1

THE SMALL AND LARGE INTESTINES

Small intestine

Starts at the pylorus and extends to the ileocecal valves. It is approximately 7 m in

length and is divided into the duodenum, jejunum and ileum.

The small bowel is present in the central and lower portion of the abdominal

cavity. Its relations consist of the greater omentum and abdominal wall anteriorly.

Posteriorly, it is fixed to the vertebral column by way of its mesentery. Fig.1

The duodenum is present

proximally and is about 25 cm in

length. It has no mesentery and

therefore, is the most fixed part

of the small bowel. It merges into

the jejunum at the

duodenojejunl flexure.

Figure 1. The relations of

small bowel

2

The reminder of the small bowel is made

up of the jejunum and ileum.

The jejunum makes up the proximal two-fifths

and is wider, thicker and more vascular than the

ileum, see Table-1. It also consists of circular folds

of mucous membrane (valvulae conniventes or

Plicae circulares) that can be used to distinguish it

from the ileum. The ileum contains larger lymph

node aggregates (Peyer,s patches), and these can

sometimes be lead points in cases in

intussusception in the young.

Table-1 Some Differences between Jejunum and Ileum

The arterial supply of the duodenum (Fig.3) consist of the superior

pancreaticoduodenal branch of the hepatic artery and the inferior

pancreaticoduodenal branch of the superior mesenteric artery. The veins drain

into the leinal and superior mesenteric.

The nerves are supplied from the coeliac plexus.

Jejunum Ileum Wall thicker Wall thinner

Lumen larger Lumen smaller

Fat on mesentery Fat on ileum and mesentery Single line of arterial arcades Several lines of arterial arcades

Prominent plicae circulares Less prominent plicae

Aggregate lymph nodules (Peyer's patches) sparse

Aggregate lymph nodules frequent

Figure 2. Anatomy of small bowel

3

The jejunum and ileum are

vascularized by superior mesenteric

artery through a rich plexus of

vessels. The veins run a similar

course. The nerves supply to the

small intestine arises from

sympathetic nerves around the

superior mesenteric artery.

Large intestine

Figure 3. The arterial supply of

duodenum

4

The large intestine (Fig.4)

extends from the ileum to

the anus. The colon is

approximately 1.5 m in

length. The large intestine

can be divide into caecum,

ascending, transvers,

descending and sigmoid

colonic segments. It is

relatively more fixed than

small bowel. It is also

differs in that it possesses

appendices epiploicae on

its surface, which are

peritoneal folds containing

fat, and the presence of

taenia, which consist of

three longitudinal bands of the outer muscle coat which do not cover the full

circumference of the colon. At the rectosigmoid junction, the three taeniae coli

become broad and fuse together so the rectum is totally invested with two

complete layers. This explains why diverticula do not form in the rectum. The

plicae semilunares are spaced, transverse, crescentic folds that separate the

tissue between the taeniae coli and form haustra. They produce a characteristic,

intermittently bulging pattern that radiologically permits differentiation of the

colon from the small intestine where the circular mucosal folds (plicae circulares)

traverse the full diameter of the small bowel lumen, thereby facilitating

radiographic distinction.

Figure 4. The large intestine

5

The blood supply of the colon (Fig.5) is derived

from ileocolic, right colic and middle colic

branches of the superior mesenteric vessels.

The descending colic receives its blood supply

from the left colic branch from the inferior

mesenteric but also communities with the

superior mesenteric system via the marginal

artery of Drummond. The veins run in a similar

distribution.

The nerve supply is derived from the

sympathetic plexus surrounding the superior

and inferiors mesenteric arteries. Visceral pain

is felt in the peri-umblical region in the proximal

colon and in the hypogastric region in the distal

colon.

Figure 5. The blood supply of large bowel

6

FUNCTIONAL ABNORMALITIES

Megacolon and non-megacolon constipation

There is no single definition of constipation; however, a bowel frequency of less

than one every 3 days would be considered abnormal by some. This group of

conditions can be divided into:

1 megacolon:

a Hirschsprung’s disease;

b non-Hirschsprung’s megarectum and megacolon;

2 non-megacolon:

a slow transit;

b normal transit

Idiopathic megarectum and megacolon

This is a rare condition and the cause is not known, although in some it may result

from poor toilet training during infancy and in others from a congenital

abnormality of the intestinal myenteric plexus.

