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COMPLICATIONS OF PEPTIC ULSER DISEASE The complications of ulcer disease are principally hemorrhage, perforation, penetration, and obstruction, in that order, with hemorrhage being the most common and perforation the most lethal. Today, these constitute the main indications for ulcer surgery and account for most deaths from ulcer disease. When emergency surgery is needed, attention is focused on rapid correction of the immediate complication. Until recently, surgery for ulcer complications often included aggressive antiulcer operations (vagotomy with partial gastric resection or drainage procedures) that markedly altered normal gastric physiology. The modern trend is toward joint medical and surgical management of the patient, with early performance of the minimum surgical procedure needed for the patient to survive the complication. Specific therapy of the underlying ulcer diathesis can be rendered postoperatively in most patients with anti-H pylori eradication therapy, elimination of ASA/NSAID use, or long-term antisecretory therapy if required. ACUTE PERFORATION Perforated duodenal ulcers The diagnosis of an acute perforation of a duodenal ulcer is suggested by the sudden onset of severe epigastric pain followed by a variable degree of shock and often slight vomiting. In the untreated patient, the condition tends to improve after a few hours, to be followed shortly thereafter by increasing prostration, pain spreading throughout the abdomen, and cardiovascular collapse. Physical examination typically reveals a board-like abdomen, with tenderness most marked in the mid- or right epigastrium. Peristalsis is absent. The temperature in the first few hours after perforation is normal. Six hours after onset of symptoms an abdominal radiograph taken in the sitting position shows free air beneath the diaphragm in about 60 per cent of cases. If the diagnosis is in doubt, Gastrografin injected through an inlying nasogastric tube will show evidence of extravasation through the perforation.
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The differential diagnosis includes acute cholecystitis, acute pancreatitis, strangulating intestinal obstruction, acute appendicitis, perforation of some other portion of the intestinal tract, and mesenteric thrombosis. A past history of ulcer disease is predictive, since the chances that the present episode is due to a perforated ulcer are greatly increased in such patients. Occasionally, a perforated ulcer seals spontaneously and the patient will continue to improve. However, these formes frustes are rare, and delay before an operation, other than to institute nasogastric suction, antibiotics, and intravenous administration of fluids and electrolytes, is dangerous. Exploratory laparotomy is often necessary to confirm the diagnosis. The size of the perforation may vary greatly, from a diameter of only 2 to 3 mm to a hole 2 to 5 cm across. When the abdomen is opened, the perforation may have sealed spontaneously, covered in most cases by adjacent omentum. Such a finding has led some surgeons to advocate the non-operative treatment of what is believed to be an acutely perforated ulcer, such treatment consisting of nasogastric suction, antibiotics, and intravenous fluids and electrolytes. The diagnosis of an abdominal catastrophe may be missed and this approach must be abandoned if the patient's condition appears to be deteriorating. This injunction means that such patients must be watched carefully and that operation may be necessary at an unfortunate hour. Although this method of therapy may produce satisfactory results in young, vigorous patients, older persons often have other serious diseases such as mesenteric thrombosis; they cannot withstand the effects of peritonitis, and spontaneous sealing of the perforation does not occur as often as in younger patients. The main indications for such treatment include patients with recent coronary occlusion or those in whom the diagnosis has been delayed and in whom the ulcer has apparently sealed spontaneously. At the time of operation for an acutely perforated duodenal ulcer the surgeon must choose between a simple closure of the perforation or a definitive procedure designed to prevent future recurrences of ulcer disease. Simple closure may be efKnowledge is the highest power Nothing to stand before it. Pandi 2

