Stomach

High Yield Anatomy

• What are the types of hiatal hernias?
• Type 1 (> 90%) - sliding
• Type 2 - purely paraesophageal (needs repair)
• Type 3 - combined sliding and paraesophageal (needs repair)
• Type 4 - entire stomach in the chest plus another organ, most commonly colon (needs repair)

• What are the types of gastric ulcers? Table 1 - Types of gastric ulcers

• What is the Siewert-Stein Classification of esophago-gastric junction (EGJ) tumors
• Type I — distal part of the esophagus (located between 1-5 cm above the anatomic EGJ)
• Type II — cardia (within 1 cm above and 2 cm below the EGJ)
• Type III — subcardial stomach (2-5 cm below EGJ) Figure 1 - Vascular anatomy of the stomach

Gastric Volvulus

• What are the features?
• Often associated with paraesophageal hernias
• High morbidity and mortality
• What are the three types?
• Organoaxial (most common) — rotation along the axis of the stomach from the GE junction to the pylorus
• Mesoaxial (less common) — rotation along short axis of stomach bisecting the lesser and greater curvature
• Combined
• How are these treated?
• Typically with emergent surgery → hernia repair, gastropexy, partial gastrectomy if devitalized
• Endoscopic decompression can be attempted in frail (risk of perforation) with double PEG tubes Gastroesophageal reflux disease (GERD)
• What are the alarm symptoms?
• Dysphagia, odynophagia, weight loss, anemia, GI bleeding
• Concern for malignancy → upper endoscopy
• How is GERD medically managed?
• Lifestyle modification: weight loss, elevate head of bed, avoid aggravating foods
• Proton pump inhibitors (PPI)
• If no improvement over several weeks on PPI → need EGD
• What are the indications for surgical evaluation?
• Failure of medical management
• Desire to avoid lifelong PPI
• Extra-esophageal manifestations - asthma, hoarseness, cough, chest pain, aspiration

If atypical symptoms and GI surgical history, think bile reflux. Work up with impedance probe and management is usually Roux-en-Y reconstruction.

• What is the pre-operative work up?
• Barium swallow
• Upper endoscopy
• Ambulatory pH testing
• Esophageal manometry to rule out underlying motility disorder (can’t do full Nissen if dysmotility)
• What are the components of 24-hour esophageal pH monitoring?
• Percent total time pH < 4
• Percent upright time pH < 4
• Percent supine time pH < 4
• Number of reflux episodes
• Number of reflux episodes ≥ 5 min
• Longest reflux episode (minutes)
• Demeester score > 14.72 = reflux
• Operative management
• What are the overall surgical goals?
• Restoration of normal anatomic position of the stomach and GE junction
• Recreation of anti-reflux valve
• Any hiatal hernia must be completely reduced → requires mediastinal dissection to ensure adequate esophageal mobilization
• Any defect in diaphragmatic crura must be adequately closed
• Complete mobilization of the fundus

• 2 cm long “floppy” fundoplication performed over large (54F) bougie

• Partial fundoplication/alternates to 360° Nissen
• Dor (anterior 180-200°)
• Toupet (posterior 270°)
• Thal (270° anterior)
• Belsey (270° anterior transthoracic)
• Lind (300° posterior)
• Hill repair
• Insufficient evidence to support one over another. Some data shows less postop dysphagia with partial wrap compared to 360° wraps, however, may have inadequate control of reflux.
• In the OR, anesthesia is having trouble ventilating patient . What are you worried about?
• Capnothorax
• Enlarge tear to avoid tension capnothorax
• Place red rubber catheter with one end into pleural tear and other end into abdomen (equalizes pressures)
• At end of procedure bring one end outside of abdomen and place to water seal while Valsalva administered
• Can also needle decompress intra-operatively - be sure to prep lower chest High end tidal CO2 during mediastinal dissection is most likely capnothorax. May also be hypoventilation, CO2 embolus, or malignant hyperthermia.
• What if the post op CXR shows a 2 cm pneumothorax?
• Don’t do anything, will self-resolve
• How do you manage these patients postoperatively?
• Schedule anti-emetics immediately postop (avoid nausea/retching)
• Soft diet for a few weeks

