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1.Symptoms. Obstruction causes symptoms of crampy abdominal pain, nausea, and vomiting. The stomach is usually markedly dilated. Prolonged vomiting due to obstruction can lead to electrolyte disorders, particularly hypokalemic metabolic alkalosis from the large hydrochloric acid losses.
2.Initial treatment consists of several days of nasogastric suction to allow the stomach to decompress.
3.Surgery. Vagotomy with antrectomy or vagotomy with drainage is the standard procedure.
V Gastritis
A Uncomplicated acute gastritis
1.Etiology. Acute diffuse gastritis can be due to a number of irritating agents, particularly aspirin and ethanol.
2.Hemorrhage can occur and be massive.
3.Treatment. Removal of the inciting agent and antacid therapy usually result in prompt healing.
B
Stress ulceration (acute hemorrhage gastritis) is another form of acute gastritis. Ischemia of the gastric mucosa is the inciting event. The injury is compounded by the effect of the intraluminal acid. Although stress ulceration is common in critically ill patients, only 5% develop significant gastric bleeding.
1.Location. Stress ulcers are characteristically shallow mucosal lesions that start in the fundus. They then spread distally and can involve the entire stomach.
2.Clinical presentation. Affected patients frequently have sepsis, multiple organ system failure, severe trauma, or a complicated postoperative course or are on assisted ventilation. Stress ulceration that occurs in burn patients is known as Curling's ulcer, and stress ulceration occurring in patients with head injury is known as Cushing's ulcer.
3.Treatment
a.Prophylaxis against stress ulceration can be achieved with antacids given as needed to keep the gastric pH above 5. H2-receptor antagonists and proton pump inhibitors are equally effective at maintaining an adequate gastric pH.
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b.Medical treatment involves correcting the underlying problems (e.g., sepsis) and vigorous use of antacids. Cimetidine is not helpful once bleeding has occurred.
c.Surgical treatment is rarely necessary and is associated with a high mortality. In the case of uncontrollable bleeding, near total gastrectomy is usually the best option.
d.Radiographic embolization can be performed to identify the main artery bleeding and stop blood flow.
VI Gastric Cancer
A Gastric tumors
Approximately 90%–95% of gastric tumors are malignant, and of the malignancies, 95% are adenocarcinomas. Other histologic types include squamous cell, carcinoid, gastrointestinal stromal tumor (GIST), and lymphoma.
B Gastric adenocarcinoma
1.The incidence of gastric adenocarcinoma has been decreasing for many years and is now stabilized. Gastric adenocarcinoma is the tenth most common cancer, with an estimated annual incidence of 22,000 cases and 13,000 deaths. The trend is increasing toward lesions more proximally located in the stomach.
2.Risk factors for gastric cancer include:
a.Age >70 years
b.Diet high in salt, smoked foods, low protein, low vitamins A and C
c.H. pylori infection
d.Previous gastric resection
e.Chronic gastritis and pernicious anemia
f.Blood group A
g.Radiation exposure
h.Tobacco use
i.Male gender
j.Low socioeconomic status
k.Adenomatous polyps
3.Symptoms include epigastric pain, anorexia, fatigue, vomiting, and weight loss. Proximal tumors can present with dysphagia, while more distal tumors may present as gastric outlet obstruction. Symptoms tend to occur late in the course of the disease. Physical signs can include palpable supraclavicular (Virchow's) or periumbilical (Sister Mary Joseph's) lymph nodes.
4.Diagnosis is suggested on UGI radiographs and is confirmed by upper endoscopy with biopsy.
5.Preoperative evaluation may include computed tomography (CT) scan to look for local extension, ascites, and distant metastases. Endoscopic ultrasound has been shown to be useful in determining the depth of penetration and in detecting nodal metastases. Staging laparoscopy may detect small peritoneal metastases and is required before most neoadjuvant protocols.
6.Involvement beyond the stomach may include direct spread to adjacent organs (e.g., spleen, diaphragm, omentum, colon); “drop metastases” to the ovary (Krukenberg's tumor) or the pelvis (Blumer's shelf tumor); or distant disease (e.g., to liver, lung).
7.Classification. Gastric carcinoma is classified according to its gross characteristics.
a.Intestinal type is a well-differentiated, glandular tumor found most commonly in the distal stomach.
b.Diffuse type is a poorly differentiated, small cell infiltrating tumor found most commonly in the proximal stomach.
8.Surgical treatment depends on nodal disease and distant metastases.
a.Potentially curable lesions
1.Potentially curable lesions are treated with subtotal or total gastrectomy, depending on tumor location.
