Made by DATEXIS (Data Science and Text-based Information Systems) at Beuth University of Applied Sciences Berlin
Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
Funded by The Federal Ministry for Economic Affairs and Energy; Grant: 01MD19013D, Smart-MD Project, Digital Technologies
Stress ulcer is suspected when there is upper gastrointestinal bleeding in the appropriate clinical setting, for example, when there is upper gastrointestinal bleeding in elderly patients in a surgical intensive care unit (ICU) with heart and lung disease, or when there is upper gastrointestinal bleeding in patients in a medical ICU who require respirators.
Stress ulcer can be diagnosed after the initial management of gastrointestinal bleeding, the diagnosis can be confirmed by upper GI endoscopy.
Stable patients presenting to A&E (accident and emergency department) or ER (emergency room) with severe abdominal pain will almost always have an abdominal x-ray and/or a CT scan. These tests can provide a differential diagnosis between simple and complex pathologies. However, in the unstable patient, fluid resuscitation and a FAST-ultrasound are done first, and if the latter is positive for free fluid, straight to surgery. They may also provide evidence to the doctor whether surgical intervention is necessary.
Patients will also most likely receive a complete blood count (or full blood count in the U.K.), looking for characteristic findings such as neutrophilia in appendicitis.
Traditionally, the use of opiates or other painkillers in patients with an acute abdomen has been discouraged before the clinical examination, because these would alter the examination. However, the scientific literature does not reveal any negative results from these alterations.
The most confirmatory investigation is endoscopy of upper gastrointestinal tract.
Laboratory
- Individuals with gastric outlet obstruction are often hypochloremic, hypokalemic, and alkalotic due to loss of hydrogen chloride and potassium. High urea and creatinine levels may also be observed if the patient is dehydrated.
Abdominal X-ray
- A gastric fluid level may be seen which would support the diagnosis.
Barium meal and follow through
- May show an enlarged stomach and pyloroduodenal stenosis.
Gastroscopy
- May help with cause and can be used therapeutically.
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 minimum reaching to the level of the submucosa (contrast with erosions, which do not involve the muscularis mucosae).
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 45 or who has other symptoms such as weight loss, because stomach cancer can cause similar symptoms. 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.
An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on people 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.
One of the reasons that blood tests are not reliable for accurate peptic ulcer diagnosis on their own is their inability to differentiate between past exposure to the bacteria and current infection. Additionally, a false negative result is possible with a blood test if the person has recently been taking certain drugs, such as antibiotics or proton-pump inhibitors.
The diagnosis of "Helicobacter pylori" can be made by:
- Urea breath test (noninvasive and does not require EGD);
- Direct culture from an EGD biopsy specimen; this is difficult to do, and can be expensive. Most labs are not set up to perform "H. pylori" cultures;
- Direct detection of urease activity in a biopsy specimen by rapid urease test;
- Measurement of antibody levels in the blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy;
- Stool antigen test;
- Histological examination and staining of an EGD biopsy.
The breath test uses radioactive carbon to detect H. pylori. To perform this exam the person will be asked to drink a tasteless liquid which contains the carbon as part of the substance that the bacteria breaks down. After an hour, the person will be asked to blow into a bag that is sealed. If the person is infected with H. pylori, the breath sample will contain radioactive carbon dioxide. This test provides the advantage of being able to monitor the response to treatment used to kill the bacteria.
The possibility of other causes of ulcers, notably malignancy (gastric cancer) needs to be kept in mind. This is especially true in ulcers of the "greater (large) curvature" of the stomach; most are also a consequence of chronic "H. pylori" infection.
If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the person stands erect, as when having a chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease.
Other radiological studies frequently used to assess patients with chronic stomach problems include a barium swallow, where a dye is consumed and pictures of the esophagus and stomach are obtained every few minutes. Other tests include a 24-hour pH study, CT scans or MRI.
The differential diagnosis of gastric outlet obstruction may include: early gastric carcinoma hiatal hernia, gastroesophageal reflux, adrenal insufficiency, and inborn errors of metabolism.
The need for medications to prevent stress ulcer among those in the intensive care unit is unclear. As of 2014, the quality of the evidence is poor. It is unclear which agent is best or if prevention is needed at all. Benefit may only occur in those who are not being fed.
