Travma 2011-1

Cilt - Volume 17

Sayı - Number 1

Ocak - January 2011

TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY

www.tjtes.org Index Medicus, Medline, EMBASE/Excerpta Medica, Science Citation Index-Expanded (SCI-E), Index Copernicus ve TÜB‹TAK-ULAKB‹M Türk Tıp Dizini’nde yer almaktadır.

Indexed in Index Medicus, Medline, EMBASE/Excerpta Medica and Science Citation Index-Expanded (SCI-E), Index Copernicus and the Turkish Medical Index of TÜB‹TAK-ULAKB‹M.

ISSN 1306 - 696x

ULUSAL TRAVMA VE AC‹L CERRAH‹ DERG‹S‹ TURKISH JOURNAL OF TRAUMA AND EMERGENCY SURGERY Editör (Editor) Recep Güloğlu

Yardımcı Editörler (Associate Editors) Kaya Sarıbeyoğlu

Hakan Yanar

Ahmet Nuray Turhan

Geçmiş Dönem Editörleri (Former Editors) Ömer Türel

Cemalettin Ertekin

Korhan Taviloğlu

ULUSAL BİLİMSEL DANIŞMA KURULU (NATIONAL EDITORIAL BOARD) Fatih Ağalar Yiğit Akçalı Yılmaz Akgün Levhi Akın Özkan Akıncı Alper Akınoğlu Mehmet Ali Akkuş Murat Aksoy Şeref Aktaş Ali Akyüz Ömer Alabaz Cem Alhan Nevzat Alkan Nilüfer Alparslan Acar Aren Cumhur Arıcı Oktar Asoğlu Mehmet Aşık Bülent Atilla Levent Avtan Yunus Aydın Erşan Aygün Mois Bahar Akın Eraslan Balcı Emre Balık Umut Barbaros Semih Baskan Mehmet Bayramiçli Ahmet Bekar Mustafa Berker Orhan Bilge Mustafa Bozbuğa Başar Cander Nuh Zafer Cantürk Münacettin Ceviz Figen Coşkun İrfan Coşkun Nahit Çakar Adnan Çalık Fehmi Çelebi Oğuz Çetinkale Orhan Çizmeci Sebahattin Çobanoğlu Ahmet Çoker Cemil Dalay Mehmet Demirhan Fatih Dikici Şükrü Dilege Osman Nuri Dilek Levent Döşemeci Murat Servan Döşoğlu Kemal Durak Koray Dural İmdat Elmas Ufuk Emekli Haluk Emir Levent Eralp

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

Yeşim Erbil Şevval Eren Hayri Erkol Metin Ertem Mehmet Eryılmaz Figen Esen Tarık Esen İrfan Esenkaya Nurperi Gazioğlu Fatih Ata Genç Niyazi Görmüş Feryal Gün Ömer Günal Nurullah Günay Haldun Gündoğdu Mahir Günşen Hakan Gürbüz Emin Gürleyik Hakan Güven Tufan Hiçdönmez Gökhan İçöz İbrahim İkizceli Murat İmer Haluk İnce Fuat İpekçi Ferda Şöhret Kahveci Selin Kapan Murat Kara Özalp Karabay Hasan Eşref Karabulut Ekrem Kaya Mehmet Yaşar Kaynar Mete Nur Kesim Yusuf Alper Kılıç Hakan Kınık Talat Kırış Haluk Kiper Hikmet Koçak Güniz Meyancı Köksal Cüneyt Köksoy İsmail Kuran Necmi Kurt Mehmet Kurtoğlu Nezihi Küçükarslan İsmail Mihmanlı Mehmet Mihmanlı Ufuk Nalbantoğlu Köksal Öner Durkaya Ören Hüseyin Öz Hüseyin Özbey Faruk Özcan Perihan Ergin Özcan Akın Özden Cemal Özçelik Niyazi Özçelik İlgin Özden

İstanbul Diyarbakır Bolu İstanbul Ankara İstanbul İstanbul Malatya İstanbul İstanbul Konya İstanbul Düzce Kayseri Ankara Adana İstanbul Bolu İstanbul Edirne İzmir Kayseri İstanbul İstanbul İzmir Bursa İstanbul Ankara İzmir İstanbul Bursa İstanbul Samsun Ankara Ankara İstanbul Eskişehir Erzurum İstanbul Ankara İstanbul İstanbul İstanbul Ankara İstanbul Sakarya İstanbul İstanbul Erzurum İstanbul İstanbul İstanbul İstanbul Denizli Diyarbakır Ankara İstanbul

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

Ankara Konya Bursa İstanbul Ankara İstanbul Mersin İstanbul İstanbul İstanbul İstanbul İstanbul Ankara Ankara İstanbul İstanbul İstanbul Kayseri İstanbul İstanbul İstanbul İstanbul Diyarbakır İstanbul İstanbul Ankara İstanbul İstanbul Ankara İstanbul Manisa İstanbul İstanbul Kocaeli Ankara İstanbul İstanbul İstanbul Kocaeli Urfa Balıkesir Adana İstanbul İstanbul İstanbul Trabzon İstanbul Ankara İstanbul İstanbul Gaziantep İstanbul Malatya Ankara İstanbul Sakarya

ULUSLARARASI BİLİMSEL DANIŞMA KURULU INTERNATIONAL EDITORIAL BOARD

Juan Asensio Zsolt Balogh Ken Boffard Fausto Catena Howard Champion Elias Degiannis Demetrios Demetriades Timothy Fabian Abe Fingerhut 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 Paris, France 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

Cape Town, S. Africa

Andrew Nicol

Cape Town, S. Africa

Hans J Oestern

Celle, Germany

Andrew Peitzman

Pittsburgh, USA

Basil A Pruitt

Peter Rhee

Pol Rommens

William Schwabb

Michael Stein

Spiros Stergiopoulos

Michael Sugrue

Liverpool, Australia

Otmar Trentz

Zurich, Switzerland

Donald Trunkey

Oregon, USA

Fernando Turegano

Madrid, Spain

Selman Uranues

Vilmos Vecsei

George Velmahos

Boston, USA

Eric J Voiglio

Lyon, France

Mauro Zago

Denver, USA

San Antonio, USA Tucson, USA Mainz, Germany Philadelphia, USA Petach-Tikva, Israel Athens, Greece

Graz, Austria Vienna, Austria

Milan, Italy

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

Başkan (President) Başkan Yardımcısı (Vice President) Genel Sekreter (Secretary General) Sayman (Treasurer) Yönetim Kurulu Üyeleri (Members)

Cemalettin Ertekin Salih Pekmezci Ahmet Nuray Turhan Recep Güloğlu Acar Aren Kaya Sarıbeyoğlu Hakan Yanar

İLETİŞİM (CORRESPONDENCE)

Ulusal Travma ve Acil Cerrahi Derneği İstanbul Üniversitesi İstanbul Tıp Fakültesi Genel Cerrahi Anabilim Dalı, Travma ve Acil Cerrahi Servisi, 34390 Çapa, İstanbul

Tel: +90 212 - 588 62 46 - 531 12 46 Faks (Fax): +90 212 - 533 18 82 e-posta (e-mail): travma@travma.org.tr Web: www.travma.org.tr

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

Ulusal Travma ve Acil Cerrahi Derneği adına Sahibi (Owner) Yazı İşleri Müdürü Amblem Yazışma adresi (Correspondence address)

Tel Faks (Fax)

Cemalettin Ertekin Recep Güloğlu Metin Ertem Ulusal Travma ve Acil Cerrahi Dergisi Sekreterliği Deniz Abdal Mah., Köprülü Mehmet Paşa Sok., Dadaşoğlu Apt., No: 25/1, 34104 Şehremini, İstanbul +90 212 - 531 12 46 - 531 09 39 +90 212 - 533 18 82

Abonelik: 2011 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) Index Medicus, Medline; EMBASE, Excerpta Medica; Science Citation Index-Expanded (SCI-E), Index Copernicus ve TÜBİTAK ULAKBİM Türk Tıp Dizini’nde yer almaktadır. (Included in Index Medicus, Medline; EMBASE, Excerpta Medica; Science Citation Index-Expanded (SCI-E), Index Copernicus and Turkish Medical Index) • Yayıncı (Publisher): KARE Yayıncılık (KARE Publishing) • Tasarım (Design): Ali Cangül • İngilizce Editörü (Linguistic Editor): Corinne Can • İstatistik (Statistician): Empiar • Online Dergi & Web (Online Manuscript & Web Management): LookUs • Baskı (Press): Yıldırım Matbaacılık • Basım tarihi (Press date): Ocak (January) 2011 • Bu dergide kullanılan kağıt ISO 9706: 1994 standardına uygundur. (This publication is printed on paper that meets the international standard ISO 9706: 1994).

Bu derginin basımı ve hekimlere ulaştırılması, bilime katkı amacıyla, Sanofi-Aventis desteğinde gerçekleştirilmektedir. İçeriğindeki tüm görüş, iddia ve açıklamalar editör ve yazarların kendilerine ait olup, hiçbir şekilde sponsor ile ilişkilendirilemez.

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.

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 190-210 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.

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. 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.

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” section, called “Upload Your Files”.

Abstract: The abstract should be structured and serve as an informative guide for the methods and results sections of the study. It must be prepared with the following subtitles: Background, Methods, Results and Conclusions. Abstracts should not exceed 200 words.

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.

References: All references should be numbered in the order of mention in the text. All reference figures in the text should be given in brackets without changing the font size. References should only include articles that have been published or accepted for publication. Reference format should conform to the “Uniform requirements for manuscripts submitted to biomedical journals” (http://www.icmje.org) and its updated versions (February 2006). Journal titles should be abbreviated according to Index Medicus. Journal references should provide inclusive page numbers. All authors, if six or fewer, should be listed; otherwise the first six should be listed, followed by “et al.” should be written. The style and punctuation of the references should follow the formats below: Journal article: Velmahos GC, Kamel E, Chan LS, Hanpeter D, Asensio JA, Murray JA, et al. Complex repair for the management of duodenal injuries. Am Surg 1999;65:972-5.

Chapter in book: Jurkovich GJ. Duodenum and pancreas. In: Mattox KL, Feliciano DV, Moore EE, editors. Trauma. 4th ed. New York: McGraw-Hill; 2000. p. 735-62.

Our journal has succeeded in being included in several indexes, in this context, we have included a search engine in our web site (www. travma.org.tr) so that you can access full-text articles of the previous issues and cite the published articles in your studies.

Review articles: Only reviews written by distinguished authors based on the editor’s invitation will be considered and evaluated. Review articles must include the title, summary, text, and references sections.

Any accompanying tables, graphics, and figures should be prepared as mentioned above.

Case reports: A limited number of case reports are published in each issue of the journal. The presented case(s) should be educative and of interest to the readers, and should reflect an exclusive rarity. Case reports should contain the title, summary, and the case, discussion, and references sections. These reports may consist of maximum five authors.

Letters to the Editor: “Letters to the Editor” are only published electronically and they do not appear in the printed version of TJTES and PUBMED. The editors do not issue an acceptance document as an original article for the ‘’letters to the editor. The letters should not exceed 500 words. The letter must clearly list the title, authors, publication date, issue number, and inclusive page numbers of the publication for which opinions are released.

Informed consent - Ethics: Manuscripts reporting the results of experimental studies on human subjects must include a statement that informed consent was obtained after the nature of the procedure(s) had been fully explained. Manuscripts describing investigations in animals must clearly indicate the steps taken to eliminate pain and suffering. Authors are advised to comply with internationally accepted guidelines, stating such compliance in their manuscripts and to include the approval by the local institutional human research committee.

ULUSAL TRAVMA VE AC‹L CERRAH‹ DERG‹S‹ TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY C‹LT - VOL. 17

SAYI - NUMBER 1

OCAK - JANUARY 2011

İçindekiler - Contents Deneysel Çalışma - Experimental Studies 1-8 The effect of glutamine on oxidative damage in an experimental abdominal compartment syndrome model in rats Sıçanlarda oluşturulan deneysel abdominal kompartman sendromunda glutaminin oksidatif hasar üzerindeki etkileri

Tihan DN, Erbil Y, Seven R, Arkaya S, Türkoğlu Ü, Hepgül G, Borucu İ 9-13 Comparison of classical surgery and sutureless repair with DuraSeal or fibrin glue for duodenal perforation in rats Sıçanlarda oluşturulan duodenum perforasyonunda klasik cerrahi ile DuraSeal ya da fibrin yapıştırıcı ile yapılan dikişsiz onarımların karşılaştırılması

Karagöz Avcı S, Yüceyar S, Aytaç E, Bayraktar O, Erenler İ, Üstün H, Uzun H, Ertürk S 14-18 Antioxidant effects of curcumin in spinal cord injury in rats Sıçanlarda spinal kord yaralanmsında curcuminin antioksidan etkileri

Şahin Kavaklı H, Koca C, Alıcı Ö

Klinik Çalışma - Original Articles 19-22 Akut apandisitte ultrasonografinin güvenilirliği Reliability of ultrasonography for diagnosing acute appendicitis

Gökçe AH, Aren A, Gökçe FS, Dursun N, Barut AY 23-28 Acil servis hekimleri tarafından düzenlenen adli raporların eksiklik ve yanlışlıklar yönünden değerlendirilmesi Evaluation of medicolegal reports written by physicians in the emergency unit with regard to deficiencies and mistakes

Serinken M, Türkçüer İ, Acar K, Özen M 29-32 Nekrotizan fasiit tanısıyla izlenen 44 olgunun klinik değerlendirmesi Clinical evaluation of forty-four patients with necrotizing fasciitis

Turhan Ö, Büyüktuna SA, İnan D, Saba R, Yalçın AN 33-40 The practice of plastic surgery in emergency trauma surgery: a retrospective glance at 10,732 patients Plastik cerrahinin acil travma cerrahisindeki yeri: 10,732 hastaya retrospektif bir bakış

Hacıkerim Karşıdağ S, Özkaya Ö, Uğurlu K, Baş L 41-45 Trakeobronşiyal yaralanmalar Tracheobronchial injuries

Aydemir B, İmamoğlu OU, Ustaalioğlu R, Okay T, Doğusoy I 46-50 Kafa travması nedeniyle tedavi edilen 954 erişkin olgunun retrospektif değerlendirilmesi: Epidemiyolojik çalışma Retrospective analysis of 954 adult patients with head injury: an epidemiological study

Işık HS, Bostancı U, Yıldız Ö, Özdemir C, Gökyar A 51-56 Fractures of the femoral head: what are the reasons for poor outcome?

Femur başı kırıkları: Tedavi stratejisi ne olmalıdır?

Özcan M, Çopuroğlu C, Sarıdoğan K

Cilt - Vol. 17 Sayı - No. 1

vii

ULUSAL TRAVMA VE AC‹L CERRAH‹ DERG‹S‹ TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY C‹LT - VOL. 17

SAYI - NUMBER 1

OCAK - JANUARY 2011

İçindekiler - Contents 57-60 The diagnosis and treatment of penile fracture: our 19-year experience Penis kırığının tanı ve tedavisi: 19 yıllık deneyim

Gedik A, Kayan D, Yamiş S, Yılmaz Y, Bircan 61-65 Factors associated with mortality in adult hospitalized burn patients in Tehran Tahran kentinde hastaneye yatırılan erişkin yanık hastalarında mortaliteye neden olan faktörler

Zarei MR, Dianat S, Eslami V, Harirchi I, Boddouhi N, Zandieh A, Rasouli MR 66-74 Tubercular bowel perforation: what to do?

Bağırsak tüberkülozu perforasyonu: Ne yapmalı?

Coccolini F, Ansaloni L, Catena F, Lazzareschi D, Puviani L, Pinna AD

Olgu Sunumu - Case Reports 75-78 Bilateral internal carotid artery and vertebral artery dissections with retinal artery occlusion after a roller coaster ride - case report and a review Lunapark trenine binmeye bağlı iki taraflı internal karotid ve vertebral arter diseksiyonu ile beraber retinal arter oklüzyonu: Olgu sunumu ve literatür incelemesi

Özkan Arat Y, Volpi J, Arat A, Klucznik R, Diaz O 79-82 Unusual penetration of a construction nail through the orbit to the cranium: a case report Bir inşaat çivisinin alışılmadık şekilde orbitayı geçerek kraniyuma saplanması: Olgu sunumu

Erkutlu İ, Alptekin M, Dokur M, Geyik M, Gök A 83-86 Rectal bleeding due to leech bite: a case report Sülük ısırığına bağlı rektal kanama: Olgu sunumu

Al B, Yenen ME, Aldemir M 87-89 Rupture of heart with all layers after a massive blunt thoracic trauma without any lesion on the bones: a case report Ağır derecede künt göğüs travması sonrası herhangi bir kemik lezyonu olmaksızın kalbin tam kat yırtılması: Olgu sunumu

Birincioğlu İ, Turan N, Can M 90-92 Gastric perforation caused by Strongyloides stercoralis: a case report Strongyloides stercoralis kaynaklı mide perforasyonu: Olgu sunumu

Öztürk G, Aydınlı B, Çelebi F, Gürsan N 93-95 Pneumomediastinum and subcutaneous emphysema caused by sigmoid diverticulum perforation secondary to blunt abdominal trauma: report of a case Künt batın travmasına sekonder gelişen sigmoid divertikül perforasyonu nedeniyle oluşan pnömomediastinum ve subkutanöz amfizem: Olgu sunumu

Yaşar NF, Kebapçı M, İhtiyar E 96 Travma ve Acil Cerrahi Bilimsel Takvim - Scientific Schedule

viii

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2010;17 (1):1-8

Experimental Study

Deneysel Çalışma doi: 10.5505/tjtes.2011.73555

The effect of glutamine on oxidative damage in an experimental abdominal compartment syndrome model in rats Sıçanlarda oluşturulan deneysel abdominal kompartman sendromunda glutaminin oksidatif hasar üzerindeki etkileri Deniz Necdet TİHAN,1 Yeşim ERBİL,1 Rıdvan SEVEN,1 Selda ARKAYA,2 Ümit TÜRKOĞLU,2 Gülçin HEPGÜL,3 İsmail BORUCU1 BACKGROUND

AMAÇ

The aim was to investigate whether or not glutamine, an antioxidant effective amino acid, improves the reperfusioninduced oxidative injury of abdominal hypertension.

Bu çalışmada, antioksidan özelliği bilinen glutaminin kullanımının iskemi-reperfüzyon sonrası oluşabilecek oksidasyon hasarı üzerindeki etkilerini araştırmayı amaçladık.

METHODS

GEREÇ VE YÖNTEM

Wistar Albino rats were used. Group 1: Abdominal compartment syndrome alone: With the rats under anesthesia, intraabdominal pressure was obtained. Three days later, the rats were sacrificed, and intestine, lung and liver samples were removed for determination of tissue malondialdehyde (MDA) and glutathione (GSH) levels as oxidative injury parameters and of myeloperoxidase (MPO) activity as an inflammatory parameter. Trunk blood was analyzed for the alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Group 2: Abdominal compartment syndrome and glutamine: intragastric glutamine was given for seven days before and three days following establishment of the abdominal compartment syndrome model. The same examination procedure was then performed. Group 3: Glutamine administration alone. Group 4: Control group.

Çalışma grubu Wistar Albino sıçanlarla oluşturuldu. Grup 1, abdominal kompartman grubuydu. Anestezi altındaki sıçanların karnına basınç uygulandı. Gaz boşaltıldıktan 3 gün sonra sıçanlar sakrifiye edildi, karaciğer, bağırsak ve akciğer doku parçalarında oksidatif hasar parametresi olarak malonildialdehit (MDA) ve glutatyon (GSH) seviyeleri ile enflamatuvar parametre olarak miyeloperoksidaz (MPO) aktivitesi ölçüldü. Alınan kan örneklerinde serum alaninaminoasit transferaz (ALT) ve aspartat-aminoasit transferaz (AST) seviyeleri ölçüldü. Grup 2, abdominal kompartman ve glutamin uygulanan gruptu. Sıçanlara 1 hafta boyunca yüksek doz glutamin mide gavajı yolu ile verildi.

Gavaj işlemi sonrası ilk gruptaki batın içi basınç uygulaması yapıldı, 3 gün daha glutamin verilen sıçanlar sakrifiye edildi, Grup 1’deki işlemlerin aynısı yapıldı. Grup 3 glutamin grubuydu. Grup 4 sham kontrol grubuydu.

RESULTS

Intraabdominal pressure significantly increased the intestine, lung and liver MDA levels and MPO activities in comparison to the control group. Glutamine was associated with decreased MDA levels and MPO activities and increased GSH levels.

BULGULAR

CONCLUSION

SONUÇ

Glutamine appears to have protective effects against reperfusion-induced oxidative damage via its anti-inflammatory and antioxidant effect.

Oksidatif hasar parametrelerine bakıldığında, glutaminin, reperfüzyon hasarını azaltıcı etkisinin antienflamatuvar ve antioksidan etkilerine bağlı olduğu düşünülmüştür.

Key Words: ������������������������������������������������� Abdominal compartment syndrome; antioxidant; glutamine; glutathione; ischemia; malondialdehyde; myeloperoxidase; oxidative stress; reperfusion.

Anahtar Sözcükler: Abdominal kompartman sendromu; antioksidan; glutamin; glutatyon; iskemi; malonildialdehit; miyeloperoksidaz; oksidatif stres; reperfüzyon.

Departments of 1General Surgery, 2Biochemistry, Istanbul University, Istanbul Faculty of Medicine, Istanbul; 3Department of General Surgery, Bagcilar Training and Research Hospital, Istanbul, Turkey.

İstanbul Üniversitesi İstanbul Tıp Fakültesi, 1Genel Cerrahi Anabilim Dalı, 2Biyokimya Anabilim Dalı, İstanbul; 3Bağcılar Eğitim ve Araştırma Hastanesi, Genel Cerrahi Kliniği, İstanbul.

Abdominal kompartman yaratılan sıçanlarda MDA düzeyi ve MPO aktivitesi kontrol grubuna göre anlamlı oranda artmıştı. Glutamin ile MDA düzeyi ve MPO aktivitesi azaldı, GSH seviyesi arttı.

Correspondence (İletişim): Deniz Necdet Tihan, M.D. İ.Ü. İstanbul Tıp Fakültesi, Genel Cerrahi Anabilim Dalı, Çapa, İstanbul, Turkey.

Tel: +90 - 212 - 589 59 70 e-mail (e-posta): dtihan@yahoo.com

1

Ulus Travma Acil Cerrahi Derg

Intraabdominal pressure (IAP) may increase in a variety of conditions ranging from trauma to abdominal surgery, from laparoscopic surgery to acute pancreatitis.[1] When IAP exceeds 15 mmHg, intraabdominal hypertension (IAH) ensues. IAH may be encountered in various clinical situations due to edema of the small intestinal wall following aggressive fluid replacement, extensive retroperitoneal bleeding, postoperative complications, acute renal failure, treatment-resistant massive ascites, serious pancreatitis, and retroperitoneal tumoral masses.[2-4] Ischemia is defined as inadequacy or cessation of blood flow to a certain tissue or organ.[5] The tissue becomes exposed to hypoxia and hypoxic tissue damage arises. Long-term ischemia threatens structural cell integrity, and even cell death ensues.[5,6] Reperfusion is re-establishment of blood flow to a certain tissue.

[5,7] When blood flow to a previously ischemic tissue is restored (reperfusion), tissue destruction is further exacerbated by free oxygen radicals released from polymorphonuclear leukocytes (PMNL) that migrate and reside in the tissue, and reperfusion-induced tissue damage occurs.[5,7-9] A variety of cells struggle against the potential hazards of free oxygen radicals by releasing enzymatic and non-enzymatic antioxidants in order to limit radical injury. Glutathione (GSH) is one of the non-enzymatic antioxidant protectors. It is well known that glutamine, which exists in blood and body fluids in high concentrations, plays a critical role in GSH biosynthesis by providing glutamate to the glutathione system.[10-12] In light of the above, considering the antioxidant effects of glutamine, we planned to investigate whether or not glutamine administration has favorable effects on serious oxidative damage that results from increased IAP. We intended to observe whether glutamine has an alleviating effect on ischemia–reperfusion injury that occurs during and following abdominal compartment syndrome (ACS) by assessing the inflammation and oxidative damage parameters obtained.

MATERIALS AND METHODS The experimental part of the study was performed in Istanbul University, Institute of Experimental Medicine and Research, between August and October 2006.

Biochemical examinations were performed in the Istanbul University Faculty of Medicine, Department of Biochemistry. Experiments were performed with permission of the Animal Ethics Committee of Istanbul University (Decision date and number: 20.09.2005 31.2005).

Subjects and Experimental Protocol Thirty-two adult male Wistar Albino rats were used for the present study. The weight range was 200-250 2

grams (g) and all rats were kept in iron cages with a 12-hour day/night cycle and 22°C room temperature.

The rats planned to undergo the IAP study were fasted the night before.

A 6 French (F) orogastric feeding tube was inserted in subjects planned for glutamine administration and then glutamine suspension, which was prepared with distilled water, was administered through gastric gavage for 10 days at a dose of 1 ml per day (1 g/kg/day).

In order to create an ACS model under ketamine anesthesia, abdomens of the rats were shaved and following application of an aseptic and antiseptic 10% povidone iodine solution, a 16-gauge sterile Angiocath was inserted intraperitoneally and 20 mmHg pressure was applied for 2 hours (h) using CO2. Rats were sacrificed using high-dose ketamine.

Three samples each of liver, small intestine and lung tissue were taken from each subject. Tissues and lumens of small intestine samples were washed twice with PBS (phosphate-buffered saline) solution at 4°C and immediately afterwards were placed into CryoTubes and stored in a deep freezer at -80°C until the date of biochemical analyses. Blood samples taken from the heart apex when apical beat was present were put into yellow cap dry biochemistry tubes and centrifuged in 3000-3500 rpm for 15 minutes (min). Serum samples that were taken from each animal were put in three different Eppendorf tubes and stored in a deep freezer at -80°C until the date of biochemical analyses.

Malondialdehyde (MDA) and GSH levels as oxidative damage parameters and myeloperoxidase (MPO) levels as an inflammatory parameter were measured in tissue samples, whereas serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured in blood samples (Table 1).

Subjects were divided into four groups as follows: Group 1 (n=8), ACS model group: Using an Angiocath, 20 mmHg constant pressure was applied for 2 h intraperitoneally to the rats, which were under anesthesia. The rats were sacrificed three days after emptying of the intraperitoneal gas, and tissue samples were taken from the liver, intestine and lung and blood sample from the heart apex.

Group 2 (n=8), ACS model and glutamine-administered group: Each rat was administered high-dose glutamine through gastric gavage for one week. Following a one-week lavage administration, intraperitoneal pressure application was performed as in Group 1. The rats were administered glutamine for three more days after emptying of the gas, were sacrificed, and then tissue and blood samples were taken as in Group 1.

Group 3 (n=8), glutamine group: Each rat was administered high-dose glutamine through gastric gaOcak - January 2011

The effect of glutamine on oxidative damage in an experimental abdominal compartment syndrome model

Examinations of Tissue Samples The liver, intestine and lung samples were weighed.

In order to detect MDA and GSH levels, their 10% homogenates were prepared by homogenizing with cold 0.15 M KCl solution in a homogenizer.

Measurement of Glutathione (GSH) Levels Measurement of GSH is based on the principal that Ellman’s reagent (5,5’-dithiobis-2 nitrobenzoic acid) is reduced by free sulfhydryl groups (-SH) of tissue homogenate. 1 mole of 2 nitro 5 thiobenzoic acid (DTNB) occurs per 1 mole of SH group, and this gives absorbance in 412 nm in spectrophotometer.

GSH levels were computed using extinction quotient and standard. Results were stated as GSH/mg protein.

Measurement of Malondialdehyde (MDA) Levels MDA (which is one of the late products of lipid peroxidation) and TBA (thiobarbituric acid) complex is measured spectrophotometrically. 10% tissue homogenates were used for this method. Results were computed using extinction quotient and standard.

MDA levels were stated as MDA/mg protein.

Protein Detection The protein amount in tissue homogenates was detected using bicinchoninic acid assay. This method is based on the principal that copper-protein complex forms chelate with bicinchoninic acid and gives absorbance in 562 nm.

Detection of Myeloperoxidase (MPO) Activity This method is based on the principal that MPO activity containing homogenate reduces o-dianisidine dihydrochloride in the presence of H2O2, and this reduced product gives absorbance in 460 nm. MPO activity was computed using o-dianisidine extinction quotient. Results were stated as U/g tissue.

Examinations of Serum Samples ALT and AST activities were examined enzymatically in serum using Roche autoanalyzer.

Statistical Analyses The results of biochemical data were stated as arithmetic average ± standard error. Statistical assessment was performed using one way analysis of variance (ANOVA), and further analysis was performed with Tukey’s test. Values of p<0.05 values were considered statistically significant.

Cilt - Vol. 17 Sayı - No. 1

Oxidative Damage and Inflammation Parameters MDA Level Lung: The MDA level was found to be significantly higher in the ACS group (Group 1) compared to controls (Group 4) (p<0.05). The MDA level of the glutamine-administered and ACS model group (Group 2) was not significantly different from controls (Group 4), whereas it was significantly lower when compared to the ACS group (Group 1) (p<0.05). There were no significant differences between the glutamine group (Group 3) and controls (Fig. 2).

Liver: The MDA level was found to be significantly higher in the ACS group (Group 1) compared to controls (Group 4) (p<0.05). The MDA level of the glutamine-administered and ACS model group (Group 2) was not significantly different from controls (Group 4), whereas it was significantly lower when compared to the ACS group (Group 1) (p<0.05). There were no significant differences between the glutamine group (Group 3) and controls (Fig. 2).

Small Intestine: The MDA level was found to be significantly higher in the ACS group (Group 1) com400 350 AST levels (U/l)

Group 4 (n=8), control group: Rats were only anesthetized without pressure application, were sacrificed, and the same tissue and blood samples were taken.

RESULTS Biochemical Analyses Serum AST and ALT Levels AST and ALT levels were found to be significantly higher in the ACS group (Group 1) compared to controls (Group 4). AST and ALT levels of the glutamineadministered and ACS model group (Group 2) were not significantly different from controls (Group 4), whereas these levels were significantly lower when compared to the ACS group (Group 1). There were no significant differences between the glutamine group (Group 3) and controls (Fig. 1).

a

300 b

250 200

b

b

Group 2

Group 3

b

b

Group 2

Group 3

150 100 50 0 160 140

ALT levels (U/l)

vage for 10 days. At the end of 10 days, the anesthetized rats were sacrificed without pressure application and the same blood and tissue samples were taken.

Group 1

Group 4

a

120 100

b

80 60 40 20 0

Group 1

Group 4

Fig. 1. Serum AST and ALT values (different letters show significance (p<0.05)).

3

Group 1

Group 2

b

Group 3

b

Group 4

a

b

Group 1

Group 2

b

Group 3

b

Group 4

600

(pmol MDA/mg protein)

b

900 800 700 600 500 400 300 200 100 0

Small intestine MDA levels

a

Liver MDA levels

800 700 600 500 400 300 200 100 0

(pmol MDA/mg protein)

Lung MDA levels

(pmol MDA/mg protein)

Ulus Travma Acil Cerrahi Derg

500

a

400 300

b

b

Group 2

Group 3

Group 4

b

b

Group 3

Group 4

b

b

Group 3

Group 4

b

200 100 0

Group 1

b

15 10 5 0

a Group 1

Group 2

Group 3

Liver GSH levels

b

b

20

b

b

a

15 10 5 0

Group 4

b

25

Group 1

Group 2

Group 3

Group 4

60

(nmol GSH/mg protein)

30

20

(nmol GSH/mg protein)

Lung GSH levels

(nmol GSH/mg protein)

25

Small intestine GSH levels

Fig. 2. Tissues MDA levels (different letters show significance (p<0.05)).

b

50 40 30

a

20 10 0

Group 1

Group 2

a a

3

Group 1

Group 2

Group 3

Group 4

2.5

a

2 1.5

b

1

b

b

0.5 0

Group 1

Group 2

Group 3

Group 4

(U/g tissue)

a

S. intestine MPO activities

a

(U/g tissue)

5 4.5 4 3.5 3 2.5 2 1.5 1 0.5 0

Liver MPO activities

(U/g tissue)

Lung MPO activities

Fig. 3. Tissues GSH levels (different letters show significance (p<0.05)).

3

a

2.5 2

b

1.5 1 0.5 0

Group 1

Group 2

Fig. 4. Tissues MPO activity (different letters show significance (p<0.05)).

pared to controls (Group 4) (p<0.05). The MDA level of the glutamine- administered and ACS model group (Group 2) was not significantly different from controls (Group 4), whereas it was significantly lower when compared to the ACS group (Group 1) (p<0.05). There were no significant differences between the glutamine group (Group 3) and controls (Fig. 2).

GSH Level Lung: The GSH level was found to be significantly higher in the ACS group (Group 1) compared to controls (Group 4) (p<0.05). The GSH level of the glutamine-administered and ACS model group (Group 2) was not significantly different from controls (Group 4), whereas it was significantly lower when compared to the ACS group (Group 1) (p<0.05). There were no significant differences between the glutamine group (Group 3) and controls (Fig. 3).

Liver: The GSH level was found to be significantly higher in the ACS group (Group 1) compared to controls (Group 4) (p<0.05). The GSH level of the glutamine-administered and ACS model group (Group 2) was not significantly different from controls (Group 4), whereas it was significantly lower when compared to the ACS group (Group 1) (p<0.05). There were no 4

significant differences between the glutamine group (Group 3) and controls (Fig. 3).

Small Intestine: The GSH level was found to be significantly higher in the ACS group (Group 1) compared to controls (Group 4) (p<0.05). The GSH level of the glutamine- administered and ACS model group (Group 2) was not significantly different from controls (Group 4), whereas it was significantly lower when compared to the ACS group (Group 1) (p<0.05). There were no significant differences between the glutamine group (Group 3) and controls (Fig. 3).

MPO Activity Lung: No significant differences were found between groups (Fig. 4).

Liver: MPO activity was found to be significantly higher in the ACS group (Group 1) compared to controls (Group 4) (p<0.05). MPO activity in the glutamine-administered and ACS model group (Group 2) was not significantly different from controls (Group 4), whereas it was significantly lower when compared to the ACS group (Group 1) (p<0.05). There were no significant differences between the glutamine group (Group 3) and controls (Fig. 4).

Ocak - January 2011

The effect of glutamine on oxidative damage in an experimental abdominal compartment syndrome model

Table 1. Mean values and standard deviations of AST and ALT (U/L), tissue GSH (nmol GSH/mg

protein) and MDA (pmol MDA/mg protein)

levels and MPO activity (U/g tissue) data in

subject groups

et al.[19] reported in an experimental study that oxidative damage occurs due to pneumoperitoneum, which was produced in order to imitate laparoscopic donor nephrectomy in rat kidneys, and this damage increases with pneumoperitoneum duration.

Groups

AST levels

ALT levels

Group 1 Group 2 Group 3 Group 4

268.1±76 153.8±30.4 148.8±29.7 158.8±71.7

118.8±21.4 88.7±7.2 70.6±28.4 67.8±15.7

Oxidative damage created by free radicals emerging from increased IAP is one of the important physiopathologic components of ACS at the cellular base.

[13] Free radicals may disrupt DNA transcription and replication by generating breaks in DNA helixes and may cause cell death in subsequent mitosis.[6,7,9] It is known that free radicals cause damage by increasing the synthesis of proinflammatory mediators like cytokines, and this oxidative damage could be demonstrated using the parameters of GSH and MDA. Serum ALT levels also increase as a result of hepatic dysfunction due to IAP increase. A continued increase in AST and ALT levels in the blood during and after the decompression period indicates tissue damage due to reperfusion. In our study, MDA levels, which indicated lipid peroxidation, were significantly higher, and GSH levels, which indicated antioxidant capacity, were significantly lower in subjects that underwent ACS model generation when compared to controls. It was observed that AST and ALT levels were high in the serum samples of the subjects in which the ACS model was generated.

Groups

GSH levels

Lung

Liver

Small intestine

Group 1 Group 2 Group 3 Group 4

4.87±1.27 12.35±2.64 15.67±2.31 15.58±4.7

15.32±3.83 23.14±4.95 24.4±2.32 21.85±2.45

26.85±3.78 44.33±14.5 49.92±9.95 46.39±9.69

Groups

MDA levels

Lung

Liver

Small intestine

Group 1 Group 2 Group 3 Group 4

624.8±101.3 430.2±115.7 437.8±73.9 421.4±85

612.9±157.6 301.9±53.7 288.9±47.3 281±49

409.8±150 246.7±103.8 240.9±97.5 225.9±113.2

Groups

MPO activities

Lung

Liver

Small intestine

3.76±0.23 3.11±1.1 2.99±0.54 3.55±0.6

2.35±0.6 1.04±0.12 1.04±0.46 0.95±0.23

2.37±0.56 1.32±0.32 0.92±0.21 0.89±0.78

Group 1 Group 2 Group 3 Group 4

Small Intestine: MPO activity was found to be significantly higher in the ACS group (Group 1) compared to controls (Group 4) (p<0.05). MPO activity of the glutamine- administered and ACS model group (Group 2) was not significantly different from controls (Group 4), whereas it was significantly lower when compared to the ACS group (Group 1) (p<0.05). There were no significant differences between the glutamine group (Group 3) and controls (Fig. 4).

DISCUSSION Abdominal compartment syndrome (ACS), which results from a sudden increase in IAP, is a frequent condition seen in clinical practice, especially in emergency surgery, trauma clinics and intensive care units, and it is sometimes fatal.[13-17] Because laparoscopic interventions increase IAP, negative effects of IAP elevation due to minimally invasive abdominal surgical interventions sometimes occur. Although Mendoza– Sagaon et al.[18] reported that laparoscopic cholecystectomy does not significantly increase stress response in pigs compared to open cholecystectomy, Akbulut Cilt - Vol. 17 Sayı - No. 1

Reperfusion causes emergence of many reactive oxygen species and related disruption of cellular function to varying degrees. Ischemia-reperfusion creates an acute inflammatory response proceeding with neutrophil activation. Proteases and cytotoxic proteins like MPO and reactive oxygen species are released from neutrophils to the extracellular fluid. It was shown in various studies that nuclear factor (NF)-κB activation ensued due to release of free oxygen radicals.

As a result of this activation, synthesis of mediators including interleukin (IL)-1, IL-6, IL-8, IL-12, tumor necrosis factor (TNF)-α, inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, intercellular adhesion molecule (ICAM), and vascular adhesion molecule (VCAM) is stimulated and an inflammatory response occurs. Therefore, the amount of proinflammatory molecules is regulated by NF-κB.[20-22] Organ failure subsequent to reperfusion proceeds with decreased microvascular permeability, edema, disordered vasoregulation, infiltration of inflammatory cells, parenchymal cell damage, and necrosis.[23] If synthesis of oxidants, cytokines and various mediators emerging in pathological settings during which tissue damage occurs cannot be prevented, sepsis and multiorgan failure may occur. If the effect of the blood-intestine barrier is considered in sepsis, the importance of prevention of oxidative damage and bacterial translocation can be recognized.[24,25] 5

Ulus Travma Acil Cerrahi Derg

As a result of ACS, cytokine activation occurs and organ damage is seen.[23] It is known that activity of the MPO enzyme, which is released from neutrophils, increases in the ischemic period seen during IAP increase. However, MPO activity is greater in the reperfusion period following decompression than in the ischemia period.[26] In our study, it was observed that as an oxidative stress parameter, MPO activity increased in tissue samples of rats in which the ACS model was generated. However, MPO activity was significantly decreased in the ACS model + glutamine administration group. No significant difference was found between groups when MPO activities in lung tissue samples taken from the rats were considered alone.

GSH is the most important defensive mechanism preventing development of oxidative damage, and it thus protects homeostasis at the cellular base.[27-29] Previous studies showed that tissue GSH levels and activities of GSH peroxidase and GSH reductase enzymes, which are critical components of the GSH redox cycle, consequently decrease when the metabolism becomes exposed to oxidative stress.[30,31] In our study, compatible with the literature, it was observed that tissue GSH levels decreased following the ischemia-reperfusion period in animal subjects in which the ACS model was generated, and this decrement could significantly be precluded in the group supplemented with glutamine.

Glutamine is a non-essential amino acid, the importance of which has been recognized in recent years. It acts as an energy source for rapidly regenerating cells like enterocytes, colonocytes and lymphocytes. It also has metabolic effects including protein synthesis and regulation of acid base balance, anabolic and trophic effects, gluconeogenesis, nucleic acid synthesis, GSH synthesis, and immunologic cell regulation. Moreover, studies have shown that glutamine regulates chemotherapy-related alterations in intestinal absorption and intestinal permeability and has favorable effects on radiation-related tissue damage.[32,33] Although glutamine is synthesized and stored in the organism, its consumption increases rapidly in catabolic conditions like major surgery, sepsis, trauma, and inflammation.[32-38] Glutamine, together with alanine and arginine, is one of a few amino acids the level of which decreases as a result of increased consumption due to a variety of inner and outer processes creating stress in metabolism and compromising homeostasis. Although it could not be statistically confirmed, it was reported that favorable results were obtained with glutamine-supplemented parenteral nutrition in intensive care patients who could not be provided nutrition via the enteral route for a long period.[12,36-40] In experimental models of sepsis, burn, radiation enteritis, ischemia-reperfusion, total parenteral nutrition, 6

and starvation, it was demonstrated that glutamine administration decreased oxidative damage and bacterial translocation and provided protection for the mucosal barrier with increasing secreted IgA levels.[20,34-38,41] It was found that glutamine reabsorption was affected, and transport of glutamine from the intestinal lumen and glutaminase activity increased in sepsis and trauma and in conditions where levels of stress hormones increased.[32,34,36,42,43] Glutamine is also responsible for NADPH and ATP production. Increased utilization of cellular glutamine delays and also prevents neutrophil apoptosis. Chang et al.[44] investigated the antiapoptotic effect of glutamine in one study about the effects of glutamine on T cells. It was found that glutamine not only regulated intracellular oxidative balance but also precluded especially T cell apoptosis. An increase in bcl-2 gene expression is thought to be the most important step of apoptosis preventing the effect of glutamine in the period following its entry into the cell.[45,46] Moreover, it is emphasized that glutamine administration to burn patients increases the bacterial killing ability of neutrophils and regulates release of free radicals.[37,47] Various studies demonstrated that ischemia reperfusion in organs is related with lipid peroxidation. The autocatalytic mechanism triggered by lipid peroxidation causes oxidative damage in the cell membrane.

Toxic and reactive metabolites, which emerge as a result of this process, cause cell death.[48,49] Because MDA is one of the latest products of the lipid peroxidation process, it is a reliable parameter for assessing the degree of peroxidation and thus oxidative damage.

There are studies in the literature demonstrating a 40% to 100% increase in MDA levels from baseline following ischemia reperfusion.[48-50] In models of ischemia-reperfusion, it was established that iNOS gene expression decreased in subjects fed a glutamine-supplemented diet.[51] It is also known that glutamine acts as an important step in GSH synthesis. On the other hand, NF-ÎşB activation is closely associated with intracellular redox balance and the GSH/GSSG ratio. Glutamine administration increased intracellular GSH and decreased NF-ÎşB release. This decrement in NF-ÎşB expression precludes dependent release of cytokines.[20,52-54] In our study, it was established that there was a significant decrease in oxidative damage parameters in glutamine- administered rats with ACS compared to those in whom ACS was generated without glutamine administration.

Various substances were tested in order to prevent and treat oxidative damage in clinical and experimental settings. Administration of protective substances including probiotics, radical scavengers, selenium, vitamin E, ascorbic acid, glutamine, taurine, betaine, Ocak - January 2011

The effect of glutamine on oxidative damage in an experimental abdominal compartment syndrome model

melatonin, alanine, curcumin, anti IL-10 receptor antibodies, and anti IL-6 receptor antibodies was found to decrease oxidative damage. Kaçmaz et al.[50] reported that octreotide application significantly decreased reperfusion-related oxidative damage in models of acute abdominal hypertension-generated rats. Protective effects of these agents are attributed to their alleviating effects on synthesis of free oxygen, nitrites and nitrate radicals.[20,24,34,35,55,56] In our study, IAP increase was found to increase the inflammatory response and reperfusion-related oxidative damage. Oxidative damage was established with an increase in MDA levels and decrease in GSH levels in the lung, liver and small intestine tissues; inflammatory response was established with an increase in MPO activity in the liver and small intestine tissues.

Glutamine was found effective when administered in order to alleviate the oxidative damage and inflammation developed in these tissues.

This study demonstrates that the favorable and protective effects of glutamine, which is also known as an antiapoptotic amino acid, on oxidative damage secondary to ACS-generated ischemia reperfusion are due to its antioxidant and antiinflammatory properties.

As a result, it was observed that glutamine diminished oxidative stress-related damage in IAP increase and ACS. This effect can be explained by glutamine’s antioxidant and antiinflammatory features. Glutamine can be applied as a therapeutic agent in confining reperfusion damage elicited by visceral ischemia due to ACS, which occurs during and/or following traumatic and surgical procedures and as a result of IAP increase generated by laparoscopic surgical techniques, which are used extensively today. Before and after clinical settings that proceed with IAP increase, glutamine should be added to nutritional supplements of patients in which ACS development is possible.

REFERENCES 1. Cullen DJ, Coyle JP, Teplick R, Long MC. Cardiovascular, pulmonary, and renal effects of massively increased intraabdominal pressure in critically ill patients. Crit Care Med 1989;17:118-21.

2. Chen RJ, Fang JF, Chen MF. Intra-abdominal pressure monitoring as a guideline in the nonoperative management of blunt hepatic trauma. J Trauma 2001;51:44-50.

3. Asensio JA, Ceballos J, Forno W. Intra-abdominal pressure monitoring. In: WC Shoemaker, GC Velhamos, D Demetriades, editors. Procedures and monitoring for the critically ill.

Philadelphia: W.B. Saunders; 2002. p. 99-103.

4. Ivatury RR, Diebel L, Porter JM, Simon RJ. Intra-abdominal hypertension and the abdominal compartment syndrome.

Surg Clin North Am 1997;77:783-800.

5. Kumar V, Cotran RS, Robbins SL. Basic pathology. Philadelphia: W.B. Saunders; 1992. p. 4-11.

6. Clarkson AN, Sutherland BA, Appleton I. The biology and pathology of hypoxia-ischemia: an update. Arch Immunol Cilt - Vol. 17 Sayı - No. 1

Ther Exp (Warsz) 2005;53:213-25.

7. de Groot H, Rauen U. Ischemia-reperfusion injury: processes in pathogenetic networks: a review. Transplant Proc 2007;39:481-4.

8. Ley K, Reutershan J. Leucocyte-endothelial interactions in health and disease. Handb Exp Pharmacol 2006:97-133.

9. Gutteridge JM, Halliwell B. Free radicals and antioxidants in the year 2000. A historical look to the future. Ann N Y Acad Sci 2000;899:136-47.

10. Rodwell VW. Metabolism of proteins and aminoacids. In: Murray RK, Granner DK, Mayes PA, Rodwell VW, editors.

Harper’s biochemistry. Appleton&Lange; 1990. p. 333-412.

11. Tapiero H, Mathé G, Couvreur P, Tew KD. II. Glutamine and glutamate. Biomed Pharmacother. 2002;56:446-57.

12. Young VR, Ajami AM. Glutamine: the emperor or his clothes? J Nutr 2001;131:2449S-87S. 13. Guloglu R, Berber E, Taviloglu K, Gunay K, Ertekin C. Clinical importance of intraabdomainal pressure in the sugical intensive care. Eur J Emerg Surg Int Care 1997;20:191-4.

14. Saggi BH, Sugerman HJ, Ivatury RR, Bloomfield GL. Abdominal compartment syndrome. J Trauma 1998;45:597-609.

15. Van Hee R. An abdominal challenge: the compartment syndrome. G Chir 2007;28:413-8.

16. Eddy V, Nunn C, Morris JA Jr. Abdominal compartment syndrome. The Nashville experience. Surg Clin North Am 1997;77:801-12.

17. Schein M, Wittmann DH, Aprahamian CC, Condon RE. The abdominal compartment syndrome: the physiological and clinical consequences of elevated intra-abdominal pressure.

J Am Coll Surg 1995;180:745-53.

18. Mendoza-Sagaon M, Hanly EJ, Talamini MA, Kutka MF, Gitzelmann CA, Herreman-Suquet K, et al. Comparison of the stress response after laparoscopic and open cholecystectomy. Surg Endosc 2000;14:1136-41.

19. Akbulut G, Polat C, Aktepe F, Yilmaz S, Kahraman A, Serteser M, et al. The oxidative effect of prolonged CO2 pneumoperitoneum on renal tissue of rats. Surg Endosc 2004;18:1384-8.

20. Huang Y, Li N, Liboni K, Neu J. Glutamine decreases lipopolysaccharide-induced IL-8 production in Caco-2 cells through a non-NF-kappaB p50 mechanism. Cytokine 2003;22:77-83.

21. Jobin C, Sartor RB. The I kappa B/NF-kappa B system: a key determinant of mucosalinflammation and protection. Am J Physiol Cell Physiol 2000;278:451-62.

22. Schmid RM, Adler G. NF-kappaB/rel/IkappaB: implications in gastrointestinal diseases. Gastroenterology.

2000;118:1208-28.

23. Oda J, Ivatury RR, Blocher CR, Malhotra AJ, Sugerman HJ. Amplified cytokine response and lung injury by sequential hemorrhagic shock and abdominal compartment syndrome in a laboratory model of ischemia-reperfusion. J Trauma 2002;52:625-32.

24. Neu J, Li N. Pathophysiology of glutamine and glutamate metabolism in premature infants. Curr Opin Clin Nutr Metab Care 2007;10:75-9.

25. Ziegler TR, Bazargan N, Leader LM, Martindale RG. Glutamine and the gastrointestinal tract. Curr Opin Clin Nutr Metab Care 2000;3:355-62.

26. Laight DW, Lad N, Woodward B, Waterfall JF. Assessment of myeloperoxidase activity in renal tissue after ischemia/reperfusion. Eur J Pharmacol 1994;292:81-8.

27. Roth E, Oehler R, Manhart N, Exner R, Wessner B, Strasser 7

Ulus Travma Acil Cerrahi Derg

E, et al. Regulative potential of glutamine--relation to glutathione metabolism. Nutrition 2002;18:217-21.

28. Valencia E, Hardy G. Practicalities of glutathione supplementation in nutritional support. Curr Opin Clin Nutr Metab Care 2002;5:321-6.

29. Fläring UB, Rooyackers OE, Wernerman J, Hammarqvist F. Glutamine attenuates post-traumatic glutathione depletion in human muscle. Clin Sci (Lond) 2003;104:275-82.

30. Reiter RJ, Tan DX, Osuna C, Gitto E. Actions of melatonin in the reduction of oxidative stress. A review. J Biomed Sci. 2000;7:444-58.

31. 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.

32. Erbil Y, Oztezcan S, Giriş M, Barbaros U, Olgaç V, Bilge H, et al. The effect of glutamine on radiation-induced organ damage. Life Sci 2005;78:376-82.

33. Daniele B, Perrone F, Gallo C, Pignata S, De Martino S, De Vivo R, et al. Oral glutamine in the prevention of fluorouracil induced intestinal toxicity: a double blind, placebo controlled, randomised trial. Gut 2001;48:28-33.

34. Labow BI, Souba WW. Glutamine. World J Surg 2000;24:1503-13.

35. Reeds PJ, Burrin DG. Glutamine and the bowel. J Nutr 2001;131:2505-24.

36. Karinch AM, Pan M, Lin CM, Strange R, Souba WW. Glutamine metabolism in sepsis and infection. J Nutr 2001;131:2535-51.

37. Peng X, Yan H, You Z, Wang P, Wang S. Effects of enteral supplementation with glutamine granules on intestinal mucosal barrier function in severe burned patients. Burns 2004;30:135-9.

38. Boelens PG, Houdijk AP, Fonk JC, Puyana JC, Haarman HJ, von Blomberg-van der Flier ME, et al. Glutamine-enriched enteral nutrition increases in vitro interferon-gamma production but does not influence the in vivo specific antibody response to KLH after severe trauma. A prospective, double blind, randomized clinical study. Clin Nutr 2004;23:391-400.

39. García-de-Lorenzo A, Zarazaga A, García-Luna PP, Gonzalez-Huix F, López-Martínez J, Miján A, et al. Clinical evidence for enteral nutritional support with glutamine: a systematic review. Nutrition 2003;19:805-11.

40. Bolotin G, Raman J, Williams U, Bacha E, Kocherginsky M, Jeevanandam V. Glutamine improves myocardial function following ischemia-reperfusion injury. Asian Cardiovasc Thorac Ann 2007;15:463-7.

41. Hulsewé KW, van Acker BA, Hameeteman W, van der Hulst RR, Vainas T, Arends JW, et al. Does glutamine-enriched parenteral nutrition really affect intestinal morphology and gut permeability? Clin Nutr 2004;23:1217-25.

42. Ikeda S, Zarzaur BL, Johnson CD, Fukatsu K, Kudsk KA.

8

Total parenteral nutrition supplementation with glutamine improves survival after gut ischemia/reperfusion. JPEN J Parenter Enteral Nutr 2002;26:169-73.

43. Yeh SL, Lai YN, Shang HF, Lin MT, Chen WJ. Effects of glutamine supplementation on innate immune response in rats with gut-derived sepsis. Br J Nutr 2004;91:423-9.

44. Chang WK, Yang KD, Chuang H, Jan JT, Shaio MF. Glutamine protects activated human T cells from apoptosis by up-regulating glutathione and Bcl-2 levels. Clin Immunol 2002;104:151-60.

45. Pithon-Curi TC, Schumacher RI, Freitas JJ, Lagranha C, Newsholme P, Palanch AC, et al. Glutamine delays spontaneous apoptosis in neutrophils. Am J Physiol Cell Physiol 2003;284:1355-61.

46. Ran Q, Liang H, Gu M, Qi W, Walter CA, Roberts LJ 2nd, et al. Transgenic mice overexpressing glutathione peroxidase 4 are protected against oxidative stress-induced apoptosis. J Biol Chem 2004;279:55137-46.

47. Kudsk KA. Current aspects of mucosal immunology and its influence by nutrition. Am J Surg 2002;183:390-8.

48. Omar R, Nomikos I, Piccorelli G, Savino J, Agarwal N. Prevention of postischaemic lipid peroxidation and liver cell injury by iron chelation. Gut 1989;30:510-4.

49. Sumimoto K, Oku J, Dohi K, Kawasaki T. Lipid peroxidation in transplanted rat liver. Transplant Proc 1990;22:2023-4.

50. 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.

51. Wasa M, Soh H, Shimizu Y, Fukuzawa M. Glutamine stimulates amino acid transport during ischemia-reperfusion in human intestinal epithelial cells. J Surg Res 2005;123:75-81.

52. Melis GC, ter Wengel N, Boelens PG, van Leeuwen PA. Glutamine: recent developments in research on the clinical significance of glutamine. Curr Opin Clin Nutr Metab Care 2004;7:59-70.

53. Bouteloup-Demange C, Claeyssens S, Maillot C, Lavoinne A, Lerebours E, Dechelotte P. Effects of enteral glutamine on gut mucosal protein synthesis in healthy humans receiving glucocorticoids. Am J Physiol Gastrointest Liver Physiol 2000;278:677-81.

54. Wischmeyer PE, Kahana M, Wolfson R, Ren H, Musch MM, Chang EB. Glutamine reduces cytokine release, organ damage, and mortality in a rat model of endotoxemia. Shock 2001;16:398-402.

55. McCauley R, Kong SE, Heel K, Hall JC. The role of glutaminase in the small intestine. Int J Biochem Cell Biol 1999;31:405-13.

56. Erman F, Balkan J, Cevikbaş U, Koçak-Toker N, Uysal M. Betaine or taurine administration prevents fibrosis and lipid peroxidation induced by rat liver by ethanol plus carbon tetrachloride intoxication. Amino Acids 2004;27:199-205.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2010;17 (1):9-13

Experimental Study

Deneysel Çalışma doi: 10.5505/tjtes.2011.13914

Comparison of classical surgery and sutureless repair with DuraSeal or fibrin glue for duodenal perforation in rats Sıçanlarda oluşturulan duodenum perforasyonunda klasik cerrahi ile DuraSeal ya da fibrin yapıştırıcı ile yapılan dikişsiz onarımların karşılaştırılması Saliha KARAGÖZ AVCI,1 Serdar YÜCEYAR,1 Erman AYTAÇ,1 Onur BAYRAKTAR,1 İlknur ERENLER,2 Hüseyin ÜSTÜN,3 Hafize UZUN,4 Süphan ERTÜRK1 BACKGROUND

AMAÇ

The purpose of the study was to compare classical primary suture repair and sutureless repair with fibrin glue or DuraSeal adhesion barrier for the closure of duodenal perforation in rats.

