25. 1 Acute pancreatitis

Вид материалаДокументы

Содержание


Normal structure
Meckel's Diverticulum
Haemorrhage per rectum
Chronic peptic ulceration
Hirschsprung's Disease
Aganglionic colon does not allow normal peristalsis to occur and functional obstruction supervenes.
Differential Diagnosis
Intestinal conditions occurring in infancy and childhood
Clinical Features
Special Investigations
Reduction by hydrostatic pressure
INTESTINAL DIVERTiCULOSIS
Jejunal Diverticula
Diverticular disease of the colon
Colonic diverticulitis
Intestinal obstruction
Surgical Treatment
Primary resection with anastomosis
Three-stage procedure A
Acute necrotising enteritis
...
Полное содержание
Подобный материал:
1   ...   10   11   12   13   14   15   16   17   ...   32

NORMAL STRUCTURE

The small intestine consists of the duodenum, jejunum and lleum. The jejunum and ileum together extend from the duodenojejunal junction to the Ileocaecal valve. The jejunum accounts for the proximal 40 per cent and the ileum for the distal 60 per cent.

The wall of the small bowel consists of the mucosa, submucosa, the muscle coat (muscularis propria) and the serosa. The mucosa is composed of an epithelial layer, a. lamina propria and a muscularis mucosa.

The small gut is suspended by its mesentery which extends from the left side of the second lumbar vertebra to the right iliac fossa. The number of arterial arcades in the mesentery increase in number from 1 to 2 in the proximal jejunum to 4 to 5 in the distal ileum, a finding that helps to distinguish the two at operation. The luminal surface of the Jejunum shows more prominent valvulae connlventes and in the lower part of the ileum they almost disappear. The mucosa has a basal layer; villi project upwards from this layer and crypts of Lieberkuhn descend downwards from it. The villous folds increase the absorptive surface. The vllli can be narrow and finger-like or broad and leaf-like. Each consists of , a core of lamina propria and a covering of epithelial cells which are either absorptive-type cells (entero-cytes) or goblet cells which secrete mucus. The crypt linings contain Paneth cells and endocrine cells in addition to the enterocytes and goblet cells. The endocrine cells contain cytoplasmic granules that contain 5 hydroxytryptamine and various peptides. Other cells containing cholecystokinin and motllin are also present. The mucosal surface is thrown up into folds (valvulae conniventes) which are visible macroscoplcally and on plain abdominal X-ray when the small bowl is distended with gas as in intestinal obstruction.

The whole of the jejunum and lleum Is supplied by the superior mesenteric artery and venous drainage is to the portal vein. The lymphatics drain to the superior mesenteric nodes.

The large bowel consists of the caecum, ascending colon, hepatic flexure, transverse colon, splenic flexure, descending colon, sigmoid colon and rectum. The caecum is the part below the Ueocaecal valve. The sigmoid colon extends from the brim of the pelvis to the rectum and the rectum starts opposite the sacral promontory.

The large bowel wall, like the small bowel wall, consists of a mucosa, a submucosa, a muscularis propria and a serosa. The epithelium of the mucosa forms tubules which are nonbranching and parallel to each other and extend down to the muscularis mucosa. There are no villl. The surface cells are mainly absorptive in type while the crypts are lined mainly by goblet cells and occasional endocrine cells.

Very few lymphatics pass through the sub­mucosa into the lamina propria and this is of Importance In the pathology of malignant disease. The muscularis propria has an inner circular and outer longitudinal layer. The longitudinal coat of muscle is condensed into three bands termed taenlae coll and the large bowel Is characterised by sacculations or haustra which appear on X-ray as Incomplete septa projecting into the gas shadow when the colon Is distended.

The colon from the caecum to the splenic flexure is supplied by the superior mesenteric artery. The rest of the colon is supplied by the inferior mesenteric artery. The rectum is supplied by the superior rectal artery (a branch of the inferior mesenteric), the middle rectal artery (a branch of the internal iliac), and the inferior rectal arteries (from the internal pudendal). Lymphatic drainage is to the epicolic, paracolic and the Intermediate nodes and then follows the course of the arteries.

Meckel's Diverticulum

The vitellointestinal duct connects the midgut to the yolk sac in embryonic life. If the proximal portion persists it forms a Meckel's diverticulum

This is present in about 2 per cent of the population and it lies on the antimesenteric border of the ileum, approximately 2 feet from the ileocaecal valve. It measures up to 2 inches in length. The tip may be connected to the umbilicus by a fibrous cord although it is usually free. A terminal branch of the superior mesenteric artery crosses the ileum to supply the diverticulum.

The muscle coat of the divertilculum Is continuous with that of the ileum. The lining mucosa is small bowel in type but may contain ectopic mucosa. The ectopic mucosa is gastric in 80 per cent of the cases, the remainder being pancreatic or colonic. Gastric epithelium may give rise to peptic ulceration either in the diverticulum or in the adjacent ileum.

Meckel's divertlculum makes itself known only by its complications. A patient with Meckel's diverticulum has about 4 per cent chance of developing a complication in a lifetime. In order of frequency, these complications are as follows.

1. Haemorrhage per rectum This Is due to peptic ulceration in the heterotopic gastric epithelium in the Meckel's diverticulum. It presents with painless, periodic, brisk and severe bleeding in childhood.

2. Intestinal obstruction Intestinal obstruction is caused by a fibrous cord or by the diverticulum inverting and causing an Intussusception or becoming incarcerated In a femoral or inguinal hernia (Littre's hernia).

3. Meckel's diverticulitis The symptoms are akin to acute appendicitis. Acute inflammation is usually associated with obstruction of the mouth of the diverticulum by oedema, food residue or foreign body. A diverticulum may perforate into the general peritoneal cavity and the clinical picture resembles a perforated duodenal ulcer. Urgent surgery is required whether or not perforation has taken place.

4. Chronic peptic ulceration Because the diver­ticulum is a part of the midgut, the pain though related to meals, is felt around the umbilicus.