Possible agents include antacids, H2-receptor blockers, sucralfate, and proton pump inhibitors (PPIs). Tentative evidence supports that PPIs may be better than H2 blockers.
Concerns with the use of stress ulcer prophylaxis agents include increased rates of pneumonia and "Clostridium difficile" colitis.
A gastric peptic ulcer is a mucosal perforation which penetrates the muscularis mucosae and lamina propria, usually produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows 4 zones: fibrinoid necrosis, inflammatory exudate, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis.
There are many tools for investigating stomach problems. The most common is endoscopy. This procedure is performed as an outpatient and utilizes a small flexible camera. The procedure does require intravenous sedation and takes about 30–45 minutes; the endoscope is inserted via the mouth and can visualize the entire swallowing tube, stomach and duodenum. The procedure also allows the physician to obtain biopsy samples. In many cases of bleeding, the surgeon can use the endoscope to treat the source of bleeding with laser, clips or other injectable drugs.
The diagnosis of hemosuccus pancreaticus can be difficult to make. Most patients who develop bleeding in the gastrointestinal tract have endoscopic procedures done to visualize the bowel in order to find and treat the source of the bleeding. With hemosuccus, the bleeding is coming from the pancreatic duct which enters into the first part of the small intestine, termed the duodenum. Typical gastroscopes used to visualize the esophagus, stomach and duodenum are designed with fiber-optic illumination that is directed in the same direction as the endoscope, meaning that visualization is in the forward direction. However, the pancreatic duct orifice is located on the side of the duodenum, meaning that it can be missed on forward-viewing endoscopy. A side-viewing endoscope (known as a "duodenoscope", or "side-viewer") used for endoscopic retrograde cholangiopancreatography (ERCP), a procedure to visualize the bile ducts and pancreatic duct on fluoroscopy, can be used to localize the bleeding to the pancreatic duct. It can be confused with bleeding from the common bile duct on endoscopy, leading to the term "pseudohematobilia".
Liver function test is normal apart from an increased serum bilirubin in the event of pancreaticobiliary reflux. Serum amylase is normal outside episodes of acute pancreatitis. It is difficult to diagnose HP because the bleeding is usually intermittent. Endoscopy is essential in ruling out other causes of upper gastrointestinal bleeding and in rare cases; active bleeding can be seen from the duodenal ampulla. Even though endoscopy may be normal, it helps to rule out other causes of upper digestive bleeding (erosive gastritis, peptic ulcers, and oesophageal and gastric fundus varices, etc.). Ultrasonography can be used to visualize pancreatic pseudocysts or aneurysm of the peripancreatic arteries. Doppler ultrasound or dynamic ultrasound has been reported to be diagnostic. Contrast-enhanced CT is an excellent modality for demonstrating the pancreatic pathology and can also demonstrate features of chronic pancreatitis, pseudocysts, and pseudoaneurysms. On precontrast CT, the characteristic finding of clotted blood in the pancreatic duct, known as the sentinel clot, is seldom seen. Computed tomography may show simultaneous opacification of an aneurysmal artery and pseudocyst or persistence of contrast within a pseudocyst after the arterial phase. Again, these findings are only suggestive of the diagnosis. Ultimately, angiography is the diagnostic reference standard. Angiography identifies the causative artery and allows for delineation of the arterial anatomy and therapeutic intervention.
Often, a diagnosis can be made based on the patient's description of their symptoms, but other methods which may be used to verify gastritis include:
- Blood tests:
- Blood cell count
- Presence of "H. pylori"
- Liver, kidney, gallbladder, or pancreas functions
- Urinalysis
- Stool sample, to look for blood in the stool
- X-rays
- ECGs
- Endoscopy, to check for stomach lining inflammation and mucous erosion
- Stomach biopsy, to test for gastritis and other conditions
People under 55 years without alarm symptoms can be treated without investigation. People over 55 years with recent onset dyspepsia or those with alarm symptoms should be urgently investigated by upper gastrointestinal endoscopy. This will rule out peptic ulcer disease, medication-related ulceration, malignancy and other rarer causes.
People under the age of 55 years with no alarm features do not need endoscopy but are considered for investigation for peptic ulcer disease caused by "Helicobacter pylori" infection. Investigation for "H. pylori" infection is usually performed when there is a moderate to high prevalence of this infection in the local community or the person with dyspepsia has other risk factors for "H. pylori" infection, related for example to ethnicity or immigration from a high-prevalence area. If infection is confirmed, it can usually be eradicated by medication.
