Esophageal diseases include:
Reflux esophagitis, esophageal varices, esophageal cancer, esophageal leiomyomas, hiatal hernia, esophageal diverticulum, corrosive esophagitis, esophageal spasm, cardia slowness, etc
Pathology
Reflux esophagitis is a malfunction of the lower esophageal sphincter muscle, in which stomach and/or duodenal contents reflux into the esophagus, causing inflammation of the esophageal mucosa.
Pathological changes: in the acute stage, mucosal hyperemia, edema, easy bleeding, erosion and superficial ulcers are formed;Fibrosis occurs in the chronic phase.
Clinical presentation
Main symptoms: Pain in the retrosternal or fossa, ranging from a burning sensation to a severe stabbing pain. Pain is often triggered or worsened when food passes through, and can sometimes be worsened by lying down or bending forward. The pain may radiate to the back. Early local spasms due to inflammation may present with intermittent dysphagia and vomiting. Later strictures due to fibrous scarring may lead to persistent dysphagia and vomiting.
Radiographic findings
Localized spasmodic contractions of the lower esophagus, blocked by barium slowing down. The mucosal folds are thickened and disturbed, and ulcers and pseudodiverticula may occur. Esophageal strictures with localized or diffuse thickening or fibrosis of the tube wall. As a result, the esophageal wall is dilated and peristalsis is diminished. Esophageal shortening, combined hiatal hernia. 
Reflux esophagitis.
Reflux esophagitis (niche opacity).
Reflux esophagitis (mucosal fold changes - pseudodiverticulum).
Reflux esophagitis (with short esophageal hiatal hernia).
Clinical historySwallowing a chemical corrosive agent can cause severe damage and inflammation of the esophagus, called corrosive esophagitis. Severe injuries can lead to esophageal rupture complicated by mediastinal barriers, while mild cases can cause esophageal scar strictures of varying degrees.
Generally, corrosive agents are divided into two categories: acid and alkali. Alkaline corrosives have strong water absorption, fat saponification and proteolytic effects, causing high swelling, ulceration and tissue necrosis of the mucosa, which can cause esophageal perforation. If it is acidic, the mucosa is black necrosis and edema is mild, but acidic people have a greater corrosive effect on the stomach and duodenum. Corrosives can destroy the esophageal mucosa and further corrode the deep tissues of the esophagus, eventually forming scars. There is a clinical history of swallowing chemical corrosive agents (strong acids, strong bases, etc.), which is easy to diagnose and differential diagnosis with other diseases.
Image performance
Acute phase (1-3 days).Paroxysmal spasms can occur due to mucosal edema and hemorrhage, weakened or absent peristalsis of the tube wall. Due to the detachment of the mucosa, the contrast agent does not attach well to the mucosal surface, and irregular light barium spots are seen.
Interim (3-10 days).: The esophagus is constricted, narrowed, and cannot be dilated. Multiple superficial or deep ulcers may be seen, and mucosal wrinkles and disorders may be seen.
Late stage: The main manifestation is lumen stenosis, which is generally long in scope, and can also be dominated by physiological stenosis. Its contrast agent is difficult to pass through. The esophagus is shortened, and dilation above the stricture may be seen. Ulceration or pseudoventricular formation may be seen in the stricture. Follow-up x-rays are important to understand the extent of the injury, the extent of the scar, and the extent of the scar.
The esophagus is irregularly narrow, and there are many niches.
Differential diagnosis:Differentiated from lower esophageal invasive carcinoma.
The stricture of the lower esophageal invasive carcinoma is clearly demarcated from the normal esophagus. The strictures of lower esophageal cancer are more rigid and less dilapidated than reflux esophagitis. In reflux esophagitis, the stricture narrows the line between the normal esophagus and the normal esophagus, rather than abrupt narrowing. Reflux esophagitis is more common with hiatal hernia, whereas esophageal cancer is not.
PathologyHiatal hernia is a condition in which part of the stomach enters the chest cavity through the diaphragmatic esophageal hiatus.
It can be divided according to its form: Congenital short esophageal type, sliding hiatal hernia, paraesophageal hiatal hernia, and mixed hiatal hernia.
Clinical presentationIt is mainly caused by irritation or erosion of the esophagus by reflux of gastric contents, and is manifested by varying degrees of discomfort, burning sensation and pain in the retrosternal upper abdomen. Usually occurs after a full meal. Symptoms worsen when lying flat immediately after eating, but may lessen when standing.
