COMPLICATIONS OF ULCER DISEASE

Complications and surgical treatment ofduodenal ulcer disease

Recurrent duodenal ulcer, when medicamentous suppression of gastric secretion does not bring to stable remission of the disease, is an indication for elective surgery. Stem vagotomy with resection of the antrum of the stomach (antrectomy) or pyloroplasty, as well as selective proximal vagotomy without stomach drainage operations are usually performed.

Stem vagotomy with antrectomy requires division of the vagus nerves with removal of the antrum by applying anastomosis with the proximal duodenum (stomach resection according to Bilroth-I) or with a loop of the jejunum (stomach resection according to Bilroth-II). This is a rather effective method of treatment of ulcer disease. The incidence of postoperative recurrence accounts for 1 %, while that of postoperative complications and lethality is somewhat higher than is seen in vagotomy with pyloroplasty.

Some surgeons would use selective vagotomy when all the gastric branches of the vagus nerves are divided, with the branches passing to the liver and appendix being preserved. In this case, postoperative recurrences and complications are less common than is seen with stem vagotomy.

Selective proximal vagotomy necessitates denervation of the fundus and body of the stomach with preservation of the branches of the vagus nerves innervating the antrum. After this type of vagotomy, pyloroplasty or another drainage operation is not necessary. (Fig 3)

Fig 3. The types of vagotomy: а) stem, b) selective, c) selective proximal.

The absolute indications for surgery are the following complications of duodenal ulcer: hemorrhage, perforation, gastric outlet stenosis, penetration.

Hemorrhage from duodenal ulcers, seen in 15-20 % of patients, may be the first clinical manifestation of almost 50 % of ulcers induced by intake of nonsteroidal antiinflammatory drugs. It may resolve spontaneously in the majority of patients. The risk of rebleeding in the patients who do not undergo antibacterial and supportive H ²- blocker therapy increases by 40 %.

The clinical picture of bleeding, when the volume of blood loss does not exceed 500 ml, does not usually have pronounced symptoms, if no significant impairments of the body’s compensatory mechanism. Reservoir blood engaged in the blood steam rapidly compensates a decrease in the volume of circulating blood. The most prominent clinical and pathophysiologic signs are seen in acute massive bleedings, when for a relatively short time period a patient loses more than 1500 ml of blood that is about 25 % of the volume of circulating blood. In these instances the clinical

picture corresponds to that of hypovolemia. The heartbeat rate increases in response to reduced venous inflow and stroke volume. Persistent bleeding results in the clinical picture of hypovolemic shock. There is noted a decrease in stroke volume and a drop in pressure due to exhaustion of compensatory mechanism, up to a critical level.

The body’s compensatory reaction to acute blood loss may include decreased renal blood flow, which is manifested by oligouria and even anuria. Hypoxia of hepatocytes and intestinal absorption of blood waste products can result in acute hepatic insufficiency or the formation of the necrotic foci in the liver. Impairment of consciousness at the presence of ulcer bleeding may be a sign of cerebrovascular insufficiency. In coronary insufficiency, patients have characteristic complaints and changes on an electrocardiogram, and even acute myocardial infarction can develop.

In massive blood loss, the release of antidiuretic hormone and aldosterone results in gradual increase in the volume of circulating blood by interstitial liquids, that is accompanied by a decrease in hematocrit and a reduce in hemoglobin concentration.

Determination of the volume of blood loss is of great importance in further diagnostic and therapy approaches. Past history, in this respect, is not informative. The amount and nature of vomitus (scarlet blood, blood clots, and characteristic “coffee grounds”), the frequency and duration of melena may only indicate the frequency of occurred bleeding. Such symptoms, as general weakness, palpitation, dizziness, collapse may also become quantitative characteristics of this complication of ulcer disease.

Objective findings give more reliable data regarding the volume of bleeding. Skin and conjunctiva pallor testifies to massive blood loss. Decreased systolic arterial pressure, below 100 mHg and increased pulse rate, above 100 p/m in the patient who has no circulatory disturbance, correspond to about 20 % loss of total blood volume. A more accurate picture of the extent of bleeding may be indicated by the estimation of circulating blood volume: 10-15 % loss of circulating blood corresponds to mild bleeding, 16-25 % - medium bleeding, above 25 % - severe bleeding.