Clinical features

It presents usually in the first 20 years with

severe constipation. Patients with idiopathic

megarectum often present with faecal

incontinence due to rectal faecal loading that

requires manual evacuation. Patients with

megacolon are more likely to present with

abdominal distension and pain. On clinical

examination, there may be a hard faecal mass

arising out of the pelvis and, on rectal

examination, there is a large faecaloma in the

lumen (Fig.6).

Figure 6

Faecaloma in colon

7

The anus is usually patulous, perianal soiling is common, and sigmoidoscopy is

usually impossible but may show melanosis coli if the patient has been taking

laxatives over many years (Fig. 7).

Investigation

Imaging

As there is an enlarged rectum, often with distension of the colon over a variable

length, a radiograph should be taken without prior bowel preparation, using a

small quantity of water-soluble contrast to prevent barium impaction.

Figure 7 Colonoscopy

Normal colon Melanosis coli

Melanosis coli, also pseudomelanosis coli, is a disorder

of pigmentation of the wall of the colon, often

identified at the time of colonoscopy. It is benign, and

may have no significant correlation with disease. The

brown pigment is lipofuscin in macrophages, not

melanin

appearance in

8

There is usually gross faecal loading of the

enlarged rectum and colon and, when a contrast

examination is carried out, the width of the colon

measured at the pelvic brim is usually more than 6.5cm

(Fig. 8).

Anorectal physiology tests

Anorectal physiology tests demonstrate delayed first

sensation and raised maximum tolerated volume. Full-

thickness rectal biopsy shows normal ganglion cells, a

finding that definitively distinguishes this condition from

Hirschsprung’s disease.

Medical treatment

This is directed at emptying the rectum and keeping it

empty with enemas, washouts and sometimes manual

evacuation under anaesthesia. Thereafter, the patient is

encouraged to develop a regular daily bowel habit, with the use of osmotic

laxatives to help the passage of semiformed stool. Rectal evacuation with

suppositories and biofeedback therapy may be useful in resistant cases.

Surgical treatment

Surgical treatment is sometimes

necessary if medical therapy fails.

Options that are available include:

1- resection of the dilated rectum and

colon (Fig. 9) back to normal-

diameter colon with normal

ganglion cells confirmed by frozen

section at the time of surgery, which

is followed by reconstruction with a coloanal anastomosis;

2-colectomy with the formation of an ileorectal anastomosis;

3 -restorative proctocolectomy;

Figure 8. Double contrast barium enema

showing megarectum

Figure 9 megacolon

9

4-vertical reduction rectoplasty, which is a new procedure designed to reduce

the volume of the rectum by at least 50%.

5- Stoma formation, which may be used either as a salvage operation for

failure of previous surgery or as a primary intervention.

Non-megacolon constipation

Although constipation is often regarded as a trivial symptom, some patients are

greatly disabled by abdominal pain, distension, reliance on laxatives and difficulty

with defaecation. However, it is extremely prevalent complaint in western

society. These are usually otherwise healthy individuals who seek help for

constipation but eat a normal diet and have a normal colon on endoscopy and

barium enema. Its cause is thought to involve slow whole-gut transit or a rectal

evacuation problem. Factors influencing bowel transit time include:

• drugs: opiates, anti-cholinergics and ferrous sulphate;

• diseases: neurological conditions (Parkinson’s disease, multiple sclerosis and

diabetic nephropathy): – hypothyroidism; – hypercalcaemia.

Investigation

Whole-gut transit time can be measured by asking the patient to stop all

laxatives and take a capsule containing radio-opaque markers (Fig. 10).

Retention of more than 80% of the

shapes, 120 hours after ingestion, is

abnormal.

Defaecating poroctography may be

helpful if the main complaint is difficulty

in evacuating stools.

Treatment

This can be done in several ways:

1 Dietary fibre. Figure 10. Abdominal transit study

10

This is the first-line treatment for people with mild constipation. Constipation

only resolves after several weeks of therapy and usually needs to be

continued in the long term.

