Ulcerative disease of the stomach and duodenum

June 22, 2024
0
0
Зміст

STOMACH AND DUODENUM

 

GASTRIC ULCER

 

The gastric ulcer is the chronic disease with polycyclic npassing. The main typical of peptic ulcer is the presence of ulcerous defect ia mucous tunic. One of basic places belongs among the gastroenterology diseases nto this pathology. Such phenomenon explained by not only considerable ndistribution of disease but also those dangerous complications which always naccompany gastric ulcers.

 

Etiology and pathogenesis

 

Frequency of morbidity non the peptic ulcer among the adult population is about 4 %. More frequent age nin patients with gastric ulcers is 50–60 years.

To development nmechanism of disease is still not enough studied. From a plenty of different theories in relation to genesis of npeptic ulcer no one able to explain the disease. So, each of such nfactors as neurogenic, mechanical, inflammatory, vascular is present in the nmechanism of development of peptic ulcer. Consider for today, that disturbance nbetween the factors of aggression and defense of mucous tunic arose peptic ulcer. To the first factors belong: nhydrochloric acid, pepsin, reverse diffusion of ions of hydrogen, products of nlipid hyperoxidizing. To the second: mucus and alkaline components of gastric njuice, property of epithelium of mucous tunic to permanent renewal, local blood nflow of mucous tunic and submucous membrane.

In the terminal stage of mechanism nof origin of gastric ulcers important role has the peptic factor and ndisturbance of trophism of gastric wall as a result of local ischemia. It nconfirmed by decreasing of blood flow in the wall of stomach at patients with nulcers on 30–35 % compared to the norm. It is proved, that a local and nfunctional ischemia more frequent arises up on small curvature of stomach ithe areas of ectopy of the antral mucous tunic in acid-forming. Exactly there nulcers appear.

Important part iulcerogenesis is acted by duodenogastric reflux and gastritis. Also, ngastrostasis can provoke hypergastrinaemia and hypersecretion and formed gastric nulcers.

Numeral scientific ndevelopments of the last years testify to the important infectious factor ithe mechanism of origin of peptic ulcer conditioned, mainly, by . helicobacter pylori.

Pathomorphology

 

Such stages of disease are ndistinguished: erosion, acute and chronic ulcers.

Erosions, mainly, are plural. Their nbottom as a result of formation of muriatic haematine is black, edges — ninfiltrated by leucocytes. A defect usually does not penetrate outside muscular ntissue of the mucous tunic. If necrosis gets to more deep layers of wall of nstomach, a acute ulcer develops. It has a nfunnel-shaped form. Bottom is also black, edges is swelled. Chronic ulcers are nmainly single, sometimes arrive to the serous layer. A nbottom is smooth, sometimes hilly, edges is like elevation, dense.

 

Classification

 

For ntoday the most known classification of gastric ulcers by Johnson (1965). There are three types of gastric ulcers are ndistinguished: I – ulcers of small curvature (for 3 cm higher from a ngoalkeeper); II– double localization of ulcers simultaneously in a stomach and nduodenum; III – ulcers of goalkeeper part of stomach (not farther as 3 cm from a ngoalkeeper). In the area of small curvature of body of stomach is localized n70,9 % ulcers, on a back wall, nearer to small curvature — 4,8 %, in the area nof cardial part – 12,9 %, in a goalkeeper part — 11,4 %. The ulcers of large ncurvature of stomach are casuistry and meet infrequently.

 

Clinical management

 

The complaints of npatients with the gastric ulcer always give valuable information about the ndisease. The detailed analysis of their anamnesis allows to pay attention to nthe possible reasons of origin of ulcer, time of the first complaints, to the nchanges of symptoms.

Pain. A pain symptom in the peptic ulcer disease is very nimportant. There are typical passing for this disease: hunger – pain – food nintake – facilitation – again hunger – pain – food intake – facilitation (so nduring all days). Night pain for the gastric ulcer is not typical. The such npatients rarely wake up in order to take a food. For diagnostics of ulcer nlocalization it is important to know the time of appearance of pain. Betweeacceptance of food and appearance of pain it is the shorter, than the higher nplaced gastric ulcer. Thus, at patients with a cardial ulcer pain arises at nonce after the food intake, with the ulcers of small curvature — in 50–60 nminutes, at pyloric localization — approximately in two hours. However this nfeature it is enough relative and some patients in general do not mark ndependence between food intake and pain. In other patients the pain attack is naccompanied by the salivation.

A epigastric regionear the xiphoid process is typical localization of pain. The irradiation of npain is not usual for gastric ulcers. Irradiation occur in patients with npenetration and depended from organ, in which an ulcer penetrates.

At the examinatioof ulcerous patient it is expedient to determine the special pain points: Boas n(pain at pressure on the left of the Х–ХII pectoral vertebrae), Mendel (pain at npercussion on the left to epigastric region).

Vomiting, the sign of disturbance of motility function of nstomach, is the second typical symptom of gastric ulcer. More frequent gastrostasis narises as a result of failure of stomach muscular, it atony which can be effect nof organ ischemia. Vomiting could arises both on empty stomach and after food nintake.

Heartburn is one of early symptoms of gastric ulcer, however at nthe prolonged passing of disease it can be hidden or quite disappear. Often it nprecedes of pain arising (initial heartburn) or accompanies a pain symptom. nMostly heartburn arises after the food intake, but can appear independently. it nis observed not only at hypersecretion of the hydrochloric acid, but at normal nsecretion, even reduced acidity of gastric juice.

The nbelching at gastric ulcers is nexamined rarely, more frequent in patients with cardial and subcardial ulcers. nIt is necessary to bind to disturbance of function of cardial valve.

The ngeneral condition of npatients with the uncomplicated gastric ulcer usually satisfactory, and in a nperiod between the attacks — even good. However for most patients lost of the nbody weight and pallor are typical. In a epigastric region hyperpigmental spots nare examined after the prolonged application of hot-water bottle. At palpatioof stomach in this area sometimes appears local painful. It is needed also to ncheck up “noise of splash”, the presence of which can be the sign of possible ngastrostasis.

At the examinatioof mouth cavity a tongue has whiter-yellow incrustation. In patients with npenetration ulcers and disturbances evacuations from a stomach examined dryness nof tongue.

Stomach, as a rule, nregular rounded shape, however during the pain attack is pulled in. There is nantiperistalsis arises during the pylorostenosis.

 The increased secretion of hydrochloric acid nin patients with gastric ulcers observed rarely and, mainly, at prepyloric nulcer localizations. Mostly secretion is normal, and in some patients is evereduced.

X-Ray nexamination. The direct signs nof ulcer at X-Ray examinations are: symptom of “Haudek’s niche” (Pic. 3.2.1), nulcerous billow and convergence of folds of mucous tunic. Indirect signs: nsymptom of “forefinger” (circular spasm of muscles), segmental nhyperperistalsis, pylorospasm, delay of evacuation from a stomach, nduodenogastric reflux, disturbance of function of cardial part n(gastroesophageal reflux).

Gastroscopy cagive important information about localization, sizes, kind of ulcer, dynamics nof its cicatrization, and also allow to perform biopsy with subsequent nhistological examination.

 

Clinical variants and ncomplication

 

The gastric ulcer npassing can be acute and chronic. Acute ulcers arise as answer for the stress nsituations, related to the nervous overstrain, trauma, loss of blood, some ninfectious and somatic diseases. By a diameter ulcers has from a few nmillimeters to centimeter, a round or oval form with even edges. Thus in most ncases clinically observed clear ulcerous clinical signs. If complications is nabsent (bleeding, perforation) such ulcers treated and mostly heal over.

G.J. Burchynskyy n(1965) such variants of clinical flow distinguished:

1. Chronic ulcer nwhich does not heal over long time.

2. Chronic ulcer nwhich after the conservative therapy heals over relatively easily, however ninclined to the relapses after the periods of remission of a different nduration.

3. Ulcers, which nlocalization are had migrant character. Observed in people with acute ulcerous nprocess of stomach.

4. Special form of ngastric ulcer passing after the already carried disease. Passed with the nexpressed pain syndrome. Characterized by the presence in place of ulcerous ndefect of scars or deformations and absence of symptom of “niche”.

There are such ncomplications can develop in patients with gastric ulcer: penetration, nstenosis, perforation, bleeding and malignization.

 

Diagnosis program

 

1. Anamnesis and nphysical examination.

2. Endoscopy.

3. X-Ray nexamination of stomach.

4. Examination of ngastric secretion by the method of aspiration of gastric contents.

5. Gastric pH nmetry.

6. Multipositiobiopsy of edges of ulcer and mucous tunic of stomach.

7. Gastric nDopplerography.

8. Sonography of nabdominal cavity organs.

9. General and nbiochemical blood analysis.

10. Coagulogram.

 

Differential diagnostics

 

Chronic gastritis, as well as at an gastric ulcer, ncharacterized by the pain syndrome, that arises after the food intake. In such npatients it is possible to observe nausea and vomiting by gastric content, nheartburn and belch. However, unlike an gastric ulcer, for gastritis typical nsymptom of “quick satiation by a food”. Unsteady emptying, diarrhea also more ninherent to gastritises. At gastric ulcer more frequent the delays are nobserved, constipation for 4–5 days.

The cancer of stomach, it is comparative with an gastric ulcer, nhas considerably more short anamnesis. The most typical clinical signs of this npathology are: absence of appetite, weight loss, rapid fatigability, depression, nunsociability, apathy. In such patients X-Ray examination expose the “defect of nfilling”, related to exophytic tumor and deformation of walls of organ. A final ndiagnosis is set after the results of multiposition biopsy of shady areas of nmucous tunic of stomach.

Differential diagnostics also needs nto be conducted with the so called precancerous states: gastritis with the nachlorhydria; chronic, continuously recurrence ulcers, poliposis and nAddison-Biermer anemia.

 

Tactic and choice of ntreatment method

 

Conservative ntreatment of gastric ulcer always nmust be complex, individually differentiated, according to the etiology, npathogeny, localization of ulcer and character of clinical signs (disturbance of nfunctions of gastroduodenal organs, complication, accompanying diseases).

Conservative ntherapy must include:

·        nOmeprazole n20 mg 2 time per day or  Н2- blocker nhistamine receptor (ranitidine) — 150 mg in the evening, famotidine — 40 mg at nnight,
nroxatidine — 150 mg in the evening

·        nantiacid ndrugs — in accordance with the results of pH-metry;

·        nreparative ndrugs (dalargin, solcoseryl, actovegin) — for 2 ml 1–2 times per days

·        nantimicrobial ndrugs (clarytromicine 500 mg twice daily, de-nol, metronidazole)

 

Treatment of npatient with a gastric ulcer must continues not less than 6–8 weeks.

Surgical treatment nmust performed in cases:

а) at the relapse nof ulcer after the course of conservative therapy;

б) in the cases whethe relapses arise during supporting antiulcer therapy;

в) when an ulcer ndoes not heal over during 1,5–2 months of intensive treatment, especially ifamilies with “ulcerous anamnesis”.

г) at the relapse nof ulcer in patients with complications (perforation or bleeding);

д) at suspicion omalignization ulcers, in case of negative cytological analysis.

