Diverticula of the intestinal tract are pockets or protrusions deriving from the lumen and extending through the wall of the gut. Diverticula that are enclosed by all layers of the bowel (serosa, muscle, and mucosa) are called ‘true’; those that lack muscle as a component of the sac are termed ‘false’. True diverticula are usually congenital, while false diverticula are acquired and usually secondary to pulsion forces within the gut. Diverticula may arise in both the small and large bowel, but this discussion will be limited to colonic diverticula.

Diverticula of the colon are generally multiple and, in the absence of inflammation, are collectively described as ‘diverticulosis’. In the presence of inflammation, the condition is termed ‘diverticulitis’. While this distinction is clear when the colon is examined surgically or histologically, symptoms of colonic dysfunction due to diverticulosis sometimes mimic those of diverticulitis. Thus, clinical distinction between the two conditions is often blurred. The term ‘diverticular disease of the colon’ may be applied to all stages of the disease from diverticulosis and its complications.

Diverticular disease of the colon has been recognized relatively recently and understanding of its manifestations has been dependent upon the twentieth century development of diagnostic radiology. Cruveilhier in 1849 described the gross anatomical findings in colonic diverticulosis, as did Habershon in 1857. Ball discussed the gross pathology of intermittent inflammation of diverticula and ascribed two cases of sigmoidovesical fistula to this cause. Graser identified oedema, fibrosis, thickening of the bowel wall and narrowing of the bowel lumen associated with inflamed diverticula that he called ‘peridiverticulitis’. Beer analysed 15 cases of diverticulitis and described associated stenosis of the sigmoid, free perforation with peritonitis, localized peritonitis with abscess formation, and sigmoidovesical fistulae. Mayo and associates reported a series of five patients who underwent resection of the colon for complications of diverticulitis; they recommended that the inflamed bowel should be resected before complications occur. They established external drainage for abscesses, constructed ‘artificial anus’ (colostomy) for obstruction and defined the terms ‘diverticulitis’ and ‘peridiverticulitis’.

In 1910 Keith contributed the important observation that the primary change in diverticular disease appears to be thickening and foreshortening of the muscular layers of the gut. Contrast meals or enemas were used for radiographic demonstration of colonic diverticula by Abbe, deQuervain, Case, and Spriggs and Marxer. Case and deQuervain independently used the term ‘diverticulosis’ to denote diverticula without evidence of inflammation. Smithwick introduced modern concepts of surgical treatment of diverticular disease.

The pathophysiology of diverticular disease is complex, involving abnormalities of anatomy and neuromuscular function, physical principles of pressure relationships within cylinders and spheres, the virulence of mixed bacterial flora of the colon, and inflammatory processes within the peritoneal cavity and in the retroperitoneal space.

Colonic muscular changes in diverticular disease first noted by Keith were further studied by Celio, Edwards, Morson, and Hughes. Thickening and foreshortening of the taeniae occur, as well as foreshortening and clustering of the circular muscle fibres with relatively weak areas in the intertineal regions and between fascicles or bands of circular fibres. Diverticula tend to extrude through these weak areas, and as Noer pointed out, these may be intimately associated with mesenteric vessels perforating through to the submucosal layers of the bowel and with the epiploic appendages.

The nature of the colonic muscular changes in diverticular disease is poorly defined. One suggested explanation has been that the bowel muscle develops work hypertrophy secondary to abnormal neuromuscular irritability. The sigmoid is the narrowest portion of the colon and functions as a partial sphincter. Its motor activity is increased by a variety of stimuli including emotional and psychological tensions, ingestion of food, cholinergic drugs, morphine, and the absence of mechanical distension. Its muscular contraction is inhibited by anticholinergic drugs and by mechanical distension. Physiological studies by Painter and his associates and by Arfwidsson and Koch have demonstrated increased irritability of the sigmoid in patients with diverticular disease, compared to normal controls. This same pattern of increased motor activity was observed by Lumsden and associates in patients with the irritable colon syndrome (Fig. 1) 1014

As the most irritable and narrowest segment of the colon, the sigmoid develops the highest intraluminal pressure per unit of muscular wall tension (Laplace's Law). Painter and Truelove have shown that patients with diverticular disease develop sigmoid globular segmentation and intraluminal pressures of 90 mmHg in response to emotional stress and also in response to the injection of morphine. These observed patterns of increased motor activity and intraluminal pressure in the sigmoid correlate well with the observed distribution of diverticula, which usually occur first in the sigmoid and propagate proximally over a period of years. Diverticulosis of the colon is accompanied by disease in the sigmoid in approximately 95 per cent of patients.

Histological and histochemical studies of the intrinsic nerves and muscle layers of the bowel in diverticular disease have not confirmed abnormal neural architecture, muscle hyperplasia, or muscle hypertrophy. Light and electron microscopy show normal muscle cells in colonic diverticular disease, neither hypertrophy nor hyperplasia being detected. These studies identified an increase in elastin content in the taeniae coli to more than 200 per cent of the level seen in normal controls. The elastin content in circular muscle was not appreciably different in diseased and normal bowel. It has been suggested that this elastosis is the basis for the foreshortening of the taeniae observed in diverticular disease.

