TJTES 2015 / 4

ISSN 1306 - 696X

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

Volume 21 | Number 4 | July 2015

www.tjtes.org

TURKISH JOURNAL of TRAUMA & EMERGENCY SURGERY Ulusal Travma ve Acil Cerrahi Dergisi Editor-in-Chief Recep Güloğlu Editors Kaya Sarıbeyoğlu (Managing Editor) M. Mahir Özmen Hakan Yanar Former Editors Ömer Türel, Cemalettin Ertekin, Korhan Taviloğlu Section Editors Anaesthesiology & ICU Güniz Meyancı Köksal, Mert Şentürk Cardiac Surgery Münacettin Ceviz, Murat Güvener Neurosurgery Ahmet Deniz Belen, Mehmet Yaşar Kaynar Ophtalmology Cem Mocan, Halil Ateş Ortopedics and Traumatology Mahmut Nedim Doral, Mehmet Can Ünlü Plastic and Reconstructive Surgery Ufuk Emekli, Figen Özgür Pediatric Surgery Aydın Yagmurlu, Ebru Yeşildağ Thoracic Surgery Alper Toker, Akif Turna Urology Ali Atan, Öner Şanlı Vascular Surgery Cüneyt Köksoy, Mehmet Kurtoğlu

www.tjtes.org

THE TURKISH ASSOCIATION OF TRAUMA AND EMERGENCY SURGERY ULUSAL TRAVMA VE ACİL CERRAHİ DERNEĞİ President (Başkan) Vice President (2. Başkan) Secretary General (Genel Sekreter) Treasurer (Sayman) Members (Yönetim Kurulu Üyeleri)

Kaya Sarıbeyoğlu M. Mahir Özmen Hakan Yanar Ali Fuat Kaan Gök Gürhan Çelik Osman Şimşek Orhan Alimoğlu

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

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

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

Tel Fax (Faks)

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

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

Publisher (Yayımcı): KARE Yayıncılık (KARE Publishing) • www.kareyayincilik.com • Design (Tasarım): Ali Cangül • Graphics (Grafikler): Edibe Çomaktekin • Linguistic Editor (İngilizce Editörü): Merve Şenol • Redaction (Redaksiyon): Erman Aytaç • Online Manuscript & Web Management (Online Dergi & Web): LookUs • Press (Baskı): Yıldırım Matbaacılık • Press date (Basım tarihi): July (Temmuz) 2015 • This publication is printed on paper that meets the international standard ISO 9706: 1994 (Bu dergide kullanılan kağıt ISO 9706: 1994 standardına uygundur.)

KARE www.tjtes.org

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

tion, called “Upload Your Files”.

As from 2001, the journal is indexed in Index Medicus and Medline, as from 2005 in Excerpta Medica and EMBASE, as from 2007 in Science Citation Index Expanded (SCI-E) and Journal Citation Reports / Science Edition, and as from 2008 in Index Copernicus. For the five-year term of 2001-2006, our impact factor in SCI-E indexed journals is 0.5.

It is cited as ‘Ulus Travma Acil Cerrahi Derg’ in PUBMED.

Figures, illustrations and tables: All figures and tables should be numbered in the order of appearance in the text. The desired position of figures and tables should be indicated in the text. Legends should be included in the relevant part of the main text and those for photomicrographs and slide preparations should indicate the magnification and the stain used. Color pictures and figures will be published if they are definitely required and with the understanding that the authors are prepared to bear the costs. Line drawings should be professionally prepared. For recognizable photographs, signed releases of the patient or of his/her legal representatives should be enclosed; otherwise, patient names or eyes must be blocked out to prevent identification.

Submission of a manuscript by electronic means implies: that the work has not been published before (except in the form of an abstract or as part of a published lecture, review, or thesis); that it is not under consideration for publication elsewhere; and that its publication in the Turkish Journal of Trauma and Emergency Surgery is approved by all co-authors. The author(s) transfer(s) the copyright to the Turkish Association of Trauma and Emergency Surgery to be effective if and when the manuscript is accepted for publication. The author(s) guarantee(s) that the manuscript will not be published elsewhere in any other language without the consent of the Association. If the manuscript has been presented at a meeting, this should be stated together with the name of the meeting, date, and the place.

Manuscripts may be submitted in Turkish or in English. All submissions are initially reviewed by the editor, and then are sent to reviewers. All manuscripts are subject to editing and, if necessary, will be returned to the authors for answered responses to outstanding questions or for addition of any missing information to be added. For accuracy and clarity, a detailed manuscript editing is undertaken for all manuscripts accepted for publication. Final galley proofs are sent to the authors for approval.

Unless specifically indicated otherwise at the time of submission, rejected manuscripts will not be returned to the authors, including accompanying materials.

TJTES is indexed in Science Citation Index-Expanded (SCI-E), Index Medicus, Medline, EMBASE, Excerpta Medica, and the Turkish Medical Index of TUBITAK-ULAKBIM. Priority of publications is given to original studies; therefore, selection criteria are more refined for reviews and case reports.

Open Access Policy: Full text access is free. There is no charge for publication or downloading the full text of printed material.

Manuscript submission: TJTES accepts only on-line submission via the official web site (please click, www.travma.org.tr/en) and refuses printed manuscript submissions by mail. All submissions are made by the on-line submission system called Journal Agent, by clicking the icon “Online manuscript submission” at the above mentioned web site homepage. The system includes directions at each step but for further information you may visit the web site (http://www.travma.org/en/ journal/).

Manuscript preparation: Manuscripts should have double-line spacing, leaving sufficient margin on both sides. The font size (12 points) and style (Times New Roman) of the main text should be uniformly taken into account. All pages of the main text should be numbered consecutively. Cover letter, manuscript title, author names and institutions and correspondence address, abstract in Turkish (for Turkish authors only), and title and abstract in English are uploaded to the Journal Agent system in the relevant steps. The main text includes Introduction, Materials and Methods, Results, Discussion, Acknowledgments, References, Tables and Figure Legends.

The cover letter must contain a brief statement that the manuscript has been read and approved by all authors, that it has not been submitted to, or is not under consideration for publication in, another journal.

It should contain the names and signatures of all authors. The cover letter is uploaded at the 10th step of the “Submit New Manuscript” sec-

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

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

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

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

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

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

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

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

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

YAZARLARA BİLGİ Ulusal Travma ve Acil Cerrahi Dergisi, Ulusal Travma ve Acil Cerrahi Derneği’nin yayın organıdır. Travma ve acil cerrahi hastalıklar konularında bilimsel birikime katkısı olan klinik ve deneysel çalışmaları, editöryel yazıları, klinik olgu sunumlarını ve bu konulardaki teknik katkılar ile son gelişmeleri yayınlar. Dergi iki ayda bir yayınlanır.

Ulusal Travma ve Acil Cerrahi Dergisi, 2001 yılından itibaren Index Medicus ve Medline’da, 2005 yılından itibaren Excerpta Medica / EMBASE indekslerinde, 2007 yılından itibaren Science Citation Index-Expanded (SCI-E) ile Journal Citation Reports / Science Edition uluslararası indekslerinde ve 2008 yılından itibaren Index Copernicus indeksinde yer almaktadır. 2001-2006 yılları arasındaki 5 yıllık dönemde SCI-E kapsamındaki dergilerdeki İmpakt faktörümüz 0,5 olmuştur. Dergide araştırma yazılarına öncelik verilmekte, bu nedenle derleme veya olgu sunumu türündeki yazılarda seçim ölçütleri daha dar tutulmaktadır. PUBMED’de dergi “Ulus Travma Acil Cerrahi Derg” kısaltması ile yer almaktadır.

Dergiye yazı teslimi, çalışmanın daha önce yayınlanmadığı (özet ya da bir sunu, inceleme, ya da tezin bir parçası şeklinde yayınlanması dışında), başka bir yerde yayınlanmasının düşünülmediği ve Ulusal Travma ve Acil Cerrahi Dergisi’nde yayınlanmasının tüm yazarlar tarafından uygun bulunduğu anlamına gelmektedir. Yazar(lar), çalışmanın yayınlanmasının kabulünden başlayarak, yazıya ait her hakkı Ulusal Travma ve Acil Cerrahi Derneği’ne devretmektedir(ler). Yazar(lar), izin almaksızın çalışmayı başka bir dilde ya da yerde yayınlamayacaklarını kabul eder(ler). Gönderilen yazı daha önce herhangi bir toplantıda sunulmuş ise, toplantı adı, tarihi ve düzenlendiği şehir belirtilmelidir.

Dergide Türkçe ve İngilizce yazılmış makaleler yayınlanabilir. Tüm yazılar önce editör tarafından ön değerlendirmeye alınır; daha sonra incelenmesi için danışma kurulu üyelerine gönderilir.

Tüm yazılarda editöryel değerlendirme ve düzeltmeye başvurulur; gerektiğinde, yazarlardan bazı soruları yanıtlanması ve eksikleri tamamlanması istenebilir. Dergide yayınlanmasına karar verilen yazılar “manuscript editing” sürecine alınır; bu aşamada tüm bilgilerin doğruluğu için ayrıntılı kontrol ve denetimden geçirilir; yayın öncesi şekline getirilerek yazarların kontrolüne ve onayına sunulur. Editörün, kabul edilmeyen yazıların bütününü ya da bir bölümünü (tablo, resim, vs.) iade etme zorunluluğu yoktur.

Açık Erişim İlkesi: Tam metinlere erişim ücretsizdir. Yayınlanan basılı materyali tam metni indirmek için herhangi bir ücret alınmaz.

Yazıların hazırlanması: Tüm yazılı metinler 12 punto büyüklükte “Times New Roman” yazı karakterinde iki satır aralıklı olarak yazılmalıdır. Sayfada her iki tarafta uygun miktarda boşluk bırakılmalı ve ana metindeki sayfalar numaralandırılmalıdır. Journal Agent sisteminde, başvuru mektubu, başlık, yazarlar ve kurumları, iletişim adresi, Türkçe özet ve yazının İngilizce başlığı ve özeti ilgili aşamalarda yüklenecektir. İngilizce yazılan çalışmalara da Türkçe özet eklenmesi gerekmektedir. Yazının ana metnindeyse şu sıra kullanılacaktır: Giriş, Gereç ve Yöntem, Bulgular, Tartışma, Teşekkür, Kaynaklar, Tablolar ve Şekiller.

Başvuru mektubu: Bu mektupta yazının tüm yazarlar tarafından okunduğu, onaylandığı ve orijinal bir çalışma ürünü olduğu ifade edilmeli ve yazar isimlerinin yanında imzaları bulunmalıdır. Başvuru mektubu ayrı bir dosya olarak, Journal Agent sisteminin “Yeni Makale Gönder” bölümünde, 10. aşamada yer alan dosya yükleme aşamasında yollanmalıdır.

Başlık sayfası: Yazının başlığı, yazarların adı, soyadı ve ünvanları, çalışmanın yapıldığı kurumun adı ve şehri, eğer varsa çalışmayı destekleyen fon ve kuruluşların açık adları bu sayfada yer almalıdır. Bu sayfaya ayrıca “yazışmadan sorumlu” yazarın isim, açık adres, telefon, faks, mobil telefon ve e-posta bilgileri eklenmelidir. Özet: Çalışmanın gereç ve yöntemini ve bulgularını tanıtıcı olmalıdır.

Türkçe özet, Amaç, Gereç ve Yöntem, Bulgular, Sonuç ve Anahtar Sözcükler başlıklarını; İngilizce özet Background, Methods, Results, Conclusion ve Key words başlıklarını içermelidir. İngilizce olarak hazırlanan çalışmalarda da Türkçe özet yer almalıdır. Özetler başlıklar hariç 190210 sözcük olmalıdır.

Tablo, şekil, grafik ve resimler: Şekillere ait numara ve açıklayıcı bilgiler ana metinde ilgili bölüme yazılmalıdır. Mikroskobik şekillerde resmi açıklayıcı bilgilere ek olarak, büyütme oranı ve kullanılan boyama tekniği de belirtilmelidir. Yazarlara ait olmayan, başka kaynaklarca daha önce yayınlanmış tüm resim, şekil ve tablolar için yayın hakkına sahip kişiler-

den izin alınmalı ve izin belgesi dergi editörlüğüne ayrıca açıklamasıyla birlikte gönderilmelidir. Hastaların görüntülendiği fotoğraflara, hastanın ve/veya velisinin imzaladığı bir izin belgesi eşlik etmeli veya fotoğrafta hastanın yüzü tanınmayacak şekilde kapatılmış olmalıdır. Renkli resim ve şekillerin basımı için karar hakemler ve editöre aittir. Yazarlar renkli baskının hazırlık aşamasındaki tutarını ödemeyi kabul etmelidirler.

Kaynaklar: Metin içindeki kullanım sırasına göre düzenlenmelidir. Makale içinde geçen kaynak numaraları köşeli parantezle ve küçültülmeden belirtilmelidir. Kaynak listesinde yalnızca yayınlanmış ya da yayınlanması kabul edilmiş çalışmalar yer almalıdır. Kaynak bildirme “Uniform Requirements for Manuscripts Submitted to Biomedical Journals” (http:// www.icmje.org) adlı kılavuzun en son güncellenmiş şekline (Şubat 2006) uymalıdır. Dergi adları Index Medicus’a uygun şekilde kısaltılmalıdır. Altı ya da daha az sayıda olduğunda tüm yazar adları verilmeli, daha çok yazar durumunda altıncı yazarın arkasından “et al.” ya da “ve ark.” eklenmelidir. Kaynakların dizilme şekli ve noktalamalar aşağıdaki örneklere uygun olmalıdır: Dergi metni için örnek: Velmahos GC, Kamel E, Chan LS, Hanpeter D, Asensio JA, Murray JA, et al. Complex repair for the management of duodenal injuries. Am Surg 1999;65:972-5.

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

Sizlerin çalışmalarınızda kaynak olarak yararlanabilmeniz için www.travma.org.tr adresli web sayfamızda eski yayınlara tam metin olarak ulaşabileceğiniz bir arama motoru vardır.

Derleme yazıları: Bu tür makaleler editörler kurulu tarafından gerek olduğunda, konu hakkında birikimi olan ve bu birikimi literatüre de yansımış kişilerden talep edilecek ve dergi yazım kurallarına uygunluğu saptandıktan sonra değerlendirmeye alınacaktır. Derleme makaleleri; başlık, Türkçe özet, İngilizce başlık ve özet, alt başlıklarla bölümlendirilmiş metin ile kaynakları içermelidir. Tablo, şekil, grafik veya resim varsa yukarıda belirtildiği şekilde gönderilmelidir.

Olgu sunumları: Derginin her sayısında sınırlı sayıda olgu sunumuna yer verilmektedir. Olgu bildirilerinin kabulünde, az görülürlük, eğitici olma, ilginç olma önemli ölçüt değerlerdir. Ayrıca bu tür yazıların olabildiğince kısa hazırlanması gerekir. Olgu sunumları başlık, Türkçe özet, İngilizce başlık ve özet, olgu sunumu, tartışma ve kaynaklar bölümlerinden oluşmalıdır. Bu tür çalışmalarda en fazla 5 yazara yer verilmesine özen gösterilmelidir.

Editöre mektuplar: Editöre mektuplar basılı dergide ve PUBMED’de yer almamakta, ancak derginin web sitesinde yayınlanmaktadır. Bu mektuplar için dergi yönetimi tarafından yayın belgesi verilmemektedir.

Daha önce basılmış yazılarla ilgili görüş, katkı, eleştiriler ya da farklı bir konu üzerindeki deneyim ve düşünceler için editöre mektup yazılabilir.

Bu tür yazılar 500 sözcüğü geçmemeli ve tıbbi etik kurallara uygun olarak kaleme alınmış olmalıdır. Mektup basılmış bir yazı hakkında ise, söz konusu yayına ait yıl, sayı, sayfa numaraları, yazı başlığı ve yazarların adları belirtilmelidir. Mektup bir konuda deneyim, düşünce hakkında ise verilen bilgiler doğrultusunda dergi kurallarına uyumlu olarak kaynaklar da belirtilmelidir.

Bilgilendirerek onay alma - Etik: Deneysel çalışmaların sonuçlarını bildiren yazılarda, çalışmanın yapıldığı gönüllü ya da hastalara uygulanacak prosedür(lerin) özelliği tümüyle anlatıldıktan sonra, onaylarının alındığını gösterir bir cümle bulunmalıdır. Yazarlar, bu tür bir çalışma söz konusu olduğunda, uluslararası alanda kabul edilen kılavuzlara ve T.C. Sağlık Bakanlığı tarafından getirilen yönetmelik ve yazılarda belirtilen hükümlere uyulduğunu belirtmeli ve kurumdan aldıkları Etik Komitesi onayını göndermelidir. Hayvanlar üzerinde yapılan çalışmalarda ağrı, acı ve rahatsızlık verilmemesi için neler yapıldığı açık bir şekilde belirtilmelidir.

Yazı gönderme - Yazıların gönderilmesi: Ulusal Travma ve Acil Cerrahi Dergisi yalnızca www.travma.org.tr adresindeki internet sitesinden on-line olarak gönderilen yazıları kabul etmekte, posta yoluyla yollanan yazıları değerlendirmeye almamaktadır. Tüm yazılar ilgili adresteki “Online Makale Gönderme” ikonuna tıklandığında ulaşılan Journal Agent sisteminden yollanmaktadır. Sistem her aşamada kullanıcıyı bilgilendiren özelliktedir.

TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY ULUSAL TRAVMA VE ACİL CERRAHİ DERGİSİ Vol. - Cilt 21

Number - Sayı 4 Temmuz - July 2015

Contents - İçindekiler

Deneysel Çalışma - Experimental Study Experimental Study - Deneysel Çalışma 235-240 The effects of erythropoietin, dextran and saline on brain edema and lipid peroxidation in experimental head trauma

Deneysel kafa travması oluşturulan sıçanlarda eritropoetin, dekstran ve salin kombinasyonunun lipid peroksidasyonu ve beyin ödemi üzerine etkileri Başarslan SK, Göçmez C, Kamaşak K, Ekici MA, Ulutabanca H, Doğu Y, Menkü A 241-247 Detection of the MicroRNA expression profile in skeletal muscles of burn trauma at the early stage in rats

Sıçanlarda yanık travmalı iskelet kaslarında erken evrede mikro-RNA ekspresyon profili Haijun Z, Yonghui Y, Jiake C, Hongjie D

Original Articles - Orijinal Çalışma 248-255 Evaluation of gunshot wounds in the emergency department

Acil serviste ateşli silah yaralanmalarının analizi Karaca MA, Kartal ND, Erbil B, Öztürk E, Kunt MM, Şahin TT, Özmen MM 256-260 Acil servise trafik kazasına bağlı künt abdominal travma ile başvuran hastalarda klinik değerlendirme, laboratuvar parametreleri ve radyolojik sonuçların tedavi kararına ve cerrahi sonuçlarına etkisi

The effect of clinical, laboratory and radiologic results on treatment decision and surgical results in patients admitted to the emergency department with blunt abdominal trauma due to traffic accident Tatar İG, Yılmaz KB, Ergun O, Balas Ş, Akıncı M, Deryol R, Şeker GE, Kulaçoğlu H, Hekimoğlu B 261-265 Evaluation of posttraumatic recurrent bacterial meningitis in adults

Erişkin posttravmatik tekrarlayan menenjitlerin değerlendirilmesi Deveci Ö, Uysal C, Varol S, Tekin R, Bozkurt F, Bekcibasi M, Hosoglu S 266-270 Choice of incision in penetrating cardiac injuries: Which one must we prefer: Thoracotomy or sternotomy?

Penetran kalp yaralanmalarında insizyon seçimi: Hangisini tercih etmeliyiz? Torakotomi mi sternotomi mi?

Beşir Y, Gökalp O, Eygi B, İner H, Peker İ, Gökalp G, Yılık L, Gürbüz A 271-278 Cerebrovascular complications of transorbital penetrating intracranial injuries

Transorbital penetran intrakraniyal travmaların serebrovasküler komplikasyonları Arat YÖ, Arat A, Aydın K 279-284 Results of surgical treatment in metacarpal shaft fractures using low profile mini plates

Düşük profilli mini plak ile metakarp cisim kırıklarının cerrahi tedavi sonuçları Aykut S, Öztürk K, Özcan Ç, Demiroğlu M, Gürün AU, Özden E

Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

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TURKISH JOURNAL OF TRAUMA & EMERGENCY SURGERY ULUSAL TRAVMA VE ACİL CERRAHİ DERGİSİ Vol. - Cilt 21

Number - Sayı 4 July - Temmuz 2015

Contents - İçindekiler

285-290 Endovascular treatment for acute traumatic thoracic aortic transection

Akut travmatik torasik aort transeksiyonunda endovasküler tedavi Ergun O, Canyiğit M, Hıdıroğlu M, Tatar İG, Birgi E, Küçüker A, Uğuz E, Durmaz HA, Çetin H, Hekimoğlu B, Şener E 291-296 Outcomes and demostration of cranial firearm injuries: A multicenter retrospective study

Kraniyal ateşli silah yaralanmalarının dağılımı ve sonuçları: Çok merkezli geriye dönük çalışma Çınar K, Seçer M, Alagöz F, Ulutaş M, Uçkun ÖM, Yıldırım AE, Gürçay AG, Güvenç Y, Çelik H, Narin F

Case Reports - Olgu Sunumu 297-299 Rarely seen complication of motor vehicle accidents: bilateral globe avulsion

Motorlu taşıt kazalarının nadir görülen bir komplikasyonu: İki taraflı glob avülsiyonu Kelahmetoğlu O, Şimşek T, Beden Ü, Aydoğdu İO, Cömert Hamzaoğlu E 300-302 Behçet hastalığına bağlı multipl ince bağırsak perforasyonu

Multiple small bowel perforations due to Behcet’s disease Eker T, Eroğlu A 303-305 Left atrial rupture due to blunt thoracic trauma

Künt toraks travmasına bağlı sol atriyal yırtık Akar İ, İnce İ, Aslan C, Çeber M, Kaya İ 306-308 Non-traumatic tension gastrothorax in a young lady

Genç bir kadında, non-travmatik tansiyon gastrotoraks Tokur M, Demiröz ŞM, Sayan M 309-314 Acute retrobulbar haemorrhage: An ophthalmologic emergency for the emergency physician

Acil hekimlerinin oftalmik acili: Akut retrobulber hemoraji Pamukcu C, Odabaşı M

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EXPERIMENTAL STUDY

The effects of erythropoietin, dextran and saline on brain edema and lipid peroxidation in experimental head trauma Seyit Kağan Başarslan, M.D.,1 Cüneyt Göçmez, M.D.,2 Kağan Kamaşak, M.D.,2 Mehmet Ali Ekici, M.D.,3 Halil Ulutabanca, M.D.,4 Yurdaer Doğu, M.D.,5 Ahmet Menkü, M.D.4 1

Department of Neurosurgery, Mustafa Kemal University Faculty of Medicine, Hatay

2

Department of Neurosurgery, Dicle University Faculty of Medicine, Diyarbakır

3

Department of Neurosurgery, Şevket Yılmaz Training and Research Hospital, Bursa

4

Department of Neurosurgery, Erciyes University Faculty of Medicine, Kayseri

5

Department of Neurosurgery, Tekten Private Hospital, Denizli

ABSTRACT BACKGROUND: The aim of this study was to investigate the protective effects of erythropoietin, dextran/saline and erythropoietin in combination with dextran/saline on brain edema and lipid peroxidation following traumatic brain injury in rats.

METHODS: In the study, 40 male 3-month-old albino Wistar rats, weighing 250–340 g, were divided into four groups, each consisting of ten rats. Traumatic brain injury was induced in all rats by the weight–drop method, and erythropoietin (5,000 U/kg) and/or dextran and saline (8 ml/kg) solutions were injected intraperitoneally ten minutes after trauma. Control animals received an equal volume of serum physiologic. All rats were sacrificed 24 hours later. Glutathione peroxidase activity and malondialdehyde levels were measured in the left hemisphere, and edema was quantitated by the wet–dry method.

RESULTS: Brain edema and the levels of malondialdehyde, the last product of lipid peroxidation in tissues, were decreased variably, and the activity of glutathione peroxidase, an antioxidant enzyme, was increased in others compared with the control group.

CONCLUSION: In this study, it was concluded that the brain edema that developed in rats on which head trauma was induced and the secondary brain damage caused by oxidative stress could be deceased using a combination of erythropoietin, dextran, and saline.

Key words: Antioxidants; brain edema; dextran; erythropoietin; saline; oxidative stress; severe head trauma.

INTRODUCTION Traumatic brain injury (TBI) is a commonly used term to describe brain damage that occurs over a larger area than the one in focal brain injury. It is one of the most devastating health problems since it can result in disabilities requiring long-term treatment and care. It is also the primary cause of death, especially in children and the young generation, throughout the world.[1,2] TBI occurs as a result of a sudden damage to the brain from an external mechanical force, possibly leading to Address for correspondence: Seyit Kağan Başarslan, M.D. Mustafa Kemal Üniversitesi, Tıp Fakültesi, Beyin Cerrahisi Anabilim Dalı, Hatay, Turkey Tel: +90 326 - 22910 00 / 3362 E-mail: kaganbasarslan@hotmail. com Qucik Response Code Ulus Travma Acil Cerrahi Derg 2015;21(4):235–240 doi: 10.5505/tjtes.2015.66502 Copyright 2015 TJTES

Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

permanent or temporary impairment of cognitive, physical, or psychosocial functions as well as a diminished or altered state of consciousness. Accelerated social and technological changes have resulted in a gradual increase in the incidence of head injuries and an accompanying increase in the risk of mortality and morbidity.

The pathology associated with TBI can mainly be divided into two parts: primary and secondary injury. Primary injury results immediately from the initial mechanical trauma; the only “treatment” for primary injury is prevention.[3] In contrast, secondary injury occurs in the hours and days following the primary injury and plays a marked role in brain damage and death that result from TBI.[4] Efforts to reduce morbidity and mortality resulting from TBI are best aimed at preventing secondary injury.[5] Secondary injury is caused by a complex cascade of physiological and biochemical mechanisms that are only partially understood.[6–8] However, since secondary injury occurs over a period of time, a window of opportunity exists during which measures can be taken to avoid further complications such as hypoxia and edema.[9] Regardless of the 235

Başarslan et al. The effects of erythropoietin, dextran and saline on brain edema and lipid peroxidation in experimental head trauma

cause of brain injury, edema almost always occurs. Edema can result in increased intracranial pressure leading to less brain perfusion, which can then contribute to ischemia exacerbating the original edema. Thus, brain edema is a central part of this vicious cycle of secondary injury in TBI. Therefore, any treatment expected to mitigate secondary injury must alleviate brain edema. The aim of this study was to assess the effect of therapeutic agents against brain edema; edema serves as the principal indicator for efficacy.

Oxygen free radicals and lipid peroxidation are believed to play crucial roles in secondary brain injury. There is extensive experimental support for the pathophysiological importance of early oxygen radical formation and cell membrane lipid peroxidation in the injured nervous system.[10,11] Previous reports of increased lipid peroxidation end products after head injury and the protective effects of free-radical scavengers are consistent with the proposed role of oxygen free radicals and lipid peroxidation in secondary brain injury.[11,12] Brain is less tolerant of hypoxia and oxidative stress than other organs. If the injured brain can be protected by antioxidants, it is expected to return to its normal physiology.[13] Accordingly, a traumatized brain should be supported by a variety of antioxidant mechanisms.

Malondialdehyde (MDA) is a reactive species that occurs naturally, which was used as a biomarker of oxidative stress in this study.[14] Glutathione peroxidase (GPx) is the general name of an enzyme family with peroxidase activity whose main biological function is to protect organisms from oxidative damage by reducing lipid hydroperoxides and free hydrogen peroxide to water. Its activity is generally accepted as a basic indicator of an antioxidant system.[15] In addition to its erythropoietic effects, erythropoietin (EPO) possesses many biological activities.[16,17] It is produced by astrocytes in response to hypoxia, suggesting that it protects neurons from ischemic damage.[18] Trials on human subjects are not conclusive regarding its ability to protect against ischemic damage. This study was undertaken as EPO had been detected in the brain as a natural response to primary hypoxic damage and might work synergistically with other agents such as dextran and hypertonic saline.

Dextran (D) is a complex of polysaccharide chains of varying lengths (3 to 2,000 kilo Daltons). It is used for a variety of reasons in intensive care units, such as preventing thrombosis, reducing blood viscosity, and expanding volume.[19] In addition, D, which can act as a potent osmotic agent, is preferred as an alternative to mannitol for urgent treatment of brain edema. The use of hypertonic saline (S) in experimentally induced brain injury has long been known to reduce the intracranial pressure. It is also used in critical care settings to maintain brain perfusion and severe hyponatremia.[20] This study investigated whether brain edema occurring in the early stages of severe head trauma could be reduced by the 236

administration of a combination of EPO, D and S in rats. If these reagents are demonstrated to reduce brain edema, the study will be expanded to include human subjects.

MATERIALS AND METHODS The approval of Erciyes University, Experimental Animal Ethics Committee was obtained for all procedure.

Animals Forty 3-month-old male Wistar albino rats, weighing 250– 340 g, were used in this study. They were kept in a windowless room where temperature and light were automatically controlled (21±1°C; 14 h light/10 h dark cycle, light on at 7 am and off at 9 pm). The humidity ranged from 50 to 54%.

The Ethical Committee of Erciyes University approved all animal procedures and the experimental protocol. All animals received proper care according to the criteria outlined in the Guide for the Care and Use of Laboratory Animals as prepared by the National Academy of Sciences and published by the National Institutes of Health.

Surgical Technique The animals were divided randomly into the following four groups of ten rats each: control, EPO, dextran-hypertonic saline (DS) and EPO+DS. The rats were anesthetized with an intraperitoneal injection of ketamine hydrochloride (70 mg/ kg) and xylazin hydrochloride (7 mg/kg). The animals maintained spontaneous breathing. The heads of the animals were fit into the head injury device with the chin resting firmly on the bottom plane. Closed head injury was created as described by Marmarou et al.[21] The cranial impact was induced at the vertex on the midline, just behind the coronal suture for all treatment groups. The free fall occurred from a height of 150 cm, preferable for producing impact energy of 0.7 J over the skull. Ten minutes after the trauma, the rats were injected intraperitoneally with EPO (5,000 U/kg) (EPO group), DS (8 ml/kg) (DS group), both EPO (5,000 U/kg) and DS (8 ml/kg) (EPO+DS group) or an equal volume of serum physiologic (control group). The rats were decapitated 24 h after the onset of injury, and brain hemispheres were removed for biochemical analysis (left hemisphere) and measurement of water content (edema) (right hemisphere).

Measurement of Brain Edema The water content of the rat brain tissues were evaluated by estimating the water content using the method described

by Hara et al.[22] Briefly, both cerebral hemispheres were immediately weighed after decapitation and kept in an oven at 70°C for 36 h until a constant weight was reached. The percentage of tissue water content was calculated using the following formula: % water content=[(wet weight-dry weight)/ wet weight]× 100.[23]

Measurement of Malondialdehyde (MDA) Level A hydroxyl radical, a typical example of free radicals, can easiUlus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

Başarslan et al. The effects of erythropoietin, dextran and saline on brain edema and lipid peroxidation in experimental head trauma

ly react with membrane phospholipids, resulting in the provocation of lipid peroxidation. MDA, as the final product of lipid peroxidation, can be identified via thiobarbituric acid (TBA) reaction. The absorptivity of the color formed by MDA with TBA was used to determine the amount of lipid peroxidation per gram of wet tissue in nmol units. After centrifugation, the color was measured at 532 nm.[24] Protein levels were measured as described by Lowry et al.

Measurement of Glutathione Peroxidase (GPx) Activity GPx activity was measured by the method of Paglia and Valentine.[25] In order to initiate enzymatic reaction, H2O2 was added to a tube containing NADPH, reduced glutathione (GSH), sodium azide, and glutathione reductase, and the change in absorbance at 340 nm was determined by spectrophotometry.

The activity was reported in units per gram protein.

Statistical Analysis All statistical analyses were performed using SPSS statistical software (SPSS for Windows, version 10.0). Using the Kolmogorov-Smirnov test, the data was determined to be normally distributed. The differences in the measured parameters among the groups were analyzed using one-way ANOVA. The Scheffe procedure was used to determine which group was significantly different. The measurable (quantitative) data distribution was defined as the average values of the x±sd, and significance level was taken as 0.05.

RESULTS Biochemical Findings Mean MDA levels and GPx activities for each group are shown in Table 1. TBI significantly increased the tissue MDA

levels and significantly decreased the tissue GPx activities when compared with controls (p<0.05). The administration of a single dose of EPO (5,000 U/kg) 10 min after the trauma resulted in significantly decreased MDA levels and significantly increased GPx activity compared with that observed for the control group (Table 1, Fig. 1).

Mean GPx activity observed in the EPO+DS group was significantly higher than that of the control group. There was also an increase in the mean GPx activity of both the EPO and DS groups compared with the control group; however, the differences were not statistically significant (Table 1, Fig. 2).

Edema Findings Tissue edema was evaluated as the percentage of water in the tissue (Table 2, Fig. 3). The rats in the DS, EPO and EPO+DS groups experienced significantly less edema than the rats in the control group. Furthermore, the rats in the EPO+DS group experienced significantly less edema than the rats in the EPO only or DS only groups. There was no significant difference between the DS and the EPO groups with respect to edema.

DISCUSSION Severe head injury, which has become one of the most important health problems worldwide, can be fatal or a disabling trauma that requires long-term treatment and care. Defense mechanism of the brain against oxidative stress has long been known to be less than that of the other organs. A traumatized brain; however, can return to its normal physiology if secondary damage caused by oxidants is prevented. Therefore, brain antioxidant mechanisms should be supported as much and as quick as possible when treating TBI.

Table 1. Tissue GPx activities and MDA levels in control and treated rats

Control (n=10)

EPO (n=10)

DS (n=10)

EPO+DS (n=10)

F

p

Mean±SD Mean±SD Mean±SD Mean±SD

GPx (Ü/ml) 287.3±13.2 311.2±40.6 338.5±39.8 373.8±22.3 13.2 0.00 MDA (µM) 2.06±0.28 1.62±0.22 1.95±0.29 1.88±0.44 3.7 0.02

Table 2. Mean Water Percent (Edema) in control and treated rats

Control (n=10)

EPO (n=10)

DS (n=10)

EPO+DS (n=10)

F

p

Mean±SD Mean±SD Mean±SD Mean±SD

Wet-weight 0.602±0.040 0.629±0.025 0.547±0.020 0.514±0.032 28.2 0.00 Dry-weight 0.190±0.014 0.229±0.010 0.196±0.010 0.207±0.018 15.8 0.00 Water% (Edema) 68.4 63.4 64.1 59.7 76.2 0.00

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2.5

70

MDA (µM/mg port)

2

66

1.5

64 62

1

60

0.5 0

58 56 Control

EPO

DS

EPO+DS

Figure 1. MDA levels in control and treated rats. The reduced MDA levels in the EPO and EPO+DS groups compared with controls suggest that EPO generates a neuroprotective and anti-edema effect by reducing lipid peroxidation.

400

GPx (nmol/min/ml)

350 300 250 200 150 100 50 0

Control

EPO

DS

EPO+DS

Figure 2. GPx activity in control and treated rats. The EPO, DS and EPO+DS groups show higher GPx activity than the control group; only the difference between the EPO+DS group and the controls was significant.

It has been shown that secondary brain injury negatively affects prognosis. The main approach to treating a traumatized brain has been to protect it from secondary injuries, including ischemia, cerebral hypoxia, cerebral edema, and raised intracranial pressure. Morbidity and mortality can only be reduced if these pathologies are prevented.[26,27] Rapidly progressive cerebral edema is usually the first step of the pathological process that follows brain trauma. Maintaining reduced brain perfusion pressure by the compression of vascular structures is one of the most important goals of treatment.[28] In response to severe trauma, the body tends to develop marked anemia and hypotension, both of which further the susceptibility to hypoxia. In addition to its erythropoietic effects, EPO also possesses many biological activities. The fact that it is produced by astrocytes in response to hypoxia suggests that EPO protects neurons from ischemic damage. Yasuda et al.[29] have demonstrated that EPO plays an important role in the development of the nervous system, and its absence results in the interruption of neurogenesis in fetal embryos. Brines et al.[30] have reported that EPO passes through 238

% Water (Edama)

68

54

Control

EPO

DS

EPO+DS

Figure 3. Edema in control and treated rats. The cerebral edema in the EPO, DS and EPO+DS groups was significantly lower than in the control group.

the blood brain barrier by a receptor-mediated mechanism and protects the brain along with the peripheral application. They have concluded that it is a safe therapeutic agent with minimal side effects. Belayev et al.[31] have histologically investigated the effects of EPO on the hypoxia induced by MCA clipping in rats and reported that EPO-treated rats developed cortical and subcortical infarction at rates that were 58% and 50% lower, respectively, compared with the controls. Ehrenreich[32] have demonstrated that EPO achieves its protective effects via its antioxidant, anti-apoptotic effects rather than by regulating disease-specific pathological mechanisms. Similarly, Kumral et al.[33] have reported that EPO increases GPx activity and decreases lipid peroxidation in neonatal rats exposed to hypoxia compared with controls. Kuzugüden et al.[34] have shown the oxidative stress induced by high doses of thinner can be reduced by EPO via a decrease in the formation of MDA and an increase in GPx activity in rat brain. In another study, Ozturk et al.[35] have investigated the antioxidant properties of EPO and propofol on closed head injury in a rat model and found that rats treated with EPO or propofol+EPO had lower serum MDA and NO levels compared with the control group. Thus, it was concluded that EPO administration during the early period of trauma caused a significant reduction in the levels of oxidative stress metabolites.

In our study, EPO showed a neuroprotective effect reducing the formation of edema and MDA and increasing the GPx activity. Taken together, these findings suggest that the neuroprotective effect of EPO is achieved by regulating enzyme activities or strengthening the antioxidant defense. It was also demonstrated that there was a significant decrease in MDA levels and a significant increase in GPx activity in the EPO and EPO+DS groups compared with that observed in the controls. These results confirm that EPO has a marked antioxidant effect. So as to take advantage of its neuroprotective effects, it is reported that EPO should be administered within the first 3 to 24 hours after trauma. Hence, EPO was administered intraperitoneally 10 minutes after the trauma occurred.

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Başarslan et al. The effects of erythropoietin, dextran and saline on brain edema and lipid peroxidation in experimental head trauma

Verdonck et al.[36] had investigated the effect of rEPO on brain edema by MRI and gravimetric methods. The model of head trauma described by Marmarau et al. was administered to Wistar albino rats, and rEPO was given 30 min later.

The measurements were obtained from the neocortex and kaudaputamen regions of rat brain, and cerebral edema was found to be significantly less in EPO-treated rats than in the controls. This provides further evidence of EPO’s positive effect on brain edema. In our study, cerebral edema was decreased in both the EPO and the DS groups compared with the controls. When EPO and DS were co-administered, there was a further decrease in edema, suggesting a synergistic antiedema effect. These results are consistent with a study by Frei et al.,[37] in which rEPO was found to significantly increase brain perfusion and improve neurological outcome by reducing cellular apoptosis, tissue inflammation and cerebral edema in rats with closed head injuries.

Thus far, the application of DS hypertonic solution has been limited to studies on hemorrhagic shock recovery. Although the results of these studies indicate that such patients may benefit from treatment with DS hypertonic solution, patients with head injury have not been included into these studies.[38] It has been shown that DS hypertonic solution reduces intracerebral pressure (ICP) in animals with head injury. Berger et al.[39] have compared the ability of hypertonic DS with that of hypertonic mannitol to reduce intracranial hypertension that develop due to focal cerebral lesions and intracranial mass and have reported that hypertonic DS provides higher brain perfusion pressure than mannitol. In addition, experimental studies have shown that S also improves cerebral perfusion pressure better than mannitol due to its potential to increase mean arterial blood pressure; in contrast, mannitol reduces mean arterial blood pressure.

Based on our findings in combination with the results of other studies, we believe that EPO should be started in clinical use, and DS might be an alternative to hypertonic mannitol in the treatment of edema in patients with severe head injury.

Based on our results and in light of the above-mentioned studies, we reached the following conclusions: 1. EPO shows a neuroprotective effect reducing the formation of edema and increasing the GPx activity, which has antioxidant effect.

2. EPO alone has an anti-edema effect equivalent to that of hypertonic DS, and this effect is increased when EPO and DS are co-administered.

3. EPO generates its neuroprotective and anti-edema effect reducing lipid peroxidation as evidenced by the reduced MDA level in EPO and EPO+DS rats compared with the controls.

4. In head injuries, lipid peroxidation causes brain edema as evidenced by the fact that brain edema is significant in the rat groups with a high level of MDA. 5. Antioxidant mechanisms play an important role in reducUlus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

ing brain edema and secondary brain damage as shown by the fact that GPx activity decreases as brain edema increases and vice versa.

6. EPO, DS and EPO+DS groups show higher GPx activity than the control group, but there was only significant difference in EPO+DS the group. This also suggests that the co-administered EPO and DS synergistically reduce brain edema and increase antioxidant activity as evidenced by the fact that the EPO, DS and EPO+DS groups all showed a higher GPx activity than the control group, but the increase was only significant for the EPO+DS. 7. Cerebral edema in the EPO, DS and EPO+DS groups was significantly lower than in the control group.

8. Dextran and saline had no effect on lipid peroxidation.

Conflict of interest: None declared.

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39. Berger S, Schürer L, Härtl R, Messmer K, Baethmann A. Reduction of post-traumatic intracranial hypertension by hypertonic/hyperoncotic saline/dextran and hypertonic.

DENEYSEL ÇALIŞMA - ÖZET OLGU SUNUMU

Deneysel kafa travması oluşturulan sıçanlarda eritropoetin, dekstran ve salin kombinasyonunun lipit peroksidasyonu ve beyin ödemi üzerine etkileri Dr. Seyit Kağan Başarslan,1 Dr. Cüneyt Göçmez,2 Dr. Kağan Kamaşak,2 Dr. Mehmet Ali Ekici,3 Dr. Halil Ulutabanca,4 Dr. Yurdaer Doğu,5 Dr. Ahmet Menkü4 Mustafa Kemal Üniversitesi Tıp Fakültesi, Beyin Cerrahisi Anabilim Dalı, Hatay Dicle Üniversitesi Tıp Fakültesi, Beyin Cerrahisi Anabilim Dalı, Diyarbakır Şevket Yılmaz Eğitim ve Araştırma Hastanesi, Beyin Cerrahi Kliniği, Bursa 4 Erciyes Üniversitesi Tıp Fakültesi, Beyin Cerrahisi Anabilim Dalı, Kayseri 5 Özel Tekten Hastanesi, Beyin Cerrahi Kliniği, Denizli 1 2 3

AMAÇ: Deneysel kafa travması oluşturulan sıçanlarda gelişen beyin hasarı ve ödemine karşı eritropoetin, dekstran ve salin kombinasyonunun koruyucu etkisini araştırmaktır.

GEREÇ VE YÖNTEM: Çalışmada ağırlıkları 250–340 g arasında değişen 40 adet Wistar Albino cinsi erkek sıçan kullanıldı. Her biri 10 adet sıçan içeren dört deney grubu oluşturuldu. Bütün sıçanlara kafa travması oluşturuldu ve ilaçlar intraperitoneal (ip) yolla travmadan 10 dk sonra verildi. Kontrol grubuna (K) diğer gruplarla eşit hacimde serum fizyolojik enjekte edildi. Birinci gruba eritropoetin (EPO) 5000 Ü/kg verildi. İkinci gruba dekstran ve salin (DS) 8 ml/kg verildi. Son gruba da aynı doz ve miktarlarda eritropoetin, dekstran ve salin (EPO+DS) beraberce verildi. Yirmi dört saat sonra sıçanlar sakrifiye edilerek beyin dokuları çıkarıldı. Sağ hemisferde yaş ve kuru ağırlık çalışıldı. Sol hemisferde glutatyon peroksidaz (GPx) aktivitesi ve malondialdehit (MDA) miktarı ölçüldü.

BULGULAR: Kontrol grubuna göre diğer gruplarda beyin ödeminin ve lipit peroksidasyonu son ürünü olan MDA’nın değişik oranlarda azaldığı, antioksidan enzim olan GPx aktivitesinin arttığı tespit edildi.

TARTIŞMA: Bu çalışmada, kafa travması oluşturulan sıçanlarda gelişen beyin ödemi ve oksidatif stresin oluşturduğu sekonder beyin hasarının eritropoetin, dekstran ve salin kombinasyonu kullanılarak azaltılabileceği sonucuna varıldı.

Anahtar sözcükler: Antioksidanlar; beyin ödemi; dekstran; eritropoetin; salin; oksidatif stres; kafa travması.

Ulus Travma Acil Cerrahi Derg 2015;21(4):235–240

240

doi: 10.5505/tjtes.2015.66502

Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

EXPERIMENTAL STUDY

Detection of the MicroRNA expression profile in skeletal muscles of burn trauma at the early stage in rats Zhang Haijun, M.D.,* Yu Yonghui, M.D.,* Chai Jiake, M.D., Duan Hongjie, M.D. Department of Burn and Plastic Surgery, First Hospital Affiliated to General Hospital of Pla, Beijing, China

ABSTRACT BACKGROUND: Severe burn injuries are associated with a persistent hypermetabolic response, which causes long-term loss of muscle mass that results in a clinical negative balance of nitrogen and muscle wasting. MicroRNAs (miRNAs) play a critical role in posttranscriptional regulation of gene expression, which negatively regulates gene expression by promoting degradation of target mRNAs or inhibiting their translation. However, the mechanisms of skeletal muscle wasting after severe burn involved in miRNAs still remain unclear.

METHODS: In this study, the alterations of miRNAs expression profile in skeletal muscles of thermal rats were detected at an early stage by microarray. All data were presented as mean±SD. Statistical analysis was determined by independent Student’s t-test and oneway ANOVA. The significance was all set at p<0.05, and fold change cut-off was 2.0 for microarray. Significant differentially expressed miRNAs were identified through Volcano Plot filtering. Hierarchical clustering was performed using MEV software (v4.6, TIGR).

