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Ca stomach

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Dr. Rahul JainDoctor at Department of Neurosurgery, AIIMS Patna

Basic anatomy with general considerations on Gastric CA, its diagnosis, Management and post gastrectomy complications.

Ca stomach

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STOMACH
Dr. RAHUL JAIN
M.S. General Surgery
Anatomy and Physiology of the
Stomach
EMBRYOLOGIC DEVELOPMENT
• The stomach arises from the embryonic endoderm and comprises a portion of the
foregut along with the esophagus, the first portion of the duodenum, as well as the
liver, bile ducts, and pancreas.
• During the fourth week of gestation, the foregut is oriented as a craniocaudal tube
with the primitive stomach and first portion of the duodenum forming the caudal
end.
• The ventral mesogastrium and the dorsal mesogastrium are attached to the
stomach anteriorly and posteriorly and suspend the stomach in the peritoneal
cavity.
• The greater and lesser curvatures of the stomach are formed because the dorsal
portion of the gastric wall grows at a faster rate than the ventral portion.
• At approximately weeks 7 and 8, as the foregut develops, it rotates 90 degrees
clockwise on its long axis so that the ventral mesogastrium is positioned to the
right of the stomach and the dorsal mesogastrium is to the left.
• The ventral mesogastrium forms the lesser
omentum comprised of the gastrohepatic and
hepatoduodenal ligaments and contains the
liver, which grows rapidly and pushes the
stomach to the left portion of the peritoneal
cavity.
• The dorsal mesogastrium develops into the
greater omentum, comprised of the
gastrophrenic, gastrosplenic, and gastrocolic
ligaments and is where the spleen is located
during development.
• This rotation also positions the left vagal nerve
trunk anterior to the stomach and the right vagal
nerve trunk in the posterior position. The
stomach descends as cephalad structures grow
and is eventually located between T10 and L3 in
the adult.
GROSS ANATOMY AND ANATOMIC
RELATIONSHIPS OF THE STOMACH
• The stomach is a dilated cylindrical J-
shaped organ that rests in the
epigastric and left hypochondrial
region of the abdomen at the level of
the first lumbar vertebra.
• It is bordered anteriorly by the left
hemidiaphragm, and the parietal
portion of the anterior abdominal wall.
• Posteriorly, the pancreas (neck, body,
and tail), left kidney, and adrenal
grand border the stomach.
• The spleen sits posterolaterally and
the transverse colon inferiorly.
• Ligamentous attachments also help to further
anchor the stomach to surrounding organs:
gastrophrenic (diaphragm),
hepatogastric or lesser omentum (liver)
gastrosplenic or gastrolienal (spleen),
gastrocolic or greater omentum (transverse colon).
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Ca stomach

  • 1. STOMACH Dr. RAHUL JAIN M.S. General Surgery
  • 2. Anatomy and Physiology of the Stomach
  • 3. EMBRYOLOGIC DEVELOPMENT • The stomach arises from the embryonic endoderm and comprises a portion of the foregut along with the esophagus, the first portion of the duodenum, as well as the liver, bile ducts, and pancreas. • During the fourth week of gestation, the foregut is oriented as a craniocaudal tube with the primitive stomach and first portion of the duodenum forming the caudal end. • The ventral mesogastrium and the dorsal mesogastrium are attached to the stomach anteriorly and posteriorly and suspend the stomach in the peritoneal cavity. • The greater and lesser curvatures of the stomach are formed because the dorsal portion of the gastric wall grows at a faster rate than the ventral portion. • At approximately weeks 7 and 8, as the foregut develops, it rotates 90 degrees clockwise on its long axis so that the ventral mesogastrium is positioned to the right of the stomach and the dorsal mesogastrium is to the left.
  • 4. • The ventral mesogastrium forms the lesser omentum comprised of the gastrohepatic and hepatoduodenal ligaments and contains the liver, which grows rapidly and pushes the stomach to the left portion of the peritoneal cavity. • The dorsal mesogastrium develops into the greater omentum, comprised of the gastrophrenic, gastrosplenic, and gastrocolic ligaments and is where the spleen is located during development. • This rotation also positions the left vagal nerve trunk anterior to the stomach and the right vagal nerve trunk in the posterior position. The stomach descends as cephalad structures grow and is eventually located between T10 and L3 in the adult.