Stimulated by the observation that some patients with diverticular disease have diffuse colonic disease with relatively less muscular abnormality in the sigmoid, Ryan has suggested that there may be a variant form of diverticular disease related to a diffuse connective tissue disorder distinct from the muscular abnormality of the sigmoid. There has been no histological confirmation of this theory, but the clinical pattern described requires further study (Fig. 2) 1015

The physical principles of pressure–tension relationships within the tubular colon or its globular segments also play an important role in the development and progression of diverticular disease. Laplace defined these relationships as follows: Equation 28

where T is tension in the gut wall, P is intraluminal pressure, and R is radius of the cylinder or sphere.

Thus in the sigmoid, where the lumen of the gut is small, muscular tension generates maximum pressures within the lumen of the bowel. These high pressures promote the extrusion of diverticula through weak areas in the gut wall: points of blood vessel penetration and the intermuscular spaces between circular smooth muscle fasicles in the inter-tineal intervals. Diets low in fibre do not distend the sigmoid and appear to promote these changes. Life-long low-residue diets in rats and rabbits produce diverticulosis of the colon, and broad-based population studies also seem to indicate a protective effect of high fibre diets on diverticular disease in man. Dietary factors may therefore play a significant role in the development and progression of diverticular disease of the colon.

The mixed and virulent bacterial flora of the colon may include E. coli, Pseudomonas, Serratia, Enterobacter, Citrobacter, Bacteroides, Enterococci, and Clostridia, most of which are facultative or obligate anaerobes. Depending upon the degree of extraluminal spread of these bacteria there may be localized inflammation with tissue necrosis, general peritonitis, or septicaemia with septic shock.

The propensity to develop diverticular disease is also partly inherited. Some families have a particularly high incidence of diverticula. Identical twins have been observed to develop diverticula at an early age and patients with multiple endocrine neoplasia syndrome type II B are prone to colonic diverticulitis. Oriental populations are more prone to right colonic diverticular disease, and diverticular disease of the colon occurs three times as frequently in Sweden as in neighbouring South Finland. The incidence of diverticular disease among young people (under age 40) may also be an expression of genetic predisposition to the condition.

The true incidence of colon diverticular disease is unknown and varies in different countries, depending upon factors such as genetic predisposition, diet, and age of the population. Among Western countries diverticular disease is uncommon before the age of 40; about 5 per cent of the population are estimated to have the disease by age 50 and approximately 70 per cent by age 85. Among those developing the disease before the age of 50 males predominate while above this age the majority of patients are female. However, there is a statistical bias since more females than males survive into the later decades of life.

In one large series, 94.6 per cent of cases of colonic diverticular disease were located in the sigmoid, while the descending colon was affected in 0.7 per cent; transverse colon, 1.0 per cent; ascending colon, 2.2 per cent; and caecum 1.5 per cent. In the same series, the age-specific incidence was 1.2 per cent in the third decade, 4.5 per cent in the fourth decade, 10.6 per cent in the fifth, 21.1 per cent in the sixth, 29.4 per cent in the seventh, 25.3 per cent in the eighth, 7.4 per cent in the ninth, 0.4 per cent in the tenth and 0.1 per cent in the eleventh decade of life among 688 cases requiring surgical treatment.

The apparently lower incidence of colonic diverticular disease in countries where high fibre diets are customary has already been mentioned. Among Oriental populations colonic diverticular disease is predominantly right-sided and the absolute frequency is lower than among western populations. However, among Orientals living in western countries the pattern of diverticular disease seems to shift more toward left-sided predominance.

The clinical manifestations of diverticular disease cover a broad spectrum. Many patients remain asymptomatic for long periods. The most frequent early symptoms are those of functional colonic disturbance—distension, cramps, diarrhoea or constipation, and local pain in the left lower abdomen. Concomitant bacterial inflammation (diverticulitis) may be associated with increased pain, left lower abdominal tenderness, palpable mass, fever, dysuria, urinary frequency and, occasionally, pneumaturia. General peritonitis and septicaemia signify more serious infection or perforation of a diverticulum. Rarely, the disease may present as septicaemia with pylephlebitis and gas in the portal venous system, or as a retroperitoneal infection dissecting upward to present as pneumomediastinum. More commonly, retroperitoneal infection tracks into the scrotum on either side, into the abdominal wall, the perineum, or into the left upper thigh. Attachment of small bowel loops to the inflammatory process in the colon may result in small bowel obstruction or development of a fistula into the small bowel. In females, diverticulitis may be associated with creation of fistulae into the fallopian tubes, uterus, or vagina, as well as into the urinary bladder (Figs. 3, 4) 1016,1017.

Diverticular disease presenting as massive rectal haemorrhage is usually seen in patients who have diffuse diverticular disease throughout the colon (Figs. 5, 6) 1018,1019. Rarely, diverticular disease may present with acute colon obstruction or with a tender, palpable mass due to a giant diverticulum of the sigmoid.

