The presence of small protruding sacs or pouches called diverticula in the intestinal wall, and the symptoms or complications caused by them. The term diverticulosis signifies the presence of diverticula in the intestine. Diverticulitis is a complication produced by inflammation in one or more diverticula.
Inflammation of diverticula (abnormal pouches) in the wall of the intestine, particularly in the colon. Diverticulitis is a form of diverticular disease and a complication of diverticulosis.
Symptoms and complications
The symptoms include fever, abdominal pain, vomiting, and rigidity of the abdomen. Intestinal haemorrhage may cause bleeding from the rectum. Diverticula may perforate, or abscesses may form in the tissue around the colon, leading to peritonitis (inflammation of the lining of the abdomen). Other complications include intestinal bleeding, narrowing in the intestine, or a fistula (an abnormal channel between one part of the intestine and another).
Diverticulitis usually subsides with bed rest and antibiotics. In severe cases, a liquid diet or intravenous infusion may be required. Surgery may be needed, in which the diseased section of the intestine is removed and the remaining sections are then joined back together. Some patients are given a temporary colostomy (an operation in which part of the colon is attached to the abdominal wall to form an opening for the discharge of faeces).
A form of diverticular disease in which diverticula (abnormal pouches) exist in the wall of the intestine, particularly in the colon. Complications of diverticulosis may include intestinal bleeding and diverticulitis. The cause is believed to be a lack of fibre in the diet. Diverticulosis is very rare in developing countries, where high-fibre foods make up much of the diet.
Symptoms occur in only a minority of people who have diverticulosis. They usually result from spasm or cramp of the intestinal muscle near diverticula. Many patients have symptoms similar to those of irritable bowel syndrome, including abdominal pain, a bloated sensation, and changes in bowel habits. In severe cases of diverticulosis, intestinal haemorrhage can lead to bleeding from the rectum.
In people with cramps, a high-fibre diet, fibre supplements, and antispasmodic drugs may relieve the symptoms.> A high-fibre diet also reduces the incidence of complications. Bleeding from diverticula usually subsides without treatment, but surgery is an option.
Diverticular Disease in more detail
Diverticula, which are herniations of mucosa through the bowel musculature, are seen most often in the sigmoid and descending colon, with prevalence <5% at age 40 years rising to 65% by age 85 in European populations, but around 0.2% in African and Asian countries. They are ascribed to a lifelong diet deficient in dietary fibre, but it is not known why some diverticula become symptomatic, although rises in intradiverticular pressure are thought to play a role in perforation.
Diverticula are usually discovered incidentally, but symptoms which are attributable to diverticular disease include colicky abdominal pain and bloating, often accompanied by a change in bowel habit with the passage of broken, pellety stools after considerable straining. All patients with such presentation should have a rigid or flexible sigmoidoscopy in addition to a barium enema or colonoscopy to exclude a rectal or sigmoid carcinoma. Treatment is with reassurance that there is no serious underlying disease, a high-fibre diet, and—for patients with pain—antispasmodics such as mebeverine. Elective resection is indicated in the few patients who have repeated severe attacks.
Complications of diverticular disease include diverticultis, pericolic abscess formation, peritonitis, intestinal obstruction, haemorrhage, and fistula formation. Acute diverticulitis typically presents with pain and tenderness over the left lower abdomen, and the patient may have pyrexia, malaise, anorexia and nausea. Treatment is with rest, antibiotics (usually cefuroxime 750 mg and metronidazole 500 mg 8-hourly) and analgesia. Resection of the sigmoid colon may be necessary if symptoms fail to resolve or recur.
