Cilt - Volume 17
Say› - Number 6
www.tjtes.org
Kas›m - November 2011
Cilt - Volume 17
Sayı - Number 6
Kasım - November 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 Yılmaz Akgün Levhi Akın Alper Akınoğlu Mehmet Ali Akkuş Murat Aksoy Şeref Aktaş Ali Akyüz Ömer Alabaz Cem Alhan Nevzat Alkan Edit Altınlı Acar Aren Cumhur Arıcı Oktar Asoğlu Mehmet Aşık Ali Atan Bülent Atilla Levent Avtan Yunus Aydın Erşan Aygün Mois Bahar Akın Eraslan Balcı Emre Balık Umut Barbaros Semih Baskan M Murad Başar Mehmet Bayramiçli Ahmet Bekar Orhan Bilge Mustafa Bozbuğa Başar Cander Nuh Zafer Cantürk Münacettin Ceviz Banu Coşar Figen Coşkun İrfan Coşkun Nahit Çakar Adnan Çalık Fehmi Çelebi Gürhan Çelik Oğuz Çetinkale M. Ercan Çetinus Sebahattin Çobanoğlu Ahmet Çoker Cemil Dalay Fatih Dikici Yalım Dikmen Osman Nuri Dilek Levent Döşemeci Murat Servan Döşoğlu Kemal Durak Koray Dural Engin Dursun Mehmet Eliçevik İmdat Elmas Ufuk Emekli
İstanbul Çanakkale İstanbul Adana Ankara İstanbul İstanbul İstanbul Adana İstanbul İstanbul İstanbul İstanbul Antalya İstanbul İstanbul Ankara Ankara İstanbul İstanbul İstanbul İstanbul Elazığ İstanbul İstanbul Ankara Kırıkkale İstanbul Bursa İstanbul Edirne Konya Kocaeli Erzurum İstanbul Ankara Edirne İstanbul Trabzon Erzurum İstanbul İstanbul İstanbul Edirne İzmir Adana İstanbul İstanbul Sakarya Antalya Düzce Bursa Ankara Ankara İstanbul İstanbul İstanbul
Haluk Emir Yeşim Erbil Şevval Eren Hayri Erkol Metin Ertem Mehmet Eryılmaz Figen Esen Tarık Esen İrfan Esenkaya Ozlem Evren Kemer Nurperi Gazioğlu Fatih Ata Genç Alper Gökçe Niyazi Görmüş Feryal Gün Ömer Günal Nurullah Günay Haldun Gündoğdu Mahir Günşen Emin Gürleyik Hakan Güven Tufan Hiçdönmez Gökhan İçöz İbrahim İkizceli Murat İmer Haluk İnce Fuat İpekçi Ferda Şöhret Kahveci Selin Kapan Murat Kara Hasan Eşref Karabulut Ekrem Kaya Mehmet Yaşar Kaynar Mete Nur Kesim Yusuf Alper Kılıç Hakan Kınık Talat Kırış Haluk Kiper Hikmet Koçak M Hakan Korkmaz Güniz Meyancı Köksal Cüneyt Köksoy İsmail Kuran Necmi Kurt Mehmet Kurtoğlu Nezihi Küçükarslan İsmail Mihmanlı Mehmet Mihmanlı Köksal Öner Durkaya Ören Hüseyin Öz Hüseyin Özbey Faruk Özcan Perihan Ergin Özcan Akın Özden Cemal Özçelik İlgin Özden
İstanbul İstanbul Diyarbakır Bolu İstanbul Ankara İstanbul İstanbul Malatya Ankara İstanbul İstanbul Tekirdağ Konya İstanbul Düzce Kayseri Ankara Adana Bolu İstanbul Edirne İzmir İstanbul İstanbul İstanbul İzmir Bursa İstanbul Ankara İstanbul Bursa İstanbul Samsun Ankara Ankara İstanbul Eskişehir Erzurum Ankara İstanbul Ankara İstanbul İstanbul İstanbul Ankara İstanbul Sakarya İstanbul Erzurum İstanbul İstanbul İstanbul İstanbul Denizli Diyarbakır İstanbul
Mehmet Özdoğan Şükrü Özer Halil Özgüç Ahmet Özkara Mahir Özmen Vahit Özmen Volkan Öztuna Niyazi Özüçelik Süleyman Özyalçın Emine Özyuvacı Salih Pekmezci İzzet Rozanes Kazım Sarı Ali Savaş İskender Sayek Tülay Özkan Seyhan Gürsel Remzi Soybir Yunus Söylet Erdoğan Sözüer Mustafa Şahin Cüneyt Şar Mert Şentürk Feridun Şirin İbrahim Taçyıldız Gül Köknel Talu Ertan Tatlıcıoğlu Gonca Tekant Cihangir Tetik Bülent Tırnaksız Mustafa Tireli Alper Toker Rıfat Tokyay Salih Topçu Turgut Tufan Fatih Tunca Akif Turna Zafer Nahit Utkan Ali Uzunköy Erol Erden Ünlüer Özgür Yağmur Müslime Yalaz Serhat Yalçın Sümer Yamaner Mustafa Yandı Nihat Yavuz Muharrem Yazıcı Cumhur Yeğen Ebru Yeşildağ 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 İstanbul Ankara Ankara İstanbul Tekirdağ İstanbul Kayseri Tokat İstanbul İstanbul İstanbul Diyarbakır İstanbul Ankara İstanbul İstanbul Ankara Manisa İstanbul İstanbul Kocaeli Ankara İstanbul İstanbul Kocaeli Urfa Balıkesir Adana İstanbul İstanbul İstanbul Trabzon İstanbul Ankara İstanbul Tekirdağ İstanbul Gaziantep İstanbul Malatya Ankara İstanbul İstanbul
ULUSLARARASI BİLİMSEL DANIŞMA KURULU INTERNATIONAL EDITORIAL BOARD
Juan Asensio Zsolt Balogh Ken Boffard Fausto Catena Howard Champion Elias Degiannis Demetrios Demetriades Timothy Fabian Rafi Gürünlüoğlu Clem W. Imrie Kenji Inaba Rao Ivatury Yoram Kluger Rifat Latifi Sten Lennquist Ari Leppaniemi Valerie Malka Ingo Marzi Kenneth L. Mattox Carlos Mesquita
Miami, USA New Castle, Australia Johannesburg, S. Africa Bologna, Italy Washington DC, USA Johannesburg, S. Africa Los Angeles, USA Memphis, USA Denver, USA Glasgow, Scotland Los Angeles, USA Richmond, USA Haifa, Israel Tucson, USA Malmö, Sweden Helsinki, Finland Sydney, Australia Frankfurt, Germany Houston, USA Coimbra, Portugal
Ernest E Moore Pradeep Navsaria Andrew Nicol Hans J Oestern Andrew Peitzman Basil A Pruitt Peter Rhee Pol Rommens William Schwabb Michael Stein Spiros Stergiopoulos Michael Sugrue Otmar Trentz Donald Trunkey Fernando Turegano Selman Uranues Vilmos Vecsei George Velmahos Eric J Voiglio Mauro Zago
Denver, USA Cape Town, S. Africa Cape Town, S. Africa Celle, Germany Pittsburgh, USA San Antonio, USA Tucson, USA Mainz, Germany Philadelphia, USA Petach-Tikva, Israel Athens, Greece Liverpool, Australia Zurich, Switzerland Oregon, USA Madrid, Spain Graz, Austria Vienna, Austria Boston, USA Lyon, France Milan, Italy
REDAKSİYON (REDACTION) Erman Aytaç
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)
Recep Güloğlu Kaya Sarıbeyoğlu Ahmet Nuray Turhan Hakan Yanar M. Mahir Özmen Ediz Altınlı Gürhan Çelik
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 (Editorial Director) Yayın Koordinatörü (Managing Editor) Amblem Yazışma adresi (Correspondence address) Tel Faks (Fax)
Recep Güloğlu Recep Güloğlu M. Mahir Özmen 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) p-ISSN 1306-696x • e-ISSN 1307-7945 • 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 (karepublishing) • 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): Kasım (November) 2011 • Bu dergide kullanılan kağıt ISO 9706: 1994 standardına uygundur. (This publication is printed on paper that meets the international standard ISO 9706: 1994).
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 6
KASIM - NOVEMBER 2011
İçindekiler - Contents Deneysel Çalışma - Experimental Studies 475-481 Determination of urinary N-acetyl-β-D glucosaminidase (NAG) levels in experimental blunt renal trauma Deneysel künt böbrek travmasında idrar N-Asetil-β-D glukozaminidaz (NAG) düzeylerinin belirlenmesi Hanbeyoğlu A, Kazez A, Üstündağ B, Akpolat N 482-487 Effect of pentoxifylline and vinpocetine on the healing of ischemic colon anastomosis: an experimental study İskemik kolon anastomozunun iyileşmesi üzerine pentoksifilin ve vinposetinin etkisi: Deneysel çalışma Sümer A, Altınlı E, Senger S, Köksal N, Onur E, Eroğlu E, Güneş P
Klinik Çalışma - Original Articles 488-492 Our new stethoscope in the Emergency Department: Handheld ultrasound Acil serviste yeni steteskopumuz: El ultrasonu Coşkun F, Akıncı E, Ceyhan MA, Kavaklı HŞ 493-496 Traumatic abdominal wall hernia Travmatik karın duvarı hernisi Gupta S, Dalal U, Sharma R, Dalal A, Attri AK 497-503 The analgesic effect of three different doses of nitroglycerine when added to lidocaine for intravenous regional anesthesia in trauma patients Travma hastalarında intravenöz rejyonel anestezi için lidokaine eklenmesi durumunda üç farklı nitrogliserin dozunun analjezik etkisi Honarmand A, Safavi M, Fatemy A 504-508 Outcome of surgically treated Lisfranc injury: A review of 34 cases Cerrahi olarak tedavi edilen Lisfranc yaralanmasının sonucu? 34 olgunun değerlendirilmesi Miswan MFM, Singh VA, Yasin NF 509-515 Outcome predictors of Glasgow Outcome Scale score in patients with severe traumatic brain injury Ağır travmatik beyin hasarlı hastalarda Glasgow Sonuç Skalası skoru sonuç belirteçleri Klemenc-Ketis Z, Bacovnik-Jansa U, Ogorevc M, Kersnik J 516-520 Özofagus perforasyonlarında tedavi: On bir olgunun analizi Treatment for esophageal perforations: analysis of 11 cases Arslan E, Şanlı M, Işık AF, Tunçözgür B, Uluşan A, Elbeyli L 521-524 Increased nutritional risk in major trauma: correlation with complications and prolonged length of stay Majör travmada artan nutrisyonel risk: Komplikasyon ve yatış süresinde uzama ile korelasyon Köseoğlu Z, Özdoğan M, Kuvvetli A, Kösenli O, Oruç C, Önel S, Das K, Akova A 525-532 Unusual emergent presentations of abdominal aortic aneurysm: Can simple blood tests predict the state of emergency? Abdominal aort anevrizmasında nadir görülen acil klinik durumlar: Basit kan testleri aciliyetin tanımlanmasında yol gösterici midir? Fedakar A, Fındık O, Kalender M, Balkanay M Cilt - Vol. 17 Sayı - No. 6
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ULUSAL TRAVMA VE AC‹L CERRAH‹ DERG‹S‹ TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY C‹LT - VOL. 17
SAYI - NUMBER 6
KASIM - NOVEMBER 2011
İçindekiler - Contents 533-538 Epidemiologic data of the patients with spinal cord injury: Seven years’ experience of a single center Omurilik yaralanması olan hastaların epidemiyolojik verileri: Tek merkezin yedi yıllık deneyimi Tuğcu İ, Tok F, Yılmaz B, Göktepe AS, Alaca R, Yazıcıoğlu K, Möhür H 539-544 The incidence of peripheral nerve injury in trauma patients in Iran İran’da travma hastalarındaki periferik sinir hasarının insidansı Saadat S, Eslami V, Rahimi-Movaghar V 545-553 Clinical management and reconstruction of isolated orbital floor fractures: The role of computed tomography during preoperative evaluation İzole orbita tabanı kırıklarına klinik yaklaşım ve ameliyat öncesi değerlendirmede bilgisayarlı tomografinin rolü Tan Başer N, Bulutoğlu R, Çelebi NU, Aslan G
Olgu Sunumu - Case Reports 554-556 Akut karına neden olan primer omentum torsiyonu: Olgu sunumu Primary omental torsion as a cause of acute abdomen: Case report Sözen S, Dölalan Ş, Yıldız F, Elkan H 557-560 Abdominal cocoon syndrome as a rare cause of mechanical bowel obstruction: report of two cases Bağırsak tıkanıklığının nadir bir sebebi olan abdominal koza sendromu: İki olgu sunumu Yeniay L, Karaca CA, Çalışkan C, Fırat Ö, Ersin SM, Akgün E 561-562 An unusual cause of cold injury: liquified petroleum gas leakage Nadir bir donma yaralanması nedeni: Sıvılaştırılmış petrol gazı sızıntısı Seyhan N, Jasharllari L, Kayapınar M, Savacı N 563-566 Post-traumatic tricuspid insufficiency: a case report Travma sonrası triküspit yetersizliği: Bir olgu sunumu Tütün U, Aksöyek A, Parlar Aİ, Çobanoğlu A 567-569 Loop formation of Meckel’s diverticulum causing small bowel obstruction in adults: report of two cases Erişkinlerde ince bağırsak tıkanıklığına neden olan Meckel divertikülüne bağlı halka oluşumu: İki olgu sunumu Singh Gupta S, Singh O 570-572 Bir olgu nedeniyle, travmatik orbital amfizemlere yaklaşım Traumatic orbital emphysema: a case report Oba E, Pamukcu C, Erdenöz S 573-578 Ulusal Travma ve Acil Cerrahi Dergisi 2011 yılı 17. cilt konu ve yazar dizini Index of volume 17
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Kasım - November 2011
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):475-481
Experimental Study
Deneysel Çalışma doi: 10.5505/tjtes.2011.57973
Determination of urinary N-acetyl-β-D glucosaminidase (NAG) levels in experimental blunt renal trauma Deneysel künt böbrek travmasında idrar N-Asetil-β-D glukozaminidaz (NAG) düzeylerinin belirlenmesi Alpaslan HANBEYOĞLU,1 Ahmet KAZEZ,1 Bilal ÜSTÜNDAĞ,2 Nusret AKPOLAT3
BACKGROUND
AMAÇ
We evaluated the applicability of urinary N-acetyl-beta-D glucosaminidase (NAG) levels in the diagnosis and followup in blunt kidney injury.
İdrar N-asetil-β-D glukozaminidaz (NAG) düzeyinin, künt böbrek yaralanmasının tanı ve takibinde kullanılabilirliği araştırıldı.
METHODS
GEREÇ VE YÖNTEM
Twenty Sprague-Dawley rats were studied. In the Sham group, left kidney exploration was made. In the Trauma group, after left kidney exploration, a 20 g weight was dropped onto the kidneys. Urine was collected for analysis with strip and determination of urinary NAG and creatinine (Cr) levels at baseline and 0-6, 12-24, 24-36 and 36-48 postoperative hours. Mann-Whitney U and Kruskal-Wallis tests were used.
Yirmi adet Sprague-Dawley cinsi genç-erişkin sıçanla çalışıldı. Sham grubunda sol böbrek eksplorasyonu yapıldı. Travma grubunda sol böbrek eksplore edildikten sonra 20 gr ağırlık böbrek üzerine düşürüldü. İşlem öncesi, işlem sonrası 0-6., 12-24., 24-36. ve 36-48. saatler arasında strip ile idrar tetkiki, idrar NAG ve kreatinin (Cr) düzeyleri için örnekler alındı. İstatistiksel analiz Mann-Whitney U ve Kruskall Wallis testleri ile yapıldı.
RESULTS
BULGULAR
Macroscopic examinations of traumatized kidneys revealed grade II and III injury, and histopathological examinations showed relevant changes. Macroscopic hematuria was observed in all traumatized rats. Urinary NAG/Cr levels in the Trauma group were found to be significantly higher than their base levels at 0-6, 12-24, 24-36, and 36-48 hours. In the Sham group, only the level of NAG/Cr at 0-6 hours was significantly higher. The increase in NAG/Cr levels at 0-6 hours was significantly higher in the Trauma group than in the Sham group.
Travma oluşturulan böbreklerin makroskopik incelemelerinde grade II ve III yaralanma olduğu, histopatolojik incelemelerinde de beklenen patolojik değişiklikler görüldü. Travma grubundaki sıçanların hepsinde makroskopik hematüri izlendi. Travma grubunda 0-6., 12-24., 24-36. ve 36-48. saatler arasındaki idrar NAG/Cr düzeyleri işlem öncesi kontrol değerlere göre anlamlı olarak yüksek bulundu. Sham grubunda ise sadece 0-6. saatteki idrar NAG/ Cr düzeyleri kontrol değerlere göre anlamlı olarak yüksekti. Sıfır-6. saatteki NAG/Cr düzeylerindeki artış travma grubunda anlamlı olarak daha fazlaydı.
CONCLUSION
SONUÇ
After isolated blunt renal trauma, urinary NAG levels increase in the early stage. However, more detailed clinical studies are needed to develop NAG levels as a criterion in the follow-up of blunt renal trauma.
İzole künt böbrek yaralanmalarından sonra erken dönemde idrar NAG düzeyleri anlamlı olarak yükselmektedir. NAG düzeylerinin künt böbrek yaralanmalarında bir ölçüt olarak kullanılabilirliği için daha kapsamlı ve klinik çalışmalarla geliştirilmesi gerekmektedir.
Key Words: NAG; renal injury; trauma.
Anahtar Sözcükler: NAG; böbrek yaralanması; travma.
Presented at the 27th Annual Meeting of Turkish Association of Pediatric Surgeons (September 30-October 3, 2009, Malatya, Turkey) and at the National Pediatric Urology Congress (April 8-10, 2010, İzmir, Turkey). Departments of 1Pediatric Surgery, 2Clinical Biochemistry, Medical Pathology, Fırat University Faculty of Medicine, Elazig, Turkey.
3
27. Türk Pediatrik Cerrahlar Derneği Yıllık Toplantısında (30 Eylül 3 Ekim 2009, Malatya) ve Ulusal Pediatrik Üroloji Kongresi’nde (8-10 Nisan 2010, İzmir) sunulmuştur. Fırat Üniversitesi Tıp Fakültesi, 1Çocuk Cerrahisi Anabilim Dalı, Klinik Biyokimya Anabilim Dalı, 3Tıbbi Patoloji Anabilim Dalı, Elazığ.
2
Correspondence (İletişim): Ahmet Kazez, M.D. Fırat Üniversitesi Fırat Üniversitesi Hastanesi, Çocuk Cerrahisi Kliniği, 23119 Elazığ, Turkey. Tel: +90 - 424 - 233 35 55 / 2907 e-mail (e-posta): akazez@firat.edu.tr
475
Ulus Travma Acil Cerrahi Derg
Although mortality and morbidity due to trauma have declined in children, injuries remain an important health problem. Most of the intraabdominal organ injuries in children occur due to blunt traumas, and approximately 10% of these injuries affect the genitourinary system.[1-4] The kidneys are the most frequently injured organs when genitourinary system injuries are considered, and renal injury is recorded in approximately 1-5% of all the injuries.[5,6] Clinical findings are not manifest in 25% of the cases with a serious renal injury.[7] Although N-acetyl-β-D glucosaminidase (NAG; 2-acetamidodeoxy-β-glucoside acetamidodeoxy glucohydrolase) has been used for the identification of renal diseases and injuries, its application in renal traumas remains an unknown issue. NAG is a stable glycolytic enzyme excreted in the urine with a molecular weight of 130,000 Dalton. It is particularly found at a high level in the lysosomes of proximal tubule cells. It cannot be filtrated through the glomerulus due to its high molecular weight; thus, the increase in the urine concentration is indicative of proximal tubular damage and loss of lysosomal integrity.[8,9] Having considered the fact that urine NAG levels can show significant changes depending on renal parenchyma and tubular damage after blunt trauma, these levels may be used as a guiding parameter in patients with suspected renal trauma. In this study, it was aimed to investigate the availability of urine NAG levels for the diagnosis and follow-up of renal trauma in rats.
MATERIALS AND METHODS This study was carried out in a University Experimental Research Center after the approval of the local Animal Ethics Committee. Young adult, male, Sprague-Dawley rats, 3 months of age and weighing 220-300 g, were included in the study. The rats were fed with standard rat food ad libitum and tap water in metabolic cages in a controlled room (temperature 20 to 25°C; humidity 70% to 80%; 12hour (h) light/dark cycle). The study was conducted on 2 groups of 10 rats each. Group 1: Rats underwent renal exploration only (Sham) Group 2: Rats were exposed to isolated blunt renal trauma (Trauma) Because basal NAG levels before the procedure would be measured, no separate control group was formed. An experimental procedure was carried out in aseptic conditions under general anesthesia of 50 mg/ kg intramuscular ketamine hydrochloride (Ketalar®, 476
Fig. 1. The trauma set prepared for the study: a 30 cm metal tube with a spoon mechanism at its lower tip and cylinder-shaped metal weights of 100, 75, 50, 40, 30, 25, 20, 15, 10 g, respectively. (Color figure can be viewed in the online issue, which is available at www.tjtes.org)
Eczacıbaşı, İstanbul, Turkey) and 4 mg/kg xylazine hydrochloride (Rompun®, Bayer, İstanbul, Turkey). Preliminary Study: Building an Experimental Isolated Renal Trauma Model A preliminary study was conducted on two rats to obtain standard renal injury. Under general anesthesia, each of the weights, 50 and 40 g respectively, was allowed to fall from a metal tube of 40 cm (i.e. from 40 cm height) in a set designed especially by the researchers (Fig. 1) onto an isolated kidney. It was observed that both of the kidneys were completely crushed and shattered (Grade V injury) for these height and weight values. The height was then lowered to 30 cm and the weight reduced to 20 g to obtain milder injuries that did not require resuscitation and surgical operation following the trauma. It was recorded that an appropriate injury model was acquired as a result of the trial performed on both kidneys applying the latter values. Both rats were sacrificed with a high dose of anesthetics after the preliminary study. Experimental Study a) Sham group: A midline laparotomy was performed under anesthesia after shaving and cleaning with antiseptic solution. The left kidney was identified and isolated from the perirenal adipose tissue and replaced into its location. Five ml of saline solution was injected into the peritoneum and the abdominal wall was closed with 4/0 continuous atraumatic silk sutures in two layers. Rats were placed into their metabolic cages, fed by standard food and water and followed-up. Kasım - October 2011
Determination of urinary N-acetyl-β-D glucosaminidase (NAG) levels in experimental blunt renal trauma
b) Trauma group: After the left kidneys were separated from the perirenal adipose tissue, they were lifted from lateral sides, and the “spoon” portion of the specially designed device for inducing trauma was inserted under the kidney. The parenchyma was targeted without causing damage to the renal pedicle, and a cylindrical metal weight of 20 g was allowed to fall once onto the kidney from a 30 cm height in vertical axis. The device was removed, and the kidney was replaced into the renal bed. Injury was observed macroscopically. Five ml of warm saline solution was injected into the abdomen, the abdomen was closed, and the rat was replaced into the metabolic cage. The same follow-up and care criteria were applied for both rat groups following procedures. Urine samples were acquired 6 h after the operation and at the intervals of 12-24, 24-36 and 36-48 h. Rats in both groups were sacrificed with high-dose anesthetic agents at the end of 48 h. The abdomen was opened, and both kidneys were removed and placed into 10% formalin solution for histopathological examination. Collecting and Evaluating Urinary Samples Urine samples accumulating in metabolic cages were taken from both groups before the procedure and were analyzed using URS-10 urine stripes (Teco Diagnostics, Anaheim, USA). Urine samples were taken to measure NAG and creatinine (Cr) levels in the urine and to calculate normal basal values before the procedure. Basal values made up the control group of the study. Urine strip examinations were carried out in urine samples of the groups that were obtained in the first 6 h following the operation and between the intervals of 12-24, 24-36 and 36-48 h. Urine samples were obtained for NAG and Cr. Urine samples were centrifuged in 3000 rpm for 5 minutes (min). Acquired supernatants were placed into Eppendorf tubes for measurements and stored at -80°C. The NAG index was calculated to eliminate the changes in urine samples that would arise due to urine volume. Urinary NAG Index (U/g): The urinary NAG index was calculated as Urine NAG activity / Urine creatinine concentration. 3-cresol-sulphophthalein method was applied to measure the NAG activity in spot urine.[10] MCP-NAG was used as substrate and the absorbance of 3-cresolsulphophthalein revealed through NAG hydrolysis was measured by Techcomp 8500 II UV/VIS spectrophotometer (Techcomp Ltd, Shanghai, China) in 580 nm. NAG 875406 kit (Roche Diagnostic GmbH, Manheim, Germany) was applied for measurements. Cr in urine was measured by Olympus AU600 autoanalyzer (Olympus Optical Co Ltd, Japan) using Olympus brand UV-kinetic kit and applying Jaffe method.[11] Cilt - Vol. 17 Sayı - No. 6
Histopathological Examination After the kidneys were fixed in 10% formalin solution 48 h after the procedure, samples that passed through the long renal axis and pelvis were taken. Hematoxylin eosin (H-E), Masson’s trichrome (MAS) and periodic acid-Schiff (PAS) stains were applied to the samples. Sections were evaluated with respect to capsule rupture, interstitial hematoma, cortical laceration, medullary laceration, glomerular damage (hematoma), tubular rupture, arcuate artery rupture, and infarction. Changes were rated between 0 and 3 for tubular rupture, subcapsular hematoma and interstitial hematoma. Accordingly, 0 expressed no pathology; 1 mild changes; 2 moderate changes; and 3 severe pathological changes. The other parameters were calculated as 0 (no pathological changes) and 1 (presence of pathology). Statistical Analysis Data acquired from the groups were expressed as mean value ± standard derivation (Mean ± SD). The Mann-Whitney U test was applied for the periodic evaluation of groups, Kruskal-Wallis test was used for period comparisons in each group, and Mann-Whitney U test was applied for dual comparisons. Lowest statistical significance level was accepted as p<0.05.
RESULTS All the rats survived until the end of the study. Grade II or III renal damage was observed in all the rats in the Trauma group. Following the procedure in the Trauma group, macroscopic hematuria was seen in all rats. Urinary Strip Analyses There were no pathological findings with regard to urine strip examinations in either group before the procedure. Further, no pathological findings were identified in urine samples received from the Sham group after the operation between the intervals of 0-6, 12-24, 24-36, and 36-48 h. Macroscopic hematuria, 2+ (80 erythrocyte/µl) and 3+ erythrocyte (200 erythrocyte/ μl) were observed in the strip test in urine samples acquired from all the rats of the Trauma group following the procedure in the interval of 0-6 h. Between 1224 h, macroscopic hematuria in 3 of the rats and 1+ (25 erythrocyte/μl) or low-level hematuria in all the rats were still present. No macroscopic hematuria was recorded in any of the rats between 24-36 h. No macroscopic hematuria was observed between 36-48 h, whereas low-level hematuria was identified in 4 rats in the strip examination. NAG Levels Control NAG values before the procedure were found to be 3.213±1.392 U/g on average in 477
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Table 1. Average NAG levels in groups Groups
NAG (U/g) Control
NAG (U/g) 0-6 h
NAG (U/g) 12-24 h
NAG (U/g) 24-36 h
NAG (U/g) 36-48 h
Sham group Trauma group
3.213±1.392 2.659±0.840
69.366±51.618* 113.00±45.109*ª
13.413±13.179 14.703±13.962*
3.805±2.590 10.027±10.362*ª
2.439±1.313 8.253±7.294*ª
*: p<0.05 between the control and time interval values in each group. ª: p<0.05 between the corresponding values of the two groups.
the Sham group. It was recorded that NAG levels (69.366±51.618 U/g) measured 0-6 h after the procedure were increased compared to control NAG values before the procedure. Further, NAG levels (13.413±13.179 U/g) measured between 12-24 h were increased compared to control values before the procedure. The increase in NAG levels was statistically significant compared to control values between 0-6 h (p<0.05), whereas the increase between 12-24 h was not significant. No significant difference was found in NAG levels (3.805±2.590; 2.439±1.313 U/g) between the intervals of 24-36 and 36-48 h compared to control values (p>0.05) (Table 1).
group compared to the Sham group (p<0.05) (Table 1, Fig. 2).
Control NAG values before the procedure were found to be 2.659±0.840 U/g on average in the Trauma group. The NAG level was measured to be 113.00±45.109 U/g for this group between 0-6 h and was higher than all the other groups. These values were measured as 14.703±13.962, 10.027±10.362, and 8.253±7.294 U/g, respectively, between the intervals of 12-24, 24-36 and 36-48 h. It was determined that all NAG levels measured between the intervals of 0-6, 12-24, 24-36, and 36-48 h were observed to be increased significantly compared to control levels before the procedure (p<0.05) (Table 1).
Pathological changes due to trauma were recorded for all the rats and are summarized in Table 2.
When the Sham group and Trauma group were compared, no significant difference was found between NAG control levels and the values between 12-24 h, whereas the increase between the intervals of 0-6, 24-36 and 36-48 h was significant in the Trauma 120 100
NAG levels of Sham group
U/g
80
NAG levels of Trauma group
60 40 20 0 Control
0-6*
12-24
24-36*
36-48*
Hours
Fig. 2. Comparison of NAG levels of the groups.
478
*p<0.05: When the same periods of the groups were compared.
Histopathological Changes No pathologic findings were observed in the Sham group on macroscopic and histopathological examination of the kidneys. In the macroscopic examination of the kidneys exposed to trauma, capsule damage, parenchymal laceration, bleeding, and perirenal bleeding were identified. Grade III injury was determined in 6 rats, whereas Grade II injury was noted in 4 rats in the Trauma group macroscopically.
DISCUSSION The measurement of the urine enzymes to diagnose kidney diseases and to reveal renal damage has a wide range of clinical application.[8,12,13] NAG, as a noninvasive test, has special importance in the diagnosis of renal damage in the early period, which occurs due to toxins or diseases, and in the follow-up of the progressive disease.[8] NAG determination is a sensitive test to measure the severity of the renal damage before renal functions regress.[14] However, there is not enough information in the literature about the changes in urine enzymes due to renal damage caused by trauma directly. The easiest means of identifying whether the genitourinary system is affected in cases with general body trauma is to analyze the urine sample of the patient and to determine whether or not hematuria has developed.[15] Sixty-five percent of the severe renal damages have macroscopic hematuria in the beginning and 32.7% of those have microscopic hematuria; no hematuria may be recorded in only 1.7% of the cases. The reason for no hematuria in these cases is either renal pedicle damage or ureteropelvic rupture, both of which are rarely observed injuries.[16] No correlation has been found between the degree of hematuria and the severity of the renal injuries. Thirty-one percent of the minor renal damages have macroscopic hematuria and 65.5% of those have microscopic hematuria; no hematuria may be recorded in 3.4% of the cases.[16-19] Macroscopic hematuria is a more significant finding Kasım - October 2011
Determination of urinary N-acetyl-β-D glucosaminidase (NAG) levels in experimental blunt renal trauma
Table 2. Histopathological examination of the kidneys in the trauma group
A
B
C
D
E
F
G
H
I
T1 T2 T3 T4 T5 T6 T7 T8 T9 T10
2 2 1 3 3 3 2 3 2 2
0 2 1 2 2 0 0 3 1 0
2 2 3 1 3 1 2 3 3 1
0 1 1 1 1 1 1 0 1 1
1 1 1 1 1 1 1 1 1 1
1 1 0 1 1 1 0 1 1 0
0 0 0 0 0 0 0 1 0 0
1 0 1 0 1 0 1 0 0 0
0 0 0 0 1 0 1 1 0 0
A: Tubular Rupture*; B: Subcapsular hematoma*; C: Interstitial hematoma*; D: Capsule rupture; E: Cortical laceration; F: Medullary laceration; G: Glomerular damage hematoma; H: Arcuate artery rupture; I: Infarction. In the first three parameters (*): 0: none, 1: mild, 2: moderate, 3: severe; other parameters are evaluated as 0: absent, 1: present.
when renal injuries are taken into account; however, major renal injury was identified in only 32% of the patients with macroscopic hematuria.[20] In this study, macroscopic hematuria was recorded in the early period in all rats of the Trauma group exposed to grade IIIII renal injuries. No hematuria was determined in rats in the Sham group in either the macroscopic or strip examinations performed in the postoperative period.
mal levels in one week, and that ESWL might cause renal damage that recovers rapidly.[25-27] In an experimental study carried out on dogs by Fortes et al.,[28] it was recorded that urine NAG levels increased 12 h after ESWL, and were decreased after 24 h. A second ESWL applied 24 h later did not increase NAG levels again. However, a NAG-related study on blunt renal trauma was not found in the literature.
Although various indicators (serum Cr and urea, Cr clearance, etc.) are used widely in routine laboratories to evaluate the glomerular damage in kidneys, biochemical indicators for the evaluation of tubular damage are limited. For his purpose, ALP (alkaline phosphatase), GGT (gamma-glutamyl transferase), LAP (leucine aminopeptidase), AAP (alanine aminopeptidase), GAL (beta galactosidase), NEP (neutral endopeptidase), and NAG measurements are used in urine. However, the stability of the molecule to be evaluated and the difficulty of collecting urine for 24 h restrict the usage of most of these indicators. Among these indicators, NAG has become prominent in the identification of renal damage.[14,21-24]
There are many study models in the literature on blunt renal injuries. Trauma models are used in which a cylinder-shaped weight attached to a pendulum in vitro is released to fall by extending it towards a side and crash to the kidney. Postmortem swine kidneys were used in other studies and biomechanics of the trauma and the final lesions were mostly emphasized. [29-31] No isolated blunt renal trauma model was found in the literature. Thus, a standard injury model was aimed to be obtained with a preliminary study. A metal tube was designed by the researchers to be used in the model. A spoon mechanism at its lower tip that could be placed under the kidney (for renal isolation) and a cylinder-shaped weight with smooth surface measuring 1 cm in diameter (for trauma) were used. The aim of the pre-study was to obtain a standard and acceptable renal injury that did not require any posttraumatic resuscitation or surgical intervention. It was found that Grade III injury, among the five- degree renal injury scale accepted by the AATS (American Association of Trauma Surgeon)[32] was observed by dropping a 20 g weight from a height of 30 cm. This trauma model was applied in rats in the Trauma group. It was determined both macroscopically and histopathologically that 4 of the rats had grade II and 6 had grade III renal injuries.
N-acetyl-β-D glucosaminidase (NAG) is the most frequently applied enzyme for the evaluation of renal tubular damage. It was reported in the literature that the stability of NAG enzyme excreted through the urine was higher and that it maintained its activity for a long period by freezing. Moreover, it was reported that this enzyme might be used in routine clinical practice by proportioning urine NAG activity to Cr and working with spot urine.[14,23,24] We also investigated the changes in urine NAG levels in the early period due to blunt renal injuries by applying the NAG/Cr ratio in order to eliminate the effects of volume changes. In clinical studies and in an experimental study conducted on rats, it was indicated that NAG levels increased just after ESWL (extra-corporeal shock wave lithotripsy), urine NAG levels returned to norCilt - Vol. 17 SayĹ - No. 6
In this study, urine NAG levels, which were recorded at 0-6, 12-24, 24-36, and 36-48 h following isolated blunt renal trauma, were found to be significantly higher with respect to urine NAG levels before the trauma. It was noted that an apparent increase was found in urine NAG levels in the first 6 h particularly 479
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and that these high levels decreased in 48 h. An increase in urine NAG levels recorded at 0-6 and 12-24 h was observed in the Sham group. The increase at 0-6 h was statistically significant. No significant difference was found for this group when urine NAG levels at 12-24, 24-36 and 36-48 h were compared to control values. In the study of Fortes et al.,[28] intravenous thionembutal was administered to dogs under anesthesia with Pentrane inhalation. Intravenous contrast material was given during the procedure and a second ESWL was applied at 24 h in the same manner. In that study, urine NAG levels before ESWL were compared to NAG levels at 12, 24, 36, and 48 h after ESWL; however, no separate control group was formed to evaluate the effects of anesthesia or contrast material. In the present study, a Sham group, which received anesthesia using ketamine and xylazine, was formed in addition to the group exposed to trauma. The apparent increase in urine NAG levels in the Sham group recorded in the first 6 h was remarkable. It was thought that this increase might be related to the anesthesia or surgical operation. In the study carried out by Fortes et al.,[28] in which ESWL was applied at 24 h with a second anesthesia and contrast administration, no increase in NAG levels was observed. This again supports the fact that the increase in urine NAG levels in the Sham group, including in our study, may be due to the surgical exploration. Additionally, when urine NAG levels of both the Trauma and Sham groups recorded at 6 h were compared, it was found that the increase in urine NAG levels of the Trauma group was significantly higher. In conclusion, urine NAG levels increase in the early period due to posttraumatic tissue damage in the kidneys. This increase is more apparent in the first 6 h and continues decreasingly to 48 h as well. The results should be supported by similar studies, and normal NAG values of various age groups should be determined for the clinical applications. Acknowledgement The authors thank FUBAP (Fırat University Research Fund), Elazığ, for financial support for this project (FUBAP project no. 1619-2009) and Ş. Kerem Özel for his linguistic overview.
REFERENCES 1. Haller JA Jr. Life-threatening injuries in children: what have we learned and what are the challenges? Bull Am Coll Surg 1995;80:8-18, 43. 2. Cooper A, Barlow B, DiScala C, String D. Mortality and truncal injury: the pediatric perspective. J Pediatr Surg 1994;29:33-8. 3. Snyder CL, Jain VN, Saltzman DA, Strate RG, Perry JF Jr, Leonard AS. Blunt trauma in adults and children: a comparative analysis. J Trauma 1990;30:1239-45. 4. Kivioja AH, Myllynen PJ, Rokkanen PU. Is the treatment of the most severe multiply injured patients worth the effort? 480
A follow-up examination 5 to 20 years after severe multiple injury. J Trauma 1990;30:480-3. 5. Baverstock R, Simons R, McLoughlin M. Severe blunt renal trauma: a 7-year retrospective review from a provincial trauma centre. Can J Urol 2001;8:1372-6. 6. Kristjánsson A, Pedersen J. Management of blunt renal trauma. Br J Urol 1993;72:692-6. 7. Başaklar AC. Genitoüriner travma. In: Başaklar AC, editor. Bebek ve çocukların cerrahi ve ürolojik hastalıkları (in Turkish). Ankara: Palme Yayıncılık; 2006. p. 1787-810. 8. Noyan T, Şekeroğlu MR, Dülger H. N-Asetil-β-D Glukozaminidaz ve böbrek hastalıklarında kullanımı. Van Tıp Dergisi 2000;7:80-3 [in Turkish]. 9. Furuhata N, Shiba K, Nara N. N-acetyl-beta-D-glucosaminidase. [Article in Japanese] Nihon Rinsho 1995;53:1267-76. 10. Price RG. The role of NAG (N-acetyl-beta-D-glucosaminidase) in the diagnosis of kidney disease including the monitoring of nephrotoxicity. Clin Nephrol 1992;38:14-9. 11. Bowers LD. Kinetic serum creatinine assays I. The role of various factors in determining specificity. Clin Chem 1980;26:551-4. 12. D’Amico G, Bazzi C. Urinary protein and enzyme excretion as markers of tubular damage. Curr Opin Nephrol Hypertens 2003;12:639-43. 13. Jung K. Enzyme activities in urine: how should we express their excretion? A critical literature review. Eur J Clin Chem Clin Biochem 1991;29:725-9. 14. Price RG. Measurement of N-acetyl-beta-glucosaminidase and its isoenzymes in urine methods and clinical applications. Eur J Clin Chem Clin Biochem 1992;30:693-705. 15. Mee SL, McAninch JW. Indications for radiographic assessment in suspected renal trauma. Urol Clin North Am 1989;16:187-92. 16. Casale AJ: Urinary tract trauma. In: Gearhart JP, Rink RC, Mouriquand PDE, editors. Pediatric urology. Philadelphia: W.B. Saunders Company; 2001. p. 923-43. 17. McAleer IM, Kaplan GW, Scherz HC, Packer MG, Lynch FP. Genitourinary trauma in the pediatric patient. Urology 1993;42:563-8. 18. Smith EM, Elder JS, Spirnak JP. Major blunt renal trauma in the pediatric population: is a nonoperative approach indicated? J Urol 1993;149:546-8. 19. Baumann L, Greenfield SP, Aker J, Brody A, Karp M, Allen J, et al. Nonoperative management of major blunt renal trauma in children: in-hospital morbidity and long-term followup. J Urol 1992;148:691-3. 20. Morey AF, Bruce JE, McAninch JW. Efficacy of radiographic imaging in pediatric blunt renal trauma. J Urol 1996;156:2014-8. 21. Viganò A, Assael BM, Dalla Villa A, Gagliardi L, Principi N, Ghezzi P, et al. N-acetyl-beta-D-glucosaminidase (NAG) and NAG isoenzymes in children with upper and lower urinary tract infections. Clin Chim Acta 1983;130:297-304. 22. Neimark A, Fidirkin A, Celovalnikova I. Enzymuria as early marker of interstitial nephritis. Int Urol Nephrol 1997;29:13740. 23. Kavukçu S, Soylu A, Türkmen M. The clinical value of urinary N-acetyl-beta-D-glucosaminidase levels in childhood age group. Acta Med Okayama 2002;56:7-11. 24. Noyan T, Şekeroğlu MR, Dülger H. Böbrek hasarı markerlerinin değerlendirilmesinde 24 saatlik ve spot idrar kullanımı arasında fark var mıdır? Klinik Laboratuar Araştırma Dergisi 2001;5:53-7 [in Turkish]. Kasım - October 2011
Determination of urinary N-acetyl-β-D glucosaminidase (NAG) levels in experimental blunt renal trauma
25. Erkizan O, Ayder AR, Minareci S, Lekili M, Dincel C. NAG, GGT, creatinine, urea and creatinine clearance before and after ESWL. Int Urol Nephrol 1994;26:259-62. 26. Uozumi J, Ueda T, Naito S, Ogata N, Yasumasu T, Koikawa Y, et al. Clinical significance of urinary enzymes and beta 2-microglobulin following ESWL. Int Urol Nephrol 1994;26:605-9. 27. Weichert-Jacobsen K, Scheidt M, Külkens C, Loch T. Morphological correlates of urinary enzyme loss after extracorporeal lithotripsy. Urol Res 1997;25:257-62. 28. Fortes MA, Andriolo A, Ortiz V, Srougi M. Effect of shock wave reapplication on urinary N-acetyl-beta-glucosaminidase in canine kidney. Int Braz J Urol 2004;30:148-54.
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29. Snedeker JG, Barnstuble BB, Iaizzo PA, Farshad M, Niederer P, Schmidlin FR. A comprehensive renal injury concept based on a validated finite element model of the human abdomen. J Trauma 2007;62:1240-9. 30. Schmitt KU, Snedeker JG. Kidney injury: an experimental investigation of blunt renal trauma. J Trauma 2006;60:880-4. 31. Bschleipfer T, Kallieris D, Hauck EW, Weidner W, Pust RA. Blunt renal trauma: biomechanics and origination of renal lesions. Eur Urol 2002;42:614-21. 32. Moore EE, Shackford SR, Pachter HL, McAninch JW, Browner BD, Champion HR, et al. Organ injury scaling: spleen, liver, and kidney. J Trauma 1989;29:1664-6.
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Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):482-487
Experimental Study
Deneysel Çalışma doi: 10.5505/tjtes.2011.75428
Effect of pentoxifylline and vinpocetine on the healing of ischemic colon anastomosis: an experimental study İskemik kolon anastomozunun iyileşmesi üzerine pentoksifilin ve vinposetinin etkisi: Deneysel çalışma Aziz SÜMER,1 Ediz ALTINLI,2 Serkan SENGER,2 Neşet KÖKSAL,2 Ender ONUR,3 Ersan EROĞLU,2 Pembegül GÜNEŞ4 BACKGROUND
AMAÇ
In the current study, we aimed to investigate the influences of pentoxifylline, which increases the flexibility, deformability and viscosity of the erythrocytes while reducing the aggregation abilities of the platelets, and vinpocetine, which has neuroprotective and antioxidant effects, on healing of colonic anastomoses.
Bu çalışmada, eritrositlerin fleksibilitesini, deformabilitesini ve akışkanlığını arttıran, aynı zamanda trombositlerin agregasyon yeteneklerini azaltan pentoksifilin ile nöroprotektif, antioksidan etkisi olan vinposetinin kolon anastomozlarında iyileşme üzerine olan etkileri araştırıldı.
METHODS
GEREÇ VE YÖNTEM
We used 30 Albino Wistar rats. Subjects were divided into three groups of 10 rats each. Colonic ischemia was established in all the groups. Following colonic transection, anastomosis was performed. Group A received intraperitoneal saline, whereas Group B and Group C received pentoxifylline and vinpocetine, respectively. The subjects were sacrificed on the postoperative 5th day by ether anesthesia, and their colonic bursting pressures were measured. The anastomotic area was excised for hydroxyproline assay and histopathologic examination.
Çalışmamızda 30 adet Albino Wistar cinsi sıçan kullanıldı. Denekler herbiri 10 adet sıçandan oluşan 3 gruba ayrıldı. Tüm gruplarda kolon iskemisi oluşturuldu. Kolon transeksiyonu sonrası anastomoz yapıldı. Grup A’ya intraperitoneal olarak serum fizyolojik, Grup B’ye pentoksifilin ve Grup C’ye ise vinposetin verildi. Cerrahi işlem sonrası 5. günde eter anestezisi ile sakrifiye edilen sıçanların kolon patlama basınçları ölçüldü. Anastomoz bölgesi hidroksiprolin ölçümü ve histopatolojik inceleme için çıkartıldı.
RESULTS
BULGULAR
According to intergroup comparisons, colonic bursting pressure was found to be higher in the treatment groups than in the control group; however, the difference was not statistically significant. Intergroup comparisons regarding tissue hydroxyproline levels showed statistically significant differences between Groups A and B, Groups A and C and Groups B and C.
Gruplararası kolon patlama basınçları kontrol grubuna göre daha yüksek ölçülmekle birlikte, istatistiksel olarak anlamlı değildi. Gruplararası doku hidroksiprolin düzeyleri açısından Grup A ile Grup B, Grup A ile Grup C ve Grup B ile Grup C arasında istatistiksel olarak anlamlı fark vardı.
CONCLUSION
SONUÇ
Similar to pentoxifylline, vinpocetine was also shown to have a beneficial effect over ischemic colon anastomoses.
Vinposetinin de pentoksifilin gibi iskemik kolon anastomozlarına olumlu etkisi olduğu gösterilmiştir.
Key Words: Colon anastomoses; ischemia; pentoxifylline; vinpocetine.
Anahtar Sözcükler: Kolon anastomozu; iskemi; pentoksifilin; vinpocetin.
Department of General Surgery, Yüzüncü Yıl Univesity, Faculty of Medicine, Van; Departments of 2General Surgery, 4Pathology, Haydarpaşa Numune Training and Research Hospital, Istanbul; 3 Department of General Surgery, Fatih Sultan Mehmet Training and Research Hospital, Istanbul, Turkey. 1
Yüzüncü Yıl Üniversitesi, Tıp Fakültesi, Genel Cerrahi Anabilim Dalı, Van; Haydarpaşa Numune Eğitim ve Araştırma Hastanesi, 2 2. Genel Cerrahi Kliniği, 4Patoloji Bölümü, İstanbul; 3Fatih Sultan Mehmet Eğitim ve Araştırma Hastanesi, Genel Cerrahi Kliniği, İstanbul.
1
Correspondence (İletişim): Aziz Sümer, M.D. Yüzüncü Yıl Üniversitesi, Tıp Fakültesi, Genel Cerrahi Kliniği, 65000 Van, Turkey. Tel: +90 - 216 - 414 45 02 / 1533 e-mail (e-posta): azizsumer2002@yahoo.com
482
Effect of pentoxifylline and vinpocetine on the healing of ischemic colon anastomosis
Colonic leaks arising from inadequate healing of the anastomosis are still deemed an important problem in colorectal surgery.[1,2] Anastomotic leak in colorectal surgery increases the morbidity and mortality rates.[3,4] Tissue blood flow and oxygenation are very significant factors contributing to the healing of colonic anastomosis, whereas ischemia and infection are known to be the most important factors interrupting the healing process.[5,6] Ischemia is one of the most influential causes leading to impaired wound healing.[7,8] The ischemic wound is known to be easily infected and to have a difficult healing process.[8,9] Prevention or reduction of ischemic damage is among the objectives of surgery. The most important elements that have an effect over organ and tissue perfusions are erythrocyte deformability and plasma viscosity. In order to remove metabolic wastes, while transporting oxygen and vital molecules to the end-organ capillaries, erythrocytes should be able to deform themselves so as to move and squeeze through narrow and sinuous areas. This ability is termed as ‘deformability’. Vasoactive drugs are known to increase tissue blood flow and oxygenation.[10] The aim of this study was to compare the effects of pentoxifylline, a xanthene derivative that reduces blood viscosity by increasing cell deformability and decreasing plasma fibrinogen concentration, while elevating blood viscosity by inhibiting platelet adhesion and aggregation, and pentoxifylline, which has antioxidant, vasodilator and neuroprotective effects, over anastomotic healing.
MATERIALS AND METHODS After gaining the approval of the ethics committee of the Haydarpasa Numune Training and Research Hospital, the study was conducted at the hospital’s animal laboratory. Our experimental study included 30 adult male and female Albino Wistar rats, weighing between 200-240 g. The rats were split into three groups in a randomized manner so as to include 10 rats in each.
lowing anesthesia, rats were weighed by an analytic balance and the weight of each rat was noted. Then, the rats were fixed on the operating table in the supine position before clipping their abdominal hair and applying povidone iodine solution. A median laparotomy was applied to all the groups. As described by Altinli et al.,[6] all the marginal arteries and vasa recti within 2 cm proximal and 2 cm distal range of the colonic segment located 3 cm proximal to the peritoneal reflection were ligated by 4/0 atraumatic silk sutures. End-to-end anastomosis was performed with polypropylene 6/0 (Fig. 1). The rats were allowed to feed at the end of 24 hours. Group A was the control group and received intraperitoneal 1 cc saline once daily for 5 days at 24-hour intervals. Group B received pentoxifylline 50 mg/kg (Vasoplan ampoule, Mustafa Nevzat İlaclari, Turkey) once daily for 5 days at 24-hour intervals. Group C received intraperitoneal vinpocetine 1 mg/kg (Cavinton ampoule, RG, Bulgaria) once daily for 5 days at 24-hour intervals. All subjects were sacrificed postoperatively on day 5 by high-dose ether anesthesia. Assessment of anastomotic healing was carried out by evaluation of bursting pressure, tissue hydroxyproline measurement, and histopathologic examination. Evaluation of Bursting Pressure The abdomen was entered through the same abdominal incision on the postoperative 5th day. Since management of adhesions formed in the anastomotic area and identified by the polyprolene sutures could lead to different measurement results, the peripheral adhesions were left untouched. Colonic content was removed from the anastomotic area. A ligature was applied 2 cm proximal to the anastomosis by 3/0 silk. An infusion pump was placed through the rectum to reach the anastomosis line and ligated by a 3/0 silk
Group A: Anastomosis in ischemic colon model Group B: Anastomosis in ischemic colon model + Intraperitoneal pentoxifylline delivery Group C: Anastomosis in ischemic colon model + Intraperitoneal vinpocetine delivery Preoperatively, each subject from all groups was fed with water and standard laboratory diet under fixed environmental conditions. Anesthesia was performed by intramuscular (IM) injection of ketamine 50 mg/ kg (Ketalar vial, Pfizer, Turkey) supported by ether inhalation, without applying any colon ��������������� cleansing.����� FolCilt - Vol. 17 Sayı - No. 6
Fig. 1. The view of the completed anastomosis. (Color figure can be viewed in the online issue, which is available at www.tjtes.org)
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Fig. 2. Bursting pressure measurement.
Fig. 3. Intense re-epithelization on colonic mucosa in the vinpocetine group.
(Color figures can be viewed in the online issue, which is available at www.tjtes.org)
so as to avoid leaks. Isotonic solution with methylene blue was administered by a syringe driver at a rate of 1 ml/min and the area of the anastomosis was monitored. The pressure value read at the first observation of methylene blue outside the anastomosis area was recognized and noted as the bursting pressure (Fig. 2). Hydroxyproline Measurement Following measurement of bursting pressure, the colon was resected longitudinally, comprising both 2 cm distal and proximal of the anastomosis. The resection segment was reduced to include 0.5 cm of both proximal and distal portions before removing one half for hydroxyproline measurement and the other half for histopathologic examination. One gram of the resected tissue was hydrolyzed for 5 hours at 121°C in an acidic buffer solution. After the hydrolysis, the samples were centrifuged at 5000 rpm for 20 minutes, which yielded the final study material. The absorbance of the final material was evaluated by colorimetric method at 560 nm and 121°C, and tissue hydroxyproline level was calculated as mg/L/g tissue by a commercially available kit (Kit: Hydroxyproline Extra [Colorimetric Determination], Lot #: 41100, Brand: Far/Italy). Histopathologic Examination Perianastomotic colonic segments were evaluated by a pathologist blindly. Preparations were evaluated in light of the parameters developed by Garcia et al.[11] Tissue samples prepared as paraffin blocks were stained with hematoxylin-eosin and examined under an Olympus CX 41 light microscope by a pathologist for presence of inflammatory cells, neovascularization, fibroblast presence, fibrosis, ischemic necrosis, continuity of the muscular layer, inflammatory infiltration in the muscular layer, and local inflammatory re484
sponse (neutrophil, lymphocyte, histiocyte, and giant cell) over the anastomotic area. Statistical Analysis The results of our study were evaluated by the Statistical Package for the Social Sciences (SPSS) for Windows 11.0 program. Intergroup comparison of the classified data was carried out by chi-square test, while Fisher’s exact test was used for unsuited data (a frequency ≤4 in the cells). Considering the small scale of the sample included in the study, nonparametric methods (Kruskal-Wallis analysis and MannWhitney U test) were applied. A p value below 0.05 at 0.95 significance level was recognized as statistically significant.
