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While most patients’ symptoms are satisfactorily controlled with PPIs and other medications, surgery remains an important option. The indications for surgery include (i) incomplete symptom control with medical management, (ii) intolerance of, or unwillingness to comply with, long-term medical therapy, (iii) regurgitation despite medication (less well amenable to PPI), (iv) presence of a large hiatus hernia, (v) complications arising from GORD, and (vi) extraoesophageal symptoms. The predictors of good surgical outcome include typical GORD symptoms, PPI responders, presence of hiatus hernia and presence of GORD complications, e.g. reflux oesophagitis (grade B or above) and non-dysplastic Barrett’s oesophagus. Factors leading to poor surgical outcomes are normal preoperative pH monitoring when performed off PPI, functional heartburn, EOO, connective tissue diseases and extreme obesity.
Recommendations from different society guidelines are summarised in Table S66.1.
TABLE S66.1 Guidelines for surgery for gastro-oesophageal reflux disease (GORD) from different societies.
American Society for Gastrointestinal and Endoscopic Surgeons (SAGES) 2010
When the diagnosis of reflux is objectively confirmed, surgical therapy should be considered if:
UK National Institute for Health and Care Excellence (NICE) 2014
Confirmed diagnosis of acid reflux and adequate symptom control with acid suppression therapy, but the patient
American College of Gastroenterology (ACG) 2013
Asian Pacific Consensus 2008/2016
International Consensus (ICARUS) 2019
Careful preoperative counselling is essential. Risks of anti-reflux surgery include a small mortality rate (0.1–0.5%), failed operation (5–10%) and side effects such as dysphagia, gas bloat or abdominal discomfort (10%). When performed well in appropriately selected patients, 80–90% of patients should be satisfied with the result of the operation.
Antireflux operations have three essential components: (i) restoration of an intra-abdominal segment of the esophagus, (ii) crural repair, and (iii) some form of reinforcement of the LOS by the upper stomach (fundoplication) or by a prosthesis placed around the intra-abdominal oesophagus.
The major types of antireflux operations were all developed in the 1950s. For many years, the relative merits of thoracic and abdominal approaches were hotly debated. With the introduction of laparoscopy, laparoscopic fundoplication with hiatal reconstruction is the standard approach. The mechanism of fundoplication is to create a ‘floppy’ valve around the OGJ and to restore the angle of His. It has the effect of increasing LOS basal pressure, lessening TLOSR and reducing the capacity of the gastric fundus, thereby enhancing gastric emptying. The different types of fundoplication have been compared extensively in clinical trials but the superiority of one over the others could not be shown.
Complete fundoplication (Nissen) is associated with a higher incidence of short-term dysphagia but is most durable in reflux control. Partial fundoplication, whether performed posteriorly (Toupet) or anteriorly (Dor, Watson), has fewer short-term side effects, although this is at the expense of a slightly higher long-term failure rate (Figure 66.16).
The most common side effect of fundoplication is short-term dysphagia, related presumably to tissue oedema and inflammation. It usually resolves within 3 months of surgery.
Figure 66.16a, b
Examples of various types of fundoplication. (a) Normal anatomy. (b) Nissen 360° fundoplication.
Some patients may experience ‘gas-bloat syndrome’, especially after a complete fundoplication. Typically, the patient would complain of gaseous distension of the abdomen and failure to belch or vomit, together with an increase in flatulence.
In the last decade, a magnetic prosthesis has become available to reinforce the LOS after hiatal reconstruction This has a similar efficacy to fundoplication in the mid-to long term and has fewer gas-bloat side effects. The magnetic ring pros- thesis consists of titanium-coated magnetic beads, connected by titanium wire. The physics of the magnets allows a lower attraction force when the beads are separated. This property of ‘relaxation’ is a more physiological sphincter to allow food passage and is less likely to create oesophageal outflow obstruction. This device is contraindicated in patients with major motility disorders, ineffective oesophageal motility or connective tissue disease.
