Marmara Medical Journal Marmara Üniversitesi Tıp Fakültesi Dergisi



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2010, Cilt 23, Sayı 2 Marmara Medical Journal Marmara Üniversitesi Tıp Fakültesi Dergisi ISSN: 1309-9469

Marmara Medical Journal Marmara Üniversitesi Tıp Fakültesi Dergisi Sahibi Marmara Üniversitesi Tıp Fakültesi adına Dekan Prof. Dr. Hasan Fevzi Batırel Editör Doç. Dr. Dilek Gogas Yavuz Editör Yardımcıları Doç. Dr. Asım Cingi Dr. Evrim Karadağ Saygı İstatistik Editörü Doç. Dr. Nural Bekiroğlu Seza Arbay, MA Koordinatörler Dr. Vera Bulgurlu Editörler Kurulu Ahmet Toprak New Orleans USA Ali Emin Denktaş, Houston USA Alex Würtz İstanbul Türkiye Ayşegül Atmaca Samsun Türkiye Arzu Denizbaşı, İstanbul, Tükiye Azra Bihorach, Florida, USA Berrak Yeğen, İstanbul, Türkiye Beste Atasoy İstanbul Türkiye Deniz Konya, İstanbul, Türkiye Fatih Durmuşoğlu İstanbul Türkiye Fahrettin Keleştimur Kayseri,Türkiye Gül Başaran, İstanbul, Türkiye Handan Kaya, İstanbul, Türkiye Hande Harmancı,Zürih İsviçre Haner Direskeneli, İstanbul, Türkiye Hülya Bilgen İstanbul Türkiye Işıl Barlan İstanbul Türkiye İpek Akman, İstanbul, Türkiye Levent Türkeri İstanbul Türkiye Mithat Erenus, İstanbul, Türkiye Murat Sungur Kayseri Türkiye Önder Ergönül, İstanbul, Türkiye Rainer W. Guillery, Londra, İngiltere Roger Lawrence Londra İngiltere Safiye Çavdar,,İstanbul Türkiye Serdar Turhal, İstanbul, Türkiye Sibel Kalaça, İstanbul, Türkiye Şule Çetinel, İstanbul, Türkiye Tufan Tarcan, İstanbul, Türkiye Volkan Topçuoğlu İstanbul Türkiye Yalçın İlker, İstanbul, Türkiye Zeynep Eti İstanbul, Türkiye

Marmara Medical Journal Marmara Üniversitesi Tıp Fakültesi Dergisi YAZARLARA BİLGİ Marmara Medical Journal Marmara Üniversitesi Tıp Fakültesi Dergisine ilginize teşekkür ederiz. Derginin elektronik ortamdaki yayınına erişim www.marmaramedicaljournal.org adresinden serbesttir. Marmara Medical Journal tıbbın klinik ve deneysel alanlarında özgün araştırmalar, olgu sunumları, derlemeler, davet edilmiş derlemeler, mektuplar, ilginç, fotoğraflı soru-cevap yazıları (photo-quiz), editöre mektup, toplantı, haber ve duyuruları, klinik haberleri ve ilginç araştırmaların özetlerini yayınlamaktadır. Yılda 3 sayı olarak Ocak, Mayıs ve Ekim aylarında yayınlanan Marmara Medical Journal hakemli ve multidisipliner bir dergidir. Gönderilen yazılar Türkçe veya İngilizce olabilir. Değerlendirme süreci Dergiye gönderilen yazılar, ilk olarak dergi standartları açısından incelenir. Derginin istediği forma uymayan yazılar, daha ileri bir incelemeye gerek görülmeksizin yazarlarına iade edilir. Zaman ve emek kaybına yol açılmaması için, yazarlar dergi kurallarını dikkatli incelemeleri önerilir. Dergi kurallarına uygunluğuna karar verilen yazılar Editörler Kurulu tarafından incelenir ve en az biri başka kurumdan olmak üzere iki ya da daha fazla hakeme gönderilir. Editör, Kurulu yazıyı reddetme ya da yazara(lara) ek değişiklikler için gönderme veya yazarları bilgilendirerek kısaltma yapmak hakkına sahiptir. Yazarlardan istenen değişiklik ve düzeltmeler yapılana kadar, yazılar yayın programına alınmamaktadır. Marmara Medical Journal gönderilen yazıları sadece online olarak http://marmaramedicaljournal.org/submit. adresinden kabul etmektedir. Yazıların bilimsel sorumluluğu yazarlara aittir. Marmara Medical Journal yazıların bilimsel sorumluluğunu kabul etmez. Makale değerlendirmek için gönderildiği sırada Yayın Hakkı Devir Formu ve çıkar çatışması formu imzalanıp dergiye iletilmelidir. Gönderilen yazıların dergide yayınlanabilmesi için daha önce başka bir bilimsel yayın organında yayınlanmamış olması gerekir. Daha önce sözlü ya da poster olarak sunulmuş çalışmalar, yazının başlık sayfasında tarihi ve yeri ile birlikte belirtilmelidir. Yayınlanması için başvuruda bulunulan makalelerin, adı geçen tüm yazarlar tarafından onaylanmış olması ve çalışmanın başka bir yerde yayınlanmamış olması ya da yayınlanmak üzere değerlendirmede olmaması gerekmektedir. Çalışma ile ilgili herhangi bir mali ya da diğer çıkar çatışması var ise çıkar çatışması formunda belirtilmelidir. Yazıların hazırlanması Derginin yayın dili İngilizce veya Türkçe dir. Türkçe yazılarda Türk Dil Kurumu Türkçe Sözlüğü (http://tdk.org.tr) esas alınmalıdır. Anatomik terimlerin ve diğer tıp terimlerinin adları Latince olmalıdır. Gönderilen yazılar, yazım kuralları açısından Uluslararası Tıp Editörleri Komitesi tarafından hazırlanan Biomedikal Dergilere Gönderilen Makalelerde Bulunması Gereken Standartlar a ( Uniform Requirements For Manuscripts Submittted to Biomedical Journals ) uygun olarak hazırlanmalıdır. (http://www. ulakbim.gov.tr /cabim/vt) Makale içinde kullanılan kısaltmalar Uluslararası kabul edilen şeklide olmalıdır (http..//www.journals.tubitak.gov.tr/kitap/ma knasyaz/) kaynağına başvurulabilir. Birimler, Ağırlıklar ve Ölçüler 11. Genel Konferansı'nda kabul edildiği şekilde Uluslararası Sistem (SI) ile uyumlu olmalıdır. Makaleler Word, WordPerfect, EPS, LaTeX, text, Postscript veya RTF formatında, şekil ve fotoğraflar ise ayrı dosyalar halinde TIFF, GIF, JPG, BMP, Postscript, veya EPS formatında kabul edilmektedir. Yazı kategorileri Yazının gönderildiği metin dosyasının içinde sırasıyla, Türkçe başlık, özet, anahtar sözcükler, İngilizce başlık, özet, İngilizce anahtar sözcükler, makalenin metini, kaynaklar, her sayfaya bir tablo olmak üzere www.marmaramedicaljournal.org

