process. Contrastingly, not manipulating blood pressure and venous pressure caused less blood to leave the body; so pH levels in the NFR group decreased subsequently to values lower than in the NS and HTS groups. Theoretically, fluids increase blood volume. However, since more blood left the body, the increase in volume was offset by a decrease in hemoglobin in goats which received NS compared to the NFR goats. Hemoglobin levels decreased because of the addition of crystalloid. Heart rates in the NFR group increased slower than in the NS group during UHS. Thus, in cases of uncontrollable hemorrhage, such as abdominal or chest cavity bleeding or pelvic fracture, for which packed red blood cells are not available, the infusion of NS may not be beneficial. Studies have demonstrated the benefits of administering hypertonic fluid to trauma patients.[7-9,35] For example, HTS has been found to facilitate cerebral perfusion, decrease intracranial pressure,[36] restore blood pressure, and improve cardiac performance.[37] In their study of mice, Bahrami et al.[38] concluded that resuscitation with hypertonic fluid decreases the inflammatory process, but neither lung tissue damage nor mortality follow the same pattern following severe UHS. Krausz et al.[39] concluded that, compared to lactated ringerâ&#x20AC;&#x2122;s solution, HTS was associated with less blood loss and improved survival in most groups of rats. Yu et al.[40] reported that limited fluid resuscitation improved the thermodynamics of pregnant rabbits, decreased inflammatory markers, and improved survival rate. In our study, using a model of UHS based on land-mine explosion and no access to packed blood cells, the infusion of HTS was the worst treatment option. HTS decreased hemoglobin levels and mean arterial pressure, and increased blood loss, heart rate, and pH severely and rapidly. No goat in the HTS group was still living after the 504

60th minute. Using HTS may be a valuable option for resuscitation in cases of controlled hemorrhagic shock, but our study demonstrated a model of UHS in which fluid therapy was not useful. Ciesla et al.[41] showed that HTS attenuates the neutrophil cytotoxic response which leads to other complications. Additionally, Watters et al.[42] suggested that any fluid therapy dose may cause dysfunctional inflammatory response, which may explain the higher blood loss in the HTS group in our study. The development of a hypercoagulable state following an injury may also explain the blood loss.[17] Fluid therapy, especially HTS, attenuates this hypercoagulability, leading to more bleeding and other complications. In addition, HTS raises blood pressure and increases blood flow. These findings are in accordance with our study, in which more bleeding and higher blood pressure were observed in the HTS group. Additionally, HTS resuscitation causes more liquid to exit the intercellular space and enhances tissue acidosis. Similarly, in our study, the arterial blood gas results for the HTS group were comparable to those of the NFR and NS groups. Our study has several limitations. We could not control for the effects of anesthesia, which would not be present in human cases of UHS. We did not use different doses of HTS or evaluate dextran. Due to the expense of goats and our limited funding, it was not possible to obtain a large number of animals for more exhaustive testing. Our study showed the role of fluids only in cases of early intervention. An extended evaluation is definitely needed to properly observe late outcomes and survival results. We limited the trial to 120 minutes, but all the goats in the HTS group died by the 60th minute. Therefore, we could not completely compare the three groups for the full two hours. However, no preliminary study using a smaller number of experimental subjects was performed. Further studies and larger randomized clinical trials are required to confirm that, in cases of UHS, the administration of fluids is detrimental. More studies are also needed to determine the physiologic reasons that HTS and NS are worse than no fluid therapy in a UHS setting. Additional studies should focus on resuscitation methods and determining the situations in which fluid administration may augment tissue oxygenation and counterbalance potential harmful effects.

Conclusion Our study shows that HTS may not be a suitable treatment for UHS when compared to NFR and NS groups, especially in settings where bleeding is uncontrollable. The NFR group had considerably better results compared to the HTS and NS groups for all features of UHS, such as hemoglobin levels, pH, bleeding time, and mean arterial pressure. NS and HTS fluids may worsen the condition in the pre-hospital field until surgical repair can be accomplished in the hospital. Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


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Acknowledgments This study was financially supported by a medical research grant of the Military Research Service Department of Iran. The authors thank Dr. Fred Naraghi for his review and critical comments. The authors would also like to thank Mrs. Pourmand (Sina Hospital, Research Development Center) for her careful edits of the manuscript.

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18. Nout YS, Mihai G, Tovar CA, Schmalbrock P, Bresnahan JC, Beattie MS. Hypertonic saline attenuates cord swelling and edema in experimental spinal cord injury: a study utilizing magnetic resonance imaging. Crit Care Med 2009;37:2160-6. 19. Patanwala AE, Amini A, Erstad BL. Use of hypertonic saline injection in trauma. Am J Health Syst Pharm 2010;67:1920-8. 20. Qureshi AI, Suarez JI, Bhardwaj A, Mirski M, Schnitzer MS, Hanley DF, et al. Use of hypertonic (3%) saline/acetate infusion in the treatment of cerebral edema: Effect on intracranial pressure and lateral displacement of the brain. Crit Care Med 1998;26:440-6. 21. Holcroft JW, Vassar MJ, Turner JE, Derlet RW, Kramer GC. 3% NaCl and 7.5% NaCl/dextran 70 in the resuscitation of severely injured patients. Ann Surg 1987;206:279-88. 22. Angle N, Hoyt DB, Coimbra R, Liu F, Herdon-Remelius C, Loomis W, et al. Hypertonic saline resuscitation diminishes lung injury by suppressing neutrophil activation after hemorrhagic shock. Shock 1998;9:164-70. 23. Wingfield WE. Veterinary emergency medicine secrets. 2nd ed. Elsevier Health Sciences; 2001. p. 431-5. 24. Greene SA. Veterinary anesthesia and pain management secrets. Elsevier Health Sciences; 2002. p. 260-3. 25. Surgeons ACo: ATLS, Advanced Trauma Life Support Program for Doctors, 7th ed., 2004. 26. Reece W. Duox physiology of domestic animals. 12 ed. Comstock; 2004. p. 50. 27. Robert MJAH. Rosen’s emergency medicine: Concepts and clinical practice. Vol. 1, 6th ed. Mosby; 2006. p. 46. 28. Committee on Trauma: Advanced Trauma Life Support Course for Physicians. Chicago: American College of Surgeons; 1993. 29. Trunkey DD. Is ALS necessary for pre-hospital trauma care? J Trauma 1984;24:86-7. 30. Krausz MM, Bar-Ziv M, Rabinovici R, Gross D. “Scoop and run” or stabilize hemorrhagic shock with normal saline or small-volume hypertonic saline? J Trauma 1992;33:6-10. 31. Turner J, Nicholl J, Webber L, Cox H, Dixon S, Yates D. A randomised controlled trial of prehospital intravenous fluid replacement therapy in serious trauma. Health Technol Assess 2000;4:1-57. 32. Sampalis JS, Tamim H, Denis R, Boukas S, Ruest SA, Nikolis A, et al. Ineffectiveness of on-site intravenous lines: is prehospital time the culprit? J Trauma 1997;43:608-17. 33. Yaghoubian A, Lewis RJ, Putnam B, De Virgilio C. Reanalysis of prehospital intravenous fluid administration in patients with penetrating truncal injury and field hypotension. Am Surg 2007;73:1027-30. 34. Kaweski SM, Sise MJ, Virgilio RW. The effect of prehospital fluids on survival in trauma patients. J Trauma 1990;30:1215-9. 35. Nolan J. Fluid resuscitation for the trauma patient. Resuscitation 2001;48:57-69. 36. Xiao HP, Gu MN, Xiao JF, Xu X, Zhao ZL. Effects of hypertonic sodium chloride hydroxyethyl starch 40 injection in treatment of acute intracranial hypertension complicated by hemorrhagic shock in dogs. [Article in Chinese] Nan Fang Yi Ke Da Xue Xue Bao 2008;28:385-8. [Abstract] 37. Kramer GC, Perron PR, Lindsey DC, Ho HS, Gunther RA, Boyle WA, et al. Small-volume resuscitation with hypertonic saline dextran solution. Surgery 1986;100:239-47. 38. Bahrami S, Zimmermann K, Szelényi Z, Hamar J, Scheiflinger F, Redl H, et al. Small-volume fluid resuscitation with hypertonic saline prevents inflammation but not mortality in a rat model of hemorrhagic shock. Shock 2006;25:283-9. 39. Krausz MM, Semenikhina L, Hirsh M. Lactated Ringer’s solution and

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saline attenuation of the neutrophil cytotoxic response is reversed upon restoration of normotonicity and reestablished by repeated hypertonic challenge. Surgery 2001;129:567-75. 42. Watters JM, Tieu BH, Todd SR, Jackson T, Muller PJ, Malinoski D, et al. Fluid resuscitation increases inflammatory gene transcription after traumatic injury. J Trauma 2006;61:300-89.

DENEYSEL ÇALIŞMA - ÖZET OLGU SUNUMU

Hipertonik salin, normal salin veya hiçbiri: Kontrol altına alınamayan hemorajik şok için en iyisi hangisi? Keçilerde deneysel çalışma Dr. Morteza Saeedi,1 Dr. Houman HajiseyedJavadi,2 Dr. Samad Shams Vahdati,2 Dr. Vahid Eslami,1 Dr. Mohamad Mokhtarpour,3 Dr. Mehdi Momeni,1 Dr. Mohammad Reza Farnia,1 Dr. Nima Hafezi Nejad1 Tahran Üniversitesi Tıp Bilimleri, Acil Tıp Bölümü, Tahran, İran Tebriz Üniversitesi Tıp Bilimleri, Acil Tıp Bölümü, Tebriz, İran 3 AJA Üniversitesi Tıp Bilimleri, Acil Tıp Bölümü, Tahran, İran 1 2

AMAÇ: Kontrol altına alınamayan hemorajik şokta değişik sıvıların etkileri değerlendirildi. Kontrol altına alınamayan hemorajik şokun en iyi tedavisinde uygun dozlar ve sıvı tiplerine ilişkin anlaşmazlıklar vardır. Bu çalışma sıvıyla resüsitasyon yapılmaksızın (NFR) kontrol altına alınamayan hemorajik şokta hipertonik (HTS) ve normal salinin (NS) etkilerini değerlendirmektedir. GEREÇ VE YÖNTEM: Otuz keçiye anestezi verilip sağ bacakları cerrahi yolla çıkartıldı. Hayvanlar eşit sayılarda NFR, HTS ve NS gruplarına randomize edildi. Kontrol altına alınmamış hemorajik şoktaki hayvanlarda hemoglobin, kalp hızı, kan kaybı, ortalama arteriyel basınç, kanama zamanı ve pH analiz edildi ve hayvanlar ablasyondan iki saat sonra öldürüldü. BULGULAR: HTS verilen keçilerin tümü 60 dakika, NS grubunda dört ve NFR grubunda ise bir keçi 120 dakika içinde öldü. NFR grubunda hemoglobin değerleri denemenin sonunda NS ve HTS grubuna göre anlamlı derecede daha yüksekti. HTS grubunda kan kaybı diğer iki gruba göre daha yüksekti (p<0.05). NS grubunda NFR grubuna göre kan kaybı daha fazlaydı (p<0.05). HTS grubunda ortalama arteriyel basınç ilk 60 dakika içinde hızla sıfıra doğru düştü. NFR ve NS gruplarında ortalama arteriyel basınç HTS grubuna göre daha yüksek olup (p<0.05), 35 dakika sonra 60 mmHg’de sabitlenmişti. Diğer iki gruba göre NFR grubunda pH değerleri daha yüksekti (p<0.05). TARTIŞMA: Çalışmamız NFR ve NS ile karşılaştırıldığında kontrol altına alınamayan hemorajik şok tedavisinde HTS’nin uygun olmadığını göstermiştir. HTS ve NS ile tedavi edilenlerle karşılaştırıldığında NFR ile tedavi edilen keçilerin hemoglobin, pH, kan basıncı ve kanama zamanı gibi tüm kontrol altına alınamayan hemorajik şok parametreleri daha iyi idi. Hastane öncesi dönemde NS veya HTS ile tedavi cerrahi onarım gerçekleşene kadar durumu kötüleştirebilmektedir. Anahtar sözcükler: Kontrol altına alınamayan hemorajik şok; sıvı; hipertonik salin; resüsitasyon; keçi. Ulus Travma Acil Cerr Derg 2013;19(6):500-506

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doi: 10.5505/tjtes.2013.31799

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EXPERIMENTAL STUDY

Antioxidant and anti-inflammatory effects of curcumin against hepatorenal oxidative injury in an experimental sepsis model in rats Gülay Yılmaz Savcun, M.D.,1 Erkan Özkan, M.D.,1 Ender Dulundu, M.D.,2 Ümit Topaloğlu, M.D.,1 Ahmet Özer Şehirli, M.D.,3 Olgu Enis Tok, M.D.,4 Feriha Ercan, M.D.,4 Göksel Şener, M.D.3 1

Department of General Surgery, Haydarpasa Numune Training and Research Hospital, Istanbul

2

Department of General Surgery, Marmara University Faculty of Medicine, Istanbul

3

Department of Pharmacology, Marmara University Faculty of Pharmacy, Istanbul

4

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

ABSTRACT BACKGROUND: To investigate the effects of curcumin, an antioxidant and anti-inflammatory agent, on free oxygen radicals and lipid peroxidation in an experimental sepsis model, as well as to determine the role of curcumin in preventing hepatorenal tissue damage caused by sepsis. METHODS: The rats were randomly divided into three groups (n=8) as follows: control group (group 1); sepsis group (group 2); and sepsis + curcumin group (group 3). Sepsis was created using the cecal ligation and perforation (CLP) method. Curcumin was administered intraperitoneally (200 mg/kg) in two equal doses just after the perforation and at twelve hours post-perforation. RESULTS: Serum TNF-a and IL-1β, and tissue MDA and MPO values were higher, whereas tissue GSH and Na+/K+-ATPase values were lower, in group 2 as compared to group 1. These values in group 3 were the inverse of those in group 2. As compared to group 1, histopathological evaluation of group 2 showed damaged hepatocytes, glomeruli, and tubules, whereas the damage was significantly reduced in group 3 as compared to group 2. CONCLUSION: The strong antioxidant and anti-inflammatory effects of curcumin against potential hepatorenal damage were shown using an experimental sepsis model in rats. Key words: Curcumin; free oxygen radicals; sepsis.

INTRODUCTION Sepsis is defined as an excessive and irregular systemic inflammatory reaction syndrome (SIRS) against infection.[1] Bacterial lipopolysaccharide endotoxins activate macrophages, triggering the release of pro-inflammatory cytokines, and thus play a role in the development of systemic inflammatory response. One of the groups of mediators that are responsible for the Address for correspondence: Erkan Özkan, M.D. Bosna Bulvarı Taşlıbayır Sok., No: 28, B Blok, Kat: 3, D: 7, Üsküdar, İstanbul, Turkey Tel: +90 216 - 414 45 02 / 1211 E-mail: dr.erkan@mynet.com Qucik Response Code

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inflammatory response is free oxygen radicals. Free oxygen radicals disrupt cell membranes by causing lipid peroxidation, inhibit ATP synthesis in the mitochondria, and cause oxidative damage to DNA and proteins.[2] Sepsis can also be defined as a harmful host response against infection. Despite aggressive surgical therapy, specific antibiotics, and other pharmacologic agents used, sepsis is the leading cause of mortality in intensive care units.[3] Curcumin, which is known as the Indian spice turmeric, is used as a spice that gives a yellow color to food. Curcumin is obtained from the yellow powder of Curcuma longa (Zingiberaceae), a tropical plant.[4] Curcumin has been widely used in Eastern populations, particularly as a traditional medicine in India and China, for the treatment of many diseases, including hepato-biliary, skin, rheumatoid, and gastrointestinal system diseases.[5] The protective features of curcumin, first and foremost its antioxidant and anti-inflammatory effects, have been shown in clinical and experimental studies.[6-9] 507


Yılmaz Savcun et al., Antioxidant and anti-inflammatory effects of curcumin against hepatorenal oxidative injury

In the present study, the antioxidant and anti-inflammatory effects of curcumin in reducing the damage caused by experimental sepsis in rats was investigated. The outcomes on clinical availability were discussed as well.

MATERIALS AND METHODS The present experimental study was conducted in the Experimental Research and Animal Laboratory of Marmara University Faculty of Medicine after obtaining approval of the Local Ethics Committee. Both genders of Wistar albino rats, weighing between 200 and 250 g, were included in the study. The rats were kept in a temperature-controlled (22±1 °C) room with a 12:12h alternating light/dark cycle. General anesthesia was induced with subcutaneous administration of ketamine HCl (50 mg/kg) and xylazine HCl (15 mg/kg). The cecal ligation and perforation (CLP) model was used to induce sepsis.[10] After shaving abdominal hair, the abdomen was entered through a 3-cm incision. Following laparotomy, the cecum was isolated and filled with feces by milking stool back from the ascending colon. The cecum was then tightly ligated with 3-0 silk at its base, below the ileocecal valve; the anterior surface of the cecum was perforated twice with an 18-gauge needle, and the cecum was replaced into the abdomen after a small amount of feces was visualized. The abdomen was closed in two layers with 3-0 continuous silk sutures. The animals were divided into 3 groups (n=8) according to the antioxidant and anti-inflammatory goals, as below. Group 1 (control group): The rats underwent anesthesia and surgery, but not CLP. Group 2 (sepsis group): Sepsis was induced by the CLP method. Group 3 (sepsis + curcumin group): Sepsis was induced by the CLP method. The rats were given curcumin (200 mg/ kg) via the intraperitoneal route in two equal doses just after surgery and at the post-operative 12th hour. All rats were sacrificed at the post-operative 24th hour. A 2-cc blood sample was obtained from the vena cava. Tissue samples were obtained from the liver and the kidney. Plasma tumor necrosis factor-alpha (TNF-α) and interleukin 1-beta (IL-1β) levels were measured. Hepatic and renal tissue malondialdehyde (MDA) and glutathione (GSH) levels, as well as myeloperoxidase (MPO) and Na+/K+-ATPase activities, were determined. The tissue samples were examined under a light microscope for histopathological changes, including interstitial inflammation and peri-hepatic and -nephritic necroses. 508

Biochemical Protocols Serum analyses Plasma TNF-α and IL-1β were quantified according to the manufacturer’s instructions and guidelines using enzymelinked immunosorbent assay (ELISA) kits (Biosource International, Nivelles, Belgium). These kits were preferred because of the high degree of sensitivity, specificity, inter- and intra-assay precision, and the small amount of plasma sample required for conducting the assay. Malondialdehyde and glutathione assays Tissue samples from the liver and kidney were homogenized in ice-cold homogenization medium containing 150 mM KCl for determination of MDA and GSH levels. The MDA levels were assayed for products of lipid peroxidation.[11] The results were expressed as nmol MDA/g tissue. GSH was determined by the spectrophotometric method using Ellman’s reagent. [12] The results were expressed as mmolGSH/g tissue. Serum MDA and GSH levels were measured by the same methods. Myeloperoxidase activity Tissue-associated MPO activity was measured using a procedure similar to the procedure documented by Hillegas et al.[13] Liver and kidney samples were homogenized in 50 mM potassium phosphate buffer (PB; pH 6.0) and centrifuged at 41,400 g for 10 min; the pellets were suspended in 50 mM PB containing 0.5% hexadecyltrimethylammonium bromide. After three freeze-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 the 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 Measurement of Na+/K+-ATPase activity is based on the measurement of inorganic phosphate that is formed from 3 mM disodium adenosine triphosphate added to the medium during the incubation period.[14] The medium was incubated in a 37 °C water bath for 5 min with a mixture of 100 mM NaCl, 5 mM KCl, 6 mM MgCl2, 0.1 mM ethylenediaminetetraacetic acid, and 30 mM Tris HCl (pH 7.4). Following the pre-incubation period, Na2ATP at a final concentration of 3 mM was added to each tube and incubated at 37 °C for 30 min. After incubation, the tubes were placed in an ice bath and the reaction was stopped. Subsequently, the level of inorganic phosphate was determined using a spectrophotometer (Shimadzu, Japan) at an excitation wavelength of 690 nm.

Histopathological Examination After the tissue samples were fixed in a 10% formaldehyde solution, they were washed with tap water for at least 3 h or overnight. The tissue samples were gradually dehydrated by passage through increasing concentrations of alcohol (15 min Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Yılmaz Savcun et al., Antioxidant and anti-inflammatory effects of curcumin against hepatorenal oxidative injury

Table 1. Serum tumor necrosis factor-alpha and interleukin 1-beta values of the control, sepsis, and sepsis + curcumin groups in the hepatorenal injury model induced by sepsis in rats

Control

Sepsis

Sepsis + Curcumin

TNF-α (pg/mL)

8.48±1.25

34.35±3.72*** 14.38±2.72+++

IL-1β (pg/mL)

9.79±1.45

32.37±3.30*** 17.19±2.66++

TNF: Tumor necrosis factor; IL: Interleukin. Data are presented as the mean ± standard deviation. ***p<0.001 as compared to the control group. ++p<0.01; +++p<0.001 as compared to the sepsis group.

with 70% alcohol, 15 min with 90% alcohol, 30 min with 96% alcohol, 30 min with 100% alcohol [twice], and 30 min with 100% toluene [twice]). Thereafter, the tissue samples were submerged in paraffin for 1 night at 60 °C and embedded in paraffin blocks the next day. After the blocking process, 5-6 µm-thick sections were obtained from the tissue samples and placed on slides. The sections were kept in toluene for 2 h to remove the paraffin. Subsequently, the sections were gradually hydrated by passage through decreasing concentrations of alcohol (2 min with 100% alcohol, 2 min with 90% alcohol, and 2 min with 70% alcohol) and placed in distilled water. After staining with hematoxylin for 15 min, the sections were rinsed in tap water for 10 min for blueing. Following staining with eosin for 5 min and washing with distilled water, the sections were again gradually dehydrated by passage through increasing concentrations of alcohol (2 min with 70% alcohol, 2 min with 90% alcohol, 2 min with 96% alcohol, and 10 min with 100% alcohol). Subsequently, the sections were washed

twice with toluene (the first wash lasted for 5 min and the second wash lasted for 10 min), then covered with Entellan. The sections were examined under a light microscope (Olympus BHX51; Tokyo, Japan).

Statistical Analysis Statistical evaluation was performed with one-way analysis of variance (ANOVA) and Tukey’s test. A p-value <0.05 was considered statistically significant. Comparison between the groups with respect to serum TNF-a and IL-1β, and hepatic and renal tissue GSH and MDA levels, as well as MPO and Na+/K+-ATPase activities were done using ANOVA; Tukey’s test was used for pairwise comparisons.

RESULTS Biochemical F indings The serum TNF-α and IL-1β levels were significantly higher

Table 2. Tissue glutathione, malondialdehyde, myeloperoxidase, and Na+/K+-ATPase values of the control, sepsis, and sepsis + curcumin groups in the hepatorenal injury model induced by sepsis in rats

Control

Sepsis

Sepsis + Curcumin

GSH (mmol/g) Liver

2.42±0.14

1.70±0.17** 2.30±0.11+

Kidney

1.66±0.16

0.77±0.12** 1.50±0.16+

MDA (nmol/g) Liver

19.55±2.16

40.70±5.79** 20.25±3.75++

Kidney

31.89±3.51

66.62±6.65*** 35.89±5.65++

MPO (U/g) Liver

12.68±1.20

46.63±5.26*** 24.43±4.43++

Kidney

9.13±1.32

29.28±4.39** 16.77±3.43+

Na /K -ATPase (mmol/mg protein/h) +

+

Liver

2.97±0.59

1.10±0.18* 2.75±0.38+

Kidney

2.25±0.28

1.12±0.15** 2.20±0.20++

GSH: Glutathione; MDA: Malondialdehyde; MPO: Myeloperoxidase. *p<0.05; **p<0.01; ***p<0.001 as compared to the control group. +p<0.05; ++p<0.01; +++p<0.001 as compared to the sepsis group.

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in group 2 compared to group 1 (p<0.001). In contrast, the TNF-α and IL-1β levels were significantly decreased in group 3 as compared to group 2 (p<0.001 and p<0.01, respectively) and approached the levels of group 1 (Table 1 and Figure 1).

(a) 40

Tissue GSH values were significantly lower in group 2 as compared to group 1 (p<0.01). Tissue GSH values were significantly increased in group 3 as compared to group 2 (p<0.05; Table 2 and Figure 2). Hepatic and renal tissue MDA values

(b) 40

***

30

20

+++

10

0

Control

Sepsis

Interlaukin 1-beta (pg/mL)

Tumor necrosis factor-alpha (pg/mL)

*** 30

10

0

Sepsis+Curcumin

++

20

Control

Sepsis

Sepsis+Curcumin

Figure 1. Serum (a) tumor necrosis factor-alpha (TNF-α) and (b) interleukin 1-beta (IL-1β) values of the control, sepsis, and sepsis + curcumin groups in the hepatorenal injury model induced by sepsis in rats. ***p<0.001 as compared to the control group; ++p<0.01; +++p<0.001 as compared to the sepsis group.

(a)

(b)

3

2 +

2

Glutathione (μmol/g)

Glutathione (μmol/g)

+

**

1

0

Control

Sepsis

0

Sepsis+Curcumin

**

1

Control

Sepsis

Sepsis+Curcumin

Figure 2. (a) Hepatic and (b) renal tissue glutathione (GSH) values of the control, sepsis, and sepsis + curcumin groups in the hepatorenal injury model induced by sepsis in rats. **p<0.01 as compared to the control group; +p<0.05 as compared to the sepsis group.

++

25

0

(b) 80

**

Control

Sepsis

Sepsis+Curcumin

Malondialdehyde (nmol/g)

Malondialdehyde (nmol/g)

(a) 30

**

60 ++

40

20

0

Control

Sepsis

Sepsis+Curcumin

Figure 3. (a) Hepatic and (b) renal tissue malondialdehyde (MDA) values of the control, sepsis, and sepsis + curcumin groups in the hepatorenal injury model induced by sepsis in rats. **p<0.01 as compared to the control group; +p<0.05; ++p<0.01 as compared to the sepsis group.

510

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Yılmaz Savcun et al., Antioxidant and anti-inflammatory effects of curcumin against hepatorenal oxidative injury

(a) 60

(b) 40 ***

**

40 ++

30 20

Myeloperoxidase (U/g)

Myeloperoxidase (U/g)

50 30

+

20

10

10 0

Control

Sepsis

0

Sepsis+Curcumin

Control

Sepsis

Sepsis+Curcumin

Figure 4. (a) Hepatic and (b) renal tissue myeloperoxidase (MPO) activities of the control, sepsis, and sepsis + curcumin groups in the hepatorenal injury model induced by sepsis in rats. **p<0.01; ***p<0.001 as compared to the control group; +p<0.05; ++p<0.01 as compared to the sepsis group.

(b)

4 + 3

2 * 1

0

Control

Sepsis

Sepsis+Curcumin

Na+-K+ATPase (mol/mg protein/h)

Na+-K+ATPase (μmol/mg protein/h)

(a)

3 ++ 2

** 1

0

Control

Sepsis

Sepsis+Curcumin

Figure 5. (a) Hepatic and (b) renal tissue Na /K -ATPase activities of the control, sepsis, and sepsis + curcumin groups in the hepatorenal injury model induced by sepsis in rats. *p<0.05; **p<0.01 as compared to the control group; +p<0.05; ++ p<0.01 as compared to the sepsis group. +

+

were significantly higher in group 2 as compared to group 1 (p<0.01 and p<0.001, respectively). Compared to group 2, the tissue MDA values were significantly lower in group 3 (p<0.01; Table 2 and Figure 3). Hepatic and renal tissue MPO activities were significantly higher in group 2 as compared to group 1 (p<0.001 and p<0.01, respectively). Compared to group 2, hepatic and renal tissue MPO activities were significantly decreased in group 3 (p<0.01 and p<0.05, respectively; Table 2 and Figure 4). Hepatic and renal tissue Na+/K+-ATPase activities were significantly decreased in group 2 compared to group 1 (p<0.05 and p<0.01, respectively). Compared to group 2, the tissue Na+/K+-ATPase activities were significantly increased in group 3 (p<0.05 and p<0.01, respectively; Table 2 and Figure 5).

Histopathological Findings Hepatocytes and sinusoids with regular morphology were observed in the hepatic parenchyma of the control group (FigUlus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

ure 6a). Severe sinusoidal dilation and congestion, damaged hepatocytes with numerous cytoplasmic vacuoles, and activated Kupffer cells were observed in the sepsis group (Figure 6b). Mild sinusoidal dilation and congestion, and hepatocytes, the majority of which showed normal morphology, were observed in the sepsis group treated with curcumin (Figure 6c). The renal cortex of the control group (Figure 7a) had glomeruli and tubules with normal morphology. In the sepsis group (Figure 7b), damaged glomeruli with disappearance of Bowman’s space, severe dilatation of the tubular lumen, and impaired tubular structure were observed. Glomerular and tubular damage were significantly reduced in the sepsis group treated with curcumin (Figure 7c).

DISCUSSION Antioxidants are substances that prevent or delay oxidation of oxidizable substrates including proteins, lipids, carbohydrates, and DNA in living cells. If the precise balance between the level of free radicals and antioxidants cannot be 511


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Figure 6. In the hepatic parenchyma of the control group (a), hepatocytes and sinusoids with regular morphology are noted. In the sepsis group (b), severe sinusoidal dilation and vascular congestion (*), damaged hepatocytes with numerous cytoplasmic vacuoles (arrowhead), and activated Kupffer cells (arrow) are noted. In the sepsis group treated with curcumin (c), hepatocytes with regular morphology (arrow) in general, mild sinusoidal dilatation, and vascular congestion (arrow) are noted. Stained with hematoxylin-eosin, original magnification: X400.

Figure 7. In the control group (a), glomeruli and tubules with normal morphology are noted. In the sepsis group (b), glomerular damage, disappearance of Bowmanâ&#x20AC;&#x2122;s space (*), severe dilation of the tubular lumen, and damaged tubules (arrow) are noted. In the sepsis group treated with curcumin (c), regular glomerular structure (arrow) in general and mild tubular damage (arrowhead) are noted. Stained with hematoxylin-eosin, original magnification: X200.

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protected, various pathologic changes that may lead to cell damage occur.[15] Although the underlying physiopathological mechanisms are quite complex in the septic response, advances in molecular biology have allowed understanding of the majority of the pathologic events in sepsis. Free oxygen radicals that are produced during sepsis cause tissue damage by causing damage to DNA, denaturing cellular proteins, and causing peroxidation of membrane lipids.[16] As the physiopathological mechanisms of sepsis have been elucidated, studies on the mechanism of action of mediators and cytokines that play a role in the process, as well as on the changes they cause in the body, have continued. As the understanding of the role of antioxidants increases, it is thought that antioxidant agents that are used to neutralize the effects of free oxygen radicals may have a role in the treatment of sepsis.[17] Curcumin, which is the active ingredient of turmeric (Curcuma longa) and has been used in the Indian medical tradition nearly for 4000 years, is a natural exogenous antioxidant. Curcumin inhibits lipid peroxidation and oxidative DNA damage, and reduces the release of arachidonic acid through lipoxygenase and cyclooxygenase inhibition. Moreover, curcumin shows an anti-inflammatory effect by inhibiting NFκB activation. Curcumin facilitates excretion of many oxygen radicals, particularly superoxide anion, nitrogen dioxide, and hydrogen radicals.[18,19] Although it is difficult to create a supportive treatment environment similar to that applied in intensive care units in animal models, experimental models are of great importance in understanding the physiopathology of septic shock and finding new therapeutic approaches prior to clinical trials. The CLP model used in the present study creates a model similar to the clinical features of septic shock and resembles human sepsis, as the CLP model displays hypodynamic and hypometabolic phases following the hypermetabolic phase.[20] Therefore, it is the closest model to the clinical situation among sepsis models in rats. Unlike the other models (models created by injection of lipopolysaccharides or by intravenous or intraperitoneal infusion of live bacteria), the CLP model has advantages such as providing continuous intraperitoneal contamination without impairing the intestinal integrity, leading to a representation of septic shock in which numerous types of microorganisms are observed (polymicrobial), thus creating a model similar to clinical septic shock (perforated appendicitis, diverticulitis, and colon perforation).[21] Pathologic changes may occur in many organs in patients with sepsis. The most commonly affected organs are the lungs, liver, kidneys, heart, and intestines.[22] These pathologic changes include changes caused by bacterial invasion, direct effect of bacterial toxins and enzymes, mediator-mediated effects, imUlus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

paired perfusion, and disseminated intravascular coagulation. In the present study, hepatic and renal pathologic changes caused by oxidative damage occurred during experimentallyinduced sepsis in rats were biochemically and histologically evaluated. The effects of curcumin, of which strong antioxidant and anti-inflammatory effects are known, against this damage were also investigated. The septic response of the organism comprises complex relationships between microbial signalling molecules, leukocytes, humoral mediators, and the vascular endothelium. Inflammatory cytokines strengthen and diversify the host response. TNF-α stimulates leukocytes and vascular endothelial cells to release other cytokines, express cell surface adhesion molecules and increase arachidonic acid turnover. Serum TNF-α levels are elevated during severe sepsis or septic shock.[23] Although TNF-α is the main mediator, it is only one of numerous cytokines that are involved in the septic process. For example, IL-1β, which has many TNF-α activities, plays a gradually increasing role in the progression of sepsis. TNF-α, IL-1β, IL-8, and other mediators show complementary effects with each other. In animal experiments, neutralizing one or several of these components can prevent the septic response. [24,25] In the present study, serum TNF-α and IL-1β levels were higher in the sepsis group as compared to the control group (p<0.001). This increase was significantly decreased in the sepsis group treated with curcumin (p<0.001 and p<0.01, respectively). Curcumin decreased TNF-α and IL-1β levels by preventing inflammation. There are several defense mechanisms against the toxic effects of free oxygen radicals. GSH is a natural antioxidant defense system. GSH is found in high concentrations in all cells and in epithelial surface fluid. GSH shows a protective effect by neutralizing free radicals and reactive oxygen intermediates. Furthermore, GSH also inactivates endogenous compounds such as prostaglandins and leukotrienes.[26,27] Ahmida[28] demonstrated an elevation in GSH levels with curcumin therapy given against renal damage induced by vancomycin in rats. Similarly, the antioxidant effect of curcumin has also been shown in a gentamicin-induced renal injury model[29] and in aflatoxin- and paracetamol-induced hepatic injury models,[30,31] and significant elevations were observed in tissue GSH levels. In the present study, hepatic and renal tissue GSH levels were lower in the sepsis group as compared to the control group (p<0.01). However, hepatic and renal tissue GSH levels were significantly increased in the sepsis group treated with curcumin as compared to the sepsis group (p<0.05). MDA is one of the highly reactive metabolic products that are produced as the result of a series of reactions due to lipid peroxidation caused by the effect of free oxygen radicals on the tissues.[32] The levels of intracellular enzymes such 513


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as MDA, which are lipid peroxidation products, are elevated in sepsis and worsen tissue damage by denaturing proteins. MDA measurement is used as an indicator of lipid peroxidation.[33] In an acetaminophen-induced renal injury model in rats, Cekmen et al.[34] showed that renal tissue MDA levels were decreased with curcumin. Moreover, tissue MDA levels were also decreased with curcumin in a renal ischemia/ reperfusion model[35] and in a methotrexate-induced hepatic injury model.[6] In the present study, hepatic and renal tissue MDA levels were found to be significantly higher in the sepsis group as compared to the control group (p<0.01 and p<0.001, respectively). It was observed that MDA levels were significantly decreased in the sepsis group treated with curcumin as compared to the sepsis group (p<0.01). Free oxygen radicals cause tissue damage directly and also lead to the accumulation of polymorphonuclear leukocytes (PMNLs) in damaged tissue. Neutrophils and monocytes express MPO. PMNLs, which migrate to the tissues after being activated, release enzymes such as MPO. Oxidation of these enzymes causes formation of toxic agents that can affect the microorganism in various ways and leads to cell death. This enzyme enhances both tissue damage and formation of radicals.[36] Tissue MPO levels have been reported to be decreased with curcumin therapy in ischemia/reperfusionand amiodarone-induced pulmonary fibrosis models.[37,38] In the present study, hepatic and renal tissue MPO levels were significantly higher in the sepsis group as compared to the control group (p<0.001 and p<0.01, respectively). MPO levels were significantly decreased in the sepsis group treated with curcumin as compared to the sepsis group (p<0.01 and p<0.05, respectively). The Na+/K+-ATPase enzyme helps to preserve cellular membrane potential and osmotic gradient and is necessary for cellular functions. The negative effects of free radicals on Na+/K+-ATPase enzyme are one of the most emphasized mechanisms that are considered to be responsible for impaired enzyme activity. It is known that transport proteins are quite susceptible to changes in reactive oxygen species. During sepsis, oxidative stress causes lipid peroxidation in erythrocyte membranes and alterations in membrane lipid composition. As a result of these alterations in erythrocyte membranes, Na+/K+-ATPase activity and membrane viscosity are decreased.[39-41] In the present study, hepatic and renal tissue Na+/K+-ATPase activities were lower in the sepsis group as compared to the control group (p<0.05 and p<0.01, respectively). However, hepatic and renal tissue Na+/K+-ATPase activities were significantly higher in the sepsis group treated with curcumin as compared to the sepsis group (p<0.05 and p<0.01, respectively). In conclusion, the present study showed strong antioxidant and anti-inflammatory effects of curcumin against the tissue damage likely caused by free oxygen radicals and lipid peroxidation induced by experimental sepsis created in rats. We 514

are of the opinion that further studies on this issue will show the benefits of curcumin in reducing or preventing the toxic effects of sepsis. Conflict of interest: None declared.

REFERENCES 1. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 1992;20:864-74. 2. Bostanoglu A, Bostanoglu S, Erverdi N, Hamamcı O, Özgen G, Dursun A, Korkmaz A. The role of oxygen free radicals in an experimental sepsis model. The Turkish Journal of Gastroenterology 1999;10:427-31. 3. Angus DC, Linde-Zwirble WT, Lidicker J, Clermont G, Carcillo J, Pinsky MR. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit Care Med 2001;29:1303-10. 4. Aggarwal BB, Sundaram C, Malani N, Ichikawa H. Curcumin: the Indian solid gold. Adv Exp Med Biol 2007;595:1-75. 5. Zhou H, Beevers CS, Huang S. The targets of curcumin. Curr Drug Targets 2011;12:332-47. 6. Hemeida RA, Mohafez OM. Curcumin attenuates methotraxate-induced hepatic oxidative damage in rats. J Egypt Natl Canc Inst 2008;20:141-8. 7. Menon VP, Sudheer AR. Antioxidant and anti-inflammatory properties of curcumin. Adv Exp Med Biol 2007;595:105-25. 8. Jacob A, Wu R, Zhou M, Wang P. Mechanism of the Anti-inflammatory Effect of Curcumin: PPAR-gamma Activation. PPAR Res 2007;2007:89369. 9. Kumar P, Padi SS, Naidu PS, Kumar A. Possible neuroprotective mechanisms of curcumin in attenuating 3-nitropropionic acid-induced neurotoxicity. Methods Find Exp Clin Pharmacol 2007;29:19-25. 10. Otero-Antón E, González-Quintela A, López-Soto A, López-Ben S, Llovo J, Pérez LF. Cecal ligation and puncture as a model of sepsis in the rat: influence of the puncture size on mortality, bacteremia, endotoxemia and tumor necrosis factor alpha levels. Eur Surg Res 2001;33:77-9. 11. Buege JA, Aust SD. Microsomal lipid peroxidation. Methods Enzymol 1978;52:302-10. 12. Beutler E. Glutathione in red blood cell metabolism. A manual of biochemical methods. New York: Grune &Stratton; 1975. p. 112-4. 13. Hillegass LM, Griswold DE, Brickson B, Albrightson-Winslow C. Assessment of myeloperoxidase activity in whole rat kidney. J Pharmacol Methods 1990;24:285-95. 14. 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;65:105-16. 15. Halliwell B, Whiteman M. Measuring reactive species and oxidative damage in vivo and in cell culture: how should you do it and what do the results mean? Br J Pharmacol 2004;142:231-55. 16. Bone RC. Gram-negative sepsis. Background, clinical features, and intervention. Chest 1991;100:802-8. 17. Del Sorbo L, Zhang H. Is there a place for N-acetylcysteine in the treatment of septic shock? Crit Care 2004;8:93-5. 18. Epstein J, Sanderson IR, Macdonald TT. Curcumin as a therapeutic agent: the evidence from in vitro, animal and human studies. Br J Nutr 2010;103:1545-57. 19. Thiyagarajan M, Sharma SS. Neuroprotective effect of curcumin in middle cerebral artery occlusion induced focal cerebral ischemia in rats. Life Sci 2004;74:969-85. 20. Rittirsch D, Hoesel LM, Ward PA. The disconnect between animal models of sepsis and human sepsis. J Leukoc Biol 2007;81:137-43. 21. İskit AB. Sepsiste deneysel modeller. Yoğun Bakım Dergisi 2005;5:1336.

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Yılmaz Savcun et al., Antioxidant and anti-inflammatory effects of curcumin against hepatorenal oxidative injury 22. Wheeler AP, Bernard GR. Treating patients with severe sepsis. N Engl J Med 1999;340:207-14. 23. Reiter RJ, Tan DX, Manchester LC, Qi W. Biochemical reactivity of melatonin with reactive oxygen and nitrogen species: a review of the evidence. Cell Biochem Biophys 2001;34:237-56. 24. Landmann R, Zimmerli W, Sansano S, Link S, Hahn A, Glauser MP, et al. Increased circulating soluble CD14 is associated with high mortality in gram-negative septic shock. J Infect Dis 1995;171:639-44. 25. Wang H, Bloom O, Zhang M, Vishnubhakat JM, Ombrellino M, Che J, et al. HMG-1 as a late mediator of endotoxin lethality in mice. Science 1999;285:248-51. 26. Çetiner M, Şener G, Demiralp. Metotreksat tedavisine bağlı ince barsakta oluşan oksidatif doku hasarında L-Karnitinin koruyucu etkisi. Turkish Journal of Haematology 2004;21 Supp. 3:50. 27. Ozkan E, Akyüz C, Sehirli AO, Topaloğlu U, Ercan F, Sener G. Montelukast, a selective cysteinyl leukotriene receptor 1 antagonist, reduces cerulein-induced pancreatic injury in rats. Pancreas 2010;39:1041-6. 28. Ahmida MH. Protective role of curcumin in nephrotoxic oxidative damage induced by vancomycin in rats. Exp Toxicol Pathol 2012;64:149-53. 29. Farombi EO, Ekor M. Curcumin attenuates gentamicin-induced renal oxidative damage in rats. Food Chem Toxicol 2006;44:1443-8. 30. El-Agamy DS. Comparative effects of curcumin and resveratrol on aflatoxin B(1)-induced liver injury in rats. Arch Toxicol 2010;84:389-96. 31. Girish C, Koner BC, Jayanthi S, Ramachandra Rao K, Rajesh B, Pradhan SC. Hepatoprotective activity of picroliv, curcumin and ellagic acid compared to silymarin on paracetamol induced liver toxicity in mice. Fundam Clin Pharmacol 2009;23:735-45. 32. Kaçmaz A, Polat A, User Y, Tilki M, Ozkan S, Sener G. Octreotide improves reperfusion-induced oxidative injury in acute abdominal hypertension in rats. J Gastrointest Surg 2004;8:113-9.

33. Akyol Ö, İşçi N, Temel İ. The relationship between plasma and erythrocyte antioxidant enzymes and lipid peroxidation in patients with rheumatoid arthritis. Joint Bone Spine 2001;68:311-7. 34. Cekmen M, Ilbey YO, Ozbek E, Simsek A, Somay A, Ersoz C. Curcumin prevents oxidative renal damage induced by acetaminophen in rats. Food Chem Toxicol 2009;47:1480-4. 35. Bayrak O, Uz E, Bayrak R, Turgut F, Atmaca AF, Sahin S, et al. Curcumin protects against ischemia/reperfusion injury in rat kidneys. World J Urol 2008;26:285-91. 36. Pascual JL, Khwaja KA, Ferri LE, Giannias B, Evans DC, Razek T, et al. Hypertonic saline resuscitation attenuates neutrophil lung sequestration and transmigration by diminishing leukocyte-endothelial interactions in a two-hit model of hemorrhagic shock and infection. J Trauma 2003;54:121-32. 37. Karatepe O, Gulcicek OB, Ugurlucan M, Adas G, Battal M, Kemik A, et al. Curcumin nutrition for the prevention of mesenteric ischemiareperfusion injury: an experimental rodent model. Transplant Proc 2009;41:3611-6. 38. Punithavathi D, Venkatesan N, Babu M. Protective effects of curcumin against amiodarone-induced pulmonary fibrosis in rats. Br J Pharmacol 2003;139:1342-50. 39. Ozkan E, Yardimci S, Dulundu E, Topaloğlu U, Sehirli O, Ercan F, et al. Protective potential of montelukast against hepatic ischemia/reperfusion injury in rats. J Surg Res 2010;159:588-94. 40. Konukoglu D, Kemerli GD, Sabuncu T, Hatemi H. Relation of erythrocyte Na+-K+ ATPase activity and cholesterol and oxidative stress in patients with type 2 diabetes mellitus. Clin Invest Med 2003;26:279-84. 41. Mahmmoud YA. Curcumin modulation of Na,K-ATPase: phosphoenzyme accumulation, decreased K+ occlusion, and inhibition of hydrolytic activity. Br J Pharmacol 2005;145:236-45.

DENEYSEL ÇALIŞMA - ÖZET OLGU SUNUMU

Sıçanlarda deneysel sepsis modelinde oluşan hepatorenal oksidatif hasara karşı curcuminin antioksidan ve antienflamatuvar etkisi Dr. Gülay Yılmaz Savcun,1 Dr. Erkan Özkan,1 Dr. Ender Dulundu,2 Dr. Ümit Topaloğlu,1 Dr. Ahmet Özer Şehirli,3 Dr. Olgu Enis Tok,4 Dr. Feriha Ercan,4 Dr. Göksel Şener3 Haydarpaşa Numune Eğitim ve Araştırma Hastanesi, Genel Cerrahi Kliniği, İstanbul Marmara Üniversitesi Tıp Fakültesi, Genel Cerrahi Anabilim Dalı, İstanbul Marmara Üniversitesi Eczacılık Fakültesi, Farmakoloji Anabilim Dalı, İstanbul 4 Marmara Üniversitesi Tıp Fakültesi, Histoloji ve Embriyoloji Anabilim Dalı, İstanbul 1 2 3

AMAÇ: Deneysel sepsis modelinde antioksidan ve antienflamatuvar bir ajan olan curcuminin serbest oksijen radikalleri, lipit peroksidasyonu üzerine olan etkileri ve sepsisin neden olduğu karaciğer ve böbrek doku hasarını önlemedeki rolü araştırıldı. GEREÇ VE YÖNTEM: Sıçanlar rastgele sekizerli üç gruba ayrıldı. Sıçanlarda sepsis çekum ligasyon perforasyon (ÇLP) yöntemiyle oluşturuldu. Gruplar, kontrol grubu (Grup 1), sepsis grubu (Grup 2), sepsis + curcumin grubu (Grup 3) şeklinde oluşturuldu. Curcumin intraperitoneal (i.p) yoldan (200 mg/kg) iki eşit dozda çekum perforasyonundan sonra 0. ve 12. saatlerde verildi. BULGULAR: Gruplar karşılaştırıldığında grup 2’de grup 1’e göre serum TNF-α, IL-1ß değerleri, doku MDA, MPO değerleri yüksek, doku GSH, Na+-K+ ATP az değerleri ise düşük bulundu. Grup 3’te ise grup 2’ye göre bu değerler tersine değiştiği belirlendi. Grup 2’de grup 1’e göre histopatolojik değerlendirmede hasarlı hepatosit, glomerulus ve tubulus yapısı görülürken grup 3’te grup 2’ye göre bu hasarların belirgin şekilde azaldığı görüldü. TARTIŞMA: Sıçanlarda deneysel sepsis modeli sonucu karaciğer ve böbrek dokusunda oluşabilecek doku hasarına karşı curcuminin güçlü antioksidan ve antienflamatuvar etkisi gösterildi. Anahtar sözcükler: Curcumin; serbest oksijen radikalleri; sepsis. Ulus Travma Acil Cerr Derg 2013;19(6):507-515

doi: 10.5505/tjtes.2013.76390

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ORIGIN A L A R T IC L E

Management of soft tissue extremity degloving injuries with full-thickness grafts obtained from the avulsed flap Özgür Pilancı, M.D.,1 Funda Aköz Saydam, M.D.,1 Karaca Başaran, M.D.,1 Aslı Datlı, M.D.,1 Erdem Güven, M.D.2 1

Department of Plastic, Reconstructive and Aesthetic Surgery, Bagcilar Research and Training Hospital, İstanbul

2

Department of Plastic, Reconstructive and Aesthetic Surgery, İstanbul University Faculty of Medicine, İstanbul

ABSTRACT BACKGROUND: A “degloving injury” is referred to as seperation of cutaneous tissue from the deeper structures of the body. Although many methods have been defined to reform the tissue integrity; defatting and readaptation of the avulsed flap still comprises one of the most effective methods. METHODS: From 2000-2012, we treated a total of nine patients with avulsed extremities with defatting and readaptation of the same flap. The fat compartment of the flaps was removed and the skin was meshed. The patients were followed-up with for an average of 12 months (range: 8-18 months). RESULTS: Total closure of the defect and healing was achieved in seven patients. Although 30% of the total surface area of the graft was lost in one patient, and 10% in another, total epithelialization was achieved later with secondary grafting. CONCLUSION: Defatting, meshing and readaptation of the same flap to its original site is still a valuable option for avulsion injuries because of the relative ease of the procedure, shorter operative times, and usability of the procedure by general surgeons. This technique might be particularly important in places where a reconstructive plastic surgeon is not available. Key words: Avulsion injuries; extremity; graft.