Radiographic findings
Direct X-ray signs of hiatal hernia: supradiaphragmatic thorax gastric supragmatic esophageal gastric ring The gastric mucosa shadow in the hernia sac can be seen in the prone right anterior oblique position, the diaphragmatic esophageal hiatus is obviously relaxed, and it is in a state of insufficiency, and the gastric contents are prone to regurgitation Short esophageal type (congenital, acquired): gastric hernia enters the chest cavity, and the short esophagus is directly connected to the stomach, and there is no hernia sac formation. Sliding type;The incidence is the highest. It usually occurs when the prone right anterior oblique position is performed for deep inspiration. Typically, three annular stenosis can be seen on the diaphragm, called the "triple ring". The superior ring is the junction of the esophagus and the upper part of the ampulla of the diaphragm-a ring;The central ring is the esophagogastric junction-B ring, and sometimes the "Z" line of the mucosal junction is visibleThe lower ring is the herniated stomach through the diaphragmatic esophageal hiatus. Paraesophageal: the esophagogastric junction is still subdiaphragm, but the fundus herniates into the chest paraesophagus. Mixed: Esophagogastric junction and fundus herniated into the thoracic cavity. 
Sliding hiatal hernia.
Short esophageal hiatal hernia.
Paraesophageal hernia Paraesophageal hernia.
Differential diagnosis:: Distinguish from the ampulla of the esophageal diaphragm.
The ampulla of the esophageal diaphragm is a normal physiological phenomenon, which is manifested by the enlargement of the lumen of the 4 5 cm section of the diaphragm in an oval shape, its edge is smooth, and it shrinks and becomes smaller as the esophageal peristalsis above it arrives When the barium is emptied, a slender mucosal fold appears.
The upper part of the ampulla of the esophageal diaphragm is directly connected to the stomach and is usually not present with a contractile ring.
The hernia sac of a hiatal hernia has the following features:
Hernia sacs vary in size, the edges may not be smooth, and the contraction of the cyst wall is not related to esophageal peristalsis.
The upper border of the hernia sac may see an esophagogastric ring.
The transverse diameter of the hernia sac is wider than that of the ampullary of the normal esophageal diaphragm.
PathologyEsophageal varices can be caused by impaired venous return at any site, which is an important complication of portal hypertension because of the formation of collateral circulation between the portal vein and superior vena cava in portal hypertension.
The specific collateral circulation pathways are as follows: portal vein-gastric coronary vein-esophageal venous plexus-azygous vein-superior vena cava.
Clinical presentationThe symptom of esophageal variceal bleeding is hematemesis, which is often sudden, and the blood is freshly poured out, or even spurted. Therefore, in acute upper gastrointestinal bleeding, such as patients with sudden shock, it is often more common in esophageal variceal bleeding caused by portal hypertension. Patients with a history of hepatitis, schistosomiasis, or chronic alcoholism, spider angiomas, abdominal wall venous distension, splenomegaly, or even ascites on physical examination, and abnormal liver function tests often indicate cirrhosis and portal hypertension.
Radiographic findings
Mild: widening or moderate tortuosity of the lower esophageal mucosal folds: as varices progress, lesions may extend into the midesophagus and appear as longitudinal toward coarse nodules or earthworm-like filling defects, and finally as beaded filling defects. Severe: varices extend to the middle and upper segments or even the entire length of the esophagus. Due to the degeneration of the muscles, the esophagus is dilated and not easy to contract, the peristalsis of the tube wall is significantly weakened, and the emptying of barium is slow, but there is no obstruction. Esophageal varices often occur in conjunction with gastric varices or can be sole. The latter manifests as grape-shaped, polyp-shaped, rounded, lobulated filling defects in the fundus and cardia. 
Mild esophageal varices.
Esophageal and gastric varices.
CT of esophageal and gastric varices
Variceal esophageal cancer with stiff walls and irregular filling defects.
Differential diagnosis:
It is different from middle and lower proliferative esophageal cancer: esophageal proliferative carcinoma is a polypoid or lobulated filling defect, the wall of the tube is stiff and cannot be expanded, and the lesion range is short and clearly demarcated from the normal esophagus. But sometimes it is necessary to be aware of the longer range, and this type of esophageal cancer is called by some peopleVarice-like esophageal cancer
Esophageal varices are extensive earthworm-like or bead-like filling defects with uneven, soft and expandable walls. Barium test: barium for esophageal proliferative carcinoma is blocked through the stricture segment and its upper end of the esophagus is dilatedBarium esophageal varices are delayed through the esophagus without obstruction.