RESULTS: Thousands of miRNAs could be examined in normal and injured tissues, but only 69 of these were significantly upregulated or down-regulated, which could be used to discriminate skeletal muscles of thermal rats from matched tissues.

CONCLUSION: The deregulated miRNAs probably play a potential role in the pathogenesis of skeletal muscle wasting in burn trauma.

Key words: Burn; microRNA; muscle wasting; profile.

INTRODUCTION Critical illnesses induce muscle wasting and muscle weakness.[1] Severe burn injuries are associated with a persistent hypermetabolic response, which causes long-term loss of muscle mass that results in a clinical negative balance of nitrogen and muscle wasting. Cutaneous burn and hind limb unloading have an additive effect on muscle atrophy, characterized by loss of muscle mass and decrease in muscle strength in both fast (PL) and slow (SL) twitch muscles.[2–5] Body weight, muscle wet weight and protein weight of rats in burn group were decreased significantly compared with sham group.[6] Following a large burn, skeletal muscle plays an *Haijun Zhang and Yonghui Yu contribute equally to this work.

Address for correspondence: Chai Jiake, M.D. 51 Fucheng Road Beijing - China Tel: +86-10-6686-7972 E-mail: cjk304@126.com Qucik Response Code

Ulus Travma Acil Cerrahi Derg 2015;21(4):241–247 doi: 10.5505/tjtes.2015.80707 Copyright 2015 TJTES

Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

important role in metabolic regulation, such as the synthesis of acute phase proteins and the deposition of new skin.[7] Growing evidence suggests that the main mechanisms underlying skeletal muscle wasting induced by severe burn include activation of ubiquitin-proteasome pathway,[8–10] myonuclear apoptosis,[1] mitochondrial dysfunction,[5,7] autophagy[1] signaling pathways driving muscle inflammation, and protein metabolism.[11] MicroRNAs (miRNAs) belong to a group of noncoding small RNAs with a length of 20–24 ribonucleotides, which play a critical role in post-transcriptional regulation of gene expression.

Most of them specifically recognize the 3’-untranslated regions (UTR) of their target mRNAs, thereby blocking the process of protein translation or causing mRNA degradation.[12,13] MiRNAs negatively regulate gene expression by promoting degradation of target mRNAs or inhibiting their translation.[14] The role of miRNAs have been confirmed for a range of common diseases connected to impaired balance of cell proliferation, differentiation and programmed death.[15] It is reported that miRNAs have been shown to play crucial roles in muscle development and in regulation of muscle cell proliferation and 241

Haijun et al. Detection of the MicroRNA expression profile in skeletal muscles of burn trauma at the early stage in rats

differentiation.[16] Growing evidence indicates that microRNAs significantly impact muscle growth, regeneration and metabolism. MicroRNAs have a great potential to become diagnostic and/or prognostic markers, therapeutic agents and therapeutic targets.[17] Recently, some research suggests that miRNAs are involved and play an important role in the pathogenesis of CKD and TWEAK induced muscle wasting.[18–21] However, the mechanisms of skeletal muscle wasting after severe burn involved in miRNAs still remain unclear. In this study, microarray analysis was used to detect the alterations of miRNAs expression profile in skeletal muscles of thermal rats at the early stage.

Further bio-informatic analysis of deregulated miRNAs will be needed to determine whether these miRNAs play a potential role in the pathogenesis of skeletal muscle wasting in burn trauma.

MATERIALS AND METHODS This study was approved by the Committee of Science and Technology of the First Hospital affiliated to the General Hospital of PLA (Beijing, China), in accordance with the protocol outlined in the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH publication no. 85–23, revised 1996).

Eight adult male Wistar rats weighing 200 to 220 g were purchased from Chinese Medical Scientific Institute (Beijing, China). A full thickness thermal injury of 30% TBSA was inflicted on the animals by immersing the back of the trunk in 94°C water for 12 s. A weight- and time-matched sham-burn group (n=4) was treated in the same way as the thermal (T) group (n=4), except that the contrast (C) group were immersed in room temperature water. After water immersion, all rats were immediately dried, administered fluid (40 ml/ kg of Ringer’s lactate solution calculated by the Parkland formula) during the post-burn period, and housed in individual cages with free access to food and water.[22] The animals were euthanized on the third day after thermal injury or sham, and their tibialis anterior (TA) muscles were harvested and stored at -80°C for RNA extraction.

MicroRNA Microarray MicroRNA arrays of Exiqon feature Tm-normalized LNA™enhanced capture probes, designed for excellent specificity and sensitivity even for AT-rich microRNAs. In addition, they offer great reproducibility with 99% correlation between arrays and a dynamic range greater than 5 orders of magnitude. The 7th generation of miRCURYTM LNA Array (v.18.0) (Exiqon) contains 3100 capture probes, covering all human, mouse and rat microRNAs annotated in miRBase 18.0, as well as all viral microRNAs related to these species. In addition, this array contains capture probes for 25 miRPlus™ human microRNAs. 242

RNA Extraction Total RNA was isolated using TRIzol (Invitrogen) and miRNeasy mini kit (QIAGEN) according to manufacturer’s instructions, which efficiently recovered all RNA species, including miRNAs. RNA quality and quantity was measured by using nanodrop spectrophotometer (ND–1000, Nanodrop Technologies) and RNA Integrity was determined by gel electrophoresis.

RNA Labeling After RNA isolation from the samples, the miRCURY™ Hy3™/Hy5™ Power labeling kit (Exiqon, Vedbaek, Denmark) was used according to the manufacturer’s guideline for miRNA labelling. One microgram of each sample was 3’-endlabeled with Hy3TM fluorescent label, using T4 RNA ligase by the following procedure: RNA in 2.0 μL of water was combined with 1.0 μL of CIP buffer and CIP (Exiqon). The mixture was incubated for 30 min at 37°C, and was terminated by incubation for 5 min at 95°C. Then 3.0 μL of labeling buffer, 1.5 μL of fluorescent label (Hy3TM), 2.0 μL of DMSO, 2.0 μL of labeling enzyme were added into the mixture. The labeling reaction was incubated for 1 h at 16°C, and terminated by incubation for 15 min at 65°C.

Array Hybridization After stopping the labeling procedure, the Hy3TM-labeled samples were hybridized on the miRCURYTM LNA Array (v.18.0) (Exiqon) according to array manual. The total 25 μL mixture from Hy3TM-labeled samples with 25 μL hybridization buffer were first denatured for 2 min at 95°C, incubated on ice for 2 min and then hybridized to the microarray for 16–20 h at 56°C in a 12-Bay Hybridization Systems (Hybridization System - Nimblegen Systems, Inc., Madison, WI, USA), which provides an active mixing action and constant incubation temperature to improve hybridization uniformity and enhance signal. Following hybridization, the slides were achieved, washed several times using Wash buffer kit (Exiqon), and finally dried by centrifugation for 5 min at 400 rpm.

Then the slides were scanned using the Axon GenePix 4000B microarray scanner (Axon Instruments, Foster City, CA).

Data Analysis Scanned images were then imported into GenePix Pro 6.0 software (Axon) for grid alignment and data extraction. Replicated miRNAs were averaged and miRNAs that intensities >=30 in all samples were chosen for calculating normalization factor. Expressed data were normalized using the Median normalization. After normalization, significant differentials expressed miRNAs were identified through Volcano Plot filtering. Hierarchical clustering was performed using MEV software (v4.6, TIGR).

Statistical Analysis All data were presented as mean±SD. Statistical analysis was Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

Haijun et al. Detection of the MicroRNA expression profile in skeletal muscles of burn trauma at the early stage in rats

RNA QC EUK 1. RNA Quantification and Quality Assurance by NanoDrop ND-1000 Sample ID

OD260/280

OD260/230

Conc. (ng/µl)

Volume (µl)

Quantity (ng)

QC result

Ratio

Ratio

Pass or Fail

1

2.00

2.30

722.96

20

14459.20

pass

4

2.00

2.31

859.83

30

25794.90

pass

5

1.91

2.38

447.36

30

13420.80

pass

6

2.02

2.28

639.62

30

19188.60

pass

37

2.02

2.24

742.03

20

14840.60

pass

39

2.03

2.21

661.48

30

19844.40

pass

41

1.98

2.41

292.58

30

8777.40

pass

41

2.02

2.21

608.70

30

18261.00

pass

• For spectrophotometer, the O.D. A260/A280 ratio should be close to 2.0 for pure RNA (ratios between 1.8 and 2.1 are avveptable). The O.D. A260/ A230 ratio should be more than 1.8.

2. RNA Integrity and gDNA contamination test by Denaturing Agarose Gel Electrophoresis

1

2

3

4

5

6

7

8

Lane 1: Lane 2: Lane 3: Lane 4: Lane 5: Lane 6: Lane 7: Lane 8:

Total RNA of sample Total RNA of sample Total RNA of sample Total RNA of sample Total RNA of sample Total RNA of sample Total RNA of sample Total RNA of sample

1 4 5 6 37 39 41 42

• The 28S 18S ribosomal RNA bands should be fairly sharp, intens bands. The intensity of the upper band should be about twice that of the lower band. Smaller, more diffuse bands representing low molecular weight RNAs (tRNA and 5S ribosomal RNA) may be present. It is normal to see a diffuse smear of ethidirum bromide staming material migrating between the 18S and 28S ribosomal bands, probably comp rised of mRNA and other heterogeneous RNA species. DNA contamination of the RNA preparation will be evident as a high molecular weight smear or band migrating above the 28S ribosomal RNA band. Degradation of the RNA will be reflected by smearing of ribosomal RNA bands.

Figure 1. Sample RNA quality controlled by Nanodrop 1000 spectrophotometer and denaturing agarose gel electrophoresis.

determined by the independent Student t test and one-way ANOVA. The significance is all set at p<0.05, and fold change cut-off is 2.0 for microarray.

RESULTS

Correlation Matrix and Scatter Plot A correlation matrix describes correlation among replicate experiments. The scatter-plot is a visualization that is useful for assessing the variation (or reproducibility) between chips (Fig. 2).

Sample RNA Quality Control Sample quality control data file from Nanodrop 1000 spectrophotometer and standard denaturing agarose gel electrophoresis is performed in Figure 1.

1e+02

1e+01

Scanned images were then imported into GenePix Pro 6.0 software (Axon) for grid alignment and data extraction. Replicated miRNAs were averaged and miRNAs that intensities >=30 in all samples were chosen for calculating median normalization factor. Expressed miRNA data were normalized using the median normalization and chosen for differentially expressed miRNAs screening.

Quality Assessment of MiRNA Data after Filtering The box plots are convenient way to quickly visualize the distribution of a dataset. They are most useful for comparing the distributions of samples. After normalization, the distributions of log2-ratios across every sample are nearly the same.

Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

T

Low Intensity Filtering and Data Normalization

1e+00

1e+01

1e+02 1e+02

1e+01

1e+00 C

1e+01

1e+02

Figure 2. The scatter-plot is for T vs C. The axes of the scatter-plot are the normalized signal values of the samples (Ratio scale).

243

Haijun et al. Detection of the MicroRNA expression profile in skeletal muscles of burn trauma at the early stage in rats

Overview of Expression Profiles of MiRNAs From the miRNA expression profiles, differentially expressed miRNAs were found between samples of skeletal muscles from thermal rats (thermal group) and sham-burn rats (control group). The expression profiles of miRNAs in paired samples were shown by calculating log fold-change Thermal

Volcano Plot (T vs C) 3.0

(p-value) –log10

2.5 2.0 1.5 1.0 0.5 0.0 -4

-2

0 Foldchange log2

2

4

Figure 3. The Volcano Plots is for T vs C. The vertical lines correspond to 2.0-fold up and down, respectively, and the horizontal line represents a p-value of 0.05. So the red point in the plot represents the differentially expressed miRNAs with statistical significance.

244

6

4

7.2 5

1.2 1

37

42

–7.1

41

The heat map diagram shows the result of the two-way hierarchical clustering of miRNAs and samples (Fig. 4). The result of hierarchical clustering shows distinguishable miRNA expression profiling among samples. Each row represents a miRNA and each column represents a sample. The miRNA clustering tree is shown on the left, and the sample clustering tree appears at the top. Cluster analysis arranges samples and miRNAs into groups based on their expression levels, which allows us to hypothesize about the relationships between miRNAs and samples.

39

Heat Map and Hierarchical Clustering

The miRNAs expression levels were compared between the injured tissues and their matched normal tissues from the microarray data and identified an average of 69 miRNAs that were significantly differentially expressed (2.0-fold) (Table 2).

The results demonstrated that thousands of miRNAs could be examined in normal and trauma tissues, but only 4 of these were significantly upregulated and 65 miRNAs were downregulated, which could be used to discriminate skeletal muscles of thermal rats from matched tissues (Tables 1, 2). Compared to normal tissues, rno-miR–628 (log2 fold-change T/C= 4.518624) was most significantly up-regulated (Table 1), while rno-miR–483–5p (log2 fold-change T/C= 0.129842) was most significantly down-regulated (Table 2). Down-regulated miRNAs were found to be more common than upregulated ones.

T c

16.689802 8.344901

0.0

Volcano Plots are useful tools for visualizing differential expression between two different conditions. They are constructed using fold-change values and p-values, and thus, allow you to visualize the relationship between fold-change (magnitude of change) and statistical significance (which takes both magnitude of change and variability into consideration).

They also allow subsets of genes to be isolated, based on those values.

8.166712

In order to identify differentially expressed miRNAs with statistical significance, a Volcano Plot filtering (Fig. 3) was performed between the two groups from the experiment. The threshold we used to screen Up or Down regulated miRNAs was Fold Change >=2.0 and p-value <=0.05.

group/Control group (T/C). Agreement was formulated as follows: fold-change cut-off: 2.0. For any fold-change, positive value indicates up-regulation and negative value indicates down-regulation. Log fold-change means log2 value of absolute fold-change. Fold-change and p-values were calculated from the normalized expression.

16.333424

Differentially Expressed MiRNAs Screening

0.0 rno–miR–133b–3p rno–miR–133a–3p rno–miR–206–3p rno–miR–126a–3p rno–miR–30a–5p rno–miR–30e–5p rno–miR–22–3p rno–miR–1–3p rno–miR–26b–5p rno–miR–30b–5p rno–miR–125b–5p rno–miR–27a–3p rno–let–7a–5p rno–let–7c–5p rno–miR–30d–5p rno–miR–136–5p rno–miR–98–5p rno–let–7b–5p rno–let–7d–5p rno–miR–126a–5p rno–miR–138–2–3p rno–miR–26a–5p rno–miR–352 rno–miR–3068–3p rno–miR–145–5p rno–let–7f–5p rno–miR–672–3p rno–miR–134–3p rno–miR–207 rno–miR–1188–3p rno–miR–3573–3p rno–miR–347 rno–let–7i–5p rno–miR–99a–5p rno–miR–10a–5p rno–miR–100–5p rno–miR–148b–3p rno–miR–336–5p rno–miR–344a/rno–miR–344a/–5p rno–miR–145–3p rno–miR–483–5p rno–miR–190b–5p rno–miR–30d–3p rno–miR–539–5p rno–miR–493–5p rno–miR–181c–5p rno–miR–183–5p rno–miR–136–3p rno–miR–9b–5p rno–miR–664–2–5p rno–miR–3072 rno–miR–760–5p rno–miR–410–5p rno–let–7b–3p rno–miR–99a–3p rno–miR–30c–2–3p rno–miR–376a–3p rno–miR–666–5p rno–miR–702–5p rno–miR–708–3p rno–miR–382–3p rno–miR–742–5p rno–miR–3558–3p rno–miR–501–3p rno–miR–678 rno–miR–222–5p rno–miR–107–5p rno–miR–201–5p rno–miR–628

Figure 4. Hierarchical clustering for Differentially Expressed miRNAs (Pass Volcano Plot) in T vs C, those miRNAs that Foreground-Background intensities are smaller than 30 in all samples have been excluded. Red indicates high relative expression, and green indicates low relative expression.

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Haijun et al. Detection of the MicroRNA expression profile in skeletal muscles of burn trauma at the early stage in rats

Table 1. Upregulated miRNAs ID

Name

Table 2.

Downregulated miRNAs (Continue)

Fold change

p-value

ID

T vs C

T vs C

Name

Fold change p-value T vs C

T vs C

146194

rno-miR–628

4.518624327

0.029565526

11182 rno-miR–98–5p

0.337921 0.009954

147536

rno-miR–107–5p

2.255367446

0.005258001

148187 rno-miR–410–5p

0.478896 0.022755

148133

rno-miR–222–5p

2.538488173

0.002218365

148417 rno-miR–1188–3p

0.482281 0.034831

0.022298433

148260 rno-miR–664–2–5p

0.342753 0.031127

14303 rno-miR–376a–3p

0.479186 0.04356

11266 rno-miR–336–5p

0.306392 0.001006

19596 rno-miR–30d–5p

0.411276 0.028727

17853 rno-miR–30d–3p

0.210027 0.008348

148472

rno-miR–201–5p

2.202553313

• Condition pairs: T vs C. • Fold Change cut-off: 2.0.

• P-value cut-off: 0.05.

• Column “ID”: array ID of the probes, each miRNA always has its unique probe, but some miRNAs may have two different probes.

• Column “Name”: the name of each miRNA. • Column “Fold change”: the ratio of normalized intensities between two conditions (use normalized data, ratio scale).

• Column “p-value”: T-test result between samples in different groups.

145968 rno-let–7d–5p

0.40086 0.010225

147592 rno-miR–3072

0.460007 0.018391

148050 rno-miR–3558–3p

0.391432 0.019711

148278 rno-miR–138-2–3p

0.365052 0.003288

148046

Table 2.

ID

Downregulated miRNAs Name

Fold change p-value T vs C

T vs C

rno-miR–344a/ rno-miR–344a–5p 0.386671 0.003028

146137 rno-miR–133a–3p

0.413985 0.029708

147198 rno-miR–26a–5p

0.496159 0.049327

42708 rno-miR–99a–5p

0.483193 0.049396

46626 rno-miR–30c–2–3p

0.338761 0.011011

17347 rno-miR–708–3p

0.486229 0.014214

147165 rno-let–7b–5p

0.46888 0.012378

9938 rno-let–7i–5p

0.353284 0.007104

28191 rno-miR–30e–5p

0.371176 0.018072

11020 rno-miR–22–3p

0.287853 0.011369

11208 rno-miR–207

0.329922 0.010157

4610 rno-miR–126a–3p

0.429071 0.042137

42686 rno-miR–136–3p

0.390576 0.009291

11007 rno-miR–206–3p

0.443065 0.036164

13485 rno-miR–10a–5p

0.426275 0.016445

145820 rno-let–7c–5p

0.467619 0.012298

0.484288 0.031295

148308 rno-miR–702–5p

0.403023 0.025969

148435 rno-miR–672–3p

0.354483 0.000445

148316 rno-miR–134–3p

0.475952 0.001026

30787 rno-miR–125b–5p

0.476592 0.024444

17752 rno-let–7f–5p

0.307114 0.000978

42511 rno-miR–99a–3p

0.480919 0.023114

146080 rno-miR–666–5p

0.320652 0.019258

11273 rno-miR–352

0.40639 0.01948

146160 rno-miR–133b–3p

0.365804 0.013484

146086 rno-miR–30a–5p

0.360244 0.021575

147162 rno-let–7a–5p

0.360995 0.0044

169132 rno-miR–382–3p

0.450157 0.049529

148348 rno-miR–3573–3p

0.456897 0.029535

46483 rno-miR–27a–3p

0.47107 0.04387

42641 rno-miR–145–5p

0.483403 0.038325

42712 rno-miR–742–5p

0.303099 0.002293

14294 rno-miR–1–3p

0.273701 0.011079

42496 rno-miR–181c–5p

0.435252 0.027404

42472 rno-miR–190b–5p

0.17921 0.013721

10943 rno-miR–136–5p

42769 rno-let–7b–3p

145943 rno-miR–100–5p

0.40957 0.034901

0.417566 0.017105

168778 rno-miR–501–3p

0.395747 0.01478

10977 rno-miR–183–5p

0.489697 0.006857

146112 rno-miR–30b–5p

0.469834 0.032755

148131 rno-miR–9b–5p

0.334163 0.041709

148309 rno-miR–3068–3p

0.412111 0.012813

46835 rno-miR–483–5p

0.129842 0.019983

148059 rno-miR–493–5p

0.444454 0.012715

14271 rno-miR–539–5p

0.404318 0.026212

42741 rno-miR–760–5p

0.385589 0.004902

146008 rno-miR–26b–5p

0.408252 0.04242

19585 rno-miR–148b–3p

0.346211 0.024874

146144 rno-miR–678

0.301297 0.022062

33596 rno-miR–126a–5p

0.421252 0.036279

42763 rno-miR–347

0.337598 0.001603

31867 rno-miR–145–3p

0.492177 0.027952

• Condition pairs: T vs C. • Fold Change cut-off: 2.0.

• P-value cut-off: 0.05.

• Column “ID”: array ID of the probes, each miRNA always has its unique probe, but some miRNAs may have two different probes.

• Column “Name”: the name of each miRNA. • Column “Fold change”: the ratio of normalized intensities between two conditions (use normalized data, ratio scale).

• Column “P-value”: T-test result between samples in different groups.

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DISCUSSION Burn trauma probably represents the largest stimulus for muscle protein catabolism. This state is characterized by an accelerated catabolism of the lean or skeletal mass that results in a clinical negative balance of nitrogen and muscle wasting.[3] Negative nitrogen balance and accelerated muscle protein breakdown are characteristics of burn injury.[9] Burn survivors experience a profound and prolonged loss of lean body mass, fat mass, and bone mineral density, associated with significant morbidity and reduced quality of life.[23] MicroRNAs (miRNAs), which regulate the stability and/or the translational efficiency of target messenger RNAs (mRNAs), have been ascribed diverse functions, including regulation of proliferation, differentiation, senescence and death.[14] Previous studies have showed that miRNAs play critical role in skeletal muscle wasting. In chronic kidney disease (CKD) induced muscle wasting, miR–29 was suppressed in muscle, which leads to higher expression of the transcription factor Ying Yang–1, thereby suppressing myogenesis.[18] FoxO1 is a dominant mediator of CKD-induced muscle wasting, and miR–486 coordinately decreases FoxO1 and PTEN to protect against this catabolic response.[19] Pharmacological agents targeting miR–486 and other miRs, involved in muscle mass regulation, could potentially be developed into therapeutic agents for muscle wasting.[20] TNF-related weak inducer of apoptosis (TWEAK) affects the expression of several genes and microRNAs involved in inflammatory response, fibrosis, extracellular matrix remodeling, and proteolytic degradation which might be responsible for TWEAK-induced skeletal muscle loss. TWEAK inhibits the expression of several miRs including muscle-specific miR–1–1, miR–1–2, miR–133a, miR133b and miR–206.[21] In the present study, the result of microarray analysis showed that thermal injury-mediated a total of 69 deregulated miRNAs in the skeletal muscles, in which 4 miRNAs were upregulated and 65 miRNAs were down-regulated. These deregulated miRNAs may potentially had an important effect in biological pathways essential for skeletal muscle dysfunction to burn trauma.

In addition, since the microarray analysis was just for roughly screening the altered miRNA, we will validate the deregulated miRNAs precisely by the quantitative real-time PCR, predict the target mRNAs of changed miRNAs and perform an deep biomathematics analysis of multiple miRNA target genes by GO and KEGG. This work may be the foundation of further research due to the pathology of muscle dysfunction in burn trauma.

Acknowledgments This work was supported by the National Natural Science Foundation of China (81120108041, 81471873 and 246

81201466), State Key Program of the General Logistics Department of PLA (BWS14J048), and Beijing Natural Science Foundation (7144250). The authors wish to thank KangChen Bio-tech Shanghai P.R. China for the microarray work.

Conflict of interest: None declared.

REFERENCES 1. Yasuhara S, Perez ME, Kanakubo E, Yasuhara Y, Shin YS, Kaneki M, et al.

Skeletal muscle apoptosis after burns is associated with activation of proapoptotic signals. Am J Physiol Endocrinol Metab 2000;279:E1114–21.

2. Wu X, Baer LA, Wolf SE, Wade CE, Walters TJ. The impact of muscle disuse on muscle atrophy in severely burned rats. J Surg Res 2010;164:e243–51.

3. Beça A, Egipto P, Carvalho D, Correia F, Oliveira B, Rodrigues A, et al.

Nitrogen balance assessment in burn patients. [Article in Portuguese] Acta Med Port 2010;23:883–90. [Abstract] 4. Herndon DN, Ramzy PI, DebRoy MA, Zheng M, Ferrando AA, Chinkes DL, et al. Muscle protein catabolism after severe burn: effects of IGF1/IGFBP-3 treatment. Ann Surg 1999;229:713–22.

5. Padfield KE, Astrakas LG, Zhang Q, Gopalan S, Dai G, Mindrinos MN, et al. Burn injury causes mitochondrial dysfunction in skeletal muscle.

Proc Natl Acad Sci U S A 2005;102:5368–73.

6. Wu X, Wolf SE, Walters TJ. Muscle contractile properties in severely burned rats. Burns 2010;36:905–11.

7. Porter C, Herndon DN, Sidossis LS, Børsheim E. The impact of severe burns on skeletal muscle mitochondrial function. Burns 2013;39:1039– 47.

8. Solomon V, Madihally S, Yarmush M, Toner M. Insulin suppresses the increased activities of lysosomal cathepsins and ubiquitin conjugation system in burn-injured rats. J Surg Res 2000;93:120–6.

9. Chai J, Wu Y, Sheng Z. The relationship between skeletal muscle proteolysis and ubiquitin-proteasome proteolytic pathway in burned rats.

Burns 2002;28:527–33.

10. Duan X, Berthiaume F, Yarmush D, Yarmush ML. Proteomic analysis of altered protein expression in skeletal muscle of rats in a hypermetabolic state induced by burn sepsis. Biochem J 2006;397:149–58.

11. Fang CH, Li B, James JH, Yahya A, Kadeer N, Guo X, et al. GSK-3beta activity is increased in skeletal muscle after burn injury in rats. Am J Physiol Regul Integr Comp Physiol 2007;293:R1545–51.

12. Baczyńska D, Michałowska D, Witkiewicz W. The role of microRNA in ischemic diseases-impact on the regulation of inflammatory, apoptosis and angiogenesis processes. [Article in Polish] Przegl Lek 2013;70:135– 42. [Abstract] 13. Huang ZP, Neppl RL Jr, Wang DZ. Application of microRNA in cardiac and skeletal muscle disease gene therapy. Methods Mol Biol 2011;709:197–210.

14. Luo W, Nie Q, Zhang X. MicroRNAs involved in skeletal muscle differentiation. J Genet Genomics 2013;40:107–16.

15. Rogaev EI, Borinskaia SA, Islamgulov DV, Grigorenko AP. Human microRNA in norm and pathology. [Article in Russian] Mol Biol (Mosk) 2008;42:751–64. [Abstract] 16. Cardinali B, Castellani L, Fasanaro P, Basso A, Alemà S, Martelli F, et al.

Microrna-221 and microrna-222 modulate differentiation and maturation of skeletal muscle cells. PLoS One 2009;4:e7607.

17. Wang XH. MicroRNA in myogenesis and muscle atrophy. Curr Opin Clin Nutr Metab Care 2013;16:258–66.

18. Wang XH, Hu Z, Klein JD, Zhang L, Fang F, Mitch WE. Decreased miR29 suppresses myogenesis in CKD. J Am Soc Nephrol 2011;22:2068–76.

19. Xu J, Li R, Workeneh B, Dong Y, Wang X, Hu Z. Transcription factor FoxO1, the dominant mediator of muscle wasting in chronic kidney dis-

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Haijun et al. Detection of the MicroRNA expression profile in skeletal muscles of burn trauma at the early stage in rats ease, is inhibited by microRNA-486. Kidney Int 2012;82:401–11.

20. Mak RH, Cheung WW. MicroRNAs: a new therapeutic frontier for muscle wasting in chronic kidney disease. Kidney Int 2012;82:373–4.

21. Panguluri SK, Bhatnagar S, Kumar A, McCarthy JJ, Srivastava AK, Cooper NG, et al. Genomic profiling of messenger RNAs and microRNAs reveals potential mechanisms of TWEAK-induced skeletal muscle wasting in mice. PLoS One 2010;5:e8760.

22. Duan H, Chai J, Sheng Z, Yao Y, Yin H, Liang L, et al. Effect of burn injury on apoptosis and expression of apoptosis-related genes/proteins in skeletal muscles of rats. Apoptosis 2009;14:52–65.

23. Pedroso FE, Spalding PB, Cheung MC, Yang R, Gutierrez JC, Bonetto A, et al. Inflammation, organomegaly, and muscle wasting despite hyperphagia in a mouse model of burn cachexia. J Cachexia Sarcopenia Muscle 2012;3:199–211.

DENEYSEL ÇALIŞMA - ÖZET OLGU SUNUMU

Sıçanlarda yanık travmalı iskelet kaslarında erken evrede mikro-RNA ekspresyon profili Dr. Zhang Haijun, Dr. Yu Yonghui, Dr. Chai Jiake, Dr. Duan Hongjie Yanık ve Plastik Cerrahi Bölümü, Pla Genel Hizmet Hastanesiyle bağlantılı İlk Hastane, Beijing, Çin

AMAÇ: Ciddi yanık travmaları kalıcı hipermetabolik yanıtla ilişkili olup kas kütlesinin uzun süreli kaybına nitrojen ile kas kaybı arasında klinik negatif dengenin bozulmasına yol açmaktradır. MikroRNA’lar (miRNA’lar) hedef mRNA’ların degradasyonunu teşvik ederek veya çevrimlerini engelleyerek gen ekspresyonunu negatif yönde post-transkripisyonel regülasyonunda kritik bir rol oynamaktadır. Ciddi yanık travmasından sonra miRNA’ların katıldığı iskelet kası kaybının mekanizmaları hâlâ anlaşılmış değildir.

GEREÇ VE YÖNTEM: Bu çalışmada mikrodizilim yöntemi kullanılarak erken evrede sıcağa maruz bırakılmış sıçanların iskelet kaslarındaki miRNA’ların ekspresyonlarındaki değişiklikler saptandı. Tüm veriler ortalama±standart sapma olarak sunuldu. İstatistiksel analizlerde bağımsız Student t-testi ve tek-yönlü ANOVA testi kullanıldı. Anlamlılık düzeyi olarak p<0.05 ve mikrodizilim yönteminde değişiklik katlarının kestirim değeri olarak 2.0 belirlendi. Eksprese edilen ve önemli farklılıklar gösteren miRNA’lar Volcano Grafik filreleme yöntemiyle belirlendi. MEV yazılım sistemi (v4.6, TIGR) kullanılarak hiyerarşik küme analizi gerçekleştirildi.

BULGULAR: Normal ve yaralanmış dokularda binlerce miRNA incelenebilmesine karşın bunların yalnızca 69’unda önemli derecede up-regülasyon veya down-regülasyona uğramıştı. Bu yöntem ısıya maruz bırakılmış sıçanların eşleştirilmiş iskelet kası dokularının ayrımında kullanılabilir.

TARTIŞMA: Yanık travmasından sonra iskelet kası kaybının patogenezinde miRNA’ların disregülasyonu potansiyel bir rol oynamaktadır.

Anahtar sözcükler: Kas kaybı; mikroRNA; profil; yanık.

Ulus Travma Acil Cerrahi Derg 2015;21(4):241–247

doi: 10.5505/tjtes.2015.80707

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ORIGIN A L A R T IC L E

Evaluation of gunshot wounds in the emergency department Mehmet Ali Karaca, M.D.,1 Nil Deniz Kartal, M.D.,1 Bülent Erbil, M.D.,1 Elif Öztürk, M.D.,1 Mehmet Mahir Kunt, M.D.,1 Tevfik Tolga Şahin, M.D.,2 Mehmet Mahir Özmen, M.D.2 1

Department of Emergency Medicine, Hacettepe University, Faculty of Medicine, Ankara

2

Department of General Surgery, Hacettepe University Faculty of Medicine, Ankara

ABSTRACT BACKGROUND: This study aimed to evaluate injury patterns of patients admitted to the emergency department with gunshot wounds, results of imaging studies, treatment modalities, outcomes, mortality ratios, and complications.

METHODS: A retrospective descriptive study was carried out including a total number of one hundred and forty-two patients admitted to Hacettepe University Emergency Department with gunshot injuries between January 1, 1999 and December 31, 2013. The Glasgow Coma Scale (GCS), Revised Trauma Score (RTS), Injury Severity Score (ISS), and theTrauma and Injury Severity Score (TRISS) probability of survival for penetrating trauma were calculated for all patients.

RESULTS: Among the one hundred and forty-two patients in the study, one hundred and twenty-eight (90.1%) were male. Mean age was 36 years. On admission, the average GCS score was 13, mean RTS was 6.64, median ISS was 5 and median TRISS probability for survival was 99.4% for penetrating trauma. Fluid was detected in three (13%) patients in FAST, whereas intra-abdominal solid organ injury and bowel injury were detected in 11 (58%) patients in abdominal CT. The pneumothorax, hemothorax and lung injuries were detected in 10 (43.5%) patients, whereas hemothorax was detected only in one patient with thoracic injury by chest X-ray. Twenty four (16.9%) patients died; eighteen patients (75%) had isolated severe intracranial injuries, two (8.9%) had thoracic injuries with head and neck injuries, and four (16.7%) patients had intra-abdominal organ injuries (one with concomitant head injury). Ten patients were brought to the ED in cardiopulmonary arrest. In dead patients, GCS, RTS and TRISS were significantly lower, and ISS were significantly higher than in surviving patients. Twenty three (95.8%) patients were in critical injury level (ISS 25–75, actually ISS >50) in the exitus group.

CONCLUSION: Mortality rates in gunshot wound patients with cranial injuries are very high. Spontaneous return is not seen in patients brought to the ED in arrest state. Bullets can cause internal organ injuries which can be greater than expected. In thoracoabdominal gunshot wound injuries, conventional X-ray and bedside FAST can be ineffective in detecting the whole extent of intrathoracic and intra-abdominal injuries. Thus, thoracic and abdominal CT should be planned early for hemodynamically stable patients in order to eliminate causes of fatality and make a timely and correct diagnosis. ISS, RTS and GCS are useful in predicting prognosis and mortality.

Especially in patients with ISS scores >50, the mortality rate can be as high as 96%.

Key words: Emergency department; GCS; gunshot injury; ISS; RTS; trauma; TRISS.

INTRODUCTION Firearms can be obtained very easily in our country as well as in the world; therefore, the injury and mortality rates due to firearms are steadily increasing. Nationwide, firearms were Address for correspondence: Mehmet Ali Karaca, M.D. Hacettepe Üniversitesi Tıp Fakültesi, Acil Tıp Anabilim Dalı, Ankara, Turkey Tel: +90 312 – 305 25 03 E-mail: mehmetalikaraca@gmail.com Qucik Response Code

Ulus Travma Acil Cerrahi Derg 2015;21(4):248–255 doi: 10.5505/tjtes.2015.64495 Copyright 2015 TJTES

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the third-leading cause of injury-related deaths following poisoning and motor vehicle accidents in 2010. In 2010, approximately 31.000 deaths occurred in the USA due to gunshot wounds. This is the equivalent of more than 85 deaths per day in the emergency department (ED). Furthermore, 73.505 Americans were treated in the ERs for non-fatal gunshot wounds in 2010.[1] Injuries are related to the energy and speed of the bullet. Bullets spin in through their route, and therefore, cause much more severe injuries than expected. Initial physical findings may not correlate to actual injuries, and the physician may be faced with a more severe case than anticipated. Many of these patients could be spending the golden hours of trauma in admission. Early evaluation and intervention in patients with gunshot injuries is, therefore, of most importance.

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Karaca et al. Evaluation of gunshot wounds in the emergency department

Table 1. Characteristic of patients

Mean (Min-Max)

Age

36 (18–77)

Systolic blood pressure (mmHg)

110 (0–239)

(<90 mmHg in 25)

Diastolic blood pressure (mmHg)

68 (0–136)

(<60 mmHg in 23)

Heart rate (beats/min)

87 (0–156)

(>120 b/min in 14)

Respiratory rate (resp/min)

18 (0–77)

(>30 resp/min in 5)

Glasgow Coma Scale

13 (3–15)

(<15 in 30)

Revised Trauma Score

6.64 (0–7.84)

(Median 7.74)

Injury Severity Score

16.34 (1–75)

(Median 5.0) (Median 99.1%)

TRISS

80.69% (0.1–99.4)

Length of stay (day)

4 (0.2–60)

Mortality ratio

16.9%

TRISS: Trauma and Injury Severity Score probability of survival rate for penetrating trauma.

This study aimed to evaluate injury patterns of patients admitted to the emergency department with gunshot wounds, results of imaging studies, treatment modalities, outcomes, mortality ratios, and complications.

MATERIALS AND METHODS A retrospective descriptive study was carried out including a total number of one hundred and forty-two patients admitted to Hacettepe University Emergency Department with gunshot injuries between January 1, 1999 and December 31, 2013. The Glasgow Coma Scale (GCS), Revised Trauma Score (RTS), Injury Severity Score (ISS), and the Trauma and Injury Severity Score (TRISS) probability of survival for blunt trauma and penetrating trauma were calculated for all patients.

The extent of injury was graded according to the ISS as: mild (1–8), moderate (9–14), severe (15–24) and critical (≥25).

[2] In the present study, the evaluated parameters included mechanism of injury, results and types of diagnostic imaging, modality of treatment, consulted departments, hospitalization ratio, length of stay and complication rate and type.

Statistical analysis was performed using the Statistical Package for Social Sciences (SPSS) version 21 for Windows, and p<0.05 was considered significant. Mean values were used and independent t test was applied in normally distributed variants, median values were used and Mann-Whitney U test was applied in non-normally distributed variants. The relations of categorical variants were evaluated with an X2 test.

RESULTS Demographic characteristics of the patients are summarized in Table 1. Among the one hundred and forty-two patients in the study, one hundred and twenty-eigh (90.1%) were male.

Mean age was 36 (range, 18–77) years.

As for the location of the injuries, the majority of injuries were detected in the lower extremities (n=68, 47.9%), the head and neck (n=44, 31%) and upper extremities (n=41, 28.9%) (Table 2). On admission, hypotension was detected in twenty-five (18%), tachycardia in fourteen (10%) and tachypnea in five (4%) patients. On admission, GCS, RTS, ISS and

Table 2. Injury area and scores Injury site n %

GCS Mean (min-max)

RTS Mean (min-max)

ISS Mean (min-max)

TRISS (%) Mean (min-max)

14.5 (12–15)

7.6 (7.11–7.84)

7 (1–11)

98.5 (96.5–99.4)

Mortality (n=24)

Lower extremity

68

48

Head and neck

44

31

9 (3–15)

4.7 (0–7.84)

34 (1–75)

50.8 (0.1–88.4)

Upper extremity

41

29

14 (13–15)

7.3 (6.47–7.84)

9 (1–14)

96.4 (88–99.4)

Thorax

36

25

13 (3–15)

6.6 (0–7.84)

20 (3–75)

77.8 (1–97.2)

2*

Abdominal

16

11

13 (3–15)

6.5 (0–7.84)

19 (2–75)

79.7 (0.1–91.3)

4†

18

GCS: Glasgow Coma Scale; RTS: Revised Trauma Score; ISS: Injury Severity Score; TRISS: Trauma and Injury Severity Score probability of survival rate for penetrating trauma (*2 patients with concomitant head and neck injury, † one patient had concomitant head trauma).

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Table 3. Injury area and imaging studies Injury site n %

Lower extremity

68

48

44

FAST Cranial CT (n=23) (n=23)

41

29

Intracranial injury

36

25

(n=20)

Bone fractures

Thorax

± bullet (n=16) Hemothorax (n=1)

Pneumo-hemothorax

Abdominal

16

Abdominal CT (n=19)

± bullet (n=22)

31

Upper extremity

Thorax CT (n=25)

Bone fractures

Head-Neck

X-Ray (n=64)

11

(n=10)

Fluid (n=3)

Solid organ and bowel

injury (n=11)

FAST: Focused assessment with sonography for trauma.

TRISS were calculated and the average GCS score was 13.

The Glasgow Coma Scale score was lower than 15 in thirty (21%) patients. Mean RTS was 6.64 (0–7.84). Mean ISS was 16.34, median ISS was 5 (1–75). Mean TRISS probability of survival was 80.6% (0.1–9.4%), and median TRISS probability for survival was 99.4% for penetrating trauma. The results of the scoring systems are summarized in Table 2.

The results of the diagnostic imaging are summarized in Table 3. The diagnostic imaging modalities and their results were evaluated. Conventional plain X-ray graphics were the most commonly utilized imaging modality. It was helpful when performed for injuries in the extremities and to detect the projectile object in the torso and extremities of the individual.

X-ray was performed in sixty-four patients, bullet fragments and bone fractures in extremities were detected in thirtyeight (59%).

Focused assessment with sonography for trauma (FAST) was

performed in twenty-three patients, and fluid was detected in three (13%) patients. Abdominal computed tomography (CT) was performed in nineteen patients and intra-abdominal solid organ injury and bowel injury were detected in eleven (58%) patients. There was superiority of abdominal CT in detecting of intra-abdominal injury in abdominal trauma patients (p<0.001). Thorax CT was performed in twenty-five patients and pneumothorax, hemothorax and lung injuries were detected in ten (43.5%) patients, whereas hemothorax was detected only in one patient with thoracic injury by chest X-ray. The sensitivity of thorax CT was much higher in detecting intra-thoracic organ injury in gunshot wounds than X-ray (p<0.001). Cranial CT was performed in twentythree patients, and major intracranial injuries were detected in twenty (87%) of these patients on cranial CT. This shows the fact that cranial CT is usually ordered in very specific conditions, and therefore, the specificity and sensitivity in detecting cranial lesions in the setting of gunshot injury is very high.

Table 4. Consultations and treatment Department

n

%

Orthopedic

72 51

Surgery

Wound care

23

33

Thoracic-Cardiovascular Surgery

52

37

12

16

Brain Surgery

27

19

15

2

Plastic & Reconstructive Surgery

26

18

8

7

General Surgery

21

15

7

4

Ear-Nose-Throat

5 3.5

3

1

Ophthalmology

2 1.4

1

Urology

2 1.4

Total

250

Procedures (n=142) Dressing 2

6

2 70 (49%)

64 (45%)

8 (6%)

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Karaca et al. Evaluation of gunshot wounds in the emergency department

Table 5. Injury area and scores Outcome n %

GCS Mean (min-max)

ISS Mean (min-max)

RTS Mean (min-max)

TRISS (%) Mean (min-max) 99.2 (97.2–99.4)

ED-discharge

55

38.7

15

4.4 (1–26)

7.82 (7.55–7.84)

Ward-discharge

49

34.5

14.4 (5–15)

11.6 (2–50)

7.41 (1.87–7.84)

91.5 (8.9–99.3)

ICU-discharge

4

2.8

12.7 (6–15)

15.7 (2–29)

7.58 (7.11–7.84)

97.3 (93.3–99.2)

Treatment refusal

7

4.9

15

5.7 (1–16)

7.63 (6.38–7.84)

98.9 (97.5–99.4)

Refer to another hospital

3

2.1

15

6.3 (4–9)

7.84

99.2 (99.1–99.3)

Exitus

24

16.9

3.5 (3–8)

57.7 (16–75)

1.77 (0–3.87)

5.8 (0.1–44)

Total

142 100

GCS: Glasgow Coma Scale; RTS: Revised Trauma Score; ISS: Injury Severity Score; TRISS: Trauma and Injury Severity Score probability of survival rate for penetrating trauma. ED: Emergency Department; ICU: Intensive Care Unit.

The consulted departments and the results are summarized in Table 4. The most frequent consultations were to orthopedics (51%), thoracic-cardiovascular surgery (37%), neurosurgery (19%), plastic surgery (18%) and general surgery (14.8%) respectively. Seventy patients (49%) underwent surgical treatment, local wound care was performed in sixtyfour (45%) and dressing was performed only in eight (6%) patients. The most frequent surgical procedures were performed by the orthopedics (n=23, 16%) and neurosurgery departments (n=15, 15%).

The outcomes of the patients are summarized in Table 5. Fifty-five (38.4%) patients were treated and discharged from the emergency department (ED), and forty-nine (34.5%) patients were hospitalized and discharged from various in-patient wards, four (2.8%) of the patients were hospitalized in the intensive care unit (ICU) and twenty-four (16.9%) patients died. The average length of stay in the hospital was 4 days.

The average lengths of stay in the ED, in-patient wards and the ICU were 10 hours, 8 days and 16 days, respectively.

Complications developed in ten (7%) patients, which are summarized in Table 6. The most frequent complication was central and peripheral nervous system injury.

Twenty four (16.9%) patients died; fifteen of these (62.5%) died within 24 hours. Eighteen of the patients that died (75%) had isolated severe intracranial injuries, two (8.9%) had thoracic injuries with head and neck injuries, and four (16.7%) patients had intra-abdominal organ injuries (one with concomitant head injury). Ten patients were brought to the ED in cardiopulmonary arrest. Twelve patients (50%) died in the ED (seven of these were brought in arrest), eight (33.3%) patients died in the Neurosurgery ICU (one of these was brought in arrest) and four patients (16.7%) died in the peri/ postoperative period in the general surgery department (two of these were brought in arrest). One patient who died in the Neurosurgery ICU was accepted as an organ donor two days following hospitalization.

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Mortality ratios of patients according to injured part of body were as follows: head and neck trauma: 41%, thorax trauma: 5.5%, abdominal trauma: 25%. In consideration of radiological findings, mortality ratios in case of critical injury were as follows: the mortality in intracranial injury was 90%, in thoracic injury it was 20% and in intra-abdominal injury it was 36%.

