57 The small and large intestines

NEIL J. McC. MORTENSEN Abdominal pain Abdominal pain arising from the alimentary canal is of two types. 1. Visceral pain. The alimentary tract is primarily a midline structure with a bilateral nerve supply. Although rotation about the midline occurs during development, nevertheless true visceral pain is referred to the midline as shown in Fig. 57.1. It is dull and poorly localised. For example, an obstructing stenosis of the terminal ileum, which is part of the midgut, would give rise to colicky periumbilical pain. 2.Peritoneal pain is of the somatic type and is much more precise, more severe and localised to the site of origin. These components account for the changes in character and site of pain which occur in appendicitis. Once the full thickness of the appendicular wall becomes inflamed the overlying peritoneum becomes involved and the patient has localised right iliac fossa pain (see Chapter 59). Surgical anatomy It is of great practical importance to be able to do the following: 1.distinguish various portions of the intestinal tract at sight; 2.know in which part of the abdomen the upper coils, as opposed to the lower coils, of small intestine lie in relationship to the anterior abdominal wall; 3.be able to decide which is the proximal and which is the distal end of any coil under consideration; 4.distinguish irrefutably large from small intestine. The following are useful tips. The mesentery of the jeiunum has only two series of arcades of blood vessels, whereas the lower ileum has several series of arcades. The mesenteric attachment runs from left to right. Provided that the gut is not twisted, the proximal small bowel lies in the upper part of the abdomen and the lower small bowel lies in the lower part of the abdomen. The large intestine can be characterised by its taenia coli and appendices epiploicae. Malformations and functional abnormalities Congenital malformations These malformations are described in the following: congenital atresia of the duodenum (see Chapter 58); congenital atresia of the small intestine (see Chapter 58); volvulus neonatorum (see Chapter 58); vascular anomalies (angiodysplasia) (see below); malrotation of the colon with failure of descent of the caecum which remains under the right lobe of the liver. This is clearly very important should the patient develop appendicitis (see Chapter 59). Megacolon and nonmegacolon constipation There is no single definition of constipation that can be described according to the character of the stools, the frequency of evacuation and the ease of evacuation.

Generally speaking a bowel frequency of less than one every 3 days would be considered abnormal. This group of conditions can be divided into: 1. megacolon: (a) Hirschsprungs disease, (b) non-Hirschsprungs megarectum and megacolon; 2. nonmegacolon: (a) slow transit, (b) normal transit.

Hirschsprungs disease
Pathology The major feature of Hirschsprungs disease is an absence of ganglion cells in the neural plexus of the intestinal wall, together with hypertrophy of the nerve trunks. This is believed to result from a failure of migration of neuroblasts into the gut from vagal nerve trunks at the end of the first trimester of foetal life. The loss of ganglion cells extends for a variable distance above the anorectal junction. In about two-thirds of patients the rectum and lower sigmoid colon are involved, but involvement of extremely short segments of the lower rectum or the whole intestinal tract have been described. The severity of symptoms is not always consistent with the length of the intestinal segment involved and may be related to the number of acetylcholinesterase-positive nerve fibres. The absence of ganglion cells gives rise to a contracted nonperistaltic segment with a dilated hypertrophied segment of normal colon above it (Fig. 57.2). Clinical features Hirschsprungs disease occurs in approximately one in 4500 live births. It shows a familial tendency and is more common in males than in females. The clinical picture varies from acute intestinal obstruction in neonates to chronic constipation in later life. 1. In neonates the delayed passage of meconium together with mild abdominal distension should alert the paediatrician to the diagnosis of Hirschsprungs disease. It is often complicated by enterocolitis which may result in perforation and septicaemia, and there is still a high mortality from Hirschsprungs disease at this age. 2. Chronic constipation starting in the first few weeks of life. The classic picture of gross abdominal distension, chronic constipation and failure to thrive should be rare with a greater awareness of the diagnosis. 3. Severe constipation without soiling in otherwise healthy children and adults can he caused by a short segment of Hirschsprungs disease. Faecal soiling is not usually a feature of the condition. Diagnosis Rectal biopsy. Confirmation of the diagnosis depends on histological demonstration of aganglionosis and hypertrophic nerve fibres in the nerve plexus. The pathologist has to be able to see a representative area of at least one nerve plexus in the biopsy. In children this can be obtained by a suction rectal biopsy or, in adults, by a formal strip, full-thickness, rectal biopsy. Specimens are usually taken from just above the anorectal junction. One is sent for biochemistry and one for histochemistry and histopathology (Fig. 57.3). Anorectal manometry. This is a useful screening test in the constipated young child or adult who is otherwise fit. The rectosphincteric inhibitory reflex is absent. It should not be carried out in ill neonates because of poor anal tone.

Radiology. Erect and supine abdominal radiographs are useful. If the large intestine is obstructed, they will show distended loops of small and large intestine with fluid levels consistent with a low intestinal obstruction. Intramural gas will indicate enterocolitis, and free peritoneal gas, a perforation. An enema using a water-soluble contrast medium will often confirm the diagnosis and indicate the length and site of involved intestine. A rectal examination should not be performed before radiology because it may dilate the abnormal segment and modify the radiological features. The contrast is instilled through a fine 5 Fr catheter under screening control with the patient in the lateral position. The coning down of the transition zone, irregularity in the mucosa and abnormal contractions of the intestine are important positive findings. Treatment This depends on the age of the patient, the length of the involved segment, the severity of symptoms and the presence of enterocolitis. In the neonate presenting with obstruction or any child or adult presenting with enterocolitis, an initial colostomy is performed. The site of the colostomy should be as low as possible in the ganglionated segment. A peroperative frozen section biopsy is taken to establish the presence of ganglia. This is important as the transition zone may be difficult to locate precisely. In the child or adult with constipation alone, the dilated intestine can be evacuated with repeat rectal saline washouts and enemas as a first step. The choice of surgical procedure to follow will depend on the length of the involved segment. Short segment disease with minimal symptoms may respond to an extended myectomy removing a strip of rectal wall up to the area where normal ganglion cells start. Long segment disease may be helped by one of the four operations shown below. The definitive operation is preceded by a temporary colostomy for a few months which allows the proximal distended colon to return to its normal calibre. If a neonate requires a colostomy the definitive operation is delayed until the child weighs approximately 10 kg when the pelvis is still shallow but wide enough to give good access. The child will be between 10 months and 1 year of age and toilet training can usually start soon after the operation. In some older children it may be possible to clear the retained faeces with enemas and laxatives; if so it may be possible to perform a one-stage operation. Duhamel operation The aganglionic segment is removed down to the level of the peritoneal reflection over the rectum. The rectum is divided and dosed. The sacral hollow is opened and the normal colon brought down to the posterior aspect of the rectal stump. With an anal retractor in place a transverse incision is made from the level in the posterior wall just above the anal sphincter. The normal colon is then grasped and sewn to the transverse incision in the rectum. The spur between the rectum and normal colon is then divided with a stapler. Swensons procedure The rectum is mobilised from above taking care to dissect immediately outside the fascia propia, preserving autonomic nerves to the bladder and seminal vesicles. The intestine is transected proximally through normal colon, the presence of ganglion cells having first been checked for by frozen section biopsy. The mobilised aganglionic segment is then everted out through the anus, the everted rectal mucosa is cleaned, and the anterior half of the junction between the top of the anal canal and the rectum is opened transversely. The proximal normal colon is then pulled through this opening

and an end-to-end anastomosis made between the colon and anal canal as the aganglionic segment is excised. Once the anastomosis is complete it is reduced hack into the anal canal. Colo-anal anastomosis This is usually reserved for older children, teenagers and adults. The rectum is mobilised as before and transected just above the level of the pelvic floor. The normal colon is then joined to the top of the anal canal either directly with a stapling tecnhique or by a sleeve technique following a mucosectomy of the upper anal canal and rectum, a procedure described by both Soave and Parks. Restorative proctocolectomy In cases of Hirichsprungs disease involving the entire colon, it is possible to reconstruct with an ileoanal pouch procedure (see Chapter 60). 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 by a congenital abnormality of the intestinal myenteric plexus. Investigation 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. Radiology. As there is an enlarged rectum often with distention of the colon over a variable length, a radiograph should he 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. 57.4). Anorectal physiology tests show abnormally large volumes inflated in the rectum to induce a feeling of rectal fullness, and inhibition of the internal and external anal sphincters is present but at much larger volumes than normal. Full-thickness rectal biopsy shows normal ganglion cells which 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 laxatives and repeated enemas as necessary. Surgical treatment Surgical treatment is necessary sometimes if medical therapy fails. Resection of the dilated rectum and colon (Fig. 57.5)back to normal diameter colon with normal ganglion cells confirmed by frozen section at the time of surgery is followed by reconstruction with a colo-anal anastomosis. Nonmegacolon 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 defecation. 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. 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. 57.6).Retention of more than 80 per cent of the shapes, 120 hours after ingestion, is abnormal. Defecating proctography may be helpful if the main complaint is difficulty in passing stools. 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. They have delayed transit using marker studies and may or may not be able to empty the rectum normally (Fig. 57.6). This is a difficult condition to treat medically; dietary measures are usually unsuccessful and surgical treatment is only justified after careful studies and when medical treatment has been exhausted. Total colectomy and ileorectal anastomosis is the preferred procedure but the results are unpredictable. One-third of patients continues to have diarrhoea or constipation and two-thirds persisting abdominal pain. It is essential to exclude underlying psychiatric or psychological problems. Obstructed defecation Some patients complain of extreme difficulty in expelling stool. They may have repeated attempts at rectal evacuation and their transit is often normal. The common feature in these patients is weakness of the pelvic floor which descends on straining. Patients may resort to digital evacuation or pressure on the perineum or within the vagina to assist defecation. The cause is not known. It may arise from damage to pelvic nerves caused by prolonged straining at stool or childbirth. Defecation proctography will show abnormal evacuation. There may be an intussusception with the upper rectum folding in to the lower rectum or an anterior rectocele where the rectum bulges forward into the posterior wall of the vagina (Fig. 57.7). Biofeedback training may be helpful in some patients; dietary therapy and laxatives are usually unsuccessful. Surgery is a last resort, and either a defunctioning ileostomy or a colostomy with colostomy irrigation is used in intractable cases.