fected with a few interrupted sutures, an omental or round ligament patch, or by suture closure reinforced with omentum. Care must be taken to avoid obstructing the duodenum with the sutures. In certain instances a more radical operation is necessary. Such cases include a giant perforation that cannot be closed by suture, a large posterior ulcer, a perforated ulcer on the anterior wall, or perforation accompanied by profuse bleeding. As was noted above, the most important indication for a definitive operation is a history of a previous ulcer. Definitive operations can be carried out successfully at the time of the great majority of operations for perforation. Appropriate procedures include gastric resection (with or without truncal vagotomy), pyloroplasty and bilateral truncal vagotomy, and proximal gastric vagotomy. Opinions vary concerning the choice of these procedures. Unless operating conditions are optimal, the surgeon must choose a simple closure of a perforation as a life-saving method; if necessary a definitive procedure can be performed later. Follow-up studies after simple plication show that nearly one-third of all patients remain free of symptoms, and about half of those with recurrent symptoms requires a definitive operation for ulcer disease later. Perforated gastric ulcers The great majority of perforated gastric ulcers are located in the immediate prepyloric area. They behave in the same way as perforated duodenal ulcers, and the same considerations are applicable. However, perforations of ulcers elsewhere in the stomach introduce the possibility of malignancy, and immediate definitive resections of the stomach are recommended. If the patient's condition is poor, and only a simple closure is contemplated, biopsy specimens should be taken of the margins of the ulcer. Non-operative management of perforated peptic ulcer
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Immediate operative repair is the most widely practised therapy for duodenal perforations and would seem to be the only conceivable course to recommend for most patients. However, most surgeons have encountered patients who refuse operations for their perforated ulcers and still recover. At operation the perforation has sometimes already been sealed off by omentum or adjacent organs and has to be reopened before it can be repaired. Indeed, the fact that non-operative treatment for perforated peptic ulcers may be successful has been recognized since 1870. In 1964 Herman Taylor reported the conservative treatment of 256 patients with perforations: only 21 patients required surgery and the overall mortality rate was 11 per cent. These results are better than those of surgical repair at the time and are comparable to most present day series. Non-operative management should only be employed if an experienced surgeon interested in this form of treatment is willing to personally supervise the patient's progress. Once the diagnosis of a perforated ulcer is made a nasogastric tube should be inserted as early as possible to empty the stomach and to reduce the leakage of gastrointestinal contents. The success of conservative treatment of perforated ulcer depends on keeping the stomach empty by nasogastric suction. Leakage from the perforation is kept to a minimum so that the omentum and surrounding organs have a chance to seal the perforation. Much attention to detail on the part of the medical and nursing staff is necessary to ensure that the tube is properly positioned in the stomach and that the stomach is properly emptied. Intravenous fluid is administered at a rate depending upon the degree of dehydration to maintain a urine output of at least 30 ml/h. In elderly patients and those in shock, central venous pressure measurements allow a more accurate assessment of fluid replacement. Broad spectrum antibiotics are also administered. The patient is carefully monitored and should be examined at least 12-hourly by the surgeon who made the initial assessment. Improvement is indicated by decrease in the pulse rate, temperature, and abdominal tenderness and by an improvement in the general well being of the patient. The surgeon must be prepared to abandon conservative management and to undertake operative intervention without delay if the patient fails to improve.