  • 5. GROSS ANATOMY AND ANATOMIC RELATIONSHIPS OF THE STOMACH • The stomach is a dilated cylindrical J- shaped organ that rests in the epigastric and left hypochondrial region of the abdomen at the level of the first lumbar vertebra. • It is bordered anteriorly by the left hemidiaphragm, and the parietal portion of the anterior abdominal wall. • Posteriorly, the pancreas (neck, body, and tail), left kidney, and adrenal grand border the stomach. • The spleen sits posterolaterally and the transverse colon inferiorly.
  • 6. • Ligamentous attachments also help to further anchor the stomach to surrounding organs: gastrophrenic (diaphragm), hepatogastric or lesser omentum (liver) gastrosplenic or gastrolienal (spleen), gastrocolic or greater omentum (transverse colon).
  • 7. • The visceral peritoneum covering the stomach forms its outermost serosal layer, which is contiguous with the lesser and greater omenta anteriorly and the anterior wall of the lesser sac posteriorly. • The muscularis externa of the stomach wall comprises three layers: the outermost longitudinal muscle layer, the middle circular muscle layer, and the innermost oblique muscle layer. • The longitudinal muscle layer of the stomach is concentrated proximally at the gastroesophageal junction and along the greater and lesser curvatures, and subsequently spreads unevenly over the corpus until joining more densely near the pylorus.
  • 8. • Deep to the longitudinal muscle fibers, the circular muscle layer covers the stomach completely and is contiguous with the LES muscle proximally and forms a thickened band at the pylorus distally. • The innermost oblique muscle layer is blended proximally with the circular muscle layer at the collar of Helvetius and splays incompletely over the anterior and posterior gastric walls. • Submucosa -the strength layer of the gastric wall, deep to the Muscularis followed by the muscularis mucosae, and finally the mucosa, which contains the lamina propria (LP) composed of connective tissue, blood vessels, and mucosal epithelium.
  • 9. VASCULAR, LYMPHATIC, AND NEURAL SUPPLY TO THE STOMACH • 4 main arteries  Left gastric – largest  Right gastric Hep A common hep  Right gastroepiploic Gastroduod  Left gastroepiploic Splenic A • Venous drainage of the stomach parallels the arterial blood supply with eventual drainage into the portal vein. • The left gastric vein (coronary vein) and right gastric vein course along the lesser curvature and drain directly into the portal vein. • The greater curvature is drained by the right gastroepiploic vein into the superior mesenteric vein and by the left gastroepiploic vein, which empties into the splenic vein.
  • 10. Gastric Adenocarcinoma Gastric cancer is 4th MC cancer in world and 2nd MCC of cancer death in world. RISK FACTORS • Helicobacter pylori infection, • a history of mucosa-associated lymphoid tissue (MALT) lymphoma, • the presence of adenomatous gastric polyps, • previous gastric operations, • pernicious anemia, • atrophic gastritis, • intestinal metaplasia, • exposure to nitrosamines from cured or smoked foods, • tobacco use, and • family history Protective Factors • Raw vegetables • Citrus fruits • Antioxidants • Selenium, Zn, iron • Green tea • Refrigeration of foods • aspirin
  • 12. PATHOLOGY • 90 to 95% of gastric cancers are adenocarcinoma with the remainder being attributed to lymphoma, gastrointestinal stromal tumors, and carcinoid tumors. • Although several histopathology classification systems exist, the most frequently used is the Lauren Classification. This classifies gastric adenocarcinomas as intestinal (well differentiated) and diffuse (poorly differentiated). • Intestinal-type adenocarcinomas are derived from the gastric mucosa and form glands. They are also more common in the distal portion of the stomach. they are associated with the H. pylori. • Diffuse-type adenocarcinoma arises from the lamina propria and spreads through the submucosa. more frequently observed in the proximal stomach
  • 13. Borrmann classification • Based on macroscopic appearance of lesion • Divides gastric ca into 5 types • Type 5 – linitis plastica – diffusely infiltrating lesion involving whole stomach
  • 14. PATHOLOGY DYSPLASIA – universal precursor to gastric adenoCA EARLY GATRIC CA • Limited to mucosa (T1a) and submucosa (T1b) • 70% well differentiated and 30% poorly diff. Morphological subtypes – 4 – Polypoid – fungating- intraluminal with ulceration – Ulcerative – Scirrhous – infiltrate enire thickness and cover very large surface area, involve entire stomach; poor prognosis • 1st two are intraluminal and in latter two bulk of tumor mass is confined to wall of stomach
