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.)
Which test most accurately assess the T stage of esophageal cancer?
A. High-resolution CT scan
B. Magnetic resonance imaging (MRI)
C. Echocardiography
D. Endoscopic ultrasonography (EUS)
E. Esophagogastroduodenoscopy (EGD)
Answer: D
For years, clinical staging, contrast radiography, endoscopy, and CT scanning formed the backbone of esophageal cancer staging.
More recently, preoperative decision making is guided by endoscopic ultrasonography (EUS) and positron emission tomography (PET) scanning.
EUS provides the most reliable method of determining depth of cancer invasion.
In the absence of enlarged LNs, the degree of wall invasion dictates surgical therapy.
(See Schwartz 10th ed., p. 1008.)
Which of the following patients would not be considered a candidate for esophagectomy?
A. A 55-year-old man with GEJ adenocarcinoma confined to the muscularis mucosa.
B. A 47-year-old woman with mid-esophageal cancer and an involved cervical LN.
C. A 60-year-old man with a large GEJ carcinoma with invasion into the pleura without a malignant effusion.
D. A 70-year-old woman with a small GEJ cancer and three pathologic LNs nearby on EUS.
Answer: B
If the tumor invades into the submucosa, without visible LN involvement, most individuals would suggest esophagectomy with LN dissection, as positive nodes can be found in 20 to 25% of those with cancer limited to the mucosa and submucosa.
If EUS demonstrates spread through the wall of the esophagus, especially if LNs are enlarged, then induction chemoradiation therapy (neoadjuvant therapy) should be strongly considered.
Lastly, when the EUS demonstrates invasion of the trachea, bronchus, aorta, or spine, then surgical resection is rarely indicated.
If there is invasion into the pleura (T4a), then surgical resection can be considered in the absence of a malignant effusion. Thus, it can be seen that the therapy of esophageal cancer is largely driven by the findings of an endoscopic ultrasonography.
It is difficult to provide modern treatment of esophageal cancer without access to this modality.
(See Schwartz 10th ed., p. 1008.)
The technique of resecting an esophageal cancer which remains symptomatic after definitive chemoradiotherapy is referred to as
A. Palliative esophagectomy
B. Savage esophagectomy
C. Rescue esophagectomy
D. None of the above, the procedure is not performed
Answer: B
Salvage esophagectomy is the nomenclature applied to esophagectomy performed after failure of definitive radiation and chemotherapy.
The most frequent scenario is one in which distant disease (bone, lung, brain, or wide LN metastases) renders the patient nonoperable at initial presentation.
Then, systemic chemotherapy, usually with radiation of the primary tumor, destroys a foci of metastasis, as demonstrated by CT and CT-PET, but the primary remains present and symptomatic.
Following a period of observation, to make sure no new disease with become evident, salvage esophagectomy is performed, usually with an open two-field approach.
Surprisingly, the cure rate of savage esophagectomy is not inconsequential. One in our patients undergoing this operation will be disease free 5 years after, despite the presence of residual cancer in the operative specimen.
Because of the dense scarring created by radiation treatment, this procedure is the most technically challenging of all esophagectomy techniques.
(See Schwartz 10th ed., p. 1011.)
Patients with dysphagia secondary to esophageal cancer treated with radiation can expect the benefit to last
A. <1month
B. 2–3months
C. 6–12months
D. >12months
Answer: B
Primary treatment with radiation therapy does not produce results comparable with those obtained with surgery.
Currently, the use of radiotherapy is restricted to patients who are not candidates for surgery, and is usually combined with chemotherapy.
Radiation alone is used for palliation of dysphagia but the benefit is short-lived, fasting only 2 to 3 months.
Furthermore, the length and course of treatment are difficult to justify in patients with a limited life expectancy.
Radiation is effective in patients who have hemorrhage from the primary tumor.
(See Schwartz 10th ed., p. 1012.)
How long after completion of neoadjuvant chemoradiotherapy should esophagectomy be performed?
A. 2weeks
B. 4–6weeks
C. 6–8 weeks
D. 8–10weeks
E. >10 weeks
Answer: C
The timing of surgery after chemoradiation induction is generally felt to be optimal between 6 and 8 weeks following the completion of induction therapy.
Earlier than this time, active inflammation may make the resection hazardous, and the patients have not had time to recover fully from the chemoradiation.
After 8 weeks, edema in the periesophageal tissue starts to turn to scar tissue, making dissection more difficult.
With chemoradiation, the complete response rates for adenocarcinoma range from 17 to 24%.
No tumor is detected in the specimen after esophagectomy.
Patients demonstrating a complete response to chemoradiation have a better survival rate than those without complete response, but distant failure remains common.
(See Schwartz 10th ed., pp. 1012–1013.)
The optimal treatment of an incidentally discovered 3 cm leiomyoma of the upper esophagus in a 45-year-old otherwise healthy man is?
A. Observation
B. Esophagectomy
C. Enucleation
D. Endoscopic resection
Answer: C
Despite their slow growth and limited potential for malignant degeneration, leiomyomas should be removed unless there are specific contraindications.
The majority can be removed by simple enucleation. If, during removal, the mucosa is inadvertently entered, the defect can be repaired primarily.
After tumor removal, the outer esophageal wall should be reconstructed by closure of the muscle layer.
The location of the lesion and the extent of surgery required will dictate the approach.
Lesions of the proximal and middle esophagus require a right thoracotomy, whereas distal esophageal lesions require a left thoracotomy.
Videothoracoscopic and laparoscopic approaches are now frequently used.
The mortality rate associated with enucleation is low, and success in relieving the dysphagia is near 100%.
Large lesions for those involving the GEJ may require esophageal resection.
(See Schwartz 10thed., pp. 1017–1018.)
Following a night of heavy drinking, a 43-year-old otherwise healthy man has sudden onset of severe chest pain after vomiting. Esophagram confirms esophageal ruptures just proximal to the GEJ. What is the preferred operative exposure?
A. Right thoracotomy
B. Right thoracotomy with laparotomy
C. Left thoracotomy
D. Left thoracotomy with laparotomy
E. Midline laparotomy
Answer: C
The key to optimum management is early diagnosis.
The most favorable outcome is obtained following primary closure of the perforation within 24 hours, resulting in 80 to 90% survival.
The most common location for the injury is the left lateral wall of the esophagus, just above the GEJ.
To get adequate exposure of the injury, a dissection similar to that described for esophageal myotomy is performed.
A flap of stomach is pulled up and the soiled fat pad at the GEJ is removed.
The edges of the injury are trimmed and closed primarily.
The closure is reinforced with the use of a pleural patch or
construction of a Nissen fundopication.
(See Schwartz 10th ed., pp. 1018–1019.)
A 34-year-old man presents to the emergency department (ED) after an episode of hematemesis. EGD confirms a Mallory-Weiss tear with no residual bleeding.
Treatment should consist of
A. Esophagectomy
B. Observation
C. Proximal gastrectomy with esophagojejunostomy
D. Injection of botulinum toxin
Answer: B
Mallory-Weiss tears are characterized by arterial bleeding, which may be massive.
Vomiting is not an obligatory factor, as there may be other causes of an acute increase in intraabdominal pressure, such as paroxysmal coughing, seizures, and retching.
The diagnosis requires a high index of suspicion, particularly in the patient who develops upper gastrointestinal (GI) bleeding following prolonged vomiting or retching.
Upper endoscopy confirms the suspicion by identifying one or more longitudinal fissures in the mucosa of the herniated stomach as the source of bleeding.
In the majority of patients, the bleeding will stop spontaneously with nonoperative management.
In addition to blood replacement, the stomach should be decompressed and antiemetics administered, as a distended stomach and continued vomiting aggravate further bleeding. A Sengstaken-Blakemore tube will not stop the bleeding, as the pressure in the balloon is not sufficient to overcome arterial pressure.
Endoscopic injection of epinephrine may be therapeutic if bleeding does not stop spontaneously.
Only occasionally will surgery be required to stop blood loss.
The procedure consists of laparotomy and high gastrotomy with oversewing of the linear tear.
Mortality is uncommon, and recurrence is rare.
(See Schwartz 10th ed., p. 1020.)
Successful treatment of a Zenker diverticulum involves
A. Diverticulopexy
B. Resection of the diverticulum
C. Observation
D. Either diverticulopexy for resection with cricopharyngeal myotomy
Answer: D
When a pharyngoesophageal diverticulum is present, localization of the pharyngoesophageal segment is easy.
The diverticulum is carefully freed from the overlying areolar tissue to expose its neck, just below the inferior pharyngeal constrictor and above the cricopharyngeus muscle.
It can be difficult to identify the cricopharyngeus muscle in the absence of a diverticulum.
A benefit of local anesthesia is that the patient can swallow and demonstrate an area of persistent narrowing at the pharyngoesophageal junction.
Furthermore, before closing the incision, gelatin can be fed to the patient to ascertain whether the symptoms have been relieved, and to inspect the opening of the previously narrowed pharyngoesophageal segment.
Under general anesthesia, and in the absence of a diverticulum, the placement of a nasogastric tube to the level of the manometrically determined cricopharyngeal sphincter helps in localization of the structures.
The myotomy is extended cephalad by dividing 1 to 2 cm of inferior constrictor muscle of the pharynx, and caudad by dividing the cricopharyngeal muscle and the cervical esophagus for a length of 4 to 5 cm.
If a diverticulum is present and is large enough to persist after a myotomy, it may be sutured in the inverted position to the prevertebra fascia using a permanent suture (ie, diverticulopexy).
If the diverticulum is excessively large so that it would be redundant if suspended, or if its walls are thickened, then a diverticulectomy should be performed.
This is best performed under general anesthesia by placing a Maloney dilator (48F) in the esophagus, after controlling the neck of the diverticulum and after myotomy.