2 Laxatives.

It is important that patients do not fall into a cycle of laxative abuse. A

number of types are available which include bulk, osmotic and stimulant

agents.

3 Biofeedback.

This involves conditioning and coordination of the abdominal and pelvic

compartments. It has been shown to be effective in those with a rectal

evacuation problem and has also been used in slow transit with some

response.

Idiopathic slow-transit constipation

This disorder is usually seen in women and results from infrequent bowel

actions, which may have been present since childhood or may suddenly

follow abdominal or pelvic surgery. Marker studies will reveal delayed

transit, and the patient may or may not be able to empty the rectum

normally (Fig. 10). This is a difficult condition to treat medically; dietary

measures are usually unsuccessful, and surgical treatment is justified only

after careful studies and when medical treatment has been exhausted. Total

colectomy and ileorectal anastomosis is the preferred procedure, but the

results are unpredictable. Studies show complications of intermittent small

bowel obstruction (60%), further surgery (30%), constipation (25%),

diarrhoea (25%) and incontinence (10%). This may be explained in part by the

argument that colectomy does not address the functional problem of the

remaining bowel. Patients need to be carefully selected for surgery. Other

types of surgery performed include stoma creation and segmental resection,

but results are variable.

11

VASCULAR ANOMALIES (ANGIODYSPLASIA)

Capillary or cavernous haemangiomas are a cause of haemorrhage from the

colon at any age. In the middle-aged or elderly patient, haemangioma needs

to be distinguished from other causes of sudden massive haemorrhage, such

as diverticulitis, ulcerative colitis (UC) or ischaemic colitis. Angiodysplasia is a

vascular malformation associated with ageing. Its true incidence is probably

not known because of the spectrum of disease severity, with ranges in the

literature from 5 to 25% over the age of 60 years. With the advent of more

sophisticated investigative tools, this may rise. Angiodysplasias occur

particularly in the ascending colon and caecum of elderly patients. The

malformations consist of dilated tortuous submucosal veins and, in severe

cases, the mucosa is replaced by massive dilated deformed vessels.

Clinical features

In the majority, the symptoms are subtle and patients can present with

anaemia. There is no gender predilection for vascular ectasia. About 10–15%

can have brisk bleeds, which may present as melaena or significant per

rectum bleeding that is often intermittent. In many patients in whom rectal

bleeding has previously been attributed to diverticular disease, bleeding was

probably, in fact, from angiodysplasia in the caecum. There is an association

with aortic stenosis.

Heyde’s syndrome describes the association of aortic valve stenosis with

gastrointestinal bleeding from colonic angiodysplasia. A mild form of von

Willebrand’s disease has been thought to be involved. This is caused by

increased breakdown of von Willebrand factor by a natural enzyme called

ADAMTS13 around sites of high shear stress such as a stenosed valve. The

coagulation abnormality resolves after aortic valve replacement.

12

Investigation

Barium enema is usually unhelpful

and should be avoided, not least because it

may mask the lesion at subsequent endoscopy.

Provided that the bleeding is not too risk,

colonoscopy may show the characteristic

lesion in the right colon. (Fig.11)

The lesions are only a few millimetres in size and appear as reddish, raised

areas at endoscopy. ‘Pill’ endoscopy is a relatively new technology that may

detect small bowel lesions. Selective superior and inferior mesenteric

angiography shows the site and extent of the lesion by a blush. If this fails, a

radioactive test using technetium-99m (99mTc)-labelled red cells may

confirm and localise the source of haemorrhage.

Treatment

The first principle is to stabilise an unstable circulation. Following this, the

bleeding needs to be localised by colonoscopy. This allows simple

therapeutic procedures such as cauterisation to be carried out. In severe

uncontrolled bleeding, surgery becomes necessary. On-table colonoscopy is

carried out to confirm the site of bleeding. Angiodysplastics lesions are

sometimes demonstrated by transillumination through the caecum.

If it is still not clear exactly which segment of the colon is involved, then a

total abdominal colectomy with ileorectal anastomosis may be necessary.