There was significant increase in mortality ratios in patients with intracranial injury (p<0.001). The mortality ratio of patients that were brought to the ED in arrest state was 100%.

Arrest state in admission to ED could be an independent risk factor for mortality in gunshot wounds.

On admission physiologic and anatomic trauma scores were calculated for each injury area of body. GCS, RTS, TRISS probability for survival were significantly lower and ISS was higher in head and neck trauma patients than other groups (GSC: 9, RTS: 4.7, TRISS: 50.8%, and ISS: 34) (p=0.001). In contrast, RTS, and TRISS were significantly higher and ISS scores significantly lower in extremity trauma patients (p=0.01) (Table 2).

Physiologic and anatomic scores were compared according to the outcome in dead and surviving patients. In dead patients, GCS, RTS and TRISS were significantly lower and ISS were significantly higher than in surviving patients (p=0.001) (Table 5).

When the patients’ outcome was compared to ISS grades; Table 6. Complications Complications n Quadriplegia/paraplegia 4 Brachial plexus and peripheral nerve palsy

2

Pneumonia 2 Wound infection

1

Amputation 1 Total 10

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Karaca et al. Evaluation of gunshot wounds in the emergency department

one patient (4.2%) was in severe injury levels (ISS 15–24) and twenty-three (95.8%) patients were in critical injury level (ISS 25–75, actually ISS>50) in the exitus group. In addition, 75% of patients treated and discharged from the ICU had in severe and critical injury grades, whereas 89.1% of the patients treated and discharged from ED had mild ISS grades (1–9).

These differences between the groups were statistically significant (p=0.001) (Table 7).

DISCUSSION While gunshot deaths were previously prevalent in the military arena, they have also become more widespread among the general public since the 1980s due to the proliferation of firearms acquired by civilians. Thus, the number of patients with gunshot wounds admitted to civil hospital emergency departments is steadily on the rise.[3] Two different types of firearms are produced with low and high bullet speeds. Bullets with high speed have high levels of energy and cause greater tissue damage than others because of cavitation formation. The bullet trajectory is curved due to gravity, and as the bullet strikes an object it slows, and its energy is transferred to the object. Thus, most bullets can be found in bone fragments. The density of tissue affects the efficiency of energy transmission. Similarly, the strength and elasticity of an object determine the degree of damage.

Solid organs are dense and have low resilience. Fluid filled hollow organs transmit energy and cause increased damage.

However, air filled organs absorb energy, and therefore, cause less damage. Air in lungs absorbs energy; the parenchyma is compressed and rebounds, thus pneumothorax or hemothorax can occur. Bone resists displacement until it shatters. The cavitational energy trapped inside the skull causes serious and lethal bleeding.[4–6] Gunshot wounds are most prevalent among males aged 30– 40. Karagoz et al. have stated the percentage as 3.75.[7] Molina et al. have stated that the mean age in patients who attempted

suicide with firearms is 46.7, whereas the mean age of gunshot victims is 34.3, the male to female ration being 5:1. The same ratio is 10:1 according to Balci et al., while Köksal et al. claim that males comprise 88.9% of all victims, and that the mean age 34.5. In our study, similarly to the data on mean age in the literature, we found the mean age to be 36 and the male to female ratio, corresponding to Balci and Köksal, to be 9:1.[8–10] Anatomical and physiological patient scores (GCS, RTS and ISS) were found to be similar to other studies while ISS scores were lower. The lower ISS results in our study are thought to be due to the prevalence of injuries in extremities.[11] The distribution of injuries on the body diagram shows a similar tendency to prevalence as in the study by Sheffy et al. who stated lower extremity injuries to be the most predominant (42%), followed by head and neck injuries (39%) and thoracic injuries (23.5%).[11] Our study similarly showed the most common injuries to be in the lower extremities (48%), followed by head and neck injuries (31%) and injuries to the thorax. Due to the prevalence of injuries to the extremities, the most frequent consultations in our study were to the orthopedics department, followed by the cardiothoracic surgery and neurosurgery departments.

In most cases of penetrating trauma, surgical treatment is necessary. Rates for this treatment vary according to the location and severity of the injury. In their study on gunshot and explosion injuries, Peleg et al. have stated surgical treatment to be necessary in 58% of gunshot wound cases.[12] Martins et al. have found the rate of surgical treatment in penetrating cranial injuries to be 58.9%.[13] The rate of surgical treatment for injuries to the extremities and femur fractures in civilian patients is 46%.[14] In the penetrating abdominal injury guide, the rate of early laparotomy in thoracoabdominal injuries is 23%, while the rate of laparotomy in general is 48%. The rate of local wound exploration is 47%.[15] Similarly to the rates in the literature, we found in our study that 49% of patients received surgical treatment. The highest rate of surgical treat-

Table 7. Outcome vs ISS grades Outcome

Mild (1-8)

Moderate (9-14)

Severe (15-24)

Critical (≥25)

Total

n % n % n % n % n %

ED-discharge

49 89.1 4 7.3 1 1.8 1 1.8 55 100

Ward-discharge

26 53.1 8 16.3 6 12.2 9 18.4 49 100

ICU-discharge

1 25 0 0 2 50 1 25 4 100

Treatment refusal

6 85.7 0 0 1 14.3 0 0 7 100

Refer to another hospital

2

66.7

1

33.3

0

0

0

0

3

100

Exitus

0 0 0 0 1 4.2 23 95.8 24 100

Total

84 59.2 13 9.2 11 7.7 34 23.9 142 100

ED: Emergency Department; ICU: Intensive Care Unit.

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Karaca et al. Evaluation of gunshot wounds in the emergency department

ment (55%) was found in the case of patients with head and neck injuries, followed by those with abdominal injuries (33%) and injuries to the extremities (32%). Local wound care was performed on 45% of the patients.

Diagnostic imaging (X-rays, USG and CT) is commonly performed in gunshot wounds to spot pathologies. X-ray imaging is very helpful in injuries to the extremities, to detect pathologies in the bone tissue, bullets, and bullet fragments.

In thoracoabdominal injuries, X-ray imaging is very valuable in detecting hemothorax, pneumothorax and injuries to the diaphragm, as well as spotting bullet fragments.[16,17] In our study, X-ray proved valuable in detecting pathologies in the bone tissue in 60% of extremity injury cases.

FAST and CT are steadily becoming more important in the diagnosis of thoracic and abdominal injuries. While bullet exit wounds are easily identifiable during physical examination, the same examination cannot detect the path of the bullet and the damage caused within the tissues.[11] Intra-abdominal free fluid and increase of fluid in the pericardial cavity can be spotted with bedside FAST imaging. In hemodynamically unstable patients, early detection of intra-abdominal injuries facilitates early diagnosis and treatment. Diaphragm injuries and vascular injuries are common in gunshot wounds due to the ballistic effect of the bullet, but hard to detect with X-ray; they can, however, be spotted with thorax CT which is also useful in detecting lung injuries, pneumothorax, hemothorax, cardiac injuries and hemopericardium (with 100% sensitivity).

In gunshot wounds to the abdomen, abdominal CT is useful for providing information on the bullet’s path through the tissue. While bedside FAST imaging is useful for detecting intraabdominal injuries, it is ineffective in spotting retroperitoneal and intestinal injuries. Abdominal CT, useful in this case, also makes non-surgical observation of gunshot wound patients possible.[15] In our study, X-ray only detected hemothorax in one of the patients with thoracic injuries while damages to the lungs and hemo-pneumothorax were found in ten of the 25 patients in the same group (40%) with thoracic CT. Similarly, FAST performed on twenty-three patients with gunshot wounds to the abdomen detected free fluid in only three of them (13%) while abdominal CT spotted damage including intra-abdominal solid organ and bowel injury in eleven of the 19 patients (58%) on whom it was performed. This shows that in hemodinamically stable gunshot wound patients, thoracoabdominal CT should be performed for timely and correct diagnosis. In the case of patients with head and neck injuries, CT is regarded as the most valuable imaging method for identifying pathologies and arriving at prognoses.[17] In our study, cranial CT performed on twenty-three patients in the group with head and neck injuries revealed intracranial injuries in 20 of them (87%).

The severity of gunshot wound cases admitted to the ED and the distribution and number of affected organs determine Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

hospitalization rates. Köksal et al. have found the hospitalization rate in gunshot wound patients to be 75% and the rate of patients treated in the ED and discharged to be 5%. Mean length of the hospital stay was found to be 9 days.[10] Peleg et al. have found the rate of ICU stays for gunshot wound patients to be 23%, with longer stays in the case of multiple wounds.[12] In our study, ICU stay rate was found to be 2.8% and the mean length of ICU stay to be four days. The comparatively short hospital stay durations are thought to be due to the low rate of patients hospitalized in the ICU. Mortality is high in gunshot wound cases and is influenced by the location of the injury and the number of organs affected. Studies have found the general mortality rate in gunshot wound cases to be between 12 and 16%. While mortality is 17% in the case of isolated injury to the chest and abdomen, it is 80% in the case of abdominal injuries with concomitant brain and lung injury. Gunshot injury deaths generally occur within the first day.[10–12] The general mortality rate in our study was %16.9 (n=24). Twelve of the patients who died (50%) did so in the ED; seven of these had been brought to the ED in the arrest state. In patients with isolated intracranial injuries, the mortality rate was 41%. One patient with cranial injury became an organ donor.

Our study found return of spontaneous breathing and circulation to be very low in the case of patients with intracranial injuries brought to the ED in the arrest state. All of these patients died. Since patients with isolated head trauma are likely candidates for organ donation, cardiopulmonary resuscitation should be performed on these patients.

There are several studies about the efficacy of scoring systems for severity of injuries, prognosis and predicting mortality in gunshot wound patients. GCS, RTS, ISS and TRISS probability for survival are the scoring systems most commonly used in these cases. Low GCS (especially <5), low RTS and ISS higher than 16 (especially 16–75) have been found to be linked to high mortality rates.[10–13,18–21] Some recent studies indicate that in numerous patient groups, evaluating ISS scores of 25–75 showing critical injury in two parts of ISS 25–48 and 50–75 would be more useful.[22] Similarly to the finding in literature, our studye found the GCS and RTS scores and TRISS levels of exitus patients to be significantly low and their ISS levels to be significantly high (GKS: 3.5, ISS: 57.7, TRISS survival for penetrating trauma: 5.8). As many as 95.8% of the exitus patients had critical injuries according to ISS. The GCS and RTS scores calculated by taking injury locations into account were significantly lower in head and neck injuries than in other injuries. These findings show that low GCS (<5) and high ISS (>50) scores are useful and serviceable in predicting prognosis and mortality in gunshot wound patients.

Complications in gunshot wound cases depend on the location and severity of the injury. Injuries affecting the neurological system and causing long-term neurological damage are 253

Karaca et al. Evaluation of gunshot wounds in the emergency department

especially important.[23] In our study, the rate of complication development was found to be 7% with the most common complications being those affecting the central and peripheral nervous system.

Conclusion Mortality rates in gunshot wound patients with cranial injuries are very high. Spontaneous return is not seen in patients brought to the ED in arrest state, but patients with isolated intracranial injuries should be considered potential organ donors and resuscitated.

Bullets have high velocity and energy, which can cause internal organ injuries greater than expected. In thoracoabdominal gunshot wound injuries, conventional X-ray and bedside FAST can be ineffective in detecting the whole extent of intrathoracic and intra-abdominal injuries. Thus, thoracic and abdominal CT should be planned early for hemodynamically stable patients in order to eliminate causes of fatality and make a timely and correct diagnosis. ISS, RTS and GCS are useful in predicting prognosis and mortality. Especially in patients with ISS scores >50, the mortality rate can be as high as 96%.

Conflict of interest: None declared.

REFERENCES 1. Statistics on Gun Deaths & Injuries (Posted on November 16, 2012).

Available at http://smartgunlaws.org/gun-deaths-and-injuries-statistics/(Accessed 12.03.2015).

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

3. Necmioğlu NS, Subaşı M. Ateşli Silah yaralanması ile oluşan uzun kemiklerin tedavisi. TOTBİD Dergisi 2003;2:3-4:118–25.

4. Yılmaz A. Ateşli silahlarla oluşan yaralanmalar. TTB Dergisi 2004;50:167–78.

5. Bartlett CS, Helfet DL, Hausman MR, Strauss E. Ballistics and gunshot wounds: effects on musculoskeletal tissues. J Am Acad Orthop Surg 2000;8:21–36.

6. Eriş S, Orak M, Al B, Güloğlu C, Aldemir M. Factors Affectıng Mortalıty In Patıents Wıth Gunshot Injurıes. Marmara Medical Journal 2009;22;181–91.

7. Karagoz YM, Karagöz SD, Atılgan M, Demircan C. An Analysis of 133 Fiream Deaths. Adli Tıp Bülteni. 1996;1:122–6.

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8. Molina DK, DiMaio VJ, Cave R. Handgun wounds: a review of range and location as pertaining to manner of death. Am J Forensic Med Pathol 2013;34:342–7.

9. Balci Y, Canogullari G, Ulupinar E. Characterization of the gunshot suicides. J Forensic Leg Med 2007;14:203–8.

10. Köksal O, Ozdemir F, Bulut M, Aydin S, Almacioğlu ML, Ozgüç H. Comparison of trauma scoring systems for predicting mortality in firearm injuries. Ulus Travma Acil Cerrahi Derg 2009;15:559–64.

11. Sheffy N, Mintz Y, Rivkind AI, Shapira SC. Terror-related injuries: a comparison of gunshot wounds versus secondary-fragments-induced injuries from explosives. J Am Coll Surg 2006;203:297–303.

12. Peleg K, Aharonson-Daniel L, Stein M, Michaelson M, Kluger Y, Simon D, et al. Gunshot and explosion injuries: characteristics, outcomes, and implications for care of terror-related injuries in Israel. Ann Surg 2004;239:311–8.

13. Martins RS, Siqueira MG, Santos MT, Zanon-Collange N, Moraes OJ. Prognostic factors and treatment of penetrating gunshot wounds to the head. Surg Neurol 2003;60:98–104.

14. Vaidya R, Sethi A, Oliphant BW, Gibson V, Sethi S, Meehan R. Civilian gunshot injuries of the humerus. Orthopedics 2014;37:307–12.

15. Biffl WL, Moore EE. Management guidelines for penetrating abdominal trauma. Curr Opin Crit Care 2010;16:609–17.

16. Öztürk H, Dokucu AI, Otcu S, Onen A. The prognostic importance of trauma scoring systems for morbidity in children with penetrating abdominal wounds: 17 years of experience. J Pediatr Surg 2002;37:93–8.

17. Reginelli A, Russo A, Maresca D, Martiniello C, Cappabianca S, Brunese L. Imaging assessment of gunshot wounds. Semin Ultrasound CT MR 2015;36:57–67.

18. Finley CJ, Hemenway D, Clifton J, Brown DR, Simons RK, Hameed SM. The demographics of significant firearm injury in Canadian trauma centres and the associated predictors of inhospital mortality. Can J Surg 2008;51:197–203.

19. Smith JE, Kehoe A, Harrisson SE, Russell R, Midwinter M. Outcome of penetrating intracranial injuries in a military setting. Injury 2014;45:874–8.

20. de Souza RB, Todeschini AB, Veiga JC, Saade N, de Aguiar GB. Traumatic brain injury by a firearm projectile: a 16 years experience of the neurosurgery service of Santa Casa de São Paulo. Rev Col Bras Cir 2013;40:300–4.

21. Eryılmaz M, Tezel O, Taş H, Arzıman I, Oğünç GI, Kaldırım U, et al.

The relationship between Injury Severity Scores and transfusion requirements of 108 consecutive cases injured with high kinetic energy weapons: a tertiary center end-mode mortality analysis. [Article in Turkish] Ulus Travma Acil Cerrahi Derg 2014;20:39–44.

22. Rozenfeld M, Radomislensky I, Freedman L, Givon A, Novikov I, Peleg K. ISS groups: are we speaking the same language? Inj Prev 2014;20:330–5.

23. Topuz AK, Eroğlu A, Atabey C, Cetinkal A. Surgical treatment outcomes ın peripheral nerve lesions due to gunshot injuries: assessment of 28 cases. [Article in Turkish] Ulus Travma Acil Cerrahi Derg 2013;19:235–40.

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Karaca et al. Evaluation of gunshot wounds in the emergency department

ORİJİNAL ÇALIŞMA - ÖZET OLGU SUNUMU

Acil serviste ateşli silah yaralanmalarının analizi Dr. Mehmet Ali Karaca,1 Dr. Nil Deniz Kartal,1 Dr. Bülent Erbil,1 Dr. Elif Öztürk,1 Dr. Mehmet Mahir Kunt,1 Dr. Tevfik Tolga Şahin,2 Dr. Mehmet Mahir Özmen2 1 2

Hacettepe Üniversitesi Tıp Fakültesi, Acil Tıp Anabilim Dalı, Ankara Hacettepe Üniversitesi Tıp Fakültesi, Genel Cerrahi Anabilim Dalı, Ankara

AMAÇ: Bu çalışmada, acil servise ateşli silah yaralanması nedeniyle başvuran hastaların yaralanma özellikleri, görüntüleme yöntemlerinin sonuçları, tedavi türleri, sonlanım, ölüm ve komplikasyon oranları araştırıldı.

GEREÇ VE YÖNTEM: Bu geriye dönük tanımlayıcı çalışmaya 1 Ocak 1999 ile 31 Aralık 2013 tarihleri arasında Hacettepe Üniversitesi Erişkin Acil Servisi’ne ateşli silah yaranması nedeniyle getirilen 142 hasta alındı. Tüm hastalar için Glaskow Koma Skalası (GKS), Revize Travma Skoru (RTS), Yaralanma Ciddiyet Skoru (ISS) ve penetran yaralanmalarda Travma ve Yaralanma Ciddiyet Skoru ve Sağkalım Olasılığı (TRISS) oranları hesaplandı.

BULGULAR: Çalışmaya alınan 142 hastanın 128’i (%90.1) erkekti. Ortalama yaş 36 olarak hesaplandı. Başvuru anında ortalama GKS skoru 13, ortalama RTS 6.64, ortanca ISS 5 ve ortanca TRISS penetran travma için sağ kalım olasılığı %99.4 hesaplandı. FAST ile hastaların üçünde (%13) karın içi serbest sıvı saptanırken abdomen bilgisayarlı tomografi (BT) ile hastaların 11’inde (%58) solid organ ve bağırsak yaralanması saptandı. Direkt akciğer grafisi ile bir hastada hemotoraks saptanırken, toraks BT ile 10 (%43.5) hastada pnömotoraks, hemotoraks ve akciğer yaralanması tespit edildi. Çalışmada 24 hasta hayatını kaybetti; 18 (%75) hastada izole intrakraniyal yaralanma, iki (%8.9) hastada baş boyun yaralanmanın eşlik ettiği toraks yaralanması, dört (%16.7) hastada karın içi organ yaralanması (bir hastada kraniyal yaralanma eşlik ediyordu) bulunuyordu. Acil servise 10 hasta kardiyopulmoner arrest olarak getirildi. Hayatını kaybeden hastalarda GKS, RTS ve TRISS yaşayan hastalara göre anlamlı derecede düşük, ISS ise anlamlı derecede yüksek saptandı. Hayatını kaybeden hastaların 23’ü (%95.8) ISS’ye göre kritik yaralanma düzeyine (ISS 25–75, aralığında ve ISS >50) sahipti.

TARTIŞMA: Ateşli silahlara bağlı kraniyal yaralanmalarda mortalite düzeyleri çok yüksektir. Acil servise arrest olarak getirilen hastalarda spontan geri dönüş görülmemektedir. Kurşuna bağlı iç organ hasarı tahmin edilenden daha fazla olmaktadır. Toraks ve abdomendeki ateşli silah yaralanmalarında direkt grafiler ve FAST tanıda yetersiz olabilmektedir. Bu nedenle bu hastalarda ölümcül olan yaralanmaların erken dönemde tespit edilmesi için toraks ve abdomen BT istemi erken dönemde planlanmalıdır. Yaralanma Ciddiyet Skoru, RTS ve GKS prognoz ve mortaliteyi öngörmede yaralıdır. Özellikle ISS >50 olgularda mortalite oranı %96’ya kadar yükselmektedir.

Anahtar sözcükler: Acil servis; GKS; ateşli silah yaralanması; ISS; RTS; travma; TRISS. Ulus Travma Acil Cerrahi Derg 2015;21(4):248–255

doi: 10.5505/tjtes.2015.64495

Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

255

K Lİ NİK Ç A LI ŞM A

Acil servise trafik kazasına bağlı künt abdominal travma ile başvuran hastalarda klinik değerlendirme, laboratuvar parametreleri ve radyolojik sonuçların tedavi kararına ve cerrahi sonuçlarına etkisi Dr. İdil Güneş Tatar,1 Dr. Kerim Bora Yılmaz,2 Dr. Onur Ergun,1 Dr. Şener Balas,2 Dr. Melih Akıncı,2 Dr. Rıza Deryol,2 Dr. Gaye Ebru Şeker,2 Dr. Hakan Kulaçoğlu,2 Dr. Baki Hekimoğlu1 1

Dışkapı Eğitim ve Araştırma Hastanesi, Radyoloji Kliniği, Ankara

2

Dışkapı Eğitim ve Araştırma Hastanesi, Genel Cerrahi Kliniği, Ankara

ÖZET AMAÇ: Acil servise trafik kazasına bağlı künt karın travması ile başvuran hastalarda klinik değerlendirme, laboratuvar parametreleri ve radyolojik sonuçların tedavi kararına ve cerrahi sonuçlarına etkisi araştırıldı.

GEREÇ VE YÖNTEM: Bu geriye dönük çalışmaya künt karın travması geçirmiş 222 hasta alındı. Pearson ki kare, Mann-Whitney U ve lojistik regresyon testleri istatistiksel analiz için kullanıldı.

BULGULAR: Tüm hastalar tam kan, biyokimya analizi, karın ultrasonografisi ile değerlendirildi. Seksen iki hasta ayrıca karın bilgisayarlı tomografisi ile incelendi. Yirmi üç hasta ameliyat edildi. Fiziksel inceleme, ultrasonografi ve bilgisayarlı tomografide pozitif bulgular, beyaz küre sayısında ve karaciğer fonksiyon testlerinde artış, hemoglobinde düşüş cerrahi girişim ihtiyacında artış ile ilişkiliydi (p<0.05).

Cerrahi girişime ihtiyaç riskini pozitif fiziksel inceleme bulguları 3.5 kat, karaciğer fonksiyon testlerinde artış 3.8 kat ve pozitif ultrasonografik bulgular 3.5 kat artırmaktaydı.

SONUÇ: Künt karın travmalı hastaların cerrahi girişim açısından değerlendirilmesinde rahatsız edici ağrıya yol açan ek yaralanmaları olan ya da şuuru kapalı hastalarda güvenilir bir fizik muayene sağlanması mümkün olmamaktadır. Laboratuvar testlerinin fiziksel inceleme ve radyolojik incelemeler ile birlikte değerlendirilmesi gerekmektedir. Radyolojik yöntemler ise künt karın travmalı hastalara yaklaşımda özellikle entübe ve yeterli fiziksel inceleme yapılamayan hastalarda karar vermede önemli bir role sahiptir.

Anahtar sözcükler: Bilgisayarlı tomografi; fizik muayene; künt travma; laboratuvar testleri; ultrasonografi.

GİRİŞ Travma, genç nüfus içinde en önemli ölüm sebepleri arasındadır. Dünya genelinde 44 yaş altındaki ölümlerin en sık sebebi travmadır ve her yıl altı milyon ölüm olgusuna yol açmaktadır.[1] On dört yaş altındaki ölümlerin %50’si, 15–24 yaş arasındaki ölümlerin %80’i ve 25–40 yaş arasındaki ölümlerin %65’i travma nedeni ile oluşmaktadır.[2] Ülkemizde, travma nedeniyle

Sorumlu yazar: Dr. İdil Güneş Tatar, Dışkapı Eğitim ve Araştırma Hastanesi, Radyoloji Bölümü, Ankara Tel: +90 312 – 596 20 00 E-posta: idilttr@yahoo.com Ulus Travma Acil Cerrahi Derg 2015;21(4):256–260 doi: 10.5505/tjtes.2015.29559 Telif hakkı 2015 TJTES

256

ölümlerde, trafik kazaları birinci sırada ve iş kazaları ise ikinci sırada yer almaktadır.[3] Travma sonrası ölümlerin %20’sinden korunulabileceği ve bu ölümlerin önemli bir kısmının kontrolsüz kanamadan kaynaklandığı hesaplanmaktadır.[4] Bu nedenle acil koşullarında ciddi karıniçi yaralanmayı tespit etmek önem taşımaktadır. İlk değerlendirme sırasında birçok yaralanma bulgu vermemektedir. Yaralanmanın mekanizmasına bağlı oluşan ilişkili ve yandaş yaralanmalar ise klinisyenin dikkatini potansiyel olarak hayatı tehdit edici yaralanmalardan uzaklaştırabilmektedir.[5] Travmaya bağlı yaralanmalar; yaş, olayın mekanizması ve yaralanma bölgesi ile ilişkilidir. Yaralanmaya bağlı ölümler üçe ayrılmıştır; olay yerinde hayat ile bağdaşmayacak düzeydeki yaralanmalar, ikincil olarak kanamaya bağlı ölümler ve geç dönemde çoklu organ yetersizliğine bağlı ölümler olarak sıralanmaktadır.[6] Acil inceleme ve tedavi kanamaya bağlı ölümUlus Travma Acil Cerrahi Derg, Temmuz 2015, Cilt. 21, Sayı. 4

Tatar ve ark. Abdominal travmada klinik, laboratuvar ve radyolojik incelemelerin cerrahi girişim ihtiyacina etkisi

lere yol açan yaralanmalar için kritiktir ve bu dönem “altın saat” olarak değerlendirilmektedir.[7] Çoklu travma hastalarına yönelik radyolojik ve laboratuvar değerlendirme yöntemleri hızla gelişmekte ve bu yöntemlerin hızlı, yeterli sonuç verici ve karar vermeye yardımcı olması beklenmektedir. Bu değerlendirmelere dayanılarak travma hastalarına yaklaşım için skorlama sistemleri ve tedavi algoritmaları geliştirilmiştir.[8] Bu çalışmada incelediğimiz faktörler bu algoritmaları geliştirirken faydalı olabilecek niteliktedir.

Bu çalışma ile bir eğitim araştırma hastanesinde trafik kazası nedeni ile acil servise başvuran 18 yaş üzerindeki erişkin hastaların; klinik muayene, laboratuvar ve radyolojik bulgularının karar alma, uygulanan cerrahi ve tedavi sonuçları üstüne etkisi araştırılmaktadır.

GEREÇ VE YÖNTEM Bu geriye dönük çalışma Ocak 2012–Aralık 2013 döneminde etik kurul izni alınarak Ankara Dışkapı Eğitim ve Araştırma Hastanesi Acil Servisi’ne trafik kazası nedeni ile başvurup, genel cerrahi konsültasyonu açılan künt karın travmalı, 18 yaş üstü erişkin 222 hastayı kapsamaktadır. Hastaların yaş, cinsiyet, travma şekli (araç içi, araç dışı, motorsiklet kazası), fiziksel inceleme bulguları, hemoglobin (Hb) takipleri, beyaz küre (BK) takipleri, karaciğer fonksiyon testi (KCFT) takipleri, ultrasonografi (USG) ve bilgisayarlı tomografi (BT) sonuçları, ek organ yaralanmaları, cerrahi işlem uygulananlarda ameliyat bulguları ve hasta sağkalım sonuçları değerlendirilip ve kayıt altına alınmıştır. Verilerine net olarak ulaşılamayan hastalar çalışma dışı bırakılmıştır.

rıca karın BT’si ile değerlendirilmişti. Radyolojik görüntüleme yöntemleri ile 29 (%13.1) hastada minimal peritoneal serbest sıvı, 26 (%11.7) hastada ise önemli derecede peritoneal serbest sıvı mevcut idi.

Hemoglobin değeri 1–2 birim düşen 60 (%27) hasta mevcut iken, 3–4 veya daha fazla birim düşen 15 (%6.8) hasta mevcut idi. Karaciğer fonksiyon testi değerleri orta derecede (<100) artış gösteren 51 (%23) hasta ve yüksek (≥100) değerleri olan 41 (%18.5) hasta bulunmaktaydı. Beyaz küre değerleri ilk başvuru anında yüksek iken takipte düşme eğilimi gösteren 50 (%22.5) hasta, yüksek iken yükselme eğilimi gösteren 58 (%26.1) hasta, normal iken yükselme eğilimi gösteren 72 (%32.4) hasta ve normal olarak saptanan 42 (%18.9) hasta mevcut idi (Tablo 1).

USG raporları analiz edildiğinde 169 (%76.1) hasta normal olarak değerlendirilirken, belirgin solid organ yaralanması olan ve cerrahi müdahale gerektirebilecek 17 (%7.7) hasta mevcut idi. Sadece minimal peritoneal serbest sıvısı olan 17 (%7.7) hasta saptanırken şüpheli bulguları olan ama takibe uyTablo 1. Hastaların biyokimya parametrelerinin analizi İnceleme sonucu

%

Hemoglobin değeri

1–2 birim düşüş

60

27

≥3–4 birim düşüş

15

6.8

Karaciğer fonksiyon testi değeri

<100 artış

51

23

≥100 artış

41

18.5

İstatistiksel analiz için “SPSS for Windows 15” programı kullanılarak tanımlayıcı istatistikler, gruplar arasındaki karşılaştırmalar için Pearson ki kare testi, Mann-Whitney U-testi ve lojistik regresyon testleri çalışılmıştır.

Beyaz küre değeri

BULGULAR

Normal

Trafik kazası nedeni ile acil servise başvuran ve karın travması ön tanısıyla genel cerrahi konsültasyonu açılan 67 (%30.2) kadın ve 155 (%69.8) erkek olmak üzere, 222 hastanın yaş ortalaması 43 (18–87) idi. Hastaların 157’si (%70.7) araç içi, 60’ı (%27) araç dışı ve beşi (%2.3) motorsiklet kazası nedeni ile başvurmuştu. On üç (%5.9) hastanın bilinç kapalılığı veya entübe olduğu için fiziksel inceleme bulguları yeterli olarak değerlendirilemezken, 159 (%71.6) hastanın karın hassasiyeti, dört (%1.8) hastanın şüpheli akut karın bulguları mevcut idi.

Karın dışı ek organ yaralanmaları sınıflandırıldığında fiziksel inceleme ve radyolojik yöntemler ile 43 (%19.4) hastada izole ekstremite/kemik yaralanması, 39 (%17.6) hastada vertebra kırığı, kot kırığı saptanmıştı. On dört (%6.3) hastanın kraniyal yaralanması mevcut iken birden çok karın dışı ek organ yaralanması olan 30 (%13.5) hasta mevcut idi.

n

Başvuruda yüksek olup düşen

50

22.5

Başvuruda yüksek olup artan

58

26.1

Başvuruda normal olup artan

72

32.4

42

18.9

Tablo 2. Hastaların radyolojik inceleme analizi İnceleme sonucu

n

%

Ultrasonografi incelemesi

222

Normal

169

76.1

Solid organ hasarı

17

7.7

Minimal serbest sıvı

17

7.7

Şüpheli bulgular

19

8.6

Bilgisayarlı tomografi incelemesi

Minimal serbest sıvı

Solid organ hasarı

Şüpheli bulgular

Normal

82 9

11

17

20.7

28

34.1

28

34.1

Tüm hastalara karın USG uygulanırken, 82 (%36.9) hasta ayUlus Travma Acil Cerrahi Derg, Temmuz 2015, Cilt. 21, Sayı. 4

257

Tatar ve ark. Abdominal travmada klinik, laboratuvar ve radyolojik incelemelerin cerrahi girişim ihtiyacina etkisi

Tablo 3. Cerrahi yaklaşım analizi Cerrahi türü

n

%

Solid organ onarımı

9

4.1

Splenektomi

7 3.2

İnce bağırsak rezeksiyonu Nefrektomi

Tanısal laparotomi Splenektomi ve nefrektomi

2

0.9

2

0.9

2

0.9

1

0.5

gun olarak değerlendirilen 19 (%8.6) hasta kayıt altına alındı.

BT çekilen hastaların dokuzunda (%11) minimal peritoneal serbest sıvı saptanırken, 17 (%20.7) hastanın sonuçları cerrahi müdahale gerektirebilecek solid organ yaralanması olarak kayıt altına alındı. Yirmi sekiz (%34.1) hastanın sonuçları ‘şüpheli bulgular ama takibe uygun’ olarak kayıt altına alındı (Tablo 2).

Yirmi üç (%10.3) hastaya cerrahi girişim uygulandı. Cerrahi uygulamaların parçası olarak dokuz (%4.1) hastaya solid organ (karaciğer veya dalak) onarımı, yedi (%3.2) hastaya splenektomi, iki hastaya (%0.9) ince bağırsak rezeksiyonu, iki hastaya (%0.9) nefrektomi, iki hastaya (%0.9) tanısal laparatomi ve bir (%0.5) hastaya ise splenektomi ile birlikte nefrektomi uygulandı (Tablo 3). On (%4.5) hasta ek organ yaralanması ve özellikle kranial ağırlıklı yaralanmalar nedeni ile takipte kaybedildi.

Fiziksel inceleme sırasında, USG veya BT ile şüpheli radyolojik bulgular (p=0.001), artmış KCFT değerleri, Hb değerlerinde düşüş ve BK değerinde artış; travma hastalarının cerrahi ihtiyacı ile anlamlı derecede ilişkiliydi (p<0.05). Fiziksel inceleme sırasındaki pozitif bulgular cerrahi gereksinimini 3.5 kat; artmış KCFT değerleri 3.8 kat ve pozitif USG bulguları ise 3.5 kat artırmaktaydı.

TARTIŞMA Karın yaralanmaları travmaya bağlı ölümlerin üçüncü en sık sebebini oluşturmaktadır.[9] Erken tanı ve tedavi mortalite oranlarını %50’lere kadar azaltabilmektedir.[10] Acil servislerde travmalı olguya yaklaşımda zamanlama ve uygulanan algoritmalar önemli olup zaman içinde değişim gösterebilmektedirler.[11,12] Yaralanmanın şiddetini kavrayabilmek için geliştirilen travma skalaları ve yaralanma şiddet skorlama sistemleri mevcuttur. Trafik kazasına bağlı künt karın travmalı hastalara ilk başvuru anında tanı koyma gereksinimi zaman ile yarışı gerektirmekte ve radyolojik yöntemler karar vermek için önemini korumaktadır. Özellikle bilinci kapalı hastalar için tedavi kararını vermek laboratuvar ve radyolojik bulgulara bağımlıdır.

Bu hasta grubunda cerrahi tedavi gerektiren bir yaralanmanın zamanında tanı alması kadar hastaların gereksiz cerrahi müdahalelerden korunması da önemlidir.[13] 258

Bu algoritmalar içinde yer alıp bir dönem geniş uygulama alanı bulan ve halen kullanılmakta olan invaziv bir işlem olan tanısal peritoneal lavaj yerini günümüzde ultrasonografi tekniklerine ‘Focused Assesment Sonography for Trauma (FAST)’ ve BT’ye bırakmıştır.[14] Künt karın yaralanmaları için ilk tercih edilen tanı yöntemi USG’dir. Bu görüntüleme yöntemi uygulayıcı bağımlı olması, içi boş organlar için düşük etkinlik göstermesi gibi dezavantajlarına rağmen rağmen halen en sık kullanılan tanı yöntemidir.[9] Ultrasonik incelemeler yatak başı uygulanabilmesi, ucuz ve non-invaziv olması ve etkinliği nedeni ile peritoneal lavaj uygulamalarının yerini almıştır.[15] Karın boşluğundaki serbest sıvının ve hemoperitoneumun saptanmasında yüksek duyarlılık ve özgüllüğü mevcuttur.[16] Bakker ve ark.

USG ile tanı alan karın travmalı hastalar için %1.7 oranında tanı gecikmesi bildirmişlerdir. Şiddetli akut karın ağrısı eşlik eden travmalı hastalar için USG tekniği ile %85 duyarlılık ve %100 özgüllük göstermekte olduğu bildirilmiştir.[17] Bilgisayarlı tomografi ise iyonizan radyasyon yayması ve kontrast madde kullanımı gerektirebilmesi gibi istenmeyen etkileri olsa bile künt karın yaralanmaları için doğru endikasyonlarda kullanıldığında en önemli görüntüleme yöntemidir.[18] Karın yaralanmaların tanı almasında, yaralanmanın sınıflandırılmasında ve en önemlisi travmaya yaklaşım sonuçlarında BT önemli yarar sağlamaktadır.[19] Ameliyatsız yaklaşım gösterilecek yaralanmaların belirlenmesi ile fiziksel inceleme ve USG sonuçları ile şüphe duyulan hastaların cerrahi tedavi kararının verilmesinde önem taşımaktadır. Karın BT görüntülemesi normal olan hastaların ek tedavi gerektirmediği bildirilmiştir.[20] Artmış KCFT değerleri, şüpheli fiziksel inceleme ve radyolojik bulgular cerrahi kararını zorlasa da karaciğer yaralanmalarına yaklaşımda konservatif tedavi yöntemlerinin faydası unutulmamalıdır. Künt karın yaralanmaları için konservatif yaklaşımlar farklı merkezlerde %50–85 gibi değişen oranlarda uygulanmakta ve başarı oranları %80’lere ulaşmaktadır.[21] Karaciğer yaralanmaları açısından; hemodinamik stabilitesi olan, peritoneal bulgular taşımayan, uzman bir radyologca değerlendirilmiş BT sonucuna göre gereklilik halinde acil şartlarda ameliyata alınma imkanı olan bir yoğun bakım ünitesine sahip olunan koşullarda basit parankimal hasarı veya intrahepatik hematomu olan ve 125 ml’den daha az intraperitoneal kanaması bulunan hastaların başka karıniçi yaralanma bulgusu göstermedikleri takdirde takip edilebileceği belirtilmiştir.[22] İntraperitoneal 500 cc’den daha az kanaması saptanan hastaların hemodinamik olarak stabil olmaları durumunda da ameliyatsız takip edilebileceği bildirilmiştir.[23] İzole karaciğer yaralanmalarının değerlendirildiği bir çalışmada ameliyatsız takip, %32 oranında başarısız olmuş ve cerrahi müdahale gerekmiştir.[24] Bu çalışmanın sonuçlarına göre artmış KCFT değerleri 3.8 kat artmış cerrahi gereksinimi ile ilişkili olarak tanımlanmış olsa bile tanı anında 92 (%41.5) hastada çeşitli oranlarda artmış KCFT değerleri saptanması, KCFT’nin tek başına karar vermek için yeterli bir parametre olamayacağını göstermektedir.

Bu çalışmanın sonuçlarına göre Hb değerlerinde düşüş ve BK değerlerinde artışın cerrahi gereksinimi ilişkisi saptanmış olmaUlus Travma Acil Cerrahi Derg, Temmuz 2015, Cilt. 21, Sayı. 4

Tatar ve ark. Abdominal travmada klinik, laboratuvar ve radyolojik incelemelerin cerrahi girişim ihtiyacina etkisi

sına rağmen laboratuvar incelemeleri tek başına hastaya yaklaşım açısından klinisyene yardımcı olmamakta; görüntüleme yöntemleri ve fiziksel inceleme bulguları ile korele edilmeleri gerekmektedir. Kardiyak enzimler, karaciğer fonksiyon testleri ve sitokinler gibi laboratuvar parametrelerinin çoklu travmalı hastaya yaklaşımdaki yeri çalışılmıştır ve bu bu testlerin fiziksel ve radyolojik incelemeler ile birlikte değerlendirilmesi gerekliliği ortaya konmuştur.[25] Geleneksel yaşamsal bulgu ölçümleri kanamanın saptanmasına spesifik olmakla beraber kanamanın saptanabilmesi için sensitif değillerdir. Yetersiz doku perfüzyonuna bağlı olarak ortaya çıkan metabolik asidoz ve özellikle baz açığının yüksek miktarda transfüzyon gerektirecek karıniçi yaralanma için önemli bir gösterge olabileceği belirtilmiştir.[5] Madsen ve ark. spesifik durumlar haricinde seri hematokrit ölçümünün rutin kullanımının majör yaralanmanın saptanmasında anlamlı yardımı olmadığını belirtmişlerdir.[26] Yine bu çalışmada ortaya çıkan fiziksel inceleme bulgularının şüpheli olması durumunda cerrahi gereksinimin arttığına dair sonuçlara karşılık literatürde izole fiziksel incelemenin, görüntüleme yöntemlerine göre yetersiz olduğunu belirten çalışmalar da mevcuttur.[27] Michetti ve ark. özellikle karın/ pelvik yaralanması olan ve negatif fiziksel inceleme bulguları gösteren %10’luk bir hasta grubunda yaralanmaların atlanabileceğini belirtmişlerdir.[28] Rahatsız edici ağrıya yol açan ek yaralanmaları olan hastalarda güvenilir bir fiziksel inceleme sağlanması mümkün olmamaktadır. Ferrera ve ark. normal fiziksel inceleme bulguları olan %7’lik hasta grubunda karıniçi yaralanma saptadıklarını bildirmişlerdir.[29] Başta kraniyal yaralanmalar olmak üzere ek organ yaralanmaları, künt karın travmalı hastalarda önemli sorunlar oluşturmaktadır. Pelvik kırıklı hastaların %40’ında aktif kanama oluşmaktadır ve morbidite ve mortalite açısından önemlidir.[30]

Çalışmanın Limitasyonları Bilgisayarlı tomografi çekilen hasta sayısındaki azlık nedeniyle BT incelemesinin cerrahi girişim kararı üzerindeki etkisi incelenememiştir.

Sonuç Travma hastalarında önemli yaralanmaların gecikmiş tanısı kadar konservatif tedavi edilebilecek hastalara yönelik gereksiz cerrahi müdahaleler de hastanın zararına olmaktadır.

Laboratuvar testlerinin fiziksel ve radyolojik incelemeler ile birlikte değerlendirilmesi gerekmektedir. Bu çalışmada cerrahi girişim riskini artıran pozitif fiziksel inceleme bulguları, karaciğer fonksiyon testlerinde artış ve pozitif USG bulguları yeni algoritmaları planlarken risk faktörleri olarak kullanılabilir.

Radyolojik yöntemler künt karın travmalı hastalara yaklaşımda özellikle entübe ve yeterli fiziksel inceleme yapılamayan hastalarda karar vermede önemli bir role sahiptir. Uygulanan tanısal laparatomi oranlarının kabul edilebilir oranlarda tutulması için hastaların yoğun bakım şartları olan, anjiyografi ile embolizasyon ve hemostaz sağlananabilen uygun travma merkezlerinde Ulus Travma Acil Cerrahi Derg, Temmuz 2015, Cilt. 21, Sayı. 4

her an cerrahi girişime alınabilecek olanakların olduğu merkezlerde takibi uygundur. Çıkar örtüşmesi: Çıkar örtüşmesi bulunmadığı belirtilmiştir.

KAYNAKLAR 1. Curry N, Davis PW. What’s new in resuscitation strategies for the patient with multiple trauma? Injury 2012;43:1021–8.

2. Ertekin C. Multipl travmalı hastaya yaklaşım. Yoğun Bakım Dergisi 2002;2:77–87.

3. T.C Başbakanlık Devlet İstatistik Enstitüsü. 1990 yılı ulaşım ve trafik kazaları istatistikleri 1991;1–45.

4. Esposito TJ, Sanddal TL, Reynolds SA, Sanddal ND. Effect of a voluntary trauma system on preventable death and inappropriate care in a rural state. J Trauma 2003;54:663–70.

5. Mofidi M, Hasani A, Kianmehr N. Determining the accuracy of base deficit in diagnosis of intra-abdominal injury in patients with blunt abdominal trauma. Am J Emerg Med 2010;28:933–6.

6. Demetriades D, Kimbrell B, Salim A, Velmahos G, Rhee P, Preston C, et al. Trauma deaths in a mature urban trauma system: is “trimodal” distribution a valid concept? J Am Coll Surg 2005;201:343–8.

7. Cowley RA. The resuscitation and stabilization of mayor multiple trauma patients in trauma center environment. Clin Med 1976;83:14–22.

8. Harrois A, Hamada S, Laplace C, Duranteau J, Vigué B. The initial management of severe trauma patients at hospital admission. Ann Fr Anesth Reanim 2013;32:483–91.

9. Shojaee M, Faridaalaee G, Yousefifard M, Yaseri M, Arhami Dolatabadi A, Sabzghabaei A, et al. New scoring system for intra-abdominal injury diagnosis after blunt trauma. Chin J Traumatol 2014;17:19–24.

10. Chardoli M, Rahimi-Movaghar V. Analysis of trauma outcome at a university hospital in Zahedan, Iran using the TRISS method. East Afr Med J 2006;83:440–2.

11. Martí De Gracia M, Artigas Martín JM, Vicente Bártulos A, Carreras Aja M. Radiological management of patients with multiple trauma: history and current practice. [Article in Spanish] Radiologia 2010;52:105–14.

[Abstract] 12. van Schuppen J, Olthof DC, Wilde JC, Beenen LF, van Rijn RR, Goslings JC. Diagnostic accuracy of a step-up imaging strategy in pediatric patients with blunt abdominal trauma. Eur J Radiol 2014;83:206–11.

13. Giannopoulos GA, Katsoulis IE, Tzanakis NE, Patsaouras PA, Digalakis MK. Non-operative management of blunt abdominal trauma. Is it safe and feasible in a district general hospital? Scand J Trauma Resusc Emerg Med 2009;17:22.

14. Gibson DE, Canfield CM, Levy PD. Selective nonoperative management of blunt abdominal trauma. J Emerg Med 2006;31:215–21.

15. Hoffman L, Pierce D, Puumala S. Clinical predictors of injuries not identified by focused abdominal sonogram for trauma (FAST) examinations.

J Emerg Med 2009;36:271–9.

