Benign esophageal tumors
Benign esophageal tumors are rare. Benign esophageal tumors can be divided into intraluminal, submucosal and intermural types according to their histogenetic origin. (1) The intraluminal type includes polyps and papillomas. The submucosal type includes hemangioma and granulocytic myoblastoma. The most common type of intramural tumor is esophageal smooth muscle tumor (esophageal leiomyoma), which occurs in the muscular layer of the esophagus. The latter accounts for about 3/4 of benign esophageal tumors.
Clinical manifestations The symptoms and signs of patients with benign esophageal tumors depend mainly on the anatomical location and size of the tumor. Larger tumors can block the esophageal lumen to varying degrees and present with symptoms such as dysphagia, vomiting and wasting. Many patients have aspiration pneumonia, pressure or pain behind the sternum. Bleeding can occur in patients with hemangioma. Patients with benign esophageal tumors, whether symptomatic or not, must be diagnosed by x-ray and endoscopy. The most frequent esophageal smooth muscle tumor occurs in the muscular layer, so the mucosa is intact and the tumor size varies, in oval, ginger or spiral shape. Barium swallow of esophageal X-ray can show “half-moon” pressure marks. Esophagoscopy can show smooth and normal mucosa on the surface of tumor. At this time, it is important not to damage the mucosa by mucosal biopsy of esophagus.
Treatment Generally speaking, regardless of the type of benign esophageal tumor, surgical resection of the lesion is required. For intramural and submucosal tumors, a blunt and sharp dissection is usually required through a thoracotomy incision to carefully protect the mucosa from breaking. The surgical results of benign esophageal tumors are satisfactory and the prognosis is good, and malignant changes are rare.
Corrosive esophageal burns
Erosive burn of esophagus is mostly caused by chemical burns of esophagus due to accidental swallowing of strong acid or strong alkali and other chemical corrosives. There are also cases of chemical burns of esophagus caused by long-term reflux esophagitis, long-term consumption of strong vinegar or long-term use of acidic drugs (such as doxycycline, tetracycline, aspirin, etc.), but they are less common. Strong bases produce more severe lysis necrosis; strong acids produce protein coagulation necrosis.
Pathology The severity of chemical burns of the esophagus is determined by the type, concentration, and dose of the chemical corrosive swallowed, the anatomical features of the esophagus accompanied by vomiting, and the duration of contact between the corrosive and the tissue.
After swallowing a chemical corrosive, the burn is often not limited to the esophagus, but often includes the oropharynx, larynx, stomach, or duodenum. The corrosive agent usually spends the longest time in contact with the three physiologically narrow segments of the esophagus and the gastric sinus, so more extensive burns often occur in these areas.
According to the pathological degree of burns, they can be generally divided into degree I, degree II and degree III burns: ① Degree I: superficial congestion and edema of esophageal mucosa, which heals in 7-8 days after the debridement period without leaving a scar. ②Degree II: The burn involves the esophageal muscle layer. In the acute stage, tissue congestion, edema, exudation, and ulcer formation after tissue necrosis and exfoliation occur within 3 to 6 weeks, and later fibrous tissue scar formation leads to stenosis. ③ Grade III: Coagulation necrosis of the whole esophagus and its surrounding tissues, which can lead to esophageal perforation and mediastinitis.
The pathological process after burn injury can be roughly divided into three stages. The first stage is the onset of inflammation, edema or necrosis within the first few days after the injury. Early signs of esophageal obstruction are often present. In the second stage, about 1 to 2 weeks after the injury, the necrotic tissue starts to fall off, soft, red granulation tissue appears, and the obstruction symptoms can often be reduced. The esophageal wall is weakest at this time and lasts for about 3-4 weeks. In the third stage scarring and strictures form and gradually worsen. The pathological evolution may proceed for weeks to months, but it is rare for strictures to reoccur after more than 1 year. The preferred site of scar stenosis is the physiological stenosis of the esophagus, i.e., the entrance to the esophagus, the plane of the tracheal bifurcation, and the lower end of the esophagus.
Clinical manifestations Immediately after accidental ingestion of corrosive agents, severe pain in the lip, mouth, pharynx, retrosternal area, and epigastrium is caused, followed by reflex vomiting, and the emesis is often bloody. If the burns involve the epiglottis, larynx and respiratory tract, coughing, hoarseness and difficulty in breathing may occur. In severe cases, coma, deficiency, fever and other toxic symptoms may occur. The formation of scar stenosis can lead to partial or complete obstruction of the esophagus, and even difficulty in swallowing saliva, malnutrition, dehydration, wasting, and anemia at a later stage due to inability to eat. The growth and development of the child is affected.