Bu çalışmada, sıçanlarda oluşturulan deneysel duodenum perforasyonunda klasik cerrahi teknikler ile adezyon bariyerleri olan DuraSeal ya da fibrin yapıştırıcıyla yapılan dikişsiz onarım tekniklerinin karşılaştırılması amaçlandı.

METHODS

GEREÇ VE YÖNTEM

Forty adult female Wistar Albino rats weighing between 250-300g were randomly divided into four equal groups.

Primary repair, primary repair and omentoplasty, or application of fibrin glue or DuraSeal adhesion barrier was performed in each of the four groups, respectively. The bursting pressure, tissue hydroxyproline levels and histopathology were evaluated.

Kırk adet yetişkin, ağırlıkları 250-300 g arasında olan, dişi Wistar Albino sıçan rastgele dört adet eşit gruba ayrıldı.

Primer onarım grubu, primer onarım ve omentoplasti grubu, fibrin yapıştırıcı uygulanan grup ve DuraSeal uygulanan grup. Doku iyileşmesini değerlendirmek amacıyla patlama basıncı, doku hidroksiprolin seviyesi ve histopatolojik inceleme parametre olarak kullanıldı.

RESULTS

BULGULAR

Bursting pressure values of the primary repair and primary repair and omentoplasty groups were significantly higher than in the fibrin glue and DuraSeal groups (p<0.001).

There were no significant differences between the experimental groups regarding hydroxyproline levels and histological parameters.

Primer onarım, primer onarım ve omentoplasti gruplarının patlama basıncı değerleri fibrin yapıştırıcı ve DuraSeal grubu patlama basıncı değerlerine göre anlamlı olarak yüksekti (p<0,001). Biyokimyasal ve histolojik parametreler açısından tüm gruplar arasında anlamlı farklılık yoktu.

CONCLUSION

Değerlendirdiğimiz dikişsiz onarım tekniklerinin konvansiyonel onarım tekniklerine üstün etkilerinin olmadığını gözlemledik. Dikişsiz onarım gruplarının sonuçları benzerdi. DuraSeal, fibrin yapıştırıcı gibi dikişsiz onarım alanında alternatif olabilir. Bu çıkarım farklı yara iyileşmesi belirteçleri ve farklı yöntemlerle planlanmış çalışmalarla desteklenmelidir.

The sutureless methods (Fibrin glue, DuraSeal) have no superior effects when compared with the conventional repair techniques. We observed similar results between the sutureless repair groups; thus, DuraSeal can be considered an alternative to fibrin glue for this purpose. This suggestion must be supported with new studies, however, which would be planned with other wound healing markers and different designs.

SONUÇ

Key Words: DuraSeal; duodenal perforation; fibrin glue; sutureless repair.

Anahtar Sözcükler: DuraSeal; duodenal perforasyon; fibrin yapıştırıcı; dikişsiz tamir.

Departments of 1General Surgery, 4Biochemistry, Istanbul University Cerrahpasa Faculty of Medicine, Istanbul; 3Department of Pathology, Ankara Training and Research Hospital, Ankara; 2Department of General Surgery, Kocaeli State Hospital, Kocaeli, Turkey.

İstanbul Üniversitesi, Cerrahpaşa Tıp Fakültesi, 1Genel Cerrahi Anabilim Dalı, 4Biyokimya Anabilim Dalı, İstanbul; 3Ankara Eğitim ve Araştırma Hastanesi, Patoloji Kliniği, Ankara; 2Kocaeli Devlet Hastanesi, Genel Cerrahi Kliniği, Kocaeli.

Correspondence (İletişim): Serdar Yüceyar, M.D. İ.Ü. Cerrahpaşa Tıp Fakültesi, Genel Cerrahi Anabilim Dalı, 34098 Fatih, İstanbul, Turkey.

Tel: +90 - 212 - 414 30 00 / 21921 Fax (Faks): +90 - 212 - 414 33 70 e-mail (e-posta): seryuce@istanbul.edu.tr

9

Ulus Travma Acil Cerrahi Derg

Duodenal perforation is an urgent situation, which usually necessitates surgical treatment.[1] Peptic ulcer disease is the most common cause of duodenal perforation.[1,2] Peptic ulcer disease is a frequent pathology that is caused by different disorders. Helicobacter pylori infection, nonsteroidal anti-inflammatory drugs, liver cirrhosis, hyperparathyroidism, and chronic pancreatitis are related to peptic ulcer disease.[3,4] Definitive surgical approaches for the management of peptic ulcer became archaic after the use of proton pump inhibitors (PPIs) and expansion of H. pylori eradication therapy. In suitable conditions, primary repair is the preferable technique for duodenal perforations.[5] Mortality and morbidity rates increase with delayed or failed surgery. Primary repair can be performed with classical open surgical technique or laparoscopy for duodenal peptic ulcer perforations. As a minimally invasive approach, sutureless repair of duodenal peptic ulcer perforation can simplify the technique and reduce the operation time.

Fibrin glue is used in clinical practice for duodenal perforations as an alternative sutureless repair via laparoscopic or endoscopic route.[6,7] Fibrin glue is obtained from human fibrinogen concentrate and used to support wound healing.[8] Fibrin glue mimics the last episode of coagulation. Thrombin and aprotinin are the main components of fibrin glue. Thrombin converts fibrinogen to fibrin. Factor XIII binds fibrin monomers with covalent links for clotting. Aprotinin is added to fibrin glue to prevent fibrinolysis.[8,9] It has been reported that fibrin glue prevents hematoma formation and supports fibroblast activity and angiogenesis.[10,11] Fibrin glue is being used in various pathologies including upper gastrointestinal tract perforations,[7,12] fistulas[13,14] and leaks.[15,16] DuraSeal, which is an absorbable synthetic hydrogel, has blue solution and limpid solution. DuraSeal is a newly introduced material aiming to minimize leaks in various organs, such as cerebrospinal fluid in neurosurgery, air in thoracic surgery and blood in vascular surgery.[17-21] The present experimental study aimed to compare the primary closure of duodenal defects by various techniques, notably primary repair, primary repair and omentoplasty, and DuraSeal or fibrin glue application.

MATERIALS AND METHODS This study was performed after approval of the Ethics Committee of the Animal Care Review Board of Istanbul University, Experimental Medicine Research Institute. Adult female Wistar Albino rats, weighing 250-300 g, were obtained from Istanbul University Cerrahpasa Medical Faculty Experimental Animals Research Laboratory. The rats were cared for in accordance with the Guide for the Care and Use of Labo10

ratory Animals (NIH Publication no. 86-23, revised 1985), maintained in colony cages (5 or 6 per cage) under controlled conditions of temperature (28°C), light (10 h light: 14 h dark) and humidity (50°F 5%). The rats were not permitted ad libitum access to standard lab chow and tap water starting from 12 hours before the surgery to the end of the experimental procedures.

10% dextrose solution (10 ml/day per rat) was given to the rats intraperitoneally during the postoperative period. Under ketamine chloride (40 mg/kg) anesthesia, the abdominal area was cleansed with povidone iodine solution after shaving. A median abdominal incision was performed. The anterior wall of the first part of the duodenum was perforated (0.2 cm) with a scalpel in every rat. The abdominal incision was closed with 3/0 silk continuous sutures as a single layer. Forty rats were divided randomly into four weight-matched equal groups as follows: primary repair (with 4/0 silk) group (n=10), primary repair and omentoplasty group (n=10), fibrin glue group (n=10) (Beriplast P combi set, ZLB Behring AG, Marburg, Germany; glue was sprayed on the perforated area without suturing), and DuraSeal group (n=10) (Confluent Surgical, Inc., Waltham, MA; DuraSeal was sprayed on the perforated area without suturing). The components of fibrin glue and DuraSeal were carefully reconstituted and prepared according to the manufacturers’ instructions. Sufficient (0.25 ml) equal volume of fibrin glue and DuraSeal to entirely cover the perforated area was applied to a target surface. For covering the perforated area surfaces, the fibrin glue and DuraSeal were sprayed using the enclosed spray-tips. The rats were sacrificed on postoperative day 4 with overdose ether inhalation. After the measurement of bursting pressure levels of the repaired duodenal perforation site, an en-bloc excision of the repaired area together with 0.5 cm proximal and distal parts of the duodenum was performed. The excised part of the duodenum was divided into two equal tissue samples for histopathological and tissue hydroxyproline level analysis. For tissue hydroxyproline level investigation, samples were immediately immersed in liquid nitrogen and stored at -70°C until being processed, and for histopathological evaluation, samples were fixed in 10% formaldehyde solution.

Measurement of Bursting Pressure The abdominal incision of the rats was opened and the adhesions around the repaired area were preserved.

The small intestine was ligated 2 cm distal from the repaired area of the duodenum. A catheter was inserted from the distal esophagus and fixed with 2/0 silk suture. The prepared system was sunk into a bowl filled with water. Air was insufflated with 6 ml/min stable speed and the bursting pressure was measured with a sphygmomanometer. The pressure level when bubbles were first seen in the water was accepted as the bursting pressure level.

Ocak - January 2011

Comparison of classical surgery and sutureless repair with DuraSeal or fibrin glue for duodenal perforation in rats

Hydroxyproline Assay The samples for hydroxyproline levels were weighed, cut into small pieces, and homogenized in a phosphate buffer to yield a 20% homogenate. Aliquots of the homogenate were added to an equal volume of 6 N hydrochloric acid, and hydrolyzed in Teflon-capped vials at 102˚C for 16 hours. The hydroxyproline content of the tissue hydroxylates was determined spectrophotometrically by using the standard addition method developed by Kivirikko et al.[22] (Hypopronosticon Kit lot/ch. B:E 92401; Organon Teknika B.V., Boxtel, Holland). Results were expressed in milligrams, such as in hydroxyproline/100 mg (wet weight).

Histopathological Evaluation Duodenal tissue slices were then fixed in 10% buffered formalin and embedded in paraffin. Each section in 4 μm thickness was stained with hematoxylin and eosin for light microscopic assessment. A certified pathologist scored samples in a blinded fashion. An arbitrary scope was given to each microscopic field at magnifications of 20x, 40x and 100x. Ten representative areas from each section consisting of inflammation, revascularization, fibroblasts and collagen were examined, and scored to obtain the mean value. The parameters were graded on a 3-grade scale; mild, moderate or marked changes were indicated by an increase or decrease of 1, 2 or 3 grades, respectively.

Statistical Evaluation All the values were expressed as the mean ± SD. The data of bursting pressure and hydroxyproline content were analyzed by ANOVA test followed by a multiple comparison post- hoc test of Tukey. MannWhitney U test was used for the evaluation of the histopathological data. Values were considered as significant when p<0.05. SPSS 12 (SPSS Inc. Chicago, IL, USA) was used for statistical analyses.

RESULTS Six rats in total died: 3 each in the fibrin glue and the DuraSeal groups. One in each of these groups died immediately after induction of anesthesia. The other 4 rats died on postoperative day 2. Macroscopic leakage was observed in 2 rats of the fibrin glue group.

However, no peritonitis and no leakage were observed in the other 2 rats in the DuraSeal group. Additional rats were included into the study to replace the rats that died. Intraabdominal adhesions were seen in all experimental groups. Bursting pressure levels are summarized in Table 1. There were no significant differences between the conventional repair groups (primary repair group, primary repair and omentoplasty group) with regard to bursting pressure levels. Bursting pressure levels of the conventional repair groups were significantly higher than in the sutureless repair groups (fibrin glue group and DuraSeal group) Cilt - Vol. 17 Sayı - No. 1

Table 1. Bursting pressure levels according to treatment groups Experimental groups

Bursting pressure (mm/Hg)

Primary repair (n=10) Primary repair+omentoplasty (n=10) Fibrin glue (n=10) DuraSeal (n=10)

166±15.78 185±42.49 84.29±11.34 ***.### 91.43±6.90 ***.###

• Significance between the primary repair group and the other groups defined with (*), (p<0.001=***).

• Significance between the primary repair+omentoplasty group and the other groups defined with (#), (p<0.001=###).

Table 2. Tissue hydroxyproline levels according to the treatment groups Experimental groups

Tissue hydroxyproline levels (μg/g wet tissue)

Primary repair (n=10) Primary repair+omentoplasty (n=10) Fibrin glue (n=10) DuraSeal (n=10)

960.79±697.67 490.45±224.97 599.12±447.35 732.73±740.11

(p<0.001). There were no significant differences between the fibrin glue and DuraSeal groups regarding bursting pressure levels.

Hydroxyproline levels of the experimental groups are summarized in Table 2. There were no significant differences between groups regarding tissue hydroxyproline levels.

Revascularization, inflammation and number of fibroblasts were similar between the primary repair and primary repair and omentoplasty groups. The collagen amount in the primary repair group was higher than in the other groups. Neoangiogenesis and number of fibroblasts were lower in the fibrin glue group. Irregular collagen arrangement was observed rarely in the DuraSeal group; however, there were no significant differences between groups with respect to histopathologic evaluation (Table 3).

DISCUSSION Surgical treatments of duodenal perforations vary from primary repair to sutureless minimally invasive approaches.[2,7,23] The technical difficulties of suturing in laparoscopic and endoscopic approaches have led to research studies about sutureless repair for duodenal perforations.[7,23,24] Application of effective sutureless repairing techniques for intestinal perforations is being studied with new chemical agents to create a proper minimally invasive technique. The effective chemicals, which have adhesive barrier functions, would add to the newest therapeutic approaches in the field of minimally invasive surgery by simplifying the procedures. However, 11

Ulus Travma Acil Cerrahi Derg

Table 3. Scores of the histopathological evaluation according to treatment groups Groups Primary repair (n=10) Primary repair + omentoplasty (n=10) Fibrin glue (n=10) DuraSeal (n=10)

Inflammation

Revascularization

Fibroblast count

Collagen value

1.5±0.53 1.6±0.7 1.5±0.53 1.6±0.7

2.1±0.55 2.1±0.74 2±0.67 2±0.82

2.5±0.53 2.2±0.63 2.5±0.53 2.33±0.57

2.5±0.53 2.3±0.43 2.5±0.53 2.3±0.89

this hypothesis should be evaluated in experimental studies initially.

The first laparoscopic repair technique was introduced with primary repair and omentoplasty in 1989.

[25] After this approach, many different methods were performed, such as omental patch with fibrin plug,[26] repair with ligamentum teres hepatis,[27] fibrin glue,[7] omental patch application with stapler,[28,29] and fibrin patch (TachoComb).[30] The beneficial effects of fibrin on wound healing have been shown.[31] It has been reported that laparoscopic fibrin glue application for duodenal ulcer perforation has similar postoperative results to primary repair or primary repair with omentoplasty. Additionally, fibrin glue application minimized the operating time.[6,7,24] Easy application and effective barrier function are the main components that reduce operating time. Lau et al.[7] suggested that sutureless repair of duodenal perforations is as safe as conventional techniques and is easy to learn for the treatment of the duodenal perforations that are smaller than 1 cm.

Prior to the present study, no data were available about the effects of DuraSeal application for gastrointestinal perforations. We observed similar results regarding histopathological and hydroxyproline levels in all the experimental groups. When we evaluated the bursting pressure levels, conventional repair methods were safer and more secure than the sutureless repair techniques. The sutureless methods that we evaluated were shown to have no superior effects to conventional repair techniques. As a foreseeable result, suturing caused physical stability in the repaired area. The serosal surface, which is the most potent layer of the intestine, is closed with suturing. In sutureless repair, the defect is clogged with a chemical agent. Especially in the early phase of the wound healing process, the physical stability could be weaker in the repaired area.

In clinical practice, physical straight is not a sine qua non parameter of the repair of duodenal perforation. In the literature, some methods, such as Taylor’s method, which require no suture application or surgical intervention, have been described for the treatment of duodenal perforations. In Taylor’s method, nasogastric aspiration, fluid resuscitation, parenteral broad-spectrum antibiotics, and antisecretory drugs are used. Taylor’s method is suggested as an alternative in selected cases of perforated gastroduodenal ulcers, the main advan12

tage being the avoidance of anesthetic and surgical stress, with their potential morbidity and mortality.[32] However, using an adhesive barrier that can repair perforations or leaks quickly and easily would be more logical for the surgeons than leaving the perforation untouched.

Fibrin glue is being used in clinical practice in the sutureless treatment of duodenal perforations.[7] All the procedures evaluated in this study have been used in clinical practice, except DuraSeal. Hydroxyproline levels and histological evaluation were similar in all the experimental groups. This result reminds us that there was no difference between groups during the wound healing process. According to this result, we suggest that DuraSeal can be considered an alternative material for the sutureless treatment of duodenal perforation, like fibrin glue, because we did not observe any harmful or worse effect of DuraSeal when compared with fibrin glue. However, this hypothesis must be supported by new studies that are planned with other wound healing markers and different designs.

REFERENCES 1. Sonnenberg A. Temporal trends and geographical variations of peptic ulcer disease. Aliment Pharmacol Ther 1995;9:312.

2. Noguiera C, Silva AS, Santos JN, Silva AG, Ferreira J, Matos E, et al. Perforated peptic ulcer: main factors of morbidity and mortality. World J Surg 2003;27:782-7.

3. Siu WT, Leong HT, Law BK, Chau CH, Li AC, Fung KH, et al. Laparoscopic repair for perforated peptic ulcer: a randomized controlled trial. Ann Surg 2002;235:313-9.

4. Christensen S, Riis A, Nørgaard M, Thomsen RW, Tønnesen EM, Larsson A, et al. Perforated peptic ulcer: use of pre-admission oral glucocorticoids and 30-day mortality. Aliment Pharmacol Ther 2006;23:45-52.

5. Wu CY, Wu CH, Wu MS, Wang CB, Cheng JS, Kuo KN, et al. A nationwide population-based cohort study shows reduced hospitalization for peptic ulcer disease associated with H pylori eradication and proton pump inhibitor use. Clin Gastroenterol Hepatol 2009;7:427-31.

6. Lau WY, Leung KL, Zhu XL, Lam YH, Chung SC, Li AK. Laparoscopic repair of perforated peptic ulcer. Br J Surg 1995;82:814-6.

7. Lau WY, Leung KL, Kwong KH, Davey IC, Robertson C, Dawson JJ, et al. A randomized study comparing laparoscopic versus open repair of perforated peptic ulcer using suture or sutureless technique. Ann Surg 1996;224:131-8.

8. Bhanot S, Alex JC. Current applications of platelet gels in facial plastic surgery. Facial Plast Surg 2002;18:27-33.

9. Joch C. The safety of fibrin sealants. Cardiovasc Surg Ocak - January 2011

Comparison of classical surgery and sutureless repair with DuraSeal or fibrin glue for duodenal perforation in rats

2003;11:23-8.

10. Akgün A, Kuru S, Uraldi C, Tekin O, Karip B, Tug T, et al.

Early effects of fibrin sealant on colonic anastomosis in rats: an experimental and case-control study. Tech Coloproctol 2006;10:208-14.

11. van der Ham AC, Kort WJ, Weijma IM, van den Ingh HF, Jeekel H. Effect of antibiotics in fibrin sealant on healing colonic anastomoses in the rat. Br J Surg 1992;79:525-8.

12. Kaya C, Demir U, Coşkun H, Kalyoncu A, Gündüz B, Eroğlu T, et al. Comparison of repair techniques in rat duodonal perforations: simple closure, simple closure and omentoplasty, and fibrin tissue adhesive. Ulus Travma Acil Cerrahi Derg 2004;10:11-6.

13. Papavramidis TS, Kotzampassi K, Kotidis E, Eleftheriadis EE, Papavramidis ST. Endoscopic fibrin sealing of gastrocutaneous fistulas after sleeve gastrectomy and biliopancreatic diversion with duodenal switch. J Gastroenterol Hepatol 2008;23:1802-5.

14. Papavramidis ST, Eleftheriadis EE, Papavramidis TS, Kotzampassi KE, Gamvros OG. Endoscopic management of gastrocutaneous fistula after bariatric surgery by using a fibrin sealant. Gastrointest Endosc 2004;59:296-300.

15. Babor R, Talbot M, Tyndal A. Treatment of upper gastrointestinal leaks with a removable, covered, self-expanding metallic stent. Surg Laparosc Endosc Percutan Tech 2009;19:1-4.

16. Silecchia G, Boru CE, Mouiel J, Rossi M, Anselmino M, Morino M, et al. The use of fibrin sealant to prevent major complications following laparoscopic gastric bypass: results of a multicenter, randomized trial. Surg Endosc 2008;22:2492-7.

17. Preul MC, Bichard WD, Spetzler RF. Toward optimal tissue sealants for neurosurgery: use of a novel hydrogel sealant in a canine durotomy repair model. Neurosurgery 2003;53:118999.

18. Hagberg RC, Safi HJ, Sabik J, Conte J, Block JE. Improved intraoperative management of anastomotic bleeding during aortic reconstruction: results of a randomized controlled trial.

Am Surg 2004;70:307-11.

19. Marien BJ, Raffetto JD, Seidman CS, LaMorte WW, Menzoian JO. Bovine pericardium vs dacron for patch angioplasty after carotid endarterectomy: a prospective randomized study. Arch Surg 2002;137:785-8.

Cilt - Vol. 17 Sayı - No. 1

20. Bennett SL, Melanson DA, Torchiana DF, Wiseman DM, Sawhney AS. Next-generation hydrogel films as tissue sealants and adhesion barriers. J Card Surg 2003;18:494-9.

21. Grotenhuis JA. Costs of postoperative cerebrospinal fluid leakage: 1-year, retrospective analysis of 412 consecutive nontrauma cases. Surg Neurol 2005;64:490-4.

22. Kivirikko KI, Laitinen O, Prockop DJ. Modifications of a specific assay for hydroxyproline in urine. Anal Biochem 1967;19:249-55.

23. Bertleff MJ, Liem RS, Bartels HL, Robinson PH, Van der Werff JF, Bonjer HJ, et al. The “stamp method”: a new treatment for perforated peptic ulcer? Surg Endosc 2006;20:7913.

24. Kubota M, Okuyama N, Hirayama Y. A new method to close an intestinal wall defect using fibrin glue and polyglycolic acid felt sealant. J Pediatr Surg 2007;42:1225-30.

25. Nathanson LK, Easter DW, Cuschieri A. Laparoscopic repair/peritoneal toilet of perforated duodenal ulcer. Surg Endosc 1990;4:232-3.

26. Mouret P, François Y, Vignal J, Barth X, Lombard-Platet R. Laparoscopic treatment of perforated peptic ulcer. Br J Surg 1990;77:1006.

27. Costalat G, Dravet F, Noel P, Alquier Y, Vernhet J. Coelioscopic treatment of perforated gastroduodenal ulcer using the ligamentum teres hepatis. Surg Endosc 1991;5:154-5.

28. Darzi A, Cheshire NJ, Somers SS, Super PA, Guillou PJ, Monson JR. Laparoscopic omental patch repair of perforated duodenal ulcer with an automated stapler. Br J Surg 1993;80:1552.

29. Nassar A. Laparoscopic omental patch repair of perforated duodenal ulcer with automated stapler. Br J Surg 1994;81:1393.

30. Sim AJW, Ashaal YE, Ramadan K, et al. Laparoscopic repair of perforated duodenal ulcers using collagen fleece coated with fibrin glue. Min Inv Ther 1995:4;215-7.

31. Feld RS, Sullivan E, Morrison P. Thrombin injection for failed stent graft repair of perforated atherosclerotic aortic ulcer. J Vasc Surg 2003;37:194-7.

32. Dascalescu C, Andriescu L, Bulat C, Danila R, Dodu L, Acornicesei M, et al. Taylor’s method: a therapeutic alternative for perforated gastroduodenal ulcer. Hepatogastroenterology 2006;53:543-6.

13

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2010;17 (1):14-18

Experimental Study

Deneysel Çalışma doi: 10.5505/tjtes.2011.31391

Antioxidant effects of curcumin in spinal cord injury in rats Sıçanlarda spinal kord yaralanmsında curcuminin antioksidan etkileri Havva ŞAHİN KAVAKLI,1 Cemile KOCA,2 Özlem ALICI3

BACKGROUND

AMAÇ

This experimental study was performed to investigate the benefit of curcumin via its antioxidant effect on spinal cord injury (SCI) in rats.

Bu deneysel çalışma, sıçanlarda spinal kord yaralanmasında curcuminin antioksidan etki yoluyla faydasını araştırmak için yapıldı.

METHODS

GEREÇ VE YÖNTEM

Twenty-four adult Wistar albino rats were randomized into three groups. SCI was performed by the weight-drop model. Group 1 underwent laminectomy followed by SCI and received no medication. Group 2 underwent laminectomy followed by SCI and received curcumin (200 mg/ kg/day orally). Group 3 underwent laminectomy followed

by SCI and received methylprednisolone (30 mg/kg intraperitoneally). Twenty-four hours later, blood samples were obtained from all rats; serum superoxide dismutase (SOD) and malondialdehyde (MDA) levels were determined, and the obtained results were compared.

Yirmi dört adet Wistar albino sıçan 3 gruba randomize edildi. Spinal kord yaralanması ağırlık düşürme modeliyle gerçekleştirildi. Grup 1’e laminektomi ardından spinal kord yaralanması uygulandı ve herhangi bir tedavi verilmedi. Grup 2’ye laminektomi ardından spinal kord yaralanması uygulandı ve curcumin verildi (200 mg/kg/gün ağızdan). Grup 3’e laminektomi ardından spinal kord yaralanması uygulandı ve metilprednizolon verildi (30 mg/kg periton içine), 24 saat sonra tüm sıçanlardan kan örnekleri alındı, sonra serum süperoksit dismutaz (SOD) ve malondialdehit (MDA) düzeyleri belirlendi ve elde edilen sonuçlar karşılaştırıldı.

RESULTS

BULGULAR

SOD level in the curcumin group was higher than in the control group (p<0.000) and methylprednisolone group (p<0.012). MDA level in the curcumin group was lower than in the control group (p<0.042). Similarly, the MDA level in the methylprednisolone group was lower than in the control group (p<0.001).

Curcumin grubunda SOD düzeyi kontrol ve metilprednizolon grubundan daha yüksekti (p<0,001 ve p<0,012).

Curcumin grubunda MDA düzeyi kontrol grubundan daha düşüktü (p<0,042). Benzer şekilde metilprednizolon grubunda MDA düzeyi kontrol grubundan daha düşüktü (p<0,001).

CONCLUSION

SONUÇ

The results of the present study show that curcumin effectively protects the spinal cord tissues against oxidative damage.

Bu çalışmanın sonuçları curcuminin etkin biçimde oksidatif hasara karşı spinal kord dokularını koruduğunu gösterir.

Key Words: Antioxidant; curcumin; malondialdehyde; spinal cord injury; superoxide dismutase.

Anahtar Sözcükler: Antioksidan; curcumin; malondialdehit; spinal kord yaralanması; süperoksit dismutaz.

1 Department af Emergency Medicine, Ankara Ataturk Training and Research Hospital, Ankara; 2Department of Biochemistry, Fatih University Faculty of Medicine, Ankara; 3Department of Infectious Diseases and Clinical Bacteriology, Medical Park Hospital, Istanbul, Turkey.

Ankara Atatürk Eğitim ve Araştırma Hastanesi, Acil Tıp Kliniği, Ankara; 2 Fatih Üniversitesi Tıp Fakültesi, Biyokimya Bölümü, Ankara; 3 Medikal Park Hastanesi, Enfeksiyon Hastalıkları ve Klinik Mikrobiyoloji Bölümü, İstanbul.

1

Correspondence (İletişim): Havva Şahin Kavaklı, M.D. Ankara Atatürk Eğitim ve Araştırma Hastanesi, Acil Tıp Kliniği, Bilkent, Ankara, Turkey.

Tel: +90 - 312 - 291 25 25 e-mail (e-posta): havvasahin1973@yahoo.com

14

Antioxidant effects of curcumin in spinal cord injury in rats

Spinal cord injury (SCI) is one of the most devastating conditions that affects both patients and society.

[1,2] SCI mainly occurs via two mechanisms as primary and secondary injury. Secondary injury after the primary impact includes different pathophysiological and biochemical events.[3-13] Oxygen-derived free radicals have been implicated in the pathogenesis of spinal cord neuronal injury after trauma. Decreasing the level of oxidative stress minimizes the secondary destruction effect after traumatic injury.[10] Methylprednisolone is a pharmacological agent that has clinically proven useful effects on functional recovery following SCI.[3,4] Additionally, curcumin has been shown to have various clinical and experimental beneficial effects. The protective effect of curcumin on induced tissue damage due to free radicals has been observed previously in a number of experimental models.[14-17] Previous studies have demonstrated that curcumin also exhibits an antioxidant property as well as anti-inflammatory, immunomodulatory, anticancer, and antiangiogenic properties via its pleiotropic effects on genes and cell-signaling pathways at multiple levels.[18] A recent experimental SCI study showed that curcumin blocked apoptosis and neuron loss, restrained astrocyte activation, and significantly improved neurologic deficit. By down-regulating glial fibrillary acidic protein expression, curcumin seems to diminish astrocyte reactivation, which may be useful for neuronal survival.[19] The objective of our study was to determine the antioxidant effects of curcumin in rats with SCI. We also aimed to compare the effects of curcumin with those of methylprednisolone.

MATERIALS AND METHODS Twenty-four male Wistar albino rats (250-270 g) were used in the study. All the protocols were approved by the institutional animal ethics committee.

The rats in each group were kept in separate cages in rooms with controlled light and temperature and were fed standard chow and water ad libitum. The animals were anesthetized by an intraperitoneal injection of 10 mg/kg xylazine (Rompun, Bayer Turk Kimya Sanayii Limited Sirketi, Istanbul, Turkey) and 50 mg/kg ketamine hydrochloride (Ketalar, Pfizer Ilacları Limited Sirketi, Istanbul, Turkey). Rats were positioned on a thermistor-controlled heating pad in the prone position and a rectal probe was inserted. Surgical procedures were performed under sterile conditions with the assistance of a surgical microscope. Following T5-12 midline skin incision and paravertebral muscle dissection, spinous processes and laminar arcs of T7-10 were removed. The dura was left intact. Weight-drop model was performed for SCI.[4,20,21] The animals were subjected to an impact of 50 g/cm to the dorsal surface Cilt - Vol. 17 Sayı - No. 1

of the spinal cord. The force was applied via a stainless steel rod (3 mm diameter tip, weight 5 g) that was rounded at the surface. The rod was dropped vertically through a 10 cm guide tube that was positioned perpendicular to the center of the spinal cord. Afterwards, the muscles and the incision were sutured with 6-0 Vicryl (Vicryl, Ethicon, Johnson & Johnson Intl, Lanneke Marelaan, Belgium).

The rats were randomized into three groups of 8 rats each. Group 1 underwent laminectomy followed

by SCI and did not receive medication. Group 2 underwent laminectomy followed by SCI and received curcumin 200 mg/kg/day orally.[22-24] Group 3 underwent laminectomy followed by SCI and received methylprednisolone (Prednol-L, Mustafa Nevzat Ilac Sanayi Anonim Sirketi, Istanbul, Turkey) intraperitoneally at a single dose of 30 mg/kg. Following the surgical procedure, the rats were placed in a warming chamber and their body temperatures were maintained at approximately 37°C until they were completely awake. In the early postoperative period, the rats received 3 ml of saline intraperitoneally to compensate for the blood loss during the surgical procedure, while the water intake was limited.

Biochemical Analysis Twenty-four hours later, blood samples were obtained from all rats. The blood samples were immediately frozen and stored in a -20°C freezer for assays of malondialdehyde (MDA) and superoxide dismutase (SOD) levels. SOD activity was assayed according to the method of Sun et al.[25] Blood samples were mixed with the same ratio of chloroform and ethanol mixture (3/5 v/v). This mixture was then centrifuged at 5000 × g for 2 hours (h). This assay for SOD activity involves xanthine oxidase used as superoxide, and the results were expressed as unit per ml. One unit of SOD is defined as the amount of protein that inhibits the rate of nitroblue tetrazolium reduction by 50%.

The levels of the end product of lipid peroxidation, serum MDA, were determined by thiobarbituric acid (TBA) test in which 1,1,3,3-tetraethoxypropane was used as standard. The TBA test is based upon the principle of calorimetrically measured concentration of the pink product at 535 nm wavelength, which is formed as a result of the reaction of TBA with lipid peroxides (MDA), which are called TBA reactive substances.

The results were expressed as nmol MDA/ml.[26] Statistical Analysis For statistical evaluation, we used the software package SPSS 15.0, and probability value of less than 0.05 was accepted as statistically significant. As the data were normally distributed and independent, statistical analysis was performed using analysis of variance (ANOVA) followed by Tukey test when com15

Ulus Travma Acil Cerrahi Derg

10

12

9

MDA (nmol MDA/ml)

SOD (U/ml)

11

10

9

8 7 6 5

8 4 7

Group 1

Group 2

Group 3

3

Group 1

Group 2

Group 3

Fig. 1. SOD level differences between groups.

Fig. 2. MDA level differences between groups.

paring groups. The results are given as the mean ± standard deviation of the mean (SD).

dative stress can result from increased reactive oxygen species (ROS) production, and/or from decreased ROS scavenging capability. The cells’ natural protective system against the devastating actions of ROS includes the protective enzymes including SOD and other antioxidants. It is believed to play important roles in reversing the pathological damage caused

by SCI. Prime targets of ROS attack are the polyunsaturated fatty acids (PUFA) in the membrane lipids causing lipid peroxidation, which may lead to disorganization of cell structure and function. Further, decomposition of peroxidized lipids yields a wide variety of end products, including MDA.[30] ROS are cleared via enzymatic, including SOD, and nonenzymatic antioxidative mechanisms. SOD is a protective enzyme that can efficiently and specifically scavenge the superoxide radical by catalyzing its dismutation to hydrogen peroxide and oxygen. Lipid peroxidation is the main cause of the further secondary damage that starts after mechanical destruction of tissues.[3,4,11,31] Lipid peroxidation products increase immediately after SCI, and the peak concentrations of ROS and nitrogen species occur within the first 24 hours.[4] In this study, we determined oxidative injury in the spinal cord during

RESULTS SOD level in the curcumin group was higher than in the control group (p<0.001) and methylprednisolone group (p<0.012) (Fig. 1). The MDA level in the curcumin group was lower than in the control group (p<0.042). Similarly, the MDA level in the methylprednisolone group was lower than in the control group (p<0.001) (Fig. 2).

For all groups, SOD and MDA levels are shown as mean ± SD in Table 1.

DISCUSSION In our study, serum SOD levels were found to be significantly increased in the curcumin group when compared to the control group and methylprednisolone group. Furthermore, curcumin reduced serum MDA, which is an indicator of lipid peroxidation, with respect to the control group. Spinal cord trauma results in a rapid and extensive oxidative stress. It has long been established that oxidative stress plays a critical role in the pathophysiology of SCI[27-29] Oxi-

Table 1. SOD and MDA levels (mean ± SD)

Group 1 (control) Group 2 (curcumin) Group 3 (methylprednisolone) p values a Group 1 and 2 p<0.000 Group 2 and 3 p<0.012

16

SOD (U/ml)

MDA (nmol MDA/ml)

8.61±0.50 10.42±0.61a 9.21±0.69

7.35±1.43b 5.75±0.82 4.49±0.57

Group 1 and 2 p<0.042 Group 1 and 3 p<0.001

b

Ocak - January 2011

Antioxidant effects of curcumin in spinal cord injury in rats

SCI by measuring MDA concentration, since it is the end product of lipid peroxidation. MDA is the breakdown product of the major chain reactions leading to the oxidation of PUFA, and thus, serves as a reliable marker of oxidative stress-mediated lipid peroxidation.[32] Measurement of SOD provides information about the antioxidant capacity of the organism.[33] Although it is difficult to limit the primary injury, there is increasing evidence of the possibility of lowering the impact of the secondary injury, using pharmacological strategies.[3,34-36] Antioxidant treatments decrease damage due to SCI by reducing oxidative stress.[4] Recent studies have shown that curcumin has neuroprotective properties.[37-41] In this study, we aimed to investigate the effect of curcumin treatment in SCI on the oxidant and anti-oxidant enzyme systems. Curcumin is a well-known neuroprotective agent. It is a phytochemical compound extracted from the rhizome of C. longa Linn. Curcumin is one of the most potent and specific antioxidants for hydroxyl radicals, and it acts as a potent scavenger of free radicals.[42] Considering these functions of curcumin, we attempted to use curcumin as a potential protector of neurons against SCI. Curcumin is easily available, inexpensive, and has proven to be non-toxic even when administered at high doses.

[43] Various studies have clearly pointed out that methylprednisolone enhances functional recovery and induces regenerative responses after SCI in humans and experimental animals,[2,4] but it is not effective enough and is sometimes associated with some side effects.

Since methylprednisolone is the only agent shown to have beneficial effects after SCI, it was used in this study to compare the treatment results with curcumin.

Our study on the oxidative stress showed that curcumin possesses significant antioxidant activity by increasing SOD and reducing MDA, which is an index of lipid peroxidation that reflects the present oxidative status. Therefore, we consider that curcumin may be used in combination with high-dose methylprednisolone in SCI. These results clearly suggest the potential effect of curcumin to reduce the damage due to SCI injury in rats.

REFERENCES 1. Ibarra A, Martiñón S. Pharmacological approaches to induce neuroregeneration in spinal cord injury: an overview. Curr Drug Discov Technol 2009;6:82-90.

2. Xu WB, Lv G, Wang YF, Lu XH, Huang T, Zhu Y, et al.

Combination of dexamethasone and aminoguanidine reduces secondary damage in compression spinal cord injury. Cell Mol Neurobiol 2009;29:683-9.

3. Hall ED, Springer JE. Neuroprotection and acute spinal cord injury: a reappraisal. NeuroRx 2004;1:80-100.

4. Yücel N, Cayli SR, Ateş O, Karadağ N, Firat S, Turköz Y. Evaluation of the neuroprotective effects of citicoline after experimental spinal cord injury: improved behavioral and neuroanatomical recovery. Neurochem Res 2006;31:767-75.

5. Guimarães JS, Freire MA, Lima RR, Souza-Rodrigues RD, Cilt - Vol. 17 Sayı - No. 1

Costa AM, dos Santos CD, et al. Mechanisms of secondary degeneration in the central nervous system during acute neural disorders and white matter damage. Rev Neurol 2009;48:304-10. [Abstract] 6. Xiong Y, Hall ED. Pharmacological evidence for a role of peroxynitrite in the pathophysiology of spinal cord injury.

Exp Neurol 2009;216:105-14.

7. Cayli SR, Kocak A, Yilmaz U, Tekiner A, Erbil M, Ozturk C, et al. Effect of combined treatment with melatonin and methylprednisolone on neurological recovery after experimental spinal cord injury. Eur Spine J 2004;13:724-32.

8. Mautes AE, Bergeron M, Sharp FR, Panter SS, Weinzierl M, Guenther K, et al. Sustained induction of heme oxygenase-1 in the traumatized spinal cord. Exp Neurol 2000;166:254-65.

9. Hamann K, Durkes A, Ouyang H, Uchida K, Pond A, Shi R. Critical role of acrolein in secondary injury following ex vivo spinal cord trauma. J Neurochem 2008;107:712-21.

10. Yazihan N, Uzuner K, Salman B, Vural M, Koken T, Arslantas A. Erythropoietin improves oxidative stress following spinal cord trauma in rats. Injury 2008;39:1408-13.

11. Michael-Titus AT. Omega-3 fatty acids and neurological injury. Prostaglandins Leukot Essent Fatty Acids 2007;77:295300.

12. Faden AI. Pharmacological treatment of central nervous system trauma. Pharmacol Toxicol 1996;78:12-7.

13. Xiong Y, Singh IN, Hall ED. Tempol protection of spinal cord mitochondria from peroxynitrite-induced oxidative damage. Free Radic Res 2009;43:604-12.

14. Zheng YY, Yu LS, Zhang YG, Ye GH, Yi JP. Effects of curcumin on malondialdehyde and c-fos protein in hypoxia ischemia brain tissue in rats. Fa Yi Xue Za Zhi 2009;25:6-8.

[Abstract] 15. Ilbey YO, Ozbek E, Cekmen M, Simsek A, Otunctemur A, Somay A. Protective effect of curcumin in cisplatin-induced oxidative injury in rat testis: mitogen-activated protein kinase and nuclear factor-kappa B signaling pathways. Hum Reprod 2009;24:1717-25.

16. Nazam Ansari M, Bhandari U, Pillai KK. Protective role of curcumin in myocardial oxidative damage induced by isoproterenol in rats. Hum Exp Toxicol 2007;26:933-8.

17. Roselló DM, Balestrasse K, Coll C, Coll S, Tallis S, Gurni A, et al. Oxidative stress and hippocampus in a low-grade hepatic encephalopathy model: protective effects of curcumin.

Hepatol Res 2008;38:1148-53.

18. Strimpakos AS, Sharma RA. Curcumin: preventive and therapeutic properties in laboratory studies and clinical trials.

Antioxid Redox Signal 2008;10:511-45.

19. Lin MS, Lee YH, Chiu WT, Hung KS. Curcumin Provides Neuroprotection After Spinal Cord Injury. J Surg Res 2009 Aug 5. [Epub ahead of print] 20. Bilginer B, Onal MB, Narin F, Ustun H, Kilinc K, Akalan N. Antiapoptotic and neuroprotective effects of mycophenolate mofetil after acute spinal cord injury in young rats. Childs Nerv Syst 2009;25:1555-61.

21. Zeman RJ, Bauman WA, Wen X, Ouyang N, Etlinger JD, Cardozo CP. Improved functional recovery with oxandrolone after spinal cord injury in rats. Neuroreport 2009;20:864-8.

22. 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.

23. Reeta KH, Mehla J, Gupta YK. Curcumin is protective against phenytoin-induced cognitive impairment and oxidative stress in rats. Brain Res 2009;1301:52-60.

17

Ulus Travma Acil Cerrahi Derg

24. Wan XH, Li YW, Luo XP. Curcumin attenuated the lipid peroxidation and apoptotic liver injury in copper-overloaded rats. Zhonghua Er Ke Za Zhi 2007;45:604-8.

25. Sun Y, Oberley LW, Li Y. A simple method for clinical assay of superoxide dismutase. Clin Chem 1988;34:497-500.

26. Yoshioka T, Kawada K, Shimada T, Mori M. Lipid peroxidation in maternal and cord blood and protective mechanism against activated-oxygen toxicity in the blood. Am J Obstet Gynecol 1979;135:372-6.

27. DeRuisseau LR, Recca DM, Mogle JA, Zoccolillo M, DeRuisseau KC. Metallothionein deficiency leads to soleus muscle contractile dysfunction following acute spinal cord injury in mice. Am J Physiol Regul Integr Comp Physiol 2009;297:R1795-802.

28. Savas M, Verit A, Ciftci H, Yeni E, Aktan E, Topal U, et al. Oxidative Stress in BPH. JNMA J Nepal Med Assoc 2009;48:41-5.

29. Christie SD, Comeau B, Myers T, Sadi D, Purdy M, Mendez I. Duration of lipid peroxidation after acute spinal cord injury in rats and the effect of methylprednisolone. Neurosurg Focus 2008;25:E5.

30. Ilhan A, Koltuksuz U, Ozen S, Uz E, Ciralik H, Akyol O. The effects of caffeic acid phenethyl ester (CAPE) on spinal cord ischemia/reperfusion injury in rabbits. Eur J Cardiothorac Surg 1999;16:458-63.

31. Golding JD, Rigley MacDonald ST, Juurlink BH, Rosser BW. The effect of glutamine on locomotor performance and skeletal muscle myosins following spinal cord injury in rats.

J Appl Physiol 2006;101:1045-52.

32. Balci M, Namuslu M, Devrim E, Durak I. Effects of computer monitor-emitted radiation on oxidant/antioxidant balance in cornea and lens from rats. Mol Vis 2009;15:2521-5.

33. Rabus M, Demirbağ R, Sezen Y, Konukoğlu O, Yildiz A, Erel O, et al. Plasma and tissue oxidative stress index in patients with rheumatic and degenerative heart valve disease.

18

Turk Kardiyol Dern Ars 2008;36:536-40.

34. Michael-Titus AT. Omega-3 fatty acids and neurological injury. Prostaglandins Leukot Essent Fatty Acids 2007;77:295300.

35. Hall ED. Pharmacological treatment of acute spinal cord injury: how do we build on past success? J Spinal Cord Med 2001;24:142-6.

36. Faden AI, Stoica B. Neuroprotection: challenges and opportunities. Arch Neurol 2007;64:794-800.

37. Yadav RS, Sankhwar ML, Shukla RK, Chandra R, Pant AB, Islam F, et al. Attenuation of arsenic neurotoxicity by curcumin in rats. Toxicol Appl Pharmacol 2009;240:367-76.

38. Wang R, Li YB, Li YH, Xu Y, Wu HL, Li XJ. Curcumin protects against glutamate excitotoxicity in rat cerebral cortical neurons by increasing brain-derived neurotrophic factor level and activating TrkB. Brain Res 2008;1210:84-91.

39. Dutta K, Ghosh D, Basu A. Curcumin protects neuronal cells from Japanese encephalitis virus-mediated cell death and also inhibits infective viral particle formation by dysregulation of ubiquitin-proteasome system. J Neuroimmune Pharmacol 2009;4:328-37.

40. Sethi P, Jyoti A, Hussain E, Sharma D. Curcumin attenuates aluminium-induced functional neurotoxicity in rats. Pharmacol Biochem Behav 2009;93:31-9.

41. Zhao J, Zhao Y, Zheng W, Lu Y, Feng G, Yu S. Neuroprotective effect of curcumin on transient focal cerebral ischemia in rats. Brain Res 2008;1229:224-32.

42. Bas M, Tugcu V, Kemahli E, Ozbek E, Uhri M, Altug T, et al. Curcumin prevents shock-wave lithotripsy-induced renal injury through inhibition of nuclear factor kappa-B and inducible nitric oxide synthase activity in rats. Urol Res 2009;37:159-64.

43. Alamdari N, O’Neal P, Hasselgren PO. Curcumin and muscle wasting: a new role for an old drug? Nutrition 2009;25:1259.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):19-22

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2011.82195

Akut apandisitte ultrasonografinin güvenilirliği Reliability of ultrasonography for diagnosing acute appendicitis Aylin Hande GÖKÇE,1 Acar AREN,1 Feridun Suat GÖKÇE,2 Nevra DURSUN,3 Abdullah Yüksel BARUT4

AMAÇ

BACKGROUND

En sık akut karın nedenlerinden birisi olan akut apandisitin tanısında öncelikle kullanılan inceleme yönteminden biri de ultrasonografidir (USG). Bu çalışmada USG’nin akut apandisit tanısındaki güvenilirliği araştırıldı.

Abdominal ultrasonography (US) is the most commonly used diagnostic tool for diagnosing acute appendicitis, which is one of the most common causes of acute surgical abdomen. In this study, we examined the reliability of US for diagnosing acute appendicitis.

GEREÇ VE YÖNTEM

METHODS

Prospektif olarak yapılan bu çalışmada 2007 yılında acil cerrahi polikliniğimize başvuran hastalarda fiziksel inceleme ve laboratuvar incelemeleri sonucu akut apandisit öntanısıyla ameliyata karar verilen 235 hastaya tüm karın USG’si yapıldı. Daha sonra bu hastalara apendektomi yapıldı; piyesler histopatolojik olarak incelendi.

In this prospective study, we performed abdominal US on 235 patients admitted to our surgical emergency department during 2007 and diagnosed as acute surgical abdomen according to the physical examination and laboratory findings. These patients were surgically treated by appendectomy, and the materials were pathologically examined.

BULGULAR

RESULTS

Bu çalışmaya 235 hasta alındı. Bu hastaların 193’ünün (%82,1) histopatolojik sonucu akut apandisit geldi, 42’sinin (%17,9) ise histopatolojik sonucu akut apandisit çıkmadı. USG sonucu akut apandisit olan 150 hastanın histopatolojik olarak 133’ünün (%88,67) akut apandisit olduğu, USG’nin normal olduğu 85 hastanın ise histopatolojik olarak 60’ının akut apandisit olduğu saptandı. Histopatolojik tanısı akut apandisit olan hastaların %31,1’ine USG ile tanı konamadı.

Two hundred thirty-five patients were admitted to this study. One hundred ninety-three of these patients (82.1%) were diagnosed as acute appendicitis, and 42 (17.9%) were diagnosed differently. One hundred thirty-three (88.67%) of 150 patients diagnosed as acute appendicitis on US examinations were also reported as acute appendicitis on histopathological examination. Sixty of 85 patients diagnosed differently on US examination were reported as acute appendicitis on histopathological examination.

SONUÇ

CONCLUSION

USG’si akut apandisit olan hastaların histopatolojisinin akut apandisit olması arasında duyarlılık %69, özgüllük %60, pozitif kestirim değeri 0,89, negatif kestirim değeri 0,30, doğruluk 0,67 bulunmuştur. USG akut apandisit tanısını koymada ancak yardımcı bir yöntem olabileceği ve USG’nin anamnez ve fiziksel incelemenin önüne geçirilmemesi gerektiği kanaatine varıldı.

The sensitivity of abdominal US for diagnosing acute appendicitis was determined as 69%. The specificity was calculated as 60%, positive predictive value as 0.89, negative predictive value as 0.30, and accuracy as 0.67. Abdominal US is a helpful diagnostic tool for diagnosing acute appendicitis. However, it should not be seen as superior to anamnesis and physical examination findings.

Anahtar Sözcükler: Akut apandisit; negatif apendektomi; ultrasonografi.

Key Words: ������������������������������������������������� Acute appendicitis; negative appendectomy; ultrasonography.

İstanbul Eğitim ve Araştırma Hastanesi, 1Genel Cerrahi Kliniği, Patoloji Kliniği, 4Radyoloji Kliniği, İstanbul; 2Balıklı Rum Hastanesi, Genel Cerrahi Kliniği, İstanbul.

Departments of 1General Surgery, 3Patholgy, 4Radiology, Istanbul Education and Research Hospital, Istanbul; 2Department of General Surgery, Balıklı Rum Hospital, Istanbul, Turkey.

3

İletişim (Correspondence): Dr. Acar Aren. Görgü Sok., No: 14, Emirgan, Sarıyer 34467 İstanbul, Turkey.

Tel: +90 - 212 - 459 62 78 e-posta (e-mail): acararen@gmail.com

19

Ulus Travma Acil Cerrahi Derg

Akut apandisit genel cerrahide en sık karşılaşılan akut karın nedenlerindendir. Tanısında öncelikli olarak fiziksel incelemeye yardımcı olarak laboratuvar incelemeleri, görüntüleme yöntemlerinden ultrasonografi (USG) ve karın tomografisi kullanılmaktadır.

Negatif apendektomi oranları %10 ile %30 arasında değişen oranlarda bildirilmekte halen ciddi bir problem olarak karşımızdadır. Perfore apandisit oranlarının %3-30 arasında değişmesi negatif apendektomileri kabul edilebilir kılabilmektedir.[1] Negatif apendektomi oranlarını azaltmak için görüntüleme yöntemleri, kan analizleri, akut faz reaktanları çeşitli klinik skorlama ve tanısal modaliteler geliştirilmiştir. Tanıda öncelikle kullanılan inceleme yöntemlerinden biri de USG’dir.

Bu çalışmada, USG’nin akut apandisit tanısındaki güvenilirliği araştırıldı.

GEREÇ VE YÖNTEM Prospektif olarak yapılan bu çalışmada 01.01.2007 ile 31.12.2007 tarihleri arasında İstanbul Eğitim ve Araştırma Hastanesi Acil Cerrahi Polikliniği’ne başvuran hastalarda fiziksel inceleme ve laboratuvar incelemesi sonucunda akut apandisit ön tanısıyla ameliyatına karar verilen 235 hastaya karın USG’si yapıldı. Tüm olgulara karın USG’si renkli Doppler USG 1024 gri skala, 12 MHz Lineer multifrekans prob ile yapıldı. Daha sonra bu hastalara McBurney insizyonla apendektomi yapıldı, piyesler histopatolojik olarak incelendi. Çalışmaya hamileler, dış merkezlerden tanısı konup hastanemize sevk edilenler ve başka bir ön tanıyla ameliyata alınıp akut karın nedeni olarak akut apandisit çıkan hastalar dahil edilmedi. USG’de apandistin ön-arka çapının 6 mm üzerinde olması, periapendiküler anekoik sıvı, periapendiküler hipoeko-

Şekil 1. Akut apandisitin ultrasonografik görünümü.

20

ik enflamasyon, çekum veya terminal ileumun duvarının diğer bağırsak segmentlerinin duvarlarından anlamlı derecede fazla kalınlaşması, apendikolit olması, nonkomprese ve aperistaltik olması akut apandisit olarak yorumlandı (Şekil 1).[2,3] Akut apandisit ön tanısı ile gönderilen materyal hastanemiz patoloji kliniğinde incelendi. Her olgudan en az iki adet örnekleme yapıldı. Histopatolojik inceleme yapıldı (Şekil 2).

Bu çalışmada istatistiksel analizler NCSS 2007 paket programı ile yapıldı. Verilerin değerlendirilmesinde tanımlayıcı istatistiksel yöntemlerin (ortalama, standart sapma) yanı sıra gruplar arası karşılaştırmalarda Kruskal-Wallis testi alt grup karşılaştırmalarında Dunn’s çoklu karşılaştırma testi, nitel verilerin karşılaştırmalarında ki-kare testi kullanıldı. Sonuçlar, anlamlılık p<0,05 düzeyinde değerlendirildi.

BULGULAR Çalışmaya alınan 235 hastanın 130’u erkek 105’i kadındı. Hastaların ortalama yaşı 28,7 idi. Fiziksel inceleme ve laboratuvar değerleriyle akut apandisit ön tanısıyla ameliyatına karar verilen 235 hastanın ameliyat öncesi yapılan karın USG’sinde; hastaların 150’sinde akut apandisit saptandı, 85’inde ise akut apandisit bulguları saptanmadı. Hastalar ameliyat edilip apendektomi piyesleri incelendi. Histopatoloji sonuçlarında hastaların 193’ünün akut apandisit olduğu, 42’sinin ise akut apandisit olmadığı saptandı. Histopatoloji sonucu akut apandisit olan 193 hastanın USG görüntülerine göre 133’ünde (%68,9) akut apandisit saptandı, 60’ında (%31,1) ise akut apandisit bulguları saptanmadı. Histopatoloji sonucu akut apandisit olmayan 42 hastanın USG görüntülerine göre 17’sinde

Şekil 2. Akut apandisitin histopatolojik görünümü.

Ocak - January 2011

Akut apandisitte ultrasonografinin güvenilirliği

Tablo 1. Akut apandisitin ultrasonografi ve histopatoloji sonuçları karşılaştırması

Ultrasonografi

Histopatoloji

Akut apandisit Negatif bulgular Toplam

Akut apandisit Negatif bulgular 133 60 193

17 25 42

Toplam 150 85 235

PKD 0,89 NKD 0,30 D 0,67

PKD: Pozitif kestirim değeri; NKD: Negatif kestirim değeri; D: Doğruluk.

(%40,48) akut apandisit saptandı, 25’inde (%59,52) ise akut apandisit bulguları saptanmadı.

Apandisitin akut olup olmaması açısından histopatoloji ve USG sonuçları karşılaştırıldığında aralarında düşük uyum bulundu (Kw: 0,27, p=0,01). Akut apandisitte USG’nin duyarlılığı 0,69, özgüllüğü 0,60, pozitif kestirim değeri 0,89, negatif kestirim değeri 0,30, doğruluğu 0,67 bulundu. USG’nin akut apandisit dediği hastada histopatoloji sonucunun akut apandisit olma olasılığı düşük (1,7) bulundu (Tablo 1).

Piyeslerin makroskopik olarak akut apandisit olarak kabul ettiğimiz olgularda seroza fibrinöz veya pürülan bir örtü ile kaplı, damarlar konjesyone olarak görüldü. Mukozada ülserasyon izlendi.

Histopatolojik incelemede apendiksteki değişiklikler minimal fokal enflamasyondan, duvarda geniş nekroza kadar değişiklikler göstermekteydi. Erken lezyonlarda epiltelde küçük bir defekt olduğundan nötrofiller bu defektin komşuluğundaki kriptin bazalinde izlendi. İlerlemiş olgularda mukoza silinmiş apendiks duvarı nekrotikti. Ayrıca bazı olgularda tromboze damarlar da vardı (Şekil 2).

