Esophagus and Diaphragm Flashcards
A 42-year-old male for whom you recently performed a
successful inguinal hernia repair, presents to your clinic
with a chief complaint of increasing difficulty swallowing some solids and occasionally liquids. He reports
this has been worsening for the last 5 months. He has
been treated by his primary care physician with daily
omeprazole, but this does not seem to be improving his
symptoms. Since you did such a good job in repairing
his hernia, he is now coming to you for advice on this
problem. He appears healthy, his vital signs are normal,
and he is maintaining his normal weight.
- The most appropriate initial study to help you sort
through the differential diagnosis of this patients
dysphagia is?
A. Contrast esophagram
B. Esophageal manometry
C. Esophagogastroduodenoscopy
D. H. pylori testing
E. Chest X-ray
A. Contrast esophagram offers the most useful information in initially sorting through this differential.
The esophagram shown essentially eliminates
diverticula and a hiatal hernia.
A contrast esophagram image is shown (showing contrast cut-off at the mid to distal esophagus).
What additional study or studies should be ordered
next in the diagnostic workup of this patient?
A. Esophageal manometry
B. Esophagogastroduodenoscopy (EGD)
C. 24-hour pH monitoring
D. 24-hour pH monitoring and EGD
E. Esophageal manometry and EGD
B.
This esophagram would typically be followed
up with an EGD.
While the esophagram shown makes the diagnosis of a diverticula or an hiatal hernia less likely, there are still several diagnoses that are not ruled out or confirmed.
An EGD would be needed to exclude anatomical causes for dysphagia, such as neoplasm or stricture.
The EGD would also be used to document any evidence of reflux or eosinophilic esophagitis.
If there is no reflux seen on EGD, a 24-hour pH study could confirm the presence of functional reflux disease.
If the 24-hour pH study is normal, then a manometry study could be done to rule out motility disorders like achalasia, diffuse esophageal spasm,
connective tissue disorders, and nutcracker esophagus.
Even if the 24-hour pH study is confirmatory, though, an esophageal manometry should be
done to rule out a concominant underlying motility disorder.
By skipping the EGD and proceeding directly to manometry, a diagnosis, such as pseudoachalasia secondary to a distal anatomic partial obstruction, may be missed.
- Upper endoscopy reveals no evidence of esophagitis, but some food is present in the distal esophagus. Manometry shows aperistalsis and a non-relaxing LES. Which initial treatment offers the patient the best chance of long term-relief?
A. Pneumatic dilation of the LES
B. Calcium channel blocker therapy
C. Esophageal myotomy with fundoplication
D. Botulinum toxin injection at LES
E. Esophagectomy
C.
This patient has achalasia. In the absence of an obstructing entity (neoplasm, hiatal hernia, diverticuli) retained food in the esophagus is suspicious for achalasia.
The diagnosis is confirmed by manometry. In patients with achalasia, the manometry demonstrates an esophagus in which there is complete absence of peristalsis and an LES pressure that is normal to moderately elevated, but fails to completely relax.
Although a hypertensive LES and an LES that fails to completely relax are often associated with achalasia, only the complete absence of peristalsis is required for the diagnosis.
The pathophysiology of achalasia is loss of ganglion cells in the myenteric plexus and interruption of inhibitory vagal nerve innervation.
The treatment for achalasia requires relaxing the hypertensive smooth muscles of the LES. In general, that can be done surgically by dividing the muscles of the LES, injecting botulinum toxin endoscopically, or dilating the LES using a balloon.
This is also done endoscopically. Surgical treatment with myotomy provides long-term treatment of achalasia with a high success rate.
Calcium channel blockers have shown inconsistent success and do not have a role in achalasia treatment.
Botulinum toxin usually requires repeated interventions every 6 to 12 months, as does
dilation. Both eventually become less effective. These may be good options in persons who are poor operative risks or in those who do not want surgery.
Esophagectomy would be required in the setting of cancer and is indicated as a last resort if multiple myotomies fail.