2.Wide margins (>6 cm) on the stomach are necessary because extensive submucosal tumor spread can occur. Lesions of the fundus and cardia may require resection of the spleen, pancreas, or transverse colon to completely remove the cancer.
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3.The role of lymphadenectomy is controversial, but for favorable lesions, there is some advantage to removing the local draining nodes. Removal of the omentum and its nodes is included. Radical lymphadenectomy that includes distant nodal basins has not been shown to improve survival and may increase morbidity. It is recommended that a least 15 regional lymph nodes be sampled to ensure adequate staging of the tumor.
b.Palliative resections are indicated in the presence of obstructing or bleeding gastric cancers. Treatment may include resection, bypass alone, or either one in conjunction with endoscopic or radiotherapeutic techniques.
9.Adjuvant chemotherapy (5-fluorouracil/leucovorin and radiation therapy) after potentially curative resection improves median survival and is the current standard of care. Neoadjuvant chemoradiation is being studied in several clinical trials
but remains unproven at this time. Unresectable tumors may show some response to chemotherapy. The addition of radiation therapy may improve results and can control bleeding symptoms.
10.Prognosis depends largely on the depth of invasion of the gastric wall, involvement of regional nodes, and presence of distant metastases but still remains poor. Overall 5-year survival after the diagnosis of gastric cancer is 10%–20%. Tumors not penetrating the serosa and not involving regional nodes are associated with a 5-year survival rate of approximately 70%. This number decreases dramatically if the tumor is through the serosa or into regional nodes. Recurrence rates after gastric resection are high, ranging from 40%–80%. Potentially curative surgical resection does offer a better 5-year prognosis; however, only 40% of patients have potentially curable disease at the time of diagnosis.
C Gastric lymphoma
The stomach is the most common site of primary intestinal lymphoma; however, gastric lymphoma is relatively uncommon, accounting for only 15% of all gastric malignancies and only 2% of lymphomas.
1.Symptoms are usually vague, namely abdominal pain, early satiety, and fatigue. Rarely ever do patients present with constitutional symptoms (i.e. “B” classification of lymphoma). Patients at risk for developing lymphomas are those who are immunocompromised or are harboring an H. pylori infection.
2.Diagnosis consists of endoscopy with biopsy and endoscopic ultrasound for staging. As with all lymphomas, assessment of distant disease should include bone marrow biopsy; CT of chest, abdomen, and pelvis; as well as an upper airway exam. Testing for H. pylori should also be performed.
3.Treatment consists of a multimodality regimen, with the role of gastric resection remaining highly controversial.
a.Medical treatment combining chemotherapy and radiation is now the most accepted first-line therapy for treating gastric lymphoma. The most common chemotherapy combination is cyclophosphamide, hydroxydaunomycin, Oncovin, and prednisone (CHOP). Some variants of lymphoma may also be treated effectively by the eradication of H. pylori infection alone.
b.Surgical treatment is now used mostly for the complications of bleeding and perforation that arise from locally advanced disease. The treatment involves the removal of all gross disease via partial gastrectomy.
4.Prognosis is good, with a 5-year survival greater than 95% when disease is localized to the stomach and 75% when local lymph nodes are involved.
D
Gastric sarcomas arise from the mesenchymal cells of the gastric wall and constitute 3% of all gastric cancers. Gastrointestinal stromal tumors (GIST) are the most common and are found predominately in the stomach.
1.Gastrointestinal stromal tumors (GIST) arise from mesenchymal cells of the GI tract, usually the pacemaker cell of
Cajal.
2.Histologic diagnosis is confirmed by immunohistochemical staining for CD 117, a cell surface antigen.
3.Presentation varies from incidental asymptomatic endoscopy or CT findings to symptomatic large tumors causing obstruction, pain, bleeding, or metastases.
4.Treatment is complete surgical removal. Clinical behavior and malignant potential are based on several factors, including mitotic count >5 per 50 high-power fields; size >5 cm; and cellular
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atypia, necrosis, or local invasion. Tumor recurrence or unresectable disease can be treated by imatinib mesylate (Gleevec), which inhibits the c-KIT gene–associated tyrosine kinase receptor responsible for tumor growth. Overall 5- year survival is 50%.
VII Benign Lesions of the Stomach
A
Gastric polyps are usually found incidentally. They often can be excised via endoscopy.
1.Hyperplastic polyps are the most common and arise most often in the setting of chronic atrophic gastritis. These polyps are non-neoplastic, and treatment consists of polypectomy.
2.Adenomatous polyps are associated with a 20% risk of malignancy, especially in those greater than 1.5 cm. Treatment consists of endoscopic polypectomy. Surgery is required for evidence of invasion on polypectomy specimen, for sessile lesions >2 cm, and polyps with symptoms of bleeding or pain.
