CHAPTER 8 Gastrectomy
Case Study
Repeat endoscopy shows a nonhealing ulcer. Biopsy of the rim of the ulcer reveals adenocarcinoma.
BACKGROUND
The stomach may be divided into four anatomic regions: the cardia, fundus, body, and antrum. The stomach derives its blood supply from four main arterial trunks: the right and left gastric arteries along the lesser curvature and the right and left gastroepiploic arteries along the greater curvature. Additional blood supply is provided by the short gastric arteries (Fig. 8-1). Given this extensive collateral vascular network, the stomach may remain viable after ligation of multiple main feeding vessels. Venous and lymphatic drainage, in general, follows the arterial supply.
INDICATIONS FOR GASTRECTOMY
I. Adenocarcinoma: Adenocarcinoma accounts for 95% of gastric malignancies and is the 14th most common cancer and the 8th leading cause of cancer-related death in the United States.
A. Gastric adenocarcinoma typically presents with nonspecific symptoms, and the diagnosis may be delayed until the disease is relatively advanced. In the absence of metastatic disease, surgical resection is indicated. Gastric adenocarcinoma frequently spreads intramurally, and the extent of disease may be masked by normal-appearing gastric mucosa; thus, resection should include 6-cm margins. Because of the high morbidity rate associated with proximal partial gastric resections, proximal tumors and midbody tumors are usually treated with total or near-total gastrectomy. In patients with distal lesions, subtotal gastrectomy is an acceptable alternative approach if appropriate margins can be obtained; otherwise, total gastrectomy is required.
B. The role of extended lymphadenectomy for gastric adenocarcinoma is controversial. A D1 dissection includes removal of perigastric nodes only; a D2 dissection includes removal of regional lymph nodes along the celiac axis (left gastric, common hepatic, and splenic arteries). A D3 dissection includes removal of additional regional nodes within the porta hepatis and next to the aorta. Numerous prospective randomized clinical trials have failed to demonstrate an improvement in 5-year survival rates with more extensive dissections. In the United States, most surgeons advocate a limited (D1 or D2) nodal dissection, harvesting at least 15 nodes for pathologic evaluation. Although once routinely performed during resection for gastric cancer, splenectomy is associated with higher perioperative morbidity and mortality rates and is no longer recommended unless there is direct invasion of the spleen or splenic hilum.
II. Other Gastric Malignancies
A. Gastric lymphoma is the second most common malignancy of the stomach. Treatment regimens vary; however, most gastric lymphomas are initially treated with chemoradiation therapy. Mucosal-associated lymphatic tissue tumors are low-grade lymphomas and are associated with Helicobacter pylori infection. Treatment aimed at eradication of the bacteria often results in tumor regression. Surgical resection of lymphomas is reserved for tumors refractory to other therapies and cases with complications, including perforation and bleeding. If indicated, the goal of resection is to obtain circumferential negative margins.
B. Gastrointestinal stromal tumors (GISTs) are mesenchymal tumors. GISTs may arise throughout the gastrointestinal (GI) tract, although the stomach is the most common site. Surgical resection with wide negative margins remains the primary treatment modality; however, encouraging results have been achieved with imatinib (Gleevec), a tyrosine kinase inhibitor, for the treatment of metastases and as an adjuvant to resection for high-risk tumors (as defined by necrosis, mitosis, and size).
C. Gastric carcinoids are rare and account for only 0.5% of all gastric tumors. Multiple gastric carcinoid tumors may be associated with enterochromaffin-like cell hyperplasia, chronic atrophic gastritis, and pernicious anemia, and have a low risk of malignancy. Solitary gastric carcinoid tumors have higher malignant potential. Resection is the mainstay of treatment.
III. Peptic Ulcer Disease: PUD results from an imbalance between physiologic acid secretion and mucosal defense mechanisms and causes erosion of either the gastric or the duodenal wall. Advances in our understanding of the pathophysiology of PUD (specifically, the implications of H. pylori infection of the gastric mucosa) as well as the development of proton pump inhibitors for the management of acid hypersecretion have made elective surgery for the treatment of PUD uncommon. Initial treatment of PUD includes lifestyle modification (e.g., avoidance of tobacco, alcohol, and nonsteroidal anti-inflammatory drugs) and a pharmacologic regimen that includes an H2 receptor antagonist or proton pump inhibitor and antibiotic therapy for H. pylori infection.
A. Indications for surgery include emergent complications of PUD (e.g., obstruction and perforation) and bleeding refractory to endoscopic intervention. Rarely, failure of medical therapy and concern about malignancy constitute additional indications. The location of the ulcer dictates the surgical approach. The modified Johnson classification categorizes gastric ulcers according to their location. Acid hypersecretion is believed to play a role in types II and III ulcers only (Table 8-1 and Fig. 8-2). Surgical therapy for these types of ulcers is therefore aimed not only at resection of the ulcer, but also at acid reduction. Treatment of types I and IV gastric ulcers, on the other hand, involves resection of the ulcer only (Fig. 8-3).