- HRM and pH monitoring are recommended investigations before consideration of surgical treatment
- pH monitoring confirms GORD and HRM assesses oesophageal body function and LOS characteristics
- Surgery should be tailored to oesophageal motility
Typically, five operating ports are inserted into the upper abdomen (Figure S66.1). The lesser omentum is incised, safeguarding any sizeable replaced left hepatic artery. The phreno-oesophageal ligament is divided to expose the cardia and lower oesophagus. The right and left crura are isolated and the abdominal oesophagus is slung for retraction. The gastric fundus is mobilised by dividing the short gastric vessels. Crural repair is first performed. In a Nissen fundoplication, the fundus is drawn behind the oesophagus and then sutured to itself in front of the oesophagus. In partial fundoplication, the fundus is drawn either behind or in front of the oesophagus and sutured to it on each side with or without anchoring to the apex of the hiatal opening/right crus, leaving a strip of exposed oesophagus either at the front or at the back. The tightness of the fundoplication or crural repair is not standardised. It is advocated to have a ‘floppy’ fundoplication to prevent dysphagia or gas-bloat syndrome. In some centres, a size 50–60Fr bougie is inserted before the creation of fundoplication to avoid too tight a wrap. The issue of oesophageal shortening continues to provoke debate. There can be no doubt that, in the presence of a large sliding hiatus hernia, the oesophagus is short, but with extensive mobilisation from the mediastinum, in most cases, it can be restored to its normal length. The extent to which severe inflammation in the wall of the oesophagus causes fibrosis and real shortening is less clear. If a good segment of the intra-abdominal oesophagus, usually at least 2–3 cm, cannot be restored without tension, an ‘oesophageal lengthening procedure’ should be performed (Figure S66.2). This produces a neo-oesophagus, around which a fundoplication can be done (Collis–Nissen operation). The hiatus can now be reconstructed or narrowed by non-absorbable braided sutures, placed behind the oesophagus. Whether a mesh should be placed to reinforce the hiatal closure is controversial.
For magnetic sphincter augmentation, after crural repair, a window is created between the posterior vagus nerve and the abdominal oesophagus, around 2 cm above the OGJ. A sizing device is then used to estimate the suitable number (13–17) of magnetic beads required. The appropriately sized device is inserted through this window and encircled around the abdominal oesophagus. With that, the anatomy of the fundus and the stomach is not disturbed, and the sizing protocol is more standardised.
Typical port sites used for laparoscopic fundoplication. The blue dots indicate the operating ports. The epigastric port is used to place a liver retractor. The two bilateral subcostal ports are used for dissecting instruments. The left lateral port is used for the assistant’s retraction. The horizontal line in the left paramedian location is the site of the camera port. In smaller patients, a subumbilical wound can be used for the camera port for better cosmesis (dotted line).
A Collis gastroplasty for oesophageal lengthening. (a) A transverse cut is made on the fundus of the stomach, then extended upwards parallel to the oesophagus. An extra length of ‘neooesophagus’ is thus made.
Complications of Antireflux Surgery and Revisional Surgery
Structurally, a wrap can be too tight or too loose. It can also be partially or completely disrupted, herniated or slipped. Structural laxity can give rise to recurrent or persistent GORD. Too long or too tight a fundoplication can give rise to dysphagia and gas-bloat syndrome. Endoscopy, contrast radiography and functional testing can assess the anatomy responsible and guide further management.
Overall, structural complications increase over time and can be classified by the Hinder and Horgan classifications (Figure S66.3).
The Hinder classification of complications post fundoplication. (a) Type I, disruption of wrap.
The Hinder classification of complications post fundoplication. (c) Type III, stomach slippage below the diaphragm. The slippage of the proximal stomach through the unbroken wrap creates a pouch below the diaphragm without recurrence of hiatus hernia.
Management strategies include a PPI for recurrent acid reflux, endoscopic dilatation of stenosis and surgical revision as a last resort. A tight complete fundoplication can be remedied by conversion to a partial fundoplication. For patients with anatomical failure and refractory symptoms, revisional surgery carries a lower chance of success; in some patients, local revision is technically impossible, as often there will be adhesion formation and altered anatomy. Transient dysphagia is common after both fundoplication and magnetic sphincter augmentation. For the latter, there may be more prolonged dysphagia requiring dilatation or, rarely, migration and ero- sion (0.15%). Removal of the device is required in 2.7% of patients; the majority can be accomplished endoscopically or laparoscopically.