TARTIŞMA Akut apandisit tanısı ve ayırıcı tanısı iyi yapılmalıdır. Hiçbir testin %100 duyarlılığı ve özgüllüğü yoktur. Çocuklarda, yaşlılarda ve premenapozal kadınlarda ilerleyen tekniklere rağmen negatif apendektomiler %25-30 gibi yüksek bir değerdedir. Negatif laparotomilerde de %5-15 oranında morbidite bildirilmiştir ve perfore apandisit oranları yaklaşık %20’dir.[4] Bu kadar yüksek değerin nedenlerinin başında cerrahi kararının geç alınması sayılabilir. Negatif laparotomi nedenlerinin başında ise tanıda gecikmeye bağlı perforasyondan korkulması gelmektedir.

Acil cerrahi servisinde akut apandisit tanısında anamnez, fiziksel inceleme ve laboratuvar incelemeleriyle üçte ikiden fazla hastanın tanısı doğru olarak yapılmaktadır.[5] Bu amaçla geliştirilen skorlama sistemleri tanı konması ve negatif laparotomileri azaltması açısından fayda sağlamaktadırlar. Bu skorlama ile negatif laparotomiler %7’ye indirilebilmiştir.[4,6] Ohmann ve Eskelinen gibi skorlar ile akut apandisit tanısını reddetCilt - Vol. 17 Sayı - No. 1

mede oldukça başarılıdırlar.[4,6] Bu durumu engelleyen başlıca faktörler klinik olarak ayırt edilemeyen patolojilerdir. Burada en yardımcı yöntemler laboratuvar ve USG devreye girmektedir.[7] Tecrübeli ellerde USG birçok patolojiyi ortaya koyması açısından doğruluğunun oldukça yüksek olduğu vurgulanmıştır.[8] Olguların çoğunda karın USG’si yardımcı teknik olarak kullanılmaktadır. USG’nin rutin incelemeler arasına sokulup sokulmaması gerektiği hala tartışmalıdır. Çeşitli yayınlara göre,[6,7,9] akut apandisit tanısında karın USG’si duyarlılık %65-90, özgüllük %90100 arasında, yeterlilik %89-95, pozitif prediktif değer %80-89 ve negatif prediktif değer %76-92 oranında değişiklik göstermektedir.

Diğer bir çalışmada[1] USG için duyarlık %55-98, özgüllük %78-100 olarak bildirilmiş ve bilgisayarlı tomografinin (BT) daha yüksek duyarlığı olduğu vurgulanmıştır.

Negatif apendektomi oranlarını azaltmak için 3540 hastayı kapsayan bir çalışmada inceleme yapılmayan olgularda negatif apendektomi oranları %9,8 verilirken, USG uygulananlarda bu oran %8,6, bilgisayarlı kesityazar uygulananlarda bu oran %4,5 e kadar inmiştir. Aynı seride yapılan araştırmada görüntüleme yöntemleri ile patoloji uyumluluğu USG için %82,4, BT için %92,3 idi. Görüntüleme yöntemleri, görüntüleme yapılmayan apendektomilere göre istatistiksel olarak anlamlı daha az negatif apendektomi yapılmasını sağlamaktadır.[10] Bizim serimizde duyarlılık %69, özgüllük %60, pozitif kestirim değeri %89, negatif kestirim değeri %30, doğruluk 0,67 değerleri ile literatüre uyumluluk göstermekle birlikte, özgüllük değeri ve negatif kestirim değerinin düşük olması düşündürücüdür.

USG ile negatif kabul edilen 85 olgunun 60’ında histopatolojik olarak apandisit bulunması radyolojik tanıda zorluktan kaynaklandığı düşünülmektedir. Özellikle erken dönem apandisit olgularında histopatolojik bulgular bile çok fokal alanlarda izlenmekte olup bu olguların görüntüleme yöntemleriyle tespit edilmesi çok zor olmaktadır.[11] Burada radyoloji uzmanının tecrübesi büyük rol oynamaktadır. Ancak, negatif tanı alan hastalarda diğer ileri incelemeler ve hastanın gözlem altında tutulması bulguların akut 21

Ulus Travma Acil Cerrahi Derg

apandisiti desteklediği durumlarda olguların ameliyat edilmesi gerekmektedir.

Radyoloji uzmanının tecrübesi arttıkça USG’nin güvenilirliği artmaktadır. Fakat, çok tecrübeli radyologların da perfore apandisitleri bile atlayabileceği unutulmamalıdır.[8] Akut apandistin medikal tedavisini ön gören bir çalışmada Turan ve arkadaşları[9] apandisit tanısını koymada sadece USG’yi yeterli görmemiş, buna BT’yi de tanı aracı olarak eklemişlerdir.

Son yıllarda Fox ve arkadaşları,[12] Kıyak ve arkadaşlarının[13] yaptığı çalışmalarda akut apandisit tanısında USG’nin özgüllük ve duyarlılığı çalışmamıza yakın oranlarda bildirilmiştir.

USG’nin serimizde pozitif prediktif değeri %89 gibi yüksek bulunmuştur. Yukarıda belirtilen her iki çalışmada da bu değerler benzer oranda izlenmiştir.

USG’de akut apandisit tanısı alan olgular büyük ihtimalle ameliyat gerektiren gerçek akut apandisittir.

Memişoğlu ve arkadaşlarının[14] çalışmasında, serilerinde negatif apendektomi oranları %17,3 olarak verilmiştir. Eğer lökosit düzeyi yüksek ve USG pozitifse bu oran %7,6’ya inmektedir. Negatif apendektomilerin ise %46’sında lökosit sayısı normal ve USG negatiftir.

SONUÇ Özellikle USG’nin negatif tanı koyduğu hastalarda, klinik bulguların devamı halinde hastanın ameliyat edilmesi gerekmektedir. Bu çalışmada, sadece USG sonucuna güvenerek akut apandisit tanısını koymanın doğru olmadığı ve faydalı bir yardımcı yöntem olan USG’nin ameliyat kararı vermede, anamnez ve fiziksel incelemenin önüne geçirilmemesi gerektiği kanısına varıldı.

KAYNAKLAR 1. Binnebösel M, Otto J, Stumpf M, Mahnken AH, Gassler N,

22

Schumpelick V, et al. Acute appendicitis. Modern diagnostics-surgical ultrasound. Chirurg 2009;80:579-87. [Abstract] 2. Rioux M. Sonographic detection of the normal and abnormal appendix. AJR Am J Roentgenol 1992;158:773-8.

3. Siegel MJ. Acute appendicitis in childhood: the role of US. Radiology 1992;185:341-2.

4. Ohmann C, Franke C, Yang Q. Clinical benefit of a diagnostic score for appendicitis: results of a prospective interventional study. German Study Group of Acute Abdominal Pain.

Arch Surg 1999;134:993-6.

5. Yacoe ME, Jeffrey RB Jr. Sonography of appendicitis and diverticulitis. Radiol Clin North Am 1994;32:899-912.

6. Sitter H, Hoffmann S, Hassan I, Zielke A. Diagnostic score in appendicitis. Validation of a diagnostic score (Eskelinen score) in patients in whom acute appendicitis is suspected.

Langenbecks Arch Surg 2004;389:213-8.

7. Saidi HS, Chavda SK. Use of a modified Alvorado score in the diagnosis of acute appendicitis. East Afr Med J 2003;80:411-4.

8. Zielke A, Sitter H, Rampp T, Bohrer T, Rothmund M. Clinical decision-making, ultrasonography, and scores for evaluation of suspected acute appendicitis. World J Surg 2001;25:57884.

9. Turan A, Kapan S, Kütükçü E, Yiğitbaş E, Hatipoğlu S, Aygün E. Comparison of operative and non operative managment of acut appendicitis. Ulusal Travma Acil Cerrahi Derg 2009;15:459-62.

10. SCOAP Collaborative, Cuschieri J, Florence M, Flum DR, Jurkovich GJ, Lin P, et al. Negative appendectomy and imaging accuracy in the Washington State Surgical Care and Outcomes Assessment Program. Ann Surg 2008;248:557-63.

11. Rosai J. Rosai and Ackerman’s surgical pathology. 9th ed.

Gastrointestinal tract-appendix. New York: Elsevier; 2004. p. 757-8.

12. Fox JC, Solley M, Anderson CL, Zlidenny A, Lahham S, Maasumi K. Prospective evaluation of emergency physician performed bedside ultrasound to detect acute appendicitis.

Eur J Emerg Med 2008;15:80-5.

13. Kiyak G, Korukluoğlu B, Ozgün Y, Devay AO, Kuşdemir A. Evaluation of Ohmann and Eskelinen scores, leukocyte count and ultrasonography findings for diagnosis of appendicitis. Ulus Travma Acil Cerrahi Derg 2009;15:77-81.

14. Memisoglu K, Karip B, Mestan M, Onur E. The value of preoperative diagnostic tests in acute appendicitis, retrospective analysis of 196 patients. World J Emerg Surg 2010;5:5.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):23-28

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2011.78989

Acil servis hekimleri tarafından düzenlenen adli raporların eksiklik ve yanlışlıklar yönünden değerlendirilmesi Evaluation of medicolegal reports written by physicians in the emergency unit with regard to deficiencies and mistakes Mustafa SERİNKEN,1 İbrahim TÜRKÇÜER,1 Kemalettin ACAR,2 Mert ÖZEN1 AMAÇ

BACKGROUND

Acil servislerde çalışan hekimler adli rapor düzenleme görevini sıklıkla yerine getirmektedir. Pek çok nedenden dolayı bu raporlarda istenmeyen hatalar bulunmakta ve bu hatalar devam eden adli işlemlerde sorunlara yol açmaktadır.

Bu çalışmada, üniversite hastanesinde belirli bir süre içinde düzenlenen adli raporlar değerlendirilerek hata ve eksiklikler yönünden gözden geçirilmesi amaçlandı.

Doctors working in emergency services often fulfill the task of preparing judicial reports. For a number of reasons, these reports have undesirable mistakes that become problematic in subsequent judicial processes. This study aimed to evaluate the judicial reports that were prepared over a certain period at a university hospital with regard to any mistakes or deficiencies.

GEREÇ VE YÖNTEM

METHODS

01.06.2005 - 30.06.2009 tarihleri arasında Pamukkale Üniversitesi Araştırma Uygulama Hastanesi Acil Servisinde düzenlenen adli raporların olgu türlerine göre dağılımları belirlendi ve içeriğindeki yanlışlık ve eksiklikler ile okunaklılığı araştırıldı. Belirlenen süre içerisinde acil servise müracaat ettiği anlaşılan 3499 adli olgudan raporuna ulaşılabilen 3219’u değerlendirmeye alındı.

The distribution of the judicial reports prepared between 01 June 2005 and 30 June 2009 in the emergency service of a University Research and Training Hospital was determined with respect to the types of cases, and their contents were studied for mistakes, deficiencies and legibility. Out of 3499 visits to the emergency service during the specified period, 3219 judicial reports that were accessible were considered in the evaluation.

BULGULAR

En sık olgu türünün trafik kazaları ile kesici-delici alet yaralanmaları olduğu, hayati tehlike kavramının doğruluğu yönünden sıkça hata yapıldığı, kimlik bilgileri ile olay saati ve muayene saati hususlarının sıkça eksik bırakıldığı tespit edildi.

SONUÇ

Hekimlerin adli rapor düzenlerken kesin rapor düzenlemekten önemli ölçüde imtina etmeleri, bilgi ve bulguların yeterli olduğu olgularda bile geçici rapor düzenleme yoluna gitme eğiliminde bulunmaları bu konudaki eğitim eksikliklerine bağlıdır. Aynı zamanda hayati tehlike, basit tıbbi girişimle giderilebilirlik gibi konulardaki yanlışlıklar da bu konudaki eğitim ve hassasiyet eksikliğinden kaynaklanmaktadır. Mezuniyet öncesi ve sonrası adli tıp eğitimi üst düzeyde önemsenmeli, hekimlerin yasal sorumlulukları konusunda farkındalık yaratılarak, bu konuda periyodik meslek içi eğitimler düzenlenmelidir.

Anahtar Sözcükler: Adli rapor; acil hekimi; hata.

Pamukkale Üniversitesi Tıp Fakültesi, 1Acil Tıp Anabilim Dalı, 2 Adli Tıp Anabilim Dalı, Denizli.

RESULTS

It was determined that the most frequent types of cases were traffic accidents and injuries by sharp and penetrating instruments. Furthermore, many mistakes were made frequently regarding the presence of life-threatening conditions, and personal identification information and times of the event and examination were often incomplete.

CONCLUSION

The fact that the doctors largely failed to prepare precise reports and tended to write unsatisfactory reports even for cases with adequate information and findings was attributed to their insufficient training in this area. At the same time, mistakes in life-threatening situations and in treatment by using simple medical interventions stem from lack of training and sensibility. Pre- and post-graduate forensic medicine education must be considered highly important, and periodic onthe-job training must be organized, creating a better awareness among doctors regarding their legal responsibilities.

Key Words: Medico-legal report; emergency physician; mistake.

Departments of 1Emergency Medicine, 2Forensic Medicine, Pamukkale University Faculty of Medicine, Denizli, Turkey.

İletişim (Correspondence): Dr. Mustafa Serinken. Pamukkale Üniversitesi Tıp Fakültesi Hastanesi Acil Servisi, 20070 Kınıklı, Denizli, Turkey.

Tel: +90 - 258 - 444 07 28 (5384) Faks (Fax): +90 - 258 - 213 49 22 e-posta (e-mail): mserinken@hotmail.com

23

Ulus Travma Acil Cerrahi Derg

Adli olgularla karşılaşıldığı durumlarda, durumun adli makamlara ihbar edilmesi ve hasta hakkında rapor düzenlenmesi, acil hekimlerinin temel görev ve sorumluluklarından birisidir. Hekimin ihbar yükümlülüğü 5237 sayılı Türk Ceza Kanunu’nun (TCK) 280. maddesinden kaynaklanmaktadır. Bu maddeye göre hekimler ve diğer sağlık çalışanları herhangi bir suç belirtisi ile karşılaştıklarında gerekli müdahalenin ardından durumu adli makamlara ihbar etmek zorundadırlar. Bu ihbar işlemini takiben, hekimin hastasının durumunu uygun dilde adli makamlara açıklayan bir medikolegal rapor düzenlemesi gerekmektedir. Acil servis hekimlerinin düzenledikleri raporlar, yargı sürecinin sağlıklı şekilde işlemesine yardımcı olmaktadır. Fakat, acil servislerde yaşanan hasta yoğunluğu ve stres, hekimlerin zaman zaman hata yapmasına neden olmaktadır. Acil hekimlerinin vardiya şeklinde çalışmaları ve çalışma saatlerinin uzun olmasının bu hataları arttırdığı düşünülmektedir.[1,2] Bunların sonucunda adli olguların muayene ve raporlanmasında birtakım yanlışlık ve eksiklikler yaşanmakta, bunun sonucunda ise adli yargılama işlemlerinde sorunlar ortaya çıkabilmektedir.[3] Ülkemizde, mezuniyet öncesi ve sonrası adli tıp eğitiminin yetersizliği ve adli tıp konularının yeterince bilinmemesi nedeniyle, acil hekimleri adli rapor düzenleme aşamasında çekingen ve tedirgin davranmaktadırlar.[4] Yaralanma sonrası düzenlenen ilk raporlardaki eksiklikler ve hatalar geri dönüşümsüz sonuçlar doğurabilmektedir. Hayatı tehlikeye sokan yaralanma veya basit tıbbı müdahale ile iyileşebilir/iyileşemez kararları verirken önemli hatalar yapılabilmektedir.[5] Acil servis hekimleri, yukarıda sayılan nedenlerden dolayı genellikle geçici adli rapor yazarak kendilerini koruduklarını düşünmektedir. Oysa bu durum gereksiz yere adli soruşturma ve kovuşturma sürecinin daha da uzaması gibi sonuçları da beraberinde getirmektedir.[6] Bu tanımlayıcı çalışmada, bir üniversite hastanesi acil servisinde düzenlenen adli raporlardaki hata ve eksiklikler araştırıldı, sorunun çözümü için veriler elde edilmeye çalışıldı.

GEREÇ VE YÖNTEM Pamukkale Üniversitesi Tıp Fakültesi Acil Servisi’ne dört yıl boyunca (01.06.2005 - 30.06.2009) başvuran erişkin ve pediyatrik adli olgular çalışma evrenini oluşturdu. Tanımlayıcı ve retrospektif olarak planlanan çalışmada raporların değerlendirilmesi bir adli tıp hekimi tarafından yapıldı. Herhangi bir nedenle hastane arşivinden adli raporuna ulaşılamayan olgular çalışma dışı bırakıldı.

Acil tıp araştırma görevlileri tarafından doldurulan adli raporlar retrospektif olarak incelendi. Adli raporlardaki bilgiler hastane dosyaları ile karşılaştırıldı.

24

Raporlardaki kimlik bilgilerine bağlı eksiklikler, olay zamanına bağlı olan eksiklikler, inceleme bulgularına bağlı eksiklikler ve kullanılan kısaltmalar tarandı. Ayrıca raporu dolduran hekimin kaşe ve imzası, raporu teslim alan görevlinin bilgileri araştırıldı.

Adli raporunda hayati tehlikesi olduğu belirtilen hastalar, Adalet Bakanlığı Adli Tıp Kurumu Başkanlığı, Adli Tıp Uzmanları Derneği ile Adli Tıp Derneği tarafından hazırlanan “Yeni Türk Ceza Kanunu Çerçevesinde Düzenlenecek Adli Raporlar İçin Kılavuz”[7] bilgileri dikkate alınarak hayati tehlike kararının doğru olup olmadığı yönünden değerlendirildi.

Son olarak adli raporlar okunabilirlik açısından değerlendirildi. Gönüllü adaylar arasından rastgele seçilen, üniversitemizde görevli bir avukattan (mesleğinin 5. yılında), bir intern doktordan ve acil servisimizde görevli bir acil tıp uzmanından adli raporları okumaları istendi. Bu üç kişi, birbirinden bağımsız olarak, tüm raporları gözden geçirdi ve okuyamadıkları raporları belirledi. Çalışmadan elde edilen tüm veriler, “Statistical Package for Social Sciences for Windows 11” adlı standart programa kaydedildi ve değerlendirmeleri yapıldı. Sayısal değişkenler ortalama ± SD, kategorik değişkenler sayı ve yüzde olarak özetlendi.

BULGULAR Çalışma süresince, acil servise başvuruda bulunan ve acil servis hekimleri tarafından adli rapor düzenlenen 3499 adli olgu olduğu belirlendi, 280 olgunun adli raporuna ulaşılamadı ve çalışma dışı bırakıldı. Kalan 3219 adli olgu çalışma evrenini oluşturdu.

Adli olguların etyolojiye göre dağılımı incelendiğinde, en büyük grubu trafik kazaları oluşturdu (%68,3 n=2201). Kesici, delici alet yaralanmaları ikinci sırada yer aldı (%12,8 n=413). Tüm adli raporların 648’i (%20,1) kesin hekim raporuydu (Tablo 1). Bu raporların büyük kısmının basit yaralanması olan (sıyrık, abrazyon, kontüzyon, kesi) hastalara ait olduğu belirlendi (n=411, %63,4). Normal fiziksel incelemesi olan hastalar ikinci büyük grubu oluşturdu (n=159, %24,5).

Etyolojiye göre kesin rapor verilme olanları araştırıldığında, zehirlenme olgularının en düşük orana sahip olduğu belirlendi (%4,4) (Tablo 1).

Adli raporlarda hayati tehlike geçirdiği belirtilen olgu sayısı 495 (%15,4) idi. Bu olguların büyük bölümü, trafik kazası sonrası oluşan çoklu travma hastalarıydı (n=314, %63,4). Yeni Türk Ceza Kanunu’nda belirtilen kriterlere göre, hayati tehlike değerlendirmesinin hekimler tarafından doğru yapılıp yapılmadığı araştırıldı. Hayati tehlikesi olduğu halde, hayati tehlike verilmeyen olguya rastlanmadı, 64 (%13,0) olguda “hayati tehlikesi vardır” kararının, hatalı olarak verildiği belirlendi. Bu olguların büyük bölümünü zehirOcak - January 2011

Acil servis hekimleri tarafından düzenlenen adli raporların eksiklik ve yanlışlıklar yönünden değerlendirilmesi

Tablo 1. Adli olguların etyolojiye göre dağılımı ve geçici/kesin rapor yazılma oranları

Tablo 2. Hayati tehlike verilen ve hayatını kaybeden

olguların etyolojiye göre dağılımları

Etyoloji

Etyoloji

n (%)

Geçici rapor Kesin rapor verilen verilen olgular olgular n (%) n (%)

2201 (68,3) 1832 (71,2) 369 (56,9) Trafik kazası Kesici, delici alet 413 (12,8) yaralanmaları 286 (11,1) 127 (19,6) 204 (6,3) Zehirlenme 195 (7,6) 9 (1,4) 149 (4,6) Darp 108 (4,2) 41 (6,3) 108 (3,3) Yüksekten düşme 85 (3,3) 23 (3,6) 53 (1,6) Ateşli silah 36 (1,4) 17 (2,6) 91 (2,8) Diğer 29 (1,2) 62 (9,6) 3219 (100,0) 2571 (100,0) 648 (100,0) Toplam

lenme vakaları oluşturdu (n=38, %59,4). Hayati tehlike verilen tüm olgular içinde, 88 olgunun daha sonraki takibinde hayatını kaybettiği saptandı (Tablo 2). Çalışma grubumuz içinde, adli raporunda hayati tehlike olmadığı belirtilen ve sonraki tedavi sürecinde hayatını kaybeden olguya rastlanmadı. İncelenen raporlarda saptanan eksiklikler Tablo 3’de özetlendi. Hayati tehlikenin mevcut olup olmadığı ve olay tarihine ilişkin bilgilerin, hekimler tarafından çok yüksek oranda yazıldığı belirlendi. Hasta yaşı ve baba adı bilgileri raporlarda en fazla saptanan eksik verilerdi (sırasıyla %84,9, %87,3). Bunları sırasıyla olay saati (%52,1) ve muayene saati (%49,9) izledi, 843 (%26,2) raporda, raporu teslim alan görevliye ait veriler yoktu (Tablo 3).

Adli raporlar okunabilirlilik açısından, bir avukat, bir intern doktor ve bir acil tıp uzmanı tarafından değerlendirildi. Avukat 846 (%26,3), intern 172 (%5,3), acil tıp uzmanı 48 (%1,5) raporda okuyamadıkları ifadeler olduğunu belirledi. Tüm raporlar kullanılan kısaltmalar yönünden de değerlendirildi. En sık kullanılan kısaltmalar “GD”, “HİHSEK”, “IR”, “USG”, “KVS”, “GİS”, “FM”, “GRF”, “EXT” olarak belirlendi. Raporlarda sık kullanılan kısaltmalar ve kullanılma oranları Tablo 4’de özetlenmiştir.

TARTIŞMA Acil servis hekimlerinin, koruyucu ve tedavi edici hekimlik görevlerinin yanı sıra adli hekimlik görevleri de bulunmaktadır. Hastanelerin acil servislerine başvuran olguların çoğunu adli olguların oluşturması nedeniyle acil servislerde yazılan adli raporların da yargı sürecinde önemi büyüktür. Ülkemizde acil servislere başvuran adli olguları konu alan araştırmalarda, olgular içinde en büyük grubun trafik kazalarına ait olduğu görülmektedir.[8,9] Bu olgular, çalışmamızda da %68 gibi yüksek bir oranla ilk sırada yer almıştır.

Cilt - Vol. 17 Sayı - No. 1

Trafik kazası Kesici, delici alet yaralanmaları Zehirlenme Darp Yüksekten düşme Ateşli silah Diğer

Hayati tehlike Hatalı olarak Takibinde verilen tüm hayati tehlike ölen olgular verilen olgular olgular n (%) n (%) n (%) 314 (63,4)

20 (31,2)

57 (64,8)

48 (9,7) 55 (11,1) 17 (3,4) 23 (4,7) 27 (5,5) 11 (2,2)

3 (4,7) 38 (59,4) 0 (0) 0 (0) 2 (3,1) 1 (1,6)

9 (10,2) 4 (4,6) 3 (3,4) 5 (5,7) 8 (9,1) 2 (2,3)

Çalışmamızda hekimlerimizin yazdığı raporların yaklaşık %20’sinin kesin rapor olduğu saptanmıştır.

Bu olguların büyük çoğunluğunun, normal fiziksel inceleme bulguları ya da basit yarası olan olgular olması düşündürücüdür. Adli raporlarla ilgili olarak sık karşılaşılan problemler arasında, hekimin kesin rapor verebilecek iken geçici rapor vermesi ilk sırada yer almaktadır.[10] Tümer ve arkadaşları[11] hekimler üzerinde yaptıkları anket çalışmasında, kesin rapor yazılmasından çekinildiği ve raporların büyük çoğunluğunun geçici rapor şeklinde hazırlandığı sonucuna ulaşmıştır.

Uygulamada sık rastlanılan bu durum aslında olası bir hatadan ve doğacak sorumluluktan kaçınmak için yapılmakta ise de, aynı zamanda hekimin temel mesleki hak ve görevlerinden vazgeçmesi anlamına da gelmektedir. Bazı hekimlerin geçici raporları “daha sonTablo 3. Raporlarda belirlenen eksiklikler

Kimlik bilgileri eksiklikleri Hastanın adı Hastanın soyadı Baba adı Doğum tarihi ya da yaşı Olay zamanına bağlı eksiklikler Olayın tarihi Olayın saati Muayene saati İnceleme bulgularına bağlı eksiklikler Genel durum Bilinç durumu Kooperasyon Sistemik inceleme bulguları Hayati tehlike Alkol düzeyi Diğer eksiklikler Hekimin kaşesi Hekimin imzası Teslim alan görevlinin bilgileri

n

%

11 14 2734 2811

4 1677 1609

0,3 0,4 84,9 87,0

560 588 624 815 2 1511

134 28 843

17,4 18,3 19,4 25,3 0,06 46,9

0,1 52,1 49,9

4,2 0,9 26,2 25

Ulus Travma Acil Cerrahi Derg

Tablo 4. Adli rapor yazımında kullanılan kısaltmalar ve oranları Kısaltma

Terim adı

Oran (n, %)

Kısaltma

Terim adı

Oran (n, %)

RT DKY NG POST LSV PNX İNF LAT PALP ABD

PROX ANT KVAH EXT

Rektal tuşe Dış kulak yolu Nazogastrik Posterior Lumbosakral vertebra Pnömotoraks İnferior Lateral Palpasyon Abdomen

Proksimal Anterior Kostavertebral açı hassasiyeti Ekstremite

28 (0,9) 27 (0,8) 35 (1,1) 54 (1,7) 58 (1,8) 65 (2,0) 89 (2,8) 90 (2,8) 95 (2,9) 102 (3,2)

119 (3,7) 122 (3,8) 812 (25,2) 1040 (32,3)

GİS IR BB BT USG KVS SOLS Y GRF HİHSEK

GKS FM N GD

Gastro intestinal sistem Işık refleksi Baş-boyun Bigisayarlı tomografi Ultrasonografi Kardiyovasküler sistem Solunum sistemi Yön Grafi Her iki hemitoraks solunuma eşit katılıyor Glaskow Koma Skoru Fizik muayene Normal Genel durum

1127 (35,0) 1148 (35,7) 1162 (36,1) 1216 (37,8) 1325 (41,2) 1335 (41,5) 1480 (46,0) 1575 (48,9) 1630 (50,6)

ra değiştirilebilir” ve “önemsiz” raporlar gibi değerlendirdikleri de bilinmektedir.[12] Geçici raporlarda yapılan hatalar, adli işlemlerin gecikmesine neden olabilmekte, bu raporların kesin rapora dönüşmesi zaman almakta ve gereksiz bir kırtasiyeciliğe yol açmaktadır.[6] Adli olgularda acil hekimlerinin kesin rapor vermemesi gerektiği yönündeki görüşün ya da eğilimin tıbbi-etik ve yasal hiçbir gerekçesi yoktur.

Adli raporlarda saptadığımız bir başka problem, olgunun hayati tehlike geçirip geçirmediği konusundadır. Hayati tehlike kararının neredeyse tüm raporlarda eksiksiz yer alması, hekimlerimizin bu ifadenin önemini bildiklerini göstermektedir. Fakat, hayati tehlike verilen olgular içinde, %13 oranında gereksiz yere hayati tehlike verildiği belirlenmiştir. Çoltu ve arkadaşları[13] bir üniversite hastanesi acil servisinde yaptıkları çalışmada, hayati tehlike kararının %6,5 oranında hatalı yapıldığını bildirmiştir. Benzer bir diğer çalışmada, bu oran %4,7 bulunmuştur. Bunların %80’inde hayati tehlike olmadığı halde hayati tehlike verildiği, kalan %20’sinde de hayati tehlike olduğu halde “hayati tehlike yoktur” şeklinde yazıldığı saptanmıştır.[14] Biz hayati tehlike geçirdiği halde, hayati tehlike verilmeyen olguya rastlamadık. “Hayati tehlikesi vardır” kararının genellikle trafik kazası sonrası oluşan çoklu travma hastalarına verildiğini ve bu olgularda yüksek oranda gereksiz yere hayati tehlike verildiğini belirledik (%31). Fakat, gereksiz yere hayati tehlike verilen olgular içinde en büyük grup, zehirlenme olgularına aitti (%59). Aynı zamanda zehirlenme olguları, en az kesin rapor verilen grubu da oluşturdu. Özetle hekimlerimizin, zehirlenme ve trafik kazaları olgularında gereksiz yere hayati tehlike verme eğiliminde olduğu görüldü.

Adli raporlarda, genel olarak acil hekiminden beklenen, istenen kişinin hayati tehlike geçirip geçirme26

1729 (53,7) 1763 (54,8) 1820 (56,5) 1931 (60,0) 1949 (60,5)

diği ve basit tıbbi müdahale ile iyileşip iyileşmeyeceği sorularıdır. 01.06.2005 tarihinde 5237 sayılı TCK ile 5271 sayılı Ceza Muhakemesi Kanunu’nun (CMK) yürürlüğe girmesini takiben Sağlık Bakanlığı Temel Sağlık Hizmetleri Genel Müdürlüğü tarafından, adli tabiplik hizmetlerinin yürütülmesinde uyulacak esasları düzenleyen 22.09.2005 tarih ve 13292 sayılı bir genelge yayınlanmıştır. Bu kanun maddelerinin içeriği ile yaralanmalarda adli raporların nasıl düzenleneceği, Adli Tıp Kurumu Başkanlığı-Adli Tıp Uzmanları Derneği ve Adli Tıp Derneği’nce hazırlanmış olan “Yeni Türk Ceza Kanunu Çerçevesinde Düzenlenecek Adli Raporlar İçin Kılavuz” adlı kitapçıkta toplanmıştır.[7] Bu kılavuzda kişinin hangi durumlarda hayatının tehlikeye gireceği, madde madde sıralanmıştır. Zehirlenme olgularındaki zorluklar da düşünülerek, bu olgular için de yaşamsal tehlike kriterleri ayrıca belirlenmiştir. Bu standartlaştırılmış listelere bakılarak, acil hekimlerince hayati tehlike kararının kolaylıkla verilebileceğini düşünmekteyiz. Burada bahsi geçen hayati tehlike kavramının olayla ilgili tüm riskleri içermeyip, olayla ilgili olarak gelişen ve hekim tarafından somut olarak saptanan durumları kapsadığı unutulmamalıdır.

Bu konuda yanlış düzenlenmiş raporlar, adli yargılama sürecinin yanlış başlamasına, yanlış ilerlemesine, davanın yanlış mahkemede görülmesine, kişilerin gereksiz yere tutuklu yargılanmasına yada hatalı cezalar almasına neden olabilmekte ve hekimler ciddi yasal yaptırımlarla karşı karşıya gelebilmektedir.

Hazırlanan kılavuzda adli raporlar hazırlanırken, bilgilerin eksiksiz olması, yazılırken anlaşılır ve sade bir dil kullanılması ve tıbbi terimlerde kısaltmalardan kaçınılması istenmektedir.[7] Çalışmamızda, kimlik bilgileri (hasta yaşı, baba adı), zaman bilgileri (olay saati, muayene saati), muayene bulguları (alkol düzeyi) ile raporu teslim alan kişiye ait bilgilerin raporlarda önemli oranda eksik olduğu tespit edilmiştir. TurOcak - January 2011

Acil servis hekimleri tarafından düzenlenen adli raporların eksiklik ve yanlışlıklar yönünden değerlendirilmesi

la ve arkadaşlarının[9] yaptığı benzer bir çalışmada, zaman bilgilerinden olay saatinin, kimlik bilgilerinden doğum tarihinin, muayene bulgularından lezyonların ayrıntılı olarak tanımlanmasının, genel durum-bilinç durumunun eksik olduğu ve raporu teslim alan kişiye ait bilgilerin hiçbir raporda kayıtlı olmadığı bildirilmiştir. Düzenlenen raporun adli makamlara iletilmesinde aksaklık yaşanması durumunda, raporun teslim edildiği kişinin bilinmemesi raporu düzenleyen acil hekimini zor durumda bırakabilir. Yasalarımız tarafından, düzenlenen adli raporların kimler tarafından ve ne şekilde adli makamlara ulaştırılacağı belirlenmiş olsa da, bu işlemin usulüne uygun yapılması raporu yazan hekimin de sorumluluğundadır.

Adli raporlar bilgisayar, daktilo veya okunaklı el yazısı ile resmi yazışma kuralları ve rapor tekniğine uygun, yalın ve hukukçuların okuyacağı düşünülerek çok fazla tıbbi terim ve kısaltma kullanmaktan kaçınarak anlaşılır şekilde yazılmalıdır.[7] Okunaksız ve düzensiz yazılan raporlar, adli raporlarda karşılaşılan en sık problemlerden biridir.[3] Çalışmamıza katılan avukatımız, raporların %26’sının bu yönde eksik olduğunu ve anlaşılır yazılmadığını belirledi. Ülkemizde doktor yazısının okunulabilirliği ile ilgili sınırlı sayıda çalışma vardır. Reçeteler üzerinde yapılan bir çalışmada, eczacıların %10,3’ünün, hekimlerin ise %11,5’inin yazılan reçetelerde okuma zorluğu çektiği saptanmıştır.[15] Diğer bir çalışmada ise hekimlerin %10’unun sıklıkla, %11,6’sının nadiren kısaltma kullandığı, %63,4’ünün çok bilinen kısaltmaları kullandığını tespit edilmiştir.[16] Çalışmamızda raporlar yazılırken tıbbi terimlerde yüksek oranda kısaltma kullanıldığı belirlenmiştir. Hekim yazısının diğer insanların yazısından farklı olmadığını ancak yazının düzgün yazılması üzerine değil de kişinin sağlığı üzerine yoğunlaştığını bildiren çalışmalarda mevcut olup genel olarak okunamayan yazılardan kurtulmak için bilgisayarlı sisteme geçilmesi önerilmektedir.[17] Raporun okunaksız ve düzensiz bir yazı ile yazılmış olması, kısaltma kelimeler kullanılması durumunda adli makamlar tarafından raporun yeniden okunaklı yazılması veya okunması için mahkemeye çağrılma durumu ile karşı karşıya kalınabilir. Bu tür sorunların çözümüne yönelik olarak, Sağlık Bakanlığı tüm sağlık kurumlarında tek tip adli rapor uygulamasına geçmeyi zorunlu hale getirmiş ve 22.09.2005 tarih ve 13292 sayılı genelge ekinde standart rapor formları yayınlamıştır. Bu raporların kullanımının yaygınlaşması, acil servislerde adli rapor düzenlenmesi esnasında hekimin unutma ya da hata yapma riskini azaltacak, ulusal bir standart sağlama ve uygulama birliğine gitme yönünden de adli işlemlerin yürütülmesinde büyük kolaylık sağlayacak ve sonuçta adaletin tecellisine büyük hizmette bulunacaktır.

Hekimlerin adli rapor düzenleme esnasında yaptığı Cilt - Vol. 17 Sayı - No. 1

yanlışlık ve eksiklikler bugüne kadar pek çok çalışmada ele alınmış olmakla birlikte, bu konunun yasal sorumluluk teşkil ettiği, hekimlerin bu nedenle ceza ve tazminat davaları ile karşılaşabilecekleri noktasına değinilmemiştir. Oysa yukarıda değinildiği gibi adli olgunun adli makamlara ihbar edilmemesi halinde hekimin TCK’nın 280. maddesi kapsamında yargılanması gerekmektedir. Üstelik hekim eğer devlet memuru olarak görev yapmakta ise TCK gerekçesinde de bahsedildiği gibi, bu maddenin daha ağır formu olan 279. maddeden yargılanacaktır.

Ayrıca hekimin adli rapor düzenlerken yapacağı her türlü yanlışlık ve eksiklik nedeniyle görevi ihmal iddiasıyla TCK 257/2. maddesinden yargılanması söz konusu olabilecektir. Bu maddede “(1) Kanunda ayrıca suç olarak tanımlanan hâller dışında, görevinin gereklerine aykırı hareket etmek suretiyle, kişilerin mağduriyetine veya kamunun zararına neden olan ya da kişilere haksız bir kazanç sağlayan kamu görevlisi, bir yıldan üç yıla kadar hapis cezası ile cezalandırılır. (2) Kanunda ayrıca suç olarak tanımlanan hâller dışında, görevinin gereklerini yapmakta ihmal veya gecikme göstererek, kişilerin mağduriyetine veya kamunun zararına neden olan ya da kişilere haksız bir kazanç sağlayan kamu görevlisi, altı aydan iki yıla kadar hapis cezası ile cezalandırılır” denilmektedir. Üstelik adli rapor düzenleme görevi adli bir görev sayılabileceği için CMK 161/5. maddesi gereğince hekimin söz konusu bu yargılanması esnasında standart soruşturma izni prosedürlerinin işletilmeyerek Cumhuriyet Savcısı tarafından doğrudan soruşturma başlatılabileceği hususu gözden kaçırılmamalı ve önemsenmelidir. Çünkü bu maddede “Kanun tarafından kendilerine verilen veya kanun dairesinde kendilerinden istenen adliye ile ilgili görev veya işlerde kötüye kullanma veya ihmalleri görülen kamu görevlileri ile Cumhuriyet Savcılarının sözlü veya yazılı istem ve emirlerini yapmakta kötüye kullanma veya ihmalleri görülen kolluk âmir ve memurları hakkında Cumhuriyet Savcılarınca doğrudan doğruya soruşturma yapılır. Vali ve kaymakamlar hakkında 2.12.1999 tarihli ve 4483 sayılı Memurlar ve Diğer Kamu Görevlilerinin Yargılanması Hakkında Kanun hükümleri, en üst dereceli kolluk amirleri hakkında ise, hâkimlerin görevlerinden dolayı tâbi oldukları yargılama usulü uygulanır” denilmektedir.

Ceza yargılamasından ayrı olarak kişilerin hekim aleyhine çeşitli tazminat davaları açması da söz konusu olabilecektir. Rapordaki yanlışlık nedeniyle cezaevinde fazladan kaldığını, maddi ve manevi kayba uğradığını iddia eden mağdur ya da fail taraf davaları ile karşılaşma ihtimalimiz vardır. Çalışmamızda ele alınan raporlardaki eksiklik ve yanlışlıklar nedeniyle hiçbir hekimin soruşturma ya da kovuşturmaya tabi tutulmadığı anlaşılmıştır. Bununla 27

Ulus Travma Acil Cerrahi Derg

birlikte bugüne değin bu konularda yasal işlem yapılmamış olması bundan sonra da hiçbir zaman olmayacağı anlamını taşımamaktadır.

Adli rapor düzenleme yasal sorumluluklar ile ilgili eğitimlerin hekimler tarafından zamanında rağbet görmediği bilinen bir gerçektir. Meslektaşlarımız bu konunun önemini ancak başları yasa ile derde girdikten sonra fark etmektedir.

Sonuç olarak, adli raporların düzenlenmesi esnasında hekimlerin yapacağı her türlü hata ve eksiklik aynen diğer malpraktis olgularında olduğu gibi kendisinin yasal olarak sorumlu tutulup, ceza ve tazminat davaları ile karşı karşıya gelmesine neden olabilecektir. Bu nedenle acil servis hekimlerinin adli olgulara nasıl yaklaşacağını, adli raporu nasıl yazacağını ve hekim sorumluluğunun neleri gerektirdiğini bilmeleri gerekmektedir. Adli raporlarda genel olarak hekimden istenen yaralanma nedeniyle kişinin hayati tehlike geçirip geçirmediği, kişinin yaralanmasının basit tıbbi müdahale ile giderilip giderilemeyeceği gibi birkaç önemli sorunun aydınlatılması olup, bu soruların çoğu temel adli tıp bilgisi ışığında ve kılavuzlardan da faydanalarak kolayca ve doğru şekilde yanıtlanabilir.

Adli raporları düzenlerken özen gösterilmesi, okunaklı ve sade ifadeler kullanılması önemlidir. Adli raporlardaki eksiklik ve hata oranlarının daha da düşürülmesi ve hatta tamamen ortadan kaldırılması için mezuniyet öncesi adli tıp eğitimine ayrılan süre ve emeğin artırılması, mezuniyet sonrası eğitimlere periyodik olarak devam edilmesi, seminerlerde bilgi kazandırmanın yanı sıra, hekimlerimize adli olgulardaki sorumluluklarını iyice kavratacak formasyonların eğitim sürecine aktarılması gerektiğine inanmaktayız. Ancak, bu konuda en önemli görev yine hekimlere düşmekte olup, bizler bu konudaki görev ve sorumluluklarımızın bilincinde olmalı, adli raporlar ve ilgili yasal mevzuat hakkında bilgilerimizi sürekli olarak güncel ve üst düzeyde tutma çabasında olmalıyız.

Bu konularda düzenlenecek meslek içi eğitimlerin takip edilmesi yanında, bu eğitimlerin kalitesinin artırılarak tutum ve davranış değişikliğini sağlayacak nitelik ve derinlikte olması sağlanmalıdır.

Ayrıca, mesleki sorumluluk sigortası kapsamla-

28

rı dikkatle incelenmeli ve adli görevleri de kapsayıp kapsamadığı noktasına dikkat edilmelidir.

KAYNAKLAR 1. Serinken M, Çımrın AH, Ergör A, Cimilli C, Bengi F. Tükenme sendromu ve acil servis hekimleri. Toplum ve Hekim Dergisi 2002;17:358-65.

2. Kurtuluş A, Acar K, Boz B. Hekimin yasal sorumlulukları.

Akademik Dizayn 2008;2:10-4.

3. Hancı H. Birinci basamak adli raporlarında yapılan hatalar.

Türkiye Klinikleri Dergisi 2004;175:4-5.

4. Yavuz MS, Aydın S. Forensic cases and reports in primary health care. Turkish Journal of Family Practice 2004;8:30-3.

5. Fedakar R, Aydiner AH, Ercan I. A comparison of “life threatening injury” concept in the Turkish Penal Code and trauma scoring systems. Ulus Travma Acil Cerrahi Derg 2007;13:192-8.

6. Çolak B, Demirbaş İ, Albayrak Ü. The importance of temporary forencis reports. STED Dergisi 2005;14:161-4.

7. Yeni Türk Ceza Kanunu Çerçevesinde Düzenlenecek Adli Raporlar İçin Kılavuz; Adli Tıp Kurumu- Adli Tıp Uzmanları Derneği- Adli Tıp Derneği. Editör: Balcıoğlu Y, Güzel S, Çetin G. İstanbul: 2005.

8. Yavuz MF, Baştürk P, Yavuz MS, Yorulmaz C. Cerrahpaşa Tıp Fakültesi Acil Servisine başvuran adli olguların değerlendirilmesi. Adli Bilimler Dergisi 2002;1:21-6.

9. Turla A, Aydin B, Sataloğlu N. Mistakes and omissions in judicial reports prepared in emergency services. Ulus Travma Acil Cerrahi Derg 2009;15:180-4.

10. Beyaztaş Y. Adli rapor konusunda hekim sorumluluğu. Anadolu Psikiyatri Dergisi 2000;1:231-4.

11. Tümer AR, Hancı H. Adli Raporlar ve Cerrahi Hekimleri, Ulusal Cerrahi Dergisi 2002; 18: 112-7.

12. Çolak B, Etiler N, Biçer Ü. Adli tıp hizmetleri kim tarafından sunulmaktır/ sunulmalıdır? Toplum ve Hekim Dergisi 2004;19:131-8.

13. Çoltu MA, Durak D, Fedakar R. Uludağ Üniversitesi Tıp Fakültesi Acil Servisinde düzenlenen adli rapor formlarının değerlendirilmesi. Adli Tıp Bülteni 2000;5:36-40.

14. Çetin V, Fedakar R. 1999-2001 Yıllarında Uludağ Üniversitesi Tıp Fakültesi Acil Servisinde düzenlenen adli rapor formlarının değerlendirilmesi. 2. Anadolu Adli Bilimler Kongresi Kitapçığı. Kayseri: 2003. s. 17.

15. Yilmaz R, Ozbay M, Koc S. Evaluation of handwriting legibility on 235 prescriptions. Turkiye Klinikleri J Foren Med 2006;3:47-52.

16. Aşıcıoğlu F, Cantürk G. Hekimlerin okunaksız el yazısının yol açtığı sorunlar: Bir anket çalısması. Adli Bilimler Dergisi 2003;2:13-22.

17. Berwick DM, Winickoff DE. The truth about doctors’ handwriting: a prospective study. BMJ 1996;313:1657-8.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):29-32

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2011.29000

Nekrotizan fasiit tanısıyla izlenen 44 olgunun klinik değerlendirmesi Clinical evaluation of forty-four patients with necrotizing fasciitis Özge TURHAN, Seyit Ali BÜYÜKTUNA, Dilara İNAN, Rabin SABA, Ata Nevzat YALÇIN AMAÇ

BACKGROUND

Nekrotizan fasiit, nadir görülen ancak hayatı tehdit eden, esas olarak yüzeyel fasiya ve deri altı dokuyu tutan bir yumuşak doku enfeksiyonudur.

Necrotizing fasciitis is a rare but life-threatening soft-tissue infection primarily involving the superficial fascia and subcutaneous tissue.

GEREÇ VE YÖNTEM

METHODS

Bu çalışmada 2004-2008 yılları arasında nekrotizan fasiit tanısıyla Akdeniz Üniversitesi Tıp Fakültesi İnfeksiyon Hastalıkları ve Klinik Mikrobiyoloji servisinde yatan ve diğer kliniklerde yatarken enfeksiyon hastalıkları ve klinik mikrobiyoloji konsültasyonlarıyla takip ve tedavi edilen 44 hasta retrospektif olarak incelendi. Hastanemizdeki etkenlerin dağılımı, yerleşim yeri, eşlik eden hastalıklar ve risk faktörlerinin ortaya konulması amaçlandı.

We conducted a retrospective study of 44 patients with necrotizing fasciitis between 2004 and 2008 in Akdeniz University Hospital, Department of Infectious Diseases and Clinical Microbiology and other departments. The aim of this study was to determine the causative agents of the necrotizing fasciitis, and the localization, predisposing factors, and comorbid conditions.

BULGULAR

RESULTS

Çalışmamız sonucunda diyabetes mellitus, travma ve cerrahi, nekrotizan fasiit oluşumunda rol oynayan predispozan faktörler arasında yer alırken en sık alt ekstremitede ve perianal bölgede yerleştiği tespit edildi. Etyolojide polimikrobiyal etkenler ilk sırada yer alırken mortalite oranı %25 olarak saptandı.

SONUÇ

Bu çalışmayla enfeksiyon acilleri arasında yer alan nekrotizan fasiit olgularının hastanemizdeki izlem sonuçları değerlendirilmiştir.

We found that diabetes mellitus, trauma and surgery were the most important predisposing factors. Moreover, the lower extremity and perianal region were the most frequently involved sites. Polymicrobial agents were the most frequent and the mortality was found as 25%.

CONCLUSION

In conclusion, necrotizing fasciitis cases followed in our hospital were evaluated in this study.

Anahtar Sözcükler: Deri yumuşak doku; fasiit; nekrotizan fasiit.

Key Words: Soft-tissue infection; fasciitis; necrotizing fasciitis. .

Nekrotizan deri yumuşak doku enfeksiyonları, yüzeyel deri enfeksiyonlarından farklı klinik bulguları, eşlik eden farklı risk faktörleri ve tedavi rejimleri olan, hızla ilerleyerek saatler içinde ölümle sonuçlanabilen enfeksiyonlardır. Bu enfeksiyonlar, fasiya ve/ veya kaslara uzanarak dokularda büyük tahribatlara neden olmaktadır. Bu klinik tablolar genellikle travma ya da cerrahi sonrası sekonder enfeksiyonlar olarak gelişmektedir.[1]

Nekrotizan deri yumuşak doku enfeksiyonlarını tutulan anatomik bölgeye, etken mikroorganizmaya veya klinik tablolara göre sınıflandırmak mümkünse de başlangıçta tanı, antimikrobiyal tedavi ve cerrahi uygulama kararı yaklaşımları bu grup enfeksiyonlarda benzerdir. Nekrotizan deri yumuşak doku enfeksiyonlarından biri olan nekrotizan fasiit, nadir görülen, yüzeyel fasiya ve deri altı yağ dokusunun akut başlayan ve hızla ilerleyen enfeksiyonudur.[1,2] Deri invaz-

*XIV. Türk Klinik Mikrobiyoloji ve İnfeksiyon Hastalıkları Kongresi’nde poster bildiri olarak sunulmuştur (25-29 Mart 2009, Antalya).

*Presented at the Turkish Congress of Clinical Microbiology and Infectious Diseases (March 25-29, 2009, Antalya, Turkey).

Akdeniz Üniversitesi Tıp Fakültesi, İnfeksiyon Hastalıkları ve Klinik Mikrobiyoloji Anabilim Dalı, Antalya.

Department of Infectious Diseases and Clinical Microbiology, Akdeniz University Faculty of Medicine, Antalya, Turkey.

İletişim (Correspondence): Dr. Özge Turhan. Akdeniz Üniversitesi Tıp Fakültesi, İnfeksiyon Hastalıkları ve Klinik Mikrobiyoloji ABD, Antalya, Turkey.

Tel: +90 - 242 - 249 67 16 e-posta (e-mail): ozgeturhan@akdeniz.edu.tr

29

Ulus Travma Acil Cerrahi Derg

yonunun derinliğine bağlı olarak lokal doku destrüksiyonundan, doku nekrozu ve septik şokla ölüme kadar ilerleyen bu klinik tabloda, acil cerrahi ve antibiyoterapi uygulamalarına rağmen mortalite oranı %6-76 arasında değişmektedir.[3] Çalışmamızda nadir görülen ancak mortalitesi oldukça yüksek olan ve enfeksiyon acilleri arasında yer alan nekrotizan fasiitin hastanemizdeki sıklığı, etkenlerin dağılımı, tutulan bölgelerin, eşlik eden hastalıklar ve risk faktörlerinin ortaya konulması amaçlandı.

GEREÇ VE YÖNTEM Antalya Üniversitesi Tıp Fakültesi Hastanesi’nde 1 Ocak 2004-31 Aralık 2008 tarihleri arasında nekrotizan fasiit tanısıyla enfeksiyon hastalıkları ve klinik mikrobiyoloji servisinde yatan ve diğer kliniklerde yatarken enfeksiyon hastalıkları ve klinik mikrobiyoloji konsültasyonlarıyla takip ve tedavi edilen 44 hasta retrospektif olarak incelendi. Çalışmamız tanımlayıcı bir araştırmadır. Verilerin yüzdeleri verilmiştir. Bu oranların verilmesi aşamasında SPSS Versiyon 16.0 (SPSS Inc.) kullanılmıştır.

BULGULAR Çalışmaya alınan hastaların %84,1’i (n=37) erkek, %15,9’ u (n=7) kadın; yaş ortalaması 54,1 (min: 9maks: 95) yıl idi. Hastaların tanısı fiziksel inceleme ile konuldu (Şekil 1). Lezyonun bulunduğu bölgede ağrı, hassasiyet, eritem, ekimoz, nekroz, ısı artışı, ödem, endurasyon, ekimotik ya da eritemli zeminde bül, cilt altı krepitasyon ve ateş bulgularından bir ya da birkaçının bir arada bulunduğu hastalara klinik olarak nekrotizan fasiit tanısı konuldu. En sık görülen risk faktörü %52,2 oranıyla diyabetes mellitus (DM) iken, bunu %9 oranıyla travma ve yine %9 oranıyla önceden geçirilmiş operasyon izledi. İki (%4,5) hastada birden fazla risk faktörü mevcutken, beş (%11,4) hastada herhangi bir risk faktörü saptanamadı. Altta yatan malignite, parapleji, gebelik, intramusküler enjeksiyon öyküsü birer hastada tespit edildi. Enfeksiyon bölgele-

ri irdelendiğinde en sık alt ekstremitede (n=14) ve perianal bölgede (n=13), daha sonra sırasıyla ürogenital (n=7), üst ekstremitede (n=5) ve gluteal bölgede (n=1) tutulum izlendi (Şekil 2).

Hastaların tedavi öncesi ve/veya tedavi sırasında alınan derin doku kültürlerinin %63,6 oranında üreme tespit edildi. On iki (%27,3) olguda polimikrobiyal üreme olurken, 4 (%9) olguda metisilin duyarlı Staphylococcus aureus (MSSA), 4 (%9) olguda Streptococcus spp., 3 (%6,8) olguda ise Pseudomonas aeruginosa üredi. Polimikrobiyal üremelerde Enterobacter spp., Aeromonas spp., Escherichia coli, Proteus spp., Klebsiella spp., Enterococcus spp., MRSA ve metisilin dirençli koagülaz negatif stafilokok (MRKNS) tespit edilen mikroorganizmalardı.

Hastaların yatırılarak takip edildiği klinikler Tablo 1’de gösterildi. Tüm hastalara empirik geniş spektrumlu antibiyoterapi ilk 24 saatte uygulandı. En sık kullanılan antibiyotikler sırasıyla karbapenemler (meropenem ya da imipenem) ve beta laktambeta laktamaz inhibitörleri (piperasilin-tazobaktam ya da sefaperazon-sulbaktam) idi. Hastaların 27’sine (%61,4) cerrahi debridman, drenaj ve/veya irrigasyon uygulandı. Hiçbir hastaya amputasyon yapılmadı. Beş olguda defektler kısmi kalınlıkta deri grefti ile örtülürken üç olguda lokal flep uygulandı. On bir (%25) hasta kaybedildi.

TARTIŞMA Nekrotizan fasiit, deri, deri altı doku ve yüzeyel fasiyayı tutan, hızla invazyon ve yayılım sonucu sistemik toksisite belirti ve bulgularıyla kendini gösteren, mortalitesi yüksek bir enfeksiyon hastalığıdır. Yapılan çalışmalarda 50-60 yaşlarında ve erkeklerde daha fazla görüldüğü ortaya konulmuştur.[4-7] Çalışmamız sonucunda da yaş ortalaması 54,1 ve erkeklerde daha fazla oranda olduğu saptanmıştır. Nekrotizan fasiitin patogenezinde önemli faktörlerden biri konaktır. İleri yaş, DM, immünsupresyon, alkolizm, travma, operasyon, yanık, ateroskleroz, obezite, kronik karaci-

%2,3

%15,9 %31,8 %20,5

%29,5

Şekil 1. Sol ayakta nekrotizan fasiit.

30

Şekil 2. Enfeksiyon bölgelerinin dağılımı.

Ocak - January 2011

Nekrotizan fasiit tanısıyla izlenen 44 olgunun klinik değerlendirmesi

Tablo 1. İzlendiği kliniklere göre hastaların dağılımı Klinik

Sayı Yüzde

Plastik ve rekonstrüktif cerrahi 10 Anestezi yoğun bakım ünitesi 7 Üroloji 6 Genel cerrahi 4 Enfeksiyon hastalıkları ve klinik mikrobiyoloji 4 Ortopedi 4 Kadın doğum 3 Genel dahiliye 2 Endokrinoloji ve metabolik hastalıklar 2 Kalp-damar cerrahisi yoğun bakımı 2 Toplam 44

22,8 15,9 13,7 9,1 9,1 9,1 6,8 4,5 4,5 4,5 100

ğer hastalığı nekrotizan deri yumuşak doku enfeksiyonlarında risk faktörleridir.[1,3,4,6,8] Çalışmamızda DM %52,2 oranında en sık rastlanan risk faktörü olarak ortaya konulmuş, bunu travma ve operasyonlar izlemiştir. Liu ve arkadaşları[7] nekrotizan fasiit tanısıyla 87 hastanın incelendiği çalışmalarında benzer olarak hastaların %50,6’sında risk faktörü olarak DM tespit ettiklerini bildirmişlerdir. Çeşitli çalışmalarda nekrotizan deri yumuşak doku enfeksiyonlarının oluşumunda DM (%12-70) en önemli risk faktörü olarak yer almaktadır.[6] Çalışmamızda tespit ettiğimiz diğer risk faktörleri de güncel literatürle uyumludur.

