Diagnosis and treatment of perforated or bleeding peptic ulcers: 2013 WSES position paper. Peptic ulcer disease (PUD), also known as a peptic ulcer or stomach ulcer, is a break in the lining of the stomach, first part of the small intestine, or occasionally. OBJECTIVE: The authors' initial experience with laparoscopic omental patch repair for perforated peptic ulcer is documented. Its results are compared with. Patients with perforated peptic ulcer (PPU) often present with acute, severe illness that carries a high risk for morbidity and mortality. Mortality ranges from 3-40%.
Perforated Duodenal Ulcer Pdf To Excel
Research from JAMA Surgery — Perforated Duodenal Ulcer — An Alternative Therapeutic Plan. A perforated ulcer, is a condition where an untreated ulcer can burn through the wall of the stomach (or other areas of the gastrointestinal tract), allowing. Summary. Perforated peptic ulcer is a common emergency condition worldwide, with associated mortality rates of up to 30%. A scarcity of high-quality studies about the.
Scoring systems for outcome prediction in patients with perforated peptic ulcer | Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. Ten different scoring systems (Table.
PPU patients were identified, including the Boey score[1. Hacettepe score[1. Jabalpur score[1. Peptic Ulcer Perforation (PULP) score[1. American Society of Anesthesiologists (ASA) score[2. Charlson comorbidity index[2. Mannheim Peritonitis Index (MPI)[2.
Acute Physiology and Chronic Health Evaluation II (APACHE II)[2. Simplified Acute Physiology Score II (SAPS II)[2. Mortality Probability Models II (MPM II)[2. Physiological and Operative Severity Score for the enumeration of Mortality and Morbidity physical sub- score (POSSUM- phys score)[2. In five studies, comparison of various scoring systems for outcome prediction was done by ROC- analyses with reporting on the area under the curve (AUC)[1. A few studies presented specificity and sensitivity, relative risks (RR) and odds ratios (OR), while most studies reported on performance by calculation of the chi square test. Table 1. Scoring systems used for outcome prediction in perforated peptic ulcer.
Boey[1. 4]1. 98. 7Patients with PPU3. Presentation ≥ or < 2. Hacettepe score[1. Patients with PPU3. Presence of serious medical illness, acute renal failure, white blood cell count, male gender. Jabalpur score[1.
Patients with PPU3. Time from perforation to operation, mean systolic blood pressure preoperatively, heart rate, serum creatinine, age, comorbidity.
PULP[1. 9]2. 01. 2Patients with PPU3. Presentation ≥ or < 2. ASA score, presence of aids, active malignancy, liver failure; serum creatinine >  1. ASA[2. 0]1. 94. 1General surgical populations. Preoperative risk assessment for surgical patients.
Degree of comorbidity and present systemic disease. Charlson comorbidity index[2. General surgical populations. Prediction of 1 year mortality for hospitalized patients. Weighting of different comorbidities. Mannheim peritonitis index[2.
General peritonitis. Peroperative prediction of outcome in patients with peritonitis. Age, gender, organ failure, duration of peritonitis, site of perforation, diffuse peritonitis, level of exudate. APACHE II[2. 4]1.
Critically ill patients. Prediction of outcome for ICU patients. Aids, metastatic cancer, liver failure, immunosuppression, chronic renal insufficiency, haemotologic malignancy, lymphoma, leukemia, age, heart rate, systolic blood pressure, respiratory rate, temperature, GCS, WBC, creatinine, blood gas, potassium, sodium, patient origin. SAPS II[2. 5]1. 99. Critically ill patients. Prediction of outcome for ICU patients.
Aids, metastatic cancer, haemotologic malignancy, age, heart rate, systolic blood pressure, temperature, GCS, urine output, WBC, bilirubin, urea, Potassium, sodium, Patient origin. MPM II[2. 6]1. 99. Critically ill patients. Prediction of outcome for ICU patients. Metastatic cancer, liver failure, chronic renal insufficiency, leukemia, age, acute renal failure, arrythmias, heart rate, GI bleeding, GCS, intracranial mass effect, cerebrovascular accident, cpr prior to admission, mechanical ventilation.
POSSUM[3. 7]1. 99. Surgical patients. Prediction of outcome (mortality) for surgical patients. Respiratory history; cardiac signs; age; heart rate; systolic blood pressure; ecg; GCS; operative severity; multiple procedures, total blood loss, peritoneal soiling, finding of peroperative malignancy; elective or acute surgery, WBC, Hb, urea, potassium, sodium.
