Small and Large intestines 1

The Small & Large Intestines

ANATOMY OF THE SMALL AND LARGE INTESTINES
Small intestine
The small intestine starts at the pylorus and extends to the ileocaecal valve. It is approximately 7 m in length and is divided into the duodenum, jejunum and ileum. Its main function is in the breakdo wn and absorption of food products. 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.
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 duodenojejunal flexure. The remainder of the small bowel is made up of the jejunum and ileum. The jejunum makes up the proximal twofifths and is wider, thicker and more vascular than the ileum. It also consists of circular folds of mucous membrane (valvulae conniventes) that can be used to distinguish it from the ileum. The ileum contains larger lymph node aggregates (Peyers patches), and these can sometimes be lead points in cases of intussusceptions in the young.
The arterial supply of the duodenum consists of the right gastric, 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. The jejunum and ileum are vascularised by the superior mesenteric artery through a rich plexus of vessels. The veins run a similar course. The nerve supply to the small intestines arises from sympathetic nerves around the superior mesenteric artery. Pathology such as obstruction causes visceral pain, which is felt in the peri-umbilical region.

Large intestine

The large intestine extends from the ileum to the anus. Rectal anatomy is described in Chapter 68. The colon is approximately 1.5 m in length. It is relatively more fixed than the small bowel. It 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 longitudinal bands of the outer muscle coat. It can be divided into the caecal, ascending, transverse, descending and sigmoid colonic segments.
The blood supply of the colon is derived from ileocolic, right colic and middle colic branches of the superior mesenteric vessels. The descending colon receives its blood supply from the left colic branch from the inferior mesenteric but also communicates 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 inferior mesenteric arteries. Visceral pain is felt in the peri-umbilical region in the proximal colon and in the hypogastric region in the distal colon.

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:
megacolon:
Hirschsprungs disease;
non-Hirschsprungs megarectum and megacolon;
non-megacolon:
slow transit;
normal transit.


Hirschsprungs disease
Hirschsprungs disease is characterised by the congenital absence of intramural ganglion cells (aganglionosis) and the presence of hypertrophic nerves in the distal large bowel. The absence of ganglion cells is due to a failure of migration of vagal neural crest cells into the developing gut. The affected gut is tonically contracted causing functional bowel obstruction. The aganglionosis is restricted to the rectum and sigmoid colon in 75% of patients (short segment), involves the proximal colon in 15% (long segment) and affects the entire colon and a portion of terminal ileum in 10% (total colonic aganglionosis). A transition zone exists between the dilated, proximal, normally innervated bowel and the narrow, distal aganglionic segment.
Hirschsprungs disease may be familial or associated with Downs syndrome or other genetic disorders. Gene mutations have been identified on chromosome 10 (involving the RET protooncogene) and on chromosome 13 in some patients. Hirschsprungs disease typically presents in the neonatal period with delayed passage of meconium, abdominal distension and bilious vomiting but it may not be diagnosed until later in childhood or even adult life, when it manifests as severe chronic constipation. Enterocolitis is a potentially fatal complication of the disease.




Figure 6.24 Barium enema in an infant showing a transition zone in the proximal sigmoid colon between the dilated proximal normally innervated bowel and the contracted aganglionic rectum.

Definitive diagnosis of Hirschsprungs disease depends on histological examination of an adequate rectal biopsy by an experienced pathologist. A contrast enema may show the extent of the aganglionic segment (Fig. 6.24). Surgery aims to remove the aganglionic segment and bring down healthy ganglionic bowel to the anus; these pull-through operations (e.g. Swenson, Duhamel, Soave and transanal procedures) can be done in a single stage or in several stages after first establishing a proximal stoma in normally innervated bowel. Most patients achieve good bowel control but a significant minority experience residual constipation and/or faecal incontinence.

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. 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.
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. 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 6.5 cm (Fig. 65.1).

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 Hirschsprungs 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:
resection of the dilated rectum and colon (Fig. 65.2) 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;
colectomy with the formation of an ileorectal anastomosis;
restorative proctocolectomy;
vertical reduction rectoplasty, which is a new procedure designed to reduce the volume of the rectum by at least 50% (Williams);
stoma formation, which may be used either as a salvage operation for failure of previous surgery or as a primary intervention.