Diverticulosis is the presence of non-inflamed diverticula, or out-pouchings from the lumen of the gut through interstices in its muscular wall, which consist of mucosa, attenuated submucosa, sparse muscular fibres, and serosal covering. Initially, these diverticula are microscopic in size but continued rhythmic peaks of intraluminal pressure due to peristaltic contractions cause them to enlarge slowly, until they become globular nodules projecting from the external surface of the bowel. These globules are usually not larger than about 1 cm in diameter, but they may become larger. Diverticula of 3 cm or more in size are called ‘giant diverticula’; these gas-filled protuberances have been recorded with a diameter of 35 cm (Fig. 7) 1020. The globular diverticula communicate with the bowel lumen by a very narrow neck, through which gas usually can pass freely; a valve-like mechanism may contribute to the formation of giant diverticula. Diverticula frequently fill with faecal material extruded from the lumen that may then become inspissated and firm. This process usually begins in the sigmoid and spreads proximally over the course of several years.

Infection and inflammation of individual diverticula is called ‘diverticulitis’. The incidence of such inflammation among patients with diverticulosis has been estimated at 15 to 25 per cent, but is not accurately known.

Factors that initiate diverticulitis are speculative. Pressure necrosis or erosion from inspissated faeces in the diverticulum has been implicated as a causative mechanism. Transmitted pressure from peristaltic contraction may cause ballooning of the diverticulum and subsequent microscopic or macroscopic rupture. Inflammation generally occurs first at the apex of the diverticulum, which is the area of poorest circulatory perfusion and is often (or perhaps always) associated with micro- or macroperforation. Gross perforation results in immediate general faecal contamination of the peritoneum. More frequently, the perforation is contained by tissues in the wall of the colon or its mesentery or is buttressed by inflammatory adhesions to the abdominal or pelvic wall or adjacent viscera; a localized abscess then forms. This may rupture back into the lumen of the colon, track along the wall or mesentery of the bowel, may be contained by the pelvic visceral surfaces or adherent small bowel loops, attach to the abdominal wall, or may dissect into the retroperitoneal tissues (Fig. 3) 1016. The abscess may resolve by local healing, persist as a localized collection, rupture free into the peritoneal cavity, or may dissect through tissue planes to drain externally by fistulization to bowel, genitourinary tract, abdominal wall, or perineum.

The mixed bacterial flora of the colon causes severe inflammation with extensive tissue necrosis and very dense scar formation on healing. Repeated bouts of localized diverticulitis may thus result in ligneous inflammatory swelling and scarring of the sigmoid and its mesentery with foreshortening and partial chronic obstruction of the bowel diminishing the efficiency of its peristaltic activity. In addition, shortening of the muscular wall of the sigmoid throws the mucosa into ridges of redundant folds that further inhibit effective stool transit. The symptomatic manifestations of diverticulitis are diverse and complex and, on clinical grounds, not always distinguishable from those of diverticulosis.

The complications of diverticular disease include sepsis, fistula (usually as a result of healed sepsis), bleeding, obstruction, and intractable painful disturbance of bowel function.

Septic complications of diverticular disease include localized inflammation within the bowel wall or mesentery, localized pelvic abscess, perforation with diffuse bacterial and/or feculent peritonitis, adherence to adjacent visceral or peritoneal surfaces, septicaemia, and septic shock. Sepsis is the indication for surgery in approximately 35 per cent of patients requiring operative treatment of colonic diverticular disease.

Fistulae form as the result of spontaneous drainage of an abscess into an adjacent viscus or to the external surface of the body. A channel communicating with the lumen of the bowel is thus created. Because of inflammation and continuing faecal contamination, fistulae rarely heal spontaneously; about 5 per cent of all operations required for diverticular disease involve treatment of fistulae.

Bleeding is intermittent and slight in approximately 10 per cent of patients with diverticular disease: this must be distinguished from bleeding caused by adenocarcinoma of the colon. Acute, massive haemorrhage from diverticular disease is of greater significance: this is not due to diverticulitis, and generally occurs in individuals with diffuse diverticulosis affecting the colon. Erosion of a small blood vessel by inspissated faeces in the diverticulum has been suggested as a cause for massive haemorrhage. An alternative mechanism may be traction and tearing of the relatively inelastic vessels when the diverticulum stretches during peristaltic contraction. Massive bleeding is the indication for surgery in approximately 10 per cent of patients requiring operative treatment of diverticular disease.

Colon obstruction secondary to diverticular disease may be partial and chronic or complete and acute. The acute presentation may be accompanied by concurrent small bowel obstruction, and should always be suspected. Operations for obstruction are somewhat less frequent than those required for massive bleeding, about 9 per cent of cases.

Patients with intractable disturbance of bowel function (distension, cramps, diarrhoea, or constipation) and persistent pain may require surgical treatment even in the absence of the more defined complications listed above. These patients require careful clinical evaluation and judgment, and comprise about 25 per cent of those undergoing surgery for diverticular disease.