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İÇİNDEKİLER Orjinal Araştırma IN-HOSPITAL MORTALITY IN PATIENTS WITH IMPAIRED FASTING GLUCOSE AND ACUTE CORONARY SYNDROMES Mehmet Uçucu, Fatma Alibaz Öner, Selen Yurdakul, Mecdi Ergüney...257 CARPAL TUNNEL SYNDROME: WHAT IS THE DIAGNOSTIC VALUE OF USG WITH HIGH RESOLUTION TRANSDUCERS? Özgür Sarıca, Arda Kayhan, Enis Öztürk, Sibel Bayramoğlu, Nurten Turan Güner, Fatma Öztora.263 MORPHOLOGICAL STUDY OF THE MENISCI OF THE KNEE JOINT IN ADULT CADAVERS OF THE SOUTH INDIAN POPULATION B.V. Murlimanju, Narga Nair, Shakuntala Pai, Mangala Pai, Chethan P, Chandni Gupta.270 ÜNİVERSİTE ÖĞRENCİLERİNİN İLAÇ/TIBBİ ÜRÜN KULLANIMINA YÖNELİK TUTUMLARININ DEĞERLENDİRMESİ Dilek Demircan, Berk Çanga, Melek Gün, Çağrı Ünal, İdris Önem, Ahmet Akıcı.276 ACİL SERVİSE BAŞVURAN HASTALARDA İNTRAVENÖZ OPİOİD UYGULAMASININ AKUT KARIN VE PERİTONEAL İRRİTASYON ÜZERİNDEKİ ETKİLERİ Payman Moharramzadeh, Samad Shams Vahdati.285 Olgu Sunumu POSSIBLE SERUM MARKERS FOR RENAL TRANSITIONAL CELL CARCINOMA: REPORT OF A CASE WITH THE REVIEW OF LITERATURE Hüsnü Tokgöz, Özlem Türksoy, Bülent Erol.290 INTRANEURAL PERINEURIOMA OF THE BRACHIAL PLEXUS Murat Sari, Aydın Sav, Zahide Mine Yazıcı, Ali Cemal Yumuşakhuylu, Mehmet Ali Sehitoğlu..293 ABDOMİNAL DESMOİD TÜMÖR:OLGU SUNUMU Gökhan Demiral, Ahmet Yılmaz, Fikret Aksoy, Özgür Ekinci, Burhan Şaban, Mustafa Kuşak, Canan Erengül..297 A RARE CAUSE OF MALE PSEUDOHERMAPHRODITISM: 46, XY GONADAL DYSGENESIS (SWYER SYNDROME) Ayhan Abacı, Tolga Unuvar, Özlem Giray, Ayfer Ulgenalp, Ece Bober, Derya Erçal, Atilla Buyukgebiz 302 Derleme ERKEK CİNSEL İŞLEV BOZUKLUKLARINDA AİLE HEKİMLİĞİ YAKLAŞIMI Çiğdem GEREKLİOĞLU, İbrahim BAŞHAN, Ersin AKPINAR.308 ANDROGEN RECEPTOR GENE AND ITS CLINICAL IMPORTANCE IN GYNECOLOGY, ONCOLOGY AND INFERTILITY Esma Sarıkaya, Tayfun Güngör, Gülnur Özakşit, Leyla Mollamahmutoğlu.316 Photo Quiz A 45-YEAR-OLD MALE WITH UPPER GASTROINTESTINAL BLEEDING AFTER ALCOHOL ABUSE Vitorino M Santos, Maria S Barcelos, Érika R N C Oliveira, Bruno CS Paz, Ana C A Almeida...323

ORIGINAL RESEARCH IN-HOSPITAL MORTALITY IN PATIENTS WITH IMPAIRED FASTING GLUCOSE AND ACUTE CORONARY SYNDROMES Mehmet Uçucu 1, Fatma Alibaz Öner 1, Selen Yurdakul 2, Mecdi Ergüney 1 1 Istanbul Education and Research Hospital, 2.Clinic of Internal Medicine, Istanbul, Turkey 2 Istanbul Education and Research Hospital, Cardiology, Istanbul, Turkey ABSTRACT Objectives: Diabetes mellitus is considered to be equivalent to coronary artery disease(chd). Both impaired fasting glucose(ifg) and impaired glucose tolerance (IGT) are risk factors for cardiovascular disease. We aimed to compare the mortality during hospitalization between IFG and diabetes in patients with acute coronary syndrome (ACS). Methods: The patients under 65 years of age, who had been diagnosed as ACS; were evaluated for mortality during the first 7 days. The patients were divided into three groups as the first group diabetic, the second group non-diabetic patients, the patients with IFG. Results: A total of 375 patients were enrolled. The mortality rate was found to be 6.7% in patients with diabetes, 2.6% in patients without diabetes, 7.0% in patients with an IFG. The mortality rate of the patients with IFG and the patients with diabetes were approximately the same and this rate was significantly higher than in those with normal blood glucose during the acute phase of ACS. Conclusion: The IFG affects mortality as much as diabetes. Fasting plasma glucose is beneficial, in determining the cardiovascular risks and in the modification of the therapy to reduce the risk of CHD. Keywords: Acute coronary syndrome, Impaired fasting glucose, Diabetes, Mortality BOZULMUŞ AÇLIK GLUKOZU OLAN AKUT KORONER SENDROMLU HASTALARDA HASTANE İÇİ MORTALİTE ÖZET Giriş: Diyabet artık koroner arter hastalığının eşdeğeri sayılmaktadır.ayrıca hem bozulmuş açlık glukozu(ifg) hemde bozulmuş karbonhidrat toleransı (IGT) kardiyovasküler hastalık için birer risk faktörüdür.bu çalışmada akut koroner sendrom (AKS) tanısı alan; diyabetli ve IFG li hastalar arasında hastane içi mortalitenin karşılaştırılması amaçlanmıştır. Yöntem: Çalışmaya akut AKS tanısı alan 65 yaş altı hastalar alındı,ilk 7 gündeki mortaliteleri değerlendirildi.hastalar açlık kan şekerine göre diyabeti olan, diyabeti olmayan ve bozulmuş açlık glukozu olanlar olmak üzere üç gruba ayrıldı. Bulgular: Toplam 375 hasta çalışmaya dahil edildi. Tüm hastalarda hospitalizasyon dönemindeki mortalite; diyabeti olan hastalarda % 6.7, diyabeti olmayanlarda % 2.6, bozulmuş açlık glukozu olanlarda %7.0 olarak bulundu.aks sonrası erken dönemde mortalite IFG ve diyabetli hastalarda yaklaşık aynı oranda tespit edildi. Bu oran normal kan şekeri olanlardan anlamlı derecede yüksek tespit edildi. Sonuç: Dolayısıyla IFG; diyabet gibi koroner kalp hastalığı için risk faktörüdür ve mortalite üzerinde onun kadar etkilidir.sonuç olarak,açlık plazma glukozu,kardiyovasküler hastalık riskinin belirlenmesinde ve koroner arter hastalık riskini azaltıcı yaklaşımların belirlenmesinde son derece faydalıdır. Anahtar Kelimeler: Akut koroner sendrom, Bozulmuş açlık glikozu, Diyabet, Mortalite İletişim Bilgileri: Fatma Alibaz Öner, M.D. Istanbul Education and Research Hospital, 2.Clinic of Internal Medicine, Istanbul, Turkey e-mail: falibaz@yahoo.com Marmara Medical Journal 2010;23(2);257-262 257