Vascular anomalies (angiodysplasia)

Capillary or cavernous haemangiomas are a cause of haemorrhage from the colon at any age presenting with colonic bleeding. In the middle-aged or elderly patient it needs to be distinguished from other causes of sudden massive haemorrhage, such as diverticulitis, ulcerative colitis or ischaemic colitis. Angiodysplasia is a vascular malformation associated with ageing. It has been recognised since the introduction of intestinal angiography and colonoscopy. Angiodysplasiasoccur particularly in the ascending colon and caecum of elderly patients over the age of 60 years and are not associated with cutaneous lesions. The malformations consist of dilated tortuous submucosal veins and in severe cases the mucosa is replaced by massive dilated deformed vessels. On histological investigation, they are made up of dilated, distorted, thin-walled vessels with only a scanty amount of muscle in their walls. Inspection of the mucosa is often unremarkable. The lesions are only a few millimetres in size and appear as reddish raised areas at endoscopy. Bleeding is usually chronic and intermittent and can be severe. Many patients previously thought to have bled from diverticular disease have probably been bleeding from angiodysplasia in the caecum. There is an association with aortic stenosis.

Barium enema is usually unhelpful and should be avoided. Provided the bleeding is not too brisk colonoscopy may show the characteristic lesion in the caecum or ascending colon. 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 (9smTc)4abelled red cells may confirm and localise the source of haemorrhage. Some angiodysplastic lesions can be treated by colonoscopic diathermy, but if bleeding is brisk and the patient seriously ill emergency surgery will be necessary. Here a catheter is placed in the appendix stump and the colon irrigated progradely with saline or water. On-table colonoscopy is carried out and the site of the bleeding can then be confirmed. Angiodysplastic lesions are sometimes demonstrated by transillumination through the caecum (Fig. 57.8).If it is still not clear exactly which segment of colon is involved then a total abdominal colectomy with ileorectal anastomosis may be necessary. Blind loop syndrome It has been shown in dogs that, if a blind loop of the small intestine is made (Fig. 57.9),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 appears, 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
One meaning of diverticulum is a wayside house of ill-fame; certainly these wayside houses live up to their evil reputation. Diverticula can occur from the stomach to the recto sigmoid. There are two varieties: 1. Congenital. All three coats of the bowel are present in the wall of the diverticulum, e.g. Meckels. 2.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 diverticulum There are two types: 1.Primary. Mostly in older patients on the inner wall of the second and third parts, these diverticula are found incidentally on barium meal and usually do not cause symptoms. They can cause problems locating the ampulla during endoscopic retrograde cholangiopancreatography (ERCP) (Fig. 57.10). 2. Secondary. Diverticula of the duodenal cap resulting from long-standing duodenal ulceration (Fig. 57.11). Jejunal diverticula These are usually of variable size and multiple (Fig. 57.12).Clinically they may (1) be symptomless, (2) give rise to abdominal pain, flatulence and borborygmi, (3)

produce a malabsorption syndrome, or (4) present as an acute abdomen with acute inflammation and occasionally rupture. They are more common in patients with connective tissue disorders. In patients with major malabsorption problems giving rise to anaemia, steatorrhoea, hypoproteinaemia or vitamin B1, deficiency; resection of the affected segment with end-to-end anastomosis can be effective. Meckels diverticulum Meckels diverticulum is present in 2 per cent of the population; it is situated on the antimesenteric border of the small intestine, commonly 60 cm from the ileocaecal valve, and is usually 35cm long. Many variations occur (2 per cent 2 feet 2 inches is a useful aidenldmoire) (Figs 57.13 and 57.14). 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. In 20 per cent of cases the mucosa contains heterotopic epithelium, namely, gastric, colonic or sometimes pancreatic tissue. When present, the abnormal mucosa lines the greater part of the proximal end of the pouch and extends sometimes for a short distance into the nearby ileum. Although Meckels diverticulum occurs with equal frequency in both sexes, symptoms usually resulting from the epithelium contained in the diverticulum predominantly occur in males. In order of frequency, these symptoms are as follows. 1. Severe haemorrhage, caused by peptic ulceration. The blood is passed per rectum, and is maroon in colour. Although the patient may vomit, the vomit does not contain blood. There is rarely any pain and sometimes the bleeding precedes perforation. An operation is 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. 2.Intussusception. In most cases, the apex of the intussusception is the swollen, inflamed, heterotopic epithelium at the mouth of the divertictilum. 3. Meckels diverticulitis, with or without perforation, may result from obstruction by food residue. The symptoms are those of acute appendicitis and, unless the appendix has already been removed, the diagnosis is impossible before operation. When a diverticulum perforates the symptoms may simulate those of a perforated duodenal ulcer. Whether or not the diverticulum is perforated urgent surgery is required. In nonperforated cases 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 midgut, the pain, although related to meals, is felt around the umbilicus. 5. Intestinal obstruction. The presence of a hand between the apex of the diverticulum and the umbilicus may cause obstruction either by the band itself or by a volvulus around it. Radiology Meckels diverticulum can he very difficult to demonstrate by contrast radiology; small bowel enema would he the most accurate investigation.Technetium-99m scanning In cases of repeated gastrointestinal haemorrhage of unknown cause where a Meckels diverticulum is suspected the abdomen is imaged with gamma camera after the injection of 30100 mic Ci (111370 x 1010 Bq) of 99Tc-labelled pertechnetate intravenously. This may localise heterotopic gastric mucosa revealing the site of a Meckels diverticulum in 90 per cent of cases. Silent Meckels diverticulum

An aphorism attributed to Dr Charles Mayo is: a Meckels diverticulum is frequently suspected, often sought for 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, provided it is wide-mouthed and the wall of the diverticulum does not feel thickened, it can he left. Where there is doubt and it can he removed without appreciable additional risk it should he resected. Exceptionally a Meckels diverticulum is found in an inguinal or a femoral hernia sac Littres hernia. Meckels diverticulectomy A Meckels diverticulum which is broad based should not he 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 where it is present. The steps of diverticulectomy are shown in Fig. 57.15. Alternatively, a linear stapler device maybe 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 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 condition is most commonly found in the sigmoid colon but the caecum can also be involved and on occasion the entire large bowel can be affected. The rectum with its complete muscle layers is not affected. In 90 per cent of cases the sigmoid colon is involved and is almost always the site of inflammation, i.e. diverticulitis. Some 5per cent of patients have associated gallstones and hiatus hernia (Saints triad). Diverticular disease is rare in Africans and Asians who eat a diet that contains natural fibre. In Western countries, wherethe roughage has been removed from flour and refined sugar forms a large part of the diet, diverticula are found in 25 per cent of barium enemas of patients over the age of 40 and the incidence increases with age. Diverticulosis It is important to distinguish between diverticulosis and the presence of diverticula which may be asymptomatic, and clinical diverticular disease where the diverticula are causing symptoms. Diverticula probably arise as a result of muscular inco ordination and spasm, resulting in increased segmentation and intraluminal pressures. Excessive segmentation in response to food, prostigmine and morphine is found in colonic motility studies, and this exaggerated response is more apparent in symptomatic than in asymptomatic individuals. 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 taeniae and the intestine develops a concertina or sawtooth appearance on barium enema (Fig. 57.16). The diverticula occur between the muscle clefts making the mucosal surface appear trabeculated. The elastin content of the taenia coli is increased compared with controls.

Diverticulitis
Diverticulitis is the result of inflammation of one or more diverticula, usually with some pericolitis. Episodes of diverticulitis may be followed by years free of symptoms, but the condition is essentially progressive the longer the duration the

worse the symptoms and the greater the risk of complications. Diverticulitis is not a precancerous condition, but cancer may coexist. 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 per cent of cases, often requiring blood transfusions; 5. fistula formation (vesicocolic, vaginocolic, enterocolic, colocutaneous) occurs in 5 per cent of cases, vesicolic being the most common. Clinical features Diverticulosis may be asymptomatic, but the disordered colonic function may cause symptoms of distension, flatulence and a sensation of heaviness in the lower abdomen, all of which may be indistinguishable from the symptoms of irritable bowel syndrome. Excessive colonic segmentation can cause severe pain in the left iliac fossa, but this must be distinguished from episodes of often subclinical inflammation in the sigmoid colon as a result of diverticulitis. Diverticulitis. Persistent lower abdominal pain, usually in the left iliac fossa with or without peritonitis in patients of either sex over the age of 40, 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. The condition has been likened to left-sided appendicitis. 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. Diagnosis Radiology. Diverticulosis, as for the irritable bowel syndrome, is a diagnosis of exclusion and symptoms should not be attributed to diverticulosis unless other diseases have been excluded by barium enema, sigmoidoscopy or colonoscopy. Although the diagnosis of acute diverticulitis is made on clinical grounds it can be confirmed during the acute phase by computerised tomography (CT). This will demonstrate not only the diverticula but also any associated pericolicabscess (Fig. 57.17). Barium enemas and sigmoidoscopy are usually reserved for patients who have recovered from an attack of acute diverticulitis for fear of causing perforation or peritonitis. Water-soluble contrast enemas may, however, be helpful in sorting out patients with large bowel obstruction. 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 saw-tooth 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.

