Friday, November 28, 2008

COLOR DOPPLER DIAGNOSIS OF ACUTE APPENDICITIS

Tai Van Le, Tai Anh Vo, Hai Thanh Phan, M.D
MEDIC Medical Center, HCM City, Vietnam


I. INTRODUCTION
  • Acute appendicitis is a common clinical problem, and one of the most common causes of acute abdominal pain requiring surgical intervention in Vietnam as well as in all other countries of the world. Accurate and prompt diagnosis is essential to minimize morbidity, especially in the case of atypical appendicitis.
  • The diagnosis of appendicitis can be based on clinical examination, laboratory findings and medical modalities imaging such as CT scanning and US scanning. In fact, ultrasound, especially color Doppler US combined with graded compression US has proved to be useful and effective in the diagnosis of acute appendicitis by its high specificity (91%), high positive predictive values (95%) and rather high accuracy (83%).

II. MATERIALS AND METHODS

  • From 12/2004 to 12/2005, a prospective study was carried out in correlation with surgical intervention results and pathologic findings on 63 patients of age from 2 to 79 (M/F: 32 /31) with clinical symptoms suspected of appendicitis.
  • Using graded compression of Puylaert [1]. Appendicitis was firstly detected with B – mode and then hyperemia within the appendiceal wall was assessed on color Doppler. The number of color Doppler signals within the appendiceal wall was classified as absent (0), sparse (1-2), moderate (3-4) or abundant (> 4). The resistive index (RI) was calculated (peak systolic velocity – end diastolic velocity/ peak systolic velocity). In cases of necrotic appendicitis with perforation, hyperemia was sought in the tissues surrouding the appendix including periappendiceal fluid, intestinal wall, greater omentum and psoas muscle. The differences were assessed between abscess, plastron, phlegmon, regional peritonitis, general peritonitis.
  • Because of the appendix as known to have variants of position was sought by US planes around the cecum which was firstly localized at its right position depending on the haustrations of the ascending colon with dirty shadowing. The ascending colon was identified by the longitudinal plane from the right hypochondria to the right iliac fossa. And the cecum is terminal haustration of the asceding colon and its variant positions may be below the right lobe of liver, at the umbilical or pelvic level.
  • Toshiba Power - Color Doppler US machine with 3.5 – 6 MHz convex and linear probes was used. Low-flow settings (lowest available pulse repetition frequency, highest color Doppler gain possible without background noise signal, low wall filter) were used.

III. RESULTS

  • There were 63 cases suspected of appendicitis, 61 cases were true appendicitis (96.8%): 60 cases were operated, 1 case was not operated because it was followed up as a plastron and 2 cases were operated but they were not appendicitis, one case was pyosalpinx, the other was cecal inflammation. There were 42 cases of non-perforated appendicitis (69%); 19 cases of perforated appendicitis (31%). The position of appendix, there were 11 retro-cecal cases (18%) (Fig. 2.g, h, i), 2 pelvic cases (3%), 1 retro-ileal case (1.5%), and 1 umbilicus-directed case (1.5%). The pathologic findings consisted of 5 cases of congestive appendicitis (submucal layer is intact), 54 cases of necrotic appendicitis or purulent appendicitis (submucal layer is necrotic a part or total). Gray- scale US showed 5 cases with intact echogenic submucosal layer, 46 cases non-intact, 8 cases with disappeared echogenic submucosal layer (Table.1).

  • There were 42 cases of nonperforated appendicitis, in which 40 cases (95%) with hyperemia: 12 cases of sparse hyperemia (30%) (Fig.2b), 5 cases of moderate hyperemia (13%), 23 cases of abundant hyperemia (57%) (Fig. 2c). There was no hyperemia in 2 cases (5%) (Fig. 2a). The velocity of flow, 7 - 33 cm/sec, was low, (mean 16 cm/s), RI (resistive index) was low: 0.43 - 0.79, (mean 0.6) (Fig.2b).
  • There were 19 cases of perforated appendicitis, 2 cases of which the appendixes were not seen because they were completely destroyed (Fig.2d), and 11 cases with hyperemia (58%) consisted of 3 cases with sparse hyperemia (27%), 2 cases with moderate hyperemia (18%), and 6 cases with abundant hyperemia (55%). There were 8 cases without hyperemia (32%) 6 cases of which had no echogenic submucosal layer corresponding to completely destroyed submucosa and 2 cases with incompletely destroyed echogenic submucosal layer (Table.2).

  • In cases of perforated appendicitis, 9 cases (47%) were abscesses with peripheral hyperemia on color Doppler (100%) (Fig.2d), 2 cases of which had peripheral and central hyperemia. In 5 cases of abscessed appendiceal plastron (phlegmon) (26%), hyperemia existed in the soft tissue around the necrotized appendix including the adjacent bowel wall, the greater omentum and the psoas muscle (Fig.2e) because of important inflammation around the perforated inflamed appendix. There were 2 cases of regional peritonitis (11%) of which only one had hyperemia. There was one case of general peritonitis (5%) without peri-hyperemia. There were 2 cases of plastron (11%) without perihyperemia (Fig.2f) because the inflammation was not severe (Table.3).