The laboratory evaluation of the volume of blood loss is more informative. For example, a decrease in hemoglobin level, up to 100g/l, from 100 up to 70g/l, and below 70g/l, correlates with mild, medium and severe blood loss, respectively (Tab. 1).

To verify the disease resulted in hemorrhage and to localize its source, it is necessary to assess the findings of the investigation and to carry out esophagogastroduodenoscopy.

Skin and visible mucous subicteritiousness in combination with dilated subcutaneous veins of the abdominal wall is characteristic of hepatic diseases with portal hypertension syndrome. The patients of this category experience frequent bleedings from varicose-dilated veins of the esophagus and cardiac portion of the

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stomach. Vomitus containing dark venous blood or blood clots becomes a differential sign of portal hemorrhage.

Table 1. Criteria for assessment of hemorrhage extent

Blood Loss Index Hemorrhage extentMILD MEDIUM SEVERE

A decrease in systolic arterial pressure (mm.Hg)

100 90-110 below 90

Loss of circulating blood volume 10-15 16-25 above 25Pulse rate p/m Up to 80 81-100 above 100Level of hemoglobin (g/l) 100 70-100 below 70Erythrocyte count (х10 ¹ ²) 3,5 2,5-3,5 below 2,5Hematocrit 30 25-30 Below 25

Manual rectum examination enables one to diagnose melena, which is signed by the presence of black feces on the glove, and also to verify a rectal tumor, when scarlet blood is discharged out on rectal hemorrhage.

Esophagogastroduodenoscopy, a more informative method of diagnosing gastrointestinal hemorrhage, allowing to: - verify the diagnosis; - localize the source of bleeding; - estimate the state of the source of bleeding (a clotted vessel, persistent bleeding and

whether recurrence is likely; - attempt secure endoscopic hemostasis; - determine treatment approach.

In some instances in order to arrest or prevent recurrent hemorrhage, the following endoscopic manipulations appear to be effective: paravessel administration of vasoconstrictive or sclerosing drugs, termocoagulation, bipolar, argon-plasma, laser coagulation, and clamping of bleeding or clotted vessel. Endoscopic monitoring is required after these procedures to control the state of the source of bleeding, carry out repeated hemostasis, and correct treatment tactics.

The use of eradication therapy, non surgical methods to arrest ulcer bleeding have allowed to reduce considerably the need for surgery.

However in the cases, when the bleeding has not stopped spontaneously and there is no possibility to secure endoscopic hemostasis (duodenal stenosis; active bleeding not allowing to visualize its source), emergency operation is indicated.

In cases with persistent duodenal bleedings, the priority is certainly given to organ-saving surgery. Taking into account the fact, that in the majority of cases bleeding ulcers are localized posteriorly on the duodenum, the operation of choice is stem vagotomy with pyloroplasty according to Finney.

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Pyloroplasty according to Finney. After applying 6-8 sero-muscular stitches between the anterior walls of the antrum of the stomach and the duodenum, their lumen is opened by means of a semilunar (curved) incision made through the pylorus. When the source of bleeding is visualized, the ulcer is sewed up by nonabsorbable stitches. Care should be taken while stitching the posterior wall of the duodenum in order to avoid the damage to the great vessels and choledoch. The final stage of pyloroplasty is applying gastro-duodenal anastomosis. For this purpose, the internal margins of the semilunar (curved) incision are sewed together, thus forming a "tongue", which prolapses into the lumen of the duodenum, plugging the ulcer of the posterior wall and serving as a valve instead of the pylorus. The external margins of the curved incision are sewed together, forming the anterior wall of anastomosis (Fig. 4).

Destruction of the pylorus is mandatory in any type of pyloroplasty, which helps prevent gastric outlet stenosis after vagotomy.

Fig 4. Pyloroplasty according to Finney.