A linear stapler is placed across the neck of the diverticulum and the diverticulum is excised distal to the staple line.
The security of this staple line and effectiveness of the myotomy may be tested before hospital discharge with a water soluble contrast esophagogram.
Postoperative complications include fistula formation, abscess, hematoma, recurrent nerve paralysis, difficulties in phonation, and Horner syndrome.
The incidence of the first two can be reduced by performing a diverticulopexy rather than diverticulectomy.
(See Schwartz 10th ed., p. 989.)
Which of the following disorders involves simultaneous nonperistaltic contractions of the esophagus?
A. Achalasia
B. Diffuse esophageal spasm (DES)
C. Hypertensive lower esophageal sphincter
D. Nutcracker esophagus
Answer: B
The classic manometric findings in these patients are characterized by the frequent occurrence of simultaneous waveforms and multipeaked esophageal contractions, which may be of abnormally high amplitude or long duration.
Key to the diagnosis of diffuse esophageal spasm (DES) is that there remain some peristaltic wave forms in excess of those seen in achalasia.
A criterion of 30% or more peristaltic wave forms out of 10 wet swallows has been used to differentiate DES from vigorous achalasia. However, this figure is arbitrary and often debated.
The LES in patients with DES usually shows a normal resting pressure and relaxation on swallowing.
A hypertensive sphincter with poor relaxation may also be present. In patients with advanced disease, the radiographic appearance of tertiary contractions appears helical, and has been termed corkscrew esophagus or pseudodiverticulosis.
Patients with segmental or DES can compartmentalize the esophagus and develop an epiphrenic or midesophageal diverticulum between two areas of high pressure occurring simultaneously.
MANOMETRIC CHARACTERISTICS
1) ACHALASIA
- Incomplete lower esophageal sphincter (LES) relaxation (<75% relaxation)
- Aperistalsis in the esophageal body
- Elevated LES pressure ≤26 mmHg
- Increased intraesophageal baseline pressures relative to gastric baseline
2) DIFFUSE ESOPHAGEAL SPASM (DES)
- Simultaneous (nonperistaltic contractions) (>20% of wet swallows)
- Repetitive and multipeaked contractions
- Spontaneous contractions
- Intermittent normal peristalsis
- Contractions may be of increased amplitude and duration
3) NUTCRACKER ESOPHAGUS
- Mean peristaltic amplitude (10 wet swallows) in distal esophagus
≥180mmHg
- Increased mean duration of contractions (>7.0 s)
- Normal peristaltic sequence
4) HYPERTENSIVE LOWER ESOPHAGEAL SPHINCTER
- Elevated LES pressure (≥26 mmHg)
- Normal LES relaxation
- Normal peristalsis in the esophageal body
5) INEFFECTIVE ESOPHAGEAL MOTILITY DISORDERS
- Decreased or absent amplitude of esophageal peristalsis (<30 mmHg)
- Increased number of nontransmitted contractions
What layer is absent in the esophagus?
The esophagus lacks a serosa.
What are the 2 nerve plexuses in the esophagus?
1) Meissner’s
- Submucosa
2) Auerbach’s
- Between muscle layers
- Responsible for peristalsis
The 3 anatomic constrictions of the esophagus?
1) Cricopharyngeal muscle
- Uppermost narrowing
- 1.5cm (narrowest)
- Main contributor to the Upper Esophageal Sphincter.
2) Crossing of left mainstem bronchus and aortic arch
- 1.6cm
3) Diaphragmatic hiatus
- 1.6 to 1.9cm
These normal constrictions tend to hold up swallowed foreign objects, and the overlying mucosa is subject to injury by the slow passage of corrosive liquids.
Pressure in the UES?
The UES is a high-pressure zone that can reach 90mmHg, and return to average resting pressure of 60mmHg when swallowing.
Pressure in the LES?
The LES has a resting pressure zone of 6 to 26mmHg.
It is 2-5cm long, and vagus-mediated relaxation occurs during normal food transit.
Pressure is increased by GASTRIN and MOTILIN.
Pressure is decreased by CCK and SECRETIN.
Blood supply of the esophagus?
1) Cervical Esophagus
- Inferior thyroid artery
2) Proximal Thoracic Esophagus
- Bronchial arteries
3) Distal Thoracic Esophagus
- Aortic branches
4) Intraabdominal Esophagus
- Ascending branch of the left gastric artery
- Inferior phrenic arteries
Discuss esophageal contractions.
Esophageal contractions are coordinated in the medulla.
1) Oral
- Voluntary
- Medial temporal lobes and limbic system
2) Pharyngeal
- Involuntary (once initiated, swallowing is an entirely reflex act.)
- Larynx closes.
3) Esophageal
- Initiated by pharyngeal activity in swallowing.
- Primary peristalsis: Becomes involuntary after initiation
- Secondary: Triggered by distension/irritation; reflux contents back.
- Tertiary: Nonprogressive, nonperistaltic, spasm
The parasympathetic innervation of the pharynx and esophagus is provided by?
Vagus nerves
Why do lesions in the cervical esophagus have less submucosal extension, and a more regionalized lymphatic spread?
The cervical esophagus has more direct segmental lymph drainage into the regional nodes.
In the upper 2/3 of the esophagus, the lymph flow is mostly cephalad.
In the lower 2/3, caudad.
In the thoracic portion, the submucosal lymph plexus extends over a long distance in a longitudinal direction before penetrating the muscle layer to enter lymph vessels in the adventitia. Consequently, a primary tumor can extend for a considerable length superiorly or inferiorly in the submucosal plexus. Free tumor cells can follow the submucosal lymphatic plexus in either direction for a long distance before they pass through the muscularis and on into the regional LNs.
Drainage of efferent lymphatics from the esophagus?
Cervical: Drain into the paratracheal and deep cervical LNs.
Upper thoracic: Empty mainly into the paratracheal LNs.
From the lower esophagus: Into the subcarinal nodes and inferior pulmonary ligament nodes
Superior gastric nodes receive lymph not only from the abdominal portion of the esophagus, but also from the adjacent lower thoracic segment.
Sequence of events during the oropharyngeal phase of swallowing?
- Elevation of tongue
- Posterior movement of tongue
- Elevation of soft palate (closing passage between oropharynx and nasopharynx)
- Elevation of hyoid
- Elevation of larynx
- Tilting of epiglottis
What are the afferent sensory nerves of the pharynx?
1) Glossopharyngeal nerve (CN IX)
2) Superior laryngeal branch 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 CN V, VII, X, XI and XII, as well as motor neurons of C1 to C3.
What is the maximum weight that the propulsive force of the esophagus can overcome?
5 to 10g
What are the 3 components of the antireflux mechanism in human beings?
1) A mechanically effective LES
2) Efficient esophageal clearance
3) An adequately functioning gastric reservoir
In what position is physiologic reflux more common?
When awake and in the upright position.
Reflux occurs 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.
Hence there are fewer opportunities for reflux in the supine position.
Second, in the upright position, there is a 12mmHg pressure gradient between the resting, positive intraabdominal 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, LES pressure in normal subjects in 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.
Neural and hormonal mechanisms affecting the LES?
INCREASE LES Pressure:
- Alpha-adrenergic neurotransmitters or beta-blockers
- Gastrin and motilin
- Bombesin, l-enkephalin, substance P
- Antacids, cholinergics, agonists, domperidone, metoclopramide, prostaglandin F2
DECREASE LES Pressure:
- Alpha-blockers and beta-stimulants
- CCK, estrogen, glucagon, progesterone, somatostatin, secretin
- Calcitonin gene-related peptide, gastric inhibitory peptide, neuropeptide Y, vasoactive intestinal polypeptide
- Anticholinergics, barbiturates, calcium channel blockers, caffeine, diazepam, dopamine, meperidine, prostaglandin E1 and E2, theophylline
- Peppermint, chocolate, coffee, ethanol, fat
Tests to detect structural abnormalities?
1) Endoscopic evaluation
- First diagnostic test (UGI Endoscopy) in any patient complaining of DYSPHAGIA.
- For initial assessment, flexible fiberoptic esophagoscope is the instrument of choice.
- GERD: Esophagitis, Barrett’s columnar-lined esophagus (CLE– columnar instead of normal squamous epithelium; histologically, intestinal metaplasia).
- Abnormalities of the gastroesophageal flap (via retroflexion): Grading of I-IV
- Hiatal hernia: Pouch lined with gastric rugal folds lying 2cm or more above the margins of the diaphragmatic crura, identified by having the patient sniff. A prominent sliding hiatal hernia is associated with increased exposure to gastric juice.
- Paraesophageal hernia: Exclude gastric (Cameron’s) ulcers or gastritis within the pouch. (Intragastric retroflex or J maneuver)
- Esophageal diverticulum: Exclude ulceration or neoplasia. Biopsy is NOT usually performed for submucosal lesions.
2) Radiographic evaluation
- Barium swallow: Assess anatomy and motility
- Hiatal hernias: Best observed prone because increased intraabdominal pressure promotes displacement of the esophagogastric junction above the diaphragm.
- Lower esophageal narrowing (rings, strictures): Fully distended views of the esophagogastric region
- Circumferential carcinomas, peptic strictures, large ulcers, hiatal hernias: Full-column technique
- Small esophageal neoplasms, mild esophagitis and esophageal varices may be missed, hence the full-column technique must be supplemented by mucosal relief or double-contrast films
- Motion recording techniques aid in evaluating functional disorders or pharyngoesophageal and esophageal phases of swallowing.
- The radiographic assessment of the esophagus is not complete unless the entire stomach and duodenum have been examined. A gastric/duodenal ulcer, partially obstructing gastric neoplasm, or scarred duodenum and pylorus may contribute to symptoms.
Grading for esophagitis?