Pathology
Esophageal cancer is a malignant tumor of the esophageal squamous epithelium and is one of the common malignant tumors. There are more in the middle and lower esophagus and the least in the upper esophagus. According to the pathological anatomy and X-ray findings, esophageal cancer was divided into four types: mushroom umbrella type, invasive type, ulcerative type and medullary type. Clinical presentation
The main symptoms are persistent and progressive dysphagia, which begins with some discomfort in the passage of food and gradually progresses to food blockage over several months. You can't eat solid food at first, then you can only eat liquids, and finally you can't eat at all. When the cancer invades the recurrent laryngeal nerve, hoarseness and dyspnea may occur. If the cancerous tissue invades the trachea and forms an esophageal tracheal fistula, it will cause choking cough when eating, which can be secondary to mediastinitis, lung abscess, aspiration pneumonia and empyema. In the advanced stage, ascites, emaciation, anemia, etc., as well as other symptoms of cachexia and cancer metastasis. Radiographic findings
Early esophageal cancer
Esophageal mucosal folds, tortuosity, interruption, single or multiple niches, localized filling defects, localized wall stiffness, slowed barium flow or transient retention, all of these are diagnostic or highly suspicious signs of early esophageal cancer, and further esophagoscopy and exfoliated cell examination are necessary if necessary.
Early esophageal cancer (small nodular cluster).
Raised early cancer.
Ulcerative early cancer.
Manifestations of advanced (intermediate and advanced) esophageal cancer
Mucosal fold disruption, filling defect;The wall of the tube is stiff, the lumen is narrow, and the passage of barium is blocked by soft tissue masses.
Advanced esophageal cancer (mass type).
Advanced esophageal cancer (ulcerative type).
Advanced esophageal cancer (sclerosis).
Advanced esophageal cancer (medullary type).
Esophageal cancer mediastinal fistula.
Manifestations of various types of intermediate and advanced esophageal cancer
Mushroom umbrella type: the tumor mainly grows into the lumen, showing irregular or cauliflower-like filling defects, combined with eccentric lumen stenosis and stiffness, the tumor area is clearly demarcated from the normal esophagus, and the esophagus above the stricture is dilated.
Infiltration: Annular stenosis is the main feature. Sometimes it is a funnel-shaped stenosis, the lesion is short, the tube wall is stiff, the tumor area is clearly demarcated from the normal esophagus, and the upper esophagus is significantly dilated.
Ulcer type: mainly long flat niches, peripheral bulges, mucosal folds destruction, stiff tube wall, poor expansion, no obvious obstruction.
Medullary type: the lesion is generally large, and a significant filling defect can be seen in the lumen, occluding the lumen and dilating the esophagus above the lesion. A fusiform soft tissue mass is seen on x-ray.
Differential diagnosis:
1.Differentiating esophageal cancer from reflux esophagitis:
Reflux esophagitis usually occurs in the lower esophagus and has persistent lumen narrowing with mild dilation and contraction without destruction of mucosal folds. Invasive carcinoma of the lower end of the esophagus, the lesion is annular stenosis, the wall of the tube is stiff and cannot be expanded, the mucosa is destroyed, and the lesion area is clearly demarcated from the normal esophagus. 2.Differentiation of esophageal cancer from esophageal leiomyoma:
The lumen of esophageal leiomyoma is a lobulated filling defect, the upper and lower ends of the tumor are indented in an arc with the normal esophagus at an acute angle, and the mucosal folds in the tumor area are flattened and disappear. Esophageal cancer is characterized by intraluminal cauliflower-like filling defects, stiff tube walls, destruction and disappearance of mucosal folds, and although the demarcation between the lesion area and the normal esophagus is clear, the upper and lower ends of the lesion lacking leiomyoma are arc-like notches and acute angles to the normal esophagus. Pathology
Esophageal leiomyomas originate from the muscular layer of the esophagus, mostly located in the lower esophagus1 and 3 segments, and the tumors are hard, expansive, and capsule-capsulated.