Diverticular disease occurs predominantly in elderly patients who have associated diseases that complicate diagnosis and influence treatment. Adenocarcinoma and polyps of the colon may coexist with diverticular disease, although a causal relationship is not recognized. Chronic ulcerative colitis or regional enterocolitis (Crohn's disease) may also occasionally affect patients with colonic diverticular disease.

Ischaemic colitis due to segmental arterial inflow restriction leading to mucosal necrosis without infarction of the muscular layers may cause pain, diarrhoea, and rectal bleeding. These changes may be confused with or may coexist with diverticular disease. Angiodysplasia, abnormal arteriovenous shunts in the colonic submucosa, especially in the right colon, may cause massive haemorrhage that must be differentiated from haemorrhage due to diverticulosis. Many patients who have colonic angiodysplasia also have diverticulosis.

Many medical diseases of the elderly weaken the immune response, predisposing patients with diverticulitis to its septic complications. These conditions include obesity, diabetes, chronic corticosteroid therapy, chronic alcoholism, asplenism, radiation therapy, cancer chemotherapy, prosthetic implants, post-transplantation immunosuppression, and AIDS. These conditions make prompt, accurate diagnosis and effective treatment of diverticular disease even more critical.

The symptoms of colon diverticular disease are diverse, and depend upon the stage of the disease. Diverticulosis may cause abdominal distension, cramps, constipation, diarrhoea, lower abdominal pain, and, rarely, massive rectal bleeding. Diverticulitis may present any or all of the above symptoms with the exception of massive rectal bleeding. Abdominal pain may be increased and fever, nausea, vomiting, dysuria, urinary frequency, pneumaturia, and external faecal fistulae may be noted. Patients with complications of diverticulitis may have chills, high fever, generalized abdominal pain, and septic shock. Symptoms may be suppressed in patients receiving chronic steroid therapy, causing significant delay in diagnosis.

Physical signs of colon diverticular disease vary according to the stage. Abdominal distension, tenderness, a palpable and tender lower abdominal mass, and normal peristaltic sounds are often observed. Fever may or may not be present. Patients with diffuse peritonitis may have diffuse abdominal tenderness, spasm, and rebound tenderness, and they are usually febrile. Rectal examination may reveal high rectal tenderness or a mass; it may also be normal.

Diagnosis may be aided by faecal occult blood test, urinalysis, leucocyte count, haematocrit, and liver function tests. If all of these tests yield normal results, however, the diagnosis of colon diverticular disease is not excluded. Patients with right-sided colon diverticulitis may have symptoms, signs, and laboratory findings indistinguishable from those of acute appendicitis.

Endoscopy has limited value in the diagnosis of acute diverticulitis, although rigid sigmoidoscopy may identify tenderness and fixation at the rectosigmoid junction. Colonoscopy is useful in identifying associated colitis, polyps, or adenocarcinoma, but spasm of the sigmoid may limit the effectiveness of the examination. Patients suffering from massive haemorrhage are not suitable candidates for colonoscopic study.

Radiographic examination is the main diagnostic technique in colonic diverticular disease. In patients with chronic or subacute symptoms, a barium enema examination may confirm the presence of diverticula, provide evidence for or against the diagnosis of diverticulitis, and help to exclude the presence of adenocarcinoma or other associated disease of the bowel. If partial obstruction of the colon is found diverticular disease may usually be distinguished from adenocarcinoma by the greater length of affected tissue, intact mucosa, muscular spasm, taper rather than blunt ends to the narrowed segment, and the presence of diverticula in the former. Diagnosis may be confirmed by colonoscopic examination.

Suspected acute diverticulitis or its complications should be investigated initially with plain and upright abdominal films and chest radiographs. Colon and/or small bowel distension may indicate obstruction. Free gas in the peritoneal cavity, retroperitoneal tissues, bladder, or portal venous system is a sign of acute diverticulitis with perforation and is a clear indication for early surgical intervention. Plain films frequently yield no diagnostic clues, and performance of a barium enema carries the risk of perforation of an inflamed diverticulum or barium contamination of the peritoneal cavity if a perforation is present. Computed tomography of the abdomen following oral administration of contrast medium (Gastrografin 10 ml in 300 ml water hourly for 3 or 4h prior to examination) has therefore become the most reliable examination for diagnosing diverticulitis of the colon. Diagnostic findings include visualization of diverticula, thickening of the bowel wall, thickening or ‘stranding’ fibrosis in the mesentery, thickening of adjacent viscera (bowel, bladder), and extraluminal mass, sinus tract, or abscess with fluid and/or gas.

Radiographic studies are important in locating the site of massive haemorrhage from the colon. Selective catheterization of superior and inferior mesenteric arteries and intra-arterial administration of contrast may disclose the site of haemorrhage, and whether this is due to diverticulosis, angiodysplasia, or other causes. Fully one-half of these bleeding points are located proximal to the splenic flexure. Intra-arterial infusion of vasopressin (0.2 U/min) will control 50 per cent of such haemorrhages and permits elective study and treatment. If haemorrhage is not controlled by vasopressin, the site of the bleeding may be identified prior to emergency resection of the appropriate bowel loop.