LA Grade A
- Mucosal break(s) ≤5 mm, without continuity across mucosal folds
LA Grade B
- Mucosal break(s) >5 mm, without continuity across mucosal folds
LA Grade C
- Mucosal break(s) continuous between ≥2 mucosal folds, involving <75% of the esophageal circumference
LA Grade D
- Mucosal break(s) involving ≥75% of the esophageal circumference
When a stricture is observed, the absence of esophagitis above a stricture suggests the possibility of a chemical-induced injury or a neoplasm. The latter should always be considered and is ruled out only by evaluation of a tissue biopsy of adequate size.
Principles in taking a biopsy from Barrett’s epithelium?
Multiple biopsy specimens should be taken in a cephalad direction to confirm the presence of intestinal metaplasia.
The earliest sign of malignant degeneration is high grade dysplasia or intramucosal adenocarcinoma. These dysplastic changes have a patchy distribution, so a minimum of 4 biopsy samples spaced 2cm apart should be taken from Barret’s lined portion of the esophagus.
Tumors occur in an area of specialized columnar epithelium near the squamocolumnar junction in 85% of patients, and within 2cm of the squamocolumnar junction in virtually all patients.
What can be employed when a patient complains of dysphagia, and no obstructing lesion is seen on the barium swallow?
Have the patient swallow a barium-impregnated marshmallow, a barium-soaked piece of bread, or a hamburger mixed with barium. This may bring out a functional disturbance in esophageal transport that can be missed when liquid barium is used.
Tests to detect functional abnormalities?
1) Esophageal motility study (EMS)
- Motor function and sphincters are evaluated
- Dysphagia, odynophagia, noncardiac chest pain, and when the barium swallow/endoscopy does not show a clear structural abnormality.
- Confirms dx of primary esophageal motility disorders (achalasia, DES, nutcracker esophagus, hypertensive LES).
- Confirms dx of motility disorders secondary to systemic disease (scleroderma, dermatomyositis, polymyositis, mixed connective tissue disease).
- GERD: Mechanically defective LES, evaluate esophageal peristalsis and contraction amplitude.
- A rise in pressure above the gastric baseline is the beginning of the LES.
2) High-Resolution Manometry
- Multiple circumferential recording sites are used to create a “map” of the esophagus and its sphincters.
- LES is a high-pressure zone that should relax at the inception of swallowing, and contract after the water or solid bolus passes through the LES.
- May detect overlooked focal motor abnormalities, predict bolus propagation and measure pressure gradients.
3) Esophageal Impedance
- Intraluminal electrical impedance catheter is used to measure GI function.
- Impedance: ratio of voltage to current, and is a measure of the electrical conductivity of a hollow organ and its contents.
- Intraluminal electrical impedance is inversely proportional to the electrical conductivity of the luminal contents and the cross-sectional area of the lumen.
- Air has very low electrical conductivity, and therefore has high impedance.
- Selectively used for dx of GERD. (24h pH monitoring has limitations– insensitive to higher pH values, can only detect abnormal acid reflux at pH <4, which is altered in those taking PPIs.
4) Esophageal Transit Scintigraphy
- Esophageal transit of a 10mL water bolus containing technetium-99m sulfur colloid can be recorded with a gamma camera. Using this technique, delayed bolus transit has been shown in patients with a variety of esophageal motor disorders, including achalasia, scleroderma, DES, and nutcracker esophagus.
5) Video and Cineradiography
- Allows re-evaluation by reviewing the studies at various speeds.
- More useful than manometry in evaluating the pharyngeal phase of swallowing.
- Manofluorography: Simultaneous computerized capture of videofluoroscopic images and manometric tracings (for complex functional abnormalities).
What is the respiratory inversion point?
The respiratory inversion point is identified when the positive excursions in the abdominal cavity that occur with breathing change to negative deflections in the thorax. This serves as a reference point at which the amplitude of the LES pressure and the length of the sphincter exposed to abdominal pressure are measured.
As the pressure-sensitive station is withdrawn into the body of the esophagus, the upper border of the LES is identified by the drop in pressure to the esophageal baseline. From these measurements, the pressure, abdominal length, and overall length of the sphincter are determined.
To account for the asymmetry of the sphincter, the pressure profile is repeated with each of the five radially oriented transducers, and the average values for sphincter pressure above gastric baseline, overall sphincter length, and abdominal length of the sphincter are calculated.
How is a mechanically defective sphincter identified?
A mechanically defective sphincter is identified by having one or more of the following:
1) Average LES pressure of <6mmHg
2) Average length exposed to the positive-pressure environment in the abdomen of ≤1cm
3) Average overall sphincter length of ≤2cm
Tests to detect increased exposure to gastric juice?
1) 24h Ambulatory pH Monitoring
- 48H* esophageal pH monitoring is the Gold standard for the diagnosis of GERD.
- the most direct method of measuring increased esophageal exposure, via an indwelling pH electrode or a radiotelemetric pH monitoring capsule
- measures the actual time the esophageal mucosa is exposed to gastric juice
- measures the ability of the esophagus to clear refluxed acid
- correlates esophageal acid exposure with the patient’s symptoms
- measurements made over 1-2 circadian cycles (24-48h)
- should NOT be considered a test for reflux, but a measurement of esophageal exposure to gastric juice,
2) Radiographic Detection of GERD
- 40% patients with classic symptoms: Spontaneous reflux
- In most patients who show spontaneous reflux on radiography, the diagnosis of increased esophageal acid exposure is confirmed by 24h esophageal pH monitoring.
- Hence the radiographic demonstration of spontaneous regurgitation of barium into the esophagus in the upright position is a reliable indicator that reflux is present.
- Failure to see this does not indicate the absence of the disease, hence this test is rarely used for clinical diagnosis.
Units used to express esophageal exposure to gastric juice?
1) Cumulative time the esophageal pH is below a chosen threshold, expressed as percentage of total, upright, and supine monitored time
2) Frequency of reflux episodes below a chosen threshold, expressed as number of episodes per 24h
3) Duration of the episodes, expressed as number of episodes >5 minutes per 24h, and the time in minutes of the longest episode recorded.
Tests of duodenogastric function?
Esophageal disorders are frequently associated with abnormalities of duodenogastric function: reflux of alkaline duodenal juice, including bile salts, pancreatic enzymes, and bicarbonate, is thought to have a role in the pathogenesis of esophagitis and complicated Barrett’s esophagus.
Functional disorders are also not confined to the esophagus but are associated with those of the rest of the foregut.
1) Gastric Emptying Study
- Radionuclide-labeled meals
- After ingestion, gamma camera images of the stomach are obtained at 5 to 15 minute intervals for 2-4hours.
- After correction for decay, the counts in the gastric area are plotted as the percentage of total counts at the start of imaging.
- The resulting emptying curve can be compared with data obtained in normal volunteers.
- Normal subjects will empty 59% of a meal within 90minutes.
What is the most specific symptom of foregut disease?
Dysphagia
It can be a sign of underlying malignancy and should be aggressively investigated until a diagnosis is established.
Oropharyngeal
- Difficulty transferring food out of the mouth into the esophagus, nasal regurgitation, and/or aspiration.
Esophageal
- Sensation of food sticking in the lower chest or epigastrium
- May or may not be accompanied by pain (odynophagia) relieved by passage of the bolus
What is the common denominator for most episodes of gastroesophageal reflux?
The loss of the high pressure zone and a decrease in the resistance it imparts to the retrograde flow of gastric juice into the esophageal body.
What characteristics of the LES work in unison to maintain its barrier function?
1) Resting LES pressure
2) Overall length
3) Intraabdominal length
As the sphincter becomes shorter, a higher amount of pressure is needed to prevent a given amount of reflux. Much like the neck of a balloon as it is inflated, as the stomach fills and distends, sphincter length decreases.
Therefore, if the overall length of the sphincter is permanently short from repeated distention of the fundus secondary to large volume meals, then with minimal episodes of gastric distention and pressure, there will be insufficient sphincter length for the barrier to remain competent, and reflux will occur.
A permanently defective sphincter is defined by one or more of the following:
1) An LES with a mean resting pressure of <6mmHg
2) An overall sphincter length of <2cm;
3) Intraabdominal sphincter length of <1cm
What is the pathophysiology of GERD?
It is believed that GERD has its origins within the stomach. Distension of the fundus occurs because of overeating and delayed gastric emptying secondary to a high-fat diet. The resultant distension causes “unrolling” of the sphincter by the expanding fundus, and this exposes the squamous epithelium in the region of the distal LES to gastric juice.
Repeated exposure results in inflammation and development of columnar epithelium at the cardia. This is the initial step in the development of carditis and explains why in early disease, esophagitis is mild and commonly limited to the very distal aspect of the esophagus. The patient attempts to compensate by increased swallowing, allowing the saliva to neutralize the refluxed gastric juice and thus, alleviate discomfort.
Increased swallowing leads to aerophagia, bloating and belching, and creates a vicious cycle of repetitive injury. Additionally, this can lead to a fibrotic mucosal ring at the squamocolumnar junction, called a “Schatzki ring” which may result in dysphagia.
This explanation for the pathophysiology of GERD is supported by the observation that severe esophagitis is almost always associated with a defective LES.
Complications of gastroesophageal reflux such as esophagitis, stricture, and Barrett’s metaplasia occur in the presence of which predisposing factors?
1) A mechanically defective LES
2) Increased esophageal exposure to fluid containing duodenal content, that includes bile and pancreatic juice
What is the incidence of metaplastic Barrett’s epithelium becoming dysplastic and progressing to adenocarcinoma?
0.2 - 0.5% per year
What is the hallmark of intestinal metaplasia?
The presence of intestinal goblet cells
What is the primary reason for performing antireflux surgery in patients with Barrett’s esophagus?
