Surgery of stomach and duodenom

1. Surgery of stomach and duodenom Martin Diva

2. Physiology • The stomach has 3 main functions: • temporary storage for food, which passes from the esophagus to the stomach where it is held for 2 hours or longer • mixing and breakdown of food by contraction and relaxation of the muscle layers in the stomach • digestion of food

3. Physiology • Gastric secretions are: • Parietal cells: contain intrinsic factor which binds to b12 to be reabsorbed in distal ileum. And hcl. • Mucous cells produce hco3 which protect the mucose lining of stomach. • Gastric secretions are high in h+,k+,cl- but low in sodium. Thats why during vomiting you can develop metabolic alkolosis and low potassium level. • Chief cells contains pepsinogen which breaks down proteins

4. Acid secretion • Controlled by 3 substances: • AcH • Histamine • Gastrin(biggest stimuli is expansion of stomach)

5. Anatomy

6. Duodenom • DUODENUM: The duodenal wall shows the standard digestive tract design with the following exceptions: • 1. The submucosa contains abundant numbers of Brunners glands which produce copious amount of an alkaline mucous (asterisks). This helps to neutralize acid chyme from the stomach. • 2. The proximal portion of the duodenum shows very few foldings of the mucosal lining. As you approach the distal end of the duodenum, the number of foldings and villi increase dramatically

7. Cogenital disorders • Pyloric stenosis: 3/100 live births. Boys are more affected 4:1, especially first born males. It is familial. • Presents: with non billous vomiting after 3 weeks of age. Baby is hunger after vomiting. If you palpate the abdomen you can feel olive mass. And you might se persistaltic waves. Patient can be dehydrated and lose weight and jaundice. Diagnose Abdominal ultrasound is test of choice , you can se thickened and elongated pyloric • Treat: Hydration, electrolites and surgery

8. Gastric Heterotopia: patches of ectopic gastric mucosa in duodenum or more distal sites. -causes bleeding and ulcerations (esp. w/Meckel’s diverticulum) • Duodenal atresia: Failure to recanalization of duodenal lumen. 1/10,000 births and associated trisomy 21. • Presents: like pyloric stenosis but with vilous vomiting and its more early (first day of life). Abdominal x ray show double bubble of stomach and proximal duodenom. Treat surgically

9. Autoimmune Gastritis (Pernicious Anemia) • About 10% of cases of Chronic gastritis. Majortiy of chronic gastritis is caused by h.pylori. • This is a type 4 hypersensitivity where you get antibodies againts parietal cells and intrinsic factor in the fundos (also called fundus type). Which cause gland destruction and mucose atrophy and intestinal metaplasia, which is risk for adenocarcinoma. • It is Associated with achlorhydria becuase knocking out parietal cells and megaloblastic anemia due to b12 deficiency. Risk for adenocarcinoma is 2-4%. This can be familial so patient can have family history of this disease. • Associated with other autoimmune

10. Autoimmune gastritis. • Patient can complain of epigastric pain, fatique, pallor and peripheral vibration sensation. • Diagnose :B12 is low and MMA is high. Macrocytic anemia, hypochlorhydria, positive antiparietal cell antibody and anti intrinsic factor antibodies. • Treat: IM b12

11. Acute gastritis • 3 most common cause of epigastric pain • Clinically hard to differentiate from PUD. • Like pud It complains epigastric pain.. Patients may present hematemesis and melana. • The cause like PUD is Nsaids and H.pylori, but unlike PUD it can be caused by alcohol, tobacoo and atrophic gastritis.

12. Acute gastritis • Stress ulcer can also be a cause of acute gastritis. Like shock, burn, sepsis, or severe trauma. (5-10% icu patient). • Cushing ulcer is when you get increase gastrin due to increase intracranial pressure (head trauma) • Curlings ulcer due to severe burn • Diagnose: if alarm symptoms you endoscope and biopsy. If no alarm symptoms go for h.pylori serology test. • Treatment. If h.pylori: PPI, amoxicillin, clarithromycin. If no h.pylori only PPI. • If low b12 and or high MMA: IM b12

13. Zollinger-ELLISON syndrome: • Tumor of functional gastrin secreting cells, located in duodenom in 50-70% of cases or pancrease 20-40%. Ulcer presents in 90-95% cases and the are multiple and can extend to jejunum • About 40% are malignant, if its in pancrease its more likely to be malignant • Presentation: Pud symptoms that is refractory to medical treatment (h2 blocker, PPI,h,pyolori antiobotic ) and surgical treatment like vagotomy and antrectomy. Patient may complain of watery diarrhea. • Think about this tumor for patient that you have tried everything to resolve PUD but failed. • Diagnose:Fasting serum gastrin level above 500 pg/dl then you follow up by a ct scan.

14. Zollinger elison syndrome:

15. Treatment of zollinger elisson syndrome: • Surgical resection only possible in 1/5 of cases. Because it is very difficult to do surgical rescton, due to tumor cells are very small and hard to find and usually have metastasis. Or you can do Total gastrictomy , to reduce acid • Malignant disesae: controll the symptoms with omperazole because you can not do anything else with it.

