29: Esophagus Flashcards
What type of hiatal hernia is characterized as a sliding hernia from dilation of the hiatus?
Type I
[UpToDate: Hiatus hernias are broadly divided into sliding and paraesophageal hernias. The most comprehensive classification scheme recognizes four types of hiatus hernia.
Type I: Sliding hernia — A type I or sliding hiatus hernia is characterized by the displacement of the gastroesophageal (GE) junction above the diaphragm. The stomach remains in its usual longitudinal alignment and the fundus remains below the GE junction.
Type II, III, IV: Paraesophageal hernias — A paraesophageal hernia is a true hernia with a hernia sac and is characterized by an upward dislocation of the gastric fundus through a defect in the phrenoesophageal membrane.
- Type II hernia results from a localized defect in the phrenoesophageal membrane where the gastric fundus serves as a lead point of herniation, while the GE junction remains fixed to the preaortic fascia and the median arcuate ligament.
- Type III hernias have elements of both types I and II hernias and are characterized by both the GE junction and the fundus herniating through the hiatus. The fundus lies above the GE junction.
- Type IV hiatus hernia is associated with a large defect in the phrenoesophageal membrane and is characterized by the presence of organs other than the stomach in the hernia sac (eg, colon, spleen, pancreas, or small intestine).]
The phrenoesophageal membrane is an extension of what?
The transversalis fascia
[UpToDate: The distal end of the esophagus is anchored to the diaphragm by the phrenoesophageal membrane, formed by the fused endothoracic and endoabdominal fascia. This elastic membrane inserts circumferentially into the esophageal musculature, very close to the squamocolumnar junction, which resides within the diaphragmatic hiatus.
This configuration is altered during swallow-initiated peristalsis, a sequenced contraction of both the longitudinal and circular muscle responsible for bolus propulsion through the esophagus. With contraction of the esophageal longitudinal muscle, the esophagus shortens and the phrenoesophageal membrane is stretched; its elastic recoil is then responsible for pulling the squamocolumnar junction back to its normal position following each swallow. This is, in effect, “physiologic herniation,” since the gastric cardia tents through the diaphragmatic hiatus with each swallow.
The globular structure seen radiographically that forms above the diaphragm and beneath the tubular esophagus during deglutition is termed the phrenic ampulla; it is bounded from above by the distal esophagus and from below by the crural diaphragm. Physiologically, the phrenic ampulla is the relaxed, effaced, and elongated lower esophageal sphincter (LES). Emptying of the ampulla occurs between inspirations in conjunction with relengthening of the esophagus and contraction of the LES.
The repetitive stress of swallowing, as well as that associated with abdominal straining and episodes of vomiting, subject the phrenoesophageal membrane to substantial wear and tear, making it a plausible target of age-related degeneration. Another potential source of stress on the phrenoesophageal membrane is tonic contraction of the esophageal longitudinal muscle induced by gastroesophageal (GE) reflux and mucosal acidification.]
What is the 2nd most common type of esophageal cancer?
Squamous cell carcinoma
[UpToDate: The incidence of esophageal SCC varies considerably among geographic regions. The highest rates are found in Northern Iran, Central Asia, and North-Central China (the so-called “esophageal cancer belt”). Geographic variation has also been reported within individual countries. Within China, for example, rates of esophageal cancer range from 1.4 to 140 per 100,000 in the Hebi and Hunyuan counties, respectively.
Several studies have described risk factors associated with esophageal SCC. Their relative importance (from a public health perspective) was estimated in a study that determined the population attributable risk for several of the major risk factors that have been identified. The authors estimated that a history of smoking, alcohol consumption, and diets low in fruits and vegetables accounted for almost 90% of esophageal SCC in the United States. The relative importance of specific risk factors may be substantially different in other parts of the world. As noted above, the major risk factors for SCC in the “esophageal cancer belt” of Iran and Asia are not well understood, but are thought to include poor nutritional status, low intake of fruits and vegetables, and drinking beverages at high temperatures.]
How must one approach endoscopy in a patient who has ingested a caustic agent?
Do not use endoscopy if perforation is suspected and do not go past a site of severe injury
[UpToDate: The absence of oropharyngeal burns does not preclude the presence of esophageal or gastric injury. Thus, upper gastrointestinal endoscopy should be performed during the first 24 hours after ingestion in order to evaluate the extent of esophageal and gastric damage, establish prognosis, and guide therapy. Endoscopy is contraindicated in patients who have evidence of perforation. In patients who are hemodynamically unstable, endoscopy should be postponed until the patient is adequately resuscitated and is once again hemodynamically stable. If severe respiratory distress is present or there are signs of severe oropharyngeal or glottic edema and/or necrosis, the patient should be intubated for airway protection prior to endoscopy. In addition, extra care should be taken when performing an endoscopy in such patients because of the risk of perforation if the esophagus is similarly damaged.]
What is the primary blood supply to the stomach following esophagectomy?
Right gastroepiploic artery
[Left gastric and short gastrics are divided during surgery]
Bloating in a previously healthy individual is concerning for what?
Aerophagia and delayed gastric emptying
[Dx: Gastric emptying study]
[UpToDate: Patients with gastroparesis can present with nausea (93%), vomiting (68-84%), abdominal pain (46-90%), early satiety (60-86%), postprandial fullness, bloating, and, in severe cases, weight loss. The vomitus may contain food ingested several hours previously.
The predominant symptom may vary based on the underlying etiology. In a retrospective study that included 416 patients with gastroparesis, patients with idiopathic gastroparesis reported more early satiety, postprandial fullness, and abdominal pain as compared with patients with diabetic gastroparesis. In contrast, patients with diabetic gastroparesis had more severe retching and vomiting.
Bloating is common in gastroparesis and is severe in many individuals. In one study of 335 individuals with gastroparesis, bloating was at least mild in 76% and severe in 41% of individuals.
While abdominal pain is a frequent symptom in patients with gastroparesis, it is rarely the predominant symptom (18%). In patients whose predominant symptom is abdominal pain, other causes should be sought. The pain is usually localized to the upper abdomen and is often described as burning, vague, or crampy. Approximately 60% report exacerbation of pain after eating. In one case series, pain interfered with sleep in 80% of patients. However, the severity of abdominal pain did not correlate with a delay in gastric emptying, suggesting that the cause of pain in this tertiary referral cohort may not have been gastroparesis.]
How long do you continue proton pump inhibitor therapy that has failed to alleviate GERD symptoms?
3-4 weeks
[Failure of PPI requires follow-up diagnostic studies]
[UpToDate:We recommend an upper endoscopy in patients with typical GERD symptoms that persist despite a therapeutic trial of four to eight weeks of twice-daily PPI therapy.
While the definition is controversial, patients who fail to respond to once-daily PPI therapy are considered to have refractory GERD and should be referred to a gastroenterologist. Expert opinion suggests that twice-daily PPI therapy should be used to improve symptom relief in patients with esophageal GERD symptoms with an unsatisfactory response to once-daily dosing. In contrast, metoclopramide as monotherapy or adjunctive therapy is not recommended in patients with esophageal or suspected extraesophageal GERD symptoms. The evaluation and management of refractory GERD and the role of surgery in patients with refractory GERD are discussed separately.]
What is the potential advantage of the transhiatal approach to esophagectomy?
May have decreased mortality from esophageal leaks with cervical anastomosis
[UpToDate: In the largest prospective database series of 2007 patients, the in-hospital mortality rate decreased in the 1998-2006 cohort (n = 944 patients) compared with the 1976-1998 cohort (1% vs 4%). In addition, the anastomotic leak rate was also lower in the 1998-2006 cohort (9% vs 14%). Other postoperative complications included atelectasis and pneumonia (2%), and intrathoracic hemorrhage, recurrent laryngeal nerve (RLN) paralysis, chylothorax, and tracheal laceration in < 1% each. Similar results have been noted in other large series.
Disadvantages include the inability to perform a full thoracic lymphadenectomy and lack of visualization of the midthoracic dissection.]
What type of hiatal hernia is characterized as a mixed or combined hernia with both sliding characteristics and paraesophageal characteristics?
Type III
[UpToDate: Type III hernias have elements of both types I (sliding) and II (paraesophageal) hernias and are characterized by both the GE junction and the fundus herniating through the hiatus. The fundus lies above the GE junction.
What are 5 risk factors for esophageal cancer?
- ETOH
- Tobacco
- Achalasia
- Caustic injury
- Nitrosamines
[UpToDate: The major risk factors for SCC of the esophagus in the United States are smoking and alcohol consumption but other risk factors may be important in specific regions of the world. The major risk factors for SCC in the “esophageal cancer belt” of Iran and Asia are not well understood, but are thought to include poor nutritional status, low intake of fruits and vegetables, and drinking beverages at high temperatures.
The major risk factors for adenocarcinoma of the esophagus are Barrett’s esophagus, gastroesophageal reflux disease, smoking, and a high body mass index.]
Hyperemia of the esophagus following caustic injury is characteristic of what grade of burn?
Grade 1 burn
[UpToDate: A grading system for esophageal injury to predict subsequent clinical outcome has been developed based upon a study of 81 patients with corrosive ingestion.
- Grade 0 – Normal
- Grade 1 – Mucosal edema and hyperemia
- Grade 2A – Superficial ulcers, bleeding, exudates
- Grade 2B – Deep focal or circumferential ulcers
- Grade 3A – Focal necrosis
- Grade 3B – Extensive necrosis
A modification of the burn classification, this system is widely used although its validity has yet to be confirmed in other prospective studies. The following correlations between endoscopic grading and prognosis have been observed:
Patients with grades 1 and 2A have an excellent prognosis without significant acute morbidity or subsequent stricture formation.
Patients with grades 2B and 3A develop strictures in 70-100% of cases.
Grade 3B carries a 65% early mortality and the need for esophageal resection with colonic or jejunal interposition in most cases. In a large retrospective study, patients with grade 3B mucosal injuries were at greater risk of prolonged hospital stay (odds ration [OR] 2.4), ICU admission (OR 10.8), and gastrointestinal and systemic complications (OR 4.2 and 4.1, respectively).
A retrospective series with 49 patients with caustic ingestion graded the degree of esophageal damage using a scoring system based on the extent of esophageal wall edema and the adjacent tissue damage on thoracoabdominal computed tomography (CT) scans. Damage to the esophagus was correlated with the presence of esophageal strictures when the extent of damage approached grades III and IV. The CT grading system resulted in a slightly larger area under the receiver operating characteristic curve (0.90) for predicting strictures compared with the endoscopic grading system (0.79).]
What are the findings on manometry in a patient with achalasia?
- Increased lower esophageal sphincter (LES) pressure
- Incomplete LES relaxation
- No peristalsis
[UpToDate: Aperistalsis in the distal two-thirds of the esophagus and incomplete LES relaxation are diagnostic findings of achalasia on conventional manometry. Elevated resting LES pressure is supportive of the diagnosis of achalasia, but is not always present and is not diagnostic.
