Diverticular disease of the colon
BYLINE: Neil Stollman a, * Dr MD,
; Jeffrey B Raskin b Prof MD
SECTION: Pg. 631 Vol. 363 No. 9409 ISSN: 0140-6736
refers to small outpouchings from the colonic lumen due to mucosal herniation
through the colonic wall at sites of vascular perforation. Abnormal colonic
motility and inadequate intake of dietary fibre have been implicated in its
pathogenesis. This acquired abnormality is typically found in developed
countries, and its prevalence rises with age. Most patients affected will
remain entirely asymptomatic; however, 10?20 of those affected can manifest
clinical syndromes, mainly diverticulitis and diverticular haemorrhage. As our
elderly population grows, we can anticipate a concomitant rise in the number of
patients with diverticular disease. Here, we review the incidence, pathophysiology,
clinical presentation, and management of diverticular disease of the colon and
Diverticulosis of the
colon is quite frequent in developed countries and prevalence rises with age.
Although up to two-thirds of people older than age 80 years are affected, most
remain asymptomatic. The causes of colonic diverticula include alterations in
colonic wall resistance, disordered colonic motility, and dietary deficiencies,
especially fibre. Clinical manifestations of this disorder range from
nonspecific intermittent abdominal pain to potentially life-threatening
complications such as diverticulitis or haemorrhage. CT scanning and
colonoscopy are important in diagnosis and management. Here, we review
epidemiology, causes, clinical presentation, and management of diverticular disease
of the colon.
Prevalence of colonic
diverticulosis is difficult to measure because most patients are asymptomatic.
In early (1920?1940) autopsy and barium enema series, rates of 2?10 were
reported.1 Data show a substantial rise in colonic diverticula within the past
few decades. Prevalence of diverticular disease increases with age, from less
than 10 in people younger than age 40 years to 50?66 in patients older than age
80 years.1?3 No sex differences seem to exist.
been labelled a disease of western civilisation because of its striking
geographic variability. The disorder is rare in rural Africa and Asia, with the
highest prevalence seen in the USA, Europe, and Australia.1 Within a given
country, the incidence of colonic diverticula can vary in ethnic groups-eg, in
Chinese inhabitants of Singapore, incidence was reported to be 0·14 cases per
million population per year versus 5·41 cases in Europeans.4 Urbanisation
within a country over time can also lead to a rise in prevalence of
diverticulosis. Follow-up in Singapore has indicated colonic diverticulosis in
19, an increase attributed mainly to dietary changes.5 Results of series of
symptomatic diverticular disease in Africa have shown a rising incidence in
increasingly urbanised communities.6,7 Cases of complicated
diverticulitis have risen 50 in Finland in the past two decades, an increase
attributed to an ageing population and reduced fibre consumption.8 Although
much of the epidemiological research mentioned is simply descriptive, understanding
and assessing these noted trends could yield insight into pathogenesis of the
disorder and help to predict disease course and complications.
typically form in parallel rows between the taeniae coli because of weakness of
the muscle wall at sites of penetration of the vasa recta supplying the mucosa.
In European and US populations, diverticula arise mainly in the distal colon,
with 90 of patients having sigmoid colon involvement and only 15 having
right-sided diverticula.3,9?11 This finding is in contrast to that
seen in Asian populations, in which right-sided involvement is more prominent.5,12
Diverticula vary from
solitary findings to many hundreds. They are typically 5?10 mm in diameter but
can exceed 2 cm. An entity of giant colonic diverticula has been described with
sizes up to 25 cm. Most are single, located in the sigmoid colon, and
asymptomatic, but can present with infection, obstruction, or perforation.13
diverticulosis is an acquired disorder, findings of observational studies
suggest that the disease pattern-eg, right-sided, pancolonic-might be
established early on and then remain constant, rather than increasing over time
in number and extent. In sequential studies with barium enema, no progression
of disease has generally been noted in most patients.14 In fact, two distinct
forms of diverticulosis might exist: one discernible by muscle thickening,
mainly in the left colon, and associated with perforation and diverticulitis;
the other due to a diffuse connective tissue abnormality, resulting in
pancolonic diverticulosis and a propensity for bleeding.15 This possibility
could, in part, account for anatomic differences described between European and
US patients and those from Asia.