Long-term relief of symptoms
Secondary goals: healing of esophageal mucosal injury and prevention of disease progression
What is the incidence of adenocarcinoma developing in Barrett’s mucosa?
It occurs at approximately 0.2 - 0.5% per year of follow-up, which represents a risk 40x that of the general population.
Most, if not all cases of adenocarcinoma of the esophagus arise in Barrett’s epithelium.
About 1/3 of all patients with BE present with malignancy.
What are some respiratory symptoms that develop in patients with GERD?
1) Laryngopharyngeal reflux-type symptoms
2) Adult-onset asthma
3) Idiopathic pulmonary fibrosis
What are the mechanisms behind reflux-induced respiratory symptoms?
1) Reflux theory
- Symptoms are the direct result of laryngopharyngeal exposure and aspiration of gastric contents
- Vagal-mediated afferent fibers result in bronchoconstriction during episodes of distal esophageal acidification.
2) Ambulatory pH testing
- Acid exposure within the proximal esophagus is more frequently identified in those with gastroesophageal reflux and respiratory symptoms, than those with gastroesophageal reflux symptoms alone.
3) Impedance testing
- A correlation between proximal fluid movement and laryngopharyngeal symptoms such as cough can be demonstrated.
4) Bronchoconstriction occurs with the infusion of acid into the distal esophagus. There is a shared embryologic origin of the tracheoesophageal tract and vagus nerve, and this reflex is though to be an afferent fiber-mediated reflex that protects the aerodigestive system from the aspiration of refluxate.
Medical therapy for GERD?
First-line:
When initially identified with mild symptoms of uncomplicated GERD, patients can be placed on 12 weeks of simple antacids before diagnostic testing is initiated.
Patients should be counseled to elevated the head of the bed, avoid tight-fitting clothing, eat small frequent meals, avoid eating the nighttime meal immediately prior to bedtime, and avoid alcohol, coffee, chocolate, and peppermint, which are known to reduce resting LES pressure and may aggravate symptoms.
Other supplements:
1) Alginic acid: may augment the relief of symptoms by creating a physical barrier to reflux, as well as by acid reduction; reacts with sodium bicarbonate in the presence of saliva to form a highly viscous solution that floats like a raft on the surface of gastric contents. When reflux occurs, this protective layer is refluxed into the esophagus, and acts as a protective barrier.
2) Metoclopramide or Domperidone: Meds to promote gastric emptying are beneficial in early disease but of little value in more severe disease.
Persistent symptoms:
Mainstay is acid suppression. High-dose regimens of hydrogen potassium PPIs, such as omeprazole (up to 40mg/d), can reduce gastric acidity by as much as 80-90%. This usually heals mild esophagitis.
In severe esophagitis, healing may occur in only one-half of the patients. In patients who reflux a combination of gastric and duodenal juice, acid-suppression therapy may give relief of symptoms, while still allowing mixed reflux to occur. This can allow persistent mucosal damage in an asymptomatic patient.
Within 6 months of discontinuation of any form of medical therapy for GERD, 80% of patients have a recurrence of symptoms, and 40% of individuals with daily GERD eventually develop symptoms that breakthrough adequately dosed PPIs. Once initiated, most patients will require lifelong treatment.
Suggested approach:
First-line therapy entails antisecretory medication, usually PPIs, in most patients. Failure of medication to adequately control GERD symptoms suggests either that the patient may have relatively severe disease, or a non-GERD cause for symptoms.
Endoscopic evaluation is recommended to assess degree of injury and presence of BE.
Treatment options entails either long term PPI use vs. antireflux surgery. Laparoscopic antireflux surgery in these patients achieves long-term control of symptoms in 85-90%. The measurement of esophageal acid exposure via 24h pH should be done when patients are considered for surgery. The status of the LES and esophageal body function should also be performed.
Key indications for antireflux surgery?
1) Objectively proven gastroesophageal reflux disease
2) Typical symptoms of gastroesophageal reflux disease (heartburn/ regurgitation) despite adequate medical management
3) Younger patient unwilling to take lifelong medication (ie, <49yo)
4) Severe endoscopic esophagitis in a symptomatic patients with a structurally defective LES
5) Development of a stricture in a patient– represents failure of medical therapy (malignancy and drug-related etiology must be ruled out, and the stricture should be progressively dilated up to a 50-60F bougie prior to surgery. If dysphagia is relieved and the amplitude of esophageal contractions is adequate, an antireflux procedure should be performed; if there is a global loss of esophageal contractility, caution should be exercised in performing an antireflux procedure, and a partial fundoplication should be considered).
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 and often develop recurrent symptoms within 1-2 years.
What is the treatment approach if high grade dysplasia or intramucosal carcinoma is found on mucosal biopsy specimens?
Treatment should be directed at the BE and the lesion, using either evaluation endoscopic ablation, endoscopic resection, or esophageal resection.
Preop evaluation for antireflux surgery?
1) Reflux objectively confirmed by 24h pH monitoring or by the presence of ulcerative esophagitis
2) Propulsive force of body of esophagus evaluated by esophageal manometry (if it has sufficient power to propel a bolus of food through a newly-constructed valve)
- Normal peristaltic contractions: consider for a 360deg Nissen fundoplication or a partial fundoplication
- Absent peristalsis: Partial fundoplication, if achalasia has been ruled out
3) Hiatal anatomy should be assessed
- Smaller hiatal hernias: Endoscopy is sufficient
- Larger hiatal hernias: Contrast radiology
Primary goal of antireflux surgery?
To safely create a new antireflux valve at the gastroesophageal junction, while preserving the patient’s ability to swallow normally and belch to relieve gaseous distention.
The aim of any fundoplication is to create a loose wrap and to maintain the position of the gastric fundus close to the distal intraabdominal esophagus, in a flap valve arrangement.
The efficacy of this relies on the close relationship between the fundus and esophagus, not the tightness of the wrap.
Basic principles in constructing the antireflux mechanism?
1) 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.
2) Operation should place an adequate length of the distal esophageal sphincter in the positive-pressure environment of the abdomen by a method that ensures its response to changes in intraabdominal pressure. The permanent restoration of 2 or more cm of abdominal esophagus ensures the preservation of the relationship between the fundus and the esophagus. All of the popular antireflux procedures increase the length of the sphincter exposed to abdominal pressure by an average of at least 1cm.
3) Operation should allow the reconstructed cardia to relax on deglutition. In normal swallowing, a vagally mediated relaxation of the distal esophageal sphincter and the gastric fundus occurs. The relaxation lasts for approximately 10 secs and is followed by a rapid recovery to the former tonicity.
4) The fundoplication should not increase the resistance of the relaxed sphincter to a level that exceeds the peristaltic power of the body of the esophagus. The resistance depends on the degree, length, and diameter of the gastric fundic wrap, and on the variation in intraabdominal pressure. A 360deg wrap should be no longer than 2cm and constructed over a large (50-60F) bougie. This will ensure that the relaxed sphincter will have adequate diameter with minimal resistance. A bougie is not necessary when constructing a partial wrap.
5) The operation should ensure that the fundoplication can be placed in the abdomen without undue tension and maintained there by approximating the crura of the diaphragm above the repair. Leaving the fundoplication in the thorax converts a sliding hernia into a PEH, with all the complications associated with that condition. Maintaining the repair in the abdomen under tension predisposes to an increased incidence of recurrence.
What factors are important to ensure relaxation of the sphincter in antireflux surgery?
1) Only the fundus of the stomach should be used to buttress the sphincter, because it is known to relax in concert with the sphincter.
2) The gastric wrap should be properly placed around the sphincter and not incorporate a portion of the stomach or be placed around the stomach itself, because the body of the stomach does not relax with swallowing.
3) Damage to the vagal nerves during dissection of the thoracic esophagus should be avoided because it may result in failure of the sphincter to relax.
Discuss Nissen fundoplication.
A 360degree fundoplication around the lower esophagus for a distance of 4-5cm, without division of the short gastric vessels (now modified– with division of vessels).
Elements common to both lap and open procedures:
1) Hiatal dissection and preservation of both vagi along their entire length
2) Circumferential esophageal mobilization
3) Hiatal closure, usually posterior to the esophagus
4) Creation of a short and floppy fundoplication over an esophageal dilator
Discuss Posterior Partial fundoplication.
Partial fundoplications were developed as an alternative to the Nissen procedure in an attempt to minimize the risk of postfundoplication side effects, such as dysphagia, inability to belch, and flatulence. The commonest approach has been a posterior partial or TOUPET fundoplication.
270-degree gastric fundoplication around the distal 4cm of esophagus.
Discuss the Anterior Partial fundoplication.
Following posterior hiatal repair, the anterior fundus is rolled over the front of the esophagus and sutured to the hiatal rim and the esophageal wall. Division of the short gastric vessels is NOT needed.
180-degree anterior partial fundoplication provides a more robust wrap and achieves an excellent longer-term outcome in 90% of patients at follow up of at least 10 years.
The fundus and esophagus are sutured to the right side of the hiatal rim to create a flap valve at the gastroesophageal junction and to stabilize a 3-4cm long intraabdominal esophagus.
Summary of antireflux surgical approaches?
1) Transoral incisionless fundoplication (TIF)
- Totally endoscopic procedure for performing a partial fundoplication using T-bar fasteners
- 270 to 290deg wrap
- Approved for hernias >2cm.
- ARS remains an option in case of TIF failure.
- Does NOT provide cruroplasty.
2) Belsey-Mark IV
- Recreates the LES while reducing an intrathoracic stomach and closing a hiatal defect.
- Approached via a left thoracotomy hence may avoid a hostile abdomen.
- Useful in the dissection of large and giant chronic paraesophageal hernias.
- 240-deg partial wrap; imbricating cardia against the distal esophagus.
3) Toupet
- 270 degree, posterior partial wrap.
