VIEWS: 28 PAGES: 7 POSTED ON: 10/7/2011
GASTRIC OUTLET OBSTRUCTION Gastric outlet obstruction (GOO) is the clinical and pathophysiological consequence of any disease process that produces a mechanical failure to gastric emptying. Clinical entities that can result in GOO generally are categorized into benign and malignant. In the past when peptic ulcer disease (PUD) was more prevalent, benign causes were the most common; however, a recent review shows that only 37% of patients with GOO have benign disease and the remaining patients have obstruction secondary to malignancy. As part of the initial workup, it is important to exclude functional obstruction such as diabetic gastroparesis. Once a mechanical obstruction is confirmed, differentiation between benign and malignant disease is important because definitive treatment is based on recognition of the specific underlying cause. Aetiology: Benigncauses include PUD, gastric polyps, ingestion of caustics, pyloric stenosis, congenital duodenal webs, gallstone obstruction (Bouveret syndrome), pancreatic pseudocysts, and bezoars. Malignant causes include pancreatic cancer as the most common malignancy causing GOO. Outlet obstruction may occur in 10-20% of patients with pancreatic carcinoma. Other tumors that may obstruct the gastric outlet include ampullary cancer, duodenal cancer, cholangiocarcinomas, and gastric cancer. Metastases to the gastric outlet also may be caused by other primary tumors PUD is a cause in approximately 5% of all patients with GOO. Ulcers within the pyloric channel and first portion of the duodenum usually are responsible for outlet obstruction. Obstruction may be acute, secondary to acute inflammation and edema or, more commonly, in a chronic, secondary to scarring and fibrosis. Helicobacter pylori has been implicated as a frequent associated finding in patients with GOO due to PUD.. In babies, pyloric stenosis constitutes the most important cause of GOO. Pyloric stenosis occurs in 1 per 750 births. It is more common in boys and first-born children and is the result of gradual hypertrophy of the circular smooth muscle of the pylorus. Pathophysiology: Intrinsic or extrinsic obstruction of the pyloric channel or duodenum causes GOO; as previously noted, the mechanism of obstruction depends upon the underlying etiology. Patients present with intermittent symptoms that progress until obstruction is complete. Vomiting is the cardinal symptom. Initially, patients may demonstrate better tolerance to liquids than solid food. In a later stage, patients develop significant weight loss due to poor intake. Malnutrition is a late sign, but it may be very profound in patients with concomitant malignancy. In the acute or chronic phase of obstruction, continuous vomiting may lead to dehydration and electrolyte abnormalities. 1 When obstruction persists, patients may develop significant and progressive gastric dilatation. The stomach eventually loses its contractility. Undigested food accumulates and may represent a constant risk for aspiration pneumonia. Clinical: Nausea and vomiting are the cardinal symptoms of GOO. Vomiting usually is described as nonbilious, and it characteristically contains undigested food particles. In the early stages of obstruction, vomiting may be intermittent and usually occurs within 1 hour of a meal. Early satiety and epigastric fullness are common. Weight loss is frequent when the condition becomes chronic and is most significant in patients with malignant disease. Abdominal pain is not frequent and usually relates to the underlying cause, eg, PUD, pancreatic cancer. Physical examination often demonstrates the presence of chronic dehydration and malnutrition. There may be visible peristalsis from left to right and a positive succussion splash particularly in GOO due to PUD. A dilated stomach may be appreciated as a tympanitic mass in the epigastric area and/or left upper quadrant. Dehydration and electrolyte abnormalities can be demonstrated by routine laboratory examinations. Increases in urea and creatinine are late features of dehydration. Prolonged vomiting causes loss of hydrochloric (HCl) acid and produces an increase of bicarbonate in the plasma to compensate for the lost chloride and sodium. The result is a hypokalemic hypochloremic metabolic alkalosis. Alkalosis shifts the intracellular potassium to the extracellular compartment, and the serum positive potassium is increased factitiously. With continued vomiting, the renal excretion of potassium increases in order to preserve sodium. The adrenocortical response to hypovolemia intensifies the exchange of potassium for sodium at the distal tubule, with subsequent aggravation of the hypokalemia. Lab Studies: Obtain a CBC. Check the hemoglobin and hematocrit to rule out the possibility of anemia. Obtain an electrolyte panel. As noted previously, identifying and correcting electrolyte abnormalities that tend to occur is essential. Liver function tests may be helpful, particularly when a malignant etiology is suspected. A test for H pylori is helpful when the diagnosis of PUD is suspected. Imaging Studies: Plain abdominal x-rays, contrast upper GI studies (Gastrografin or barium), and CT scans with oral contrast are helpful. 