INTRODUCTION Degloving injuries are characterized by avulsion of the cutaneous and subcutaneous skin tissue of the extremity from more rigid deep structures as a result of trauma. Such degloving may occur on a deep fascia, muscle or bone surface. [1,2] After damage in the musculocutaneous perforators of cutaneous and subcutaneous tissues, viability of such tissues becomes compromised. Hidalgo divides degloving injuries into three main groups. Type 1 is an average avulsion injury, which is the most common type and is characterized by a laceration and visible Address for correspondence: Erdem Güven, M.D. İstanbul Üniversitesi İstanbul Tıp Fakültesi, Plastik, Rekonstrüktif ve Estetik Cerrahi Anabilim Dalı, 34093 İstanbul, Turkey Tel: +90 212 - 635 11 84 E-mail: guvenmd@istanbul.edu.tr Qucik Response Code

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avulsed areas. Type 2 injuries are referred to as atypical avulsion injuries. At first sight, there is no serious trauma sign; however, there is actually an avulsion in a wide area. Type 3 injuries are referred to as avulsion injuries of specific areas. Such types of injuries include the plantar area and the scalp. Revascularization and replantation are required for most of these injuries.[3] In extremity avulsion injuries, serious damage may occur in deeply located tissues, such as muscles, bones, or neurovascular structures. In these cases, the manifestation becomes more serious. If the treatment is not initiated promptly, severe complications such as wound infection, sepsis, and disseminated tissue necrosis may develop.[4-6] Today, treatment used in cases of complex extremity injuries includes immediate debridement of the devitalized tissues and repairing the defect with the healthy soft tissue.[7] Such principles also apply to avulsion-type injuries.[6] However, it might not always be possible to assess the viability of the avulsed flap.[6,8] Therefore, various procedures have been defined, including re-adaption of the flap, reconstruction with grafts, free or local flaps, revascularizations, replantations, etc.[1,6,9-13] Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Pilanc覺 et al., Management of soft tissue extremity degloving injuries with full-thickness grafts obtained from the avulsed flap

The most simple and effective treatment option is to convert the avulsed flap into a graft and re-adapt it to its original place. In this study, we present the approach of reapplying the avulsed flap after defatting as a full-thickness graft, which has been underestimated as a treatment option, but provides promising outcomes.

MATERIALS AND METHODS A total of nine patients with degloving injuries of extremities were admitted to our clinic between 2010 and 2012. The age range was 6-33 years (mean age: 16 years). Seven patients had degloving injuries due to traffic accidents, while two patients had occupational accidents. Injury was at the upper extremity in three patients and in the lower extremity in six patients. Two patients had an accompanying trauma (Table 1). Since all patients had common-type avulsion injuries, the avulsed areas were easily visible (Figure 1a, b). Patients had an infection and tetanus prophylaxis before surgery. An effective irrigation was performed using physiological saline to minimize contamination with bacteria. Subcutaneous fat tissue was excised to obtain a full-thickness skin graft while protecting the contact between the avulsed flaps and the underlying tissue (Figure 1c). The grafts were meshed to ensure draining of hematoma and seroma. Then, the grafts were sutured to their original locations. Multiple full layers of sutures were placed on the wound in order to increase stabilization. The graft was immobilized using compressed dressing and a resting splint. Dressing was changed on the 3rd postoperative day. Immobilization was maintained until the 10th postoperative day.

RESULTS Patients were followed for 12 months on average (range: 8-18 months). Mean hospitalization period was 9 days. Almost all

of the grafts were intact in seven patients. In one patient, 30% of the total surface area of the graft was lost, while 10% was lost in another. Secondary grafting was done in these patients with partial split-thickness skin grafts obtained from the lateral thigh. There was minimal graft loss in one patient, which was handled with conservative measures. A local wound infection, controlled with wound care, was noted in one patient. A hypertrophic scar developed in two patients. These patients were treated with compressed wound dressings and silicon scar gel.

DISCUSSION In extremity avulsion injuries, it is crucial to select the treatment modality while considering the viability of the avulsed flap. Many techniques have been defined to assess the viability of the avulsed flap in literature.[1,8,14,15] The most important issue is deciding which tissues will be protected and which tissues will be removed.[2] Degloving injuries are most commonly caused by traumas, where musculocutaneuos perforators are ruptured but the skin cover is often intact.[16] Although at first sight, a direct adaptation of the avulsed flap at its original site seems as the most functional and cosmetic treatment, it was reported that a readapted flap may lead to a necrosis.[1,8] The effects of various agents in increasing the viability of the avulsed flap have been studied in the literature. For example, Milcheski et al.[17] administered intraperitoneal pentoxifylline and allopurinol in two distinct groups after adaptation of the flap at its original site in the experimental degloving rat model. Researchers determined that flap viability was higher in the test group compared to the control group. Although successful results were obtained in the experimental studies, primary repair in clinical settings often causes surgical disappointment due to venous circulation, even if the arterial flap supply was sufficient initially.[10,14] Therefore, tests demonstrating arterial sup-

Table 1. Patient characteristics Patient

Age

Gender

Manner of injury

Type of injury

1

17

Male

Occupational accident

Common

Site

Accompanying injury

Right hand - forearm

Not available

dorsal 2

33

Female

Traffic accident

Common

Right foot dorsal

1st finger subtotal amputation

3

6

Male

Traffic accident

Common

Right foot dorsal

Not available

4

8

Male

Traffic accident

Common

Left foot-ankle dorsal

Not available

5

9

Female

Traffic accident

Common

Right foot dorsal

Not available

6

24

Male

Traffic accident

Common

Left hand 3rd -4th -5th

4th finger mid- phalanx fracture

finger dorsal

7

11

Male

Traffic accident

Common

Left cruris circular

Not available

8

23

Female

Traffic accident

Common

Right foot dorsal

Not available

9

18

Male

Occupational accident

Common

Right forearm volar side

Not available

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(a)

(b)

(c)

Figure 1. (a) A case of a foot avulsion. Post-operative 13th month result with defatting and adaptation of the same flap to its original site. (b) Same technique applied for a hand avulsion. Post-operative 14th month results. (c) Defatting and transformation of the flaps to full thickness grafts.

ply, such as the fluorescein test, may not be very useful for the fate of the flap in cases of degloving injuries.[18] Microsurgical techniques have been applied to protect the avulsed flap as much as possible. Waikakul et al.,[10] categorized the avulsed flaps into three groups in his 32-patient series. The first 9-patient group included the patients with serious damage to the flap skin and subcutaneous tissue. In this group, the graft obtained from the flap was used for reconstruction. All patients in this group reported a graft loss of 5-35%. The second group included patients with visible veins in the subcutaneous tissue who did not have venous backflow. In this group, arterializations were applied and full perfusion was achieved in 4 of 13 patients. In the third group, venous re-anastomosis was done since there was no venous backflow. Flap loss occurred in 2 of 10 patients in this group. The author stated that the group that had the graft applied recovered and became ambulatory faster despite the advantages of the microsurgery technique applied. In addition, the author reported that the flap should immediately be used as graft if perfusion cannot be achieved after arterialization 518

and venous anastomosis.[10] A microsurgical revascularization is not always technically possible and its success rates vary; it requires advanced training and equipment, which may be considered drawbacks of the method.[19] Flaps might be another option for covering the degloving injury defects. For example, Graf et al.[11] treated two cases of foot degloving injuries using revascularization and dorsalis pedis flap methods, respectively. Authors reported that the foot treated with revascularization was more stable and had more physiological load distribution. Rautio et al.[12] reported that free flaps made after degloving injuries of lower extremities may experience necrosis in time due to load-bearing. They suggested that the long-term results are more promising in these types of injuries when the free flaps are made neurosensorial. Lai et al.[13] reported a reverse flow lateral arm adipofascial flap application in one case of an avulsion injury and achieved promising results. Elshahat et al.[9] repaired the pediatric feet avulsion injury defects with bipedicled “delay flaps” designed from the adjacent wound area. Drawbacks of the technique were the 2-week delay and requirement for an Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Pilancı et al., Management of soft tissue extremity degloving injuries with full-thickness grafts obtained from the avulsed flap

additional graft at the donor site. Reconstructions with flaps can extend the time of recovery and hospitalization. Theoretically, nasocomial infections may occur due to extended treatments.[20] In addition, reconstructions with flaps have the disadvantage of sacrificing the intact structures for wound closure.[21,22] Thus, repair with flap should be restricted to the cases where direct bone, joint, or neurovascular structures are exposed. Today, many surgeons suggest the early adaptation of the avulsed flap to its original site after defatting.[1,6,15] Forming a full-thickness skin graft from the avulsed skin and the defect closure was first reported by Farmer in 1939.[23] In the studies conducted by Kudsk and Ziv, no significant difference was observed between the full-thickness and partial-thickness grafts in terms of graft viability.[8,24] However, full thickness grafts yield better cosmetic results.[16,25] Jeng et al.[6] applied full-thickness grafts obtained from the flap to all 42 patients with degloving injuries at the lower extremities and reported a success rate of 91%. Common-type avulsion injuries were present in 90% of the patients, while 10% of patients had atypical avulsion injuries. Graft loss occurred in 12 patients and wastreated using secondary grafts. Minimal flexion contracture at the knee was observed in 4 patients. No patients developed functional loss, and all patients were satisfied with the cosmetic outcome. Jeng et al.[6] suggested the use of avulsed flap as a full-thickness graft as a safe and rapid repair method. Çelebioğlu et al applied the same method on their six-case series and reported success in all cases without the need for a secondary operation. In the cases where the flap is used as the graft, success is mainly associated with an immobilization of the graft.[6] The use of a vacuum-assisted closure (VAC) was proposed for graft immobilization to increase the viability of the graft by eliminating the problems that may occur with movement of the graft.[4] Wolter et al.[5] applied artificial bilayered dermal substitute to the defect following a debridement and then repaired it using a graft. However, such methods cause an additional cost burden. Jeng et al.[6] proposed another procedure, which includes opening drainage holes on the full-thickness grafts and fixing multiple grafts on the receptor bed. They achieved a considerably high graft survival rate using this simple method. In our study, we achieved results similar to the literature. Seven of the nine patients recovered without any secondary operations. Partial losses were observed in two patients and were treated with a secondary partial-thickness skin grafting. None of our patients developed any late complications such as joint contractures. Immediate graft applications have shortened hospitalization time (9 days on average). This was an economical and a reliable method for eliminating sophisticated flap applications. In this technique, the damaged area was covered with its original tissue. Since the graft obtained is Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

a full-thickness graft, it possesses all dermal components. This contributes to a decreased risk of contracture development. Finally, forming a full-thickness skin graft from the flap in degloving injuries is an important advantage in terms of having fast wound coverage. Defatting decreases the infection risk since it also ensures debridement. Early repair with a graft speeds up recovery and shortens hospitalization time. Thus, the need for secondary reconstructions is prevented. In conclusion, the avulsed flap in avulsion injuries might be immediately converted into a graft by removing its subcutaneous fat tissues. This is particulary important if there is even a slight suspicion about the viability of the avulsed flap. This method provides efficient, safe, simple, and long-term acceptable outcomes. Conflict of interest: None declared.

REFERENCES 1. de Korte N, Dwars BJ, van der Werff JF. Degloving injury of an extremity. Is primary closure obsolete? J Trauma 2009;67:60-1. 2. Arnez ZM, Khan U, Tyler MP. Classification of soft-tissue degloving in limb trauma. J Plast Reconstr Aesthet Surg 2010;63:1865-9. 3. Hidalgo DA. Lower extremity avulsion injuries. Clin Plast Surg 1986;13:701-10. 4. Dini M, Quercioli F, Mori A, Romano GF, Lee AQ, Agostini T. Vacuumassisted closure, dermal regeneration template and degloved cryopreserved skin as useful tools in subtotal degloving of the lower limb. Injury 2012;43:957-9. 5. Wolter TP, Noah EM, Pallua N. The use of Integra in an upper extremity avulsion injury. Br J Plast Surg. 2005;58:416-8. 6. Jeng SF, Wei FC. Technical refinement in the management of circumferentially avulsed skin of the leg. Plast Reconstr Surg 1997;100:1434-41. 7. Naique SB, Pearse M, Nanchahal J. Management of severe open tibial fractures: the need for combined orthopaedic and plastic surgical treatment in specialist centres. J Bone Joint Surg Br 2006;88:351-7. 8. Kudsk KA, Sheldon GF, Walton RL. Degloving injuries of the extremities and torso. J Trauma 1981;21:835-9. 9. Elshahat A. Management of complex avulsion injuries of the dorsum of the foot and ankle in pediatric patients by using local delayed flaps and skin grafts. Eplasty 2010;10:64. 10. Waikakul S. Revascularization of degloving injuries of the limbs. Injury 1997;28:271-4. 11. Graf P, Kalpen A, Biemer E. Revascularisation versus reconstruction of degloving injuries of the heel: case report. Microsurgery 1995;16:149-54. 12. Rautio J. Resurfacing and sensory recovery of the sole. Clin Plast Surg 1991;18:615-26. 13. Lai CS, Tsai CC, Liao KB, Lin SD. The reverse lateral arm adipofascial flap for elbow coverage. Ann Plast Surg 1997;39:196-200. 14. McGrouther DA, Sully L. Degloving injuries of the limbs: long-term review and management based on whole-body fluorescence. Br J Plast Surg 1980;33:9-24. 15. Çelebioğlu S, Keser A, Arifoğlu K, Ortak T, Koçer U. Ekstremite avülsiyon yaralanmalarında klinik deneyimlerimiz. Acta Orthop Traumatol Turc 1997;31:141-4.

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Pilancı et al., Management of soft tissue extremity degloving injuries with full-thickness grafts obtained from the avulsed flap 16. Nogueira A, Martínez MJ, Arriaga MJ, Pérez A, Tévar aF. Delayed fullthickness autografting of cryopreserved avulsed skin in degloving injuries of the extremities. Plast Reconstr Surg 2001;107:1009-13. 17. Milcheski DA, Nakamoto HA, Tuma P Jr, Nóbrega L, Ferreira MC. Experimental model of degloving injury in rats: effect of allopurinol and pentoxifylline in improving viability of avulsed flaps. Ann Plast Surg 2013;70:366-9. 18. Huygen RE, Hovius SE, van der Meulen JC. Treatment of extensive avulsions of the skin and soft tissues of the extremities. [Article in Dutch] Ned Tijdschr Geneeskd 1986;130:1836-40. [Abstarct] 19. Suliman MT. Distally based adipofascial flaps for dorsal foot and ankle soft tissue defects. J Foot Ankle Surg 2007;46:464-9. 20. Park SH, Silva M, Bahk WJ, McKellop H, Lieberman JR. Effect of re-

peated irrigation and debridement on fracture healing in an animal model. J Orthop Res 2002;20:1197-204. 21. Lee YH, Rah SK, Choi SJ, Chung MS, Baek GH. Distally based lateral supramalleolar adipofascial flap for reconstruction of the dorsum of the foot and ankle. Plast Reconstr Surg 2004;114:1478-85. 22. Uysal AC, Alagöz MS, Sensöz O. Distally based lateral supramalleolar adipofascial flap. Plast Reconstr Surg 2006;117:685-6. 23. Farmer AW. Treatment of avulsed skin flaps. Ann Surg 1939;110:951-9. 24. Ziv I, Zeligowski A, Mosheiff R, Lowe J, Wexler MR, Segal D. Splitthickness skin excision in severe open fractures. J Bone Joint Surg Br 1988;70:23-6. 25. Goris RJ, Nicolai JP. A simple method of taking skin grafts from the avulsed flap in degloving injuries. Br J Plast Surg 1982;35:58-9.

KLİNİK ÇALIŞMA - ÖZET OLGU SUNUMU

Yumuşak doku ekstremite avülzyon (degloving) yaralanmalarının avülze flepten elde edilmiş tam kalınlıklı deri grefti ile onarımı Dr. Özgür Pilancı,1 Dr. Funda Aköz Saydam,1 Dr. Karaca Basaran,1 Dr. Aslı Datlı,1 Dr. Erdem Güven2 1 2

Bağcılar Egitim ve Araştırma Hastanesi, Plastik Rekonstrüktif ve Estetik Cerrahi Kliniği, İstanbul İstanbul Üniversitesi İstanbul Tıp Fakültesi, Plastik Rekonstrüktif ve Estetik Cerrahi Anabilim Dalı, İstanbul

AMAÇ: Deri ve subkütan dokunun muskulofasyal tabaka sağlam kalacak şekilde derindeki yapılardan ayrılmasına avülzyon (degloving) yaralanması denir. Doku bütünlüğünün yeniden sağlanması için birçok yöntem tanımlanmış olsa da, avülze flebin yağ dokudan arındırılarak yeniden yerine adaptasyonu hala en etkili yöntemlerden birisidir. GEREÇ VE YÖNTEM: Kliniğimizde 2000-2012 yılları arasında ekstremite avülzyon yaralanması mevcut dokuz hastada avülze flebi yağ dokudan arındırdık. Grefte yamalar açarak yeniden yerine adapte ettik. Hastalar ortalama 12 ay takip edildi (dağılım, 8-18 ay). BULGULAR: Yedi hastada tamama yakın iyileşme elde ettik. Bir hastada greftin %30’unda, diğerinde ise %10’a yakın kayıp gözlemledik. Fakat bu hastalar sekonder greftlemelerle epitelizasyon sağlanarak sorunsuz tedavi edildi. TARTIŞMA: Avülzyon yaralanmalarında yağ doku uzaklaştırılarak, greftin yama ile eski yerine adaptasyonu hala değerini korumaktadır. Bunun başlıca sebebi, yöntemin genel cerrahlar tarafından da kısa sürede kolaylıkla uygulanabilir olmasıdır. Bu da plastik cerrahlara ulaşmanın zor olduğu durumlarda önem arz edebilir. Anahtar sözcükler: Avülzyon yaralanmaları; ekstremite; greft. Ulus Travma Acil Cerr Derg 2013;19(6):516-520

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ORIGIN A L A R T IC L E

Functional outcomes after treatment of traumatic brachial plexus injuries: clinical study Yavuz Aras, M.D, Aydın Aydoseli, M.D, Pulat Akın Sabancı, M.D, Mehmet Osman Akçakaya, M.D, Görkem Alkır, Murat İmer, M.D Department of Neurosurgery, Istanbul University Istanbul Faculty of Medicine, Istanbul

ABSTRACT BACKGROUND: The aim of this study is to evaluate functional outcome and quality of life using statistically validated tools. METHODS: Participating patients were called and asked questions from the Short Form 36 (SF-36), the Disability of the Arm, Shoulder and Hand (DASH) questionnaire, a pain scale and an additional question on their satisfaction with surgery. RESULTS: A total of 33 patients were operated by a single surgeon (MI) between 1997 and 2010 at the Neurosurgery Department of Istanbul School of Medicine. Three of these patients refused to participate and three other patients were excluded, leaving 27 patients, with an average follow-up of 79,6 months, for review. The most common cause of traumatic brachial plexus injuries (TBPI) was motor vehicle accidents. Fourteen patients had isolated supraclavicular injuries and three patients had infraclavicular injuries. The remaining 10 patients’ injuries were both supra- and infraclavicular. Avulsion was encountered in three patients. The patients who were operated within the first six months after trauma represented significantly better scores in DASH, SF-36 and pain scale. CONCLUSION: Statistically validated tests like DASH and SF-36 questionnaires are valuable tools for evaluating TBPI patients. Centers specialized in treating TBPI with surgery may use these tests pre- and postoperatively which lead to objective personalized evaluation of patients’ subjective symptoms. Key words: Brachial plexus, functional outcome; nerve injury, quality of life.

INTRODUCTION Traumatic brachial plexus injuries (TBPI) tend to occur in young, otherwise healthy and active individuals. While brachial plexus injuries themselves are not fatal, they can cause disability and can be very difficult to reverse.[1] In addition to motor and sensory deficits, they may also cause pain and functional limitations.[2] Over the years, opinions concerning the treatment of lesions of the brachial plexus have changed. [3] The development of microsurgery and associated technology renewed interest in surgical reconstruction, and has given rise to more favorable results in comparison to earlier studies.[3-5]

Address for correspondence: Mehmet Osman Akçakaya, M.D. İstanbul Tıp Fakültesi Nörolojik Bilimler Binası, Nöroşirürji Anabilim Dalı 6. Kat Çapa, Fatih, 34340 İstanbul, Turkey Tel: +90 212 - 414 20 00 / 32599 E-mail: moakcakaya@gmail.com Qucik Response Code

Ulus Travma Acil Cerr Derg 2013;19(6):521-528 doi: 10.5505/tjtes.2013.48107 Copyright 2013 TJTES

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In most of the studies, surgical results were assessed only by means of motor or sensory recovery,[1,6-9] which does not always correlate with functional status. Functional outcomes and quality of life (QOL) were evaluated only in a few series.[2,10,11] The recent development of statistically validated functional and QOL assessment tools has improved the ability of clinicians to quantify these outcomes.[2] According to Kretschmer et al.[11] 87% of patients operated for TBPI were satisfied and 83% would undergo the procedure again. Despite a high satisfaction rate, patients remained considerably disabled and half of the patients were unable to return to work. Thus, there is a discordance between patient satisfaction and disability. In the present study, the functional outcomes of a TBPI patient series operated by a single surgeon were evaluated by using Short From 36 (SF-36) and the Disability of the Arm, Shoulder and Hand (DASH) questionnaire and by assessing of pre- and postoperative pain. The goal of this study is to present our clinical experience by analyzing the influence of demographic features, injury type, timing of surgery, side and location of injury, preoperative motor examination, surgical approach, technique, and additional injury to QOL with functional outcomes of the TBPI patients by using these scales. 521


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MATERIALS AND METHODS Thirty-three patients underwent surgery to treat a TBPI between 1997 and 2010 in Department of Neurosurgery, İstanbul School of Medicine by a single surgeon (MI). All of the patients were contacted by phone except one, who was deceased secondary to a myocardial infarction three years ago. One other patient had been diagnosed with non small cell lung cancer and was excluded from the study with this additional diagnosis. Another patient experienced a TBPI while falling during a suicide attempt. Hospital records indicated that the patient was diagnosed with major depressive disorder. His answers were thought to be subjective due to his possible ongoing depression. Three patients from the remaining 30 patients refused to participate in the study. The remaining 27 participant patients were asked to give answers on phone for DASH and SF-36 questionnaires. They were asked to give a number between 0 and 100 for the pain they suffered before the surgery and at the moment of conversation. The medical records of these 27 patients were reviewed retrospectively for demographic data, location, side, type and mechanism of injury, preoperative and early postoperative neurological status of the patient, surgical technique, presence of avulsion, additional injury, time interval between injury and surgery and electrophysiological findings. Data was recorded in an SPSS spreadsheet (SPSS version 13.0 for Windows; SPSS, Inc., Chicago, IL). The location of the TBPI was classified as supraclavicular if the injured elements were roots or trunks. It was infraclavicular if cords or main terminal branches were affected. If both supra and infraclavicular elements were affected they were grouped as both.

Questionnaires The DASH Outcome Measure is a 30-item, self-report questionnaire designed to measure physical function and symptoms in people with any of several musculoskeletal disorders of the upper limb.[14] The tool gives clinicians and researchers the advantage of having a single, reliable instrument that can be used to assess any or all joints in the upper extremity. Every question can be answered on a scale from 1 to 5 and with a total minimum score of 30 and maximum 150. Lower scores indicate better results.[2,12,13] The hand or arm the patient uses to perform a particular activity does not influence the response; answers must be based on the ability to perform the activity, regardless of how the activity was performed. The SF-36 is a multi-purpose, short-form health survey with only 36 questions. It yields an eight-scale profile of functional health and well-being scores as well as a psychometricallybased physical and mental health summary measures and a 522

preference-based health utility index. It is a generic measure, as opposed to one that targets a specific age, disease or treatment group. Accordingly, the SF-36 has proven useful in surveys of general and specific populations, comparing the relative burden of diseases and in differentiating the health benefits produced by a wide range of different treatments. [15,16] The results are separated into eight subscale profiles; energy and vitality, physical function, social function, role limitations caused by physical problems, role limitations caused by emotional problems, bodily pain, mental health, general perception of health. The results can be demonstrated as physical and mental summary scores. Higher scores indicate better results.[2] For the evaluation of pain that patients suffer, they were asked to give a number from 0 to 100. The idea was to mimic the Visual Analogue Pain Scale (VAPS) on the phone. All of the questions were asked by a secretary/non-physician in order to eliminate any effect of pressure on the patient’s response.

Statistical Analysis Data was entered and analyzed using statistical software (SPSS version 13.0 for Windows). The SF-36 results were linearly transformed to a scale of 0 to 100 and were compared with the normative scores of the general population.[17,18] All samples were analyzed using Student’s t test for parametric data and the Mann-Whitney U-test for non-parametric data. One-way analysis of variance was used for comparing patients in the three injury location subgroups. Spearman’s ρ correlation coefficients were calculated between the scores on the decision making question as well as the time delay to surgery and each of the DASH questionnaire, the SF-36 subscales and the pain scale.

RESULTS From the 33 TBPI patients who underwent surgery 27 agreed to participate in the study (1 patient died, 2 patients were excluded, 3 patients refused to enroll in the study). There were 7 females and 20 males. Their mean age was 31.7 years old (range 10-66 yrs.). The mean time from injury to surgery was 6.6 months (range 2-17 mos.). The mean follow-up period from surgery to the telephone contact was 79.6 months (range 17-150 mos.). In the current study, the most common cause of TBPI was motor vehicle accidents which was concordant with the previous literature.[1,11] Motor vehicle accidents, pedestrian accidents and penetrating injuries are the major causes of all trauma. Motorcycle accidents, falls and occupational accidents are subsequent causes of BPI (Table 1). Associated injuries were encountered in six patients. Two patients had thoracal vertebra fractures, one had spinal epidural hematoma at the third cervical vertebra level and a left tibia fracture, Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Aras et al., Functional outcomes after brachial plexus surgery

Table 1. Characteristics of TBPI Description Type of injury Motor vehicle accident Pedestrain accident Falls Motorcycle accident Penetrating injury Firearm injury Glass Knife Occupational accident Location of injury Supracalvicular Infraclavicular Both Avulsion Present Absent Associated injuries* Spinal fracture Extremity fracture Hemopneumothorax Spinal epidural hematoma Abdominal trauma Clavicula fracture No associated injury

No. of patients 7 7 3 2 3 2 1 2 14 3 10 3 24

Internal neurolysis was added to external neurolysis according to the perioperative observations of the surgeon. If the nerve was found to be extremely compressed and the fascicle was thought to be tighten by adhesions then internal neurolysis was performed. The process of internal neurolysis involves division with or without removal of the external epineurium and then dissection in the plane of investing extrafascicular internal epineurium. Removal of extrafascicular connective tissue is performed, taking care not to enter the fascicular perineurium (Fig. 3).[24] If there was not a defect in the anatomic continuity of the brachial plexus and only nerve compression was found, the operation was finalized by performing neurolysis. If a problem on the continuity of the nerve was detected, end to end

(a)

(b)

2 2 1 1 1 2 21

*Some of the patients had multipl additional injuries.

Figure 1. External neurolysis. (a) Nerve contained within surrounding scar. (b) Nerve is dissected from scar in plane around the external epineurium.

one had a hemopneumothorax, two patients had clavicular fractures, and one patient had a firearm injury in abdomen and a left radius fracture (Table 1). Fourteen patients had isolated supraclavicular and three patients had infraclavicular injuries. The remaining 10 patientsâ&#x20AC;&#x2122; injuries were both supraclavicular and infraclavicular. Three patients were diagnosed with an avulsion.

Surgical Technique Patients were operated according to their neurological examination and electromyographic findings. MRI was also used in some of the patients with root avulsions in order to evaluate the presence of meningocele.

Figure 2. Transposition. Nerve is transposed to a location that is not subject to repetitive mechanical trauma.

(a)

(b)

(c)

All of the patients received general anesthesia during surgery. Operations were done according to the approaches demonstrated in the previous literature.[19,20,21] An anterior approach was selected for all of the cases.[22,23] Exploration of the brachial plexus and external neurolysis were performed in every case. When a chronically injured nerve is surgically exposed, it is typically scarred and adherent to surrounding tissue. External neurolysis can is a technique in which the nerve is released from its local tethering (Fig. 1). And if feasible, the nerve is translocated to a site that is not mechanically traumatized (Fig. 2). This process does not intentionally violate the epineurium and vascular supply of the nerve.[24] Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

Figure 3. Internal neurolysis. (a) The external epineurium is removed using microsurgical technique. (b) The scarred internal epineurium is dissected, separating the individual fascicles, taking care not to violate the perineurium. (c) The dissected fascicles with some residual epineural scar.

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Time Delay To Surgery

Table 2. Operation types and numbers Operation method

Number

Ex Neu Ex + In Neu Ex + In Neu End to end Single n An Ex + In Neu + Fasiculus An Ex + In Neu+ Sural n G of avulsed C5 root Ex + In Neu+ Neuroma Exc + Neur G Ex + In Neu+ IC n Neurotisation

16 5 2 1 1 1 1

Ex: External; In: Internal; Neu: Neurolysis; An: Anastomsis; Exc: Excision; IC: Intercostal; n: Nerve; Neur: Neurogen; G: Grafting.

anastomosis was performed. The most common intraoperative finding was compression of the neural elements due surrounding fibrotic tissue. The total number of each type of operation are given in Table 2. Patient 11 underwent surgery in another clinic 2 months ago before her admission to our department; it was learned that she had undergone an ulnar to second intercostal nerve anastomosis. An exploration and external neurolysis was performed in our clinic, however her intractable neuropathic pain did not resolved. An additional DREZ operation was performed for pain control, seven months later.

Fifteen patients underwent surgery in less than six months following the injury, 12 patients had surgery later than six months. The patients who were operated in the first six months after trauma represented significantly better scores in DASH, SF-36 and pain scale; pre-operative pain scale scores (PSS) were similar for both groups (p<0.05) (Table 4).

Presence of Avulsion

Avulsion was present in three cases (Figure 4). These patientsâ&#x20AC;&#x2122; preoperative PSS scores were significantly higher compared to the ones without avulsion. Although the preoperative scores were higher in the patients with avulsion, the long term postoperative PSS scores were not significantly different than the other group of patients (Table 5). All the parameters related with DASH and SF-36 were not significantly different between patients with and without avulsions.

Localization of Injury When comparing the functional outcome results for different types of injuries, there was not a difference between supraclavicular, infraclavicular, or both types of injuries (Table 3).

Table 3. Patient demographics Pat. No Age/Sex Location Side 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27

50/F 51/M 25/M 20/M 66/M 41/M 47/M 44/M 10/M 26/M 37/F 33/F 26/M 18/M 46/M 23/M 15/M 37/M 24/F 28/M 21/F 27/M 30/M 30/M 44/F 20/M 17/F

Supra Both Supra Both Supra Both Infra Infra Supra Both Both Both Supra Supra Infra Both Supra Both Both Supra Supra Supra Supra Both Supra Supra Supra

Main limitation (weakness <3/5)

R AAb, EEb, EFc L AAb, EE, EF, WE, WFc, Gc L Flail arm L Flail arm L Flail arm R Flail arm L EEb L EE, WE, WE, G L AAb, EF, WEc L EE, EF, WE, WF, G R Flail arm L AAbb, EEc, EF, WE, WF, G L AAb, EE, EF, WEc, WFc, Gc L AAbb, EF, EE, WE, WF, G L EE, EFb, WE, WF, G R AAb, EE, EF, WE R AAb, EEb, EF, WEc, WFb, Gc L AAbc, EFc, WEb, WFc R EEb, EFc, WE, WFb L AAb, EEc, EF, WFc L AAbc, Gc L Flail arm L AAb, EE, EF, WEb, WFb, Gc R Flail arm L AAbb, EE, EF, WE, WF R EEb, EFb, WEc L AAbb, WFc, WE, G

Injury to OR Foll. Up DASH (mo) (mo) 12 8 6 5 7 3 2 3 9 2 6 6 3 8 2 3 2 2 3 4 13 8 17 15 12 5 12

48 50 54 68 58 64 81 71 102 98 120 102 120 123 121 132 159 158 156 34 28 26 22 20 17 19 98

SF-36 SF-36 PCS MCS

PSS PSS Pre-op Now

59.4 40.7 36.5 70.6 40.4 32.4 54.3 44.5 26.5 70.6 37.5 22.8 95.8 27.3 28.6 67.2 31.5 24.7 52.5 39.8 26.8 27.5 46.3 45.7 39.2 47.5 47.4 55 25.0 34.6 68.1 35.1 22.8 40 41.8 37.4 51.7 40.8 25.6 81.8 35.1 21.8 12.9 58.9 51.4 74.2 26.4 26.3 29.2 50.2 48.1 21.7 46.1 48.4 24.2 46.6 50 20.0 47.0 41.6 24.1 54.6 54.7 69.8 36.7 42.9 79.3 25.4 22.3 65.5 36.9 25.0 81.8 35.3 22.8 18.1 48.3 43.3 26.7 47.5 47.6

70 10 10 60 80 70 30 70 10 30 80 20 10 90 70 90 70 85 10 20 80 40 70 70 90 60 30

30 10 10 40 50 50 70 20 10 20 100 10 10 20 0 40 10 15 10 10 10 40 70 50 90 20 10

R: Right; L: Left; Supra: Supraclavicular; Infra: Infraclavicular; M: Male; F: Female; mo: Months; DASH: Disability of the Arm, Shoulder and Hand; SF-36: Short Form 36; PCS: Physical component summary; MCS: Mental component summary; OR: Operation; AAb: Abduction of the arm; EE: Elbow extension; EF: Elbow flexion; WF: Wrist flexion; WE: Wrist extension; G: Grip; bPower was 3/5, cPower was 4/5.

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was not a statistically significantly difference for DASH and SF-36 scores.

The Effect of Additional Injuries Six patients had additional injuries other than Brachial Plexus Injury. The presence of additional injuries did not significantly change the scores of the DASH, SF-36 and PSS assessments.

Side

Figure 4. Operation photograph of a patient with penetrating glass injury. A. Two tips of the avulsed upper truncus. B. Middle truncus.

The Effect of Weakness on Outcome For analyzing the effect of preoperative weakness on outcome; the patients were grouped to two groups; patients having BMRC grade 0/5, 1/5, 2/5 and patients having BMRC grade 3/5, 4/5, 5/5 for each muscle group. Deltoid, triceps, biceps, wrist flexors, wrist extensors and distal interosseous muscle group’s strengths were evaluated. For only the distal interosseous muscle group, it was found that patients having muscle strength less than 3/5 preoperatively have significantly worse results for post PSS 0.03 (Mann-Whitney U). There

There were 8 patients with right side TBPI and 19 patients with left side TBPI. All of the patients were right handed. No statistical differences were seen between the two groups on the DASH or SF-36 scores. Neither questionnaire focuses on the side of the injury. Answers are based on the ability to perform the activity, regardless of how the activity was performed. So there is potential bias for the patients with an injury on the nondominant side. This is a particular concern in the DASH questionnaire, as the questions had been chosen for those tasks in which both hands/arms/shoulders must be used like “ Can you open a tight or new jar? ” or “ Can you use a knife to cut food? ”. Another aspect of this study is to determine the effect of TBPI surgery’s effect on the life of the patient. So, comparing the right and left side would also be important from this point of view. It is possible that a greater number of patients are needed to make an objective comparison, because not all of the right and left dominant patients had a homogenous distribution. But according to these results, as all of the patients were right hand dominant, left sided BPI patients had better results than the opposite side.

DISCUSSION With the contribution of modern technology to the medi-

Table 4. Mann-Whitney U test Patients operated in 0-6 months of injury Patients operated after 6 months of injury p (Mean±SD) (Mean±SD) DASH

42.2±21.6

62.4±22.6 0.026

PCS (SF-36)

51.3±7.0

41.8±9.4

0.015

MCS (SF-36)

46.9±12.0

39.4±11.9

0.032

Pre-op APS

55.3±30.5

55.9±29.9

0.173

Post-op APS

13.0±5.9

34.1±26.4

0.020

DASH: Disability of the Arm, Shoulder and Hand; SF-36: Short Form 36; PCS: Physical component summary; MCS: Mental component summary; APS: Analog pain scale.

Table 5. Mann-Whitney U test

Patients with avulsion Patients without avulsion (Mean±SD) (Mean±SD)

p

Pre-op analog pain scale

85.0±8.7

51.9±29.4

0.029

Post-op analog pain scale

13.3±5.8

23.5±21.7

0.463

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Aras et al., Functional outcomes after brachial plexus surgery

cine, a parallel increase is obtained in the success of peripheral nerve surgery. The usage of an operating microscope has increased the success rates in all divisions of neurosurgery including peripheral nerve surgery. TBPI lesions are mostly seen in young adults who were otherwise healthy and this injury limits the social and professional life of the victim. As a common mistake of physicians, we generally consider the objective findings of the patients like muscle strength and sensory performance instead of subjective symptoms like pain or feeling of well-being. But a patient may have a normal motor and sensory function with intractable pain. In contrast, a patient’s severe pain may be relieved but his/her motor status may not improve. Thus, when evaluating the success of a surgical procedure, like BPI surgery, we must also take into account the subjective changes in the patients’ feelings such as pain status, emotional state and desire to return to work. There are few studies regarding TBPI patients’ functional outcomes, feelings and QOL in the literature.[2,10,11] There is an increased need for evaluating the QOL of these patients. In this study we want to represent our clinical experience with analyzing our patients’ QOL assessment. Compatible with the literature,[2,6,25-27] the results of this study demonstrated that patients who underwent surgery for BPI within the first six months of injury have better functional outcomes compared with patient who waited longer. In the current series, patients operated in the first six months of trauma scored significantly better results in SF36, DASH and PSS assessments. According to our clinical practice, immediate surgery, without waiting for electrophysiological evaluation should be performed on the patients who had a penetrating TBPI. Neurologists who carry out electrophysiological tests recommend to perform these tests 21 days after trauma.[28,29] The initial three weeks of healing prior to testing theoretically decreases testing artefacts. In the light of these data, we think the best timing for a blunt BPI surgery is between 3 weeks and 6 months after trauma. Perhaps future studies can be designed to investigate the comparable outcomes of patients operated in the first 3 months and 4th to 6th months of trauma. In the present study, the mean time from trauma to surgery was 6.6 months. Considering that the six month window is a critical period for a BPI patient to undergo surgery, referral of these patients needs to be improved. This is a common problem involving both patients and physicians in treatment of TBPI.[2,6] An epidemiological study by Midha stated that 78% of multitrauma patients with BPI were diagnosed within the first 3 days of injury.[30] Thus, this problem may be overcome by increasing the awareness of this pathology among the physicians in other disciplines who infrequently encounter this 526

pathology. Flores stated that they improved this problem by means of workshops and discussions related to the necessity of early investigation of the cases among other physicians.[27] Some authors, like Magalon et al.,[31] advocate for very early surgery for TBPI patients, as they believe regardless of associated vascular or bone injuries, brachial plexus lesions should be repaired within the first 7 days after injury. They stated that it is easier to operate early because relatively shorter grafts can be used. While this can be true for penetrating injuries, some patients may be unnecessarily operated on due to the inability to perform neurophysiological tests in the early days after injury.[6,31] From the point of localization, there is a debate in the literature. Some authors stated that supraclavicular elements are injured more severely and have a worse prognosis.[30,32] Whereas others disagree with this argument.[6,11] We did not find a significant difference between the SF-36, DASH and APS scores of patients with supraclavicular, infraclavicular or mixed type of injury localization. Flores advocated that normal or near normal post-traumatic motor function status of the hand is one of the most important preoperative parameters for obtaining good outcomes. [27] For the current study this was not the case. The preoperative strength of each muscle group were analyzed according to the scores the patients reported and there was not a significant difference in any muscle group for PSS/DASH/SF-36 assessments. The preoperative PSS of the patients with avulsions were significantly higher compared to the ones without avulsion. Although their preoperative scores were higher, the long term postoperative PSS were not significantly different than the patients without avulsion. This finding is concordant with the results of Labib’s studies.[2] They also found that patients with avulsions had worse scores for pain and SF-36. Since this main tissue which is strived on is nerve, evaluation of the success of the TBI surgery must depend on long follow-up periods. This period is estimated as 2-3 years according to some authors[5,33] and 4 years for others.[34] The mean follow-up period for the current study is 79 months which is quite long enough. According to our experience, patients who were operated for BPI benefit more from the point of pain than muscle strength. In other words, patients who were underwent surgery may not have a significant improvement in their muscle strength but they have significantly less pain after the operation. This was also stressed in the previous literature.[11] The importance of informing patients about this issue preoperatively is important in providing an adequate expectation and satisfaction from the operation and prevent frustration.[11] Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Aras et al., Functional outcomes after brachial plexus surgery

One of the limitations of the present study is the absence of preoperative SF-36 and DASH scores of the patients, ideally these scores could be compared with current scores. Also, another limitation of this study is the lack of current neurological examination of the patients, as we do not exactly know their muscle strengths. All of the patients at least had an external neurolysis procedure in this study. Only a small number of patients had nerve grafting. Comparing with the literature, our rate of grafting is lower than the average. We attributed this finding to late referral. The mean time for admission from injury was 6.6 months in the present study. We believe nerve grafting is more efficient when performed shortly after injury, thus, in our patients who were referred months after injury, nerve grafting was performed only for a small number. Nevertheless, external neurolysis was performed for the management of pain in all cases. The importance of delayed referral of BPI patients to specialized centers has been stressed in previous literature.[6,35,36] Norkus et al.[26] published a study of 14 patients and concluded that neurolysis or nerve transfer in the early stage (first 12 months) and tendon transfer in the late stage of brachial plexus injury may result in significant improvement. In the present study, there is an insufficient number of patients for comparing the operation methods as only three patients underwent an anastomosis, two patients underwent nerve transfers and one patient underwent neurotisation. Studies examining the correlation between patient’s self-assessment and physician’s examination can be designed in the future.

Conclusions Statistically validated tests like SF-36 and DAS questionnaires are valuable tools for evaluating the BPI patients. Specialized centers dealing with TBPI surgery may use these tests preand postoperatively which will lead to an objective personalized evaluation of each patient’s subjective symptoms.

4. Millesi H. Surgical management of brachial plexus injuries. J Hand Surg Am 1977;2:367-78. 5. Narakas A. Brachial plexus surgery. Orthop Clin North Am 1981;12:30323. 6. Dubuisson AS, Kline DG. Brachial plexus injury: a survey of 100 consecutive cases from a single service. Neurosurgery 2002;51:673-83. 7. Kandenwein JA, Kretschmer T, Engelhardt M, Richter HP, Antoniadis G. Surgical interventions for traumatic lesions of the brachial plexus: a retrospective study of 134 cases. J Neurosurg 2005;103:614-21. 8. Kline DG, Tiel RL. Direct plexus repair by grafts supplemented by nerve transfers. Hand Clin 2005;21:55-69. 9. Secer HI, Solmaz I, Anik I, Izci Y, Duz B, Daneyemez MK, et al. Surgical outcomes of the brachial plexus lesions caused by gunshot wounds in adults. J Brachial Plex Peripher Nerve Inj 2009;4:11. 10. Choi PD, Novak CB, Mackinnon SE, Kline DG. Quality of life and functional outcome following brachial plexus injury. J Hand Surg Am 1997;22:605-12. 11. Kretschmer T, Ihle S, Antoniadis G, Seidel JA, Heinen C, Börm W, et al. Patient satisfaction and disability after brachial plexus surgery. Neurosurgery 2009;65:189-96. 12. Solway S, Beaton DE, McConnell S, Bombardier C. The DASH outcome measure user’s manual. 2nd ed. Toronto: Institute for Work & Health; 2002. 13. Beaton DE, Davis AM, Hudak P, McConnell S. The DASH (Disabilities of the Arm, Shoulder and Hand) outcome measure: what do we know about it now? British Journal of Hand Therapy 2001;6:109-18. 14. About the DASH. http://www.dash.iwh.on.ca/about.htm. Accessed February 25, 2006. 15. McHorney CA, Ware JE Jr, Lu JF, Sherbourne CD. The MOS 36-item Short-Form Health Survey (SF-36): III. Tests of data quality, scaling assumptions, and reliability across diverse patient groups. Med Care 1994;32:40-66. 16. McHorney CA, Ware JE Jr, Raczek AE. The MOS 36-Item ShortForm Health Survey (SF-36): II. Psychometric and clinical tests of validity in measuring physical and mental health constructs. Med Care 1993;31:247-63. 17. Hunsaker FG, Cioffi DA, Amadio PC, Wright JG, Caughlin B. The American academy of orthopaedic surgeons outcomes instruments: normative values from the general population. J Bone Joint Surg Am 2002;84-2:208-15. 18. Ware JE Jr, Sherbourne CD. The MOS 36-item short-form health survey (SF-36). I. Conceptual framework and item selection. Med Care 1992;30:473-83.

Acknowledgements

19. Birch R, Bonney G, Wynn Parry CB. Surgical disorders of the peripheral nerves. Edinburgh: Churchill Livingstone; 1998.

The present work was not supported by any fund or organization.

20. Kline DG, Hudson AR. Nerve injuries: operative results for major nerve injuries, entrapments, and tumors. Philadelphia: W.B. Saunders; 1995.

REFERENCES

22. Davis DH, Onofrio BM, MacCarty CS. Brachial plexus injuries. Mayo Clin Proc 1978;53:799-807.

1. Kim DH, Cho YJ, Tiel RL, Kline DG. Outcomes of surgery in 1019 brachial plexus lesions treated at Louisiana State University Health Sciences Center. J Neurosurg 2003;98:1005-16. 2. Ahmed-Labib M, Golan JD, Jacques L. Functional outcome of brachial plexus reconstruction after trauma. Neurosurgery 2007;61:1016-23. 3. Ricardo M. Surgical treatment of brachial plexus injuries in adults. Int Orthop 2005;29:351-4.

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21. Leffert RD. Brachial plexus injuries. New York: Churchill Livingstone; 1985.

23. Kline DG, Judice DJ. Operative management of selected brachial plexus lesions. J Neurosurg 1983;58:631-49. 24. Burchiel KJ, Ochoa JL. Surgical management of post-traumatic neuropathic pain. In: Burchiel KJ, editor. Neurosurgery Clinics of North America. Surgical Management of Peripheral Nerve Injury and Entrapment. Philadelphia: W.B. Saunders; 1991. p. 117-21. 25. Jivan S, Kumar N, Wiberg M, Kay S. The influence of pre-surgical delay

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31. Magalon G, Bordeaux J, Legre R, Aubert JP. Emergency versus delayed repair of severe brachial plexus injuries. Clin Orthop Relat Res 1988;237:32-5. 32. Narakas AO. The treatment of brachial plexus injuries. Int Orthop 1985;9:29-36. 33. Terzis JK, Papakonstantinou KC. The surgical treatment of brachial plexus injuries in adults. Plast Reconstr Surg 2000;106:1097-1124. 34. Samii M, Carvalho GA, Nikkhah G, Penkert G. Surgical reconstruction of the musculocutaneous nerve in traumatic brachial plexus injuries. J Neurosurg 1997;87:881-6. 35. Kanaya F, Gonzalez M, Park CM, Kutz JE, Kleinert HE, Tsai TM. Improvement in motor function after brachial plexus surgery. J Hand Surg Am 1990;15:30-6. 36. McGillicuddy JE. Clinical decision making in brachial plexus injuries. Neurosurg Clin N Am 1991;2:137-50.

KLİNİK ÇALIŞMA - ÖZET OLGU SUNUMU

Travmatik brakiyal plesus yaralanmaları cerrahisi sonrası fonksiyonel sonuçlar: Klinik çalışma Dr. Yavuz Aras, Dr. Aydın Aydoseli, Dr. Pulat Akın Sabancı, Dr. Mehmet Osman Akçakaya, Dr. Görkem Alkır, Dr. Murat İmer İstanbul Üniversitesi İstanbul Tıp Fakültesi, Nöroşirürji Anabilim Dalı, İstanbul

AMAÇ: Bu çalışmanın amacı istatistiksel geçerliliği olan değerlendirme araçları kullanılarak fonksiyonel sonuçları ve hastaların yaşam kalitesini incelemektir. GEREÇ VE YÖNTEM: Hastalar telefon ile arandı. Kısa form-36 (SF-36), el-kol ve omuz maluliyet değerlendirme anketi (DASH), bir ağrı derecelendirme testi hastalar tarafından dolduruldu ve hastaların uygulanan cerrahi ile ilgili memnuniyeti sorgulandı. BULGULAR: İ.Ü. İstanbul Tıp Fakültesi, Nöroşirürji Kliniği’nde 1997-2010 yılları arasında travmatik brakiyal pleksus yaralanması (TBPY) tanısıyla toplam 33 hasta tek bir cerrah tarafından (MI) ameliyat edildi. Üç hasta değerlendirmeye katılmayı reddetti ve üç hasta çalışmaya alınmadı. Toplamda 27 hasta, ortalama 79.6 aylık takip süresi ile çalışmaya alındı. TBPY’nin en sık nedeni motorlu araç kazaları idi. On dört hastada izole supraklaviküler, üç hastada ise infraklaviküler yaralanma vardı. Kalan 10 hastada yaralanmalar hem supra- hem infraklavikülerdi. Üç hastada kök avülsiyonuna rastlandı. Travma sonrası ilk altı ay içinde ameliyat edilen hastaların SF-36, DASH testleri ve ağrı dereceleri, diğer hastalara göre belirgin şekilde daha iyi olarak bulundu. TARTIŞMA: SF-36 ve DASH gibi istatistiksel geçerliliği olan testler TBPY hastalarının değerlenmesinde kullanılabilecek değerli araçlardır. TBPY ile ilgilenen özelleşmiş merkezler için, bu testlerin ameliyat öncesi ve sonrası dönemde uygulanmasıyla hastaların öznel şikayetlerinin nesnel olarak değerlendirilmesi mümkündür. Anahtar sözcükler: Brakiyal pleksus; fonksiyonel sonuçlar; sinir yaralanması; yaşam kalitesi. Ulus Travma Acil Cerr Derg 2013;19(6):521-528

528

doi: 10.5505/tjtes.2013.48107

Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


ORIGIN A L A R T IC L E

Factors affecting mortality caused by falls from height Mustafa İçer, M.D., Cahfer Güloğlu, M.D., Murat Orak, M.D., Mehmet Üstündağ, M.D. Department of Emergency Medicine, Dicle University Faculty of Medicine, Diyarbakır

ABSTRACT BACKGROUND: Falls from height are among the most common trauma cases presenting to emergency departments and often cause mortality and morbidity. In the present study, we aimed to determine the factors that effectively reduce mortality caused by falls from height. METHODS: Data from 2252 trauma patients who presented to Dicle University Emergency Service between January 2005 and December 2008 due to falling from height in the Southeastern Anatolia region were retrospectively analyzed. We analyzed the parameters that are considered to have a positive effect on mortality, which included the following: month of fall; age; gender; etiology; place of fall; type of ground on which the patient fell; height of fall; intubation; hypotension; tachycardia; neck, head, thoracal, abdominal, pelvic, and extremity injuries; Glasgow Coma Score (GCS); Injury Severity Score (ISS); and Revised Trauma Score (RTS). RESULTS: There were 1435 males (63.7%) and 817 females (36.3%) included in the study. Two thousand thirty-one (94.6%) patients survived the fall while 121(5.4%) died. The mean age of the surviving patients was 15.55±18.60 years, while the patients who died had a mean age of 29.59±28.93 years. The mean height of the fall of the survivors’ was 3.09 meters, and the mean height of the fall for those that died was 6.61±5.73 meters (p<0.001). CONCLUSION: The mean fatal height of the fall in falls from height is 6.61 m. Age, attempted suicide, height of fall, type of ground on which the patient fell, place of fall, and head, thoracic, and abdominal trauma are the primary factors affecting mortality caused by falls from height. Key words: Fall from height; height of fall; hemopneumothorax; mortality; subarachnoid hemorrhage.