Perforating duodenal ulcer develops in 2-3 % of ulcer patients, with 5-10 % of them being previously asymptomatic; and in 10 % - perforation is accompanied by bleeding. A thinned-wall of the duodenum plays an important role in pathogenesis of perforating ulcer. Physical exertion and overeating provoke the disease.

Duodenal ulcer perforates more often (90%) into a free abdominal cavity. The disease usually develops suddenly, but a thorough study of a case history often reveals anticipating symptoms of exacerbation of ulcer disease. 30 % of patients have reported that epigastric pain may considerably increase just prior to perforation; then nausea, causeless vomiting and fever develop. The most typical symptoms of perforation are a sharp knife-like pain in the abdomen, board-like muscular tension of the anterior abdominal wall, positive Shetkin-Blumberg’s symptom, disappearance of hepatic dullness on abdominal percussion, bradycardia and skin pallor. Vomiting is a rare sign. On physical examination attention is paid to a forced position – lateral position with the legs pulled up to the abdomen and an appearance - a pale face expressing a feeling of fear and pain. During the first hours from the development of perforation, stool and gas passage may present, but meteorism and gas retention increase later.

Peritonitis develops in 6-8 hours after perforation of the ulcer. The general condition of the patient deteriorates quickly: collapse is likely, pulse becomes accelerated and thready; fever and dynamic intestinal obstruction develop, leykocytosis increases. The dullness of percussion sound in the lateral quadrants of the abdomen testifies to the presence of free liquid in the abdominal cavity.

Plain abdominal X-ray is a reliable diagnostic method of perforating ulcers - a crescent strip of gas between the diaphragm dome and liver is defined in 85-90 % of patients.

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The concealed perforation of duodenal ulcers occurs in 2-10 % of cases and is characterized by ulcer defect obstruction by the neighboring organs (the omentum, liver, gall bladder) or gastric contents (particles of food, mucus). The obstruction of the perforated aperture may be long or short-lasting or permanent. In the last, if the patient didn’t undergo esophagogastroduodenoscopy (during which the air is sucked into the stomach), the obstruction is self-healing. The onset of concealed perforation is as sudden as that of perforation into a free abdominal cavity. However the patient’s condition may significantly improve sometimes later. The pain subsides, but does not disappear completely and is still felt in the epigastrium and right part of the abdomen. Abdominal palpation reveals protective rigidity, and pneumoperitoneum is seen on X-ray.

Atypical perforation of duodenal ulcers is seen in 3-5 % of patients and is characterized by the perforation of duodenal contents into the retroperitoneum or any limited space, but not into a free abdominal cavity. These situations may develop in perforation of the ulcers located posteriorly on the duodenum, or when the ulcer perforates into the space, formed by postoperative adhesions. The clinical features are vague without acute onset of the disease. The patients complain of the abdominal pains, which can not be definitely localized. The muscular tension of the abdominal wall is not expressed. The patient’s condition starts to deteriorate significantly when the phlegmones of the retroperitoneal space or abscesses of the abdominal cavity start developing.

Conservative treatment at the presence of perforating ulcer is carried out only in cases when surgical treatment is not possible due to a grave patient’s condition, or when a patient refuses to undergo surgery. These situations necessitate constant aspiration of gastric contents through a nasogastric tube, infusion therapy with intravenous administration of the drugs suppressing gastric secretion, and antibiotics.

Modern approaches to the choice of operative treatment of perforating duodenal ulcers are based on a high efficiency of medicamentous treatment of the disease after surgical correction of the occurred complication. This means, that the operation at the presence of perforating duodenal ulcer is aimed at eliminating the source of peritonitis. For this purpose, one should perform laparotomy, closure of the perforated aperture, sanation and drainage of the abdominal cavity.

The use of laparoscopy technologies in surgery enables one to carry out laparoscopy or laparoscopy-assisted stitching of the perforating ulcers from a mini-laparotomic access in most patients.

It is necessary to take into account, that stitching is indicated only after esophagogastroduodenoscopy, which makes it possible to exclude the simultaneous presence of other ulcer complications: pylorostenosis, intraluminal bleeding from a perforating or so-called "kissing" ulcer of the posterior wall of the duodenum, a circular ulcer.

