Definition

 Peptic ulcer of a and (ICD 10: K25-26)– chronic disease with polycyclic behaviour, which chracterized by secretoric, motoric and trophic modifications this organs and development ulcerous defects of its mucose.  Contrary to general belief, more peptic ulcers arise in the duodenum, than in the stomach.  About 4% of stomach ulcers are caused by a malignant tumor, so multiple are needed to make sure, duodenal ulcers are generally benign. Gastric ulcer

 The gastric ulcer is a chronic disease.  The main features of peptic ulcer is the presence of ulcer defect in the mucosa.  It forms the basis of pathology of many gastroenterological diseases.  Such phenomenon is explained by not only considerable distribution of disease but also the dangerous complications which always accompany gastric ulcers. Etiology and pathogenesis

 Frequency of morbidity of the peptic ulcer among the adult population is about 4 %.  It is more frequently seen patients in age group between 50 - 60 years.  Disturbance between the factors of aggression and defense mechanism of mucosa leads to peptic ulcer. Etiology and pathogenesis

Aggression factors:  hydrochloric acid (HCl),  pepsin,  reverse diffusion of ions of hydrogen (H+),  products of lipid hyperoxidizing. Aggressive factors (hydrochloric acid and pepsin) Parietal cells secrete hydrogen ions in concentration which is three times as high as the concentration of hydrogen ions present in the blood. Each secreted hydrogen ion combines with a chlorine ion.  The final step in the secretion of hydrogen ions is performed by means of the proton pump which includes the specific K+, H+-ATPase occuring on the membranes of microvilli.  This K+, H+-ATPase exchanges hydrogen for potassium across the microvillus membrane.  The parietal cells produce a pure solution of HCl which mixes with the secretion of non-parietal cells.  The HCl secretion is regulated by chemical, nervous and humoral factors.  The membrane of parietal cells harbours specific receptors (H2- receptors) responding to histamin released from the neigbouring mast cells.  Then there are receptors sensitive to muscarine effects of acetylcholine which is released by the vagus nerve’s endings.  Parietal cells contain receptors which respond to endogenous circulating gastrin. Etiology and pathogenesis

Defense mechanism:  and alkaline components of gastric juice,  property of epithelium of mucosa to permanent renewal,  local blood flow of mucosa and submucosa. Etiology and pathogenesis

 Numerous scientific developments of the past testify to the important infectious factor in the mechanism of origin of peptic ulcer, mainly, by pylori. Etiology Scientific classification Kingdom:Bacteria Phylum:Proteobacteria Class:Epsilon Proteobacteria Order:Campylobacterales Family:Helicobacteraceae Genus:Helicobacter Species:H. pylori Binomial name The bacterium was discovered in 1979 by Australian pathologist Robin Warren, who did further research on it with Barry Marshall beginning in 1981; they isolated the organisms from mucosal specimens from human stomachs and were the first to successfully culture them. In their original paper, Warren and Marshall contended that most stomach ulcers and were caused by by this bacterium and not by stress or spicy food as had been assumed before. Etiology

Immunohistochemical staining of H. pylori from a gastric .

H. pylori colonized on the surface of regenerative epithelium (Warthin-Starry's silver) Stomach disease

 An ulcer is a crater-like lesion on the skin or mucous membrane caused by an inflammatory, infectious, or malignant condition. Jonson’s classification (1965)

 Type I - ulcers of lesser curvature (3 cm higher than the pylorus) 13%  Type II - double localization of ulcers simultaneously in the 71% stomach and duodenum  Type III - ulcers of pyloric and of stomach (not farther than 3 cm from 11% the pylorus). Clinical management

 Pain. The pain symptom in the is very important.  There are typical staging for this disease: hunger - pain - food intake - facilitation - again hunger - pain - food intake - facilitation (so during all days). Clinical management

 Patients with the cardial ulcer pain arises at once after the food intake, with the ulcers of lesser curvature - in 50-60 minutes, in pyloric localization - approximately in two hours.  In other patients the pain attack is accompanied by salivation. Clinical management

 Vomiting, the sign of disturbance of gastric motility, is the second typical symptom of gastric ulcer.  More frequent gastrostasis arises as a result of failure of stomach muscul, it's atony which can be due to ischemia.  Vomiting could arise both on empty stomach and after food intake. Clinical management

is one of the early symptoms of gastric ulcer, however in prolonged disease it can be hidden or disappear.  Often it precedes pain (initial heartburn) or accompanies a pain symptom.  Mostly heartburn arises after the food intake, but can appear independently. Diagnosis programme

 Anamnesis and physical examination.  General and biochemical blood analysis.  Coagulogram.  Examination of gastric secretion by the method of aspiration of gastric contents.  .  Gastric pH-metry.  Multi position biopsy of edges of ulcer and mucosa of stomach.  Gastric Dopplerography.  Sonography of abdominal cavity organs.  X-Ray examination of stomach. FEGDScopy

This picture displays the endoscope detecting a gastric ulcer Differential diagnosis

 Chronic gastritis, like gastric ulcer is characterized by the pain syndrome, that arises after the food intake. In such patients it is possible to observe and vomiting of gastric content, heartburn and belching. However, unlike gastric ulcer, in gastritis typical symptom of "quick satiation by food is seen. Unsteady emptying, are also more inherent to gastritis. In gastric ulcer frequently the delay in gastric empting leads to for 4-5 days. Differential diagnosis  The cancer of stomach, it is comparative with gastric ulcer, has considerably more short anamnesis.  The most typical clinical signs of this pathology are: absence of appetite, weight loss, rapid fatigability, depression, unsociability, apathy.  In such patients X-Ray examination expose the "defect of filling", related to exophytic tumor and deformation of walls of organ.  A final diagnosis is set after the results of multi position biopsy of shady areas of mucosa of stomach. Tactic and choice of treatment method