INTRODUCTION

MATERIALS AND METHODS

Falls from height are a leading cause of traumas, second only to traffic accidents. They are the most common cause of trauma in childhood, and are responsible for 5.90% of all deaths during childhood in developed countries.[1] In addition, falls rank first among admissions to emergency services related to trauma and injuries,[2] and account for 25-34% of admissions to the emergency room in the United States of America.[3] Falls from height cause blunt body trauma. Many factors can affect the prognosis, such as age, fall height, cause of fall, type of ground on which the patient fell, the injured body parts, and organ injury. In this study, we aimed to examine the factors affecting mortality caused by falls from height.

Data from 2252 trauma patients who presented to Dicle University Emergency Service between January 2005 and December 2008 due to falling from height in the Southeastern Anatolia region were retrospectively analyzed. Patients were consecutively enrolled. All patients were examined by emergency services. All patients were resuscitated according to the ATLS (Advanced Trauma Life Support) program and were diagnosed and treated in compliance with available protocols. Detailed information about the trauma was obtained from the patient, the patient’s family, paramedics, police records, or witnesses. Patient data were recorded on standard forms. Patients with incomplete or missing data or those having trauma from simple falls, falls from moving vehicles (cars, bicycle, horse-donkey), electric shock, or those who were dead at presentation were excluded from the study.

Address for correspondence: Mustafa İçer, M.D. Dicle Üniversitesi Tıp Fakültesi Acil Tıp Anabilim Dalı, 21280 Diyarbakır, Turkey Tel: +90 412 - 248 85 38 E-mail: drmicer@mynet.com Qucik Response Code

Ulus Travma Acil Cerr Derg 2013;19(6):529-535 doi: 10.5505/tjtes.2013.77535 Copyright 2013 TJTES

Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

To assess mortality rate, patients were divided into the following two groups: survivors and those that died. We examined parameters considered important for mortality as follows: month of fall; age; gender; cause of fall (workplace accident, suicide, other accidents); place of fall (fall off the roof, balcony, window, stairs, tree, domestic furniture, construction scaffold, hammock, lap); other types of fall (fall into 529


İçer et al., Factors affecting mortality caused by falls from height

a hole, stairwell, elevator shaft, well, fall off the wall, cliffs); type of ground on which the patient fell; fall height; intubation; hypotension; tachycardia; neck, head, thoracic, pelvic, abdominal, and extremity injuries; GCS; ISS; and RTS.

Table 1. Demographic characteristics of cases with fall from height

n

%

0-3

495

22

4-6

521

23

7-15

552

25

16-25

204

9

26-54

303

13

≥55

177

8

82

3.64

Univariate analyses were performed using the Chi-Square test (X2) for categorical variables and the Student’s t test for continuous variables. Multivariate logistic regression analysis (Backward-Wald Step-Wise Model) was used to detect risk factors for mortality. Continuous variables are presented as Mean ± SD (Standard Deviation). A p value less than 0.05 was considered statistically significant.

Age distribution (years)

RESULTS

Seasonal distribution

Among the 2252 trauma patients presenting with fall from height, 1435 (63.70%) were male and 817 (36.30%) were female. Two thousand one hundred and thirty-one (94.60%) patients survived and 121 (5.40%) died. Among those who died, 84 (69.40%) were male and 37 (30.60%) were female (Table 2). The patients ranged in age from 1 month to 95 years, with 48% between 4-15 years of age. The greatest number of presentations occurred in August, and the most common mode of fall was falling off the roof. Table 1 presents the patient distribution in terms of age, season, place, cause, and type of ground on which the falls occurred. Assessing the patient mortality in terms of age revealed that those patients between 7-15 years and 4-6 years had the lowest mortality (2.35%, p=0.001; 3.45%, p=0.015, respectively) while patients aged 55 years or greater had the highest mortality (19.20%, p=0.001). Suicidal falls had the highest mortality (20.50%, p=0.001). Furthermore, 79.50% of suicidal falls were from greater than 7 meters and 46.20% were from more than 10 meters. Mortality rates in terms of place of fall, in descending order, were falls from roofs, balcony/windows, and construction scaffolds (p=0.001, p=0.018, and p=0.023, respectively). Also, the outcomes of patients falling on solid grounds compared to those falling on soft grounds were statistically significant (p<0.001). The effects of fall height were also statistically significant, with mortality increasing as fall height increases. Among the 71 patients already intubated at admission, 24 (33.80%) survived and 47 (66.20%) died. Forty-eight (65.80%) of the 73 patients who presented with hypotension survived while 25 (34.20%) died. Among 264 tachycardic patients, 191 (72.30%) survived and 73 (27.70%) died. Mortality was higher among intubated, hypotensive, and tachycardic patients (p<0.001). Clinical and demographic data of the patients that died and those that survived are presented in Table 2. The ratios of system injuries in surviving and dying patients are presented in Table 3. The effect of head, thoracic, abdominal, and maxillofacial trauma on mortality was statistically signifi530

January February

71

3.15

March

121

5.37

April

164

7.28

May

189

8.39

June

272

12.07

July

336

14.96

August

386

17.14

September

244

10.83

October

191

8.48

November

81

3.59

December

115

5.10

Cause of fall

Workplace accident

Suicide

Other accidents

153

7

39

2

2060

91

Place of fall Roof

1056

46.90

98

4.35

Stairs

162

7.19

Tree

104

4.61

Balcony/window

Domestic furniture

78

3.46

Construction scaffold

103

4.57

Hammock

20

0.90

Lap

21

0.90

Others

608

27

Soft

493

21.90

Hard

1759

78.10

Ground of fall

cant (p<0.001, p=0.003). Among pathologies related to head trauma, neurologic deficit, cerebral edema, cranial fracture, epidural hematoma (EDH), subdural hematoma (SDH), subarachnoid hemorrhage (SAH), intracerebral hematoma (ICH), cerebral contusion, and pneumocephalus had a statistically significant effect on mortality. (p=0.008, p<0.001, p=0.006, Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


İçer et al., Factors affecting mortality caused by falls from height

Table 2. Clinical and demographic data of patients that died and those that survived

Survived

n

%

Died

Total

n %

n %

p

Gender distribution Male

1351 94.10

84 5.90

1435 100

Female

780 95.50

37 4.50

817 100

Total

2131 94.60

121 5.40

2252 100

0-3

468 94.55

27 5.45

495 100

0.501

4-6

503 96.55

18 3.45

521 100

0.015

7-15

539 97.65

13 2.35

552 100

0.001

16-25

193 94.60

11 5.40

204 100

0.544

26-54

285 94.05

18 5.95

303 100

0.359

≥55

143 80.80

34 19.20

177 100

0.001

140

13 8.50

153 100

0.091

0.206

Age distribution (years)

Cause of fall

Workplace accident

91.50

Suicide

31 79.50

39 100

0.001

Others

1960 95.10

100 4.90

8 20.50

2060 100

0.001

981 92.90

75 7.10

1056 100

0.001

Balcony/window

87 88.80

11 11.20

98 100

0.018

Stairs

156 96.30

6 3.70

162 100

0.467

Place of fall Roof

Tree

103

99

1 1

104 100

0.041

Domestic furniture

77

98.70

1 1.30

78 100

0.124

Construction scaffold

92

89.30

11 10.70

103 100

0.023

2 10

20 100

0.292

Hammock

18 90

Lap

21 100

0 0

21 100

0.625

Others

594 97.70

14 2.30

608 100

<0.001

Soft

491 99.60

2 0.40

493 100

<0.001

Hard

1640 93.20

119 6.80

1759 100

Ground of fall

Fall height

3 m or lower

1663

97.70

39 2.30

1702 100

<0.001

3.1-6 m

345

88.70

44 11.30

389 100

<0.001

6.1-9.9 m

57

85

10 15

67 100

0.003

10 m or higher

66

70.20

28 29.80

94 100

<0.001

Intubation

24 33.80

47 66.20

71 100

<0.001

Hypotension

48 65.80

25 34.20

73 100

<0.001

Tachycardia

191 72.30

73 27.70

264 100

<0.001

p=0.002, p=0.001). The effect of orbital fracture in maxillofacial trauma on mortality was statistically significant (p=0.021). Among thoracic injuries, rib fracture, pneumothorax, lung contusion, and hemopneumothorax had a statistically significant effect on mortality (p<0.001). Intraabdominal free fluid presence in abdominal trauma was significantly associated Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

with mortality (p<0.001). The effect of pelvic fracture in extremity traumas on mortality was also significant (p<0.05). Surviving patients (n=2131) had a mean age of 15.55±18.60 years, a mean fall height of 3.09 meters, a mean RTS of 11.90±0.46, a mean ISS of 8.76±7.63, and a mean GCS of 531


İçer et al., Factors affecting mortality caused by falls from height

Table 3. Distribution of patients that died and those that survived by system injuries

Survived

%

n %

Total

p

n %

Head trauma

505 85

89 15

594 100

<0.001

Neurologic deficit

19

79.20

5

20.80

24

100

0.008

Diffuse axonal injury

2

67.70

1

33.30

3

100

0.153

Cerebral edema

140

79.10

37

20.90

177

100

<0.001

Cranial fracture

372

86.30

59

13.70

431

100

<0.001

Epidural hematoma (EDH)

66

86.80

10

13.20

76

100

0.006

Subdural hematoma (SDH)

54

68.40

25

31.60

79

100

<0.001

Subarachnoid hemorrhage (SAH)

22

37.90

36

62.10

58

100

<0.001 0.002

Intracerebral hematoma (ICH)

19

76

6

24

25

100

Cerebral contusion

61

84.70

11

15.30

72

100

0.001

Pneumocephalus

56 77.80

16 22.20

72 100

<0.001

Maxillofacial trauma

114

92.70

9

7.30

123

100

0.003

Maxillar fracture

26

86.70

4

13.30

30

100

0.074

Mandibular fracture

25

92.60

2

7.40

27

100

0.654

Orbital fracture

46

86.80

7

13.20

53

100

0.021

Nasal fracture

28

96.60

1

3.40

29

100

1

Thoracic trauma

92

76.70

28

23.30

120

100

<0.001

Rib fracture

42

75

14

25

56

100

<0.001

Sternal fracture

0

0

1

100

1

100

0.054

Hemothorax

27 81.80

6 18.20

33 100

0.070

Pneumothorax

25 69.40

11 30.60

36 100

<0.001

25

10

35

<0.001

Lung contusion

Hemopneumothorax

532

n

Died

71.40

8 61.50

28.60

100

5 38.50

13 100

<0.001

Abdominal trauma

300

89.30

36

10.70

336

100

<0.001

Intraabdominal free fluid

281

89.50

33

10.50

314

100

<0.001

Hepatic injury

34

87.20

5

12.80

39

100

0.055

Splenic injury

53

91.40

5

8.60

58

100

0.237

Retroperitoneal hematoma

2

66.70

1

33.30

3

100

0.153

Renal injury

22

91.70

2

8.30

24

100

0.373

Urinary bladder injury

1

50

1

50

2

100

0.105

Extremity trauma

563

95.30

28

4.70

591

100

0.459

Cervical vertebral fracture

10

83.30

2

16.70

12

100

0.133

Thoracic vertebral fracture

46

93.90

3

6.10

49

100

0.745

Lumbal vertebral fracture

81

94.20

5

5.80

86

100

0.806

Sacral vertebral fracture

6

100

0

0

6

100

1

Scapular fracture

16

18.80

3

81.20

16

100

0.051

Clavicular fracture

21

84

4

16

25

100

0.042

Humeral fracture

111

94.10

7

5.90

118

100

0.678

Radial fracture

153

96.20

6

3.80

159

100

0.465

Ulnar fracture

92

95.80

4

4.20

96

100

0.816

Femoral fracture

165

93.20

12

6.80

177

100

0.384

Tibial fracture

56

94.90

3

5.10

59

100

1

Fibular fracture

40

95.20

2

4.80

42

100

1

Metacarpal fracture

6

100

0

0

6

100

1

Metatarsal fracture

5

100

0

0

5

100

1

Calcaneal fracture

51

91.10

5

8.90

56

100

0.223

Pelvic fracture

79

88.80

10

11.20

89

100

0.026

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İçer et al., Factors affecting mortality caused by falls from height

Table 4. Mean values of age, fall height, and trauma scores

Result

n Mean SD*

Age

Died

Survived 2131 15.55 18.60

Fall height (m)

Died

Survived 2131 3.09 2.77

p

121 29.59 28.93 <0.001 121

6.61

5.73

RTS

Died

Survived 2131 11.90 0.46

<0.001

121 8.14 3.55 <0.001

ISS

Died

Survived 2131 8.76 7.63

121 24.72 9.13 <0.001

GCS

Died

Survived 2131 14.37 1.82

121 7.74 4.29 <0.001

SD: Standard deviation.

14.37±1.82. The 121 patients that died had a mean age of 29.59±28.93 years, a mean fall height of 6.61±5.73 meters, a mean RTS of 8.14±3.55, a mean ISS of 24.72±9.13, and a mean GCS of 7.74±4.29. Fall height, age, RTS, ISS, and GCS had statistically significant effects on mortality (p<0.001) (Table 4). All variables shown in univariate analyses to be effective on mortality (p<0.05) were included in logistic regression. In multivariate analysis, hemopneumothorax (95% confidence interval=9.621-939.915, Odds Ratio=9509.23, p=0.009), and SAH (95% confidence interval=4.747-157.928, Odds Ratio=2737.96, p=0.015) were the most significant independent variables affecting mortality.

DISCUSSION Falls from height constitute a large number of trauma patients presenting to emergency services. The factors affecting mortality in falls are very complex. Injuries due to falls from height are usually severe multi-organ injuries related to the skeletal muscles and solid organs.[4] The mortality risk is affected by the fall height, the body part hitting the ground, and the type of ground on which the fall occurred.[5] Mortality and morbidity of trauma in falls from height depend on impact velocity, the injured organ(s), and the resulting pathologies.[6-8] Deaths due to falls from height result from multiple blunt traumas, especially head trauma.[9] A1 et al.[10] reported a mortality rate of 2.20% due to falls from height. That study included all cases presenting with trauma due to a fall, as did our current study. Falls from higher heights often have greater mortality than those that are from lower heights. Liu et al.[11] reported a mortality rate of 22.70% due to falls from above 6 m, while Lapostolle et al.[12] reported a mortality rate of 33.80% due to falls from above 3 m. In our study, the mortality rate due to falls from above 10 m was similar to the figures derived from those studies. Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

In the study by Yagmur et al.[13] 67 of 1220 patients died from falls from height, and 29 of these patients were older than 15 years. Goren et al.[14] studied 484 postmortem cases, and found that their mean age was 27.05 years (range 4-100 years). Agalar et al.[15] reported that age was one of the important prognostic factors affecting the severity of the trauma after vertical free fall. Lapostolle et al.[12] found that age was one of the independent prognostic variables in those who died from falls from height. Another study reported that children younger than 3 years sustained fewer injuries than did older children falling from the same height. The authors hypothesized that this is because the younger children have more fat and cartilage and a lesser amount of muscular tissue, which leads to a better transfer of energy.[16] Driscoll et al.[17] reported that 44% of patients older than 75 years had fatal falls from height and that the mortality risk increased as age increased above 55 years. We also found that mortality was the highest in those older than 55 years, while the mortality rates were significantly lower in those patients between 4-6 years and 7-15 years. We believe that the anatomic and physiologic differences between children and the elderly may cause the significant differences in mortality between these groups. In the study by Goren et al.,[14] of the 484 postmortem cases examined, 431 were related to accidents while 53 were related to suicide attempts. In the study by Lapostolle et al.,[12] 123 of 287 cases were due to suicide and 45.50% of them died. In our study, the rate of mortality in suicide cases was lower than that reported by Laposotlle et al. This is most likely because the patients in that study fell from a height ≥ 3 m. We speculate that the increased fall height was an important factor for the relationship between the suicide cases and mortality. Yagmur et al.[13] reported a mortality rate of 5.80% in 1643 cases that fell off the roof. Goren et al.[14] found that the majority of deaths due to falls were due to falls from the roof 533


İçer et al., Factors affecting mortality caused by falls from height

(56, 36.7%), balcony (108, 25.1%), and stairs (57, 13.2%). Falls off the rooftops, balcony/windows, and construction scaffolds are most likely more fatal since they often occur from an increased fall height, land on a solid ground, and lead to a higher rate of life-threatening injuries such as head, thoracic, and abdominal injuries. The type of ground on which the fall occurs, the mode of the fall, and the general health status of the victim are the most important factors influencing the severity of the injury.[12,18] In our study, falling on solid ground increased severity of trauma and organ damage, and therefore we determined that it was a major factor affecting mortality. The severity of the injury is typically proportional to the fall height.[19] Most childhood fatalities from falls occur from floor 3 or above.[20,21] Scalea et al.[22] reported a mortality rate of 4.90% in patients falling from 3 meters or above. In a retrospective study, Liu et al.[11] reported a mortality rate of 22.70% in 66 patients falling from 6 meters or above. Hawley et al.[23] reported a significantly increased mortality in patients falling from 6 meters and reported a threshold of 6 meters for fatal fall heights for individuals below 15 years of age. In our study, compared with mortality of falls from 3 m or below, the mortality rates associated with falls from 3-6 m, 6-10 m, and 10 m and above were increased 5, 6.50, and 13 times, respectively (Table 2). Based on this data, we predict a lower mortality in falls from 3 m or below but expect a higher mortality in falls from 6-10 m and above. An association between hypotension and tachycardia, which are important symptoms of blood loss in major trauma, and mortality has been reported in literature.[24] Many studies have reported an increased mortality in intubated patients. [25-27] The mortality rates of patients in our study who arrived intubated, hypotensive, and tachycardic were consistent with the literature findings. Goren et al.[14] found that the most frequently affected body part was the head (91%) in 484 postmortem cases that had fallen or jumped from height. The other effected body parts, in descending order, were thorax (54%), abdomen (37%), extremities (36%), and neck (17%). A study from India that autopsied 80 patients who died from falls from height reported that head traumas were associated with the highest mortality. [28] Multiple organ failure and brain injury were the most common causes of death in another study examining falls from height.[29] Consistent with the literature, in our study, the patients who died most commonly had head trauma. Goodacre et al.[30] reported head trauma as a factor affecting mortality. Lapostolle et al.[12] identified age, fall height, ground of fall, and the first body part hitting the ground as the independent prognostic factors affecting mortality in cases falling from above 3 m. Liu et al.[11] reported head trauma and chest trauma as mortality factors, and reported severe head 534

trauma as an independent prognostic mortality factor. These studies reported an association between the affected body part and mortality, but did not report a relationship between the clinical diagnosis at the affected part and mortality. We examined both the affected body part and the relationship between the clinical diagnoses and mortality and found that SAH and hemopneumothorax were independent prognostic factors affecting mortality. In conclusion, the mean fatal height in falls from height is 6.61 m. Age, suicide, fall height, type of ground on which the fall took place, place of fall, as well as head, thoracic, and abdominal trauma affect mortality. Hemopneumothorax and SAH were the most important independent factors affecting mortality in our study. Conflict of interest: None declared.

REFERENCES 1. Taviloğlu K, Aydin A, Cuhali BD, Demiralp T, Güloğlu R, Ertekin C. The evaluation of the suitability of our cases for referral to a level I trauma center. Ulus Travma Derg 2001;7:146-50. 2. CeylanS, Açıkel CH, Dündaröz R, Yaşar M, Güleç M, Özışık T. Bir eğitimhastanesi acil servisine travma nedeniyle başvuran hastaların sıklığının ve travma özelliklerinin saptanması. Türkiye Klinikleri Tıp Bilimleri 2002;22:156-61. 3. Park SH, Cho BM, Oh SM. Head injuries from falls in preschool children. Yonsei Med J 2004;45:229-32. 4. Lowenstein SR, Yaron M, Carrero R, Devereux D, Jacobs LM. Vertical trauma: injuries to patients who fall and land on their feet. Ann Emerg Med 1989;18:161-5. 5. Chalmers DJ, Marshall SW, Langley JD, Evans MJ, Brunton CR, Kelly AM, et al. Height and surfacing as risk factors for injury in falls from playground equipment: a case-control study. Inj Prev 1996;2:98-104. 6. Mathis RD, Levine SH, Phifer S. An analysis of accidental free falls from a height: the ‘spring break’ syndrome. J Trauma 1993;34:123-6. 7. Warner KG, Demling RH. The pathophysiology of free-fall injury. Ann Emerg Med 1986;15:1088-93. 8. Lehman D, Schonfeld N. Falls from heights: a problem not just in the northeast. Pediatrics 1993;92:121-4. 9. Türk EE, Tsokos M. Blunt cardiac trauma caused by fatal falls from height: an autopsy-based assessment of the injury pattern. J Trauma 2004;57:301-4. 10. Al B, Yildirim C, Coban S. Falls from heights in and around the city of Batman. Ulus Travma Acil Cerrahi Derg 2009;15:141-7. 11. Liu CC, Wang CY, Shih HC, Wen YS, Wu JJ, Huang CI, et al. Prognostic factors for mortality following falls from height. Injury 2009;40:595-7. 12. Lapostolle F, Gere C, Borron SW, Pétrovic T, Dallemagne F, Beruben A, et al. Prognostic factors in victims of falls from height. Crit Care Med 2005;33:1239-42. 13. Yagmur Y, Güloğlu C, Aldemir M, Orak M. Falls from flat-roofed houses: a surgical experience of 1643 patients. Injury 2004;35:425-8. 14. Goren S, Subasi M, Týrasci Y, Gurkan F. Fatal falls from heights in and around Diyarbakir, Turkey. Forensic Sci Int 2003;137:37-40. 15. Agalar F, Cakmakci M, Sayek I. Factors effecting mortality in urban vertical free falls: evaluation of 180 cases. Int Surg 1999;84:271-4. 16. Meller JL, Shermeta DW. Falls in urban children. A problem revisited.

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İçer et al., Factors affecting mortality caused by falls from height Am J Dis Child 1987;141:1271-5. 17. Driscoll TR, Mitchell RJ, Hendrie AL, Healey SH, Mandryk JA, Hull BP. Unintentional fatal injuries arising from unpaid work at home. Inj Prev 2003;9:15-9. 18. Mc Swain NE. Kinematics of trauma. In: Mattox KL, Feliciano DV, Moore EE, editors. Trauma 4th ed. NewYork: McGraw-Hill; 2000. p. 127-51. 19. McSwain NE, Shaftan GW. Blunt trauma after vertical deceleration. Postgrad Surg 1990;2:140-5. 20. Sieben RL, Leavitt JD, French JH. Falls as childhood accidents: an increasing urban risk. Pediatrics 1971;47:886-92. 21. Spiegel CN, Lindaman FC. Children can’t fly: a program to prevent childhood morbidity and mortality from window falls. Am J Public Health 1977;67:1143-7. 22. Scalea T, Goldstein A, Phillips T, Sclafani SJ, Panetta T, McAuley J, et al. An analysis of 161 falls from a height: the ‘jumper syndrome’. J Trauma 1986;26:706-12. 23. Hawley CA, Ward AB, Long J, Owen DW, Magnay AR. Prevalence of traumatic brain injury amongst children admitted to hospital in one health district: a population-based study. Injury 2003;34:256-60. 24. Spahn DR, Cerny V, Coats TJ, Jacques Duranteau J, Mondéjar EF, Gordini G, et al. Management of bleeding following major trauma: a Euro-

pean guideline. Critical Care 2007;11:1-22. 25. Denninghoff KR, Griffin MJ, Bartolucci AA, Lobello SG, Fine PR. Emergent endotracheal intubation and mortality in traumatic brain injury. West J Emerg Med 2008;9:184-9. 26. Davis DP, Peay J, Sise MJ, Vilke GM, Kennedy F, Eastman AB, et al. The impact of prehospital endotracheal intubation on outcome in moderate to severe traumatic brain injury. J Trauma 2005;58:933-9. 27. Arbabi S, Jurkovich GJ, Wahl WL, Franklin GA, Hemmila MR, Taheri PA, et al. A comparison of prehospital and hospital data in trauma patients. J Trauma 2004;56:1029-32. 28. Venkatesh VT, Kumar MV, Jagannatha SR, Radhika RH, Pushpalatha K. Pattern of skeletal injuries in cases of falls from a height. Med Sci Law 2007;47:330-4. 29. Aufmkolk M, Voggenreiter G, Majetschak M, Neudeck F, Schmit-Neuerburg KP, Obertacke U. Injuries due to falls from a great height. A comparative analysis of injuries and their outcome following suicide-related and accidental falls. [Article in German] Unfallchirurg 1999;102:525-30. [Abstract] 30. Goodacre S, Than M, Goyder EC, Joseph AP. Can the distance fallen predict serious injury after a fall from a height? J Trauma 1999;46:1055-8.

KLİNİK ÇALIŞMA - ÖZET OLGU SUNUMU

Yüksekten düşmelerde mortaliteyi etkileyen faktörler Dr. Mustafa İçer, Dr. Cahfer Güloğlu, Dr. Murat Orak, Dr. Mehmet Üstündağ Dicle Üniversitesi Tıp Fakültesi, Acil Tıp Anabilim Dalı, Diyarbakır

AMAÇ: Acil servislere başvuran travma hastaları içinde yüksekten düşmeler ilk sırada yer alır ve önemli oranlarda morbidite ve mortaliteye neden olur. Çalışmamızda yüksekten düşmelerde mortalite üzerine etkili faktörleri araştırmayı amaçladık. GEREÇ VE YÖNTEM: Bu çalışmada Ocak 2005 ile Aralık 2008 tarihleri arasında Güneydoğu Anadolu bölgesinde yüksekten düşme ile gelen ve Dicle Üniversitesi Hastanesi Acil Servisinde tedavi edilen 2252 travmalı hastaya ait veriler geriye dönük olarak analiz edildi. Mortalite üzerinde etkili olabileceğini düşündüğümüz; düşmenin olduğu ay, yaş, cinsiyet, düşme nedeni, düşme yeri, düşme zemini, düşme yüksekliği, entübasyon, hipotansiyon, taşikardi, baş boyun, göğüs, karın, pelvis, ekstremite yaralanması, Glasgow Koma Skalası (GKS), Injury Severity Score (ISS) ve Revize Travma Skoru’nu (RTS) içeren parametreleri inceledik. BULGULAR: Çalışmaya alınan hastaların 1435’i (%63.7) erkek, 817’si (%36.3) kadındı. Hastaların 2131’i (%94.6) yaşadı, 121’i (%5.4) öldü. Yaşayan hastaların yaş ortalaması 15.55±18.60 yıl, düşme yüksekliği ortalaması 3.09 metre iken, ölen hastaların yaş ortalaması 29.59±28.93 yıl, düşme yüksekliği ortalaması 6.61±5.73 metre idi (p<0.001). TARTIŞMA: Yüksekten düşmelerde ölümcül düşme yüksekliği ortalaması 6.61 m’dir. Yaş, intihar, düşme yüksekliği, düşme zemini, düşme yeri, kafa travması, göğüs travması ve karın travması mortaliteyi etkileyen faktörlerdir. Anahtar sözcükler: Yüksekten düşme; düşme yüksekliği; hemopnomotoraks; mortalite; subaraknoid kanama. Ulus Travma Acil Cerr Derg 2013;19(6):529-535

doi: 10.5505/tjtes.2013.77535

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ORIGIN A L A R T IC L E

An analysis of firearms-related deaths between 1993-2010: a retrospective study Mehmet Toygar, M.D.,1 Türker Türker, M.D.,2 Murat Eroğlu, M.D.,3 Ümit Kaldırım, M.D.,4 Yavuz Poyrazoğlu, M.D.,5 Yusuf Emrah Eyi, M.D.,6 Murat Durusu, M.D.,4 Mehmet Eryılmaz, M.D.4 1

Department of Forensic Medicine, GMMA School of Medicine, Ankara

2

Department of Public Health, GMMA School of Medicine, Ankara

3

Department of Emergency Medicine, GMMA Haydarpaşa Training Hospital, İstanbul

4

Department of Emergency Medicine, GMMA School of Medicine, Ankara

5

Department of General Surgery, Mevki Military Hospital, Ankara

6

Department of Emergency Medicine, Hakkari Military Hospital, Hakkari

ABSTRACT BACKGROUND: Firearm injuries (FI) are the most common cause of death among military personnel. In this study, postmortem examination and autopsy records of deaths resulting from firearm injuries recorded in the Department of Forensic Medicine of Gulhane Military Medical Academy between 1993-2010 were examined retrospectively. METHODS: We evaluated the characteristics of 153 firearm deaths accounting for 36.6% of all medical-legal autopsies. The cases included 152 men (99.3%) and 1 woman (0.7%). RESULTS: The mean age of the cases was 23.1 years (±4.7; range, 20-43 years). The manner of death was determined in all cases with 41.8% of cases identified as suicide and 39.9% as homicide. The most common sites of firearm entrance wounds were the head and neck region (n=109, 71.2%), the chest (n=26, 17%), or the abdomen (n=14, 9.2%). The type of firearm was not clear in most cases. CONCLUSION: In conclusion, complete forensic and medical records will facilitate the rapid and accurate conclusion of the legal process and will enhance future retrospective studies. Key words: Firearm deaths; homicide; suicide.

INTRODUCTION Firearm injury (FI) is one of the most important causes of death among military personnel.[1] According to the World Health Organization, firearms are used in two thirds of all homicide cases and one fifth of suicide cases.[2] According to data from the World Health Organization (WHO), 2.3 million people have died as a result of violence worldwide and 26% of these deaths were war-related deaths. Interpersonal violence, self-mutilation and injuries as a result of war are the Address for correspondence: Mehmet Toygar, M.D. Gülhane Askeri Tıp Akademisi, Adli Tıp Anabilim Dalı, Ankara, Turkey Tel: +90 312 - 304 48 64 E-mail: mehmetoygar@yahoo.com Qucik Response Code

Ulus Travma Acil Cerr Derg 2013;19(6):536-542 doi: 10.5505/tjtes.2013.70120 Copyright 2013 TJTES

536

most common causes of death in the 15-44 year age population all over the world.[2] In the USA, there are 30,000 firearm-related deaths every year.[3] In a study in Italy, while 27.7% of forensic autopsies were of deaths resulting from firearm injuries,[4] in India it has been reported that only 1.5% of forensic autopsies are of deaths resulting from firearm injuries.[5] In Turkey according to the data of National Statistical Institute (TurkStat), firearm injuries are the most common cause of homicides and the third cause of suicides following poisoning and hanging.[6,7] According to the 2008 data of TurkStat, 0.3% (749/215.562) of deaths were caused by firearms apart from deaths in warfare.[6] In our country, studies evaluating forensic cases have stated mortality rates of 8.2-27.7% from firearms injuries.[8-12] This study aimed to analyze the demographic data of cases of firearms injury which underwent an autopsy in our department and to compare that data with other studies. Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Toygar et al., An analysis of firearms-related deaths between 1993-2010

MATERIALS AND METHODS A retrospective examination was made of postmortem examination and autopsy records in the Department of Forensic Medicine of Gulhane Military Medical Academy of deaths resulting from firearms injuries between 1993-2010. Approval for the study was granted by the Local Ethics Committee. It was determined that examination and autopsy were conducted on a total of 417 forensic qualified cases. The records were examined of 153 (36.6%) of these deaths, which were firearms related. Explosive substance-related deaths were not included in the study. Cases were evaluated according to the autopsy records, age, gender, manner of death, site of entrance wound, exit wound location, length of stay in hospital, range of fire, type of firearm, whether bullets were obtained from the corpse or not, the number of bullets that hit the body and toxicological examinations.

RESULTS Demographic Characteristics In this study, examination and autopsy processes were conducted on 417 forensic qualified cases including 153 firearmsrelated death cases. These cases were 152 male (99.3%) and 1 female (0.7%) with a mean age of 23.1Âą4.7 years (range, 20-43 years).

Manner of Death Cases were examined according to the manner of death

and it was determined that 41.8% of the cases were suicide, 39.9% were homicide, 9.2% were accident and 9.2% were from other causes (non-specific origin in the medical and investigative documents).

Types of Firearms The type of firearm used was not clear in 59.5% of all cases. It was interesting that the type of firearm could not be determined in all the cases in which the manner of death could not be determined (Table 1).

Wound Characteristics The distribution of firearm entry wounds were evaluated according to the body parts; entry wound was in head and neck region of 109 (71.2%) of victims, in chest of 26 (17%), in abdomen of 14 (9.2%) and in lower extremity of 4 (2.6%). In the cases with multiple-entry wound, the vital localizations of entry wounds were considered. When the distribution of firearm exit wound of cases was evaluated according to the body parts. The exit wound was in the head and neck region of 96 (62.7%) cases, in the back of 30 (19.6%), in the abdomen of 8 (5.2%) and in the lower extremity of 4 (2.6%). It was also detected that 9 cases had no exit wound and in 6 cases the exit wound could not be defined because of atypical wound characteristics. In the cases with multiple-exit wounds, the vital localization of the exit wounds was considered.

Table 1. The type of firearm used according to the manner of death Types of firearms

Homicide

Suicide

Accident

Not-Specified

Total

n %

n %

n %

n %

n %

Long-barrelled

10 16.4

34 53.1

2 14.3

0 0

46 30.1

Short-barrelled 4 6.6 7 10.9 5 35.7 0 0 16 10.4 Not-Specified

47 77

Total

61 100 64 100 14 100 14 100 153 100

23 35.9

7 50

14 100

91 59.5

39.9 41.8 9.2 9.2 100

Table 2. Entry wound localization according to the manner of death Entry area

Homicide

n %

n %

n %

n %

Head-neck

44 72.1

45 70.3

9 64.3

11 78.6

Chest

10 16.4 11 17.2 3 21.4 2 14.3 26 17

Abdomen

5 8.2

8 12.5

1 7.1

0 0

14 9.2

Lower extremity

2 3.3

0 0

1 7.1

1 7.1

4 2.6

Total

61 100 64 100 14 100 14 100 153 100

Suicide

Accident

Not-Specified

Total n % 109 71.2

39.9 41.8 9.2 9.2 100

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Toygar et al., An analysis of firearms-related deaths between 1993-2010

When the entry wound localization was examined according to the manner of death, the head and neck was the most frequent site of wounding regardless of the manner of death (Table 2).

In the analysis of the type of weapon according to the range of fire, it was observed that cases in which the type of the weapon could not be determined, mostly consisted of cases in which the range of fire could not be determined (Table 3). When the range of fire was examined according to the manner of death of cases, it was striking that the range of fire could not be determined in most of the accidental firearm deaths (Table 4).

Range of Fire When the cases were evaluated according to the range of fire, while it was not clear in 43.1% of cases, there was, a contact/ near contact shot in 44.4%, a close shot in 4.6% and a distant shot in 7.8%. In the autopsy reports, the range of fire could not be defined in 43.1% of all cases and in 78.6% of accidental cases. This was because the shot was made to a clothed area or there had been medical intervention to the entry wound(s) (the identification of the features of the entry wounds were not made in the medical records before medical intervention, and the information about analysis results in terms of range of fire of perforated clothing was not found from the available data of shots made to a clothed area) (Table 3).

The Entry Wound Localization According to the Range of Fire When the entry wound localization of cases was examined according to the range of fire, the entry wound was in the head area in 62.4% of the cases with an undetermined shot (Table 5). It is interesting that cases with gunshot wounds in the chest and abdomen were not wounded with short-barrelled guns.

Table 3. The range of fire according to the type of firearm Range of fire

Long barrelled

Short barrelled

Not-specified

Total

n %

n %

n %

n %

Contact/near contact

26

38.2

8

11.8

34

50

68

44.4

Close

2

28.6

0

1.6

5

71.4

7

4.6

Distant

4 33.3

1 8.3

7 58.4

12 7.8

Undetermined

14 21.2

7 10.6

45 68.2

66 43.1

Total

46 30.1

16 10.4

91 59.5

153 100

Table 4. The range of fire according to the manner of death Range of fire

Homicide

Suicide

n %

n %

n %

n %

n %

Contact/near contact 18 29.5

42 65.6

2 14.3

6 42.9

68 44.4

1

1

2

7

4.9

Accident

1.6

Close

3

12 19.7 0 0 0 0 0 0 12 7.8

Undetermined

28 45.9

Total

61 100 64 100 14 100 14 100 153 100

11 78.6

14.3

Total

Distant

21 32.8

7.1

Not-Specified

6 42.9

4.6

66 43.1

Table 5. The entry wound localization according to the type of firearm Range of fire

538

Long barrelled

Short barrelled

Not-specified

Total

n %

n %

n %

Head-neck

26 23.8

15 13.8

68 62.4

109 71.2

Chest

13 50.0

0

-

13 50.0

26 17.0

Abdomen

6 42.9

0 -

8 67.1

14 9.2

Lower extremity

1

Total

46

25.0

1

25.0

16

2

50.0

91

n %

4

2.6

153 100

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Toygar et al., An analysis of firearms-related deaths between 1993-2010

Toxicological Review In the autopsy reports of firearm-related deaths, no toxic substance was determined in 55.6% of materials and xycain, ethyl alcohol, prilocaine, lidocaine, barbiturates, benzodiazepines and atropine were found in 3.9%. No toxicological review was applied to 39.9% of cases because of lengthy hospitalization and medical treatment.

Bullets When the cases were evaluated according to the number of bullets that hit the body, it was determined that 86.9% died with one bullet injury, 7.2% with two bullet injuries and 5.9% with three or more bullet injuries. Bullets were not retrieved in the autopsy of 94.8% of cases who died as a result of firearms injury, and were rerieved from 5.2% of cases and were handed over to the judicial authorities.

Death from Complications 61.4% of the cases died at the crime scene, during transport on the road or in the emergency services. In 55.3% of cases, the weapon type could not be ascertained, 35.1% were shot with a long-barrelled weapon and 9.6% with a short-barrelled weapon. Analysis of the cases who died at the crime scene, during transport on the road or in the emergency services determined the following data; 68.1% were injured in the head area, 21.3% in the chest and 9.6% in the abdomen; 63.8% were shot from a contact/near contact shot, 6.4% from a close shot,10.6% from a distant shot and the range of fire could not be determined in 19.1% of these cases; the origin was homicide in 36.2%, suicide in 46.8% and no clear origin was determined in 10.6%. In this study, the duration of hospitalization and medical treatment ranged from 1 day to 630 days. Hospitalization was less than 90 days in 96.1% of cases.

DISCUSSION In this study covering a period of 17 years between 19932010, 153 (36.6%) of the 417 forensic qualified cases that underwent examination and autopsy procedures originated from firearms. Previous studies in our country have reported this rate as between 7.4%- 27.7%.[8-12] In a study by Norton and Langley in New Zealand, this rate was 0.3%,[13] Nizamo et al[14] reported this rate as 8.7% in Mozambique, and Biago Solarino[4] determined this rate to be 27.7% in Italy. In the current study, this ratio is higher because the population served by our health center has access to firearms. Studies evaluating deaths from firearms injuries have shown that these deaths especially concern the 20-40 year group.[912] Parallel to literature, the cases in the current study ranged Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

from 20-43 years of age. In a study by Azmak et al in Edirne, the cases were primarily in the 21-30 years age group, followed by the 31-40 years age group.[8] In other studies in Iran (38.2%),[15] in Africa[16] and in India (46.7%) in a study by Kohli et al[5] it has been stated that cases were most common in the 20-30 years age group. Other studies in other regions such as Sweden, Germany, the United States and South Africa have also yielded similar results.[5,15-21] A contact/near contact shot is the range of fire in the majority of suicide cases,[8,22-25] while a close or distant shot has been the range of fire determined in the majority of homicide cases.[23,26] Druid identified that firearm wounds in homicides were made from a contact/near contact shot or a close shot and in 99% of suicide cases it was a close shot.[27] In a study by Azmak et al it was determined that the range of fire was mostly a distant shot, was not detected in 8% of cases, and was a contact shot in almost all suicide cases.[8] The range of fire could not be determined in 32.8% of suicide cases, because the shot had been made to a clothed area or there had been medical intervention to the entry wound. Definition of the entry wound features had not been entered in the medical records before medical intervention, so there was insufficient information in terms of range of fire in the data obtained from the analysis results of perforated clothing in a shot made to a clothed area. It is estimated that the majority of these cases were from a distant shot. When the cases of the current study were evaluated according to origin, it was determined that 39.9% were homicide. Although several studies have stated this rate as ranging between 62.2%-71.80%, it was determined by Solarino et al[4] as 88.4%, by Kellermann[28] as 88%, by Guileyardo[29] as 65%, by Riddick[30] as 53%, by Al Ragheb[31] as 51%, by Verzeletti et al[32] as 35.9%, and by Druid[27] as 18.7%. While the results of the current study are similar to those of some previous studies, they are also different from those of some others. In the current study, 41.8% were suicide cases. In several studies in our country this rate has been reported as between 11.70-32.7%[6,8,33-35] and in studies in other countries as 6.5-73.9%.[5,27,32] Researchers have reported a strong relationship between access to firearms and suicide.[36-38] In the current study, the suicide rate is higher than in other studies, which may be due to a high rate of accessibility to firearms of the study population. In the current study, 9.2% were accidental cases. This rate has been reported as ranging between 0.13-24% in previous studies.[4-6,8,11,33-35] Copeland and Ornehult made a detailed study of accidental firearms deaths together with crime scene investigation and it was reported that the firearms accidents could have occured as a result of playing with firearms, showing the weapon others or because of faulty firearms.[39,40] These features are similar to the findings of accidental deaths in the current study. 539


Toygar et al., An analysis of firearms-related deaths between 1993-2010

In studies by Azmak,[8] Al Ragheb,[31] Riddick,[30] Muscat,[41] Verzeletti[32] and Solarino[4] short barrelled weapon types were determined to have been used in homicide cases. In contrast, Druid stated that the weapon type most used in homicide cases was a shotgun and secondly, rifles. However, attention was also drawn to the fact that in 44% of homicide cases information about the weapon type could not be obtained.[27] In the current study, in most of the homicide cases (77%), the type of firearm could not be determined because information about the weapon type was not available (terrorism, medical intervention to patients in more than one place, attempts to firstly rescue the patients rather than assessing the judicial aspect of cases and therefore no record of the type of weapon in judicial records etc.). In the current study, the type of the firearm could not be determined in all cases in which the manner of death could not be determined. This may suggest a strong relationship between these two factors. In a study by Azmak et al,[8] the weapon type used in 50% of suicide cases was reported to be a handgun. In other studies, similar results have also been reported.[4,8,32,38] Al Ragheb,[31] Riddick[30] and Muscat[41] reported that while the handgun was common in suicide cases in the civil population, rifled weapons were common in military populations. The preferred weapon type in suicide cases of the current study was mostly long barrelled (53.1%), which is due to a higher rate of use of long barrelled weapons in the study population. In a study of homicides by Amiri, the most common entry wound site was reported as 42.6% head, 42.6% chest and 16.7% back,[15] which conforms with the results of previous studies.[8,15,30,31,35,41-44] Azmak reported that the entry wound was in the head (right temporal area, left temporal area and neck) in 65%, in the chest in 25% and in the abdomen in 10% of suicide cases.[8] AÄ&#x;ritmiĹ&#x;[46] reported that the most common entry wound localization is in the head-neck, chest and abdomen in children and adolescents. Similar findings have been reported in previous studies.[15,30,31,36,42,47] Di Maio[47] stated that in suicide cases with handguns and long barrelled weapons, the most common entry wound localization was in the head area, and this result is compatible with the findings of the current study. The gun type was identified when the entry wound localization was in the head-neck area in all cases of homicide. It can be seen that almost all the findings of the current study conform with the findings of other studies. Muscat[41] reported that the most commonly seen entry wound localization in homicide with a handgun is the headneck area. In homicide cases where a long-barrelled weapon had been used the most common entry wound localization has been reported as the chest area.[41] 540

Rates of single entry wound have been reported by Fedakar[35] as 70.9% of cases, by Amiri[15] as 65.2%, by Verzeletti[32] as 74.8%, by Kohli[5] as 77%, and by Azmak[8] as 74.1%. When the current study was evaluated according to single entry wound, the findings are consistent with literature. Azmak,[8] Kohli[5] and Goren[34] reported that the majority of cases that died as a result of firearms injury died at the crime scene, during transportation or in the emergency services. Similar to the findings of other studies, the majority of the cases in the current study died within 24 hours. Verzeletti[32] detected alcohol, amphetamines, opiates, cannabinoid, and cocaine in 35% of cases and Ĺ&#x17E;am[6] detected substances such as ethyl alcohol, stimulants, narcotics or psychoactivants in 24% of cases. Galea[48] identified positive drug results in more than half of cases and the most detected substances (24.2%) were cannabis (19.5%), opiates (9.6%), and alcohol (26.9%). Druid[27] identified an association between alcohol and the majority of murder and suicide cases. Bilban[49] identified alcohol in 68.8% of suicide cases who died as a result of firearms injury. Bosnar[50] reported significantly high blood alcohol concentrations in suicide cases that occurred with firearms in time of war. Alcohol has been found in 62% of homicide cases in Sweden[51] and 68.6% of murder cases in Norway.[52] According to literature, in the current study, substances were identified at very low rates in the toxicological analysis. The reason for this low rate is that the study group was living in an environment which was often checked in respect of substance abuse and where alcohol or other harmful substances were not permitted.

Conclusion As our department serves people who have been authorized to use firearms, firearms injuries are a more frequently encountered issue in our department than in other institutions relevant to the subject. However, it can be seen that there is no great difference in terms of demographic data. As the most common injury areas in firearms-related death and injury cases are localized in the head-neck and chest, taking precautions (hard hat, protective clothing etc.) in these areas is thought to decrease the number of injuries and deaths. The results of this study suggest a strong relationship between criminal findings such as non-identification of the type of firearm and range of fire and the manner of death and clarification of the incident. Attempting to make a medical intervention quite rightly to save life and thus focusing on a therapeutic direction creates problems in keeping detailed and proper records of medical interventions in these type of forensic cases and in the clarification of investigations. This leads to a prolonged legislative process and leaves some questions unanswered that should be answered by the official authorities. We think that keeping complete forensic and medical records will lead to a more rapid and accurate conclusion Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Toygar et al., An analysis of firearms-related deaths between 1993-2010

of the legal process and thus future retrospective research will be able to reflect more accurate and objective results. Conflict of interest: None declared.

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for discrimination between suicidal and homicidal gunshot injuries. Int J Legal Med 2002;116:273-8. 24. Stone IC. Characteristics of firearms and gunshot wounds as markers of suicide. Am J Forensic Med Pathol 1992;13:275-80. 25. Karlsson T. Multivariate analysis (‘forensiometrics’)--a new tool in forensic medicine. Differentiation between firearm-related homicides and suicides. Forensic Sci Int 1999;101:131-40. 26. Thomsen JL, Albrektsen SB. An investigation of the pattern of firearms fatalities before and after the introduction of new legislation in Denmark. Med Sci Law 1991;31:162-6.

3. Denton JS, Segovia A, Filkins JA. Practical pathology of gunshot wounds. Arch Pathol Lab Med 2006;130:1283-9.

27. Druid H. Site of entrance wound and direction of bullet path in firearm fatalities as indicators of homicide versus suicide. Forensic Sci Int 1997;88:147-62.

4. Solarino B, Nicoletti EM, Di Vella G. Fatal firearm wounds: a retrospective study in Bari (Italy) between 1988 and 2003. Forensic Sci Int 2007;168:95-101.

28. Kellermann AL, Rivara FP, Lee RK, Banton JG, Cummings P, Hackman BB, et al. Injuries due to firearms in three cities. N Engl J Med 1996;335:1438-44.

5. Kohli A, Aggarwal NK. Firearm fatalities in Delhi, India. Leg Med (Tokyo) 2006;8:264-8.

29. Guileyardo JM, Carmody TJ, Lene WJ, Stone IC. Racial and ethnic patterns in firearms deaths. Am J Forensic Med Pathol 1994;15:328-30.

6. Şam B, Kaya E.A, Özdemir M, Arpak B.B, Makça C. İstanbul’da 20032007 yılları arasında gerçekleşmiş ateşli silah yaralanmasına bağlı ölümler. 1. Uluslararası Avrasya Adli Bilimler Kongresi.

30. Riddick L, Wanger GP, Fackler ML, Carter RD, Hoff CJ, Jinks JM, et al. Gunshot injuries in Mobile County, Alabama: 1985-1987. Am J Forensic Med Pathol 1993;14:215-25.