RESULTS No deaths were observed due to anesthesia or surgery. Two rats died in Group B at 3 and 4 days after the anastomosis. Necropsies revealed strong anastomoses. However, dilatation was observed in the intestinal loops over the proximal portion of anastomoses and these were evaluated to be consistent with ileus. The subjects that died were excluded from the study and replaced with new subjects in order to complete the study. Bursting Pressure In all subjects, the bursting was observed at the anastomotic line. Average anastomotic bursting pressures were 73.5±14.15 mmHg in Group A, 77.2±11.97 mmHg in Group B, and 87.4±15.66 mmHg in Group C. While colonic bursting pressures were higher in Groups B and C in comparison to Group A, the differences between groups were statistically insignificant (p=0.86). The anastomotic bursting pressures and standard deviations are shown in Table 1. Kasım - October 2011
Effect of pentoxifylline and vinpocetine on the healing of ischemic colon anastomosis
Table 1. Colon bursting pressure of the groups and standard deviation Colon bursting pressure Mean±SD
Group A (mmHg)
Group B (mmHg)
Group C (mmHg)
160 106 91 13 60 15 64 41 79 88 73.5±14.15
88 82 77 89 86 21 73 149 82 98 77.2±11.97
147 55 74 26 32 43 137 161 112 87 87.4±15.66
Table 2. Tissue hydroxyproline level of the groups and standard deviation Hydroxyproline level Mean±SD
Group A (mg/L/g tissue)
Group B (mg/L/g tissue)
Group C (mg/L/g tissue)
130.0 139.0 136.0 72.0 34.0 146.0 58.0 162.0 154.0 252.0 128.3±19.61
549.0 263.0 226.0 156.0 347.0 311.0 464.0 272.0 317.0 371.0 327.6±36.1
1016.0 480.0 488.0 923.0 827.0 695.0 462.0 464.0 330.0 536.0 622.1±72.61
Tissue Hydroxyproline Level Average hydroxyproline levels were 128.3±19.61 mg/L/g tissue in Group A, 327.6±36.1 mg/L/g tissue in Group B, and 622.1±72.61 mg/L/g tissue in Group C. Intergroup difference was statistically significant (p=0.00001). Paired comparisons of the groups revealed statistically significant differences (pA-B=0.00001; pA-C=0.00001; pB-C=0.001). Distribution and statistical analysis results are shown in Table 2. Histopathologic Examination Wound healing, granulation tissue formation, and histological changes in local inflammatory responses in anastomoses were evaluated according to the parameters modified by Garcia et al.[11] The intergroup differences between the subjects with regard to mucosal re-epithelization grading were statistically significant (p=0.009). The vinpocetine group demonstrated a good degree of re-epithelization in the colonic mucosa (Fig. 3). There was no statistically significant intergroup difference among the study subjects with regard to neovascularization, fibroblasts, continuity of the musCilt - Vol. 17 Sayı - No. 6
cular layer, inflammation of the muscular layer, polymorphonuclear leukocytes (PNL) at the anastomotic site, lymphocyte infiltration, and grading of histiocyte and giant cells (p=0.422, p=0.42, p=0.105, p=0.274, p=0.171, p=0.059, p=0.19, p=0.538, respectively). The difference between the groups in terms of fibrosis grading was statistically significant (p=0.023).
DISCUSSION The most common complication of gastrointestinal operations, which are performed frequently, is anastomotic leaks, with high morbidity and mortality. In colorectal anastomoses, the anastomotic leak rate is reported to be 10-20%. Although the incidence of this complication has been significantly reduced with the application of modern surgical techniques, it is still an important complication.[4,9,12-14] As with all anastomoses, tissue blood flow and oxygenation are considerable factors in colonic anastomoses.[5,12] In comparison with other gastrointestinal components, the colon is known to present higher anastomotic leak rates due to its certain anatomical 485
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and biological characteristics, such as low collagen content, high collagenase activity, reduced collateral circulation, and absence of a serosa in the extraperitoneal rectum.[15]
were not statistically significant. This difference was thought to be associated with the fact that the number of subjects in our study was one-third of the abovementioned study.
There have been numerous experimental studies regarding colonic anastomotic healing. In those studies, many agents have been used, such as hyperbaric oxygen, glucan, erythropoietin, bosentan, growth hormone, and H2-receptor antagonists like famotidine. The common denominator of all those studies was the effort to reduce ischemia.[4,5,12,14,16,17] Benacerraf et al.[18] reported 100% anastomotic leak in cases where perianastomotic oxygen pressure was below 20 mmHg, while denoting that the anastomotic leak rate was reduced by elevation of oxygen pressure. In the current study, we used pentoxifylline and vinpocetine to reduce ischemia. Consistent with previous studies in the literature, hydroxyproline levels and bursting pressures were determined to be higher in groups in which such agents were used when compared with the control group.
In the study of Abdel Salam et al.,[19,20] vinpocetine and pentoxifylline were shown to have positive effects over ischemic hepatic tissue induced by carbon tetrachloride. The result of this study can be deemed as supportive of a likely positive influence of pentoxifylline and vinpocetine over colonic anastomosis because of their evident positive effects in organ ischemia.
Bursting pressure and hydroxyproline determinations are measures that offer insight into the anastomosis healing process. Bursting pressure reveals the mechanical parameters of a colonic anastomosis and reflects growing anastomotic strength. Biochemical parameters of anastomotic healing are reflected by the collagen content in perianastomotic tissues, as determined by hydroxyproline content.[4] In this study, comparison of the control and treatment groups with regard to bursting pressure revealed a high, but not statistically significant, difference. Hydroxyproline levels were found to be higher in the treatment groups than in the control group. The elevated levels of bursting pressure and hydroxyproline were associated with the reduction of collagenase activity induced by vinpocetine and pentoxifylline. In the study of Parra-Membrives et al.[9] focusing on the effects of pentoxifylline over ischemic colorectal anastomoses, pentoxifylline and control groups showed similar mucosal re-epithelization; presence of inflammatory cells in the granulation tissue; and lymphocyte, histiocyte, and fibroblast infiltration. No significant alteration was observed with regard to destruction of the muscular layer. The control group demonstrated a significantly high amount of neutrophils over the anastomosis line. The underlying reason for the reduction in grading of perianastomotic fibrosis was claimed to be ischemia and neovascularization. In the current study, unlike the investigation of Parra-Membrives et al.,[9] we determined a higher level of mucosal re-epithelization in the vinpocetine and pentoxifylline groups. However, despite higher values for inflammatory cells, neovascularization, muscular layer continuity, and PNL presence, the differences 486
In conclusion, we observed a positive influence of vinpocetine, similar to that of pentoxifylline, over healing of ischemic colonic anastomosis.
REFERENCES 1. Schilling JA. Wound healing. Surg Clin North Am 1976;56:859-74. 2. Carrico TJ, Mehrhof AI Jr, Cohen IK. Biology of wound healing. Surg Clin North Am 1984;64:721-33. 3. Kirsner RS, Eaglstein WH. The wound healing process. Dermatol Clin 1993;11:629-40. 4. Inan A, Sen M, Sürgit O, Ergin M, Bozer M. Effects of the histamine H2 receptor antagonist famotidine on the healing of colonic anastomosis in rats. Clinics (Sao Paulo) 2009;64:567-70. 5. Guzel S, Sunamak O, AS A, Celik V, Ferahman M, Nuri MM, et al. Effects of hyperbaric oxygen and Pgg-glucan on ischemic colon anastomosis. World J Gastroenterol 2006;12:1421-5. 6. Altinli E, Saribeyoğlu K, Karahasanoğlu T, Hamzaoğlu I, Aydoğan F, Karabiçak I, et al. Are clips useful in the surgical repair of colonic perforations? Acta Chir Belg 2005;105:4102. 7. Stoop MJ, Dirksen R, Hendriks T. Advanced age alone does not suppress anastomotic healing in the intestine. Surgery 1996;119:15-9. 8. Uluocak K. Kolon anastomoz yetmezliklerinin sebepleri ve önlenmesi. Dirim 1992;67:34-42. 9. Parra-Membrives P, Ruiz-Luque V, Escudero-Severín C, Aguilar-Luque J, Méndez-García V. Effect of pentoxifylline on the healing of ischemic colorectal anastomoses. Dis Colon Rectum 2007;50:369-75. 10. Erdoğan C, Erdem A, Akıncı S.B, Dikmeoğlu N, Başgül E, Balkancı, Aypar Ü. Midazolamın sıçanlarda eritrosit deformabilitesi ve plazma viskositesi üzerine etkisi. Anestezi Dergisi 2005;13:205-8. 11. Garcia JC, Arias C, Garcia C, Vara E, Balibrea JL. Modificacio´n de los mediadores inflamatorios en isquemiareperfusio´n intestinal en unmodelo de diabetes tipo II. Cir Esp 2002;71:276-86. [Abstract] 12. Moran M, Ozmen MM, Duzgun AP, Gok R, Renda N, Seckin S, et al. The effect of erythropoietin on healing of obstructive vs nonobstructive left colonic anastomosis: an experimental study. World J Emerg Surg 2007;2:13. doi:10.1186/17497922-2-13. 13. Thornton FJ, Barbul A. Healing in the gastrointestinal tract. Surg Clin North Am 1997;77:549-73. 14. Cetinkaya Z, Esen K, Ozercan IH, Ustundag B, Ayten R, Aygen E. The effect of Bosentan on healing of colonic anastoKasım - October 2011
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mosis. World J Emerg Surg 2006;1:37. 15. Kılıç Y, Avar B, Kamalı S, Güven H, Sungur F. Kolon anastomozlarında stapler ve el dikiştekniklerinin kısa süreli komplikasyonlar açısından karşılaştırılması. Kolon Rektum Hast Derg 1991;1:45-50. 16. Cağlikülekçi M, Ozçay N, Oruğ T, Aydoğ G, Renda N, Atalay F. The effect of recombinant growth hormone on intestinal anastomotic wound healing in rats with obstructive jaundice. Turk J Gastroenterol 2002;13:17-23. 17. Karahasanoglu T, Altinli E, Hamzaoglu I, Paksoy M, Yeşildere T, Alemdaroglu K. Effect of growth hormone treat-
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ment on the healing of left colonic anastomoses in proteinmalnourished rats. Br J Surg 1998;85:931-3. 18. Benacerraf B, Sebestyen MM. Effect of bacterial endotoxins on the reticuloendothelial system. Fed Proc 1957;16:860-7. 19. Abdel Salam OM, Oraby FH, Hassan NS. Vinpocetine ameliorates acute hepatic damage caused by administration of carbon tetrachloride in rats. Acta Biol Hung 2007;58:411-9. 20. Abdel Salam OM, Baiuomy AR, El-Shenawy SM, Hassan NS. Effect of pentoxifylline on hepatic injury caused in the rat by the administration of carbon tetrachloride or acetaminophen. Pharmacol Rep 2005;57:596-603.
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Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):488-492
Original Article
Klinik Çalışma doi: 10.5505/tjtes.2011.89914
Our new stethoscope in the Emergency Department: Handheld ultrasound Acil serviste yeni steteskopumuz: El ultrasonu Figen COŞKUN,1 Emine AKINCI,1 Mehmet Ali CEYHAN,2 Havva ŞAHİN KAVAKLI3
BACKGROUND
AMAÇ
The concept of Focused Assessment with Ultrasound for Trauma (FAST), which was introduced by Rozycki et al. in 1996, has started a new era in the management of trauma patients. Today, Advanced Trauma Life Support (ATLS) suggests bedside ultrasonography (USG) evaluation of trauma patients. We aimed to investigate the usability and the reliability of handheld ultrasound (Vscan) in determining free fluid during the initial evaluation of trauma patients. METHODS
1996 yılında Rozycki ve arkadaşları tarafından önerilen Focused Assesment with Ultrasound for Trauma (FAST) kavramıyla travma hastalarına yaklaşımda yeni bir dönem başlamıştır. Günümüzde travma hastalarında yatak başı ultrasonografi (USG) değerlendirilmesi Advanced Trauma Life Support (ATLS) içine dahil edilmiştir. Bu çalışmada, acil servise başvuran travma hastalarının ilk değerlendirilmesinde el ultrasonunun (Vscan) karıniçi serbest sıvı varlığının saptanmasında kullanılabilirliğini ve güvenilirliğini araştırmayı amaçladık.
This was a multi-center, prospective study involving multiple trauma patients who presented to three hospital emergency departments (EDs). FAST was completed using Vscan by an emergency physician and an abdominal USG was performed by a radiologist on all patients. Results of Vscan, abdominal USG and other radiological studies, if performed, were compared.
GEREÇ VE YÖNTEM
Bu çalışma, çok merkezli ve prospektiftir. Üç eğitim hastanesinin acil servisine başvuran çoklu travma hastaları değerlendirildi. Acil tıp uzmanı tarafından Vscan aracılığı ile FAST ve radyoloji uzmanı tarafından karın USG’si yapıldı. Vscan sonuçları, karın USG sonuçları ve yapıldıysa diğer görüntüleme yöntemi ile karşılaştırıldı.
RESULTS
BULGULAR
A total of 216 patients were included in the study. Of those, 203 had negative Vscan results, while 13 had positive results. When USG performed by a radiologist was considered as the gold standard, Vscan sensitivity for FAST was 88.9%, specificity was 97.6%, negative predictive value was 99.5%, and positive predictive value was 61.5% in our study.
Çalışmaya 216 hasta alınmış olup, 203 hastada Vscan ile yapılan FAST negatifken, 13 hastada pozitifti. Radyoloji uzmanı tarafından yapılan USG altın standart olarak kabul edildiğinde, FAST’in duyarlılığı %88,9, özgüllüğü %97,6, negatif tahmini değeri 99,5, pozitif tahmini değeri ise %61,5 olarak saptandı.
CONCLUSION
SONUÇ
Vscan, as the smallest portable imaging device, seems to have a promising future as an indispensable gadget, equal to stethoscopes, in evaluating trauma and other critical patients.
Taşınabilir görüntüleme cihazlarının en küçüğü olan Vscan acil serviste gerek travma hastaları gerekse kritik hasta değerlendirilmesi sırasında boynumuzda taşıyabildiğimiz steteskopumuz kadar vazgeçilmez bir araç olacaktır.
Key Words: Emergency department; FAST; handheld ultrasound; Vscan.
Anahtar Sözcükler: Acil servis; FAST; el ultrasonu; Vscan.
1 Ankara Training and Research Hospital, Ankara; Ankara Numune Training and Research Hospital, Ankara; 3 Ankara Atatürk Training and Research Hospital, Ankara, Turkey. 2
1 Ankara Eğitim ve Araştırma Hastanesi, Ankara; Ankara Numune Eğitim ve Araştırma Hastanesi, Ankara; 3 Ankara Atatürk Eğitim ve Araştırma Hastanesi, Ankara.
2
Correspondence (İletişim): Emine Akıncı, M.D. Şenlik Mah., Baldıran Sok., No: 40/18, Keçiören 06310 Ankara. Tel: +90 - 312 - 355 22 19 e-mail (e-posta): emineakinci@yahoo.com
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Handheld ultrasound
When managing trauma patients, a rapid diagnosis and the most appropriate treatment are crucial. For abdominal trauma patients, computed tomography (CT) and ultrasonography (USG) are the two major diagnostic tools used to determine the need for laparotomy. Bedside applicability, speed, cost-effectiveness, and high sensitivity for determining intraabdominal free fluid make USG a tool-of-choice for the evaluation of unstable trauma patients.[1] The concept of Focused Assessment with Ultrasound for Trauma (FAST), which was introduced by Rozycki et al.[2] in 1996, began a new era in the management of trauma patients. Today, bedside USG FAST evaluation of trauma patients is recommended in the Advanced Trauma Life Support (ATLS) guidelines. We used Vscan as the handheld USG. Vscan is a portable imaging device, which can be used easily in emergency departments (EDs). It weighs 320 grams and measures 13x7x3 cm and allows abdominal, cardiac and obstetric evaluation of patients. This study reports on the usability and reliability of handheld ultrasound (Vscan) in determining the existence of free intra-abdominal fluid during the initial evaluation of trauma patients in EDs by emergency physicians.
MATERIALS AND METHODS This research was undertaken at three hospitals. The sample was selected from multiple trauma patients who presented at Ankara Training and Research Hospital, Ankara Numune Training and Research Hospital or Ankara Atatürk Training and Research Hospital EDs in Turkey, from June 1 to June 30, 2010. Only the trauma patients who were evaluated to have abdominal trauma findings and who agreed to participate were included in the study. Patients under 16 years of age, pregnant patients and those without abdominal trauma were excluded from the study.
ing and Research Hospital and Siemens Sonoline G4 at Ankara Atatürk Training and Research Hospital. The time between two evaluations averaged 10 minutes. All of those EDs see 500 to 600 patients per day on average. Even though the numbers vary between the weekdays and weekends, the average number of trauma patients seen daily in each of those EDs is around 100. Radiologists were residents with one or more years of practical experience and an average of 20 abdominal USG examinations of trauma patients per day. All participating radiologists average six ED shifts per month. The results of the Vscan, ��������������������������� abdominal������������������ USG and other radiological studies, if performed, were compared. The demographic information, physical examination and FAST findings were recorded in standardized forms. Vscan is a pocket-sized visualization tool providing black and white anatomic and color-coded blood flow images in real-time. The images are generated based on ultrasound technology. Harmonic imaging, B-mode and color-flow are the standard modes of Vscan. The device has a battery that provides one-hour uninterrupted scanning. Vscan allows longitudinal measurement and can scan to a maximum depth of 24 cm (Fig. 1). Statistical Analysis Kappa statistics were used in the comparison of the FAST examination and radiology results. Pearson’s chi-square and Fisher’s exact tests were used for the analysis of the differences. The area under the curve (AUC) value and its confidence interval (CI) were calculated for the performance evaluation of FAST diagnosis. The Mann-Whitney U test was used for the analysis of the time differences between positive and negative FAST outcomes and Vscan times. Calculated p values less than 0.05 were considered as statistically significant. All data were evaluated using MedCalc 11.2.1 software.
Approval for the study was obtained from the Local Ethics Committee. All of the EDs in the participating hospitals are equipped with radiological imaging tools and X-ray equipment. Furthermore, the USG and CT devices are within easy reach in the ED. All the emergency physicians who used Vscan during the study underwent a 4-hour didactic training about the properties of the device and FAST techniques, as well as 4 hours of manikin and real-time patient evaluation training prior to the study. All patients were evaluated according to the ATLS principles. FAST was completed using Vscan by an emergency physician. All patients were then evaluated by a radiologist in the radiology examination room. The ultrasound machines used by the radiologists were Toshiba SSA660A at Ankara Training and Research Hospital, Toshiba Nemio 10 at Ankara Numune TrainCilt - Vol. 17 Sayı - No. 6
Fig. 1. Vscan picture. (Color figure can be viewed in the online issue, which is available at www.tjtes.org)
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Fig. 3. Receiver Operating Characteristic (ROC) curve analysis for accuracy of diagnosis using FAST. (Color figure can be viewed in the online issue, which is available at www.tjtes.org)
Fig. 2. Free fluid (black stripe, indicated by red arrows) within Morison’s pouch.
RESULTS A total of 216 patients were included in the study, of which 110 (51%) had been involved in a motor vehicle accident, 43 (20%) had fallen from height, 41 (19%) had been the victim of assault, and 22 (10%) had work-related injuries. Two hundred and three patients had negative Vscan results, while 13 had positive results (Table 1) (Fig. 2). The average FAST time for the emergency physicians was 2.5 minutes, and radiologists completed the FAST exam in 2 minutes. A statistically significant relevance was noted when USG performed by a radiologist was considered as the gold standard (kappa=0.713; p<0.001). FAST sensitivity was calculated as 88.9% (95 CI%: 51.8%-99.7%), specificity as 97.6% (95% CI: 94.5%-99.2%) and AUC value as 0.93 (95% CI: 0.89-0.96; p<0.001). The negative predictive value for FAST was calculated as 99.5% and the positive predictive value as 61.5%. Fig. 3 shows the ROC (receiver operating characteristics) analysis for the accuracy of diagnosis using FAST.
We found a statistically significant correlation between the results of FAST performed by emergency physicians using Vscan and the results of the abdominal USG performed by radiologists (p<0.001) (Table 2). Five patients in the study had positive Vscan FAST results but negative USG results. The abdominal CT proved to be negative for intraabdominal injuries in two of those patients and they were discharged following an observation period. Two patients had intraabdominal solid organ injuries detected by abdominal CT. They were monitored conservatively and were discharged after 6.8 days without the need for surgical intervention. The last of the five patients were unstable upon presentation and underwent emergency splenectomy for ruptured spleen. One patient had a negative Vscan FAST result but a positive USG. An abdominal CT was performed to finalize the diagnosis and the result was negative, confirming the Vscan result. This patient was discharged following observation for 24 hours (Table 2).
DISCUSSION The development of diagnostic ultrasound devices accelerated in the ‘90s and portable, laptop-like small and light devices began to be produced. These
Table 1. Correlation between FAST examination results and USG examination results FAST – FAST + Total 490
Abdominal USG –
Abdominal USG +
Fisher’s Exact Test p value
202 (97.6%) 5 (2.4%) 207 (100%)
1 (11.1%) 8 (88.9%) 9 (100%)
<0.001
Kasım - November 2011
Handheld ultrasound
Table 2. Crosstabs FAST with Vscan by emergency physicians USG FAST negative FAST positive Total
Count % within FAST % within Count % within FAST % within
Normal
Pathology
Total
202 99.5% 97.6% 5 38.5% 2.4% 207 95.8% 100.0%
1 .5% 11.1% 8 61.5% 88.9% 9 4.2% 100.0%
203 100.0% 94.0% 13 100.0% 6.0% 216 100.0% 100.0%
*USG performed by a radiologist using FAST.
portable ultrasound devices allowed users to perform FAST, echocardiography, obstetric USG, and Doppler evaluations on patients.[3-5] These technological advancements allowed medical practitioners other than radiologists, as well as nurses and paramedics, to perform in- and out-of-hospital (ambulance, helicopter, military applications, disaster triage, etc.) USG exams. [6,7] The current literature reveals a large number of articles on the feasibility and areas of use of portable ultrasound devices including the bedside USG evaluation of trauma patients in an ED. Trauma is the leading cause of mortality in young people worldwide.[8] The majority of trauma-related deaths occur during the first hour following the trauma, which is known as the “Golden Hour”. In order to reduce deaths during the golden hour, rapid and accurate interventions during the pre-hospital, triage and early ED phases should be provided.[8] Abdominal injuries are the third deadliest injuries following head and chest trauma.[9] USG has proven useful in the management of abdominal trauma patients over the past 30 years. The introduction of FAST in the ’90s has made USG a popular tool, especially in the ED.[9,10] In Turkey, in the ED, the FAST examination is administered to trauma patients simultaneously with the ATLS care. There is ample support in the literature for use of FAST in trauma patients. Smith et al.,[11] in 2010, stated that abdominal assessment with FAST was a time-saving procedure for definitive treatment and other advanced examinations in developing countries. In another study of 500 patients, McGahan et al.,[12] in 1997, compared USG findings with laparotomy and abdominal CT in hemoperitoneum and organ injuries. They found a USG sensitivity of 63% and specificity of 95% in detecting these particular injuries. Nelson et al.,[3,13] in their 2008 study, summarized studies on outof-hospital uses of portable USG devices. They determined that portable USG devices are not only useful for FAST, but can also be successfully used to determine cardiac activity and pericardial tamponade by emergency medical services (EMS) providers in their Cilt - Vol. 17 Sayı - No. 6
ACLS algorithms, in Germany and Italy. As the smallest portable imaging device, Vscan can image cardiac activity as well as abdominal structures. We believe that Vscan will prove useful not only in performing FAST and abdominal evaluations in the EDs, but also in evaluating and observing critical patients. We have not found any publication related to Vscan in the literature; however, this device has been made available only recently. Vscan is a handheld device and enables personalized use at the point of care. It can be used by physicians, as well as possibly by nurses, paramedics or even medical students under the supervision of a physician. It can be integrated easily into physical examinations, allowing physicians to add a visual inspection of the body. The clinical applications of Vscan include cardiac, abdominal, urinary, bladder, obstetrics and gynecology, thoracic/pleural fluid, and motion detection. In conclusion, Vscan, as the smallest portable imaging device, seems to have a promising future as an indispensable gadget which, like the stethoscope, could be used by all medical practitioners and assist in the evaluation of trauma and other critical patients in the ED. Disclosure The authors declare that they have no actual or potential competing financial interests.
REFERENCES 1. Rose JS. Ultrasound in abdominal trauma. Emerg Med Clin N Am 2004;22:581-99. 2. Rozycki GS, Ochsner MG, Schmidt JA, Frankel HL, Davis TP, Wang D, et al. A prospective study of surgeon-performed ultrasound as the primary adjuvant modality for injured patient assessment. J Trauma 1995;39:492-8; discussion 498500. 3. Nelson BP, Chason K. Use of ultrasound by emergency medical services: a review. Int J Emerg Med 2008;1:253-9. 4. Kirkpatrick AW, Sirois M, Laupland KB, Goldstein L, Brown DR, Simons RK, et al. Prospective evaluation of hand-held focused abdominal sonography for trauma (FAST) in blunt 491
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abdominal trauma. Can J Surg 2005;48:453-60. 5. Rugolotto M, Hu BS, Liang DH, Schnittger I. Rapid assessment of cardiac anatomy and function with a new hand-carried ultrasound device (OptiGo): a comparison with standard echocardiography. Eur J Echocardiogr 2001;2:262-9. 6. Lapostolle F, Petrovic T, Lenoir G, Catineau J, Galinski M, Metzger J, et al. Usefulness of hand-held ultrasound devices in out-of-hospital diagnosis performed by emergency physicians. Am J Emerg Med 2006;24:237-42. 7. Walcher F, Weinlich M, Conrad G, Schweigkofler U, Breitkreutz R, Kirschning T, et al. Prehospital ultrasound imaging improves management of abdominal trauma. Br J Surg 2006;93:238-42. 8. Davis JH, Pruitt JH, Pruitt BA Jr. History. In: Mattox KL, Feliciano DV, Moore EE, editors. Trauma. 4th ed., New York: McGraw Hill; 2000. p. 3-19.
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9. Tsui CL, Fung HT, Chung KL, Kam CW. Focused abdominal sonography for trauma in the emergency department for blunt abdominal trauma. Int J Emerg Med 2008;1:183-7. 10. Chung KL, Kam CW. Emergency ultrasonography in a patient of blunt traumatic haemoperitoneum. Hong Kong Journal Emerg Med 1995;2:104-7. 11. Smith ZA, Postma N, Wood D. FAST scanning in the developing world emergency department. S Afr Med J 2010;100:105-8. 12. McGahan JP, Rose J, Coates TL, Wisner DH, Newberry P. Use of ultrasonography in the patient with acute abdominal trauma. J Ultrasound Med 1997;16:653-62 13. Heegaard W, Plummer D, Dries D, Frascone RJ, Pippert G, Steel D, et al. Ultrasound for the air medical clinician. Air Med J 2004;23:20-3.
Kas覺m - November 2011
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):493-496
Original Article
Klinik Çalışma doi: 10.5505/tjtes.2011.40225
Traumatic abdominal wall hernia Travmatik karın duvarı hernisi Sanjay GUPTA, Usha DALAL, Rajeev SHARMA, Ashwani DALAL, Ashok Kumar ATTRI
BACKGROUND
AMAÇ
Traumatic abdominal wall hernia (TAWH) is uncommonly encountered despite the high prevalence of blunt abdominal trauma. The diagnosis is often difficult because of its varied presentation along with lack of awareness of this entity.
Künt karın travmasının yüksek prevalansına karşın, travmatik karın duvarı hernisi (TKDH) ile nadiren karşılaşılmaktadır. Değişken prezantasyonu ile birlikte bu antiteye ilişkin farkındalığın azlığı nedeniyle tanısı güçlükle konulmaktadır.
METHODS
The case files of all patients with TAWH who were operated at our hospital were retrospectively reviewed and analyzed. RESULTS
A total of 11 patients with TAWH were analyzed (8 males, 3 females). The clinical presentation was varied, with a palpable defect and a reducible swelling (6 patients), localized area of irreducible swelling (3 patients), surgical emphysema (2 patients), and cellulitis/abscess formation (2 patients). All of these patients were operated within 24 hours of hospital admission. Except for the 3 patients who presented late, there was a favorable outcome in all the others. The cause of mortality was septicemia, possibly due to incarceration of bowel in the defect leading to strangulation and perforation.
GEREÇ VE YÖNTEM
Hastanemizde ameliyat edilen TKDH’li bütün hastaların dosyaları, retrospektif olarak gözden geçirildi ve analiz edildi. BULGULAR
TKDH’li toplam 11 hasta değerlendirildi (8 erkek, 3 kadın). Klinik tablo çeşitliydi; palpe edilebilen bir defekt ve redükte edilebilir şişlik (n=6), redükte edilemeyen şişliğe ilişkin lokalize alan (n=3), cerrahi amfizem (n=2) ve sellülit/apse formasyonu (n=2). Hastaların tamamı, hastaneye yatırılmalarından itibaren 24 saat içinde ameliyat edildi. Geç başvuran 3 hasta dışında kalanlarda, sonuç olumlu idi. Mortalite nedeni muhtemelen bağırsağın boğulması ile gelişen perforasyona bağlı septisemi idi. SONUÇ
CONCLUSION
TAWH, although uncommon, is associated with significant morbidity and mortality when there is a delay in diagnosis and intervention. Early intervention leads to a significantly better outcome.
Nadir olmakla birlikte TKDH, tanı ve müdahalede bir gecikme olması durumunda anlamlı morbidite ve mortalite ile birliktedir. Erken girişim sonucu anlamlı olarak iyileştirmektedir.
Key Words: Abdominal wall; blunt trauma; hernia.
Anahtar Sözcükler: Karın duvarı; künt travma; herni.
Although abdominal trauma is frequently encountered, abdominal wall herniation consequent to such trauma is a rare occurrence as compared to injury to the intraabdominal organs. These herniae can range from small defects to disruption of most of the anterior abdominal wall, and at times can be associated with significant internal injuries that can divert the attention of the clinician.
It was Selby[1] who reported the first such case of traumatic abdominal wall hernia (TAWH) in 1906, but even after so many years, the diagnosis of TAWH is often delayed or missed completely. The reported prevalence among trauma patients, even at dedicated trauma centers with the best of facilities, is less than 1%.[2] In the present communication, an effort was made to highlight the clinical presentation of TAWH
Department of Surgery, Government Medical College and Hospital, Chandigarh, India.
Devlet Tıp Koleji ve Hastanesi, Genel Cerrahi Anabilim Dalı, Chandigarh, Hindistan.
Correspondence (İletişim): Sanjay Gupta, M.D. 1221, Sector 32b, 160030 Chandigarh, India. Tel: +91 - 172 - 2661213 e-mail (e-posta): sandiv99@yahoo.co.uk
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and to determine the factors that can affect the outcome of these patients.
MATERIALS AND METHODS The case records of all trauma patients admitted to our emergency department over a period of nearly six years (December 2002 to August 2009) were retrospectively reviewed. The patients who were diagnosed as TAWH were identified and their records analyzed for the mode of injury, preoperative clinical features, time elapsed between injury and surgery, site of TAWH, associated injury, and outcome. RESULTS Since 2002, when our first patient with TAWH was diagnosed[3] (reported in 2004), we identified 10 more such cases, for a total of 11 cases of TAWH seen in our Institute. The details of these patients are tabulated in Table 1. Of these 11 patients, 8 were males and 3 were females, with a mean age of 42.4 years (range: 12-70 years). Eight of them sustained injury by blunt trauma, and 3 were involved in a road traffic accident. The site of injury was the right lower quadrant (5 patients), left lower quadrant (5 patients) and left upper quadrant (1 patient). None of these patients gave a history of any previous reducible abdominal wall swelling. A palpable defect was present in the anterior abdominal wall with a reducible swelling in 6 patients; in 3, there was an irreducible swelling. Two had surgical emphysema along the site of injury, and 2 had cellulitis around the injury site. All the patients were operated within 24 hours of admission, but due to delayed presentation, 3 patients were operated on the 4th and 5th days following the injury. The decision to operate was taken on the ba-
Fig. 1. Contrast-enhanced computer tomographic (CECT) film of a patient showing the defect in the muscle layer above the left iliac crest, with bowel loop seen in the defect.
sis of (i) clinical features, i.e. palpable defect in 4 patients, reducible swelling in 2 patients; (ii) radiological features, i.e. presence of free air under the dome of the diaphragm on X-ray in 1 patient and computerized tomography (CT) scan suggesting TAWH in 2 patients (Fig. 1); and (iii) on the basis of intervention (in 2 patients), i.e. aspiration of fecal fluid and presence of fecal material upon incision in patients who presented with localized area of cellulitis. Most of these patients were explored through a midline incision. Perioperatively, defects of variable size (range: 6-15 cm) were seen, with a complete disruption of all layers of muscle (Fig. 2). The skin, however, was intact in all these patients. The defect was closed primarily or in layers after debridement of surrounding
Table 1. Traumatic abdominal wall hernia - patient data No Age Mode of injury (yrs)
Location Clinical presentation of TAWH
Time of surgical Associated injury intervention
1 2 3 4
60 22 12 60
Fall of ceiling MVA MVA Hit by Bullock cart
LLQ LLQ RLQ LLQ
Palpable defect with visible peristalsis Palpable defect Palpable defect Cellulitic changes left flank
<24 hrs <24 hrs <24 hrs 4th day
5
70
Hit by cart
RLQ
6 7
65 45
Fall on blunt object Fall on blunt object
RLQ RLQ
8
30
Hit by cart
LUQ
Reducible swelling with localized crepitation Irreducible swelling Swelling with localized crepitation Abscess formation
9 10 11
40 35 28
Hit by cow MVA Fall on blunt object from height
RLQ LLQ LLQ
Tender irreducible swelling Reducible swelling Generalized tenderness with palpable defect
Outcome Died due to MI Discharged well Discharged well Died due to sepsis
5th day
None Transected descending colon Liver laceration Perforated sigmoid colon lying in subcutaneous plane Caecal perforation
<24 hrs <24 hrs
None Perforated bowel
Discharged well Discharged well
3rd day
Perforated splenic flexure of colon present in the defect None None Small bowel mesenteric injury
Died due to sepsis
<24 hrs <24 hrs <24 hrs
Died due to sepsis
Discharged well Discharged well Discharged well
TAWH: Traumatic abdominal wall hernia; MVA: Motor vehicle accident; LLQ: Left lower quadrant; RLQ: Right lower quadrant; LUQ: Left upper quadrant.
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Traumatic abdominal wall hernia
region of the abdominal wall, but is most commonly seen in the lower quadrants, just lateral to the rectus sheath. A possible explanation for this is the absence of a posterior rectus sheath in this region.
Fig. 2. Perioperative photograph showing the defect in the muscle layer, with transected descending colon. (Color figure can be viewed in the online issue, which is available at www.tjtes.org)
devitalized tissue. However, in 1 case where primary closure was not possible, a fascia lata graft was taken from the thigh to close the wound. No prosthetic mesh was used in any of the other patients. Any associated bowel injury was managed by primary repair or exteriorization depending on the time of presentation, fecal contamination and condition of the patient. Four patients died in the postoperative period: 1 due to myocardial infarction and the other 3 due to septicemia (all 3 had presented late after sustaining injury).
DISCUSSION Traumatic abdominal wall hernia (TAWH) is one of uncommon injuries seen in trauma patients. Various criteria have been laid down from time to time to define TAWH, but of prime importance is the presence of intact skin at the site of herniation, and the absence of any hernia at the site prior to the trauma. [4,5] TAWH usually occurs as result of a direct blow to the abdominal wall, which results in disruption of the muscle layers, but the skin remains intact since the force was not sufficient enough to penetrate the skin. A tangential shearing force associated with increase in abdominal pressure has also been hypothesized to be responsible for muscle or fascial disruption.[6] Wood et al.[7] categorized TAWH into three categories: small defects caused by impact against the blunt objects, e.g. handle bars (also known as handle bar hernia); larger defects sustained during motor vehicle accidents; and, rarely, intraabdominal bowel herniation that is seen associated with deceleration injury. However, the force of the impact is also important in deciding the size of the defect, as all of our patients had sizable defect, but only three of them were involved in a motor vehicle accident. TAWH can occur in any Cilt - Vol. 17 SayÄą - No. 6
Disruption of abdominal musculature and associated intraabdominal injury may not be evident on physical examination, as these patients are often difficult to examine and have a varied clinical presentation. Such defects may be palpable, with a reducible or irreducible swelling, or may be present over a large area with visible peristalsis or surgical emphysema. Delayed presentation can further worsen the picture since incarceration of a gut loop in the defect with subsequent perforation or strangulation may be â&#x20AC;&#x2DC;containedâ&#x20AC;&#x2122;, and may present with minimal signs of peritonitis. In such cases, a plain X-ray of the abdomen and/or a CT scan may help to establish the diagnosis. A lateral or oblique X-ray film may show a gas-filled loop outside the abdominal cavity. It may also help to reveal an associated injury such as pneumoperitoneum or diaphragmatic herniation. CT of the abdomen has been found to be more useful in defining the anatomy of the disrupted muscles, differentiating swelling from the hematoma and evaluating the associated injuries.[8] In our series, six patients were diagnosed clinically, on the basis of the presence of a palpable defect or reducible swelling. In two patients, the diagnosis was established on CT scan of the abdomen, while in the rest, the diagnosis was made intraoperatively (1 operated for pneumoperitoneum on X-ray and 2 for the presence of fecal matter at local site). The mortality associated with isolated TAWH is rare. It is usually the associated injury that can lead to mortality in such patients. A similar observation was made in the present series, as three patients died of septicemia subsequent to bowel injury. The exact incidence of mortality associated with TAWH cannot be commented upon as most of the existing literature is in the form of case reports. All patients who are diagnosed with TAWH should be explored as early as possible because of chances of early as well as late incarceration of the bowel in the defect, leading to the subsequent perforation or strangulation. This has been well documented to have a worse effect on the outcome. Early exploration, preferably through a midline incision, also helps to deal with other associated injuries, which have been reported in up to 100% of cases. In addition, mesenteric and bowel injuries that are liable to be missed on CT scan can also be managed well in time.[9] The surgical treatment includes primary closure of the defect in layers, with debridement of any surrounding devitalized tissue. Though we did not require the use of a prosthetic mesh for the closure of the defect, 495
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it is to be considered only in those cases where there is no hollow viscus injury or where a tension-free repair of the tissue is not possible.[10] The mesh has also been used by some as an onlay graft over the sutured repair to prevent recurrence. However, the exact rate of recurrence with sutured or mesh repair is not known. The use of laparoscopy has also been advocated by some, especially in hemodynamically stable patients and with equivocal CT scan. This has been found to be helpful in preventing negative laparotomies, in diagnosing any associated injury, and in planning the incision. Laparoscopic repair of such injuries has also been reported.[11] To conclude, TAWH, though rare in trauma patients, has been found to be associated with significant mortality and morbidity. A high index of suspicion is required for the diagnosis of this condition. Apart from associated injuries, a delay in the diagnosis and intervention can significantly affect the outcome of these patients.
REFERENCES 1. Selby CD. Direct abdominal hernia of traumatic origin. JAMA 1906;47:1485. 2. Netto FA, Hamilton P, Rizoli SB, Nascimento B Jr,
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Brenneman FD, Tien H, et al. Traumatic abdominal wall hernia: epidemiology and clinical implications. J Trauma 2006;61:1058-61. 3. Singh R, Kaushik R, Attri AK. Traumatic abdominal wall hernia. Yonsei Med J 2004;45:552-4. 4. Mc Whorter GL. Inguinal hernia due to direct trauma: technique of operation. Am J Surg 1939;45:316-19. 5. Holland JH. Hernia from the compensation insurance standpoint. NEJM 1933;209:579-85. 6. Guly HR, Stewart IP. Traumatic hernia. J Trauma 1983;23:250-2. 7. Wood RJ, Ney AL, Bubrick MP. Traumatic abdominal hernia: a case report and review of the literature. Am Surg 1988;54:648-51. 8. Hickey NA, Ryan MF, Hamilton PA, Bloom C, Murphy JP, Brenneman F. Computed tomography of traumatic abdominal wall hernia and associated deceleration injuries. Can Assoc Radiol J 2002;53:153-9. 9. Brenneman FD, Boulanger BR, Antonyshyn O. Surgical management of abdominal wall disruption after blunt trauma. J Trauma 1995;39:539-44. 10. Drago SP, Nuzzo M, Grassi GB. Traumatic ventral hernia: report of a case, with special reference to surgical treatment. Surg Today 1999;29:1111-4. 11. Aucar JA, Biggers B, Silliman WR, Losanoff JE. Traumatic abdominal wall hernia: same-admission laparoscopic repair. Surg Laparosc Endosc Percutan Tech 2004;14:98-100.
Kas覺m - November 2011
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):497-503
Original Article
Klinik Çalışma doi: 10.5505/tjtes.2011.30643
The analgesic effect of three different doses of nitroglycerine when added to lidocaine for intravenous regional anesthesia in trauma patients Travma hastalarında intravenöz rejyonel anestezi için lidokaine eklenmesi durumunda üç farklı nitrogliserin dozunun analjezik etkisi Azim HONARMAND, Mohammadreza SAFAVI, Abbas FATEMY BACKGROUND
AMAÇ
Nitroglycerine (NTG) has analgesic properties. The aim of the present study was to assess the analgesic effect of three different doses of NTG (200 µg, 300 µg and 400 µg) when added to lidocaine in intravenous regional anesthesia (IVRA) in trauma patients.
Nitrogliserin (NTG), analjezik özelliklere sahiptir. Mevcut çalışmanın amacı, travma hastalarında intravenöz rejyonel anestezide (IVRA) lidokain eklendikten sonra üç farklı NTG dozunun (200 µg, 300 µg ve 400 µg) analjezik etkisini değerlendirmektir.
METHODS
GEREÇ VE YÖNTEM
One hundred patients undergoing hand surgery were randomly allocated to four groups to receive 3 mg/kg 2% lidocaine diluted with saline to a total dose of 40 mL in the control group (Group LS, n = 25) or 200, 300, 400 µg NTG plus 3 mg/kg 2% lidocaine diluted with saline to a total dose of 40 mL in the NTG group (Groups LN1, LN2, LN3 respectively; n = 25 in each group). Before and after the tourniquet application, hemodynamic variables, tourniquet pain, sedation, and analgesic use were recorded.
El cerrahisi uygulanan 100 hasta rastgele dört gruba ayrıldı: Kontrol grubunda serum fizyolojik ile toplam 40 mL’lik bir doza dilüe edilen 3 mg/kg %2 lidokain (Grup LS, n=25) veya NTG grubunda serum fizyolojik ile toplam 40 mL’lik bir doza dilüe edilen 200, 300, 400 µg NTG + 3 mg/kg 2% lidokain (sırasıyla Grup LN1, Grup LN2, Grup LN3; her bir grupta n=25) uygulandı. Turnike uygulamasından önce ve sonra, hemodinamik değişkenler, turnike ağrısı, sedasyon ve kullanılan analjezik kullanımı kaydedildi.
RESULTS
BULGULAR
Sensory and motor block onset times were significantly shorter in the LN3 group compared with Groups LN1, LN2, and LS (p<0.05). Sensory and motor block recovery times were statistically prolonged in the LN3 group when compared with Groups LN1 and LS (p<0.05). Postoperative visual analogue scale (VAS) scores were significantly lower at 2, 4, 8, 12, and 24 hours after tourniquet release in Group LN3 compared with Group LS (p<0.05).
Duysal ve motor bloğun başlama zamanları, LN1, LN2 ve LS gruplarına göre LN3 grubunda anlamlı şekilde daha kısaydı (p<0,05). Duysal ve motor bloğun geriye dönme zamanları, LN1, LN2 ve LS gruplarına kıyasla LN3 grubunda anlamlı şekilde daha uzundu (p<0,05). Ameliyat sonrası vizüel analog skala (VAS) skorları, LS-grubuna kıyasla LN3 grubunda turnikenin gevşetilmesinden 2., 4., 8., 12. ve 24. saat sonra anlamlı şekilde daha düşüktü (p<0,05).
CONCLUSION
SONUÇ
The addition of 400 µg NTG to lidocaine in IVRA shortens the onset of sensory and motor block in trauma patients and improves the quality of anesthesia and perioperative analgesia better than the addition of 200 µg or 300 µg NTG, without causing side effects.
IVRA’da lidokaine 400 µg NTG’nin eklenmesi, 200 µg veya 300 µg NTG’nin eklenmesine göre, travma hastalarında yan etkilere yol açmaksızın, duysal ve motor bloğun başlama zamanını kısaltır, anestezi kalitesini ve perioperatif analjeziyi artırır.
Key Words: Anesthetic techniques; lidocaine; nitroglycerin; tourniquet pain; trauma patients.
Anahtar Sözcükler: Anestetik teknikler; lidokain; nitrogliserin; turnike ağrısı; travma hastaları.
Anesthesiology and Critical Care Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
İsfahan Tıbbi Bilimler Üniversitesi, Anesteziyoloji ve Yoğun Bakım Araştırma Merkezi, İsfahan, İran.
Correspondence (İletişim): Mohammadreza Safavi, M.D. Department of Anesthesiology and Intensive Care, Isfahan University of Medical Sciences, Isfahan, Iran. Tel: +98 - 913 - 3152416 e-mail (e-posta): safavi@med.mui.ac.ir
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The majority of patients with trauma have tendon rupture of the hands or feet. Furthermore, there are crush injuries in the hands and feet that require orthopedic surgeries. Relieving postoperative pain is an important issue that must be considered. Intravenous regional anesthesia (IVRA) is a technically simple, reliable and cost-effective method of regional anesthesia for short operative procedures of the extremities performed on an ambulatory basis in trauma patients.[1,2] IVRA has disadvantages that include local anesthetic (LA) toxicity, slow-onset poor muscle relaxation, tourniquet pain, and the inability to provide prolonged postoperative analgesia.[1,3] Different additives such as opioids, tramadol, nonsteroidal antiinflammatory drugs, dexmedetomidine, and muscle relaxant have been combined with LAs to improve block quality, prolong post-deflation analgesia and decrease tourniquet pain.[1,3,4] Sen and colleagues[5] showed that the addition of 200 µg nitroglycerine (NTG) to lidocaine for IVRA improves sensory and motor block, tourniquet pain and postoperative analgesia without side effects. They emphasized that more studies with different doses must be performed to determine a relevant conclusion before the routine use of NTG. We thus designed the present study to evaluate the effect of three different doses of NTG (200 µg, 300 µg and 400 µg) on sensory and motor block onset and recovery time, the quality of anesthesia, intraoperative and postoperative hemodynamic variables, intraoperative and postoperative pain, tourniquet pain, and the side effects of NTG when added to lidocaine for IVRA in trauma patients.
MATERIALS AND METHODS One hundred American Society of Anesthesiologists (ASA) physical status I-II trauma patients, aged 18-65 years old, scheduled for elective hand or forearm surgery gave written informed consent to participate in this randomized prospective double-blind study, which was approved by the Ethics Committee of our institute. Exclusion criteria were patients with Reynaud disease or sickle cell anemia and those with a history of allergy to any drug used. After arrival of patients to the operating room, mean arterial pressure (MAP), peripheral oxygen saturation (SpO2) and heart rate (HR) were monitored. The operative arm was elevated for 3 minutes (min), after which it was exsanguinated with an Esmarch bandage. A 10 cm pneumatic padded doubletourniquet was then placed around the upper arm and the proximal cuff was inflated to 250 mmHg. Circulatory isolation of the arm was confirmed by skin blanching, absence of radial pulse and loss of pulse oximetry tracing in the ipsilateral index finger. 498
A randomization list was generated and identical syringes containing each drug were prepared by an anesthesiologist who was blinded to the study. A resident of anesthesiology blinded to the group and drug allocation applied the concealed syringes and recorded all data. IVRA was administered with 3 mg/kg 2% lidocaine diluted with saline to a total dose of 40 ml in the control group (Group LS, n=25) or with 200, 300, 400 µg NTG plus 3 mg/kg 2% lidocaine diluted with saline to a total dose of 40 ml in the NTG groups (Groups LN1, LN2, LN3, respectively; n=25 in each group). The solution was administered over 90 seconds (s) by an anesthesiologist blinded to the group assignments. The sensory block was assessed continuously at 30 s intervals by a pinprick performed with a 22 gauge short beveled needle. Motor function was evaluated by asking the patient to flex and extend his/her wrist and fingers, and complete motor block was noted when voluntary movement was impossible. Onset of sensory block (defined as the time elapsed from injection of the study drug to sensory block achieved in all dermatomes) and onset of motor block (defined as the time elapsed from injection of the study drug to complete motor block) were recorded. After completion of sensory and motor block, the distal cuff was inflated to 250 mmHg, and the proximal tourniquet was released. Then, the operation was started. MAP, HR, SpO2, visual analogue scale (VAS) scores (0 = no pain and 10 = worst pain imaginable), and degree of sedation (scale 1-5, 1 = completely awake, 2 = awake but drowsy, 3 = asleep but responsive to verbal commands, 4 = asleep but responsive to tactile stimulus, 5 = asleep and not responsive to any stimulus)[6] were recorded before and after tourniquet inflation at 1, 5, 10, 20, and 30 min after the injection of study drugs and at 1, 3, 5, 10, 15, and 30 min after tourniquet release. Hypotension (30% decrease from baseline value) was treated with IV ephedrine (5- to 10-mg bolus), bradycardia (30% decrease from baseline value) was treated with IV atropine 0.5 mg, and arterial oxygen saturation less than 90% was treated with O2 supplementation via a face mask. During the intraoperative period, boluses of fentanyl 1 µg/kg were administered for tourniquet pain treatment when VAS was more than 3 and total fentanyl consumption was recorded. The time elapsed after tourniquet inflation to the first patient request for fentanyl was also recorded. Tourniquet duration was defined as time from initial proximal tourniquet inflation until deflation of the distal tourniquet at the end of the operation. Data were recorded postoperatively at 2, 4, 8, 12, and 24 hours (h). Postoperatively, when VAS was more Kasım - November 2011
IV regional anesthesia and nitroglycerine in trauma patients
than 3, 75 mg of suppository diclofenac were administered and total diclofenac consumption was recorded. The time elapsed after tourniquet release to the first patient request for diclofenac was also recorded. All assessments were performed by an anesthesia resident blinded to the study.
group t-test with a 0.050 two-sided significance level.
After the operation, qualification of the operative condition such as disturbing movement of the arm and excessive bleeding was done by the surgeon, who was unaware of the group allocation, according to the following numeric scale: 0 = unsuccessful, 1 = poor, 2 = acceptable, and 3 = perfect.
Sedation score and the quality of the anesthesia between the four groups were compared using the Kruskal-Wallis test. Values are given as number (%), mean (SD) or median (range). A value of p<0.05 was considered statistically significant.
In addition, in the postoperative period, the patients were asked to qualify the operative conditions according to following numeric scale: 4 (excellent) = no complaint from patient, 3 (good) = minor complaint with no need for supplemental analgesics, 2 (moderate) = complaint that required supplemental analgesics, and 1 (unsuccessful) = patient given general anesthesia.[7] Sensory recovery time (defined as the time elapsed after tourniquet deflation up to recovery of pain in all dermatomes determined by pinprick test) was recorded. Motor block recovery time (defined as the time elapsed after tourniquet deflation up to movement of fingers) was also recorded. Throughout the study period, the patients were asked about any side effects (tinnitus, skin rash, gastric discomfort, vertigo, headache, nausea, and other side effects). Measurements and data recording in all patients were performed by the same person. The statistical analysis was done using the Statistical Package for the Social Sciences (SPSS) 15 statistical software package. Based on Sen et al.’s study,[5] a sample size of 25 in each group will have 80% power to detect a difference in the mean amount of intraoperative fentanyl requirement of 17.9 µg using a two-
Statistical comparisons for quantitative data were performed using two-way ANOVA, followed by unpaired t-tests with Bonferroni correction. Nominal or categorical data were analyzed and compared using the χ2 test.
RESULTS One hundred trauma patients were enrolled in the study. No patient was excluded from the study due to technical failure. There was no significant difference between the four groups with respect to the demographic data, type of surgical procedure and duration of surgery and tourniquet time (Table 1). There was no significant difference between the four groups in HR, MAP and SpO2 at any time interval during surgery or in the postoperative period. As Table 2 shows, sensory and motor block onset times were significantly shorter in Groups LN1, LN2 and LN3 compared with Group LS (p<0.05). Sensory and motor block recovery times were also statistically prolonged in these three groups (p<0.05) (Table 2). Sensory and motor block onset times were significantly shorter in Group LN3 compared with Groups LN1 and LN2 (p<0.05). Sensory and motor block recovery times were statistically prolonged in Group LN3 when compared with Group LN1 (p<0.05) (Table 2). The initial time for beginning tourniquet and postoperative pain was significantly longer in Groups LN1, LN2 and LN3 compared with Group LS (p<0.05) (Table 2). This variable was significantly longer in Group LN3 compared with Groups LN1 and LN2 (p<0.05). The to-
Table 1. Patient characteristics, type of surgery, and operation and tourniquet times according to groups Variable
Group LN1 (n=25)
Group LN2 (n=25)
Group LN3 (n=25)
Group LS (n=25)
Age (yr) Gender (F/M) Weight (Kg) ASA (I/II) Duration of surgery (min) Tourniquet time (min) Types of surgery (n) Carpal tunnel syndrome Trigger finger Tendon release
34.6±10.4 6/19 68.8±5.2 21/4 67.7±4.1 74.2±5.6
30.4±9.2 3/22 68.6±9.6 23/2 70.3±5.1 78.0±5.4
33.2±9.8 7/18 69.5±4.9 22/3 69.8±5.2 76.6±5.3
32.6±10.6 8/17 67.2±5.7 20/5 68.2±5.8 75.7±6.1
5 6 14
7 5 13
4 6 15
4 9 12
Values are presented as number or mean±SD. Group LN1 = Lidocaine-nitroglycerin 200µ group; Group LN2 = Lidocaine-nitroglycerin 300 µ group; Group LN3 = Lidocaine-nitroglycerin 400µ group; Group LS = Lidocaine-saline group. There were no significant differences between the four groups.
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Table 2. Onset and recovery times of sensory and motor block, initial time of tourniquet and postoperative pain, and the amount of intraoperative and postoperative analgesic requirements according to the groups Variable
Group LN1 (n=25)
Group LN2 (n=25)
Group LN3 (n=25)
Group LS (n=25)
p
Sensory block onset time (min) Sensory block recovery time (min) Motor block onset time (min) Motor block recovery time (min) The first time of tourniquet pain (min) Intraoperative fentanyl requirement (µg) The first time of postoperative pain (min) Postoperative diclofenac requirement (mg)
4.1±0.9 6.6±0.7 5.4±0.7 6.4±0.7 23.5 ±11.1 57.9 ±14.2 261.9±49.7 75.0±0.0
3.5±0.8 7.9±0.9 4.8±0.6 7.8±1.1 30.6±8.2 32.2±12.2 331.0± 87.9 75.0±0.0
2.8±0.6† 8.4±0.8‡ 3.8±0.7† 8.4±1.0‡ 53.7±6.3† 25.0±0.0‡ 461.7 ±147.0† 75.0± 0.0
5.0±1.2 ٭ 3.3±0.5 ٭ 6.2±0.8 ٭ 3.7±0.7 ٭ 12.6±4.5 ٭ 75.0±26.3 ٭ 134.8±18.9 ٭ 120.2±39.2 ٭
0.000 0.000 0.000 0.000 0.000 0.000 0.000 0.000
Values are presented as mean±SD. Group LN1 = Lidocaine-nitroglycerin 200µ group; Group LN2 = Lidocaine-nitroglycerin 300µ group; Group LN3 = Lidocainenitroglycerin 400µ group; Group LS = Lidocaine-saline group. ٭p<0.05 vs. Groups LN1, LN2, LN3; † p<0.05 vs. Group LN1, LN2; ‡ p<0.05 vs. Group LN1.
tal dosage of fentanyl administration for relieving tourniquet pain was significantly less in Groups LN1, LN2 and LN3 compared with Group LS (p<0.05) (Table 2). This variable was significantly less in Group LN3 when compared with Group LN1 (p<0.05). The median (range) sedation values at any intraoperative and postoperative period were not statistically different between the four groups. VAS scores for tourniquet pain were significantly lower at 5, 10, 20, and 30 min after tourniquet inflation in Groups LN1, LN2 and LN3 compared with Group LS during the intraoperative period (p<0.05) (Fig. 1). This variable was significantly less in Group LN3 when compared with Group LN1 at 5, 10, 20, and 30 min (p<0.05) (Fig. 1). The total dosage of diclofenac administration for relieving postoperative pain was significantly less in Groups LN1, LN2 and LN3 compared with Group LS (p<0.05) (Table 2). Postoperative VAS scores were significantly lower at 1, 3, 5, 10, 15, and 30 min after tourniquet deflation in Groups LN1, LN2 and LN3
compared with Group LS (p<0.05) (Fig. 2). This variable was significantly less in Group LN3 when compared with Group LN1 at all the above-mentioned times (p<0.05) (Fig. 2). Postoperative VAS scores were significantly lower at 2, 4, 8, 12, and 24 h after tourniquet release in Group LN3 compared with Group LS (p<0.05) (Fig. 3). This variable was significantly less in Group LN3 when compared with Group LN1 at all the above-mentioned times (p<0.05) (Fig. 3). In Group LN2, postoperative VAS scores were significantly lower at 2, 4, 8, and 12 h after tourniquet release when compared with Group LS (p<0.05) (Fig. 3). Postoperative VAS scores in Group LN3 were significantly lower at 12 and 24 h after tourniquet deflation when compared with Group LN2 (p<0.05) (Fig. 3). Anesthesia quality as assessed by the patient and the surgeon was significantly better in Groups LN1, LS
LN1
LN2
LN3
5 Visual Analogue Scores (cm)
4.5 4
* *
3.5
† *
3
*
*
* † *
*
* † *
2.5
† *
2 1.5
LN2
LN3
*
*
4
*
*
*
*
*
* *
*
*
*
3.5 † *
3 2.5
† *
† *
† *
† *
*
2 1.5 1 0.5
1
0
0.5
1 min ATR
0 1 min ATI
5 min ATI
10 min ATI
20 min ATI
30 min ATI
Timing of measurement
Fig. 1. Intraoperative (tourniquet pain) visual analogue scale scores. Data are presented as mean (SD). Group LN1 = lidocaine-nitroglycerin 200µ group; Group LN2 = lidocaine-nitroglycerin 300µ group; Group LN3 = lidocaine-nitroglycerin 400µ group; Group LS = lidocaine-saline group. ATI = after tourniquet inflation. ٭ p<0.05 vs. group LS; † p<0.05 vs. group LN1. 500
Visual Analogue Scores (cm)
4.5 LS
LN1
5
3 min ATR
5 min ATR
10 min ATR
15 min ATR
30 min ATR
Timing of measurement
Fig. 2. Postoperative visual analogue scale scores at 1, 3, 5, 10, 15, and 30 minutes after tourniquet release. Data are presented as mean (SD). Group LN1 = Lidocainenitroglycerin 200µ group; Group LN2 = Lidocainenitroglycerin 300µ group; Group LN3 = Lidocaine-nitroglycerin 400µ group; Group LS = Lidocaine-saline group. ATR: After tourniquet release. ٭p<0.05 vs. Group LS; † p<0.05 vs. Group LN1. Kasım - November 2011
IV regional anesthesia and nitroglycerine in trauma patients
Table 3. Quality of anesthesia as evaluated by patients and surgeon Variable Quality of anesthesia (Patient) Quality of anesthesia (Surgeon)
Group LN1 (n=25)
Group LN2 (n=25)
Group LN3 (n=25)
3 (2-4) * 3 (2-4) *
3 (2-4) * 3 (2-4) *
4 (3-4) *† 4 (3-4) *†
Group LS p (n=25) 2 (2-3) 2 (2-3)
0.000 0.000
Values are presented as median (range). * p<0.05 vs. Group LS; † p<0.05 vs. Group LN1 and Group LN2.