The POEM or per oral endoscopic myotomy technique involves dividing the LES muscle endoscopically. This has the advantage of avoiding most surgical risks. The long-term success rate, though, is unknown and is not yet considered the equivalent of a surgical myotomy.
Suppose in this same patient, that the results of the manometry do not show achalasia. Instead, the standard esophageal manometry shows 10/10 normal propagated swallows with a mean distal esophageal amplitude pressure of 293mm Hg.
The lower esophageal sphincter pressure is normal and relaxes completely. The results of ambulatory pH monitoring and EGD were both normal.
What is the most likely diagnosis?
A. Achalasia
B. Pseudoachalsia
C. Diffuse esophageal spasm
D. Nutcracker esophagus
D.
Manometry is used to rule out esophagility motility disorders. Not only does it measure how well food travels down the esophagus into the stomach, it also measures the pressure inside the esophagus and the LES.
The normal pressure of an LES is 10 to 15 mmHg.
Patients with GERD will often have a hypotensive LES with a pressure of around 5 to 8 mm Hg and normal to moderately abnormal peristalsis. The low
LES pressure is thought to allow gastric contents to reflux back into the esophagus.
Twenty-four-hour ambulatory manometry can be used to diagnose spastic disorders such as Diffuse Esophageal Spasm (DES), nutcracker esophagus, or hypercontractile esophageal motility disorder is a rare cause of dysphagia.
The nutcracker esophagus is characterized by very high LES pressures (>50 mm Hg) during swallowing with otherwise normal peristalsis.
DES would be characterized by high pressures throughout the esophagus (25-50 mm Hg) and poor peristalsis.
Pseudoachalasia would show a slightly hypertensive but relaxing LES and abnormal but not absent peristalsis.
Connective tissue disorders, like scleroderma, would be hallmarked by poor peristalsis and a normal LES.
Locations of anatomic narrowing of the esophagus seen on an esophagram include all of the following EXCEPT
A. Lower esophageal sphincter
B. Crossing of the left mainstem bronchus and aortic arch
C. Thoracic outlet
D. Cricopharyngeal muscle
Answer: C
Three normal areas of esophagea narrowing are evident on the barium esophagogram or during esophagoscopy.
The uppermost narrowing is located at the entrance into the esophagus and is caused by the cricopharyngeal muscle. Its luminal diameter is 1.5 cm, and it is the narrowest point of the esophagus.
The middle narrowing is due to an indenta- tion of the anterior and left lateral esophagea wall caused by the crossing of the left main stem bronchus and aortic arch. The luminal diameter at this point is 1.6 cm.
The lowermost narrowing is at the hiatus of the diaphragm and is caused by the gastroesophageal sphincter mechanism. The luminal diameter at this point varies somewhat, depending on the distention of the esophagus by the passage of food, but has been measured at 1.6 to 1.9 cm.
These norma constrictions tend to hold up swallowed foreign objects, and the overying mucosa is subject to injury by swallowed corrosive liquids because of their slow passage through these areas.
(See Schwartz 10th ed., p. 942.)
The cervical esophagus receives its blood supply primarily from the
A. Internal carotid artery
B. Inferior thyroid artery
C. Superior thyroid artery
D. Inferior cervical artery
E. Facial artery
Answer: B
The cervical portion of the esophagus receives its main blood supply from the inferior thyroid artery.
The thoracic portion receives its blood supply from the bronchial arteries, with 75% of individuals having one right-sided and two left-sided branches.
Two esophageal branches arise directly from the aorta.
The abdominal portion of the esophagus receives its bood supply from the ascending branch of the left gastric artery and from inferior phrenic arteries. On entering the wall of the esophagus, the arteries assume a T-shaped division to form a longitudinal plexus, giving rise to an intramural vascular network in the muscular and submucosal layers. As a consequence, the esophagus can be mobilized from the stomach to the level of the aortic arch without fear of devascularization and ischemic necrosis.
Caution should be exercised as to the extent of esophageal mobilization in patients who have had a previous thyroidectomy with ligation of the inferior thyroid arteries proximal to the origin of the esophageal branches.
(See Schwartz 10th ed., pp. 945–946.)