16. Leenen LP. Abdominal trauma: from operative to nonoperative management. Injury 2009;40 Suppl 4:S62–8.

17. Bakker J, Genders R, Mali W, Leenen L. Sonography as the primary screening method in evaluating blunt abdominal trauma. J Clin Ultrasound 2005;33:155–63.

18. Gunes Tatar I, Aydin H, Kizilgoz V, Yilmaz KB, Hekimoglu B. Appropriateness of selection criteria for CT examinations performed at an emergency department. Emerg Radiol 2014;21:583–8.

19. Mullinix AJ, Foley WD. Multidetector computed tomography and blunt thoracoabdominal trauma. J Comput Assist Tomogr 2004;28 Suppl 1:20–7.

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21. Lin BC, Fang JF, Chen RJ, Wong YC, Hsu YP. Surgical management and outcome of blunt major liver injuries: experience of damage control laparotomy with perihepatic packing in one trauma centre. Injury 2014;45:122–7.

22. Meyer AA, Crass RA, Lim RC Jr, Jeffrey RB, Federle MP, Trunkey DD. Selective nonoperative management of blunt liver injury using computed tomography. Arch Surg 1985;120:550–4.

23. Feliciano DV. Continuing evolution in the approach to severe liver trauma. Ann Surg 1992;216:521–3.

24. Azzam AZ, Gazal AH, Kassem MI, Souror MA. The role of non-operative management (NOM) in blunt hepatic trauma. Alexandria J of Med 2013;49:223–7.

25. Karakuş A, Kekeç Z, Akçan R, Seydaoğlu G. The relationship of trauma severity and mortality with cardiac enzymes and cytokines at multiple trauma patients. Ulus Travma Acil Cerrahi Derg 2012;18:289–95.

26. Madsen T, Dawson M, Bledsoe J, Bossart P. Serial hematocrit testing does not identify major injuries in trauma patients in an observation unit.

Am J Emerg Med 2010;28:472–6.

27. Soyuncu S, Cete Y, Bozan H, Kartal M, Akyol AJ. Accuracy of physical and ultrasonographic examinations by emergency physicians for the early diagnosis of intraabdominal haemorrhage in blunt abdominal trauma.

Injury 2007;38:564–9.

28. Michetti CP, Sakran JV, Grabowski JG, Thompson EV, Bennett K, Fakhry SM. Physical examination is a poor screening test for abdominal-pelvic injury in adult blunt trauma patients. J Surg Res 2010;159:456–61.

29. Ferrera PC, Verdile VP, Bartfield JM, Snyder HS, Salluzzo RF. Injuries distracting from intraabdominal injuries after blunt trauma. Am J Emerg Med 1998;16:145–9.

30. Hallinan JT, Tan CH, Pua U. Emergency computed tomography for acute pelvic trauma: where is the bleeder? Clin Radiol 2014;69:529–37.

ORIGINAL ARTICLE - ABSTRACT OLGU SUNUMU

The effect of clinical, laboratory and radiologic results on treatment decision and surgical results in patients admitted to the emergency department with blunt abdominal trauma due to traffic accident İdil Güneş Tatar, M.D.,1 Kerim Bora Yılmaz, M.D.,2 Onur Ergun, M.D.,1 Şener Balas, M.D.,2 Melih Akıncı, M.D.,2 Rıza Deryol, M.D.,2 Gaye Ebru Şeker, M.D.,2 Hakan Kulaçoğlu, M.D.,2 Baki Hekimoğlu, M.D.1 1 2

Department of Radiology, Dışkapı Training and Research Hopital, Ankara Department of General Surgery, Dışkapı Training and Research Hopital, Ankara

BACKGROUND: The purpose of this study was to evaluate the effect of clinical, laboratory and radiological results on treatment decision and surgical results in patients with blunt abdominal trauma, who were admitted to the emergency department due to traffic accident.

METHODS: Two hundred and twenty-two patients with blunt abdominal trauma were included into this retrospective study. Pearson chi square, Mann-Whitney U test and logistic regression methods were used for statistical analysis.

RESULTS: All patients were analyzed by complete blood count and biochemistry and abdominal sonography. Eighty-two patients were also evaluated by CT. Twenty-three patients underwent surgery. Positive findings on physical examination, sonography and CT, increased white blood cell count and liver function tests, decreased hemoglobin were associated with the need for surgery.

DISCUSSION: For the surgical evaluation of patients with blunt abdominal trauma, a reliable physical examination is not possible when the patients have concomitant injuries causing disturbing pain, or when the patients are unconscious. Laboratory tests should be interpreted with the clinical and radiologic analysis. Radiologic procedures play an important role in the management of patients with blunt abdominal trauma, especially for intubated patients.

Key words: Computed tomography; blunt trauma; laboratory tests; physical examination; ultrasonography.

Ulus Travma Acil Cerrahi Derg 2015;21(4):256–260

260

doi: 10.5505/tjtes.2015.29559

Ulus Travma Acil Cerrahi Derg, Temmuz 2015, Cilt. 21, Sayı. 4

ORIGIN A L A R T IC L E

Evaluation of posttraumatic recurrent bacterial meningitis in adults Özcan Deveci, M.D.,1 Cem Uysal, M.D.,2 Sefer Varol, M.D.,3 Recep Tekin, M.D.,1 Fatma Bozkurt, M.D.,1 Muhammed Bekçibaşı, M.D.,4 Salih Hoşoğlu, M.D.1 1

Department of Infectious Diseases and Clinical Microbiology, Dicle University Faculty of Medicine, Diyarbakir

2

Department of Forensic Medicine, Dicle University Faculty of Medicine, Diyarbakir

3

Department of Neurology, Dicle University Faculty of Medicine, Diyarbakir

4

Department of Infectious Diseases and Clinical Microbiology, Bismil State Hospital, Diyarbakir

ABSTRACT BACKGROUND: Acute bacterial meningitis may develop as a complication after head trauma. The aim of this study was to present the demographic, clinical, microbiological and radiological characteristics of adult patients who presented with recurrent bacterial meningitis attacks after trauma.

METHODS: Using a retrospective approach, the medical records of patients with acute recurrent bacterial meningitis (RBM) were reviewed, and those who had a history of trauma were included into the study. RBM was diagnosed based on clinical, bacteriologic and laboratory results. Demographic characteristics, clinical course, laboratory test results including cerebrospinal fluid analysis (CSF), radiological images, and the applied treatments were evaluated.

RESULTS: A total of two hundred and twelve patients with acute bacterial meningitis were included into the study. RBM was diagnosed in twenty-five patients (11.8%), and in 18 of these patients (8.5%), the attacks had occurred subsequent to a trauma. In the CSF cultures of four patients, S. pneumoniae growth was observed. CT cisternography indicated CSF leaks in eleven patients. Moreover, bone fractures were observed in the CT images of ten patients. Ceftriaxone therapy was prescribed to 83% of the patients. Eight patients had a history of a fall in childhood, and five were involved in traffic accidents before acute bacterial meningitis. Four of the patients developed epilepsy and one developed deafness as sequelae.

CONCLUSION: Since RBM attacks are frequently observed following trauma, in patients with a history of trauma who present with meningitis, the risk of recurrence should be considered.

Key words: Meningitis; posttraumatic; recurrent.

INTRODUCTION Acute bacterial meningitis is a life-threatening infection that may cause significant morbidity in the cranial and spinal leptomeninges.[1] Recurrent bacterial meningitis (RBM) is defined as the recurrence of the symptoms and clinical and laboratory findings of bacterial meningitis in spite of an adequate Address for correspondence: Özcan Deveci, M.D. Dicle Üniversitesi Tıp Fakültesi, Enfeksiyon Hastalıkları ve Klinik Mikrobiyoloji Anabilim Dalı, Diyarbakır, Turkey Tel: +90 412 – 248 80 01 E-mail: ozcandeveci1@hotmail.com Qucik Response Code

Ulus Travma Acil Cerrahi Derg 2015;21(4):261–265 doi: 10.5505/tjtes.2015.02651 Copyright 2015 TJTES

Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

and successful treatment of the previous meningitis attack.[2,3] RBM is a rare entity, suggesting the existence of predisposing causes, among which traumatic causes appear to be the most frequent.[4] Developmental or traumatic disorders may give bacteria access to the subarachnoid space, resulting in RBM. Additionally, undiagnosed immune deficiencies may lead to a susceptibility to the bacteria causing meningitis in affected individuals. Various predisposing factors have been reported.

Therefore, the causes paving the way for RBM should be comprehensively investigated.[2] Pneumococcal RBM is usually caused by an intracranial seeding of bacteria via direct communication with an extracranial source. This condition frequently manifests with constant or intermittent cerebrospinal fluid (CSF) rhinorrhoea due to various etiologies.[5] Early diagnosis of any underlying pathologies in patients with recurrent bacterial meningitis is important to prevent further attacks and improve the general outcome in affected patients.

Posttraumatic recurrent bacterial meningitis has primarily 261

Deveci et al. Evaluation of posttraumatic recurrent bacterial meningitis in adults

been described in case series of pediatric patients. Studies conducted on adult patients with posttraumatic recurrent bacterial meningitis are limited in number. Since the majority of the previous studies on RBM have included fewer than ten patients, our study may shed greater light to the understanding and management of posttraumatic RBM with the larger number of patients featured. The aim of the present study was to present the demographic, clinical, microbiological, and radiological characteristics of adult patients who presented with recurrent bacterial meningitis attacks after trauma.

MATERIALS AND METHODS The study was conducted at the Dicle University Hospital, which is a 1,275-bed tertiary referral center that provides care for the vast majority of patients with bacterial meningitis in south-eastern Turkey. Patients who presented to the Dicle University Hospital with symptoms including headache, fever, nausea and vomiting, and nuchal rigidity during physical examination pointing to meningitis between the years 2003 and 2012 were included into the study in a retrospective manner.

After neurology consultation to exclude any cerebrovascular events, the patients were admitted to the Department of Infectious Diseases with a pre-diagnosis of meningitis. Lumbar punctures were performed and the cerebrospinal fluid (CSF) was tested. Patients with a leukocyte count >1000/mm3 (dominance of polymorphonuclear leukocytes), CSF glucose <50% of blood glucose, CSF protein >50 mg/dl, and/or positive CSF culture were diagnosed with acute bacterial meningitis.

All patients were asked about any previous history of meningitis and trauma preceding the attacks. Recurrent bacterial meningitis was defined as a case of meningitis that developed due to the same or a different microorganism more than three weeks after the completion of the treatment for the initial meningitis attack. The diagnosis of RBM was based on clinical, bacteriological and laboratory results. Patients with ventriculo-peritoneal shunts or immune deficiency were excluded from the study. Since the patients had a history of trauma, cranial tomography (CT), cranial magnetic resonance imaging (MRI) and ventriculo-cisternography results were recorded in patients with risk factors. The mean age, gender, and CSF results of the patients were evaluated. The prescribed antimicrobial treatments were also taken into consideration.

The consent of the Dicle University Medical Faculty Ethics Committee was obtained for this study.

RESULTS The total number of patients with acute bacterial meningitis during the study period was two hundred and twelve. Recurrent bacterial meningitis was diagnosed in twenty-five (11.8%) of them. Post-traumatic RBM was diagnosed in eighteen (72%) of the recurrent meningitis patients. The age range of these patients was between 17 and 63 years, and the mean age 262

was 28 years. Among the patients, eight were female while ten were male. A total of eighteen patients with forty-three meningitis episodes were recorded. The mean number of the episodes was 2.6Âą0.8 (range, 2â&#x20AC;&#x201C;5 episodes). Seven patients had a history of fall from height during their childhood, and five had a history of traffic accident.

When the CSF test results of the patients were assessed, CSF pressure was observed to be increased in the majority of the patients. CSF was turbid, and the mean CSF glucose was lower than 50% of the blood glucose level. These CSF results were consistent with acute bacterial meningitis. Grampositive growth was the most frequently observed growth type. S. pneumoniae growth was observed in the CSF cultures of four patients. Gram staining indicated gram-positive diplococcus in four patients (Table 1).

Radiological imaging results of the patients showed bone fractures and dural contrast enhancement in the brain CT images of seven patients, dural contrast enhancement in the brain MRI of thirteen (72.2%) patients, and bone fractures in ten (55.6%) patients. Among the fifteen patients who had undergone cisternographies, eleven had dural defects and eleven had CSF leaks (Table 2). In terms of antibiotic treatment, fourteen out of the eighteen patients (77.8%) received ceftriaxone while four patients (22.2%) received ceftriaxone+vancomycin. No patients with RBM died during the episodes. Four patients had complications, where three of them developed epilepsy and one developed hearing loss. None of our patients had been on prophylactic antibiotherapy.

Table 1. CSF test results Findings

n %

Turbid

17 94

Protein level too high to be measured

13

CSF glucose/blood glucose <50%

16

88

Gram positive diplococcus

4

22

S. pneumoniae growth in the culture

4

22

n

%

Brain CT dural contrasting

7

39

Brain CT bone fracture

10

55

Brain MRI dural contrasting

13

72

Brain MRI bone fracture

10

55

CSF leak in CT cisternography

11

61

72

CSF: Cerebrospinal fluid.

Table 2. Radiological findings Radiological findings

CSF: Cerebrospinal fluid.

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Deveci et al. Evaluation of posttraumatic recurrent bacterial meningitis in adults

DISCUSSION Post-traumatic meningitis is an important condition due to its potential for recurrences and sequelae. In some cases, it may even prove fatal. This study underlined that patients with post-traumatic meningitis should be assessed for CSF leakage and the risk of recurrence. Furthermore, healthcare professionals should consider the risk of recurrence in all bacterial meningitis cases.

In a retrospective study evaluating meningitis patients among the general population, 6% of the patients have been found to have recurrent meningitis.[6] Adriani et al.[7] have conducted a prospective study on meningitis patients among the population in the Netherlands and reported this rate as 5%. However, the rate may be lower in children. In a study by Drummond et al.,[8] conducted on pediatric meningitis patients during a ten-year period, the rate of recurrent meningitis has been observed to be only 1.3%. In another study conducted in a tertiary pediatric training and research hospital in Turkey, a rate as high as 6.2% has been observed for recurrent meningitis,[9] which is higher compared to the previous studies. In our study, radiological assessment pointed out CSF leaks and skull fractures due to trauma. In a study previously conducted at our hospital, Hosoglu et al.[10] had evaluated two hundred and eighteen meningitis episodes in adult patients and reported head trauma as a risk factor for meningitis in seventeen (7.8%) patients. They had also reported S. pneumoniae as the most prevalent causative agent. In an RBM series from our hospital, twenty-two RBM episodes had been reported in ten patients. Head trauma was a predisposing factor in four of these patients.[11] The spectrum of predisposing factors in RBM is not wide. In a study focusing on patients with recurrent meningitis, 21% of them has had immune deficiency and 74% has had congenital, traumatic, or surgical CSF fistulas as predisposing factors.[12] In the literature, there are several case reports on patients with late onset CSF leaks due to head trauma. These fistulas have become apparent within the first month in the majority of cases.[13] In a retrospective study conducted on one hundred and sixty patients with CSF leak due to head trauma, the risk of developing meningitis within the first week following the head trauma has been found as 9.1%.[14] In our study, the rate of CSF leaks in patients with posttraumatic RBM was observed to be high, which emphasizes the role of trauma in RBM. In a review of case reports on RBM, CSF fistulas due to head trauma have been found to trigger the majority of the recurrent meningitis attacks. According to this review, 28.1% (102 out of 363 patients) of the recurrent bacterial meningitis cases has occurred secondary to head traumas.

However, this review did not distinguish between pediatric and adult patients.[3] The majority of the articles on RBM are either case reports or studies conducted on a limited number of patients. The patients are evaluated as a general study group including both pediatric and adult patients. Only five Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

reports comprised more than five patients.[7,13,15,16] In this respect, our study features a comparatively higher number of adult patients.

In a review by Tebruegge et al., S. pneumoniae has been detected in one hundred (89%) out of one hundred and twentytwo culture-positive episodes following a head trauma. It is followed by H. influenzae and N. meningitidis with 6% and 4%, respectively. When we look at the general causes of recurrent bacterial meningitis, S. pneumoniae was also the leading agent in 72% of the patients in the same study.[3] In another study from our country conducted on fourteen pediatric RBM patients, eight out of the eleven patients (72.7%) with bacterial growth had S. pneumoniae in the culture. In the same study, S. pneumoniae growth was also observed in three patients in whom RBM had developed due to a trauma.[9] We also obtained similar results in terms of the causative agents in our study, and S. pneumoniae was the most frequently detected causative agent in culture-positive patients.

Radiological imaging methods are useful to detect CSF fistulas. These methods include CT scans, CT cisternography, radionucleotide cisternography, and MRI. CT cisternography is based on the demonstration of the fistula defect through a contrast agent, and its sensitivity has been reported to be around 55â&#x20AC;&#x201C;77%.[16,17] MRI shows the cerebral tissue and soft tissue thoroughly, which is especially important in case of encephalocele.[18] In a study conducted on twenty-four patients, MRI has been reported to be 100% sensitive in demonstrating CSF leaks.[19] In an extensive review, all of the CSF leaks detected through MRI have been surgically verified.[3] In our study, CT cisternography was used to show CSF leaks, which were detected at a high rate.

In terms of treatment, in the study by Tuygun et al.[9] in which fourteen pediatric recurrent meningitis patients have been evaluated, all patients have been administered a combination of ceftriaxone and vancomycin. In our study, all patients initially received ceftriaxone. When no response to the initial treatment was observed in four patients, vancomycin was later added to the regimen. Prophylactic antibiotic use in patients with skull base fractures and CSF fistula is controversial.[20,21] In a large-scale study that evaluated the causes of cranial trauma in Turkey, falls from height and traffic accidents were reported as the most common causes. Falls were predominantly observed in male patients. Also in our study, similar causes were observed in terms of the etiology of the cranial trauma.[22] Another review has emphasized the importance of falls during the childhood.[23] Similarly, falls from height and traffic accidents were found as the most frequent causes in our study. Moreover, six out of our seven patients with a history of fall were male. Treatment of CSF fistulas can be surgical or medical. The majority of the CSF leaks are self-limiting and stop spontaneously within 2â&#x20AC;&#x201C;7 days the after the trauma. Failure of the conservative treatment is an indication for surgical repair. Profuse leaks, Pneumocephalus, 263

Deveci et al. Evaluation of posttraumatic recurrent bacterial meningitis in adults

delayed and intermittent leaks and recurrent meningitis are absolute indications for surgical treatment.[24] In case of CSF fistulas irresponsive to the medical treatment, surgical treatment should be taken into consideration. Prognosis is very good in patients with spontaneously or surgically closed CSF fistulas.[25] This study has certain limitations due to its retrospective design. In some patients, the history of trauma was based on the statement of the patient or next of kin. In addition, the data on antibiotic treatment before the admission to the hospital was insufficient in some patients.

In case of RBM, patients should be inquired about and examined for any developmental or traumatic anatomic defects or immune deficiency. Since recurrent bacterial meningitis attacks are frequently observed following a trauma, in patients who present with symptoms including headache, nausea, vomiting, and nuchal rigidity, meningitis should be considered in the differential diagnosis. History of any trauma in childhood should be taken seriously since the risk of meningitis might continue throughout the patient’s lifetime. After the recovery from the acute phase of bacterial meningitis, the patient should be evaluated for predisposing factors of RBM. Conflict of interest: None declared.

REFERENCES 1. Kendirli T, Unay B, Tosun F, Hacihamdioğlu B, Akin R, Ozkaptan Y, et al. Recurrent Streptococcus pneumoniae meningitis in a child with traumatic anterior cranial base defect. Pediatr Int 2006;48:91–3.

2. Lieb G, Krauss J, Collmann H, Schrod L, Sörensen N. Recurrent bacterial meningitis. Eur J Pediatr 1996;155:26–30.

3. Tebruegge M, Curtis N. Epidemiology, etiology, pathogenesis, and diagnosis of recurrent bacterial meningitis. Clin Microbiol Rev 2008;21:519– 37.

4. Fyfe DA, Rothner DA, Orlowski J, Cook SA. Recurrent meningitis with brain abscess in infancy. Am J Dis Child 1983;137:912–3.

5. Pappas DG Jr, Hammerschlag PE, Hammerschlag M. Cerebrospinal fluid rhinorrhea and recurrent meningitis. Clin Infect Dis 1993;17:364–8.

6. Durand ML, Calderwood SB, Weber DJ, Miller SI, Southwick FS, Caviness VS Jr, et al. Acute bacterial meningitis in adults. A review of 493 episodes. N Engl J Med 1993;328:21–8.

7. Adriani KS, van de Beek D, Brouwer MC, Spanjaard L, de Gans J. Community-acquired recurrent bacterial meningitis in adults. Clin Infect Dis

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2007;45:46–51.

8. Drummond DS, de Jong AL, Giannoni C, Sulek M, Friedman EM. Recurrent meningitis in the pediatric patient-the otolaryngologist’s role. Int J Pediatr Otorhinolaryngol 1999;48:199–208.

9. Tuygun N, Tanir G, Aytekin C. Recurrent bacterial meningitis in children: our experience with 14 cases. Turk J Pediatr 2010;52:348–53.

10. Hoşoğlu S, Ayaz C, Geyik MF, Kökoglu OF, Ozen A. Acute bacterial meningitis in adults: analysis of 218 episodes. Ir J Med Sci 1997;166:231–4.

11. Hoşoğlu S, Ayaz C, Ceviz A, Cümen B, Geyik MF, Kökoğlu OF. Recurrent bacterial meningitis: a 6-year experience in adult patients. J Infect 1997;35:55–62.

12. Kline MW. Review of recurrent bacterial meningitis. Pediatr Infect Dis J 1989;8:630–4.

13. Friedman JA, Ebersold MJ, Quast LM. Persistent posttraumatic cerebrospinal fluid leakage. Neurosurg Focus 2000;9:1.

14. Dunne DW, Quagliarello V. Group B streptococcal meningitis in adults.

Medicine (Baltimore) 1993;72:1–10.

15. Eljamel MS, Foy PM. Acute traumatic CSF fistulae: the risk of intracranial infection. Br J Neurosurg 1990;4:381–5.

16. Maitra S, Ghosh SK. Recurrent pyogenic meningitis-a retrospective study. Q J Med 1989;73:919–29.

17. Schick B, Weber R, Kahle G, Draf W, Lackmann GM. Late manifestations of traumatic lesions of the anterior skull base. Skull Base Surg 1997;7:77–83.

18. Chow JM1, Goodman D, Mafee MF. Evaluation of CSF rhinorrhea by computerized tomography with metrizamide. Otolaryngol Head Neck Surg 1989;100:99–105.

19. Manelfe C, Cellerier P, Sobel D, Prevost C, Bonafé A. Cerebrospinal fluid rhinorrhea: evaluation with metrizamide cisternography. AJR Am J Roentgenol 1982;138:471–6.

20. Giunta G, Piazza I. Recurrent bacterial meningitis occurring five years after closed head injury and caused by an intranasal post-traumatic meningo-encephalocele. Postgrad Med J 1991;67:377–9.

21. Johnson DB, Brennan P, Toland J, O’Dwyer AJ. Magnetic resonance imaging in the evaluation of cerebrospinal fluid fistulae. Clin Radiol 1996;51:837–41.

22. Işık HS, Gökyar A, Yıldız O, Bostancı U, Ozdemir C. Pediatric head injuries, retrospective analysis of 851 patients: an epidemiological study.

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23. Ongel K, Katirci E, Uludag H, Mergen H, Uzun E, Kisioglu AN. Assesment of fall from high level patients according to publications. Tıp Araştırmaları Dergisi 2008;6:175–80.

24. Marentette LJ, Valentino J. Traumatic anterior fossa cerebrospinal fluid fistulae and craniofacial considerations. Otolaryngol Clin North Am 1991;24:151–63.

25. Coşkuner T, Kubilay U, Dalbayrak S, Ünver Ş. Approach to patients with CSF rhinorrhea. J Kartal Tr 2002;13:204–6.

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KLİNİK ÇALIŞMA - ÖZET OLGU SUNUMU

Erişkin posttravmatik tekrarlayan menenjitlerin değerlendirilmesi Dr. Özcan Deveci,1 Dr. Cem Uysal,2 Dr. Sefer Varol,3 Dr. Recep Tekin,1 Dr. Fatma Bozkurt,1 Dr. Muhammed Bekçibaşı,4 Dr. Salih Hoşoğlu1 Dicle Üniversitesi Tıp Fakültesi, Enfeksiyon Hastalıkları ve Klinik Mikrobiyoloji Anabilim Dalı, Diyarbakır Dicle Üniversitesi Tıp Fakültesi, Adli Tıp Anabilim Dalı, Diyarbakır Dicle Üniversitesi Tıp Fakültesi, Nöroloji Anabilim Dalı, Diyarbakır 4 Bismil Devlet Hastanesi, Enfeksiyon Hastalıkları ve Klinik Mikrobiyoloji Kliniği, Diyarbakır 1 2 3

AMAÇ: Akut bakteriyel menenjit kafa travmalarının bir komplikasyonu olarak gelişebilir. Bu çalışmanın amacı kafa travmaları sonrası gelişen erişkin tekrarlayan bakteriyel menenjit (TBM) olgularının demografik, klinik, mikrobiyolojik ve radyolojik özelliklerini sunmaktır.

GEREÇ VE YÖNTEM: Çalışma geriye dönük olarak yapıldı. TBM gelişen olguların medikal kayıtları değerlendirildi. Bunlardan kafa travması öyküsü olanlar çalışmaya alındı. TBM tanısı klinik, bakteriyolojik ve laboratuvar testleri kullanılarak konuldu. Hastaların demografik özellikleri, klinik gidişi, beyin omurilik sıvısı (BOS) test sonuçları, radyolojik görüntüleme ve hastaların tedavileri değerlendirildi.

BULGULAR: Toplam 212 akut bakteriyel menenjitli hasta çalışmaya dahil edildi. TBM hastaların sayısı 25 idi (%11.8). Bunların da 18’i travmayı takiben gelişen ataklardı. Dört hastanın BOS kültüründe S. pneumonia üremesi gözlendi. Beyin tomografisi (BT) sisternografisi 11 hastada kaçağı gösterdi. Ayrıca on hastanın BT incelemesinde kemik kırığı gözlendi. Hastaların %83’üne seftriakson tedavi olarak verildi. Akut bakteriyel menenjit öncesi sekiz hastada çocukluk çağında düşme ve beş hastada trafik kazası öyküsü vardı. Dört hastada epilepsi ve bir hastada sağırlık gelişti.

TARTIŞMA: Tekrarlayan bakteriyel menenjit sıklıkla travmayı takiben geliştiğinden dolayı, travma hikayesi olan menenjitli hastaların tekrar gelişme riski açısından göz önünde bulundurulması gerekir.

Anahtar sözcükler: Menenjit; posttravmatik; tekrarlayan.

Ulus Travma Acil Cerrahi Derg 2015;21(4):261–265

doi: 10.5505/tjtes.2015.02651

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ORIGIN A L A R T IC L E

Choice of incision in penetrating cardiac injuries: Which one must we prefer: Thoracotomy or sternotomy?

Yüksel Beşir, M.D.,1 Orhan Gökalp, M.D.,2 Börteçin Eygi, M.D.,1 Hasan İner, M.D.,1 İhsan Peker, M.D.,1 Gamze Gökalp, M.D.,3 Levent Yılık, M.D.,2 Ali Gürbüz, M.D.1 1

Department of Cardiovascular Surgery, Katip Celebi University Ataturk Training and Reseacrh Hospital, Izmir

2

Department of Cardiovascular Surgery, Katip Celebi University Faculty of Medicine, Izmir

3

Department of Paediatric Emergency, Tepecik Training and Research Hospital, Izmir

ABSTRACT BACKGROUND: Penetrating cardiac injuries are high-risk, high-mortality injuries considering the outcomes. Therefore, it is important to choose the appropriate incision. In general clinical settings, thoracotomy and median sternotomy are choices of incisions to explore the injury. In this study, the results of median sternotomy and thoracotomy in penetrating cardiac injuries were compared.

METHODS: Between January 2003 and December 2013, forty patients, who underwent either thoracotomy or median sternotomy for penetrating cardiac injury, were retrospectively analyzed, and the collected data were compared. Twenty-six patients underwent thoracotomy (Group 1), and fourteen patients underwent median sternotomy (Group 2).

RESULTS: There was no statistically significant gender difference between the groups. However, the mean age in Group 2 was found to be significantly higher than the one in Group 1 (p<0.05).

CONCLUSION: There were no significant survival differences between the groups in the long term. Incision choice should be determined considering the site of injury and whether there is an accompanying pulmonary injury or not. On the other hand, thoracotomy has some draw backs compared to median sternotomy.

Key words: Cardiac; median sternotomy; penetrating; thoracotomy.

INTRODUCTION Firearms and sharp weapons are general causes of penetrating cardiac injuries in most cases. Only 10.4% of the trauma cases in need of immediate surgical intervention happen to be in the thorax, and 1% of these cases are cardiac injuries.

[1] Although cardiac injuries are rare, they are highly fatal injuries compared to the other types. It is really important to transfer these patients to the nearest facility in time, make sure they get immediate diagnosis and proper resuscitation until they are ready to be taken into the operating room for exploration. Median sternotomy and thoracotomy are two Address for correspondence: Yüksel Beşir, M.D. İzmir Katip Çelebi Üniversitesi Atatürk Eğitim ve Araştırma Hastanesi, Kalp Damar Cerrahisi Kliniği, İzmir, Turkey Tel: +90 232 – 243 43 43 E-mail: yukselbesir@hotmail.com Qucik Response Code

Ulus Travma Acil Cerrahi Derg 2015;21(4):266–270 doi: 10.5505/tjtes.2015.52882 Copyright 2015 TJTES

266

options to explore any trauma to the chest.[2] Surgeon generally decides the technique of approach in the operating room considering the site of injury and presence of an accompanying pulmonary injury. In this study, the results of thoracotomy and median sternotomy were compared.

MATERIALS AND METHODS Forty patients who underwent surgical intervention due to penetrating cardiac injury were retrospectively analyzed between January 2003 and December 2013. The data were collected from hospital archives. Twenty-six (65%) patients underwent thoracotomy (Group 1) while fourteen of them (35%) underwent median sternotomy (Group 2).

The data regarding demographics, etiology and perioperative findings were analyzed.

Computerized tomography, physical exam, chest x-ray and echocardiography were the tools of investigation in the preoperative setting. On the other hand, some of these tools had to be ignored due to hemodynamic instability of the patients, and they were taken to the operating room right away.

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Beşir et al. Choice of incision in penetrating cardiac injuries

Table 1. Characteristics of age and gender Group 1 Group 2 p Male Sex (n, %)

25

Age (Mean±SD)

30.12±12.54

96.2

11

78.6

0.115

40.86±17.06

0.026

15–63 19–77

Operating physicians decided the exploration technique according to the site of injury and presence of a possible pulmonary injury. In case of pulmonary involvement, they went for thoracotomy. When there was a suspicion of posterior cardiac wall involvement and an accompanying pulmonary injury, thoracotomy was the chosen technique. In case of any anterior cardiac involvement without suspicion of pulmonary injury, the chosen technique was median sternotomy. Some patients with thoracotomy had also received median sternotomy where the cardiac injuries could not be repaired through thoracotomy. Moreover, some patients with median sternotomy also received additional thoracotomy due to their pulmonary injuries. Hemodynamic instability was not a factor for choosing the exploration technique. There was no immediate thoracotomy in the emergency room. Cardiopulmonary bypass was never used in these patients.

Injuries other than in the thorax were assessed and treated after repairing the thoracic injuries.

Patients with cardiac arrest and the ones who were unresponsive to resuscitation were excluded from the study.

Statistical analysis Data analysis was performed using SPSS 15.0 for Windows with a 95% confidence interval. Pearson Chi-Square and Fisher’s Exact test were used for analyzing the categorical data

comparison between the groups. Mann-Whitney U statistical analysis was used for the comparison of continuous variables.

P<0.05 is accepted as the minimum statistical significant value.

RESULTS There were twenty-five (96%) male patients and one (4%) female patient in Group 1. The mean age of Group 1 was 30.1±12.5 (15–63) years; there were eleven (78%) male patients and three (22%) female patients in Group 2, and the mean age of this group was 40.86±17.06 (19–77) years. There was no statistically significant gender difference between the groups (p=0.11). In Group 2, mean age was statistically significantly different than the mean age in Group 1 (p=0.02) (Table 1).

In Group 1, twenty-one patients had sharp weapon injuries and five had firearm injuries. In Group 2, seven patients had sharp weapon injuries, two patients had firearm injuries and five patients had injuries due to medical interventions. There was a significant difference for medical interventional injuries in Group 2 (p=0.005). There was no significant difference comparing the other etiologic factors. As for the additional operations in Group 1, there were eleven pulmonary repairs, three internal mammary artery ligations, four abdominal exploration, and two primary repairs of great vessels (descending aorta and pulmonary artery). In Group 2, one pulmonary repair, three abdominal explorations, and two repairs of great vessels (ascending aorta, right subclavian artery) were additionally performed. Statistically, the pulmonary repair rate was found significantly higher in Group 1 than in Group 2 (p=0.03). Seventeen patients in Group 1 and four patients in Group 2 had additional surgical intervention, and this finding was statistically significant (p=0.026) (Table 2).

Twenty-one patients received left antero-lateral thoracotomy, two received left postero-lateral thoracotomy and three received right anterior thoracotomy. In thoracotomy patients, three patients additionally received median sternotomy due

Table 2. Etiology and additional operations

Group 1 Group 2

n

%

n

%

Etiology

0.005

Sharp weapon injuries

20

76.9

Firearm injuries

6

23.1

2

14.3

Complications of medical interventions

0

0

5

35.7

Additional operation

17

65.4

4

28.6

0.026

Lung repair

11

42.3

1

7.1

0.030

Inter mamarian artery ligation

3

11.5

0

0

0.539

Great vessel repair

2

7.7

2

14.3

0.602

Abdomen exploration

4

15.4

3

21.4

0.679

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7

p

50

267

Beşir et al. Choice of incision in penetrating cardiac injuries

Table 3. Localization of cardiac injuries

Group 1

Group 2

p

Right ventricle

11

10

0.006

Left ventricle

11

4

0.392

Right atrium

8

2

0.446

to exposure problems of the injuries. In sternotomy patients, two received additional thoracotomy due to pulmonary injuries. Cardiopulmonary by-pass was never used in both groups.

In Group 1, there were eleven patients with right ventricle injury, eleven with left ventricle injury, eight with right atrial injury, and four patients had multiple injury sites. In Group 2, there were ten right ventricle injuries, four left ventricle injuries, two right atrial injuries, and two patients had multiple injury sites. There was no left atrial injury at all. There was no statistically significant difference in the groups for injury sites (p>0.05) (Table 3). The injuries of three patients in Group 1 and two patients in Group 2 were repaired with pericardial grafts and synthetic grafts. Injuries in all the other patients were repaired with immediate primary suturing.

The mean duration of operations in Group 1 was found significantly higher than the durations in Group 2 (p=0.020).

Total perioperative blood transfusions in Group 1 were higher than the total number of transfusions in Group 2 (p=0.003). When the durations of ICU stays were compared, there was no statistically significant difference between the groups (p=0.662). On the other hand, mean length of hospital stay was found significantly higher in Group 1 (p=0.008).

There were seven (26.9%) mortalities in Group 1 and two (14.2%) in group 2, but there was no statistical significance (p=0.453). One patient in Group 1 had a reoperation due to bleeding (Table 4).

DISCUSSION Penetrating cardiac injuries make up 10% of all thoracic trauma cases though they are found to be the most common cause of mortality.[1,3,4] Patient profile in this group of trauma cases is generally young males.[3,4] In our study, the mean age

in Group 1 was 30.1±12.5 and 40.86±17.06 in Group 2, and that is slightly different from the data in the literature. The mean age was found higher in Group 2 than in Group 1, which is thought to be due to the higher rate of patients undergoing complicated percutaneous interventions in this group. In this study, there was a male predominance, which is concordant with the general literature.

Sharp object injuries and firearm injuries are general causes for penetrating cardiac injuries in many studies.[5,6] Most common cause of penetrating cardiac injuries in the United States is firearms, and in the rest of the world, the leading cause of penetrating cardiac injuries is sharp objects. There are also some rare causes like fracture of sternum and percutaneous interventions.[6] Most common reasons for iatrogenic cardiac injuries are implantation or explantation of pacemaker leads, radiofrequency ablation, percutaneous transluminal coronary angiography, central venous catheters, and pulmonary artery catheterizations.[6,7] In this study, also it was also found that the most common reasons for penetrating cardiac injuries are sharp objects and firearm injuries. In the sternotomy group; however, the rate of iatrogenic injuries was found to be higher. In our institution, operating theaters and angiography suits are on the same floor. In case of a complication, the patients can be transferred into the theaters immediately and such patients usually receive median sternotomy since the underlying pathology is expected to be heart related. These patients have almost always sole cardiac injuries so median sternotomy is the chosen technique.

Mortality in penetrating cardiac injuries is also closely related to adjacent organ injuries.[3,8] Rate of accompanying Intraabdominal injuries that require laparotomy is 10% as stated by many authors.[9,10] Manduz et al. have reported in one of their studies that the extra cardiac injuries accompany 35% of cardiac injuries.[3] In this study, ten patients had pulmonary injuries, one patient had liver injury, and one patient had colon injury. Firearm injuries also possess greater risk for additional extra cardiac injuries.[4,11] In our study, extra cardiac injuries in the thoracotomy group were found higher than in the sternotomy group since eligible patients for this group generally admitted with pulmonary injuries already. Considering patients with non-pulmonary extra cardiac injuries, there was no statistical difference between the groups.

Table 4. Perioperative data

Duration of operation (minute)

Group 2

p

160.38±89.35 (55–385)

103.93±28.16 (60–180)

0.02

Blood transfusion (unit)

4.73±2.69 (2–11)

2.43±1.7 (1–6)

0.003

Length of hospital stay (day)

6.5±2.25 (4–12)

4.56±1.01 (3–6)

0.008

Duration of intensive care unit (day)

3.17±3.55 (1–17)

2.62±0.96 (2–5)

0.662

7 (26.9%)

2 (14.2%)

0.453

Mortality

268

Group 1

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Beşir et al. Choice of incision in penetrating cardiac injuries

As reported by many authors, the most commonly involved chamber is the right ventricle (RV), followed by the left ventricle (LV), and the left atrium (LA) has been found to be rarely involved.[6,12] Kang et al. have reported the following involvement rates: RV 43%, LV 34%, RA 18%, LA 5%. Involvement of multiple chambers is 18–35%.[4,6] In our study, the most commonly involved chamber was RV, followed by LV and RA, respectively. These findings also correlate with the published data. Involvement rates of multiple cardiac chambers in our study are as follows: 15% in Group 1, 14% in Group 2.

Incision and approach to injuries vary among institutions.

There are numerous publications about different approaches as published data though there is no consensus. There are studies showing significant survival rates in emergent antero-lateral thoracotomy for cardiac injuries admitted to emergency room.[1,13] On the other hand, some authors have reported that thoracotomy for penetrating cardiac injuries should only be performed by experienced and well-equipped teams to achieve favorable results.[6,14] In our study, the patients were transferred to the operating rooms immediately since the ER is located in close proximity to ORs. There are some studies suggesting median sternotomy in the first place for hemodynamically stable patients admitted to the ER.[1] When sternum saw is available, sternotomy can be managed very fast and effectively yielding great exposure to the heart and great vessels.[1,6,15] Sternotomy results in less pain compared to thoracotomy so pulmonary functions are minimally depressed and patient can be weaned easily. Sternotomy, on the other hand, can be very disadvantageous in cases of descending aortic injuries and esophageal injuries, in these cases, cardiopulmonary by-pass is generally established.[1,15] In suspicion of posterior cardiac injury or/and esophageal injury, thoracotomy can be chosen in the first place. The initial plans for the approach cannot yield proper exposure to the injury site and an additional sternotomy or a thoracotomy can be needed sometimes. Mitchell et al. have reported 20% sternotomy in thoracotomy patients and a 3% thoracotomy in sternotomy patients in their study.[15] In our study, 11% of the thoracotomy patients needed additional sternotomy and 14% of the sternotomy patients needed additional thoracotomy.

Additional incisions are unfavorable due to excessive pain and cosmetic issues so it is important to avoid extra incisions.

It is to our belief that preoperative imaging is the key point and should be carefully performed as long as the patient is hemodynamically stable enough. In some cases; however, it is inevitable to perform additional incisions no matter how hard imaging modalities have been instituted to make a decision.

Survival rates in penetrating cardiac injuries can vary between 3% and 84% in published studies.[6,16] Tyburski et al. have reported the following variables as mortality factors: hemodynamic instability, mechanism of injury (firearm injuries are the most fatal injuries), presence of cardiac tamponade at admission, presence of great vessel injury and presence of multiple injuries.[16] The best prognosis is reported for the right venUlus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

tricle injuries.[4,17] In published studies, authors have generally compared thoracotomies performed in the ER and the thoracotomies performed in the OR for prognosis. In our study, the mortality rates between the thoracotomy group and the sternotomy group were compared, and no statistically significant difference was found. Similar comparisons were not found in the literature as published studies. On the other hand, duration of operation, transfusions and length of hospital stay were found significantly different in two groups. The thoracotomy group showed increased rates for transfusion, hospital stay and duration of operation because this group had additional injuries to primary cardiac injuries. Number of patients and retrospective nature of this study are the general limitations along with the inhomogeneous etiologies of injuries for the two groups.

Thoracotomy and sternotomy are two different approaches in suspected penetrating cardiac injuries. There is no significant difference in prognosis between the groups. Even though thoracotomy is generally considered favorable in multiple injuries, we believe thoracotomy can be disadvantageous in yielding proper operative exposure in some cases.

Conflict of interest: None declared.

REFERENCES 1. Dereli Y, Ozdemir R, Ağrış M, Oncel M, Hoşgör K, Ozdiş AS. Penetrating cardiac injuries: assessment of 21 patients. Ulus Travma Acil Cerrahi Derg 2012;18:441–5. [Abstract] 2. Asensio JA, Soto SN, Forno W, Roldán G, Petrone P, Gambaro E, et al. Penetrating cardiac injuries: a complex challenge. Surg Today 2001;31:1041–53.

3. Manduz S, Katrancıoğlu N, Bingol H, Atlı H, Dogan K. Penetrating cardiac injuries. Turkish J Thorac Cardiovasc Surg 2008;16:228–231.

4. Gormus N, Dereli Y, Tanyeli O. Blunt and Penetrating Cardiac Injurie.

Turkiye Klinikleri J Cardiovasc Surg-Special Topics 2013;5:5–10.

5. Asensio JA, Garcia-Nunez LM, Petrone P. Penetrating cardiac injuries in America-predictors of outcome in 2016 patients from the National Trauma Data Bank; in preparation. As quoted by Asensio JA, Garcia-Nunez LM, Petrone P. Trauma to the heart. In: Feliciano DV, Mattox KL Moore EE, editors. Trauma. 6th ed. New York: McGraw Hill; 2008. p. 569–88.

6. Kang N, Hsee L, Rizoli S, Alison P. Penetrating cardiac injury: overcoming the limits set by Nature. Injury 2009;40:919–27.

7. Fasseas P, Orford JL, Panetta CJ, Bell MR, Denktas AE, Lennon RJ, et al. Incidence, correlates, management, and clinical outcome of coronary perforation: analysis of 16,298 procedures. Am Heart J 2004;147:140–5.

8. Campbell NC, Thomson SR, Muckart DJ, Meumann CM, Van Middelkoop I, Botha JB. Review of 1198 cases of penetrating cardiac trauma. Br J Surg 1997;84:1737–40.

9. Degiannis E, Bowley DM, Westaby S. Penetrating cardiac injury. Ann R Coll Surg Engl 2005;87:61–3.

10. Saadia R, Levy RD, Degiannis E, Velmahos GC. Penetrating cardiac injuries: clinical classification and management strategy. Br J Surg 1994;81:1572–5.

11. Buckman RF Jr, Badellino MM, Mauro LH, Asensio JA, Caputo C, Gass J, et al. Penetrating cardiac wounds: prospective study of factors influenc-

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12. Çikirikçioglu M, Yagdi T, Posacioglu H, Ozkisacik E, Calkavur T, Atay Y, et al. Penetran cardiac injury. Ulus Travma Acil Cerrahi Derg 2000;6;189–92.

13. Hardikar AA, Thakur SS, Karmakar PS, Ambike VS, Kanetkar AV, Golhar KB. Penetrating cardiac injury due to ball pointpen. Asian Cardiovasc Thorac Ann 1999;7:158–60.

14. Working Group, Ad Hoc Subcommittee on Outcomes, American College of Surgeons. Committee on Trauma. Practice management guidelines for emergency department thoracotomy. Working Group, Ad Hoc

Subcommittee on Outcomes, American College of Surgeons-Committee on Trauma. J Am Coll Surg 2001;193:303–9.

15. Mitchell ME, Muakkassa FF, Poole GV, Rhodes RS, Griswold JA. Surgical approach of choice for penetrating cardiac wounds. J Trauma 1993;34:17–20.

16. Tyburski JG, Astra L, Wilson RF, Dente C, Steffes C. Factors affecting prognosis with penetrating wounds of the heart. J Trauma 2000;48:587– 91.

17. Attar S, Suter CM, Hankins JR, Sequeira A, McLaughlin JS. Penetrating cardiac injuries. Ann Thorac Surg 1991;51:711–6.

KLİNİK ÇALIŞMA - ÖZET OLGU SUNUMU

Penetran kalp yaralanmalarında insizyon seçimi: Hangisini tercih etmeliyiz?

Torakotomi mi sternotomi mi?

