THE SRI LANKA JOURNAL OF SURGERY April 2015 Volume 33, No.1 ISSN 1391-491X In this issue Stoma care training for nurses in Sri Lanka Hand Injuries Symposium on gastro-oesophageal reflux disease Botox in pelvic floor dyssynergia The College of Surgeons of Sri Lanka <Full page ad space - Front inner cover> Marketed by nurturing life CIC Holdings PLC Contact: Kasun : 0773 470 307 Romesh : 0777 317 010 Journal of The College of Surgeons of Sri Lanka. April 2015 Volume 33, No.1 - Quarterly. ISSN 1391-491X e - journal ISSN 2279 2201 Mission: “To reach the highest standard of scientific surgical practice by dissemination of high quality scientific information and to foster and promote the growth of scientific surgery in Sri Lanka and in the region” EDITORIAL BOARD Ajith P. Malalasekera Editor-in-Chief Kemal I. Deen Sivasuriya Sivaganesh Ruvini Abeygunaratne Satish Goonesinghe Rohan Siriwardena Chandika Liyanage Nalaka Gunawansa Hiran Amarasekara Dulantha De Silva Pramodh Chandrasinghe INTERNATIONAL ADVISORY BOARD Ian Pearce (UK) Tom R DeMeester (USA) Peter Hutchinson (UK) Konstantina Karabatsou (UK) EMERITUS EDITORS Naomal M. A. Perera Pradeep A. Fernando Serozsha A. S. Goonewardena Suren C. Paul S. J. Stephen E. D. Rodrigo C. S. Sinnatamby EDITORIAL OFFICE Dakshitha Wickramasinghe A. Faidh Ramzee Editorial Assistant The College of Surgeons of Sri Lanka No.6, Independence Avenue Colombo 07 Eardley Norton Phone : 0094- 11 - 2682290 Fax : 0094- 11 - 2695080 Email : [email protected] Printed by Ananda Press 82/5, Sri Ratnajothi Saravanamuttu Mawatha Colombo 13 THE COLLEGE OF SURGEONS OF SRI LANKA QUARTERLY ISSN 1391-49X Sponsored advertisement by Lanka Hospitals, Colombo. Sponsored advertisement by Lanka Hospitals, Colombo. April 2015 Volume 33, No.1 Contents Editorial The surgeon should assume a prominent role in the diagnosis and treatment of gastro-oesophageal reflux disease William C. Dengler 1 Scientific articles Establishment of a stoma care training program for nurses in Sri Lanka and evaluation of its effectiveness D.P. Wickramasinghe, A.M.P. Samarasekera, S. Senaratne, C.S. Perera, A. Tissera, D.N. Samarasekera 4 Continuing medical education Management of the injured hand - basic principles of care K. Karunadasa 9 Symposium on GORD Diagnosis and management of gastro-oesophageal reflux disease 14 N.P. Dinamithra, N.M.M. Nawarathne Oesophageal manometry and pH-impedance studies in gastro-oesophageal reflux disease S.U.B. Dassanayake, A.N.R. Fernandopulle 20 Nissen fundoplication: how I do it C.A.H Liyanage, S. Kumarage 24 Technical note Botulinum toxin injection to the puborectalis in the management of pelvic floor dyssynergia H.D.S Pradeep, P.C Chandrasinghe, S.A.S.R Siriwardana, S.K Kumarage 27 Case reports A Sri Lankan family with cerebellar hemangioblastoma due to a heterozygous nonsense mutation in the von Hippel-Lindau tumor suppressor, E3 ubiquitin protein ligase (VHL) gene P.K.D.C.T. Somadasa, N.D. Sirisena, V.H.W. Dissanayake 30 Laparoscopic resection with minilaparotomy anastomosis for pancreatico-duodenectomy K.B. Galketiya, V. Pinto, R. Rohankumar, B.G. Jayawickrama, A. Herath 33 Axial torsion and gangrene of a giant Meckel's diverticulum causing small bowel obstruction S.N. Deshmukh, S.P. Jadhav, A.G. Asole 35 Incisional hernia after ventriculoperitoneal shunt M. Jayant, R. Kaushik 37 Epidermal splenic cyst G.H.M. Pinsara, N. Liyanage, P.G.K. Anuradha, P.M. Lambiyas, H. Gamage 41 Selected abstracts 45 EDITORIAL The surgeon should assume a prominent role in the diagnosis and treatment of gastro-oesophageal reflux disease A few months ago, in February, I had the privilege of participating in a panel discussion in front of members of the College of Surgeons of Sri Lanka as well as pathologists where questions regarding the diagnosis and management of gastro-oesophageal reflux disease (GORD) were discussed. It was quite apparent from the questions presented, that a great deal of thought and insight existed on the part of College members about the important issues in caring for the GORD patient. Central to the discussion was the question, “What is the role of the general surgeon in the management of this disease?” In the United States, we are taught that GORD is a disease of the western world, primarily seen in the US and Europe due to diet, the epidemic of obesity and other factors. It is the most common gastrointestinal disorder seen by both primary care physicians and gastroenterologists. We are also taught that reflux disease is rarely seen in Asia and other eastern countries such as Sri Lanka. However, it became quite apparent that GORD is seen with increasing frequency in Sri Lanka and the same problematic questions regarding efficient diagnosis and management that we struggle with in the US, also exist in this nation. The evolution of GORD management in the United States has unfortunately led to an undesirable “status quo”. A patient presents, usually to the primary care physician with symptoms such as heartburn, regurgitation or any other foregut complaint. The physician concludes that the symptom source is possibly reflux disease and the patient is placed on empiric proton pump inhibitor therapy (PPIs) and sent on his way. If symptoms resolve, patients are left on their PPIs, often indefinitely. Persistent symptoms are often further investigated by a gastroenterologist with an endoscopy, which usually is without significant findings. Patients are typically continued on PPIs and returned to the care of the primary care physician without resolution of their problem. This method of management has led to runaway PPI costs, exceeding 10 billion dollars annually. We have continued this approach and watched the incidence of reflux-induced oesophageal adenocarcinoma increase more then 600% in the past 40 years [1] and millions continue to suffer under medical therapy often augmenting their PPIs with antacids and H2 blockers without relief. The present approach is failing and based on the medical literature, that should be of no surprise. Making the diagnosis of GORD based on patient symptoms alone is fraught with hazard. Some 30-40% of patients, including those presenting with typical symptoms of heartburn and regurgitation, are found not to have reflux disease after undergoing pH testing. Furthermore, while upper endoscopy is necessary to rule out other disorders, it is a terrible test for the presence or absence of GORD with objective findings of reflux (erosive oesophagitis, stricture or Barrett's oesophagus) present in only 20% of patients [2]. Symptomatic response to PPI therapy also incorrectly predicts the presence or absence of reflux disease in as many as 50% of patients [3]. Yet these are the “tools” typically used in the diagnosis of reflux that have led to the unsatisfactory management we observe today. The availability in recent years of over the counter PPIs, allowing patients to self medicate has made this problem even greater. From a therapeutic standpoint, more problems are seen. Upon their introduction, PPIs were thought to be the panacea due to their powerful acid suppressive effects. However, we now understand that approximately 40% of GORD patients continue to have breakthrough symptoms on PPIs [4]. Continued symptomatic complaints are frequently ignored by medical physicians or addressed by escalating the dose of these medications, often without benefit. The immense experience with PPIs over the years, has unmasked disturbing side effects. These include an increased risk of hip fractures and increased risk of C. difficile colitis, both of which have prompted Food and Drug Administration alerts in the US. Hypomagnesemia, increases in community acquired pneumonias and other side effects are of concern. Many patients are also never told that this medical therapy is usually necessary for life and other options such as surgery are never discussed or offered. One must question the desirability of a therapy that requires daily medications for life, is extremely costly, has significant side effects and resolves a patient's symptoms only about 60% of the time. Certainly, The Sri Lanka Journal of Surgery 2015; 33(1): 1-3 1 specific efforts in developing an approach where other therapeutic choices, including surgery, could provide great patient benefit. The endemic use of PPIs may also be playing a role in the dramatic and disturbing rise in the incidence adenocarcinoma of the oesophagus. Even the American Gastroenterological Association in its 2011 Guidelines on the management of Barrett's oesophagus acknowledged the possibility that PPI-induced gastric pH changes could possibly be adversely altering the chemistry of the refluxate and contribute to the rise in reflux-induced cancer [5]. This should be an alarming concept, yet it is infrequently discussed and has not significantly affected PPI use. In that same publication, the possibility that anti-reflux surgery may protect against development of cancer by stopping the reflux was also discussed. Despite the above considerations, the present empiric medical approach seems entrenched in the United States and significant change will be very difficult. However, as more and more GORD is seen in Sri Lanka, a different course, recognizing these problematic issues could be taken. Involvement of the surgeon in both the diagnostic and therapeutic aspects of GORD would allow a more effective approach to this disease that would greatly benefit patients. The surgeon, however, must position himself not as an individual interested in only performing an operation, but as someone with a true understanding of reflux and oesophageal disease, capable of proper diagnostic evaluations, patient education and familiarity with all potential therapies. Only the surgeon can offer all options and tailor such offerings to each specific patient. Anti-reflux surgery has been proven to be an effective long-term therapy for GORD [6]. In expert hands, it provides symptomatic relief, eliminates the need for acid suppressive medications and may decrease the likelihood of a patient developing of oesophageal adenocarcinoma. It is the only approach that actually stops the reflux and this had been confirmed with postoperative pH study normalization in 80-90% of patients. Although there are known side effects, these are minimal in the majority of patients if a proper pre-operative evaluation is performed. Persistent dysphagia should be seen in no more than 2-5%. Surgery tends to be offered to the most severely symptomatic patients and even in this group, satisfaction is high with symptom resolution in over 80% [7]. This exceeds efficacy and satisfaction with the entire group of PPI patients, many of whom have relatively minimal symptoms. Conceptually, the surgical approach makes sense as it directly addresses the cause of the disease by re-establishing the integrity of the lower oesophageal sphincter (LOS) and stopping the reflux. Medical therapy with PPIs does absolutely nothing for the LOS and the reflux is not reduced. Only the composition of the refluxate is changed and for many patients this is not sufficient. As noted above, it could possibly be quite harmful. The efficacy of laparoscopic Nissen fundoplication has been proven and the concept of a therapy that directly restores the function of the LOS has prompted the development of a host of endoscopic approaches over recent years. Most have come and gone due to lack of efficacy. The Stretta procedure and transoral intraluminal fundoplication (TIF) remain available, but their efficacy is debated and neither has demonstrated predictable improvement in distal oesophageal acid exposure. They do not predictably decrease reflux and therefore their efficacy in positively influencing a dysfunctional LOS is questioned. LINX (Torax Medical, Minneapolis, MN, USA) is a relatively new procedure that has been available for several years. A small ring of titanium magnetic beads is placed around the LOS using a laparoscopic procedure that takes approximately 30 minutes and requires minimal dissection. The procedure can be done as an outpatient. The ring does not compress the LOS. It is placed loosely and “augments” the LOS. The beads separate when a food bolus is passed into the stomach and then the magnets return to their resting state providing augmentation to the damaged LOS thereby preventing reflux. Over 3000 LINX procedures have been performed worldwide and follow up of greater than 5 years is available. LINX provides predictable symptom resolution in >80% without the side effects seen with Nissen fundoplication. Normalization of pH is seen in the majority of patients confirming the desired result [8]. Sphincter augmentation with LINX results in restoration of the barrier to reflux. Medications can usually be completely discontinued. Exclusion criteria include hiatus hernia >3cm. The Sri Lanka Journal of Surgery 2015; 33(1): 1-3 2 Only the surgeon can offer all of the treatment options. To do so effectively, he must understand and apply knowledge of all aspects of GORD. This includes a meticulous evaluation of patients and incorporation of pH testing and high resolution oesophageal manometry. Understanding the utilization and interpretation of these diagnostics are essential in the logical management of GORD. This requires quite a commitment on the part of the surgeon but will translate into optimal patient care with proper utilization of both medical and surgical therapy. To achieve this end, I propose the establishment of a “Reflux Center” for the evaluation and treatment of GORD and oesophageal disease. This entity should be overseen by the general surgeon or collaboratively with gastroenterologists who want to advance beyond the “scope and a pill, one size fits all” approach. Symptomatic patients would undergo complete evaluation including endoscopy, biopsies, pH testing and high resolution manometry, providing an objective diagnosis for each. For many, GORD will be ruled out. Some will be found to have a primary oesophageal motility disorder such as achalasia or nutcracker oesophagus. GORD patients failing medical therapy or desiring an alternative will be educated and offered a surgical approach. The incidence of GORD in Sri Lanka is likely to increase and for the benefit of your patients a logical, programmatic approach is encouraged with the general surgeon taking a lead role. William C. Dengler, MD, FACS [email protected] References: 1. 2. 3. 4. 5. 6. 7. 8. Chandrasoma PT, DeMeester TR. GERD: From Reflux to Adenocarcinoma. 1st ed. Burlington MA, USA: Academic Press 2006 Richter JE, Pandolfino JE, Vela MF, Kahrials PJ, Lacy BE, Ganz R, Dengler W, Oelschlager BK, Peters J, DeVault KR, Fass R,GyawaliCP, Conklin J, DeMeester T. Utilization of wireless pH monitoring technologies:a summary of the proceedingsfrom the Esophageal Diagnostic Working Group. Dis Esophagus 2013;26(8):755-765. Bytzer P, Jones R, Vakil N, Junghard O, Lind T, Wernersson B, Dent J. Limited ability of the proton-pump inhibitor test to identify patients with gastroesophagealreflux disease. ClinGastroenterolHepatol 2012;10 (12):1360-1366. AGA Institute: GERD patient study: patients and their medications. Harris Interactive 2008 Spechler SJ, Souza RF, Inadomi JA, Shaheen N, Allen JI, Brill J, Pruitt RE, Kahrilas PJ, Peters J, Nix K, Montgomery EA, MitchellDB, Yao J. American Gastroenterological Association medical position statement and technical review on the management of Barrett's Esophagus. Gastro 2011; 140 (3): 1084-1091. Katz PO, Gerson LB, Vela MF. Guide lines for the diagnosis and management of gastroesophagealreflux disease. Am J Gastroenterol 2013; 108 (3): 308-28. Oelschlager BK, Ma KC, Soares RV, Montenovo MI, Munoz Oca JE, Pellegrini CA. A broad assessment of clinical outcomes after laparoscopic anti-reflux surgery. Ann Surg 2012;256 (1):87-94. Bonavina L, Saino G, Bona D, Sironi A, Lazzari V. One hundred consecutive patients treated with magnetic sphincter augmentation for gastroesophageal reflux disease: 6 years of clinical experience from a single center. J AmColl Surg 2013; 217 (4): 577-85. The Sri Lanka Journal of Surgery 2015; 33(1): 1-3 3 SCIENTIFIC ARTICLES Establishment of a stoma care training program for nurses in Sri Lanka and evaluation of its effectiveness D.P. Wickramasinghe1, A.M.P. Samarasekera1, S. Senaratne1, C.S. Perera2, A. Tissera3, D.N. Samarasekera1 1 Department of Surgery, Faculty of Medicine, University of Colombo, Sri Lanka 2 Faculty of Medicine, Sir John Kotelawala Defence University, Sri Lanka 3 Education, Training and Research Unit, Ministry of Health, Sri Lanka Key words: Stoma care nurse; training; developing country; effectiveness Abstract Introduction In June 2012, the Ministry of Health with the Department of Surgery of the Faculty of Medicine, University of Colombo conducted the first certificate course in stoma therapy for nurses in Sri Lanka. We aim to evaluate the success of the course in enhancing the knowledge and skills of the participants. Methods We evaluated 15 domains of patient care in the 61 participants using a self-administered validated questionnaire administered before the onset and after completion of the course. Data were analysed using Wilcoxon signed-rank test. Results Of the 61, 37 (60.6%) were females. The mean age was 31.5 (SD±5.5) years. All 15 domains of patient care had improved at the end of the program. The biggest increase was seen in staff confidence category. The 3 domains that had the biggest improvement were; confidence to select different appliances to suit different conditions (90% improvement in score), having material for proper patient teaching (88.6%) and confidence in educating patients (77.6%). There were no statistically significant correlation between age, gender or years in nursing and the improvement in any of the measured domains. Correspondence: D.N. Samarasekera E-mail: [email protected] The Sri Lanka Journal of Surgery 2015; 33(1): 4-8 Conclusion The program was successful in allowing the participants to function independently. It was conducted with local resource personnel and minimal cost. Introduction Sri Lanka with a population of nearly 21 million [1] is one of the few developing countries in the world which still maintains a government sponsored free health care service. The health services expenditure was 2.9% of the GDP in 2010 [1] which is comparable with other countries in the region like India, Bangladesh and Singapore. There are approximately 60,000 beds for inpatient care (3 per 1000 persons) and 19,000 nurses in the free health service in Sri Lanka [2]. Though the traditional role of the in-ward nurse has largely persisted in Sri Lanka, the new trend towards specialized nurses is slowly emerging. Stoma care is a specialized area in nursing, and a trained stoma care nurse is an important member in the colorectal surgical team [3-5]. Their role in patient rehabilitation is multi fold; from pre-operative services to post-operative and community care [6-8]. The National Health Service (NHS) in the United Kingdom has identified the importance of the involvement of nurses in the management of patients with colorectal cancer and has made several recommendations about their role in the diagnosis, treatment and support of patients [9]. In Sri Lanka there were only 3 trained stoma care nurses available in the state health care service. There were 447 documented cases of patients with anorectal cancer referred to the National Cancer Institute in 2005 [10]. In addition the prevalence of Inflammatory Bowel Disease such as ulcerative colitis and Crohn's disease which may need ostomies are also increasing in Sri Lanka (incidence 5.3/100,000 and 1.2/100,000 respectively [11]. Hence, the need for specialized stoma 4 therapy nurses was promptly identified by the Ministry of Health. The authors were invited to plan and supervise the training program. The aim was to provide at least one trained stoma care nurse to each teaching and general hospital. Material and methods Outline of the course The course was designed to cover the important aspects of stomas created in the gastro intestinal and genito urinary systems. Tracheostomy was not included in the course due to the different management strategies involved. It was designed as a 4 week full time certificate course. Key competencies recognized by previous authors [12] including stoma assessment, pouch fitting, pouch emptying, access to resources and supplies, and basic problem-solving skills as well as other content considered necessary by the local resource personnel were included in the curriculum. The course involved lectures and discussions by the experts in the respective fields in the country. The anatomical and physiological aspects, disease processes, medical and surgical management and clinical decision making components were taught by clinicians. The nursing component was taught by the second author. Formal teaching-learning activities included lectures, discussions, ward visits and clinic duties. In addition, the participants were asked to select a stoma patient and follow them up for the duration of the course. They were instructed to identify health and non-health problems of the patient and potential interventions were suggested. The end of course assessment included a report and a case presentation by each group. A panel of experts reviewed their reports and gave a feedback on changes and improvements. The entire program, except interaction with patients, was conducted in English. Ethical clearance for the study was obtained from the Ethics Review Committee of the National Hospital of Sri Lanka (NHSL). Participation The participants were selected from teaching and general hospitals from the entire country. From nearly 300 applicants, 61 participants were selected. They The Sri Lanka Journal of Surgery 2015; 33(1): 4-8 were subsequently grouped into groups of 10 for ward and clinic rotations. The feedback received indicated that participants engaged actively in the teachinglearning activities. After 6 months, the trainees participated in a 1-day sequel in which their knowledge, skills and patient records were assessed. They also presented short case scenarios of their patients with management dilemmas which were then discussed by the content experts. Analysis of effectiveness Participants completed a validated questionnaire [13] which evaluated basic demographic details and some aspects of patient care (staff confidence, staff resources and patient preparedness for discharge). The questions were derived from the “Survey of Ostomy Care questionnaire” which was a self-administered questionnaire used in a previous publication by Gemmil et al [13]. It contained a 15-item Likert scale (1-Strongly disagree, 5-Strongly agree) addressing confidence of the staff nurse and attitudes about the ability to care for patients with an ostomy. The questionnaire was administered on the first day of the program and at the completion. All surveys were anonymous and did not include identifying information. Continuous data were analysed using the mean, median and standard deviation. Repeated measure data were analysed using the Wilcoxon Signed Rank test. Correlations were identified using the Spearman correlation. Results Of the total 61 participants, 37 (60.6%) were females. The mean age was 34.5 (±5.5) years. The mean years in nursing profession was 9.5 (±5.5) years. All 15 domains of patient care that were measured had improved at the end of the program (Table 1). The biggest increase was seen in staff confidence category (average increase in score 63.5%) followed by staff resource (55.1%) and patient preparedness for discharge (43.8%). The 5 domains that had the biggest improvement in descending order are; the confidence to select different appliances to suit different conditions (P<0.0001), having material for proper patient teaching (P<0.001), confidence in educating patients ( P<0.001), confidence in having adequate knowledge (P<0.001) and confidence in assessing the stoma (P<0.001). 