Figure 65.1 Double-contrast barium enema showing megarectum and a huge megasigmoid with normal left colon alongside for comparison (courtesy of Dr D. Nolan, John Radcliffe Hospital, Oxford, UK).



Figure 65.2 Megacolon.
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. Some reports have put the annual prescription sales for laxatives in the UK at just under 50 million. 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 (Parkinsons 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. 65.3). Retention of more than 80% of the shapes, 120 hours after ingestion, is abnormal. Defaecating proctography may be helpful if the main complaint is difficulty in evacuating stools.


Treatment
This can be done in several ways:
Dietary fibre. 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.
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.
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. 65.3).
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.



Figure 65.3 Whole-gut transit studied using radio-opaque markers. More than 80% should have passed by day 5, demonstrating delayed transit here (courtesy of Dr D. Nolan, John Radcliffe Hospital, Oxford, UK).

VASCULAR ANOMALIES (ANGIODYSPLASIA)

Capillary or cavernous haemangiomas are a cause of haemorrhagefrom 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 presentwith anaemia. About 1015% 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. Heydes syndrome describes the association of aortic valve stenosis with gastrointestinal bleeding from colonic angiodysplasia. A mild form of von Willebrands 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.

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 brisk, colonoscopy may show the characteristic lesion in the right colon. 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. Angiodysplastic lesions are sometimes demonstrated by transillumination through the caecum (Fig. 65.4). 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.



Figure 65.4 Angiodysplasia of the caecum demonstrated by transillumination with a colonoscope intraoperatively.

BLIND LOOP SYNDROME

It has been shown in dogs that, if a blind loop of the small intestine is made (Fig. 65.5), defects of absorption will appear. If this occurs in the upper intestine, the defect is chiefly of fat absorption; if in the lower intestine, there is vitamin B12 deficiency. This has been found to occur in humans and is referred to as the blind loop syndrome.
Essentially, the stasis produces an abnormal bacterial flora, which prevents proper breakdown of the food (especially fat) and mops up the vitamins that are present. Sometimes, the only manifestation is anaemia, resulting from vitamin B12 deficiency but, if steatorrhoea occurs, other serious malabsorption features follow. 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:
Congenital. All three coats of the bowel are present in the wall of the diverticulum, e.g. Meckels diverticulum.
Acquired. The wall of the diverticulum lacks a proper muscular coat. Most alimentary diverticula are thought to be acquired.

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.
Duodenal diverticula
There are two types:
Primary. Mostly occurring in older patients on the inner wall of the second and third parts (Fig. 65.6), these diverticula are found incidentally on barium meal and are usually asymptomatic. They can cause problems locating the ampulla during endoscopic retrograde cholangiopancreatography (ERCP).
Secondary. Diverticula of the duodenal cap result from longstanding duodenal ulceration (Fig. 65.7).


Jejunal diverticula
These are usually of variable size and multiple (Fig. 65.8). 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, resection of the affected segment with end-to-end anastomosis can be effective.

Meckels diverticulum

Meckels diverticulum is present in 2% of the population; it is situated on the anti-mesenteric border of the small intestine, commonly 60 cm from the ileocaecal valve, and is usually 35 cm long. Many variations occur (2% 2 feet 2 inches is a useful aide-mmoire) (Figs 65.9 and 65.10). It represents the patent intestinal end of the vitellointestinal duct (Summary box 65.1).

Summary box 65.1Meckels diverticulum

Occurs in 2% of patients, are usually 2 inches (5 cm) in length and are situated 2 feet (60 cm) from the ileocaecal valve
It should be sought when a normal appendix is found at surgery for suspected appendicitis
If a silent Meckels 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 65.8 Jejunal diverticula. Figure 65.9 Meckels diverticulum.



Figure 65.10 Gangrenous Meckels diverticulitis.
A Meckels diverticulum possesses all three coats of the intestinal wall and has its own blood supply. 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 Meckels 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, these symptoms are as follows:


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 150 cm of ileum should be carefully inspected.

Intussusception. In most cases, the apex of the intussusceptions is the swollen, inflamed, heterotopic epithelium at the mouth of the diverticulum.

Meckels 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.

Chronic peptic ulceration. As the diverticulum is part of the mid-gut, the pain, although related to meals, is felt around the umbilicus.

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.

