Diagnostic Atlas of Gastroesophageal Reflux Disease: A New Histology-based Method
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The mucosal layer is normally composed of nonkeratinized stratified squamous epithelium, as opposed to the stomach where columnar epithelium is present. In the distal aspect of the esophagus within the lower esophageal sphincter, repeated exposure of the squamous epithelium to gastric contents can result in metaplasia of esophageal squamous mucosa to a columnar epithelium called cardiac mucosa.
This nomenclature was originally used to describe what was mistakenly thought to be the proximal stomach or cardia, but there is now convincing evidence that this is in fact metaplastic esophageal mucosa. Alternatively, cardiac mucosa can also differentiate further to acquire parietal cells and is known as oxyntocardiac mucosa. A critical layer within the mucosa for determining the biologic behavior of a superficial cancer is the muscularis mucosa.
This thin, poorly developed layer lies below the basement membrane and above the submucosa. It is often duplicated in patients with Barrett esophagus, and can lead to confusion during pathologic evaluation of the depth of tumor invasion in endoscopic resection ER specimens. The submucosa is characterized by a rich lymphatic plexus that extends throughout the esophagus. Lymphatic collecting branches arise from within the submucosa and pierce the muscularis propria to communicate with regional lymph nodes and the thoracic duct outside of the esophagus.
This network of lymphatics allow for significant longitudinal spread of esophageal cancers and a high rate of skip metastases. These glands are helpful for determining the true extent of the esophagus when metaplasia of the mucosa occurs. The muscularis propria is composed of an inner circular layer and an outer longitudinal layer. The muscles are striated in the upper portion and transition to completely smooth muscle near the upper third of the esophagus. The longitudinal muscle layer courses down in an elongated spiral pattern, turning approximately 90 degrees as it descends to the stomach.
The circular muscle layer is thicker than the longitudinal layer, which also takes on an elliptical or spiral orientation Fig. This arrangement of muscle is responsible for the wormlike drive of peristalsis. The cervical portion of the esophagus receives its main blood supply from the inferior thyroid artery.
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The thoracic portion receives blood from the bronchial and esophageal arteries. Seventy-five percent of individuals have one right-sided and two left-sided bronchial arteries, and usually two esophageal branches arise directly from the aorta. There are rarely aortic branches directly to the esophagus in the lower half of the esophagus in the chest, allowing the surgeon to perform an en bloc dissection of all of the periesophageal tissue directly off the plane of the aortic adventitia from the right to the left pleural spaces.
The blood supply of the abdominal portion of the esophagus comes from the ascending branch of the left gastric artery and from the right and left inferior phrenic arteries Fig. After the vessels have entered the muscular wall of the esophagus, branching occurs at right angles to provide an extensive longitudinal vascular plexus. The rich blood supply provided by this vascular plexus allows mobilization of the esophagus from the stomach to the aortic arch without causing ischemic injury.
Endoscopic view of esophageal muscle layers during a peroral endoscopic myotomy POEM for achalasia. The endoscopic knife is lifting and cutting the circumferential circular muscle fibers, leaving the longitudinal muscle fibers intact. Arterial anatomy of the esophagus. The capillaries of the esophagus drain into a submucosal and periesophageal venous plexus, from which the esophageal veins originate. In the cervical region, the esophageal veins empty into the inferior thyroid vein; in the thoracic region, they empty into the bronchial, azygos, or hemiazygos veins; and in the abdominal region, they empty into the coronary vein Fig.
The lymphatic channels are located almost exclusively below the muscularis mucosa in the submucosa of the esophagus, constituting a dense and interconnected plexus with more lymph vessels than blood capillaries Fig. Lymph flow in the submucosal plexus runs in a longitudinal direction, and after the injection of a contrast medium, the longitudinal spread is six times that of the transverse spread. In the upper two-thirds of the esophagus, the lymphatic flow is mostly cephalad; in the lower third, it is mostly caudal.