Surgical technique of laparoscopy-assisted stitching of perforating ulcer from a mini-laparotomic access. Under laparoscope control one should define the area of

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projection of the perforating ulcer onto the anterior abdominal wall. Minilaparotomy is performed with the incision of 3-4cm long in this area. A perforated aperture is stitched up hermetically. Laparoscopic sanation and drainage of the abdominal cavity is performed after stitching the minilaparatomic wound.

With associated complications of ulcer disease, with perforation being one of them, surgical tactics changes to extensive operations. Stem vagotomy with pyloroplasty according to Jadd is a method of choice in these cases.

Surgical technique of pyloroplasty according to Jadd. The anterior wall of the duodenum with a perforating ulcer is excised by means of a rhomboid incision, with the medial corner of the incision destroying the pylorus. The posterior wall of the duodenum is inspected through the aperture. At the presence of a "kissing" ulcer, regardless of bleeding, the ulcer is stitched. The formed defect of the duodenum is sewed transversely with two-row stitches (a Fig. 5).

Fig. 5 Pyloroplasty according to Jadd.

A high traumatic rate and technical difficulties arising in stomach resection enable one to use this type of surgical treatment of perforating ulcers, if only there are strict indications. For example, stomach resection according to Bilroth II is indicated in early referral of a patient with a perforating duodenal ulcer, the absence of purulent peritonitis and the presence of such concomitant complication of the disease as decompensated cicatrical pyloric stenosis with expressed ectasia and impaired gastric motility, or the presence of a circular ulcer of the duodenum. These situations should not be confined to stitching of perforating ulcer or pyloroplasty with vagotomy. Non-eliminated pyloric stenosis will result in the development of recurrent duodenal ulcer in the nearest terms after the operation, while closure of the perforated aperture of a circular ulcer may end in either the parting of the suture or the formation of a cicatricial gastric outlet stenosis. Vagotomy with pyloroplasty executed for perforating ulcers at the presence of decompensated gastric motility will progress to evacuatory disorders and an early recurrence of the disease.

Gastric outlet stenosis is the final stage of chronic ulcer disease in 2-4 % of patients. Gradual development of cicatricial narrowing of the pylorus is accompanied by an increase in gastric motor-evacuator disturbances. Duodenal ulcer results in stenosis in 90 % of cases.

Classification of pyloroduodenal stenoses ( J.M.Pantsyrev et al., 1977)

I stage - forming stenosis,II stage - compensated stenosis,III stage - subcompensated stenosis,IV stage - decompensated stenosis.

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Stenosis may be organic, as the consequence of cicatricial process, and functional, combined with a spasm and edema of the pyloric channel. Functional stenosis may develop in almost all patients at the phase of exacerbation of ulcer disease.

In compensated pyloroduodenal stenosis the patients complain of sensations of heaviness and fullness in the upper abdomen, nausea after a meal; they often induce vomiting themselves. The vomiting brings relieve. This condition is accompanied by electrolyte and fluid loss, hemoconcentration, a decreased volume of circulating blood, diuresis, and elevated specific gravity of urine. X-ray reveals moderate gastric ectasia, hyperperistalsis.

Subcompensated stage of stenosis is characterized by an expressed sensation of heaviness and fullness of the stomach, sometimes with the accompanying pain, frequent foul-smelling acidic belching of gases and gastric contents. Vomiting occurs almost every day; it arises at once or within 1,5-2 hours after a meal following increased epigastric pain with arising sensation of fullness in the stomach. Anti ulcer therapy does not seem to arrest vomiting. The patient significantly loses weight. Radiological signs of subcompensated stenosis are as follows: decreased tonicity, moderate ectasia, hyperperistalsis, and a significant delay of contrast evacuation into the duodenum.