Dr. Yüksel Beşir,1 Dr. Orhan Gökalp,2 Dr. Börteçin Eygi,1 Dr. Hasan İner,1 Dr. İhsan Peker,1 Dr. Gamze Gökalp,3 Dr. Levent Yılık,2 Dr. Ali Gürbüz1 1 2 3

İzmir Katip Çelebi Üniversitesi Atatürk Eğitim ve Araştırma Hastanesi, Kalp Damar Cerrahisi Kliniği, İzmi̇ r İzmir Katip Çelebi Üniversitesi Tıp Fakültesi, Kalp Damar Cerrahisi Anabilim Dalı, İzmi̇ r Tepecik Eğitim ve Araştırma Hastanesi, Çocuk Acil Kliniği, İzmir

AMAÇ: Penetran kalp yaralanmaları klinik sonuçları sebebiyle yüksek mortaliteye sahip ciddi yaralanmalardır. Bu yaralanmalardaki en önemli problemlerden biri ekplorasyon için uygun yöntemi seçmektir. Genel olarak yaralanma bölgesine göre torakotomi ya da mediyan sternotomi yöntemlerinden birisi kullanılarak eksplorasyon gerçekleştirilir. Bu çalışmada penetran kalp yaralanması olan hastalarda yapılan mediyan sternotomi ve torakotomi sonuçları karşılaştırılmıştır.

GEREÇ VE YÖNTEM: Ocak 2003 ile Aralık 2013 arasında kliniğimizde penetran kalp yaralanması sebebiyle ameliyat edilmiş toplam 40 hasta geriye dönük olarak incelendi. Bu hastaların 26 tanesine torakotomi (Grup 1) 14 tanesine de mediyan sternotomi (Grup 2) uygulandı. Her iki grup ameliyat öncesi ve ameliyat sırasında veriler açısından karşılaştırıldı.

BULGULAR: İki grup arasında cinsiyet açısından fark yoktu. Ancak yaş ortalaması Grup 2’de diğerine göre istatistiksel olarak daha yüksek idi (p<0.05). Etiyolojik faktörlere bakıldığında ise Grup 1’de delici kesici alet ile yaralanma oranı Grup 2’den yüksek, Grup 2’de de girişimsel işlem komplikasyonuna bağlı yaralanma oranı Grup 1’den yüksek bulundu (p<0.05). Ameliyat sırasında verilerden ise ek olarak akciğer yaralanması ve diğer başka bölgede cerrahi müdahale oranı Grup 1’de Grup 2’ye göre istatistiksel olarak daha yüksek bulundu (p<0.05). Kullanılan kan miktarı, operasyon süresi ve hastaneden taburcu olma süresi de Grup 1’de istatistiksel olarak daha yüksek bulundu (p<0.05).

TARTIŞMA: Penetran kalp yaralanmalarında eksplorasyon için kullanılacak yönteme karar verilirken dikkate alınan esas parametreler yaralanma bölgesi ve akciğer yaralanması olup olmadığıdır. Bununla birlikte etkinliği çok iyi bilinen torakotomi ve mediyan sternotomi arasında sağ kalım açısından herhangi bir fark yoktur. Ancak torakotominin mediyan sternotomiye göre bazı ameliyat sırasında parametreler açısından dezavantajları olduğu da akılda bulunmalıdır.

Anahtar sözcükler: Kalp; mediyan sternotomi; penetran; torakotomi.

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doi: 10.5505/tjtes.2015.52882

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ORIGIN A L A R T IC L E

Cerebrovascular complications of transorbital penetrating intracranial injuries Yonca Özkan Arat, M.D.,1,2 Anıl Arat, M.D.,3 Kubilay Aydın, M.D.4 1

Department of Ophthalmology, Baskent University Faculty of Medicine, Ankara

2

Department of Ophthalmology and Visual Sciences, University of Wisconsin, Madison, WI, USA

3

Department of Radiology, Section of Interventional Neuroradiology, Hacettepe University Faculty of Medicine, Ankara

4

Department of Radiology, Section of Interventional Neuroradiology, Istanbul University Istanbul Faculty of Medicine, Istanbul

ABSTRACT BACKGROUND: Cerebrovascular trauma secondary to transorbital intracranial penetrating injury (TIPVI) is rare. Relatively benign initial presentation may mask the underlying life-threatening vascular injury in transorbital intracranial penetrations. The aim of this study was to evaluate clinical features and endovascular treatment of TIPVI. METHODS: Six patients with angiographic documentation of TIPVI in subacute/chronic phase were reviewed retrospectively. Five were treated endovascularly; however endovascular treatment was aborted in one and conservative management was pursued.

RESULTS: Except for one case presenting with vision loss and mild stroke, no significant neurologic deficit was present. Vascular lesions included two cases of carotid-cavernous fistulas, three traumatic aneurysms of cavernous carotid, anterior and middle cerebral arteries and a unique case of coalescing cavernous aneurysms following a through-and-through injury in which the aneurysms united within the thrombosed cavernous sinus on follow up. Fistulas were treated with covered stents, aneurysms with parent artery occlusion or flow diverters. All patients had uneventful recoveries.

CONCLUSION: TIPVI may present in a delayed fashion after a seemingly benign presentation. A high index of suspicion is critical to rule out TIPVI with vascular imaging. Transcatheter angiographic techniques allow for both diagnosis and treatment of TIPVI with favorable results.

Key words: Cerebrovascular injury; fistula; penetrating intracranial injury; transorbital injury; traumatic aneurysm.

INTRODUCTION Penetrating head injuries (PHI) represent about 0.4% of head injuries.[1] Compared with closed head injuries, PHIs are usually more severe and result in higher mortality and morbidity.

[2,3] They have historically been seen in military settings, but over the past two decades, civilian cases of PHI have been reported more frequently. PHIs are usually high-velocity type in military settings and low-velocity type including predominantly accidental injuries in the civilian settings.[2,3] Transor-

Address for correspondence: Anil Arat, M.D. Hacettepe Üniversitesi Hastanesi, Radyoloji Anabilim Dalı, Hacettepe Mahallesi, 06230 Ankara, Turkey Tel: +90 312 – 305 44 01 E-mail: anilarat@hotmail.com Qucik Response Code

Ulus Travma Acil Cerrahi Derg 2015;21(4):271–278 doi: 10.5505/tjtes.2015.48839 Copyright 2015 TJTES

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bital penetrating intracranial injury (TIPI) is aparticular type of PHI in this regard, as the orbit forms a ‘low-resistance’ pathway for the more commonly encountered low-velocity injuries in daily life.[4] It represents an uncommon type of injury,[5,6] it occurs more frequently in children,[7,8] and its management has been reported to be a challenge.[9] Although uncommon, TIPI may result in grave complications such as cerebrovascular injury, central nervous system infections, cerebrospinal fluid fistulas, and venous thrombosis.

[10–12] Among these complications, transorbital intracranial penetrating vascular injury (TIPVI) stands out as a risk factor for imminent death or disability.[13] Very limited data exist regarding the incidence and management of vascular injuries in TIPI. There are only a handful of cases of vascular complications after TIPI described in the literature. Due to their rare occurrence and diversity of mechanisms or patterns of such injury,[14,15] no standards exist regarding the management of these injuries. This series aimed to reviewthe presentation and endovascular management of TIPI cases with vascular complications we encountered, which were treated by neurointerventional procedures.

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MATERIALS AND METHODS This manuscript is related to cerebrovascular trauma secondary to low and high velocity transorbital intracranial penetrating injury. TIPI was described by Van Duinen[10] as entry of objects whose diameter is much smaller than the diameter of the anterior orbital opening, from the orbit into the intracranial space. He put forward that the orbital rim should remain intact, and he excluded high velocity injuries although he admitted that a clear cut-off between low and high velocity injuries is not clear. This point is also highlighted by other authors.[16] In his thesis about TIPI, Welman[17] also excluded high velocity injuries but included all penetrating trauma with an object that either traverses or is suspected to have traversed the orbital space. In this article, due to the lack of a clear distinction between high and low velocity impacts,[10] all penetrating injuries were included, provided that there was not extensive craniofacial injury and the penetrating injury primarily involved the compartment bordered by the skull bones forming the orbital walls. In this article, TIPVI is defined as vascular injuries caused by TIPI and includes traumatic aneurysms, caroticocavernous fistulas (CCF), cavernous sinus thrombosis and arterial occlusions. This is a retrospective review of six cases with TIPVI which the corresponding author encountered throughout his practice. In five of these cases, he was the primary operator for the endovascular treatment; however, in one patient, he was involved through case consultation and the third author was the primary interventionist.

All patients had a cerebral digital subtraction angiogram delineating the vascular injury and an endovascular treatment was attempted in all of the patients. Endovascular treatment was performed in all cases under general anesthesia and systemic heparinization via femoral percutaneous approach. In three cases treated by stents (stent grafts or flow diverter stents), patients were loaded with Clopidogrel and Aspirin at least 1 week prior to the procedure and patients were asked to continue antiplatelet medication for 6 months. For two of these patients who were above 50 kg (Case 4 and 6), the maintenance dose was 75 mg/day for Clopidogrel, 300 mg/day for Aspirin, and for the third patient who was 4 years old (Case 3) the patients family was asked to give the patient a quarter of a 75 mg tablet of Clopidogrel and 100 mg of Aspirin daily.

RESULTS There were a total of six patients (1 female, 5 male) with vascular injuries secondary to transorbital intracranial injury. All except one were children; mean age was 13.3 years (range, 2–27 years). Only the adult case had a high-velocity injury (Case 6). Both of the young children (Cases 3 and 5) had an accidental injury with a knitting needle, and all the other patients had an assault with sharp objects or shot guns.

One patient (Case 2) had an injury with multiple pellets that passed through both orbits resulting in bilateral open globe injury with no light perception vision. Otherwise, none of 272

the remaining cases had a globe injury. Endovascular treatment was successful in Cases 2 to 6. In the first patient, it appeared very feasible to finish the endovascular procedure with deployment of a stent during the procedure; however, the patient was noncompliant with medical advice. In order not to put the patient under the risk of a thromboembolic event based on her anticipated noncompliance to antiplatelet medication after discharge, the procedure was aborted and the patient was followed. In four out of six patients (67%), the involved artery was occluded either intentionally or during follow-up, without any clinical consequences.

The following includes the pertinent findings of patients in this series: Case 1– 15-year-old female was assaulted and presented to the emergency department with a right orbital pellet injury and frontal lobe hematoma. After evacuation of frontal hematoma, based on the initial CT scan which showed a fracture in the right and left nasal superior orbital rim and multiple pellets in the cranium without major injury to the globe, vascular imaging was requested. Since the pellets in close proximity of the ICA precluded a thorough visualization of the artery on CT angiogram, an angiogram was performed to rule out a vascular injury. The cerebral angiogram revealed a 3 mm bilobulated traumatic cavernous aneurysm. An attempt for primary coiling of the aneurysm failed. Since the patient was not compliant with medical advice and stent placement would entail strict adherence to antiplatelet medication, it was decided not to proceed with stent placement and follow the aneurysm conservatively. One year follow-up angiogram showed a decrease in the size and lobulation of the aneurysm.

Case 2– A 16-year-old male presented to the emergency room after being shot through the orbit with a shotgun. On examination, there was bilateral open globe injury with no light perception vision and orbital soft tissue injury. He was also noted to have pellets in close proximity of the right internal carotid artery (ICA) on CT scan, which prompted a cerebral angiogram. On angiogram, there were 3 tiny aneurysms of the cavernous ICA and no evidence of a carotid cavernous fistula (Fig. 1a). A repeat angiogram obtained after 8 days, on the day of the endovascular treatment of the aneurysms, showed interval enlargement of the aneurysms (Fig. 1b). Selective coiling was attempted, but it was realized that the two of the larger aneurysms had coalesced within the cavernous sinus, still in the absence of a carotid cavernous fistula (Fig. 1c). Stent reconstruction of the artery was unsuccessful and based on the presence of very good collateral flow through the Circle of Willis, the patient was treated with parent artery occlusion (Fig. 1d). The patient’s family denied a follow-up angiogram, patient had no significant neurologic deficits except for bilateral blindness at 6 months.

Case 3– A 4-year-old boy presented to the emergency room after an accidental injury caused by a knitting needle penUlus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

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(a)

(b)

(c)

(d)

Figure 1. Case 2; (a) Magnified views of the right carotid angiogram in lateral projection obtained after the assault reveals three tiny aneurysms of the cavernous carotid artery measuring approximately 1 to 1.5 mm in size and mild contour abnormality of the inferior border of the proximal cavernous carotid artery. (b) Follow-up angiogram in lateral view demonstrates interval growth of the aneurysm at the level of the dural ring. The 2 more proximal aneurysms have coalesced into a larger, approximately 5 mm aneurysm. Although the through-and through injury of the carotid artery involves the cavernous segment no evidence of a fistula at this site is noted. (c) Roadmap capture during embolization reveals that microcatheter used to catheterize the aneurysm (arrow) projecting posteriorly from the genu reentered the internal carotid artery from wall the defect at the orifice of the most proximal aneurysm. A balloon catheter was placed in the carotid artery (arrowhead) to protect the patency of the internal carotid artery but was removed later, upon recognition of the “multihole” injury of the carotid artery. (d) Lateral radiogram at the end of parent artery sacrifice. The carotid artery was coiled first in a retrograde fashion through the microcatheter reentering the artery proximally. As the catheter kicked back into the ICA, coiling was continued to complete occlusion of the carotid artery. An Amplatzer Vascular Plug (St. Jude Medical, St. Paul, MN) was placed proximally and stagnation of the contrast medium below the plug is evident.

etrating the right orbit. The needle was removed at the site of the accident. On examination, the entry wound was noted at the medial canthus. The patient had no neurologic deficit except for right abducence and facial nerve paresis. CT of the head revealed right retroorbital and subarachnoid hemorrhage. Since the patient had right pulsatile exophtalmus and subarachnoid hemorrhage, he underwent a carotid angiogram which revealed a right CCF (Fig. 2a). The patient was treated endovascularly. A detachable balloon was navigated to the site of the fistula and inflated (Fig. 2b). Due to the extent of the tear in the carotid artery, this was not sufficient to seal the site of the fistula. The wall defect was then covered by placement of two 4.5 mm polytetrafluoroethylene-covered

(a)

(b)

stent grafts (Jomed, Helsingborg, Sweden) at the site of the fistula that resulted in immediate occlusion of the fistula without any procedure related complications (Fig. 2c). Six month follow-up carotid angiography incidentally revealed interval occlusion of the right internal carotid artery and robust collateral flow through the Circle of Willis supplying the right ICA territory.

Case 4– A 16-year-old male was referred with complaints of headache. He had a history of a ‘pencil injury’ in the classroom three months before the presentation. The pencil entered the orbit superiorly without damaging the globe.

There was no neurologic deficit, but the patient had signifi-

(c)

Figure 2. Case 3; (a) Preoperative right carotid angiogram in anteroposterior view demonstrates the carotid-cavernous fistula. (b) Lateral view of internal carotid angiogram obtained during attempted embolization with detachable balloon shows that the inflated balloon was not able to seal off the tear in the carotid artery and that residual fistula remains. (c) Lateral projection of carotid angiogram obtained after placement of two stent grafts shows elimination of the fistula and restoration of the flow in the right internal carotid artery.

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(a)

(b)

(c)

(d)

Figure 3. Case 5; (a) Base view obtained from 3D rendering of head CT reveals a focal bony defect of the medial aspect of the orbital roof which corresponds to the entry point of the knitting needle to the cranium. (b) 3D rendering of the CTA demonstrating the defect of the orbital roof (arrow) and the aneurysm (open arrow) as seen from above. (c) Lateral view of right internal carotid angiogram shows the distal anterior cerebral artery traumatic aneurysm. (d) Lateral view of the right internal carotid angiogram after endovascular treatment reveals almost total obliteration of the aneurysm with coils. Due to the traumatic nature of the aneurysm, there was recurrence on follow-up, which was treated with endovascular parent artery sacrifice.

cant retroorbital headaches immediately after the accident which gradually worsened over the 3 months and converted to cephalalgia. A CT scan revealed a mass lesion of the middle cranial fossa. A CT angiogram showed the lesion to be a giant dissecting aneurysm of the proximal segment of middle cerebral artery. The aneurysm was treated by placement of Silk (Balt, Montmercy, France) flow diverter stents within a larger Leo (Balt, Montmercy, France) intracranial stent. 3-month CT angiogram demonstrated a patent middle cerebral artery and almost total occlusion of the aneurysm. The patient remained neurologically intact.

Case 5– A 2-year-old girl had an impalement injury to her right eye with a knitting needle. The needle entered the anterior cranial fossa by passing through the orbital roof. A CT scan revealed focal subarachnoid blood between the frontal lobes anteriorly and the entry site of the needle (Fig. 3a). She was neurologically intact and a decision was made to follow her closely without further intervention. Three days after the 274

accident, she suddenly deteriorated. After a seizure, she developed drowsiness and left sided hemiparesis. A repeat CT scan was significant for a newly developed 3 cm hematoma at the location of the previous subarachnoid hemorrhage. CTA revealed a 6 mm pseudoaneurysm of the distal anterior cerebral artery (Fig. 3b). The aneurysm was coiled (Figs. 3c, d), and then, the hematoma was evacuated surgically. At 2 months, there was recurrence of the pseudoaneurysm which was then treated with endovascular parent artery occlusion.

There was no clinical sequela. The patient remained asymptomatic at 21 months after the accident without recurrence of the aneurysm on magnetic resonance angiography.

Case 6– A 27-year-old male was referred with complaints of headache, proptosis and redness of the right eye developing immediately after a gunshot injury through the inferomedial aspect of the contralateral orbit (Fig. 4a) without any globe injury. There was restriction of abduction and adduction of the right eye. The carotid angiogram obtained 35 days later Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

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(a)

(b)

(c)

Figure 4. Case 6; (a) Photograph of patient 6 when he returned for a control angiogram 5 months after the injury and 4 months after treatment. The arrow marks the entry site of the bullet at the inferomedial rim of the left orbit which has healed with mild discoloration. (b) Pre-procedure right common carotid angiogram in right oblique projection shows simultaneous opacification of bilateral ophthalmic and angular veins secondary to the carotid-cavernous fistula as well as the internal carotid circulation arteries. Noted is the bullet that has traversed to the right. (c) Follow-up right common carotid angiogram 4 months after treatment in anteroposterior view shows no evidence of residual fistula and patency of the stent graft in the internal carotid artery.

revealed a right sided traumatic CCF (Fig. 4b), which was treated with 2 covered stents (Jostent Graftmaster Abbott Vascular Inc, CA, USA). The first stent opened more distally than anticipated and to cover the proximal leak into the fistula a second one was placed. There was immediate occlusion of the fistula. At 4 months, the internal carotid artery was patent, the fistula was obliterated and the patient was asymptomatic (Fig. 4c).

DISCUSSION Vascular complications of penetrating brain injury include traumatic aneurysms, traumatic occlusions, subarachnoid hemorrhage, vasospasm, and traumatic fistulas.[10,18] According to the recently published large series on vascular complications of penetrating head injury by Bodanapally et al.,[13] true incidence of vascular injuries after penetrating head injury is not clearly known because this condition is associated with a high rate of mortality before patients are able to receive medical care. These authors state that the incidence among survivors ranges from 3 to 42%, and they emphasize that previous reports mainly focus on the aneurysms. Despite the contradicting epidemiologic and etiologic data about these aneurysms,[19] it is put forward that among all intracranial aneurysms, only 0.4 to 0.7 percent are traumatic and only one fifth of these traumatic aneurysms are secondary to penetration of the head.[18] The incidence of cavernous fistula secondary to penetrating head injury is even more obscure and appears to be even lower compared to aneurysms.[12,20,21] Periorbital penetrating trauma accounts for 30 to 50% of eye trauma,[22] but the penetrating object usually does not reach the brain. The occurrence of transorbital penetrating brain Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

injury is, therefore, uncommon.[6] On the other hand, it is rare to encounter traumatic vascular injury after any kind of penetrating brain injury[19] so it is ostensible that TIPVI is very rare. As a matter of fact, in a series of 35 patients with penetrating orbitocranial gunshot injuries, no vascular injury has been noted.[23] In another study reviewing non-missile orbitocranial penetrations, only one case of a CCF and no aneurysms have been found.[24] Turbin et al. reviewed all cases of low-velocity TIPIs from 1980 to 2002 and could not find any traumatic aneurysms in the literature.[2] CCF appears to be rare but still more common compared to aneurysms after TIPI. To date, some CCF cases have been reported secondary to TIPI.[10,17,24–26] The most comprehensive studies on TIPI include a book by Van Duinen published in 2000[10] and a thesis by Welman presented in 2004.[17] It is quite likely that TIPI cases are included in large series of penetrating cranial trauma,[12,27] but a distinct transorbital route is not defined in these large series.

We went over the citations provided by Van Duinen[10] and Welman et al.[17] to search for the traumatic aneurysms secondary to low-velocity TIPI, and then, we also searched the literature from 1999 to date to find additional cases of low velocity TIPVI. We were able to identify only 15 documented cases during the last two centuries since the early 1800s.

[10,17,19,28–30] Interestingly, in four of these 14 cases, the anterior cerebral artery was involved, the internal carotid artery/anterior choroidal artery was involved in 4, we were not able to ascertain the exact location of the aneurysms in 7 cases from the data available. As for high velocity injury, we were able to identify only four cases of intracranial aneurysms/transections secondary to high velocity TIPI since 1999.[31–34] All were “centrally” located; one on the anterior cerebral artery, two 275

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on basilar artery and one on M1 segment of middle cerebral artery. All the vascular locations listed above are “central” (that is to say close to midline) in location. This is contrary to the more commonly encountered “peripheral” location of vascular injury secondary to PHI in general.[19] In this series, all of the vascular injuries were central (internal carotid, anterior cerebral, proximal middle cerebral).

The three most frequent trajectories by which foreign objects penetrate the brain are through the orbital roof, the superior orbital fissure, or the optic canal.[5,6] The most frequent path is via the roof of the orbit since the superior orbital plate of the frontal bone is fragile, and during the injury, patients extend their heads backwards, exposing the orbital roof. The next most common route is via the superior orbital fissure.

The objects that enter the orbit at a low velocity are directed by the bony anatomy toward the superior orbital fissure. A third trajectory of penetration is the optic canal.[5,6] Penetrating objects may have been directed centrally because of the funneling of low-velocity objects centrally as they can make their way into the skull through the low-resistance pathways mentioned above.

Superior orbital fissure penetration is more likely to result in lesions around cavernous sinus,[28] which are represented by cavernous sinus thrombosis or rarely carotid-cavernous fistula and very rarely, isolated cavernous aneurysms. In our literature search, we found reports on cavernous sinus thrombosis,[2] scattered reports on CCFs[17,10,24–26] and a scant number of ICA aneurysms around the cavernous portion of the ICA[10] secondary to TIPI. We are unaware of the occurrence of a case, regardless of the type or site of the trauma, similar to the one we presented in which there were coalescing aneurysms of the cavernous ICA secondary to multi-hole penetration of the ICA (Case 2). We think that cavernous sinus thrombosis secondary to the indwelling pellets concealed the multiple vessel wall defects of the ICA within the cavernous ICA, and as the thrombus around these defects resolved, there was coalition of the pseudoaneurysms within the sinus.

Another interesting fact about this case was the presence of an asymptomatic small cerebral infarction in the distal cerebrovascular territory. Occurrence of cerebral infarcts as a sequela to penetrating ICA injury has been reported rarely in the literature.[35,36] The clinical importance of TIPVI arises from the following: 1) The orbit is a pathway for low-velocity, small-sized objects to reach the brain, which was the case in five out of six patients in our series, and in three of these, the penetrating pen or knitting needle would be unlikely to enter the brain had the injury occurred in other parts of the skull. The effect of this low-energy injury may appear to be deceivingly local.[2] Again in five out of six of our cases, findings were confined to the orbitofacial region concealing the underlying vascular brain injury. At times, even the orbitofacial entry wounds of sizable penetrating objects may be missed in TIPI.[2,37,38] Furthermore, 276

the globe, not uncommonly, is pushed sideways and the presence of vision as noted in some of our patients may provide false relief. 2) The incidence of vascular injury in TIPI may be too low for the emergency medicine physician or the ophthalmologist to bring to mind. 3) Cerebral arteries have very thin adventitia and no internal elastic lamina. Consequently, initially small traumatic pseudoaneurysm may quickly enlarge, rupture and re-rupture in 30 to 50% of cases causing mortality or significant morbidity. That is to say, TIPVI is a morbid injury without a straightforward diagnosis.

High-velocity objects like bullets tend to transect the vessels, and low-velocity penetrating injury is more likely to result in traumatic intracranial aneurysms.[33] Either high-velocity impacts or the secondary occlusion and/or dissection of vessels are more straightforward to diagnose. Since low-velocity objects can reach the cerebral vessels relatively easily through the orbit, a high index of suspicion is needed for detection of traumatic intracranial aneurysms due to low-velocity penetrating trauma. These lesions are insidious,[19] may result in the so called “talk and die” type of injury[22] or tend to rupture later in the subacute phase or even go into chronic phase undetected. Cases 2 and 5 are examples of enlarging/rupturing traumatic intracranial aneurysms, Case 1 is an example that was followed into the chronic phase.

The suggested management of TIPI is to leave the penetrating object in situ and immediately transfer the patient to a trauma or tertiary care center.[11] It was reported to be unsafe and unnecessary to delay vascular imaging in these cases.

[12] Although TIPVI is not common after TIPI, detecting a vascular injury would be life-saving. We believe that given the widespread availability of multislice CT imaging, TIPI patients should undergo a cerebral CT angiogram in addition to a routine non-contrast head CT. Despite the fact that CT angiogram lacks the sensitivity of the digital subtraction angiogram (DSA), its ability to detect traumatic intracranial aneurysms is very accurate.[13] Risk factors for vascular injury include orbitobasal (including transorbital) entry site, subarachnoid or intraventricular hemorrhage, trajectory within 2 cm or less to the Circle of Willis[13] and blast injury with Glascow Coma Scale 8 or less.[39] These findings should prompt a DSA. Based on our case and our literature review, there appears a vulnerability of central arteries in TIPI. These arteries are the anterior cerebral, internal carotid, basilar and proximal middle cerebral arteries which should be well scrutinized on vascular imaging.

There is no standard treatment for TIPVI. Surgical and endovascular treatments and in selected cases, conservative management have been utilized.[19,39,40] We managed one aneurysm conservatively because the patient was not compliant with her medications including antiplatelet drugs. Selective coiling had failed and the tiny cavernous aneurysm had diminished in size during follow-up. Otherwise, for the most part, interventional treatment of cavernous injuries is endovascular. In this arterial Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

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segment, various endovascular techniques including selective occlusion with balloons or coils, placement of stents or stent grafts have been utilized for the treatment of non-traumatic lesions or those due to blunt trauma.[19,40,41] We found only one case of TIPVI treated endovascularly[19] but expected that favorable results obtained in other traumatic aneurysms will also hold true for TIPVI. The traumatic aneurysms within the subarachnoid space have been managed either surgically or endovascularly.[39,19] As a traumatic cerebral aneurysm lacks an aneurysm wall and is actually a pseudoaneurysm confined by the surrounding subarachnoid clot, conventional clipping or coiling is associated with re-rupture or a high rate of recurrence.[39] Whenever feasible, we prefer to perform endovascular parent artery occlusion for these aneurysms. With improvements in stent technology, smaller stents and flowdiverter stents are available. These devices allow for the healing of the aneurysmal wall defect over the stent struts even in very fragile, dissecting type aneurysms[42] and decrease the rate of recurrences. We used a flow diverter in one of our patients and believe these devices will be used more frequently in traumatic intracranial aneurysms in the future.

One point to underscore is that repeat vascular imaging is critical in the management of TIPVI and other traumatic intracranial aneurysms. We suggest performing a repeat CT angiogram or DSA after an initially negative imaging study in high risk patients, which enables the physician to catch the aneurysms that had been concealed by the initial vasospasm or that had demonstrated interval growth. Regardless of the treatment modality employed, repeat vascular imaging is critical to detect recurrences in these lesions which are prone to recur without significant signs or symptoms.

TIPVI is a rare but devastating complication of TIPI. Since low velocity injury may cause intracranial penetration and vascular damage without significant symptoms or findings, a high level of suspicion is needed to detect TIPVI. Vascular imaging should be used liberally in cases of TIPI. Transcatheter angiographic techniques allow for both unequivocal diagnosis and also treatment of TIPVI with good results.

Conflict of interest: None declared.

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10. Martin Th A van Duinen, editor. The transorbital intracranial penetrating injury: a review of the literature from a neurosurgical viewpoint. Boston: Kluwer Academic Publishers, 163. p. 2000.

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12. du Trevou MD, van Dellen JR. Penetrating stab wounds to the brain: the timing of angiography in patients presenting with the weapon already removed. Neurosurgery 1992;31:905–12.

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16. Perez EA. Penetrating Trauma. In: Bucholz RW, Heckman CD, CourtBrown CM, editors. Rockwood and Green’s Fractures in Adults. 6th ed.

Philadelphia: Lippincott Williams & Wilkins; 2006. p. 446–75.

17. Welman C. A review of the Groote Schuur hospital experience of lowvelocity non-missile penetrating orbital and transorbital stab wounds [dissertation]. University of Cape Town, 2004.

18. Vascular complications of penetrating brain injury. J Trauma 2001;51(2 Suppl):26–8.

19. Cohen JE, Gomori JM, Segal R, Spivak A, Margolin E, Sviri G, et al.

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20. Fields CE, Cassano AD, Dattilo JB, Yelon JA, Ivatury RR, Broderick TJ. Indirect carotid-cavernous sinus fistula after shotgun injury. J Trauma 2000;48:338–41.

21. Fabian TS, Woody JD, Ciraulo DL, Lett ED, Phlegar RF, Barker DE, et al. Posttraumatic carotid cavernous fistula: frequency analysis of signs, symptoms, and disability outcomes after angiographic embolization. J Trauma 1999;47:275–81.

22. Erkol Z, Bilal S, Bayram M. An orbitocranial penetration case with a perforating body. [Article in Turkish] Ulus Travma Acil Cerrahi Derg 1996;2:47–50.

23. Gönül E, Erdoğan E, Taşar M, Yetişer S, Akay KM, Düz B, et al. Penetrating orbitocranial gunshot injuries. Surg Neurol 2005;63:24–31.

24. Chibbaro S, Tacconi L. Orbito-cranial injuries caused by penetrating non-missile foreign bodies. Experience with eighteen patients. Acta Neurochir (Wien) 2006;148:937–42.

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26. Khalil N, Elwany MN, Miller JD. Transcranial stab wounds: morbidity and medicolegal awareness. Surg Neurol 1991;35:294–9.

27. Bodanapally UK, Saksobhavivat N, Shanmuganathan K, Aarabi B, Roy AK. Arterial injuries after penetrating brain injury in civilians: risk factors on admission head computed tomography. J Neurosurg 2015;122:219– 26.

28. Kim MS, Sim SY. Traumatic aneurysm of the callosomarginal arterycortical artery junction from penetrating injury by scissors. J Korean Neurosurg Soc 2014;55:222–5.

29. Kawata H, Ohba M, Hikage F, Ohguro H. Transorbital cerebral injury in two children. Jpn J Clin Ophthalmol 2009;63:665–9.

30. Greene KA, Dickman CA, Smith KA, Kinder EJ, Zabramski JM. Selfinflicted orbital and intracranial injury with a retained foreign body, associated with psychotic depression: case report and review. Surg Neurol 1993;40:499–503.

31. Tokdemir M, Türkçüoğlu P, Kafadar H, Türkoğlu A. Sudden death following periorbital pellet injury. Brain Inj 2007;21:997–9.

32. Brenke C, Fontana J, Schmieder K, Barth M. Surgical management of basilar artery laceration caused by transorbital penetrating injury: case report. J Neurol Surg A Cent Eur Neurosurg 2013;74 Suppl 1:239–41.

33. Horowitz MB, Kopitnik TA, Landreneau F, Ramnani DM, Rushing EJ, George E, et al. Multidisciplinary approach to traumatic intracranial aneurysms secondary to shotgun and handgun wounds. Surg Neurol 1999;51:31–42.

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35. Hiraishi T, Kawaguchi T, Kobayashi T, Tomikawa M, Ito Y, Fujii Y. Unstable stenosis of the internal carotid artery caused by a craniofacial nailgun injury-case report-. Neurol Med Chir (Tokyo) 2009;49:590–3.

36. Song JK, Srinivasan J, Gordon DS, Newell DW, Baxter AB. Internal carotid pseudoaneurysm and cerebral infarction from shotgun pellet penetration and embolization. AJR Am J Roentgenol 1999;173:1116.

37. Abdelaziz L, Barbara R, Scullion D, Cosgrave E, Metcalfe T. A minor lid laceration concealing a potentially life-threatening injury. BMJ Case Rep 2012.

38. Vaqas B, Kopniczky Z, Haliasos N, Namnyak S, Pollock J. An occult intracranial foreign body introduced via a conjunctival wound. Trauma 2013;15:252–6.

39. Bell RS, Vo AH, Roberts R, Wanebo J, Armonda RA. Wartime traumatic aneurysms: acute presentation, diagnosis, and multimodal treatment of 64 craniocervical arterial injuries. Neurosurgery 2010;66:66–79.

40. Fulkerson DH, Voorhies JM, McCanna SP, Payner TD, Leipzig TJ, Scott JA, et al. Endovascular treatment and radiographic follow-up of proximal traumatic intracranial aneurysms in adolescents: case series and review of the literature. Childs Nerv Syst 2010;26:613–20.

41. Archondakis E, Pero G, Valvassori L, Boccardi E, Scialfa G. Angiographic follow-up of traumatic carotid cavernous fistulas treated with endovascular stent graft placement. AJNR Am J Neuroradiol 2007;28:342–7.

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Treatment of ruptured blood blister-like aneurysms with flow diverter SILK stents. J Neurointerv Surg 2015;7:202–9.

ORİJİNAL ÇALIŞMA - ÖZET OLGU SUNUMU

Transorbital penetran intrakraniyal travmaların serebrovasküler komplikasyonları Dr. Yonca Ozkan Arat,1,2 Dr. Anil Arat,3 Dr. Kubilay Aydın4 Başkent Üniversitesi Tıp Fakültesi, Göz Hastalıkları Anabilim Dalı, Ankara Wisconsin Üniversitesi, Göz Hastalıkları ve Görme Bilimleri Bölümü, Madison, WI, ABD Hacettepe Üniversitesi Tıp Fakültesi, Radyoloji Anabilim Dalı, Girişimsel Nöroradyoloji Birimi, Ankara 4 İstanbul Üniversitesi İstanbul Tıp Fakültesi, Radyoloji Anabilim Dalı, Girişimsel Nöroradyoloji Birimi, İstanbul 1 2 3

AMAÇ: Transorbital intrakraniyal penetran travmayı takiben gelişen serebrovasküler travma (TIPVT) nadirdir. Bu olgularda ilk muayene tablosunun göreceli olarak hafif olması altta yatan ve yaşamsal tehlikesi olan vasküler travmayı maskeleyebilir. Bu çalışmada amacımız, TIPVT olgularını ve endovasküler tedavi sonuçlarımızı incelemektir.

GEREÇ VE YÖNTEM: Subakut veya kronik fazda anjiyografik olarak dokümente edilmiş altı TIPVT olgusu geriye dönük olarak incelendi. Altı hastanın beşinde endovasküler tedavi uygulandı, bir olguda endovasküler tedavi denendi ancak konservatif tedavi kararı verildi.

BULGULAR: Tam görme kaybı ve hafif inme sonrası tedaviye alınan bir hasta haricinde hiçbir hastada nörolojik kayıp izlenmedi. İki olguda karotikokavernöz fistül, üç olguda anterior serebral, orta serebral ve kavernöz karotis arter anevrizmaları, bir olguda tromboze kavernöz sinüs içinde koalisyon gösteren kavernöz anevrizmalar izlendi. Fistüller kaplı stentlerle, anevrizmalar parent arter oklüzyonu veya akım yönlendiricilerle tedavi edildi. Tüm hastalarda komplikasyonsuz bir iyileşme süreci izlendi.

TARTIŞMA: TIPVT olguları hafif görünen yanıltıcı başvuru tablosundan sonra geç dönemde kendisini gösterebilir. Bu olguların atlanmaması için en küçük şüphede vasküler görüntüleme yapılmalıdır. Transkateter anjiyografik teknikler, TIPVT olgularının teşhisine olduğu gibi iyi sonuçlarla tedavisine de olanak sağlamaktadır.

Anahtar sözcükler: Serebrovasküler travma; fistül; penetran intrakraniyal travma; transorbital travma; travmatik anevrizma.

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ORIGIN A L A R T IC L E

Results of surgical treatment in metacarpal shaft fractures using low profile mini plates Serkan Aykut, M.D.,1 Kahraman Öztürk, M.D.,1 Çağrı Özcan, M.D.,2 Murat Demiroğlu, M.D.,1 Ahmet Utku Gürün, M.D.,1 Erdem Özden, M.D.1 1

Department of Hand and Upper Extremity Surgery, Metin Sabancı Baltalimani Bone Diseases Training and Research Hospital, Istanbul

2

Department of Orthopedics and Traumatology, Metin Sabancı Baltalimani Bone Diseases Training and Research Hospital, Istanbul

ABSTRACT BACKGROUND: Metacarpal fractures are among the most common fractures of the hand. They may lead to loss of function if treated improperly. These injuries can be treated conservatively. However, if significant shortening, rotational deformity and angulation occur, surgical treatment is required. In this article, results of metacarpal fractures treated with open reduction and internal fixation with mini plates were presented.

METHODS: We retrospectively reviewed the clinical and radiologic records of twenty-nine consecutive patients with 37 metacarpal fractures treated by open reduction and internal fixation with low profile mini plate fixation between 2006 and 2013. Surgical treatment with dorsal approach was planned for cases with unacceptable shortening, rotational deformity, and angulation. Early active motion was begun in all cases postoperatively. Patients were permitted to use their hands in daily activities four weeks after surgery. For objective assessment, total range of joint motion was measured. Rotational deformity of the fingers was assessed. Grip strength and quick DASH scores were compared with the uninjured side. Metacarpal shortening was evaluated radiologically, and angulation was measured.

RESULTS: Mean age was 35.1 years (19–61 years) and mean follow-up period was 32 months (6–39 months). While mean operation time was 8.48 days (2–23 days), mean shortening was 7.58 (2–30) mm. In cases with radiologically documented union, mean angulation in the posteroanterior plane was 8.13 (0–42) degrees preoperatively and 3.55 (0–28) degrees postoperatively. In lateral X-rays, mean angulation was 8.22 (0–39) degrees preoperatively and 3.66 (0–28) degrees postoperatively. Mean quick DASH score was 3.6 (0–11.4).

Mean grip strength measurements by Jamar hand dynamometer were 41.05 (±8.3) kg for fractured hands, 44.7 (±9) kg for normal hands. No significant relationship was found between normal hand and fracture hand by Mann-Whitney U test.

CONCLUSION: As in general fracture treatment principles, goals in metacarpal fracture treatment are obtaining an anatomical and stable reduction, fracture union and beginning early movement to avoid loss of function. Open reduction and low profile titanium plate application in metacarpal fractures is the choice of treatment in suitable cases as it meets the above mentioned treatment principles.

Key words: Low profile; metacarpal shaft fractures; miniplate; osteosynthesis.

INTRODUCTION Metacarpal fractures constitute 30% of hand fractures.[1] Fractures of the metacarpal shaft occur as a result of axial loading, torsion, or direct falls and are classified as transverse, oblique, or comminuted.[1–9] The fractures of all metacarpals from the Address for correspondence: Serkan Aykut, M.D. Rumeli Hisarı Caddesi, No: 62, 34470 Baltalimanı, İstanbul, Turkey Tel: +90 212 - 323 70 70 E-mail: aykutserkan@yahoo.com Qucik Response Code

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second to the fifth are characterized by edema and deformity, and inappropriate treatment may result in functional loss in the hand and disability.[4,9–11] The goals of treatment are restoration of length, correction of rotational deformity, if present, establishing adequate stability, proper soft tissue management, and early initiation of movement. The treatment of metacarpal shaft fractures can be further sub-classified as transverse, oblique, spiral, or comminuted based on the fracture geometry. Stepping on hand or ball shock, as examples of direct trauma, mostly causes transverse and comminuted fracture, whereas sprain injuries like falling on the outstretched arm causes spiral and oblique fracture.[4,12,13,14] Most metacarpal fractures are treated conservatively.[1–3,9,11,15–21] If closed methods fail to achieve or maintain reduction when there is angulation, rotation or shortness because of the location (intra articular vs. extra articular), surgery could be used. Oblique and spiral fractures are prone to malrotation so operative 279

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fixation could be necessary, whereas comminuted fractures with or without segmental bone loss demand restoring and maintaining metacarpal length.[2–4,6,11,13,15,20,22,23] Surgical methods include percutaneous or open Kirschner wire fixation, intramedullary fixation, open or percutaneous interfragmentary screw fixation, and external fixation.[1,2,10,16,24,25] Kirschner wires are the most commonly used fixation materials after closed or open reduction.[2,15] However, late initiation of movement resulting in a stiff hand, pin tract infection, and pin migration are the disadvantages of this method.[2,3,26] Plate and screws provide a stable fixation in metacarpal fractures, and thus, allow for early motion and contribute significantly to the outcome. K-wire is a stable method in cases where soft tissue is intact. Soft tissues support the power of fracture fixation. Plate fixation is used in comminuted metacarpal fractures.[1,2,11,16,17,20,26–28] A stable fixation allows for passive and active movements in intrinsic muscles affected by the trauma, significantly improving hand functions. Preservation of the anatomic reduction prevents rotational deformity.[11,24,27] In patients treated with plate and screw osteosynthesis, an adequate stability was achieved and early motion was initiated. All patients returned to their preinjury occupations, and none had angulation or rotational deformities.[17,26] The aim of this study was to assess the clinical and radiologic outcomes of patients with metacarpal fractures, who underwent open anatomic reduction and fixation with low profile titanium plates in our department.

We planned to show that by using plate osteosynthesis in metacarpal body fractures, good functional results could be obtained with early initiation of motion, good results could be achieved radiologically, and rotational deformity could be corrected, shortness could be totally prevented, and thereby, extensor lag could be avoided; however, complications such as tendon irritation could develop.

MATERIALS AND METHODS A retrospective analysis of the clinical and radiologic data of 37 metacarpal fractures in twenty-nine patients operated in our department with low profile 2.0 mm non-locking titanium miniplates and screws between 2006–2013 was carried out. Open, thumb metacarpal, intra articular fracture, metacarpal neck fracture, and patients with other fractures in the same upper extremity were excluded.

2–5 mm shortness, rotational deformity, angulation greater than 20° for index and long finger; greater than 30° for ring finger and greater than 40° for little finger were indications for surgery[23,29] that was unacceptable after closed reduction and casting in clam digger position. All patients were operated in supine position and under infraclavicular block. After the tourniquet was inflated, the forearm was placed in prona280

tion, a dorsal longitudinal incision was made, and the fracture was exposed with adequate soft tissue dissection. Excessive soft tissue dissection and periosteal sleeving was avoided. A low profile 2.0 mm titanium miniplate was applied with fixation of at least four cortices, two on each side of the fracture.

In oblique or spiral type of fractures, those fractures suitable for interfragmentary screw fixation were initially fixed with interfragmentary screws, and then, by plate fixation (Fig. 1af). Metacarpal alignment and angulation were confirmed with fluoroscopy. The plate and screws were covered with periosteum and soft tissues.

After the operation, a short arm splint was applied in functional position until the edema and pain subsided, and the extremity was elevated for the first 24–48 hours. Depending on the general condition of the patient, type of fracture and fixation method, active finger and metacarpophalangeal joint motion was initiated on the second postoperative day. Based on these same factors, the patients were allowed to use their hands in daily activities after the fourth postoperative week and in activities requiring force after the sixth week.

During the final follow up, total range of motion was assessed, grip power was measured and compared with the normal extremity. Quick DASH scoring was performed in all patients. Union, angulation, and shortness were assessed on PA, lateral, and 30 to 45° pronation and/or supination oblique X rays that were taken on postoperative first, third and sixth months and final follow up. The complications were noted.

RESULTS There were twenty-five male and four female patients, and the fracture was located in the left hand in eighteen patients and in the right in eleven. Six of the patients had multiple fractures. The fractures were caused by falling on the hand in eighteen patients, fisting in five, crush injury in four, sports injury in one, and traffic accident in one. Mean age was 35.1 (19–61) years and mean follow up was 32 (6–93) months.

Mean interval between the injury and operation was 8.48 (2–23). The fracture was in the 2nd metacarpal in 12 fractures, 3rd in 9, 4th in 9, and 5th in 7. The type of fracture was oblique in twenty-eight, transverse in six, and comminuted in three patients (Table 1). 2.0 mm adaptation plate was used for six transverse, T shaped plate for twenty-eight oblique, and three for comminuted fractures with bridge technique preferred by AO.[30] Surgery was considered necessary due to angulation in eighteen patients, and shortness in eleven.

Total range of motion was 271.1 (245–275) degrees. Mean grip strength, measured with Jamar’s hand dynamometer, was 41.05 (±8.3) in the fractured side, and 44.7(±9) kg on the normal side. Strength of firm hand and fracture was evaluated

by Mann-Whitney U test with IBM SPSS 22.0 program, and a significance level of p<0.05 was accepted. No significant relaUlus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

Aykut et al. Results of surgical treatment in metacarpal shaft fractures using low profile mini plates

(a)

(b)

(d)

(c)

(e)

(f)

Figure 1. Nineteen year old patient’s X-ray of left hand and fingers (a) AP / (b) oblique / (c) lateral shows oblique fracture of 4th metacarpal with rotational deformity and shortening at the fracture site. Postoperative 6th month (d) AP / (e) oblique / (f) lateral x-rays show perfect reduction was achieved with use of low-profile mini-plate and screws.

tionship was found between the firm hand and fracture hand

by Mann-Whitney U test (p=0.203).

Mean quick DASH score was 3.6 (0–11.4). Radiologic union was achieved in all patients. Mean angulations before and after the operation were 8.13 (0–42) and 3.55 (0–28) degrees in the anteroposterior plane; and 8.22 (0–39) and 3.66 (0–28) degrees in the sagittal plane, respectively. Only one patient

developed a rotation problem which was later corrected.