LN2 and LN3 compared with Group LS (p<0.05) (Table 3). This variable was significantly better in Group LN3 when compared with Groups LN1 and LN2 (p<0.05) (Table 3). The incidence [number (%)] of hypotension was not significantly different among the four groups [3(12), 3(12), 1(4), 0(0) in Groups LN4, LN3, LN2 and LN1, respectively, p>0.05]. The incidences of tachycardia [0(0), 1(4), 1(4), 0(0)], hypertension [0(0), 0(0), 0(0), 2(8)], vertigo [2(8), 1(4), 0(0), 0(0)], headache [0(0), 0(0), 0(0), 1(4)], and nausea [2(8), 0(0), 0(0), 0(0)] in Groups LN4, LN3, LN2 and LN1, respectively, were not significantly different between the four groups (p>0.05 for all).
DISCUSSION Providing satisfactory and prolonged analgesia is an important goal in the management of postoperative pain in trauma patients. IVRA is a technique that is mostly used for providing anesthesia and analgesia during the operation. Using additives with lidocaine may prolong the duration of postoperative analgesia. Our study showed that the addition of 400 µg NTG to lidocaine for IVRA in trauma patients improved the LS
LN1
LN2
* *
Visual Analogue Scores (cm)
5 4
*
*
†*
* ‡† *
‡† *
* † *
† *
3 2 1 0 2h ATR
4h ATR
8h ATR
12h ATR
24h ATR
Timing of measurement
Fig. 3. Postoperative visual analogue scale scores at 2, 4, 8, 12, and 24 hours after tourniquet release. Data are presented as mean (SD). Group LN1 = Lidocaine-nitroglycerin 200µ group; Group LN2 = Lidocaine-nitroglycerin 300µ group; Group LN3 = Lidocaine-nitroglycerin 400µ group; Group LS = Lidocaine-saline group. ATR: After tourniquet release. ٭p<0.05 vs. Group LS; † p<0.05 vs. Group LN1. ‡ p<0.05 vs. Group LN2. Cilt - Vol. 17 Sayı - No. 6
The first study on adding NTG to IVRA for hand and forearm surgery was performed by Sen and colleagues.[5] They reported that postoperative VAS scores were significantly lower for the first 4 h postoperatively in Group NTG, in which 200 µg NTG was added to IVRA. The limitation of their study was using only one low dose of NTG (200 µg). The duration of effect of NTG with this dosage was also short (4 h). They recommended further study with the other dosages of NTG. Our study showed that increasing the dosage of NTG to 400 µg significantly decreased postoperative VAS scores for 24 h after tourniquet release. There are a variety of proposed sites for action of IVRA. Raj et al.[6] showed that the action of LA is on major nerve trunks, probably reaching the nerve trunk through small venules within the nerve core, while Rosenberg[7] provided strong evidence regarding a peripheral site. It is currently accepted that both the nerve endings and trunks are affected.[8] The favorable effects of NTG, which we confirmed in the present study, might be influenced by a direct potent vasodilatory effect that promotes distribution of lidocaine to nerves,[9] and it seems it was dose-dependent. This would explain the more rapid onset of sensory and motor block that was seen in Group LN3.
LN3
6
speed of onset and the quality of anesthesia and decreased tourniquet pain and intraoperative and postoperative analgesic consumption better than the addition of the other two doses of NTG (200 µg or 300 µg), while causing no significant side effects.
Nitroglycerine (NTG) is metabolized to nitric oxide (NO) in the cell.[10] NO synthesis was first discovered in vascular endothelial cells,[11] central and peripheral nerve cells and fibers,[12] and macrophages.[13] NO causes an increase in the intracellular concentration of cyclic guanosine monophosphate, which generates pain modulation in the central and peripheral nervous system.[9] Activation of the NO-cyclic guanosine monophosphate signal transduction system causes sensitization of wide-dynamic-range neurons located in the superficial and deep dorsal horns and concurrently attenuates the inhibition of the same neurons produced by stimulation in the periaqueductal gray, resulting in the transmission of painful stimuli.[14] 501
Ulus Travma Acil Cerrahi Derg
Nozaki et al.’s[15] study showed that peripherally applied NO donors have no analgesic effects themselves but augment the analgesic effects of peripherally administered analgesics during inflammation. This would explain the lower VAS scores and analgesic administration in groups receiving NTG, which also seems dose-dependent. In addition, NO generators induce antiinflammatory effects and analgesia by blocking hyperalgesia and the neurogenic component of inflammatory edema with topical application.[16,17] An additional possible mechanism includes an analgesic effect through the direct stimulation of peripheral fibers imitating the actions of locally applied acetylcholine.[18] Ultimately, molecular pharmacology modulation may be suggested for the mechanism of synergistic interaction between µ-opioid receptors and NO.[19] NO has also been described to have direct modulatory effects on N-methyl-D-aspartate receptors [20] and gamma-aminobutyric acid-A receptors.[21] The mechanisms discussed above, or their combinations, possibly contribute to the analgesic effects of NTG added to lidocaine in IVRA. The clinical efficiency of transdermal NTG for acute pain relief has been demonstrated in several previous studies.[22,23] NTG was found to be beneficial in the treatment of shoulder pain,[24] chronic thoracotomy pain[25] and thrombophlebitis[26] and for augmenting the effect of spinal sufentanil or neostigmine,[27] or epidural S(+)-ketamine.[28] In these investigations, the analgesic effects of transdermal NTG were investigated, while in our study, the efficiency of IV NTG was documented with the mechanism similar to that of transdermal NTG. While a variety of adjuvants have been proposed for improving intraoperative and postoperative analgesia and maintaining better operative conditions, these adjuvants may possibly cause complications such as nausea, vomiting, sedation, dizziness, wound hematoma, skin rash, and hypotension.[1-4,29] NTG may possibly cause dose-dependent side effects such as hypotension, tachycardia or headache as well.[27] In the present study, there was no significant difference in side effects between groups. Nitroglycerine (NTG) has a very short half-life.[10] These techniques, combined with the short half-life of NTG, may diminish the incidence and severity of unwanted side effects. In conclusion, the addition of 400 µg NTG to lidocaine in IVRA in trauma patients shortened sensory and motor block onset times, prolonged sensory and motor block recovery times, and improved tourniquet pain, while prolonging the time for the first analgesic requirement, decreasing the total amount of analgesic, 502
and enhancing patient satisfaction better than the addition of 200 µg or 300 µg NTG, without side effects. Our study showed that the analgesic effect of NTG was dose-dependent. This point needs further investigation before a final conclusion can be elicited.
REFERENCES 1. Choyce A, Peng P. A systematic review of adjuncts for intravenous regional anesthesia for surgical procedures. Can J Anaesth 2002;49:32-45. 2. Turan A, Karamanlýoglu B, Memis D, Kaya G, Pamukçu Z. Intravenous regional anesthesia using prilocaine and neostigmine. Anesth Analg 2002;95:1419-22. 3. Estèbe JP, Gentili ME, Langlois G, Mouilleron P, Bernard F, Ecoffey C. Lidocaine priming reduces tourniquet pain during intravenous regional anesthesia: A preliminary study. Reg Anesth Pain Med 2003;28:120-3. 4. Memiş D, Turan A, Karamanlioğlu B, Pamukçu Z, Kurt I. Adding dexmedetomidine to lidocaine for intravenous regional anesthesia. Anesth Analg 2004;98:835-40. 5. Sen S, Ugur B, Aydin ON, Ogurlu M, Gursoy F, Savk O. The analgesic effect of nitroglycerin added to lidocaine on intravenous regional anesthesia. Anesth Analg 2006;102:916-20. 6. Raj PP, Garcia CE, Burleson JW, Jenkins MT. The site of action of intravenous regional anesthesia. Anesth Analg 1972;51:776-86. 7. Rosenberg PH. Intravenous regional anesthesia: nerve block by multiple mechanisms. Reg Anesth 1993;18:1-5. 8. Brill S, Middleton W, Brill G, Fisher A. Bier’s block; 100 years old and still going strong! Acta Anaesthesiol Scand 2004;48:117-22. 9. Lauretti GR, Perez MV, Reis MP, Pereira NL. Double-blind evaluation of transdermal nitroglycerine as adjuvant to oral morphine for cancer pain management. J Clin Anesth 2002;14:83-6. 10. Hashimoto S, Kobayashi A. Clinical pharmacokinetics and pharmacodynamics of glyceryl trinitrate and its metabolites. Clin Pharmacokinet 2003;42:205-21. 11. Furchgott RF, Zawadzki JV. The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine. Nature 1980;288:373-6. 12. Bredt DS, Snyder SH. Isolation of nitric oxide synthetase, a calmodulin-requiring enzyme. Proc Natl Acad Sci U S A 1990;87:682-5. 13. Hevel JM, White KA, Marletta MA. Purification of the inducible murine macrophage nitric oxide synthase. Identification as a flavoprotein. J Biol Chem 1991;266:22789-91. 14. Lin Q, Peng YB, Wu J, Willis WD. Involvement of cGMP in nociceptive processing by and sensitization of spinothalamic neurons in primates. J Neurosci 1997;17:3293-302. 15. Nozaki-Taguchi N, Yamamoto T. The interaction of FK409, a novel nitric oxide releaser, and peripherally administered morphine during experimental inflammation. Anesth Analg 1998;86:367-73. 16. Berrazueta JR, Fleitas M, Salas E, Amado JA, Poveda JJ, Ochoteco A, et al. Local transdermal glyceryl trinitrate has an antiinflammatory action on thrombophlebitis induced by sclerosis of leg varicose veins. Angiology 1994;45:347-51. 17. Ferreira SH, Lorenzetti BB, Faccioli LH. Blockade of hyperalgesia and neurogenic oedema by topical application of nitroglycerin. Eur J Pharmacol 1992;217:207-9. 18. Durate ID, Lorenzetti BB, Ferreira SH. Peripheral analgesia and activation of the nitric oxide-cyclic GMP pathway. Eur J Kasım - November 2011
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Pharmacol 1990;186:289-93. 19. Toda N, Kishioka S, Hatano Y, Toda H. Modulation of opioid actions by nitric oxide signaling. Anesthesiology 2009;110:166-81. 20. Bogdanov MB, Wurtman RJ. Possible involvement of nitric oxide in NMDA-induced glutamate release in the rat striatum: an in vivo microdialysis study. Neurosci Lett 1997;221:197-201. 21. Fukami S, Uchida I, Mashimo T, Takenoshita M, Yoshiya I. Gamma subunit dependent modulation by nitric oxide (NO) in recombinant GABAA receptor. Neuroreport 1998;9:1089-92. 22. Prado WA, Schiavon VF, Cunha FQ. Dual effect of local application of nitric oxide donors in a model of incision pain in rats. Eur J Pharmacol 2002;441:57-65. 23. Turan A, Karamanlioğlu B, Memiş D, Pamukçu Z. Alternative application site of transdermal nitroglycerin and the reduction of pain on propofol injection. Eur J Anaesthesiol 2003;20:170-2. 24. Berrazueta JR, Losada A, Poveda J, Ochoteco A, Riestra A, Salas E, et al. Successful treatment of shoulder pain syndrome due to supraspinatus tendinitis with transdermal nitro-
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glycerin. A double blind study. Pain 1996;66:63-7. 25. Glantz L, Godovic G, Lekar M, Kramer M, Eidelman LA. Efficacy of transdermal nitroglycerin combined with etodolac for the treatment of chronic post-thoracotomy pain: an open-label prospective clinical trial. J Pain Symptom Manage 2004;27:277-81. 26. Lauretti GR, Oliveira AP, Julião MC, Reis MP, Pereira NL. Transdermal nitroglycerine enhances spinal neostigmine postoperative analgesia following gynecological surgery. Anesthesiology 2000;93:943-6. 27. Berrazueta JR, Poveda JJ, Ochoteco J, Amado JA, Puebla F, Salas E, et al. The anti-inflammatory and analgesic action of transdermal glyceryltrinitrate in the treatment of infusionrelated thrombophlebitis. Postgrad Med J 1993;69:37-40. 28. Lauretti GR, Oliveira AP, Rodrigues AM, Paccola CA. The effect of transdermal nitroglycerin on spinal S(+)-ketamine antinociception following orthopedic surgery. J Clin Anesth 2001;13:576-81. 29. Turan A, Memiş D, Karamanlioğlu B, Güler T, Pamukçu Z. Intravenous regional anesthesia using lidocaine and magnesium. Anesth Analg 2005;100:1189-92.
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Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):504-508
Original Article
Klinik Çalışma doi: 10.5505/tjtes.2011.04809
Outcome of surgically treated Lisfranc injury: A review of 34 cases Cerrahi olarak tedavi edilen Lisfranc yaralanmasının sonucu? 34 olgunun değerlendirilmesi Mohd Fairudz Mohd MISWAN, Vivek Ajit SINGH, Nor Faissal YASIN
BACKGROUND
AMAÇ
We reviewed cases with Lisfranc injuries who presented to our center in order to study the adequacy of the treatment method and their final functional outcome.
Merkezimize başvuran Lisfranc yaralanması olan olgular, tedavi yöntemi ve nihai fonksiyonel sonuçları incelenerek değerlendirildi.
METHODS
GEREÇ VE YÖNTEM
This is a retrospective review of 34 cases diagnosed with Lisfranc injuries treated at our center from 2000 to 2006. This review is aimed to determine the demography and functional outcome of all patients with Lisfranc injury treated during this period.
Bu retrospektif çalışmada, merkezimizde 2000 ile 2006 yılları arasında Lisfarnc yaralanması tanısıyla tedavi edilen 34 olgunun sonuçları değerlendirildi. Bu yazıyla, bu dönemde tedavi edilen Lisfranc yaralanması olan tüm hastaların demografik ve fonksiyonel sonucun belirlenmesi amaçlandı.
RESULTS
BULGULAR
The injury was classified based on the "Hardcastle and Associates Classification". In our review, we found that the commonest Lisfranc injury was type B2 (41%). These injuries are mostly fixed with K-wires (76.5%). All patients assessed with Bristol Foot Score (BFS) had a good score in all categories, with a total score ranging from 16 to 25.
Yaralanmalar “Hardcastle ve Arkadaşlarının Sınıflaması”na göre sınıflandırıldı. En yaygın Lisfranc yaralanması tipi, tip B2 (%41) oldu. Bu yaralanmalar, çoğunlukla K-telleri ile sabitlendi (%76,5). Bristol Foot Skoru (BFS) ile değerlendirilen hastalar, 16 ile 25 arasında değişen toplam skor ile bütün kategorilerde iyi bir skora sahipti.
CONCLUSION
SONUÇ
We concluded that all Lisfranc injuries, whether treated with closed or open fixation methods, demonstrated a good long-term functional outcome.
İster kapalı ister açık fiksasyon yöntemleri ile tedavi edilsin, bütün Lisfranc yaralanmalarının iyi bir uzun süreli fonksiyonel sonuç gösterdiğini düşünüyoruz.
Key Words: Lisfranc injuries; functional outcome.
Anahtar Sözcükler: Lisfranc yaralanmaları; fonksiyonel sonuç.
Fracture dislocation of the tarsometatarsal joint of the foot (Lisfranc injury) is a serious injury. It is rare, with less than 1% ever reported in the literature.[1-4] However, the true incidence is probably higher and is increasing daily due to the increased number of motor vehicle accidents, industrial accidents and sports
injuries. Traumatic tarsometatarsal injuries are usually accompanied by multiple other injuries and may be caused by a high-energy motor vehicle or industrial accident. These injuries can be caused by a direct or indirect mechanism. They normally present as open fractures and are associated with soft tissue injuries,
Department of Orthopaedics, University Malaya Medical Center, Kuala Lumpur, Malaysia.
Malaya Tıp Merkezi, Ortopedi Bölümü, Kuala Lumpur, Malezya.
Correspondence (İletişim): Vivek Ajit Singh, M.D. Lembah Pantai, 46000 Kuala Lumpur, Malaysia. Tel: +060164940600 e-mail (e-posta): drvivek69@gmail.com
504
Outcome of surgically treated Lisfranc injury
such as degloving injuries and bone and cartilage loss.
Radiographs taken of the injured foot would reveal an abnormal space between the bases of the first and second metatarsal. This can be easily missed in the Accident and Emergency setting. Failure to recognize this can lead to chronic pain and impairment.[1] A good outcome to this injury depends on accurate anatomical reduction.[1,2,4] Lisfranc injuries are mostly treated with percutaneous K-wire fixation or temporary screw fixation whether using closed or open reduction technique. The reported results are related to the accuracy of reduction and also to the severity of associated articular and soft tissue damage. Conservative casting of the injuries without fixation has not proven to be effective. We reviewed cases of Lisfranc injuries presenting to our center in order to study the adequacy of the treatment method and their final functional outcome.
MATERIALS AND METHODS This was a retrospective study carried out from 1 January 2000 to 31 December 2006. Patients were identified by reviewing the operating theater records. Patients’ records were then traced from the records department and the X-rays were traced from the Radiology���������������������������������������� Department. The radiographs were evaluated by an independent reviewer from the Radiology Department. The radiographs taken at diagnosis and initial follow-up are usually in three views, as anterior-posterior, lateral and oblique. Once the injury had
16 14 No. of patients
Isolated Lisfranc injuries are more common in sports injuries and occur as a result of a sudden torque applied to the foot when a portion of it is fixed or by axial loading of the foot in a vertical position. The Lisfranc joint consist of articulation of first and second metatarsal bases with the first and second cuneiform bones. It is held together by the Lisfranc ligament, which is a band of ligamentous tissue that connects the medial cuneiform and the base of the second metatarsal. Thus, the Lisfranc joint is considered the “keystone” of the midfoot due to the wedging of the second metatarsal into the second cuneiform space. The joint is also the focal point of all tarsometatarsal articulation.[3-6]
12 10 8 6 4 2 0
A
B1
B2
C1
C2
Fig. 1. Distribution of patients according to Hardcastle classification.
healed, weight-bearing stress radiographs were taken to determine any subtle instability. All cases had a radiograph of the affected foot taken at their last followup. These injuries were classically evaluated with the Hardcastle Classification.[1] We used the Modified Hardcastle Classification[7] for this study (Table 1). Patients were then contacted for further evaluation, and all data were entered in the data collection form. This qualitative assessment was developed based on an evaluation performed using the Bristol Foot Score (BFS).[8] As it is a self-administered assessment, there are no inter-observer variations. The entire questionnaire can be completed within 3 to 5 minutes, encouraging better response levels. It consists of questions regarding the function, i.e. mobility, pain, footwear, foot health, and disability, and self-perception as a result of the foot problems. We also repeated radiographs of the affected foot during the evaluation to study the current status of the injury.
RESULTS Over this study, we identified 34 patients with Lisfranc injuries. The majority of the patients were males, with only one female. The average age of our patients was 30 years, with the majority (85%) between 18 to 45 years old. Two cases were younger than 18 years of age and three were older than 45 years of age. The mean follow-up was 48 months (range: 8-72 months). These injuries were sustained via motor vehicle ac-
Table 1. Hardcastle classification Type A (total incongruity) Type B1 (partial incongruity) Type B2 (partial incongruity) Type C1 (divergent/partial displacement) Type C2 (divergent/total displacement) Cilt - Vol. 17 Sayı - No. 6
All five metatarsals are displaced as a unit. The first metatarsal is displaced medially with or without displacement of one or more of the other metatarsals. The first metatarsal remains intact whereas there is lateral displacement of one or more other metatarsals. The first metatarsal is displaced medially with less than four of the other metatarsals displaced laterally. The first metatarsal is displaced medially and all the others are displaced laterally. 505
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cident in 21 cases, industrial accident in 8 and sports injury in 1; in 4 cases, they were due to other causes. There was almost equal involvement of both feet (right foot: 18 cases, left foot: 16 cases). There were 20 cases of isolated injury and 14 cases related with polytrauma. Twenty-five patients (74%) had closed injuries and 9 (26%) open injuries. In our series, 4 patients sustained type A injury, 5 type B1, 14 type B2, 3 type C1, and 8 type C2 injury, based on Hardcastle Classification (Fig. 1). All the patients were treated surgically. For closed isolated injuries, the surgery was carried out on an elective basis within two days of injury and for cases of polytrauma, the reduction was done as soon as possible on an emergency basis. There was only one case that was initially treated conservatively by closed manual reduction (conservative), but the post-reduction radiograph showed that there was still displacement and the patient was subsequently stabilized operatively. In
Table 2. Distribution of patients according to type of fixation Type of fixation
No. of patients
Closed reduction & percutaneous K-wire Open reduction & K-wire fixation Open reduction & screw fixation Open reduction with K-wire & screw fixation
11 15 5 3
all patients, the operated foot was immobilized in a below-knee back slab for eight weeks postoperatively. After eight weeks, the K-wires were removed and these patients were allowed partial weight-bearing for the subsequent three weeks, followed by full weightbearing. The methods of fixation used are shown in Table 2, and consisted of close manual reduction with percutaneous K-wire, open reduction with K-wire or screw fixation (as shown in Fig. 2) or both K-wire and screw
Table 3. Patient demographics No
Age
Sex
Etiology
Site
Nature of injury
Hardcastle classification
Operation done
BFS
Isolated of polytrauma
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34
57 43 17 24 25 55 18 27 44 21 28 21 25 33 23 22 23 29 35 48 37 21 19 23 28 28 20 34 34 22 29 32 36 30
Male Male Male Male Male Male Male Male Male Male Male Male Male Male Male Male Male Male Female Male Male Male Male Male Male Male Male Male Male Male Male Male Male Male
Fall MVA Sports Industrial MVA MVA MVA MVA MVA MVA MVA MVA MVA Industrial MVA Industrial Industrial Industrial Fall MVA MVA Industrial Fall MVA MVA MVA Industrial MVA Fall MVA Industrial MVA MVA MVA
Right Right Right Left Left Right Left Right Right Right Left Left Left Right Left Right Right Right Left Left Left Right Right Right Right Right Left Right Left Left Left Left Right Right
Closed Open Closed Closed Closed Closed Closed Open Open Open Closed Closed Closed Closed Closed Closed Open Closed Closed Open Closed Closed Closed Open Open Closed Closed Closed Closed Closed Closed Open Closed Closed
B1 B1 B2 B2 C2 B2 B2 B2 C2 B2 B1 C2 B2 B2 B2 A C2 C2 B2 C1 C1 A B1 C2 C2 C2 B2 B2 B2 A A B1 B2 C1
ORIF, screw & K-wire CMR, p/c K-wire CMR, p/c K-wire OR & K-wire OR & K-wire ORIF & screw fix CMR, p/c K-wire OR & K-wire OR & K-wire OR & K-wire ORIF, screw & K-wire ORIF, screw & K-wire ORIF & screw fix ORIF & screw fix OR & K-wire CMR, p/c K-wire OR & K-wire CMR, p/c K-wire CMR, p/c K-wire OR & K-wire OR & K-wire CMR, p/c K-wire OR & K-wire OR & K-wire OR & K-wire CMR, p/c K-wire ORIF & screw fix CMR, p/c K-wire CMR, p/c K-wire ORIF & screw fix CMR, p/c K-wire OR & K-wire OR & K-wire OR & K-wire
23 24 20 24 25 24 15 24 16 15 23 25 16 20 18 20 23 18 16 25 20 15 16 24 23 16 18 20 25 23 15 16 25 24
Isolated Polytrauma Isolated Isolated Isolated Isolated Polytrauma Polytrauma Isolated Polytrauma Polytrauma Isolated Isolated Isolated Isolated Polytrauma Isolated Isolated Isolated Polytrauma Isolated Isolated Polytrauma Polytrauma Isolated Polytrauma Polytrauma Polytrauma Isolated Polytrauma Isolated Isolated Isolated Polytrauma
MVA: Motor vehicle accident; ORIF: Open reduction internal fixation; CMR: Closed manipulative reduction; p/c: Percutaneous; OR: Open reduction.
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Outcome of surgically treated Lisfranc injury
Fig. 2. Type B Lisfranc injury fixed with screw fixation. Type B: Pre and post reduction.
fixation. The majority of the patients (44%) were treated with open reduction and K-wire fixation. In our series, an average of 2 K-wires or 2 screws were used for the fixation. In unstable cases, a combination of 2 screws and 2 K-wires was used. There were no cases of displacement of the Lisfranc injury as of the latest follow-up. Functional outcome was assessed using the BFS. All patients assessed with BFS had a good score in all categories, with a total score ranging from 16 to 25 (scores ranging from 15 to 42 were considered as a good functional outcome). Details are shown in Table 3. There was only one patient in our series with symptoms of osteoarthritis.
DISCUSSION The etiology of Lisfranc injuries has changed over time. The commonest cause of Lisfranc injuries in our series was motor vehicle accident, followed by industrial accidents. These injuries are a result of direct crushing force or an indirect pronation force acting on a fixed forefoot in equines. The commonest type encountered in our center was type B2 (41%), followed by type C2 (23%), type B1 (15%), type A (12%), and the least common, type C1 (9%). This is in contrast to a series reported by Aitken and Poulson,[5] in which there was dorsolateral displacement of all five metatarsals, or the series reported by Wilppula,[9] in which dorsolateral displacement of four lateral metatarsals was the commonest injury. We treated the majority (76.5%) of these injuries with reduction and K-wiring either percutaneously or via the open method. None of our patients experienced any displacement of the reduction, and the method of fixation was adequate until healing occurred. We removed all the K-wires at the postoperative eighth week. This is similar to the protocol used by Rajapakse.[10] However, in his series, he also removed the screws after six months, which we did not do. This is in contrast to what has been reported by Aitken.[5] In his series, he felt that temporary fixation with K-wires was inadequate as it led to eventual displacement. Gaweda[11] reported, in his series of 41 patients with Cilt - Vol. 17 Sayı - No. 6
acute and chronic Lisfranc injuries followed for 16 years, that the best results were achieved after closed reduction and percutaneous K-wire fixation in acute cases. Teng et al.[12] analyzed the gait of the injured foot and the control foot in cases of Lisfranc injury with anatomic reduction, and showed no significant difference in the parameters. Therefore, anatomic reduction of the Lisfranc injury is essential to restore normal function of the foot. In our series, we did not encounter any major complication, such as vascular impairment, compartment syndrome, redisplacement of the Lisfranc injury postfixation, or skin complications. We had only one case that had immediate displacement after closed manual reduction and casting, which had to be fixed electively with closed K-wiring. Jeifreys[13] reported in his series that osteoarthritis is almost an inevitable sequela of Lisfranc injury, and Hardcastle[1] reported in his series an osteoarthritis rate of 30%. We encountered only one patient with signs and symptoms of osteoarthritis in our series - a 44-year-old male who presented with an isolated open Lisfranc injury (type C2). His injury was fixed with open reduction and K-wiring. He developed symptoms of osteoarthritis 13 months after the surgery. In our study, we used the Modified Hardcastle Classification to classify the Lisfranc injuries. Talarico[14] studied the interrater reliability of this classification and concluded that there is moderate interrater agreement among clinicians when using this scale for interpreting Lisfranc injuries. For the functional score, we used the BFS, which is a useful tool for evaluating the efficacy of interventions and for describing foot health within populations. The BFS was designed to produce a measure that quantifies, from the patient’s rather than the clinician’s perspective, the impact that foot problems has on their everyday life. This will enable the health services to provide more responsive and equitable care. It also displays good internal reliability, loading predominantly on a single factor that addresses the feet and perceived disability. The BFS provide a valuable additional contribution to professional foot-health status scores and potentially uncovers subtle psychological factors that influence behavior and outcomes.[7] All the patients in our series scored within the range of good functional outcome (15-42) regardless of the fixation methods used or type of Lisfranc injury sustained. In conclusion, all Lisfranc injuries treated in our center, regardless of the severity of the injury or method of treatment, demonstrated a good long-term functional outcome based on the BFS. We found that both K-wire and screw fixation were adequate in achieving an acceptable anatomical reduction until the injury healing occurred. 507
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REFERENCES 1. Hardcastle PH, Reschauer R, Kutscha-Lissberg E, Schoffmann W. Injuries to the tarsometatarsal joint. Incidence, classification and treatment. J Bone Joint Surg [Br] 1982;64:34956. 2. Yuen JS, Yung SW, Wong MK. Open reduction and temporary rigid internal fixation of Lisfranc fracture-dislocations. Singapore Med J 2001;42:255-8. 3. Cassebaum WH. Lisfranc fracture-dislocations. Clin Orthop Relat Res 1963;30:116-29. 4. Wilson DW. Injuries of the tarso-metatarsal joints. Etiology, classification and results of treatment. J Bone Joint Surg [Br] 1972;54:677-86. 5. Aitken AP, Poulson D. Dislocations of the tarsometatarsal joint. J Bone Joint Surg [Am] 1963;45-A:246-60. 6. Wiley JJ. The mechanism of tarso-metatarsal joint injuries. J Bone Joint Surg Br 1971;53:474-82. 7. Myerson MS, Fisher RT, Burgess AR, Kenzora JE. Fracture dislocations of the tarsometatarsal joints: end results correlated with pathology and treatment. Foot Ankle 1986;6:22542.
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8. Barnett S, Campbell R, Harvey I. The Bristol Foot Score: developing a patient-based foot-health measure. J Am Podiatr Med Assoc 2005;95:264-72. 9. Wilppula E. Tarsometatarsal fracture-dislocation. Late results in 26 patients. Acta Orthop Scand 1973;44:335-45. 10. Rajapakse B, Edwards A, Hong T. A single surgeon’s experience of treatment of Lisfranc joint injuries. Injury 2006;37:914-21. 11. Gaweda K, Tarczyńska M, Modrzewski K, Turzańska K. An analysis of pathomorphic forms and diagnostic difficulties in tarso-metatarsal joint injuries. Int Orthop 2008;32:705-10. 12. Teng AL, Pinzur MS, Lomasney L, Mahoney L, Havey R. Functional outcome following anatomic restoration of tarsalmetatarsal fracture dislocation. Foot Ankle Int 2002;23:922-6. 13. Jeifreys TE. Lisfranc’s fracture-dislocation: a clinical and experimental study of tarso-metatarsal dislocations and fracture-dislocations. J Bone Joint Surg [Br] I963:45:546-51. 14. Talarico RH, Hamilton GA, Ford LA, Rush SM. Fracture dislocations of the tarsometatarsal joints: Analysis of interrater reliability in using the modified Hardcastle classification system. J Foot Ankle Surg 2006;45:300-3.
Kasım - November 2011
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):509-515
Original Article
Klinik Çalışma doi: 10.5505/tjtes.2011.35336
Outcome predictors of Glasgow Outcome Scale score in patients with severe traumatic brain injury Ağır travmatik beyin hasarlı hastalarda Glasgow Sonuç Skalası skoru sonuç belirteçleri Zalika KLEMENC-KETIS,1 Urska BACOVNIK-JANSA,2 Marko OGOREVC,3 Janko KERSNIK2
BACKGROUND
AMAÇ
Traumatic brain injury is a major public health problem due to high mortality and morbidity among survivors.
Travmatik beyin hasarı, sağ kalan kişilerde yüksek mortalite ve morbiditeye neden olan majör bir kamu sağlığı problemidir.
METHODS
We performed a retrospective cohort study of patients with severe traumatic brain injury. We recorded the attending physician’s evaluation of the patient’s consciousness, the patient’s demographics, routine physical measurements, and medical interventions. We used Glasgow Coma Scale and Extended Glasgow Outcome Scale.
GEREÇ VE YÖNTEM
RESULTS
Ağır travmatik beyin hasarına sahip olan hastalara ilişkin retrospektif bir kohort çalışması gerçekleştirdik. Tedavi eden doktorun hastanın bilincine ilişkin değerlendirmesi, hastanın demografik özellikleri, rutin fiziksel ölçümleri ve tıbbi girişimler kaydedildi. Glasgow Koma Skalası ve genişletilmiş Glasgow Sonuç Skalası kullanıldı.
We included 60 patients (83.3% males, mean age: 49.5 years). The Glasgow Coma Scale score was 4.8±1.9 and the Extended Glasgow Outcome Scale score was 2.9±2.5 points. Linear regression for higher Extended Glasgow Outcome Scale score explained 59.8% of the variance and revealed the duration of hospital stay and the presence of epidural hematoma as significant predictors. The classification tree for the higher Extended Glasgow Outcome Scale score revealed the following variables to be important: the duration of hospital stay, Glasgow Coma Scale score, partial pressure of carbon dioxide, surgery, response time of out-of-hospital emergency team, systolic and diastolic blood pressure, fall, and basis fracture.
BULGULAR
Bu çalışmaya 60 hasta (%83,3 erkek, ortalama yaş 49,5 yıl) dahil edildi. Glasgow Koma Skalası skoru 4,8±1,9 ve genişletilmiş Glasgow Sonuç Skalası skoru 2,9±2,5 puan idi. Daha yüksek genişletilmiş Glasgow Sonuç Skalası skoruna yönelik lineer regresyon, varyansın %59,8’ini açıkladı ve önemli prediktörler olarak epidural hematomanın varlığını gösterdi. Daha yüksek genişletilmiş Glasgow Sonuç Skalası skoruna yönelik sınıflama ağacı, şu değişkenlerin önemli olabileceğini gösterdi: Hastanede kalma süresi, Glasgow Koma Skalası skoru, parsiyel karbondioksit basıncı, cerrahi, hastane dışı acil ekibinin yanıt zamanı, sistolik ve diyastolik kan basıncı, düşme ve kafa kaidesi kırığı.
CONCLUSION
SONUÇ
Standardized inpatient protocol on monitoring, intervention and outcome recording should be adopted to make future comparisons more useful and to promote benchmarking between trauma centers in order to improve care for patients with severe traumatic brain injury.
Ağır travmatik beyin hasarlı hastalara yönelik bakımı geliştirmek için travma merkezleri arasında gelecekte daha yararlı karşılaştırmalar yapmak ve karşılaştırmalı değerlendirmeyi ilerletmek üzere; izleme, girişim ve sonuç kaydı ile ilgili standardize yatılı tedavi protokolü benimsenmelidir.
Key Words: Traumatic brain injury/outcome/predictors.
Anahtar Sözcükler: Travmatik beyin hasarı/sonuç/prediktörler.
Department of Family Medicine, Medical School, University of Maribor, Maribor, Slovenia; 2Department of Family Medicine, Medical School, University of Ljubljana, Ljubljana, Slovenia; 3 Institute for Economic Research, Ljubljana, Slovenia.
1
Maribor Üniversitesi Tıp Fakültesi, Aile Hekimliği Anabilim Dalı, Maribor, Slovenya; Ljubljana Üniversitesi Tıp Fakültesi, Aile Hekimliği Anabilim Dalı, Ljubljana, Slovenia; Ekonomik Araştırma Enstitüsü, Ljubljana, Slovenya.
Correspondence (İletişim): Zalika Klemenc-Ketis, M.D. Kersnikova cesta, 1 3320 Velenje, Slovenia. Tel: +038638963122 e-mail (e-posta): zalika.klemenc-ketis@uni-mb.si
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Traumatic brain injury (TBI) remains a major public health problem due to the high mortality and the long-term morbidity and disability among survivors. The incidence of severe TBI ranges (depending somewhat also on the study design) from 9 to 17 per 100,000 inhabitants.[1-3] According to the severity of head trauma, patients can be grouped into mild TBI (in 30-91%), moderate TBI (in 4-30%) and severe TBI (in 5-40%) groups.[2,4-6] Traumatic brain injury (TBI) patients are prevailingly male (58-74%).[1-3] However, females were 1.8 times more likely to die of their brain injury and 1.6 times more likely to experience poorer outcomes (that is, severe disability or persistent vegetative state) than males.[7] On the contrary, a study from Australia showed that women with severe TBI, after matching for initial injury severity and age at injury, demonstrated a better early outcome as indicated by their Glasgow Outcome Scale (GOS) scores than men (OR 4.2 points) and had a shorter duration of hospital stay (OR 9.0 days).[8,9] Age is an exceedingly important parameter affecting recovery from TBI. The mean age of TBI victims varies from 32 to 49 years.[1,3,9] Older patients, after isolated TBI, have poorer functional status at discharge and make less improvement at one year compared to all other patients. These worse outcomes occur despite less severe TBI in elderly patients as measured by a higher Glasgow Coma Scale (GCS) score upon admission.[10] Patients between 18 and 29 years of age had the lowest mean score on GOS, which correlated with the low admission GCS score because of polytrauma associated with severe TBI.[10] Ethnic minorities had significantly worse long-term functional outcomes after TBI, which was related to a lack of health insurance.[11] Better outcomes of patients after TBI is ensured by early intubation[12,13] and surgery.[1,14] Recovery of neurological patients is usually long, and TBI patients can gradually improve even after several months.[15] Early intensive rehabilitation may improve the functional outcome of patients with TBI Table 1. Extended Glasgow Outcome Scale (GOSE)* Score outcome
Category
Dead Vegetative state Lower severe disability Upper severe disability Lower moderate disability Upper moderate disability Lower good recovery Upper good recovery
1 2 3 4 5 6 7 8
* Patient’s overall rating is based on lowest outcome category indicated on the scale.
510
in the early months after injury and hence increase the chance of their returning to work early.[16,17] Only 4.9% of patients hospitalized due to TBI had hospital neurorehabilitation, 68% within one month after injury. Patients were classified as: 10.9% severe, 23.4% moderate and 65.7% mild TBI, and 5% were younger than 16 years and 25% older than 65 years. (2) Extended Glasgow Outcome Scale (GOSE) proved to be a useful tool for measuring disability even 10 years after TBI and was also proven to correlate well with other measures of human functioning.[18] In Slovenia, there are more than 300 deaths due to TBI (among 2 million population) per year, and outof-hospital emergency services in the country have a trained doctor on the staff at all times to provide recommended procedures in TBI patients, and there are reports on the beneficial outcomes when applied.[12,13] We thus wanted to test which factors predict outcomes in severe TBI patients.
MATERIALS AND METHODS We performed a retrospective cohort study of severe TBI patients injured in Celje district who were admitted to the hospital from January 1, 2004 to December 31, 2008. Patients who were recognized as dead in the field were excluded due to lack of reliable data about the cause of death. The emergency medical service (EMS) of Celje covers a population of 125,000 inhabitants. On average, 4.6 emergency interventions are performed per day. We extracted data from routine EMS reports, which are routinely filled in by the attending physician. The physician’s evaluation of the patient’s consciousness, the patient’s demographics, routine physical measurements, and medical interventions were recorded. An experienced attending physician assessed the patient’s health status. Early outcome of patients was assessed by GCS. Only TBI patients with a GCS<9 as assessed i the field were included. Appropriate intervention according to the emergency care protocol was administered in each case and the interventions recorded. We used GOSE (Table 1), which is a global assessment of independent living and social reintegration that is widely used as an outcome measure in brain injury research, to analyze long-term functional outcome. The assessment was carried out using the structured interview for the GOSE, with questions covering the following areas: 1) consciousness; 2) independence inside and outside the home; 3) resumption of normal social roles (work, social and leisure activities, personal relationships); and 4) residual symptoms interfering with daily life. The GOSE does not require a detailed psychological or neurologic examination and can be administered by professionals from different backgrounds. The GOS consists of five categoKasım - November 2011
Outcome predictors of Glasgow Outcome Scale score in patients with severe traumatic brain injury
Table 2. The demographic and clinical characteristics of the patients in the sample Characteristic
Fig. 1. Flow chart of TBI patients. [Figure legend: TBI: Traumatic brain injury; STBI: Severe traumatic brain injury; Confirmed: STBI confirmed in hospital by imaging and exclusion of intoxication or other causes for GCS<9 at trauma site.]
ries: dead, vegetative state, severe disability (conscious, but disabled), moderate disability (disabled, but independent), and good recovery. For the GOSE, the latter three categories are divided into upper and lower bands. The scales include the outcome categories “dead” and “vegetative state,” but only the categories of conscious survival were applicable in the current study. For the purposes of analysis, any patients disabled before the injury were treated as severely disabled and not separately identified.[19] The GOSE score of each survivor was obtained using a structured telephone interview by the severe TBI patient’s family physician using a standardized data form containing nine yes/no questions, which proved to be reliable for GOS assessment in neurologically injured patients.[20] We reviewed the patients’ out-of-hospital protocols of EMS intervention and hospital charts for surgery performed, length of hospital stay, discharge, rehabilitation, and other outcomes. The data were analyzed using the Statistical Package for the Social Sciences (SPSS) 13.0 statistical package (SPSS Inc., Chicago, IL, USA). We calculated the descriptive statistics. Spearman’s correlation coefficient (r) was used to analyze the association between Cilt - Vol. 17 Sayı - No. 6
Sex Male Female Causes for severe TBI Fall Traffic accident Gunshot Consequence of severe TBI Cerebral edema Subdural hematoma Subarachnoidal bleeding Skull fracture Basis fracture Contusion of the brain Epidural hematoma Intracerebral bleeding Hematocephalus Pneumocephalus Skin injury Surgery Presence of alcohol in the blood Intubation Resuscitation Polytrauma Hospital rehabilitation Epileptic seizures during hospital stay Drugs during resuscitation or hospital stay Analgesic Anesthetic, sedative Liquids Antiemetic Relaxant Hospital pneumonia
Number
%
50 10
83.3 16.7
16 39 4
26.7 65.0 6.7
36 15 29 31 7 40 4 10 7 4 11 24 8 51 3 25 17 10
60.0 25.0 48.3 51.7 11.7 66.7 6.7 16.7 11.7 6.7 18.3 40.0 13.3 85.0 5.0 41.7 28.3 16.7
24 45 52 2 25 26
40.0 75.0 86.7 3.3 41.7 43.3
TBI: Traumatic brain injury.
the different variables. We used independent samples t-test. Values of p<0.05 were considered to be statistically significant. Multiple logistic regression and classification tree analysis were performed to identify predictive factors of different outcomes after TBI.
RESULTS In the observed period, EMS took care of 1,101 patients: 143 (13.0%) of them for TBI and 60 (5.5%) for severe TBI (Fig. 1). Among 60 patients, 50 (83.3%) were males (Table 2). The average age of the patients was 49.5±20.8 years. The average response time of the out-of-hospital emergency team was 10.3±5.4 minutes. The GCS score was 4.8±1.9 and the GOSE score was 2.9±2.5 points. The average saturation of blood with oxygen was 85.0±12.5, the average pCO2 in the arterial blood was 35.5±13.0 kPa, and the average systolic and diastolic blood pressures were 118.5±37.5 mmHg and 511
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Table 3. Linear regression analysis for the higher GOSE score Dependent variable
Independent variable
GOSE score
Age (years) GCS score Duration of hospital stay (days) Brain contusion Epidural hematoma Intracerebral bleeding Gunshot Surgery Resuscitation Anesthetic, sedative Antiemetic Hospital pneumonia
B -0.009 0.336 0.029 1.099 2.761 -0.592 -0.277 0.866 -1.237 0.474 -0.488 0.451
Lower 95% C.I. for B
Higher 95% C.I. for B
-0.034 0.000 0.007 -0.135 0.493 -2.157 -2.376 -0.277 -3.498 -0.940 -4.516 -0.791
0.016 0.672 0.052 2.333 5.030 0.974 1.822 2.009 1.023 1.889 3.540 1.693
p 0.501 0.050 0.013 0.079 0.018 0.450 0.791 0.134 0.276 0.502 0.808 0.468
GOSE: Extended Glasgow Outcome Scale; GCS: Glasgow Coma Scale; CI: Confidence interval.
75.0±23.0 mmHg, respectively. The duration of hospital stay was 19.8±27.2 days. The GOSE score was negatively correlated with the age of the patients (r=-0.259, p=0.048) and positively correlated with GCS score (r=0.290, p=0.024) and with the duration of hospital stay (r=0.475, p<0.001). Patients with brain contusion had higher GOSE score in comparison to others (3.3±2.7 vs. 2.1±1.6, p=0.033). Patients with epidural hematoma had higher GOSE score in comparison to others (6.8±1.5 vs. 2.6±2.3, p=0.001). Patients with intracerebral bleeding had lower GOSE score in comparison to others (1.7±1.6 vs. 3.1±2.5, p=0.039). Patients who were injured by a gunshot had lower GOSE score than others (1.0±0 vs. 3.0±2.5, p<0.001). Patients that underwent surgery had higher GOSE score than others (3.8±2.6 vs. 2.7±2.2, p=0.015). In patients in whom resuscitation was needed, the GOSE score was lower than in other patients (1.0±0 vs. 3.0±2.5, p<0.001). Patients that received anesthetics or sedatives had higher GOSE scores than others (3.3±2.6 vs. 1.7±1.5, p=0.005). Patients that received antiemetics had lower GOSE scores than others (1.0±0 vs. 2.9±2.5, p<0.001). Patients with nosocomial pneumonia had higher GOSE scores than others (4.2±2.4 vs. 1.9±2.0, p<0.001). Linear regression for higher GOSE score explained 59.8% of the variance and revealed the duration of hospital stay and the presence of epidural hematoma as significant predictors (Table 3). The classification tree for higher GOSE score revealed the following variables to be important in explaining a better GOSE: longer hospital stay, higher initial GCS score, higher pCO2, surgery, shorter response time of the out-of-hospital emergency team, low systolic and diastolic blood pressure, patient fall as cause of TBI, and cranial basis fracture (Fig. 2).
DISCUSSION The independent predictors for higher GOSE sco512
re were higher GCS score at the site of the injury, longer stay in the hospital and the presence of epidural hematoma. Similarly, the classification tree proved results of linear regression statistics that the duration of hospital stay was most important in predicting the outcome after severe TBI. Namely, patients that stayed in the hospital more than 12 days scored on average 3.5 more points on the GOSE scale as compared to those with a shorter stay (Node 2: 4.9±2.1 vs. Node 1: 1.4±1.5). This may indicate that many patients die during the first days after severe TBI, which might be due to the severity of the TBI itself or due to concomitant polytrauma or hospital complications. We can support this assumption also by our finding that in all patients with a shorter hospital stay (except in 2), the GOSE score was 1 (they died during the hospital stay or in the first 6 months after severe TBI). As is evident from the left branch of the classification tree, the second and third most important factors for better GOSE outcome were higher on-site GSC and the presence of surgery, which might have played a key role in a satisfying outcome for these two survivors. The favorable effect of surgery was also demonstrated in other studies.[14] If we follow the right branch of the classification tree, we can see that the second most important factor for better outcome after severe TBI was pCO2; a level higher than 34 mmHg improved the GOSE score by two points (Node 5: 3.2±2.1 vs. Node 6: 5.2±1.9). This is not unexpected because higher pCO2 is an indicator of a better cardiac output and hence better brain blood circulation.[21] In those with adequate circulation (systolic blood pressure over 95 mmHg), GOSE improved by three points (Node 11: 2.7±1.5 vs. Node 12: 5.7±1.7), showing that patients with hypovolemia or other causes of low systolic systemic blood pressure have worse outcomes, which was also shown in other studies.[15,17] On the other hand, lower values of diastolic blood pressure (below 65 mmHg) improved Kasım - November 2011
Outcome predictors of Glasgow Outcome Scale score in patients with severe traumatic brain injury
GOSE by more than two points (Node 14: 5.1±1.5 vs. Node 13: 7.2±0.8), probably indicating that this might improve brain circulation in anticipated raised intrac-
ranial pressure. In the next step, we found the best outcome in those patients with severe TBI without skull fracture (7.5 points), followed by patients who suffe-
GOS-E Node 0 Mean Std. Dev. n % Predicted
2.867 2.460 60 100.0 2.867
Duration of hospital stay (days) Improvement=2.996
≤12
>12
Node 1
Node 1
Mean Std. Dev. n % Predicted
Mean Std. Dev. n % Predicted
1.353 1.454 34 56.7 1.353
pCO2 (kPa) Improvement=0.393
GCS Improvement=0.409
≤7.5
>7.5
Node 3
Node 4
Mean Std. Dev. n % Predicted
1.000 0.000 29 48.3 1.000
Mean Std. Dev. n % Predicted
≤34
Yes
Mean Std. Dev. n % Predicted
3.400 3.362 5 8.3 3.400
Mean Std. Dev. n % Predicted
Node 6
3.200 2.049 5 8.3 3.200
Mean Std. Dev. n % Predicted
Response time (minutes) Improvement=0.180
No
7.000 1.414 2 3.3 7.000
>34
Node 5
Surgery Improvement=0.720
Node 7
4.846 2.073 26 43.3 4.846
Mean Std. Dev. n % Predicted
1.000 0.000 3 5.0 1.000
Node 9 Mean Std. Dev. n % Predicted
Systolic blood pressure (mmHg) Improvement=0.386
>12
≤12
Node 8
≤95
Node 10
2.000 1.732 3 5.0 2.000
5.238 1.921 21 35 5.238
Mean Std. Dev. n % Predicted
>95
Node 11
5.000 0.000 2 3.3 5.000
Mean Std. Dev. n % Predicted
Node 12
2.667 1.528 3 5.0 2.667
Mean Std. Dev. n % Predicted
5.667 1.645 18 30.0 5.667
Dyastolic blood pressure (mmHg) Improvement=0.271
≤65
> 65
Node 13 Mean Std. Dev. n % Predicted
Node 14
7.200 0.837 5 8.3 7.200
Mean Std. Dev. n % Predicted
Cranium basis fracture Improvement=0.030
Yes
Mean Std. Dev. n % Predicted
Fall Improvement=0.171
Yes
Node 15 7.500 0.577 4 6.7 7.500
5.077 1.498 13 21.7 5.077
Yes
Node 16 Mean Std. Dev. n % Predicted
6.000 1 1 6.000
No
Node 17 Mean Std. Dev. n % Predicted
4.375 1.302 8 13.3 4.375
Node 18 Mean Std. Dev. n % Predicted
6.200 1.095 5 8.3 6.200
Fig. 2. The classification tree for higher GOSE score. [GOSE: Extended Glasgow Outcome Scale; GCS: Glasgow Coma Scale.] Cilt - Vol. 17 Sayı - No. 6
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red severe TBI after a fall (6.2 points), patients with skull fracture (6.0 points), and those with causes of severe TBI other than fall (4.0 points). The mean age of the patients in our sample at the time of injury was 49.5 years, older than in a recent Swedish and Australian study (31.2 years and 31.4 years, respectively).[9,18] In the majority of the cases, the injury was caused by traffic accidents (65%). As reported in a Swiss study,[3] none of our gunshot victims (6.7%) survived. The length of hospital stay in our study (20 days) is consistent with the findings of other researchers.[3] Post-traumatic epilepsy is one of the most important complications after TBI,[22] and our finding that 16.7% of patients suffered from posttraumatic epilepsy is consistent with the findings of Andelic and co-workers.[9,18] The overall in-hospital mortality was 58%, which is consistent with the findings of Elm and co-workers (52% mortality rate).[3] The average GOSE score after severe TBI in our sample was 2.9±2.5 points. The majority of patients (70%) had a bad outcome and 30% made good recovery, which is consistent with the findings of Hawley and co-workers,[23] who at follow-up found 26% of patients with severe disability, 44% with moderate disability and 30% with good recovery. The strengths of our study were the inclusion of all eligible patients, which minimizes the risk for selection bias, the use of standardized scales in assessing patients, and the fact that patients on the field were assessed by an experienced and well-trained attending EMS physician. The main limitation is the relatively small sample. Another limitation is also the retrospective design of the study. Further studies should have a prospective design and should aim at a larger sample. In conclusion, adequate out-of-hospital and inhospital treatments proved to play a role in better outcomes as measured in GOSE scores. A decision tree provides a good insight into the hierarchy of measures that improve long-term outcomes after severe TBI. It could present the basis for the development of a standardized inpatient protocol on monitoring, intervention and outcome recordings. Such a protocol would make future comparisons more useful and also promote benchmarking between the trauma centers in order to improve care for severe TBI patients. Acknowledgements We thank all the doctors who provided the interviews with severe TBI patients. We acknowledge the valuable support from Andrej Zmavc, MD, head of EMS Celje, in the development of the EMS and in this research.