In decompensated stage of stenosis food does not pass into the duodenum. Vomiting arises not only after every meal, but also in the intervals between meals; gastric pain becomes persistent. A sensation of heaviness and fullness of the stomach disappears only after vomiting or washing out of the stomach. The patient’s general condition significantly deteriorates, then dehydration and exhaustion augment with spasms and symptoms of uremia to follow (weakness, headache, loss of appetite, feeling of thirst, a smelly breath, oligouria). Hypocloremia and alkalosis develop. Abdominal palpation reveals a “splashing sound”. Ectased stomach can be frequently outlined in the epigastric and umbilical areas through a thinned abdominal wall. Rentgenological investigation shows a stomach in the shape of a hook-like stretched sack with sharply weakened peristalsis and a sharply reduced or a complete absence of evacuation. Processes of putrefactive fermentation in the stomach in these patients result in expressed contamination of mucous membrane.

The patients with I-II stage of pyloroduodenal stenosis are allowed to undergo an operation after a 5-7 day preoperative preparation where the basic aids are antiulcer therapy and periodic stomach decompression. In cases with acute ulcer, operative treatment is more justified after a 2-3 weeks’ antiulcer therapy course, which leads to regression of the inflammatory process, when even cicatrisation of an ulcer is likely.

Patients with III-IV stage of stenosis require a more prolonged and massive preoperative preparation including:1) Restoration of fluid-electrolyte and acid-base balances by means of transfusion of a large amount of solutions containing potassium, sodium and chlorine ions;

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2) Intensive parenteral feeding covering energy expenditures, daily requirements of proteins, vitamins, microelements;3) Conservative antiulcer treatment, when caution is paid to the use of atropine and anticholinergic drugs producing negative effect on gastric motility;4) Regular stomach decompression.

Operative treatment of the patients with sub- and decompensated stenosis can be executed only after obtaining the proved findings of efficiency of the fulfilled therapy, which include a significant reduce in the amount of aspirated gastric contents; normalization of volumetric parameters, electrolyte and acid-base balances in blood; improved renal function and decreased azotemia. Critical situations, when there are no positive results from the therapy within several days and the general patient’s condition continues to deteriorate, require urgent surgery. The extent of surgical intervention in these cases should be minimal and aimed at providing an adequate evacuation of the stomach.

The choice of operation in ulcer pyloroduodenal stenosis depends on the following factors: staging of stenosis, duration of ulcer in the past history, the presence of other ulcer complications, the age of patient, the extent of prominent concomitant pathology.

Gastrojejunostomy – is quite a simple and slightly traumatic operative intervention. The indications to perform are a high operational risk in the patients of senile age with decompensated stenosis and severe accompanying diseases with expressed electrolyte-fluid imbalances; the absence of ulcer clinical manifestations, endoscopic and radiological signs of active ulcer process at the presence of low gastric secretion in the elderly patients with cicatricial pyloroduodenal stenosis. Of a large number of methods to perform gastrojejunostomy, the priority should be given to retro-colonic anastomosis on an extremely short loop.

Stem vagotomy with stomach drainage operations (including gastrojejunostomy) is a pathophysiologically substantiated operation in ulcer pyloric stenosis.

Pyloroplasty according to Heineke-Mikulicz is simpler and less traumatic, which enables one to eliminate cicatricial pyloric stenosis. After longitudinal division of a stenosed pylorus, the anterior wall of the duodenum is sewed transversely with the anterior wall of pyloric channel. As a result, the diameter of the pyloric channel and the initial portion of the duodenum considerably increase (Fig 6).

Fig 6. Pyloroplasty according to Heineke-Mikulicz

Gastroduodenostomy by Jaboulay is carried out at the presence of extended pyloroduodenal stenosis with expressed cicatricial deformity of the upper horizontal part of the duodenum, when pyloroplasty is impossible. When the duodenum is mobilized according to Kocher, that makes it possible to compare its descending portion with the antral stomach, gastroduodenoanastomosis should be placed (Fig 7).

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Fig 7. Gastroduodenostomy by Jaboulay

The resection of 2/3d of the stomach in pyloroduodenal stenosis is recommended: - in patients of young and middle age groups with a low operational risk, at the presence of an active ulcer with high secretion and expressed gastric motility disturbances (stomach resection according to Bilroth-II modified by Hofmeister-Finsterer);-if cicatricial stenosis is associated with gastric ulcer or duodenostasis(stomach resection by Roux).