  • 15. DIAGNOSIS • Signs and symptoms of gastric cancer are non-specific. • Symptoms include epigastric pain, early satiety, and weight loss, nausea, vomiting, bloating. • Chronic occult blood loss presenting as IDA and heme-positive stool. • Pain associated with gastric cancer is constant, non radiating and not relieved by eating. • Physical exam findings are also nonspecific, but may include palpable lymph nodes such as the Sister Mary Joseph node (periumbilical region), the Virchow node (left supraclavicular region), or the Blumer shelf (prerectal drop metastases) evident on digital rectal exam. Development of a palpable abdominal mass or ascites are findings of advanced disease
  • 16. • Markers may be elevated in the setting of gastric cancer, including carcinoembryonic antigen (CEA), CA-125, CA 19-9, and β-HCG. These biomarkers, however, lack sufficient sensitivity and specificity to establish a diagnosis. • Imaging with computed tomography (CT) of the chest, abdomen, and pelvis with oral and intravenous contrast should be obtained, but the diagnosis is established definitively with an upper endoscopy and biopsy confirmation of an adenocarcinoma. • Endoscopic ultrasound (EUS) accurately assesses the depth of tumor invasion and enlargement of perigastric lymph nodes,. • Cross-sectional imaging with CT scan or magnetic resonance imaging (MRI) is useful for the evaluation of metastatic disease. • Positron emission tomography (PET) may also be used, as most gastric cancers are PET avid. • If metastatic disease is identified, human epidermal growth factor receptor 2 (HER2-neu) testing is recommended
  • 17. • AJCC TNM is most widely used staging system. • Siewert classification system – based on anatomic location of adenoCa that are in close proximity to GE junction. – Type I - tumors of the distal esophagus, within 1 to 5 cm above the GE junction; – type II - tumors center located from 1 cm above the GE junction to 2 cm below – type III - tumors are termed subcardinal, located between 2 and 5 cm caudad to the GE junction. • R status - first described by Hermanek in 1994 – to describe tumor status after resection – R0 - microscopically margin-negative resection – R1 indicates removal of all macroscopic disease, but microscopic margins are positive. – R2 indicates gross residual disease.
  • 19. LYMPHADENECTOMY • Dissection of stations 1 to 6, a D1 lymphadenectomy, refers to dissection of the perigastric lymph nodes. • A D2 lymphadenectomy includes stations 1 to 11 and involves removal of the perigastric lymph nodes as well as the lymph nodes extending along the hepatic, left gastric, celiac, and splenic arteries. • A D3 lymphadenectomy includes stations 1 to 16 and removes the nodal stations listed previously as well as the periaortic and porta hepatic lymph nodes.
  • 21. TUMOR MANAGEMENT • Stage IA tumors may be managed endoscopically with endoscopic mucosal resection (EMR) or endoscopic submucosal dissection (ESD), • stage IB to stage IIIC tumors are potentially curable with multimodality therapy. • Tumors that appear locoregionally advanced on cross-sectional imaging are not candidates for surgical resection for curative intent. Findings consistent with locoregionally advanced tumors exhibit disease infiltration at the root of the mesentery, have paraaortic lymph node involvement on imaging or biopsy, and invasion or encasement of major vascular structures excluding the splenic vessels. • In addition, the presence of distant metastases or peritoneal seeding (stage IV tumors) negates the potential for operative cure, and these patients should receive chemotherapy
  • 22. EMR • most significant advantage of endoscopic resection is avoiding the need for gastrectomy. • major disadvantage is incomplete resection because of tumor size or unrecognized lymph node metastases. • general guidelines for endoscopic resection of early gastric cancer are as follows: (1) tumor limited to the mucosa, (2) no lymphovascular invasion, (3) tumor smaller than 2 cm, (4) no ulceration, and (5) well or moderately well differentiated histopathology. • larger tumors or tumors with SM1(limited submucosal) invasion can be managed with ESD.
  • 24. SURGERY • Goal – resection of all tumor i.e., R0 and adequate lymphadenectomy. • achieve margin negative resection intragastric margins of 5 cm are recommended; In addition, an omentectomy and lymph node dissection should be conducted. • more than 15 resected lymph nodes are required for adequate staging purposes and quality of care. • Standard operation – radical subtotal gastrectomy • Reconstruction with a Billroth I gastroduodenostomy is the reconstruction of choice because it preserves natural enteric flow. • Loop gastrojejunostomy (Billroth II) is an alternative reconstruction that is performed frequently.