Marmara Medical Journal 2010;23(2);257-262 Mehmet Uçucu, et al. In-hospital mortality in patients with impaired fasting glucose and acute coronary syndromes INTRODUCTION Diabetes mellitus is an important cardiovascular risk factor. The rate of death due to cardiovascular disease in diabetic patients is 2 4 times higher than in nondiabetic population. In diabetics, 70-80% of deaths occur because of cardiovascular diseases. Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) are conditions where the plasma glucose level is lower than the required level for diabetes mellitus(dm) diagnosis but higher than normal. The etiology of type 2 DM and IGT is abdominal obesity, insulin resistance and impaired insulin secretion, but the etiology of IFG has not yet been determined. IGT and IFG are believed to be two different disorders affecting two different populations, and these disorders are risk factors for diabetes and cardiovascular disease development 1. In this study, we aimed to investigate the mortality during the hospitalization period (the first 7 days) by dividing patients admitted to coronary intensive care unit due to acute coronary syndrome (ACS) into three groups as the patients with diabetes, patients without diabetes, and patients with IFG. MATERIAL AND METHOD Three hundred seventy five patients admitted with acute coronary syndrome (ACS) diagnosis to the coronary intensive care unit between January 2006 January 2007 were included in the study. As diabetes prevalence is higher in the population aged 65 and older, the patients in this age group were not included in the study. The blood samples of the patients were taken the first morning following admission. The blood samples were analyzed using standard biochemistry tubes in the biochemistry laboratory of our hospital. The age, gender, diagnosis, anamnesis, medical history, fasting blood glucose level and course of the MI in the acute phase (in the first 7 days) of each patient were recorded. The blood sugar levels of the patients were grouped into three groups according to the results : Normal group; patients with no previous diagnosis of diabetes and with a fasting glucose level of <100 mg/dl; IFG group; patients with a fasting glucose level of 100 125 mg/dl; and DM group; patients with a fasting glucose level of >125 mg/dl. The patients in these three groups were monitored during their hospitalization periods (7 days on average) and mortality was investigated. The SPSS for the Windows 10.0 statistical package program was used in the evaluation of the data. The quantitative data of the groups were compared using ANOVA and Tukey s HSD and the qualitative data were compared using chi-square tests. P<0.05 was considered significant. Our study was approved by local ethic commite of our hospital. RESULTS A total of 375 patients, 66 women (17.6%) and 309 men (72.4%) under the age of 65, who were hospitalized for ACS diagnosis in the coronary intensive care unit were included in the study. 18.4% of the patients were under 45 years of age (69), 59.73% of the patients were between 45-60 years of age (224) and 21.86% of the patients were between 60-65 years of age (82). Of these patients, 72 (19.2%) had a previous diagnosis of diabetes, 17 (4.53%) were newly diagnosed with diabetes and in 56 (14.93%) patients impaired fasting glucose and in 230 patients (61.33%) normal blood glucose was detected(table I). Sixteen patients died during the hospitalization period. The number of men (309) was significantly higher than the number of women (66). Although 72.4% of the patients were male, diabetes was more common in women with acute myocardial infarction (p < 0.028). While the prevalence of diabetes for all patients was 19.2% during the first admission, it was 23.73% after the study. Among the patients with ACS, 83.8% had myocardial infarction (MI) with ST elevation, 6.1% had MI without ST elevation and 10% had unstable angina pectoris(usap). With respect to the ACS classification no statistically significant difference in mortality 258

Marmara Medical Journal 2010;23(2);257-262 Mehmet Uçucu, et al. In-hospital mortality in patients with impaired fasting glucose and acute coronary syndromes was seen during the hospitalization period (p = 0.532). It was found that the mortality in all patients during the hospitalization period was 6.7% in patients with diabetes, 2.6% in patients without diabetes and 7.0% in patients with impaired fasting glucose(table II). In conclusion, mortality in the diabetic patients during the acute phase (first 7 days) of acute coronary syndrome was significantly increased compared to the patients without diabetes. However, no statistically significant differences were found between the patients with impaired fasting glucose and the diabetic patients with respect to the mortality in the acute phase of MI. ( p = 0.192 ) Table I: The clinical and demographic characteristics of patients Non DM IFG DM Age 52,3±8.3 54.98±7.43 52.9 ±8.64 FPG 88.67 ±21.5 117.82 ±5.75 219.21±75.07 Total cholesterol(mg/dl) 195,1±44,97 195±43,8 197±40,3 Triglycerides(mg/dl) 167,29±102,16 165±100,5 250±42,5* Low densitiy cholesterol(mg/dl) 113,43±38,56 100,55±18,93 165±28,93* High densitiy cholesterol(mg/dl) 40,11±10,69 38,05±10,09 42±18,9 Smoking (%) 34 35 31 Body mass index (kg/m²) 27,61± 5,47 26,09±3,09 32,03±3,2* SAB(mm/hg) 115,7±7,39 113±8,13 139± 6,35* DAB(mm/hg) 69,3±5,79 71,55±8,31 88±5,9* *The parameters are significantly higher in diabetic group (p<0,05). (SAB:sistolic arterial pressure, DAB:diastolic arterial pressure) Table II: Mortality rate of patients Non DM IFG DM n % n % n % Patients who survived 224 97.4 52 93 83 93.3 Patients who died 6 2.6 4 7 6 6.7 2=3,91 p=0,192 259