Penetration is an ulcer lesion of the entire wall of the duodenum (or the stomach), when ulcer penetrates into the surrounding organs and tissues. Penetrating ulcers develop in 3 stages: 1) Penetrations through all the layers of the duodenum (or the stomach),2) Fibrous adhesions with adjacent organ,3) Complete penetration into the tissue of the adjacent organ.

If penetration affects all the layers, with no organ or tissue adjacent to that part of the duodenum, ulcer perforates into the abdominal cavity. Ulcers of the posterior and lower walls of the upper horizontal portion of the duodenum, as well as lower (post-bulbar) ulcers often penetrates into the head of the pancreas, liver, hepato-duodenal ligament. Penetration can result in the formation of pathologic anastomosis - choledochoduodenal, cholecystoduodenal, duodenocolonic fistulas.

In penetrating ulcers the course of the disease becomes more severe. The clinical picture is manifested by the presence of additional signs. There arise symptoms characteristic of the diseases of the organs involved in the pathologic process (pancreatitis, cholecystitis, periduodenitis). Gastric pain becomes persistent, intensive; it is unrelated to eating. Nausea increases, vomiting becomes frequent, there is noted a subfebrile temperature, leukocytosis, increased erythrocyte sedimentation rate (ESR). In the area where penetration is localized, palpation reveals expressed tenderness and inflammatory infiltrate.

Ulcers penetrating into the pancreas are characterized by constant persistent back pains, which intensify after eating and at night: they fail to be arrested by antacids and spasmolytics. The epigastric pain radiates into the back, and sometimes the pain becomes girdle. In ulcers penetrating into the mesentery and mesocolon the pain extends to the lower abdomen.

The formation of internal fistulas results in reduced intensity of a pain syndrome that is associated with buffer action of bile or intestinal contents on gastric juice.

X-Ray reveals a deep "niche" and a limited mobility of a penetration area. Endoscopic study shows, that penetration appears as round, deep abrupt crater with high shaft-like edges, which are well-defined from the underlying mucous membrane.

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Penetrating ulcer frequently recurs, that result in pathologic changes to progress in the wall of the duodenum and surrounding tissues. In cases when penetrating ulcers are present or suspected, stomach resection or vagotomy is indicated.

Complications of gastric ulcersMalignancy is a process of ulcer regeneration into a cancer to which only

gastric ulcers are subject to. The clinical features of malignancy are as follows: - Pains, which are not associated with eating, become persistent;- Decreased intensity, and sometimes a complete disappearance of a pain syndrome;- Loss of appetite and weight;- Anemia, increased erythrocyte sedimentation rate (ESR);- Decreased gastric secretion, when even achlorhydria may develop.

Ulcers of giant sizes, callous gastric ulcers, those located in the cardial stomach and on the greater curve frequently become malignant. Cancer can develop even at the place of the cicatrix remained after the ulcer has healed.

Modern diagnostic methods have given the possibility to reduce significantly the number of operations, previously performed because of suspicion of malignant gastric ulcers. Histological confirmations of malignancy are the indications for stomach resection, provided the oncological principles have been met.

Bleeding from gastric ulcers is 4-5 times less common than the one from the duodenal ulcers. Surgery is indicated if hemostatic therapy and endoscopic manipulations are not effective. If malignancy of a bleeding ulcer is suspected in patients with a low operational risk, stomach resection is indicated. Gastric bleeding in patients with a high operational risk can be arrested by a less traumatic way, i.e. by stitching a bleeding ulcer through a gastrotomic access with the ligation of the left gastric artery in combination with vagotomy and drainage operation (pyoroplasty or gastrojejunostomy).

Penetration of gastric ulcer occurs in to the lesser omentum or the body of the pancreas in most cases. In penetration into the lesser omentum the pain from epigastric area radiates to the right subcostal area. If ulcer penetrates at the direction towards the diaphragm, the pain radiates to the substernal area, neck, shoulder, and the subscapular area. Quite often it mimics stenocardia. The presence of this complication is the indication for stomach resection or vagotomy.