All of the following cranial nerves are involved in the swallowing mechanism EXCEPT
A. V
B. VII
C. VIII
D. X
E. XI
F. XII
Answer: C
Swallowing can be started at will, or it can be reflexively elicited by the stimulation of areas in the mouth and pharynx, among them the anterior and posterior tonsillar pillars or the posterior lateral walls of the hypopharynx.
The afferent sensory nerves of the pharynx are the glossopharyngeal nerves and the superior laryngeal branches of the vagus nerves.
Once aroused by stimuli entering via these nerves, the swallowing center in the medulla coordinates the complete act of swallowing by discharging impulses through cranial nerves V, VII, X, XI, and XII, as well as the motor neurons of C1 to C3.
Discharges through these nerves occur in a rather specific pattern and last for approximately 0.5 seconds. Little is known about the organization of the swallowing center, except that it can trigger swallowing after a variety of different inputs, but the response is always a rigidly ordered pattern of outflow.
Following a cerebrovascular accident, this coordinated outflow may be altered, causing mild to severe abnormalities of
swallowing.
In more severe injury, swallowing can be grossly disrupted, leading to repetitive aspiration.
(See Schwartz 10th ed., p. 948.)
All of these are parts of the human antireflux mechanism EXCEPT
A. Adequate gastric reservoir
B. Mechanically functioning lower esophageal sphincter (LES)
C. Mucus secreting cells of the distal esophagus
D. Efficient esophageal clearance
Answer: C
If the pharyngeal swallow does not initiate a peristaltic contraction, then the coincident relaxation of the lower esophageal sphincter (LES) is unguarded and reflux of gastric juice can occur.
This may be an explanation for the observation of spontaneous lower esophageal relaxation, thought by some to be a causative factor in gastroesophageal reflux disease (GERD).
The power of the worm-drive pump of the esophageal body is insufficient to force open a valve that does not relax.
In dogs, a bilateral cervical parasympathetic blockade abolishes the relaxation of the LES that occurs with pharyngeal swallowing or distention of the esophagus. Consequenty, vagal function appears to be important in coordinating the relaxation of the LES with esophageal contraction.
The antireflux mechanism in human beings is composed of three components: a mechanically effective LES, efficient esophageal clearance, and an adequately functioning gastric reservoir.
A defect of any one of these three components can lead to increased esophageal exposure to gastric juice and the deveopment of mucosal injury.
(See Schwartz 10thed.,p.949.)
Physiologic reflux happens most commonly when a person is
A. Awake and supine
B. Awake and upright
C. Asleep and supine
D. Asleep and semi-erect
Answer: B
On 24-hour esophageal pH monitoring, healthy individuals have occasional episodes of gastroesophageal reflux.
This physiologic reflux is more common when awake and in the upright position than during sleep in the supine position.
When reflux of gastric juice occurs, normal subjects rapidly clear the acid gastric juice from the esophagus regardless of their position.
There are several explanations for the observation that physiologic reflux in norma subjects is more common when they are awake and in the upright position than during sleep in the supine position.
First, reflux episodes occur in healthy volunteers primarily during transient losses of the gastroesophageal
barrier, which may be due to a relaxation of the LES or intragastric pressure overcoming sphincter pressure.
Gastric juice can also reflux when a swallow-induced relaxation of the LES is not protected by an oncoming peristaltic wave.
The average frequency of these “unguarded moments” or of transient losses of the gastroesophageal barrier is far less while asleep and in the supine position than while awake and in the upright position. Consequently, there are fewer opportunities for reflux to occur in the supine position.
Second, in the upright position, there is a 12-mm Hg pressure gradient between the resting, positive intra-abdominal pressure measured in the stomach and the most negative intrathoracic pressure measured in the esophagus at midthoracic level. This gradient favors the flow of gastric juice up into the thoracic esophagus when upright. The gradient diminishes in the supine position.
Third, the LES pressure in normal subjects is significantly higher in the supine position than in the upright position. This is due to the apposition of the hydrostatic pressure of the abdomen to the abdominal portion of the sphincter when supine.