B. Patients with free perforation or hemorrhage are often systemically ill and hemodynamically unstable. A focused surgical approach is appropriate in such settings; perforated ulcers are typically patched with omentum (i.e., Graham patch) and bleeding vessels are oversewn. In the stable patient, optimal treatment for a bleeding or perforated gastric ulcer includes resection (distal gastrectomy or antrectomy). Proximal ulcers are treated with wedge resection.
| Johnson Classification | Location | Acid Hypersecretion |
|---|---|---|
| Type I | Lesser curve | No |
| Type II | Lesser curve and duodenum | Yes |
| Type III | Prepyloric | Yes |
| Type IV | Proximal lesser curve near gastroesophageal junction | No |
PREOPERATIVE EVALUATION
I. Laboratory testing should include a complete blood count, blood chemistry, liver function tests, coagulation studies, and blood type and screen in anticipation of surgical blood loss. Patients are often anemic as a result of chronic blood loss within the GI tract. Elevated liver function tests may reflect the presence of hepatic metastases.
II. Esophagogastroduodenoscopy is required for the diagnosis and localization of gastric malignancies and PUD. Endoscopic ultrasound can be used to assess depth of tumor invasion and nodal involvement.
III. Barium swallow may provide additional information about the size and location of a gastric lesion. It is especially useful in the evaluation of large tumors that preclude passage of an endoscope.
IV. Computed tomography (CT) of the abdomen and pelvis may identify visceral metastases or malignant ascites, either of which render the disease unresectable. CT is sensitive in detecting liver metastases larger than 5 mm, but may miss smaller lesions. Additionally, CT does not reliably detect peritoneal metastases and is inferior to endoscopic ultrasound in assessing nodal disease.
COMPONENTS OF THE OPERATION AND APPLIED ANATOMY
Total gastrectomy is described below. Unique features of partial resections (Fig. 8-4), including reconstructive options, are discussed in the subsequent section on additional operative considerations.
Figure 8-4 The levels of transection of the stomach for total, subtotal, or distal gastrectomy.
(From Khatri VP, Asensio JA: Operative Surgery Manual. Philadelphia, Saunders, 2003.)
Patient Positioning and Preparation
Preoperative Considerations
Exposure and Dissection: Total Gastrectomy
I. After the abdomen is entered, the greater omentum is retracted upward and dissected away from the transverse colon to enter the lesser sac (Fig. 8-5).
II. The left gastroepiploic vessels are ligated along the greater curve of the stomach, and the short gastric arteries are ligated within the gastrosplenic ligament (Fig. 8-6).
III. The stomach is retracted cephalad, exposing the aorta and celiac trunk. The celiac lymph tissue is dissected up toward the stomach, starting at the superior border of the pancreas.
IV. The left gastric artery is identified and is ligated near its origin from the celiac trunk (Fig. 8-7).
V. The pylorus is mobilized, and branches of the right gastroepiploic vessels are identified inferiorly and ligated. Similarly, the right gastric artery is identified as it courses superior to the pylorus and is divided (Fig. 8-8).
VI. The duodenum is mobilized by sharply dissecting its lateral retroperitoneal and posterior pancreatic attachments.
VII. The first portion of the duodenum is divided approximately 2 to 3 cm distal to the pylorus using a thoracoabdominal stapler, leaving a closed duodenal stump.
VIII. The gastrohepatic ligament is divided near the liver, and the left hepatic lobe is retracted laterally, exposing the esophagus.
Reconstruction: Roux-en-Y Anastomosis
II. After an appropriate jejunal transection point is identified, an opening in the mesentery is created immediately adjacent to the bowel. A gastrointestinal anastomosis surgical stapler is placed around the bowel, with the lower jaw inserted through the mesenteric opening. The stapler is fired, leaving two closed ends of transected bowel.
III. The distal end of transected jejunum is brought up to the esophagus. The jejunal limb can be placed in an antecolic (i.e., in front of the transverse colon) or retrocolic (i.e., behind the transverse colon through a defect in the mesocolon) position.
IV. An end-to-side anastomosis between the esophagus and the distal segment of jejunum is performed.
Additional Operative Considerations
I. Partial Gastrectomy: Partial gastrectomy may be indicated for the treatment of distal tumors or benign gastric ulcer disease. The initial dissection required for a subtotal gastrectomy is similar to that described for total gastrectomy. Of note, during partial gastrectomy, only the most distal short gastric arteries are ligated because the proximal short gastric vessels serve as the blood supply to the gastric remnant.
II. Reconstruction: After total gastrectomy, GI continuity is most often re-established with a Roux-en-Y esophagojejunostomy (as described in the previous section). After partial gastrectomy, however, multiple reconstructive options exist. A Billroth I reconstruction involves anastomosis of the distal stomach to the proximal divided duodenum (Fig. 8-10). An alternative is a Billroth II reconstruction, in which a loop of jejunum is mobilized and anastomosed to the gastric remnant (Fig. 8-11).
