| disease | Achalasia |
Achalasia is a primary esophageal motility disorder characterized by (1) absence of peristalsis in the esophageal body, (2) failure or incomplete relaxation of the lower esophageal sphincter during swallowing, and (3) elevated resting pressure of the lower esophageal sphincter. Although achalasia is a benign condition, it significantly impacts quality of life, health, and longevity. Due to dysphagia, patients may resort to various measures such as adjusting posture, drinking water, or repeated swallowing, which can make them feel embarrassed about eating in public and prefer dining alone. This creates psychological stress and severely affects social activities.
bubble_chart Etiology
The disease manifests as stenosis of the distal esophagus, dilation, curvature, and elongation of the esophageal body, thickening of the muscular layer—particularly the circular muscle—which is most pronounced. Histological examination reveals a reduction in ganglion cells, mononuclear cell infiltration, and fibrosis in the myenteric plexus of the esophageal body. The number of ganglion cells is decreased in the distal esophagus. Vagal nerve fibers exhibit ruptured myelin sheaths, fragmented neurofilaments, swollen axoplasm, and separation between the axon-Schwann membrane and the axonal membrane. The dorsal motor nucleus of the vagus nerve shows abnormalities in both the number and structure of neurons. Ultrastructural examination of esophageal smooth muscle reveals shedding of microfilaments. Thus, it is evident that degenerative changes occur from the brainstem, vagal nerve fibers, and myenteric plexus all the way to the muscle nerve fibers, leading to denervation of the esophagus. However, the mechanisms by which viruses, exotoxins, tumors, Chinese Taxillus Herb parasites, and gastrin exert their effects, as well as the location of the primary lesion, remain unclear.
bubble_chart Clinical ManifestationsThe incidence rate is low, approximately 1/100,000, and there may be a family history. The main symptoms include difficulty swallowing, regurgitation, and chest pain, with symptoms generally persisting for a long time. However, symptoms in young children are often nonspecific and easily confused, which will be discussed later in the section on pediatric achalasia.
1. Difficulty swallowing has the following characteristics: (1) Difficulty swallowing does not occur immediately at the beginning of a meal but becomes noticeable as food intake increases due to impaired esophageal emptying. (2) It occurs with both solid and liquid foods, though sometimes the difficulty is markedly different with liquids. (3) The severity of dysphagia is inversely proportional to the degree of esophageal dilation—the more dilated the esophagus, the milder the dysphagia. (4) Esophageal emptying primarily relies on gravity, so patients may adopt various methods, such as standing while eating, walking continuously, drinking large amounts of liquids, forceful swallowing, repeated swallowing, or holding their breath after deep exhalation, mainly to increase intra-esophageal pressure and force food into the stomach. (5) Rapid eating, consuming excessively cold or hot foods, or emotional stress can worsen swallowing difficulties.
2. Regurgitation Regurgitation symptoms appear later than dysphagia. As the disease progresses, the timing and content of regurgitation vary. In the initial stage, about 90% of patients experience regurgitation during or after meals, with small amounts of recently consumed food. As the esophageal body continues to dilate, its capacity gradually increases, sometimes exceeding 1L. The frequency of regurgitation decreases, occurring perhaps once every 2–3 days, but the volume increases, and regurgitated material may include food consumed the previous night or even several days earlier, with a foul odor. Approximately 57% of patients experience regurgitation while lying down, waking to find regurgitated material on their pillow or bedding. Some patients may dismiss this, but experienced doctors should inquire carefully to understand the condition thoroughly. They should also ask whether nocturnal regurgitation causes aspiration, leading to intolerable choking or coughing that forces the patient to sit up. This is especially important for patients with recurrent bronchitis, lung infections, lung abscesses, or bronchiectasis, as these may result from esophageal regurgitation. The presence of blood in regurgitated material should raise concern for possible cancer, as about 3% of these patients develop malignancies.
4. Weight loss and bleeding Due to dysphagia, patients often fear eating, leading to insufficient nutrient intake and varying degrees of weight loss and malnutrition. Bleeding is uncommon and usually results from esophageal inflammation, but the possibility of cancer should not be overlooked.
﹝Auxiliary examinations﹞
1. X-ray examination X-ray examination is crucial for diagnosing achalasia, with both plain chest films and esophagography showing distinctive features.