5 There were no statistically significant correlation between age, gender or years in nursing and the improvement in any of the measured domains. Score before participation Score after participation Improvement Sign ificance (%) Staff confidence 1. I feel confident that I can assess my patient’s ostomy well enough to care for my patient with an ostomy at this time. I feel confident that I have the skills to size, fit, and apply an ostomy appliance at this time. 2.8 4.57 63.2 <0.005 3.1 4.69 51.2 <0.005 I feel confident that I can advise my patients on community resources for supplies, education, and support well enough at this time. 2.5 4.44 77.6 <0.005 I feel confident that I have the background, knowledge, and experience in ostomy care to sufficiently care for my patients at this time. 2.7 4.41 63.3 <0.005 5. I feel confident that I can teach my patients well enough to care for themselves at home at this time. 3 4.57 52.3 <0.005 6. I feel confident that I know enough about the different types of appliances for the various ostomies and patients’ conditions to adequately select the proper ones for my patient at this time. 2 .3 3 4.43 90.1 <0.005 I care for ostomy patients often enough to keep up my skills in ostomy car e. 2 .9 5 4.34 47.1 <0.005 2. 3. 4. 7. Staff resources 8. I know who to call for answers about ostomy care should I encounter a problem. 2 .6 7 4.25 59.1 <0.005 9. I have the proper patient teaching materials (booklets, pamphlets, videos, etc.) to teach my patients/family about ostomy care. 1 .9 3 3.64 88.6 <0.005 10. If I am unsure about any aspect of ostomy care, there is someone available who can answer my questions. 3 .0 3 4.02 32.6 <0.005 11. I have enough time during my shift to teach ostomy care to my patient/family. 2 .6 6 3.52 32.3 <0.005 2 .3 3 3.79 62.6 <0.005 13. Patients are well infor med about what to expect regarding their condition, expected changes, and care at home at the time they leave the hospital. 2.8 4.1 46.4 <0.005 14. I feel that patients will get adequate follow-up care and teaching after they leave the hospital. 2 .8 9 3.98 37.7 <0.005 15. Patients are well prepared to care for themselves at home at the time they leave the hospital. 2 .7 9 4.11 47.3 <0.005 12. There is adequate staff education or in-service opportunities to keep my knowledge up-to-date on ostomy care. Patient preparedness for discharge Table 1. Improvements in different domains The Sri Lanka Journal of Surgery 2015; 33(1): 4-8 6 Discussion Stoma care nurses fulfil a variety of needs in patients with stomas; from pre-operative services such as counselling regarding the surgical procedure, the impact of an ostomy, ostomy management, sexual counselling and stoma site selection to postoperative services such as advising the family in ostomy care, diet, provide long-term follow-up and on-going counselling, education, surveillance for complications and community care [6]. Thus, their knowledge and skills directly affect the care and education of the patients [13] and patient satisfaction [14,15]. Nurses who perceive themselves to have high competence and a favourable perception of the ostomy patient were found to have had significantly more education [15]. Given the diversity of these requirements, their training and approach also need to be similarly comprehensive. Even in well-established colorectal health care services, there are deficiencies in nursing care [16]. Clayton et al [17] have also identified that patients whose surgery resulted in stomas are also less satisfied with health care delivery. Our initial assessment as well as the follow-up 1-day course revealed that the course was successful in delivering the necessary knowledge and skills for them to function independently. Knowles et al described a similar educational program in Scotland which achieved a significant improvement in disease-related knowledge, best practice statements for nursing issues and general issues and including attitudes that were maintained at four months [18]. They observed that the program achieved an increased index of achievement in almost all the areas concerned. A program conducted in the USA has also reported an improvement in the quality of care as the competency increased [17]. Cost effectiveness is a very important criterion in the assessment of the success of a training program. Even in Europe, Foubert et al [19] reported that cost and the need for frequent modifications of skills and knowledge are the principle limitations. Our program utilized local resource personnel and existing facilities and as a result required very little additional funding. We also noted that the improvement observed did not depend on the age, gender or the experience, indicating that this program is equally effective for a wide range of participants. The Sri Lanka Journal of Surgery 2015; 33(1): 4-8 In summary, our results suggest that a 4 week course provides adequate knowledge and confidence for trained nurses to function as stoma care nurses. The staff confidence domain having the biggest increase indicates that the program was successful in making them confident in managing stoma patients and functioning independently when required. Seeing an increase in all measured domains indicates that the program was successful in providing a comprehensive training and a holistic approach for the participants. A major factor affecting stoma care nurses in the west is the infrequency of interaction with patients with stoma and that their confidence is greatly influenced by an opportunity to practice the skills learned [13]. The 6 month post-workshop review proved that our participants were actively involved in stoma care patient management on a daily basis and therefore this is less likely to be a concern in our system. Another important component of the course was training the participants in patient education. Nurses are generally trained to care for the patient than carry out patient education [13]. Training nurses in how to educate patients during their regular shift recognizes the important role of patient education in patient retention of information. Teaching nurses how to teach also enhances nurses' confidence in their ability to teach. Conclusions We conclude that a 4 week full time program for trained nurses would suffice to impart the necessary knowledge and skills for a stoma therapy nurse. The entire program was carried out with the help of local resource persons with minimal cost. There was no statistically significant correlation between age, gender or years in nursing and the improvement in any of the measured domains. The findings would encourage health care providers from other developing countries to explore the possibility of training stoma care nurses. Authors' contributions DPW, AMPS, AT and DNS were involved in the study conception and design. DPW, SS and CS did the data acquisition, analysis and interpretation of data. DPW, SS, CS and DNS drafted the manuscript. All authors were involved in critical revisions of the manuscript. 7 References 1. Organizarion WH. Country Information: World Health Organization; 2012 [cited 2012]. Available from: http://www.who.int/countries/lka/en/index.html. 2. Jayasekara RS. Issues, challenges and vision for the future of the nursing profession in Sri Lanka: a review. Int Nurs Rev 2009;56(1):21-7. 3. Toth PE. Ostomy care and rehabilitation in colorectal cancer. Semin Oncol Nurs 2006;22(3):174-7. 4. Taylor C. Best practice in colorectal cancer care. Nurs Times 2012;108(12):22-5. 5. Porrett T. Extending the role of the stoma care nurse. Nurs Stand 1996;10(27):33-5. 6. Doughty D. Role of the enterostomal therapy nurse in ostomy patient rehabilitation. Cancer 1992;70(5 Suppl):1390-2. 7. Escueta NA. Role of the enterostomal therapy nurse in the care of ostomy patients. Philipp J Nurs 1991;61(3-4):147. 8. Comb J. Role of the stoma care nurse: patients with cancer and colostomy. Br J Nurs 2003;12(14):852-6. 9. Melville A. Why nurses must get involved in colorectal cancer management. Nurs Times 1998;94(11):56-8. 10. Programme NCC. Cancer Incidence Data: Sri Lanka Year 2001-2005. 2009. 11. Niriella MA, De Silva AP, Dayaratne AH, Ariyasinghe MH, Navarathne MM, Peiris RS, et al. Prevalence of inflammatory bowel disease in two districts of Sri Lanka: The Sri Lanka Journal of Surgery 2015; 33(1): 4-8 a hospital based survey. BMC Gastroenterol 2010;10:32. 12. Boarini JC, McNichol, J. L., Carmel, J., Goldberg, M., & Pruitt, L. . Fecal and urinary diversions: Management principles. J. C. Colwell MTG, & J. E. Carmel, editor. St. Louis, MO: Mosby; 2004. 13. Gemmill R, Kravits K, Ortiz M, Anderson C, Lai L, Grant M. What do surgical oncology staff nurses know about colorectal cancer ostomy care? J Contin Educ Nurs 2011;42(2):81-8. 14. Jackson AL, Pokorny ME, Vincent P. Relative satisfaction with nursing care of patients with ostomies. J ET Nurs 1993;20(6):233-8. 15. Moore S, Grant E, Katz B. Nurse perceptions of ostomy patients & their ostomy care competence. Home Care Provid 1998;3(4):214-20. 16. Lynch BM, Hawkes AL, Steginga SK, Leggett B, Aitken JF. Stoma surgery for colorectal cancer: a populationbased study of patient concerns. J Wound Ostomy Continence Nurs 2008;35(4):424-8. 17. Clayton HA, Boudreau L, Rodman R, Bak S, Embry K, Fortier J. Development of an ostomy competency. Medsurg Nurs 1997;6(5):256-67; quiz 68-9. 18. Knowles G, Hutchison C, Smith G, Philp ID, McCormick K, Preston E. Implementation and evaluation of a pilot education programme in colorectal cancer management for nurses in Scotland. Nurse Educ Today 2008;28(1):1523. 19. Foubert J, Faithfull S. Education in Europe: are cancer nurses ready for the future? J BUON 2006;11(3):281-4. 8 CONTINUING MEDICAL EDUCATION Management of the injured hand - basic principles of care K. Karunadasa Plastic and Reconstructive Surgical Unit, North Colombo Teaching Hospital, Ragama Introduction The aim of this second article is to introduce basic principles in the management of injured hand. It is difficult to provide a uniform guideline with “one injury–one solution” approach, as every case is different and unique. Detailed description of the management and surgical techniques of each structure is beyond the scope of this article. Hand injuries present either as an isolated injury or as a component of multiple injuries. In poly-traumatized patients hand injuries are not uncommon; often these patients are referred late. Resuscitation, stabilization and dealing with potentially life threatening injuries take priority over the injured hand. Haemostasis and initial wound irrigation along with a scrub of the injured hand is an acceptable during the initial management of multi trauma patient. Surgical management of the hand can be deferred till the patient is stabilized. However, there can be a significant negative impact on long-term quality of life if the hand injuries are not treated or significantly delayed [1]. Initial care Thorough assessment of the injured hand is performed and documented. This is aided with digital photography as a means communication, teaching and recording. The only potential life threatening problem in the injured hand is bleeding. Haemorrhage can be controlled initially with direct, firm compression and elevation unless there is a coagulopathy. Initial wound irrigation and dressing is performed at the emergency department. Elevation of the injured hand is vital to minimize the development of oedema. Emergency room splinting is a useful adjunct to reduce pain. Adequate regular analgesia should be provided. If local anaesthetic blocks are to be administered, it is essential Correspondence: K. Karunadasa E-mail: [email protected] The Sri Lanka Journal of Surgery 2015; 33(1): 9-13 that a neurological examination is carried and documented, prior to blocks. Immunization status for tetanus is assessed and addressed accordingly. Prophylactic antibiotics are started depending on the degree of contamination and should be used judiciously. Prophylactic antibiotics are not indicated in uncomplicated hand injuries without contamination [2]. Use of antibiotics should never replace the role of meticulous debridement and wound irrigation, which is the key in preventing infection [3]. Plain radiographs of two views should be the routine investigation in any injured hand. It is important to have true lateral and true antero-posterior views of the fingers, as rotated or angulated views might hide apparently minor fractures, as avulsion fractures and dislocations. In a true lateral view the radial and ulnar condyles of the phalangeal bones should overlap. An oblique view often provides additional information but cannot replace a true lateral view. Radiographs without a splint are the ideal as the splints mask details of bony injury. Further radiologic evaluation is indicated in selected cases by the expert. Management of open wound Wound debridement or wound excision, is the most important initial step that determines the functional outcome of the injured hand. This vital step should not be done by the junior surgeon in the team as proper wound excision requires experience and judgment. An adequate form of anaesthesia, tourniquet and magnification are essential prerequisites in operating on an injured hand. The affected area is irrigated with saline irrigation under anaesthesia. This step will not only help the mechanical debridement but also clean the whole region as the patient may not get a chance to wash the hand for a considerable period of time after the operation. Macroscopic contamination is carefully removed and devitalized tissue is debrided with sharp instruments. Loose strands of crushed and frayed tendons are carefully debrided preserving the healthy 9 length. In debriding the injured nerves and tendons it is important to be conservative than to be radical. At the end of the debridement and thorough irrigation, tourniquet is deflated to assess the viability of the tissue and haemostasis is completed with bipolar diathermy, clips or ligatures. Achieving adequate surgical access is mandatory in identifying the injured structures. These access incisions should be placed carefully and generally follows Brunner incisions, and are the extensions from the existing wounds. Skin flaps are raised with sharp dissection, guided by the palmar fascial bands and maintaining an adequate thickness. Narrow acute angled skin flaps are likely to become ischaemic. Straight line incisions on the volar aspect of fingers are strongly condemned as they will heal with contractures. It is important to remember that neurovascular bundles are just deep to the transversely oriented fibres of the palmar fascia in the palm. In the fingers the neurovascular bundles are subcutaneous in relation to mid lateral lines. Management of vascular injury Revascularization of digits, hands or wrist-proximal injuries require microsurgical expertise and appropriate cases need to be transferred to equipped centres. Prompt recognition of vascular compromise in partial amputations and crush injuries is imperative to avoid delay. Duration of ischaemia is critical for the long term recovery of small muscle function and nerve recovery. Thorough debridement, adequate exposure, bone shortening and achieving skeletal stability are essential prerequisites prior to anastomosing injured vessels. The revascularised hand can be functionally useless, unless all the nerves and tendons are repaired. The surgeon should select the indicated cases as some amputations may not be technically possible as in severe crush injuries, and unstable patients with concomitant severe injuries [4]. Soft tissue cover Soft tissue coverage is crucial in terms of achieving healing without infection and to protect the repairs underneath. Majority of open hand trauma are amenable for immediate closure. In the presence of significant contamination, a subsequent debridement may be indicated with an interval of 24 to 48 hours. Primary closure is the best form of achieving early wound The Sri Lanka Journal of Surgery 2015; 33(1): 9-13 closure which is the usual case in cut injuries and majority of lacerations. In the case of soft tissue loss as in significant crush injuries and degloving injuries, soft tissue coverage has to be achieved. If the wound is a graftable, vascularised bed a skin graft can be used. A popular myth is that “one should wait till the wound is granulated as a requirement for a skin graft”. In fact, primarily skin grafted hands do better than with a delayed graft. Definitive cover in the form of a graft or flap should ideally be provided within few days rather than weeks. The delay in achieving cover will promote granulation tissue that is destined to form scar, which is considered the enemy of a well-functioning hand. There are absolute indications for a flap (vascularised tissue); exposed bone devoid of periosteum, bare tendon without paratenon, exposed cartilage and joints and exposed neurovascular structures. A wound with these structures exposed should be referred to a plastic surgical unit without delay. The ultimate aim of soft tissue coverage is to achieve healed wounds with stable and durable coverage. It is best the coverage over the tips and volar aspect to be sensate [5, 6]. Skeletal injury Fractures and dislocations of small bones of the hand are difficult and often unforgiving injuries. Many different fracture patterns are described in hand bones. Comprehensive discussion of each fracture is beyond the scope of this article. Stabilisation of the bony skeleton of the hand is essential prior to neurovascular or tendon repairs. General principles of fracture management apply to hand fractures as for other bones in the body. But special attention should be paid in meticulous and gentle tissue handling around these small bones. The impact of scar formation and the development of stiffness is significantly high in hand fractures. Relatively thin soft tissue envelope makes access easy, but maintaining cover for the injured bone is difficult. Majority of closed, stable fractures heal with splinting for 3–4 weeks followed by active moving [7,8]. Significant displacement, angulation and rotation have to be treated by closed manipulation or open reduction. Indications for operative intervention exist for individual fractures. In finger fractures, correction of significant rotational deformity is mandatory to avoid overriding and scissoring of fingers [9]. The aim of surgical intervention is to correct the deformity and to achieve stable fixation to allow early movement. Here the benefit of surgical intervention is weighed against 10 the surgical trauma and its consequences. Wounds with open fractures should be thoroughly and promptly debrided and early soft tissue cover should be achieved. K-wires are widely used fixation devices which are cheap, quick and easily inserted. It is used after open or closed reduction and inserted percutaneously with radiologic guidance. K-wires involve less tissue dissection and operative trauma compared with plate and screw fixation. The K-wires are removed in the clinic after 3-4 weeks. The drawback with K wires is that the stability of fixation may not be adequate to allow early active movement. Rigid fixations are favoured as this will allow early active movements of the fingers. They include plate and screws, lag screws, intraosseous wiring and rarely intramedullary nails. These involve significant tissue dissection and subsequent scar formation and stiffness [10,11]. Tendon injury Primary repair of tendon injuries are the standard practice. Tendon injuries should be repaired early as the wound is easy to manage, the tendon ends are fresh, undue delay lead to changes in tendon ends and proximally in the muscle belly. In delayed cases the repair is technically difficult and sometimes primary repair may be impossible, and interposition tendon graft or staged tendon reconstruction would be the option. In flexor tendon injuries all the tendons must be repaired, and in the finger preferably both Flexor Digitorum Profundus (FDP) and Flexor Digitorum Superficialis (FDS) tendons are repaired. Isolated FDP repair, excising the FDS, is considered in occasions with severely injured, unclean or ragged tendon ends or insufficient tendons. In zone one injuries tendon to bone repairs are performed, traditionally with a core suture in the proximal tendon passed through the base of the distal phalanx or around it using the needle drill technique. The suture is tied on the nail dorsally to be removed in six weeks. Development of suture anchors has replaced this technique but in the authors setup the traditional method is