The choice of nmethod of surgical treatment of gastric ulcer depended from localization and nsizes of ulcer, presence of gastro- and duodenostasis, accompanying gastritis, ncomplications of peptic ulcer (penetration, stenosis, perforation, bleeding, nmalignization), age of patient, general condition and accompanying diseases. Ipatients with cardial localization of ulcer the operation of choice is the proximal nresection of stomach, which, from one side, allows to remove an ulcer, and from nother — to save considerable part of organ, providing it functional ability n(Pic. 3.2.2). In case with large cardial ulcers, when the vagus nerves pulled nin the inflammatory infiltrate and it is impossible to save integrity even one nof them, operatioeeds to be complemented by pyloroplasty. It will give npossibility to warn pylorospasm and gastrostasis, which in an early npostoperative period can be the reason of anastomosis insufficiency and other ncomplications.

At the choice of nmethod of surgical treatment of gastric ulcers with subcardial localization osmall curvature without duodenostasis it is better to apply the methods of nstomach resection with saving of passage through a duodenum.

For this purpose we nare developed the method of segmental resection of stomach with additioselective proximal vagotomy. The redistribution of gastric blood nflow between the functional nparts of stomach as reply to medicinal vagotomy (intravenous introduction 1,0 ml 0,1 % solution of natropine of sulfate) is studied. Hyperemia of acid-forming part of stomach ncomes after introduction of preparation. The functional scopes of stomach parts nare determined. The border between acid-forming and antral parts are the most frequent localization of gastric nulcers.

During this noperation middle laparotomy is performed, intravenously entered 1,0 ml 0,1 % nsolution of atropine, then the scopes of functional stomach parts are nidentified and by stitches-holders is marked a intermedial segment. Selective proximal vagotomy is performed. After mobilization of large curvature nof stomach within the limits of intermedial segment it resection is performed. nAfter that gastro-gastro anastomosis “end-to-end” is formed (Pic. 3.2.3).

The analysis of nsupervisions of the patients operated by such method in postoperative period nhas good results. It allows to recommend this operation for clinical practice, nin case of gastric ulcers of subcardial localizations, without duodenostasis, npenetration, malignization or nerves Latarjet damaging.

The operation of nchoice in patients with subcardial ulcers and duodenostasis is gastric nresection by Billroth II.

the tubular nresection of stomach on  the Більрота-II nmethod.

At the choice of nmethod of surgical treatment of ulcers which are localized in upper and middle nthird of stomach, it is necessary to consider such factors, as absence of npenetration in a small omentum and absence of the duodenostasis. In such npatients is performed segmental resection of stomach with ulcer removing with nselective proximal vagotomy. In case of penetration ulcer in a small omentum nwith involvement in infiltrate Latarjet nerves, such operation is impossible nbecause of future spasm of pylorus and gastrostasis. If duodenostasis is nabsence than better to apply pylorus-saving resection by Maki-Shalimov. Ipatients with duodenostasis better to apply gastric resection by Billroth II.the nпілорозберігаючу resection of stomach for Макі-Шалімовим (rice. 3.2.4), and at npatients with present стазом in a duodenum — resection of stomach after the nБільрота-ІІ method (rice. 3.2.5).

 

At the border of ngastric resectioear pyloric sphincter can be spasm and gastrostasis in a npostoperative period . Avoiding such complication is possible, if this border nof gastric resection passes no more than 1,5 cm from a pyloric nsphincter (M.M. Risaev, 1986). So, at a resection, that passes higher than 2,0 cm from a npylorus, integrity of both loops is kept.

Patients with nantral ulcers without the duodenostasis performed the gastric resection by Billroth nI (Pic. 3.2.6), and on presence of duodenostasis – Billroth II.the nпілорозберігаючу resection of stomach for Макі-Шалімовим (rice. 3.2.4), and at npatients with present стазом in a duodenum — resection of stomach after the nБільрота-ІІ method (rice. 3.2.5).

 

Prepiloric ulcers nis similar to the ulcers of duodenum. Such localization of gastric ulcers nwithout malignization allow to perform selective proximal vagotomy. However, at large prepyloric ulcers with penetration without duodenostasis is nbetter to perform the gastric resection by Billroth I and on presence of nduodenostasis – by Billroth II.

Більротом-I, nand with the дуоденостазуБільротом-ІІ phenomena.

By ncontra-indication to operations with saving of food passing through the nduodenum are also decompensated pylorostenosis , functional gastrostasis and nduodenostasis. In such patients it is better to perform gastric resection by nBillroth II.

 

DUODENAL ULCER

 

The duodenal ulcer is the chronic recurrent disease nwhich characterized by ulcerous defect on a mucous tunic of duodenum. Pathology noften makes progress with complications development.

 

Etiology and npathogenesis

 

There are some netiologic factors of the duodenal ulcer: Helicobacter pylori, emotion tensioand neuropsychic stress overstrain, heredity and genetic inclination, presence nof chronic gastroduodenitis, disturbance of diet and harmful habits (alcohol, nsmoking). In pathogenesis of peptic ulcer a leading role is played disturbance nof equilibrium between aggressive and projective properties of secret of nstomach and it mucous tunic. The aggressive factors are vagus hyperfunctioning nand hypergastrinemia; hyperproduction of hydrochloric acid and pepsin, and also nreverse diffusion of the ions Н+, action of bilious acids and isoleucine, ntoxins and enzymes of helicobacter pylori (HP). There are factors which are ncontribute to ulcerogenic action: disturbance of motility of stomach and nduodenum, ischemia of duodenum, and metaplasia of the epithelium.

 

Pathomorphology

 

Morphogenesis of duodenal ulcer nfundamentally does not differ from ulcer in a stomach. Chronic ulcers are nmainly single, is localized on the front or back wall of bulb (bulbar ulcer) nand only in 7–8 % cases – below it (postbulbar ulcer). The plural ulcers of nduodenum are met in 25 % cases.

 

 

Classification

(by A.L.Hrebenev, A.O.Sheptulin, 1989)

 

The duodenal ulcer nis divided:

I. By etiology: n

А. True duodenal nulcer.

Б. Symptomatic ulcers.

II. By passing nof disease:

1. Acute (first nexposed ulcer).

2. Chronic:

a) with the rare exacerbation; n

b) with the annual nexacerbation;

c) with the nfrequent exacerbation (2 times per a year and more frequent).

III. By the nstages of disease:

1. Exacerbation.

2. Scarring:

a) stage of “red” nscar;

b) stage of “white” nscar.

3. Remission.

IV. By nlocalization:

1. Ulcers of bulb nof duodenum.

2. Low postbulbar nulcers.

3. Combined ulcers nof duodenum and stomach.

V. By sizes: n

1. Small ulcers up nto 0,5 cm. n

2. Middle — up 1,5 cm.

3. Large — up to 3 cm;

4. Giant ulcers nover 3 cm. n

VI. By the npresence of complications:

1. Bleeding.

2. Perforation.

3. Penetration.

4. Organic nstenosis.

5. Periduodenitis.

6. Malignization.

 

Clinical management

 

Pain in the epigastric nregion is the most expressed symptom of duodenal ulcer, often with displacement nto the right in the projection area of bulb of duodenum and gall-bladder. Also nfor this pathology is typical the pain, that arises in 1,5–2 hours after food nintake, “hungry” and nightly pain. As a rule, it is acute, sometimes nunendurable, and is halted only after the use of food or water. Such patients ncomplains for the seasonal exacerbation, more frequent in spring and in autumn. nHowever exacerbation can be also in winter or in summer. In the acute period of ndisease heartburn often increases. However heartburn is the frequent symptom of ncardial insufficiency and gastroesophageal reflux. For an duodenal ulcer the nacute burning feeling of acid in a esophagus, pharynx and even in the cavity of nmouth is especially typical. Often are belch by air or sour content, excessive nsalivation. Vomiting is not a typical symptom for duodenal ulcer. More typical nsign is nausea. Sometimes for facilitation patients wilfully cause vomiting. nThese symptoms, arises in the late periods of passing of duodenal ulcer.

Intensity of paiand dyspepsia syndromes depends both on the depth of penetration and from ndistribution of ulcerous and periulcerous processes. Superficial ulceratiowithin the mucous tunic, as a rule, does not cause the pain because it does not nhave sensible receptors. However, more deep layers of wall (muscular and nespecially serous) have plural sensible vegetative receptors. Therefore, odeepening and distribution of process arises visceral pain. At evident nperiulcerous processes and penetration of ulcers to neighboring organs and ntissues, usually, a parietal peritoneum, that has spinal innervation, is pulled nin. Pain becomes viscero-somatic, more intensive. A such pain syndrome (with airradiation in the back) is typical for low postbulbar ulcers and bulbous nulcers of back wall, which penetrates in a pancreas and hepato-duodenal nligament. Usually such patients has good appetite. Some of them limit nthemselves in acceptance of ordinary food, go into to the dietary feed by small nportions, and some — even hold back from a food, being afraid to provoke pain, nand as a result of it weight is lost. Some of patients feeds more intensive and noften.

The psychical nstatus of patients often are changed as a asthenoneurotic syndrome: irritates, ndecline of working capacity, indisposition, hypochondria, abusiveness.

An inspection, as a nrule, gives insignificant information. In many cases on the abdominal skin it nis possible to notice hyperpigmentation after application of hot-water bottle. nDuring the pain attack patients often occupy the forced position. At nsuperficial palpation on the abdominal wall determined hyperesthesia in ulcer nprojection. In the epigastric region, during deep palpation, it is possible to ndefine pain and muscular tension, mostly moderate intensity. There is important nsymptom of local percussion painful (Mendel’s symptom): percussion by fingers nin the symmetric epigastric areas provoke pain in the ulcer, which is increased nafter the deep breath. The roentgenologic and endoscopic are main diagnostic nmethods. The symptom of ulcerous “niche” is a classic roentgenologic sign. It nis depot of contrast agent, which is corresponded to ulcerous defect, with nclear contours and light bank to which converged fold mucus. Cicatricial ndeformation of bulb of duodenum as a shamrock, butterfly, narrowing, tube, ndiverticulum and other forms is the important sign of chronic ulcerous process. nA roentgenologic method is especially important for determination of nconfiguration and sizes of stomach and duodenum, and also for estimation of nmotility functions. X-Ray examination is the main method at the peptic ulcer ncomplicated by stenosis, with disturbance of evacuation, duodenostasis, nduodenal-gastric reflux, gastroesophageal reflux, diverticulum. But by X-Ray nexamination is difficult to diagnose small superficial ulcers, acute ulcers, nerosions, gastritises and duodenitises. The most informing method in such cases nit endoscopy.

During endoscopy nexamination it is possible to define localization, form, sizes and depth of nulcer. During bleeding grumes, trickle or pulsating of blood are observed. By nirrigation by styptic solutions, by cryocoagulation, by laser coagulatioendoscopy allows to secure hemostasis. Endoscopy allows to perform the biopsy nof ulcer tissues for determination of possible malignization.

 

Clinical variants and ncomplication

 

In patients with nlow postbulbar ulcers the clinical signs are more expressed. It characterized nby late (in 2–3 hours after food intake) and intensive “hungry” and nightly npain, that often irradiate to the back and to the right hypochondrium. The npostbulbar ulcers are inclined to more frequent exacerbation, and also to more nfrequent complications, such, as penetration, stenosis and bleeding.

The are more nfrequent ulcerous bleeding (the bulbous happen in 20–25 % cases, postbulbar — nin 50–75 %), perforations (10–15 % cases). Penetration, stenosis and nmalignization in patients with duodenal ulcers are observed rarely.