5. The diverticulum may be found at the proximal end of the discharging umbilical sinus in 5 per cent of the cases. -•

Investigations

A firm preoperative diagnosis of Meckel's diver­ticulum is unusual except in children with rectal bleeding or in the case of an umbilical fistula. In rectal bleeding, radioisotope scanning has been found useful. Tc99m pertechnetate is Injected intravenously. The isotope is taken up by the gastric mucoid cells and will show as a hot spot, usually in the lower abdomen to the right of the umbilicus. It is difficult to identify a diverticulum on routine barium examination because of the overlying loops of bowel and because the diverticulum is self emptying.

Management

The suggested management of Meckel's divertt-culum is outlined in Chart 45.1.

1. Diverticulum is excised together with a wedge resection of the adjacent ileum.

2. It should not be amputated at its base and invaginated in the same way as a vermiform appendix because of the risk of stricture and it may act as an apex of intussusception.

3. Moreover, it does not remove the heterotopic epithelium completely if such be present. It Is better to resect a small segment of ileum containing the diverticulum because it is here that the ectopic gastric mucosa and ulceration is often situated, rather than in the diverticulum Itself. After resection, the bowel continuity Is restored by end-to-end anastomosis.


Hirschsprung's Disease (Congenital Megacolon)

During normal embryonic development, pre-ganglionic parasympathettc nerve fibres from both the vagal and sacral outflow grow into the bowel. Ganglion cells later migrate from the neural crest and pass along these fibres to take up their place in the submucosal and intermuscular plexus. In Hirschsprung's disease, there is a partial failure of ganglion cell migration and the ganglion cells in a segment of large bowel are absent.

Hirschsprung's disease shows a familial tendency and occurs in about one in 20,000 births. Males are affected five times more than females. Most cases of agangllonosis involve the rectum and rectosigmoid but longer segments of absent ganglion cells may also occur, and total colonic aganglionosis, although rare, is also seen.

Aganglionic colon does not allow normal peristalsis to occur and functional obstruction supervenes.

Clinical Features

The patient usually comes in Infancy, sometimes In early childhood and occasionally in adult life.

Infants The infant fails to pass meconium during the first 2 or 3 days of life. By the third day. the abdominal distension is obvious and complete obstruction may occur. As a rule, the relief is given by a small enema or by passing a greased examining finger (with expulsion of stool and flatus).

At times, there is chronic obstruction characterised by chronic constipation alternated by episodes of diarrhoea associated with passage of large amounts of foul smelling gas.

Children The Infants who survive may present during childhood as (i) constipation dating from birth. The stools are hard and likened to "goat pellet" (ii) malnutrition, and (ill) abdominal distension. The abdomen has a characteristic appearance. Abdominal muscles become thin from stretching and there are prominent veins on it. Impacted stools in the greatly dilated sigmoid colon can be palpated across the lower abdomen.

Rectal examination reveals a normal or contracted anus and a rectum without faeces.

Adults Very occasionally, the symptoms become severe as late as in the adult life when the patient seeks advice.

Diognosis

Plain abdominal X-rays in infants show dilated loops of bowel, but it is difficult to distinguish between small and large bowels in infancy. A barium (in saline) enema X-ray should be per­formed. It is done in an unprepared bowel (as the preliminary washout often minimises the dilatation of the gut above the obstruction). The barium enema should be prepared with normal saline (not with water) because the megacolon absorbs water much more rapidly than normal colon and this may result in water intoxication. In infants, the barium is retained for 24 hours or more and delayed films after 24 hours are necessary.

In children, the characteristic radiological finding is a narrow agangllonic segment, the funnel shaped transitional zone, and the increasingly dilated proximal colon.

Rectal biopsy Definitive diagnosis is made on either a full thickness rectal biopsy or a partial thickness suction biopsy. Partial thickness "mucosal" biopsy may be taken from the posterior rectal wall with a suction biopsy capsule, without anaesthesia. If the histology findings are equivocal, it Is necessary to take a 1x2 cm full thickness rectal biopsy from the posterior rectum proximal to the dentate line, .under anaesthesia. The two cardinal features are a complete absence of ganglion cells and an increase in nonmyelinated nerve fibres in the submucosa and In the Inter -muscular plane. Since these nerves are chollnergic, an increase in acetylcholine activity in specially stained sections is helpful In diagnosis and even superficial biopsies in expert hands may be diagnosed. The site of biopsy must be about 2 cm above the dentate line.

Differential Diagnosis

The main differential diagnosis is with idlopathic megacolon (functional constipation). It occurs in older children or in adults. The dilatation extends up to the anus which means that the rectum is also dilated. This may be a result of habitual constipation. Rectal examination reveals a loaded rectum. Treatment consists of regularisation of bowel habits.

Complications

1. Death rate of untreated agangllonic megacolon In infancy may be very high. A serious complication is the development of enterocolitls.

2. Ischaemic necrosis and perforation of the bowel above the agangllonic segment may develop and cause a presentation similar to neonatal necrotlsing enterocolitls.

Treatment

The aim of surgery Is to excise the whole length of the agangllonic segment (which Is the cause of the functional obstruction) and to restore continuity. In other words, the upper limit of resection must include the transitional zone and a little of healthy dilated colon above it while the lower limit should be so designed as to preserve the anal canal with Its sphincters.

The majority of patients are neonates or infants and in these an emergency colostomy Is required to save life and the definitive operation of resection has to be postponed to a later date. One stage surgery is only done for those who are In moderately fair health and over the age of 2 years.

Colostomy may be either left iliac or transverse colostomy. During the operation of colostomy, it is always advisable to put a marker with black silk at the lowermost limit of the dilated ganglionic segment and it helps during the operation of resection.

Definitive operation Three type of operation are practised.