 Conservative treatment of gastric ulcer always must be complex, individually differentiated, according to the etiology.  Conservative therapy must include: anticholinergic drugs (atropine, methacin, platyphyllin) and myolitics (papaverine, halidor, nospanum); antiacid drugs - in accordance with the results of pH-metry; Conservative therapy  Proton pump inhibitors: These drugs are potent inhibitors of H+,K+-ATPase. This , located in the apical secretory membrane of the parietal cell, plays a key role in the secretion of H+ (protons). These drugs can completely inhibit acid secretion and have a long duration of action. They promote ulcer healing and are also key components of H. pylori eradication regimens. Proton pump inhibitors have replaced H2-blockers in most clinical situations because of greater rapidity of action and efficacy. Conservative therapy

 Proton pump inhibitors include esomeprazole (NEXIUM), lansoprazole (PREVACID), and pantoprazole (PROTONIX) , all available orally and IV, and omeprazole (PRILOSEC) and rabeprazole, available only orally in the US. Omeprazole (PRILOSEC) is available without a prescription in the US.  Long-term proton pump inhibitor therapy produces elevated gastrin levels, which lead to enterochromaffin- like cell hyperplasia. However, there is no evidence of dysplasia or malignant transformation in patients receiving this treatment. Some may develop vitamin B12 . Conservative therapy

 H2 blockers: These drugs cimetidine (TAGAMET), , ranitidine (ZANTAC), famotidine (PEPCID), , available IV and orally; and nizatidine (AXID) (available orally) are competitive inhibitors of histamine at the H2 receptor, thus suppressing gastrin- stimulated acid secretion and proportionately reducing gastric juice volume. Histamine- mediated pepsin secretion is also decreased. Conservative therapy

 H2 blockers are well absorbed from the GI tract, with onset of action 30 to 60 min after ingestion and peak effects at 1 to 2 h. IV administration produces a more rapid onset of action. Duration of action is proportional to dose and ranges from 6 to 20 h. Doses should often be reduced in elderly patients. Conservative therapy

 For duodenal ulcers, once daily oral administration of cimetidine 800 mg, ranitidine 300 mg, famotidine 40 mg, or nizatidine 300 mg given at bedtime or after dinner for 6 to 8 wk is effective. Gastric ulcers may respond to the same regimen continued for 8 to 12 wk, but because nocturnal acid secretion is less important, morning administration may be equally or more effective. Children ≥ 40 kg may receive adult doses. Below that weight, the oral dosage is ranitidine 2 mg/kg q 12 h and cimetidine 10 mg/kg q 12 h. For GERD, H2 blockers are now mostly used for pain management. Gastritis heals with famotidine or ranitidine given bid for 8 to 12 wk. Conservative therapy

 Cimetidine and, to a lesser extent, other H2- blockers interact with the P-450 microsomal enzyme system and may delay metabolism of other drugs eliminated through this system (eg, phenytoin /DILANTIN/), warfarin (COUMADIN) , theophylline (ELIXOPHYLLIN, THEO-DUR) , diazepam (VALIUM) , lidocaine (XYLOCAINE). Conservative therapy

 Antacids relieve symptoms, promote ulcer healing, and reduce recurrence. They are relatively inexpensive but must be taken 5 to 7 times/day. The optimal antacid regimen for ulcer healing seems to be 15 to 30 mL of liquid or 2 to 4 tablets 1 h and 3 h after each meal and at bedtime. The total daily dosage of antacids should provide 200 to 400 mEq neutralizing capacity.  In general, there are two types of antacids: absorbable and nonabsorbable. Absorbable antacids (eg, Na bicarbonate, Ca carbonate) provide rapid, complete neutralization but may cause alkalosis and should be used only briefly (1 or 2 days). Nonabsorbable antacids (eg, aluminum or Mg hydroxide) cause fewer systemic adverse effects and are preferred. Surgery Surgical treatment must be performed in cases:  of relapse of ulcer after the course of conservative therapy;  in the cases when the relapses arise during supportive antiulcer therapy;  when an ulcer does not heal during 1,5-2 months of intensive treatment, especially in families with "ulcer anamnesis“;  in relapse of ulcer in patients with complications (perforation or bleeding);  suspected malignancy of ulcers, in case of negative cytological analysis. Surgery

Resection of stomach by Billroth I: 1. Scopes of resection; 2. Gastroduodeno- anastomosis. Surgery

Resection of stomach by Billroth II in the Finsterer modification: 1 - scopes of resection; 2 - sewn up stump of duodenum; 3 - completed view of the operated stomach. Duodenal ulcer

 The duodenal ulcer is the chronic recurrent disease which is characterized by ulcer defect on a mucosa of the duodenum. Pathology often leads to development of complications. Duodenal ulcer Etiology and pathogenesis  Helicobacter pylori,  emotional stress and neuropsychic stress,  overstrain,  heredity and genetic inclination,  presence of chronic gastroduodenitis,  disturbance of diet and harmful habits (alcohol, smoking). Duodenal ulcer  In pathogenesis of peptic ulcer a leading role is played by disturbance of equilibrium between aggressive and projective properties of secretion of stomach and its mucosa. The aggressive factors are hyperfunctioning vagus and hypergastrinemia; hyperproduction of hydrochloric acid and pepsin, and also reverse diffusion of the ions H+, action of bilious acids and isoleucine, toxins and of helicobacter pylori (HP). There are factors which contribute to ulcerogenic action like disturbance of motility of stomach and duodenum, ischemia of duodenum, and metaplasia of the epithelium. Primary hyperparathyreosis (PHPT)

 The enhanceable concentration of calcium in blood increases a secretion and instrumental in development of ulcerous illness (more frequent in a duodenum) with frequent relapses.  Because a starting mechanism is saved, ulcers continue to recidive. Pathology

 Morphogenesis of duodenal ulcer fundamentally does not differ from that of ulcer in the stomach.  Chronic ulcers are mainly single, is localized on the anterior or posterior wall of bulb (bulbar ulcer) and only in 7-8 % cases - below it (postbulbar ulcer).  Multiple ulcers of duodenum are met in 25 % cases. Classification (by A.L.Hrebenev, A.O.Sheptulin, 1989) The duodenal ulcer is divided:  I. By etiology: A. True duodenal ulcer.  B. Symptomatic ulcers.  II.By onset of disease:  Acute (first exposed ulcer).  Chronic: a) with the rare exacerbation;  with the annual exacerbation;  with the frequent exacerbation (2 times per a year and more frequent).  III.By the stages of disease:  Exacerbation.  Scarring: a) stage of "red" scar;  b) stage of "white" scar.  3.Remission.  IV. By localization:  Ulcers of bulb of duodenum.  Low postbulbar ulcers.  Combined ulcers of duodenum and stomach.