Clinical presentation
When the course of the disease is generally long, ranging from months to years. Begins to present with retrosternal discomfort or a strange sensation in the larynx. The tumor gradually grows, causing a partial blockage of the esophageal lumen, which produces symptoms of swallowing obstruction. Dysphagia is usually not severe, sometimes intermittent, and usually does not interfere with normal eating. Radiographic findings
Intermural type: The tumor grows intraluminal or both out-of-luminal and can grow on both sides at the same time. Tangent, manifested as a semicircular or lobulated protrusion into the cavity, a filling defect with sharp edges, and a clear demarcation between the lesion and the normal esophagus, with an arc-like indentation and an acute angle;In anteroposterior position, the tumour appears as a circular filling defect. When the barium is passed, the tumor is surrounded by barium, and it appears as an arcuate or annular shadow on the upper and lower edges of the tumor, which is called the "annular sign", which is a typical manifestation of the disease. Outgrowth of the wall: large in size, can cause a soft tissue mass within the mediastinum that matches the extent of the filling defect within the esophagus, and the mass can be mistaken for a mediastinal tumor. The mucosal folds in the tumor area were flattened and disappeared, the mucosal folds around the tumor were normal, and irregular niches could be seen on the surface of some tumors. Differential diagnosis:
It needs to be differentiated from esophageal cancer. The main distinguishing point is that the filling defect of esophageal cancer is irregular, the surface mucosa is destroyed, and most of them have irregular niches, often causing lumen stenosis and obstruction.
Esophageal leiomyomas.
Pathology
Esophageal achalasia is characterized by the simultaneous presence of functional strictures of the cardia tubes and pathological dilation of the esophagus. This condition used to be called cardia spasm. It is more common in women. It is believed that the degeneration and reduction of ganglion cells in the lower muscle wall of the esophagus hinders the transmission of normal nerve impulses, and the lower esophageal cardia cannot relax, which constitutes the cause of this disease. Clinical presentation
The onset is usually slow and the course of the disease is long. The main symptoms are hypopharyngeal obstruction and a feeling of heaviness or obstruction behind the sternum. When the esophagus is severe, it can cause compressive symptoms such as palpitations and dyspnea. Radiographic findings
Plain chest x-ray: the superior mediastinum is widened, fluid level is visible within it, and the barium slowly sinks in the form of snowflakes.
Barium esophagus swallow imaging:
1.The esophagus is highly dilated with uniformity, 4 to 5 times that of the normal esophagus.
2.The lower end of the esophagus becomes tapered and appears in the shape of a bird's beak or large radish root. A small number of esophagus lie transversely on the diaphragm in the shape of a pouch, peristalsis is weakened or absent, and no regular contraction is seen.
3.After the barium reaches the stenosis end, the cardia is slightly open due to gravity, and a small amount of barium is ejected into the stomach.
4.The luminal morphology of the esophageal stricture changes with breathing.
Mild. Moderate.
Severe. Differential diagnosis:
It needs to be distinguished from lower esophageal invasive carcinoma: The stricture segment of lower esophageal invasive carcinoma is short, clearly demarcated from the normal esophagus, the wall of the tube is stiff and cannot expand, and the mucosa is destroyed. The morphology of the stricture segment of the lower esophageal invasive carcinoma does not change with respiratory movements. A narrow segment of cardia spasm with a smooth and soft wall that expands intermittently without mucosal destruction. Pathology
Esophageal diverticulum can be divided into pharyngeal esophageal diverticulum, septal upper esophageal diverticulum, and middle esophageal diverticulum.
The first two are internally baric diverticula that lack muscularis except for a mucosal and submucosal layerThe latter is a traction diverticulum with a tissue structure of the esophagus.
Clinical presentation
Most are asymptomatic and are only incidentally detected on x-rays, and a few patients have swallowing obstruction or a sense of swallowing.
Large diverticulums can cause symptoms such as food retention and food reflux. When diverticulitis is complicated, the obstruction is often worsened, and chest and back discomfort or pain are often present.
Occasionally, perforation occurs, causing mediastinitis or esophagotracheal fistula.
Radiographic findingsBarium esophagus swallow imaging:
Esophageal diverticulum and supraphragmatic esophageal diverticulum: the former is located in the pharynx, and the latter is located in the esophagus 5 to 6 cm above the diaphragm. Diverticulum appears as a drooping sac-like pouch that protrudes more often toward the left side of the esophagus, with smooth edges and large diameters.
Middle esophageal diverticulum: It mostly occurs at the bronchial or pulmonary artery indentation, and is mostly caused by adhesions between adjacent lymphadenitis (mostly tuberculous), and the diverticulum is generally small in diameter and smooth or irregular in shape.
Mixed diverticulum: It is a traction plus internal pressure diverticulum, which generally occurs in the middle of the esophagus and rarely occurs in the supraphragmatic esophagus, and is shaped like a tent, flask, funnel, or cylindrical shape, mostly protruding anteriorly, and the apex is drooping.
Upper esophageal diverticulum (pharyngeal esophageal diverticulum) Upper esophageal diverticulum (pharyngeal esophageal diverticulum).
Multiple diverticulum of the esophagus Multiple diverticulum of the esophagus.
