One of the esophageal cancers is squamous cell carcinoma that develops often also with the help of tobacco and alcohol in the normal squamous cell lining of the esophagus. This cancer may be treated by radiotherapy or surgery. The incidence of this cancer is increasing in North America especially in white males, and adenocarcinomas do not respond well to radiation treatment.
Esophagitis is commonly treated with medications to control acid production or secretion primarily proton pump inhibitors. Proton pump inhibitors PPIs are recognized as the most powerful and effective drugs used to inhibit acid secretion and allow healing of tissue damage in the esophagus. Early detection or prevention of cancer is discussed below.
Guidelines from the American College of Gastroenterology recommend periodic check-ups surveillance or action as follows:. Continued research is needed. Early detection and prevention of cancer are difficult.
Studies have suggested that risk of esophageal cancer is amplified by factors that either increase reflux e. Measures that may be protective include lifestyle modifications emphasizing controlling reflux, tobacco cessation, improvements in diet e. Surgical removal of the abnormal tissue would remove the cancer risk.
Cancer detection programs employ periodic endoscopic examination of the esophagus and the procurement of tiny tissue samples biopsies for the pathologist to examine. In newly detected cases the abnormal segment is systematically biopsied in four quadrants at 2-cm intervals within the metaplastic esophagus. Severe dysplasia seen at multiple sites in a young person may prompt the physician to suggest surgical removal of the lower esophagus esophagectomy.
For those individuals for whom surgery is considered too risky, close observation at three-month intervals may be a safer alternative.
If low-grade dysplasia persists after adequate treatment of the esophagitis, the patient should be followed yearly with endoscopy and biopsy. Otherwise, all affected persons should be endoscoped and have the affected area biopsied at 18 to 24 month intervals.
Not all the experts subscribe to such an aggressive and expensive program, nor has it yet been shown to save lives or improve quality of life.
Some risk factors can be avoided e. Avoiding risk factors and increasing protective factors that can be controlled may decrease chances of developing a disease. Unless there is severe esophagitis, this change can be recognized during an endoscopy. If these changes persist and are severe high-grade dysplasia , aggressive treatment is necessary to prevent development of adenocarcinoma.
When esophageal atresia is suspected, a nasogastric tube insertion should be attempted. If atresia is present, an inserted nasogastric tube will typically stop at 10 to 12 cm. The atretic upper esophagus ends in a blind pouch, and the trachea communicates with the distal esophagus.
Air enters the GI tract via the tracheoesophageal fistula and the newborn presents clinically with a gas-filled abdomen and frequent aspiration pneumonias due to gastric reflux into the respiratory tract through the fistula. Confirmation of the type of esophageal atresia is obtained by esophagography with or without bronchoscopy. Treatment of esophageal atresia and tracheoesophageal fistula is surgical, and the procedure depends on the type of esophageal atresia and the distance between the two esophageal segments.
Thus, if the distance between the esophageal segments is short, end-to-end anastomosis is the preferred surgical procedure. If the distance between segments is long, lengthening of the upper esophageal segments in some cases can be achieved using bougienage or intraoperative myotomy.
The results of surgical correction are generally excellent when the esophageal malformation is an isolated anomaly. Overall outcome is determined by the associated genetic malformation, age of infant, and birth weight. Long-term outcome after esophageal atresia repair indicates that the most significant problems are GI and respiratory symptoms. Gastroesophageal reflux disease symptoms may be alleviated by pharmacologic treatment or with time, owing to the patient's accommodation with the medical condition, but there is a higher risk of developing chronic esophagitis and Barrett's metaplasia compared to the normal population.
The aesthetic aspects of the surgical treatment are now becoming more important in adults with esophageal atresia owing to good functional results of applied treatments. Congenital esophageal stenosis represents narrowing of the esophageal lumen. It can be located at any level of the esophagus, but is more frequent in the distal third. It appears either as a web membranous diaphragm or a long segment of esophagus with a threadlike lumen fibromuscular stenosis. Usually, the esophageal stenosis results from incomplete esophageal recanalization during the eighth week of human embryologic development, but it also may result from failure of esophageal blood vessels to develop in the affected area.
The incidence of esophageal stenosis is low, occurring in 1 in every 25, live births. Patients may present with aspiration and recurrent pneumonia in early infancy.
Dysphagia and regurgitation of solid food are symptoms that appear later in childhood, when more solid foods are added to the child's diet. If the esophageal stenosis is not severe, its diagnosis may be postponed until adulthood, when a history of long-standing solid foods dysphagia could be documented.