Sigmoidoscopy. The mucosa may be normal and in acute attacks the sigmoidoscopy will be painful and the mucosa inflamed. Colonoscopy or flexible sigmoidoscopy is more helpful (Fig. 57.18). The necks of diverticula can be seen and the 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 endoscopy. Management Diverticulosis should be treated with a high-residue diet containing roughage in the form of wholemeal bread, flour, fruit and vegetables. Bulk formers such as bran, Celevac, Isogel and Fybogel may be given until the stools are soft. Painful diverticular disease may require bed rest and 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 carried out. Operative procedures for diverticular disease. Some 10 per cent 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. At this operation the sigmoid loop is often found adherent in the pouch of Douglas. Careful dissection will allow eventual mobilisation of the recto sigmoid 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 Hartmanns operation is the procedure of choice. The involved area is resected. The rectum is closed at the penitoneal 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, placing a urinarycatheter through the appendix stump and washing the colon with physiological saline or water for irrigation. This makes subsequent restoration and bowel continuity with an anastomosis much safer (Fig. 57.19a, h). 3.In acute perforation, peritonitis soon becomes general and may be purulent, which has a mortality rate of about 15 per cent. Gross faecal peritonitis carries more than a 50 per cent mortality rate and pneumoperitoneum is usually present; the diagnosis may not be confirmed until emergency laparotomy. There is a choice of procedures: (a) primary resection and Hartmanns 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, now rarely used; (d) suture of the perforation with drainage with or without proximal defunction. In selected cases with a small leak and minimal soiling. 4. Fistulae can only be cured 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 on occasion.

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. Diverticular disease and carcinoma coexist in 12 per cent of cases. Exploration may be necessary but, even then, differentiation may be difficult until histological investigations are available (Table 57.1). Weight loss, falling haemoglobin and persistently positive occult blood are sinister features. Solitary diverticulum of the caecum and ascending colon is rare and is congenital, and may present with symptoms and signs identical to those of acute appendicitis. Extensive diverticular disease can sometimes affect the right colon. This, however, is rare in the West hut more common in Eastern countries. In Japan, China, Malaysia and Korea, right-sided disease is twice as common as left-sided disease. Ulcerative colitis Aetiology The cause of ulcerative colitis is unknown; its prevalence among first-degree relatives of patients is 15 times that of the general population but there is no clear Mendelian pattern of inheritance. 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. Some cases are allergic to milk protein. Smoking seems to have a protective effect and there have been anecdotal reports of remission of the disease with smoking or the use of nicotine chewing gum. 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 the normal population. There remain three main hypotheses, none of which has been proved: 1. a mucosal immunological reaction; 2. a weakened mucous barrier; 3. defective mucosal metabolism of butyrates. Epidemiology There are 1015 new cases per 100 000 population a year in the UK. The disease has been rare in Eastern populations hut 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; it is uncommon before the age of 10 and most patients are between the ages of 20 and 40 at diagnosis. Pathology In 95 per cent of cases the disease starts in the rectum and spreads proximally. When the ileocaecal valve is incompetent, retrograde (backwash) ileitis involving the last 30 cm of the ileum is likely to occur. It is a nonspecific 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 per cent of cases and may be numerous. They result from previous episodes of ulceration heaving islands of spared mucosa which will remain prominent when the adjacent mucosa heals. In severe fulminant colitis a section of the colon, usually the transverse colon, may become acutely dilated and the intestinal wall then becomes extremely thin and may perforate (toxic megacolon). On microscopic investigation there is an increase of inflammatory cells in the lamina propia, the walls of crypts are infiltrated by

inflammatory cells and there are crypt abscesses. There is depletion of goblet cell mucin. The crypts are reduced in number and appear to be atrophic and irregularly spaced. With time these changes become severe and precancerous changes can develop (r~ severe dysplasia or carcinoma in situ). Symptoms The first symptom is watery or bloody diarrhoea; there may be a rectal discharge of mucus which 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 bad 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 Inflammation confined to the rectum accounts for about 25 per cent of all cases. As most of the colon is healthy the stool is formed or semi-formed and the patient is often severely troubled by tenesmus and urgency. The risk of cancer in these cases is low. In 510 per cent there is spread to involve the rest of the colon. Left-sided and total colitis (Fig. 57.20) Diarrhoea usually implies that there is active disease proximal to the rectum. Approximately 15 per cent of patients have left-sided colitis, and 25 per cent have total colitis extending beyond the midtransverse colon. 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: 1.mild rectal bleeding or diarrhoea with four or fewer motions per day and the absence of systemic signs of disease; 2. moderate more than four motions per day but no systemic signs of illness; 3. severe more than four motions a day together with one or more signs of systemic illness: fever over 37.50C, tachycardia more than 90/minute, hypoalbuminaemia less than 30 g/litre, weight loss more than 3 kg. Complications of severe disease Fulminating colitis and toxic dilatation (megacolon) (Fig. 57.21). Patientswith severe disease should he admitted to hospital. Dilatation should he 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. The diagnosis is confirmed by the presence on a plain abdominal radiograph of the colon with a diameter more than 6 cm. The condition must be differentiated from dysentery, typhoid and amoebic colitis. Plain abdominal radiographs should he obtained daily in patients with severe colitis and a progressive increase in diameter in spite of medical therapy is an indication for surgery (Fig. 57.22). Perforation. Colonic perforation in ulcerative colitis is a gravecomplication with a mortality rate of 50 per cent 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 only present in parts of the colon that are normal or only mildly inflamed. Mucosal islands

can sometimes be seen and have been mentioned. Small bowel loops in the right lower quadrant may be a sign of severe disease. Barium enema The principal signs are (Fig. 57.23): 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. 57.24). 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, bleeds on touch and there may be a pus-like exudate. Later tiny ulcers may be seen and appear to coalesce. This is different from the picture of amoebic dysentery where there are large deep ulcers with intervening normal mucosa. Colonoscopy and biopsy This has an important place in management: 1. to establish the extent of inflammation; 2. to distinguish between ulcerative colitis and Crohns colitis; 3. to monitor response to treatment; 4. to assess long-standing 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. The cancer risk in colitis Although this is an important complication the overall risk is only about 3.5 per cent. It is much less in early cases but increases with duration of disease. Thus, after 20 years of colitis the risk may be as much as 12 per cent. Carcinoma is more likely to occur where the whole colon is involved and where the disease started in early life (Fig. 57.25). 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, even if the disease is clinically quiescent. If on biopsy there is severe epithelial dysplasia, surgery is indicated. Annual colonoscopy and biopsy is then part of cancer surveillance. In the rare cases with a fibrous stricture these should be examined especially carefully for the presence of an underlying carcinoma. Extraintestinal manifestations Arthritis occurs in around 15 per cent of patients and is of the large joint polyarthropathy type, affecting knees, ankles, elbows and wrists. Sacroileitis and ankylosing spondylitis are 20 times more common in patients with ulcerative colitis. Skin lesions: erythema nodosum, pyoderma gangrenosum or aphthous ulceration. Eye problems: iritis. Liver disease: sclerosing cholangitis has been reported in up to 70 per cent of cases. Diagnosis is by ERCP which demonstrates the characteristic alternating stricturing and bleeding of the intrahepatic and extrahepatic ducts. Bile duct cancer is a rare complication and colectomy does not appear to reduce the risk of subsequent bile duct cancer or sclerosing cholangitis.

Treatment 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. Sulphasalazine and other 5-aminosalicylic acid (5-ASA) derivates, for example, mesalazine and olsalazine, can be given both topically and systemically. Their main function is in maintaining remission rather than treating an acute attack. Nonspecific antidiarrhoeal agents have no place in the routine management of ulcerative colitis. 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/day is given over a 34-week period. Sulphasalazine 1 g three times a day or one of the newer 5-ASA compounds should be given concurrently. Moderate attacks These patients should be treated with oral prednisolone 40 mg/day, 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 with particular reference to the presence of signs of peritonism. Their abdominal girth is measured and liver dullness should be percussed regularly. 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 on plain radiographs (see Fig. 57.22), increasing colonic diameter or a sudden increase in pulse and temperature may indicate a colonic perforation. A stool chart helps in the assessment of response to therapy, and careful medical/surgical joint management is essential. Fluid and electrolyte balance is maintained, anaemia is corrected and adequate nutrition provided, sometimes in severe cases with intravenous nutrition. The patient is maintained nil by mouth and 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 cyclosporin A to induce remission, If there is failure to gain an improvement within 57 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 per cent overall, ranging from 5 per cent in those patients with proctitis to 50 per cent in those patients with a very severe attack: 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 on review colonoscopy have severe dysplasia; extraintestinal manifestations; rarely, severe haemorrhage or stenosis causing obstruction.

Operations I. In the emergency situation the first-aid procedure is a total abdominal colectomy and ileostomy. The rectum can either he 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 he 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. 2. Proctocolectomy and ileostomy: this is the procedure associated with the least compilcation rate. The patient is left with a permanent ileostomy There is, however, a 20 per cent long-term risk of adhesion obstruction, and 510 per cent of the perineal wounds are very slow to heal. The late result will be a chronic perineal sinus which may require repeated currettage or excision. The obvious disadvantage is an ileostomy and although many patients cope remarkably well there is a psychological and social cost. Rectal and anal dissection. Refinements of the procedure have included a close rectal dissection to minimise damage to the nervi erigentis and hence erectile dysfunction which may occur in 0.52 per cent, and inter sphincteric excision of the anus which results in a smaller perineal wound and fewer healing problems. 3. Restorative proctocolectomy with an ileoanal pouch (Parks). In this operation a pouch or reservoir is made out of ileum (Fig. 57.26) as a substitute for the rectum and sewn or stapled to the anal canal. Various pouch designs have been described, hut the J is the most popular and the most easily made using staplers (Fig. 57.27). 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 mucosectomv 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 a double stapled anastomosis 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 he carried out in one, two or three stages. In selected cases a covering loop ileostomy is omitted hut is usually used. Complications include pelvic sepsis usually resulting from a leak of 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. Although associated with a higher complication rate, it is rapidly becoming the operation of choice in younger patients, avoiding a permanent ileostomy. About 20 per cent of patients have an episode of pouchitis, that is, inflammation of the reservoir, at some time. It usually responds to treatment with metronidazole. 4. Colectomy and ileorectal anastomosis: if there is minimal rectal inflammation this can occasionally he used; it has largely been superseded by restorative proctocolectomy. 5. ileostomy with a continent intra-abdominal pouch (Kocks procedure). A reservoir is made 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; now rarely used.