16. H.Pylori infection • Helicobacter pylori infection: • Most important cause of chronic gastritis -90% of patients. It causes inflammtion of antrum (sometime called antrum type) H.pylori Colonizes 50% of persons over age 50, most of which are asymptomatic. H.pylor is a gram negativ with produces urease to produce ammonia and it buffer gastric acid. Basically weakens the mucosall wall to cause gastritis or ulcers. Complication of h.pylori infection is gastric adenocarcenoma in the antrum and Maltoma. •

17. Peptic ulcer disease • Solitary mucosal ulcer involving proximal duodenom (90%) or distal stomach (10%). • Patient complains: Post prandial epigastric pain, stomach ulcer is usually worse after eating and duodenal ulcer are better after eating. Epigastric pain that awakes patient at night and melana. • Causes: Nsaids is most common cause. For duodenal ulcer its about 90% and for stomach about 75%. Ze is another cause. Alcohol and tobaco does not cause ulcer but worse the healing.

18. Peptic ulcer • Diagnose: Patient with alarm symptos, do endoscopy and biopsy. Without alarm symptoms do serology test. All patients should be put on Ppi, but if postive for H.pylori Clarithromycin and amoxicillin is added . Typical ulcer are small less then 3 cm, sharpyl demarcated and surrounded by radiating folds of mucosa • Malignant ulcers are larger, irregular with heaped up margins

19. Surgery of peptic ulcer disease • Surgery is usually only required for complications such as hemorrhage, perforation and pyloric stenosis, or it may be considered in case patients doesn’t tolerate the medical therapy. • Options are: • Vagotomy • Gastrectomy • In emergency surgery: Haemorrhage: may be controlled endoscopically by adrenaline injection, diathermy, laser coagulation or heat probe . Perforation: laparoscopic repair is as good or better than open repair. Pyloric stenosis: endoscopic balloon dilatation, followed by maximal acid suppression. If this is not effective: drainage procedure (eg gastro-enterostomy) + highly selective vagotomy may be performed (often laparoscopically)

20. Complications of PUD • Perforation: The pain is worse, signs of peritoneal inflammation (generalized, very sensitive to touch, rebound tenderness, guarding), abdominal distension, fever and shock. This is a surgical emergency!! • Gastric adenocarcinoma and Maltoma: Diagnose on biopsy and should be surgical resected • Gastric outlet obstruction: Symptoms early satiety, weightloss, vomiting. diagnos endoscopy and treat surgically

21. Complications of Surgery for Peptic Ulcer: • Early complications: duodenal stump leakage, gastric retention, hemorrhage may develop in the immediate postoperative period. • Late complications: recurrent ulcer, gastrojejunocolic and gastrocolic fistula, dumping syndrome, anemia

22. Dumping syndrome

23. Gastric polyps • Any nodule or mass projecting above mucosa; uncommon (0.4%), 3-5% in Japan. Majority are non-neoplastic (90%) and represent hyperplastic lesions Due to chronic inflammation such as due to chronic gastritis or celiac disease. • They are usually asymptomatic and discovered coincidentally on EGD. If you see multiple polyps it can be due to familial polyposis syndromes. • All gastric polyps over 1 cm in diameter should be removed for biopsy. Polyps over 2 cm will be surgically removed. • Types of Gastric polyps: • Fundic gland polyps: People with PPIS can get it, they are usually small • True adenomas: 5 to 10% of gastric polyps; have dysplastic epithelium and malignant potential. They can transfer to an adenocarcinoma. Most males have this. They carry 20% risk of malignancy. The risk of malignincy increases with size. • Hyperplastic polyps: Associated chronic inflammation like celiac and chronic gastritis. Biopsy should taken for h.pylori • Treatment: antibiotics may be recommended to help reduce the size of polyps or in case of large polyps: surgery (like endoscopy or partial gastrectomy)

24. Gastric Carcinoma: • 95 % of all gastric cancers • Risk factors are: Male over 70, blood group A , diet in high smoked/salty food, tobacco, chronic gastritis, h.pylori , adenomatous polyps • Symptoms: epigastric pain, fatique, early satiety, anorexia, dysphagia, vomiting, supraclavicular node, sister mary joseph nodule (periumbilical). Rarely lesser trelat . • Diagnos: Endoscopy with biopsy ,when it is diagnosed do endoscopic ultrasound and Ct to see depth and local extension and metastasis

25. Sister mary joseph nodule

26. Morphology: • Intestinal type (most common): due to intestinal metaplasia from h.pylori, and autoimmune gastritis. Nitrosamine in smoked food(japan), blood type A • Diffuse type:Not assiocaited with h.pylori, autoimmune,nitrosamine. Linitis plastica (signet cels in the wall of stomach causes thickening of stomach). This cause significant early satiety

27. Metastasis • Gastric cancer can spread direcly or hematogenously • Spleen, diaphragm, omentum,liver, lung, transverse colon • Ovary ( Kruckenburg tumor). Classic for signet cells. • Rectouterine pouch (blumer’s shelf tumor) • Survival is bad and depend on invasion

28. Treatment • Surgical resection is the only curative treatment: 85% of patients are operable, and in 50% the lesions are amenable to resection; of the resectable lesions, half are potentially curable. • Partial gastrectomy for distal tumors. -If more proximal: total gastrectomy may be needed (eg linitis plastica) -Combination of chemotherapy appears to increase survival in advanced disease.

29. Sources • Robbins pathology • Current Diagnosis and Treatment - Gerard Doherty.

30. Thanks!