In the thoracic portion of the esophagus, 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. As a consequence of this nonsegmental lymph drainage, the lymphatic spread of tumor cells can extend for a considerable distance superiorly and inferiorly within the submucosal lymphatics before the cells pass through lymphatic channels in the muscularis and on into the regional lymph nodes. There is a high rate of skip metastases in esophageal cancer due to this arrangement. By contrast, the cervical esophagus has a more segmental lymph drainage into the regional lymph nodes, and as a result, tumors in this portion of the esophagus have less submucosal extension.
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Lymph from the cervical esophagus drains into the paratracheal and deep cervical lymph nodes, whereas lymph from the upper thoracic esophagus flows mainly into the paratracheal lymph nodes. The lymph from the lower thoracic esophagus drains into the subcarinal and inferior pulmonary nodes. Lymph from the distal thoracic and abdominal portion of the esophagus drains into the parahiatal and perigastric nodes.
Venous anatomy of the esophagus. The parasympathetic innervation of the pharynx and esophagus is provided mainly by cranial nerve X or the vagus nerves. The constrictor muscles of the pharynx receive branches from the pharyngeal plexus, which is located on the posterior lateral surface of the middle constrictor muscle and is formed by pharyngeal branches of the vagus nerve, with a small contribution from cranial nerves IX and XI.
The cricopharyngeal sphincter and the cervical portion of the esophagus receive branches from both the right and left recurrent laryngeal nerves originating from the vagus nerves Fig. Damage to these recurrent nerves interferes not only with the movement of the vocal cords but also with the function of the cricopharyngeal sphincter and the motility of the cervical esophagus, predisposing the patient to pulmonary aspiration on swallowing. The upper thoracic esophagus receives innervation from the left recurrent laryngeal nerve and both vagus nerves. As the right and left vagus nerves descend into the mediastinum, they join the outer surface of the esophagus.
The esophageal plexus, which is formed by the branches of the right and left vagus nerves and thoracic sympathetic chain, lies on the anterior and posterior walls of the esophagus and innervates the lower thoracic portion. Afferent visceral sensory fibers from the esophagus end without synapse in the first four segments of the thoracic spinal cord by a combination of sympathetic and vagal pathways. These pathways are also occupied by afferent visceral sensory fibers from the heart, which explains the similarity of symptoms in esophageal and cardiac diseases.
To comprehend the mechanics of alimentation, it is useful to visualize the gullet as a series of pumps and valves. In the pharyngeal segment, the tongue and pharyngeal muscle function as pumps, whereas the soft palate, the epiglottis, and the cricopharyngeus serve as the valves that regulate flow. In the esophageal segment, the esophageal body functions as the pump to propel the food bolus, whereas the lower esophageal sphincter serves as a valve to allow transport into the stomach and to prevent the flow of gastric contents back into the esophagus.
Swallowing can be started at will, or it can be reflexively elicited by the stimulation of 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 vagal nerves. Once it is aroused by stimuli entering through 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 and the motor neurons of C1 through C3.
Discharges through these nerves always occur in a specific pattern and last for approximately 0. Little is known about the swallowing center except that it can trigger swallowing after a variety of different inputs. Once it is triggered, the swallow response is always a rigidly ordered pattern of outflow neurogenic impulses. The act of alimentation requires the passage of food and drink from the mouth into the stomach. Food is taken into the mouth in a variety of bite sizes, after which it is broken up by the teeth, mixed with saliva, and lubricated.
When food is ready for swallowing, the tongue, acting as a pump, moves the bolus into the posterior oropharynx and forces it into the hypopharynx Fig. Concomitantly with the posterior movement of the tongue, the soft palate is elevated, thereby closing the passage between the oropharynx and nasopharynx.
With the initiation of the swallow, the hyoid moves superiorly and anteriorly, thereby elevating the larynx and enlarging the retropharyngeal space. At the same time, the epiglottis covers the laryngeal inlet to prevent aspiration. Lymphatic anatomy of the esophagus. During swallowing, the pressure in the hypopharynx rises abruptly to 60 mm Hg as a result of the backward movement of the tongue and contraction of the posterior pharyngeal constrictors. A sizable pressure difference develops between the hypopharyngeal pressure and the subatmospheric midesophageal or intrathoracic pressure Fig.
