Week 13: GI part 1/3: Esophagus & Stomach

This patient is presenting with Boerhaave’s syndrome, which refers to esophageal rupture, usually due to forceful vomiting resulting in a full-thickness tear. Patients present with severe, persistent chest pain. Subcutaneous emphysema may be present on physical examination. In patients with mediastinal emphysema, mediastinal crackling with each heartbeat may be heard on auscultation. This is known as Hamman’s sign. Chest X-ray findings may include a left pneumothorax, a left pleural effusion, mediastinal emphysema, and a widened mediastinum. Diagnosis should be confirmed with an esophagram using water-soluble oral contrast. Emergent surgical consult should be obtained and broad-spectrum antibiotics should be started. Because significant morbidity and mortality occur very rapidly due to sepsis, it is necessary to determine early whether the patient is a surgical candidate. Patients with free perforation likely require emergency surgery, whereas stable patients with a contained perforation may be able to be managed with intravenous antibiotics and maintaining NPO status.
Because Boerhaave’s syndrome is a surgical emergency, surgical consultation should not be delayed to obtain a CT chest with IV contrast (A). Endoscopy (C) could help in diagnosing Boerhaave’s syndrome, but could also worsen the perforation. Therefore, endoscopy is not indicated, and surgical evaluation should be immediate. Nasogastric tube placement (D) is contraindicated with esophageal tears and should be avoided.

The X-ray demonstrates a foreign body in the esophagus that should be removed under direct visualization by an endoscopist. Pediatric patients account for 75% of all ingestions with coins being the most commonly ingested foreign body. The esophagus has four natural areas where it narrows and these are the most likely places for foreign bodies to become stuck. The four areas are at the upper esophageal sphincter, the aortic arch, the left main stem bronchus and the lower esophageal sphincter. Patients are often asymptomatic on presentation if the foreign body is in the esophagus. Anteroposterior and lateral X-rays of the neck and chest should be performed. An esophageal coin can be differentiated from a tracheal coin on X-ray based on orientation. Coins will appear “en face” on anteroposterior X-ray if they are in the esophagus.
Removal under direct laryngoscopy (A) is not recommended as the coin is too deep to be reached this way. Removal with a Foley catheter (C) may be effective in esophageal foreign bodies. If the coin remains in the esophagus, it should be removed and not observed for passage (D).

This patient presents with a perforated peptic ulcer requiring evaluation for emergent surgery. Perforation is one of the serious complications of peptic ulcer disease in addition to hemorrhage and gastric outlet obstruction. Up to 10% of patients with ulcers can develop perforation and it most commonly occurs in the anterior wall of the duodenum. Perforation typically presents with an acute onset of severe abdominal pain and should be preceded by symptoms consistent with peptic ulcer disease (burning or gnawing pain). The acute pain often radiates to the back and the patient may experience referred pain to the shoulder as a result of air sitting under the diaphragm. Upright chest X-ray and abdominal X-ray with decubitus views will often, but not always, show pneumoperitoneum. This finding should prompt immediate surgical consultation as the patient will require operative management.

Clarithromycin, amoxicillin and a proton-pump inhibitor (A) can be used to treat H. pylori. A CT scan of the abdomen and pelvis (B) is helpful in a patient with symptoms suggestive of perforation and negative plain radiographs. Ultrasound of the right upper quadrant (D) is useful in the diagnosis of biliary pathology.

Esophageal varices are dilated veins in the esophagus that result from increased pressure in the portal system usually secondary to liver cirrhosis. They are diagnosed with esophagogastroduodenoscopy and have an increased risk of bleeding. Variceal rupture can cause massive hemorrhaging and be acutely life threatening. The immediate treatment of acute variceal hemorrhage is volume resuscitation, intubation for airway protection if needed, and correction of any underlying coagulopathy. Beyond the immediate resuscitation, there are several pharmacologic treatments for variceal bleeding. However, ceftriaxone and IV antibiotics have shown to decrease mortality by reducing the infectious complications. It is common for patients with variceal bleeding to have concomitant bacterial infections from translocation of gut bacteria. Common antibiotics used are third generation cephalosporins or fluoroquinolones. This should be given as soon as possible and ideally before endoscopy.

Octreotide (C) is an analog of somatostatin that is used to reduce blood flow through the gastric mucosa and cause splanchnic vasoconstriction. The literature shows that octreotide will help achieve hemostasis and prevent rebleeding; however, it has no clear benefit in mortality. Pantoprazole (D) and other proton pump inhibitors are frequently used in undifferentiated upper gastrointestinal bleeding, but benefits are typically seen in patients with peptic ulcer bleeding. Erythromycin (B) is a promotility agent that is used to enhance endoscopic visualization but is not recommended for routine use. All variceal bleeding will need early endoscopy for definitive treatment with ligation or sclerotherapy.