REFERENCES 1. Leitgeb J, Erb K, Mauritz W, Janciak I, Wilbacher I, Rus514
nak M; Australian Severe TBI Study Investigators. Severe traumatic brain injury in Austria V: CT findings and surgical management. Wien Klin Wochenschr 2007;119:56-63. 2. von Wild KR; Hannover, Münster TBI Study Council. Posttraumatic rehabilitation and one year outcome following acute traumatic brain injury (TBI): data from the well defined population based German Prospective Study 20002002. Acta Neurochir Suppl 2008;101:55-60. 3. von Elm E, Osterwalder JJ, Graber C, Schoettker P, Stocker R, Zangger P, et al. Severe traumatic brain injury in Switzerland - feasibility and first results of a cohort study. Swiss Med Wkly 2008;138:327-34. 4. MRC CRASH Trial National Coordinators. Update on progress in the international, multicenter, randomized, controlled trial of corticosteroids after significant head injury (Medical Research Council CRASH Trial). Curr Opin Crit Care 2003;9:92-7. 5. Marshall LF, Gautille GM, Klauber MR, Eisenberg HM, Jane JA, Leurssen TG et al. The outcome of severe closed head injury. J Neurosurg 1991;75:S28-S36. 6. Jiang JY, Gao GY, Li WP, Yu MK, Zhu C. Early indicators of prognosis in 846 cases of severe traumatic brain injury. J Neurotrauma 2002;19:869-74. 7. Kraus JF, Peek-Asa C, McArthur D. The independent effect of gender on outcomes following traumatic brain injury: a preliminary investigation. Neurosurg Focus 2000;8:e5. 8. Slewa-Younan S, Baguley IJ, Heriseanu R, Cameron ID, Pitsiavas V, Mudaliar Y, et al. Do men and women differ in their course following traumatic brain injury? A preliminary prospective investigation of early outcome. Brain Inj 2008;22:183-91. 9. Andelic N, Hammergren N, Bautz-Holter E, Sveen U, Brunborg C, Røe C. Functional outcome and health-related quality of life 10 years after moderate-to-severe traumatic brain injury. Acta Neurol Scand 2009;120:16-23. 10. Livingston DH, Lavery RF, Mosenthal AC, Knudson MM, Lee S, Morabito D, et al. Recovery at one year following isolated traumatic brain injury: a Western Trauma Association prospective multicenter trial. J Trauma 2005;59:1298304. 11. Shafi S, Marquez de la Plata C, Diaz-Arrastia R, Shipman K, Carlile M, Frankel H, et al. Racial disparities in long-term functional outcome after traumatic brain injury. J Trauma 2007;63:1263-70. 12. Klemen P, Golub M, Grmec S. Combination of quantitative capnometry, N-terminal pro-brain natriuretic peptide, and clinical assessment in differentiating acute heart failure from pulmonary disease as cause of acute dyspnea in pre-hospital emergency setting: study of diagnostic accuracy. Croat Med J 2009;50:133-42. 13. Slovenian society for intensive medicine. The guidelines for treatment of patients with severe head trauma. Zdrav Vestn 2004;73:31-6. 14. Howard JL, Cipolle MD, Anderson M, Sabella V, Shollenberger D, Li PM, et al. Outcome after decompresive craniotomy for the treatment of severe traumatic brain injury. J Trauma 2008;65:380-6. 15. Corral L, Ventura JL, Herrero JI, Monfort JL, Juncadella M, Gabarrós A, et al. Improvement in GOS and GOSE scores 6 and 12 months after severe traumatic brain injury. Brain Inj 2007;21:1225-31. 16. Zhu XL, Poon WS, Chan CC, Chan SS. Does intensive rehabilitation improve the functional outcome of patients with traumatic brain injury (TBI)? A randomized controlled trial. Kasım - November 2011
Outcome predictors of Glasgow Outcome Scale score in patients with severe traumatic brain injury
Brain Inj 2007;21:681-90. 17. Sörbo A, Rydenhag B, Sunnerhagen KS, Blomqvist M, Svensson S, Emanuelson I. Outcome after severe brain damage, what makes the difference? Brain Inj 2005;19:493-503. 18. Ponsford J, Draper K, Schönberger M. Functional outcome 10 years after traumatic brain injury: its relationship with demographic, injury severity, and cognitive and emotional status. J Int Neuropsychol Soc 2008;14:233-42. 19. Pettigrew LE, Wilson JT, Teasdale GM. Reliability of ratings on the Glasgow Outcome Scales from in-person and telephone structured interviews. J Head Trauma Rehabil 2003;18:252-8. 20. LeGrand SA, Hindman BJ, Dexter F, Moss LG, Todd MM. Reliability of a telephone-based Glasgow Outcome
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Scale assessment using a structured interview in a heterogenous population of patients and examiners. J Neurotrauma 2007;24:1437-46. 21. Kolar M, Krizmaric M, Klemen P, Grmec S. Partial pressure of end-tidal carbon dioxide successful predicts cardiopulmonary resuscitation in the field: a prospective observational study. Crit Care 2008;12:R115. 22. Asikainen I, Kaste M, Sarna S. Early and late posttraumatic seizures in traumatic brain injury rehabilitation patients: brain injury factors causing late seizures and influence of seizures on long-term outcome. Epilepsia 1999;40:584-9. 23. Hawley CA, Joseph S. Predictors of positive growth after traumatic brain injury: a longitudinal study. Brain Inj 2008;22:427-35.
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Ulus Travma Acil Cerrahi Derg 2011;17 (6):516-520
Original Article
Klinik Çalışma doi: 10.5505/tjtes.2011.41882
Özofagus perforasyonlarında tedavi: On bir olgunun analizi Treatment for esophageal perforations: analysis of 11 cases Ersin ARSLAN, Maruf ŞANLI, Ahmet Feridun IŞIK, Bülent TUNÇÖZGÜR, Ahmet ULUŞAN, Levent ELBEYLİ
AMAÇ
BACKGROUND
Kliniğimizde tedavi uygulanan özofagus perforasyonlu 11 olgu, özellikle cerrahi tedavinin önemini vurgulamak için sunuldu.
We present 11 cases with esophageal perforations who were treated in our department, with the intent of underlining the importance of surgical intervention.
GEREÇ VE YÖNTEM
METHODS
Bu çalışmada, 2005-2010 yılları arasında özofagus perforasyonu nedeni ile tedavi uygulanan 11 olgu geriye dönük olarak incelendi. İlk 24 saat içerisinde tanı konulan olgular erken, daha sonra tanı konulanlar ise geç tanı olarak değerlendirildi.
We retrospectively analyzed 11 cases of esophageal perforation who were treated from 2005 to 2010. The cases diagnosed within the first 24 hours were regarded as early diagnoses; those diagnosed later than this period were regarded as late diagnoses.
BULGULAR
RESULTS
Olguların yaş ortalaması 45,8 idi. Olgulardan 3’üne perforasyon oluştuktan sonra erken, diğerlerine ise geç dönemde tanı konuldu. Erken tanı konulan 3 olguya primer onarım, geç tanı konulan 8 olgunun 4’üne primer onarım, 2’sine kolon interpozisyonu, 1’ine stent uygulama ve 1 olguya ise medikal tedavi uygulandı. Geç tanı konulan olguların tümüne drenaj yapıldı. Erken tedavi edilen 3 olgu komplikasyonsuz olarak iyileşti. Diğer 8 olgunun 1’inde anastomoz kaçağı, 1’inde ise fistül gelişti. İki olgu hayatını kaybetti. Mortalite %18,1 olarak bulundu.
The mean age of the patients was 45.8 years. Following the perforation, 3 of the patients had early diagnoses and the others had late diagnoses. Of the 3 cases with early diagnosis, all had primary repair; of the late diagnosis cases, 4 had primary repair, 2 had colonic interposition, 1 had stent implantation, and 1 received medical treatment. All the cases with late diagnoses underwent drainage. The 3 cases who received early treatment recovered without complications. Of the other 8 cases, 1 had leakage from the anastomosis and 1 developed a fistula. Two (18.1%) of our patients died.
SONUÇ
CONCLUSION
Özofagus perforasyonlarında mediastinit gelişmeden yapılacak olan müdahale hayat kurtarıcıdır. Yaralanmadan sonra 72 saate kadar yapılacak olan ve primer onarımı içeren cerrahi tedavinin iyi sonuçlar verdiğini düşünmekteyiz.
Treatments performed before the development of mediastinitis are lifesaving in esophageal perforation patients. We think that surgical treatment performed within the first 72 hours that includes primary repair would yield favorable results.
Anahtar Sözcükler: Fistül; özofagus perforasyonu; primer onarım.
Key Words: Fistula; esophageal perforation; primary repair.
Gaziantep Üniversitesi Tıp Fakültesi, Göğüs Cerrahisi Anabilim Dalı, Gaziantep.
Department of Thoracic Surgery, Gaziantep University Faculty of Medicine, Gaziantep, Turkey.
İletişim (Correspondence): Dr. Maruf Şanlı. Gaziantep Üniversitesi, Tıp Fakültesi Göğüs Cerrahisi AD, 27310 Gaziantep, Turkey. Tel: +90 - 342 - 360 60 60 e-posta (e-mail): sanli@gantep.edu.tr
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Özofagus perforasyonlarında tedavi
Özofagus perforasyonları nadir görülür, fakat özofagusa yönelik tanı ve tedavi ile ilgili invaziv girişimlerin artması nedeni ile sıklığı giderek artmaktadır.[1,2] Özofagus perforasyonu kısa sürede mediastinal ve/veya plevral enflamasyon ve enfeksiyon, ardından sepsis gelişmesine neden olduğundan, bu olgularda morbidite ve mortalite yüksektir.[3] Özofagus perforasyonunda yakınma ve bulgular, perforasyonun yeri, gelişme şekli ve saptanma süresine bağlı olarak değişir.[3,4] Akciğer ve özofagus pasaj grafisi yararlı olmakla birlikte, kesin tanı perforasyonun endoskopik olarak görülmesi ile konur. Özofagoskopi ile hem rüptürün seviyesi belirlenir hem de tedavi yöntemine karar verilir. Bu olgularda iyi sağkalım için ilk 24 saat içerisinde tanı konulması ve tedaviye başlanması önemlidir.[2,5] İlk 24 saat sonrası bu olgularda mortalite 2 katına kadar çıkar.[1,6] Bu yazıda, kliniğimizde tedavi uygulanan özofagus perforasyonlu 11 olguda, perforasyon nedeni, yerleşim yeri, klinik özellikleri, uygulanan tedavi yöntemleri ve komplikasyonlar irdelenerek son durumları ile sunuldu.
GEREÇ VE YÖNTEM Kliniğimizde 2005-2010 yılları arasında, özofagus perforasyonu nedeni ile tedavi uygulanan ve bilgilerine ulaşılan 11 olgu geriye dönük olarak incelendi. İlk 24 saat içerisinde tanı konulan olgular erken, daha sonra tanı konulanlar ise geç tanı olarak değerlendirildi. Olgular demografik özellikleri, yaralanma yeri, şekli ve zamanı, yakınmalar, fiziksel inceleme ve radyolojik bulgular, tanı yöntemleri, uygulanan tedavi yöntemleri, morbidite ve mortalite yönünden değerlendirildi. Olgulara göğüs radyografisi, göğüs bilgisayarlı tomografisi (BT) yapılırken, bir kısmında kontrastlı radyolojik incelemeler (özofagus pasaj grafisi) yapıldı. Olguların tümünde özofagoskopi ile perforasyon tanısı kondu. BULGULAR Olguların yaş ortalaması 45,8 olarak bulundu. En genç olgu 2 yaşında iken, en yaşlı olgu 78 yaşındaydı (Tablo 1). Olgular etyolojik olarak incelendiğinde; 7’sinde iyatrojenik (5’inde özofageal dilatasyon, 1’inde trakeotomi, 1’inde ses cihazı yerleştirme), 3’ünde yabancı cisim, 1’inde ise spontan (Boerheave sendromu) nedenli özofagus perforasyonu geliştiği görüldü. Olguların 3’ünde perforasyon oluştuktan sonra ilk 24 saat içerisinde, 6’sında 24-72 saat içerisinde, 2’sinde ise daha geç dönemde tanı konuldu. İlk 24 saatte tanı konulan 3 olgunun 2’sinde yabancı cisim nedeniyle yapılan özofagoskopi, diğerinde ise akalazya nedeniyle yapılan dilatasyon sırasında rüptür gelişmişti. Olgularımızda özofagus perforasyonun yerleşimi, nedeni ve tedavi uygulamaları Tablo 2’de gösterilmiştir. Cilt - Vol. 17 Sayı - No. 6
Tablo 1. Olguların demografik özellikleri, semptom ve bulguları, radyolojik özellikler ve mevcut primer patolojiler
Olgu sayısı
Cinsiyet Erkek Kadın Yaş Yaş aralığı Ortalama Semptom ve bulgular Göğüs ağrısı Ateş Yutma güçlüğü Nefes darlığı Cilt altı amfizem Boyunda hassasiyet Radyolojik bulgular Pnömotoraks Medyastinal amfizem Plevral efüzyon Primer patoloji Koroziv özofajit Yabancı cisim Akalazya Boerhave sendromu Larenks karsinomu (Ses protezi) Akciğerde kitle (Trakeotomi)
6 5 2-78 45,8 7 6 6 5 3 2 8 7 4 4 3 1 1 1 1
Olgulardaki en belirgin radyolojik bulgu pnömotoraks (n=8) ve mediastinal amfizemdi (n=7). Klinik ve radyolojik olarak özofagus rüptüründen şüphelenilen olguların tümünde tanı, özofagoskopi ile kesinleştirildi. Kontrastlı pasaj grafisi, geç olgularda ve suda eriyen kontrast madde kullanılarak yapıldı (Şekil 1). Olgulara tanı konulma süresine bağlı olarak giri-
(a)
(b)
Şekil 1. (a) Kontrast maddenin özofagustan geçişi. (b) Aynı olguda plevral sıvıda kontrast maddenin görünümü. 517
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Tablo 2. Perforasyonun yerleşim yeri, nedeni ve tedavi şekli
Perforasyon nedeni İyatrojenik Dilatasyon Trakeotomi Ses protezi Yabancı cisim Spontan Perforasyon yerleşimi Torakal Servikal Abdominal Tedavi şekli Primer onarım Drenaj + primer onarım Kolon interpozisyonu + jejunostomi Drenaj + primer onarım + jejunostomi Drenaj + stent + jejunostomi Drenaj + medikal
Olgu sayısı
5 1 1 3 1 6 4 1 3 3 2 1 1 1
şim uygulandı. Erken tanı konulan 3 olgu, doğrudan operasyona alınarak primer tamir uygulandı (Şekil 2). Geç olguların 4’üne primer tamir, 2’sine kolon interpozisyonu, 1’ine stent yerleştirme, 1’ine ise medikal tedavi uygulandı. Geç tanı alan olguların tümünde plevral ve/veya mediastinal drenaj uygulandı. Olguların 3’ünde enteral beslenme için jejunostomi açılırken, diğerleri total parenteral nutrisyon (TPN) ile beslendi. Erken cerrahi uygulanan üç olgu komplikasyonsuz olarak iyileşti. Diğer sekiz olgunun birinde anastomoz kaçağı, bir diğerinde ise fistül gelişti. Koroziv darlık nedeniyle uygulanan dilatasyon sırasında rüptür gelişen ve kolon interpozisyonu uygulanan olgudaki anastomoz kaçağı, medikal tedavi ile iyileşti. Larenks
karsinomu olan ve eksternal ses cihazı takılırken rüptür gelişen olgu ise fistül sonucu tedavinin 2. ayında sepsis ve solunum yetmezliği nedeni ile öldü. Koroziv darlık nedeniyle dilatasyon uygulanan 2 yaşındaki olguda gelişen perforasyon, 48. saatte primer onarıldı. Solunum yetersizliği ve sepsis gelişen olgu operasyon sonrası 3. gün öldü. Serimizin mortalite oranı %18,1’dir. Diğer 9 olgu ise ortalama 32,8 (dağılım 6-72 ay) aydır kliniğimizde takip edilmektedir.
TARTIŞMA Özofagus perforasyonları nadir görülen, gelişen invaziv girişimlere bağlı olarak görülme sıklığı giderek artan, erken dönemde tanı konulup tedavi edilmez ise yüksek mortaliteye sahip bir sorundur. İyatrojenik yaralanmalar özofageal perforasyonlarının en sık nedenidir.[4,6] Ayrıca, yabancı cisime bağlı, spontan, travma, kostik yaralanma, malignite ve barotravma sonucu da özofagusta perforasyon oluşabilir.[1,3] Olgularımızda da en sık sebep, 7 olgu (%63) ile iyatrojenik yaralanmalardı. Bu olgulardan 5’inde dilatasyon sonucu rüptür geliştiği belirlendi. Günümüzde sıklıkla kullanılan terapötik endoskopilerde %1-10 arasında,[2] dilatasyonlarda ise %0,1 oranında[7] özofagus perforasyonu görüldüğü bildirilmektedir. En sık görülen semptom ve bulgular; ağrı, ateş, yutma güçlüğü, nefes darlığı ve cilt altı amfizemidir.[1] Ayrıca taşikardi, hidropnömotoraks, mediastinal amfizem ve şok belirtileri de görülebilir.[4] Olgularımızda göğüs ağrısı, ateş ve yutma güçlüğü öne çıkan yakınmalardı. Ayrıca, pnömotoraks, plevral sıvı veya mediastinal amfizem bulgularından en az biri mevcuttu. Olgularda semptom ve bulgular perforasyonun nedenine, yerleşimine ve oluş zamanına göre değişebilir. Özellikle iyatrojenik gelişen ve oral alımın olmadığı olgularda patolojik bulgu saptanmayabilir. Perforasyonun üzerinden zaman geçmesi, perforasyondan sonra oral gıda alınması durumunda ise, genel durum kötüleşmesi, ateş, takipne ve hipotansiyon gibi sepsis bulgula-
Şekil 2. (a) Özofagusta perforasyonun görünümü. (b) Mukozanın ve (c) kasın ayrı ve tek tek dikilmesi. 518
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Özofagus perforasyonlarında tedavi
rı ortaya çıkar.[3] Bu nedenle risk faktörü olan olgular çok küçük kuşku olsa bile dikkatli bir şekilde, hızla değerlendirilmelidir. Erken tanı ve yapılacak girişimin hayat kurtarıcı olabileceği unutulmamalı, acil tedavi planlanmalıdır. Akciğer grafisi, göğüs BT’si, radyoopak madde ile çekilen pasaj grafisi tanıda yardımcı olsa bile, kesin tanı endoskopi ile konur.[4] Olgularımızın hepsinde perforasyon, özofagoskopi ile görüldü. Sadece 3 olguya ilk 24 saatte tanı konulabildi. Erken tanı konulan olgulardaki perforasyon, işlem esnasında (yabancı cisim çıkarma veya dilatasyon) görüldüğü için bu olgularda kontrastlı madde ile özofagografi yapılmadı. Geç tanı konulan 8 olgudaki tanısal işlemler içinde, suda eriyen kontrast madde kullanılarak çekilen özofagografide yer aldı. Başka kliniklerde incelenen bu 8 olguda mediastinit bulguları ortaya çıkana kadar perforasyondan şüphelenilmediği, olguların kliniğimizde geç konsülte edildiği ve tanının geciktiği belirlendi. Tedavide amaç, enfeksiyon kaynağının ortadan kaldırılması, yeterli drenaj, vücut savunmasının arttırılması, gastrointestinal sistemin devamlığı ve yeterli beslenmenin sağlanmasıdır.[4] Bu amaçla öncelikle oral alım kesilir ve gelişecek olan mediastiniti kontrol altına almak için geniş spektrumlu antibiyotik tedavisi başlanır. Plevral ve/veya mediastinal drenaj uygulanır, parenteral veya jejunostomi ile enteral beslenme sağlanır. Olgularımızda oral alım kesildi ve geniş spektrumlu antibiyoterapi başlandı. Geç tanı konulan olgulara tüp torakostomi ile plevral drenaj uygulandı. Dört olguya jejunostomi yapılırken, 7 olguya TPN ile beslenme sağlandı. Özofagus perforasyonunun tedavisinde standart bir yaklaşım yoktur. Tedavi seçeneği perforasyon nedeni, lokalizasyon, özofageal hastalığın varlığı, tanı zamanı, çevre organ yaralanması, hastanın genel durumu ve yaşına bağlı olarak değişir. Konservatif tedavi sadece seçilmiş olgularda uygulanır. Erken tanı konulan, oral almamış, özofagus lümeninin içine drene olan perforasyonlarda, abdominal özofagus perforasyonu olmaması durumlarında konservatif tedavi seçilebilir.[3] Ancak konservatif tedavi uygulanırken eldeki cerrahi seçeneğinin kaybedilebileceği unutulmamalıdır. Küçük servikal yaralanmalarda tek başına drenajın, bazen yeterli olabileceği belirtilmektedir.[3] Başka bir merkezde özofagus 1. darlıktan yabancı cisim (metal para) çıkarılırken perforasyon gelişen ve kliniğimize boyun ağrısı ve ciltaltı amfizemi nedeniyle perforasyondan 48 saat sonra tüp torakostomili olarak gönderilen çocuk olgumuzda; özofagoskopi ile özofagus 1. darlıkta yaklaşık 0,3 cm’lik yaralanma bölgesi görüldü. Özofagoskopi eşliğinde nazogastrik sonda takıldı, oral alım kesildi. Bu olgu, klinik olarak herhangi bir mediastinit bulgusu gelişmemesi ve boyun ağrısı ve ciltaltı amfizeminin giderek kaybolması üzerine medikal olarak Cilt - Vol. 17 Sayı - No. 6
takip edildi ve 11. gün sorunsuz olarak taburcu edildi. Erken tanı ve cerrahi uygulanması ile sağkalım %93 olarak bildirilmiştir.[8] Bu olgularda en sık seçilen cerrahi yöntem primer onarımdır.[3] Bizim erken cerrahi ile primer onarım uyguladığımız 3 olguda sağkalım %100’dü. Olgularımızda primer onarım mukoza ve kas tabakası ayrı ayrı olmak üzere emilebilir materyalle yapıldı. Geç tanılarda ve ciddi mediastinit bulguları olan olgularda ise yaralanma sahasının çıkarılması ile özofageal diversiyon, gastrostomi/jejunostomi ve geç rekonstrüksiyon yöntemleri önerilmektedir. [3,9] Geç tanı konulan olguların 2’sinde drenajı içeren tedavi yapılarak, mediastinit bulguları kaybolduktan sonra kolon interpozisyonu uygulandı. Geç tanı konulan diğer bir olgumuzda (Boerheave sendromu tanısı olan olgumuz), ciddi mediastinit bulguları olduğu için önce drenaj yapıldı ve genel durumu ameliyat için uygun olmadığından özofageal stent yerleştirildi. Bu olguda işlem sonrası 3. ayda yapılan özofagoskopide, perforasyonun granülasyon dokusu ile kapandığı görüldü ve stent çıkarıldı. Onarım bölgesinin doku flepleri ile güçlendirilmesinin fistül gelişimini %13’ten %6’ya, mortaliteyi %39’dan, %25’e azalttığı bildirilmektedir.[10] Geç tanı konulan 3 olguda primer onarım uygulandı. Bunlardan yaralanma bölgesi servikalde olan olguda onarım bölgesi pektoral kas, toraksta olan 2 olguda ise plevra ile güçlendirildi. Geç tanı konulan olguların 1’inde anastomoz kaçağı, 1’inde fistül geliştiği görüldü. Anastomoz kaçağı koroziv darlık nedeni ile dilatasyon sırasında rüptür gelişen ve kolon interpozisyonu uygulanan olguda izlendi. Bu olguda oral alım kesildi, jejunostomi ile enteral beslenme sağlandı ve anastomoz boyunda olduğu için takip edildi. Fistül operasyon sonrası 20. gün iyileşti. Özofagus cerrahisi sonrası en önemli sorunlardan olan anastomoz kaçağının tedavisinde stent uygulaması, önerilen yaklaşımlardandır.[2] Eksternal ses cihazı yerleştirilirken perforasyon gelişen ve primer onarım uygulanan olguda, ameliyat sonrası dönemde fistül gelişerek mediastinit ve ampiyem oluştu. Olgudaki onarım bölgesi 1. darlık seviyesinde olduğu için stent uygulanamadı. Bu olgu operasyon sonrası 2. ay sepsis ve solunum yetersizliği nedeni ile hayatını kaybetti. Özofagus perforasyonu gelişen olgularda tüm tedavi yöntemlerine rağmen mortalite %10-23 arasındadır.[1,6,10,11] Olgularımızın 2’sinde mortalite gelişti ve mortalite oranı %18,1 olarak bulundu. Sonuç olarak, özofagus perforasyonlarında erken tanı ve tedavi hayat kurtarıcıdır. Bu olgularda mortalitenin en önemli nedenlerinden olan mediastiniti önlemek için yeterli drenaj sağlanmalı ve geniş spektrumlu antibiyoterapiye başlanmalıdır. Mediastinal ve plevral kirlenme gelişmeden tanının konulması, tedavinin 519
Ulus Travma Acil Cerrahi Derg
başarı şansını arttırır. Biz özellikle ilk 72 saate kadar olan perforasyonlarda primer onarım uygulanabileceği ve canlı dokular ile anastomoz hattının güçlendirilmesinin fistül gelişimini azaltabileceği düşüncesindeyiz.
KAYNAKLAR 1. Chirica M, Champault A, Dray X, Sulpice L, Munoz-Bongrand N, Sarfati E, et al. Esophageal perforations. J Visc Surg 2010;147:117-28. 2. Erdoğan A, Öz N, Sarper A, Dertsiz L, Demircan A, Işın E. Özofagus perforasyonları; 11 olgunun analizi. GKDC Dergisi 1999;7:57-62. 3. Yenigün B, Çelik A, Cangır KA. Özofagus yaralanmaları. TTD Toraks Cerrahisi Bülteni 2010;1:60-73. 4. Eroğlu A, Türkyılmaz A, Başoğlu A. Özofagus yaralanmaları. Türkiye Klinikleri J Surg Med Sci 2007;3:29-37. 5. Roan JN, Wu MH. Esophageal perforation caused by external air-blast injury. J Cardiothorac Surg 2010;5:130. 6. Hermansson M, Johansson J, Gudbjartsson T, Hambreus G,
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Jönsson P, Lillo-Gil R, et al. Esophageal perforation in South of Sweden: results of surgical treatment in 125 consecutive patients. BMC Surg 2010;10:31. 7. Wolfsen HC, Hemminger LL, Achem SR, Loeb DS, Stark ME, Bouras EP, et al. Complications of endoscopy of the upper gastrointestinal tract: a single-center experience. Mayo Clin Proc 2004;79:1264-7. 8. Kiernan PD, Sheridan MJ, Elster E, Rhee J, Collazo L, Byrne WD, et al. Thoracic esophageal perforations. South Med J 2003;96:158-63. 9. Richardson JD. Management of esophageal perforations: the value of aggressive surgical treatment. Am J Surg 2005;190:161-5. 10. Lawrence DR, Ohri SK, Moxon RE, Townsend ER, Fountain SW. Primary esophageal repair for Boerhaave’s syndrome. Ann Thorac Surg 1999;67:818-20. 11. Eroglu A, Can Kürkçüogu I, Karaoganogu N, Tekinbaş C, Yimaz O, Başog M. Esophageal perforation: the importance of early diagnosis and primary repair. Dis Esophagus 2004;17:91-4.
Kasım - November 2011
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):521-524
Original Article
Klinik Çalışma doi: 10.5505/tjtes.2011.28582
Increased nutritional risk in major trauma: correlation with complications and prolonged length of stay Majör travmada artan nutrisyonel risk: Komplikasyon ve yatış süresinde uzama ile korelasyon Zikret KÖSEOĞLU,1 Mehmet ÖZDOĞAN2 Adnan KUVVETLİ,2 Ozgün KÖSENLİ,1 Cem ORUÇ,2 Safa ÖNEL,2 Koray DAS,2 Atilla AKOVA,2 BACKGROUND
AMAÇ
Acute Physiology and Chronic Health Evaluation II (APACHE II) and the Trauma Injury Severity Score (TRISS) are physiological and anatomical severity scores to predict trauma outcome. Nutritional Risk Screening (NRS-2002) is used for the screening of nutritional risk, which can affect outcome adversely. The objective of this study was to determine the reliability of these scales to predict disease severity, complications and mortality, and to compare the reliability of the NRS-2002 in predicting outcome with different scoring systems in trauma–intensive care unit (ICU) patients.
Akut Fizyoloji ve Kronik Sağlık Değerlendirmesi II (APACHE II) ve Travma Yaralanma Şiddet Skoru (TRISS), travma sonucunu tahmin etmek için kullanılan fizyolojik ve anatomik şiddet skorlama skalalarıdır. Nutrisyonel Risk Skorlaması (NRS-2002), nutrisyonel riskin taraması için kullanılır. Bu çalışmanın amacı, hastalığın şiddetini, komplikasyonları ve mortalite tahmini için bu skorlama sistemlerinin güvenilirliğini belirlemek ve travma yoğun bakım hastaları için sonuçların tahmininde farklı skorlama sistemleri ile NRS-2002’nin güvenilirliğini karşılaştırmaktır.
METHODS
Bu çalışmaya altı aylık çalışma süresinde (1 Temmuz 2008 ile 1 Ocak 2009) travma sonrasında bir eğitim hastanesi yoğun bakım ünitesine (YBÜ) kabul edilen 100 ardışık hasta dahil edildi. Skorlama sistemlerinin diskriminasyon özellikleri alıcı işletim karakteristiği (receiver operating characteristic-ROC) eğrileri kullanılarak değerlendirildi.
The study enrolled 100 consecutive patients who were admitted to the ICU in a training hospital due to trauma in the six-month study period (1 July 2008 and 1 January 2009). Discrimination characteristics of the scoring systems were evaluated using receiver operating characteristic (ROC) curves.
GEREÇ VE YÖNTEM
BULGULAR
Overall mortality was 14%, and the complication rate was 22%. Nutritional risk at admission was found to be increased in 58% of the patients. The NRS-2002 score was increased in patients with complication. ISS, TRISS and APACHE II at admission had a reliable power of discrimination (AUC>0.8) for mortality and complication prediction. The NRS-2002 score had moderate discrimination power for complication prediction (AUC=0.708) but showed high correlation with increased length of stay (LOS).
Genel mortalite %14 ve komplikasyon oranı %22 idi. Hastaneye başvuru sırasında hastaların %58’inde nutrisyonel riskin artmış olduğu saptandı. Komplikasyon gelişen hastalarda NRS-2002 skorunun artığı saptandı. Başvurudaki ISS, TRISS ve APACHE II skorlarının mortalite ve komplikasyon tahmini için diskriminasyon gücü güvenilir seviyede (AUC >0,8) idi. NRS-2002 skorunun komplikasyon tahmini için orta derecede diskriminasyon gücü (AUC=0,708) olduğu saptandı. NRS-2002 skoru ile hastanede kalış süresi arasında yüksek korelasyon mevcuttu.
CONCLUSION
SONUÇ
RESULTS
A significant percent of trauma patients are at nutritional risk. The NRS-2002 score can be useful in predicting complication and prolonged LOS in trauma patients.
Travma hastalarının önemli bir yüzdesi nutrisyonel risk altındadır. NRS-2002 skoru travma hastalarında komplikasyon artışı ve yatış süresinde uzama tahmininde yararlı olabilir.
Key Words: Nutritional Risk Screening (NRS)-2002; trauma score/ outcome; critical care; nutritional risk.
Anahtar Sözcükler: Beslenme Risk Taraması (NRS) -2002; travma skoru/sonucu; yoğun bakım; beslenme riski.
Departments of 1Emergency Medicine, 2General Surgery, Adana Numune Training and Research Hospital, Adana, Turkey.
Adana Numune Eğitim ve Araştırma Hastanesi, 1Acil Tıp Kliniği, 2 Genel Cerrahi Kliniği, Adana.
Correspondence (İletişim): Zikret Köseoğlu, M.D. Adana Numune Eğitim ve Arşt Hastanesi, Acil Tıp Servis, Seyhan, 01170 Adana, Turkey. Tel: +090 - 322 - 226 03 31 / 1181 e-mail (e-posta): drzikret@yahoo.com
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Ulus Travma Acil Cerrahi Derg
There are several scoring systems in general use for outcome prediction in hospitalized patients. The rationale behind the common use of these scales is to score illness severity to yield comparisons between patient groups, intensive care units (ICUs) or interventions. [1,2] However, they have also been used to assess or to predict the risk in specific patient groups for mortality, complication and length of hospital stay (LOS). In the context of trauma patients, there are three main groups of scoring systems for risk prediction. 1: Anatomical scores, which provide an overall score based on grades of multiple injuries. The most commonly used anatomical score is the Injury Severity Score (ISS). 2: Physiological scores are calculated by evaluating the physiological variables of the patient without taking the anatomical injuries into account. One of the most widely used physiological prognostic models in the ICU is the Acute Physiology and Chronic Health Evaluation II (APACHE II) system. It incorporates the chronic health evaluation (e.g. diabetes mellitus, cirrhosis) with the acute physiological status of the patient. 3: Combined anatomical and physiological scores assess both anatomical injury variables and physiological parameters to increase the predictive power. The Trauma Injury Severity Score (TRISS) method, the most widely used combined system, provided improvements in the ability to predict outcome after trauma.[3] As expressed by Osler,[4] the outcome prediction algorithm can be usefully summarized as follows: Outcome = anatomical injury + physiological injury + patient reserve. Nutritional status is one of the most important components of the patient’s reserve. Of note, one of the drawbacks of all the above-mentioned systems is that they all ignore the nutritional status. They do not take the nutritional risk into account as an independent predictive variable. However, malnutrition at admission has been known to be associated with increased rates of complications, LOS and mortality.[5,6] The Nutritional Risk Screening 2002 (NRS-2002) score was introduced by the European Society for Clinical Nutrition and Metabolism (ESPEN) as a useful method for the screening of nutritional risk in hospitalized patients.[7] It consists of a nutritional score, a disease severity score and an age adjustment for patients aged >70 years. The total score is calculated and patients are classified as being at no risk to high risk. When the NRS-2002 score is ≥3, patients are accepted as under risk from a nutritional point of view. The primary aim of the present study was to investigate the reliability of systems designed to predict disease severity and the probability of mortality and 522
complications, and to compare the reliability of NRS2002 in predicting outcome with different scoring systems in trauma - ICU patients. To our knowledge, the present study is the first study in the English literature comparing the reliability of a nutritional risk screening index with that of prognostic trauma scores. The secondary aim was to determine the nutritional risk of trauma patients in the region at the time of hospital admission.
MATERIALS AND METHODS The study enrolled 100 consecutive patients who were admitted to the ICU due to trauma between 1 June 2008 and 1 January 2009 in the Training and Research Hospital, which is a 910-bed tertiary care hospital with an annual census of 330,000 patients (only emergency department [ED]). The hospital is a tertiary care referral center for a hinterland in the north-eastern Mediterranean region populated by around 6 million people. The main outcome measures were mortality, complications and LOS. Complications that were taken into the analysis included: wound-related (surgical site infection, evisceration, and dehiscence), cardiac (arrhythmias, ischemic events), pulmonary (atelectasis, respiratory failure, adult respiratory distress syndrome, and pneumonia), and gastrointestinal (leaks, fistulas, and intraabdominal abscesses) complications and other events (acute renal failure, acalculous cholecystitis, and pressure ulcer). Records of the Prehospital Emergency Medical Service, hospital emergency department and trauma– ICU were reviewed. Radiological and operative findings were evaluated. APACHE II, ISS and NRS-2002 scores were calculated. APACHE II score and the predicted mortality rates according to TRISS methodology were calculated using open-access web sites (http:// www.akademikcerrahi.com/apache.html and http:// www.sfar.org/scores2/triss2.html). Data Analysis The term “discrimination” refers to the ability of a model to distinguish patients who experienced an event from those who did not. Therefore, it defines the overall predictive power of a model. Discrimination was measured by the receiver operating characteristic (ROC) curves. The area under the curve (AUC) represents the probability that a patient who experienced the event had a higher predicted probability of having that event than a patient who did not.[8] The higher the true-positive rate is compared to the false-positive rate, the greater the AUC. The discrimination power of a model is considered perfect if AUC=1, good if AUC>0.8, moderate if AUC is between 0.6 and 0.8, and poor if AUC<0.6. Kasım - November 2011
Increased nutritional risk in major trauma
Table 1. Patient information (age and LOS are presented as mean ± SD) Number Age ICU LOS (day) Hospital LOS (day) Patients with complications Reoperation
Total
Survivors
Non-survivors
p
100 32.88±12.44 2.71±2.39 5.02±3.06 22 5
86 33.10±12.99 2.91±2.51 5.59±2.90 14 –
14 31.50±8.53 1.50±0.76 1.50±0.76 8 5
– NS 0.04 0.0001 0.002 NS
NS: Nonsignificant; ICU: Intensive care unit; LOS: Length of stay.
Continuous variables were presented as means ± SD and were compared using ANOVA. Categorical values were analyzed using the chi-square test. Correlations were evaluated by Pearson’s correlation. A value of p<0.05 was considered as statistically significant. Statistical evaluation was performed by using the Statistical Package for the Social Sciences (SPSS) 11.0 statistical package.
RESULTS Data on survivors and non-survivors are presented in Table 1. A total of 100 patients (41 penetrating, 59 blunt trauma patients), with a mean age of 32.88±12.44 years (range: 15-65) were included in the study. Overall mortality was 14%, and at least one complication was observed in 22% of the patients. When the NRS2002 score is ≥3, patients are accepted as at risk from a nutritional point of view. In the present study, the NRS-2002 score was found to be ≥3 in 58% of the patients. Table 2 shows overall scores and the differences between survivors and non-survivors and patients with or without complications. Increased ISS and APACHE II scores and the predicted mortality rate with the TRISS method were found to be significantly associated with both mortality and complication development. The NRS-2002 score was significantly increased in patients with complication; however, no association was found between the NRS-2002 and mortality. Discrimination values of the scoring systems revealed findings consistent with the statistical evaluation. ISS, TRISS and APACHE II scores recorded on admission had a reliable power of discrimination
(AUC >0.8) for mortality and complication prediction. The NRS-2002 score was found to be insufficient for mortality prediction (AUC=0.504). However, the NRS-2002 score had acceptable discrimination power for complication prediction (AUC=0.708) (Table 3). The NRS-2002 score showed a correlation with both increased intensive care and hospital LOS (Table 4).
DISCUSSION Published research showed that nearly one-third of hospitalized patients suffer from malnutrition.[9,10] There are few reports about the incidence of malnutrition in trauma patients. The findings in the present study pointed out that more than half of the patients are subject to increased nutritional risk at trauma-ICU admission. In accordance with this finding, a recent study demonstrated that 40% of trauma patients had moderate malnutrition at hospital admission according to the Subjective Global Assessment (SGA) model.[11] These observations are important since trauma paTable 3. Discrimination and calibration statistics of the evaluated scoring systems for outcome variables* ISS TRISS APACHE II NRS-2002
Mortality AUC (p)
Complication AUC (p)
0.878 (<0.001) 0.926 (<0.001) 0.920 (<0.001) 0.504 (0.920)
0.861 (<0.001) 0.902 (<0.001) 0.867 (<0.001) 0.708 (=0.001)
ISS: Injury Severity Score; TRISS: Trauma Injury Severity Score; APACHE II: Acute Physiology and Chronic Health Evaluation II; NRS: Nutritional Risk Screening. *(The areas under the ROC curves [AUC] for outcome variables and their significance)
Table 2. The relation between scores and mortality and complication development (mean ± SD) ISS TRISS APACHE II NRS-2002
Total
Survivors
Non-survivors
p
Patients without complication
Patients with complication
p
15.85±13.07 9.32±21.88 6.48±5.01 2.55±1.57
12.63±8.76 2.25±3.00 5.0±2.95 2.53±1.65
35.64±17.54 52.75±35.01 15.64±5.43 2.64±1.01
<0.001 <0.001 <0.001 0.813
12.46±10.50 6.66±20.11 5.14±4.18 2.28±1.56
27.86±14.38 18.76±25.58 11.23±4.92 3.5±1.23
<0.001 0.021 <0.001 0.001
ISS: Injury Severity Score; TRISS: Trauma Injury Severity Score; APACHE II: Acute Physiology and Chronic Health Evaluation II; NRS: Nutritional Risk Screening.
Cilt - Vol. 17 Sayı - No. 6
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Ulus Travma Acil Cerrahi Derg
Table 4. Correlations between scoring systems and LOS (Pearson correlation) ISS TRISS APACHE II NRS-2002 Hospital LOS (day) ICU LOS (day)
ISS
TRISS
APACHE II
NRS-2002
Hospital LOS (day)
ICU LOS (day)
1 .772* .743* .183 .000 .081
.772* 1 .755* -.012 -.348* -.156
.743* .755* 1 .126 -.132 .076
.183 -.012 .126 1 .542* .527*
.000 -.348* -.132 .542* 1 .752*
.081 -.156 .076 .527* .752* 1
ISS: Injury Severity Score; TRISS: Trauma Injury Severity Score; APACHE II: Acute Physiology and Chronic Health Evaluation II; NRS: Nutritional Risk Screening; LOS: Length of stay; ICU: Intensive care unit. * Correlation is significant at 0.01 level (2-tailed).
tients are usually young and productive persons. Although the NRS-2002 has not been specifically devised for use in trauma and surgical patients, it was found as an accurate screening tool in patients undergoing major elective surgery, and a high NRS-2002 score is associated with an increased complication rate and prolonged LOS.[12,13] The purpose of nutritional screening is to predict the probability of a better or worse outcome due to nutritional factors and whether nutritional treatment is likely to be influential.[7] Therefore, an ideal nutritional screening tool is supposed to predict postoperative mortality and complication rates in surgical patients, so that nutritional intervention can be provided in high-risk patients. To our knowledge, this is the first study in the English literature comparing the reliability of a nutritional risk screening index with that of prognostic trauma scores and severity of illness scores. The present data indicate sufficient discrimination statistics and predictive power of the NRS-2002 for complication and prolonged LOS prediction in trauma-ICU patients. The predictive powers of anatomical, physiological and combined trauma scoring systems for mortality and prediction differ. It appears that currently there is no ideal and universally applicable scoring system. [3] An ideal scoring system should incorporate all variables��������������������������������������������� of anatomical injury, physiological derangement and patient reserve into an outcome prediction score. “Patient reserve” plays a very important role in outcome, and this concept includes age, comorbidities, immunological and genetic properties, and the nutritional status of the patient. None of the currently available systems takes the nutritional risk into account as an independent predictive variable. As demonstrated before,[3] the ISS, APACHE II and TRISS systems were found to have sufficient predictive power for mortality and complication in the present study. Although the NRS-2002 score incorporates age, nutritional status and preexisting comorbidities, ROC analysis indicated that it has inadequate predictive power for mortality. Although trauma is a disease of the young and 524
healthy population, a significant percent of trauma patients in our region are at nutritional risk. The NRS2002 score can be useful and practical in predicting complication risk and prolonged hospital stay in trauma patients.
REFERENCES 1. Blackburn GL, Benotti PN, Bistrian BR, Bothe A, Maini BS, Schlamm HT, et al. Nutritional assessment and treatment of hospital malnutrition. Infusionsther Klin Ernahr 1979;6:23850. 2. Boyd O, Jackson N. How is risk defined in high-risk surgical patient management? Crit Care 2005;9:390-6. 3. Chawda MN, Hildebrand F, Pape HC, Giannoudis PV. Predicting outcome after multiple trauma: which scoring system? Injury 2004;35:347-58. 4. Correia MI, Waitzberg DL. The impact of malnutrition on morbidity, mortality, length of hospital stay and costs evaluated through a multivariate model analysis. Clin Nutr 2003;22:235-9. 5. Goiburu ME, Goiburu MM, Bianco H, Díaz JR, Alderete F, Palacios MC, et al. The impact of malnutrition on morbidity, mortality and length of hospital stay in trauma patients. Nutr Hosp 2006;21:604-10. 6. Hanley JA, McNeil BJ. The meaning and use of the area under a receiver operating characteristic (ROC) curve. Radiology 1982;143:29-36. 7. Kondrup J, Allison SP, Elia M, Vellas B, Plauth M; Educational and Clinical Practice Committee, European Society of Parenteral and Enteral Nutrition (ESPEN). ESPEN guidelines for nutrition screening 2002. Clin Nutr 2003;22:415-21. 8. Le Gall JR. The use of severity scores in the intensive care unit. Intensive Care Med 2005;31:1618-23. 9. Osler T. Injury severity scoring: perspectives in development and future directions. Am J Surg 1993;165:43-51. [Abstract] 10. Pirlich M, Schütz T, Norman K, Gastell S, Lübke HJ, Bischoff SC, et al. The German hospital malnutrition study. Clin Nutr 2006;25:563-72. 11. Schiesser M, Müller S, Kirchhoff P, Breitenstein S, Schäfer M, Clavien PA. Assessment of a novel screening score for nutritional risk in predicting complications in gastro-intestinal surgery. Clin Nutr 2008;27:565-70. 12. Schneider SM, Veyres P, Pivot X, Soummer AM, Jambou P, Filippi J, et al. Malnutrition is an independent factor associated with nosocomial infections. Br J Nutr 2004;92:105-11. 13. Sorensen J, Kondrup J, Prokopowicz J, Schiesser M, Krähenbühl L, Meier R, et al. EuroOOPS: an international, multicentre study to implement nutritional risk screening and evaluate clinical outcome. Clin Nutr 2008;27:340-9. Kasım - November 2011
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):525-532
Original Article
Klinik Çalışma doi: 10.5505/tjtes.2011.65983
Unusual emergent presentations of abdominal aortic aneurysm: Can simple blood tests predict the state of emergency? Abdominal aort anevrizmasında nadir görülen acil klinik durumlar: Basit kan testleri aciliyetin tanımlanmasında yol gösterici midir? Ali FEDAKAR,1 Orhan FINDIK,2 Mehmet KALENDER,1 Mehmet BALKANAY1
BACKGROUND
AMAÇ
This paper attempts to see if simple blood test results can predict the state of an emergency aneurysm as being nonruptured, contained leak or free rupture.
Bu çalışmada, basit kan testlerinin acil abdominal aort anevrizmasının (AAA) klinik sunumu ile ilişkisinin araştırılması amaçlandı.
METHODS
GEREÇ VE YÖNTEM
Ninety-three patients who presented to our emergency room and were operated for abdominal aortic aneurysm (AAA) between January 1999 and March 2009 were evaluated retrospectively. Cases were classified as: chronic contained rupture (Group I), impending rupture (Group II), dissecting rupture (Group III), and free rupture (Group IV).
Ocak 1999 - Mart 2009 tarihleri arasında kliniğimiz acil servisine müracaat etmiş ve hastaneye AAA tanısı ile yatırılmış olan toplam 93 hasta geriye dönük olarak incelendi. Kronik sınırlandırılmış rüptür olguları “Grup I”, rüptür tehdidi olguları, “Grup II”, disekan rüptür olguları “Grup III” ve gerçek (serbest) rüptür olguları ise “Grup IV” olarak sınıflandırıldı.
RESULTS
BULGULAR
Chronic contained rupture was determined in 15 (16.1%), impending rupture in 31 (33.3%), dissecting rupture in 14 (15.1%), and true (free) rupture in 27 (29%) cases. Aortocaval fistula was present in 3 (3.2%) patients, aortoenteric fistula in 2 (2.2%) and aorto biliary fistula in 1 (1.1%). Group IV was significantly different from Groups I, II and III with regard to hematocrit levels, white blood cell counts, neutrophils and lymphocyte rates, bicarbonate levels, and mortality rates.
Kronik sınırlandırılmış rüptür hastaların 15’inde (%16,1), rüptür tehdidi 31’inde (%33), disekan rüptür 14’ünde (%15,1) ve gerçek (serbest) rüptür 27’sinde (%29) saptandı. Hastaların üçünde (%3,2) aortokaval fistül, ikisinde (%2,2) aortoenterik fistül, birinde (%1,1) aortobiliyer fistül tanımlandı. Grup IV hemotokrit seviyesi, beyaz küre sayısı, nötrofil ve lenfosit oranları, bikarbonat seviyesi ve mortalite oranları açısından Grup I, II ve III’e göre istatiksel olarak anlamlı olan farklı parametrelere sahipti.
CONCLUSION
SONUÇ
To avoid a delay in diagnosis, it is important to know the different presentations of emergency AAA. In the emergency room, simple laboratory parameters may be highly directive in suspicion of ruptured AAA.
Tanıda gecikmeyi önlemek için AAA’nın acil kliniğinin değişkenlik gösterdiğinin bilinmesi önemlidir. Acil odasında alınan basit kan testleri serbest rüptür açısından oldukça yönlendirici olabilmektedir.
Key Words: Abdominal aortic aneurysm; emergency; clinical presentations.
Anahtar Sözcükler: Abdominal aort anevrizması; acil; klinik bulgular.
1 Department of Cardiac Surgery; Kartal Kosuyolu Education and Research Hospital, İstanbul; 2Department of Cardiac Surgery; Derince Education and Research Hospital, Kocaeli, Turkey.
Kartal Koşuyolu Yüksek İhtisas Hastanesi, Kalp ve Damar Cerrahisi Kliniği, İstanbul; 2Derince Eğitim ve Araştırma Hastanesi, Kalp ve Damar Cerrahisi Kliniği, Kocaeli.
1
Correspondence (İletişim): Ali Fedakar, M.D. Kartal Kosuyolu Yüksek İhtisas Eğitim ve Araştırma Hastanesi, 34846 İstanbul, Turkey. Tel: +90 - 216 - 459 44 40 e-mail (e-posta): alfdkr67@hotmail.com
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Abdominal aortic aneurysm (AAA) is an important cause of morbidity and mortality especially in male patients over the age of 65, and its prevalence is 1.0-8.9% in the general population.[1] Its incidence is reported to be increasing in the last 20 years.[2,3] It is estimated that there are 8000 deaths in England and 15000 deaths in the United States annually related to rupture of AAA.[1,4] The treatment of ruptured AAA is emergent surgery or endovascular repair. The mortality rate is dependent on the hemodynamic condition of the patient during the intervention. The reported operative mortality is 30-70% in ruptured AAA.[5,6] The mortality of ruptured AAA is unchanged despite the advances in surgical procedure, anesthetic management and medical care in conventional operations for ruptured AAA. [6] However, in recent years, there have been encouraging studies reporting good results with endovascular stent graft treatment in patients with ruptured aortic aneurysms.[7,8] The classic triad of ruptured AAA is abdominal or back pain, hemodynamic shock and pulsatile abdominal mass. The clinical presentation depends on the localization and degree of the rupture. The rupture is from the anterolateral wall of the abdominal aorta to the peritoneal cavity in 12% of the cases.[9,10] Rupture from the posterolateral wall to the retroperitoneal area constitutes 88% of cases and has a less mortal course than anterolateral wall rupture.[9,10] These groups of patients can reach health centers and operating rooms. However, an initially limited rupture with a small blood loss may progress into a large rupture within hours. Rarely, the ruptures can fistulize into the inferior vena cava, duodenum or biliary tract.[11] It is important to note that emergency AAA encompasses a spectrum of disease from symptomatic nonruptured aneurysms to the classic free intraperitoneal rupture. In the emergency room, the diagnosis of the ruptured AAA is established clinically, but also by ultrasound or computed tomography (CT) scan. There may be difficulties in obtaining correct hemodynamic data and laboratory results in a patient presenting with shock. Shock before surgery has been shown by univariate and multivariate analyses to be associated with increased mortality.[6,7] A pragmatic approach would dictate that prompt and correct diagnosis of emergency AAA in hemodynamically stable patients is vital to reduce the incidence of the development of shock before surgical intervention.[6] The purpose of this study was to detect subtle clinical and laboratory values for the early detection of ruptured AAA. We evaluated clinical and laboratory parameters and investigated whether these variables affected mortality in patients who present to the emergency room with ruptured and unusual forms of non-ruptured AAA. 526
MATERIALS AND METHODS The study was approved by the Local Ethics Committee. The data collection methodology and data analysis strategies for this study were applied according to our institutional retrospective research practice. Ninety-three patients who were admitted to our emergency room and underwent operation for AAA between January 1999 and March 2009 were evaluated retrospectively. Three of the cases had aortocaval fistula, two had aortoenteric fistula and one had aorta biliary fistula. These patients with fistulae were excluded from the statistical analysis due to the insufficient number of cases. Patients were evaluated for demographic data, clinical presentation, operative findings, and rupture morphology. The patients who were diagnosed as emergency AAA were basically classified according to CT, and the diagnosis was confirmed by operative findings. In the operative findings, if the aneurysm wall was ripped and the retroperitoneal and peritoneal cavity were filled with massive blood, it was recognized as “free rupture”; if the rupture was limited with organized hematoma outside the aorta contained in a pseudoaneurysmal wall of retroperitoneal connective tissue, we recognized it as “chronic contained rupture” (Fig. 1). When the blood drained into the inferior vena cava, it was designated as “aortocaval fistula” (Fig. 2), while blood draining into the intestinal system was designated as “aortoenteric fistula” and to the biliary tract as “aorto biliary fistula”. Respectively, an “impending rupture” is a symptomatic aneurysm that is about to rupture (Fig. 3). When the wall of the AAA was dissected, it was recognized as a “dissected rupture of AAA”. Cases were classified into four groups. Patients fulfilling criteria set by Jones and colleagues in 1986[12] for contained rupture constituted Group I (n=15), impending rupture[13,14] (acutely symptomatic non-rup-
Fig. 1. Computed tomographic view of the chronic contained rupture of AAA. Kasım - November 2011
Unusual emergent presentations of abdominal aortic aneurysm
Fig. 2. Computed tomographic view of dilated iliac veins due to aortocaval fistula.
tured AAA) Group II (n=31), dissecting rupture Group III (n=14) (while forming this group, patients with intramural thrombus and/or hematoma were selected, with no distinction between chronic or acute dissection), and free rupture Group IV (n=27). Three of the cases had aortocaval fistula, two had aortoenteric fistula and one had aorta biliary fistula. These patients with fistulae were excluded from the statistical analysis due to the insufficient number of cases, and 87 patients were included in the final analysis. The clinical findings and laboratory parameters (hematocrit, white blood cell count, neutrophils, lymphocytes, blood pH, bicarbonate, base deficit, urea, and C-reactive protein [CRP] levels) that were measured during the admission to the emergency room and mortality rates were compared between the study groups. Freely ruptured AAAs were used as a “gold standard” for comparison with contained or impending ruptured cases. Statistical Analysis The Number Cruncher Statistical System (NCSS) 2007 and PASS 2008 statistical software (Utah, USA) were used for statistical analysis of data. For quantitative variables, in addition to descriptive statisti-
Fig. 3. Discontinuity of aortic wall calcifications and highattenuating crescents in the wall of AAAs on unenhanced computed tomographic scans are signs of impending rupture of the AAA.[14] This patient admitted to the emergency room with abdominal pain and was taken to the operating room before rupture.
cal methods (mean and standard deviation), one way ANOVA test was used for the comparison of normally distributed parameters, and the Tukey HSD test was used to detect the group that caused difference. The Kruskal-Wallis test was used to compare non-normally distributed parameters, and the Mann-Whitney U test was used to detect the group that caused difference. A chi-square test was used for comparison of qualitative variables. P values <0.05 were considered statistically significant in the 95% confidence interval.
RESULTS No significant difference was found between the groups in terms of age and gender (Table 1). The mean diameter of the aneurysm, median duration of symptoms, time interval before the operation, duration of hospital stay, mean arterial systolic and diastolic blood pressures, and known concomitant illnesses are summarized in Table 2. Hypertension was detected in 36 cases, chronic obstructive pulmonary disease (COPD)
Table 1. The distribution of AAA cases according to age, gender and deaths in groups
Group I Mean±SD
Group II Mean±SD
Group III Mean±SD
Group IV Mean±SD
p
Age Gender Deaths (30-day mortality)
Male Female
64.40±9.33 n (%) 14 (93.3) 1 (6.7)
67.67±6.98 n (%) 28 (90.3) 3 (9.7)
63.71±8.01 n (%) 11 (78.6) 3 (21.4)
69.70±8.86 n (%) 26 (96.3) 1 (3.7)
0.083
No Yes
15 (100.0) 0 (0.0)
27 (90.0) 3 (10.0)
12 (92.3) 1 (7.7)
16 (59.3) 11 (40.7)
0.307 0.002**
+One way ANOVA test; ++Chi-square test; **p<0.01.