  • 25. • Siewert III – total gastrectomy + Roux-en-Y esophagojejunostomy • Proximal subtotal gastric resection with esophagogastric anastomosis can be done but has poor outcome. • Due to distal denervated gastric segment, Pyloroplasty if done guarantees bile esophagitis and if pylorus is left intact gastric emptying may be problematic.
  • 26. PROPHYLACTIC GASTRECTOMY • Overall, 1% to 3% of gastric cancers are hereditary in nature, with the most common type being hereditary diffuse gastric cancer. This is characterized by an autosomal dominant inheritance pattern and diffuse signet ring cells due to a germline mutation in CDH1 (E-cadherin). • Guidelines for screening include: 1. a known mutation in a gastric cancer susceptibility gene within the family, 2. gastric cancer in one family member before age 40, 3. gastric cancer in two first-degree or second-degree relatives with at least one case diagnosed before age 50, 4. gastric cancer in three or more first-degree or second degree relatives regardless of the age of onset, 5. gastric cancer and breast cancer in one patient with one diagnosis before age 50, or 6. gastric cancer in one patient and breast cancer in onefirst-degree or second- degree relative with one diagnosis before age 50.
  • 27. • Once the mutation has been diagnosed, prophylactic gastrectomy is recommended for asymptomatic carriers between the ages of 18 and 40. Annual surveillance endoscopy with biopsy should be performed for those patients who elect not to undergo prophylactic gastrectomy,
  • 28. Postgastrectomy Syndromes DUMPING SYNDROME • DS is a constellation of GI and vasomotor symptoms, which present postprandially due to rapid gastric emptying. It is caused by loss of pyloric regulation of gastric emptying and/or decreased gastric compliance. • Early dumping – 20 to 30 mins after meals, is attributable to bowel distention, relative hypovolemia, GI hormone hypersecretion, and autonomic dysregulation. • has more GI and less CVS effects. Systemic manifestations include palpitations, tachycardia, fatigue, a need to lie down following meals, flushing or pallor, diaphoresis, possibly syncope. Abdominal symptoms include early satiety, epigastric fullness or pain, diarrhea, nausea, cramps, bloating, and borborygmi • Dumping symptoms are triggered by rapid gastric emptying of hyperosmolar voluminous chyme that causes bowel distention, hypermotility, and splanchnic blood pooling.
  • 29. • Late dumping occur 2 to 3 hours postprandially. Due to rapid gastric emptying related specifically to carbohydrates. • Symptoms of late dumping consist of perspiration, faintness, decreased concentration, and altered levels of consciousness. Late dumping involves a reactive hypoglycemia brought on by the rapid and high initial glucose load presented to and absorbed by the small intestine, leading to a GLP-1–mediated inappropriately high insulin response and hypoglycemia • Medical treatment – dietary modification and octreotide. • Surgery – Roux-en-Y GJ associated with delayed gastric emptying is employed I dumping syndrome.
  • 30. POSTVAGOTOMY DIARRHEA • Truncal vagotomy is associated with clinically significant diarrhea in 5% to 10% of patients. It occurs soon after surgery and usually is not associated with other GI or systemic symptoms, a fact that helps to distinguish it from dumping. • The symptoms tend to improve over the months and years after the index operation. • Some patients respond to cholestyramine while others to codeine or loperamide.
  • 31. • The operation of choice is probably a 10-cm reversed jejunal interposition placed in continuity 100 cm distal to the ligament of Treitz • Another option is the onlay antiperistaltic distal ileal graft. • Both operations can cause obstructive symptoms and/or bacterial overgrowth.
  • 32. GASTRIC STASIS • Chronic gastric stasis following gastric surgery may be due to a problem with gastric motor function or be caused by an obstruction. • presents with vomiting (often of undigested food), bloating, epigastric pain, and weight loss. Symptoms are usually improved by a liquid diet and always improved by prolonged fasting. • Obstruction may be mechanical (e.g., anastomotic stricture, efferent limb kink from adhesions or constricting mesocolon, or a proximal small-bowel obstruction) or functional (e.g., retrograde peristalsis in a Roux limb). • The evaluation includes esophagogastroduodenoscopy (EGD), upper GI series, gastric emptying scan (scintigraphy), and gastric motor testing. Endoscopy shows gastritis and retained food or bezoar in the stomach. • Management consists of dietary modification and promotility agents. One of several gastrokinetic agents, such as metoclopramide, domperidone, and erythromycin, will generally prove efficacious in a given patient.