Marmara Medical Journal 2010;23(2);257-262 Mehmet Uçucu, et al. In-hospital mortality in patients with impaired fasting glucose and acute coronary syndromes DISCUSSION It is reported that dyslipidemia, hypertension, obesity, and cerebrovascular and coronary artery diseases are commonly seen in diabetic patients. In diabetics, coronary artery atherosclerosis is aggressive and has an earlyonset 2. It is thought that in the pathogenesis of diabetes, long before overt hyperglycemia occurs and diabetes is diagnosed, there is a long period of insulin resistance, when the blood glucose is maintained at normal levels by compensatory hyperinsulinemia. Events associated with atherosclerosis start to develop long before the stages when this can be detected as IFG and IGT 3. It was demonstrated that cardiovascular risk increases also in this prediabetic period 4,5. Detecting patients in this stage and protecting them against the harmful effects of insulin resistance helps to prevent coronary heart disease. Also in our study, the early stage mortality rates of the acute MI patients with diabetes (6.7%) and with IFG (7.0%) were almost the same and significantly higher compared to patients without diabetes (2.6%). This shows that the atherosclerotic process starts well before the impaired fasting glucose stage, which is the earliest stage of DM. The risk of cardiac mortality in type 2 diabetes patients is at a similar level with the risk in patients who have had myocardial infarction 6. The fact that complications develop in the prediabetic period in an important proportion of the patients has increased the interest in impaired fasting glucose, impaired glucose tolerance and postprandial hyperglycemia 7. The high cardiovascular disease risk in these patients is the result of atherosclerosis development 8. The cause of the accelerated atherosclerosis development observed in diabetes is multifactorial; hyperglycemia, dyslipidemia and high oxidative stress were demonstrated to play important roles in the etiology. 9,10 The fact that impairments are observed in the endothelial functions in individuals with cardiovascular risk factors before overt cardiovascular disease development shows that the endothelial dysfunction is the main factor in atherosclerosis development 11. In the hyperinsulinemia period before type 2 diabetes occurs, endothelial dysfunction and proliferation in the vascular smooth muscle occurs with the effect of increasing levels of insulin and insulin-like growth factors in the blood. Endothelial dysfunction is an important factor in thrombosis formation and contributes to increased coronary artery disease risk in individuals with impaired fasting glucose and impaired glucose tolerance. Although hyperinsulinemia was shown to cause endothelial dysfunction in healthy persons, it was found that the insulin treatment given to diabetic patients corrects endothelial dysfunction. In UKPDS study, it was reported that no significant change was observed in the macrovascular disease incidence, while a decrease was observed in the incidence of microvascular disease with the aggressive insulin treatment given to diabetic patients. The study which provided the most comprehensive information about the diabetes macrovascular disease relationship, is the DECODE study 12. In this study, which aimed to determine the diabetes prevalence as well as to demonstrate all-cause mortality and cardiovascular prognosis, it was found that there was a linear relationship between postprandial glucose level and coronary heart disease, and cardiovascular mortality. It was found that mortality increased if the postprandial glucose level exceeded 200 mg/dl 13. In some studies in the literature, fasting blood glucose level alone is inadequate in indicating the mortality risk associated with hyperglycemia and it was stated that oral glucose tolerance test(ogtt) would provide additional prognostic information indicating impaired glucose tolerance 14. In a FUNAGATA study, it was suggested that impaired glucose tolerance presents a cardiovascular risk while impaired fasting glucose does not cause any risk 15. In the study they conducted, Nurkalem Z. and Sargın M. investigated acute coronary syndrome cases. As a result of this study, they found a correlation between the number of 260

Marmara Medical Journal 2010;23(2);257-262 Mehmet Uçucu, et al. In-hospital mortality in patients with impaired fasting glucose and acute coronary syndromes affected coronary arteries and both IGT and diabetes frequency. They also detected a positive correlation between the number of involved coronary arteries and the postprandial glucose level 16. The studies published in other countries also show that the prevalence of previously undiagnosed diabetes is increasing. This demonstrated that impaired glucose tolerance and undiagnosed diabetes is an important public health problem 17. Considering the fact that IGT and IFG present similar cardiovascular risks and IGT is detected in nearly 50% of patients with IFG, similar results are expected in patient groups with IFG. As previously discussed, how IFG and IGT causes coronary artery disease has not been clarified yet. In many patients, IGT is accompanied by risk factors such as hypertension, obesity and dyslipidemia. In a study conducted in Japan, it was demonstrated that in 225 cases on whom coronary angiography was performed, the proportion of diabetic patients and IGT patients who developed coronary artery disease was higher compared to non-diabetic patients and it was claimed that in the IGT group, hypertension and hypertrigliceridemia played an important role in the atherosclerosis development 18. Moreover, hyperglycemia may also represent an individual risk factor. Hyperglycemia causes changes in the coagulation mechanism, which again causes thrombosis.in hyperglycemic patients, increases in prothrombin, fibrinopeptide A and factor 7 levels together with an increase in platelet aggregation are observed 19,20. Consequently, in our study it was interesting to observe that the rate of impaired fasting glucose was higher in patients with ACS than in the normal population. The findings that in the early phase after the ACS (hospitalization phase) the mortality rate was almost the same in patients with IFG and diabetes and that this rate was significantly higher when compared to the patients with normal fasting glucose are important. Recognizing that the atherosclerosis process has already started in the IFG period, which is the earliest phase of diabetes and that it presents a cardiovascular risk, early detection of patients with IFG would be a useful approach in the determination of the cardiovascular risks and modification of the treatment. It is recommended that more aggressive treatment approaches should be used in diabetics or in patients with IFG, also considering the concomitant risk factors such as hypertension, dyslipidemia and obesity. It is thought that when this is provided, the complications may be prevented more successfully. In individuals with risk factors for diabetes (obesity, family history of diabetes, history of giving birth to a macrosomic baby), it is beneficial to determine whether IFG is present by testing the fasting blood sugar, to prevent or delay the development of diabetes with recommended treatment approaches in patients with detected IGT by OGTT if necessary will be beneficial in reduction of the CHD risk. Our study showed that; in patients hospitalized in our coronary intensive care unit with a diagnosis of acute myocardial infarction, the prevalence of diabetes and IFG was higher compared to that of the normal population. In the early phase after AMI, the rate of mortality was approximately the same in patients with IFG and diabetes, and this rate was significantly higher compared to the individuals with normal glucose levels and therefore like diabetes, IFG was also a risk factor for CHD and it affected mortality as much as diabetes. REFERENCES 1. American Diabetes Association.Diagnosis and classification of diabetes mellitus. By Diabetes Care 2004;27: 5-10, 2. Abacı A, Oğuzhan A, Karaman S, et al. Effects of diabetes mellitus on formatıon of coronary vessels. Circulatıon 1999; 99 : 2239-2242. 3. Zimmet P, Albertik KGMM.The changing face of macrovascular disease in noninsulin dependent diabetes mellitus in different cultures : an epidemic in progress Lancet 1997; 350 :S1-S4. 4. Haffner SM, Stern M, Hazuda HP, et al. Cardiovascular risk factor in confirmed prediabetıc individuals. Does the clock for coronary artery disease start ticking before the onset of clinical diabetes. JAMA 1990; 263: 2893-2898. 5. Wheathcoft SB, Williams IL, Shah AM, et al. Pathophisiological impications of insulin resistance on vasculer endothelial function diabetic medicine 2003; 20: 255-268 261

