1. The middle third of the esophagus is accessed through the left chest.
   
2. The esophagus has two layers of muscle surrounded by serosa.
   
3. The recurrent laryngeal nerve runs posterior to the esophagus.
   
4. The cricopharyngeus functions as the upper esophageal sphincter.
   
5. The lower esophagus courses to the right of the spine to pass through the diaphragm.

The esophagus begins at the 6^th cervical vertebrae and travels down to the 11^th thoracic vertebra, approximately 25 cm in distance. It has 2 layers. The inner mucosal layer is lined proximally with squamous epithelium that transitions to columnar epithelium near the gastroesophageal junction. The outer muscular layer is composed of an inner circular muscle layer and an outer longitudinal muscle layer. There is no serosal layer to the esophagus. There are four anatomic segments of the esophagus.

The cervical esophagus is located between the hypopharynx and the thoracic inlet. The recurrent laryngeal nerve can be found in tracheoesophageal groove. The location of the nerve is more consistent in the left neck. Therefore, the cervical esophagus is approached through a left neck incision. The cricopharyngeus is located in this segment and acts, along with the inferior constrictor, as the upper esophageal sphincter.

The upper thoracic esophagus is located between the thoracic inlet and the lower border of the azygous vein. The middle thoracic esophagus then begins and extends to the inferior pulmonary veins. Finally, the lower thoracic esophagus begins and extends inferiorly to the stomach. As the esophagus approaches the thoracic inlet, it deviates to the left before returning to a midline position at approximately the T5 vertebrae. It again courses to the left as it approaches the diaphragmatic hiatus. The middle third of the esophagus is approached typically through the right chest while the distal esophagus is exposed with a left thoracotomy.

Besides the upper esophageal sphincter, there are two other areas of increased pressure and narrowing. There is an area of increase pressure as the esophagus passes posterior to the left mainstem bronchus. The last area is the lower esophageal sphincter, which is a physiologic sphincter contributed to by multiple components, including abdominal esophageal length and pressure, the diaphragmatic hiatus, and the Angle of His.

Answer: D

Patti, M., Gantert, W., Way, L. (1997) Surgery of the esophagus: anatomy and physiology. The Surgical Clinics of North America , 77, 959–970.

1. The most common cause of perforation is malignancy.
   
2. Esophagogastroduodenoscopy is the diagnostic test of choice.
   
3. Early, broad‐spectrum antibiotics is the mainstay of treatment.
   
4. The most common site of perforation is cervical near the cricopharyngeus.
   
5. There is no role for conservative, nonoperative management of perforation.

Iatrogenic injury is the most common cause of esophageal perforation. The most common site of perforation is at the narrowing caused by the cricopharyngeus. Patients should be asked about recent instrumentation of the esophagus. Patients will often present with dysphagia, chest pain, back pain, or epigastric abdominal pain. Physical exam may reveal crepitus and diminished lung sounds. Chest radiographs may show a left pleural effusion for proximal or distal perforations or a right pleural effusion for midesophageal perforations. Saliva or food particle return after chest tube placement is diagnostic.

If esophageal perforation is suspected, upper endoscopy can be performed but is not the first test of choice as it may worsen the injury. Either CT scan with PO contrast or esophagography with water‐soluble contrast followed by thin barium should be used to diagnose the injury.

Early operative management is the mainstay of treatment for esophageal perforation. Delay in treatment leads to a high incidence of morbidity and mortality. For some contained perforations without signs of sepsis, conservative management may be attempted. This may include endoscopic stenting or clipping. Obstructive pathology or malignancy is a contraindication to conservative management. Antibiotic coverage should include aerobe, anaerobe, and fungal coverage.

Answer: D

Chirica, M., Kelly, M.D., Siboni, S., et al. (2019) Esophageal emergencies: WSES guidelines. World Journal of Emergency Surgery , 14, 26.

Nirula, R. (2014) Esophageal perforation. Surgical Clinics of North America , 94, (1) 35–41.

1. There is no role in postoperative antibiotic use.
   
2. Band ligation is first‐line therapy for bleeding esophageal varices.
   
3. Tamponade with a Sengstaken–Blakemore tube is often successful for long‐term control.
   
4. Surgical portosystemic shunts should be pursued early to prevent bleeding.
   
5. Upper endoscopy should be avoided to prevent provoked bleeding.

Gastroesophageal varices are the result of portal hypertension, most often the result of cirrhosis. In patients with cirrhosis, varices form at a rate of approximately 8% per year. The most common acute presentation is gastrointestinal hemorrhage. If a patient presents with suspected bleeding varices, other signs of portal hypertension and cirrhosis, such as spider nevi, jaundice, and ascites, may be present.