Penetration is nfrequent complication of “low” and postbulbar ulcers of duodenum, which are nplaced on posterior, posterior superior and posterior inferior walls. nPenetrates, usually, deep chronic ulcers, by passing through all layers of nduodenum ieighboring organs and tissues (head of pancreas, hepato-duodenal nligament, small and large omentum, gall-bladder, liver). Such penetration is naccompanied by development of inflammatory process in the neighboring organs nand surrounding tissues and forming of cicatrical adhesions. A pain syndrome nbecomes more intensive, permanent and often pain irradiated in the back. nSometimes in the area of penetration it is possible to palpate painfully ninfiltrate.

 

Diagnostic program

 

1. Anamnesis and nphysical examination.

2. Endoscopy.

3. X-Ray nexamination of stomach and duodenum.

4. General and nbiochemical blood analysis.

5. Coagulogram.

 

Differential diagnostics

 

The duodenal ulcer must be ndifferentiated from acute and chroniccholecystitis, pancreatitis, ngastroduodenitis. Endoscopy is help to diagnose duodenal ulcer.

 

Tactic and choice of ntreatment method

 

Conservative ntreatment. In most patients after nconservative treatment an ulcer heals over in 4–6 weeks. Warning of relapses ncan be carried out by only supporting therapy during many years.

The best therapy of nduodenal ulcer is associated with a helicobacter infection, there is the use of nantagonists of Н2- receptors of histamine (renitidine— 300 mg in the evening or n150 mg twice for days; famotidine— 40 mg in the evening or 20 mg twice for ndays; nisatidine — 300 mg in the evening or 150 mg twice for days; roxatidine — n150 mg in the evening) in combination with sucralfate (venter) — for 1 г three times for ndays and antacid (almagel, maalox or gaviscon —1 dessert-spoon in a 1 hour nafter food intake). To this complex it is needed to add antibacterial npreparations (De-nol – 1 tabl. 4 times per a day during 4–6 weeks + oxacylline nfor 0,5 g n4 times per a day — 10 days + Tryhopol (metronidazole) for 0,5 g 4 times per a nday — 15 days).

In treatment of nduodenal ulcer used chinolitics and miolitics (atropine, methacin, nplatyphyllin), and also mesoprostol (200 mg 4 times per days) and omeprasole n(20 or 40 mg on days).

Such treatment of npatients with the duodenal ulcer must be 4–6 weeks. If complications absents nthere is no necessity in the special diet.

Because of nappearance of new pharmaceutical preparations and modern therapeutic treatment, nindication to the operative methods narrowed. But the number of acute ncomplications of duodenal ulcer does not go down, especially bleeding and nperforations which require the urgent surgery.

Indications nto the elective operation:

1. Passing of nduodenal ulcer with the frequent relapses which could not treated nconservatively.

2. Repeated nulcerous bleeding.

3. Stenosis of noutcome part of stomach.

4. Chronic penetratioulcers with the pain syndrome.

5. Suspicion for nmalignization ulcers.

Methods nof surgical treatment.

At patients with nthe duodenal ulcer three types of operations are distinguished:

— organ-saving noperations;

— organ-sparing noperations;

— resection.

From them the nbetter are: organ-saving operations with vagotomy, excision of ulcer and ndrainage operation.

Types nof vagotomy: trunk (TrV) n(Pic.. 3.2.7), selective (SV) (Pic. 3.2.8), selective proximal (SPV) (Pic. n3.2.9). Selective proximal vagotomy is optimal in the elective surgery of nduodenal ulcer. However in urgent surgery a trunk, selective or selective nproximal is often used in combination with drainage operations.

Drainage of the nstomach operations are: Heineke-Mikulicz pyloroplasty, Finney pyloroplasty, nsubmucous pyloroplasty by Diver-Barden-Shalimov, gastroduodenostomy by nJaboulay, gastroenteroanastomosis.

пілоропластику for Гейнеке-Мікулічем (rice. 3.2.10), for Фіннеєм (rice. 3.2.11), підслизову пілоропластику after the Дівера-Бардена-Шалімова method, гастродуоденостомію, offered Жабуле (rice. 3.2.12), nгастроентероанастомоз and ін.

_It is necessary to mark nthat “clean isolated” SPV, performed in patients with duodenal ulcer, often (i15–20 % cases) results in the relapses. The considerably less number of nrelapses (8–10 %) is observed after SPV in combinations with drainage noperations. Especially dangerous is the relapses of the ulcers placed in the nprojection of large duodenal papilla, after gastroduodenostomy by Jaboulay.

The least number of nrelapses of duodenal ulcer is observed after organ-saving operations, that ncombine SPV and ulcer excision.

If ulcer localized non the anterior surface of duodenal bulb it can be performed by the method Jade n(Pic. 3.2.13) with subsequent to the pyloroplasty by Heineke-Mikulich.

At patients with ndecompensate stenosis and expressed dilatation and by the atony of stomach it nis needed to apply the classic resection of stomach depending on possible ndamping-syndrome by Billroth -I or Billroth -II.

The choice of nsubtotal resection of stomach needs to be done at suspicion for malignizatioor at histological confirmed malignization ulcers. In a duodenum this process nhappens very rarely.

 

 

ULCEROUS STENOSIS

 

Ulcerous stenosis is complication of Peptic ulcer or nduodenum, which characterized by narrowing.

 

Etiology and npathogenesis

 

Stenosis of noutgoing part of stomach and duodenum of ulcerous origin arises as a result of nscarring and common morphological changes around an ulcer. Narrowing, ndisturbance of the coordinated motility of goalkeeper come as a result of it nand creates the obstacle to the even moving of stomach content to the duodenum.

 

Pathomorphology

 

Such pathology in the compensation stage narises hypertrophy of the stomach walls. The pyloric ring has a 0,5–0,7 cm idiameter. The mucous tunic of pyloric part of stomach is thickened, with rough nfolds. Muscular fibers are hypertrophied and solid. Histological hyperplasia of npyloric glands is observed.

During decompensation the muscular nlayer of stomach higher stenosis becomes thinner, tone of him goes down, and a npyloric ring narrows to a few millimetres. Microscopically present atrophy of nmucous tunic and muscular fibers, vessels sclerosis. A stomach collects the nform of the stretched sack which goes down to the level of small pelvis.

 

Classification

(by О.О. Shalimov nand V.F.Saenko, 1987)

 

Three clinical stages nof stenosis are distinguished:

I — compensated;

II — nsubcompensated;

III — ndecompensated.

The morphological nchanges in the initial part of stomach and duodenum are represented by the nclassification offered by M.I. Kusin (1985). On the basis of clinical, nroentgenologic, endoscopic, electrogastrographical and intraoperative methods nthe examinations distinguished three stages of stenosis:

I — inflammatory;

II — ncicatricial-ulcerous;

III — cicatricial.

In accordance with nlocalization, by V.F.Saenko (1988) distinguished three types of stenosis:

I — stenosis of ngoalkeeper;

II — stenosis of nbulb of duodenum;

III — postbulbar nduodenal stenosis.

First two types of nstenosis are similar by functional and the organic changes. It united them by none name — pyloroduodenal, or high duodenal stenosis. The second group is npostbulbar duodenal stenosis. Feature of them is that a goalkeeper does not ntake participation in the cicatricial- ulcerous process and it function is not nbroken.

 

Clinical management

 

The nfirst signs of stenosis can be exposed already in eight-ten years from the nbeginning of the peptic ulcer disease., Mainly, this is narrowing and rigidity nand disturbance of retractive activity of goalkeeper, which create a barrier nfor transition of stomach content to the duodenum.

In the stage of the ncompensated stenosis hypertrophy of wall of stomach develops and tone of nmuscular shell rises. Hereupon gastric content, slowly, but passes through the nnarrowed area of stomach output. In this stage patients, usually, complained nabout feeling of plenitude in a epigastric area after food intake, periodic nvomitings by sour gastric content. On empty a stomach by a stomach pump 200–300 nml gastric content is removed.

In the subcompensated nstage muscular layer of stomach becomes thinner. Tone of him goes down, a nperistalsis relaxes, and it looks like the stretched sack. Evacuation disorders nis increased. Fermentation and rotting developed in stagnant gastric content. nOn this stage of disease development patients, usually, complain for the npermanent feeling of weight in epigastric region and regurgitation with aunpleasant “rotten” smell of sulphuretted hydrogen.

Vomiting becomes nsystematic (once or twice on a day) up to half of liter per day. On empty a nstomach it possible to aspirate from it more 500 ml of content with the food nused the day before.

In the decompensatiostage of the clinical sighn make progress quickly. There are heavy ndisturbances of the general condition of patient, considerable loss of weight n(to 30–40 %), acutely expressed dehydration of organism, hypoproteinemia, nhypokalemia, azotemia and alkalosis. In case of the protracted neglected ndisease, as a result of progress of disturbances of metabolism, there can be a nconvulsive syndrome (gastric tetany). Vomiting in this stage not always can be nconsidered by a typical sign, in fact patients often renounce to adopt a food, nand a stomach acquires considerable sizes, overdistension form, it tone is nviolated and atrophy of wall comes. In such patients in a epigastric area it is npossible to define the contours of the stretched stomach, with a slow nperistalsis,. In the distance it is possible to hearken the splash. By a probe nfrom a stomach to 1.5-2litres of food with a putrid smell are removed. There ncan be gastric tetany at considerable disturbances of electrolyte metabolism.

A diagnosis is set naccording to a typical syndrome, results of sounding of stomach, rontgenoscopy, nat which by contrasting of a barium expose stenosis of initial part of stomach nor duodenum, determines it origin and estimate a degree.

Roentgenologically in the compensation stage stomach iormal sizes, it nperistalsis deep, increased, evacuation of content proceeds no more than 6 nhours. In the stage of subcompensation a stomach is megascopic, a peristalsis nis loosened, evacuation stays too long to 24 hours. During decompensation a nstomach is considerably extended as a sack, deformed, the waves of nantiperistalsis can take place, a contrast stays too long more than 24–48 nhours. The method of the double contrasting by a barium and air considerably nfacilitates diagnostics.

Determination of nstomach motility has not only diagnostic but also prognostic value for the nchoice of method of operation.

In the stage of ncompensation motility of stomach is well-kept, often even increased. With the nincreasing the degree of stenosis the motility disturbance increased, up to ngastroplegia.

In the biochemical nblood test is marked the decline of content of albumen to 54–48 g/l; potassium n— to 2,9–2,5 mmol/l; chlorides — to 85–87 mmol/l. The changes of such indexes nare most expressed at patients with gastrogenous tetany.

The study of nsecretory function of stomach allows to define the degree of compensation of nstenosis and importent at the choice of adequate method of operation.

Gastroscopy with a nbiopsy is the enough informing method of examination of such patients. By this nmethod is possible to determine a reason and degree of stenosis, and also state nof mucous tunic of stomach.

 

Diagnosis program

 

1. Complaints of npatient and anamnesis of disease.

3. Sounding of nstomach and examination of gastric content.

4. Fibergastroduodenoscopy, nbiopsy.

5. Intragastric nрНmetry.

6. Study of motility nof stomach.

7. Roentgenologic nexamination of stomach and duodenum (structural features, passage).

8. Sonography.

 

Differential diagnostics

 

Stenosis of the output part of nstomach and duodenum of ulcerous origin it is needed to differentiate with nfunctional gastrostasis and narrowing of tumour and chemical genesis.