Marmara Medical Journal 2010;23(2);257-262 Mehmet Uçucu, et al. In-hospital mortality in patients with impaired fasting glucose and acute coronary syndromes 6. Peterson DT, Greene WC, Reaven GM. Effect of experimental diabetes mellitus on kidney ribosomal protein synthesis. Diabetes 1971;20:649-54. 7. Ryden L, Armstrong PW, Cleland JG, et al. Efficacy and safety of high-dose lisinopril in chronic heart failure patients at high cardiovascular risk, including those with diabetes mellitus. Result from the ATLAS trial. Eur Heart J 2000;21:1967-1978. 8. Ledru F, Ducimetieve P,Battoglia S, et al. New Diagnostic criteria for diabetes coronery artery disease insights from an angiographic study. I Am Coll Cardiol 2001, 37 :1543-1550. 9. Laakso M. Hyperglisemia and cardiovascular disease in type 2 diabetes. Diabetes 1999;48:937-942. 10. Hsueh WA, Laur RE. Cardiovascular risk continuum : implications of insulin resistance and diabetes AMJ Med 1998; 105: 4-14. 11. Schachiner V, Britten MB,Zeiher AM. Prognostic impact of coronary vasodilator dysfunction on adverse long-term outcome of coronary heart disease. Circulation 2000; 101:1899-1906. 12. Yılmaz MT, Salman S. Diabetik hastada postprandial glukoz düzeyinin önemi. Aktüel Tıp Derg 2003;8 :14-18. 13. Haffner SM, Lehta S, Ronnemaa T, Pyorala K, Laakso M. Mortality from coronary heart disease in subjects with type 2 diabetes and in and in nondiabetic subjects with and without prior myocardial infarction. Engl J Med 1998, 339 :229-234. 14. Rodriguez BL,Curb JD, Burcfiel CM, et al. Impaired glucose tolerance diabetes and cardiovascular disease risk factor profiles. The Honolulu Heart Program. Diabetes Care 1996;19: 587-590. 15. Tominago M, Eguchi H, Monaka H, Igarahi H, Kato T, Sekikama A. Impaired glucose tolerance is a risk factor for cardiovascular disease, but not impaired fasting glocose. The FURAGATO diabetes study. Diabetes Care 1999; 22 : 920-924. 16. Nurkalem Z, Sargın M, Alper A, et al. Nondiabetik AKS vakalarında postprandial hipergliseminin koroner lezyonlarla ilişkisinin araştırılması. Endokrinolojide Yönelişler 2003;12 : 175-179. 17. Hanefeld M, Koehler C, Schaper F, Fuecker K, Henkel E, Temelkova T, Postprandial plasma glucose is an independent risk factor for increased carotid intima media thickness in non-diabetic individuals. Atherosclerosis 1998;144 : 229-235. 18. Balkau B, Bertrais S, Ducimetieve P, Eschvege E. Is there a glycemic threshold for mortality risk. Jpn Heart J 1991;31 : 35-43. 19. Alain D,Baron MD. Vascular reactivity. Am J Cardiol 1999; 84: 251-271. 20. Kawano H, Motoyama T, Hirashima O, et al. Hyperglicemia rapidly surresses flow mediated endothelium-dependent vasodilatation of brachial artery. J Am Coll Cardiol 1999; 34 : 146-154. 262

ORIGINAL RESEARCH CARPAL TUNNEL SYNDROME: WHAT IS THE DIAGNOSTIC VALUE OF USG WITH HIGH RESOLUTION TRANSDUCERS? Özgür Sarıca 1, Arda Kayhan 2, Enis Öztürk 3, Sibel Bayramoğlu 3, Nurten Turan Güner 3, Fatma Öztora 4 1 Taksim İlk Yardım Eğitim ve Araştırma Hastanesi, Radyoloji Kliniği, İstanbul, Türkiye 2 Namık Kemal Üniversitesi Tıp Fakültesi, Radyoloji Anabilim Dalı, Tekirdağ, Türkiye 3 Bakırköy Dr. Sadi Konuk Eğitim ve Araştırma Hastanesi, Radyoloji Kliniği, İstanbul, Türkiye 4 Niğde Devlet Hastanesi, Radyoloji Kliniği, Niğde, Türkiye ABSTRACT Objective: Carpal tunnel syndrome (CTS) is a common peripheral entrapment neuropathy, caused by the entrapment of the median nerve. Ultrasonography (USG) has been used as a cost-effective and comfortable technique in the examination of the carpal tunnel and the median nerve in the last decade. Material and Methods: Thirty-five wrists of 21 patients with the signs, symptoms and electromyelography (EMG) confirmed diagnosis of CTS and 40 wrists of healthy adults were evaluated by ultrasonography (USG), performed with a 7.5-12 MHz transducer. Results: All of the 35 wrists of 21 patients with CTS diagnosed by EMG and 40 wrists of 20 healthy adults were diagnosed accurately. Conclusion: USG may be performed as a first step test in the diagnosis of suspected CTS. Keywords: Carpal tunnel syndrome, EMG, High resolution USG ÖZET KARPAL TÜNEL SENDROMU: YÜKSEK REZOLÜSYONLU USG NİN TANISAL DEĞERİ NEDİR? Amaç: Karpal Tünel Sendromu (KTS), median sinir tuzağına bağlı sık görülen periferal tuzak nöropatidir. Ultrasonografi (USG), son yıllarda karpal tünel ve median sinirin değerlendirilmesinde kullanılan ucuz ve rahat uygulanabilen bir tekniktir. Yöntem: KTS bulgusu, semptomları ve elektromyelografik tanısı olan 21 hastada 35 ve 20 sağlıklı olguda 40 el bileği 7.5-12 MHz prob kullanılarak USG eşliğinde değerlendirildi. Bulgular: 21 KTS li olguda 35 el bileğinin tamamı ve sağlıklı 20 sağlıklı olguda 40 el bileği doğru olarak değerlendirildi. Sonuç: Yüksek rezolüsyonlu USG, KTS tanısında tercih edilecek ilk basamak görüntüleme tekniği olabilir. Anahtar Kelimeler: Karpal Tünel Sendromu, EMG, Yüksek rezolüsyonlu USG İletişim Bilgileri: Arda Kayhan, M.D. Namık Kemal Üniversitesi Tıp Fakültesi, Radyoloji Anabilim Dalı, Tekirdağ, Türkiye e-mail: arda_kayhan@yahoo.com Marmara Medical Journal 2010;23(2);263-269 263