Cause and pathogenesis
Colonic wall resistance
descriptions of diverticular colons typically noted thickening of muscle wall
and shortening of the taeniae coli, with resultant concertina-like bunching of
haustral folds. Although muscle contraction is noted, routine histology has not
generally indicated muscle hypertrophy. Findings of electron microscopic
studies have shown that diverticular colonic walls consist of structurally
normal muscle cells but elastin deposition is amplified by more than 200 in
muscle cells in the taenia coli compared with those without diverticula.16
Elastin is laid down in a contracted form, resulting in shortening of the
taenia coli and bunching of circular muscle. Age-related changes in collagen
composition could have a causal role in weakening of wall resistance. An
increase in type III collagen synthesis has been described.17,18
Further, changes in collagen crosslinking have been shown in animal and human
models.19,20 The importance of gut wall connective tissue is
underscored by early development of diverticula in patients with connective
tissue disorders such as Marfan's and Ehlers-Danlos
In the 1960s,
Arfwidsson22 did manometry on patients with or without sigmoid diverticula and
showed higher resting, postprandial, and neostigmine-stimulated luminal
pressures in diverticular patients than in controls. Painter and colleagues23,24
confirmed these findings in response to neostigmine or morphine in individuals
with sigmoid diverticula (intraluminal hypertension) and did simultaneous
cineradiography. Painter suggested a theory of segmentation in which
contraction of the colon causes a series of discrete "little
bladders" (figure 1). He proposed that this segmentation had a
physiological role in delaying of transport and augmentation of water
reabsorption but could also generate excessively high pressures within every
bladder, favouring herniation. This effect might be amplified by dietary fibre
deficiency.25 Subsequently, patients with symptomatic diverticulosis have been
shown to have higher motility indices than either asymptomatic patients or healthy
controls.26 High right-sided pressures have also been recorded in patients with
right-colon diverticulosis, suggesting that abnormal motility could also have a
role in pathogenesis of proximal diverticula.27 A preponderance of excitatory
cholinergic nerves and a diminution of action of non-adrenergic,
non-cholinergic inhibitory nerves by nitric oxide have been noted in
diverticular colons compared with controls.28 These findings suggest that an
imbalance in usual excitatory and inhibitory influences could favour enhanced
tonicity. Whether altered motility and intraluminal hypertension are a cause of
disease or symptoms, or an effect of same, is uncertain.
variability of diverticular disease and correlation with a western diet have
long suggested a dietary factor as fundamental in pathogenesis of the disorder.
Burkitt and Painter1 were the most eloquent proponents of this theory,
labelling diverticulosis a deficiency disease that, like scurvy, could be
avoided with dietary changes. They recorded transit times and stool weights
from more than 1200 individuals in the UK and rural Uganda.29 The UK patients,
eating a low fibre diet, had transit times of about 80 h and mean stool weights
of 110 g/day. By contrast, rural Ugandans, eating very high fibre diets, had
times of 34 h and weights of more than 450 g/day. The longer transit time and
smaller stool volumes were thought to increase intraluminal pressure,
predisposing to diverticular herniation. As reasonable as this hypothesis
seems, results of studies in western populations comparing transit times and
stool volumes in patients with and without diverticular disease have failed to
show significant differences. Nonetheless, corroborative data in animals do
exist, most notably in rats fed diets of various fibre content throughout their
lifespan.30 45 of rats on the lowest fibre diet developed diverticula compared
with only 9 of those fed the highest fibre diet. Furthermore, in another animal
model, high fibre diets protected against collagen crosslinking and were
associated with reduced frequency of diverticulosis.19
The asymptomatic patient
diverticular disease is frequently an incidental finding during assessment of a
patient for another reason, such as routine screening for colon cancer. No
treatment or follow-up needs to be offered to this large population, most of
whom will remain asymptomatic, although findings of one study suggested a
possible prophylactic benefit of a high-fibre diet. In a prospective study of
51529 US male health professionals followed up for more than 4 years, 385 new
cases of symptomatic diverticular disease were identified.31 A significant
inverse association was recorded between dietary fibre intake and risk of
development of clinically evident diverticular disease. Insoluble fibre from
fruits and vegetables was noted to be more protective than cereal fibres.32
These results provide support for a recommendation that patients with
asymptomatic diverticular disease might benefit from increasing their fruit and
vegetable fibre intake, a stance endorsed by the American Dietetic
The symptomatic patient
Patients can present
with non-specific abdominal complaints-eg, lower abdominal pain, usually left-sided-and
subsequently be shown to have diverticulosis coli; a causal relation is
sometimes difficult to establish. Such patients do not usually manifest signs
of inflammation, such as pyrexia or neutrophilia, which could indicate
diverticulitis. Pain is generally exacerbated by eating and diminished with
defecation or flatus, which suggests colonic wall tension due to raised
intraluminal pressure. Patients might also report other symptoms such as
bloating or constipation. Assessment can indicate fullness or mild tenderness
in the left lower quadrant, but frank rebound or guarding should be absent. A
guaiac-positive stool in this setting should never be attributed to
diverticulosis without complete colonic assessment. Findings of laboratory
studies should be normal.