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The majority, however, will dramatically improve within 12 to 24 h. Oral fluids may be started when all signs of peritonitis disappear and intestinal activity returns. Normal diet is resumed within a few days. The patient should be treated with H2receptor blocking drugs. Upper gastrointestinal endoscopy is performed 6 weeks later: evidence of healed duodenal ulceration will be seen in the great majority of patients. A decision is then made, depending on the individual circumstances, to stop medical treatment or to continue long-term maintenance H2 blockade. An upper gastrointestinal series using water-soluble contrast material is a useful adjunct for the definitive diagnosis and treatment of these patients. The demonstration of an ulcer crater without leakage in a patient with a typical history and peritonitis is reassuring and provides circumstantial evidence that the cause of peritonitis is indeed a perforated ulcer. It also suggests that spontaneous sealing has probably occurred. Free leakage of contrast into the peritoneal cavity indicates that the crisis is not yet over and a high degree of vigilance needs to be maintained. It was hoped that conservative treatment may improve the outlook for frail elderly patients who may be too ill to withstand general anaesthesia. Unfortunately this is not so: perforations are less likely to seal spontaneously in elderly patients. The greater omentum is atrophic in the elderly and is presumably less effective in sealing perforations. In addition, the elderly patient withstands continued intra-abdominal sepsis poorly. Early laparotomy after adequate resuscitation offers the best chance of recovery in these high risk patients. HAEMORRHAGE Clinical features: the history and physical examination provide crucial information for the initial evaluation of a patient presenting with a gastrointestinal tract hemorrhage. The history findings can be extremely helpful in determining the location of the gastrointestinal hemorrhage. The differential diagnosis includes: gastric ulcer, duodenal ulcer, esophageal varices, gastric varices, mallory-weiss tear, esophagitis, neoplasm, hemorrhagic gastritis, angiodysplasia, hemobilia, pancreatic pseudocyst, pancreatic pseudoaneurysm, aortoenteric fistula.
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Hematemesis and melena are the most common presentations of acute upper gastrointestinal bleeding, and patients may present with both symptoms. Occasionally, a brisk upper gastrointestinal bleeding manifests as hematochezia. History and physical examination findings in acute upper gastrointestinal bleeding at presentation include: hematemesis - 40-50%, melena - 70-80%, hematochezia - 15-20%, either hematochezia or melena - 90-98%, syncope - 14.4%, presyncope - 43.2%, dyspepsia - 18%, epigastric pain - 41%, heartburn - 21%, diffuse abdominal pain - 10%, dysphagia - 5%, weight loss - 12%, jaundice - 5.2%. Some prognostic indicators that can be detected from the history and physical examination findings are helpful for developing a scoring system to assess the risk of poor outcome with upper gastrointestinal bleeding. These factors include age, heart rate, systolic blood pressure (SBP) upon admission, orthostatic changes in blood pressure or pulse rate, and the use of any anticoagulants. Worrisome clinical signs and symptoms of hemodynamic compromise include tachycardia of more than 100 beats per minute (bpm), systolic blood pressure of less than 90 mm Hg, cool extremities, syncope, and other obvious signs of shock such as ongoing brisk hematemesis or maroon or bright-red stools, which requires rapid blood transfusion. Age older than 60 years is an independent marker for a poor outcome. The mortality rate increases to 12-25% in those older than 60 years compared to a mortality rate of less than 10% for patients younger than 60 years. Patients who present in hemorrhagic shock have an increased mortality rate of up to 30%. Hemorrhage may be classified based on the amount of blood loss, as noted in the following table (American College of Surgeons Committee on Trauma, 1997). Table 2. Estimated Fluid and Blood Losses in Shock
Class 1 Blood Loss, mL Blood Loss, blood volume Pulse Rate, bpm % Up to 750 Up to 15% <100 Class 2 750-1500 15-30% >100 Class 3 1500-2000 30-40% >120 Class 4 >2000 >40% >140 6