Diverticular Disease in great detail
The term diverticular disease was first described in the medical literature at the turn of the 20th century. The first case of resection for a complication of diverticular disease was documented by Mayo in 1907. Autopsy studies in the United Kingdom and Australia have shown that the prevalence of colonic diverticula increases with age. It is less than 5% at the age of 40 years; at the age of 60 it is 30% and rises to 65% by the age of 85. Subtle gender differences have also been observed. In Edinburgh, 23% of all barium enemas demonstrated diverticula. The annual incidence increased from 0.17 in 1000 in those under 45 years to 5.7 in 1000 in those over 75 years of age. Women were affected more than men. A study in eastern England measured the incidence of perforation secondary to diverticular disease. They observed that there was increase in perforation with age and after adjusting for age there was a higher incidence in males (5.1 in 100 000 per year male and 3.6 in 100 000 per year female). In spite of the introduction of high-fibre diets, there is no evidence that the incidence of diverticular disease is declining. A recent review has observed a slight rise in the prevalence of perforated diverticular disease in Western countries from 2.4 in 100 000 in 1986 to 3.8 in 100 000 in 2000.
On the other hand, colonic diverticulosis is very rare in African and Asian countries where the prevalence is 0.2%. Interestingly, in a review of 600 Japanese patients with diverticular disease, right-sided colonic disease was demonstrated in 70%. This geographical distribution is not simply due to genetic factors and race, as Asian and African migrants moving to the United Kingdom or the United States of America have acquired the prevalence of disease seen in the native white population, which suggests an environmental risk factor, thought to be dietary. This is in agreement with the observation that patients presenting with complicated diverticular disease have a low intake of dietary fibre, and vegetarians have a low incidence of the disease.
Diverticular disease is said to be a disease of the 20th century and in the United Kingdom there is a correlation between the rising incidence at the beginning of the 20th century and an increased consumption of refined flour and sugar. Sugar consumption has trebled since 1860, and in the late 1870s the stone grinding of flour was replaced by roller milling, which removes more fibre. Modern white bread and some brown breads contain little fibre compared with the amount in wholemeal bread, which was previously a staple part of the diet.
The development of diverticula can therefore be ascribed to a lifelong diet deficient in dietary fibre. A high-fibre diet is related to reduced gut transit times, with less strain on the colon. Modern, fibre-deficient diets on the other hand give rise to stiff, viscous stools that need high intracolonic pressures to propel them. High luminal pressures cause a protrusion of the mucosa through vulnerable points in the sigmoid and descending colon. They usually occur at the site where colonic blood vessels penetrate the wall. This hypothesis is supported by the observation that, although basal intracolonic pressures are similar in health and diverticular disease, when the diseased colon is activated by emotion, eating, mechanical stimuli, or drugs such as morphine or prostigmine, high pressures are generated in those segments that have diverticula. This is due to hypersegmentation by the colonic smooth muscle, and the difference has been recorded in the earliest stage of disease and may explain its progressive nature. In symptomatic patients an increase in dietary fibre causes a relief of symptoms in many cases.
Changes in the colon wall also play a part. With age, and following episodes of diverticulitis, the colonic wall becomes stiff and less distensible, aggravating the effects of raised intracolonic pressure. An increase in elastin and changes in collagen have been reported. Diabetic patients are prone to diverticular disease at an earlier stage, suggesting a defect in glycolysation of colonic collagen with advancing age. In those with connective tissue disorders such as Ehlers–Danlos syndrome or Marfan’s disease, diverticula are also seen at an unusually early age.
Pathogenesis of diverticular complications
The distinction between symptomatic and asymptomatic diverticular disease is important, for although something is known about the formation of diverticula it is not known why some diverticula become symptomatic.
A large American cohort study has shown that high red meat intake and a diet deficient in fruit and vegetables multiplied the risk of developing symptomatic diverticular disease threefold. The benefits of fibre are thought to be secondary to their effect in reducing gut transit times and colonic segmentation. Secondly, there may be a symbiotic effect related to the formation of short-chain fatty acids, which are released after bacterial action on fibre. On the other hand, certain chemicals in cooked meat such as hetrocyclic amines are thought to trigger cytotoxicity of colonocytes.