In the upright position, the abdominal pressure surrounding the sphincter is negative compared with atmospheric pressure, and, as expected, the abdominal pressure gradually increases the more caudally it is measured.
This pressure gradient tends to move the gastric contents toward the cardia and encourages the occurrence of reflux into the esophagus when the individual is upright.
In contrast, in the supine position, the gastro- esophageal pressure gradient diminishes, and the abdominal hydrostatic pressure under the diaphragm increases, causing an increase in sphincter pressure and a more competent cardia.
(See Schwartz 10th ed., p. 949
All of the following hormones decrease LES tone EXCEPT
A. Gastrin
B. Estrogen
C. Somatostatin
D. CCK
E. Glucagon
Answer: A
The LES has intrinsic myogenic tone, which is modulated by neural and hormonal mechanisms.
Alpha-adrenergic neurotransmitters or beta-blockers stimulate the LES, and alpha-blockers and beta-stimulants decrease its pressure.
It is not clear to what extent cholinergic nerve activity controls LES pressure.
The vagus nerve carries both excitatory and inhibitory fibers to the esophagus and sphincter.
The hormones gastrin and motilin have been shown to increase LES pressure; and cholecystokinin, estrogen, glucagon, progesterone, somatostatin, and secretin decrease LES pressure.
The peptides bombesin, l-enkephalin, and substance P increase LES pressure; and calcitonin gene-related peptide, gastric inhibitory peptide, neuropeptide Y, and vasoactive intestinal polypeptide decrease LES pressure.
Some pharmacologic agents such as antacids, cholinergics, agonists, domperidone, metoclopramide, and prostaglandin F2 are known to increase LES pressure; and anticholinergics, barbiturates, calcium channel blockers, caffeine, diazepam, dopamine, meperidine, prostaglandin E1 and E2, and theophylline decrease LES pressure.
Peppermint, chocolate, coffee, ethanol, and fat are all associated with decreased LES pressure and may be responsible for esophageal symptoms after a sumptuous meal.
(See Schwartz 10th ed., pp. 949–950.)
The most common cause of a deficient LES is
A. Inadequate length
B. Mean resting pressure >6mmHg
C. Inadequate intraabdominal length
D. Failure of receptive relaxation
Answer: C
It is important that a portion of the total length of the LES be exposed to the effects of an intraabdominal pressure.
That is, during periods of elevated intraabdominal pressure, the resistance of the barrier would be overcome if pressure were not applied equally to both the LES and stomach simultaneously.
Thus, in the presence of a hiatal hernia, the sphincter resides entirely within the chest cavity and cannot respond to an increase in intra abdominal pressure, because the pinch valve mechanism is lost and gastroesophageal reflux is more liable to occur.
Therefore, a permanently defective sphincter is defined by one or more of the following characteristics:
1) An LES with a mean resting pressure of <6mmHg;
2) an overall sphincter length of <2cm; and
3) intraabdominal sphincter length of <1cm.
Compared to normal subjects without GERD, these values are below the 2.5 percentile for each parameter.
The most common cause of a defective sphincter is an inadequate abdominal length.
Maximal esophageal mucosal damage is caused by exposure to
A. Acidic fluid alone
B. Acidic fluid, food contents, and pepsin
C. Acidic fluid, trypsin, and food contents
D. Acidic fluid, pepsin, and bile salts
E. Neutral fluid, pepsin, and trypsin
Answer: D
The potential injurious components that reflux into the esophagus include gastric secretions such as acid and pepsin, as well as biliary and pancreatic secretions that regurgitate from the duodenum into the stomach.
There is a considerable body of experimental evidence to indicate that maximal epithelial injury occurs during exposure to bile salts combined with acid and pepsin.
These studies have shown that acid alone does minimal damage to the esophageal mucosa, but the combination of acid and pepsin is highly deleterious.
Similarly, the reflux of duodenal juice alone does little damage to the mucosa, although the combination of duodenal juice and gastric acid is particularly noxious.
(See Schwartz 10th ed., p. 967.)
