**3.2 Bleeding**

The occurrence of hemorrhage complication is clearly higher than perforation. The evaluation of annual incidence of bleeding shows a large range of variation from 36 to 44%, followed by perforation with the range from 6 to 14% [22]. Bleeding complications can develop with various degrees of severity. Peptic ulcers cause almost half of all cases of upper gastrointestinal hemorrhage. The more serious events of bleeding usually are due to chronic duodenal ulcers; however, both gastric and duodenal ulcers have the overlappable trend to bleed. Gastroduodenal bleeding from peptic ulcer is a well-known clinical occurrence, in some cases with high morbidity. The reason of major severity of this complication in the duodenal ulcer is connected to anatomical condition: the ulcer situated on the posterior wall of duodenal bulb penetrates and exposes the gastroduodenal artery, which can be eroded followed usually by copious hemorrhage. In the other sites of the duodenal bulb, as anterior wall, there are no major blood vessels. The peptic ulcers in the second portion of duodenum, so-called postbulbar ulcers, are less usual than bulbar ulcers; however, bleeding complication is frequent also in this site. The clinical manifestation of bleeding is characterized by the amount and speed of hemorrhage. The massive and sudden bleeding appears with hematemesis, followed by melena, can cause hypovolemic condition and, in some cases, hypovolemic shock. Blood loss that develops less rapidly manifests with melena, also accompanied in some cases by hemodynamic alterations. In other cases continuous and moderate blood loss induces chronic anemia. Clinical data achieve the evaluation of the severity of hemorrhage and the general conditions, as hemodynamic stability, hypovolemic status, etc. The knowledge of these findings is central for the starting of urgent resuscitation therapy. However, the diagnosis must be completed by endoscopy to define the pathological features of bleeding ulcer, essential notion to perform the correct therapeutic approach: medical, endoscopic, surgical therapy. In the context of hemorrhagic complication, the control of possible active blood losses is necessary by checking stably the nasogastric tube, the stool, and the value of hematocrit and hemoglobin level. After the bleeding has stopped, rebleeding is possible, also within a short period of time. The urgent and current therapeutic approach in the patients with bleeding peptic ulcer includes fluid resuscitation, intravenous proton pump inhibitor (PPI) therapy, blood transfusions in some cases if necessary, therapeutic endoscopic procedures, if required. Usually this approach stops bleeding and cures the ulcer. However, the evolution of the bleeding complication is not favorable in the minority of patients, and the therapeutic resolution demands the surgical procedures. There are some clinical conditions that require surgery: patient with hypovolemic status and hemodynamic alteration not responding to powerful fluid resuscitation therapy; recurrent bleeding after early interruption, in most cases after unsuccessful further endoscopic treatment; finally in the patients with moderate, small, but continuous hemorrhage that needs prolonged fluid infusion and repeated blood transfusion.

#### **3.3 Perforation**

The global frequency of perforation in the evolution of peptic ulcer disease ranges between 2 and 10%. However, the sites of lesion, in the gastroduodenal tract, show different occurrence chance of the complication. The major frequency of perforation is in duodenal ulcer, reaching 60%; in the antral and gastric body site, the ulcer perforation develops by 20% [23, 24]. This clinical event is spontaneous. The free perforation in the peritoneal cavity causes upper abdominal pain; typically this pain is sudden, that is, the patient recalls precisely its onset and associates it with what he was doing. The first step of the peritoneal flogosis is a chemical peritonitis due to the gastric and biliopancreatic secretions. However, the reaction of peritoneal serous mitigates the gastroduodenal irritants with the light exudate, and the abdominal pain can ameliorate for a short frame time. This first phase is followed quickly by the return of the severe epigastric and then diffuse abdominal pain. The patient appears very suffering and reduces the movements of the abdominal wall with short breaths and bending off the thighs upward. The objective abdominal examination shows hypomobility of the wall, usually its board-like rigidity; with percussion tympanic sound instead of the normal dullness over the liver, because of the air leaking from the stomach; on auscultation, peristaltic sound is weak or absent. There are also atypical or less typical clinical presentations of peptic ulcer perforations. A small duodenal perforation with a small amount of gastroduodenal secretion flowing out along the right parietocolic douche can simulate acute appendicitis. Anyway in some patients the clinical appearance of perforation can be less pronounced with little symptomatological evidence and possible diagnostic pitfall. Finally, the so-called covered or sealed perforation is possible, due to the closure