7. Turkish Statistical Institute. Death Statistics Province and District Centers 2008.

31. Al Ragheb SY. Firearm fatalities in Jordan. Med Sci Law 1984;24:21321.

8. Azmak D, Altun G, Bilgi S, Yilmaz A. Firearm fatalities in Edirne, 19841997. Forensic Sci Int 1998;95:231-9.

32. Verzeletti A, Astorri P, De Ferrari F. Firearm-related deaths in Brescia (Northern Italy) between 1994 and 2006: a retrospective study. J Forensic Leg Med 2009;16:325-31.

9. Salaçin S. An analysis of the medicolegal autopsies performed in Adana, Turkey, in 1983-1988. Am J Forensic Med Pathol 1991;12:191-3. 10. Çoltu A, Durak D. A retrospective examination of forensic autopsies of 141 firearm wound cases. J Forensic Med (in Turkish) 1992;8:49-51.

33. Günaydın G, Demirci S. Konya’da 1991-2000 yılları arasında atesli silah yaralanması nedeniyle ölen 248 olgunun degerlendirilmesi. Yıllık Adli Tıp Toplantıları Antalya 2002, 2002. s. 308-13.

11. Karagöz YM, Karagöz SD, Atilgan M, Demircan C. An analysis of 133 firearm deaths. In: 2nd Congress of Forensic Sciences, Bursa, May 13-16, 1996.

34. Goren S, Subasi M, Tirasci Y, Kemaloglu S. Firearm-related mortality: a review of four hundred-forty four deaths in Diyarbakir, Turkey between 1996 and 2001. Tohoku J Exp Med 2003;201:139-45.

12. Ertürk S, Ege B, Karaali H. Different ways of firearm injuries in forensic medicine. J Forensic Med (in Turkish) 1989;5:27-32.

35. Fedakar R, Gündoğmuş UN, Türkmen N. Firearm-related deaths in two industrial cities of Turkey and their province. Leg Med (Tokyo) 2007;9:14-21.

13. Norton R, Langley J. Firearm related deaths in New Zealand 1978-87. N Z Med J 1993;106:463-5. 14. Nizamo H, Meyrowitsch DW, Zacarias E, Konradsen F. Mortality due to injuries in Maputo City, Mozambique. Int J Inj Contr Saf Promot 2006;13:1-6. 15. Amiri A, Sanaei-Zadeh H, Towfighi Zavarei H, Rezvani Ardestani F, Savoji N. Firearm fatalities. A preliminary study report from Iran. J Clin Forensic Med 2003;10:159-63.

36. Avis SP. Suicidal gunshot wounds. Forensic Sci Int 1994;67:41-7. 37. Wiebe DJ. Homicide and suicide risks associated with firearms in the home: a national case-control study. Ann Emerg Med 2003;41:771-82. 38. Boyd JH. The increasing rate of suicide by firearms. N Engl J Med 1983;308:872-4. 39. Copeland AR. Accidental death by gunshot wound--fact or fiction. Forensic Sci Int 1984;26:25-32.

16. Meel B. Trends in firearm-related deaths in the Transkei region of South Africa. Am J Forensic Med Pathol 2007;28:86-90.

40. Ornehult L, Eriksson A. Fatal firearm accidents in Sweden. Forensic Sci Int 1987;34:257-66.

17. Meel BL. Firearm fatalities in the Transkei region of South Africa, 19932004. S Afr Med J 2005;95:963-7.

41. Muscat JE, Huncharek MS. Firearms and adult, domestic homicides. The role of alcohol and the victim. Am J Forensic Med Pathol 1991;12:105-10.

18. Karger B, Billeb E, Koops E. Accidental firearm fatalities. Forensic and preventive implications. Int J Legal Med 2002;116:350-3.

42. Selway R. Gunshot suicides in Victoria, Australia, 1988. Med Sci Law 1991;31:76-80.

19. Onuminya JE, Ohwowhiagbese E. Pattern of civilian gunshot injuries in Irrua, Nigeria. S Afr J Surg 2005;43:170-2.

43. Selway R. Firearm fatalities in Victoria, Australia 1988. Med Sci Law 1991;31:167-74.

20. Ikeda RM, Gorwitz R, James SP, Powell KE, Mercy JA. Trends in fatal firearm-related injuries, United States, 1962-1993. Am J Prev Med 1997;13:396-400.

44. Rammelsberg JO, Nowak R. Homicide by gunshot. An evaluation of 50 homicides with reference to gunshot wound site. [Article in German] Arch Kriminol 1999;203:65-72. [Abstract]

21. Hardt-Madsen M, Simonsen J. Firearms fatalities in Denmark 19701979. Forensic Sci Int 1983;23:93-8.

45. Betz P, Peschel O, Eisenmenger W. Suicidal gunshot wounds--site and characteristics. [Article in German] Arch Kriminol 1994;193:65-71. [Abstract]

22. Ropohl D, Koberne F. Fatal shotgun use in peace time. [Article in German] Beitr Gerichtl Med 1990;48:339-48. [Abstract] 23. Karger B, Billeb E, Koops E, Brinkmann B. Autopsy features relevant

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46. Ağritmiş H, Yayci N, Colak B, Aksoy E. Suicidal deaths in childhood and adolescence. Forensic Sci Int 2004;142:25-31.

541


Toygar et al., An analysis of firearms-related deaths between 1993-2010 47. Di Maio VJM. Gunshot wounds – practical aspects of firearms, ballistics and forensic techniques. New York: Elsevier; 1985. p. 294-7. 48. Galea S, Ahern J, Tardiff K, Leon AC, Vlahov D. Drugs and firearm deaths in New York City, 1990-1998. J Urban Health 2002;79:70-86. 49. Bilban M, Skibin L. Presence of alcohol in suicide victims. Forensic Sci Int 2005;147:9-12. 50. Bosnar A, Stemberga V, Coklo M, Koncar GZ, Definis-Gojanovic M,

Sendula-Jengic V, et al. Suicide and the war in Croatia. Forensic Sci Int 2005;147 Suppl:13-6. 51. Sjögren H, Eriksson A, Broström G, Ahlm K. Quantification of alcoholrelated mortality in Sweden. Alcohol Alcohol 2000;35:601-11. 52. Nordrum I, Eide TJ, JŁrgensen L. Alcohol in a series of medico-legally autopsied deaths in northern Norway 1973-1992. Forensic Sci Int 2000;110:127-37.

KLİNİK ÇALIŞMA - ÖZET OLGU SUNUMU

1993-2010 yılları arasında gerçekleşmiş ateşli silah yaralanmasına bağlı ölümler: Geriye dönük çalışma Dr. Mehmet Toygar,1 Dr. Türker Türker,2 Dr. Murat Eroğlu,3 Dr. Ümit Kaldırım,4 Dr. Yavuz Poyrazoğlu,5 Dr. Yusuf Emrah Eyi,6 Dr. Murat Durusu,4 Dr. Mehmet Eryılmaz4 Gülhane Askeri Tıp Akademisi, Adli Tıp Anabilim Dalı, Ankara Gülhane Askeri Tıp Akademisi, Halk Sağlığı Anabilim Dalı, Ankara 3 Gülhane Askeri Tıp Akademisi Haydarpaşa Eğitim Hastanesi, Acil Tıp Anabilim Dalı, İstanbul 4 Gülhane Askeri Tıp Akademisi, Acil Tıp Anabilim Dalı, Ankara 5 Mevki Asker Hastanesi, Genel Cerrahi Kliniği, Ankara 6 Hakkari Asker Hastanesi, Acil Tıp Kliniği, Hakkari 1 2

AMAÇ: Ateşli silah yaralanmaları (ASY) askeri personelin en sık ölüm sebebidir. Bu çalışmada, Gülhane Askeri Tıp Akademisi Adlı Tıp Anabilim Dalı’na 1993-2010 yılları arasında ateşli silah yaralanmasına bağlı ölümlere ait postmortem muayene ve otopsi kayıtlarının geriye dönük analizi amaçlandı. GEREÇ VE YÖNTEM: Olguların 153’ünün (%36.6) ateşli silah kaynaklı olduğu gözlendi. Olguların %99.3’ü erkek (n=152), %0.7’si kadın idi (n=1). Yaş ortalaması 23.1±4.7 yıl (20-43 yıl) idi. BULGULAR: Olgular ölüm biçimine göre değerlendirildiğinde %41.8’i intihar, %39.9’u cinayetti. En sık atesli silah giriş bölgesi sırasıyla baş-boyun 109 (%71.2), toraks 26 (%17) ve abdomen 14 (%9.2) idi. Olguların çoğunda ateşli silah tipi belli değildi. TARTIŞMA: Sonuç olarak adli ve tıbbi kayıtların tam ve düzgün tutulmasının yasal sürecin doğru ve hızlı sonuçlanmasına ve ileride yapılacak geriye dönük araştırmalarda daha doğru ve objektif sonuçların yansıtılmasına neden olacağı kanaatindeyiz. Anahtar sözcükler: Ateşli silah ölümleri; cinayet; intihar. Ulus Travma Acil Cerr Derg 2013;19(6):536-542

542

doi: 10.5505/tjtes.2013.70120

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ORIGIN A L A R T IC L E

A new application technique of circular fixator for the treatment of open tibial fractures: circular fixator-hinge technique Bilal Demir, M.D., Sami Sökücü, M.D., Erdem Özden, M.D., Umut Yavuz, M.D., Serda Duman, Yavuz Selim Kabukçuoğlu, M.D. Department of Orthopedics and Traumatology, Metin Sabancı Baltalimani Bone and Joint Disease Hospital, Istanbul

ABSTRACT BACKGROUND: The purpose of this study is to present and validate a hinge-fixator technique for the treatment of open tibial fractures, which has advantages in application and the follow up period. METHODS: The technique was used in open tibia fractures of 14 adult patients. Using this method, initial anatomic reduction was achieved and temporary stability was obtained on the hinge-fixator after applications were completed. Patients’ radiological and clinical results were analyzed using the Paley’s criteria at the time of the last follow-up. RESULTS: Patients were brought in for followed up analysis over a 5.4 year period. According to Paley, two patients had ‘good’ and 12 patients had ‘excellent’ radiological results, while the functional result were excellent (n=13) and good (n=1), respectively. CONCLUSION: The hinge-fixator technique is a fast and easy method that contributes to shorter operation times, reduced radiation exposure, and more comfortable treatment periods. Key words: Circular fixator; hinge technique; tibia fracture.

INTRODUCTION External fixators have long been used for fracture treatment. Since the introduction of the Ilizarov method, these fixators have gained the widespread use. Nevertheless, the basic principles of fixation techniques have not been changed, although intensive technologic developments have been recorded.[1-4] Even though the circular fixators are not the first choice for the treatment of simple fractures, they are often preferred for complex fractures associated with soft tissue damage. [5,6] One of the greatest advantages of the circular fixators are their application to various traumatic extremities with a reduction in infection rates.[7,8] The most important disadvanAddress for correspondence: Bilal Demir, M.D. 67. Ada 4/11, Kardelen Sitesi, Daire.19, Ataşehir 34758 Istanbul, Turkey Tel: +90 212 - 323 70 75 E-mail: bilalbirkandemir@yahoo.com Qucik Response Code

Ulus Travma Acil Cerr Derg 2013;19(6):543-547 doi: 10.5505/tjtes.2013.47936 Copyright 2013 TJTES

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tages of the method are patient discomfort during the follow up, patient compliance adjustments are needed, and external fixation devices are more difficult to learn compared to other methods.[9-11] The purpose of this study is to present the circular fixator technique for the treatment of open tibial fractures. Our findings demonstrate that the circular fixator technique has major advantages in application and in the follow up period for treating open tibial fractures. Using this technique, the fragments are fixated to a simple hinge-fixator frame and the final stabilization is performed after the fracture is reduced. In addition, the duration of the operation can be shortened and the traction of the pins and wires harming the soft tissue by tension is minimized. Thus a more comfortable treatment option is facilitated.

MATERIALS AND METHODS The method was used in open tibial fractures of 14 adult patients. Ten of the patients were male and four were female with the mean age of 41.3 years (range 24-58). Tibial fractures were located on the right side in 10 patients and on the left side in four patients. Based on the AO classification system, there was one patient with type A2, one A3, one B1, five B2, two B3, two C1 and two C2 fractures, respectively. 543


Demir et al., Circular fixator-hinge technique

Figure 1. Hinge system was obtained by combining three offsets where each offset is perpendicular to the former one. The hinges can freely move in coronal, sagittal and transverse planes as a natural result of this binding style (The numbers 1,2,3 depicts offsets and Schanz pin in the picture). One hinge is prepared for each major fragment.

According to the Gustilo-Anderson classification, there were three cases of grade 2 fractures, three cases of grade 3a, six cases of grade 3b, and two cases of grade 3b. The most frequent etiologic factors for fractures were motorbike and car accidents. Standard anterior-posterior (AP) and lateral graphics were obtained for surgical planning as well as for the follow-up. The lengths of the extremities were evaluated by comparing with the opposing tibia if the fractures were comminuted or segmented. All patients underwent operative treatment within an average of 10.7 hours after the injury (range from five hours to seven days). All operations were performed in supine position, under fluoroscopic guidance by the same surgical team on a radiolucent operating table. 10 patients had general anesthesia whereas four had spinal block anesthesia. A tourniquet was not used in any of the patients. In two Gustilo-Anderson grade 3b fracture cases, flap coverage of the skin defects were performed before the fixator application. Duration of operation, intra-operative fluoroscopy time, and number of maneuvers performed for reduction of the fractures were recorded in the operation theater. The accompanying fractures were also treated in the same session but the data were collected just for the tibial fractures. The time spent in the external fixator and time-to-weight bearing/walking were also recorded. All data were collected by reviewing the patients’ medical records. Patients’ radiological and clinical results were evaluated according to the Paley’s criteria at the time of last follow-up. [12,13] On the plain radiographs, angles between the anatomic axis of the proximal and distal segments were evaluated, 544

Figure 2. Fragments are fixed by Schanz pins sent through the hinges. The picture shows a-a` and b-b` as amount of fracture displacement. At this stage, reduction was still not performed.

while varus-valgus or procurvation-recurvation deformities were recorded. Complications were also recorded according to Paley’s complication classification.[14]

Surgical Technique In this hinge-fixator system, first the standard circular fixator frames were prepared. The hinge system was obtained by combining three offsets (a standard component of fixator elements), where each offset was connected perpendicular to the former one. As a result, the hinge system was able to perform free rotational movement in coronal, sagittal, and transverse planes (Figure 1). Separate hinge systems were prepared and connected to the medial side of the rings for each fracture segment. These segments were fixed with Schanz screws inserted through the hinge system (Figure 2). Reduction of the fracture site was obtained by longitudinal traction. Rotation was controlled by checking the alignment of the anterior tibial crest of the distal fragment with the proximal part. After achieving anatomical reduction (which

Figure 3. The photograph of leg after reduction, the fracture is fixed temporarily on the hinge-fixator. Antero posterior and lateral views showed a nearly anatomic reduction.

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Demir et al., Circular fixator-hinge technique

was confirmed by fluoroscopy), the screws of the hinge system were tightened. Thus, the fracture was fixated in an anatomic position with the fixator frame (Figure 3). Subsequently, the stabilization was achieved by applying the wires and completing the fixator application (Figure 4). If the fracture was segmented, a separate fixator-hinge level was used for the middle major fragment. For these types of fractures, reduction was applied for each segment, and the length of the extremity was adjusted according to the opposing tibia or according to the fibular length.

a wire break and fortunately did not require any additional surgery. Solid osseous union was achieved with all patients. Patients were followed up 5.4 (3-8) years. At the final visit, patients were graded according to Paleyâ&#x20AC;&#x2122;s radiologic scale.

(a)

(b)

(c)

(d)

RESULTS The mean duration of the operation was 61.14 (45-100) minutes, and the intra-operative fluoroscopy usage was 6.4 (5-12) images/patient. The average number of maneuvers performed for the reduction of the fractures was 2.7 (2-4) times. The average post-operative hospitalization period was 3.5 (2-8) days. None of the patients required additional reduction after surgery. Time to full weight bearing walking after surgery was 2.78 days. The number of postoperative follow up visits was 3.9 (3-7) times. The mean time spent in external fixator was 5.1 (4-5.8) months. According to pin tract infection classification of Paley, 12 patients had grade 1 (inflammation) and five patients had grade 2 (soft tissue infection) pin tract infection. One patient had

Figure 4. After reduction, the desired stabilization is obtained by completing the fixator application. Antero posterior and lateral graphics of a cruris at postoperative four months which reveals union.

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Figure 5. Fixator should be modified according to surgical procedure. (a) Radiologic anterior-posterior view, (b) pre-operative photograph of the cruris (c) a modified fixator applied and (d) follow up imaging.

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Two patients were good (one patient had 10 degrees translation deformity and one patient had 15 degrees recurvation deformity) and 12 patients were excellent. According to the clinical evaluation, 13 patients were excellent and one patient was good (2 cm shortness). No rotational deformity was detected in any of the patients. As stated above, a single patient with segmental tibia fracture showed 10 degrees of translation deformity, while another showed 15 degrees of recurvation deformity, but no additional treatment was required in both patients.

DISCUSSION One of the most important advantages of the hinge-fixator technique is that the reduction of the fracture is made at the initial stage. Thus, soft tissues re-locate to their original positions, and pins and wires do not lead to tractions in soft tissues. The size and weight of fixators are one of the major factors that affect patient’s compliance and comfort.[10,14] In our practice, fracture reduction is made just after inserting the first Schanz screws, and so the stabilization can be obtained by a smaller fixator. In addition, if a local or distant flap is applied for the patient’s soft tissue coverage, fixator may be modified according to the condition of the leg so that it may improve patient compliance and comfort (Figure 5). Although anatomic reduction may be obtained in the treatment of fractures by open reduction and internal fixation, there are some disadvantages of this procedure such as healing delay, infection, and soft tissue damage.[15-17] In conservative treatment methods, some of these listed disadvantages can be eliminated, but obtaining good reduction and stable fixation still pose a problem.[18] On the other hand, treatment of fractures with external fixators can be considered as a “semi-conservative” method between surgical treatment and conservative methods. From this point of view choosing circular external fixators in the treatment of severe open fractures may prevent many possible complications.[18-20] There is a general consensus that better reduction result in earlier and stronger union outcomes.[5,17,21] In conservative treatment methods, plasters or braces have limited effects on maintaining stable reduction. From this point of view, hingefixator systems may be accepted as a “sophisticated brace”. In this method, reduction may be protected in a stable way, where functional use of extremity can also be possible during the treatment period.[1,4,7] Reduction of the fracture is mainly based on applying traction and manipulation. In order to achieve a successful reduction, soft tissue contracture may not have been developed. Therefore, the affectivity of traction and manipulation is being diminished by the time passes after the fracture.[7,10,14] In our patient group, the operations were performed within 5 hours to 7 days (average 10.7 hours) from admission to the hospital. If a patient has not undergone operation within 7 days after

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the initial trauma due to a concomitant disease or other additional pathologies, classic gradual reduction methods should be preferred rather than this method. One of the most important problems encountered using the fixator during the treatment of a patient’s fracture is pin-site infection. Soft tissue irritation resulting from the pushes and tractions of wires and pins frequently facilitates pin-site infections.[2,14,22] Soft tissue healing is faster in reduced fractures and irritation around pins and wires becomes lower. Thus, as an advantage follow-up control intervals can be in longer periods. In our patient group, the average number of control visits after discharge from hospital was 3.9 (3-7)/times/patient. In the classical application techniques, reduction is made during or after the application of fixator frames. It requires using more fixator elements which results in a larger and a heavier fixator. Furthermore, radiation exposure is higher during the reduction process. Fixator manipulations during application lead to decreases in the stability of the construct.[23,24] In our method, fluoroscopy is used only at the reduction stage. There is no need for fluoroscopy, after reduction has been achieved. Thus, in the hinge-fixator technique radiation exposure of surgical team is also reduced. In our patient group, the mean number of fluoroscopy images is 6.4 (4-12) images. We demonstrate that the hinge-fixator method in the treatment of tibia fractures is fast and easy with a shorter operation time, lesser radiation exposure, shorter hospital stay, longer follow up visit intervals, and a more comfortable treatment period. It also leads to excellent radiologic and clinical outcomes. Conflicts of interest: The authors did not receive grants or outside funding in support of their research or preparation of this manuscript. They did not receive payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, educational institution, or other charitable or nonprofit organization with which the authors are affiliated or associated.

REFERENCES 1. Al-Sayyad MJ. Taylor Spatial Frame in the treatment of pediatric and adolescent tibial shaft fractures. J Pediatr Orthop 2006;26:164-70. 2. Kai H, Yokoyama K, Shindo M, Itoman M. Problems of various fixation methods for open tibia fractures: experience in a Japanese level I trauma center. Am J Orthop (Belle Mead NJ) 1998;27:631-6. 3. Monsell FP, Howells NR, Lawniczak D, Jeffcote B, Mitchell SR. Highenergy open tibial fractures in children: treatment with a programmable circular external fixator. J Bone Joint Surg Br 2012;94:989-93. 4. Zeman J, Matejka J. Use of a hybrid external fixator for treatment of tibial fractures. [Article in Czech] Acta Chir Orthop Traumatol Cech 2005;72:337-43. [Abstract] 5. Browner BD, Alberta FG, Mastella DJ. A new era in orthopedic trauma

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Demir et al., Circular fixator-hinge technique care. Surg Clin North Am 1999;79:1431-48. 6. Müller TS, Sommer C. Minimally invasive plate osteosynthesis of the distal tibia. [Article in German] Oper Orthop Traumatol 2012;24:35467. [Abstract] 7. Demir B, Gursu S, Oke R, Konya NM, Ozturk K, Sahin V. Shortening and secondary relengthening for chronically infected tibial pseudarthroses with poor soft tissues. J Orthop Sci 2009;14:525-34. 8. Oztürkmen Y, Karamehmetoğlu M, Karadeniz H, Azboy I, Caniklioğlu M. Acute treatment of segmental tibial fractures with the Ilizarov method. Injury 2009;40:321-6. 9. Chin TY, Bardana D, Bailey M, Williamson OD, Miller R, Edwards ER, et al. Functional outcome of tibial plateau fractures treated with the finewire fixator. Injury 2005;36:1467-75. 10. Demir B, Ozturk K, Oke R, Gursu S, Aydin KB, Sahin V. A modified technique of internal bone transport. Acta Orthop Belg 2008;74:216-21. 11. Zalavras CG, Patzakis MJ, Thordarson DB, Shah S, Sherman R, Holtom P. Infected fractures of the distal tibial metaphysis and plafond: achievement of limb salvage with free muscle flaps, bone grafting, and ankle fusion. Clin Orthop Relat Res 2004;427:57-62. 12. Paley D, Catagni MA, Argnani F, Villa A, Benedetti GB, Cattaneo R. Ilizarov treatment of tibial nonunions with bone loss. Clin Orthop Relat Res 1989;241:146-65. 13. Paley D, Maar DC. Ilizarov bone transport treatment for tibial defects. J Orthop Trauma 2000;14:76-85. 14. Paley D. Problems, obstacles, and complications of limb lengthening by the Ilizarov technique. Clin Orthop Relat Res 1990;250:81-104. 15. Eralp L, Kocaoglu M, Rashid H. Reconstruction of segmental bone defects due to chronic osteomyelitis with use of an external fixator and an

intramedullary nail. Surgical technique. J Bone Joint Surg Am 2007;95. 16. Howard JL, Agel J, Barei DP, Benirschke SK, Nork SE. A prospective study evaluating incision placement and wound healing for tibial plafond fractures. J Orthop Trauma 2008;22:299-306. 17. Schwarz C, Wulsten D, Ellinghaus A, Lienau J, Willie BM, Duda GN. Mechanical load modulates the stimulatory effect of BMP2 in a rat nonunion model. Tissue Eng Part A 2013;19:247-54. 18. Dewijze M, Pe M, Tondeur G. Sarmiento’s method of conservative treatment of leg fractures. [Article in French] Acta Chir Belg 1985;85:37-41. [Abstract] 19. Fujita M, Yokoyama K, Nakamura K, Uchino M, Wakita R, Itoman M. Tibial fractures associated with crush injuries to the soft tissues of the dorsal foot in children. Injury 2004;35:272-7. 20. Hall JA, Beuerlein MJ, McKee MD; Canadian Orthopaedic Trauma Society. Open reduction and internal fixation compared with circular fixator application for bicondylar tibial plateau fractures. Surgical technique. J Bone Joint Surg Am 2009;91:74-88. 21. Augat P, Simon U, Liedert A, Claes L. Mechanics and mechano-biology of fracture healing in normal and osteoporotic bone. Osteoporos Int 2005;16:S36-43. 22. Saw A, Chua YP, Hossain G, Sengupta S. Rates of pin site infection during distraction osteogenesis based on monthly observations: a pilot study. J Orthop Surg (Hong Kong) 2012;20:181-4. 23. Kesemenli C, Subasi M, Necmioglu S, Kapukaya A. Treatment of multifragmentary fractures of the femur by indirect reduction (biological) and plate fixation. Injury 2002;33:691-9. 24. Seide K, Weinrich N, Wenzl ME, Wolter D, Jürgens C. Three-dimensional load measurements in an external fixator. J Biomech 2004;37:1361-9.

KLİNİK ÇALIŞMA - ÖZET OLGU SUNUMU

Açık tibia kırıklarının sirküler fiksatörler ile tedavisinde yeni bir uygulama tekniği: Fiksatör-menteşe yöntemi Dr. Bilal Demir, Dr. Sami Sökücü, Dr. Erdem Özden, Dr. Umut Yavuz, Dr. Serda Duman, Dr. Yavuz Selim Kabukçuoğlu Baltalimanı Kemik ve Eklem Hastalıkları Hastanesi, Ortopedi ve Travmatoloji Kliniği, İstanbul

AMAÇ: Bu çalışmada, sirküler fiksatör-menteşe kombinasyonu ile daha kolay ve hızlı fiksatör uygulaması sağlayan, klinik ve radyolojik sonuçları geliştiren yeni bir uygulama yöntemi anlatıldı. GEREÇ VE YÖNTEM: Önerdiğimiz uygulama yöntemi ile 14 tibia kırığı olgusu tedavi edildi. Hastaların 10’u erkek, dördü kadın ve ortalama yaş 41.3 (dağılım, 24-58) yıl idi. Sirküler fiksatör menteşe tekniği kullanılarak, öncelikle hızlı anatomik redüksiyon ve geçici kırık stabilizasyonu sağlandı. Skopi kontrolünden sonra fiksatör uygulaması tamamlanarak gerçek kırık stabilizasyonu yapıldı. Hastalardan elde edilen veriler ve son kontrollerde alınan klinik ve radyolojik sonuçlar Paley kriterlerine göre değerlendirildi. BULGULAR: Tüm hastalarda solid osseoz kaynama elde edilerek, ortalama 5.4 (dağılım, 3-8) yıl boyunca takip yapıldı. Son değerlendirmede Paley’e göre radyolojik olarak 2 iyi, 12 mükemmel ve klinik olarak da 13 mükemmel, 1 iyi sonuç elde edildi. TARTIŞMA: Kırıkların sirküler fiksatör-menteşe yöntemi ile tedavisinde hızlı ve kolay bir uygulama imkanı sağlanmaktadır. Bu yöntemde daha kısa cerrahi süresi, daha az radyasyon maruziyeti, daha kısa hastane yatış süreleri ve daha seyrek hastene kontrolleri ile birlikte daha konforlu bir tedavi süreci sağlanmaktadır. Anahtar sözcükler: Sirküler fiksatör; menteşe yöntemi; tibia kırığı. Ulus Travma Acil Cerr Derg 2013;19(6):543-547

doi: 10.5505/tjtes.2013.47936

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ORIGIN A L A R T IC L E

Cemented calcar replacement versus cementless hemiarthroplasty for unstable intertrochanteric femur fractures in the elderly Deniz Çankaya, M.D., Bülent Özkurt, M.D., Abdullah Yalçın Tabak, M.D. Department of Orthopaedics and Traumatology, Ankara Numune Training and Research Hospital, Ankara

ABSTRACT BACKGROUND: Unstable intertrochanteric fractures remain a challenging problem in elderly individuals due to high failure rates associated with internal fixation. Hemiarthroplasty is one treatment option for intertrochanteric femur fractures in elderly patients. The aim of the present study was to compare the reliability of cementless and cemented hemiarthroplasty for unstable intertrochanteric femur fractures in elderly patients. METHODS: Elderly patients with AO type 31-A2 intertrochanteric femur fractures were treated with cemented (n=40) or cementless (n=46) hemiarthroplasty. Duration of surgery, amount of blood loss and blood transfusion, Harris hip scores, rate of loosening of the femoral component, duration of hospital stay after surgery and mortality rates were recorded. RESULTS: There were no significant differences between the groups in length of hospital stays, Harris hip scores, amount of blood transfusions, implant loosening and follow-up mortality rates. Walking ability was better in the cemented group in the early follow-up period. Duration of surgery, amount of blood loss and perioperative mortality rates were significantly lower in the cementless group than in the cemented group. CONCLUSION: Cementless hemiarthroplasty is a reliable treatment choice for unstable intertrochanteric femur fractures in elderly patients with early mobilization, acceptable functional results, low implant loosening rates, shorter surgery time, lesser blood loss and lower perioperative mortality rate. Key words: Cementless hemiarthroplasty; elderly; intertrochanteric femur fractures; mortality.

INTRODUCTION Hip fractures present a common source of morbidity and mortality among elderly people worldwide. Globally, the mean age of the population is increasing, and the number of hip fractures is expected to triple in the next 50 years.[1] Intertrochanteric hip fractures are extracapsular fractures common in elderly people with poor bone quality.[2] Classifications of these fractures are unreliable and therefore not useful in determining treatments. In general, fractures with comminution of the posteromedial cortex and subtrochanteric extension Address for correspondence: Deniz Cankaya, M.D. Ankara Numune Eğitim ve Araştırma Hastanesi, Ortopedi ve Travmatoloji Kliniği, 06100 Altındağ, Ankara, Turkey Tel: +90 312 - 508 51 41 E-mail: cankayadeniz78@gmail.com Qucik Response Code

Ulus Travma Acil Cerr Derg 2013;19(6):548-553 doi: 10.5505/tjtes.2013.57615 Copyright 2013 TJTES

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are considered unstable.[3] The treatment of unstable intertrochanteric femur fractures is very challenging and is still a matter of discussion, especially in elderly patients.[4] Studies comparing internal fixation and hemiarthroplasty for unstable intertrochanteric femur fractures in elderly patients state that hemiarthroplasty is an alternative treatment with earlier mobilization and the same functional outcome compared to internal fixation.[4,5] Although hemiarthroplasty has become popular for intertrochanteric femur fractures in elderly patients, there is no consensus whether cementless or cemented hemiarthroplasty is a better option. Cementation is associated with an increase in intramedullary pressure, consequently leading to fat embolization, which increases the mortality rates in cemented hemiarthroplasty. Bone cement implantation syndrome is a challenging problem, especially in patients with multiple comorbidities. Several studies examined the effects of cementing on morbidity and mortality with controversial results and pointed out the need for future studies.[6-9] Although the outcomes of cemented and cementless Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Çankaya et al., Cemented calcar replacement vs cementless hemiarthroplasty for unstable intertrochanteric femur fractures in the elderly

hemiarthroplasty were reported individually,[2,10-12] to our knowledge, there has been no study comparing cemented and cementless hemiarthroplasty for intertrochanteric femur fractures in elderly patients. In the present study, we aimed to compare the reliability of cementless and cemented hemiarthroplasty for unstable intertrochanteric femur fractures in elderly patients.

MATERIALS AND METHODS Between 2008 and 2010, 86 patients with AO type 31-A2 intertrochanteric femur fractures were included in this prospective study. Patients with pathological fractures, previous contralateral hip fractures, stable fractures and reverse oblique fractures were excluded from the study. Of the eligible patients, 46 of them underwent cemented hemiarthroplasty (Group I), and 40 of them underwent cementless hemiarthroplasty (Group II). Group I included 10 male and 36 female patients with an average age of 78 years (range 6695 years). Group II included 8 male and 32 female patients with an average age of 76 years (range 65-92 years). There were no significant differences between the groups in age and gender (Table 1). The comorbidity scores of the patients according to the American Society of Anesthesiologists (ASA) criteria were recorded before the surgery. One operating surgeon performed the cemented and cementless operations with the same surgical technique. In Group I, cemented calcar replacement stems designed for proximal femur (Biomet Inc. Warsaw, IN, USA) were used (Figure 1). In Group II, PPF and taperloc femoral stems of the same company (Biomet Inc. Warsaw, IN, USA) were used (Figure 2). The modified Watson-Jones anterolateral approach with the same surgical technique was used for all patients. According to the amount of displacement and bone quality, displaced trochanteric fractures were secured by Dall-Miles cable or pds suture in both techniques. Surgery time, amount of blood loss and blood transfusion were recorded. The perioperative interval was considered as the time between hospitalization and 72 hours postoperatively.

Follow-up visits were performed at 6 weeks, then at 3, 6 and 12 months and every year thereafter. Harris hip scores and walking ability of the patients were recorded during followup visits. Hip radiographs were evaluated for loosening of the femoral stem. Any change in the position of the stem, or a continuous radiolucent line wider than 2 mm at the bone-cement or bone-implant interface in at least two Gruen zones were accepted as loosening. Mortality rates of the groups in the follow-up period were recorded and reported as the perioperative, 3-month, 1-year and 2-year mortality rates.

Statistical Analysis Statistical calculations were performed with SPSS 13.0 (SPSS Inc, Chicago IL, USA) and the results are expressed in mean and standard deviation. Comparisons between the groups were done with the Student t-test and chi-square test. A p value <0.05 was considered to indicate a statistically significant difference.

RESULTS In Group I, six patients died perioperatively. During the follow-up period, 18 patients in Group I and 17 patients in Group II died. After 2 years of follow-up, 22 patients in Group I and 23 patients in Group II were alive. The mean follow-up period in Group I and II were 38 months (range 24-51 months) and 32 months (range 24-45 months), respectively. The number of patients with lower ASA scores (ASA 1 or 2) and higher ASA scores (ASA 3 or 4) were 17/29 and 11/23, respectively. There was no significant difference between the groups in comorbidy scores (p=0.600). The mean surgical time was 89.13 (±8.51) minutes for Group I and 83.10 (±9.50) minutes for Group II. The surgical time was significantly shorter in Group II (p=0.004). The average number of units of packed red cells (PRCs) transfused were 1.10 and 1.24 in Group 1 and Group 2, respectively. Postoperative transfusion rates were similar in the groups (p=0.338). The amount of postoperative drainage was 540 (±119) ml and 469

Table 1. Demographic and clinical data of the patients

Cemented group

Number

Cementless group

46

Age (years) Sex (Female / Male) ASA 1-2/3-4

p

40

78 (7.11)

76 (7.52)

0.317

36 / 10

32 / 8

0.843

17 / 29

17 / 23

0.600

Operating times (minutes)

89 (8.51)

83 (9.50)

0.004

Blood transfusion (packet)

1.28 (0.72)

1.43 (0.68)

0.338

Blood loss (ml)

540 (118)

468 (131)

0.012

Hospital stay (days)

9.10 (2.34)

9.80 (2.45)

0.195

The values are given as the mean and the number of patients with the standard deviation in parentheses.

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Çankaya et al., Cemented calcar replacement vs cementless hemiarthroplasty for unstable intertrochanteric femur fractures in the elderly

(a)

(b)

Figure 1. (a) Anteroposterior preoperative radiograph of the patient with unstable intertrochateric fracture and (b) postoperative radiograph after cementless hemiarthroplasty.

(a)

(b)

Figure 2. (a) Anteroposterior preoperative radiograph of the patient with unstable intertrochateric fracture and (b) postoperative radiograph after cementless hemiarthroplasty.

(±131) ml in Groups I and II, respectively. The amount of postoperative blood loss was significantly lower in Group II (p=0.012). The mean duration of hospital stay was 9.10 days and 9.80 days, respectively (p=0.195). All patients were ambulatory during discharge. The mean Harris hip scores at the 3-month and 1-year follow-ups were 77.13 (±5.60) and 81.52 (±6.12) for Group I and 75.97 (±5.20) and 80.81 (±6.66) for Group II. At the last follow-up, the mean Harris hip scores increased to 83.27 (±6.33) and 82.78 (±5.88), respectively. 550

There were no significant differences between the groups regarding the Harris hip scores during the follow-up period (Table 2). Before surgery, 35 patients of Group I and 30 patients of Group II walked without support (p=0.907). At the 3-month follow-up, the number of patients who were able to walk without support was 12 and 5, respectively. Group II had a significantly better outcome in walking ability (p=0.039). After Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Ă&#x2021;ankaya et al., Cemented calcar replacement vs cementless hemiarthroplasty for unstable intertrochanteric femur fractures in the elderly

Table 2. Functional outcome during the follow-up

Cemented group

Cementless group

p

77.13 (5.59)

75.97 (5.20)

0.397

Harris Hip Score (100) HHS at 3 months HHS at 12 months

81.52 (6.21)

80.81 (6.66)

0.695

HHS at 24 months

83.27 (6.33)

82.76 (5.88)

0.789

Pre-operative WWS

35/46

30/40

0.907

WWS at 3 months

12/31

5/32

0.039

WWS at 12 months

14/25

11/27

0.271

WWS at 24 months

14/22

13/23

0.626

Walking without support (WWS)

The values are given as the mean with the standard deviation in parentheses for HHS and the number of patients for WWS.

Table 3. Mortality rates in follow-up

Cemented group n

%

Perioperative

6/46 13

0-3 months

9/40

3-12 months

6/31

12-24 months

3/25

Cementless group

p

n % 0/40 0

0.028

23

8/40

20

0.785

19

5/32

16

0.697

12

4/27

15

0.766

The values are given as the number of patients.

the 2-year follow-up, the number of patients who were able to walk without support was 14 and 13, respectively and there was no significant difference between the groups (p=0.626) (Table 2). Radiographs of the operated hip were taken in every follow-up to evaluate loosening of the femoral stem. There was no osteolysis or implant failure, and as displaced fragments were secured, there was no nonunion of trochanteric major fracture in both groups during regular follow-up.

ment of the greater and lesser trochanters, unstable intertrochanteric fractures are one of the most complex forms of hip fracture in elderly patients. Additionally, elderly patients have weak/porous bones that do not usually provide adequate purchase for internal fixation, leading to early biomechanical failure. Due to the high rate of failure, the best strategy for the treatment of unstable trochanteric femur fractures in elderly patients is still a matter of debate.

While six patients in Group I died perioperatively, none of the patients died in Group II, and the perioperative mortality rate was significantly higher in Group I compared to that of Group II (p=0.028). The number of deaths was 15 and 13, respectively, at the 1-year follow-up. Between the first and the second years, three patients from Group I and four patients from Group II died. Regarding the follow-up mortality rates, there were no significant differences between the groups (Table 3).

The first endoprostheses used in hip fractures were designed for cementless use, but cemented fixation has become the preferred technique thereafter.[1] Several studies showed that cemented hemiarthroplasty with or without calcar replacement was a good option in elderly patients with intertrochanteric femur fracture.[13-16] As cemented hemiarthroplasty is more commonly used, the effect of cementation on mortality, caused by elevating the intramedullary pressure which leads to fat embolization, has become one of the main concerns of physicians.[6-8,17,18] Contradictory results were obtained in these studies. Elmaraghy et al.[6] suggested that cemented hemiarthroplasty had no effect on the formation of fat emboli, but Christie et al.[7] showed that cemented arthroplasty caused greater and more prolonged embolic cascades than did uncemented arthroplasty. In another study, Donaldson et al.[8] suggested that morbidity and mortality might be minimized by preferring cementless arthroplasty

DISCUSSION As life expectancy increases with better medical care, hip fractures have become a common source of morbidity and mortality worldwide.[1] Hip fractures in elderly patients tend to present significant comminution and displacement due to inevitable osteoporosis in elderly patients. With the involveUlus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

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Çankaya et al., Cemented calcar replacement vs cementless hemiarthroplasty for unstable intertrochanteric femur fractures in the elderly

in high-risk patients. A review article on 7,774 patients with hip fractures concluded that cemented arthroplasty caused significantly higher mortality.[17] Hossain et al.[18] reported eight cases of perioperative death after cemented hemiarthroplasty in elderly patients. Our results supported these studies, which suggested serious adverse effects of cement on mortality. Among 46 patients in the cemented group, 6 patients died during the perioperative period while there was no death among patients who had cementless hemiarthroplasty. The present study showed that cementation significantly increased the perioperative mortality rate, similar to the majority of the studies in the literature. As cementless hemiarthroplasty appears to be an alternative treatment choice for intertrochanteric femur fractures in elderly patients, the reliability of cementless hemiarthroplasty in this age group has become the main concern of recent studies.[2,5,10-13] The main argument against cementless hemiarthroplasty was the possible low osseointegration in osteoporotic patients leading to instability of the implant. Two recent studies reported an implant survival rate of about 100% after total hip arthroplasty after more than 5 years follow-up in patients older than 75 years of age.[19,20] No implant failure was reported in the studies, which evaluated cementless hemiarthroplasty for unstable intertrochanteric fractures in elderly patients.[2,4,5,10,11] Even in cementless modular hip arthroplasty after failed trochanteric fracture fixation, none of the patients required reoperation due to the loosening of femoral prosthesis.[21] Our current study also supported the results reported in the literature and no implant loosening or failure was observed during 2 years follow-up. To our knowledge, there is no comparative study between cemented and cementless calcar replacement hemiarthroplasty for unstable intertrochanteric fractures in elderly patients. In our current comparative study, we found that cemented hemiarthroplasty was associated with better outcomes only in walking without support during the early follow-up period. However, during the first year of follow-up, this advantage disappeared. Cementless hemiarthroplasty had shorter surgical time and lesser blood loss compared to cemented hemiarthroplasty; however those differences did not alter the transfusion rate. Regarding the functional outcomes, there was no difference between cemented and cementless hemiarthroplasty. The most important result of the present study was the significantly higher perioperative mortality rates after cemented arthroplasty.

Conclusion Cementless hemiarthroplasty is a reliable treatment choice for intertrochanteric femur fractures in older age-group patients with early mobilization, acceptable functional results, low implant loosening rates, shorter surgery time, lesser blood loss and lower perioperative mortality rate. 552

Conflict of interest: None declared.

REFERENCES 1. Miyamoto RG, Kaplan KM, Levine BR, Egol KA, Zuckerman JD. Surgical management of hip fractures: an evidence-based review of the literature. I: femoral neck fractures. J Am Acad Orthop Surg 2008;16:596607. 2. Choy WS, Ahn JH, Ko JH, Kam BS, Lee DH. Cementless bipolar hemiarthroplasty for unstable intertrochanteric fractures in elderly patients. Clin Orthop Surg 2010;2:221-6. 3. Kaplan K, Miyamoto R, Levine BR, Egol KA, Zuckerman JD. Surgical management of hip fractures: an evidence-based review of the literature. II: intertrochanteric fractures. J Am Acad Orthop Surg 2008;16:665-73. 4. Kim SY, Kim YG, Hwang JK. Cementless calcar-replacement hemiarthroplasty compared with intramedullary fixation of unstable intertrochanteric fractures. A prospective, randomized study. J Bone Joint Surg Am 2005;87:2186-92. 5. Kayali C, Agus H, Ozluk S, Sanli C. Treatment for unstable intertrochanteric fractures in elderly patients: internal fixation versus cone hemiarthroplasty. J Orthop Surg 2006;14:240-4. 6. Elmaraghy AW, Humeniuk B, Anderson GI, Schemitsch EH, Richards RR. The role of methylmethacrylate monomer in the formation and haemodynamic outcome of pulmonary fat emboli. J Bone Joint Surg Br 1998;80:156-61. 7. Christie J, Burnett R, Potts HR, Pell AC. Echocardiography of transatrial embolism during cemented and uncemented hemiarthroplasty of the hip. J Bone Joint Surg Br 1994;76:409-12. 8. Donaldson AJ, Thomson HE, Harper NJ, Kenny NW. Bone cement implantation syndrome. Br J Anaesth 2009;102:12-22. 9. Taylor F, Wright M, Zhu M. Hemiarthroplasty of the hip with and without cement: a randomized clinical trial. J Bone Joint Surg Am 2012;94:577-83. 10. Sinno K, Sakr M, Girard J, Khatib H. The effectiveness of primary bipolar arthroplasty in treatment of unstable intertrochanteric fractures in elderly patients. N Am J Med Sci 2010;2:561-8. 11. Lee YK, Ha YC, Chang BK, Kim KC, Kim TY, Koo KH. Cementless bipolar hemiarthroplasty using a hydroxyapatite-coated long stem for osteoporotic unstable intertrochanteric fractures. J Arthroplasty 2011;26:626-32. 12. Rodop O, Kiral A, Kaplan H, Akmaz I. Primary bipolar hemiprosthesis for unstable intertrochanteric fractures. Int Orthop 2002;26:233-7. 13. Haentjens P, Casteleyn PP, De Boeck H, Handelberg F, Opdecam P. Treatment of unstable intertrochanteric and subtrochanteric fractures in elderly patients. Primary bipolar arthroplasty compared with internal fixation. J Bone Joint Surg Am 1989;71:1214-25. 14. Abdelkhalek M, Ali AM, Abdelwahab M. Cemented bipolar hemiarthroplasty with a cerclage cable technique for unstable intertrochanteric hip fractures in elderly patients. Eur J Orthop Surg Traumatol 2013;23:443-8. 15. Kesemenli C, Subaşi M, Arslan H, Kirkgöz T, Necmioğlu S. Treatment of intertrochanteric fractures in elderly patients with Leinbach type endoprostheses. Ulus Travma Derg 2001;7:254-7. 16. Akman S, Sen C, Asik M, Akpınar S, Gedik HK. Our experience with leinbach prosthesis in intertrochanteric femoral fractures. Ulus Travma Acil Cerrahi Derg 1999;5:208-212. 17. Parvizi J, Ereth MH, Lewallen DG. Thirty-day mortality following hip arthroplasty for acute fracture. J Bone Joint Surg Am 2004;86-A:1983-8. 18. Hossain M, Andrew JG. Is there a difference in perioperative mortality

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Çankaya et al., Cemented calcar replacement vs cementless hemiarthroplasty for unstable intertrochanteric femur fractures in the elderly between cemented and uncemented implants in hip fracture surgery? Injury 2012;43:2161-4.

throplasty in patients older than 80 years of age. J Bone Joint Surg Br 2003;85:641-5.

19. Berend KR, Lombardi AV, Mallory TH, Dodds KL, Adams JB. Cementless double-tapered total hip arthroplasty in patients 75 years of age and older. J Arthroplasty 2004;19:288-95.

21. Thakur RR, Deshmukh AJ, Goyal A, Ranawat AS, Rasquinha VJ, Rodriguez JA. Management of failed trochanteric fracture fixation with cementless modular hip arthroplasty using a distally fixing stem. J Arthroplasty 2011;26:398-403.

20. Pieringer H, Labek G, Auersperg V, Böhler N. Cementless total hip ar-

KLİNİK ÇALIŞMA - ÖZET OLGU SUNUMU

Yaşlı hastalarda görülen dengesiz intertrokanterik kırıkların tedavisinde, çimentosuz ve çimentolu kalkar replasmanlı hemiartroplastinin karşılaştırılması Dr. Deniz Çankaya, Dr. Bülent Özkurt, Dr. Abdullah Yalçın Tabak Ankara Numune Eğitim ve Arastırma Hastanesi, Ortopedi ve Travmatoloji Kliniği, Ankara

AMAÇ: İnstabil (dengesiz) intertrokanterik femur kırıklarının yaşlılardaki tedavisi, içten tespitteki yüksek başarısızlık oranları nedeniyle halen üzerinde görüş birliği olmayan bir sorundur. Hemiartroplasti, yaşlı hastalarda tercih edilen tedavi seçeneklerinden biridir. Bu çalışmada, yaşlı hastalarda görülen dengesiz intertrokanterik femur kırıkları için, çimentosuz ve çimentolu parsiyel artroplastilerin güvenilirlikleri karşılaştırıldı. GEREÇ VE YÖNTEM: 2008 ile 2010 yılları arasında AO sınıflamasına göre 31 A2 tipi intertrokanterik femur kırığı olan 86 yaşlı hastaya, çimentosuz (n=40) ve çimentolu (n=46) parsiyel artroplasti uygulandı. Hastaların cerrahi süreleri, kan kayıpları, kan transfüzyonları, Harris kalça skorları, femoral komponentlerin gevşemeleri, hastanede kalma süreleri ve ölüm oranları kaydedildi. BULGULAR: Gruplar arasında, kan transfüzyonu, hastanede kalış süresi, implant gevşeme oranları, Harris kalça skorları ve takiplerdeki ölüm oranları açısından fark yoktu. Yürüme yeterliliği erken dönemde çimentolu grupta daha iyiydi. Cerrahi zamanı, kan kaybı ve perioperatif ölüm oranları çimentosuz grupta anlamlı derecede düşüktü. TARTIŞMA: Çimentosuz hemiartroplasti ileri yaş grubundaki hastalarda görülen dengesiz intertrokanterik femur kırıklarının tedavisinde erken mobilizasyona olanak tanımasıyla, kabul edilebilir fonksiyonel sonuçlarıyla, düşük implant gevşeme oranlarıyla, daha kısa cerrahi süresiyle, daha az kanamayla ve daha düşük perioperatif ölüm oranıyla güvenilir bir tedavi seçeneğidir. Anahtar sözcükler: Çimentosuz hemiartroplasti; ileri yaş; intertrokanterik femur kırığı; yaşlı. Ulus Travma Acil Cerr Derg 2013;19(6):548-553

doi: 10.5505/tjtes.2013.57615

Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

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K Lİ NİK Ç A LI ŞM A

Çocuk apandisitlerinde risk faktörlerinin analizi Dr. Turan Yıldız,1 Dr. Zehra Bozdağ,2 Dr. Ünal Erkorkmaz,3 Dr. Arif Emre,4 Dr. Taner Turgut,5 Dr. Zekeriya İlçe1 1

Sakarya Üniversitesi Tıp Fakültesi, Çocuk Cerrahi Anabilim Dalı, Sakarya

2

Gaziantep Üniversitesi Tıp Fakültesi, Tıbbi Patoloji Anabilim Dalı, Gaziantep

3

Sakarya Üniversitesi Tıp Fakültesi, Biyoistatistik Anabilim Dalı, Sakarya

4

Gebze Fatih Devlet Hastanesi, Genel Cerrahi Kliniği, Kocaeli

5

Derince Eğitim ve Araştırma Hastanesi, Genel Cerrahi Kliniği, Kocaeli

ÖZET AMAÇ: Apandisit çocuklardaki en sık cerrahi karın ağrısı nedenidir. Biz bu çalışmada apandektomilerin histopatolojileri üzerine yaş, cinsiyet, mevsim ve ailesel faktörlerin etkisini araştırdık. GEREÇ VE YÖNTEM: Akut apandisit nedeni ile Eylül 2009-2011 yılları arasında ameliyat edilen 588 hasta çalışmaya alındı. Hastalar histopatolojik bulgularına göre akut, perfore ve negatif apandektomi olarak üç gruba ayrıldı. Bu gruplar üzerine yaş, cinsiyet, mevsim ve ailesel faktörlerin etkinliği araştırıldı. BULGULAR: Hastaların ortalama yaşı 11.8±3.26 yıl (dağılım, 1-16 yıl) idi. Hastaların analizinde 10 yaşından sonra apandisit 2.41 kez sık görüldü. Erkeklerde apandisit kızlara göre 4.63 kez daha sık bulundu. Negatif apendektomi ile 10 yaşından sonra daha sık karşılaşıldı. Aile hikayesi ve mevsimlerin apandisit üzerine etkisi oransal olarak saptandı fakat bu etki anlamlı değildi (p>0.05). SONUÇ: Apandisit cerrahisi planlarken yaş ve cinsiyet dikkate alınmalıdır. Çünkü doğru tanı yaş ve cinsiyet ile ilişkilidir. Ayrıca apandisit histopatolojisi ailesel ve çevresel faktörlerden etkilenir. Anahtar sözcükler: Apandisit; cinsiyet; çocuk; heredite; mevsim; yaş.