The incidence of metaplastic Barrett esophagus (BE) progressing to adenocarcinoma is
A. Less than 0.1% per year
B. 0.2 to 0.5% per year
C. 1 to 3% per year
D. 3 to 5% per year
E. Greater than 5% per year
Answer: B
If reflux of gastric juice is allowed to persist, and sustained or repetitive esophageal injury occurs, two sequelae can result.
First, a luminal stricture can develop from submucosa and eventually intramural fibrosis.
Second, the tubular esophagus may become replaced with columnar epithelium. The columnar epithelium is resistant to acid and is associated with the alleviation of the complaint of heartburn. This columnar epithelium often becomes intestinalized, identified histologically by the presence of goblet cells. This specialized intestinal metaplasia (IM) is currently required for the diagnosis of Barrett esophagus (BE).
Endoscopically, BE can be quiescent or associated with complications of esophagitis, stricture, Barrett ulceration, and dysplasia. The complications associated with BE may be due to the continuous irritation from refluxed duodenogastric juice.
This continued injury is pH-dependent and may be modified by medical therapy.
The incidence of metaplastic Barrett epithelium becoming dysplastic and progressing to adenocarcinoma is approximatey 0.2 to 0.5% per year.
(See Schwartz 10th ed., pp. 968–969.)
The histologic hallmark of BE is
A. Columnar epithelium
B. Goblet cells
C. Parietal cells
D. Cuboidal epithelium
Answer: B
The definition of BE has evolved considerably over the past decade. Traditionally, BE was identified by the presence of columnar mucosa extending at least 3 cm into the esophagus.
It is now recognized that the specialized, intestinal type epitheium found in the Barrett mucosa is the only tissue predisposed to malignant degeneration.
Consequently, the diagnosis of BE is presently made given any length of endoscopically identifiable columnar mucosa that proves, on biopsy, to show IM.
Although long segments of columnar mucosa without IM do occur, they are uncommon and might be congenital in origin.
The hallmark of IM is the presence of intestinal goblet cells. There is a high prevalence of biopsy-demonstrated IM at the cardia, on the gastric side of the squamocolumnar junction, in the absence of endoscopic evidence of a columnar-lined esophagus (CLE).
Evidence is accumulating that these patches of what appears to be Barrett in the cardia have a similar malignant potential as in the longer segments, and are precursors for carcinoma of the cardia.
(See Schwartz 10thed.,p.969.)
Relief from respiratory symptoms can be expected in approximately what percent of patients with reflux associated asthma with medical therapy?
A. <10%
B. 25%
C. 50%
D. 75%
Answer: C
Once the diagnosis is established, treatment may be initiated with either proton pump inhibitor (PPI) therapy or antireflux surgery.
A trial of high-dose PPI therapy may help establish the facts that reflux is partly or completely responsible for the respiratory symptoms.
It is important to note that the persistence of symptoms in the face of aggressive PPI treatment does not necessarily rule out reflux as a possible cofactor or sole etiology.
Although there is probably some elements of a placebo effect, relief of respiratory symptoms can be anticipated in up to 50% of patients with reflux-induced asthma treated with antisecretory medications.
However, when examined objectively, <15% of patients can be expected to have improvement in their pulmonary function with medical therapy.
In properly selected patients, antireflux surgery improves respiratory symptoms in nearly 90% of children and 70% of adults with asthma and reflux disease.
Improvements in pulmonary function can be demonstrated in around 30% of patients.
Uncontrolled studies of the two forms of therapy (PPI and surgery) and the evidence from the two randomized controlled trials of medical versus surgical therapy indicate that surgical valve reconstruction is the most effective therapy for reflux-induced asthma.
The superiority of the surgery over PPI is most noticeable in the supine position, which corresponds with the nadir of PPI blood levels and resultant acid breakthrough and is the time in the circadian cycle when asthma symptoms are at their worst.
(See Schwartz 10th ed., p. 971.)