Perforation of gastric ulcers is an extremely rare complication of gastric ulcer. These ulcers, as a rule, are located in the antral stomach, closely against the pylorus. The technique of surgical treatment of perforating gastric ulcers, therefore corresponds to the one used in perforating duodenal ulcers.

Complications of surgical treatment of ulcer diseaseRecurrent ulcer. The incidence of postoperative recurrent ulcers accounts for

3-10% of duodenal ulcers and 2% of gastric ulcers. Recurrence after vagotomy with pyloroplasty and selective proximal vagotomy is of a more frequent occurrence than after vagotomy with resection of the antral stomach.

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After stomach resection, recurrent ulcer is usually localized on the anastomosis or right behind it inside the jejunum, and is frequently manifested by epigastric pain. In comparison with the pain in duodenal ulcer, this pain is more persistent and increases faster than before the operation.

It is considered, that occurrence of an ulcer at the place of anastomosis testifies to incomplete vagotomy. In fact, persistent Helicobacter pylori may be of crucial importance. It may be observed less after antrectomy, since bile inflow into the stomach suppresses bacterial reproduction. However, after placing Y-shaped anastomosis by Roux, which prevents reflux of bile into the stomach stump, the infection may recur. Incomplete stomach resection without vagotomy can also result in recurrent ulcer.

The sensitivity of contrast radiological study in diagnosing ulcer of anastomosis does not exceed 50-60 %. Cicatricial deformity of anastomosis can mimic or conceal the ulcer defect. If recurrent ulcer is suspected, endoscopic study, as a more sensitive and accurate method, is used.

If recurrent ulcer is caused by incomplete vagotomy, then thoracoscopic vagotomy or repeated (reconstructive) operation on the stomach (stem vagotomy, stomach resection by Roux) may be effective. To determine the completeness of vagotomy, Hollander’s insulin test may be used besides a 24-hour intragastric рН-measuring. The use of insulin enables one to investigate the influence of the vagus nerves on gastric secretion.

Insulin test. After a tube is introduced into the stomach, gastric contents are being aspirated for an hour. Then insulin is administered intravenously at a ratio of 2 Units/10 kg of the weight of the patient. Gastric contents aspirated during the 3d hour of the study (2 portions collected in separate graduated flasks) are subject to the analysis. (for 30 minutes each). Insulin test is considered to be positive, i.e. testifying to incomplete vagotomy if:1 – there is a rise in the index of free hydrochloric acid by 20 mmol/l in any sample received after insulin administration, in comparison with the index of basal secretions;2 – there is an increase in stimulated secretions of hydrochloric acid up to 10 mmol/l at the presence of basal achlorhydria in any portion of gastric juice received after insulin administration.

There are some cases when during the operation not all the branches of the vagus nerve have been divided, but it has appeared to be sufficient for reducing the level of acidity and cicatrisation of the ulcer. In these patients after insulin administration, stimulated secretion of hydrochloric acid does not exceed the value of 5 mmol/l compared to basal secretion.

Afferent loop syndrome. After stomach resection according to Bilroth-II, there may sometimes arise partial obstruction of the afferent loop of gastrojejunoanastomosis. Patients complain of distended abdomen and the pain arising in 20-60 minutes after eating, which is quite often accompanied by nausea and vomiting. Vomitus frequently contains plenty of bile, but vomiting brings relief. The

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blood analysis reveals a slight or moderate increase in amylase level. The clinical manifestations of the syndrome are likely to be caused by the distention of the afferent loop of the jejunum by pancreatic juice and bile, whose prolonged congestion results in accelerated growth of bacteria, fat and vitamin malabsorption.

Endoscopic and radiological studies of the stomach enable one to assess the extent of obstruction, morphological and functional condition of the afferent loop. Treatment consists of surgical elimination of the obstruction. The method of choice, as a rule, is the creation of gastrojejuno-and duodenojejunoanastomosis by Roux.