Typical conventional manometric findings:
- Aperistalsis in the distal two-thirds of the esophagus – In patients with achalasia, aperistalsis is seen in the smooth muscle portion of the body of the esophagus. Swallows may elicit no esophageal contraction or may be followed by simultaneous contractions with amplitudes <40 mmHg.
- Incomplete LES relaxation – Incomplete LES relaxation distinguishes achalasia from other disorders associated with aperistalsis. In normal individuals, there is complete relaxation of the LES after a swallow (to a level <8 mmHg above gastric pressure). In contrast, in patients with achalasia, LES relaxation in response to a swallow may be incomplete or absent with a mean swallow-induced fall in resting LES pressure to a nadir value of >8 mmHg above gastric pressure.
- Elevated resting LES pressure – Loss of inhibitory neurons in patients with achalasia can cause resting LES pressures to rise to hypertensive levels (above 45 mmHg).
Atypical manometric findings – A number of atypical manometric findings have been reported in patients with achalasia, including achalasia with preserved peristalsis, cases with occasional complete or partial LES relaxation, and vigorous achalasia. Vigorous achalasia is an outdated term that has been used for patients who have simultaneous esophageal body contractions with amplitudes >40 mmHg in the presence of a non-relaxing LES on conventional manometry, sometimes associated with spastic esophageal activity on barium swallow. Preserved peristalsis with esophageal contractions >40 mmHg also has been described in patients with vigorous achalasia. The distinction between vigorous and classic achalasia appears to have little clinical significance. Some patients diagnosed with vigorous achalasia by conventional manometry have type III achalasia by high-resolution manometry (HRM).]
From which side is the appropriate surgical approach for the cervical esophagus?
Left
[UpToDate: A left neck exposure is preferred for the esophagogastric anastomosis, since this approach reduces the risk of injury to the recurrent laryngeal nerve (RLN). The left RLN recurs lower (around the aortic arch) than the right RLN, which recurs around the subclavian artery and is therefore more likely to be injured from a right neck approach.]
Deep ulcers, charring, and lumen narrowing of the esophagus following caustic injury is characteristic of what kind of burn?
Grade 3 burn
[UpToDate: A grading system for esophageal injury to predict subsequent clinical outcome has been developed based upon a study of 81 patients with corrosive ingestion.
- Grade 0 – Normal
- Grade 1 – Mucosal edema and hyperemia
- Grade 2A – Superficial ulcers, bleeding, exudates
- Grade 2B – Deep focal or circumferential ulcers
- Grade 3A – Focal necrosis
- Grade 3B – Extensive necrosis
A modification of the burn classification, this system is widely used although its validity has yet to be confirmed in other prospective studies. The following correlations between endoscopic grading and prognosis have been observed:
Patients with grades 1 and 2A have an excellent prognosis without significant acute morbidity or subsequent stricture formation.
Patients with grades 2B and 3A develop strictures in 70-100% of cases.
Grade 3B carries a 65% early mortality and the need for esophageal resection with colonic or jejunal interposition in most cases. In a large retrospective study, patients with grade 3B mucosal injuries were at greater risk of prolonged hospital stay (odds ration [OR] 2.4), ICU admission (OR 10.8), and gastrointestinal and systemic complications (OR 4.2 and 4.1, respectively).
A retrospective series with 49 patients with caustic ingestion graded the degree of esophageal damage using a scoring system based on the extent of esophageal wall edema and the adjacent tissue damage on thoracoabdominal computed tomography (CT) scans. Damage to the esophagus was correlated with the presence of esophageal strictures when the extent of damage approached grades III and IV. The CT grading system resulted in a slightly larger area under the receiver operating characteristic curve (0.90) for predicting strictures compared with the endoscopic grading system (0.79).]
Which disease causes dysphagia and loss of lower esophageal sphincter tone with massive reflux and strictures?
Scleroderma
[UpToDate: Nearly 90% of patients with either subtype of SSc (diffuse cutaneous SSc [dcSSc] or limited cutaneous SSc [lcSSc]) have evidence of gastrointestinal involvement. Nearly half of these patients may have no symptoms. These issues are discussed in detail separately but will be briefly reviewed here.
Esophageal hypomotility and incompetence of the lower esophageal sphincter disease were the earliest described visceral manifestations of SSc. Symptoms principally result from chronic gastroesophageal reflux, with subsequent chronic esophagitis and stricture formation, Barrett’s esophagus, and pulmonary microaspiration.
Any part of the gastrointestinal tract from mouth to anus may be affected in SSc. Common symptoms of gastrointestinal involvement include dysphagia and choking, heartburn, hoarseness, cough after swallowing, bloating, alternating constipation and diarrhea, pseudo-obstruction and bacterial small bowel overgrowth with malabsorption, and fecal incontinence. Chronic gastroesophageal reflux and recurrent episodes of microaspiration may contribute to the development or progression of interstitial lung disease. Vascular ectasia (angiodysplasia) in the antrum of the stomach (“watermelon stomach”) is frequent and may be a cause of chronic gastrointestinal bleeding and anemia.]
How does one diagnose Boerhaave’s syndrome?
Gastrografin swallow
[UpToDate: Boerhaave syndrome is often diagnosed incidentally in a patient being evaluated for chest pain. The diagnosis of Boerhaave syndrome should be suspected in patients with severe chest, neck, or upper abdominal pain after an episode of severe retching and vomiting or other causes of increased intrathoracic pressure, and the presence of subcutaneous emphysema on physical exam. While thoracic and cervical radiography can be supportive of the diagnosis, the diagnosis is established by contrast esophagram or computed tomography (CT) scan.
Delay in the diagnosis is associated with a higher risk of complications and mortality, which ranges between 16% and 51%]
Manometry showing high-amplitude peristaltic contractions with normal relaxation of the lower esophageal sphincter is characteristic of what?
Nutcracker esophagus
[Nutcracker esophagus, or Hypertensive peristalsis, is a disorder of the movement of the esophagus characterized by contractions in the smooth muscle of the esophagus in a normal sequence but at an excessive amplitude or duration.]
[UpToDate: Nutcracker esophagus is characterized by normal sequential contractions in the smooth muscle esophagus of excessive amplitude or duration. On conventional manometry, nutcracker esophagus is defined by high amplitude peristaltic contractions in the distal 10 cm of the esophagus, with average distal esophageal peristaltic pressures exceeding 220 mmHg after 10 5 mL liquid swallows. On HRM with EPT, these high pressure contractions are identified by distal contractile integral (DCI) >8000x mmHgscm. Other terms for hypertensive peristalsis include “spastic nutcracker” or “jackhammer esophagus”.
Nutcracker esophagus may overlap with other esophageal motility disorders. Many patients with nutcracker esophagus also have a hypertensive or poorly relaxing LES. One study using ambulatory 24-hour esophageal manometry found that patterns of DES or nutcracker esophagus on stationary manometry frequently interchanged during episodes of chest pain.]
Manometry showing strong non-peristaltic unorganized contractions and normal relaxation of the lower esophageal sphincter is characteristic of what?
Diffuse esophageal spasm
[UpToDate: Patients with diffuse (distal) esophageal spasm (DES) are symptomatic and present with dysphagia for solids and liquids. Patients have esophageal dysphagia, which is characterized by difficulty swallowing several seconds after initiating a swallow and a sensation of food getting stuck in the esophagus. The dysphagia may occur in association with retrosternal chest pain. In some cases, patients have symptoms of heartburn or regurgitation. In contrast with DES, only a small proportion of patients with nutcracker esophagus and hypertensive lower esophageal sphincter (LES) are symptomatic. In all three disorders, symptoms do not necessarily correlate with manometric abnormalities and may be due to concurrent gastroesophageal reflux disease (GERD) or heightened visceral sensitivity.
DES is characterized by increased simultaneous contractions in the distal esophagus. On conventional manometry, DES is defined by 20% or more simultaneous contractions (with amplitude >30 mmHg). On high resolution manometry (HRM) with esophageal pressure topography (EPT), DES is defined by ≥20% premature contractions (distal latency <4.5 seconds).
It is important to note that DES is intermittent, and manometric findings may be seen with only some of a series of test swallows or only on some days of testing. Patients with DES may also have a variety of other nonspecific manometric findings, including repetitive and prolonged duration contractions. Although most patients with DES usually have normal relaxation of the LES, approximately one-third of patients may have high resting pressure or incomplete relaxation. Patients with DES who present with chest pain have higher amplitudes and better transit of swallowed boluses on impedance testing as compared with those who present with dysphagia.]
Where is esophageal perforation most likely to occur in patients with Boerhaave’s syndrome?
Left lateral wall of esophagus, 3-5 cm above the GE junction
[UpToDate: Boerhaave syndrome usually occurs in patients with a normal underlying esophagus. However, a subset of patients with Boerhaave syndrome has underlying eosinophilic esophagitis, medication-induced esophagitis, Barrett’s or infectious ulcers. Sudden increase in intraesophageal pressure combined with negative intrathoracic pressure such as that associated with severe straining or vomiting, and less frequently with childbirth, seizure, prolonged coughing or laughing, or weightlifting, results in a longitudinal esophageal perforation.
The esophageal perforation usually involves the left posterolateral aspect of the distal intrathoracic esophagus and extends for several centimeters. However, the rupture can occur in the cervical or intra-abdominal esophagus. Rupture of the intrathoracic esophagus results in contamination of the mediastinal cavity with gastric contents. This leads to chemical mediastinitis with mediastinal emphysema and inflammation, and subsequently bacterial infection and mediastinal necrosis. Rupture of the overlying pleura by mediastinal inflammation or by the initial perforation directly contaminates the pleural cavity, and pleural effusion results. Although pericardial tamponade and infected pericardial effusions due to Boerhaave syndrome have been reported, they are rare. If untreated, sepsis and organ failure result.
Effort rupture of the cervical esophagus leads to a localized cervical perforation and has a more benign course, as the spread of contamination to the mediastinum through the retroesophageal space is slow and attachments of the esophagus to the prevertebral fascia limit the lateral dissemination of esophageal flora.]
What is the treatment for esophageal manifestations of scleroderma?
Esophagectomy (if severe)
[UpToDate: We manage esophageal disease with a primary focus on the amelioration of reflux, hypomotility, and the symptoms of strictures; oral and esophageal candidiasis is treated with antifungal agents. We treat reflux with both lifestyle modifications, such as bed elevation and avoidance of late meals, and antisecretory agents, usually a proton pump inhibitor.
In patients with hypomotility, we use prokinetic drugs, such as cisapride or metoclopramide, and avoid nonsteroidal antiinflammatory drugs (NSAIDs) or calcium channel blockers, if possible. Coadministration of cisapride with erythromycin, clarithromycin, or imidazoles should be avoided because of potentially fatal drug interactions. Treatment for esophageal strictures involves use of both proton pump inhibitors and dilatation when needed.]