Mean shortness was 7.58 (2–30) mm. Four patients (13.7%) had restricted movement in the follow up on the sixth week, which resolved with the lengthening of the rehabilitation program. Four of the patients had difficulty in movement and also signs of tenosynovitis, and hence, the hardware was removed with a second operation in these patients. One patient

Table 1. Type of the fractures

2. Metacarpal

3. Metacarpal

4. Metacarpal

5. Metacarpal

Total

Oblique 8 6 8 6 28 Transverse 3 1 1 1 6 Comminuted 1 2 – – 3

12

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9

7

37

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(3.44%) had 3 mm shortness, 30° angulation, and rotational deformity that interfered with function of the fifth finger. A revision operation was performed. All patients returned back to their preoperative occupations.

DISCUSSION In this study, metacarpal body fractures were operated on using low profile titanium plates and based on AO principles.[30] Adequate stability was achieved in all patients, allowing early movement. All patients could return to their preoperative occupations. Except for the patient who underwent revision surgery, none of the patients had displacement, angulation, and rotational deformity. Due to irritation of plaque material and tendon adhesion after dorsal approach, material extraction could be done after surgical treatment of metacarpal fracture. In a study of Mumtaz et al. including forty cases, rate of material extraction has been 20%.[20] In our study; only four of the patients (%13) required hardware removal due to plate irritation, which we believe to be a relatively low rate owing to the use of low profile plates and respect to soft tissues.

Respect to soft tissue or tissue damage that occur during fracture are milestones of healing and stabilization of the fracture. In a cadaveric study of Ouellette et al., metacarpal fractures plaqued by dorsal approach have been compared biomechanically with soft tissues completely peeled off and intact. Fixation strength has been found significantly different in soft tissue intact group.[28] Kato et al., have shown that minimizing soft tissue damage in comminuted fractures during surgery causes no significant difference in rigidity of the fixated anatomically bone to bone with completely peeled of soft tissue, even to be non-reducted anatomically after internal fixation.[31] In our study, minimally invasive surgical approach was used as recommended by AO. A dorsal approach was used in all patients, and excessive soft tissue or periosteal dissection was avoided. The plates were applied from the dorsal aspect of the metacarpals and to four cortices, with two on each side of the fracture. An additional interfragmentary compression screw was applied in especially long oblique fractures.[30] Lack of agreement in surgical management of metacarpal fractures, retrospective nature of most studies, and handling of these fractures together with phalangeal fractures are the limitations of this topic. We believe that prospective multicenter studies that compare various surgical methods will provide evidence based data.

The metacarpal bones are the longest tubular bones in the hand and form a stable platform for the fingers and the crucial anatomic structures on the volar aspect.[1] Fibrocartilagenous volar plates and deep intermetacarpal ligaments form a strong construct between the metacarpals and prevent shortness in metacarpal fractures. Most transverse fractures angulate dorsally due to unbalanced traction of the interosseous muscles 282

and the effects of the extrinsic extensor tendons on the distal fracture segment. This dorsal angulation may be tolerated up to 10° in the second metacarpal and 20° in the third, which are relatively immobile, and up to 30° in the fourth metacarpal and 40 degrees in the fifth, which have greater mobility at the carpometacarpal joints. Oblique and spiral fractures of the metacarpals are less stable fractures and have a tendency for shortness and rotation. Therefore, angulations in metacarpal fractures must be measured and should be evaluated according to which metacarpal bone is fractured. Every 2 mm of shortness results in a 7° extensor lag.[32] Similarly, the metacarpals are very intolerant to any rotational deformity.

Only 5° of malrotation results in 1.5 cm overlap when the fingers are in flexion. Therefore, when deciding for surgery, the type of the fracture, angulation, shortness, and rotation should be assessed, and a decision should be made separately for each metacarpal.

Since most metacarpal fractures are stable, they can be managed successfully after reduction using conservative methods such as splinting.[1–3,15–18,20,21,24] After closed reduction, immobilization should be made in the intrinsic-plus or “clam-digger” position (wrist in 30–40 degrees extension, metacarpophalangeal joints in 80–90 degrees of flexion, and the interphalangeal joints in full extension) with a thermoplastic splint, plaster or fiberglass short-arm cast. If metacarpal rotation, length, and angulation cannot be obtained or maintained, operative stabilization is necessary. These latter types of fractures constitute a relatively smaller fraction of metacarpal fractures.

There are various alternatives in the surgical treatment of unstable or displaced metacarpal fractures, which are K wire fixation, cerclage wires or intramedullary wiring with or without K wires, locking or nonlocking miniplates and screws, and external fixation.[1–4,10,24,25] In vitro biomechanical comparative studies have shown that dorsal plating is the most stable fixation method.[2,10,33,34] K wire fixation may be made percutaneously in a cross, transverse, or intramedullary manner.

K wires are easily available in the operating rooms, and are easily applied. They can be introduced percutaneously, which may protect from the problems related to open surgery.[1] Percutaneous insertion; however, may result in tendon adhesions or even ruptures.[3] K wires cannot provide adequate biomechanical stability and are prone to complications including restricted motion and stiffness.[3] Wire ends are left outside the skin, commonly resulting in problems such as implant loosening and infection. Kaiser et al. have published a series of children treated with a single elastic stable intramedullary wire, and only one patient needed wire removal for skin irritation, and none of the remaining patients had an infection or secondary surgery.[18] Ozer et al. have compared intramedullary nailing with plate and screw fixation in a series of thirty-eight patients and found that although the two groups were similar with respect to the clinical results, the operative times were shorter in the intramedullary nail group.[35] On the other hand, reduction loss, penetration of Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

Aykut et al. Results of surgical treatment in metacarpal shaft fractures using low profile mini plates

material into the metacarpophalangeal joint, and secondary surgery for removal of the material were higher in the intramedullary nail group.[27] Dorsal mini plating with steel or titanium plates is a method with increasing popularity. Lateral plating of metacarpal fractures is not appropriate because it is biomechanically very weak compared to dorsal plating.[34] When compared with the wiring method, it provides a stable fixation when at least 2 or 3 bicortical screws are inserted to each side of the fracture.[1,10,34] Early initiation of active and passive motion can prevent intrinsic tightness. On the other hand, complications such as material failure and irritation, infection, and nonunion have been reported to be as high as 35%.[22,36] These series handled phalangeal fractures together with metacarpal fractures, and more recent studies involving only metacarpal fractures have reported lower complication rates.[11,21,22,26,36] We believe that the reason for the relatively lower complication rates in our series was the inclusion of only metacarpal fractures, performance of minimal soft tissue and periosteal stripping, and use of low profile plates.

The use of low profile titanium plates in metacarpal fractures provides a stable fixation and allows early movement, which are significant advantages over other methods.

Conflict of interest: None declared.

REFERENCES 1. Diaz-Garcia R, Waljee JF. Current management of metacarpal fractures.

Hand Clin 2013;29:507–18.

12. Ochman S, Doht S, Paletta J, Langer M, Raschke MJ, Meffert RH. Comparison between locking and non-locking plates for fixation of metacarpal fractures in an animal model. J Hand Surg Am 2010;35:597–603.

13. Rhee PC, Becker HA, Rizzo M. Update on the Treatment of Metacarpal Fractures. Curr Orthop Pract 2012;23:289–95.

14. Gereli A, Nalbantoğlu U, Türkmen M. Sporcularda görülen metakarp ve falanks kırıkları TOTBİD Dergisi 2012;11:220–7.

15. Al-Qattan MM. Outcome of conservative management of spiral/long oblique fractures of the metacarpal shaft of the fingers using a palmar wrist splint and immediate mobilisation of the fingers. J Hand Surg Eur Vol 2008;33:723–7.

16. Baldwin PC, Wolf JM. Outcomes of hand fracture treatments. Hand Clin 2013;29:621–30.

17. Ford DJ, el-Hadidi S, Lunn PG, Burke FD. Fractures of the metacarpals: treatment by A. O. screw and plate fixation. J Hand Surg Br 1987;12:34– 7.

18. Kaiser MM, Tafazzoli K, Theilen TM, Schulz AP, Paech A, Wessel LM. Intramedullary nailing for metacarpal 2-5 fractures. J Pediatr Orthop B 2009;18:296–301.

19. Meals C, Meals R. Hand fractures: a review of current treatment strategies. J Hand Surg Am 2013;38:1021–31.

20. Mumtaz MU, Farooq MA, Rasool AA, Kawoosa AA, Badoo AR, Dhar SA. Unstable metacarpal and phalangeal fractures: treatment by internal fixation using AO mini-fragment plates and screws. Ulus Travma Acil Cerrahi Derg 2010;16:334–8.

21. Nalbantoğlu U, Gereli A, Uçar BY, Kocaoğlu B, Doğan T. Treatment of metacarpal fractures with open reduction and low-profile plate and screw fixation. [Article in Turkish] Acta Orthop Traumatol Turc 2008;42:303– 9.

22. Page SM, Stern PJ. Complications and range of motion following plate fixation of metacarpal and phalangeal fractures. J Hand Surg Am 1998;23:827–32.

23. Green’s Operative Hand surgery Fifth Edition 2005;1:283–5.

2. Adams JE, Miller T, Rizzo M. The biomechanics of fixation techniques for hand fractures. Hand Clin 2013;29:493–500.

24. Ouellette EA, Freeland AE. Use of the minicondylar plate in metacarpal and phalangeal fractures. Clin Orthop Relat Res 1996;327:38–46.

3. Blazar PE, Leven D. Intramedullary nail fixation for metacarpal fractures.

Hand Clin 2010;26:321–5.

25. Margić K. External fixation of closed metacarpal and phalangeal fractures of digits. A prospective study of one hundred consecutive patients. J Hand Surg Br 2006;31:30–40.

4. Dean BJF, Little C. Fractures of the metacarpals and phalanges. Orthopedics and Trauma 2011;25:43–56.

5. Henry MH. Fractures of the proximal phalanx and metacarpals in the hand: preferred methods of stabilization. J Am Acad Orthop Surg 2008;16:586–95.

6. McNemar TB, Howell JW, Chang E. Management of metacarpal fractures. J Hand Ther 2003;16:143–51.

7. Nakashian MN, Pointer L, Owens BD, Wolf JM. Incidence of metacarpal fractures in the US population. Hand (N Y) 2012;7:426–30.

8. Soong M, Got C, Katarincic J. Ring and little finger metacarpal fractures: mechanisms, locations, and radiographic parameters. J Hand Surg Am 2010;35:1256–9.

9. Sennet BJ. Operative treatment of metacarpal fractures of the hand (excluding thumb metacarpal fractures). Operative Techniques in Orthopaedics 1997;7:127–33.

10. Black D, Mann RJ, Constine R, Daniels AU. Comparison of internal fixation techniques in metacarpal fractures. J Hand Surg Am 1985;10:466– 72.

11. Fusetti C, Garavaglia G, Papaloïzos M. Re: Souer JS, Mudgal CS. Plate fixation in closed ipsilateral multiple metacarpal fractures. J Hand Surg Eur 2008;33:740-4. J Hand Surg Eur Vol 2009;34:560–2.

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26. Kumar S, Mohanta S. Treatment of unstable metacarpal fractures by miniplate and screws. J Clin Orthop Trauma 2010:66–70.

27. Ozer K, Gillani S, Williams A, Peterson SL, Morgan S. Comparison of intramedullary nailing versus plate-screw fixation of extra-articular metacarpal fractures. J Hand Surg Am 2008;33:1724–31.

28. Ouellette EA, Dennis JJ, Milne EL, Latta LL, Makowski AL. Role of soft tissues in metacarpal fracture fixation. Clin Orthop Relat Res 2003;412:169–75.

29. C McCarty, JB Samora, HM Awan. Metacarpal shaft fractures: A review.

OA Orthopaedics 2014;2:12.

30. Rüedi TP, Buckley RE, Moran CCAO. Principles of Fracture Management Second edition Part 2:685–7.

31. Kato S, Latta L, Burkhalter W. Mechanical evulation of external and internal fixation for metacarpal fracture. Trans Orthop Res Soc 1986;11:316.

32. Freeland AE, Geissler WB, Weiss AP. Surgical treatment of common displaced and unstable fractures of the hand. Instr Course Lect 2002;51:185–201.

33. Dumont C, Fuchs M, Burchhardt H, Appelt D, Bohr S, Stürmer KM. Clinical results of absorbable plates for displaced metacarpal fractures. J

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Hand Surg Am 2007;32:491–6.

34. Vanik RK, Weber RC, Matloub HS, Sanger JR, Gingrass RP. The comparative strengths of internal fixation techniques. J Hand Surg Am 1984;9:216–21.

35. Ozer K, Gillani S, Williams A, Peterson SL, Morgan S. Comparison of

36. Fusetti C, Meyer H, Borisch N, Stern R, Santa DD, Papaloïzos M. Complications of plate fixation in metacarpal fractures. J Trauma 2002;52:535–9.

ORİJİNAL ÇALIŞMA - ÖZET OLGU SUNUMU

Düşük profilli mini plak ile metakarp cisim kırıklarının cerrahi tedavi sonuçları Dr. Serkan Aykut,1 Dr. Kahraman Öztürk,1 Dr. Çağrı Özcan,2 Dr. Murat Demiroğlu,1 Dr. Ahmet Utku Gürün,1 Dr. Erdem Özden1 1 2

Metin Sabancı Kemik Hastalıkları Eğitim ve Araştırma Hastanesi, El Cerrahisi Kliniği, İstanbul Metin Sabancı Kemik Hastalıkları Eğitim ve Araştırma Hastanesi, Ortopedi ve Travmatoloji Kliniği, İstanbul

AMAÇ: Metakarpal kırıklar elde en sık rastlanan kırıklardandır. Uygun tedavi edilmedikleri takdirde fonksiyon kaybına neden olabilirler. Bu yaralanmaların çoğu konservatif olarak tedavi edilebilir. Ancak belirgin kısalma, rotasyonel deformite ve açılanma oluştuğunda cerrahi tedavi gereklidir. Bu yazıda metakarp kırıklarının açık redüksiyon ve mini plaklar ile tespitinin sonuçlarının sunulması amaçlandı.

GEREÇ VE YÖNTEM: Kliniğimizde 2006 ve 2013 yılları arasında düşük profilli mini plak osteosentezi yapılmış, klinik ve radyolojik takibi olan 29 hastanın 37 metakarp kırığı geriye dönük olarak incelendi. Kabul edilemeyen kısalık, rotasyonal deformite ve açılanma olan olgulara dorsal girişimle cerrahi girişim planlandı. Tüm hastalara ameliyat sonrası erken hareket başlandı. Hastalara ameliyattan dört hafta sonra günlük aktivitelerde ellerini kullanmalarına izin verildi. Objektif değerlendirmede toplam eklem hareket açıklığı ölçüldü. Parmakların rotasyonel deformitesi değerlendirildi.

Kavrama gücü ve QuickDASH skorları yaralanmamış taraf ile karşılaştırıldı. Metakarpal kısalık radyolojik olarak ölçüldü ve açılanma hesaplandı.

BULGULAR: Ortalama yaş 35.1 (19–61) yıl, ortalama takip süresi 32 (6–39) aydı. Travma sonrası ameliyata kadar geçen süre ortalama 8.48 (2–23) gündü. Ortalama kısalık 7.58 (2–30) mm olarak ölçüldü. Radyolojik kaynamanın görüldüğü olgularda posteroanterior planda ortalama açılanma ameliyat öncesi 8.13 (0–42) derece, ameliyat sonrası 3.55 (0–28) derece olarak ölçüldü. Lateral grafilerde ortalama açılanma ameliyat öncesi 8.22 (0–39) derece, ameliyat sonrası 3.66 (0–28) derece olarak not edildi. Ortalama QuickDASH skoru 3.6 (0–11.4) tü. Ortalama kavrama gücü kırık elde Jamar el dinamometrisi ile 41.05 (±8.3) kg, etkilenmemiş tarafta 44.7 (±9) kg olarak ölçüldü. Sağlam el ile kırık el arasında kavrama gücü açısından Mann-Whitney U testine göre istatistiksel olarak anlamlı bir fark elde edilmedi (p<0.05). Ortalama eklem hareket açıklığı 271.1 (245–275) dereceydi. Dört olguda (%13.7) hareket kısıtlılığı vardı, rehabilitasyon programı uzatılarak çözüldü. Yine dört hastada (%13.7) irritasyona bağlı plak çıkarılmasına neden olan hareket kısıtlılığı ve tenosinovit gelişmişti. Bir hastada (%3.44) rotasyon ve kısalık ile kaynama gözlendi. Revizyon cerrahisi planlandı.

TARTIŞMA: Genel kırık prensiplerinde olduğu gibi metakarp kırıklarında da hedef kırığın uygun anatomik ve stabil redüksiyonunun sağlanarak tedavi edilmesi, kırığın kaynamasının sağlanması ve fonksiyon kaybından kaçınabilmek için erken hareket başlanmasıdır. Yukarıda sayılan tedavi prensiplerini karşılayabildiğinden uygun olgularda açık redüksiyon ve düşük profilli mini titanyum plak uygulaması metakarp kırıklarının tedavisinde tedavi seçeneklerinden biridir.

Anahtar sözcükler: Düşük profilli; metakarp cisim kırıkları; mini plak; osteosentez.

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doi: 10.5505/tjtes.2015.01651

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ORIGIN A L A R T IC L E

Endovascular treatment for acute traumatic thoracic aortic transection Onur Ergun, M.D.,1 Murat Canyiğit, M.D.,2 Mete Hıdıroğlu, M.D.,3 İdil Güneş Tatar, M.D.,1 Erdem Birgi, M.D.,1 Aslıhan Küçüker, M.D.,3 Emrah Uğuz, M.D.,3 Hasan Ali Durmaz, M.D.,1 Hüseyin Çetin, M.D.,2 Baki Hekimoğlu, M.D.,1 Erol Şener, M.D.3 1

Department of Radiology, Diskapi Yildirim Beyazit Training and Research Hospital, Ankara

2

Department of Radiology, Ataturk Training and Research Hospital, Ankara

3

Department of Cardiovascular Surgery, Ataturk Training and Research Hospital, Ankara

ABSTRACT BACKGROUND: This study aimed to present our experience in patients with acute traumatic thoracic aortic transection treated by endovascular stent-graft.

METHODS: From October 2011 to October 2014, eleven patients were brought to our hospitals after suffering motor vehicle accident or fall from height. Computed tomography revealed acute traumatic transection of the thoracic aorta at the aortic isthmus just distal to the left subclavian artery in nine patients, at the middle or distal thoracic aorta in two, and both aortic isthmus and middle thoracic aorta in one. Endovascular technique was preferred as the treatment modality. All patients, except one, were treated within twelve hours of diagnosis.

RESULTS: Deployment of stent-grafts was successful in all cases. The stent-grafts were oversized between 10% and 20%. The origin of left subclavian artery was covered with stent-graft in six patients to achieve adequate proximal landing zone. In two of them, carotico-subclavian bypass and periscope graft placement were applied to maintain subclavian artery blood flow. There were no procedure related deaths, paraplegia or ischemic complications. A patient with cardiac arrest, on whom cardiopulmonary resuscitation and transient aortic balloon occlusion within the aorta were applied in the angiography suit died at the postoperative twelve hours. Mean hospital stay after procedures was 14.8 days (range, 4–60 days). Mean follow-up time of ten patients was 16.6 months (range, 1–36 months).

CONCLUSION: Our study supports that thoracic endovascular aortic stenting for acute transection is promising in terms of shortand mid-term results similar to other studies in the literature.

Key words: Aortic rupture; aortic stent-graft; aortic transection; endovascular treatment.

INTRODUCTION Traumatic aortic transection is a rare but often fatal injury that generally occurs due to motor vehicle accidents, which is also associated with other life-threatening injuries.

Mortality rates are extremely high, and most patients die before arriving at the hospital.[1] The mechanism of injury Address for correspondence: Onur Ergun, M.D. Dışkapı Yıldırım Beyazıt Eğitim ve Araştırma Hastanesi, Radyoloji Kliniği, Dışkapı, Ankara, Turkey Tel: +90 312 – 596 26 18 E-mail: onurergun@yahoo.com Qucik Response Code

Ulus Travma Acil Cerrahi Derg 2015;21(4):285–290 doi: 10.5505/tjtes.2015.21556 Copyright 2015 TJTES

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after blunt thoracic trauma has been shown as high-speed deceleration in the anterior-posterior and lateral directions resulting in torsion, bending, shearing and increase in intravascular pressure. Depending on all these factors, transverse tears occur mostly at the level of the aortic isthmus and also at the aortic root and diaphragm.[2] Current diagnosis of traumatic aortic transection is mainly made by contrast-enhanced computed tomography (CT).[2] Treatment options include open thoracic surgery and endovascular repair.

This study aimed to present our treatment experience and short- and mid-term results in patients with acute traumatic thoracic aortic transection treated by endovascular stent-graft.

MATERIALS AND METHODS From October 2011 to October 2014, eleven patients (eight 285

Ergun et al. Endovascular treatment for acute traumatic thoracic aortic transection

male and three female) were brought to our hospitals after suffering motor vehicle accident or fall from height. Mean age of the patients was 46.7 years (range, 15–66). All of the cases first underwent CT imaging of the thorax and abdomen. CT revealed acute traumatic transection of the thoracic aorta at the aortic isthmus just distal to the left subclavian artery in nine patients, at the middle or distal thoracic aorta in two, and both aortic isthmus and middle thoracic aorta in one. Moreover, CT demonstrated at least two or more associated injuries such as pulmonary contusion, pleural effusion, pneumothorax, pericardial effusion, left-sided hemothorax, rib fractures, fractured pelvis, intraabdominal hemorrhage, and thoracolumbar vertebra compression fractures.

Endovascular technique was preferred as the treatment modality. Full informed written consent was obtained from all patients or patients’ first-degree relatives, and they were informed about the risks of the procedure. Ten of the eleven patients were treated within the twelve hours of diagnosis.

One patient with a history of traffic accident ten days prior was admitted to hospital with severe backache. This patient was treated on that admittance. In all patients, arterial access for stent-grafts was provided by right-sided femoral cut-down under general anesthesia. In an urgent status like cardiothoracic shock, an aortic balloon was transiently dilated within the aorta at the just distal the subclavian artery by using the left femoral artery.

All of the procedures were performed under systematical heparinization with 3000IU heparin, which is a lower dose than in elective endovascular stenting cases as recommended.

[3] Diagnostic digital subtraction angiography (DSA) was performed to establish the anatomy of the aortic arch and confirm the location of the transection in all patients. Arterial access for diagnostic catheters was achieved from left common femoral artery in eight patients and from left brachial artery in three. Both vertebral arteries were initially evaluated in patients who had a transection line with less than 15 mm distance to the left subclavian artery in the CT examination and the left subclavian artery needed to be closed. If the right vertebral artery was hypoplasic or atretic, preprocedural surgical carotico-subclavian bypass or revascularization of the left subclavian artery with parallel grafting during the endovascular procedure was performed. All patients were treated with thoracic aortic stent-grafts. None of our patients received prophylactic spinal drainage, which is not recommended due to the reasons such as proximal location of the injury, limited coverage of the thoracic aorta, and the risk of epidural hematoma.[3] The patients were discharged with 300 mg acetylsalicylic acid medication alone. Follow-up examinations were performed with CT angiography carried out before discharge from the hospital, and at three, six and twelve months postoperatively and yearly thereafter.

286

RESULTS Deployment of stent-grafts was successful in all cases (technical success: 100%). The mean aortic diameter was 24.09 mm (range, 19–28 mm). The mean stent-graft diameter was 27.63 mm (range, 22–32 mm). The stent-grafts were oversized between 10% and 20%. Patient data and stent-graft details were demonstrated in Table 1.

The origin of left subclavian artery was covered with stentgraft in six patients to achieve adequate proximal landing zone. While left carotid-subclavian bypass was performed in one of the two patients with right vertebral artery hypoplasia in the angiography suit, periscope graft technique for subclavian artery blood supply was applied in the other patient during the procedure. A 9x150 mm heparin coated self-expandable covered stent (Viabahn, WL Gore and Associates Inc. Flagstaff, Ariz) was used as a periscope graft.

In one patient with pelvic fractures, selective internal iliac embolization was performed to stop active bleeding from the internal iliac artery branches by using multiple coils and Amplatzer Vascular Plug (AGA Medical Corporation, Birmingham, UK) just after the aortic stent-graft procedure.

There were no procedure related deaths, left upper extremity ischemic complications, cerebrovascular events, or paraplegia in any of the patients. A patient with cardiac arrest on whom cardiopulmonary resuscitation and transient aortic balloon occlusion within the aorta at the just distal of the subclavian artery were applied in the angiography suit was deceased at the postoperative twelve hours (Figs. 1a-d).

Postoperative CT images confirmed technical success in exclusion of the transection without any types of endoleak. Mean hospital stay after procedures was 14.8 days (range, 4–60 days).

Mean follow-up time of ten patients was 16.6 months (range 1–36 months). The stent-grafts were patent with no evidence of endoleak, stent-graft collapse or migration. Besides, carotico-subclavian bypass graft and periscope graft were also patent at the postoperative first year CT angiography, respectively.

DISCUSSION Traumatic transection of the aorta is often a fatal injury that arises after high-energy blunt trauma with a mortality rate of 86.2% outside the hospital. Aortic transection is the second most common cause of death following head injury (intracranial hemorrhage) with a rate of occurrence between 13% and 20% after blunt trauma.[3,4] Most patients with acute traumatic aortic transection show no evidence of aortic injury until hemodynamic instability occurs.[2] In high impact motor vehicle accidents, rapid deceleration causes aortic arch injury mostly at the level of the isthmus.[5] Patients with aortic injury also have concomitant traumas. It is important to evaluate Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

Ergun et al. Endovascular treatment for acute traumatic thoracic aortic transection

Table 1. Patient data and stent-graft details No Sex Age Mechanism Location of

(year) of injury transection

1

Male

49

Motor vehicle

Aortic isthmus

Distance Stent-graft from left subclavian artery (mm) 8

Aortic Graft size Follow diameter (mm) -up (mm) (month)

Cook-Zenith

27

32x32x160

18

accident 2

Male

43

Fall from height

Aortic isthmus

10

Medtronic-Talent

27

32x32x100

8

3

Male

54

Motor vehicle

Distal thoracic

90

Medtronic-Talent

26

30x30x100

7

accident

aorta

4

Female

15

Fall from height

Aortic isthmus

0

Medtronic- Vailant

20

22x22x112

36

5

Male

42

Motor vehicle

Aortic isthmus

20

Cook-Zenith

21

24x24x80

36

Aortic isthmus

18

Gore- TAG

19

22x22x100

24

accident 6

Female

45

Motor vehicle

accident 7

Male

48

Fall from height

Aortic isthmus

10

Cook-Zenith

25

28x28x140

12

8

Male

48

Motor vehicle

Middle thoracic

40

Cook-Zenith

28

32x32x140

Exitus

Aortic isthmus

8

Cook-Zenith

25

28x28x140

12

Aortic isthmus

3

Cook-Zenith

22

26x26x134

12

7

Cook-Zenith

25

28x28x140

1

accident 9

Male

66

Motor vehicle

aorta

accident 10

Female

43

Motor vehicle

accident 11

Male

61

Fall from height Both aortic isthmus

and middle

thoracic aorta

whether hemodynamic instability is aorta-related or not. In case of acute massive mediastinal hematoma, active bleeding or left sided hemothorax; endovascular approach must be performed immediately. Otherwise, non-aorta-related life threatening injuries must be treated first and endovascular repair is suggested to be performed within 24 hours.[4] While open surgical repair has been performed as conventional treatment of traumatic aortic transection for years, endovascular stents have started to be used with low rates of morbidity and mortality by the rapid development of aortic stent-grafts in the last two decades.[1] The first clinical experience of endovascular stent-grafting in abdominal aortic aneurysms was described in 1991 by Parodi et al.[6] It is now a well-established method of treatment as an alternative to open surgery. There are some clear advantages of endovascular treatment over open surgery, including avoidance of left thoracotomy, single lung ventilation, aortic cross-clamping and cardiopulmonary bypass, reduced surgery time and reduced blood loss.[2,4] Mortality rates of endovascular treatment are between 0% and 20%, which is more favorable when compared to open surgery. After open surgical repair of traumatic aortic injuries, 30-day mortality rates are between 15% Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

and 50%.[2] The risks of death and spinal cord ischemia are significantly lower in all age groups after endovascular treatment compared with surgery.[3] There were no procedure related deaths in our patient group. Our 30-day mortality rate was 9.1%.

Paraplegia is the most serious complication of treatment and is seen postoperatively with an incidence of 2.3% to 25.5%.

[4] The low risk of paraplegia is an advantage of the endovascular procedure when compared with open surgery.[4] Other short-term complications of endovascular treatment include stroke, access-site complications, stent collapse and recurrent laryngeal nerve damage, with morbidity ranging 3% to 36%.[2] In a literature review, the incidence of stroke or transient ischemic attack has been reported as 1.2%.[7] We didnâ&#x20AC;&#x2122;t observe paraplegia or any ischemic complications in our patient group. In the same review, the incidence of early and late endoleak after endovascular treatment has been reported as 4.2% and 0.9%, respectively.[7] Our technical success was 100% without any types of endoleak.

Due to technical success and lower early and late complication rates, endovascular stenting for aortic transection 287

Ergun et al. Endovascular treatment for acute traumatic thoracic aortic transection

(a)

(c)

(b)

(d)

Figure 1. (a-d) Axial thoracic computed tomography angiography image (a) shows a pseudoaneurysm from the anterolateral aspect of the proximal thoracic aorta (white arrow) compatible with aortic transection in a motor vehicle accidentâ&#x20AC;&#x2122;s patient. Cardiac arrest was developed in the angiography suit, and cardiopulmonary resuscitation and transient aortic balloon occlusion (b) within the aorta at the just distal of the subclavian artery were applied. Aortogram obtained just after the balloon deflation and stent-graft insertion (c) reveals a pseudoaneurysm at the proximal thoracic aorta (white arrow). Aortogram after stent-graft deployment (d) demonstrated successful exclusion of the pseudoaneursym.

has replaced open surgical repair as the primary treatment modality in many centers. Endovascular aortic stenting may reduce mortality and paraplegia rates by half compared with open surgery, whichmakes endovascular treatment the firstline therapy for blunt thoracic aortic trauma.[7] Rates of stent-graft collapse after endovascular treatment has been reported between 0.03% and 10% in the literature.[4] Excessive oversizing of the stent-graft and acute angle of the aortic arch are the factors that can lead to stent collapse.

[4] Caudal migration of stent-graft can also occur with an in288

cidence of 1% to 2.8%.[8] Together with tortuous seal zone anatomy, excessive oversizing is also a predisposing factor for caudal migration.[8] Accordingly, oversizing is an important problem for endovascular treatment due to lack of small-caliber stent-grafts for use in young patients with usually smaller aorta diameters. We didnâ&#x20AC;&#x2122;t observe any stent collapse or caudal migration of the stent-graft in our limited patient group in the follow up.

Aortic transections occur mostly at the level of the aortic isthmus. Therefore, it is usually difficult to find enough space Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

Ergun et al. Endovascular treatment for acute traumatic thoracic aortic transection

from the origin of the left subclavian artery for proximal landing zone of stent-graft. If there is not adequate proximal landing zone, left subclavian artery may be sacrificed. At that point, the dominancy of vertebral arteries becomes important. If the right vertebral artery is atretic or hypoplastic without intact posterior communicating arteries, surgical carotid-subclavian bypass should be performed.[3] Also recently, endovascular revascularization procedures such as modified chimney and periscope graft techniques have been introduced as an alternative to surgery.[9] Extra-anatomical bypass surgery is a well established method with high patency rates, but long-term durability of these new endovascular techniques is not clearly known yet.[10] We had to cover the origin of the left subclavian artery in six of our patients to achieve adequate proximal landing zone. In two patients, right vertebral artery was hypoplastic. Surgical left carotid-subclavian bypass was performed in one of the patients in the angiography suit and endovascular periscope graft technique for left subclavian artery blood supply was applied in the other patient during the endovascular procedure. These patients did not develop any ischemic complications.

Covering of the left subclavian artery may also lead to higher incidence of upper extremity ischemia and stroke. Left upper extremity symptoms have occurred in up to 15.8% of patients, in which left subclavian artery was covered during thoracic endovascular repair, but intervention was required in only 5.8% of patients in one study.[11] In addition, Leong Tan et al. have reported that they covered the left subclavian artery with the stent-graft in five of their six patients during endovascular stenting for traumatic thoracic aortic injury and none of the patients had any upper extremity ischemic complications or cerebrovascular events. However, authors stated that in all five patients, right vertebral artery was dominant.[12] We also didn’t observe any ischemic complications in four patients with dominant right vertebral artery, in whom the left subclavian artery was covered with stent-graft.

Our study has some limitations including the limited number of patients and lack of long-term follow-up of our patients.

Open surgical repair for aortic transection is associated with considerable rate of perioperative morbidity and mortality.

Endovascular treatment has replaced open surgical repair as the primary treatment modality in many centers. Yet, there

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are no randomized controlled trials comparing open surgery with endovascular treatment for aortic transection. Similar to our study, retrospective studies indicate that short and mid-term results of thoracic endovascular aortic stenting for transection are promising, but prospective long-term studies are mandatory to assess durability of the stent-grafts since the majority of the patients are at a young age.

Conflict of interest: None declared.

REFERENCES 1. Chung-Yu Lo, Chun-Che Shih. Endovascular Treatment for Traumatic Aortic Rupture. Acta Cardiol Sin 2008;24:97–9.

2. Steenburg SD, Ravenel JG, Ikonomidis JS, Schönholz C, Reeves S. Acute traumatic aortic injury: imaging evaluation and management. Radiology 2008;248:748–62.

3. Lee WA, Matsumura JS, Mitchell RS, Farber MA, Greenberg RK, Azizzadeh A, et al. Endovascular repair of traumatic thoracic aortic injury: clinical practice guidelines of the Society for Vascular Surgery. J Vasc Surg 2011;53:187–92.

4. Chalvatzoulis E, Megalopoulos A, Trellopoulos G, Ananiadou O, Papoulidis P, Kemanetzi I, et al. Endovascular repair of traumatic aortic transection. Interact Cardiovasc Thorac Surg 2010;11:238–42.

5. Asmat A, Tan L, Caleb MG, Lee CN, Robless PA. Endovascular management of traumatic thoracic aortic transection. Asian Cardiovasc Thorac Ann 2009;17:458–61.

6. Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 1991;5:491–9.

7. Hoffer EK, Forauer AR, Silas AM, Gemery JM. Endovascular stent-graft or open surgical repair for blunt thoracic aortic trauma: systematic review.

J Vasc Interv Radiol 2008;19:1153–64.

8. Wang GJ, Fairman RM. Endovascular repair of the thoracic aorta. Semin Intervent Radiol 2009;26:17–24.

9. Lachat M, Mayer D, Pfammatter T, Criado FJ, Rancic Z, Larzon T, et al. Periscope endograft technique to revascularize the left subclavian artery during thoracic endovascular aortic repair. J Endovasc Ther 2013;20:728–34.

10. Kucuker A, Hidiroglu M, Cetin L. The results of carotid-subclavian bypass in a single institute. Damar Cer Derg 2013;22:285–91.

11. Riesenman PJ, Farber MA, Mendes RR, Marston WA, Fulton JJ, Keagy BA. Coverage of the left subclavian artery during thoracic endovascular aortic repair. J Vasc Surg 2007;45:90–5.

12. Leong Tan GW, Pek CH, Wong D, Punamiya S, Chiu MT, Appasamy V, et al. Management of blunt traumatic thoracic aorta injuries with endovascular stent-grafts in a tertiary hospital in an urban Asian city. Ann Vasc Surg 2011;25:605–11.

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ORİJİNAL ÇALIŞMA - ÖZET OLGU SUNUMU

Akut travmatik torasik aort transeksiyonunda endovasküler tedavi Dr. Onur Ergun,1 Dr. Murat Canyiğit,2 Dr. Mete Hıdıroğlu,3 Dr. İdil Güneş Tatar,1 Dr. Erdem Birgi,1 Dr. Aslıhan Küçüker,3 Dr. Emrah Uğuz,3 Dr. Hasan Ali Durmaz,1 Dr. Hüseyin Çetin,2 Dr. Baki Hekimoğlu,1 Dr. Erol Şener3 1 2 3

Dışkapı Yıldırım Beyazıt Eğitim ve Araştırma Hastanesi, Radyoloji Kliniği, Ankara Atatürk Eğitim ve Araştırma Hastanesi, Radyoloji Kliniği, Ankara Atatürk Eğitim ve Araştırma Hastanesi, Kalp ve Damar Cerrahisi Kliniği, Ankara

AMAÇ: Biz bu çalışmada endovasküler stent-greft ile tedavi ettiğimiz akut travmatik torasik aort transeksiyonu hastalarındaki deneyimimizi sunmayı amaçladık.

GEREÇ VE YÖNTEM: Eylül 2011 ile Eylül 2014 tarihleri arasında trafik kazası veya yüksekten düşme sonrası hastanelerimize getirilen on bir hasta çalışmaya dahil edildi. Bilgisayarlı tomografi ile dokuz hastada aortik istmusta, iki hastada orta-distal torasik aortada, bir hastada ise hem aortik istmusta hem de orta torasik aortada akut aortik transeksiyon görüldü. Tedavi yöntemi olarak endovasküler yöntem tercih edildi. Bir hasta haricindeki tüm hastalar tanı sonrası 12 saat içerisinde tedavi edildi.

BULGULAR: Stent-greftler tüm olgularda başarıyla yerine yerleştirildi. Stent-greftler hedef damar çapına oranla %10 ila %20 oranında daha geniş çapta kullanıldı. Altı hastada stentin tutunması için yeterli proksimal alan sağlanması için sol subklavyen arterin orijini stent-greft ile kapatıldı. Bu hastaların ikisinde sol subklavyen arterdeki akımın devam etmesi için cerrahi karotiko-subklavyen by-pass ve endovasküler periskop stent-greft yöntemleri kullanıldı. İşleme bağlı ölüm, parapleji veya iskemik bulgu hiçbir hastada izlenmedi. Anjiyografi odasında kardiyopulmoner resüsitasyon ve aortada geçici balon oklüzyonu uygulanan kardiyak arrestli bir hasta işlem sonrası 12. saatte hayatını kaybetti. Hastaların operasyon sonrası ortalama hastanede kalış süresi 14.8 gün (4 ila 60 gün) olarak hesaplandı. On hastanın ortalama takip süresi 16.6 ay idi (1 ila 36 ay).

TARTIŞMA: Bizim çalışmamızda elde ettiğimiz sonuçlar literatürdeki diğer çalışmalara benzer şekilde akut aort transeksiyonunda endovasküler stent-greft tedavisinin kısa ve orta vadede başarılı ve umut verici olduğunu desteklemektedir.

Anahtar sözcükler: Aort ruptürü; aortik stent-greft; aort transeksiyonu; endovasküler tedavi.

Ulus Travma Acil Cerrahi Derg 2015;21(4):285–290

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ORIGIN A L A R T IC L E

Outcomes and demostration of cranial firearm injuries: A multicenter retrospective study Kadir Çınar, M.D.,1 Mehmet Seçer, M.D.,2 Fatih Alagöz, M.D.,3 Murat Ulutaş, M.D.,4 Özhan Merzuk Uçkun, M.D.,3 Ali Erdem Yıldırım, M.D.,3 Ahmet Gürhan Gürçay, M.D.,5 Yahya Güvenç, M.D.,6 Haydar Çelik, M.D.,7 Fırat Narin, M.D.8 1

Department of Neurosurgery, Şehitkamil State Hospital, Gaziantep

2

Department of Neurosurgery, Deva Hospital, Gaziantep

3

Department of Neurosurgery, Ankara Numune Training and Research Hospital, Ankara

4

Department of Neurosurgery, Sanko University Konukoglu Hospital, Gaziantep

5

Department of Neurosurgery, Ankara Ataturk Training and Research Hospital, Ankara

6

Department of Neurosurgery, Dr. R.K. Sincan State Hospital, Ankara

7

Department of Neurosurgery, Ankara Training and Research Hospital, Ankara

8

Department of Neurosurgery, Ankara Memorial Hospital, Ankara

ABSTRACT BACKGROUND: Cranial firearm injuries (CFAI) are associated with significant morbidity and mortality.This study was aimed to determine the factors affecting mortality of CFAI cases managed in our institution by a retrospective analysis of CT scans and clinical data.

METHODS: This multicenter retrospective study examined two hundred and nineteen patients presenting to neurosurgery clinics after CFAI between January 2012 and November 2014. Age, sex, Glasgow Coma Score (GCS), CT findings, and mortality and morbidity rates of the patients were analyzed to determine the factors affecting mortality.

RESULTS: Mean age of the study population was 24.19±12.25 years, 85.8% of them were male. The most common CT findings were fracture (100%), intracranial hemorrhage (61.2%), and an intracranially located foreign body (44.3%). A cranial operation was performed in 64.8% of the victims. Mean GCS on admission was 8±3.9, which increased in survivors (p<0.05).

CONCLUSION: CFAIs are associated with increased mortality and morbidity. We determined that many factors affected morbidity and mortality rates, and patient age, presence of intracranial hemorrhage, GCS, and treatment protocols were significantly associated with mortality.

Key words: Cranial firearm injuries; intracranial hemorrhage; morbidity; mortality.

INTRODUCTION Firearm injuries (FAI) are common injuries with high mortality.[1,2] Head and neck regions are the most commonly injured areas in FAI, and 14% of all deaths due to head trauma are caused by FAIs.[3–5] Address for correspondence: Ali Erdem Yıldırım, M.D. Ankara Numune Eğitim ve Araştırma Hastanesi, Nöroşirürji Kliniği; Talatpaşa Bulvarı, Altındag, 06100 Ankara, Turkey Tel: +90 312 – 508 52 76 E-mail: alierdemyildirim@gmail.com Qucik Response Code

Ulus Travma Acil Cerrahi Derg 2015;21(4):291–296 doi: 10.5505/tjtes.2015.84883 Copyright 2015 TJTES

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FAIs are high-energy traumas.[5] The extent of cerebral parenchymal injury depends on the type of the firearm, the shooting range, and the angle of entry, mass, and velocity of the bullet.[5–7] While the majority of subjects exposed to FAI die at the scene, the mortality rate of those who can survive until hospital can be reduced by application of appropriate and aggressive efforts.[8,9] No consensus has been reached yet regarding an appropriate CFAI classification and the indications for operation.[10] Some authors have recommended aggressive surgery and rapid treatment.[11–15] although some others have advocated a conservative treatment in the case of multilobular injury and a GCS less than 5.[15–17] Our study explored age, sex, Glasgow Coma Score (GCS), CT findings, and mortality and morbidity rates in patients 291

Çınar et al. Outcomes and demostration of cranial firearm injuries: a multicenter retrospective study

presenting to neurosurgery centers after CFAIs and analyzed the factors affecting mortality and morbidity.

Table 1. CT Findings of the patients

MATERIALS AND METHODS This multicenter study retrospectively evaluated patients who presented with CFAIs between January 2012 and November 2014, which included two hundred ans nineteen patients with penetrating intracranial injury. Age, sex, GCS score, CT findings, and mortality and morbidity rates were analyzed. The factors affecting mortality were analyzed. Mean age of the study population was 24.19±12.25 (range, 1–66) years and 85.8% of them were male. In 37.5% of the patients, the foreign body responsible for intracranial injury was located in the cranial cavity.

n

%

Fracture type

Single bone

Multiple bones

129

58.9

Entry-Exit

51 23.2

Base fracture

39 17.8

Depression

17

7.7

Sinus fragmentation

2

.9

Total*

90 41.1

Hemorrhage type

Intracerebral hematoma

78

35.6

The study data were stored digitally and analyzed using SPSS (Statistical Package for Social Sciences) Version 16.0 software. The normality of distribution of the descriptive variables was tested with Kolmogorov Smirnov test. Logistic regression and Wilcoxon tests were used for the comparison of study data. The results were evaluated within a confidence interval of 95%, and a p value less than 0.05 was considered significant.

SAH

39

17.8

Ventricular hemorrhage

27

12.3

Subdural hematoma

16

7.3

Epidural hematoma

12

5.5

Hemorrhage along the trajectory

7

3.2

Cerebellar hematoma

6

2.7

RESULTS

Shrapnel

68 31.1

Bone fragment

23

10.5

Undefined foreign body

The findings of CT scans were assessed in all subjects. The scans revealed a fracture in a single bone in one hundred and twenty-three (56.2%) patients, intracranial hemorrhage (subarachnoid hemorrhage, lobar hemorrhage and hemorrhage along the trajectory) in one hundred and thirty-four (61.2%), intracranial foreign body in ninety-seven (44.3%), edema in thirty-six (16.4%), contusion outside the trajectory in fifteen (6.8%), pneumocephaly in seven (3.2%), and cerebrospinal fluid (CSF) fistula in five (2.3%) (Table 1).

Total *

134

61.2

Foreign body*

10

4.6

Bullet

4

1.8

Total*

97

44.3

Edema

36

16.4

Contusion

15

6.8

Pneumocephaly

7 3.2

CSF fistula

5

2.3

There are inconsistencies between the number of the individual cells and the total numbers due to the presence of more than a lesion in a given patient.

*

Medical therapy was applied in 35.2% of the patients while an intracranial operation was performed in 64.8%. Duraplasty (54.8%) and decompression (46.1%) were the most commonly performed surgical operations (Table 2).

Mean GCS on admission was 8±3.9 in the overall study population. The mean GCS of the surviving patients was 14.6±1.3.

GCS increased in one hundred and forty-two patients while it remained stable in thirteen (p<0.05).

Fifty-six (36.1%) of the survivors developed morbidity, of which paresis/plegia were the most common pathologies (n=26, 16.8%) (Table 3).