Initial management of bleeding varices involves appropriate resuscitation. In patients with altered mental status, intubation may be necessary to prevent aspiration. Upper endoscopy is necessary for accurate diagnosis and treatment. Band ligation is the first‐line treatment for bleeding esophageal varices. This treatment modality has a success rate of over 70% and can be repeated as necessary. Continuing antibiotics in the postprocedural period has been shown to decrease rates of rebleeding. Sengstaken–Blakemore tubes may be used to temporarily control bleeding not alleviated by initial endoscopic treatment. However, the treatment is only temporary and has a high rate of complications including aspiration and esophageal rupture. Portosystemic shunts may be considered for bleeding that does not resolve with primary or secondary treatments. Transjugular intrahepatic portosystemic shunt (TIPS) may be attempted, while surgical portosystemic shunts only be used when other modalities have failed.

Answer: B

Sharma, M., Singh, S., Desai, V., et al. (2019) Comparison of therapies for primary prevention of esophageal variceal bleeding: a systematic review and network meta‐analysis. Hepatology , 69, (4) 1657–1675.

Seo, Y.S. (2018) Prevention and management of gastroesophageal varices. Clinical and Molecular Hepatology , 24, (1) 20–42.

Garcia‐Tsao, G., Bosch, J. (2010) Management of varices and variceal hemorrhage in cirrhosis. New England Journal of Medicine , 362, (9) 823–832.

1. Esophagogastroduodenoscopy is indicated in symptomatic patients without evidence of perforation.
   
2. Acid ingestion causes deeper esophageal injury than alkali ingestion.
   
3. Neutralizing agents are contraindicated in treatment.
   
4. The most common late complication is esophageal stricture.
   
5. Early enteral feeding is not contraindicated in low‐grade injuries.

Household cleaner ingestions are a common occurrence. While children with accidental exposure are likely to vomit and limit the amount of substance and contact time, purposeful ingestion for self‐harm is associated with larger volume of substance and more serious injury. Acid ingestion is associated with coagulative necrosis, while alkali ingestions lead to liquefactive necrosis that causes a deeper injury. Therefore, alkali ingestions have a higher morbidity and mortality.

Patients with ingestions should be evaluated based on clinical symptoms. They should be resuscitated and evaluated for signs of perforation. If patients have no overt signs of perforation, upper endoscopy should be performed to evaluate the extent of injury. Grade 1 injuries only show edema and hyperemia. Grade 2A and 2B have superficial or deep ulceration, respectively. Grade 3A demonstrates focal necrosis while Grade 3B has extensive necrosis. Grade 1 and 2A have good prognosis, 2B and 3A have a high rate of stricture, and 3B has a high rate of mortality.

Emetics should not be used as they cause re‐exposure of the esophagus to the agent upon regurgitation. Likewise, neutralizing agents should not be used as they cause an exothermic reaction that also can worsen the injury. In patients with low‐grade injuries can be started on a liquid diet early and advanced as tolerated.

Answer: B

Hoffman, R.S., Burns, M.M., Gosselin, S. (2020) Ingestion of caustic substances. New England Journal of Medicine , 382, (18) 1739–1748.

1. Blunt injuries are more common to the cervical esophagus than penetrating.
   
2. A negative physical exam is adequate to rule out an esophageal injury.
   
3. The injury to the mucosal layer is never larger than the injury to the muscular layer.
   
4. Full strength barium is the initial contrast of choice in evaluating for injury.
   
5. Esophagoscopy has a high negative predictive value.

Diagnosis and management of esophageal injury is imperative as delay in diagnosis significantly worsens patient outcomes. Injuries to the esophagus are most often associated with penetrating wounds. Blunt cervical esophageal injuries are often associated with impact on a hyperextended neck. Rupture may also occur with rapidly increased pressure.

While hard signs such as saliva in the wound are indicative of injury, lack of physical exam signs of injury are not adequate to rule out injury. Diagnostic modalities include an upper GI study with water‐soluble contrast. If this study is negative, it should be followed by a study with thin barium for confirmation. Full strength barium should be avoided as it can cause mediastinitis and mediastinal fibrosis. Esophagoscopy is also a component of diagnosis and has a high negative predictive value.