Scoring systems aimed at prediction of outcome in PPUThe Boey score was the first score directly aimed at mortality prediction for perforated peptic ulcer[1. The original work by Boey et al stated that delay of surgery after onset of symptoms for more than 4. Eventually, the delay of surgery was adjusted to 2. Hong Kong[1. 4, 2. The Hacettepe score was also developed for PPU patients and comprises four factors (Table. This study evaluated 1.
Turkey and found the Hacettepe score to be equivalent to the Mannheim Peritonitis Index (MPI), with a sensitivity of 8. The sensitivity for the MPI in this study was 7. Eventually, this score was used in a study from India, as elaborated below[1. The Jabalpur score was based on a study on 1.
India, with a mean age of 3. This score takes into account six factors, which are all assessable preoperatively.
Both morbidity and mortality were predicted accurately, based on a high AUC value (Table. Table 2. Scoring accuracy of mortality prediction in PPU patients. ASA 0. 9. 1 0. 7. Boey. 0. 8. 50. 8. Apache II 0. 8. 7 0.
SAPS II 0. 8. 6 MPM II 0. Hacateppe score. 0. Jabalpur score. 0. MPI 0. 8. 4 Modified Apache II0. Modified MPI0. 8. PULP 0. 8. 3 Sepsis score 0.
Most recently, the Peptic Ulcer Perforation (PULP) score has been introduced as a scoring system for perforated peptic ulcer. This score is based on a nationwide study from Denmark and included 2. PPU patients with a median age of 7. Seven factors are taken into account, with weighted points applicable for each factor, with a maximum sum of 1. The optimal cut- off point was found to be 7 points, which gives a positive predictive value (PPV) of 2. PPV of 3. 8% for the group with 8 or more points[1. The PULP study also compared different systems elaborated below.
General scores of comorbidity. The ASA score introduced in 1. ASA score is frequently reported together with other descriptive patient data including age, gender, and various physiologic parameters, but this classification has no specific role in outcome prediction of patients with PPU per se.
The Charlson comorbidity index was developed to stratify comorbidity into different risk groups by assigning scores to various illnesses[2. The Charlson index is a widely used scoring system and considers 1. Cerebrovascular disease is given 1 point, severe liver disease 3 points and metastatic cancer and AIDS are given 6 points.
The Charlson index was initially suggested for prediction of long- term mortality. However, later studies have found it to be useful also in prediction of in- hospital morbidity and mortality[3. One study also used the Charlson comorbidity index to predict outcome in PPU patients. A highly significant association between a medium or high Charlson score and 3.
OR) of 4. 1. 7 for high score (3 or more points on the Charlson score) and an OR of 3. Charlson score)[3. However, identification of any other PPU studies to confirm the obtained results by use of this particular score was not possible. The Sepsis criteria are easy to calculate preoperatively and the presence of sepsis is fulfilled if two or more of the following parameters are present, when infection is confirmed or highly likely; temperature > 3. °C or < 3. 6°C respiratory rate >  2. PCO2 <  4. Pa, heart rate >  9.
White cell count >  1. ×1. 09 or <  4. ×1. 09[3. 3]. Obviously this system is widely used in several aspects of medicine, but has also been applied to predict outcome in a PPU cohort, as elaborated below[2. The Mannheim Peritonitis Index (MPI) consists of seven factors that are more directly related to the operative findings. As the name implies, the design was specifically intended for surgical patients presenting with peritonitis.
It comprises both preoperative and perioperative conditions, and has been found to predict morbidity well, but less so in prediction of mortality for PPU patients[1. Intensive care unit (ICU) systems. The Acute physiology and chronic health evaluation II (APACHE II) score is a common score globally and the most used ICU scoring system in the USA. It comprises twelve different physiological measurements, age and previous health status, and was originally designed to categorize ICU patients according to risk. The system gives an increasing amount of points for extreme values (high or low), between 0 (3. °C - 3. 8. 4. °C) and 4 (≥4.
°C and ≤2. 9. 9. °C). Originally this score was found to perform well amongst ICU patients[2. Later, it was also applied to predict outcome in PPU patients. One study from the USA[3. PPU patients with scores less than 1. Others have tried different cut- off values without finding these to be more useful.
However the APACHE II score is a rather complex system needing mathematical equations to calculate and a minimum of 2. This may pose implications and concerns for its clinical usefulness and availability. Nevertheless, APACHE II has been shown to predict outcome well also for PPU patients[1. The Simplified acute physiology score II (SAPS II) is designed for predicting outcome in ICU patients and consists of 1. It was developed in the 8.