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Table 2. Some clinical features of emergency AAA cases
Range
Mean±SD
Diameter of aneurysm (mm) 40-130 73.11±21.11 Pulse (bpm) 11-130 81.38±25.38 The median duration of symptoms (day) 1-720 54.12±143.79 The time interval before the operation (hour) 0.40-16.0 4.32±4.08 Length of hospital stay (day) 1-60 10.08±9.80 Systolic blood pressure (mmHg) 20-216 121.90±41.44 Diastolic blood pressure (mmHg) 0-123 71.92±29.69 Hypertension Chronic obstructive pulmonary disease Coronary artery disease
Yes n (%)
No n (%)
36 (41.9)
50 (58.1)
34 (39.1) 36 (41.4)
53 (60.9) 51 (58.6)
in 34 cases and coronary artery disease in 36 cases (Table 2). The numbers of deaths in the study groups are presented in Table 1 (3 deaths in Group II, 1 in Group III and 11 in Group IV). There were no deaths in Group I. When groups were compared according to rate of mortality, a highly significant difference was detected between the groups (p=0.001). As an expected finding, Group IV, which was established from totally ruptured patients, had a significantly higher mortality rate than the other groups. Seven patients had a delay in diagnosis and re-
sultant free rupture. These patients were evaluated in Group IV. Five patients had clinical impeding rupture, 2 patients contained rupture and 1 patient dissected rupture. All of them progressed to free rupture in the emergency room or intensive care unit, and three patients died. The laboratory parameters were compared with the reference values and classified as normal, high or low. The distributions of these values according to groups are presented in Table 3. All parameters in Group IV were abnormal (Fig. 4). Hematocrit levels lower than normal reference values were seen in 100% of patients in Group IV, 32% in Group III, 67% in Group II, and 53% in Group I. The white blood cell count was higher than normal reference values in 100% in Group IV, 42% in Group III, 58% in Group II, and 53% in Group I. All parameters, the number of patients and percentages are presented in Table 3. The distributions of the levels of the laboratory parameters according to groups are presented in Table 4. The levels of hematocrit, white blood cell count, percentages of neutrophils and lymphocytes, and bicarbonate levels in blood were compared between the groups. Results of the Tukey HSD test showed that there was significant statistical difference between Group IV and the others (p: 0.001; p: 0.001; p: 0.01; p<0.01). The levels of hematocrit, number of white blood cells, percents of neutrophils and lymphocytes, and bicarbonate levels did not show differences between Groups I, II and III (p>0.05).
Table 3. The distribution of laboratory parameter levels in groups Hematocrit (39-50%)* White blood cell (4.3-10.3 x109/L)* Neutrophil (41-73%)* Lymphocyte (19-44.9%)* Base deficit (0-2.5 mEq/L)* CRP (0-0.74 mEq/L)*
Group I n (%)
Group II n (%)
Group III n (%)
Group IV n (%)
Sum n (%)
Low Normal
8 (53.3) 7 (46.7)
21 (67.7) 10 (32.3)
13 (92.9) 1 (7.1)
27 (100) 0 (0)
69 (79.3) 18 (20.7)
Low Normal High
0 (0) 7 (46.7) 8 (53.3)
1 (3.2) 12 (38.7) 18 (58.1)
0 (0) 8 (57.1) 6 (42.9)
0 (0) 0 (0) 27 (100)
1 (1.1) 27 (31) 59 (67.8)
Normal High
4 (26.7) 11 (73.3)
10 (32.3) 21 (67.7)
3 (21.4) 11 (78.6)
0 (0) 27 (100)
17 (19.5) 70 (80.5)
Low Normal
11 (73.3) 4 (26.7)
23 (74.2) 8 (25.8)
10 (71.4) 4 (28.6)
27 (100) 0 (0)
71 (81.6) 16 (18.4)
Normal High
7 (46.7) 8 (53.3)
14 (45.2) 17 (54.8)
5 (35.7) 9 (64.3)
2 (7.4) 25 (92.6)
28 (32.2) 59 (67.8)
Normal High
6 (40) 9 (60)
7 (22.6) 24 (77.4)
0 (0) 14 (100)
0 (0) 27 (100)
13 (14.9) 74 (85.1)
*Normal reference values; CRP: C-reactive protein.
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Table 4. The mean values of laboratory parameters in groups Hematocrit (%)+ White blood cell (x109/L)+ Neutrophil (%)+ Lymphocyte (%)++ Blood pH Bicarbonate (mEq/L)+ Base deficit (mEq/L)++ Urea (mg/dL)++ CRP (mg/dL)++
Group I Mean±SD
Group II Mean±SD
Group III Mean±SD
Group IV Mean±SD
p
38.13±5.12 11.69±5.29 76.27±12.62 16.29±9.79 7.40±0.05 23.11±2.63 2.48±1.46 46.73±23.67 0.89±0.44
36.51±3.83 12.83±5.79 79.19±10.80 13.94±10.71 7.39±0.05 22.15±3.47 3.15±1.80 62.23±29.67 1.31±0.65
33.71±5.31 10.30±3.07 76.71±9.28 14.39±6.15 7.39±0.05 22.27±3.08 3.54±2.28 63.14±21.04 1.52±0.71
24.08±5.75 18.42±3.47 88.11±4.35 8.43±2.67 6.73±1.94 16.58±3.39 9.98±4.45 87.87±52.34 4.22±1.36
0.001** 0.001** 0.001** 0.006** 0.087 0.001** 0.001** 0.006** 0.001**
+One way ANOVA test; ++Kruskal-Wallis test; **p<0.01.
Blood pH levels were lower in Group IV than the others. However, there was no significant difference between the other three groups. Base deficit levels were found significantly different between the groups, and Mann-Whitney U test detected that this difference came from Group IV. The levels of base deficit did not differ between Groups I, II and III (p>0.05). The levels of urea showed significant difference between the groups (p<0.01). The Mann-Whitney U test was performed to detect the group that caused difference. The levels of urea in Group IV were significantly higher than in Groups I and II (p: 0.001; p: 0.036, respectively). The urea levels of Group III were significantly higher than in Group I (p: 0.046; p<0.05). There were no differences between the levels of urea in the other groups. The levels of CRP differed significantly between the groups (p<0.01). The Mann-Whitney U test was
Percentage of low hematocrit
performed to detect the group that caused difference. The levels of CRP in Groups IV and III were significantly higher than in Group I (p: 0.001; p: 0.001; p<0.01). It was also found that the levels of CRP in Group IV were significantly higher than in Groups II and III (p: 0.001; p<0.01, respectively). There were no differences between the levels of CRP in the other groups (p>0.05).
DISCUSSION Our data show that patients with emergency AAA presented unusual forms by a majority. Eighty-seven patients who were admitted as emergency AAA were basically classified according to operative findings. Contained rupture was determined in 15 (17.2%), impending rupture in 31 (35.6%), dissecting rupture in 14 (16.1%), and true (free) rupture in 27 (31.1%) cases. Clinical presentation of emergency AAA is not typical every time. Therefore, misdiagnoses and de-
Abnormal base deficit
Elevated CRP levels
100
100
100
80
80
80
60
60
60
40
40
40
20
20
20
0
0
I
II
III
IV
Groups
Percentage of high WBC
I
II
III
IV
Groups
Decreased percentage of neutrophil
0
100
100
80
80
80
60
60
60
40
40
40
20
20
20
I
II
III
IV
Groups
0
I
II
III
IV
II
III
IV
Groups
Elevated percentage of lymphocyte
100
0
I
Groups
0
I
II
III
IV
Groups
Fig. 4. The percentages of abnormal laboratory parameters in groups. Cilt - Vol. 17 Sayı - No. 6
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lays in the diagnosis are possible.[15,16] Davidovich et al.[17] presented a study of 41 cases with unusual forms in a series of 506 cases with ruptured AAA within a 14-year period. Eleven patients had chronic contained rupture, 5 aortoduodenal fistula, and 25 aortocaval fistula. The correct preoperative diagnosis was established in 6 (of 11) cases of chronic contained rupture, in 2 (of 5) cases of primary aortoduodenal fistula, and in 13 (of 25) cases of aortocaval fistula. They classified and investigated only ruptured aneurysms and unusual forms of ruptured AAA and did not focus on emergency presentations of AAA. Campbell et al.[18] presented a 25-year study of emergency surgical admissions. This study documented the changes over 25 years in a district general hospital, and showed a progressive increase in ruptured aortic aneurysm. It is important to note that emergency AAA encompasses a spectrum of disease from symptomatic non-ruptured aneurysms to the classic free intraperitoneal rupture. There is a dilemma about the effect of misdiagnoses and delays in the diagnosis on mortality. Some studies have shown an increased mortality among patients with emergency AAA who were misdiagnosed. Several other studies have shown that misdiagnosis at presentation had no effect on mortality.[19-21] In a recent study, Gaughan et al.[6] reported that initially hemodynamically stable AAA patients who deteriorate after admission to the hospital had a poor prognosis. The 30-day mortality was 49% in that study, which emphasized the importance of starting prompt treatment with a correct diagnosis in reducing the mortality rates. One study investigated 98 patients; 56 of 98 patients were stable during the admission, and there were more misdiagnoses in this latter group compared to the group of patients presenting with shock.[6] Seven patients had delay in diagnosis and resultant free rupture in our series and three cases resulted in mortality. Hans and Huang[22] retrospectively analyzed the records of 101 ruptured AAA patients. A better outcome was obtained in patients younger than 70 years, with a hematocrit of more than 35% at presentation and with emergency department to operating room time of less than 120 minutes. In the study of the Tochii et al.,[23] the rate of hospital deaths was 25.6% in 43 patients who underwent emergency operation for AAA. In our study, the mortality rate was low, at 6.25%, in the hemodynamically stable groups (Groups I, II, III). However, in patients with true rupture, the mortality rate was significantly higher than in these groups (40.7%). These findings suggest that the mortality rate can be reduced if hemodynamically stable patients who lack the classic signs of rupture are diagnosed and managed without delay before the aneurysms have ruptured. Usually, ruptured or non-ruptured AAA has to be 530
decided in the emergency room. The clinical examination plays an important part in the detection of AAAs and has moderate overall sensitivity; however, it cannot be relied upon to exclude them, especially if rupture is a possibility.[24] The accuracy of the physical examination in the diagnosis of AAA has a sensitivity of 68% and a specificity of 75%.[25] Ultrasound is substantially less accurate in the diagnosis of rupture, with a high false-positive rate of 33% and low specificity of 62%.[26] In cases of suspected rupture, CT has a sensitivity of 88% and a specificity of 88%.[27] However, CT is more time-consuming, and there is usually not enough time. The present study investigated whether any laboratory parameter could be used as a guide for differentiating a ruptured or non-ruptured emergency AAA. The correct diagnosis of emergency AAA is difficult, and the reports from autopsy findings and retrospective studies reveal that there are misdiagnosed cases even in the most advanced medical centers.[28] The diagnosis can be missed especially when the patients present with atypical clinical symptoms such as hip pain,[29] groin pain,[24] hematuria, tenesmus, and hydronephrosis.[25] These atypical clinical symptoms can lead to diagnostic error, such as urethral colic, lumbar disc herniation, sciatica, acute myocardial infarction, perforated peptic ulcer, acute pancreatitis, acute cholecystitis, mesenteric vascular occlusion, and acute diverticulitis.[28] Most patients who survive to be admitted to the emergency department are hemodynamically stable. We evaluated a series of patients with and without AAA rupture to determine which, if any, laboratory parameters may be used as a guide for differentiating ruptured or non-ruptured emergency AAA. The laboratory parameters were compared with the reference values and were classified as normal, high or low. The distributions of these values according to groups are presented in Table 3. All parameters in the free rupture group were abnormal (Fig. 4). Hematocrit levels lower than normal reference values were seen in 100% of patients in the free rupture group, 32% in the dissecting rupture group, 67% in the impeding rupture group, and 53% in the chronic contained group. Our data show that the hematocrit levels were not definitive for the rupture, as nearly 50% of the other groups also had abnormal hematocrit levels. The white blood cell count was higher than normal reference values in 100% in the free ruptured group, 42% in the dissected group, 58% in the impeding rupture group, and 53% in the chronic contained rupture group. High base deficit was present in 92.6% of patients in the free rupture group, and low hematocrit, high white blood cell count, elevated rate of neutrophil and decreased lymphocytes rates, and elevated CRP levels were present in all of the patients. Therefore, we can claim that our study, as expected, showed that increased base deficit, Kas覺m - November 2011
Unusual emergent presentations of abdominal aortic aneurysm
low hematocrit, high white blood cell count, elevated neutrophil and decreased lymphocytes rates, and elevated CRP levels are relevant to the severity of the patient’s condition of ruptured AAA. Especially when classic signs of rupture are lacking, simple hematological and biochemical tests can be directive in determining the timing of life-saving surgery in emergent AAA patients.[30] Vainas et al.[31] reported that high sensitive CRP levels are associated with AAA size (CRP: 3.23 (2.96) mg/dl), and they hypothesized that CRP may be released from the aneurysmatic area. In Parry’s paper,[32] it was reported that the aneurysmatic region is a inflammatory site, and they had documented elevated CRP levels (2.07 vs 1.29 ng/dl, p=0.005). However, Domanovits[33] found acute phase reactants showing inflammatory increase only in symptomatic AAA patients (p=.002). In our study, we found high CRP levels in almost all groups (reference CRP levels 0-0.74 mEq/ ml, p=0.001), but when the scenario worsened, we observed a greater increase in CRP levels (Tables 3, 4). The results of our study revealed lower mortality rates in hemodynamically stable patients compared to patients presenting with free rupture. Free rupture represents a serious clinical scenario with deteriorated laboratory parameters prompting early surgery, which can provide a low mortality rate in this group. With this study, we also attempted to attract attention to an acute phase reactant (CRP) and its association with AAAs. Outcomes similar to those reported in other clinical trials were also observed in our study. Our study has some limitations. First, it is a retrospective study. Second, we did not consider the possible differences in the skill levels of surgeons and anesthetists. Third, the study was not designed in a blinded fashion, so observer bias cannot be excluded. Fourth, the included patients are only those who were operated. It would seem that in this group the diagnosis is obvious. Freely ruptured AAAs could be used as a type of “gold standard” for comparison with contained or impending ruptured cases. However, a difference in lab parameters for a group with a clear clinical presentation is not particularly helpful for diagnosis. In conclusion, emergency AAA represents a spectrum of disease from symptomatic non-ruptured aneurysm to free intraperitoneal rupture, which has significantly worse outcomes in patients with shock before surgery. Even before shock presents, laboratory parameters may indicate the extent of the threat in ruptured patients. Among groups, the worst laboratory parameters were determined in the free rupture group. Hematocrit level was lower, neutrophils dominated, white blood cell counts were higher, CRP levels were elevated, and blood pH deteriorated toward acidosis. Cilt - Vol. 17 Sayı - No. 6
We conclude that especially when classic signs of rupture are lacking, simple hematological and biochemical tests can be directive in determining the timing of life-saving surgery in emergent AAA patients.
REFERENCES 1. Sakalihasan N, Limet R, Defawe OD. Abdominal aortic aneurysm. Lancet 2005;365:1577-89. 2. Fowkes FG, Macintyre CC, Ruckley CV. Increasing incidence of aortic aneurysms in England and Wales. BMJ 1989;298:33-5. 3. Acosta S, Ogren M, Bengtsson H, Bergqvist D, Lindblad B, Zdanowski Z. Increasing incidence of ruptured abdominal aortic aneurysm: a population-based study. J Vasc Surg 2006;44:237-43. 4. Ashton HA, Buxton MJ, Day NE, Kim LG, Marteau TM, Scott RA, et al. The Multicentre Aneurysm Screening Study (MASS) into the effect of abdominal aortic aneurysm screening on mortality in men: a randomised controlled trial. Lancet 2002;360:1531-9. 5. Bown MJ, Sutton AJ, Bell PR, Sayers RD. A meta-analysis of 50 years of ruptured abdominal aortic aneurysm repair. Br J Surg 2002;89:714-30. 6. Gaughan M, McIntosh D, Brown A, Laws D. Emergency abdominal aortic aneurysm presenting without haemodynamic shock is associated with misdiagnosis and delay in appropriate clinical management. Emerg Med J 2009;26:334-9. 7. Moore R, Nutley M, Cina CS, Motamedi M, Faris P, Abuznadah W. Improved survival after introduction of an emergency endovascular therapy protocol for ruptured abdominal aortic aneurysms. J Vasc Surg 2007;45:443-50. 8. Cayne NS, Veith FJ. Ruptured abdominal aortic aneurysms: role of endovascular therapy. Mt Sinai J Med 2010;77:250-5. 9. Brimacombe J, Berry A. Haemodynamic management in ruptured abdominal aortic aneurysm. Postgrad Med J 1994;70:252-6. 10. Johansson G, Swedenborg J. Ruptured abdominal aortic aneurysms: a study of incidence and mortality. Br J Surg 1986;73:101-3. 11. Halpern VJ, Kline RG, D’Angelo AJ, Cohen JR. Factors that affect the survival rate of patients with ruptured abdominal aortic aneurysms. J Vasc Surg 1997;26:939-48. 12. Jones CS, Reilly MK, Dalsing MC, Glover JL. Chronic contained rupture of abdominal aortic aneurysms. Arch Surg 1986;121:542-6. 13. Rakita D, Newatia A, Hines JJ, Siegel DN, Friedman B. Spectrum of CT findings in rupture and impending rupture of abdominal aortic aneurysms. Radiographics 2007;27:497507. 14. Gonsalves CF. The hyperattenuating crescent sign. Radiology 1999;211:37-8. 15. Marston WA, Ahlquist R, Johnson G Jr, Meyer AA. Misdiagnosis of ruptured abdominal aortic aneurysms. J Vasc Surg 1992;16:17-22. 16. Hoffman M, Avellone JC, Plecha FR, Rhodes RS, Donovan DL, Beven EG, et al. Operation for ruptured abdominal aortic aneurysms: a community-wide experience. Surgery 1982;91:597-602. 17. Davidović LB, Marković MD, Jakovljević NS, Cvetković D, Kuzmanović IB, Marković DM. Unusual forms of ruptured abdominal aortic aneurysms. Vascular 2008;16:17-24. 18. Campbell WB, Lee EJ, Van de Sijpe K, Gooding J, Cooper MJ. A 25-year study of emergency surgical admissions. Ann 531
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R Coll Surg Engl 2002;84:273-7. 19. Akkersdijk GJ, van Bockel JH. Ruptured abdominal aortic aneurysm: initial misdiagnosis and the effect on treatment. Eur J Surg 1998;164:29-34. 20. Acheson AG, Graham AN, Weir C, Lee B. Prospective study on factors delaying surgery in ruptured abdominal aortic aneurysms. J R Coll Surg Edinb 1998;43:182-4. 21. Weinstein ES, Cooper M, Hammond S, Carlson R, Guber M, Maloy J. The “stable” ruptured abdominal aortic aneurysm gives a false sense of security. Am J Surg 1999;178:133-5. 22. Hans SS, Huang RR. Results of 101 ruptured abdominal aortic aneurysm repairs from a single surgical practice. Arch Surg 2003;138:898-901. 23. Tochii M, Ogino H, Matsuda H, Minatoya K, Sasaki H, Kitamura S. Is prompt surgical treatment of an abdominal aortic aneurysm justified for someone in their eighties? Ann Thorac Cardiovasc Surg 2009;15:23-30. 24. Lynch RM. Ruptured abdominal aortic aneurysm presenting as groin pain. Br J Gen Pract 2002;52:320-1. 25. Fink HA, Lederle FA, Roth CS, Bowles CA, Nelson DB, Haas MA. The accuracy of physical examination to detect abdominal aortic aneurysm. Arch Intern Med 2000;160:8336. 26. Lindholt JS, Vammen S, Juul S, Henneberg EW, Fasting H. The validity of ultrasonographic scanning as screening method for abdominal aortic aneurysm. Eur J Vasc Endovasc Surg
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1999;17:472-5. 27. Shih CC, Lai ST, Chang Y. Computed tomography in the determination of surgical emergency for symptomatic abdominal aortic aneurysm. Zhonghua Yi Xue Za Zhi (Taipei) 1998;61:210-5. 28. Banerjee A. Atypical manifestations of ruptured abdominal aortic aneurysms. Postgrad Med J 1993;69:6-11. 29. Vaidyanathan S, Wadhawan H, Welch P, El-Salamani M. Ruptured abdominal aortic aneurysm masquerading as isolated hip pain: an unusual presentation. CJEM 2008;10:2514. 30. Yien RLC, Yip J, Yuen WC. Atypical presentations of ruptured abdominal aortic aneurysm: Case reports. Surgical Practice 2008;12:126-28. 31. Vainas T, Lubbers T, Stassen FR, Herngreen SB, van Dieijen-Visser MP, Bruggeman CA, et al. Serum C-reactive protein level is associated with abdominal aortic aneurysm size and may be produced by aneurysmal tissue. Circulation 2003;107:1103-5. 32. Parry DJ, Al-Barjas HS, Chappell L, Rashid ST, Ariëns RA, Scott DJ. Markers of inflammation in men with small abdominal aortic aneurysm. J Vasc Surg 2010;52:145-51. 33. Domanovits H, Schillinger M, Müllner M, Hölzenbein T, Janata K, Bayegan K, et al. Acute phase reactants in patients with abdominal aortic aneurysm. Atherosclerosis 2002;163:297-302.
Kasım - November 2011
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):533-538
Original Article
Klinik Çalışma doi: 10.5505/tjtes.2011.95676
Epidemiologic data of the patients with spinal cord injury: Seven years’ experience of a single center Omurilik yaralanması olan hastaların epidemiyolojik verileri: Tek merkezin yedi yıllık deneyimi İlknur TUĞCU,1 Fatih TOK,2 Bilge YILMAZ,1 Ahmet S GÖKTEPE,1 Rıdvan ALACA,1 Kamil YAZICIOĞLU,1 Haydar MÖHÜR3 BACKGROUND
AMAÇ
We aimed to present the demographic and epidemiologic data on spinal cord injury (SCI) patients who were rehabilitated at our hospital, to identify high-risk groups and etiological factors, and to evaluate the factors that affect the duration of hospitalization (DOH).
Bu çalışmada, hastanemizde rehabilite edilmiş omurilik yaralanması olan hastaların demografik ve epidemiyolojik verilerinin sunulması, yüksek risk gruplarının ve etyolojik faktörlerinin belirlenmesi ve hastanede yatış süresine etki eden faktörlerin değerlendirilmesi amaçlanmıştır.
METHODS
GEREÇ VE YÖNTEM
Data on 905 SCI patients treated on an inpatient basis between December 2000 and June 2007 at our hospital were retrospectively evaluated. Patient age, sex, etiology of injury, DOH, neurologic level, and functional grouping were analyzed. Additionally, the effects of age and sex on DOH were evaluated.
Aralık 2000 ile Haziran 2007 yılları arasında hastanemizde yatarak tedavi görmüş 905 hastanın verileri retrospektif olarak incelendi. Hastaların yaşları, cinsiyetleri, yaralanma etyolojisi, hastanede yatış süresi, nörolojik seviye ve fonksiyonel grupları analiz edildi. Hastanede yatış süresini etkileyen faktörler değerlendirildi.
RESULTS
BULGULAR
In total, 661 (73%) of the patients were male and 244 (27%) were female. The mean age of the patients was 33.4±15.0 years; 51.27% of the patients were 20-33 years of age. The mean DOH was 73.6±49.8 days. In all, 304 (33.5%) of the patients were tetraplegic and 601 (66.5%) were paraplegic. Motor vehicle collisions were the most common cause of injury (n=318, 35.1%), followed by falls from an elevated height (n=170, 18.8%). DOH was significantly higher among the tetraplegia American Spinal Injury Association (ASIA) A-B patients than among the other patients (p<0.01).
Hastaların 661’i (%73) erkek, 244’ü (%27) kadındı. Ortalama yaşları 33,4±15,0 ve hastaların %51,27’si 20-33 yaş arasındaydı. Hastanede yatış süresi ortalama 73.6±49.8 gündü. Hastaların 304’ü (%33,5) tetraplejik, 601’i (%66,5) paraplejikti. Motorlu araç çarpışmaları kazaların en sık nedeniydi (n=318, %35,1), bunu yüksekten düşme (n=170, %18.8) takip etti. Tetrapleji ASIA (American Spinal Injury Association) A-B hastaların yatış süresi diğer hastalardan anlamlı derecede daha fazlaydı (p<0,01).
CONCLUSION
Omurilik yaralanmalarının çoğu önlenebilir nedenlerden kaynaklanmıştı. Omurilik yaralanmalarının epidemiyolojik, demografik ve patolojik özelliklerinin anlaşılması yüksek risk gruplarının berirlenmesi, yaralanmayı öneleycek bireysel ve toplumsal önlemlerin alınmasına katkı sağlayacaktır.
It is clear that most of the SCIs we observed were preventable. Comprehensive identification of the epidemiologic, demographic and pathologic features of SCIs contributes to identifying high-risk groups, thereby making it possible to pay personal and communal attention to precautions for SCIs. Key Words: Spinal cord injury/etiology/epidemiology. 1 Department of Physical Medicine and Rehabilitation, Gulhane Military Medical Academy, Turkish Armed Forces Rehabilitation Center, Ankara; 2 Physical Medicine and Rehabilitation Service, İskenderun Military Hospital, Iskenderun; 3Department of Physical Medicine and Rehabilitation, Gazi University Faculty of Medicine, Ankara, Turkey.
SONUÇ
Anahtar Sözcükler: Omurilik yaralanması/etyoloji/epidemiyoloji. Gülhane Askeri Tıp Akademisi, Fiziksel Tıp ve Rehabilitasyon Anabilim Dalı, Türk Silahlı Kuvvetleri Rehabilitasyon Merkezi, Ankara; 2 İskenderun Asker Hastanesi, Fiziksel Tıp ve Rehabilitasyon Kliniği, İskenderun; 3Gazi Üniversitesi Tıp Fakültesi, Fiziksel Tıp ve Rehabilitasyon Anabilim Dalı, Ankara.
1
Correspondence (İletişim): Fatih Tok, M.D. İskenderun Asker Hastanesi, İskenderun 31200 Hatay, Turkey. Tel: +90 - 326 - 618 99 49 e-mail (e-posta): drfatihtok@gmail.com
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Spinal cord injuries (SCIs) are rarely seen, but are associated with devastating physical psychological and economic consequences. These injuries are usually seen in young persons of productive age.[1] SCIs are among the most important causes of disability, morbidity, mortality, and economic loss.[2] Rehabilitation of SCI patients requires lifetime care and a multidisciplinary rehabilitation that addresses the associated functional, physiological, social, and economic problems. The aim of rehabilitation is to help patients regain as much of their pre-injury productivity as possible, with medical, social, occupational, and physiological support. The purpose of sufficient health support and precaution from SCI is to reduce to a minimum the incidence and effects of SCI. SCIs also occur due to accidents and carelessness, as with most other injuries; thus, epidemiologic and demographic studies are important for identifying risk groups and the factors that cause injury. Nonetheless, epidemiological data on SCI in Turkey are insufficient. One of the few such studies reported an annual incidence of SCI in Turkey as 12.7/1,000,000. [3] The incidence of SCI in developed countries was reported as 6-56/1,000,000, with an annual prevalence in the United States estimated at 250,000.[4,5] The present study aimed to present the demographic and epidemiologic data on SCI patients who were rehabilitated in our hospital, to identify high-risk groups and etiological factors, and to evaluate the factors that affect the duration of hospitalization (DOH).
MATERIALS AND METHODS Data on patients who were treated on an inpatient basis between December 2000 and June 2007 at the Turkish Army Forces Rehabilitation Center for Acute Care and Spinal Cord Injury Rehabilitation Department were scanned. In all, the records of 905 SCI patients who were treated on an inpatient basis in our hospital during this time were retrospectively analyzed. Patient age at the time of injury, sex, injury etiology, DOH, neurologic level, and functional grouping were analyzed. The American Spinal Injury Association (ASIA) classification was used to determine the neurologic level and functional grouping; patients were classified into the following three functional groups: 1. Tetraplegia ASIA A-B; 2. Paraplegia ASIA A-B; 3. Tetraplegia and paraplegia: ASIA C-D-E. In determining DOH, ASIA neurologic level and functional grouping for patients who were hospitalized more than once, data from the first hospitalization were used. Additionally, the effects of age, sex and functional grouping on DOH were statistically evaluated. The Statistical Package for the Social Sciences (SPSS) v.16.0 for Windows was used for statistical analysis. 534
RESULTS In total, 661 (73%) of the patients were male and 244 (27%) were female. The mean age of the patients was 33.4±15.0 years (range: 3-83 years). In all, 51.27% of the patients were 20-33 years of age and 70.02% were 15-44 years of age (Table 1). The mean DOH was 73.6 ± 49.8 days (range: 3-424 days). Injury etiology analysis showed that motor vehicle collisions (while inside the vehicle) (IMVC) were the most common cause of injury (n=318, 35.1%), followed by fall from a height (FFH) (n=170, 18.8%), and gunshot wounds (GW) (n=110, 12.2%). Injury etiologies are presented in Table 2. Among the patients, 304 (33.5%) were tetraplegic Table 1. Age distribution of the patients Age (years) 0-10 11-14 15-19 20-33 34-44 45-60 61-83
n
%
14 12 64 464 151 142 58
1.54 1.32 7.07 51.27 16.68 15.69 6.40
Table 2. Distribution of patients according to neurologic level, ASIA classification, functional grouping, and etiology Tetraplegia Paraplegia C3-C8 T1-T12 L1-L4 ASIA-A ASIA-B ASIA-C ASIA-D ASIA-E Functional group 1 Functional group 2 Functional group 3 IMVC FFH GW TM DSW Tumors OMVC EHW KW Other etiologies Total
n
%
304 601 304 457 144 485 158 135 122 5 197 256 452 318 170 110 65 42 41 40 27 2 90 905
33.5 66.5 33.5 50.5 16 53.6 17.5 14.9 13.5 0.6 21.8 28.3 49.9 47.5 18.8 12.2 7.2 4.6 4.5 4.4 3.0 0.2 9.9 100
Kasım - November 2011
Epidemiologic data of the patients with spinal cord injury
3. Tetraplegia and paraplegia, ASIA C-D-E: 452 (49.9%) patients.
120
Patient count
100
The distribution of patients according to ASIA neurologic level and functional grouping are presented in Table 2. The most common neurologic level was cervical-5 (n=109) (distribution is presented in Fig. 1), followed by thoracic-12 (n=84), cervical-6 (n=83), and thoracic-10 and thoracic-11 (n=70 patients).
80 60 40 20 0
C3 C4 C5 C6 C7 C8 T1 T2 T3 T4 T5 T6 T7 T8 T9 T10 T11T12 L1 L2 L3 L4
Neurologic level
The distribution of neurologic level among male and female patients is presented in Figure 2. IMVC was the most common etiology among both sexes, followed by FFH. While GW was the third most common etiology among the male patients (15.4%), it was the sixth most common etiology among the females (3.3%). IMVC was the cause of SCI in 5 patients in 2000, 41 patients in 2001, 45 patients in 2002, 56 patients in 2003, 70 patients in 2004, 57 patients in 2005, 54 patients in 2006, and 30 patients in 2007. The small number of patients injured due to IMVC in 2000 and 2007 might be attributed to the dates of the study period, which ran from December 2000-June 2007.
Fig. 1. Patient distribution according to neurologic level. 250
Male
Female
Patient count
200 150 100 50
s er
s
W
th O
K
Tu m
or
W
C
EH
V M
TM
O
W
SW
G
D
H FF
IM
V
C
0
Etiology
Fig. 2. Distribution of male and female SCI patients according to etiology. IMVC: Motor vehicle collision (inside the vehicle); FFH: Fall from a height; GW: Gunshot wound; DSW: Diving into shallow water; OMVC: Motor vehicle collision (outside the vehicle); EHW: Exposure to high weight; KW: Knife wound.
and 601 (66.5%) were paraplegic. Distribution of patients according to ASIA functional grouping was as follows: 1. Tetraplegia, ASIA A-B: 197 (21.8%) patients. 2. Paraplegia, ASIA A-B: 256 (28.3%) patients.
Neurologic levels according to the etiology are presented in Table 3. With reference to this table, cervical levels were common in cases of diving into shallow water (DSW) and IMVC, and thoracic levels were common in cases of FFH, GW, knife wounds (KW), and exposure to heavy weight (EHW). When we separated the SCI patients into etiological subgroups, the mean age at injury among 110 patients injured due to GW was 26.3±8.1 years (range: 13-52 years). Age distribution of the GW-injured patients is presented in Figure 3. The densest age accumulation among the GW-injured patients was between 20 and 30 years, with 81 (73.6%) patients in this age group. The mean age of the patients injured due to IMVC was 30.6±12.3 years (range: 3-70 years) and the age distribution is presented in Figure 4. The most common age group among the IMVC-injured patients was
Table 3. The relationship between SCI etiology and neurologic level SCI etiology IMVC FFH GW Transverse myelitis DSW Tumors OMVC EHW KW Others
The 4 most common neurologic levels C-5 (13.2%) T-12 (17.1%) T-12 (14.5%) C-5 (15.4%) C-6 (35.7%) C-5 (9.8%) C-6 (15%) T-11 (22.2%) T-9 (50%) C-6 (14.4%)
C-6 (9.7%) T-10 (10.0%) T-10 (11.8%) L-2 (13.8%) C-5 (33.3%) T-12 (9.8%) C-5 (12.5%) T-10 (11.1%) T-11 (50%) C-5 (13.3%)
T-11 (8.5%) T-11 (10.0%) L-1 (9.1%) C-6 (12.3%) C-4 (19.0%) L-2 (9.8%) T-10 (10.0%) L-2 (11.1%) L-2 (13.3%)
C-4 (7.9%) C-5 (8.2%) T-4 (9.1%) L-1 (9.2%) C-7 (7.1%) T-6 (9.8%) T-12 (10.0%) C-5 (11.1%) T-10 (8.9%)
IMVC: Motor vehicle collision (inside the vehicle); FFH: Fall from a height; GW: Gunshot wound; DSW: Diving into shallow water; OMVC: Motor vehicle collision (outside the vehicle); EHW: Exposure to heavy weight; KW: Knife wound.
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30
Patient count
25 20 15 10 5 0 13 15 16 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 39 40 41 42 43 46 47 48 49 52
Age
Fig. 3. Distribution of gunshot wound (GW) SCI patients according to age.
19-45 years of age (n=259, 81.4%). Age distribution was more heterogeneic among patients injured due to MVCs (outside of the vehicle, OMVCs), and the highest density was between 20 and 30 years of age (Fig. 5). The mean age of the 42 patients injured due to DSW was 23.9±8.8 years (range: 13-64 years), and 33 of these patients were 17-28 years of age. All the patients injured due to DSW were tetraplegic. The neurologic level in 14 of these patients was cervical-5, versus cervical-6 in 15 patients; 69% of the patients injured due to DSW had a neurologic level of cervical-5 and 6. Analysis of the factors that affected DOH among the
SCI patients showed that there was no meaningful correlation between patient age (p=0.41) or sex (p=0.36) and DOH. Post-hoc Bonferroni testing was applied after determining high significance (p<0.0001) in variance analysis in order to evaluate the efficacy of functional groups on DOH. The results showed that there was a statistically significant difference (p<0.0001) between the effect of functional group 1 and that of functional groups 2 and 3 on DOH, whereas the difference (p=0.27) between the effect of functional groups 2 and 3 on DOH was not significant (DOH according to functional groups is presented in Table 2). When we investigated the effects of etiology on DOH, we grouped GW and KW under the heading “wounds”, and in the same way grouped IMVC and OMVC under “MVC”; however, other traumatic causes were grouped as “traumatic other”, and other etiologies without trauma were grouped as “non-traumatic”. The wound group included 112 patients with a mean DOH of 65.9±49 days (range: 6-310 days), the MVC group included 358 patients with a mean DOH of 80.9±53.4 days (range: 3-316 days), the traumatic other group included 239 patients with a mean DOH of 72±38.1 days (range: 3-195 days), and the non-traumatic group included 196 patients with a mean DOH of 66.4 ± 54.2 days (range: 6-424 days). After this grouping, we determined high significance (p<0.002) in order to evaluate group effects on DOH with vari-
35
Patient count
30 25 20 15 10 5 0
3 4 5 6 7 10 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 49 52 53 54 56 57 58 59 60 61 63 66 70
Age
Fig. 4. Distribution of motor vehicle collision (inside the vehicle) (IMVC) SCI patients according to age. 16 14
Patient count
12 10 8 6 4 2 0
14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 43 44 45 46 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 70 72 73 76 77
Age
Fig. 5. Distribution of fall from height (FFH) SCI patients according to age. 536
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Epidemiologic data of the patients with spinal cord injury
ance analysis. Based on post-hoc Bonferroni testing, DOH in the MVC group was significantly longer than in the wound (p=0.03) and non-traumatic (p=0.006) groups; however, there was no significant difference in DOH between the traumatic other group and the MVC group (p=0.19). Furthermore, there was no significant difference in DOH between the three groups except MVC (p>0.5).
DISCUSSION Spinal cord injury (SCI) is an important problem due to its associated physical, psychological, social, and economic consequences. We think that comprehensive identification of the epidemiologic, demographic and pathologic features of SCI contributes to identifying high-risk groups, thereby making it possible to pay personal and communal attention to precautions for SCIs. The present study presents epidemiologic data on SCI patients who were treated on an inpatient basis at our hospital, which is a tertiary care center, from December 2000 to June 2007. Motor vehicle collision (MVC) was the most common etiology in the present study, followed by FFH, as in many other studies;[3,6-11] however, the ratio of SCI etiologies varies according to country. For example, O’Connor et al.[12] reported that they did not observe any SCIs due to GW or KW in Ireland due to Ireland’s strict weapons control laws. The high incidence of SCI due to GW in the young population in the present study was probably due to the fact that our hospital primarily serves veterans; however, SCIs due to GW among females and civilians calls into question the efficacy of Turkish laws related to obtaining and carrying guns. A bimodal age distribution was observed in the present study; 51.27% of the patients were 20-33 years of age. MVC was the first common etiology in this age group, as it was among the other age groups. O’Connor et al.[12] concluded that higher SCI incidence rates due to MVC are seen in less developed countries with poor road safety and a primarily agricultural economy. Gwynedd et al.[13] observed a relationship between traffic accidents and traffic laws, and emphasized that if the incidence of traffic accidents could not be reduced, the incidence of SCI might be reduced with effective first aid, evacuation from the vehicle and transport to hospital. During these operations, SCI and traumatic brain injury should be remembered firstly. Burke et al.[8] reported that MVC caused 35% and FFH caused 31% of SCIs, whereas in the present study, IMVC and OMVC caused 51.1% and FFH caused 18.8% of SCIs. These results indicate that Turkish traffic laws and first aid operations must be critically reviewed and modified. In the present study, we determined that 70 patients were injured due to MVC in Cilt - Vol. 17 Sayı - No. 6
2004, followed by 57 in 2005, and 56 in 2003; however, it was reported that there were 455,667 accidents in 2003, 537,384 in 2004, 621,183 in 2005, 728,756 in 2006, and 825,583 in 2007 (Report of Traffic Accidents, Turkish Republic General Directorate of Highways, October 2007).[14] In the present study, C-5 was the most common neurological level (Fig. 1). This result is compatible with Da Burkes’ findings; however, Gur et al. reported that the most frequent neurological level was L-1 and Karacan et al. reported that the most frequent neurological level was T-12.[3,4,8] We determined that C-5 was the most common neurological level in patients injured due to IMVC, tumors and transverse myelitis and the second most common neurologic level among those injured due to OMVC, DSW and other injuries (Table 3). The present study’s results show that DOH was longer among the patients injured due to IMVC and OMVC than among the other patients. This situation can be explained with multiple traumas due to traffic accidents. Moreover, we observed that DOH in the traumatic group was longer than in the non-traumatic group. The present study has a few limitations. The study was not an incidence study and such studies have not been conducted recently in Turkey. We did not collect any data concerning whether passengers in traffic accidents used safety belts, if drivers had used alcohol, or where individuals were sitting in the vehicle at the time of the accident. Another limitation was the lack of data collection concerning the circumstances associated with FFH (work accident, fall from a tree, suicide attempt, etc.). Lack of information about stabilization operations and factors affecting DOH were other limitations. It is clear that most SCIs we observed were preventable. We think etiologies such as IMVC, OMVC and GW can be prevented with amended traffic laws, changes to the procedures for obtaining and carrying guns, and increasing audits and educational programs. On the other hand, etiologies like FFH and DSW are also preventable with a high education level and social consciousness, and with a greater mass of people learning how to administer first aid to injured patients after accidents. SCI studies that aim to determine costeffective preventative measures are needed, as is critical analysis of the risk factors and of how, when, and where SCIs occur. Moreover, epidemiological data on SCIs and multi-centered studies are warranted.
REFERENCES 1. Devivo MJ. Epidemiology of traumatic spinal cod injury. In: Kirshblum SC, Campagnolo D, DeLisa JE, editors. Spinal cord medicine. Phidelphia: Lippincott Williams and Wilkins; 537
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2002. p. 69-81. 2. DeVivo MJ. Causes and costs of spinal cord injury in the United States. Spinal Cord 1997;35:809-13. 3. Karacan I, Koyuncu H, Pekel O, Sümbüloglu G, Kirnap M, Dursun H, et al. Traumatic spinal cord injuries in Turkey: a nation-wide epidemiological study. Spinal Cord 2000;38:697-701. 4. Gur A, Kemaloglu MS, Cevik R, Sarac AJ, Nas K, Kapukaya A, et al. Characteristics of traumatic spinal cord injuries in south-eastern Anatolia, Turkey: a comparative approach to 10 years’ experience. Int J Rehabil Res 2005;28:57-62. 5. Pickett W, Simpson K, Walker J, Brison RJ. Traumatic spinal cord injury in Ontario, Canada. J Trauma 2003;55:1070-6. 6. van Asbeck FW, Post MW, Pangalila RF. An epidemiological description of spinal cord injuries in The Netherlands in 1994. Spinal Cord 2000;38:420-4. 7. Prasad VS, Schwartz A, Bhutani R, Sharkey PW, Schwartz ML. Characteristics of injuries to the cervical spine and spinal cord in polytrauma patient population: experience from a
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regional trauma unit. Spinal Cord 1999;37:560-8. 8. Burke DA, Linden RD, Zhang YP, Maiste AC, Shields CB. Incidence rates and populations at risk for spinal cord injury: A regional study. Spinal Cord 2001;39:274-8. 9. Dixon GS, Danesh JN, Caradoc-Davies TH. Epidemiology of spinal cord injury in New Zealand. Neuroepidemiology 1993;12:88-95. 10. Biering-Sørensen E, Pedersen V, Clausen S. Epidemiology of spinal cord lesions in Denmark. Paraplegia 1990;28:10518. 11. Gjone R, Nordlie L. Incidence of traumatic paraplegia and tetraplegia in Norway: a statistical survey of the years 1974 and 1975. Paraplegia 1978;16:88-93. 12. O’Connor RJ, Murray PC. Review of spinal cord injuries in Ireland. Spinal Cord 2006;44:445-8. 13. Pickett GE, Campos-Benitez M, Keller JL, Duggal N. Epidemiology of traumatic spinal cord injury in Canada. Spine (Phila Pa 1976) 2006;31:799-805. 14. http://www.kgm.gov.tr/kaza2k.asp.
Kasım - November 2011
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):539-544
Original Article
Klinik Çalışma doi: 10.5505/tjtes.2011.75735
The incidence of peripheral nerve injury in trauma patients in Iran İran’da travma hastalarındaki periferik sinir hasarının insidansı Soheil SAADAT, Vahid ESLAMI, Vafa RAHIMI-MOVAGHAR
BACKGROUND
AMAÇ
In patients aged 1-34 years, injury is the leading cause of mortality, disability and health care costs. Two to 3% of Level I trauma patients have peripheral nerve injury (PNI).
Bir-34 yaşındaki hastalarda yaralanma önde gelen mortalite, sakatlık ve sağlık bakım gideri nedenidir. Birinci seviye travma hastalarının %2’si ile %3’ü periferik sinir hasarına (PSH) sahiptir.
METHODS
GEREÇ VE YÖNTEM
Data were collected from the Iran National Trauma Registry database, compiled according to the International Classification of Diseases, 9th revision (ICD9) codes, from August 1999 to February 2004. The information included demography, mechanism, levels and regions of PNI, associated injuries, Abbreviated Injury Scale, duration of hospital stay, and costs.
Veriler Ağustos 1999’dan Şubat 2004’e kadar olan zaman aralığı içinde ICD9-kodlarına göre İran Ulusal Travma Kayıt veritabanından toplandı. Bilgiler demografi, PSH’ye ilişkin mekanizma, seviyeler ve bölgeler ile eşlik eden hasarlar, Kısaltılmış Hasar Skalası, hastanede kalma süresi ve hastane giderlerini içerdi.
RESULTS
16,753 hastanın 219’u (%1,3) PSH’li ve 182’si (%83,1) erkek idi. PSH’li hastaların ortalama yaşı, sinir hasarı olmayan hastalarınkine göre daha düşük bulundu (28.6±14.45 ve 33±21,08 yaş; p<0,001). En yaygın PSH nedeni, keskin cisimden kaynaklanan direkt laserasyondu (%61) bunu karayolu trafik kazaları (%22) izledi. Penetran travma, penetran yaralanmalara göre daha yaygındı (%5,6 ve %0,4, p<0,001). En sık PSH, dirsek ile el bölgesinde görüldü. (%10). Ulnar sinir, en sık olarak yaralanan sinirdi. Ulnar sinir yaralanmasına ilişkin en yaygın alan, ön kol oldu (%15,3).
Of 16,753 patients, 219 (1.3%) had PNI; 182 (83.1%) were male. The mean age of the patients with PNI was lower than of those without nerve injury (28.6±14.45 vs. 33±21.08 years; p<0.001). The most common cause of PNI was direct laceration from a sharp object (61%) followed by road traffic crashes (22%). Penetrating trauma was more common than non-penetrating injuries (5.6% vs. 0.4%, p<0.001). The most frequent PNI location was from the elbow to the hand (10%). The ulnar nerve was the most commonly injured nerve. The most common area of ulnar nerve injury was at the forearm (15.3%). CONCLUSION
BULGULAR
SONUÇ
Sharp laceration and road traffic crash have the highest rates of PNI, which are more common in young males. Open wounds from the elbow to the hand should raise suspicion of PNI in triage. Although injuries leading to PNI are rare, their outcomes and disabilities require further research.
Keskin laserasyon ve trafik kazası, genç yaş erkeklerde daha sık olan PSH’ye ilişkin en yüksek oranlara sahiptir. Dirsekten itibaren ele doğru olan açık yaralar, triyajda PSH’ye ilişkin kuşkuyu artırmalıdır. PSH’ye yol açan yaralanmalar nadir olmakla birlikte, bunların sonuçları ve sakatlıkları daha ileri araştırma gerektirmektedir.
Key Words: Extremity trauma; incidence; peripheral nerve injury; road traffic crashes.
Anahtar Sözcükler: Ekstremite travması; insidans; periferik sinir yaralanması; karayolu trafik kazaları.
Sina Trauma and Surgery Research Center, Tehran University of Medical Sciences, Tehran, Iran.
Sina Travma ve Cerrahi Araştırma Merkezi, Tahran Üniversitesi Tıp Bilimleri, Tahran, İran.
Correspondence (İletişim): Vafa Rahimi-movaghar, M.D. Sina Trauma and Surgery Research Center, Sina Hospital, Tehran University of Medical Sciences, Tehran 11365-3876, Iran. Tel: +98 - 915 342 2682 e-mail (e-posta): v_rahimi@sina.tums.ac.ir
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80
60
The AIS scores were used to classify injury severity and were assigned to all traumas noted in the diagnostic record of hospitalized patients with PNI.[5-7]
40
20
In this study, the incidence of PNI and the related factors in trauma patients in Iran are discussed.
MATERIALS AND METHODS Our research is a retrospective cross-sectional study. The data were collected from the Iran National Trauma Registry database from August 1999 to February 2004. The data were acquired from important hospitals in eight major cities of Iran. Each case that was admitted because of trauma and had a hospitalization period of more than 24 hours was included in the database. A PNI was defined as an injury to a nerve in the upper or lower extremities. The PNI, associated injuries and mechanism of trauma were classified based on the International Classification of Diseases, 9th revision (ICD-9) from S00 to S99 for a single region and T00 to T07 for multiple regions. Patients with exclusively nerve root, brachial or lumbar plexus were excluded. Diagnosis of a PNI was made by neurologic examination of general physicians in the emergency room and confirmed by specialists and electrodiagnostic evaluations. The information obtained from the original database included the patients’ general characteristics, mechanism of trauma (such as RTC, fall, cuts from a sharp object), traumas (such as open wounds, fractures), levels and regions of PNIs, Abbreviated Injury Scale (AIS), duration of hospital stay, and final disposition/outcome.
Female Male
Count
Trauma is the most common cause of death among people 1 to 34 years of age, a chief cause of disability and years of life lost, and a main contributor to health care costs.[1] Trauma to the peripheral nerve results in significant disability across the world.[2] The most causative factor for trauma entirely,[3] and of peripheral nerve injury (PNI) specifically, is road traffic crash (RTC). Data from developed countries are useful but insufficient for strategic long-term planning in developing countries.[4]
0
0-10
11-20 21-30 31-40 41-50 51-60 61-70
70+
Fig. 1. Number of peripheral nerve injuries for each age-sex category.
The Injury Severity Score (ISS) was computed by the sum of squares of the highest AIS score in the three body regions with the most injury. Statistical analysis was conducted consisting of Student’s t test and non-parametric tests including the Mann-Whitney U test and Kruskal-Wallis test to compare means and chi-square testing, where appropriate. The significance level was set at 0.05. Statistical analyses were conducted using the Statistical Package for the Social Sciences (SPSS) 14.0 (SPSS Inc, Illinois, USA) and STATA 10 (Statacorp, Texas, USA).
RESULTS The study subjects consisted of 16,753 trauma patients. They presented with 23,729 traumas. Ninety percent of the patients were younger than 50 years. The two most common mechanisms of trauma were RTC (58%) and fall (25%). Distribution of extremity traumas in age groups are displayed in Table 1. Two hundred and nineteen patients (1.3%) were found to have PNI. Of these, 182 (83.1%) were male and 37 (16.9%) female. The mean age of patients with PNI was lower than of those without nerve injury (28.6±14.45 vs. 33±21.08 years, p<0.001). Distribution of PNI among age groups in both sexes is depicted in Figure 1. PNI
Table 1. Distribution of extremity traumas according to age group Age Total, % Open wound, % Fracture, % Joint/ligament, % Nerves, % Blood vessels, % Muscle tendons, % Crushing, % group n=16709 n=3878 n=10,497 n=878 n=235 n=216 n=874 n=131 (100%) (23.2%) (62.8%) (5.3%) (1.4%) (1.3%) (5.2%) (0.8%) 0-10 11-20 21-30 31-40 41-50 51-60 61-70 71+ 540
8.6 24.1 25.4 13.6 8.7 6.6 7.1 6.0
6.6 26.5 33.5 15.1 8.0 4.6 4.1 1.8
10.2 22.6 20.6 12.6 9.3 7.5 8.8 8.4
4.1 21.4 29.0 15.9 9.9 8.7 7.1 3.9
5.5 26.0 33.6 17.0 8.5 4.3 3.8 1.3
6.5 31.0 35.6 17.1 2.8 2.8 2.8 1.4
3.4 31.0 39.0 14.6 5.7 3.0 2.1 1.1
8.4 29.0 25.2 21.4 5.3 6.1 2.3 2.3
Kasım - November 2011
The incidence of peripheral nerve injury in trauma patients in Iran
Intoxication Gunshot 2%
Others 2%
12
Road traffic crash 20%
Open wound Fracture
10 8 Fall 8%
6
Sharp object cutting 60%
4
Trauma of blunt object 6%
2
Fig. 2. Mechanism of trauma in peripheral nerve-injured patients.
Regions Peripheral nerve injury (PNI) was more common in the upper extremities (83.9%) than lower extremities. The ulnar nerve was most commonly injured at the forearm level. The ulnar nerve injury at the forearm Cilt - Vol. 17 Sayı - No. 6
Knee & Lower leg
Ankle & Foot
Fig. 3. Distribution of peripheral nerve injuries in different extremity regions and the association with fractures and open wounds.
60
Open wound Fracture
50 40 30 20 10 0
ln ar ed ia n Ra di M a l us cu Axi l lo cu lary ta n Cu eou ta s D neo i D ig gita us ita l l n n. . o of fo th er Sc ia ti Ti b Co ial m m on La D ee te ra p l pe ro ne al
Specific Anatomical Nerves Nerves: The ulnar nerve was the most commonly injured nerve (Fig. 4). In the upper extremity, the order of the most frequently injured nerves was ulnar, digital, median, and radial. In the lower limbs, the most commonly injured nerves were the common peroneal nerve followed by tibial nerve. Distribution of PNIs and associations with fractures and open wounds are shown in Figure 4.
Hip & Thigh
Extremity
U
Trauma Eleven percent of all traumas were penetrating (2,642 out of 23,720). However, in PNI patients, the frequency of penetrating trauma was more than of nonpenetrating injuries (5.6% vs. 0.4%; p<0.001). PNI was associated with 4.9% of open wounds and 0.4% of fractures (Table 3). Figure 3 shows the distribution of these lesions in the extremities of PNI patients. The most common open wounds associated with PNI were wounds from the elbow to the hand region (Fig. 3).
Wrist & Hand
M
Mechanism of Trauma The most common mechanism of trauma in patients who experienced PNI was sharp object laceration (61%) followed by RTC (22%) (Fig. 2). Considering all RTC patients (9,717), the most common victims were pedestrians (41%). However, PNI-related RTCs were most common in car occupants (N=78; 0.8%). Among car occupants, PNI was more common in front seat passengers.
Shoulder Elbow &Upper &Fore arm arm
Count
was most common in the 21-30 years of age group (34%).
0
Nerve
Fig. 4. Distribution of peripheral nerve injuries and the association with fractures and open wounds.
level (S 54.0) alone constituted 15.3% of all PNIs. Injury Severity Score (ISS) The PNI patients presented with lower ISS than other trauma patients (5.5±5.8 vs. 7.1±7.5), and the difference was statistically significant (p<0.001). In PNI patients, the highest ISS was associated with the tibial nerve (Table 2). Length of hospital stay and expenses The average length of hospital stay for all trauma 541
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Table 2. ISS in different nerve injures Upper extremity
Lower extremity
Nerve
ISS
Nerve
ISS
Ulnar Median Radial Axillary Digital, thumb Digital, others
5.09±2.30 6.73±13.10 5.64±2.55 4.50±0.71 2.00±1.73 2.87±1.93
Sciatic Tibial Peroneal Deep peroneal
6.29±3.86 8.25±2.22 7.40±2.38 5.67±2.89
patients was 5.92±6.19 days and the mean hospital expenses were 1,656,428±3,287,094 Rials. The mean hospital stay in PNI patients was less than in other trauma patients (6.0±6.02 vs. 6.8±7.9 days; p<0.05). Hospital duration and expenses with different nerve injuries are summarized in Table 4.