Diagnosis In the early stage, the diagnosis is mainly based on the history of swallowing corrosive agents and the above-mentioned clinical manifestations, and the diagnosis can be established when the physical examination reveals the manifestation of burning in the oropharynx. However, sometimes the presence or absence of burns in the oropharynx does not necessarily prove the presence or absence of burns in the esophagus, so the diagnosis should be confirmed by iodine oil imaging of the esophagus if necessary. Posterior sternal pain, back or abdominal pain should exclude esophageal or gastric perforation. In advanced stages, an esophagogram can clarify the location and extent of the stricture.
Treatment
1. Emergency treatment procedures are as follows: ① Take a brief medical history, including the type, time, concentration and amount of corrosive agent taken. ② Quickly determine the general condition of the patient, especially the condition of the respiratory system and circulatory system. Keep the airway unobstructed, tracheotomy if necessary. Establish intravenous access as soon as possible. ③ Swallow vegetable oil or protein water as early as possible to protect the esophagus and gastric mucosa. Even swallow saline or water for dilution if unconditionally. There are existing controversies about the previous methods of neutralizing alkaline substances with weak acid solutions and neutralizing acid substances with alkaline solutions. Some believe that this method is not only unhelpful, but also harmful, because the heat generated by the chemical reaction can cause re-injury. ④ Actively manage complications, including laryngeal edema, shock, gastric perforation, mediastinitis, etc. ⑤ Prevention of esophageal stricture and early use of adrenocorticosteroids and antibiotics can reduce inflammatory response, prevent infection, fibrous tissue proliferation and scar formation. Hormones are prohibited for suspected esophageal and gastric perforation. It is controversial whether to place a tube in the lumen for endoluminal stenting of the esophagus or esophageal pressure method to prevent stenosis.
2.Dilatation therapy should be performed 2-3 weeks after the acute inflammation and edema of the esophagus begins to subside. For mild circumferential stenosis, dilation with a probe strip under esophagoscope can be used; for long tubular stenosis, dilation with a swallowed wire pulled out through the gastrostomy opening and a tethered dilator in the downward or reverse direction is recommended. In some cases, plastic strips are used for dilation. Esophageal dilation should be repeated periodically.
3.Surgical treatment For severe long stenosis and failure of dilatation therapy, surgical treatment can be used. The esophagus is cut off above the stenosis and replaced with an anastomosis of the stomach, jejunum or colon, depending on the situation. The stenotic segment of the esophagus is left open or removed. The gastric or intestinal segment can be elevated via the pleural cavity, posterior sternum or anterior sternum subcutaneously, depending on the patient’s specific situation.
Cardia achalasia
achalasia of cardia or cardiospasm is the absence of peristalsis in the body of the esophagus during swallowing and poor relaxation of the cardia sphincter. It is usually seen in 20-50 years old, with a slight increase in women.
Etiology and pathology The etiology is still unknown. It is generally believed that the disease is due to degeneration, reduction or absence of ganglion in the esophageal muscle layer and loss of normal propulsion of the esophagus. The lower esophageal sphincter and cardia cannot relax, resulting in the retention of food in the esophagus. Over time, the esophagus becomes dilated, hypertrophied, elongated, flexed, and loses muscle tone. Food stagnation, chronic irritation of the esophageal mucosa, resulting in congestion, inflammation, and even ulceration. After a long time, cancer may occur in a few patients.
Clinical manifestations The main symptoms are difficulty in swallowing and a feeling of heaviness or obstruction behind the sternum. Most of them have a long duration, and the symptoms are sometimes mild and severe, and the attacks are often related to mental factors. Hot food is easier to pass than cold food, and sometimes solid food can be passed because it can form a certain pressure. Initially, the attacks are intermittent, but as the disease progresses, it becomes persistent difficulty in eating. When the esophagus is significantly enlarged, it can accommodate large amounts of liquid and food. Tracheal aspiration can occur at night and be complicated by pneumonia.
Diagnosis Barium swallow imaging of the esophagus is characterized by loss of peristalsis in the body of the esophagus, a bird’s beak shape at the lower end of the esophagus and the cardia with neat and smooth edges, and a markedly dilated esophagus at the upper end, which may have a liquid surface. The barium cannot pass through the cardia. Esophageal fiberscopy can confirm the diagnosis and exclude cancer.
Treatment
1.Non-surgical treatment If the disease is short and mild, antispasmodic drugs can be used. Eat less and more meals, chew slowly and avoid eating too hot or too cold food. Some early patients with mild disease can try to perform esophageal dilatation first. The method of dilation can be mechanical, water bladder, air bladder, barium bladder, etc. It can relieve the symptoms. However, attention should be paid to prevent the complications of strong dilation, such as esophageal perforation and bleeding.