4) Dor
- 180 degree, anterior partial warp.
5) Hill
- Creation of a gastroesophageal flap valve, in an attempt to recreate normal anatomy.
6) Gastropexy
- For highest risk patients with hernias at risk for volvulus.
- May include a percutaneous endoscopic gastrostomy tube.
Management of Barrett’s Esophagus following antireflux surgery?
1) Low-grade dysplasia
- Biopsy specimens should be repeated after 12 weeks of high-dose acid suppression therapy.
2) High-grade dysplasia or Intramucosal cancer in >1 biopsy specimen
- If invasive CA (stage T1b or deeper) is present, or for multifocal long segment BE in younger and fit patients, in whom endoscopic treatments are unlikely to be adequate: ESOPHAGEAL RESECTION.
- For smaller intramucosal tumors to be removed with clear pathology margins, to obtain better pathological staging as a “big biopsy”, or to excise shorter segments of BE piecemeal: ENDOSCOPIC MUCOSAL RESECTION.
- To reduce the rate of progression from high grade dysplasia to invasive cancer by 50%: RF ABLATION.
3) Indeterminate/lower grade
- Suppress dysplasia by a course of acid suppression therapy in high doses for 2-3 months, followed by rebiopsy of the Barrett’s segment.
Most frequent cause of failure after open antireflux procedures?
Placement of the wrap around the stomach
Most frequent cause of failure after laparoscopic antireflux procedures?
Herniation of repair into the chest
Indications for esophageal resection in patients with failed antireflux repair?
When dysphagia is associated with poor motility and multiple previous repairs, further revision fundoplication is unlikely to be successful, and in otherwise fit patients it is appropriate to seriously consider esophageal resection.
Types of esophageal hiatal hernia?
Type I: Sliding hernia
- Upward dislocation of the cardia in the posterior mediastinum
- 48 years old
Type II: Rolling or Paraesophageal Hernia (PEH/Giant hiatal hernia)
- Upward dislocation of gastric fundus alongside a normally positioned cardia
- 61 years old
- women > men (4:1)
Type III: Combined sliding-rolling/mixed hernia
- Upward dislocation of both cardia and gastric fundus
- The end stage of type I and type II hernias occurs when the whole stomach migrates up into the chest by rotating 180deg around its longitudinal axis, with the cardia and pylorus as fixed points (intrathoracic stomach).
Type IV: When an additional organ, usually the colon, herniates as well.
Types II-IV are also known as paraesophageal hernias, as a portion of the stomach is situated adjacent to the esophagus, above the gastroesophageal junction.
What is the cause of dyspnea in the presence of a giant PEH?
Traditionally, it is believed that dysphagia and postprandial fullness are caused by compression of the adjacent esophagus by a distended cardia, or twisting of the GEJ by the torsion of the stomach that occurs as it becomes progressively displaced in the chest. Respiratory complications ensure from aspiration.
New research demonstrates that the cause of dyspnea in the presence of a giant PEH is more likely to be left atrial compression, decreasing cardiac output, than a restrictive pulmonary effect.
How would a patient with dysphagia secondary to a sliding hiatal hernia manifest manometrically?
This is reflected by a double-humped high-pressure zone at the GEJ.
The first pressure rise is due to diaphragmatic impingement on the herniated stomach.
The second is due to the true distal esophageal sphincter.
How to diagnose a hiatal hernia?
1) Upright CXR
- Air fluid level behind the cardiac shadow
- Caused by a PEH or intrathoracic stomach
2) Upper GI barium study
- Greater accuracy for a paraesophageal hernia (sliding hernias can spontaneously reduce)
3) Fiber-optic esophagoscopy
- Sliding: Gastric pouch lined with rugal folds extending above the impression caused by the crura of the diaphragm (or measuring at least 2cm between the crura), identified by having the patient sniff, and the squamocolumnar junction on withdrawal of the scope.
- PEH: On retroversion of the scope, there is a separate orifice adjacent to the GEJ into which gastric rugal folds ascend.
- Sliding-Rolling/Mixed: Gastric pouch lined with rugal folds above the diaphgram, with the GEJ entering about midway up the side of the pouch.
Pathophysiology of hiatal hernias?
24h esophageal pH monitoring shows that
- PEH: 60% with increased esophageal exposure to gastric acid
- Sliding: 71% with increased esophageal exposure to gastric acid
Hence it is now recognized that paraesophageal hiatal hernia can be associated with pathologic gastroesophageal reflux.
The competency of the cardia depends on an interrelationship between:
1) distal esophageal sphincter pressure
2) length of sphincter exposed to positive-pressure environment of abdomen
3) overall sphincter length
A deficiency in any one of these is associated with incompetency of the cardia regardless of whether a hernia is present.
Indications for surgical repair for hiatal hernias?
Patients with PEH are generally counseled to have elective repair, especially if symptomatic.
Why do most surgeons advocate routine addition of an antireflux procedure following repair of the hernia defect?
1) Physiologic testing with 24h esophageal pH monitoring has shown increased esophageal exposure to acid gastric juice in 60-70% of patients with a PEH, and 71% in those with a sliding hernia.
2) There is no relation between symptoms experienced by the patient with a PEH and the competency of the cardia.
3) A dissection of the gastroesophageal esophagus may lead to postoperative reflux despite a negative preoperative pH score.
What is a short esophagus?
The failure to achieve 2.5cm of intraabdominal esophagus with standard mediastinal dissection techniques.
What is Collis gastroplasty?
A procedure to achieve esophageal lengthening by the creation of a neoesophagus using the gastric cardia.
What is the most common cause of anatomic failure following laparoscopic Nissen fundoplication done for GERD?
Recurrent hiatal hernia (5-10%)
What is the management for asymptomatic recurrent hernias?
Asymptomatic recurrent hernias, like primary PEH, do not need to be repaired. The risk of incarceration, strangulation, or obstruction is minimal.
What is Schatzki’s ring?
Schatzki’s ring is a thin submucosal circumferential ring in the lower esophagus at the squamocolumnar junction, often associated with a hiatal hernia.
Stiennon believed the ring to be a pleat of mucosa formed by infolding of redundant esophageal mucosa due to shortening of the esophagus. Others believe it to be congenital, and still others suggest it is an early stricture resulting from inflammation of the esophageal mucosa caused by chronic reflux.
Symptoms include brief episodes of dysphagia during hurried ingestion of solid foods.
Majority of Schatzki’s ring patients without proven reflux have a history of ingestion of drugs known to be damaging to the esophageal mucosa.
Treatment of Schatzki’s ring?
The best form of treatment of a symptomatic Schatzki’s ring in patients who do not have reflux consists of esophageal dilation for relief of the obstructive symptoms.
In patients with a ring who have proven reflux and a mechanically defective sphincter, an antireflux procedure is necessary to obtain relief and avoid repeated dilation.
What is scleroderma
Scleroderma is a systemic and primarily neurogenic disorder, involving small vessel inflammation and subsequent perivascular deposition of normal collagen, leading to vascular compromise. It is accompanied by esophageal abnormalities in 80% of patients.
In the GI tract, the predominant feature is smooth muscle atrophy. In early scleroderma, an adrenergic overactivity may be present that causes parasympathetic inhibition, supporting a neurogenic mechanism for the disease. Clinically, this manifests in the patient as having a poor esophageal pump and a poor valve.
How is scleroderma diagnosed?
The diagnosis of scleroderma can be made manometrically by the observation of normal peristalsis in the proximal striated esophagus, with absent peristalsis in the distal smooth muscle portion.
LES pressure is progressively weakened as the disease advances.
Gastroesophageal reflux occurs in patients with scleroderma because they have both hypotensive sphincters and poor esophageal clearance. This combined defect can lead to severe esophagitis and stricture formation.
The typical barium swallow shows a dilated, barium-filled esophagus, stomach, and duodenum, or a hiatal hernia with distal esophageal stricture and proximal dilatation..
How is scleroderma treated?
Traditionally, esophageal symptoms have been treated with PPIs, antacids, elevation of the head of bed, and multiple dilations for strictures, with unsatisfactory results. Scleroderma patients have frequently had numerous dilations before they are referred to the surgeon.
The surgical management is controversial, but majority recommend a partial fundoplication (anterior or posterior) performed laparoscopically. Esophageal shortening may require a Collis gastroplasty in combination with a partial fundoplication.
If esophagitis is severe, or there has been a previous failed antireflux procedure and the disease is associated with delayed gastric emptying, a gastric resection with Roux-en-Y gastrojejunostomy has proved the best option.
What is eosinophilic esophagitis?
A condition with immunologic similarity to asthma, a form of allergic esophagitis.
Normally presents with chest pain (often postprandial) and dysphagia, most commonly to solids.
Unlike GERD, it does not respond to proton pump inhibitors.
A barium swallow should be the first test obtained in the patient with dysphagia. EE has a characteristic finding called the “ringed esophagus” or the “feline esophagus” as the esophageal rings are felt to look like the stripes of a housecat.
Histologically, the pathologist should see a minimum of 15 eosinophils per hpf, usually at the base of the epithelium.
How is Eosinophilic Esophagitis treated?
Treatment is symptomatic, and includes testing for food allergies and elimination of identified items from the diet.
Second-line therapy includes inhaled or ingested corticosteroids as would be used to treat asthma. If dysphagia is not relieved by steroids, it may be necessary to dilate the esophagus.
What are the causes of motility disorders of the pharynx and upper esophagus?
Termed transit dysphagia, this is usually congenital or results from acquired disease involving the central and peripheral nervous system (CVA, brainstem tumors, poliomyelitis, multiple sclerosis, Parkinson’s disease, pseudobulbar palsy, peripheral neuropathy, and operative damage to cranial nerves involved in swallowing).