（1）Plain chest X-ray: About 85% of patients show absence of the gastric bubble. A posteroanterior view may reveal a tortuous, dilated esophagus protruding into the right thoracic cavity, widening the mediastinal shadow near the superior vena cava and right atrium. Sometimes, a fluid level can be seen within the dilated esophageal shadow. A lateral chest film shows the enlarged, thickened esophagus and fluid level in the posterior mediastinum, with the trachea displaced anteriorly. In some cases, inflammatory changes may be present in the lung fields.
(2) Esophagography: The following preparations should be made before performing esophagography: (1) If a routine chest X-ray reveals significant retention in the esophagus, insert a gastric tube before the contrast study to aspirate the retained material to avoid affecting the observation of the esophageal wall and motility. (2) Prepare medications that may be needed during the examination, such as amyl nitrite, so they can be administered immediately if required during observation. (3) Prepare video recording equipment to allow repeated review of the esophageal morphology and its motor function and emptying capacity in various positions, including upright, horizontal, right anterior oblique, etc. Special attention should be paid to the supine position, which evaluates emptying capacity excluding the influence of gravity. Based on esophagography findings, achalasia can be broadly classified as follows: Grade I achalasia: The lower esophagus shows significant narrowing with smooth margins, marked dilation above the narrowing, and only minimal passage of barium. The esophageal dilation does not exceed 4 cm in diameter. The proximal third of the esophagus may exhibit normal peristalsis, the middle third lacks effective peristalsis, and the distal third shows disordered or vigorous contractions. The sphincter fails to relax, and barium is retained in the middle third of the esophagus. The esophagus may appear spindle-shaped, bird-beak-shaped, or resemble fistula disease. The gastric bubble is minimal or absent.
2. Gastroscopy Endoscopy is highly helpful in diagnosing this condition. In addition to observing the dilated esophagus, passing the gastroscope through the cardia sphincter is not difficult, and the lack of significant resistance does not necessarily indicate a problem. However, it is indispensable for differential diagnosis and the subsequent correct formulation of treatment plans, especially when there is blood in the reflux. Endoscopy can detect pseudoachalasia caused by cardiac cancer. In cases of severe retention esophagitis, the esophageal mucosa becomes extremely hyperplastic, with polypoid changes or ulcer formation that may be difficult to distinguish from cancer. In such cases, a biopsy or brush cytology can be performed for histological or cytological examination to clarify the diagnosis. If secondary inflammatory changes in the esophagus are found, such as reddened and eroded mucosa, ulcers, mucosal leukoplakia, or candidal esophagitis, this provides clear guidance for the selection of treatment methods and timing for achalasia. When the esophagus is inflamed, the tissue is fragile due to edema, making esophageal dilation prone to perforation, and myotomy may easily tear the mucosa, leading to esophageal fistula. Therefore, conservative treatment should be administered first, and surgery should be performed only after the inflammation subsides. If leukoplakia is present in the mucosa, there is a risk of malignant transformation, which warrants vigilance. Treatment should consider this possibility and take appropriate measures, including surgical resection if necessary during seasonal epidemics. For candidal esophagitis, antifungal medications such as nystatin or amphotericin B should be used first.
3. Esophageal Manometry From the esophageal manometry curve, it can be observed that the lower esophageal sphincter loses its normal wavy pattern—a curve wave that is initially low-pressure followed by high-pressure (caused by the lower esophageal sphincter's initial relaxation and post-relaxation contraction)—and instead becomes an irregular, unevenly spaced waveform curve rising from the baseline with normal or elevated pressure. Occasionally, irregular low-pressure curves of shorter duration than normal may be seen. The esophageal body loses the rhythmic peristaltic contraction waves that normally occur during swallowing, instead exhibiting tertiary contractions or very low-amplitude pressure waves. When the esophagus is extremely dilated, these may not even be recordable. In cases of vigorous achalasia, the pressure waves are repetitive, not sequential from top to bottom, and spontaneous, with amplitudes that may be normal or abnormally high, possibly due to solid or liquid retention in the esophageal lumen. The resting pressure of the esophagus increases from the normal atmospheric pressure to 2.67 kPa (20 mmHg), equaling the pressure in the gastric fundus.
bubble_chart Treatment Measures
1. Principles of Treatment Currently, there are three methods for treating this condition: medication, dilation, and esophageal myotomy. Regardless of the method, the goal is to alleviate the resistance caused by the failure of the lower esophageal sphincter to relax, its lack of coordination, and its spasmodic contractions, thereby facilitating esophageal emptying.
