Disease of esophagus
Esophageal diverticula
The esophageal diverticula are the sacciform outpouchings of the esophageal wall, which filled with mucus and undigested food.
Etiology and pathogenesis
The conducting pathogenic moment in occurrence of esophageal diverticula is the increase of intraesophageal pressure proximal to muscle sphincters, which gradually results in herniation in weak sites of the esophageal wall. Such mechanism of formation is characteristic for pulsion diverticula. Traction diverticula are formed as a result of paraesophageal inflammatory and sclerotic processes, which tract esophagus to other organs, more often – with the right bronchus. During their motions owing to a traction esophageal diverticula also are gained.
Zenker’s diverticula in advanced cases are great in size. There are three stages in their development:
1) outpouching of mucosa;
2) formation of a globular sack;
3) enlargement of diverticulum with further descending in mediastinum.
Pathology
The restricted blind herniation of the wall of esophagus could be single or multiple, ring-shaped, cylindrical, oval or sacciform-shaped. The muscle coat atrophies, that makes difficult differentiation between true and false diverticula. The latter caused by inflammatory processes. In such cases the paraesophageal scarring resulting from extrapharyngeal abscesses, mediastinitis, specific and nonspecific inflammatory processes of bifurcational lymph nodes (traction diverticula) are revealed.
The small size of the opening of pouch, for example, in globular diverticula, leads to congestion of contents with the further development of inflammation (diverticulitis erosive, catarrhal, gangrenous, purulent).
Classification
1. According to the origin:
a) congenital;
b) acquired.
2. According to number:
a) single;
b) multiple.
3. According to histological structure:
a) true (have all layers of esophageal wall);
b) false (absent muscular layer of esophageal wall).
4. According to localization:
a) pharyngoesophageal (Zenker’s);
b) bifurcational;
c) epiphrenic.
5. According to the clinical course:
a) complicated;
b) uncomplicated.
Types of diverticula:
1 – pharyngoesophageal (Zenker’s)
2 – bifurcational
3 – epiphrenic
Symptomatology and clinical course
Clinical manifestation of the esophageal diverticula, as a rule, connected with the occurrence of complications.
The symptomatology of Zenker’s diverticula depends on the stage of development and their size.
A Zenker diverticulum, which is seen in the images below, is formed by the herniation of mucosa through an area of weakness in the posterior wall of the hypopharynx (the Killian triangle).
Sometimes Zenker diverticula are called pharyngoesophageal diverticula because of their close proximity to the cervical esophagus; however, this is somewhat of a misnomer because the diverticula actually arise from the hypopharynx rather than from the esophagus.
Of the diverticula discussed in this article, Zenker diverticula are the most common type to cause symptoms.
Zenker diverticula are an acquired pulsion-type of diverticula that probably develop because of the aging process. They form in the posterior hypopharynx at a point where a defect in the muscular wall, between the inferior pharyngeal constrictor muscle and the cricopharyngeal sphincter (Killian triangle), usually exists.
Zenker diverticula are believed to occur because of an outflow obstruction caused when loss of coordination of the buccal squirt (ie, swallowing movement of the tongue posteriorly with contraction of the oropharyngeal muscles) and opening of the cricopharyngeus (ie, the upper esophageal sphincter) occurs. The noncompliant cricopharyngeus muscle becomes fibrotic over time.
Oropharyngeal dysphagia, usually to solids and to liquids, is the most common symptom. Retention of food material and secretions in the diverticulum, particularly when diverticula are large, can result in regurgitation of undigested food, halitosis, cough, and even aspiration pneumonia. The patient may note food on the pillow upon awakening in the morning. With very large diverticula, a mass in the neck occasionally can be detected. Cancer rarely has been reported in association with Zenker diverticula.
Salivation, cervical dysphagia, difficult swallowing and cough usually occur in advanced stages of the diverticulum.
The dysphagia is frequently caused by congestion of food in diverticulum. Also a compressible mass in the neck usually on the left side is frequently revealed. The patients should press this mass to swallow the food and sometimes make unusual movements by neck in order to empty the diverticulum. The gurgling sound when the patient is eating and foul-smell from the mouth resulting from decay of undigested food in diverticulum cause the patient to alter social activities.
The sign “of a wet pillow” results from increased salivation and nocturnal discharge of saliva and mucus from the mouth.
Diverticula of the esophageal body are relatively rare. They primarily occur in the middle and distal esophagus (see the image below).
Bifurcational diverticula are usually less
Diverticula that occur in the distal esophagus, in the lower 6-
The epiphrenal diverticula can achieve considerably size, and more frequently complicated by diverticulitis. Being filled with food, such diverticulum can compress cervical organs, and sometimes is complicated with achalasia.
Diverticula of the mid and distal esophagus may have various etiologies. For instance, some diverticula in the mid esophagus are congenital in origin; others are of the traction variety. With the latter, diverticula develop by traction from contiguous mediastinal inflammation and adenopathy, eg, pulmonary tuberculosis and histoplasmosis. The diverticula that develop by traction and adenopathy usually are asymptomatic.
Retention of undigested food in large diverticula occasionally results in regurgitation, nocturnal cough, and aspiration pneumonia.
Occasional epiphrenic diverticula occur in the setting of long-standing peptic esophagitis and strictures, and they rarely are symptomatic. Other rare causes of diverticula of the mid and distal esophagus include iatrogenic surgical injury to the esophagus and Ehlers-Danlos syndrome (weakness of collagen). Perhaps the most common causes of mid esophageal and epiphrenic diverticula are motility disorders of the esophageal body, including achalasia, diffuse esophageal spasm, and hypertensive lower esophageal sphincter.
Dysphagia is the most common symptom associated with mid esophageal and epiphrenic diverticula, although it usually is related more to the underlying motility disturbance than to the diverticulum per se. However, on occasion, the diverticulum may be responsible for the dysphagia, particularly if it is very large and filled with food or a bezoar. Regurgitation and aspiration may be related to large mid esophageal and epiphrenic diverticula; however, in patients with achalasia, regurgitation and aspiration are more likely to be related to poor esophageal emptying from the underlying motility disturbance (eg, hypertensive lower esophageal sphincter that fails to relax, absence of esophageal body peristalsis).
The diagnosis is confirmed by the findings of barium swallow, and also esophagoscopy.
Pharyngoesophageal (Zenker’s) diverticulum)
Variants of clinical course and complications
Diverticulitis. The anginal pain, or the pain in epigastric region, which can resemble stenocardia or gastric disorders, belching, are the chief manifestations. Sometimes observed nausea and vomiting.
The perforation of diverticulum can be directed into pleural space, trachea, bronchus or pericardium. The clinical picture depends on the place of perforation. In part the perforation in trachea or bronchus results in occurrence of esophago-bronchial fistula. Clinically such complication is commonly shown by cough during meal. An everlasting esophago-bronchial fistula can cause the aspiration pneumonia with the further abscessing.
Bleeding from diverticula frequently results from erosion of esophageal mucosa on the background of diverticulitis. Nevertheless such bleedings, as a rule, are not profuse and rather easily stopped by conservative treatment.
Malignancy rarely occurs and most often as the outcome of recurrent diverticulites.
The diagnostic program
1. Anamnesis and objective examination.
2. General blood and urine analyses.
3. Coagulogram.
4. Chest X-radiography.
5. Roentgenoscopy of esophagus and gastrointestinal tract.
Radiographic studies and upper GI endoscopy detect many esophageal diverticula incidentally because esophageal diverticula often are asymptomatic.
On standard chest radiographs and CT scans, large diverticula of the esophagus and hypopharynx also may manifest as air-filled and/or fluid-filled structures communicating with the esophagus.
Barium radiography (ie, barium esophagography, barium swallow) generally is the diagnostic procedure of choice. In addition to being excellent at defining the structural appearance of diverticula, barium swallow also may provide clues to underlying motility disturbances that may be involved in diverticular formation. However, if the patient has dysphagia or odynophagia or has alarm symptoms, then upper endoscopy is indicated.
Barium swallow is a useful study in patients who are symptomatic and have mid esophageal and epiphrenic diverticula.
Diagnosis of esophageal intramural pseudodiverticulosis is made best using barium radiography.