 Small ulcers up to 0,5 cm.  Middle - up 1,5 cm.  Large - up to 3 cm;  Giant ulcers over 3 cm.  VI. By the presence of complications:  Bleeding.  Perforation.  Penetration.  Organic stenosis.  Periduodenitis.  Malignant transformation. Complications Clinical management

 For this pathology is typical the pain, that arises in 1,5-2 hours after food intake, "hunger" and nightly pain. As a rule, it is acute, sometimes unendurable, and relived only by intake food or water. Such patients complains of seasonal exacerbation, more frequent in spring and in autumn. However exacerbation can be also in winter or in summer. In the acute phase of the disease heartburn often increases. However heartburn is the frequent symptom of cardiac insufficiency and gastroesophageal reflux. For a duodenal ulcer the acute burning feeling of acid in a , and even in the cavity of mouth is especially typical. Often belching of air or sour content, excessive salivation. Clinical management

 Vomiting is not a typical symptom for duodenal ulcer. More typical sign is nausea. Sometimes for relief patients wilfully cause vomiting. These symptoms, arises in the late periods of duodenal ulcer.  There is an important symptom on local percussion (Mendel's symptom): percussion by fingers in the symmetric epigastric areas provoke pain in the ulcer, which is increased after the deep breath. DIAGNOSE

 The roentgenologic and endoscopic examination are main diagnostic methods.

NB!!! X-Ray examination is the main method in peptic ulcer complicated by stenosis with disturbance of evacuation, duodenostasis, duodenal-gastric reflux, gastroesophageal reflux, diverticulum. Esophagogastroduodenoscopy (EGD)

The procedure called gastroscopy involves the placing of an endoscope (a small flexible tube with a camera and light) into the stomach and duodenum to search for abnormalities. Tissue samples may be obtained to check for H. pylori bacteria, a cause of many peptic ulcers. An actively bleeding ulcer may also be cauterized (blood vessels are sealed with a burning tool) during a gastroscopy procedure. Esophagogastroduodenoscopy X-Ray and Endoscopy

 But by X-Ray examination it is difficult to diagnose small superficial ulcers, acute ulcers, erosions, gastritis and . The most informative method of investigation in such cases is endoscopy. During endoscopy examination it is possible to define localization, form, sizes and depth of ulcer. During bleeding grumes, trickle or pulsating of blood are observed. By irrigation by styptic solutions, by cryocoagulation, by laser coagulation endoscopy allows to secure hemosta-sis. Endoscopy allows to perform the biopsy of ulcer tissues for determina-tion of possible malignization. X-Ray X-Ray Differential diagnosis

 The duodenal ulcer must be differentiated from acute and chronic , , gastroduodenitis.  Endoscopy helps to diagnose duodenal ulcer. Conservative treatment

 In most patients after conservative treatment the ulcer heals in 4-6 weeks. Relapses can be prevented by supportive therapy for many years.  The best therapy of duodenal ulcer is associated with the treatment of helicobacter infection — the use of antagonists of H2- receptors of histamine (ranitidine- 300 mg in the evening or 150 mg twice daily; famotidine- 40 mg in the evening or 20 mg twice daily; nisatidine - 300 mg in the evening or 150 mg twice daily; roxatidine - 150 mg in the evening) in combination with sucralfate (venter) — for 1 gm trice daily and antacid (almagel, maalox or gaviscon - 1 table-spoon 1 hour after food intake). To this treatment it is added antibacterial preparations (De-nol - 1 tabl. 4 times a day for 4-6 weeks + oxacylline 0,5 g 4 times a day for 10 days + Tryhopol (metronidazole) for 0,5 g 4 times a day for 15 days. Indications to elective operation:

 1. Staging of duodenal ulcer with the frequent relapses which could not be treated conservatively.  2. Repeated ulcer bleeding.  3. Stenosis of piloric part of stomach.  4. Chronic penetration ulcers with the pain syndrome.  5. Suspicion malignant change. Methods of surgical treatment

In patients with the duodenal ulcer three types of operations are performed:  organ-saving operations;  organ-sparing operations;  resection. Methods of surgical treatment

Partiel gastrectomy - reduction of parietal cell mass by removal of part of the stomach, (a) Billroth I gastrectomy, (b) Polya (or Billroth II) gastrectomy, (c) Vagotomy - can be either (i) truncal, or (ii) highly selective with preservation of the antral and pyloric innervation Organ-saving operations

 Among the best surgical methods are: organ- saving operations with vagotomy, excision of ulcer and drainage operation.  Types of vagotomy: trunk (TrV), selective (SV) . selective proximal (SPV).  Selective proximal vagotomy is optimal in the elective surgery of duodenal ulcer. Vagotomy Types of vagotomy

Trunk vagotomy: 1) Selective vagotomy: 1) esophagus; 2) cutting schematic image; 2) of the front vagus cutting of gastric branches nerve; 3) back vagus of the vagus nerve and the nerve. Latarjet nerve Drainage of the stomach operations

Selective proximal vagotomy: Heineke-Mikulicz pyloroplasty: 1)front vagus nerve; 1) pyloroduodenotomy; 2)"goose paw" of the Latarjet 2) suturing of incision, which cut in nerve. transversal direction; first row of sutures; 3) completed view, second row of serous- serous sutures.