They can be categorized into one or a combination of the ff abnormalities:
1) inadequate oropharyngeal bolus transport
2) inability to pressurize the pharynx
3) inability to elevate the larynx
4) discoordination of pharyngeal contraction and cricopharyngeal relaxation
5) decreased compliance of the pharyngoesophageal segment secondary to neuromuscular disease
What are the requirements for a successful pharyngoesophageal myotomy?
1) Adequate oropharyngeal bolus transport
2) Intact swallowing reflex
3) Reasonable coordination of pharyngeal pressurization with cricopharyngeal relaxation
4) Cricopharyngeal bar, Zenker’s diverticulum, or a narrowed pharyngoesophageal segment on videoesophagogram and/or presence of excessive pharyngoesophageal shoulder pressure on motility study.
What is Zenker’s diverticulum?
Zenker’s diverticulum signifies cricopharyngeal dysfunction, enlarging progressively due to the decreasing compliance of the skeletal portion of the cervical esophagus that occurs with aging.
Symptoms include dysphagia associated with spontaneous regurgitation of undigested, bland material, often interrupting eating or drinking. Occasionally this can be severe enough to cause debilitation and significant weight loss. Chronic aspiration and repetitive respiratory infection are common.
Once suspected, the diagnosis is established by a barium swallow.
Treatment of Zenker’s diverticulum?
The low morbidity and mortality associated with cricopharyngeal and upper esophageal myotomy have encouraged its use for almost any problem in the oropharyngeal phase of swallowing.
If a diverticulum is large enough to persist after a myotomy, it may be sutured in the inverted position to the prevertebral fascia using a permanent suture (ie, diverticulopexy).
If the diverticulum is excessively large, or if its walls are thickened, a diverticulectomy should be performed.
Endoscopic stapled cricopharyngotomy and diverticulotomy are also effective for larger diverticular (>2cm).
Prognosis of Zenker’s diverticulum?
Recurrence of a Zenker’s diverticulum may occur with long follow-up and is more common after diverticulectomy without myotomy, presumably due to persistence of the underlying loss of compliance of the cervical esophagus when a myotomy is not performed.
What are esophageal motility disorders?
Esophageal motility disorders should be looked at as a spectrum of abnormalities that reflect various stages of destruction of esophageal motor function.
These result from abnormalities in the propulsive pump action of the esophageal body or relaxation of the LES. They result from either primary esophageal abnormalities, or from generalized neural, muscular, or collagen vascular disease.
PRIMARY ESOPHAGEAL MOTILITY DISORDERS Achalasia, "vigorous" achalasia Diffuse and segmental esophageal spasm Nutcracker esophagus Hypertensive lower esophageal sphincter Nonspecific esophageal motility disorders
SECONDARY ESOPHAGEAL MOTILITY DISORDERS
Collagen vascular diseases: progressive systemic sclerosis, polymyositis and dermatomyositis, mixed connective tissue disease, SLE
Chronic idiopathic intestinal pseudoobstruction
Neuromuscular diseases
Endocrine and metastatic disorders
Incidence of achalasia?
6 in 100,000 population per year
Pathophysiology of achalasia?
Although complete absence of peristalsis in the esophageal body has been proposed as the major abnormality, present evidence indicates achalasia is a primary disorder of the LES.
The pathogenesis of achalasia is presumed to be a neurogenic degeneration, which is either idiopathic or due to infection.
This degeneration leads to hypertension of the LES, a failure of the sphincter to relax on swallowing, elevation of intraluminal esophageal pressure, esophageal dilatation, and a subsequent loss of progressive peristalsis in the body of the esophagus.
The esophageal dilatation results from the combination of a nonrelaxing sphincter, which causes a functional retention of ingested material in the esophagus, and elevation of intraluminal pressure from repetitive pharyngeal air swallowing.
With time, the functional disorder results in anatomic alterations seen on radiographic studies, such as a dilated esophagus with a tapering “bird’s beak”-like narrowing of the distal end.
There is usually an air-fluid level in the esophagus from the retained food and saliva, the height of which reflects the degree of resistance imposed by the nonrelaxing sphincter. As the disease progresses, the esophagus becomes massively dilated and tortuous.
What is vigorous achalasia?
A subgroup of patients with otherwise typical features of classic achalasia has simultaneous contractions of their esophageal body that can be of high amplitude.
This manometric pattern has been termed vigorous achalasia, and chest pain episodes are a common finding in these patients. Since the development of high resolution esophageal manometry technology, the term vigorous achalasia has been replaced with Chicago type 3 achalasia.
Differentiation of type 3 achalasia from DES can be difficult. In both diseases, videographic examination may show a corkscrew deformity of the esophagus and diverticulum formation.
What is DES?
Diffuse Esophageal Spasm (DES) is characterized by substernal chest pain and/or dysphagia. It differs from classic achalasia in that it is primarily a disease of the esophageal body, produces a lesser degree of dysphagia, causes more chest pain, and has less effect on the patient’s general condition.
Nonetheless, it is impossible to differentiate achalasia from DES on the basis of symptoms alone. Esophagogram and esophageal manometry are required to distinguish these two entities. True symptomatic DES is a rare condition, occurring about 5x less frequently than achalasia.
What is the pathophysiology of DES?
The cause and neuromuscular pathophysiology of DES are unclear. The basic motor abnormality is rapid wave progression down the esophagus secondary to an abnormality in the latency gradient.
Hypertrophy of the muscular layer of the esophageal wall and degeneration of the esophageal branches of the vagus nerve have been observed in this disease, although these are not constant findings.
Manometric abnormalities in DES may be present over the total length of the esophageal body, but are usually confined to the distal 2/3.
In segmental esophageal spasm, the manometric abnormalities are confined to a short segment of the esophagus.
Manometric characteristics of Achalasia?
ACHALASIA
1) Incomplete LES relaxation (<75% relaxation)
2) Aperistalsis in the esophageal body
3) Elevated LES pressure ≤26mmHg
4) Increased intraesophageal baseline pressures relative to gastric baseline
Manometric characteristics of Diffuse Esophageal Spasm (DES)?
DES
1) Simultaneous nonperistaltic contractions >20% of wet swallows
2) Repetitive and multipeaked contractions
3) Spontaneous contractions
4) Intermittent normal peristalsis
5) Contractions may be of increased amplitude and duration
Key to the diagnosis of DES is that there remain some peristaltic waveforms in excess of those seen in achalasia.
The LES shows a normal resting pressure and relaxation on swallowing.
In patients with advanced disease, the radiographic appearance of tertiary contractions appears helical and has been termed “corkscrew esophagus” or “pseudodiverticulosis” (patients with segmental or diffuse esophageal spasm can compartmentalize the esophagus and develop an epiphrenic or midesophageal diverticulum between two areas of high pressure occuring simultaneously).
Manometric characteristics of Nutcracker Esophagus?
NUTCRACKER ESOPHAGUS
1) Mean peristaltic amplitude (10 wet swallows) in distal esophagus ≥180mmHg
2) Increased mean duration of contractions (>7.0s)
3) Normal peristaltic sequence
Manometric characteristics of Hypertensive Lower Esophageal Sphincter?
HYPERTENSIVE LES
1) Elevated LES pressure ≥26mmHg
2) Normal LES relaxation
3) Normal peristalsis in the esophageal body
Manometric characteristics of nonspecific/ineffective esophageal motility disorders?
INEFFECTIVE/NONSPECIFIC ESOPHAGEAL MOTILITY DISORDERS
1) Decreased or absent amplitude of esophageal peristalsis (<30mmHg)
2) Increased number of nontransmitted contractions
3) Increased number of multipeaked/repetitive contractions
4) Contractions of prolonged duration
5) Contractions of low amplitude
The finding of a nonspecific esophageal motility disorder may represent only a manometric marker of an intermittent, more severe esophageal motor abnormality.
High amplitude peristalsis (nutcracker esophagus) and low-amplitude peristalsis (ineffective esophageal motility) are frequently associated with GERD.
Surgery plays no role in these disorders, unless there is an associated diverticulum.
What is the most common of the primary esophageal motility disorders?
Nutcracker Esophagus
What is a Nutcracker Esophagus?
Nutcracker or supersqueezer esophagus is a manometric abnormality in patients who are characterized by peristaltic esophageal contractions with peak amplitudes greater than two SDs above the normal values. Contraction amplitudes can easily be above 400mmHg.
Treatment should be aimed at the treatment of GERD. Chest pain symptoms (at the lower end of peak pressure) may be related to GERD rather than intraluminal hypertension.
At the high end (peak pressures >300mmHg), chest pain may be the result of the nutcracker physiology, as treatment directed at reducing intraluminal pressure is more effective than when used for those with lower peak pressures.
What is Hypertensive Lower Esophageal Sphincter?
Hypertensive LES is characterized by an elevated basal pressure of the LES with normal relaxation and normal propulsion in the esophageal body.
About one-half of these patients, however, have associated motility disorders of the esophageal body, particularly hypertensive peristalsis and simultaneous waveforms. In the remainder, the disorder exists as an isolated abnormality.
Dysphagia in these patients may be cause by a lack of compliance of the sphincter, even in its relaxed state.
Myotomy of the LES may be indicated in patients unresponsive to medical therapy of dilation.
When the symptom contribution of the hypertensive sphincter is in doubt, it is possible to inject the LES with botulinum toxin, endoscopically. If symptoms are relieved (temporarily) with this technique, then it is likely that myotomy will provide more permanent benefit.
What are the causes behind secondary esophageal motility disorders?
Connective tissue disease (scleroderma, CREST syndrome) and infants treated for Esophageal atresia often develop motility disorders that manifest later in life.
Symptoms include heartburn and dysphagia. The latter may be a result of a peptic stricture rather than the esophageal dysmotility.
An esophageal motility study will usually show severely reduced or absent LES pressure.