Diagnosis of Zenker diverticulum is made best using barium swallow, which should include lateral views of the pharyngoesophageal junction. It also can be made using careful upper endoscopy by an experienced endoscopist.
6. Fibrogastroduodenoscopy.
Esophageal diverticula Fibrogastroduodenoscopy
Differential diagnostics
Functional diverticula (pseudodiverticula). Their clinical manifestations resemble a diffuse idiopathic esophagospasm. Intermittent dysphagia, which usually arises after meal or strong excitements, are the sings of pseudodiverticula. A retrosternal pain, which accompanied them, can result in misdiagnosis of stenocardia.
Stenocardia. It is characterized by pain attacks with irradiation in the left arm and left scapula, feeling of fear. After taking of nitroglycerin the pain, and fear, as a rule, disappear. In contrast with stenocardia, the retrosternal pain caused by a spastic stricture or diverticulum of esophagus, is characterized by feeling of compression deeply inside, which usually more expressed in the back. There is no obvious sensation of fear, irradiation of pain in arm and relief after nitroglycerin. Usually it is accompanied by disturbances of swallowing, sometimes vomiting, after that the pain frequently disappears.
Tactics and choice of treatment
The treatment of pharyngoesophageal diverticula is surgical. Conservative therapy is indicated in case of severe concomitant pathology, the patient’s refusal of operation or there are no conditions for its performance. In such cases mechanically sparing diet with washing down of solid food.
Asymptomatic and minimally symptomatic esophageal body diverticula do not require treatment.
In many patients with mid esophageal and epiphrenic diverticula, dysphagia is related to underlying dysmotility; thus, treatment should be directed to the motility disorder when feasible. For instance, achalasia can be treated with pneumatic dilation, botulinum toxin injection into the lower esophageal sphincter, or surgical Heller esophagomyotomy.
Treatment of esophageal intramural pseudodiverticulosis is directed toward underlying strictures or dysmotility.
The bifurcational diverticula require operative treatment only in one patient in ten. The indications for such operation are frequently recurrent diverticulites, bleeding, perforation, esophago-bronchial fistula or suspicion on malignancy.
Treatment of Zenker diverticulum traditionally has been surgical, although the specific operation used still is controversial. Surgical options include diverticulectomy with cricopharyngeal myotomy, diverticular suspension (diverticulopexy) with cricopharyngeal myotomy, and cricopharyngeal myotomy alone.
Consider diverticulectomy when esophageal body diverticula are believed to be the cause of aspiration. An abdominal laparoscopic approach may be feasible for some patients with epiphrenic diverticula. Case reports of endoscopic treatment of giant midesophageal diverticula have been reported. However, patients who are being considered for diverticulectomy should first undergo careful study with barium swallow, flexible endoscopy, and esophageal manometry. Treatment directed at an underlying esophageal motility disorder, such as achalasia, cannot be ignored.
Diverticulectomy usually is not performed by itself because it does not correct the defect in cricopharyngeal function that usually contributes to the formation of a Zenker diverticulum.
While the transcervical approach has been used traditionally, the transoral route using a rigid esophagoscope also may be used.
Good results have been obtained by performing a diverticulotomy using a flexible endoscope and needle-knife papillotome to cut the common wall between the diverticulum and the oropharynx as well as the cricopharyngeus while the patient is consciously sedated. Data suggest that this technique offers good results with a relatively high success rate, but it should be performed in large centers with surgeons who are experienced with this technique. In some variations of this technique, the diverticulum is stapled.
Other novel techniques are being developed. Flexible endoscopic diverticulotomy approaches have been explored using various techniques, including argon plasma coagulation, monopolar coagulation forceps, and needle-knife incision. These techniques typically use a cap or hood attached to the endoscope. The goal of these techniques is the division of the septum between the diverticulum and the esophagus, thus performing a cricopharyngeal myotomy.
Increased efforts to a laparoscopic approach to repair both epiphrenic diverticula and Zenker diverticula have been explored. The literature supports open surgery and a laparoscopic approach as appropriate methods of repair. The laparoscopic technique uses stapler closure, and multiple case reports cite wound leakage from stapler failure as a complication. With complication rates as high as 20%, a skilled surgeon with experience in this procedure is beneficial. Benefits of the laparoscopic approach include decreased morbidity because of no thoracotomy wounds and chest tubes and a less invasive approach.
A study of 229 endoscopic diverticulotomies (in 189 patients), conducted by Kos et al, indicated that better results can be achieved using a combination of CO2 laser and Acuspot in the endoscopic procedure than by employing endoscopic diverticulotomy with electrocautery or with a carbon dioxide (CO2) laser alone. The investigators reported the following postsurgical results:
· Endoscopy with CO2 laser
· Dysphagia – Absent following 78.4% of procedures
· Repeat surgery – Required following 19.6% of procedures
· Endoscopy with electrocautery
· Dysphagia – Absent following 72% of procedures
· Repeat surgery – Required following 24.3% of procedures
· Endoscopy with CO2 laser and Acuspot
· Dysphagia – Absent following 84.6% of procedures
· Repeat surgery – Required following 13% of procedures
Accesses. In order to expose pharyngoesophageal diverticula the cervical access along the anterior border of the sternocleidomastoid muscle is applied; in case of bifurcational diverticula right-sided posterolateral thoracotomy in ІV intercostal space is performed; in epiphrenal diverticula – left-sided posterolateral thoracotomy in VІІ intercostal space .
The essence of the operation consists of the following: the esophagus mobilized proximal and distal to diverticulum; after the exposure the latter is sutured or stapled near its basis and cut off. The line of suturing is covered by muscular layer of esophageal wall.
Accesses for diverticula
Cervical
Right-sided posterolateral thoracotomy in ІV intercostal space
Left-sided posterolateral thoracotomy in VІІ intercostal space
Steps of operation for esophageal diverticulum:
Mobilization of esophageal diverticulum
Suturing of diverticulum base
Suturing of esophageal muscles over the site of diverticulum
Achalasia of the cardia
Achalasia of the cardia is the disease, which is characterized by failure of the lower esophageal sphincter to relax with swallowing.
Etiology
The cause of this disease is still unknown. Among the underlying mechanisms are the psycho-emotional trauma, disturbance of parasympathetic and sympathetic innervation and influence of vegetotrophic substances on muscular fibers.
Pathology
Morphological changes depend on the stage of the disease, character of inflammation and mainly concerervous and muscle fibers. Thus the phenomena of the thickening of axial cylinders of nervous fibers progressively increase, with the development of their fragmentation and vacuolization. The working hypertrophy of muscular fibers is finished by the dystrophy of myocytes and the development of sclerosis. The latter is contributed by inflammation, mainly of immune character. In final stage a mediastinal pleura, paraesophageal fat and diaphragm consolidate and knitted together.
LES pressure and relaxation are regulated by excitatory (eg, acetylcholine, substance P) and inhibitory (eg, nitric oxide, vasoactive intestinal peptide) neurotransmitters. Persons with achalasia lack nonadrenergic, noncholinergic, inhibitory ganglion cells, causing an imbalance in excitatory and inhibitory neurotransmission. The result is a hypertensive nonrelaxed esophageal sphincter.
Frequency
Sex
The male-to-female ratio of achalasia is 1:1.
Age
Achalasia typically occurs in adults aged 25-60 years. Less than 5% of cases occur in children.
Classification
Four stages of the disease are distinguished:
1) functional spasm without esophageal dilation;
2) constant spasm with a moderate esophageal dilation and maintained peristalsis;
3) cicatrical changes of the wall with expressed esophageal dilation, the peristalsis is absent;
4) considerable esophageal dilation with sigmoid-shaped elongation and the presence of erosive changes of esophageal mucosa.
Symptomatology and clinical course
Dysphagia in the onset of the disease wears a temporary intermittent character with further permanent interchange. The passing of food after several swallows delayed on the level of a lower part of breastbone. In some cases during meal the dysphagia arises suddenly without any cause. The majority of the patients with dysphagia swallow better warm or hot food.
Esophageal vomiting (regurgitation) is the outcome of accumulation in esophagus of two and more l. of fluid. In initial stages of the disease the regurgitation can arise during or at once after meal and is accompanied by discomfort pain sensations. In advanced stages observed regurgitation with a rotten smell. The regurgitation can occur during sleeping – the sign “of a wet pillow”.
