Gastrectomy usually means removal of part of the stomach and anastomosis of the gastric remnant with either the duodenum (Billroth I) or a loop of proximal jejunum (Billroth II). These operations typically are performed as surgical treatment of peptic ulcer disease or cancer of the stomach. Rarely, the entire stomach is removed.
Removal of part or all of the stomach can be associated with a variety of consequences and complications. These may range in severity from a simple inability to eat large meals, due to loss of the reservoir function of the stomach, to more serious complications, such as severe dumping and profound nutritional sequelae.
Pathogenesis. The dumping syndrome develops as a result of the loss of pyloric regulation of gastric emptying. Thus, strictly speaking, a portion of the stomach does not necessarily have to be removed; a pyloroplasty alone can lead to the dumping syndrome. After a pyloroplasty or an antrectomy, hyperosmolar food is «dumped» rapidly into the proximal small intestine.
During the early phase of the dumping syndrome, the hyperosmolar small-bowel contents draw water into the lumen, stimulate bowel motility, and release vasoactive agents, such as serotonin, bradykinin, neurotensin, substance P, and vasoactive intestinal peptide from the bowel wall. Patients experience abdominal cramps, diarrhea, sweating, tachycardia, palpitations, hypotension, and light-headedness. These effects typically occur within 1 hour after eating.
In the late phase, because of the absorption of a large amount of glucose after the meal, plasma insulin rises excessively and blood sugar may plummet. Consequently, the patient may experience tachycardia, light-headedness, and sweatiness 1 to 3 hours after a meal.
The typical symptoms and signs in the setting of gastric surgery usually are sufficient to make the diagnosis of dumping syndrome. A blood sugar determination several hours after a meal when symptoms are at their worst may be helpful in confirming the late phase.
Patients are advised to eat small meals six to eight times a day. Carbohydrates are restricted to minimize glucose absorption. Medications to reduce bowel motility, such as diphenoxylate or loperamide, may be helpful. In rare instances, surgical revision with anastomosis of the gastric remnant to an antiperistaltic segment of jejunum may be necessary.
Pathogenesis. About 1% to 3% of patients who have undergone partial gastrectomy for ulcer disease develop a recurrent ulcer. Recurrent ulcers nearly always occur in small intestinal mucosa adjacent to the anastomosis (duodenal mucosa in a Billroth I, jejunal mucosa in a Billroth II). The factors that contribute to the development of a recurrent ulcer are similar to those that contributed to the original ulcer disease. A recurrent ulcer after surgery raises the question of the adequacy of the operation. Also, the possibility of an acid hypersecretory syndrome (e.g., gastrinoma or retained antrum) must be considered.
Diagnosis. Patients with recurrent ulcers usually experience abdominal pain that may or may not be similar to their original ulcer pain. Typically, the pain is relieved by food, although in some patients the pain is aggravated by eating. As in ordinary ulcer disease, bleeding, obstruction, and perforation can occur. The diagnosis is established by endoscopy. Because of the surgical deformity at the anastomosis, the endoscopist must be especially attentive to examining the folds and crevices in the vicinity of the anastomosis.
|TABLE. COMPLICATIONS OF GASTRIC SURGERY|
The documentation of a recurrent ulcer is an indication for at least a fasting serum gastrin determination. Formal acid secretory testing may not be reliable because of the loss of acid through the widely patent anastomosis. If the ratio of basal acid output to maximal acid output exceeds 60%, that is suggestive of a gastrinoma or another acid hypersecretory syndrome, but a low ratio does not exclude such a syndrome. If suspicion is high for a Zollinger-Ellison-like syndrome, a secretin stimulation test should be performed.
Treatment. Conventional ulcer therapy may be sufficient. Some patients require chronic treatment with acid-suppressive drugs. Those in whom such therapy fails may benefit from more extensive surgery. A demonstrated acid hypersecretory condition may require more specific treatment.
Nutritional and metabolic sequelae
The weight loss that commonly occurs after gastric surgery is multifactorial. First, the storage capacity of the postsurgical stomach is limited, thereby restricting the amount of food that can be consumed at one meal. Second, if the dumping syndrome is present, the patient may reduce food intake to avoid unpleasant consequences. Thus, malabsorption may contribute to weight loss due to failure to absorb adequate calories and nutrients.
The causes of malabsorption are numerous.
The reduction in gastric acid contributes to the malabsorption of dietary iron. If the patient has a gastrojejunal anastomosis (Billroth II), bypass of the duodenum also results in poor absorption of iron, calcium, and folate. Thus, iron- or folate-deficiency anemia or a manifestation of calcium deficiency, such as osteoporosis, may develop.
Bypass of the duodenum also means that food-stimulated secretin and cholecystokinin release is diminished, resulting in delayed and attenuated bile and pancreatic secretions. Furthermore, the digestive enzymes mix poorly with the food as they «chase» it down the small intestine.
Rarely, bacterial overgrowth develops within the afferent loop after Billroth II surgery, causing deconjugation of bile acids and contributing to the fat malabsorption. The dumping syndrome, if present, adds to poor mixing, even in patients with a gastroduodenal anastomosis (Billroth I).