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7 Blood Pressure Respiratory Rate Urine mL/h Output, StaNormal Normal Decreased Decreased 30-40 Anxious, fused Crystalloid blood Decreased Decreased >35 con- Confused, lethargic and Crystalloid blood and

Normal or InDecreased creased 14-20 Slightly anxious 20-30 Mildly anxious Crystalloid

CNS/Mental tus

Fluid ReplaceCrystalloid ment, 3-for-1 rule

Acute massive haemorrhage A patient who has required 5 units of blood during a single hospital admission by definition has a massive haemorrhage. When a patient enters with serious upper gastrointestinal bleeding, the source can usually be determined with reasonable certainty on clinical grounds. Nearly two-thirds of all cases of severe upper gastrointestinal haemorrhage are due to ulcers of the stomach or duodenum. A past history of ulcer disease, a recent history of ingestion of gastric irritants such as aspirin or ibuprofen, sudden profuse vomiting of blood, and later haematochezia are typical. The other major causes of massive upper gastrointestinal bleeding&mdash;portal hypertension and oesophageal varices&mdash;can usually be eliminated by history and physical examination, but the frequency of concomitant ulcer disease makes other early diagnostic procedures essential. At times, a bleeding duodenal ulcer is manifested merely by tarry stools. Early upper gastrointestinal endoscopy is the most valuable diagnostic study. However, profuse bleeding may make it useless, since such patients must be taken directly to the operating room. Selective angiography can be helpful but is not always available. On the other hand injection of 99 m-technetium-labelled erythrocytes is not useful because of the heavy background radiation in the upper abdomen. Although barium contrast studies often show the ulcer, they should not be used before angiography because residual barium might prevent further imaging studies.
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The diagnosis of the source of bleeding must often be made by laparotomy. An adequate incision and careful observation of the abdominal contents should indicate the probable site of bleeding. A wide gastrotomy incision that extends across the pylorus, if necessary, gives the best exposure to help find the source. Therapeutic measures for acute massive bleeding include injection of vasopressin into a peripheral vein, irrigation of the stomach for removal of blood clots, continued nasogastric suction, elimination or oral intake, and intravenous replacement of blood, fluid, and electrolytes. Until an operation is performed or the patient recovers, a careful chart of the vital signs and repeated assays of the haematocrit are essential. Massive bleeding is not well tolerated in patients over 60 years of age: under that age, mortality is not increased by delay and attempts to control the bleeding by endoscopic techniques such as electrocoagulation or laser. Older patients respond much better to early operation. Early operation is indicated in patients bleeding from the gastroduodenal artery or a gastric ulcer. Angiographic embolization of the gastroduodenal or the left gastric arteries may be effective, but there are dangers involved. A foreign body may slip from the gastroduodenal into the hepatic artery and lead to hepatic necrosis; one in the left gastric artery may lead to necrosis of the upper portion of the stomach. Operations for massively bleeding duodenal ulcers The site of bleeding must be determined. If the source is the gastroduodenal artery, it must be ligated as the first step. This procedure involves suture of the artery, either above the duodenum as it emerges from the hepatic artery or within the duodenal lumen, suture of the caudal portion of the artery within the duodenum or of the two major branches the superior pancreatoduodenal and the right gastroepiploic and of the transverse pancreatic artery. Heavy, non-absorbable sutures are used. In other instances the duodenum may be boggy and bleeding from multiple areas; in such instances it may be impossible to identify single vessels to ligate.
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As soon as bleeding has been controlled, a definitive operation can be carried out. We believe that hemigastrectomy and truncal vagotomy followed by a Billroth II anastomosis is best; others prefer the simpler pyloroplasty and truncal vagotomy. A major determinant in the selection is the experience of the surgeon. Gastric resection is more difficult, but gives slightly better control of bleeding because it removes areas of gastritis and duodenitis that are potential sources of postoperative bleeding. Operations for bleeding gastric ulcers Gastric resection is preferred for bleeding gastric ulcers. A truncal vagotomy should be added if the ulcer is in the prepyloric area or if the patient has a history of a duodenal ulcer. Either a Billroth I or II anastomosis can be made. In some patients who are very poor operative risks, a local excision of the ulcer may be performed. However, the chances of recurrence within a year approach nearly 50 per cent. The most difficult stomach ulcer to treat is one located in the proximal portion. In older patients who are poor risks, a distal resection, ligation of the left gastric artery, and intragastric plication of the ulcer is recommended. Minor haemorrhages Repetitive minor haemorrhage is another indication for operation. The source of such bleeding is more likely to be ulcer disease associated with gastritis or duodenitis; major vessels, such as the left gastric or gastroduodenal are not involved. The symptoms usually consist of repeated episodes of tarry stools, which may not be associated with pain. Other sites of occult bleeding may need to be investigated, and endoscopy during a bleeding episode is essential to confirm the diagnosis. Otherwise, this difficult diagnostic problem may require such measures as preoperative arteriography and intraoperative endoscopy.
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When the symptoms are not controlled by medical measures, operation is necessary. Gastric resection with bilateral truncal vagotomy is preferred; the antrum should be completely excised. Careful examination of the entire gastrointestinal tract at the time of operation is essential. OBSTRUCTION Gastric outlet obstruction is one of the important indications for surgery for an ulcer of the stomach or duodenum. Such complications must be regarded with care, because gastric cancer may be present, but is difficult to diagnose in these circumstances. Clinical features: nausea and vomiting are the cardinal symptoms of gastric outlet obstruction. Vomiting usually is described as nonbilious, and it characteristically contains undigested food particles. In the early stages of obstruction, vomiting may be intermittent and usually occurs within 1 hour of a meal. Early satiety and epigastric fullness are common. Weight loss is frequent when the condition approaches chronicity and is most significant in patients with malignant disease. Abdominal pain is not frequent and usually relates to the underlying cause, eg, peptic ulcer diseases, pancreatic cancer. Physical examination often demonstrates the presence of chronic dehydration and malnutrition. A dilated stomach may be appreciated as a tympanitic mass in the epigastric area and/or left upper quadrant. Dehydration and electrolyte abnormalities can be demonstrated by routine laboratory examinations. Increases in BUN and creatinine are late features of dehydration. Prolonged vomiting causes loss of hydrochloric (HCl) acid and produces an increase of bicarbonate in the plasma to compensate for the lost chloride and sodium. The result is a hypokalemic hypochloremic metabolic alkalosis. Alkalosis shifts the intracellular potassium to the extracellular compartment, and the serum positive potassium is increased factitiously. With continued vomiting, the renal excretion of potassium increases in order to preserve sodium. The adrenocortical reKnowledge is the highest power Nothing to stand before it. Pandi 10

