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Diverticular disease
Best Practice & Research Clinical Gastroenterology Vol. 16, No. 1, pp. 135±148, 2002
doi:10.1053/bega.2002.0270, available online at http://www.idealibrary.com on
9 Diverticular disease Ronald J. Place
MD, FACS
Chief, Section of Colon and Rectal Surgery Department of Surgery, Madigan Army Medical Center, Ft. Lewis, WA 98431, USA
Cliord L. Simmang*
MD, FACS, FASCRS
Associate Professor of Surgery and Program Director of Colon and Rectal Surgery Department of Surgery, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 95390-9156, USA
Diverticular disease is a common ®nding in Western countries with an increasing prevalence with age. Many patients with the disorder remain asymptomatic. However, up to 30% of those aected may show clinical signs including pain, bleeding, obstruction, abscess, ®stulae and perforation. The purpose of this chapter is to review the epidemiology, pathogenesis, clinical presentation, diagnostic regimens and treatment options for this disorder. Key words: diverticulosis; diverticulitis; gastrointestinal haemorrhage; abscess; peritonitis.
INTRODUCTION Epidemiology Colonic diverticular disease includes a constellation of symptoms that ranges from mild irregularities in defaecatory function to bleeding and severe intra-abdominal in¯ammation. The incidence of diverticula rises within a society as it reduces its dietary ®bre intake. Animal studies con®rm these data, since 45% of rats fed a low ®bre diet developed diverticulitis compared with 9% fed a high ®bre diet.1 Historically, geographical location has been an important predictor of the prevalence, with diverticula being common in Western countries, less so in South America and rare in Africa and the Orient. As economic development and the adoption of a Western diet has increased, the diverticular disease prevalence has risen as well.2,3 Diverticulosis is uncommon before the age of 40 and increases in frequency with age.4 Post-mortem reports suggest that it is found in up to half of adults over the age of 60.5 The anatomical distribution of diverticula varies with geographical location. Industrialized countries with a Western diet have predominantly left-sided diverticula. Right-sided diverticulosis is more common and appears to have fewer clinical complications than left-sided disease in Japan.6 As left-sided diverticular disease increases in societies of previously low prevalence, right-sided colonic diverticulosis persists.7 These variations in anatomical distribution among ethnic groups support a multi-factorial basis for the disease. *All correspondence to: Dr Cliord L. Simmang, Tel: +1 (214) 648-9467; Fax: +1 (214) 648-2301; E-mail: [email protected] 1521±6918/02/01013514 $35.00/00
c 2002 Harcourt Publishers Ltd. *
136 R. J. Place and C. L. Simmang
Pathology The majority of colonic diverticula are histologically pseudodiverticula, consisting of herniations of the mucosa and submucosa through the muscular wall of the colon. Although true diverticula containing all bowel wall layers do occur as congenital anomalies, the more common pulsion pseudodiverticula are acquired. The outer longitudinal muscle ®bres form discrete taeniae, leaving the colonic wall predominantly a single layer of circular muscle ®bres. Diverticula develop in rows between the mesenteric and lateral taenia. The points of greatest muscular weakness are where the intramural vasa recta penetrate the circular muscle to the submucosa.8 In most patients with sigmoid diverticulosis, both muscle layers are greatly increased in thickness. This is associated with shortening of the taeniae producing a deformity called myochosis, which narrows the colonic lumen, allowing muscle contractions to obliterate the lumen and divide the bowel into isolated segments. These changes facilitate the transmission of higher pressures to the mucosa via the vasa recta. Luminal narrowing may be secondary to the shortening of the sigmoid musculature as well as pericolic ®brosis.9 Histological abnormalities include the presence of excess elastin in the taeniae that is not seen in the circular muscle.10 Elastosis may contribute to sacculation, with contraction of the sigmoid colon as elastin ®bres in the remaining circular muscle deteriorate with age. Tensile strength in the bowel wall decreases with senescence.11 Alterations in collagen structure appear to be due to increases in the cross-linking of colonic collagen with age, rather than a decrease in the total collagen content.12 The possibility of myenteric neural injury has also been explored. Preliminary data show that recombinant human brain-derived neurotrophic factor (rHuBDNF) accelerates colonic transit and increases stool frequency in healthy adults.13 In addition, recombinant human neurotrophin-3 (rHuNT-3) accelerates orocaecal and colonic transit in constipated patients.14 Research relating any speci®c neurohormonal relationship to diverticulosis is lacking.15 Functional abnormalities Extensive studies by Painter have implicated the hypersegmentation resulting in intraluminal hypertension from the low bulk Western diet as the primary cause of diverticular disease.16 Intraluminal manometry shows that intracolonic pressures may exceed 90 mmHg when segmentation allows the motor work of the colonic musculature to be transmitted to the bowel wall rather than producing faecal transit. Fibre increases stool weight, lowers colonic pressures and improves transit time. This may prevent muscular hypertrophy and decrease the likelihood of segmentation and its resulting intraluminal hypertension. This hypothesis is supported in epidemiological studies by the inverse relationship between dietary ®bre and the presence of colonic diverticula.17 An additional protective eect is seen from increased physical activity.18 No studies support the concept of whole ®bre (nuts, seeds, etc) becoming entrapped in a diverticulum and leading to diverticulitis. DIVERTICULOSIS Clinical manifestation and dierential diagnosis The majority of patients with diverticulosis either have no symptoms, or symptoms of such a minor nature that they never seek medical attention.19 Some patients have
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symptoms of intermittent abdominal pain, bloating, excessive ¯atulence and irregular defaecation. Nausea, anorexia, passage of pellet-like stools or attacks of diarrhoea may also be present. Many conditions, especially those associated with altered intestinal motility, may be confused with diverticulosis. The most common of these is the irritable bowel syndrome (IBD), although the most important entity to consider is colorectal carcinoma.20 Both diverticular disease and colorectal carcinoma may have similar clinical presentations. Both conditions are common and are most frequently seen in the elderly. Any segment of the colon can be involved, but these conditions are most commonly found in the left colon, especially the sigmoid. Late manifestations of both diseases can result in luminal narrowing, obstruction, perforation, or the development of a ®stula. Also, both may be clinically silent for a long period of time. Patients with IBD present with intestinal symptoms, but evaluation fails to reveal an anatomical abnormality. It has been suggested that IBD may precede the development of diverticular disease, but no evidence has been found for a causal relationship between the two conditions.21 Either way, the management of uncomplicated diverticular disease and IBD are similar. Diagnostic studies In patients with diverticulosis, plain abdominal radiographs are normal. Colonic evaluation is performed as much to rule out neoplasm as to con®rm diverticulosis. The diagnosis is most often established with a barium enema, since this is the best way to determine the extent and severity of diverticulosis. However, the accuracy of barium enema in diagnosing concomitant lesions has been reported to be as low as 50%.22,23 Reasons for this include a redundant and overlapping sigmoid colon obscuring visualization, or a narrowed spastic segment in which the intraluminal outline is dicult to visualize. Also, diverticula may masquerade as polyps by inversion or due to an adherent ball of stool.24,25 Lower gastrointestinal endoscopy is more useful for evaluating the large bowel for concomitant pathology than for diverticulosis. Rigid sigmoidoscopy usually can not be advanced beyond the rectosigmoid junction and only rarely will visualize diverticular ori®ces. By contrast, ¯exible sigmoidoscopy may allow identi®cation of the ori®ces. Patient discomfort and diculty with advancement of the endoscope may limit this examination. Sigmoid tortuosity and thickened rugae suggest previous episodes of diverticulitis.26 Colonoscopy has proved useful in dierentiating diverticular disease from carcinoma. However, attempts to visualize the diseased segments seen on barium enema have been possible in only 50±73% of patients secondary to oedema or strictures.27,28 An evaluation of 125 patients with complicated diverticular disease identi®ed an associated carcinoma in 17% and an additional diagnosis in 32%.29 The presence of bleeding is a signi®cant risk factor for the presence of a concomitant lesion. In a group of 135 patients with persistent bleeding in whom barium enema showed only diverticular disease, 11% had carcinoma and an additional diagnosis was made in 37%.21 These ®ndings strongly suggest that colonoscopic evaluation in patients with diverticular disease, especially complicated diverticular disease, should be performed. Treatment The principle treatment for patients with diverticular disease has revolved around a high ®bre diet. A diet with a high bulk content reduces colonic pressure and may
138 R. J. Place and C. L. Simmang