BLIND LOOP SYNDROME

The blind loop syndrome is caused by stasis of the intestinal contents with

subsequent bacterial overgrowth. This stasis can be caused by a number of

abnormalities, including stricture, stenosis, fistula, diverticulum, or the

Figure 11. Angiodysplasia of the caecum

13

formation of a blind pouch. The syndrome is characterized by by steatorrhea,

diarrhea, anemia, weight loss, abdominal pain, multiple vitamin deficiencies,

joint pain and occasionally neurological disorders. The steatorrhea is the

result of bile salt deconjugation in the stagnant fluid in the blind loop of

bowel. Megaloblastic anaemia is probably a result of successful competition

by bacteria for vitamin B12. The Schilling test here is corrected by the

administration of tetracycline not the intrinsic factor. In general, high loops

produce steatorrhoea, whereas low loops tend to produce anaemia.

Temporary improvement will follow the use of antibiotics to destroy the

bacteria causing the trouble, but the main treatment is surgical extirpation of

the cause of the stasis where applicable.

DIVERTICULAR DISEASE

Types

Diverticula can occur in a wide number of positions in the gut, from the

oesophagus to the rectosigmoid. There are two varieties:

1- Congenital.

All three coats of the bowel are present in the wall of the diverticulum, e.g.

Meckel’s diverticulum.

2- Acquired.

The wall of the diverticulum lacks a proper muscular coat. Most alimentary

diverticula are thought to be acquired.

14

Small intestine

Most of these diverticula arise from the mesenteric side of the bowel, probably

as the result of mucosal herniation through the point of entry of blood vessels. So

they are false diverticula because their wall consist of mucosa and submucosa and

lack complete muscularis.

➢ Duodenal diverticula

There are two types:

1 Primary. Mostly occurring in older patients on the inner wall of the second and

third parts (Fig.12), these diverticula are found incidentally on barium meal and

are usually asymptomatic. They can cause problems locating the ampulla during

endoscopic retrograde cholangiopancreatography (ERCP). (Fig.13)

Figure 12

Barium meal study viewing duodenal diverticulum

Figure 13. Endoscopic appearance of duodenal

diverticulum

15

2 Secondary. Diverticula of the

duodenal cap result from longstanding

duodenal ulceration (Fig.9).

➢ Jejuna diverticula

These are usually of variable size and multiple (Fig.15).

Clinically, they may (1) be symptomless, (2) give rise to abdominal pain, (3)

produce a malabsorption syndrome or (4) present as an acute abdomen with

acute inflammation and occasionally

perforation.

They are more common in patients

with connective tissue disorders. In

patients with major malabsorption

problems giving rise to anaemia,

steatorrhoea, hypoproteinaemia or

vitamin B12 deficiency.

Treatment:

Resection of the

affected segment with end-to-end

anastomosis can be effective.

Figure 14. Duodenal Ulcer and Pseudo Diverticulum

Figure 15. Jejuna diverticula

16

➢ Meckel’s diverticulum

Meckel’s diverticulum is the most prevalent congenital anomaly of the GI tract

affecting approximately 2% of the population; it is situated on the anti-mesenteric

border of the small intestine, commonly 60cm from the ileocaecal valve, and is

usually 3–5cm long. Many variations occur. A useful, although crude mnemonic

describing Meckel’s diverticula is the “rule of two” (2% prevalence, 2:1 female

predominance, location 2feet proximal to ileocecal valve in adults, 2 inches in

length, and one half of the those who are symptomatic are under 2 years of age)

(Figs 16 and 17). It represents the patent intestinal end of the vitellointestinal

duct. (Fig. 18) (Summary box 1).

s

Summary box 1

Meckel’s diverticulum

■ It should be sought when a normal appendix is found at surgery for suspected appendicitis

■ If a silent Meckel’s is found incidentally during the course of an operation, it can be left alone provided it is

wide mouthed and not thickened

■ If ectopic gastric epithelium is present within the diverticulum, it may be the source of gastrointestinal bleeding

Figure 16. Meckel’s diverticulum Figure 17. Meckel’s diverticulum with attached band

17

A Meckel’s diverticulum possesses all three coats

of the intestinal wall has its own blood supply.

(Fig.19).