Complications of ulcer disease  Perforated ulcer (anterior. surface) with sudden onset of the pain, a chemical followed by bacterial peritonitis  Posterior penetration (posterior. surface), may be to =>increased amylase- pain=>radiating to back, unrelated to meals.  Hemorrhage (post. surface), bleeding from Gasteroduodenal artery.  Gastric Outlet Obstruction (GOO) which happens usually because of edema or scarring, most often occurs in the setting of duodenal or pyloric channel ulcers. Bleeding gastroduodenal ulcers  Bleeding gastroduodenal ulcers are due to bleeding in the gastro-intestinal tract cavity as a result of increasing necrosis in the ulcer area with blood vessels, with the subsequent damage of their walls.  The ulcer bleeding comprises of 60 % of the acute bleeding from the upper parts of . Ulcer emergencies

Vomiting of a substance that resembles coffee grounds, or the presence of black tarry stools, may indicate serious bleeding. Bleeding gastroduodenal ulcers

 In men ulcer is complicated by bleeding twice as more, than in women.  Its important to note that 80 % of patients who had bleeding from ulcer and was treated by conservative methods, are under permanent threat of recurrent bleeding. Bleeding gastroduodenal ulcers

 Pathomorphology: Increase in the process of necrosis are leading factors in the development of the ulcer bleeding in the area of ulcer crater with penetration into the vessel and subsequent damage of the vascular wall;  activation of fibrinolysis in tissues of stomach and duodenum;  ischemia of tissues of wall of stomach. Bleeding gastroduodenal ulcers: Classification Bleeding gastroduodenal ulcers according to blood loss (by O.O. Shalimov and V.F. Saenko, 1987) are divided into:  I degree - observed with loss at 20 % volume of circulatory blood (at a patient with weight of body 70 kg it is up to 1000 ml);  II degree - is loss 20 to 30 % volume of circulatory blood (1000- 1500 ml);  The III degree - is observed with blood loss of more than 30 % volume of circulatory blood (1500-2500 ml). MALT lymphoma

 Gastric MALT lymphoma is frequently associated (72-98%) with chronic inflammation as a result of the presence of Helicobacter pylori.  If the disease is limited to the stomach (which is assessed with computed tomography), then 70-80% of patients will have a complete regression on treatment with antibiotic eradication of H. pylori.  Others may be effectively controlled with the use of radiotherapy, or surgery. Both modalities may be curative in localized disease.  In contrast, if the disease has spread or has been refractory on antibiotics, chemotherapy may need to be considered. Bleeding gastroduodenal ulcers: Clinical management  Vomiting can be the first sign, mostly, with gastric localization of ulcers. Vomitus, as a rule, is "coffee-ground" in appearence. Sometimes they are like fresh blood.  The black tar-like stools are the permanent symptom of ulcer bleeding, with an unpleasant smell (""), that can take place few times in a days.  Bloody vomiting and "melena" is accompanied by worsening of the general condition of patient. Bleeding gastroduodenal ulcers: Anamnesis

 Patients tell, that pain is in upper part of which occured a few days prior to bleeding, suddenly disappears the onset of bleeding (the Bergmann's symptom) . Bleeding gastroduodenal ulcers

 In patients with ulcer bleeding there are typical changes of hemodynamic indexes: the pulse is rapid, weak filling and tension, arterial pressure is mostly reduced. These indexes need to be observed in the dynam- ics, as they can change during the short interval of time.  Alhover’s index (AI): PS/AP sist. Nornal value 0.5, at bleeding AI will increase. Bleeding gastroduodenal ulcers: Clinicaly

 For loss of blood I degree typically there is rabid pulse to 90-100, decrease of arterial pressure of to 90/60 mm Hg. The excitability of patient changes by lethargy, however consciousness is clear, breathing is frequent. After the bleeding stops and in absence of hemorrhagic compensation the disturbances of circulation of blood is not observed. Bleeding gastroduodenal ulcers: Clinicaly

 In patients with the II degree of hemorrhage the general condition needs to be estimated as average. Expressed pallor of skin, sticky sweat, lethargy. Pulse - 120-130 per min., weak filling and tension, arterial pressure - 90-80/50 mm Hg. In the first few hours the spasm of vessels (centralization of circulation of blood) arises after bleeding, that predetermines normal or increased, arterial pressure. However, as a result of the massive bleeding compensatory mechanisms of arterial pressure are exhausted and can acutely go down at any point.  Without the proper compensation of hemorrhage such patients can survive, however almost always there are considerable disturbances of blood circulation with distur- bance of functions of and kidneys. Bleeding gastroduodenal ulcers: Clinicaly

 The III degree of hemorrhage characterizes clinical stage with heavy bleeding. The pulse in such patients 130- 140 per min., and arterial pressure - from 60 to 0 mm Hg.  Consciousness is almost always darkened, acutely expressed adynamy. Central vein pressure is low. Oliguria is observed, that can change to anuria.  Without active and directed correction of hemorrhage the patient can die. Bleeding gastroduodenal ulcers: Diagnosis program

 Anamnesis and physical examination.  Digital examination of .  General analysis of blood.  Coagulogram.  Biochemical blood test.  Gastroduodenoscopy.  X-Ray examination of gastrointestinal tract.  Electrocardiography. Bleeding gastroduodenal ulcers: Laboratory

 Important information about such pathology is given by haematological indexes.  Decreased number of red corpuscles and haemoglobin, decrease of haematocrit is observed in such patients.  However always remember, that initially after bleeding haematological indexes can change insignificantly. Conducting of general analysis of blood in dynamics in every few hours is more informative. Bleeding gastroduodenal ulcers: diagnosis

 The deciding value in establishment of diagnosis is the endoscopic examination.  Fiber-gastroduodenoscopy enables not only to deny or confirm the presence of bleeding but also, it is especially important, to set its reason and source.  Often a negative result is obtained if the stomach and duodenum content blood. In such cases it is necessary to remove blood or other content by gastric lavage, and to repeat endoscopic examination. During the examination area of bleeding with fresh blood from the bottom of ulcer or ulcer defect with one or a few erosive and thrombosed vessels is revealed (stopped bleeding). The floor of ulcer can be filled with blood. Bleeding gastroduodenal ulcers MALT lymphoma

MALT lymphoma is a form of non-Hodgkin lymphoma (NHL) involving the mucosa- associated lymphoid tissue (MALT), frequently of the stomach, but virtually any mucosal site can be afflicted. It is a cancer originating from B cells in the marginal zone of the MALT.