Splashing sounds and gurgling behind breastbone are rarely observed.
The sign of nocturnal cough arises owing to aspiration of fluid from esophagus into trachea. Thereby, the patients try to sleep in a sedentary position.
Pain and sense of tightness in the chest is the result of spasm and esophageal distention. With the developing of esophagitis, the pain wears a burning character.
Loss of weight is the outcome of prolonged disturbed food intake.
It is necessary to consider roentgenological contrast examination with barium swallow as the chief method, which enables to confirm the diagnosis. In the beginning of the disease revealed an inappreciable esophageal dilation and temporary delay of barium above the level of the inferior esophageal sphincter. In advanced stages of the disease observed a considerable esophageal dilation and elongation with a long delay of barium. Contours of a distal constricted part of esophagus described as the “rat tail” or “bird-beak” sign, without filling defects .
Esophageal achalasia
The endoscopic procedure reveals erosive changes of esophageal mucosa and enables to take a biopsy to rule out malignancy. Frequently in advanced stages it is failed to pass by endoscope a constricted part of esophagus and cardia.
Variants of clinical course and complications
The disease is characterized by remittent course with the change of the periods of dysphagia – from inappreciable to intensive. Even in advanced stages in minority of patients observed a latent course with complete disappearance of dysphagia in considerable esophageal dilation and cicatrical stenosis of cardia. Nevertheless later (from several months to several years) there comes an exacerbation of the disease with more severe course.
The bleeding arises owing to complications of erosive esophagitis at long duration of the disease.
The malignancy occurs in the patients with phenomena of a chronic esophagitis and chronic character of the disease.
Pneumonia, abscesses, bronchiectases, atelectases and pneumosclerosis are frequently the outcomes of decreasing pulmonary excursion which results from compression by dilated esophagus.
The diagnostic program
1. Anamnesis and physical findings.
2. General blood and urine analyses.
3. Chest X-radiography.
4. Esophagogastroscopy.
5. Contrast roentgenoscopy (barium swallow).
The esophagus appears dilated, and contrast material passes slowly into the stomach as the LES opens intermittently. The distal esophagus is narrowed and has been described as resembling a bird’s beak
Esophageal achalasia
Esophageal achalasia
Differential diagnostics
Cancer of the lower part of esophagus and cardial part of stomach. The predominant place in differential diagnostics possesses X-ray examination. As opposed to achalasia, the cancer is characterized by irregular contours of constricted part of esophagus with filling defect. Endoscopic examination and biopsy allows to confirm the diagnosis.
Diaphragmatic hypotonia with inflection of esophagus also can be accompanied with dysphagia. However chest X-radiography enables to find out high standing of the left dome of diaphragm.
Pneumothorax. On the plain chest X-radiography the edge of dilated esophagus can resemble the edge of collapsed lung. Nevertheless in the patient with pneumothorax on the roentgenogram the lung pattern is absent.
Tactics and choice of treatment
The goal of therapy for achalasia is to relieve symptoms by eliminating the outflow resistance caused by the hypertensive and nonrelaxing LES. Once the obstruction is relieved, the food bolus can travel through the aperistaltic body of the esophagus by gravity.
Calcium channel blockers and nitrates are used to decrease LES pressure. Approximately 10% of patients benefit from this treatment. This treatment is used primarily in elderly patients who have contraindications to either pneumatic dilatation or surgery.
Endoscopic treatment includes an intrasphincteric injection of botulinum toxin to block the release of acetylcholine at the level of the LES, thereby restoring the balance between excitatory and inhibitory neurotransmitters. This treatment has limited value. Only 30% of patients treated endoscopically still have relief of dysphagia 1 year after treatment. Most patients need repeated botulinum toxin injections, with short-lasting clinical benefits. This treatment can cause an inflammatory reaction at the level of the gastroesophageal junction, making a subsequent myotomy very difficult. Compared with pneumatic dilation, botulinum toxin injection is associated with significantly higher symptom recurrence rates at 12 months. Similarly, this treatment modality is less effective than laparoscopic Heller myotomy at 2-year follow-up. Use this treatment in elderly patients who are poor candidates for dilatation or surgery.
Pneumatic dilatation performed by a qualified gastroenterologist is the recommended treatment in those sporadic cases in which surgery is not appropriate. A balloon is inflated at the level of the gastroesophageal junction to blindly rupture the muscle fibers while leaving the mucosa intact. The success rate is 70-80%, and the perforation rate is approximately 5%. If a perforation occurs, emergency surgery is needed to close the perforation and to perform a myotomy. As many as 50% of patients may require more than 1 dilatation. The incidence of pathologic gastroesophageal reflux after the procedure is approximately 30%.
A laparoscopic Heller myotomy is considered by many to be the appropriate primary treatment of patients with achalasia (see Surgical Care). A Heller myotomy and a partial fundoplication performed from the chest (thoracoscopic) have a high incidence of gastroesophageal reflux.
Peroral endoscopic myotomy (POEM) has been recently introduced as a novel approach to achalasia. This procedure is performed under general anesthesia with endotracheal intubation. A 2-cm longitudinal mucosal incision is made on the mucosal surface to create a mucosal entry to the submucosal space. An anterior submucosal tunnel is created downwards, passing the gastroesophageal junction and about
Several potential advantages of POEM compared with laparoscopic Heller myotomy have been proposed. The endoscopic approach should theoretically minimize postoperative pain. A longer myotomy can be performed, extending to the medium third of the esophagus, just below the aortic arch. A concomitant antireflux surgery may not be required because of the selective section of the circular muscle fibers without any dissection at the level of the gastroesophageal junction. In current practice, few data are available regarding clinical outcomes in small series of patients over very short follow-up periods.
Based on the limited evidence available, POEM seems to be a promising new procedure. However, there are some concerns about this new technique. Endoscopic myotomy is a very demanding procedure, requiring major skills, with a very long learning curve. Even though several studies have reported significant reduction of LES pressure as demonstrated by manometry, the LES pressure was often between 15 and
Diet. The food should be semisoft, without pungent relishes, chemically inactive and enriched with proteins, fat, carbohydrates and vitamins.
The medicament treatment should include local anesthetics, spasmolytics, and sedative drugs. Atropin and other anticholinergic agents only increase the spasm of a cardial sphincter, therefrom their usage is undesirable. The medicament treatment results only in temporary relief.
Cardiodilatation is indicated in І-ІІ stage of achalasia. It is one of the chief methods of the treatment of this pathology. The treatment is performed as follows: under local anesthesia by aerosol or solution of anesthetic agent (lidocain, trimecain) through constricted part of the cardia under roentgenological check cardiodilatator (metal, pneumatic) is passed. The air is pumped up in balloon making pressure 200-
Surgical treatment is managed in ІІІ-ІV stage of achalasia or in recurrence of the disease after dilatation.
Because of excellent results, a short hospital stay, and a fast recovery time, the primary treatment is considered by many to be a laparoscopic Heller myotomy and partial fundoplication. In the author’s experience and in the experience of many authors, this treatment provides a fine balance in relieving symptoms of dysphagia by performing the myotomy and in preventing gastroesophageal reflux by adding a partial wrap. A prospective, randomized study from Vanderbilt University indicated that there is significantly less risk of postoperative reflux following a Heller myotomy plus a partial fundoplication than there is after a Heller myotomy alone. The authors of this study also showed that in patients with achalasia, adding a partial fundoplicatioot only is more effective in preventing postoperative reflux but also is more cost-effective at a time horizon of 10 years.
A partial fundoplication added to the myotomy entails better functional results when compared with a total fundoplication, with a lower risk of persistent or recurrent dysphagia. Recently, a multicenter, randomized controlled trial comparing partial anterior (Dor) with partial posterior (Toupet) fundoplication did not find significant differences in terms of postoperative incidence of gastroesophageal reflux. In current practice, a partial anterior fundoplication is more frequently performed since it is simpler to perform and covers the exposed esophageal mucosa.