Technical error when performing stomach resection according to Bilroth-II may be incomplete removal of the mucous membrane of the antral stomach remaining in the duodenal stump. Having no contact with hydrochloric acid, the remaining mucous of the stomach produces a large amount of gastrin. It results in hyperchlorhydria and recurrent gastric ulcers. Only resection of the duodenal stump is able to produce cure.

Removal of the pylorus in stomach resection or its excision in pyloroplasty results in the development of duodenogastric reflux, thus causing reflux -gastritis . Patients complain of rapid satiation, unpleasant sensations in the abdomen and vomiting. Endoscopic study reveals reflux of bile into the stomach and hyperemic mucous coating. Conservative treatment with the use of the drugs improving gastric motility (motilium, cizaprid) may be helpful in some patients. Persistent course of the disease requires Y-shaped anastomosis by Roux.

The clinical picture of early dumping syndrome develops 20-30 minutes after eating and is manifested by vasomotor disorders: palpitation, tachycardia, dizziness, sweating, occasional ortostatic hypotonia, unpleasant sensations in the abdomen, vomiting. Fast inflow of hypersmolar gastric contents into the proximal jejunum results in its distention and reduction in plasma volume. Reflexes are likely to influence the distention of the jejunum or the release of intestinal hormones and vasoactive substances in blood.

The later dumping syndrome develops in 1,5-3 hours after a meal and is manifested by general weakness, dizziness, tachycardia, sweating, mental confusion, collapses. These symptoms arise after eating sweetened products. Quickly entering the jejunum, mono-and disaccharide cause glucose level to increase in blood, insulin release and jet hypoglycemia. Treatment of dumping syndrome consists of correction of diet. Oktreotid (50 mkg, 3 times a day) is prescribed in severe cases.

Postvagotomy diarrhea is seen 2 hours after eating in some patients who have had stem vagotomy. The pathogenesis of this phenomenon still remains unclear. This condition is likely to arise as the consequence of impaired parasympatic innervation of the inter organs. Destruction of the pylorus regulating gastric evacuation results in a quick inflow of gastric contents into the jejunum. Food acts as osmotic laxative causing diarrhea.

Carcinoma of gastric stump. There is a rising incidence of the development of adenocarcinoma in 15 years’ time after stomach resection executed on duodenal ulcer.

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The presence of the symptoms characteristic of gastric ulcer or carcinoma of stomach are indications to perform urgent examination.

Malabsorption syndrome. Digestion disorder and malabsorption of food in patients who have undergone operative treatment of gastric ulcer arise as the consequence of accelerated gastric emptying, poor digestion, decreased bile concentration in the intestine, accelerated passage of chyme along the jejunum, decreased or delayed secretion of pancreatic juice in response on eating.

After operation there often arises a slight steatorrhea, which can be revealed by feces analysis only. Weight loss develops more often after stomach resection (60% of patients) than after vagotomy, which is also associated with reduced consumption of food. Steatorrhea and weight loss can be caused by superfluous colonization of the intestine.

Osteoporosis and osteomalacia are seen more often after stomach resection than after vagotomy with pyloroplasty, and are caused by calcium and vitamin D malabsorptions. Radiological signs of osteoporosis are seen only some years later after the operation. Patients may experience pain in the bones or pathologic fractures. Osteomalacia is usually characterized by elevated activity of alkaline phosphatase and decreased level of calcium in blood serum. Such patients should intake calcium and vitamin D preperations.

Hematologic complications . Anemia in patients after stomach resection according to Bilroth-II increases gradually and is manifested only some years later after the operation, probably due to iron or folic acid malabsorptions. But, iron salts absorption is normal, and therefore, they may be successfully prescribed for oral intake.

Parietal cells of the stomach secrete Castle’s intrinsic factor 100 times more than needed for vitamin B ¹ ² absorption in the distal ileum. Therefore, vitamin B ¹ ² deficiency does not arise after stomach resection. Nevertheless, some patients may frequently develop decreased level of vitamin B ¹ ² in blood due to reduced absorption.

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