Imaging

Meckels diverticulum can be very difficult to demonstrate by contrast radiology; small bowel enema would be the most accurate investigation. Technetium-99m scanning may be useful in identifying Meckels diverticulum as a source of gastrointestinal bleeding.

Silent Meckels diverticulum

An aphorism attributed to Dr Charles Mayo is: a Meckels diverticulum is frequently suspected, often sought and seldom found. A Meckels diverticulum usually remains symptomless throughout life and is found only at necropsy. When a silent Meckels 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 Meckels diverticulum is found in an inguinal or a femoral hernia sac Littres hernia.

Meckels diverticulectomy

A Meckels 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. The steps of diverticulectomy are shown in Figure 65.11. Alternatively, 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.





Colon
Introduction
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.

Aetiology

Diverticula of the colon 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 strips of longitudinal muscle, sometimes partly covered by appendices epiploicae. The rectum with its complete muscle layers is not affected. 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.

Diverticulosis

It is important to distinguish between diverticulosis, which may be asymptomatic, and clinical diverticular disease in which the diverticula are causing symptoms. 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. 65.12).



Figure 65.12 Barium enema showing sigmoid diverticular disease saw-teeth and diverticula (courtesy of Dr D. Nolan, John Radcliffe Hospital, Oxford, UK).

Diverticulitis

Diverticulitis is the result of inflammation of one or more diverticula, usually with some pericolitis. It is not a precancerous condition, but cancer may coexist (Summary box 65.2).

Summary box 65.2Complications of diverticular disease

Diverticulitis
Pericolic abscess
Peritonitis
Intestinal obstruction
Haemorrhage
Fistula formation

The complications are the following:
Recurrent periodic inflammation and pain in some patients, these episodes may be clinically silent.
Perforation leading to general peritonitis or local (pericolic) abscess formation.
Intestinal obstruction:
in the sigmoid as a result of progressive fibrosis causing stenosis;
in the small intestine caused by adherent loops of small intestine on the pericolitis.
Haemorrhage: diverticulitis may present with profuse colonic haemorrhage in 17% of cases, often requiring blood transfusions.
Fistula formation (vesicocolic, vaginocolic, enterocolic, colocutaneous) occurs in 5% of cases, with vesicocolic being the most common.


Clinical features
Elective
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

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 65.1).

Table 65.1 Classification of diverticulitis

StageSeverityPainSystemicInvestigationManagement1Pericolic abscess or phlegmonLIFPossibly no changeDelayed barium
enema, endoscopyBowel rest, IV antibiotic, DVT prophylaxis and fluids2Pelvic or intra-abdominal abscessSevere, fullness in LIFMild toxicCTPercutaneous drainage3Non-faeculent peritonitisPeritonitisToxicCTResuscitation + operation4Faeculent peritonitisPeritonitisSevere toxicity, shockProceed to operationResuscitation + immediate operationDVT, deep venous thrombosis; IV, intravenous; CT, computerised tomography; LIF, left iliac fossa.

Diagnosis

Radiology
Although the diagnosis of acute diverticulitis is made on clinical grounds, it can be confirmed during the acute phase by computerized tomography (CT). It is particularly good at identifying bowel wall thickening, abscess formation and extraluminal disease. The specificity is high and it is able to demonstrate other pathology. It has revolutionised the assessment of complicated diverticular disease. 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. 65.13) 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, Crohns disease (CD), tuberculosis and actinomycosis.

Colonoscopy

Colonoscopy may reveal the necks of diverticula within the bowel lumen (Fig. 65.14). 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.





Figure 65.13 Barium enema showing a large filling defect in the sigmoid colon caused by a pericolic abscess (courtesy of Dr D. Nolan, John Radcliffe Hospital, Oxford, UK).




Figure 65.14 Colonoscopic view of sigmoid diverticula. Note the mouths of diverticula between the hypertrophied colonic walls.
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.

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 65.3).

Summary box 65.3Principles 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, Hartmanns 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 (للإطلاع فقط)

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 inflammation. Some 10% of patients require an operation either for recurrent attacks, which make life a misery, or for the complications of diverticulitis.
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.
If there is obstruction, inflammatory oedema and adhesions or the bowel is loaded with faeces, a Hartmanns operation is the bprocedure of choice (Fig. 65.15). 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.
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:
primary resection and Hartmanns procedure (see above);
primary resection and anastomosis after on-table lavage in selected cases;
exteriorisation of the affected bowel, which is then opened as a colostomy, a procedure now rarely used.
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.
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 65.2). 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.