GİRİŞ Apandisit apandiks vermiformisin enflamasyonudur. Çocuklardaki en sık cerrahi karın ağrısı nedenidir.[1,2] İnsanların %7’si hayatları boyunca apandisit nedeni ile ameliyat edilir. Bununla birlikte doğru tanı %72-94 oranında kalmaktadır. Bu oranlar tanının hala zor olduğunun göstergesidir.[3,4] Çocuklarda ise zor iletişim kurulması, fiziksel incelemenin zorluğu, obezite ve bazen genç kızlardaki jinekolojik hastalıklar doğru tanı oranlarını daha da düşürebilmektedir.[5,6] Bu amaçla yaş, cinsiyet, mevsim ve genetik faktörler irdelenip, doğru tanıdaki yerleri ortaya koyulmaya çalışılmıştır. Ancak bazı faktörler üzerinde tartışmalar hala devam etmektedir.[7,8] Bu amaçla değişik bölgelerde

Sorumlu yazar: Dr. Turan Yıldız, Sakarya Üniversitesi Tıp Fakültesi, Çocuk Cerrahi Anabilim Dalı, Sakarya Tel: +90 422 - 326 15 69 / 72 E-posta: tyildiz44@hotmail.com Ulus Travma Acil Cerr Derg 2013;19(6):554-558 doi: 10.5505/tjtes.2013.52059 Telif hakkı 2013 TJTES

554

çalışmalar yapılmıştır. Ancak bizim çalışmayı yaptığımız Malatya bölgesinde bu konuda yapılmış bir çalışma bulunmamaktadır. Bu çalışmada, Malatya bölgesinde yapılan apendektomilerin histopatolojisi üzerine yaş, cinsiyet, mevsim ve ailesel faktörlerin etkisi araştırıldı.

GEREÇ VE YÖNTEM Eylül 2009-Eylül 2011 yılları arasında Malatya Devlet Hastanesi Çocuk Cerrahi Kliniği’nde apandisit ön tanısı ile ameliyat edilen 588 hastanın demografik verileri ve alınan apendiksin histopatolojik verileri “SPSS for Windows 20.0” programına kaydedildi. Hastaların yaşı, cinsiyeti, ailesel yatkınlığı (1. derece) ve cerrahinin gerçekleştiği mevsim apendektomi materyallerinin histopatolojik sonuçları ile ilişkili olarak incelendi. Histopatolojik sonuçlar normal apendiks (NA), akut apandisit (AA) ve perfore apandisit (PA) olarak ayırt edildi. NA saptanan hastalarda ek patoloji mevcut ise appendektomi yapılmadı. Çalışmaya 0-16 yaşında olan ve ameliyat öncesi tanısı apandisit olarak kabul edilen tüm hastalar alındı. İnsidental apendektomiler çalışmaya alınmadı. Tüm materyaller tek bir patolog tarafından değerlendirildi. Bu çalışma için yerel etik kurul onayı alındı. Ulus Travma Acil Cerr Derg, Kasım 2013, Cilt. 19, Sayı. 6


Yıldız ve ark., Çocuk apandisitlerinde risk faktörlerinin analizi

liyat edilen hastaların regression analizinde 10 yaşından sonra apandisit 2.41 kez artmış olarak bulundu (OR: 2.406; %95 GA: 1.064-5.436). Multipl logistik regresyon analizine göre erkeklerde apandisit kızlara göre 4.63 kez daha sık bulundu (OR: 4.63; %95 GA: 2.051-10.474).

Histopatolojik Değerlendirme Hasta kayıtlarından patoloji protokol numaraları tespit edilen hastalara ait hematoksilen eozin (H-E) boyalı doku kesitleri binoküler ışık mikroskobunda incelenmiş ve değerlendirilmiştir. Apendiks lümeninde ve duvarında nötrofil lökosit infiltrasyonu bulunan olgular AA olarak değerlendirilmiş, perforasyonun eşlik ettiği olgular ayrıca belirtilmiştir. Enflamasyonun görülmediği olgular NA olarak değerlendirilmiştir.

Ameliyat edilen hastaların 404’ünde AA, 118’inde PA, 66’sında NA tespit edildi. AA en sık apendektomi nedeniydi (%68.7). Daha sıklıkla erkek çocuklarda (%65.8) görüldü. Yaş ortalaması 12.2±3.04 yıl dı (Şekil 1). İkinci dekadda PA’ya göre sıklığının arttığı tespit edildi (p=0.001).

İstatistiksel Analiz Yaş gruplarını karşılaştırmak için iki bağımsız grupların t-testi veya tek yönlü varyans analizi (ANOVA) kullanıldı. ANOVA sonuçları dikkate değer olduğunda, ikili karşılaştırmada levene homogenistik testin sonuçlarına göre tamhane test kullanıldı. Yaşlar ortalama±standart sapma olarak sunuldu. Kategorik değişkenler ki-kare testi ile karşılaştırıldı. Veriler sayı ve yüzde olarak sunuldu. Multivaryant lojistik regresyon analizi apandisit ile yaş, cinsiyet ve aile öyküsü ilişkisini tespit etmek amacıyla kullanıldı. p<0.05 anlamlı olarak kabul edildi. İstatistiki analizler ticari yazılım kullanılarak yapıldı (IBM SPSS Statistics 20, SPSS inc., an IBM Co., Somers, NY).

Perfore apandisit apendektomilerin %20.1’i idi. Erkek çocuklarda daha sıklıkla görüldü. PA görülme yaşı AA’lara göre daha düşüktü. Yaş ortalaması 10.4±3.65 dü (Şekil 2). Özellikle beş yaş ve daha küçük çocukların %56.5’inde (n=13) PA görülmekle birlikte istatistiki olarak anlamlı fark görülmedi. Ameliyat edilen hastaların %11.2’sinde apendiks normaldi. Bu hastaların yaş ortalaması 12.45±3.13 idi. NA’lı hastaların %75.8’i (n=50) 10 yaşından sonra görüldü. Bu hastaların 10 yaşından sonra AA ve PA’ya göre görülme sıklığı arttı (p=0.001). NA kızlarda (%63.6) daha sık idi (Şekil 3). Bu kızların 21’inde (%50) ameliyat esnasında jinekolojik patoloji (over kisti, over kist rüptürü, kist torsiyonu gibi) ile karşılaşıldı. Ayrıca NA’lı görülen hastaların histopatolojik incelemeleri sonucunda dokuz hastada Enterobius vermicularis yumurtası ve bir hastada ise Taenia saginata yumurtası ile karşılaşıldı.

BULGULAR Hastaların verileri Tablo 1’de gösterilmiştir. Bu çalışma 370’i (%63) erkek toplam 588 hasta ile yapıldı. Hastaların ortalama yaşı 11.8±3.26 yıl (dağılım, 1-16 yıl) idi. Hastaların 194’ü (%33) 0-10 yaşında, 394’ü (%67) 11-16 yaşında ameliyat edildi. Ame-

Tablo 1. Akut, perfore ve negatif apendektomilerin dağılımı

Negatif

n %

Yaş

Akut n %

Perfore

p

n %

12.45±3.13

12.21±3.04

10.43±3.65

0-10

16 24.2

122 30.2

56 47.5

11-17

50 75.8

282 69.8

62 52.5

24

266

80

<0.001b.c

Yaş grupları 0.001b.c

Cinsiyet

Erkek

Kız

36.4

65.8

67.8

42 63.6

138 34.2

38 32.2

25 37.9

113 28

36 30.8

<0.001a.b

Mevsim İlkbahar Yaz

6 9.1

86 21.3

29 24.8

Sonbahar

19 28.8

118 29.2

35 29.9

Kış

16 24.2

87 21.5

18 15.2

Negatif

31 93.9

111 88.1

27 81.8

Pozitif

2 6.1

15 11.9

6 18.2

0.125

Aile hikayesi 0.316

Veriler ortalama±standard sapma ve yüzde n (%) olarak gösterildi. a: Negatif ve akut apandisit grubu arasında anlamlı fark görüldü. b: Negatif ve perfore apandisit grubu arasında anlamlı fark görüldü. c: Akut ve perfore apandisit grubu arasında anlamlı fark görüldü.

Ulus Travma Acil Cerr Derg, Kasım 2013, Cilt. 19, Sayı. 6

555


Yıldız ve ark., Çocuk apandisitlerinde risk faktörlerinin analizi

50

Erkek Kız

45 40

Hasta sayısı

35 30 25 20 15 10 5 0

1

2

3

4

5

6

7

8 9 Yaş

10 11 12 13 14 15 16

Şekil 1. Kız ve erkek çocuklarda akut apandisitin yaşa göre dağılımı.

14

Hasta sayısı

10 8 6 4 2 0

1

2

3

4

5

6

7

8 9 Yaş

10 11 12 13 14 15 16

Şekil 2. Kız ve erkek çocuklarda perfore apandisitin yaşa göre dağılımı.

12

Erkek Kız

10

Hasta sayısı

8 6 4 2 0

1

2

3

Akut apandisit, PA ve NA ile mevsimler arasında görülme sıklığı açısından istatistiki bir fark görülmedi (p=0.125). Ayrıca total olarak tüm apandisitlerin görülmesi ile mevsimler arasında ilişki tespit edilmedi. Ancak AA bahar aylarında oransal olarak daha sık görüldü (%29.6-29.3). NA yaz aylarında azaldığını tespit ettik (%9.1).

TARTIŞMA Apandisit çocuklardaki en sık akut karın nedenidir.[4] Çok sık karşılaşılmasına rağmen zamanında ve doğru tanı koyulmasında halen sıkıntılar mevcuttur.[5,6] Zamanında yapılamayan tanı sonucu perforasyon oluşmakta ve takiben bazı komplikasyonlar ortaya çıkmaktadır (ileus, karıniçi apse, infertilite gibi).[9] Veya gereksiz laparatomiye bağlı olarak negatif apendektomi yapılmakta ve komplikasyonlar oluşmaktadır. Yapılan çalışmalar sonucunda çocuklardaki apandisitlerin yaklaşık %36’sı perfore, %10-30’unun NA olduğu bildirilmektedir.[4,10] Özellikle çocuk apandisitlerinin tanısında hikaye, fizik muayene ve yakın takip önemlidir.[11]

Erkek Kız

12

4

5

6

7

8 9 Yaş

10 11 12 13 14 15 16

Şekil 3. Kız ve erkek çocuklarda negatif apendektomilerin dağılımı.

Aile hikayesi sorgulanmış olan 192 hastanın 23’ünde (%11.9) birinci derece akrabalarından en az birinin apandisit nedeni ile ameliyat edildiği tespit edildi. Bu hastaların beşinin ailesinde birden fazla kişi apandisit nedeni ile ameliyat edilmişti. Ailesel öyküsü olanların (AÖP) 21’inde (%91.3) apandisit (16 AA, 5 556

PA) ve 2 (%8.6) NA ile karşılaşıldı. Ailesinde birden fazla kişide AÖP olanların dördü AA, biride PA’ydı. Diğer 169 hastanın aile öyküsü negatifti (AÖN). Bu hastalardan 138’inde (%81.6) apandisit (111 AA, 27 PA) ve 31’inde (%18.3) NA görüldü. AÖP olan hastalarda apandisit daha sıklıkla görülmekle birlikte AÖN olanlarla arasında istatistiki olarak anlamlı bir fark görülmedi (p=0.316).

Akut apandisit 10 yaşından sonra erkek çocuklarda sıktır. Erkeklerde 1.1 ile 2.9 kat daha sık apandisit görülmüştür.[12] Yapılan çalışmalarda AA’nın 10-19 yaşları arasında belirgin olarak arttığı tespit edilmiştir.[13,14] Bizim çalışmamızda erkekler de kızlara nazaran belirgin olarak daha sık apandisit ile karşılaşıldı. Ayrıca hastalarımızda 10 yaşından sonra hem erkeklerde hemde kızlarda AA sıklığının arttığını tespit edildi. Sonuçlarımız literatür ile uyumludur.[12-14] Perfore apandisit, AA’nın tanısında gecikme sonucu oluşmaktadır. Yapılan çalışmaların çoğunda erkeklerde kızlara oranla daha sıktır. Ancak AA’da olduğu kadar bariz bir fark görülmemiştir.[13,15] Çalışmamızda erkeklerde daha sıktı. Yaş ile PA oranları arasında küçük değişiklikler görüldü.[15-17] Bununla birlikte bir kısım çalışmada özellikle iletişim kurulmanın ve muayenenin zor olduğu küçük çocuklarda PA’nın arttığı gözlenmiştir.[5,6,18,19] Lee ve ark.[15] yaptıkları çalışmada 5-14 yaş grubunda PA’nın pik yaptığını tespit etmişlerdir. Bizim çalışmamızda PA yaş ortalaması AA’ya göre daha küçüktü. Ayrıca beş yaş ve altındaki çocukların %56.5’inde perfore apandiksi tespit ettik. Bunun nedeninin küçük çocukların kendisini daha zor ifade etmeleri ve muayenenin zor yapılmasına bağlı olduğunu düşünmekteyiz. Negatif eksplorasyon oranı %24’lere kadar yükselebilmektedir.[20] Hastalarımızın %11.2’sinde NA vardı. Kızlarda daha sıktı (%63.6). Kız çocuklarında puberte ve postpubertal jineUlus Travma Acil Cerr Derg, Kasım 2013, Cilt. 19, Sayı. 6


Yıldız ve ark., Çocuk apandisitlerinde risk faktörlerinin analizi

kolojik problemler normal apandiks oranlarını artırmaktadır. [21] Bizde bu yaş grubu hastalarda jinekolojik patolojilere sık rastladık. Bu hastaların çoğunun gerçek patolojisi over kisti, kist rüptürü veya kist torsiyonu gibi jinekolojik patolojiler olduğunu gördük. Bu nedenle negatif apendektomi oranlarının hastanın yaşı ve cinsiyeti ile yakından ilişkili olduğunu düşünmekteyiz. Apandisit nedeni ile ameliyat edilen hastaların ailesel yatkınlığı konusunda yapılan çalışmalarda hastaların yaklaşık %10’unda AÖP bulunmuştur.[22] Karın ağrısı ile başvuran AÖP hastalarda 1.4 ile üç kat daha fazla apandisit ile karşılaşıldığı tespit edilmiştir.[23,24] Bunun nedeni olarak spesifik bakteriyel enfeksiyonlar, benzer diyet alışkanlıkları gibi çevresel faktörler sorumlu tutulmaktadır.[22] Çalışmamızda AÖP olan hastalarda AÖN tanılılara göre daha sık apandisit saptadık (91.3/81.6). Çalışmamızda iki grup arasında anlamlı fark saptamadık. Bunun nedeni olgu sayısı ile ilişkili olabilir. Konuyla ilgili kapsamlı çalışmalara ihtiyaç vardır. Apandisitin görülme sıklığı ile mevsimler arasında ilişki saptanmış olmakla birlikte hangi mevsimde daha sık görüldüğüne dair bir tartışma söz konusudur. Çalışmalarda AA yaz aylarında sık görülmekte iken, bir kısmında da kış aylarında daha sık görülmektedir.[2,13,15,17] Çalışmamızda AA sonbahar ve ilkbahar mevsiminde daha sık görülmekle birlikte istatistiki fark görmedik. Birçok çalışmada PA kış ve sonbahar aylarında daha sık bildirilmiştir.[13,21] Çalışmamızda PA’nın görülme dönemleri arasında fark görülmedi. Çalışmamız ile literatür arasındaki bu çelişkinin, çalışmayı yaptığımız bölgeyle diğer çalışmalar arasındaki iklim farkından kaynaklandığını düşünmekteyiz. Çalışmamız ve birçok diğer çalışmalarda apandisitin mevsimsel farkları apandisit oluşumunda hava sıcaklığından çok, çalışmanın yapıldığı bölgelerin nem, yağış gibi farklı iklimsel özelliklerinden veya bu mevsimlerle artan bakteri veya virüs enfeksiyonların etkili olduğunu düşündürtmektedir. Yine negatif apandiks görülme oranları yaz aylarında düşmekle beraber fark anlamlı bulunmadı. Yaz aylarındaki negatif appendektominin azalış nedeninin okul gibi stres faktörlerinin ortadan kalkmasıyla ilgili olabilir. Ancak bu konuda daha ayrıntılı çalışmalara ihtiyaç olduğunu düşünüyoruz. Sonuç olarak, apandisit etiyolojisi çok faktörlü olmakla birlikte birçok öncü faktörden etkilenmektedir. Bu nedenle karın ağrısı ile başvuran çocuklarda yaş, cinsiyet, ailesel yatkınlık ve bölgenin mevsimsel özelliklerinin göz önünde bulundurulup değerlendirilmesi tanıya yardımcı olacaktır. Ayrıca negatif eksplorasyon sıklığı puberte döneminde kız çocuklarda artmaktadır. Bu nedenle pubertedeki kız çocuklarının ayırıcı tanısında diğer yardımcı tanı ve tedavi yöntemlerinden (USG, BT ve laparaskopi gibi) daha fazla yararlanılması gerektiğini düşünüyoruz. Çıkar örtüşmesi: Çıkar örtüşmesi bulunmadığı belirtilmiştir. Ulus Travma Acil Cerr Derg, Kasım 2013, Cilt. 19, Sayı. 6

KAYNAKLAR 1. Karabulut R, Sonmez K, Turkyilmaz Z, Demirogullari B, Ozen IO, Demirtola A, et al. Negative appendectomy experience in children. Ir J Med Sci 2011;180:55-8. 2. Deng Y, Chang DC, Zhang Y, Webb J, Gabre-Kidan A, Abdullah F. Seasonal and day of the week variations of perforated appendicitis in US children. Pediatr Surg Int 2010;26:691-6. 3. Ates M, Coban S, Sevil S, Terzi A. The efficacy of laparoscopic surgery in patients with peritonitis. Surg Laparosc Endosc Percutan Tech 2008;18:453-6. 4. Pearl RH, Hale DA, Molloy M, Schutt DC, Jaques DP. Pediatric appendectomy. J Pediatr Surg 1995;30:173-81. 5. Rothrock SG, Skeoch G, Rush JJ, Johnson NE. Clinical features of misdiagnosed appendicitis in children. Ann Emerg Med 1991;20:45-50. 6. Horwitz JR, Gursoy M, Jaksic T, Lally KP. Importance of diarrhea as a presenting symptom of appendicitis in very young children. Am J Surg 1997;173:80-2. 7. Oguntola AS, Adeoti ML, Oyemolade TA. Appendicitis: Trends in incidence, age, sex, and seasonal variations in South-Western Nigeria. Ann Afr Med 2010;9:213-7. 8. Kulik DM, Uleryk EM, Maguire JL. Does this child have appendicitis? A systematic review of clinical prediction rules for children with acute abdominal pain. J Clin Epidemiol 2013;66:95-104. 9. Mueller BA, Daling JR, Moore DE, Weiss NS, Spadoni LR, Stadel BV, et al. Appendectomy and the risk of tubal infertility. N Engl J Med 1986;315:1506-8. 10. Morrow SE, Newman KD. Current management of appendicitis. Semin Pediatr Surg 2007;16:34-40. 11. Noh H, Chang SJ, Han A. The diagnostic values of preoperative laboratory markers in children with complicated appendicitis. J Korean Surg Soc 2012;83:237-41. 12. Shrestha R, Ranabhat SR, Tiwari M. Histopathologic analysis of appendectomy specimens. Journal of Pathology of Nepal 2012;2:215-9. 13. Sulu B, Günerhan Y, Palanci Y, Işler B, Cağlayan K. Epidemiological and demographic features of appendicitis and influences of several environmental factors. Ulus Travma Acil Cerrahi Derg 2010;16:38-42. 14. Al-Omran M, Mamdani M, McLeod RS. Epidemiologic features of acute appendicitis in Ontario, Canada. Can J Surg 2003;46:263-8. 15. Lee JH, Park YS, Choi JS. The epidemiology of appendicitis and appendectomy in South Korea: national registry data. J Epidemiol 2010;20:97105. 16. Addiss DG, Shaffer N, Fowler BS, Tauxe RV. The epidemiology of appendicitis and appendectomy in the United States. Am J Epidemiol 1990;132:910-25. 17. Luckmann R, Davis P. The epidemiology of acute appendicitis in California: racial, gender, and seasonal variation. Epidemiology 1991;2:323-30. 18. Hardin DM Jr. Acute appendicitis: review and update. Am Fam Physician 1999;60:2027-34. 19. Tobe T. inapparent virus infection as a trigger of appendicitis. Lancet 1965;1:1343-6. 20. Smink DS, Finkelstein JA, Kleinman K, Fishman SJ. The effect of hospital volume of pediatric appendectomies on the misdiagnosis of appendicitis in children. Pediatrics 2004;113:18-23. 21. Stein GY, Rath-Wolfson L, Zeidman A, Atar E, Marcus O, Joubran S, et al. Sex differences in the epidemiology, seasonal variation, and trends in the management of patients with acute appendicitis. Langenbecks Arch Surg 2012;397:1087-92. 22. Ergul E. Heredity and familial tendency of acute appendicitis. Scand J

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24. Gauderer MW, Crane MM, Green JA, DeCou JM, Abrams RS. Acute appendicitis in children: the importance of family history. J Pediatr Surg 2001;36:1214-7.

ORIGINAL ARTICLE - ABSTRACT OLGU SUNUMU

Analysis of risk factors for the development of pediatric appendicitis Turan Yıldız,1 M.D., Zehra Bozdağ, M.D.,2 Ünal Erkorkmaz, M.D.,3 Arif Emre, M.D.,4 Taner Turgut, M.D.,5 Zekeriya İlçe, M.D.1 Department of Pediatric Surgery, Sakarya University Faculty of Medicine, Sakarya Department of Pathology, Gaziantep University Faculty of Medicine, Gaziantep 3 Department of Biostatics, Sakarya University Faculty of Medicine, Sakarya 4 Department of General Surgery, Gebze Fatih State Hospital, Kocaeli 5 Department of General Surgery, Derince Training and Reseach Hospital, Kocaeli 1 2

BACKGROUND: Appendicitis is the most common form of abdominal pain requiring surgery among children. This study evaluates the association of age, sex, seasonal, and familial factors with the histopathology of appendectomies. METHODS: 588 patients who underwent operations for acute appendicitis between 2009 and 2011 were included in this study. The patients were classified in one of three groups based on histopathological results: acute, perforated, and negative appendectomy. This study evaluates the association between age, sex, seasonal, and familial factors and the histopathological classification. RESULTS: The mean age of the patients was 11.8±3.26 years (range 1 to 16 years). Among these patients, appendicitis was 2.41 times more common in children greater than 10 years old. Appendicitis occurred 4.63 times more often among males than in females. Negative appendectomy occurred more often in children greater than 10 years of age. Appendicitis was associated with both seasonal factors and family history; however this association did not meet the threshold for statistical significance (p>0.05). CONCLUSION: The age and sex of the patient should be taken into account when considering appendicitis surgery to improve the accuracy of the diagnosis. In addition, the histopathology of appendicitis is influenced by familial and environmental factors. Key words: Age; appendicitis; child; gender; heredity; season. Ulus Travma Acil Cerr Derg 2013;19(6):554-558

558

doi: 10.5505/tjtes.2013.52059

Ulus Travma Acil Cerr Derg, Kasım 2013, Cilt. 19, Sayı. 6


K Lİ NİK Ç A LI ŞM A

Karıniçi basınç artışına yol açabilen hastalıkların tedavisi intravezikal basınç ölçümü kontrolü altında daha güvenle yapılabilir mi?* Dr. Emre Divarcı,1 Dr. Orkan Ergün,1 Dr. Bülent Karapınar,2 Dr. Mehmet Yalaz,3 Dr. Ahmet Çelik1 1

Ege Üniversitesi Tıp Fakültesi, Çocuk Cerrahisi Anabilim Dalı, İzmir

2

Ege Üniversitesi Tıp Fakültesi, Çocuk Sağlığı Anabilim Dalı Yoğun Bakım Ünitesi, İzmir

3

Ege Üniversitesi Tıp Fakültesi, Çocuk Sağlığı Anabilim Dalı, Neonatoloji Bilim Dalı, İzmir

ÖZET AMAÇ: Karıniçi basınç artışına bağlı ilerleyici organ yetersizliği gelişebilmektedir. Travma, adheziv ileus, karın ön duvarı defektleri ve septik şokta sıvı resüsitasyonu çocukluk çağında karıniçi basınç artışına neden olabilen hastalıklardan bazılarıdır. Bu hastalıkların tedavisi karıniçi (intraabdominal) basınç (İAB) ölçümü kontrolü altında daha güvenle yapılabilir mi? GEREÇ VE YÖNTEM: Aralık 2009 - Ekim 2010 tarihleri arasında ileriye yönelik bir çalışma uygulandı. İAB saptanmasında intravezikal basınç (İVB) ölçümü kullanıldı. Tedavi stratejilerinin belirlenmesinde karıniçi hipertansiyon (İAB >12 mmHg) ve abdominal kompartman sendromu (İAB >15 mmHg + yeni gelişen organ disfonksiyonu) eşik değerler olarak kullanıldı. BULGULAR: Abdominal travma (n=14), karın ön duvarı defektleri (n=8), septik şokta sıvı resüsitasyonu (n=7) ve adheziv ileuslu (n=6) 35 hasta çalışmaya alındı. Travmalı hastaların %14’ünde AKS saptandı ve cerrahi gerekti. İAH/AKS karın ön duvarı defektli hastaların %38’inde defektin kapatılması sonrasında saptandı ve kapatma stratejileri değiştirildi. Septik şokta sıvı resüsitasyonu sırasında hastaların %43’ünde İAH gözlendi ve dekompresif girişimler uygulandı. İAH/AKS saptanan adheziv ileuslu üç hastada (%50) cerrahi girişim kararında basınç yüksekliklerinin katkısı oldu. SONUÇ: İntravezikal basınç ölçümü, izlem ve tedavileri sırasında İAB artışına yol açabilen hastalıkların tedavilerinin yönlendirilmesi ve girişim gerekliliğinin karar verilmesinde önemli katkılar sağlayabilmektedir. Riskli hastalık gruplarında İVB ölçümü, kolay ve güvenle uygulanabilecek yardımcı bir yöntemdir. Anahtar sözcükler: Abdominal kompartman sendromu; çocuk; ileus; intraabdominal basınç; karıniçi hipertansiyon; intravezikal basınç ölçümü; karın ön duvarı defekti; septik şokta sıvı resüsitasyonu; travma.

GİRİŞ Karıniçi basınç artışı çeşitli mekanizmalarla ilerleyici organ işlev bozukluğu yaratabilen klinik bir durumdur. Artmış karıniçi (intraabdominal) basınç (İAB) majör damarlara basıya bağlı kardiyak debiyi düşürmekte, diyafragmanın yükselmesine Sorumlu yazar: Dr. Ahmet Çelik, Ege Üniversitesi Tıp Fakültesi Hastanesi, Çocuk Cerrahisi Kliniği, Bornova, 35100 İzmir Tel: +90 444 1 343 E-posta: ahmet.celik@ege.edu.tr 29. Ulusal Çocuk Cerrahisi Kongresi’nde sunulmuştur (16-19 Mayıs 2011, İstanbul).

*

Ulus Travma Acil Cerr Derg 2013;19(6):559-563 doi: 10.5505/tjtes.2013.35478 Telif hakkı 2013 TJTES

Ulus Travma Acil Cerr Derg, Kasım 2013, Cilt. 19, Sayı. 6

neden olarak pulmoner oksijenizasyonu bozmakta ve dolaşım bozukluğu sonucunda renal yetersizliğe neden olabilmektedir (Şekil 1). Sonuçta gelişen çoklu organ yetersizliği tablosu, çocuklarda yüksek oranda mortaliteye yol açabilen abdominal kompartman sendromu (AKS) olarak adlandırılmaktadır (%50-60).[1- 3] İntravezikal basınç (İVB) ölçümü, İAB’nin saptanmasında klinik kullanımı kolay ve güvenilir bir yöntem olması nedeniyle öncelikle tercih edilmektedir.[4] Çocuklarda çeşitli klinik durumların izlem ve tedavileri sırasında İAB artışı gelişebilmektedir. Abdominal travma, karın ön duvarı defektleri, adheziv bağırsak tıkanıklığı ve septik şokta sıvı resüsitasyonu çocukluk çağında karıniçi basınç artışına neden olabilen yüksek riskli hastalıklardan bazılarıdır. İzlem ve tedavileri sırasında gelişebilen İAB artışı çoklu organ yetersizliğine yol açabilmektedir. Bu hastalıkların tedavisi İVB ölçümü kontrolü altında daha etkin ve güvenilir bir şekilde yapılabilir mi? 559


Divarcı ve ark., Karıniçi basınç artışına yol açabilen hastalıkların tedavisi ve intravezikal basınç ölçümü

evredir. İAH, İAB’nin birden çok ölçümde 12 mmHg’nın üzerinde saptanması olarak tanımlanmaktadır.[4]

GEREÇ VE YÖNTEM Kliniğimiz çocuk ve yenidoğan yoğun bakım ünitelerinde Aralık 2009 - Ekim 2010 tarihleri arasında karın travması, adheziv bağırsak tıkanıklığı, septik şokta sıvı resüsitasyonu ve karın ön duvarı defekti nedeniyle tedavi edilen hastalar ileriye yönelik olarak çalışmaya alındı. Hastanemiz etik kurulundan onay alındı. Karıniçi basıncın saptanması için klinik kullanımı kolay ve güvenilir bir yöntem olarak kabul edilen İVB ölçümü kullanıldı.

İntravezikal Basınç Ölçüm Tekniği İdrar sondası klemplendikten sonra, sonda girişim yerinden enjektör ile mesaneye 1 cc/kg (maksimum 20 cc) serum fizyolojik (SF) enjekte edilir. Sonrasında enjektör çıkarılıp içerisinden SF geçirilmiş düz serum seti iğnesiyle sondaya bağlanır. Enjeksiyon sonrası 30-60 sn beklendikten sonra düz serum seti plastik serum torbasına yakın bir noktadan kesilip içindeki SF’nin yerçekimi ile aşağı inmesi beklenir. Cetvelin alt ucu symphisis pubis seviyesinde tutularak sıvı sütunun son yüksekliği cm olarak ölçülüp mmHg’ya çevrilerek kaydedilir (1 mmHg=1,36 cm H2O). Çalışma grupları travma, karın ön duvarı defektleri, adheziv bağırsak tıkanıklığı ve septik şokta sıvı resüsitasyonu olarak belirlendi. Yüksek riskli hastalıkların yoğun bakım ünitelerindeki izlemleri sırasında düzenli İVB ölçümü yapıldı. Tedavi stratejileri belirlenirken karıniçi (intraabdominal) hipertansiyon (İAH) ve AKS eşik değerler olarak kabul edildi. Bu hastaların tedavileri İAH ve AKS’nin etkin şekilde tedavi edilmesi için yeniden düzenlendi.

İntraabdominal Hipertansiyon Tanısı İntraabdominal hipertansiyon, AKS gelişmeden önceki klinik İAB artışı Doku ödeminde artış

Hava yolu basınçlarında artış

Kapiller kaçak

Hiperkapni

Oligüri Viseral hipoperfüzyon

Pulmoner ventilasyonda bozulma

İskemi Kardiyak debide düşme

Şekil 1. İntraabdominal basınç artışının yarattığı patofizyolojik döngü.

560

Abdominal Kompartman Sendromu Tanısı Ölçüm sırasında intraabdominal basıncın 15 mmHg’nın üzerinde saptanmasına ek olarak aşağıdaki organ işlev bozukluğu ölçütlerinden bir veya daha fazlasının geliştiği hastalar AKS olarak kabul edildi: • Hacim genişleticilere veya diüretiklere refrakter oligüri (<1 ml/kg/saat) veya anüri. • Hemodinamik instabilite veya volüm genişleticilere refrakter hipotansiyon. • PCO2 artımı ve daha fazla FiO2 ve yüksek ventilasyon basıncı gereksinimi, normal solunumdaki hastada mekanik ventilatör gereksinimi gelişmesi. • ≥6 mmol baz defisiti ile giden metabolik asidoz. Metot olarak yüksek riskli hastalıkların tedavileri İVB ölçümlerine göre yapılması planlandı. Karın travmalı hastaların izlemleri İVB ölçümleri kontrolü altında yapılmaya çalışıldı. İAH/ AKS gelişimi durumunda ek girişim yapılması amaçlandı. Karın ön duvarı defektleri İVB monitorizasyonu altında kapatıldı. Yüksek İAB saptanması durumunda primer kapatmadan vazgeçilerek tedavi stratejisinin değiştirilmesi planlandı. Adheziv bağırsak tıkanıklığı olan hastaların izleminde ameliyat kararının verilmesinde yüksek İVB basınçlarının kullanılması amaçlandı. Septik şokta sıvı resüsitasyonunda ise aşırı IV sıvı verilmesinden kaçınmak için düzenli İVB ölçümü yapılması ve gerekirse karın içindeki serbest sıvının boşaltılması hedeflendi.

BULGULAR Abdominal travma (n=14), karın ön duvarı defekti (n=8), septik şokta sıvı resüsitasyonu (n=7) ve adheziv bağırsak tıkanıklığı (n=6) tanılarıyla çalışmaya alınan toplam 35 hastanın tedavisi İVB ölçümü kontrolü altında yapıldı. Hastalarda İAH/ AKS gelişimine göre tercih edilen tedavi stratejileri ve sonuçları Tablo 1’de ayrıntılı olarak belirtildi. Abdominal travma nedeniyle izlenen 14 hastanın üçünde İAH veya AKS gelişti (%21). Travma nedeniyle izlenen hastalarda ameliyat kararı verilmesinde AKS ve hemodinamik instabilite majör endikasyonlar olarak kabul edildi. On dört hastanın ikisinde AKS ve hemodinamik instabilite nedeniyle cerrahi tedavi uygulanması gerekti. Ameliyatsız izlenen hastaların ortalama en yüksek İAB değeri 7±3 mmHg iken, ameliyat edilen her iki hastada 22 mmHg olarak saptandı (Tablo 1). AKS tanısı, İAB’nin 15 mmHg’dan yüksek olmasına ek olarak anüri ve yüksek ventilasyon basınçları gereksinimi ile konuldu. Ameliyat sırasında dalakta arter, ven yaralanması izlenmedi. Dalak rüptürü saptananlara splenektomi yapıldı. Karıniçi kanama boşaltıldı, kan boşaltıldıktan sonra AKS düzeldi ve mortalite gelişmedi. AKS’li iki hastada da ameliyat sonrası İAB değeri 22 Ulus Travma Acil Cerr Derg, Kasım 2013, Cilt. 19, Sayı. 6


Divarcı ve ark., Karın içi basınç artışına yol açabilen hastalıkların tedavisi ve intravezikal basınç ölçümü

Tablo 1. Yüksek riskli hastalıklarda İAH/AKS gelişimine göre tercih edilen tedavi stratejileri ve tedavi sonrası İAB değerlerindeki değişim Tanı

Hasta sayısı (n)

Tedavi stratejisi

Tedavi öncesi İAB (mmHg)

Tedavi sonrası İAB (mmHg)

Travma (n=14)

İAH/AKS (-)

11

İzlem

6.5±2.5

6.2±2.3

İAH (+)

1

Sıvı kısıtlaması

13

9

AKS (+)

2

Dekompresif laparotomi ile splenektomi

22

9

Karın ön duvarı defektleri (n=8)

İAH/ AKS (-)

5

Primer kapatma

8.2±3.7

6±2.1

İAH (+)

2

Yama ile evreli onarım

13

7

AKS (+)

1

Dekompresif laparotomi ile

18

7

7

7

14.2

8.5

24

7

bağırsak rezeksiyonu Adheziv bağırsak obstrüksiyonu (n=6)

İAH/AKS (-)

3

İzlem

İAH (+)

2

Bridektomi

AKS (+)

1

Dekompresif laparotomi ile total bağırsak rezeksiyonu

Septik şokta sıvı resüssitasyonu (n=7)

İAH/AKS (-)

3

İzlem

8.6±1.1

8.5±1.1

İAH (+)

3

Parasentez/ultrafiltrasyon

14.5±3.2

9.5±4.7

İAH: İntraabdominal hipertansiyon; AKS: Abdominal kompartman sendromu; İAB: İntraabdominal basınç.

mmHg’dan 9 mmHg’ya geriledi. İAH saptanan hastada ise IV sıvı tedavisi düzenlenerek aşırı sıvı resüsitasyonundan kaçınılmaya çalışıldı. İzleminde AKS’ye gidiş olmadan, İAH tablosu düzeldi. Karın ön duvarı defektleri IVB ölçümleri kontrolü altında kapatıldı. Ameliyat sonrası sekiz saat aralıklarla İVB ölçümü yapıldı. Sekiz hastanın üçünde defektin kapatılması sonrasında İAH veya AKS gelişti (%38). İAH/AKS saptanmayan hastaların maksimum İAB değeri 8.2±3.7 mmHg olarak saptandı. İAH gelişen iki hastanın ameliyat öncesi düşük olan İAB değerleri kapatma sonrası 14 ve 13 mmHg’ya yükseldi. Bu iki hastada primer kapatmadan vazgeçilip yama ile evreli onarım yöntemine geçildi. İAB değerleri yama uygulaması sonrası 8 ve 7 mmHg’ya kadar geriledi. Yama günler içinde aralıklı olarak dikilerek daraltıldı ve defekt güvenli olarak kapatılabildi. Primer kapatma sonrası AKS gelişen hastada ise 18 mmHg’ya yükselen İAB değeri dekompresif laparotomi sonrası 5 mmHg’ya kadar geriledi. Dekompresif laparotomi sırasında yaklaşık 30 cm nekroze bağırsak segmenti rezeksiyonu yapılması gerekti. Rezeksiyon sonrası karın rahat olarak kapatılabildiği için yama konulmasına gerek görülmedi. Dekompresif işlem sonrası AKS düzeldi, mortalite gözlenmedi. Karın ön duvarı defektli tüm hastalarda defekt onarılarak etkin tedavi elde edildi. Ulus Travma Acil Cerr Derg, Kasım 2013, Cilt. 19, Sayı. 6

Septik şokta sıvı resüsitasyonu uygulanan yedi hastanın üçünde yüksek miktarda intravenöz sıvı verilmesine bağlı üçüncü boşlukta sıvı toplanmasına bağlı İAH gelişti (%43). İAH gelişen hastaların maksimum İAB değeri 14.5±3.2 mmHg iken gelişmeyen hastalarda 8.6±1.1 mmHg olarak saptandı. Dekompresif girişim olarak iki hastada parasentez, bir hastada ise ultrafiltrasyon uygulanarak serbest sıvı karın içinden uzaklaştırıldı. İAB değeri dekompresif işlem sonrası 14.5 mmHg’dan 9.5 mmHg’ya geriledi. Tüm hastalarda İAH evresinde müdahale edilerek AKS’ye gidiş önlendi. Adheziv bağırsak tıkanıklığı tanısıyla kliniğimize yatırılan altı hastanın üçünün izleminde İAH/AKS gelişti (%50). İAH/AKS gelişen hastaların maksimum İAB değeri 17.5±5.9 mmHg iken gelişmeyen hastalarda 8.1±2.4 mmHg saptandı. İAH/AKS saptanan hastalarda cerrahi tedavi uygulanması gerekti. İAH/ AKS saptanmayan hastaların ise izlem sonrasında bağırsak tıkanıklığı tablosu düzeldi. Yalnızca İAH/AKS gelişen hastalarda ameliyat gerekli oldu. Ameliyat sonrası maksimum İAB değeri 17.5±5.9 mmHg’dan 8±1.7 mmHg’ya geriledi. Cerrahi tedavi olarak İAH’li iki hastada bridektomi yeterli olurken, AKS gelişen hastada total intestinal ve kolonik rezeksiyon yapılması gerekti. AKS nedeni olarak, brid basısına bağlı gelişen tam tıkanıklığın geç fark edilmesi ve sonucunda enteral beslenmenin devam edilerek intestinal distansiyonun belirgin artması düşü561


Divarcı ve ark., Karıniçi basınç artışına yol açabilen hastalıkların tedavisi ve intravezikal basınç ölçümü

nüldü. Ani ve aşırı artan İAB intestinal dolaşımı bozarak total bağırsak nekrozuna yol açtığı belirlendi. AKS’li hastada ameliyat sonrası kısa bağırsak sendromu gelişti ve uzun dönemde kolestaz ve sepsise bağlı olarak kaybedildi (Tablo 1). İAH’li hastalarda ise tıkanıklık tablosu düzeldi, mortalite izlenmedi.

TARTIŞMA Artmış İAB’nin zararlı etkileri ilk olarak 1800’lü yıllarda tanımlanmıştır. İAB artışı sonucu ortaya çıkan İAH ve AKS’de kardiyak, renal, pulmoner, hepatik ve gastrointestinal sistem gibi çeşitli sistemlerde son organ işlev bozuklukları görülmektedir. [5-8] Çocuklarda AKS’ye bağlı yüksek oranda mortalite gelişmektedir (% 50-60).[1-3] İntraabdominal basıncı artışı diyafragmayı yükseltmekte, bu da intratorasik ve plevral basınçları artırarak akciğer ve göğüs duvarı kompliyansında ilerleyici bir azalmaya yol açmaktadır. [9-11] Artmış intratorasik basınç ve akciğer basısına bağlı gelişen hipoksik pulmoner vazokonstriksiyon pulmoner hipertansiyona neden olmaktadır. İnferior vena kava ve portal vene direkt basıya bağlı kardiyak venöz dönüş azalmaktadır. Artmış intratorasik basınç kalbe bası oluşturmakta ve kardiyak debiyi düşürmektedir. Kardiyak debide düşme ve direkt renal basıya bağlı renal disfonksiyon gelişmektedir.[12] Artmış İAB splanknik ve hepatik dolaşımda hipoperfüzyona yol açmaktadır. İAB artışında hemodinamik belirtilerin ortaya çıkmasından çok önce viseral dolaşımın bozulduğu gösterilmiştir.[13-15] Çocuk cerrahisinde artmış İAB’nin zararlı etkileri ilk olarak Gross tarafından karın ön duvarı defektli hastaların tedavisinde bildirilmiş ve evreli onarım önerilmiştir.[16] Sonrasında İAB kontrolü altında primer kapatma yıllar içinde daha sıklıkla kullanılmaya başlanmıştır. Chin ve arkadaşları[17] İVB 20 mmHg’nın üzerinde olan karın ön duvarı defektli hastalarda asit kaçağı, ventral herni oluşumu, ödem ve oligürinin daha sık olduğunu rapor etmiştir. Rizzo ve arkadaşları[18] karın ön duvarı defektli hastalarda primer kapatmanın İVB ölçümü eşliğinde yapılması durumunda hastanede kalış süresinin kısaldığını ve maliyetin düştüğünü belirtmişlerdir. Artmış İAB’nin primer kapatma sonrası nekrotizan enterokolit gelişiminde etkili olduğu da bildirilmiştir.[19,20] Bizim çalışmamızda da karın ön duvarı defektlerinin tedavisi İVB ölçümü kontrolü altında düzenlenmiştir. Primer kapatma sonrasında İAB artışına bağlı İAH veya AKS gelişen hastaların tedavi stratejisi yeniden düzenlenmelidir. Bu klinik durumların düzelmesi için primer kapatmadan vazgeçilip yama ile evreli onarıma geçilmelidir. AKS’ye bağlı intestinal nekroz gelişen hastalarda ise dekompresif laparotomi ve gerekirse bağırsak rezeksiyonu yapılmalıdır. Aralıklı İVB ölçümleri altında defektin kapatılması, İAH ve AKS’ye bağlı morbidite ve mortalite oranlarında belirgin düşme sağlayacaktır. Travma sonrası karıniçi kanamaya bağlı İAB artışı gelişebilmektedir. Çocuklarda batın travmasına bağlı solid organ yaralanması gelişen hastaların çoğunluğunun tedavisinde ameliyatsız 562

izlem yeterli olmaktadır. Çalışmamızda travmalı 14 hastanın ikisinde AKS, birinde İAH gelişmiştir (%21). İAH’li hastanın izleminde İAB değerleri gerilemiştir. AKS gelişen hastaların ise beraberinde hemodinamik instabilite olması nedeniyle ameliyata alınması gerekmiştir. Travmalı hastaların izlemi sırasında aralıklı İVB ölçümü yapılarak İAB takip edilmelidir. Karıniçi kanaması devam eden hastalarda İAB’de artış saptanmaktadır. Bu sayede kanaması devam eden hastalarda hemodinamide belirgin bozukluk gelişmeden daha erken müdahale edilebilecektir. Karın travması sonrası ameliyatsız izlem veya cerrahi tedavi kararının verilmesinde aralıklı İVB ölçümü ile İAB araştırılması güvenle uygulanabilecek etkili bir yöntemdir. Karıniçi basınç artışına neden olabilecek yüksek riskli hastalıklardan bir diğeri septik şokta sıvı resüsitasyonu uygulanan hastalardır. Çocuk yoğun bakım hastalarında sepsis, travma, yanık gibi hastalıkların tedavisinde yüksek miktarda intravenöz sıvı verilebilmektedir. Aşırı resüsitasyon sonrasında üçüncü boşluğa sıvı kaçışına bağlı İAH gelişmektedir.[21,22] Çalışmamızda septik şokta sıvı resüsitasyonu uygulanan toplam yedi hastanın üçünde İAH gelişmiştir (%43). Hastaların ikisinde parasentez birinde ultrafiltrasyon uygulanarak serbest sıvı karıniçi kompartmandan uzaklaştırılmıştır. Sonrasında tüm hastaların İAB değerlerinde anlamlı düşme ve vital fonksiyonlarında işlem öncesine göre belirgin düzelme izlenmiştir. Tüm hastalarda İAH düzeltilerek AKS’ye gidiş önlenmiştir. Şokta sıvı resüsitasyonu uygulanan hastalarda düzenli ve sık İVB ölçümü, İAH evresinde müdahale edilerek AKS’ye ilerlemenin önlenmesini sağlamaktadır. Çocuklarda da erişkinlerde belirtildiği gibi, septik şokta sıvı resüsitasyonu sırasında sık ve düzenli İVB ölçümleri yapılmalıdır. Adheziv bağırsak tıkanıklığı ile başvuran her hastada ameliyat gerekli olmamaktadır. Bazı hastaların izlemleri sırasında obstrüksiyon tablosu düzelebilmektedir. Ameliyat kararı ne kadar izlem sonrasında, hangi hastalarda verilmelidir? Adheziv ileusa bağlı abdominal distansiyon ve İAB artışı gelişmektedir. Çalışmamızda adheziv ileuslu altı hastanın üçünde İAH veya AKS saptanmıştır. AKS gelişen hastada dekompresif laparotomi amaçlı acil ameliyat uygulanmıştır. İAH’li hastalarda ise beraberinde NG sondadan devam eden safralı drenaj ve batın distansiyonu olması nedeniyle ameliyat gerekli görülmüştür. İAH/ AKS gelişmeyen hastaların izlemleri sonrası tıkanıklık tablosu düzelmiştir. Adheziv bağırsak tıkanıklığı olan hastaların klinik izlemi sırasında aralıklı İVB ölçümü yapılarak İAH veya AKS araştırılmalıdır. Ameliyat kararı ve zamanlaması İVB ölçümü kontrolü altında daha güvenle yapılabilmektedir. Tıkanıklığın düzelip düzelmeyeceği konusunda İVB ölçümleri ölçülebilir bir parametre olarak kullanılabilir.