In patients with intracranial hemorrhage, mortality was higher among those who had ventricular hemorrhage or a hemorrhage along the trajectory. The patients having epidural hemorrhage, on the other hand, had a lower mortality (p<0.05) (Table 4).

292

Table 2. Treatment approaches in FAIs

n

Medical therapy

77

% 35.2

Surgical therapy Duraplasty

120 54.8

Decompression

101 46.1

Craniotomy

53 24.2

Hematoma drainage

12

5.5

Shrapnel removal

5

2.3

4

1.8

142

64.8

Craniectomy Total *

There are inconsistencies between the number of the individual cells and the total numbers due to the presence of more than a lesion in a given patient.

*

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Çınar et al. Outcomes and demostration of cranial firearm injuries: a multicenter retrospective study

DISCUSSION

Table 3. The pathologies responsible for patient morbidity

n

%

Paresis/plegia

26 16.8

Optic nerve injury

19

12.3

Dysphasia

8

5.2

Facial nerve injury

2

1.3

6. nerve injury

2

1.3

No auditory functions

1

0.6

Vegetative form

1

0.6

Total*

56

36.1

There are inconsistencies between the number of the individual cells and the total numbers due to the presence of more than a lesion in a given patient.

*

While the mortality of single bone injury, depression fractures, and base fractures was lower, it was higher for lesions with entry and exit points (p<0.05) (Table 5).

Sixty-four (29.2%) FAI victims died. Considering the factors causing mortality, mortality rates in patients with a lower GCS on admission, multiple fractures, hemorrhage, edema, and undergoing medical treatment were higher (p<0.05) (Table 6).

Firearm injuries are very important pathologies for neurosurgery practice due to their higher mortality and morbidity rates as well as the potential for improved patient outcomes with timely and appropriate surgical interventions.[1,2,8] As a result of escalating tension and civil wars in various regions of the Middle East beginning in 2010, a significant rise in terror incidents has been witnessed, leading to both an increased number and severity of FAI cases admitted to hospitals in our country.[3,16] Previous studies have reported that the patients admitted for FAI were usually 20–35 years old and predominantly male.

[4,8,10,16,18] In agreement with the literature, our study found that predominantly young males were the victims of FAIs. Computed tomography should be ordered as an initial step in FAIs, and it is noted that lesions on tomography are correlated to prognosis.[19] CT allows evaluation of bullet position and localization in cranium; it also provides information regarding the status of bone structures and brain parenchyma. The extent of tissue injury inflicted by FAIs depends on many factors, of which foreign body’s velocity is the most important one.

[5–7] Depending on these factors, a foreign body may remain in the scalp or it may tear dura and injure intracranial structures.

Table 4. The effect of hemorrhage type on mortality

Mortality p

Survived Died

n % n %

Ventricular hemorrhage

8

Intracerebral hematoma

51 32.9 27 42.2 0.192

Hemorrhage along the trajectory

1

5.2 0.6

19 6

29.7 9.4

<0.001 0.001

Cerebellar hematoma

5 3.2 1 1.6 0.493

SAH

23 14.9 16 25.0 0.077

Epidural

35 22.6 4 6.3 0.004

Subdural

10 6.5 6 9.4 0.458

Table 5. The relationship between the bone structure and mortality

Mortality p Survived Died

n % n %

Single bone

88 56.8 25 29.1 0.017

Entry-Exit

23 14.8 28 43.8 <0.001

Depression

16 10.3 1 1.6 0.028

Base

35 22.6 4 6.3 0.004

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Çınar et al. Outcomes and demostration of cranial firearm injuries: a multicenter retrospective study

Table 6. Factors causing mortality

B

S.E.

Wald Df Sig. Exp(B)

Age

-0.047 0.023 4.258 1 0.039 .954

Sex

1.467

GCS

-1.083 0.206 27.642 1 0.000 .339

Hemorrhage

1.982

Bone fracture

0.857 2.930 1 0.087 4.335 0.701 7.981 1 0.005 7.255

1.100

0.576

3.654

1

0.056

3.005

-16.539

14494.254

0.000

1

0.999

.000

Foreign body

0.146

0.565

0.067

1

0.796

1.157

Edema

-0.887 0.846 1.100 1 0.294 .412

CSF fistula

Contusion

1.379

Pneumocephaly

-1.053 1.819 0.336 1 0.562 .349

1.304 1.118 1 0.290 3.970

Treatment modality

-1.199

0.335

12.795

Constant

4.934

1.822

7.337 1 0.007 138.953

Carey et al. and Kirkpatrick et al. have reported that mortality is related to the affected region, secondary injuries, and lesions of brain stem.[13,21] Martins et al. have reported that 17% of bullets did not penetrate dura; the authors attributed this finding primarily to lower shooting velocities of non-military firearms.[4] Bone fragments and bullets cause direct injury on tissue although they also lead to injury of distant brain tissues via short time shockwaves.[5] Aarabi et al. have reported that the most common pathologic lesion is intraventricular bleeding (49%)[22] while Çırak et al. most commonly observed intracerebral hemorrhage (19%). Various studies have reported a SAH rate of 31–80%.[23–26] In our study, no fracture was observed in 8% of patients, a lower figure than that reported

by Martins et al., probably because of the use of military firearms in this region. In this study, intracerebral hemorrhage was the most common type of hemorrhage since brain tissue occupies the largest space within the intracranial cavity. We believe that the rate of shrapnel injuries was high owing to the mine injuries during crossing the borders illegally and the use of cluster bombs to damage as many people as possible during armed conflicts. We also suggest that parenchymal injury may have been worsened by high-energy shrapnel impacts causing cranial bone fragmentation with fragments penetrating cranial cavity.

[10,11,17,20]

1

0.000

.302

open depression or multiple fractures, CSF fistula, active hemorrhage, progressive neurological deficit, and increased intracranial pressure.[19] Some authors have advocated a less aggressive cleaning procedure preserving as much brain tissue as possible[27,28] while some others have suggested a more aggressive approach consisting of debridement of necrotic tissue, hematoma evacuation, removal of bone fragments and foreign material as much as possible, establishing hemostasis, and dural closure.[11–15,29–32] Surgical intervention is not recommended for multilobular injuries and a GCS below 5 owing to lack of survival benefit.[15,32] Grahm et al. do not recommend surgery in the absence of any significant hematoma or a bihemispheric or multilobar injury, or when GCS is above 6–8.[30] Çırak et al.,[19] Ziyal et al.,[9] and Stone et al.[32] have operated 86%, 35%, and 31% of their patients, respectively, most commonly with duraplasty. Our rate of surgical intervention was higher than many former studies, primarily owing to a better clinical condition and a higher GCS in our patients. We believe that duraplasty application is common since firm dural closure is a component of all intracranial operations although a few exceptions exist.

We suggest that the mortality rate may have been increased by intracranial pressure alterations due to hemorrhages opening into ventricular cavity, augmented brain tissue injury along the bullet trajectory, and injury to important neural tissues.

We also think that serious parenchymal injury caused by entry and exit lesions that crossed the midline may have boosted mortality rates. To our opinion, the mortality rate associated with epidural hemorrhage was lower since these lesions were easily decompressed and did not cause any parenchymal injury.

Patients may develop hemiparesis, cranial nerve palsy, and seizure after FAI.[34] Ziyal et al. have reported a morbidity rate of 47%, with mono/hemiparesis being the most common morbidities.[9] Former studies have suggested that morbidity rate increases when hemorrhage developes near the ventricle.[4,35] The morbidity rate in our study was 36.1%, with visual loss being the most common pathology. To our opinion, the morbidity rate is dependent on lesion site and the applied treatment. Furthermore, in our study, the likelihood of optic nerve injury may have been higher owing to a higher rate of complex fractures while a lower morbidity rate may have stemmed from a lower rate of hemorrhages opening into the ventricle.

Discussions concerning emergency procedures applied for FAIs exist. The indications for surgical intervention include

Studies from different centers have reported mortality rates ranging between 7.7% and 93%[4,12,15,17,18,30,32] while our mortal-

294

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Çınar et al. Outcomes and demostration of cranial firearm injuries: a multicenter retrospective study

ity rate was 29.6%. The mortality rates have possibly been affected by equipment, expertise, and treatment protocols at the treating centers.

There is no consensus concerning the prognostic importance of age in FAIs involving the head. Some authors have reported a lower mortality with increasing age,[37] whereas some others have demonstrated otherwise.[12,17,38] We detected an inverse correlation between age and mortality. The likely reason of this observation may be the relatively young age of the victims who engaged in armed conflicts and the increased lethality of firearms used in such conflicts.

GCS determines the treatment planning and long-term outcomes of the patient.[5] Çırak et al.[19] have reported that a patient’s prognosis can be predicted on the basis of CT findings and GCS. Aarabi et al.[22] and Hoppe et al.[39] have reported mean admission GCSs of 7.8 and 13.5, respectively. They noted that GCS was inversely proportional to prognosis. Aldrich et al. have reported that GCS usually improves following resuscitation.[23] Kim et al. have reported an adequate improvement in all but one patient with GCS >8 whereas those having GCS<8 has had increased mortality and morbidity.[35] Former studies have reported that GCS was inversely proportional to mortality.[4,10,12,16,18,30,3335,36] Complying with the literature data, an inverse relationship between GCS and mortality was also detected.

It has been reported that there is a linear relationship between the extent of brain injury and mortality and morbidity rates.[3,10] Williams et al, and Raul et al. have reported that the ballistic trajectory and the extent of injury affect the rates of morbidity and mortality.[40,41] Various studies have particularly stressed that intraventricular hemorrhages are associated with poor prognosis.[13,35] Gressot et al. have reported that patients having a hematoma had a higher mortality rate.[18] In our study, the presence of hemorrhage was an important predictor of mortality. Hemorrhage leads to deranged tissue integrity, impaired local circulation, and ischemia; it is therefore a predictor of brain damage and death.

In patients with intracerebral hematoma, clinical status is determined by the location of hematoma and its rate of accumulation.[5] In patients hospitalized with FAI, favorable outcomes can be obtained by appropriate interventions performed before irreversible changes develop.[10] Some authors do not recommend surgery for patients with very low GCS. [15,16,30,37] Hence, the higher mortality in medically managed patients in our study may have resulted from avoiding surgery in patients with a GCS of 3.

Firearm injuries are associated with significant morbidity and mortality. It was determined in this study that many factors affected morbidity and mortality rates, and the mortality rate was particularly affected by patient age, presence of hemorrhage, GCS, and treatment protocols applied.

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Conflict of interest: None declared.

REFERENCES 1. Martins RS, Siqueira MG, Santos MT, Zanon-Collange N, Moraes OJ. Prognostic factors and treatment of penetrating gunshot wounds to the head. Surg Neurol 2003;60:98–104.

2. Cooper PR. Gunshot wounds of the brain, in Copper PR (ed): Head Injury. Baltimore, Williams and Wilkins, Sec ed. p. 1987;313–26.

3. Miller JD, Butterworth JF, Gudeman SK, Faulkner JE, Choi SC, Selhorst JB, et al. Further experience in the management of severe head injury. J Neurosurg 1981;54:289–99.

4. Brandt F, Roosen K, Weiler G, Grote W. Neurosurgical management of gunshot injuries to the head. [Article in German] Neurochirurgia (Stuttg). 1983;26:164–71. [Abstract] 5. Raul JS, Deck C, Meyer F, Geraut A, Willinger R, Ludes B. A finite element model investigation of gunshot injury. Int J Legal Med 2007;121:143–6.

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

7. Brandvold B, Levi L, Feinsod M, George ED. Penetrating craniocerebral injuries in the Israeli involvement in the Lebanese conflict, 1982–1985.

Analysis of a less aggressive surgical approach. J Neurosurg 1990;72:15– 21.

8. Kaufman HH, Makela ME, Lee KF, Haid RW Jr, Gildenberg PL. Gunshot wounds to the head: a perspective. Neurosurgery 1986;18:689–95.

9. Williams AJ, Ling GS, Tortella FC. Severity level and injury track determine outcome following a penetrating ballistic-like brain injury in the rat.

Neurosci Lett 2006;408:183–8.

10. Aarabi B, Tofighi B, Kufera JA, Hadley J, Ahn ES, Cooper C, et al. Predictors of outcome in civilian gunshot wounds to the head. J Neurosurg 2014;120:1138–46.

11. Ziyal IB. Kılınçoğlu BF, Şahin Y, Aydın Y. Penetrating Craniocerebral Gunshot Wounds. Ulusal Travma Derg 1999;5:238–41.

12. Harsh GR III, Harsh GR IV. Penetrating wounds of the head, in Wilkins RH, Rengachary SS (eds): Neurosurgery. New York. McGraw-Hill. p.

1985;1670–8.

13. Kaufman HH, Sadhu VK, Clifton GL, Handel SF. Delayed intracerebral hematoma due to traumatic aneurysm caused by a shotgun wound: a problem in prophylaxis. Neurosurgery 1980;6:181–4.

14. Gönül E, Baysefer A, Kahraman S, Ciklatekerlioğlu O, Gezen F, Yayla O, et al. Causes of infections and management results in penetrating craniocerebral injuries. Neurosurg Rev 1997;20:177–81.

15. Grahm TW, Williams FC Jr, Harrington T, Spetzler RF. Civilian gunshot wounds to the head: a prospective study. Neurosurgery 1990;27:696– 700.

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

17. Paret G, Dekel B, Yellin A, Hadani M, Weissman D, Vardi A, et al. Pediatric craniocerebral wounds from plastic bullets: prognostic implications, course, and outcome. J Trauma 1996;41:859–63.

18. Aras M, Altaş M, Yilmaz A, Serarslan Y, Yilmaz N, Yengil E, et al. Being a neighbor to Syria: a retrospective analysis of patients brought to our clinic for cranial gunshot wounds in the Syrian civil war. Clin Neurol Neurosurg 2014;125:222–8.

19. Önder A, Kadıoğlu HHM, Aydın İH. Kranioserebral Ateşli Silah Yaralanmaları Atatürk Üniversitesi Tıp Bülteni 1991;23:201–10.

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21. Mut M. Penetran balistik beyin hasarında deneysel çalışmaların yeri: güncel literatür seçmelerinin incelenmesi Turk Noroşirürji Derneği Nörotravma Bülteni 2007;2:5–8.

22. Berker M. Atış bilimi (balistik) ve ateşli silahla yaralanmanın biyomekaniği (yara balistiği). Turk Noroşirürji derneği nörotravma bülteni 2007;2:3–4.

23. Demirci Ş, Doğan KH, Deniz İ, Büken B, Erkol Z. Konya’da çocukluk çağında meydana gelen ateşli silah yaralanmasına bağlı ölümler. Adli Tıp Bülteni:2009;14(l):22–9.

24. Carey ME, Sarna GS, Farrell JB, Happel LT. Experimental missile wound to the brain. J Neurosurg 1989;71:754–64.

25. Siccardi D, Cavaliere R, Pau A, Lubinu F, Turtas S, Viale GL. Penetrating craniocerebral missile injuries in civilians: a retrospective analysis of 314 cases. Surg Neurol 1991;35:455–60.

26. Jacobs DG, Brandt CP, Piotrowski JJ, McHenry CR. Transcranial gunshot wounds: cost and consequences. Am Surg 1995;61:647–54.

27. Yaman O, Dağlı AT, Güvercin AR, Kuzeyli K. Gunshot Wound to Head.

Sinir Sistemi Cerrahisi Derg 2014;4:69–73.

28. Clark WC, Muhlbauer MS, Watridge CB, Ray MW. Analysis of 76 civilian craniocerebral gunshot wounds. J Neurosurg 1986;65:9–14.

29. Selden BS, Goodman JM, Cordell W, Rodman GH Jr, Schnitzer PG. Outcome of self-inflicted gunshot wounds of the brain. Ann Emerg Med 1988;17:247–53.

30. Nagib MG, Rockswold GL, Sherman RS, Lagaard MW. Civilian gunshot wounds to the brain: prognosis and management. Neurosurgery 1986;18:533–7.

31. Kirkpatrick JB, Di Maio V. Civilian gunshot wounds of the brain. J Neurosurg 1978;49:185–98.

32. Shoung HM, Sichez JP, Pertuiset B. The early prognosis of craniocerebral gunshot wounds in civilian practice as an aid to the choice of treatment. A series of 56 cases studied by the computerized tomography. Acta Neurochir (Wien) 1985;74:27–30.

33. Kennedy F, Gonzalez P, Dang C, Fleming A, Sterling-Scott R. The Glasgow Coma Scale and prognosis in gunshot wounds to the brain. J Trauma 1993;35:75–7.

34. Levy ML, Masri LS, Lavine S, Apuzzo ML. Outcome prediction after penetrating craniocerebral injury in a civilian population: aggressive surgical management in patients with admission Glasgow Coma Scale scores of 3, 4, or 5. Neurosurgery 1994;35:77–85.

35. Aldrich EF, Eisenberg HM, Saydjari C, Foulkes MA, Jane JA, Marshall LF, et al. Predictors of mortality in severely head-injured patients with civilian gunshot wounds: a report from the NIH Traumatic Coma Data Bank. Surg Neurol 1992;38:418–23.

36. Cirak B, Güven MB, Kiymaz N, Işik S. Cranial gunshot injuries and treatment approaches. [Article in Turkish] Ulus Travma Derg 2000;6:241–3.

37. Levy ML, Rezai A, Masri LS, Litofsky SN, Giannotta SL, Apuzzo ML, et al. The significance of subarachnoid hemorrhage after penetrating craniocerebral injury: correlations with angiography and outcome in a civilian population. Neurosurgery 1993;32:532–40.

38. Stone JL, Lichtor T, Fitzgerald LF. Gunshot wounds to the head in civilian practice. Neurosurgery 1995;37:1104–12.

39. Gressot LV, Chamoun RB, Patel AJ, Valadka AB, Suki D, Robertson CS, et al. Predictors of outcome in civilians with gunshot wounds to the head upon presentation. J Neurosurg 2014;121:645–52.

40. Kim TW, Lee JK, Moon KS, Kwak HJ, Joo SP, Kim JH, et al. Penetrating gunshot injuries to the brain. J Trauma 2007;62:1446–51.

41. Hoppe IC, Kordahi AM, Paik AM, Lee ES, Granick MS. Pediatric facial fractures as a result of gunshot injuries: an examination of associated injuries and trends in management. J Craniofac Surg 2014;25:400–5.

ORİJİNAL ÇALIŞMA - ÖZET OLGU SUNUMU

Kraniyal ateşli silah yaralanmalarının dağılımı ve sonuçları: Çok merkezli geriye dönük çalışma Dr. Kadir Çınar,1 Dr. Mehmet Seçer,2 Dr. Fatih Alagöz,3 Dr. Murat Ulutaş,4 Dr. Özhan Merzuk Uçkun,3 Dr. Ali Erdem Yıldırım,3 Dr. Ahmet Gürhan Gürçay,5 Dr. Yahya Güvenç,6 Dr. Haydar Çelik,7 Dr. Fırat Narin8 Şehit Kamil Devlet Hastanesi, Nöroşirürji Kliniği, Gaziantep Deva Hastanesi, Nöroşirürji Kliniği, Gaziantep Ankara Numune Eğitim ve Araştırma Hastanesi, Nöroşirürji Kliniği; Ankara 4 Sanko Üniversitesi Hastanesi, Nöroşirürji Kliniği, Gaziantep 5 Ankara Atatürk Eğitim ve Araştırma Hastanesi, Nöroşirürji Kliniği; Ankara 6 Dr. N.K. Sincan Devlet Hastanesi, Nöroşirürji Kliniği, Ankara 7 Ankara Eğitim ve Araştırma Hastanesi, Nöroşirürji Kliniği; Ankara 8 Ankara Memorial Hastanesi, Nöroşirürji Kliniği; Ankara 1 2 3

AMAÇ: Kraniyal ateşli silah yaralanmaları (KASY) sonucu hastanemizde tedavi edilen olgular, bilgisayarlı tomografi (BT) sonucu ve klinik verilerine göre incelendi, mortalite üzerine etkili faktörleri belirlemek için veriler geriye dönük olarak değerlendirildi.

GEREÇ VE YÖNTEM: Çok merkezli çalışmamızda beyin cerrahisi kliniklerine KASY sebebi ile Ocak 2012–Kasım 2014 tarihleri arasında başvuran 219 hasta geriye dönük olarak değerlendirildi. Hastaların yaş, cinsiyet, Glascow Coma Skala (GKS) skoru, BT bulguları, morbidite ve mortalite durumları incelendi. Mortaliye etki eden faktörler analiz edildi.

BULGULAR: Hastaların yaş ortalaması 24.19±12.25 yıl olup, %85.8’i erkekti. Bilgisayarlı tomografide belirlenen en sık bulgular kırık (%100), intrakraniyal kanama (%61.2) ve intrakraniyal yabancı cisimdi (%44.3). Hastaların %64.8’ine intrakraniyal operasyon uygulandı. Hastane başvurusu esnasında ortalama GKS puanı 8±3.9, yaşayan hastaların ortalama GKS puanının arttığı saptandı (p<0.005). Hastaların mortalite oranı %29.2 ve morbidite oranı %36.1 idi. Mortaliteye etki eden faktörlerin GKS, kırık tipi, kanama, ödem ve tedavi şekliydi (p<0.05).

TARTIŞMA: Ateşli silah yaralanmaları morbiditesi ve mortalitesi yüksek yaralanmalardır. Morbidite ve mortalite üzerine birçok faktörün etki ettiği ve özellikle mortalite üzerine hastanın yaşı, kanamanın varlığı, GKS ve tedavi protokollerinin etki ettiğini saptadık.

Anahtar sözcükler: Kraniyal ateşli silah yaralanmaları; intrakraniyal kanama; morbidite; mortalite.

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Rarely seen complication of motor vehicle accidents: Bilateral globe avulsion Osman Kelahmetoğlu, M.D.,1* Tekin Şimşek, M.D.,2 Ümit Beden, M.D.,3 İlhami Oğuzhan Aydoğdu, M.D.,2 Ebru Cömert Hamzaoğlu, M.D.3 1

Department of Plastic, Reconstructive and Aesthetic Surgery, Tarsus State Hospital, Mersin

2

Department of Plastic, Reconstructive and Aesthetic Surgery, Ondokuz Mayıs University Faculty of Medicine, Samsun

3

Department of Ophthalmology, Ondokuz Mayıs University Faculty of Medicine, Samsun

ABSTRACT Avulsion of the globe is a rare condition that can occur with severe maxillofacial trauma. A few bilateral cases have been reported.

The objective of this study was to present a case of this challenging condition in a 15-year-old male patient who was admitted to the emergency service after a motor vehicle accident.

Key words: Avulsion; globe; bilateral; luxation; trauma.

INTRODUCTION Traffic accidents are the most common causes of maxillofacial trauma. Depending on the severity of the trauma, a wide spectrum of fracture patterns and unexpected conditions may be encountered like avulsion of the globe. Subluxation of the globe is extremely rare, and we found few reported cases.

[1–3] This study presented the case of a patient with this rare condition, who was followed-up for one year postoperatively.

CASE REPORT A 15-year-old male was admitted to the emergency service after a car accident. He had been sitting in the back seat.

On examination, his entire face was edematous, the left up-

Presented at the 32th National Turkish Society of Plastic Reconstructive and Aesthetic Surgeons Congress as a Poster Presentation (September 15-19, 2010, Trabzon, Turkey). *Current affiliation: Department of Plastic, Reconstructive and Aesthetic Surgery, Bezmialem Vakif University Faculty of Medicine, Istanbul.

Address for correspondence: Osman Kelahmetoğlu, M.D. Bezmialem Vakıf Üniversitesi Tıp Fakültesi, Plastik, Rekonstrüktif ve Estetik Cerrahi Anabilim Dalı, Vatan Cad., No: 1, İstanbul, Turkey Tel: +90 212 – 453 17 00 E-mail: osmankelahmetoglu@gmail.com Qucik Response Code

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per lid had a deep laceration and both globes were luxated out of the orbital sockets (Figs. 1a,b). There were no light reflexes or any eye movement. Computed tomography (CT) showed complete laceration of both optic nerves (Fig. 1c).

There were also multiple fractures corresponding to a Le Fort III pattern with Le Fort II components with frontal sinus anterior wall fractures. Neurosurgery consultation revealed no brain injury other than minor edema. The surgical team included an ophthalmologic surgeon. Radiological examination revealed no sign of systemic trauma, except minor brain swelling and pneumocephalus. There was no cervical injury.

After the initial evaluation in the emergency room, the patient was transferred to the operating room. The left globe was completely out of the orbit and there was retrobulbar hemorrhage; all extraocular muscles and optic nerve were ruptured. As the left globe was unsuitable for repositioning, it was enucleated. The right globe was also out of the orbit and had findings similar to the left globe, except there was no retrobulbar hemorrhage. The stumps of the medial and inferior rectus muscles were found. After repairing the medial and inferior rectus muscles and performing a right lateral canthoplasty, the globe was repositioned. The facial fractures were immobilized with plates and screws (Fig. 1d). Postoperatively, the patient was observed in the intensive care unit for two days. He was discharged on the fifth postoperative day.

Four months postoperatively, the patient presented to the outpatient clinic with left periorbital cellulitis. He was treated with oral antibiotics. At six months, an ocular prosthesis was placed 297

KelahmetoÄ&#x;lu et al. A rarely seen complication of motor vehicle acci-dents: bilateral globe avulsion

(a)

(c)

(b)

(d)

(e)

Figure 1. (a) Preoperative anterior view in the emergency room. (b) Preoperative lateral view in the emergency room. (c) Preoperative computed tomography scan imaging shows complete laceration of both optic nerves (red arrows). (d) Immediate postoperative 3D computed tomography imaging shows repaired facial fractures. (e) One year postoperative imaging shows no major facial deformity.

in the left orbit. One year postoperatively, the patient was reevaluated and there was no major facial deformity (Fig. 1e).

DISCUSSION A variety of orbital and periorbital soft tissue injuries can be seen with craniofacial fractures, including contusion, avulsion, muscle entrapment, optic nerve damage, and globe rupture.

[1] The optic nerve and globe are usually resilient to mild-tomoderate ocular trauma, while high-energy trauma can lead to multiple fractures that reduce the orbital volume significantly, facilitating avulsion of the globe from its socket.[4] Globe avulsion is a rare condition usually resulting from severe trauma to the orbit and face.[3] The term describes globes that have been pulled out of their normal anatomical position by an external force.[5] Morris et al. have identified three mechanisms: (a) an elongated object enters the medial orbit, propelling the globe forward; (b) a wedge-shaped object enters the orbit medially, displacing the globe anteriorly; and (c) a penetrating object transects the optic nerve directly.[5] Song and Carter have described abrupt deceleration as a cause of bilateral globe subluxation.[3] Therefore, passengers in the back seats can experience more abrupt deceleration.

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Optic nerve transection is well-documented, and it is the major reason for globe subluxation.[2â&#x20AC;&#x201C;6] An isolated ruptured optic nerve is classified as incomplete while it is complete when there is disruption of the extraocular muscles and optic nerve, resulting in total luxation of the ocular bulb.[1] Cases with intact extraocular muscles have been reported.

[2â&#x20AC;&#x201C;6] The extraocular muscles injured and avulsed most commonly are the medial, inferior, superior, and lateral recti and the obliques, respectively.[7] Imaging studies of the head and orbit are advisable before surgery to assess the extent of orbital and ocular injuries. Brain and orbital CT are required to exclude intracranial bleeding, optic chiasma injury, and bone fractures.[6] Some authors have reported normal CT images in the presence of optic nerve avulsion.

In this case, multiple fractures of the orbital walls and abrupt deceleration likely caused the bilateral globe avulsion. The patient had bilateral transected optic nerves, and none of the extraocular muscles in either globe were intact. He also had multiple fractures corresponding to a Le Fort III pattern with Le Fort II components with frontal sinus anterior wall fractures. There was minor brain edema.

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Kelahmetoğlu et al. A rarely seen complication of motor vehicle acci-dents: bilateral globe avulsion

The management of an avulsed globe is controversial. Some authors advocate primary enucleation to treat ocular globe luxation with optic nerve avulsion because there is no visual recovery.[1] Others suggest that repositioning the globe and retaining the eye can offer psychological and cosmetic benefits to the patient[1,2] and enhance the subsequent cosmetic outcome of an ocular prosthesis.[1] Moreover, in children, the maintenance of the ocular globe assists in adequate facial bone development.[8] In this case, the left globe was unsuitable for repositioning, it was enucleated. Then, the right globe was repositioned after repairing the medial and inferior rectus muscles and performing a right lateral canthoplasty. Facial fractures were repaired with plates and screws. The possible mechanism of the survival of the right globe was out of the orbit with soft tissue attachments to the orbital walls and the periorbital soft tissues. At the end of the one year period, there was not any sign of phtisis bulbi, which was due to possible source of the blood supply in the soft tissue attachments. At six months, an ocular prosthesis was placed in the left orbit.

Conclusion Globe avulsion is an extremely rare, challenging and unexpected complication of maxillofacial trauma. Patients with severe maxillofacial trauma should be observed meticulously for globe avulsion. Well-repaired fractures and repositioning of the globes prevent facial deformity in children and might reduce the patient’s psychological stress

due to the concurrent blindness.

No grants and funding have been received for this study.

None of the authors has financial interest related to this study to disclose.

Conflict of interest: None declared.

REFERENCES 1. Unal S, Argin A, Arslan E, Demirkan F, Aksoy A. Bilateral complete avulsion of ocular globes in a Le Fort III maxillofacial fracture: a case report and review of the literature. Eur J Ophthalmol 2005;15:123–5.

2. Razmjua H, Masjedi M. Traumatic bilateral globe avulsion (case report).

J Res Med Sci 2009;14:259–60.

3. Song A, Carter KD. Bilateral traumatic globe subluxation. Ophthal Plast Reconstr Surg 2006;22:136–7.

4. Bajaj MS, Kedar S, Sethi A, Gupta V. Traumatic globe luxation with optic nerve transection. Orbit 2000;19:165–170.

5. Morris WR, Osborn FD, Fleming JC. Traumatic evulsion of the globe.

Ophthal Plast Reconstr Surg 2002;18:261–7.

6. de Santana Santos T, Vajgel A, Ribeiro CF, de Santana Júnior JR, Andrade Filho ES. Avulsion of globe following maxillofacial trauma. J Craniofac Surg 2012;23:1097–100.

7. Mailer CM. Avulsion of the inferior rectus. Can J Ophthalmol.

1974;9:262–6.

8. Pereira FJ, Bettega RB, Velasco e Cruz AA. Management of globe luxation followed by traumatic liquoric fistula: case report. Arq Bras Oftalmol 2011;74:58–60.

OLGU SUNUMU - ÖZET

Motorlu taşıt kazalarının nadir görülen bir komplikasyonu: İki taraflı glob avülsiyonu Dr. Osman Kelahmetoğlu,1* Dr. Tekin Şimşek,2 Dr. Ümit Beden,3 Dr. İlhami Oğuzhan Aydoğdu,2 Dr. Ebru Cömert Hamzaoğlu3 1 2 3

Tarsus Devlet Hastanesi, Plastik, Rekonstrüktif ve Estetik Cerrahi Kliniği, Mersin Ondokuz Mayıs Üniversitesi Tıp Fakültesi, Plastik, Rekonstrüktf ve Estetik Cerrahi Anabilim Dalı, Samsun Ondokuz Mayıs Üniversitesi Tıp Fakültesi, Göz Hastalıkları Anabilim Dalı, Samsun

Glob avülsiyonu, ağır maksillofasiyal travmalar sonucu oluşabilen nadir bir durumdur. Birkaç tane iki taraflı olarak rapor edilmiş olgular mevcuttur.

Bu yazıda, motorlu taşıt kazası sonrası acil servise getirilen bu zorlu duruma sahip 15 yaşında erkek hasta sunuldu.

Anahtar sözcükler: Avülsiyon; glob; iki taraflı; luksasyon; travma. *Şimdiki Kurumu: Bezmialem Vakıf Üniversitesi Tıp Fakültesi, Plastik, Rekonstrüktif ve Estetik Cerrahi Anabilim Dalı, İstanbul Ulus Travma Acil Cerrahi Derg 2015;21(4):297–299

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OLGU SUNUMU

Behçet hastalığına bağlı multipl ince bağırsak perforasyonu Dr. Tevfik Eker,1 Dr. Aydan Eroğlu2 1

Yakın Doğu Üniversitesi Tıp Fakültesi, Genel Cerrahi Anabilim Dalı, Lefkoşa, Kuzey Kıbrıs

2

Ankara Üniversitesi Tıp Fakültesi, Genel Cerrahi Anabilim Dalı, Ankara

ÖZET Behçet hastalığı, kronik, nükslerle seyreden, pek çok sistemi tutan, idiyopatik enflamatuvar bir hastalıktır. Gastrointestinal sistemde ağızdan sonra en sık tutulum yeri ileoçekal bölgedir. Behçet hastalığının neden olduğu intestinal ülserlerler, perforasyonlara neden olabilmektedir. On dokuz yaşında erkek hasta Behçet hastalığı tanısı ile hastanemize kabul edildi. Hastada akut karın gelişmesi üzerine kliniğimizde ameliyat edildi ve laparotomi sırasında terminal ileumda multipl perforasyonlar olduğu saptandı. Hastaya parsiyel ileum rezeksiyonu yapıldı. Ameliyat sonrası dönemi sorunsuz seyreden hasta taburcu edildi. Hastanın ileostomisi ilk ameliyattan sonraki ikinci ayda kapatıldı. On altı aylık izlem periyodunda hastada klinik olarak önemli bir sorun görülmedi. Bu yazıda Behçet hastalığının tanısı sırasında nadiren görülen bir komplikasyon olan multipl ileum perforasyonu sunuldu ve yayınlanmış olguların bilgisi altında tartışıldı.

Anahtar sözcükler: Behçet sendromu; enterobehçet; faktör V Leiden; intestinal perforasyon; MTHFR; tombofili.

GİRİŞ Behçet hastalığı (BH) ilk kez 1937 yılında Prof. Dr. Hulusi Behçet tarafından tanımlanan sistemik inflamasyonlarla karakterli bir vaskülittir.[1] Oral ve genital ülserler, BH’nin en sık görülen belirtileridir. Dil, dudak, yanak mukozası, farinks ve diş etinde, kadınlarda vulva ve vajinal mukoza, erkeklerde skrotum ve penis, inguinal bölge ve perineum ülserlerin en sık yerleştiği bölgelerdir.[2] İntestinal mukozal ülserler gastrointestinal sistemin (GİS) herhangi bir yerinde görülebilir.[3] Yüzeysel veya derin olabilirler. Bu ülserlerden spontan perforasyonlar bildirilmiştir. Karın ağrısı, ishal, özofajite sekonder pirozis ve retrosternal yanma, peri anal fistül belirtileri görülebilir. Gastrointestinal tutulum, bağırsak duvarının küçük damarlarında, sıklıkla da venlerinde vaskülit oluşumu nedeniyle gelişir. En sık tutulum yeri terminal ileum ve çekumdur. Özofagus ve daha nadiren mide de tutulabilir.[3]

İletişim adresi: Dr. Tevfik Eker, Yakın Doğu Üniversitesi Tıp Fakültesi, Genel Cerrahi Anabilim Dalı, Lefkoşa, K.K.T.C. Tel: +90 312 – 508 31 67 E-mail: tevfikeker@yahoo.com Qucik Response Code

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Behçet hastalığının enterik tutulumuna bağlı multipl ileum perforasyonu gelişen olgumuzu sunduğumuz bu makalede, BH’nin enterik tutulumunun klinik ve laboratuvar özelliklerini, komplikasyonlarını ve cerrahi tedavisini literatür eşliğinde tartışmayı amaçladık.

OLGU SUNUMU On dokuz yaşında erkek hasta görme bulanıklığı yakınması ile başvurduğu göz hastalıkları kliniğinde Behçet hastalığı ön tanısı ile hospitalize edildiği sırada meydana gelen karın ağrısı nedeni ile Şubat 2011 tarihinde kliniğimize konsülte edildi. Hastanın yapılan fiziksel incelemesinde oral ve genital bölgedeki ülseröz lezyonların dışında, karında yaygın hassasiyet, defans, sağ ve sol alt kadranlarda rebound saptandı. Ateş ve taşikardisi bulunan olgunun laboratuvar bulgularında lökosit: 31.6x109/L, hemoglobin 8.8 g/dl, trombosit 884x109/L olup biyokimyasal değerleri normal sınırlarda idi. Karın ultrasonografisinde pelviste serbest sıvı olduğu, pelvik yağ dokunun ödemli ve sağ alt kadranda çift duvar kalınlığı 13–19 mm arasında değişen, komprese olmayan, aperistaltik yapının komplike apandisit lehine değerlendirilmesi üzerine hasta perfore apandisit ön tanısı ile ameliyata alındı. Şekil 1’de hastanın ayakta direkt karın grafisinde ince bağırsaklara ait hava sıvı seviyeleri görülmektedir. Yapılan laparotomide apandiksin sağlam olduğu ancak ileoçekal valvden itibaren 80 cm proksimaline kadar uzanan ince bağırsak segmenti boyunca multipl perforasyonların bulunduğu, karın içerisinde bağırsak segmentleri arası ve pelvik bölgede yoğun intestinal içerik olduğu görüldü. 80 cm’lik ileum segmenti rezeke edildi, karın içerisi kirli kabul edilerek Ulus Travma Acil Cerrahi Derg, Temmuz 2015, Cilt. 21, Sayı. 4

Eker ve ark. Behçet hastalığına bağlı multipl ince bağırsak perforasyonu

dan dört–altı yıl sonra ortaya çıkmaktadır. Chou ve ark.nın kendi kliniklerinde Behçet hastalığına bağlı intestinal perforasyon nedeni ile opere ettikleri 21 hastayı inceledikleri geriye dönük çalışmalarında ve Kasahara ve ark.nın Behçet hastalığına bağlı 136 perforasyon olgusunun verilerinin geriye dönük incelenmesinde de BH’nin sistemik bulgularının ve tanısının ortalama üçüncü dekatta koyulduğu ve GİS tutulumu ve perforasyonlar ile en sık dördüncü dekatta karşılaşıldığı saptanmıştır.[9,10] Bizim burada sunduğumuz olgunun hem 19 yaşında olması, hem de tanı ile eşzamanlı olarak intestinal tutulum ve perforasyon olması ilgi çekicidir.

Şekil 1. Hastanın ayakta direkt karın grafisinde ince bağırsaklara ait hava sıvı seviyeleri görülmektedir.

proksimal ve distal bağırsak uçları tüfek namlusu şeklinde ileostomi oluşturuldu. Ameliyat sonrası klinik takiplerinde bir sıkıntı gelişmeyen hasta 10. günde taburcu edildi. Yaklaşık iki ay sonra elektif şartlarda ileostomisi kapatıldı. Hastanın trombofilik polimorfizmlerinin araştırılmasında faktör V Leiden (FVL) GG, protrombin (PT) G20210A GG ve metilentetrahidrofolat redüktaz (MTHFR) C677T ise CT olduğu saptandı.

MTHFR C677T heterozigot olarak tespit edildi ancak olgunun serum homosistein düzeyi normal sınırlarda bulundu.

TARTIŞMA Behçet hastalığının Dr. Hulusi Behçet tarafından tanımlanmasından günümüze kadar geçen 74 yıllık dönemde, bu hastalığın multisistemik olduğu ve cilt, eklem, gastrointestinal, ürogenital, kardiyopulmoner sistemleri tutması ile ilgili çalışmalar yayınlanmaktadır. Behçet hastalığı, GİS’nin herhangi bir yerini tutabilir. Özofagus ve mide nadir tutulmakla birlikte, oral bölge dışında en sık tutulum yeri terminal ileum ve çekumdur.

Behçet hastalığılığı gastrointestinal sistemde iki tip ülser meydana gelir; lokalize veya diffüz tip ülserler. Lokalize ülserler ileoçekal bölgede sık görülür ve derindir. Sıklıkla serozal yüzeye penetre olup perforasyonla komplike olurlar. Buna karşılık diffüz ülserler sıklıkla kolonda görülürler ve ayrı ayrı çok sayıda ülserlerdir.[4,5] Behçet hastalığı tarihi ipek yolu üzerindeki ülkelerde (Japonya, Kuzey Çin’den Akdeniz ülkeleri arasındaki bölge) daha sık görülür ve GİS tutulumun gerçek sıklığı bilinmemekle birlikte (endoskopik incelemeler semptomatik bireylerde yapıldığı için) etnik farklılıklar taşımaktadır; Japonlar’da, Koreliler’de ve Çinliler’de daha fazla görülürken Türkler’de GİS tutulumu daha azdır (Çinliler’de %15 Japonlar’da %50–60 iken Türkler’de %0–5).[6–8] Gastrointestinal tutulumu sıklıkla oral ülserlerin başlamasınUlus Travma Acil Cerrahi Derg, Temmuz 2015, Cilt. 21, Sayı. 4

Enterobehçet vasküler tutulumun bir sonucu olup, geniş damarların yanı sıra küçük damarların tutulması, trombozu ile intestinal iskemi ve infarktlar ile sonuçlanır. Perforasyon nedeniyle ileokolik rezeksiyon geçirmiş Enterobehçet olgularında spesmenin histolojik incelemesinde küçük damarlarda fibrointimal obliterasyon, nötrofil infiltrasyonu içeren derin ülserler olurken, buna komşu mukoza ise rölatif olarak normaldir.

Son yıllarda FVL ile göz tutulumu arasındaki ilişki, PT G20210A mutasyonu ile BH’de tromboz gelişimi için risk faktörü olduğuna dair çalışmalar yayınlanmaktadır.[11,12] Tursen ve ark.nın BH olan 21 olguluk çalışmasında PT G20210A mutasyonu sağlıklı popülasyona göre daha yüksek bulunmuştur.[13] Slingardi ve ark. 118 İtalyan BH’sinde (hiç birisinde enteroBehçet saptanmamış) FVL ve PT G20210A polimorfizmi açısından sağlıklı kontrol grubuna göre farklılık olmadığını göstermişlerdir. Sadece göz tutulumu açısından PT G20210A mutasyonu olmasının anlamlı olabileceği ileri sürülmüştür.[14] Behçet hastalığında bu trombüs formasyonunun patogenezisi tam olarak anlaşılamamıştır. Protein C, protein S, anti-trombin eksikliği, anti-fosfalipid antikorlar, FVL, PT gen mutasyonları, hiperhomosisteinemi gibi trombofilik parametrelerin etkinliği araştırılmaktadır. Ancak trombofilianın BH gelişiminde etkisi tartışmalıdır.[15,16] Her ne kadar genetik trombotik defektler, bozulmuş koagülasyon/fibrinolizis, endotel hasarı ya da disfonksiyonu ile birlikte diğer immüno enflamatuvar moleküllerin hepsinin katkısı olsa da BH’de trombotik durumun altta yatan nedeni tam olarak bilinmemektedir. Aksu ve ark.nın araştırmasında, BH’de plazma homosistein konsantrasyonu sağlıklı popülasyona göre anlamlı olarak daha yüksektir.[17] Başka bir çalışmada ise homosistein düzeyi derin ven trombozu (DVT) olan BH grubunda DVT olmayan Behçet hastalarından ve sağlıklı popülasyondan daha yüksek bulunmasına rağmen MTHFR genotip dağılımında anlamlı olarak farklılık saptanmamıştır.[18] Ayrıca MTHFR C677T polimorfizmi tek başına homosistein regülasyonunda rol oynayamaz. Bizim olgumuzda araştırılan trombofilik polimorfizmlerden MTHFR 677CT olduğu görüldü, ancak serum homosistein düzeyi normal olarak bulundu.

Enterobehçet’e bağlı perforasyon gelişen hastalarda uygulanan sınırlı rezeksiyonlarda anastomoz proksimalinden tekrar perforasyon gelişebileceğini ve perforasyon tekrarını önlemek 301

Eker ve ark. Behçet hastalığına bağlı multipl ince bağırsak perforasyonu

için literatürde geniş rezeksiyonlar öneren kaynaklar mevcuttur.[9,10] Biz olgumuzda sağlam cerrahi sınırlar bırakılacak şekilde parsiyel ince bağırsak rezeksiyonu uyguladık ve karın içerisi kirli olduğundan dolayı primer anastomoz yerine tüfek namlusu ileostomi oluşturarak operasyonu sonlandırdık. Rezeksiyon sonrası primer anastomoz yerine ileostomi tercih edilmesi ve elektif ileostomi kapatılması, hastalığın aktive olduğu bu dönemde uygulanan primer anastomoz sonrası görülen perianastomotik reperforasyon komplikasyonu oranlarını da azaltabileceğini düşündürse de, bu cerrahi tekniğin başarı oranlarını ortaya koymak için geniş olgu çalışmalarına ihtiyaç vardır. Çıkar örtüşmesi: Çıkar örtüşmesi bulunmadığı belirtilmiştir.

KAYNAKLAR 1. Alpsoy E. Behçet hastalığının deri ve mukoza belirtileri. Türkderm 2003;37:92–9.

2. Bang D. Clinical spectrum of Behçet’s disease. J Dermatol 2001;28:610– 3.

3. Ebert EC. Gastrointestinal manifestations of Behçet’s disease. Dig Dis Sci 2009;54:201–7.

4. Jung YS, Yoon JY, Lee JH, Jeon SM, Hong SP, Kim TI, et al. Prognostic factors and long-term clinical outcomes for surgical patients with intestinal Behcet’s disease. Inflamm Bowel Dis 2011;17:1594–602.

5. Choi IJ, Kim JS, Cha SD, Jung HC, Park JG, Song IS, et al. Long-term clinical course and prognostic factors in intestinal Behçet’s disease. Dis Colon Rectum 2000;43:692–700.

6. Sakane T, Takeno M, Suzuki N, Inaba G. Behçet’s disease. N Engl J Med 1999;341:1284–91.

7. Ng FH, Cheung TC, Chow KC, Wong SY, Ng WF, Chan HC, et al.

Repeated intestinal perforation caused by an incomplete form of Behçet’s

syndrome. J Gastroenterol Hepatol 2001;16:935–9.