2 Plain x-rays, the obstruction series (supine abdomen, upright abdomen, and chest posteroanterior [PA]), can demonstrate the presence of gastric dilatation and may be helpful with distinguishing the differential diagnosis. Diagnostic Procedures: Upper endoscopy can help visualize the gastric outlet and may provide a tissue diagnosis when the obstruction is intraluminal. The sodium chloride load test is a traditional clinical nonimaging study that may be helpful. o The traditional sodium chloride load test is performed by infusing 750 cc of sodium chloride solution into the stomach via a nasogastric tube (NGT). o A diagnosis of GOO is made if more than 400 cc remain in the stomach after 30 minutes. Nuclear gastric emptying studies measure the passage of orally administered radionuclide over time. Unfortunately, both the nuclear test and saline load test may produce abnormal results in functional states. Barium upper GI studies are very helpful because they can delineate the gastric silhouette and demonstrate the site of obstruction. An enlarged stomach with a narrowing of the pyloric channel or first portion of the duodenum helps differentiate GOO from gastroparesis. The specific cause may be identified as an ulcer mass or intrinsic tumor. In the presence of PUD, perform endoscopic biopsy to rule out the presence of malignancy. In the case of peripancreatic malignancy, CT scan–guided biopsy may be helpful in establishing a preoperative diagnosis. Needle-guided biopsy also may be helpful in establishing the presence of metastatic disease. This knowledge may impact the magnitude of the procedure planned to alleviate the GOO. Histologic Findings: Histologic findings relate to the individual underlying cause. Management: Treatment of patients with GOO due to benign ulcer disease may be medical if results of imaging studies or endoscopy determine that acute inflammation and edema are the principle causes of the outlet obstruction (as opposed to scarring and fibrosis, which may be fixed). If medical therapy conducted for a reasonable period fails to alleviate the obstruction, then surgical intervention becomes appropriate. The choice of surgical procedure depends upon the patient's particular circumstances; however, 3 vagotomy and antrectomy should be considered the gold standard against which the efficacy of other procedures should be measured. Weigh the extent of surgical intervention for the relief of GOO against the type and extent of malignancy and the patient's anticipated long-term prognosis. As a guiding principle, undertake major tumor resections in the absence of metastatic disease in a patient who can withstand such a procedure from a nutritional standpoint. In patients with largely metastatic disease, determine the degree of surgical intervention for palliation in light of the patient's realistic prognosis and personal wishes The stomach is located mainly in the left upper quadrant beneath the diaphragm and is attached superiorly to the esophagus and distally to the duodenum. The stomach is divided into 4 portions, the cardia, the body, the antrum, and the pylorus. Inflammation, scarring, or infiltration of the antrum and pylorus are associated with the development of GOO. The duodenum begins immediately beyond the pylorus and mostly is a retroperitoneal structure, wrapping around the head of the pancreas. The duodenum classically is divided into 4 portions. It is intimately related to the gallbladder, liver, and pancreas; therefore, a malignant process of any adjacent structure may cause outlet obstruction due to extrinsic compression. Contraindications: Contraindications for surgery relate to the underlying medical condition. Most patients benefit from an initial period of gastric decompression, hydration, and correction of electrolyte imbalances. In patients who are severely malnourished, postponing surgical intervention until the nutritional status has been optimized may be wise. In selective cases, some patients may benefit from total parenteral