ULCERATIVE COLITIS

Aetiology
The cause of UC is unknown. There is probably a genetic contribution with no clear Mendelian pattern of inheritance. It has been shown that 15% of patients with UC have a first-degree relative with inflammatory bowel disease. UC is more common in Caucasians than in blacks or Asians. In spite of intensive bacteriological studies, no organisms or group of organisms can be incriminated. Relapse of colitis has, however, been reported in association with bacterial dysenteries. Smoking seems to have a protective effect. Patients often comment that relapses are associated with periods of stress at home or at work, but personality and psychiatric profiles are the same as those of the normal population.
Studies show that mucosal permeability increases with the presence of inflammation. This may be due to a combination of genetic susceptibility or damage by toxins. The resulting passage of antigens that trigger inflammation may cause an influx of neutrophils and lymphocytes. This inflammation is usually dampened down in normal tissue, but this is lost in UC. There may be loss of tolerance to self-antigens. UC is thought to be an immune disorder in individuals with yet unknown susceptibility genes or a hypersensitivity reaction to an external antigen.

Table 65.2 Differentiation of diverticulitis from carcinoma of the colon

DiverticulitusCarcinomaHistoryLongShortPainMore common25% painlessMass25% have tendernessBleeding17% often profuse, periodic65% usually small amounts persistentlyRadiographDiffuse changeLocalised: no relaxation with propantheline bromideSigmoidoscopyInflammatory change over an areaNo inflammation until ulcer reachedColonoscopyNo carcinoma seenCarcinoma seen and biopsied
Epidemiology
There are 1015 new cases per 100 000 population a year in the UK. This is higher in people of Jewish origin. The prevalence is 160 per 100 000 population. There are approximately 96 000 people with UC in the UK. The incidence has not changed over the last 20 years. The disease has been rare in eastern populations but is now being reported more commonly, suggesting an environmental cause that has developed as a result of an increasing westernisation of diet and/or social habits and better diagnostic facilities. The sex ratio is equal in the first four decades of life. From the age of 40 years, the incidence in females falls whereas it remains the same in males. It is uncommon before the age of 10 years, and most patients are between the ages of 20 and 40 years at diagnosis.

Pathology

In 95% of cases, the disease starts in the rectum and spreads proximally. The rectum is involved in all circumstances except in those using topical rectal preparations (rectal sparing). It is a diffuse inflammatory disease, primarily affecting the mucosa and superficial submucosa, and only in severe disease are the deeper layers of the intestinal wall affected. There are multiple minute ulcers, and microscopic evidence proves that the ulceration is almost always more severe and extensive than the gross appearance indicates. When the disease is chronic, inflammatory polyps (pseudopolyps) occur in up to 20% of cases and may be numerous. In severe fulminant colitis, a section of the colon, usually the transverse colon, may become acutely dilated, with the risk of perforation (toxic megacolon). On microscopic investigation, there is an increase in inflammatory cells in the lamina propria, the walls of crypts are infiltrated by inflammatory cells and there are crypt abscesses. There is depletion of goblet cell mucin. With time, these changes become severe, and precancerous changes can develop (= severe dysplasia or carcinoma in situ).


Symptoms
The first symptom is watery or bloody diarrhoea; there may be a rectal discharge of mucus that is either blood-stained or purulent. Pain as an early symptom is unusual. In most cases, the disease is chronic and characterised by relapses and remissions. In general, a poor prognosis is indicated by (1) a severe initial attack, (2) disease involving the whole colon and (3) increasing age, especially after 60 years. If the disease remains confined to the left colon, the outlook is better.

Proctitis

About 50% have rectal inflammation. As most of the colon is healthy, the stool is formed or semiformed, and the patient is often severely troubled by tenesmus and urgency. There is usually no systemic upset, no effect on growth in children, and extra-alimentary manifestations are rare. In 510%, there is spread to involve the rest of the colon.