What procedure must accompany an esophagectomy?
Pyloromyotomy
[UpToDate: The role of a pyloroplasty or pyloromyotomy to reduce the risk of gastric outlet obstruction following a gastric pull-up procedure has been challenged by prospective studies and randomized trials, including:
- A prospective study of 242 patients undergoing an esophagectomy with gastric conduit found that patients with a pyloromyotomy (n = 159) did not have significantly lower rates of gastric outlet obstruction compared with those without a pyloromyotomy (9.6% vs 18.2%). In addition, there was no significant difference for rates of pneumonia or mortality (27.7% vs 19.5%, and 2.4% vs 2.5%, respectively). Management with pyloric dilation was effective in relieving symptoms in approximately 97% of symptomatic patients.
- A meta-analysis of nine trials and 553 esophagectomy patients randomized to pyloromyotomy versus none found a lower risk of gastric outlet obstruction for patients treated with a pyloromyotomy (OR 0.18, 0.03-0.97, p<0.046) [144]. There was no difference for operative mortality, esophagogastric anastomotic leaks, pulmonary morbidity, or fatal pulmonary aspiration.]
The upper 1/3 of the esophagus is composed of what type of muscle?
Striated muscle
Where are the incisions made in the 3-hole approach to esophagectomy?
Abdominal, thoracic, and cervical incisions
[UpToDate: The tri-incisional esophagectomy combines the transhiatal and transthoracic approaches into a transthoracic total esophagectomy with a thoracic lymphadenectomy and cervical esophagogastric anastomosis. The three-incisional technique allows the surgeon to perform a complete two-field (mediastinal and upper abdominal) lymphadenectomy under direct vision and a cervical esophagogastric anastomosis. We prefer a thorascopic approach to the chest rather than a thoracotomy to minimize the risk of respiratory complications.
Thoracotomy – A right posterolateral thoracotomy or a thoracoscopy is performed first to assess resectability and exclude local invasion of contiguous structures. An en bloc resection is performed that includes the esophagus and mediastinal and upper abdominal lymph nodes, including the right paratracheal, subcarinal, periesophageal and celiac axis lymph nodes.
Laparotomy – The abdomen is explored to exclude metastatic disease, and the stomach is mobilized in preparation for the construction of the gastric conduit.
Neck incision – A left neck exposure is preferred for the esophagogastric anastomosis, since this approach reduces the risk of injury to the recurrent laryngeal nerve (RLN). The left RLN recurs lower (around the aortic arch) than the right RLN, which recurs around the subclavian artery and is therefore more likely to be injured from a right neck approach.]
Where are the incisions made in the Ivor Lewis approach to esophagectomy?
Abdominal incision and a right thoracotomy
[UpToDate: The Ivor-Lewis transthoracic esophagectomy can be used to resect cancers in the lower third of the esophagus but is not the optimal approach for cancers located in the middle third because of the limited proximal margin that can be achieved. This procedure combines a laparotomy with a right thoracotomy and an intrathoracic esophagogastric anastomosis. This approach permits direct visualization of the thoracic esophagus and allows the surgeon to perform a full thoracic lymphadenectomy. We prefer a minimally invasive Ivor-Lewis approach to a thoracotomy.
A modification of the Ivor-Lewis transthoracic esophagectomy includes a left thoracoabdominal incision with a gastric pull-up and an esophagogastric anastomosis in the left chest. This approach is most useful for tumors involving the gastroesophageal junction. Only one incision is required, but disadvantages include a high incidence of complications such as postoperative reflux and limitation of the proximal esophageal margin by the aortic arch.]
Where do epiphrenic diverticula typically occur?
Distal 10cm of the esophagus
What is the name of the procedure characterized by stapling along the stomach cardia to create “new” esophagus because there is not enough esophagus to pull down into the abdomen during a nissen fundoplication?
Collis gastroplasty
[UpToDate: Patients with a shortened esophagus from chronic inflammation or altered anatomy present a unique challenge to the surgeon. A Collis (esophageal lengthening) gastroplasty combined with an intra-abdominal or intra-thoracic fundoplication should be performed in these settings; however, opinions vary regarding what constitutes adequate esophageal mobilization. Trans-thoracic approaches should be considered for the patient with concurrent pulmonary disease requiring evaluation or extensive prior abdominal surgery.]
When is surgery indicated for the treatment of GERD?
- Failure of medical treatment
- Avoidance of lifetime medication
- Young patient
[UpToDate: Antireflux surgery should be considered in patients who require high doses of proton pump inhibitors to control symptoms, particularly in young patients who may require lifelong therapy. Whether surgery is beneficial in patients who have failed PPI therapy remains controversial. Surgery is not recommended in patients who demonstrate a complete lack of response to PPI therapy.
In one study, refractory GERD was the most common (88%) indication for antireflux surgery and a number of surgical studies have suggested that fundoplication may be of benefit in patients with refractory GERD. However, many of these reports had important methodologic limitations such as variable definitions of “refractory” GERD, different clinical end points, and accounting for dropouts. Furthermore, patients who have undergone fundoplication may continue to use antisecretory medications (ranging from 10% to almost two-thirds of patients in a systematic review). The predictors of successful outcomes following fundoplication also remain poorly defined.
Another surgical approach is laparoscopic sphincter augmentation using a device comprised of a string of magnetized beads. The device is implanted at the lower esophageal sphincter to maintain closure of a weak lower esophageal sphincter, preventing reflux. The beads then separate when the patient swallows to allow passage of a food or liquid bolus. In one prospective study, 100 patients with GERD that was partially responsive to PPIs underwent implantation of a magnetic esophageal sphincter device. At three-year follow-up, a 50% or greater reduction in esophageal acid exposure was achieved in 64% of patients and 87% of patients reported complete cessation of PPI use. The most frequent adverse event was dysphagia, which occurred in 68% of patients. Serious side effects occurred in 6% of individuals. However, randomized controlled trials are needed to confirm these results and to assess the long-term safety of magnetic devices to treat refractory GERD.]
What is the treatment for epiphrenic diverticula?
Diverticulectomy, and if symptomatic, esophageal myotomy on the side opposite the diverticulectomy
[NCBI: laparoscopic treatment is successful and should be the method of choice. The diverticular neck can be exposed satisfactorily from the abdomen; a stapler inserted from this angle is better orientated to transect the neck than one inserted through a thoracoscopic approach. Furthermore, the myotomy and fundoplication are much more easily performed from the abdomen than from alternative approaches.]
What is the second most common benign tumor of the esophagus?
Esophageal polyps
Dysphagia, regurgitation, weight loss, and respiratory symptoms caused by a lack of peristalsis and failure of the lower esophageal sphincter to relax after a food bolus is characteristic of which disorder?
Achalasia
[UpToDate: Achalasia results from progressive degeneration of ganglion cells in the myenteric plexus in the esophageal wall, leading to failure of relaxation of the lower esophageal sphincter, accompanied by a loss of peristalsis in the distal esophagus.
Achalasia is an uncommon disorder with an annual incidence of approximately 1.6 cases per 100,000 individuals and prevalence of 10 cases per 100,000 individuals. Men and women are affected with equal frequency. The disease can occur at any age, but onset before adolescence is rare. Achalasia is usually diagnosed in patients between the ages of 25 and 60 years.
Achalasia may occur in association with adrenal insufficiency and alacrima in patients with triple A syndrome or Allgrove syndrome, a rare autosomal recessive genetic disorder.
The etiology of primary or idiopathic achalasia is unknown. Secondary achalasia is due to diseases that cause esophageal motor abnormalities similar or identical to those of primary achalasia. In Chagas disease, which occurs predominantly in Central and South America, esophageal infection with the protozoan parasite Trypanosoma cruzi can result in a loss of intramural ganglion cells, leading to aperistalsis and incomplete lower esophageal sphincter relaxation. Other diseases that have been associated with achalasia-like motor abnormalities include amyloidosis, sarcoidosis, neurofibromatosis, eosinophilic esophagitis, multiple endocrine neoplasia type 2B, juvenile Sjögren syndrome, chronic idiopathic intestinal pseudo-obstruction, and Fabry disease.]
Where does squamous cell carcinoma of the esophagus occur?
Upper 2/3 of esophagus
[UpToDate: The majority of SCCs are located in the midportion of the esophagus. SCC arises from small polypoid excrescences, denuded epithelium, or plaques. These early lesions are usually subtle, and can easily be missed on endoscopy. In a series from Linxian China (where SCC is endemic), 25 of 31 patients had biopsy specimens containing moderately dysplastic changes or cancer that were obtained from sites classified as having either “friability, a focal red area, erosion, plaque, or nodule”. Furthermore, 15 of 16 patients (94%) with moderate dysplasia or carcinoma would have been identified had biopsies been restricted to only these visibly abnormal areas.
Tissue staining with Lugol iodide solution during endoscopy (chromoendoscopy) may facilitate diagnosis of early lesions, although the technique is uncommonly used in clinical practice. Lugol solution is a compound iodine solution that stains normal squamous epithelium containing glycogen. Malignant squamous cells do not stain since they are usually devoid of glycogen.
More advanced lesions are characterized by infiltrating and ulcerated masses, which may be circumferential. SCC invades the submucosa at an early stage, and extends along the wall of the esophagus usually in a cephalad direction. Local lymph node invasion occurs early and quickly because the lymphatics in the esophagus are located in the lamina propria, in contrast to the rest of the gastrointestinal tract, in which they are located beneath the muscularis mucosa. The tumor spreads to regional lymph nodes along the esophagus, the celiac area, and adjacent to the aorta. Invasion of local structures may result in fistula formation (such as to the trachea). Erosion into the aorta can be associated with massive upper gastrointestinal hemorrhage.
Distant metastases to the liver, bone, and lung are seen in nearly 30% of patients. In addition, bone marrow invasion can be detected in 40% when monoclonal antibodies are used to stain for malignant cells.]
Is nodal disease outside the area of resection (IE supraclavicular or celiac nodes) a contraindication to esophagectomy?
Yes
[UpToDate: The presence of peritoneal, lung, bone, adrenal, brain, or liver metastases or extraregional lymph node spread (eg, paraaortic or mesenteric lymphadenopathy) precludes an attempt at resection.
The finding of a malignant node in the celiac area remote from the primary tumor (eg, for a SCC in the upper or middle thoracic esophagus) was previously thought to be a sign of unresectability and considered metastatic disease. However, celiac nodal metastases are scored as regional nodal disease in the new 2010 edition of the TNM staging system, regardless of the primary tumor location or histology, and they no longer carry the connotation of distant metastatic disease. Nevertheless, prognosis is poor in such cases, even if the primary tumor is located in the distal esophagus or EGJ. In one series, the two-year survival rate of patients with celiac node involvement who underwent surgery as a component of therapy was approximately 10%.