Malignant squamous cell carcinoma of the esophageal diverticulum Malignant squamous cell carcinoma of the esophagus diverticulum.
Esophageal spasms are divided into diffuse and localized. Diffuse esophageal spasm is a temporary narrowing of the esophagus due to a motor disturbance in the esophagus. The pathological manifestation is diffuse esophageal muscle thickening, and the number of ganglion cells is not reduced, and some scholars call it esophageal functional diverticulum. It can occur at any age, both men and women, and intermittent dysphagia can occur. If angina is discharged clinically, esophageal pH monitoring and manometry should be performed to detect gastroesophageal reflux or abnormal movement. If the esophageal contraction is causing pain, in principle, it should be confirmed with manometry, and a high amplitude of synchronized contractions can be observed at the onset of pain over a long period of time. Endoscopic diffuse esophageal spasm typically appears as spiral spasm. It can be induced by taking choline inhibitors (such as tensilon) or pulling the esophagus with an inflated balloon. Imaging testsPredominantly, barium swallow can show signs of diffuse esophageal spasm.
X-rays show esophageal spasm leading to barium passage that is intermittent and typically characterized by symmetrical wavy changes on both sides of the esophagus, multiple annular contractions in the lower esophagus, and smooth, soft esophageal walls with normal mucosal folds.
Barium passes slowly through the middle and lower esophagus, and sometimes diffuse filling defects of varying sizes can be seen in the middle and lower segments. It is caused by the accumulation of esophageal debris and the mixing of barium residues.
Diffuse esophageal spasm.
Localized esophageal spasm.
Differential diagnosis:
1. Distinguish it from esophageal cancer from the following aspects:
Filling defect: The so-called filling defect of diffuse esophageal spasm is mainly caused by the retention of food debris, and its changes in number, shape and location are different from the important signs of filling defect in esophageal cancerEsophageal stricture: The esophageal stricture of diffuse esophageal spasm is frequent and unconstant, while esophageal cancer, especially invasive esophageal cancer, is localized, generally single, and the stricture form is fixedClinical changes: diffuse esophageal spasm is non-progressive dysphagia, whereas dysphagia in esophageal cancer is progressively worsening. 2. Distinguish from the third peristaltic wave
The third peristaltic wave is a type of esophageal dysfunction that is common in older people and can also be a secondary manifestation of cardia retardation. X-rays show irregular, tightly packed contractile rings in the middle and lower esophagus that are asymmetrically distributed. This contraction ring can appear one after the other, and after a few seconds the phenomenon disappears and the esophagus returns to normal. Barium swallow fluoroscopy shows that the edge of the esophagus is irregular, undulating, concave in depth, and the protrusions are asymmetrical, which can be round and blunt or sharp. Thirdly, peristaltic waves appear for a short period of time, and the degree of margin irregularity is less than that of diffuse esophageal spasm. Pathology
Esophageal foreign bodies are often encountered in clinical emergency work, mostly in children who ingest coins and small metals, in **, it is more common in the accidental ingestion of bone fragments or fish bones, and in the elderly, it is more common in swallowing lost dentures, all of which are X-ray opaque foreign bodies. Most foreign bodies tend to lodge in esophageal entrance strictures and aortic arch indentations, or in left main bronchial indentations. Clinical presentation
Clinically, there is a clear history of swallowing a foreign body, which is mainly manifested by a feeling of obstruction when swallowing, dysphagia and pain, often at the site of the foreign body. If secondary infection occurs, the pain will worsen and lead to periesophageitis, which can even lead to a periesophageal abscess, which can produce more complex clinical symptoms. Radiographic findings
History and nature of the foreign body should be known prior to examination Large radiopaque foreign bodies can usually be detected and localized. Small foreign bodies (eg, fine bone spurs) or x-opaque foreign bodies should be checked for barium swallowing, and barium will adhere to the x-opaque foreign body and be visualized. The fish bones should be checked by swallowing barium cotton, which hangs on the foreign body, and can still stay in place after repeated swallowing or even drinking. Diagnosed. If the suspicious foreign body is near the aortic arch and barium cotton examination is needed to identify, it is better to swallow a small amount of barium cotton multiple times, such as swallowing a large amount of barium at one time may pull the foreign body to the esophageal perforation, or even involve the large blood vessels and cause massive bleeding, endangering the patient's life. If the soft tissue around the esophagus is swollen or even the air-fluid level is seen in the foreign body on the radiograph or on the radiograph, it indicates inflammation, infection or even abscess formation at the esophageal foreign body. CT is necessary.
Esophageal foreign body: silver lock.
Esophageal foreign body: chicken bone.