III. Vagotomy: In patients undergoing a gastric resection for refractory type II or III gastric ulcers, a truncal vagotomy may be performed to reduce acid secretion. This procedure involves the ligation of the left and right vagus nerves above the take-off of the hepatic and celiac branches just proximal to the gastroesophageal junction (Fig. 8-12A). Selective vagotomy, which preserves the hepatic and celiac branches of the vagal nerves (Fig. 8-12B), has few advantages over standard truncal vagotomy and is rarely performed. Both of these approaches may compromise gastric emptying and are typically performed in combination with a distal gastrectomy or pyloroplasty. Highly selective vagotomy, or parietal cell vagotomy, involves the selective ligation of only those vagal branches supplying the parietal, acid-producing cells; because innervation to the antrum and pylorus is preserved, this procedure has less effect on gastric emptying than does truncal vagotomy. When performed with a distal gastrectomy or antrectomy, the highly selective approach has little advantage over truncal vagotomy (Fig. 8-12C).
IV. Splenectomy: Clinical trials have shown a significant increase in perioperative morbidity when splenectomy is performed with gastrectomy for malignancy. The spleen should be removed only if there is evidence of direct tumor invasion of the splenic hilum or parenchyma.
V. Frozen Sections: The diffuse intramural growth pattern of gastric adenocarcinoma makes it difficult to assess resection margins clinically. Intraoperative frozen sections are routinely obtained to ensure negative margins.
VI. Enteral Access: Many surgeons advocate routine insertion of a tube jejunostomy after total gastrectomy to facilitate the administration of postoperative nutritional support.
VII. Drainage: Placement of a closed-suction drain in the resection bed may facilitate surveillance for an anastomotic leak in the postoperative period and is advocated by some surgeons.
Figure 8-10 Partial gastrectomy with Billroth I reconstruction.
(From Dempsey D, Pathak A: Antrectomy. Op Tech Gen Surg 5:86–100, 2003.)
EARLY COMPLICATIONS
I. Anastomotic Leak: A leak may develop at any newly constructed anastamoses or from the divided duodenal stump. Leaks usually present between the fifth and seventh postoperative days and may be heralded by fever, abdominal pain, leukocytosis, and enteric or bilous drainage. An upper GI contrast study or CT scan may be used to confirm the diagnosis. Duodenal stump leaks generally require prompt re-exploration. Anastomotic leaks may sometimes be managed with bowel rest, intravenous antibiotics, and observation, assuming that the patient is stable without signs of peritonitis. If a fluid collection is present, percutaneous drainage is indicated. Clinical deterioration after nonoperative management of an anastomotic leak mandates surgical exploration.
II. Hemorrhage: Postoperative bleeding may be extraluminal or intraluminal. intraluminal bleeding can present with upper (hematemesis) or lower (hematochezia) GI bleeding. Endoscopy can be used to both diagnose and treat anastomotic bleeding. Rarely, reoperation is required to control postoperative hemorrhage.
III. Obstruction: Afferent limb obstruction refers to obstruction of the bowel proximal to the gastrojejunostomy after a Billroth II anastomosis and classically presents with pain and bilious emesis (Fig. 8-13). Initial treatment typically involves endoscopic decompression and placement of an NGT. The majority of these obstructions are functional in etiology. Mechanical obstruction or refractory functional obstruction requires reoperation. The latter may be treated with conversion of the Billroth II reconstruction to a Roux-en-Y anastomosis. Gastric outlet obstruction after distal gastrectomy is typically functional in nature and resolves with temporary nasogastric decompression and promotility agents.
LATE COMPLICATIONS
I. Dumping syndrome refers to a constellation of symptoms (fatigue, lightheadedness, flushing, diaphoresis) followed by cramping and diarrhea that occur after eating a meal. “Early” dumping syndrome occurs approximately 30 minutes after eating and is caused by dysregulation of GI hormone secretion. Treatment involves dietary modification (avoidance of hyperosmolar liquids and fiber supplementation) and octreotide. “Late” dumping occurs approximately 2 hours after a meal and is caused by hyperinsulinemia that results in hypoglycemia. Administration of sugar is generally sufficient treatment.
II. Bile reflux gastritis occurs after a partial gastrectomy with Billroth I or II reconstruction. Patients may present with pain, nausea, and bilious emesis. Severely symptomatic patients may require reoperation and conversion of the Billroth I or II reconstruction to a Roux-en-Y gastrojejunal reconstruction.
III. Metabolic abnormalities may result from gastric resection. Resection of the proximal stomach and parietal cell mass results in decreased intrinsic factor secretion and vitamin B12 deficiency; this may manifest with megaloblastic anemia. The achlorhydria associated with partial gastrectomy may also result in bacterial overgrowth, malabsorption of nutrients and vitamins, and diarrhea. After Billroth II reconstruction in particular, inadequate mixing of digestive enzymes, and ingested fats may lead to fat and calcium malabsorption, steatorrhea, and osteopenia.