Exposure of esophageal injury is dependent on the location. Cervical injuries are approached from the left neck, mid‐esophageal injuries from the right chest, and distal injuries from the left chest. The muscle should be divided past the area of injury to expose the full extent of the mucosal injury as this often extends further than the muscular injury. The edges of the wound should be debrided of necrotic and nonviable tissue. The esophagus is repaired in two layers and should be buttressed with a muscle flap. Inspection for a through‐and‐through injury should also be done, either through the operative field or by intraoperative endoscopy.

Answer: E

Chirica, M., Kelly, M.D., Siboni, S., et al. (2019) Esophageal emergencies: WSES guidelines. World Journal of Emergency Surgery , 14, 26.

Biffl, W.L., Moore, E.E., Feliciano, D.V., et al. (2015) Western Trauma Association critical decisions in trauma: diagnosis and management of esophageal injuries. Journal of Trauma and Acute Care Surgery , 79, (6) 1089–1095.

1. Monitor for passage of the foreign body
   
2. Emergent endoscopy
   
3. Administration of emetics to clear foreign body
   
4. CT scan of the chest
   
5. Emergent bronchoscopy

Ingestions of foreign bodies are common occurrences in children. Most foreign body ingestions do not require treatment and will pass on their own. However, if the patient is symptomatic or the identity of the foreign body is unknown, further investigation is necessary. Ingestions of coin batteries represent an emergent situation and require prompt action to prevent further complications. Coin batteries, when in contact with surrounding tissue, produce hydrochloric acid and, if left untreated, will lead to ulcerating and perforation. Patients may present with dysphagia, drooling, or PO intolerance.

Plain films of the chest may show the presence of the foreign body if it is in the esophagus. While coins will show up as round objects on imaging, coin batteries have a classic double halo appearance when viewed en face and a step‐off appearance on lateral views.

Suspected or known ingestion of a coin battery should prompt immediate removal. This is accomplished with upper endoscopy. When the diagnosis is made on plain film imaging, no further radiographic studies are needed.

Answer: B

Torrecillas, V., Meier, J.D. (2020) History and radiographic findings as predictors for esophageal coins versus button batteries. International Journal of Pediatric Otorhinolaryngology , 137, 110208.

Wright, C.W., Closson, F.T. (2013) Updates in pediatric gastrointestinal foreign bodies. Pediatric Clinics of North America , 60, (5) 1221–1239.

1. The gastrosplenic ligament contains the short gastric arteries.
   
2. The pylorus receives its blood supply from the left gastric artery.
   
3. The stomach is acidified by hydrochloric acid production in the parietal cells.
   
4. Total gastrectomy places patients at risk for pernicious anemia.
   
5. The right gastric artery most often arises from the proper hepatic artery.

The stomach is located in the left upper quadrant of the abdomen, although its exact location can vary based on patient positioning and the amount of gastric contents at the time. The stomach is attached to surrounding structures laterally by the gastrosplenic ligament, which contains the short gastric arteries, medially by the gastrohepatic ligament and retroperitoneal duodenum, and cephalad by the gastrophrenic ligament. The stomach is loosely attached to the transverse colon by the gastrocolic ligament.

The stomach receives its rich blood supply from the left and right gastric arteries, the left and right gastroepiploic arteries, and the short gastric arteries. The left gastric artery most often arises from the celiac axis, but variants may originate from the common hepatic artery, splenic artery, aorta, or superior mesenteric artery. The right gastric artery originates from the proper hepatic artery the majority of the time, but also can come from the left hepatic artery or common hepatic artery. The right gastroepiploic artery is a branch of the gastroduodenal artery, while the left gastroepiploic artery is most often a branch of the splenic artery. The pylorus receives arterial supply from the gastroduodenal artery.

The gastric mucosa is made up of columnar cells. Parietal cells produce hydrochloric acid to acidify the stomach. Parietal cells also produce intrinsic factor, which is necessary for the absorption of vitamin B₁₂. Following gastrectomy patients are at risk for pernicious anemia secondary to intrinsic factor deficiency. Gastrin, which is produced by G cells in the antrum, stimulates acid secretion.

Answer: B

Soybel, D.I. (2005) Anatomy and physiology of the stomach. Surgical Clinics of North America , 85

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