If fistulization to the genitourinary tract is suspected, diagnostic studies should include urine culture, intravenous pyelography, and cystoscopy.

Uncomplicated diverticular disease can be managed by dietary manipulation, including provision of supplementary dietary fibre, stool softeners, and anticholinergic drugs to inhibit peristaltic cramps. High fibre intake results in a larger, softer stool which distends the colon and undergoes more rapid transit through the gut. The extra force is optimally provided by a diet rich in fruit, vegetables, and whole grain cereals, with generous water intake. Supplementary bulk may be supplied with 10 to 20 g of wheat bran daily. Softening and moisturization of the stool may be aided by ingestion of powdered psyllium seed husks (5–10 g daily). Drugs that may inhibit peristalsis (such as propantheline bromide 7.5–15 mg thrice daily) may give symptomatic relief. Morphine causes increased intracolonic pressure and should be avoided: if narcotic medication is required, meperidine hydrochloride (50–75 mg) may be used.

The pathophysiology, symptoms, complications, and methods of diagnosis of diverticulitis and its sequelae have been discussed in preceding sections and diverticulitis itself will be regarded here as a complication of diverticular disease. The accurate diagnosis of complications such as sepsis (including fistula as a late manifestation), bleeding, obstruction, and intractable pain with functional bowel disturbance is essential to enable effective treatment. Many methods of treatment, both surgical and non-surgical, have been used in the past and have been found to be inadequate or have been replaced by more effective procedures. In this section emphasis will be given to treatments that are currently considered safest and most effective.

Patients with acute diverticulitis should be treated by restriction of oral intake and by intravenous administration of fluids and antibiotics with a broad spectrum of activity against enteric pathogens. A regimen including cefotetan, 1.0 g every 12 h and metro-nidazole, 250 mg every 6 h intravenously is appropriate; other combinations of appropriate antibiotics may be equally effective. Many patients treated in this manner will improve rapidly, with resolution of the signs of local inflammation and ileus within a few days. When the gut function is restored (as marked by passage of flatus or stool) it is safe to resume oral feeding and, usually, to switch to oral administration of metronidazole (250 mg every 6 h). Following resolution of the local inflammation, a barium enema examination should be performed to assess the disease more accurately. The patient should be placed on a high fibre diet. Such treatment is sufficient in approximately 65 per cent of patients admitted to hospital for acute diverticulitis; the remainder will require some kind of surgical intervention.

Patients who remain febrile and tender and exhibit evidence of systemic illness after 12 to 24 h of treatment as outlined above should be re-examined: fever, leucocytosis and abdominal or rectal tenderness or mass are highly suggestive of a pericolic or pelvic abscess. Ultrasonography or repeat CT scan are useful for confirmation (Fig. 13) 1026 but on clinical grounds, such a patient is a candidate for surgical exploration.

If the abscess is wholly contained within the bowel wall and mesentery and can be extirpated with a segmental resection, and if the (unprepared) bowel is relatively empty and free of inflammation, a one-stage resection and end-to-end anastomosis may be considered. Such patients are uncommon, and a safer course is to resect the inflamed segment of bowel, close the distal resected end (usually rectum), and pull the proximal resected end through the abdominal wall as a colostomy. Drains may or may not be left in the pelvis, depending on the clinical indications. Patients who are treated in this way are candidates for anastomosis after they have made a complete recovery—generally in 3 months.

An alternative treatment that may be considered when the facilities are available is initial CT-guided percutaneous drainage of the abscess, continued antibiotic treatment, and resection of the involved segment with primary end-to-end anastomosis 7 to 10 days later (Figs. 14, 15) 1027,1028. If severe inflammation or residual abscess is found at this time the anastomosis should be abandoned in favour of resection, rectal turn-in, and colostomy. About 40 per cent of patients who require operations for diverticular disease have localized or pelvic abscesses. The expected mortality rate among such patients is approximately 2.5 per cent.

The most serious septic complication of diverticular disease is free perforation of the colon with bacterial or faecal peritonitis. The majority of patients presenting with this clinical picture have coexisting severe illnesses, and many are immunosuppressed. In addition to cefotetan and metronidazole these patients should receive an aminoglycoside such as gentamicin, 1 to 1.5 mg/kg intravenously every 8 h, and serum levels (peak 8–12 &mgr;g/ml, trough < 2 &mgr;g/ml) should be monitored daily until they are stable. Patients with general peritonitis must be closely monitored for respiratory, renal, and liver failure, septic shock, and for coagulopathy. Patients receiving chronic steroid therapy should be given increased supplementary doses (hydrocortisone, 300 mg/day) and intravenous fluids should be administered to assure adequate urine output (approximately 50 ml/h). As soon as the patient is haemodynamically stable resection of the perforated bowel segment, rectal turn-in and end-colostomy of the descending colon should be performed. All pus and debris should be irrigated from the peritoneal cavity. If there is gross contamination, delayed primary closure of skin and subcutaneous fascia decreases the risk of wound sepsis.