The role of antireflux surgery under these conditions is controversial but if performed, should be limited to partial fundoplication, as full Nissen fundoplication may result in severe dysphagia.
What are pulsion diverticula?
Pulsion diverticula are those associated with motor disorders. They occur most commonly with nonspecific motility disorders, but can occur also with primary motility disorders.
In primary motility disorders, the motility disorder is usually diagnosed before the development of the diverticulum. When associated with achalasia, the development of a diverticulum may temporarily alleviate the symptom of dysphagia by becoming a receptacle for ingested food and substitute the symptom of dysphagia for postprandial pain and regurgitation of undigested food.
If a motility abnormality of the esophageal body or LES cannot be identified, a traction or congenital cause for the diverticulum should be considered.
What are epiphrenic diverticula?
Traditionally, diverticula were considered a primary abnormality. Hence they were categorized based on location.
Epiphrenic diverticula arise from the terminal third of the thoracic esophagus and are usually found adjacent to the diaphragm. They have been associated with distal esophageal muscular hypertrophy, esophageal motility abnormalities, and increased luminal pressure. They are pulsion diverticula and are associated with diffuse spasm, achalasia, or nonspecific motor abnormalities in the esophageal body.
What is the treatment for pulsion diverticula?
When diverticula are associated with esophageal motility disorders, esophageal myotomy from the proximal extent of the diverticulum to the stomach should be combined with diverticulectomy. (If diverticulectomy alone is performed, one can expect a high incidence of suture line rupture due to the same intraluminal pressure that initially gave rise to the diverticulum.)
If the diverticulum is suspended to the prevertebral fascia of the thoracic vertebra, a myotomy is begun at the neck of the diverticulum and extended across the LES. If the diverticulum is excised by dividing the neck, the muscle is closed over the excision site, and a myotomy is performed on the opposite esophageal wall, starting just above the level of the diverticulum or at the proximal extent of the spastic segment of the esophagus if high resolution motility is used. If complete, the myotomy will cross the LES, reducing distal esophageal peak pressure, and it will increase the likelihood that dysphagia will be replaced with GERD symptoms.
Increasingly, partial fundoplication is performed after LES myotomy to decrease the frequency of disabling GERD developing after myotomy and diverticulectomy.
When a large diverticulum is associated with a hiatal hernia, then hiatal hernia repair is added.
What are traction diverticula?
Midesophageal or traction diverticula were theorized to come from adhesions forming between the inflamed mediastinal nodes and esophagus of TB patients. By contraction, the adhesions exerted traction on the esophageal wall and led to a localized diverticulum.
Most of these are asymptomatic and incidentally discovered during investigation of nonesophageal complaints. In such patients, the radiologic abnormality may be ignored. Those with dysphagia, regurgitation, chest pain, or aspiration should be thoroughly investigated for an esophageal motor abnormality.
Occasionally, a patient will present with a bronchoesophageal fistula manifested by a chronic cough on ingestion of meals. The diverticulum in such patients is most likely to have an inflammatory etiology.
What is the treatment for traction diverticula?
The indication for surgery is dictated by the degree of symptomatic disability.
Usually, midesophageal diverticula can be suspended due to their proximity to the spine.
If a motor abnormality is documented, a myotomy should be performed as described for an epiphrenic diverticulum.
Indications for a long esophageal myotomy?
Used for motor disorders of the esophageal body. Indicated for dysphagia caused by any motor disorder characterized by segmental or generalized simultaneous waveforms in a patient whose symptoms are not relieved by medical therapy.
Diffuse and segmental esophageal spasm, vigorous or type 3 achalasia, and nonspecific motility disorders associated with a mid- or epiphrenic esophageal diverticulum.
What is POEM?
Peroral Endoscopic Myotomy (POEM) allows a long myotomy to be performed entirely from the lumen of the esophagus with an endoscope. It is minimally invasive and can be done outpatient.
This procedure may be used for those with type 3 achalasia (vigorous achalasia), where it is necessary to divide the esophagogastric circular muscle on both sides of the diaphragm to the extent that might not be possible with laparoscopy or thoracoscopy alone.
The major downside of POEM is that an effective antireflux valve cannot be created, exposing the patient to a 40-50% risk of GERD post procedure.
What is Heller Myotomy?
Heller Myotomy or Myotomy of the Lower Esophageal Sphincter (LES) aims to relieve the functional outflow obstruction secondary to loss of relaxation and compliance of the LES in achalasia (ie, reducing sphincter pressure to <10mmHg).
Other options for addressing LES include hydrostatic balloon dilation (similar outcome with surgical myotomy), botulinum toxin injection.
What is the most common functional disorder second to GERD?
Achalasia
Treatment options for Achalasia?
MEDICAL OR SURGICAL?
For newly diagnosed patients, pneumatic dilation achieves adequate relief of dysphagia and pharyngeal regurgitation in 50-60% of patients. If dilation fails, myotomy is indicated.
For those with a dilated and tortuous esophagus or an associated hiatal hernia, balloon dilation is dangerous and surgery (surgical myotomy) is the better option.
The best treatment for achalasia is a laparoscopic Heller myotomy with partial fundoplication.
APPROACH
In the absence of a previous upper abdominal surgery, most surgeons prefer the abdominal approach (less pain, shorter length of stay). It is also a bit easier to ensure a long gastric myotomy when the approach is transabdominal.
ARS
Excellent results have been reported following meticulously performed myotomy without an antireflux component. If an antireflux procedure is used as an adjunct to esophageal myotomy, a complete 360-deg fundoplication should be avoided. Rather, a 270-deg Belsey fundoplication, a Toupet posterior 180-deg fundoplication, or a Dor anterior 180-deg fundoplication should be used to avoid the long term esophageal dysfunction secondary to outflow obstruction afforded by the fundoplication itself.
PROGNOSIS
The earlier an effective reduction in outflow resistance can be accomplished, the better the outcome will be, and the more likely some esophageal body function can be restored.
Principles in performing a surgical myotomy of the LES?
1) Complete division of all circular and collar-sling muscle fibers
2) Adequate distal myotomy to reduce outflow resistance
3) Undermining of the muscularis to allow wide separation of the esophageal muscle
4) Prevention of postoperative reflux
What antireflux procedures are used to follow completion of a laparoscopic Heller myotomy?
Either an anterior hemifundoplication augmenting the angle of His (Dor) or posterior partial fundoplication (Toupet) can be performed.
The Dor type is slightly easier to perform, and does not require disruption of the normal posterior gastroesophageal attachments (theoretical advantage in preventing postoperative reflux).
In most RCTs, laparoscopic Heller myotomy and partial fundoplication was superior to the alternative treatments.
What is the most common esophageal carcinoma worldwide?
Squamous carcinoma of the esophagus
Risk factors for SCC of the esophagus?
Additives (nitrous compounds in pickled vegetables and smoked meat)
Mineral deficiencies (zinc and molybdenum)
Smoking
Alcohol
Long-standing achalasia
Lye strictures
Tylosis (autosomal dominant disorder with keratosis of palms and soles)
HPV
Most important etiologic factor in the development of adenocarcinoma of the esophagus?
Metaplastic, columnar-lined or Barrett’s esophagus
occurs in 10-15% of patients with GERD
Why does dysphagia present late in esophageal cancer?
Dysphagia usually presents late in the natural history of the disease because the lack of a serosal layer on the esophagus allows the smooth muscle to dilate with ease. As a result, the dysphagia becomes severe enough for the patient to seek medical advice only when more than 60% of the esophageal circumference is infiltrated with cancer.
General approach to Esophageal Cancer?
Esophageal cancer is diagnosed with endoscopic biopsy and is staged with CT of the chest and abdomen, EUS, and PET scan for all patients with CT or EUS evidence of advanced disease (T2 or greater, N1-2 or NX).
T in situ, T1a, intramucosal cancer
- Endoscopic treatment (EMR)
T1-T2, N0: Confined to esophagus (submucosal invasion)
- Esophagectomy with LN dissection
T1-T3, N1: Locally advanced
- Multimodality approach
(neoadjuvant chemo + surgery)
(chemoRT + surgery)
Any T, Any N, M1: Disseminated
- Palliation (RT, endoscopic placement of expandable esophageal stent)
Most common sites of esophageal CA mets?
Lung Liver Peritoneal surfaces Omentum Small bowel mesentery
Indications for curative resection based on endoscopic ultrasound of the esophagus?
EUS provides the most reliable method of determining cancer depth of invasion. A curative resection should be encouraged if EUS indicates that the tumor has not invaded adjacent organs (T4b), and/or fewer than 6 enlarged LNs are imaged.
AJCC Staging for Esophageal Cancer?
TX: Primary tumor cannot be assessed.
T0: No evidence of primary tumor.
Tis: High-grade dysplasia
T1: Tumor invades lamina propria, muscularis mucosae, or submucosa.
- T1a: Tumor invades lamina propria or muscularis mucosae.
- T1b: Tumor invades submucosa
T2: Tumor invades muscularis propria.
T3: Tumor invades adventitia.
T4: Tumor invades adjacent structures.
- T4a: Resectable tumor invading pleura, pericardium, or diaphragm.
- T4b: Unresectable tumor invading other adjacent structures, such as aorta, vertebral body, trachea, etc.
NX: Regional LN cannot be assessed. N0: No regional LN mets. N1: Mets in 1-2 regional LNs. N2: Mets in 3-6 regional LNs. N3: Mets in ≥7 regional LNs.
M0: No distant mets.
M1: Distant mets.
Clinical Staging for Squamous Cell CA of the Esophagus?
Esophageal SCC
Stage
0: Tis N0 M0
I: T1 N0-1 M0
II: T2 N0-1 M0
T3 N0 M0
III: T3 N1 M0
T1-3 N2 M0
IVA: T4 N0-2 M0
Any T N3 M0
IVB: Any T Any N M1
Clinical Staging for Adenocarcinoma of the Esophagus?