  • 33. • Gastroparesis following vagotomy and drainage procedures may be treated with subtotal (75%) gastrectomy. • Billroth II anastomosis with Braun enteroenterostomy
  • 34. AFFERENT LOOP OBSTRUCTION The etiologies of afferent loop obstruction include: (1) entrapment, compression, and kinking of the afferent loop by postoperative adhesions; (2) internal herniation, volvulus, and intussusception of the afferent loop; (3) scarring due to marginal ulceration of the GJ; (4) locoregional recurrence of cancer (lymph nodes, peritoneum, gastric remnant, anastomotic sites); (5) radiation enteritis of the afferent loop; and (6) enteroliths, bezoars, and foreign bodies impacted in the afferent loop.
  • 35. • The classic presentation of chronic afferent loop syndrome is postprandial abdominal pain relieved by bilious vomiting, • A meal elicits pancreatic, biliary, and duodenal secretion into the obstructed afferent limb. As the volume of these secretions increases, the obstructed duodenum and proximal jejunum become more distended. Eventually the pressure in the partially obstructed afferent limb overcomes . • the obstruction (usually 30 to 60 minutes postprandially), delivering a large volume of bilious secretions into the stomach or Roux limb. This leads to bilious vomiting and prompt relief of the pain, which was caused by the afferent limb distention.
  • 36. • . • If the obstruction is high grade or complete, the distended afferent loop may not sufficiently decompress. In this scenario, vomiting, if present, will be nonbilious, and a clinical picture of “closed loop obstruction” manifested as an acute abdomen will result. If this condition is not recognized early, the afferent loop may actually perforate and result in peritonitis. • The operations most commonly associated with afferent loop obstruction are Billroth II • At operation the primary cause of afferent loop obstruction should be confirmed and treated. This may include resection for tumor or marginal ulcer, lysis of adhesions, or repair of internal hernia.
  • 37. • Procedures to consider include addition of a Braun anastomosis in a former Billroth II reconstruction, • excision of the redundant loop and conversion of Billroth II to Roux-en-Y GJ or bilroth I • excision of the redundant loop and reconstruction of the former Roux-en-Y jejunojejunostomy
  • 38. ALKALINE (BILE) REFLUX GASTRITIS • presumably caused by the longstanding presence of an abnormal amount of duodenal content in the stomach or gastric remnant. • Histologic bile gastritis is more common after Billroth II (40% to 85%) than Billroth I anastomosis (29% to 48%) or gastric drainage operations (pyloroplasty or loop GJ, 15%).Rarely cholecystectomy is associated with the clinical syndrome,possibly due to the loss of bile reservoir function, resulting in a continuous flow of bile into the duodenum with the potential for duodenogastric reflux in the setting of pyloric dysfunction. • The most common symptoms attributed to chronic bile gastritis are abdominal pain and bilious vomiting. • The pain is midepigastric burning abdominal pain, often associated with nausea, and characteristically unrelieved by antacids or acid suppressive medication. Unlike afferent limb syndrome, the pain does not resolve after vomiting. Weight loss and anemia are common.
  • 39. • The diagnosis of alkaline reflux gastritis is essentially a diagnosis of exclusion. • The first step in patient evaluation is endoscopy. • Mucosal biopsies will show the characteristic histologic features of reflux: foveolar hyperplasia, glandular cystic degeneration, edema of the lamina propria, and vasocongestion of the mucosal capillaries, all in association with minimal inflammatory cell infiltration. • Medical management has limited success in relieving symptoms. • Roux-en-Y GJ is the surgical reconstruction most frequently chosen. • Conversion to Roux-en- Y GJ with a 60-cm Roux limb reliably diverts intestinal contents from the gastric remnant and improves symptoms (endoscopic findings also)
  • 40. • The Henley procedure is an infrequently used technique for the management of alkaline reflux gastritis. Gastrojejunoduodenostomy (i.e., isoperistaltic jejunal interposition between the gastric remnant and the duodenum ). The jejunal segment should be approximately 40 cm in length to minimize enterogastric reflux.
  • 41. • The biliary diversion and the suprapapillary duodenojejunostomy — the so-called duodenal switch. • Biliary diversion achieves complete elimination of bile salts from the gastric/duodenal lumen by the choledochojejunostomy, and therefore symptoms associated with enterogastric reflux are alleviated.