Sonuç İntravezikal basınç ölçümü batın travması, adheziv bağırsak tıkanıklığı, septik şokta sıvı resüsitasyonu ve karın ön duvarı defektleri gibi izlem ve tedavileri sırasında karıniçi basınç artışına yol açabilen hastalıkların tedavilerinin yönlendirilmesi ve girişim gerekliliğinin karar verilmesinde önemli katkılar Ulus Travma Acil Cerr Derg, Kasım 2013, Cilt. 19, Sayı. 6


Divarcı ve ark., Karın içi basınç artışına yol açabilen hastalıkların tedavisi ve intravezikal basınç ölçümü

sağlayabilmektedir. Yüksek riskli hastalıklarda düzenli ve sık İVB ölçümü yapılarak erken dönemde İAB artışı saptanmaya çalışılmalı ve gerekirse kompresif işlemler uygulanmalıdır. Çıkar örtüşmesi: Çıkar örtüşmesi bulunmadığı belirtilmiştir.

KAYNAKLAR 1. Beck R, Halberthal M, Zonis Z, Shoshani G, Hayari L, Bar-Joseph G. Abdominal compartment syndrome in children. Pediatr Crit Care Med 2001;2:51-6. 2. Ejike JC, Humbert S, Bahjri K, Mathur M. Outcomes of children with abdominal compartment syndrome. Acta Clin Belg Suppl 2007;1:141-8. 3. Pearson EG, Rollins MD, Vogler SA, Mills MK, Lehman EL, Jacques E, et al. Decompressive laparotomy for abdominal compartment syndrome in children: before it is too late. J Pediatr Surg 2010;45:1324-9. 4. Malbrain ML, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med 2006;32:1722-32. 5. Saggi BH, Sugerman HJ, Ivatury RR, Bloomfield GL. Abdominal compartment syndrome. J Trauma 1998;45:597-609. 6. Eddy V, Nunn C, Morris JA Jr. Abdominal compartment syndrome. The Nashville experience. Surg Clin North Am 1997;77:801-12. 7. Fahy BG, Barnas GM, Flowers JL, Nagle SE, Njoku MJ. The effects of increased abdominal pressure on lung and chest wall mechanics during laparoscopic surgery. Anesth Analg 1995;81:744-50. 8. Fietsam R Jr, Villalba M, Glover JL, Clark K. Intra-abdominal compartment syndrome as a complication of ruptured abdominal aortic aneurysm repair. Am Surg 1989;55:396-402. 9. Bongard F, Pianim N, Dubecz S, Klein SR. Adverse consequences of increased intra-abdominal pressure on bowel tissue oxygen. J Trauma 1995;39:519-25. 10. Puri GD, Singh H. Ventilatory effects of laparoscopy under general anaesthesia. Br J Anaesth 1992;68:211-3. 11. Johannsen G, Andersen M, Juhl B. The effect of general anaesthesia on the haemodynamic events during laparoscopy with CO2-insufflation.

Acta Anaesthesiol Scand 1989;33:132-6. 12. Doty JM, Saggi BH, Blocher CR, Fakhry I, Gehr T, Sica D, et al. Effects of increased renal parenchymal pressure on renal function. J Trauma 2000;48:874-7. 13. Diebel LN, Wilson RF, Dulchavsky SA, Saxe J. Effect of increased intraabdominal pressure on hepatic arterial, portal venous, and hepatic microcirculatory blood flow. J Trauma 1992;33:279-83. 14. Schwarte LA, Scheeren TW, Lorenz C, De Bruyne F, Fournell A. Moderate increase in intraabdominal pressure attenuates gastric mucosal oxygen saturation in patients undergoing laparoscopy. Anesthesiology 2004;100:1081-7. 15. Kologlu M, Sayek I, Kologlu LB, Onat D. Effect of persistently elevated intraabdominal pressure on healing of colonic anastomoses. Am J Surg 1999;178:293-7. 16. Gross RE. A new method for surgical treatment of large omphaloceles. Surgery 1948;24:277-92. 17. Chin T, Wei C. Prediction of outcome in omphalocele and gastroschisis by intraoperative measurement of intravesical pressure. J Formos Med Assoc 1994;93:691-3. 18. Rizzo A, Davis PC, Hamm CR, Powell RW. Tntraoperative vesical pressure measurements as a guide in the closure of abdominal wall defects. Am Surg 1996;62:192-6. 19. Oldham KT, Coran AG, Drongowski RA, Baker PJ, Wesley JR, Polley TZ Jr. The development of necrotizing enterocolitis following repair of gastroschisis: a surprisingly high incidence. J Pediatr Surg 1988;23:9459. 20. Blane CE, Wesley JR, DiPietro MA, White SJ, Coran AG. Gastrointestinal complications of gastroschisis. AJR Am J Roentgenol 1985;144:58991. 21. Wilson MD, Dziewulski P. Severe gastrointestinal haemorrhage and ischaemic necrosis of the small bowel in a child with 70% full-thickness burns: a case report. Burns 2001;27:763-6. 22. Morrell BJ, Vinden C, Singh RN, Kornecki A, Fraser DD. Secondary abdominal compartment syndrome in a case of pediatric trauma shock resuscitation. Pediatr Crit Care Med 2007;8:67-70.

ORIGINAL ARTICLE - ABSTRACT OLGU SUNUMU

Can increased intra-abdominal pressure (IAP) be treated more effectively with intravesical pressure measurement in high-risk patients? Emre Divarcı, M.D.,1 Orkan Ergün, M.D.,1 Bülent Karapınar, M.D.,2 Mehmet Yalaz, M.D.,3 Ahmet Çelik, M.D.1 Department of Pediatric Surgery, Ege University Faculty of Medicine, Izmir; Department of Pediatrics, Intensive Care Unit, Ege University Faculty of Medicine, Izmir; 3 Department of Pediatrics, Division of Neonatology, Ege University Faculty of Medicine, Izmir 1 2

BACKGROUND: Increased intra-abdominal pressure (IAP) can result in multiorgan failure. Trauma, mechanical bowel obstruction (MBO), abdominal wall defects (AWD) and fluid resuscitation in septic shock are conditions associated with a high risk of increased IAP in children. It may be possible to treat these conditions more effectively using intravesical pressure measurement. METHODS: This prospective study was performed between December 2009 and October 2010. Intravesical pressure (IVP) measurement was used to determine IAP. The presence of Intra-abdominal hypertension (IAP >12 mmHg) and abdominal compartment syndrome (IAP >15 mmHg + new organ dysfunction) was evaluated in all clinical decisions. RESULTS: IVP monitoring was applied in all patients with abdominal trauma (14), AWD (8), fluid resuscitation for septic shock (7), and MBO (6). A diagnosis of ACS was determined in 14% of trauma patients and required surgery. IAH/ACS occurred in 38% of AWD cases, which required closure. IAH occurred in 43% of patients undergoing fluid resuscitation for septic shock, requiring decompressive intervention. IAH/ACS occurred in 50 % of MBO patients, all of whom required surgery. CONCLUSION: IVP measurement is a useful method to identify candidates for surgical treatment in cases of trauma and MBO. Similarly, IVP monitoring can facilitate the closure of abdominal wall defects and the application of fluid resuscitation in septic shock. Key words: Abdominal compartment syndrome; children; ileus; intraabdominal pressure; intraabdominal hypertension; Intravesical pressure measurement; abdominal wall defects; fluid resuscitation in septic shock; trauma. Ulus Travma Acil Cerr Derg 2013;19(5):559-563

doi: 10.5505/tjtes.2013.35478

Ulus Travma Acil Cerr Derg, Kasım 2013, Cilt. 19, Sayı. 6

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CAS E R EP O RT

Iliopsoas hematoma due to muscular rupture following defibrillation Artan Jahollari, M.D.,1 Raif Cavolli, M.D.,1 Murat Tavlasoglu, M.D.,2 Ferat Sallahu, M.D.,3 Shkelzen Muriqi, M.D.4 1

Department of Cardiovascular Surgery, International Medicine Hospital, Pristina, Kosova

2

Department of Cardiovascular Surgery, Diyarbakir Military Hospital, Diyarbakir, Turkey

3

Department of General Surgery, International Medicine Hospital, Pristina, Kosova

4

Department of Anaesthesia, International Medicine Hospital, Pristina, Kosova

ABSTRACT We describe a 62 year old patient who presented with acute anterior ischemia and subsequently developed an iliopsoas hematoma. The patient was treated surgically due to rapid progression and femoral neuropathy, and the iliopsoas muscle rupture was diagnosed intraoperatively. The rupture was related to the external electrical defibrillation the patient had on admission. This was a rare case, and we hope the report would help to raise physiciansâ&#x20AC;&#x2122; awareness regarding this complication and treatment. Key words: Defibrillation; hematoma; iliopsoas rupture.

INTRODUCTION Iliopsoas hematoma is a rarely seen form of retroperitoneal hemorrhage. The causes are various and the treatment differs based on the underlying pathology and clinical situations of the patient. We herein report the case of a patient who was admitted with acute anterior ischemia and afterward developed an iliopsoas hematoma. The patient underwent an operation and identified with an iliopsoas rupture, which was related to external electrical defibrillation. We could not find a similar case reported in the medical literature, and we think that our case report may be the first of its kind to be published.

CASE REPORT A 62-year-old male patient, who presented with severe Address for correspondence: Artan Jahollari, M.D. Preoc 10000 Magjistralja Prishtine-shkup Pristina - Kosovo Tel: +377 44 936 720 E-mail: artanjahollari@gmail.com Qucik Response Code

Ulus Travma Acil Cerr Derg 2013;19(6):564-566 doi: 10.5505/tjtes.2013.74152 Copyright 2013 TJTES

564

retrosternal pain, was diagnosed with acute anteroseptal ischemia. Several minutes after his admission he experienced ventricular fibrillation and was immediately converted with a single 200 joule shock of a biphasic defibrillator. Emergent coronary angiography via the right femoral artery was performed, revealing total thrombotic occlusion of the proximal LAD (left anterior descending artery) which was treated successfully with PCI (percutaneous coronary intervention). 5000 IU of unfractioned heparin was administered intravenously during the procedure and the following treatment included subcutaneous LMWH (low molecular weight heparin, enoxaparine sodium 6000 anti-Xa IU/0.6 ml, twice a day), aspirin 100 mg /day and clopidogrel 75 mg/day. On the 2nd day he complained of left flank pain and a decrease in hemoglobin was observed. An abdominal ultrasound revealed the presence of a left retroperitoneal hematoma. The magnetic resonance imaging (MRI) showed a large hematoma of the left iliopsoas muscle (Figure 1). Anticoagulants and antiagreggants were immediately stopped and the patient was followed conservatively, supplied with fresh frozen plasma and fresh blood. Despite ruling out active gross hemorrhage by a radial angiogram, the progressive decrease of hemoglobin persisted and the pain severity increased, radiating to the left leg. He developed abdominal defense and paresis of the left leg, which was attributed to femoral neuropathy. Urgent surgery consisting of a laparatomic exploration was performed on the 4th day. Approximately 1000 ml of aspirated fluid was collected from the retroperitoneal area. The psoas fascia was incised and a Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Jahollari et al., Iliopsoas hematoma due to muscular rupture following defibrillation

Figure 1. Axial view of MRI showing large hematoma of left iliopsoas muscle.

Figure 2. Intraoperative view of the ruptured iliopsoas.

mixture of 1000 ml of liquefied and clotted blood was removed. Rupture of the muscle fibers was observed and intact muscle parts were sutured together (Figure 2). During the postoperative period he was treated with LMWH (enoxaparine sodium 6000 anti-Xa IU/0.6 ml, daily). He had a rapid recovery and was discharged after 5 days on antiaggregant therapy (aspirin 100 mg /day and clopidogrel 75 mg/day).

DISCUSSION Hematoma of the iliopsoas muscle is a rare and challenging condition. Anticoagulant use, hemophilia, trauma, alcoholic cirrhosis, etc. appear to be some of the main causes.[1-3] However, the nature of this pathology is not fully understood and a many cases develop spontaneously.[4] Clinical manifestation includes abdominal and flank pain, abdominal distention and defense, hemorrhagic shock features, and leg or groin pain in presence of femoral nerve compression. Abdominal ultrasound provides a first glance and quick information about the ongoing condition. However, more specific tools, such as MRI and CT-scan, are necessary to confirm the pathology and help to make a proper decision. Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

There are different treatment modalities for iliopsoas hematomas. Good outcomes of conservative therapy have been successfully reported, and we agree that this is the first choice in stable patients. Patients suffering from hemophilia or that are under anticoagulant therapy seem to benefit the most from this choice. Local puncture can also be applied to drain the hematoma, but it carries the risk of further complications and is not helpful in removing clotted blood. Selective embolization of active branch bleeding is an option in selected patients and requires expertise. However, the definite treatment in complicated and unstable patients remains surgery. The presence of severe pain and the development of neurologic symptoms due to compression and hemorrhagic shock are some of the main indications for surgical decompression. Different sources strongly support the evacuation of the hematoma immediately after the onset of femoral neuropathy, and associate it with a great likelihood of a return to pre-event neurological status.[5-7] In our case, surgery was obligatory by abdominal defense, femoral neuropathy, and hemodynamic progression; all together compromising the general situation. Despite the delicate heart condition, our patient tolerated the surgery well and recovered quickly. During the surgery we discovered that rupture of the iliopsoas was the reason for the hematoma. Although it helped to increase the hemorrhage, anticoagulant usage cannot be blamed, as it does not explain the rupture of the muscle. On the other hand, defibrillation was the only physical trauma the patient experienced and it is a well-known fact that it provokes skeletal muscle contractions.[8] The psoas major muscle itself originates at the vertebral bodies of T12 and L1-L5 and their associated intervertebral discs, a region anatomically close to the apical defibrillator pad. External electrical defibrillation is an old and safe treatment modality in ventricular fibrillation, and very few cases with mechanical complications of external defibrillation have been reported. Most complications include skin burns, but bone and muscle involvement have also been described, including sternal[9] and vertebral fractures,[10] myocardial lesions,[11] and pectoral muscle necrosis.[12] Iliopsoas rupture due to defibrillation has not been previously reported and although it is a rare complication, it must be kept in mind owing to its potential severity. As a result, we herein described a rare case of iliopsoas hematoma due to muscular rupture. We strongly believe that the rupture resulted as a complication of external defibrillation. Conservative treatment is the therapy of choice in iliopsoas hematomas. However, surgery should be considered in rapidly progressing, neurologically complicated and hemodynamically unstable cases. Conflict of interest: None declared.

REFERENCES 1. Zago G, Appel-da-Silva MC, Danzmann LC. Iliopsoas muscle hema-

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6.

toma during treatment with warfarin. [Article in Portuguese] Arq Bras Cardiol 2010;94:1-3. [Abstract] Dauty M, Sigaud M, Trossaërt M, Fressinaud E, Letenneur J, Dubois C. Iliopsoas hematoma in patients with hemophilia: a single-center study. Joint Bone Spine 2007;74:179-83. Sugiyama C, Akai A, Yamakita N, Ikeda T, Yasuda K. Muscle hematoma: a critically important complication of alcoholic liver cirrhosis. World J Gastroenterol 2009;15:4457-60. Marquardt G, Barduzal Angles S, Leheta F, Seifert V. Spontaneous haematoma of the iliac psoas muscle: a case report and review of the literature. Arch Orthop Trauma Surg 2002;122:109-11. Parmer SS, Carpenter JP, Fairman RM, Velazquez OC, Mitchell ME. Femoral neuropathy following retroperitoneal hemorrhage: case series and review of the literature. Ann Vasc Surg 2006;20:536-40. Nakao A, Sakagami K, Mitsuoka S, Uda M, Tanaka N. Retroperitoneal hematoma associated with femoral neuropathy: a complication under antiplatelets therapy. Acta Med Okayama 2001;55:363-6.

7. Guivarc’h M. Hematoma of the iliac psoas muscle. 29 cases. [Article in French] J Chir (Paris) 1997;134:382-9. [Abstract] 8. Kim Y, Schimpf PH. Electrical behavior of defibrillation and pacing electrodes. Proceedings of the IEEE 1996;84:446-56. 9. Vollmann D, Lüthje L, Seegers J, Sohns C, Dorenkamp M, Vafa A, et al. Sternal fracture after elective electrical cardioversion of atrial fibrillation. Clin Res Cardiol 2011;100:261-2. 10. Giacomoni P, Cremonini R, Cristoferi E, Guardigli C, Gulinelli E, Matarazzo V, et al. Vertebral fracture caused by electric cardioversion. [Article in Italian] G Ital Cardiol 1987;17:543-5. [Abstract] 11. Liaudet L, Kehtari R, Enrico JF. Myocardial lesion secondary to defibrillation. Literature review and practical implications. [Article in French] Rev Med Suisse Romande 1993;113:933-43. [Abstract] 12. Vogel U, Wanner T, Bültmann B. Extensive pectoral muscle necrosis after defibrillation: nonthermal skeletal muscle damage caused by electroporation. Intensive Care Med 1998;24:743-5.

OLGU SUNUMU - ÖZET

Defibrilasyon sonrası gelişen kas yırtığına bağlı iliopsoas hematomu Dr. Artan Jahollari,1 Dr. Raif Cavolli,1 Dr. Murat Tavlasoglu,2 Dr. Ferat Sallahu,3 Dr. Shkelzen Muriqi4 International Medicine Hospital, Kalp ve Damar Cerrahisi Bölümü, Pristina, Kosova Diyarbakır Asker Hastanesi, Kalp ve Damar Cerrahisi Bölümü, Diyarbakır, Türkiye 3 International Medicine Hospital, Genel Cerrahi Bölümü, Pristina, Kosova 4 International Medicine Hospital, Anestezi Bölümü, Pristina, Kosova 1 2

Bu yazıda, akut anterior iskemi ile başvuran ve ardında iliopsoas hematomu gelişen 62 yaşında bir hasta sunuldu. Çabuk ilerleme ve femoral nöropati gelişmesi nedeniyle hasta cerrahi olarak tedavi edildi ve ameliyat sırasında iliopsoas kas yırtığı tespit edildi. Kas yırtığı, kabul esnasında uygulanan eksternal elektrik defibrilasyonla ilişkilendirildi. Bu nadir olgu sunumunun bu komplikasyon ve tedavisinin hakkında hekimlerin farkındalığını artıracağını ummuyoruz. Anahtar sözcükler: Defibrilasyon; hematom; iliopsoas yırtığı. Ulus Travma Acil Cerr Derg 2013;19(6):564-566

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Trauma-associated bleeding from the bilateral internal iliac arteries resolved using angiographic embolization Ali Aygün, M.D.,1 Yunus Karaca, M.D.,2 Emin Ayan, M.D.,3 Türkmen Suha, M.D.,1 Hasan Dinç, M.D.3 1

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

2

Department of Emergency Medicine, Kanuni State Hospital, Trabzon

3

Department of Radiology, Karadeniz Technical University Faculty of Medicine, Trabzon

ABSTRACT Pelvic fracture is associated with high mortality. The management of major pelvic injuries remains one of the most important issues in modern trauma care. A 39-year-old male patient presented at the emergency department after being hit with a 500 kg load. His general condition was average with unstable vital signs. Pelvic tomography revealed fractured bone structure, thickening secondary to hematoma in both iliopsoas muscles, and hemorrhage-related active extravasation in the left internal iliac trace. The patient’s hemodynamics worsened despite fluid and blood replacement, and angiographic embolization was scheduled. Bilateral embolization of the iliac artery was performed. Control angiography confirmed that full embolization was established. The patient was monitored in intensive care, but expired after three days due to acute kidney failure, disseminated intravascular coagulation, and multi-organ failure. Angiographic embolization is a technique improves hemorrhage control in pelvic trauma but can also increase risk of complications such as ischemia and necrosis. Key words: Angiography; embolization; bilateral internal iliac artery; hemorrhage; trauma.

INTRODUCTION

CASE REPORT

Pelvic factures are associated with high mortality. Extensive fractures may cause injury to the surrounding blood vessels, nerves, and urogenital and gastrointestinal organs. Post-traumatic arterial injuries generally result in the demise of the patient prior to arrival at the hospital. The management of major pelvic injuries remains one of the most important challenges in modern trauma care.[1] This report describes a case of bilateral internal iliac artery injury subsequent to pelvic fracture caused by trauma and bleeding in a patient undergoing hemodynamic stabilization using angiographic embolization.

A 39-year-old male patient presented at the emergency department after a 500-kg load fell on him. The patient was lucid and his general condition was rated as average. Blood pressure was 80/50 mmHg, pulse 120/min and respiratory rate 22/min. Physical examination revealed sensitivity in the pelvic region, ecchymosis in the scrotum, and deformity and sensitivity in the right femur. Pelvic radiography indicated a displaced fracture of the right femoral shaft, fracture of the bilateral iliac wings, separation of both sacroiliac joints, separation of the symphysis pubis, and a displaced fracture in both the left superior and inferior pubic ramus (Figure 1a). Following abdominal CT, we observed a linear displacement fracture in the right and left iliac wings, a fragmented displacement fracture extending to the sacroiliac joint in both sacral areas, linear displaced fracture in the left inferior and superior pubic ramus, increased symphysis in the pubis joint space, thickening secondary to hematoma in both iliopsoas muscles, and active extravasation in the left internal iliac artery trace (Figure 1b). Skin traction was applied to the right femur fracture and a pelvic bandage was applied for pelvic stabilization. The patient had shock-related hemodynamic impairment and was intubated and sent to the interventional radiology department. Angiography revealed active extravasation in the bilateral iliac artery truncus. The bilateral iliac artery was embolized us-

Address for correspondence: Ali Aygün, M.D. Karadeniz Teknik Üniversitesi Tıp Fakültesi, Acil Tıp Anabilim Dalı, 61080 Trabzon, Turkey Tel: +90 462 - 377 52 02 E-mail: dr_aliaygun@hotmail.com Qucik Response Code

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(a)

(b)

(c)

Figure 1. (a) Pelvic radiogram. (b) Active extravasation of contrast material administered by catheterization of the distal abdominal aorta from both internal iliac arteries (before embolization). (c) Appearance of the injury after embolization of the right and left iliac arteries.

ing a combination of NBCA-lipidol mixture and a coil artery occluder device (Figure 1c). Control angiography confirmed that full embolization had been established. Following the procedure, the patient was transferred to the intensive care unit for monitoring. Ischemia and gangrenous changes developed in the scrotal and gluteal regions. The patient expired on the third day as a result of acute kidney failure, disseminated intravascular coagulation, and multi-organ failure.

DISCUSSION Hemorrhaging in pelvic fractures is largely retroperitoneal leakage from the bone surfaces and the small vessels. Major arterial bleeding occurs in approximately 20% of cases. [2] Angiography is useful for the diagnosis and treatment of arterial bleeding subsequent to fracture injury. Ligation of the internal iliac arteries is an essential component in the treatment of unstable patients with massive pelvic bleeding. [1] Costantini et al.[3] identified active arterial extravasation in 18 of 31 patients with pelvic fracture who underwent angiography. Although negative angiography findings were obtained in the remaining 13 patients, therapeutic embolization was impossible in four cases due to the presence of hematoma in the fracture. In the present case, active arterial extravasation was identified and the embolization procedure was successfully performed. Early fracture stabilization and early angiography with embolization, and peritoneal pelvic packing can be performed in hemodynamically unstable patients with pelvic fractures. Angiography performs both diagnostic and therapeutic functions. It may be applied as a primary treatment in patients with serious and complex injuries. Intervention with angiography and embolization in patients with multiple bleeding foci avoids the potential side effects of laparotomy. In addition, arterial hemorrhage control prior to laparotomy prevents the aggravation of bleeding during laparotomy due to the decreasing tamponade effect. Angio-embolization has a success rate of 85-100% when conducted by experienced medical personnel.[4] Internal iliac artery ligation increases the risk of ischemic 568

complication in both the acute phase and during long-term follow up. Travis et al.[5] reported no significant difference in the incidence of skin necrosis, pelvic perineal infection, and nerve damage in the first 30 days in patients who underwent embolization compared to those who did not. However, a high incidence of hip and perineal region paresthesia was reported among the embolization patients. In a separate study by DuBose et al., no ischemic sequelae were observed during the course of hospitalization among patients who underwent iliac artery ligation.[1] In the present case, ischemic and gangrenous changes were observed in the scrotal and gluteal regions following angiographic embolization. The patient expired as a result of acute kidney failure and multiorgan failure on the third post-procedural day. In a study by Karadimas et al.[6] of patients undergoing angiographic embolization, five patients expired in the first 24 h due to hypotension and hemorrhage two as a result of multi-organ trauma, while one patient succumbed to pulmonary injury and another to multiple organ failure within days of the procedure. In a study by DuBose et al., 18 patients undergoing bilateral internal iliac ligation died. Seven of these patients died as a result of severe head trauma, another six died of cardiac arrest during surgery and five as a result of septic complications.[1]

Conclusion While angiographic embolization is a powerful technique for suppressing bleeding in pelvic trauma, it is associated with serious complications including ischemic necrosis. Conflict of interest: None declared.

REFERENCES 1. DuBose J, Inaba K, Barmparas G, Teixeira PG, SchnĂźriger B, Talving P, et al. Bilateral internal iliac artery ligation as a damage control approach in massive retroperitoneal bleeding after pelvic fracture. J Trauma 2010;69:1507-14. 2. Star AJ, Malekzadeh AS. Fractures of the pelvic ring. In: Bucholz RW, Heckman JD, Court-Brown CM, editors. Rockwood & Greenâ&#x20AC;&#x2122;s fractures in adults. Volume 2, 6th ed. Philadelphia: Lippincott Williams &

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Aygün et al., Trauma-associated bleeding from the bilateral internal iliac arteries resolved using angiographic embolization Wilkins; 2006. p. 1585-663. 3. Costantini TW, Bosarge PL, Fortlage D, Bansal V, Coimbra R. Arterial embolization for pelvic fractures after blunt trauma: are we all talk? Am J Surg 2010;200:752-8. 4. Fang JF, Shih LY, Wong YC, Lin BC, Hsu YP. Angioembolization and laparotomy for patients with concomitant pelvic arterial hemorrhage and blunt abdominal trauma. Langenbecks Arch Surg 2011;396:243-50.

5. Travis T, Monsky WL, London J, Danielson M, Brock J, Wegelin J, et al. Evaluation of short-term and long-term complications after emergent internal iliac artery embolization in patients with pelvic trauma. J Vasc Interv Radiol 2008;19:840-7. 6. Karadimas EJ, Nicolson T, Kakagia DD, Matthews SJ, Richards PJ, Giannoudis PV. Angiographic embolisation of pelvic ring injuries. Treatment algorithm and review of the literature. Int Orthop 2011;35:1381-90.

OLGU SUNUMU - ÖZET

Travma sonucu oluşmuş bilateral internal iliyak arter kanamasının anjiyografik embolizasyon ile sonlandırılması Dr. Ali Aygün,1 Dr. Yunus Karaca,2 Dr. Emin Ayan,3 Dr. Türkmen Suha,1 Dr. Hasan Dinç3 Karadeniz Teknik Üniverstesi Tıp Fakültesi, Acil Tıp Anabilim Dalı, Trabzon Kanuni Eğitim Araştırma Hastanesi, Acil Tıp Servisi, Trabzon 3 Karadeniz Teknik Üniverstesi Tıp Fakültesi, Radyoloji Anabilim Dalı, Trabzon 1 2

Pelvis kırıkları mortalitesi yüksek tarvmalardır. Majör pelvis yaralanmalarının yönetimi halen modern travma bakımının en önemli sorunlarından biridir. Otuz dokuz yaşında erkek hasta yaklaşık 500 kg ağırlığındaki yükün üzerine düşmesi nedeniyle acil servise getirildi. Hastanın genel durumu orta, vital bulguları dengesizdi. Pelvis tomografisinde kemik yapılarda kırıklar ile her iki iliopsoas kasında hematoma bağlı kalınlaşma ve sol internal iliak trasesinde kanamaya ait aktif ekstravazasyon vardı. Mayi ve kan replasmanına rağmen hemodinamisi bozulan hastaya anjiyografik embolizasyon uygulandı. Hastaya iki taraflı iliak arter embolizasyonu yapıldı. Embolizasyon sonrası yapılan kontrol anjiyografide tam embolizasyon sağlandığı görüldü. Hasta yoğun bakımında takibe alındı. Hasta takibinin üçüncü gününde akut böbrek yetersizliği ve dissemine intravasküler koagülasyon ve çoklu organ yetersizliği nedeniyle kaybedildi. Pelvik travmada anjiyografik embolizasyon kanama kontrolü açısından başrılı sonuçlar alınan bir yöntem olup iskemi nekroz gibi ciddi komlikasyonları beraberinde getirebilir. Anahtar sözcükler: Anjiyografi; embolizasyon; iki taraflı internal iliak arter, kanama, travma. Ulus Travma Acil Cerr Derg 2013;19(6):567-569

doi: 10.5505/tjtes.2013.00836

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A rare cause of acute appendicitis: an ingested foreign body Batuhan Hazer, M.D.,1 Özgür Dandin, M.D.,2 Dursun Özgür Karakaş, M.D.3 1

Department of General Surgery, Kasımpaşa Military Hospital, İstanbul

2

Department of General Surgery, Bursa Military Hospital, Bursa

3

Department of General Surgery, Ağrı Military Hospital, Ağrı

ABSTRACT Various kinds of foreign bodies causing appendicitis have been reported. However, a needle contained in the appendix is very rare, especially in adults. We report an unusual case of a twenty year old man who had ingested a needle ten days prior and presented with signs and symptoms of acute abdominal pain. An abdominal computed tomography scan revealed acute appendicitis. The patient was successfully treated with laparoscopic surgical intervention. In cases of a foreign body in the gastrointestinal tract that cannot be removed endoscopically, the emergence of non-specific symptoms may be early symptoms of acute problems in the abdomen. Key words: Appendicitis; foreign body; ingestion; needle.

INTRODUCTION

CASE REPORT

Foreign body ingestions are frequent in children, but rare in adults. Patients with mental disorders and prisoners are the individuals that comprise this group. Foreign bodies generally do not cause complications and pass through the gastrointestinal tract spontaneously, but perforation can occur by sharp or pointed foreign bodies or gastrointestinal erosions and abrasions can occur with retained foreign bodies which can cause bleeding.[1] Acute appendicitis caused by foreign bodies is a very rare condition.[2] The prevalence of appendicitis due to foreign bodies is approximately 0.0005%.[3] Various kinds of foreign bodies such as a needle, tongue stud, screw, crown post, tooth root, and pin can cause appendicitis.[2-7] Foreign bodies go into the appendiceal lumen and cause an inflammatory reaction with or without perforation.[4]

Address for correspondence: Dursun Özgür Karakaş, M.D. Ağrı Asker Hastanesi Baştabipliği, 04100 Ağrı, Turkey Tel: +90 472 - 215 11 29 E-mail: drdok1978@hotmail.com

A 20-year-old man was admitted with periumbilical pain and loss of appetite over duration of 24 hours. On physical examination, pain and defense was found on deep palpation of the right lower quadrant and the periumbilical region. The patient did not have a fever. White blood cells were 14,000×103/μL with an absolute neutrophil count of 80%. A metallic foreign body in the right lower quadrant was found upon abdominal X-ray and a needle in the appendix with local signs of appendicitis was found upon examination of a computed tomography (CT) scan (Figure 1). According to patient’s clinical signs and symptoms and CT scan we decided to perform a laparoscopic exploration. A slightly thickened and inflamed appendix was found during the exploration and an appendectomy was performed laparoscopically. Dissection of the appendicitis revealed a needle that represented the foreign body identified in the previous imaging studies (Figure 2a). The cause of appendicitis was not obstruction of lumen, but more likely due to the erosion of the needle close to the neck of the appendix. Pathologic evaluation was reported as a 7-cm long and 0.9-cm wide appendix with a macroscopic needle inside (Figure 2b) and an ulcerative appendicitis microscopically. The patient was discharged 3 days following surgery, with no postoperative complications.

Qucik Response Code

DISCUSSION

In this case we report about a 20-year-old man who underwent laparoscopic appendectomy for acute appendicitis due to foreign body ingestion.

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Complications usually depend on the size and shape of the foreign bodies. Blunt foreign bodies cause appendicitis through obstruction of the appendiceal lumen and remain dormant for longer periods. Elongated, sharp foreign bodies (75% of foreign bodies in the appendix) are more likely to cause perforations, appendicular abscesses and peritonitis.[2,9,10]

foreign bodies is estimated as less than 1%.[1,8]

The symptoms may vary from asymptomatic to abdominal pain, with or without vomiting or diarrhea. Ingestion of the foreign body history, low grade pyrexia and/or tenderness/ peritonism in the lower abdomen on examination and increased white cells and inflammatory markers on laboratory can be found. Radio opaque foreign bodies and/or free intraperitoneal air can be seen upon examination of the abdominal X-ray. Usually, a computed tomography would be required to confirm the diagnosis.[9]

It was reported that various foreign bodies have been discovered including sewing needles, retained shot pellets, tongue studs, endodontic files, drill bits, dog hair, toothbrush bristle, toothpicks, fishing lines, mercury (after ingestion of the bulb of a thermometer) and condom fragments in the appendix. [2,7,9,10] However, a needle in the appendix is a very rare condition.[10]

The management of ingested foreign bodies includes serial abdominal X-rays during follow up, endoscopic removal and surgery. Due to the risk of perforation if there is no spontaneous drainage of the foreign body or unsuccessful endoscopy, open or laparoscopic appendectomy is necessary to remove the needle.[10]

Figure 1. Computed tomographic images of foreign body in appendix.

Ingested foreign bodies may remain immobile in the appendix without stimulating an inflammatory response for extended periods or an inflammatory reaction with or without perforation.[4,10] The clinical presentation can vary from hours to years.[2,10] The prevalence of appendicitis due to foreign bodies is approximately 0.0005%.[3] Collins et al.[9] has reported that of the 51.8% of 71,000 appendectomies caused by foreign body, only 5.5% were due to unusual foreign bodies.

(a)

Foreign bodies that are asymptomatic and in the distal part of the small intestine can be monitored by conservative treatment. We did not have information related to swallowing a needle in our case. There were no classic abdominal examination findings of acute appendicitis. During the investigation of the etiology of abdominal pain, it was diagnosed as in the early stages of acute appendicitis. In conclusion, in cases of a foreign body in the gastrointestinal tract that cannot be removed endoscopically, and followed up

(b)

Figure 2. (a) Laparoscopic images of needle in appendix. (b) Macroscopic image of needle in appendix.

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with conservative treatment, the emergence of non-specific symptoms may be the early symptoms of acute problems in the abdomen. Conflict of interest: None declared.

REFERENCES 1. Ozkan Z, Kement M, Kargı AB, Censur Z, Gezen FC, Vural S, et al. An interesting journey of an ingested needle: a case report and review of the literature on extra-abdominal migration of ingested foreign bodies. J Cardiothorac Surg 2011;6:77. 2. Song YS, Covarrubias DA, Nardi PM. Foreign body appendicitis. AJR Am J Roentgenol 2009;193:W154-5. 3. Simkovic D, Hladík P, Lochman P. Unusual cause of the acute appendicitis. [Article in Czech] Rozhl Chir 2004;83:365-7. [Abstract]

4. Fischer CD, Mukherjee A. Appendicitis due to tongue stud ingestion: a case study and review of management plans. S D J Med 2004;57:19-22. 5. York GL. A unique case of foreign-body appendicitis. AJR Am J Roentgenol 2003;181:1431-2. 6. Kumar R, Bawa M, Ragavan M. Ingested metallic screw causing appendicitis in an infant--the metallic ‘Screw Appendicitis’. Indian J Pediatr 2010;77:337. 7. Abbey RK, Gupta R, Sharma RK, Sood PC. Acute appendicitis--an unusual cause. Indian J Med Sci 1999;53:108-10. 8. Moorjani V, Wong C, Lam A. Ingested foreign body mimicking an appendicolith in a child. Br J Radiol 2006;79:173-4. 9. Sar S, Mahawar KK, Marsh R, Small PK. Recurrent appendicitis following successful conservative management of an appendicular mass in association with a foreign body: a case report. Cases J 2009;2:7776. 10. Benizri EI, Cohen C, Bereder JM, Rahili A, Benchimol D. Swallowing a safety pin: Report of a case. World J Gastrointest Surg 2012;4:20-2.

OLGU SUNUMU - ÖZET

Akut apandisitin nadir bir nedeni: Yabancı cisim yutulması Dr. Batuhan Hazer,1 Dr. Özgür Dandin,2 Dr. Dursun Özgür Karakaş3 Kasımpaşa Asker Hastanesi, Genel Cerrahi Kliniği, İstanbul Bursa Asker Hastanesi, Genel Cerrahi Kliniği, Bursa 3 Ağrı Asker Hastanesi, Genel Cerrahi Kliniği, Ağrı 1 2

Çeşitli yabancı cisimlerin akut apandisite neden olduğu bildirilmiştir. Ancak apandikste iğne bulunması özellikle yetişkinlerde çok nadir görülmektedir. Bu yazıda, nadir bir olgu olan, 10 gün önce iğne yutan ve akut karın semptom ve bulguları ile başvuran 20 yaşındaki erkek hasta sunuldu. Karın BT görüntülerinde akut apandisit raporlanan hasta laparoskopik cerrahi girişim ile başarılı bir şekilde tedavi edildi. Endoskopik olarak çıkarılamayan ve konservatif tedavi ile takip edilen gastrointestinal sistemde yabancı cisim olan olgularda, nonspesifik semptomların ortaya çıkması akut karının erken dönem bulguları olabilir. Anahtar sözcükler: Apandisit; yabancı cisim; iğne; yutma. Ulus Travma Acil Cerr Derg 2013;19(6):570-572

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Acute intestinal obstruction secondary to left paraduodenal hernia: a case report Merve Busra Cengiz, M.D., Mustafa Hasbahçeci, M.D., Gökhan Cipe, M.D., Oğuzhan Karatepe, M.D., Mahmut Müslümanoğlu M.D. Department of General Surgery, Bezmialem Vakif University Faculty of Medicine, Istanbul

ABSTRACT Paraduodenal hernia, the most common type of internal herniation, is rare in the etiology of intestinal obstruction. Delayed diagnosis and surgical intervention may result in significant morbidity and mortality risk. This report presents a case of left paraduodenal hernia resulting in acute intestinal obstruction. A 43-year old male patient was admitted with a diagnosis of acute intestinal obstruction. A left paraduodenal hernia was identified by computed tomography findings of an encapsulated cluster of dilated small bowel loops occupying the left upper quadrant between the stomach and pancreas, and the presence of an engorged and displaced vascular pedicle at the orifice of the hernia. Upon further investigation, the dilated proximal jejunal segments were found in the left paraduodenal fossa, enclosed in a hernia sac. After reducing the intestinal segments to the abdominal cavity, the orifice of the hernia sac was closed by suturing to the retroperitoneum. Paraduodenal hernia should be considered as a possible etiology in cases of acute intestinal obstruction with unremarkable presentations. Physicians should be familiar with the demonstrative imaging findings of computed tomography of a paraduodenal hernia. Early surgical intervention is critical to prevent the significant morbidity and mortality associated with this condition. Key words: Internal hernia; intestinal obstruction; paraduodenal hernia.

INTRODUCTION Small bowel obstruction may be caused by internal herniation, or a protrusion of a viscus through a normal or abnormal peritoneal or mesenteric aperture within the confines of the peritoneal cavity. Internal herniation may be acquired or congenital.[1,2] Internal herniations are classified according to their location, and paraduodenal hernias are the most common type.[1] Although the reported incidence of internal hernia is less than 1%, internal hernia may account for the underlying pathology in up to 5% of cases of acute intestinal obstruction. In cases where diagnosis is delayed, intestinal strangulation and gangrene develop and result in a mortality rate of greater than 50%.[1,3] Address for correspondence: Mustafa Hasbahceci, M.D. Hırkai Şerif Mahallesi, Keçeci Çeşmesi Sokak, Doktorlar Sitesi, B Blok, No: 6/7, Fatih, İstanbul, Turkey Tel: +90 212 - 621 94 99 E-mail: hasbahceci@yahoo.com Qucik Response Code

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Widespread use of computed tomography (CT) in acute intestinal obstruction may aid physicians in diagnosing internal herniation through demonstrative preoperative imaging.[2,3] Prompt surgical intervention is essential to reduce the morbidity and mortality associated with internal herniation. In this paper, we aim to present a case of left paraduodenal hernia causing an acute intestinal obstruction, with particular regard to the associated imaging findings.

CASE REPORT A 43-year old male patient was admitted to our emergency department with abdominal pain, distention, nausea, vomiting, and obstipation for one day. The patient history revealed no systemic disease. He had previously undergone appendectomy and laparoscopic cholecystectomy. All vital signs were stable. Physical examination revealed marked abdominal distension, rebound tenderness, and abdominal guarding, especially in the left upper quadrant. Multiple air-fluid levels were observed on the abdominal X-ray. Laboratory analyses including complete blood count and biochemical analysis of the biliary and urinary systems were all normal except for an elevated leukocyte count of 14.0003/μL. An abdominal CT scan demonstrated an encapsulated cluster of dilated small bowel loops primarily occupying the left upper quadrant between 573


Cengiz et al., Acute intestinal obstruction secondary to left paraduodenal hernia

Figure 1. A coronal CT scan showing an encapsulated (between arrows) cluster of dilated small bowel loops occupying the left upper quadrant.

the stomach and the pancreas (Figure 1), and the presence of an engorged and displaced vascular pedicle at the orifice of the hernia (Figure 2). The patient underwent emergent laparotomy with a diagnosis of left paraduodenal hernia. On surgical exploration, the dilated proximal jejunal segments were found in the left paraduodenal fossa, which was enclosed in a hernia sac. After reducing the intestinal segments to the abdominal cavity, the orifice of the hernia sac was closed by suturing the retroperitomeum. The patient was discharged following an uneventful recovery.

DISCUSSION Internal hernia, which may be either acquired or congenital, is the protrusion of a viscus through a normal or abnormal peritoneal or mesenteric aperture within the confines of the peritoneal cavity.[1] The orifice of the hernia is either a preexisting anatomic structure, such as the foramen of Winslow, or a pathologic defect caused by a congenital or acquired etiology.[2,3] There are several distinct types on internal herniation with varying prevalence: left or right paraduodenal (53%), pericecal (13%), foramen of Winslow (8%), trans-mesenteric and trans-mesocolic (8%), intersigmoid (6%), and retroanastomotic (5%). Among these, paraduodenal hernia is the most common pathology. While paraduodenal hernias are 3 times more common in men, other types of internal herniation.[1] Although this type of hernia is congenital, presentation usually occurs in the 4th through 6th decades of life, as in this case.[4,5] Demographic features of the case presented in this study are consistent with the known risk factors for internal hernia. Despite past history of previous surgeries, these interventions are unlikely to be significant in the etiology of left paraduodenal hernia. However, it is important to note that the incidence of trans-mesenteric or trans-mesocolic hernia 574

Figure 2. An axial CT scan showing engorged and displaced vascular pedicle (thin arrow) at the orifice of the hernia, and dilated small bowel loops around this vascular pedicle in a hernia sac (thick arrow).

derived from the use of novel surgical procedures has increased in recent years and differential diagnosis should take this into consideration.[1] Paraduodenal hernias are classified in two categories according to their left or right side localization. Left paraduodenal hernia is defined as the herniation of the bowel through Landzertâ&#x20AC;&#x2122;s fossa, an aperture found in approximately 2% of the population.[3] Left sided paraduodenal hernia is more common than right-sided hernia, accounting for approximately 40-50% of all internal hernias. Landzertâ&#x20AC;&#x2122;s fossa is a hole through the mesocolon of the transverse colon located behind the ascending or fourth segment of the duodenum formed by the lifting of the peritoneal fold by the inferior mesenteric vein and ascending left colic artery running along the lateral fossa.[1,6] The most common presentation of internal herniation is acute small bowel obstruction with pain on the left upper segment of the abdomen, distention, nausea, vomiting, and obstipation. Some patients may experience recurrent symptomatic episodes that are often postprandial and relieved in the supine position.[7] Diagnosis of paraduodenal hernia is often difficult due to variable presentation and unremarkable findings during the physical examination. However, paraduodenal hernia should be considered in cases of acute intestinal obstruction in male patients with no prior history of abdominal surgery. Radiological imaging systems are essential for early diagnosis and facilitate planning of surgical treatment. Intestinal obstruction is typically diagnosed by abdominal X-ray.[8] However, CT is emerging as the most effective method for the diagnosis of paraduodenal hernia.[6] Encapsulated clustering of bowel loops at the duodenojejunal junction between the stomach and the pancreas to the left of the ligament of Treitz Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Cengiz et al., Acute intestinal obstruction secondary to left paraduodenal hernia

or behind the pancreatic tail itself and the left displacement of the inferior mesenteric vein are the major descriptive imaging features. Depression of duodenojejunal junction causing dilatation and air-fluid levels in the trapped loops, and the engorgement and crowding of the mesenteric vessels are characteristic features. Preoperative diagnosis of paraduodenal hernia was possible in this case as a result of several published reports describing diagnostic imaging characteristics.[2,7] Surgical treatment of left paraduodenal hernia follows the basic principles of hernia surgery: reduction of the contents, restoration of normal anatomy, and repair of the defect.[7] However, prompt surgical intervention is required for the prevention of strangulation and gangrene in cases with acute intestinal obstruction. After removal of the contents of the hernia sac, the viability of the bowel should be determined. During closure of the defect with non-absorbable sutures, attention should be given to avoid injury to the inferior mesenteric vein, located just anterior and lateral within the orifice. In cases where a defect prevents repair using sutures, widening of the defect may be performed to avoid future herniation.[5] In conclusion, internal herniation, and specifically paraduodenal hernia, is an unusual cause of acute intestinal obstruction. Internal herniation should be considered as the possible etiology of acute intestinal obstruction due to the unremarkable and nonspecific presentation. CT is a valuable imaging technique for patients with acute abdominal pain. Physicians

should be familiar with the characteristic imaging findings for internal herniation. Early surgical intervention is critical to avoid the morbidity and the mortality associated with this condition. Conflict of interest: None declared.

REFERENCES 1. Martin LC, Merkle EM, Thompson WM. Review of internal hernias: radiographic and clinical findings. AJR Am J Roentgenol 2006;186:70317. 2. Selçuk D, Kantarci F, Oğüt G, Korman U. Radiological evaluation of internal abdominal hernias. Turk J Gastroenterol 2005;16:57-64. 3. Fernández-Rey CL, Martínez-Álvarez C, Concejo-Cutoli P. Acute abdomen secondary to left paraduodenal hernia: diagnostic by multislice computer tomography. Rev Esp Enferm Dig 2011;103:38-9. 4. Bittner JG 4th, Edwards MA, Harrison SJ, Li K, Karmin PN, Mellinger JD. Laparoscopic repair of a right paraduodenal hernia. JSLS 2009;13:242-9. 5. Huang YM, Chou AS, Wu YK, Wu CC, Lee MC, Chen HT, et al. Left paraduodenal hernia presenting as recurrent small bowel obstruction. World J Gastroenterol 2005;11:6557-9. 6. Al-Khyatt W, Aggarwal S, Birchall J, Rowlands TE. Acute intestinal obstruction secondary to left paraduodenal hernia: a case report and literature review. World J Emerg Surg 2013;8:5. 7. Yun MY, Choi YM, Choi SK, Kim SJ, Ahn SI, Kim KR. Left paraduodenal hernia presenting with atypical symptoms. Yonsei Med J 2010;51:787-9. 8. Sen M, Inan A, Dener C, Bozer M. Paraduodenal internal hernias: clinical analysis of two cases. Ulus Travma Acil Cerrahi Derg 2007;13:232-6.

OLGU SUNUMU - ÖZET

Sol paraduodenal fıtığa bağlı akut intestinal tıkanıklık: Olgu sunumu Dr. Merve Busra Cengiz, Dr. Mustafa Hasbahçeci, Dr. Gökhan Cipe, Dr. Oğuzhan Karatepe, Dr. Mahmut Müslümanoğlu Bezmialem Vakıf Üniversitesi Tıp Fakültesi, Genel Cerrahi Anabilim Dalı, İstanbul

Paraduodenal fıtık, internal fıtığın en sık görülen tipi olarak akut intestinal tıkanıklığın nadir bir sebebidir. Tanı ve cerrahi tedavideki gecikmeler yüksek morbidite ve mortalite için önemli olabilir. Bu yazıda, akut intestinal tıkanıklığa sebep olan bir sol paraduodenal fıtık olgusu sunuldu. Kırk üç yaşındaki bir erkek hasta akut intestinal tıkanıklık ön tanısı ile başvurdu. Bilgisayarlı tomografide saptanan, mide ile pankreas arasında özellikle sol üst kadranı dolduran enkapsüle dilate ince bağırsak segmentleri kümesi ve fıtık açıklığında bulunan genişlemiş ve yer değiştirmiş ince bağırsak vasküler pedikülü bulguları ile sol paraduodenal herni tanısı kondu. Eksplorasyonda, sol paraduodenal fossa yerleşimli bir fıtık kesesi içerisinde sınırlanmış dilate proksimal ince bağırsak segmentlerinin olduğu görüldü. Bağırsak segmentleri karın içi boşluğa redükte edildikten sonra, fıtık açıklığı retroperitona dikilerek kapatıldı. Paraduodenal fıtık, belirgin olmayan başvuru şekli nedeniyle akut intestinal tıkanıklığın olası bir sebebi olarak düşünülmelidir. Hekimler bilgisayarlı tomografi ile elde edilebilen tanısal görüntüleme bulgularına aşina olmalıdır. Erken cerrahi girişim, bu hastalık ile ilişkili morbidite ve mortalitenin azaltılması için önemlidir. Anahtar sözcükler: İnternal fıtık; intestinal tıkanıklık; paraduodenal fıtık. Ulus Travma Acil Cerr Derg 2013;19(6):573-575

doi: 10.5505/tjtes.2013.30776

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OLGU SUNUMU

Travma sonrası geç prezente olmuş pulmoner arteriyovenöz fistülün septal tıkayıcı cihaz ile kapatılması Dr. Bülent Güçyetmez,1 Dr. Ece Salihoğlu,2 Dr. Aykut Ayyıldız,3 Dr. Levent Saltık,4 Dr. Lütfi Telci5 1

International Hospital, Genel Yoğun Bakım Ünitesi, İstanbul

2

Acıbadem Üniversitesi Tıp Fakültesi, Kalp Damar Cerrahisi Anabilim Dalı, İstanbul

3

Maslak Acıbadem Hastanesi, Genel Yoğun Bakım Ünitesi, İstanbul

4

İstanbul Üniversitesi Cerrahpaşa Tıp Fakültesi, Çocuk Hastalıkları Anabilim Dalı, İstanbul

5

İstanbul Üniversitesi İstanbul Tıp Fakültesi, Anesteziyoloji Anabilim Dalı, İstanbul

ÖZET Travmatik pulmoner arteriyovenöz fistül (PAVF) genelde penetran yaralanmalardan sonra gelişen nadir bir komplikasyondur. Yıllarca semptomsuz kalarak geç dönemde tespit edilebilir. Bu yazıda altı yıl önce geçirilmiş penetran toraks travması sonrası gelişen ve septal tıkayıcı cihaz ile kapatılan PAVF olgusu sunuldu. Penetran toraks travmalarında bilgisayarlı tomografik anjiyografi ve pulmoner arteriyografinin rutin olarak kullanılması geç dönemde oluşabilecek semptomatik PAVF tespitinde önemlidir. Yeni nesil tıkayıcı cihazlar sayesinde daha geniş ve yüksek basınçlı defektlerin kapatılmasında transkateter yaklaşım uygun olgularda cerrahi tedaviye alternatif olabilir. Anahtar sözcükler: Penetran toraks travması; pulmoner arteriyovenöz fistül; septal tıkayıcı cihaz.