This pressure gradient speeds the movement of food from the hypopharynx into the esophagus when the cricopharyngeus or UES relaxes. The bolus is both propelled by the peristaltic contraction of the posterior pharyngeal constrictors and sucked into the thoracic esophagus by this pressure gradient.
Critical to receiving the bolus is the compliance of the cervical esophageal muscle and the timing and degree of relaxation of the UES. Abnormalities of compliance and UES opening can result in pharyngeal dysphagia. During the transfer of the bolus from the mouth into the esophagus, the UES is mechanically pulled open. Elevation of the larynx by muscles attached to the hyoid bone pulls the UES open at the same time that relaxation of the UES is occurring.
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The active relaxation of the UES is caused by a reduction in the tone of the tonic constriction of the cricopharyngeus muscle, and it is dependent on a neurologically mediated reflex. This is an all-or-nothing event; partial relaxation does not normally occur. The UES closes within 0. The postrelaxation contraction continues down the esophagus as a peristaltic wave Fig. The high closing pressure and the initiation of the peristaltic wave prevent reflux of the bolus from the esophagus into the pharynx.
After completion of the swallow, the pressure of the UES returns to its normal resting pressure. The pharyngeal activity in swallowing initiates the esophageal phase of swallowing. Because of the helical arrangement of its circular muscles, the body of the esophagus functions as a worm-drive propulsive pump, and it is responsible for transmitting a bolus of food into the stomach. During the esophageal phase of swallowing, the bolus is moved into the stomach over a gradient of 12 mm Hg i. Effective and coordinated smooth muscle function in the lower two-thirds of the esophageal body is important to allow this movement to occur.
Relationship of the esophagus to the vagus nerves and their branches.
Esophageal Anatomy and Physiology and Gastroesophageal Reflux Disease
The peristaltic wave generates an occlusive pressure that varies from 30 to mm Hg. The wave rises to a peak in 1 second, remains at the peak for about 0. The whole course of the rise and fall of an occlusive contraction may occupy one point in the esophagus for 3 to 5 seconds. The lower esophageal sphincter relaxes at the initiation of the peristaltic wave and remains open until the peristaltic wave passes through the body and into the sphincter muscle, and this is followed by a distinctive postrelaxation contraction of the lower esophageal sphincter.
A consecutive swallow after 20 seconds produces a similar primary peristaltic wave; however, if repetitive swallowing occurs sooner, the esophagus becomes unresponsive deglutitive inhibition. Overview of the act of swallowing. Pressure profile of the esophagus in the neck, chest, and abdomen. Foregut motor disorders and their surgical management. Med Clin North Am ;, with permission. Overview of esophageal body peristalsis. To be effective, peristaltic contractions must be of sufficient amplitude to occlude the esophageal lumen and sufficiently organized in a peristaltic waveform to propel a bolus toward the stomach.
Low-amplitude contractions that do not occlude the lumen merely indent a semisolid bolus rather than propel it, and simultaneous contractions throughout the body of the esophagus result in splitting the bolus or propelling it orally which can be observed on a barium esophagram as bolus segmentation or cephalic escape. Clinically, defects in peristalsis occur in three broad categories, depending on which major feature is the most impaired.
First, there is a neural abnormality that results in the defective organization of the peristaltic wave; this is recognized by the presence of simultaneous contractions with a loss of the peristaltic sequence and results in typical primary motility disorders e. The second category defect is evident when there is a reduction of the amplitude of the contraction but the peristaltic sequence remains; this is usually due to muscle damage and the formation of fibrous tissue within the muscle. Examples include end-stage gastroesophageal reflux disease GERD and connective tissue disorders such as scleroderma.
The third category defect results from altered anatomy of the esophageal body. A loss in the efficiency of the peristaltic sequence can result when the esophagus is not anchored distally, as occurs with a large paraesophageal hernia PEH ; which can result in the appearance of an accordion esophagus on a barium swallow esophagram with ineffective clearance of barium.