Minimally invasive surgery for achalasia is performed under general anesthesia with the use of 5 trocars. A controlled division of the muscle fibers (myotomy) of the lower esophagus (
Heller’s method (esophagomyotomy). Operation is performed through upper median laparotomy or left thoracotomy in VІІ intercostal space. After exposing of constricted part of esophagus and taking it on tourniquets a muscular layer of anterior wall of esophagus dissected down to mucosa. The myotomy performed from dilated part of esophagus to cardial part of stomach. The complete transsection of all muscular layer of esophagus, particularly its circular fibers, is the requirement of relapse prevention.
Heller’s operation:
Myotomia of the cardia (1 – muscles, 2– mucosa)
Shift of stomach fundus to the esophageal cardia
Nissen fundoplication
The defect of a muscular layer of esophageal wall is covered with a gastric fundus or by means of interrupted suture or diaphragmatic flap.
Patients remain hospitalized for 24-48 hours and return to regular activities in about 2 weeks.
The operation relieves symptoms in 85-95% of patients, and the incidence of postoperative reflux is about 20%.
For patients in whom surgery fails, they may be treated with an endoscopic dilatation first. If this fails, a second operation (extending the previous myotomy onto the anterior gastric wall) can be attempted once the cause of failure has been identified with imaging studies. The last resort is to surgically remove the esophagus (ie, esophagectomy).
Treatment options vary for patients with different degrees of illness severity. A study by Reynoso et al suggests that among hospitalized patients with minor/moderate illness severity, laparoscopic myotomy for achalasia showed comparable or better outcomes than esophageal dilation. For major/extreme illness severity, dilation showed a comparable or better profile for hospitalized patients with achalasia.
Esophagectomy was the standard treatment in patients with achalasia and a markedly dilated or sigmoid-shaped esophagus, with Heller myotomy considered to be ineffective in such cases. However, in a study by Sweet and colleagues of 113 patients with achalasia, the investigators reported that (1) in most of the study’s patients, even those with achalasia and a dilated esophagus, a laparoscopic Heller myotomy relieved dysphagia; (2) additional treatment was needed in about 20% of patients; and (3) in the end, 90% of patients had attained good swallowing ability. Esophagectomy was not required in any of the patients to maintain clinically adequate swallowing.
Cowgill et al reported on outcomes in 47 patients more than 10 years after laparoscopic Heller myotomy for achalasia. They found that notable complications were infrequent following the procedure and that no perioperative deaths had occurred. One patient underwent a second myotomy 5 years after the first, because of symptom recurrence. There were 33 surviving patients at the time of the study; the authors reported that the other patients died from causes unrelated to myotomy. Using a Likert scale and a Wilcoxon matched-pairs test to assess patients’ symptoms before and after laparoscopic myotomy, Cowgill et al found significant postsurgery decreases in the frequency and severity scores for dysphagia, chest pain, vomiting, regurgitation, choking, and heartburn. They concluded that “the symptoms of achalasia are durably ameliorated by laparoscopic Heller myotomy during long-term follow-up evaluation.”
Compared with pneumatic dilatation, laparoscopic Heller myotomy is associated with better results in terms of dysphagia improvement and postoperative gastroesophageal reflux rates, with a significantly lower risk of re-intervention. While the results are similar at a short-term follow-up, long-term follow-up shows that most patients after surgery are asymptomatic, compared with only 50% of patients even after multiple pneumatic dilatations.
Several studies have shown better outcomes after laparoscopic Heller myotomy than pneumatic dilatation in patients younger than 40 years. In addition, previous endoscopic treatment, such as botulinum toxin injection or pneumatic dilatation, may compromise the clinical outcome of laparoscopic Heller myotomy. Higher intraoperative complications rates and poorer long-term outcomes after laparoscopic Heller myotomy have been reported in several series of patients previously treated with endoscopic treatments. These findings may be related to scar tissue at the level of the gastroesophageal junction, which makes surgical dissection of the anatomic planes much more difficult.
In 2011, Boeckxstaens et al[22] reported the results of a multicenter, randomized trial comparing pneumatic dilatation (95 patients) to laparoscopic Heller myotomy with Dor fundoplication (106 patients) for untreated esophageal achalasia. The perforation rate during pneumatic dilatation and laparoscopic Heller myotomy was 4% and 12%, respectively. Therapeutic success was defined as a drop in Eckardt score below 3. The study showed similar success rates after laparoscopic Heller myotomy (90%) and pneumatic dilatation (86%) over a 2-year follow-up period.
In conclusion, while pneumatic dilatation was considered the main treatment modality for patients with achalasia in the 1980s, with surgery having a secondary role in case of dilatation failure, in current practice pneumatic dilatation should be reserved for when surgical expertise is not available and for the treatment of recurrent dysphagia after myotomy.
One study only has compared in a retrospective fashion POEM and laparoscopic Heller myotomy.[28] Eighteen patients undergoing POEM were compared in a nonrandomized fashion to 55 patients treated by laparoscopic Heller myotomy. No differences were observed in terms of length of the myotomy, complication rate, and length of hospital stay. Veress needle decompression of the pneumoperitoneum was required intraoperatively in 7 (39%) patients undergoing POEM. Treatment success (Eckardt score ≤3) after POEM was achieved in 16 (89%) patients at median 6-month follow-up. Six weeks after POEM, routine follow-up manometry and timed-esophagram showed normalization of esophagogastric junction pressures and contrast column heights.
Only long-term follow-up and prospective trials comparing POEM with laparoscopic Heller myotomy and fundoplication will determine the role of this new technique in the treatment of esophageal achalasia.
Helerovsky’s method. The operation is indicated for the patients with ІІІ-ІV stage of the disease in case of considerable esophageal dilation, when performance of Heller’s operation is impossible owing to cicatrical changes. However the indication for this operation should be restricted, because of frequent development of expressed esophagitis in postoperative period. The same accesses, as in Heller’s operation are applied. Constricted part of esophagus to its dilation exposed and cardial part of stomach is mobilized. Dilated part of the esophagus is anastomosed with the fundus of stomach.
Esophageal sticture
The cicatrical esophageal stenosis can arise owing to chemical, thermal and radial burns, and as a result of esophagitis or peptic ulcers. The most frequent cause of cicatrical strictures is considered to be chemical burns of esophagus, which are usually the result of accidentally or purposely (suicide) drink of acids or alkalis.
Disease processes that can produce esophageal strictures can be grouped into 3 general categories: (1) intrinsic diseases that narrow the esophageal lumen through inflammation, fibrosis, or neoplasia; (2) extrinsic diseases that compromise the esophageal lumen by direct invasion or lymph node enlargement; and (3) diseases that disrupt esophageal peristalsis and/or lower esophageal sphincter (LES) function by their effects on esophageal smooth muscle and its innervation.
Many diseases can cause esophageal stricture formation. These include acid peptic, autoimmune, infectious, caustic, congenital, iatrogenic, medication-induced, radiation-induced, malignant, and idiopathic disease processes.
The etiology of esophageal stricture can usually be identified using radiologic and endoscopic modalities and can be confirmed by endoscopic visualization and tissue biopsy. Use of manometry can be diagnostic when dysmotility is suspected as the primary process. Computed tomography (CT) scanning and endoscopic ultrasonography are valuable aids in the staging of malignant stricture. Fortunately, most benign esophageal strictures are amenable to pharmacologic, endoscopic, and/or surgical interventions.
Because peptic strictures account for 70-80% of all cases of esophageal stricture, peptic stricture is the focus of this article. A detailed discussion of possible benign and malignant processes associated with esophageal stricture and its management is beyond the scope of this article.
Frequency
United States Gastroesophageal reflux affects approximately 40% of adults. Esophageal strictures are estimated to occur in 7-23% of untreated patients with reflux disease.
Gastroesophageal reflux disease accounts for approximately 70-80% of all cases of esophageal stricture. Postoperative strictures account for about 10%, and corrosive strictures account for less than 5%.
The overall frequency of initial and subsequent dilations for peptic stricture appears to have decreased gradually since the introduction of proton pump inhibitors (PPIs) in the market in 1989. This has been borne out by data at the author’s institution and in 2 large community hospitals in
Mortality/Morbidity
The mortality rate of peptic strictures is not increased unless a procedure-related perforation occurs or the stricture is malignant. However, the morbidity for peptic strictures is significant.
Most patients undergo a chronic relapsing course with an increased risk of food impaction and pulmonary aspiration.