Ileostomy End ileostomy (Brooke). In those patients with a permanent ileostomy there must be scrupulous attention to detail during the operation to ensure that the patient has a good functional result. The position of the ileostomy should be carefully chosen by the patient with the help of a stoma care nursing specialist. The ileum is normally brought through the lateral edge of the rectus abdominis muscle. The use of a spout (Fig. 57.28) was originally described by Bryan Brooke and it 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. ileostomy care During the first few postoperative days, fluid and electrolyte balance must he adjusted with great care. There may he an ileostomy flux while the ileum adapts to the loss of the colon, and the fluid losses can amount to 4 or 5litres/day. The stools thicken in a few weeks and are semisolid in a few months. The help, skill and advice of the stoma care nursing specialist are essential. Modern appliances have transformed stoma care and skin problems are unusual (Fig. 57.29). Complications of an ileostomy include prolapse, retraction, stenosis, bleeding and paraileostomy hernia.Loop ileostomy. This is often used to defunction a pouch ileoanal procedure or even a low anterior resection. 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. Crohns disease (regional enteritis) Crohns disease became widely recognised following the report in 1932 by Crohn, Ginzburg and Oppenheimer describing young adults with a chronic inflammatory disease of the ileum. It can affect any part of the gastrointestinal tract from the lips to the anal margin, but ileocolonic disease is the most common presentation. Epidemiology It is most common in North America and northern Europe. Prevalence rates as high as 56 per 100 000 have been reported in the UK. Over the last four decades there seems to have been a rise in the incidence which cannot be accounted for by increased diagnosis. It is slightly more common in females than in males but is most commonly diagnosed in young patients between the ages of 25 and 40. There does, however, seem to be a second peak of incidence around the age of 17. Aetiology Although Crohns disease has some features suggesting chronic infection, no causative organism has ever been found; similarities between Crohns disease and tuberculosis have focused attention on mycobacteria. Focal ischaemia has also been postulated as a causative factor, possibly originating from a vasculitis arising through an immunological process. A wide variety of foods has now been implicated but none conclusively. Smoking increases the risk threefold. About 10 per cent of patients have a first-degree relative with the disease and there is an association with ankylosing spondylitis. Cell-mediated immune function may be defective in patients with Crohns disease but it is not known whether this is a consequence of the disease itself or the effects of malnutrition and medical therapy. As with ulcerative colitis it is now believed that Crohns disease can predispose to

cancer, although the incidence of malignant change is not nearly as high as in ulcerative colitis and is most manifest in the ileum. Pathology Ileal disease is the most common accounting for 60 per cent of cases; 30 per cent of cases are limited to the large intestine and the remainder consists of patients with ileal disease alone or more proximal small bowel involvement. Anal lesions are common. Crohns disease of the mouth, oesophagus, and stomach and duodenum are uncommon. Resection specimens show a fibrotic thickening of the intestinal wall with a narrow lumen (Fig. 57.30). There is usually dilated gut just proximal to the stricture and, in the strictured area, there are deep mucosal ulcerations with linear or snake-like patterns. Oedema in the mucosa between the ulcers gives rise to a cobblestone appearance. The transmural inflammation leads to adhesions, inflammatory masses with mesenteric abscesses and fistulae into adjacent organs. The serosa is usually opaque, there is thickening in the mesentery and mesenteric lymph nodes are enlarged. The condition is discontinuous with inflamed areas separated from normal intestine; these are sometimes called skip lesions. Under the microscope there are focal areas of chronic inflammation involving all layers of the intestinal wall. There are noncaseating giant cell granulomas but these are only found in 60 per cent of patients. They are most common in anorectal disease. The earliest mucosal lesions are discrete aphthous ulcers. Recent studies have also shown multifocal arterial occlusions in the muscularis propia. Clinical features Presentation depends upon the area of involvement. Acute Crohns disease Acute Crohns disease occurs in only 5 per cent of cases. Symptoms and signs resemble those of acute appendicitis but there is usually diarrhoea preceding the attack. Rarely there could be a free perforation of the small intestine, resulting in a local or diffuse peritonitis. Acute colitis with or without toxic megacolon can occur in Crohns disease but is less common than in ulcerative colitis. Chronic Crohns disease There is often a history of mild diarrhoea extending over many months occurring in bouts accompanied by intestinal colic. Patients may complain of pain, particularly in the right iliac fossa, and there may be a tender mass palpable. Intermittent fevers, secondary anaemia and weight loss are common. A perianal abscess or fissure may be the first presenting feature of Crohns disease; the cause is often an infected anal crypt associated with concomitant diarrhoea, but as the disease becomes chronic specific fistulae resulting from the Crohns disease itself can develop. After months of repeated attacks with acute inflammation the affected area of intestine begins to narrow with fibrosis causing abdominal pain on eating, giving rise to what has been described as food fear. Children developing the illness before puberty may have retarded growth and sexual development. With progression of the disease adhesions and transmural fissuring, intra-abdominal abscesses and fistula tracts can develop. 1.Entero-enteric fistulae can occur into adjacent small bowel loops or the pelvic colon and entero-vesical fistulae may cause repeated urinary tract infections and pneumaturia. 2. Entero-cutaneous fistulae rarely occur spontaneously and usually follow previous surgery. Anal disease (see Chapter 58)

In the presence of active disease, the penianal skin appears bluish. Three or more oedematous pinky-blue fleshy tags protrude from the anal margin; they may have superficial ulceration on the inner surface extending into the anal canal. Superficial ulcers with undermined edges are relatively painless and can heal with bridging of epithelium. Deep cavitating ulcers are usually found in the upper anal canal; they can be painful and cause perianal abscesses and fistulae, discharging around the anus and sometimes forwards into the genitalia. The most distressing feature of anal disease is sepsis from secondary abscesses and perianal fistulae. Remarkably the rectal mucosa is often spared and may feel normal on rectal examination. If it is involved, however, it will feel thickened, nodular and irregular. Investigation Sigmoidoscopic examination Sigmoidoscopic examination may be normal or show minimal involvement. Ulceration in the anal canal will, however, be readily seen. Colonoscopy As a result of the discontinuous nature of Crohns disease there will be areas of normal colon or rectum. In between these there are areas of inflamed mucosa which are irregular, ulcerated with a mucopurulent exudate. The earliest appearances are aphthoid-like ulcers surrounded by a rim of erythematous mucosa. These become larger and deeper with increasing severity of disease. In colonic Crohns disease there may be stricturing and it is important to exclude malignancy in these sites (Fig. 57.31). At the ileo-colic anastomosis of a patient having had previous ileocaecal resection, recurrent disease is usually seen on the ileal side of the anastomosis. Radiology Barium enema will show similar features to those of colonoscopy in the colon. The best investigation of the small intestine is small bowel enema (Fig. 57.32). This will show up areas of delay and dilatation characterising partial obstruction. The involved areas tend to be narrowed, irregular and sometimes, when a length of terminal ileum is involved, there may be the string sign of Kantor. Sinograms are useful in patients with entero-cutaneous fistulae. CT scans are used in patients with fistulae and those with intra-abdominal abscesses and complex involvement. Magnetic resonance imaging (MRI) has been shown to be useful in assessing perianal disease. Treatment Medical therapy Steroids are the mainstay of treatment. Patients with a relapse of their Crohns disease are treated with up to 40 mg prednisolone orally, daily supplemented by 5-ASA cornpounds in those patients with colonic involvement, although there is some evidence that this may help small bowel disease as well. Those who have symptoms and signs of a mass or an abscess are also treated with antibiotics. Azathioprine is used for its additive and steroid-sparing effect. Nutritional support is essential. Severely malnourished people may require intravenous feeding or nasoenteric feeding regimens. Anaemia, hypoproteinaemia, electrolyte, vitamin and metabolic bone problems must all be addressed. Indications for surgery Surgical resection will not cure Crohns disease. Surgery is therefore focused on complications of the disease. As many of these indications for surgery may be relative, joint management by an aggressive physician arid a conservative surgeon is thought to be ideal. These complications include: recurrent intestinal obstruction;

bleeding; perforation; failure of medical therapy; intestinal fistula; fulminant colitis; malignant change; perianal disease. Surgery To preserve functional gut length, resection is kept to a minimum so as to deal with the local problem. The whole of the gastrointestinal tract has to be examined carefully at the time of laparotomy. If on occasion Crohns disease is diagnosed during the course of an operation for suspected appendicitis, the appendix should be removed. If the ileum is thick, rigid and pipe-like, senior help should be sought so that an ileocaecal resection can be carried out. The course of the disease after surgery is unpredictable but recurrence is common. It does not seem to be related to the presence of disease at the resection line. Recurrence rates vary from site to site hut the cumulative probability of recurrence requiring surgery for ileal disease is of the order of 20, 40, 60 and 80 per cent at 5, 10, 15 and 20 years, respectively, after previous resection. Restorative operations have a higher incidence of recurrence than, for example, proctocolectomy and ileostomy. 1. Ileocaecal resection is the usual procedure for ileocaecal disease with a primary anastomosis between the ileum and the transverse colon. 2. Segmental resection: short segments of small or large bowel involvement can he treated by segmental resection. 3. Colectomy and ileorectal anastomosis. In patients with widespread colonic disease with rectal sparing and a normal anus this can be a useful option. 4. Temporary loop ileostomy. This can be used either in patients with acute distal Crohns disease allowing remission and later restoration of continuity or in patients with severe penianal or rectal disease. 5.Proctocolectomy. Patients with colonic and anal disease failing to respond to medical treatment or defunction will eventually require a permanent ileostomy. 6.Strictureplasty. Multiple strictured areas of Crohns disease (Fig. 57.33) can be treated by a local widening procedure, strictureplasty, to avoid excessive small bowel resection (Fig. 57.34) (Lee). 7. Anal disease is usually treated conservatively by simple drainage of abscesses, placing setons around any fistulae, and occasionally in patients with inactive disease primary repair of a recto-vaginal or high fistula in ano could be attempted. Infections Intestinal amoebiasis. Amoebiasis is an infestation with Entamoeba histolytica. This parasite has a world-wide distribution. Life history of the parasite. The active form of the parasite or trophozoite lives in the intestinal mucous membrane where it ingests red blood corpuscles and other cells and multiples by mitosis. Should the parasite become pathogenic, it makes its way into the follicles ofLieberkuhn and, by dissolving into glandular tissue via the cytolysins, submucous loculi are produced. Some of these burst through the mucous membrane to become amoebic ulcers. While the trophozoites continue their activities in the base of the ulcer, others cease to feed, migrate towards the surface and become transformed into cysts which pass into the outer world with the faeces. Amoebiasis is transmitted mainly in contaminated drinking water.