nutrition (TPN) or distal tube feeding (eg, placed via a percutaneous jejunostomy). One of the relative contraindications for surgery is the presence of advanced malignancy; in these cases, life expectancy may be limited to a few months. Overall, every patient with GOO deserves evaluation by a surgeon. Even if the patient has unresectable disease, other palliative surgical measures may improve the quality of life. Medical therapy: Initial management of GOO should be the same regardless of the primary cause. After a diagnosis is made, admit patients for hydration and correction of electrolyte abnormalities. Remembering that the metabolic alkalosis of GOO responds to the administration of chloride is important; therefore, sodium chloride solution should be the initial IV fluid of choice. Potassium deficits are corrected after repletion of volume status, and after the chloride has been replaced. Place a NGT to decompress the stomach. Occasionally, a large tube is required because the undigested food blocks tubes with small diameters. 4 Further treatment is tailored to the underlying cause; this is where the distinction between benign and malignant disease becomes important. Surgical therapy: Management of benign disease When acute PUD has been identified as a primary cause of GOO, focus treatment on reduction of acid production. Histamine 2 (H2) blockers and proton pump inhibitors comprise the mainstay of treatment. Treat H pylori infection, when identified, according to current recommendations. Although most patients improve temporarily with treatment, scarring and fibrosis may worsen over time. These patients are likely to present with recurrent GOO. More than 75% of patients presenting with GOO eventually require surgical intervention (Doberneck, 1987). Surgical intervention usually provides definitive treatment for GOO, but it may result in its own comorbid consequences. Operative management should offer both relief of obstruction and correction of the acid problem. The most common surgical procedures performed for GOO related to PUD are vagotomy and antrectomy, vagotomy and pyloroplasty, truncal vagotomy and gastrojejunostomy, pyloroplasty, and laparoscopic variants of the aforementioned procedures. Of these, vagotomy and antrectomy with Billroth II reconstruction (gastrojejunostomy) seems to offer the best results. Vagotomy and pyloroplasty and pyloroplasty alone, although used with some success, can be technically difficult to perform due to scarring at the gastric outlet. A combination of balloon dilatation and highly selective vagotomy has been described, but it is associated with gastroparesis and a high recurrence rate. The role of laparoscopic approach in the treatment of GOO is under investigation and may represent a valid form of therapy with low morbidity. Pneumatic balloon dilatation of a chronic benign stricture can be performed via endoscopy. Published series utilizing this technique report success rates over 65% after multiple dilatations (Gibson, 2000). Patients treated with balloon dilatation, without treatment for H pylori infection, have a high rate of failure. Patients who are negative for H pylori do not respond favorably to balloon dilatation and should be considered for surgical treatment early in the process (Gouma, 1999). Management of malignant disease The management of GOO secondary to malignancy is controversial. Of patients with periampullary cancer, 30-50% present with nausea and vomiting at the time of diagnosis (Jaffin, 1985; Khullar, 1996). Most of these tumors are unresectable (approximately 40% of the gastric cancers and 80-90% of the periampullary cancers [Kurtz, 1996; Lillemoe, 1993]). When tumors are found to be unresectable, 13-20% of patients eventually develop GOO before they succumb to their disease. The 1-year survival rate is poor. Gastrojejunostomy remains the surgical treatment of choice for GOO secondary to malignancy. Although surgeons traditionally have preferred an antecolic anastomosis to prevent further obstruction by advancing tumor growth, a recent publication evaluating 5 the retrocolic anastomosis in this setting challenges conventional wisdom (Lillemoe, 1999). Results demonstrate that a retrocolic anastomosis may be associated with decreased incidences of delayed gastric emptying (6% versus 17%) and late GOO (2% versus 9%). Recently, metallic stents have been used for treatment of GOO in a malignant setting. Metallic stents previously have been used successfully to treat stenosis of areas such as blood vessels, bile duct, esophagus, and the trachea. With the development of newer stents and delivery