Nekrotizan fasiit, sıklıkla gövde, ekstremiteler (özellikle alt ekstremite) ve perine bölgesinde görülmektedir.[1,3,5] Çalışmamızda en sık tutulan bölgelerin alt ekstremite ve perianal bölge olduğu tespit edilmiştir. Farklı çalışmalarda tutulan bölge sıklıkları hasta gruplarına ve risk faktörlerine göre değişmektedir. Özgenel ve arkadaşları[4] en sık anorektal bölgede tutulum saptarken Demir ve arkadaşları[5] çalışmasında perine bölgesi en sık tutulan bölge olarak bildirilmiştir. Benzer olarak Canbaz ve arkadaşları[6] Fournier gangrenli hastaları değerlendirdikleri çalışmalarında anorektal bölgenin en sık tutulduğunu tespit etmişlerdir. Liu ve arkadaşları[7] çalışmasında ise bizim çalışmamızda olduğu gibi alt ekstremite nekrotizan fasiitin en sık görüldüğü yer olarak bildirilmiştir.

Nekrotizan fasitte izole edilen mikroorganizmaların tipi ve sayısı değişkenlik gösterebilmektedir. Monomikrobiyal formda Streptococcus pyogenes, Staphylococcus aureus ve diğer stafiloloklar, Vibrio vulnificus, Aeromonas hydrophila, anaerobik (örn. Peptostreptococcus spp.) ve diğer streptokoklar yer alırken polimikrobiyal formda çok çeşitli anaerobik ve aerobik mikroorganizmalar izole edilebilir.[1,2,9] Çalışmamızda polimikrobiyal etken üremeleri ön plandayken anaerop kültür yapılmadığı için hiç anaerobik mikroorganizma izole edilememiştir. Bu da çalışmamızı kısıtlayıcı bir faktördür. Yine hasta gruplarına ve risk faktörlerine göre değişmekle birlikte diğer çalışmalarCilt - Vol. 17 Sayı - No. 1

da da bizim çalışmamıza benzer etkenler bildirilmiştir.

[5-7,10] Farklı olarak Özgenel ve arkadaşları[4] yara kültürlerinde en sık (%50) Pseudomonas aeruginosa üremesi saptarken bizim çalışmamızda olguların sadece %6,8’inde Pseudomonas aeruginosa izole edilmiştir.

Liu ve arkadaşları[7] ise en sık etken olarak Klebsiella pneumoniae’yi bildirmişlerdir. Nekrotizan fasiit tedavisinde tüm etken patojenler göz önüne alınarak en kısa sürede geniş spektrumlu tekli ya da kombine antimikrobiyal tedavi başlanmalıdır. Kültür alındıktan sonra hızlı bir şekilde empirik başlanan bu tedavi rejimlerinde anaerop mikroorganizmalara da etkili antimikrobiyaller yer almalıdır.[1-3] Karbapenemler (imipenem, meropenem, ertapenem), ampisilin-sulbaktam ya da piperasilin-tazobaktam + klindamisin, geniş spektumlu sefalosporinler + metronidazol ya da klindamisin vb. antimikrobiyaller empirik tedavide önerilmektedir.[1,2] Kültür sonuçlarına göre antimikrobiyal tedavi yeniden düzenlenebilir. Çalışmamızda önerilere paralel olarak antimikrobiyal tedavide en sık karbapenemlerin (meropenem ya da imipenem) ve beta laktam-beta laktamaz inhibitörlerinin (piperasilintazobaktam ya da sefaperazon-sulbaktam) kullanıldığı tespit edilmiştir. Nekrotizan fasiit tedavisinin en önemli kısmı erken ve yaygın cerrahi eksplorasyon ve tüm nekrotik dokuların kanlanmanın iyi olduğu seviyeye kadar debridmanıdır.[11] Enfekte bölgenin ilerlemesi, çok yaygın ve dirençli olması durumlarında birden fazla debridman önerilmektedir.[6,11,12] Yaygın cerrahi eksplorasyon ve tutulan tüm dokuların radikal uzaklaştırılması ve aynı seansta bol yıkama yaradaki ilerlemeyi durdurmaya yardımcı olur.[11] Nekrotizan fasiitin erken tanısı ve hastalara hastaneye yattıktan sonraki ilk 24 saat içinde erken cerrahi debridman yapılması mortaliteyi azaltabilen en önemli yaklaşımdır.[12] Kuşkulu nekrotizan deri yumuşak doku enfeksiyonlarında zaman kaybetmeden ameliyat kararı verilmelidir. Özellikle hastada sistemik toksisite bulguları, hipotansiyon, ateş, antibiyoterapiye rağmen hızlı bir ilerleme, enfekte bölgede ekimoz, nekroz, hemorajik bül, ağrı ya da hipoestezi ve gaz varsa hastaya derhal cerrahi dedridman uygulanmalıdır.[1] Debridmanlarda özellikle avasküler dokular alınmalı ve kanlanan dokuya kadar hasarlı ve nekrotik dokular uzaklaştırılmalıdır. Enfeksiyonun tümüyle gerilemesi ve granülasyon dokusunun gelişmesiyle beraber yaralar deri grefti ya da flep ile kapatılabilir. Yaşamsal tehdit söz konusu olduğunda ekstremite ya da organ ampüte edilmelidir.[11] Çalışmamızda hastaların çoğunluğuna hızlı ve uygun cerrahi girişimlerin uygulandığı tespit edilmiştir. Hastanemizde gerek enfeksiyon hastalıkları ve klinik mikrobiyoloji servisinde gerekse tüm cerrahi birimlerde ve yoğun bakımlarda izlenen nekrotizan deri yumuşak doku enfeksiyonu bulunan hastalarda multidisipliner bir yaklaşım söz konusudur. Bölümümüz kendi ya da konsültasyon hastalarını günlük 31

Ulus Travma Acil Cerrahi Derg

olarak klinik ve laboratuvar olarak izlemekte, antibiyoterapi rejimlerini düzenlemektedir. Nekrotizan fasiitin yerleşimine ve gerektirdiği cerrahi tekniğe (flep vb) göre de farklı cerrahi bölümlerde hastalarımız takip ve tedavi edilmiştir. Çalışmamız sonucunda mortalite oranı %25 olarak saptanmıştır. Ülkemizde yapılan çalışmalarda mortalite oranları %14,3-33,3 arasında değişmektedir.[5,6,10] Light ve arkadaşları[8] nekrotizan fasiitli hastaların uzun dönem sonuçlarını bildirdikleri çalışmalarında mortalite oranlarını çalışmamızla aynı oranda (%25) bildirmişlerdir. Klasik bilgi olarak %80’lere ulaşabilen mortalite oranlarının bizim ve benzer çalışmalarda bu düzeye ulaşmaması, günümüzde hızlı bir yaklaşımla uygun antibiyoterapilerin uygulandığını ve erken geniş cerrahi debridmanların yapıldığını düşündürmektedir.

Sonuç olarak, nekrotizan fasiit, erken tanı, erken geniş cerrahi debridman ve geniş spektrumlu antibiyoterapi gerektiren, hızlı ilerleyen ve mortal seyredebilen bir hastalıktır. Hastalarda altta yatan hastalıklar ve risk faktörleri mutlaka değerlendirilmelidir. Bu çalışmayla nekrotizan fasiitin hastanemizdeki izlem sonuçları ortaya konmaya çalışılmıştır.

Teşekkür Bu çalışma Akdeniz Üniversitesi Bilimsel Araştırma Projeleri Koordinasyon Birimi tarafından desteklenmiştir.

KAYNAKLAR 1. Stevens DL, Bisno AL, Chambers HF, Everett ED, Dellinger P, Goldstein EJ, et al. Practice guidelines for the diagnosis

32

and management of skin and soft-tissue infections. Clin Infect Dis 2005;41:1373-406.

2. Swartz MN, Pasternack MS. Cellulitis, necrotizing fasciitis, and subcutaneous tissue infections. In: Mandell GL, Bennett JE, Dolin R, editors. Principles and practice of infectious diseases. 7th ed. New York: Churchill Livingstone; 2010. p.

1289-312.

3. Yamazhan T. Yumuşak dokunun nekrotizan enfeksiyonları. In: Gündeş S, editör. Deri, yumuşak doku, eklem ve kemik enfeksiyonları. Ankara: Bilimsel Tıp Yayınevi; 2008. p. 277-85.

4. Ozgenel GY, Akin S, Kahveci R, Ozbek S, Ozcan M. Clinical evaluation and treatment results of 30 patients with necrotizing fasciitis. Ulus Travma Acil Cerrahi Derg 2004;10:110-4.

5. Demir CY, Kunt A. Nekrotizan yumuşak doku enfeksiyonları: klinik sonuçlarımız. İnönü Üniversitesi Tıp Fakültesi Dergisi 2003;10:187-90.

6. Canbaz H, Cağlikülekçi M, Altun U, Dirlik M, Türkmenoğlu O, Taşdelen B, et al. Fournier’s gangrene: analysis of risk factors affecting the prognosis and cost of therapy in 18 cases. Ulus Travma Acil Cerrahi Derg 2010;16:71-6.

7. Liu YM, Chi CY, Ho MW, Chen CM, Liao WC, Ho CM, et al. Microbiology and factors affecting mortality in necrotizing fasciitis. J Microbiol Immunol Infect 2005;38:430-5.

8. Light TD, Choi KC, Thomsen TA, Skeete DA, Latenser BA, Born JM, et al. Long-term outcomes of patients with necrotizing fasciitis. J Burn Care Res 2010;31:93-9.

9. Napolitano LM. Severe soft tissue infections. Infect Dis Clin North Am 2009;23:571-91.

10. Erdogan O, Arıcı C, Colak T, Yıldız S, Ogus M, Akaydın M. Necrotizing soft tissue infections and the risk factors for mortality. Ulus Travma Acil Cerrahi Derg 1999;5:184-8.

11. Ağır H. Doku grefti: Endikasyon ve teknikleri. In: Gündeş S, ed. Deri, yumuşak doku, eklem ve kemik enfeksiyonları.

Ankara: Bilimsel Tıp Yayınevi; 2008. p. 153-79.

12. Terzi C. Yumuşak doku infeksiyonlarında mortaliteyi etkileyen faktörler. Ankem Derg 2005;19:97-100.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):33-40

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2011.99083

The practice of plastic surgery in emergency trauma surgery: a retrospective glance at 10,732 patients Plastik cerrahinin acil travma cerrahisindeki yeri: 10,732 hastaya retrospektif bir bakış Semra HACIKERİM KARŞIDAĞ,1 Özay ÖZKAYA,2 Kemal UĞURLU,1 Lütfü BAŞ1

BACKGROUND

AMAÇ

The number of patients applying to the emergency Plastic and Reconstructive Surgery outpatient clinic varies considerably depending on the sociocultural profiles of societies.

Due to the abundance of anatomic regions comprising the targets of this field of specialization, plastic surgery is continuously gaining in importance in emergency traumatology.

Acil plastik cerrahi polikliniğine başvuran hasta sayısı toplumların sosyokültürel özelliklerine bağlı olarak ciddi farklılıklar göstermektedir. Çalışma bölgesinin yaygınlığı nedeni ile de plastik cerrahinin acil travmatolojideki önemi giderek artmaktadır.

METHODS

Bu çalışmada, 2000-2004 yılları arasında Şişli Etfal Eğitim ve Araştırma Hastanesi Acil Plastik Cerrahi polikliniğine başvuran 10,732 hastanın etyoloji, cinsiyet, yaş dağılımı, yaralanma özellikleri ve tedavileri retrospektif olarak değerlendirildi.

In this study, 10,732 patients admitted to the outpatient clinic of Emergency Plastic Surgery in Şişli Etfal Training and Research Hospital were evaluated retrospectively regarding etiology, sex, age distribution, injury characteristics, and treatment.

RESULTS

GEREÇ VE YÖNTEM

BULGULAR

While 64% of all patients had forearm and hand injuries, 28% had maxillofacial injuries, and 8% had tissue defects.

There was a male: female ratio of 4: 1, and the mean age of all patients was 22.9 years. The mean age of patients (males 81%) admitted with upper extremity injuries was 22.3 years. Most of the upper extremity injuries were due to glassware cuts (33%). The mean age of patients admitted with maxillofacial trauma was 23.2 years. Among the patients with head-and-neck injuries, the most frequent cause of trauma was traffic accidents (38%).

Başvuran hastaların %64’ünde ön kol ve el yaralanmaları, %28’inde maksillofasyal yaralanma ve %8’inde doku defektleri vardı. Hastalarda 4/1 oranında erkek baskınlığı vardı, yaş ortalaması 22,9 idi. Üst ekstremite yaralanması ile başvuran hastaların %81’i erkek ve yaş ortalamaları 22,3 olarak bulundu. Üst ekstremite yaralanması olan hastalarda en sık etyolojik neden, %33 ile cam kesisi idi. Maksillofasyal travma nedeniyle başvuran hastaların yaş ortalaması 23,2 olarak saptandı. Baş-boyun yaralanması olan hastaların %38’inde travma sebebi trafik kazası idi.

CONCLUSION

SONUÇ

Regarding the frequency and characteristics of the patients treated, we suggest that plastic surgery shows a progressively increasing significance and widening field of practice in emergency traumatology and, as no similar study currently exists, ours will contribute significantly to the literature.

Tedavi edilen hasta sıklığı ve özelliği göz önüne alındığında plastik cerrahinin acil travmatolojideki yeri ve öneminin her geçen gün artmakta olduğunu ve benzer bir çalışma olmadığı için bu çalışmanın literatüre katkısı olacağını düşünmekteyiz.

Key Words: Emergency; plastic surgery; trauma surgery.

Anahtar Sözcükler: Acil; plastik cerrahi; travma cerrahisi.

Department of Plastic Reconstructive and Aesthetic Surgery, Şişli Etfal Training and Research Hospital, Istanbul; 2 Department of Plastic Reconstructive and Aesthetic Surgery, Yalova State Hospital, Yalova, Turkey.

1

Şişli Etfal Eğitim ve Araştırma Hastanesi, Plastik Rekonstrüktif ve Estetik Cerrahi Kliniği, İstanbul; 2 Yalova Devlet Hastanesi, 1. Plastik Rekonstrüktif ve Estetik Cerrahi Kliniği, Yalova.

1

Correspondence (İletişim): Özay Özkaya, M.D. Okmeydanı Eğitim ve Araştırma Hastanesi, Plastik Rekonstrüktif ve Estetik Cerrahi Kliniği, Şişli, İstanbul, Turkey.

Tel: +90 - 212 - 221 77 77 e-mail (e-posta): oozozay@yahoo.com

33

Ulus Travma Acil Cerrahi Derg

In the literature, few studies have focused on the role of plastic and reconstructive surgery in trauma centers.[1] According to the organization of some hospitals, plastic and reconstructive surgery particularly provides closure of tissue defects, while in others, surgery in the upper extremities and the head-and-neck region is also intensively performed. Progresses in microsurgery and their adaptation to trauma surgery have contributed considerably to the increasing significance of plastic and reconstructive surgery in trauma surgery. In two studies done in Israel, it was stressed that plastic surgery has an important role in large-scale injuries related to terrorist attacks.[2,3] In addition, a study was published reporting the role of plastic surgery in repair of tissue defects following aircraft injuries.[4] A report from the United States stressed the critical importance of plastic surgery in emergency conditions requiring reconstructive interventions in all regions of the body.[1] With a frequency of 38%, upper extremity injuries constitute the largest patient group in emergency plastic surgery, followed in frequency by head-and-neck injuries (25%), lower extremity injuries (25%) and chest trauma (12%).[1] As the forearm and hand have their unique anatomies due to their complex functions, their injuries are also commonly combined injuries.[5] Likewise, maxillofacial traumas vary regarding their etiologies and the fractured facial bones, and various treatment protocols are required depending on these factors.

Traumatic injuries significantly affect the patients socially, functionally and financially. Injuries within the field of practice of emergency plastic surgery, unless causing prominent hemodynamic instabilities as in cases of amputations and main artery injuries, are usually not life-threatening. However, injuries related to plastic surgery may result in considerable disability and loss of life quality.[6,7] Our review of the literature revealed a few studies in which the issues within the field of interest of emergency plastic surgery, such as upper extremity surgery, head-and-neck traumas, and soft tissue traumas, were examined individually; however, no publication involved every field of practice of emergency plastic surgery. Therefore, retrospectively reviewing 10,732 patients admitted to the Emergency Plastic Surgery Department in Şişli Etfal Training and Research Hospital between 2000 and 2004, we aimed to construct a reference study stressing the significance of emergency plastic and reconstructive surgery in trauma centers.

MATERIALS AND METHODS A total of 10,732 patients admitted to and treated in the Emergency Plastic Surgery Clinic in Şişli Etfal Training and Research Hospital between 2000 and 2004 were evaluated retrospectively regarding their 34

age and sex distributions, etiology and type of injury, and treatment protocols. The age distributions of patients according to gender were investigated. The patients were evaluated in three major classes according to their cause of admission, namely upper extremity injuries, head-and-neck trauma and soft tissue injuries.

Upper extremity injuries: The age and sex distributions of 6,869 patients admitted with upper extremity injuries were studied, and the injuries were evaluated in 6 subgroups according to etiology, namely glassware cuts, falls, traffic accidents, household accidents, labor accidents, and miscellaneous (e.g., stabbing and bites). The distribution of etiology in the different age groups was investigated. Patients admitted with glassware cuts were classified as accidental injury and self-inflicted trauma during moments of aggression. In addition, injuries were studied in 4 groups according to the wound types, namely, isolated skin injuries, isolated tendon injuries, fractures-dislocations, and combined injuries (nerve, blood vessel, and tendon incisions, and bone pathologies). The pathologies developing with different etiologies were analyzed.

The patients were classified according to the treatment protocols as those treated in the emergency wards with local anesthesia and those treated in operation theaters under general anesthesia. Treatments in the emergency wards were classified as those accomplished under emergency conditions and those requiring secondary interventions under elective conditions.

Likewise, patients treated in the operation theater were studied in groups such as combined injuries (e.g., tendon, nerve and vascular structure repair), replantation, fractures, open fasciotomy, major artery injuries, and miscellaneous.

Head-and-neck injuries: A total of 3005 patients admitted with head-and-neck trauma were evaluated regarding age and sex distributions. The patients were classified according to their cause of admission as traffic accidents, sports injuries, game injuries, injuries during daily activities, assaults, falls, and labor injuries. The distribution of the etiologic factors in age groups was studied. The head-and-neck injuries were evaluated in two groups according to the injured tissue contents as soft tissue injuries and bone fractures.

Accompanying additional pathologies and systemic injuries were also investigated.

The cases with fractures were classified according to sex and etiology. Fractures were studied according to their anatomic locations as mandible, zygomatic bone, orbit base, and maxillary, nasal and frontal fractures. The mandibular fractures were classified further according to the fracture localization as symphysisparasymphysis, condylar, angular, trunk, ramus, and coronoid fractures. Likewise, maxillary fractures were Ocak - January 2011

The practice of plastic surgery in emergency trauma surgery

classified as Le Fort I, II, III and sagittal fractures.

Patients admitted with head-and-neck injuries were studied in two groups according to time of treatment in the early and late periods, and factors influencing the time of treatment were investigated. Furthermore, treatment modalities of patients with fractures were examined.

Soft tissue injuries: Age and sex distributions of 858 patients admitted with soft tissue injuries were evaluated. The patients were studied via classification according to their etiologies, namely, falls, traffic accidents, gunshot wounds, burns, and infections. The distributions of etiologies by age groups were examined.

The injury sites, the anatomic distributions of lower extremity defects, and the anatomic distributions of defects according to etiologies were studied. Coexistence of defects with fractures and the treatment modalities of fractures were investigated, and finally, the treatment modalities of defects located on the trunk and lower extremities were examined.

RESULTS Between 2000 and 2004, a total of 10,732 patients were admitted under emergency conditions to the Emergency Plastic Surgery Clinic in Ĺ&#x17E;iĹ&#x;li Etfal Training and Research Hospital. Of the patients, 7902 (73.6%) were males and 2830 (26.4%) were females.

The mean age of the patients was 22.9 years (range: 2 months-93 years). Analysis of the age distribution of patients revealed that 64% of the patients were aged 11-35 years, with a male predominance. The second most common age group was 0-10 years, with nearly equal gender distribution. We observed that the male predominance was most common among patients aged 21-35 years, while there was a progressive decline in male predominance with increasing age above 36 years. The age distributions in both sexes are displayed in Table 1.

The cause of admission was upper extremity injuries in 6869 patients (64%), head-and-neck injuries in 3005 patients (28%), and soft tissue traumas in 858 patients (8%). While males with upper extremity injuries demonstrated a 4-fold predominance over females, the M:F ratio was approximately 1.5:1 among the cases of head-and-neck and soft tissue injuries (Table 2).

Upper extremity injuries: Of the 6869 patients admitted with upper extremity injuries, 5564 (81%) were males and 1305 (19%) were females (Table 2).

The mean age of the patients was 22.3 years (range: 2 months-88 years). Evaluation of the distributions of upper extremity injuries according to sex and age groups (Table 3) revealed that 70% of the patients were aged 11-35 years. This age group was followed in frequency by the 0-10 years group. The frequenCilt - Vol. 17 SayÄą - No. 1

cy decreased progressively with age above 35 years.

There was also a prominent male predominance among patients aged 11-35 years, who constituted the group with the highest admission rate.

The upper extremity injuries were evaluated in 6 groups according to etiology, namely, glassware cuts, falls, traffic accidents, household accidents, labor accidents, and miscellaneous injuries (e.g., stabbing and bites). While 2267 patients (33%) were admitted with the complaints of glassware cuts, the cause of admission was falls in 1442 patients (21%), traffic accidents in 824 patients (12%), household accidents in 412 patients (6%), and labor accidents in 687 patients (10%) (Table 4).

Among the patients, 70% of those admitted with glassware cuts were aged 16-35 years, while 54% of those admitted with falls were 21-35 years, and 22.5% of them were aged 0-10 years. Among patients admitted due to traffic accidents, 68% were aged 16-50 years, while 67% of those with household accidents were aged 0-10 years, and 84% of those with labor accidents were aged 16-50 years.

Patients with self-inflicted trauma due to punching glass during a bout of aggression constituted 76% of all cases of glassware cuts. Among the patients punching glass, 84% were males, and 79% were aged 16-35 years. Isolated skin cuts, isolated tendon cuts, fractures-dislocations, and combined injuries (blood vessel, nerve, tendon, and bone) constituted 38%, 27%, 14%, and 21% of the patients, respectively (Table 5).

In the cases of glassware cuts, combined injuries were found in 46%, and isolated tendon cuts were present in 32% of the patients. Among the patients admitted due to traffic accidents, 53% had isolated skin incisions.

Isolated cutaneous incisions constituted 32% and combined incisions 31% of the patients admitted with labor accidents. While the fall cases had comparable rates of isolated skin cuts, isolated tendon cuts, and fractures, the combined injury rates were very low. While 43% of the household accidents were isolated cutaneous incisions, 28% of them were combined injuries.

The cases were studied in two groups according to the treatment being accomplished in emergency conditions or requiring secondary treatment under elective conditions. The treatments were accomplished during the initial admission in 4396 patients (64%).

These patients were also grouped according to where the treatment was undertaken, namely, those treated with local anesthesia in the emergency ward and those treated under general anesthesia in the operation theater. Surgery under general anesthesia in the operation theater was required under emergency conditions on the first admission in 187 patients (0.37%).

Analysis of the types of injuries in the 187 patients 35

Ulus Travma Acil Cerrahi Derg

operated under general anesthesia in the operation theater on first admission revealed that 64 patients (34%) were treated for combined injuries, while 38 (20%) required replantation, 26 (14%) required fixation for serious fractures, 21 (11%) required open fasciotomy, and 17 (9%) underwent repair of major artery injuries.

Head-and-Neck injuries: The 3005 patients admitted with maxillofacial trauma constituted 28% of all patients. There were 1202 females and 1803 males, with the male:female ratio being 1.5:1.

At the time of the injuries, the mean age of patients was 23.2 (range: 1-93) years. While 511 patients (17%) were younger than 10 years, 1683 (56%) were 10-35 years, 661 (22%) were 35-50 years, and 150 (5%) were older than 50 years (Table 6).

Traffic accidents constituted 38% of all cases with head-and-neck injuries. In the first 10 years of life, game injuries (35%) and falls (29%) were the most important causes of trauma. In the group aged 10-20 years, sports injuries were the most common etiology, at a rate of 30%, followed in frequency by traffic accidents, at a rate of 26%, and injuries during games and daily activities in 23% of the cases. Traffic accidents constituted the most frequent cause of injuries in the group aged 20-50 years. The etiologic factors were more equally distributed in the group aged over 50 years, with 27% of the patients being injured during daily activities, followed by falls, assaults, traffic accidents, and labor accidents, at rates of 23%, 18%, 15%, and 12%, respectively (Table 7).

While 68% of the 3005 patients admitted with head-and-neck injuries had soft tissue injuries only, bone fractures were present in 32%. In 41% of the 961 patients admitted with bone fractures, the fractures were accompanied by soft tissue injuries. In 21.4% of the cases, the head-and-neck injuries were accompanied by other problems such as traumas of the head, chest, abdomen, or extremities.

Fractures were present in 37.2% of the males and 24.1% of the females, while 51.8% of the traffic accidents with injuries in the head-and-neck region resulted in fractures. Furthermore, fractures occurred in 40.2% of the patients admitted due to assaults, 21.4% of the labor accidents, 18.6% of the falls, 12.3% of the sports injuries, and 11.8% of the patients injured during games and daily activities (Table 8).

While fractures were more commonly encountered in patients aged 20-50 years, at a rate of 74%, in patients aged <10 or >50 years, soft tissue injuries were prominent.

In the 961 patients with fractures, there were a total of 1883 fractures. Among these 961 patients, 67.6% 36

(649 patients) had multiple and 32.4% (312 patients) had solitary fractures.

Anatomic classification of the fractures revealed that 921 fractures (48.9%) were located in the mandible, followed in frequency by the zygomatic bone (364 fractures, 19.3%), base of orbit (299 fractures, 15.9%), nose (122 fractures, 6.5%), maxilla (113 fractures, 6%), and frontal bone (64 fractures, 3.4%) (Table 9).

The mandibular fractures were distributed according to fracture location as 408 (44.3%) in the symphysis-parasymphysis, 236 (25.6%) in the condyle, 138 (15%) in the angulus, 102 (11.1%) in the trunk, 29 (3.1%) in the ramus, and 8 (0.9%) coronoid fractures (Table 10).

Among the maxillary fractures, 45 (39.8%) were in the form of Le Fort II, 43 (38%) Le Fort I, and 17 (15%) Le Fort III, and 8 (7.2%) were sagittal fractures.

Of the 2044 patients admitted with soft tissue injuries, 91.3% (1866 patients) were followed up after their initial treatments, while in the remaining 178 (8.7%), fatal pathologies were controlled primarily, with the soft tissue repairs being deferred to a later date.

In the 921 patients with mandibular fractures, 63 (6.8%) were followed without any open or closed reductions. While 512 patients (55.6%) were treated with closed reduction, 356 (38.6%) underwent open reduction and rigid fixation.

While 298 (81.8%) of the zygomatic bone fractures and 258 (86.2%) of the orbital fractures were treated with open reduction, the remaining cases were only followed. Among the maxillary fractures, open reduction was performed in 62 (54.6%) and closed reduction in 24 (21.2%) of the cases, while the remaining 27 (24.2%) were followed without any intervention.

Closed reduction was the mode of treatment in 115 (94.2%) of the nasal fractures, and 35 (55%) of the frontal bone fractures were followed without any intervention.

Soft tissue traumas: The 858 patients admitted with soft tissue traumas constituted 8% of all patients (Table 2). Among these patients, 323 (37.7%) were females and the remaining 535 (62.3%) were males.

The mean age of the patients was 26.65 years (range: 6 months-90 years). The distributions of patients among age groups are displayed in Table 11.

Analysis of the causes of soft tissue injuries revealed that 66.2% of the cases were traffic accidents, followed in frequency by burns (19.5%), gunshot wounds (5.6%), falls (4.7%), and infections (4%). The patients admitted with infectious wounds had uncontrolled diabetes.

Ocak - January 2011

The practice of plastic surgery in emergency trauma surgery

Table 1. Age distribution of patients according to gender Age group

Males

M/F

Total

689 555 861 456 240 29 2830

982 1797 3695 1028 456 44 7902

1.3 3.2 4.3 2.3 1.9 1.5 2.8

1571 2352 4556 1484 696 73 10732

Upper extremity injuries Head-and-Neck injuries Soft tissue injuries Total

Distribution of etiologies among age groups

Glassware Falls Traffic Household Labor Miscel- Total cuts accidents accidents accidents laneous

0-10 11-15 16-20 21-35 36-50 51↑ Total

153 85 608 988 303 130 2267

Table 7.

325 53 164 780 43 77 1442

75 124 127 325 105 68 824

278 48 17 21 20 28 412

- 28 116 308 154 81 687

54 885 58 396 112 1144 868 3290 45 670 100 484 1237 6869

179 83 81 39 41 423

61 95 636 327 23 1142

71 107 247 81 6 512

52 21 171 90 27 361

- 18 121 79 18 238

148 34 67 45 35 329

511 358 1325 661 150 3005

Females Males M/F Total 1305 1202 323 2830

5564 1803 535 7902

4.26 6869 1.50 3005 1.65 858 2.79 10732

Table 6.

Isolated Isolated Fracture Combined Total skin tendon dislocation

Glassware Cuts 451 Falls 527 Traffic Accidents 435 Household Accidents 178 Labor Accidents 217 Other (stabbing, bites, etc.) 802 Total 2610

727 416 244 96 133 239 1855

153 478 103 23 126 179 962

1036 21 42 115 211 17 1442

592 144 51 61 63

1142 361 238 329 512

51.8 40.2 21.4 18.6 12.3

50 961

423 3005

11.8 32

Females

Males

M/F

Total

364 238 376 163 150 14 1305

521 1302 2914 507 301 19 5564

1.4 5.5 7.8 3.1 2.0 1.35 4.26

885 1540 3290 670 451 33 6869

The age and sex distributions of patients admitted with head-and-neck injuries Females

Males

M/F

Total

255 250 277 250 110 34 17 9 1202

256 400 451 357 249 46 30 14 1803

1 1.60 1.61 1.42 2.26 1.35 1.76 1.56 1.50

511 650 728 607 359 80 47 23 3005

0 - 10 11 - 20 21 - 30 31 - 40 41 - 50 51 - 60 61 - 70 71↑ Total Table 9.

Number of cases Total Percentage with fractures number

Traffic accidents Assaults Labor accidents Falls Sports injuries Injuries during games /daily activities Total

2267 1442 824 412 687 1237 6869

The distribution of fractures according to etiologies

Age and sex distributions of patients admitted with upper extremity injuries

0 - 10 11 - 20 21 - 35 36 - 50 51 - 70 71 ↑ Total

Classification of the pathologies according to the etiology in upper extremity injuries

Table 8.

The distribution of etiologies among age groups in head-and-neck injuries

Injuries Traffic Sport Assaults Labor Falls Total during accidents injuries

accidents games and daily activities

<10 years 10 - 20 20 - 35 35 - 50 50 + Total

Table 5.

Table 3.

Distribution of causes of admission according to gender

Females

0-10 11-20 21-35 36-50 51-70 71 ↑ Total

Table 4.

Table 2.

Percentage of fractures according to anatomic locations

Fracture location

Number

Percentage

Mandible Zygomatic bone Orbit Maxilla Nose Frontal bone

921 364 299 113 122 64

48.9 19.3 15.9 6 6.5 3.4

Table 10. Distribution of the anatomic locations of

mandibular fractures and frequencies (%)

Table 11. The distribution of patients admitted with soft tissue traumas by age groups

Table 12. The sex distributions of the causes of soft

tissue traumas

Fracture location

Symphysis-parasymphysis Condyle Angulus Trunk Ramus Coronoid

Number

Percentage

408 236 138 102 29 8

44.3 25.6 15 11.1 3.1 0.9

Table 13. Causes and age distributions of soft tissue

injury patients

0 - 10 11 - 20 21 - 30 31 - 40 41 - 50 51 - 60 61 - 70 70 + Total

Males

M/F

Total

70 67 64 48 29 28 21 6 323

105 95 98 81 66 50 29 11 535

1.50 1.41 1.53 1.69 2.27 1.79 1.38 1.83 1.65

175 162 162 129 95 78 50 17 858

Traffic accidents 182 Burns 81 Gunshot wounds 19 Falls 23 Infections 18 Total 323

Table 14. The etiologic distribution of tissue injury sites

Burns

Traffic accidents

Falls

Gunshot wounds

Infections

Total

0 - 5 6 -15 16-35 36-50 51 + Total

19 27 14 13 8 81

11 14 24 57 89 172 24 78 34 65 182 386

4 7 8 7 9 3 2 1 - - 23 18

- 2 2 7 8 11 5 6 4 3 19 29

- - - - 2 1 7 7 9 8 18 16

85 167 318 153 145 858

Lower extremities Trunk Combined Total

28 25 9 10 14 86

Females

Traffic Burns Falls Gunshot Infections Total accidents

wounds 392 104 72 568

92 71 4 167

26 13 2 41

33 15 - 48

32 - 2 34

575 203 80 858

Table 16. Anatomic distribution of the lower extremity defects by frequency (%)

Table 17. Anatomic distributions of the lower extremity defects according to etiology

Fracture location

Thigh Knee Crux Ankle Heel Dorsum of the foot Base of the foot Combined Total

Number

Percentage

46 7 197 33 72 151 52 97 655

7 1 30 5 11 23 8 15 100

Thigh Knee Crux Ankle Heel Dorsum of foot Base of foot Combined Total

Males

M/F

Total

386 86 29 18 16 535

2.12 1.06 1.53 0.78 0.89 1.65

568 167 48 41 34 858

Table 15. Anatomic locations of defects by frequency (%)

Lower extremities Trunk Total

Number

Percentage

655 283 938

70 30 100

Among the traffic accidents, 46% occurred in patients aged 169 5 18 46 35 years, while 59% of the burns oc- 1 - 7 9 11 3 197 curred in patients aged 0-15 years, - 2 - 33 2 9 - 72 and 58% of the gunshot wounds oc- 5 2 151 5 - 4 52 curred in patients aged 16-35 years.

3 - 7 97 28 33 34 655 Infectious wounds were not encountered in patients younger than 15 years, while 91% of these patients with infections were older than 36 years (Table 13).

Analysis of the causes of soft tissue injuries among patient aged 0-5 years revealed that burns constituted the largest group, at a rate of 55%. Among the sexes, burns occurred in females at a rate of 56% and in males at a rate of 55%.

Traffic Burns Falls Gunshot Infections Total accidents

wounds 5 4 158 19 50 131 33 64 464

While males constituted 68% of the cases of traffic accidents and 60% of the gunshot wound cases, the rates of infectious wounds and burns were comparable among males and females, and 56% of the patients injured due to falling were females. The sex distributions of the causes of soft tissue injuries are displayed in Table 12.

Cilt - Vol. 17 Sayı - No. 1

Females

9 2 16 12 11 13 10 23 96

37

Ulus Travma Acil Cerrahi Derg

Traffic accidents were observed at a rate of 29.4%, while falls and gunshot wounds were found at rates of 13% and 2.4%, respectively (Table 13). Traffic accidents were the most common causes of soft tissue injuries in patients aged 6-15 years, at a rate of 48.5%.

Males constituted 70% of the cases of traffic accidents in this age group. The second most common etiologic factor was burns, at a rate of 31%.

tion, plastic surgeons have a significant role, particularly in the treatment of an important group of patients with critical injuries. In our review of the literature regarding the practice of emergency plastic surgery, we found that the significance of plastic surgery in warand terror-related injuries was usually stressed,[2-4] whereas no reports other than one publication with a limited number of cases[1] were found.

Traffic accidents occurred at a rate of 82% among patients aged 16-35 years, and males constituted 66% of these cases (Table 13). The most common causes of soft tissue injuries in patients older than 36 years were traffic accidents (67%) and burns (15%) (Table 13).

Though dependent on the structure of hospitals, emergency plastic surgery has a very wide field of practice. Furthermore, patients may be referred to emergency plastic surgery particularly by general/ trauma surgeons and orthopedists as well as neurosurgeons, urologists, pediatric surgeons, ophthalmologists, otorhinolaryngologists, and obstetrics and gynecology specialists.[1]

Combined injuries constituted 9% of the injuries (Table 14). When the defects of patients with more than one injury were considered, there were a total of 938 defects among 858 patients, 70% (655/938) of which were located in the lower extremities (Table 15).

Analysis of the anatomic distributions of lower extremity defects revealed that 30% (161/535) were located in the crux, while 23% (123/535) were located on the dorsum of the foot, and 12% (65/535) were located both in the crux and dorsum of the foot (Table 16).

The anatomic distributions of defects according to the etiologies are displayed in Table 17. In the patients admitted with lower extremity tissue defects, 34% (158/464) of the defects were located at the crux, and 28% (131/464) were located on the dorsum of the foot, while among the patients admitted with infectious wounds, 53% (18/34) of the defects were located in the thigh.

While 275 (42%) of the defects were accompanied by fractures, there were no fractures in the remaining 380 (58%). While 19% of the fractures were followed with immobilizer splints, 22% underwent fixation with Kirschner wires, 15.5% underwent plate-screw fixation, and 43.5% underwent external fixation.

While 15.5% of the lower extremity soft tissue defects were treated with primary suturing, 4% were treated with secondary healing, 51% required grafting, and 17% were treated with local flaps; free tissue transfer was performed in the remaining 12.5%. While 62% of the tissue defects occurring in the trunk were caused by traffic accidents, 26.5% were due to burns (Table 14). Among these defects, 11% were left to secondary healing, while 24% were treated with primary suturing, 47% required grafting, and 18% were repaired with local flaps.

DISCUSSION Trauma patients constitute the most important patient group in which a multidisciplinary approach is performed. While the trauma surgeon, neurosurgeon and orthopedist form the main team of this collabora38

Upper extremity injuries constitute the most common patient group of emergency plastic surgery, with an encounter frequency of 38% according to the limited data in the literature.[1] Among the 10,732 cases admitted to our emergency outpatient clinic between 2000 and 2004, upper extremity injuries were present in 64% of the patients. Twenty-five percent of the patients admitted to emergency plastic surgery clinics had head-and-neck injuries, and 37% had tissue defects of the lower extremities and trunk.[1] In harmony with the literature, head-and-neck injuries were present in 28% of our patients, whereas the percentage of the patients with tissue defects, which was 8% in our cases, is considerably lower as compared with those reported in previous publications. This low rate might be due to the fact that patients with simple soft tissue injuries may also be treated in hospitals without emergency plastic surgery clinics.

As the forearm and hand have complex functions and unique anatomic structures, their injuries are commonly of combined type.[5] In studies regarding emergency upper extremity injuries, male predominance has been found as 60-62%[8,9] and 82%,[5] while it was 81% among our cases.

In our study, the rates of labor accidents, household accidents and glassware cuts were 9.8%, 6.3% and 33.3%, respectively. These rates greatly differ from those in a previous study of our clinic conducted between 1995 and 1997 in which emergency upper extremity injuries were investigated. In that study, the rates were 40%, 38% and 13% for labor accidents, household accidents and glassware cuts, respectively.[5] This indicates that the etiologies may change over time.

Patients with self-inflicted trauma via punching through glass during a bout of aggression constituted 76% of all glassware cuts. Of these patients, 84% were males, and 79% were aged 16-35 years. Other than the previous report of our clinic,[5] we found no descripOcak - January 2011

The practice of plastic surgery in emergency trauma surgery

tion of patients with this type of self-inflicted trauma in the literature, nor was there any statistical data regarding this issue.

The rates of isolated cutaneous incisions, which we found to be 38%, were close to those previously reported, as 35-45%.[5,8,9] Though we found the rate of isolated tendon cuts to be 27%, it has been reported to be much lower, ranging from 2 to 5% in various studies.[5,9] In one study, it was reported that 2% of the cases with hand injuries should be referred to a clinic for treatment, and the rate of tendon incisions was reported to increase up to 29% among these cases.[5] While the mean age of patients with head-andneck injuries was reported to range from 20-29 years in the literature,[10-12] the mean age in our cases was 23.2, which was compatible with those of the previous reports. In the literature, female:male ratios ranging from 2:1 to 9:1 have been reported,[10-12] whereas in our study, the male:female ratio was found to be 1.5:1.

While head-and-neck injuries were reported as most commonly occurring during games and daily activities, at a rate of 38%,[11] this etiologic factor was encountered at a rate of 14% in our cases. While traffic accidents were the most common causes of injury in our cases, with a rate of 38%, only 12% of the headand-neck injuries in the literature were caused by traffic accidents.[11] In the literature, traffic accidents have also been reported as being the cause in as high as 75% of the cases.[10] Reports in which assaults were found to be the most common cause, with a rate of 48% of the cases, have also been published.[13] The rates of assaults, sport accidents, labor accidents, and falls in our study were compatible with those in the literature.[11] While only soft tissue injuries were present in 68% of the patients with head-and-neck injuries, there were accompanying bone fractures in 961 patients (32%).

These results were similar to those in the literature.

[11] While the male:female ratio of patients with fractures has been reported to be 2.5:1,[11,12] it was 2:1 in our study, supporting the earlier results. Other serious wounds accompany head-and-neck injuries in 10-15% of the cases.[14] In our study, this rate was found to be 8.7%.

While the fracture was in the mandible in 48.9% of our cases, this rate shows a great variability in the literature, ranging from 24% to 75%.[10-13] The rates of fractures elsewhere in the face in our study were compatible with those in the literature.[10-12] In our cases, the most frequent fractures were those of the symphysis-parasymphysis, with a rate of 44.3%, while they were reported to be seen at a rate of 29.3% in the literature as the second most common fractures.[12] In various reports, the most common mandibular fracture was reported to be that of the condyle, at a rate of Cilt - Vol. 17 Say覺 - No. 1

32%, whereas condyle fractures were found to be the second most common fracture type in our study, with a rate of 25.3%. The frequencies of other mandibular fracture types in our study were similar to those in the literature.[11,12] Maxillofacial traumas vary in both their etiologies and the fractured facial bones, and require various treatment protocols depending on these factors. Likewise, the patients with mandible fractures were treated with closed reduction in 55.6%, and with open reduction and rigid fixation in 38.6% of the cases, in harmony with the literature.[10-12] However, 81.8% of the cases of zygomatic bone fractures and 86.2% of the cases with orbital fractures in our study were treated with open reduction, both of which were higher than the rates reported in the literature.[11,12] While males have been reported to constitute 66% of the patients with lower extremity soft tissue injuries, males constituted 62% in our cases, supporting the literature. The mean age of patients in our study was also compatible with that in the literature. While traffic accidents were reported in the literature to be the most common cause, with a rate of 82%, this rate was 62% in our cases, with traffic accidents still being the most common cause.

While males constituted 68% of the cases of traffic accidents and 60% of the cases of gunshot wounds in our study, no comparable publication in the literature with the same parameters was found. Likewise, the lower extremity defects in our study were distributed anatomically to the crux in 30%, dorsum of the foot in 23%, and both the crux and the dorsum of the foot in 12% of the cases; however, we failed to make any comparisons due to the scarcity of publications.[15] Fractures were present in 42% of the cases admitted to our emergency clinic with lower extremity injuries. While 43% of these fractures were treated with external fixation, 22% underwent intramedullary fixation. These rates were comparable to the external fixation and intramedullary fixation rates previously published, as 51% and 36%, respectively.[16] Among our cases of lower extremity soft tissue defects, 51% were treated with grafting, while local flaps were used in 17%, and free tissue transplantation was required in 12.5% of the cases. Although the literature is devoid of large series and the present publications are scarce, it has been reported in a few studies that these rates were 30% for repair with skin grafts, 27% for repair with local flaps, and 10% for free tissue transplantation.[1] Traffic accidents were the cause in 62% of our cases with tissue defects of the trunk, while another 26.5% were caused by burns. Further, 47% of these defects were treated with grafts, and 18% were treated 39

Ulus Travma Acil Cerrahi Derg

with local flaps. As no publication regarding patients admitted to emergency plastic surgery clinics with defects on the chest has yet been published, we were unable to make any comparisons.

Injuries requiring emergency plastic surgery interventions are usually not life-threatening unless there is a prominent hemodynamic instability due to a large vessel injury or trauma causing massive tissue damage. As a result, it is possible to complete the treatment under elective conditions in patients whose emergency situation is under control. However, complicated injuries, unless treated appropriately, may cause serious loss of function, and this may lead to considerable disability and reduced life quality.[6,7] In the structure of various centers, there are two different rooms, namely an intervention room for plastic surgery and an operation theater. In the event there is no life-threatening situation and repair under local anesthesia is possible, many patients can be treated in the intervention room.

Reports have been published stating that 67% of the patients were treated in the intervention room, while the remaining 33% were treated in the operation theater.[17] In our series, 67% of the patients underwent treatment in the intervention room, while 1% were referred urgently to the operation theater, where their treatments were accomplished. The remaining 32% underwent their emergency treatments in the intervention room, while their elective treatments were deferred to a later date. The causes were patient-related and circumstance-related. Coexisting serious injuries and in part social problems were the patient-related factors, while circumstance-related factors included the unavailability of the common central operation theater due to treatment of other, more fatally injured patients, since the lives of emergency plastic surgery patients are usually not threatened.

In view of the frequencies and characteristics of the treated patients, the importance and practice of plastic surgery in emergency traumatology is progressively increasing. However, particularly complicated injuries, unless appropriately treated, may lead to serious function losses and prominent disability, with reduction in life quality. We suggest that the conditions of emergency intervention rooms and operation theaters, which cannot provide immediate treatment of every patient under current conditions, should be revised according to the current situation. In addition, we suggest that this report will contribute greatly to the literature, as no extensive study in which the issues within the field of practice of emergency plastic surgery (up-

40

per extremity surgery, head-and-neck trauma, and soft tissue traumas) has yet been published.

REFERENCES 1. Peterson SL, Moore EE. The integral role of the plastic surgeon at a level I trauma center. Plast Reconstr Surg 2003;112:1371-8.

2. Golan J, Golan E, Alder J, Sternberg N, Zagher U, Rosenberg B, et al. Plastic surgery and civilian casualties due to “terrorist” activities. Ann Plast Surg 1982;8:359-62.

3. Cohen M, Kluger Y, Klausner J, Avital S, Shafir R. Recommended guidelines for optimal design of a plastic surgery service during mass casualty events. J Trauma 1998;45:9608.

4. Greenberg BM, Brewer BW. Avianca flight No. 052 accident: a plastic surgical perspective. Plast Reconstr Surg 1991;88:529-35.

5. Karasoy A, Sakinsel A, Gözü A, Kuran I, Baş L. Our experience in emergency hand injuries. Ulus Travma Derg 1998;4:266-9.

6. Dowrick AS, Gabbe BJ, Williamson OD. Does the presence of an upper extremity injury affect outcomes after major trauma? J Trauma 2005;58:1175-8.

7. Butcher JL, MacKenzie EJ, Cushing B, Jurkovich G, Morris J, Burgess A, et al. Long-term outcomes after lower extremity trauma. J Trauma. 1996;41:4-9.

8. Nieminen S, Nurmi M, Isberg U. Hand injuries in Finland.

Scand J Plast Reconstr Surg 1981;15:57-60.

9. Angermann P, Lohmann M. Injuries to the hand and wrist. A study of 50,272 injuries. J Hand Surg Br 1993;18:642-4.

10. Al Ahmed HE, Jaber MA, Abu Fanas SH, Karas M. The pattern of maxillofacial fractures in Sharjah, United Arab Emirates: a review of 230 cases. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2004;98:166-70.

11. Gassner R, Tuli T, Hächl O, Rudisch A, Ulmer H. Craniomaxillofacial trauma: a 10 year review of 9,543 cases with 21,067 injuries. J Craniomaxillofac Surg 2003;31:51-61.

12. Motamedi MH. An assessment of maxillofacial fractures: a 5-year study of 237 patients. J Oral Maxillofac Surg 2003;61:61-4.

13. Kelley P, Crawford M, Higuera S, Hollier LH. Two hundred ninety-four consecutive facial fractures in an urban trauma center: lessons learned. Plast Reconstr Surg 2005;116:42e49e.

14. Hogg NJ, Stewart TC, Armstrong JE, Girotti MJ. Epidemiology of maxillofacial injuries at trauma hospitals in Ontario, Canada, between 1992 and 1997. J Trauma 2000;49:425-32.

15. Suri M, Patel A, Vora H, Raibagkar S, at al. Post-traumatic posterior heel soft tissue defect reconstruction. Indian J Plastic Surg 2005;38:138-42.

16. Pinsolle V, Reau AF, Pelissier P, Martin D, Baudet J. Softtissue reconstruction of the distal lower leg and foot: are free flaps the only choice? Review of 215 cases. J Plast Reconstr Aesthet Surg 2006;59:912-8.

17. Anandan SM, Agrawal K, Panda K. The major role of a minor plastic surgery operation theater. Ann Plast Surg 2006;56:703-4.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):41-45

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2011.32391

Trakeobronşiyal yaralanmalar Tracheobronchial injuries Bülent AYDEMİR, Oya Uncu İMAMOĞLU, Recep USTAALİOĞLU, Tamer OKAY, Ilgaz DOĞUSOY

AMAÇ

BACKGROUND

Bu çalışmada, trakeobronşiyal yaralanmaların tanı ve tedavisinde kullanılan yöntemleri araştırdık ve literatürle karşılaştırmayı amaçladık.

We aimed in this study to investigate and compare the diagnostic and therapeutic methods in tracheobronchial injuries.

GEREÇ VE YÖNTEM

METHODS

Kliniğimizde 2003-2008 yılları arasında trakeobronşiyal yaralanma nedeni ile ameliyat edilen 9 olgu (7 erkek, 2 kadın) çalışmaya dahil edildi. Travma sonrası trakeobronşiyal yaralanma nedeni ile ameliyat edilen 7 olgu ile entübasyon sonrası trakeal yaralanma görülen 2 olgu incelendi. Olgular, yaş, cinsiyet, travma tipi, klinik bulgular, yaralanma bölgesi, uygulanan girişim ve sonuçları açısından değerlendirildi.

Nine cases (7 male, 2 female) operated between 2003 and 2008 because of tracheobronchial injury were included in the study. The cause of tracheobronchial injury was trauma in 7 cases and postintubation laceration in 2 cases. The cases were evaluated in terms of age, sex, type of trauma, clinical findings, localization of injury, performed diagnostic and therapeutic methods, and results.

BULGULAR

Yaralanma 6 olguda künt travma, 1 olguda penetran travma sonucu gerçekleşirken, 2 olguda ise iyatrojenikti. Yaralanma 5 olguda trakeal, 4 olguda ise bronşiyal seviyede idi.

Bir olguya üst bilobektomi, bir olguya trakeal rezeksiyon ve ucuca anastamoz, 3 olguya uçuca anastomoz ve 4 olguya ise primer tamir yapıldı. Bir olgu ameliyat sırasında, bir olgu ise ameliyat sonrası erken dönemde kaybedildi.

The causes of tracheobronchial laceration were blunt trauma in 6 cases, penetrating trauma in 1 case and iatrogenic (postintubation) in 2 cases. Lacerations were in the trachea in 5 cases and at the bronchial level in 4 cases. Operations included right upper bilobectomy in 1 case, tracheal resection and end to end anastomosis in 1 case, end to end anastomosis in 3 cases, and primary repair in 4 cases. One case died during the operation and 1 case died postoperatively.

SONUÇ

CONCLUSION

Trakeobronşiyal yaralanmalarda erken tanı önemlidir. Yaralanmanın yerinin ve şeklini belirlenmesi için kullanılan en önemli tanı aracı bronkoskopidir. Tedavide rezeksiyondan mümkün olduğunca kaçınılmalı ve primer onarım tercih edilmelidir.

In tracheobronchial injuries, early diagnosis and treatment are very important. The most useful method is bronchoscopy for determining the type and localization of the injury.

In treatment, primary repair should be preferred over anatomical resections whenever possible.

Anahtar Sözcükler: Travma; trakeobronşial yaralanma.

Key Words: Trauma; tracheobronchial injuries.

Dr. Siyami Ersek Göğüs Kalp ve Damar Cerrahi Hastanesi, İstanbul.

RESULTS

Dr. Siyami Ersek Thoracic and Cardiovascular Surgery Hospital, Istanbul, Turkey.

İletişim (Correspondence): Dr. Bülent Aydemir. Dr. Siyami Ersek Göğüs Kalp ve Damar Cerrahi Hastanesi, Tıbbiye Cad., Haydarpaşa, İstanbul, Turkey.

Tel: +90 - 216 - 542 44 44 e-posta (e-mail): aydemirb@hotmail.com

41

Ulus Travma Acil Cerrahi Derg

Tüm travmaya bağlı ölümlerin %25’i toraks travmaları nedeniyledir.[1] Trakeobronşiyal yaralanmalar ise travma sonrası görülen nadir (%1-4), fakat hayatı tehdit eden patolojilerdir.[1,2] Sıklıkla künt travmalar sonucu görülseler de penetran veya ateşli silah yaralanmaları, eksplorasyon yaralanmaları ve iyatrojenik yaralanmalar nedeni ile de oluşabilir.[3,4] Trakeobronşiyal yaralanmalar, membranöz yüzde basit bir yırtıktan, tam ayrılmaya kadar değişen derece ve bölgelerde enine, uzunlamasına ve kompleks olarak görülebilmektedirler.[1] Standart tedavi yöntemi cerrahidir.

[4] Trakeobronşiyal yaralanma gelişen olgularda bulgular, lezyonun plevral boşlukla ilişkili olup olmamasına göre değişiklik gösterir. Sıklıkla hayatı tehdit eden dramatik klinik durumlar oluşsa da, peritrakeal fasya veya mediastinal plevranın intakt olduğu durumlarda hastanın ventilasyonu bozulmayabilir ve klinik tablonun net olmadığı bu hastalarda tanı atlanabilir.[3] Bu çalışmada, trakeobronşiyal travma nedeni ile ameliyat edilen olgular retrospektif olarak değerlendirilerek literatür eşliğinde tartışıldı.

GEREÇ VE YÖNTEM 2003-2008 yılları arasında hastanemiz acil polikliniğine toraks travması nedeni ile başvuran 4500 olgu incelendiğinde, 610’u yatırılarak tedavi edilen bu olguların 72’si ameliyat edilmişti. Trakeobronşiyal yaralanma nedeni ile ameliyat edilen 7 olgu (%1,14) ve entübasyon sonrası trakeal yaralanma görülen 2 olgu geriye dönük olarak incelendi. Olgular yaş, cinsiyet, travma tipi, klinik bulgular, yaralanma lokalizasyonu, uygulanan girişim ve sonuçları açısından değerlendirildi.

Tablo 1. Künt ve penetran travmalı olguların klinik ve radyolojik bulgulara göre dağılımı

Klinik bulgular Solunum sıkıntısı Ciltaltı amfizemi Hemoptizi Masif hava kaçağı Radyolojik bulgular Pnömotoraks Mediastinal amfizem Hemopnömotoraks Ciltaltı amfizemi

Sayı

4 6 1 2

5 5 1 6

Yüzde 57,1 85,7 14,2 28,5 71,4 71,4 14,2 85,7

Cerrahi Teknik Trakeobronşiyal yaralanma tanısı ile ameliyat edilen tüm olgular tek lümenli tüp ile entübe edildi. Posterolateral torakotomi ile toraksa girildi. Trakeal seviyede yaralanma olan olgulardan tam kesi olan ve doku kaybı nedeni ile trakeal rezeksiyon yapılan olguda trakea distal ucu dışarıdan entübe edilerek steril ventilasyon hattına bağlandı. Membranöz trakeaya kontinü dikişler, trakeanın kartilaj kısmına separe dikişler konarak hazırlandı. Dışarıdan trakeanın distal kısmını ventile eden tüp çekilerek orotrakeal tüp ilerletildi ve ventilasyon sağlandı. Anastomoz dikişleri bağlanarak anastomoz tamamlandı. Bazı olgularda nonabsorbabl monoflament dikiş materyali (polipropilen) bazı olgularda ise absorbabl monoflamanet dikişler (polidioksanon) tercih edildi.