All of the following patients are good candidates for reflux surgery EXCEPT
A. A 31-year-old man with typical GERD with disease becoming resistant to medical therapy.
B. A 55-year-old woman with disease well-controlled with PPIs who wishes to discontinue medical therapy.
C. A 75-year-old man with new onset heartburn which is not relieved by PPIs.
D. A 52-year-old man with volume reflux and a large paraesophageal hernia.
Answer: C
Studies of the natural history of GERD indicate that most patients have a relatively benign form of the disease that is responsive to lifestyle changes and dietary and medical therapy, and do not need surgical treatment.
Approximately 25 to 50% of the patients with GERD have persistent or progressive disease, and it is this patient population that is best suited to surgical therapy.
In the past, the presence of esophagitis and a structurally defective LES were the primary indications for surgical treatment, and many internists and surgeons were reluctant to recommend operative procedures in their absence. However, one should not be deterred from considering antireflux surgery in a symptomatic patient with or without esophagitis or a defective sphincter, provided the disease process has been objectively documented by 24-hour pH monitoring.
This is particularly true in patients who have become dependent upon therapy with PPIs, or require increasing doses to control their symptoms.
It is important to note that a good response to medical therapy in this group of patients predicts an excellent outcome following antireflux surgery.
In general, the key indications for antireflux surgery are:
(a) objectively proven gastroesophageal reflux disease, and
(b) typical symptoms of gastroesophageal reflux disease (heartburn and/or regurgitation) despite adequate medical management, or
(c) a younger patient unwilling to take life-long medication.
In addition, a structurally defective LES can also predict which patients are more likely to fail with medical therapy.
Patients with normal sphincter pressures tend to remain well-controlled with medical therapy, whereas patients with a structurally defective LES may not respond as well to medical therapy, and often develop recurrent symptoms within 1 to 2 years of beginning therapy.
Such patients should be considered for an antireflux operation, regardless of the presence or absence of endoscopic esophagitis.
(See Schwartz 10th ed., p. 972.)
Preoperative testing for anti-reflux surgery typically includes all of the following EXCEPT
A. Computed tomography (CT) scan of the chest and abdomen
B. Contrast esophagram
C. 24 hour pH probe
D. Esophageal manometry
E. Esophagogastroduodenostomy
Answer: A
Before proceeding with an antireflux operation, several factors should be evaluated.
The clinical symptoms should be consistent with the diagnosis of gastroesophageal reflux.
Patients presenting with the typical symptoms of heartburn and/or regurgitation who have responded, at least partly, to PPI therapy, will generally do well following surgery, whereas patients with atypical symptoms have a less predictable response.
Reflux should also be objectively confirmed by either the presence of ulcerative esophagitis or an abnormal 24-hour pH study.
The propulsive force of the body of the esophagus should be evaluated by esophageal manometry to determine if it has sufficient power to propel a bolus of food through a newly reconstructed valve.
Patients with normal peristaltic contractions can be considered for a 360° Nissen fundoplication or a partial fundoplication, depending on patient and surgeon preferences.
When peristalsis is absent a partial fundoplication is probably the procedure of choice, but only if achalasia has been ruled out.
Hiatal anatomy should also be assessed. In patients with smaller hiatal hernias endoscopy evaluation usually provides sufficient information.
However, when patients present with a very large hiatus hernia or for revision surgery after previous antireflux surgery, contrast radiology provides better anatomical information.
The concept of anatomic shortening of the esophagus is controversial, with divergent opinions held about how common this problem is.
Believers claim that anatomic shortening of the esophagus compromises the ability of the surgeon to perform an adequate repair without tension, and that this can lead to an increased incidence of breakdown or thoracic displacement of the repair.
Some of those who hold this view claim that esophageal shortening is present when a barium swallow X-ray identifies a sliding hiatal hernia that will not reduce in the upright position, or that measures more than 5 cm in length at endoscopy.
When identified these surgeons usually undertake add a gastroplasty to the antireflux procedure.
Others claim that esophageal shortening is overdiagnosed and rarely seen, and that the morbidity of adding a gastroplasty outweighs any benefits.
These surgeons would recommend a standard antireflux procedure in a patients undergoing primary surgery.
(See Schwartz 10th ed., pp. 972–973.)