Marmara Medical Journal 2010;23(2);263-269 Özgür Sarıca, et al. Carpal tunnel syndrome: What is the diagnostic value of USG with high resolution transducers? INTRODUCTION Carpal tunnel syndrome (CTS) is a common peripheral entrapment neuropathy, including a group of signs and symptoms, caused by the entrapment of the median nerve as it passes through the carpal tunnel. The diagnosis of CTS is usually based on a combination of clinical signs and physical examination findings. Additional nerve conduction studies may be required for confirmation. The most reliable method for confirming a clinical diagnosis of CTS, is electrodiagnostic testing, but false negatives and false positives may occur, even when the most sensitive methods are used 1-3. Although the electrodiagnostic studies are usually not comfortable and badly tolerated by the patients, they are still accepted as the gold standard in a CTS diagnosis. Magnetic resonance imaging and high resolution ultrasonography (USG) have been shown to be useful diagnostic tools in CTS providing information about the median nerve and surrounding structures 4,5. Sonography has been used as a cost-effective and comfortable technique in the examination of the carpal tunnel and the median nerve in the last decade, with a sensitivity of 49-84% and spesificity of over 95% 6. Our aim is to review the efficacy of high resolution USG in the diagnosis of CTS. MATERIAL AND METHOD Twenty-one patients diagnosed with CTS, confirmed by clinical signs, symptoms and electromyelography (EMG) were included in this study. All the patients were informed about the procedure and an informed consent from all the participants was obtained. Patients with only idiopathic CTS were included in the patient group and 35 of the 21 patients wrists were examined. Patients with a history of trauma, surgery or steroid injection and patients with systemic disease such as uncontrolled diabetes, gout, or renal insufficiency were also excluded. Three patients with wrists with a previous history of CTS on the contralateral right side were excluded. We also excluded a patient s left wrist diagnosed as bifid median nerve and persistant median artery, detected during our USG examination. Another patient with CTS symptoms on the right wrist was also excluded after a ganglion cyst was detected. In one patient, only the right wrist was examined, due to only right sided symptoms. The control group included the patients who had no known systemic disease, wrist trauma history or symptoms related to the wrist. The sensory and motor nerve conduction studies and needle EMG examinations of the median and ulnar nerve in the patients symptomatic wrists were applied using standard techniques. The prolongation of the 2nd finger sensory response latency, equal to or more than 1 millisecond compared to the 5th finger ulnar response latency, the pathologic decrease in the velocity of sensory transmission between the wrist and the 2nd finger, a sensory response amplitude of the 2nd finger below 10 microvolt, a median ulnar sensory response latency difference over 0,4 millisecond in the 4th finger (the prolongation of median sensory response latency), a normal median nerve motor transmission velocity in the forearm segment but a pathological prolongation in the distal motor transmission period in between the tenar muscles and wrist were used as CTS criteria in the EMG examination. USG examinations were performed by a radiologist experienced in musculoskeletal system sonography. During the examination, a 7.5-12-MHz linear array transducer (TOSHIBA Applio) was used and the patients were in supine -neutral position while the observer was on the right lateral side and the patient facing the examiner. The examination was supported by using a gel standoff pad. The median nerve in and proximal to the carpal tunnel was scanned in the transverse axial plane initially. The presence of ganglion cysts, anatomic variations, etc. and fluid accumulations in the tendons neighbouring the nerve (tendinitis-tenosynovitis) were investigated and patients with such findings were excluded. The course of the median nerve was followed through its trace from the 264

Marmara Medical Journal 2010;23(2); 263-269 Özgür Sarıca, et al. Carpal tunnel syndrome: What is the diagnostic value of UGS with high resolution transducers? most distal palmar region to the distal 1/3 of forearm. The examination began with an evaluation of the nerve and the neighbouring anatomical structures and it was followed by the assesment of the structure, contour and internal echogenicity of the median nerve. The anteroposterior (AP) and transverse diameters of the median nerve were measured at the level of the radiocarpal joint and the proximal carpal bones. At the level of the proximal carpal bones, the flattening ratio (FR) was calculated using the diameter measurements of the mid- median nerve (FR=Transverse diameter/ AP diameter). The cross-sectional area of the median nerve at the level of the radiocarpal joint proximal median nerve area (PMNA) and at the level of proximal carpal bones mid- median nerve area (MMNA) were also measured. The manual trace method in the USG equipment was used in the area measurements and the hyperechogenic rim was not included. In the overall measurements, millimetersquare unit was used for area measurements and millimeter unit was used for the length measurements. The final measurement was obtained following three trials, and by calculating the arithmetical mean. The measurement was carefully performed to demarcate the nerve to be in the transverse projection of the imaging plane. Palmar displacement or volar bulging may be defined as the farthest distance between the flexor retinaculum and an imaginary line tangent to the trapezium and hamate at the level of the distal carpal bones. We also measured the palmar displacement at the level of the distal carpal bones. The statistical analysis was evaluated by performing the SPSS 10.0 for windows programme, using Student s t, q square, Fisher exact square and ROC Curve tests. A p value of less than 0.05 was considered statistically significant. All of the values were defined as percent with mean+/- standard deviation and n. RESULTS The patients were aged 32-74 years ( mean age 48,00 +/-10,24). The patient group consisted of 1 male (4,8%) and 20 females (95,2%). The control group consisted of 17 females (85%) and 3 males ( 15%) aged 26-51 years ( mean 37,45 +/- 8,99). The duration of the symptoms was at least 1 month and not more than 24 months. Of 21 patients, 15 were housewives, (71,4%), 4 were tailors (19.0%), 1 was a waiter (4,8%) and 1 was a butcher (4,8%). We detected the typical reticular echo pattern in the control group. There was no significant difference between the diameters of the median nerve at the level of the radiocarpal joint and at the level of the proximal carpal bones. In all patients with CTS; the median nerve at the wrist region was hypoechogenic. We also detected the loss of thin reticular echogenicities which are formed by the epineurium layers surrounding the neural fascicles. Mean PMNA at the level of the radiocarpal joint was 6,97±1,09 mm 2 and the mid level cross-sectional area of the MMNA at the level of the proximal carpal bones was 7,70±1,06 mm 2 in the control group. There was no significant increase in the values of MMNA compared to PMNA in the control group. Mean PMNA at the level of the radiocarpal joint was 12,71±5,2 mm 2 and MMNA at the level of proximal carpal bones was 16,02±6,65 mm 2 in the patient group. There was a significant increase in the values of both PMNA and MMNA compared to the control group(p<0.001). There was no significant difference between PMNA and MMNA in the control group, whereas MMNA showed a significant increase compared to PMNA in the patient group (Table I). The thickening ratio (TR) (TR = MMNA / PMNA) was 1,12±0,21 in the control group and 1,30±0,31 in the patient group. The TR ratios of the patient group was increased in the patient group and there was a significant difference compared to the control group (p<0.05) (Table II). The FR of the control and patient groups were calculated using the dimension of the median nerve obtained at the level of the proximal 265