BULGULAR Trakeobronşiyal yaralanma nedeni ile ameliyat edilen 9 olgunun 2’si kadın 7’si erkekti. Olgular 3 ile 66 arasında değişen farklı yaş guruplarındandı. Yaralanma 6 olguda künt travma, 1 olguda penetran travma sonucu gerçekleşirken, 2 olguda ise iyatrojenikti. İntratorasik ameliyat sırasında endotrakeal entübasyona bağlı iyatrojenik trakeal yırtık görülen 2 olgu dışındaki toplam 7 olgunun klinik durumları değerlendirildi. Sadece travmanın 2. günü hastanemize trakeobronşiyal yırtık şüphesiyle dış merkezden gönderilen bir olgu entübeydi ve O2 satürasyonu düşüktü. Cilt altı amfizemi (%85,7) ve solunum sıkıntısı (%57,1) en sık saptanan bulgulardı (Tablo 1).

Yedi olgu arka-ön akciğer grafisi ve toraks bilgisayarlı tomografi (BT) ile değerlendirilirken bir olguya 3 boyutlu rekonstrüksiyon BT ile sanal bronkoskopi yapıldı (Şekil 1). Cilt altı amfizemi (%85,7) ve pnömotoraks (%71,4) en sık rastlanan radyolojik bulgulardı.

(Tablo 1) (Şekil 2, 3).

Şekil 1. Bronş rüptürü olan olgunun toraks BT ve sanal bronkoskopi görüntüleri.

42

Kesin tanı 7 olguda bronkoskopi ile, 2 olguda ise torasik operasyon sırasında konuldu. Bronkoskopi ile tanı konan 7 olgudan 2’sine rijit bronkoskopi, 3’üne Ocak - January 2011

Trakeobronşiyal yaralanmalar

fiberoptik bronkoskopi, 2 olguya da hem rijit hem fiberoptik bronkoskopi yapıldı. Ameliyat sırasında tanı konan 2 olgu ise elektif operasyonlar için entübasyon yapılan ve bu sırada iyatrojenik olarak yırtık (posterior membran) geliştiği görülen olgulardı. Bu olgulardan ilki planjon guatr nedeniyle torakotomi yapılan olguda saptandı. Bu olgunun ameliyat öncesi hazırlık döneminde yapılan bronkoskopisinde trakeanın sağdan kitle tarafından itildiği ve oldukça malazik olduğu görüldü. Ameliyat sırasında kitle eksplore edilirken kitlenin hemen altında çift lümenli endotrakeal tüpün trakeal kafının trakeanın posterior membranını yırtarak dışarı protrüze olduğu görüldü. İkinci olgu ise trakeal stenoz nedeni ile ameliyat edilen bir olgu idi. Koller insizyonu ile başlanarak trakea diseksiyonu tamamlanıp trakeanın stenotik segmentinin rezeksiyonunu takiben distal trakeanın entübasyonu sırasında posterior membranda karinaya kadar uzanan uzunlamasına yırtık oluştuğu görüldü.

Tablo 2. Olguların travma tipi, lokalizasyon ve uygulanan tedaviye göre dağılımı

Lokalizasyon Trakea Sol bronşiyal sistem Sağ bronşiyal sistem Travma tipi Künt Penetran İyatrojenik Tedavi Primer tamir Uç-uca anastamoz Rezeksiyon

Sayı

5 1 3

6 1 2

4 4 1

Yüzde 55,5 11,1 33,3 66,6 11,1 22,2 44,4 44,4 11,1

Yaralanma 5 olguda trakeal seviyede, 3 olguda sağ bronşiyal sistemde, 1 olgu ise sol bronşiyal sistemde idi.

Yedi trakeobronşiyal yaralanmalı olgu travma günü ameliyat edilirken, künt travma sonucu trakeobronşiyal yaralanma gelişen 2 olgu ise 2. ve 3. günler ameliyat edildi. Bütün olgulara posterolateral torakotomi yapıldı. Sağ üst lob ve orta lob bronşunda parçalı laserasyon görülen 1 olguya üst bilobektomi, 3 olguya ucuca anastamoz, 1 olguya trakeal rezeksiyon + uçuca anastamoz, 4 olguya ise primer tamir yapıldı (Tablo 2).

Şekil 2. Künt travma sonucu trakea posterior membranda laserasyon gelişen olgunun toraks BT kesitleri. Laserasyon torasik innetten başlayıp sağ ana bronşa dek uzanmaktadır.

Şekil 3. Ateşli silah yaralanması sonucu trakeal yırtık gelişen olgunun toraks BT kesitleri.

Cilt - Vol. 17 Sayı - No. 1

İki olguda yara yeri enfeksiyonu, bir olguda ise pnömoni, ampiyem ve trakeoözefageal fistül gelişti.

Bir olgu operasyon sırasında hipoksi nedeni ile kaybedilirken, trakeoözofageal fistül gelişen olgu mediastinit ve sepsis nedeni ile kaybedildi. İki olgu ile mortalite oranı %22,2 idi.

TARTIŞMA Tüm travmaların %25’ini toraks travmaları oluşturur. Trakeobronşiyal travmalar hayatı tehdit eden travmalar olmakla birlikte nadir görülen olgulardır. Travmatik trakeobronşiyal yırtık gelişen birçok olgu acil kliniklerine getirilmeden önce kaybedilmekte[5] ve hastane dışı mortalitenin %30’un üzerinde olduğu bildirilmektedir.[4] Bu nedenle doğru insidansı saptamak zor olmakla birlikte tüm toraks travmaları içerisinde %1-2’lik bir orana sahip olduğu söylenebilir. Literatürlerde bu oran %4’e kadar çıkmaktadır.[4] İyatrojenik trakeal yaralanmalar ise daha da nadir görülen yaralanmalardır. Orotrakeal entübasyonlardan sonra görülen iyatrojenik trakeal yırtıkların %0,005, çift lümenli tüp ile entübasyon sonrası görülen trakeal yırtıkların ise %0,05 ile %1 oranında görüldüğü bildirilmiştir.[4,6] Hastanemiz göğüs cerrahisi kliniği acil polikliniğine aynı dönemde toraks travması nedeni ile başvuran 4500 olgu değerlendirildiğinde bu olguların sade43

Ulus Travma Acil Cerrahi Derg

ce 7’sinde (%0,15) trakeobronşiyal yırtık saptanarak tedavi edilmiştir. Hastanemizde yatırılarak tedavi edilen toraks travmalı olgular esas alındığında trakeobronşiyal yaralanma sıklığı %1,14’dür. İyatrojenik trakeal yırtık sıklığı ise 2 olgu ile %0,13’dür.

Trakeobronşiyal yaralanmalar genellikle künt travmalar nedeni ile oluşurlar. Penetran travma sonucu oluşan trakeobronşiyal yaralanmalar olguların sadece %6-10’unu oluşturur.[4] Bizim olgularımızın içinde sadece birinde penetran travma nedeni ile trakea yırtığı gelişmişti (%14,2). İyatrojenik trakeobronşiyal yaralanmalar genellikle entübasyon sonrası, dilatasyon trakeostomileri sırasında veya endobronşiyal tedaviler sırasında oluşmaktadır.[6] Bizim olgularımızın ikisi de entübasyon sonrası görülmüştür.

Travma sonrası ilk fiziksel bulgular çok belirsiz olabilir. Bununla birlikte bazı fiziksel bulgular tanı için şüphe çekmelidir. Fiziksel incelemede en sık saptanan bulgular; solunum sıkıntısı, siyanoz, hemoptizi, hemotoraks, pnömotoraks ve ciltaltı, mediastinal veya servikal amfizemdir.[4] Kaptanoğlu ve arkadaşlarının[1] serilerinde %60, Balcı ve arkadaşlarının[5] serisinde %25, Gómez-Caro ve arkadaşlarının[4] serilerinde ise %66,7 ile en sık bulgu cilt altı amfizemi olarak bildirilmiştir. Bizim serimizde de en sık saptanan bulgu ve radyolojik sonuçlar ciltaltı amfizemiydi (%85,7).

Akciğer röntgeninde pnömomediastinum ve servikal amfizem trakeobronşiyal yırtıklar için en spesifik görüntüdür.[7] Klinik durum, yaralanma ile plevra arasındaki bağlantı ile ilişkilidir. Trakea yaralanması görülen iki olguda hemoptizi, mediastinal amfizem ve iki taraflı pnömotoraks olmakla birlikte toraks tüplerinden hava drenajı minimaldi ve akciğerler ekspanse idi. Yaralanmanın büyüklüğü ile karşılaştırıldığında semptomlar oldukça hafifti. Bir olguda 5 cm’lik trakea posterior membran yırtığı olmasına rağmen peritrakeal fasyanın ve mediastinal plevranın sağlam kalması nedeniyle solunum sıkıntısı yoktu. Ateşli silah yaralanması nedeni ile trakeal yırtık oluşan diğer olguda da yaralanma bölgesindeki hematomun masif hava kaçağını önlemesi, ventilasyonun bozulmasına engel olmuştu.

Trakeobronşiyal yaralanmaların kesin tanısında bronkoskopi altın standarttır.[2] Toraks travmalı olgularda trakeobronşiyal travma için spesifik bronkoskopi endikasyonları; hemoptizi, pnömomediastinum, servikal amfizem ve tüp torakostomi ile drenaja rağmen devam eden pnömotorakstır.[7] Şüpheli olgularda BT çekilmesi, zaman ve olanaklar elverişli ise üç boyutlu rekonstrüksiyon ve sanal bronkoskopi yapılması tanıda yardımcı olmaktadır.[8] Travma sonrası trakeobronşiyal yaralanma tanısı 7 44

olguda bronkoskopi ile konuldu. Tüm olgular aynı zamanda toraks BT’si ile değerlendirilirken bir olguya 3 boyutlu rekonstrüksiyon BT ile sanal bronkoskopi yapıldı.

Trakea ve ana bronşlar kartilaj halkaları tarafından desteklenen kas ve mukozadan yapılmıştır. Esnek ve katlanabilir özelliktedirler. Gerilme basınçları düşüktür. Bundan dolayı travmalara karşı dayanıklılığı azdır. Künt travma sonrası oluşan trakeobronşiyal yaralanmalar olguların %80’inden fazlasında karinanın 2,5 cm etrafında görülür.[9] Sıklıkla da membranöz duvarda lineer laserasyonlar şeklindedir. En sık yaralanmanın sol bronşiyal seviyede olduğunu bildiren seriler olduğu gibi sağ bronşiyal sistemin ağırlıkta olduğu seriler de vardır.[1] Özellikle 259 olgunun değerlendirildiği Kiser’in çalışmasında sağ bronşiyal sistem künt travmadan en çok etkilenen bölge olarak görülmüştür.[10] Olguların %76’sında yaralanma karinaya 2 cm mesafede, yaklaşık olarak yarısı da sağ ana bronşta görülmüştür.[10] Olgularımızın 5’inde yaralanma trakeal seviyede olması (%55), bu olgulara entübasyon sonrası görülen yaralanmaların daha çok trakeada oluşmasıyla açıklanabilir. Entübasyon sonrası görülen yaralanmalar çıkarıldığında trakeobronşiyal yaralanmaların %57,1’i bronşiyal seviyede görülmüştür. Olgularımızda sağ bronşiyal sistem ise en çok etkilenen lokalizasyon olarak gözükmektedir.

Genel durumu stabil olan hastalarda trakeadaki yırtık küçükse ve akciğerin ekspansiyonu tüp torakostomi ile sağlanabiliyorsa konservatif yaklaşım tercih edilebilir.[1] Torakotomi yapılan toraks travmalı olguların %1-2’sinde pnömonektomi yapılırken trakeobronşiyal yaralanmalı olgularda bu oran %12’ye kadar çıkmaktadır.[1] Kiser’in çalışmasında cerrahi olarak tedavi edilen bronşiyal seviyedeki yaralanmalarda rezeksiyon oranı %24 dür.[10] Ancak, trakeobronşiyal yaralanmaların tedavisinde altın standart primer tamirdir.[11,12] Sıklıkla polipropilen daha az sıklıkla polidioksanon dikişler tercih edilmektedir.[13] Olgularımızın tamamına cerrahi tedavi uygulanmıştır. Sadece sağ üst lob ve orta lob bronşunda parçalı laserasyon görülen 1 olguya rezeksiyon uygulanmıştır (%11,1). Ateşli silah yaralanması nedeni ile trakeada doku kaybı ile beraber olan trakeal yaralanmaya ise trakeal rezeksiyon ve uç-uca anastomoz yapılmıştır. Olgularımızın büyük çoğunluğunda trakeobronşiyal yaralanma bronkoplastik tekniklerle onarılmıştır (%88). İki olguda yara yeri enfeksiyonu gelişti. Bir olguda ise etkin fizyoterapi ile düzelen atelektazi, bir olguda ise pnömoni, ampiyem ve trakeoözefageal fistül gelişti.

Mortalite iki taraflı bronşiyal yaralanmalarda %60, trakeal yaralanmalarda ise %26 olarak bulunmuştur.[10] Trakeobronşiyal yaralanmalarda erken yüksek mortaOcak - January 2011

Trakeobronşiyal yaralanmalar

litenin diğer yandaş travmalarla ilişkili olduğu söylenebilir. Balcı ve arkadaşlarının[5] serilerinde cerrahi mortalite %19,3 bulunmuştur.

Bizim serimizde bir olgu ameliyat sırasında hipoksi nedeni ile kaybedilirken, bir olgu da erken dönem gelişen trakeoözofageal fistül sonrası mediastinit ve sepsis nedeni ile kaybedildi. İki olgu ile mortalite oranı %22,2 idi.

Mediastinal plevranın sağlam kalması, trakeada oluşan büyük laserasyonların bile asemptomatik kalmasına sebep olabilir. Konservatif yötemlerle iyileşmesi çok zor olan bu lezyonların kesin tanısı için olgular dikkatle değerlendirilmeli ve yapılacak bronkoskopinin tedaviyi doğru yönlendirerek hayat kurtarıcı olacağı unutulmamalıdır.

KAYNAKLAR 1. Kaptanoğlu M, Nadir A, Erbaş E, Gönlügür U, Seyfikli Z, Doğan K ve ark. Trakeobronşiyal yaralanmalar: 15 olguluk bir serinin değerlendirilmesi. Toraks Dergisi 2001;2:54-59.

2. Ishibashi H, Ohta S, Hirose M, Akimoto T. Blunt tracheal transection and long tear in posterior membranous trachea.

Eur J Cardiothorac Surg 2006;30:945-7.

3. Gabor S, Renner H, Pinter H, Sankin O, Maier A, Tomaselli F, et al. Indications for surgery in tracheobronchial ruptures.

Eur J Cardiothorac Surg 2001;20:399-404.

4. Gómez-Caro A, Ausín P, Moradiellos FJ, Díaz-Hellín V, Lar-

Cilt - Vol. 17 Sayı - No. 1

rú E, Pérez JA, et al. Role of conservative medical management of tracheobronchial injuries. J Trauma 2006;61:142635.

5. Balci AE, Eren N, Eren S, Ulkü R. Surgical treatment of post-traumatic tracheobronchial injuries: 14-year experience.

Eur J Cardiothorac Surg 2002;22:984-9.

6. Schneider T, Storz K, Dienemann H, Hoffmann H. Management of iatrogenic tracheobronchial injuries: a retrospective analysis of 29 cases. Ann Thorac Surg 2007;83:1960-4.

7. Narci H, Gündüz K, Yandi M. Isolated tracheal rupture caused by blunt trauma and the importance of early diagnosis: a case report. Eur J Emerg Med 2004;11:217-9.

8. Oto Ö, Açıkel Ü, Tüzün E, Silistreli E, Gürcan U, Karabay Ö ve ark. Genç bir olguda bronş rüptürü onarımı ve tanısal tekniklerde yeni ufuklar. GKDC Dergisi 1997;455:292-5.

9. Johnson SB. Tracheobronchial injury. Semin Thorac Cardiovasc Surg 2008;20:52-7.

10. Kiser AC, O’Brien SM, Detterbeck FC. Blunt tracheobronchial injuries: treatment and outcomes. Ann Thorac Surg 2001;71:2059-65.

11. Minambres E, Gonzalez-Castro A, Buron J, Suberviola B, Ballesteros MA, Ortiz-melon F Management of postintubation tracheobronchial rupture: Our experiense and a review of the literature. Eur J Emergency Medicine 2007;14:177-9.

12. Rossbach MM, Johnson SB, Gomez MA, Sako EY, Miller OL, Calhoon JH. Management of major tracheobronchial injuries: a 28-year experience. Ann Thorac Surg 1998;65:182-6.

13. Richardson JD. Outcome of tracheobronchial injuries: a long-term perspective. J Trauma 2004;56:30-6.

45

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):46-50

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2011.57431

Kafa travması nedeniyle tedavi edilen 954 erişkin olgunun retrospektif değerlendirilmesi: Epidemiyolojik çalışma Retrospective analysis of 954 adult patients with head injury: an epidemiological study Hasan Serdar IŞIK,1 Uğur BOSTANCI,2 Ömer YILDIZ,2 Cengiz ÖZDEMİR,2 Ahmet GÖKYAR3

AMAÇ

BACKGROUND

Kafa travmaları, özellikle kentlerde ve genç nüfusta en sık görülen morbidite ve mortalite sebeplerinden biridir. Bu retrospektif çalışmayla, kafa travmaları ile ilgili ülkemiz epidemiyolojik veritabanına katkıda bulunmayı amaçladık.

Head traumas are among the most common causes of mortality and morbidity among young adults in urban areas. We aimed to contribute to the epidemiological database of our country with regard to head traumas.

GEREÇ VE YÖNTEM

METHODS

Ocak 2003-Haziran 2008 tarihleri arasında, Samsun Mehmet Aydın Eğitim ve Araştırma Hastanesi Nöroşirürji kliniğinde tedavi edilen 15 yaş ve üstü 954 hasta retrospektif olarak incelendi. Hastaların 721’i (%75,5) erkek, 233’ü (%24,5) kadındı. Hastaların %52,5’i 15-40 yaş arası genç nüfustu.

BULGULAR

Trafik kazaları (%75) en sık tespit edilen travma nedeniydi. Giriş Glasgow Koma Skoruna (GKS) göre hastaların %48’inde hafif (GKS 13-15), %31’inde orta (GKS 9-12) ve %21’inde ise ağır (GKS 3-8) kafa travması mevcuttu.

Hastaların 177’si (%18,5) ameliyat edildi. Yapılan ameliyatlar en sık subdural hematom ve epidural hematom nedeniyleydi. Serimizde mortalite %19,4 (n=185) olarak bulundu. Bu hastaların travma nedeni incelendiğinde, trafik kazaları yine ilk sırada yer almıştır.

SONUÇ

Kafa travmaları ile ilgili epidemiyolojik çalışma ve verilerin artması, travmanın oluşmadan engellenebilmesi açısından önem taşır. Serimizde, özellikle erkek hakimiyeti, travma sıklığının en yüksek olduğu yaş grupları, travma ve mortalite sebepleri açısından ülkemizde yapılan diğer çalışmalara benzer veriler elde edilmiştir. Ancak, merkez bir hastane olmamız sebebiyle orta ve ağır kafa travmalarının oransal fazlalığı, mortalitemizi de etkilemiştir.

Anahtar Sözcükler: Epidemiyoloji; kafa travması; mortalite.

1 Ordu Üniversitesi Tıp Fakültesi Nöroşirürji Anabilim Dalı, Ordu; Samsun Mehmet Aydın Eğitim ve Araştırma Hastanesi Nöroşirürji Kliniği, Samsun; 3Samsun Medical Park Hastanesi Nöroşirürji Kliniği, Samsun.

2

We retrospectively analyzed 954 patients older than 15 years with head trauma who were treated in the Neurosurgery Department of Samsun Mehmet Aydın Education and Research Hospital between January 2003 and June 2008.

Seven hundred twenty-one (75.5%) patients were male and 233 (24.5%) were female. Five hundred twenty-one (52.5%) were between 15-40 years old.

RESULTS

Traffic accident (75%) was the most common cause of head trauma. According to Glasgow Coma Score (GCS), 48% of the patients had mild (13-15), 31% moderate (912) and 21% severe (3-8) head injury. One hundred seventy-seven (18.5%) patients were operated. The commonest operations were performed for subdural and epidural hematomas. Mortality was 19.4% (185). Common causes of mortality were traffic accidents (77%) and gunshot injuries.

CONCLUSION

It is important to have local epidemiological studies and data about head traumas in order to prevent these traumas. In this study, the predominance of young men and the causes of trauma and mortality were similar to that reported in the related literature.

Key Words: Epidemiology; head injury; mortality.

Department of Neurosurgery, Ordu University Faculty of Medicine, Ordu; 2 Department of Neurosurgery, Mehmet Aydın Education and Research Hospital, Samsun; 3Department of Neurosurgery, Medical Park Hospital, Samsun, Turkey.

1

İletişim (Correspondence): Dr. Hasan Serdar Işık. Durugöl Mah., 1068. Sok., Zirvekent Sitesi, 6/C Blok Da: 4, Ordu, Turkey.

Tel: +90 - 452 - 234 50 10 / 1060 e-posta (e-mail): serdarisik1@hotmail.com

46

Kafa travması nedeniyle tedavi edilen 954 erişkin olgunun retrospektif değerlendirilmesi

Kafa travmaları, ciddi morbidite ve mortalite sebebi olarak sadece tedavi edilmesi gereken bir sağlık sorunu olmayıp, aynı zamanda önlenebilir olmaları açısından da değerlendirilmesi gereken sosyoekonomik bir sorundur. Özellikle az gelişmiş ve gelişmekte olan ülkelerde ve genç nüfusta, ölüm sebeplerinin arasında ilk sırada travmalar ve yarıdan fazlasında da kafa travmaları bulunmaktadır.[1-7] Kafa travması sonucu meydana gelen kalıcı sakatlıklar, sadece hasta ve ailesini etkilemekle kalmayıp, ülke ekonomileri için de ciddi tahribat sebebi olmaktadır. Bu nedenlerle, travmanın oluşmadan önlenmesi ciddi önem arzetmektedir. Bunu sağlamak için, konu ile ilgili epidemiyolojik verilere ve sonucunda da eğitim ve eksik olduğu tespit edilen noktalarda kurallar oluşturma gereksinimi vardır. Rutland-Brown ve arkadaşlarının[8] yaptığı bir çalışmaya göre, Amerika Birleşik Devletlerinde her yıl yaklaşık 1,1 milyon kişi kafa travması nedeniyle hastaneye başvurmakta, 235.000 hasta yatırılarak tedavi edilmekte ve 50.000 kişi de hayatını kaybetmektedir. Ülkeler hatta bölgeler arasında değişmekle birlikte literatürde bildirilen kafa travması insidansı 2000-3000/1,000,000 civarında verilmektedir.[4,9,10] Ülkemizde kafa travması insidansı ve epidemiyolojisi ile ilgili yeterli çalışma bulunmamaktadır. Yapılan az sayıda çalışmada, tüm dünyada olduğu gibi ülkemizde de şehirleşme ve endüstrileşmenin bir sonucu olarak trafik kazaları, iş kazaları (yüksekten düşme gibi) ve bireysel silahlanmanın sonucu olarak da ateşli silah yaralanmaları kafa travmalarının en sık görülen sebepleridir.[1,3,4,6,11] Nedenleri ve sonuçları bölgesel değişiklikler de gösterebilen kafa travmalarını önleyici, ya da oluştuktan sonra hızlı ve etkin tedavilerin sağlanabilmesi amacıyla bu çalışmaların artırılması gerekmektedir.

Tablo 2. Hastaların travma nedenlerine göre dağılımı Travma nedeni

Sayı

Yüzde

Trafik kazaları Araç içi trafik kazası Araç dışı trafik kazası Düşmeler Yüksekten düşme Diğer düşmeler Darp Ateşli silah yaralanması

719 436 283 121 47 74 70 44

75 46 29 12,5 5 7,5 7,5 5

Tablo 3. Hastaların başvuru zamanına göre dağılımı Başvuru zamanı

Sayı

Yüzde

0-2 saat 2-6 saat 6-24 saat 24 saatten fazla

325 416 137 76

34,1 43,6 14,4 7,9

maları, operasyonları, Glasgow Çıkış Skorları (GÇS) ve mortalite sebepleri açısından retrospektif olarak incelendi ve değerlendirildi. On beş yaş altında olan ve izole spinal travma sebebi ile yatırılan hastalar çalışmaya dahil edilmedi.

Bu çalışma, Samsun Mehmet Aydın Eğitim ve Araştırma Hastanesi, Yerel Etik Komitesinin onayıyla yapıldı.

BULGULAR Kliniğimizde Ocak 2003-Haziran 2008 tarihleri arasında toplam 1805 hasta kafa travması nedeniyle yatırılarak tedavi edilmiş olup, bu hastaların 954’ü (%53) 15 yaş ve üstü olan hastalardı, 954 hastanın 721’i (%75,5) erkek, 233’ü (%24,5) kadın olarak bulundu. Çalışmaya dahil edilen yaş grupları 15 yaş ve üstü olup (15-94) en fazla yoğunluk %52,5 ile 15-40 yaş arasında idi (Tablo 1).

Biz bu çalışmada, Orta Karadenizde travma açısından merkez bir hastane konumunda olan Samsun Mehmet Aydın Eğitim ve Araştırma Hastanesinde yatarak tedavi edilen erişkin 954 hastayı retrospektif olarak inceleyerek, ülkemizin epidemiyolojik veri tabanına katkıda bulunmayı amaçladık.

Kafa travmasının etyolojik nedenleri incelendiğinde trafik kazaları (%75) ilk sırada, sonrasında ise sırasıyla düşmeler (%12,5), darp (%7,5) ve ateşli silah yaralanmaları (%5) yer almaktaydı (Tablo 2). Travma sonrası hastaneye başvuru zamanları açısından yapılan değerlendirilmede, %34 hasta ilk iki saatte, toplamda %78 hasta ise ilk 6 saatte hastanemiz acil servisine kabul edilmişti (Tablo 3). Hastalara gerekli incelemeler ve konsültasyonlar acil serviste yapıl-

GEREÇ VE YÖNTEM Ocak 2003-Haziran 2008 tarihleri arasında Samsun Mehmet Aydın Eğitim ve Araştırma Hastanesi Nöroşirürji Kliniğinde, 15 yaş ve üstü 954 hasta yatırılarak tedavi edildi. Bu hastalar yaş, cinsiyet, travma sebepleri, travmadan sonra hastaneye başvuru zamanları, başvuru Glasgow Koma Skorları (GKS), ek travTablo 1. Hastaların yaş gruplarına göre dağılımı

Yaş aralığı Sayı Yüzde

Yaş aralığı 15-20

21-30

31-40

41-50

51-60

61-70

71-80

≥81

Toplam

106 11,1

207 21,7

188 19,7

176 18,4

97 10,2

94 9,9

67 7,0

19 2

954 100

Cilt - Vol. 17 Sayı - No. 1

47

Ulus Travma Acil Cerrahi Derg

Tablo 4. Hastaların giriş ve çıkış Glasgow Koma Skalasına göre dağılımı

Giriş Glasgow Koma Skalası

13-15 (Hafif)

9-12 (Orta)

3-8 (Ağır)

456 48

297 31

201 21

Sayı Yüzde

Tablo 5. Eşlik eden diğer travmaların dağılımı Eşlik eden travmalar

Sayı

Yüzde

Ortopedik Toraks Batın Maksillofasiyal Diğer (KBB, göz vs.)

162 64 28 46 22

17 7 3 5 2

dı. Bilgisayarlı Beyin Tomografisi (BBT) yatırılması planlanan tüm hastalara rutin olarak çektirildi. Giriş GKS’sine göre, hastaların %48’inde hafif (13-15), %31’inde orta (9-12) ve %21’inde ise ağır (3-8) kafa travması mevcuttu (Tablo 4). Hastaların kafa travması dışında tespit edilen ek patolojileri arasında ilk sırayı ortopedik travmalar (%17), ikinci sırada ise toraks travmaları (%7) yer almaktaydı (Tablo 5). Yapılan incelemeler ve BBT sonrası acil ameliyat gerektiren hasta sayısı 177 (%18,5) olup, ameliyatlar en sık subdural ve epidural hematomlar nedeniyle gerçekleştirildi (Tablo 6). Çalışmamızda GÇS’ye göre yapılan değerlendirmede ise tam iyileşme ile taburcu edilen hasta sayısı 654 (%68,55) iken, mortalite 185 (%19,4) olarak tespit edildi (Tablo 4). Hayatını kaybeden hastaların 128’i (%69) ilk 3 günde kaybedildi. Etyolojileri incelendiğinde ise ilk sırayı yine trafik kazaları alırken, ikinci sırada ateşli silah yaralanmaları yer almıştır (Tablo 7). Yaş aralıklarına göre ölüm oranları da Tablo 8’de özetlenmiştir.

TARTIŞMA Tüm dünyada olduğu gibi ülkemizde de, kentleşme ve endüstrileşmenin ortaya koyduğu en ciddi sorunlardan biri travmalardır. Dünya Sağlık Örgütü verilerine göre travmalara bağlı ölüm oranı tüm dünya için 100,000’de 83,7 iken, ülkemizde bu oran 100,000’de 120 olarak bildirilmektedir.[12] Kafa travmalarına bağlı ölüm oranları, tüm travmalar içinde 1/3 oranında verilmektedir.[6,12] Oluşan sakatlıklar, iş gücü kaybı, teda-

Glasgow Çıkış Skalası Tam Orta Ciddi Bitkisel iyileşme derecede derecede yaşam

sakatlık sakatlık 654 68,5

81 8,5

34 3,5

– –

Ölüm

185 19,5

vi giderleri gibi faktörler de değerlendirildiğinde, durum ciddi bir halk sağlığı sorunu olarak karşımıza çıkmaktadır.

Oransal olarak az gelişmiş ve gelişmekte olan ülkelerde daha sık olsa da tüm dünyada çalışan nüfus gençler ve erkekler olduğundan, kafa travmalarına en çok bu grup maruz kalmaktadır. Çalışmamızda hastalarımızın %75,5’inin erkek olması ve %52,5 oranında 15-40 yaş aralığında bulunması literatür verileriyle uyum göstermektedir.[1,3,4,6,11] Ülkemizde son yıllarda ambulans hizmetlerinde ciddi gelişmeler kaydedilmiştir. Sağlık Bakanlığı ve diğer kurumların ambulans sayılarını artırmaları, teknik iç donanımları ve personel sayı ve kalitesini uygun hale getirmeleri, telefonla çağrı için tek numara sistemine geçilmesi, hasta-ambulans merkezi ve hastaneler arasında etkin ve hızlı bir koordinasyonun sağlanması, tüm ülke sathında olmasa bile büyük merkezlerde, hastaların olay yeri müdahalesi ve doğru hastaneye kısa zamanda ulaşabilmesi açısından önemli katkılar sağlamaktadır. Özellikle trafik kazaları ile ilgili genel istatistikler incelendiğinde, ölümlerin %10’u ilk 5 dakika, %50’si ilk 30 dakika ve %80’i ilk 1 saatte olmaktadır.[3,13] Sadece bu rakamlar bile travmadan sonra oluşan yaralanmaya hızlı, etkin ve doğru merkezde yapılacak müdahaleyi planlamak ve en kısa sürede gerçekleştirmek gereğini ortaya koymaktadır. Çalışmamızda, hastanemiz çevre ilçe ve illerden çok sayıda hasta sevk edilen merkez bir hastane olmasına rağmen, hastaların %78’i travmadan sonra ilk 6 saat sonra acil servisimize getirilmişlerdir. Kesin bir kayıt olmasa da getirilen hastaların büyük çoğunluğu adı geçen ambulans hizmetlerinden faydalanmışlardır. Çalışmamızda kafa travmaları etyolojileri değerlendirilmesinde trafik kazaları %75 gibi oldukça yüksek bir oranda bulunmuştur. Bunun da %46’sı araç içi trafik kazasıdır. Ülkemizde yapılan diğer epidemiyolojik çalışmalarda kafa travması nedeni olan trafik kazası oranları %28 ile %50,6 arasında bildirilmektedir.

Tablo 6. Hastaların ameliyat nedenlerine göre dağılımı

Sayı Yüzde 48

Subdural hematom Epidural hematom Ateşli silah yaralanması Çökme kırığı İntraserebral hematom 86 43

63 31,5

25 12,5

16 8

10 5 Ocak - January 2011

Kafa travması nedeniyle tedavi edilen 954 erişkin olgunun retrospektif değerlendirilmesi

daha yüksek oranlarda bulunmasının sebebini, hastanemizin bölgesel bir travma merkezi şeklinde çalışıyor olmasından kaynaklandığı inancındayız.

Tablo 7. Hayatını kaybeden hastaların travma nedenlerine göre dağılımı Travma nedeni

Sayı

Yüzde

Trafik kazası Ateşli silah yaralanması Düşme Darp Toplam

142 24 12 7 185

77 13,5 6 3,5 100

Hastaların kafa travması yanı sıra etkilenmiş oldukları diğer vücut patolojileri açısından yapılan değerlendirmede, ilk sırada ortopedik kırıklar (%17) ve toraks travmaları (%7) yer almaktaydı. Bu bulgular yapılan diğer çalışmalar ile benzerlik göstermektedir.

[1,3,4,6,13]

Ayrıca İstanbul üniversitesinde yapılan iki ayrı çalışmada araç dışı trafik kazaları, araç içi olanlardan daha fazla bulunmuştur.[4,6] Bir başka nokta ise, literatürdeki diğer çalışmalarda düşmelerin, yüksekten düşmeler de dahil olmak üzere, trafik kazalarına yakın oranlarda olduğudur.[1,3,6] Ancak, bu çalışmaların hepsinde, kafa travması geçirmiş tüm hastaların çalışmaya dahil edildiği görülmüştür. Bizim serimizde, sadece 15 yaş ve üstü erişkin hastaların bulunmasının bu farkı ortaya çıkardığı inancındayız. Kliniğimizde yaptığımız bir başka çalışmada, 851 çocukluk çağı (14 yaş ve altı) kafa travmalı hasta incelenmiş, düşmelerin oranının %70 olduğu tespit edilmiştir. Sonuçta bu iki veri birleştirildiğinde literatürle benzer sonuçlara ulaşılmaktadır. Ancak, görülmüştür ki, ülkemizde ve dünyada, özellikle genç erkek nüfusda trafik kazaları, kafa travmaları ve genel vücut travmalarının en önemli sebeplerinden biridir. Günümüzde bu sebepten, dünyada her 50 saniyede 1 kişi ölmekte, her 2 saniyede 1 kişi yaralanmaktadır.[13] Trafik kazalarının gelişmekte olan ülkelere bedeli 1,4-2 milyar ABD Dolar civarında bildirilmektedir.[13] Ülkemizdeki trafik kazaları istatistiklerine bakıldığında, trafik kazasına neden olan kusurların %98,07’sinin sürücülere ait olduğu ve bunların da %61’inin ilk ve ortaokul mezunu olduğu görülmektedir.[14] Bu anlamda, konu ile ilgili kişisel ve toplumsal eğitime ve trafik kurallarına uyulması adına daha caydırıcı önlemlere ihtiyaç olduğu açıktır.

[1,3,4,6,11]

Hastaların acil serviste yapılan ilk muayeneleri sonucu tespit edilen giriş GKS’leri incelendiğinde hafif (13-15) travmaların %48, orta ve ağır (3-12) travmaların oranı ise %52 olarak tespit edilmiştir. Ülkemizde yapılan diğer epidemiyolojik çalışmalar incelendiğinde orta ve ağır kafa travması oranı Kırış ve arkadaşları tarafından %40,3, Karasu tarafından %36 ve Ökten tarafından ise %34 olarak bildirilmektedir.[1,4,6] Bizim çalışmamızda orta ve ağır travmaların literatüre göre

Çalışmamızda 177 (%18,5) hastaya toplam 200 ameliyat uygulandı. Yirmi üç hasta çeşitli nedenlerle 2 kez ameliyat edildiler. Ameliyatlar en sık subdural ve epidural hematomlar nedeniyle uygulandı. Literatüre göre ameliyat sayısı ile ilgili oranlarımız benzerdir.[1,4,6] Ancak, ameliyat türleri değerlendirildiğinde ise epidural ve çökme kırığı nedeniyle gerçekleştirilen ameliyat oranı azlığımızı da yine bu çalışmadaki yaş grup farklılığı ile açıklamaktayız.

Hastalar GÇS’leri açısından değerlendirildiğinde, tam iyileşme ile taburcu olan hastaların oranı %68,55’dir. Mortalite oranı ise %19,4 olarak bulunmuştur. Hastaların %12’si ise çeşitli oranlarda sakatlıklar ile taburcu edilmiştir. Bu oranlar literatür ile uyum göstermektedir.[1,4,6,13] Bu çalışmada hayatını kaybedenlerin sayısı 185 (%19,4) olarak bulunmuştur. Literatür verileri incelendiğinde bu oran %3 ile 18 arasında bildirilmektedir.

[1,4,6,13] Yüz dokuz (%59) hasta ilk 24 saat içinde kaybedilmiştir. Bu rakamlar göstermektedir ki, mortalite oranımız literatüre göre yüksek olmakla birlikte, serimizdeki orta ve ağır kafa travmalarının diğer çalışmalara göre oransal fazlalığı ve çalışmaya yalnızca erişkin hastaların dahil olması bu şekilde bir sonuç doğurmuştur. Yine kliniğimizde yapılan ve pediatrik 851 kafa travmalı hastayı içeren çalışmamızda mortalite oranımız %3,8 bulunmuştur. Yaş grupları ile mortalite ilişkisi incelendiğinde ise, özellikle 60 yaş üstündeki hastaların oranı %31,3’dür. Bu oran oldukça dikkat çekicidir. Yaşlı hastalarda geçirilen travma dışında, mevcut diğer sistemik sorunlar çocuk ve gençlere oranla mortaliteyi olumsuz etkilediğini anlaşılmaktadır. Literatürde, yaşlı hastalarda geçirilen travmaların sonuçlarının gençlere göre daha olumsuz seyrettiği bildirilmektedir.[4,13,15] Hayatını kaybeden hastaların travma etyolojile-

Tablo 8. Hastaların yaş aralıklarına göre mortalite sayı ve yüzdeleri

Yaş aralığı

15-20

21-30

31-40

41-50

51-60

61-70

71-80

≥81

Toplam

Sayı Mortalite sayısı Yüzde

106 14 13,2

206 32 15,5

186 32 17,2

177 29 15,6

97 21 21,6

96 21 21,8

67 26 38,8

19 10 52,6

954 185 100

Cilt - Vol. 17 Sayı - No. 1

49

Ulus Travma Acil Cerrahi Derg

ri değerlendirilmesinde, ilk sırayı %77 ile trafik kazaları alırken, ikinci sırada ateşli silah yaralanmaları (%13,5) yer almıştır. Bu oranlar ülkemizde yapılan diğer epidemiyolojik çalışmalarla benzer olmakla beraber, ateşli silah yaralanmalarının sayısı ve mortalite oranı daha yüksektir.[1,4,6] Bunun nedenini, son yıllarda ülkemizde ve dünyada oldukça arttığı gözlenen bireysel silahlanmanın bir sonucu olarak değerlendirmekteyiz. Emniyet Genel Müdürlüğü ve Jandarma Genel Komutanlığı verilerine göre Umut Vakfı tarafından hazırlanan “Türkiye’de bireysel silahlanmaya ait istatistikler” isimli rapora göre, Türkiye’de toplam ruhsatlı silah sayısı yaklaşık 2,5 milyon olup, ruhsatsız silahlar da dikkate alındığında (kuru sıkı silahlar hariç olmak üzere) bu rakam 7 ile 10 milyon arasında bildirilmektedir. Bu rapora göre, ruhsatsız ve kuru sıkı silah sayısının hızla arttığı ve suçlarda çok yaygın olarak kullanıldığı açıkça tespit edilmektedir.[16] Sonuç olarak, kafa travmalarının sebep olduğu ölüm ve sakatlıkların bir çoğunun önlenebilir nedenlerden kaynaklandığı gözlenmektedir. Bu çalışma ve literatürdeki diğer epidemiyolojik çalışmalar göstermiştir ki, gerek trafik kazaları, iş kazaları ve gerekse bireysel silahlanmaya karşı alınacak etkin ve ciddi önlemler ile birlikte eğitim çalışmaları, travma sayıları ile sebep olduğu ölüm ve sakatlıkları azaltabilecekdir. Ayrıca, son yıllarda, oluşan travma sonrası hızlı ve etkin tedavi ve bakım koşulları giderek düzelmekle birlikte, tam teşekküllü travma merkezlerinin yaygınlaşması, ambulans, yoğun bakım ve nitelikli personel sayılarını artırılması bahsedilen üzücü sonuçları azaltmada etkili olacağı inancındayız.

KAYNAKLAR 1. Kırış T, İş M, İmer M, Güleç İ, Hepgül K, Ünal F ve ark.

Nöroşirürjide travma pratiği, prospektif epidemiyolojik çalışma. Ulus Travma Derg 1998;4:281-4.

50

2. Jennett B. Epidemiology of head injury. J Neurol Neurosurg Psychiatry 1996;60:362-9.

3. Çırak B, Güven MB, Işık S, Kıymaz N, Demir Ö. Acil servise başvuran travma hastaları ile ilgili epidemiyolojik bir çalışma. Ulus Travma Derg 1999;5:157-9.

4. Ökten Aİ, Ergün R, Akdemir G, Okay Ö, Duyar M, Anasız H ve ark. Kafa travmalarının epidemiyolojisi: 1450 olgunun verileri. Ulus Travma Derg 1997;3:291-7.

5. Gennarelli TA, Thibault LE. Biomechanism of head injury.

In: Wilkins RH, Rengachary SS, editors. Neurosurgery. Vol 1. 1st ed. Mc Graw-Hill Book Co; 1985. p. 1531-6.

6. Karasu A, Sabanci PA, Cansever T, Hepgül KT, Imer M, Dolaş I, et al. Epidemiological study in head injury patients.

Ulus Travma Acil Cerrahi Derg 2009;15:159-63.

7. Markogiannakis H, Sanidas E, Messaris E, Koutentakis D, Alpantaki K, Kafetzakis A, et al. Predictors of in-hospital mortality of trauma patients injured in vehicle accidents.

Ulus Travma Acil Cerrahi Derg 2008;14:125-31.

8. Rutland-Brown W, Langlois JA, Thomas KE, Xi YL. Incidence of traumatic brain injury in the United States, 2003. J Head Trauma Rehabil 2006;21:544-8.

9. Sencer A, İmer M. Günümüzde kafa travmasına genel bir bakış. Türkiye Klinikleri Cerrahi 2004;9:188-95.

10. World Health Organization manual of the international statistic classification of diseases, injuries and causes of death. 9th revision. Genova: WHO, 1975.

11. Çırak B, Berker M, Özcan OE, Özgen T. Kafa travmalarının etken ve sonuçlarına bir bakış: Epidemiyolojik bir çalışma.

Ulus Travma Derg 1999;5:90-2.

12. Peden M, Mc Gee K, Sharma G. The injury chart book: a graphical overview of the global burden of injuries. Genova, WHO, 2002.

13. Sabuncuoğlu H. Trafik kazaları ve istatistiklerle Türkiye gerçeği. Nörotravma ve Yoğun Bakım 2009;4:11-5.

14. Temel F, Özcebe H. Türkiye’de karayollarında trafik kazaları.

Sürekli Tıp Eğitimi Dergisi 2006;15:192-7.

15. Stranjalis G, Bouras T, Korfias S, Andrianakis I, Pitaridis M, Tsamandouraki K, et al. Outcome in 1,000 head injury hospital admissions: the Athens head trauma registry. J Trauma 2008;65:789-93.

16. Türkiye’de bireysel silahlanmaya ilişkin istatistikler. Umut Vakfı. www.umut.org.tr./public-raporlar.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):51-56

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2011.99267

Fractures of the femoral head: what are the reasons for poor outcome?

Femur başı kırıkları: Tedavi stratejisi ne olmalıdır?

Mert ÖZCAN, Cem ÇOPUROĞLU, Kenan SARIDOĞAN

BACKGROUND

AMAÇ

In this article, we aimed to discuss treatment strategies in fracture of the femoral head, which is a very rare injury.

Bu yazıda, çok nadir bir yaralanma olan femur başı kırıklarında tedavi stratejilerinin tartışılması amaçlandı.

METHODS

GEREÇ VE YÖNTEM

We reviewed five patients (six fractures) who admitted to our emergency department due to femoral head fracture between March 2006 and December 2007. Functional outcomes of the patients who were treated operatively and nonoperatively were compared.

Mart 2006 ile Aralık 2007 arasında acil servise femur başı kırığı ile başvuran beş hastanın altı kırığı incelendi. Cerrahi ve cerrahi dışı yöntemlerle tedavi edilen hastaların fonksiyonel sonuçları karşılaştırıldı.

RESULTS

Hastaların yarısı cerrahi yöntemle, yarısı da cerrahi dışı yöntemlerle tedavi edildi. Mükemmel ve iyi sonuçların oranı %50 bulundu. İki taraflı yaralanması bulunan hastada avasküler nekroz gelişti. Bu hastada fonksiyonel sonuçlar kötü bulundu. Cerrahi ile tedavi edilen hastalardan birinde erken posttravmatik artrit görüldü, bu hastanın fonksiyonel sonuçları orta bulundu.

Half of the fractures were treated nonoperatively and half of them surgically. We observed a rate of 50% excellent to good results. Avascular necrosis developed in a patient with bilateral injury. The functional results were poor for this patient. Early posttraumatic arthritis was observed in a patient who was treated surgically; this patient had moderate results.

CONCLUSION

BULGULAR

SONUÇ

We should aim at anatomic reduction of the fragments with minimum soft tissue injury. The best approach should be chosen for excellent view of the fragments. We should not forget that half of these patients will have a poor outcome despite all treatment strategies.

Minimum yumuşak doku travması ile anatomik redüksiyonun sağlanması bu kırıkların tedavisindeki amacımız olmalıdır. Parçaların en iyi görüntüsü hangi yaklaşımla sağlanacaksa o yaklaşım tercih edilmelidir. Şu unutulmamalıdır ki, tüm tedavi seçeneklerine rağmen bu hastaların fonksiyonel sonuçları kötü olabilmektedir.

Key Words: Femur head; fracture; Pipkin; outcome.

Anahtar Sözcükler: Femur başı; kırık; Pipkin; sonuçlar.

Femoral head fractures are seen in multitraumatized patients, especially after motor vehicle accidents.

[1] They are very rare injuries. Keely and Lipscomb[2] reported that the occurrence rate of femoral head fracture is two cases per one million per year. Therefore, more attention should be paid to the treatment of these patients.

The most common mechanism is dashboard injuries, in which the forces are transmitted through the shaft of the femur to the femoral head and acetabulum.

[1] Traumatic posterior hip dislocations and femoral head injuries are common in this type of injury.[3] The association of traumatic hip dislocation and femoral head fracture is variable in the literature (4-17%).[4-12]

Department of Orthopaedics and Traumatology, Trakya University Faculty of Medicine, Edirne, Turkey.

Trakya Üniversitesi Tıp Fakültesi, Ortopedi ve Travmatoloji Anabilim Dalı, Edirne.

Correspondence (İletişim): Mert Özcan, M.D. Trakya Üniversitesi Tıp Fakültesi Ortopedi ve Travmatoloji Anabilim Dalı, 22030 Edirne, Turkey.

Tel: +90 - 284 - 235 76 41 / 4700 e-mail (e-posta): mertozcan@trakya.edu.tr

51

Ulus Travma Acil Cerrahi Derg

Treatment strategies in femoral head fractures are also controversial due to the low incidence of these fractures and the different classification systems used in the literature.[1,13] In the past 20 months, we had six cases of femoral head fracture with or without acetabulum fracture.

This is a very high incidence in this short time period.

Therefore, we decided to discuss the treatment strategies based on our own experience to help optimize the treatment strategies of these fractures, in view of the controversies remaining in the literature on the classification and outcome of these injuries.

MATERIALS AND METHODS We reviewed five patients (six fractures) who admitted to our emergency department due to femoral head fracture between March 2006 and December 2007. Medical data and radiographs including computerized tomography (CT), bone scan and magnetic resonance imaging (MRI) of the patients were reviewed for analysis. During the last follow-up, femoral head viability was investigated with MRI or bone scan. Each fracture was classified according to Pipkin,[14] Brumback[13] and AO[15] classifications in order to evaluate the patients more precisely. Functional outcome was evaluated with the Merle dâ&#x20AC;&#x2122;Aubigne and Postel score[16] and the Thompson and Epstein score.

(a)

(c)

(b)

The Merle dâ&#x20AC;&#x2122;Aubigne and Postel score evaluates the hip function in three categories: pain, mobility and walking, with each section having a maximum score of 6 points. Eighteen points indicate excellent, 15-17 points good, 12-14 points fair, and <12 points poor results. The Thompson and Epstein score evaluates functional and radiological outcome. Numeric scores are not used in this scoring system. Each of the functional and radiological outcome measurements are described as excellent, good, moderate or poor.

[17]

Complications like heterotopic ossification, avascular necrosis (AVN) and posttraumatic arthritis were also documented.

RESULTS Five patients with six femoral head fractures were treated in our hospital between March 2006 and December 2007. Three of the fractures were stable with minimum displacement; therefore, they were treated nonoperatively (Figs. 1, 2), while three of them were treated with open reduction and internal fixation (ORIF) (Fig. 3). The average age at the time of injury was 28 (20-36) years. Most of the fractures were due to traffic accident; only one patient sustained injury from a motor vehicle accident. The fractures were classified and are summarized in Table 1 according to AO, Brumback and Pipkin classifications. All femoral head dislocations were reduced within the first 24 hours. We used Kocher-Langenbeck approach. The minimum follow-up was 16 months. One type I and two type II fracture dislocations according to Pipkin classification were treated nonoperatively. Two patients with Pipkin type II and one patient with type IV injury were treated with ORIF.

(d)

Fig. 1. This 21-year-old male patient was treated conservatively. Preoperative X-ray (a) and CT (b) of the patient showed the fractures on both sides (arrows). After one-year follow-up, we observed that the fractures were united (c); however, bilateral avascular necrosis of the femoral head was observed in the patient as seen in MRI (d). This patient had poor functional outcome.

52

The overall outcomes were excellentgood in 3 fractures, fair in 1 and poor in 2 (Table 1). No sciatic nerve injury, deep wound infection or heterotopic ossification was observed.

AVN was seen in 2 hips.

This patient had bilateral injury and was treated nonoperatively. This paOcak - January 2011

Fractures of the femoral head: what are the reasons for poor outcome?

(a)

(b)

(c)

Fig. 2. This 29-year-old male patient was treated conservatively. Preoperative X-ray (a) and CT (b) of the patient showed Pipkin type II fracture (arrow). This patient healed without any complication with excellent functional outcome.

tient also had bilateral deep vein thrombosis despite low molecular weight heparin prophylaxis. All the fractures were united. In one of the operated patients, early posttraumatic arthritis developed. This patient is still being followed, and may require arthroplasty in the future.

(a)

(d)

(g)

(b)

DISCUSSION Femoral head fractures are serious injuries. They are commonly seen after high-energy trauma following traumatic hip dislocation. Femoral head fracture dislocations are one of the few orthopedic emergen-

(c)

(e)

(f)

(h)

(覺)

Fig. 3. This 20-year-old female patient had fracture dislocation of the hip joint. She had both acetabular fracture and fracture of the femoral head (Pipkin type IV). (a) The initial X-ray of the patient before the reduction of the hip joint. After reduction, we observed displaced femoral head fracture (b, c). Figs. (d-f) are intraoperative photographs of the patient. The fracture, reduction and fixation with two countersunk screws are seen. Figure (g) and (h) are postoperative X-rays of the patient.

The anatomic reduction and fixation of the fragment can be seen. Postoperative CT also supports the quality of fixation (i).

Cilt - Vol. 17 Say覺 - No. 1

53

Ulus Travma Acil Cerrahi Derg

Table 1. Demographic data and results of the patients No Age/Sex Pipkin/Side Brumback AO 1 2 3 4 5 5

29/M 34/M 36/M 20/F 21/M 21/M

II/R II/R II/L IV/L II/L I/R

2A 2B 2A 2A 2A 1A

Treatment

C13 Nonoperative C13 ORIF C13 ORIF C13 ORIF C13 Nonoperative C12 Nonoperative

Approach Complication Follow-up M. d’Aub. – KL KL KL – –

– PTA – – AVN AVN

28 m 16 m 16 m 32 m 16 m 16 m

T&E

Excellent Excellent Fair Fair Good Good Excellent Excellent Poor Poor Poor Poor

M. d’Aub: Merle d’Aubigne score; T&E: Thompson and Epstein score; M: Male, F: Female; ORIF: Open reduction internal fixation; KL: Kocher-Langenbeck; PTA: Post traumatic arthritis; AVN: Avascular necrosis; m: Months.

cies, and reduction must be done as soon as possible under general anesthesia with good muscle relaxation to prevent further damage. After reduction, careful examination on small-cut CT scans should be performed for reduction quality, comminution and free intraarticular fragments.[18] MRI could also be added to the diagnostic tools for further evaluation of soft tissues, blood flow to the femoral head and cartilage damage.

[19,20] The information provided by these radiologic diagnostic modalities allows a complete understanding of the fracture pattern for the planning of further treatment.

Data about the outcome of the femoral head fractures reported in the literature are not evident. Similar to the literature, our series of femoral head fractures involved different fracture types and different treatment modalities. Since this trauma is rarely seen, the published series are small in number (5 patients in our series); Henle[21] reported 12 patients over an 8-year period. Therefore, making a statistical analysis or any recommendation is almost impossible. For the same reason, prospective trials regarding outcome and treatment modalities are also not possible.

Definitive treatment should be planned according to the expectations, physiological status and well-being of the patient. Conservative treatment is accepted only when postreduction CT demonstrates anatomical reduction.[21] Closed nonoperative treatment can be the best option for Pipkin type I and type II fractures. If closed reduction is not appropriate, ORIF should be the choice of treatment, excision of the fragments is the worst of all.[1] These fractures are intraarticular fractures requiring anatomical reduction and stable fixation. Most of the patients will benefit more or less from surgical treatment. However, surgical treatment has some disadvantages. According to the literature, excellent and good results in Pipkin type I and type II fractures are achieved in more than 75% after closed treatment, while ORIF yields similar results in 65% of the cases. However, good or excellent results are achieved in only 50% of cases after excision of the fragments.[8,9,11-13,22-27] Over the past decades, rates of excellent or good results of 40-70% have been published in the litera54

ture.[8,22-24,28-31] Our rate of excellent and good results was 50%, which was similar to the literature. Two of the three patients who had excellent and good results were treated with ORIF. On the other hand, AVN was seen in two fractures; this patient was treated conservatively and had poor results. Therefore, we can say that the treatment modality is not associated with functional outcome in these injuries.

One of the factors affecting the outcome is surgical exposure. Although initial damage to the cartilage is the main factor in the determination of final outcome in femoral head fractures, poor results in many cases are related to the difficulties encountered in obtaining adequate exposure, reduction and osteosynthesis.

[1] Three surgical approaches are advocated in the literature: anterolateral (Watson-Jones),[22,24,32] anterior (Smith-Patterson)[24,25,31] and posterior (Kocher-Langenbeck).[26] Anterior approaches are related with high rates of heterotopic ossification, but obtain an optimal exposure of the fragments of the femoral head.[1] Swiontkowski et al.[33] compared anterior versus posterior approach in the treatment of Pipkin type I and II fractures. They found that anterior approach caused less blood loss, shorter operation time and better visualization but more heterotopic ossification. Another criticism of the anterior approach is that it will damage the remaining anterior blood supply.[6,7,29] We treated three patients (50%) operatively. We used posterior Kocher-Langenbeck approach for operations. Although it is reported that the anterior (Smith-Patterson) approach is associated with less blood loss, shorter operation time and better visualization, the functional outcomes were identical for both procedures.[33] One of the disadvantages of the anterior approach is deterioration of the remaining anterior blood circulation after posterior dislocation and the associated posterior circulatory loss;[29] however, Stockenhuber et al.[22] showed that there is little or no interference with the blood supply of the femoral head via this approach. On the other hand, the posterior approach is associated with additional damage to the posterior circulation, which was deteriorated after posterior dislocation and has potential for AVN. However, the posterior approach is recommended for Ocak - January 2011

Fractures of the femoral head: what are the reasons for poor outcome?

Pipkin type IV fractures. Simultaneous repair of both the posterior wall of the acetabulum and femoral head can be achieved in this way.[28,32] We used the posterior approach for the operations without any major intraoperative complications. AVN was not seen in our operatively treated patients. We also observed no postoperative heterotopic ossification. In our opinion, the experience of the surgeon is the key point for the success of the operation rather than the technique itself.