prevent the development of diverticula.17,30 Daily ingestion of 20±30 g of bran is necessary to achieve a therapeutic eect.31 Coarse bran has been shown to be more eective than ®ne bran in increasing stool weight, speeding transit time and reducing intraluminal pressure in the colon.32 Many people ®nd it dicult to ingest the needed ®bre from dietary foods. The addition of commercial bulk forming agents such as psyllium provides a suitable substitute. DIVERTICULAR BLEEDING Dierential diagnosis Painless rectal bleeding is associated with diverticulosis in up to 30% of patients.33 Although this bleeding is usually of minor clinical signi®cance, massive bleeding from colonic diverticula may occur in 5% of patients with diverticulosis.34 Because most diverticular bleeding does not require therapy, the importance of the evaluation of bleeding in patients with known diverticular disease is to diagnose concurrent causes, including colitis and carcinoma. Diverticulosis is so common in the adult population that the attribution of bleeding to diverticular disease must be a diagnosis of exclusion. The cause of diverticular bleeding appears to be chronic injury to the vasa recta adjacent to the lumen of the diverticulum.35 The mechanism leading to intimal thickening with fragmentation of the internal elastic lamina and thinning of the media is not known. The predilection for right-sided diverticula to bleed may be related to a larger lumen, which exposes more of the vasa recta to potential disruption.35 The importance of angiodysplasia of the right colon has now been recognized as of nearly equal importance in causing severe lower gastrointestinal haemorrhage.36 In the elderly population in particular, the most frequent location of massive angiodysplastic bleeding is the right colon.37 Fortuitously, most bleeding diverticula are also found in the right colon. Patients presenting with profuse rectal bleeding often have no antecedent history of diverticular complications. In an elderly patient, the sudden onset of painless, brisk haematochezia may quickly lead to hypotension. This demands a prompt and organized evaluation concurrent with resuscitation. Although physical examination may be unrewarding, sigmoidoscopy may reveal the rare rectal cancer or identify the patient with acute colitis that presents with massive bleeding. The usual resuscitative measures should be performed including establishing large bore intravenous access, placement of an indwelling urinary catheter and passage of a nasogastric tube to rule out a massive upper bleeding source.38 Blood should be obtained for type and cross-match, determination of electrolytes and coagulation studies. Further invasive diagnostic techniques depend upon the rate of blood loss, the medical condition of the patient and the prompt availability of these procedures. A barium enema is no longer considered a useful initial study, since its sensitivity and speci®city are both inadequate and residual barium will obscure subsequent assessment. Diagnostic studies Nuclear scanning techniques using Technetium 99m sulphur colloid and Technetiumtagged red blood cells may be useful in patients with a slow rate of bleeding. The cost, limited availability and morbidity of emergency arteriography initially prompted enthusiasm for radionucleotide imaging, at least as a screening test prior to angiography.39 In animal studies, bleeding scans can detect very low bleeding rates
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(0.1 ml/min) and are more likely to detect intermittent bleeding.40 However, a bleeding scan alone may not be speci®c enough to plan operative strategy.41 In patients with brisk bleeding, emergency angiography has become the initial procedure of choice. Angiography is both speci®c and highly sensitive if the rate of bleeding is sucient (0.5±1.0 ml/min).34 The superior mesenteric artery is studied ®rst, since the incidence of acute bleeding is highest from the right side of the colon. Next, the inferior mesenteric artery is studied, followed by a coeliac axis injection, which may show an unsuspected upper intestinal bleeding site. The speci®city of angiography is high if the study is positive and may reveal tumours, diuse mucosal bleeding, or the characteristic angiographic signs of angiodysplasia including delayed venous emptying, vascular tufts, or an early ®lling vein.42 A patient with a positive scan but negative arteriogram may be a good candidate for prompt colonoscopy. Bleeding sites have been identi®ed in up to 85% of patients.43 The technical compromise of emergency colonoscopy can be overcome when the bowel preparation and procedure are performed in the intensive care unit setting by an expert endoscopist.44 Treatment One advantage of diagnostic angiography is the option to attempt therapy by either infusion of vasospastic substances or selective embolization. Intra-arterial vasopressin can be temporarily eective in controlling diverticular haemorrhage.37 Unfortunately, rebleeding will occur in up to half of these patients following withdrawal of vasopressin.34 In addition, the use of vasopressin in these patients has several disadvantages including its eect on coronary perfusion, hypertension and arrhythmias. Embolization with autologous blood or Gelfoam1 is also eective. However, post-embolic colonic infarction is a signi®cant risk.45 In patients who fail angiographic treatment, mortality is increased. This may be due to a delay in eventual surgical treatment.46 Consequently, transcatheter embolization should probably be reserved for those patients at prohibitive surgical risk. Colonoscopic intervention is useful when the bleeding site can be visualized by this technique. Success has been reported with electrocoagulation of arterio-venous malformations.47 Like angiography, colonoscopic localization is extremely valuable in planning surgical treatment, even if endoscopic therapy ultimately proves unsuccessful. Surgery is clearly indicated in the treatment of persistent or recurrent diverticular bleeding. The most important factor in both safety and ecacy of surgery is a clear de®nition of the bleeding site during pre-operative investigations. Appropriate segmental colectomy yields a very low rebleeding rate.34,37,46,48 Considerable controversy continues regarding the procedural selection for the declining number of patients who come to operation for massive bleeding without pre-operative localization. Historically, total abdominal colectomy with ileoproctostomy was the procedure of choice, since a rebleeding rate of 30% was noted following blind segmental resection.49 The relatively high morbidity following emergency total colectomy may re¯ect other surgical risk factors such as multiple transfusions, age and coagulopathy in this subset of patients, rather than the technical aspects of the procedure. The indications are poorly de®ned for elective resection to prevent recurrent bleeding in patients who avoid initial operation. Recurrence of bleeding after one episode has been estimated at 20±30%, with a re-admission rate for further bleeding of 5% per year.48,50 Patients presenting with a second diverticular bleed have a greater than 50% risk of further recurrences.51 A conservative approach is probably warranted in most patients who
140 R. J. Place and C. L. Simmang
have a single bleed with a low transfusion requirement. However, resection after two or more episodes of bleeding requiring transfusion may be considered if the source of bleeding has been clearly identi®ed and the operative risk is acceptable. The morbidity and mortality of elective colon resection is much lower than the risks of emergency surgery, which continues to have a mortality of over 20% in bleeding patients.46,52,53
DIVERTICULITIS Diverticulitis results from in¯ammation and subsequent perforation of a colonic diverticulum. Occurring in 10±25% of patients with diverticulosis, diverticulitis represents the most common complication.33 The initial event is a microperforation that results in a peridiverticulitis and/or phlegmon, which is referred to as uncomplicated diverticulitis. Complicated diverticulitis ensues when continuation of the in¯ammatory and septic process is associated with obstruction, free perforation, ®stula, or abscess.54 Pathogenesis The mechanism of diverticulitis is felt to be the result of faecal material that has become inspissated within a diverticulum, producing a faecalith. This faecalith then becomes impacted or abrades the mucosal lining to produce a low grade chronic in¯ammation.9 It usually involves a single diverticulum in the sigmoid colon. This in¯ammatory process may proceed to either a micro- or macroperforation.21 With microperforation, peridiverticulitis ensues and is contained locally by pericolonic fat, mesentery or adjacent organs. With repeated episodes the phlegmonous reaction becomes more extensive. With healing, a ®brotic reaction may ensheathe the colon and produce segmental narrowing, stricture, or even obstruction.55 Macroperforation leads to either free perforation with generalized peritonitis, or a walled o and locally contained pericolonic abscess. The septic process can then erode into adjacent structures and produce a ®stula. The most common ®stula is the colovesical ®stula.56 Other ®stulae that may be commonly seen include colocutaneous, colovaginal and coloenteric ®stula.56±58 Uncommon ®stulae that have been reported include ®stulae between the colon and ureter, uterus, Fallopian tubes, perineum and even the venous system.59,60 Clinical features The most common presenting symptoms include left lower quadrant pain, fever and leukocytosis. If there has been progression of the disease process, the patient may present with symptoms of complicated diverticulitis such as a recurrent urinary tract infection, pneumaturia as a result of a colovesical ®stula, or a faeculent vaginal discharge from a colovaginal ®stula. The patient with free perforation and peritonitis will present with acute peritoneal signs. The most common ®nding on physical examination is tenderness in the left lower quadrant. Signs of localized peritoneal in¯ammation may be present with involuntary guarding and localized percussion tenderness. A tender mass representing the phlegmon can occasionally be palpated. Rectal examination often reveals tenderness in the pelvis.
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Diagnostic studies Initial laboratory studies that are often helpful include a complete blood count, urinalysis as well as abdominal ¯at and upright X-rays. Usually, the white blood cell count is elevated with a predominance of polymorphonuclear leukocytes. Urinalysis may reveal the presence of white blood cells if the in¯ammatory process is adjacent to either the ureter or bladder. Finding bacteria in the urine consistent with urinary infection is suggestive of a colovesical ®stula. If the clinical picture is clear, the diagnosis of diverticulitis can be made on the basis of laboratory and clinical criteria. If in doubt, computed tomography (CT) scanning of the abdomen and pelvis, ultrasonography and contrast enema may be used to help con®rm the diagnosis. Abdominal CT and ultrasonography are non-invasive tests that can demonstrate thickened colonic wall and an associated abscess. CT is usually the test of choice to con®rm diverticulitis, since it reliably detects the location and extent of the in¯ammation.60 It also provides valuable accessory information such as the presence of an abscess, urethral obstruction, or a ®stula between the colon and urinary bladder.61,62 Air in the bladder of a patient who has not had urinary tract manipulations is diagnostic of a ®stula from the intestinal tract.62 If an abscess is present, percutaneous drainage under CT guidance is a valuable therapeutic procedure.63 Ultrasonography can reveal thickened, hypoechoic in¯amed colonic wall or an abscess. Percutaneous drainage of an abscess can also be accomplished with ultrasonic guidance.64 The performance of a contrast enema for the evaluation of acute diverticulitis has diminished since the introduction of CT.