Figure 2: US Images for Illustration

IV. DISCUSSIONS
  • In almost cases of acute appendicitis, there was hyperemia within the wall of the appendix due to vasodilatation in inflammatory structure accounting for 84% of the cases of non-perforated appendicitis and 58% of those of perforated appendicitis. The velocity of flow was low, RI was low because of high velocity of diastolic flow due to vasodilatation. Congestive appendicitis (with intact of submucal layer) is allways hyperemia; necrotic appendicitis if the submucal is destroyed completely resulting of absent hyperemia, these were corresponding almost blood vessel is distributed within submucal layer. These results are similiar to those in the literature [2]. Therefore Color Doppler aids gray-scale in cases of acute appendicitis at early stage.
  • In cases of acute appendicitis with perforation causing abscess, 100% had peripheral hyperemia; this helped us differenciate appendiceal abscess from other types of fluid collection, especially for the cases of necrotic appendicitis in which the appendixes were completely destroyed.
  • In addition, hyperemia also helped us differentiate between the plastron (without hyperemia) with phlegmon, regional peritonitis (with hyperemia within tissues around necrotic appendix with perforation). Thanks to this, there were prompt and exact surgical indications. Plastron needed only conservative treatment and delayed surgery, whereas phlegmon and regional peritonitis had to be surgically intervened promptly.
  • The method of localization of cecal positions mentioned above proved to be effective and useful in detection of appendix depending on characteristic US haustral pattern of the acending colon. In practice, this helped to improve the accuracy of diagnosis of appendicitis (96.8%).

V. CONCLUSIONS

  • Color Doppler shows hyperemia in almost acute appendicitis; spectrum shows low velocity, high diastolic flow, low resistive index (RI). Color Doppler aids gray-scale in cases of acute appendicitis at early stage. Hyperemia in the soft tissue around the perforated appendix often help us to differentiate abscess from plastron, phlegmon, regional and general peritonitis. Peripheral hyperemia in appendiceal abscess has a high specificity (100%).
  • Exact determination of position of cecum is very useful in the detection of appendix and therefore helps improve the accuracy of diagnosis of acute appendicitis.

    REFERENCES
  1. Puylaert JBCM. Acute appendicitis: US evaluation using grade compression. Radiology 1986; 58:355--360.
  2. Patriquin HP et al. Appendicitis in children and young aldules: Doppler sonography- phathologic correlation. AJR 1996; 166:629--633.
  3. Quiilin SP, Siegel MJ. Diagnosis of appendiceal abscess in children with acute appendicitis: value of color sonography. AJR 1995; 164:1251--1254

Wednesday, November 26, 2008

Case report: THORACIC KIDNEY

  • Thận lạc chỗ hiếm gặp, có những trường hợp rất khó phát hiện, dễ bỏ sót, do lạc chỗ ở những vị trí hiếm gặp (làm cho chúng ta ít nghĩ để tìm), hay ở những vị trí dễ bị che khuất. Chúng tôi xin trình bày trường hợp hiếm nhất trong các trường hợp thận lạc chỗ: Thận lạc chỗ cao (thoracic kidney).
  • Bé trai 2 tuổi. Sốt 3 ngày, nhập viện điều trị nhiễm trùng tiểu, 2 ngày sau hết sốt. Siêu âm: 2 lần đầu không thấy thận (T). Sau đó bệnh nhân được làm xạ hình SPECT (Tc-99m) thấy 2 thận bài tiết thuốc bình thường. Siêu âm lần 3: thận trái lạc chỗ cao trên lách dưới cơ hoành (T).
Hình siêu âm cho thấy thận (T) vị trí cao
trên lách ngay dưới cơ hoành (T).




BÀN LUẬN
  • Thận hình thành từ nụ niệu quản (ureteric bud), từ tuần thứ 7--9 thai kỳ, đi lên trên. Sự đi lên quá mức: thận ở vị trí cao (thoracic kidney). Sự đi lên bị cản trở kết quả: thận ở vùng chậu, tiểu khung, vị trí thấp. Thận di chuyển ngang sang phía đối bên, thường dính với thận đối bên, hay riêng biệt. Hai thận khác bên kết hợp cho thận hình móng ngựa. Thận lạc chỗ hiếm gặp, thoracic kidney hiếm gặp nhất, ít hơn 5% trong toàn bộ thận lạc chỗ. Sự đi lên quá mức và tuỳ thuộc vào sự hình thành cơ hoành: hoàn chỉnh hay thoát vị hoành: thận đội lên cơ hoành (hình ảnh nhão cơ hoành) hay chui lên lồng ngực khi có thoát vị hoành bẩm sinh. Thoracic kidney gặp bên trái nhiều hơn bên phải, nam nhiều hơn nữ (nam/nữ = 2/1). Không có triệu chứng, chức năng bình thường. Có thể gây giảm sản một phần phổi do bị thận chèn ép.
  • XQ tim phổi: có thể có hình ảnh nhão cơ hoành, u trong ngực, u trung thất.
  • CT, DSA: giúp chẩn đoán xác định.
  • ECHO: chưa tìm thấy đề cặp. Khi siêu âm thấy 1 thận: Thận to bù trừ thường là thận độc nhất, 1 số rất ít thận còn lại thiểu sản hay teo nhỏ. Khi không thấy to bù trừ thì chắc chắn còn 1 thận lạc chỗ ở đâu đó.
  • Thoracic kidney rất hiếm gặp, dễ bỏ sót. Tuy nhiên nếu nghĩ tới khi làm siêu âm sẽ phát hiện được và có chẩn đoán chính xác.

    REFERENCE
    Yusuf K. Yalcinbas. Thoracic left kidney: a differential diagnostic dilemma for thoracic surgeons. Ann Thorac Surg 2001;72:281-283