GİRİŞ Pulmoner arteriyovenöz fistül (PAVF) pulmoner arter ile pulmoner ven arasında direkt bağlantı olmasıdır ve anatomik sağ-sol şanta neden olur.[1,2] Ülkemizde 16 olgu sunumu bildirilmiştir.[3] Doğuştan PAVF olgularının %80-90’ı herediter hemorajik telenjiektazi (HHT) ile birliktelik gösterir ve Osler Weber Sendromu olarak tanımlanır.[4] Sonradan gelişen PAVF ise siroz, metastatik troit karsinom, “schistosomiasis”, “actinomycosis”, fanconi sendromu, mitral stenoz ve penetran toraks travması sonrası oluşabilmektedir.[5] Penetran toraks travması sonrası akut dönemde veya geç dönemde PAVF oluştuğuna dair olgular bildirilmiştir.[6,7] En sık raslanan semptom %21-71 ile efor dispnesidir. Hipokseminin şiddeti şantın boyutu ile ilişkilidir.[1,6] Fiziksel incelemede ise en sık siyanoz, çomak

İletişim adresi: Dr. Bülent Güçyetmez, International Hospital, İstanbul Caddesi, No: 82, Yeşilköy, İstanbul Tel: +90 212 - 468 41 44 E-mail: drbulentgucyetmez@yahoo.com Qucik Response Code

Ulus Travma Acil Cerr Derg 2013;19(6):576-580 doi: 10.5505/tjtes.2013.06432 Telif hakkı 2013 TJTES

576

parmak ve pulmoner vasküler üfürüm, HHT’lerde ayrıca cilt lezyonları saptanır.[2,8] Tanıda akciğer grafisi, ekokardiyografi ve BT-Anjiyografi, pulmoner arteriyografi kullanılır. Tedavide lokalizasyon ve fistülün çapı önemlidir. Patolojiye göre cerrahi veya transkateter yöntemler uygulanabilir.[6,9,10] Bu yazıda, altı yıl önce geçirilmiş penetran toraks travmasına bağlı gelişen ve septal tıkatıcı cihaz ile kapatılan PAVF olgusu sunuldu.

OLGU SUNUMU Altı yıl önce toraks nafiz ateşli silah yaralanması ile hastanemiz acil servisine başvuran 37 yaşında kadın hastanın karın tomografisinde solid organ yaralanması tespit edilmemiş, toraks tomografisinde ise sol akciğerde bir, sağ akciğerde ikisi santral yerleşimli üç adet kurşun, akciğer kontüzyonu, iki taraflı hemopnömotoraks, sağ 6-7. kot kırığı saptanarak yoğun bakım ünitemize alınmıştır. Solunum yetersizliği olan hastaya iki taraflı toraks dreni takılmış ve mekanik ventilasyon desteğine başlanmıştır. Üç gün mekanik ventilasyon desteğinde takip edilen hasta üçüncü gün ekstübe edilmiş, yedinci gün toraks drenleri çekilmiştir. Sonraki günler aralıklı non-invaziv mekanik ventilayon (NIMV) desteği sağlanarak 10. günde spontan solunumda nazal oksijen desteğinde (2lt/dk), SpO2 %98 ve hemodinamik parametreleri stabil halde kata transUlus Travma Acil Cerrahi Derg, Kasım 2013, Vol. 19, No. 6


Güçyetmez ve ark., Travma sonrası geç prezente olmuş pulmoner arteriyovenöz fistülün septal tıkayıcı cihaz ile kapatılması

450 400 350 300 250 200 150 100 50 0

PaO2/FiO2

400

274 203 167

169

156

178

222

235 173

1. gün 2. gün 3. gün 4. gün 5. gün 6. gün 7. gün 8. gün 9. gün 10. gün

Şekil 1. Yoğun bakım süresince PaO2/FiO2 oranının günlük seyri.

105 100 95 90 85

SpO2 (ort.)

80

SpO2 (min.)

75

fer edilmiştir. Yoğun bakım yatışı süresince günlük minimum “Harowitz oranı” (PaO2/FiO2 oranı), ortalama ve minimum periferik satürasyon (SpO2) değerleri Şekil 1 ve Şekil 2’de gösterilmiştir.

1. gün 2. gün 3. gün 4. gün 5. gün 6. gün 7. gün 8. gün 9. gün 10. gün

Şekil 2. Yoğun bakım süresince ortalama ve minimum SpO2 seyri.

On üçüncü günde solunum sıkıntısı gelişen hastada pulmoner emboliden şüphelenilerek çekilen akciğer grafisi ve BT anjiyografi görüntüleri radyoloji tarafından normal olarak değerlendirilmiştir (Şekil 3). Bronkodilatör tedavi ile klinik tablosu düzelen (oda havasında SpO2 %98) hasta travmanın 20. gününde taburcu edilmiştir. Altı yıl sonra, son bir yıl içinde giderek artan halsizlik, ellerde uyuşma, baş ağrısı ve efor dispnesi ile tekrar hastanemize başvuran hastanın yapılan muayenesinde dudaklarda siyanoz ve çomak parmak tespit edilmiştir. Hemodinamik parametreleri stabil olan hastanın oda havasında SpO2 %85 ölçülmesi üzerine alınan arter ve ven kan gazları arasında fark olmadığı görülmüştür. %100 oksijen altında satürasyonda artma olmayan hastaya BT anjiyografi yapılmıştır. BT anjiyografide pulmoner kapiller yatak kontrastla boyanmadan pulmoner

Yoğun bakım yatışı

13. gün

6 yıl sonra

Şekil 3. Radyolojik görüntülemeler (yoğun bakım girişi, yoğun bakım çıkışı, endovasküler tedavi öncesi).

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Güçyetmez ve ark., Travma sonrası geç prezente olmuş pulmoner arteriyovenöz fistülün septal tıkayıcı cihaz ile kapatılması

120

100 103

98.5

97.9

100

95

83.5

80 SaO2

PaO2

90 60

85

50.6

40

84.3

20

80

0

75

80

105 69.6

70 60

100

58

48

40 30

SpO2

PvO2

50

90 85

20

85

80

10 0

99

98

95

Yoğun bakım çıkışı

Endovasküler tedavi Endovasküler tedavi öncesi sonrası

75

Yoğun bakım çıkışı Endovasküler tedavi Endovasküler tedavi öncesi sonrası

Şekil 4. Endovasküler tedavi yanıtı.

ven, pulmoner arter ve sol atriyumun eş zamanlı kontrast ile boyandığı görülerek PAVF tanısı konmuştur. BT anjiyografide defektin boyutu 2.15 cm olarak tespit edilmiştir. Geriye dönük olarak altı yıl önceki BT anjiyografi tekrar incelendiğinde boyutu 0.97 cm olan PAVF tespit edilmiştir (Şekil 3). Kalp damar cerrahisi ve kardiyoloji departmanlarının yaptığı değerlendirme sonrası fistülün yeri ve çapı endovasküler tedaviye uygun bulunarak septal tıkayıcı cihaz ile kapatılmasına karar verilmiştir (Şekil 4). Hasta kateter laboratuvarında lokal anestezi altında direkt pulmoner arteriyografi yapılarak fistül boyutu tam olarak ölçülmüş, uygun ebatta septal tıkayıcı cihaz ile kapatılmıştır. Septal tıkayıcı cihaz uygulamasını takiben klinik, kan gazı ve satürasyon değerleri düzelen hasta 24 saat klinik izlem sonrası taburcu edilmiştir. Hasta halen işlem sonrası ikinci yılında oda havasında SpO2 %97 ile kardiyoloji tarafından klinik olarak takip edilmektedir ve yıllık yapılan ekokardiyografi kontrollerinde rekanalizasyon tespit edilmemiştir.

TARTIŞMA Penetran toraks travması tüm toraks travmalarının %30’unu oluşturur ve hemotoraks, pnömotoraks ve hemopnömotoraks en sık görülen komplikasyonlardır.[11] Buna ek olarak nadir de olsa PAVF oluşabilir. PAVF patogenezinde terminal arterlerde oluşan defekt ile ince duvarlı kapiller keselerin dilatasyonu ileri sürülmektedir.[12] Tek veya çoklu olabilen PAVF yerleşim yeri sıklıkla alt loblardır. İki taraflı görülme oranı %8-20 arasında bildirilmiştir.[2] Santral penetran toraks yaralanmaları ventriküler septal defekt (VSD) ile birliktelik 578

gösterebilir.[9] Olgumuz santral penetran toraks yaralanması olmasına rağmen VSD ile birliktelik göstermeyen bir PAVF’dir. Penetran toraks travmalarından sonra oluşan PAVF’lerin %1355’i semptomsuz seyretmektedir ve bu olgularda PAVF boyutu 2 cm’nin altındadır.[2,13] Olgumuz boyutu 0.97 cm olan ve yaklaşık beş yıl kadar semptomsuz seyreden bir PAVF olgusudur (Şekil 3). Semptomsuz PAVF’ler yıllar içinde büyüme eğilimi göstererek semptomatik hale gelebilir.[14] Gebelik gibi kan hacmi, kan akımı ve pulmoner kan akımı artışı ile hormon değişimine neden olan durumların PAVF’nin dilatasyonuna ve büyümesine neden olduğu ileri sürülmektedir.[2] Olgumuzun son bir yıl içinde ağır egzersize başlamış olmasının PAVF’nin semptomatik hale gelmesinin nedeni olduğu düşünülmüştür. Defektin boyutu 2 cm’yi aştığı zaman “platipne” (dik pozisyonda dispnenin artması) ve “ortodeksia” (dik pozisyonda oksijen satürasyonunun düşmesi) gözlenebilir. Hastaların %43 ile %67’sinde migren tarzı baş ağrısı, vertigo, parezi, uyuşma, senkop, konfüzyon refrakter hipoksemi, siyanoz, çomak parmak ve efor dispnesi görülebilir.[2,15] Defektin boyutu 2.15 cm’ye ulaşan olgumuzda da başağrısı, ellerde uyuşma gibi nörolojik bulgular ile birlikte siyanoz, çomak parmak ve efor dispnesi geliştiği görülmüştür. PAVF oluşumuna bağlı gelişen anatomik sağ-sol şant refrakter hipoksemi nedenidir.[5,16] Refrakter hipoksemi %100 oksijen desteğine rağmen PaO2 ve SpO2 değerlerinin yükselmemesi olarak tanımlanabilir.[16] Olgumuzda istirahat halinde PaO2 50.6 mmHg, PvO2 48 mmHg, SaO2 %84.3 ve SpO2 %84 olarak görülmüş ve %100 oksijen ile bu değerlerin yükselmedikleri gözlenmiştir. PAVF tanısında direkt grafilerin tanı niteliği taşımadığı ve tanının pulmoner anjiografi ile konulduğuna dair yayınlar bulunmaktadır.[17] Bazı yayınlar Ulus Travma Acil Cerrahi Derg, Kasım 2013, Vol. 19, No. 6


Güçyetmez ve ark., Travma sonrası geç prezente olmuş pulmoner arteriyovenöz fistülün septal tıkayıcı cihaz ile kapatılması

görülmektedir.[21,25] Son yıllarda tıbbi mühendislik alanındaki gelişmelerle embolizasyon araçları da yenilenmektedir. Diğer ‘coil’ tipi basit tıkayıcı tellerden daha komplike bir yapısı olan bu yeni nesil aparatlar kafes tipi bir dokuya ve açıldıklarında mantar benzeri bir görüntüye sahiptir (Şekil 5). Bu sistem ‘coil’den farklı olarak sadece defektin içini doldurmayıp, açıldığında mantarın boyun kısmı defekti doldururken, her iki taraftaki mantar yapının başını oluşturan bölüm çevredeki sağlam dokuyu destek alarak dışarı doğru taşar; böylece hem defektin tamamen kapatılması hem de yerleştirilen aparatın çevre dokuya sabitlenmesi sağlanır (Şekil 6). Günümüzde kalp içi defektelerin kapatılmasında tercih edilen sistemler ile geniş ve yüksek basınçlı defektlerin basit kateter yöntemleri kullanılarak güvenli bir şekilde kapatılması mümkün olmaktadır.[24] Bu yöntemin daha sık rastlanan doğumsal PAVF tedavisi ile ilgili iyi tecrübeler mevcuttur.[23,24,26]

Şekil 5. Septal tıkayıcı cihazın görünümü.

Sağlam doku kenarı

Septal tıkayıcı cihaz

Şekil 6. Septal tıkayıcı cihazın defekt içine yerleşmiş hali.

ise akciğer grafisinde nodüller görülebildiğini BT anjiyografi, kontrastlı ekokardiyografi ve pulmoner arteriyografide ise şant bölgesinde kontrast geçişi gözlendiğini belirtmektedir.[18] Akciğer grafisinde nodül görünümü olmayan olgumuzda BT anjiyografi ile kontrast geçişi görülerek defektin yeri ve boyutu belirlenmiştir. Bu nedenle tanıda akciğer grafisinin belirleyici olmadığını; BT anjiyografi ve pulmoner arteriyografinin ise tanı koydurucu olduğunu düşünmekteyiz. PAVF tedavisi lezyonun yerleşimi ve çapına göre değişkenlik göstermektedir. Küçük çaplı fistüllerde embolizasyon ile başarılı sonuçlar elde edilmektedir ancak lezyonun büyük ve santral yerleşimli olduğu olgularda cerrahi tedavi daha ön planda yer almaktadır.[19-21] Cerrahide yaklaşım, fistülün çapına göre basit fistül kapatılmasından lobektomiye kadar giden geniş bir yelpazede yer alır.[21,22] Transkateter yaklaşımda sıklıkla kullanılan basit ‘coil’ tipi tıkayıcılarla rekanalizasyon, migrasyon, trombüs gibi sorunlar bildirilmiştir.[23] Buna karşılık bu yöntem ile akciğer parenkiminin korunması, torakotomiye bağlı komplikasyon riskinden uzaklaşma, genel anestezi ve cerrahi insizyon gerektirmemesi, iyileşme sürecinin kısa ve hızlı olması gibi önemli avantajları sebebi ile uygun vakalarda ilk tercih edilen yöntem olmuştur.[24] Ancak travma sonrası oluşan fistüllerde defektin genellikle yüksek basınçlı ve geniş çaplı olması nedeni ile ‘coil’ ile kapatılma yerine cerrahi tedavinin tercih edildiği Ulus Travma Acil Cerrahi Derg, Kasım 2013, Vol. 19, No. 6

Bu olguda da bu tip bir aparat kullanılarak hastanın defekti kapatılmış ve hasta noninvaziv bir yöntemle akciğer parenkim kaybı olmaksızın sağlığına kavuşmuştur. Bu olgu aynı zamanda penetran toraks travması sonrası gelişen fistül kapatılmasında ülkemizde septal tıkayıcının kullanıldığı ilk olgudur. Sonuç olarak, penetran toraks travmasında erken dönemde oluşacak refrakter hipoksemi akla PAVF getirmelidir. Daha önemlisi penetran toraks travması sonrası asemptomatik seyredebilen PAVF’nin erken dönemde tespit edilmesidir. Bu nedenle penetran toraks travması sonrası hastalar semptomsuz dahi olsalar BT anjiyografi ve pulmoner arteriyografi ile PAVF yönünden detaylı olarak araştırılmalıdır. Tespit edilen PAVF’nin yeri ve çapının uygun olması durumunda; akciğer parenkimini koruyan transkateter yöntemlerin uygulanabileceği göz önünde bulundurulmalıdır. Çıkar örtüşmesi: Çıkar örtüşmesi bulunmadığı belirtilmiştir.

KAYNAKLAR 1. Ghersin E, Hildoer DJ, Fishman JE. Pulmonary arteriovenous fistula within a pulmonary cyst - evaluation with CT pulmonary angiography. Br J Radiol 2010;83:114-7. 2. Khurshid I, Downie GH. Pulmonary arteriovenous malformation. Postgrad Med J 2002;78:191-7. 3. Kartaloğlu Z, Okutan O, Kunter E, Ciftçi F, Ilvan A, Tunç H. A case of arteriovenous malformation seen as an endobronchial lesion. Tuberk Toraks 2004;52:175-8. 4. Szopiński J, Kamiński Z, Bestry I, Bogdan J. Pulmonary arteriovenous fistulas. [Article in Polish] Pneumonol Alergol Pol 1994;62:634-9. [Abstract] 5. Khalil A, Parrot A, Hammoudi N, Korzec J, Fartoukh M, Carette MF. Severe refractory hypoxemia 16 years after a gunshot injury: Multidetector CT-angiography pattern and endovascular treatment. Circulation 2010;121:27-8. 6. Dairywala IT, Lokhandwala J, Patrick H, Talucci R, Jain D. Severe refractory hypoxemia following a gunshot injury. Chest 2005;127:398-401. 7. Arom KV, Lyons GW. Traumatic pulmonary arteriovenous fistula. J Thorac Cardiovasc Surg 1975;70:918-20. 8. Mager JJ, Westermann CJ. Value of capillary microscopy in the diagnosis

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Güçyetmez ve ark., Travma sonrası geç prezente olmuş pulmoner arteriyovenöz fistülün septal tıkayıcı cihaz ile kapatılması of hereditary hemorrhagic telangiectasia. Arch Dermatol 2000;136:7324. 9. Antunes MJ, Fernandes LE, Oliveira JM. Ventricular septal defects and arteriovenous fistulas, with and without valvular lesions, resulting from penetrating injury of the heart and aorta. J Thorac Cardiovasc Surg 1988;95:902-7. 10. Mills T, Gupta S, Helmcke F, Lopera J, Harrison L, Martinez J, et al. Posttraumatic pulmonary arteriovenous fistula presenting as multiple embolic strokes. Echocardiography 2007;24:79-82. 11. Yekta Altemur K, Ilkay Y, Mustafa K, Rüstem M, Yoruk Y. 13-year experience with penetrating trauma patients. Trakya Univ Tip Fak Derg 2009;26:232-6. 12. Gossage JR, Kanj G. Pulmonary arteriovenous malformations. A state of the art review. Am J Respir Crit Care Med 1998;158:643-61. 13. Yüksel M, Laçin T. Travmalı hastaya yaklaşım. İçinde: Yüksel M, Çetin G, editörler. Toraks travmaları. İstanbul: Turgut Yayıncılık; 2003. s. 1-14. 14. Swanson KL, Prakash UB, Stanson AW. Pulmonary arteriovenous fistulas: Mayo Clinic experience, 1982-1997. Mayo Clin Proc 1999;74:67180. 15. Sheikhzadeh A, Paydar MH, Ghabussi P, Hashemian M, Yazdanyar A, Hakim HS. Pulmonary arteriovenous fistulas. Case presentations and clinical recognition. Herz 1983;8:179-86. 16. Baik S. Traumatic pulmonary arteriovenous fistula due to shotgun wound to the chest. Am J Forensic Med Pathol 1984;5:161-4. 17. Kerr A, Sauter D. Acquired traumatic pulmonary arteriovenous fistula: case report. J Trauma 1993;35:484-6. 18. Shovlin CL, Jackson JE. Pulmonary arteriovenous malformations and other pulmonary vascular abnormalities. In: Mason RJ, Broaddus VC, Martin TR, King TE, Schraufnagel DE, Murray JF, et al., editors. Ma-

son Murray and Nadel’s textbook of respiratory medicine. Vol 1., 5th ed. Philadelphia: Saunders Elsevier; 2010. p. 2963-89. 19. Ando K, Mochizuki A, Kurimoto N, Yokote K, Nakajima Y, Osada H, et al. Coil embolization for pulmonary arteriovenous malformation as an organ-sparing therapy: outcome of long-term follow-up. Ann Thorac Cardiovasc Surg 2011;17:118-23. 20. Chilvers ER, Whyte MK, Jackson JE, Allison DJ, Hughes JM. Effect of percutaneous transcatheter embolization on pulmonary function, rightto-left shunt, and arterial oxygenation in patients with pulmonary arteriovenous malformations. Am Rev Respir Dis 1990;142:420-5. 21. Ploch PJ, Datta S, Thompson JH, Raghavendran K. Posttraumatic pulmonary arteriovenous fistula: is resection the procedure of choice? A case report and review of literature. J Trauma 2009;66:554-7. 22. Kanauchi N, Sato T, Abiko M, Takahashi N. Surgically treated cases of pulmonary arteriovenous fistula. [Article in Japanese] Kyobu Geka 2001;54:517-20. [Abstract] 23. Uthaman B, Al-Qbandi M, Abushaban L, Rathinasamy J. Transcatheter closure of large pulmonary arteriovenous fistula including pulmonary artery to left atrial fistula with Amplatzer septal occluder. Catheter Cardiovasc Interv 2007;70:422-8. 24. Grosso M, Groppo Marchisio F, Testa F, Gallarato G, Balderi A, Lingua G, et al. Pulmonary arteriovenous malformations: percutaneous treatment preserving parenchyma in high-flow fistulae. Radiol Med 2008;113:395-413. 25. Pejhan S, Rahmanijoo N, Farzanegan R, Rahimi M. Surgically treatable pulmonary arteriovenous fistula. Ann Thorac Cardiovasc Surg 2012;18:36-8. 26. Ergül Y, Nişli K, Aydoğan U. Transcatheter closure of a fistula between the right pulmonary artery and left atrium using the Amplatzer septal occluder. Turk Kardiyol Dern Ars 2011;39:231-4.

CASE R E P O R T - ABSTRACT

Late presentation of posttraumatic pulmonary arteriovenous fistulea occlusion with septal occluder device Bülent Güçyetmez, M.D.,1 Ece Salihoğlu, M.D.,2 Aykut Ayyıldız, M.D.,3 Levent Saltık, M.D.,4 Lütfi Telci, M.D.5 Department of Intensive Care Unit, International Hospital, Istanbul Department of Cardiovascular Surgery, Acıbadem University Faculty of Medicine, Istanbul 3 Department of Intensive Care Unit, Maslak Acıbadem Hospital, Istanbul 4 Department of Pediatric Cardiology, Istanbul University Cerrahpasa Faculty of Medicine, Istanbul 5 Department of Anaesthesiology, Istanbul University Istanbul Faculty of Medicine, Istanbul 1 2

ABSTRACT Posttraumatic pulmonary arteriovenous fistula is a rare complication of penetrating injury. Cases may remain asymptomatic for years prior to diagnosis. We present a case of pulmonary arteriovenous fistula related to a penetrating injury of the thorax 6 years previously that was occluded with a septal occluder device. Consistent use of CT or conventional catheter pulmonary angiography following penetrating injury to the thorax is essential to the early diagnosis of pulmonary arteriovenous fistula during the asymptomatic stage. Modern occlude devices facilitate the transcatheter approach as a viable alternative to surgery for the closure large, high pressure defects. Key words: Penetrating thoracic trauma; pulmonary arteriovenous fistulea; septal occluder device. Ulus Travma Acil Cerr Derg 2013;19(6):576-580

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OLGU SUNUMU

Mediastinoskopi ile çıkarılan mediastinal yabancı cisim (saçma çekirdeği): Olgu sunumu∗ Dr. Bayram Metin,1 Dr. Halil Tözüm,2 Dr. Serkan Kaya1 1

Ağrı Devlet Hastanesi, Göğüs Cerrahi Servisi, Ağrı

2

Medeniyet Üniversitesi Tıp Fakültesi, Göğüs Cerrahi Kliniği, İstanbul

ÖZET Toraksa yönelik ateşli silah yaralanmalarında sakatlık ve ölüm oranı yüksektir. Ancak “toraks içinde kalıp herhangi bir patolojiye neden olmayan yabancı cisimlerin akıbeti” konusu literatürde az rastlanır bir durumdur. Bu yazıda, boyun bölgesinden ateşli silah yaralanması sonucu acil servise getirilen ve erken dönemde komplikasyon gelişmeyen fakat takip sürecinde boyun bölgesindeki saçma çekirdeğinin mediastene doğru hareket ettiği tespit edilen ve trakeal fistül yaratma riski nedeni ile de mediastinoskopi ile saçma çekirdeğinin çıkarıldığı bir olgu sunuldu. Anahtar sözcükler: Mediastinal yabancı cisim; mediatinoskopi; torasik travma; trakeal fistül.

GİRİŞ Travma, genç erişkinlerde en sık görülen ölüm nedenidir. Göğüs travmaları, kafa ve ekstremite travmalarından sonra üçüncü sıklıkta görülür. Göğüs travmalarında doğru ve hızlı tanı ve uygun cerrahi yaklaşım sakatlık ve ölüm riskinin azaltılmasının temelini oluşturur.[1] Göğüs travmalarının %70’ini künt, %30’unu ise penetran yaralanmalar oluşturmaktadır. Künt yaralanmaların en sık görülen nedeni motorlu taşıt kazaları, penetran yaralanmaların en sık görülen nedenleri ise ateşli silah yaralanmaları ve delici-kesici aletlerle olan yaralanmalardır. Penetran göğüs yaralanmalarında ölüm oranı, künt göğüs travmalarına göre daha düşüktür. Bunun nedeni, bu yaralanmaların etkilediği alanın daha küçük olması ve eşlik eden organ yaralanmalarının daha az olmasıdır. Penetran yaralanmalar içinde ise ateşli silahlarla meydana gelen yaralanmaların ölüm oranı, diğer delici ve kesici aletlerle meydana gelen yaralanmalara göre iki kat daha fazladır. Güİletişim adresi: Dr. Halil Tözüm Göztepe Eğitim ve Araştırma Hastanesi, Göğüs Cerrahi Polikliniği, Merdivenköy, Kadıköy, İstanbul Tel: +90 216 - 566 40 00 E-posta: dr.thorax@gmail.com TÜSAD 33. Ulusal Kongresi’nde sunulmuştur (15-19 Ekim 2011, Çeşme, İzmir).

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nümüzde, bu tip yaralanmalarda nasıl bir cerrahi tedavi yaklaşımının izleneceğinin belirlenmesi büyük önem taşımaktadır. Klinik çalışmalar, deneyimli bir ekip tarafından zamanında müdahale edilmediğinde, ateşli silahlarla meydana gelen göğüs yaralanmalarında ölüm riskinin artacağını göstermiştir.

OLGU SUNUMU Ateşli silah yaralanmasına maruz kalarak hastanemiz acil servisine getirilen 27 yaşında erkek hastanın biri boyun bölgesinde olmak üzere çeşitli yerlerinde saçma yaralanmaları vardı. Erken travma sürecinde mediastende hava izlenen ve mediastinit riskine karşı geniş spekturumlu antibiyotik tedavisi verilen hasta, komplikasyon gelişmemesi üzerine, takibe alınarak taburcu edildi (Şekil 1). Bu dönemde vücudun değişik bölgelerine dağılmış olan saçma taneciklerinin çıkarılmasına gerek görülmedi (Şekil 2). Yaklaşık bir ay süren takip sonrasında boyun bölgesindeki saçma taneciğinin ilerleyerek trakea alt ucuna bası yapmaya başladığı görüldü (Şekil 3a, b). Saçma taneciğinin hareket ettiği görüldüğünden, başka bir hayati dokuya migrasyonunu ya da trakea içine doğru hareket etmesini engelleyebilmek için, çıkarılmasına karar verildi. Hasta sırt üstü yatar pozisyonda ameliyata alındı. Boyun ekstansiyona getirilerek skopi ile saçma taneciğinin tam yeri saptandı. Klasik mediastinoskopi insizyonu ile pretrakeal fasyaya kadar diseksiyon ilerletildi. Pretrakeal fasya açılarak mediastinoskop yerleştirildi. Superior mediastende trakea arka duvarına dogru ilerlenerek, skopi yardımı ile saçma taneciği bulundu ve forceps ile tutularak çıkartıldı (Şekil 4a, b). 581


Metin ve ark., Mediastinoskopi ile çıkarılan mediastinal yabancı cisim

lardan uzakta bulunan yabancı cismin etrafında zamanla oluşan yabancı cisim reaksiyonu ve skar dokusu sonucu cismin o bölgeye hapsolmasıdır. Bazen bu yabancı cisimler hareket ederek kalp, ana vasküler yapılar, bronşlar ya da akciğer parankimine doğru yer değiştirebilir. Böyle bir durumda yıllardır semptomsuz olan hastada, hemoptizi, dispne, göğüs ağrısı ve prodüktif öksürük gibi semptomlar görülebilir, hatta ölümcül sonuçlarla bile karşılaşılabilir.[1,2] Ancak küçük bir saçma tanesini çıkartmaya çalışmak; gereğinden fazla sağlam doku travmasına yol açacak, hatta önemli vasküler yapılarda ya da çevre dokularda tahribata yol açabilecektir. Burada olası zarar ve yarar hesabı iyi yapılmalı, çıkartma endikasyonu konulmadan önce hasta ve planlanan ameliyat tekrar tekrar gözden geçirilmelidir.

Şekil 1. Bilgisayarlı tomografi kesitinde saçma taneciği ve mediastinal amfizem.

Ameliyat sonrası herhangi bir komplikasyon gelişmeyen hasta, ikinci gün taburcu edildi. On yedi aydır takipte olan hasta, sorunsuz olarak takipten çıkartıldı.

TARTIŞMA Penetran toraks travmalarını takiben geç dönemde toraks içinde en sık tespit edilen yabancı cisimler kurşun, saçma, cam, metal ve şarapnel parçalarıdır. Bu tip yabancı cisimler, akut dönemde müdahale gerektiren intratorasik patolojiye neden olmadıkları durumlarda genellikle semptomsuz seyir gösterirler. Bunun nedeni de kalp, bronş, damarlar gibi yaşamsal yapı-

Mermi çekirdeklerinin gömleksiz yapıda olanlarında, aralıklı röntgen takiplerinin yapılması veya herhangi bir nedenle gerçekleştirilecek radyolojik incelemelerde, değerlendirmeyi yapacak hekimin konu ile ilgili uyarılması gerekmektedir.[3] Bunun yanında saplanıp kalan mermi veya şarapnel parçacıkları, manyetik rezonans incelemesinin yapılmasını sakıncalı kılmaktadır. Bu sakınca, ilgili metal parçacıkların yüksek manyetik alan ve güçlü radyo frekans dalgaları nedeniyle ısınması, içinde bulunduğu dokularda yanıklara sebebiyet vermeleri, küçük parçacıkların yerinden oynayarak doku zedelenmesi ve kanamalara yol açmasındandır.[4] İntratorasik yabancı cisimlere yaklaşım konusunda sınırlı literatür bilgisi mevcuttur ve standart bir yaklaşım biçimi yoktur. İntratorakal semptomsuz olan bir merminin çıkarılıp çıkarılmayacağı konusu her zaman tartışmalıdır. Ateşli silahlarla meydana

Şekil 2. Toraks ve ekstremitelerdeki saçma tanecikleri. Toraks bilgisayarlı tomografide sağda trakeanın posterioruna yakın yerleşimli metalik saçma görülüyor.

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(a)

(b)

Şekil 3. (a) Arka-ön akciğer grafisinde torakal 3. vertebra hizasında görülen saçma görüntüsü. (b) Saçma taneciğinin yer değiştirmesi ile trakeal bası görünümü.

gelen toraks travması olgularında hemodinamik açıdan sorun yoksa rutin grafilerle ön değerlendirme yapılır. Bu değerlendirmede bir patoloji saptanmazsa olgu izleme alınır. Acil incelemeden sonraki altıncı saatte göğüs grafisi tekrarlanır. Hasta hala semptomsuz ve grafi normalse geç komplikasyon görülme olasılığı düşüktür. Çoğunlukla düşük hızlı silah ve bıçak yaralanmaları ameliyata gerek olmadan tedavi edilebilirler. Bu yaklaşım toraksın delici yaralanmalarında altı saat kuralı olarak anılır.[5] Toraks travmalarında endoskopik cerrahi teknik ve aletlerin yaygın kullanımı ile video destekli torakoskopik cerrahi de geniş kullanım alanı bulmuştur. Özellikle travma sonrası şüpheli diyafram yaralanmalarında, drene olamayan veya devam eden hemotoraksta, düzelmeyen pnömotoraksta yaygın olarak kullanılmaktadır.[6] İntratorasik yabancı cisim parçaları torakotomiye gerek duyulmadan VATS (video-assisted thoracoscopy) ile çıkarılabilir.[7,8]

(a)

Transmediastinal ateşli silahla yaralanmalar son derece ölümcül olgular olduğundan bu konuda yayınlanmış çalışmalar da oldukça azdır. Selinger ve ark.[9] ateşli silah yaralanması sonrası sol ventrikül ile sağ atriyum arasında fistül gelişen bir olgunun 52 yıl semptomsuz kaldığını, konjestif kalp yetersizliği sonrası tanı konduğunu ve tedavi edildiğini bildirmektedir. Mediastinoskopi teknik olarak, servikal bölgede sternal çentikten 1 cm yukarıda, orta hatta 4 cm uzunluğunda transvers insizyon sonrası pretrakael fasyaya ulaşıldıktan sonra pretrakeal fasya açılarak mediastinoskopun fasya altına yerleştirilmesi ve trakea üstünden ilerletilmesi şeklinde yapılan bir işlemdir. Mediastinoskop karinaya kadar ilerletilir, mediastinoskop önündeki dokular aspiratör yardımıyla künt diseksiyon ile iyice belirlenir. Böylece birçok mediastinal lenf nodu bölgesinden örnekler alınabilir. Mediastinoskopi sıklıkla akciğer kanserinin cerrahi girişim endikasyonunu ve

(b)

Şekil 4. (a) Ameliyat esnasında skopi yardımı ile saçma çekirdeğinin yerinin belirlenmesi sırasındaki görüntüsü. (b) Çıkarılan şaçma çekirdeği.

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evrelemesini değerlendirmek için uygulanan tanısal bir yöntemdir. Kanserden başka lenfoma, tüberküloz ve sarkoidoz gibi birçok hastalığa bağlı gelişen lenfadanopatilerin tanısında da kullanılmaktadır. Tüm bunların yanısıra, özellikle superior mediastendeki kistik ve solid lezyonların tedavisinde de kullanıldığı yolunda birçok yayın vardır.[10] Özellikle son dönemde sıklıkla uygulanan video-mediastinoskopinin, daha iyi bir görüntüleme sağlayarak, olgumuz benzeri olgularda çok daha efektif kullanılabileceğine inanmakla beraber, şartlar dahilinde hareket etmenin bir cerrahın en önemli prensiplerinden biri olması gerektiğini düşünüyoruz. Bu noktada, hastanemizde video-mediastinoskop olmamasına rağmen, yine de minimal invaziv bir yaklaşım ile saçma taneciğini çıkartmak mümkün oldu. Her ne kadar tanısal bir işlem olarak öne çıkmış olsa da, mediastinoskopinin olgumuzda da olduğu gibi bazı seçilmiş olgularda mediastende yer alan lezyonların ya da yabancı cisimlerin çıkarılmasında kullanılabileceğini belirtmek istedik. Sonuç olarak, mediastinal yabancı cisimlerin çıkarılması için planlama doğru bir şekilde yapılmalı ve mediastinoskopinin bu amaçla kullanılabileceği akılda tutulmalıdır. Çıkar örtüşmesi: Çıkar örtüşmesi bulunmadığı belirtilmiştir.

KAYNAKLAR 1. Yüksel M, Laçin T. Travmalı hastaya yaklaşım. İçinde: Yüksel M, Çetin G, editörler. Toraks travmaları. İstanbul: Turgut Yayıncılık; 2003. s. 1-14. 2. Karakuş A, Güngör A, Damgacı K, Kandiş H, Apaydın OÖ. Komplikasyonsuz toraks içi yabancı cisim (mermi çekirdeği): Olgu sunumu. Akademik Acil Tıp Derg 2011;10:138-40. 3. Oyar O, Yavuz MS, Köroğlu M. Vücut içerisine kalmış ve zamanla değişime uğramış bir mermi çekirdeği. Adli Bilimler Dergisi 2004;3:415. 4. Henkelman RM. Image artifacts. In: Stark DD, Bradley WG, editors. Magnetic resonance imaging. St. Louis: Mosby Year Book; 1992. s. 245. 5. Kerr TM, Sood R, Buckman RF Jr, Gelman J, Grosh J. Prospective trial of the six hour rule in stab wounds of the chest. Surg Gynecol Obstet 1989;169:223-5. 6. Bilgin M, Kahraman AY, Oğuzkaya F, Şahin A. Türk Göğüs Kalp Damar Cerrahisi Dergisi 1998;6:347-50. 7. Marsico GA, Almeida AL, Azevedo DE, Venturini GC, Azevedo AE, Marsico Pdos S. Video-assisted thoracoscopic removal of foreign bodies from the pleural cavity. [Article in English, Portuguese] J Bras Pneumol 2008;34:241-4. 8. Dinka T, Kovács O, Kotsis L. Emergency video-assisted thoracoscopic surgery for intrathoracic foreign bodies. [Article in Hungarian] Magy Seb 2004;57:346-50. [Abstract] 9. Selinger L, Werner K, Silber R, Nellessen U, Inselmann G. Natural history of a ventriculoatrial fistula after a gunshot injury in 1945. Ann Thorac Surg 1998;65:1137-8. 10. Smythe WR, Bavaria JE, Kaiser LR. Mediastinoscopic subtotal removal of mediastinal cysts. Chest 1998;114:614-7.

CASE R E P O R T - ABSTRACT

Removal of mediastinal foreign body (steel shot) using mediastinoscopy: case report Bayram Metin, M.D.,1 Halil Tözüm, M.D.,2 Serkan Kaya, M.D.1 1 2

Department of Thoracic Surgery, Ağrı State Hospital, Ağrı Department of Thoracic Surgery, Medeniyet University Faculty of Medicine, İstanbul

ABSTRACT Morbidity and mortality is high in patients with gunshot wounds to the chest. Only in rare cases do foreign bodies persist in the thorax without significant pathology. At this study, we present a case in which steel shot was removed through the mediastinum using mediastinoscopy due to the risk of tracheal fistula. Key words: Foreign body of mediastinium; mediastinoscopy; thoracic injury, tracheal fistula. Ulus Travma Acil Cerr Derg 2013;19(6):581-584

584

doi: 10.5505/tjtes.2013.85453

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Ulusal Travma ve Acil Cerrahi Dergisi 2013 Yılı 19. Cilt Konu Dizini Abdominal kompartman sendromu bkz. 2013;19(5):559-563 Acil bkz. 2013;19 (1):41-44 bkz. 2013;19 (3):241-245 cerrahi bkz. 2013;19(5):405-410 ortopedik travma bkz. 2013;19 (2):157-163 Acil servis bkz. 2013;19 (1):25-28 bkz. 2013;19 (2):180-182 bkz. 2013;19 (3):205-214 bkz. 2013;19 (3):251-255 bkz. 2013;19 (4):320-326 bkz. 2013;19 (4):327-332 bkz. 2013;19(5):423-428 Acil şiddet indeksi bkz. 2013;19 (3):205-214 Acil tıp bkz. 2013;19 (3):205-214 bkz. 2013;19(5):398-404 Açık apendektomi bkz. 2013;19 (3):200-204 Adezyon bkz. 2013;19 (4):305-312 Ağrı bkz. 2013;19(5):417-422 Ağrı skoru bkz. 2013;19 (3):200-204 Akrep sokması bkz. 2013;19(5):417-422 Aksonal travma bkz. 2013;19 (1):77-79 Akut ağrı bkz. 2013;19(5):398-404 Akut apandisit bkz. 2013;19 (1):13-19 bkz. 2013;19 (1):20-24 Akut pankreatit bkz. 2013;19 (2):103-108 Akut sinir greftlemesi bkz. 2013;19 (2):109-114 Albendazol bkz. 2013;19 (2):119-122 Algoritma bkz. 2013;19 (3):223-228 Alvarado skoru bkz. 2013;19 (1):13-19 Ameliyat sonrası komplikasyonlar bkz. 2013;19 (4):305-312 Amyand fıtığı bkz. 2013;19(5):488-490 Analiz bkz. 2013;19 (2):152-156 Anjiyografi bkz. 2013;19(6):567-569 Ankaferd kan durdurucu bkz. 2013;19 (1):1-7 Anket bkz. 2013;19(5):463-468 Antibiyotik bkz. 2013;19 (3):189-194 Antitrombotik tedavi bkz. 2013;19 (3):223-228 Aortobifemoral baypas bkz. 2013;19 (2):164-166 Apandisit bkz. 2013;19 (1):83-85 bkz. 2013;19 (1):86-88

bkz. 2013;19 (3):200-204 bkz. 2013;19 (4):380-382 bkz. 2013;19(6):554-558 bkz. 2013;19(6):570-572 Apendektomi bkz. 2013;19 (1):20-24 bkz. 2013;19(5):488-490 Apopitozis bkz. 2013;19(6):491-499 bkz. 2013;19 (4):313-319 Appendiks testis torsiyonu bkz. 2013;19 (4):333-336 Appendiks vemiformis bkz. 2013;19 (1):83-85 bkz. 2013;19 (4):385-386 Aseptik gevşeme bkz. 2013;19 (2):98-102 At nalı bkz. 2013;19 (4):385-386 Ateşli silah lezyonu bkz. 2013;19 (4):371-374 ölümleri bkz. 2013;19(6):536-542 yaralanmaları bkz. 2013;19(5):392-397 yaralanması bkz. 2013;19 (3):235-240 yaralanması bkz. 2013;19(5):429-433 Atlanmış tanılar bkz. 2013;19 (2):157-163 Avulsiyon bkz. 2013;19 (3):277-281 Avülzyon yaralanmaları bkz. 2013;19(6):516-520

Cinayet bkz. 2013;19(6):536-542 Cinsiyet bkz. 2013;19(6):554-558 Curcumin bkz. 2013;19(6):507-515

Ç

adır bkz. 2013;19 (3):251-255 Çimentosuz hemiartroplasti bkz. 2013;19(6):548-553 Çocuk bkz. 2013;19 (3):246-250 bkz. 2013;19 (4):357-362 bkz. 2013;19 (4):366-370 bkz. 2013;19(5):488-490 bkz. 2013;19(5):559-563 bkz. 2013;19(6):554-558 hasta popülasyonu bkz. 2013;19(5):411-416 Çocuklar bkz. 2013;19 (2):123-126 bkz. 2013;19 (2):183-185 bkz. 2013;19 (3):229-234 Çocuklarda travma bkz. 2013;19 (4):363-365 Çocuklarda yutulmuş mıknatıs bkz. 2013;19 (2):177-179 Çocukluk çağı bkz. 2013;19 (3):261-266 Çok kesitli bilgisayarlı tomografi bkz. 2013;19 (4):375-379 Çoklu kırık bkz. 2013;19(5):475-479 Çoklu travma ağırsak darlığı bkz. 2013;19 (2):183-185 bkz. 2013;19 (4):327-332 Bağışıklık durumu bkz. 2013;19 (4):320-326 bkz. 2013;19(6):491-499 Bakteriyel translokasyon bkz. 2013;19(6):491-499 Baryum bkz. 2013;19 (1):86-88 abigatran bkz. 2013;19(5):469-471 Baryum taşı bkz. 2013;19 (1):86-88 Dalak yaralanması bkz. 2013;19 (3):195-199 Beyin ödemi Damar yaralanması bkz. 2013;19(5):405-410 bkz. 2013;19 (2):89-97 De Garengeot fıtığı bkz. 2013;19 (4):380-382 bkz. 2013;19 (4):294-298 Defibrilasyon bkz. 2013;19(6):564-566 Beyin travması bkz. 2013;19 (1):77-79 Demografi bkz. 2013;19(5):449-455 Bilgisayarlı tomografi Deprem bkz. 2013;19 (3):251-255 bkz. 2013;19 (1):33-40 Deri grefti bkz. 2013;19 (3):215-218 bkz. 2013;19 (1):80-82 Derin doku yaralanması bkz. 2013;19 (1):1-7 bkz. 2013;19 (2):157-163 Dieulafoy lezyonu bkz. 2013;19 (2):133-139 hastalığın şiddeti indeksi Diffüz idiopatik skeletal hiperosteozis bkz. 2013;19 (2):103-108 bkz. 2013;19 (1):73-76 Blastik travma bkz. 2013;19 (3):271-273 Direkt trombin inhibitörü Boğulmuş kasık fıtığı bkz. 2013;19(5):488-490 bkz. 2013;19(5):469-471 Bouveret sendromu bkz. 2013;19 (4):375-379 Diş bkz. 2013;19 (3):246-250 Brakiyal pleksus bkz. 2013;19(6):521-528 Disfaji bkz. 2013;19 (1):73-76 Brakiyal pleksus kesisi bkz. 2013;19(5):485-487 Diyafram ve perikart rüptürü Burun bkz. 2013;19 (2):152-156 bkz. 2013;19 (4):363-365

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Ulus Travma Acil Cerrahi Derg, Kasım 2013, Vol. 19, No. 6

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Ulusal Travma ve Acil Cerrahi Dergisi 2013 Yılı 19. Cilt Konu ve Yazar Dizini

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Diyafram yaralanması bkz. 2013;19 (1):45-48 acettepe acil triyaj sistemi Diyagnostik laparoskopi bkz. 2013;19 (1):53-57 bkz. 2013;19 (3):205-214 Duplikasyon bkz. 2013;19 (1):83-85 Hematom bkz. 2013;19(6):564-566 Düşme yüksekliği bkz. 2013;19(6):529-535 Hemopnömotoraks Düşük doz metotreksat bkz. 2013;19 (4):285-293 bkz. 2013;19 (3):274-276 bkz. 2013;19(6):529-535 klemiçi kırıklar bkz. 2013;19 (2):145-151 Hemostaz Eksternal boyun travması bkz. 2013;19 (1):1-7 bkz. 2013;19 (3):271-273 bkz. 2013;19 (3):195-199 Ekstremite Hepatik kist hidatik bkz. 2013;19 (2):119-122 bkz. 2013;19 (1):25-28 Hepatobiliyer iminodiasetik asit tarama bkz. 2013;19(6):516-520 bkz. 2013;19(5):480-484 El bkz. 2013;19 (1):58-64 Heredite bkz. 2013;19(6):554-558 El bileği bkz. 2013;19 (1):58-64 Hifema bkz. 2013;19 (4):357-362 Elektromiyografik inceleme Hipertonik salin bkz. 2013;19(6):500-506 bkz. 2013;19 (3):235-240 Hipertonik tuz bkz. 2013;19 (2):89-97 Embolizasyon bkz. 2013;19(6):567-569 Hipofarenks perforasyonu Endoskopi bkz. 2013;19(5):434-440 bkz. 2013;19 (3):271-273 Endoskopik asistans bkz. 2013;19(5):434-440 HIV bkz. 2013;19 (3):267-270 Endoskopik tedavi bkz. 2013;19 (2):133-139 Hiyoid kırığı Enjeksiyon tedavisi bkz. 2013;19 (1):29-32 bkz. 2013;19 (3):271-273 Epidemiyoloji bkz. 2013;19 (3):282-284 bkz. 2013;19 (1):49-52 bkz. 2013;19(5):417-422 ğne bkz. 2013;19(6):570-572 bkz. 2013;19(5):449-455 İki taraflı epidural hematom Epididimo-orşit bkz. 2013;19 (4):333-336 bkz. 2013;19 (3):267-270 Ergotamin bağımlılığı bkz. 2013;19(5):475-479 İki taraflı internal iliak arter Erişkinler bkz. 2013;19 (3):229-234 bkz. 2013;19(6):567-569 Etyoloji İkodekstrin bkz. 2013;19 (4):305-312 bkz. 2013;19 (2):152-156 İleri yaş bkz. 2013;19(6):548-553 bkz. 2013;19 (4):348-356 İleus bkz. 2013;19(5):559-563 İliopsoas yırtığı bkz. 2013;19(6):564-566 ekalit bkz. 2013;19 (1):86-88 İmipenem bkz. 2013;19 (3):189-194 Femoral fıtık bkz. 2013;19 (4):380-382 İmmünsupresyon bkz. 2013;19 (1):65-68 Femur boynu bkz. 2013;19(5):456-462 İnce bağırsak bkz. 2013;19(5):387-391 Fetüs bkz. 2013;19 (4):371-374 İncir yaprağı bkz. 2013;19 (4):383-384 Fistül bkz. 2013;19 (4):375-379 İnferior çıkık bkz. 2013;19 (1):41-44 Fitofotodermatit bkz. 2013;19 (4):383-384 İnterlökin bkz. 2013;19(6):491-499 Fıtık bkz. 2013;19 (4):380-382 İntermaksiller fiksasyon 2013;19 (4):299-304 Fonksiyonel sonuçlar bkz. 2013;19(6):521-528 İnternal fıtık bkz. 2013;19(6):573-575 Forestier hastalığı bkz. 2013;19 (1):73-76 İnternal herniasyon bkz. 2013;19 (2):164-166 Forrest sınıflaması bkz. 2013;19 (1):29-32 İntertrokanterik femur kırığı Fournier gangreni bkz. 2013;19 (3):215-218 bkz. 2013;19(6):548-553 Futbol bkz. 2013;19 (3):219-222 İntestinal perforasyon bkz. 2013;19 (1):33-40 İntestinal tıkanıklık bkz. 2013;19(6):573-575 ebelik İntihar bkz. 2013;19(6):536-542 bkz. 2013;19 (1):20-24 İntraabdominal basınç bkz. 2013;19(5):559-563 bkz. 2013;19 (2):119-122 İntrauterin yaralanma bkz. 2013;19 (4):371-374 bkz. 2013;19 (4):371-374 İntravezikal basınç ölçümü Genel cerrah bkz. 2013;19(5):463-468 bkz. 2013;19(5):559-563 Genotoksisite 2013;19 (4):299-304 İskemi bkz. 2013;19(5):387-391 Gizli kırık bkz. 2013;19 (2):157-163 İstismara bağlı kafa travması Glukozamin bkz. 2013;19 (1):8-12 bkz. 2013;19 (3):261-266 Göğüs travması İzole bkz. 2013;19(5):485-487 bkz. 2013;19 (2):173-176 İzole hepatik kanal yaralanması bkz. 2013;19(6):491-499 bkz. 2013;19(5):480-484 Görme prognozu bkz. 2013;19 (4):357-362 İzole nervus vagus yaralanması Göz içi basıncı yükselmesi bkz. 2013;19 (2):180-182 bkz. 2013;19 (2):115-118 Greft bkz. 2013;19(6):516-520