Medical treatment Severity of the in¯ammatory and infectious process determines the treatment for diverticulitis. Patients with minimal symptoms or signs of peritonitis may be treated on an outpatient basis. A clear liquid diet is recommended and broad-spectrum antibiotics are continued for 7±10 days. This has become the standard of care, despite the lack of a randomized placebo-controlled trial documenting the necessity of antibiotics and the known previous resolution of acute diverticulitis in a high percentage of patients not treated with antibiotics.65 Patients with signs of signi®cant in¯ammation should be hospitalized for bowel rest, intravenous ¯uids and broad-spectrum intravenous antibiotics. If pain medication is required, meperidine is an appropriate analgesic as it has been shown to decrease intraluminal pressure.66 Morphine should be avoided as it has been shown to increase intracolonic pressure. Unless there is a signi®cant ileus or obstructive component, nasogastric suction is usually not required. Improvement in most patients will occur in the ®rst 48±72 h. As the in¯ammatory process continues to resolve, diet is resumed and the patient may be discharged to complete a 7±10 day course of antibiotics as an outpatient. Investigative studies are usually performed 4±6 weeks after resolution of symptoms. The patient's colon should be evaluated by either colonoscopy or barium contrast enema. Following recovery from the ®rst episode of simple uncomplicated diverticulitis, surgery is seldom indicated, since only 20±30% of patients will have recurrent episodes of diverticulitis.33 A high ®bre diet is recommended. If the patient suers a second attack of diverticulitis requiring antibiotic therapy, it should initially be treated in the same way as the ®rst episode. However, elective surgical intervention is recommended 4±6 weeks following resolution of the in¯ammation, since the chance of a third episode in these patients is greater than 50%.55
142 R. J. Place and C. L. Simmang
Patients less than 40 years of age who present with acute diverticulitis often have a more aggressive course of diverticulitis. The initial diagnosis may be confused with appendicitis and may be correct in only 50±60% of patients.67,68 Complicated diverticulitis requiring urgent surgery is found in up to 75% of younger patients, compared to only 30% of older patients.67,68 These observations led to the recommendation for resection after the ®rst attack in young patients. However, recent investigators have pointed out errors in the methodology of the older studies and they are hesitant to oer surgery after the ®rst attack.65,69 An additional special group is immunocompromised patients. These patients have a higher rate of perforation (43% versus 14%), need for surgery (58% versus 33%), and post-operative mortality (39% versus 2%) than non-compromised patients.70 Due to this risk, some authorities have advocated elective resection after one attack in an immunosuppressed patient or prior to transplant if medically feasible.71 SURGICAL OPTIONS Although several options are available, the extent of resection should be the same in each. It is felt that a major cause of recurrent diverticulitis following sigmoidectomy is the failure to completely resect all of the abnormal colon at the rectosigmoid junction. Although it is seldom necessary to mobilize the rectum distally beyond 2 cm below the sacral promontory, the distal line of transection must be below the con¯uence of the taenia of the colon on the rectum.72 The proximal margin of resection is proximal to any abnormally thickened colon wall. Although diverticula may be present throughout the large intestine, it is not necessary to remove all diverticula-containing colon. Resection and primary anastomosis (one-stage procedure) is the most common operation employed for patients who can undergo bowel preparation prior to surgery. For patients with recurrent uncomplicated diverticulitis, this is the standard operation. It is also commonly used in patients with ®stula, or those who have undergone preoperative percutaneous drainage of an abscess when intra-operative contamination will be minimized. Currently, a great deal of enthusiasm exists for the use of laparoscopic techniques to facilitate this procedure.33,73 Relative contra-indications to a one-stage procedure include patients with signi®cant intra-abdominal contamination, or patients in whom bowel preparation of the proximal colon cannot be performed. Sigmoid resection with descending colostomy and rectal stump closure with subsequent colostomy closure (two-stage procedure) has become the most common operation for the emergency treatment of diverticulitis. The advantage of this procedure is that the septic focus is removed by the primary operation and the source of continued contamination is eliminated. The wisdom of resection of the perforated segment is underlined by a review of 57 publications dealing with a total of 1282 patients undergoing emergency surgery for perforated diverticulitis.74 Of these, 61% had some form of conservative operation (drainage, perforation closure, proximal colostomy only) with a 25% mortality. In contrast, those patients who underwent resection of the perforated segment had a mortality of 11%. After 3±6 months to allow the intra-abdominal in¯ammatory process to subside, the colostomy can be taken down and anastomosed to the rectal stump to restore intestinal continuity. Performance of a transverse colostomy and drainage as the ®rst operation (threestage procedure) was the traditional recommendation for patients with perforated sigmoid diverticulitis and abscess formation. With rare exceptions, this has been supplanted by one of the above procedures.
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Generalized peritonitis Free perforation from diverticulitis into the peritoneal cavity results in generalized peritonitis. Intra-abdominal ®ndings are classi®ed as purulent peritonitis, or the more devastating form of faeculent peritonitis. Purulent peritonitis may arise from the sudden rupture of a previously walled-o abscess, or from a persistently leaking diverticular perforation. The site of perforation may not always be identi®ed. Patients will complain of severe abdominal pain that is often acute in onset. Abdominal radiographs may reveal intra-peritoneal free air, but the absence of free air does not exclude the diagnosis. Leukocytosis with a left shift is generally observed, although in some cases leukopenia may accompany instances of severe sepsis, especially in patients who are elderly or immunocompromised. Patients presenting with colonic perforation are often septic or soon will be depending on the time from perforation to emergency room evaluation. Before an operation can be performed safely, the patient must be resuscitated in order to withstand general anaesthesia and surgery. Prompt resuscitation and urgent coeliotomy are then performed. Emergency operations on patients with generalized peritonitis secondary to perforated diverticulitis should limit the extent of resection to the perforated segment to avoid opening further avenues of sepsis from extensive peritoneal dissection or colonic mobilization. The distal colon can be stapled and a mucous ®stula avoided. Prior to closure of the abdomen, the specimen should be opened so that if a malignancy is found, a wider resection can be considered if the patient's overall condition is satisfactory. Following resection, the peritoneal cavity should be copiously irrigated with warm saline solution. If an abscess cavity is present, closed suction drains are used. An end descending colostomy is usually performed. Primary resection and anastomosis has been used on selected patients in recent years, but is not widely accepted.75 The principles concerning the extent of the resection should be applied during the second stage when the colostomy is taken down and intestinal continuity restored. The most catastrophic, but least common, manifestation of perforated diverticulitis is faeculent peritonitis. In this situation, the patient rapidly develops a generalized peritonitis from the spillage of faecal material. Mortality for patients with diuse purulent peritonitis has been reported at 6% compared to 35% for those with faeculent peritonitis.74,76 Aggressive resuscitation followed by emergent resection without anastomosis remains the preferred treatment.76 Abscess As a result of perforation, an abscess may develop. A localized abscess is a walled-o perforation contained within the pericolic region or within the colonic mesentery. This is the most common complication of sigmoid diverticulitis. A pelvic abscess results from perforation that is contained and walled-o within the pelvis by adjacent organs. The patient with a localized pericolic or intra-mesenteric abscess presents with clinical manifestations con®ned to the left lower quadrant, including pain and localized peritoneal signs. Tachycardia and leukocytosis may be present and correlate with the degree of in¯ammation. Abdominal examination often reveals a tender fullness or mass in the left lower quadrant. Initial management consists of broad-spectrum antibiotic therapy and bowel rest. An abscess may be dierentiated from a phlegmon with ultrasonography or CT scanning. The application of CT scanning and ultrasonography to localize and percutaneously drain these abscesses has been successful in converting an emergency situation to a semi-elective one.63,64,77,78 Once the abscess is drained,
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injection of water soluble contrast can be performed to evaluate for resolution of the abscess cavity as well as to detect a colonic ®stula. For abscesses with ®stulae, early resection is performed 7±14 days after drainage of the abscess cavity while broadspectrum antibiotics are continued. This time-frame is needed for the in¯ammatory process to resolve and to permit an operative procedure that is more likely to be completed safely in one stage. If no ®stula is demonstrated and a delayed operative procedure is selected, the patient is allowed to resume oral intake. The catheter is left within the collapsed abscess cavity, in the event that resumption of oral intake would result in recurrence of colonic leakage and subsequent ®stula. If no new drainage is noted, the catheter may be removed. The operation is then performed 6±12 weeks later to allow the in¯ammatory process to subside and to yield a safer operation. The clinical presentation and management of pelvic abscesses is similar to those in the abdomen. However, the signs and symptoms may be diminished due to protection from contiguous structures masking the presence of the abscess. Rectal or vaginal examination may reveal a tender bulging mass. If the abscess is located in the mid to upper pelvis, no mass may be palpable. In the event that trans-abdominal drainage of the pelvic abscess is technically dicult, trans-rectal or trans-vaginal drainage can be performed. This may be guided by either trans-vaginal or trans-rectal ultrasound to clearly localize the abscess cavity and permit safe drainage. Fistula The formation of a diverticular ®stula results from diverticulitis with an associated abscess that erodes into an adjacent organ. A tract is established between the source of the abscess (perforated sigmoid diverticulum) and secondarily involved adjacent organ. This is a relatively frequent complication of diverticulitis and has been reported in 5±33% of patients with diverticular disease requiring an operation. Although diverticulitis is the most common cause of a colovesical ®stula, sigmoid carcinoma is second and should be remembered during the evaluation and management process.56,59 Colonoscopy should be used to directly visualize the sigmoid mucosa and to exclude carcinoma, since the potentially curative surgical treatment of a colovesical ®stula from cancer involves wider surgical resection (especially of the bladder), than would be recommended for a patient with diverticulitis. Crohn's disease is another aetiology of ®stula that could be discovered by colonoscopy. Colovesical ®stulas are far more common in men than women with ratios ranging from 2:1 to 6:1.56,79 In women, the uterus is interposed between the bladder and the colon and presumably acts as a protective shield. Most women (83%) who develop a colovaginal ®stula have had a previous hysterectomy.56 The clinical presentation of a diverticular ®stula may be consistent with diverticulitis or just the ®stula. Patients with colovesical ®stulae will often present with symptoms of urinary tract infection and pneumaturia. CT scanning most accurately con®rms a colovesical ®stula by demonstrating air within the bladder. This test is also useful in assessing the extent and degree of pericolonic in¯ammation that aids in both diagnosis as well as pre-operative surgical planning. Cystograms have been shown to demonstrate the ®stula in approximately 30% of cases.21 Cystoscopy demonstrates bullous oedema or localized cystitis in the area of a ®stula in 90% of patients.56 Coloenteric ®stulas can usually be demonstrated by contrast enema. A vaginogram may demonstrate a colovaginal ®stula and hysterogram may demonstrate a colouterine ®stula. Roughly 95% of colocutaneous ®stulas associated with diverticulitis develop post-operatively, whereas only 5% develop spontaneously.57
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Emergency surgical intervention is seldom required in the presence of a ®stula caused by diverticulitis. Often the formation of a ®stula results in an improvement in the patient's condition, since it allows natural drainage of the abscess. The initial treatment should be directed towards the identi®cation and control of associated sepsis. The general principle of treating ®stulae is to remove the oending organ and origin. The majority of these patients can undergo pre-operative bowel preparation following control of sepsis and will be suitable for a one-stage resection.56 Careful and meticulous dissection must be performed when mobilizing the left colon in order to avoid injury to the left ureter. The use of a pre-operative ureteral stent should be considered. The colon usually can be pinched o the bladder and seldom is it necessary to resect a portion of the bladder. Although the wall of the bladder surrounding the ®stula connection will often be indurated, the ®stula is pinpoint and the actual opening is often not clearly seen. It is unnecessary to resect the indurated portion of the bladder, since this will resolve once the colon has been excised. If an opening is present, it can be closed in two layers. Post-operative urinary drainage should be continued for several days. A cystogram may be performed prior to removal of the urinary catheter to insure that there is no bladder leakage. After the diseased bowel is resected, a primary anastomosis is constructed attempting to leave the site of the anastomosis separated from the region of the prior ®stula and in¯ammation. Omental interposition can be performed to further segregate the new anastomosis from the area of in¯ammation if suitable omentum is available. Similarly, in the presence of a colouterine ®stula, no treatment of the uterus is required. However, for appropriate indications, an elective hysterectomy may be performed as a concomitant procedure. Following resection of a colovaginal ®stula, the apex of the vaginal vault may be closed or left open as closure is often unnecessary. Again, omental interposition should be considered. When resecting a coloenteric ®stula, the small bowel may be primarily closed if the bowel surrounding the ®stula is soft and supple.56 If indurated, a segmental small bowel resection with primary anastomosis should be performed.