8. Shin SJ, Lee SK, Kim TI, Cheon JH, Kim ES, Kim BC, et al. Chronological changes in the systemic manifestations of intestinal Behcet’s disease and their significance in diagnosis. Int J Colorectal Dis 2010;25:1371–6.

9. Chou SJ, Chen VT, Jan HC, Lou MA, Liu YM. Intestinal perforations in Behçet’s disease. J Gastrointest Surg 2007;11:508–14.

10. Kasahara Y, Tanaka S, Nishino M, Umemura H, Shiraha S, Kuyama T. Intestinal involvement in Behçet’s disease: review of 136 surgical cases in the Japanese literature. Dis Colon Rectum 1981;24:103–6.

11. Salvarani C, Calamia K, Silingardi M, Ghirarduzzi A, Olivieri I. Thrombosis associated with the prothrombin G-->A20210 mutation in Behçet’s disease. J Rheumatol 2000;27:515–6.

12. Vayá A, Forner MJ, Estellés A, Villa P, Mira Y, Ferrando F, et al. Intracardiac thrombosis in a case of Behcet’s disease associated with the prothrombin 20210G-A mutation. Haematologica 2000;85:425–8.

13. Tursen U, Kaya TI, Eskandari G, Gunduz O, Yazar M, Ikizoglu G, et al. Association of factor V Leiden and prothrombin gene mutation with Behçet’s disease. Arch Dermatol Res 2001;293:537–9.

14. Silingardi M, Salvarani C, Boiardi L, Accardo P, Iorio A, Olivieri I, et al. Factor V Leiden and prothrombin gene G20210A mutations in Italian patients with Behçet’s disease and deep vein thrombosis. Arthritis Rheum 2004;51:177–83.

15. Leiba M, Seligsohn U, Sidi Y, Harats D, Sela BA, Griffin JH, et al.

Thrombophilic factors are not the leading cause of thrombosis in Behçet’s disease. Ann Rheum Dis 2004;63:1445–9.

16. Ateş A, Düzgün N, Ulu A, Tiryaki AO, Akar N. Factor V gene (1691A and 4070G) and prothrombin gene 20210A mutations in patients with Behçet’s disease. Pathophysiol Haemost Thromb 2003;33:157–63.

17. Aksu K, Turgan N, Oksel F, Keser G, Ozmen D, Kitapçioğlu G, et al.

Hyperhomocysteinaemia in Behçet’s disease. Rheumatology (Oxford) 2001;40:687–90.

18. Canataroglu A, Tanriverdi K, Inal T, Seydaoglu G, Arslan D, Ozbek S, et al. Methylenetetrahydrofolate reductase gene C677T mutation and plasma homocysteine level in Behçet’s disease. Rheumatol Int 2003;23:236– 40.

CASE REPORT - ABSTRACT

Multiple small bowel perforations due to Behcet’s disease Tevfik Eker, M.D.,1 Aydan Eroğlu, M.D.2 1 2

Department of General Surgery, Near East University Faculty of Medicine, Nicosia, Northern Cyprus Department of General Surgery, Ankara University Faculty of Medicine, Ankara

Behcet’s disease is a chronic, relapsing, multisystemic, idiopathic, and inflammatory disease. A common gastrointestinal site other than the mouth is the ileocecal region. Intestinal ulcers, due to Behcet’s disease, can cause perforation. A 19-year-old male patient was admitted to our hospital for Behcet’s disease. The patient developed acute abdomen, and laparotomy revealed multiple perforations throughout the terminal ileum. He underwent partial ileum resection. Postoperative period was uneventful, and the patient was discharged. The patient’s ileostomy was closed two months after the first operation. He was clinically well during the 16-month follow-up period. This study aimed to report multiple ileum perforations as an unusual complication of Behcet’s disease at the time of presentation and review of the current literature of reported cases.

Key words: Behcet’s Disease; Entero-Behcet; factor V Leiden; intestinal perforation; MTHFR; thrombophylism.

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CA S E R EP O RT

Left atrial rupture due to blunt thoracic trauma İlker Akar, M.D.,1 İlker İnce, M.D.,1 Cemal Aslan, M.D.,1 Mehmet Çeber, M.D.,1 İlker Kaya, M.D.2 1

Department of Cardiovascular Surgery, Gaziosmanpasa University Faculty of Medicine, Tokat

2

Department of Cardiovascular Surgery, Tokat State Hospital, Tokat

ABSTRACT Blunt traumatic cardiac rupture is rare and associated with high mortality. The most popular theory of cardiac rupture after blunt thoracic trauma is rapid deceleration with disruption of the atria from their connections to the vena cava and pulmonary veins. In cases with both massive hemothorax and hemopericardium, injury can usually originate from the heart and/or major vessels. Surgical approach through the median sternotomy can provide convenience to repair the defect. In this article, successful treatment with median sternotomy of a 33-year-old male case with a rupture of the left atrium after blunt thoracic trauma was reported.

Key words: Blunt thoracic trauma; left atrium; rupture.

INTRODUCTION The incidence of cardiac rupture after blunt thoracic trauma ranges from approximately 0.16–2%. Left atrial rupture, among cardiac injuries, is also rare and a catastrophic event associated with high mortality rates. Several mechanisms of blunt traumatic cardiac rupture have been described. The most popular theory of cardiac rupture after blunt thoracic trauma is rapid deceleration with resultant disruption of the atria from their connections to the vena cava and pulmonary veins.[1] This study reported the case of 33-year-old man with a rupture of the left atrium-right superior pulmonary vein connection after blunt thoracic trauma.

CASE REPORT A 33-year-old male was brought to the emergency service after a fall from height. He was awake, alert, and oriented to person, place, and time. He was only suffering from backAddress for correspondence: İlker Akar, M.D. Kaleardı Mah., Muhittin Fisunoğlu Cad., Ali Şevki Erek Yerleşkesi Tıp Fakültesi, 60100 Tokat, Turkey Tel: +90 356 – 212 95 00 / 1270 E-mail: ilkerakar16@yahoo.com Qucik Response Code

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ache. On physical examination, there were small bruises on his chest. Cardiovascular evaluation revealed only distantsounding heart sounds, without hypotension or distended jugular veins. His respiratory rate was 20 breaths per minute, pulse rate was 120 beats per minute, and blood pressure was 100/50 mmHg. Chest X-ray radiography showed an enlarged cardiac silhouette with mediastinal widening and right pleural effusion. In thoracoabdominal computed angiography tomography (CAT), the hemopericardium and right hemothorax were seen (Fig. 1). Major vessels of the mediastinum were normal. In echocardiography, there was markedly pericardial effusion. The patient was taken to the operating room with a pre-diagnosis of cardiac rupture. After midline sternotomy and pericardial incision, 400 ml fibrin blood gushed out. On the examination of the heart, left atrial rupture was detected at the pulmonary vein-atrial junction (Fig. 2). Under partial cardiopulmonary bypass, the defect was sutured with a pledgeted 4–0 polypropylene suture. After opening the right pleura, approximately 1200 ml blood was aspirated. There was no bleeding source at the right hemithorax. After weaning from the cardiopulmonary bypass, transeusophageal echocardiography was performed and no defect was seen at interatrial and interventricular septum. The postoperative period was uneventful, and the patient was discharged on the postoperative six day without any complications.

DISCUSSION The incidence of cardiac injury after blunt chest trauma varies from 8% to 86% in reported series.[2-4] Cardiac rupture was detected in 96.9% of the fatalities caused by a blunt mechanism among 160 trauma autopsies with cardiac injury.[4] The 303

Akar et al. Left atrial rupture due to blunt thoracic trauma

cava-atrial and pulmonary vein-atrial junctions.[8] In our case, there was a self limited rupture with hematoma at the junction of the right superior pulmonary vein-left atrium due to the accidental fall which caused to deceleration trauma.

Figure 1. Computed tomography angiography image of hemopericardium and hemothorax.

Figure 2. Intraoperative scene of the left atrial rupture.

spectrum of potential injuries to the heart after blunt chest trauma is wide, including myocardial contusion, free wall or septal rupture, valvular disruptions, and injury to the great vessels.[4,5]. Chamber rupture has high mortality, and most patients cannot reach to the emergency room.[6] The National Trauma Data Bank reports that chamber rupture represents 0.041% of all trauma cases and has 89.2% mortality rate.[7] Cardiac rupture is predominantly observed in the relatively weaker right side of the heart than in the left side. In a report, the anatomic distribution of chamber injuries were: right atrium, twenty-one patients (50%); right ventricle, seven patients (17%); left atrium, ten patients (24%) and left ventricle, four patients (9%). The underlying mechanisms of blunt cardiac rupture were as follows: (i) direct precordial impact, (ii) compression of the heart between the sternum and vertebral column, (iii) rapidly increased hydrostatic venous pressure transferred from the abdomen or lower extremities to the heart, (iv) acceleration/ deceleration force, and (v) direct penetration by the sternum or rib fractures.[6] A rapidly increased hydrostatic pressure usually affects the right atrium, and deceleration force usually causes a disruption of the vena 304

The clinical situation in blunt cardiac injuries varies from simple myocardial contusion without symptoms to cardiogenic shock because of cardiac tamponade. In asymptomatic patients, elevated cardiac enzymes can be seen. In chest trauma patients presenting with no clinical signs, the diagnosis of blunt cardiac injury is often difficult and requires several diagnostic tests.[9] If there is mediastinal widening with left or right hemothorax in chest graphy, cardiac injury should be considered and further investigations as echocardiography and computed tomography have to be performed. In our case, there was no symptom suggesting cardiac injury.

In chest X-ray graphy, the right hemothorax and mediastinal widening were detected. In echocardiography, there was markedly pericardial effusion. The right hemothorax and hemopericardium were detected at CTA. The mediastinal main vessels were normal. The patient was taken to the operating room with the diagnosis of cardiac rupture.

After blunt thoracic injuries, at the present of massive hemothorax, most non-cardiac surgeons tend to do thoracotomy rather than median sternotomy, but thoracotomy only provides limited surgical exposure of the heart and ascending aorta. Leavitt et al. have found an equal incidence of the initial types of incisions in their review, with 48% median sternotomies and 45% left thoracotomies.[6] However, median sternotomy provides good exposure of the entire heart and the ascending aorta, and it is suitable for a cardiopulmonary bypass and extracorporeal life support. Yu-Yun Non et al. have prefered sternotomy upon thoracotomy as the initial approach for suspected blunt traumatic cardiac rupture in their series of patients (8/11, 72.7%). The additional two have been shifted from initial thoracotomy to sternotomy to facilitate cardiac repair[1] In our patient, median sternotomy was preferred instead of thoracotomy. We repaired the defect at the junction of the left atrium and right superior pulmonary vein under partial cardiopulmonary bypass due to hemodynamic instability.

Cardiac rupture is an infrequent, but frequently a fatal sequelae of blunt thoracic trauma. When no external wound is visible and vital signs are relatively stable, the possibility of cardiac rupture after blunt trauma is easily overlooked.

If there is any suspicion of cardiac rupture, expeditious diagnostic protocols and appropriate surgical management are essential to get a better outcome.

Conflict of interest: None declared.

REFERENCES 1. Nan YY, Lu MS, Liu KS, Huang YK, Tsai FC, Chu JJ, et al. Blunt traumatic cardiac rupture: therapeutic options and outcomes. Injury 2009;40:938â&#x20AC;&#x201C;45.

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Akar et al. Left atrial rupture due to blunt thoracic trauma 2. Schultz JM, Trunkey DD. Blunt cardiac injury. Crit Care Clin 2004;20:57–70.

3. El-Chami MF, Nicholson W, Helmy T. Blunt cardiac trauma. J Emerg Med 2008;35:127–33.

4. Fedakar R, Türkmen N, Durak D, Gündoğmuş UN. Fatal traumatic heart wounds: review of 160 autopsy cases. Isr Med Assoc J 2005;7:498–501.

5. Thors A, Guarneri R, Costantini EN, Richmond GJ. Atrial septal rupture, flail tricuspid valve, and complete heart block due to nonpenetrating chest trauma. Ann Thorac Surg 2007;83:2207–10.

6. Leavitt BJ, Meyer JA, Morton JR, Clark DE, Herbert WE, Hiebert CA. Survival following nonpenetrating traumatic rupture of cardiac chambers. Ann Thorac Surg 1987;44:532–5.

7. Teixeira PG, Inaba K, Oncel D, DuBose J, Chan L, Rhee P, et al. Blunt cardiac rupture: a 5-year NTDB analysis. J Trauma 2009;67:788–91.

8. Martin TD, Flynn TC, Rowlands BJ, Ward RE, Fischer RP. Blunt cardiac rupture. J Trauma 1984;24:287–90.

9. Sybrandy KC, Cramer MJ, Burgersdijk C. Diagnosing cardiac contusion: old wisdom and new insights. Heart 2003;89:485–9.

OLGU SUNUMU - ÖZET

Künt toraks travmasına bağlı sol atriyal yırtık Dr. İlker Akar,1 Dr. İlker İnce,1 Dr. Cemal Aslan,1 Dr. Mehmet Çeber,1 Dr. İlker Kaya2 1 2

Gaziosmanpaşa Üniversitesi Tıp Fakültesi, Kalp ve Damar Cerrahisi Anabilim Dalı, Tokat Tokat Devlet Hastanesi, Kalp ve Damar Cerrahisi Kliniği, Tokat

Künt travmatik kardiyak yaralanma nadir olmakla birlikte yüksek mortalite ile ilişkilidir. Künt toraks travması sonrası kalp yırtığının oluşmasındaki en geçerli teori; hızlı deselerasyona bağlı atriumların vena kava ve pulmoner venler ile birleşme yerlerinden oluşacak yırtılmadır. Hemotoraks ve hemoperikardiyumun birlikte olduğu olgularda yaralanma genellikle kalp ve/veya büyük damarlardan kaynaklanabileceğinden median sternotomi ile olan yaklaşım yaralanmanın tamiri için kolaylık sağlar. Bu yazıda, 33 yaşında bir erkek olguda künt toraks travması sonrası oluşan sol atriyal yırtığın mediyan sternotomi ile başarılı bir şekilde tedavisi sunuldu.

Anahtar sözcükler: Künt toraks travması; sol atriyum; yırtık.

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CA S E R EP O RT

Non-traumatic tension gastrothorax in a young lady Mahmut Tokur, M.D.,1 Ş. Mustafa Demiröz, M.D.,1 Muhammet Sayan, M.D.2 1

Department of Thoracic Surgery, Kahramanmaras Sutcu Imam University Faculty of Medicine, Kahramanmaras

2

Department of Thoracic Surgery, Aksaray State Hospital, Aksaray

ABSTRACT Tension gastrothorax is a very rare but potentially fatal clinical condition in which the stomach that herniates through a diaphragmatic defect into the thorax is massively distended by trapped air. It leads to severe symptoms due to the compression of the lung and mediastinum. A 27-year-old female, who had no prior trauma history, applied to the emergency service with the complaint of respiratory disorder, and was consulted by the department of thoracic surgery. Thorax CT revealed presence of gastrothorax in the left hemithorax.

Thus, the patient went into cardiopulmonary arrest and was resuscitated. Emergency thoracotomy was performed, abdominal organs were reduced and diaphragmatic defect was repaired. She was discharged on the fifth postoperative day without any complications.

Key words: Diaphragmatic rupture; emergency thoracotomy; tension gastrothorax.

INTRODUCTION Tension gastrothorax is a very rare and life-threatening condition which radiologically mimics tension pneumothorax.

[1] Visceral organs that herniate into the thorax through a diaphragmatic defect lead to this clinical condition. This diaphragmatic defect may be congenital or secondary to blunt or penetrating thoracic traumas, or it may also be iatrogenic.

[2] Surgery is the choice of treatment; early gastric decompression applied in the emergency setting may save life.[3]

CASE REPORT A 27-year-old female was admitted to the emergency service with the complaints of nausea, shortness of breath and abdominal pain existing for five days. Physical examination revealed hypotension, tachycardia, and loss of respiratory sounds on the left hemithorax. On chest X-ray, there was no lung parenchyma on the left side and mediastinal shift to the right side was present (Fig. 1). Thorax CT revealed toAddress for correspondence: Ş. Mustafa Demiröz, M.D. Kahramanmaraş Sütçü İmam Üniversitesi Tıp Fakültesi, Avşar Kampüsü, Göğüs Cerrahisi Anabilim Dalı, Kahramanmaraş, Turkey Tel: +90 340 – 280 33 80 E-mail: demirozsm@gmail.com Qucik Response Code

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tal gastric herniation through a left side diaphragmatic defect (Fig. 2). Thus, cardiopulmonary arrest developed on the CT table, the patient was resuscitated, and an emergency thoracotomy was performed. Herniated organs were reduced and diaphragmatic defect was primarily repaired. Postoperative chest x ray showed expanded left lung and improved mediastinal shift (Fig. 3). Postoperative course was uneventful. The patient was discharged on the fifth postoperative day.

DISCUSSION Tension gastrothorax is a clinical condition which defines the herniation of some abdominal organs, especially the stomach, into the thorax due to several disorders, mimicking tension pneumothorax by causing contralateral mediastinal shift and hemodynamic instability.[1] This entity is thought to be a late complication of unrecognized traumatic diaphragmatic hernia.

Therefore, determining the real incidence is difficult.[4] Tension gastrothorax develops through congenital diaphragmatic defects, iatrogenic defects (tube thoracostomy, esophageal interventions, diaphragmatic plication, and etc.) or traumatic diaphragmatic ruptures. In several reports, traumatic diaphragmatic defects have been notified to be seen in 3–5% and 10– 15% respectively after blunt and penetrating traumas, mostly on the left (3 times as much as the right side). However, traumatic gastrothorax is very rare.[2] In the index case, there was no history of trauma or former surgical intervention, and therefore, herniation through a congenital defect was thought in the etiology. In the diagnosis of such a rare entity, clinical suspicion is very important because there are no pathognomonic findings of diaphragmatic rupture and gastrothorax.[4] Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

Tokur et al. Non-traumatic tension gastrothorax in a young lady

Clinically, it may mimic tension pneumothorax. Findings such dyspnea, hypotension (secondary to mediastinal vascular compression), tachycardia, intestinal sounds on the left hemithorax may be seen.[1] Late cases may admit by progressive left side pain, shortness of breath, and vomiting. In addition, cardiopulmonary arrest may occur due to mediastinal compression and acute venous return failure.[4] Kao Y and colleagues have reported a patient with tension gastrothorax as a late complication of a prior blunt thoracic trauma, who had abdominal distension, epigastric pain and persistent hiccup at the time of admission.[2] In our case, symptoms on admission were shortness of breath, epigastric pain and nausea. These symptoms and our findings (hypotension, tachycardia and loss of respiratory sounds on left hemithorax) were in accordance with the literature.

Figure 3. Postoperative chest X-ray.

In another case report of gastrothorax secondary to blunt trauma by McCann and colleagues, there were gas bubbles, diaphragm contour abnormality, diaphragmatic elevation and compression atelectasis of the left lower lobe found on chest X-ray.[1] In another case report, there were only findings of tension pneumothorax on chest X-ray.[5] Rathinam and colleagues have reported fluid-gas level on the left hemithorax in a pediatric patient with tension gastrothorax.[4] In index case, only findings of tension pneumothorax were seen on chest X-ray.

Figure 1. Chest X-ray upon hospital admission, showing findings of tension pneumothorax.

The improvement in symptoms by nasogastric decompression and sighting of nasogastric catheter in the thorax on chest X-ray may bring tension gastrothorax into mind.[3] Thorax CT findings include the presence of diaphragmatic rupture or defect, herniated abdominal organs into the thorax, contralateral mediastinal shift, compression atelectasis on the left lung, and concomitant thoracic or abdominal organ injuries.[1,5] In treatment, emergency nasogastric catheter insertion may be lifesaving besides general medical preventions.[1] Some authors suggest gastric decompression by transthoracic needle aspiration to gain time for surgery and obtain clinical stability when nasogastric decompression fails.[3,5] The optimal choice of treatment for traumatic diaphragmatic hernias is surgery. Correct diagnosis and urgent surgical treatment decrease morbidity and mortality rates.[2,6] For surgical treatment, thoracotomy, laparotomy or both may be performed. Abdominal organ reduction and primary diaphragmatic repair are performed. Rapid expansion of the left lung may lead re-expansion pulmonary edema.[4,5]

Conclusion Figure 2. Thorax CT scan reveal findings of gastrothorax.

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Tension gastrothorax is a very rare clinical entity. An accurate 307

Tokur et al. Non-traumatic tension gastrothorax in a young lady

differential diagnosis with tension pneumothorax is required.

Treatment is based on general medical preventions and nasogastric decompression followed by surgical therapy. As in our case, it may occur as a late complication of congenital diaphragmatic defect without any history of prior trauma or operation.

Conflict of interest: None declared.

2. Kao Y, Lee WJ, Lin HJ. Tension gastrothorax: a life-threatening cause of acute abdominal pain. CMAJ 2009;180:983.

3. Slater RG. Tension gastrothorax complicating acute traumatic diaphragmatic rupture. J Emerg Med 1992;10:25–30.

4. Rathinam S, Margabanthu G, Jothivel G, Bavanisanker T. Tension gastrothorax causing cardiac arrest in a child. Interact Cardiovasc Thorac Surg 2002;1:99–101.

5. Salim F, Ramesh V. Tension gastrothorax: a rare complication. J Coll Physicians Surg Pak 2009;19:325–6.

REFERENCES 1. McCann B, O’Gara A. Tension viscerothorax: an important differential for tension pneumothorax. Emerg Med J 2005;22:220–1.

6. Akhtar MS, Beg MH, Kumar A. Isolated Traumatic Giant Diaphragmatic Hernia Mimicking a Haemopneumothorax: A Report of Two Cases. Chest Dis Allied Sci 2012;54:259–61.

OLGU SUNUMU - ÖZET

Genç bir kadında, non-travmatik tansiyon gastrotoraks Dr. Mahmut Tokur,1 Dr. Ş. Mustafa Demiröz,1 Dr. Muhammet Sayan2 1 2

Kahramanmaraş Sütçü İmam Üniversitesi Tıp Fakültesi, Göğüs Cerrahisi Anabilim Dalı, Kahramanmaraş Aksaray Devlet Hastanesi, Göğüs Cerrahisi Kliniği, Aksaray

Bir diyafragmatik defektten toraksa herniye olarak masif distansiyona uğrayan mide dokusunun neden olduğu tansiyon gastrotoraks oldukça nadir, ancak ölümcül olabilen bir klinik durumdur. Akciğer ve mediasten basısına bağlı ciddi semptomlara neden olur. Nefes darlığı şikayeti ile acil servise başvuran ve travma öyküsü olmayan 27 yaşında kadın hasta, ilk değerlendirme sonrası göğüs cerrahisi kliniğine konsülte edildi. Toraks bilgisayarlı tomografide sol hemitoraksda gastrotoraks tespit edildi. Hastanın arrest olması nedeniyle resüsitasyona başlandı ve acil sol torakotomi yapılarak abdominal organlar redükte edildi ve diyafragmatik defekt primer onarıldı. Hasta operasyon sonrası beşinci gün sorunsuz şekilde taburcu edildi.

Anahtar sözcükler: Diyafragma ruptürü; acil torakotomi; tansiyon gastrotoraks.

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CA S E R EP O RT

Acute retrobulbar haemorrhage: An ophthalmologic emergency for the emergency physician Can Pamukcu, M.D.,1 Mahmut Odabaşı, M.D.2 1

Department of Ophthalmology, Şehitkamil Goverment Hospital, Gaziantep

2

Department of Ophthalmology, Sişli Etfal Training and Research Hospital, Istanbul

ABSTRACT Acute retrobulbar haemorrhage (ARBH) is a rare ophthalmic emergency observed following blunt eye trauma. Multiple trauma and loss of consciousness can hide symptoms of ARBH. Rapid diagnosis and immediate lateral canthotomy and cantholysis must be performed to prevent permanent visual loss in patients. Medical treatment can be added to surgical therapy. Lateral canthotomy and cantholysis are simple procedures that can be performed by emergency physicians. In this report, it was aimed to present a case with post-traumatic ARBH and provide general knowledge about the diagnosis, follow-up and treatment of ARBH. Key words: Maxillofacial trauma; orbital compartment syndrome; retrobulbar haemorrhage.

INTRODUCTION Acute retrobulbar haemorrhage (ARBH) is a rare complication observed following blunt orbital trauma. ARBH concerns both emergency physicians and ophthalmologists. ARBH may result in loss of vision at various levels that may progress to permanent visual loss unless early treatment is provided. Loss of vision can be prevented through early diagnosis and treatment.[1] Therefore, follow-up examinations of vision should be performed in emergency patients who develop proptosis after craniofacial trauma. In addition, visual loss can develop in patients with facial trauma for various reasons. In one study, in 67% of 727 patients with facial fracture, ocular damage was observed at different levels and it was reported that 3% of these damages resulted in complete loss of vision.[2] Therefore, all patients with periorbital trauma should be evaluated in terms of potential globe damage. Dutton have reported the importance of measuring and recording the visual acuity of all patients referring to the emergency with facial trauma.[3] As immediate and right approach is essential in the treatment Address for correspondence: Can Pamukcu, M.D. Halıcıoğlı Çıksalın Çakırbeyler Sokak, No: 10/14, İstanbul, Turkey.

Tel: +90 342 – 324 67 67 E-mail: cpamukcu@gmail.com Qucik Response Code

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of ARBH, medical personnel should recognize the signs of ARBH, treat it and have a sufficient level of training in patient care for patients with facial trauma.

In this article, we aimed to present a patient who developed ARBH, and provide general review regarding ARBH.

CASE REPORT A 45-year-old male patient exposed to blunt orbital trauma referred to the emergency with complaints of pain and loss of vision in the left eye. He stated that one hour prior, his left eye was exposed to an impact by a solid object. On his first examination, visual acuity was normal in the right eye and counting fingers from a 1-meter distance in the left eye. Ocular movements were limited to every direction in the left eye.

Afferent pupillary defect was detected; the patient also had left periorbital edema, ecchymosis and proptosis. After blunt trauma, he got a non-penetrating laceration on his upper left eyelid on the region consistent with the orbital rim line. Furtherrmore, the patient stated that he had nasal congestion in the left side of his nose. In biomicroscopic examination, his right eye was normal; whereas there was corneal edema, subconjunctival hemorrhage and chemosis in the left eye. In the fundus examination, the right eye was normal; whereas the posterior segment in the left eye could not be clearly evaluated because of corneal edema. Intraocular pressure (IOP) was measured as 60 mmHg. The patient referred to our clinic following blunt orbital trauma was diagnosed with ARBH and the patient’s condition was conveyed to the radi309

Pamukcu et al. Acute retrobulbar haemorrhage: an ophthalmologic emergency for the emergency physician

ology unit. Axial and coronal orbital computerized tomography (CT) was performed immediately. Upon assessment

by CT, fracture of the left medial orbital wall, haemorrhage within the retrobulbar space, nasal fracture and suspicious fracture at the level of infraorbital canal were detected (Fig. 1). The patient was laid down with head up at an angle of 45°. Intravenous (IV) mannitol and topical dorzolamide-timolol were administered to the patient and lateral canthotomy and cantholysis were performed. The left lower eyelid was completely released with lateral canthotomy and cantholysis (LCC) (Fig. 2). Skin laceration on the left upper eyelid was left to primary healing. Soon after LCC, IOP decreased to 30 mmHg and the patient’s visual acuity improved to 4/10. The eye was not closed for follow-up examination and pressure dressing was not used. Oral prophylactic antibiotic treatment was initiated. IOP decreased to 18 mmHg after 8 hours. In visual examination, the patient’s vision was detected to be at the level of 8/10 and globe movements were normal. The patient had complaints of nasal congestion but was told not to blow his nose in order to prevent the development of orbital emphysema. In his evaluation on day 10, the patient had no visual loss. In this follow-up, lower eyelid reconstruction with lateral canthal sling was performed due to lower eyelid ectropion (Fig. 3).

Figure 2. After canthotomy and cantholysis: Frontal view in the figure above, lateral view in the figure below. The release of the lower eyelid is clearly observed in the picture below.

ARBH is not a commonly encountered condition. It may develop after orbital surgery, endoscopic sinus surgery, retrobulbar and peribulbar injection, spontaneously with facial and craniofacial traumas or trauma surgery.[4–12] As a complication

(a)

Figure 3. Patient’s appearance in the follow-up examination on day 10.

(b)

of orbital or periorbital surgery, orbital hemorrhage may develop particularly when the orbital septum is passed.[13,14]

DISCUSSION The rate of development of ARBH after retrobulbar and peribulbar injection is less than 2%.[6,7] The incidence of orbital haemorrhage development with blepharoplasty has been reported as 0.055% (1:2,000) and after zygomatic fracture repair as 0.3%.[12,14] Figure 1. (a) Retrobulbar haemorrhage is observed in coronal orbital CT; fracture in the left medial orbital wall (small arrows), suspicious fracture at the level of infraorbital canal (big arrow). (b) Fracture in the nasal bone in axial orbital CT (arrow).

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The orbital space is comprised of three compartments, namely subperiosteal space, intraconal space and extraconal space. In case haemorrhage is observed in one of these compartments, the orbital space does not comply with the Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

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increase in volume. Therefore, a forward protrusion of the globe is observed leading to clinical appearance of proptosis.

The orbital bone structure is open only at the front. However, as the eyelids are attached to the orbital rim by the canthal tendons in this segment, essentially it is also limited at the front. Even though minor volumetric increases in the orbit are compensated, rapid elevations in volume increases intraorbital pressure and the globe displaces forwardly.[15,16] As the intraorbital pressure increases, interstitial pressure also increases and perfusion pressure decreases. The globe, pushed backwards by the eyelids at the front, is simultaneously pushed forward from behind with the effect of increasing orbital pressure. IOP increases, and the perfusion of the eye deteriorates. As in our case, IOP may increase to 60 mmHg or further. Normal IOP value is 8–21 mmHg.[17] The orbit acts as a closed box; as in the other compartments of the body, there is a similar pressure-volume relationship in orbital fissures and foramina. Therefore, there is the risk of development of compartment syndrome. Compartment syndrome develops in the orbital area, and as a result of the increasing tissue pressure, perfusion pressure decreases.[18] In the elevation of orbital pressure, the posterior ciliary artery is affected more than the central retinal artery (CRA) is. The CRA can be protected due to being covered by the optical nerve. High systolic pressure is also one of the mechanisms protecting the CRA. There is no similar protection in other blood vessels inside the muscular cone or in the ones entering the eye around the optical nerve. Hence, complete visual loss has been reported due to the CRA occlusion as well as anterior ischemic optic neuropathy.[18] Venous pooling is observed due to increasing intraorbital pressure after retrobulbar haemorrhage leading to a further increase in the orbital pressure. As the pressure on the tissues increases, arterial flow will stop.[19,20] If the vasa nervorum is affected, optical nerve involvement is expected as well. When the orbital pressure exceeds the CRA pressure, retina begins to be affected. Basically, with an increase in the orbital pressure and decrease in perfusion, damage starts and pathology establishes. Further, the optical nerve may be damaged due to compression and tension.[21] Visual loss generally develops as a result of the CRA occlusion, direct compression to the optical nerve or to the blood vessels feeding the optical nerve.

[8] It should also be kept in mind that visual loss may also develop after blunt ocular trauma due to retinal detachment, hyphema, rupture of the globe and vitreous haemorrhage. Although the mechanism of visual loss is not clear, recovery of vision after decompression suggests that ischemia and reperfusion lie under the pathogenesis of this condition.[22,23] Vision is the most valuable criterion in diagnosis and follow-up. Level of vision is correlated with optical nerve and retinal perfusion. In our case, improvement in vision from the level of counting fingers from a 1–meter to the 4/10 level after lateral canthotomy and inferior cantholysis supports this argument.

When retrobulbar pressure increases to a critical level, irreversible optical nerve and retinal ischemia develop in 60 Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

minutes and resistant visual loss in 1.5 to 2 hours.[1,24–27] It was reported that healing in retinal ischemia lasting no longer than 90 minutes was good; whereas the response to ischemia exceeding 105 minutes was poor; therefore, it was emphasized that surgery should be performed in the first 90 minutes.[26] Our case had referred to our clinic in 1 hour. The patient’s diagnosis was made immediately and his condition was conveyed to radiology. Axial and coronal CT scan of the orbit was performed immediately. As the diagnosis was confirmed by the CT scan, lateral canthotomy and inferior cantholysis were performed under emergency room conditions.

The time to lateral canthotomy and inferior cantholysis was approximately 30 minutes. Total time, including this, was 90 minutes after the trauma. The level of vision was 4/10 postsurgery and 8/10 after 8 hours. In cases when imaging cannot be performed immediately, if clinical diagnosis of retrobulbar haemorrhage is made, performing lateral canthotomy and inferior cantholysis, which are simple and safe methods, without imaging would be the right approach.

When diagnosing a patient with orbital trauma, visual acuity and frontal segment examination should be performed and reactions to light should be carefully evaluated. Evaluation of the patient’s reactions to light is of major importance regarding optical nerve function. Pupil dilation and fundus examination should be reserved after light reflex examination. In case of optical nerve pathology or cranial pathology are suspected, fundus examination may be delayed. During the assessment of light reactions, when one eye is exposed to light, bilateral pupils constrict, indicating that afferent system (signal to the brain) and efferent system (signal from the brain) are not damaged. If there is afferent pupillary defect, when the damaged eye is exposed to light both pupils stay dilated. Constriction of both pupils indicates that the optical nerve in the eye exposed to trauma is not damaged.

It is sometimes difficult to make a complete evaluation in traumatic patients. The patients are generally confused, agitated or unresponsive. Proptosis is the first marked finding in cases when visual acuity assessment cannot be performed.

The main clinical features of ARBH are decrease in visual acuity, pain, proptosis and ophthalmoplegia. In unresponsive and agitated patients, it may not be easy to assess pain and ophthalmoplegia. In unresponsive and unconscious patients, globe movements can be evaluated by forced duction test.

The evidence of elevated orbital pressure is tight lids, resistance to retropulsion and tight orbit. The course of intraocular pressure in ARBH is high.[17] Chemosis and subconjunctival haemorrhage may occur in orbital haemorrhage. Periorbital crepitus may be present in orbital emphysema.[28,29] In case of fundus examination can be performed, optical disc edema, retinal venous congestion, CRA pulsation or occlusion and retinal edema may be observed.[30] Even though orbital tissue pressure can be measured directly by manometer, clinically, it is not used very commonly. Nor311

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mal orbital pressure is 3–6 mmHg.[15,16] In a patient exposed to periorbital trauma, the intraocular pressure bears an alerting character. Elevated IOP is the most substantial finding that will indicate compartment syndrome if the patient is unconscious or non-cooperating. The normal value of IOP ranges between 8–21 mmHg.[17] In a patient with increased IOP, complaints such as pain in the eye, decrease in vision and changes in perceptions of colour are observed. If IOP is ≥40 mmHg in the proptotic eye, this is an important indication concerning ischemia and requires immediate treatment. As our patient’s eyes could be partially opened and his cooperation was good, intraocular pressure could be measured. In patients with facial trauma, measuring intraocular pressure may not always be possible, so increase in intraocular pressure can be examined by palpation of the globe. It may sometimes be difficult to decide whether the globe is solid or not under emergency conditions. Palpation is a subjective method and may prove dangerous in cases with suspected perforation.

Whatever the IOP is, visual loss and relative afferent pupil defects indicate the need for immediate treatment.

ARBH diagnosis can easily be made in the presence of proptosis, abnormally reactive pupils and swelling in the disc.

Proptosis is the most prominent sign in a traumatic patient.

It sometimes develops due to a secondary edema in the retrobulbar tissues and compartment syndrome may be a part of the phenomenon. In some cases, it is difficult to make a diagnosis of proptosis because edema in the periorbital region may conceal proptosis. An objective diagnosis of proptosis can be made by an exophthalmometer.

Within 1–3 hours following ARBH, the probability of irreversible exposition to damage in retina increases,[1,6,7,24–27,29] As ARBH may be observed after an orbital surgery; orbital pain, visual acuity, proptosis, direct light reaction and pupil size should be evaluated and recorded in the postoperative follow-up. If pathology is detected, immediate action should be taken for diagnosis and treatment. Caution should be taken regarding retrobulbar haemorrhage in a patient with tense and proptotic eye with complete visual loss and nonreactive pupillary response after facial trauma. In one study, it was emphasized that the most common reason of visual loss after facial fracture repair was the increase in the orbital pressure developing after the haemorrhage.[10] This condition also requires immediate surgery. Performing immediate surgical decompression shall prevent visual loss.

Orbital examination of patients referring for head and face trauma should not be ignored. Rupture in globe, optical nerve damage, intraorbital haemorrhage, foreign objects, periorbital and orbital apex fractures can easily be differentiated.

Imaging methods are useful in showing the severity, cause, location and pathology of the condition. The connection between the presence of orbital fracture and hematoma should be assessed by CT scan. Diagnosis can also be confirmed by ultrasonography (USG).[31,32] Magnetic resonance imaging is 312

often performed later. In the USG scan, retrobulbar hematoma can be observed in front of the orbital bone and behind the globe as a hypoechoic lesion. Tension in the optical nerve after proptosis can be viewed by CT scan. Further, in the CT scan, distortion in the posterior segment of the globe can be observed to some extent due to retrobulbar hemorrhage.[31] Patients referring to the emergency with orbital trauma should be told that due to sino-orbital connections, exhaling from their noses forcibly will carry the risk of orbital haemorrhage and emphysema due to valsalva and cough.[28] The patient with orbital trauma should be laid down with an angle of 45°. In these patients, eye dressings and pressure dressing should not be used; pressure dressing can increase intraorbital pressure, and also covering can delay early diagnosis.[32] Our patient’s eye was not covered. Our patient with medial orbital wall fracture on the left had nasal congestion as well.

Therefore, the patient was told not to blow his nose to prevent the development of orbital emphysema.

Medical treatment has a role before and/or after the surgical treatment of ARBH. Medical treatment has a supplementary contribution to surgical decompression. Osmotic agents, carbonic anhydrase inhibitors, high-dose steroids and β-blockers are used in medical treatment.[1,32] Using osmotic agents such as mannitol increases the osmolarity of blood and creates osmotic gradient thereby providing a reduction in IOP. Further, using carbonic anhydrase inhibitors such as acetazolamide, helps decrease IOP by reducing aqueous humor production.

Osmotic agents decrease IOP by reducing the water content of the vitreous. Mannitol is a rapid acting agent; however, mannitol and acetazolamide should not be used in hypovolemic shock. Anti-inflammatory and anti-oxidant activities of corticosteroids are utilized. It has been shown that high dose corticosteroids have a protective effect on traumatic optic neuropathy.[32] Steroids stabilize the cell membrane against ischemic damage by reducing inflammation.[33] Timolol maleate also reduces the production of aqueous humor.[32] Hence, it has a role in medical treatment. In the medical treatment of ARBH, i.v. 20% mannitol 2 g/kg q.i.d., i.v. acetazolamide 250 mg q.i.d., i.v. methylprednisolone 250 mg q.i.d. and topical timolol maleate one drop b.i.d. are recommended.[1,32] Certain amount of time should pass in order for the medical treatment to reduce orbital pressure. Further, we think that medical treatment has a limited effect on reducing the orbital pressure. Therefore, we think that it may only be used as an adjuvant therapy. There are publications contrary to this opinion. A case with complete recovery of vision has been reported without the need of surgery after the medical treatment.[34] There is also a publication recommending surgical intervention in case the vision is not recovered in 30–45 minutes.[11] However, we think that as a certain amount of time will pass from the moment of the incident to the patient’s arrival to the emergency room and also time is required for the medical treatment to show effect and additionally since we think that medical treatment has a limited effect in reducing Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4

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the orbital pressure, we recommend that medical treatment and LCC should be performed concurrently. LCC will reduce the pressure exerted on the orbit by the eyelids which limit the orbit in the front. Firstly, a sudden intraorbital pressure reduction will occur in consequence of the removal of the limiting effect of the eyelid on the orbit. Then, a slow orbital pressure reduction will occur as a result of the reduction in pressure in the foramina and veins, decrease in venous congestion and resolution of edema. Intraocular pressure measured 60 mmHg in our patient, decreased to 30 mmHg postoperatively and to 18 mmHg in 8 hours. There are also authors adopting surgery as the first choice resembling our approach. Goodhall et al.[4] reported that when they performed LCC alone, it was effective in improving visual acuity and preventing permanent visual loss and that they had performed surgery concurrent with intravenous acetazolamide in two cases.

ered for a few days, and soon after the swellings are resolved, it can be repaired or be left to heal spontaneously. If IOP is still elevated after the LCC, hematoma should be discharged with decompression surgery. Should lateral canthotomy and inferior cantholysis fail, the upper leg of the lateral canthal tendon can be released. With medial, lateral and basal surgery, a space can be formed where the volume can expand in the orbital area. Burkat has described inferolateral anterior orbitotomy for the discharge of hematoma or compressed air.[6]

LCC as surgical treatment is a well-documented approach in the treatment of ARBH.[8] Lateral canthotomy and inferior cantholysis were recommended in many studies.[4,8,32] Canthotomy and inferior cantholysis can easily be performed under the conditions of a simple outpatient clinic or emergency room under local anesthesia.[4,8] It is favourable that decompression surgery is performed by an ophthalmologist.

However, under emergency conditions if an ophthalmologist cannot be reached, LCC should be performed immediately by a trained medical doctor.[35,36] Suner et al.[36] have defined a training model of lateral canthotomy and cantholysis for emergency physicians. Lateral canthotomy is the procedure of separating lateral canthal tendon in two by cutting it up to the orbital rim. Afterwards, inferior cantholysis is performed by releasing the lower leg of the canthal tendon. Following inferior cantholysis, the lower leg of the lateral chantal tendon is entirely separated, consequently the lower eyelid is completely mobile (Fig. 2). Even though chantotomy can be performed alone or with cantholysis, some authors recommend performing cantholysis with lateral chantotomy.[4,8] Inferior chantolysis is more effective than chantotomy in decreasing the IOP.[37] However, concurrent lateral canthotomy and cantholysis reduce orbital pressure more effectively. In a study where orbital pressure was increased by administering saline solution to a sheep’s eye, concurrent canthotomy and cantholysis (30.4 mmHg) provided more reduction in the intraocular pressure compared to canthotomy (14.2 mmHg) and cantholysis (19.2 mmHg) alone.[37] In our experience, lateral canthotomy and cantholysis technique, when combined with intravenous corticosteroids mannitol and acetazolamide, is a much more successful method. In another case who had retrobulbar haemorrhage symptoms after retrobulbar anesthesia, after decompression with lateral canthotomy and inferior cantholysis IOP decreased from 50 mmHg to 30 mmHg.[38] The efficacy of the technique is also observed in our case.

As a conclusion, ARBH may cause permanent visual defect.

LCC should be performed immediately in patients diagnosed with ARBH in the presence of elevated intraocular pressure, proptosis and decrease in visual acuity. Further, we think that starting medical treatment shall provide a supplemental contribution to reducing orbital pressure.

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The potential complications of LCC are ectropion, lacrimal gland damage and post-operative infection. Lateral canthal incision then can be sutured or more often left open to heal with granulation.[4,18] In our case, eyelid repair with lateral canthal sling was performed due to ectropion in the lower eyelid.

Conflict of interest: None declared.

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3. Dutton GN, al-Qurainy I, Stassen LF, Titterington DM, Moos KF, elAttar A. Ophthalmic consequences of mid-facial trauma. Eye (Lond) 1992;6:86–9.

4. Goodall KL, Brahma A, Bates A, Leatherbarrow B. Lateral canthotomy and inferior cantholysis: an effective method of urgent orbital decompression for sight threatening acute retrobulbar haemorrhage. Injury 1999;30:485–90.

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8. Vassallo S, Hartstein M, Howard D, Stetz J. Traumatic retrobulbar hemorrhage: emergent decompression by lateral canthotomy and cantholysis.

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9. Kulkarni AR, Aggarwal SP, Kulkarni RR, Deshpande MD, Walimbe PB, Labhsetwar AS. Ocular manifestations of head injury: a clinical study.

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10. Girotto JA, Gamble WB, Robertson B, Redett R, Muehlberger T, Mayer M, et al. Blindness after reduction of facial fractures. Plast Reconstr Surg 1998;102:1821–34.

11. Ord RA. Post-operative retrobulbar haemorrhage and blindness complicating trauma surgery. Br J Oral Surg 1981;19:202–7.

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OLGU SUNUMU - ÖZET

Acil hekimlerinin oftalmik acili: Akut retrobulber hemoraji Dr. Can Pamukcu,1 Dr. Mahmut Odabaşı2 1 2

Şehitkamil Devlet Hastanesi, Göz Kliniği, Gaziantep Şişli Etfal Eğitim ve Araştırma Hastanesi, Göz Kliniği, İstanbul

Akut retrobulber hemoraji (ARBH) künt göz travması sonrası görülen nadir bir oftalmik acildir. Hastanın çoklu travmatik hasarı ve bilinç kaybı varsa semptomlar gizlenebilir. Hastada kalıcı görme kaybını önlemek için hızlı tanı konup zaman kaybetmeden lateral kantotomi, kantoliz yapılmalıdır.

Medikal tedavi cerrahi tedaviye ek olarak başlanabilir. Lateral kantotomi ve kantoliz acil hekimleri tarafından uygulanabilecek kolay bir prosedürdür.

Bu makalede travma sonrası retrobulber hemoraji gelişen bir olgumuzu sunarken, retrobulber hemorajinin tanısı, tedavisi ve takibi hakkında genel bilgi verilmiştir.

Anahtar sözcükler: Maksillofasiyal travma; orbital kompartman sendromu; retrobulber hemoraji.

Ulus Travma Acil Cerrahi Derg 2015;21(4):309–314

314

doi: 10.5505/tjtes.2015.16768

Ulus Travma Acil Cerrahi Derg, July 2015, Vol. 21, No. 4