Endoscopic image of gastric MALT lymphoma taken in body of stomach in patient who presented with upper GI hemorrhage. Appearance is similar to gastric ulcer with adherent clot. FEGDS Classification of intesivity bleeding by J.A.Forrest, 1974 y

 F Іа -  F Ib -  F ІІа –  F ІІb -  F ІІс -  F III - Bleeding gastroduodenal ulcers: Differential diagnosis  For bleeding from the varicose veins of esophagus in patients with with of liver the acute onset without pain is characteristic, like during exacerbation of ulcer disease.  This type of bleeding is massive and leading to considerable hemorrhage. Vomiting of fresh blood, expressed tachycardia, falling of arterial pressure are observed. In such patients it is possible to find the signs of cirrhosis of liver and portal hypertension ("head of jelly-fish", hypersplenism, ascites, icterus). Bleeding gastroduodenal ulcers: Differential diagnosis

 The cancer of stomach in the destruction stage can be also complicated by bleeding. However, such bleeding are massive, and chronic character is carried mostly with gradual growth of anaemia.  In this pathology there is inherent worsening of the general condition of patient, loss of weight of body, decrease of appetite and waiver of meat. At the roent- genologic examination the "defect of filling" is seen in the stomach. Bleeding gastroduodenal ulcers: Differential diagnosis

 Other diseases to be differenciated from ulcer bleeding are:  the Mallory-Weiss syndrome (acute linear break of the mucosa of the esophagus and cardiac part of stomach) ,  benign tumours of stomach and duodenum (more frequent leiomyoma),  hemorrhagic gastritis,  acute (stress) erosive defects of stomach,  arteriovenous fistula of mucosa. Conservative treatment of bleeding is rotined:

 1. Bed rest, hunger.  2. Cannulation of two veins, one of which must be central.  3. Transfusion of mass of red corpuscles, plasma.  4. Introduction of hemostatics (fibrinogen, aminocaprony acid, cryoprecipitate, plasma, chloride of calcium, vicasoly).  5. Intravenous introduction of inhibitirs of proteasis (contrical, trasilol).  6. Oppression of gastric secretion (to the atropine sulfate, blocks of H2- receptors).  7. Oppression of fibrinolytic activity (aminocaprony acid perorally).  8. Guided low blood pressure (arfonad, pentamin).  9. Proceeding in VCB is due to haemocorectors.  10. Local hypothermia (washing of stomach by cold water).  11. In case of stopping of bleeding is a diet of Meylengrakhta (sour cream, raw frappe eggs).  12. Local stop of bleeding. Bleeding gastroduodenal ulcers: Tactic and choice of treatment method

 The conservative therapy is indicated for patients of I degree and whom bleeding has stopped; for patients of II-III degrees with heavy accompanying pathology, because of operative risk.  Conservative therapy must include: - prescription of hemostatic preparations (intravenously the aminocapronic acid 5 % - 200-400 ml, chlorous calcium 10 % - 10,0 ml, vicasol 1 % -3,0 ml);  increase the volume of circulatory blood (gelatin, poliglukine, salt blood substitutes); Bleeding gastroduodenal ulcers: The conservative therapy

 preparations of blood (fibrinogen - 2-3 g, cryoprecipitate);  blood substitutes therapy (red corpuscles mass, washed red corpuscles, plasma of blood);  antiulcer preparations - blocker of H2- receptor (ranitidine, roxatidine, nasatidine- for 150 mg 1- 2 times per days);  antacid and adsorbents (almagel, phosphalugel, maalox- for 1-2 dessert-spoons through 1 hour after food intake). Ht -N Ht -N Ht - Hb-N Hb-N Hb-

НОРМА КРОВОТЕЧЕНИЕ ГЕМОДИЛЮЦИЯ Bleeding gastroduodenal ulcers: The conservative therapy

 It is important to wash stomach with ice water and the use 5 % solution of aminocapronic acid 1 tablespoon every 20-30 minutes. Local stop of bleeding

 During the leadthrough of EFGDS it is possible natively to stop bleeding by electro-coagulation, photocoagulation a laser, application of glue of KL-3.  Methods of endoscopic stop of bleeding: 1. Cryocautery. 2. Diathermo-coagulation. 3. Electro-coagulation. 4. Laser coagulation. Bleeding gastroduodenal ulcers: Surgery Absolute indications to surgical treatment are: 1) prolonged bleeding I degree; 2) recurrent bleeding after hemorrhage I degree; 3) bleeding of the II-III degrees; 4) stopped bleeding with hemorrhage of the II-III degrees with endoscopically exposed ulcer defect with the presence of throm bosed vessels or erosive vessels filled with clotted blood, in the floor of the ulcer. Bleeding gastroduodenal ulcers: Surgery

 The choice of method of surgical treatment always needs to be decided individually.  Today the best tactic which gives advantage to organ-saving and organosparing methods of operations.  The removal of ulcer as a source of bleeding must be an obligatory condition. Bleeding gastroduodenal ulcers: Surgery