1. Swenson's operation

2. Duhamel's operation

3. Soave's operation

1. Swenson's operation It is a combined abdominal and anal approach. The inferior mesenteric artery Is divided and the sigmold colon and rectum are mobilised to as far down as possible. During mobilisation, dissection is done as close to the wall of the gut as possible, in order to avoid injury to the pelvic nerves, etc. A line of junction between the ganglionic and the aganglionic segments is made out and the gut is divided a little proximal to this junction. The distal cut end is closed in the form of a stump. A long artery forceps is now introduced per anus and the stump is held with the tip of the forceps. As the artery forceps is withdrawn, the distal loop of gut containing agangllonic segment and the normally Innervated anal canal, are everted. A transverse Incision is made on the anterior wall of this everted loop, 2 cm from the anus. Through this opening, the long forceps Is reintroduced and the proximal divided end of the colon is pulled through It. The anal canal is completely divided along the same line in which it was Incised on Its anterior wall. Thus, the whole length of the agangllonic segment is resected. To the cut end of the anal canal. Is anastomosed the cut end of the "pulled through" colon. The suture line together with the anal canal Is Inverted through the anus.

The above is the historical description of the original Swenson procedure. With the use of the stapling device, there Is no need to evert the anal and end-to-end anastomosis is possible within the pelvis.

2.. Duhamel's Operation In Swenson's, the normal rectal sensation Is lost In the absence of the rectum. In Duhamel's, only the aganglionic segment of the colon is excised per abdomen and the rectum is preserved. The cut end of the rectum is closed. The upper cut end of the colon is brought down behind the rectum. It is then made to traverse through the posterior wall of the anal canal between the fibres of the internal sphincter, so that it finally emerges at the anus posteriorly, but in the submucous plane (i.e. not in the anal lumen). After an interval of 3 weeks an enterotribe is used to crush the partition between the two lumens.

The end of the proximal colon is anastomosed to an incision made in the posterior wall of the rectum, 1 cm above the dentate line. The intervening spur of rectum and bowel is divided and a side-to-anastomosis is made with a stapler to form a common rectal reservoir.

3. Soave's operation It also retains the rectum, excising only the aganglionic part of the colon. The rectum is denuded of its mucous mem­brane. Thereafter, the proximal colon is pulled ' through the lumen of the rectum and the anal canal, and is sutured to the anus .

INTESTINAL CONDITIONS OCCURRING IN INFANCY AND CHILDHOOD

Neonatal Necrotising Enterocolitis

This condition usually affects premature infants, in the first week of life, who have often undergone some form of stress such as perinatal hypoxia.

The aetiology is unknown. The most likely explanation is that the bowel becomes ischaemic and is then secondarily invaded by the bacterial flora of the bowel lumen. The reason for the ischasmia is uncertain although it is possible that blood is redistributed away from the splanchnic circulation during periods of perinatal stress, resulting in mesenteric hypoperfusion.

The terminal ileum and right colon are the most commonly affected sites and show gross vascular congestion with mucosal haemorrhages, ulceration and necrosis. Small submucosal gas bubbles may be seen on careful naked eye examination.

Microscopically, there is marked vascular congestion and oedema with necrosis of the mucosa. A pseudomembrane of necrotic epithelium and debris is commonly present. Gas bubbles appear as cyst-like spaces in the submucosa and are important in diagnosis, both radiologically and microscopically. Surgical resection may be required and in those patients who survive without resection, a stricture may form in the affected part of the bowel.

Intussusception

Intussusception is the invagination of one part of the small or large bowel into the next part. It almost invariably occurs in a forward direction. Very rarely indeed is an intussusception retrograde.

There are two distinct categories:

1. There is a definite cause for intussusception such as an intestinal polyp, an inverted Meckel's diverticulum or a food bolus. Adults and older children are usually the victims. This is not very common.

2. There is no definite cause. Majority of cases of intussusception belong to this group which is known as idiopathic intussusception. Most of the cases occur in children between the sixth and the eleventh months of age. Boys are affected more. It is more common in spring and autumn and in fat rather than thin infants.

The aetiology of intussusception in children is not clear. The most likely explanation is that the hypertrophy of the lymphoid tissue of Peyer's patches acts as a starting point for the intussusception. This view Is substantiated by the fact that Idiopathic intussusception most commonly occurs in the terminal part of the lleum which is rich in Peyer's patches. As to the cause of the inflammation of the lymphoid tissue, there are the following views.

1. Change in the intestinal flora, caused by the change in the child's diet at the age of about 1 year.

2. Infection, secondary to upper respiratory infection and mostly viral. Adenovirus antibodies have been Isolated In most cases of Intussusception.

Intussusception can be lleoileal, ileocolic (more than 70%) or jejunal.

The invaglnated segment is termed the tatus-susceptum and the receiving segment is termed the intussuscepiens. That part which advances is the apex. The blood supply of the inner layer (intus-susceptum) is impaired due to pressure on the invaginated mesentery (causing occlusion of veins Initially) with resultant haemorrhagic infarction of the bowel.

Clinical Features

Except for those where there is a definite cause, the majority affect the healthy, first born male child between the age of six to eleven months.

-The child gets paroxysms of abdominal pain, draws up the legs and screams. The pain occurs at intervals of 15-20 minutes, and the child is often lethargic, pale, and refuses feeds. Vomiting is late to appear because the obstruction is in the lower gut. In the early stages a normal stool is frequently passed, later blood and mucus (the "red currant jelly" stool) is passed.

On examination, the abdomen is not distended. The mass of intussusception (a palpable abdominal tumour) in the left hypochondrium may be made out by gentle palpation. There is said to be a feeling of emptiness in the right iliac fossa (Dance's sign) which is caused by the shifting of its contents. On rectal examination, the examining finger is smeared with red-currant jelly. Occasionally, the intussusception may be felt at the tip of the finger, like the cervix uteri in the vagina. Unrelieved, the pain becomes continuous. After a day or two, the abdomen commences to distend and vomiting becomes copious. Only 20 per cent of children present in this typical manner (in approximately 35% a mass is not palpable, in 35% rectal blood and mucus are absent, and in 20% there is no obvious colic). The diagnosis is often not made until the condition is well advanced, by which time the intussuscepted bowel may be gangrenous.

Special Investigations

Straight X-ray of the abdomen shows increased gas shadows in the small intestine and caecal gas shadow is not seen.