Relationship between esophageal motility and severity of gas : Medicine
The LES represents the barrier that confines the gastric juice to the stomach and protects the acid-sensitive squamous esophageal mucosa from injury by refluxed gastric juice. As is true for any valve, failure of the LES can occur in two completely opposite ways, which lead to two distinct clinical disease entities. Regardless of the type of LES failure, the secondary effects are produced proximally in the esophagus.
Failure of the LES to relax or to open appropriately leads to the inability of the esophagus to propel food into the stomach, esophageal distention, and the condition known as achalasia. On the other hand, failure of the LES to remain closed leads to an increased exposure of the squamous epithelium to gastric juice and the condition known as GERD. The LES has no anatomic landmarks and cannot be seen endoscopically; it is identified on manometry as a rise in pressure over gastric baseline pressure.
This high-pressure zone is normally present except in two situations: 1 after a swallow, when it is momentarily dissipated or relaxes to allow passage of food into the stomach; and 2 during a belch, when it allows gas to be vented from a distended fundus. The common denominator for virtually all episodes of gastroesophageal reflux is the loss of this normal high-pressure zone or barrier. When the barrier is absent, resistance to the flow of gastric juice from an environment of higher pressure the stomach to an environment of lower pressure the esophagus is lost.
In early GERD, this is usually caused by a transient loss of the barrier. In advanced GERD, there is usually a permanent loss of the barrier. There are three characteristics of the LES or high-pressure zone that maintain its function as a barrier to intragastric and intra-abdominal pressure challenges. Two of these characteristics — the overall length and pressure of the LES — work together and depend on each other to provide resistance to the flow of gastric juice from the stomach into the esophagus. A fundamental principle for surgeons to understand is that the length of the barrier or LES is critical to its function.
Relationship of the length and pressure of the lower esophageal sphincter in maintaining competence of the gastroesophageal barrier. With excessive gastric distention e. In this situation, competency of the barrier is an ever-constant clinical problem. The observation that gastric distention results in shortening of the LES down to a critical length so that the pressure dissipates, the lumen opens, and reflux occurs provides a mechanical explanation for transient LES relaxations without invoking a neuromuscular reflex.
If only the LES pressure and not its length is measured e. Variations in the anatomy of the cardia, from a normal acute angle of His to an abnormal dome architecture of a sliding hiatal hernia, influence the ease with which the sphincter is shortened by gastric distention. A hernia can result from the pulsion force of abdominal pressure on the esophageal hiatus or from the traction produced by inflammatory fibrosis of the esophageal body.
The resulting alteration in the geometry of the cardia places the sphincter at a mechanical disadvantage in maintaining its length with progressive degrees of gastric distention. Greater gastric distention is necessary to open the barrier in patients with an intact angle of His than in those with a hiatal hernia.
Kahrilas et al. Patients with hiatal hernias had significantly more transient LES relaxations per hour than did control subjects without hernias. The reduction in length became significant 20 to 30 minutes after the beginning of air infusion and occurred in a distal to cephalad direction before a loss of LES pressure was observed. Effect of increasing gastric volume on the shortening of the lower esophageal sphincter length.
As the stomach expands, the gastric body takes up the inferior aspect of the sphincter causing its length to shorten. Nissen fundoplication prevents shortening of the sphincter during gastric distention. Arch Surg ;—, with permission. Representation of the loss of competence of the lower esophageal sphincter with shortening of its length.
As a critical length is reached, there is a precipitous drop in sphincter pressure reflecting loss of competence. The lower esophageal sphincter: mechanisms of opening and closure. Surgery ;—, with permission. The third characteristic of the LES high-pressure zone is its position. A portion of the overall length of the high-pressure zone is normally exposed to the positive intra-abdominal pressure environment and is commonly referred to as the abdominal length of the LES.
When the abdominal length of the LES is inadequate, increases in intra-abdominal pressure will be applied to the stomach but not the LES thereby encouraging reflux to occur. Studies have shown that the critical length of abdominal LES is 1 cm, below which almost no LES pressure will be sufficient to maintain competency of the sphincter. In the fasting state deficits in LES pressure, overall length, or abdominal length will lead to an increased likelihood of sphincter incompetence.