Recently, favorable results with trochanteric flip osteotomy and ORIF of the femoral head have been published; however, their overall excellent or good results did not differ much from the literature.[1,21] The increased morbidity of this operation should also be remembered. Therefore, we can say that every fracture of the femoral head should not promptly be treated with ORIF. Additional damage done during surgical interventions must not be forgotten. The treatment of choice should be well explained to the patient and expectations of the patients should be taken into consideration. ORIF does not mean excellent results; patients may also benefit from conservative treatment strategies. We should not forget that we cannot control the injury at the time of impaction. Perhaps that is the main key of all treatment strategies; this must be investigated further.

Fixation methods are variable. We used 2 mm countersunk titanium minifragment screws for the fixation in our patients without any problem. Some authors[23,34] advocated titanium or Herbert screws for MRI compatibility. Biodegradable screws have also been used successfully.[9] Total hip replacement should be chosen for elderly patients with Pipkin type III fractures. Excision of the fragment was recommended by Epstein[6,7,29] in the 1970s, however, maintaining joint congruity is a prerequisite for a good outcome, which is reinforced by more recent studies.[5,8,24,25] We believe that the poor outcome of these patients is mostly due to major complications. These complications included AVN of the femoral head (0-24%), posttraumatic osteoarthritis (0-72%), peripheral nerve damage (7-27%). and heterotopic ossification (254%).[1,21] In our patient group, AVN was seen in two fractures and posttraumatic arthritis in one. AVN can be caused by the damage at the time of impaction or it can be iatrogenic. Care should be taken during reduction of the hip with gentle maneuvers to prevent further vascular impairment.

AVN and posttraumatic arthritis are serious complications and can be treated with joint replacement.

Some authors even recommend total hip replacement as the initial treatment for Pipkin type III fractures; however, this is justifiable only for older patients. Total joint replacement or hip arthrodesis can only be Cilt - Vol. 17 Say覺 - No. 1

recommended after the failure of ORIF. We are still following our patients who had serious complications, and they may require further surgery.

Although we observed no heterotopic ossification, its incidence is not low.[35] It is mostly seen after intracranial injury in multitrauma patients. These patients can be treated with indomethacin or low-dose irradiation for prophylaxis.

It is believed that every effort should be attempted for the preservation of the joint. Despite the modern treatment modalities and increased technology, most of these patients develop some degree of joint arthritis or joint pain. If we cannot protect the joint, hip arthrodesis is the best option for young patients; for the elderly, total hip replacement seems to be the best choice.

We think that functional results are not directly related to the treatment modality. The severity of the injury, general health of the patient, timing of the surgery, timing of admission to the hospital, timing of reduction of the hip dislocation, injury at the time of impaction, cartilage injury, and subchondral collapse are all important factors that affect the outcome in these patients.

In conclusion, we believe that newer technologies and techniques will improve the outcome of femoral head fractures in the coming decades. In the treatment, we should aim at anatomic reduction of the fragments with minimum soft tissue injury. When surgery is required, we should choose the best approach for excellent view of the fragments. Lastly, we should not forget that half of these patients will have a poor outcome despite all treatment strategies.

REFERENCES 1. Kloen P, Siebenrock KA, Raaymakers ELFB, Marti RK, Ganz R. Femoral head feactures revisited. European Journal of Trauma 2002;4:221-3.

2. Kelly PJ, Lipscomb PR. Primary vitallium-mold arthroplasty for posterior dislocation of the hip with fracture of the femoral head. J Bone Joint Surg [Am] 1958;40:675-80.

3. Funsten RV, Kinser P, Frankel CJ. Dashboard dislocation of the hip: a report of twenty cases of traumatic dislocation. J Bone Joint Surg 1938;20:124-32.

4. Armstrong JR. Traumatic dislocation of the hip joint; review of 101 dislocations. J Bone Joint Surg [Br] 1948;30:430-45.

5. Butler JE. Pipkin Type-II fractures of the femoral head. J Bone Joint Surg Am 1981;63:1292-6.

6. Epstein HC. Posterior fracture-dislocations of the hip; longterm follow-up. J Bone Joint Surg [Am] 1974;56:1103-27.

7. Epstein HC. Posterior fracture dislocations of the hip. J Bone Joint Surg [Am] 1961;43:1079-1098 8. Hougaard K, Thomsen PB. Traumatic posterior fracture-dislocation of the hip with fracture of the femoral head or neck, or both. J Bone Joint Surg [Am] 1988;70:233-9.

9. Jukkala-Partio K, Partio EK, Hirvensalo E, Rokkanen P. Absorbable fixation of femoral head fractures. A prospective 55

Ulus Travma Acil Cerrahi Derg

study of six cases. Ann Chir Gynaecol 1998;87:44-8.

10. Kelly RP, Yarbrough SH 3rd. Posterior fracture-dislocation of the femoral head with retained medial head fragment. J Trauma 1971;11:97-108.

11. Lang-Stevenson A, Getty GJM. The Pipkin fracture dislocation of the hip. Injury 1987;18:264-69.

12. Roeder LF Jr, DeLee JC. Femoral head fractures associated with posterior hip dislocation. Clin Orthop Relat Res 1980:121-30.

13. Brumback RJ, Kenzora JE, Levitt LE, Burgess AR, Poka A. Fractures of the femoral head. Hip 1987:181-206.

14. Pipkin G. Treatment of grade IV fracture-dislocation of the hip. J Bone Joint Surg [Am] 1957;39:1027-42 15. Ganz R. Proximal femur. In: Müller ME, Allgöwer M, Schneider R, Willenegger H, editors. Manual of internal fixation.

Techniques recommended by the AO-ASIF group. Berlin: Springer; 1992. p. 519-21.

16. Merle d’Aubigné R, Postel M. Functional hip arthroplasty with acrylic prosthesis. J Bone Joint Surg [Br] 1954;36:45175.

17. Thompson VP, Epstein HC. Traumatic dislocation of the hip; a survey of two hundred and four cases covering a period of twenty-one years. J Bone Joint Surg [Am] 1951;33:746-78.

18. Moed BR, Maxey JW. Evaluation of fractures of the femoral head using the CT-directed pelvic oblique radiograph. Clin Orthop Relat Res 1993:161-7.

19. Potter HG, Montgomery KD, Heise CW, Helfet DL. MR imaging of acetabular fractures: value in detecting femoral head injury, intraarticular fragments, and sciatic nerve injury. AJR Am J Roentgenol 1994;163:881-6.

20. Horii M, Kubo T, Hirasawa Y. Radial MRI of the hip with moderate osteoarthritis. J Bone Joint Surg [Br] 2000;82:364-8.

21. Henle P, Kloen P, Siebenrock KA. Femoral head injuries: Which treatment strategy can be recommended? Injury 2007;38:478-88.

22. Stockenhuber N, Schweighofer F, Seibert FJ. Diagnosis, therapy and prognosis of Pipkin fractures (femur head dislocation fractures) Chirurg 1994;65:976-82. [Abstract] 23. Marchetti ME, Steinberg GG, Coumas JM. Intermediateterm experience of Pipkin fracture-dislocations of the hip. J

56

Orthop Trauma 1996;10:455-61.

24. Schönweiss T, Wagner S, Mayr E, Rüter A. Late results after fracture of the femoral head. Unfallchirurg 1999;102:776-83.

[Abstract] 25. Mowery C, Gershuni DH. Fracture dislocation of the femoral head treated by open reduction and internal fixation. J Trauma 1986;26:1041-4.

26. Vermeiren JA, van Hoye M. Three cases of femoral head fracture in a single car accident. J Trauma 1991;31:579-81.

27. Weigand H. Combination injuries of the hip joint including shear fractures of the femoral head. Aktuelle Traumatol 1980;10:1-8.

28. Dreinhöfer KE, Schwarzkopf SR, Haas NP, Tscherne H. Femur head dislocation fractures. Long-term outcome of conservative and surgical therapy. Unfallchirurg 1996;99:400-9.

[Abstract] 29. Epstein HC, Wiss DA, Cozen L. Posterior fracture dislocation of the hip with fractures of the femoral head. Clin Orthop Relat Res 1985;(201):9-17.

30. Sahin V, Karakaş ES, Aksu S, Atlihan D, Turk CY, Halici M. Traumatic dislocation and fracture-dislocation of the hip: a long-term follow-up study. J Trauma 2003;54:520-9.

31. Stannard JP, Harris HW, Volgas DA, Alonso JE. Functional outcome of patients with femoral head fractures associated with hip dislocations. Clin Orthop Relat Res 2000:44-56.

32. Duquennoy A, Decoulx J, Capron JC, Torabi DJ. Traumatic dislocations of the hip with fracture of the femur head. Apropos of 28 cases. Rev Chir Orthop Reparatrice Appar Mot 1975;61:209-19. [Abstract] 33. Swiontkowski MF, Thorpe M, Seiler JG, Hansen ST. Operative management of displaced femoral head fractures: casematched comparison of anterior versus posterior approaches for Pipkin I and Pipkin II fractures. J Orthop Trauma 1992;6:437-42.

34. Murray P, McGee HM, Mulvihill N. Fixation of femoral head fractures using the Herbert screw. Injury 1988;19:220-1.

35. Boes M, Kain M, Kakar S, Nicholls F, Cullinane D, Gerstenfeld L, et al. Osteogenic effects of traumatic brain injury on experimental fracture-healing. J Bone Joint Surg [Am] 2006;88:738-43.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):57-60

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2011.93763

The diagnosis and treatment of penile fracture: our 19-year experience Penis kırığının tanı ve tedavisi: 19 yıllık deneyim Abdullah GEDİK, Devrim KAYAN, Sait YAMİŞ, Yakup YILMAZ, Kamuran BİRCAN

BACKGROUND

AMAÇ

The aim of this study was to retrospectively evaluate our approach to the diagnosis and treatment of penile fracture.

Bu çalışmada, penis kırıkların tanı ve tedavisine yaklaşımlar retrospektif olarak değerlendirildi.

METHODS

GEREÇ VE YÖNTEM

We retrospectively evaluated the results of 107 patients with penile fracture treated in our clinic between January 1990 and January 2009. Patient age, etiology of each fracture, history, physical examination results, radiologic findings, type of treatment, and postoperative complications were recorded. In 5 cases cavernosography was performed and in 8 cases retrograde urethrography.

Ocak 1990 ile Ocak 2009 tarihleri arasında kliniğimize penis kırığı nedeniyle başvuran 107 hasta retrospektif olarak değerlendirildi. Hastaların yaşı, kırığın nedeni, kırığın oluş zamanı, fiziksel inceleme bulguları, radyolojik bulgular, uygulanan tedavi şekli ve ameliyat sonrası komplikasyonlar kaydedildi. Beş hastaya kavernozografi ve 8 hastaya retrograd üretrografi yapıldı.

RESULTS

BULGULAR

The most common etiologies of penile fracture were coitus and manually bending the penis for detumescence. Diagnoses were made based on history and physical examination in 102 patients and cavernosography in 5 patients. In order to evaluate urethral injury in 8 cases, retrograde urethrography was performed. Rupture was repaired surgically in 101 patients, but 6 patients were treated conservatively. Among the 6 conservatively treated patients, 3 developed penile curvature 6 months post-treatment; no complications occurred in the surgically treated patients.

Cinsel ilişki ve uygunsuz ortamda erekte peniste detümesansı sağlamak için elle bükme penis kırığının en sık nedenleri olarak bulundu. Tanı 102 hastada anamnez ve fiziksel incelemeyle kondu. Kavernozografi 5 hastada yapıldı. Üretral yaralanma düşünülen 8 hastaya retrograd üretrografi yapıldı. Yırtıklar 101 hastada cerrahi olarak onarıldı, 6 hastaya ise konservatif tedavi yapıldı. Ameliyattan sonraki 6. ayda yapılan kontrollerde konservatif tedavi yapılan 6 hastanın 3’ünde penil kurvatur gelişirken cerrahi yapılan hastalarda hiçbir komplikasyon gelişmedi.

CONCLUSION

SONUÇ

Cavernosography should be performed only when history and physical examination are insufficient for diagnosis, and retrograde urethrography should be performed when urethral injury is suspected. In order to prevent the development of penile curvature and to ensure rapid recovery, early surgical repair is advised.

Anamnez ve fiziksel inceleme ile kesin tanı konulamayan hastalarda kavernozografi, üretra yaralanması şüphesi olanlara ise üretrografi yapılmalıdır. Penis kırığının erken cerrahi onarımı penis kurvatur gelişimini önlemek ve hızlı iyileşmeyi sağlamak için önerilmektedir.

Key Words: Cavernosography; conservative treatment; penile fracture; surgical treatment.

Anahtar Sözcükler: Kavernozografi; konservatif tedavi; penil kırık; cerrahi tedavi.

Department of Urology, Dicle University Faculty of Medicine, Diyarbakır, Turkey.

Dicle Üniversitesi Tıp Fakültesi, Üroloji Anabilim Dalı, Diyarbakır.

Correspondence (İletişim): Abdullah Gedik, M.D. Dicle Üniversitesi Tıp Fakültesi Üroloji Anabilim Dalı, 21280 Diyarbakır, Turkey.

Tel: +90 - 412 - 248 80 01 e-mail (e-posta): abgedik@gmail.com

57

Ulus Travma Acil Cerrahi Derg

Penile fracture is the rupture of the tunica albuginea surrounding the corpus cavernosum. Its etiology is generally blunt trauma that occurs while the penis is erect. Manually bending an erect penis, some forms of coitus, masturbation, and falling out of bed can cause penile fracture.[1,2] Anamnesis and physical examination are the most important diagnostic tools. Anamnesis typically includes sudden detumescence and ecchymotic swelling of the penis following a cracking sound while the penis is erect.[3] A large penile hematoma can be seen on the physical examination. The hematoma can sometimes spread to the scrotum and pubic area, and generally the penis deviates to the opposite side.

Anamnesis and physical examination are generally adequate for diagnosis, but if these two methods are insufficient, then cavernosography becomes necessary for the diagnosis.[4,5] Sometimes corpus spongiosum and urethral injury are seen as adjacent injuries. It was reported that adjacent urethral injury is seen in 10%-33% of penile fractures, and when present, gross hematuria or urethrorrhagia with voiding difficulty are additional clinical findings.[6,7] Retrograde urethrography is necessary for the diagnosis of urethral injury.

MATERIALS AND METHODS All cases of penile fracture that presented to our hospital between January 1990 and January 2009 were retrospectively evaluated. The etiological factors, elapsed time from trauma to presentation, size and location of penile hematomas, penile deviation, urethrorrhagia, and the location and size of ruptures were recorded.

When the patient history and physical examination were insufficient for diagnosing penile fracture, the diagnosis was confirmed by cavernosography. In patients with microscopic or gross hematuria with or without urethrorrhagia retrograde urethrography was performed to confirm urethral injury.

In surgically treated patients, wide-spectrum antibiotics were prophylactically administered. Urethral Foley catheters were placed in all patients intraoperatively, and elastic bandages with light pressure were applied in all patients postoperatively. For conservative treatment, bed rest, elastic bandages, penoscrotal elevation, and prophylactic antibiotics were used.

All patients were followed up at three and six months post-treatment.

RESULTS All 107 patients presented to the hospital due to penile pain, penile ecchymotic swelling following sudden detumescence, or following blunt trauma to an erect penis. Mean age of the patients was 28Âą11 years (range: 17-56 years). The most common types 58

of trauma were coitus and manually bending the erect penis. The types of trauma that caused penile fracture are summarized in Table 1.

The mean elapsed time from trauma to presentation to hospital was 6Âą4 hours (range: 1-24 hours).

On the physical examination, urethrorrhagia was observed in 2 patients and localized hematoma was seen in 5 patients. Large hematomas caused penile deviation in 73 patients. In 29 patients, there was a large hematoma extending to the scrotum and pubic area.

It was possible to palpate the rupture in 83 patients, but palpation was not possible in 19 patients because of large hematomas and severe pain. In the remaining 5 patients with localized hematomas (they did not describe hearing a cracking sound), cavernosography was performed to observe the rupture and diagnose penile fracture.

In 6 patients with a microscopic hematuria and in 2 patients with urethrorrhagia, retrograde urethrography was performed in order to determine if there was adjacent urethral and corpus spongiosum injury. Two patients had incomplete urethral injury and urethrorrhagia, but 6 patients with a microscopic hematuria did not have urethral injury.

With the exception of the 8 patients that underwent urethrography and the 5 that underwent cavernosography, no additional diagnostic imaging was performed.

Table 1. Etiological factors of penile fracture according to patient reports Etiology Coitus Manually bending the penis Rolling over in bed during sleep Masturbation Falling on an erect penis No explanation Total

Number of Patients 46 (43%) 26 (24.3%) 23 (21.5%) 6 (5.6%) 3 (2.8%) 3 (2.8%) 107 (100%)

Table 2. Clinical findings of surgically repaired patients

n

Localization of the lesion Left corpus cavernosum 55 (54.5%) Right corpus cavernosum 42 (41.6%) Both corpora cavernosa 4 (3.9%) Length of rupture (cm) 0.5-1 36 (35.7%) 1-2 61 (60.4%) 2-4 4 (3.9%) Total number of patients 101 (100%) Adjacent injuries Urethra and corpus spongiosum 2 (1.87%) Ocak - January 2011

The diagnosis and treatment of penile fracture

In 101 of the 107 patients, surgical repair was performed under spinal anesthesia. The clinical findings of these 101 patients are summarized in Table 2.

In 87 patients, a subcoronal circular incision was used, whereas in 14 patients in whom it was possible to palpate the rupture, a semicircular incision was made over the rupture. Following the evacuation of the hematoma, the rupture in the cavernosal body was sutured with 2/0 interrupted Vicryl sutures. In patients with adjacent urethral injury, the urethra was repaired with 4/0 interrupted Vicryl sutures. No drainage was necessary in any of the cases. All catheters placed preoperatively were removed the following day, except in 2 patients with urethral injury, in which case the catheter was removed 3 weeks postoperatively after performing pericatheter urethrography to determine patency of the urethra. All patients were discharged the day after catheter removal and were advised to refrain from coitus for 6 weeks.

Mean length of hospitalization in the surgically treated patients was 1.2 days (range: 1-4 days). No early postoperative complications were seen in any of the patients. Conservative treatment was administered in 3 patients who refused surgery and in 3 patients with minimal extravasation in cavernosography. Mean length of hospitalization in the conservatively treated patients was 5 days (range: 4-7 days).

In all, 89 (88%) of the surgically treated patients and 6 (100%) of the conservatively treated patients presented for the three-month follow-up, while 76 (75%) and 4 (66%), respectively, presented for the sixmonth follow-up.

At the three-month follow-up of the surgical patients, 18 (17.8%) complained of slight loss of sensation in the penis and in the glans, which had completely resolved at the six-month follow-up. At the three-month follow-up of the conservatively treated patients, 2 of the 3 patients who refused surgery and 1 of the 3 patients with minimal extravasation reported minor pain and penile curvature of less than 30 degrees, which were not problematic; at the six-month follow-up, none of the patients was experiencing pain, but penile curvature persisted.

DISCUSSION Penile fracture is a rare urologic emergency. It is the rupture of the tunica albuginea of the corpus cavernosum, which generally develops after blunt trauma while the penis is erect. The tunica albuginea is 2 mm thick in a flaccid penis, but decreases to 0.25 mm during an erection, and a sudden increase in intracorporeal pressure due to blunt trauma during an erection could easily result in rupture.[4] According to hospital statistics in the United States, the incidence of penile Cilt - Vol. 17 Sayı - No. 1

fracture is 1/175,000.[8] In total, 1,331 penile fracture cases were reported in 183 papers between 1935 and 2001, and most were reported from countries of the Mediterranean and Middle East. Coitus as the etiological factor of penile fracture was reported in 33% and 60% of cases.[9,10] Zargooshi[11] published the largest series of penile fractures (172 cases) and reported that in 69.1% of cases, the etiological factor was manually bending an erected penis for detumescence while in 8.1% of cases, the etiological factor was coitus. Özen et al.,[12] Asgari et al.[13] and el-Sherif et al.[14] reported that penile fractures were caused by manually bending the penis for detumescence in 64% of cases (16 of 25 patients), 78% of cases (25 of 32 patients), and 61.9% of cases (13 of 21 patients), respectively.

The most frequent etiological factor in the present series was coitus (43%). The incidence of manually bending the penis for detumescence in the present series was 24.3% (26 patients). The reported incidence of the various etiological factors for penile fracture varies because patients do not always accurately report the cause, probably due to embarrassment. One of our patients from a rural area presented to a primary care center and reported that he had suffered a scorpion bite on his penis. He was treated with scorpion antiserum prior to being referred to our clinic. Even after repairing his 1.5-cm rupture, he still did not reveal the actual cause of his penile fracture.

In the present study, 3 patients refused to report the cause of fracture. Possible etiological factors other than coitus and manual bending were turning over during sleep, falling out of bed, masturbation, and being kicked by an animal. Despite the difficulty in determining the etiological factor, the diagnosis of penile fracture is not difficult. Patients complain about penile pain, deviation and ecchymotic swelling following sudden detumescence of the penis, accompanied by a cracking sound. Some authors suggest that cavernosography should be routinely performed in order to differentiate penile fracture from dorsal vein rupture,[15] but one should always consider that anaphylactic reactions can occur in response to use of opaque material, and extravasation of opaque material could result in fibrosis. During cavernosography of large hematomas, determination of the length of rupture can sometimes be limited and cause false-negative results.

We performed cavernosography in 5 of our patients with small hematomas, as they were not sure if they heard a cracking sound. In 2 of these patients, the extravasation was quite large and we repaired the rupture surgically. The other 3 patients with minimal extravasation were treated conservatively.

It is reported that urethral injury could be an adjacent injury in 10%-33% of penile fractures.[6,7] The incidence of adjacent urethral injury was low in reports 59

Ulus Travma Acil Cerrahi Derg

from Iran, Persian Gulf countries and Japan (0-3%), but high in reports from European countries (20%38%).[11] This variation in the incidence of urethral injury is probably due to differences in etiological factors between countries. The incidence of urethral injury in the present study was 1.8% (2 patients), and both cases had urethrorrhagia and difficulty voiding.

We performed retrograde urethrography in these 2 patients as well as in patients with microscopic hematuria. In the present study, urethral injury was diagnosed in only 2 patients who had urethrorrhagia and difficulty voiding; therefore, we suggest performing retrograde urethrography only in patients with difficulty voiding and/or urethrorrhagia, and not in those with only microscopic hematuria.

Early reports suggested that penile fractures should be treated conservatively with elastic bandages, cold compress, antibiotics, fibrinolytics, and anti-inflammatory drugs; however, with long-term follow-up, it was observed that conservatively treated patients experienced complications such as penile pain, penile curvature, arteriovenous fistulas, and erectile dysfunction, at the rate of 10%-53%.[9,16,17] Muentener et al.[3] compared surgical and conservative treatments and reported success rates of 92% and 59%, respectively.

We treated 6 of our patients conservatively and during the long-term follow-up, 3 of them developed penile curvature of less than 30 degrees and penile pain, which did not interfere with coitus. The length of hospitalization was also longer among the conservatively treated patients. Thus, based on our results, we no longer advise conservative treatment because penile curvature developed even in our patients with minimal extravasation.

In the treatment of penile fractures, early surgical repair is generally preferred in order to avoid complications such as penile curvature, the development of fibrotic plaques and painful erection. Early surgical repair might also preserve sexual function and decrease the length of hospitalization.[9,11,13] For surgical repair, we primarily used subcoronal circular incision. This incision facilitates successful repair of the rupture and evaluation of the other cavernosal body and corpus spongiosum. Intraoperative examination with this type of incision helped us to indentify overlooked adjacent injuries. In some of our patients, we used a semicircular incision over the rupture line when it could be clearly palpated. It is possible to successfully repair the rupture with this type of incision, but this incision is inadequate for evaluating the other cavernosal body and corpus spongiosum.

Despite the fact that it is easy to change the semicircular incision to a circular one, based on our experience,

60

we recommend the primary use of circular incision.

In conclusion, anamnesis and physical examination are the main diagnostic tools for penile fracture.

When these methods fail to yield definitive diagnosis, cavernosography should be performed in order to confirm the diagnosis. If there is difficulty voiding and/ or urethrorrhagia, retrograde urethrography should be performed in order to visualize the urethral injury. In the treatment of penile fractures, we believe that early surgical repair is the only treatment option for all ruptures, regardless of size.

REFERENCES 1. Cecchi M, Pagni GL, Ippolito C, Summonti D, Sepich CA, Fiorentini L. Fracture of the penis: description of a case.

Arch Ital Urol Androl 1997;69:137-9. [Abstract] 2. Schrama J, Skjetne O, Vada K. Penis fracture. Tidsskr Nor Laegeforen 1998;118:2017-8. [Abstract] 3. Muentener M, Suter S, Hauri D, Sulser T. Long-term experience with surgical and conservative treatment of penile fracture. J Urol 2004;172:576-9.

4. Kowalczyk J, Athens A, Grimaldi A. Penile fracture: an unusual presentation with lacerations of bilateral corpora cavernosa and partial disruption of the urethra. Urology 1994;44:599-601.

5. Nymark J, Kristensen JK. Fracture of the penis with urethral rupture. J Urol 1983;129:147-8.

6. Karadeniz T, Topsakal M, Ariman A, Erton H, Basak D. Penile fracture: differential diagnosis, management and outcome. Br J Urol 1996;77:279-81.

7. Mydlo JH, Harris CF, Brown JG. Blunt, penetrating and ischemic injuries to the penis. J Urol 2002;168:1433-5.

8. Mc Aninc JW, Santucci RA. GenitourÄąnary trauma: In: Walsh PC, Retik AB, Vaughan E D, Wein AJ, editors. Campbellâ&#x20AC;&#x2122;s Urology. 8th ed. Philadelphia: Saunders; 2004. p. 3707-40.

9. El-Bahnasawy MS, Gomha MA. Penile fractures: the successful outcome of immediate surgical intervention. Int J Impot Res 2000;12:273-7.

10. Tsang T, Demby AM. Penile fracture with urethral injury. J Urol 1992;147:466-8.

11. Zargooshi J. Penile fracture in Kermanshah, Iran: report of 172 cases. J Urol 2000;164:364-6.

12. Ozen HA, Erkan I, Alkibay T, Kendi S, Remzi D. Fracture of the penis and long-term results of surgical treatment. Br J Urol 1986;58:551-2.

13. Asgari MA, Hosseini SY, Safarinejad MR, Samadzadeh B, Bardideh AR. Penile fractures: evaluation, therapeutic approaches and long-term results. J Urol 1996;155:149.

14. el-Sherif AE, Dauleh M, Allowneh N, Vijayan P. Management of fracture of the penis in Qatar. Br J Urol 1991;68:6225.

15. Dever DP, Saraf PG, Catanese RP, Feinstein MJ, Davis RS. Penile fracture: operative management and cavernosography.

Urology 1983;22:394-6.

16. Mydlo JH. Surgeon experience with penile fracture. J Urol 2001;166:526-9.

17. Mydlo JH, Gershbein AB, Macchia RJ. Nonoperative treatment of patients with presumed penile fracture. J Urol 2001;165:424-5.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):61-65

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2011.22129

Factors associated with mortality in adult hospitalized burn patients in Tehran Tahran kentinde hastaneye yatırılan erişkin yanık hastalarında mortaliteye neden olan faktörler Mohammad-Reza ZAREI,1,2 Seyedsaied DIANAT,2 Vahid ESLAMI,2 Iraj HARIRCHI,3 Nosratollah BODDOUHI,4 Ali ZANDIEH,2 Mohammad R. RASOULI2 BACKGROUND

AMAÇ

The mortality rate following burn is an important outcome parameter. This study aimed to identify factors associated with mortality in adult hospitalized burn patients in Tehran, Iran.

Yanığı takiben ortaya çıkan mortalite oranı, önemli bir sonuç parametresidir. Bu çalışmada, Tahran’da hastaneye yatırılan erişkin yanıklı hastalarda mortalite ile birlikte olan faktörlerin belirlenmesi amaçlandı.

METHODS

GEREÇ VE YÖNTEM

This cross-sectional study was performed during a oneyear period in two referral burn centers in Tehran. During the study period, 1321 adult (>15 years) hospitalized burn patients were enrolled. Univariate and multivariate (logistic regression) analyses were performed to identify factors associated with mortality.

Bu çapraz karşılaştırmalı çalışma, Tahran’daki iki yanık başvuru merkezinde bir yıllık periyotta yapıldı. Çalışma periyodunda hastaneye yatırılan 1321 erişkin (>15 yaş) yanıklı hasta çalışmaya kaydedildi. Mortalite ile birlikte olan faktörleri belirlemek üzere, tek değişkenli analiz ve çok değişkenli (lojistik regresyon) analiz yapıldı.

RESULTS

BULGULAR

The mean age of the patients was 33.1±14.9 years. By far, the majority of burns were accidental (n=1076, 81.5%).

Regarding the mechanism of burn, burn with petroleum products was the most frequent. Mean percent burned total body surface area (TBSA) was 39.9%±25.8%. The mortality rate was 33%. Sepsis was the most common cause of mortality. The results of the present study indicated that non work-related burns, burned TBSA and body surface area affected by second- or third-degree burns were independent determinants of mortality among adult hospitalized burn patients.

Hastaların ortalama yaşı 33,1±14,9 yıl idi. Yanıkların büyük çoğunluğu kazaya bağlıydı (n=1076, %81,5). Yanık mekanizması ile ilgili olarak, petrol ürünleri ile en sık yanık nedeni idi. Ortalama yüzde yanık toplam vücut yüzey alanı (TVYA) %39,9±%25,8 idi. Mortalite oranı %33 oldu. Sepsis, en sık mortalite nedeniydi. Bu çalışmanın sonuçlarına göre erişkin yanık hastalarında iş kazası olmayan yanıklar, yanık olan TVYA ve ikinci ve üçüncü derece yanıktan etkilenmiş yüzey alanı mortalitenin bağımsız belirleycileridir.

CONCLUSION

The present study showed a high mortality rate in the studied burn centers. Patients with identified risk factors should be categorized as high risk at the time of admission and need special attention and care during hospitalization.

Bu çalışma, çalışılan yanık merkezlerinde yüksek bir mortalite oranı olduğunu göstermiştir. Belirlenen risk faktörleri olan hastalar, yatışları sırasında yüksek riskli hastalar olarak sınıflandırılmalı ve bu hastalara hastanede kalış süresince özel ilgi ve bakım gösterilmelidir.

Key Words: Burn; Iran; mortality; risk factor; total body surface area.

Anahtar Sözcükler: Yanık; İran; mortalite, risk faktörü; toplam vücut yüzey alanı.

Department of Emergency Medicine, Imam Khomeini Hospital, Tehran University of Medical Sciences; 2Sina Trauma and Surgery Resaerch Center, Sina Hospital, Tehran University of Medical Sciences; 3 Department of Surgery, Tehran University of Medical Sciences; 4 Division of Plastic Surgery, Shahid Motahari Hospital, Tehran University of Medical Sciences, all in Tehran, Iran.

1 Tahran Tıbbi Bilimler Üniversitesi, İmam Humeyni Hastanesi, Acil Tıp Bölümü; 2Tahran Tıbbi Bilimler Üniversitesi, Sina Hastanesi, Sina Travma ve Cerrahi Araştırma Merkezi; 3Tahran Tıbbi Bilimler Üniversitesi, Cerrahi Bölümü; 4Tahran Tıbbi Bilimler Üniversitesi, Shahid Motahari Hastanesi, Plastik Cerrahi Bölümü, Tahran, İran.

1

SONUÇ

Correspondence (İletişim): Mohammad R. Rasouli, M.D. Sina Hospital, Hassan-abad Sq., Tehran - Iran.

Tel: +0098 - 2166718311 e-mail (e-posta): mhr_rasouli@yahoo.com

61

Ulus Travma Acil Cerrahi Derg

62

700 600 500 400 300 200

O th er

io n os

am

e

Ex pl

Fl

bu rn al

m ic

Ch e

ho t

liq

ui d

ca tri ec

0

l

100

nd

The following data were obtained for each patient: age, sex, mechanism of burn, total percent of burned total body surface area (TBSA) and percent of TBSA affected by each burn degree (first-, second- and thirddegree), procedures performed in patients including escharotomy, debridement, and tracheal intubation,

The upper extremity was the most frequently burned site, affected in 1230 cases. Fig. 2 demonstrates the frequency of the involved body site. Mean burned

El

MATERIALS AND METHODS After approval of the ethical committee on human research of Tehran University of Medical Sciences, a cross-sectional study was performed during a one-year period in two referral burn centers in Tehran (Tohid and Motahhari Hospitals). For this study, all adult (age >15 years) burn patients hospitalized within the period of the study were enrolled. Data were collected by trained physicians, who completed a prepared questionnaire for each patient at the time of emergency room admission. They also followed the patients during hospitalization and collected the required data.

or a

To the best of our knowledge, there is no report from Iran to introduce a comprehensive model to predict mortality in hospitalized burn patients. In this study, besides demonstrating the epidemiologic profile of adult hospitalized burn patients in two burn centers in Tehran, we aimed to identify risk factors for mortality in these patients.

RESULTS During the study period, 1321 patients (964 males [73%]) were enrolled into the study. Six hundred seventy-seven (51.2%) and 644 (48.8%) successive cases were from Tohid and Motahari hospitals, respectively.

The mean age of the patients was 33.1Âą14.9 years.

Burns had most commonly occurred in homes and factories, accounting for 762 (57.7%) and 232 (17.6%) of cases, respectively. By far, the majority of burns were accidental (n=1076, 81.5%) followed by deliberate self-burn (n=159, 12%) and assault (n=51, 3.9%).

Work-related burns accounted for 287 (21.7%) of the burns. Regarding the mechanism of burn, burns with petroleum products were the most frequent. Fig. 1 depicts the details.

Va p

According to previous reports from Iran,[7,8] the mortality rate of hospitalized burn patients is much higher than in developed countries.[9-13] As most of the introduced models have been designed based on data from developed countries, these models may not be fully compatible with the situation of burn care in developing countries like Iran.[14-17]

Statistical analysis was performed using SPSS (SPSS Inc., Chicago, IL, version 16) and MedCalc (Maria-kerke, Belgium, version 9.2). All quantitative data were expressed as mean Âą standard deviation. The patients were categorized into two groups, as survivors and non-survivors. Univariate analysis was performed using independent samples t test and chi-square analysis for quantitative and qualitative variables successively. Multivariate analysis (logistic regression) was carried out to determine risk factors for mortality. For this purpose, receiver operating characteristic (ROC) analysis was done to identify cut-off values for burned TBSA and TBSA affected by second- and third-degree burns. These variables were then categorized into two groups based on the obtained cut-off points and entered into the multivariate analysis. The body surface areas were categorized into two groups based on cut-off values obtained from ROC analysis. For logistic regression analysis, age was categorized into four groups as follows: <50, 5064, 65-80, and >80 years.[18]

G as

Advances in burn care and understanding some aspects of the pathophysiologic process of burns have motivated researchers to identify risk factors for mortality in burn patients, resulting in the development of several models for the prediction of mortality following burn.[3-5] These models are of great value, enabling the physician to recognize patients who are more likely to recover fully or those with determinant factors that are life-threatening. Development of these models can be used as an effective tool for management and triage of burn patients in burn care centers and in general hospitals, so that patients with higher risk of mortality can be referred to specialized burn care centers for more effective management after initial resuscitation.[6]

outcome of the injury (death or survival), and cause of death.

Pe pr trol od eu uc m ts

Burns are a global public health concern affecting about 1% of the general population annually. In addition to the physical and psychological morbidity that burns impose upon the injured patients and their families, these types of injuries are associated with a huge financial burden on the medical care system.[1,2]

Fig. 1. The frequency of each mechanism of burn.

Ocak - January 2011

Factors associated with mortality in adult hospitalized burn patients in Tehran

Table 1. Risk factors for mortality in univariate analysis Variable

Sex

Escharotomy

Work-related burn

Tracheal intubation

Male Female Yes No Yes No Yes No

Outcome (dead) (n=437)

p

274 (62.7%) 163 (37.3%) 50 (11.5%) 384 (88.5%) 59 (13.5%) 378 (86.5%) 10 (90.9%) 1 (9.1%)

<0.001† <0.001† <0.001† <0.001‡

Chi-square; ‡Fishers exact test.

†

TBSA was 39.9%±25.8%. Debridement and escharotomy were carried out in 89 (6.7%) and 74 (5.6%) of the cases, respectively. Eleven subjects (0.8%) underwent tracheal intubation while only one case (0.1%) required tracheostomy.

Four hundred thirty-seven cases (33.1%) died.

Sepsis was the most common cause of mortality, occurring in 277 cases (63.6%), followed by respiratory failure in 109 (24.9%) and renal failure in 12 (2.7%).

The mean age of the patients classified as non-survivors and survivors was 34.3±16.8 and 32.5±14 years, respectively, which was not statistically significant (p=0.055). Univariate analysis revealed a significant association between mortality and sex, non work-related burns, not performing escharotomy, burned TBSA, and second- and third-degree burned body surface area (Tables 1, 2). Further, burn with petroleum products accounted for 62% (n=271) of mortalities (p<0.001).

We also found some cut-off values for burned TBSA using ROC analysis. These cut-off values were 35.5%, 13% and 43%, respectively, for second-degree, thirddegree and burned TBSA. These variables were categorized into two groups based on these values and then entered into multivariate analysis.

Logistic regression analysis showed the association between mortality and burned TBSA, burned body surface area with second- and third-degree burns, and non work-related burn injuries (Table 3).

1400 1200 1000 800 600 400 200 0

Head&Neck

Trunk

Upper Extremity

Lower Extremity

Fig. 2. Distribution of burned sites of the body among the patients.

Cilt - Vol. 17 Sayı - No. 1

DISCUSSION The results of the present study indicated that non work-related burns, burned TBSA and body surface area affected by second- or third-degree burns are independent determinant factors of mortality among adult hospitalized burn patients.

The mortality rate in our series of patients was 33%, which is higher than in most of the reports from other countries.[9,10,12,13,19] However, it is relatively similar to the mortality rates that have been reported from Iran.

In a study by Soltani et al.[20] conducted in Tehran, the mortality rate was 51% in males and 69% in females.

Another report by Groohi et al.[21] revealed that overall case fatality rate among patients admitted to burn units in Kurdistan was 33.4%. The high rate of mortality in hospitalized burn patients in our study may be explained in part by the lack of a sufficient number of burn care centers in Tehran and surrounding cities, leading to a high number of patients admitted in these centers, thereby making the management of these patients difficult. Another issue is the delayed or inefficient management of burn patients in general hospitals and delayed referral of those severely injured patients who need more specialized care in burn care centers.

The high rate of pseudomonas infection among hospitalized burn patients in Iranian burn care centers has been reported previously and may have an important impact on the high mortality rate.[22] Cause of death in hospitalized burn patients varies in different studies, and sepsis, multiple organ failure and inhalation injury have been reported as the main causes of death in burn patients.[16,19,23] The most common cause of death in our study was sepsis. This was similar to another study in Kuwait.[19] In a study on major burns in Tokyo, cause of early death within 30 days of admission was shock and inhalation injury. In addition, long-term cause of mortality was multiple organ failure.[23] In another study by Ryan et al.,[16] the most frequent cause of death was multiple organ failure.

There are extensive studies investigating the role of various risk factors for mortality following burn injury. Some authors have consistently reported age, TBSA and inhalation injury as risk factors of mortality in burn patients.[7,16,23-26] We did not find an association between age and mortality in our study, which is consistent with a study conducted in the Netherlands.[27] In accord with previous reports on the role of TBSA as an independent risk factor for mortality,[7,16,23,24] we similarly found a significant association between TBSA and mortality. We have also proposed some cut-off values for second- and third-degree and burned TBSA for prediction of mortality in burn patients. We found that burned TBSA of more than 43% has a significant association with mortality. Ryan et al.[16] also demon63

Ulus Travma Acil Cerrahi Derg

Table 2. Percent of burned total body surface area and percent of body surface area

affected by second- and third-degree burns Variable (mean ± SD)

Non-survivors (n=437)

Survivors (n=884)

p

55.1±24.0 34.5±27.5 66.2±21.3

24.7±14.9 6.9±6.1 26.1±14.9

<0.001 <0.001 <0.001

Percent area of second-degree burn Percent area of third-degree burn Percent TBSA SD: Standard deviation; TBSA: Total body surface area.

Table 3. Variables having significant association with mortality in multivariate analysis Variable

β

p

Exp (β)

Upper

Lower

1.383 3.267 3.049 1.305 -5.335

0.024 <0.001 <0.001 0.019 <0.001

3.987 26.241 21.087 3.687 0.005

1.199 8.859 6.257 1.237 –

13.260 77.728 71.072 10.995 –

Second-degree TBSA Third-degree TBSA Percent TBSA Non work-related Constant

95%CI

CI: Confidence interval; TBSA: Total body surface area.

strated that TBSA of more than 40% is a significant risk factor for mortality in burn patients. In our study, those patients requiring tracheal intubation had a higher rate of morality compared with those in whom tracheal intubation was not needed. Although we do not have the rate of inhalation injury in our study, this may be an indicator of inhalation injury necessitating tracheal intubations, which has been reported as a risk factor for mortality.[16] Non work-related burn was a risk factor for mortality in our study. Similarly, in a study by Bang et al.,[19] domestic accidental burn was detected as a risk factor for mortality. In addition, we found that those with need for escharotomy had lower rate of mortality; however, no significant difference was detected after logistic regression analysis. Similar to our study, Ryan et al.[16] found no significant association between need for escharotomy and mortality. However, in another study on patients with severe burns, need for escharotomy was a significant predictor of mortality.[28] There is controversy about gender differences in the mortality of burn patients. Some investigators have demonstrated that female gender is a risk factor for mortality in burn patients.[6,29,30] In a study by McGwin et al.,[14] female burn patients aged less than 60 years had an increased risk of death compared with males. This association persisted following adjustment for burn size, burn depth and inhalation injury.

On the other hand, some researchers have found no significant association between gender differences and mortality in burn patients.[23] In a larger study by Brusselaers al.,[31] a higher but statistically insignificant mortality rate was observed in male burn patients (1.6% male, 1.1% female). Similar to the last report 64

by Blot et al., we identified a higher mortality rate in male burn patients. However, this association was not persistent following multivariate logistic regression analysis, indicating no independent role of gender on mortality in burn patients. This may suggest that other confounding factors affect this association.

This study had some limitations, perhaps the most important of which was the lack of data on inhalation injury.

In conclusion, the present study showed a high mortality rate in the studied burn centers, which may be due to the lack of a sufficient number of burn care centers in Tehran and surrounding cities, the lack of a suitable multidisciplinary approach and delayed referral to burn centers of burn patients from the emergency ward of general hospitals. In the present study, non work-related burns, burned TBSA, and body surface area affected by second- or third- degree burns were independent predictors of mortality. The patients with these risk factors should be categorized as high risk at the time of admission and need special attention and care during hospitalization.

Acknowledgement This study was supported by a grant from Sina Trauma and Surgery Research Center, Tehran University of Medical Sciences.

REFERENCES 1. Macedo JL, Santos JB. Predictive factors of mortality in burn patients. Rev Inst Med Trop Sao Paulo 2007;49:365-70.

2. Mashreky SR, Rahman A, Chowdhury SM, Giashuddin S, SvanstrOm L, Linnan M, et al. Epidemiology of childhood burn: yield of largest community based injury survey in Bangladesh. Burns 2008;34:856-62.

Ocak - January 2011

Factors associated with mortality in adult hospitalized burn patients in Tehran

3. Hilal A, Cekin N, Arslan M, Gulmen M. Deaths due to burns in Adana, Turkey. Burns 2008;34:982-5.

4. Belgian Outcome in Burn Injury Study Group. Development and validation of a model for prediction of mortality in patients with acute burn injury. Br J Surg 2009;96:111-7.

5. McGwin G Jr, George RL, Cross JM, Rue LW. Improving the ability to predict mortality among burn patients. Burns 2008;34:320-7.

6. Gomez M, Wong DT, Stewart TE, Redelmeier DA, Fish JS. The FLAMES score accurately predicts mortality risk in burn patients. J Trauma 2008;65:636-45.

7. Panjeshahin MR, Lari AR, Talei A, Shamsnia J, Alaghehbandan R. Epidemiology and mortality of burns in the South West of Iran. Burns 2001;27:219-26.

8. Lari AR, Alaghehbandan R, Nikui R. Epidemiological study of 3341 burns patients during three years in Tehran, Iran.

Burns 2000;26:49-53.

9. Barret JP, Gomez P, Solano I, Gonzalez-Dorrego M, Crisol FJ. Epidemiology and mortality of adult burns in Catalonia.

Burns 1999;25:325-9.

10. Rimdeika R, Kazanavicius M, Kubilius D. Epidemiology of burns in Lithuania during 1991-2004. Medicina (Kaunas) 2008;44:541-7.

11. da Silva PN, Amarante J, Costa-Ferreira A, Silva A, Reis J. Burn patients in Portugal: analysis of 14,797 cases during 1993-1999. Burns 2003;29:265-9.

12. De-Souza DA, Marchesan WG, Greene LJ. Epidemiological data and mortality rate of patients hospitalized with burns in Brazil. Burns 1998;24:433-8.

13. Garner WL, Reiss M. Burn care in Los Angeles, California: LAC+USC experience 1994-2004. Burns 2005;31:S32-5.

14. McGwin G Jr, George RL, Cross JM, Reiff DA, Chaudry IH, Rue LW 3rd. Gender differences in mortality following burn injury. Shock 2002;18:311-5.

15. George RL, McGwin G Jr, Schwacha MG, Metzger J, Cross JM, Chaudry IH, et al. The association between sex and mortality among burn patients as modified by age. J Burn Care Rehabil 2005;26:416-21.

16. Ryan CM, Schoenfeld DA, Thorpe WP, Sheridan RL, Cassem EH, Tompkins RG. Objective estimates of the probability of death from burn injuries. N Engl J Med 1998;338:362-6.

17. Pham TN, Kramer CB, Wang J, Rivara FP, Heimbach DM,

Cilt - Vol. 17 Sayı - No. 1

Gibran NS, et al. Epidemiology and outcomes of older adults with burn injury: an analysis of the National Burn Repository. J Burn Care Res 2009;30:30-6.

18. Belgian Outcome in Burn Injury Study Group. Development and validation of a model for prediction of mortality in patients with acute burn injury. Br J Surg 2009;96:111-7.

19. Bang RL, Sharma PN, Gang RK, Ghoneim IE, Ebrahim MK. Burn mortality during 1982 to 1997 in Kuwait. Eur J Epidemiol 2000;16:731-9.

20. Soltani K, Zand R, Mirghasemi A. Epidemiology and mortality of burns in Tehran, Iran. Burns 1998;24:325-8.

21. Groohi B, Alaghehbandan R, Lari AR. Analysis of 1089 burn patients in province of Kurdistan, Iran. Burns 2002;28:56974.

22. Lari AR, Alaghehbandan R. Nosocomial infections in an Iranian burn care center. Burns 2000;26:737-40.

23. Kobayashi K, Ikeda H, Higuchi R, Nozaki M, Yamamoto Y, Urabe M, et al. Epidemiological and outcome characteristics of major burns in Tokyo. Burns 2005;31 Suppl 1:S3-S11.

24. Laloë V. Epidemiology and mortality of burns in a general hospital of Eastern Sri Lanka. Burns 2002;28:778-81.

25. Waller AE, Marshall SW, Langley JD. Adult thermal injuries in New Zealand resulting in death and hospitalization. Burns 1998;24:245-51.

26. Han TH, Kim JH, Yang MS, Han KW, Han SH, Jung JA, et al. A retrospective analysis of 19,157 burns patients: 18-year experience from Hallym Burn Center in Seoul, Korea. Burns 2005;31:465-70.

27. Bloemsma GC, Dokter J, Boxma H, Oen IM. Mortality and causes of death in a burn centre. Burns 2008;34:1103-7.

28. Ryan CM, Sheridan RL, Schoenfeld DA, Warshaw AL, Tompkins RG. Postburn pancreatitis. Ann Surg 1995;222:163-70.

29. Muller MJ, Pegg SP, Rule MR. Determinants of death following burn injury. Br J Surg 2001;88:583-7.

30. O’Keefe GE, Hunt JL, Purdue GF. An evaluation of risk factors for mortality after burn trauma and the identification of gender-dependent differences in outcomes. J Am Coll Surg 2001;192:153-60.

31. Brusselaers N, Juhász I, Erdei I, Monstrey S, Blot S. Evaluation of mortality following severe burns injury in Hungary: external validation of a prediction model developed on Belgian burn data. Burns 2009;35:1009-14.

65

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):66-74

Original Article

Klinik Çalışma doi: 10.5505/tjtes.2011.39145

Tubercular bowel perforation: what to do?

Bağırsak tüberkülozu perforasyonu: Ne yapmalı?

Federico COCCOLINI,1 Luca ANSALONI,1 Fausto CATENA,1 Daniel LAZZARESCHI,2 Lorenza PUVIANI,1 Antonio Daniele PINNA1

BACKGROUND

AMAÇ

The incidence of abdominal tuberculosis (TB) is increasing in western and developed countries. This pathology has several complications, including free intestinal perforation.

The aim of this study was to analytically summarize all the pertinent literature discussing the various treatments for TB-related perforations.

Abdominal tüberküloz (TB) insidansı, Batı ülkeleri ile gelişmiş ülkelerde artmaktadır. Bu patoloji, serbest intestinal perforasyonu da içeren birkaç komplikasyona sahiptir. Bu çalışmanın amacı, tüberkülozla ilişkili perforasyonlara yönelik çeşitli tedavileri tartışan ilgili tüm literatürü analitik olarak özetlemektir.

METHODS

GEREÇ VE YÖNTEM

We reviewed the patient database of the Emergency Surgery Department of the Bologna University Hospital, checking the last 13 years. A retrospective review was conducted of all reported cases of intestinal perforation due to intestinal TB published through 3 March 2009.

Bologna Üniversite Hastanesi Acil Servis Departmanı’nın son 13 yıldaki kayıtlarını sorgulayan hasta veritabanı gözden geçirildi. 3 Mart 2009 tarihine kadar bildirilmiş olan intestinal TB’ye bağlı raporlanan bütün intestinal perforasyonu olguları geriye dönük olarak değerlendirildi.

RESULTS

BULGULAR

119 cases of abdominal TB presenting with intestinal perforation were published. There are no standardized guidelines regarding the surgical treatment. Of the 119 reported cases, 40 (33.6%) were treated with resection and anastomosis, 17 (14.2%) with direct sutures, 4 (3.3%) with a simple drain, and in 57, the treatment was not reported.

İntestinal perforasyon ile başvuran 119 abdominal tüberküloz olgusu yayınlanmıştır. Cerrahi tedavi ile ilgili standardize kılavuzlar bulunmamaktadır. Bildirilen 119 olgudan, 40’ı (%33,6) rezeksiyon ve anastomozla, 17’si (%14,2) doğrudan dikişlerle, 4’ü (%3,3) basit bir drenle tedavi edilmiş ve 57 olgunun tedavisi de rapor edilmemiştir.

CONCLUSION

SONUÇ

No clinical evidence has been available for analysis to discern the optimal surgical strategy for treating intestinal perforations induced by TB. The direct closure of the perforation typically correlates with poor morbidity and mortality results. The better treatment seems to be the surgical resection of the perforated part with anastomosis. However, pharmacological therapy remains the essential pillar of treatment.

TB’ye bağlı bağırsak delinmelerinin cerrahi tedavisi için en uygun stratejiyi analizle ayırt edilecek hiçbir klinik kanıt saptanmadı. Perforasyonun doğrudan kapatılması, tipik olarak yüksek morbidite ve mortaliteyle korelasyon göstermektedir. Perfore kısmın rezeksiyonu ile birlikte anastomoz gerçekleştirilmesi daha iyi tedavi gibi görünmektedir. Yine de, farmakolojik tedavi, tedavinin esas ayağı olarak kalmaya devam etmektedir.

Key Words: Perforation; surgery; treatment; tuberculosis.

Anahtar Sözcükler: Perforasyon; cerrahi; tedavi; tüberküloz.

Department of Surgery, Bologna University, St. Orsola Hospital, Bologna, Italy; 2University of California-Berkeley, Ca, USA.

1

Bologna Üniversitesi, St Orsola Hastanesi, Cerrahi Birimi, Bologna, İtalya; 2 Kaliforniya Berkeley Üniversitesi, Ca, ABD.

Correspondence (İletişim): Federico Coccolini, M.D. Via Massarenti, 9 40138 Bologna, Italy.

Tel: +0039 - 051 - 636 3235 / 3597 e-mail (e-posta): fedecocco@iol.it

66

Tubercular bowel perforation

Tubercular infection can involve the chest as well as many parts of the human body, namely the abdomen, peritoneum and bowel. Although the entire gut can be involved, the ileocecal area is most commonly affected.[1-3] Abdominal tuberculosis (TB) is the sixth most frequent extra-pulmonary location[3,4] and it is relatively rare in the industrialized world. On the other hand, the incidence of abdominal TB is increasing in western and developed countries due to immigration from developing countries, aging populations, increasing incidence of human immunodeficiency virus (HIV) infection, and misdiagnosis with ineffectual treatment.[4,5] For these reasons, abdominal TB represents an interesting challenge for surgeons in developed countries as well.

Abdominal TB typically presents itself in three major forms as well as with several less common symptoms: (I) the ascitic type, (II) the plastic type, which causes intestinal obstruction, and (III) the glandular type, which involves the mesenteric nodules. It is less common to observe tuberculous strictures, nodules, fistulae, or an interconnected association of these manifestations.[3,6] There are several complications involving intestinal TB, including bowel obstruction (31.7%), intestinal perforation (4.9%), enterocutaneous fistula (2.4%), and small bowel volvulus resulting from mesenteric lymphadenitis (2.4%).[7] Different studies typically denote different percentages for these complications.

[8] Free intestinal perforation is an uncommon complication of intestinal TB due to a reactive thickening of the peritoneum and subsequent adhesion formations with surrounding tissues.[9] It accounts for 1-10% of abdominal TB cases and has a poor prognosis, with a mortality rate higher than 30%.[10-12] To date, there has been no clinical evidence available to assess the best surgical means to treat intestinal perforations due to TB. The main cause of such unavailability is the extremely rare nature of this complication.

MATERIALS AND METHODS We reviewed the patient database of the Emergency Surgery Department of the Bologna University Hospital, checking the last 13 years (1995-2008).

Then, a retrospective review was conducted of all reported cases of intestinal perforation due to intestinal TB published through 3 March 2009. On PubMed (1966-2009), using the key words “tuberculosis and intestinal perforation”, we found 216 articles. For purposes of practicality, we excluded from the compilation process 49 different articles that were written in languages other than English, Italian, Spanish, or French. Of the remaining articles, 103 were excluded Cilt - Vol. 17 Sayı - No. 1

because they did not address the topic of interest. In the end, we definitively considered 54 articles (25%), including case reports, case series and reviews. In particular, we searched for the methods used to diagnose and treat tuberculous intestinal perforation.

RESULTS Case Report In the analysis of the patient database of our Unit, we found 5 cases of abdominal TB, only one (20%) of which presented with perforation.

A 53-year-old woman from Eritrea was admitted to the Department of Internal Medicine four months prior with a one-month history of minor epigastric pain, progressive abdominal distension, and hyperpyrexia. On her physical examination, the patient looked ill and febrile (temperature 38.8°C). Abdominal examination showed no evidence of peritonitis, and her blood profile showed hemoglobin 11.5 g/dl, leukocyte count 9.0 x 103/uL (neutrophils 85.5%), ESR (erythrocyte sedimentation rate) 83 mm/hr, Ca-125 585 u/ml, and albumin 2.5 g/dl. All hepatitis markers were negative, and all liver and renal function tests and electrolytes appeared normal. Chest radiography assessments were normal and esophagogastroduodenoscopy (EGDS) showed only a sliding hiatal hernia.

Colonoscopy was negative up to the hepatic flexure.

An abdominal ultrasonography (US) scan detected ascites without hepatopathies or portal hypertension, and an evacuative paracentesis of about 4 liters (L) was consequently performed. A cytologic examination of the ascitic fluid showed normal mesothelial cells and rare granulocytes, neutrophils, lymphocytes, and histiocytes, followed by a negative microbiological exam for bacteria and mycobacteria. The computed tomography (CT) scan showed pleural bilateral effusion, ascites and enlarged mesenteric lymph nodes (Fig. 1). The Mantoux intradermic reaction was negative.

Treatment was thereby commenced with an empirical antibiotic therapy using third-generation cephalosporin after hemoculture tested positive for Staphylococcus haemolyticus, and a slight improvement in the pa-

Fig. 1. CT scan shows mesenteric lymph node enlargement.