Postoperatively, these patients require intensive monitoring and support of all vital systems. However, removal of the septic focus usually results in prompt improvement as long as this has been treated soon after perforation. Delay is associated with increased morbidity and mortality. Patients with general peritonitis comprise about 10 per cent of those requiring operation for diverticular disease; their expected mortality is approximately 45 per cent.

Fistulae are late manifestations of septic complications of diverticular disease and represent the end-stage of spontaneous drainage of an abscess into adjacent viscera or to the skin surface. In descending order of frequency, fistulae may be colovesical, coloenteric, colovaginal, colocutaneous (abdominal wall), colouterine, colosalpingeal, colocolonic, coloureteral, or colocutaneous (perineum or thigh). Operations for fistula are elective and permit preliminary mechanical and antibiotic preparation of the colon. An effective regimen is the administration of 240 ml of magnesium citrate by mouth 2 days prior to and on the day before operation. On the day preceding surgery erythromycin base 1.0 g and neomycin 1.0 g are given by mouth at 12 noon, 1.00 p.m. and 9.00 p.m. An enema is given on the night before surgery.

Intravenous cefotetan and metronidazole are administered just prior to surgery, and these may be continued for 24 h or more postoperatively, depending upon the surgical findings. During the operation the degree of inflammation and scarring in the sigmoid and at the site of the fistula is assessed. A one-stage resection of the sigmoid colon, including the fistula and a segment of the fistulized organ (bladder, small bowel, etc.), with primary anastomosis of the colon and suture of the fistulized viscus, can be performed in about 25 per cent of patients. In the remainder, it will be safer to perform a loop colostomy in the right transverse colon, close the incision, and allow 3 months for the pelvic inflammation to subside. A second stage operation is then required to resect the sigmoid colon and the fistula and to create an anastomosis between the descending colon and the rectum. After another month a barium enema should be performed to assure the integrity of the anastomosis. Thereafter, the colostomy may be closed. Operations for fistula account for about 9 per cent of operations required for diverticular disease. The expected mortality rate in this group of patients is less than 1 per cent.

Massive bleeding is the indication for approximately 9 per cent of operations for colon diverticular disease. Patients with this presentation often have diffuse diverticulosis and usually do not have associated diverticulitis with pain and tenderness as localizing markers. Confounding conditions such as angiodysplasia and ischaemic colitis may also obscure the diagnosis. Endoscopy is not generally helpful in such cases and it is better to proceed promptly with selective angiography of the superior and inferior mesenteric arteries. If bleeding continues at a rate of 0.5 ml/min the locus of bleeding can frequently be identified. With the arterial catheter in the feeding artery, infusion of vasopressin (0.2 U/min for 24–48 h) may control the haemorrhage. If the patient recovers and only diverticular disease is present, appropriate treatment is a high fibre diet, as for chronic diverticular disease; if bleeding is not controlled or recurs, surgical intervention is required.

When the bleeding site is identified, a segmental resection with end-to-end anastomosis is the operation of choice. If the site cannot be located, subtotal colectomy with ileorectal anastomosis should be performed as an emergency procedure. Since there is no time for preoperative preparation of the bowel, these patients should receive broad-spectrum antibiotics intravenously pre- and postoperatively, as well as appropriate blood replacement. The expected mortality rate in this group of patients is approximately 10 per cent.

Obstruction in colonic diverticular disease may be chronic, due to postinfection scarring as well as to muscular narrowing of the sigmoid. Acute obstruction is usually associated with active diverticulitis or associated abscess and may be accompanied by obstruction of adherent small bowel loops.

Patient with chronic obstruction generally tolerate preoperative mechanical and antibiotic preparation of the bowel and may undergo semi-elective surgery. One-stage resection and anastomosis under intravenous perioperative antibiotic cover may be performed in most of these patients.

Acute colonic obstruction is usually superimposed on acute diverticulitis and, as described, is frequently associated with abscess or small bowel adhesions. These seriously ill patients require nasogastric suction, broad-spectrum triple antibiotics, intravenous fluids, and prompt surgical intervention. The optimum operative procedure in these patients is lysis of the small bowel adhesions, drainage of abscesses, resection of the inflamed strictured segment, rectal turn-in, and end-descending colostomy. Bowel continuity should be restored at a second procedure after an interval of 3 months.

Colon obstruction is the indication for about 8 per cent of operations for diverticular disease, and the mortality rate is about 2 per cent. Acute obstruction occurs in one in eight of such patients.

Many patients with colon diverticular disease have chronic lower abdominal pain, distension, cramps, and diarrhoea, or constipation, with the last two sometimes alternating. Barium enema will confirm the presence of diverticulosis and may show marked irregular deformity of the sigmoid and descending colon due to muscular thickening and shortening. Although there is no organic stricture, symptoms may suggest partial functional obstruction. Colonoscopy may help to exclude other causes of symptoms such as inflammatory bowel disease or adenocarcinoma, but spasm and narrowing of the sigmoid often make the procedure difficult and of limited value.