2. Medical Treatment There are few medications available for treating achalasia. The more effective ones are nitrates and heart pain medication, whose pharmacological action is to reduce the pressure of the lower esophageal sphincter, aiding esophageal emptying. However, their effects are short-lived, and they may be ineffective or poorly effective for some patients. In such cases, dilation or myotomy must be considered.
3. Dilation Therapy Esophageal dilation for achalasia has long been widely used. With advancements in technology, dilation techniques have continuously improved and innovated, moving toward higher efficiency, safety, and comfort, expanding their applicability. Except for cases with concurrent esophagitis, this procedure can be performed on almost all patients. In cases of esophagitis, the inflamed mucous membrane becomes fragile and prone to tearing, leading to perforation. Therefore, it is safer to first control the inflammation medically before performing the procedure. On the night before the procedure, the patient should fast and cleanse the esophagus, using a thick gastric tube to rinse and remove residual food to prevent aspiration during the procedure and facilitate observation. To improve the efficacy of dilation, in addition to the traditional olive-tip dilators, pneumatic or hydrostatic forced dilation is now used, transforming the previously short-lived effects requiring repeated dilation into long-term symptom relief. Under fluoroscopic guidance, an esophagoscope and guidewire are used to safely place the dilator, effectively preventing perforation risks. Preoperative atropine, appropriate sedatives, and analgesics are administered. Under local anesthesia and fluoroscopy, the pneumatic or hydrostatic dilator is inserted into the esophagus, positioning the dilation balloon across the esophagogastric junction before applying pressure. The effectiveness of dilation determines whether a second or multiple sessions are needed.
Pneumatic dilation is relatively safe, with only a few cases of perforation or bleeding, usually minor, presenting as hematemesis or melena. Aspiration and gastroesophageal reflux (often occurring after repeated dilations) may also occur. The most severe complication is esophageal perforation, with an incidence of about 3%. Perforations can be classified as acute or subacute based on timing. Acute perforations occur immediately post-procedure. Clinically, if persistent pain worsens or fails to subside within an hour after dilation, perforation should be suspected. Symptoms such as dyspnea and subcutaneous emphysema should prompt a chest X-ray; if mediastinal emphysema or hydropneumothorax is detected, the diagnosis is confirmed. Swallowing contrast medium revealing extravasation confirms the diagnosis. Once diagnosed, immediate surgical repair is required. Perforations typically occur on the posterior lateral wall of the lower esophagus, requiring fistula repair followed by myotomy on the opposite wall to prevent postoperative reflux esophagitis. Anti-reflux procedures may also be performed. Subacute perforations are detected later, often presenting as mediastinal abscesses or empyema, requiring drainage. If occult perforation is suspected or confirmed by esophagography without abscess or empyema, conservative treatment with antibiotics, fasting, IV fluids, and nasogastric tube feeding is initiated. If symptoms resolve or perforation heals within a week, oral intake can resume.
4. Esophageal Myotomy This surgery aims to relieve the non-relaxing lower esophageal sphincter, effectively improving esophageal emptying. It is simple, easy to perform, has few complications, and low mortality, making it suitable for all ages. Since the 1950s, it has been a standard treatment for achalasia.
(1) Surgical Indications
(1) Severe achalasia requires a more aggressive esophageal myotomy to relieve symptoms.
(2) Cases where long-term conservative therapy is ineffective.
(3) Severe achalasia with significant esophageal dilation and severe curvature, making dilatation difficult and risky, or when dilatation is impossible or fails.
(4) Frequent severe aspiration pneumonia.
(5) Infants, young children, adolescents, or patients with vigorous achalasia who can achieve good long-term outcomes.
(6) Patients who cannot tolerate or are unwilling to undergo repeated dilatation therapy.
(2) Surgical Contraindications
(1) Severe cardiopulmonary insufficiency.