Medication-related dyspepsia is usually related to NSAIDs and can be complicated by bleeding or ulceration with perforation of stomach wall.
Treatment of hemosuccus pancreaticus depends on the source of the hemorrhage. If the bleeding is identified on angiography to be coming from a vessel that is small enough to occlude, embolization through angiography may stop the bleeding. Both coils in the end-artery and stents across the area of bleeding have been used to control the hemorrhage. However, the bleeding may be refractory to the embolization, which would necessitate surgery to remove the pancreas at the source of hemorrhage. Also, the cause of bleeding may be too diffuse to be treated with embolization (such as with pancreatitis or with pancreatic cancer). This may also require surgical therapy, and usually a distal pancreatectomy, or removal of the part of the pancreas from the area of bleeding to the tail, is required.
A perforated ulcer, is a condition in which untreated ulcer can burn through the wall of the stomach (or other areas of the gastrointestinal tract), allowing digestive juices and food to leak into the abdominal cavity. Treatment generally requires immediate surgery. The ulcer is known initially as a peptic ulcer before the ulcer burns through the full thickness of the stomach or duodenal wall. A diagnosis is made by taking an erect abdominal/chest X-ray (seeking air under the diaphragm). This is in fact one of the very few occasions in modern times where surgery is undertaken to treat an ulcer. Many perforated ulcers have been attributed to the bacterium "Helicobacter pylori". The incidence of perforated ulcer is steadily declining, though there are still incidents where it occurs. Causes include smoking and nonsteroidal anti-inflammatory drugs (NSAIDs). A perforated ulcer can be grouped into a stercoral perforation which involves a number of different things that causes perforation of the intestine wall. The first symptom of a perforated peptic ulcer is usually sudden, severe, sharp pain in the abdomen. The experience is typically so intense that most people precisely recall the exact moment the pain began. The pain is typically at its maximum immediately and persists. It is characteristically made worse by any movement, and greatly intensifies with coughing or sneezing.
A diagnosis of peritonitis is based primarily on the clinical manifestations described above. Rigidity (involuntary contraction of the abdominal muscles) is the most specific exam finding for diagnosing peritonitis (+ likelihood ratio: 3.9). If peritonitis is strongly suspected, then surgery is performed without further delay for other investigations. Leukocytosis, hypokalemia, hypernatremia, and acidosis may be present, but they are not specific findings. Abdominal X-rays may reveal dilated, edematous intestines, although such X-rays are mainly useful to look for pneumoperitoneum, an indicator of gastrointestinal perforation. The role of whole-abdomen ultrasound examination is under study and is likely to expand in the future. Computed tomography (CT or CAT scanning) may be useful in differentiating causes of abdominal pain. If reasonable doubt still persists, an exploratory peritoneal lavage or laparoscopy may be performed. In patients with ascites, a diagnosis of peritonitis is made via paracentesis (abdominal tap): More than 250 polymorphonucleate cells per μL is considered diagnostic. In addition, Gram stain is almost always negative, whereas culture of the peritoneal fluid can determine the microorganism responsible and determine their sensitivity to antimicrobial agents.
The symptoms due to bleeding are hematemesis and/or melena.
A Dieulafoy's lesion is difficult to diagnose, because of the intermittent pattern of bleeding. Endoscopically it is not easy to recognize and therefore sometimes multiple views have to be performed over a longer period. Today angiography is a good additional diagnostic, but then it can only be seen during a bleeding at that exact time.
Hematemesis is treated as a medical emergency. The most vital distinction is whether there is blood loss sufficient to cause shock.
In predicting the prognosis, there are several scoring indices that have been used as predictors of survival. Two such scoring systems are the Ranson criteria and APACHE II (Acute Physiology and Chronic Health Evaluation) indices. Most, but not all studies report that the Apache score may be more accurate. In the negative study of the APACHE-II, the APACHE-II 24-hour score was used rather than the 48-hour score. In addition, all patients in the study received an ultrasound twice which may have influenced allocation of co-interventions. Regardless, only the APACHE-II can be fully calculated upon admission. As the APACHE-II is more cumbersome to calculate, presumably patients whose only laboratory abnormality is an elevated lipase or amylase do not need assessment with the APACHE-II; however, this approach is not studied. The APACHE-II score can be calculated at www.sfar.org.