For tumors of the cervical esophagus (which extends from the hypopharynx to the sternal notch), infiltration into the prevertebral fascia or posterior larynx, invasion of the membranous trachea to the level of the carina, or significant bilateral encasement of major neurovascular structures precludes surgical resection. Regardless of apparent resectability, however, tumors of the cervical esophagus are rarely resected due to the resultant functional deficits and impairment of quality of life. They are more often treated in a similar manner to head and neck SCCs.]
What is the most common cause of esophageal perforation?
EGD
[UpToDate: Most esophageal perforations are iatrogenic following esophageal instrumentation. The most common cause of non-iatrogenic esophageal perforation is spontaneous rupture, followed by foreign body ingestion, trauma, and malignancy.]
What type of hiatal hernia is characterized by the entire stomach plus another organ entering the chest?
Type IV
[UpToDate: Type IV hiatus hernia is associated with a large defect in the phrenoesophageal membrane and is characterized by the presence of organs other than the stomach in the hernia sac (eg, colon, spleen, pancreas, or small intestine).]
Where do ingested acidic agents cause most of their damage?
Stomach
[UpToDate: Acid ingestion typically produces a superficial coagulation necrosis that thromboses the underlying mucosal blood vessels and consolidates the connective tissue, thereby forming a protective eschar. Because acid solutions cause pain upon contact with the oropharynx, the amount of acid ingested tends to be limited. In addition, in contrast to the more viscous alkaline solutions, acid preparations tend to pass quickly into the stomach, causing less esophageal damage.
As the acid flows along the lesser curvature of the stomach toward the pylorus, pylorospasm impairs emptying into the duodenum producing stagnation and injury that is particularly prominent in the antrum. Food in the stomach tends to provide a protective effect. Nevertheless, acid ingestion in sufficient concentration can cause esophageal and gastric perforation with peritonitis.]
What is the normal lower esophageal sphincter (LES) pressure at rest?
15mmHg
[Normal LES pressure with food bolus is 0 mm Hg. UES pressures are 60 mmHg and 15 mmHg at rest and with food bolus respectively.]
The upper esophageal sphincter is composed of which muscle?
Cricopharyngeus muscle
The thoracic duct travels from right to left at what level as it ascends the mediastinum?
T4-5
Where are the incisions made in the transhiatal approach to esophagectomy?
Abdomen and neck
[UpToDate: A transhiatal esophagectomy (THE) can be performed to resect cervical, thoracic, and esophagogastric junction (EGJ) esophageal cancers; it is performed through an upper midline laparotomy incision and a left neck incision, typically without a thoracotomy. The thoracic esophagus is bluntly dissected through the diaphragmatic hiatus superiorly and via the neck inferiorly. A cervical anastomosis is created most often with a gastric pull-up approach.]
Traction diverticula of the esophagus are true diverticula that usually lie to which side of the esophagus (anterior, posterior, or lateral)?
Lateral
[UpToDate: The classification of esophageal diverticula depends upon their location. They predominantly occur in three areas:
- Immediately above the upper esophageal sphincter (Zenker’s diverticulum)
- Near the midpoint of the esophagus (traction diverticulum)
- Immediately above the lower esophageal sphincter (epiphrenic diverticulum)
Traction diverticula were originally thought to be due to scarring and traction on the walls of the esophagus (hence the name) from external inflammatory processes (such as fungal infections or tuberculosis). However, more recent evidence has demonstrated that many mid-esophageal diverticula are associated with esophageal motility abnormalities including spasm, achalasia, lower esophageal sphincter hypertension, or nonspecific abnormalities.]
What is the normal upper esophageal sphincter (UES) pressure at rest?
60mmHg
[Normal UES pressure with food bolus is 15 mm Hg. LES pressures are 15 mmHg and 0 mmHg at rest and with food bolus respectively.]
What is the most common cause of dysphagia following nissen fundoplication?
Wrap is too tight
[UpToDate: Management of patients after fundoplication depends upon symptoms related to the size and tightness of the wrap.
Most patients have some degree of postoperative dysphagia and require a period of modified dietary intake primarily consisting of liquids from 2-12 weeks. The most common predictor of postoperative dysphagia is the presence of preoperative dysphagia. Such patients should be counseled appropriately before surgery.
Some patients describe a “sticking” sensation in their lower or mid chest that they mistakenly attribute to recurrent gastroesophageal reflux disease (GERD). Such patients often resume antisecretory medications. However, it is unlikely that patients whose fundoplication is functionally intact have persistent gastroesophageal reflux. Thus, we suggest that they be studied radiographically prior to restarting antisecretory medications to identify those who require dilation or a revision.
Dysphagia that persists for more than 12 weeks requires evaluation, which typically begins with a barium swallow to assess the anatomic placement of the fundoplication. Patients should be asked to swallow a 13 mm barium tablet. Patients with dysphagia in whom the 13 mm barium tablet passes slowly through the esophagus and who had normal motility preoperatively should be considered candidates for dilation after 12 weeks. Approximately 6 to 12 percent of patients with fundoplication required dilation in various reports.
There is no consensus on the optimal dilation technique (ie, bougie versus guidewire dilation versus pneumatic dilations). The author performs direct bougie dilation, with or without endoscopic guidance. In the author’s experience, the procedure is extremely well tolerated and produces good results. Tortuous pathways through the fundic wrap are best managed by guidewire dilation. Pneumatic dilation is rarely needed.
Patients who have a 360 degree fundoplication may be candidates for revision to a partial fundoplication if dysphagia persists and effective barium tablet passage cannot be established.]
From which side is the appropriate surgical approach for the lower 1/3 thoracic esophagus?
Left (left-sided course in this region)
[UpToDate: The Ivor-Lewis transthoracic esophagectomy can be used to resect cancers in the lower third of the esophagus but is not the optimal approach for cancers located in the middle third because of the limited proximal margin that can be achieved. This procedure combines a laparotomy with a right thoracotomy and an intrathoracic esophagogastric anastomosis. This approach permits direct visualization of the thoracic esophagus and allows the surgeon to perform a full thoracic lymphadenectomy. We prefer a minimally invasive Ivor-Lewis approach to a thoracotomy.
Disadvantages of the transthoracic esophagectomy include a limitation to the length of proximal esophagus that can be resected to achieve a histologically negative resection margin, an intrathoracic location of the esophagogastric anastomosis, and a 3-20% risk of severe bile reflux. A leak occurring at the intrathoracic anastomosis has been associated with morbidity and mortality rates as high as 64%. With current technique, mortality rates are substantially lower.
Many centers report favorable results using the conventional Ivor-Lewis esophagectomy with a right thoracic anastomosis. Prospective comparisons, plus at least one meta-analysis, suggest similar long-term outcomes compared with THE. In one of the largest series of 228 patients undergoing an Ivor-Lewis subtotal esophagectomy, the perioperative mortality rate was 4%, and major respiratory, cardiovascular and/or thromboembolic complications occurred in 17% and 7%, respectively. Nine patients (4%) developed a mediastinal leak, which was anastomotic in five, and due to either an ischemic gastric conduit or gastrotomy dehiscence in the remainder. Only one patient developed a chyle leak.
Modified Ivor-Lewis transthoracic esophagectomy — A modification of the Ivor-Lewis transthoracic esophagectomy includes a left thoracoabdominal incision with a gastric pull-up and an esophagogastric anastomosis in the left chest. This approach is most useful for tumors involving the gastroesophageal junction. Only one incision is required, but disadvantages include a high incidence of complications such as postoperative reflux and limitation of the proximal esophageal margin by the aortic arch.]
Where does squamous cell carcinoma of the esophagus most frequently metastasize?
Lung
[UpToDate: The most common sites of distant metastases in patients with esophageal cancer are the liver, lungs, bone, and adrenal glands. Adenocarcinomas most frequently metastasize to intraabdominal sites (liver, peritoneum), while metastases from SCCs are usually intrathoracic.]
Which two veins drain blood from the esophagus?
- Azygous vein
- Hemi-azygous vein
Severe Barrett’s esophageal dysplasia is an indication for what treatment?
Esophagectomy
[UpToDate: Estimates of the annual cancer incidence in patients with Barrett’s esophagus have ranged from 0.1-3%, with more recent studies suggesting rates closer to 0.1-0.4% per year. Although the risk of developing esophageal cancer is increased at least 30-fold above that of the general population, the absolute risk of developing cancer for a patient with nondysplastic Barrett’s esophagus is very low. The risk of developing cancer is higher among men, older patients, and patients with long segments of Barrett’s mucosa or dysplasia.
Patients with Barrett’s esophagus most often die from causes unrelated to esophageal cancer. This is likely because many patients with Barrett’s esophagus are older, overweight, and succumb to common diseases, such as coronary artery disease, before developing esophageal adenocarcinoma. In a meta-analysis with 50 studies that included 14,109 patients, the mortality rate due to esophageal adenocarcinoma was 3.0 per 1000 person-years, whereas the mortality rate due to other causes was 37.1 per 1000 person-years.
Esophagectomy is the only therapy for high-grade dysplasia that removes all of the neoplastic epithelium along with any occult malignancy and regional lymph nodes. However, it also has the highest rates of procedure-related mortality and long-term morbidity. The mortality rates for esophagectomy among institutions vary inversely with the frequency with which the operation is performed. In a study of data from the Dutch National Medical Registry, the mortality rates for esophagectomy were 12.1%, 7.5%, and 4.9% at centers performing 1-10, 11-20, and more than 50 esophagectomies per year, respectively. With the development of effective endoscopic therapies, esophagectomy can now often be avoided.
The average hospital stay for open esophagectomy is approximately two weeks, and 30-50% of patients develop at least one serious postoperative complication such as pneumonia, arrhythmia, myocardial infarction, heart failure, wound infection, or anastomotic leak. Esophagectomy is frequently associated with long-term problems such as dysphagia, weight loss, gastroesophageal reflux, and dumping. Some of these complications are related to transection of the vagal nerve and may be reduced with a vagal-sparing esophagectomy.]
Where do Zenker’s diverticula occur?
Posteriorly between the pharyngeal constrictors and the cricopharyngeus
[UpToDate: Zenker’s diverticula (ZD) emerge from a defect in the muscular wall of the hypopharynx in a natural area of weakness known as Killian’s triangle, which is formed by the oblique fibers of the inferior pharyngeal constrictor muscle and the cricopharyngeal sphincter. Autopsy series suggest Killian’s triangle is more prevalent in males (60%) and is associated with the dimensions of the body and with the length and the descensus of the larynx.]
Which nerve innervates the cricopharyngeus muscle?
Recurrent laryngeal nerve
Which nerve exits the chest and becomes the celiac plexus?
