Peptic Ulcers

Peptic Ulcers


Centers for Disease Control (2005) describes a peptic ulcer as a sore or hole in the lining of the stomach or duodenum. It is also called peptic ulcer disease or PUD. It can develop at any age and studies say it will develop in more than 25 million Americans at one point in their lives. Most PUDs are caused by a bacterium, called helicobacter pylori or h. pylori, which is curable by antibiotics. The most common symptom is burning pain in the stomach (CDC). The purpose of this paper is to know more about PUD as it afflicts some members of the family.

Of the approximately 500,000 persons who develop PUD every year, 70% are between 24 and 64 years old (Howden, 2003). More ulcers occur in the stomach and proximal duodenum than elsewhere. The H. pylori bacterium and the use of non-steroidal inflammatory drugs or NSAIDs are the most frequent causes and occur in 48% and 24%, respectively. Destroying the bacterium will greatly reduce the probability of recurrence from 67% to 6% for duodenal ulcers and from 59% to 4% for gastric ulcers. Symptoms of PUD include episodic pain, which is relieved by eating and pain upon awakening at night. There is no abdominal pain in at least 30% of sufferers (Howden).

PUD is rare in children and mostly affecting those 8-17 years old (Lie, 2007). Duodenal ulcers are most common in these cases, in which the bacterium is the primary cause. Major and alarming symptoms include anemia, hematemesis, melena, anorexia and Hemoccult-positive stool. It is a rare cause of obstruction, accounting for 5-8% of such cases, and may hint at malignancy. A patient older than 55 years old should be promptly referred for endoscopy. Those younger without the alarming symptoms should be tested for the bacterium and discontinue using NSADs. The serum enzyme-linked immunosorbent assay, urea test, stool antigen test or endoscopic biopsy can be used to test for the bacterium. With a positive test for the infection, antibiotics should be administered for 10-14 days and an anti-secretory regimen for 4 weeks. Endoscopy should be used to confirm healing of gastric ulcers and rule out malignancy. PPIs are the choice for superior acid suppression, increasing healing rates and providing relief for symptoms better than histamine blockers. PPIs heal 95% of duodenal ulcers and 80-90% of gastric ulcers in 4 weeks (Lie).

About 25% of NSAID-using patients with gastric ulcers may need to be on PPI treatment for more than 8 weeks (Lie, 2007). Those at high risk for complications, such as recipients of transplants, may require surgery. Truncal vagotomy and drainage, selective vagotomy and drainage, highly selective vegotomy and partial gastrectomy are among the surgical options. Endoscopic balloon dilatation or surgery is an approach to relieve chronic obstruction. Injection of epinephrine, alcohol or scleroant, coagulation through endoscopy with ligation and angiographic embolization with vagotomy and drainage and partial gastrectomy are surgical options after stabilization (Lie).

Bleeding, perforation and gastric outlet obstructions are the serious complications of PUD (Lie, 2007). Ulcer perforation occurs in 2-10% of cases. In 60% of the cases, the anterior wall of the duodenum is affects, the antral at 20% and the lesser curve at 20% for gastric ulcers. The Rockall risk scoring scheme is used to assess risks for age, shock, co-morbid illness, diagnosis and recent bleeding. A score higher than 4 points signals a 25% risk for recurrence of bleeding and 20% mortality. Management includes nasogastric decompression, histamine blockers, PPIs and destruction of the H. pylori bacterium (Lie).

Complexities, Origin and Level of Concern

For over a century, PUD was customarily managed with surgery, which often incurred high morbidity and mortality rates (Yuan, Padol and Hunt, 2006). Histamine H2-receptor antagonists became the popular and effective choice to suppress gastric acid secretion in the 70s. This led to the decline of surgery to 85% in the 80s. This was followed by the introduction of proton pump inhibitors for the same purpose. More than a decade hence today, three main issues remain unresolved. One is the optimal way of eradicating the bacterium as failure rates rise. Another is to find the best prevention to ulcer development and recurrence among NSAI users. And the third is to devise treatment for non-NSAID, non-H-pylori-associated peptic ulcers (Yuan, et al.).