The pathogenesis of diverticular perforation is not clear. However, rises in intradiverticular pressure are thought to play a role. This may be secondary to a blockage of the mouth with faecal material or colonic segmentation. Once the pressure rises over a critical threshold, focal ischaemia leading to necrosis occurs. This would then allow the passage of luminal bacteria into the local pericolic tissue. With time this would mature into a local abscess. In cases of failure of local tissue to contain the infection, there may be a progression to a faecal peritonitis. This spectrum of diverticular complications can be classified into the four stages as proposed by Hinchey. See table below:
|Table: Hinchey classification of sepsis/contamination in diverticulitis|
|2||Contained pelvic, retroperitoneal or distant intraperitoneal abscess|
|3||Generalized purulent peritonitis, no communication with bowel lumen|
|4||Generalized purulent peritonitis, communication with bowel lumen
The sigmoid colon, which is less compliant than other colonic segments, is where intraluminal colonic pressures are highest. This reflects the observation that the sigmoid colon is the commonest area in the colon to develop diverticular disease and also secondary complications such as perforation. It has also been noted that diverticula are very distensible and other factors are thought to play a role in whether complications such as perforation occur. Pathology reveals that diverticula consists mainly of a mucosal layer and any factor that results in changes of the integrity of the mucosal barrier will result in alteration of the ability microbial population to pass into the local tissues. This can be divided into factors affecting the microbial flora (antibiotics and fibre deficiency), mucin secretion (nonsteroidal anti-inflammatory drugs (NSAIDs) and fibre), epithelial cell insult (NSAIDs) and immune activity in the colonic wall (age, drugs such as corticosteroids and immunosuppressants).
There is growing body of evidence that NSAIDs have a role to play in complicated diverticular disease. Two prospective case–control studies have shown patients with complications of diverticular disease were more likely to be taking NSAIDs than age-matched controls. Another study compared 115 cases with complicated diverticular disease with 77 with uncomplicated disease. NSAIDS and corticosteroids were found to be associated with development of peritonitis and abscess formation. Also, a large American cohort study following over 35 000 male health professional showed that individuals on NSAIDS had a relative risk of 2.2 of developing symptoms of abdominal pain, bleeding, or change in bowel habit secondary to diverticular disease. The action of NSAIDs may be secondary to a reduction in mucosal blood flow as a result of modulation of prostaglandin levels.
A diverticulum consists of a herniation of mucosa through the colonic musculature. As it enlarges its muscular covering atrophies, so that the fully developed diverticulum consists of mucosa, connective tissue, and peritoneum. The striking abnormality is in the thickening of the circular and longitudinal muscle, which both narrows the colonic lumen and shortens the sigmoid like a concertina to give a sawtooth appearance on barium enema. The diverticula occur as slit-like apertures between the muscle clefts.
Inflammation in diverticular disease is the result of infection around diverticula, which spreads within the pericolic fat to form a dissecting abscess. Usually a single diverticulum is the cause of a pericolic abscess, perhaps initiated by the presence of a faecolith. Involvement of the peritoneum results in local peritonitis, which may become generalized in the event of a perforation. This may also give rise to intraabdominal abscesses or fistulas to the bladder, small bowel, vagina, or uterus. Repeated episodes of diverticulitis lead to a contracted, narrowed sigmoid colon surrounded by fibrous tissue. Bleeding in diverticular disease can often be traced to an infected diverticulum. This may cause either the erosion of a vessel in its wall or the formation of granulation tissue inside the diverticulum, which then bleeds.
Only 10 to 15% of cases of diverticular disease result in symptoms, of which 75% develop diverticultis. They are usually discovered incidentally. The symptoms usually result from disordered motility rather than secondary complications of the disease.
Uncomplicated diverticular disease
Symptoms which are attributable to diverticular disease include colicky abdominal pain and bloating. Pain can be felt along the course of the colon, particularly over the sigmoid, and is often accompanied by a change in bowel habit with the passage of broken, pellety stools after considerable straining. Examination may reveal some tenderness over the sigmoid colon without guarding or evidence of systemic upset. These symptoms may be indistinguishable from those of the irritable bowel syndrome. The passage of blood with an unformed stool needs to be investigated thoroughly to exclude more sinister pathology.