It is therefore vulnerable to infection and

obstruction in the same way as the appendix.

Indeed, when a normal appendix is found at

surgery for suspected appendicitis, a Meckel’s

diverticulum should be sought by inspection of an

appropriate length of terminal ileum. In 20% of

cases, the mucosa contains heterotopic epithelium

, namely gastric, colonic or sometimes pancreatic tissue in order of frequency.

Clinical problems are most often seen in paediatric population.

These symptoms are as follows:

1 severe haemorrhage, caused by peptic ulceration. Painless bleeding occurs per

rectum and is maroon in colour. An operation is sometimes required for serious

progressive gastrointestinal bleeding. When no lesion in the stomach or

duodenum can be found, the terminal 150cm of ileum should be carefully

inspected.

Figure 18. Development of Meckel’s diverticulum

Figure 19. Meckel’s diverticulum with its

own blood supply

18

2 Intussusception. In most cases, the apex of the intussusception is the swollen,

inflamed, heterotopic epithelium at the mouth of the diverticulum.

3 Meckel’s diverticulitis may be difficult to distinguish from the symptoms of

acute appendicitis. When a diverticulum perforates, the symptoms may simulate

those of a perforated duodenal ulcer. At operation, an inflamed diverticulum

should be sought as soon as it has been demonstrated that the appendix and

fallopian tubes are not at fault.

4 Chronic peptic ulceration. As the diverticulum is part of the mid-gut, the pain,

although related to meals, is felt around the umbilicus.

5 Intestinal obstruction. The presence of a band between the apex of the

diverticulum and the umbilicus may cause obstruction either by the band itself or

by a volvulus around it. (Fig. 17)

➢ Imaging

Meckel’s diverticulum can be very difficult to

demonstrate by contrast radiology; small bowel

enema would be the most accurate investigation.

(Fig.20)

Technetium-99m scanning

may be useful in identifying

Meckel’s diverticulum as a

source of gastrointestinal bleeding. (Fig.21)

Figure 20. Small bowel enema diagnosing

Meckel’s diverticulum

19

‘Silent’ Meckel’s diverticulum

An aphorism attributed to Dr. Charles Mayo is: ‘a

Meckel’s diverticulum is frequently suspected,

often sought and seldom found’. A Meckel’s

diverticulum usually remains symptomless

throughout life and is found only at necropsy.

When a silent Meckel’s diverticulum is

encountered in the course of an abdominal

operation, it can be left provided it is wide

mouthed and the wall of the diverticulum does not

feel thickened. Where there is doubt and it can be

removed without appreciable additional risk,

it should be resected. Exceptionally,

a Meckel’s diverticulum is found in an inguinal or a femoral hernia sac – Littre’s

hernia.

Meckel’s diverticulectomy

A Meckel’s diverticulum that is broad based should not be amputated at its base

and invaginated in the same way as a vermiform appendix, because of the risk of

stricture. Furthermore, this does not remove heterotopic epithelium when it is

present. A linear stapler device may be used. Where there is induration of the

base of the diverticulum extending into the adjacent ileum, it is advisable to

resect a short segment of ileum containing the diverticulum, restoring continuity

with an end-to-end anastomosis.

Figure 21. Technetium-99m scanning

20

Colon

• Introduction

Diverticular disease is a clinical term used to describe the presence of symptomatic

diverticula. The prevalence of diverticular disease in the western world is 60% over

the age of 60 years. The condition is found in the sigmoid colon in 90% of cases, but

the caecum can also be involved and, on occasion, the entire large bowel can be

affected. Interestingly in South-east Asia, right-sided diverticular disease is twice as

common as the left. The main morbidity of the disease is due to sepsis.

Diverticulosis refers to the presence of diverticula without inflammation.

Diverticulitis refers to inflammation and infection associated with diverticula.