 Palliative operations (incision of ulcer, forming of roundabout anastomosis) can be justified only by taking into account the general condition of patient.  In bleeding ulcers of duodenum it is better to excise the ulcer or exteriorize it with other methods. For extraordinarily heavy patients of palliative operations is justified:

 1) sewing of bleeding vessel is from the side of mucus;  2) V-like carving of ulcer;  3) embolization of bleeding vessels;  4) sewing of wall of stomach through on the perimeter of ulcer with next imposition of serous-muscular guy-sutures by Kartavin;  5) inseaming of bleeding gastric and duodenum ulcer. Postoperative treatment

Basic principles: 1. Proceeding in VCB. 2. A fight is against postbleeding anaemia. 3. Improvement of reologic properties of blood. 4. Prophylaxis or treatment of hepatic-kidney insufficiency. 5. Infusion therapy. 6. Antiulcerous therapy which includes for itself block ofgastric secretion. 7. Decompression of stomach is to proceeding in a peristalsis and arcade of intestinal maintenance. 8. Fight against paresis of intestine, leadthrough of cleansing enemas. 9. Vitaminterapy. 10. Symptomatic therapy. 11. Antibiotic therapy is after indications. Perforated ulcer gastroduodenal ulcers

 The typical perforation of gastric or duodenal ulcer is due to increase of necrotic process in the area of ulcer with subsequent disturbance of integrity of the wall, that result in the permanent flow of gastroduodenal content and air in the free abdominal cavity. Perforated ulcer gastroduodenal ulcers

 Peptic ulcers may lead to emergency situations. Severe with or without evidence of bleeding may indicate a perforation of the ulcer through the stomach or duodenum.

Perforated ulcer gastroduodenal ulcers Etiology and pathogenesis

1. 50,7 % cases of duodenal ulcer perforates and 42,8 % ulcers of pyloric part of stomach, 4,8 % ulcers of lesser curvature of body of stomach and 0,7 % cardial ulcers lead to perforation. 2. The causes of ulcers perforation are: exacerbation of peptic ulcer, harmful habits, stress, professional, athletic overexertion, alcohol abuse. Perforated ulcer gastroduodenal ulcers: Classification by V.S. Savelev, 1986) Perforated gastroduoden al ulcers are divided according to:  1. etiology: ulcer;unulcer.  2. localization: gastric (lesser curvature, cardial, antral, prepyloric, pyloric) ulcer, anterior and posterior walls; ulcers of duodenum (anterior and posterior walls).  3. type of perforation: perforated in an abdominal cavity; covered perforations; atypical perforations. Perforated ulcer gastroduodenal ulcers: Clinical management Clinically the perforations are distinguished into three phases: shock, transitory phase, peritonitis (Mondor,1939).  The phase of shock last for about 6 hours and the typical symptom is acute pain in the epigastric region (Delafua compares it to pain due to stabbing with a dagger) with an radiation to the right shoulder and collarbone, the face is pale, with expression of strong fear, lines become acute (facies abdominalis), skin is cold and clammy. The pulse at first is slow (vagus pulse), later becomes frequent. Sometime the reflex vomiting and delay of gases is seen. Arterial pressure is reduced. On examination stomach is pulled in, and does not take part in respiration. On palpation the stomach is "wooden belly", especially in an upper part, where usually there is more pain. Positive Blumberg's sign. On percussion there is absence of hepatic dullness (the Spizharnyy symptom). On rectal examination there is tenderness in the area of rectouterine or rectovesical pouch (the Kulenkampff's symptom). Perforated ulcer gastroduodenal ulcers: Clinical management

 The phase of shock is followed by transient recovery, when the reflex signs decrease: the general condition of patient gets better, the pulse becomes normal, arterial pressure rises, the stomach-ache diminishes partly.  However tension of muscles of anterior abdominal wall is present, positive Blumberg's sign. Perforated ulcer gastroduodenal ulcers: Clinical management

 The phase of "recovery transition" lasts for 6-12 hours and then followed by the phase of peritonitis where the pulse is rapid, the stomach is distended, bowel sounds are not audible, the face acquires a specific look -facies Hippocratica - the eyes fall back, lips turn blue, the nose becomes sharp, the becomes dry and furred, breathing is superficial and frequent, the temperature rises. Diagnosis programme

1. Anamnesis and physical examination. 2. Analysis of blood and urine, biochemical blood test, coagulogram. 3. X-Ray examination of abdominal cavity organs for presence offree gas (). 4. Pneumogastrography, contrasting pneumogastrography. 5. Fiber-gastroduodenoscopy. 6. Sonography of abdominal cavity organs. 7. Laparocentesis with the Neymark diagnostic test (to 2- 3 ml of abdominal cavity exudate add 4-5 drops of the 10 % solution of iodine. If the admixtures of gastric content appear in exudate, then under action of iodine gastric content gets a dirty-dark blue color). 8. Laparoscopy. X-ray X-ray Tactic and choice of treatment method

 The diagnosed perforated gastric and duodenum ulcer is an absolute indication to operation. Preoperative preparation must include: in I phase antishock treatment; in the II and III phases - reanimation, introductions of antibiotics for 2-3 hours before operation, correction of hypovolemia by salt blood substitutes (solution of chlorous sodium), solutions of dext-ran (polyhlukine, reopolihlukine, hemodes). Amount of liquid necessary for correction of hypovolemia, is calculated after hematokrit by central vein pressure. Taking the normal of hematokrit as 40 %, on each 5 % increase, 1000,0 ml of fluids is to be prescribed. Conservative treatment

Conservative treatment (method of Tejlor, 1946) can be justified when the refuses for operation, or when surgery contraindicated 1. Conservative management includes: 2. Permanent nasogastral aspiration of gastric content; 3. Introduction of preparations which decrease gastric secretion (atropine, H2- blockers and others like that); 4. Introduction of antibiotics; 5. Correction of metabolism; 6. Laparocentesis with drainage and closed lavage of the abdominal cavity. Surgery: Palliative operation