(2) Complicated by advanced-stage esophageal cancer.
(3) Preoperative Preparation
(1) Correct typical edema and electrolyte imbalances.
(2) Fully treat pulmonary complications and wait for the acute phase to subside.
(3) In cases of severe retention esophagitis, the mucosa and submucosal tissues are fragile and prone to perforation. Medical treatment for 3–4 weeks is required, and surgery should only be considered after endoscopic confirmation of mucosal healing.
(4) Administer metronidazole 0.2g orally three times daily for 3 days before surgery to cleanse the esophagus.
(5) Place a non-side-hole gastric tube the night before surgery and on the morning of the procedure to remove accumulated food, debris, and secretions from the esophagus. Retain the gastric tube to reduce the risk of aspiration during anesthesia induction.
(6) Administer a sedative intramuscularly the night before surgery.
(4) Choice of Incision: The approach for esophageal myotomy includes transthoracic and transabdominal routes. Sometimes the transthoracic approach is preferable, sometimes the transabdominal, and occasionally both are suitable. Correctly selecting the incision is crucial for surgical success.
(1) Transthoracic Approach: The transthoracic incision provides better exposure of the cardia compared to the abdominal incision, making muscle layer incision and dissection easier and more thorough. It allows for a longer myotomy, with unrestricted upper muscle layer incision and fewer risks of mucosal injury. This is especially beneficial for patients with fragile scar tissue at the lower esophagus. The diaphragmatic esophageal hiatus remains uninjured, preventing postoperative diaphragmatic hernia. It also allows for a broader selection of anti-reflux techniques and concurrent treatment of associated conditions such as esophageal leiomyoma, diverticulum, or cancer.
(2) Transabdominal Approach: The abdominal incision offers simplicity, minimal injury, and faster postoperative recovery. It is less risky for elderly or frail patients and allows for abdominal examination and concurrent treatment of any detected pathologies. However, exposure can be challenging, especially in obese patients. Extensive dissection in the cardia region may not provide sufficient visibility. Due to limitations in the upper muscle layer incision, dissection of the cardia is often necessary, potentially compromising its structure and leading to reflux. Thus, an anti-reflux procedure like Nissen fundoplication must be considered. However, in achalasia with absent esophageal peristalsis, a full fundoplication may cause excessive obstruction.
(5) Surgical Methods
(1) Transthoracic approach esophageal myotomy: The surgery is performed through the 7th or 8th intercostal space via a posterolateral thoracotomy. The lung is pushed forward and upward, and the inferior pulmonary ligament is divided until the inferior pulmonary vein is reached. The mediastinal pleura is incised longitudinally, carefully preserving the vagus nerves. The proximal end extends to the aortic arch, while the distal end reaches the diaphragm. The esophagus is exposed, freed, and lifted with a gauze tape. The abdominal segment of the esophagus and a short portion of the gastroesophageal junction are pulled into the thoracic cavity, usually without the need to incise the hiatus. In rare cases where the gastroesophageal junction cannot be pulled into the thoracic cavity, a small incision can be made on the anterolateral part of the hiatus. However, after completing the myotomy, this incision must be sutured closed to prevent herniation of abdominal contents into the thoracic cavity. Holding the esophagus with the left hand, a small longitudinal incision is made in the esophageal muscle layer between the left and right vagus nerves, down to the submucosal layer. A blunt-tipped forceps is then used to extend the myotomy upward and downward through blunt dissection. The proximal end of the myotomy should extend at least 2 cm beyond the narrowed segment of the esophagus, while the distal end should reach the gastroesophageal junction and extend slightly onto the gastric wall, not exceeding 1 cm (a few millimeters is sufficient). A small transverse vein at the gastroesophageal junction serves as a landmark; the incision must not extend beyond this vein to avoid postoperative reflux. After completing the myotomy, the incised muscle edges are freed laterally to cover at least half or more of the esophageal circumference. This ensures that the esophageal mucosa naturally bulges out from the incision, reducing the likelihood of postoperative scarring and re-adhesion of the myotomy. Some authors advocate removing a strip of the freed muscle flap. Throughout the procedure, care must be taken to protect the vagus nerves and avoid perforating the mucosa. Once the myotomy is completed, air is injected through a gastric tube to test for mucosal perforation. If no fistula is confirmed, meticulous hemostasis is performed, even for minor bleeding points, to prevent clot organization and subsequent stricture. After these steps, the esophagus is repositioned in the mediastinum, restoring the gastroesophageal junction to its normal intra-abdominal location. The mediastinal pleura is closed with interrupted sutures, a closed drainage tube is routinely placed, and the thoracotomy is closed.