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sponse to hypovolemia intensifies the exchange of potassium for sodium at the distal tubule, with subsequent aggravation of the hypokalemia. Laboratory studies:

Obtain a complete blood count. Check the hemoglobin and hematocrit Obtain an electrolyte panel. As noted previously, identifying and corLiver function tests may be helpful, particularly when a malignant etiA test for H pylori is helpful when the diagnosis of peptic ulcer dis-

to rule out the possibility of anemia.

recting electrolyte abnormalities that tend to occur is essential.

ology is suspected.

eases is suspected. Imaging Studies:

Plain abdominal radiographs, contrast upper gastrointestinal studies Plain radiographs, the obstruction series (supine abdomen, upright ab-

(Gastrografin or barium), and CT scans with oral contrast are helpful.

domen, and chest posteroanterior), can demonstrate the presence of gastric dilatation and may be helpful with distinguishing the differential diagnosis. Diagnostic Procedures:

Upper endoscopy can help visualize the gastric outlet and may provide The sodium chloride load test is a traditional clinical nonimaging study

a tissue diagnosis when the obstruction is intraluminal.

that may be helpful. The traditional sodium chloride load test is performed by infusing 750 cc of sodium chloride solution into the stomach via a nasogastric tube. A diagnosis of gastric outlet obstruction is made if more than 400 cc remain in the stomach after 30 minutes.

Nuclear gastric emptying studies measure the passage of orally admin-

istered radionuclide over time. Unfortunately, both the nuclear test and saline load test may produce abnormal results in functional states.

Barium upper GI studies are very helpful because they can delineate
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the gastric silhouette and demonstrate the site of obstruction. An enlarged stomach

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with a narrowing of the pyloric channel or first portion of the duodenum helps differentiate gastric outlet obstruction from gastroparesis.

The specific cause may be identified as an ulcer mass or intrinsic tuIn the presence of peptic ulcer diseases, perform endoscopic biopsy to In the case of peripancreatic malignancy, CT scanguided biopsy may Needle-guided biopsy also may be helpful in establishing the presence

mor.

rule out the presence of malignancy.

be helpful in establishing a preoperative diagnosis.