Once suspicion of congenital esophageal stenosis is raised, an upper endoscopy with biopsy and pH monitoring of the esophagus help with diagnosis and eliminate the possibility of a stricture secondary to gastroesophageal reflux. Barium swallow typically demonstrates narrowing of the esophagus lumen. The first approach to treatment is with dilation, which may include bougienage or pneumatic dilation under fluoroscopic guidance.
Dilation may be diagnostic and therapeutic. Although pneumatic dilation expands and stretches a fibromuscular stenosis, a persistent "waist" in the balloon may indicate a cartilaginous ring and the necessity for surgical resection. The efficacy of dilatation seems to be limited and may even result in severe complications such as chest pain, mucosal tears, or esophageal rupture. When pneumatic dilation fails, surgical treatment may be required for removal of the abnormal segment.
Laser lyses of webs or stenosis stenting have been described and may be attempted in selected cases. When respiratory tissue is present on esophageal stenosis biopsy, surgical removal of the involved segment is necessary owing to high risk of malignant transformation. Foregut duplications include esophageal cysts tubular duplications and bronchogenic cysts. They originate from failure of the primitive foregut to become completely vacuolated during the embryonic life. These cyst- or tube-like structures develop independently and rarely are in continuity with the esophagus.
They can be associated with other congenital malformations, such as tracheoesophageal fistulas, spinal abnormalities, esophageal atresia distal to duplication, and other segmental GI duplications small bowel is more frequent. Duplications of the GI tract have three common characteristics:. The congenital duplication cysts represent 0. They are lined by squamous columnar, cuboid, or ciliated epithelium, surrounded by two layers of smooth muscle.
Usually they are accidentally discovered on chest computed tomography CT scans and are asymptomatic. Cysts may become symptomatic owing to complications such as respiratory system compression causing stridor, cough, or tachypnea , digestive system compression causing chest pain or dysphagia , cardiac compression causing cardiac arrhythmias , infarction, rupture, or, rarely, neoplastic dysplasia. Congenital esophageal duplications may be separated from the esophagus or may share a common wall.
Duplications may also contain gastric mucosa. Duplications of the esophagus can be associated with vertebral anomalies and intraspinal cysts and often are associated with intraabdominal intestinal duplications. A chest x-ray may demonstrate a soft tissue mass with a mediastinal shift. Barium swallow can detect tubular esophageal duplication, but miss the esophageal cyst that does not communicate with the esophageal lumen.
A CT scan delineates anatomy of the mass prior to surgical resection, and a nuclear technetium scan may help identify ectopic gastric mucosa. Definitive treatment involves complete surgical resection of the duplication, even for asymptomatic cysts. The congenital esophageal ring is a concentric extension of the normal esophageal tissue, usually consisting of different anatomic layers including mucosa, submucosa, and sometimes muscles.
The location is variable, but most are found in the distal esophagus. There are three types of esophageal rings: types A, B. Esophageal rings may originate from incomplete vacuolization of the esophageal columnar epithelium during early embryonic life; however, they are also associated with immunologic 63 or inflammatory conditions such as scleroderma, chronic graft-versus-host disease , 64, 65 and gastroesophageal reflux.
The type A esophageal ring is a muscular ring located roughly 2 cm proximal to the squamocolumnar junction and it represents a proliferation of the proximal border of the LES. It consisting of three layers: mucosa, submucosa, and muscularis propria. It is the least frequent type and usually asymptomatic. The type B or Schatzki's ring is a mucosal ring located at the squamocolumnar junction.
Because it is difficult to exactly localize the squamocolumnar junction and the LES , the exact anatomic relationship between the Schatzki's ring and squamocolumnar junction remains controversial. Typically it is associated with the proximal margin of a hiatal hernia.
It consists of two layers, mucosa and submucosa, having squamous epithelium on its upper surface and columnar epithelium on its lower surface. No differences in the prevalence of rings based on gender has been noticed, but they appear to be more common in subjects over 40 years old. Esophageal rings usually exist as a single lesion but can be multiple. Owing to its mucosal nature, Schatzki's ring has been proposed to be caused by GERD , but no clinical association had been found.
The type C esophageal ring is an indentation caused by the diaphragmatic crura, sometimes seen on radiographic studies. It is never symptomatic.
Routine upper GI series, including barium radiography and upper esophagogastric endoscopy are diagnostic for this type of ring. The prognosis is good, and patients with symptoms are advised to change their dietary habits and to cut and chew all food carefully. If no improvement in the symptoms is noticed, serial progressive dilations are recommended. The congenital esophageal web is defined as a thin, usually eccentric, transverse membrane.
It consists of two layers, mucosa and submucosa, and is formed from connective tissue covered by normal squamous epithelium. Its location is variable, but most frequently is found in the cervical esophagus, where it is frequently associated with heterotopic gastric mucosa.