All patients should have a rigid or flexible sigmoidoscopy in addition to a barium enema to exclude a rectal or sigmoid carcinoma. They should be reassured that there is no serious underlying disease and a high-fibre diet should be recommended. Exercise and high dietary fibre have been shown to be prevent the development of diverticular disease in prospective studies. However, evidence for the efficacy of dietary fibre for treatment of established diverticular disease is not conclusive, as shown by two randomized controlled trials where only one showed improved symptoms. Current dietary recommendations include wholemeal bread, wholewheat breakfast cereals, rough porridge or muesli, and fresh fruit and vegetables daily. Fibre increases stool bulk in three ways—by holding water, by proliferation of bacteria, and from the by-products of bacterial fermentation. The coarser the fibre the greater is the faecal bulk, but also the greater the unpalatability. Although cooking bran improves its taste, it reduces its water-holding capacity. A good clinical response is usually achieved by including two tablespoons of bran with the morning cereal, but about one-half of patients will experience gaseous distension or cramps on starting the high-fibre diet. It is worth warning them that this is likely to happen and that it will resolve within a month or so if they persist with the diet.
More recent studies looking at pharmacological agents have shown some benefit with rifamaxin (a derivative of rifamycin) and fibre. Mesalazine has also been associated with a decreased recurrence of symptoms over placebo. However this study also showed that abdominal pain was more common in the treatment group. A case–control study has shown that mesalazine is associated with reduced intracolonic pressure and a reduction in the perforation rate. A reduction in perforation rate was also observed with the use of calcium channel blockers. This is thought to act via the mechanism of reducing intracolonic pressure. Long term use of opioids may be detrimental in such patients, resulting in an increased the risk of developing perforation. More research needs to be done in this field.
In patients with pain, antispasmodics such as mebeverine may be useful, and in a minority with repeated severe attacks an elective resection is then indicated. See table below:
|Table: Indications for surgery|
This is probably more effective than sigmoid myotomy, an operation that became popular in the mid-1960s. In this procedure the circular muscle is divided with a longitudinal incision to widen the colonic lumen. The incision is made through the taenia so as to avoid opening diverticula, and is deepened until the mucosa is just seen. The operation lowers the sigmoid intraluminal pressures and improves symptoms but, after 3 years, pressures return to their former levels. The need for myotomy has declined but it may still be useful in some elderly or obese patients.
Complicated diverticular disease
Complications of diverticular disease include diverticultis, percolic abscess formation, peritonitis, intestinal obstruction, haemorrhage, and fistula formation. This results in the significant morbidity and mortality in this subgroup of patients. This has obvious cost implications in terms of expenditure in health services across the Western world. It is important to distinguish the minority of patients who suffer from a febrile attack with left iliac fossa peritonism, sometimes called left-sided appendicitis, from those with chronic pain and diarrhoea. The inflammation may settle with minimal symptoms or develop into a pericolic abscess or peritonitis.
Pain is felt over the left lower abdomen, and the patient may have pyrexia, malaise, anorexia, and nausea which evidence of systemic upset. The neutrophil count is raised. This is as a result of localized bacterial infection in the colonic wall causing an inflammatory infiltrate thus resulting in systemic manifestations. In certain cases, right iliac fossa tenderness may be present due to sigmoid colon looping to the right side of the abdomen. This may be diagnosed at laparoscopy for right iliac pain.
Treatment is with rest, antibiotics, usually coamoxiclav 1.2 g and metronidazole 500 mg 8-hourly (effective against Gram-negative bacteria and anaerobes), and analgesia. Most cases settle within a few days and the diagnosis can be confirmed after 2 to 3 weeks by barium enema. A narrow segment can sometimes be difficult to distinguish from a carcinoma and any doubtful cases can be clarified by subsequent colonoscopy.
