25. 1 Acute pancreatitis
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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 disorders (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 gastrointestinal 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.
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.
1. Local 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.
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 ileum.
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 ileitis supervenes.
The commonest presentation of chronic ileitis 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.
Ulcerative 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.
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.
NORMAL STRUCTURE AND FUNCTION
The stomach consists of fundus, body. pyloric part and pylorus. The fundus Is the part which projects upwards in contact with the left dome of the diaphragm above the level of the cardiac orifice. It is usually full of gas. The body extends from the fundus to the level of the angular notch (angular incisure), a constant notch in the lower part of the lesser curvature. The pyloric part extends from this level, consisting of the proximal antrum which narrows gradually towards the pylorus as the pyloric canal. The pylorus is thicker than the rest of the stomach wall because of the thickened circular muscle (pyloric sphincter). The pylorus is normally open; when a wave of gastric contraction reaches here, it contracts to squirt some pyloric contents into the duodenum, but some contents are also squeezed back into the stomach to help mixing of the contents.
Gastric epithelial cells lining the stomach secrete mucus and are responsible for the lubrication of contents. Parietal cells (oxyntic cells) occur in the body of the stomach and secrete acid. The chief cells lie mainly in the fundic mucosa and secrete pepsinogen. The antrum (pyloric gland area) secretes a thick, viscid relatively alkaline mucus and the hormone gastrin and somatostatln.
The histologlcal division between the body and antral mucosa does not correspond to the anatomical division, but is more irregular. Normally, a tongue of antrum extends up the lesser curve.
The blood supply of the stomach is from the coellac axis. The main arteries are the left and right gastric arteries and the left and right gastroepiplolc arteries The short gastric arteries (from the splenic artery) supply the fundus. The veins corresponding to the right and left gastric arteries terminate in the portal vein. Those corresponding to the left gastroepiploic artery and vasa brevia Join the splenic vein, while the right gastroepiploic vein empties into the superior mesenteric vein. The prepyloric vein of Mayo is a helpful landmark in distinguishing the pyloric canal from the first part of the duodenum.
The lymphatic drainage runs with the arterial supply to the left and right gastric nodes, the subpyloric nodes, the splenic nodes and the right gastroepiploic nodes. From there, it drains to the coeliac nodes.
GASTRIC SECRETION
Acid is produced by the parietal (oxyntic) cells and pepsin is produced by the chief cells. Gastrin is released from antral G cells in response to the mechanical distension of the antrum. After release from the G cells, gastrin reaches the parietal cell via the systemic circulation. Secretion of the acid is controlled by negative feedback; when intragastric pH falls considerably, the release of gastrin is inhibited. Gastrin increases acid secretion through histamine, which stimulates H receptors on the parietal cell wall to produce cyclic AMP. The cyclic AMP in turn causes acid secretion by a mechanism not fully understood.
Prostaglandins antagonise the release of acid by stomach. It spares the anterior and posterior nerves of Latarjet, but divides all the vagal branches that terminate on the proximal two-thirds of the stomach. Since antral inner vation is preserved, gastric emptying is relatively unimpaired, and a drainage procedure is unnecessary. It must not be carried out if the pylorus is narrowed by scarring. The recurrent ulceration rate is higher than with the truncal vagotomy.
Vagotomy and antrectomy This entails a distal gastrectomy of 50 per cent of the stomach along with truncal vagotomy. With the line of stomach transection carried high on the lesser curve to conform with the boundary of the gastrin producing mucosa. The gastrointestinal continuity is restored by Billroth I technique (the proximal remnant is reanastomosed to the duodenum) or by the Billroth II method (the proximal remnant, is anastomosed to the side of the proximal jejunum)
Vagotomy and antrectomy has a low incidence of stomal ulceration, but the operation is more major with increased risk of immediate complications from anastomatic leakage.
Subtotal gastrectomy This consists of resection of two-third to three-fourth of the distal stomach. Physiologically, it removes the major source of gastrin (the antrum) and about half of the parietal cell area of the stomach. This is not much practised nowadays. The long-term sequelae (dumping, nutritional disturbances, bilious vomiting, etc.) are regarded as too heavy a price to pay for a relatively benign condition.