  • 42. ROUX STASIS SYNDROME • After distal gastrectomy with Roux-en-Y reconstruction, subset of patients experience symptomatic delayed gastric emptying of solids. This phenomenon has been termed the Roux syndrome or Roux stasis syndrome because it has generally been attributed to measurable abnormalities in Roux limb motility. Peristalsis is abnormal in a Roux limb, with a significant number of propulsive contractile waves proceeding in the proximal direction (i.e., toward the stomach). • Roux syndrome is more common in the presence of a large gastric remnant or after vagotomy. • Symptoms of Roux syndrome include abdominal pain and distention, postprandial bloating, nausea, and vomiting. Typically the vomitus contains solid food and is nonbilious. Bacterial overgrowth, with diarrhea and nutrient malabsorption, may result. • Most patients with the Roux syndrome can be successfully managed conservatively with dietary manipulations and use of prokinetic agents.
  • 43. • In general, if the original gastrectomy removed less than half the stomach, consideration can be given to subtotal gastrectomy with anastomosis to a new Roux limb (usually the original Roux should be resected), or with B2 reconstruction and Braun enteroenterostomy. • However, bile reflux gastritis and esophagitis remain a risk with the latter procedure. Although the addition of a “TA” staple line in the afferent limb distal to the Braun anastomosis and proximal to the B2 GJ preserves normal small bowel motility in the efferent limb and eliminates bile from the stomach
  • 44. MARGINAL ULCERS • Marginal ulceration (i.e., juxtaanastomotic ulceration) is a well-described complication of GJ • It is more common after Roux- en-Y anastomosis than after Billroth II because the former arrangement lacks the buffering afferent limb contents that counteract the noxious effect of gastric acid on the jejunal mucosa (usually the ulceration is on the jejunal side of the anastomosis).
  • 45. • Chronic ischemia and permanent suture material may also be contributing factors. • NSAIDs (including aspirin) and smoking predispose to marginal ulcer. Incomplete vagotomy, Helicobacter infection, and hypergastrinemia must • also be considered. • Presentation may be acute (usually perforation) or chronic. Symptoms include abdominal pain, vomiting, and various signs and symptoms of chronic or acute blood loss. • In most cases, marginal ulcers can be adequately treated with PPIs, the elimination of NSAIDs, Helicobacter treatment, and smoking cessation.
  • 46. GALLSTONES • Following gastrectomy for cancer, 25% of patients will develop cholelithiasis within 2 years and 6% will ultimately undergo cholecystectomy for symptoms. • It is more likely to occur after radical gastrectomy (30%) than after simple gastrectomy (5%). • Denervation of the gallbladder can occur through truncal vagotomy or selective division of the hepatic branches of the left vagus. Also, nodal dissection can lead to transection of the nerves controlling gallbladder motility. This may explain the higher risk and earlier occurrence of gallstone formation after total gastrectomy than after distal gastrectomy and after extended lymphadenectomy compared to more limited perigastric lymphadenectomy. • Other factors that affect gallstone formation include changes in the secretions of gut hormones, including cholecystokinin (CCK). • The exclusion of food passage through the duodenum after Roux-en-Y reconstruction results in decreased secretion of CCK with a resultant decrease in gallbladder motility, which explains the higher incidence of stone formation when Roux-en-Y reconstruction is performed.
  • 47. • Other contributing factors include weight loss, leading to mobilization of cholesterol stores and supersaturation of biliary cholesterol, and the presence of edema or inflammation around the bile ducts with resultant biliary stasis. NUTRITIONAL ABNORMALITIES • Weight loss • Anemia-This is generally secondary to nutrient malabsorption but can also be by decreased nutrient intake or chronic blood loss due to ulcer, tumor, or mucosal inflammation. Iron, vitamin B12, and folate deficiencies are the most common cause of chronic nutritional anemia after gastric surgery. Iron absorption takes place primarily in the duodenum and proximal jejunum and is facilitated by an acidic environment in the stomach. Intrinsic factor, essential for the enteric absorption of vitamin B12, is made by the parietal cells of the stomach • CHRONIC CALCIUM DEFICIT AND OSTEOPOROSIS-Calcium absorption occurs primarily in the duodenum, so any gastric operation that diverts the food stream away from the duodenum will disturb calcium homeostasis.