Colitis (Fig. 65.16)

Diarrhoea usually implies that there is active disease proximal to the rectum. There is an increased tendency to systemic upset. Protein loss is associated with bleeding, which results in weight loss. There is a greater risk of extra-alimentary manifestations and cancer. Approximately 30% of patients have inflammation extending to the sigmoid colon, and spread proximal to the splenic flexure occurs in 20%. The clinical pattern is one of recurrent severe attacks of bloody diarrhoea up to 20 times a day, dehydration and fluid electrolyte losses. Anaemia and hypoproteinaemia are common.

Disease severity

Disease severity can be graded as:
mild rectal bleeding or diarrhoea with four or fewer motions per day and the absence of systemic signs of disease;

moderate more than four motions per day but no systemic signs of illness;

severe more than four motions a day together with one or more signs of systemic illness: fever over 37.5C, tachycardia more than 90 min1, hypoalbuminaemia less than 30 g l1, weight loss more than 3 kg.

Complications of severe disease

Fulminating colitis and toxic dilatation (megacolon) (Fig. 65.17)
Patients with severe disease should be admitted to hospital for intensive treatment. This occurs in 510% of patients. The patient will have severe rectal symptoms with systemic upset such as weight loss and dehydration. A third will come to urgent surgery. Dilatation should be suspected in patients with active colitis who develop severe abdominal pain. It is an indication that inflammation has gone through all the muscle layers of the colon. In patients on intensive treatment such as steroids, there may be few symptoms. The diagnosis is confirmed by the presence on a plain abdominal radiograph of the colon with a diameter of more than 6 cm. The condition must be differentiated from dysentery, typhoid and amoebic colitis. Plain abdominal radiographs should be obtained daily in patients with severe colitis, and a progressive increase in diameter in spite of medical therapy is an indication for surgery (Summary box 65.4; Fig. 65.18).


Summary box 65.4Complications of UC
Acute
Toxic dilatation
Perforation
Haemorrhage
Chronic
Cancer
Extra-alimentary manifestations: skin lesions, eye problems, liver disease


Perforation

Colonic perforation in UC is a grave complication with a mortality rate of 50% or more. Steroids may mask the physical signs. Perforation can sometimes occur without toxic dilatation. Generally, patients with severe attacks should be managed so that they do not develop these complications.

Severe haemorrhage

Severe rectal bleeding is uncommon and may occasionally require transfusion and, rarely, surgery.

Investigations

A plain abdominal film can often show the severity of disease. Faeces are present only in parts of the colon that are normal or only mildly inflamed. Mucosal islands can sometimes be seen. Small bowel loops in the right lower quadrant may be a sign of severe disease.



Figure 65.18 Supine abdominal radiograph in toxic megacolon. The transverse colon is dilated (7 cm), there is no formed residue in the colon, and large mucosal islands are present in the ascending colon and hepatic flexure. No haustration is present in the transverse colon, which distinguishes this from ileus of obstruction. Mucosal islands are due to oedematous remnants or mucosa where there has been extensive ulceration (courtesy of Dr C. Bartram, St Marks Hospital, London, UK).


Barium enema
The principal signs are (Fig. 65.19):
loss of haustration, especially in the distal colon;
mucosal changes caused by granularity;
pseudopolyps;
in chronic cases, a narrow contracted colon.
In some centres, an instant enema is used with a water-soluble medium for contrast instead of barium and no bowel preparation to avoid aggravating any underlying colitis (Fig. 65.20).

Sigmoidoscopy

Sigmoidoscopy is essential for diagnosis of early cases and mild disease not showing up on a barium enema. The initial findings are those of proctitis: the mucosa is hyperaemic and bleeds on touch, and there may be a pus-like exudate. Where there has been remission and relapse, there may be the presence of regeneration nodules or pseudopolyps. Later, tiny ulcers may be seen that appear to coalesce. This is different from the picture of amoebic dysentery, in which there are large, deep ulcers with intervening normal mucosa.



Figure 65.19 Double-contrast barium enema showing left-sided ulcerative colitis with a tubular left colon compared with a normal right colon (courtesy of Dr D. Nolan, John Radcliffe Hospital, Oxford, UK).

Colonoscopy and biopsy

This has an important place in management:
to establish the extent of inflammation;
to distinguish between UC and Crohns colitis;
to monitor response to treatment;
to assess longstanding cases for malignant change.
Although it may occasionally be helpful, colonoscopy is not usually used in acute cases for fear of aggravating the disease or perforation.