still in practice. Zone two injures are the most challenging as both FDS and FDP tendons are running in the crowded flexor sheath and inherent with a higher chances of poor outcome. Zone 3, 4, and 5 flexor tendon injuries are treated with the same principles as for zone two, but these are more spacious and technically easy [12,13]. Anatomic multi strand locking suture techniques are The Sri Lanka Journal of Surgery 2015; 33(1): 9-13 favoured as they allow early active range of movement exercise. Repair suture should consist of a core suture and an epitendinous suture. In selecting a core suture, material used, caliber, number of strands crossing the repair, knot placement and suture locking are the important aspects to consider [14]. Epitendinous suture of fine non absorbable material would add the fine finishing touch to the repair site and helps to increase the strength. Polyester, polypropylene, and nylon are the commonly used material [15,16]. Repair site bunching and gap formations should be avoided. Bulky repair site may trap under a pulley. Poor repair can lead to gap formation and is associated with increased risk of repair rupture. The authors preferred technique is for strand locking core suture and circumferential epitendionus suture with non-absorbable material as polyester or polypropylene. Atraumatic surgical technique in retrieving and handling the tendons is essential to minimize subsequent scar formation. In retrieving the tendon ends several windows are made in the fibrous flexor sheath without damaging the full length of the pulleys. Maximal preservation of the A2 and A 4 pulleys is important to prevent bowstringing. In the case of severely injured pulleys can be reconstructed. Fine hypodermic needles are used to transfix the tendons in stabilizing the ends for the repair. The troublesome adhesion formation is minimized with early active movement of the fingers. Hence strict adherence to rehabilitation protocols is recommended for a good outcome [17,18]. Flexor tendon injuries remain a difficult problem in hand trauma, in terms of achieving optimal functional recovery. Hence these should not be left to be repaired by the inexperienced junior operator. Undesirable outcomes as stiffness, repair rupture, flexion contractures and adhesions should be managed by experts with the involvement of the hand therapist. Tendon repair re-explorations, tenolysis and staged tendon reconstruction should be done carefully in indicated patients and are not the operations for the occasional hand surgeon [19,20]. Extensor tendons are easily accessed as their subcutaneous location. Extensor retinaculum, juncturae, sagittal bands and retinacula ligaments are the structures that keep the extensor tendons in place. As extensor tendons are thin in calibre and flat distally the repair techniques are modified accordingly and standard core suture is impossible. Running suture or cross-stich is used in these areas. Proximally they become thick and 11 a core suture is indicated especially in wrist and forearm. Different therapy protocols are used to suit the zone of the injury. Traditionally zone 1 and 2 injuries are immobilized with splints for 6 weeks [21,22]. Further details of the rehabilitation of tendon injuries will be discussed in the third article. Nerve injury Early repair of injured nerves is essential for re-innervation of specific muscles and restoration of sensibility in the hand which are imperative for reasonable function. Proximal injury of the upper extremity nerves are notorious for long lasting disabilities as, loss of fine sensory and motor function. Recovery of sensation requires a long time to reach the optimum and undue delay is likely to compromise the ultimate sensibility of the hand. Often protective sensibility recovers following nerve repair but tactile discriminative function seldom recovers. Microsurgical technique including magnification is essential in handling peripheral nerves. Tension free nerve repairs should be performed with micro sutures such as 8-0 or 9-0 non absorbable monofilament. In sharp cut injuries primary repair is easy, since there is no loss of nerve tissue. Positional changes as flexing a joint to gain length for a primary repair, in the case of segmental nerve loss are not recommended. Inadvertent dissection or mobilization of a nerve over a significant length is strongly discouraged as this can potentially devascularise the nerve and stimulate formation of scar tissue. Epineurial repair is the commonly practiced technique where fascicular arrangement should be matched under magnification. Cross sectional anatomy and the pattern of vasa nervorum is the guide for the proper match. Poor repair technique often lead to fascicular escape and neuroma formation, resulting in poor sensory and motor recovery as well as a symptomatic neuroma [23]. In the case of a segmental nerve loss, interposition nerve grafts should be used. In the case of extensive soft tissue loss or severe contamination, primary nerve repair may be delayed till the rest of the wound is stabilized. In unsuitable wound bed, as in established infection or the presence of tissue with questionable viability, primary nerve grafting should be deferred. In such occasions, delayed reconstructive procedures as, delayed nerve grafting, nerve transfers, tendon transfers or joint fusions are indicated. Post-operative therapy is invaluable in The Sri Lanka Journal of Surgery 2015; 33(1): 9-13 sensory and motor re-education and rehabilitation. Early active movements within a protective splint facilitate nerve gliding. Desensitisation is useful in managing hypersensitive areas. Lack of nerve regeneration, chronic paraesthesia, symptomatic neuroma and complex regional pain can complicate the recovery after a nerve injury [24]. Fingertip injury Fingertip injuries are unique in that they are seemingly minor but inherently associated with specialised problems. The priority is to provide the best possible coverage with good quality skin which is sensate. They are commonly managed with local nerve blocks except in small children. Crushed fingertip is probably the commonest hand injury in the paediatric group. Simple pulp lacerations are often primarily repaired but when there is a significant pulp loss it should be reconstructed. In the presence of exposed distal phalanx bone a flap is indicated, while a hypothenar graft can be used in replacing the pulp skin. The amount of remaining tissue and its configuration determines the reconstructive option. Nail bed injuries require careful repair with fine absorbable suture. Nail plate or a substitute is placed as a splint after nail bed repair. Minor skin loss is often managed with dressings, although they take at least two to three weeks to heal. A distal phalanx tuft fracture is often present in tip crush injuries which are generally managed only with a soft tissue repair. Even though a large number of flaps are described for the reconstruction of tissue loss of the fingertip, they are generally managed with less traumatic surgical techniques. More proximal injuries with non-salvageable tips require proper amputation with primary repair. The potential secondary deformities of the fingertip injury can cause a great deal of inconvenience to the patient preventing the use of their hand [25]. Immediate post-operative care Local anaesthetic nerve blocks are an essential part in alleviating post-operative pain. Regular and adequate analgesia is mandatory in hand injury as this is the key to allow early rehabilitation. The dressing and the splints used at the end of the operation should be tailored according to the injury and the repairs done. Elevation of the hand is essential in reducing the inevitable oedema. Rehabilitation of the injured hand is critical to 12 ensure the best outcome after any form of trauma. Any hand injury management is incomplete without appropriate rehabilitation in the post repair period. Conclusion Hand is a complex anatomical organ which is frequently exposed to injuries. Complex and severe hand injuries can potentially exclude young people from their professional life, often contributed to by improper management. Detailed assessment of the injured hand is the key for the successful repair of the damaged structures. The outcome depends primarily on the prompt and skilled treatment. The treating surgeon should have a sound understanding of the rehabilitation of the injured hand and be patient enough to complete the appropriate therapy programs. References 1. Ciclamini D, Panero B, Titolo P, et al. Particularities of hand and wrist complex injuries in polytrauma management. Injury 45:448-51, 2014. 2. Al-Nammari SS, Reid AJ. Towards evidence based emergency medicine: best BETs from the Manchester Royal Infirmary. Prophylactic antibiotics are not indicated in uncomplicated hand lacerations. Emerg Med J 24:218, 2007. 3. Tsai E, Failla JH. Hand infections in the trauma patient. Hand Clin15 :373-86, 1999. 4. Prucz RB, Friedrich JB. Upper extremity replantation: current concepts. PlastReconstrSurg133 :333-42, 2014. 5. Rockwell WB, Lister GD. Soft tissue reconstruction. Coverage of hand injuries. OrthopClin North Am 24 :41124,1993. 6. Sabapathy SR, Bajantri B. Indications, selection, and use of distant pedicled flap for upper limb reconstruction. Hand Clin 30:185-99, 2014. 7. Gregory S, Lalonde DH, Fung Leung LT. Minimally invasive finger fracture management: wide-awake closed reduction, K-wire fixation, and early protected movement. Hand Clin 30 :7-15, 2014 8. Bloom JM, Hammert WC. Evidence-based medicine: metacarpal fractures. PlastReconstrSurg 133:1252-60, 2014. 9. Shah CM, Sommerkamp TG. Fracture dislocation of the The Sri Lanka Journal of Surgery 2015; 33(1): 9-13 finger joints. J Hand Surg Am 39 :792-802, 2014. 10. Shaftel ND, Capo JT. Fractures of the digits and metacarpals: when to splint and when to repair? Sports Med Arthrosc 22 :2-11,2014. 11. Kollitz KM, Hammert WC, VedderNB,et al. Metacarpal fractures: treatment and complications. Hand 9:1623,2014. 12. Wong JK, Peck F. Improving results of flexor tendon repair and rehabilitation. PlastReconstrSurg 134:913-25, 2014. 13. Neumeister MW, Amalfi A, Neumeister E. Evidencebased medicine: Flexor tendon repair. PlastReconstrSurg 133 :1222-33, 2014. 14. Hardwicke JT, Tan JJ, Foster MA, et al. A systematic review of 2-strand versus multistrand core suture techniques and functional outcome after digital flexor tendon repair. J Hand Surg Am 39 :686-695, 2014. 15. Tolerton SK, Lawson RD, Tonkin MA. Management of flexor tendon injuries - Part 2: current practice in Australia and guidelines for training young surgeons. Hand Surg 19 :305-10, 2014. 16. Savage R. The search for the ideal tendon repair in zone 2: strand number, anchor points and suture thickness. J Hand Surg (Eur) 39:20-9,2014. 17. Lutsky KF, Giang EL, Matzon JL. Flexor tendon injury, repair and rehabilitation. OrthopClin North Am 46 :6776, 2015. 18. Sandvall BK, Kuhlman-Wood K, Recor C, et al. Flexor tendon repair, rehabilitation, and reconstruction. PlastReconstrSurg 132:1493-503,2013. 19. Elliot D, Giesen T. Avoidance of unfavourable results f o l l o w i n g p r i m a r y f l e x o r t e n d o n s u r g e r y. Indian J PlastSurg 46:312-24, 2013. 20. Dy CJ, Hernandez-Soria A, Ma Y, et al. Complications after flexor tendon repair: a systematic review and meta-analysis. J Hand Surg (Am) 37:543-551,2012. 21. Amirtharajah M, Lattanza L. Open Extensor Tendon Injuries. J Hand SurgAm 40 :391-397, 2015. 22. Matzon JL, Bozentka DJ.Extensor tendon injuries. J Hand Surg Am 35 :854-61, 2010. 23. S l o a n E P. N e r v e i n j u r i e s i n t h e h a n d . Emerg Med Clin North Am 11:651-70,1993. 24. Lundborg G, Rosén B. Hand function after nerve repair. ActaPhysiol (Oxf) 189:207-17, 2007. 25. Lemmon JA, Janis JE, Rohrich RJ. Soft-tissue injuries of the fingertip: methods of evaluation and treatment. An algorithmic approach. PlastReconstrSurg 122:105e117e, 2008. 13 SYMPOSIUM ON GORD Diagnosis and management of gastro-oesophageal reflux disease N.P. Dinamithra, N.M.M. Nawarathne Gastro-enterology and Hepatology Unit, National Hospital of Sri Lanka Introduction Gastro-oesophageal reflux disease (GORD) is a common disease encountered by both gastroenterologists and generalists alike. This article will provide an overview of GORD and its presentation, extra oesophageal manifestations, complications and recommendations for an approach to the diagnosis and management of this important disease. Epidemiology Epidemiologic estimates of the prevalence of GORD are based primarily on the typical symptoms of heartburn and regurgitation. A systematic review found the prevalence of GORD to be 10 –20 percent in the Western world [2]. Community prevalence of GORD in Sri Lanka is not known but a single study done by Nawarathne et al found it closer to 15% [1]. While clinically troublesome heartburn is seen in about 6 percent of the population [3], chest pain may be the sole presenting complaint of GORD [4,5]. It is imperative to distinguish cardiac from non-cardiac chest pain, before considering GORD as the cause of chest pain. Although the symptom of dysphagia can be associated with uncomplicated GORD, its presence warrants investigation for a potential complication including motility disorders, ring, stricture or malignancy [6] A systematic review found that 38 % of the general population has dyspepsia. Dyspepsia was more frequent in patients with GORD than those without. The symptoms of epigastric pain, early satiety, belching and bloating were more likely to be PPI-responsive compared to nausea. In general, these symptoms can be considered to be a part of GORD if they respond to a PPI trial [7]. Symptoms at night have a greater impact on quality of life (QOL) when compared to day symptoms. Correspondence: N.P. Dinamithra E-mail: [email protected] The Sri Lanka Journal of Surgery 2015; 33(1): 14-19 Therefore, nocturnal symptoms and sleep disturbances are important to elucidate when dealing with GORD patients [8]. Aging increases the prevalence of erosive oesophagitis, i.e. Los Angeles (LA) grades C and D [9]. Barrett's oesophagus increases in prevalence after age 50, especially in Caucasian males [10].The patients with erosive oesophagitis are more likely to be men. Women are more likely to have non erosive reflux disease (NERD). Barrett's oesophagus is more frequent in men compared to women [11]. The male to female, gender ratio for oesophageal adenocarcinoma is estimated to be 8:1 [10]. There is a definite link between GORD and obesity. Several meta-analysis found an association between body mass index (BMI), waist circumference, weight gain and the presence of symptoms and complications of GORD including erosive reflux disease (ERD) and Barrett ' s oesophagus [12,13]. Establishing the diagnosis of GORD The diagnosis of GORD is mainly clinical but it is made using a combination of symptom presentation, objective testing with endoscopy, ambulatory reflux monitoring, and response to a trial of anti-secretory therapy. The symptoms of heartburn and regurgitation are the most reliable to arrive at a presumptive diagnosis based on history alone. However, these are not as sensitive as most believe. Empiric PPI therapy (a PPI trial) is a reasonable approach to confirm GORD when it is suspected in patients with typical symptoms. It has a sensitivity of 78 percent and specificity of 54 percent. Dysphagia has historically been an alarm symptom and an indication for early endoscopy. Based on retrospective case control studies respiratory symptoms have been associated with GORD. In addition, dental erosions, sinusitis, chronic laryngitis and voice disturbance have similarly been associated with GORD. Endoscopic findings of GORD include erosive 14 oesophagitis, strictures, and a columnar lined oesophagus or Barrett's oesophagus. As such, endoscopy has excellent specificity for the diagnosis of GORD especially when erosive oesophagitis is seen. In a study done on Sri Lankan patients who had symptoms suggestive of GORD, hiatus hernia (HH), columnar lined oesophagus (CLO) and reflux oesophagitis (RO) were found in 14.3%, 9.5% and 13.3% respectively [1]. Based on current literature the use of routine biopsy of the oesophagus to diagnose GORD cannot be recommended in a patient with heart- burn and a normal endoscopy. In addition, the practice of obtaining mucosal biopsies from a normal appearing gastro-oesophageal junction (GOJ) has not been demonstrated to be useful in GORD patients [14]. Oesophageal manometry is of limited value in the primary diagnosis of GORD. Neither a decreased lower oesophageal sphincter pressure, nor the presence of a motility abnormality is specific enough to make a diagnosis of GORD. Manometry should be used to aid placement of the transnasal pH-impedance probes and is also recommended before consideration of antireflux surgery, primarily to rule out achalasia or severe hypomotility. Ambulatory reflux monitoring (pH or impedance-pH) is the only test that allows for determining the presence of abnormal oesophageal acid exposure, reflux frequency and symptom association with reflux episodes. GORD is common during pregnancy and manifests as heartburn, and may begin in any trimester. One study found its onset to be around 50 percent in the first trimester, 40 percent in the second trimester, and 10 percent in the third trimester [15]. Severity also increased throughout pregnancy. Despite its frequent occurrence during pregnancy, heartburn usually resolves after delivery [16]. In the occasional pregnant patient who does require testing, upper GI endoscopy is the test of choice, but should be reserved for patients whose symptoms are refractory to medical therapy or who have suspected complications. If possible however, upper GI endoscopy should be delayed until after the first trimester. Management of GORD Lifestyle interventions are part of therapy for GORD. Counseling is often provided regarding weight loss, elevation of head end of bed, tobacco and alcohol cessation, avoidance of late-night meals, and cessation The Sri Lanka Journal of Surgery 2015; 33(1): 14-19 of foods that can potentially aggravate reflux symptoms including caffeine, coffee, chocolate, spicy foods, highly acidic foods such as oranges and tomatoes, and foods with high fat content. There was an increase in oesophageal acid exposure times with tobacco and alcohol consumption in addition to ingestion of chocolate and fatty foods. However, tobacco and alcohol cessation (4 trials) were not shown to raise lower oesophageal sphincter pressure (LOSP), improve oesophageal pH, or improve GORD symptoms. A recent systematic review concluded that there was lack of evidence that consumption of carbonated beverages causes or provokes GORD [17]. Weight gain even in subjects with a normal BMI has been associated with new onset of GORD symptoms [18]. Multiple cohort studies have demonstrated reduction in GORD symptoms with weight loss [19, 20]. A large case control study based on a Nurses Health Cohort demonstrated a 40 percent reduction in frequent GORD symptoms for women who reduced their BMI by 3.5 or more compared with controls [18]. Assumption of the recumbent position has been associated with worsening of oesophageal pH values and GORD symptoms. Three randomized controlled trials have demonstrated improvement in GORD symptoms and oesophageal pH values with head end elevation of the bed [21, 22]. Medical options for patients failing lifestyle modifications include antacids, histamine-receptor antagonists (H2RA), or PPI therapy. PPI therapy has been associated with superior healing rates and decreased relapse rates compared with H2RAs and placebo for patients with erosive oesophagitis [24]. A 1997 meta-analysis demonstrated superior healing rates for all grades of erosive oesophagitis using PPI therapy compared with H2RAs, sucralfate, or placebo [25]. PPIs showed a significantly faster healing rate (12%) vs. H2RAs (6%) and placebo (3%). A Cochrane systematic review in patients with non-erosive reflux disease demonstrated superiority for PPI therapy compared with H2RAs and prokinetics for heartburn relief [26]. There are seven PPIs available in the market at present. Meta-analyses fail to show significant difference in efficacy for symptom relief between PPIs [27]. All of the PPIs with the exception of omeprazole- sodium bicarbonate 15 and dexlansoprazole, should be administered 30–60 minute before meals to assure maximal efficacy. It would be expected that 70 – 80 percent of patients with ERD and 60 percent of patients with NERD would demonstrate complete relief on PPI therapy. Risk factors for lack of symptom control have included patients with longer duration of disease, presence of hiatal hernia, extra oesophageal symptoms, and lack of compliance [28]. Maintenance PPI therapy should be administered for GORD patients who continue to have symptoms after PPI is discontinued and in patients with complications including erosive oesophagitis and Barrett's oesophagus (BO). In patients found to have any length of BO, retrospective studies have suggested a decreased risk for dysplasia in patients continuing PPI usage [29]. Medical options for GORD patients with incomplete response to PPI therapy are limited. The addition of bedtime H2RA has been recommended for patients with symptoms refractory to PPI. Prokinetic therapy with metoclopramide in addition to PPI therapy is another option often considered for these patients. Combination therapy of Metoclopramide with H2RA has not been shown to be more effective compared with H2RA or prokinetic therapy alone [30]. The other option is to use baclofen for refractory GORD patients. Baclofen, a GABA (b) agonist, has been demonstrated to be effective in GERD by its ability to reduce transient LOS relaxations [31], and reflux episodes [32]. Potential surgical options for GORD include laparoscopic fundoplication or bariatric surgery in the obese. Reasons to refer GORD patients for surgery may include desire to discontinue medical therapy, non-compliance, side-effects associated with medical therapy, the presence of a large hiatal hernia, oesophagitis refractory to medical therapy, or persistent symptoms documented to be caused by refractory GORD. With the introduction of oesophageal pH-impedance monitoring, patients found to have abnormal amounts of non-acid reflux on PPI therapy with good symptom correlation may be considered for surgery [34]. Refractory dyspeptic symptoms including nausea, vomiting and epigastric pain are less likely to demonstrate symptomatic response. The highest surgical responses are seen in patients with typical symptoms of heartburn and/or regurgitation that demonstrate good response to PPI therapy. Surgical options, its recommendation and The Sri Lanka Journal of Surgery 2015; 33(1): 14-19 evidence are shown in table 1. 