SUMMARY Diverticulosis is a common problem, increasing in incidence with age and associated with a low ®bre diet. Most patients are asymptomatic. For those with symptoms, colonic evaluation should be performed and a high ®bre diet recommended. Diverticular bleeding is usually of minor signi®cance. If massive bleeding or recurrent bleeding requiring transfusions occurs, colectomy guided by localization studies is suitable for most patients. Diverticulitis is the most common complication of diverticula. The diagnosis may be made with clinical or radiographical criteria. Ultrasound and CT often Practice points . colonoscopic evaluation should be performed in patients with non-emergency symptomatic diverticular disease . the recommendation for sigmoidectomy for patients younger than age 40 with a single episode of diverticulitis is controversial . early use of non-invasive tests such as CT scanning and ultrasonography con®rm the diagnosis and show additional complications such as abscesses or ®stulae
146 R. J. Place and C. L. Simmang
Research agenda . detailed studies pertaining to the role of neurohormones in the development of diverticulosis are needed . the role of laparoscopic surgery for diverticular disease needs to be de®ned
provide additional information with complicated diverticulitis and provide a means to drain abscesses. Resection is performed for patients with recurrent disease. Other indications include stricture, perforation, abscess, ®stula and immunocompromised patients. Although usually performed as a single procedure, the speci®c operation, including the use of laparoscopy, should be tailored to the individual patient.
REFERENCES 1. Fisher N, Berry CS, Fearn T et al. Cereal dietary ®ber consumption and diverticular disease: a lifespan study in rats. American Journal of Clinical Nutrition 1985; 43: 788±804. 2. Madiba TE & Mokeona T. Pattern of diverticular disease among Africans. East African Medical Journal 1994; 71: 644±646. 3. Suginara K, Muto T, Morioka Y et al. Diverticular disease of the colon in Japan: a review of 615 cases. Diseases of the Colon and Rectum 1984; 27: 531. 4. Parks TG. Natural history of diverticular disease of the colon. Clinical Gastroenterology 1975; 4: 53±69. * 5. Painter NS & Burkitt DP. Diverticular disease of the colon, a 20th century problem. Clinical Gastroenterology 1975; 4: 3±21. 6. Nakada I, Ubukata H, Goto Y et al. Diverticular disease of the colon at a regional general hospital in Japan. Diseases of the Colon and Rectum 1995; 38: 755±759. 7. Goenka MK, Nagi B, Kochar R et al. Colonic diverticulosis in India: the changing scene. Indian Journal of Gastroenterology 1994; 13: 86±88. 8. Slack WW. The anatomy, pathology, and some clinical features of diverticulitis of the colon. British Journal of Surgery 1962; 50: 185. 9. Morson BC. Pathology of diverticular disease of the colon. Clinical Gastroenterology 1975; 4: 37±52. 10. Whiteway J & Morson BC. Elastosis in diverticular disease of the sigmoid colon. Gut 1985; 26: 258±266. 11. Bornstein P. Disorders of connective tissue function and the aging process: a synthesis and review of current concepts and ®ndings. Mechanisms of Ageing and Development 1976; 5: 305±314. 12. Wess L, Eastwood MA, Wess TJ et al. Cross-linking of collagen is decreased in colonic diverticulosis. Gut 1995; 37: 91±94. 13. Coulie B, Camilleri M, Burton D et al. Recombinant human brain derived neurotrophic factor accelerates colonic transit in humans. Gastroenterology 1999; 116: A979. 14. Szarka L, Camilleri M, Burton D et al. Recombinant human neurotrophin-3 accelerates small bowel and colonic transit in healthy humans and patients with constipation. Gastroenterology 1999; 116: A1089. *15. Camelleri M, Lee JS, Viramontes B et al. Insights into the pathophysiology and mechanisms of constipation, irritable bowel syndrome, and diverticulosis in older people. Journal of the American Geriatrics Society 2000; 48: 1142. 16. Painter NS. The cause of diverticular disease of the colon; its symptoms and its complications. Journal of the Royal College of Surgeons of Edinburgh 1985; 30: 118±122. 17. Gear JSS, Ware A, Fursdon P et al. Symptomless diverticular disease and intake of dietary ®bre. Lancet 1979; 1: 511±514. 18. Aldoori WH, Giovannucci EL, Rimm EB et al. A prospective study of alcohol, smoking, caeine, and the risk of symptomatic diverticular disease in men. Annals of Epidemiology 1995; 5: 221±228. 19. Thompson WG. Do colonic diverticula cause symptoms? American Journal of Gastroenterology 1968; 81: 613. 20. Otte JJ, Lanses L & Andersen R. Irritable bowel syndrome and symptomatic diverticular disease ± dierent diseases? American Journal of Gastroenterology 1968; 81: 529±531. 21. Gordon PH. Diverticular disease of the colon. In Principles and Practice of Surgery for the Colon, Rectum, and Anus, pp 739±797. St. Louis: Quality Medical Publishing, 1992.
Diverticular disease 147 22. Schnyder P, Moss AA, Thoeni RF et al. A double-blind study of radiologic accuracy in diverticulitis, diverticulosis, and carcinoma of the sigmoid colon. Journal of Clinical Gastroenterology 1979; 1: 55±66. 23. Boulos PB, Cowen AP, Karamoils PG et al. Early detection of carcinoma in sigmoid diverticular disease. Annals of Surgery 1985; 202: 607±609. 24. Freeny PC & Walker JH. Inverted diverticula of the gastrointestinal tract. Gastrointestinal Radiology 1979; 4: 57±59. 25. Lappas JC, Maglinte DD, Kopecky KK et al. Diverticular disease: imaging with post contrast sigmoid ¯ush. Radiology 1988; 168: 35. 26. Pemberton JH, Armstrong DN & Dietzer CD. Diverticulitis. In Yamada T (ed.) Textbook of Gastroenterology, 2nd edn, pp 1876±1890. Philadelphia: JB Lippincott Co, 1992. 27. Dean ACB & Newell JP. Colonoscopy in the dierential diagnosis of carcinoma from diverticulitis of the sigmoid colon. British Journal of Surgery 1973; 60: 633±635. 28. Max MH & Knudson CO. Colonoscopy in patients with in¯ammatory colonic strictures. Surgery 1978; 84: 551±556. 29. Hunt HR. The role of colonoscopy in complicated diverticular disease: a review. Acta Chirurgica Belgica 1979; 78: 349±353. 30. Hodgson WJB. An interim report on the production of colonic diverticula in the rabbit. Gut 1972; 13: 802. 31. Thompson WG & Patel DG. Clinical picture of diverticular disease of the colon. Clinical Gastroenterology 1986; 15: 903±916. 32. Smith AN, Drummond E & Eastwood MA. The eect of course and ®ne Canadian red spring wheat and French soft white bran on colonic motility in patients with diverticular disease. American Journal of Clinical Nutrition 1981; 34: 2460±2463. *33. Young-Fadok TM, Roberts PL, Spencer MP & Wol BG. Colonic diverticular disease. Current Problems in Surgery 2000; 37: 457±514. 34. Browder W, Cerise EJ & Litwin MS. Impact of emergency angiography in massive lower gastrointestinal bleeding. Annals of Surgery 1986; 204: 530±536. 35. Meyers MA, Alonso DR, Gray GF et al. Pathogenesis of bleeding diverticulosis. Gastroenterology 1976; 71: 577±583. 36. Welch CE, Athanasoulis CSA & Galdabini JJ. Hemorrhage from the large bowel with special reference to angiodysplasia and diverticular disease. World Journal of Surgery 1978; 2: 73±83. 37. Boley SJ, DiBiase A & Brandt LJ. Lower intestinal bleeding in the elderly. American Journal of Surgery 1979; 137: 57±64. 38. Jensen DM & Machiacado GA. Emergent colonoscopy in patients with severe lower gastrointestinal bleeding. Gastroenterology 1981; 80: 1184. 39. Winzelberg GG, Froelich JW, McKusick KA et al. Radionuclide localization of lower gastrointestinal hemorrhage. Radiology 1981; 139: 465±469. 40. Gupta S, Luna E, Kingley S et al. Detection of gastrointestinal bleeding by radionuclide scintigraphy. American Journal of Gastroenterology 1984; 79: 26±31. 41. Bentley DE & Richardson JD. The role of tagged red blood cell imaging in the localization of gastrointestinal bleeding. Archives of Surgery 1991; 126: 821±824. 42. Boley SJ, Brandt LJ & Frank MS. Severe lower intestinal bleeding: diagnosis and treatment. Clinical Gastroenterology 1981; 10: 65±91. 43. Forde KA. Colonoscopy in acute rectal bleeding. Gastrointestinal Endoscopy 1981; 27: 219±220. 44. Jensen DM & Machiacado AM. Diagnosis and treatment of severe hematochezia: the role of urgent colonoscopy after purge. Gastroenterology 1988; 95: 1569±1574. 45. Rosenkrantz H, Bookstein JJ, Rosen RJ et al. Postembolic colonic infarction. Radiology 1982; 142: 47±51. 46. Leitman M, Paull DE & Shires GT III. Evaluation and management of massive lower gastrointestinal hemorrhage. Annals of Surgery 1989; 175±180 47. Brandt LJ & Boley SJ. The role of colonoscopy in the diagnosis and management of lower intestinal bleeding. Scandinavian Journal of Gastroenterology 1984; 19: 61±70. *48. McGuire HH. Bleeding colonic diverticula: a reappraisal of natural history and management. Annals of Surgery 1994; 220: 653±656. 49. Drapanas T, Pennington DG, Kappelman M et al. Emergency subtotal colectomy: preferred approach to management of massive bleeding diverticular disease. Annals of Surgery 1973; 177: 519±526. *50. Sarin S & Boulos PB. Long-term outcome of patients presenting with acute complications of diverticular disease. Annals of the Royal College of Surgeons of England 1994; 76: 117±120. 51. McGuire HH Jr & Haynes BW Jr. Massive hemorrhage from diverticulosis of the colon: guidelines for therapy based on bleeding patterns observed in ®fty cases. Annals of Surgery 1972; 175: 847±855. 52. Britt LG, Warren L & Moore OF. Selective management of lower gastrointestinal bleeding. American Surgeon 1983; 49: 121±125.