Barium enema is diagnostic for Ileocolic intussusception. The enema stops as it reaches the intussusceptum and gives a horseshoe deformity.

Treatment

Hypovolaemia and dehydration must be corrected by fluids. In the absence of peritonitis and intestinal obstruction, the initial treatment may be by hydrostatic barium enema which is successful in 50% of the cases. Operative reduction becomes necessary when the hydrostatic reduction is Incomplete, uncertain or contraindicated (signs of bowel perforation and peritonitis). If the history is longer than 48 hours, the hydrostatic reduction may not succeed.

Reduction by hydrostatic pressure Barium enema should not be attempted until the patient has been resuscitated enough to allow an operative procedure to be performed safely. The baby is sedated. The barium is given under X-ray control in an effort to distend the intussuscipiens and reduce the Intus­susceptum. The enema column should not be raised more than 75 cm above the patient. The buttocks are strapped to prevent the expulsion of barium. Complete reduction is confirmed when the contrast is seen to flow fieely and reach the terminal ileum. The abdominal mass, if present should disappear. If the first enema is unsuccessful, it should be repeated. Barium enema, however, will not reduce gangrenous bowel.

Operative reduction The abdomen Is opened through a right transverse incision placed about 1 cm above the umbilicus. The reduction is accomplished by squeezing the lowest part of the sausage like mass. The last part is the most difficult to reduce. In case of difficulty reduction may be achieved by the following.

1. Dissecting gently the adhesions at the neck between the intussusceptum and intussuscipiens

2. Squeezing on the intussusception by fingers in order to displace the oedema from the region of the ileocaecal valve.

3. At no time should traction be applied to the proximal ileum.

Resection and anastomosis The indications are (i) gangrenous change, (ii) impossible reduction, and (lli) badly injured gut during the process of reduction.

In the usual type (Ueocolic), a right hemicolec-tomy has to be performed. Primary anastomosis is recommended but a Mikulicz resection may be necessary in critically ill patients.

Recurrence following successful management of an Intussusception is about 3%.

Mortality is related to delay in diagnosis.

INTESTINAL DIVERTiCULOSIS

Two types of divertlcula, congenital and acquired, are seen in the Intestinal tract. Apart from the Meckel's divertlculum, congenital diverticula are produced as a result of reduplication of the gastrointestinal tract. The acquired diverticula of pulsion type are more common and are produced as a result of mucosal hemiation through a defect in the muscular wall at the point of entrance of a blood vessel. Pulsion diverticula are found in the duodenum and the proximal jejunum and colon. • Duodenal Diverticula

They are found in older patients on the Inner wall of the second and third parts of the duodenum. They may be an incidental finding on barium meal and usually do not cause symptoms. The most common site is near the ampulla of Vater. It is claimed that duodenal diverticula may occasionally obstruct the termination of the common bile duct or even the pancreatic duct. However, it is unusual for duodenal diverticula to be operated on, though there are reports of haemorrhage occurring as a complication.

Jejunal Diverticula

They are seen usually in middle-aged males, and about 5-10 diverticula are located along the mesenteric border of the proximal 18 inches of the jejunum. The diverticula are mucosal hemiations and are devoid of any muscular wall. Clinically, they may (i) be symptomless, (ii) give rise to abdominal pain and flatulence, or (ill) lead to attacks of acute abdominal pain. Many cases develop. acute intestinal obstruction due to jejunal volvulus secondary to these diverticula. As the diverticula are devoid of any muscular wall, they result in stasis of food particles. The diverticulum may perforate and give rise to peritonitis.

Treatment

If jejunal diverticulosis is asymptomatic, no active surgical treatment is necessary. In the majority of cases resection and end-to-end anastomosis gives good results.

DIVERTICULAR DISEASE OF THE COLON

They are the acquired herniations of mucosa protruding through the circular muscle at the points where the blood vessels penetrate the colonic wall. They are devoid of any muscle in the wall. Diverticula vary from a few millimetres to several centimeters in diameter, the necks may be narrow or wide, and some contain inspissated faecal matter. The condition may be localised to one part of the colon, usually the sigmoid colon.

While diverticulosis of the colon is so common in the West, it is rare in the Indian subcontinent. This rarity is partly due to the high residue diet of Indians, as compared to the refined low residue diet of Europeans. High intraluminal pressure and weakness of the colonic wall may be two factors important in the pathogenesis of diverticula.

Diverticulosis remains asymptomatic in most people and is detected incidently on barium enema X-rays. In addition to diverticula, barium enema films may show segmental spasm and muscular thickening that narrow the lumen and give it a "saw tooth" appearance .

In some, the disordered colonic function may cause symptoms of distension, flatulence and a sensation of heaviness in the lower abdomen. Excessive colonic segmentation can cause severe colic pain in the left iliac fossa. This pain waxes and wanes rapidly and is in fact due to spastic obstruction of the colon.

Diverticulosis should be treated with a high residue diet. It is. however, not certain that complications of diverticulosis can be so avoided. Breakfast cereals are the most convenient agents to use. Pain may require antispasmodics. Habitual purgation should be avoided.

Colonoscopy may become necessary for massive haemorrhage to rule out carcinoma.

COLONIC DIVERTICULITIS

It either occurs with perforation due to raised intraluminal pressure or begins as an infection in a diverticulum. Only one diverticulum is involved at a time, usually in the sigmoid colon. Episodes of diverticulltis may be followed by years free of symptoms, but the condition is essentially progressive — the longer the duration, the worse are the symptoms and the greater the risk of complications.Clinical Features

The acute attack consists of localised abdominal pain that is mild to severe. It resembles acute appendicitis except that it is situated In the left lower quadrant. The patient may pass loose stools or may be constipated. Abdominal distension may be relieved by passage of flatus. Inflammation adjacent to the urinary bladder may produce dysuria. Nausea and vomiting depend on the location and severity of the inflammation. Physical findings Include low grade fever, mild abdominal distension, left lower quadrant tenderness, and a left lower quadrant or pelvic mass.

Complications

These Include the following.