DISCUSSION This study showed that the incidence of PNI is 1.3% in trauma patients in trauma hospitals in Iran. The PNI incidence rate has been determined as 13.9 per 100,000 person years.[8] In other studies, 2-3% of Level I trauma patients have PNI,[9-11] and the incidence of PNIs following limb trauma was 1.64%.[10] Fractures of adjacent bones are generally associated with PNI.[2,12] Most of the PNIs are single rather than multiple nerve injuries.[13] The high incidence of PNI in male patients is reflected in other sources in the literature.[9,10,13-16] The exception for this rule can be seen in the study of Taylor et al.,[6] which reported almost equal PNI in males and females. Additionally, Ahrari et al.[9] reported 52% of male injury in the Bam earthquake, which may be due to almost similar involvement of both sexes in disasters. The higher incidence of PNI in males could be related to high-risk occupations and cultural issues. In addition, women are not accustomed to riding motorcycle in Iran.[4]
Our study showed that 90% of the trauma patients were under 50 years old, and the peak frequency of PNI was identified in the 21-30-year-old age group, which shows the higher vulnerability of the youth. [9,10,13,17]
Lower ISS and hospital stay were both suggestive of less severity of trauma in PNI patients versus those without nerve injury. This indicates that PNI is not restricted to severe injuries and its probability should not be ignored in non-severe trauma patients.[9] In our study, laceration by a sharp object was the most common mechanism of trauma in PNI patients. The same finding can be seen in the literature, in which penetrating trauma involved PNI more than non-penetrating injury.[18] Meanwhile, the outcome of extremity function is better in penetrating injuries.[19] PNI in association with vascular trauma is very critical. The combination of vascular injury and non-penetratingrelated PNI may result in permanent limb dysfunction. [19,20]
In our study, the upper extremity was involved more than the lower extremity in PNI. This finding was similar to many other studies.[8,9,16,21] However, in our study, the ratio of upper to lower extremity PNI was higher than that reported in previous studies. In other situations such as sports, PNI is also more common in the upper than the lower extremities.[22,23]
Table 3. Peripheral nerve injury (PNI) prevalence according to the fractured bone Leg and Lower Limb
Shoulder and Upper Limb
Hand
Bone name
Bone name
Bone name
Femur Tibia Fibula Multiple (tibia & fibula) 542
PNI Rate (%) 0.1 0.5 0.4 0.0
Clavicle Scapula Humerus Multiple (Clavicle, Scapula, Humerus) Ulna Radius Multiple (radius & ulna)
PNI Rate (%)
Foot PNI Rate (%)
Bone name
PNI Rate (%)
0.9 1.4 2.0 50.0
Scaphoid Other carpals Metacarpal, 1 Metacarpal, Others
0.0 5.3 0.0 2.5
Calcaneus Talus Tarsal, others Metatarsal
0.0 0.0 0.0 1.9
1.7 1.4 1.0
Metacarpal, Multiple Thumb Fingers, Other Fingers, multiple
0.0 6.1 2.4 7.5
Toe, great Toe, others Foot, multiple
0.0 0.0 4.3
Kasım - November 2011
The incidence of peripheral nerve injury in trauma patients in Iran
Table 4. Hospital duration and expenses and the mean patients age in different nerve injuries Nerve name
Age (years)±SD
Hospitalization duration (days) ±SD
Medical expenses (Rials) ±SD
Ulnar Median Radial Axillary Musculocutaneous Digital, thumb Digital, others Sciatic Tibia Common peroneal Lateral plantar Deep peroneal
30±14 22±9 30±16 30±22 27 26±14 27±12 43±17 37±30 31±17 56 29±8
5.54±5.53 5.15±5.57 6.25±7.94 1.50±0.71 1.00 4.00±4.36 4.01±3.96 11.86±8.57 8.00±6.38 8.06±6.68 30.00 5.43±4.56
2.068.551±5.503.734 1.291.550±1.313.244 1.205.524±1.706.899 516.092±517.732 1.367.740±914.933 495.731±731.094 1.086.928±1.044.594 2.375.426±1.375.710 2.834.179±253.8915 1.964.645±1.213.409 3.900.512 1.691.296±1.646.828
According to the Central Bank of Iran, the mean exchange of $USD was 4891 Rials during the study period: http://www.cbi.ir/exratesadv/exratesadv_en.aspx accessed on April 6, 2010.
In some other studies, lower extremity injury was more common than the upper extremity injury.[10,17] A higher incidence of lower extremity injury was reported in the recent earthquake victims, which could be attributed to the position of the wounded when the earthquake occurred or to incorrect evacuation and transportation of the victims.[17] In two studies, the most frequently injured nerve in the upper extremity was the radial nerve.[9,17] However, our study demonstrated that the ulnar, median and radial nerves were the most frequently injured major nerves. This sequence was also identified in other studies.[13,16] Asplund et al.[4] showed that the majority of PNIs occurred in the wrist and hand region. However, in our study, the forearm was the most frequently involved area, followed by the wrist and hand. This higher involvement of nerves in the forearm, wrist and hand is due to their superficial location and the exposure of these regions in daily work with sharp cutting objects.[13] In the lower extremity, our findings concur with those of Kouyoumdjian’s study[11] in which the peroneal nerve was the most commonly injured nerve. However, in two studies, the sciatic nerve was the most frequently injured nerve,[16,17] followed by the peroneal nerve.[16] In conclusion, laceration by a sharp object and RTC contribute to the highest rates of PNI, which are more common in young males. Open wounds from the elbow to the hand should raise suspicion of PNI in the triage. Although injuries leading to PNI are rare, their outcomes, physical and social disabilities and impact on health system management are areas requiring further research. Cilt - Vol. 17 Sayı - No. 6
REFERENCES 1. Rivara FP, Grossman DC, Cummings P. Injury prevention. First of two parts. N Engl J Med 1997;337:543-8. 2. Robinson LR. Traumatic injury to peripheral nerves. Muscle Nerve 2000;23:863-73. 3. Beyer FR, Ker K. Street lighting for preventing road traffic injuries. Cochrane Database Syst Rev 2009:CD004728. 4. Asplund M, Nilsson M, Jacobsson A, von Holst H. Incidence of traumatic peripheral nerve injuries and amputations in Sweden between 1998 and 2006. Neuroepidemiology 2009;32:217-28. 5. Noble J, Munro CA, Prasad VS, Midha R. Analysis of upper and lower extremity peripheral nerve injuries in a population of patients with multiple injuries. J Trauma 1998;45:116-22. 6. Taylor CA, Braza D, Rice JB, Dillingham T. The incidence of peripheral nerve injury in extremity trauma. Am J Phys Med Rehabil 2008;87:381-5. 7. Selecki BR, Ring IT, Simpson DA, Vanderfield GK, Sewell MF. Trauma to the central and peripheral nervous systems. Part II: A statistical profile of surgical treatment New South Wales 1977. Aust N Z J Surg 1982;52:111-6. 8. Eser F, Aktekin LA, Bodur H, Atan C. Etiological factors of traumatic peripheral nerve injuries. Neurol India 2009;57:434-7. 9. Ahrari MN, Zangiabadi N, Asadi A, Sarafi Nejad A. Prevalence and distribution of peripheral nerve injuries in victims of Bam earthquake. Electromyogr Clin Neurophysiol 2006;46:59-62. 10. Kushwaha VP, Garland DG. Extremity fractures in the patient with a traumatic brain injury. J Am Acad Orthop Surg 1998;6:298-307. 11. Kouyoumdjian JA. Peripheral nerve injuries: a retrospective survey of 456 cases. Muscle Nerve 2006;34:785-8. 12. Heidari P, Zarei MR, Rasouli MR, Vaccaro AR, RahimiMovaghar V. Spinal fractures resulting from traumatic injuries. Chin J Traumatol 2010;13:3-9. 13. Civil ID, Schwab CW. The Abbreviated Injury Scale, 1985 revision: a condensed chart for clinical use. J Trauma 1988;28:87-90. 14. MacKenzie EJ, Steinwachs DM, Shankar B. Classifying trauma severity based on hospital discharge diagnoses. Validation of an ICD-9CM to AIS-85 conversion table. Med Care 1989;27:412-22. 543
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15. MacKenzie EJ, Siegel JH, Shapiro S, Moody M, Smith RT. Functional recovery and medical costs of trauma: an analysis by type and severity of injury. J Trauma 1988;28:281-97. 16. Stone L, Keenan MA. Peripheral nerve injuries in the adult with traumatic brain injury. Clin Orthop Relat Res 1988:136-44. 17. Heidari P, Zarei MR, Rasouli MR, Vaccaro AR, RahimiMovaghar V. Spinal fractures resulting from traumatic injuries. Chin J Traumatol 2010;13:3-9. 18. Babar SM. Peripheral nerve injuries in a Third World country. Cent Afr J Med 1993;39:120-5. 19. Creagh TA, Broe PJ, Grace PA, Bouchier-Hayes DJ. Blunt
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trauma-induced upper extremity vascular injuries. J R Coll Surg Edinb 1991;36:158-60. 20. Nichols JS, Lillehei KO. Nerve injury associated with acute vascular trauma. Surg Clin North Am 1988;68:837-52. 21. Visser PA, Hermreck AS, Pierce GE, Thomas JH, Hardin CA. Prognosis of nerve injuries incurred during acute trauma to peripheral arteries. Am J Surg 1980;140:596-9. 22. Feinberg JH, Nadler SF, Krivickas LS. Peripheral nerve injuries in the athlete. Sports Med 1997;24:385-408. 23. Frey U. The relationship between anatomical site of injury and particular sports. Proc R Soc Med 1969;62:917-9.
Kas覺m - November 2011
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):545-553
Original Article
Klinik Çalışma doi: 10.5505/tjtes.2011.47135
Clinical management and reconstruction of isolated orbital floor fractures: The role of computed tomography during preoperative evaluation İzole orbita tabanı kırıklarına klinik yaklaşım ve ameliyat öncesi değerlendirmede bilgisayarlı tomografinin rolü Nesrin TAN BAŞER,1 Refika BULUTOĞLU,2 Nihal Uzun ÇELEBİ,1 Gürcan ASLAN1
BACKGROUND
AMAÇ
A common consent regarding repair indications, timing of repair and choice of reconstruction materials for isolated orbital base fractures does not yet exist.
İzole orbita taban kırıklarının cerrahi endikasyonu, zamanlaması, kullanılacak rekonstrüksiyon materyali hakkında halen görüş birliği yoktur.
METHODS
GEREÇ VE YÖNTEM
We retrospectively reviewed our patients (41 male, 13 female) who were operated due to a diagnosis of isolated orbital floor fracture between 2002 and 2010.
2002-2010 yılları arasında izole orbita taban kırığı tanısı alarak ameliyat edilen hastalar (41 erkek, 13 kadın) geriye dönük olarak değerlendirildi.
RESULTS
BULGULAR
Fifty-four patients diagnosed with isolated orbital base fracture were found; 49 of 54 patients required surgery. The indications for surgery were restricted ocular motility and marked enophthalmos in 20.4% of the patients, whereas in 79.6%, surgical intervention was decided largely based on the coronal computed tomography images. 36.7% of the cases were operated earliest, in the first 16 hours, and 10.2% were operated the latest, in 72-96 hours. Ultra-thin porous polyethylene was used in the orbital base repair. Twelve patients contacted for this study were evaluated. Enophthalmia and exophthalmia were in normal limits in patients, and none of the patients displayed ectropion or scleral show findings or reported any complaints related to scar formation.
İzole orbita taban kırığı tanısı alan 54 hastadan, ameliyat edilen 49 hastanın cerrahi endikasyonuna bakıldığında, %20,4’ünde göz hareketlerinde kısıtlılık ve belirgin enoftalmi, %79,6’sında koronal planda çekilen bilgisayarlı tomografi görüntülerinin etkili olduğu görüldü. Hastaların %36,7’si ilk 16 saat içinde %10,2’si en geç 72-96 saat içinde ameliyat edildi. Orbita taban onarımı için ultra ince poröz polyetilen kullanıldı. Bu çalışma nedeniyle kendilerine ulaşılan 12 hastanın enoftalmi-egzoftalmi açısından normal sınırlarda olduğu, hiçbir hastada ektropiyon ya da skleral show bulgusu olmadığı, hastaların skara bağlı herhangi bir şikayetlerinin olmadığı görüldü.
CONCLUSION
SONUÇ
When not treated in a timely manner and with appropriate materials, orbital base fractures might result in enophthalmia and diplopia. We believe that a good prognosis of orbital base fractures relies on the right decision for surgical indication, early surgical intervention, and repair with appropriate material.
Tedavi edilmediğinde enoftalmi ve çift görme ile sonuçlanabilecek olan orbita taban kırığında, iyi prognoz doğru cerrahi endikasyon, erken cerrahi girişim ve uygun materyal ile onarıma bağlı olduğunu düşünmekteyiz.
Key Words: Computed tomography; orbital fractures; orbital implants; X-ray.
Anahtar Sözcükler: Bilgisayarlı tomografi; orbita kırıkları; orbita implantları; X-ışınları.
2nd Department of Plastic Recostructive and Aesthetic Surgery, Ankara Traning and Research Hospital, Ankara; 2 Burdur State Hospital, Burdur, Turkey.
1 Ankara Eğitim ve Araştırma Hastanesi, 2. Plastik Rekonstrüktif ve Estetik Cerrahi Kliniği, Ankara; 2 Burdur Devlet Hastanesi, Burdur.
1
Correspondence (İletişim): Nesrin Tan Baser, M.D. Koru Mah., 2558. Sok., Arı Sitesi, No: 46, Çayyolu 06810 Ankara, Turkey. Tel: +90 - 312 - 595 36 62 e-mail (e-posta): drntanbaser@gmail.com
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Orbital floor fractures are commonly encountered injuries in facial traumas. Anatomically, the anteromedial one-third of the orbital floor comprises the orbital face of the maxilla, whereas the posteromedial one-third is formed by the palatine bone and the lateral one-third is formed by the zygomatic bone. Generally, fracture occurs over the medial wall and floor of the orbit following trauma.[1] There are various identifications of orbital fractures based on the inclusion or exclusion of the orbital rim. The fractures comprising only the orbital floor are termed as indirect orbital floor fracture, blowout fracture, pure internal
Number (n)
25 20 15 10 5 0 Assault
Traffic accident
Fall
Striking object
Sports injury
Other
Number (n)
Fig. 1. Injury etiology.
20 18 16 14 12 10 8 6 4 2 0 1-16
17-24
Fall
24-48
49-72
>96
Time (h)
Number (n)
Fig. 2. Distribution of the interval between trauma and surgical repair.
20 18 16 14 12 10 8 6 4 2 IA
IB
IIA
IIB
IIIA
IIIB
Harris classification
Fig. 3. Distribution of the orbital floor fractures relative to Harris classification. 546
Age 0-10 11-20 21-30 31-40 41-50 51-60 >60 Total cases
Woman
Man
Case
1 1 2 3 3 2 1 13
1 2 12 8 9 5 4 41
2 3 14 11 12 7 5 54
orbital floor fracture, or isolated orbital floor fracture. [2] Among all maxillofacial fractures, the incidence of orbital fractures is 57.4% and the incidence of isolated orbital floor fractures is 21.4%.[3]
30
0
Table 1. Distribution of the isolated orbital fractures relative to age and gender
The management of isolated orbital floor fractures has been a contentious issue. Despite many articles published on orbital floor fractures, there is no consensus as yet on many subjects, including the indications for surgery, timing of surgery, surgical method, and choice of reconstruction material. Recent studies and meta-analyses appear to have differing conclusions on the subject.[2,4-6] Because of the varying views on the management of isolated orbital floor fractures, we decided to evaluate the efficacy of our method of clinical management. Therefore, we retrospectively reviewed our patients who had been operated on with the diagnosis of isolated orbital floor fracture between 2002 and 2010. In this study, we aimed to discuss the efficacy of our management method in cases of isolated orbital floor fractures by reevaluating our indications for surgery, timing of surgery, preferred surgical method, and choice of repair material in light of the recent data collected from our contacted patients and the outcomes of the similar studies in the literature.
MATERIALS AND METHODS The study population included patients who presented to our Emergency Room and were diagnosed with isolated orbital floor fracture. The patients with an accompanying maxillofacial fracture were excluded from the study. The following medical data concerning the patients included in our study were reviewed retrospectively: injury etiology, preoperative physical examination findings, computed tomography (CT) results, the interval between the trauma and the surgery, surgical approach, material used in the repair of the orbital floor, and postoperative complications (Figs. 1-3, Tables 1, 2). We evaluated the coronal orbital CT images according to the classification system defined by Harris and colleagues[7] while establishing diagnosis and determining indications for surgery. Kas覺m - November 2011
Clinical management and reconstruction of isolated orbital floor fractures
Table 2. Preoperative and early postoperative period findings of the patients Findings
Time
Diplopia Hypoesthesia Enophthalmia Restricted ocular motility Periorbital ecchymosis
Case
Preoperative Postoperative First 15 days 1st month 3rd month 6th month Preoperative Postoperative First 15 days 1st month 3rd month 6th month Preoperative Postoperative First 15 days 1st month 3rd month 6th month Preoperative Postoperative First 15 days 1st month 3rd month 6th month Preoperative
7 9 4 1 – 18 18 10 2 – 4 – – – – 6 – – – – 47
The 2-mm-thick coronal CT images of the study population were assessed based on these criteria, and a graphic showing the fracture types was created (Fig. 3). All the patients were evaluated by an ophthalmolo-
gist upon admittance to the Emergency Room. The patients who had indications for surgery were examined for any systemic problem that could complicate the operation prior to the surgery. Intraoperatively, the tissues entrapped between the fractured bone fragments were released, and the defect in the orbital floor was repaired. According to our clinical routine, patients with an orbital floor fracture are operated on and discharged 3 days postoperatively with a prescribed oral antibiotic, called for a follow-up assessment at 5 days for removal of the sutures, and checked once again at 1 week, according to which they are either removed from the follow-up list if everything is normal, or referred to the polyclinic in the event of a problem. The patients that we succeeded in contacting were invited for an up-to-date follow-up assessment. Those patients were evaluated in terms of ocular motility, diplopia, orbital position of the globe, scarring, ectropion, and complications associated with the implant (Table 3). The orbital position of both normal and traumatized globes was measured by an ophthalmologist using a Hertel exophthalmometer.
RESULTS We included 54 patients (41 male, 13 female) with an isolated orbital fracture treated within the specified period. The age range of the patients was 6-65 years, and the mean age was 37.5 years (Table 1). The most common causes of fracture were assault (n=24, 44.4%), traffic accident (n=10, 18.5%), fall (n=8, 14.8%), striking an object (n=5, 9.2%), sports injury (n=3, 5.5%), and other causes (n=4, 7.4%) (Fig. 1). The distribution of the clinical signs and symptoms among the patients was as follows: periorbital edema-ecchymosis (87.0%), diplopia (12.96%), enophthalmos (7.4%), restricted ocular motility (11.1%), and hypoesthesia in the infraorbital region (33.3%) (Table 2).
Table 3. Late postoperative findings of the contacted patients
First PE findings/late-period PE findings
No
Fracture type*
Interval# (hours)
Causes of fractures
1 2 3 4 5 6 7 8 9 10 11 12
IB IIA IIA IIIA IIIB IIIA IIA IIB IIIA IIB IIB IIIA
6 Not operated 28 9 42 72 25 20 80 8 12 27
Striking object Fall Assault Traffic accident Assault Fall Assault Fall Assault Assault Assault Traffic accident
Diplopia
ROM
Enophthalmos (mm)
Yes/No Yes/No No/No No/No No/No No/No Yes/No Yes/No No/No Yes/No Yes/No No/No
Upgaze/No No/No No/No No/No No/No No/No No/No Upgaze/No No/No No/No No/No No/No
No/+0.30 No/-0.10 No/-0.20 Yes/-0,50 Yes/-0.70 No/-0.60 No/+0,35 No/-0.40 No/-0.60 No/-0.40 No/-0.10 No/-0.50
Incision-rel. Ectropion compliant No – Itching No No No No No No No No No
No – No No No No No No No No No No
Implant-rel. compliant
Postop. time (months)
No – No No No No No No No No No No
72 P. traumatic 50 8 76 78 65 27 32 53 58 36 19
*: According to Harris classification[7]; PE: Physical examination; ROM: Restricted ocular motility; ₫: The orbital position of both normal and traumatized globes was measured by Hertel exophthalmometer. Differences in the measurements between the affected and normal eyes are given. #: Interval between the trauma and surgery.
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(a)
(b)
(c)
(d)
Fig. 4. (a) Type IA fracture with no surgical repair. (b) Type IB fracture. Tissue entrapment is shown by the arrow. (c) Type IIA fracture without surgical indication. Soft tissue is not displaced into the maxillary sinus. (d) Type IIB fracture where there is a marked tissue herniation towards the maxillary sinus.
Forty-nine of 54 patients required surgery. The indications for surgery in our 49 isolated orbital floor fracture cases were restricted ocular motility in 6 patients and marked enophthalmos in 4 patients, whereas in the remaining cases, surgical intervention was decided largely based on the coronal CT images. There was no indication for surgery in 2 patients with a type IA fracture due to presence of a fissure fracture and in 3 patients with type IIA fracture due to absence of soft tissue herniation towards the maxillary sinus, and no problem was experienced in the follow-up of those patients (Fig. 4a, 4c). In terms of the interval between the trauma and the surgery, 36.7% of the cases were operated within the first 16 hours and 10.2% at the latest, within 72-96 hours (Fig. 2). Subciliary incision was the preferred surgical approach in all the operated cases. In 6 of the 8 patients with a trapdoor fracture (type IB), bone was reduced to its former place after releasing the soft tissues (Fig. 4b). In 43 patients, ultra-thin porous polyethylene (0.85 mm x 38 mm x 50 mm Medpor簧, Porex Surgical, Inc., College Park, GA) implant was used for orbital floor reconstruction. Depending on the size of the orbital floor defect, the implant material was cut in a circle and placed accordingly; it was not fixated except in 6 patients with a large defect (Fig. 5). Prior to finalizing the operation, all patients were subjected to forced duction test, and the movement capability of the eye was checked in all directions. Regarding the early postoperative follow-ups, the follow-up period was observed to range between 4-12 weeks. None of the patients demonstrated restricted ocular motility or enophthalmos except 1 in 9 diplopia patients who experienced diplopia until postopera548
(a)
(b)
(c)
Fig. 5. (a) Type IIB fracture over the right orbital floor. (b) Round porous polyethylene implant. (c) Appearance of the implant material and orbital floor at postoperative 2 months [The right side appears to vary due to printing of the CT images in the opposite direction].
tive 12 weeks. Hypoesthesia was present in some patients but it resolved by the 6th month (Table 2). Three (6.12%) patients developed incision-related ectropion, and in 2 patients, ectropion was resolved by massage within 4-6 weeks, whereas 1 patient required surgery. During the postoperative first week, 1 patient developed infection following surgery. The infection was controlled with broad spectrum intravenous (i.v.) antibiotic therapy. The infection regressed and the patient did not require removal of the implant. This patient developed ectropion resulting from the contraction over the suture line. Since it was a severe ectropion case, the patient was operated on and a full-thickness skin graft was placed over this region. None of the patients showed a complication involving displacement or extrusion of the porous polyethylene implant. We were able to contact only 18 of the 54 patients chosen for the assessment of late sequelae. However, only 12 of those patients agreed to participate in the late postoperative assessment. The findings involving the late postoperative assessment of those 12 patients are shown in Table 3. The postoperative time for the patients included in the assessment ranged between 8 months - 6.5 years. Late assessment of 2 patients, who had marked enophthalmos prior to the operation, revealed no difference between the affected and normal eyes in the measurements performed using Hertel exophthalmometer. Late-period assessment of the patients who had diplopia or restricted ocular motility prior to the surgery revealed that those pathologies were resolved. None of the patients exhibited ectropion. No patient had a complaint about the subciliary incision. The implant placed over the orbital floor showed no extrusion. Kas覺m - November 2011
Clinical management and reconstruction of isolated orbital floor fractures
DISCUSSION According to the current literature, isolated orbital floor fractures are recognized as an indication for emergency surgery. Burnstine[4] conducted a metaanalysis in 2002 and listed the indications for emergency surgery as follows: entrapped muscle or soft tissue on CT images with concurrent diplopia, accompanying oculocardiac reflex (bradycardia, cardiac block, nausea, vomiting, or syncope), mild presence or absence of edema, ecchymosis, markedly limited extraocular motility, and white-eyed blowout fractures that indicate orbital floor fractures shown by CT along with muscle or perimuscular soft tissue entrapment in patients under 18 years of age. The meta-analysis of Gonzales and colleagues[2] on isolated orbital floor fractures listed the same indications for emergency (within 24-48 hours) repair. There is no controversial or contentious point in the literature concerning the surgical indication or timing of surgery under the above-mentioned conditions. The main ambiguity is experienced while determining surgery and the timing of the surgery in conditions other than the those listed above. Dal Canto et al.[8] compared the patients (n=58) who had been operated on early (1-14 days) and late (15-29 days), and found no statistically significant difference between the postoperative diplopia and enophthalmos rates, while observing no statistically significant difference between the two groups with regard to strabismus surgery or use of special glasses. Thus, they reported effective outcomes in surgeries performed in 15-29 days and noted that waiting for the diplopia to resolve could spare the patients from unnecessary interventions.
of the herniating tissue as well as availability of a less traumatic intervention, with low diplopia and enophthalmos incidences during the early period.[9-14] In our case series, except for the 6 patients showing an indication for emergency surgery, patients exhibiting an indication for surgery were operated on within a time range of 6 - 92 hours (Fig. 2).
Simon et al.[5] published a study in 2009 and noted that this waiting period should be even longer. In their study including 50 patients (36 cases were isolated orbital floor fractures) in which they compared early repairs (performed within the first 2 weeks) and late repairs (performed within 1 month - 3.5 years), they found no difference with regard to postoperative surgical outcome. In light of their findings, except emergency cases, they recommended early repair only in the presence of symptomatic diplopia, positive forced duction test and large orbital floor fractures that would result in enophthalmos, and they noted that in cases other than those, surgery should be delayed for 6-9 months until the resolution of the diplopia. However, when the article is analyzed, it can be seen that there is no difference between the two groups in terms of visual acuity and ocular motility, whereas it can be observed that the enophthalmos rate was higher in the late surgery group than in the early surgery group. Contrary to the studies recommending waiting for a certain period of time, there are surgeons who advocate early surgery because of the more flexible nature of the fracture line and the easy-to-release character
Limited anteroposterior healing of the eye due to extraocular muscle contraction or fibrosis of the orbital tissue is cited as responsible for late enophthalmos. [15,17] Correction of late enophthalmos is more difficult than prevention of enophthalmos with early surgery. As reported in many studies, dissection becomes more difficult due to progressing fibrosis.[10,14,18] Unlike Simon et al., Dulley and Fells[19] found the postoperative enophthalmos incidence as 72%, and reported that 40% of those required additional surgery.
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We believe that timing of the reconstruction bears great importance in reestablishing the globe support that is lost in orbital floor fractures and in retaining the orbital volume in order to prevent possible functional and cosmetic problems. The fact that none of the patients showed enophthalmos values requiring surgery supports our point of view (Table 3). In our clinic, we do not apply forced duction test as a diagnostic preoperative assessment. This test might be embarrassing when applied on awake patients. Moreover, according to Hollier and Thornton,[15] it may not be successful in acute cases. It is claimed that this test does not indicate whether restricted eye motility in the early period arises from a mechanic muscle entrapment or edema and hemorrhage.[16] Generally, early enophthalmos occurs due to detachment of the periosteum of the orbital floor, leading to herniation of the content into the maxillary sinus or elevated orbital volume associated with the posterior displacement of the orbital floor. Early enophthalmos can be masked by traumatic hemorrhage and edema.[17] For these reasons, we believe that preoperative measurement of enophthalmos would not provide accurate data in those patients. Therefore, clinically, the degree of enophthalmos is not measured preoperatively.
Many studies have reported inadequate assessment of restricted ocular motility, diplopia and enophthalmos during the early period because of edema.[20,21] This swelling may also limit the extraocular muscle movements, which would appear like tissue entrapment within the orbital floor defect. Therefore, we believe that 2-mm-thick coronal CT imaging bears great importance in the diagnosis and decision for surgery. Coronal CT imaging is recognized as the best modality in determination of the location and size of the orbital fractures, globe prolapse, accompanying fractures, and likely optical nerve damages as well as being the 549
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most helpful method in preoperative assessment.[6,10,20] There are studies published on calculation of the orbital volume on 3D orbital tomography images or concerning measurement of the related areas on 2D coronal images.[18,20,22] The downside of those quantitative CT analyses is noted to be the influence of soft tissue changes such as edema, hemorrhage and emphysema on the measurement results.[23] Moreover, these measurements require additional software and technical equipment. Harris et al.[7] categorized the isolated orbital floor fractures with the help of CT images based on the relationship between fractured bone fragments and the soft tissues as 3 main types and 6 subtypes. This classification is outlined below: Type I. Trap-door fractures in which bone fragments realign. Type IA. No orbital soft tissue is visible within the maxillary sinus (Fig. 4a). Type IB. Orbital soft tissue is visible within the maxillary sinus (Fig. 4b). Type II. Bone fragments are distracted and soft tissue is displaced towards the maxillary sinus through spaces between those fragments.
future occurrence of diplopia and enophthalmos in our cases. Successful orbital floor reconstruction depends on meticulous preoperative planning, careful dissection and the accurate selection of reconstruction material. The ideal implant should be of an inert and easily malleable character; should allow tissue in-growth and form no fibrous capsule; and should have low infection, inflammation, migration, and removal rates.[5,18] Various materials are used in reconstruction of the orbital floor, such as autogenic grafts (bone, cartilage, fascia, etc.),[26-31] allogenic grafts,[32,33] and alloplastic materials (silicone, polytetrafluoroethylene, hydroxylapatite, porous polyethylene, titanium, and Vitallium mesh).[34-41] There are studies outlining their advantages, disadvantages and success rates. Cadaver-based allogenic bone grafts are not preferred due to risk of viral infection transmission, resorption rate and their costly nature.[31] Among some of the advantages of alloplastic materials are the absence of donor-site morbidity, ready availability, and wide range of options, whereas foreign body reaction and infection are noted among their disadvantages.[39] The upsides of autogenous grafts (calvaria, nasal septal bone, cartilage, etc.)
Type IIA. There is no herniation of soft tissue or the displacement of the soft tissue is less than the distracted bone fragment. Type IIB. The herniation of soft tissue is greater than the distracted bone fragment. Type III. Displaced bone fragments surround displaced soft tissue. Type IIIA. Soft tissue and bone are moderately displaced towards the maxillary sinus (Fig. 6a). Type IIIB. Soft tissue and bone are markedly displaced towards the maxillary sinus (Fig. 6b). We believe that evaluation of patients based on the CT images and Harris classification is adequate for determining whether surgery is indicated.[7,10,24] In our case series, enophthalmos was detected by physical examination only in 4 patients in the early period following injury. While 1 patient had Type IIIA fracture, the remaining 3 had Type IIIB fracture. The other 13 cases diagnosed as Type IIIA and Type IIIB fractures based on the CT images demonstrated no enophthalmos or restricted ocular motility during the physical examination. In one study, the incidence of enophthalmos after weeks or months of injury was noted as 8-54%.[25] Based on those CT images, the patients were subjected to early surgery. In our study, the mean operative time was 34 hours for 49 isolated orbital floor fracture cases. We think that performing early surgery reduced the surgical trauma by avoiding fat atrophy, fibrosis and contraction, and thus prevented 550
(a)
(b) Fig. 6. (a) Type IIIA fracture with displacement of bone and soft tissues into the maxillary sinus. (b) Type IIIB fracture with marked displacement of the osseous and soft tissues into the maxillary sinus. Kas覺m - November 2011
Clinical management and reconstruction of isolated orbital floor fractures
are rapid vascularization, bone formation and low resorption, whereas their downsides are donor-site morbidity, hardly malleable nature and prolonged operative time.[39,42] Maybe the most important disadvantage of autogenous grafts is the unpredictable resorption rate and likelihood of late enophthalmos associated with reduced graft volume.[42] There is still no consensus among the surgeons in the selection of the reconstruction material between autogenous and alloplastic grafts. Ilankovan[43] studied a case series of 222 patients and reported successful esthetic and functional outcomes by using calvarial bone graft. Shetty et al.[44] compared the autogenous graft [calvarial bone graft] and alloplastic material (Prolene and titanium) in a case series including 10 patients, and found both materials appropriate for reconstruction, but noted the need for further studies with larger study populations. Prowse et al.[36] conducted a study on a case series of 81 patients by employing silicone implant, titanium mesh, Lactosorb, Resorb X, and autogenous bone and cartilage, and reported that contrary to the literature, silicone implants could be used because of low infection and excursion rates as well as high patient satisfaction. Morrison et al.[45] found the rate of removal of implant due to infection or excursion as 12%. Currently, the most commonly used alloplastic implant materials are titanium and porous polyethylene. Porous polyethylene is composed of high-density micropores connected to each other, which allow fibrovascular tissues to advance into the implant. This structure provides a certain rigidity to the polyethylene and allows it to automatically fixate itself to the adjacent tissues. There are many studies showing the superiority of porous polyethylene over other graft materials.[34,35,41] Ng et al.[13] performed a study on 30 orbital floor fracture cases treated by porous polyethylene, and none of the patients exhibited a need for removal of the implant within a follow-up period of 9 months. They described the porous polyethylene layer as a strong and easily malleable material preventing donor-site morbidity. Moreover, orbital volume was found to be increased in orbital reconstruction with porous polyethylene; however, the difference was not statistically significant compared with those of the other orbits. One of the largest studies in the literature on complications of porous polyethylene belongs to Lee and colleagues.[46] They reconstructed 170 cases of orbital floor fracture by porous polyethylene and reported the complication rate as 6.4%. They noted a low complication rate along with perfect functional and cosmetic outcomes in their reconstructions performed with porous polyethylene. Our experiences suggest that porous polyethylene enables rapid repair of the floor fracture, establishing stability in a short time owing to the fast ingrowth of Cilt - Vol. 17 Say覺 - No. 6
the fibrovascular tissue within the implant. No implant fixation was applied except in 6 patients with markedly large defects, and no problem was encountered. In our study, only 1 patient developed infection, which regressed with i.v. antibiotic therapy. No sign of implant-related early extrusion, enophthalmos or exophthalmos related to elevated volume was determined. When we analyzed the measurements obtained by Hertel exophthalmometer while reviewing the late follow-up assessments of the 12 patients, development of late enophthalmos associated with reduced volume appears to be impossible with this material because it does not display resorption, which is known to be the most important downside of autogenous materials. In some patients, orbital volume was elevated; however, when the orbital position of the globe was compared between the affected and contralateral orbits, this increase was observed to be insignificant and unrelated to exophthalmos (Table 3). In the literature, surgical complications of orbital floor fractures are listed as optic nerve injury, retrobulbar hemorrhage and edema-related loss of vision (0.24-3.1%), infection or displacement of the implant material, postoperative mydriasis, epiphora, and eyelid malposition.[6] Ellis et al.[47] advocates that when correct implant material is used in the orbital reconstruction, the complications are not associated with the implant material. In our clinic, we used 0.85-mm-thick porous polyethylene for all the orbital floor defects in patients treated with implants. In 2 of 6 patients with a markedly large defect, the implant material was fixated to the orbital floor by microscrews, while in other patients, the implant was fixated to the periosteum by Prolene sutures. The remaining patients received no fixation. None of the patients complained of implant displacement or migration. We preferred ultra-thin porous polyethylene implant due to its malleable, thin, inert, and infection-resistant nature, requiring no fixation or additional surgical procedures. Another focus of ongoing discussion concerning orbital floor fractures is the type of incision. In recent studies, the transconjunctival approach is more commonly preferred, whereas subciliary incision is mentioned with high complication rates. The transconjunctival approach is known to be more successful than the subciliary approach with regard to ectropion. [5,48,49] However, one should bear in mind that the transconjunctival approach may require lateral canthotomy for better vision, and this procedure carries the risk of entropion and canthal displacement. In 3 (6.1%) of 49 patients who received subciliary incision for insertion of the implant, ectropion was encountered. While in 2 of them, ectropion was resolved with massage at 3 months, 1 patient required surgery. 551
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The mean follow-up period of the 12 patients that we succeeded in contacting ranged between 8 months - 6.5 years. These patients were evaluated in terms of enophthalmos, exophthalmos, diplopia, restricted ocular motility, ectropion, and scarring. In light of our measurements, the patients were observed to be within normal range with regard to enophthalmos-exophthalmos, while no sign of ectropion or scleral show was observed. Moreover, the patients had no complaint associated with scarring. In conclusion, the diagnosis and treatment of orbital floor fractures bear great importance because they may result in enophthalmos and diplopia if not treated in a timely manner and with the appropriate construction material. This study showed that good prognosis in orbital floor fractures depends on accurate determination of the indications of surgery, early surgical intervention and selection of proper reconstruction material. The evaluation of enophthalmos, diplopia and ocular motility is not easy in the early period due to the presence of edema. Therefore, assessment of the coronal CT images and experience level of the surgeon play as significant a role as the clinical symptoms of the patient in deciding on surgery. In our opinion, detection of bone fragments within the maxillary sinus or herniation of the orbital content into the maxillary sinus both constitute an indication for surgery. This retrospective study reflects our eight-year experience on isolated orbital fractures and shows that early surgery for insertion of porous polyethylene implants by the subciliary approach can be performed with low complication rates and high patient satisfaction. We believe that early surgery prevents late enophthalmos and diplopia complications.
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tive computed tomography and postoperative ocular motility. Trans Am Ophthalmol Soc 1998;96:329-53. 8. Dal Canto AJ, Linberg JV. Comparison of orbital fracture repair performed within 14 days versus 15 to 29 days after trauma. Ophthal Plast Reconstr Surg 2008;24:437-43. 9. Dutton JJ. Management of blow-out fractures of the orbital floor. Surv Ophthalmol 1991;35:279-80. 10. Harris GJ. Orbital blow-out fractures: surgical timing and technique. Eye (Lond) 2006;20:1207-12. 11. Nam SB, Bae YC, Moon JS, Kang YS. Analysis of the postoperative outcome in 405 cases of orbital fracture using 2 synthetic orbital implants. Ann Plast Surg 2006;56:263-7. 12. Bansagi ZC, Meyer DR. Internal orbital fractures in the pediatric age group: characterization and management. Ophthalmology 2000;107:829-36. 13. Ng SG, Madill SA, Inkster CF, Maloof AJ, Leatherbarrow B. Medpor porous polyethylene implants in orbital blowout fracture repair. Eye (Lond) 2001;15:578-82. 14. Hoşal BM, Beatty RL. Diplopia and enophthalmos after surgical repair of blowout fracture. Orbit 2002;21:27-33. 15. Hollier L, Thornton J. Facial fractures I: Upper two thirds. Selected Read Plast Surg 2002;9:1-34. 16. Ansons AM, Davis H. Mechanical disordere of ocular motility. In: Ansons AM, Davis H, editors. Diagnosis and management of ocular motility disorders. 3rd ed. Malden: Blackwell Science Ltd; 2001. p. 420-74. 17. Ball JB Jr. Direct oblique sagittal CT of orbital wall fractures. AJR Am J Roentgenol 1987;148:601-8. 18. Ye J, Kook KH, Lee SY. Evaluation of computer-based volume measurement and porous polyethylene channel implants in reconstruction of large orbital wall fractures. Invest Ophthalmol Vis Sci 2006;47:509-13. 19. Dulley B, Fells P. Long-term follow-up of orbital blow-out fractures with and without surgery. Mod Probl Ophthalmol 1975;14:467-70. 20. Ploder O, Oeckher M, Klug C, Voracek M, Wagner A, Burggasser G, et al. Follow-up study of treatment of orbital floor fractures: relation of clinical data and software-based CTanalysis. Int J Oral Maxillofac Surg 2003;32:257-62. 21. Whitehouse RW, Batterbury M, Jackson A, Noble JL. Prediction of enophthalmos by computed tomography after ‘blow out’ orbital fracture. Br J Ophthalmol 1994;78:618-20. 22. Charteris DG, Chan CH, Whitehouse RW, Noble JL. Orbital volume measurement in the management of pure blowout fractures of the orbital floor. Br J Ophthalmol 1993;77:100-2. 23. Manson PN, Iliff N. Management of blow-out fractures of the orbital floor. II. Early repair for selected injuries. Surv Ophthalmol 1991;35:280-92. 24. Harris GJ, Garcia GH, Logani SC, Murphy ML. Correlation of preoperative computed tomography and postoperative ocular motility in orbital blowout fractures. Ophthal Plast Reconstr Surg 2000;16:179-87. 25. Stasior OG, Roen JL. Traumatic enophthalmos. Ophthalmology 1982;89:1267-73. 26. Girdler NM, Hosseini M. Orbital floor reconstruction with autogenous bone harvested from the mandibular lingual cortex. Br J Oral Maxillofac Surg 1992;30:36-8. 27. Harsha BC, Turvey TA, Powers SK. Use of autogenous cranial bone grafts in maxillofacial surgery: a preliminary report. J Oral Maxillofac Surg 1986;44:11-5. 28. Krishnan V, Johnson JV. Orbital floor reconstruction with autogenous mandibular symphyseal bone grafts. J Oral Maxillofac Surg 1997;55:327-32. Kasım - November 2011
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29. Johnson PE, Raftopoulos I. In situ splitting of a rib graft for reconstruction of the orbital floor. Plast Reconstr Surg 1999;103:1709-11. 30. Cavusoglu T, Vargel I, Yazici I, Cavusoglu M, Vural AC. Reconstruction of orbital floor fractures using autologous nasal septal bone graft. Ann Plast Surg 2010;64:41-6. 31. Baran CN, Ulusoy MG, Sungur N, Koçer U, Şensöz Ö. Reconstruction of orbital floor defects with auricular conchal cartilage grafts. Turkiye Klinikleri J Med Sci 2003;23:442-9. 32. Yavuzer R, Tuncer S, Başterzi Y, Işik I, Sari A, Latifoğlu O. Reconstruction of orbital floor fracture using solvent-preserved bone graft. Plast Reconstr Surg 2004;113:34-44. 33. Celiköz B, Duman H, Selmanpakoğlu N. Reconstruction of the orbital floor with lyophilized tensor fascia lata. J Oral Maxillofac Surg 1997;55:240-4. 34. Yilmaz M, Vayvada H, Aydin E, Menderes A, Atabey A. Repair of fractures of the orbital floor with porous polyethylene implants. Br J Oral Maxillofac Surg 2007;45:640-4. 35. Ozturk S, Sengezer M, Isik S, Turegun M, Deveci M, Cil Y. Long-term outcomes of ultra-thin porous polyethylene implants used for reconstruction of orbital floor defects. J Craniofac Surg 2005;16:973-7. 36. Prowse SJ, Hold PM, Gilmour RF, Pratap U, Mah E, Kimble FW. Orbital floor reconstruction: a case for silicone. A 12 year experience. J Plast Reconstr Aesthet Surg 2010;63:1105-9. 37. Ng JD, Huynh TH, Burgett R. Complications of bioabsorbable orbital implants and fixation plates. Ophthal Plast Reconstr Surg 2004;20:85-6. 38. Tuncer S, Yavuzer R, Kandal S, Demir YH, Ozmen S, Latifoglu O, et al. Reconstruction of traumatic orbital floor fractures with resorbable mesh plate. J Craniofac Surg 2007;18:598605. 39. Chowdhury K, Krause GE. Selection of materials for orbital floor reconstruction. Arch Otolaryngol Head Neck Surg
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1998;124:1398-401. 40. Dietz A, Ziegler CM, Dacho A, Althof F, Conradt C, Kolling G, et al. Effectiveness of a new perforated 0.15 mm poly-pdioxanon-foil versus titanium-dynamic mesh in reconstruction of the orbital floor. J Craniomaxillofac Surg 2001;29:828. 41. Aygıt CA, Demiralay A, Bayçın N. Reconstructıon of orbital blow-out fractures bone defects with porous polyethylene implants. Ulus Travma Acil Cerrahi Derg 1999;5:175-9. 42. Goiato MC, Demathé A, Suzuki T, dos Santos DM, Dekon SF. Management of orbital reconstruction. J Craniofac Surg 2010;21:1834-6. 43. Ilankovan V, Jackson IT. Experience in the use of calvarial bone grafts in orbital reconstruction. Br J Oral Maxillofac Surg 1992;30:92-6. 44. Shetty P, Kumar SG, Baliga M, Uppal N. Options in orbital flor reconstruction in blowout fractures: a review of ten cases. J Maxillofac Oral Surg 2009;8:137-40. 45. Morrison AD, Sanderson RC, Moos KF. The use of silastic as an orbital implant for reconstruction of orbital wall defects: review of 311 cases treated over 20 years. J Oral Maxillofac Surg 1995;53:412-7. 46. Lee S, Maronian N, Whipple ME, Most SP, Whipple ME, McCulloch TM, et al. Porous high-density polietilen for orbital reconstruction. Arch Otolaryngol Head Neck Surg 2005;131:466-50. 47. Ellis E 3rd, Tan Y. Assessment of internal orbital reconstructions for pure blowout fractures: cranial bone grafts versus titanium mesh. J Oral Maxillofac Surg 2003;61:442-53. 48. Tadj A, Kimble FW. Fractured zygomas. ANZ J Surg 2003;73:49-54. 49. Rohrich RJ, Janis JE, Adams WP Jr. Subciliary versus subtarsal approaches to orbitozygomatic fractures. Plast Reconstr Surg 2003;111:1708-14.
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Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):554-556
Case Report
Olgu Sunumu doi: 10.5505/tjtes.2011.40222
Akut karına neden olan primer omentum torsiyonu: Olgu sunumu Primary omental torsion as a cause of acute abdomen: Case report Selim SÖZEN,1 Şükrü DÖLALAN,2 Fahrettin YILDIZ,3 Hasan ELKAN2
Omental infarkt, yaklaşık yüz yıl önce tanımlanmış, nadir görülen bir patolojidir. Akut karın ağrısına neden olan omental torsiyonlu hastamız literatür verileri ile birlikte değerlendirildi. Primer torsiyonda iskemik omentumun eksizyonu ideal tedavi şeklidir.
Torsion of the omentum is a rare pathology that was described 100 years ago. The characteristic appearance of omental torsion and a review of the literature are presented with respect to a case of primary omental torsion that was causing acute abdomen. Excision of the ischemic omentum is the proper treatment for omental torsion.
Anahtar Sözcükler: Akut karın; omental torsiyon.
Key Words: Acute abdomen; omental torsion.
Omental infarkt, omentum majusun perfüzyonunun bozulması sonucu gelişen, klinik bulgularıyla hemen her akut karını taklit edebilen, nadir görülen bir patolojidir. Yerleşimine göre akut apandisit, akut kolesistit, renal kolik veya divertikülit ile karışabilir.[1]
torsiyonda iskemik omentumun eksizyonu ideal tedavidir.
Omental infarkt, yaklaşık yüz yıl önce tanımlanmış, nadir görülen bir patolojidir. Son yıllarda geliştirilen kesitsel tanı yöntemlerinin akut patolojilerde kullanılmaya başlanmasıyla bilindiğinden daha sık bir patoloji olduğu anlaşılmıştır.[2] Omental infarkt, en sık dördüncü beşinci dekadlarda görülür. Erkek-kadın oranı 2:1’dir. Olguların sadece %15’i pediatrik yaş grubundadır. Hastaların çoğu obezdir.[3] Omental infarktın doğal patolojik seyri enflamatuvar sürecin retraksiyon, fibrozis ve son olarak da komplet rezolüsyon veya otoamputasyon şeklinde sonlanmasıdır.[4] Sepsis, apse formasyonu ve adezyon gelişimi geç komplikasyonlardandır.[4] Her nekadar bazı araştırmacılar tarafından konservatif tedavi yaklaşımının yeterli olacağı ileri sürülmüş olsa da primer
Adana Numune Eğitim ve Araştırma Hastanesi, Adana; 2 Balıklıgöl Devlet Hastanesi, Şanlıurfa; 3 Harran Üniversitesi Tıp Fakültesi, Şanlıurfa.
1
Biz bu çalışmamızda akut karın nedeni ile ameliyat ettiğimiz olguyu literatür verileri ışığı altında değerlendirdik.
OLGU SUNUMU Yirmi dört yaşında, erkek hasta, yaklaşık 2 gün önce başlayan karın ağrısı, bulantı ve kusma şikayeti ile hastanemizin acil cerrahi servisine başvurdu. Hastanın özgeçmişinde 2 yıldır mide şikayetleri nedeni ile proton pompa inhibitörleri kullanması dışında bir özellik yoktu. Benzer şikayetler ile başvurduğu başka bir merkezde yapılan ultrasonografide (USG) karın içi organlarda herhangi bir patoloji saptanmamış. Bu merkezde aynı şikayetler nedeni ile yapılan üst gastrointestinal sistem endoskopisinde antral gastrit saptanmış. Hastaya ilaç tedavi verilerek taburcu edilmiş. Hastanın fiziksel incelemesinde sağ üst kadran, epigastrium ve sağ alt kadranda hassasiyet, defans, ribaund mevcut. Laboratuvar incelemede beyaz küre sa-
Adana Numune Training and Research Hospital, Adana; 2 Balıklıgöl State Hospital, Sanliurfa; Harran University Faculty of Medicine, Sanliurfa, Turkey. 1
3
İletişim (Correspondence): Dr. Selim Sözen. Yurt Mah., 71335 Sok. No: 13/19, İrfan Altaş Apt., Çukurova, Adana, Turkey. Tel: +90 - 424 - 314 84 10 e-posta (e-mail): selimsozen63@yahoo.com
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Akut karına neden olan primer omentum torsiyonu
Şekil 1. Omental torsion.
yısında artış (15000/ mm3) biyokimyasal parametrelerinde ise ALT: 81 AST: 48 dışında patoloji saptanmadı. ADBG özellik yoktu. Hasta bu şikayetler ve fiziksel inceleme bulguları ile kliniğimize yatırıldı. Sekiz saatlik gözlem ve medikal tedaviye rağmen şikayetlerinde gerileme olmayan hasta akut karın tablosunda, peptik ulcus perferasyonu veya akut kolesistit ön tanıları düşünülerek ameliyata alındı. Özellikle sağ üst kadran ve epigastriumda defans ve ribaund pozitif olması nedeni ile kapalı perforasyon veya akut kolesitit olabileceği düşüncesi ile sağ paramedian kesiyle karına girildi. Laporotomide karında serohemorajik mayi mevcuttu. Apendiks doğaldı. Omentum parsiyel olarak nekrotik ve kanamalıydı. Nekroze olan omentumun vasküler pedikülüne klemp konularak parsiyel olarak çıkarıldı (Şekil 1). Histopatolojik inceleme sonucunda, omentumda hemoraji ve infarktüs odakları mevcuttu. Mikroskopik inceleme sonucunda ise infarkte odaklar akut enflamatuvar hücreler tarafından işgal edilmişti. Ameliyat sonrası dönemde patoloji saptanmayan hasta ameliyattan sonra 3. günde şifa ile taburcu edildi.
TARTIŞMA Omentum torsiyonu omentumun uzun aksiyal ekseni etrafında dönmesi ve vasküler yapısını komprese etmesi sonucu oluşur. Vasküler patolojiler, hiperkoagülasyon durumları ve herniler gibi değişik nedenlere sekonder olabileceği gibi idiyopatik (primer) olarak da gelişebilir. Primer omental infarktın nedenleri hala bilinmemektedir. Vasküler yapılardaki anatomik varyasyonlar, staz veya tromboza neden olabilecek venöz malformasyonlar, aşırı-ağır yemek sonrası gelişen venöz konjesyon öne sürülen nedenlerdendir.[5] Erkekler kadınlara göre iki kat daha fazla bu hastalığa yakalanırlar. Ayrıca obez bireylerde bu hastalık daha fazla görülür.[2,3] Ağrı genelde sağ alt kadrana yerleşimlidir. Orta derecede lökositoz ateş ve kusma tabloya eşlik edebilir. Cilt - Vol. 17 Sayı - No. 6
Bizim olgumuzda hem alt ve üst kadran ağrısı tabloya eşlik etmekteydi. Olgumuz literatürlere uygun şekilde obez bireydi. Orta derecede lökositoz ve ateş mevcuttu. Akut karınlı hastalarda, değişik ön tanılarla yapılan USG ve bilgisayarlı tomografi (BT) incelemelerde omentumun da dikkatlice değerlendirilmesi ile tanısı kolayca konabilir. USG incelemede maksimum hassasiyet olan bölgede, karın ön duvarının hemen altında, komprese edilemeyen, oval şekilli, büyük, hiperekoik solid kitle lezyonu saptanır.[5,6] Apendiks normaldir. Minimal asit bulunabilir.[3] Benzer bulgular epiploik apendajitte de izlenebilir. USG’de omental infarktla benzer şekilde, maksimum hassasiyetin olduğu bölgede, komprese edilemeyen, oval, hiperekoik, solid kitle mevcuttur. Farklı olarak, komşu bağırsak duvarında kitle etkisi ve kalınlaşma, paryetal peritonda yapışıklık ve kalınlaşma saptanır. Lezyon genellikle hipoekoik bir halka ile sarılıdır. Bizim olgumuzda dış merkezde yapılan USG’de patoloji saptanmamıştı. Yerleşimine göre akut apandisit, akut kolesistit, renal kolik veya divertikülit ile karışabilir.[1] Bizim olgumuzda hem alt ve üst kadranda hassasiyet mevcuttu. Tablo akut kolesistit ve gastrit tablosu ile klinik olarak benzerlik göstermekteydi. Hatta başka merkezde yapılan üst sindirim sistemi endoskopisinde antral gastrit saptanmıştı. Non invasiv tanı yöntemleri ile tanı konup, konservatif olarakta tedavi edilmesine rağmen, akut karın ön tanısı ile ameliyata alınan olgularda rezeksiyon yapılabilir. Medikal tedavi apse formasyonu, sepsis ve karın içi adezif bant oluşumu riskini cerrahiye göre arttırmaktadır. Puylaert[5] ve Vriesman,[6] konservatif yöntemle tedavi ettikleri hastalarda komplikasyon gelişmediğini bildirmişlerdir. Omental infarktlı hastaların tedavisi konusunda görüş birliği sağlanamamıştır. Bir kısım yazarlar, gelişebilecek komplikasyonları öne sürerek cerrahi tedavi gerektiğini savunurken, bir kısmı da, geç komplikasyonların aslında sanıldığı kadar sık olmadığını ve sadece analjezik ilaçlar uygulanarak yapılacak konservatif tedavinin yeterli olacağını savunmaktadır.[5-8] 555
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Rezeksiyon laparoskopik ya da konvansiyonel teknik ile yap覺labilir. Akut kar覺n tablosu ile ameliyat edilen olgularda saptanan omentum torsiyonu rezeksiyon ile tedavi edilebilir.
KAYNAKLAR 1. McClure MJ, Khalili K, Sarrazin J, Hanbidge A. Radiological features of epiploic appendagitis and segmental omental infarction. Clin Radiol 2001;56:819-27. 2. Schwartzman GJ, Jacobs JE, Birnbaum BA. Omental infarction as a delayed complication of abdominal surgery. Clin Imaging 2001;25:341-3. 3. Helmrath MA, Dorfman SR, Minifee PK, Bloss RS, Brandt ML, DeBakey ME. Right lower quadrant pain in children
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caused by omental infarction. Am J Surg 2001;182:729-32. 4. Stella DL, Schelleman TG. Segmental infarction of the omentum secondary to torsion: ultrasound and computed tomography diagnosis. Australas Radiol 2000;44:212-5. 5. Puylaert JB. Right-sided segmental infarction of the omentum: clinical, US, and CT findings. Radiology 1992;185:16972. 6. van Breda Vriesman AC, de Mol van Otterloo AJ, Puylaert JB. Epiploic appendagitis and omental infarction. Eur J Surg 2001;167:723-7. 7. Karak PK, Millmond SH, Neumann D, Yamase HT, Ramsby G. Omental infarction: report of three cases and review of the literature. Abdom Imaging 1998;23:96-8. 8. Wiesner W, Kaplan V, Bongartz G. Omental infarction associated with right-sided heart failure. Eur Radiol 2000;10:11302.