67

Ulus Travma Acil Cerrahi Derg

nodules covered by normal mucosa. A new Mantoux intradermic reaction was performed, and it showed negative results. The day after the contrast meal, the patient exhibited an acute abdomen with signs of peritonitis. A CT scan was then performed which showed barium in the abdominal cavity.

Fig. 2. Jejunum-colic fistula (frontal view).

tient’s general subjective condition was observed. The patient was then discharged one month later with the provisional diagnosis of “unknown-origin ascites”.

Three months later, the woman was readmitted to the hospital with hyperpyrexia, asthenia, weight loss, ascites, and night sweating. Her blood profile showed hemoglobin 8 g/dl, leukocyte count 16.98 x 103/uL (neutrophils 83.3%), ESR 24 mm/hr, and albumin 2.3 g/dl. A chest X-ray revealed right pleural effusion while the US abdominal scan showed ascites.

A barium meal revealed a jejunum-colic fistula when a portion of the contrast meal seemed to precociously enter the ascending part of the colon (Fig. 2). A complete colonoscopy, performed to verify the hypothesis of an inflammatory bowel disease (IBD), yielded three

Fig. 3. Yellow-white nodules covering the entire peritoneal (parietal and visceral) surface.

68

The patient was then transferred to the emergency surgery unit where a laparotomy was performed. During the laparotomy, about 1 L of fecaloid fluid was drawn from the abdominal cavity. The entire visceral and parietal surfaces of the peritoneum were full of yellow-white nodules (ranging from 1 to 5 mm in size) (Fig. 3). A biopsy was taken. The entire cavity was affected by the infection; the small bowel was firmly attached to the omentum and adhesiolysis was consequently performed to free the stomach, right and left colon, rectum, and uterus, including Fallopian tubes and ovaries. Although all these structures were affected by the inflammatory process, no perforation was evident. As checking for a perforation could have been difficult and dangerous, the dissection was stopped without probing for evidence of perforation. A thorough washing of the entire abdominal cavity was performed, five drains were placed, and the abdomen was closed. A few days later, the histopathological examination of the nodules revealed a chronic flogistic granulomatous process with a giant-cellular reaction (Fig. 4). Although an official diagnosis of tubercular peritonitis had not yet been confirmed, treatment commenced with an ex-juvantibus anti-tubercular therapy (pyrazinamide 5 mg po three times a day, isoniazid 300 mg IV once a day, rifampin 600 mg IV once a day, and ethambutol 500 mg IV twice a day) alongside a total parenteral nutrition (TPN) regimen.

One week after beginning the treatment therapy, a new Mantoux intradermic reaction yielded a positive result. Three weeks after the surgical intervention, an

Fig. 4. Histology: chronic flogistic granulomatous process with a giant-cellular reaction.

Ocak - January 2011

Tubercular bowel perforation

Table 1. Summary of all published papers Authors

No. of patients with No. of patients with Site of abdominal TB intestinal perforation perforation

Diagnosis

Treatment

Outcome

12 simple suture 2 drain 6 NR* 1 simple suture

15 survived 5 died (suture group) 1 survived

16 resection + anastomosis 5 simple suture 3 simple suture 4 resection + anastomosis

NR*

4 resection + anastomosis 2 simple drain 1 resection + anastomosis 1 colonic stoma NR*

6 survived

3 resection + anastomosis NR*

1 died

7 simple suture 5 resection + anastomosis NR* 2 resection + anastomosis NR*

9 survived 3 died

Sweetman WR (1958) [50]

70

20

NR*

Laparotomy histology

Gleason T (1979) [51]

49

1

1 duodenum

Ecgleston FC (1983) [52]

137

21

Gilinsky NH (1986) [53]

52

7

Kapoor VK (1986) [43]

45

6

15 ileum 3 jejunum 3 multiple 4 ileum 2 colon 1 appendix 1 rectum 4 ileum 2 not found

Laparotomy histology Laparotomy

Dorè P (1990) [54]

2

2

1 ileum 1 colon

Laparotomy histology

Uygur-B. O (2003) [18]

31

3

NR*

Rahman A (2003) [55]

3

3

3 ileum

Tanrikulu CA (2005) [4]

39

3

3 ileum

Cengiz A (2005) [56]

12

12

10 ileum 2 jejunum

Laparotomy histology (60.8%) Ex-juvantibus therapy (28.8%) Laparotomy histology Ascitic fluid culture (8%) Histology (20%) Laparotomy histology

Jhobta RS (2006) [41] Leung VKS (2006) [57]

20 22

20 2

Clarke DL (2007) [12]

67

5

Leone V (2007) [58]

6

1

Tan KK (2008) [44]

57

6

20 small bowel 2 ileum Laparotomy histology 4 jejunum Laparotomy 1 stomach histology 1 ileum Laparotomy histology 3 ileum Laparotomy 2 colon histology (71.9%) 1 duodenum Clinical (28.1%)

Et al. [22,59-62]

5

5

4 ileum 1 colon

Laparotomy histology

Present study

5

1

1 not found

622

119

Laparotomy histology

Total

Laparotomy histology Laparotomy histology

1 resection + anastomosis 2 resection + anastomosis 1 appendectomy 1 drainage 2 NR* 4 resection + anastomosis 1 simple suture 1 simple drain

6 survived 1 died (suture group)

2 died NR*

3 survived

NR* 2 survived 3 died 2 survived 1 survived 4 survived 2 died (resection + anastomosis group) 4 survived 1 died (suture group) 1 survived

54 survived - 18 died

NR: Not reported.

abdominal X-ray with Gastrografin® meal showed neither fistulas nor perforations and no abdominal effusion was detected by a CT contrast scan. The patient’s condition continued to improve during the admission period; no obstructive episodes occurred and the peritonitis appeared to heal satisfactorily. Intestinal transit was resumed 16 days after the intervention, and the first drain was removed 22 days after the surgery. Twenty-five days after the operation, the patient began a combined nutritional regimen, thereby transitioning away from the parenteral nutrition (PN) treatment. On the 30th day after the surgical procedure, the PN was fully discontinued and an abdominal X-ray with Gastrografin® was performed, yielding negative results. Fifty days after the surgical intervention, the last drain was removed Cilt - Vol. 17 Sayı - No. 1

and the patient was discharged. After 7 months of antiTB therapy, the follow-up CT was negative and monitored parameters including Ca-125 (8 U/ml) resulted in the improvement of the patient’s condition. The patient was checked one and a half years after the surgery during a routine examination, and appeared to be in good health with no recurrences or complications.

Literature Review The aim of this study was to analytically summarize all pertinent literature discussing the various treatments for TB-related pathology. We also attempted to stress the difficulty of performing a differential diagnosis among a confounding plethora of non-specific and unclear signs and symptoms.

69

Ulus Travma Acil Cerrahi Derg

Fig. 5. Site of tubercular perforation.

Fig. 6. Type of treatment for tubercular perforation.

In the reviewed literature, we found 54 relevant articles including case reports, case series, and reviews.

A total of 622 patients with abdominal TB were considered, among them 119 presenting with intestinal perforation (Table 1). Of the 119 cases reported, in 92 (77.3%), the diagnosis was reached via laparotomy and histology; the remaining 27 (22.7%) were diagnosed by different methods such as ex-juvantibus therapy, clinical findings and ascitic fluid culture.

rope and the United States has become evident since the mid 1980s.[13] The resurgence of this pathology is directly related to the increasing number of individuals infected with HIV.[2] It has been estimated that a person infected with both HIV and TB has a 7% to 10% chance per year of developing active TB, as opposed to the 10% lifetime chance of someone who is infected with only TB.[14] Over the last four decades, a number of audits on abdominal TB from many parts of the world have been conducted.[8,11,12,15-19] However, many of these audits were conducted during the preHIV era. With the global diffusion of HIV, the clinical manifestation of abdominal TB differs greatly from its description in these early reports.

Analyzing the sites of perforation, we observed 2 perforations of the duodenum, 9 of the jejunum, 50 of the ileum, and 7 of the colon-rectum. The others were localized as: 1 in the stomach and 1 in the appendix, and 3 were multiple. In 3 cases, the surgeons were not able to identify the exact site of perforation, and in 43, the authors failed to report these sites (Fig. 5). We can conclude, in accordance with the reviewed literature, that the most frequent site of perforation is the ileocecal area.

Many of the published papers do not include the description of the methods used to treat the perforation and many of the treatment outcomes are omitted.

Forty cases (33.6%) were treated with resection and anastomosis, 17 (14.2%) with simple suture of the perforation, and 4 (3.3%) with the simple positioning of a drain; in 57 cases, the method of treatment was not reported (Fig. 6). Mortality was only reported in a few cases, as seen in Table 1. This lack in reporting the outcomes of the various surgical treatments does not help to establish the best way to treat this rare form of perforation. In fact, the outcome was reported in 72 cases (60.5%), and the total mortality was 25%. Dividing results into the different treatment groups, it is clear how the direct suture gained poorer results, with a mortality of 41.1%, against the resection with anastomosis group, in which mortality reached 21%.

DISCUSSION Although TB remains relatively rare in developed countries, especially the type involving the gastrointestinal tract, an increase in the number of cases in Eu70

Abdominal TB is a disease that predominantly affects young adults.[3,4,20] Two-thirds of all cases involve patients between 21 and 40 years of age. There is no difference in the incidence rate between male and female subjects, although some studies suggest a slightly increased female predisposition.[3,12,21] Clinical presentation can be acute, chronic, or both acute and chronic. In the majority of cases, constitutional symptoms are present, including fever (4070%), pain (80-95%), diarrhea (11-20%), constipation, alternating constipation and diarrhea, weight loss (40-90%), anorexia, malaise, ascites, abdominal distension, night sweating, and hematochezia.[3,4,12] Despite a popular misconception that intestinal complications are often linked to pulmonary TB, only 1520% of the patients with gastrointestinal tubercular complications have concomitantly active pulmonary TB. Thirty to 50% of patients with abdominal TB have a normal chest film[12] and the tuberculin skin test is positive in only 42% of patients. Given these statistics, such assessments cannot be used as reliable predictors of disease. It should be mentioned that, in areas where TB is endemic, this test has been known to have high false-positive rates, and typically has a lower specificity for abdominal disease than pulmonary TB.[20] For these reasons, they could not be used Ocak - January 2011

Tubercular bowel perforation

to establish the diagnosis in our case as well. Furthermore, tuberculin skin tests cannot accurately differentiate between active disease and previous sensitization by contact or vaccination.[21] Many papers published on abdominal TB emphasize the difficulty of diagnosing this enigmatic pathology. Unfortunately, the tests that clinicians and surgeons rely on are often not sufficiently conclusive to guarantee a reasonably definitive diagnosis. The primary problem is not diagnosing the intestinal perforation, as this is often straightforward enough. Instead, the problem lies in properly identifying the cause, in this case intestinal TB. In any case, intestinal perforation caused by primary abdominal TB is relatively rare.[22] The instrumental modalities used during investigation include: chest X-rays, small bowel barium meal, barium enema, US, CT, and colonoscopy. Laboratory, immunological, microbiological, and clinical modalities include: ascitic fluid examination, ELISA, peritoneal biopsies, acid-fast bacilli research in the sputum, hematic tests, and tuberculin skin test.[3,4,12,23-25] All of these diagnostic instruments demonstrate a different grade of reliability and confidence, but none of them yields a conclusive diagnosis with any definitive certainty.

We now will try to discuss our case, considering the review of the literature, trying to underline eventual mistakes or misunderstandings in the diagnostictherapeutic circuit.

Paracentesis has a low diagnostic yield. Direct smears for the Ziehl-Neelsen stain are typically ineffectual, with reported sensitivity ranging from 0% [18,26,27] to 6%.[2,28-30] Cultures of ascitic fluid take a considerable amount of time before results are available, with most tuberculous ascites cases culminating in negative results.[17,24,30] However, it should be noted that the rate of positive culture results could be improved by obtaining 1 L of ascitic fluid concentrated via centrifugation.[24,28] Our hospital microbiologist did not concentrate the ascitic fluid via centrifugation.

Several authors suggest that C-reactive protein (CRP) of ascitic fluid obtained by US-guided fine needle aspiration is the diagnostic method of choice for patients with a strong suspicion of intestinal TB. They also asserted that it should always be performed prior to any surgical intervention.[23] In our case, before the urgent surgical intervention, there was not a strong enough suspicion of abdominal TB to perform CRP analysis in the ascitic fluid. If a concentration via centrifugation had been performed, a mycobacteria may have been found, thus leading to a modification in the therapeutic circuit.

Other authors describe the evaluation of adenosine deaminase (ADA) in ascitic fluid[31] as a useful diagCilt - Vol. 17 Say覺 - No. 1

nostic tool. This enzyme level is proportional to the level of T-lymphocyte activity. T-cells are stimulated by microbacterial antigens. The level of ADA in tuberculous ascites is significantly higher than it is in cirrhotic or malignant ascites.[3,20] In the event of coinfection with HIV, ADA values could be either normal or slightly below average.[3] However, even if the patient was not HIV-positive, the possibility of using ADA had not been considered.

Many reports have shown strong correlations between tuberculous peritonitis and high Ca-125 serum levels. An elevated serum level of Ca-125 is often indicative of the peritoneal diffusion of ovarian carcinomas. The elevation of this marker in the serum, especially in unclear or convoluted cases, should be examined considering the possibility of peritoneal TB.[32-35] There also seems to be a direct association between serum Ca-125 levels and the resulting efficacy of antituberculous therapy.[33] In our patients, the dosing of Ca-125 was performed about 4 months before the admission in our Operative Unit. It has not been considered as a strong indicator of peritoneal involvement or suggestive for tubercular peritonitis in the absence of signs of other malignancies.

Radiology is very helpful with respect to modern imaging, even without a high grade of specificity. CT scanning is often unable to differentiate this pathology from other intra-abdominal disorders. However, CT scanning is adept at detecting various intra-abdominal features typical of abdominal TB, including thickening of the intestinal mucosa, stranding and thickening of the small bowel mesentery, and the retroperitoneal lymphadenopathy.

Endoscopic techniques like colonoscopy are extremely useful, principally for detecting lesions of the terminal ileum and colon.[3] This kind of examination helps to differentiate between other colon-related pathologies that could present with unspecified bowel symptoms. In the case we explain, a colonoscopy was performed to verify the suspicion of an IBD, and the only findings reported were three nodules covered by apparently normal mucosa, of which the endoscopist decided not to perform a biopsy.

Although both clinicians and surgeons of modern medicine have access to and experience with the aforementioned facilities and techniques, the diagnosis of abdominal TB remains principally a surgical endeavor. Many authors have suggested a laparotomy as the best way to obtain an adequate amount of tissue for a definitive diagnosis of abdominal TB.[8,12,15,16] Four out of five reviews published between 1972 and 2007[12,15,16,18,19] argue that a precise diagnosis can only be reached intraoperatively or by observing the effects of drug treatment. These reviews primarily dis71

Ulus Travma Acil Cerrahi Derg

cussed cases from 1962. Although technological advancement since 1962 has had a profound effect on the medical field, the methods of diagnosing intestinal TB remain relatively unchanged. Beginning roughly 10 years ago, laparoscopies began being utilized to investigate the peritoneal cavity for signs of abdominal TB. Even if this technique enabled inspection of the peritoneal cavity without overly invasive maneuvers, it did not reduce dependence on open surgery. Clarke et al.[12] explained how they were only able to establish a conclusive diagnosis and definitive therapeutic intervention in one out of five patients that underwent laparoscopy. Laparoscopies have been hailed as being particularly useful for obtaining quality samples for microbiological analysis. However, laparoscopic investigation of tuberculous peritonitis has failed in 1% to 16% of cases,[29,36,37] and is not without risk.

The major complication is intestinal perforation,[38,39] which was originally thought to be more common in the fibro-adhesive form.[29] Five case series investigated the use of laparoscopy in 257 cases of tubercular peritonitis.[29,37-40] They investigated morbidity and complications linked to the use of this technique. Four cases of major complications (intestinal perforation) and three minor complications (ascites oozing through laparoscopic wound and omental hemorrhage) were reported. Obviously, the use of diagnostic laparoscopy is not feasible in urgent settings.

Even if a patient presents with all the appropriate signs and symptoms, there is little conclusive evidence that alludes to intestinal TB perforation. The percentage of intestinal perforation due to abdominal TB is very low, even in countries with high TB incidence. In 2006, Jhobta et al.[41] reported that 3.9% of peritonitis cases in a series of 504 consecutive intestinal perforations resulted from TB-induced intestinal perforation.

Another article, considering a series of 204 consecutive patients, reported only 4 cases (1.9%) of intestinal perforation resulting from TB.[42] It should be pointed out that incidence rates have decreased significantly in the past 20 years. In 1986, Kapoor et al.[43] reported a series of 6 cases with an incidence of TB-induced perforation of 13.3%. In those years, the percentages of TB-induced intestinal perforations ranged from 7.5% to 12.2%.[9,10,43] The clinical presentation of these cases is rather characteristic of the pathology. The diagnosis of intestinal perforation is not difficult in most cases. For the surgeon, the difficulty arises when trying to reach an intra-operative diagnosis and when subsequently planning appropriate treatment for the patient.

Surgical treatment of tuberculous perforations is rather controversial. Although pharmacological treatment remains the central pillar of abdominal TB, emergency surgery is often required for its acute com72

plications,[44] particularly for perforations. There is very little scientific evidence with which to base an argument for the best way to treat these complications of abdominal TB, and the noticeable lack of literature in this field certainly does not help. The bulk of this topicâ&#x20AC;&#x2122;s background is derived from a series of case reports and case series published in a 40-year period. In all, 119 cases have been described, with various means of treatment. In many of the reported cases, the surgical treatment and the outcomes were not adequately described (Table 1). However, direct closure of the perforation with or without bypass is generally associated with poorer results.[45] Resection and anastomosis is therefore recommended,[46] especially if combined with postoperative anti-tubercular therapy.[47-49] However, regardless of the surgical procedure, the mortality rate is relatively high, ranging from 30%[45,46] to 60%.[12] This high rate of mortality is principally due to the poor clinical perioperative conditions of patients undergoing surgery. In addition to already being a highly debilitating pathology, the peritonitis resulting from the perforation overwhelms the patientâ&#x20AC;&#x2122;s capacity to bear surgical stress. In all the reviewed literature, not a single report was found that resembled our case.

We believe that our course of action in this case was a safe and responsible way to approach the problem.

In the presence of extensive adhesions, no attempt should be made to locate the perforation, as injury to the adherent intestinal loops is likely and focal fistula may result in the postoperative period.[43] In this case, it is possible to place drains and immediately begin an ex-juvantibus anti-tubercular therapy once the surgical intervention has been completed. In our experience, this approach resulted in a complete restoration of health within a reasonable recovery period, even in a very weak patient.

In conclusion, intestinal TB should always be considered when deliberating the possible cause of intestinal perforation. There are no standardized guidelines regarding the surgical treatment of this complication, as it is relatively rare in developed countries, and the chance of making a correct preoperative diagnosis is often unlikely. Many clinical, radiological or laboratory methods can often be employed. Although laparoscopy is a useful technique, the only way of reaching a conclusive diagnosis involves a laparotomy with subsequent histological examination.

The mortality rates seem to be significantly higher when intestinal perforations are treated with simple sutures.[45] Intestinal resection and primary anastomosis seems to be the better way to treat TB-induced intestinal perforation. However, anti-tubercular therapy undisputedly remains the essential pillar of treatment for abdominal TB. Lastly, when searching for the perforation becomes invasive and dangerous or when Ocak - January 2011

Tubercular bowel perforation

the exact site simply cannot be conclusively located, placement of drains and immediate ex-juvantibus antitubercular therapy is probably the best solution.

Concluding, the lack of proper research on this topic as demonstrated by incomplete and often inconclusive literature requires further studies to comprehensively investigate ideal treatment for TB perforations. More complete studies performed by centers experienced with this kind of pathology are necessary in order to define standardized guidelines regarding the treatment of this complication.

REFERENCES 1. Aston NO. Abdominal tuberculosis. World J Surg 1997;21:492-9.

2. Marshall JB. Tuberculosis of the gastrointestinal tract and peritoneum. Am J Gastroenterol 1993;88:989-99.

3. Sharma MP, Bhatia V. Abdominal tuberculosis. Indian J Med Res 2004;120:305-15.

4. Tanrikulu AC, Aldemir M, Gurkan F, Suner A, Dagli CE, Ece A. Clinical review of tuberculous peritonitis in 39 patients in Diyarbakir, Turkey. J Gastroenterol Hepatol 2005;20:906-9.

5. Lingenfelser T, Zak J, Marks IN, Steyn E, Halkett J, Price SK. Abdominal tuberculosis: still a potentially lethal disease.

Am J Gastroenterol 1993;88:744-50.

6. King M, Bewes P, Cairns J, Thornton J. Chap. 29. In Primary surgery, Vol. 1., (non-trauma). Oxford medical publications, Oxford, UK, 2009. p. 496-507.

7. Akinoğlu A, Bilgin I. Tuberculous enteritis and peritonitis.

Can J Surg 1988;31:55-8.

8. Marks IN. Abdominal tuberculosis. Ballieres Clin Med Comunicable Dis 1988;3:329-48.

9. Kakar A, Aranya RC, Nair SK. Acute perforation of small intestine due to tuberculosis. Aust N Z J Surg 1983;53:381-3.

10. Bhansali SK. Abdominal tuberculosis. Experiences with 300 cases. Am J Gastroenterol 1977;67:324-37.

11. Segal I, Tim LO, Mirwis J, Hamilton DG, Mannell A. Pitfalls in the diagnosis of gastrointestinal tuberculosis. Am J Gastroenterol 1981;75:30-5.

12. Clarke DL, Thomson SR, Bissetty T, Madiba TE, Buccimazza I, Anderson F. A single surgical unit’s experience with abdominal tuberculosis in the HIV/AIDS era. World J Surg 2007;31:1087-98.

13. Raviglione MC, Snider DE Jr, Kochi A. Global epidemiology of tuberculosis. Morbidity and mortality of a worldwide epidemic. JAMA 1995;273:220-6.

14. CDC Division of tuberculosis elimination. Centers for Disease Control and Prevention. Trends in tuberculosis morbidity and mortality. Epidemiology and statistics unit. October 2000. Available at: www.cdc.gov/nchstp/tb/surv.

15. Gilinsky NH, Marks IN, Kottler RE, Price SK. Abdominal tuberculosis. A 10-year review. S Afr Med J 1983;64:849-57.

16. Novis BH, Bank S, Marks IN. Gastro-intestinal and peritoneal tuberculosis. A study of cases at Groote Schuur Hospital 1962-1971. S Afr Med J 1973;47:365-72.

17. Manohar A, Simjee AE, Haffejee AA, Pettengell KE. Symptoms and investigative findings in 145 patients with tuberculous peritonitis diagnosed by peritoneoscopy and biopsy over a five year period. Gut 1990;31:1130-2.

18. Uygur-Bayramicli O, Dabak G, Dabak R. A clinical dilemma: abdominal tuberculosis. World J Gastroenterol 2003;9:1098Cilt - Vol. 17 Sayı - No. 1

101.

19. Gunn A, Keddie NC. Abdominal tuberculosis. Br J Surg 1972;59:597-602.

20. Hassan I, Brilakis ES, Thompson RL, Que FG. Surgical management of abdominal tuberculosis. J Gastrointest Surg 2002;6:862-7.

21. Kapoor VK. Abdominal tuberculosis. Postgrad Med J 1998;74:459-67.

22. Sefr R, Rotterová P, Konecný J. Perforation peritonitis in primary intestinal tuberculosis. Dig Surg 2001;18:475-9.

23. Uzunkoy A, Harma M, Harma M. Diagnosis of abdominal tuberculosis: experience from 11 cases and review of the literature. World J Gastroenterol 2004;10:3647-9.

24. Chow KM, Chow VC, Szeto CC. Indication for peritoneal biopsy in tuberculous peritonitis. Am J Surg 2003;185:567-73.

25. Wang WN, Wallack MK, Barnhart S, Kalani AD, Storrs SL. Tuberculous peritonitis: definitive diagnosis by laparoscopic peritoneal biopsy. Am Surg 2008;74:1223-4.

26. Wang HK, Hsueh PR, Hung CC, Chang SC, Luh KT, Hsieh WC. Tuberculous peritonitis: analysis of 35 cases. J Microbiol Immunol Infect 1998;31:113-8.

27. Shakil AO, Korula J, Kanel GC, Murray NG, Reynolds TB. Diagnostic features of tuberculous peritonitis in the absence and presence of chronic liver disease: a case control study.

Am J Med 1996;100:179-85.

28. Singh MM, Bhargava AN, Jain KP.Tuberculous peritonitis. An evaluation of pathogenetic mechanisms, diagnostic procedures and therapeutic measures.N Engl J Med 1969;281:1091-4.

29. Nafeh MA, Medhat A, Abdul-Hameed AG, Ahmad YA, Rashwan NM, Strickland GT. Tuberculous peritonitis in Egypt: the value of laparoscopy in diagnosis. Am J Trop Med Hyg 1992;47:470-7.

30. Muneef MA, Memish Z, Mahmoud SA, Sadoon SA, Bannatyne R, Khan Y. Tuberculosis in the belly: a review of forty-six cases involving the gastrointestinal tract and peritoneum. Scand J Gastroenterol 2001;36:528-32.

31. Voigt MD, Kalvaria I, Trey C, Berman P, Lombard C, Kirsch RE. Diagnostic value of ascites adenosine deaminase in tuberculous peritonitis. Lancet 1989;1:751-4.

32. Panoskaltsis TA, Moore DA, Haidopoulos DA, McIndoe AG. Tuberculous peritonitis: part of the differential diagnosis in ovarian cancer. Am J Obstet Gynecol 2000;182:740-2.

33. Mas MR, Cömert B, Sağlamkaya U, Yamanel L, Kuzhan O, Ateşkan U, et al. CA-125; a new marker for diagnosis and follow-up of patients with tuberculous peritonitis. Dig Liver Dis 2000;32:595-7.

34. Thakur V, Mukherjee U, Kumar K. Elevated serum cancer antigen 125 levels in advanced abdominal tuberculosis. Med Oncol 2001;18:289-91.

35. Simsek H, Savas MC, Kadayifci A, Tatar G. Elevated serum CA 125 concentration in patients with tuberculous peritonitis: a case-control study. Am J Gastroenterol 1997;92:1174-6.

36. Mimica M. Usefulness and limitations of laparoscopy in the diagnosis of tuberculous peritonitis. Endoscopy 1992;24:58891.

37. Bhargava DK, Shriniwas, Chopra P, Nijhawan S, Dasarathy S, Kushwaha AK.Peritoneal tuberculosis: laparoscopic patterns and its diagnostic accuracy. Am J Gastroenterol 1992;87:109-12.

38. Chu CM, Lin SM, Peng SM, Wu CS, Liaw YF. The role of laparoscopy in the evaluation of ascites of unknown origin.

Gastrointest Endosc 1994;40:285-9.

73

Ulus Travma Acil Cerrahi Derg

39. Sandikçi MU, Colakoglu S, Ergun Y, Unal S, Akkiz H, Sandikçi S, et al. Presentation and role of peritoneoscopy in the diagnosis of tuberculous peritonitis. J Gastroenterol Hepatol 1992;7:298-301.

40. Hossain J, al-Aska AK, al Mofleh I. Laparoscopy in tuberculous peritonitis. J R Soc Med 1992;85:89-91.

41. Jhobta RS, Attri AK, Kaushik R, Sharma R, Jhobta A. Spectrum of perforation peritonitis in India-review of 504 consecutive cases. World J Emerg Surg 2006;1:26.

42. Khanna AK, Misra MK. Typhoid perforation of the gut. Postgrad Med J 1984;60:523-5.

43. Kapoor VK, Kriplani AK, Chattopadhyay TK, Sharma LK. Tuberculous perforations of the small intestine. Ind J Tub 1986;33:188-9.

44. Tan KK, Chen K, Sim R. The spectrum of abdominal tuberculosis in a developed country: a single institution’s experience over 7 years. J Gastrointest Surg 2009;13:142-7.

45. Bhansali SK, Desai AN, Dhaboowala CB. Tuberculous perforation of the small intestine. A clinical analysis of 19 cases.

J Assoc Physicians India 1968;16:351-5.

46. Aston NO, de Costa AM. Tuberculous perforation of the small bowel. Postgrad Med J 1985;61:251-2.

47. Salvati V, Fumo F, D’Armiento FP, Fumo M, Cerrone C. Primary intestinal tuberculosis. Minerva Chir 1996;51:567-71.

48. Shah S, Thomas V, Mathan M, Chacko A, Chandy G, Ramakrishna BS, et al. Colonoscopic study of 50 patients with colonic tuberculosis. Gut 1992;33:347-51.

49. Wake PN, Humphrey C, Walker R. Long term intravenous rifampicin after massive small bowel resection. Tubercle 1980;61:109-11.

50. Sweetman WR, Wise RA. Acute perforated tuberculous enteritits:surgical treatment. Ann of Surg 1959;149:143-8.

51. Gleason T, Prinz RA, Kirsch EP, Jablokow V, Greenlee HB. Tuberculosis of the duodenum. Am J Gastroenterol

74

1979;72:36-40.

52. Ecgleston FC, Deodhar MC, Kumar A. Surgery in abdominal tuberculosis - results in 137 cases. Ind J Tub 1983;30:139.

53. Gilinsky NH, Voigt MD, Bass DH, Marks IN. Tuberculous perforation of the bowel. A report of 8 cases. S Afr Med J 1986;70:44-6.

54. Doré P, Meurice JC, Rouffineau J, Carretier M, Babin P, Barbier J, et al. Intestinal perforation occurring at the beginning of treatment: a severe complication of bacillary tuberculosis.

Rev Pneumol Clin 1990;46:49-54.

55. Rahman A. Spontaneous ileal perforation: an experience of 33 cases. J Postgrad Med Inst 2003;17:105-10.

56. Ara C, Sogutlu G, Yildiz R, Kocak O, Isik B, Yilmaz S, et al. Spontaneous small bowel perforations due to intestinal tuberculosis should not be repaired by simple closure. J Gastrointest Surg 2005;9:514-7.

57. Leung VK, Law ST, Lam CW, Luk IS, Chau TN, Loke TK, et al. Intestinal tuberculosis in a regional hospital in Hong Kong: a 10-year experience. Hong Kong Med J 2006;12:26471.

58. Leone V, Misuri D, Fazio C, Cardini S.Abdominal tuberculosis: clinical features, diagnosis and role of surgery. Minerva Chir 2007;62:25-31.

59. Gupta NM, Motup T, Joshi K. Isolated colonic tuberculous perforation as a rare cause of peritonitis: report of a case.

Surg Today 1999;29:273-5.

60. McElvanna K, Skelly RT, O’Neill C, Spence GM. Miliary tuberculosis causing multiple intestinal perforations in an immigrant worker. Ulster Med J 2008;77:206-8.

61. Prout WG. Multiple tuberculous perforations of ileum. Gut 1968;9:381-2.

62. Gupta NM, Motup T, Joshi K. Isolated colonic tuberculous perforation as a rare cause of peritonitis: report of a case.

Surg Today 1999;29:273-5.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):75-78

Case Report

Olgu Sunumu doi: 10.5505/tjtes.2011.53189

Bilateral internal carotid artery and vertebral artery dissections with retinal artery occlusion after a roller coaster ride - case report and a review Lunapark trenine binmeye bağlı iki taraflı internal karotid ve vertebral arter diseksiyonu ile beraber retinal arter oklüzyonu: Olgu sunumu ve literatür incelemesi Yonca ÖZKAN ARAT,1 John VOLPI,2 Anil ARAT,3 Richard KLUCZNIK,4 Orlando DIAZ4 We present the first case of a woman with no significant medical history who developed dissections of bilateral carotid and bilateral vertebral arteries, as well as a retinal artery occlusion, after a roller coaster ride. A 35-year-old woman developed right-sided neck pain followed by a frontal headache immediately after a roller coaster ride. Five days after the incident, she developed complete loss of vision in her right eye for two hours. Subsequently, the vision improved but remained significantly decreased. On presentation, her visual acuity was 20/200 in the right and 20/20 in the left eye. Her fundus exam revealed retinal edema in the superotemporal retinal artery distribution without any visible emboli. Her neurological exam was otherwise normal. The cerebral angiogram showed bilateral internal carotid and vertebral artery dissections. The patient remained stable with conservative therapy without further worsening of vision or any new neurological deficits. Outcomes for cervicocephalic arterial dissection are usually favorable, but early diagnosis is critical for initiation of appropriate treatment of possible complications. Physicians must have a high index of suspicion for arterial dissection when patients note any headache, neck pain or vertigo triggered by violent motion after leisure activities such as roller coaster rides.

Bu yazıda, lunapark trenine (roller coaster) binmesini takiben iki taraflı internal karotid ve iki taraflı vertebral arter diseksiyonu ile beraber retinal arter oklüzyonu gelişen, bilgilerimize göre, literatürdeki ilk olguyu sunuyoruz. Otuz beş yaşında sağlıklı bir kadın hastada, lunapark trenine binmesini takiben, sağ taraflı boyun ağrısı ve frontal başağrısı gelişmiştir. Bundan beş gün sonra hastanın sağ gözünde 2 saat süren tam görme kaybını takiben, bu gözde görme düzelmiş fakat normale göre çok düşük düzeyde kalmıştır. Hastanın ilk muayenesinde sağ gözde görmesi 20/200 ve sol gözde 20/20 düzeyinde bulunmuştur. Fundus muayenesinde üst temporal arter boyunca ödem izlenmiş, emboli görülmemiştir. Hastanın bunun dışında nörolojik muayenesi normaldi. Yapılan beyin anjiyografisinde, iki taraflı internal karotid ve iki taraflı vertebral arter diseksiyonu görülmüştür. Hasta, konservatif tedavi ile stabil olarak kalmış ve görmesinde daha fazla düşme veya yeni nörolojik kayıp izlenmemiştir. Baş-boyun arter diseksiyonlarında prognoz çogunlukla iyidir, fakat olası komplikasyonların önlenmesi için erken teşhis çok önelidir. Lunapark treni gibi ani ve hızlı hareketlere maruz kalınmasını takiben başağrısı, boyun ağrısı, baş dönmesi gibi şikayetler gelişen hastalarda arteriyel diseksiyon için yüksek şüphe bulunmalıdır.

Key Words: Carotid artery; dissection; retinal artery; vertebral artery.

Anahtar Sözcükler: Karotid arter; diseksiyon; retinal arter; vertebral arter.

CASE REPORT A 35-year-old woman with no significant medical history developed right-sided neck pain followed by a frontal headache immediately after a roller coaster

ride, which was not relieved with acetaminophen/ propoxyphene (Darvocet-N®100). Five days after the incident, she developed complete loss of vision in her right eye for two hours. Subsequently, the vision

Department of Ophthalmology, University of Wisconsin, Madison, WI; 2 Department of Neurology, The Methodist Hospital, Houston, TX; 3 Department of Radiology, University of Wisconsin, Madison, Wisconsin; 4 Department of Radiology, The Methodist Hospital, Houston, TX, USA. 1

Wisconsin Üniversitesi, Göz Hastalıkları Anabilim Dalı, Madison, WI; 2 Methodist Hastanesi, Nöroloji Anabilim Dalı, Houston, TX; 3 Wisconsin Üniversitesi, Radyoloji Anabilim Dalı, Madison, WI; 4 Methodist Hastanesi, Radyoloji Anabilim Dalı, Houston, TX, A.B.D.

1

Correspondence (İletişim): Yonca Ozkan Arat, M.D. 301 S. Yelowstone Dr. #400 53705 Madison-Wisconsin, United States.

Tel: +001 - 608 - 4458942 e-mail (e-posta): yoncaozkan@hotmail.com

75

Ulus Travma Acil Cerrahi Derg

improved but remained significantly decreased compared to baseline. She was admitted to our hospital for evaluation and treatment. On presentation, her visual acuity was 20/200 in the right eye and 20/20 in the left eye. She had an afferent pupillary defect on the right. Her fundus exam revealed retinal edema in the superotemporal retinal artery distribution without any visible emboli. Her neurological exam was otherwise normal without any other neurological deficit. The patient underwent a cerebral angiogram, which demonstrated occlusion of the right internal carotid artery (Fig. 1a) and dissections involving the left internal carotid and both vertebral arteries (Fig. 1b-d). The left internal carotid artery injection showed preferential opacification of all intracranial arteries from the left internal carotid artery (Fig. 2). There was complete occlusion of the right internal carotid artery with retrograde perfusion of the right ophthalmic artery.

Conservative management was offered to the patient based on the angiogram, and she was started on anticoagulation with 12 units/kg-hr intravenous heparin infusion for four days followed by oral Coumadin for three months. The patient (a) then remained stable without further (c) worsening of vision or development of any new neurological deficits.

DISCUSSION Among all patients admitted to the hospital for blunt trauma, the incidence of carotid artery injury is approximately 0.1%,[1] and that of vertebral artery injury approximately 0.5%.[2] Four-vessel cervical dissections are extremely rare, and there have been about seven cases reported in the literature.[3-9] Furthermore, our case also had retinal artery occlusion associated with ipsilateral ophthalmic artery occlusion secondary to internal carotid artery dissection. There have been only a few reports of central/ branch retinal artery occlusion associated with cervical dissections.[10-18] To our knowledge, we are reporting the first case of a woman with no history of collagen vascular disease who developed dissections of both carotid and both vertebral arteries, as well as a retinal artery occlusion, after a roller coaster ride.

Arterial dissection is the most common etiology for stroke in a young per76

son.[19] Trauma and connective tissue disorders represent the major risk factors.[20] Most cervical dissections are atraumatic or associated with only mild trauma.[3] Traumas due to roller coaster rides have been rarely associated with cervical arterial dissections. There have been five cases of vertebral artery dissection and seven cases of internal carotid artery dissection

(b) (d)

Fig. 1. (a) Right common carotid arteriogram showing total occlusion of the internal carotid artery at its origin. (b) Left common carotid arteriogram demonstrates a small dissection flap (arrow) on the posterior wall of the internal carotid artery. (c) Right subclavian arteriogram shows dissection flap and a small pseudoaneurysm at approximately the C7-T1 level; distal cervical vertebral artery is involved to a lesser extent. (d) Left subclavian artery shows a similar involvement of the vertebral artery on the right side.

Ocak - January 2011

Bilateral internal carotid artery and vertebral artery dissections with retinal artery occlusion

weighted magnetic resonance imaging (MRI) with fat saturation can be used to image the neck vessels. MRI has been shown to be a sensitive, noninvasive modality for diagnosis.[28] However, conventional cerebral angiography remains the gold standard.[29] In general, the outcomes for cervicocephalic arterial dissections are usually favorable with either anticoagulant or antiplatelet therapy, but early diagnosis is crucial for initiation of appropriate treatment and monitoring of potential complications.[21]

Fig. 2. Left internal carotid arteriogram shows preferential opacification of the contralateral carotid circulation through the anterior communicating artery. The vertebrobasilar circulation distal to the midbasilar segment also opacifies in this injection via the posterior communicating arteries bilaterally.

reported after roller coaster rides.[21-26] None of these cases had involvement of both bilateral vertebral and carotid arteries. The complex and abrupt changes in motion have the potential to cause sudden hyperextension, hyperflexion or rotation of the neck, which may cause injury to the carotid or vertebral arteries and create intimal tears.[21,24] These rides can generate force in excess of 4 gravitational forces (Gs), which in combination with neck movements could potentially rip the carotid intima.[22] Subintimal penetration of blood with subsequent longitudinal extension of intraluminal hematoma may cause vessel narrowing that may progress to complete obstruction, aneurysm formation, or both.[24] Certain people, such as those with underlying connective tissue disorders, may be more susceptible to arterial dissection. However, there is evidence to suggest that patients who are phenotypically normal may have ultrastructural abnormalities of connective tissue.[27] In our patient, the work-up for an underlying connective tissue disease was negative.

It should be noted that recognition of cervicocephalic arterial dissections is often delayed since the presenting symptoms, including headache, vertigo and neck pain, are non-specific, and the diagnosis may not be considered until there is evidence of neurological impairment. A high index of suspicion is therefore necessary for the diagnosis in the presence of nonspecific symptoms that usually precede the neurological deficits for up to three weeks or more.[23,24] If the diagnosis is suspected, targeted investigations such as axial T1Cilt - Vol. 17 Say覺 - No. 1

Internal carotid artery dissections may be associated with ocular complications such as ophthalmoplegia, Horner syndrome, ischemic optic neuropathy, and arterial vessel occlusions.[11] Central retinal artery occlusions caused by carotid artery dissections are exceedingly rare compared with the other ophthalmologic signs in these patients. Most authors believe it results from ocular hypoperfusion rather than an embolic process because of the existence of reversal of the ophthalmic flow.[11,14] There have been only a few reports of branch retinal artery or cilioretinal artery occlusion associated with a visible emboli.[13,17] Our patient had retinal edema in the superotemporal retinal artery distribution without any visible emboli. We believe that she either had reperfused central retinal artery occlusion with retrograde flow with evidence of increased retinal insult superotemporally or branch retinal artery occlusion. The recognition of an internal carotid artery dissection is of utmost importance because a risk of hemispheric stroke exists in one-third of the patients, usually within the first week.[11] Early diagnosis and treatment of internal carotid artery dissection are important to reduce the risk of hemispheric stroke. All patients with central retinal artery occlusion should be questioned about associated pain or other extraocular symptoms, such as tinnitus, preceding the occurrence of central retinal artery occlusion.[14] In conclusion, outcomes in cervicocephalic arterial dissection are usually favorable with anticoagulant therapy, but early diagnosis is critical for initiation of appropriate treatment of possible complications. Physicians must have a high index of suspicion for arterial dissection when patients note any headache, neck pain, vertigo, or tinnitus triggered by violent motion after leisure activities such as roller coaster rides.

REFERENCES 1. Biffl WL, Moore EE, Ryu RK, Offner PJ, Novak Z, Coldwell DM, et al. The unrecognized epidemic of blunt carotid arterial injuries: early diagnosis improves neurologic outcome.

Ann Surg 1998;228:462-70.

2. Biffl WL, Moore EE, Elliott JP, Ray C, Offner PJ, Franciose RJ, et al. The devastating potential of blunt vertebral arterial injuries. Ann Surg 2000;231:672-81.

3. Chakrapani AL, Zink W, Zimmerman R, Riina H, Benitez R. Bilateral carotid and bilateral vertebral artery dissection following facial massage. Angiology 2008;59:761-4.

77

Ulus Travma Acil Cerrahi Derg

4. Marshman LA, Ball L, Jadun CK. Spontaneous bilateral carotid and vertebral artery dissections associated with multiple disparate intracranial aneurysms, subarachnoid hemorrhage and spontaneous resolution. Case report and literature review. Clin Neurol Neurosurg 2007;109:816-20.

5. Yong RL, Heran NS. Traumatic carotid cavernous fistula with bilateral carotid artery and vertebral artery dissections.

Acta Neurochir (Wien) 2005;147:1109-13.

6. Nadgir RN, Loevner LA, Ahmed T, Moonis G, Chalela J, Slawek K, et al. Simultaneous bilateral internal carotid and vertebral artery dissection following chiropractic manipulation: case report and review of the literature. Neuroradiology 2003;45:311-4.

7. Coric D, Wilson JA, Regan JD, Bell DA. Primary stenting of the extracranial internal carotid artery in a patient with multiple cervical dissections: technical case report. Neurosurgery 1998;43:956-9.

8. Rees JH, Valentine AR, Llewelyn JG. Spontaneous bilateral carotid and vertebral artery dissection presenting as a ColletSicard syndrome. Br J Radiol 1997;70:856-8.

9. Grau AJ, Brandt T, Forsting M, Winter R, Hacke W. Infection-associated cervical artery dissection. Three cases. Stroke 1997;28:453-5.

10. Rao TH, Schneider LB, Patel M, Libman RB. Central retinal artery occlusion from carotid dissection diagnosed by cervical computed tomography. Stroke 1994;25:1271-2.

11. Biousse V, Touboul PJ, Dâ&#x20AC;&#x2122;Anglejan-Chatillon J, LĂŠvy C, Schaison M, Bousser MG. Ophthalmologic manifestations of internal carotid artery dissection. Am J Ophthalmol 1998;126:565-77.

12. Godfrey DG, Biousse V, Newman NJ. Delayed branch retinal artery occlusion following presumed blunt common carotid dissection. Arch Ophthalmol 1998;116:1120-1.

13. McDonough RL, Forteza AM, Flynn HW Jr. Internal carotid artery dissection causing a branch retinal artery occlusion in a young adult. Am J Ophthalmol 1998;125:706-8.

14. Mokhtari F, Massin P, Paques M, Biousse V, Houdart E, Blain P, et al. Central retinal artery occlusion associated with head or neck pain revealing spontaneous internal carotid artery dissection. Am J Ophthalmol 2000;129:108-9.

15. Lubin J, Capparella J, Vecchione M. Acute monocular blindness associated with spontaneous common carotid artery dis-

78

section. Ann Emerg Med 2001;38:332-5.

16. Schneider U, Hermann A, Ernemann U, Bartz-Schmidt KU. Central retinal artery occlusion secondary to spontaneous internal carotid artery dissection. Retina 2004;24:979-81.

17. Hwang JF, Chen SN, Chiu SL, Wu SL. Embolic cilioretinal artery occlusion due to carotid artery dissection. Am J Ophthalmol 2004;138:496-8.

18. Akiyama Y, Tanaka M, Hayashi J, Fujimoto M, Harada K, Nakahara I, et al. Internal carotid artery obstruction derived from persistent arterial wall dissection associated with old trivial trauma. Neurol Med Chir (Tokyo) 2006;46:395-7.

19. Leys D, Lucas C, Gobert M, Deklunder G, Pruvo JP. Cervical artery dissections. Eur Neurol 1997;37:3-12.

20. Schievink WI, Mokri B, Whisnant JP. Internal carotid artery dissection in a community. Rochester, Minnesota, 19871992. Stroke 1993;24:1678-80.

21. Schneck M, Simionescu M, Bijari A. Bilateral vertebral artery dissection possibly precipitated in delayed fashion as a result of roller coaster rides. J Stroke Cerebrovasc Dis 2008;17:39-41.

22. Blacker DJ, Wijdicks EF. A ripping roller coaster ride. Neurology 2003;61:1255.

23. Stahlfeld KR, Roozrokh HC. Traumatic bilateral ECCA injury in a roller coaster enthusiast. Ann Vasc Surg 2002;16:505-8.

24. Lascelles K, Hewes D, Ganesan V. An unexpected consequence of a roller coaster ride. J Neurol Neurosurg Psychiatry 2001;71:704-5.

25. Kettaneh A, Biousse V, Bousser MG. Neurological complications after roller coaster rides: an emerging new risk?

Presse Med 2000;29:175-80. [Abstract] 26. Burneo JG, Shatz R, Papamitsakis NI, Mitsias PD. Neuroimages: amusement park stroke. Neurology 2000;55:564.

27. Brandt T, Hausser I, Orberk E, Grau A, Hartschuh W, AntonLamprecht I, et al. Ultrastructural connective tissue abnormalities in patients with spontaneous cervicocerebral artery dissections. Ann Neurol 1998;44:281-5.

28. Ozdoba C, Sturzenegger M, Schroth G. Internal carotid artery dissection: MR imaging features and clinical radiological correlation. Radiology 1996;199:191-8.

29. Ganesan V, Savvy L, Chong WK, Kirkham FJ. Conventional cerebral angiography in children with ischemic stroke. Pediatr Neurol 1999;20:38-42.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):79-82

Case Report

Olgu Sunumu doi: 10.5505/tjtes.2011.49092

Unusual penetration of a construction nail through the orbit to the cranium: a case report Bir inşaat çivisinin alışılmadık şekilde orbitayı geçerek kraniyuma saplanması: Olgu sunumu İbrahim ERKUTLU,1 Mehmet ALPTEKİN,1 Mehmet DOKUR,2 Murat GEYİK,1 Abdulvahap GÖK1 Penetrating head and neck trauma with construction nails are uncommon life-threatening injuries and an important problem in developing countries. Assessment of the neurovascular and systemic physical status is a first requirement, and the decision concerning which surgical approach to perform for the removal of the nail is of critical importance. A 10-year-old girl was presented one hour after a fall injury with complaint of a swelling and foreign body lodgment on the left forehead. Neurological and systemic physical examinations were normal except for weak direct pupillary light reflex on the left side and the patient’s state of uneasiness. Radiological investigations showed that the head of the nail had entered from the left infraorbital region and become lodged through the orbital roof, below the frontal bone. Surgical extraction of the nail in the operating room was performed successfully using left pterional craniotomy and lateral orbitotomy technique, and there was no complication after surgery. Here, we report a case with a rare craniocerebral penetrating wound and type, with the head of the nail lodged in the anterior fossa through the orbital roof, which may be defined as ‘reverse penetration of the nail’.

İnşaat çivileriyle oluşan delici baş ve boyun yaralanmaları, nadiren gözlenen, ölümcül ve gelişmekte olan ülkelerin önemli bir problemidir. Hastanın nörovasküler durumu ve sistemik fiziksel incelemesi ilk bilinmesi gereken durumdur, çivinin çıkarılmasında cerrahi ve/veya medikal olarak hangi yaklaşımın uygulanacağı kritik önem taşır. On yaşında, yüksekten düştükten 1 saat sonra sol alnında şişlik ve yabancı cisim batması şikayetiyle başvuran bir kız çocuğu sunuldu. Sol göz ışık refleksindeki zayıflık ve huzursuzluğu dışında nörolojik ve sistemik muayenesi normal idi.

Radyolojik araştırmalar çivi başının sol supraorbital bölgeden girdiğini ve orbital tavan boyunca ilerleyerek frontal kemiğin altından ilerleyerek saplandığını gösterdi. Çivi sol piterional kraniyotomi ve lateral orbitotomi tekniği kullanılarak başarıyla çıkarıldı ve cerrahi sonrası herhangi bir komplikasyon gelişmedi. Biz burada belkide “çivinin ters penetrasyonu” olarak tanımlanabilecek nadir bir kraniyoserebral delici yaralanmayı ve orbital tavan boyunca ilerleyerek anterior fossaya baş kısmıyla saplanan bir yaralanma tipini sunduk. Ek olarak bu tip yaralanmalarda çivi baş tarafından kraniyuma saplandıysa ameliyat öncesi ve sonrası alınması gereken önlem ve tedavi stratejileri tartıştışıldı.

Key Words: Craniocerebral penetrating injury; nail; surgery; treatment options.

Anahtar Sözcükler: Kraniyoserebral delici yaralanma; çivi; cerrahi; tedavi seçenekleri.

Penetrating orbito-cranial injuries are quite common in military practice, but they are very rarely seen in civilian life, where they are predominantly accidental injuries. Penetrating object injuries occurring by falling onto a penetrating object such as a nail are rarely encountered cases, although a number of head injuries associated with construction nails have been reported previously.[1-5] These types of injuries can be life-threatening, depending on the patient’s age, the injury location and vascular and other complications

of the injury.[4,5] The most common delayed complications are cerebrospinal fluid (CSF) leakage, infectious complications such as meningitis, orbital cellulitis and cerebral abscess, and vascular injuries such as traumatic aneurysm and progressive intravascular thrombosis.

[2-4,6] However, their true incidence is not clear.[4]

Department of Neurosurgery, Gaziantep Faculty of Medicine, Gaziantep; Department of Emergency Medicine, Kilis State Hospital, Kilis, Turkey.

1

2

Due to the risk of significant neurological and vascular complications, it is important to clarify where the foreign body is located, and it is vital to determine Gaziantep Üniversitesi Tıp Fakültesi Nöroşirürji Anabilim Dalı, Gaziantep; 2 Kilis Devlet Hastanesi, Acil Tıp Kliniği, Kilis.

1

Correspondence (İletişim): İbrahim Erkutlu, M.D. Kolejtepe Mah., Mehmet Dai Sok., Dr. Bülent Aksoy Apt., No: 48/3, Gaziantep, Turkey.

Tel: +90 - 342 - 360 39 10 / 7723 e-mail (e-posta): erkutlu@gantep.edu.tr

79

Ulus Travma Acil Cerrahi Derg

the most appropriate surgical approach to remove the object and overcome potential complications.

We report a patient who fell onto a rusty nail that lodged head-first deeply into the anterior cranial fossa through the orbital roof, and we discuss the treatment strategies.

CASE REPORT In this case presentation, we carried out the surgical analysis of a 10-year-old female child who was admitted to our clinic from another hospital with the anamnesis of falling from a first floor height onto a rusty nail 7-8 cm in length, resulting in a serious lodgment into the left orbital region. Edema and a sharppointed metal object were observed on the left eyelid, protruding 0.5 cm from the skin. Although her verbal response was confused, she was able to obey commands for the examination. Glasgow Coma Scale was 15 (E4-M6-V5), and direct pupillary light reflex was positive in the right eye and weak in the left eye.

There was no active bleeding from the wound, which was on the lateral edge of the left eyebrow (Fig. 1d).

Cranial X-rays and computerized tomography (CT) showed that the nail had entered from the lateral edge of the left orbital roof. The nail head was lodged in

the left anterior cranial fossa. The head of the nail was very close to the paraophthalmic segment of the left internal carotid artery and the left optic nerve (Fig. 1ac). Since the neurological and radiological investigations showed no vascular injury, we decided to extract the nail surgically (Fig 2a-c). The patient was taken to the operating room immediately. A left pterional craniotomy was performed through a standard frontotemporal skin incision and then lateral orbitotomy was added to this approach. Following craniotomy, the nail was exposed extradurally. We observed that the head of the nail penetrated the cranium, orbital roof, periorbital adipose tissue, and dura mater. The dura was opened over the proximal sylvian fissure. After sylvian dissection, the nail was exposed intradurally and extradurally. The head of the nail was observed to press on the internal carotid artery without any penetration. Although the head of the nail was very close to the paraophthalmic segment of the left internal carotid artery and the left optic nerve, it was quite far from the pituitary gland, 3rd cranial nerve and stalk; therefore, no abnormality in pituitary functions or the 3rd cranial nerve was observed. Intraoperatively, no injury to these structures was seen. We also interpreted the cause of the pupillary dysfunction as perhaps being related to the trauma to the globe.

The patient received analgesic medication, prophylactic antibiotics and tetanus prophylaxis. She showed no additional clinical abnormality after the operation except for weak pupillary light reflex. Her follow-up cerebral CT was normal during the postoperative period (Fig. 2d). She was discharged on the 7th postoperative day.

(a)

(c)

(b)

(d)

Fig. 1. Antero-posterior (a) and lateral (b) cranial plain radiographs of the patient show the nail and its location. Axial CT image shows the intracranial portion of the nail.

The head of the nail was very close to the left carotid artery and optic nerve (c).

Note that the sharp tip of the nail protrudes from the cranium (white arrow) (d).

80

DISCUSSION In the literature, this type of injury has mostly been reported as nail gun injuries.[1,5] The foremost priority, which is critical in assessing penetrating craniocerebral injuries, is to determine if any vascular injuries have occurred and to eliminate any problem that could affect vital functions.[1-3,5] Many algorithms concerning diagnostic and therapeutic approaches have been published previously on this subject.[7] We report this case for several reasons. First, the patientâ&#x20AC;&#x2122;s Ocak - January 2011

Unusual penetration of a construction nail through the orbit to the cranium

presentation was unusual with respect to the penetration of the rusty nail, that is to say, it may be described as a “reverse penetration”.

One of the interesting subjects about this trauma is how deeply the nail was able to penetrate the cranial structure. Complete penetration of nails into the cranial cavity is rather rare.[8] Similar to other studies, the entry point in our case was also the orbital roof. The orbital roof is seen in many series as the point of entry; its mechanism can be explained by patients’ extending their head backwards during injury, thus exposing the orbital roof. In addition, the orbital roof is a very thin, bony plate, offering little resistance.[6] Second, reverse penetration of the nail is very important in terms of the surgical removal. If the object is removed suddenly during surgery, it may drag the neurovascular structures together with the head of the nail and may cause fatal injuries. This situation forms the important distinction between the present case and the more common types of injuries where the nail lodges tip-first.

Treatment of penetrating craniocerebral wounds with nails at the skull base is problematic, due to difficulties regarding surgical exposure. The anterior fossa contains important neurovascular structures such as the internal carotid artery and branches, the optic nerve and orbital structures.[9] If it is possible, and had

(a)

(c)

(b)

(d)

the patient exhibited signs of vascular injury, vascular monitoring in the neck and even proximal-distal monitoring intracranially would have been required.

Trauma to the cerebrovascular system (both penetrating and non-penetrating) can cause injuries such as arterial dissection, pseudoaneurysm, arterial or venous rupture or thrombosis, and arteriovenous fistula.