Malabsorption of vitamin B12 may occur. Normally, intrinsic factor is secreted by gastric parietal cells in excess of what is needed to complex with dietary vitamin B12. An acid-reducing operation by itself is not sufficient to compromise vitamin B12 absorption. However, most patients who have undergone partial gastrectomy have chronic gastritis, presumably because of reflux of small-intestinal contents, which can result in gastric atrophy and loss of parietal cells over several years. Secretion of intrinsic factor diminishes, and the neurologic or hematologic consequences of pernicious anemia may develop.
Diagnosis. Many of the nutritional and metabolic manifestations of the postgastrectomy state are self-evident. Routine hematologic studies plus serum iron, ferritin, and vitamin B12 levels help in determining the cause of anemia and in planning appropriate treatment. Because of normal homeostatic mechanisms, serum calcium usually remains normal.
A quantitative stool fat determination may document the severity of malabsorption. However, even patients who do well after gastric surgery typically have mild elevations in stool fat in the range of 5 to 10 g per day. An abnormal vitamin B12 absorption test (Schilling test) without intrinsic factor, which normalizes with added intrinsic factor, can document the lack of intrinsic factor in patients with macrocytic or mixed anemia. Endoscopic biopsy showing atrophic gastritis lacking parietal cells confirms the diagnosis.
Treatment. The patient is advised to consume frequent small feedings to accommodate the small gastric remnant. Antidiarrheal agents may be helpful. If fat malabsorption is a prominent feature, a low-fat diet, perhaps supplemented with medium-chain triglycerides (which do not require bile acids for absorption) should be prescribed. In patients with fat malabsorption, an empiric trial of tetracycline, 250 mg four times daily for 7 to 10 days, is justified because documentation of bacterial overgrowth in the afferent loop is difficult.
Afferent loop syndrome
- Pathogenesis. The afferent loop syndrome may occur in patients with a gastrojejunostomy. This term does not refer to the blind loop syndrome. Occasionally this is a point of some confusion. The blind loop syndrome, which means bacterial overgrowth in a blind or stagnant loop of bowel or within a diverticulum with consequent bile acid deconjugation and fat malabsorption, certainly can occur in the afferent loop.
- The afferent loop syndrome develops because of a stricture or kinking of the afferent, or proximal, loop of a Billroth II anastomosis. This defect impairs the egress of fluid from the duodenum. When the patient eats, biliary, pancreatic, and duodenal secretions enter the duodenum. If these secretions cannot pass easily to the gastrojejunal anastomosis, the afferent loop becomes distended, causing severe epigastric pain. As the pressure within the loop increases, the obstruction is suddenly overcome, culminating in vomiting and prompt relief of pain.
- Diagnosis. The clinical story of severe abdominal pain developing during or shortly after eating and relieved promptly by vomiting in a patient with a Billroth II anastomosis is highly suggestive. Documentation by objective testing is difficult. HIDA scanning may help confirm the diagnosis if isotope is seen to fill and distend the afferent loop during development of typical pain, without entry into the stomach or distal jejunum. The patient should undergo endoscopy to look for an anastomotic ulcer or a constriction within the afferent loop. However, kinking of the loop is difficult to determine by endoscopy. Although an upper gastrointestinal x-ray series usually is not helpful, it may suggest kinking of the loop and can indicate the length of the afferent loop and its position in the abdomen. The diagnosis of afferent loop syndrome is made after much deliberation in patients who have symptoms consistent with the diagnosis and in whom another cause for the symptoms cannot be found.
- Treatment. Medical management of the afferent loop syndrome usually is unsatisfactory. Sometimes frequent small feedings prevent symptoms. If an anastomotic ulcer is discovered, that can be treated. An occasional patient improves with the passage of time. The definitive treatment is surgical and consists of either relieving adhesive bands or shortening the afferent loop and reforming the anastomosis.
Chronic gastritis and carcinoma in the gastric remnant
- Pathogenesis. In some studies, patients who have undergone partial gastrectomy appear to be at increased risk to develop adenocarcinoma within the remnant 15 years or more after surgery. The first estimates of the prevalence of this complication were about 5%, but subsequent evidence indicates that the risk may be much lower. Postgastrectomy adenocarcinoma usually occurs in the gastric mucosa at the anastomosis. The pathogenesis is thought to be related to the chronic gastritis that invariably develops and is most severe at the anastomosis.
- Diagnosis. In view of the evidence that the risk of adenocarcinoma arising in the gastric remnant may be considerably less than originally estimated, routine surveillance endoscopy in asymptomatic patients does not appear to be cost effective and thus is not recommended. However, the physician should be attentive to changes in symptoms or clinical status in postgastrectomy patients that may indicate the development of neoplasia. These include the development of new or different abdominal symptoms, anorexia, vomiting, weight loss, and gross or occult gastrointestinal bleeding. The appropriate diagnostic study is endoscopy with biopsy of the anastomosis.