Kas覺m - November 2011
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):557-560
Case Report
Olgu Sunumu doi: 10.5505/tjtes.2011.39018
Abdominal cocoon syndrome as a rare cause of mechanical bowel obstruction: report of two cases Bağırsak tıkanıklığının nadir bir sebebi olan abdominal koza sendromu: İki olgu sunumu Levent YENİAY, Can Avni KARACA, Cemil ÇALIŞKAN, Özgür FIRAT, Sinan Muhtar ERSİN, Erhan AKGÜN
An abdominal cocoon is an extremely rare condition, and has been reported mainly in young adolescent women as a cause of small bowel obstruction. In these patients, the small bowel is encased in a fibrous sac called an abdominal cocoon. We hereby present two cases who were diagnosed only by laparotomy and their correlation with the literature. They both received early intervention, thus preventing the need for bowel resection. The pathology of both membranes showed inflammation.
Abdominal koza literatürde genelde genç adölesan kadınlarda ince bağırsak tıkanıklığının bir nedeni olarak bildirilen nadir bir durumdur. Bu hastalarda ince bağırsak “abdominal koza” olarak adlandırılan fibröz bir kese içine sarılmıştır. Biz burada tanısı ancak laparotomi ile konulabilen iki olguyu literatürdeki bilgilerle birlikte sunuyoruz. Her iki olguya da erken dönemde müdahale edilerek bağırsak rezeksiyonundan kaçınılmıştır. Her iki olguda da membranın patolojik incelemesi enflamatuvar bir sürece işaret etmiştir.
Key Words: Abdominal cocoon; peritoneal encapsulation.
Anahtar Sözcükler: Abdominal koza; periton kapsülleme.
Abdominal cocoon syndrome describes the condition of partial or total encapsulation of abdominal viscera within a dense fibrous membrane, and was first described by Foo et al.[1] in 1978. The majority of the cases are reported from tropical and subtropical climate belts of the world. To our best knowledge, the only case reported from a non-tropical zone is from England, in which the case was born in Pakistan.[2]
CASE REPORTS Case 1- A 26-year-old female patient was admitted to the emergency department with the complaints of colic abdominal pain and vomiting persisting for two days. There were similar episodes with spontaneous symptomatic relief in the detailed history of the patient. Anamnesis revealed no history of chronic illness, chronic medication or previous operation.
Several theories have been suggested regarding the etiology of the disease, but the majority of the cases are of unknown etiology.[3] Herein, we present two cases of idiopathic abdominal cocoon syndrome who were treated successfully in our surgery department, together with a brief review of the literature.
In the physical examination, there were signs of peritoneal irritation especially in the lower quadrants of the abdomen with rebound tenderness. No distention was observed and the bowel sounds were attenuated. Air fluid levels were seen in plain abdominal X-rays, and a computerized tomography revealed distended small bowels to the level of the terminal ileum.
Department of General Surgery, Ege University Faculty of Medicine, Izmir, Turkey.
Ege Üniversitesi Tıp Fakültesi Genel Cerrahi Anabilim Dalı, İzmir.
Correspondence (İletişim): Can Avni Karaca, M.D. 252. Sok., No: 40 Da: 1, Izmir, Turkey. Tel: +90 - 232 - 390 50 50 e-mail (e-posta): acankaraca@gmail.com
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(a)
(b)
Fig. 1. Case 1. (a) Bowels and the abdominal viscera were found to be under a thick and dense membrane. (b) The appendix was firmly adhered to the cecal wall. (Color figure can be viewed in the online issue, which is available at www.tjtes.org)
Blood chemistry, total blood count and urine analysis showed no abnormality except a slight elevation of Creactive protein. The patient was then explored based on the diagnosis of acute abdomen. In the operational observation, bowels and the abdominal viscera were found to be under a thick and dense membrane, and the obstruction site causing the symptoms was a short small bowel segment adjacent to the ileocecal valve (Fig. 1a). The appendix was firmly adhered to the cecal wall (Fig. 1b). There was no major omentum present. The patient underwent simply bridectomy; no resection was performed. After the incision of the membrane, the bowels were freed, leaving no narrowed segment. The postoperative course was uncomplicated. The patient was allowed to feed via oral route by the 3rd postoperative day, and stool discharge occurred on the 4th postoperative day.
(a)
The diagnosis was made perioperatively, and the patient was further questioned regarding secondary causes of abdominal cocoon syndrome. There was no positive history of these causes, which are reviewed in the Discussion section. The patient was discharged on the 6th postoperative day. The histopathologic analysis of the specimen was reported as fibrosis, inflammation and fibrin exudation. The patient is doing well on follow-up, with no symptoms of bowel obstruction. Case 2- A 71-year-old male patient was admitted to the emergency department with the complaint of profuse vomiting after meals and absence of gas discharge for nearly two days. He described three similar episodes with spontaneous symptomatic relief within three months. He had no chronic disease.
(b)
Fig. 2. Case 2. A cardinal symptom of mechanical bowel obstruction. (Color figure can be viewed in the online issue, which is available at www.tjtes.org) 558
Kas覺m - November 2011
Abdominal cocoon syndrome as a rare cause of mechanical bowel obstruction
Palpation of the upper quadrants of the abdomen was painful with rebound tenderness. There was a soft palpable mass located in the left quadrants of the abdomen. No distention was observed, and the bowel sounds were not altered. Plain X-rays of the abdomen showed no significant pathologic sign. Abdominal computerized tomography revealed distention of stomach, duodenum and a short segment of the proximal jejunum with a small amount of fluid collection around the stomach. The tomography reported a clustering of bowels to the left quadrants of the abdomen. The blood chemistry and total blood count showed no abnormality.
sexuality factors.[6,7] None of these secondary pathogenetic factors was encountered in our cases. The absence of the major omentum in both of our cases may suggest the association of some unknown genetic factors that play a role in the pathogenesis of idiopathic disease.[8]
The patient underwent an emergency laparotomy with a diagnosis of acute abdomen. During the operational evaluation, the bowels were found to be encapsulated in a thick membrane causing obstruction, but preventing the distention, which is a cardinal symptom of mechanical bowel obstruction (Fig. 2a, b). As observed in the first case, the major omentum was missing.
A relatively young female patient without an obvious cause of bowel obstruction.
The patient underwent simple bridectomy, and the adhesions were freed by careful dissections in order to prevent iatrogenic bowel injuries, which are frequently reported in the literature in similar cases. The postoperative course was uneventful. Enteral feeding started on the 2nd postoperative day, and stool discharge occurred on the 6th postoperative day. As in the first case, the diagnosis was done perioperatively. Since there was no positive history of secondary causes, the case was admitted as primary abdominal cocoon syndrome. The patient was discharged on the 8th postoperative day. The histopathologic analysis of the specimen revealed fibrosis and granulomatous inflammation. Follow-up of the patient was unproblematic, with no symptoms of bowel obstruction.
DISCUSSION An abdominal cocoon was first described and named by Foo et al.[1] in 1978. An abdominal cocoon is a form of intestinal encapsulation, which is mostly observed in young girls living in tropical and subtropical regions.[1,4,5] In contrast to peritoneal encapsulation, the encasing membrane is an opaque fibrous structure, which is not covered by a mesothelium. In the vast majority of the cases, the histological evaluation of the membrane shows inflammation. The pathogenesis of abdominal cocoon syndrome remains unknown; however, the etiopathogenesis correlates to congenital dysplasia, chronic asymptomatic peritonitis, some medicines (e.g., practolol), continuous ambulatory peritoneal dialysis, and district and Cilt - Vol. 17 Sayı - No. 6
The clinical presentation of the abdominal cocoon syndrome mostly occurs as acute abdomen, which, in most cases, requires surgical intervention. Preoperative������������������������������������������ diagnosis of the syndrome is usually difficult. There are four main clinical features suggested in the literature by Yip and Lee[9] for preoperative diagnosis. These are:
Past history of similar episodes with symptomatic relief. Presentation with symptoms suggestive of bowel obstruction but absence of cardinal symptoms such as distention. Presence of soft non-tender abdominal mass. Our first case fits most of the features above except for the presence of a palpable mass. The latter also fits these features except for the patient being an elderly male patient. All these clinical features allowed us to suspect the diagnosis of abdominal cocoon syndrome. This led us to decide laparotomy earlier, thus preventing strangulation and resection of the bowel. However, the definitive diagnosis is achieved under laparotomy. In the literature, typically, the appearance of the abdomen is described as the bowels being in a coil-like pattern with a dense thick membrane covering the small bowels totally or partially.[10] In some distinct cases, this membrane can cover the large intestine and even solid organs. In both of our cases, the membrane fully covered both the small and large intestine, but left the solid viscera uncovered.[10] The treatment of choice for abdominal cocoon syndrome is lysis of adhesions or total removal of the membrane. In summary, abdominal cocoon syndrome is rare and difficult to diagnose. A better awareness of the entity, plus a combination of clinical examination and radiologic studies, may facilitate the preoperative diagnosis. Suitable and early surgery and appropriate perioperative treatment can improve patient prognosis in this rare condition.
REFERENCES 1. Foo KT, Ng KC, Rauff A, Foong WC, Sinniah R. Unusual small intestinal obstruction in adolescent girls: the abdominal cocoon. Br J Surg 1978;65:427-30. 2. Macklin J, Hall C, Feldman MA. Unusual cause of small 559
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3. 4. 5. 6.
bowel obstruction in adolescent girls: the abdominal cocoon. J R Coll Surg Edinb 1991;36:50-2. Kumar M, Deb M, Parshad R. Abdominal cocoon: report of a case. Surg Today 2000;30:950-3. Bhatnagar A, Pathania OP, Malik V, Chowdhry A. Abdominal cocoon causing small bowel obstruction. Indian J Gastroenterol 1987;6:55-6. Ahmed MN, Kaur S, Zargar HU. Abdominal cocoon: an unusual intestinal obstruction (a case report). J Postgrad Med 1984;30:62-3. Afthentopoulos IE, Passadakis P, Oreopoulos DG, Bargman J. Sclerosing peritonitis in continuous ambulatory peritoneal dialysis patients: one centerâ&#x20AC;&#x2122;s experience and review of the
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literature. Adv Ren Replace Ther 1998;5:157-67. 7. Mann RD. An instructive example of a long-latency adverse drug reaction--sclerosing peritonitis due to practolol. Pharmacoepidemiol Drug Saf 2007;16:1211-6. 8. Wei B, Wei HB, Guo WP, Zheng ZH, Huang Y, Hu BG, et al. Diagnosis and treatment of abdominal cocoon: a report of 24 cases. Am J Surg 2009;198:348-53. 9. Yip FW, Lee SH. The abdominal cocoon. Aust N Z J Surg 1992;62:638-42. 10. Sieck JO, Cowgill R, Larkworthy W. Peritoneal encapsulation and abdominal cocoon. Case reports and a review of the literature. Gastroenterology 1983;84:1597-1601.
KasÄąm - November 2011
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):561-562
Case Report
Olgu Sunumu doi: 10.5505/tjtes.2011.79836
An unusual cause of cold injury: liquified petroleum gas leakage Nadir bir donma yaralanması nedeni: Sıvılaştırılmış petrol gazı sızıntısı Nevra SEYHAN, Lorenc JASHARLLARI, Muhammed KAYAPINAR, Nedim SAVACI
Liquefied petroleum gas (LPG) is an odorless and colorless gas that is a mixture of hydrocarbons (propane and butane). It is now more commonly preferred among drivers as an autogas throughout the world because it is cheaper than petrol or diesel and produces the same amount of energy. Because of its rapid vaporization and consequent lowering of temperature, it may cause severe cold injuries. A 33-year-old male who suffered from hand burn due to LPG is presented in this article. In LPG-converted cars, if the conversion has not been done properly, LPG may leak. Thus, the public must be informed of this potential danger while undertaking repairs of their vehicles.
Sıvılaştırılmış petrol gazı (SPG) renksiz ve kokusuz bir gaz olup propan ve bütan hidrokarbonlarının bir karışımıdır. Petrol ve dizelden daha ucuz olduğu ve aynı enerjiyi sağladığı için tüm dünyada yaygın olarak tercih edilmektedir. Hızlı buharlaşabilme ve buna bağlı ısıyı düşürebilme özelliğinden dolayı şiddetli donuk yaralanmalarına neden olabilir. Bu yazıda, SPG dönüşümlü arabasını onarmaya çalışırken ellerinde donuk yanığı meydana gelen 33 yaşında erkek hasta sunuldu. SPG’li araçlarda dönüşüm standartlara uygun yapılmadığı takdirde gaz sızıntısı olabilir ve donma yaralanmalarına yol açabilir. Bu potansiyel tehlikeye karşı LPG’li araçların tamiri sırasında oldukça dikkatli olunmalıdır.
Key Words: Autogas; burn; cold injury; LPG.
Anahtar Sözcükler: Gaz; yanık; donma yaralanması; LPG.
Liquefied petroleum gas (LPG) is the generic name for mixtures of hydrocarbons (mainly 60% propane and 40% butane). When these mixtures are lightly compressed, they change from a gaseous state to a liquid. The pressure at which LPG becomes liquid, called its vapor pressure, likewise varies depending on composition and temperature. LPG is colorless, odorless and heavier than air. LPG burns readily in air, and has an energy content similar to petrol and a heat energy twice that of natural gas. This makes it an excellent fuel for heating, cooking and for automotive use.
than petrol or diesel. It burns more cleanly than petrol or diesel and is especially free of the particulates from the latter, thus making it more environmentally friendly.
Liquefied petroleum gas (LPG) comes from two sources. It can be obtained from the refining of crude oil and can also be extracted from natural gas or crude oil streams coming from underground reservoirs. Today, 60% of LPG in the world is produced from the underground reservoir sources, whereas 40% is extracted from the refining of crude oil. LPG is much cheaper
Department of Plastic and Reconstructive Surgery, Selcuk University Meram Medical School, Konya, Turkey.
One of the dangers of LPG is its rapid vaporization and consequent lowering of temperature (the boiling point is between -42° and 0°C, depending on the hydrocarbon mix). LPG can cause severe cold injuries if brought into contact with exposed skin.[1] A case of cold injury following skin contact with LPG is presented in this article.
CASE REPORT A 33-year-old male applied to the emergency department with burn on both his hands. He was consulted to our clinic. He was a teacher and reported that he was trying to repair his LPG-converted car on his own. He checked the solenoid cut-off valve in order to
Selçuk Üniversitesi Meram Tıp Fakültesi Plastik Rekonstrüktif Estetik Cerrahi Anabilim Dalı, Konya.
Correspondence (İletişim): Nevra Seyhan, M.D. Köyceğiz Cad., Konuk Sok., No: 21, 42680 Konya, Turkey. Tel: +90 - 332 - 223 67 06 e-mail (e-posta): nevraseyhan@hotmail.com
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understand if there was anything wrong with the system. The engine was running at the time, and there had been a fuel leakage at the point of connection between the pipes and the solenoid valve. He did not realize the gas escape at first. The contact of his exposed hands with the gas lasted only a few seconds. Later, he had the sensations of chill and pain and recognized that his hands had become white. He did not receive any first aid and came directly to the hospital. On his physical examination, he had second-degree superficial burn on the dorsum of both hands with generalized erythema and blisters. His palms were partially involved, not in the usual circumferential pattern that would raise suspicion about a compartment syndrome, and all of his fingers were well perfused. Based on his history, he was diagnosed as frostbite injury with LPG. We applied antibiotic ointment to his hands daily and he was given analgesics for pain relief, and his hands were kept in elevation. The blisters burst spontaneously a few days after his hospitalization. Complete healing was achieved on day 14. Re-epithelization occurred, excluding the need for skin grafting, and he was discharged. On his routine follow-ups, the only abnormality was skin hyperpigmentation of the involved areas. An informed consent was obtained from the patient for the presentation of this case.
DISCUSSION The use of LPG as an energy source has increased in many countries. Its cheaper price and its property of being less hazardous to the ozone layer are the main reasons for its increasing popularity as a car fuel. Motor vehicles can now be converted from running on petrol or diesel to LPG. In the United Kingdom, government grants cover up to 40-75% of the conversion costs.[2] In LPG-converted cars, an isolating valve (solenoid) is positioned between the cylinder and the vaporizer, which automatically closes the gas flow from the tank to the engine compartment. This solenoid valve is closed when the engine is stopped. The tank, which is located at the back of the car, is connected to this valve by copper tubes. The autogas is sent through the
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copper tubes to the vaporizer, which reduces the pressure of the LPG and thus changes its state from liquid to vapor form. This is then supplied to the engine.[3] Leakage at the connection site of the tubes to the safety shut-off valve is probably due to an improper installation of the LPG kit. Evaporating LPG cools and causes cold burns to the skin. Cold injuries with LPG have been reported previously.[1,2] In these cases, patients were filling their LPG-converted vehicles at the filling station, and the vapor leak was between the gun nozzle and the fuel tank. In our case, the leak was related to the LPG conversion system of the automobile. The vehicle fuel system should be inspected regularly in order to ensure safety, and the installation must be done according to government-approved standards. In Turkey, there are no current laws addressing individuals who perform substandard and illegal conversion. There are reports about burns caused by explosion of the LPG tanks,[4] but dangers of cold burns from LPG must also be taken into account.[5] Our patient was a teacher and had no knowledge about the cooling effect of the autogas, and thus did not take any preventive measure like wearing gloves while trying to repair the car. In the event of any malfunction, owners should take their vehicle to a LPG-licensed mechanic rather than attempting any repair on their own in an effort to avoid such injuries.
REFERENCES 1. Wright TC, Kim JB, Currie LJ, Kay AR, Burge TS. Leakage of liquefied petroleum gas during motor vehicle refuelling-a new cause of cold injury. Burns 2006;32:132-3. 2. Murugkar PM, Jones NW, Shokrollahi K, Potokar TS, Drew PJ, Dickson WA. Hand burns sustained whilst refuelling car with LPG (liquefied petroleum gas). Burns 2006;32:515-6. 3. Gümüş M. The effect of LPG using ratio on performance and emission characteristics in a spark ignition engine with dual fuel injection. J Fac Eng Arch Gazi Univ 2009;24:265-73. 4. Bozkurt M, Kulahci Y, Zor F, Kapi E. Burn injuries related to liquefied petroleum gas-powered cars. J Burn Care Res 2008;29:897-901. 5. Bonamonte D, Profeta G, Conserva A, Mazzoccoli S, Foti C, Angelini G. Cold burn from contact with a propane and butane gas blend inside a spray canister used as a hooter. Contact Dermatitis 2008;59:61-2.
Kasım - November 2011
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):563-566
Case Report
Olgu Sunumu doi: 10.5505/tjtes.2011.02212
Post-traumatic tricuspid insufficiency: a case report Travma sonrası triküspit yetersizliği: Bir olgu sunumu Ufuk TÜTÜN, Ayşen AKSÖYEK, Ali İhsan PARLAR, Adnan ÇOBANOĞLU
Post-traumatic tricuspid insufficiency is a rare complication of chest trauma. An 18-year-old male patient was injured in a bicycle accident from his abdominal and anterior chest wall. The tear on the inferior diaphragmatic surface of the heart was repaired with primary sutures by the attending surgeon. Eighteen years later, he was admitted to the hospital with severe tricuspid regurgitation (3+/4+). During the operation, the valve was determined unsuitable for repair and was replaced with a bioprosthesis. The hemodynamic aberrations relevant to an isolated tricuspid valve injury are very often well-tolerated. Reconstructive surgery may be possible in the early period. In the late cases, repair is sometimes not feasible due to degeneration of the valvular apparatus. Replacement with a biological prosthesis may give the best long-term results in longstanding cases.
Travma sonrası triküspit yetersizliği göğüs travmasının nadir bir komplikasyonudur. On sekiz yaşında erkek hastanın bisiklet kazasında karın ve göğüs duvarının ön kısmı yaralanıyor. Kalbin inferior diyafragmatik yüzeyindeki yırtık tedavisini yapan doktor tarafından primer dikişle onarılıyor. On sekiz yıl sonra, ciddi triküspit yetersizliği (3+/4+) ile hastaneye başvurdu. Operasyonda, kapak onarıma uygun değildi ve biyoprotez kapak ile değiştirildi. İzole triküspit kapak hasarıyla ilgili hemodinamik bozulma sıklıkla iyi tolere edilir. Rekonstrüktif cerrahi erken periyotta mümkün olabilir. Gecikmiş olgularda, onarım valvüler yapıların dejenerasyonuna bağlı bazı durumlarda uygun olmayabilir. Biyolojik protezler ile replasman uzun süreli olgularda uzun dönemde en iyi sonucu verebilir.
Key Words: Trauma; tricuspid valve insufficiency.
Anahtar Sözcükler: Travma; triküspit kapak yetersizliği.
Post-traumatic tricuspid insufficiency is a rare complication of chest trauma. Todd et al.[1] reported the first case regarding traumatic tricuspid insufficiency in 1848. However, it has been reported with increasing frequency during the last 45 years. Over 100 cases have been reported thus far in the literature. Along with the advent of high- speed transportation, the frequency of cardiac injuries, including those of the tricuspid valve, has been rising. Traffic accidents are the leading causes of traumatic tricuspid valve regurgitation, but other unusual mishaps have also been incriminated.[2-5] The great majority of patients were subjects of closed chest trauma. Recently, post-traumatic tricuspid insufficiency has been reported with the deployment of airbags.[6]
injuries are not dramatic in nature. The hemodynamic aberrations relevant to an isolated tricuspid valve injury are very often well-tolerated.
The hemodynamic alterations related to tricuspid
Department of Cardiovascular Surgery, Turkiye Yuksek Ihtisas Hospital, Ankara, Turkey.
In this article, we present a case of post-traumatic tricuspid valve injury that was successfully managed with valve replacement.
CASE REPORT An 18-year-old male, apparently in perfect health, was involved in an accident while riding a bicycle. He had extensive multiple injures to the face, thoracic cage and abdomen. His abdominal and anterior chest areas were injured by the handlebar of his bicycle. He was transported to a nearby local hospital, and after preliminary resuscitative measures, underwent an emergency laparotomy for the penetrating abdominal
Türkiye Yüksek İhtisas Hastanesi, Kalp Damar Cerrahisi Kliniği, Ankara.
Correspondence (İletişim): Ufuk Tütün, M.D. Doktorlar 91 Sitesi 688. Sok., No: 11/11 Ümitköy Çayyolu, Yenimahalle 06530 Ankara, Turkey. Tel: +90 - 312 - 466 56 88 e-mail (e-posta): ufuktutun@yahoo.com
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and thoracic injuries. A tear on the inferior diaphragmatic surface of the heart was repaired with primary sutures by the attending surgeon.
(a)
Eighteen years later, he was admitted to our institution with nausea and palpitation. On physical examination, marked pulsations were observed in the distended veins of the neck. The right ventricular pulsation was palpable along the left sternal border. On auscultation, a holosystolic murmur and early diastolic rumble were audible at the left parasternal area. There was also mild pulsatile hepatomegaly and peripheral edema. X-ray evaluation of the chest revealed an increase in the cardiothoracic ratio. A transthoracic echocardiography (TTE) demonstrated diastolic fluttering and wide diastolic excursion of the anterior leaflet of the tricuspid valve. The TTE revealed severe tricuspid regurgitation (3+/4+), with well-preserved systolic function of the right ventricle. Both the aortic and mitral valves were noted to be completely competent. A TTE study to investigate Ebsteinâ&#x20AC;&#x2122;s malformation was unsuccessful.
(b)
(c)
(d) Fig. 1. (a) One of the major anterior chordae detached from its papillary muscle head. (b) The arrow shows a fibrotic and scarred myocardial tissue on the anterior endocardial wall of the right ventricle under the anterior leaflet of the tricuspid valve. (c) The valve was replaced with a bioprosthesis. (d) The heart was reduced in size on the postoperative chest X-ray taken two months later (left corner: preoperative, right corner: postoperative). 564
During the operation, the tricuspid valve annulus was found to be dilated, with the chordae attached to the anterior and posterior leaflets avulsed from their papillary muscles. Must of the free edges of the leaflets were hanging freely and prolapsing into the right atrium. A portion of the anterior leaflet had been pulled in with contraction of the area towards a fibrotic zone in the anterior right ventricular wall. One of the major anterior chordae had detached from its papillary muscle head (Fig. 1a). There was a fibrotic scarred myocardial tissue (1x1 cm2) on the anterior endocardial wall of the right ventricle under the anterior leaflet of the tricuspid valve that probably initially caused increasing regurgitation due to contraction of the leaflet (Fig. 1b). The valve was replaced with a 31 mm bioprosthesis (Fig. 1c). The postoperative course was uneventful. Postoperatively, the patient improved significantly. He was discharged on the postoperative 6th day on digitalis and diuretics. During the follow-up in the outpatient clinic, the patient had normal physical findings, and the heart had decreased in size on chest X-ray two months later (Fig. 1d).
DISCUSSION Tricuspid regurgitation is a rare complication of blunt or penetrating chest trauma. The true incidence of tricuspid valve injury is hard to estimate. Parmley et al.[7] reported that they had determined eight cases of tricuspid valve injury in necropsy specimens of 546 cardiac injuries. Traumatic tricuspid rupture involves a sudden increase of the right ventricular intracavitary pressure KasÄąm - November 2011
Post-traumatic tricuspid insufficiency
during the isometric systolic phase, when the valve is closed.[8] The frequency of this disease is probably underestimated because isolated chronic tricuspid regurgitation is usually well-tolerated. Most patients experience few or no symptoms after the trauma.[9] In general, acute insufficiency of the tricuspid valve following trauma is subtle and insidious. Because of its subclinical course, progressive dilatation of the tricuspid annulus occurs, and the right ventricular dilatation and dysfunction eventually develop before surgery. Finally, annular dilatation, secondary to the right ventricular enlargement, usually intervenes and contributes to the worsening of the regurgitation. There is an interaction between the right ventricular end diastolic volume and the left ventricular function in conditions of right ventricular volume overload. There is an elevation in the left ventricular end diastolic pressure, which in turn may lead to left ventricular functional impairment, and this has been thought to be due to a change in the left ventricular geometry secondary to a leftward displacement of the stiff interventricular septum. As the right-sided pressures rise during the course of the disease process, the foramen ovale may re-open with resultant right-to-left shunting and finally irreversible myocardial damage.[10] Two major concerns have been raised with regard to the traditional management: the timing of the operation and the surgical procedure.[11] The proper timing of surgery has remained controversial. Of course, surgery before serious myocardial damage carries a lower risk. An early operation allows preservation of myocardial reserve by preventing the secondary myocardial changes. An early operation facilitates faster regression of the myocardial changes, if present. Some authors believe that early surgery yields better life quality and expectancy.[10-12] With favorable surgical anatomy, reconstruction of the tricuspid valve is the preferred treatment. If reconstruction is not feasible, valve replacement may be considered. A bioprosthesis is usually preferred on the right side. Alfieri et al.[13] described that the operative technique is dictated primarily by the specific anatomical lesions encountered at the time of surgery. Early operation facilitates repair of the valve. Repair of the tricuspid valve has been more frequent in recent years. In our case, the extensive annular dilatation and very extensive changes in the leaflets and chordae made repair impossible, with an expectation of good longterm results. The most frequently reported injury is chordal rupture (55% of the cases), followed by rupture of the anterior papillary muscle (27%) and tear of the leaflets (15%).[14] Some surgeons prefer reconstructive surgery. Implantation of artificial chordae, quadrangular resection of the flail segment, chordal Cilt - Vol. 17 Say覺 - No. 6
transposition, and papillary muscle reimplantation have been suggested in the presence of chordal rupture or papillary muscle rupture, allowing a successful repair in about 45% of the cases. Significant residual regurgitation after surgery was not unusual. Allfieri et al.[10] adopted a new surgical approach that consists of stitching together the middle point of the free edges of the tricuspid leaflets, producing a clover-shaped valve (Clover technique). Surgery continues to be the most recommended curative modality. Clinically overt heart failure has been the traditional indication for surgery, which usually consists of tricuspid valve replacement.[11] Delayed repair can result in excessive fibrosis and shortening or elongation of the chordae and damages the leaflets beyond repair, necessitating replacement of the valve. If the pathology of the tricuspid valve is not favorable for reconstructive surgery, replacement with a bioprosthesis is usually undertaken. As in this patient, it should be kept in mind that the degenerative process may be less pronounced on the right side of the heart with respect to the left due to the hemodynamic properties of the right side of the heart. As a result, reconstructive surgical therapy may be appropriate in post-traumatic tricuspid insufficiencies if early surgical intervention can be undertaken. As irreversible cardiac pathologies like chordal changes, fibrosis and leaflet degeneration develop during the course of the disease process in the late period, we think that valve replacement with a biological prosthesis may give the best long-term results in longstanding cases.
REFERENCES 1. Todd RB. A case of rupture of the chordae tendineae of the tricuspid valve of the heart with remarks. Duplin Quart J Med Sci 1848;5:1-11. 2. Hirata K, Kyushima M, Asato H, Mototake H, Ie T, Henzan E, et al. Tricuspid regurgitation due to blunt chest trauma. Report of a case and review of the literature. Jpn Heart J 1993;34:361-75. 3. Mary DA, Day JB, Pakrashi BC, Ionescu MI. Isolated tricuspid incompetence after penetrating trauma. Am J Cardiol 1973;31:792-5. 4. Pate JW, Richardson RL Jr. Penetrating wounds of cardiac valves. JAMA 1969;207:309-11. 5. Gerry JL Jr, Bulkley BH, Hutchins GM. Rupture of the papillary muscle of the tricuspid valve. A complication of cardiopulmonary resuscitation and a rare cause of tricuspid insufficiency. Am J Cardiol 1977;40:825-8. 6. Sharma OP, Mousset XR. Review of tricuspid valve injury after airbag deployment: presentation of a case and discussion of mechanism of injury. J Trauma 2000;48:152-6. 7. Parmley LF, Manion WC, Mattingly TW. Nonpenetrating traumatic injury of the heart. Circulation 1958;18:371-96. 8. Naja I, Pomar JL, Barriuso C, Mestres C, Mulet J. Traumatic tricuspid regurgitation. J Cardiovasc Surg (Torino) 1992;33:256-8. 9. Cahill NS, Beller BM, Linhart JW, Early RG. Isolated trau565
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matic tricuspid regurgitation: prolonged survival without operative intervention. Chest 1972;61:689-91. 10. Shahidnoorai S, Ameli M. Post traumatic tricuspid insufficiency: when to intervene? J Cardiovasc Surg (Torino) 1991;32:585-8. 11. van Son JA, Danielson GK, Schaff HV, Miller FA Jr. Traumatic tricuspid valve insufficiency. Experience in thirteen patients. J Thorac Cardiovasc Surg 1994;108:893-8. 12. Fracasso A, Pothen P, Gallucci V. Tricuspid regurgitation caused by blunt chest trauma in association with pericar-
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dial agenesis: surgical correction after eight years. Thorax 1982;37:75-6. 13. Dounis G, Matsakas E, Poularas J, Papakonstantinou K, Kalogeromitros A, Karabinis A. Traumatic tricuspid insufficiency: a case report with a review of the literature. Eur J Emerg Med 2002;9:258-61. 14. Alfieri O, De Bonis M, Lapenna E, Agricola E, Quarti A, Maisano F. The “clover technique” as a novel approach for correction of post-traumatic tricuspid regurgitation. J Thorac Cardiovasc Surg 2003;126:75-9.
Kasım - November 2011
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):567-569
Case Report
Olgu Sunumu doi: 10.5505/tjtes.2011.54533
Loop formation of Meckel’s diverticulum causing small bowel obstruction in adults: report of two cases Erişkinlerde ince bağırsak tıkanıklığına neden olan Meckel divertikülüne bağlı halka oluşumu: İki olgu sunumu Shilpi SINGH GUPTA, Onkar SINGH Meckel’s diverticulum is the most common congenital anomaly of the gastrointestinal tract, and in the majority of cases it remains asymptomatic. The total lifetime rate of complications is 4%. It is an uncommon cause of intestinal obstruction in adults. Loop formation of Meckel’s diverticulum leading to small bowel obstruction is an extremely rare event. We report two such cases in which the bowel became obstructed and strangulated in a loop formed by adhesion of the distal end of the Meckel’s diverticulum to the proximal ileum and mesentery.
Meckel divertikülü olguların çoğunluğunda asemptomatik olarak kalan en yaygın konjenital gastrointestinal sistem anomalisidir. Yaşam boyu komplikasyon oranı %4’dür. Erişkinlerde nadir bir intestinal tıkanıklık nedenidir. İnce bağırsak tıkanıklığına neden olan Meckel divertikülüne ilişkin halka oluşumu oldukça enderdir. Biz, Meckel divertikülünün distal ucu ile proksimal ileum ve mezenter arasında halka şeklinde adezyonlar oluşmasıyla bağırsağın tıkandığı ve strangülasyona uğradığı iki olguyu sunuyoruz.
Key Words: Adults; intestinal obstruction; Meckel’s diverticulum.
Anahtar Sözcükler: Erişkinler; intestinal tıkanıklık; Meckel divertikülü.
Meckel’s diverticulum is an uncommon cause of intestinal obstruction in adult life.[1] Rarely, Meckel’s diverticulum may form a loop due to adhesions between its distal end and the bowel itself or the mesentery.[2-6] Adhesion of the diverticulum to the bowel wall, thus creating a loop and causing obstruction, has been reported only twice.[5,6] Bowel loops may become entangled in this loop and strangulated. The condition is usually not suspected before exploration, but may lead to gangrene of the bowel and high mortality if the treatment is delayed.
rigidity throughout. Bowel sounds were increased. Ultrasonography (USG) of the abdomen revealed hyperperistaltic dilated small bowel loops. Erect radiograph of the abdomen showed multiple air fluid levels situated in the central abdomen and to the left (Fig. 1). A nasogastric tube was inserted, which drained bilious secretion. The patient was taken for exploratory laparotomy, and a proximal ileal segment was found, compressed by a loop formed by adhesion of the tip of the Meckel’s diverticulum to the antimesenteric border of the terminal ileum (Fig. 2a). Proximal bowel loops were dilated, but fortunately not gangrenous. The Meckel’s diverticulum and adhesion were excised, and the small bowel freed and decompressed. The base of the diverticulum was inflamed (Fig. 2b). Continuity was restored with end-to-end anastomosis. The patient made an uneventful recovery after the surgery and was asymptomatic at the last follow-up.
CASE REPORTS Case 1- A 32-year-old male with no previous history of abdominal surgery presented with a history of abdominal pain and vomiting of two days’ duration. History of absolute constipation was present for one day. There was no history of similar pain in the past. On examination, his vital signs were within normal limits, but signs of dehydration were present. The abdomen was distended, with muscle guarding and M.G.M Medical College & M.Y. Hospital, Indore, India.
Case 2- A 28-year-old male presented with a history of abdominal pain, vomiting and constipation of M.G.M. Tıp Koleji ve M.Y. Hastanesi, Indore, Hindistan.
Correspondence (İletişim): Shilpi Singh Gupta, M.D. VPO-Sangowal, Tehsil-Nakodar 144041, Jalandhar, India. Tel: +91 - 7552740240 e-mail (e-posta): drguptashilpi@gmail.com
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Fig. 1. Case 1 - Erect abdominal radiograph showing multiple air-fluid levels predominantly in the central abdomen and to the left.
Fig. 3. Case 2 - Erect abdominal radiograph showing multiple air-fluid levels predominantly in the central abdomen and to the left.
three days’ duration. There was no history of a previous similar pain or of previous surgery. The abdomen was distended, with tenderness and guarding throughout. Total leukocyte count was 19,600/cmm. Renal function tests were normal. USG of the abdomen revealed hyperperistaltic dilated small bowel loops with a small amount of free fluid in the abdomen. Plain X-ray of the abdomen revealed multiple air-fluid levels (Fig. 3). Exploratory laparotomy was planned. Intra-operatively, the Meckel’s diverticulum with gangrenous base was found attached to mesentery by its distal end, thus forming a loop (Fig. 4). A segment of the terminal ileum was compressed in this
loop with proximal dilatation. A proximal 8” segment of the ileum was gangrenous. En-bloc resection of the gangrenous segment of bowel and Meckel’s diverticulum was performed, and continuity was maintained with end-to-end anastomosis. The patient had an uneventful postoperative recovery.
(a)
DISCUSSION Meckel’s diverticulum is a congenital outpouching arising from the antimesenteric border of the distal ileum that is present in 1-3% of the general population. It is a remnant of the vitellointestinal duct that connects the primitive gut to the yolk sac during devel-
(b)
Fig. 2. Case 1 - (a) Obstruction of the ileal segment by a loop formed by adhesion of the tip of the Meckel’s diverticulum to the antimesenteric border of the terminal ileum; (b) The resected specimen of the Meckel’s diverticulum. (Color figure can be viewed in the online issue, which is available at www.tjtes.org) 568
Kasım - November 2011
Loop formation of Meckel’s diverticulum
be treated as an emergency condition with immediate exploratory laparotomy after initial resuscitation. The main aim of surgery is to remove the Meckel’s diverticulum along with resection of the gangrenous segment of the bowel, if gangrene is present.[11] Recently, laparoscopy has proved useful to resolve small bowel obstruction associated with Meckel’s diverticulum.[12] Both the cases reported herein were young adult males presenting with acute colicky abdominal pain. There was no history in either patient that would have suggested any common etiology leading to acute intestinal obstruction.
Fig. 4. Case 2 - The Meckel’s diverticulum with gangrenous base attached to the mesentery by its distal end, thus forming a loop. (Color figure can be viewed in the online issue, which is available at www.tjtes.org)
opment. The majority of cases remain asymptomatic, but complications include hemorrhage, intestinal obstruction, diverticulitis, umbilical discharge, perforation, and peritonitis.[7] Only about 4% of patients with Meckel’s diverticulum are symptomatic.[8] The total lifetime rate of complications is widely accepted at 4%, with a male-to-female ratio ranging from 1.8:1 to 3:1.2 While in adults, the most common complication is intestinal obstruction,[5] Meckel’s diverticulum is an infrequent cause of intestinal obstruction.[1,5] Various mechanisms of small intestinal obstruction from Meckel’s diverticulum include diverticular intussusception, which is the most common mechanism, volvulus from persistent attachment to the umbilicus, congenital meso-diverticular bands, Littre’s hernias, foreign body impaction, diverticulitis, and adhesions or neoplasms.[2,4,9] Other very rare causes of obstruction from Meckel’s diverticulum include formation of a loop between the end of a Meckel’s diverticulum and the adjacent mesentery or bowel wall.[2-4,9] Loop formation as a result of the development of adhesions between the distal end of the diverticulum and the mesentery or the bowel is an extremely rare finding.[24,10] The former finding of adhesion of the diverticulum to the mesentery, thus forming a loop and leading to an obstructive case in adults, is very rarely reported; formation of a loop due to adhesion of the tip of the Meckel’s diverticulum to the bowel has been reported only twice in the literature.[5,6] Preoperative diagnosis of intestinal obstruction because of Meckel’s diverticulum may be challenging and requires a high degree of suspicion.[11] If such a case is left untreated, it leads to strangulation and ischemic necrosis of the bowel loop. Hence, it should Cilt - Vol. 17 Sayı - No. 6
In conclusion, loop formation due to adhesions between the distal end of the Meckel’s diverticulum and the intestine or the mesentery is an infrequent phenomenon and is even rarer in adults. The condition requires a high degree of suspicion, and should be included in the differential diagnosis of small bowel obstruction in adults.
REFERENCES 1. Nath DS, Morris TA. Small bowel obstruction in an adolescent: a case of Meckel’s diverticulum. Minn Med 2004;87:46-8. 2. Dumper J, Mackenzie S, Mitchell P, Sutherland F, Quan ML, Mew D. Complications of Meckel’s diverticula in adults. Can J Surg 2006;49:353-7. 3. Piñero A, Martínez-Barba E, Canteras M, Rodriguez JM, Castellanos G, Parrilla P. Surgical management and complications of Meckel’s diverticulum in 90 patients. Eur J Surg 2002;168:8-12. 4. Tomikawa M, Taomoto J, Saku M, Takeshita M, Yoshida K, Sugimachi K. A loop formation of Meckel’s diverticulum: a case with obstruction of the ileum. Ulus Travma Acil Cerrahi Derg 2003;9:134-6. 5. Prall RT, Bannon MP, Bharucha AE. Meckel’s diverticulum causing intestinal obstruction. Am J Gastroenterol 2001;96:3426-7. 6. Devanaboyna G, Singh-Ranger D, Shami S. Meckel’s diverticulum causing mechanical small bowel obstruction. Can J Surg 2008;51:156. 7. Kusumoto H, Yoshida M, Takahashi I, Anai H, Maehara Y, Sugimachi K. Complications and diagnosis of Meckel’s diverticulum in 776 patients. Am J Surg 1992;164:382-3. 8. You JS, Chung SP, Park YS, Yu JS, Park YA. A case of strangulated small bowel obstruction caused by Meckel’s diverticulum in an adult. J Emerg Med 2007;33:133-5. 9. Karadeniz Cakmak G, Emre AU, Tascilar O, Bektaş S, Uçan BH, Irkorucu O, et al. Lipoma within inverted Meckel’s diverticulum as a cause of recurrent partial intestinal obstruction and hemorrhage: a case report and review of literature. World J Gastroenterol 2007;13:1141-3. 10. Karatepe O, Dural C, Erçetin C, Citlak G, Samaslıoğlu A, Gülçiçek OB, et al. Rare complication of Meckel’s diverticulum: loop formation of diverticulum. Turk J Med Sci 2008;38: 91-3. 11. Sharma RK, Jain VK. Emergency surgery for Meckel’s diverticulum. World J Emerg Surg 2008;3:27. 12. Tashjian DB, Moriarty KP. Laparoscopy for treating a small bowel obstruction due to a Meckel’s diverticulum. JSLS 2003;7:253-5. 569
Turkish Journal of Trauma & Emergency Surgery
Ulus Travma Acil Cerrahi Derg 2011;17 (6):570-572
Case Report
Olgu Sunumu doi: 10.5505/tjtes.2011.79069
Bir olgu nedeniyle, travmatik orbital amfizemlere yaklaşım Traumatic orbital emphysema: a case report Ersin OBA, Can PAMUKCU, Serkan ERDENÖZ
Otuz yaşında erkek hasta, sümkürme sonrası sağ gözde gelişen, ani ağrı, şişme, az görme ve çift görme şikayetleri ile başvurdu. Üç gün önce künt orbital travma hikayesi olan hastanın görmesi sağda 6/10, solda 10/10 idi. Ön segment ve fundus incelemesinde özellik saptanmadı. Sağ gözünde yukarı bakış kısıtlılığı tespit edildi. Yukarı ve aşağı bakışları sırasında diplopi mevcuttu. Göz içi basıncı sağda 21 mmHg, solda 16 mmHg idi. Hertel ekzoftalmometre değerleri sağda 21 mm, solda 19 mm idi. Orbital bilgisayarlı tomografi incelemesinde sağ inferior orbital duvar kırığı ve orbital amfizem saptandı. Proflaktik antibiyotik tedavisi başlandı. Üçüncü gün kontrolünde herhangi bir şikayeti bulunmayan hasta intranazal basınç artışına neden olabilecek uygulamalardan kaçınması konusunda uyarıldı. Takipte herhangi bir patolojik bulgu ortaya çıkmadı.
A 30-year-old male presented with sudden diminution of vision, orbital pain, diplopia, and swelling of the eyelid of the right eye after blowing his nose within three days after a blunt ocular trauma. His best-corrected visual acuities were 6/10 in the right eye and 10/10 in the left eye. Anterior segment and fundus examination were normal bilaterally. Limitation of upward ocular motility was noticed in the right eye. Diplopia was detected in both upward and downward motilities. Intraocular pressures were 21 mmHg in OD and 16 mmHg in OS. Hertel exophthalmometry measurements were 21 mm for the right eye and 19 mm for the left eye. The direct computerized tomography image displayed the inferior orbital wall fracture and orbital emphysema in the right orbit. Prophylactic antibiotherapy was applied. The patient was advised not to blow his nose. He had no complaints on the third day after the trauma. Follow-up examinations showed no ophthalmological complications.
Anahtar Sözcükler: Inferior orbital duvar kırığı; orbital amfizem; orbital travma.
Key Words: Inferior orbital wall fracture; orbital emphysema; orbital trauma.
Orbital amfizem orbitayı içine alan paranazal sinüs kırıklarıyla birliktelik gösterir. Orbital kırıklarda sümkürme sonrası subkutan amfizem iyi tanımlanmış olup buna eşlik eden görme kaybı ender rastlanmaktadır. Orbital travma sonrası ani vizyon kaybı genellikle retrobulber hemoraji nedeniyle olur.
Bu yazıda, orbital travma sonrası gelişen orbital amfizem olgusuna yaklaşım irdelenmiştir.
Orbital amfizem, travma hikayesi olan hastada palpasyon ve radyolojik inceleme ile değerlendirilir. Orbital duvar kırığı olan hastalarda intranazal hava basıncının artması ile maksiller, etmoid ve daha az sıklıkla frontal sinüsten orbital alana hava girer.[3]
OLGU SUNUMU Otuz yaşında erkek hasta sağ göz kapağında şişme, ağrı, az görme ve çift görme şikayeti ile başvurdu. Üç gün önce arkadaşının omzuna çarptığını söyleyen hasta şikayetlerinin sabah sümkürme sonrası başladığını ifade etti. Yapılan incelemesinde görmeleri sağda 6/10 solda 10/10 idi. Ön segment ve fundus incelemesinde patoloji saptanmadı. Sağ gözde yukarı bakış kısıtlılığı vardı (Şekil 1). Yukarı ve aşağı bakışlarında diplopisi mevcuttu. Göz içi basınçları sağda 21 mmHg, solda 16 mmHg idi. Hertel ekzoftalmometre değerleri sağ 21 mm, sol 19 mm idi. Orbital bilgisayarlı tomografi (BT) incelemesinde sağda inferior orbital duvar kırığı,
Şişli Etfal Eğitim ve Araştırma Hastanesi, 2. Göz Kliniği, İstanbul.
Department of Ophthalmology, Sisli Etfal Training and Research Hospital, Istanbul, Turkey.
Orbital amfizem, orbital duvarların dahil olduğu paranazal sinüs fraktürlerinde genelde ilk 24 saat içinde ortaya çıkar.[1] Benign, geçici bir fenomen olan orbital amfizemin spontan absorbsiyonu iki hafta içinde gerçekleşir.[2]
İletişim (Correspondence): Dr. Ersin Oba. Şişli Etfal Eğitim ve Araştırma Hastanesi, 2. Göz Kliniği, İstanbul, Turkey. Tel: +90 - 212 - 231 22 09 / 5146 e-posta (e-mail): pamukcu.can@gmail.com
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Travmatik orbital amfizemlere yaklaşım
Şekil 1. Sağ gözde yukarı bakış kısıtlılığı.
Şekil 3. Kapak şişliği gerilemiş, glob hareketleri serbestleşmiş.
Renkli şekiller derginin çevrimiçi sayısında görülebilir (www.tjtes.org)
orbital amfizem ve sağ maksiller sinüste hemoraji tespit edildi (Şekil 2a, b). İnferior rektus kasının ise kırık hattına girdiği gözlendi (Şekil 2c). Proflaktik antibiyotik tedavisi başlandı. Üçüncü gün kontrolünde vizyonlar sağ ve solda 10/10, göz içi basınçları iki taraflı eşit ve 15 mmHg saptandı. Kapak şişliğinin gerilediği, glob hareketlerinin serbestleştiği görüldü (Şekil 3). Hertel ekzoftalmometrik ölçümü ise sağ 18 mm sol ise 19 mm olarak kaydedildi. Sümkürme ve hapşırma sonrası bu durumun olabileceği hastaya anlatıldı. Daha sonraki takiplerde herhangi bir patoloji saptanmadı.
TARTIŞMA Orbital amfizemlerin tanısı genellikle anamnez, fiziksel inceleme ve orbital BT incelemesi ile konur ve tedavisiz resorbe olur.[2] Periorbital hasarlı hastalarda,
görme keskinliği ve ekstraoküler kas fonksiyonu en önemli oftalmolojik muayenelerdir. İnferior orbital kırık bulunan olgumuzda, artan orbita içi basıncın inferior rektus kasını kırık hattına ittiği görülmektedir (Şekil 2c). Bunun sonucu olarak glob hareketinin yukarı bakış sırasında kısıtlandığını saptadık (Şekil 1). Orbital amfizem genelde benign, geçici bir fenomen olarak tanımlanmış olup, küçük orbital duvar kırıkları ile birlikte görüldüğü bildirilmiştir.[4] Fizyopatolojik açıdan orbital amfizem, intranazal hava basıncının artması ile, (özellikle hastanın hapşırması, sümkürmesi gibi) maksiller, etmoid ve daha az sıklıkla frontal sinüsten orbital alana giren hava ile ortaya çıkmaktadır.[3] Mukozal yırtık olduğu zaman mukozadan kaynaklanan kanama paranazal sinüs içine akar. Paranazal sinüs mukozasının destrüksiyonu ve kırık hattının valf benzeri bir etki yapması ile hava orbita içi-
(a)
(c)
(b) Cilt - Vol. 17 Sayı - No. 6
Şekil 2. (a) Koronal orbital BT, sağda inferior orbital duvar kırığı ve sağ maksiller sinüste hemoraji. (b) Aksiyel orbital BT, sağda orbital amfizem. (c) Koronal orbital BT, inferior rektus kasının görünümü. 571
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ne girer ve valf mekanizmasının havanın çıkmasını engellemesi de orbital amfizemin temelini oluşturur. [5] Mukozal yırtık olduğunda paranazal sinüs içine kanama olur. Paranazal sinüs içindeki kanamalar hiatus semilunaris içinden meatus nasi mediusa akar ve burun tıkanıklığına yol açabilir ve hasta sümkürme ihtiyacı hisseder.[6] Nazal tıkanıklık kanama dışında nazal mukozanın enflamasyon ve ödemine de bağlı olabilir. Hastalar burun tıkanıklığı olması nedeniyle sümkürme ihtiyacı hissederler. Böylece paranazal sinüste hemoraji varlığı olan hastalarda mukozal yırtığında eşlik etmesi nedeniyle orbital amfizem açısından riskli hasta grubunu oluştururlar. Olgumuzda paranazal sinüste hemoraji varlığı orbital amfizemin gelişimine katkıda bulunduğunu düşünmekteyiz. Orbital alana hava girişi olan hastalarda yüzde şişme, göz kapaklarında kapanma ve ekstraorbital subkutan amfizem klinik semptomları ortaya çıkar. Subkonjonktival hemoraji, krepitasyon, hassasiyet ve ağrı olabilir.[7] Nadiren orbital amfizem sonucu orbital kompartman sendromu gelişerek santral retinal arter oklüzyonu gelişebilir. Orbital alana giren hava santral retinal arter üzerine kitle etlisi yaparak oklüzyona ve görme kaybı yapabilir.[5] Hastamızda yüzde şişme, göz kapaklarında kapanma ve ekstraorbital subkutan amfizem, subkonjonktival hemoraji, krepitasyon, hassasiyet ve ağrı da ortaya çıkmıştır (Şekil 1). Olgumuz nedeniyle orbital travma geçiren hastaların farklı kliniklerde (Plastik cerrahi, KBB vb.) tanı alsalar da mutlaka göz hastalıkları kliniği ile konsülte edilmesinin yararı ortaya çıkmaktadır. Hastalar gelişebilecek görsel komplikasyonlar riski nedeniyle yakından takip edilmelidir.[2] Silver ve arkadaşları orbital amfizemi evrelendirip bir tedavi protokolü önermişlerdir (Tablo 1).[8] Silver ve arkadaşları her hastaya antibiyotik tedavisi önermişlerdir. Görme kaybı halinde bu tedaviye ilave olarak steroid tedavisinin eklenmesini önermişlerdir. Bazı yayınlarda yüksek intraoküler basınç varlığında ve/veya oftalmopleji oluştuğunda optik siniri doğrudan veya iskemik hasardan korumak için hastalara cerrahi girişim yapılması önerilmiştir.[9]
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Tablo 1. Orbital amfizemin tedavi algoritması Evre
Belirtiler
Tedavi
I II III
Diplopi / proptozis Vizyon kaybı Orbital kompartman sendromu / oftalmopleji
Antibiyotik tedavisi ile gözlem Ek olarak kortizon Ek cerrahi girişim
Mukoza yırtığına bağlı amfizem gelişimi yüksek intraoküler/intraorbital basınç artışına ve görme kaybına neden olabilir. Sinüs içine hemoraji bulunduğunda hastalar orbital amfizem gelişimi için risk altında olmaları nedeniyle özellikle ilk 7-10 gün boyunca sümkürme ve hapşırmama konusunda uyarılmalıdır, Orbital amfizem olan her hastaya proflaktik antibiyotik tedavisi verilmelidir. Bu dönemde hastalar sıkı takip edilmelidir.
KAYNAKLAR 1. Papadimitriou P, Ntomouchtsis A, Antoniades K. Delayed traumatic ocular emphysema: a case report. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;102:e18-20. 2. Mohan B, Singh KP. Bilateral subcutaneous emphysema of the orbits following nose blowing. J Laryngol Otol 2001;115:319-20. 3. Ord RA, Le May M, Duncan JG, Moos KF. Computerized tomography and B-scan ultrasonography in the diagnosis of fractures of the medial orbital wall. Plast Reconstr Surg 1981;67:281-8. 4. Lee HJ, Jilani M, Frohman L, Baker S. CT of orbital trauma. Emerg Radiol 2004;10:168-72. 5. Dobler AA, Nathenson AL, Cameron JD, Carpel ET, Janda AM, Pederson JE. A case of orbital emphysema as an ocular emergency. Retina 1993;13:166-8. 6. Shinohara H, Shirota Y, Fujita K. Implication of differences in the incidence of orbital emphysema in ethmoidal and maxillary sinus fractures. Ann Plast Surg 2004;53:565-9. 7. Paquette M, Terezhalmy GT, Moore WS. Subcutaneous emphysema. Quintessence Int 2002;33:478-9. 8. Silver HS, Fucci MJ, Flanagan JC, Lowry LD. Severe orbital infection as a complication of orbital fracture. Arch Otolaryngol Head Neck Surg 1992;118:845-8; discussion 882. 9. Frenkel RE, Spoor TC. Diagnosis and management of traumatic optic neuropathies. Adv Ophthalmic Plast Reconstr Surg 1987;6:71-90.