2.Surgical treatment usually adopts transabdominal or left chest for lower esophageal cardia myotomy (Heller operation), which is a simple method with good results. The myotomy should be thorough until the mucosa expands. The extent of myotomy is about half of the circumference of the esophagus. However, care should be taken to prevent cutting through the mucosa or damaging the vagus nerve. Anti-reflux surgery, such as fundoplication and pyloroplasty, is also performed on top of this procedure.
Esophageal diverticulum
A restricted bulge of one or all layers of the esophageal wall, forming a pouch that communicates with the esophageal lumen, is called diverticulum of the esophagus. According to its pathogenesis, it can be divided into two types: traction type and bulging type. The traction type mostly occurs near the bifurcation of the trachea, mostly due to adhesions and scar contraction with the nearby esophageal wall after lymph node inflammation or lymph node tuberculosis infection there. The bulging type is mostly due to pressure difference between the inside and outside of the esophagus and herniation of the esophageal mucosa through weak points in the muscular layer, mostly in the pharynx and 5-10 cm above the diaphragm (Figure 31-4). The traction type is called true diverticulum because the whole esophagus is pulled outward; the bulging type is called pseudodiverticulum because only the mucosa is bulging.
I. Pharyngoesophageal diverticulum
Etiology and pathology Because there is a weak triangle between the subpharyngeal constrictor muscle and cricopharyngeal muscle, coupled with the uncoordinated muscle activity, that is, when the subpharyngeal constrictor muscle contracts to push down the food, the cricopharyngeal muscle does not relax or contract prematurely, resulting in the esophageal mucosa from the weak area bulging out, is bulging type of pseudodiverticulum.
Clinical manifestations and diagnosis There are no symptoms in the early stage. When the diverticulum increases in size, there may be a gurgling sound during swallowing. If there is food retention in the diverticulum, it can cause pressure in the neck. Stagnant food decomposition and decay can lead to foul odor and mucosal inflammation and edema, causing difficulty in swallowing. On physical examination, a soft mass can sometimes be found in the neck, and there is a gurgling sound when pressure is applied. Huge diverticula may compress the recurrent laryngeal nerve and cause hoarseness. Pulmonary infection can be complicated by aspiration of refluxed food into the lungs.
Diagnosis is mainly confirmed by barium x-ray examination of the esophagus. This can show the location, size, and connections of the diverticulum.
Treatment Surgery can be considered for symptomatic patients. The diverticulum is removed and the esophageal wall incision is closed in layers. If the general condition is not suitable for surgery, we can push the diverticulum during each meal to reduce food accumulation, and drink warm water to rinse the food residue inside the diverticulum after eating.
B. Middle esophageal diverticulum
Etiology and pathology Inflammation of the tracheal bifurcation or lymph nodes near the pulmonary hilum, forming a scar that pulls the whole esophagus. The size is usually 1 to 2 cm, and can be single or multiple. The diverticulum neck opening is mostly large and does not easily stagnate food.
Clinical presentation and diagnosis Often asymptomatic. If inflammatory edema occurs, there may be a sensation of gagging or pain in the back of the sternum or back.
Diagnosis mainly relies on barium swallow X-ray to confirm the diagnosis. Sometimes esophagoscopy is performed to exclude cancerous lesions.
Treatment Clinically asymptomatic patients do not require surgery. If there is inflammation and edema, anti-inflammatory and antispasmodic drugs can be included to relieve the symptoms. If there is bleeding, perforation or obvious symptoms, surgery can be considered. The esophageal wall is freed and the diverticulum is repositioned or removed.
Supradiaphragmatic diverticulum
Etiology and pathology The lower part of the esophagus near the upper part of the septum, from a weak point of the smooth muscle layer, for some reason such as cardia failure, esophageal hiatus hernia, etc., caused by increased pressure in the esophagus, resulting in mucosal bulging. It occurs in the lower esophagus on the posterior right side. In a few cases, the whole esophagus is bulged to form a true diverticulum.
Clinical manifestations and diagnosis The main symptom is pain behind the sternum or in the upper abdomen. Sometimes there is difficulty in swallowing or food reflux. The diagnosis mainly relies on barium swallow x-ray of the esophagus, which can show the diverticular sac, diverticular neck and its location and direction.
Treatment For those with obvious symptoms or food sludge, resection of the diverticulum can be considered, while other diseases of the esophagus and diaphragm can be managed.