148 R. J. Place and C. L. Simmang 53. Irvin GL, Hersley JS & Caruanci JA. The morbidity and mortality of emergent operations for colorectal disease. Annals of Surgery 1984; 199: 598±603. *54. Roberts P, Abel M & Rosen L. Practice parameters for sigmoid diverticulitis. Diseases of the Colon and Rectum 1995; 38: 125±132. *55. Rege RV & Nahrwald DL. Diverticular disease. Current Problems in Surgery 1989; 26: 138±189. 56. Woods RJ, Lavey IC, Fazio VW et al. Internal ®stulas in diverticular disease. Diseases of the Colon and Rectum 1988; 31: 591±596. 57. Fazio VW, Church JM, Jagelman DG et al. Colocutaneous ®stula complicating diverticulitis. Diseases of the Colon and Rectum 1987; 30: 89±94. 58. Grissom R & Snyder TE. Colovaginal ®stula secondary to diverticular disease. Diseases of the Colon and Rectum 1991; 34: 1043±1049. 59. Colcock BP & Stahlman FD. Fistulas complicating diverticular disease of the sigmoid colon. Annals of Surgery 1972; 175: 838±846. 60. Sonnershein MA, Cone LA & Alexander RM. Diverticulitis with colovenous ®stula and portal venous gas. Journal of Clinical Gastroenterology 1986; 8: 195±198. 61. Birnbaum BA & Balthazar EJ. CT of appendicitis and diverticulitis. Radiologic Clinics of North America 1994; 32: 885±898. 62. Labs JD, Sarr MG, Fishman EK et al. Complications of acute diverticulitis of the colon: improved early diagnosis with computerized tomography. American Journal of Surgery 1988; 155: 331±336. *63. Stabile BE, Puccio E, van Sonnenberg E et al. Preoperative percutaneous drainage of diverticular abscesses. American Journal of Surgery 1990; 159: 99±104. 64. Schwerk WB, Schwarz S & Rothmud M. Sonography in acute colonic diverticulitis. Diseases of the Colon and Rectum 1992; 35: 1077±1084. *65. Schoetz DJ. Diverticular disease of the colon: a century-old problem. Diseases of the Colon and Rectum 1999; 42: 703±709. 66. Almy TP & Howell DA. Diverticula of the colon. New England Journal of Medicine 1980; 302: 324±331. 67. Konvolinka CW. Acute diverticulitis under age forty. American Journal of Surgery 1994; 167: 562±565. 68. Schauer PR, Ramos R, Ghiatas AA et al. Virulent diverticular disease in young obese men. American Journal of Surgery 1992; 164: 443±448. 69. Vignati PV, Welch JP & Cohen JL. Long-term management of diverticulitis in young patients. Diseases of the Colon and Rectum 1995; 38: 627±629. *70. Tygues ES, Prystowsky JB, Joehl RJ et al. Acute diverticulitis: a complicated problem in the immunocompromised patient. Archives of Surgery 1991; 126: 855±859. 71. Schoetz DJ. Uncomplicated diverticulitis: indications for surgery and surgical management. Surgical Clinics of North America 1993; 73: 965±974. 72. Benn PL, Wol BG & Ilstrop DM. Level of anastomosis and recurrent colonic diverticulitis. American Journal of Surgery 1986; 151: 269±271. 73. Eijsbouts QAJ, de Haan J, Berends F et al. Laparoscopic elective treatment of diverticular disease. Surgical Endoscopy 2000; 14: 726±730. 74. Krukowski ZH & Matheson NA. Emergency surgery for diverticular disease complicated by generalized and faecal peritonitis. British Journal of Surgery 1984; 7: 921±927. 75. Alanis A, Papanicolaou GK, Tadros R et al. Primary resection and anastomosis for treatment of acute diverticulitis. Diseases of the Colon and Rectum 1989; 32: 933±939. 76. Tudor RG & Keighley MRB. The options in surgical treatment of diverticular disease. Surgery Annual 1987; 19: 135±149. 77. Mueller PR, Saini S, Wittenburg J et al. Sigmoid diverticular abscesses: percutaneous drainage as an adjunct to surgical resection in 24 cases. Radiology 1987; 164: 321±325. 78. Ne CC, van Sonneberg E, Casola G et al. Diverticular abscesses: percutaneous drainage. Radiology 1987; 163: 15±18. 79. Krompier A, Howard R, Macewen A et al. Vesicocolonic ®stulas in diverticulitis. Journal of Urology 1976; 115: 664±666.
doi:10.1053/bega.2002.0270, available online at http://www.idealibrary.com on
9 Diverticular disease Ronald J. Place
MD, FACS
Chief, Section of Colon and Rectal Surgery Department of Surgery, Madigan Army Medical Center, Ft. Lewis, WA 98431, USA
Cliord L. Simmang*
MD, FACS, FASCRS
Associate Professor of Surgery and Program Director of Colon and Rectal Surgery Department of Surgery, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 95390-9156, USA
Diverticular disease is a common ®nding in Western countries with an increasing prevalence with age. Many patients with the disorder remain asymptomatic. However, up to 30% of those aected may show clinical signs including pain, bleeding, obstruction, abscess, ®stulae and perforation. The purpose of this chapter is to review the epidemiology, pathogenesis, clinical presentation, diagnostic regimens and treatment options for this disorder. Key words: diverticulosis; diverticulitis; gastrointestinal haemorrhage; abscess; peritonitis.