• Avoid meat, raw vegetables, bread, carbonated beverages for 4-6 weeks

• What is the management of postop dysphagia?
• Very common
• Severe dysphagia → esophagram
• Dysphagia persisting past 6 weeks postop → esophagram (concern for recurrent hernia, slipped wrap) → if not present, dilation Hiatal Hernia
• How are these diagnosed?
• Often seen on CXR
• Barium swallow, CT chest, and EGD and are used in various combinations depending on individual patient presentation .
• What is the management?
• Repair of type I in the absence of reflux disease is not indicated → same operative indications as for GERD
• All symptomatic paraesophageal hernias (types 2-4) should be repaired, especially those with obstructive symptoms or those that have volvulized Type I = sliding, Type II = paraesophageal, Type III - both, Type IV = another organ
• Asymptomatic paraesophageal hernias should be repaired on a routine, elective basis if the patient is a good surgical candidate
• Watchful waiting is an option for asymptomatic or minimally symptomatic patients who are poor surgical candidates
• Laparoscopic repair is the preferred approach, although may also be repaired via open or trans-thoracic approach
• Hernia sac needs to be mobilized and excised (key step that decreases early recurrence)
• Use of mesh in large (> 5-8 cm) hiatal hernia decreases short-term recurrence . However, many questions remain regarding the long-term safety.

Currently, insufficient evidence to recommend one way or the other regarding routine use of mesh reinforcement, but probably reasonable with large defects .

• Permanent suture to close crura
• Fundoplication should be performed at time of repair (same principles as when done for GERD regarding mediastinal mobilization and length of intra- abdominal esophagus needed) → Collis gastroplasty (esophageal lengthening)
• Gastropexy or gastrostomy tube may be added if needed if not bad enough to need extra length Gastroduodenal Ulcer Disease
• What is the association with H . pylori?
• H . pylori is found in 75% of gastric ulcer disease and 95% of duodenal ulcer patients
• What is the treatment?
• Triple therapy
• PPI
• Clarithromycin
• Amoxicillin or metronidazole
• Gastroduodenal Ulcers
• What are the management principles for bleeding gastric and duodenal ulcers?
• First step is typical resuscitative measures and early endoscopy, NG tube placement
• Rapid upper endoscopy is usually diagnostic and therapeutic
• Endoscopic clips, thermal coagulation, injection of vasoactive or sclerosing agent

• Endoscopic interventions are 90% effective for controlling initial bleeding

• What is the risk of rebleeding?
• Actively bleeding pulsatile vessel — up to 80%
• Visible vessel — up to 50%
• Adherent clot — 15-25%
• Clean base — <5%
• Gastric Ulcer
• What is important in treating gastric ulcers?
• Biopsy ulcer to evaluate for malignancy as well as obtain antral biopsies to test for H . pylori .
• MC cause of gastric bleeding = H . pylori and NSAIDs
• Underlying malignancy present in approximately 5% of gastric ulcers
• What do you do if patient rebleeds after 1st endoscopic intervention?
• Repeat endoscopy (angiography also an option)
• Once bleeding is controlled, etiology has to be identified and treated
• Stop NSAIDS, tobacco cessation, PPI, H . Pylori treatment, etc .
• When do you operate?
• For bleeding that cannot be controlled endoscopically or hemorrhagic shock → midline laparotomy, anterior gastrotomy, oversew bleeding area, biopsy, and close gastrotomy
• Duodenal Ulcer
• What is the management of a bleeding duodenal ulcer?