Frequently, coexistent Barrett esophagus and its attendant complications occur.
The need for repeated dilatation potentially increases the risk of perforation.
Race
Peptic strictures are 10-fold more common in whites than blacks or Asians. However, this is controversial as a recent retrospective study reported comparable frequencies between blacks and non-Hispanic whites. The authors reported that distribution of reflux esophagitis and grade and frequency of reflux-related esophageal ulcer and hiatal hernia were also similar ion-Hispanic whites and blacks. However, heartburn was more frequent and nausea/vomiting less frequent ion-Hispanic whites compared with blacks with erosive esophagitis or its complications.[2]
Sex
Peptic strictures are 2- to 3-fold more common in men than in women.
Age
Patients with peptic stricture tend to be older, with a longer duration of reflux symptoms.
Pathology
Peptic esophageal strictures are sequelae of gastroesophageal reflux -induced esophagitis, and they usually originate from the squamocolumnar junction and average 1-
Two major factors involved in the development of a peptic esophageal stricture are as follows:
Dysfunctional lower esophageal sphincter: Mean LES pressures are lower in patients with peptic strictures compared with healthy controls or patients with milder degrees of reflux disease. A study by Ahtaridis et al showed that patients with peptic esophageal strictures had a mean LES pressure of
Disordered motility resulting in poor esophageal clearance: In the same study, Ahtaridis et al demonstrated that 64% of patients with strictures had motility disorders compared with 32% of patients without strictures.
Other possible associated factors include the following:
Presence of a hiatal hernia: Hiatal hernias are found in 10-15% of the general population, 42% of patients with reflux symptoms and no esophagitis, 63% of patients with esophagitis, and 85% of patients with peptic esophageal strictures. This suggests that hiatal hernias may play a significant role.
Acid and pepsin secretion: This does not appear to be a major factor. Patients with peptic esophageal strictures have been demonstrated to have the same acid and pepsin secretion rates as sex-matched and age-matched controls with esophagitis but no stricture formation. In fact, some authors believe that alkaline reflux may play an important role.
Gastric emptying: No good evidence suggests that delayed emptying plays a role in peptic esophageal strictures.
The morphological changes in esophageal burns pass four stages:
І – stage of acute esophagitis. Lasts from one to two months. It is characterized by edema and divestment of necrotic tissues. This stage is hazardous for erosive bleedings.
ІІ – stage of chronic esophagitis. The ulcers of different sizes with granulating tissue in their bottom, focal constrictions of esophageal lumen are formed.
ІІІ – stage of cicatrical stricture of esophagus. Begins from 2-4th month and lasts to 2 years.
ІV – stage of late complications. Develops in two years after the burn and is characterized by formed cicatrical stricture of esophagus.
Classification
According to the clinical course:
I. The period of acute manifestation has three degrees of severity:
1 – mild;
2 – moderate;
3 – severe.
ІІ. The latent period (false improvement).
ІІІ. The period of cicatrization.
According to the depth of lesion:
I degree – superficial burn with the damage of epithelial layer of esophagus;
ІІ degree – the burn with the damage of entire mucosa of esophagus;
ІІІ degree – the burn damage of all layers of esophagus;
ІV degree – the spread of postburecrosis on paraesophageal tissue and adjacent organs.
Symptomatology and clinical course
The clinical signs of esophageal burn directly depend on the period of lesion and degree of gravity.
Acute period
The mild degree of clinical course manifests by satisfactory general state of the patient. At swallowing the patient feels a moderate pain, sometimes salivation, hoarseness. Roentgenologically – the lumen of esophagus without changes, with free passage of barium, the mucous folds with regular contours, but in some places it is possible to observe its graduation. The esophageal peristalsis is maintained. As a rule, in 5-7 days the clinical manifestations of the burn disappear.
The moderate degree of gravity of acute period is characterized by acute substernal and pharyngeal pain at swallowing, repeated vomiting, feeling of fear and excitement. Tachycardia – 120-130 beats/min. The body temperature rises to
Severe degree is characterized by the clinic of shock. Pulse of weak filling and tension, expressed tachycardia, acute substernal pain. The excitement of the patient is accompanied by feeling of fear, further transmits into adynamia, frequently the patients are unconsciousness. The skin is pale, covered with cold sweat. One patient in four except esophageal burns, suffers from burn of the stomach. The clinical course of the disease is worsened by oliguria, which can transfer into anuria, and also occurrence of other complications. It determines the unfavorable forecast.
The barium swallow in the majority of patients is problematic. Nevertheless if the general state of the patient allows to carry out it, on the first day after a burn already have been observed expressed manifestations of esophagitis: the esophagus dilated, mucosal folds are failed to reveal. The deposits of destructive changed tissues in the lumen of esophagus resemble the picture of filling defects; the peristalsis is absent, complete atony.
Latent period
This period is connected with replacement of necrotic tissues by granulations. The general state of the patient is improved. The acute signs disappear. The patient swallows freely, without feeling of discomfort at passage of food.
Period of cicatrize
It frequently lasts from 1 to 12 months. It is connected with replacement of granulations by cicatrical tissue that results in progressing of esophageal stricture and disturbance of swallowing at first of solid, and further of liquid food. Such strictures develop at the orifice of esophagus, in projection of tracheal bifurcation and in the place of gastroesophageal juncture. The passage of food through the constricted regions of esophagus is possible at first only due to careful grinding and watering, but further it is inefficient. Thereafter food delay in esophagus, choking, salivation, belching and vomiting develop. If the stricture is located in the lower part of esophagus, the vomitis can be of putrefactive character. Progressing loss of weight observed, which without correction can transfer into cachexia. The level and degree of the stricture, its extension circumstantiated after X-ray examination.
Cicatrical stricture of the lower esophagus
Variants of clinical course and complications
The esophageal burns in 30 % of cases are accompanied by disturbances of valvular function of epiglottis. It in reinforced salivation causes the aspiration of fluid in trachea, infection of airways, development of bronchitis and pneumonia.
In 25 % of the patients the esophageal burn combined with gastric burn, mainly of its pyloric part. It can result in lot of complications, which sometimes prevail on the manifestations of esophageal burn. Especially dangerous among such complications of the early period is the gastric bleeding and perforation. The postburn stricture of pylorus belongs to the late complications.
Gastrointestinal bleedings usually occur in 3-10 days after the burn and are characteristic for the stage of formation of ulcers and granulations. Despite the rare arrosion of major vessels in such pathology, these bleedings are accompanied by considerable hemorrhage, because bleeds a considerable surface of the mucous membrane of esophagus or stomach.
Mediastinitis is mostly observed in deep burns of ІІІ-ІV degree. It can be the outcome of perforation of esophagus or of hematogenic or lymphogenic spread of infection to mediastinum. The clinical manifestations mainly caused by a septic state of the patient and severe intoxication. The fever, difficult respiration, chest pain and tachycardia to 130 and more beats/min are observed. Temperature rises to 39-40°С and has hectic character. Roentgenologically observed distention of the mediastinal shadow, sometimes detached mediastinal pleura. Pleurisy, pericarditis and lung abscesses can arise as the early complications of esophageal burns. To the late complications, except cicatrical stricture, it is necessary to regard tracheo-esophageal and broncho- esophageal fistula, and also malignancy of the cicatrical changed esophagus.
History
Patients with peptic strictures may present with heartburn, dysphagia, odynophagia, food impaction, weight loss, and chest pain.
Progressive dysphagia for solids is the most common presenting symptom. This may progress to include liquids.
Atypical presentations include chronic cough and asthma secondary to aspiration of food or acid.
The clinician cannot rely on the presence or absence of heartburn to definitely determine whether dysphagia is secondary to a peptic esophageal stricture.
· Of patients with peptic esophageal strictures, 25% have no previous history of heartburn.
· Heartburn may resolve with worsening of a peptic stricture.
· Approximately two thirds of patients with adenocarcinoma in Barrett esophagus have a history of long-standing heartburn.
· The abnormal esophageal motor activity in achalasia can produce a heartburn sensation.
Important points regarding dysphagia
· The obstruction is usually perceived at a point that is either above or at the level of the lesion.
· Dysphagia for solids and liquids simultaneously should alert the clinician to the possibility of a motility disorder such as achalasia or collagen vascular disorders.