• Aetiology

The majority of colonic diverticula are false diverticula in which the mucosa and

muscularis mucosa have herniated through the colonic wall so they are acquired

herniations of colonic mucosa, protruding through the circular muscle at the

points where the blood vessels penetrate the colonic wall. They tend to occur in

rows between the taeniae coli, sometimes partly covered by appendices

epiploicae. The rectum with its complete muscle layers is not affected. They are

thought to be pulsion diverticula resulting from high intraluminal pressure. It is

thought to be related to reduced fibre in the western diet. This results in low stool

bulk with resulting segmentation and hypertrophy of the colonic wall

musculature, thus causing increased intraluminal pressure. Diverticular disease is

rare in Africans and Asians, who eat a diet that is rich in natural fibre.

True diverticula, which comprise all layres of bowel wall, are rare and are usually

congenital in origin.

21

Diverticulosis

It is important to distinguish between diverticulosis, which may be asymptomatic,

and clinical diverticular disease in which the diverticula are causing symptoms. It

is extremely common in the United States and Europe. The sigmoid colon is the

most common site of diverticulosis. Diverticulosis is thought to be an acquired

disorder, but the etiology is poorly understood. The most accepted theory is that

a lack of dietary results in smaller stool volume, requiring high intraluminal

pressure and high colonic wall tension for propulsion. Chronic contraction then

results in muscular hypertrophy and

development of the process of segmentation in

which the colon acts like separate segments

instead of functioning as a continuous tube. As

segmentation progress, the high pressures are

directed radially toward the colonic wall rather

than to development of propulsive waves that

moves stool distally. The high radial pressures

directed against the bowel wall create pulsion

diverticula. On histological investigation, the

diverticulum consists of a protrusion of mucous

membranes covered with peritoneum. There is

thickening of the circular muscle fibres of the

intestine, which develops a concertina or

saw-tooth appearance on barium enema (Fig.22).

Figure 22. Saw-tooth appearance of diverticular

disease

22

Diverticulitis

Diverticulitis is the result of inflammation of one or more diverticula, usually with

some pericolitis and estimated to occur in 10 to 25% of people with diverticulosis

It is not a precancerous condition, but cancer may coexist (Summary box 2).

The complications are the following:

1- Recurrent periodic inflammation and pain – in some patients, these episodes

may be clinically silent.

2- Perforation leading to general peritonitis or local (pericolic) abscess formation.

3- Intestinal obstruction:

a- in the sigmoid as a result of progressive fibrosis causing stenosis;

b- in the small intestine caused by adherent loops of small intestine on the

pericolitis.

4- Haemorrhage: diverticulitis may present with profuse colonic haemorrhage in

17% of cases, often requiring blood transfusions.

5- Fistula formation (vesicocolic, vaginocolic, enterocolic, colocutaneous) occurs

in 5% of cases, with vesicocolic being the most common.

Summary box 2

Complications of diverticular disease

■ Diverticulitis

■ Pericolic abscess

■ Peritonitis

■ Intestinal obstruction

■ Haemorrhage

■ Fistula formation

23

➢ Clinical features

Elective or uncomplicated diverticulitis

In mild cases, symptoms such as distension, flatulence and a sensation of heaviness

in the lower abdomen may be indistinguishable from those of irritable bowel

syndrome.

Emergency or complicated diverticulitis

Persistent lower abdominal pain, usually in the left iliac fossa, with or without

peritonitis, could be caused by diverticulitis. Fever, malaise and leucocytosis can

differentiate diverticulitis from painful diverticulosis. The patient may pass loose

stools or may be constipated; the lower abdomen is tender, especially on the left,

but occasionally also in the right iliac fossa if the sigmoid loop lies across the

midline. The sigmoid colon is often palpable, tender and thickened. Rectal

examination may, but does not usually, reveal a tender mass. Any urinary

symptoms may herald the formation of a vesicocolic fistula, which leads to

pneumaturia (flatus in the urine) and even faeces in the urine.

Classification of contamination Studies have shown that the degree of sepsis has a major impact on outcome.

Those with inflammatory masses have a lower mortality than those with

perforation (3% vs. 33%). Classification systems have been developed for acute

diverticulitis, of which Hinchey is the most commonly used (Table 2).