1. Perforation Small-sized perforation may lead to localised inflammation In the colonic wall or paracollc tissues. Macroperforation results in more extensive bacterial contamination and more serious infection such as an abscess or generalised peritonitis.

2. Fistula formation An abscess may be confined by adjacent structures or may enlarge and spread; it may reabsorb with antibiotic treatment or drain spontaneously into the lumen of the bowel or into an adjacent viscus to form a fistula. Coloveslcal fistula is the commonest type which typically presents as pncumaturia. Patients rarely pass urine per rectum as the colonic pressure is higher than the bladder pressure.

3. Intestinal obstruction Small bowel may adhere to an inflamed area and cause small bowel obstruction.

4. Haemorrhage Haemorrhage usually occurs in diverticulosis rather than divertlculitis. Since the divertlcula protrude through the colonic wall where blood vessels enter, it is perhaps not surprising that erosion or ulceratlon of the wall of the divertlculum will lead to massive haemorrhage.

/ Investigations

Plain X-ray abdomen may show free abdominal air if a divertlculum has perforated into the general peritoneal cavity. If inflammation is localised, there is a picture of ileus, multiple fluid levels, etc.

CT-scan is proving to be more useful than water soluble contrast enema. Contrast enhanced CT may show perlcolic abscess or fistula. The location of an abscess accessible for percutaneous drainage provides a major therapeutic advantage.

Barium enema is contralndicated during the initial stages of an acute attack lest barium leaks into the peritoneal cavity. Water soluble contrast media used under low pressure is, however, safe. It is preferable to defer the barium enema until the episode of acute diverticulitis has settled.

Flexible sigmoidoscopy and colonoscopy should also be avoided during an attack. It is, however, useful in the later stages to evaluate other abnormalities. Cystoscopy may reveal oedematous change in the bladder area adjacent to diverticulitis.

Differential Diagnosis

Free perforation of a diverticulum with generalised peritonitis may be dificult to differentiate from the other causes of perforation.

Acute localised diverticulitis may simulate appendicitis except that the pain is on the left side. Amoebic colitis may present as pain and tenderness in the left iliac fossa.

A difficult differentiation lies between diver­ticulitis and carcinoma of the colon. Persistent bleeding should not be attributed to diverticular disease until malignancy has been excluded.

Management

Generally, nothing is given by mouth, nasogastric suction is instituted, intravenous fluids are given and, parenteral antibiotics administered. Analgesics are prescribed. As acute manifestations subside, oral feeding is resumed gradually. The diagnosis must be confirmed by an Investigative work-out.

Surgical Treatment

Immediate operation is required if generalised peritonitis is present. Abdominal pain. mass, fever or leucocytosis that fells to improve after 3-4 days of medical therapy also Indicates surgical intervention.

At laparotomy, the peritoneal fluid varies from turbid to purulent to grossly faecal. The extent of colonic inflammation, the amount of peritonitis, the patient's general condition, and the surgeon's experience and preferences determine the type of operation to be performed.

1. Primary resection with anastomosis It is not safe, if the bowel is oedematous or there is gross infection in the surgical field because of the risk of anastomotic leakage.

Resection for sigmold diverticulitis should include the rectosigmoid distally to the point where the taenlae become confluent;

anastomosis being performed to the proximal rectum, which is always free of diverticula. The distal descending colon is removed but there Is no need to resect too much proximally even if involved with diverticula; they do not become symptomatic in the absence of the high pressure zone of the sigmoid.

2. Primary resection without anastomosis (2 stage procedure) The diseased bowel is removed, the proximal end is brought out as a temporary colostomy, and the distal colonic stump is closed (Hartmann procedure). Intestinal continuity being restored In a second operation after the inflammation subsides.

3. Three-stage procedure A preliminary trans­verse colostomy can be done as a first stage and the paracollc abscess is drained; in the second stage operation the left colon is resected; and after further two weeks the colostomy is closed. Colovesical fistula may cause surprisingly little disturbance to the patient. Pneumaturia may be recollected only in response to direct questioning. A fistula requires surgical treatment only if it persists and there is never a need for emergency operation. Diverticulitis is managed by bluntly dissecting the colon from the bladder, resecting the colon, and performing a primary anastomosis.

ACUTE NECROTISING ENTERITIS

It is a distinct cllnlcopathological entity primarily affecting the Jejunum. This is different from necrotising enterocolitis of infancy and ischaemic enteritis of old age. These patients mostly come from a low socioeconomic background — labourers and farmers. They live in unhygienic surroundings and consume a poor and unbalanced diet. The possible factors responsible for this disease may be prolonged malnutrition and protein deficiency, reducing pancreatic and other digestive proteases. If this individual is now exposed to the contaminated food, there is failure of proteolysis of the organisms and their toxins. The whole brunt of the attack falls on the jejunum.

Pathology

Jejunum Is the principal site of affection. In the early stage, lesions are patchy and spread out. hi later stage they may be confluent and affect 2-4 feet of jejunum. The mucosa shows continuous areas of necrotic mucous membrane. In late stages, areas of frank gangrene are seen on the surface. Mesenteric vessels are normal and pulsatile. The peritoneal cavitvcontains fluid which may be serous or seropurulent. Frank peritonitis is seen when gangrene supervenes.

Clinical Features

The disease is common in summer and affects males more often than females. Majority of cases are seen in the age group of 25-50 years. The patient suffers from acute abdominal pain, vomiting and mild fever. He develops abdominal distension and diarrhoea. Frank melaena is seen in many cases. In the later stages, the patient develops high fever and becomes toxic. Abdominal tenderness is generalised but more marked in the left upper abdomen. Rigidity, guarding and rebound tenderness are present. Peristalsis is normal or slightly increased in the initial stages and absent later.

Clinically, the patient presents a mixed picture of intestinal obstruction and acute peritonitis of varying severity. Plain X-ray of the abdomen shows dilated loops of the small intestine.

Treatment

The patient is treated conservatively with bed rest, nasogastric suction, IV fluids and electrolytes, antibiotics and metronidazole. The indications for surgery are rising pulse rate, appearance of abdominal rigidity, a palpable lump, severe bloody diarrhoea and toxaemia.