· Dysphagia secondary to a Schatzki ring is usually intermittent and nonprogressive.
· Dysphagia for solids and liquids early in the course of disease should alert the clinician to the possibility of achalasia as an etiology of a peptic esophageal stricture.
· Benign esophageal strictures usually produce dysphagia with slow and insidious progression (ie, months to years) of frequency and severity with minimal weight loss.
· Malignant esophageal strictures result in a rapid progression (ie, weeks to months) of severity and frequency of dysphagia and are associated frequently with significant weight loss.
Determining whether the patient takes any medications known to cause pill esophagitis is important.
Determining whether a history of collagen vascular disease or immunosuppression exists may provide clues to the underlying etiology.
Physical
Physical examination frequently does not provide clues to the cause of dysphagia.
Assessing the patient’s nutritional status is important.
Patients with collagen vascular diseases may exhibit joint abnormalities, calcinosis, telangiectasias, sclerodactyly, or rashes.
The presence of atypical gastroesophageal reflux disease may be suggested by hoarse voice, posterior oropharyngeal erythema, diffuse dental erosions, wheezing, or epigastric tenderness.
Patients with adenocarcinoma of the gastroesophageal junction may have left supraclavicular lymphadenopathy (Virchow node).
Causes
Proximal or mid esophageal strictures
· Caustic ingestion (acid or alkali)
· Malignancy
· Radiation therapy[3, 4]
· Infectious esophagitis -Candida, herpes simplex virus (HSV), cytomegalovirus (CMV), human immunodeficiency virus (HIV)
· Acquired immunodeficiency syndrome (AIDS) and immunosuppression in patients who have received a transplant
· Medication-induced stricture (pill esophagitis) – Alendronate, ferrous sulfate, nonsteroidal anti-inflammatory drugs (NSAIDs), phenytoin, potassium chloride, quinidine, tetracycline, ascorbic acid.[5] Drug-induced esophagitis often occurs at the anatomic site of narrowing, with the middle one-third behind the left atrium predominating in 75.6%.[6]
· Diseases of the skin – Pemphigus vulgaris, benign mucous membrane (cicatricial) pemphigoid, epidermolysis bullosa dystrophica
· Graft versus host disease
· Idiopathic eosinophilic esophagitis
· Extrinsic compression
· Squamous cell carcinoma
· Sequela of endoscopic submucosal dissection for superficial squamous cell neoplasms.[7]
· Miscellaneous – Trauma to the esophagus from external forces, foreign body, surgical anastomosis/postoperative stricture, congenital esophageal stenosis
Distal esophageal strictures
· Peptic stricture – Gastroesophageal reflux disease, Zollinger-Ellison syndrome
· Adenocarcinoma
· Collagen vascular disease – Scleroderma, systemic lupus erythematosus (SLE), rheumatoid arthritis
· Extrinsic compression
· Alkaline reflux following gastric resection
· Sclerotherapy and prolonged nasogastric intubation
· Crohn disease
The diagnostic program
1. Anamnesis and physical findings.
2. X-ray examination of esophagus and stomach.
· Barium esophagram provides an objective baseline record of the esophagus before medical therapy or endoscopic intervention.
· This study also provides information about the location, length, and diameter of the stricture and the smoothness or irregularity of the esophageal wall (road map).
· The information obtained can complement endoscopic findings.
· Lesions, such as diverticula and paraesophageal hernias, that potentially may lead to increased risk of complications during endoscopy can be identified.
· This study may be more sensitive than endoscopy for detection of subtle narrowings of the esophagus such as those caused by rings and peptic strictures that are greater than
· This study has 100% sensitivity with luminal diameter less than
3. Chest X-radiography.
· Chest radiograph, posteroanterior (PA) and lateral: Chest radiography should be used as an adjunct if extrinsic compression is considered a possible etiology of esophageal stricture.
CT scanning
· CT scans can be used to stage malignancies that produce esophageal strictures.
· Accuracy in estimating the depth of tumor invasion is 60-69%.
· Accuracy in determining spread to other organs is 82%.
4. Endoscopic examination of esophagus, stomach and duodenum.
· This procedure can be used to establish or confirm the diagnosis of esophageal stricture, to seek evidence of esophagitis, to exclude malignancy, to obtain biopsy and brush cytology specimens, and to implement therapy.
· EGD is more sensitive than barium esophagram in the identification of subtle mucosal lesions.
· Subtle strictures may be missed when smaller and thinner endoscopes are employed, especially in the setting of minimal sedation.
5. General blood analysis.
6. Coagulogram.
7. Biochemical investigation of plasma.
· Complete blood cell (CBC) count: Usually, the results of a CBC are within the reference range; however, anemia may develop due to chronic bleeding from severe esophagitis or carcinoma.
· Liver profile: Usually, the findings are within the reference range; however, the liver profile may be abnormal if metastatic disease in underlying malignancy is present.
· Complete metabolic panel: This study may allow assessment of the patient’s nutritional status, especially in conjunction with weight loss.
8. Histologic Findings
· Initial histologic changes in the peptic stricture process include edema, cellular infiltration, basal cell hyperplasia, and vascular changes with a slight increase in type III collagen deposition on healing.
· If untreated, the process can lead to progressive inflammation and ulceration involving the submucosa and muscularis mucosa. This can lead to damage of the muscular layer and the intrinsic nervous system of the esophagus, resulting in deposition of type I collagen with subsequent formation of scar tissue and stricture formation.
Differential diagnostics
It is necessary in advanced stages of esophageal and gastric strictures.
As there is the similar symptomatology, such cicatrical changes of the pyloroantral part of stomach can suggest pylorostenosis caused by peptic ulcer. The differential diagnosis is based on careful analysis of the history and endoscopic investigation of esophagus and stomach.
Esophageal cancer. As this pathology can have the similar roentgenological picture, it requires thorough differential diagnostics. Besides anamnesis and clinical manifestations, the question of the diagnosis finally confirmed by histological investigation of a biopsy material, obtained during endoscopy.
Tactics and choice of treatment
The treatment of esophageal burns first of all should be guided to save the life of the patient, and also to prevent the development of esophageal strictures. The first aid must be given as soon as possible after taking of the chemical substance, which have caused the burn. In such cases by means of gastric tube and great amount of water (to 10-
The further aid – the treatment of shock and hypovolemia by massive intravenous infusions (up to 4-
Antibacterial therapy is nominated for prevention of infection complications.
In first two days after the burn the patients get parenteral feeding. Nevertheless, if the swallowing is not disturbed, it is possible to add feeding by grinding cold food. The early application of enteric feeding can be as a weak bougienage of esophagus and simultaneous prophylaxis of cicatrical strictures. The development of complications requires the treatment of their liquidation.
In the third period of the course of disease it is important not to miss a possible formation of cicatrical stenosis of esophagus. In overwhelming majority at timely and correct performance of esophageal dilatation it is possible to achieve positive effect and avoid multistep and hazardous operations. The dilatation is carried out by special elastic thermolabile bougies. The first procedures of bougienage are necessary to carry out under the roentgenological check. It enables to prevent perforation of esophagus. The latter, as the complication of esophageal bougienage, can occur not only in places of cicatrical stricture, but also in the region of piriform sinus. Thereby the bougie penetrates in mediastinum and can result in mediastinitis. With the purpose of prevention of such complication the esophageal bougienage is better to carry out with conductor. It can be represented by a cord (thick thread), passed through the mouth and gastrostoma. The bougie should have the canal for conductor, nevertheless it is possible to apply the usual one with the loop, on its end.
Diet
The usual antireflux precautions and lifestyle modifications should be reinforced, although no published data exist showing that these measures are efficacious in peptic strictures.
· Patients are told to avoid fatty and spicy foods, alcohol, tobacco, chocolate, and peppermint.
· Patients should eat smaller meals, avoid eating in a hurried fashion, and chew their food well.
· Patients should be encouraged not to eat at least 2-3 hours before bedtime.
· Weight reduction should be encouraged.
· Ill-fitting dentures or poor dentition should be corrected if possible.
Traditionally, more emphasis has been placed on mechanical dilatation, and coexistent esophagitis has been relatively ignored. However, several studies have demonstrated that aggressive acid suppression using PPIs is extremely beneficial in the initial treatment of esophageal stricture, as well as long-term management.