Mallory-Weiss syndrome is characterized by longitudinal mucosal lacerations in the distal esophagus and proximal stomach, commonly associated with violent or repeated vomiting. The lacerations lead to bleeding from submucosal arteries. Mallory-Weiss syndrome is common, representing 8–15% of upper gastrointestinal (GI) bleeding. Symptoms include dysphagia, odynophagia, and upper GI bleeding. Bleeding is usually mild to moderate, often resolving spontaneously. Risk factors include alcoholism, hiatal hernia, and gastritis or esophagitis. The diagnostic study of choice in patients with continued bleeding is endoscopy. All patients with Mallory-Weiss syndrome should be treated with proton pump inhibitors for acid suppression and antiemetics. For patients with actively bleeding, endoscopic therapy (thermal coagulation, hemoclips, or endoscopic band ligation) is indicated.

Boerhaave’s syndrome (A) is a full-thickness esophageal perforation and a surgical emergency. Patients typically present with severe chest pain that begins acutely after vomiting. The patient in this question does not have any pain and is feeling better, making this an unlikely diagnosis. Diverticulosis (B) is a common cause of lower gastrointestinal bleeding but does not cause hematemesis. Peptic ulcer disease (D) is mostly commonly the result of Helicobacter pylori infection and nonsteroidal anti-inflammatory drug usage. Patients will present with vague epigastric pain that may radiate to the back.

Swallowed foreign bodies most commonly obstruct at the level of C6, the cricopharyngeus muscle, one of the four natural areas of luminal narrowing in the esophagus. The cricopharyngeus is the muscle of the upper esophageal sphincter (UES). Depending on the type of material, a plain radiograph may not reveal the object, particularly with food bolus obstructions. Pediatric patients often swallow objects like coins, and it may be difficult to ascertain whether a coin is in the trachea or esophagus. On a soft tissue X-ray, a coin located in the esophagus appears in the coronal plane, “en face,” as opposed to appearing sagitally when in the trachea. Most foreign bodies less than 2 cm x 5 cm will pass spontaneously through the GI tract. If the patient is without severe symptoms, foreign bodies less than this size are observed for 24 hours as only 10-20% require endoscopic removal. Fewer than 1% will require surgical removal. Pediatric patients account for more than 75% of esophageal foreign bodies. Other at risk patients include edentulous persons, those with psychiatric disease and prisoners, and those with underlying structural abnormalities of the esophagus (rings, strictures, diverticula, malignancy).

The aortic arch (A) at the level of T4 is the second most common location for foreign body obstruction in the esophagus. The gastroesophageal junction (C) at T11 is third most common. The tracheal bifurcation (D) at T6 is the fourth most common site, particularly as the left mainstem bronchus pushes against the esophagus. The thoracic inlet at T1 is the least common location for obstruction.

This patient is presenting with peptic ulcer disease secondary to Helicobacter pylori infection. It is estimated that 30%–40% of the US population is infected with H. pylori, although many will never develop peptic ulcer disease. It is usually acquired through the fecal-oral route, typically in childhood. It is estimated that the majority of patients with duodenal and gastric ulcers are infected with H. pylori. Its presence causes mucosal inflammation and disrupts the normal defense mechanism of the stomach lining, leading to ulceration. Methods of testing include urea breath test, urea blood test, blood antibody testing, stool antigen testing, and biopsy during endoscopy. Triple therapy withclarithromycin 500 mg BID, amoxicillin 1 g BID (metronidazole 500 mg BID if allergic to penicillin), and a proton pump inhibitor (such as lansoprazole 30 mg BID) for 10–14 days is currently recommended for all patients with confirmed H. pylori infection.

Amoxicillin 1 g BID, metronidazole 500 mg BID, lansoprazole 30 mg BID for 10–14 days (A) is incorrect as you need the addition of clarithromycin; clarithromycin 500 mg BID, amoxicillin 1 g BID, metronidazole 500 mg BID for 10–14 days (C) is incorrect as you have not used a PPI; and clarithromycin 500 mg BID, amoxicillin 1 g BID, metronidazole 500 mg BID, lansoprazole 30 mg BID for 10–14 days (D) is incorrect as you have treated the patient with too many medications.

Esophageal varices occur in patients with cirrhotic liver disease and portal hypertension. Over time, varices develop in the lower portion of the esophagus and may acutely bleed leading to massive upper GI bleeding. Octreotide is a somatostatin analog which causes splanchnic vasoconstriction when administered intravenously. As a result of splanchnic vasoconstriction, hypertension of the portal system may decrease leading to decreased bleeding. In an acute GI bleed from varices, a bolus of 50 to 100 micrograms is administered followed by a continuous infusion of 50 micrograms/hour.