For years, barium
enema was the standard investigation in diverticulosis patients, and although
it provides information on number and location of colonic diverticula, it
cannot discern clinical relevance. However, inaccurate findings have been
reported in nearly a third of patients with diverticulosis.34 This disorder
has, in the past, been regarded as a contraindication to colonoscopy for fear
of causing a perforation.35,36 Further data and extensive clinical
experience, however, have shown that colonoscopy is safe in this population,
although the diverticular colon can be difficult to examine because of spasm,
luminal narrowing, and fixation.37
Brodribb38 did a
randomised double-blind trial of a high-fibre diet in 18 patients with
symptomatic diverticular disease. A significant placebo effect was noted at 1
month; however, by 3 months, a significant reduction in bowel symptoms was seen
in patients on the high-fibre diet. These findings suggest that patients should
gradually increase their dietary fibre over weeks, and be aware that their
symptoms might initially worsen before they improve, which could take months.
In a subsequent study,39 no improvement in symptom endpoints was reported
despite a decline in transit times and increases in stool weight and frequency.
Despite these conflicting data, some amelioration of symptoms in patients with
uncomplicated disease can be reasonably expected with a high-fibre diet.
Hypermotility of the
diverticular colon suggests that anticholinergic or antispasmodic drugs might
improve symptoms by diminishing muscular contraction. Nonetheless, no
adequately controlled therapeutic trials have shown a benefit. No rationale
exists for use of antibiotics or narcotic analgesics in uncomplicated
perhaps 75?80, with anatomical diverticulosis will remain asymptomatic
throughout their lifetime. Of the few who develop complications,
diverticulitis-and its difficulties such as abscesses, fistulas, or obstruction-is
the most usual manifestation, followed by diverticular haemorrhage, both of
which are addressed below.
Complicated diverticular disease
diverticulitis generally present with left lower quadrant pain, indicating the
propensity for this disorder to arise in the sigmoid colon in western
countries, although individuals with redundant sigmoid colons can manifest
suprapubic or right-sided pain. Asian patients have predominantly right-sided
diverticula and will usually present with right lower quadrant pain.42 Pain may
be intermittent or constant and is sometimes associated with a change in bowel
habits.43 Haematochezia is rare, although anorexia, nausea, and vomiting can
arise. Physical examination usually discloses localised tenderness and,
occasionally, a palpable mass. Bowel sounds are typically depressed but can be
normal in mild cases or enhanced in the presence of obstruction. Rectal
examination may reveal tenderness or a mass, especially with a low-lying pelvic
abscess. Fever is present in most patients, although hypotension and shock are
unusual. White blood cell count is sometimes raised.43
diagnosis of this presentation includes acute appendicitis, especially in Asian
patients or those with redundant sigmoid colons.42 Aphthous ulcers, anorectal
involvement, and chronic diarrhoea suggest a possible diagnosis of Crohn's
colitis. Colon carcinoma, like diverticulosis, affects colons of ageing
westerners, and a causal relation has been postulated. Most probably, colon
cancer and diverticulosis are both results of the same environmental effects,
mainly dietary. Chronic symptoms of weight loss or bleeding should raise suspicion
for carcinoma. Surgical investigation and resection could be necessary to make
a precise diagnosis. In uncomplicated cases, elective colonoscopy after acute
inflammation has resolved will allow for exclusion of malignant disease.
Elderly people with diverticulosis are also at risk for ischaemic colitis.
Features helpful to differentiate between these disorders include presence of
thumbprinting on abdominal radiographs and haematochezia, both suggesting
ischaemia. Gynaecological disorders, such as ruptured ovarian cysts, ovarian
torsion, ectopic pregnancy, or pelvic inflammatory disease, can resemble acute
diverticulitis in female patients. Pelvic ultrasound can be helpful in
obtaining an accurate diagnosis. Other forms of colitis, such as pseudomembranous
or amoebic, can also mimic diverticulitis.