24

Table 2. Classification of diverticulitis Stage Severity Pain Systemic Investigation Management

1 Pericolic abscess LIF Possibly no change Delayed barium Bowel rest,IV Ab

or phlegmon enema, endoscopy DVT prophylaxis,

and fluids

2 Pelvic or intra- Severe, fullness Mild toxic CT PC drainage

abdominal abscess. in LIF

3 Non-faeculent Peritonitis Toxic CT Resuscitation + operation

Peritonitis

4 Faeculent Peritonitis Severe toxicity, Proceed Resuscitation+immediate

peritonitis shock to operation operation

Diagnosis • Radiology

Although the diagnosis of acute

diverticulitis is made on clinical

grounds, it can be confirmed during

the acute phase by computerised tomography (CT). It is particularly good

at identifying bowel wall thickening,

abscess formation and extraluminal

disease. (Fig. 23) The specificity is high

and it is able to demonstrate other

pathology.

It has revolutionised the assessment of

complicated diverticular disease. Figure 23. Computed tomography in diverticulitis

25

On identification of abscesses in stable patients, drainage may be carried out

percutaneously. Such an option may delay or postpone further operative

procedures. Barium enemas (Fig.24)

and sigmoidoscopy are usually reserved for patients who have

recovered from an attack of acute

diverticulitis, for fear of causing

perforation or peritonitis.

Watersoluble contrast enemas may,

however, be helpful in sorting out

patients with large bowel obstruction.

In the acute situation, it is good at

detecting intraluminal changes and

leakage. The sensitivity for this is of

the order of 90%. Barium radiology is

carried out to exclude a carcinoma and

to assess the extent of the disease.

Where the sigmoid colon is thickened

and narrowed, a ‘sawtooth’

appearance may be seen. Some

strictures can be very difficult to

distinguish by radiology alone and, in

those circumstances, colonoscopy will

be necessary to rule out a carcinoma.

Vesicocolic fistulae should be

evaluated

with cystoscopy and biopsy

in addition to colonoscopy.

Contrast examinations may show the

fistula itself. The differential diagnosis

for vesicocolic fistulae (and other fistulae)

includes cancer, radiation damage, Crohn’s disease (CD), tuberculosis and

actinomycosis.

Figure 24. Barium Enema. There is an abscess in the left lower

quadrant which is producing compression on the barium-

filled sigmoid (red arrow), and there is evidence of

extraluminal contrast (red arrow) from a perforated

diverticulum

26

• Colonoscopy

Colonoscopy may reveal the necks of

diverticula within the bowel lumen

(Fig. 25). A narrowed area of

diverticulitis can be entered but, on

occasion, not passed because of the

severity of disease.

The differential diagnosis from a

carcinoma can be impossible if a tight

stenosis prevents colonoscopy. In

equivocal cases, biopsies may be taken.

Management

Non-complicated Diverticulosis should be treated with a high-residue diet

containing roughage in the form of wholemeal bread, flour, fruit and vegetables.

The evidence for this is not of a high quality. Bulk formers such as bran, Celevac,

Isogel and Fybogel may be given until the stools are soft. Painful diverticular

disease may require antispasmodics. Most patients with uncomplicated

diverticulitis will recover without surgery, and 50 to 70% will have no further

episodes. But the risk of complications increases with recurrent disease.

Acute diverticulitis is treated by bed rest and intravenous antibiotics (usually

cefuroxime and metronidazole). After the acute attack has subsided, and if the

diagnosis has not already been confirmed by CT, a barium enema should be

administered (Summary box .3)

Figure 25. Colonoscopy findings in diverticulosis and diverticulitis

27

Summary box 3

Principles of surgical management of diverticular disease

■ In elective cases with full bowel preparation, resection and primary

anastomosis is usually possible

■ If there is obstruction, oedema, adhesions or perforation, Hartmann’s

procedure is usually the operation of choice

■ In selected cases, resection and anastomosis after on-table lavage may be

possible

■ Laparoscopic assessment has been described but is controversial

■ In cases of minimal peritoneal contamination, peritoneal lavage followed by

suture of a small perforation can also be performed

Operative procedures for diverticular disease

The aim of surgery is to control sepsis in the peritoneum and circulation.

Indications for operation include general peritonitis and failure to resolve on

conservative treatment. Surgery, especially in the acute setting, has considerable

risk. Postoperative mortality and reoperation rate for elective resection are 5%

and 12%, respectively, which compares with 17% and 16% for emergency surgery.