Esophageal AdenoCA
Stage
0: Tis N0 M0
I: T1 N0 M0
IIA: T1 N1 M0
IIB: T2 N0 M0
III: T2 N1 M0
T3 N0-1 M0
T4a N0-1 M0
IVA: T1-4a N2 M0
T4b N0-2 M0
Any T N3 M0
IVB: Any T Any N M1
Approach to cervical esophageal cancer?
8% of primary malignant tumors of the esophagus occur in the cervical portion, and are almost always SCC. They are more common in females.
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 LNs with minimal flow in a longitudinal direction.
Cervical esophageal CA is frequently unresectable because of early invasion of the larynx, great vessels, or trachea. Hence stereotactic radiation with concomittant chemotherapy is the most desirable treatment.
Approach to esophageal CA in the middle third (midthoracic)?
These are mostly SCC, and are frequently associated with LN mets.
Generally, T1 and T2 cancers without LN mets are treated with resection only, but there is more and more data to suggest LN involvement or transmural cancer (T3) warrants treatment with neoadjuvant chemoradiation therapy followed by resection.
Although some surgeons prefer a transhiatal esophagectomy, most surgeons believe that resection of midesophageal cancer should be performed under direct vision with either thoracoscopy (VATS) or thoracotomy.
Approach to esophageal CA in the lower esophagus and cardia?
These are usually adenocarcinomas. Unless staging demonstrates an incurable lesion, resection in continuity with a LN dissection should be performed.
Because of the propensity of GI tumors to spread for long distances submucosally, long lengths of grossly normal GI tract should be resected.
The longitudinal lymph flow in the esophagus can result in skip areas, with small foci of tumor above the primary lesion, which underscores the importance of a wide resection of esophageal tumors. (*Wong has shown that local recurrence at the anastomosis can be prevented by obtaining a 10cm margin of normal esophagus above the tumor. Also, there is no submucosal lymphatic barrier between the esophagus, stomach and cardia, hence 50% of local recurrences post resection occur in the intrathoracic stomach along the line of gastric resection.)
How long is the esophagus?
17-25cm
What does a curative resection for distal esophageal lesions entail?
A curative resection requires a cervical division of the esophagus and a >50% proximal gastrectomy in most patients with carcinoma of the distal esophagus or cardia.
How does age factor in when approaching esophageal CA?
Resection for cure of esophageal CA in a patient older than 80 years old is rarely indicated because of the additional operative risk and the shorter life expectancy. However octogenarians with a high-performance status and excellent cardiopulmonary reserve may be considered candidates for esophagectomy.
Incidence of esophageal carcinoma by location?
Cervical 8% Upper thoracic 3% Middle thoracic 32% Lower thoracic 25% Cardia 32%
Functional grades of dysphagia?
I: Eating normally (11%)
II: Requires liquids with meals (21%)
III: Able to take semisolids but unable to take solid food (30%)
IV: Able to take liquids only (40%)
V: Unable to take liquids, but able to swallow saliva (7%)
VI: Unable to swallow saliva (12%)
Grades I-III can generally be palliated with RT, in combination with chemotherapy (definitive chemoradiation therapy, meaning surgery is not anticipated in the future). Radiation is increased from 45 Gy to 60 Gy, administered over 8 weeks, rather than 4 weeks for induction therapy.
Grade IV and higher necessitates additional treatment, the mainstay of which is indwelling esophageal stents. However, if cancers involve the GEJ, a stent may cause disabling reflux and heartburn; hence RT may be preferable for cancers at this level. If feeding access is desirable, laparoscopic jejunostomy is the procedure of choice.
How does cardiopulmonary reserve factor in when approaching esophageal CA?
Cardiopulmonary reserve is assessed with FEV in 1 second (≥ 2L).
A patient with an FEV in 1 second of <1.25L is a poor candidate for esophageal resection.
Poor pulmonary reserve: TRANSHIATAL Esophagectomy (less pulmonary morbidity)
Most individuals who can climb 3 flights of stairs without stopping will do well with two-field open esophagectomy especially with an epidural catheter for postoperative pain relief.
What is the factor most predictive of postoperative complications in esophageal resection?
Nutritional status. Profound weight loss (>20lb) with hypoalbuminemia (albumin <3.5g/dL) is associated with a much higher rate of complications and mortality.
Because most malnourished patients have locally advanced esophageal cancer, placement of a feeding tube prior to induction chemoRT should be considered.
Clinical indications of advanced esophageal carcinoma (poor candidates for surgery)?
Recurrence nerve paralysis Horner's syndrome Persistent spinal pain Paralysis of the diaphragm Fistula formation Malignant effusion Tumor >8cm in length Abnormal axis of the esophagus on barium >4 enlarged LNs in CT Weight loss >20% Loss of appetite
Quickest surgical procedure to perform for esophageal cancer?
Open transhiatal esophagectomy
Most radical resection?
Ivor-Lewis (En Bloc) Esophagectomy
The operation is started in the abdomen with an upper midline laparotomy and extensive LN dissection. Following closure of the abdominal incision, the patient is placed in the left lateral decubitus position, and an anterolateral thoracotomy is performed through the 6th ICS.
Because this is the most radical of dissections, complications are most common, including pneumonia, respiratory failure, AF, chylothorax, anastomotic leak, conduit necrosis, fistula, recurrent laryngeal nerve injury. However this also has a long-term outcome with the greatest survival.
What is salvage esophagectomy?
Salvage esophagectomy is the term used for esophagectomy performed after failure of definitive RT and chemotherapy. This is often done when distant disease renders the patient nonoperable at initial presentation. Then, systemic chemo destroys all foci of mets as shown by CT and PET, but the primary remains symptomatic and present.
1 in 4 patients undergoing this operation will be disease-free 5 years later.
Because of dense scarring by radiation treatment, this is the most challenging technically among all esophagectomy techniques.
What type of tumor constitutes more than 50% of benign esophageal tumors?
Leiomyomas constitute more than 50% of benign esophageal tumors. The average age at presentation is 38, and these are twice as common in males.
These are usually solitary and usually intramural, with 90% located in the lower 2/3. The overlying mucosa is freely movable and normal in appearance, with dysphagia and pain as the most common complaints.
A barium swallow is the most useful method to demonstrate a leiomyoma of the esophagus (smooth, semilunar, or crescent-shaped filling defect that moves with swallowing, sharply demarcated, covered and surrounded by normal mucosa).
Esophagoscopy should also be performed to exclude the reported observation of a coexistence with carcinoma.
Biopsy should NOT be done (increased chance of mucosal perforation). Endoscopic ultrasound is also a useful adjunct in the workup of leiomyomas.
Leiomyomas should be removed by simple enucleation.
What is the surgical approach for leiomyomas of the esophagus?
Lesions of the proximal and middle esophagus require a right thoracotomy, whereas distal esophageal lesions require a left thoracotomy.
Large lesions or those involving the GEJ may require esophageal resection.
Discuss esophageal cysts.
Congenital cysts are lined wholly or partly by columnar ciliated respiratory-type epithelium, glandular gastric-type epithelium, squamous epithelium, or transitional epithelium.
Acquired retention cysts also occur probably secondary to obstruction of the excretory ducts of the esophageal glands.
Enteric and bronchogenic cysts are the most common secondary to developmental abnormalities during the formation and differentiation of the lower respiratory tract, esophagus and stomach from the foregut.
Cysts are usually located intramurally in the middle to lower third of the esophagus, and present clinically similar to leiomyomas.
Surgical excision by enucleation is the preferred treatment. During removal, a fistulous tract connecting the cysts to the airways should be sought, especially in patients with repeated bronchopulmonary infections.
How do you diagnose esophageal perforation?
Perforation of the esophagus constitutes a true emergency. Spontaneous perforation, known as Boerhaave’s syndrome, comprises only 15% of cases of esophageal perforation (14% FB, 10% trauma).
Pain is a striking and consistent symptom and strongly suggests rupture (cervical area following instrumentation of the esophagus, or substernally in a patient with a history of resisting vomiting). If subcutaneous emphysema is present, the diagnosis is almost certain.
CXR may show air or an effusion in the pleural space (abnormalities may differ based on time interval, site of perforation, and integrity of mediastinal pleura):
TIME
Mediastinal emphysema, strong indicator of perforation, takes at least 1 hour to be demonstrated and is present in only 40% of patients. Mediastinal widening secondary to edema may not occur for several hours. Air in the deep muscles (erector spinae) of the neck is often the earliest sign of perforation and can be present without evidence of air in the mediastinum.
SITE
Cervical perforation: Cervical emphysema
Thoracic perforation: Mediastinal emphysema
INTEGRITY OF MEDIASTINAL PLEURA Pleural rupture results in a PNEUMOTHORAX (77%) 2/3: Left-sided perforation 1/5: Right-sided perforation 1/10: Bilateral
Intact pleura results in MEDIASTINAL EMPHYSEMA
A pleural effusion secondary to inflammation of the mediastinum occurs late.
In 9% of patients, CXR is normal.
Diagnosis is confirmed with a CONTRAST ESOPHAGOGRAM (Extravasation in 90% of patients). The use of a water-soluble medium such as Gastrografin is preferred (ideally in right lateral decubitus position– if upright, there is a 10% false negative rate as the passage of contrast can be too rapid).
Elevation of pleural amylase may occur from extrusion of saliva through the perforation.
Common locations for esophageal perforation?
Into the left pleural cavity or just above the GEJ. The most common location is the left lateral wall of the esophagus, just above the GEJ.
50% of patients have concomitant GERD, suggesting that minimal resistance to the transmission of abdominal pressure into the thoracic esophagus is a factor in the pathophysiology of the lesion.