INTRODUCTION Epidemiology Colonic diverticular disease includes a constellation of symptoms that ranges from mild irregularities in defaecatory function to bleeding and severe intra-abdominal in¯ammation. The incidence of diverticula rises within a society as it reduces its dietary ®bre intake. Animal studies con®rm these data, since 45% of rats fed a low ®bre diet developed diverticulitis compared with 9% fed a high ®bre diet.1 Historically, geographical location has been an important predictor of the prevalence, with diverticula being common in Western countries, less so in South America and rare in Africa and the Orient. As economic development and the adoption of a Western diet has increased, the diverticular disease prevalence has risen as well.2,3 Diverticulosis is uncommon before the age of 40 and increases in frequency with age.4 Post-mortem reports suggest that it is found in up to half of adults over the age of 60.5 The anatomical distribution of diverticula varies with geographical location. Industrialized countries with a Western diet have predominantly left-sided diverticula. Right-sided diverticulosis is more common and appears to have fewer clinical complications than left-sided disease in Japan.6 As left-sided diverticular disease increases in societies of previously low prevalence, right-sided colonic diverticulosis persists.7 These variations in anatomical distribution among ethnic groups support a multi-factorial basis for the disease. *All correspondence to: Dr Cliord L. Simmang, Tel: +1 (214) 648-9467; Fax: +1 (214) 648-2301; E-mail: [email protected] 1521±6918/02/01013514 $35.00/00
c 2002 Harcourt Publishers Ltd. *
136 R. J. Place and C. L. Simmang
Pathology The majority of colonic diverticula are histologically pseudodiverticula, consisting of herniations of the mucosa and submucosa through the muscular wall of the colon. Although true diverticula containing all bowel wall layers do occur as congenital anomalies, the more common pulsion pseudodiverticula are acquired. The outer longitudinal muscle ®bres form discrete taeniae, leaving the colonic wall predominantly a single layer of circular muscle ®bres. Diverticula develop in rows between the mesenteric and lateral taenia. The points of greatest muscular weakness are where the intramural vasa recta penetrate the circular muscle to the submucosa.8 In most patients with sigmoid diverticulosis, both muscle layers are greatly increased in thickness. This is associated with shortening of the taeniae producing a deformity called myochosis, which narrows the colonic lumen, allowing muscle contractions to obliterate the lumen and divide the bowel into isolated segments. These changes facilitate the transmission of higher pressures to the mucosa via the vasa recta. Luminal narrowing may be secondary to the shortening of the sigmoid musculature as well as pericolic ®brosis.9 Histological abnormalities include the presence of excess elastin in the taeniae that is not seen in the circular muscle.10 Elastosis may contribute to sacculation, with contraction of the sigmoid colon as elastin ®bres in the remaining circular muscle deteriorate with age. Tensile strength in the bowel wall decreases with senescence.11 Alterations in collagen structure appear to be due to increases in the cross-linking of colonic collagen with age, rather than a decrease in the total collagen content.12 The possibility of myenteric neural injury has also been explored. Preliminary data show that recombinant human brain-derived neurotrophic factor (rHuBDNF) accelerates colonic transit and increases stool frequency in healthy adults.13 In addition, recombinant human neurotrophin-3 (rHuNT-3) accelerates orocaecal and colonic transit in constipated patients.14 Research relating any speci®c neurohormonal relationship to diverticulosis is lacking.15 Functional abnormalities Extensive studies by Painter have implicated the hypersegmentation resulting in intraluminal hypertension from the low bulk Western diet as the primary cause of diverticular disease.16 Intraluminal manometry shows that intracolonic pressures may exceed 90 mmHg when segmentation allows the motor work of the colonic musculature to be transmitted to the bowel wall rather than producing faecal transit. Fibre increases stool weight, lowers colonic pressures and improves transit time. This may prevent muscular hypertrophy and decrease the likelihood of segmentation and its resulting intraluminal hypertension. This hypothesis is supported in epidemiological studies by the inverse relationship between dietary ®bre and the presence of colonic diverticula.17 An additional protective eect is seen from increased physical activity.18 No studies support the concept of whole ®bre (nuts, seeds, etc) becoming entrapped in a diverticulum and leading to diverticulitis. DIVERTICULOSIS Clinical manifestation and dierential diagnosis The majority of patients with diverticulosis either have no symptoms, or symptoms of such a minor nature that they never seek medical attention.19 Some patients have
Diverticular disease 137
symptoms of intermittent abdominal pain, bloating, excessive ¯atulence and irregular defaecation. Nausea, anorexia, passage of pellet-like stools or attacks of diarrhoea may also be present. Many conditions, especially those associated with altered intestinal motility, may be confused with diverticulosis. The most common of these is the irritable bowel syndrome (IBD), although the most important entity to consider is colorectal carcinoma.20 Both diverticular disease and colorectal carcinoma may have similar clinical presentations. Both conditions are common and are most frequently seen in the elderly. Any segment of the colon can be involved, but these conditions are most commonly found in the left colon, especially the sigmoid. Late manifestations of both diseases can result in luminal narrowing, obstruction, perforation, or the development of a ®stula. Also, both may be clinically silent for a long period of time. Patients with IBD present with intestinal symptoms, but evaluation fails to reveal an anatomical abnormality. It has been suggested that IBD may precede the development of diverticular disease, but no evidence has been found for a causal relationship between the two conditions.21 Either way, the management of uncomplicated diverticular disease and IBD are similar. Diagnostic studies In patients with diverticulosis, plain abdominal radiographs are normal. Colonic evaluation is performed as much to rule out neoplasm as to con®rm diverticulosis. The diagnosis is most often established with a barium enema, since this is the best way to determine the extent and severity of diverticulosis. However, the accuracy of barium enema in diagnosing concomitant lesions has been reported to be as low as 50%.22,23 Reasons for this include a redundant and overlapping sigmoid colon obscuring visualization, or a narrowed spastic segment in which the intraluminal outline is dicult to visualize. Also, diverticula may masquerade as polyps by inversion or due to an adherent ball of stool.24,25 Lower gastrointestinal endoscopy is more useful for evaluating the large bowel for concomitant pathology than for diverticulosis. Rigid sigmoidoscopy usually can not be advanced beyond the rectosigmoid junction and only rarely will visualize diverticular ori®ces. By contrast, ¯exible sigmoidoscopy may allow identi®cation of the ori®ces. Patient discomfort and diculty with advancement of the endoscope may limit this examination. Sigmoid tortuosity and thickened rugae suggest previous episodes of diverticulitis.26 Colonoscopy has proved useful in dierentiating diverticular disease from carcinoma. However, attempts to visualize the diseased segments seen on barium enema have been possible in only 50±73% of patients secondary to oedema or strictures.27,28 An evaluation of 125 patients with complicated diverticular disease identi®ed an associated carcinoma in 17% and an additional diagnosis in 32%.29 The presence of bleeding is a signi®cant risk factor for the presence of a concomitant lesion. In a group of 135 patients with persistent bleeding in whom barium enema showed only diverticular disease, 11% had carcinoma and an additional diagnosis was made in 37%.21 These ®ndings strongly suggest that colonoscopic evaluation in patients with diverticular disease, especially complicated diverticular disease, should be performed. Treatment The principle treatment for patients with diverticular disease has revolved around a high ®bre diet. A diet with a high bulk content reduces colonic pressure and may
138 R. J. Place and C. L. Simmang
prevent the development of diverticula.17,30 Daily ingestion of 20±30 g of bran is necessary to achieve a therapeutic eect.31 Coarse bran has been shown to be more eective than ®ne bran in increasing stool weight, speeding transit time and reducing intraluminal pressure in the colon.32 Many people ®nd it dicult to ingest the needed ®bre from dietary foods. The addition of commercial bulk forming agents such as psyllium provides a suitable substitute. DIVERTICULAR BLEEDING Dierential diagnosis Painless rectal bleeding is associated with diverticulosis in up to 30% of patients.33 Although this bleeding is usually of minor clinical signi®cance, massive bleeding from colonic diverticula may occur in 5% of patients with diverticulosis.34 Because most diverticular bleeding does not require therapy, the importance of the evaluation of bleeding in patients with known diverticular disease is to diagnose concurrent causes, including colitis and carcinoma. Diverticulosis is so common in the adult population that the attribution of bleeding to diverticular disease must be a diagnosis of exclusion. The cause of diverticular bleeding appears to be chronic injury to the vasa recta adjacent to the lumen of the diverticulum.35 The mechanism leading to intimal thickening with fragmentation of the internal elastic lamina and thinning of the media is not known. The predilection for right-sided diverticula to bleed may be related to a larger lumen, which exposes more of the vasa recta to potential disruption.35 The importance of angiodysplasia of the right colon has now been recognized as of nearly equal importance in causing severe lower gastrointestinal haemorrhage.36 In the elderly population in particular, the most frequent location of massive angiodysplastic bleeding is the right colon.37 Fortuitously, most bleeding diverticula are also found in the right colon. Patients presenting with profuse rectal bleeding often have no antecedent history of diverticular complications. In an elderly patient, the sudden onset of painless, brisk haematochezia may quickly lead to hypotension. This demands a prompt and organized evaluation concurrent with resuscitation. Although physical examination may be unrewarding, sigmoidoscopy may reveal the rare rectal cancer or identify the patient with acute colitis that presents with massive bleeding. The usual resuscitative measures should be performed including establishing large bore intravenous access, placement of an indwelling urinary catheter and passage of a nasogastric tube to rule out a massive upper bleeding source.38 Blood should be obtained for type and cross-match, determination of electrolytes and coagulation studies. Further invasive diagnostic techniques depend upon the rate of blood loss, the medical condition of the patient and the prompt availability of these procedures. A barium enema is no longer considered a useful initial study, since its sensitivity and speci®city are both inadequate and residual barium will obscure subsequent assessment. Diagnostic studies Nuclear scanning techniques using Technetium 99m sulphur colloid and Technetiumtagged red blood cells may be useful in patients with a slow rate of bleeding. The cost, limited availability and morbidity of emergency arteriography initially prompted enthusiasm for radionucleotide imaging, at least as a screening test prior to angiography.39 In animal studies, bleeding scans can detect very low bleeding rates
Diverticular disease 139