The SAPS II system is frequently used for outcome prediction in critically ill patients in Europe and Scandinavia, and has many similarities with the APACHE II system[2. Both systems are rather complex, with a number of factors incorporated in the calculations, including physiologic parameters. The SAPS II system predicts mortality and morbidity well, but also seems more suitable for ICU patients. Nevertheless, this score performed well for outcome prediction of PPU patients[1.
The Mortality probability models II (MPM II) was designed for prediction of outcome in ICU patients. MPM II assesses the presence or not of 1. The MPM II predicted mortality better then both SAPS II and APACHE II in one study[1. However this study was rather small and skewed with basically younger male patients, which is in contrast to current PPU cohorts. While some studies from Asia and Africa have presented similar patient characteristics[3. Scandinavia and Northern Europe have presented data with a 1: 1 male/female ratio and median age close to 7. Moreover, the MPM II is a rather complex system, thus suboptimal for a pre- operative calculation in the clinical context PPU patients present.
The Physiological and Operative Severity Score for Enumeration of Mortality and Morbidity (POSSUM score) consists of 1. These factors are then entered into two mathematical equations for risk assessment[3.
Peptic ulcer - Wikipedia, the free encyclopedia. Peptic ulcer disease (PUD), also known as a peptic ulcer or stomach ulcer, is a break in the lining of the stomach, first part of the small intestine, or occasionally the lower esophagus.[1][2] An ulcer in the stomach is known as a gastric ulcer while that in the first part of the intestines is known as a duodenal ulcer. The most common symptoms are waking at night with upper abdominal pain or upper abdominal pain that improves with eating. The pain is often described as a burning or dull ache. Other symptoms include belching, vomiting, weight loss, or poor appetite. About a third of older people have no symptoms.[1] Complications may include bleeding, perforation, and blockage of the stomach. Bleeding occurs in as many as 1.
Common causes include the bacteria, Helicobacter pylori and non- steroidal anti- inflammatory drugs (NSAIDs).[1] Other less common causes include tobacco smoking, stress due to serious illness, Behcet disease, Zollinger- Ellison syndrome, Crohn disease and liver cirrhosis, among others.[1][4] Older people are more sensitive to the ulcer causing effects of NSAIDs. The diagnosis is typically suspected due to the presenting symptoms with confirmation by either endoscopy or barium swallow.
H. pylori can be diagnosed by testing the blood for antibodies, a urea breath test, testing the stool for signs of the bacteria, or a biopsy of the stomach. Other conditions that produce similar symptoms include stomach cancer, coronary heart disease, and inflammation of the stomach lining or gallbladder.[1]Diet does not play an important role in either causing or preventing ulcers.[5] Treatment includes stopping smoking, stopping NSAIDs, stopping alcohol, and medications to decrease stomach acid. The medication used to decrease acid is usually either a proton pump inhibitor (PPI) or an H2 blocker with four weeks of treatment initially recommended.[1] Ulcers due to H. PPI. Antibiotic resistance is increasing and thus treatment may not always be effective.[6] Bleeding ulcers may be treated by endoscopy, with open surgery typically only used in cases in which it is not successful.[3]Peptic ulcers are present in around 4% of the population.[1] They newly began in around 5. About 1. 0% of people develop a peptic ulcer at some point in their life.[8] They resulted in 3. The first description of a perforated peptic ulcer was in 1. Princess Henrietta of England.[3]H.
Barry Marshall and Robin Warren in the late 2. Nobel Prize in 2. Signs and symptoms[edit]Signs and symptoms of a peptic ulcer can include one or more of the following: abdominal pain, classically epigastric strongly correlated to mealtimes. In case of duodenal ulcers the pain appears about three hours after taking a meal; bloating and abdominal fullness; waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus - although this is more associated with gastroesophageal reflux disease); nausea, and copious vomiting; loss of appetite and weight loss; hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcer, or from damage to the esophagus from severe/continuing vomiting. A history of heartburn, gastroesophageal reflux disease (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer include NSAIDs (non- steroid anti- inflammatory drugs) that inhibit cyclooxygenase, and most glucocorticoids (e.
In patients over 4. The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers: A gastric ulcer would give epigastric pain during the meal, as gastric acid production is increased as food enters the stomach. Symptoms of duodenal ulcers would initially be relieved by a meal, as the pyloric sphincter closes to concentrate the stomach contents, therefore acid is not reaching the duodenum. Duodenal ulcer pain would manifest mostly 2–3 hours after the meal, when the stomach begins to release digested food and acid into the duodenum. Also, the symptoms of peptic ulcers may vary with the location of the ulcer and the patient's age.