[10] Angiography should be immediately performed, and any probable vascular damages should be investigated. If the lesion caused by the penetrating object has already affected the venous structures, the patient unquestionably should be evaluated by preoperative angiography, CT and/or magnetic resonance imaging (MRI) due to the potential for an unexpected air embolism.[2,3,8] Postoperatively, a second vascular study should always follow 2-3 weeks after a negative one to detect the possibility of the formation of a pseudoaneurysm.[2,4,5] The guidelines for the management of these aneurysms are not well defined, especially with regards to asymptomatic patients. There are several different methods for the management of these injuries.

[4] A foreign body that has completely penetrated into the brain needs to be removed via craniotomy. Some authors have advised that if angiography is negative for vascular injury and the patient is asymptomatic, the nail should be extracted via closed gentle traction.

They also have advocated that intervention involving craniotomy and/or an endovascular approach should be reserved for those presenting with symptoms of vascular involvement and also when the nail has no extracranial extension, due to possible unnecessary complications.[7,9,11]

Fig. 2. Intraoperative images show cranio-orbital approach (a) and the nail located between the left periorbita and the sylvian fissure (b). The nail was 7-8 cm in length (c). Early postoperative axial CT image demonstrates that there was no lesion in the surgical area (d).

Cilt - Vol. 17 Sayı - No. 1

Third, the priority is selection of the most logical treatment strategy to overcome these injuries. Many authors have advised previously that the most appropriate treatment in cerebral penetrating injuries is surgical intervention, if possible.

[8] At this point, the question remains: what should we do or which treatment strategy should we choose if the vascular injury is beyond repair? In this problematic situation, endovascular management or extracranial-intracranial vascular bypass procedures would have had to be considered.[9] There was no injury to the neurovascular structures in our case because of blunt compression by the head of the 81

Ulus Travma Acil Cerrahi Derg

nail. However, we believe that, in cases of penetrating cranium injuries, the object should be removed in the operating room due to the high risks of neurovascular injury. One of the most important reasons for neurovascular injury during surgery is a wrongly selected or inadequate surgical approach. A wide surgical exposure along with careful manipulation of the embedded nail is of importance to avoid unexpected injury to the surrounding brain and related structures. The cranio-orbital approach has been used for many years to treat some vascular and tumoral lesions in neurosurgical practice. This technique also provides a wide and safe surgical corridor in anterior fossa lesions and necessitates less retraction of the vital neurovascular structures.[12,13] Finally, surgical operations should not be attempted in centers having no experience in craniotomy and vascular operations because the anterior fossa contains major vessels and cranial nerves. Such procedures can lead to various unexpected fatal complications and morbidity. Although the entry point of the nail in this case was on the infraorbital region, the optic nerve, internal carotid artery and branches were intact, and the neurological examination was normal except for a weak pupillary light reflex on the left side. The periorbital tissue and osseous part of the orbital roof were injured. After physical examination and radiological investigations, we considered that immediate surgical intervention would be more reliable, given the finding that the nail had not seriously damaged any neurovascular structures at the moment of entry. In this case, we did not perform cerebral angiography preoperatively because the patient had no neurological or radiological abnormalities. While we decided not to perform angiography in this patient, we nevertheless believe that this procedure is absolutely necessary in these types of injuries.

In conclusion, penetrating injuries with construction nails are uncommon but life-threatening injuries.

Appropriate imaging studies include CT scan of the head, with or without angiography, and therapeutic embolization. Neurosurgical and otolaryngologic approaches are most commonly used to extract these foreign bodies from the face, skull base and parenchyma. Appropriate diagnosis is crucial to avoid potential complications such as CSF leakage, intracra-

82

nial infection and hemorrhage. Thorough knowledge of the neuro-anatomic relationships within the injured region is the most important criterion in such procedures. We believe that physicians should not attempt to remove foreign bodies and should refer the patient to neurosurgeons who are experienced in neurovascular surgery. In addition, medical precautions such as antibiotherapy and tetanus prophylaxis should not be neglected. Families in developing countries should be taught how to limit accidents and to protect children from danger.

REFERENCES 1. Agrillo A, Sassano P, Mustazza MC, Filiaci F. Complex-type penetrating injuries of craniomaxillofacial region. J Craniofac Surg 2006;17:442-6.

2. Bilotta F, Rosa G, Delfini R, Pinto R, Fiorani B. Unrecognized periorbital penetrating nail in the brain: case report.

Am J Emerg Med 2007;25:198-9.

3. Bragg S. Head trauma from a nail gun. J Emerg Nurs 2006;32:329.

4. Lee AD, Oh YS. Unusual delayed presentation of a nail gun injury through the skull base. Laryngoscope 2007;117:977-80.

5. Panourias IG, Slatinopoulos VK, Arvanitis DL. Penetrating craniocerebral injury caused by a pneumatic nail gun: an unsuccessful attempt of suicide. Clin Neurol Neurosurg 2006;108:490-2.

6. Türkçüoğlu P, Aydoğan S. Intracranial foreign body in a globe-perforating injury. Can J Ophthalmol 2006;41:504-5.

7. Selvanathan S, Goldschlager T, McMillen J, Campbell S. Penetrating craniocerebral injuries from nail-gun use. J Clin Neurosci 2007;14:678-83.

8. Chibbaro S, Tacconi L. Orbito-cranial injuries caused by penetrating non-missile foreign bodies. Experience with eighteen patients. Acta Neurochir (Wien) 2006;148:937-42.

9. Cosan TE, Arslantas A, Guner AI, Vural M, Kaya T, Tel E. Injury caused by deeply penetrating knife blade lodged in infratemporal fossa. Eur J Emerg Med 2001;8:51-4.

10. Buchalter GM, Johnson LP, Reichman MV, Jacobs J. Penetrating trauma to the head and neck from a nail gun: a unique mechanism of injury. Ear Nose Throat J 2002;81:779-83.

11. Nitsch A, Verheggen R, Merten HA. Penetrating pneumatic nail-gun injury to skull base. Br J Oral Maxillofac Surg 2007;45:692.

12. Gonzalez LF, Crawford NR, Horgan MA, Deshmukh P, Zabramski JM, Spetzler RF. Working area and angle of attack in three cranial base approaches: pterional, orbitozygomatic, and maxillary extension of the orbitozygomatic approach. Neurosurgery 2002;50:550-7.

13. Zabramski JM, Kiriş T, Sankhla SK, Cabiol J, Spetzler RF. Orbitozygomatic craniotomy. Technical note. J Neurosurg 1998;89:336-41.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):83-86

Case Report

Olgu Sunumu doi: 10.5505/tjtes.2011.75318

Rectal bleeding due to leech bite: a case report Sülük ısırığına bağlı rektal kanama: Olgu sunumu Behçet AL,1 Mehmet Emin YENEN,2 Mustafa ALDEMİR3 We present herein a case with a four-day history of fresh rectal bleeding due to leech bite. The cause was found to be a leech in the rectum by anoscope. This pathological condition is extremely rare in urban areas. Leech endoparasitism, although rare, may cause serious, even lethal, complications. Suspicion of leech infestation should be kept in mind when faced with intermittent or severe rectal bleeding in humans, and should be investigated surgically as with all other foreign bodies. In the current study, we present a patient who admitted with rectal bleeding due to leech bite. The leech was removed by hand examination (by forceps) without requiring any surgical attempt.

Bu yazıda, sülük ısırığına bağlı oluşan dört günlük taze rektal kanamalı olgu sunuldu. Kanamının nedeni anoskopla rektumda olduğu saptanan sülüktü. Bu patolojik durum şehir alanlarında oldukça azdır. Sülük endoparasitizmi az olmasına rağmen, ciddi ve hatta ölümcül komplikasyonlara neden olmaktadır. İnsanlarda aralıklı veya ciddi rektal kanama ile karşılaştığında sülük infestasyon şüphesi akılda tutulmalıdır ve diğer tüm yabancı cisimlerde olduğu gibi cerrahi olarak incelenmelidir. Burada sülük ısırığına bağlı rektal kanama ile başvuran bir hastayı sunduk. Sülük, herhangi bir cerrahi girişim yapılmaksızın el değerlendirmesi ile (forseps ile) çıkarıldı.

Key Words: Anoscope; clamp; forceps; hand evaluation; leeches; rectal bleeding.

Anahtar Sözcükler: Anaoskop; klemp; forseps; el ile değerlendirme; sülük; rektal kanama.

Leeches are blood-sucking hermaphroditic parasites that vary in color and range in length from a few millimeters to half a meter; they are cylindrical or leaflike in shape, depending on the contraction of their bodies.[1] Leech infestation primarily occurs in tropical areas, such as in Mediterranean countries, Africa and Asia.[2] They have a mouth, tentacles, three jaws, and suckers specially adapted for attaching to and sucking blood from the skin and mucosal surface of mammalian species.[3] However, as an endoparasite, the leech can cause serious, even lethal, complications, though it is rare. When lodged in the rectum, the parasite can simulate the symptoms of gastrointestinal hemorrhage. Leeches are usually taken into the human body while bathing or drinking unfiltered water or while swimming in contaminated water. They localize on the mucosa of the oropharynx, nasopharynx, tonsils, esophagus, or nose, but rarely in the rectal mucosa.[4-7] Leeches are not harmful to humans at all times, and rarely, they are used in replantation and flap survival, especially in the head[8] and also neck regions.[9]

We report a case with leech in the rectum who complained of fresh rectal bleeding. We used an easy and innovative method to remove the parasite with a local anesthetic injection while the patient was in the knee-elbow position.

Department of Emergency Medicine, Gaziantep University Faculty of Medicine, Gaziantep; 2Department of General Surgery, Batman State Hospital, Batman; 3Department of Emergency Medicine, Dicle University Faculty of Medicine, Diyarbakır, Turkey.

1

CASE REPORT A previously healthy 33-year-old male from a rural community in Batman, southeastern Turkey, presented with a four-day history of fresh rectal bleeding. Two days before the onset of bleeding, he had been aware of anorectal discomfort and a sensation of wanting to defecate. The rectal bleeding was independent from defecation. Twenty-four hours before admission to our Emergency Department, his rectal bleeding increased, and he was evaluated in another medical center for this complaint. His clinical and conventional radiological examination of the chest and gastrointestinal system revealed no pathological finding. He was thus sent to the Emergency Department of Batman State Hospital for further evaluation. On admission, he was pale, his Gaziantep Üniversitesi Tıp Fakültesi, Acil Tıp Anabilim Dalı, Gaziantep; 2 Batman Devlet Hastanesi, Genel Cerrahi Kliniği, Batman; 3 Dicle Üniversitesi Tıp Fakültesi, Acil Tıp Anabilim Dalı, Diyarbakır.

1

Correspondence (İletişim): Behçet Al, M.D. Gaziantep Üniversitesi Tıp Fakültesi, Acil Servisi, 02710 Gaziantep, Turkey.

Tel: +90 - 342 - 360 60 60 e-mail (e-posta): behcetal@gmail.com

83

Ulus Travma Acil Cerrahi Derg

pulse rate was 87/min, and blood pressure was 110/70 mmHg. The complete blood count revealed a hypochromic microcytic anemia. The results of blood count were as follows: erythrocyte count 3.4 million per mm3 (reference range [r.r.]: 4.2-5.9 million per cu mm3); hematocrit 31% (r.r.: 39-49%); hemoglobin 10 g/100 ml (r.r.: 13-18 g/100 ml); mean corpuscular volume 75 µm3 (r.r.: 80-100 µm3); mean corpuscular hemoglobin 24 pg (r.r.=27-32 pg); and mean corpuscular hemoglobin concentration 28% (r.r.: 32-36%). The platelet count was 210 K/µL. Total white blood cell count was 5400/µL with 16% eosinophils. A thick blood film for malaria parasites was negative. The international normalized ratio (INR) and partial thromboplastin time (PTT) were both normal. The remaining examination did not reveal any abnormalities, in particular no obvious bleeding sites, lymphadenopathy or hepatosplenomegaly. In the knee-elbow position, anoscope examination revealed first degree internal hemorrhoid. We found a dark brown, smooth foreign body just above the internal hemorrhoidal swelling. It was a small parasite that proved to be an aquatic leech (family Hirudinidae; order Gnathobdellida; class Hirudinea; phylum Annelida) (Figs. 1, 2). Direct extraction of the worm with forceps failed because of the worm’s slippery body surface. Several attempts at spraying 4% lidocaine solution onto the worm failed to anesthetize it. After we clamped its mouth, and waited for four minutes, it stopped moving and was removed easily from the rectal mucosa with forceps. The worm with a blood-sucker was identified as a leech, which measured about 5.5 cm in length. It was still alive. After the leech was removed, due to continued oozing of blood from the lesion, compression with a tampon was performed. After a period of 8 hours, the blood oozing stopped. Flexible rectoscopy was performed for other probable parasites, and no other leeches were found.

DISCUSSION The leech is a blood-sucking worm, belonging to the phylum Annelida, class Hirudinea.[10] Leeches that attack man may be divided into two classes (aquatic and land). Land leeches have powerful jaws that can penetrate the skin so that they can attach anywhere on the external surface of the body. Land leeches are common in Southeast Asia, the Pacific Islands and South America. Aquatic leeches have weak jaws and require soft tissues, such as the mucosa of the upper aerodigestive tractus, to feed on; they have a worldwide distribution.[11] Aquatic types are acquired while bathing or drinking unfiltered water or swimming in contaminated pools. Due to this mode of transmission, almost all cases have been reported from lessdeveloped countries where use of safe water is often a problem, especially in rural areas.[12] Aquatic leeches live exclusively in fresh water. They have been described in sites like the esophagus,[11] mouth/pharynx/ larynx,[12] conjunctiva,[13] nose,[14] trachea/bronchi,[15] vagina,[16] bladder,[17] and rectum.[18] When attached to the mucous membrane, they ingest blood averaging 890% of their weight.[19] In this regard, aquatic leeches are more dangerous than land leeches because they are more likely to cause severe anemia, which may require blood transfusion.[1] Cundall et al.[20] reported three patients with severe anemia, one of whom died.

Our patient had suffered from weakness and anorectal pain for approximately four days, and a hypochromic microcytic anemia had developed, but he did not require blood transfusion.

According to the patient’s history, he had swum in a contaminated pool six days previously. The patient recovered promptly and showed no more signs or symptoms of rectal bleeding or anemia. He was discharged one day later. A long-term follow-up was not possible due to the local circumstances.

The most common mode of presentation in leech endoparasitism is nasal infestation.[21] In the stomach, the leech is usually destroyed by gastric acid.[11] Therefore, it has not been described in the lower intestines, although it can pass from outside through the anal sphincter into the rectum.[18] However, the presence of a leech in the rectum has been reported in a limited number of articles. In the last 35 years, there were only two case reports on this issue.[18] When the leech is present in the rectum, patients present with intermittent or severe rectal bleeding, anorectal discom-

Fig. 1. A lateral view of the leech.

Fig. 2. An anteroposterior view of the leech with the oral opening on the left (length 5.5 cm; diameter 7 mm).

84

Ocak - January 2011

Rectal bleeding due to leech bite

fort, a sensation of wanting to defecate, and sensation of a moving foreign body in the rectum.[18] Cases of leech-induced bleeding from the vagina, bladder and pharynx have been reported but, to the best of our knowledge, this is only the third reported case of rectal bleeding and certainly the first to be managed by anoscope and hand evaluation. In earlier reports, the first from China, the patient was treated conservatively with hemostatic drugs, and bleeding only stopped on the second day after the diagnosis was made. In the second case, from Malaysia, the patient was managed endoscopically, and electrocoagulation was applied to stop the bleeding.[22] The possibility of leech endoparasitism should not be overlooked in patients (especially in children) presenting with epistaxis, rectal bleeding or hemoptysis, and a history of recent contact with fresh water lakes or streams in areas where aquatic leeches are commonly found.[18,19,21] Diagnosis is easy when the leech is in the rectum. However, when lodged in the anorectal mucosa, an examination without general anesthesia may be required. In this location, the differential diagnosis should necessarily include other anorectal or colorectal lesions, such as hemorrhoids, anorectal polyp, malignant tumors, and angiodysplasia.[23,24] Leech bites are painless and result in a triradiate wound that remains open for a long time and heals slowly.[25] As was seen in our case, the commonest complication of leech application is oozing. The amount and duration of bleeding vary according to the area bitten, with bleeding from the vagina, rectum, urinary bladder, and pharynx having been reported.[18,25] Faust et al.[24] reported that prolonged hemorrhage might result in anemia and death. The mean duration of bleeding from a leech bite wound was reported as 10 hours in one study (range: 6.5-23). In our patient, the bleeding continued for six hours and persisted intermittently for the next two hours, in spite of application of a compression tampon. However, he did not have any hematological problems. After the leech was removed, the amount of oozing blood was not excessive, so no other method (hemostatic drugs, electrocoagulation, etc.) was needed to stop it completely.

Compression with a tampon was sufficient to control the oozing in this case.

Since a leech attaches strongly with its suckers and has a soft and slippery body surface that ruptures easily, it is difficult to hold and remove a leech with force.[26] If the leech is attached too tightly to the mucosa and resists mechanical removal, then hypertonic sodium chloride solution (more suitable in older children) or cocaine/lidocaine can be applied, which releases the hold of the leech or paralyses it, respectively. Afterwards, it can be removed easily. In our case, we removed the leech mechanically (with clamp and Cilt - Vol. 17 Sayı - No. 1

forceps) after it was paralyzed with lidocaine. Then, flexible rectoscopy was performed to search for other parasites, but no other leeches were found.

In summary, rectal bleeding seems to be an uncommon complication of leech bite that can be managed with simple examination such as by inspection, anoscope or hand evaluation. The case should be considered as an emergency, and all precautions should be taken to avoid more bleeding. To prevent this type of disease, people have to be taught more effectively about the necessity to use clean, safe water, and local and government officials must support health education and facilitate access to safe water. Leech infestation should be kept in mind when faced with intermittent or severe rectal bleeding in patients who recount a recent history of swimming in possibly contaminated waters.

REFERENCES 1. el-Awad ME, Patil K. Haematemesis due to leech infestation.

Ann Trop Paediatr 1990;10:61-2.

2. Uygur K, Yasan H, Yavuz L, Dogru H. Removal of a laryngeal leech: A safe and effective method. Am J Otolaryngol 2003;24:338-40.

3. Eldor A, Orevi M, Rigbi M. The role of the leech in medical therapeutics. Blood Rev 1996;10:201-9.

4. Bilgen C, Karci B, Uluöz U. A nasopharyngeal mass: leech in the nasopharynx. Int J Pediatr Otorhinolaryngol 2002;64:736.

5. Kaygusuz I, Yalçin S, Keleş E. Leeches in the larynx. Eur Arch Otorhinolaryngol 2001;258:455-7.

6. Mohammad Y, Rostum M, Dubaybo BA. Laryngeal hirudiniasis: an unusual cause of airway obstruction and hemoptysis.

Pediatr Pulmonol 2002;33:224-6.

7. Güloğlu C, Al B, Özhasenekler A, Güllü N, Aldemir M. Üst solunum yolu obstrüksiyonu, burun kanaması ve kronik aneminin nadir bir sebebi olarak sülük: iki olguluk deneyimimiz.

Tıp Araştırmaları Dergisi (In Turkish) 2004;2:45-8.

8. García AC, Martín AM, De Luna Gijón CA, Martín Anaya AS, Mondéjar AR. Leech in the epiglottis: an unusual discovery in our times. Am J Otolaryngol 2002;23:91-2.

9. Irish JC, Gullane PJ, Mulholland S, Neligan PC. Medicinal leech in head and neck reconstruction. J Otolaryngol 2000;29:327-32.

10. Labadi MH, Jamal MN. Leeches in the larynx. J Laryngol Otol 1997;111:980-1.

11. White GB. Leeches and leech infestation. In: Cook GC, editor. Manson’s tropical diseases. 20th ed. London: Saunders; 1998. p. 1523-5.

12. Solomon E. Leech-an unusual cause of (laryngo-tracheal) obstruction. Ethiop Med J 1991;29:141-2.

13. Alcelik T, Cekic O, Totan Y. Ocular leech infestation in a child. Am J Ophthalmol 1997;124:110-2.

14. Campbell JR, Hart FL, Purnomo. Nasal leech infestation of man. Trop Geogr Med 1987;39:94-5.

15. Ahmadizadeh A. Leech infestation as a potential cause of hemoptysis in childhood. Arch Otolaryngol Head Neck Surg 2002;128:92.

16. Lepage P, Serufilira A, Bossuyt M. Severe anaemia due to leech in the vagina. Ann Trop Paediatr 1981;1:189-90.

85

Ulus Travma Acil Cerrahi Derg

17. Deka PM, Rajeev TP. Unusual cause of hematuria. Urol Int 2001;66:41-2.

18. Raj SM, Radzi M, Tee MH. Severe rectal bleeding due to leech bite. Am J Gastroenterol 2000;95:1607.

19. al-Hadrani A, Debry C, Faucon F, Fingerhut A. Hoarseness due to leech ingestion. J Laryngol Otol 2000;114:145-6.

20. Cundall DB, Whitehead SM, Hechtel FO. Severe anaemia and death due to the pharyngeal leech Myxobdella africana.

Trans R Soc Trop Med Hyg 1986;80:940-4.

21. Bergua A, Vizmanos F, Monzón FJ, Blasco RM. Unavoidable epistaxis in the nasal infestation of leeches. Acta Otorrinolaringol Esp 1993;44:391-3. [Abstract]

86

22. Ji-Tuan X. Four misdiagnosed cases of visceral bleeding caused by Haemadipha japonica. Southeast Asian J Trop Med Public Health 1997;28:673-4.

23. Adams SL. The emergency management of a medicinal leech bite. Ann Emerg Med 1989;18:316-9.

24. Faust EC, Russel PF, Jurg RC. Craig and Faust’s clinical parasitology. 8th ed. Philadelphia: Lea & Febiger; 1970. p.

563-70.

25. Pandey CK, Sharma R, Baronia A, Agarwal A, Singh N. An unusual cause of respiratory distress: live leech in the larynx.

Anesth Analg 2000;90:1227-8.

26. Litch JA, Bishop RA. Saturated aqueous sodium chloride solution for the removal of leeches. Trop Doct 2000;30:102.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):87-89

Case Report

Olgu Sunumu doi: 10.5505/tjtes.2011.79027

Rupture of heart with all layers after a massive blunt thoracic trauma without any lesion on the bones: a case report Ağır derecede künt göğüs travması sonrası herhangi bir kemik lezyonu olmaksızın kalbin tam kat yırtılması: Olgu sunumu İsmail BİRİNCİOĞLU,1 Nurşen TURAN,1 Muhammet CAN2 Our case is a male student which was dead because of traffic accident as passenger in October, 01, 2007. His heart was found to be lacerated and ruptured horizontally from atrioventricular region through all layer of the wall at autopsy.

There were not any changes of skeletal system. Our case is considered as a rare and interesting case because there was no lesion on the bones, though the case was exposed to so massive trauma that cause rupture of heart from all layers.

Trafik kazası sonucu olay yerinde hayatını kaybeden yolcu, 18 yaşında, erkek, üniversite öğrencisidir. 01.10.2007 tarihinde yapılan otopsisinde kalbin atrio-ventriküler bölgeden yatay olarak tam kat yırtılmış ve kopmuş olduğu saptandı, iskelet sisteminde herhangi bir lezyon yoktu. Bu olgu kalpte tam kat yırtılmaya neden olabilecek derecede ağır bir travmaya maruz kalmasına rağmen hiçbir kemik lezyonu olmaması açısından nadir olgu olarak değerlendirildi.

Key Words: Blunt thoracic trauma; heart laceration.

Anahtar Sözcükler: Künt göğüs travması; kalp laserasyonu.

Thorax trauma is a leading cause of traumatic deaths, accounting for 20-25% of all traumatic deaths in the first 30 years of life.[1,2] Cardiac, lung and big vessel injury may occur in thorax traumas. Lung and cardiac injuries aggravate perfusion and oxygenation of the body and lead to increased morbidity and mortality.[1] Males are more frequently subjected to thorax traumas than females.[1-3]

Autopsy: The autopsy was performed on 10 January 2007.

Fatal cardiac lacerations due to blunt thorax trauma are generally diagnosed at autopsy.[4,5]

CASE REPORT Report of Death Scene and External Physical Examination: The case was 18 years of age and a university student. He was sitting in the passenger side of the vehicle beside the driver who caused the accident.

The victim’s body was found 10 meters away from the vehicle, which was thrown out on 10 January 2007.

The body was sent to the state hospital for external physical examination. Some parts of his body were covered with black motor oil. Except for a few small ecchymoses and lacerations, no lesion or fracture was defined (Fig. 1a, b). No rupture in his t-shirt, athlete or blue jeans was detected.

Department of Forensic Medicine, Karadeniz Technical University Faculty of Medicine, Trabzon; 2Department of Forensic Medicine, Balıkesir University Faculty of Medicine, Balıkesir, Turkey.

1

External Examination: The case was 25 years old, with a height of 182 cm and weight of 80 kg on examination. Rigor mortis had not formed but onset of livor mortis was observed on the patient’s back. One abrasion on the abdomen, 8 abrasions measuring 1 cm on his back, one small abrasion on his right cheek, and motor oil contamination on the face, thorax and arms were reported.

Internal Examination: No macroscopic pathology was seen on his head. Both right and left thoracic cavities were filled with blood. The heart was ruptured from the atrioventricular region horizontally. The ventricular region of the heart was found separated in the thoracic cavity (Fig. 2). The abdominal cavity was also filled with blood. The liver and spleen had multiple small lacerations. No skeletal pathology was determined.

Laboratory Examinations: Blood taken via vessel at autopsy was investigated for alcohol and hypnotic and narcotic drugs. No toxic substance was detected from the blood sample.

1 Karadeniz Teknik Üniversitesi Tıp Fakültesi, Adli Tıp Anabilim Dalı, Trabzon; 2Balıkesir Üniversitesi Tıp Fakültesi Adli Tıp Anabilim Dalı, Balıkesir.

Correspondence (İletişim): İsmail Birincioğlu, M.D. Karadeniz Teknik Üniversitesi Tıp Fakültesi Adli Tıp Anabilim Dalı, 61080 Trabzon, Turkey.

Tel: +90 - 462 - 377 55 08 e-mail (e-posta): ismbir@yahoo.com

87

Ulus Travma Acil Cerrahi Derg

(a)

(b)

Fig. 1. (a) Frontal view of the victimâ&#x20AC;&#x2122;s body. (b) Posterior view of the victimâ&#x20AC;&#x2122;s body.

cases may be as high as 85%.[14] Cardiac rupture incidence resulting from blunt thoracic trauma is lower in children (0-43%) than in adults (16-76%).[15] Cardiac contusion due to blunt thorax trauma is more frequent in children compared to adults. Because the right ventricle wall is thinner than the left, right ventricle injury is more frequent.[10] Aorta rupture incidence is 13-16% in traffic accidents, and mortality rate in these cases is 70-85%.[16] Result of Report: The cause of death was determined to be due to organ laceration and internal hemorrhage due to general body trauma.

DISCUSSION In recent years, thoracic trauma cases have increased in conjunction with the increase in the incidences of violence and traffic and occupational accidents.[6] It has been noted that rib and sternum fractures occurring during cardiopulmonary resuscitation may cause cardiac and lung lacerations, and rarely, cardiac rupture and liver laceration.[7] After blunt thoracic trauma, the trachea and bronchus are rarely injured.

Penetrative injuries result in organ laceration in many cases.[8] The incidence of cardiac laceration in patients with blunt thoracic trauma has been reported in various studies as 2%,[9] more than 7%,[10,11] and more than 15%.[12,13] Cardiac rupture because of one blunt thoracic trauma is very rare. Thoracic traumas causing cardiac laceration have more than one bone fracture (e.g. costae and sternum fractures).[5,10] This type of injury has a wide range of clinical expression, from no clinical finding to serious life-threatening findings like arrhythmia, conduction anomalies, congestive heart failure, cardiogenic shock, hemo-pericardium, pericardial tamponade, valvular rupture, intraventricular thrombus, thromboemboli, air emboli, coronary artery occlusion, ventricular aneurysm, and constructive pericarditis.[12,13] Blunt thoracic traumas causing cardiac rupture have a high mortality rate. It has been shown in some studies that the mortality rate in these 88

Cardiac injury frequently occurs in traffic, sportive and occupational accidents and due to intentional trauma. Recently, blunt cardiac injuries have mostly resulted from traffic accidents.[3,10-12,17] Cardiac injuries have been found to occur more frequently with penetrative injury than with blunt injury.[12] A few cases of simultaneous rupture of mitral and tricuspid valves caused by blunt chest trauma have been reported. Papillary muscle rupture is the most common cause of traumatic mitral regurgitation, fol-

Fig. 2. Cardiac rupture from all layers of the wall.

Ocak - January 2011

Rupture of heart with all layers after a massive blunt thoracic trauma without any lesion on the bones

lowed by rupture of the chordae tendineae and leaflet tears. In traumatic injury of the tricuspid valve, chordal rupture occurs most frequently, followed by anterior papillary muscle rupture and leaflet tears. Papillary muscle rupture has been purported to occur due to ventricular compression between the sternum and the spine during the period of isovolumic contraction when the cardiac valves are closed.[18] Depending on the mechanism and severity of the trauma, the cardiac injury ranges from a mild contusion to rupture of the cardiac wall. Though rupture of the heart is rare, it is the commonest form of deadly cardiac injury from blunt trauma. Interestingly, the cardiac ruptures are usually discovered at autopsy.

The mechanisms of cardiac injury in blunt trauma may be summarized as 1) direct blow to the anterior chest (most common cause of ventricular rupture); 2) indirect injury that causes a sudden increase in preload, resulting in atrial rupture; 3) compression of the heart between the sternum and vertebral bodies; 4) acceleration/deceleration of the heart and great vessels; 5) blast injury, and 6) penetrating injury of a cardiac chamber by a fractured rib or the sternum. The heart may be ruptured by compression or from a blow or a fall, usually on its right side and towards its base.[5] In conclusion, contusions or lacerations of the heart may also be produced by blows from a blunt weapon or by compression of the chest, even without fracturing any bone of the thorax and without visible marks of external injury. Therefore, there is always a possibility of fatal cardiac injuries going unnoticed and leading to a fatal outcome.

REFERENCES 1. Altunkaya A, Aktunc E, Kutluk AC, Buyukates M, Demircan N, Demir AS, et al. Evaluation of 282 cases with thoracic trauma. Türk Göğüs Kalp Damar Cer Derg 2007;15:127-32.

2. Vougiouklakis T, Peschos D, Doulis A, Batistatou A, Mitselou A, Agnantis NJ. Sudden death from contusion of the right atrium after blunt chest trauma: case report. Int J Care Injured 2005;36:213-7.

Cilt - Vol. 17 Sayı - No. 1

3. Harel Y, Szeinberg A, Scott WA, Frand M, Vered Z, Smolinski A, et al. Ruptured interventricular septum after blunt chest trauma: ultrasonographic diagnosis. Pediatr Cardiol 1995;16:127-30.

4. Savolainen HO, Järvinen AA, Vihtonen KM. Left atrial rupture following blunt thoracic injury. Case report. Scand J Thorac Cardiovasc Surg 1991;25:231-4.

5. Meera TH, Nabachandra H. A postmortem study of blunt cardiac injuries. JIAFM 2005;27:82-4.

6. Cobanoglu U. Thoracic trauma: analysis of 110 cases. Toraks Dergisi 2006;7:162-9.

7. Boz B, Erdur B, Acar K, Ergin A, Turkcuer I, Ergin N. Incidence of thoracic cage injury due to cardiopulmonary resuscitation: forensic autopsy results. Ulusal Travma Acil Cerrahi Derg 2008;14:216-20.

8. Helmy N, Platz A, Stocker R, Trentz O. Bronchus rupture in multiply injured patients with blunt chest trauma. Eur J Trauma 2002;1:31-4.

9. De Amicis V, Rossi M, Monaco M, Di Lello F. Right luxation of the heart after pericardial rupture caused by blunt trauma.

Tex Heart Inst J 2003;30:140-2.

10. Darok M, Beham-Schmid C, Gatternig R, Roll P. Sudden death from myocardial contusion following an isolated blunt force trauma to the chest. Int J Legal Med 2001;115:85-9.

11. Gölbaşi I, Türkay C, Sahin N, Erdoğan A, Gülmez H, Erbasan O, et al. Heart wounds. Ulus Travma Derg 2001;7:167-71.

12 Cobanoglu U. Investigation of cardiac changes of 70 cases with thoracic trauma. Toraks Dergisi 2007;8:59-68.

13. Markovchick V, Wolfe R. Cardiovascular trauma. In: Morris PJ, Wood WC, editors. Oxford textbook of surgery. 2nd ed.

London: Oxford University Pres.; 2001. p. 527-45.

14. Colline EMB, Rodriguez A, Turney SZ, Dunham CM, Cowley RA. Blunt traumatic cardiac rupture: a 5-year experience.

Ann Surg 1990;701-4.

15. Baum VC. Cardiac trauma in children. Paediatr Anaesth 2002;12:110-7.

16. von Oppell UO, Thierfelder CF, Beningfield SJ, Brink JG, Odell JA. Traumatic rupture of the descending thoracic aorta.

S Afr Med J 1991;79:595-8.

17. Bruschi G, Agati S, Iorio F, Vitali E. Papillary muscle rupture and pericardial injuries after blunt chest trauma. Eur J Cardiothorac Surg 2001;20:200-2.

18. Choi JS, Kim EJ. Simultaneous rupture of the mitral and tricuspid valves with left ventricular rupture caused by blunt trauma. Ann Thorac Surg 2008;86:1371-3.

89

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):90-92

Case Report

Olgu Sunumu doi: 10.5505/tjtes.2011.51196

Gastric perforation caused by Strongyloides stercoralis: a case report Strongyloides stercoralis kaynaklı mide perforasyonu: Olgu sunumu Gürkan ÖZTÜRK,1 Bülent AYDINLI,1 Fehmi ÇELEBİ,1 Nesrin GÜRSAN2 Strongyloidiasis is a parasitosis caused by the female nematode of the Strongyloides stercoralis. S. stercoralis causes a chronic infection that is asymptomatic in 50% of chronically infected patients, and it can also affect the stomach.

Gastric involvement causes symptoms mostly mimicking gastritis. We report herein a case of gastric perforation in a 37-year-old woman, which was thought to be caused by S. stercoralis.

Stronglodiasis, Strongyloides stercoralis’in dişi nematodları tarafından oluşturulan bir parazitozdur. S. stercoralis olguların %50’sinde asemptomatik olan ve mideyi etkileyebilen kronik bir enfeksiyon oluşturur. Mide tutulumu genelde gastriti taklit eden bulgulara neden olur. Biz burada 37 yaşındaki kadın hastada S. stercoralis’e bağlı oluştuğunu düşündüğümüz bir mide delinmesi olgusunu sunuyoruz.

Key Words: Strongyloides stercoralis; gastric involvement; perforation.

Anahtar Sözcükler: Strongyloides stercoralis; mide tutulumu; delinme.

Strongyloidiasis is a parasitosis caused by the female nematode of the Strongyloides stercoralis. It is mainly a dermatologic and gastrointestinal disease.[1-5] We report herein a case of gastric perforation caused

by S. stercoralis.

vels and free air under the right hemi-diaphragm (Fig. 1). Ultrasound examination revealed mild to moderate free intraperitoneal fluid and dilated intestinal loops. The patient underwent emergent laparotomy with the preoperative diagnosis of gastrointestinal perforation. During the exploration, a 0.5 cm perforation was found on the posterior wall of the gastric corpus, at the base of a 2 cm in diameter gastric ulcer. The ulcer was excised with a 0.5 cm margin and sent for frozen section. The result of the frozen section was tumor negative. The defect at the posterior wall was then closed primarily.

CASE REPORT A 37-year-old otherwise healthy woman from a rural area admitted to the emergency room with an acute abdominal pain. Her history revealed that she had experienced epigastric pain, heartburn, nausea, vomiting, and abdominal discomfort for the last five months and had received treatment for suspected gastritis. The abdominal pain had become more intense in the last 12 hours and gained in severity hourly. It was initially epigastric but hours later became diffuse and spread to the entire abdomen. She also had vomiting and nausea. On the physical examination, she had fever (38.5°C), diffuse tenderness on the entire abdomen, rebound tenderness, and strong muscular defense. Leukocyte count was 15000/mm3 with lymphocyte predominance and eosinophilia. Plain abdominal radiographs revealed dilated intestinal loops with air-fluid leDepartments of 1General Surgery, 2Pathology, Atatürk University Faculty of Medicine, Erzurum, Turkey.

The postoperative period was uneventful. Pathological examination of the excised ulcer revealed inflammatory changes and adult form of S. stercoralis at the site of perforation (Figs. 2, 3). The patient was consulted with the Department of Infectious Diseases and was evaluated for any immunodeficiency. The immunologic status of the patient was normal. Albendazole treatment at a dose of 10 mg/kg was recommended.

The patient was discharged on the 10th day. She refused to take any further medication for the treatment of the disease or to present during the follow-up period.

Atatürk Üniversitesi Tıp Fakültesi, 1Genel Cerrahi Anabilim Dalı, 2 Patoloji Anabilim Dalı, Erzurum.

Correspondence (İletişim): Gürkan Öztürk, M.D. Atatürk Üniversitesi Tıp Fakültesi Aziziye Araştırma Hastanesi Genel Cerrahi S Blok, Eruzurm, Turkey.

Tel: +90 - 442 - 316 63 33 / 2255 e-mail (e-posta): gurkanoztrk@yahoo.com

90

S. stercoralis-caused gastric perforation

rogenic or disease-related immune deficiency causes hyperinfection and disseminated strongyloidiasis.[2-6,8] It is reported that gastrointestinal involvement is commonly seen in patients with immunodeficiency, but Thompson et al.[7] reported two cases that were immunocompetent.[1,7,9] We investigated the immunological status of our patient, after the pathologic examination revealed S. stercoralis, and found that she was not immunocompromised. Further analyses for possible human immunodeficiency virus (HIV) infection were also negative.

Fig. 1. Plain radiograph of the patient revealing bilateral subdiaphragmatic free air.

It is reported that S. stercoralis can affect the stomach.[1,2,7,9-11] Clinically, gastric involvement causes symptoms such as epigastric pain and tenderness, nausea and vomiting.[1,3,6,7] All these also existed in the history of our patient. She received medical treatment for a suspected gastritis. The common feature of gastric mucosal injury is destruction of the mucosa, but gastric perforation was not reported previously, although the pathologic route of disseminated disease is invasion and ulceration of the wall.[6]

S. stercoralis causes a chronic infection, which is asymptomatic in 50% of chronically infected patients.

[2,6] This chronic state of the infection is caused by the autoinfection cycle of the parasite. This state can be accelerated with deficiency in the immune system. Iat-

The diagnosis of this disease is commonly made on the basis of suspicion because the signs and symptoms are quite non-specific. Examination of a single stool sample will detect rhabdoid larvae 25% of the time.

The sensitivity of the stool test can be elevated to 85% by using several tests.[3] However, some other authors suggest that the diagnostic yield is not higher than 46%, even after three stool examinations.[7] We, however, performed only a single stool test and this was negative. Enzyme-linked immunosorbent assay could also be used for the diagnosis of strongyloidiasis with a sensitivity ranging from 68% to 95%.[3,7] Endoscopic assessment and pathological examination, however, are very important. Reported endoscopic features for gastritis strongyloidiasis are small ulcerations and antral erythema and edema of the antrum, pylorus and duodenum.[1,7] S. stercoralis (filariform larvae) is fo-

Fig. 2. Gastric biopsy revealed a moderate inflammatory infiltrate in the gastric mucosa.

Fig. 3. Numerous filariform larvae consistent with Strongyloides stercoralis.

DISCUSSION S. stercoralis is a helminth that infects the small intestine of humans, particularly the duodenum and the upper jejunum.[1,6,7] It is widely distributed throughout tropical and subtropical regions of the world. Risk groups for acquiring the infection include residents and travelers to Southern, Eastern and Central Europe, Latin America, sub-Saharan Africa, and the Caribbean islands.[3,5-8] Our patient was not from these regions and had not traveled outside the East Anatolian region of Turkey.

Cilt - Vol. 17 Say覺 - No. 1

91

Ulus Travma Acil Cerrahi Derg

und on microscopic examination of gastric specimens and causes inflammatory infiltration of the mucosa, mimicking gastric mucosal inflammation, ulceration and hypertrophic pyloric stenosis.[1,7,9] These findings were also observed in our patient.

Treatment of S. stercoralis consists of orally administered ivermectin, thiabendazole and albendazole[3,7,9] treatments. We could not determine the effectiveness of the medical treatment because the patient refused to take any further oral treatment.

In summary, it is important to recognize that disseminated strongyloidiasis is most commonly seen in immunocompromised patients, but this case is an exception because it presented as a perforation in a patient who was not immunocompromised or living in an endemic area.

REFERENCES 1. Meine GC, Dietz J, Rocha M, Mattos T, de Souza AR, Conteletti FR. Atypical gastric presentation of strongyloidiasis in HIV-infected patient-case report. Dig Liver Dis 2004;36:7602.

2. Tzanetou K, Tsiodra P, Delis V, Frangia K, Karakatsani E, Efstratopoulos A, et al. Coinfection of Schistosoma mansoni and Strongyloides stercoralis in a patient with variceal bleeding. Infection 2005;33:292-4.

3. Concha R, Harrington W Jr, Rogers AI. Intestinal strongy-

92

loidiasis: recognition, management, and determinants of outcome. J Clin Gastroenterol 2005;39:203-11.

4. Isotalo PA, Toye B, Eidus L. Human T-lymphotropic virus 1 adult T-cell lymphoma with Giardia and Strongyloides parasitism. Arch Pathol Lab Med 2000;124:1241.

5. Satoh M, Futami A, Takahira K, Kodaira M, Tanaka T, Kuriki K, et al. Severe strongyloidiasis complicated by meningitis and hydrocephalus in an HTLV-1 carrier with increased proviral load. J Infect Chemother 2003;9:355-7.

6. Daubenton JD, Buys HA, Hartley PS. Disseminated strongyloidiasis in a child with lymphoblastic lymphoma. J Pediatr Hematol Oncol 1998;20:260-3.

7. Thompson BF, Fry LC, Wells CD, Olmos M, Lee DH, Lazenby AJ, et al. The spectrum of GI strongyloidiasis: an endoscopic-pathologic study. Gastrointest Endosc 2004;59:90610.

8. Chieffi PP, Chiattone CS, Feltrim EN, Alves RC, Paschoalotti MA. Coinfection by Strongyloides stercoralis in blood donors infected with human T-cell leukemia/lymphoma virus type 1 in S達o Paulo City, Brazil. Mem Inst Oswaldo Cruz 2000;95:711-2.

9. Lambertucci JR, Le達o FC, Barbosa AJ. Gastric strongyloidiasis and infection by the human T cell lymphotropic virus type 1 (HTLV-1). Rev Soc Bras Med Trop 2003;36:541-2.

10. Dees A, Batenburg PL, Umar HM, Menon RS, Verweij J. Strongyloides stercoralis associated with a bleeding gastric ulcer. Gut 1990;31:1414-5.

11. Wurtz R, Mirot M, Fronda G, Peters C, Kocka F. Short report: gastric infection by Strongyloides stercoralis. Am J Trop Med Hyg 1994;51:339-40.

Ocak - January 2011

Turkish Journal of Trauma & Emergency Surgery

Ulus Travma Acil Cerrahi Derg 2011;17 (1):93-95

Case Report

Olgu Sunumu doi: 10.5505/tjtes.2011.69783

Pneumomediastinum and subcutaneous emphysema caused by sigmoid diverticulum perforation secondary to blunt abdominal trauma: report of a case Künt batın travmasına sekonder gelişen sigmoid divertikül perforasyonu nedeniyle oluşan pnömomediastinum ve subkutanöz amfizem: Olgu sunumu Necdet Fatih YAŞAR,1 Mahmut KEBAPÇI,2 Enver İHTİYAR1 Pneumomediastinum and subcutaneous emphysema are very rare reported signs of colonic perforation most often associated with diverticulitis, toxic megacolon and colonoscopy. We report a case of a 60-year-old man with subcutaneous emphysema and pneumomediastinum, which developed three days after a car accident without pneumothorax. A computed tomography scan demonstrated perforation of a sigmoid diverticulum in conjunction with air. A laparotomy was performed and revealed a perforated sigmoid diverticulum, fistulized into the retroperitoneal cavity. We suspect that this diverticular perforation was caused by the deterioration of the sigmoid mesocolon secondary to the blunt abdominal trauma. To our knowledge, this is the first report in the literature about pneumomediastinum and subcutaneous emphysema caused by sigmoid diverticular rupture following mesosigmoid trauma.

Pnömomediastinum ve subkutanöz amfizem divertikülit, toksik megakolon ve kolonoskopi sonrası görülebilen kolon perforasyonunun çok nadir bir komplikasyonu olarak meydana gelebilir. Burada, geçirdiği trafik kazasından sonra ilk muayenesinde yokken, 3 gün sonra pnömotoraks olmaksızın pnömomediastinum ve subkutanöz amfizem gelişen 60 yaşında erkek hasta sunuldu. Çekilen bilgisayarlı tomografide sigmoid divertikül perforasyonu ile devamlılık gösteren serbest hava gözlendi. Laparotomide retroperitoneal kaviteye fistülize olmuş perfore sigmoid divertikülü saptandı. Bu divertiküler perforasyonun künt karın travmasına sekonder gelişen sigmoid mezokolon yaralanmasından kaynaklandığını düşünmekteyiz. Tüm literatür taramamızda mezosigmoid travması sonrası sigmoid divertikül perforasyonu nedeniyle ortaya çıkmış pnömomediastinum ve subkutanöz amfizem olgusuna rastlayamadık. Bu nedenle bu olgu bu konuda literatürdeki ilk olacaktır.

Key Words: Perforation; pneumomediastinum; sigmoid diverticulum; trauma.

Anahtar Sözcükler: Perforasyon; pnömomediastinum; sigmoid divertikülü; travma.

Pneumomediastinum and subcutaneous emphysema are uncommon clinical entities that occur when air leaks from the lungs or any of the luminal organs, such as the bronchial tube, larynx, trachea, esophagus, and very rarely, the colon, with subsequent dissection into the mediastinum. The continuum of fascial planes connecting cervical soft tissues with the mediastinum and retroperitoneum permits this dissection.[1] We describe herein a patient presenting with subcutaneous emphysema and pneumomediastinum caused by sigmoid diverticulum perforation three days after a blunt abdominal trauma.

CASE REPORT A 60-year-old man presented to the Emergency Department with severe pain in his left groin and left forearm after a car accident. On admission, his blood pressure was 110/70 mmHg with a regular heart rate of 80/min. The initial clinical evaluation revealed a deformity on the left forearm and tenderness to palpation of the left groin accompanied by restricted motion of the left hip. He had minimal abdominal tenderness on palpation and no signs of respiratory distress. His vital signs and hemoglobin level remained stable during the follow-up in the Emergency Department. Fractures of

Departments of 1General Surgery, 2Radiology, Eskisehir Osmangazi University, Faculty of Medicine, Eskişehir, Turkey.

Eskişehir Osmangazi Üniversitesi Tıp Fakültesi, 1Genel Cerrahi Anabilim Dalı, 2Radyoloji Anabilim Dalı, Eskişehir.

Correspondence (İletişim): Necdet Fatih Yaşar, M.D. Eskişehir Osmangazi Üniversitesi, Tıp Fakültesi, Genel Cerrahi Anabilim Dalı, Meşelik Kampüsü 26480 Eskişehir, Turkey.

Tel: +90 - 222 - 239 29 79 / 2600 e-mail (e-posta): fatih_yasar@yahoo.com

93

Ulus Travma Acil Cerrahi Derg

(a)

(b)

Fig. 1. (a) (axial) and (b) (coronal). The first tomography after the trauma: mesenteric fibrofatty changes in the sigmoid mesocolon and multiple sigmoid diverticula are observed.

the left acetabulum and fracture of both bones of the left forearm were documented on the radiography. Bilateral anterior fractures of the 8th rib, which involved the costochondral junction, and bilateral minimal pleural effusions were identified by a thoracic tomographic scan. Neither pneumothorax nor pneumomediastinum was observed. An abdominal tomographic scan revealed mesenteric and mural thickening of the sigmoid colon, multiple sigmoid diverticula (Fig. 1a, b) and minimal perihepatic and perisplenic fluid collection. After traction was applied to the left leg and the left arm was immobilized in a cast, the patient was transferred to the Department of Orthopedics. On the third day of the hospitalization, subcutaneous emphysema developed in the right upper quadrant of the abdomen and disseminated up to the level of the 7th rib on the right side and down to the scrotum within 10 hours. He had no abdominal tenderness on palpation but he became febrile and confused. The initial total leukocyte count of 17300/mmÂł on admission was increased to 19600/mmÂł. A new chest radiograph showed a left-sided pneumomediastinum without pneumothorax. A second thoracoabdominopelvic computed to(a)

mography scan revealed extraperitoneal free air in the mediastinum, retroperitoneal space and subcutaneous tissue. In addition to these findings, perforation of a sigmoid diverticulum was identified (Fig. 2a, b). During the tomography scan, contrast medium was applied orally to visualize any possible perforation site of the esophagus. Images of lower parts of the pelvis were also taken to examine the rectum. No other possible cause of the extraperitoneal air except the diverticular perforation was found. After the tomography, laparotomy was performed. The abdominal exploration revealed that the sigmoid mesocolon and sigmoid colon were edematous and fragile, possibly due to the trauma. The sigmoid diverticulum perforation was confirmed, forming an abscess that was fistulized into the retroperitoneal space without any leakage into the peritoneum. After aspirating the pus and irrigating the area with saline, the necrotic tissue around the abscess was debrided and Hartmannâ&#x20AC;&#x2122;s procedure was performed. On the 5th postoperative day, he was able to be extubated and enteral feeding was begun. In spite of medical management and noninvasive respiratory support, respiratory distress syndrome developed two (b)

Fig. 2. (a) (Axial) and (b) (coronal): The second computed tomography on the 3rd day of the hospitalization,: free air in the retroperitoneal space and subcutaneous tissue with perforation of a sigmoid diverticulum are identified.

94

Ocak - January 2011

Pneumomediastinum and subcutaneous emphysema

weeks after the extubation and the patient was reintubated and died on the 24th postoperative day.

sigmoid diverticulum perforation secondary to blunt abdominal trauma.

DISCUSSION Pneumomediastinum and subcutaneous emphysema may be observed after intrathoracic pressure changes, leading to alveolar rupture and dissection of air along the tracheobronchial tree due to emesis or asthma flare-ups and sometimes spontaneously without any specific reason.[2,3] Emesis may also cause esophageal rupture, which may lead to pneumomediastinum and subcutaneous emphysema.[4] Aspiration of a foreign body is also described in the possible etiology by puncturing the airway or by increasing the pressure.[5] Our patient did not have any of these in his history. Blunt chest trauma may also be a cause of pneumomediastinum by tearing the tracheobronchial and esophageal structures.[6-8] Pneumothorax usually accompanies these findings depending on the type of the injury. In our case, pneumothorax was not observed in the early and late radiography and computed tomography scan. The tracheobronchial tree was intact and no contrast medium leakage from the esophagus was observed on the tomography scan. Pneumomediastinum and subcutaneous emphysema are also very rare signs of colonic perforation, which is usually secondary to diverticulitis,[9,10] toxic megacolon in ulcerative colitis,[11] colonoscopy,[12] endoscopic polypectomy,[13] and very rarely, spontaneously.[14] In our case, it was thought that the pneumomediastinum, pneumoretroperitoneum and subcutaneous emphysema were due to the perforation of a sigmoid diverticulum, which was documented by both tomography scans and abdominal exploration. However, it is interesting that in the first tomography images, there was no sign of perforation but multiple sigmoid diverticula and mesenteric and mural thickening of the sigmoid colon secondary to the injury. The second tomography identified the diverticulum perforation on the third day of his hospitalization. During the laparotomy, we noticed that the sigmoid colon and mesocolon were edematous and fragile, walled off by an abscess that was fistulized into the retroperitoneal space. We concluded that this diverticulum perforation resulted in subcutaneous emphysema and pneumomediastinum. To our knowledge, this is the first report in the literature about pneumomediastinum and subcutaneous emphysema caused by

1. Maunder RJ, Pierson DJ, Hudson LD. Subcutaneous and mediastinal emphysema. Pathophysiology, diagnosis, and management. Arch Intern Med 1984;144:1447-53.

2. Caceres M, Ali SZ, Braud R, Weiman D, Garrett HE Jr. Spontaneous pneumomediastinum: a comparative study and review of the literature. Ann Thorac Surg 2008;86:962-6.

3. Macia I, Moya J, Ramos R, Morera R, Escobar I, Saumench J, Spontaneous pneumomediastinum: 41 cases. Eur J Cardiothorac Surg 2007;31:1110-4.

4. Forshaw MJ, Khan AZ, Strauss DC, Botha AJ, Mason RC. Vomiting-induced pneumomediastinum and subcutaneous emphysema does not always indicate Boerhaave’s syndrome: report of six cases. Surg Today 2007;37:888-92.

5. Ramadan HH, Bu-Saba N, Baraka A, Mroueh S. Management of an unusual presentation of foreign body aspiration. J Laryngol Otol 1992;106:751-2.

6. Nugteren P, Paul MA, Plötz FB. Rupture of the right main bronchus: a case of a 4-year-old girl. Eur J Emerg Med 2007;14:97-9.

7. Martel G, Al-Sabti H, Mulder DS, Sirois C, Evans DC. Acute tracheoesophageal burst injury after blunt chest trauma: case report and review of the literature. J Trauma 2007;62:236-42.

8. Okutani D, Aoe M, Yamane M, Hatoh S, Toyooka S, Sano Y, et al. Extensive traumatic pneumomediastinum. without injuries of organs in the thorax: report of a case. Kyobu Geka 2007;60:942-5. [Abstract] 9. Besic N, Zgajnar J, Kocijancic I. Pneumomediastinum, pneumopericardium, and pneumoperitoneum caused by peridiverticulitis of the colon: report of a case. Dis Colon Rectum 2004;47:766-8.

10. Soliani G, Dominici M, Bergossi L, Basaglia E, Pauli S, Carcoforo P. Acute colon diverticulitis in multiple myeloma patient: an unusual presentation of a colonic perforation. Case report. Ann Ital Chir 2002;73:643-6.

11. Mogan GR, Sachar DB, Bauer J, Salky B, Janowitz HD. Toxic megacolon in ulcerative colitis complicated by pneumomediastinum: report of two cases. Gastroenterology 1980;79:559-62.

12. Goerg KJ, Düber C. Retroperitoneal, mediastinal and subcutaneous emphysema with pneumothorax after colonoscopy.

Dtsch Med Wochenschr 1996;121:693-6. [Abstract] 13. Ho HC, Burchell S, Morris P, Yu M. Colon perforation, bilateral pneumothoraces, pneumopericardium, pneumomediastinum, and subcutaneous emphysema complicating endoscopic polypectomy: anatomic and management considerations.

Am Surg 1996;62:770-4.

14. Prêtre R, Rohner A. Pneumomediastinum and subcutaneous cervical emphysema as signs of rectosigmoid perforation.

Gastroenterol Clin Biol 1992;16:460-2. [Abstract]

Cilt - Vol. 17 Sayı - No. 1

REFERENCES

95

Ulus Travma Acil Cerrahi Derg

TRAVMA VE ACİL CERRAHİ BİLİMSEL TAKVİM YURTİÇİ TOPLANTILAR 4. Uludağ Üniversitesi Genel Cerrahide Güncel Yaklaşımlar Toplantısı......... 17 - 20 Mart 2011

Grand Yazıcı Otel - Uludağ 10. Hepato Pankreato Bilier Cerrahi Kongresi.................................................. 7 - 9 Nisan 2011

Antalya 10. Ulusal Endoskopik-Laparoskopik Cerrahi Kongresi.................................. 27 Nisan 2011

Antalya 8. Ulusal Travma ve Acil Cerrahi Kongresi........................................................ 14 - 18 Eylül 2011

Mardan Palace - Antalya

YURTDIŞI TOPLANTILAR 3rd National Conference: Emergency Medicine 2011........... ........................... 14 Ocak 2011

Londra, İngiltere 12th European Congress of Trauma & Emergency Surgery ........................... 27 - 30 Nisan 2011

Milano, İtalya ASGBI 2011 International Surgical Congress .................................................. 11 - 13 Mayıs 2011

Bournemouth, İngiltere European Burns Association Congress 2011.................................................... 14 - 17 Eylül 2011

Hague, Hollanda 13th European Congress of Trauma & Emergency Surgery ........................... 12 - 15 Mayıs 2012

Basel, İsviçre

96

Ocak - January 2011