(0.1 ml/min) and are more likely to detect intermittent bleeding.40 However, a bleeding scan alone may not be speci®c enough to plan operative strategy.41 In patients with brisk bleeding, emergency angiography has become the initial procedure of choice. Angiography is both speci®c and highly sensitive if the rate of bleeding is sucient (0.5±1.0 ml/min).34 The superior mesenteric artery is studied ®rst, since the incidence of acute bleeding is highest from the right side of the colon. Next, the inferior mesenteric artery is studied, followed by a coeliac axis injection, which may show an unsuspected upper intestinal bleeding site. The speci®city of angiography is high if the study is positive and may reveal tumours, diuse mucosal bleeding, or the characteristic angiographic signs of angiodysplasia including delayed venous emptying, vascular tufts, or an early ®lling vein.42 A patient with a positive scan but negative arteriogram may be a good candidate for prompt colonoscopy. Bleeding sites have been identi®ed in up to 85% of patients.43 The technical compromise of emergency colonoscopy can be overcome when the bowel preparation and procedure are performed in the intensive care unit setting by an expert endoscopist.44 Treatment One advantage of diagnostic angiography is the option to attempt therapy by either infusion of vasospastic substances or selective embolization. Intra-arterial vasopressin can be temporarily eective in controlling diverticular haemorrhage.37 Unfortunately, rebleeding will occur in up to half of these patients following withdrawal of vasopressin.34 In addition, the use of vasopressin in these patients has several disadvantages including its eect on coronary perfusion, hypertension and arrhythmias. Embolization with autologous blood or Gelfoam1 is also eective. However, post-embolic colonic infarction is a signi®cant risk.45 In patients who fail angiographic treatment, mortality is increased. This may be due to a delay in eventual surgical treatment.46 Consequently, transcatheter embolization should probably be reserved for those patients at prohibitive surgical risk. Colonoscopic intervention is useful when the bleeding site can be visualized by this technique. Success has been reported with electrocoagulation of arterio-venous malformations.47 Like angiography, colonoscopic localization is extremely valuable in planning surgical treatment, even if endoscopic therapy ultimately proves unsuccessful. Surgery is clearly indicated in the treatment of persistent or recurrent diverticular bleeding. The most important factor in both safety and ecacy of surgery is a clear de®nition of the bleeding site during pre-operative investigations. Appropriate segmental colectomy yields a very low rebleeding rate.34,37,46,48 Considerable controversy continues regarding the procedural selection for the declining number of patients who come to operation for massive bleeding without pre-operative localization. Historically, total abdominal colectomy with ileoproctostomy was the procedure of choice, since a rebleeding rate of 30% was noted following blind segmental resection.49 The relatively high morbidity following emergency total colectomy may re¯ect other surgical risk factors such as multiple transfusions, age and coagulopathy in this subset of patients, rather than the technical aspects of the procedure. The indications are poorly de®ned for elective resection to prevent recurrent bleeding in patients who avoid initial operation. Recurrence of bleeding after one episode has been estimated at 20±30%, with a re-admission rate for further bleeding of 5% per year.48,50 Patients presenting with a second diverticular bleed have a greater than 50% risk of further recurrences.51 A conservative approach is probably warranted in most patients who
140 R. J. Place and C. L. Simmang
have a single bleed with a low transfusion requirement. However, resection after two or more episodes of bleeding requiring transfusion may be considered if the source of bleeding has been clearly identi®ed and the operative risk is acceptable. The morbidity and mortality of elective colon resection is much lower than the risks of emergency surgery, which continues to have a mortality of over 20% in bleeding patients.46,52,53
DIVERTICULITIS Diverticulitis results from in¯ammation and subsequent perforation of a colonic diverticulum. Occurring in 10±25% of patients with diverticulosis, diverticulitis represents the most common complication.33 The initial event is a microperforation that results in a peridiverticulitis and/or phlegmon, which is referred to as uncomplicated diverticulitis. Complicated diverticulitis ensues when continuation of the in¯ammatory and septic process is associated with obstruction, free perforation, ®stula, or abscess.54 Pathogenesis The mechanism of diverticulitis is felt to be the result of faecal material that has become inspissated within a diverticulum, producing a faecalith. This faecalith then becomes impacted or abrades the mucosal lining to produce a low grade chronic in¯ammation.9 It usually involves a single diverticulum in the sigmoid colon. This in¯ammatory process may proceed to either a micro- or macroperforation.21 With microperforation, peridiverticulitis ensues and is contained locally by pericolonic fat, mesentery or adjacent organs. With repeated episodes the phlegmonous reaction becomes more extensive. With healing, a ®brotic reaction may ensheathe the colon and produce segmental narrowing, stricture, or even obstruction.55 Macroperforation leads to either free perforation with generalized peritonitis, or a walled o and locally contained pericolonic abscess. The septic process can then erode into adjacent structures and produce a ®stula. The most common ®stula is the colovesical ®stula.56 Other ®stulae that may be commonly seen include colocutaneous, colovaginal and coloenteric ®stula.56±58 Uncommon ®stulae that have been reported include ®stulae between the colon and ureter, uterus, Fallopian tubes, perineum and even the venous system.59,60 Clinical features The most common presenting symptoms include left lower quadrant pain, fever and leukocytosis. If there has been progression of the disease process, the patient may present with symptoms of complicated diverticulitis such as a recurrent urinary tract infection, pneumaturia as a result of a colovesical ®stula, or a faeculent vaginal discharge from a colovaginal ®stula. The patient with free perforation and peritonitis will present with acute peritoneal signs. The most common ®nding on physical examination is tenderness in the left lower quadrant. Signs of localized peritoneal in¯ammation may be present with involuntary guarding and localized percussion tenderness. A tender mass representing the phlegmon can occasionally be palpated. Rectal examination often reveals tenderness in the pelvis.
Diverticular disease 141
Diagnostic studies Initial laboratory studies that are often helpful include a complete blood count, urinalysis as well as abdominal ¯at and upright X-rays. Usually, the white blood cell count is elevated with a predominance of polymorphonuclear leukocytes. Urinalysis may reveal the presence of white blood cells if the in¯ammatory process is adjacent to either the ureter or bladder. Finding bacteria in the urine consistent with urinary infection is suggestive of a colovesical ®stula. If the clinical picture is clear, the diagnosis of diverticulitis can be made on the basis of laboratory and clinical criteria. If in doubt, computed tomography (CT) scanning of the abdomen and pelvis, ultrasonography and contrast enema may be used to help con®rm the diagnosis. Abdominal CT and ultrasonography are non-invasive tests that can demonstrate thickened colonic wall and an associated abscess. CT is usually the test of choice to con®rm diverticulitis, since it reliably detects the location and extent of the in¯ammation.60 It also provides valuable accessory information such as the presence of an abscess, urethral obstruction, or a ®stula between the colon and urinary bladder.61,62 Air in the bladder of a patient who has not had urinary tract manipulations is diagnostic of a ®stula from the intestinal tract.62 If an abscess is present, percutaneous drainage under CT guidance is a valuable therapeutic procedure.63 Ultrasonography can reveal thickened, hypoechoic in¯amed colonic wall or an abscess. Percutaneous drainage of an abscess can also be accomplished with ultrasonic guidance.64 The performance of a contrast enema for the evaluation of acute diverticulitis has diminished since the introduction of CT.
Medical treatment Severity of the in¯ammatory and infectious process determines the treatment for diverticulitis. Patients with minimal symptoms or signs of peritonitis may be treated on an outpatient basis. A clear liquid diet is recommended and broad-spectrum antibiotics are continued for 7±10 days. This has become the standard of care, despite the lack of a randomized placebo-controlled trial documenting the necessity of antibiotics and the known previous resolution of acute diverticulitis in a high percentage of patients not treated with antibiotics.65 Patients with signs of signi®cant in¯ammation should be hospitalized for bowel rest, intravenous ¯uids and broad-spectrum intravenous antibiotics. If pain medication is required, meperidine is an appropriate analgesic as it has been shown to decrease intraluminal pressure.66 Morphine should be avoided as it has been shown to increase intracolonic pressure. Unless there is a signi®cant ileus or obstructive component, nasogastric suction is usually not required. Improvement in most patients will occur in the ®rst 48±72 h. As the in¯ammatory process continues to resolve, diet is resumed and the patient may be discharged to complete a 7±10 day course of antibiotics as an outpatient. Investigative studies are usually performed 4±6 weeks after resolution of symptoms. The patient's colon should be evaluated by either colonoscopy or barium contrast enema. Following recovery from the ®rst episode of simple uncomplicated diverticulitis, surgery is seldom indicated, since only 20±30% of patients will have recurrent episodes of diverticulitis.33 A high ®bre diet is recommended. If the patient suers a second attack of diverticulitis requiring antibiotic therapy, it should initially be treated in the same way as the ®rst episode. However, elective surgical intervention is recommended 4±6 weeks following resolution of the in¯ammation, since the chance of a third episode in these patients is greater than 50%.55
142 R. J. Place and C. L. Simmang
Patients less than 40 years of age who present with acute diverticulitis often have a more aggressive course of diverticulitis. The initial diagnosis may be confused with appendicitis and may be correct in only 50±60% of patients.67,68 Complicated diverticulitis requiring urgent surgery is found in up to 75% of younger patients, compared to only 30% of older patients.67,68 These observations led to the recommendation for resection after the ®rst attack in young patients. However, recent investigators have pointed out errors in the methodology of the older studies and they are hesitant to oer surgery after the ®rst attack.65,69 An additional special group is immunocompromised patients. These patients have a higher rate of perforation (43% versus 14%), need for surgery (58% versus 33%), and post-operative mortality (39% versus 2%) than non-compromised patients.70 Due to this risk, some authorities have advocated elective resection after one attack in an immunosuppressed patient or prior to transplant if medically feasible.71 SURGICAL OPTIONS Although several options are available, the extent of resection should be the same in each. It is felt that a major cause of recurrent diverticulitis following sigmoidectomy is the failure to completely resect all of the abnormal colon at the rectosigmoid junction. Although it is seldom necessary to mobilize the rectum distally beyond 2 cm below the sacral promontory, the distal line of transection must be below the con¯uence of the taenia of the colon on the rectum.72 The proximal margin of resection is proximal to any abnormally thickened colon wall. Although diverticula may be present throughout the large intestine, it is not necessary to remove all diverticula-containing colon. Resection and primary anastomosis (one-stage procedure) is the most common operation employed for patients who can undergo bowel preparation prior to surgery. For patients with recurrent uncomplicated diverticulitis, this is the standard operation. It is also commonly used in patients with ®stula, or those who have undergone preoperative percutaneous drainage of an abscess when intra-operative contamination will be minimized. Currently, a great deal of enthusiasm exists for the use of laparoscopic techniques to facilitate this procedure.33,73 Relative contra-indications to a one-stage procedure include patients with signi®cant intra-abdominal contamination, or patients in whom bowel preparation of the proximal colon cannot be performed. Sigmoid resection with descending colostomy and rectal stump closure with subsequent colostomy closure (two-stage procedure) has become the most common operation for the emergency treatment of diverticulitis. The advantage of this procedure is that the septic focus is removed by the primary operation and the source of continued contamination is eliminated. The wisdom of resection of the perforated segment is underlined by a review of 57 publications dealing with a total of 1282 patients undergoing emergency surgery for perforated diverticulitis.74 Of these, 61% had some form of conservative operation (drainage, perforation closure, proximal colostomy only) with a 25% mortality. In contrast, those patients who underwent resection of the perforated segment had a mortality of 11%. After 3±6 months to allow the intra-abdominal in¯ammatory process to subside, the colostomy can be taken down and anastomosed to the rectal stump to restore intestinal continuity. Performance of a transverse colostomy and drainage as the ®rst operation (threestage procedure) was the traditional recommendation for patients with perforated sigmoid diverticulitis and abscess formation. With rare exceptions, this has been supplanted by one of the above procedures.