1. Surgical therapy is a treatment option for long-term therapy in GORD patients. (Strong recommendation, h i g h l e v e l o f e v i d e n c e ) 2. Surgical therapy is generally not recommended in patients who do not respond to PPI therapy. (Strong recommendation, high level of evidence) 3. Preoperative ambulatory pH monitoring is mandatory in patients without evidence of erosive oesophagitis. All patients should undergo preoperative manometry to rule out achalasia or scleroderma-like esophagus. (Strong recommendation, moderate level of evidence) 4. Surgical therapy is as effective as medical therapy for carefully selected patients with chronic GORD when performed by an experienced surgeon. (Strong recommendation, high level of evidence) 5. Obese patients contemplating surgical therapy for GORD should be considered for bariatric surgery. Gastric bypass would be the preferred operation in these patients. (Conditional recommendation, m o d e r a t e l e v e l o f e v i d e n c e ) 6. The usage of current endoscopic therapy or transoral incisionless fundoplication cannot be recommended as an alternative to medical or traditional surgical t h e r a p y. ( C o n d i t i o n a l r e c o m m e n d a t i o n , m o d e r a t e l e v e l o f e v i d e n c e ) Table 1. Surgical options for GORD [33] Extra oesophageal presentations of GORD The spectrum of clinical presentations attributed to GORD has expanded from typical oesophageal symptoms of heartburn and regurgitation, to an assortment of extra oesophageal manifestations including respiratory and laryngeal symptoms. A number of epidemiological studies have identified an association between GORD and these extra oesophageal symptoms, but causality cannot be concluded from these studies. A systematic review of 28 studies found that symptoms of GORD and abnormal 24-hour pH monitoring were present in 59 and 51% of asthma patients, but concluded that there was little data to clarify the direction of causality [35]. Cohort studies suggest that GORD may be the cause in 21–41 percent of chronic nonspecific cough [36]. GORD refractory to treatment with PPIs We are seeing increasing numbers of patients treated empirically with PPIs for symptoms that are suspected to be due to GORD, but who do not respond to these medications. The term refractory GORD encompasses 16 a heterogeneous group of patients that may differ in symptom frequency and severity, PPI dosing regimen (once or twice daily), and response to therapy (from partial to absent). Dealing with this category of patients is shown in table 2 and figure 1 [33] with the level of evidence and degree of recommendation. 1. The first step in management of refractory GORD i s o p t i m i z a t i o n o f P P I t h e r a p y. ( S t r o n g recommendation, low level of evidence) 2. Upper endoscopy should be performed in refractory patients with typical or dyspeptic symptoms principally to exclude non-GORD etiologies. (Conditional recommendation, low level of evidence) 3. In patients in whom oextraesophageal symptoms of GORD persist despite PPI optimization, assessment for other etiologies should be pursued through concomitant evaluation by ENT, pulmonary, and allergy specialists (Strong recommendation, low level of evidence) 4. Patients with refractory GORD and negative evaluation by endoscopy (typical symptoms) or evaluation by ENT, pulmonary, and allergy specialists (extra oesophageal symptoms), should undergo ambulatory reflux monitoring (Strong recommendation, low level of evidence) 5. Reflux monitoring off medication can be performed by any available modality (pH or impedance-pH) (Conditional recommendation, moderate level of evidence). Testing on medication should be performed with impedance-pH monitoring in order to enable measurement of nonacid reflux. (Strong recommendation, moderate level of evidence) 6. Refractory patients with objective evidence of ongoing reflux as the cause of symptoms should be considered for additional anti reflux therapies that may include surgery. (Conditional recommendation, low level of evidence). Patients with negative testing are unlikely to have GORD and PPI therapy should be discontinued. (Strong recommendation, low level of evidence) Table 2. Management of "refractory" GORD [33] Complications associated with GORD Numerous “complications” have been associated with GORD including erosive oesophagitis, stricture, and Barrett's oesophagus (BO). Obesity has been demonstrated to be a risk factor for symptoms, ERD, BO, and adenocarcinoma. It may be that the presence of an abnormal waist-to-hip ratio is the greatest risk factor for the presence of BO [37]. There are limited data to suggest that a columnar lined The Sri Lanka Journal of Surgery 2015; 33(1): 14-19 Figure 1. Algorithm for the evaluation of refractory gastroesophageal reflux disease (GORD) [33]. oesophagus (Barrett's oesophagus) can be obscured by any grade of erosive oesophagitis, most commonly it is obscured by grades C and D [38,39] . On the basis of these data, a repeat endoscopy after a minimum 8-week course of PPI therapy is recommended in patients with grades C and D oesophagitis but also can be considered in lower grades. Peptic strictures are infrequent in practice, and are likely related to the widespread use of anti-secretory therapy. Strictures tend to occur most often in Caucasians, older patients with a longer duration of untreated symptoms, and in the setting of abnormal oesophageal motility. Intra lesional corticosteroids (40 mg of triamcinolone injected in four 1 ml aliquots) in a four quadrant pattern can be considered in peptic strictures refractory to dilation. Barrett's oesophagus is the only complication of GORD with malignant potential. BO can be found in 5 to 15 percent of patients who undergo endoscopy for symptoms of GORD [40] and tends to be seen at the higher end of this range in patients with long duration of symptoms, who are over the age of 50, male, and Caucasian. Conclusion In summary, refractory GORD remains a difficult clinical challenge. Many pathological mechanisms have 17 been proposed as causes of refractory symptoms but, in most cases, data supporting the hypotheses remain equivocal. The work-up of a refractory patient should clearly include a careful history, and the consideration of alternative diseases that require alternative treatments is paramount. Reflux monitoring studies are helpful in determining the presence or absence of GORD, and reflux–symptom analysis is a very important tool that presently requires further refinement and better outcome studies to aid our interpretation. References 1. Navarathne M. M. Navarathne & Vasitha Abeysuriya & A. Ileperuma & U. L. Thoufeek. Endoscopic observations around the gastroesophageal junction in patients with symptomatic gastroesophageal reflux disease in South Asia. Indian J Gastroenterol (2010) 29:184–186 2. Dent J ,El Serag HB, Wallander M A et al. Epidemiology of gastrooesophageal reflux disease: a systematic review. Gut 2005 ; 54 : 710 – 7. 3. Camilleri M ,Dubois D ,Coulie B et al. Prevalence and socioeconomic impact of upper gastrointestinal disorders in the United States: results of the US Upper Gastrointestinal Study. Clin Gastroenterol Hepatol 2005 ; 3 : 543 – 52 4. Atkins D, Briss PA, Eccles M et al. Systems for grading the quality of evidence and the strength of recommendations II: pilot study of a new system. BMC Health Serv Res 2005;5:25–36 5. Vakil N, van Zanten SV, Kahrilas P et al. The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus. Am J Gastroenterol 2006; 101:1900 – 20. 6. Vakil NB, Traxler B, Levine. Dysphagia in patients with erosive esophagitis: prevalence, severity, and response to proton pump inhibitor treatment. Clin Gastroenterol Hepatol 2004;2:665–8. 7. Gerson LB, Kahrilas PJ, Fass R. Insights into gastroesophageal reflux disease-associated dyspeptic symptoms. Clin Gastroenterol Hepatol 2011;9: 824–33. 8. Gerson LB, Fass R. A systematic review of the definitions, prevalence, and response to treatment of nocturnal gastroesophageal reflux diseas. Clin Gastroenterol Hepatol 2009;7:372–8 . 9. Johnson DA, Fennerty MB. Heartburn severity underestimates erosive esophagitis severity in elderly patients with gastroesophageal reflux disease. Gastroenterology 2004; 126:660 –4 . 10. Rubenstein JH, Scheiman JM, Sadeghi S et al. Esophageal adenocarcinoma incidence in individuals with gastroesophageal reflux: synthesis and estimates from population studies .Am J Gastroenterol 2011;106:254 – 60. The Sri Lanka Journal of Surgery 2015; 33(1): 14-19 11.Lin M, Gerson LB, Lascar R et al. Features of gastroesophageal reflux disease in women. Am J Gastroenterol 2004; 99:1442–7 . 12.Corley D A, Kubo A. Body mass index and gastroesophageal reflux disease: a systematic review and meta-analysis . Am J Gastroenterol 2006 ; 101 : 2619–28. 13.Hampel H, Abraham NS, ElSerag HB. Meta-analysis: obesity and the risk for gastroesophageal reflux disease and its complications. Ann Intern Med 2005;143:199– 211. 14. Takubo K, Honma N, Aryal G et al. Is there a set of histologic changes that are invariably refl ux associated? Arch Pathol Lab Med 2005 ; 129 : 159 – 63 . 15. Olans LB, Wolf J. Gastroesophageal reflux in pregnancy. Gastrointest Endosc Clin N Am 1994 ; 4 : 699 – 712 . 16. Richter J. Review article: the management of heartburn in pregnancy. Aliment Pharmacol Th er 2005 ; 22 : 749 – 57 . 17.Johnson T, Gerson L, Hershcovici T et al. Systematic review: the effects of carbonated beverages on gastrooesophageal reflux disease. Aliment Pharmacol Ther 2010 ; 31 : 607 – 14 . 18. Jacobson BC, Somers SC, Fuchs CS et al. Body-mass index and symptoms of gastroesophageal reflux in women. N Engl J Med 2006 ; 354 : 2340– 8 . 19. Fraser-Moodie CA, Norton B, Gornall C et al. W eight loss has an independent beneficial effect on symptoms of gastro-oesophageal reflux in patients who are overweight. Scand J Gastroenterol 1999; 34 : 337– 40. 20. Mathus-Vliegen L M, T ytgat G N. Twenty-four-hour pH measurements in morbid obesity: effects of massive overweight, weight loss and gastric distension. Eur J Gastroenterol Hepatol 1996 ; 8 : 635 – 40 . 21. Gagne DJ, Dovec E, Urbandt JE. Laparoscopic revision of vertical banded gastroplasty to Roux-en-Y gastric bypass: outcomes of 105 patients . Surg Obes Relat Dis 2 011; 7 : 4 93– 9 . 22. Stanciu C, Bennett JR. Effects of posture on gastrooesophageal reflux . Digestion 1977 ; 15 : 104 – 9. 23. Pollmann H, Zillessen E, Pohl J et al. Effect of elevated head position in bed in therapy of gastroesophageal reflux . Z Gastroenterol 1996 ; 34(Suppl 2) : 93 – 9 . 24. Labenz J, Malfertheine P. Treatment of uncomplicated reflux disease . World J Gastroenterol 2005 ; 11 : 4291 – 9 25. Chiba N, De Gara CJ, Wilkinson JM et al. Speed of healing and symptom relief in grade II to IV gastroesophageal reflux disease: a meta-analysis .Gastroenterology 1997 ; 112 : 1798 – 810 . 26. Van Pinxteren B, Sigterman K E, Bonis P et al. Short-term treatment with proton pump inhibitors, H2-receptor antagonists and prokinetics for gastro-oesophageal reflux disease-like symptoms and endoscopy negative reflux disease Cochrane Database Syst Rev : Cd002095. 27. Gralnek IM, Dulai GS, Fennerty MB et al. Esomeprazole versus other proton pump inhibitors in erosive esophagitis: a meta-analysis of randomized clinical trials. Clin Gastroenterol Hepatol 2 006; 4 : 1 452– 8 . 28. Dickman R, Boaz M, Aizic S et al. Comparison of clinical characteristics of patients with gastroesophageal reflux disease who failed proton pump inhibitor therapy versus 18 those who fully responded. J Neurogastroenterol Motil 2011; 17: 387– 94. 29. El-Serag HB, Aguirre TV, Davis S et al. Proton pump inhibitors are associated with reduced incidence of dysplasia in Barrett's esophagus. Am J Gastroenterol 2004 ; 99 : 1877 – 83 . 30. Richter J E, Sabesin S M, Kogut D G et al. Omeprazole versus ranitidine or ranitidine/metoclopramide in poorly responsive symptomatic gastro-esophageal reflux disease . Am J Gastroenterol 1996 ; 91 : 1766 – 72 . 7 31. Grossi L, Spezzaferro M, Sacco LF et al. Effect of baclofen on oesophageal motility and transient lower oesophageal sphincter relaxations in GORD patients: a 48-h manometric study. Neurogastroenterol Motil 2008 ; 20 : 760 –6 . 32. Koek GH , Sifrim D , Lerut T et al. Effect of the GABA(B) agonist baclofen in patients with symptoms and duodenogastro-oesophageal reflux refractory to proton pump inhibitors. Gut 2003 ; 52 : 1397 – 402 . 33. Katz et al. Guidelines for the Diagnosis and Management of Gastroesophageal Reflux Disease. Am J Gastroenterol 2013; 108:308 – 328 . 34. del Genio G, Tolone S , del Genio F et al. Prospective The Sri Lanka Journal of Surgery 2015; 33(1): 14-19 assessment of patient selection for antireflux surgery by combined multichannel intraluminal impedance pH monitoring. J Gastrointest Surg 2008 ; 12 : 1491 – 6 35. Havemann BD, Henderson CA, El-Serag HB. The association between gastro-oesophageal reflux disease and asthma: a systematic review. Gut 2007 ; 56 : 1654–64. 36. Irwin RS, Curley FJ, French CL. Chronic cough. The spectrum and frequency of causes, key components of the diagnostic evaluation, and outcome of specific therapy. Am Rev Respir Dis 1990; 1 41: 6 40– 7 . 37. Havemann BD, Henderson CA, El-Serag HB. The association between gastro-oesophageal reflux disease and asthma: a systematic review. Gut 2007 ; 56 : 1654 – 64 . 38. Modiano N, Gerson LB. Risk factors for the detection of Barrett's esophagus in patients with erosive esophagitis. Gastrointest Endosc 2009; 69: 1014– 20. 39. Hanna S, Rastogi A, Weston AP et al. Detection of Barrett's esophagus after endoscopic healing of erosive esophagitis. Am J Gastroenterol 2006 ; 101 : 1416 – 20 . 40. Westhoff B , Brotze S , Weston A et al. The frequency of Barrett’s esophagus in high-risk patients with chronic GERD . Gastrointest Endosc 2005:61:226-31 19 SYMPOSIUM ON GORD Oesophageal manometry and pH-impedance studies in gastro-oesophageal reflux disease 1 2 SUB Dassanayake , ANR Fernandopulle 1 Gastroenterology & Hepatology unit, National Hospital of Sri Lanka, 2 Teachng Hospital, Jaffna Introduction disorders. Gastro-oesophageal reflux disease (GORD) is probably the most common disease encountered by the gastroenterologist physician and surgeon. Its diagnosis is mainly clinical and based on symptoms of heartburn and reflux. Upper gastrointestinal endoscopy when done may show evidence of reflux oesophagitis. Oesophageal pH and manometry are used mainly for a specific group of patients who are resistant to routine medication and prior to surgery. Ambulatory reflux monitoring is the only test that can assess reflux symptom association. On the other hand, oeosophageal manometry is recommended for preoperative evaluation, but has no role in the diagnosis of GORD. These rapidly evolving and highly technical fields of study have provided major insights into our understanding of the pathophysiology of GORD, and have become an integral part of its evaluation in the modern era. The first attempts at measuring the pH changes in GORD were made by Tuttle et al, who in 1960 used a glass pH electrode to demonstrate a gradual sloping gradient in the gastro-oesophageal pH in patients with oesophagitis in contrast to a sharp one in normal subjects [1]. Later, Johnson and DeMeester developed a dependable external electrode in 1974, successfully using it to measure oesophageal pH changes for up to 24 hours [2]. During the last decade, further studies demonstrated that the use of combined pH-impedance monitoring was more effective compared to pH monitoring alone in clinical practice. Kronecker and Meltzer performed the first oesophageal manometric studies using a balloon kymograph in 1894, but its clinical use was demonstrated by an atlas of oesophageal manometry published by Code et al in 1958 [3]. When optimally utilized, a manometric evaluation provides an accurate description of oesophageal contractile function, and is useful in characterizing a variety of oesophageal motility Correspondence: A.N.R. Fernandopulle E-mail: [email protected] The Sri Lanka Journal of Surgery 2015; 33(1): 20-23 Technical details pH monitoring Intra-oesophageal acidity can be measured via a trans-nasal catheter with a pH sensitive electrode placed in the oesophagus (for 24h) or a telemetry capsule (for 48h). Detection of periods of oesophageal acidification allows for a direct diagnosis of episodes of gastro-oesophageal reflux and quantification of the exposure of the distal oesophagus to acid [2]. For ambulatory monitoring, the basic equipment should include a data logger and an event marker to signal symptoms and other events during the period of recording. Reflux is defined as a drop in pH below 4. The number of episodes of reflux and the acid exposure time (the % of time with the pH <4) is recorded. The acid exposure time has been shown to positively correlate with the degree of mucosal damage. Although routine studies are performed with one distal pH sensor, experimental studies using multiple pH sensors allow evaluation of the proximal extent of the reflux [4]. However, pH studies do not give a measurement of the volume of the reflux. Wireless pH monitoring using a capsule is a fairly recent advancement which is more tolerable to the patient, but is limited by cost. Intraluminal impedance monitoring Impedance monitoring includes the concurrent measurement of impedance from multiple intraluminal recording segments of an impedance catheter positioned 20 within the oesophageal body [5]. The different patterns of electrical conductivity of gas, liquid or mixed content allows their distinction. It is also possible to distinguish between resting states, bolus transit, and wall contraction. The sequence of impedance changes allow recognition of flow in either aboral (swallow related) or oral (reflux) directions [6]. Gastro-oesophageal reflux is demonstrated as a liquid or mixed bolus moving in the oral direction during impedance studies, without any measurement of the pH. The most distal electrode is placed 2-3cm from the lower oesophageal sphincter (LOS) to detect restricted reflux episodes not reaching 5cm beyond the LOS [5]. Combined pH-impedance electrodes allow measurement of both parameters and their structure combines the two principles (figure 1). With the combination, reflux can be categorized as acid (nadir pH<4) or non-acid (nadir pH>4). In ambulatory subjects off proton-pump inhibitor (PPI) therapy, approximately two-thirds of reflux episodes are acidic and one-third is weakly acidic [7]. Conversely, if patients are on PPI therapy, approximately 90% of reflux episodes are weakly acidic (nadir pH 4-7) and are still responsible for the majority of symptoms [8]. Ambulatory reflux monitoring (pH or impedance-pH) is the only test that allows for determining the presence of abnormal oesophageal acid exposure, reflux frequency, and symptom association with reflux episodes. Figure 1. Schematic representation of a combined i m p e d a n c e - p H c a t h e t e r. T h e r e i s o n e a n t i m o n y electrode placed 5cm above the LOS and six pairs of impedance electrodes set at 2cm intervals . The Sri Lanka Journal of Surgery 2015; 33(1): 20-23 Manometry Manometry quantifies intraluminal oesophageal and LOS pressure during swallowing to detect abnormalities of peristalsis and sphincter relaxation. Stationary oesophageal manometry is performed by water-perfused catheters with volume displacement transducers or strain gauge transducers with solid-state circuitry. Water-perfused catheters are in wider use due to their lower cost, reusability and versatility, but require skilled personnel for maintenance. A perfused sleeve assembly is commonly used to hold the catheter in place during oesophageal shortening with swallowing. High resolution manometry (HRM) is a relatively recent advancement, which is characterized by the use of catheters which have a large number of sensors (21-36 sensors) which are very closely spaced (1-2cm). Data from HRM is usually illustrated as an oesophageal pressure topography (OPT) plot. OPT plots utilize colours to illustrate different pressure domains, and can be used to clearly demonstrate the gastro-oesophageal junction (GOJ) and the functional anatomy of the oesophagus [10]. Use in gastro-oesophageal reflux pH/impedance-pH monitoring pH monitoring in patients with endoscopy proven erosive oesophagitis has been shown to have excellent sensitivity (77–100%) and specificity (85–100%); however, the sensitivity is lower in those with endoscopy-negative reflux symptoms (<71%) [11]. The differentiation between physiological and pathological reflux is thought to be best achieved by recording the percentage of time the pH is < 4 [12]. The temporal relationship between the symptoms and reflux episodes is expressed using the symptom index (SI) or symptom association probability (SAP). A positive SI and/or SAP indicates a high probability that the relationship between reflux and symptoms did not occur due to chance and thus suggests causality [13]. Both these indices have been used in patients off PPI therapy who are experiencing heartburn. For patient management, a strongly positive SI or SAP may suggest the need for a therapeutic intervention and a negative result supports the notion that the patients symptoms are unlikely to be due to reflux [14]. However, a major shortcoming is that these depend on the patient 21 identifying and reporting all symptoms completely. Additionally reflux episodes that occur as prolonged rather than transitory events may not be reported correctly [11]. According to current guidelines, indications for ambulatory pH monitoring in GORD are [14.15]: 1.In the evaluation of patients refractory to PPI therapy. 