During exploration, early lesions may be left alone. Advanced lesions may need resection. In presence of frank gangrene and peritonitis, the prognosis is grave.

INFLAMMATORY BOWEL DISEASE (CROHN'S DISEASE AND ULCERATIVE COLITIS)

Inflammatory bowel disease is the term commonly used to include ulcerative colitis and Crohn's disease. It Is rare in the tropical countries, but more common In Northern Europe, the UK and the USA. Though excluded from this category, a number of inflammatory disordes (e.g. tuberculosis or amoebic colitis) are far more common, in the Indian sub­continent and Africa, than ulcerative colitis and Crohn's disease. Salmonella enteritis may mimic an acute episode of ulcerative colitis. With the rise In. air travel, the spectrum of disease has certainly lost its clear definition and tropical infective causes need to be excluded so that inappropriate surgery can be avoided.

Crohn's Disease

This is a nonspecific chronic granulomatous condition. It may affect any part of the gastrotntestinal tract although it has a propensity to occur In the small bowel, especially the terminal ileum and colon. The small bowel alone is affected in 66 per cent of the cases, small and large bowel together In 17 per cent, and the large bowel alone in 17 per cent. hi about 10-25 per cent of cases, there are 'skip' lesions in other parts of the intestinal tract.

The disease is slightly more common in women than men. It Is commonest in the second and third decades. There is evidence that heredity is a factor.

The commonest clinical presentation is a gradual onset of diarrhoea with or without a right iliac fossa mass. Abdominal pain is not uncommon.

Aetiology

The aetiology is not clear. Certain suggestions are enumerated in Table 45.1.

Suggested Cause Comment

Viral Infection and Mycobacterlum Kansasll Incriminated but not proved.

Diet and food allergy suggested but not proved. Increased Incidence of autoantlbodles. The most convincing aetiology till date.

Psychological problems are a consequence rather than a cause.

Pathology

The earliest feature is small punched-out ulcers on an otherwise normal mucosa. Later, deep linear ulcers are seen but in contrast to ulceratlve colitis the intervening mucosa is often normal. The mucosa eventually becomes thickened and oedematous but is not as friable as in ulcerative colitis. The affected bowel is thick and oedematous. The serosal surface often has a fibrlnous exudate and there is a tendency for several loops of gut to be matted together, possibly with concomitant abscess and fistula formation. The associated mesentery is often oedematous with enlarged lymph nodes caused by reactive hyperplasia.

The disease may lead to local or remote complications.

t Loco/ Complications

The inflammation involves all the coats and there are deep fissures and this may lead to perforation and peritonitis but more often, the process leads to local abscess formation which may lead to internal fistula, either to other loops of bowel or to the urinary bladder. External flstulae usually follow abdominal surgery. Chronic anal fissures, anal fistulae, or pararectal abscesses are seen in some cases.

In the colon, deep ulceratlons lead to toxic dilatation. Occasionally, massive haemorrhage occurs Into the wall or into the lumen of the bowel.

In long-standing Crohn's disease, malignant change has been recorded.

Remote Complications

These are similar to those associated with ulcerative colitis.

1. There is a higher incidence of other allergy related diseases, e.g. asthma and eczema.

2. There is a higher Incidence of fleeting joint pains and ankylosing spondylitis.

3. Eye disease (uveitis) may occur.

4. Sclerosing cholangitis and liver disorders, leading to cirrhosis are recognised in some patients.

5. Skin problems usually take the form of erythema nodosum associated with an acute exacerbation;

less often, skin necrosis (pyoderma gangrenosa) occurs.

Rectal bleeding is unusual In Crohn's disease but common in chronic ulcerative colitis. The findings of abdominal mass and complications are common in Crohn's disease.

Investigations

Barium study may show areas of the disease. The characteristic small bowel changes include areas of luminal narrowing with an Irregular thick bowel wall. There may be multiple skip lesions and areas of dilatation associated with obstruction. Deep fissuring ulcers or even fissuring may be demonstrated. The string sign of Kantor is due to narrowing of the terminal Ueum.

Blood tests including ESR and C-reactive protein give an Indication of the disease activity.

Management

A disease that may affect any part of the gastro-intestinal tract and is subject to recurrence is best treated by medical means. Complications and occasionally the severity of symptoms may require surgery in many cases.

Nutritional support is essential and anaemia is corrected. Medical management aims to control the Inflammatory process and allow remission. The principal agents used are sulphasalazine and steroids. Sulphasalazine is far more useful in preventing relapse in ulcerative colitis but its value is less certain in colonic Crohn's disease and unproved in small bowel Crohn's. Steroids bring acute, nonspecific colitis under control. This requires a high dosage which should be reduced as quickly as possible. Metronidazole particularly for small bowel disease may be exhibited.

Patients with extensive Intestinal involvement or sepsis may be severely malnourished. The serum albumin and the degree of weight loss may provide a rough estimate to the degree of nutritional depletion. Enteral feeding or in some even total parenteral nutrition may be necessary.

In cases with stricture causing obstruction and fistula or abscess formation, surgery Is Invariably necessary.

There Is as yet no effective adjuvant drug treatment which would reduce the long-term recurrence rate.

Individual Regional Involvement

Heal Crohn's disease The difficulties of distin­guishing acute Crohn's disease from acute appendicitis though exaggerated are still there. Should the abdomen be opened on the mistaken diagnosis of acute appendicitis and Crohn's disease is found, the one thing not to do is to remove the appendix. This may result in an external faecal fistula. Occasionally the condition resolves completely, more often chronic ileltis supervenes.

The commonest presentation of chronic lleitis is ill-defined abdominal pain and slightly increased frequency of stools. The diagnosis may be confirmed by small bowel barium contrast examination which may show a thin trickle of barium (Kantor's string sign) through the terminal ileum.

Most patients of chronic Heal disease will require surgical treatment. A reasonable surgical approach is a conservative bowel resection, 10 cm above the manifest disease and if colon is affected, the right hemicolectomy may be added.