• Initial management same as any upper GI bleed → resuscitate, NG tube, rapid EGD for diagnosis/ treatment

• Endoscopy is 1st and 2nd line (like gastric ulcers) → possibly angiography → surgery reserved for uncontrolled bleeding with above and hemodynamic instability
• What operation?
• Longitudinal anterior duodenotomy, control bleeding with sutures placed superior and inferior to ulcer taking care to avoid CBD (can ligate GDA above duodenum if bleeding continues) → approximate ulcer crater → close duodenotomy transversely
• How do you treat perforated ulcers?
• Initiate fluid resuscitation, NG decompression, acid suppression, and antibiotics for empiric coverage of gram-negative rods, oral flora, anaerobes, and fungus (e .g . ampicillin, ceftriaxone, metronidazole, fluconazole)
• Omental patch repair
• May be performed open or laparoscopically
• Close perforation with seromuscular bite if able to approximate and then secure tongue of omentum over site of perforation with 3-4 sutures A small amount of free air and stable patient may have a contained perforation that does not require OR. However, not a common exam scenario.
• If patient undergoing operation for complication of gastroduodenal ulcer disease and has hx of treatment with PPI and/or eradication of h . pylori (i .e . refractory ulcer disease), what else should you consider?
• Acid reducing procedure
• Truncal vagotomy and pyloroplasty

• Highly selective vagotomy (HSV) - Preserves motor innervation to pylorus, eliminating need for drainage procedure

• Vagotomy and antrectomy — Higher morbidity (2/2 need for Bilroth reconstruction) than vagotomy and pyloroplasty or HSV, therefore, reserved for stable patients with anatomic indications (large antral ulcers, pyloric scarring) Marginal ulcer after bariatric surgery perforation treated the same as duodenal ulcer. Gastric Cancer
• What are the risk factors?
• H . pylori, smoking, heavy ETOH intake, high salt, nitrates
• Typically classified as intestinal type or diffuse type (Lauren Classification)
• Most are sporadic, 5-10% familial component, 3-5% inherited syndrome
• Hereditary diffuse gastric cancer
• Autosomal dominant disorder 2/2 germline mutation in CDH1
• How do you treat these patients?
• Prophylactic gastrectomy recommended between age 18-40 for CDH1 carriers
• Women with CDH1 are at increased risk of breast CA similar to BRCA patients
• What are other hereditary syndromes with increased risk of gastric CA?
• Lynch syndrome (DNA mismatch genes)
• Juvenile polyposis syndrome (SMAD4)
• Peutz-Jehgers Syndrome
• Familial adenomatous polyposis (APC gene on 5q21)
• How do you stage these?

• Routine labs, CT chest/abdomen/pelvis, EUS with FNA, PET/CT

• What is the role of staging laparoscopy?
• NCCN recommends laparoscopic staging with peritoneal washing for clinical stage > T1b tumors if chemoradiation or surgery being considered (not needed if known metastasis and undergoing definitive chemoradiation or palliative options)
• Staging Pearls —
• T stage
• T1
• T1a invades lamina propria or muscularis mucosa
• T1b invades submucosa
• T2 invades muscularis propria
• T3 invades subserosa
• T4 invades through serosa or into adjacent structures
• N status
• N1 involves 1-2 nodes
• N2 involves 3-6 nodes
• N3 involves 7 or more nodes
• M1 = distant metastasis Staging similar to esophageal cancer, but esophagus has no serosa.
• What is unresectable disease?
• Peritoneal involvement, distal metastases, root of mesentery involvement or para-aortic nodal disease confirmed by biopsy, encasement of major vascular structure (excluding splenic vessels)
• Who gets neoadjuvant therapy?