2.Before consideration of endoscopic or surgical therapy in patients with non-erosive disease. 3.Where the diagnosis of GORD is in question. On patients refractory to PPI therapy, cessation of treatment prior to pH monitoring (7-14 days) is commonly done [15]. However, it is difficult to make recommendations on the “off vs on PPI” approaches according to the available evidence in centers where impedance-pH testing is available [14]. If reflux monitoring off medication is negative, the probability of GORD is very low, while a positive reflux test offers objective evidence to support the diagnosis. However, it does not provide information on the reason for the poor response to therapy. If pH monitoring alone is used in refractory patients while on PPI therapy, up to 96% may show normal acid exposure levels [16]. The use of combined pH-impedance monitoring is useful in these cases to detect non-acid reflux, which may increase the sensitivity up to 90% in endoscopy negative patients [5]. In patients with extra-oesophageal manifestations of GORD (mainly laryngeal and respiratory), a negative reflux monitoring test will point towards non-GORD aetiologies for the symptoms. The presence of abnormal pH monitoring results in patients with extraoesophageal symptoms vary widely in reports [17]. 24-hour pH monitoring also provides important prognostic information on patient selection for antireflux surgery [15]. It has been shown to be the strongest outcome predictor of laparoscopic Nissen fundoplication, although this is probably based more on the correct identification of the disease than on its severity [18]. The Sri Lanka Journal of Surgery 2015; 33(1): 20-23 Manometry During oesophageal manometry, gastro-oesophageal reflux is signified by the occurrence of absent LOS pressure with a common cavity phenomenon which is ended by primary and secondary peristalsis [19]. A common cavity phenomenon is identified by the rapid increase of intra-oesophageal pressure to match the intra gastric pressure, which signifies the relaxation of both the LOS and the crural diaphragm [20]. However, this phenomenon is technically difficult to detect with a low volume refluxate and is a relatively insensitive and nonspecific method of measuring reflux [5]. Due to these reasons, manometry is not considered important in establishing the diagnosis of GORD. However, manometry is recommended prior to antireflux surgical procedures to exclude other dysmotility disorders. GORD may co-exist with undiagnosed conditions such as achalasia, scleroderma oesophagus or non-reflux induced oesophageal spasm, which are best diagnosed by manometry [21]. The association between post-surgical dysphagia and preoperative peristaltic dysfunction detected by manometry has been a controversial issue, although current data do not support it [22]. Conclusion Gastro-oesophageal reflux disease remains one of the commonest conditions seen in our practice and should be diagnosed based on its common symptoms. While oesophageal manometry and pH studies help in the diagnosis and management of GORD they should not be routinely done for all patients. If used selectively and in the proper setting, they will help alleviate some of the most troublesome symptoms seen in the population. References 1. Tuttle SG, Rufin F, Bettarello A. The physiology of heartburn. Ann intern med [internet] 1961 aug 1;55(2):292–300. 2. Johnson LF, demeester TR. Development of the 24-hour intraoesophagealph monitoring composite scoring system. J Clin Gastroenterol 1986;8 Suppl 1:52–8. 3. Kahrilas, Clouse PJ, Ray E. Hogan WJ. An American Gastroenterological Association Medical Position Statement on the Clinical Use of Oesophageal Manometry. Gastroenterology 1994;107:1865–84. 4. Weusten BL, Akkermans LM, vanberge-Henegouwen 22 GP, Smout AJ. Spatiotemporal characteristics of physiological gastrooesophageal reflux. Am J Physiol 1994 Mar;266(3 Pt 1):G357–62. 5. Sifrim D, Castell D, Dent J, Kahrilas PJ. Gastrooesophageal reflux monitoring: review and consensus report on detection and definitions of acid, non-acid, and gas reflux. Gut 2004;53(February):1024–31. 6. Nguyen HN, Silny J, Matern S. Multiple intraluminal electrical impedancometry for recording of upper gastrointestinal motility: current results and further implications. Am J Gastroenterol 1999 Feb;94(2):306–17. 7. Bredenoord AJ, Weusten BLAM, Timmer R, Smout AJPM. Characteristics of gastrooesophageal reflux in symptomatic patients with and without excessive oesophageal acid exposure. Am J Gastroenterol 2006 Nov;101(11):2470–5. 8. Mainie I, Tutuian R, Shay S, Vela M, Zhang X, Sifrim D, et al. Acid and non-acid reflux in patients with persistent symptoms despite acid suppressive therapy: a multicentre study using combined ambulatory impedance-ph monitoring. Gut 2006;55:1398–402. 9. Hirano I, Richter JE. ACG practice guidelines: esophageal reflux testing. Am J Gastroenterol 2007;102:668–685. 10. Roman S, Pandolfino J, Mion F. High-resolution manometry: A new gold standard to diagnose oesophageal dysmotility? Gastroenterol Clin Biol [Internet] Elsevier Masson SAS; 2009;33(12):1061–7. 11. Hirano I, Richter JE, Fass R, Baroni DS, Bernstein DE, Bharucha AE, et al. ACG practice guidelines: Oesophageal reflux testing. Am J Gastroenterol 2007;102(6):668–85. 12. Pandolfino JE, Vela MF. Oesophageal-reflux monitoring. Gastrointest Endosc [Internet] Elsevier; 2009 Feb 21;69(4):917–30.e1. 13. Bredenoord a. J. Impedance-ph monitoring: New standard for measuring gastro-ooesophageal reflux. Neurogastroenterol Motil 2008;20:434–9. 14. Katz PO, Gerson LB, Vela MF. Guidelines for the The Sri Lanka Journal of Surgery 2015; 33(1): 20-23 diagnosis and management of gastrooesophageal reflux disease. Am J Gastroenterol [Internet]. Nature Publishing Group; 2013;108(3):308–28; quiz 329. 15. Fuchs KH, Babic B, Breithaupt W, Dallemagne B, Fingerhut A, Furnee E, et al. EAES recommendations for the management of gastrooesophageal reflux disease. Surg Endosc [Internet] 2014;28:1753–73. 16. Charbel S, Khandwala F, Vaezi MF. The role of oesophagealph monitoring in symptomatic patients on PPI therapy. Am J Gastroenterol United States; 2005 Feb;100(2):283–9. 17. Saritas Yuksel E, Vaezi MF. New Developments in Extraoesophageal Reflux Disease. Gastroenterol Hepatol (N Y) [Internet] Millennium Medical Publishing; 2012 Sep;8(9):590–9. 18. Csendes a. Multivariate analysis of factors predicting outcome after laparoscopic Nissen fundoplication. J Gastrointest Surg [Internet] 1998;4:650. 19. Wyman JB, Dent J, Holloway RH. Changes in ooesophagealph associated with gastro-ooesophageal reflux. Are traditional criteria sensitive for detection of reflux? Scand J Gastroenterol NORWAY; 1993 Sep;28(9):827–32. 20. Dent J, Dodds WJ, Friedman RH, Sekiguchi T, Hogan WJ, Arndorfer RC, et al. Mechanism of gastrooesophageal reflux in recumbent asymptomatic human subjects. J Clin Invest 1980;65(February):256–67. 21. Pandolfino JE, Kahrilas PJ. AGA technical review on the c l i n i c a l u s e o f o e s o p h a g e a l m a n o m e t r y. Gastroenterology 2005;128:209–24. 22. Mughal MM, Bancewicz J, Marples M. Ooesophageal manometry and ph recording does not predict the bad results of Nissen fundoplication. Br J Surg ENGLAND; 1990 Jan;77(1):43–5. 23. Zerbib F, Bruley Des Varannes S, Roman S, Pouderoux P, Artigue F, Chaput U, et al. Normal values and day-to-day variability of 24-h ambulatory ooesophageal impedanceph monitoring in a Belgian-French cohort of healthy subjects. Aliment Pharmacol Ther 2005;22:1011–21. 23 SYMPOSIUM ON GORD Nissen fundoplication: how I do it C.A.H Liyanage, S. Kumarage University Surgical Unit, North Colombo Teaching Hospital, Ragama, Sri Lanka Introduction Contraindications Laparoscopic Nissen fundoplication is now the standard approach for treatment of severe gastro-oesophageal reflux disease (GORD), not responding to medical treatment [1]. GORD affects 10% of the population and it causes significant morbidity to this group of people. The main cause for GORD is the dysfunctional lower oesophageal sphincter (LOS) rather than an over production of acid [2]. Open fundoplication is now almost an unacceptable procedure. The contraindications for laparoscopic fundoplication are, Rudolph Nissen (1896-1981) described the first fundoplication in 1950 [3,4]. The procedure has been revised many times and currently laparoscopic Nissen fundoplication is the gold standard for symptomatic GORD [5]. In Sri Lanka the procedure is offered to a very selective group of patients as pH and manometric studies are not freely available. The preceding two articles by our medical colleagues describe the value and the importance of evaluating symptomatic GORD patients. 1. Portal hypertension. 2. Contraindication for general anaesthesia. 3. Coagulopathy. 4. Inexperienced surgeon. Previous surgery, short esophagus and morbid obesity (BMI>35kg/m2) will make it a risky operation. For patients with BMI of >35kg/m2 it is recommended to do a gastric bypass surgery. Patients with esophageal dysmotility disorders should also be excluded from the procedure. The learning curve for a laparoscopic Nissen fundoplication would be at least 20 mentored procedures [6]. Procedure Indication The indications for surgery for a patient with GORD are, 1. Ineffective medical management. 2. Need for long term medical treatment: The long term treatment with proton pump inhibitors can cause undesirable side effects. In addition patients can have a poor quality of life due to long term drug treatment. 3. Alarming signs - asthma, chest pain, aspiration, hoarseness. 4. Para-oesophageal hernia. 5. Recurrent reflux. 6. Complications after previous antireflux surgery. Correspondence: Chandika Liyanage E-mail: [email protected] The Sri Lanka Journal of Surgery 2015; 33(1): 24-26 Prior to the procedure it is important to do an upper GI endoscopy by the operating surgeon at which he should measure the length of the gastro-oesophageal junction (GOJ). In addition 24-hour pH monitoring, oesophageal manometry, impedance monitoring, fluoroscopic real time swallowing studies and gastric emptying testing are important. Technique After the patient is anaesthetised, patient is placed in Lloyd Davies stirrups in the reverse Trendelenburg position. The operating surgeon stands in between the legs of the patient and the camera holding surgeon will stand on the left of the patient while the assistant stands on the right. We use an optical guided trocar for placement of the camera port at the paramedian region above and lateral 24 to the umbilicus. A 10mm port is used for the camera. If the falciform ligament is bulky and redundant, we use a percutaneously placed and laparoscopically guided suspension suture. Further four 5mm ports are placed; 2 ports are on the left and one on the right side of the abdomen and one epigastric port (Figure 1). can be made on a bougie to prevent narrowing, we do not use this technique. Where there is a short oesophagus, the thoracic oesophagus has to be mobilized and pulled down prior to forming the wrap. In addition, there are additional procedures to lengthen the GOJ. Where there is a large hiatus hernia the repair can be augmented by a mesh. Post-operative period Patient is then managed with anti-emetics and pureed food for 2 days and gradually introduced to more solid food. Figure 1. Laparosopic port sites at Nissen fundoplication We use an improvised technique to retract the liver utilising a laparoscopic needle holder through the epigastric port. The left lobe of the liver is retracted and held up with the sheath of the needle holder and the jaw of the needle holder is used to pinch the diaphragm. Further, the pars flaccida is divided using an ultrasonic shear (Harmonic Scalpel, Ethicon endosurgery) and the right crus of the diaphragm is defined. The oesophagus is then mobilized along the crus. Retro-oesophageal dissection is done lifting the posterior vagus nerve along with the oesophagus, up to the lateral border of left crus and a tunnel is made between the posterior to the oesophagus. The vagus nerve is protected which is retracted superiorly with the oesophagus. The fundus of the stomach is mobilized along the greater curvature of the stomach dividing the short gastric vessels with the Harmonic scalpel. The crural defect is then sutured using 2/0 silk sutures. The fundus is pulled behind the GOJ and the fundal wrap is formed with 2/0 silk sutures. We perform a 3600 degree wrap. There are other centres which perform 2700wraps and Dor wraps. Patients do complain of “tightness” on swallowing but with pre-operative counselling and reassurance that this feeling will disappear as time progresses, the patient usually overcomes this fear. Early post-operative symptoms include abdominal discomfort and fullness, mild dysphagia, and post prandial discomfort. These are mainly due to swelling around the fundus and GOJ and usually resolve in 2-6 weeks. Post-surgical pneumothorax and surrounding structural damage to the spleen or vagus nerve are very rare. Dysphagia lasting more than 12 weeks will require further evaluation. About 5-10% of patients who undergo Nissen fundoplication will require re-do surgery. Conclusion Laparoscopic Nissen Fundoplication is effective for carefully selected patients with severe GORD who are refractory to medical treatment. When performed by an experienced surgeon in appropriately selected patients laparoscopic anti-reflux surgery is cost effective than life long medical treatment. However, there is no evidence that laparoscopic fundoplication reverses the metaplasia in Barrett oesophagus. Furthermore there is no evidence to suggest that fundoplication reduces the incidence of adenocarcinoma in patients with Barrett oesophagus. Acknowledgement : Dr. Prasad Madushanka for secretarial assistance. The new fundal wrap and the tightness of the GOJ is checked using on-table endoscopy. Though the wrap The Sri Lanka Journal of Surgery 2015; 33(1): 24-26 25 References 1. Adam R, Adam CA, Akerstorm G, el al: Gastrooesophageal reflux disease. Surgical treatment 2001; 1:68-78,. 2. Singhal V, Khaitan L: Gastroesophageal reflux disease: diagnosis and patient selection. Indian Journal of Surgery 2 014; 76(6):453-460. 3. Nissen, R. Eine einfache Operation zur Beeinflussung der Refluxoesophagitis. Schweiz Med Wochenschr. The Sri Lanka Journal of Surgery 2015; 33(1): 24-26 1956;86:590–592. 4. Niebisch S, Peters JH: Update on fundoplication for the treatment of GERD. CurrGastroenterol Rep 2012; 14(3):186-96. 5. Ranmnik V, Jackson P, De coppi P, et al: Laparoscopic Nissen fundoplication and gastrostomy for a giant hiatal hernia in an infant with situsinversustotalis. BMJ 2013;10:1136,. 6. Lafullarde T, David I, Watson, et al: Laparoscopic Nissen Fundoplication: Five year results and beyond. JAMA 2001; 136(2): 180-184. 26 TECHNICAL NOTE Botulinum toxin injection to the puborectalis in the management of pelvic floor dyssynergia. I.H.D.S Pradeep1, P.C Chandrasinghe2, S.A.S.R Siriwardana3, S.K Kumarage2 1 Professorial Surgical Unit, Colombo North Teaching Hospital, Ragama. 2 Department of Surgery, University of Kelaniya, Ragama. 3 Department of Radiology, Colombo North Teaching Hospital, Ragama. Introduction Pelvic floor dyssynergia (spastic pelvic floor) is a functional disorder that causes difficulty in evacuation of the rectum [1]. This entity is an under diagnosed condition which requires dynamic pelvic MRI as the current investigation of choice. Treatment includes biofeedback therapy, injection of botulinum toxin in to puborectalis ring and surgical division of the puborectalis ring. Surgical division of puborectalis ring has irreversible effects and has a risk of causing incontinence [2]. Botulism toxin injection provides a reversible paralysis of the puborectalis allowing the chance of diagnosis and treatment in short term. perianal lesions such as fistulae, fissures or hemorrhoids. On digital rectal examination anal tone was normal. She underwent colonoscopy which was normal. A dynamic pelvic MRI was done which revealed a prominent puborectalis with impingement at the anorectal angle (paradoxic movement) while straining indicating spastic pelvic floor. A grade I rectocele was also present (Figure 1; a & b). Considering the clinical scenario it was decided to proceed with botulinum toxin injection under ultra sound guidance to the puborectalis sling as a short term therapeutic trial. This brief report describes the technique of Botulinum toxin injection to puborectalis sling in a patient diagnosed with pelvic floor dyssynergia. Clinical diagnosis A 37 year old mother of two children presented with a history of recurrent anal fissures with chronic anal pain and difficulty in evacuation of the rectum for two years duration. There was sensation of incomplete bowel emptying and tightness of the perineum. She had adopted an unusual position to defecate in order to overcome the difficulty and had to strain more than thirty minutes at a time. She had undergone lateral internal anal sphincterotomy and didn't have significant improvement. She didn't have a past history of abdominal or pelvic surgeries. She had two normal vaginal deliveries and there was no history of obstetric complications or instrumental delivery. On examination there was no rectal prolapse, perineal floor descent or Correspondence: I.H.D.S Pradeep E-mail: [email protected] The Sri Lanka Journal of Surgery 2015; 33(1): 27-29 Figure 1. Dynamic pelvic MRI at rest (a) and increased anorectal angle during straining (b) Technique After taking written informed consent the patient was positioned in the lithotomy position under spinal anesthesia. Perineum and upper thigh were cleaned with 10% povidone iodine and draped with perineal towels. Real time perineal ultrasound scan was performed using a high frequency (10 MHz ) linear probe to demonstrate the anatomical structures. In visualizing the structures the probe was held perpendicular to the perineum on either side of the anus and at the perineal body. The anal sphincter complex and the puborectalis ring were 27 identified (Figure 2). The anal sphincter complex appears on ultrasonography as a hypoechoic ring shadow. The puborectalis appears as a 'V' shaped mixed echogenic shadow encircling the spinchters. With sonographic guidance a 26g needle was introduced in to the puborectalis sling and 50 units of botulinum toxin was injected in to each limb of the puborectalis sling under sonographic guidance. Although the needle cannot be visualized sonographically the movement of muscle fibres with the penetration of the needle is used as a guide. Post operatively the patient was managed with oral analgesia and syrup lactulose 30 ml nocte. She was advised to have a fibre rich diet and adequate amount of water. Using of a squatting pan for the act of defecation was recommended as the pelvic floor muscles are maximally relaxed in this position. Patient was discharged on post procedure day one and reviewed at post procedure two weeks. Patient had dramatic improvement of symptoms with biofeedback, two weeks after the procedure. On further follow up her symptoms reappeared at 1 month following the procedure. Injection of botulinum toxin was done for the second time in the same manner. Figure 2. Ultrasonographic view of the puborectalis muscle (arrow) Discussion Pelvic floor dyssynergia (anismus) is a functional disorder due to spastic pelvic floor leading to defective relaxation of pelvic floor muscles resulting in evacuation difficulty during the act of defecation. The exact etiology for this is not well recognized. Chronic straining is thought to be the main cause resulting in the The Sri Lanka Journal of Surgery 2015; 33(1): 27-29 loss of muscle coordination specifically of the puborectalis part of the levator ani. These patients are often misdiagnosed and continue to have constipation and evacuation difficulty for a long period of time. In analyzing their symptoms these patients fulfill the ROME II criteria for functional constipation. Currently the dynamic pelvic MRI is the choice of imaging which shows defective relaxation of puborectalis sling and pelvic floor muscles causing an acute ano rectal angle during evacuation causing obstructed defaecation [8]. Other available investigations are defaecation proctography, balloon expulsion, anorectal manometry and electromyography of the pelvic floor muscles. Lower GI endoscopy is mandatory to exclude colonic pathology. Validated standard questionnaires (PAC- SYM, PAC-QOL) are used to assess the severity of the symptoms and response following treatment. Treatment modalities consist of Biofeedback therapy, botulinum toxin injection to the puborectalis sling and surgical division of the puborectalis muscle. Bio feedback therapy is morbidity free effective therapy for well motivated patients diagnosed of having this condition. Gadel Hak et al. reported 91.6% subjectively overall improvement of symptoms in a group of 60 patients who underwent biofeedback therapy [5]. Although it has been shown to have limited therapeutic effect in clinical practice [6] botulinum toxin injection is useful in relieving symptoms in the short term which causes transient relaxation of puborectalis sling allowing confirmation of the diagnosis. It has higher success rates compared to biofeedback training alone [7]. Muscle coordination can be regained once the spasticity is relieved with botulinum toxin. Symptoms tend to return in few months when the effect of the drug weans off. There has been no severe side effect observed following injection of botulinum toxin to treat benign anal conditions [4]. Farid M and El Monem et al compared biofeed back therapy over Botulinum toxin injection in forty eight patients with anismus [3]. Patients were assessed for initial improvement at one month and long term success rate at one year in this study. Patients who had biofeedback(BF) therapy had 50% initial improvement and 25% long term success rate and patients had Botulinum toxin had 70.8% initial improvement with 33.3% long term success rate. They concluded highlighting the limited therapeutic effect of biofeedback therapy and higher temporary success rate 28 of botulinum injection (BI). Partial surgical division (PSD) of the puborectalis sling bilaterally is the definitive surgical treatment indicated for anismus. This procedure is found to be an effective method with low morbidity and higher success rates compared to non pharmacological methods. Previous authors have administered botulinum toxin with the assistance of endoanal ultrasound or electromyography of the puborectalis, methods which are not freely available in the local setting [12]. We describe the technique performed with the use of perineal ultrasound scanning which is a non-invasive freely available modality. The drawback of surgical division is the risk of causing irreversible incontinence. Faried M et al conducted a study on 60 patients who were randomly allocated to receive either one of the three modalities of treatment with a follow up of up to one year [3]. The groups differed significantly with regard to functional outcome at 1 month (50% - BF, 75% - BI, 95% - PSD). The difference persisted at one year post procedure. They concluded that bilateral PSD of puborectalis has higher success rate with less morbidity in the long run. Incontinent for flatus or faeces (13%) and pelvic floor descent (26%) were the complications observed in this series with PSD. It was decided to proceed with PSD of puborectalis in our patient as the method of relieving her recurrent symptoms, which was proven to be effective with less morbidity in long term basis. In conclusion botulinum injection to the puborectalis can be effectively administered under perineal ultrasound scan guidance. Modality of treatment should be decided based on each case to have best outcome and minimize post procedure complications. References 1. Wexner SD, Bartolo DC (eds) (1995) Constipation: etiology, evaluation and management. ButterworthHeinemann, Oxford, pp 1–272 2. Kamm MA, Hawely PR, Lennard-Jones JE (1988) Lateral The Sri Lanka Journal of Surgery 2015; 33(1): 27-29 division of puborectalis muscle in the management of severe constipation. Br J Surg 75:661–663 3. Farid M, Youssef T, Mahdy T, Omar W, Ayman M, Abdul H, El Nakeeb A, Youssef M. Comparative study between botulinum toxin injection and partial division of puborectalis for treating anismus. Int J Colorectal Dis 2009 Mar;24(3):327-34. 