Right vagus nerve
Which kind of caustic substance (Alkali or acidic) causes deep liquefactive necrosis?
Alkali substance
[UpToDate: Ingestion of alkali (such as ammonia or sodium hydroxide) acutely results in a penetrating injury called liquefactive necrosis. The injury extends rapidly (within seconds) through the mucosa and wall of the esophagus towards the mediastinum until tissue fluids buffer the alkali. In the stomach, partial neutralization of the ingested alkali by gastric acid may result in a more limited injury. Duodenal injury is much less common, occurring in 30% in one series, in contrast to 100% and 94% involvement of the esophagus and stomach, respectively.
Extensive transmural damage may result in esophageal, gastric, or duodenal perforation, mediastinitis, peritonitis, and death. This is most likely to occur with liquid preparations that coat larger mucosal surfaces. In contrast, solid lye preparations, such as disc batteries, induce more localized injury to the esophagus.
The process of liquefactive necrosis usually lasts three to four days and is associated with vascular thrombosis and mucosal inflammation, resulting in focal or extensive sloughing and ulceration. Over the ensuing two weeks, the esophageal wall becomes progressively thinner because of sloughing and the development of granulation tissue and fibrosis. Re-epithelialization is usually complete one to three months later.
The likelihood of stricture formation depends upon the depth of damage and degree of collagen deposition. Death and severe complications primarily occur in patients with severe second-degree and third-degree burns.]
What is the best single test for determing resectability of esophageal cancer?
Chest and abdominal CT
[UpToDate: Once the diagnosis of an esophageal cancer is established, staging usually begins with a CT scan of the chest and upper abdomen to both evaluate the region of the primary tumor and to search for distant metastatic disease. However, CT is of limited value for locoregional tumor staging. Although it can accurately show enlarged nodes, sensitivity for celiac axis nodal disease is poor, and it is not consistently able to differentiate the depth of primary tumor invasion. In one study, local tumor staging was correctly predicted by CT in only 42% of patients. Endoscopic ultrasound (EUS) is more accurate and has replaced CT as the locoregional tumor staging modality of choice.
Another disadvantage of CT is its limited sensitivity for small metastases (particularly within the peritoneum). PET scans are more sensitive than CT for detecting metastatic disease and are now widely used for preoperative staging in patients who lack evidence of distant disease on CT. In general, the addition of preoperative PET to the staging evaluation results in a change in management (usually avoidance of unnecessary surgery) in up to 20% of patients with esophageal cancer.
Like CT, PET scans (with or without integrated CT) have low accuracy for staging locoregional disease extent, particularly nodal status. This may be due, at least in part, to high FDG uptake in the primary esophageal malignancy that obscures increased FDG uptake in the regional nodes and/or low sensitivity for small involved lymph nodes.]
The middle and lower thirds of the esophagus are composed of what type of muscle?
Smooth muscle
Epigastric pain in a previously healthy individual is concerning for what?
- Peptic ulcer
- Tumor
What are the 3 anatomic areas of esophageal narrowing?
- Cricopharyngeus muscle
- Compression by the left mainstem bronchus and aortic arch
- Diaphragm
What is the treatment for a grade 2 burn of the esophagus due to a caustic agent?
Prolonged observation and conservative therapy (IVF, spitting, antibiotics, oral intake after 3-4 days)
[Indications for esophagectomy include: Sepsis, peritonitis, mediastinitis, free air, mediastinal or stomach wall air, crepitance, contrast extravasation, pneumothorax, larger effusion]
[UpToDate: Grade 2A – Superficial ulcers, bleeding, exudates. Grade 2B – Deep focal or circumferential ulcers.
If the patient is asymptomatic and gives a reliable history of a low-volume, accidental ingestion of low-concentration acid or alkali, endoscopy may not be necessary. Such patients may be discharged and followed as outpatients.
In all other instances, the patient should be hospitalized, kept fasting, and have serial chest and abdominal films taken. If the patient is hypotensive, intravenous fluids and blood products should be administered. Gastric acid suppression with intravenous proton pump inhibitors is often used to prevent stress ulcers of the stomach. Adequate pain relief with intravenous narcotics needs to be maintained continuously until the patient improves. Clinical signs of perforation, mediastinitis, or peritonitis are indications for emergency surgery. Broad spectrum antibiotics (such as third generation cephalosporins) are often given for patients with Grade 3 caustic injury or when there is a high suspicion for esophageal perforation.
For patients in respiratory distress, laryngoscopy should be performed in order to evaluate the need for tracheostomy. Patients with oropharyngeal injury should be monitored closely for the possible development of airway obstruction. Examination of the oropharynx may reveal edema, erosions, or deep necrosis with grayish pseudomembranes. If the epiglottis or the larynx is edematous, endotracheal intubation is contraindicated and a tracheostomy should be performed for airway control.
It is also important to recognize that certain agents and procedures are contraindicated in the presence of caustic ingestions:
Use of emetics is contraindicated because vomiting re-exposes the esophagus and the oropharynx to the caustic agent, further aggravating injury.
Neutralizing agents (weakly acidic or basic substances) should not be administered because damage is generally instantaneous. Furthermore, neutralization releases heat that adds thermal injury to the ongoing chemical destruction of tissue.
Nasogastric intubation to remove any remaining caustic material is contraindicated because it may induce retching and vomiting, which can compound injury and possibly lead to perforation of the weakened esophagus or stomach.]
Where does adenocarcinoma of the esophagus occur?
Lower 1/3 of esophagus
[UpToDate: Much more is known about the early pathology of adenocarcinoma of the esophagus because of recognition of early cancer during surveillance of patients with Barrett’s esophagus. The majority of cases are located near the gastroesophageal junction and are associated with endoscopic evidence of Barrett’s esophagus. Adenocarcinoma arising in Barrett’s esophagus may present as an ulcer, a nodule, an altered mucosal pattern, or no visible endoscopic abnormality. Early adenocarcinoma not associated with Barrett’s esophagus arises from an ulcer, plaque, or nodule near the gastroesophageal junction.]
What is the best test for dysphagia?
Esophogram
[UpToDate: Patients with esophageal dysphagia should be referred for an upper endoscopy. In addition to its diagnostic value, endoscopy offers an opportunity to obtain tissue samples to determine the etiology, and to perform a therapeutic intervention (eg, dilation of an esophageal ring).
We perform a barium swallow in the following patients:
- As the initial test (prior to upper endoscopy) in patients with a history or clinical features suggestive of a proximal esophageal lesion (eg, surgery for laryngeal or esophageal cancer, Zenker’s diverticulum, or radiation therapy), a known complex (tortuous) stricture (eg, post-caustic injury or radiation therapy). In these patients, the blind intubation of the proximal esophagus during upper endoscopy may be associated with the risk of perforation due to upper esophageal pathology. However, it is important to note that performing a barium swallow prior to an upper endoscopy in such patients has not been demonstrated to decrease the rate of endoscopic complications or improve outcomes.
- Following a negative upper endoscopy in patients in whom a mechanical obstruction is still suspected, as lower esophageal rings or extrinsic esophageal compression can be missed by an upper endoscopy.
Patients should be instructed to drink barium in the prone-oblique position; maximal distension of the esophagogastric junction is achieved by having the patient swallow barium rapidly in association with a variety of respiratory maneuvers. In addition, asking the patient to swallow 13 mm barium tablets or a solid bolus, such as a marshmallow or bread, may be helpful for demonstrating subtle lesions in patients with persistent or intermittent solid food dysphagia.
Motility testing should be performed in patients with dysphagia in whom upper endoscopy is unrevealing and/or an esophageal motility disorder is suspected. Although certain motility disorders (eg, achalasia) can be strongly suspected based upon their characteristic radiographic appearance when in advanced stages, confirmation with a motility study is required to establish the diagnosis. A nonspecific motility disorder or achalasia can be detected in up to 50% of patients with nonstructural dysphagia.]
From which side is the appropriate surgical approach for the upper 2/3 thoracic esophagus?
Right (avoids the aorta)
[UpToDate: The tri-incisional esophagectomy combines the transhiatal and transthoracic approaches into a transthoracic total esophagectomy with a thoracic lymphadenectomy and cervical esophagogastric anastomosis. The three-incisional technique allows the surgeon to perform a complete two-field (mediastinal and upper abdominal) lymphadenectomy under direct vision and a cervical esophagogastric anastomosis. We prefer a thorascopic approach to the chest rather than a thoracotomy to minimize the risk of respiratory complications.
Thoracotomy – A right posterolateral thoracotomy or a thoracoscopy is performed first to assess resectability and exclude local invasion of contiguous structures. An en bloc resection is performed that includes the esophagus and mediastinal and upper abdominal lymph nodes, including the right paratracheal, subcarinal, periesophageal and celiac axis lymph nodes.
Laparotomy – The abdomen is explored to exclude metastatic disease, and the stomach is mobilized in preparation for the construction of the gastric conduit.
Neck incision – A left neck exposure is preferred for the esophagogastric anastomosis, since this approach reduces the risk of injury to the recurrent laryngeal nerve (RLN). The left RLN recurs lower (around the aortic arch) than the right RLN, which recurs around the subclavian artery and is therefore more likely to be injured from a right neck approach.
The advantages of a neck anastomosis include easier management of a possible anastomotic leak, lower incidence of reflux, more extensive proximal resection margin, and location outside of radiation ports if administered preoperatively.]
What is the treatment for uncomplicated Barrett’s esophagus?
Treat like GERD with PPI or nissen
[Patients need careful follow-up with EGD for lifetime, even after nissen. Surgery will decrease esophagitis and prevent further metaplasia but it will not prevent malignancy or cause regression of the columnar lining.]
[UpToDate: The recommendations that follow are generally consistent with guidelines from the British Society of Gastroenterology, the American Society of Gastrointestinal Endoscopy, and the American Gastroenterological Association, as well as a 2015 international consensus statement. However, it should be noted that many of the issues related to the surveillance and management of Barrett’s esophagus remain controversial, with considerable disagreement among experts.
The risk of developing esophageal adenocarcinoma in patients with nondysplastic Barrett’s esophagus is estimated to be 0.1-0.4% per year. Although this risk is increased at least 30-fold above that of the general population, the absolute risk for any individual patient with nondysplastic Barrett’s esophagus is low.
We suggest that all patients with Barrett’s esophagus receive treatment with a proton pump inhibitor (PPI) rather than reserving treatment only for patients who are symptomatic (Grade 2B). We typically start patients on a standard dose of a PPI once daily (eg, omeprazole 20 mg daily), and only increase the dose if it is required to eliminate gastroesophageal reflux disease symptoms or to heal reflux esophagitis.