The valve created during an antireflux procedure should be at least
A. 1cm
B. 2cm
C. 3cm
D. 4cm
E. 5cm
Answer: C
The primary goal of antireflux surgery is to safely create a new antireflux valve at the gastroesophageal junction (GEJ), while preserving the patient’s ability to swallow normally and to belch to relieve gaseous distention.
Regardless of the choice of the procedure, this goal can be achieved if attention is paid to some basic principles when reconstructing the antireflux mechanism.
First, the operation should create a flap valve which prevents regurgitation of gastric contents into the esophagus.
This will result in an increase in the pressure of the distal esophageal sphincter region. Following a Nissen fundopication, the expected increase is to a level twice the resting gastric pressure (ie, 12 mm Hg or a gastric pressure oF 6 mm Hg).
The extent of the pressure rise is often less following a partial fundoplication, although with all types of fundoplication the length of the reconstructed valve should be at least 3 cm.
This not only augments sphincter characteristics in patients in whom they are reduced before surgery, but prevents unfolding of a normal sphincter in response to gastric distention.
Preoperative and postoperative esophageal manometry measurements have shown that the resting sphincter pressure and the overall sphincter length can be surgically augmented over preoperative values, and that the change in the former is a function of the degree of gastric wrap around the esophagus.
However, the aim of any fundoplication is to create a loose wrap, and to maintain the position of the gastric fundus close to the distal intra-abdominal esophagus, in a flap valve arrangement.
The efficacy of this relies on the close relationship between the fundus and the esophagus, not the“tightness” of the wrap.
(SeeSchwartz10thed.,p.973.)
A Toupet fundoplication involves
A. A 180° anterior wrap
B. A 90° posterior wrap
C. A 180° posterior wrap
D. A 270° posterior wrap
Answer: D
Partial fundoplications were developed as an alternative to the Nissen procedure in an attempt to minimize the risk of post fundoplication side effects, such as dysphagia, inability to belch, and flatulence.
The commonest approach has been a posterior partial or Toupet fundoplication. Some surgeons use this type of procedure for all patients presenting for anti-reflux surgery, whereas others apply a tailored approach in which a partial fundoplication is constructed in patients with impaired esophagea motility, in which the propulsive force of the esophagus is thought to be insufficient to overcome the outflow obstruction of a complete fundoplication.
The Toupet posterior partial fundoplication consists of a 270° gastric fundoplication around the distal 4 cm of esophagus.
It is usually stabilized by anchoring the wrap posteriorly to the hiatal rim.
(See Schwartz 10th ed., pp. 975–976.)
What percentage of patients should be expected to have relief of symptoms at 5 years out from antireflux surgery?
A. <50%
B. 50–60%
C. 60–80%
D. 80–90%
E. >90%
Answer: D
Studies of long-term outcome following both open and laparoscopic fundoplication document the ability of laparoscopic fundoplication to relieve typical reflux symptoms
(heartburn, regurgitation, and dysphagia) in more than 90% of patients at follow-up intervals averaging 2 to 3 years, and 80 to 90% of patients 5 years or more following surgery.
This incudes evidence-based reviews of antireflux surgery, prospective randomized trials comparing antireflux surgery to PPI therapy and open to laparoscopic fundoplication
and analysis of U.S. national trends in use and outcomes.
(See Schwartz 10th ed., p. 977.)
An upward dislocation of both the cardia and gastric fundus is which type of hiatal hernia?
A. I
B. II
C. III
D. IV
Answer: C
With the advent of clinical radiology, it became evident that a diaphragmatic hernia was a relatively common abnormality and was not always accompanied by symptoms.
Three types of esophageal hiatal hernia were identified:
(a) the sliding hernia, type I, characterized by an upward dislocation of the cardia in the posterior mediastinum;
(b) the rolling or paraesophageal hernia (PEH), type II, characterized by an upward dislocation of the gastric fundus alongside a normally positioned cardia; and
(c) the combined sliding-rolling or mixed hernia, type III, characterized by an upward dislocation of both the cardia and the gastric fundus.