4. Madaliński MH, Sławek J, Duzyński W, Zbytek B, Jagiełło K, Adrich Z, Kryszewski A. Side effects of botulinum toxin injection for benign anal disorders. Eur J Gastroenterol Hepatol 2002 Aug;14(8):853-6. 5. Gadel-Hak N, El-Hemaly M, Hamdy E, El-Raouf AA, Atef E, Salah T, El-Hanafy E, Sultan A, Haleem M, Hamed H. Pelvic floor dyssynergia: efficacy of biofeedback training. Arab J Gastroenterol 2011 Mar;12(1):15-9. 6. Farid M, El Monem HA, Omar W, El Nakeeb A, Fikry A, Youssef T, Yousef M, Ghazy H, Fouda E, El Metwally T, Khafagy W, Ahmed S, El Awady S, Morshed M, El Lithy R. Comparative study between biofeedback retraining and botulinum neurotoxin in the treatment of anismus patients. Int J Colorectal Dis 2009 Jan;24(1):115-20. 7. Faried M, El Nakeeb A, Youssef M, Omar W, El Monem HA. Comparative study between surgical and nonsurgical treatment of anismus in patients with symptoms of obstructed defecation: a prospective randomized study. J Gastrointest Surg 2010 Aug;14(8):1235-43. 8. C S Reiner, MD, R Tutuian, MD, A E Solopova, MD, D Pohl, MD, B Marincek, MD, and D Weishaupt, MD. MR defecography in patients with dyssynergic defecation: spectrum of imaging findings and diagnostic value. Br J Radiol Feb 2011; 84(998): 136–144. 9. Ron Y, Avni Y, Lukovetski A, Wardi J, Geva D, BirkenfeldS,Halpern Z. Botulinum toxin type-A in therapy of patients with anismus. Dis Colon Rectum 2001;44:1821-1826. 10. Andromanakos N, Skandalakis P, Troupis T, FilippouD.Constipation of anorectal outlet obstruction: pathophysiology,evaluation and management. J Gastroenterol Hepatol 2006;21(4):638–646. 11. Maria G, Brisinda G, Bentivoglio AR, Cassetta E, Albanese A.Botulinuxn toxin in the treatment of outlet obstruction constipationcaused by puborectalis syndrome. Dis Colon Rectum 2000;43:376-380. 12. Yong Zhang, Zhen-Ning Wang, Lei He, GeGao, Qing Zhai, Zhi-Tao Yin, Xian-Dong Zeng. Botulinum toxin type-A injection to treat patients with intractable anismus unresponsive to simple biofeedback training. World J Gastroenterol 2014 September 21; 20(35): 12602-12607 29 CASE REPORTS A Sri Lankan family with cerebellar hemangioblastoma due to a heterozygous nonsense mutation in the von Hippel-Lindau tumor suppressor, E3 ubiquitin protein ligase (VHL) gene. P.K.D. Channa T. Somadasa1, Nirmala D. Sirisena1, L. Suresh C. De Silva2, Vajira H.W. Dissanayake1,2 1 Human Genetics Unit, Faculty of Medicine, University of Colombo, Sri Lanka, 2 Asiri Centre for Genomic and Regenerative Medicine, Asiri Surgical Hospital, Colombo, Sri Lanka Key words: Genetics; hemangioblastoma; VHL gene; Von Hippel-Lindau disease Abstract Mutations in the von Hippel-Lindau tumor suppressor, E3 ubiquitin protein ligase (VHL) gene cause a variety of phenotypes including von Hippel-Lindau (VHL) disease. This report describes a Sri Lankan family with three siblings with cerebellar haemangioblastoma due to a nonsense mutation in the VHL gene. A heterozygous nucleotide substitution in exon 3 was identified in all three siblings resulting in a stop codon at amino acid position 175 leading to a truncated non-functional VHL protein [NM_000551.3(VHL):c.525C>G;p.Tyr175Ter; rs5030835C>G]. Patients with rare tumours characteristic of VHL should undergo clinical and genetic evaluation for VHL. Introduction The von Hippel-Lindau tumor suppressor, E3 ubiquitin protein ligase (VHL) gene [GenBank: NG_008212.3, OMIM# 193300], is a tumor suppressor gene which spans a 14.25-kb genomic region at 3p25.3. It encodes for two alternatively spliced transcript variants. Transcript variant 1 (NM_000551.3) which is encoded by all 3 exons is translated to a protein with 213 amino acid residues (NP_000542.1) while transcript variant 2 (NM_198156.2) is translated to a protein with 172 acid residues (NP_937799.1) [1] . Mutations in the VHL tumor suppresser gene cause a variety of phenotypes including von Hippel-Lindau disease (VHL), familial phaeochromocytoma and inherited polycythaemia [2]. VHL is an autosomal dominantly inherited familial cancer syndrome Correspondence: Vajira H. W. Dissanayake E-mail: [email protected] The Sri Lanka Journal of Surgery 2015; 33(1): 30-32 predisposing to a variety of malignant and benign tumors [3] such as haemangioblastomas of the cerebellum, spinal cord, brainstem and retina, clear cell renal carcinomas, pheochromocytomas, endolymphatic sac tumours, pancreatic islet cell tumours, haemangiomas of the adrenals, liver and lungs, epididymal and broad ligament papillary cyst adenomas as well as visceral cysts in the kidneys and pancreas [4]. A germline mutation of the VHL gene is the basis of familial inheritance of VHL syndrome. According to Knudson's (“Two Hit”) hypothesis, both alleles of a tumor suppresser gene need to be mutated in order for a tumour to develop, therefore a patient who manifests a tumour, inherits one mutation from a parent, and develops the second mutation in the same gene in the affected organ as a somatic mutation, at which point the tumour begins to manifest [5]. To date, more than 300 mutations have been identified in families with VHL disease, consisting of partial and whole gene deletions, frameshift, nonsense, missense, and splice site mutations [6]. About 20% of cases are due to de novo mutations. This report describes a Sri Lankan family with 3 siblings with cerebellar haemangioblastoma due to a heterozygous nonsense mutation in the VHL gene. The Family A 28 year old female who was clinically diagnosed with a cerebellar hemangioblastoma was referred to the Human Genetics Unit for genetic evaluation. The patient was clinically diagnosed with cerebellar haemangioblastoma at the age of 13 years, since then, she had undergone four surgeries for removal of the recurrent tumour in the posterior cranial fossa. In addition, a tumor arising from the fourth ventricle of the brain was also surgically removed. She also developed a 30 cervical spinal cord haemangioblastoma (Figure 1). Two of her male siblings were also diagnosed with cerebellar hemangioblastoma. The CT scan of one of the brothers showed dilatation and a cystic mass in the lateral third ventricle as well as a renal cyst. Figure 2 shows the pedigree of the family with VHL disease. Figure 1. (a) T2 weighted sagittal MRI brain of the female proband showing the recurrent cerebellar haemangioblastoma and (b) T1 weighted post contrast sagittal MRI of the cervical spine showing spinal haemangioblastoma. comparison of the nucleotide sequences generated from the patients and to confirm the presence of any mutations. A heterozygous nonsense mutation was identified in all 3 individuals in exon 3 of the VHL gene. A single nucleotide substitution at position 13214 (NG_008212.3.g13214C>G) replaced the codon for amino acid tyrosine (UAC) in transcript variant 1 (NM_000551.3.c525C>G) to a stop codon (UAG) resulting in premature termination of the VHL protein at amino acid position 175 (NP_000542.1.pTyr175Ter). This mutation has previously been reported in other families and documented in the dbSNP database and assigned the SNPID rs5030835 (http://www.ncbi.nlm.nih.gov/projects/SNP/rs=50308 35). Figure 3 shows the partial electropherogram with the point mutation at position 13214 of the VHL gene. Figure 3. Partial electropherogram of the patient showing the heterozygous nonsense mutation in the VHL gene. Discussion Figure 2. Pedigree of the family with VHL disease showing the familial mutation in the three siblings. Genotyping The VHL gene was sequenced in the patient and her 2 siblings after obtaining their written informed consent. DNA was extracted from peripheral blood using QIAamp blood DNA midi kit from Qiagen. All 3 exons and flanking intronic regions of the VHL gene were sequenced using an ABI PRISM 3130 Genetic A n a l y z e r. T h e p u b l i s h e d h u m a n V H L g e n e Reference Sequence file obtained from GenBank (http://www.ncbi.nlm.nih.gov) was used for The Sri Lanka Journal of Surgery 2015; 33(1): 30-32 This report describes a Sri Lankan family with three siblings with cerebellar haemangioblastoma due to a heterozygous nonsense mutation in the VHL gene. VHL mutations are associated with various benign and malignant tumours resulting in high morbidity and mortality rates. Mutations in the VHL gene are known to cause haemangioblastomas of the central nervous system (CNS) in 60-80% of VHL patients [6,7]. A study conducted by van der Harst et al. in 1998 reported that 8 out 68 patients with pheochromocytoma had mutations in the VHL gene. Among these patients, two were relatives and had a familial mutation [8]. Familial mutations in the VHL gene have also been reported in VHL families presenting with clear cell renal cell carcinoma. Recent advances in understanding the genetic basis of VHL disease has resulted in improved diagnosis of VHL disease and provided greater insights into the molecular pathogenesis of the disease [1]. The 31 prognosis can be improved through early screening, diagnosis and surveillance [9]. Molecular genetic testing coupled with genetic counseling is now considered standard for the evaluation of patients and families with suspected VHL [10]. Acknowledgments We would like to express our thanks to Dr. Udari Liyanage, Senior Lecturer & Consultant Radiologist, Department of Anatomy, Medical Faculty, Colombo for providing radiological information and Mr. Sanka P. Bandara of the Audio-Visual Unit, Medical Faculty, Colombo for preparing the radiological photographs. References 1. Maher, E.R., H.P. Neumann, and S. Richard, von HippelLindau disease: a clinical and scientific review. Eur J Hum Genet 2011, 19(6): p. 617-23. 2. Maher, E.R, Von Hippel-Lindau disease. Curr Mol Med 2004, 4(8): p. 833-42. 3. Pastore, Y., et al., Mutations of von Hippel-Lindau tumor- suppressor gene and congenital polycythemia. Am J Hum Genet 2003, 73(2): p. 412-9.1 4. Kaelin, W.G., Jr., The von Hippel-Lindau tumour s u p p r e s s o r p r o t e i n : O 2 s e n s i n g a n d c a n c e r. Nat Rev Cancer 2008, 8(11): p. 865-73. 5. Berger, A.H., A.G. Knudson, and P.P. Pandolfi, A continuum model for tumour suppression. Nature 2011, 476(7359): p. 163-9. 6. Hasani-Ranjbar, S., et al., Mutation screening of VHL gene in a family with malignant bilateral pheochromocytoma: from isolated familial pheochromocytoma to von Hippel-Lindau disease. Fam Cancer 2009, 8(4): p. 465-71. 7. Tootee, A. and S. Hasani-Ranjbar, Von hippel-lindau disease: a new approach to an old problem. Int J Endocrinol Metab 2012, 10(4): p. 619-24. 8. Van der Harst, E., et al., Germline mutations in the vhl gene in patients presenting with phaeochromocytomas. Int J Cancer 1998, 77(3): p. 337-40. 9. Gallou, C., et al., Mutations of the VHL gene in sporadic renal cell carcinoma: definition of a risk factor for VHL patients to develop an RCC. Hum Mutat 1999, 13(6): p. 464-75. 10. Friedrich, C. Genotype-phenotype correlation in von Hippel-Lindau syndrome. Human Molecular Genetics 2001, 10(7): p. 763-767. Key Points: Mutations in the VHL gene are known to predispose to haemangioblastomas of the central nervous system in 60-80% of patients with VHL disease. Molecular genetic testing coupled with genetic counseling should be offered to patients and families with suspected VHL disease. The prognosis can be improved through early screening, diagnosis and surveillance. The Sri Lanka Journal of Surgery 2015; 33(1): 30-32 32 CASE REPORTS Laparoscopic resection with minilaparotomy anastomosis for pancreatico-duodenectomy K B Galketiya, V Pinto, R Rohankumar, B G Jayawickrama, A Herath Teaching Hospital Peradeniya, Kandy, Sri Lanka. Key words: Pancreatico-duodenectomy; laparoscopy Introduction Pancreatico-duodenectomy is the surgical treatment of choice for carcinoma of the periampullary region and head of pancreas. The open procedure is associated with considerable morbidity and occasional mortality. The long incision, continuous handling and prolonged use of retractors can result in post operative respiratory inadequacy due to severe pain and ileus. There is often significant blood loss. Laparoscopic assisted Whipples resection is an achievable alternative minimizing postoperative complications, thus facilitating early feeding, mobilization and discharge from hospital [1,2,4,6]. However literature indicates the need of further studies to recommend its routine use [4,5,6,7,8]. the mid transverse colon to caecum. The duodenum was identified and 'kocherized' and the inferior vena cava was exposed until the left renal vein crossed the abdominal aorta . Mobilization of the duodenum was continued until the ligament of Treitz was divided allowing the jejunum to be pulled freely to the right side. The portal vein was exposed to the neck of pancreas and the dissection continued until the common bile duct and common hepatic artery hepatic artery and gastroduodenal artery were exposed. The gastro-duodenal artery was divided in between clips. The stomach was transected with a stapler. The pancreas was divided in front of the portal vein. Case Report A year 50 year old male presented with obstructive jaundice who was deeply icteric with a palpable Gall bladder. Imaging were suggestive of a periampullary carcinoma which was confirmed by endoscopy and b i o p s y. L a p a r o s c o p i c a s s i s t e d p a n c r e a t i c o duodenectomy was planned. Patient was evaluated for co-morbidities and optimized as required. His weight was 58kg with a BMI of 25.1kg/m2 . Procedure was carried out under general anaesthesia with invasive monitoring and supplemented by epidural analgesia. The patient was placed in reverse-trendelenburg 20 degrees and rotated to the left by 30 degrees with legs abducted to 60 degrees. Five ports were used. Pneumoperitoneum was created by insufflation of CO2 at a pressure of 14 mmHg. The gastro-colic omentum was divided, entering in to lesser sac exposing the pancreas. Colon was mobilized from The jejunum was transected with a stapler. The divided pancreas and uncinate process were taken off from the portal vein. The common bile duct was transected and the resection was complete. The time for resection was 330 minutes with a blood loss of 400ml. The patient was stable during procedure and did not require blood transfusion. Correspondence: K.B. Galketiya E-mail: [email protected] A mid line laparotomy of about 10 cm was made to retrieve the specimen and perform the anastomoses - The Sri Lanka Journal of Surgery 2015; 33(1): 33-34 Figure1. Picture showing transected stomach and pancreas being divided in front of the portal vein 33 pancreatico-jejunostomy, hepatico-jejunostomy and gastro-jejunostomy. The respiratory and cardiovascular parameters were monitored carefully and were stable. Following extubation, the patient was managed in the ICU. Pain relief was provided using the epidural catheter for the first day. Subsequently the patient was comfortable with diclofenac sodium suppositoies100mg twice a day. He was mobilized after twenty four hours and started on oral sips forty eight hours after surgery. Semisolids were started after four days and a normal diet by the sixth day. He was discharged on the eighth post operative day. Discussion Laparoscopic pancreatico-duodenectomy creates a new learning curve for the gastrointestinal surgeon. The patient positioning, port placement, adequate retraction, traction and counter traction, precise appreciation of anatomy and tissue planes are all required for successful completion. Adherence to meticulous haemostasis is crucial. We successfully completed the laparoscopic resection in this patient. This was after conversion to open surgery at various stages of resection in seventeen patients. For the reconstruction, we opted for a minilaparotomy [3]. Anastomoses could be performed laparoscopicaly, for which a skill in laparoscopic suturing is essential. The next goal to achieve is performing the hepaticojejunostomy laparoscopically. Then the pancreas can be anastomsed to the posterior wall of the stomach. This and the gastro-jejunostomy could be performed with a mini incision of about 5cm. The meticulous fluid balance, monitoring and vigilance reduced complications due to altered physiology owing to pneumoperitonium, position, abdominal compartment syndrome with aorto- caval compression leading to impediment of perfusion to organs, possibility of gas embolism during this surgery which took 330 minutes [9]. Conclusion Laparoscopic pancreatico-duodenectomy may well be performed safely with minimum blood loss in an acceptable time with minimal complications and speedy post operative recovery. Persistence during the learning curve is a must in reaching the goal. References 1. Gagner M, Palermo M.Laparoscopic Whipple procedure: review of the literature J HepatobiliaryPancreat Surg. 2009;16(6):726-30. doi:10.1007/s00534-009-0142-2. Epub 2009 Jul 28. 2. Dulucq JL, Wintringer P, Stabilini C, Feryn T, Perissat J, Mahajna A. Are major laparoscopic pancreatic resections worthwhile? A prospective study of 32 patients in a single institution. SurgEndosc. 2005 Aug;19(8):1028-34. Epub 2005 May 26 3. Lee JS, Han JH, Na GH, Choi HJ, Hong TH, You YK, Kim DG.Laparoscopic pancreaticoduodenectomy assisted by mini-laparotomy.JSLS. 2013 JanMar;17(1):68-73. 4. Lei P, Wei B, Guo W, Wei H. Minimally Invasive Surgical Approach Compared With Open Pancreaticoduodenectomy: A Systematic Review and Meta-analysis on the Feasibility and Safety. Surg Laparosc Endosc Percutan Tech. 2014 Apr 16. [Epub ahead of 5. Tan-Tam C, Chung SW.Minireview on laparoscopic h e p a t o b i l i a r y a n d p a n c r e a t i c s u r g e r y. World J Gastrointest Endosc. 2014 Mar 16;6(3):60-67. 6. Nigri G1, Petrucciani N2, La Torre M2, Magistri P2, Va l a b r e g a S 2 , A u r e l l o P 2 , R a m a c c i a t o G2.Duodenopancreatectomy: Open or minimally invasive approach? Surgeon. 2014 Feb 10. pii: S1479666X(14)00012-2. doi: 10.1016/j.surge.2014.01.006. [Epub ahead of print] 7. Bao PQ1, Mazirka PO, Watkins KT.Retrospective Comparison of Robot-Assisted Minimally Invasive Ve r s u s O p e n P a n c r e a t i c o d u o d e n e c t o m y f o r Periampullary Neoplasms. J Gastrointest Surg. 2013 Nov 15. [Epub ahead of print] 8. Zenoni SA1, Arnoletti JP2, de la Fuente SG2.Recent developments in surgery: minimally invasive approaches for patients requiring pancreaticoduodenectomy. JAMA Surg. 2013 Dec;148(12):1154-7. doi: 10.1001/jamasurg.2013.366. 9. Gerges FJ, Kanazi G, Jabbour-khoury S. Anesthesia for laparoscopy: a review. J Clin Anesth. 