In patients with multiple strictures In whom resection might lead to the possibility of short bowel syndrome, strictureplasty offers relief of obstruction without the need for resection.

When associated larger abscesses are present, it is advisable to merely drain them, some surgeons advise bypassing the inflammatory area by a defunctioning ileotransverse colostomy.

Colonic Crohn's disease The commonest pre­sentation is chronic diarrhoea, usually associated with bleeding and weight loss. Endoscopic examination may show patchy Inflammation, the ulcers in Crohn's disease often have a linear and deep appearance. Radiological study is helpful.

•Patients with acute Crohn's colitis (diarrhoea of 'sudden onset and with bleeding) should be distinguished from infective colitis; ischaemic colitis and diverticulitis. In tropical countries, amoebiasis is a far more common cause of colitis but is uncommon in Europe and the USA.

Parenteral nutrition and steroids are prescribed for acute colitis. If there is no response in 3-4 days, surgery is advocated. In less severe cases, medical treatment may be continued.

For patients in whom medical treatment has failed to control the chronic disease, surgical treatment is indicated. Diffuse colonic disease with involvement of the rectum requires proctocolectomy with ileostomy. In patients with little or no evidence of anal or rectal disease, but with extensive colonic involvement, a total colectomy with ileorectal anastomosis has a definite place.

Anal and rectal disease Over half the patients with large bowel Crohn's have an anal lesion. Fissure is the commonest problem and may heal with medical management or become chronic. A fistula in ano may develop, sometimes multiple, and may heal with conservative treatment. Occasionally conser­vative surgery with drainage of abscess cavities may be necessary. In more resistant cases defunctioning colostomy or proctectomy may be necessary.

Ulceratlve Colitis

It is more common in the United States and northern Europe than in Africa and India. It has a peak incidence in early adult life. Close relatives of patients with ulcerative colitis have an increased incidence of the disease. In spite of intensive bacteriological studies, no organisms or groups of organisms can be incriminated. There is some evidence that patients with ulcerative colitis have an intrinsic abnormality of the immune system.

During the last 30 years, more and more cases have been seen and reported in the Indian literature. The difficulty in Identifying the true cases of ulcerative colitis lies in the fact that several cases suffer from bacillary and amoebic colitis and the suspicion of ulcerative colitis is raised only when repeated stool examinations fail to show any causative organisms and there is no response to antlamoebic treatment.

Pathology

Almost always the disease starts in the rectum and extends proximally. The disease is confined to the rectum and distal sigmoid in 60% of the cases, extension to the splenic flexure is seen in a further 25% and in the remaining 15%. total colitis may occur and these are more at risk of developing toxic dilatation. If the ileocaecal valve is incompetent, retrograde extension into the terminal ileum (backwash ileitis) is liable to occur.

The disease is characterised by the appearance of multiple minute ulcers. As time goes on, the small ulcers are apt to coalesce to form larger ones. When the ulceration extends into the submucosa it causes reflex muscle spasm and the appearance of a stricture. In long-standing cases there is always considerable intramural fibres is. In addition, attempts at healing may produce epithelial thickening between the ulcers —the so called pseudopolyps.

Cases in which it is not possible, histologically, to differentiate ulcerative colitis from Crohn's disease are designated as indeterminate colitis. Indeterminate colitis behaves more like ulcerative colitis than Crohn's disease.

In longstanding colitis, epithelial dysplasia may occur, and when this is severe, carcinoma is frequently found at other sites in the colon.

Clinical Features

It has a peak incidence in early adult life. The disease is more common in women than men. The first symptom is watery diarrhoea, occurring day and night, in a person of previously normal bowel habit. The disease starts suddenly. There is a rectal discharge, commonly mucoid and sometimes purulent. Pain is usually absent. Two clinical types are encountered.

Fulminating type (5%) There Is Incessant diarrhoea, the stools containing blood, mucus and pus. There may be abdominal distension due to acute dilatation of the colon. With the onset of colonic dilatation, diarrhoea may give way to features of intestinal obstruction.

Chronic type (95%) The initial attack Is of moderate severity. Thereafter, at variable intervals, the patient gets bouts of diarrhoea. During the attack, stools are passed, ten to twenty times in 24 hours. There is an associated tenesmus. The number of stools and the days of suffering depend on the length of the colon involved. With each episode, the patient gets emaciated and anaemic and when the whole colon is involved, the patient may be so weak as to be partially or wholly bedridden.

Ulcerative colitis runs a considerably milder course in an Indian than in the Western population. In only a few, total colon involvement Is seen. Backwash ileitis is almost unknown and such local complications as pseudopolyposis, narrowing of the lumen and pipe-stem deformity, perforation and haemorrhage are not so often seen. It is rare to find complications such as acute dilatation. Fulminating type of disease is only occasionally seen in India.

Differential Diagnosis

The differential diagnosis includes Crohn's disease, ischaemic colitis, diverticular disease, carcinoma, irritable bowel syndrome, pseudomembranous colitis, bacillary dysentery and amoebic colitis. Corticosterolds must never be given to a patient with presumed idlopathic ulceratlve colitis until amoebiasis has been excluded.

Special Investigations

Barium enema study This is avoided in the fulminating type. The loss of normal colonic haustrations is the earliest change and is seen in the distal colon to begin with. The colon is narrow and contracted (pipe stem colon). Pseudopolyposis, characterised by small filling defects may be well demonstrated in some cases.

SIgmoldoscopy The initial findings are those of proctitis. The early changes observed are redness of the mucosa. In more severe disease, diffuse small ulcers on a red granular mucosa are seen, the mucosa Is friable and bleeds on touch. In amoebic dysentery, there are large deep ulcers with the intervening mucosa comparatively healthy.

Colonoscopy It may be a primary Investigation and is also used for assessing stricutres, in cases of doubtful radiology, and for multiple biopsies around the colon.

Both sigmoldoscopy and colonoscopy are avoided la patients with severe acute colitis. Because of the danger of perforation, due care is observed in an active case.