E

İ

F

G

586

Kaburga kırığı bkz. 2013;19 (3):274-276 Kaçırılan kırıklar bkz. 2013;19 (1):25-28 Kafa travması bkz. 2013;19 (1):69-72 Kalkaneus kırıkları bkz. 2013;19 (2):145-151 Kalkaneus plakları bkz. 2013;19 (2):145-151 Kalsiyum alginat bkz. 2013;19 (3):195-199 Kan beyin bariyeri bkz. 2013;19 (4):294-298 Kanama bkz. 2013;19 (2):133-139 Kanama bkz. 2013;19 (2):167-172 bkz. 2013;19(6):567-569 Kapalı göz travması bkz. 2013;19 (3):219-222 Kapalı redüksiyon bkz. 2013;19 (1):41-44 Karaciğer bkz. 2013;19 (2):119-122 bkz. 2013;19 (2):167-172 Karbonatlı içecekler bkz. 2013;19 (3):256-260 Kardeş kromatit değişimi 2013;19 (4):299-304 Kardiyak herniasyon bkz. 2013;19 (4):363-365 Karın ön duvarı defekti bkz. 2013;19(5):559-563 Karıniçi hipertansiyon bkz. 2013;19(5):559-563 Karıniçi yapışıklık bkz. 2013;19 (3):189-194 Keçi bkz. 2013;19(6):500-506 Kemik bkz. 2013;19 (1):8-12 Kırık bkz. 2013;19 (2):152-156 bkz. 2013;19 (3):241-245 bkz. 2013;19(5):456-462 Kırık iyileşmesi bkz. 2013;19 (1):8-12 Klinik şiddet bkz. 2013;19(5):441-448 Koagülopati bkz. 2013;19(5):469-471 Koagülopati sürecinin çevrimi bkz. 2013;19(5):469-471 Kolon perforasyonu bkz. 2013;19 (1):65-68 Kolostomi bkz. 2013;19 (1):65-68 Komplikasyon bkz. 2013;19 (2):119-122 bkz. 2013;19 (3):229-234 bkz. 2013;19(5):441-448 Komplike olmayan apandisit bkz. 2013;19 (3):200-204 Kontrol altına alınamayan hemorajik şok bkz. 2013;19(6):500-506 Kontüzyon bkz. 2013;19 (3):219-222 Koroner arter diseksiyonu bkz. 2013;19 (2):173-176 Koruma bkz. 2013;19 (3):219-222 Kronik aortik anevrizma bkz. 2013;19 (4):343-347 Künt bkz. 2013;19 (4):343-347 Künt karın travması bkz. 2013;19 (2):183-185 Künt travma bkz. 2013;19 (2):127-132 bkz. 2013;19 (3):282-284 bkz. 2013;19 (4):357-362 bkz. 2013;19 (4):366-370

Laparoskopi bkz. 2013;19 (1):20-24 Laparoskopik apendektomi bkz. 2013;19 (3):200-204

Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Ulusal Travma ve Acil Cerrahi Dergisi 2013 Yılı 19. Cilt Konu ve Yazar Dizini Lintula skoru bkz. 2013;19 (1):13-19 Lornoksikam bkz. 2013;19 (4):294-298 Luksasyo erekta bkz. 2013;19 (1):41-44

Serbest doku aktarımı bkz. 2013;19(5):411-416 Serbest düşen mermi çekirdeği bkz. 2013;19(5):392-397 Serbest oksijen radikalleri agnezyum sülfat bkz. 2013;19 (4):313-319 bkz. 2013;19(6):507-515 Maksillofasial travma bkz. 2013;19 (4):348-356 Sıkıştırılmış şişe kapağı bkz. 2013;19 (3):256-260 Malformasyon bkz. 2013;19 (4):385-386 Sıvı bkz. 2013;19(6):500-506 Maliyet bkz. 2013;19 (1):13-19 Sindirim sistemi kanaması bkz. 2013;19 (1):29-32 Mandibula kırığı bkz. 2013;19 (3):271-273 Sinir dokusunun korunması Mandibula kırıkları bkz. 2013;19 (4):348-356 bkz. 2013;19 (4):313-319 Sinir yaralanması bkz. 2013;19(6):521-528 Manyetik rezonans kolonanjiyografi bkz. 2013;19 (4):375-379 Sirküler fiksatör bkz. 2013;19(6):543-547 Sistemik enflamatuvar yanıt sendromu Manyetik rezonans venogram bkz. 2013;19 (1):69-72 bkz. 2013;19(6):491-499 Siyanoakrilat bkz. 2013;19 (3):215-218 Mediastinal yabancı cisim Siyatik sinir bkz. 2013;19 (2):109-114 bkz. 2013;19(6):581-584 Skafoid bkz. 2013;19 (3):241-245 Mediatinoskopi bkz. 2013;19(6):581-584 Skalp bkz. 2013;19 (3):277-281 Menteşe yöntemi bkz. 2013;19(6):543-547 Skor bkz. 2013;19 (1):13-19 Metilprednisolon bkz. 2013;19 (4):285-293 Skrotum bkz. 2013;19 (4):333-336 Metronidazol bkz. 2013;19 (3):189-194 Spinal travma Mevsim bkz. 2013;19(6):554-558 bkz. 2013;19 (1):49-52 Mezenter ven bkz. 2013;19 (3):223-228 bkz. 2013;19(5):441-448 Mezenter yaralanması bkz. 2013;19 (2):183-185 Spiral bilgisayarlı tomografi Mide bkz. 2013;19 (2):133-139 bkz. 2013;19 (1):33-40 Mide çıkım obstrüksiyonu Strangüle inguinal herni bkz. 2013;19 (4):333-336 bkz. 2013;19 (4):375-379 Subaraknoid kanama bkz. 2013;19(6):529-535 Migren bkz. 2013;19(5):475-479 Subdural hematom bkz. 2013;19 (3):261-266 Morbidite adial sinir duyusal dalı Subkondil kırığı bkz. 2013;19(5):434-440 bkz. 2013;19 (1):45-48 bkz. 2013;19 (2):186-188 bkz. 2013;19 (2):103-108 Radyofrekans ablasyon bkz. 2013;19 (2):167-172 Subkondiler kırık bkz. 2013;19(5):434-440 Suriyeli olgu bkz. 2013;19(5):429-433 Mortalite Radyografi bkz. 2013;19 (1):45-48 bkz. 2013;19 (1):25-28 bkz. 2013;19 (2):103-108 bkz. 2013;19 (2):157-163 -drenaj bkz. 2013;19 (2):119-122 bkz. 2013;19 (2):127-132 Randomize kontrollü çalışma Tanısal laparotomi bkz. 2013;19 (1):53-57 bkz. 2013;19(6):529-535 Termoelastik gerilme analizi bkz. 2013;19(5):398-404 Motorsiklet kazaları bkz. 2013;19(5):423-428 bkz. 2013;19 (2):98-102 Reperfüzyon bkz. 2013;19(5):387-391 Replantasyon bkz. 2013;19 (3):277-281 Testis torsiyonu bkz. 2013;19 (4):333-336 ekroz bkz. 2013;19 (4):313-319 Resüsitasyon bkz. 2013;19(6):500-506 Tetanoz bkz. 2013;19 (4):320-326 Nikel-krom alaşımı 2013;19 (4):299-304 Retinal hemoraji bkz. 2013;19 (3):261-266 TEVAR bkz. 2013;19 (4):343-347 Nöroma bkz. 2013;19 (2):186-188 Tibia kırığı bkz. 2013;19(6):543-547 Retroçekal apandisit bkz. 2013;19 (1):80-82 Rotasyonel açısal akselerasyon Titanyum bkz. 2013;19 (4):299-304 küler travma bkz. 2013;19 (1):77-79 Titanyum miniplak osteosentezi bkz. 2013;19 (2):115-118 bkz. 2013;19 (4):299-304 bkz. 2013;19 (3):256-260 afra kesesi bkz. 2013;19 (4):375-379 Torasik travma Omurilik yaralanması Safra taşı bkz. 2013;19 (4):375-379 bkz. 2013;19 (2):127-132 bkz. 2013;19 (4):285-293 Safra yolları bkz. 2013;19 (4):375-379 bkz. 2013;19(6):581-584 bkz. 2013;19 (4):313-319 Sagittal sinüs trombozu bkz. 2013;19 (1):69-72 Total diz replasmanı bkz. 2013;19 (2):98-102 Omuz bkz. 2013;19 (1):41-44 Sağlık maliyetleri bkz. 2013;19(5):423-428 Trafik kazası bkz. 2013;19 (1):77-79 Orafasiyel travma bkz. 2013;19 (3):246-250 Sanders sınıflaması bkz. 2013;19 (2):145-151 Trakeal fistül bkz. 2013;19(6):581-584 Orbita kırığı bkz. 2013;19(5):449-455 Santral kord sendromu bkz. 2013;19 (1):73-76 Travma Osteoblast bkz. 2013;19 (1):8-12 Sarsılmış bebek sendromu bkz. 2013;19 (1):41-44 bkz. 2013;19 (3):261-266 bkz. 2013;19 (1):73-76 bkz. 2013;19 (2):140-144 Sefazolin bkz. 2013;19 (3):189-194 lüm bkz. 2013;19 (1):29-32 bkz. 2013;19 (3):274-276 Önkol sinir yaralanması bkz. 2013;19 (2):186-188 Seftriakson bkz. 2013;19 (3):189-194 bkz. 2013;19 (4):343-347 Selektif non-operatif yönetim Önlenebilir maliyet bkz. 2013;19(5):429-433 bkz. 2013;19(5):463-468 bkz. 2013;19(5):423-428 Özofagus bkz. 2013;19 (3):229-234 bkz. 2013;19(5):449-455 Sepsis bkz. 2013;19(6):507-515 bkz. 2013;19(5):472-474 Septal tıkayıcı cihaz bkz. 2013;19(6):576-580 araduodenal fıtık bkz. 2013;19(6):573-575 bkz. 2013;19(5):559-563 Parça etkili patlayıcılar bkz. 2013;19 (2):140-144 Septik şokta sıvı resüsitasyonu bkz. 2013;19(5):559-563 bkz. 2013;19(6):567-569 Parsiyel protez bkz. 2013;19(5):456-462

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Pediatrik bkz. 2013;19 (2):140-144 bkz. 2013;19(5):485-487 Pediatrik travma skoru bkz. 2013;19 (2):140-144 Penetran karın travması bkz. 2013;19 (1):53-57 bkz. 2013;19(5):463-468 Penetran oküler yaralanma bkz. 2013;19 (2):115-118 Penetran toraks travması bkz. 2013;19(6):576-580 Penetran yaralanma bkz. 2013;19(5):405-410 Penetrasyon yaralanması bkz. 2013;19 (1):58-64 Perforatör flepler bkz. 2013;19(5):411-416 Periferik sinir bkz. 2013;19 (3):235-240 Periferik sinir yaralanmaları bkz. 2013;19 (2):109-114 Perioperatif kanama bkz. 2013;19(5):469-471 Peritoneal lavaj bkz. 2013;19 (3):189-194 Perkütan koroner girişim bkz. 2013;19 (2):173-176 Piperin bkz. 2013;19(5):387-391 Pnömotoraks bkz. 2013;19 (4):327-332 Prognoz bkz. 2013;19(5):441-448 Pulmoner arteriyovenöz fistül bkz. 2013;19(6):576-580

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Ulusal Travma ve Acil Cerrahi Dergisi 2013 Yılı 19. Cilt Konu ve Yazar Dizini Travma değerlendirilmesi bkz. 2013;19 (2):180-182 Travma şiddet indeksleri bkz. 2013;19 (2):127-132 Travmatik beyin hasarı bkz. 2013;19 (2):89-97 bkz. 2013;19 (4):294-298 Travmatik glokom bkz. 2013;19 (2):115-118 Travmatik renal arter oklüzyonu bkz. 2013;19 (4):366-370 Triküspit kapak hasarı bkz. 2013;19(5):472-474 Triyaj bkz. 2013;19 (3):205-214 Tromboz bkz. 2013;19 (3):223-228

Ultrasonografi bkz. 2013;19 (1):80-82 Ultrasonografi bkz. 2013;19 (4):327-332

588

Üst ekstremite bkz. 2013;19(5):405-410 Üst kadran ağrısı bkz. 2013;19 (1):80-82

Vazospazm bkz. 2013;19(5):475-479 Velpeau bandajı bkz. 2013;19 (3):274-276

Y

abancı cisim bkz. 2013;19 (1):58-64 bkz. 2013;19 (3):229-234 bkz. 2013;19(6):570-572 Yaklaşım bkz. 2013;19(5):456-462 Yanık bkz. 2013;19 (3):251-255 Yanık epidemiolojisi bkz. 2013;19 (2):123-126 Yanıklar bkz. 2013;19 (2):123-126 bkz. 2013;19 (4):383-384

Yara balistiği bkz. 2013;19(5):392-397 Yaralanma bkz. 2013;19 (2):152-156 Yaş bkz. 2013;19(6):554-558 Yaşam kalitesi bkz. 2013;19 (3):200-204 bkz. 2013;19(6):521-528 Yaşlı bkz. 2013;19(6):548-553 Yatakbaşı ultrasonografi bkz. 2013;19 (3):241-245 Yeniden kanama bkz. 2013;19 (1):29-32 Yutma bkz. 2013;19(6):570-572 Yutulan yabancı cisimler bkz. 2013;19 (2):177-179 Yüksek kinetik enerji bkz. 2013;19 (2):140-144 Yüksekten düşme bkz. 2013;19(6):529-535

Z-LEDH-FMK bkz. 2013;19 (4):313-319

Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


DİZİN - I ND E X

Ulusal Travma ve Acil Cerrahi Dergisi 2013 Yılı 19. Cilt Yazar Dizini Abbasi S bkz. 2013;19(5):398-404 Acar E bkz. 2013;19 (2):180-182 Acar U bkz. 2013;19 (2):115-118 Ağalar F bkz. 2013;19(5):463-468 Ağcaoğlu O bkz. 2013;19 (3):223-228 Akbulut S bkz. 2013;19(5):417-422 Akça H bkz. 2013;19 (4):305-312 Akçakaya MO bkz. 2013;19 (4):313-319 Akçakaya MO bkz. 2013;19(6):521-528 Akçal A bkz. 2013;19(5):411-416 Akcan A bkz. 2013;19(5):387-391 Akdağ A bkz. 2013;19(6):491-499 Akdemir HU bkz. 2013;19(5):441-448 Akdemir O bkz. 2013;19 (3):267-270 Akgül O bkz. 2013;19 (2):89-97 Akgün İ bkz. 2013;19 (2):164-166 Akhmedov A bkz. 2013;19 (1):58-64 Akkapulu N bkz. 2013;19 (4):380-382 Akkaya H bkz. 2013;19 (4):371-374 Akkaya N bkz. 2013;19 (2):186-188 Akkücük S bkz. 2013;19(5):429-433 Akoğlu E bkz. 2013;19(5):423-428 Akoğlu H bkz. 2013;19(5):423-428 Aksakal İA bkz. 2013;19(5):434-440 Aksakal N bkz. 2013;19 (3):223-228 Aksoy M bkz. 2013;19 (3):223-228 Aksoy N bkz. 2013;19 (4):333-336 Akyıldız HY bkz. 2013;19(5):387-391 Akyüz F bkz. 2013;19 (2):89-97 Akyüz M bkz. 2013;19(5):387-391 Algın O bkz. 2013;19 (1):80-82 Algın O bkz. 2013;19 (4):375-379 Ali Y bkz. 2013;19 (1):69-72 Alimoğlu O bkz. 2013;19 (2):127-132 Alış H bkz. 2013;19 (1):20-24 Alış H bkz. 2013;19 (1):29-32 Alış H bkz. 2013;19 (3):200-204 Alkır G bkz. 2013;19(6):521-528 Alper A bkz. 2013;19 (2):119-122 Altaf R bkz. 2013;19 (1):69-72 Altıparmak M bkz. 2013;19 (4):348-356 Altıparmak UE bkz. 2013;19 (2):115-118 Altuntaş M bkz. 2013;19(5):441-448 Andjelkov K bkz. 2013;19 (4):383-384 Ankaralı S bkz. 2013;19 (3):195-199 Anlar M bkz. 2013;19 (2):89-97 Anlaş Demir S bkz. 2013;19 (1):49-52 Aras F bkz. 2013;19 (4):294-298 Aras Y bkz. 2013;19 (4):313-319

Aras Y bkz. 2013;19(6):521-528 Aren A bkz. 2013;19 (3):246-250 Aren G bkz. 2013;19 (3):246-250 Arı Ş bkz. 2013;19 (4):357-362 Armağan E bkz. 2013;19 (4):320-326 Arslan E bkz. 2013;19 (4):363-365 Arslan ED bkz. 2013;19(5):417-422 Arslan H bkz. 2013;19 (2):123-126 Aslan O bkz. 2013;19(5):434-440 Atabey C bkz. 2013;19 (3):235-240 Atamanalp SS bkz. 2013;19 (1):45-48 Avcı CC bkz. 2013;19 (2):145-151 Ayan E bkz. 2013;19(6):491-499 Ayan E bkz. 2013;19(6):567-569 Ayçiçek A bkz. 2013;19 (1):73-76 Aydede H bkz. 2013;19 (1):83-85 Aydemir B bkz. 2013;19 (3):229-234 Aydil BA bkz. 2013;19 (4):299-304 Aydın AE bkz. 2013;19 (1):65-68 Aydın M bkz. 2013;19 (3):195-199 Aydın Y bkz. 2013;19 (1):45-48 Aydınlı B bkz. 2013;19 (1):45-48 Aydoseli A bkz. 2013;19 (4):313-319 Aydoseli A bkz. 2013;19(6):521-528 Aygen E bkz. 2013;19 (1):13-19 Aygün A bkz. 2013;19(6):567-569 Aygün D bkz. 2013;19 (2):180-182 Aygün D bkz. 2013;19(5):441-448 Aytekin H bkz. 2013;19 (2):89-97 Ayyıldız A bkz. 2013;19(6):576-580 Azboy İ bkz. 2013;19(5):456-462

Bakan V bkz. 2013;19 (1):1-7 Bakar B bkz. 2013;19 (4):285-293 Bakkaloğlu H bkz. 2013;19 (1):65-68 Bali BS bkz. 2013;19 (2):103-108 Bali İ bkz. 2013;19 (1):53-57 Başak F bkz. 2013;19 (2):127-132 Basaran K bkz. 2013;19(6):516-520 Başkıran A bkz. 2013;19 (1):86-88 Bat O bkz. 2013;19 (3):195-199 Bayraktaroğlu S bkz. 2013;19 (4):327-332 Bayram E bkz. 2013;19 (4):294-298 Bektaş G bkz. 2013;19 (3):277-281 Beyazit Y bkz. 2013;19 (2):133-139 Bilge O bkz. 2013;19 (2):119-122 Bilgen MS bkz. 2013;19(5):475-479 Binnetoğlu K bkz. 2013;19 (1):13-19 Boyacı MG bkz. 2013;19 (1):73-76

Ulus Travma Acil Cerrahi Derg, Kasım 2013, Vol. 19, No. 6

Boydak B bkz. 2013;19 (4):327-332 Bozaxhiu D bkz. 2013;19 (1):77-79 Bozdağ Z bkz. 2013;19(6):554-558 Bozkurt MA bkz. 2013;19 (1):20-24 Bozkurt MA bkz. 2013;19 (1):29-32 Bozkurt MA bkz. 2013;19 (3):200-204 Bulut G bkz. 2013;19 (2):145-151 Burcu A bkz. 2013;19 (2):115-118 Bülbüller N bkz. 2013;19 (1):13-19

Can H bkz. 2013;19 (4):313-319 Canbek U bkz. 2013;19 (2):157-163 Canbolat A bkz. 2013;19 (4):313-319 Cavolli R bkz. 2013;19(6):564-566 Cefye K 2013;19 (4):299-304 Cengiz MB bkz. 2013;19(6):573-575 Cevik C bkz. 2013;19(5):429-433 Ceylan E bkz. 2013;19 (3):215-218 Ceylan OM bkz. 2013;19 (3):219-222 Ceylan OM bkz. 2013;19 (3):256-260 Cingü K bkz. 2013;19 (4):357-362 Cinpolat A bkz. 2013;19 (3):277-281 Cipe G bkz. 2013;19(6):573-575 Copçu E bkz. 2013;19 (3):215-218

Çaça İ bkz. 2013;19 (4):357-362 Çağatay HH bkz. 2013;19(5):449-455 Çakır C bkz. 2013;19 (3):251-255 Çal MA bkz. 2013;19 (3):267-270 Çalışkan M bkz. 2013;19 (2):127-132 Çam OH bkz. 2013;19 (3):271-273 Çankaya D bkz. 2013;19(6):548-553 Çelik A bkz. 2013;19 (2):177-179 Çelik A bkz. 2013;19(5):559-563 Çelik S bkz. 2013;19 (3):229-234 Çetin İ bkz. 2013;19 (4):294-298 Çetinkal A bkz. 2013;19 (3):235-240 Çetinkale O bkz. 2013;19 (2):123-126 Çetinkaya Şardan Y bkz. 2013;19 (3):205-214 Çetinus Ebkz. 2013;19 (1):8-12 Çevrim Ö bkz. 2013;19 (4):327-332 Çil Y bkz. 2013;19 (2):152-156 Çitgez B bkz. 2013;19 (2):164-166 Çivi M bkz. 2013;19 (4):294-298 Çığşar EB bkz. 2013;19(5):488-490 Çınar Y bkz. 2013;19 (4):357-362 Çıralık H bkz. 2013;19 (1):1-7 Çokluk C bkz. 2013;19(5):441-448 Çolak Ş bkz. 2013;19 (1):49-52

589


Ulusal Travma ve Acil Cerrahi Dergisi 2013 Yılı 19. Cilt Konu ve Yazar Dizini Çömelekoğlu Ü bkz. 2013;19 (4):305-312 Çoruh A bkz. 2013;19 (4):348-356 Çoşkun K bkz. 2013;19(5):392-397

Dağ A bkz. 2013;19 (4):305-312 Dandin Ö bkz. 2013;19(6):570-572 Daş K bkz. 2013;19 (1):53-57 Daş K bkz. 2013;19(5):463-468 Datlı A bkz. 2013;19(6):516-520 Demir A bkz. 2013;19(5):417-422 Demir B bkz. 2013;19(6):543-547 Demir M bkz. 2013;19(6):491-499 Demirbağ S bkz. 2013;19 (2):140-144 Demirbaş E bkz. 2013;19 (1):8-12 Demircan Y bkz. 2013;19 (4):333-336 Demirdöver C bkz. 2013;19 (2):109-114 Demirli Çaylan N bkz. 2013;19 (3):261-266 DeMuro JP bkz. 2013;19(5):469-471 Denizbaşı A bkz. 2013;19(5):423-428 Derebaşınlıoğlu H bkz. 2013;19 (2):123-126 Dikici F bkz. 2013;19 (1):8-12 Dinç H bkz. 2013;19(6):567-569 Dirlik MM bkz. 2013;19 (4):305-312 Dişibeyaz S bkz. 2013;19 (2):133-139 Divarcı E bkz. 2013;19(5):559-563 Doğan Y bkz. 2013;19 (1):58-64 Doğusoy I bkz. 2013;19 (3):229-234 Dokucu Aİ bkz. 2013;19(5):488-490 Dulundu E bkz. 2013;19(6):507-515 Duman S bkz. 2013;19(6):543-547 Durak K bkz. 2013;19(5):475-479 Durak VA bkz. 2013;19 (4):320-326 Durdu T bkz. 2013;19(5):417-422 Dursun A bkz. 2013;19 (4):333-336 Dursun R bkz. 2013;19 (3):251-255 Durukan AH bkz. 2013;19 (3):219-222 Durukan AH bkz. 2013;19 (3):256-260 Durusu M bkz. 2013;19(6):536-542

Ekici U bkz. 2013;19 (2):164-166 Ekinci M bkz. 2013;19(5):449-455 Ekmekçi C bkz. 2013;19 (2):173-176 Elbeyli L bkz. 2013;19 (4):363-365 Eldegez CU bkz. 2013;19 (1):65-68 Elmalı M bkz. 2013;19 (1):33-40 Emre A bkz. 2013;19 (2):119-122 Emre A bkz. 2013;19(6):554-558 Ener BK bkz. 2013;19 (2):127-132 Enis Tok O bkz. 2013;19(6):507-515 Er E bkz. 2013;19 (1):25-28 Eraybar Pozam S bkz. 2013;19 (4):320-326 Erbil B bkz. 2013;19 (3):205-214 Ercan F bkz. 2013;19(6):507-515 Erçetin C bkz. 2013;19 (2):119-122 Erdem M bkz. 2013;19 (2):145-151 Erden S bkz. 2013;19(6):491-499 Erdoğan B bkz. 2013;19 (3):282-284 Erdoğan MÖ bkz. 2013;19 (1):49-52 Erdoğan MÖ bkz. 2013;19 (3):282-284 Erdurman FC bkz. 2013;19 (3):219-222

590

Erdurman FC bkz. 2013;19 (3):256-260 Erer M bkz. 2013;19 (1):58-64 Ergin M bkz. 2013;19 (3):274-276 Ergintürk ACAR D bkz. 2013;19 (2):115-118 Ergün O bkz. 2013;19(5):559-563 Erhan Y bkz. 2013;19 (1):83-85 Erikci VS bkz. 2013;19 (4):333-336 Erkal H 2013;19 (4):299-304 Erkekel Ş bkz. 2013;19 (1):80-82 Erkorkmaz Ü bkz. 2013;19(6):554-558 Eroğlu A bkz. 2013;19 (3):235-240 Eroğlu L bkz. 2013;19(5):434-440 Eroğlu M bkz. 2013;19(6):536-542 Eroğlu SE bkz. 2013;19(5):423-428 Ersel M bkz. 2013;19 (4):327-332 Ersoy PE bkz. 2013;19 (4):375-379 Ersöz G bkz. 2013;19(6):491-499 Ertekin C bkz. 2013;19 (3):246-250 Ertekin C bkz. 2013;19(5):463-468 Eryılmaz M bkz. 2013;19 (2):140-144 Eryılmaz M bkz. 2013;19(5):392-397 Eryılmaz M bkz. 2013;19(6):536-542 Eser O bkz. 2013;19 (1):73-76 Eskitaşcıoğlu T bkz. 2013;19 (4):348-356 Eslami V bkz. 2013;19(6):500-506 Eyi YE bkz. 2013;19(6):536-542

Farnia MR bkz. 2013;19(6):500-506 Farsi D bkz. 2013;19(5):398-404 Ficklscherer A bkz. 2013;19 (2):98-102 Furqan N bkz. 2013;19 (1):69-72 Garge S bkz. 2013;19 (4):366-370 Garge S bkz. 2013;19(5):480-484 Gemici E bkz. 2013;19 (3):200-204 Genç B bkz. 2013;19 (4):343-347 Genişol İ bkz. 2013;19 (4):333-336 Gök AFK bkz. 2013;19 (3):223-228 Gökalan KARA İ bkz. 2013;19 (2):186-188 Gökçe G bkz. 2013;19 (3):219-222 Gökler C bkz. 2013;19 (1):53-57 Gölcük Y bkz. 2013;19 (1):41-44 Gömleksiz C bkz. 2013;19 (4):313-319 Gönenç M bkz. 2013;19 (1):20-24 Gönenç M bkz. 2013;19 (1):29-32 Gönenç M bkz. 2013;19 (3):200-204 Görmeli CA bkz. 2013;19 (3):251-255 Görmeli G bkz. 2013;19 (3):251-255 Güçiz Doğan B bkz. 2013;19 (3):205-214 Güçyetmez B bkz. 2013;19(6):576-580 Gülabi D bkz. 2013;19 (2):145-151 Gülnerman YC bkz. 2013;19 (1):53-57 Güloğlu C bkz. 2013;19(6):529-535 Güloğlu R bkz. 2013;19 (3):246-250 Gümüş LT bkz. 2013;19 (4):305-312 Gümüşalan Y bkz. 2013;19 (1):1-7 Gümüşer G bkz. 2013;19 (4):294-298 Gün F bkz. 2013;19 (2):177-179 Günay GK bkz. 2013;19 (4):348-356 Gündoğmuş ÜN bkz. 2013;19 (4):371-374

Günendi T bkz. 2013;19 (2):177-179 Gürlek K bkz. 2013;19 (3):274-276 Güven E bkz. 2013;19(6):516-520 Güven K bkz. 2013;19 (2):119-122 Güzel E bkz. 2013;19 (1):8-12

Hafezimoghadam P bkz. 2013;19(5):398-404 HajiseyedJavadi H bkz. 2013;19(6):500-506 Halm JA bkz. 2013;19(5):405-410 Hasbahçeci M bkz. 2013;19 (2):127-132 Hasbahceci M bkz. 2013;19(6):573-575 Hazer B bkz. 2013;19(6):570-572 Heper Y bkz. 2013;19 (4):320-326 Hocaoğlu E bkz. 2013;19 (1):58-64 Hoşgör M bkz. 2013;19 (4):333-336 Hürmeriç V bkz. 2013;19 (3):256-260

Ilgar M bkz. 2013;19 (1):33-40 Işık AF bkz. 2013;19 (4):363-365 Işık B bkz. 2013;19 (1):86-88 Işık Ö bkz. 2013;19 (4):385-386 Işık Y bkz. 2013;19 (3):251-255 İçer M bkz. 2013;19(6):529-535 İlçe Z bkz. 2013;19(6):554-558 İlhan YS bkz. 2013;19 (1):13-19 İmamoğlu M bkz. 2013;19 (2):183-185 İmer M bkz. 2013;19(6):521-528 İmerci A bkz. 2013;19 (1):41-44 İmerci A bkz. 2013;19 (2):157-163 İnce V bkz. 2013;19 (1):86-88 İpek EG bkz. 2013;19(5):472-474 İrkören S bkz. 2013;19 (3):215-218 İş M bkz. 2013;19 (2):89-97 İyibozkurt C bkz. 2013;19 (2):119-122

Jahollari A bkz. 2013;19(6):564-566 Jain A bkz. 2013;19 (1):69-72 Jansson V bkz. 2013;19 (2):98-102

Kabukçuoğlu YS bkz. 2013;19(6):543-547 Kahraman E bkz. 2013;19 (2):152-156 Kahyaoğlu OS bkz. 2013;19 (4):385-386 Kalaycı MU bkz. 2013;19 (1):29-32 Kaldırım Ü bkz. 2013;19(6):536-542 Kalender AM bkz. 2013;19 (1):1-7 Kalogeropoulou C bkz. 2013;19 (2):167-172 Kanık EA bkz. 2013;19 (4):305-312 Kanojia R bkz. 2013;19 (4):366-370 Kapan S bkz. 2013;19 (1):20-24 Kapan S bkz. 2013;19 (1):29-32 Kara PH bkz. 2013;19 (1):25-28 Karabacak A bkz. 2013;19(5):387-391 Karabulut K bkz. 2013;19 (1):13-19 Karabulut M bkz. 2013;19 (3):200-204 Karaca C bkz. 2013;19 (2):109-114 Karaca MA bkz. 2013;19 (3):205-214 Karaca Y bkz. 2013;19(6):567-569 Karacan CD bkz. 2013;19 (3):261-266 Karaçelik M bkz. 2013;19 (2):173-176

Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6


Ulusal Travma ve Acil Cerrahi Dergisi 2013 Yılı 19. Cilt Konu ve Yazar Dizini Karadağ ÇA bkz. 2013;19(5):488-490 Karadaş S bkz. 2013;19 (3):251-255 Karagöz A bkz. 2013;19 (3):241-245 Karagöz H bkz. 2013;19(5):485-487 Karakaş DÖ bkz. 2013;19(6):570-572 Karakuş A bkz. 2013;19(5):429-433 Karancı T bkz. 2013;19 (3):267-270 Karaoğlan A bkz. 2013;19 (3):267-270 Karaoğlanoğlu M bkz. 2013;19 (1):80-82 Karaoğlanoğlu M bkz. 2013;19 (4):375-379 Karapınar B bkz. 2013;19(5):559-563 Karateke F bkz. 2013;19 (1):53-57 Karateke F bkz. 2013;19(5):463-468 Karatepe O bkz. 2013;19(6):573-575 Karavelioğlu E bkz. 2013;19 (1):73-76 Karavias D bkz. 2013;19 (2):167-172 Karbeyaz K bkz. 2013;19 (4):371-374 Karşıdağ S bkz. 2013;19(5):411-416 Karşıdağ S bkz. 2013;19(5):449-455 Kartal A bkz. 2013;19 (2):164-166 Kasımcan MÖ bkz. 2013;19 (4):285-293 Katı C bkz. 2013;19(5):441-448 Kavalci C bkz. 2013;19(5):417-422 Kavasoğlu K bkz. 2013;19 (4):343-347 Kaya A bkz. 2013;19 (2):157-163 Kaya B bkz. 2013;19 (3):195-199 Kaya İ bkz. 2013;19 (1):8-12 Kaya S bkz. 2013;19(6):581-584 Kayaoğlu HA bkz. 2013;19 (3):189-194 Kaytancı E bkz. 2013;19 (3):271-273 Keleş MK bkz. 2013;19(5):434-440 Kelten B bkz. 2013;19 (3):267-270 Keskin A bkz. 2013;19 (4):371-374 Keskin M bkz. 2013;19 (1):65-68 Khursheed N bkz. 2013;19 (1):69-72 Kılıç B bkz. 2013;19 (2):177-179 Kılınç K bkz. 2013;19 (4):285-293 Kırkıl C bkz. 2013;19 (1):13-19 Kısaoğlu A bkz. 2013;19 (1):45-48 Kıyan S bkz. 2013;19 (4):327-332 Koç C bkz. 2013;19 (1):86-88 Koç O bkz. 2013;19 (4):305-312 Koçak Berberoğlu H 2013;19 (4):299-304 Kocataş A bkz. 2013;19 (3):200-204 Koksel O bkz. 2013;19(6):491-499 Korkusuz P bkz. 2013;19 (1):8-12 Koşargelir M bkz. 2013;19 (1):49-52 Koşargelir M bkz. 2013;19 (3):282-284 Kozanoğlu E bkz. 2013;19 (1):58-64 Köksal Ö bkz. 2013;19 (4):320-326 Köse EA bkz. 2013;19 (4):285-293 Köseoğlu A bkz. 2013;19 (4):385-386 Köseoğlu RD bkz. 2013;19 (3):189-194 Kul B bkz. 2013;19 (2):123-126 Kunt MM bkz. 2013;19 (3):205-214 Kupana AYVA Ş bkz. 2013;19 (4):285-293 Kurtoğlu M bkz. 2013;19 (3):223-228 Kuru S bkz. 2013;19 (3):246-250 Kuvat SV bkz. 2013;19 (1):58-64 Küçükalp A bkz. 2013;19(5):475-479

Külahçı Y bkz. 2013;19(5):485-487

Lafçı G bkz. 2013;19 (4):343-347 Maroulis I bkz. 2013;19 (2):167-172 Menderes A bkz. 2013;19 (2):109-114 Menekşe E bkz. 2013;19 (1):53-57 Menekşe E bkz. 2013;19(5):463-468 Meriç K bkz. 2013;19 (3):282-284 Mesci A bkz. 2013;19 (2):140-144 Mete FS bkz. 2013;19 (1):58-64 Metin B bkz. 2013;19(6):581-584 Metin MR bkz. 2013;19 (4):375-379 Mir MA bkz. 2013;19 (2):103-108 Mir RA bkz. 2013;19 (2):103-108 Mitrushi A bkz. 2013;19 (1):77-79 Mokhtarpour M bkz. 2013;19(6):500-506 Momeni M bkz. 2013;19(6):500-506 Movahedi M bkz. 2013;19(5):398-404 Muriqi S bkz. 2013;19(6):564-566 Muslumanoglu M bkz. 2013;19(6):573-575 Müller PE bkz. 2013;19 (2):98-102

Narasimhan KL bkz. 2013;19(5):480-484 Navsaria PH bkz. 2013;19(5):405-410 Nejad NH bkz. 2013;19(6):500-506 Nicol AJ bkz. 2013;19(5):405-410 NiethammerT bkz. 2013;19 (2):98-102 Nural MS bkz. 2013;19 (1):33-40

Oba ME bkz. 2013;19(5):449-455 Okay T bkz. 2013;19 (3):229-234 Okumuş M bkz. 2013;19 (1):1-7 Okur Ö bkz. 2013;19 (4):333-336 Onur A bkz. 2013;19 (1):86-88 Onur ÖE bkz. 2013;19(5):423-428 Orak M bkz. 2013;19(6):529-535 Oral R bkz. 2013;19 (3):261-266 Oruç C bkz. 2013;19 (4):385-386 Oyar O bkz. 2013;19 (1):25-28 Öcal AK bkz. 2013;19 (4):305-312 Öğünç Gİ bkz. 2013;19(5):392-397 Öksüz S bkz. 2013;19(5):485-487 Önel S bkz. 2013;19 (1):53-57 Önel S bkz. 2013;19(5):463-468 Öner OZ bkz. 2013;19 (1):29-32 Örnek Y bkz. 2013;19 (4):333-336 Özalp B bkz. 2013;19 (1):58-64 Özaydın İ bkz. 2013;19 (3):195-199 Özbağ D bkz. 2013;19 (1):1-7 Özbek C bkz. 2013;19 (2):173-176 Özbilen Acar G bkz. 2013;19 (3):271-273 Özcan AA bkz. 2013;19(5):449-455 Özcan AŞ bkz. 2013;19 (1):80-82 Özcan HR bkz. 2013;19 (2):186-188 Özçete E bkz. 2013;19 (4):327-332 Özçınar B bkz. 2013;19 (3):223-228 Özden E bkz. 2013;19(6):543-547 Özden İ bkz. 2013;19 (2):119-122

Ulus Travma Acil Cerrahi Derg, Kasım 2013, Vol. 19, No. 6

Özdoğan M bkz. 2013;19 (1):53-57 Özdoğan M bkz. 2013;19(5):463-468 Özdoğan Ö bkz. 2013;19 (2):173-176 Özdülger A bkz. 2013;19(6):491-499 Özer MT bkz. 2013;19(5):392-397 Özkan E bkz. 2013;19(6):507-515 Özkan N bkz. 2013;19 (3):189-194 Özkan Ö bkz. 2013;19 (3):277-281 Özkan Ö bkz. 2013;19 (3):277-281 Özkurt B bkz. 2013;19(6):548-553 Özkurt E bkz. 2013;19 (3):223-228 Özmen E bkz. 2013;19 (1):80-82 Özmen E bkz. 2013;19 (4):375-379 Özmen MM bkz. 2013;19 (3):205-214 Özmen MM bkz. 2013;19(5):463-468 Özoğul B bkz. 2013;19 (1):45-48 Özpek A bkz. 2013;19 (2):127-132 Özpolat Ç bkz. 2013;19(5):423-428 Öztürk E bkz. 2013;19 (1):49-52 Öztürk G bkz. 2013;19 (1):45-48 Öztürk Ş 2013;19 (4):299-304 Özüçelik DN bkz. 2013;19 (3):205-214 Özyazgan İ bkz. 2013;19 (4):348-356 Özyazıcı S bkz. 2013;19 (1):53-57 Özyazıcı S bkz. 2013;19(5):463-468

Paç M bkz. 2013;19 (4):343-347 Palandüz Ş 2013;19 (4):299-304 Pamukcu C bkz. 2013;19(5):449-455 Parlak E bkz. 2013;19 (2):133-139 Peker Y bkz. 2013;19 (2):140-144 Pellumbi A bkz. 2013;19 (3):256-260 Pietschmann MF bkz. 2013;19 (2):98-102 Pilancı Ö bkz. 2013;19(6):516-520 Pınar Erdem A bkz. 2013;19 (3):246-250 Polat A bkz. 2013;19(6):491-499 Poyrazoğlu Y bkz. 2013;19(6):536-542 Purnak T bkz. 2013;19 (2):133-139

Rahimi-Movaghar V bkz. 2013;19(5):398-404 Rao K bkz. 2013;19 (4):366-370

Sabancı PA bkz. 2013;19(6):521-528 Saeedi M bkz. 2013;19(6):500-506 Sağlam F bkz. 2013;19 (2):145-151 Salihoğlu E bkz. 2013;19(6):576-580 Sallahu F bkz. 2013;19(6):564-566 Saltık L bkz. 2013;19(6):576-580 Sarı F bkz. 2013;19 (2):145-151 Sarıcı İS bkz. 2013;19 (3):223-228 Sarıhan H bkz. 2013;19 (2):183-185 Sarkarati B bkz. 2013;19 (4):285-293 Savcun GY bkz. 2013;19(6):507-515 Savran A bkz. 2013;19 (1):41-44 Savran A bkz. 2013;19 (2):157-163 Saydam FA bkz. 2013;19(6):516-520 Sekhon V bkz. 2013;19(5):480-484 Sencer A bkz. 2013;19 (4):313-319 Sepet E bkz. 2013;19 (3):246-250 Serin K bkz. 2013;19 (2):119-122 591


Ulusal Travma ve Acil Cerrahi Dergisi 2013 Yılı 19. Cilt Konu ve Yazar Dizini Serin KR bkz. 2013;19 (1):65-68 Serinsöz E bkz. 2013;19 (4):305-312 Sert DE bkz. 2013;19 (4):343-347 Sever N bkz. 2013;19(5):488-490 Sforza M bkz. 2013;19 (4):383-384 Shahlaee A bkz. 2013;19(5):398-404 Sipahioğlu S bkz. 2013;19(5):456-462 Sivri B bkz. 2013;19 (3):205-214 Sivrioğlu N bkz. 2013;19 (3):215-218 Sobacı G bkz. 2013;19 (3):219-222 Sobacı G bkz. 2013;19 (3):256-260 Sökücü S bkz. 2013;19(6):543-547 Sonel AM bkz. 2013;19 (3):215-218 Sözüer E bkz. 2013;19(5):387-391 Spyropoulos C bkz. 2013;19 (2):167-172 Sucu DÖ bkz. 2013;19(5):411-416 Suha T bkz. 2013;19(6):567-569 Suvak B bkz. 2013;19 (2):133-139 Sürer L bkz. 2013;19 (1):41-44 Sürer L bkz. 2013;19 (2):157-163

Şahin A bkz. 2013;19 (3):205-214 Şahin A bkz. 2013;19 (4):357-362 Şahin E bkz. 2013;19(5):456-462 Şahin F bkz. 2013;19 (2):186-188 Şahin M bkz. 2013;19 (4):357-362 Şanlı M bkz. 2013;19 (4):363-365 Şehirli AÖ bkz. 2013;19(6):507-515 Şen C bkz. 2013;19 (2):145-151 Şen Tanrıkulu C bkz. 2013;19 (4):380-382 Şener G bkz. 2013;19(6):507-515 Şimşek G bkz. 2013;19 (4):320-326 Şimşek T bkz. 2013;19(5):434-440 Tabak AY bkz. 2013;19(6):548-553 Tamer L bkz. 2013;19(6):491-499 Tanrıkulu H bkz. 2013;19 (3):229-234 Tanrıkulu Y bkz. 2013;19 (4):380-382 Taş H bkz. 2013;19 (2):140-144 Taşkın AK bkz. 2013;19 (3):195-199 Taşoğlu İ bkz. 2013;19 (4):343-347 Tavlasoglu M bkz. 2013;19(6):564-566 Tekant Y bkz. 2013;19 (2):119-122 Tekin M bkz. 2013;19 (3):271-273 Telci L bkz. 2013;19(6):576-580

592

Temiz C bkz. 2013;19 (4):294-298 Tolgay CG bkz. 2013;19 (3):246-250 Topaloğlu Ü bkz. 2013;19(6):507-515 Topçu İ bkz. 2013;19 (4):294-298 Toprak SN bkz. 2013;19(5):423-428 Topuz AK bkz. 2013;19 (3):235-240 Torun S bkz. 2013;19 (2):133-139 Toygar M bkz. 2013;19(6):536-542 Tözüm H bkz. 2013;19(6):581-584 Troshani B bkz. 2013;19 (1):77-79 Trouillier H bkz. 2013;19 (2):98-102 Tunca F bkz. 2013;19 (1):65-68 Turgut G bkz. 2013;19(5):411-416 Turgut T bkz. 2013;19(6):554-558 Turhan AN bkz. 2013;19 (1):20-24 Tutcu Şahin S bkz. 2013;19 (1):83-85 Türkcü FM bkz. 2013;19 (4):357-362 Türker T bkz. 2013;19(6):536-542

Vermeulen J bkz. 2013;19(5):405-410 Verschuren RCM bkz. 2013;19(5):405-410 Vroon LC bkz. 2013;19(5):405-410 Vyshka G bkz. 2013;19 (1):77-79

Wani A bkz. 2013;19 (1):69-72 Wani H bkz. 2013;19 (2):103-108 Wegener B bkz. 2013;19 (2):98-102

Vahdati SS bkz. 2013;19(6):500-506

Yağmur Ç bkz. 2013;19(5):434-440 Yalaz M bkz. 2013;19(5):559-563 Yalnız Akkaya Z bkz. 2013;19 (2):115-118 Yanar F bkz. 2013;19 (3):223-228 Yar Ü bkz. 2013;19(5):456-462 Yaroğlu HY bkz. 2013;19(6):491-499 Yaşar M bkz. 2013;19 (3):195-199 Yavuz U bkz. 2013;19(6):543-547 Yeginsu A bkz. 2013;19 (3):274-276 Yel C bkz. 2013;19(5):417-422 Yengil E bkz. 2013;19(5):429-433 Yenidoğan E bkz. 2013;19 (3):189-194 Yetkin G bkz. 2013;19 (2):164-166 Yiğit T bkz. 2013;19 (2):140-144 Yıldırım A bkz. 2013;19 (3):241-245 Yıldırım A bkz. 2013;19 (4):357-362 Yıldırım Ü bkz. 2013;19 (3):195-199 Yıldız EH bkz. 2013;19 (2):115-118 Yıldız M bkz. 2013;19 (4):333-336 Yılmaz F bkz. 2013;19(5):417-422 Yılmaz G bkz. 2013;19 (3):261-266 Yılmaz M bkz. 2013;19 (2):109-114 Yılmaz MS bkz. 2013;19(5):417-422 Yılmaz Z bkz. 2013;19 (1):1-7 Yıydırgan Mİ bkz. 2013;19 (1):45-48 Yontar Y bkz. 2013;19 (4):348-356 Yorulmaz R bkz. 2013;19 (3):282-284 Yur M bkz. 2013;19 (1):13-19 Yüksel H bkz. 2013;19 (4):357-362 Yüksel KZ bkz. 2013;19 (1):1-7 Yürüktümen A bkz. 2013;19 (4):327-332

Van Lieshout EMM bkz. 2013;19(5):405-410 Van Waes OJF bkz. 2013;19(5):405-410 Vandenberk N bkz. 2013;19 (3):241-245 Vayvada H bkz. 2013;19 (2):109-114 Verma S bkz. 2013;19(5):480-484

Zaccheddu R bkz. 2013;19 (4):383-384 Zehir S bkz. 2013;19(5):456-462 Zeren C bkz. 2013;19(5):429-433 Zorlu P bkz. 2013;19 (3):261-266

Uğraş A bkz. 2013;19 (1):8-12 Uğur SG bkz. 2013;19 (1):41-44 Uğurlu K bkz. 2013;19(5):411-416 Uludağ M bkz. 2013;19 (2):164-166 Ulus AT bkz. 2013;19 (4):343-347 Uluşan A bkz. 2013;19 (4):363-365 Ursavaş HT bkz. 2013;19 (1):41-44 Uruc V bkz. 2013;19(5):429-433 Uslu A bkz. 2013;19(5):485-487 Uz İ bkz. 2013;19 (4):327-332 Uzar Aİ bkz. 2013;19(5):392-397 Ülkür E bkz. 2013;19(5):485-487 Ünlü N bkz. 2013;19 (2):115-118 Ünlüer EE bkz. 2013;19 (1):25-28 Ünlüer EE bkz. 2013;19 (3):241-245 Üreyen O bkz. 2013;19 (4):385-386 Üstündağ M bkz. 2013;19(6):529-535

Ulus Travma Acil Cerr Derg, November 2013, Vol. 19, No. 6

Travma 2013 6  
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