2006;18:67-78. Key Points: Laproscopic pancreatico-duodenectomy is a treatment method which leads to reduced perioperative complications and speedy recovery. However there is a steep learning curve to be negotiated before it becomes standard practice. The Sri Lanka Journal of Surgery 2015; 33(1): 33-34 34 CASE REPORTS Axial torsion and gangrene of a giant Meckel's diverticulum causing small bowel obstruction. S. N. Deshmukh, S. P. Jadhav, A. G. Asole Dr. Vaishampayan Memorial Government Medical College, Solapur, Maharashtra, India. Key words: Meckel's diverticulum; torsion; gangrene; small bowel obstruction Introduction Meckel's diverticulum is the most prevalent congenital anomaly of the gastrointestinal tract, affecting approximately 2% of the general population [1]. It results from incomplete obliteration of the most proximal portion of the vitelline or omphalomesenteric duct [2]. Bleeding, obstruction, and inflammation are the three most common complications of Meckel's diverticulum [3]. Here, we report a case of axial torsion and gangrene of Meckel's diverticulum which is the rarest complication. Case history A 13-year-old girl presented with abdominal pain, vomiting, distension and constipation of 2 days duration. On physical examination her abdomen was distended, tender and guarding was present. There was no history of previous abdominal surgery. Per rectal examination was unremarkable. Plain abdominal radiograph depicted multiple air-fluid levels suggesting small bowel obstruction. All the laboratory parameters were within normal limits except elevated leucocyte count. Emergency exploratory laparotomy was performed. At exploration the loop of the ileum was found entrapped due to axially torsed gangrenous Meckel's diverticulum leading to small bowel obstruction (Figure 1). The tip of the Meckel's diverticulum was found adherent to the umbilicus (Figure 2). Simple diverticulectomy was performed. The diverticulum measured 8cm x 1.5cm. Postoperative course was uneventful. Histopathological examination confirmed acute Meckel's diverticulitis with focal gangrenous change. Figure 1. Ileal loop entrapped by axially torsed gangrenous Meckel's diverticulum. Figure 2. Gangrenous Meckel's diverticulum with tip adherent to the umbilicus. Correspondence: S.N. Deshmukh E-mail: [email protected] The Sri Lanka Journal of Surgery 2015; 33(1): 35-36 35 Discussion Meckel's diverticulum was first described by Fabricius Hildanus in 1598 and later named after Johann Friedrich Meckel, a German comparative anatomist who first recognized its developmental origin in 1809 [3]. It is a true diverticulum containing all the layers of the small bowel wall [3]. It is invariably found on the antimesenteric border of the ileum, with 90% located within 90 cm of the ileocaecal valve [2]. Meckel's Diverticula are called giant when they are longer than 5cm [4]. Majority of Meckel's diverticula are clinically silent and are incidentally identified at surgery or at autopsy. The lifetime risk of complications is estimated to be 4% with most of the complications occurring in adults [2]. Gangrene due to axial torsion of a Meckel's diverticulum is the rarest of the complications that have been reported, particularly in children [5]. Predisposing factors for axial torsion include, presence of mesodiverticular bands, a narrow base, excessive length, and associated neoplastic growth or inflammation of the diverticulum [2]. The correct diagnosis of Meckel's diverticulum before surgery is often difficult because a complicated form of this condition may be clinically indistinguishable from a variety of other intra-abdominal diseases such as acute appendicitis, inflammatory bowel disease, or other causes of small bowel obstruction [3]. Therefore high index of suspicion is warranted to correct and expeditious diagnosis especially in patients with atypical presentation [5]. The management of incidentally found (asymptomatic ) Meckel's diverticulum is controversial [1]. Treatment of complicated Meckel's diverticulum is always surgical and includes simple diverticulectomy or ileal resection either by open or laparoscopic approach [3]. Segmental ileal resection may be necessary if the diverticulum contains tumour or if the base of the diverticulum is inflamed or perforated [1]. References 1. Tavakkolizadeh A, Whang EE, Ashley SW, Zinner M. Small intestine. In: Brunicardi FC, Anderson DK, (eds): Schwartz's principles of surgery New York: McGraw Hill, 2010; 1002-1004. 2. Seth A, Seth J. Axial torsion as a rare and unusual complication of a Meckel's diverticulum: a case report and review of the literature. Journal of Medical Case Reports 2011;(5):118 3. Cartanese C, Petitti T, Marinelli E, et al. Intestinal obstruction caused by torsed gangrenous Meckel's diverticulum encircling terminal ileum. World J Gastrointest Surg 2011; 4. Ruiz VA, Camacho LA, Diaz DC. Giant Meckel's diverticula with necrosis due to axial torsion. Rev Col Gastroenterol 2010; 25(4):398–400. 5. Limas C, Seretis K, Soultanidis C, Anagnostoulis S. Axial torsion and gangrene of a giant Meckel's diverticulum Gastrointestin Liver Dis 2006;15:67-68. Key Points: Axial torsion and gangrene of a Meckel's diverticulum is a rare complication. It can rarely account for small bowel osbtruction. Treatment of complicated Meckel's diverticulum is always surgical and includes simple diverticulectomy or ileal resection. The Sri Lanka Journal of Surgery 2015; 33(1): 35-36 36 CASE REPORTS Incisional hernia after ventriculoperitoneal shunt M. Jayant, R. Kaushik Department of Surgery, Government Medical College and Hospital, Chandigarh, India Abstract Ventriculoperitoneal (VP) shunt is a common neurosurgical procedure that is performed to drain the cerebrospinal fluid (CSF) into the peritoneal cavity. Although a relatively safe procedure, at times, it can be associated with a variety of complications at the abdominal end such as displacement, cyst formation, inguinal hernia, hydrocele, perforation of intraabdominal organs, or extrusion. Rarely, an incisional hernia may occur at the abdominal incision. We present a rare case of an incisional hernia occurring at the abdominal site of shunt insertion and highlight the problems faced while repairing it. Introduction Since the first reports by Kausch in the early part of the 20th century of the use of the peritoneal cavity for diverting CSF, ventriculoperitoneal (VP) shunts have become the standard procedure for the treatment of hydrocephalus [1,2]. Like any surgical procedure, VP shunting is also associated with complications; the most common causes of shunt malfunction are proximal obstruction and infection [1] and these usually present with headache, changes in the mental status, and vomiting [3]. Complications that occur at the distal (abdominal) end are also a cause of significant morbidity, and in various series, nearly 5 - 47 % of all shunt failures are thought to be due to malfunction of the distal catheter [4-7] with a higher incidence in patients with scoliosis, obesity and those who have undergone prior abdominal surgery [4,8]. Abdominal complications that have been reported are; shunt infection, development of an inguinal hernia, subcutaneous collections of CSF, peritoneal or omental cyst formation, mesenteric pseudotumors, bowel perforation, intestinal volvulus around the shunt tubing, Correspondence: Dr. Robin Kaushik E-mail: [email protected] The Sri Lanka Journal of Surgery 2015; 33(1): 37-40 catheter disconnection; and various types of catheter migrations such as extraperitoneal retraction and displacement, migration of the catheter into the pleural cavity or heart, or protrusion of the catheter through the mouth, umbilicus, bladder, vagina, anus, or scrotum. Knotting of the shunt has also been reported on occasion [1–7], as have been other less common complications such as adhesive bowel obstruction, intra-abdominal abscesses, cerebrospinal–enteric fistula and intractable CSF ascites [1,3]. The development of an incisional hernia at the abdominal end after shunt placement is an extremely rare complication. Theoretically, any abdominal operation has the potential for developing into an incisional hernia, but the incidence of this problem after a VP shunt is quite low. Although many reviews on the topic of complications or abdominal complications after shunt do mention this complication, we could come across only two actual reports of incisional hernia occurring at the abdominal end [9,10], and we present another such case, highlighting the various problems we faced while dealing with this rare type of hernia. Case Report This 23 years old gentleman came to our outpatient department with swelling and pain in the upper abdomen. The swelling gave a typical history of a hernia, with increase in size on exertion and reduction while lying down. The patient gave history of surgery about a year and a half back, when he underwent VP shunt insertion followed by endoscopic surgery for a third ventricular colloid cyst. He remained well for nearly a year, after which he noticed this gradually increasing swelling over his upper abdomen. On examination, there was a visible, horizontal scar in the epigastrium, with a palpable soft lump that showed cough impulse, and reduced in size on lying down. A defect of approximately 2x2 cms was palpable in the 37 abdominal wall here. The VP shunt could also be palpated to the left of this defect (Figure 1). The patient was worked up for elective surgery for the incisional hernia, and a neurosurgical opinion was taken for the removal of VP shunt. The neurosurgical team felt that it would be better if the shunt remained in situ, and advised avoidance of injury to the shunt while operating the hernia. Figure1. Photograph showing incisional hernia at the abdominal site of VP shunt insertion Surgery was performed under general anesthesia. Scar tissue from the previous surgery was excised and the incision was extended on either side. Carefully, the skin flaps were mobilized, repeatedly palpating the shunt and taking care not to damage it as it ran in the subcutaneous planes onto its point of entry into the peritoneal cavity. The muscle sheath was mobilized all around, as was the hernial sac. The sac was invaginated, and an incision was given onto the muscle sheath parallel to the closure. The free edges of the sheath were sutured together to provide additional support, as well as to reduce tension on the closure. A polypropylene mesh was then used to cover the area and was sutured to the margins of the sheath all around. Closure was performed over a drain. The patient remained well in the post-operative period, The Sri Lanka Journal of Surgery 2015; 33(1): 37-40 and is well on a short follow up, with no recurrence of the hernia. Discussion An incisional hernia can occur after any type of abdominal wall incision, although the highest incidence is seen with midline and transverse incisions. Multiple risk factors are implicated in the development of an incisional hernia, and can be broadly classified into surgical or technical factors (expertise, choice of suture material, technique of closure, closure under excessive tension, wound infections, emergent surgery, postoperative infections, etc.), and patient factors (advanced age, malnutrition, obesity, ascites, corticosteroid usage, diabetes, cigarette smoking, obesity, other illnesses, etc.) [11]. In our patient, it was quite possibly a combination of increased intra-abdominal pressure (due to CSF drainage into the peritoneal cavity) and a compromised technique of abdominal wound closure that contributed to the formation of his incisional hernia. Surprisingly, an exhaustive search through the internet, various databases and cross referencing through article bibliographies (even a search for articles on the etiology of incisional hernias) did not yield much information about the occurrence of incisional hernia after VP shunt surgery. Although many series mention incisional hernia at the abdominal end of the shunt as a complication of the procedure, despite going through a large amount of literature available on VP shunts (and its complications), we found only two reports that actually reported the occurrence incisional hernia in their patients [9,10].We accept the fact that given the vast amount of literature on the topic of VP shunts, despite our efforts, we still might have missed some reports on this topic, but even then, the development of an incisional hernia after VP shunt remains the rarest of complications. Quite possibly, the rarity of this complication in comparison to the other reported abdominal complications after VP shunt is responsible for the paucity of information on this topic. Unfortunately, this translates into very practical problems while managing such cases since there is not much evidence or guidelines to go on except one's own experience in dealing with incisional hernias. We felt that the continued presence of the shunt tubing at the hernia site, and the point of its entry into the 38 peritoneal cavity would always act as a weak point in the anterior abdominal wall and a potential site of herniation. Therefore, to our minds, removal of the shunt if it was no longer required, and repair of the incisional hernia was the best option, but this had already been vetoed by the treating neurosurgeons who wanted to keep the shunt in place. The second option that we discussed was re-positioning of the abdominal end of the shunt through another area and mesh repair of the incisional hernia, both laparoscopically, but the patient was not willing for this since (a) he did not want any manipulation of the shunt, and (b), the costs of this procedure in our set up are quite high and were unaffordable for him. In the end, we were left with no other option but to perform an open hernioplasty, taking care not to damage the shunt during surgery. Not surprisingly, laparoscopy has found application in VP shunts also, not only to deal with the complications of the procedure, but also initially, at the time of performing the shunt. With its advantage of better vision and less tissue trauma, laparoscopic placement of the abdominal end of the shunt is rapidly becoming accepted as a procedure of choice, and has reportedly brought down the incidence of complications at the distal end [3,4,6,8–10]. In addition, laparoscopic placement of the shunts allows for confirmation of shunt patency and function by direct visualization of CSF flow from the shunt tubing [10]. The advantages of the laparoscopic approach also include a shorter hospital stay, less post-operative pain, lower chance of incisional hernia formation, and, since the catheter is positioned under direct vision with minimal bowel manipulation, there is a much lower chance of bowel injury and adhesion formation [6,8]. Even when dealing with complications, laparoscopy offers a distinct advantage over laparotomy, especially in terms of superior visualization of the peritoneal cavity, retrieval of displaced shunts, lysis of adhesions, culture of abdominal fluid, repositioning of displaced tubings, and assessing the abdomen for any other pathology [2-4,6,8, 10]. However, the flip side is that separate incisions (for port and shunt placement) as well as two separate teams (neurosurgical and laparoscopic) are required, which may not be available everywhere. Being unable to perform laparoscopic surgery in our patient, we proceeded with open, onlay hernioplasty. The Sri Lanka Journal of Surgery 2015; 33(1): 37-40 Marking of the shunt pre-operatively, repeated digital palpation, careful dissection, and taking care not to pass the suture needle through the shunt tubing at the time of fixing the mesh were important steps that we took to avoid inadvertent damage to the shunt tubing during surgery, which could have had disastrous consequences. As we mentioned above, the application of laparoscopic surgery in VP shunt placement will further reduce the incidence of incisional hernia after VP shunting, but we hope that our experience with open repair of such a rare hernia might help those who may occasionally come across such cases who do not have access to laparoscopic facilities. References 1. Chung JJ, Yu JS, Kim JH, et al. Intraabdominal complications secondary to ventriculoperitoneal shunts: CT findings and review of the literature. AJR Am J Roentgenol 2009;193:1311-7 2. Acharya R, Ramachandran CS, Singh S. Laparoscopic management of abdominal complications in ventriculoperitoneal shunt surgery. J LaparoendoscAdvSurg Tech A 2001; 11:167-70 3. Popa F, Grigorean VT, Onose G, et al. Laparoscopic treatment of abdominal complications following ventriculoperitoneal shunt. J Med Life 2009; 2: 426 - 36 4. RaysiDehcordi S, De Tommasi C, Ricci A, et al. Laparoscopy-assisted ventriculoperitoneal shunt surgery: personal experience and review of the literature. Neurosurg Rev 2011; 34:363-70; discussion 370-1 5. Coley BD, Kosnik EJ. Abdominal complications of ventriculoperitoneal shunts in children. Semin Ultrasound CT MR 2006; 27: 152 – 60 6. Nfonsam V, Chand B, Rosenblatt S, et al. Laparoscopic management of distal ventriculoperitoneal shunt complications. SurgEndosc 2008; 22:1866 – 70 7. Agha FP, Amendola MA, Shirazi KK, et al. Unusual abdominal complications of ventriculo-peritoneal shunts. Radiology1983; 146:323- 6 8. Park YS, Park IS, Park KB, et al. Laparotomy versus Laparoscopic Placement of Distal Catheter in Ventriculoperitoneal Shunt Procedure. J Korean NeurosurgSoc 2010; 48: 325-329 9. Jea A, Al-Otibi M, Bonnard A, Drake JM. Laparoscopy-assisted ventriculoperitoneal shunt surgery in children: a series of 11 cases. J Neurosurg 2007; 106:421-5 10. Kavic SM, Segan RD, Taylor MD, Roth JS. Laparoscopic Management of Ventriculoperitoneal and Lumboperitoneal Shunt Complications. JSLS 2007; 11:14–19 11. Javid JP, Greenberg JA, Brook DC. Hernias. In: Zinner MJ, Ashley SW Jr. (Eds.) Maingot's Abdominal Operations, 12th Edition, 2012 McGraw-Hill Professional, New York 39 Incisional hernia after VP shunt insertion is a rare complication at the abdominal end. Treatment options include: -Removal of the shunt if it is no longer required, and repair of the incisional hernia. -Laparoscopic re-positioning of the abdominal end of the shunt through another area and mesh repair of the incisional hernia. -Open, onlay hernioplasty, avoiding inadvertent damage to the shunt tubing during surgery. The Sri Lanka Journal of Surgery 2015; 33(1): 37-40 40 CASE REPORTS Epidermal splenic cyst G. H. M. Pinsara, N. Liyanage, P. G. K. Anuradha, P.M. Lambiyas, H. Gamage Gastrointestinal Surgical Unit, Teaching Hospital Karapitiya, Galle. Key words: Epithelial cysts; splenectomy; spleen 1. A cyst arising from the pancreas Abstract 2. A cyst arising from the spleen We report a case of a large epithelial cyst of the spleen of an 18 year old man who was treated with splenectomy. The management of splenic cysts has changed from total splenectomy to splenic preservation surgery. But complete splenectomy is reserved for cases in which cyst excision cannot be done. Introduction Splenic cysts are rare lesions with 800 cases reported in the world literature [1]. Splenic cysts are classified into primary (true) or secondary (false) cysts on the basis of presence or absence of cellular lining of the cystic wall [2]. The true incidence of splenic cysts is unknown. The prevalence of splenic cysts has increased recently secondary to increased detection with the computerized tomography and the non-operative management of certain types of splenic injury [3]. Here we present a case of non-parasitic large epithelial cyst. Case report An 18 year old man presented with left sided abdominal distension for 4 years. There was no history of abdominal pain, history of trauma, significant medical illness or surgical intervention in the past. Abdominal examination revealed a large mass in the left hypochondrium extending to the umbilical region and epigastrium. The patient had a contrast enhanced CT scan of the abdomen which showed a large cystic lesion measuring 20×20×21cm in relation to the pancreas. Based on imaging, the following diagnoses were considered; In order to determine whether it was a pancreatic cyst or a splenic cyst an ultrasound guided aspiration of the cyst was arranged and the aspirate was sent for amylase, carcino-embryonic antigen (CEA), CA 19-9 and cytology. Cytology revealed a straw coloured proteinaceous fluid with no evidence of micro-organism growth or malignant cells. CEA, CA 19-9 and amylase levels were normal. Other haematological investigations were unremarkable. This makes the diagnosis more in favour of a cyst arising from the spleen. Exploratory laparotomy was planned. As there was a possibility of a splenectomy he was referred to the haematology unit and he was given polyvalent pneumococcal and meningcoccal vaccines. At laparotomy a large splenic cyst was found in relation to the hilum of the spleen. The spleen was elongated, flattened and was sandwiched between the anterolateral abdominal wall and the cyst. Stomach and left kidney were displaced towards the right side. There were adhesions with the tail of the pancreas and also dense inseparable adhesions with the diaphragm. Firstly, reduction of cyst with intraoperative drainage of approximately 3 litres of straw coloured fluid was carried out. It was followed by complete splenectomy due to the large size of the cyst, cyst location and presence of adhesions with adjacent structures. Histologically it was a unilocular cyst with dense fibrous cyst wall lined by flattened epithelium. Therefore the histopathological diagnosis was primary splenic (epithelial) cyst. Post-operative clinical course was satisfactory and at follow up the patient was asymptomatic and was started on lifelong penicillin prophylaxis. Correspondence: Dr. Prageeth Lambiyas E-mail: [email protected] The Sri Lanka Journal of Surgery 2015; 33(1): 41-44 41 Figure 1. CECT abdomen showing a large cyst compressing the surrounding structure. Figure 4. Specimen of the aspirated cyst removed from the patient Figure5. Interior appearance of the cyst Figure 2. Sagittal section of the CECT abdomen Discussion Figure 3. Intraoperative picture of the cyst The spleen plays an important role in haemopoiesis, immune function and protection against infections and malignancies. Splenic cysts are very rare. They are classified as primary (true) or secondary (pseudo/false) cyst. Primary cysts have a cellular lining in the cyst wall and are parasitic or non-parasitic in origin. Non parasitic type primary cysts are further classified as congenital or neoplastic. Congenital splenic cysts are also called epidermoid or epithelial cysts. They are uncommon and account for only 10% of all splenic cysts. 