Bacteriology
Campylobacter is the commonest cause of infective colitis in the UK. Pathologically, it is difficult to distinguish from UC. A stool specimen needs to be sent for microbiology analysis when UC is suspected. Other infective causes include Shigella and amoebiasis. Pseudomembranous colitis occurs in hospital patients on antibiotic treatment and non-steroidal anti-inflammatory drugs (NSAIDs). The causative organism is Clostridium difficile. Immunocompromised patients are at risk of infective proctocolitis from cytomegalovirus and cryptosporidia.

The cancer risk in colitis

Although this is an important complication, the overall risk is only about 3.5%. It is much less in early cases but increases with duration of disease. At 10 years, the risk of cancer in all patients with UC, irrespective of disease extent, is 2%. This increases to 8% at 20 years and 18% at 30 years. Carcinoma is more likely to occur if the whole colon is involved and if the disease started in early life (Fig. 65.21). Carcinomatous change, often atypical and high grade, may occur at many sites at once. The colon is involved rather than the rectum, and the maximal incidence is during the fourth decade.
The golden rule is that, when the disease has been present for 10 years or more, regular colonoscopic checks must be carried out to check for dysplasia, even if the disease is clinically quiescent. If on biopsy, there is severe epithelial dysplasia, which is a marker for impending or frank carcinomatous change, surgery is indicated. Annual colonoscopy and biopsy is then part of cancer surveillance. In the rare patients with a fibrous stricture, the stricture should be examined especially carefully for the presence of an underlying carcinoma.



Figure 65.20 Instant enema in acute ulcerative colitis. The rectum shows a granular mucosa with ulceration extending from the proximal sigmoid into the splenic flexure region. The ulcers are seen tangentially as collar-stud projections from the mucosal line. Formed residue is present in the ascending colon and hepatic flexure. The colitis extends into the mid-transverse colon but is most active in the descending colon (courtesy of Dr C. Bartram, St Marks Hospital, London, UK).

Extraintestinal manifestations

Arthritis occurs in around 15% of patients and is of the large joint polyarthropathy type, affecting knees, ankles, elbows and wrists. Sacroiliitis and ankylosing spondylitis are 20 times more common in patients with UC.
Bile duct cancer is a rare complication, and colectomy does not appear to reduce the risk of subsequent bile duct cancer or sclerosing cholangitis. Other manifestations include:
skin lesions: erythema nodosum, pyoderma gangrenosum or aphthous ulceration;
eye problems: iritis;
liver disease: sclerosing cholangitis has been reported in up to 70% of cases. Diagnosis is by ERCP, which demonstrates the characteristic alternating stricturing and bleeding of the intrahepatic and extrahepatic ducts.


Figure 65.21 Resection specimen from a patient with longstanding ulcerative colitis showing a narrow tubular colon with areas of cancerous change in the rectum and sigmoid (courtesy of Dr B. Warren, John Radcliffe Hospital, Oxford, UK).

Treatment

It is important to appreciate the multidisciplinary approach to the management of UC. This involves the gastroenterologist, nurses, nutritionist, stomatherapist and social worker as well as the surgeon.
Medical treatment of an acute attack
Corticosteroids are the most useful drugs and can be given either locally for inflammation of the rectum or systemically when the disease is more extensive. One of the 5-aminosalicylic acid (5- ASA) derivatives can be given both topically and systemically. Their main function is in maintaining remission rather than treating an acute attack. Non-specific anti-diarrhoeal agents have no place in the routine management of UC (Summary box 65.5).


Summary box 65.5Principles of management of UC
Many patients can be adequately maintained for years on medical therapy
Toxic dilatation must be suspected in any colitic patient who develops severe abdominal pain; missed colonic perforation is associated with a high mortality
Colitic patients are at increased risk of developing cancer; those with pancolitis of long duration are most at risk

Mild attacks
Patients with a mild attack and limited disease will usually respond to rectally administered steroids. In those with more extensive disease, oral prednisolone 2040 mg day1 is given over a 3- to 4-week period. One of the 5-ASA compounds should be given concurrently.

Moderate attacks

These patients should be treated with oral prednisolone 40 mg day1, twice-daily steroid enemas and 5-ASA. Failure to achieve remission as an out-patient is an indication for admission.