Most cases are asymptomatic. Intermittent dysphagia for solid food is the usually complaint. Esophageal web occurs more frequently in females. As for congenital esophageal rings, it is thought that webs result from incomplete vacuolization of the esophageal columnar epithelium during early embryonic life.
They were also associated with iron-deficiency conditions, blistering skin diseases such as epidermolysis bullosa , 69 heterotopic gastric mucosa in the upper esophagus, 70 and gastroesophageal reflux. Radiographic techniques are the most sensitive diagnostic methods and esophageal webs may be confused with esophageal stenosis. Treatment consists of bougienage, and rarely transendoscopic incision or surgical resection is necessary.
This page has been archived and is no longer updated Jump to main content Jump to navigation nature. Search Advanced search. Top of page Key Points The adult human esophagus is an to cm long muscular tube that has cervical, thoracic, and abdominal parts.
The esophagus wall is composed of striated muscle in the upper part, smooth muscle in the lower part, and a mixture of the two in the middle.
The myenteric plexus is well developed in the smooth muscle, but is also present in the striated muscle part of the esophagus. The function of the myenteric plexus in the striated esophagus is not well understood.
Esophagus develops from foregut and by week 10 is lined by ciliated epithelial cells. Beginning at 4 months, the ciliated epithelium starts to be replaced by squamous epithelium. At either end of the esophagus the ciliated epithelium gives rise to esophageal glands.
The upper esophagus is derived from branchial arches 4, 5, and 6, but the derivation of the lower esophagus is not known. The development of various elements of esophageal wall requires coordination of a variety of genes and mediators. Esophageal peristalsis appears in the first trimester, and gastroesophageal reflux can be documented in the second trimester. Top of page Introduction From mouth to stomach, the food conduit consists of the oral cavity, pharynx, and esophagus.
Top of page Embryology The first stages of life are divided into the embryonic and fetal periods. Figure 1: Primordial gut. Top of page Adult Anatomy Gross Anatomy The esophagus is a flattened muscular tube of 18 to 26 cm from the upper sphincter to the lower sphincter. Blood Supply The rich arterial supply of the esophagus is segmental Figure 2.
Figure 2: Arterial blood supply of the esophagus. Figure 3: Venous drainage of the esophagus. Innervation The esophagus, like the rest of the viscera, receives dual sensory innervation, traditionally referred to as parasympathetic and sympathetic, but more properly based on the actual nerves, vagal, and spinal 21 Figure 4. Figure 4: Parasympathetic and sympathetic innervation of the esophagus.
Lymphatics Lymphatic drainage in the esophagus consists of two systems: the lymph channels and lymph nodules. Figure 5: Lymphatic drainage. Top of page Musculature of the Esophagus The muscular coat consists of an external layer of longitudinal fibers and an internal layer of circular fibers Figure 6. Figure 6: Musculature of the esophagus. Top of page Upper Esophageal Sphincter The upper esophageal sphincter UES is a high-pressure zone situated between the pharynx and the cervical esophagus Figure 7.
Figure 7: Upper esophageal sphincter and upper esophageal musculature. Top of page Lower Esophageal Sphincter The lower esophageal sphincter is a high-pressure zone located where the esophagus merges with the stomach Figure 8.
Figure 9: Diaphragmatic crura and esophageal opening viewed from below a and as viewed from above b. Top of page Histology Light Microscopy The wall of the esophagus consists of four layers: mucosa, submucosa, muscularis propria, and adventitia. It consists of three sublayers: Mucous membrane: a nonkeratinized squamous epithelium. It covers the entire inner surface of the esophagus, except the LES , where both squamous and columnar epithelium may coexist.
The mucous membrane is composed of stratum basale, including basophilic cells that can divide and replenish the superficial layers stratum intermedium stratum superficialis. Lamina propria: a thin layer of connective tissue Muscularis mucosa: a thin layer of longitudinally, irregularly arranged smooth muscle fibers. The muscularis mucosa extends through the entire esophagus and continues into the rest of the GI tract, being much thinner in the proximal part of the esophagus than in its distal part.
Caudally, approaching the cardiac orifice, the muscularis mucosa forms a thick layer. The muscularis mucosa separates the lamina propria from the submucosa and retracts when it is sectioned during surgical procedures.
Submucosa The submucosa contains connective tissue as well as lymphocytes, plasma cells, nerve cells Meissner's plexus , vascular network Heller plexus , and mucous glands. Muscularis Propria The muscularis propria is responsible for motor function. Adventitia The adventitia is an external fibrous layer that covers the esophagus, connecting it with neighboring structures.
Top of page Developmental Anomalies Tracheoesophageal Fistula and Atresia Tracheoesophageal fistula and esophageal atresia are the most frequent congenital esophageal abnormalities. Figure Main types of tracheoesophageal fistulae.