Functional gastrostasis more frequent meets at women. Basic, that ndistinguishes it from other pathologies, there is absence of some organic nchanges in the area of pyloric part of stomach or in a duodenum, that can be nexposed during fibergastroscopy.

Differential diagnostics of stenosis nof tumour genesis, as a rule, also does not cause the special ndifficulties. A diagnosis is finally confirmed by histological examinations of nthe biopsy material taken during endoscopy.

Postburn stenosis of piloroantral narea of stomach observed, from data of statistics, more than in 25 % cases of npatients with the burn of esophagus. In anamnesis in each of such patients ntakes place by mistake or the intentionally taken an a swig at acid, alkali or nother chemical matter. Some diagnostic difficulties can arise up at the nisolated postburn stenosis of pyloric part of stomach. The however attentively ncollected anamnesis and professionally conducted endoscopic examination enable nto set a correct diagnosis.

 

Tactic and choice of ntreatment method

 

Treatment of ulcerous nstenosis of piloroantral part of stomach and duodenum must be exceptionally noperative. A method depend on many factors: degree of stenosis, these secretory nand motility functions of stomach, age of patient, presence of accompanying ndiseases and others like that. In the compensated and subcompensated stages of nstenosis and at enough well-kept functions of stomach it is possible to perform nof organ-saving operations (vagotomy with drainage stomach operations, economy nresection of stomach). At growth of the signs of stenosis and disturbance of nbasic functions of stomach, the volume of operation must be increased up nresection by the Bilroth’s second method.

At the patients and nolder age persons with heavy accompanying pathology is performed minimum surgery n—gastroenteroanastomosis.

Preoperative npreparation must be strictly individual.

At patients with ninsignificant disturbances of gastric motor activity (stage of compensation, nsubcompensations) and with good level of metabolism indexes it is better to nshorten preoperative preparation in time. Such patients, usually, operated o3–4 day. Preparation before operation at patients with decompensated npilorostenosis must be directed for the correction of metabolism disturbances. nSuch patients must receive transfusion of liquid up to 2,5–3 l per day with ncontent of the ions К+, Na+, Са++, amino acid and glucose; plasma, albumen. nTwice on days performed decompression and washing of stomach and anti-ulcerous ntherapy. Effective preoperative preparation in such patients requires 5–7 days, nsometimes more.

 

 

 

PERFORATED GASTRODUODENAL ULCERS

 

The typical nperforation of gastric or duodenum ulcer is strengthening of necrosis process ithe area of ulcerous crater with subsequent disturbance of integrity of wall, nthat result to the permanent effluence of gastroduodenal content and air in a nfree abdominal cavity.

 

 

Etiology and npathogenesis

 

In 50,7 % cases perforates nthe ulcers of duodenum, in 42,8 % are ulcers of pyloric part of stomach, in 4,8 n% are ulcers of small curvature of body of stomach and in 0,7 % are cardial nulcers.

Ulcers, which lie non the front wall of stomach and duodenum more frequent give the perforatiowith general peritonitis, while ulcers on a back wall — perforation with nadhesive inflammation.

The reasons of nulcers perforation are: exacerbation of peptic ulcer, harmful habits, stresses, nprofessional, athletic overexertion, faults in the feed and abuses by strong nwaters.

 

Pathomorphology

 

In pathogeny of acute perforatioimportant: progressive necrosis processes in the area of ulcerous crater with activating nof virulent infection; hyperergic type of local vaculo-stromal reaction with nthe thrombosis of veins of stomach and duodenum; local manifestation of nautoimmune conflict with accumulation of sour mucopolysaccharides on periphery nof ulcer and high coefficient of plasmatization of mucous tunic (К.I. Mishkin, nА.А. Frankfurt, 1971).

 

Classification

(by V.S. Savelev, n1986)

 

Perforated ngastroduodenal ulcers are divided:

1. nAfter etiology:

— ulcerous;

— unulcerous.

2. nAfter localization:

— gastric (small ncurvature, cardial, antral, prepyloric, pyloric) ulcer, front and back walls;

— ulcers of nduodenum (front and back walls).

3. nAfter passing:

— perforated in aabdominal cavity;

— covered nperforations;

— atypical nperforations.

 

Clinical management

 

The clinical npicture of perforation is very typical and depends on distribution of ninflammatory process and infection of abdominal cavity. In clinical passing of nthe perforations distinguish three phases: shock, “imaginary prosperity” and nperitonitis (Mondor, 1939).

For the phase of shock (to 6 hours nlast) typical very acute pain in epigastric region (Delafua compares it to paifrom the stab with a dagger) with an irradiation in a right shoulder and ncollar-bone, a face is pale, with expression of strong fear, lines become n(facies abdominalis) acute, a death-damp irrigates skin covers. A pulse is at nfirst slow (vagus pulse), later becomes frequent and less filling. Sometime nobserved the reflex vomiting and delay of gases. Arterial pressure is reduced. nOn examination stomach is pulls in, does not take part in the act of breathing. nAt palpation is “wooden belly stomach”, especially in an upper part, where, nusually, there is most pain. Positive Blumberg’s nsign. At percussion is ndisappearance of hepatic dullness (the Spizharnyy symptom). At rectal examination expose painful in the area of rectouterine or rectovesical npouch (the nKulenkampff’s symptom).

The phase of shock nchanges by the phase of “imaginary prosperity”, when the reflex signs go down: nthe general condition of patient gets better, a pulse becomes normal, arterial pressure nrises, a stomach-ache diminishes partly. However observed tension of muscles of nfront abdominal wall, positive Blumberg’s sign.

The phase of n“imaginary prosperity” in 6–12 hours from the moment of perforation changes by nthe phase of peritonitis: a pulse is frequent, a stomach is swollen through ngrowing flatulence, intestinal noises are not listened, a face acquires the nspecific kind — facies Hippocratica —the eyes fall back, lips turn blue, a nose nbecomes sharp, a tongue becomes dry and furred, breathing superficial and nfrequent, a temperature rises.

 

Variants of clinical passing nand complication

 

Covered perforation (А.М. Shnicler, 1912). At this npathology the perforative hole after a perforation is closed by a fibrin, by a omentum, nby the fate of liver, sometimes — piece of food. After that some amount of nstomach content and air gets in an abdominal cavity. After the protection a nstomach-ache diminishes, but proof tension of muscles of front abdominal wall, nespecially overhead quadrant of stomach is kept. At percussion hepatic dullness nis doubtful. During x-Ray examination it is not always possible to mark gas iright hypochondrium (Pic. 3.2.14).

Consequences of npassing of the covered perforation: the repeated perforation with development of classic nclinical signs can come; at separation of process from a free abdominal cavity na subdiaphragmatic or subhepatic abscess is formed; complete closing of defect nby surrounding tissue with gradual convalescence of patient.

The atypical perforation is the perforation, at which gastric nor intestinal content gets not to the abdominal cavity, but in retroperitoneal nspace (ulcers of back wall of duodenum), large or small omentum (ulcers of small ncurvature of stomach), hepato-duodenal ligament.

In such patients nduring a perforation pain is not acutely expressed. During palpation observed ninsignificant rigidity of muscles of front abdominal wall. On occasion, nespecially on the late stages of disease, there can be hypodermic emphysema and ncrepitation.

 

Diagnosis program

 

1. Anamnesis and nphysical examination.

2. Global analysis nof blood and urine, biochemical blood test,

coagulogram.

3. X-Ray nexamination of abdominal cavity organs for presence of free gas n(pneumoperitoneum).

4. nPneumogastrography, contrasting pneumogastrography.

5. nFiber-gastroduodenoscopy.

6. Sonography of nabdominal cavity organs.

7. Laparocentesis with nthe Neymark diagnostic test (to the 2–3 ml of abdominal cavity exudate adds 4–5 ndrops of the 10 % solution of iodine. If the admixtures of gastric content nappear in exudate, then under action of iodine gastric content gets a ndirtily-dark blue color).

8. Laparoscopy.

 

Tactic and choice of ntreatment method

 

The diagnosed nperforated gastric and duodenum ulcer is an absolute indications to operation. nPreoperative preparation must include: in I phase are antishock action; in the nII and III phases — reanimation preparations, introductions of antibiotics for n2–3 hours before operation, liquidation of hypovolemia by salt blood nsubstitutes (solution of chlorous sodium), solutions of dextran (polyhlukine, nreopolihlukine, hemodes). Amount of liquid necessary for correction of hypovolemia, ncalculate after hematokrit by central vein pressure. Taking for the norm of nhematokrit 40 %, on each 5 % higher norms need to be poured 1000,0 ml liquids.

Conservative ntreatment (method of Tejlor, 1946) can be justified at the refusal of patient from noperation or in default of conditions for its implementation.

It must include:

— permanent nnasogastral aspiration of gastric content;

— introduction of npreparations which brake a gastric secretion (atropine, Н2- blockers and others nlike that);

— introduction of nantibiotics;

— correction of nmetabolism;

— laparocentesis nwith drainage and closed lavage of the abdominal cavity.

In the decision of nquestion about the choice of method of operative treatment of perforated ngastroduodenal ulcers the important value has the following factors: nlocalization of ulcer, clinico-morphological description of ulcer (perforatioof acute or chronic ulcer), connected with the perforation such complications nof ulcer, as bleeding, cicatricial-ulcerous stenosis, penetration, degree of nrisk of operation and feature of clinical situation.

Operative ntreatments at a perforated ulcer divide into palliative and radical.

 

Palliative operations

 

Palliative operations nare: closure of the perforative hole of ulcer, tamponade of the perforative nhole by a omentum on a leg by В.А. Oppel – P.N.Polikarpov – М.А.Pidhorbunskyy n(1896, 1927, 1948) (Pic. 3.2.15). Indications and terms for their nimplementation are:

— perforation of nacute duodenal ulcer in youth and young age without anamnesis;

— perforation of nacute ulcer in the II–III phases of passing;

— perforation of ncallous gastric ulcer in the II–III phases of passing;

— expressed and nhigh degrees of risk of operation.

 

Radical operations

 

The radical noperations at perforated ulcers are: resection of stomach and excision of the nperforative hole of ulcer in combination with pyloroplasty and StV, SV or SPV.

Indications and nterms for implementation of resection of stomach are:

— perforation of ncallous gastric ulcer in I phase of clinical passing;

— repeated nperforation of ulcer;

— perforation of nulcer in I phase of clinical passing in combination with stenosis and bleeding nof ulcer;

— perforation of nduodenal ulcer in I phase of passing in combination with a gastric ulcer;

— unexpressed and nmoderate degree of risk of operation;

— sufficient nqualification of surgeon and material resources of operating-anaesthetic nbrigade.

Indications for nimplementation of operation of excision of the perforative hole of ulcer with npyloroplasty, StV, SV and SPV are: perforation of ulcer of front wall of nduodenum or pyloric part of stomach in the I–II phases of passing;

— perforation of nulcer of front wall of duodenum in the I–II phases of passing in combinatiowith the bleeding ulcer of back wall;

— perforation of nduodenal ulcer in the I–II phases of passing in combination with the ncompensated stenosis of outgoing part of stomach;

— increased gastric nsecretion;

— insignificant and nmoderate degree of risk of operation;

   nsufficient nqualification and technical preparedness of surgeon.

 

 

BLEEDING GASTRODUODENAL nULCERS

 

Bleeding gastroduodenal ulcers are outpouring of blood in the ngastrointestinal tract cavity as a result of strengthening and distribution of nnecrosis process in the ulcer area to vessels with the subsequent melting of ntheir walls.