(2) Transabdominal esophageal myotomy: A longitudinal midline incision or left paramedian incision is made between the xiphoid process and the umbilicus. The triangular ligament is divided, and the left lobe of the liver is retracted downward and to the right to expose the cardia and the diaphragmatic hiatus. The peritoneum covering the abdominal segment of the esophagus is incised, and the esophagus is mobilized. A tape is passed around the distal esophagus and pulled downward to expose the area between the vagus nerves. The esophageal muscle layer is then incised, with the method being largely similar to that of transthoracic esophageal myotomy. Due to the deep position of the esophagus and poor exposure, extending the myotomy proximally over a longer segment is more challenging.
(3) Transthoracic esophageal myotomy combined with anti-reflux procedure: After completing the esophageal myotomy, the tape around the esophagus is pulled upward to elevate the esophagus from the posterior mediastinum. The attachments of the hiatus at the gastroesophageal junction are divided, along with the anterior reflection of the phrenoesophageal membrane, the posterior peritoneum, fat, and the abdominal cavity. The gastroesophageal junction is freed from its diaphragmatic attachments, and the ascending branches of the left gastric artery and the branches of the inferior phrenic artery are ligated and divided. At this point, the entire gastroesophageal junction and part of the gastric fundus can be pulled into the thoracic cavity, and the fat pad at the gastroesophageal junction is excised.
Construction of the Mark IV anti-reflux procedure: The anterior part of the hiatus is retracted to expose the tendinous portion of the right crus of the diaphragm. Four thick sutures are placed posterior to the esophagus through the hiatus but are not tied yet. The distal 5 cm of the esophagus is wrapped by the gastric fundus for two-thirds of its circumference. The fundus is fixed in two rows of interrupted mattress sutures, placed 2 cm and 5 cm away from the gastroesophageal junction, respectively. After tying the second row of sutures, the sutures are not cut but are instead passed from the abdominal side to the thoracic side through the tendinous portion of the diaphragm on both sides. The anti-reflux mechanism is positioned below the diaphragm, and the two sutures are tightened and tied. Finally, the four crural sutures are tied, leaving a gap in the hiatus wide enough to admit one finger. A closed drainage tube is placed, and the thoracotomy is closed layer by layer.
(4) Transabdominal esophageal myotomy combined with anti-reflux procedure: After completing the esophageal myotomy, three to four thick sutures are placed in the right crus of the diaphragm posterior to the esophagus.
(6) Surgical complications and preventive measures
(1) Symptoms not relieved; Persistent dysphagia after myotomy or early recurrence is often due to inadequate myotomy, residual circular muscle fibers, or small vessels outside the submucosa not being divided, resulting in incomplete natural bulging of the submucosa. This situation can be detected during surgery by carefully examining the esophagus after myotomy and freeing it, then inflating the submucosa like a tire using a side-hole-free gastric tube. If any circular muscle fibers or small vessels remain uncut, even just a few strands, they can form a constricting band or strip causing obstruction, which should be completely divided during the operation. Additionally, if the myotomy length is insufficient, or the narrowed area at the cardia is not fully released, or the proximal esophageal stricture is not completely relieved, the myotomy may be too low if performed via the abdomen, or if performed via the chest, it may fail to reach the esophagogastric junction while preserving the normal anatomical relationship between the cardia and the hiatus. To address insufficient myotomy length, it is essential to strictly follow the guideline that the proximal end of the myotomy should extend at least 2 cm above the transition line between the narrowed and dilated esophagus, while the distal end should reach 1 cm beyond the esophagogastric junction, using the small vein anterior to the cardia as a landmark. Another reason for unresolved symptoms is adhesion and healing of the myotomy edges. Therefore, during surgery, the muscle flaps must be dissected beyond half the circumference of the esophagus, and hemostasis must be thorough—even minor bleeding points should be addressed. Only after confirming no active bleeding should the chest be closed, with effective drainage established. Accidental injury to the vagus nerve during surgery can lead to pyloric spasm, impairing gastric emptying and increasing reflux. An effective preventive measure is to identify and isolate the vagus nerve, marking it with a tape. When incising the mediastinal pleura, stay close to the pleura to avoid cutting too deep and damaging the vagus nerve. Blunt dissection is preferred when freeing the esophagogastric junction. Lastly, another cause of unresolved symptoms is misdiagnosis, such as mistaking reflux esophagitis-induced peptic stricture for achalasia.
