gastric perforation

INTRODUCTION

Gaster is a part of the gastrointestinal tract that is located between the esophagus and duodenum. In anatomy consists of gastric cardia, fundus, corpus, antrum and pylorus.
Gastric ulcers can be divided into three classifications based Daintree kaegori Johnson`n, namely:

     Type I: Gastric ulcer on the lesser curvature
     Type II: The combination of gastric ulcer and duodenal ulcer
     Type III: Ulcers prepylori

Type 1, or primary, characterized ulcers located on the lesser curvature in the relationship between the fundus and antruum, occurs in older patients and is rarely associated with type hiposekresi stomach acid.

Type 2, or a combination, duodenal ulcers and gastric lesions in the lesser curvature that occurs in conjunction with duadenal ulcer disease is active or silent
Ulcer type 3 is on prepylorik
Mortality and morbidity
There are several factors that affect mortality and morbidity in the state of gastric perforation, such as:
· Shock at the time of hospital admission
· Comorbid disease
· Late surgery (over> 24 hours)
· Operation of gastric resection
· Postoperative infections and surgical wound infections
Fungus Infection on peritoneal
· To assess mortality and morbidity, there are several scores that can be used include the SCORE Boey (1982)

risk factors					score
Old perforation					0
<24 hours					1
> 24 hours					0
Preoperative systolic blood pressure					1
> 100 mmHg					0
<100 mmHg					1
Systemic disease (heart, kidney, lung, diabetes, etc.)
there is
None
The total score		The risk of morbidity
1		0%
2		10 – 46 %
3		100%

Pathophysiology
Helicobacter pylori infection and the use of non-steroidal anti-inflammatory are the two main factors in the pathogenesis of peptic ulcer. H. pylori infection occurs in 76% of cases and 90% of gastric ulcers occur in cases of duodenal ulcer. Other factors that also play a role is the use of steroids, smoking, alcohol or coffee, stress, and others.
Disease or condition associated with increased risk factors for gastric ulcers is cirrhosis, chronic lung disease, renal failure and kidney transplantation.
Pathophysiology of H. pylori infection remains unclear. The mechanisms through which H. pylori is now known to trigger the formation of ulcers include stimulation of the release of gastrin, vagal reflex inhibition interruption, inhibition of gastrin release, and inhibition of bicarbonate secretion gastroduadenal.
Recent studies confirm the association between NSAID ulcers peptikim. Improvement of gastrointestinal complications due to these drugs can be achieved through consultations provided to patients to limit or stop the use, concurrent use of other drugs to minimize the side effects on the gastrointestinal tract (eg antibiotics for H.pylori, prostaglandins, and anti secretion), and the selection of NSAID drugs that have minimal side effects most of the gastrointestinal tract in patients who have an increased risk of peptic ulcer complications. Peptic ulcers usually occur when mucosal damage is more or equal to 3 mm (Levine, 2000)
CLINICAL SYMPTOMS
Symptoms vary, typically jekas limitless pain occurs and occurs 30 minutes to 3 hours, or less than 2 hours after a meal, is located in the epigastrium, such as burning. But pain can also be felt in the right upper quadrant of the abdomen, chest or back. Anorexia, weight loss, nausea, chest burning possibilities may also occur. Vomiting associated with obstruction occurring, either partial or complete. Hematemasis or melena is a manifestation of gastrointestinal bleeding.
Physical examination found in incomplete gastric ulcers are not specific. The prisoners on the epigastrium can be found. Melena was found in acute gastrointestinal bleeding and subacute. If a perforated gastric ulcer occurs it will be acute peritonitis, where the patient looks great pain, such as feeling stabbed in the stomach. Sudden onset of pain, especially in the epigastric aderah because peritoneal stimulation by gastric acid, bile or pancreatic enzymes. Gastric fluid into the winding parakolika mengakir right, cause lower right abdominal pain, then mnyebar throughout the abdomen.
In early perforation no bacterial infection, called peritonitis phase chemistry. The presence of pain in the shoulder showed peritoneal stimulation below the diaphragm. Peritoneal stimulation defans cause tenderness and muscular. Liver dullness may disappear as a result of free air under the diaphragm. Decreased intestinal peristalsis to disappear due to temporary paralysis of the bowel. If there has been a bacterial peritonitis, body temperature will rise, tachycardia, hypotension, and lethargy.
Stimulation of peritoneal cause pain in every movement that causes a shift in the peritoneum. Subjective pain sufferers of pain at the time of moving, like walking, breathing, coughing, and straining. Pain objective of pain if moved as palpation, rebound tenderness, rectal, test psoas, obturator tests and others.
MANAGEMENT
Principles of antibiotic treatment of peptic ulcers are H. pylori gastritis, the use of antacids, H2 antagonists and reassessment to determine recovery after 6-8 weeks. Indications of surgery if gastric ulcer near the pylorus and kenaikann related to gastric acid, gastric acid if the elevation does not happen performed partial gastrectomy. In perforation or bleeding gastrectomy can also be selected if the resection was not possible because the patient's condition
COMPLICATIONS
Bleeding occurs in 20-30% of gastric ulcers, endoscopy is an option with a sensitivity of> 90%. Double-contrast barium can be used in 75% of cases. Filling defect caused by a blood clot can be seen at the base of the contrast-filled ulcer.
Gastric obstruction occurred in 5% of cases, is more common in duodenal ulcer, but may also occur in antral ulcer perforation or canell pylori occurred in 10% of peptic ulcer. Most are from the anterior duodenal perforation.