Congenital Esophageal Stenosis Congenital esophageal stenosis represents narrowing of the esophageal lumen. Congenital Esophageal Duplication and Duplication Cyst Foregut duplications include esophageal cysts tubular duplications and bronchogenic cysts.
They are lined by alimentary epithelium. They have smooth muscle in theirs walls. Congenital Esophageal Rings The congenital esophageal ring is a concentric extension of the normal esophageal tissue, usually consisting of different anatomic layers including mucosa, submucosa, and sometimes muscles. Congenital Esophageal Webs The congenital esophageal web is defined as a thin, usually eccentric, transverse membrane. Top of page Ancillary details. Top of page References Larsen W.
It contains oesophageal glands, that secrete mucus to help ease the passage of swallowed food. The muscularis externa layer in the top third of the oesophagus contains skeletal muscle, in the middle, it is a mixture of smooth and skeletal muscle, and in the bottom third it is entirely smooth.
This photograph shows an example of the muscle layers from the upper oesophagus. Oesophagus Function of the Oesophagus The oesophagus is a muscular tube through which food is carried from the pharynx to the stomach. Layers of the Oesophagus. Oesophageal Epithelium. Oesophogeal Mucosa. In slide , locate the cardio-esophageal junction W pg , Note the abrupt transition from the mucosa of the esophagus with its stratified squamous epithelium to the glandular mucosa of the stomach.
The cardiac gastric glands View Image are present only in a very small segment of the stomach mucosa adjacent to this junction. Since the cardiac gastric glands are primarily mucous, they can also be be demonstrated with the PAS stain, as shown in slide In this slide, the cells lining the gastric pits View Image stain very intensely with PAS due to the carbohydrate-rich, viscous mucus they secrete. The secretion of the cardiac glands is a bit more watery so they do not stain quite as intensely.
Gastric glands W pg , At low magnification, notice that the gastric pits are relatively more shallow here View Image and the tubular gastric or fundic glands are relatively much longer than those in the cardia or pylorus. Observe that the tall columnar cells lining the luminal surface and pits have basally located nuclei and lightly staining cytoplasm. Most of these cells secrete mucus, that is stored in the apical cytoplasm. You can see these cells in the stomach preparation stained with PAS which will stain mucus and other glycoproteins in slide In this slide, the mucous cells of the gastic pits stain quite intensely.
Also identifiable are lighter-staining "mucous neck cells" present in the neck region of the gastric glands and mucus-secreting cells of the cardiac glands found near the gastro-espophageal junction. Parietal cells are large, ovoid to pyramidal shaped cells with their broad side adjacent to the basement membrane.
Each cell contains a round, centrally located nucleus and reveals a lightly eosinophilic cytoplasm that appears granular due to the presence of many mitochondria. The chief cells are present in the lower one-third to one-half of the gastric glands.
However, in other preparations slides and , the pepsinogen has been extracted and the empty secretory granules resemble many glass beads in the supranuclear cytoplasm. The base of the cytoplasm, on the other hand, is distinctly basophilic. Other cells of the gastric glands, such as undifferentiated stem cells and various endocrine cells, will NOT be studied in this laboratory session as they are not readily identifiable in the stomach, but you should be aware of their general characteristics.
Notice the presence of a large number of lymphocytes and plasma cells in the lamina propria between the gastric glands, and, in some areas, aggregated as lymphoid nodules View Image which will be studied in greater detail along with other lymphatic tissues but you should at least be able to identify them here.
Also, notice that the strands of smooth muscle fibers from the inner layer of the muscularis mucosae extend between the glands toward the surface.
The contraction of these strands may help the emptying of the glands. Pyloric glands W pgs , In slide , you can see the transition from pylorus of the stomach to duodenum of the small intestine. The pyloric region of the stomach is characterized by a thick wall due to the presence of the pyloric sphincter muscle View Image , which is comprised primarily of the inner circular layer of the muscularis externa.
Compare its wall thickness with that of the adjacent duodenum W pg , An occasional parietal cell may be also found. Note that the bases of the pyloric glands abut the muscularis mucosae whereas in the duodenum, you will see abundant glands Brunner's glands DEEP to the muscularis mucosae i. Just in case you are worried about identifying cardiac glands versus pyloric glands, it is admittedly very difficult to tell these two apart based only on high-mag views, but you can always use contextual information to help you out: cardiac glands will be right near the gastro-esophageal junction whereas pyloric glands are at the gastro-duodenal junction.
This is the lining of the esophagus, where it is no longer necessary to have an outer keratinized layer to protect against desiccation, as it was for skin. Thus, the outermost layer is still cellular and contains a nucleus.
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