Marmara Medical Journal 2010;23(2); 263-269 Özgür Sarıca, et al. Carpal tunnel syndrome: What is the diagnostic value of UGS with high resolution transducers? carpal bones (FR = Transverse diameter / PA diameter). The FR in the control group was calculated as 2,27±0,50 and the FR in the patient group was calculated as 2,86±0,61. The FR of the patient group was significantly increased compared to that of the control group (p<0.05) (Table III). In palmar displacement (PD) measurements at the level of the trapezium-hamate, we observed a significant difference between the control group and the patient group. The PD values were calculated as 3,09±0,81 mm in thecontrol group and 4,98±0,69 mm in the patient group. The PD value of the patient group shows significant increase compared to the control group( p<0.05) ( Table IV). We determined the MMNA as the major criterion in CTS. In comparison of the patient and control groups, the sensitivity of USG was 91,40% and the spesificity was 92,50% in the diagnosis of CTS. The sensitivity of palmar displacement and flattening ratio which we used as minor criteria was 97,10% and 88,60% and the spesificity was 60,00% and 67,50% respectively. Table I. The values of PMNA at the level of the radiocarpal joint and the values of MMNA at the level of proximal carpal bones Area (mm 2 ) PMNA MMNA Group n X±SD X±SD Control 40 6,97±1,09 7,70±1,06 Patient 35 12,71±5,2 P<0.001 16,02±6,65 P<0.001 Table II. The thickening ratio of the control and patient groups (TR = MMNA / PMNA) TR Group n X±SD Control 40 1,12±0,21 Patient 35 1,30±0,31 P<0.05 Table III: The flattening ratio of the control and patient groups (FR) FR Group n X±SD Control 40 2,27±0,50 Patient 35 2,86±0,61 P<0.05 266

Marmara Medical Journal 2010;23(2); 263-269 Özgür Sarıca, et al. Carpal tunnel syndrome: What is the diagnostic value of UGS with high resolution transducers? Table IV. The palmar displacement values of the control and patient groups (PD) PD Group n X±SD Control 40 3,09±0,81 Patient 35 4,98±0,69 P<0.05 Fig 1: The USG image of a normal median nerve. The typical reticular pattern of the median nerve, formed by hypoechogenic areas surrounded by hyperechogenic bands. Fig 2:Extensive increase in the cross-sectional area of the median nerve and loss of reticular pattern in a patient with CTS 267

Marmara Medical Journal 2010;23(2); 263-269 Özgür Sarıca, et al. Carpal tunnel syndrome: What is the diagnostic value of UGS with high resolution transducers? DISCUSSION The diagnosis of CTS is made by history and physical examination in some patients, whereas in others some additional confirming studies are required. 7. In the last few years, many reports have stated that US has high sensitivity and specificity in CTS diagnosis, but many of these studies considered EMG as the gold standard for inclusion criteria 8,9. The conventional electrophysiological tests are expensive, time-consuming and are not well tolerated by the patients 9. Technical factors such as filter adjustment or the voltage of the stimulator may effect the quality of the test. Though EMG can detect the presence and the extent of CTS, it cannot give information about the cause of the disease and the anatomical details of the median nerve and neighbouring structures. The median nerve, its variations and the structures in the wrist region (ganglion cyst neighbouring median nerve, bifid median nerve accompanied by persistant median artery) can be accurately detected by USG. USG may also be helpful in determining the cause of the disease. The accuracy of the diagnosis is increased and the treatment protocol is accurately planned by USG. Additionally, USG has an important role in the treatment of entrapment neuropathies. It can be used as a guide during endoscopic surgery and in postoperative complication follow-up 9. Decreased median nerve echogenicity and loss of reticular pattern in USG have been reported in most studies, though these findings are not diagnostic criteria for CTS 8,10,11. The evaluation of nerve echogenicity is a subjective criterion which is observer dependent and even the variations in the angle of the transducer can effect the echogenicity of the nerve. The poor diagnostic value of the nerve echogenicity has also been stated by Wong et al. 12. Although it was present in all our cases, decreased nerve echogenicity and loss of reticular pattern were not accepted as diagnostic criteria since we believe that they are subjective findings. The diagnostic criterion in our study was the cross-sectional area of median nerve. The most sensitive measurements are obtained at the level of the pisiformis, because the increased diameter of the nerve due to edema is most remarkable at this plane 4. We obtained the area measurements at the level of the radiocarpal joint and proximal carpal bones. In many studies, the critical crosssectional area is stated as 9.0-14.0 mm 2. We accepted the values over 9.5 mm 2 as pathologic. In some series, this value is found as high as 15.0 mm 2. In our study, we detected the mean cross-sectional area of median nerve as 16.02±6.65 mm 2 (sensitivity = 91.4% specifity = 92.5%). Wong et al. calculated the cross-sectional area of median nerve in left and right hands seperately in both the control and the patient Group 12. In patient the group, it was calculated as 11.0±4.0 mm 2 in the right, 10.0±3.0 mm 2 in the left wrist and in the control group 8.0±2.0 mm 2 in the right 8.0±1.0 mm 2 in the left wrist. It was stated that the statistical results in the patients with a cross-sectional area of median nerve equal to or higher than 9.8 mm 2 at the entrance of the carpal tunnel are corresponding to the EMG findings. Lin-Yi Wang et al stated that the most useful diagnostic criterion in high resolution US was a 9.875 mm median nerve CSA of 2 at the pisiform level 13. Leonard et al. stated the mean values of area measurements in the patient group as 11.6 mm 2 and in the control group as 7.8 mm 2 at the level of the pisiformis 14. In our study, we detected the mean cross-sectional area of the median nerve as 7,70±1,06 mm 2 at the level of the pisiformis in the control group and 16,02±6,65 mm 2 in the patient group. There was a significant difference in the values of the control and the patient group(p<0.05). We observed that there was no significant increase in the cross-sectional area at the level of the pisiformis in the control group and in the patient group, there was a remarkable increase due to the edema of the median nerve. All these findings are concordant with the literature 11,12,14,15. 268