Most patients with
diverticulitis present with signs and symptoms sufficient to justify clinical
diagnosis and institute empiric treatment, although a thorough physical
examination and basic laboratory studies, such as white blood cell count,
should be done in patients coming to clinical attention. Further studies should
be reserved for individuals in whom diagnosis remains uncertain, response to
empiric treatment is suboptimal, or a complication is suspected.
Chest and abdominal
radiographs should generally be done in patients with clinically significant
abdominal pain. A chest radiograph taken while the patient is upright can aid
detection of pneumoperitoneum and help to assess cardiopulmonary status.
Abdominal radiographs can show abnormal findings in 30?50 of patients,44,45
which include small or large bowel dilation or ileus, pneumoperitoneum, bowel
obstruction, or soft-tissue densities suggesting abscesses.
the diagnostic standard-are limited by the fact that diverticulitis is mainly
an extraluminal process. If they are to be undertaken, water-soluble contrast
material should be used and a low-pressure single-contrast study done. Findings
deemed highly suggestive of diverticulitis include extravasated contrast
material outlining an abscess cavity, intramural sinus tract, or fistula
(figure 2).9,46 Absence of any diverticula should provoke
reconsideration of the diagnosis. In retrospective analyses, contrast enema has
been shown to have a sensitivity of 62?94, with false-negative results in 2?15.47,48
CT scanning has an
increasing role in diagnosis, and should be regarded as the diagnostic
procedure of choice. Abdominal and pelvic scanning is done with intravenous,
oral, and rectal contrast. Criteria suggestive of diverticulitis include
pericolic infiltration of fatty tissue, colonic wall thickening, and abscess
formation (figure 3). In many trials comparing CT with barium enema in
suspected diverticulitis, sensitivities for CT of 93?98 and specificities of
75?100 have been consistently reported, significantly more accurate than
Because of risk of
perforation from either the device or air insufflation, endoscopy is generally
avoided in initial assessment of the patient with acute diverticulitis. Its use
should be restricted to situations in which diagnosis of diverticulitis is
unclear. In such cases, limited sigmoidoscopy with minimum insufflation can be
helpful to exclude other diagnoses, such as inflammatory, infectious, or
Need for admission is
the initial decision to be made in uncomplicated diverticulitis, which is based
on patient's presentation, their ability to tolerate oral intake, severity of
illness, comorbid disease, and adequate outpatient support. Outpatients should
be treated with a clear liquid diet and a broad-spectrum oral antibiotic with
activity against anaerobes and gram-negative rods (in particular,
Escherichia coli and Bacteroides fragilis).52
Symptomatic improvement should generally be evident within 2?3 days, at which
time diet can be slowly advanced. Antibiotic treatment should be continued for
7?10 days. Patients needing admission should have clear liquids or nothing by
mouth and intravenous fluids. Intravenous antibiotics should be started, aimed
mainly at colonic anaerobic and gram-negative flora.52 Improvement of symptoms
should be expected within 2?4 days, at which point diet can be advanced. If
improvement continues, patients may be discharged to complete a 7?10 day oral
antibiotic course. Failure of conservative medical treatment warrants a
diligent search for complications, consideration of alternative diagnoses, and
surgical consultation. Most patients admitted with acute diverticulitis will
respond to conservative treatment, but 15?30 will need surgery during that
time.9,48,53 Free perforation with generalised peritonitis, although
uncommon, carries a high mortality rate (up to 35) and needs urgent surgical
For most patients who
respond well to conservative treatment, an important clinical question
subsequently revolves around likelihood of recurrence and role of prophylactic
surgical resection. Risk of recurrent symptoms after an attack of acute
diverticulitis has been reported between 7 and 45; a third is a reasonable
approximation.9,48,53 Recurrent attacks are less likely to respond
to medical treatment and have a high mortality rate;48,53 thus, most
authorities agree that elective resection is indicated after two attacks of
uncomplicated diverticulitis.54?56 The risk-benefit analysis of such
an approach must be tailored with consideration of severity and responsiveness
of the episode, general health of the patient, and risk of subsequent
occurrence. Risk of resection is an evolving factor, with reports of
increasingly favourable experiences with laparoscopic resections for
diverticular disease.57?62 This approach might reduce the threshold
for resection in some patients by lowering operative morbidity. However, some
patients will still have symptoms after surgical resection.