Kasım - November 2011
Ulusal Travma ve Acil Cerrahi Dergisi 2011 yılı 17. cilt konu ve yazar dizini
ULUSAL TRAVMA VE ACİL CERRAHİ DERGİSİ 2011 YILI 17. CİLT KONU DİZİNİ
Abdominal aort anevrizması
bkz. 2011;17 (6):525-532 Abdominal kompartman sendromu bkz. 2011;17 (1):1-8 bkz. 2011;17 (2):183-185 Abdominal koza bkz. 2011;17 (6):557-560 Acil bkz. 2011;17 (1):33-40 2011;17 (6):525-532 Acil hekimi bkz. 2011;17 (1):23-28 Acil servis bkz. 2011;17 (2):113-116 bkz. 2011;17 (3):243-247 bkz. 2011;17 (6):488-492 Acil tıp bkz. 2011;17 (3):248-252 Acil tıp teknisyeni bkz. 2011;17 (2):113-116 Açık göz küresi yaralanması bkz. 2011;17 (5):413-418 Açık göz yaralanması bkz. 2011;17 (4):334-339 Adezyon bariyeri bkz. 2011;17 (5):377-382 Adezyon bkz. 2011;17 (3):205-209 bkz. 2011;17 (4):308-312 Adli olgu bkz. 2011;17 (5):470-472 Adli rapor bkz. 2011;17 (1):23-28 Agar bkz. 2011;17 (2):108-112 Akciğer fonksiyonu bkz. 2011;17 (2):103-107 Akut apandisit bkz. 2011;17 (1):19-22 bkz. 2011;17 (5):396-400 Akut karın bkz. 2011;17 (3):210-214 bkz. 2011;17 (6):554-556 Akut mezenter iskemi bkz. 2011;17 (3):193-198 Akut pankreatit bkz. 2011;17 (5):383-389 Alfa lipoik asit bkz. 2011;17 (5):383-389 Alvarado skoru bkz. 2011;17 (5):396-400 Amyand fıtığı bkz. 2011;17 (5):467-469 Anal oto-erotizm bkz. 2011;17 (4):374-376 Anaoskop bkz. 2011;17 (1):83-86 Anatomik bölge bkz. 2011;17 (4):313-317 Anestetik teknikler bkz. 2011;17 (6):497-503 Anjiyografi bkz. 2011;17 (2):152-158 Anjiyotensin bkz. 2011;17 (2):97-102 Ankaferd bkz. 2011;17 (4):308-312 Antikoagülasyon bkz. 2011;17 (3):210-214 Antioksidan bkz. 2011;17 (1):1-8 bkz. 2011;17 (1):14-18 Aort diseksiyonu bkz. 2011;17 (5):458-460 Apandisit bkz. 2011;17 (3):267-268 Aspirasyon bkz. 2011;17 (5):470-472 AT1 bkz. 2011;17 (2):97-102
Cilt - Vol. 17 Sayı - No. 6
Ateşli silah yaralanmaları bkz. 2011;17 (5):401-406 bkz. 2011;17 (5):450-454 bkz. 2011;17 (5):464-466 Atlanan yaralanma bkz. 2011;17 (3):215-219
Bağırsak rezeksiyonu
bkz. 2011;17 (4):344-348 Bağırsak tıkanıklığı bkz. 2011;17 (3):277-279 Beslenme Risk Taraması bkz. 2011;17 (6):521-524 Beslenme riski bkz. 2011;17 (6):521-524 Beta glukan bkz.2011;17 (4):303-307 Bilgisayarlı tomografi bkz. 2011;17 (3):215-219 bkz. 2011;17 (6):545-553 Bilimsel yayın bkz. 2011;17 (3):248-252 Biyolojik içten tespit bkz. 2011;17 (2):159-165 Biyolojik protez bkz. 2011;17 (4):354-358 Böbrek yaralanması bkz. 2011;17 (6):475-481 Boğa boynuzu bkz. 2011;17 (4):374-376 Bouveret sendromu bkz. 2011;17 (5):461-463 Bozulmuş ceset bkz. 2011;17 (4):340-343 BT tarama bkz. 2011;17 (3):267-268 Büyük damar yaralanması bkz. 2011;17 (5):423-429
Celox
bkz. 2011;17 (3):199-204 Cerrahi bkz. 2011;17 (1):66-74 bkz. 2011;17 (1):79-82 bkz. 2011;17 (2):180-182 bkz. 2011;17 (2):189-191 Cerrahi bölgesi enfeksiyonu bkz. 2011;17 (4):354-358 Cerrahi tedavi bkz. 2011;17 (1):57-60 bkz. 2011;17 (5):467-469 Cerrahi teknik bkz. 2011;17 (4):354-358 Cerrahi yapışıklık bkz. 2011;17 (2):108-112 Curcumin bkz. 2011;17 (1):14-18 ®
Çivi bkz. 2011;17 (1):79-82
Çocuk bkz. 2011;17 (2):173-176 bkz. 2011;17 (4):318-322 bkz. 2011;17 (4):365-367 Çocuk istismarı bkz. 2011;17 (5):430-434 Çocuklar bkz. 2011;17 (5):419-422 Çocukluk çağı bkz. 2011;17 (2):166-172 Çok kesitli bilgisayarlı tomografi bkz. 2011;17 (5):461-463
Debridman bkz. 2011;17 (4):323-328
Delici-kesici alet yaralanmaları bkz. 2011;17 (5):401-406 Delinme bkz. 2011;17 (1):90-92 Deri yumuşak doku bkz. 2011;17 (1):29-32 Dikişsiz tamir bkz. 2011;17 (1):9-13 Diseksiyon bkz. 2011;17 (1):75-78 bkz. 2011;17 (4):371-373 Divertikül bkz. 2011;17 (4):365-367 Diyafram hernisi bkz. 2011;17 (5):435-439 Donma yaralanması bkz. 2011;17 (6):561-562 Döhle cisimciği bkz. 2011;17 (2):128-132 Duodenal perforasyon bkz. 2011;17 (1):9-13 DuraSeal bkz. 2011;17 (1):9-13
Eğitim bkz. 2011;17 (5):430-434
Eğitim düzeyi bkz. 2011;17 (5):445-449 Eksternal fiksatörler bkz. 2011;17 (5):407-412 Ekstremite amputasyonu bkz. 2011;17 (4):323-328 Ekstremite travması bkz. 2011;17 (6):539-544 El bkz. 2011;17 (3):253-260 El ile değerlendirme bkz. 2011;17 (1):83-86 El ultrasonu bkz. 2011;17 (6):488-492 Elektrik çarpması bkz. 2011;17 (4):349-353 Ender çivileri bkz. 2011;17 (5):407-412 Enfekte alanlar bkz. 2011;17 (4):354-358 Enstrümantasyon bkz. 2011;17 (2):141-148 Epidemiyoloji bkz. 2011;17 (1):46-50 bkz. 2011;17 (2):166-172 bkz. 2011;17 (3):231-237 Epilepsi bkz. 2011;17 (4):359-362 Ergen bkz. 2011;17 (4):318-322 Erişkinler bkz. 2011;17 (6):567-570 Erken rezolüsyon bkz. 2011;17 (3):283-285 Ev kazaları bkz. 2011;17 (5):445-449
Fasiit bkz. 2011;17 (1):29-32
FAST bkz. 2011;17 (6):488-492 Fekal diversiyon bkz. 2011;17 (2):123-127 Femur başı bkz. 2011;17 (1):51-56 Femur cisim kırığı bkz. 2011;17 (2):159-165 Fibrin yapıştırıcı bkz. 2011;17 (1):9-13 Fibroblast bkz. 2011;17 (2):97-102 Fistül bkz. 2011;17 (6):516-520 Flep sürvisi bkz. 2011;17 (2):97-102 Fonksiyonel sonuç bkz. 2011;17 (6):504-508 Forseps bkz. 2011;17 (1):83-86 Fosfor bkz. 2011;17 (3):193-198 Futbol bkz. 2011;17 (2):180-182 bkz. 2011;17 (4):313-317 bkz. 2011;17 (4):371-373
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Gastrointestinal kanama
Kalça bkz. 2011;17 (5):455-457 Kalça kırıkları bkz. 2011;17 (5):407-412 bkz. 2011;17 (2):173-176 Kalp laserasyonu bkz. 2011;17 (1):87-89 Gaz bkz. 2011;17 (6):561-562 Kalp yaralanması bkz. 2011;17 (5):423-429 Gecikmiş tanı bkz. 2011;17 (5):435-439 Kan yayması bkz. 2011;17 (2):128-132 Genel cerrah bkz. 2011;17 (3):225-230 Kanama bkz. 2011;17 (2):183-185 Glutamin bkz. 2011;17 (1):1-8 Kanama kontrolü bkz. 2011;17 (3):199-204 Glutatyon Karaciğer bkz. 2011;17 (4):308-312 bkz. 2011;17 (1):1-8 Karaciğer hasarı bkz.2011;17 (4):303-307 bkz. 2011;17 (4):293-297 Karayolu trafik kazaları Göğüs travması bkz. 2011;17 (5):423-429 bkz. 2011;17 (6):539-544 Greftleme bkz. 2011;17 (4):323-328 Karın bkz. 2011;17 (4):363-364 Güdük bkz. 2011;17 (3):267-268 Karın cerrahisi bkz. 2011;17 (2):108-112 aşlanma bkz. 2011;17 (5):419-422 bkz. 2011;17 (5):377-382 Hastane bkz. 2011;17 (2):113-116 Karın duvarı bkz. 2011;17 (6):493-496 Hata bkz. 2011;17 (1):23-28 Hemopnömotoraks bkz. 2011;17 (3):280-282 Karın travması bkz. 2011;17 (2):113-116 Karın yaralanması bkz. 2011;17 (2):180-182 Hemotoraks bkz. 2011;17 (2):117-122 Karotid arter bkz. 2011;17 (1):75-78 Hemşire bkz. 2011;17 (2):113-116 Kaspaz 3 bkz. 2011;17 (5):390-395 Herni bkz. 2011;17 (6):493-496 Kavernozografi bkz. 2011;17 (1):57-60 Hipotermi bkz. 2011;17 (3):199-204 Kayısı çekirdeği bkz. 2011;17 (3):286-288 Hizmet içi eğitim bkz. 2011;17 (5):430-434 Kazalar bkz. 2011;17 (2):149-151 Hücresel morfolojik değişiklikler Kırık bkz. 2011;17 (1):51-56 bkz. 2011;17 (2):128-132 Kırık bkz. 2011;17 (3):253-260 Kırık tespiti bkz. 2011;17 (5):407-412 hmal edilmiş rektal yabancı cisim Kırsal bkz. 2011;17 (3):231-237 bkz. 2011;17 (4):374-376 Kilitli intramedüller çivi İlk yardım bkz. 2011;17 (5):445-449 bkz. 2011;17 (2):159-165 İnce bağırsak delinmesi Kirschner teli bkz. 2011;17 (3):253-260 bkz. 2011;17 (3):286-288 Klemp bkz. 2011;17 (1):83-86 İnferior orbital duvar kırığı Klinik bulgular bkz. 2011;17 (6):525-532 bkz. 2011;17 (6):570-572 Kolon anastomozu bkz. 2011;17 (6):482-487 İnguinal defekt bkz. 2011;17 (3):273-276 İnkarsere intestinal fıtık bkz. 2011;17 (4):344-8 Kolostomi bkz. 2011;17 (5):401-406 Komplikasyon bkz. 2011;17 (3):220-224 İnterlökin-6 Komplikasyon oranları bkz. 2011;17 (4):298-302 bkz. 2011;17 (5):450-454 bkz. 2011;17 (5):390-395 Komplikasyonlar bkz. 2011;17 (4):349-353 İnterlökin-1β bkz. 2011;17 (4):298-302 Konservatif tedavi bkz. 2011;17 (1):57-60 İnternal karotid arter Kortizol bkz. 2011;17 (5):390-395 bkz. 2011;17 (4):371-373 İntestinal tıkanıklık bkz. 2011;17 (6):567-570 Köpek kedi ısırıkları bkz. 2011;17 (2):133-140 İran bkz. 2011;17 (1):61-65 Kraniyal epidural hematom İskemi bkz. 2011;17 (3):283-285 bkz. 2011;17 (1):1-8 Kraniyoserebral delici yaralanma bkz. 2011;17 (6):482-487 bkz. 2011;17 (1):79-82 İskemi reperfüzyon bkz. 2011;17 (2):97-102 Künt abdominal travma İskemik flep bkz. 2011;17 (2):97-102 bkz. 2011;17 (3):215-219 İyatrojenik bkz. 2011;17 (4):359-362 Künt göğüs travması bkz. 2011;17 (1):87-89 Künt toraks travması adınlar bkz. 2011;17 (5):445-449 bkz. 2011;17 (3):269-272 Kafa tabanı Künt travma bkz. 2011;17 (2):149-151 bkz. 2011;17 (4):363-364 bkz. 2011;17 (2):149-151 bkz. 2011;17 (6):493-496 Kafa travması Kurşun yaralanması bkz. 2011;17 (5):455-457 bkz. 2011;17 (1):46-50 bkz. 2011;17 (2):149-151 aparoskopi bkz. 2011;17 (3):267-268 bkz. 2011;17 (2):166-172 Laparotomi bkz. 2011;17 (3):215-219 Kafatası kırığı Leptin bkz. 2011;17 (4):298-302 bkz. 2011;17 (2):149-151 bkz. 2011;17 (3):283-285 Lidokain bkz. 2011;17 (6):497-503
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K
L
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Lintula skoru bkz. 2011;17 (5):396-400 Lisfranc yaralanmaları bkz. 2011;17 (6):504-508 Losartan bkz. 2011;17 (2):97-102 LPG bkz. 2011;17 (6):561-562
Malondialdehid
bkz. 2011;17 (4):293-297 bkz. 2011;17 (1):14-18 bkz. 2011;17 (1):1-8 Meckel divertikülü bkz. 2011;17 (6):567-570 Mediasten bkz. 2011;17 (4):368-370 Mediastinal amfizem bkz. 2011;17 (4):368-370 Mesane bkz. 2011;17 (4):365-367 bkz. 2011;17 (5):455-457 Metilen mavisi bkz. 2011;17 (3):205-209 Mide tutulumu bkz. 2011;17 (1):90-92 Minör kafa travması bkz. 2011;17 (2):186-188 Miyeloperoksidaz bkz. 2011;17 (1):1-8 Mor granül bkz. 2011;17 (2):128-132 Morbidite bkz. 2011;17 (3):220-224 2011;17 (4):344-348 bkz. 2011;17 (5):440-444 Mortalite bkz. 2011;17 (1):46-50 bkz. 2011;17 (1):61-65 bkz. 2011;17 (4):329-333 bkz. 2011;17 (4):344-348 bkz. 2011;17 (5):440-444
N-asetilsistein bkz. 2011;17 (4):293-297
NAG bkz. 2011;17 (6):475-481 Negatif apendektomi bkz. 2011;17 (1):19-22 Nekrotizan fasiit bkz. 2011;17 (1):29-32 Nitrogliserin bkz. 2011;17 (6):497-503 Non-operatif tedavi bkz. 2011;17 (3):238-242
Obturator herni bkz. 2011;17 (3):277-279
Oksidatif stres bkz. 2011;17 (1):1-8 Omental torsiyon bkz. 2011;17 (6):554-556 Omurga sabitleme bkz. 2011;17 (2):103-107 Omurilik yaralanması bkz. 2011;17 (6):533-538 Orbita implantları bkz. 2011;17 (6):545-553 Orbita kırıkları bkz. 2011;17 (6):545-553 Orbital amfizem bkz. 2011;17 (6):570-572 Orbital travma bkz. 2011;17 (6):570-572 Otopsi bkz. 2011;17 (4):340-343
Özofagus perforasyonu
bkz. 2011;17 (6):516-520
Pediyatrik hasta bkz. 2011;17 (2):186-188
Pediyatrik travma bkz. 2011;17 (3):243-247 Pelvis kırıkları bkz. 2011;17 (3):261-266 Penetran kalp yaralanması bkz. 2011;17 (3):225-230
Kasım - November 2011
Ulusal Travma ve Acil Cerrahi Dergisi 2011 yılı 17. cilt konu ve yazar dizini Penetran karın travma indeksi bkz. 2011;17 (5):450-454 Penetran pelvis travması bkz. 2011;17 (5):455-457 Penetran yaralanma bkz. 2011;17 (5):413-418 Penis kırık bkz. 2011;17 (1):57-60 Penis protezi bkz. 2011;17 (5):464-466 Penis travması bkz. 2011;17 (5):464-466 Pentoksifilin bkz. 2011;17 (6):482-487 Perforasyon bkz. 2011;17 (1):66-74 Perforasyon bkz. 2011;17 (1):93-95 Periferik sinir yaralanması bkz. 2011;17 (6):539-544 Perine yanıkları bkz. 2011;17 (2):123-127 Periton kapsülleme bkz. 2011;17 (6):557-560 Peritonit bkz. 2011;17 (3):205-209 bkz. 2011;17 (4):365-367 bkz. 2011;17 (5):390-395 Perkütan tedavi bkz. 2011;17 (3):261-266 Pipkin bkz. 2011;17 (1):51-56 Plak ve vida bkz. 2011;17 (2):159-165 Planlı repalarotomi bkz. 2011;17 (5):390-395 Plastik cerrahi bkz. 2011;17 (1):33-40 Pnömobili bkz. 2011;17 (4):363-364 Pnömomediastinum bkz. 2011;17 (1):93-95 Pnömotoraks bkz. 2011;17 (3):280-282 Primer onarım bkz. 2011;17 (6):516-520 Prognostik faktörler bkz. 2011;17 (4):329-333 Prognoz bkz. 2011;17 (4):334-339 Prokalsitonin bkz. 2011;17 (3):193-198 Proksimal falanks bkz. 2011;17 (3):253-260 Pseudomonas aeruginosa bkz. 2011;17 (4):323-328 Psödomeningosel bkz. 2011;17 (2):189-191
Rektal bkz. 2011;17 (2):173-176
Rektal kanama bkz. 2011;17 (1):83-86 Rektal onarım bkz. 2011;17 (5):401-406 Rektal yaralanma bkz. 2011;17 (5):401-406 Rektus abdominis kas flebi bkz. 2011;17 (3):273-276 Rektus kılıfı hematomu bkz. 2011;17 (3):210-214 Reperfüzyon bkz. 2011;17 (1):1-8 Reperfüzyon hasarı bkz. 2011;17 (2):97-102 Replantasyon bkz. 2011;17 (2):177-179 Retinal arter bkz. 2011;17 (1):75-78 Retroperitoneal bkz. 2011;17 (2):183-185 Risk faktörü bkz. 2011;17 (1):61-65
Safra taşı ileusu bkz. 2011;17 (5):461-463 Sağlık personeli bkz. 2011;17 (5):430-434 Sarsılmış bebek sendromu bkz. 2011;17 (5):430-434 Sepsis bkz. 2011;17 (4):293-297 Serbest oksijen radikalleri bkz. 2011;17 (5):383-389 Serebral iskemi bkz. 2011;17 (2):186-188 Serulein bkz. 2011;17 (5):383-389
Cilt - Vol. 17 Sayı - No. 6
Sigmoid divertikülü bkz. 2011;17 (1):93-95 Sinir kökleri tuzaklanması bkz. 2011;17 (2):189-191 Sitokinler bkz. 2011;17 (5):383-389 Siyatik herni bkz. 2011;17 (3):277-279 Skalp bkz. 2011;17 (2):177-179 Sol taraf bkz. 2011;17 (5):467-469 Solid organ yaralanması bkz. 2011;17 (3):215-219 Soliter bkz. 2011;17 (2):173-176 Spinal kanal bkz. 2011;17 (2):141-148 Spinal kırık bkz. 2011;17 (2):141-148 Spinal kord yaralanması bkz. 2011;17 (1):14-18 Splenektomi bkz. 2011;17 (3):238-242 Splenik travma bkz. 2011;17 (3):238-242 Spondilolistezis bkz. 2011;17 (5):458-460 Spontan pnömomediastinum bkz. 2011;17 (4):368-370 Strongyloides stercoralis bkz. 2011;17 (1):90-92 Sülük bkz. 2011;17 (1):83-86 Süperoksit dismutaz bkz. 2011;17 (1):14-18 Süt yanığı bkz. 2011;17 (5):419-422
Tandır yanığı bkz. 2011;17 (4):323-328
Tecrübe bkz. 2011;17 (3):225-230 Tedavi bkz. 2011;17 (1):66-74 Tedavi seçenekleri bkz. 2011;17 (1):79-82 Tedavi/sonucu bkz. 2011;17 (2):141-148 Tıkanma sarılığı bkz.2011;17 (4):303-307 Toksik granülasyon bkz. 2011;17 (2):128-132 Topikal hemostaz bkz. 2011;17 (4):308-312 Toplam vücut yüzey alanı bkz. 2011;17 (1):61-65 Toplum sağlığı bkz. 2011;17 (2):133-140 Toraks travması bkz. 2011;17 (4):329-333 Trafik kazaları bkz. 2011;17 (4):318-322 Trafik kazası bkz. 2011;17 (3):243-247 Trakeobronşial yaralanma bkz. 2011;17 (1):41-45 Travma bkz. 2011;17 (1):41-45 bkz. 2011;17 (1):93-95 bkz. 2011;17 (3):231-237 bkz. 2011;17 (4):340-343 bkz. 2011;17 (6):475-481 bkz. 2011;17 (6):563-566 Travma cerrahisi bkz. 2011;17 (1):33-40 Travma hastaları bkz. 2011;17 (6):497-503 Travma skoru bkz. 2011;17 (4):329-333 bkz. 2011;17 (6):521-524 Travma sonrası bkz. 2011;17 (5):435-439 Travma tahtası bkz. 2011;17 (2):103-107 Travma yeleği bkz. 2011;17 (2):103-107 Travmatik beyin hasarı bkz. 2011;17 (4):298-302 Travmatik beyin hasarı bkz. 2011;17 (6):509-515
Travmatik diyafram yaralanması bkz. 2011;17 (5):435-439 Travmatik pulmoner psödokist bkz. 2011;17 (3):269-272 Tren kazası bkz. 2011;17 (5):440-444 Triküspit kapak yetersizliği bkz. 2011;17 (6):563-566 TRISS yöntemi bkz. 2011;17 (4):329-333 Turnike ağrısı bkz. 2011;17 (6):497-503 Tüberküloz bkz. 2011;17 (1):66-74 Tümör nekroz faktör-α bkz. 2011;17 (4):293-297 bkz. 2011;17 (4):298-302 Türkiye bkz. 2011;17 (3):231-237 bkz. 2011;17 (3):248-252 bkz. 2011;17 (4):334-339
Ultrasonografi
bkz. 2011;17 (1):19-22 bkz. 2011;17 (2):113-116 bkz. 2011;17 (3):248-252
Ülser bkz. 2011;17 (2):173-176 Varfarin bkz. 2011;17 (3):199-204
Vasküler anomali bkz. 2011;17 (3):280-282 Vasküler cerrahi girişimler bkz. 2011;17 (2):152-158 Vasküler yaralanma bkz. 2011;17 (3):273-276 Vertebra bkz. 2011;17 (2):141-148 Vertebral arter bkz. 2011;17 (1):75-78 Vinpocetin bkz. 2011;17 (6):482-487 Vscan bkz. 2011;17 (6):488-492
Yabancı cisim aspirasyonu
bkz. 2011;17 (4):359-362 Yabancı cisim bkz. 2011;17 (3):286-288 bkz. 2011;17 (5):470-472 Yanık bkz. 2011;17 (1):61-65 bkz. 2011;17 (2):128-132 bkz. 2011;17 (3):220-224 bkz. 2011;17 (4):323-328 bkz. 2011;17 (6):561-562 Yara bkz. 2011;17 (2):133-140 Yaralanma bkz. 2011;17 (4):313-317 Yaşlı bkz. 2011;17 (5):396-400 bkz. 2011;17 (5):413-418 Yoğun bakım bkz. 2011;17 (6):521-524 Yüksek voltaj bkz. 2011;17 (4):349-353
575
Ulus Travma Acil Cerrahi Derg
ULUSAL TRAVMA VE ACİL CERRAHİ DERGİSİ 2011 YILI 17. CİLT YAZAR DİZİNİ A Samir H bkz. 2011;17 (3):267-268 Acar HA bkz. 2011;17 (2):123-127 Acar K bkz. 2011;17 (1):23-28 Acar YA bkz. 2011;17 (3):248-252 Acaroğlu RE bkz. 2011;17 (3):261-266 Açıkgöz M bkz. 2011;17 (4):371-373 Acıman E bkz. 2011;17 (4):371-373 Aggarwal G bkz. 2011;17 (4):374-376 Ağalar C bkz. 2011;17 (5):390-395 Ağalar F bkz. 2011;17 (5):390-395 Ahmad M bkz. 2011;17 (3):277-279 Akan A bkz. 2011;17 (3):225-230 Akarsu C bkz. 2011;17 (4):308-312 Akataş C bkz. 2011;17 (2):103-107 Akçora B bkz. 2011;17 (4):365-367 Akdemir O bkz. 2011;17 (4):298-302 Akgün E bkz. 2011;17 (6):557-560 Akıncı E bkz. 2011;17 (6):488-492 Akkaş M bkz. 2011;17 (5):440-444 Akkaya S bkz. 2011;17 (5):445-449 Akköse Ş A bkz. 2011;17 (4):329-333 Akoğlu H bkz. 2011;17 (2):113-116 Akova A bkz. 2011;17 (6):521-524 Akpınar F bkz. 2011;17 (5):430-434 Akpolat N bkz. 2011;17 (6):475-481 Aksakal N bkz. 2011;17 (2):123-127 Aksöyek A bkz. 2011;17 (6):563-566 Al B bkz. 2011;17 (1):83-86 Al-Bashir M bkz. 2011;17 (3):267-268 Alaca R bkz. 2011;17 (6):533-538 Alavi SA bkz. 2011;17 (2):108-112 Albayrak A bkz. 2011;17 (4):323-328 Albayrak Y bkz. 2011;17 (4):323-328 Aldemir M bkz. 2011;17 (1):83-86 Alıcı Ö bkz. 2011;17 (1):14-18 Alimoğlu O bkz. 2011;17 (5):435-439 Alkan Ö bkz. 2011;17 (5):461-463 Alptekin M bkz. 2011;17 (1):79-82 Altay M bkz. 2011;17 (2):141-148 Altay MA bkz. 2011;17 (5):407-412 Altınkaya N bkz. 2011;17 (5):461-463 Altınlı E bkz. 2011;17 (5):377-382 Altınlı E bkz. 2011;17 (6):482-487 Altıntaş L bkz. 2011;17 (4):334-339 Altıntaş Ö bkz. 2011;17 (4):334-339 Ansaloni L bkz. 2011;17 (1):66-74 Ansaloni L bkz. 2011;17 (4):354-358 Arat A bkz. 2011;17 (1):75-78 Aren A bkz. 2011;17 (1):19-22 Arıtürk E bkz. 2011;17 (2):173-176 Arkaya S bkz. 2011;17 (1):1-8 Arslan E bkz. 2011;17 (6):516-520 Arzıman İ bkz. 2011;17 (3):248-252 Aslan G bkz. 2011;17 (6):545-553 Asrar S bkz. 2011;17 (3):277-279 Atak İ bkz. 2011;17 (5):455-457
576
Atik E bkz. 2011;17 (4):365-367 Atilla K bkz. 2011;17 (3):286-288 Attri AK bkz. 2011;17 (6):493-496 Ay D bkz. 2011;17 (2):103-107 Ay D bkz. 2011;17 (5):440-444 Ayan M bkz. 2011;17 (4):293-297 Aydemir B bkz. 2011;17 (1):41-45 Aydın S D bkz. 2011;17 (4):340-343 Aydın H bkz. 2011;17 (2):152-158 Aydın MS bkz. 2011;17 (5):458-460 Aydın MT bkz. 2011;17 (3):225-230 Aydınlı B bkz. 2011;17 (1):90-92 Aydınuraz K bkz. 2011;17 (5):390-395 Aylu B bkz. 2011;17 (4):323-328 Aytaç E bkz. 2011;17 (1):9-13 Ayvaz M bkz. 2011;17 (3):261-266 Bacovnik UJ bkz. 2011;17 (6):509-515 Balcı E bkz. 2011;17 (5):430-434 Balcı Y bkz. 2011;17 (2):133-140 Balkanay M bkz. 2011;17 (6):525-532 Bardak Y bkz. 2011;17 (5):413-418 Barış S bkz. 2011;17 (2):173-176 Barlas İS bkz. 2011;17 (2):123-127 Barut AY bkz. 2011;17 (1):19-22 Baş G bkz. 2011;17 (5):435-439 Baş L bkz. 2011;17 (1):33-40 Başaran K bkz. 2011;17 (2):177-179 Baykan H bkz. 2011;17 (2):128-132 Bayraktar B bkz. 2011;17 (4):313-317 Bayraktar O bkz. 2011;17 (1):9-13 Baysungur V bkz. 2011;17 (3):280-282 Baysungur V bkz. 2011;17 (4):368-370 Bayyurt S bkz. 2011;17 (2):159-165 Belli S bkz. 2011;17 (4):344-348 Belli S bkz. 2011;17 (5):461-463 Biçer A bkz. 2011;17 (3):273-276 Bilgen MS bkz. 2011;17 (2):159-165 Bircan K bkz. 2011;17 (1):57-60 Birincioğlu İ bkz. 2011;17 (1):87-89 Birincioğlu İ bkz. 2011;17 (5):470-472 Boddouhi N bkz. 2011;17 (1):61-65 Bora S bkz. 2011;17 (3):286-288 Boraie M bkz. 2011;17 (2):183-185 Borucu İ bkz. 2011;17 (1):1-8 Bostancı U bkz. 2011;17 (1):46-50 Bostancı U bkz. 2011;17 (2):166-172 Bozgeyik M bkz. 2011;17 (3):231-237 Bozkurt M bkz. 2011;17 (2):128-132 Bozkurt M bkz. 2011;17 (3):220-224 Böyük A bkz. 2011;17 (5):401-406 Bu-Ali O bkz. 2011;17 (3):267-268 Bulut M bkz. 2011;17 (4):329-333 Bulut NE bkz. 2011;17 (5):383-389 Bulutoğlu R bkz. 2011;17 (6):545-553 Büyükaşık O bkz.2011;17 (4):303-307
Büyükkoçak U bkz. 2011;17 (5):390-395 Das K bkz. 2011;17 (6):521-524 Büyüktuna SA bkz. 2011;17 (1):29-32 Demir Ş bkz. 2011;17 (5):461-463 Demirhan R bkz. 2011;17 (5):423-429 C Misra M bkz. 2011;17 (3):238-242 Demirkol AH bkz. 2011;17 (5):458-460 Can M bkz. 2011;17 (1):87-89 Dianat S bkz. 2011;17 (1):61-65 Can M bkz. 2011;17 (5):470-472 Diaz O bkz. 2011;17 (1):75-78 Canbaz H bkz. 2011;17 (3):210-214 Dinç C bkz. 2011;17 (4):313-317 Canbaz Y bkz. 2011;17 (4):349-353 Dirlik M bkz. 2011;17 (3):210-214 Cander B bkz. 2011;17 (3):193-198 Dirlik M bkz. 2011;17 (4):340-343 Cander B bkz. 2011;17 (4):293-297 Doğusoy I bkz. 2011;17 (1):41-45 Catena F bkz. 2011;17 (1):66-74 Dokur M bkz. 2011;17 (1):79-82 Catena F bkz. 2011;17 (4):354-358 Dokur M bkz. 2011;17 (3):248-252 Cavit IY bkz. 2011;17 (4):318-322 Dolgun H bkz. 2011;17 (3):283-285 Cece H bkz. 2011;17 (4):363-364 Dom S bkz. 2011;17 (5):390-395 Ceyhan MA bkz. 2011;17 (6):488-492 Dölalan Ş bkz. 2011;17 (6):554-556 Chen K-T bkz. 2011;17 (3):215-219 Dulundu E bkz. 2011;17 (5):383-389 Cingöz G bkz. 2011;17 (4):340-343 Durak K bkz. 2011;17 (2):159-165 Coccolini F bkz. 2011;17 (1):66-74 Dural K bkz. 2011;17 (2):152-158 Coccollini F bkz. 2011;17 (4):354-358 Dursun N bkz. 2011;17 (1):19-22 Coşkun F bkz. 2011;17 (6):488-492 Dündür ZD bkz. 2011;17 (3):193-198 Düzci U bkz. 2011;17 (2):123-127 Çağlar Ö bkz. 2011;17 (3):261-266 Çağlar Y bkz. 2011;17 (4):334-339 Edirne Y bkz. 2011;17 (5):470-472 Çağlayan O bkz. 2011;17 (5):390-395 Ekem S bkz. 2011;17 (4):371-373 Çağman B bkz. 2011;17 (5):407-412 Ekinci O bkz. 2011;17 (5):383-389 Çakır C bkz. 2011;17 (4):323-328 Elbeyli L bkz. 2011;17 (6):516-520 Çal MA bkz. 2011;17 (4):298-302 Elçioğlu Ö bkz. 2011;17 (2):133-140 Çalışkan C bkz. 2011;17 (6):557-560 Elkan H bkz. 2011;17 (6):554-556 Çalışkan K bkz. 2011;17 (4):344-348 Emekli U bkz. 2011;17 (2):177-179 Çalışkan M bkz. 2011;17 (5):455-457 Emircan Ş bkz. 2011;17 (4):329-333 Çam Etez B bkz. 2011;17 (3):199-204 Eraslan E bkz. 2011;17 (5):413-418 Çardak Ç bkz. 2011;17 (3):280-282 Erayman İ bkz. 2011;17 (4):293-297 Çaylak H bkz. 2011;17 (3):269-272 Erbil Y bkz. 2011;17 (1):1-8 Çelebi F bkz. 2011;17 (1):90-92 Ercan F bkz. 2011;17 (5):383-389 Çelebi NU bkz. 2011;17 (6):545-553 Erçin U bkz. 2011;17 (3):205-209 Çelik A bkz. 2011;17 (5):377-382 Erdem S bkz. 2011;17 (4):293-297 Çetin A bkz. 2011;17 (2):103-107 Erdenöz S bkz. 2011;17 (6):570-572 Çetin A bkz. 2011;17 (5):467-469 Erel Ö bkz. 2011;17 (4):340-343 Çınar N bkz. 2011;17 (4):298-302 Erenler İ bkz. 2011;17 (1):9-13 Çınar O bkz. 2011;17 (3):248-252 Ergün BR bkz. 2011;17 (3):283-285 Çoban S bkz. 2011;17 (4):363-364 Ergüngör MF bkz. 2011;17 (2):189-191 Çobanoğlu A bkz. 2011;17 (6):563-566 Erkol H bkz. 2011;17 (3):231-237 Çobanoğlu U bkz. 2011;17 (2):117-122 Erkol H bkz.2011;17 (4):303-307 Çobanoğlu U bkz. 2011;17 (5):470-472 Erkutlu İ bkz. 2011;17 (1):79-82 Çoker A bkz. 2011;17 (2):180-182 Eroğlu E bkz. 2011;17 (5):377-382 Çolak A bkz. 2011;17 (4):298-302 Eroğlu E bkz. 2011;17 (6):482-487 Çolak T bkz. 2011;17 (3):210-214 Eroğlu HE bkz. 2011;17 (3):205-209 Çolakoğlu T bkz. 2011;17 (4):344-348 Ersin S bkz. 2011;17 (2):180-182 Çopuroğlu C bkz. 2011;17 (1):51-56 Ersin SM bkz. 2011;17 (6):557-560 Ertürk C bkz. 2011;17 (5):407-412 Dağ A bkz. 2011;17 (3):210-214 Ertürk S bkz. 2011;17 (1):9-13 Dalal A bkz. 2011;17 (6):493-496 Eryılmaz M bkz. 2011;17 (5):450-454 Dalal U bkz. 2011;17 (6):493-496 Eryılmaz R bkz. 2011;17 (5):435-439 Dalgıç A bkz. 2011;17 (2):189-191 Eslami V bkz. 2011;17 (1):61-65 Daphan Ç bkz. 2011;17 (5):390-395 Eslami V bkz. 2011;17 (6):539-544 Dar TI bkz. 2011;17 (3):277-279 Evin A bkz. 2011;17 (4):313-317
Kasım - November 2011
Ulusal Travma ve Acil Cerrahi Dergisi 2011 yılı 17. cilt konu ve yazar dizini Evren İ bkz. 2011;17 (5):455-457 Ezer A bkz. 2011;17 (4):344-348 Fatemy A bkz. 2011;17 (6):497-503 Fedakar A bkz. 2011;17 (6):525-532 Fındık O bkz. 2011;17 (6):525-532 Fırat Ö bkz. 2011;17 (6):557-560 Foo N-P bkz. 2011;17 (3):215-219 Gazzotti F bkz. 2011;17 (4):354-358 Gedik A bkz. 2011;17 (1):57-60 Gedik E bkz. 2011;17 (3):220-224 Genç O bkz. 2011;17 (3):269-272 Geyik M bkz. 2011;17 (1):79-82 Gezen C bkz. 2011;17 (2):123-127 Gezici AR bkz. 2011;17 (2):189-191 Girgin S bkz. 2011;17 (5):401-406 Girişgin S bkz. 2011;17 (4):293-297 Gler S bkz. 2011;17 (3):286-288 Gourgiotis S bkz. 2011;17 (4):289-292 Gök A bkz. 2011;17 (1):79-82 Gökcan R bkz. 2011;17 (5):455-457 Gökçe AH bkz. 2011;17 (1):19-22 Gökçe FS bkz. 2011;17 (1):19-22 Gökçek B bkz. 2011;17 (4):308-312 Göktepe AS bkz. 2011;17 (6):533-538 Gökyar A bkz. 2011;17 (1):46-50 Gökyar A bkz. 2011;17 (2):166-172 Gönüllü H bkz. 2011;17 (4):349-353 Göz M bkz. 2011;17 (5):458-460 Guo H-R bkz. 2011;17 (3):215-219 Gupta A bkz. 2011;17 (3):238-242 Gupta S bkz. 2011;17 (6):493-496 Gül M bkz. 2011;17 (3):193-198 Gül M bkz. 2011;17 (4):293-297 Gül S bkz. 2011;17 (4):371-373 Gülay H bkz. 2011;17 (3):286-288 Gülgösteren M bkz. 2011;17 (4):359-362 Gümrükçü G bkz. 2011;17 (5):377-382 Gümüş M bkz. 2011;17 (5):401-406 Gün İ bkz. 2011;17 (5):430-434 Günalp M bkz. 2011;17 (5):440-444 Günay MC bkz. 2011;17 (2):141-148 Günay O bkz. 2011;17 (5):430-434 Gündüz T bkz. 2011;17 (2):133-140 Güneş P bkz. 2011;17 (6):482-487 Gürbüz N bkz. 2011;17 (3):231-237 Gürsan N bkz. 2011;17 (1):90-92 Güven E bkz. 2011;17 (2):177-179 Güvendik Gİ bkz. 2011;17 (3):261-266 Güzey D bkz. 2011;17 (5):435-439
Işık AF bkz. 2011;17 (6):516-520 Işık D bkz. 2011;17 (4):349-353 Işık HS bkz. 2011;17 (1):46-50 Işık HS bkz. 2011;17 (2):166-172 Işıkan UE bkz. 2011;17 (5):407-412 İçöz G bkz. 2011;17 (2):180-182 İhtiyar E bkz. 2011;17 (1):93-95 İlktaç A bkz. 2011;17 (5):464-466 İmamoğlu OU bkz. 2011;17 (1):41-45 İşbil N B bkz. 2011;17 (3):199-204 Jasharllari L bkz. 2011;17 (6):561-562 Jawas A bkz. 2011;17 (2):183-185 Jen C-C bkz. 2011;17 (3):215-219
Kabak İ bkz. 2011;17 (5):455-457 Kabalak AA bkz. 2011;17 (5):419-422 Kaçağan F bkz. 2011;17 (3):253-260 Kahramansoy N bkz. 2011;17 (3):231-7 Kahramansoy N bkz.2011;17 (4):303-7 Kalaycı MU bkz. 2011;17 (3):205-209 Kalaycı MU bkz. 2011;17 (4):308-312 Kalender M bkz. 2011;17 (6):525-532 Kalkan S bkz. 2011;17 (5):464-466 Kamalı S bkz. 2011;17 (3):225-230 Kapan M bkz. 2011;17 (5):401-406 Kapı E bkz. 2011;17 (3):220-224 Kapı E bkz. 2011;17 (2):128-132 Kara E bkz. 2011;17 (2):180-182 Kara PH bkz. 2011;17 (2):113-116 Karabağ H bkz. 2011;17 (5):458-460 Karabulut K bkz. 2011;17 (3):193-198 Karaca CA bkz. 2011;17 (6):557-560 Karaca K bkz. 2011;17 (3):210-214 Karadaş S bkz. 2011;17 (4):349-353 Karagöz Avcı S bkz. 2011;17 (1):9-13 Karakoç D bkz. 2011;17 (5):396-400 Karakol P bkz. 2011;17 (2):128-132 Karaman Mİ bkz. 2011;17 (5):464-466 Karaoğlan A bkz. 2011;17 (4):298-302 Karatepe O bkz. 2011;17 (3):225-230 Karcıoğlu Ö bkz. 2011;17 (5):445-449 Kavaklı HŞ bkz. 2011;17 (6):488-492 Kavaklı K bkz. 2011;17 (3):269-272 Kaya C bkz. 2011;17 (5):464-466 Kayan D bkz. 2011;17 (1):57-60 Kayapınar M bkz. 2011;17 (6):561-562 Kayayurt K bkz. 2011;17 (2):113-116 Kaynaroğlu V bkz. 2011;17 (5):396-400 Kazez A bkz. 2011;17 (6):475-481 Kebabçı M bkz. 2011;17 (1):93-95 Hacıkerim SK bkz. 2011;17 (1):33-40 Keklik B bkz. 2011;17 (2):177-179 Halezeroğlu S bkz. 2011;17 (3):280-282 Kelten B bkz. 2011;17 (4):298-302 Halezeroğlu S bkz. 2011;17 (4):368-370 Kement M bkz. 2011;17 (2):123-127 Hamzaoğlu O bkz. 2011;17 (4):318-322 Kersnik J bkz. 2011;17 (6):509-515 Hanbeyoğlu A bkz. 2011;17 (6):475-481 Kertmen H bkz. 2011;17 (3):283-285 Harirchi I bkz. 2011;17 (1):61-65 Kılıç TY bkz. 2011;17 (2):113-116 Hayran M bkz. 2011;17 (5):396-400 Kılıç YA bkz. 2011;17 (5):396-400 Hepgül G bkz. 2011;17 (1):1-8 Kıyan A bkz. 2011;17 (3):231-237 Honarmand A bkz. 2011;17 (6):497-503 Kıyançiçek S bkz. 2011;17 (2):113-116 Klemenc ZK bkz. 2011;17 (6):509-515
Cilt - Vol. 17 Sayı - No. 6
Klucznik R bkz. 2011;17 (1):75-78 Koç O bkz. 2011;17 (5):419-422 Koç Z bkz. 2011;17 (5):461-463 Koca C bkz. 2011;17 (1):14-18 Koca O bkz. 2011;17 (5):464-466 Koca YS bkz. 2011;17 (3):205-209 Konan A bkz. 2011;17 (5):396-400 Kordon Ö bkz.2011;17 (4):303-307 Köksal N bkz. 2011;17 (5):377-382 Köksal N bkz. 2011;17 (6):482-487 Köksal Ö bkz. 2011;17 (3):199-204 Köksal Ö bkz. 2011;17 (4):329-333 Kösenli O bkz. 2011;17 (6):521-524 Köseoğlu E bkz. 2011;17 (2):159-165 Köseoğlu Z bkz. 2011;17 (6):521-524 Kubilay D bkz. 2011;17 (3):205-209 Kumar S bkz. 2011;17 (3):238-242 Kuo W-Y bkz. 2011;17 (3):215-219 Kurban S bkz. 2011;17 (3):193-198 Kurt F bkz. 2011;17 (3):231-237 Kuvat SV bkz. 2011;17 (2):128-132 Kuvat SV bkz. 2011;17 (3):220-224 Kuvat SV bkz. 2011;17 (3):273-276 Kuvvetli A bkz. 2011;17 (6):521-524 Küçükalp A bkz. 2011;17 (2):159-165
Öncel M bkz. 2011;17 (2):123-127 Öncü MR bkz. 2011;17 (4):349-353 Önder A bkz. 2011;17 (5):401-406 Önel S bkz. 2011;17 (6):521-524 Örnek F bkz. 2011;17 (5):413-418 Öz K bkz. 2011;17 (5):423-429 Özalp B bkz. 2011;17 (3):273-276 Özcan M bkz. 2011;17 (1):51-56 Özcan T bkz. 2011;17 (3):210-214 Özçelik D bkz. 2011;17 (3):253-260 Özdemir C bkz. 2011;17 (1):46-50 Özdemir C bkz. 2011;17 (2):166-172 Özdemir F bkz. 2011;17 (3):199-204 Özdemir F bkz. 2011;17 (4):329-333 Özdenkaya Y bkz. 2011;17 (4):308-312 Özdoğan ES bkz. 2011;17 (2):103-107 Özdoğan M bkz. 2011;17 (6):521-524 Özel A bkz. 2011;17 (2):128-132 Özen B bkz. 2011;17 (4):371-373 Özen M bkz. 2011;17 (1):23-28 Özen M bkz. 2011;17 (3):243-247 Özgüç H bkz. 2011;17 (4):329-333 Özkan Arat Y bkz. 2011;17 (1):75-78 Özkan B bkz. 2011;17 (4):334-339 Özkan E bkz. 2011;17 (5):383-389 Özkan S bkz. 2011;17 (4):359-362 Lazzareschi D bkz. 2011;17 (1):66-74 Özkara S bkz. 2011;17 (4):308-312 Lazzereschi D bkz. 2011;17 (4):354-358 Özkaya D bkz. 2011;17 (5):413-418 Lin H-J bkz. 2011;17 (3):215-219 Özkaya Ö bkz. 2011;17 (1):33-40 Öztürk A bkz. 2011;17 (5):430-434 M. Abu-Zidan F bkz. 2011;17 (2):183-185 Öztürk CN bkz. 2011;17 (2):97-102 M. Abu-Zidan F bkz. 2011;17 (3):267-268 Öztürk G bkz. 2011;17 (1):90-92 Malik AA bkz. 2011;17 (3):277-279 Öztürk Mİ bkz. 2011;17 (5):464-466 Mamoudieh M bkz. 2011;17 (2):108-112 Mathur R bkz. 2011;17 (4):374-376 Pamukcu C bkz. 2011;17 (6):570-572 Melek M bkz. 2011;17 (5):470-472 Parlakgümüş A bkz. 2011;17 (4):344-348 Mergan D bkz. 2011;17 (2):117-122 Parlar Aİ bkz. 2011;17 (6):563-566 Mesci A bkz. 2011;17 (5):450-454 Pehlivanlı F bkz. 2011;17 (5):390-395 Metin Aksu N bkz. 2011;17 (5):440-444 Pekdemir M bkz. 2011;17 (2):186-188 Meyzin İ bkz. 2011;17 (2):177-179 Peker Y bkz. 2011;17 (5):450-454 Mirkheshti N bkz. 2011;17 (2):108-112 Pinha AD bkz. 2011;17 (4):354-358 Mishra B bkz. 2011;17 (3):238-242 Pinna AD bkz. 2011;17 (1):66-74 Miswan MFM bkz. 2011;17 (6):504-508 Pirhan D bkz. 2011;17 (4):334-339 Mordeniz C bkz. 2011;17 (5):458-460 Pirhan Y bkz. 2011;17 (5):467-469 Möhür H bkz. 2011;17 (6):533-538 Puviani L bkz. 2011;17 (1):66-74 Mutlu Şarlı Ş bkz. 2011;17 (5):430-434 Q Parray F bkz. 2011;17 (3):277-279 N Khan R bkz. 2011;17 (3):238-242 Neri F bkz. 2011;17 (4):354-358 R. Rasouli M bkz. 2011;17 (1):61-65 R. Rasouli M bkz. 2011;17 (2):149-151 Oba E bkz. 2011;17 (6):570-572 Rahimi V M bkz. 2011;17 (2):149-151 Ogorevc M bkz. 2011;17 (6):509-515 Rahimi V M bkz. 2011;17 (6):539-544 Okan İ bkz. 2011;17 (5):435-439 Raikwar R bkz. 2011;17 (4):374-376 Okay T bkz. 2011;17 (1):41-45 Rashidi N Rbkz. 2011;17 (2):149-151 Okçu O bkz. 2011;17 (2):152-158 Rather SA bkz. 2011;17 (3):277-279 Okur E bkz. 2011;17 (3):280-282 Okur E bkz. 2011;17 (4):368-370 Saadat S bkz. 2011;17 (2):149-151 Onan B bkz. 2011;17 (5):423-429 Saadat S bkz. 2011;17 (6):539-544 Onan İS bkz. 2011;17 (5):423-429 Saba R bkz. 2011;17 (1):29-32 Onur E bkz. 2011;17 (5):377-382 Safavi M bkz. 2011;17 (6):497-503 Onur E bkz. 2011;17 (6):482-487 Sagar S bkz. 2011;17 (3):238-242 Oruç C bkz. 2011;17 (6):521-524 Sakıncı Ü bkz. 2011;17 (2):152-158
577
Ulus Travma Acil Cerrahi Derg Sancak B bkz. 2011;17 (3):205-209 Sapmaz E bkz. 2011;17 (3):269-272 Sarı A bkz. 2011;17 (3):225-230 Sarıbay R bkz. 2011;17 (3):210-214 Sarıdoğan K bkz. 2011;17 (1):51-56 Sarıkaya S bkz. 2011;17 (2):103-107 Sarısoy HT bkz. 2011;17 (2):186-188 Satsangi B bkz. 2011;17 (4):374-376 Saurabh G bkz. 2011;17 (3):238-242 Savacı N bkz. 2011;17 (6):561-562 Saygun O bkz. 2011;17 (5):390-395 Sayır F bkz. 2011;17 (2):117-122 Sazak H bkz. 2011;17 (4):359-362 Schmidt R bkz. 2011;17 (4):289-292 Seçer M bkz. 2011;17 (2):189-191 Senger S bkz. 2011;17 (5):377-382 Senger S bkz. 2011;17 (6):482-487 Serin E bkz.2011;17 (4):303-307 Serinken M bkz. 2011;17 (1):23-28 Serinken M bkz. 2011;17 (3):243-247 Serinken M bkz. 2011;17 (5):445-449 Seven R bkz. 2011;17 (1):1-8 Seydanoğlu A bkz. 2011;17 (4):293-297 Seyhan N bkz. 2011;17 (6):561-562 Sharma R bkz. 2011;17 (6):493-496 Shukla S bkz. 2011;17 (4):374-376 Sığırlı D bkz. 2011;17 (3):199-204 Singh S G bkz. 2011;17 (6):567-570 Singh O bkz. 2011;17 (6):567-570 Singh VA bkz. 2011;17 (6):504-508 Singhal M bkz. 2011;17 (3):238-242 Smer A bkz. 2011;17 (5):377-382 Soylu A bkz. 2011;17 (3):205-209 Sönmez Y bkz. 2011;17 (5):413-418 Sözen S bkz. 2011;17 (6):554-556 Sümer A bkz. 2011;17 (6):482-487
Tan Başer N bkz. 2011;17 (6):545-553 Tander B bkz. 2011;17 (2):173-176 Tarım A bkz. 2011;17 (4):344-348 Taş H bkz. 2011;17 (5):450-454 Taşçılar N bkz. 2011;17 (4):371-373 Temiz A bkz. 2011;17 (2):173-176 Temiz A bkz. 2011;17 (4):365-367 Temiz M bkz. 2011;17 (2):173-176 Terzi A bkz. 2011;17 (4):363-364 Tezel Ç bkz. 2011;17 (3):280-282 Tezel Ç bkz. 2011;17 (4):368-370 Tezel E bkz. 2011;17 (2):97-102 Tezel O bkz. 2011;17 (3):248-252 Tihan DN bkz. 2011;17 (1):1-8 Tok F bkz. 2011;17 (6):533-538 Topalan M bkz. 2011;17 (3):273-276 Topaloğlu Ü bkz. 2011;17 (5):383-389 Topçuoğlu G bkz. 2011;17 (4):359-362 Toplu G bkz. 2011;17 (3):253-260 Torun MF bkz. 2011;17 (5):458-460 Toy H bkz. 2011;17 (3):193-198 Tök L bkz. 2011;17 (5):413-418 Tuğcu İ bkz. 2011;17 (6):533-538 Tunçer S bkz. 2011;17 (3):273-276 Tunçözgür B bkz. 2011;17 (6):516-520 Turan N bkz. 2011;17 (1):87-89 Turanlı S bkz. 2011;17 (5):467-469 Turhan Ö bkz. 2011;17 (1):29-32 Türkçüer İ bkz. 2011;17 (1):23-28 Türkçüer İ bkz. 2011;17 (5):445-449 Türker HB bkz. 2011;17 (2):141-148 Türkmenoğlu Ö bkz. 2011;17 (3):210-214 Türkoğlu E bkz. 2011;17 (3):283-285 Türkoğlu Ü bkz. 2011;17 (1):1-8 Tütün U bkz. 2011;17 (6):563-566
Şahin Kavaklı H bkz. 2011;17 (1):14-18 Şahiner T bkz. 2011;17 (5):390-395 Şanlı M bkz. 2011;17 (6):516-520 Şavkılıoğlu E bkz. 2011;17 (4):359-362 Şehirli AÖ bkz. 2011;17 (5):383-389 Şekerci Z bkz. 2011;17 (3):283-285 Şenel E bkz. 2011;17 (5):419-422 Şener G bkz. 2011;17 (5):383-389 Şenyuva CTG bkz. 2011;17 (3):253-260
U. Ahmed M bkz. 2011;17 (2):183-185 Uğurlu K bkz. 2011;17 (1):33-40 Uğurluoğlu C bkz. 2011;17 (3):205-209 Ulaş N bkz.2011;17 (4):303-307 Uluşan A bkz. 2011;17 (6):516-520 Uyanık E bkz. 2011;17 (5):445-449 Uzun H bkz. 2011;17 (1):9-13 Uzun H bkz. 2011;17 (4):298-302 Uzunkoy A bkz. 2011;17 (4):363-364 Ustaalioğlu R bkz. 2011;17 (1):41-45
Tabak AY bkz. 2011;17 (2):141-148 Taçyıldız İ bkz. 2011;17 (5):401-406
Ünlüer EE bkz. 2011;17 (2):113-116 Ünveren T bkz. 2011;17 (3):253-260
578
Üstün H bkz. 2011;17 (1):9-13 Üstündağ B bkz. 2011;17 (6):475-481 Vandenberk N bkz. 2011;17 (2):113-116 Vaper P bkz. 2011;17 (4):368-370 Volpi J bkz. 2011;17 (1):75-78 Yağmur F bkz. 2011;17 (5):430-434 Yaka E bkz. 2011;17 (2):186-188 Yalçın AN bkz. 2011;17 (1):29-32 Yalçın Ö bkz. 2011;17 (2):97-102 Yalçın O bkz. 2011;17 (4):308-312 Yalçın Tök Ö bkz. 2011;17 (5):413-418 Yamiş S bkz. 2011;17 (1):57-60 Yanar H bkz. 2011;17 (3):273-276 Yasin NF bkz. 2011;17 (6):504-508 Yastı AÇ bkz. 2011;17 (5):419-422 Yaşar NF bkz. 2011;17 (1):93-95 Yavaşi Ö bkz. 2011;17 (2):113-116 Yavuz E bkz. 2011;17 (4):308-312 Yazıcı Ü bkz. 2011;17 (4):359-362 Yazıcıoğlu K bkz. 2011;17 (6):533-538 Yenen ME bkz. 2011;17 (1):83-86 Yeniay L bkz. 2011;17 (6):557-560 Yeşilyurt S bkz. 2011;17 (2):103-107 Yıldız F bkz. 2011;17 (4):363-364 Yıldız F bkz. 2011;17 (6):554-556 Yıldız Ö bkz. 2011;17 (1):46-50 Yıldız Ö bkz. 2011;17 (2):166-172 Yılmaz B bkz. 2011;17 (6):533-538 Yılmaz C bkz. 2011;17 (2):113-116 Yılmaz ER bkz. 2011;17 (3):283-285 Yılmaz G bkz. 2011;17 (3):261-266 Yılmaz S bkz. 2011;17 (2):186-188 Yılmaz Y bkz. 2011;17 (1):57-60 Yücel O bkz. 2011;17 (3):269-272 Yücesir İ bkz. 2011;17 (4):313-317 Yüceyar S bkz. 2011;17 (1):9-13 Yüksel MU bkz. 2011;17 (5):467-469 Yüksel N bkz. 2011;17 (4):334-339 Yüney E bkz. 2011;17 (3):225-230 Zandieh A bkz. 2011;17 (1):61-65 Zarei M-R bkz. 2011;17 (1):61-65 Zeybek N bkz. 2011;17 (5):450-454 Zilan A bkz. 2011;17 (5):435-439 Ziyade S bkz. 2011;17 (5):435-439
Kasım - November 2011