Marmara Medical Journal 2010;23(2); 263-269 Özgür Sarıca, et al. Carpal tunnel syndrome: What is the diagnostic value of UGS with high resolution transducers? The FR and PD are also evaluated in the literature 8,10,11,16 but the diagnostic importance of these findings is controversial. In their study, Nakamichi and Tachibana stated that in the control group, the flattening ratios are increased at the level of the distal end of flexor retinaculum and hamate, whereas, in the patient group they are increased at wrist flection 16. Wong at al. declared that the evaluation of the flattening ratio and palmar bowing is based on subjective interpretation, so these findings have poor diagnostic value 12. In our study, we examined the significant increase in both values and we believe that these findings can be used as contributory minor criteria in the diagnosis of CTS. We detected that; 21 of 35 patients had wrists with CTS diagnosed by EMG, and 37 of 40 healthy patients wrists were diagnosed accurately. According to this determination, USG has a sensitivity of 91.4% and spesificity of 92.5%. The statistical findings of our study, in which we accepted the critical value of cross-sectional area of the median nerve at the pisiformis level as 9.5 mm 2 is parallel to the literature 15,17. In conclusion, USG is a modality of low cost, short duration, and availability. It is painless and noninvasive. Although it is operator dependent, it shows high reproducibility after adequate training of the operators. Highresolution USG, with measurement of the median nerve cross-sectional area at the proximal carpal tunnel inlet, can be used as a first step test in the diagnosis of suspected CTS, and EMG should be applied when the physical examination and USG findings are not sufficient. REFERENCES 1. Nathan PA, Keniston RC, Meadows KD, et al. Predictive value of nerve conduction measurements at the carpal tunnel. Muscle Nerve 1993;16:1377 1382. 2. Atroshi I, Gummesson C, Johnsson R, et al. Diagnostic properties of nerve conduction tests in population-based carpal tunnel syndrome. BMC Musculoskelet Disord 2003;4:9 ( Epub 2003 May 7). 3. Lew HL, Date ES, Pan SS, et al. Sensitivity, specificity, and variability of nerve conduction velocity measurements in carpal tunnel syndrome. Arch Phys Med Rehabil 2005; 86:12 16. 4. Beekman R, Visser LH. Sonography in the diagnosis of carpal tunnel syndrome: a critical review of the literature. Muscle&Nerve 2003; 27:26 33. 5. Uchiyama S, Itsubo T, Yasutomi T, et al. Quantitative MRI of the wrist and nerve conduction studies in patients with idiopathic carpal tunnel syndrome. J Neurol Neurosurg Psychiatry 2005; 76:1103 1108. 6. Anonymous: Practice parameter for electrodiagnostic studies in carpal tunnel syndrome: summary statement. American Association of Electrodiagnostic Medicine, American Academy of Physical Medicine and Rehabilitation. Muscle&Nerve 1993; 16:1390-1391. 7. Kulick R.. Carpal tunnel syndrome: Orth Clin North Am 1996; 27:345-354. 8. Lee D, van Holsbeeck MT, Janevski PK, et al. Diagnosis of carpal tunnel syndrome. Ultrasound versus electromyography. Radiol Clin North Am 1999 ; 37:859-872. 9. Zenbilci N. Elektromiyografi. Sinir Sistemi Hastalıkları. 2.Baskı. İstanbul:Cerrahpaşa Tıp Fakültesi Yayınları, 198:95-109. 10. Martinoli C., Bianchi S, Gandolfo N, et al. US of nerve entrapments in osteofibrous tunnels of the lower limbs. Radiographics 2000; 20:199-217. 11. Nakamichi KI, Tachibana S. Ultrasonographic measurement of median nerve cross-sectional area in idiopathic carpal tunnel syndrome: Diagnostic accuracy. Muscle&Nerve 2002; 26:798-803. 12. Wong S.M, Griffith J.F, Hui A.C.F, et al. Discriminatory sonographic criteria for the diagnosis of carpal tunnel syndrome. Arthritis & Rheumatism 2002; 46:1914-1921. 13. Wang LY, Leong CP, Huang YC, et al. Best diagnostic criterion in high-resolution ultrasonography for carpal tunnel syndrome. Chang Gung Med J 2008;31:469-476. 14. Leonard L, Rangan A, Doyle G, et al. Carpal Tunnel Syndrome-is high-frequency ultrasound a useful diagnostic tool? J Hand Surg (British and European volume) 2003; 28B 1: 77-79. 15. Bayrak IK, Bayrak AO, Tilki HE, et al. Ultrasonography in Carpal Tunnel Syndrome: Comparison with electrophysiological stage and motor unit number estimate. Muscle&Nerve 2007;35:344 348. 16. Nakamichi KI, Tachibana S. Enlarged median nerve in idiopathic carpal tunnel syndrome. Muscle&Nerve 2000 ;23:1713-1718. 17. Wiesler ER, Chloros GD, Cartwright MS, et al. The use of diagnostic ultrasound in carpal tunnel syndrome. J Hand Surg Am 2006; 31:726-732. 269

ORIGINAL RESEARCH MORPHOLOGICAL STUDY OF THE MENISCI OF THE KNEE JOINT IN ADULT CADAVERS OF THE SOUTH INDIAN POPULATION B.V. Murlimanju 1, Narga Nair 2, Shakuntala Pai 2, Mangala Pai 1, Chethan P 1, Chandni Gupta 2 1 Manipal University, Anatomy, Mangalore, Hindistan 2 Manipal University, Anatomy, Manipal, Hindistan ABSTRACT Objective: To estimate the incidence of different shapes of the medial and lateral meniscus and the incidence of discoid meniscus in the South Indian population. Methods: The study included 108 menisci from 54 adult cadaveric knee joints which were preserved in 10% formaldehyde solution. After the dissection procedure, the morphological variants of the shapes of menisci were macroscopically noted and classified. The medial meniscus was subgrouped as crescent-shaped, sided U-shaped, sided V-shaped, sickle-shaped and C-shaped. The lateral meniscus was subgrouped as crescentshaped, C-shaped and discoid-shaped. Results and Conclusion: From our observations, 50% of the medial menisci were cresent- shaped, 38.9% were sided V-shaped and 11.1% were sided U-shaped. The percentages of the different types of lateral menisci were 61.1%, C-shaped and 38.9%, crescent-shaped. No discoid medial or lateral meniscus (0%) was observed in the study. Keywords: Knee, Lateral meniscus, Medial meniscus, Shape, Side GÜNEY HİNDİSTANLI YETİŞKİN KADAVRA POPÜLASYONUNDA DİZ EKLEMİ MENİSKÜSLERİNİN MORFOLOJİK DEĞERLENDİRİLMESİ ÖZET Amaç: Güney Hindistan popülasyonunda, medial ve lateral menisküs şekil farkı ve diskoid menisküs görülme oranının tahmin edilmesi. Yöntem: Çalışmada, %10 formaldehid solüsyonunda korunmuş olan, 54 yetişkin kadavra dizinden elde edilmiş 108 adet menisküs kullanılmıştır. Diseksiyon prosedüründen sonra çıkarılan menisküslerin şekillerindeki morfolojik varyasyonlar makroskopik olarak incelenip sınıflandırılmıştır. Medial menisküs için, hilal biçimli, kenarlı U biçimi, kenarlı V biçimi, orak biçimi ve C biçimi alt gruplama yapılmıştır. Lateral menisküs için ise hilal biçimi, C biçimi ve diskoid biçimi alt gruplaması yapılmıştır. Bulgular ve Sonuç: Yaptığımız gözlemler sonucu, medial menisküslerin % 50 si hilal biçimli, %38,9 u kenarlı V biçimli, %11.1 i kenarlı U biçimli bulunmuş; lateral menisküs şekillerindeki yüzdeler ise %61.1 C biçimli, %38.9 hilal biçimli bulunmuştur. Çalışmada diskoid yapıda lateral veya medial menisküs e rastlanmamıştır. Anahtar Kelimeler: Diz, Lateral menisküs, Medial menisküs, Kenar, Şekil İletişim Bilgileri: B.V. Murlimanju, M.D. Manipal University, Anatomy, Mangalore, Hindistan e-mail: drmanju_22@rediffmail.com Marmara Medical Journal 2010;23(2);270-275 270