· A dysphagia score developed by Dakkak et al in a study of 64 patients revealed that the stricture diameter only contributed to 30% of the dysphagia score and that esophagitis and other factors accounted for 70% of the score. A linear association existed between the dysphagia score only when the luminal diameter was less than
· Smith et al showed in a randomized study of 366 patients that omeprazole 20 mg/d was superior to ranitidine 300 mg twice a day in preventing stricture recurrence with redilation rates of 30% and 46%, respectively, at 12 months (P < 0.01)
· Marks et al showed that the redilation rate in patients treated with omeprazole 20-40 mg/d was 41% versus 73% in patients treated with ranitidine 150-300 mg twice per day and almost reached significance (P < 0.07).[10] However, the omeprazole group showed higher rates of dysphagia relief and healing of esophagitis when compared with histamine 2 (H2) blockers.
· In contrast, 2 other studies by Swarbrick et al and Silvis et al did not show any significant differences in the redilation rates at 12 and 10 months, respectively.
· PPI treatment of patients with esophageal stricture is also more cost effective than H2 blocker therapy. Marks et al found that over a 6-month period, the cost of omeprazole therapy was $1744 compared with $2957 with H2 blockers.
· H2 blockers have not been shown to be any better than placebo in various trials, and no reliable data on prokinetic agents exist.
Surgical Care
In advanced cases if failed to reach the restore of esophageal patency by a bougienage, the esophagoplasty by stomach, small and large intestine is applied.
The following discussion concerns the endoscopic and surgical modalities employed for the management of peptic esophageal stricture. The choice of dilator and technique is dependent on many factors, the most important being stricture characteristics. It is also based on other factors, including patient tolerance, operator preference, and experience. No clear consensus on the optimal end point exists. In summary, dilation therapy should be tailored individually.
Endoscopic dilation dates to the 16th century, when physicians used wax wands for esophageal dilation.[13, 14] The word bougie is derived from Boujiyah, an Algerian city that was the center of the medieval candle trade. The following 3 types of dilators are used:
· Mercury-filled bougies – Maloney or
o These dilators are indicated in uncomplicated strictures with diameters greater than 10-
o They are inexpensive and simple to perform without fluoroscopic guidance.
o Minimal or no sedation is necessary.
o Self-bougienage may be performed at home.
· Wire-guided polyvinyl bougies – Savary-Gilliard and American dilators
o These dilators are relatively stiff and better suited to longer, tighter, and irregular strictures.
o The need for fluoroscopy is variable.
o The range is 5-
o Drawbacks include trauma to the laryngeal wall and patient discomfort.
o American dilators are shorter, less tapered, and impregnated with barium for better fluoroscopic visualization.
· Through-the-scope (TTS) balloon dilators
o These dilators are used through the endoscope, and they allow for direct visualization.
o These are relatively expensive and not reusable.
o Fluoroscopy is not mandatory, but it is useful in difficult cases.
o Studies conflict about the benefits of balloon dilators compared with Savary dilators.
A prospective, randomized study with 17 patients in each arm comparing balloon dilators with Savary dilators was performed by Saeed et al over a 2-year period, with the end point being
· Stricture recurrence was similar in the first year but lower in the second year for balloons.
· Fewer sessions were needed for balloons, 1.1 sessions +/- 0.1 versus 1.7 sessions +/- 0.2, and less procedural discomfort occurred (P < 0.05).
· Both devices were effective in relieving dysphagia.
Another prospective, randomized study by Scolapio et al included 251 patients with peptic strictures. Schatzki rings did not show any differences in complications, the degree of immediate relief, or the time to recurrent dysphagia.
· General rules of esophageal dilation
o Many authors have questioned the need for mandatory fluoroscopy, and no published data exist to advocate safety of fluoroscopy. However, one may consider using fluoroscopy in complicated strictures, especially in guiding the blind passage of a guidewire.
o Rule of 3s: The first bougie passed should be approximately equal to the estimated diameter of the stricture. Pass no more than 3 consecutive bougies of progressively increasing size after the first one that meets moderate resistance during any one dilation session. The rule of 3s has been questioned because of a lack of data verifying the increased efficacy or safety if one adheres to this rule. This rule was formulated for dilation using mercury-filled bougies resulting in dilatioo greater than
o A study by Kozarek et al showed only one perforation in 400 patients dilated with polyvinyl dilators to greater than
o Balloon dilators frequently dilate greater than that prescribed by the rule of 3s without any increased risk of complications.
· No consensus exists regarding the end point of esophageal dilation for peptic strictures.
o Most patients experience complete relief when dilated to 40-
o In summary, the extent of the dilatation should be individualized based on symptomatic response and technical difficulty encountered during therapy.
· Intralesional steroid injection
o Limited anecdotal data exist showing that intralesional steroid injection of peptic strictures may be beneficial. The mechanism is unclear; it may inhibit collagen formation and enhance collagen degradation, thus increasing stricture compliance.
o Triamcinolone 10 mg/mL in 0.5 mL aliquots was injected in 4 quadrants in 2 patients with a successful outcome as reported by Kirsch et al.
o Lee at al showed a higher rate of achieving greater luminal diameters and duration between dilations in a nonrandomized cohort of patients with strictures of varying etiologies.[20] Similar results were obtained by Kochhar et al in 71 patients, although 8 injections of 20 mg of triamcinolone in 0.5-mL aliquots were given at the proximal margin and into the stricture itself.
o A randomized prospective trial of Savary dilation with or without intralesional steroids was conducted in 42 patients by Dunne et al ; it demonstrated a decreased need for second dilations in the steroid group (1.95 vs 5.5) at 1 year. Similar results were seen in a study by Ramage et al in 30 patients, but the latter study was also double blinded with a sham group. Two patients (13%) in the steroid group and 9 patients (60%) in the sham group needed repeat dilation over a 12-month period.
o Therefore, a trial of steroid injection may be reasonable in patients with benign strictures who experience no significant relief of dysphagia despite repeated dilations and aggressive antireflux therapy. Hishiki et al reported the use of repeated endoscopic dilatation with systemic steroids in a child with severe esophageal anastomotic stricture that did not respond to endoscopic dilatation and local steroid injection of the stricture. At 18 months follow-up,the child remained asymptomatic without any further endoscopic dilations.
· Endoscopic stricturoplasty: Two case series described a technique using a needle knife to make 4 quadrant incisions followed by Savary dilation. This was successful in 8 of 8 patients as reported by Raijman et al[25] and 5 of 6 patients as reported by Hagiwara et al.
· Pharyngoesophageal puncture is a term recently coined by Tang et al to describe the technique of endoscopic dilation of radiation-induced severe or complete pharyngoesophageal strictures. A combination of guide wires, endoscopic balloons, puncture and techniques learned from ERCP were successfully applied to 3 patients with severe/complete stenosis.
· Expandable polyester silicone-covered stent: Repici et al presented a case series of 15 patients whose condition had failed endoscopic therapy. A temporary placement of a stent for 6 weeks was successful in 12 patients over a long-term period (mean follow-up, 22.7 mo). However, the exact duration for stent placement remains unclear, as strictures can recur following stent removal. Furthermore, a variety of complications have been described following stent deployment. More recently, biodegradable stents have shown some promise in animal studies and were used to treat severe corrosive esophageal stenosis in a child.[32]
· The role of surgical treatment in peptic stricture remains in dispute. Indications include failed aggressive medical therapy or an unsuitable candidate for aggressive medical therapy. This is usually a rare occurrence in the era of PPI therapy. Various procedures advocated include the following:
o Esophageal-sparing procedures – Standard antireflux surgery (Nissen total or Belsey partial fundoplication), esophageal lengthening with antireflux surgery (Collis-Nissen or Belsey gastroplasty)
o Esophageal resection and reconstruction – Gastric or colon interposition or jejunal segment
· If the benign peptic stricture is dilatable, an esophageal-sparing operation is performed.
o If the length of the esophagus is normal, standard antireflux surgery and postoperative dilation as necessary is recommended.
o If the esophagus is short, performing Collis gastroplasty and postoperative dilation as necessary is recommended.
o If the stricture is undilatable, esophageal resection and interposition is recommended.