Severe attacks

These patients must be regarded as medical emergencies and require immediate admission to hospital. Their appearance is often misleading, and they must be examined at least twice a day. It is important to monitor vital signs (pulse, temperature and blood pressure). Weight needs to be recorded at admission and twice a week while in hospital. A stool chart should be kept. Increasing abdominal girth is a potential sign of megacolon developing. A plain abdominal radiograph is taken daily and inspected for dilatation of the transverse colon of more than 5.5 cm. The presence of mucosal islands or intramural gas on plain radiographs (see Fig. 65.18), increasing colonic diameter or a sudden increase in pulse and temperature may indicate a colonic perforation. Fluid and electrolyte balance is maintained, anaemia is corrected and adequate nutrition is provided, sometimes intravenously in severe cases. If the patient is not having immediate surgery, then oral nutrition is important. High calories are required. If severe malnourishment is present, then parenteral nutrition may be indicated. The patient is treated with intravenous hydrocortisone 100200 mg four times daily. This can be supplemented with a rectal infusion of prednisolone. There is no evidence that antibiotics modify the course of a severe attack. Some patients are treated with azathioprine or ciclosporin A to induce remission. If there is failure to gain an improvement within 35 days, then surgery must be seriously considered. Prolonged high-dose intravenous steroid therapy is fraught with danger. Patients who have had weeks of treatment, during which the colonic wall has become friable and disintegrates at laparotomy, are now fortunately rare.

Indications for surgery

The risk of colectomy is 20% overall, ranging from 5% in those patients with proctitis to 50% in those patients with a very severe attack. The need for surgery is highest in the first year after the disease onset, for:
severe or fulminating disease failing to respond to medical therapy;
chronic disease with anaemia, frequent stools, urgency and tenesmus;
steroid-dependent disease here, the disease is not severe but remission cannot be maintained without substantial doses of steroids;
the risk of neoplastic change: patients who have severe dysplasia on review colonoscopy;
extraintestinal manifestations;
rarely, severe haemorrhage or stenosis causing obstruction.


Operations (للإطلاع فقط)
The patient is placed in a position to allow access to the rectum. In the emergency situation, the first aid procedure is a total abdominal colectomy and ileostomy. The rectal stump is left long but runs the risk of on-going haemorrhage. The rectum can either be brought out at the lower end of the wound as a mucous fistula or closed just beneath the skin. This has the advantage that the patient recovers quickly, the histology of the resected colon can be checked, and restorative surgery can be contemplated at a later date when the patient is no longer on steroids and in optimal nutritional condition. The alternative, division of the rectum below the sacral promontory, can result in breakdown and pelvic abscess, and makes subsequent identification of the stump more difficult. This is more likely to occur in patients in a poor condition or those on long-term steroids.

Proctocolectomy and ileostomy

This is the procedure associated with the lowest complication rate. It is indicated in patients who are not candidates for restoration. The patient is left with a permanent ileostomy. There is, however, a 20% long-term risk of adhesional obstruction (the
reoperation rate is, however, very low) and 510% of the perineal wounds are slow to heal. The late result will be a chronic perineal sinus that may require repeated currettage or excision. The obvious disadvantage is an ileostomy and, although many patients cope remarkably well with satisfactory objective measures of quality of life, there is a psychological and social cost. Problems that may arise with a stoma include stricture formation, prolapse, retraction and herniation.

Rectal and anal dissection

Refinements of the procedure have included a close rectal dissection to minimise damage to the nervi erigenti and hence erectile dysfunction, which may occur in 0.52%, and intersphincteric excision of the anus, which results in a smaller perineal wound and fewer healing problems.

Restorative proctocolectomy with an ileoanal pouch (Parks)