Complication of npeptic or duodenal ulcer by bleeding is critical situation which threatens to nlife of patient and requires from the surgeon of immediate and decisive actions nfor clarification of reasons of bleeding and choice of tactic of treatment. The nulcerous bleeding has 60 % of the acute bleeding from the upper parts of ngastrointestinal tract.

 

Etiology and npathogenesis

 

The origin of the ngastrointestinal bleeding at patients with a gastric or duodenal ulcer almost nis always related to exacerbation of ulcerous process. The reason of bleeding nis a erosive vessel, that is on the bottom of ulcer. The expressed inflammatory nand sclerotic processes round the damaged vessel embarrassed its contraction, nthat diminishes chances on the spontaneous stop of bleeding.

Gastric ulcers, ncompare with the ulcers of duodenum, complicated by bleeding more frequent. nBleeding at gastric ulcers are more expressed, profuse, with heavy passing.

At the duodenal nulcer bleeding more frequent complicate the ulcers of back wall, which npenetrates in the head of pancreas.

At the men ulcer is ncomplicated by bleeding twice more frequent, than at women. It costs to mark nthat 80 % patients which carried bleeding from an ulcer and treated oneself by nconservative preparations, are under the permanent threat of the recurrent nbleeding.

 

Pathomorphology

 

Strengthening of necrosis process nare leading factors in the origin of the ulcerous bleeding in the area of nulcerous crater with distribution of this process to a vessel and subsequent nmelting of vascular wall; activation of fibrinolysis in tissues of stomach and nduodenum; ischemia of tissues of wall of stomach.

 

Classification

 

Bleeding ngastroduodenal ulcers after the degree of weight of loss of blood (by О.О. nShalimov and V.F.Saenko, 1987) are divided:

I degree is easy n— observed at the loss to 20 % volume of circulatory blood (at a patient nwith weight of body 70kg it is up to 1000 ml);

II degree — middle nweight is loss from 20 to 30 % volume of circulatory blood (1000–1500 ml);

The III degree is heavy n— is observed at loss of blood more than 30 % volume of circulatory blood n(1500–2500 ml).

 

Clinical management

 

At patients with apeptic ulcer disease, bleeding pops up, mainly at night. Vomiting can be the first nsign of it, mostly, at gastric localization of ulcers. Vomiting masses, as a nrule, looks like “coffee-grounds”. Sometimes they are as a fresh red blood or nits grume.

The black tar-like nemptying are the permanent symptom of the ulcerous bleeding, with an unpleasant nsmell (“melena”), that can take place to a few times per days.

Bloody vomiting and nemptying as “melena” is accompanied by worsening of the general condition of npatient. A acute weakness, dizziness, noise in a head and darkening in eyes, nsometimes — loss of consciousness. A collapse with the signs of hemorrhagic nshock can also develop. Exactly with a such clinical picture the such patients nget to the hospital. It is needed to remember, that for diagnostics anamnesis nis very important. Find out often, that at a patient an peptic ulcer was nalready diagnosed once. It appears sometimes, that bleeding is repeated or nsurgery concerning a perforated ulcer took place in the past. At some patients na gastric or duodenum ulcer is was not diagnosed before, the however nattentively collected anamnesis exposed, that at a patient had a stomach-ache. nThus it communication with acceptance of food and seasonality is typical (more nfrequent appears in spring and in autumn). Patients tell, that pain in overhead npart of abdomen which disturbed a few days prior to bleeding suddenly ndisappeared after first its displays (the Bergmann’s symptom).

At patients with nthe ulcerous bleeding there are the typical changes of hemodynamic indexes: a npulse is frequent, weak filling and tension, arterial pressure is mostly nreduced. These indexes need to be observed in a dynamics, as they can change nduring the short interval of time.

There is the pallor nof skin and visible mucous tunics at a examination. A stomach sometimes is nmoderately exaggerated, but more frequent is pulled in, soft at palpation. Ioverhead part it is possible to notice hyperpigmental spots — tracks from the nprotracted application of hot-water bottle. Painful at deep palpation in the narea of right hypochondrium (duodenal ulcer) or in a epigastric area (gastric nulcer) it is possible to observe at penetrated ulcers. Important symptom of nMendel also — painful at percussion in the projection of piloroduodenal area.

At the examinatioof patients with the gastrointestinal bleeding finger examination of rectum is nobligatory. It needs to be performed at the first examination, because ninformation about the presence of black excrement (“melena”) more frequent get naccording to a patient anamnesis, that can result in erroneous conclusions. nFinger examination of rectum allows to expose tracks of black excrement or nblood. In addition, it is sometimes possible to expose the tumour of rectum or nhaemorrhoidal knots which also are the source of bleeding.

The deciding value nin establishment of diagnosis has the endoscopic examination. nFiber-gastroduodenoscopy enables not only to deny or confirm the presence of nbleeding but also, that it is especially important, to set its reason and nsource. Often embarrassed the examination of stomach and duodenum present in it nblood and content. In such cases it is necessary to remove blood or content, by ngastric lavage, and to repeat endoscopic examination. During the examinatiooften exposed the bleeding with fresh blood from the bottom of ulcer or nulcerous defect with one or a few erosive and thrombosed vessels (stopped nbleeding). The bottom of ulcer can be covered by the package of blood.

Important ninformation about such pathology is given by haematological indexes also. nDiminishment of number of red corpuscles and haemoglobin of blood, decline of nhaematocritis is observed in such patients. However always needed to remember, nthat at first time after bleeding haematological indexes can change ninsignificantly. Conducting of global analysis of blood in a dynamics in every na few hours is more informing.

Variants of clinical npassing and complication

 

It is necessary always nto remember that complication of peptic ulcer by bleeding happens considerably nmore frequent, than is diagnosed. Usually, to 50–55 % moderate bleeding n(microbleeding) have the hidden passing. The massive bleeding meet considerably nrarer, however almost always run across with the brightly expressed clinical nsigns which often carries dramatic character. In fact profuse bleeding with the nloss 50–60 % to the volume of circulatory blood could stop the heart and cause nthe death of patient.

The clinical signs nand passing of disease depend on the degree of lost of blood (О.О. Shalimov and nV.F.Saenko, 1987).

For nlost of blood I degree ntypical there is a frequent pulse to 90–100, decline of arterial pressure of to n90/60 mm Hg. The excitability of patient changes by lethargy, however clear nconsciousness is, breathing some frequent. After the stop of bleeding and iabsent of hemorrhage compensation the expressed disturbances of circulation of nblood does not observe.

At patients with nthe II degree of hemorrhage the general conditioeeds to be estimated as naverage. Expressed pallor of skin, sticky sweat, lethargy. Pulse — 120–130 per nmin., weak filling and tension, arterial pressure — 90–80/50 mm Hg. At first nhours the spasm of vessels (centralization of circulation of blood) comes after nbleeding, that predetermines normal or increased, arterial pressure. However, nas a result of the protracted bleeding compensate mechanisms of arterial npressure are exhausted and can acutely go down at any point. Without the proper ncompensation of hemorrhage the such patients can survive, however almost always nthere are considerable disturbances of blood circulation with disturbance of nfunctions of liver and kidneys.

The III degree of nhemorrhage characterizes heavy clinical passing. There is a pulse in such npatients — 130–140 per min., and arterial pressure — from 60 to 0 mm Hg. Consciousness nis almost always darkened, acutely expressed adynamy. Central vein pressure is nlow. Oliguria is observed, that can change by anuria. Without active and ndirected correction of hemorrhage a patient can die.

But, not always nweight of bleeding which is conditioned by the degree of hemorrhage correspond nthe general condition of patient. On occasion the considerable loss of blood nduring the set time is accompanied by the relatively satisfactory condition of npatient. And vice versa, moderate hemorrhage can bring to the considerable nworsening of general condition. It can depend both on compensate possibilities nof organism and from the presence of accompanying pathology.

It is needed to nremember, that the ulcerous bleeding can accompanying with the perforation of nulcer. During perforation ulcers are often accompanied by bleeding. Correct ndiagnostics of these two complications has the important value in tactical napproach and in the choice of method of surgical treatment. In fact simple nsuturing of perforated and bleeding ulcer can complicated in postoperative nperiod by the profuse bleeding and cause the necessity of the repeated noperation.

 

 

Diagnosis program

 

1.     Anamnesis and physical examination.

2.     Finger examination of rectum.

3.     Gastroduodenoscopy.

4.     Global analysis of blood.

5.     Coagulogram.

6.     7. Biochemical blood test.

7.     X-Ray examination of gastrointestinal tract.

8.     Electrocardiography.

 

 

Differential diagnostics

 

At wide introduction of ngastroduodenoscopy of question of differential diagnostics of bleeding lost the nactuality. However much a problem arises up at impossibility to execute this nexamination through the heavy general condition of patient or taking into naccount other reasons. Differential diagnostics is conducted with bleeding of nunulcerous origin, which arise up in different parts of digestive tract.

For bleeding from the varicose extended veins of nesophagus during portal hypertension at patients with the cirrhosis of nliver the acute beginning without pain is characteristic, like during nexacerbation of ulcerous disease. These bleeding differ by the special nmassiveness and considerable hemorrhage. Vomiting by fresh blood, expressed ntachycardia, falling of arterial pressure are observed. In such patients it is npossible to find the signs of cirrhosis of liver and portal hypertension (“head nof jelly-fish”, hypersplenism, ascites, often is icterus).

Sliding hernia of the esophagus nopening of diaphragm can be naccompanied by formation of ulcers in the place of clench of the stomach by the nlegs of diaphragm and bleeding from them. However for this pathology are more ntypical microbleeding, that is hidden. In such patients often the present nprotracted anaemia which can achieve the critical values. Sometimes in them nobserve more expressed bleeding with “classic” vomiting “coffee-grounds” and nmelena. During the roentgenologic examination with barium is possible to expose nthe signs of sliding hernia of the esophagus opening: the obtuse cardial angle, nabsence or diminishment of gas bubble of stomach or “ringing symptom”.

The cancer tumour of stomach in the ndestruction stage can be also complicated by bleeding. However, such bleeding nare massive, and chronic character is carried mostly with gradual growth of nanaemia. For this pathology there are the inherent worsenings of the general ncondition of patient, loss of weight of body, decline of appetite and waiver of nmeat food. At the roentgenologic examination the “defect of filling” is exposed nin a stomach.

The gastric bleeding can be related nto the diseases of the cardio-vascular system (atherosclerosis, hypertensive ndisease), however such happens mainly in the older years people. Clearly, that nin such patients during the endoscopic examination the source of bleeding nexposing is not succeeded.

Among other diseases, with which it nis necessary to differentiate the ulcerous bleeding, it is needed to remember nthe Mallory-Weiss syndrome, benign tumours of stomach and duodenum (more nfrequent leiomyoma), hemorrhagic gastritis, acute (stress) erosive defeats of nstomach, arteriovenous fistula of mucous tunic.

Often differential diagnostics nperformed according to the level of localization of source of bleeding idifferent parts of gastrointestinal tract. For the upper parts of digestive ntract (esophagus and stomach) typical there is vomiting by grume or n“coffee-grounds” content and emptying by “melena”. The farther aboral placed nsource of bleeding, the bloody emptying changes the more so. During the nbleeding from a thin bowel excrement looks as “melena”. In case of such npathology of colon (polypuses, tumours, unspecific ulcerous colitis) emptying nhave the appearance of fresh red blood, mostly as packages.