If symptoms fail to resolve, or recur, resection of the sigmoid colon may be necessary. When it is necessary to resect an acutely inflamed and unprepared colon, a Hartmann’s operation may be safer than a primary anastomosis.
However complications will normally develop during the primary episode with further episodes having less inflammatory sequelae. Risk of recurrence after the first episode ranges from 7 to 45%. For recurrent diverticulitis operated electively, a primary anastomosis would be ideal. The accepted management policy for recurrent diverticulitis is elective surgery after two episodes of uncomplicated diverticulitis in order to reduce the morbidity and mortality risk associated with admission for complicated diverticulitis. However this needs to be tempered by the observation from a population-based study that only 25% of patients with perforated diverticulitis actually had a previous history of diverticular disease. This is in agreement with other studies which puts the range at 3 to 30%. Furthermore following elective operation, 10% develop recurrent diverticulitis. Patients being consented for elective operations therefore need to be fully informed of risk and benefits.
Acute diverticulitis can lead to a local peritonitis with abscess formation, either in the paracolic or pelvic area. There may be a palpable mass and a swinging fever. When in doubt the diagnosis can be confirmed by CT scanning with rectal contrast. The latter investigation is excellent at demonstrating bowel wall thickening, abscess formation, and extraluminal disease. The specificity is high. The size of the abscess can be measured. Small abscesses less than 5 cm in size can be treated with antibiotics with good outcome. Those less than 2 cm in size can be treated with antibiotics in the community.
It is wise to let an abscess localize whilst treating the patient with rest, antibiotics, and analgesia. Some abscesses will be amenable to drainage by direct incision, either over them or via the rectum or vagina. More complicated collections are best drained by CT-guided aspiration or drain placement. There is rarely any need to do a proximal transverse colostomy. If drainage persists, an elective sigmoid colectomy with primary anastomosis can be done at a later time. Even when an abscess is localized, however, the condition remains potentially dangerous as it may rupture into the peritoneal cavity giving rise to peritonitis.
Acute diverticulitis can be complicated by generalized purulent peritonitis, either by direct spread from the inflamed colon or by rupture of a peridiverticular abscess. The clinical picture is of severe intraperitoneal sepsis with toxaemia, ileus, and abdominal pain, and septicaemia will often follow. Before surgery such patients need to be intensively resuscitated with intravenous colloids together with administration of systemic antibiotics. Once stabilized, they require emergency laparotomy.
Other causes of the acute abdomen that may not require surgery should be excluded, including pelvic inflammatory disease, ureteric calculus, and even pulmonary embolus. In these circumstances a CT scan is invaluable.
Surgical options include a defunctioning transverse colostomy, Hartmann’s procedure—removing the diseased sigmoid, oversewing the distal rectum, and bringing out an end colostomy—or colonic resection and primary anastomosis. The first option tends to be performed by more junior surgeons in the middle of the night; however, this is associated with complications of ongoing sepsis secondary to the ongoing faecal stream through the septic colon. Historically, complicated diverticular disease was managed in three stages in which initially the sepsis was drained together with the formation of transverse loop colostomy. This was then followed by resection of the diseased segment and end colostomy followed by reversal. However, this required three hospital admissions and resulted in considerable morbidity. The reduction to two-stage (Hartmann’s) resulted in a drop in mortality rates. More recent studies suggest that in a selected case group a one-stage process involving primary anastomosis is not associated with increased mortality rates. This has the added advantages of reducing hospital re-admissions, although there is a risk of potential leak. There has been a shift away from the more conservative procedures in this situation due to the residual ‘septic colon’ and the further problem of the unsuspected carcinoma within the inflammatory mass. For these reasons more radical measures are favoured by experienced surgeons. Hartmann’s operation is the procedure most frequently used.
Hartmann’s procedure is safe and effective and removes the postoperative risk of anastomotic leak, although subsequent reconnection may involve a major operation in older patients. Purulent peritonitis carries a mortality of around 15%.