• cT2 or higher and any N Similar to esophageal and rectal cancer

• What are the surgical principles?
• Resection with at least 4 cm margins and lymph node harvest of at least 15
• Type of resection (total vs subtotal gastrectomy) and extent of lymph node dissection (D1 vs D2) is somewhat controversial
• Subtotal gastrectomy is preferred for distal lesions (Siewert III)
• Proximal tumors (Siewert II) will generally need total gastrectomy with esophagojejunostomy, distal portion of esophagus may need to be resected for adequate margins
• Tumors crossing GE junction are classified and treated as esophageal cancer
• NO prophylactic splenectomy (only if spleen or hilum grossly involved with tumor)
• T4 tumors require en bloc resection of involved structures
• What are the types of lymph node dissection?
• D1 dissection = removal of N1 nodes (perigastric nodes along greater/lesser curve, stations 1-6)
• D2 dissection = removal of N1 and N2 nodes (nodes along left gastric, common hepatic, celiac and splenic arteries, stations 7-11)
• Gastrectomy with D2 dissection is the standard in Asia, however, Western studies have failed to demonstrate survival benefit of D2 dissection over D1 dissection, and D2 dissection may be associated with increased morbidity/mortality → current NCCN recommendation is for R0 resection with at least D1 or modified D2 lymph node dissection
• R0 = negative microscopic margin
• R1 = negative gross margin, positive microscopic margin

• R2 = positive gross margin

• When is adjuvant therapy recommended?
• Adjuvant 5-fluorouracil for T3, T4, or node positive disease following R0 resection Post Gastrectomy Syndromes
• What is retained antrum syndrome?
• Retained antral tissue within duodenal stump after gastric resection
• G cells bathed in alkaline fluid → continuous gastrin release → acid production in proximal stomach remnant and ulceration Check gastrin levels to rule out a gastrin-secreting tumor.
• Treatment = PPI; vagotomy and resection of retained antrum
• What is dumping syndrome?
• Tachycardia, diaphoresis, dizziness, flushing
• Early dumping syndrome (20-30 min after meal)
• Occurs due to abrupt hyperosmolar load to small intestine
• Late dumping syndrome (1-4 hours after meal)
• Due to rapid carbohydrate load to small intestine resulting in large insulin surge and rebound hypoglycemia
• Majority managed with small meals, no sugary drinks → for refractory dumping syndrome try octreotide
• What is alkaline reflux gastritis?
• After Bilroth I and Bilroth II reconstructions
• Diagnosis = impedance studies
• What is medical management?
• Pro kinetic agents, bile acid binding resins
• What is surgical management?
• Conversion to RNY

At least 50 cm for Roux limb will avoid recurrent bile reflux.

• What is the Braun enterostomy?
• Anastomosis between afferent and efferent limb
• What is afferent limb syndrome?
• Acute or chronic obstruction of afferent jejunal limb following Bilroth II reconstruction
• Increased luminal pressure of afferent limb can result in what symptoms?
• Obstructive jaundice, cholangitis, pancreatitis from back pressure up biliopancreatic system
• Duodenal stump blow out
• Bacterial overgrowth in afferent limb → bacteria deconjugate bile acids → steatorrhea, malnutrition, and vitamin B-12 deficiency leading to megaloblastic anemia .
• Treatment = conversion to Roux-en-Y or Bilroth I; bacterial overgrowth can be managed first with antibiotics (high relapse rate though) If B2 patient presents with bowel obstruction, no NGT and decompression → emergent surgery. Similar to bypass patients with internal hernia.

Figure 2 - Gastric reconstruction options with associated complications Quick Hits

• What do you do if you need more esophageal length during paraesophageal hernia repair?
• Collis gastroplasty
• Unable to swallow secretions after Nissen, what’s the problem and management?
• Wrap too tight, return to OR
• Types of ulcer associated with increased acid output?
• Type II and III
• Types of ulcer associated with decreased mucosal protection?
• Type I and IV
• Hiatal hernia discovered at time of sleeve gastrectomy . What do you do?
• Repair
• Patient with history of antrectomy and Bilroth II reconstruction in distant past presents with intermittent abdominal pain and

distention which is relieved after bilious emesis, megaloblastic anemia on laboratory work up . What is this?

• Afferent limb syndrome
• What is the diagnosis for a patient with multiple duodenal ulcers and gastrin levels >1000 pg/ml?
• Zollinger Ellison syndrome
• Gastric mass with biopsy showing expansion of the marginal zone compartment with development of sheets of neoplastic small lymphoid cells . Diagnosis and treatment?
• Maltoma
• Treatment = antibiotics (triple therapy for H . pylori)
• Will typically regress once H . pylori is eradicated

Figures