Complex Gastro-oesophageal Reflux Disease
Peptic strictures and dilatation
Reflux-induced strictures are relatively rare in the era of PPIs as most patients will be treated empirically before long-term complications occur. These strictures generally respond well to dilatation and long-term treatment with a PPI. Antireflux surgery is an alternative to long-term PPI treatment, just as in uncomplicated GORD. Most patients do not require anything other than a standard operation.
Hiatus hernia and paraoesophageal (‘rolling’) hernia
Hiatus hernia is a condition in which the abdominal contents migrate through the hiatal opening of the diaphragm into the mediastinum. There are four types of hiatus hernia (Figure 66.18): (i) the sliding hernia (type I), accounting for most hiatus hernias (85–95%), where the OGJ is herniated upwards; (ii) the true paraoesophageal/rolling hernia (type II), where there is asymmetrical herniation of the stomach next to the oesophagus and the OGJ remains in its normal intra- abdominal position (this is relatively uncommon); (iii) the more common mixed sliding and paraoesophageal hernia (type III); and (iv) when abdominal viscera other than the stomach migrate into the hernia sac, it is classified as type IV. Hiatus hernia is closely related to advanced age and obesity.
A sliding hiatus hernia predisposes to GORD and is usually diagnosed in the presence of reflux symptoms. For asymptomatic patients, it can be an incidental finding on plain chest radiographs or CT as an intrathoracic gas bubble or fluid level (Figure 66.19). A paraoesophageal hernia, especially when large, presents more with obstructive symptoms. The term ‘giant paraoesophageal hernia’ is present when more than half of the stomach has herniated into the thoracic cavity (Figure 66.20). This may present as a surgical emergency if gastric volvulus occurs. It is more common for the stomach to rotate along its longitudinal axis, termed organoaxial volvulus. When the stomach rotates around the transverse axis, it is called mesentericoaxial volvulus.
Gastric volvulus can produce symptoms such as dysphagia and chest pain. In severe cases, it can cause obstruction, strangulation, ischaemia, perforation and compression on the lungs, leading to impaired lung function. Emergency presentation and operation with any of these complications carries a high morbidity rate on account of a combination of late diagnosis, advanced patient age, comorbidities and the complexity of surgery involved. Therefore, all symptomatic paraoesophageal hiatus hernias should be repaired. The decision to repair an asymptomatic paraoesophageal hernia needs to balance risk with the patient’s age and comorbidities, as the annual risk of developing acute symptoms requiring emergency surgery is probably less than 2%.
Patients who present acutely should first be resuscitated, followed by nasogastric tube decompression. Immediate surgery is needed if there is suspicion of ischaemia, perforation or unresolved obstruction. The surgical principle is similar to that of sliding hiatus hernia repair but more technically demanding. The steps include reduction of any herniated organ, extensive mediastinal dissection to restore the intra- abdominal length of the oesophagus, excision of the hernia sac to prevent a recurrence, repair of the crura in a tension-free manner and some form of fixation of the stomach in the abdomen.
Manoeuvres such as oesophageal lengthening and a diaphragmatic relaxing incision with mesh may also apply. Some surgeons perform a fundoplication as an effective means of maintaining reduction and dealing with the associated GORD at the same time. Some prefer anterior gastropexy or placement of a gastrostomy tube to prevent a recurrence. Laparoscopic or robotic-assisted repair has become popular. Full anatomical repair of a large rolling hernia can be difficult and requires considerable expertise. Even in expert hands, the anatomical recurrence rate can be as high as 46%, though not all are symptomatic.
Chest radiograph showing a gastric bubble in the lower mediastinum behind the heart corresponding to a hiatus hernia.