#### *Introductory Chapter: Complications of Gastroduodenal Ulcers DOI: http://dx.doi.org/10.5772/intechopen.101478*

by the omentum or by the liver, or also the posterior, retroperitoneal perforation (epiploon retrocavity); these start with discrete clinical symptoms. However, the septic focus is active and usually develops in circumscribed peritonitis, as subhepatic or subdiaphragmatic abscess and also in generalized peritonitis [25, 26]. Within the laboratory findings, there is evidence of leukocytosis, with mild level in the early phases, after some hours more elevated. In the imaging studies, plain X-rays, with patient upright, of the lower chest and the abdomen reveal in most cases (plus than 80%) free subdiaphragmatic air. The clinical and this imaging data allow the diagnosis of ulcer perforation [27]. If the free intrabdominal air cannot be detected, the imaging study may be completed by US and CT. Both these exams can demonstrate also little amount of free air or fluid; the small fluid collection can be detected in the pelvic space. In particular there is evidence of the possible findings of little leaks through perforated ulcer by CT with oral contrast [27]. The early management of perforated peptic ulcer encloses fluid infusion, intravenous proton pump inhibitor, antibiotics with wide antimicrobial activity, and positioning of the nasogastric tube. The central therapeutic role in the peptic ulcer perforation is played by surgery, usually by mini-invasive approach, following one of several procedures of surgical ulcer closure [23, 24, 28]. The altered conditions in the patients with every free perforation are indication to urgent surgery. In the patients with little leaks through perforated ulcer or spontaneous closing of perforation, localized intraperitoneal inflammatory disease and well stable clinical conditions can be performed by nonoperative treatment by nasogastric tube, PPI, and antibiotics. However, the conservative management should allow a quick amelioration, that is, within 24 hours; but any delay in the improvement or also small deterioration of clinical condition requires urgent surgical procedure [29, 30].

## **3.4 Pyloric obstruction**

The stenosis is the less frequent complication of the peptic ulcer, based on the evolution of the disease due to inflammation, edema, muscular spasm, followed by repair process with scaring. The detected frequency ranges between 5 and 8%. In detail, the development of this complication comprises various factors, some functional, other pathological. The functional factors are spasm, pyloric dysmotility, decrease of gastric motility, due to peptic ulcer disease; the pathological factors are inflammation, edema, fibrosis, and finally, scarring and stenosis. The first phase of dysfunction with edema and inflammation causes the reversible gastric obstruction, the following phase of fibrosis and scarring induces the irreversible obstruction [23]. The majority of patients who complain symptoms of gastric outlet obstruction have an history of peptic ulcer disease. The clinical appearance is characterized by anorexia, nausea, early satiety, epigastric pain, vomiting. This long untreated clinical condition is followed by weight loss and deterioration of general condition. A typical symptom is the decreased efficacy of antiacid drugs. This is the clue for the indication of altered acid gastric secretion condition: pyloric obstruction conducts to stasis with increase in the gastric pH, following rise of gastrin issue and overflow of acid secretion. Usually the diagnosis of stenosis and exclusion of malignancy are achieved by endoscopy, endobiopsy, and imaging exams, such as conventional radiography and CT scan. The initial medical management is based on re-establishment of hydroelectrolytic balance and gastric decompression by nasogastric tube for 48–72 hours. In some cases these procedures allow the resumption of oral diet and recovery of nutritional status. There are some studies that report the positive role of the treatment of *H. pylori* infection on the resolution of the outlet obstruction [31]. Also the NSAIDs use has been detected to cause gastropyloric obstruction and the favorable role of drug's suspension on the resolution of complication [32]. The

operative treatment of gastric obstruction includes endoscopic procedures such as balloon dilation and surgical treatment as highly selective vagotomy with pyloroplasty, truncal vagotomy with gastrojejunostomy, or antrectomy.
