Muralto first described duodenal ulcers at autopsy in 1688. Crisp published a landmark paper in which he described symptomatology of perforated peptic ulcers in 1843. Therapy of perforated ulcer has been a hallmark of General Surgical practice for well over 100 years. Virtually, every American Board of Surgery candidate can rely on seeing a question in their oral examination regarding management of this entity; however, our understanding of the problem has changed drastically over the last 20 years. The last 10 years of the 20th century witnessed a scientific revolution in our
recognition of the role that infection with Helicobacter pylori plays in producing the gastric acid hypersecretion that characterizes peptic ulcer. This hypersecretion, and attempts to control it, had in fact been the subject of a previous scientific revolution during the 1950s and 1960s that had shepherded a transition from surgical therapy that focused on resection of acid-secreting mucosa via subtotal gastrectomy to eliminating the hypersecretion by section of the vagus nerves. This revolution was best summarized by the Nobel Prize-nominated vagotomy pioneer, Lester Reynolds Dragstedt, whose philosophy regarding the controversy between the choice of resection versus vagotomy was best summarized in his remark that “the stomach is a mighty handy organ to take to the dinner table”. This is a reminder that is even more valid today. This concept of duodenal ulcer as an infectious disease, not to mention the wide “over the counter” availability of H₂ blockers and proton pump inhibitors, has led to a marked decrease in the incidence of complications such as: intractability and/or gastric outlet obstruction that formerly might have led to surgery. Unfortunately, our new understanding has not yet led to any detectable changes in incidence of ulcer perforation. Thus, ulcer perforation continues to be an important, even if somewhat diminished, staple of surgical practice. Opportunities for prevention must necessarily focus on the two etiologies most responsible for perforations: treatment of H. pylori infection and use of nonsteroidal anti-inflammatory drugs (NSAID). However, this is a formidable undertaking when one considers that ∼50% of the population of the United States harbors H. pylori infection and that there is a ubiquitous availability of NSAIDs as over-the-counter remedies. Any prospects for improvement in prognosis probably lie with general advances in acute surgery. The decrease in the incidence of uncomplicated duodenal ulcers over the past three to four decades has been somewhat attributable to our increased understanding of the multiple etiologies, risk factors, and epidemiology of duodenal ulcer disease, however, honest observers will note that the decrease in duodenal ulcer disease predated our understanding of its infectious nature as well as the remarkable therapeutic medications that are now so widely available.

These have been said to include NSAID use, cigarette smoking, excessive alcohol intake, and extreme emotional or physical stress. In the Western countries, it is estimated that up to 30% of regular NSAIDs users have one or more ulcers. Both NSAIDs and aspirin interfere with the protective mucus layer by inhibiting mucosal cyclooxygenase activity and reducing levels of mucosal prostaglandins. Gastric acid also exacerbates NSAID injury and conversely, gastric acid suppression has been shown to partially protect against NSAID injury. However, the exact mechanism by which NSAIDs cause duodenal perforation has not been clearly defined.

NSAID use has been reported to increase the risk of ulcer perforation by five to eight times that of nonusers (Svanes) and NSAID is a factor in between one-fifth to one-third of perforations, the proportion increasing with increasing age.

Cigarette smoking is a risk factor for PUD and its complications. Furthermore, cigarette smoking may adversely affect the healing of peptic ulcerations and, in the absence of treatment for H. pylori, may predispose to relapses. Cigarette smoking does not appear to influence the relapse rate for peptic ulceration if H. pylori in patients has been eradicated. Nevertheless, at least one study has disputed the association between smoking and PUD. Smoking probably promotes peptic ulceration by increasing gastric acidity and maximal acid output and enhancing H. pylori proliferation. Smokers have been found to have decreased prostaglandin concentrations in their gastric and duodenal mucosa and smoking has been shown to inhibit acid-stimulated duodenal mucosal bicarbonate secretion. It is not clear which, if any, of these proposed mechanisms contributes to peptic ulceration in cigarette smokers.

Alcohol has also been thought to be a strong risk factor for peptic ulcer although there is little hard data to support this. While the prevalence of ulcers is higher in alcoholic cirrhotics, no association has been demonstrated in drinkers without cirrhosis.

Ulcer patients commonly describe dyspepsia with ingestion of certain foods, but there is no evidence that such foods cause ulcers. Coffee (caffeinated and decaffeinated), tea, and colas are all potent acid secretagogues. It was once popular to prescribe a bland diet for ulcer patients; however, they are generally conceded to exert no benefit.

Ulcers have long been associated in the public’s mind with emotional stress; however, this association has been disparaged since the appreciation of the role of H. pylori infection and NSAID use. Emotional stress is apparently probably not sufficient to cause ulcers in most patients since eradication of H. pylori and elimination of NSAIDs generally prevent ulcer recurrence despite the patient’s emotional state.

There are some suggestions that genetic factors may predispose patient to peptic ulcer. The incidence among identical twins is higher than that for nonidentical twins and there is an increase in first-degree relatives of ulcer patients. The genes responsible are unknown. Some of this increased susceptibility may be due to a high rate of H. pylori infection among family members. It was initially thought that elevated serum levels of serum pepsinogen I might be a genetic marker, but this now appears to be a consequence of H. pylori infection, which disappears with eradication. Other proposed markers include O blood group, lack of secretion of blood group antigens in saliva, and the presence of certain HLA subtypes; however, it now appears that these associations relate more to susceptibility to H. pylori infection.

Perforated PUD typically causes sudden and severe epigastric abdominal pain that may progress to involve the entire abdomen. The pain caused by the spillage of highly caustic gastric secretions into the peritoneum rapidly reaches peak intensity and remain constant. Many patients can state the exact time of onset of their symptoms. Radiation to the right scapula region is common because of right subphrenic collection of gastric contents. Occasionally, pain is sensed in the lower abdomen if gastric contents travel caudally through the paracolic gutter. Peritoneal irritation is usually intense, and most patients avoid movement to minimize discomfort. The degree of peritoneal findings, however, is strongly influenced by a number of factors:

Physical examination reveals low-grade fever, diminished bowel sounds, and rigidity of the abdominal wall musculature. The patient can also demonstrate signs and symptoms of:

Other indicators of toxicity (such as peritoneal irritation, fever, and increased white blood cell count with left shift) may actually be absent in both elderly and immunocompromised patients. Furthermore, other acute conditions, such as myocardial infarction, dissecting aortic aneurysm, cholecystitis, pancreatitis, diverticulitis, appendicitis, and renal colic can mimic the symptomatology of perforated PUD.

It has been argued that, in general, laboratory studies are of little value in evaluating a patient with suspected duodenal ulcer perforation, but such tests as complete blood cell count, amylase and lipase determinations, and liver functions tests may be useful in excluding other causes of upper abdominal pain.