 

Tactic and choice of ntreatment method

 

The conservative ntherapy indicated to patients with the stopped bleeding of I degree and nbleeding of the II–III degrees at patients which have heavy accompanying npathology, because of operative risk.

Conservative ntherapy must include:

— prescription of nhemostatic preparations (intravenously the aminocapronic acid 5 % — 200–400 ml, nchlorous calcium 10 % — 10,0 ml, vicasol 1 % — 3,0 ml);

— addition to the nvolume of circulatory blood (gelatin, poliglukine, salt blood substitutes);

— preparations of nblood (fibrinogen — 2–3 г, cryoprecipitate);

— blood substitutes ntherapy (red corpuscles mass, washed red corpuscles, plasma of blood);

— antiulcerous npreparations — blocker of Н2- receptor (ranitidine, roxatidine, nasatidine— for n150 mg 1–2 times per days);

— antacid and nadsorbents (almagel, phosphalugel, maalox— for 1–2 dessert-spoons through 1 nhour after food intake).

It is expedient to napply washing of stomach by water with ice and the use 5 % solution of naminocapronic acid inward for to a 1 soupspoon in every 20–30 minutes.

The endoscopic nmethods of stop of bleeding are used also. Among them most effective is a laser nand electro-coagulation.

Absolute indications nto surgical treatment are: 1) lasting bleeding I degree; 2) recurrent nbleeding after hemorrhage I degree; 3) bleeding of the II–III degrees; 4) nstopped bleeding with hemorrhage of the II–III degrees at the endoscopically nexposed ulcerous defect with a presence on the ulcer bottom thrombosed vessels or erosive vessels ncovered by the package of blood.

The choice of nmethod of surgical treatment always needs to be decided individually. Otoday the best tactic which gives advantage to organ-saving and organоsparing nmethods of operations. The removing ulcer as sources of bleeding must be aobligatory condition. The methods of sewing of bleeding vessels or edging of nulcer and bandaging of vessels which feed a stomach and duodenum did not njustify itself through the real threat of relapse of bleeding already in aearly postoperative period (9–12 days).

Palliative noperations (cutting of ulcer, forming of roundabout anastomosis) can be njustified only taking into account the general condition of patient and on a nnecessity as possible quick and least traumatically to make off operation.

At the bleeding nulcers of duodenum it is better to apply excision of ulcer or it nexteritirization after methods, developed by V.Zajtsev and Velihotskyy. nOperation complemented by one of types of vagotomy, it is better by a selective nproximal with piliroplastic. The resection of stomach on the second or first nmethod of Bilroth can be realized only in the stable general condition of npatient. During the resection of stomach in case of low bleeding duodenal nulcers it is better to execute mobilization of duodenum and suturing of its nstump on transcholedochus drainage which formed as transcholedochus duodenotomy n(Laqey, 1942). This method warns the possible intraoperative damages of ncholedoch, that are the possible at low duodenal ulcers. Transcholedochus nduodenotomy by performing the decompression of stump of duodenum, warns ninsufficiency of its stitches, that can arise up in an early postoperative nperiod.

In case of bleeding ngastric ulcers, the resection methods of operations are also usable. Only ooccasion, when patients has the grave general condition, it is possible to nassume the wedge cutting of ulcer.

 

MALIGNIZATION

CANCER OF STOMACH

 

The cancer of stomach is a malignant formation, that develops nfrom epithelium tissue of mucus stomach. Among the tumours of organs of ndigestion this pathology takes first place and is the most frequent, by the nreason of death from malignant formations in many countries of world. Frequency nof it at the last 30 years considerably diminished in the countries of WesterEurope and North America, but yet remains high in Japan, China, countries of nEast Europe and South America.

 

Etiology and npathogenesis

Etiology of cancer nof stomach is unknown. It is known that, as other diseases of gastrointestinal ntract, a cancer damages a stomach. According to statistical information, it nmeets approximately in 40 % of all localizations of cancer.

The factors of nexternal environment has the substantial influencing on frequency of this npathology. Above all things, feed, smoke food, salting, freezing of products nand their contamination of aflatoxin. Consider that a “food factor” can be: a) nby a carcinogen; b) by the solvent of carcinogens; c) to grow into a carcinogein the process of digestion; d) to be instrumental in action of carcinogens; e) nnot enough to neutralize carcinogens.

In the USA and countries of WesterEurope frequency of cancer of stomach in 2 times more large in the lower nsocio-economic groups of population. Some professional groups also can it n(miners, farmers, works of rubber, woodworking and asbestine industry). High ncorrelation communication is set between frequency of cancer of stomach and use nof alcohol and smoking. The value of genetic factors (heredity, blood type) is nnot led to.

The cancer of stomach arises up nmainly in age 60 years and above, more frequent men are ill.

Precancer. The precancer diseases of stomach are: a) chronic metaplastic ndisregenerator gastritis conditioned by helicobacter pylori; b) villous npolypuses of stomach and chronic ulcers; c) nutritional anemia due to vitamiB12 deficiency (pernicious); d) resected stomach concerning an ulcer.

The presence of precancer changes of nmucous tunic of stomach has substantial influence for frequency of stomach ncancer. In those countries, where morbidity on the cancer of stomach is higher, nconsiderably more frequent chronic gastritises are diagnosed. Lately in etiology nof chronic gastritises take the important value helicоbacter pylori. In Japan, nwhere the cancer of stomach is in 40 % cases is the reason of death, chronic ngastritis appears in 80 % cases of resected stomach, concerning a cancer.

Connection between polypuses, nchronic gastric ulcers and possible it malignization comes into question iliterature during many decades. Most authors consider that polypuses could be malignant differently. There are nthree histological types of polypuses: hyperplastic, villous and hamartoma. There are hyperplastic polypuses, but it not nmalignant.

Hamartoma is accumulation of cells of normal mucous tunic of nstomach. They never becomes malignant.

Villous polypuses are potentially nmalignant in 40 % cases, but it happen in 10 times less, than hyperplastic. The npossibility of malignization of chronic gastric ulcers is not proved. The nAmerican scientists support a hypothesis, that the cancer of stomach can be nulcerous often, but malignization of ulcers takes place rarely (no more than 3 n%). From data of the Japanese scientists, on 50–70th there was higher ncorrelation connection between chronic gastric ulcers and cancer of stomach. nThe frequent decline of this correlation is lately noticed (70 % on 50–70th and n10 % on 80th).

Frequency of cancer of stomach at npatients with pernicious anaemia hesitates within the 5–10 %, that in 20 times nhigher, compare with control population. In patients with a resected stomach nafter peptic ulcers is multiplied the risk of origin of stomach cancer in 2–3 ntimes (duration of latent period hesitates from 15 to 40 years). The reason of nsuch dependence is not found out, but there is a version, that this is linked nwith a gastric epithelium metaplasia by an intestinal type.

 

Pathomorphology

 

From all malignant formations of the nstomach in 95 % adenocarcinoma is observed. Epidermoid cancer, adeno-acanthoma and carcinoid tumours do not exceed 1 %. Frequency of nleiomyosarcoma hesitates within the limits of 1–3 %. Lymphoma of gastrointestinal tract is localized in a nstomach.

The prognosis of localizatiodepends on the degree of invasion, histological variants of tumour.

 The macroscopic forms of cancer of stomach idifferent times were described variously. More than 60 years ago the Germapathologist Bermann described 5 macroscopic forms of cancer of stomach: 1) npolypoid or mushroom-like; 2) saucer-shaped or with ulcerous and expressly nsalient edges; 3) with ulcerous and infiltration of walls of stomach; 4) ndiffuse -infiltrate; 5) unclassified.

American pathopsychologs is selected n4 forms. The tumours of stomach with ulcerous are the most frequent macroscopic nform of cancer of stomach and arise up on soil of chronic ulcer. The signs nsuspicious on malignization are: the sizes of ulcer more than 2 cm in a diameter, nappearance of the heightened edges.

The polypoid tumours of stomach observed only in 10 %. These ntumours can achieve considerable sizes without an invasion and metastasis. nScirrhous carcinoma is the third macroscopic type. This category of tumours nalso does not exceed 10 %. The scirrhous carcinoma is the signs of infiltratioby anaplastic cancer cells, diffusely developed connecting tissue which results nin the bulge and rigidity of wall of stomach. So called “small cancers” belong nto the fourth macroscopic type. It meet comparative rarely (no more than 5 %) and nis characterized by superficial accumulation of cancer cells which substitute nfor normal mucus in such kind: a) superficial flat layer which does not rise nabove the level of mucus; b) salient (bursting) formation; c) erosions.

Mainly (more than 50 %) tumours narise up in a antral part or in distal (lower) third of stomach, rarer (to 15 n%) — in a body and in cardia (to 25 %).

However, lately more often observed ncardioesophageal cancers and diminishment of frequency of tumours of distal nparts of stomach. In 2 % cases meet the multicentric focuses of growth, but nfrom data of some authors, this percent could be multiplied in 10 times after ncarefully histological inspection of the resected stomaches. This assertion is nbased on the theory of the “tumour field” (D.I. Holovin, 1992). Especially this ntypically for patients which has pernicious anaemia or chronic metaplastic ndisregenerative gastritis.

Metastasis is carried out by nlymphogenic, hematogenic and implantation ways mostly. Three (from data of some nauthors, four) pools of lymphogenic metastasis are selected: left gastric n(knots on passing of small curvature of stomach in a gastro-subgastric ligament nand pericardial); splenic (mainly, suprainfrapancreatic knots); hepatic (knots nin a hepato-duodenal ligament, right gastric omentum that lower pyloric groups, nright gastric and supraраpyloric groups, pancreatoduodenal group).

However, the such way of lymphogenic nmetastasis is conditional and incomplete, as at presence of block lymph flow passes nretrograde metastasis, so called “jumping metastases” which predetermine the norigin of remote lymphogenic metastases in left supraclavicular lymph nodes n(Virhov metastasis) appear, in Lymph nodes of left axillar and inguinal areas, nmetastases in a umbilicus.

Direct distribution: small and large nomentum, esophagus and duodenum; liver and diaphragm; pancreas, spleen, bile nducts.

Front wall of stomach: colon bowel nand mesocolon; organs and tissues of retroperitoneal space.

Lymphogenic metastasis: regional nlymph nodes, remote lymph nodes, left supraclavicular lymph node (Virhov), nlymph node of axillar area (Irish); in a umbilicus (sisters Joseph).

Hematogenic metastasis: liver, nlungs, bones, cerebrum.

Peritoneal metastasis: peritoneum, novarium (the Krukenberg metastasis), Duglas space (the Shnicler metastasis).

 

Classification (by nsystem of ТNM)

 

Т— primary tumour.

Т0 is a primary ntumour is not determined.

Тх — not enough ndata for estimation of primary tumour.

Тis is invasive ncarcinoma: intraepithelial tumour without the invasion of own shell mucus n(Carcinoma in situ).

Т1 is a tumour ninfiltrate the wall of stomach to the submucous layer.

Т2 is a tumour ndamages mucus, submucous and muscular layers.

Т3 is a tumour ngerminates in a serous shell.

Т4 is a tumour npasses to the neighbouring structures.

N are regional nlymphatic nodes.

Nх — not enough ninformation for the damage assessment of lymphatic nodes.

Nо — metastases iregional lymph nodes are not present.

N1 are damaged nperigastral lymph nodes in the distance no more than 3 cm from a primary ntumour along small or large curvature of stomach.