Practice guidelines state:
Stercoral ulcer is an ulcer of the colon due to pressure and irritation resulting from severe, prolonged constipation due to large bowel obstruction. It is most commonly located in the rectum. Individuals with this condition are at risk for stercoral perforation.
The Ranson criteria are a clinical prediction rule for predicting the severity of acute pancreatitis. They were introduced in 1974.
Vascular disorders are more likely to affect the small bowel than the large bowel. Arterial supply to the intestines is provided by the superior and inferior mesenteric arteries (SMA and IMA respectively), both of which are direct branches of the aorta.
The superior mesenteric artery supplies:
1. Small bowel
2. Ascending and proximal two-thirds of the transverse colon
The inferior mesenteric artery supplies:
1. Distal one-third of the transverse colon
2. Descending colon
3. Sigmoid colon
Of note, the splenic flexure, or the junction between the transverse and descending colon, is supplied by the most distal portions of both the inferior mesenteric artery and superior mesenteric artery, and is thus referred to medically as a watershed area, or an area especially vulnerable to ischemia during periods of systemic hypoperfusion, such as in shock.
Acute abdomen of the ischemic variety is usually due to:
1. A thromboembolism from the left side of the heart, such as may be generated during atrial fibrillation, occluding the SMA.
2. Nonocclusive ischemia, such as that seen in hypotension secondary to heart failure, may also contribute, but usually results in a mucosal or mural infarct, as contrasted with the typically transmural infarct seen in thromboembolus of the SMA.
3. Primary mesenteric vein thromboses may also cause ischemic acute abdomen, usually precipitated by hypercoagulable states such as polycythemia vera.
Clinically, patients present with diffuse abdominal pain, bowel distention, and bloody diarrhea. On physical exam, bowel sounds will be absent. Laboratory tests reveal a neutrophilic leukocytosis, sometimes with a left shift, and increased serum amylase. Abdominal radiography will show many air-fluid levels, as well as widespread edema.
Acute ischemic abdomen is a surgical emergency. Typically, treatment involves removal of the region of the bowel that has undergone infarction, and subsequent anastomosis of the remaining healthy tissue.
In normal conditions, the peritoneum appears greyish and glistening; it becomes dull 2–4 hours after the onset of peritonitis, initially with scarce serous or slightly turbid fluid. Later on, the exudate becomes creamy and evidently suppurative; in dehydrated patients, it also becomes very inspissated. The quantity of accumulated exudate varies widely. It may be spread to the whole peritoneum, or be walled off by the omentum and viscera. Inflammation features infiltration by neutrophils with fibrino-purulent exudation.
Functional and undifferentiated dyspepsia have similar treatments. Drug therapy decisions are difficult because trials included heartburn in the definition of dyspepsia. This led to the results favoring proton pump inhibitors (PPIs), which are effective for the treatment of heartburn.
Traditional therapies used for this diagnosis include lifestyle modification, antacids, H-receptor antagonists (H2-RAs), prokinetic agents, and antiflatulents. It has been noted that one of the most frustrating aspects of treating functional dyspepsia is that these traditional agents have been shown to have little or no efficacy.
If this is not the case, the patient is generally administered a proton pump inhibitor (e.g. omeprazole), given blood transfusions (if the level of hemoglobin is extremely low, that is less than 8.0 g/dL or 4.5–5.0 mmol/L), and kept NPO, which stands for "nil per os" (Latin for "nothing by mouth", or no eating or drinking) until endoscopy can be arranged. Adequate venous access (large-bore cannulas or a central venous catheter) is generally obtained in case the patient suffers a further bleed and becomes unstable.
Antacids are a common treatment for mild to medium gastritis. When antacids do not provide enough relief, medications such as H blockers and proton-pump inhibitors that help reduce the amount of acid are often prescribed.
Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine. They include the medications sucralfate and misoprostol. If NSAIDs are being taken regularly, one of these medications to protect the stomach may also be taken. Another cytoprotective agent is bismuth subsalicylate.
Several regimens are used to treat "H. pylori" infection. Most use a combination of two antibiotics and a proton pump inhibitor. Sometimes bismuth is added to the regimen.