Pathology.The ulcers, which have been described as bottlenecked because of their considerably undermined edges, have a yellow necrotic floor, from which blood and pus exude. Although on rare occasions the ulcers are scattered throughout the large intestine, in 75 per cent they are confined to the lower sigmoid and upper rectum. Biopsy.Endoscopic biopsies or fresh hot stools are examined carefully to look for the presence of amoebae. It is important to emphasise, however, that the presence of the parasite does not indicate that it is pathogenic (Fig. 57.35). Clinical features. Dysentery is the principal manifestation of the disease but it may come in various other guises. Appendicitis or amoebic caecal mass. In tropical countries where amoebiasis is endemic, this is a constantly recurring problem. To operate on a patient with amoebic dysentery without the precautions subsequently described is to invite an exacerbation of amoebiasis which may prove fatal. The bowel is friable and satisfactory closure of the appendix stump becomes difficult or impossible, especially in cases where a palpable mass is present. When there is an amoebic mass there tends to be tenderness on deep palpation over the caecum and the sigmoid. Perforation.The most common sites are the caecum and recto-sigmoid; usually perforation occurs into a confined space where adhesions have previously formed and a pericolic abscess results which eventually needs draining. When there is sudden faecal flooding in the general peritoneal cavity, drainage of the region of the perforation, gastrointestinal aspiration, intravenous fluid, antibiotics and a full course of emetine are sometimes successful. Severe rectal haemorrhage as a result of separation of the slough is liable to occur. Granuloma.Progressive amoebic invasion of the wall of the rectum or colon, with secondary inflammation, can produce a granulomatous mass indistinguishable from a carcinoma. Fibrous stricture may follow the healing of extensive amoebic ulcers. Intestinal obstruction is a common complication of amoebiasis, and the obstruction is the result of adhesions associated with pericolitis and large granuloma. Paracolic abscess, ischiorectal abscess and fistula occur from perforation by amoebae of the intestinal wall followed by secondary infection. Ulcerative colitis. A search for amoebae should always be made in the stools of patients believed to have ulcerative colitis. Treatment.High-dose intravenous steroids in this situation can he catastrophic. Metronidazole (Flagyl) is the first-line drug, 800 mg three times daily for 710 days. Diloxanide furoate is best for chronic infections associated with the passage of cysts in stools. Intestinal antibiotics improve the results of the chronic stages, probably by coping with superadded infection. Typhoid and paratyphoid. Surgical complications. Paralytic ileus is the most common complication of typhoid. Intestinal haemorrhage may be the leading symptom. Perforation.Perforation of a typhoid ulcer usually occurs during the third week and is occasionally the first sign of the disease. The ulcer is parallel to the long axis of the gut and is usually situated in the lower ileum. Paratyphoid B. Perforation of the large intestine sometimes occurs. Vigorous intravenous antibiotic therapy is given; occasionally surgery is required to defunction the colon or in late cases remove the colon as for ulcerative colitis. Cholecystitis.Acute typhoid cholecystitis is not uncommon and perforation can occur; gallstones occasionally contain typhoid bacilli and some patients may become typhoid carriers.

Phlebitis.Venous thrombosis, particularly of the left common iliac vein, is an occasional complication of typhoid fever. Genitourinary complications. Typhoid cystitis, pyelitis and epididymo-orchitis may all occur. Joints.All degrees of arthritis, from a mild effusion to suppuration, occur as a complication of this disease. Bone.Typhoid osteomyelitis and typhoid of the spine occur. Tuberculosis of the intestine. Tuberculosis can affect any part of the gastrointestinal tract from the mouth to the anus. The sites affected most often are the ileum, proximal colon and peritoneum. There are two principal types. Ulcerative tuberculosis is secondary to pulmonary tuberculosis and arises as a result of swallowing tubercle bacilli. There are multiple ulcers in the terminal ileum, lying transversely, and the overlying serosa is thickened, reddened and covered in tubercles. Clinical features. Diarrhoea and weight loss are the predominant symptoms and usually the patient will be receiving treatment for pulmonary tuberculosis. Radiology.A barium meal and follow-through or small bowel enema will show the absence of filling of the lower ileum, caecum and most of the ascending colon as a result of narrowing and hypermotility of the ulcerated segment (Fig. 57.36). Treatment.A course of chemotherapy is given. Healing often occurs provided the pulmonary tuberculosis is adequately treated. An operation is only required in the rare event of a perforation or intestinal obstruction. Hyperplastic tuberculosis. This usually occurs in the ileocaecal region although solitary and multiple lesions in the lower ileum are sometimes seen. This is caused by the ingestion of Mycobacterium tuberculosis by patients with a high resistance to the organism. The infection establishes itself in lymphoid follicles, and the resulting chronic inflammation causes thickening of the intestinal wall and narrowing of the lumen. There is early involvement of the regional lymph nodes which may caseate. Unlike Crohns disease, with which it shares many similarities, abscess and fistula formation is rare. Untreated, sooner or later subacute intestinal obstruction will supervene often together with the impaction of an enterolith in the narrowed lumen. Clinical features. Attacks of abdominal pain with intermittent diarrhoea are the usual symptoms. The ileum above the partial obstruction is distended, and the stasis and consequent infection lead to steatorrhoea, anaemia and loss of weight. Sometimes the presenting picture is of a mass in the right iliac fossa in a patent with vague ill health. The differential diagnosis is that of an appendix mass, carcinoma of the caecum, Crohns disease, tuberculosis or actinomycosis of the caecum. Radiology.A barium follow-through or small bowel enema will show a long narrow filling defect in the terminal ileum. Treatment.When the diagnosis is certain and the patient has not yet developed obstructive symptoms, treatment with chemotherapy is advised and may cure the condition. Where obstruction is present, operative treatment is required and ileocaecal resection is best. Actinomycosis of the ileocaecal region. Abdominal actinomycosis is rare. Unlike intestinal tuberculosis, narrowing of the lumen of the intestine does not occur and mesenteric nodes do not become involved. A local abscess, however, spreads to the retroperitoneal tissues and the adjacent abdominal wall, becoming the seat of multiple indurated discharging sinuses. The liver may become involved via the portal vein. Clinical features. The usual history is that appendicectomy has been carried out for an appendicitis. Some 3 weeks after surgery a mass is palpable in the right iliac fossa and

soon afterwards the wound begins to discharge. At first this is thin and watery, and then later it becomes thicker and malodorous. Other sinuses may form and a secondary faecal fistula develop. Pus should be sent for bacteriological examination where the characteristic sulphur granules can be seen. Treatment.Penicillin or cotrimoxazole has to be prolonged and high dosage. Tumours of small intestine Compared with the large intestine, the small intestine is rarely the seat of a neoplasm and these become progressively less common from the duodenum to the terminal ileum. Benign. Adenoma, submucous lipoma and leiomyoma occur from time to time, and sometimes reveal themselves by causing an intussusception. The second most common complication is intestinal bleeding from an adenoma in which event the diagnosis is frequently long delayed because the tumour is overlooked at barium radiology, endoscopy and even surgery. PeutzJeghers syndrome consists of: familial intestinal hamartomatous polyposis affecting the jejunum, where it is a cause of haemorrhage, and often intussusception; melanosis of the oral mucous membrane and the lips. The melanosis takes the form of melanin spots sometimes present on the digits and the perianal skin, but the pigmentation of the lips is the sine qua non (Fig. 57.37). Histology.The polyps can be likened to trees. The trunk and branches are smooth muscle fibres and the foliage is virtually normal mucosa. Treatment.As malignant change rarely occurs, resection is necessary only for serious bleeding or intussusception. Large single polyps can be removed by enterotomy or short lengths of heavily involved intestine can be resected. Those lesions within reach can be snared by colonoscopy. Malignant. Lymphoma. There are three main types as follows. 1.Western type lymphoma. These are annular ulcerating lesions, which are sometimes multiple. They are now thought to he non-Hodgkins B-cell lymphoma in origin. They may present with obstruction and bleeding, perforation, anorexia and weight loss. 2. Primary lymphoma associated with coeliac disease. There is an increased incidence of lymphoma in patients with coeliac disease; this is now regarded as a T-cell lymphoma. Worsening of the patients diarrhoea, with pyrexia of unknown - origin together with local obstructive symptoms, is the usual feature. 3.Mediterranean lymphoma. This is found mostly in North Africa and the Middle East and is associated with alpha-chain disease. Unless there are particular surgical complications these conditions are usually treated with chemotherapy. Carcinoma.As with other small bowel tumours these can present with obstruction, bleeding or diarrhoea. Complete resection offers the only hope of cure (Fig. 57.38). Carcinoid tumour. These tumours occur throughout the gastrointestinal tract, most commonly in the appendix, ileum and rectum in decreasing order of frequency. They arise from neuroendocrine cells at the base of intestinal crypts. The primary is usually small but when they metastasise, the liver is usually involved with numerous secondaries, which are larger and more yellow than the primary, and when this has occurred the carcinoid syndrome will become evident. The tumours can produce a number of vasoactive peptides, most commonly 5-hydrox-ytryptamine (serotonin), which may be present as 5-hydroxyindoleacetic acid in the urine during attacks.