N2 are damaged nperigastral lymph nodes in the distance more than 3 cm from a primary tumour, nwhich can be remoted during operation, including lymph nodes placed along left ngastric, splenic, abdominal and general hepatic arteries.

М is remote nmetastases.

Мх — not enough ninformation for estimation of remote metastases.

Мо — remote nmetastases are not present.

М1 is presence of nremote metastases.

 

Groupment by stages

 

Stage 0 Т No Mo.

Stage I Т1-2 No Mo.

Stage II T2-3 No nMo.

Stage III T1-4 N1-2 nMo.

Stage IV any T, any nN M1.

Except for clinical nclassification (ТNM or сTNM), for the most detailed study pathological nclassification (postsurgical, posthistological) which is signed рТNМ.

G — nhistopathological differentiation:

G1 is the well ndifferentiated tumour;

G2 is the nmoderately differentiated tumour;

G3-4 — it is badly nor undifferentiated tumour.

 

Clinical management

 

All authors which nare engaged in the study of problem of cancer of stomach underline absence or nvagueness, no specificity of symptoms, especially on the early stages of ndisease. The displays of cancer of stomach are very various and depend olocalization of tumour, character of its growth, morphological structure, ndistribution on contiguous organs and tissues. At localization of tumour in a ncardial part patient complains firstly, as a rule, for appearance of dysphagy.

At careful, npurposeful collection of anamnesis it is not succeeded to expose some other, nmost early symptoms, which precedes to dysphagy and forces a patient to appeal nto the doctor. The unpleasant feeling behind a breastbone and feeling of nunpassing of hard food on a esophagus appear at the beginning of disease. After nsome time (as a rule, it is enough quickly, during a few weeks, sometimes evedays) a hard food does not pass (it is to wash down by water or other liquid). nThis period can be during 1–3 months. Patients address a doctor exactly in this nperiod. Other symptoms appear to this time: regurgitation, pain behind a nbreastbone, loss of mass of body, sometimes even exhaustion, the grey colouring nof person, a skin is dry, quickly grows general weakness. Sometimes patients naddress a doctor, when already with large effort a spoon-meat passes only or ncomplete stenosis came.

At localization of ntumour in the antral part of stomach the first complaints, as a rule, are up to nappearance of feeling of weight in epigastric region after the reception of nfood (even in a two-bit), “feeling of saturation” (after the reception of glass nof water), belch (at first it is simple by air, and then with a smell). Feeling nof weight grows for a day, patients forced to cause vomiting. In the morning nthere can be vomiting by mucus with the admixtures of “coffee-grounds” (so ncalled “cancer” water). Patients loses weight (mass of body is lost), a nweakness, anaemia grows.

Tumours localized nin the body of stomach show up either a pain syndrome or syndrome of so called n“small signs” (А.I. Savitskyy, 1947), which is characterized by appearance of namotivational general weakness, decline of capacity, rapid fatigueability, ndepression (by the loss of interest to the environment), proof decline of nappetite, gastric discomfort, making progress weight lost.

The carried chronic ndiseases of stomach, for which typical seasonality, can influence on the nclinical sign of cancer of stomach. At appearance of “gastric” complaints out nof season or in absent of effect from the got therapy concerning the nexacerbation of “gastritis”, “ulcers” must guard a patient and doctor (symptom nof “precipice” of gastric anamnesis).

In case of noccurring of “gastric” symptoms first in persons in age 50 years and older it nis foremost necessary to eliminate the cancer of stomach.

In parts of npatients cancer of stomach shows up only the metastatic damage of other organs nor complications. More than twenty so called “atypical” forms, which are ncharacterized by “causeless” anaemia, ascites, icterus, fever, edemata, nhormonal disturbances, changes of carbohydrate exchange, intestinal symptoms, nare distinguished.

During the nexamination of patients with the cancer of stomach the pallor of skin covers n(at anaemia) is observed, ieglected case is “frog” stomach (sign of nascites).

During palpatiodetermined painful in a epigastric area, sometimes possible to palpate the ntumour.

During auscultatioof patients with pylorostenosis it is possible to define “noise of splash”.

Laboratory ninformation: hypochromic anaemia, neutrophilic leukocytosis, megascopic ESR; nduring examination of gastric secretion: hypo- and anacidity and achlorhydria.

Gastroduodenoscopy nenables to diagnose a tumour even smaller 5 mm and conduct an aiming nbiopsy with histological examination of the taken material.

Roentgenoscopy and nroentgenography examination of stomach. Basic signs: defect of filling, local nabsence of peristalsis, “malignant” relief of mucous tunic (Pic. 3.2.18).

Ultrasonic examination: npresence of metastases in a liver, pancreas.

Computer tomography nallows to estimate the basic parameters of tumour, germination ieighbouring norgans and presence of metastases.

It is expedient to napply laparoscopy, mainly, for the decision of question about operable of ntumour (diagnostics of metastatic defeat of organs of abdominal cavity).

 

Diagnosis program

 

1. Anamnesis and nphysical methods of examination.

2. Roentgenologic nexamination of stomach.

3. Endoscopic examinatiowith a biopsy (if necessary from a few places and even repeatedly), cytologic nand histological examination.

4. Sonography, ncomputer tomography.

5. Laboratory, nradioisotope methods of examination.

6. Laparoscopy.

7. Diagnostic n(therapeutic) laparotomy.

 

Differential diagnostics

 

At an early cancer complaints depend non the previous gastric diseases. Therefore, on the basis of clinical ninformation, suspecting a tumour is possible only on occasion, when in patients nnext to clear pain symptoms an appetite goes down, appear anaemia, general nweakness. In practice an early cancer is recognized at purposeful screening, nand also in the process of endoscopic or roentgenologic examination of gastric npatients.

A differential diagnosis is nconducted with an peptic ulcer, gastritis, polyposis, other gastric and nungastric diseases. For a cancer there is typical firmness of symptoms, instead nof their seasonality (typical syndrome of “precipice” of gastric anamnesis) or ntendency to their gradual progress.

The row of diseases, with which the ncancer of stomach is to differentiate to the doctor, depends from character of ncomplaints of patients.

Five basic clinical syndromes are nselected:

1) pain;

2) gastric discomfort;

3) anaemic;

4) dysphagic;

5) disturbance of evacuation from a nstomach.

At patients, at what cancer of nstomach shows up a pain syndrome and syndrome of gastric discomfort, a ndifferential diagnosis is conducted with the peptic ulcer, gastritis, cancer of nbody of pancreas.

It is oriented on features dynamics nof development of pain syndrome, ingravescent of the general condition, change nof character of complaints.

A question about character of nanaemia, source and nature of bleeding decides at an anaemic syndrome. In the nprocess of examination attention is paid to the state of bottom of stomach, nwhere bleeding malignant formations can be.

At a dysphagic syndrome a ndifferential diagnosis is conducted with the cicatrical narrowing, achalasia of nesophagus. For malignant formations testify short anamnesis, gradual progress nof symptoms, signs of gastric discomfort, general weakness, weight lost.

At disturbance of evacuation from a nstomach during stenosis of pyloric part, absence of ulcerous anamnesis, ndeclining years of patients, relatively quick (weeks, months) growth of nstenosis testify for tumor.

 

Tactic and choice of nmethod of surgical treatment

 

The presence of ncancer of stomach is a indications for surgical treatment. However, counting osuccess is possible only at presence of the limited tumours (within the limits nof the 0–II stages). At the III stage of disease implementation of the nwidespread combined operations in a radical volume is possible, however most npatients die during 1–2 years. A distal or proximal subtotal resection (Pic. n3.2.19) and total gastrectomy (Pic. 3.2.20) is performed with removing of large nand small omentumes and regional areas of metastasis with obligatory nhistological examination of stomach on the lines of resections.

During the combined noperations organs which are pulled in to the pathological process are removed.

In case of IV stage nof disease and satisfactory state of patient palliative operations which nimprove quality of life of patient are performed.

In case of presence nof complications (mainly stenosis) and grave common condition of patient nperform symptomatic operative treatments.

Symptomatic is noperations which will liquidate one of symptoms of cancer of stomach. In this ngroup of operations include: 1) roundabout gastrojejunoanastomosis (Pic. n3.2.21) and jejunostoma (in case of the stenosis tumours of stomach output); 2) ngastrostoma (Pic. 3.2.22) in case of the cancer of cardial part of stomach with ndisturbance of patency; 3) edging of bleedingх vessels in case of complicatioof cancer by bleeding; 4) tamponade by omentum during the perforation of ntumour.

The value of radial ntherapy and chemotherapy, as independent methods of treatment of cancer of nstomach, is limited. Radial therapy is indicated for patients with cardial ncancer as preoperative course or as palliative treatment. Adjuvant mono- or npolychemotherapy (mainly by 5-phtoruracil) is conducted in a postoperative nperiod as combined therapy and in case of dissemination of the tumours.

Prognosis. The indexes of five-year survival of patients with nthe cancer of stomach hesitate within the limits of 5–30 %, but, from data of nmost authors, they do not exceed 10 %.

        

REFERENCES

1.   Bliss, D. W., and Stabile, B. E.: The impact of ulcerogenic drugs non surgery for the treatment of peptic ulcer disease. Arch. Surg., 126:609, n1991.

2.   Bloom, B., and Kroch, E.: Time trends in peptic ulcer disease and nin gastritis and duodenitis: Morbidity, utilization, and disability in the nUnited States. J. Clin. Gastroenterol., 17:333, 1993.

3.   Boey, J., Choi, S. K. Y., Alagaratnam, T. T., and Poon, A.: Risk nstratification in perforated duodenal ulcers: A prospective validation of npredictive factors. Ann. Surg., 205:22, 1987.

4.   Burch, J. M., Cox, C. L., Feliciano, D. V., Richardson, R. J., and nMartin, R. R.: Management of the difficult duodenal stump. Am. J. Surg., n162:522, 1991.

5.   Cheng, C. A., Geoghegan, J. G., Lawson, D. C., Berlangieri, S. U., nAkwari, O., and Pappas, T. N.: Central and peripheral effects of CCK receptor nantagonists L-365, 260 and MK-329 on satiety in dogs. Am. J. Physiol., 246:219, n1993.

6.   Chey, W. Y., Kim, M. S., Lee, K. Y., and Chang, T. M.: Secretin is nan enterogastrone in the dog. Am. J. Physiol., 240:G239, 1981.

7.   Colin-Jones, D. G., Ireland, A., and Gear, P.: Reducing overnight nsecretion of acid to heal duodenal ulcers: Comparison of standard divided dose nof ranitidine with a single dose administered at night. Am. J. Med., 77:116, n1984.

8.   Crofts, T. J., Park, K. G. M., Steele, R. J. C., Chung, S. S. C., nand Li, A. K. C.: A randomized trial of nonoperative treatment for perforated npeptic ulcer. N. Engl. J. Med., 320:970, 1989.

9.   Cullen, J. J., and Kelly, K. A.: Gastric motor physiology and npathophysiology. Surg. Clin. North Am., 73:1145, 1993.

10. Debas, H. T., Farooq, O., and Grossman, M. I.: Inhibition of gastric nemptying is a physiological action of cholecystokinin. Gastroenterology, n68:1211, 1975.

11. Dragstedt, L. R.: Vagotomy for gastroduodenal ulcer. Ann. Surg., n122:973, 1949.

12. Feldman, M.: Gastric bicarbonate secretion in humans: Effect of npentagastrin, bethanechol, and 11,16,16-trimethyl prostagladin E 2. J. Clin. nInvest., 72:295, 1983.