Diverticulitis in special situations
seen in about 2?5 of people younger than 40 years old,9,53 mainly in
males.9,63,64 Disease is more virulent in young patients, with 66?88
needing urgent surgery during their initial attack, with a high risk of
recurrences or complications.9,63,65,66 Obesity can also be an
important risk factor in young people.67 For these reasons, and because of the
low operative risk of an elective procedure in an otherwise healthy young
patient, resection is generally indicated after one well-documented episode of
uncomplicated diverticulitis.48,54 Others, however, have questioned
patients with diverticulitis may present with more subtle signs and symptoms
than those who are immunocompetent and represent a difficult diagnostic
challenge. They are less likely to benefit from medical treatment and have a
higher rate of free perforation, need for surgery, and postoperative mortality
than non-compromised patients.70,71 Because of this high risk, some
authorities have advocated elective resection after one episode in an immunosuppressed
Diverticulitis is the
most usual clinical complication of diverticular disease, affecting 10?25 of
patients with diverticula.3 The process by which diverticulitis arises has been
likened to that of appendicitis, with a diverticulum becoming obstructed by
inspissated stool in its neck.40 This faecalith abrades the mucosa of the sac,
causing inflammation and expansion of usual bacterial flora, with diminished
venous outflow and localised ischaemia. Bacteria may breach the mucosa and
extend the process through the full wall thickness, ultimately leading to
perforation.41 Extent and localisation of the perforation will establish its
clinical behaviour. Microperforations can remain contained by pericolic fat and
mesentery and cause small pericolic abscesses. Large perforations can result in
an extensive abscess, which could continue around the bowel wall and form a
large inflammatory mass or extend to other organs. Free perforation into the
peritoneum causing frank peritonitis can be life-threatening but is rare.
When perforation of a
diverticulum takes place, a localised phlegmon initially develops; further
spread can lead to formation of large local or distant abscesses. Clinical
signs suggesting abscess formation include a tender mass on investigation or
persistent fever despite an adequate trial of antibiotics. When an abscess is
suspected, CT scanning is the best modality for making the diagnosis and
following its course.
abscesses can generally be treated conservatively with continued antibiotics
and bowel rest.56,72 In patients in whom surgery is needed, a
single-stage resection and anastomosis can generally be done. For those with distant
or unresolving abscesses, drainage is indicated. Surgery was previously the
main option, but CT-guided percutaneous drainage of abdominal abscesses is now
used in preference when feasible. The advantage of percutaneous catheter
drainage is rapid control of sepsis and patient stabilisation. Further,
drainage might eliminate need for a two-stage procedure with interval
colostomy, instead allowing temporary palliative drainage and subsequent
When a diverticular
phlegmon or abscess extends or ruptures into an adjacent organ, fistulas can
arise, the most typical being colovesicular.75 Such fistulas have a two to one
male predominance, attributable to protection of the bladder by the uterus and
50 rate of hysterectomy in female patients with colovesical fistulas.
Pneumaturia and faecaluria are suggestive signs.76 Cystoscopy, cystography, and
contrast radiographs or methylene blue studies can show fistula tracts.
Single-stage operative resection with fistula closure can be undertaken in most
patients.75,76 Colovaginal fistulas are the next most frequent,
representing about 25 of all cases.75 Passage of stool or flatus via the vagina
is pathognomonic. Frequent vaginal infections or copious discharge should
prompt consideration of a colovaginal fistula. Treatment is surgical resection
of the diseased colon with repair of the contiguous organ.56 Coloenteric,
colouterine, coloureteral, and colocutaneous fistulas arise much less
During an episode of
acute diverticulitis, partial colonic obstruction can happen because of
relative lumenal narrowing from pericolic inflammation or compression from
abscess formation. Colonic pseudo-obstruction can also take place. Acute
diverticulitis might cause small bowel obstruction or ileus if a loop of small
intestine becomes incorporated into the inflammatory mass. These presentations
usually improve as inflammation subsides with effective treatment; failure to
do so should prompt surgical consultation.