 Sewing of omentum on a leg by the Oppel-Polikarpov Surgery: Palliative operation Radical operations The radical operations in perforated ulcers are: resection of stomach and excision of the perforationin combination with pyloroplasty and StV, SV or SPV. Indications and terms for implementation of resection of stomach are: 1. perforation of callous gastric ulcer in I phase of clinical staging; 2. repeated perforation of ulcer; 3. perforation of ulcer in I phase of clinical staging in combination with stenosis and bleeding of ulcer; 4. perforation of duodenal ulcer in I phase of staging in combination with a gastric ulcer; 5. unexpressed and moderate degree of risk of operation; 6. sufficient qualification of surgeon, availability of material resources for operating. Gastric outlet obstruction

 The two common causes of gastric outlet obstruction are: - Gastric cancer - secondary to peptic ulceration Ulcer stenosis

Obstruction:  Gastric outlet obstruction is the least frequent ulcer complication.  Most cases are associated with duodenal or pyloric channel ulceration, with gastric ulceration accounting for only 5 percent of cases. Ulcer stenosis: phases in development of scars narrowing Ulcer stenosis

"Kissing" ulcers of the anterior and posterior wall in the duodenal bulb, bleeding slowly. In the past most situations like this required emergency surgery and removal of part of the stomach. Now with our newer technology, many bleeding ulcers can be cauterized which stops the bleeding. In many cases, surgery can now be avoided. Ulcer stenosis: classification Classification (by A.A.Shalimov and V.F.Saenko(Ukraine), 1987)

Three clinical stages of stenosis are distinguished:  I - compensated;  II - subcompensated;  III - decompensated. Ulcer stenosis In accordance with localization, by V.F.Saenko (1988) distinguished three types of stenosis:

 I - stenosis of pylorus;  II - stenosis of bulb of duodenum;  III- postbulbar duodenal stenosis. Pyloric stenosis: a diagnose

 Roentgenologically in the compensation stage stomach is normal in sizes, its peristalsis is deep, increased, evacuation of contents takes no more than 6 hours.  In the stage of subcompensation the stomach is megascopic, peristalsis is decreased, evacuation take up to 24 hours.  During decompensation the stomach is considerably dilated like a sack and deformed, the waves of antiperistalsis can take place, the contrast stays for long to more than 24-48 hours.  The method of the double contrasting by a barium and air considerably facilitates diagnosis. Pyloric Stenosis

78 year-old woman with chronic ulcer disease, who developed symptomatic gastric outlet obstruction. Her early satiety, postprandial vomiting and weight loss failed to improve after two sessions of endoscopic balloon dilation of the pylorus, necessitating surgery

57 year-old woman with long-standing ulcer disease, whose symptomatic pyloric stenosis responded promptly and completely to endoscopic balloon dilation of the pylorus. Pyloric stenosis: a differential diagnose

 1. Functional gastrostasis is more frequently seen in women. In that there is absence of some organic changes in the area of pyloric part of stomach or in a duodenum, that can be exposed during fibergastroscopy.  2. Differential diagnosis of stenosis of tumour genesis, as a rule also does not cause the special difficulties. A diagnosis is finally confirmed by histological examinations of the biopsy material taken during endoscopy. Duodenal Stricture

Benign inflammatory post-bulbar duodenal stricture in a 79 year-old man with a history of peptic ulcer disease, and symptoms of partial gastric outlet obstruction.

Post-bulbar duodenal stricture in a 61 year-old woman with a history of peptic ulcer disease, who had presented with symptoms suggestive of partial gastric outlet obstruction. Pyloric stenosis: a differential diagnose

 3. Postburn stenosis of piloroantral area of stomach is observed from data of statistics in more than 25 % of cases of patients with the burn of esophagus. Some diagnostic difficulties can arise with isolated postburn stenosis of pyloric part of stomach. However carefully history taking and professionally conducted endoscopic examination enables to set the correct diagnosis. Pyloric stenosis: a treatment

 1. Treatment of ulcer stenosis of pyloroantral part of stomach and duodenum must be exclusion ally operative.  2. In the compensated and subcompen- sated stages of stenosis and when functions of stomach is preserved it is possible to perform organ-saving operations (vagotomy with drainage operations, minimal resection of stomach). Pyloric stenosis: a treatment

 3. With increase in the signs of stenosis and disturbance of basic functions of stomach, the volume of operation must be increased to resection by the Bilroth's second method.  4. An older age persons with severe accompanying pathology minimum surgery of gastroenteroanastomosis is performed. Preoperative preparation

 Must be strictly individual.  In patients with insignificant disturbances of gastric motor activity (stage of compensation, subcompensations) and with good level of metabolism indexes it is better to shorten preoperative preparation in time. Such patients are usually, operated on 3-4 day.  Preoperative preparation of patients with decompensated pylorostenosis must be directed to the correction of metabolic disturbances. Such patients must receive transfusion of fluids up to 2,5-3 1 per day which contain the ions K+, Na+, Ca++, amino acid and glucose; plasma, albumen. Twice daily decompression and washing of stomach with anti-ulcer therapy is done. Effective preoperative preparation in such patients requires 5-7 days, sometimes even more. Penetrating Ulcer

72 year-old woman with (vomiting blood) and melena (black, tarry stools). Endoscopy revealed this large gastric ulcer, shown here at retroflexion, which was penetrating into the liver.

53 year-old man with hematemesis, melena and severe anemia. Endoscopy revealed a rather deep gastric ulcer, with a prominent visible vessel which bled intermittently. Bleeding could not be controlled endoscopically. At surgery, the ulcer was found to be penetrating into the pancreas. Malignant Gastric Ulcer

46 year-old man with no prior gastrointestinal symptoms, presented with five days of epigastric pain. Initial studies revealed iron-deficiency anemia and blood in the stool. Endoscopy demonstrated this lesion on the lesser curvature which appeared to be edematous folds with a central ulceration, but which on biopsy proved to be a poorly differentiated adenocarcinoma, signet ring cell type.