B
Ectopic pancreas occurs during development and is rare. The majority of cases are found in the stomach, duodenum, and jejunum. The most common presenting symptoms are abdominal pain, nausea and vomiting, and bleeding. Surgical excision is the recommended treatment.
C
Ménétrier's disease (hypoproteinemic hypertrophic gastropathy) is a premaliganant abnormality of the gastric mucosa with an unknown etiology.
1.Characteristics include the following:
a.A hypertrophic gastric mucosa is seen by radiographic or endoscopic evaluation.
1.Giant rugae are characteristic.
2.Mucous cells are increased in number.
3.Parietal and chief cells are decreased in number.
b.There is gastric hypersecretion of mucus as well as excessive protein loss and hypochlorhydra.
2.Treatment consists of anticholinergics, acid suppression, octreotide, and H. pylori eradication. Total gastrectomy is required in patients with severe hypoproteinemia despite maximal medical therapy.
D
Mallory-Weiss tears are linear mucosal lesions found at the gastroesophageal junction and are related to repeated forceful vomiting. These tears account for 15% of all upper GI bleeds. Massive hemorrhage is rare but is greater in those with preexisting portal hypertension. Most cases of bleeding can be controlled by endoscopic interventions, intra-arterial infusions, or transcatheter embolization. Only 10% of patients require surgery to stop the bleeding, which consists of oversewing the mucosal tear (see Chapter 10, VI).
E
Dieulafoy's gastric lesion is caused by an abnormally large tortuous artery located in the submucosa. The classic presentation is a sudden onset of massive upper GI bleeding with associated hypotension. Endoscopy is both diagnostic and therapeutic. Surgery is rarely needed.
F
Gastric volvulus is an uncommon entity. The volvulus may be intermittent. It is caused by laxity of the ligaments supporting the stomach and is frequently associated with congenital diaphragmatic defects, traumatic injuries to the diaphragm, and paraesophageal hernias.
1.Types
a.Organoaxial volvulus is a rotation around the cardiopyloric line, a line drawn along the length of the stomach between the cardia and pylorus (most common).
b.Mesentericoaxial volvulus occurs around a line perpendicular to the cardiopyloric line.
c.Volvulus may also occur as a combination of these two types.
2.The sudden onset of constant, severe abdominal pain, wretching without vomitus, and the inability to pass a nasogastric tube constitutes Borchardt's triad.
3.Surgical treatment includes reducing the torsion and fixation of the stomach.
G
Bezoars are agglutinated masses of hair (trichobezoars occur most commonly in young, neurotic women), vegetable matter (phytobezoars are seen after a partial gastric resection and
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tend to be more common in older men), or a combination of the two that form within the stomach.
1.Symptoms of a bezoar include nausea, vomiting, weight loss, and abdominal pain. Complications include obstruction and ulceration.
2.Treatment generally requires endoscopic or surgical removal, although enzymatic dissolution of some bezoars has been successful.
VIII Duodenal Tumors
A
Malignant tumors are usually adenocarcinomas. Treatment of resectable lesions is pancreaticoduodenectomy (Whipple's procedure). Other tumors include carcinoids, GISTs, gastrinomas, and parcomas.
B
Benign tumors include lipomas, benign GISTs, hamartomas, and adenomas. Surgical resection is the treatment of choice.
IX Miscellaneous Disorders of the Stomach and Duodenum
A Gastric outlet obstruction (see IV B 6 c)
B Superior mesenteric artery syndrome Especially in young, thin women, the third portion of the duodenum can be obstructed by the superior mesenteric artery, which takes a sharp angle from the aorta and courses over the duodenum. This anatomic configuration is combined with predisposing factors, such as a lack of the retroperitoneal fat cushion, prolonged immobilization, and pressure (e.g., from a body cast). The syndrome is also known as cast syndrome because of its association with patients in body casts.
1.Symptoms include vomiting and postprandial pain.
2.Treatment
a.Medical treatment consists of eliminating all contributing factors, such as casts, girdles, and lying in the supine position. Weight gain may alleviate symptoms. Increasing oral intake, enteral feeding beyond the ligament of Treitz, and parenteral supplementation may be tried.
b.Surgical treatment includes either releasing the ligament of Treitz, which moves the duodenum out from beneath the superior mesenteric artery, or bypassing the obstruction.
C
Duodenal (pulsion) diverticula are frequently asymptomatic. The most common location is opposite the ampulla of Vater. Severe hemorrhage or perforation can occur; but in the absence of such complications, no treatment is indicated.