The placement of a nasogastric tube (A) will not have a therapeutic outcome in the management of upper GI bleeding due to esophageal varices. Nasogastric tubes may be placed to help prevent vomiting in patients with ongoing bleeding. Additionally, in cases where the presence of bleeding is unclear, a tube may be inserted diagnostically although the sensitivity of this limits its usefulness. Some argue that caution must be taken in the presence of variceal bleeding for fear of worsening bleeding from the trauma of tube insertion. Propranolol (C) is a beta-blocker used prophylactically in patients with known esophageal varices in order to maintain blood pressure and heart rate control. The medication has no role in the acute management of a variceal bleeding. Ranitidine (D) is an H2-antagonist used in the suppression of acid production. The pathophysiology of variceal bleeding is not due to increased acid production nor worsened by the presence of acid and these agents are not indicated. In upper GI bleeding due to peptic ulcer disease, proton pump inhibitors may have some benefit in preventing re-bleeding after the initial episode and are often part of the management of those patients.

Gastroesophageal reflux disease (GERD) is caused by damage to the mucosa of the esophagus from reflux of gastric acid. It is further subdivided into erosive and non-erosive GERD based on endoscopic identification of visible esophageal damage. GERD typically manifests as heartburn that occurs after eating and is worse in the supine position. However, it may also present with epigastric pain, indigestion, nausea, and eructation. Reflux may even extend to the oral cavity and lungs, causing sore throat, cough, and wheezing. While GERD can be diagnosed clinically, pharmaceutically refractory cases and those patients in whom alternative diagnoses are a consideration warrant further objective evaluation. Esophageal pH monitoring is appropriate for patients without alarm symptoms. The presence of dysphagia, odynophagia, or other alarming symptoms should be evaluated by endoscopy. Lifestyle changes including weight loss, elevating the head of the bed, and avoiding food triggers (e.g., caffeine, alcohol, and acidic foods) are all important interventions. Mild, intermittent disease can be treated with antacids as needed, whereas patients with more severe disease require treatment with either an H2 blocker or a proton pump inhibitor (PPI). Erosive GERD should be treated with a PPI (e.g., omeprazole and lansoprazole), whereas non-erosive disease can be treated with either an H2 blocker or a PPI. However, studies have shown the use of PPI results in better response as well as faster healing and resolution of symptoms compared to H2 blockers. Accordingly, PPIs are recommended as first-line for gastroesophageal reflux disease where financial issues are not a factor. H. pylori infection is a consideration in patients with peptic ulcer disease, but patients with GERD and a positive H. pylori test should also be treated. Initial triple therapy with lansoprazole, amoxicillin, and clarithromycin for 10 days is one treatment option.

Bismuth subsalicylate, metronidazole, and doxycycline (A) is not a treatment for H. pylori. The substitution of tetracycline for doxycycline would make it appropriate. Continuing famotidine and adding sucralfate (B) is not appropriate as the patient has tested positive for H. pylori. Triple therapy should be offered even in the absence of peptic ulcer disease. Additionally, sucralfate is not recommended for GERD treatment in the non-pregnant patient. Stopping famotidine and starting omeprazole (D) would be appropriate for a patient with objectively diagnosed GERD and a negative H. pylori result.

This patient presents with infectious esophagitis secondary to a candidal infection and can be treated with fluconazole. Esophagitis is defined as inflammation of the esophagus and can be caused by a number of mechanisms including infection, allergy related (eosinophillic) or pills. Infectious esophagitis typically occurs in patients that are immunocompromised (diabetes, HIV/AIDS, chronic steroids etc.). Esophageal candidiasis is common in the HIV/AIDS population and is considered an AIDS-defining illness. In addition to candida, it can be caused by HSV1 and CMV. Patients with infectious esophagitis present with severe odynophagia that may be to solids, liquids or both. They may also have chest pain, nausea and dyspepsia. Dehydration is common secondary to pain. Diagnosis can be made based on clinical presentation but an endoscopy can be performed to confirm the diagnosis. In immunocompromised patients with candidal esophagitis, treatment should be with fluconazole for 14 to 21 days. If they are unable to tolerate oral medications, intravenous fluconazole can be given.

Acylovir (A) is used in the treatment of herpes esophagitis. Clotrimazole troches (B) can be used in the treatment of mild oropharyngeal candidiasis in immunocompetent patients. CT scan of the neck (C) is unnecessary and is unlikely to show the pathology in the esophagus.