Furthermore, typical ulcers tend to heal and recur and as a result the pain may occur for few days and weeks and then wane or disappear.[1. Usually, children and the elderly do not develop any symptoms unless complications have arisen. Burning or gnawing feeling in the stomach area lasting between 3. This pain can be misinterpreted as hunger, indigestion or heartburn. Pain is usually caused by the ulcer but it may be aggravated by the stomach acid when it comes into contact with the ulcerated area.
The pain caused by peptic ulcers can be felt anywhere from the navel up to the sternum, it may last from few minutes to several hours and it may be worse when the stomach is empty. Also, sometimes the pain may flare at night and it can commonly be temporarily relieved by eating foods that buffer stomach acid or by taking anti- acid medication.[1. However, peptic ulcer disease symptoms may be different for every sufferer.[1.
Complications[edit]Gastrointestinal bleeding is the most common complication. Sudden large bleeding can be life- threatening.[1.
It occurs when the ulcer erodes one of the blood vessels, such as the gastroduodenal artery. Perforation (a hole in the wall of the gastrointestinal tract) often leads to catastrophic consequences if left untreated. Erosion of the gastro- intestinal wall by the ulcer leads to spillage of stomach or intestinal content into the abdominal cavity.
Perforation at the anterior surface of the stomach leads to acute peritonitis, initially chemical and later bacterial peritonitis. The first sign is often sudden intense abdominal pain; an example is Valentino's syndrome, named after the silent- film actor who experienced this pain before his death. Posterior wall perforation leads to bleeding due to involvement of gastroduodenal artery that lies posterior to the 1st part of duodenum. Penetration is a form of perforation in which the hole leads to and the ulcer continues into adjacent organs such as the liver and pancreas.[1. Gastric outlet obstruction is the narrowing of pyloric canal by scarring and swelling of gastric antrum and duodenum due to peptic ulcers. Patient often presents with severe vomiting without bile. Cancer is included in the differential diagnosis (elucidated by biopsy), Helicobacter pylori as the etiological factor making it 3 to 6 times more likely to develop stomach cancer from the ulcer.[1.
H. pylori[edit]A major causative factor (6. Helicobacter pylori that colonizes the antralmucosa.[1. The immune system is unable to clear the infection, despite the appearance of antibodies.
Thus, the bacterium can cause a chronic active gastritis (type B gastritis). Gastrin stimulates the production of gastric acid by parietal cells. In H. pylori colonization responses to increased gastrin, the increase in acid can contribute to the erosion of the mucosa and therefore ulcer formation.
Another major cause is the use of NSAIDs. The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox- 1), which is essential for the production of these prostaglandins. COX- 2 selective anti- inflammatories (such as celecoxib or the since withdrawn rofecoxib) preferentially inhibit cox- 2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID- related gastric ulceration. Stress due to serious health problems such as those requiring treatment in an intensive care unit is well described as a cause of peptic ulcers, which are termed stress ulcers.[4]While chronic life stress was once believed to be the main cause of ulcers, this is no longer the case.[1.
It is, however, still occasionally believed to play a role.[1. This may be by increasing the risk in those with other causes such as H. NSAID use.[1. 9]Dietary factors such as spice consumption, were hypothesized to cause ulcers until late in the 2. Caffeine and coffee, also commonly thought to cause or exacerbate ulcers, appear to have little effect.[2. Similarly, while studies have found that alcohol consumption increases risk when associated with H.
Even when coupled with H. Although some studies have found correlations between smoking and ulcer formation,[2.
H. pylori infection.[2. Gastrinomas (Zollinger–Ellison syndrome), rare gastrin- secreting tumors, also cause multiple and difficult- to- heal ulcers. Diagnosis[edit]. Endoscopic image of gastric ulcer, biopsy proven to be gastric cancer.
The diagnosis is mainly established based on the characteristic symptoms. Stomach pain is usually the first signal of a peptic ulcer. In some cases, doctors may treat ulcers without diagnosing them with specific tests and observe whether the symptoms resolve, thus indicating that their primary diagnosis was accurate. More specifically, peptic ulcers erode the muscularis mucosae, at least to the level of the submucosa (contrast with erosions, which do not involve the muscularis mucosae).[2. Confirmation of the diagnosis is made with the help of tests such as endoscopies or barium contrast x- rays. The tests are typically ordered if the symptoms do not resolve after a few weeks of treatment, or when they first appear in a person who is over age 4.
Also, when severe ulcers resist treatment, particularly if a person has several ulcers or the ulcers are in unusual places, a doctor may suspect an underlying condition that causes the stomach to overproduce acid.[1. An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described.
Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.