X Postgastrectomy Syndromes
These symptom complexes can be disabling.
A
Alkaline reflux gastritis is the most common problem after a gastrectomy, occurring in about 25% of all patients.
1.Symptoms are postprandial epigastric pain, nausea, vomiting, and weight loss.
2.Diagnosis. Endoscopy demonstrates the gastritis and a free reflux of bile.
3.Treatment is conversion of the Billroth I or II gastrectomy (Fig. 11-4A,B) to a Roux-en-Y anastomosis (Fig. 11-4F).
B
Afferent loop syndrome is caused by intermittent mechanical obstruction of the afferent loop of a gastrojejunostomy.
1.Symptoms include early postprandial distention, pain, and nausea, which are relieved by vomiting of bilious material not mixed with food.
2.Treatment consists of providing good drainage of the afferent loop, usually by conversion to a Roux-en-Y anastomosis.
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C
Dumping syndrome affects most postgastrectomy patients but is a significant problem in only a few. It exists in either an early or late form with the former occurring more frequently.
1.Early dumping syndrome occurs within 20–30 minutes following ingestion of a meal. It is more common after partial gastrectomy with Billroth II reconstruction. It results from the rapid movement of a hypertonic food bolus into the small intestine. Rapid fluid shifts into the small bowel cause distention and a subsequent autonomic response along with the release of several humoral agents.
2.Late dumping syndrome occurs 2–3 hours after a meal and is far less common. The large carbohydrate load passed into the small intestine causes on over-release of insulin resulting in profound hypoglycemia. This stimulates the adrenal gland to release a large amount of catecholamines producing confusion tachycardia, lightheadedness and tremulousness.
3.Signs and symptoms may include epigastric fullness or pain, nausea, palpitations, dizziness, diarrhea, tachycardia, and elevated blood pressure.
4.Treatment
a.Conservative nonsurgical measures include octreotide to control symptoms. Patients are advised to avoid a high-carbohydrate diet and not to drink fluids with meals.
b.Surgical treatment is used to delay gastric emptying, including interposition of an antiperistaltic jejunal loop between the stomach and small bowel or conversion to a long limb Roux-en-Y reconstruction.
D
Postvagotomy diarrhea is common in its mild form but seldom is a disabling problem. Symptoms usually improve during the first year after surgery.
Chapter 12
Small Intestine
Karen A. Chojnacki
David J. Maron
I Introduction
AAnatomy
1.External structure. The small intestine is the length of bowel that extends from the pylorus to the cecum.
a.The duodenum, which is retroperitoneal, extends from the pylorus to the ligament of Treitz.
b.The jejunum (proximal 40%) and ileum (distal 60%), which are intraperitoneal, make up the remainder of the small intestine.
c.The total length of small bowel is approximately 3 m (the duodenum measures 30 cm; the jejunum is 110 cm; and the ileum is 160 cm).
2.Vasculature. The arterial supply to the small intestine is primarily from the jejunal and ileal branches of the superior mesenteric artery (except the duodenum, which is also supplied by the branches of the celiac axis).
a.Jejunal mesenteric arteries have only one or two arcades and a long vasa recta (the small arteries directly adjacent to the bowel wall).
b.Ileal arteries have multiple arcades that extend closer to the bowel and have short vasa recta.
3.Layers of the wall of the small intestine
a.The mucosa consists mostly of absorptive columnar epithelium and mucous-producing goblet cells. The absorption of nutrients takes place through the epithelial cells that cover the intestinal villi and have a total surface area of approximately 500 m2. Mucosal cells proliferate rapidly and have a life span of 5 days.
b.The submucosa is the strongest layer and provides strength to an intestinal anastomosis. It contains nerves, Meissner's plexus, blood vessels, lymphoid tissue (Peyer patches), and fibrous and elastic tissue.
c.The muscularis—the muscle layer—consists of an outer longitudinal layer and an inner circular layer with Auerbach's myenteric plexus of ganglion cells in between.
d.The serosa is the outermost layer and derives embryologically from the peritoneum.
4.Internal structure
a.Spiral folds of mucosa and submucosa, also known as plicae circulares or valvulae conniventes, are more prominent proximally.
b.The jejunum is larger in diameter, thicker walled, has more prominent plicae circulares, and has less mesenteric fat than the ileum.
c.The lymphoid tissue (Peyer patches) becomes more prominent distally in the ileum.
BPhysiology
The primary functions of the small intestine are digestion and absorption. All ingested food and fluid, plus secretions from the stomach, liver, and pancreas, reach the small intestine. The total volume may reach 9 L/day, and all except 1–2 L will be absorbed.
1. Motility