The clinical syndrome itself consists of reddish-blue cyanosis, flushing attacks, diarrhoea, borborygmi, asthmatic attacks and, eventually, sometimes pulmonary and tricuspid stenosis. Classically the flushing attacks are induced by alcohol. Treatment.Most patients with gastrointestinal carcinoids do not have carcinoid syndrome. Surgical resection is usually sufficient. In the cases found incidentally at appendicectomy nothing further is required. In patients with metastatic disease, multiple enucleations of hepatic metastases or even partial hepatectomy can he carried out. The treatment has been transformed by the use of octreotide (a somatostatin analogue) which reduces both flushing and diarrhoea, and octreotide cover is usually used in patients with a carcinoid syndrome who have surgery to prevent a carcinoid crisis. Carcinoid tumours generally grow more slowly than most metastatic malignancies; the patients may live with the syndrome of metatastic disease for many years. Tumours of the large intestine Benign The term polyp is a clinical description of any elevated tumour. It covers a variety of histologically different tumours shown in Table 57.2. Polyps can occur either singly, synchronously in small numbers or as part of a polyposis syndrome. In familial adenomatous polyposis, more than 100 adenomas are present. It is important to be sure of the histological diagnosis because adenomas have significant malignant potential. Adenomatous polyps Adenomatous polyps vary from a tubular adenoma (Fig. 57.39), rather like a raspberry on a stalk, to the villous adenoma, a flat spreading lesion. Solitary adenomas are usually found during the investigation of colonic bleeding or sometimes fortuitously. Villous tumours more usually give symptoms of diarrhoea, mucus discharge and occasionally hypokalaemia. The risk of malignancy developing in an adenoma increases with increasing size of tumour, for example, in 1-cm diameter tubular adenomas there is a 10 per cent risk of cancer, whereas in villous adenomas over 2 cm in diameter there may be a 15 per cent chance of carcinoma. Adenomas larger than 5mm in diameter are usually treated because of their malignant potential. Colonoscopic snare polypectomy or diathermy obliteration with hot biopsy forceps can be used. Huge villous adenomas of the rectum can be difficult to remove even with techniques per anus and occasionally proctectomy is required; the anal sphincter can usually be preserved. Hamartomatous polyps PeutzJeghers polyps may occur in the colon as either solitary or multiple lesions. Juvenile polyps may occur as multiple lesions in the colon often associated with a congenital defect such as a malrotation or Meckels diverticulum. They have minimal malignant potential and ate only removed if they are causing troublesome pain, bleeding or hypoproteinaemia. Haemangioma A localised submucous telangiectasis is often the cause of bleeding which may be profuse. If bleeding is continuing, both angiography and colonoscopy can help to localise the source. If found by colonoscopy the lesion can be removed endoscopically, whereas arteriographic detection can be followed by the use of vasopressin or microspheres to stop the haemorrhage. Often the only method of detecting it is to operate while the bleeding is in progress. The distribution of blood

within the intestine is noted; scrutiny of the blood-containing portion of the colon may reveal the lesion but on-table colonoscopy could be necessary. The tumour is resected once located. Lipoma Lipoma is less frequently encountered in the large than in the small intestine. In the large intestine it is almost always confined to the caecum. The tumour is submucous and in more than half the cases it is the cause of an intussusception. On occasion a lipoma at the ileocaecal valve can be confused with a caecal cancer. Familial adenomatous polyposis Familial adenomatous polyposis (FAP) is a general neoplastic disorder of the intestine. Although the large bowel is mainly affected polyps can occur in the stomach, duodenum and small intestine. The main risk is large bowel cancer, but duodenal and ampullary tumours have been reported. It is inherited as a Mendelian dominant and the gene responsible (APC gene) has now been identified on the short arm of chromosome 5 (Bodmer). Males and females are equally affected. It can also occur sporadically without any previous sign or history, presumably by new mutations. There is often, in these cases, a history of large bowel cancer occurring in young adulthood or middle age suggesting preexisting adenomatosis. FAP can be associated with benign mesodermal tumours such as desmoid tumours and osteomas. Epidermoid cysts can also occur (Gardners syndrome); desmoid tumours in the abdomen invade locally to involve the intestinal mesentery and although nonmetastasising they can become unresectable. Clinical features. Polyps are usually visible on sigmoidoscopy by the age of 15 years and will almost always be visible by the age of 30. Carcinoma of the large bowel occurs 1020 years after the onset of the polyposis. One or more cancers will already be present in two-thirds of those patients presenting with symptoms. Symptomatic patients. These are either new proposition or those from an affected family who have not been screened. They may have loose stools, lower abdominal pain, weight loss, diarrhoea and the passage of blood and mucus. Polyps are seen on sigmoidoscopy, and the number and distribution of polyps, and usually cancers if they ate symptomatic, are shown on a double-contrast barium enema. If in doubt colonoscopy is performed with biopsies to establish the number and histological type of polyps. If over 100 adenomas (Fig. 57.40) ate present the diagnosis can be made confidently but it is important not to confuse this with nonneoplastic forms of polyposis. Asymptomatic patients. Usually members of affected families attend for screening. As yet there is no reliable means of knowing whether an individual is affected unless adenomas develop. If there are no adenomas by the age of 30, FAP is unlikely. Pigmented spots in the retina (CHIRPES) and deoxyribonucleic acid (DNA) tests for the FAP gene should make screening mote reliable in the future. If the diagnosis is made during adolescence, operation is deferred usually to the age of 17 or 18. Screening policy. 1. All members of the family should be examined at the age of 1012 years, repeated every 12 years. 2. Most of those who are going to get polyps will have them at 20 and these requite operation. 3. If there are no polyps at 20, continue with 5-yearly examination until age 50; if there are still no polyps there is probably no inherited gene. Carcinomatous change may exceptionally occur before the age of 20. Examination of blood relatives,

including cousins, nephews and nieces, is essential and a family tree should be constructed and a register of affected families maintained. Treatment. Colectomy with ileorectal anastomosis has in the past been the usual operation because it avoids an ileostomy in a young patient. The rectum is subsequently cleared of polyps by snaring or fulguration. The patients ate examined by flexible sigmoidoscopy at 6-monthly intervals thereafter. In spite of this, a proportion of patients develops carcinoma in the rectal stump. The risk of carcinoma in the St Marks series was 10 per cent over a period of 30 years. The alternative and now more common operation is a restorative proctocolectomy with an ileoanal anastomosis. This has a higher complication rate than ileorectal anastomosis. It is indicated in patients with serious rectal involvement with polyps, those who are likely to be poor at attending for follow-up and those with an established cancer of the rectum or sigmoid. However, it is now used mote frequently for less severe cases. Malignant Adenocarcinoma of the colon Pathology. Microscopically, the neoplasm is a columnar cell carcinoma originating in the colonic epithelium. Macroscopically the tumour may take one of four forms (Fig. 57.41). Type 4 is the least malignant form. It is likely that all carcinomas start as a benign adenoma, the so-called adenomacarcinoma sequence. The annular variety tends togive rise to obstructive symptoms whereas the others more commonly will present with bleeding. Site and distribution of cases of cancer are shown in Fig. 57.42. Tumours are more common in the left colon and rectum. The spread of carcinoma of the colon. Generally this is a comparatively slow growing neoplasm. Local spread The tumour is limited to the bowel for a considerable time; it spreads round the intestinal wall and usually causes intestinal obstruction before it invades adjacent structures. The ulcerative type mote commonly invades locally and an internal fistula may result, for example, into the bladder. There may also be a local perforation with an abscess or even an external faecal fistula. The progression of invasion occurs across the submucosa into the musculatis propia and thence out into the serosa and fat, lymphatics and veins in the mesentery alongside the bowel wall. Lymphatic spread Lymph nodes draining the colon are grouped as follows: N1 nodes in the immediate vicinity of the bowel wall; N2 nodes arranged along the ileo-colic, right colic, midcolic, left colic and sigmoid arteries; N3 the apical nodes around the superior and inferior mesenteric vessels where they arise from the abdominal aorta. Involvement of the lymph nodes by the tumour progresses in a gradual manner from those closest to the growth along the course of the lymphatic vessels to those placed centrally. Bloodstream spread This accounts for a large proportion (3040 per cent) of late deaths. Metastases are carried to the liver via the portal system sometimes at an early stage before clinical or operative evidence is detected (occult hepatic metastases). Staging colon cancer. Dukes classification was originally described for rectal tumours (see Chapter 60) but has been adopted for histopathological reporting of colon cancer as well. There have been numerous modifications of the original system