Diverticular disease 143
Generalized peritonitis Free perforation from diverticulitis into the peritoneal cavity results in generalized peritonitis. Intra-abdominal ®ndings are classi®ed as purulent peritonitis, or the more devastating form of faeculent peritonitis. Purulent peritonitis may arise from the sudden rupture of a previously walled-o abscess, or from a persistently leaking diverticular perforation. The site of perforation may not always be identi®ed. Patients will complain of severe abdominal pain that is often acute in onset. Abdominal radiographs may reveal intra-peritoneal free air, but the absence of free air does not exclude the diagnosis. Leukocytosis with a left shift is generally observed, although in some cases leukopenia may accompany instances of severe sepsis, especially in patients who are elderly or immunocompromised. Patients presenting with colonic perforation are often septic or soon will be depending on the time from perforation to emergency room evaluation. Before an operation can be performed safely, the patient must be resuscitated in order to withstand general anaesthesia and surgery. Prompt resuscitation and urgent coeliotomy are then performed. Emergency operations on patients with generalized peritonitis secondary to perforated diverticulitis should limit the extent of resection to the perforated segment to avoid opening further avenues of sepsis from extensive peritoneal dissection or colonic mobilization. The distal colon can be stapled and a mucous ®stula avoided. Prior to closure of the abdomen, the specimen should be opened so that if a malignancy is found, a wider resection can be considered if the patient's overall condition is satisfactory. Following resection, the peritoneal cavity should be copiously irrigated with warm saline solution. If an abscess cavity is present, closed suction drains are used. An end descending colostomy is usually performed. Primary resection and anastomosis has been used on selected patients in recent years, but is not widely accepted.75 The principles concerning the extent of the resection should be applied during the second stage when the colostomy is taken down and intestinal continuity restored. The most catastrophic, but least common, manifestation of perforated diverticulitis is faeculent peritonitis. In this situation, the patient rapidly develops a generalized peritonitis from the spillage of faecal material. Mortality for patients with diuse purulent peritonitis has been reported at 6% compared to 35% for those with faeculent peritonitis.74,76 Aggressive resuscitation followed by emergent resection without anastomosis remains the preferred treatment.76 Abscess As a result of perforation, an abscess may develop. A localized abscess is a walled-o perforation contained within the pericolic region or within the colonic mesentery. This is the most common complication of sigmoid diverticulitis. A pelvic abscess results from perforation that is contained and walled-o within the pelvis by adjacent organs. The patient with a localized pericolic or intra-mesenteric abscess presents with clinical manifestations con®ned to the left lower quadrant, including pain and localized peritoneal signs. Tachycardia and leukocytosis may be present and correlate with the degree of in¯ammation. Abdominal examination often reveals a tender fullness or mass in the left lower quadrant. Initial management consists of broad-spectrum antibiotic therapy and bowel rest. An abscess may be dierentiated from a phlegmon with ultrasonography or CT scanning. The application of CT scanning and ultrasonography to localize and percutaneously drain these abscesses has been successful in converting an emergency situation to a semi-elective one.63,64,77,78 Once the abscess is drained,
144 R. J. Place and C. L. Simmang
injection of water soluble contrast can be performed to evaluate for resolution of the abscess cavity as well as to detect a colonic ®stula. For abscesses with ®stulae, early resection is performed 7±14 days after drainage of the abscess cavity while broadspectrum antibiotics are continued. This time-frame is needed for the in¯ammatory process to resolve and to permit an operative procedure that is more likely to be completed safely in one stage. If no ®stula is demonstrated and a delayed operative procedure is selected, the patient is allowed to resume oral intake. The catheter is left within the collapsed abscess cavity, in the event that resumption of oral intake would result in recurrence of colonic leakage and subsequent ®stula. If no new drainage is noted, the catheter may be removed. The operation is then performed 6±12 weeks later to allow the in¯ammatory process to subside and to yield a safer operation. The clinical presentation and management of pelvic abscesses is similar to those in the abdomen. However, the signs and symptoms may be diminished due to protection from contiguous structures masking the presence of the abscess. Rectal or vaginal examination may reveal a tender bulging mass. If the abscess is located in the mid to upper pelvis, no mass may be palpable. In the event that trans-abdominal drainage of the pelvic abscess is technically dicult, trans-rectal or trans-vaginal drainage can be performed. This may be guided by either trans-vaginal or trans-rectal ultrasound to clearly localize the abscess cavity and permit safe drainage. Fistula The formation of a diverticular ®stula results from diverticulitis with an associated abscess that erodes into an adjacent organ. A tract is established between the source of the abscess (perforated sigmoid diverticulum) and secondarily involved adjacent organ. This is a relatively frequent complication of diverticulitis and has been reported in 5±33% of patients with diverticular disease requiring an operation. Although diverticulitis is the most common cause of a colovesical ®stula, sigmoid carcinoma is second and should be remembered during the evaluation and management process.56,59 Colonoscopy should be used to directly visualize the sigmoid mucosa and to exclude carcinoma, since the potentially curative surgical treatment of a colovesical ®stula from cancer involves wider surgical resection (especially of the bladder), than would be recommended for a patient with diverticulitis. Crohn's disease is another aetiology of ®stula that could be discovered by colonoscopy. Colovesical ®stulas are far more common in men than women with ratios ranging from 2:1 to 6:1.56,79 In women, the uterus is interposed between the bladder and the colon and presumably acts as a protective shield. Most women (83%) who develop a colovaginal ®stula have had a previous hysterectomy.56 The clinical presentation of a diverticular ®stula may be consistent with diverticulitis or just the ®stula. Patients with colovesical ®stulae will often present with symptoms of urinary tract infection and pneumaturia. CT scanning most accurately con®rms a colovesical ®stula by demonstrating air within the bladder. This test is also useful in assessing the extent and degree of pericolonic in¯ammation that aids in both diagnosis as well as pre-operative surgical planning. Cystograms have been shown to demonstrate the ®stula in approximately 30% of cases.21 Cystoscopy demonstrates bullous oedema or localized cystitis in the area of a ®stula in 90% of patients.56 Coloenteric ®stulas can usually be demonstrated by contrast enema. A vaginogram may demonstrate a colovaginal ®stula and hysterogram may demonstrate a colouterine ®stula. Roughly 95% of colocutaneous ®stulas associated with diverticulitis develop post-operatively, whereas only 5% develop spontaneously.57
Diverticular disease 145
Emergency surgical intervention is seldom required in the presence of a ®stula caused by diverticulitis. Often the formation of a ®stula results in an improvement in the patient's condition, since it allows natural drainage of the abscess. The initial treatment should be directed towards the identi®cation and control of associated sepsis. The general principle of treating ®stulae is to remove the oending organ and origin. The majority of these patients can undergo pre-operative bowel preparation following control of sepsis and will be suitable for a one-stage resection.56 Careful and meticulous dissection must be performed when mobilizing the left colon in order to avoid injury to the left ureter. The use of a pre-operative ureteral stent should be considered. The colon usually can be pinched o the bladder and seldom is it necessary to resect a portion of the bladder. Although the wall of the bladder surrounding the ®stula connection will often be indurated, the ®stula is pinpoint and the actual opening is often not clearly seen. It is unnecessary to resect the indurated portion of the bladder, since this will resolve once the colon has been excised. If an opening is present, it can be closed in two layers. Post-operative urinary drainage should be continued for several days. A cystogram may be performed prior to removal of the urinary catheter to insure that there is no bladder leakage. After the diseased bowel is resected, a primary anastomosis is constructed attempting to leave the site of the anastomosis separated from the region of the prior ®stula and in¯ammation. Omental interposition can be performed to further segregate the new anastomosis from the area of in¯ammation if suitable omentum is available. Similarly, in the presence of a colouterine ®stula, no treatment of the uterus is required. However, for appropriate indications, an elective hysterectomy may be performed as a concomitant procedure. Following resection of a colovaginal ®stula, the apex of the vaginal vault may be closed or left open as closure is often unnecessary. Again, omental interposition should be considered. When resecting a coloenteric ®stula, the small bowel may be primarily closed if the bowel surrounding the ®stula is soft and supple.56 If indurated, a segmental small bowel resection with primary anastomosis should be performed.
SUMMARY Diverticulosis is a common problem, increasing in incidence with age and associated with a low ®bre diet. Most patients are asymptomatic. For those with symptoms, colonic evaluation should be performed and a high ®bre diet recommended. Diverticular bleeding is usually of minor signi®cance. If massive bleeding or recurrent bleeding requiring transfusions occurs, colectomy guided by localization studies is suitable for most patients. Diverticulitis is the most common complication of diverticula. The diagnosis may be made with clinical or radiographical criteria. Ultrasound and CT often Practice points . colonoscopic evaluation should be performed in patients with non-emergency symptomatic diverticular disease . the recommendation for sigmoidectomy for patients younger than age 40 with a single episode of diverticulitis is controversial . early use of non-invasive tests such as CT scanning and ultrasonography con®rm the diagnosis and show additional complications such as abscesses or ®stulae
146 R. J. Place and C. L. Simmang
Research agenda . detailed studies pertaining to the role of neurohormones in the development of diverticulosis are needed . the role of laparoscopic surgery for diverticular disease needs to be de®ned
provide additional information with complicated diverticulitis and provide a means to drain abscesses. Resection is performed for patients with recurrent disease. Other indications include stricture, perforation, abscess, ®stula and immunocompromised patients. Although usually performed as a single procedure, the speci®c operation, including the use of laparoscopy, should be tailored to the individual patient.
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