An LES defective in all three parameters is particularly likely to be associated with increased reflux of gastric juice into the esophagus. This reflux can result in inflammatory injury to the mucosa and ultimately to the muscularis propria of the esophageal body, thereby causing a reduced contraction amplitude of the esophageal body and interrupted or dropped peristaltic sequences.
Continued reflux can lead to progressive loss of effective esophageal clearance, protracted esophageal exposure to the refluxed material and ultimately further organ injury Fig. Early GERD is initiated by increased transient losses of the barrier as a result of gastric overdistention from excessive air and food ingestion. With overeating, a critical length is reached usually about 1 to 2 cm at which the sphincter gives way; its pressure drops precipitously, and reflux occurs Fig. If the swallowed air is vented, gastric distention is reduced, the length of the LES is restored, and competency returns until subsequent distention again shortens it and further reflux occurs.
Aerophagia is common in patients with GERD because they swallow their saliva more frequently to neutralize the acidic gastric juice that is refluxed into the esophagus. The high prevalence of the disease in the Western world is thought to be a result of the eating habits of Western society. Surgical correction with a fundoplication prevents the shortening of the barrier with progressive degrees of gastric distention by diverting the forces that pull on the gastroesophageal junction.
Overview of the progressive nature of GERD and the effect of the lower esophageal sphincter and esophageal body on reflux in the upright and supine positions. In advanced GERD, permanent loss of sphincter length occurs from inflammatory injury that extends from the mucosa into the muscular layers of the LES. Fletcher et al. This proximal movement exposes the distal esophageal squamous mucosa to acid and results in the formation of cardiac mucosa.
Cardiac mucosa is an acquired mucosa that replaces chronically injured squamous mucosa in the terminal esophagus. For clinicians, the finding of a permanently defective LES has several implications. First, symptoms in patients with a defective LES can be difficult to manage, and mucosal damage may persist with medical therapy. It has been shown repeatedly that a laparoscopic Nissen fundoplication can consistently restore the length and pressure of the LES to normal parameters.
Third, a permanently defective LES and the loss of effective esophageal clearance can lead to mucosal injury such as erosive esophagitis or Barrett metaplasia, repetitive regurgitation and aspiration events and ultimately pulmonary fibrosis. Without reestablishing a barrier, chronic use of acid suppression therapy may simply mask the symptoms due to modification of the pH; however, in the setting of a structurally defective LES, reflux will continue unabated. The diagnostic tests that are employed to evaluate the esophagus are those used to visualize structural abnormalities, to detect functional abnormalities, and to measure esophageal exposure to gastric juice.
Radiographic assessment of the anatomy and function of the esophagus and stomach is one of the most important aspects of the esophageal evaluation, provided the surgeon has a working knowledge of esophageal physiology. Classically, the barium esophagram has been described as a road map for the esophagus. The first diagnostic test in patients with suspected esophageal disease should be a barium swallow that includes a full assessment of the stomach and the duodenum.
The study also provides anatomic information, such as the presence of obstructing lesions and structural abnormalities of the foregut. The pharynx and the UES are evaluated in the upright position, allowing assessment of the timing and coordination of the events of pharyngeal transit. It readily identifies a diverticulum, stasis of the contrast medium in the valleculae, cricopharyngeal bar, or narrowing of the pharyngoesophageal segment.
These are anatomic manifestations of neuromuscular disease and result from the loss of muscle compliance from the deinnervation of the skeletal muscle of the pharynx and the cervical esophagus. The assessment of bolus transport on video esophagography often adds to or complements the information obtained by esophageal manometry.
Esophageal clearance is optimally assessed by observing several individual swallows of barium with the patient in both the upright and supine positions; the study can be performed with both liquid and solid bolus material.
During normal swallowing, a primary peristaltic wave is generated that completely strips the bolus out of the esophagus and into the stomach. Residual material rarely stimulates a secondary peristaltic wave; rather, an additional pharyngeal swallow is usually required. Normal subjects can also clear a solid barium bolus with four or fewer swallows in the upright position. Motility disorders with disorganized or simultaneous esophageal contraction give a segmented appearance to the barium column.