(2) Symptom recurrence after esophageal myotomy; After a symptom-free period following esophageal myotomy, symptoms may reappear due to insufficient myotomy or re-healing, post-inflammatory scar formation around the esophagus, fibrosis caused by scarring leading to retention esophagitis, postoperative reflux resulting in reflux esophagitis and subsequent stenosis, or complications such as cancerous obstruction. Most patients with "S"-shaped tortuous esophageal dilation may experience improvement after surgery, but the outcomes are poorer compared to those with milder conditions. This is due to further degeneration of neuromuscular function, exacerbating achalasia and causing symptom recurrence. Persistent symptoms or postoperative recurrence require objective examination to determine the cause. Depending on the findings, medical treatment or dilation therapy may be attempted. Surgery is considered only if these methods fail. Preoperative preparation for esophageal resection and colonic reconstruction is essential, as some underlying causes may only be identified during intraoperative exploration. If the original myotomy was insufficient or has healed, the incision may be extended or a new myotomy performed. For cancerous obstruction, esophageal resection is necessary. For "S"-shaped dilation and tortuosity, a cervical and abdominal incision with esophageal stripping and cervical esophagogastric anastomosis is required. For peptic stenosis, some authors perform distal esophageal and gastric fundus side-to-side anastomosis via the abdomen, combined with complete fundoplication. Alternatively, resection of the stenotic segment or interpositional intestinal graft reconstruction may be performed.
(3) Mucosal perforation; Mucosal perforation may occur during myotomy or lateral esophageal dissection due to inadvertent cuts, electrocautery for hemostasis, or postoperative severe vomiting. Therefore, during myotomy, haste should be avoided. Carefully split the esophageal sides with a vertical blade, cutting and separating gradually to clearly visualize the tissue being incised. When nearing the submucosal layer, slightly tilt the blade to reduce its sharpness, preventing deep penetration that could lead to uncontrollable perforation. During lateral dissection, inflammatory adhesions may pose challenges. Dissection should stay close to the outer muscular layer of the mucosa, leaving small muscle fragments rather than risking mucosal breach. After most of the dissection is complete, remove these fragments for safer outcomes. For mucosal bleeding, finger pressure is preferable to electrocautery or suturing, as the latter increases perforation risk. If a fistula is detected intraoperatively, repair it with atraumatic sutures. Shao Lingfang advocates inverting the mucosa and tying knots intraluminally. A commonly overlooked sign is localized mucosal bulging resembling a diverticulum during air insufflation, indicating excessive thinning and impending perforation. In such cases, reinforcing the area with surrounding tissue is crucial. Postoperatively, gastrointestinal decompression and avoiding vomiting are essential, with delayed oral intake. If a fistula is confirmed within 12 hours, immediate surgical repair is advised. If delayed and empyema has formed, closed thoracic drainage or open wound management is necessary until spontaneous healing occurs.
(4) Esophageal hiatal hernia and diaphragmatic hernia; Hiatal hernia occurs when the hiatus is inadvertently incised or its supporting structures are damaged during esophageal myotomy, leaving the defect unaddressed. Increased abdominal pressure may push abdominal contents through the hiatus into the thorax, retracting upon pressure reduction. Prevention involves suturing the left and right diaphragmatic crura posteriorly with thick silk sutures (3–4 stitches) to narrow the hiatus, followed by fixing the cardia and esophagus to the diaphragm with additional sutures.