There is controversy as to whether a more radical approach should be adopted.

Historically, data have shown that mortality was lower in patients in whom the

inflamed colon was resected. However, two randomised comparative trials have

shown that mortality is lower in the group in which a proximal defunctioning

stoma is performed. The decision needs to be made by the individual surgeon

based on the general state of the patient. The risk of recurrence in patients with

moderate diverticulitis is only 14%. This compares with 39% for severe

diverticulitis. Therefore, a policy of monitoring can be used in elderly patients

following an acute attack that settles. Younger patients unfortunately have a

higher risk of recurrence (below the age of 50 years, the risk of recurrence is

25%). Surgery may be indicated for young patients with more than two attacks of

28

inflammation. Some 10% of patients require an operation either for recurrent

attacks, which make life a misery, or for the complications of diverticulitis

1- The ideal operation carried out as an interval procedure after careful

preparation of the gut is a one-stage resection. This involves removal of the

affected segment and restoration of continuity by end-to-end anastomosis.

Careful dissection will allow eventual mobilisation of the rectosigmoid out of the

pelvis exposing the normal rectum, and greater mobility will allow an easier

anastomosis.

2- If there is obstruction,

inflammatory oedema and

adhesions or the bowel is

loaded with faeces, a

Hartmann’s operation is the

procedure of choice (Fig.26)

This removes the risk of

anastomotic leak.

However, complications may

ensue if the stoma is under

tension, or the rectal stump

breaks down. The involved area is

resected. The rectum is closed at the peritoneal reflection, and the left colon

brought out as a left iliac fossa colostomy. The once popular staged procedures

using a preliminary transverse colostomy are now rarely used except by

inexperienced surgeons because of the high mortality associated with them. In

selected obstructed cases, the bowel can be cleaned by on-table lavage, making

anastomosis much safer.

3- In acute perforation, peritonitis soon becomes general and may be purulent,

with a mortality rate of about 15%. Gross faecal peritonitis carries a mortality rate

of more than 50% and pneumoperitoneum is usually present; the diagnosis may

not be confirmed until emergency laparotomy.

There is a choice of procedures:

Figure 26. Hartmann’ operation

29

a primary resection and Hartmann’s procedure (see above);

b primary resection and anastomosis after on-table lavage in selected cases;

c exteriorisation of the affected bowel, which is then opened as a colostomy, a

procedure now rarely used.

4-Fistulae can be cured only by resection of the diseased bowel and closure of the

fistula. In the case of a colovesical fistula, it is usually possible to ‘pinch off’ the

affected bowel from the bladder, close it and then resect the sigmoid. In very

difficult cases, a staged procedure with a preliminary defunctioning stoma may be

necessary.

5- Haemorrhage from diverticulitis must be distinguished from angiodysplasia. It

usually responds to conservative management and occasionally requires resection.

On-table lavage and colonoscopy may be necessary to localise the bleeding site. If

the source cannot be located, then subtotal colectomy and ileostomy is the safest

option.

Diverticular disease and carcinoma coexist in 12% of cases. Exploration may be

necessary but, even then, differentiation may be difficult until histological

investigations are available (Table 3). Weight loss, falling haemoglobin and

persistently positive occult blood are sinister features. Solitary diverticulum of the

caecum and ascending colon is rare and congenital, and may present with

symptoms and signs identical to those of acute appendicitis.

Laparoscopic surgery

In selected cases, laparoscopic surgery has been used for sigmoid resection. This

has the benefit of decreased hospital stay and costs. However, there is little high-

quality research in the field to advocate its true merits.

30

Table 3. Differentiation of diverticulitis from carcinoma of the colon

Diverticulitis Carcinoma

History: Long Short

Pain: More common 25% painless

Mass: 25% have tenderness

Bleeding: 17% often profuse, periodic 65% – usually small amounts persistently

Radiograph: Diffuse change Localized: no relaxation with propantheline bromide

Sigmoidoscopy: Inflammatory change over an area No inflammation until ulcer reached

Colonoscopy: No carcinoma seen Carcinoma seen and biopsied