In patients with suspected Barrett’s esophagus, we perform endoscopic four-quadrant biopsies every 2 cm. Any mucosal irregularities in the Barrett’s segment should be removed with endoscopic resection, and the resected specimen should be sent for evaluation by a pathologist with expertise in esophageal histopathology. Subsequent recommendations depend on whether dysplasia is seen on histology. Any diagnosis of dysplasia should be confirmed by a second pathologist with expertise in esophageal pathology.]
What is the most common site of esophageal perforation?
Cricopharyngeus muscle (usually occurs with EGD)
[UpToDate: Zenker’s diverticula (ZD) and epiphrenic diverticula are thought to be caused by motor abnormalities of the esophagus. In contrast, traction diverticula were originally thought to be due to scarring and traction on the walls of the esophagus (hence the name) from external inflammatory processes (such as fungal infections or tuberculosis). However, more recent evidence has demonstrated that many mid-esophageal diverticula are also associated with esophageal motility abnormalities including spasm, achalasia, lower esophageal sphincter hypertension, or nonspecific abnormalities.
ZD emerge from a defect in the muscular wall of the hypopharynx in a natural area of weakness known as Killian’s triangle, which is formed by the oblique fibers of the inferior pharyngeal constrictor muscle and the cricopharyngeal sphincter. Autopsy series suggest Killian’s triangle is more prevalent in males (60%) and is associated with the dimensions of the body and with the length and the descensus of the larynx. Evagination of the sphincter is thought to result from chronic increased pressure on the weakened area, which may be due to two causes:
- High intrabolus pressures during swallowing
- Resistance to swallowing due to abnormalities of the upper esophageal sphincter (UES).]
What organism can cause symptoms similar to achalasia?
Trypanasoma Cruzi
[UpToDate: The etiology of primary or idiopathic achalasia is unknown. Secondary achalasia is due to diseases that cause esophageal motor abnormalities similar or identical to those of primary achalasia. In Chagas disease, which occurs predominantly in Central and South America, esophageal infection with the protozoan parasite Trypanosoma cruzi can result in a loss of intramural ganglion cells, leading to aperistalsis and incomplete lower esophageal sphincter relaxation. Other diseases that have been associated with achalasia-like motor abnormalities include amyloidosis, sarcoidosis, neurofibromatosis, eosinophilic esophagitis, multiple endocrine neoplasia type 2B, juvenile Sjögren syndrome, chronic idiopathic intestinal pseudo-obstruction, and Fabry disease.]
Which vein does the thoracic duct insert into?
Left subclavian vein
What are the treatments of diffuse esophageal spasm?
- Calcium channel blockers
- Nitrates
[Upper and lower esophagus Heller myotomy if those fail.]
[UpToDate: In patients whose primary symptom is dysphagia, we suggest initial treatment with a calcium channel blocker (eg, diltiazem 180 to 240 mg/day). In patients whose primary symptom is chest pain, we suggest a calcium channel blocker or a tricyclic antidepressant (eg, imipramine 25 to 50 mg at bedtime) as the initial treatment. For patients who do not respond to initial treatment, treatment options include botulinum toxin or a nitric oxide contributing drug (eg, isosorbide 10 mg or sildenafil 50 mg on an as needed basis for pain).]
Which imaging tests are indicated in a patient who has ingested a caustic agent?
- Plain films
- Chest and abdominal CT
[To look for free air and signs of perforation]
[UpToDate: The absence of oropharyngeal burns does not preclude the presence of esophageal or gastric injury. Thus, upper gastrointestinal endoscopy should be performed during the first 24 hours after ingestion in order to evaluate the extent of esophageal and gastric damage, establish prognosis, and guide therapy. Endoscopy is contraindicated in patients who have evidence of perforation. In patients who are hemodynamically unstable, endoscopy should be postponed until the patient is adequately resuscitated and is once again hemodynamically stable. If severe respiratory distress is present or there are signs of severe oropharyngeal or glottic edema and/or necrosis, the patient should be intubated for airway protection prior to endoscopy. In addition, extra care should be taken when performing an endoscopy in such patients because of the risk of perforation if the esophagus is similarly damaged.]
What type of hiatal hernia is characterized as paraesophageal (a hole in the diaphragm alongside the esophagus and a normal GE junction)?
Type II
[UpToDate: A paraesophageal hernia is a true hernia with a hernia sac and is characterized by an upward dislocation of the gastric fundus through a defect in the phrenoesophageal membrane.
Type II hernia results from a localized defect in the phrenoesophageal membrane where the gastric fundus serves as a lead point of herniation, while the GE junction remains fixed to the preaortic fascia and the median arcuate ligament.]
What is the treatment for a non-contained esophageal perforation with minimal contamination that gets diagnosed early?
Primary repair with drains
[Requires longitudinal myotomy to see full extent of injury. Consider intercostal muscle flaps to cover repair]
[UpToDate: Primary repair of esophageal injuries can be performed whenever there is an ability to get a closure of healthy tissue without tension. The esophagus should be debrided to healthy tissue and repaired.
Most low grade (I through III) traumatic esophageal perforations can be repaired primarily, or repaired over a drain. If primary repair is not possible because of contamination or hemodynamic instability, but there is only a small amount of tissue loss, an effective strategy is to repair the esophagus around a large T-tube, but this is rarely needed with the availability of esophageal stents. This creates a controlled esophageal-cutaneous fistula, which may close spontaneously after edema resolves and the T-tube is removed. Alternatively, an esophageal stent could be used to cover the defect.
The esophagus should be debrided to healthy tissue and the mucosal defect should be completely exposed, even if this requires enlarging the muscular defect. Failure to close the mucosa will most assuredly result in failure of the repair. Intraoperative endoscopy can be helpful for identifying the extent of the defect. The mucosal defect should be closed first, followed by a second layer closure of the muscularis layer. There are no studies comparing the techniques. Some recommend absorbable suture with knots on the outside to avoid granuloma formation, but this has not been subjected to rigorous evaluation.
Larger defects or those involving significant devascularization (IV, V) require more challenging surgical management. Typically in the traumatic circumstance, esophagectomy with reconstruction is not indicated due to the length and technical nature of the procedure as well as the patient’s hemodynamic status. Rather, esophageal diversion may be required. This includes creation of an end cervical esophagostomy and division of the esophagus at the gastroesophageal junction to exclude the site of injury. If the patient is hemodynamically stable, removal of the thoracic esophagus should be performed. In the unstable patient, the thoracic esophagus may be left in situ with removal later once the patient is stable. While in the abdomen, a gastrostomy is recommended but should be placed strategically so as to not damage the subsequent formation of a gastric tube for reconstruction of the gastrointestinal tract. Feeding jejunostomy is also recommended, although only in stable patients. Delayed esophageal reconstruction is planned months later.]
How does a Heller myotomy differ in the treatment of achalasia and diffuse esophageal spasm?
- Achalasia requires only myotomy of the lower esophagus
- Diffuse esophageal spasm requires myotomy of the upper and lower esophagus
Barrett’s esophagus is characterized histologically by what?
Squamous metaplasia to columnar epithelium
[UpToDate: Endoscopic examination generally is required to diagnose Barrett’s esophagus. Two criteria must be fulfilled:
The endoscopist must document that columnar epithelium lines the distal esophagus.
Histologic examination of biopsy specimens from that columnar epithelium must reveal intestinal metaplasia. Some data suggest that gastric cardiac-type epithelium in the esophagus also might predispose to cancer and thus might be considered “Barrett’s esophagus,” but most authorities still require the presence of intestinal metaplasia for an unequivocal diagnosis.]
What is the treatment for a grade 3 burn of the esophagus due to a caustic agent?
Esophagectomy
[Caustic esophageal perforations require esophagectomy and are not repaired due to extensive damage]
[UpToDate: Grade 3A – Focal necrosis. Grade 3B – Extensive necrosis.
If the patient is asymptomatic and gives a reliable history of a low-volume, accidental ingestion of low-concentration acid or alkali, endoscopy may not be necessary. Such patients may be discharged and followed as outpatients.
In all other instances, the patient should be hospitalized, kept fasting, and have serial chest and abdominal films taken. If the patient is hypotensive, intravenous fluids and blood products should be administered. Gastric acid suppression with intravenous proton pump inhibitors is often used to prevent stress ulcers of the stomach. Adequate pain relief with intravenous narcotics needs to be maintained continuously until the patient improves. Clinical signs of perforation, mediastinitis, or peritonitis are indications for emergency surgery. Broad spectrum antibiotics (such as third generation cephalosporins) are often given for patients with Grade 3 caustic injury or when there is a high suspicion for esophageal perforation.
For patients in respiratory distress, laryngoscopy should be performed in order to evaluate the need for tracheostomy. Patients with oropharyngeal injury should be monitored closely for the possible development of airway obstruction. Examination of the oropharynx may reveal edema, erosions, or deep necrosis with grayish pseudomembranes. If the epiglottis or the larynx is edematous, endotracheal intubation is contraindicated and a tracheostomy should be performed for airway control.
It is also important to recognize that certain agents and procedures are contraindicated in the presence of caustic ingestions:
Use of emetics is contraindicated because vomiting re-exposes the esophagus and the oropharynx to the caustic agent, further aggravating injury.
Neutralizing agents (weakly acidic or basic substances) should not be administered because damage is generally instantaneous. Furthermore, neutralization releases heat that adds thermal injury to the ongoing chemical destruction of tissue.
Nasogastric intubation to remove any remaining caustic material is contraindicated because it may induce retching and vomiting, which can compound injury and possibly lead to perforation of the weakened esophagus or stomach.]
What is the most common type of hiatal hernia?
Type I
[Sliding hernia from dilation of the hiatus]
[UpToDate: A type I or sliding hiatus hernia is characterized by the displacement of the gastroesophageal (GE) junction above the diaphragm. The stomach remains in its usual longitudinal alignment and the fundus remains below the GE junction.]
What is the treatment for a grade 1 burn of the esophagus due to a caustic agent?
Observation and conservative therapy
[Conservative therapy: IVF, spitting, antibiotics, oral intake after 3-4 days]
[UpToDate: Grade 0 – Normal. Grade 1 – Mucosal edema and hyperemia
If the patient is asymptomatic and gives a reliable history of a low-volume, accidental ingestion of low-concentration acid or alkali, endoscopy may not be necessary. Such patients may be discharged and followed as outpatients.
In all other instances, the patient should be hospitalized, kept fasting, and have serial chest and abdominal films taken. If the patient is hypotensive, intravenous fluids and blood products should be administered. Gastric acid suppression with intravenous proton pump inhibitors is often used to prevent stress ulcers of the stomach. Adequate pain relief with intravenous narcotics needs to be maintained continuously until the patient improves. Clinical signs of perforation, mediastinitis, or peritonitis are indications for emergency surgery. Broad spectrum antibiotics (such as third generation cephalosporins) are often given for patients with Grade 3 caustic injury or when there is a high suspicion for esophageal perforation.