Complications

Toxic megacolon It occurs in the fulminating type of disease and may result in perforation. Both require immediate surgery. The underlying cause is unknown although predisposing factors such as antidiarrhoeal agents, antic holinergic drugs and barium enema examination have been implicated. At operation, a dilated bowel, usually the transverse colon and less commonly the sigmoid colon Is seen. The serosa is dull and congested. It can be classically likened to a wet blotting paper. Histologically, there is gross ulceration with deep penetrating clefts. The muscle layer shows extensive lysis.

Perforation Any severely diseased colon may perforate but patients with toxic megacolon are especially vulnerable. Systemic therapy (cortico-steroids) may mask the development of this complication.

Massive haemorrhage It is an uncommon but life-threatening complication.

Cancer Patients with extensive ulcerative colitis of more than ten years standing, have an increased risk of developing colorectal cancer. The risk of developing cancer is greater in patients who develop the disease at an early age. Microscopically, they are adenocarcinomas and are often poorly differentiated. The screening of patients of ulceratlve colitis by annual rectal biopsy is recommended starting five years after the onset of symptoms. In addition, endoscopy at 1-3 year intervals may be performed. Proctocolectomy is carried out if severe dysplasia is seen.

Extralntestlnal Manifestations

Liver Cirrhosis occurs in 1 to 5 per cent cases of ulce­ratlve colitis. Sclerosing cholangltis and carcinoma of the bile ducts are important complications.

Skin Erythema nodosum appears as raised, red, tender nodules classically on the anterior tibial aspect of the leg in 2-4 per cent of patients with ulcerative colitis. Pyoderma gangrenosum, also occurs commonly in ulcerative colitis and appears as a large, deep ulcer with central necrosis. It usually, but not always, improves with colectomy.

Joints Patients with ulceratlve colitis may develop arthritis. This usually occurs during exacerbation of colitis and runs a self-limiting course. The knees are most frequently affected and in general, the joints are asymmetrically affected. Between 2 to 6 per cent of cases of both ulceratlve colitis and Crohn's disease are associated with ankylosing spondylitls.

Eye Iritis may occur, hi India, systemic compli­cations like arthritis have been seen but complications like erythema nodosum, pyoderma gangrenosum, skin rashes, eye lesions and ankylosing spondylltis have not been seen so often.

Treatment of Ulceratlve Colitis

All cases are to be treated by a rigid course of medical treatment unless there is specific contraindication to It. Surgery is reserved for those cases which fail to respond to medical treatment or where complications set in. The general line of treatment is as follows:

1. Maintenance of fluid and electrolyte balance

2. Correction of anaemia

3. Adequate nutrition

4. Sedatives and tranqulllsers.

Steroids are used to induce remission and Salazopyrine to maintain it. Sulphasalazine (Salazopyrin) is a combination of sulphapyridlne and 5-aminosallcylic acid. It is poorly absorbed in the small intestine and split by bacterial action in the colon to liberate the active 5-aminosalicyllc acid which has an anti-inflammatory property. The sulphapyridlne fraction Is responsible for most of the side effects which include dyspepsia, skin rash, etc. Patients who cannot tolerate the drug can be given an enteric coated preparation or the recently developed preparation that contains 5-amlnosallcylate alone (e.g. mesalazlne).

For a quiescent case Salazopyrin is given orally, 4 to 6 gm In divided doses for 7 days. Thereafter, the dose is reduced to 2 gm/day and is continued for long In order to prevent relapse.

For mild to moderate relapse Increased dose of salazopyrine (4-6 gm daily) is given. Retention enema of prednlsolone phosphate, 20 mg in 100 ml daily is commenced.

For on acute fulminating case These cases require hospitalisation. Nasogastric suction is required in patients with colonic dilatation or those at risk of developing this complication. Steroids are given intravenously (prednisolone 20-80 mg/daily). Alter­natively ACTH may be administered as an intra­venous drip. Steroids are given orally when oral feeding is resumed and the dose tapered gradually over a period of 1 -3 months. Sulphasalazine is given orally if the patient is allowed to eat; but the seriously 111 may require Intravenous broad-spectrum antibiotics. One should be careful in using antlchollnerglcs and opiates because these may precipitate acute dilatation of the colon.

If there is no response to steroids In 4 weeks or so, the continued use of steroids may be dangerous. It may Increase the risk of haemorrhage or perforation and even colectomy may be Impossible to perform in view of an extensively friable colon. Moreover, steroid therapy renders the patient more susceptible to pyogenic infection.

Indications for surgery In India, the disease runs a mild course and majority of cases can be controlled by medical treatment. The indications for surgery, however, are the following.

1. In chronic cases

a. Progressive disability in spite of conservative treatment.

I. When persistent diarrhoea limits the ability to work

II. frequent exacerbations. b. Chronic invalidism resulting from

malnutrition, anaemia and liver damage. c. Advent of complications.

i. Local stricture, abscess, fistula 11. Systemic eye complications, arthritis, skin lesions ;

d. Risk of neoplastic change in pseudopolyposis. e. When the onset is in the childhood.

2. In acute cases

a. If remission is not achieved within 3 weeks of steroid therapy.

b. Advent of complications — massive haemor­rhage, perforation, toxic megacolon.

Surgical treatment When surgical treatment is advised, about six days intensive preoperative preparation is carried out. Total proctocolectomy with permanent ileostomy is the procedure favoured by the majority of surgeons. Some advocate total colectomy with immediate or subsequent ileorectal anastomosis. It should, however, not be performed If perianal complications are present.

Total proctocolectomy and ileoanal pouch (reservoir) is now being practised in some centres. In this procedure the ileum (made into a reservoir or pouch. is brought into the pelvis and anastomosed to the anal canal just above the dentate line. The anastomosis protected temporarily by a loop ileostomy.

Secondary Deposits

The small intestine may become involved by a number of secondary cancers.

Endometrlosis

It has been estimated that endometriotic foci occur in about 4% of menstruating women but symptoms are few. They may produce obstruction. Treatment by danazol 200 mg twice daily may be used, as long-term prophylaxis, in those producing symptoms.

Endometriotic Invasion regresses after the ovaries have stopped functioning or have been removed.