Recurrent episodes of
diverticulitis, sometimes subclinical, can initiate progressive fibrosis and
stricturing of the colonic wall without persisting inflammation. Ultimately,
high-grade or complete obstruction can happen, needing surgery. An insidious
presentation with non-specific symptoms is typical. Generally, a stricture with
uncertain cause is identified on barium enema. The important issue is to
distinguish between a diverticular stricture and a stenosing neoplasm. Doctors
should attempt to make this differentiation by colonoscopy with biopsy, but
this procedure is not always possible.77 Strictures in which malignant disease
cannot be excluded should undergo surgical en bloc resection. A trial of
endoscopic treatment with balloon dilation can be attempted in patients in whom
neoplasm is judged sufficiently excluded.78?80 Early work with
colonic metal stents has suggested that they might have a role in colonic
obstruction due to diverticular disease. Stenting can provide temporary
decompression, allowing for bowel preparation and subsequent single-stage
resection without diversion.81,82
resected specimens from patients with bleeding diverticula shows intimal
thickening and medial thinning of the vasa recta as it courses over the dome of
the diverticulum.90 These changes arise asymetrically towards the lumen and
lead to segmental weakening of the artery, predisposing to rupture. Factors
that initiate this arterial change are unknown, although inflammation does not
seem to be a contributing factor. This finding accords with the clinical
impression that bleeding rarely complicates diverticulitis.
The association of
use of non-steroidal anti-inflammatories (NSAIDs) with ulcer disease and upper
gastrointestinal bleeding is well documented, but data have also implicated
these drugs in diverticular bleeding. In a large prospective series of patients
with lower gastrointestinal bleeding (in whom 50 were diver-ticular), a
bleeding risk with NSAIDs was reported that was equal to that of duodenal
ulcer.94 In the Health Professionals Follow-up Study,95 regular NSAID use was
associated with raised risk of diverticular bleeding. Whether patients with
diverticulosis should be counselled to avoid NSAIDs-as is done for ulcer
patients-or use COX2 selective agents-is still conjecture.
of diverticular haemorrhage is usually one of an abrupt painless onset. The
patient can have mild lower abdominal cramps or the urge to defecate, followed
by passage of voluminous red or maroon blood or clots. While melaena can
sometimes happen with a slowly bleeding right colon lesion, the arterial nature
of diverticular bleeding makes this presentation uncommon. Presence of colonic
diverticula should not be judged an adequate explanation for a positive faecal
occult blood test or as a cause of iron deficiency anaemia. Haemorrhage ceases
spontaneously in 70?80 of patients, and rebleeding rates range from 22 to 38.88,89,92
The chance of a third bleeding episode can be as high as 50, leading many
doctors to recommend surgical resection after a second bleeding episode,
similar to recommendations made for recurrent divericulitis.54,88
Diagnosis and management
Overall management of
lower gastrointestinal bleeding is beyond the scope of this review, but is
described in other articles.89,96
Fluid and blood product
resuscitation needs immediate attention. Exclusion of an upper gastrointestinal
source by endoscopy is warranted, because 10?15 of patients with haematochezia
will have an upper gastrointestinal tract cause. Flexible sigmoidoscopy is an
appropriate initial approach to rule out an obvious rectosigmoid lesion, and
can be done either unprepared or after enema administration. If no cause is
identified, further assessment with non-invasive (nuclear scintigraphy) or
invasive (angiography, colonoscopy) techniques can be undertaken in an attempt
to localise and treat the bleeding source.
several theoretical advantages in assessment of lower gastrointestinal
bleeding. It is non-invasive and sensitive to bleeding rates as low as 0·1
mL/min. Furthermore, once labelled, red cells remain active for up to 24 h,
permitting repeat imaging in the patient with intermittent bleeding.97 At best,
however, nuclear scans provide information only about the anatomic site of
bleeding, not its cause, and have no therapeutic potential. Further, accuracy
of predicting the bleeding site has been questioned.98 In view of the high
sensitivity and relative simplicity of scintigraphy, however, many centres use
this method as a screening test before angiography, to keep the number of
negative angiograms to a minimum and allow for selection of a specific artery
Angiography has a
sensitivity for lower gastrointestinal bleeding at a rate of 0·5 mL/min,
although this value is from animal work.83 An important use of diagnostic
angiography is to identify the site of bleeding with enough accuracy to allow
selective hemicolectomy, rather than empirical subtotal colectomy, although
accuracy has been questioned.99 An additional role for angiography rests in its
therapeutic potential. Intra-arterial vasopressin can control haemorrhage in
more than 90 of patients.100 This treatment is usually only temporary, however,
because up to half of treated people will rebleed with discontinuation of
infusion. Nonetheless, even temporary control of bleeding can allow
semielective surgical procedure in a well-prepared patient, rather than
emergency resection, with concomitant reduction in surgical morbidity.100
Angiographic embolisation of very distal bleeding branches (subselective) is
also effective and safe.101
For most patients,
diverticular bleeding is self-limited. Subsequent colonoscopy should be done to
elucidate the bleeding source and to exclude neoplasia.9,102?104
role of colonoscopy during episodes of lower gastrointestinal bleeding is being
A rapid oral purge with electrolyte solution to
prepare the colon for emergent colonoscopy has been shown to be safe and
In small series, endoscopy has been used to
control acute bleeding (figure 4).110?118
In a cohort of 48 patients
with lower gastrointestinal bleeding,118 ten had definite signs of diverticular
haemorrhage and were treated endoscopi-cally, and none had recurrent bleeding.