For patients in respiratory distress, laryngoscopy should be performed in order to evaluate the need for tracheostomy. Patients with oropharyngeal injury should be monitored closely for the possible development of airway obstruction. Examination of the oropharynx may reveal edema, erosions, or deep necrosis with grayish pseudomembranes. If the epiglottis or the larynx is edematous, endotracheal intubation is contraindicated and a tracheostomy should be performed for airway control.
It is also important to recognize that certain agents and procedures are contraindicated in the presence of caustic ingestions:
Use of emetics is contraindicated because vomiting re-exposes the esophagus and the oropharynx to the caustic agent, further aggravating injury.
Neutralizing agents (weakly acidic or basic substances) should not be administered because damage is generally instantaneous. Furthermore, neutralization releases heat that adds thermal injury to the ongoing chemical destruction of tissue.
Nasogastric intubation to remove any remaining caustic material is contraindicated because it may induce retching and vomiting, which can compound injury and possibly lead to perforation of the weakened esophagus or stomach.]
Where do the right and left vagus nerves travel with respect to the stomach?
- Right travels posterior to the stomach
- Left travels anterior to the stomach
What is the most common type of esophageal cancer?
Adenocarcinoma
[UpToDate: For most of the twentieth century, SCC comprised the vast majority of esophageal cancers globally. For the past three decades, however, the frequency of adenocarcinoma of the esophagus, esophagogastric junction (EGJ) and gastric cardia has increased dramatically, a finding initially observed in Western countries and more recently in some Eastern countries as well. In many epidemiologic series, the incidence of adenocarcinoma has overtaken that of the previously more common SCC. As an example, a study of a cancer registry in the United States estimated that the age-adjusted incidence rates of esophageal adenocarcinoma rose progressively from 1.8 per 100,000 in 1987 to 1991 to 2.5 per 100,000 during 1992 to 1996. Whites were affected five times more often than blacks, and men eight times more often than women, although the incidence among white women has also increased. A significant increase in the incidence was observed among persons aged 45 to 65.]
What method of esophagectomy may be the preferred choice in young patients because it preserves gastric function?
Colonic interposition
[NCBI: Almost a century ago, Kelling and Vuillet introduced the use of the colon as an esophageal substitute. Since then, several modifications to this approach have been described, using the left, the right, or the transverse colon as an interposition graft. Interposition of the left colon became the most popular procedure. It requires wide mobilization of the entire colon, ligation of the middle colic artery, and transection of the colon at the right flexure and somewhere between the left flexure and the midportion of the descending colon, depending on the patient’s anatomy.
This preference for left colic interposition is based on the vascular anatomy and its natural variation in the colon. According to several autopsy studies, the arterial anastomoses (marginal artery) between the ileocolic and right colic vessels are absent in up to 70% of patients, whereas the collaterals between the left and right colic artery are mostly sufficient. Corresponding differences can be found with venous collaterals in the colon. In the left colon, the marginal venous anastomoses are excellent, but ileocolic venous collaterals are insufficient in 20% to 30% of patients.
Mesenteric angiography does not always confirm these autopsy results. In patients scheduled for colonic interposition, a discontinuity of the superior–inferior mesenteric artery anastomosis at the left flexure was seen in 48%; discontinuity of the marginal artery between the middle and right colic artery was seen in 70%. However, the relevance of these angiography findings for the selection of the colon graft is questionable: intraoperative trial clamping rarely demonstrates an inadequate collateral flow through arterial anastomoses at the splenic flexure.
Clinical results appear to support the superiority of left to right colonic interposition. A combined evaluation of studies that allow a separate analysis of left or right colon grafts revealed a rate of colon necrosis or ischemia of 4.6% (20/438) with use of the left colon and of 10.8% (13/120) with use of the right.
However, even an almost 5% rate of left colonic graft failure cannot be considered optimal, because this complication is potentially life-threatening and adds to the significant general risk of the procedure.]
What is the appropriate diagnostic test for Zenker’s diverticulum?
Barium swallow or manometry
[Risk for perforation with EGD]
[UpToDate: Zenker’s diverticula are usually diagnosed with barium swallowing examinations, preferably combined with dynamic continuous fluoroscopy during the swallowing process. In some patients, the entire first glass of barium taken will disappear into the confines of an especially large diverticulum. However, small diverticula can be missed if they are superimposed on the main column of barium in the esophagus. This can be avoided by rotating the patient during the examination. In our experience, a second diverticulum is present in approximately 1-2% of patients but is usually much smaller than the first. Esophageal manometry is typically not required; however, it may help to illuminate the pathogenesis of the diverticulum. An alternative method to diagnose ZD and to differentiate from a thyroid or neck mass is transcutaneous ultrasound. This technique might be a good alternative in people who experience difficulties in swallowing barium, provided the technique is in experienced hands.]
Which tests should be employed to diagnose esophageal perforation?
CXR (looking for free air) followed by gastrografin swallow and then barium swallow
[UpToDate: An esophageal perforation should be suspected in patients who develop significant neck, chest, or abdominal pain following endoscopy. Generally, the evaluation starts with an examination for signs of a perforation (eg, subcutaneous emphysema), followed by plain thoracic and cervical radiographs. If needed, contrast esophagography or computed tomographic (CT) scanning may be obtained to confirm the diagnosis or to look for intrathoracic and intra-abdominal collections that require drainage.
Because delays in diagnosis are associated with higher complication and mortality rates, early diagnosis is essential. As an example, in a summary of 390 patients from 11 series, the overall mortality rate for patients who did not receive treatment within 24 hours was 27% (range 0-46%), whereas it was 14% (range 0-28%) for patients who were treated within 24 hours.
Patients with a suspected perforation should undergo thoracic and cervical radiographs (posterior-anterior and lateral films). In addition, if an intra-abdominal perforation is suspected, upright abdominal films should be obtained. Radiographic evidence of emphysema is found subcutaneously in the neck in approximately 95% of patients with cervical perforations, and in the mediastinum in approximately 40% of patients with intrathoracic perforations. Other findings suggestive of an esophageal perforation include pleural effusions, mediastinal widening, hydrothorax, hydropneumothorax, or subdiaphragmatic air. Mediastinal emphysema may not become visible radiographically for an hour, and pleural effusions and mediastinal widening may take several hours to develop.
Contrast esophagography (Gastrografin or barium swallow) — Contrast esophagography usually establishes the diagnosis. The sensitivity of contrast studies depends upon the size and location of the perforation, and the technique used for the study. The studies should be carried out with the patient in the right lateral decubitus position. In many centers, water-soluble contrast agents (eg, Gastrografin) are used initially. Esophagography with water-soluble contrast will show extravasation on radiograph in 50% of patients with cervical perforations and 75-80% of patients with thoracic perforations. Water-soluble contrast must be used with care in patients at risk for aspiration, as it can cause severe pneumonitis. In such patients, dilute barium is preferred as the initial contrast agent. In addition, water-soluble contrast should not be used in patients with known or suspected fistulas between the esophagus and the respiratory tract or if respiratory tract perforation is suspected.
If the water-soluble contrast study is negative, a barium study should be performed. Barium studies will detect 60% of cervical perforations and 90% of intrathoracic perforations. Although barium is superior to water-soluble contrast for demonstrating small perforations, it causes an inflammatory response in mediastinal or pleural cavities and is therefore not used as the primary diagnostic study.]
Which nerve can cause persistently high acid levels postoperatively if left undivided after a vagotomy?
Criminal nerve of Grassi (branch of the right posterior vagus nerve)
[UpToDate: Vagotomy is a procedure that transects or removes a portion of the vagus nerves or branches of the vagus nerves to decrease gastric acid secretion. Vagotomy eliminates direct cholinergic stimulation of acid secretion and renders the acid-producing parietal cells less responsive to histamine and gastrin. Vagotomy also abolishes the vagal stimulus for release of antral gastrin. Vagotomy can be performed by sectioning the vagal trunks (ie, truncal vagotomy), sectioning distal nerve fibers (referred to as highly selective vagotomy, parietal cell vagotomy, or proximal gastric vagotomy), or a combination of techniques. It can be performed in an open or laparoscopic fashion.
Truncal vagotomy is the simplest procedure to perform. Basal and stimulated acid secretions are reduced by 80% and 50%, respectively. However, truncal vagotomy sacrifices innervation to the pancreas, small intestine, proximal colon, and hepatobiliary tree, and alters gastric physiology requiring some form of gastric emptying procedure (pyloroplasty or gastroenterostomy). Highly selective vagotomy reduces basal and stimulated acid secretion by more than 75% and 50%, respectively, while minimizing the effects of vagotomy on gastric emptying. However, surgeons-in-training have less exposure to the more technically demanding procedures, like highly selective vagotomy (parietal cell vagotomy), because of the decrease in the hospitalization rate for peptic ulcer disease.]
What is the initial treatment for GERD?
Proton pump inhibitor
[Omeprazole is 99% effective]
[UpToDate: We suggest lifestyle and dietary modification in all patients with GERD (Grade 2C).
In patients with mild and intermittent (less than two episodes per week) symptoms of GERD who are naïve to treatment, we suggest as needed low-dose histamine 2 receptor antagonists (H2RAs).
Concomitant antacids are appropriate if symptoms occur less than once a week. In patients with continued symptoms, we increase the dose of H2RAs to standard dose, twice daily for a minimum of two weeks.
If symptoms of GERD persist, we discontinue H2RAs and initiate once-daily proton pump inhibitors (PPIs) at a low dose (Grade 2B) and then increase to standard doses if required for symptom control.
We make gradual incremental changes in therapy at two- to four-week intervals. Once symptoms are controlled, therapy should be continued for at least eight weeks.
In patients with erosive esophagitis, we recommend initial acid suppressive therapy with standard-dose PPI once daily.]
What is the most common benign tumor of the esophagus?
Leiomyoma
[UpToDate: The classic or usual GI tract leiomyoma has a similar morphologic appearance to leiomyomas in other organs. In the gut, they are usually small and well circumscribed. The tumors typically arise from the muscularis propria; growth may be intraluminal, extraluminal, or a combination with a dumb-bell shape. Leiomyomas can range in size from less than 0.5 cm (microleiomyomas) to as large as 30 cm.
Microscopically, leiomyomas are formed of fascicles of benign-appearing spindle cells without nuclear atypia; mitoses are sparse or absent, and necrosis virtually never occurs. The nucleus is centrally located and oval but may be displaced to one side by distinct vacuoles suggesting signet-ring cells. These vacuoles do not contain fat or mucosubstances, which differentiates them from liposarcomas and carcinomas.]
What is the best test for diagnosing GERD?
pH probe
[The current gold standard for diagnosis of GERD is esophageal pH monitoring. It is the most objective test to diagnose the reflux disease and allows monitoring GERD patients in their response to medical or surgical treatment. One practice for diagnosis of GERD is a short-term treatment with proton-pump inhibitors, with improvement in symptoms suggesting a positive diagnosis. Other tests include: endoscopy, histology, manometry. Fiser also states that EGD is the best test for heartburn because it can directly visualize esophagitis.]