Relevance to Nursing

Duodenal cancers are dominant in Western populations while gastric ulcers are prevalent in Asia, especially in Japan (Yuan, et al., 2006). Despite the decline of PUD in Western countries, 1 out of 10 Americans remains afflicted with it today. This incidence exacts an annual direct and indirect financial burden of U.S.$3.4 billion in the U.S. It peaks in the elderly and is thus expected to assert a global impact on health-care delivery, health economics and the quality of life itself in the patient (Yuan, et al.)..

Existing Literature

Current literature in 2005 to 2006 addresses dyspepsia, the treatment of PUD, h. pylori and NSAID gastro-enteropathy (Louw, 2006). One discussed the triaging of dyspeptic subjects, information on new proton pump inhibitor drugs and h.pylori eradication "rescue regimens." The COX-2 debacle is presented for the prevention of NSAID gastropathy. At the same time, it questions the use of anti-platelet agents as safe substitutes for aspirin cardio prophylaxis. It also addresses the safety of proton pump inhibitors and non-steroidal anti-inflammatory drug enteropathy (Louw).

A systematic review of related studies before 1997 and between 1997 and 2008 presented data on 61,067 cases of whom 5,001 (Straube, Tramer, Moor, Derry & McQuay, 2009). The mortality rates in all the cases significantly fell at 95% from 11.6% before 1997 to 7.4% since 1997. The studies also reported an increase in the mortality among 5,526 NSAID and aspirin-using patients from 14.7% before 1997 to 20.9% since 1997. The data suggest that deaths from upper gastrointestinal bleeding or fallen decreased from 1 to 13 but remained higher among NSAID and aspirin users at 1 out of 5 (Straube, et al.). Bleeding of the upper gastrointestinal tract has been found to occur in 15-20% of PUD patients, a most common cause of death (Lie, 2007). About 20% of these death arise from asymptomatic ulcers (Lie).

Resolutions of the PUD Issue

A separate study assessed the effect of community h. pylori screening and treatment of dyspepsia, aimed at reducing the incidence of gastric cancer (Hansen, Wildner-Christensen, Hellas & Schaffalitzky de Muckadell, 2008). At the same time, it tested for the prevalence of dyspepsia and quality of life. The sampling consisted of 12,540 with a 94% response. It was the first population-based, randomized, controlled trial of H. pylori screening and treatment for the purpose. The study also provided insight into the incidence of PUD in a middle-aged population (Hansen, et al.).

The findings revealed that the community H. pylori and treatment program had a limited and insignificant effort on the rate of dyspepsia, on the consultation rate of a GP and sick leave days for dyspepsia (Hansen, et al., 2008). The prescription rate of ulcer drugs had no significant effect on the quality of life of the respondents. The health costs involved were likewise insignificant. Lower incidence of proven ulcers and fewer complicated ulcers were found in the screened group. A 10-year follow-up was planned to determine whether the incidence of PUD would increase as the same population grew older (Hansen, et al.).

Another review sought to gain a better understanding and management of dyspepsia, using and comparing four management strategies (Louw & Marks, 2003). Two of these strategies were "test-and-treat"-based and the other two were PPI-based. The "test-and-treat" strategies were recommended with endoscopy for treatment failures or with a trial of proton pump inhibitor therapy for clinical failures and endoscopy in case of failures in acid suppression. The proton pump inhibitor or PPI-based therapy was followed by endoscopy for treatment failures, with test and treat for those who failed the PPI trial and endoscopy for failures in the test-and-treat strategy. It found that the H. pylori antigen test was not as reliable as the urea breath test. It also revealed that what was considered the most promising "new" therapy for H. pylori was not new but only a mix of older drugs presented in four management strategies. The combination, however, showed some promise (Louw & Marks).


PUD remains a common problem in the primary and specialist care in the U.S. (Howden, 2003). Knowledge about peptic ulcer dramatically changed in the 80s with the introduction of a causal link between PUD and the H. pylori bacterium. Although it was at first viewed with much skepticism, it eventually gained universal acceptance. Test for the bacterium in all patients with an active ulcer or a past history of ulcer disease. PUD was thus considered a treatable chronic bacterial infection. But in recent years, there have been patients with peptic ulcers who showed no evidence of the bacterium. This suggested risks other than H. pylori (Howden)

Incidence of H. pylori-negative ulcer appeared to be higher in the U.S. than in…