Gastric outlet obstruction

Gastric outlet obstruction occurs in approximately 2% of patients with PUD and is usually caused by ulcer-related inflammation or scar formation near the peripyloric region. Signs and symptoms of outlet obstruction include early satiety after meals, nausea, vomiting, abdominal pain, and weight loss. Ulcer healing with conventional acid-suppressive therapy is the primary treatment, but if this is unsuccessful then an endoscopic procedure (e.g., balloon dilation) is required. 

Peled N et al Gastric-outlet obstruction induced by prostaglandin therapy in neonates. N Engl J Med 1992 327 505. [PMID 1635565]... 

All NSAIDs have the potential to cause gastric and duodenal ulcers and bleeding through direct (topical) or indirect (systemic) mechanisms. Risk factors for NSAID-associated ulcers and ulcer complications (perforation, gastric outlet obstruction, GI bleeding) include increased age, comorbid medical conditions (e.g., cardiovascular disease), concomitant corticosteroid or anticoagulant therapy, and history of peptic ulcer disease or upper Gl bleeding. 

Enteric coating reduces the rate of absorption of aspirin. In cases of severe overdosage this can cause difficulties in diagnosis and treatment, since early plasma salicylate measurements are unreliable, maximum blood concentrations sometimes not being reached until 60 or 70 hours after overdose (94,95). Another complication of the use of enteric-coated aspirin is the risk of gastric outlet obstruction and the resulting accumulation of tablets because of subclinical pyloric stenosis. 

Modified-release formulations of nifedipine have been associated in case reports with the formation of bezoars, concretions of undigested material within the gastrointestinal tract, mostly in the stomach. An unusual case of tablet impaction in the duodenum, with gastric outlet obstruction, was discovered 1 year after the patient stopped taking a modified-release formulation of nifedipine (27). 

Co-administration of misoprostol and NSAIDs significantly reduced the frequency of NSAID-induced gastric ulcer in patients with osteoarthritis (118) and misoprostol reduced serious upper gastrointestinal complications (perforation, gastric outlet obstruction, and perhaps bleeding) by 40% compared with placebo in older patients with rheumatoid arthritis treated with NSAIDs (110,119). 

Mechanical gastric outlet obstruction Peptic ulcer disease Gastric carcinoma Pancreatic disease Motility disorders Gastroparesis... 

The most common adverse effects of NSAIDs involve the gastrointestinal tract. Minor complaints (nausea, dyspepsia, anorexia, and abdominal pain) are common (up to 60% of patients). Serious GI complications associated with NSAIDs including perforations, gastric outlet obstruction, and GI bleeding, occur in 1.5% to 4% of patients per year. 

The most common sites of GI injmy are the gastric and duodenal mucosae." The incidence of gastric ulcers with NSAID use is approximately 11% to 13%, and that for duodenal ulcers is 7% to 10%. Serious GI complications associated with NSAIDs, including perforations, gastric outlet obstruction, and GI bleeding, occur in 1.5% to 4% of patients per year. NSAIDs are so widely used that these small percentages translate into substantial morbidity and mortality. " Moreover, the risk increases to 9% per year for patients with the risk factors of advanced age, history of peptic ulcer or GI bleeding, or cardiovascular disease. Consequently, about 16,500 deaths are associated annually with NSAID use in rheumatoid arthritis or OA patients. 

To study effects on clinically important GI complications with celecoxib, the CLASS study used celecoxib (400 mg twice daily, or twice the highest FDA-approved dose) compared to diclofenac and ibuprofen at standard dose. Celecoxib use was reported to be associated with a reduced incidence for the combined end point of symptomatic ulcers and ulcer complications (perforations, gastric outlet obstruction, or bleeding). Some subjects also used aspirin for car-dioprotection, but there is concern that GI safety of COX-2 inhibitors is blunted with use of concomitant aspirin (even 30 mg of aspirin can suppress gastric prostaglandin prodnction)." For patients taking aspirin and celecoxib, nicer complications were higher than with celecoxib only, but lower than with traditional NSAIDs. 

With achlorhydria, H2-antagonist therapy, gastric cancer, or gastric outlet obstruction, bacterial counts may rise to 10 /mt. 

Aluminum-containing antacids are used cautiously in patients with gastric outlet obstruction. M iesium- and aluminum-containing antacids are used cautiously in l atients with decreased kidney function. The calcium-containing antacids are used cautiously in patients witli resiiiratoiy insufficiency, renal impairment, or cardiac disease Antacids are classified as Rr iancy Category C dru and should be used witli caution during pr nancy. 

Babyn P, Peled N, Manson D et al (1995) Radiologic features of gastric outlet obstruction in infants after long-term prostaglandin administration. Pediatr Radiol 25 41-43... 

A barium study (Fig. 3.16) will demonstrate narrowing of the antropyloric region (occurring in up to 16% of patients) (Griscom et al. 1974) secondary to chronic inflammation and fibrosis, which can eventually lead to gastric outlet obstruction. In some cases, the proximal duodenum will also be involved. Ultrasound will also reveal a thickening of the antropyloric wall, simulating HPS. Most patients, however, will be older than the typical HPS patient. 

Di Sario JA, Fennerty MB, Tietze CC (1994) Endoscopic balloon dilatation for ulcer-induced gastric outlet obstruction. Am J Gastroenterol 89 868-871 Dohmoto M (1991) New method-endoscopic implantation of rectal stent in palliative treatment of malignant stenosis. Endoscopia Digestiva 3 1507-1512 Eckhauser ML (1992) Laser therapy of colorectal carcinoma. 

---