Diaphragm hernia occurs when the diaphragm is incised during esophageal myotomy or anti-reflux procedures without proper repair, or when sudden increases in intra-abdominal pressure due to severe coughing or vomiting cause the sutures to loosen. During the procedure, manual exploration should be performed to check for any gaps or weak areas, which should be reinforced immediately. If a hiatal hernia or diaphragm hernia is confirmed postoperatively, it should be repaired. If incarceration is suspected, surgical exploration is necessary.
(5) Reflux esophagitis: Postoperative manifestations of reflux or reflux esophagitis, such as retrosternal pain or a burning sensation in the upper abdomen, acid regurgitation or hematemesis, inability to bend forward or lower the head after eating, and even refusal to eat due to pain. Esophagoscopy often reveals localized congestion, edema, erosion, or superficial ulcers in the lower esophagus. Preventive measures: During surgery, the integrity of the diaphragmatic esophageal hiatus and the esophageal diaphragmatic ligament should be maintained; the vagus nerve should be protected; the length of the myotomy should strictly adhere to the prescribed landmarks, and the lower end should not extend beyond the small transverse veins on the gastric wall beneath the submucosa. Ellis firmly believed that as long as the length of the gastric wall myotomy is strictly controlled, additional anti-reflux surgery is unnecessary. However, he also pointed out that for patients with concurrent ulcer disease, performing only a myotomy without additional acid-reducing surgical methods is inappropriate. Most scholars agree that enhancing the anti-reflux mechanism is necessary, but there is still controversy over the method of wrapping the esophagus 360° with an obstructive mechanism.
(7) Surgical outcomes: The postoperative mortality rate for this condition is extremely low, with the vast majority of authors reporting no postoperative deaths, indicating that the Heller procedure is a safe surgery. The ideal surgical outcome should ensure esophageal emptying without gastroesophageal reflux and provide long-term symptom relief. Factors affecting the outcome, aside from surgical technique, include the natural remission phase of the disease and the progressive worsening due to neuromuscular degeneration. Additionally, the surgery only relieves the obstruction at the cardia, while the effective peristalsis of the esophagus is not restored, so symptoms may still occur with rapid swallowing postoperatively. The severity of the disease also impacts the efficacy. In cases of excessive esophageal dilation, severe muscular fibrosis, or tight submucosal adhesions, even after myotomy relieves the obstruction, the dilated esophagus may not return to its original diameter, remaining twisted and enlarged. Without effective peristalsis as a propulsive pump, emptying disorders persist, making symptom recurrence unsurprising. Therefore, while symptoms may improve in advanced-stage patients, the outcomes are often not excellent. In contrast, surgery rarely fails in patients with mild symptoms, highlighting the benefits of early surgical intervention for better outcomes. Bingben The disease's natural remission phase and the progressive worsening due to neuromuscular degeneration also play a role. Moreover, the surgery only addresses the obstruction at the cardia, without restoring effective esophageal motility. Thus, rapid swallowing postoperatively may still cause symptoms. The severity of the disease further affects outcomes. In cases of excessive esophageal dilation, severe muscular fibrosis, or tight submucosal adhesions, even after myotomy relieves the obstruction, the dilated esophagus may not return to its original diameter, remaining twisted and enlarged. Without effective peristalsis as a propulsive pump, emptying disorders persist, making symptom recurrence unsurprising. Therefore, while symptoms may improve in advanced-stage patients, the outcomes are often not excellent. In contrast, surgery rarely fails in patients with mild symptoms, highlighting the benefits of early surgical intervention for better outcomes.
(8) Achalasia is a benign disease with an unclear etiology. Current treatments, including medication, dilation, and surgery, are symptomatic. Drug therapy is ineffective and short-acting, with only two effective medications available. Thus, the primary effective treatments for this condition are esophageal dilation and surgery.
Various anti-reflux mechanisms have been developed based on the Heller procedure, such as gastric fundoplication, vagotomy and pyloroplasty, the Nissen fundoplication (360° wrap or partial 2/3 wrap), and the Mark IV procedure, each with its own applications and effectiveness in controlling reflux. Concerns have been raised that the Nissen procedure's 360° wrap might cause physiological obstruction. Some evidence suggests that short-term 360° wrapping does not cause obstruction, but whether it impairs esophageal emptying as achalasia worsens with neuromuscular degeneration requires further long-term investigation.