72 year-old man with hematemesis, with active bleeding from a malignant ulcer in the gastric fundus, seen here at retroflexion.

87 year-old woman was found to be anemic and to have occult blood in the stool; she had no gastrointestinal symptoms of any kind. Endoscopy revealed this ulcerated, sessile, polypoid mass which proved to be adenocarcinoma on biopsy. Malignant Gastric Ulcer

82 year-old woman who presented with early satiety and postprandial vomiting, suggestive of gastric outlet obstruction, along with weight loss and anemia. Endoscopy demonstrated an ulcerated mass with prominent folds, which did not obstruct the gastric outlet. The lesion was an adenocarcinoma of the signet ring cell type.

54 year-old woman with abdominal pain. Biopsies of this ulcer, with raised margins, revealed poorly differentiated adenocarcinoma, signet-ring type. Gastric Foreign Body

25 year-old man presenting with nausea and abdominal discomfort, who had ingested dozens of interlocked safety pins.

77 year-old woman with dementia, undergoing endoscopy for insertion of a feeding gastrostomy tube. An incidental finding was this cloth-covered elastic hair accessory which the patient had apparently recently ingested. Gastrointestinal bleeding of unulcer etiology: The Mallory-Weiss Syndrome

 This is origin of acute linear break of the mucosa of the esophagus and cardiac part of stomach, which is accompanied by bleeding of a varying degree into the gastrointestinal tract lumen, and is named as Mallory-Weiss Syndrome.  First described by K. Mallory and C. Weiss in 1929. This type of gastroduodenal bleeding is observed in 10 % cases, and patients between the 30-50 years of age are mainly affected. Mallory-Weiss syndrome

A linear mucosal laceration caused by the force of vomiting, generally at or just below the esophagogastric junction, resulting in bleeding. Seen here is an elliptical-shaped mucosal tear which has stopped bleeding, from the forward view (on the left) and from the retroflexed position (on the right).

66 year-old women with a self-induced, intraprocedural Mallory-Weiss caused by retching during the exam. Bleeding was self-limited; shown here are fresh blood coating mucosa, and the clot forming at the point of bleeding just below the esophagogastric junction, seen at retroflexion. The Mallory-Weiss Syndrome Etiology and pathogenesis 1.The predetermining factors: - attacks of cough, - physical overstrain after the surplus food and alcohol intake with vomiting, - chronic diseases of stomach, with the acute increase of intragastric pressure. Mallory-Weiss syndrome

This thin linear mucosal tear is seen on a retroflexed view, looking back up at the esophagogastric junction.

Close up of the mucosal tear from the photo at left, showing the separation of the mucosa.

Deep, wide mucosal tear beginning just above the squamocolumnar junction, extending rightward in this photo, in a 51 year-old man presenting with hematemesis (vomiting blood). Bleeding was self-limited once the vomiting was brought under control. The Mallory-Weiss Syndrome

 The increase of intragastric pressure causes change of blood flow in the walls of the distended stomach.  Spontaneous damage of mucosa of cardiac part of stomach, is accompanied by bleeding in the gastrointestinal tract lumen.  The damage involves not only the mucosa but also the muscular layer.  Most often the damage is localized on lesser curvature, on the posterior wall of stomach and esophagus. The Mallory-Weiss Syndrome: Classification  By localization of injury: a) esophagus; b) cardio- esophageal; c) cardiac.  By the amount of injury: a) single; b) multiple.  By the depth of injury: a) superficial (I degree), which penetrate to the submucosal layer; ) deep (II degree), which take mucus and submucosal layer; in) complete break (III degree) which is characterized by the break of all layers of organ.  By the degree of hemorrhage: a) mild; b) moderate; c) massive.  By clinical staging: 1) simple form,  2) delirious form: a) with the signs of acute hepatic insufficiency; b ) without the signs of acute hepatic insufficiency. The Mallory-Weiss Syndrome: Clinical management  The main symptom of syndrome is "bloody" vomiting with the dyspeptic signs preceded by nausea and vomiting.  Amount of bleeding depends on length and depth of damage and caliber of the damaged vessels. In some cases initially patients vomits by dark blood and only on the repeated vomiting the vomitus has bright red blood. And in some cases there is vomiting of bright red blood. The Mallory-Weiss Syndrome Diagnosis programme  1. Anamnesis and physical examination.  2. Esophagogastroscopy.  3. General analysis of blood.  4. Coagulogram.  5. Blood group and Rhesus factor.

Urgent esophagogastroscopy is the basic method of diagnosis. During the process in the cardiac part of stomach or esophagus single or multiple fissures are diagnosed, which are placed longitudinally, often with bleeding. The edges of mucosa round the fissures are edematous, elevated and covered by fibrin. Often the muscular layer of stomach or esophagus forms the base of the fissure. The Mallory-Weiss Syndrome: treatment

 Conservative treatment of the Mallory-Weiss syndrome is indicated when there is small break in the mucosa of the stomach or absence of bleeding.  Treatment of patients is begun with active conservative therapy, which includes blood transfusion, infusion of hemostatic, application of antacid drugs.  With rupture of the I-II degrees as indicated by endoscopy a monopolar electrocoagulation of the fissure and closureof the fissure by aerosol film- forming preparation Lifusol is used. The Mallory-Weiss Syndrome: treatment

 Operative treatment is indicated in deep large ruptures of mucosa and muscular layers, cardiac part of stomach, which are complicated by bleeding.  In such cases gastrotomy and suturing of ruptures by interrupted suture or 8-shaped stitch by applying nonabsorbable filaments is preferred.  Repair of ruptures of mucosa of stomach is often supplemented with vagotomy and pyloroplasty. In deep, and multiple ruptures which are accompanied by the edema of tissues, repair is supplemented with ligation of left gastric artery.