leading to some confusion but in its most basic form Dukes classification for colon cancer is as follows. Dukes A confined to bowel wall; B through the bowel wall but not involving the free peritoneal serosal surface; C lymph nodes involved. Dukes himself never described a D stage, but this is often used to describe either advanced local disease or metastases to the liver. TNM classification. The TNM classification is more detailed and accurate but more demanding. T tumour stage: into submucosa; T2 into muscularis propria; into pericolic fat but-not breaching serosa; breaches serosa or directly involving another organ. N nodal stage: N0 no nodes involved; N1 12 nodes involved; N2 3 or more nodes. M metastases: no metastases; metastases. Ly lymphatic invasion: L0 no lymphatic vessels involved; lymphatics involved. V venous invasion: V0 no vessel invasion; Vi vessels invaded. R residual tumour: R0 no residual tumour; margins involved, residual tumour present. Clinical features. Carcinoma of the colon usually occurs in patients over 50 years of age but it is not rare earlier in adult life. Twenty per cent of cases present as an emergency with intestinal obstruction or peritonitis. In any case of colonic bleeding in patients over the age of 40 a complete investigation of the colon is required. A careful family history should be taken. Those with first-degree relatives who have developed colorectal cancer at the age of 45 or below are at high risk and may be part of one of the colorectal cancer family syndromes. Carcinoma of the left side of the colon Most tumours occur in this location. They ate usually of the stenosing variety. The main symptoms are those of increasing intestinal obstruction. Pain is referred to the suprapubic area. Patients will have episodes of colic; a constant ache may suggest an advanced tumour. Alteration of bowel habit. An adult previously having a predictably regular bowel habit suddenly develops irregularity. There may be increasing difficulty in getting the bowels to move, requiring laxatives. The episodes of constipation may be followed by attacks of diarrhoea. Palpable lump. The lump that is felt on abdominal, rectal or bimanual palpation is sometimes not the tumour itself, but impacted faeces above it. When the tumour is

situated in a pendulous pelvic colon, a hard movable swelling may be felt in the rectovesical pouch on rectal examination. Distension. Lower abdominal distension is not uncommon and, as with the pain, is relieved by passing flatus. Carcinoma of the sigmoid This follows the general pattern of the above, with these differences. Pain is usually colicky from the outset. Tenesmus. Low tumours may give rise to a feeling of the need for evacuation which may result in tenesmus accompanied by the passage of mucus and blood, especially in the early morning. Bladder symptoms are not unusual and in some instances may herald a colovesical fistula. Carcinoma of the transverse colon This may be mistaken for a carcinoma of the stomach because of the position of the tumour together with anaemia and lassitude. Carcinoma of the caecum and ascending colon This may present with the following. Anaemia, severe and unyielding to treatment; there may be a palpable tumour present. The presence of a mass in the right iliac fossa. Colonoscopy may be needed to confirm the diagnosis. Caecal carcinoma is sometimes discovered unexpectedly at operation for acute appendicitis or for an appendix abscess failing to resolve. On rare occasions the appendix is inflamed, or even gangrenous, from the obstruction to its lumen by the tumour. A carcinoma of the caecum can be the apex of an intussusception presenting with the symptoms of intermittent obstruction. Metastatic disease Patients may present for the first time with liver metastases and an enlarged liver, ascitis from carcinomatosis peritonei and, more rarely, rnetastases to the lung, skin, bone and brain. Methods of investigation Sigmoidoscopy. This is part of the routine investigation of patients passing blood and mucus that is really limited to the rectum. Flexible sigmoidoscopy. The 60-cm, fibre-optic, flexible sigmoidoscope is being used increasingly in the out-patient clinic or in special rectal bleeding clinics. The patient is prepared with a disposable enema and sedation is not usually necessary. Colonoscopy. This has the advantage of not only picking up a primary cancer but also having the ability to detect synchronous polyps or even multiple carcinomas which occur in 5 per cent of cases. It tends to be used in patients with bleeding as their main presenting symptom, those with known polyps and those in whom there is doubtful radiology. Ideally every case should be proven histologically before surgery. Full bowel preparation and sedation are necessary. Radiology. Double-contrast barium enema is used routinely now. It shows a cancer of the colon as a constant irregular filling defect (Fig. 57.43). It is the investigation of choice in patients with predominant change in bowel habit as their presenting symptom. Ultrasonography is often used as a screening investigation for liver metastases, and CT is used in patients with large palpable abdominal masses to determine local invasion and is particularly used in the pelvis in the assessment of rectal cancer.

Treatment Preoperative preparation. Full mechanical bowel preparation before colonic surgery is essential. The most commonly used method is dietary restriction to fluids only for 48 hours before surgery; on the day before operation two sachets of Picolax (sodium picosulphate) are taken to purge the colon. In addition a rectal washout may be necessary. Alternatives include prograde lavage via a nasogastric tube using water or balanced electrolyte solutions. A stoma site is carefully discussed with the stoma care nursing specialist and antiembolus stockings are fitted; the patient is started on prophylactic subcutaneous heparin and intravenous prophylactic antibiotics are given at the start of surgery. When intestinal obstruction is present, preparation in this way may precipitate abdominal pain and it may be safer to save preparation to the time of the operation using an on table lavage technique. Operations The test of operability. The abdomen is opened and the tumour assessed for resectability. 1. The liver is palpated for secondary deposits, the presence of which is not necessarily a contraindication to resection because the best palliative treatment for carcinoma of the colon is removal of the tumour. 2. The peritoneum, particularly the pelvic peritoneum, is inspected for signs of small, white, seed-like, neoplastic implantations. Similar changes can occur in the omentum. 3. The various groups of lymph nodes that drain the involved segment are palpated. Their enlargement does not necessarily mean that they are invaded by metastases because the enlargement may be inflammatory. 4. The neoplasm is examined with a view to mobility and operability. Local fixation, however, does not always imply local invasion because some tumours excite a brisk inflammatory response. The operations to be described are designed to remove the primary tumour and its draining locoregional lymph nodes which may be involved by metastases. Lesser resections are indicated, however, should hepatic rnetastases render the condition curable nonsurgically. There is some evidence that early division of major blood vessels supplying the involved colon (no-touch technique Turnbull) can slightly improve the number of curative operations. Carcinoma of the caecum or ascending colon (Fig. 57.44) is treated when resectable by right hemicolectomy (Fig. 57.45). The abdomen is opened, the peritoneum lateral to the ascending colon is incised and the incision carried around the hepatic flexure. The right colon is elevated, with the leaf of peritoneum containing its vessels and lymph nodes, from the posterior abdominal wall, taking care not to injure the ureter, spermatic vessels in the male or the duodenum. The peritoneum is separated medially neat the origin of the ileo-colic artery, which is divided together with the right colic artery when this has a separate origin from the superior mesenteric. The mesentery of the last 30 cm of ileum, and the leaf of raised peritoneum attached to the caecum, ascending colon and hepatic flexure, after ligation of the mesenteric blood vessels, is divided as far as the proximal third of the transverse colon. When it is cleat that there is an adequate blood supply at the resection margins, the right colon is resected and an end-to-end anastomosis fashioned between the ileum and transverse colon. Carcinoma of the hepatic flexure. When the hepatic flexure is involved the resection must be extended correspondingly (Fig. 57.46).

Carcinoma of the transverse colon. When there is no obstruction, excision of the transverse colon and the two flexures together with the transverse mesocolon and the greater omentum, followed by end-to-end anastomosis, can be used. An alternative is an extended right hemicolectomy (Fig. 57.46). Carcinoma of the splenic flexure or descending colon. The extent of the resection is from right colon to descending colon. Sometimes removal of the colon up to the ileum, with an ileorectal anastomosis, is preferable. Carcinoma of the pelvic colon. The left half of the colon is mobilised completely (Fig. 57.47). So that the operation is radical, the inferior mesenteric artery below its left colic branch, together with the related paracolic lymph nodes, must be included in the resection. This entails carrying the dissection as far as the upper third of the rectum. Many surgeons advocate flush ligation of the inferior mesenteric artery on the aorta (high litigation). Provided that there is no obstruction primary anastomosis is the rule. Occasionally a protecting upstream stoma may be necessary. The methods of dealing with large bowel obstruction as a result of colon cancer are described in Chapter 58. When a growth is found to be inoperable. In the upper part of the left colon, a transverse colostomy is performed. In the pelvic colon, a left iliac fossa colostomy is preferable. With an inoperable growth in the ascending colon a bypass using an ileocolic anastomosis is the best procedure. Over 95 per cent of colonic carcinomas can, however, be resected. Adjuvant therapy See Chapter 60. Hepatic metastases It is important to biopsy hepatic metastases for histological diagnosis. Unless they are on the very surface and edge of the liver, they are not usually resected at the time of colonic surgery. Patients with up to two or three liver metastases confined to one lobe of the liver may be offered hepatic resection. Multiple painful hepatic metastases can be palliated by cytotoxic drugs, cryosurgery or laser therapy (Fig. 57.48). Other disorders Traumatic rupture The intestine can be ruptured with or without an external wound so-called blunt trauma (Fig. 57.49). The most common cause of this is a blow on the abdomen which crushes the bowel against the vertebral column or sacrum; also a rupture is more likely to occur where part of the gut has been fixed, for example, in a hernia, or where a fixed part of the gut joins a mobile one such as the duodenojejunal flexure. Here the damage may be retroperitoneal and easily overlooked.In small perforations the mucosa may prolapse through the hole and partly seal it, making the early signs misleading. In addition there may be a laceration in the mesentery. The patient will then have a combination of intra-abdominal bleeding and release of intestinal contents into the abdominal cavity, giving rise to peritonitis. Traumatic rupture of the large intestine is much less common. In blast injuries of the abdomen following the detonation of a bomb, the pelvic colon is particularly at risk of rupture. Compressed air rupture can follow the dangerous practical joke where an airline carrying compressed air is turned on near the victims anus. Rupture of the upper rectum can occur during sigmoidoscopy and occasionally during the placement of rectal catheters for barium radiology. Traumatic rupture of the colon can occur during colonoscopy. The most common site is the sigmoid colon where the