This is a catastrophic complication with a mortality of around 50%, particularly in older patients. A diverticulum ruptures, often with little or no inflammation, liberating quantities of faeces into the peritoneal cavity. Rapid and severe shock with septicaemia ensues. Energetic resuscitation is necessary, followed promptly by surgery and a Hartmann’s operation. These patients often need to be stabilized in an intensive care unit postoperatively.
Recurrent inflammation with fibrosis and muscular hypertrophy can lead to progressive stenosis and colonic obstruction, which is usually chronic but may present acutely. Conservative treatment is worth trying at first, provided a carcinoma has been excluded. With the aid of a stool softener the symptoms may resolve and the stricture gradually dilate. If these measures fail, the bowel should be prepared for a resection, with care taken not to aggravate the obstruction.
Small-bowel obstruction is sometimes a complication of acute diverticulitis, as the bowel may adhere to the inflammatory mass. It usually resolves as the inflammation subsides but on occasion a laparotomy and division of adhesions or even a small-bowel resection may be necessary.
A colovesical fistula usually presents with recurrent urinary tract infections, together with pneumaturia or faecuria. The fistula arises in the sigmoid, which has often folded over into the pouch of Douglas, and adheres to the apex of the bladder. This is the most frequent cause of colovesical fistula but carcinoma and Crohn’s disease should be excluded.
Fistulas may also occur between the sigmoid and vagina, uterus, ureter, and ileum. They seldom heal spontaneously but do not always give rise to disabling symptoms and so represent a relative indication for surgery. Sigmoid colectomy as a one-stage procedure is the best option, and colostomy is rarely required. A fistula into the bladder is simply closed and urethral catheter drainage continued for a week.
Major haemorrhage is an uncommon but well-recognized complication. Bleeding from the colon only accounts for 20% of gastrointestinal haemorrhages, of which 50% are diverticular in origin. It is important that other more common causes for bleeding such as polyps and angiodysplasia are excluded by angiographic studies and colonoscopy. Most patients who present tend to be elderly. Massive bleeding is defined when over 40% of blood volume is lost. This can be catastrophic in older patients who have a reduced physiological capacity to maintain vital organ perfusions.
Massive bleeds tend to present as fresh rectal bleeding. Up to 80% will settle down spontaneously and require only transfusion and supportive measures. The initial management of these patients includes oxygen therapy with adequate venous access. Disorders of coagulation need to be identified and corrected during the ongoing resuscitation process. It is important to exclude upper gastrointestinal bleeding by way of endoscopy. Colonoscopy in the immediate aftermath of a bleed can be difficult but in experienced hands the diagnostic yield can be high as 70%. The endoscope needs to have a wide-bore suction channel and excessive insufflation needs to be avoided due to the risk of causing a re-bleed. In units with access to vascular services, mesenteric angiography can be performed. Localization of the bleeding point needs to be at least 1 to 1.5 ml/h. Therapeutic interventions that are available include vasopressin injection and selective embolization. Radiolabelling is usually reserved for patients who are haemodynamically stable, with no access to vascular radiology and failure to establish a diagnosis during endoscopy. However, in circumstances where there is accelerated transit if blood, localization can be poor. As the haemorrhage can be from any part of the colon, good localization is an essential prelude to any operation. Blind colonic resections have a particularly poor record and if the site of bleeding has still not been located, on-table colonic lavage via the appendix stump and intraoperative colonoscopy will usually target the bleeding segment.
A study published in the New England Journal of Medicine reported the results of urgent colonoscopy in bleeding diverticular disease. Instead of the traditional conservative measures patients were given bowel preparation and colonoscoped within 12 h. Bleeding sites thus identified were treated by colonoscopic diathermy and the number of major bleeds, blood transfusions, and operations was reduced together with length of hospital stay. It remains to be seen whether this will result in a major shift of emphasis in management.