80% of epithelial splenic cysts occur in patients aged under 20 year but can occur in children and infants [4,5]. The Sri Lanka Journal of Surgery 2015; 33(1): 41-44 42 Secondary cysts without cellular lining usually occur following blunt trauma to the upper abdomen and is considered responsible for 75% of secondary cysts [6]. Both types of splenic cysts usually do not produce any specific symptoms until they reach a significant size and may remain asymptomatic in 30–60% of patients [7]. Splenic cysts may present with localized or referred pain, splenomegaly, abdominal distension and symptoms and signs relating to compression of nearby structures. The latter include early satiety, dysphagia, nausea, vomiting, atelectasis and left lower lobe pneumonia [8]. Cysts may also be an incidental finding on abdominal imaging for another purpose. A comprehensive differential diagnosis includes cystic lesions of adjacent structures (eg: pancreas, liver, omentum), intrasplenic aneurysms, benign & malignant splenic tumours, pyogenic splenic abscesses and rare parasitic ecchinococcal disease which is more common in Africa and Central America [9]. Physical examination is usually normal apart from the abdominal distension with abdominal mass. Routine haemotological and biochemical investigations are also within normal range. Tumour markers such as CEA and CA19.9 levels are usually elevated in the true cyst and rarely high in pseudo cysts due to the absence of epithelial lining [10,11]. But CA 19.9 and CEA levels were in the normal range in our case. Indications for operative intervention of the splenic cysts include symptomatic splenic cysts and cysts with a diameter >5 cm because of increased risk of complications [12]. Surgical intervention aims to eradicate the cyst and prevent recurrence. Operative methods include both open and laparoscopic techniques. Traditionally splenic cysts have been treated with the open complete splenectomy. Currently the trend is to more conservative surgery preserving the spleen with the demonstration of life long risk of overwhelming post splenectomy sepsis (OPSI). Post splenectomy patient has 5% life time risk of developing OPSI which carries a mortality rate of 38-69 % [13]. Options available for the splenic preservation include total cystectomy, marsupialization, cyst decapsulation (unroofing) or partial splenectomy; accessed either by open laparotomy or laparoscopy. Other conservative The Sri Lanka Journal of Surgery 2015; 33(1): 41-44 methods include sclerosis or drainage using radiological guidance. The incidence of recurrence of these methods has been reported high as 100% [3]. Partial splenectomy preserves more than 25% splenic parenchyma which is the minimal splenic tissue to preserve immunological protection without increasing the risk of recurrence [14]. In unroofing/ partial splenic cystectomy, the cyst wall should be resected as much as possible to prevent recurrence of the cyst. Marsupialization is another conservative surgery which reduces the duration of surgery and carries no risk of recurrence. But it is difficult to perform any type of conservative surgery if the cyst is very large; if it is completely covered by the splenic parenchyma (intrasplenic cyst); if it is located in the hilum of the spleen, if there are multiple cysts (polycystic cases) or dense vesicular adhesions to adjacent structures; in these situations, a complete splenectomy should be performed using open or laparoscopic approach [15] In our case it was impossible to manage with percutaneous drainage and sclerosis technique due to the large size of the cyst. We had to treat a very large cyst located in the splenic hilum with dense inflammatory adhesions around the spleen, whereas splenic parenchyma consisted of rim of tissue pushed to periphery making any possibility of splenic preservation surgery highly unlikely. Therefore the patient was treated with open complete splenectomy. References 1. 2. 3. 4. 5. 6. Geraghty M, Khan IZ, Conlon KC. Large primary splenic cyst: a laparoscopic technique. J Minim Access Surg 2009; 5:14-6. Martin JW. Congenital splenic cysts. Am J Surg 1958; 96:302–8 Wu H, Kortbeek J. Management of splenic pseudo cysts following trauma: A retrospective case series. Am J Surg 2006;5:631–4. Carpenter G, Cotter PW, Davidson JRM. Epidermoid cyst of the spleen. Aust N Z J Surg 1986;56:365-8. Sakamoto Y, Yunotani S, Edakuni G, Mori M, Iyama A, Miyazaki K. Laparoscopic splenectomy for a giant splenic epidermoid cyst: report of a case. Surg Today 1999;29:1268–72. Pachter HL, Hofstetter SR, Elkowitz A, Harris L, Liang HG. The role of cystectomy and splenic preservation: Experience with seven consecutive patients. J Trauma 43 1993;35:430–6. 7. Labruzzo C, Haritopoulos KN, Tayar AR, Hakim NS. Posttraumatic cyst of the spleen: A case report and review of the literature. Int Surg 2002;82:152–6. 8. Gibeily GJ, Eisenberg BL. Splenic cysts-diagnosis and management. West j Med 1988;148:464-6. 9. Sellers GJ, Starker PM. Laparoscopic treatment of benign splenic cysts. Surg Endoscopy 1997;11:766–8. 10. Walz MK, Metz KA, Sastry M, Eigler FW, Leder LD. Benign mesothelial splenic cyst may cause high serum concentrations of CA-19-9. Eur J Surg 1994;160:389–91. 11. Madia C, Lumachi F, Veroux M, Fiamingo P, Gringeri E, 12. 13. 14. 15. Brolese A, et al. Giant splenic epithelial cyst with elevated serum markers CEA and CA 19-9 levels: an incidental association. Anticancer Res 2003;23:773-6. Till H, Schaarschmidt K. Partial laparoscopic decapsulation of congenital splenic cysts. SurgEndosc 2004;18:626–8. Davidson RN, Wall RA. Prevention and management of infections in patients without a spleen. ClinMicrobiol Infect 2001;12:657–60. Hansen MB, Moller AC. Splenic cysts. SurgLaparoscEndoscPercutan Tech 2004;14:316–22. Avital S, Kashtan H. A large epithelial splenic cyst. N Engl J Med 2003; 349: 2173-2174. Key Points: Splenic cysts are a rare phenomenon now increasingly identified due to increased imaging Symptomatic and large cysts are an indication for surgery Splenic preservation surgery is the treatment of choice when possible The Sri Lanka Journal of Surgery 2015; 33(1): 41-44 44 SELECTED ABSTRACTS C-reactive protein to predict the need for surgical intervention in acute renal colic McSorley ST et al. Journal of Clinical Urology 2014; 7(6):380-383. Objectives C-reactive protein (CRP) is a serum marker of systemic inflammation which has been suggested to predict need for emergent surgical intervention in patients with acute renal colic at a value of > 28 mg/l on admission. We aimed to determine if this applied to our patients. Patients and methods We prospectively collected data from all patients admitted with symptomatic urolithiasis, confirmed by CT-KUB, over three months. Fifty-nine patients were included; however, four were excluded because of comorbidites which could influence CRP, or recent urological surgery, giving N = 55, age 50.0±14.6 years (mean±SD), M:F 40:15. The decision to proceed to intervention was made by each patient's clinical team and not by the authors; however, there was no blinding to CRP. Commentary Ajith Malalasekera Consultant urological surgeon and senior lecturer in anatomy Faculty of Medicine, University of Colombo This study reinforces the importance of assessing for the presence of sepsis in patients with renal colic. Apart from clinical evidence of infection, CRP, especially rising CRP will, according to this study, add to the information that will identify those requiring intervention. While this marker rises in response to inflammation in the patient, it is not specific to the site nor a particular cause. Clinicians must be aware of factors which may raise the CRP (e.g. inflammation, trauma, infection) when utilising this information in the management of renal colic patients. Use of drains versus no drains after burr-hole evacuation of chronic subdural haematoma: a randomised controlled trial. Santarius T et al. Lancet 2009 Sep 26;374(9695):106773. Results Background A total of 24 of 55 patients required intervention on their index admission (22 retrograde ureteric stent, one nephrostomy, one ureteroscopic stone extraction), and 31 were managed conservatively. Those undergoing intervention had higher CRP on admission (mean 16.3 vs 9.4 mg/l, p = 0.06) and higher maximum CRP (mean 94.7 vs 25.7 mg/l, p < 0.001) than those managed conservatively. Nineteen (79%) of those requiring intervention had CRP < 28 mg/l on admission. There were no deaths, no intensive care admissions and all were discharged to outpatient follow-up. Chronic subdural haematoma causes serious morbidity and mortality. It recurs after surgical evacuation in 5-30% of patients. Drains might reduce recurrence but are not used routinely. Our aim was to investigate the effect of drains on recurrence rates and clinical outcomes. Conclusion Rising CRP during admission is a strong predictor of the need for emergency surgical intervention in patients with acute renal colic; however, CRP at admission is less useful. The Sri Lanka Journal of Surgery 2015; 33(1): 45-49 Methods We did a randomised controlled trial at one UK centre between November, 2004, and November, 2007. 269 patients aged 18 years and older with a chronic subdural haematoma for burr-hole drainage were assessed for eligibility. 108 were randomly assigned by block randomisation to receive a drain inserted into the subdural space and 107 to no drain after evacuation. The primary endpoint was recurrence needing redrainage. The trial was stopped early because of a significant 45 benefit in reduction of recurrence. Analyses were done on an intention-to-treat basis. This study is registered with the International Standard Randomised Controlled Trial Register (ISRCTN 97314294). Findings cytoreductive surgery (CCRS) of colorectal peritoneal carcinomatosis (PC) followed by intraperitoneal chemotherapy (IPC) are completeness of the resection and extent of the disease. This study aimed to determine a threshold value above which CCRS plus IPC may not offer survival benefit compared with systemic chemotherapy. Recurrence occurred in ten of 108 (9.3%) people with a drain, and 26 of 107 (24%) without (p=0.003; 95% CI 0.14-0.70). At 6 months mortality was nine of 105 (8.6%) and 19 of 105 (18.1%), respectively (p=0.042; 95% CI 0.1-0.99). Medical and surgical complications were much the same between the study groups. Between March 2000 and May 2010, 180 patients underwent surgery for PC from colorectal cancer with intended performance of CCRS plus IPC. Intrpretation Results Use of a drain after burr-hole drainage of chronic subdural haematomas is safe and associated with reduced recurrence and mortality at 6 months Among the 180 patients, CCRS plus IPC could be performed for 139 patients (curative group, 77%), whereas it could not be performed for 41 patients (palliative group, 23%). The two groups were comparable in terms of age, gender, primary tumor characteristics, and pre and postoperative systemic chemotherapy. The mean peritoneal cancer index (PCI) was lower in the curative group (11±7) than in the palliative group (23±7) (p < 0.0001). After a median follow-up period of 60 months (range 47–74 months), the 3-year overall survival (OS) rate was 52 % [95% confidence interval (CI) 43–61%] in the curative group compared with 7% (95% CI 2–25%) in the palliative group. Comparison of the survivals for each PCI (ranging from 5 to 36) shows that OS did not differ significantly between the two groups of patients when the PCI was higher than 17 (hazard ratio 0.64; range 0.38–1.09). Commentary Ruvini Abeygunaratne Consultant Neurosurgeon Hope hospital, Manchester and Lanka hospitals, Colombo This is a landmark paper in neurosurgery dealing with a common but important condition with a high mortality and morbidity. Chronic subdural haematomas are common and generally affect the elderly population who suffer from a number of pre-existing pathologies. Therefore there are risks associated with recurrent surgery, and thereby morbidity and mortality increases. The most effective treatment is that which involves one surgical procedure which is quick and safely done with measures taken to reduce the incidence of recurrence. This randomised trial demonstrates that the use of subdural drains routinely reduces the rate of recurrence and the 6 month mortality. Extent of colorectal peritoneal carcinomatosis: Attempt to define a threshold above which HIPEC does not offer survival benefit: a comparative study Goéré D et al. Annals of Surgical Oncology 2015; (Online First) 1-7 Background The main prognostic factors after complete The Sri Lanka Journal of Surgery 2015; 33(1): 45-49 Methods Conclusion This study confirmed the major prognostic impact of PC extent. When the PCI exceeds 17 in PC of colorectal origin, CCRS plus IPC does not seem to offer any survival benefit. Commentary Dulantha de Silva Senior Lecturer in Surgery General Sir John Kotelawala Defence University Presence of peritoneal metastases in colorectal cancer has been generally associated with dismal prognosis, conferring a virtual death sentence on the sufferer. In the 46 last two decades however, the introduction of Cytoreductive Surgery (CRS) combined with hyperthermic intra-peritoneal chemotherapy (HIPEC) has given rise to 5-year survival rates of up to 30-50% in select groups of patients. controversial. The purpose of this study is to conduct a systematic review of randomized clinical trials assessing the results of hemiarthroplasty and total hip replacement in patients undergoing either alternative using meta-analysis. This prospective study from a centre with significant experience in this technique is an attempt to further define the group of patients with potential to benefit from this treatment strategy. Two major factors affecting outcome in these patients are the completeness of cytoreduction i.e. removal of all macroscopic tumour nodules greater than 1mm and the extent of peritoneal metastases as defined by the peritoneal carcinomatosis index (PCI score). Methods Evidence has long indicated that inability to achieve complete cytoreduction is associated with poor prognosis with survival no better than with palliative chemotherapy. The data from this study supports that contention. The study also shows an impressive overall 3-year survival rate of 52% for complete CRS and HIPEC. However sub-group analysis does indicate that with PCI scores greater than 17, it confers no survival advantage even in the presence of complete cytoreduction. The data from this study adds to the evidence that in patients with relatively limited peritoneal disease, CCRS and HIPEC can be associated with significant survival benefits. The place of this technique is still controversial among some authorities, perhaps due to the paucity of good quality randomised control trials evaluating its efficacy. Nevertheless, it is hard to ignore the potential promise of this procedure in offering a chance of survival in a number of patients otherwise condemned to palliation. Outcome of hemiarthroplasty and total hip replacement for active elderly patients with displaced femoral neck fractures: A meta-analysis of 8 randomized clinical trials Yiqiong Zhao, A Meta-Analysis of 8 Randomized Clinical Trials. PLoS ONE 9(5):e98071. Background Displaced fracture of the femoral neck has been a common clinical problem, especially in aged patients. However, the optimal treatment choice remains The Sri Lanka Journal of Surgery 2015; 33(1): 45-49 A literature search for randomized clinical trials was conducted through Medline, Embase and Cochrane library between 1969 and 2013 with no restrictions. Additional relevant articles were referred as source of information by way of manual searches on major orthopedic journals. Upon the search, two authors independently evaluated study quality and relevant data was extracted. Results A total of 8 studies with 983 patients were included in this meta-analysis. After pooling the available data, a significant dominance of Harris hip score was found for total hip replacement compared with hemiarthroplasty ( S M D : 2 7 . 11 , 9 5 % : 2 1 0 . 7 0 , 2 3 . 5 3 ) o n e y e a r postoperatively and the advantage kept over (SMD: 26.91, 95%:212.98, 20.85) two years after surgery. A trend toward a higher dislocation rate was found in total hip replacement group (RR: 0.46, 95%: 0.21,1.02), of which the difference was considered insignificant. The risk of revision in group hemiarthroplasty appeared to be more than two fold higher than that after total hip replacement (RR: 4.14, 95%CI: 2.09, 8.19). Conclusion Even though there is a higher rate of dislocation after total hip replacement, this disadvantage could be accounted for, on the basis of a better functional score and the lower revision rate. However, from the results, it stands to reason that total hip replacement should be strongly suggested in elderly active patients with femoral neck fracture. Commentary Hiran Amarasekera Consultant Orthopaedic Surgeon Neville Fernando Teaching Hospital Malabe The treatment of choice for sub capital femoral neck fractures in last decades has been hemi arthroplasty. 47 Either cementless (Austin-Moore) or cemented (Thompson) type prosthesis has been widely used. However with increasing life expectancy and increased active lifestyle in the elderly total hip replacement (THR) has been preferred as the first line of treatment by some orthopaedic surgeons. Where is the evidence helping orthopaedic surgeons to make that decision? Zhao et al has combined eight randomized control trials in this meta-analysis to answer this question. Eight randomised trials done in Germany, Italy, Sweden, Holland, UK and USA with a total of 983 patients were included in the meta-analysis. Authors conclude that apart from a slightly higher dislocation rate the benefits of a total hip replacement in the active elderly outweigh the risks and suggest this as the treatment of choice. As all these studies have been done in developed countries the information should be cautiously applied in a developing country such as Sri Lanka. Points to consider in our setting are the cost difference between the two implants, time taken for the surgery, expertise level available in the health service, workload of the surgeon, age and activity level of the patient. Cost difference between the two implants is significant, a THR costing 10 to 15 times that of a h e m i a r t h r o p l a s t y. S k i l l l e v e l n e e d e d f o r hemiarthroplasty is less than for a THR enabling junior surgeons such as SHOs and trainees to do them. Time taken for a hemiarthroplasty is far less than for a THR a key factor in a setting with a high workload and limited theatre time. The activity level and demand for independent mobility of Sri Lankans may be less than that of the European patients. Nevertheless the times are changing with increasing life expectancy, and increasing number of elderly living alone, leading to increased demand for THR over the years. However if we were to adopt THR as primary treatment for femoral neck fractures our own criteria should be developed considering above factors to suite the Sri Lankan setting. Prior to developing these criteria it will be interesting to know the percentage of hemi arthroplasties that are revised for a THR and the indication for the revision. A research project to find this information is essential to move forward in the right direction The Sri Lanka Journal of Surgery 2015; 33(1): 45-49 The Society for Vascular Surgery lower extremity threatened limb classification system based on wound, ischemia, and foot infection (WIfI) correlates with risk of major amputation and time to wound healing Zhan, Luke X. et al. Journal of Vascular Surgery, Volume 61, Issue 4 , 939 - 944 Objective The purpose of this study was to evaluate whether the new Society for Vascular Surgery (SVS) Wound, Ischemia, and foot Infection (WIfI) classification system correlates with important clinical outcomes for limb salvage and wound healing. Methods A total of 201 consecutive patients with threatened limbs treated from 2010 to 2011 in an academic medical center were analyzed. These patients were stratified into clinical stages 1 to 4 on the basis of the SVS WIfI classification. The SVS objective performance goals of major amputation, 1-year amputation-free survival (AFS) rate, and wound healing time (WHT) according to WIfI clinical stages were compared. Results The mean age was 58 years (79% male, 93% with diabetes). Forty-two patients required major amputation (21%); 159 (78%) had limb salvage. The amputation group had a significantly higher prevalence of advanced stage 4 patients (P < .001), whereas the limb salvage group presented predominantly as stages 1 to 3. Patients in clinical stages 3 and 4 had a significantly higher incidence of amputation (P < .001), decreased AFS (P < .001), and delayed WHT (P < .002) compared with those in stages 1 and 2. Among patients presenting with stage 3, primarily as a result of wound and ischemia grades, revascularization resulted in accelerated WHT (P = .008). Conclusions These data support the underlying concept of the SVS WIfI, that an appropriate classification system correlates with important clinical outcomes for limb salvage and wound healing. As the clinical stage progresses, the risk of major amputation increases, 48 1-year AFS declines, and WHT is prolonged. We further demonstrated benefit of revascularization to improve WHT in selected patients, especially those in stage 3. Future efforts are warranted to incorporate the SVS WIfI classification into clinical decision-making algorithms in conjunction with a comorbidity index and anatomic classification. Commentary Dr. Nalaka Gunawansa Consultant Vascular and Transplant Surgeon National Institute for Nephrology Dialysis and Transplantation National Hospital of Sri Lanka Salvaging the infected diabetic foot and preventing major amputation is a tremendous challenge to all general and vascular surgeons worldwide. Deciding which patient can be safely salvaged without major amputation and which patient will benefit with a revascularization procedure to attempt such limb salvage has been an ongoing debate even amongst vascular surgeons. While not all diabetic foot ulcers The Sri Lanka Journal of Surgery 2015; 33(1): 45-49 with infection warrant amputation, neither do all ischaemic diabetic feet benefit by revascularization, especially if the infection has destroyed the tissue beyond a point of potential salvage. The Society of Vascular Surgery (SVS) has thus introduced a scoring system that incorporates the three main determinants of such limb salvage (wound extent, degree of limb ischaemia and degree of foot infection) to shed some light and guidelines in this area of controversy. This study was the first major study that adopted the said scoring system in clinical practice to assess its applicability across a wide spectrum of patients suffering from different degrees of ischamic diabetic foot ulcers. Although the sample size was relatively small to be used as a benchmark for future revascularization attempts, the study has shown the clinical applicability and use of such a scoring system to predict limb salvage and amputation free survival rates. This will invariably assist in the decision making process of clinicians before embarking on revascularization or condemning for major amputation. 49 The Sri Lanka Journal of Surgery can now be viewed online. Please visit: www.lankasurgeons.org or Sri Lanka Journals online (http://sljs.sljol.info/) <Full page ad space - back outer cover>
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