formation of a sigmoid loop pushes against the antimesenteric border of the sigmoid colon, stretching it out and eventually perforating it. Gun shot wounds and impalement injuries to the bowel have mote serious consequences because of the introduction of debris from the patients clothing or the missile itself mixing with the bacteria in the patients gut. High-velocity missiles may cause extensive damage of the bowel over a much wider area than just the entry and exit wounds. Treatment Where rupture is suspected a plain radiograph in the erect or lateral decubitus position will demonstrate the presence of free air in the peritoneal cavity or indeed in the retroperitoneal tissues. In almost all cases an abdominal exploration must be performed and, in many instances, simple closure of the perforation is all that is required. In others, for example, where the mesentery is lacerated and the bowel is not viable, resection may be necessary. In the case of the large intestine small clean tears can be closed primarily, if there is a large tear with damage to the surrounding structures to the adjacent mesentery resection, exteriorisation may be used. Much depends on the amount of intra-abdominal soiling. In the case of retroperitoneal portions of the intestine, for example, the duodenum, perforations can involve the front and back walls and the duodenum in particular has to be carefully mobilised to check that a concealed tear is not overlooked. In all cases the abdomen is washed out with saline and broad-spectrum intravenous antibiotics are given. Pneumatosis cystoides intestinalis This is a rate condition in which gas-filled cysts ate found in the subserosa or submucosa of the small intestine or colon. They ate usually translucent, thin-walled, range in size between 1 and 2 cm and contain gas, mainly nitrogen, but also an increased content of hydrogen, and have a lining of flattened cells. The cause is not known; there is an association with chronic obstructive pulmonary disease but an increased local production of intestinal gas is a mote probable cause. It has been seen in patients with necrotising enteritis, entetocolitis and diverticulitis. The cysts ate usually symptomless but occasionally can give rise to intestinal obstruction and rectal bleeding, diarrhoea or mucus in the stool. The cysts may be recognised at sigmoidoscopy or seen on plain abdominal films, barium studies (Fig. 57.50) and even CT scans. Management of the uncomplicated primary disease is conservative. When symptoms demand treatment the first line is intermittent high-flow oxygen therapy providing a concentration of 70 per cent continuously for 5 days by nasal specula. The cysts may also resolve with antibiotic treatment, particularly metronidazole. In resistant cases maintenance treatment with sulphasalazine may be helpful. Enterocutaneous or faecal fistula An external fistula communicating with the caecum sometimes follows an operation for gangrenous appendicitis or the draining of an appendix abscess. A faecal fistula can occur from necrosis of a gangrenous patch of intestine after the relief of a strangulated hernia, or from a leak from an intestinal anastomosis. The opening of an abscess connected with chronic diverticulitis or carcinoma of the colon frequently results in faecal fistula. Radiation damage is also another cause of fistula formation. The most common cause of enterocutaneous fistula is, however, previous surgery. This happens most often in patients with adhesions following previous operations. Damage to the small intestine occurs inadvertently during dissection of the adhesions

and, because of an associated subacute obstruction or abscess, the fistula blows postoperatively. Enterocutaneous flstulae can be divided into: those with a high output, more than 1 litre/day; those with a low output, less than 1 litre/day. They can also be described anatomically as simple, with a direct communication between the gut and the skin, or complex, that is, those with one or more tracts that are tortuous and sometimes associated with an intervening abscess cavity half-way along the tract. The discharge from a fistula connected with the duodenum or jejunum is bile stained and causes severe excoriation of the skin. When the ileum or caecum is involved the discharge is fluid faecal matter; when the distal colon is the affected site it is solid or semisolid faecal matter. The site of leakage and the length of the fistula can be determined by small bowel enema and barium enema, by fistulography and most importantly CT of the abdomen will show up any associated abscesses (Fig. 57.51). Treatment This can be very challenging in patients with a high-output fistula. Low-output fistulae can be expected to heal spontaneously, provided there is no obstruction beyond the fistula opening. Reasons for failure of spontaneous healing also include: epithelial continuity between the gut and the skin; the presence of active disease where, for example, there is Crohns disease or carcinoma at the site of the anastomosis or in the tract; an associated complex abscess. The abdominal wall must be protected from erosion by the use of appliances. The patient must remain nil by mouth, intravenous nutrition is started and signs of a decrease in the fistula output are sought. The higher the fistula in the intestinal tract the more skin excoriation must be expected, and this is worst in the case of a duodenal fistula. High-output fistulae cause rapid dehydration and hypoproteinaemia. Vigorous fluid replacement and nutritional support are essential. The drainage of an intraabdominal abscess can be life saving. This can be achieved by either CT-guided drainage or occasionally laparotomy. In patients with a complex fistula it may be necessary to bring out a defunctioning stoma upstream of the fistula site, even if this results in a high-output stoma. Treatment with a somatostatin analogue (octreotide) may be useful in these cases to reduce fistula output and stoma output. Operative treatment Operative repair should only be attempted after a trial of conservative management. The surgery can on occasion be technically extremely demanding and anastomosis should not be fashioned in the presence of continuing intra abdominal sepsis or when the patient is hypoproteinaemic. Stomas Colostomy A colostomy is an artificial opening made in the large bowel to divert faeces and flatus to the exterior, where it can be collected in an external appliance. Depending on the purpose for which the diversion has been necessary a colostomy may be temporary or permanent. Temporary colostomy This is most commonly established to defunction an anastomosis after an anterior resection, to prevent faecal peritonitis developing following traumatic injury to the rectum or colon, and to facilitate the operative treatment of a high fistula in ano. It is

now less commonly used for patients with distal obstruction of the sigmoid colon as a result of carcinoma or diverticular disease. A temporary colostomy is made bringing a loop of colon to the surface (loop colostomy) where it is held in place by a plastic bridge passed through the mesentery. Once the abdomen has been closed the colostomy is opened and the edges of the colonic incision are sutured to the adjacent skin margin (Fig. 57.52). When firm adhesion of the colostomy to the abdominal wall has taken place, after 7 days the bridge can be removed. A loop of colon can most easily be brought to the surface using large bowel that has a mesentery. Most loop colostomies are made in the transverse colon but the sigmoid colon can also be suitable. Following the surgical cure or healing of the distal lesion for which the temporary stoma was constructed, the colostomy can be closed. It is usual to perform a contrast examination (distal loopogram) to check that there is no distal obstruction or continuing problem at the site of previous surgery. Colostomy closure is most easily and safely accomplished if the stoma is mature, that is, after the colostomy has been established for 2 months. Closure is usually performed by an intraperitoneal technique which is accompanied by fewer closure breakdowns with faecal fistulae. Double-barrelled colostomy This colostomy was designed so that it could be closed by crushing the intervening spur using an enterotome or a stapling device. It is rarely used now but occasionally the colon is divided so that both ends can be brought separately to the surface ensuring that the distal segment is completely defuntioned. Permanent colostomy This is usually formed after excision of the rectum for a carcinoma by the abdominoperineal technique. It is formed by bringing the distal end (end colostomy) of the divided colon to the surface in the left iliac fossa, where it is sutured in place joining the colonic margin to the surrounding skin. The point at which the colon is brought to the surface must be carefully selected to allow a colostomy bag to be applied without impinging on the bony prominence of the anterosuperior iliac spine. The best site is usually through the lateral edge of the rectus sheath, 6 cm above and medial to the bony prominence (Fig. 57.53). An important point after the colostomy has been made is to close the lateral space between the intraperitoneal segment of the sigmoid colon and the peritoneum of the pelvic wall, to prevent internal herniation of strangulation of loops of small bowel through the deficiency. Alternatively a retroperitoneal tunnel for the colostomy avoids creating lateral space. Colostomy bags and appliances (Fig. 57.54) Faeces from a permanent colostomy ate collected in disposable adhesive bags. A wide range of such bags is currently available. Many now incorporate a stomahesive backing, which can be left in place for several days. In most hospitals a stoma care service is available to offer advice to patients and to acquaint them with the latest appliances, and the appropriate psychological and practical help. Complications of colostomies The following complications can occur to any colostomy but are more common after poor technique: prolapse; retraction; necrosis of the distal end;

stenosis of the orifice; colostomy hernia; bleeding (usually from granulomas around the margin of the colostomy); colostomy diarrhoea: this is usually an infective enteritis and will respond to oral metronidazole 200 mg three times daily. Many of these complications require revision of the colostomy. Sometimes this can be achieved with an incision immediately around the stoma but on occasion reopening the abdomen and freeing up the colostomy may be necessary. Occasionally transfer to the opposite side of the abdomen may be necessary. Loop ileostomy An ileostomy is used by some surgeons as an alternative to colostomy, particularly for defunctioning a low rectal anastomosis. The creation of a loop ileostomy from a knuckle of terminal ileum has already been described. The advantages of a loop ileostomy over a loop colostomy are the ease with which the bowel can be brought to the surface and the absence of odour. Care is needed, when the ileostomy is closed, that suture line obstruction does not occur. Caecostomy This is rarely used now. In desperately ill patients with advanced obstruction, a caecostomy may be useful. In late cases of obstruction the caecum may become so distended and ischaemic that rupture ofthe caecal wall may be anticipated. This can occur spontaneously giving rise to faecal peritonitis or at operation when an incision in the abdominal wall reduces its supportive role and allows the caecum to expand. In such a situation it should be decompressed by suction as soon as the abdomen is opened. In thin patients it may then be possible to carry out direct suture of the incised or perforated caecal wall to the abdominal skin of the tight iliac fossa, although a resection of this area is really the best treatment. Following on-table lavage, via the appendix stump the irrigating catheter can be left in place as a tube caecostomy. Caecostomy is only a short-term measure to allow a few days for the condition of the patient to improve. Reoperation should normally follow fairly soon thereafter and a proper surgical procedure carried out. Further reading Allan, R.N., Keigliley, M.R.B., Alexander, J. and Hawkins, E. (1990) Inflammatory Bowel Diseases, Churchill Livingstone, Edinburgh. Keighley, M.R.B. and Williams, N.S. (1999) Surgery of the Anus, Rectum and Colon, 2nd edn, WB. Saunders, London.