Dietary management, anticholinergic medication, and stool conditioners may fail to provide relief, and some patients will require surgical resection of the affected bowel. Since the operation in these cases is semi-elective, preoperative mechanical and antibiotic preparation of the bowel can be undertaken. Perioperative intravenous antibiotics should be administered. Primary resection and anastomosis should be performed in nearly all of these patients. However, if unexpected inflammation or scarring make the dissection dangerous the bowel should be divided, with the proximal end converted to a colostomy and the distal end turned in. Re-resection and anastomosis should be planned after an interval of 3 months.

Resection for intractable dysfunction and pain accounts for about 25 per cent of patients undergoing surgery for diverticular disease. The expected mortality rate for these patients is less than 1 per cent.

Although 95 per cent of operations for diverticular disease are performed in the sigmoid and descending colon, in 1 per cent of cases the transverse colon is affected and in 2 per cent each the ascending colon and the caecum is affected. The same principles of bowel preparation and antibiotic usage that have been discussed previously also apply in these instances. When operation is required local excision of the inflamed diverticulum may occasionally be feasible, but in most instances segmental resection and primary anastomosis preferable. Diverticulitis of the caecum may mimic acute appendicitis except that the clinical course may be less fulminant and nausea less common. If a caecal inflammatory mass is encountered ileocaecal resection to remove the mass en bloc with primary reanastomosis of the bowel is the preferred treatment.

Complications for diverticular disease and their associated mortality rates are so severe that attempts have been made to define groups of patients who should benefit from elective colon resection to pre-empt these complications. These include patients with

(1)recurrent attacks of local inflammation (two or more);

(2)persistent tender abdominal mass;

(3)narrowing or marked deformity of the sigmoid on radiographic examination;

(4)dysuria associated with diverticulosis;

(5)rapid progression of symptoms from time of onset;

(6)clinical or radiographic signs that do not definitely exclude carcinoma;

(7)relative young age.

The age of the patient is particularly important in considering elective operation. All patients less than 50 years of age may be expected to suffer from repeated attacks of diverticulitis and progressive complications. These patients should therefore be encouraged to undergo resection of the affected segment as an elective procedure under the safest possible conditions.

The few patients who present with giant diverticula should also be treated by elective colon resection. Candidates for organ transplantation who have diverticular disease should be considered for elective colon resection prior to the transplantation procedure. Overall mortality rates for emergency operations for diverticular disease exceed those for elective operations by more than 5 to 1.

Operative treatment of colon diverticular disease is technically demanding and should be undertaken only by experienced surgeons. Sepsis, scarring, foreshortening, thickening and narrowing of the bowel, associated abscesses, obstruction, and fistulae present challenges that require both technical expertise and mature judgement. In addition, decisions have to be made regarding avoidance of injury to adjacent structures, the length of bowel to be resected, primary anastomosis or diversion of the faecal stream, the security of bowel anastomosis, the advisability of colostomy proximal to an anastomosis, and the appropriateness and placement of drains.

The spleen and the left ureter are particularly at risk of damage during operations for diverticular disease. Accidental splenic injury and subsequent splenectomy create a risk of venous thromboembolic complications and may permanently impair immunity. The left ureter may be adherent to the sigmoid mesentery or bound in dense scar in the region of the pelvic brim, sometimes with partial ureteral obstruction. Preoperative placement of a left ureteral catheter as a stent may help to identify the ureter in an area of inflammation or dense scar. Ureteral injury can be avoided by dissecting the mesentery of the descending colon from Gerrota's fascia, identifying the ureter near the renal pelvis, then dissecting downward through the difficult area, keeping the ureter in a posterior position and always in view.

The choice of abdominal incision is important for a safe and convenient resection of the left colon. Although a midline or a left paramedian incision is the more conventional approach, an oblique curved incision that begins at the lateral border of the right rectus muscle 4 cm above the symphysis pubis crosses both rectus muscles and curves upward to the costal margin in the left flank gives ideal exposure of both the spleen and the depths of the pelvis. The use of the Trendelenberg position and tilting of the table to the right permit the small bowel to be packed into the right upper abdomen, leaving the field clearly exposed from the splenic flexure to the cul-de-sac. Closure of the wound in layers and reapproximation of the rectus muscles by figure-of-eight synthetic absorbable sutures gives reliable and comfortable healing and essentially removes the risk of incisional herniation. If a sigmoid or descending colostomy is required the bowel may be brought through a separate incision above and medial to the incision to create a stoma at the level of the umbilicus. Transverse colostomy may be accomplished easily by lifting the abdominal wall with the left hand within the abdomen and making a transverse right upper quadrant incision through which a loop of right transverse colon may be drawn (Figs. 16–19) 1029,1030,1031,1032.