systems, metallic stents may have a role in the nonsurgical treatment of gastroduodenal obstruction. Stents may allow the physician to avoid complicated surgical procedures. A recent literature review reports data from 11 different studies in which 91 patients with unresectable GOO secondary to malignancy were treated with metallic stents. Immediate relief was observed in 81 patients (89%); 17 patients had recurrent obstruction (21%) (Mauro, 2000). The promising results suggest that stents eventually may replace surgery as palliative intervention for unresectable periampullary malignancies. Preoperative details: Perform standard preoperative evaluation in these patients. Correct fluid and electrolyte abnormalities prior to surgery. Perform gastric decompression by NGT and suction and alert the anesthesiologist to the potential risk for aspiration upon induction. Perform a preoperative nutritional evaluation and initiate appropriate nutritional therapy (TPN or enteral feedings via a percutaneous jejunostomy placed distal to the obstruction) as soon as possible. Intraoperative details: Intraoperative details depend upon the etiology of the underlying disease and the reason that the specific surgical procedure is undertaken. Postoperative details: Admit patients to a monitor unit after the procedure. Pay special attention to fluid and electrolyte status. Most surgeons agree that perioperative antibiotics are advisable but may be limited to use during the immediate perioperative period in the absence of intervening infection. If a gastric reconstruction is performed, an NGT is recommended. The length of time that the NGT should remain in place is controversial; however, remembering that a previously dilated stomach, the performance of a vagotomy, and the presence of metastatic cancer all may contribute to decreased gastric motility is important. An anatomically patent gastrojejunostomy may fail to empty for days. This syndrome of delayed gastric emptying is a well-known entity and requires surgical patience. Aggressive pulmonary toilet, deep venous thrombosis (DVT) prophylaxis, and early ambulation are advisable. Follow-up care: Closely monitor patients after surgery and upon discharge. After relief of GOO, patients may continue to experience gastric dysmotility and may require medication to stimulate gastric emptying and motility. 6 In patients with malignancy, the potential for progressive and recurrent disease always remains. These patients should be monitored by a surgeon or an oncologist. Closely monitor patients whose treatment consisted of balloon dilatation because most of these patients require subsequent dilatations in order to achieve satisfactory results Complications: Although the risk is small, patients undergoing endoscopic treatment with either balloon dilatation or stenting are at risk for perforation. Several literature reports exist regarding migration of the stents and reocclusion requiring further intervention. Operative complications in patients undergoing surgery for GOO often are related to the nutritional status of the patients. Commencing nutritional support upon recognition of the presence of GOO is important. If surgery is anticipated, delaying the surgery or any intervention until TPN has been instituted for at least 1 week often is prudent. Acute intervention may be technically difficult because of significant gastric dilatation and gastric wall edema. This circumstance may increase the rate of anastomotic leak. On occasion, delaying surgical intervention for several days while the stomach is decompressed by nasogastric suction may be prudent. Alert patients undergoing gastric resection for benign or malignant disease to the possibility of well-known postgastrectomy syndromes such as dumping, alkaline gastritis, and afferent loop syndrome. Severe symptoms may be present in 1-2% of patients. GOO is a clinical condition that may result from a number of underlying causes, both benign and malignant. Despite medical advances in the acid suppression mechanism, the incidence of GOO remains a prevalent clinical problem in benign PUD. Also, an increase in the number of cases of GOO seems to be noted secondary to malignancy; this possibly is due to improvements in cancer therapy, which allow patients to live long enough to develop this complication. Orient initial management to identification of the primary underlying cause and to the correction of volume and electrolyte abnormalities. Barium swallow studies and upper endoscopy are the main tests utilized to make the diagnosis. Tailor treatment to the specific cause . 7
"GASTRIC OUTLET OBSTRUCTION"