In this operation, a pouch is made out of ileum (Fig. 65.22) as a substitute for the rectum and sewn or stapled to the anal canal. This avoids a permanent stoma. It is reserved for patients with adequate anal sphincters and should be avoided when CD is a possibility. It should not initially be considered for poorly patients. Various pouch designs have been described, but the J is the most popular and the most easily made using staplers (Fig. 65.23). The S (three loop) has been associated with evacuation difficulties due to the short efferent spout. The W (four loop) pouch has a larger reservoir, which results in less bowel frequency. There is some controversy over the correct technique for ileoanal anastomosis. In the earliest operations, the mucosa from the dentate line up to midrectum was stripped off the underlying muscle, but it is now known that a long muscle cuff is not needed. A mucosectomy of the upper anal canal with an anastomosis at the dentate line is claimed to remove all of the at-risk mucosa and any problem of subsequent cancer. It may also result in imperfect continence with nocturnal seepage. The alternative is an anastomosis double-stapled to the top of the anal canal, preserving the upper anal canal mucosa. Continence appears to be better, but the theoretical risk of leaving inflamed mucosa remains. The procedure can be carried out in stages. In most cases, a covering loop ileostomy is used. Complications include pelvic sepsis usually resulting from a leak at the ileoanal anastomosis small bowel obstruction and pouch vaginal fistula. Frequency of evacuation is determined by pouch volume, completeness of emptying, reservoir inflammation and intrinsic small bowel motility, but can be between three and six evacuations daily. Increased frequency, urgency and faecal incontinence can be seen (20%, 5% and 5% respectively), but these reduce with time. Although associated with a higher complication rate, it is rapidly becoming the operation of choice in younger patients, avoiding a permanent ileostomy. The failure rate in the first year is 515%, the main reasons being pelvic sepsis (50%), poor function (30%) and pouchitis or inflammation of the pouch (10%). It is also important for women to realise that they may suffer from reduced fertility. So women yet to have children may elect for a colectomy with ileostomy or colectomy and ileorectal anastomosis if the rectum is spared in the first instance. There are much higher failure rates in CD when compared with UC (50% vs. 10%), and the operation is not
to be recommended in this disease.

Colectomy and ileorectal anastomosis

If there is minimal rectal inflammation, this can occasionally be used, although the surgeon should not be falsely reassured that the rectum has been relatively spared in a patient using steroid enemas. If the rectum is preserved, then annual rectal inspection is advocated. Although it has the advantage of stoma avoidance and minimal risk to sexual function associated with rectal dissection, it has largely been superseded by restorative proctocolectomy. A number of series have shown low mortality and morbidity, but it has fallen out of favour due to the on-going risk of persisting inflammation and malignancy.

Ileostomy with a continent intra-abdominal pouch (Kocks procedure)

A reservoir is made from 30 cm of ileum and, just beyond this, a spout is made by inverting the efferent ileum into itself to give a continent valve just below skin level. The pouch is emptied by the patient inserting a catheter through the valve; this procedure is now rarely used. Complications include early leak with formation of fistulae, which can occur in 1020%, and late subluxation of the valve, which can occur in 20%. Pouch survival at 10 years was 87% in one study.

Ileostomy

End-ileostomy (Brooke)
In those patients with a permanent ileostomy, there must be scrupulous attention to detail during the operation to ensure a good functional result. The position of the ileostomy should be carefully chosen by the patient with the help of a stoma care nurse specialist. There is an argument for making the trephine incision before entering the abdomen to prevent any problems of distortion of the abdominal wall after opening. The ileum is normally brought through the rectus abdominis muscle. Careful attention to the terminal ileal mesentery should be taken to ensure that it is supplied by the marginal artery in order to reduce mesenteric bulk. The use of a spout (Fig. 65.24) was originally described by Bryan Brooke; this should project some 4 cm from the skin surface. A disposable appliance is placed over the ileostomy so that it is a snug fit at skin level.


Loop ileostomy
This is often used to defunction a pouch ileoanal procedure. A knuckle of ileum is pulled out through a skin trephine in the right iliac fossa. An incision is made in the distal part of the knuckle, and this is then pulled over the top of the more proximal part to create a spout on the proximal side of the loop with a flush distal side still in continuity. This allows near-perfect defunction, but also the possibility of restoration of continuity by taking down the spout and reanastomosing the partially divided ileum.

Ileostomy care

During the first few postoperative days, fluid and electrolyte balance must be adjusted with great care. There may be an ileostomy flux while the ileum adapts to the loss of the colon, and the fluid losses can amount to 4 or 5 litres day1. The stools thicken in a few weeks and are semisolid in a few months. The help, skill and advice of the stoma care nurse specialist are essential. Modern appliances have transformed stoma care, and skin problems are unusual (Fig. 65.25).
Complications of an ileostomy include prolapse, retraction, stenosis, bleeding, fistula and paraileostomy hernia.

THE END

Printed By:
Haider Hashim

7th of December 2011










The small & large intestines Lecture (1 & 2)

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