of metastatic disease. This knowledge may impact the magnitude of the procedure planned to alleviate the gastric outlet obstruction. Initial management of gastric outlet obstruction should be the same regardless of the primary cause. After a diagnosis is made, admit patients for hydration and correction of electrolyte abnormalities. Remembering that the metabolic alkalosis of gastric outlet obstruction responds to the administration of chloride is important; therefore, sodium chloride solution should be the initial fluid of choice. Potassium deficits are corrected after repletion of volume status, and after the chloride has been replaced. Place a nasogastric tube to decompress the stomach. Occasionally, a large tube is required because the undigested food blocks tubes with small diameters. Duodenal ulcers cause obstruction for two reasons: in young patients acute ulcers are associated with much surrounding inflammation and oedema; in the elderly fibrosis develops about an old ulcer. Differentiation between the two modes of obstruction usually can be made by observation during several days of nasogastric suction, intravenous administration of H2-receptor antagonists, and intravenous alimentation. Oedema usually subsides within a few days, while fibrotic obstruction continues to produce large quantities of gastric aspirate. In either case the prognosis is poor without operation. However, obstruction due to oedema that subsides rapidly can be treated conservatively for a few weeks, at which time the operation will be much easier and safer.
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The operation chosen depends on the condition of the patient. Gastric resection combined with vagotomy is our preference in young patients, although vagotomy and gastroenterostomy may be performed if inflammation about the pylorus is severe. Proximal gastric vagotomy is contraindicated. Older patients in poor condition who are considered to have fibrotic obstruction and burned-out ulcers, can be treated if necessary by gastroenterostomy under local anaesthesia. A gastric resection will generally be tolerated, but the addition of a vagotomy may lead to a prolonged period of gastric atony, and should be avoided. Obstructing gastric ulcers should be treated by gastric resection combined with truncal vagotomy. PENETRATION Unlike perforation, ulcer penetration into an adjacent viscus, such as the liver, pancreas, or biliary system, is rarely dramatic. Rather, it presents with gradual exacerbation of pain, loss of rhythmicity, increase in local tenderness, increasing requirement for medication, or the development of features of an additional disease process, such as pancreatitis or cholangitis. Its most common manifestation is pancreatitis. The association of pancreatitis and duodenal ulcer is more common than can be accounted for by the presence of penetration. The complication of penetration is rarely catastrophic and responds, in most cases, to intensive medical therapy. Only a minority of cases require surgery. FISTULAE SECONDARY TO ULCER DISEASE Gastric ulcers can perforate into the transverse colon, producing a gastrocolic fistula, the symptoms of which include vomiting of faeces and severe diarrhoea. Exactly the same type of fistula and symptoms can occur if the underlying disease is either gastric or colonic cancer. The diagnosis of a fistula may be made by barium contrast radiographs or endoscopy. However, endoscopic observation and biopsy to rule out cancer are indicated. If the lesion is benign, gastric and colonic resecKnowledge is the highest power Nothing to stand before it. Pandi 13

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tions are necessary; malignancy of either the stomach or colon requires more extensive resection. Duodenal ulcers may penetrate into the common bile duct or the ascending or transverse colon; involvement of any other organ is rare. Although the general principles of therapy are the same as for gastric ulcers, choledochoduodenal fistulae furnish special problems. This problem may arise either from a duodenal ulcer in the second portion of the duodenum or from primary disease of the biliary tree. If biliary tract disease can be ruled out and the dissection promises to be dangerous, a low ulcer can be treated by a Billroth II resection; the duodenal stump can be closed cephalad to the fistula, leaving it in place. A vagotomy is added. INTRACTABILITY Intractability implies that a patient with an ulcer has been treated with the best available medical therapy but is still symptomatic. Such ulcers are usually duodenal or prepyloric. It is important that a gastrinoma is ruled out by appropriate tests. The patient should undergo endoscopy while symptoms are most severe; if an ulcer is present, and further medical therapy only leads to temporary relief, a standard ulcer operation should be performed. There are many patients who complain of ulcer-like symptoms, but in whom no objective evidence of an ulcer can be found: other causes of epigastric distress should be investigated. These patients should be examined carefully by endoscopy and by barium contrast radiography before an operation is undertaken. To do otherwise may mean that the operative findings will be unimpressive and that the patient will complain of the same symptoms postoperatively. In these patients full medical therapy is recommended before embarking on any possibly curative operation. Under these circumstances the least that can be done is the best. A proximal gastric vagotomy will be the least likely to subject the patient to new, more serious postoperative symptoms, provided that the procedure is uncomplicated.
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