This can often give a beading or corkscrew appearance to the barium within the esophagus.
In patients with dysphagia, the use of a barium-impregnated marshmallow, piece of bread, or hamburger can identify an esophageal transport disturbance that is not evident on the liquid barium study. A mm barium tablet is another useful adjunct that can be used to determine how well solid material can clear the esophagus, and identify areas of clinically significant narrowing since solid food dysphagia typically is present with luminal narrowing below 13 mm.
A hiatal hernia is present in a high percentage of patients with gastroesophageal reflux. The hiatal hernia is an important component of the underlying pathophysiology of reflux. The diagnosis of reflux disease is not accurately made on video esophagram. Spontaneous reflux to the level of the thoracic inlet seems to correlate with a positive pH test, but evoked reflux and spontaneous reflux into the distal esophagus are not. Moreover, failure to observe reflux during a video esophagram does not indicate the absence of disease.
A full-column technique with distention of the esophageal wall can discern extrinsic compression of the esophagus, and a fully distended esophagogastric region is necessary to identify narrowing from a Schatzki ring, stricture, or obstructing lesion. Mucosal relief or double-contrast films can be obtained to enhance the detection of small neoplasms, esophagitis, and varices.
Assessment of the stomach and duodenum during the barium study is helpful for the evaluation of the patient with esophageal symptoms ESs. A gastric or duodenal ulcer, a neoplasm, or poor gastroduodenal transit can mimic many of the symptoms that are suggestive of an esophageal disorder. Endoscopic evaluation of the esophagus is essentially the physical examination of the foregut. It is a critical part of the assessment of a patient with esophageal disease and is indicated in essentially every patient who is being evaluated for GERD.
A barium study obtained before esophagoscopy is helpful to the endoscopist by directing attention to locations of subtle change and alerting the examiner to such potential danger spots as a cervical vertebral osteophyte, an esophageal diverticulum, a deeply penetrating ulcer, or a carcinoma. Adenocarcinoma of the esophagus and gastric cardia is now the most rapidly increasing cancer type in the Western world. At present, there is no histologic test that has any practical value in the diagnosis of reflux disease.
The only histologic diagnostic criteria are related to changes in the squamous epithelium which are too insensitive and nonspecific for effective patient management. It is widely recognized that columnar metaplasia of the esophagus manifest histologically as cardiac, oxyntocardiac and intestinal epithelia is caused by reflux.
However, except for intestinal metaplasia, which is diagnostic for Barrett esophagus, these columnar epithelia are not used to diagnose reflux disease in biopsies. The reason for this is that these epithelial types are indistinguishable from "normal" "gastric" cardiac mucosa. In standard histology texts, this "normal gastric cardia" is cm long. In the mids, Dr. Chandrasoma and his team at USC produced autopsy data suggesting that cardiac and oxyntocardiac mucosa is normally absent from this region and that their presence in biopsies was histologic evidence of reflux disease.
From this data, they determined that the presence of cardiac mucosa was a pathologic entity caused by reflux and could therefore be used as a highly specific and sensitive diagnostic criterion for the histologic diagnosis of reflux disease. They call this entity "reflux carditis".
In addition, the length of these metaplastic columnar epithelia in the esophagus was an accurate measure of the severity of reflux disease in a given patient. At present, there is some controversy over whether cardiac mucosa is totally absent or present normally to the extent of mm. While this should not be a deterrent to changing criteria which are dependent on there normally being cm of cardiac mucosa, there has been little mainstream attempt to change existing endoscopic and pathologic diagnostic criteria in the mainstream of either gastroenterology or pathology.
The ATLAS will be the source of easily digestible practical information for pathologists faced with biopsies from this region. It will also guide gastroenterologists as they biopsy these patients. ISBN: Autori: Chandrasoma. Editore: Elsevier - Academic Press. Edizione: Lingua: Inglese. Finitura: Copertina rigida. Pagine: Per inviare la segnalazione inserisci il tuo nome e l'indirizzo email del destinatario. Per segnalare la pagina devi prima inserire la sequenza di caratteri mostrata in figura.
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