The length of colon to be resected depends upon the extent of muscular abnormalities in the gut wall as well as the extent of the inflammatory changes. The distal resection margin should be at the level of the intraperitoneal rectum, which is usually the distal extent of diverticular disease. The rectum may be effectively brought upward by blunt retroperitoneal dissection from the hollow of the sacrum, making division and anastomosis technically easier. The resected specimen should include all the narrowed and inflamed segment, as well as the area of muscular thickening and foreshortening: in most instances this will require resection of a length of at least 25 cm. The splenic flexure should be freed and the left colic artery and vein divided and ligated near their origins to permit the splenic flexure or left transverse colon to be brought to the rectum without tension. The anastomosis may be stapled or hand-sewn but must be accurate, without tension and in well perfused bowel. If the anastomosis is not technically perfect, a right transverse colostomy should be added and, in selected cases, pelvic drainage will be required.

Operative complications of treatment of colonic diverticular disease include splenic injuries (2 per cent), intraoperative haemorrhage (2 per cent), colonoscopic perforation (1 per cent), and ureteral injury (0.6 per cent).

Postoperative complications include respiratory failure (6 per cent), wound abscess (4 per cent), anastomotic leak (2.5 per cent), renal failure (2 per cent), peritonitis (2 per cent), incisional hernia (2 per cent), haemorrhagic shock (2 per cent), ileus (2 per cent), thrombocytopenia (2 per cent), small bowel obstruction (1.5 per cent), and sigmoidocutaneous fistula (1 per cent). Many other conditions occur with a frequency of less than 1 per cent.

Anastomotic leak is a serious postoperative complication which needs to be identified promptly and is treated by abdominal re-exploration, transverse colostomy, and external drainage of the contaminated area. All such patients are gravely ill and require triple antibiotic coverage (metronidazole, ampicillin, and gentamicin) with careful metabolic monitoring and support. There is a 10 per cent mortality rate associated with this complication. All patients who recover have long, complex, and costly illnesses necessitating multiple additional operative procedures. Re-resection of the area of failed anastomosis is mandatory and effective healing should be demonstrated by barium enema prior to attempted closure of the transverse colostomy.

Postoperative abscesses may be subphrenic, pelvic, or intermesenteric. These abscesses can often be treated by percutaneous catheter drainage; if treatment is not successful, open drainage is required.

Intestinal obstruction should be treated by nasogastric decompression and intravenous administration of fluids, including intravenous hyperalimentation. This will permit resolution of the obstruction without re-exploration in most instances. If pain, distension, and leucocytosis do not resolve quickly, surgical re-exploration of the abdomen should be carried out.

Intravenous hyperalimentation by means of a central line is an important adjunct to treatment of postoperative complications in patients in whom oral feedings must be restricted for more than 5 to 7 days. Nutrition, effective antibiotic therapy, fluid intake to maintain renal function, defunctioning of the bowel, and adequate drainage of sepsis are critical to the recovery of such patients.

Overall mortality rates for patients requiring operation for colon diverticular disease are in the range of 5 per cent. Mortality among patients requiring emergency surgery for complications of the disease is more than five times greater than among those undergoing elective procedures. Patients need an average of 1.5 operations for successful treatment, but those with severe complications often require several staged procedures before recovery.

Complications of operations are frequent (approximately 30 per cent overall), often serious, and usually related to sepsis. Multiple organ failure may follow septic shock, which occurs either as a manifestation of the primary disease or as a postoperative complication. Morbidity among patients with postoperative complications tends to be prolonged, often lasting for several months.

The high mortality and morbidity rates among patients treated for complications of diverticular disease support the recommendation that those who are at high risk of developing complications should undergo elective colon resection. Unfortunately, 50 per cent of those who require emergency operations for complications of diverticular disease have had symptoms for less than 30 days at the time of the presenting illness.

Long-term results of colon resection for diverticular disease are excellent. Most patients are relieved of their chronic bowel complaints and all the septic sequelae of the disease, although they tend to have slightly more frequent stools (2–3 per day) as compared to their preoperative status. Patients who require ileorectal anastomosis for massive haemorrhage may have troublesome diarrhoea that generally responds to medical management. Recurrent diverticulitis is rare following adequate resection of the diseased bowel segment, and affects less than 5 per cent of patients overall. However, among patients who have had incompleted staged operative treatment and who may be left with a colostomy and defunctioned sigmoid or rectum, the disease and its complications may continue in the defunctioned segment.

Diverticular disease of the colon is a disease increasing in frequency as the average age of Western populations increases. While its causes are multifactorial, at least one prophylactic measure appears to be the provision of a diet high in fibre, causing a relatively short transit time of stool in the gut.

The complications of diverticular disease are severe and are associated with significant morbidity and mortality. Surgical resection of affected colon segments is effective treatment but is hazardous if sepsis is present.

Improved results of treatment depend upon skilled judgment, technical expertise, and effective antibiotic and metabolic management. Elective operation should be considered for patients with repeated attacks of diverticulitis, those under the age of 50, and for patients with diverticular disease who have reduced immunological competence or who may be candidates for organ transplantation.

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