13. Fennerty, M.: Helicobacter pylori. Arch. Intern. Med., 154:721, n1994.

14. Gantz, I., Schaffer, M., DelValle, J., Logsdon, C., Campbell, V., nUhler, M., and Yamada, T.: Molecular cloning of a gene encoding the histamine H n2 receptor. Proc. Natl. Acad. Sci., 88:429, 1991.

15. Gitlin, N., McCullough, A. J., Smith, J. L., Mantell, G., and nBerman, R.: A multicenter, double-blind, randomized, placebo-controlled ncomparison of nocturnal and twice-a-day famotidine in the treatment of active nduodenal ulcer disease. Gastroenterology, 92:48, 1987.

16. Göke, R., Fehmann, H.-C., and Göke, B.: Glucagon-like npeptide-1(7-36) amide is a new incretin/enterogastrone candidate. Curr. J. nClin. Invest., 21:135, 1991.

17. Gray, J. L., Debas, H. T., and Mulvihill, S. J.: Control of dumping nsyndromes by somatostatin analogue in patients after gastric surgery. Arch. nSurg., 126:1231, 1991.

18. Griffith, C. A., and Harkins, H. N.: Partial gastric vagotomy: Aexperimental study. Gastroenterology, 32:96, 1957.

19. Hamby, L. S., Zweng, T. N., and Strodel, W. E.: Perforated gastric nand duodenal ulcer: An analysis of prognostic factors. Am. Surg., 59:319, 1993.

20. Hoffman, J., Olesen, A., and Jensen, H. E.: Prospective 14- to n18-year follow-up study after parietal cell vagotomy. Br. J. Surg., 74:1056, n1987.

21. Hui, W. M., Ng, M. M. T., Lok, A. S. F., Lai, C. L., Lau, Y. N., and nLam, S. K.: A randomized comparative study of laser photocoagulation, heater nprobe, and bipolar electrocoagulation in the treatment of actively bleeding nulcers. Gastrointest. Endosc., 37:299, 1991.

22. Isenberg, J. I., Selling, J. A., Hogan, D. L., and Koss, M. A.: nImpaired proximal duodenal mucosal bicarbonate secretion in patients with nduodenal ulcer. N. Engl. J. Med., 316:374, 1987.

23. Jaffin, B. W., and Kaye, M. D.: The prognosis of gastric outlet nobstruction. Ann. Surg., 201:176, 1985.

24. Johansson, C., and Kollberg, B.: Stimulation by intragastrically nadministered E 2 prostaglandins of human gastric mucus output. Eur. J. Clin. nInvest., 9:229, 1979.

25. Katkhouda, N., and Mouiel, J.: Laparoscopic treatment of peptic nulcer disease. In Hunter, J., and Sackier, J. (Eds.): Minimally Invasive nSurgery. New York, McGraw-Hill, 1993, p. 123.

26. Keane, T. E., Dillon, B., Afdhal, N. H., and McCormack, C. J.: nConservative management of perforated duodenal ulcer. Br. J. Surg., 75:583, n1988.

27. Knuhtsen, S., Holst, J. J., Knigge, U., Olesen, M., and Nielsen, O. nV.: Radioimmunoassay, pharmacokinetics, and neuronal release of ngastrin-releasing peptide in anesthetized pigs. Gastroenterology, 87:372, 1984.

28. Koness, R. J., Cutitar, M., and Burchard, K. W.: Perforated peptic nulcer: Determinants of morbidity and mortality. Ann. Surg., 56:280, 1990.

29. Kozarek, R. A., Botoman, V. A., and Patterson, D. J.: Long-term nfollow-up in patients who have undergone balloon dilatation for gastric outlet nobstruction. Gastrointest. Endosc., 36:558, 1990.

30. Kulber, D., Hartunian, S., Schiller, D., and Morgenstern, L.: The ncurrent spectrum of peptic ulcer disease in the older age groups. Am. Surg., n56:737, 1990.

31. Marshall, B.: Unidentified curved bacilli in gastric epithelium iactive chronic gastritis. Lancet, 1:1273, 1983.

32. Marshall, B., and Warren, J.: Unidentified curved bacilli in the nstomach of patients with gastritis and peptic ulceration. Lancet, 1:1311, 1984.

33. Meisner, S., Jorgensen, L. N., and Jensen, H.: The Kaplan and Meier nand the Nelson estimate for probability of ulcer recurrence 10 and 15 years nafter parietal cell vagotomy. Ann. Surg., 207:1, 1988.

34. Meyer, J. H., Elashoff, J., Porter-Fink, V., Dressman, J., and nAmidon, G. L.: Human postprandial gastric emptying of 1–3-millimeter spheres. nGastroenterology, 94:1315, 1988.

35. Millat, B., Hay, J., Valleur, P., Fingerhut, A., Fagniez, P., and nthe French Associations for Surgical Research: Emergency surgical treatment for nbleeding duodenal ulcer: Oversewing plus vagotomy versus gastric resection, a ncontrolled randomized trial. World J. Surg., 17:468, 1993.

36. Mistiaen, W., Van Hee, R., Blockx, P., and Hubens, A.: Gastric nemptying for solids in patients with duodenal ulcer before and after highly nselective vagotomy. Dig. Dis. Sci., 35:310, 1990.

37. Mullan, F. J., Wilson, H. K., Majury, C. W., Mills, J. O. M., nCromie, A. J., Campbell, G. R., and McKelvey, S. T. D.: Bile acids and the nincreased risk of colorectal tumours after truncal vagotomy. Br. J. Surg., n77:1085, 1990.

38. Negulescu, P. A., Reenstra, W. W., and Machen, T. E.: Intracellular nCa requirement for stimula-secretion coupling in parietal cell. Am. J. nPhysiol., 256:C241, 1989.

39. NIH Consensus Conference: Therapeutic endoscopy and bleeding ulcers. nJAMA, 262:1369, 1989.

40. Pappas, T. N., Chang, A. M., Debas, H. T., and Taylor, I. L.: nPeptide YY release by fatty acids insufficient to inhibit gastric emptying idogs. Gastroenterology, 91:1386, 1986.

41. Pappas, T. N., and Debas, H. T.: Complications of peptic ulcer ndisease: Perforation and obstruction. In Taylor, M. B. (Ed.): Gastrointestinal nEmergencies. Baltimore, Williams & Wilkins, 1992, p. 83.

42. Pappas, T. N., Debas, H. T., and Taylor, I. L.: Entergastrone-like neffect of peptide YY is vagally mediated in the dog. J. Clin. Invest., 77:49, n1986.

43. Pappas, T. N., Mulvihill, S. J., Goto, Y., and Debas, H. T.: nAdvances in drug therapy for peptic ulcer disease. Arch. Surg., 122:447, 1987.

44. Pappas, T. N., Tache, Y., and Debas, H. T.: Opposing central and nperipheral actions of brain-gut peptides: A basis for regulation of gastric nfunction. Surgery, 98:183, 1985.

45. Pappas, T. N., Taylor, I. L., and Debas, H. T.: Postprandial nneurohormonal control of gastric emptying. Am. J. Surg., 155:98, 1988.

46. Peterson, W. L.: Helicobacter pylori and peptic ulcer disease. N. nEngl. J. Med., 324:1043, 1991.

47. Poitras, P.: Motilin is a digestive hormone in the dog. nGastroenterology, 87:909, 1984.

48. Poxon, V. A., Keighley, M. R. B., Dykes, P. W., Heppinstall, K., and nJaderberg, M.: Comparison of minimal and conventional surgery in patients with nbleeding peptic ulcer: A multicentre trial. Br. J. Surg., 78:1344, 1991.

49. Quigley, R. L., Pruitt, S. K., Pappas, T. N., and Akwari, O.: nPrimary hypertrophic pyloric stenosis in the adult. Arch. Surg., 125:1219, n1990.

50. Ritchie, W. P.: Alkaline reflux gastritis: Late results on a ncontrolled trial of diagnosis and treatment. Ann. Surg., 203:537, 1986.

51. Sachs, G., and Wallmark, B.: The gastric H+, K+-ATPase: The site of naction of omeprazole. Scand. J. Gastroenterol., 24(suppl. 166):3, 1989.

52. Schirmer, B. D.: Current status of proximal gastric vagotomy. Ann. nSurg., 209:131, 1989.

53. Schoon, I., Mellstrom, D., Oden, A., and Bengt-Olof, Y.: Peptic nulcer disease in older age groups in Gothenburg in 1985: The association with nsmoking. Age Ageing, 20:371, 1991.

54. Soll, A. H.: Pathogenesis of peptic ulcer and implications for therapy. nN. Engl. J. Med., 322:909, 1990.

55. Soll, A. H., and Wollin, A.: Histamine and cyclic AMP in isolated ncanine parietal cells. Am. J. Physiol., 237:E444, 1979.

56. Sontag, S., Graham, D. Y., Belsito, A., et al.: Cimetidine, ncigarette smoking, and recurrence of duodenal ulcer. N. Engl. J. Med., 311:689, n1984.

57. Taylor, T., and Bhandarkar, D.: Laparoscopic vagotomy: An operatiofor the 1990s? Ann. R. Coll. Surg. Engl., 75:385, 1993.

58. Toftgaard, C.: Gastric cancer after peptic ulcer surgery: A historic nprospective cohort investigation. Ann. Surg., 210:159, 1989.

59. Turner, W. W., Thompson, W. M., and Thal, E. R.: Perforated gastric nulcers. Arch. Surg., 123:960, 1988.

60. Tzu-Ming, C., Stabile, B. E., and Passaro, E., Jr.: Gastrinoma: nCurrent medical and surgical therapy. Contemp. Surg., 29:32, 1986.

61. Valen, B.,  Dregelid, E., nTonder, B., and Svanes, K.: Proximal gastric vagotomy for peptic ulcer disease: nFollow-up of 483 patients for 3 to 14 years. Surgery, 110:824, 1991.

62. Walsh, J. H., and Mayer, E. A.: Gastrointestinal hormones. ISleisenger, M. H., and Fordtran, J. S. (Eds.): Gastrointestinal Diseases, 5th ned. Philadelphia, W.B. Saunders, 1993, p. 18.

63. Wara, P.: Endoscopic prediction of major rebleeding—a prospective nstudy of stigmata of hemorrhage in bleeding ulcer. Gastroenterology, 88:1209, n1985.

64. Yamada, T.: Local regulatory actions of gastrointestinal peptides. nIn Johnson, L. R., Christensen, J., Jacobson, M. J., and Walsh, J. H. (Eds.): nPhysiology of the Gastrointestinal Tract. New York, Raven Press, 1987, p. 131.

65. Yovos, J. G., O’Dorisio, T. M., Pappas, T. N., et al.: Effects of namino acids and gastric inhibitory polypeptide on insulin release in dogs. Am. nJ. Physiol., 242:E53, 1982.

66. Zollinger, R. M.: Gastrinoma: The Zollinger-Ellison syndrome. Semin. nOncol., 14:247, 1987.

67. Zollinger, R. M., and Ellison, E. H.: Primary peptic ulcerations of nthe jejunum associated with islet cell tumors of the pancreas. Ann. Surg., n142:709, 1955.

 

Leave a Reply

Your email address will not be published. Required fields are marked *

Приєднуйся до нас!
Підписатись на новини:
Наші соц мережі