The end stage of type I and type II hernias occurs when the whole stomach migrates up into the chest by rotating 180° around its longitudinal axis, with the cardia and pylorus as fixed points.
In this situation the abnormality is usually referred to as an intrathoracic stomach (Fig. 25-1).
In some taxonomies, a type IV hiatal hernia is declared when an additional organ, usually the colon, herniates as well. Type II-IV hiatal hernias are also referred to as paraesophageal hernia (PEH), as a portion of the stomach is situated adjacent to the esophagus, above the GEJ.
(See Schwartz 10th ed., Figure 25-39D, pp. 980–981.)
The most common form of esophageal cancer diagnosed in the United States is
A. Adenocarcinoma
B. Squamous carcinoma
C. Anaplastic carcinoma
D. Leiomyosarcoma
Answer: A
Adenocarcinoma of the esophagus, once an unusual malignancy, is diagnosed with increasing frequency and now accounts or more than 50% of esophageal cancer in most Western countries.
The shift in the epidemiology of esophageal cancer from predominantly squamous carcinoma seen in association with smoking and alcohol, to adenocarcinoma in the setting of BE, is one of the most dramatic changes that have occurred in the history of human neoplasia.
Although esophageal carcinoma is a relatively uncommon malignancy, its prevalence is exploding, largely secondary to the well-established association between gastroesophageal reflux, BE, and esophageal adenocarcinoma.
Once a nearly uniformly lethal disease, survival has improved slightly because of advances in the understanding of its molecular biology, screening and surveillance practices, improved staging, minimally invasive surgical techniques, and neoadjuvant therapy.
(See Schwartz 10th ed., p. 1003.)
Squamous cell carcinomas of the esophagus most commonly occur
A. At the GEJ
B. In the cervical and upper thoracic esophagus
C. In the lower thoracic esophagus
D. Evenly distributed throughout the esophagus
Answer: B
It is estimated that 8% of the primary malignant tumors of the esophagus occur in the cervical portion.
They are almost always squamous cell cancer, with a rare adenocarcinoma arising from a congenital inlet patch or columnar lining.
These tumors, particularly those in the postcricoid area, represent a separate pathologic entity or two reasons: (a) They are more common in women and appear to be a unique entity in this regard; and (b) the efferent lymphatics from the cervical esophagus drain completely differently from those of the thoracic esophagus.
The latter drain directly into the paratracheal and deep cervical or internal jugular lymph nodes (LNs) with minimal flow in a longitudinal direction.
Except in advanced disease, it is unusual for intrathoracic LNs to be involved.
(See Schwartz 10th ed., p. 1005.)
The preoperative test most heavily correlated with the ability to tolerate an esophagectomy is:
A. DLCO
B. FEV1
C. Ability to climb a flight of stairs
D. FVC
Answer: B
Patients undergoing esophageal resection should have sufficient cardiopulmonary reserve to tolerate the proposed procedure.
The respiratory function is best assessed with the forced expiratory volume in 1 second, which ideally should be 2L or more.
Any patient with a forced expiratory volume in 1 second of <1.25 L is a poor candidate for thoracotomy, because he or she has a 40% risk of dying from respiratory insufficiency within 4 years.
In patients with poor pulmonary reserve, the transhiatal esophagectomy should be considered, as the pulmonary morbidity of this operation is less than is seen following thoracotomy.
Clinical evaluation and electrocardiogram are not sufficient indicators of cardiac reserve.
Echocardiography and dipyridamole-thallium imaging provide accurate in formation on wall motion, ejection fraction, and myocardial blood flow.
A defect on thallium imaging may require further evaluation with preoperative coronary angiography. Arresting ejection fraction of <40%, particularly if there is no increase with exercise, is an ominous sign.
In the absence of invasive testing, observed stair-climbing is an economical (albeit not quantitative) method of assessing cardiopulmonary reserve.
Most individuals who can climb three flights of stairs without stopping will do well with two-sided open esophagectomy, especially if an epidural catheter is used for postoperative pain relief.
(See Schwartz 10th ed., p. 1007.)