· In the literature, some anecdotal reports exist of minimally invasive surgery, including laparoscopic transhiatal esophagectomy and laparoscopic Collis gastroplasty with Nissen fundoplication. With continuing advances in technology, whether or not minimally invasive surgery would play a major role in the surgical management of peptic stricture remains to be determined.
Esophageal plastic
By stomach
By large intestine
By small intestine
Esophageal cancer
Esophageal cancer is cancer that occurs in the esophagus — a long, hollow tube that runs from your throat to your stomach. Your esophagus carries food you swallow to your stomach to be digested.
Esophageal cancer usually begins in the cells that line the inside of the esophagus. Esophageal cancer can occur anywhere along the esophagus, but in people in the
Esophageal cancer isn’t common in the
Etiology
It’s not clear what causes esophageal cancer. Esophageal cancer occurs when cells in your esophagus develop errors (mutations) in their DNA. The errors make cells grow and divide out of control. The accumulating abnormal cells form a tumor in the esophagus that can grow to invade nearby structures and spread to other parts of the body.
Types of esophageal cancer
Esophageal cancer is classified according to the type of cells that are involved. The type of esophageal cancer you have helps determine your treatment options. Types of esophageal cancer include:
· Adenocarcinoma. Adenocarcinoma begins in the cells of mucus-secreting glands in the esophagus. Adenocarcinoma occurs most often in the lower portion of the esophagus. Adenocarcinoma is the most common form of esophageal cancer in the
· Squamous cell carcinoma. The squamous cells are flat, thin cells that line the surface of the esophagus. Squamous cell carcinoma occurs most often in the middle of the esophagus. Squamous cell carcinoma is the most prevalent esophageal cancer worldwide.
· Other rare types. Rare forms of esophageal cancer include choriocarcinoma, lymphoma, melanoma, sarcoma and small cell
Risk factors
It’s thought that chronic irritation of your esophagus may contribute to the DNA changes that cause esophageal cancer. Factors that cause irritation in the cells of your esophagus and increase your risk of esophageal cancer include:
· Drinking alcohol
· Having bile reflux
· Chewing tobacco
· Having difficulty swallowing because of an esophageal sphincter that won’t relax (achalasia)
· Drinking very hot liquids
· Eating few fruits and vegetables
· Eating foods preserved in lye, such as lutefisk, a Nordic recipe made from whitefish, and some olive recipes
· Having gastroesophageal reflux disease (GERD)
· Being obese
· Having precancerous changes in the cells of the esophagus (Barrett’s esophagus)
· Undergoing radiation treatment to the chest or upper abdomen
· Smoking
Other risk factors include
· Being male
· Being between the ages of 45 and 70
Signs and symptoms
· Difficulty swallowing (dysphagia)
· Weight loss without trying
· Chest pain, pressure or burning
· Fatigue
· Frequent choking while eating
· Indigestion or heartburn
· Coughing or hoarseness
Early esophageal cancer typically causes no signs or symptoms.
If you’ve been diagnosed with Barrett’s esophagus, a precancerous condition that increases your risk of esophageal cancer caused by chronic acid reflux, ask your doctor what signs and symptoms to watch for that may signal that your condition is worsening.
Screening for esophageal cancer isn’t done routinely because of a lack of an easily identifiable high-risk group and the possible risks associated with endoscopy. If you have Barrett’s esophagus, discuss the pros and cons of screening with your doctor.
Diagnostic
Using a scope to examine your esophagus (endoscopy). During endoscopy, your doctor passes a hollow tube equipped with a lens (endoscope) down your throat and into your esophagus. Using the endoscope, your doctor examines your esophagus looking for cancer or areas of irritation.
X-rays of your esophagus. Sometimes called a barium swallow, an upper gastrointestinal series or an esophagram, this series of X-rays is used to examine your esophagus. During the test, you drink a thick liquid (barium) that temporarily coats the lining of your esophagus, so the lining shows up clearly on the X-rays.
Collecting a sample of tissue for testing (biopsy). A special scope passed down your throat into your esophagus (endoscope) or down your windpipe and into your lungs (bronchoscope) can be used to collect a sample of suspicious tissue (biopsy). What type of biopsy procedure you undergo depends on your situation. The tissue sample is sent to a laboratory to look for cancer cells.
Esophageal cancer staging
When you’re diagnosed with esophageal cancer, your doctor works to determine the extent (stage) of the cancer. Your cancer’s stage helps determine your treatment options. Tests used in staging esophageal cancer include computerized tomography (CT) and positron emission tomography (PET).
The stages of esophageal cancer are:
Stage I. This cancer occurs only in the top layer of cells lining your esophagus.
Stage II. The cancer has invaded deeper layers of your esophagus lining and may have spread to nearby lymph nodes.
Stage III. The cancer has spread to the deepest layers of the wall of your esophagus and to nearby tissues or lymph nodes.
Stage IV. The cancer has spread to other parts of your body.
Surgery
Surgery to remove the cancer can be used alone or in combination with other treatments. Operations used to treat esophageal cancer include:
Surgery to remove very small tumors. If your cancer is very small, confined to the superficial layers of your esophagus and hasn’t spread, your surgeon may recommend removing the cancer and margin of healthy tissue that surrounds it. Surgery for very early-stage cancers can be done using an endoscope passed down your throat and into your esophagus.
Surgery to remove a portion of the esophagus (esophagectomy). Your surgeon removes the portion of your esophagus that contains the tumor and nearby lymph nodes. The remaining esophagus is reconnected to your stomach. Usually this is done by pulling the stomach up to meet the remaining esophagus. In some situations, a portion of the colon is used to replace the missing section of esophagus.
Surgery to remove part of your esophagus and the upper portion of your stomach (esophagogastrectomy). Your surgeon removes part of your esophagus, nearby lymph nodes and the upper part of your stomach. The remainder of your stomach is then pulled up and reattached to your esophagus. If necessary, part of your colon is used to help join the two.
Esophageal cancer surgery carries a risk of serious complications, such as infection, bleeding and leakage from the area where the remaining esophagus is reattached. Surgery to remove your esophagus can be performed as an open procedure using large incisions or with special surgical tools inserted through several small incisions in your skin (laparoscopically). How your surgery is performed depends on your situation and your surgeon’s experience and preferences.
Surgery for supportive care
Besides treating the disease, surgery can help relieve symptoms or allow you to eat.
Relieving esophageal obstruction. A number of treatments are available to relieve esophageal obstruction. One option includes using an endoscope and special tools to widen the esophagus and place a metal tube (stent) to hold the esophagus open. Other options include surgery, radiation therapy, chemotherapy, laser therapy and photodynamic therapy.
Providing nutrition. A surgeon inserts a feeding tube (percutaneous gastronomy) so you can receive nutrition directly into your stomach or intestine. This is usually temporary until the surgical site heals or until you’re finished with chemotherapy and radiation therapy.
Chemotherapy
Chemotherapy is drug treatment that uses chemicals to kill cancer cells. Chemotherapy drugs are typically used before (neoadjuvant) or after (adjuvant) surgery in people with esophageal cancer. Chemotherapy can also be combined with radiation therapy. In people with advanced cancer that has spread beyond the esophagus, chemotherapy may be used alone to help relieve signs and symptoms caused by the cancer.
The chemotherapy side effects you experience depend on which chemotherapy drugs you receive.
Radiation therapy
Radiation therapy uses high-powered energy beams to kill cancer cells. Radiation can come from a machine outside your body that aims the beams at your cancer (external beam radiation). Or radiation can be placed inside your body near the cancer (brachytherapy).
Radiation therapy is most often combined with chemotherapy in people with esophageal cancer. It can be used before or after surgery. Radiation therapy is also used to relieve complications of advanced esophageal cancer, such as when a tumor grows large enough to stop food from passing to your stomach.
Side effects of radiation to the esophagus include sunburn-like skin reactions, painful or difficult swallowing, and accidental damage to nearby organs, such as the lungs and heart.
Combined chemotherapy and radiation
Combining chemotherapy and radiation therapy may enhance the effectiveness of each treatment. Combined chemotherapy and radiation may be the only treatment you receive, or combined therapy can be used before surgery. But combining chemotherapy and radiation treatments increases the likelihood and severity of side effects.