In a historical control group of 17 patients not treated with colonoscopy,119
nine had additional bleeding. Although such treatment may be applicable to only
a few patients with lower intestinal bleeding, colonoscopic haemostasis will
probably have an increasing role in the future.
Surgery in lower
gastrointestinal bleeding is usually reserved until endoscopic or angiographic
treatments fail. Segmental resection is most usually done if the bleeding site
is clearly identified from a therapeutically unsuccessful angiographic or
endoscopic procedure. Rebleeding is seen in about 6 of patients.100 In people
with persistent bleeding and no angiographic or endoscopic identification of a
definite bleeding site, subtotal colectomy could be needed.
gastrointestinal bleeding can be caused by diverticula, vascular ectasias,
colitis, or neoplasms.10,83?85
Diverticular sources have been
reported to be the most typically identified cause, accounting for greater than
40 of lower gastrointestinal bleeding episodes.86,87
haemorrhage can arise in 3?5 of patients with diverticulosis.10,88,89
Despite the fact that most diverticula are in the left colon in western
individuals, the site of bleeding may more often be located in the proximal
Search strategy and selection criteria
Sources of information included: authors' published work and research;
and original research, reviews, and practice guidelines identified by computer
database search-eg, MEDLINE, LexisNexis, The Cochrane Library, and
Science Citation Index. Most recent publications were prioritised. Search terms
included: "diverticulosis", "diverticulitis",
"diverticular disease", "diverticular hemorrhage",
"gastrointestinal bleeding", "diverticular abscess",
"diverticular fistula", "colonoscopy",
"endoscopy", "epidemiology", "pathogenesis",
"motility", "fiber", "computerized tomography",
"CT-scanning", "surgery", "laparoscopic",
"ultrasound", "ultrasonography", "barium enema",
"contrast enema", "NSAID", and "non-steroidal
anti-inflammatory", with Boolean operators AND and OR. Human and animal
studies in the English language were reviewed and manually
Conflict of interest statement
No funding was
received for this Seminar.
CONTACT: *Correspondence to: Dr Neil Stollman, Division of
Gastroenterology, San Francisco General Hospital, 1001 Potrero Avenue, Suite
3-D, San Francisco, CA 94110, USA
LOAD-DATE: October 20, 2005
a Division of Gastroenterology, San Francisco General
Hospital, and University of California San Francisco, San Francisco, CA, USA;
b Division of Gastroenterology, University of Miami School of
Medicine, Jackson Memorial Medical Center, Miami, FL, USA
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GRAPHIC: Figure 1, Segmentation of colon by contractions producing little
bladders Modified from reference 24
with permission of the Royal College of Surgeons of England, 1964.
Figure 2, Barium
enemas of manifestations of diverticulitis (A) Acute diverticulitis with
oedema (arrow) of the bowel wall. (B) Intramural sinus tract (arrow) in acute
diverticulitis. (C) Confined perforation or abscess (arrow) in acute
diverticulitis. All figures courtesy of Javier Casillas.
Figure 3, CT
scans of manifestations of diverticulitis
(A) Contained abscess (arrow) in severe sigmoid diverticulitis. (B)
Large air-containing abscess (arrow) in subacute diverticulitis. (C) Large
diverticular abscess (arrow) with penetration into retroperitoneal structures
and extending through abdominal wall into subcutaneous tissue. All figures
courtesy of Javier Casillas.
Endoscopic pictures of diverticulum
(A) Diverticulum with visible vessel. (B) Oozing during epinephrine
injection. (C) Diverticulum post injection. All photos courtesy of Francisco C
DOCUMENT-TYPE: Review article
PUBLICATION-TYPE: Other (Journal)
Copyright 2004 Elsevier Ltd
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