[UpToDate: The diagnosis of gastroesophageal reflux disease (GERD) can be based upon clinical symptoms alone. Response to antisecretory therapy is not a diagnostic criterion for GERD. A meta-analysis of diagnostic test characteristics found that a response to proton pump inhibitors (PPIs) did not correlate well with objective measures of GERD such as ambulatory pH monitoring. Pooled sensitivity was 78% while specificity was 54%. Thus, a response to PPIs does not correspond to a GERD diagnosis based on reflux testing. However, the observation that 40-90% of patients with symptoms suggestive of GERD have a symptomatic response to PPIs raises the question of which diagnostic approach is more relevant in practice. Clearly, it is neither necessary nor practical to initiate an invasive diagnostic evaluation in every patient with heartburn.
However, in a subset of patients, diagnostic testing is required to confirm the diagnosis of GERD and to rule out other diagnoses
The goal of additional testing is to confirm the diagnosis of gastroesophageal reflux disease (GERD) in patients refractory to therapy, assess for complications of GERD, or to establish alternative diagnoses.
According to a guideline issued by the American Gastroenterological Association (AGA), endoscopy with biopsy should be done at presentation for patients with an esophageal GERD syndrome with troublesome dysphagia and to evaluate patients with a suspected esophageal GERD syndrome who have not responded to an empirical trial of twice-daily PPI therapy.
Other potentially useful tests are ambulatory pH monitoring and manometry. Ambulatory pH monitoring is useful for confirming gastroesophageal reflux disease in those with persistent symptoms (whether typical or atypical) who do not have evidence for mucosal damage on endoscopy, particularly if a trial of twice-daily PPI has failed or to monitor the adequacy of treatment in those with continued symptoms. In this setting, pH monitoring should be done while withholding PPI therapy. Manometry is useful in ensuring that ambulatory pH probes are placed correctly, to evaluate peristaltic function before antireflux surgery, and to exclude major motor disorders as an alternative diagnosis in patients with chest pain and/or dysphagia.
Biliary tract ultrasonography should be considered in patients with nausea and/or epigastric pain. Double contrast barium swallow is used infrequently. When data from barium radiography and endoscopy were compared, the diagnostic accuracy of radiography was 25% with mild esophagitis, 82% with moderate esophagitis, and 99% with severe esophagitis. The demonstration of reflux of barium during the study is of dubious significance since it can be provoked in 25-71% of symptomatic patients compared with 20% of normal controls.
Unexplained chest pain should be evaluated with at least an electrocardiogram and exercise stress test prior to a gastrointestinal evaluation.]
What causes Zenker’s diverticula?
Failure of the cricopharyngeus to relax
[UpToDate: Zenker’s diverticula (ZD) and epiphrenic diverticula are thought to be caused by motor abnormalities of the esophagus. In contrast, traction diverticula were originally thought to be due to scarring and traction on the walls of the esophagus (hence the name) from external inflammatory processes (such as fungal infections or tuberculosis). However, more recent evidence has demonstrated that many mid-esophageal diverticula are also associated with esophageal motility abnormalities including spasm, achalasia, lower esophageal sphincter hypertension, or nonspecific abnormalities.
Evagination of the sphincter is thought to result from chronic increased pressure on the weakened area, which may be due to two causes:
- High intrabolus pressures during swallowing
- Resistance to swallowing due to abnormalities of the upper esophageal sphincter (UES)
The data supporting these hypotheses have been based upon manometric pressure recordings in patients with ZD. However, studies evaluating UES pressures in these patients have been inconsistent. The technical challenges of manometric data collection for UES function may account for such varied results. They may also reflect potentially heterogeneous defects that could result in a ZD and the variable methods used to record UES pressures. Furthermore, the presence of a diverticulum, particularly a larger one, may distort the pressure profile such that it no longer represents the conditions that originally favored diverticulum formation.]
Epiphrenic diverticula are rare and occur in association with what?
Esophageal motility disorders (I.E. Achalasia)
[UpToDate: The classification of esophageal diverticula depends upon their location. They predominantly occur in three areas:
- Immediately above the upper esophageal sphincter (Zenker’s diverticulum)
- Near the midpoint of the esophagus (traction diverticulum)
- Immediately above the lower esophageal sphincter (epiphrenic diverticulum)
Zenker’s diverticula (ZD) and epiphrenic diverticula are thought to be caused by motor abnormalities of the esophagus. In contrast, traction diverticula were originally thought to be due to scarring and traction on the walls of the esophagus (hence the name) from external inflammatory processes (such as fungal infections or tuberculosis). However, more recent evidence has demonstrated that many mid-esophageal diverticula are also associated with esophageal motility abnormalities including spasm, achalasia, lower esophageal sphincter hypertension, or nonspecific abnormalities . ]
Which artery supplies the cervical esophagus?
Inferior thyroid artery
What are the treatments for nutcracker esophagus?
- Calcium channel blocker
- Nitrates
[Upper and lower esophagus Heller myotomy if those fail]
[UpToDate: In patients whose primary symptom is dysphagia, we suggest initial treatment with a calcium channel blocker (eg, diltiazem 180 to 240 mg/day). In patients whose primary symptom is chest pain, we suggest a calcium channel blocker or a tricyclic antidepressant (eg, imipramine 25 to 50 mg at bedtime) as the initial treatment. For patients who do not respond to initial treatment, treatment options include botulinum toxin or a nitric oxide contributing drug (eg, isosorbide 10 mg or sildenafil 50 mg on an as needed basis for pain).]
What is the treatment for Schatzki’s ring?
Dilatation of the ring and a proton pump inhibitor
[Do not resect]
[UpToDate: In a series of 104 patients with a Schatzki ring, a single dilation with a large bougie dilator was effective and safe. The dilator chosen was at least 2 mm larger than the estimated size of the residual lumen (range 2-9 mm larger). All patients had relief of their dysphagia following dilation, and there were no complications.]
Dysphagia/odynophagia in a previously healthy individual are concerning for what?
Tumor
Which two arteries supply the abdominal esophagus?
- Left gastric artery
- Inferior phrenic artery
Which part of the esophagus lymphatically drains cephalad and caudad?
- Upper 2/3 drains cephalad
- Lower 1/3 drains caudad
What is the surgical treatment for GERD?
Nissen fundoplication
[Divide short gastrics, pull esophagus into abdomen, approximate crura, 270 (partial) or 360 (full) degree gastric fundus wrap]
[UpToDate: A variety of antireflux procedures have been described for the treatment of gastroesophageal reflux disease (GERD). The most common procedures (Nissen fundoplication, Belsey Mark IV, and Hill repair) claim about an 85% success rate in relieving symptoms and healing esophagitis. Long-term mortality of surgical management is quite low.
Many surgical approaches focus on restoring a physiologic equivalent to the normal LES. Manometric studies of the lower esophageal sphincter (LES) have documented that reflux is correlated with a lower mean LES pressure, shorter mean intra-abdominal LES length, and shorter overall sphincter length. Each of these problems can be corrected by specific surgical procedures.
The Nissen fundoplication has, in many series, been found superior to other procedures, with symptomatic improvement occurring in 85-90% of patients. This procedure originally involved passage of the gastric fundus behind the esophagus to encircle the distal 6 cm of the esophagus. However, many variations and modifications have been described, and a “Nissen fundoplication” may be performed differently by different surgeons. Variables include: approach (transthoracic or abdominal); portion of stomach wall used (anterior and posterior or anterior only); combination with other procedures (eg, vagotomy or gastroplasty); the looseness of the wrap; the completeness of the wrap; and the length of the wrap. Most surgeons choose to perform a loose (“floppy”) Nissen fundic wrap that is about 1-2 cm in length including a posterior crural repair.
Nissen fundoplication can also be effectively performed laparoscopically. Although there have been few long-term studies, a number of observational studies of laparoscopic fundoplication demonstrate comparable safety, short-term efficacy, and patient satisfaction, as well as shorter hospital stays and recuperative times than with open operation. A prospective, randomized trial comparing open with laparoscopic fundoplication in 110 consecutive patients found, at up to 11 years follow-up, similar benefits on symptoms but a significantly higher incidence of incisional hernias and defective fundic wraps in the open group.]
What condition is characterized as a narrowing of the lower esophagus that can cause dysphagia?
Schatzki’s ring
[UpToDate: B ring – Mucosal structure precisely at the squamocolumnar junction that is smooth and thin (<4 mm in axial length). A B ring can be demonstrated in approximately 15% of individuals on a barium swallow radiograph. When the caliber of a B ring is less than 12.5 mm, it is called a Schatzki ring, which is a common cause of solid food dysphagia. Owing to its location, a B ring is covered with squamous mucosa proximally and columnar epithelium distally.
B rings are found in 6-14% of routine barium esophagrams, but in the vast majority of patients they are asymptomatic. Schatzki rings (a subset of B rings) are less commonly identified during endoscopy (4% of patients undergoing upper endoscopy for various indications in one study.
Schatzki rings are almost always associated with hiatal hernias. In a study of 167 patients with a Schatzki ring, a hiatal hernia was detected in 97%. Schatzki rings have also been associated with eosinophilic esophagitis. However, more often patients with eosinophilic esophagitis have multiple proximal esophageal rings, long strictured segments, linear furrows in the mucosa, and eosinophilic abscesses that appear as white papules.]
What is the best test for dysphagia or odynophagia?
Barium swallow (better at picking up masses)
[UpToDate: We perform a barium swallow in the following patients:
- As the initial test (prior to upper endoscopy) in patients with a history or clinical features suggestive of a proximal esophageal lesion (eg, surgery for laryngeal or esophageal cancer, Zenker’s diverticulum, or radiation therapy), a known complex (tortuous) stricture (eg, post-caustic injury or radiation therapy). In these patients, the blind intubation of the proximal esophagus during upper endoscopy may be associated with the risk of perforation due to upper esophageal pathology. However, it is important to note that performing a barium swallow prior to an upper endoscopy in such patients has not been demonstrated to decrease the rate of endoscopic complications or improve outcomes.
- Following a negative upper endoscopy in patients in whom a mechanical obstruction is still suspected, as lower esophageal rings or extrinsic esophageal compression can be missed by an upper endoscopy.
Patients should be instructed to drink barium in the prone-oblique position; maximal distension of the esophagogastric junction is achieved by having the patient swallow barium rapidly in association with a variety of respiratory maneuvers. In addition, asking the patient to swallow 13 mm barium tablets or a solid bolus, such as a marshmallow or bread, may be helpful for demonstrating subtle lesions in patients with persistent or intermittent solid food dysphagia.]