- Type I sliding hernia predisposes to GORD
- Types II/III/IV paraoesophageal hernia present mainly with obstructive symptoms
- Volvulus and strangulation require emergency surgical treatment
Diagnosis and definitions
Barrett’s oesophagus is a known complication of GORD. First described in 1950 as peptic ulceration in a tubular organ lined by columnar epithelium, it was interpreted as an intrathoracic tubular stomach with a congenitally short oesophagus. Later it was correctly identified as ‘oesophagus lined with a gastric mucous membrane’. Currently, the commonly agreed definition of Barrett’s oesophagus is the proximal migration of columnar epithelium (salmon-coloured mucosa) in the lower oesophagus extending more than 1 cm above the OGJ. The additional criterion of the biopsy-proven presence of mucus-secreting goblet cells or intestinal metaplasia is controversial.
The American Gastroenterology Association 2011 position statement and the American College of Gastroenterology 2016 guideline required biopsy confirmation of intestinal metaplasia as mandatory because it is the only type of oesophageal columnar epithelium that predisposes to malignancy. On the other hand, the British Society of Gastroenterology guideline 2014 and the Asia-Pacific consensus 2016 both addressed the importance of intestinal metaplasia as a clinical consideration for guiding treatment and surveillance. However, this was not included in the definition because of the possibility of sampling error and the lack of reliable markers to distinguish between intestinal metaplasia of the cardia and oesophagus. Therefore, endoscopy plays an important role in the diagnosis, identifying the important anatomical landmarks and taking accurate biopsies for histological assessment.
Endoscopically, the OGJ is defined as the proximal end of the longitudinal gastric folds under minimal air insufflation. It should not be confused with the diaphragmatic hiatal pinch or the squamocolumnar junction. The Prague C&M Classifica- tion for Barrett’s length is based on validated, explicit, consensus-driven criteria, including assessment of the circumferential (C) and maximal (M) extent of the endoscopically visualised Barrett’s segment (Figure 66.21). The length of Barrett’s oesophagus is a risk factor for developing neoplasia.
Prague C&M criteria to report endoscopic Barrett’s oesophagus. The location of the oesophagogastric junction is defined by the top of the gastric folds (36 cm). Prague criteria of Barrett’s oesophagus are expressed in C (circumferential), in this case 33–36 cm (3 cm), and M (maximum extent), in this case 28–36 cm (8 cm). This patient therefore has Prague C3 M8 Barrett’s oesophagus.
When Barrett’s oesophagus is discovered, the treatment is that of the underlying GORD. Pharmacological therapy generally is the same as treatment of symptomatic GORD patients. Antireflux surgery is indicated if it is associated with GORD symptoms. A randomised trial suggested that aspirin, as a chemoprevention agent, in combination with a high-dose PPI, may improve outcomes in patients with Barrett’s oesophagus measured by progression to cancer and mortality.
In patients with dysplastic Barrett’s oesophagus without suspicion of invasive cancer, the epithelium can be ablated or resected. Indication for such procedures in non-dysplastic Barrett’s oesophagus is controversial. Ablative therapy aims to completely eradicate all intestinal metaplasia. When the mucosa regenerates after ablation in a non-acidic environment (when a high-dose PPI is prescribed), a ‘neosquamous’ lining is formed. Ablative approaches that are supported by evidence include photodynamic therapy, RFA and cryotherapy. Among these methods, RFA is most popular because there is evidence of its effectiveness, cost and side-effect profile. EMR by the cap method or multiband technique can be done to remove the whole segment of the mucosa. When this is applied to circumferential Barrett’s oesophagus, the stricture rate is high when healing occurs. The procedure can be performed in stages, allowing mucosal healing to occur first in one half of the oesophagus before a second stage to remove the other half, thus lessening the chance of stenosis. In contrast, the incidence of stricture formation is low following RFA, because the depth of ablation extends to the muscularis mucosae only (S66.4a-f).
Endoscopic ablation should only be applied to flat lesions without nodularity, ulceration or irregular contour. Such features are suggestive of invasive neoplasm that should be investigated and treated by EMR or endoscopic submucosal dissection (ESD). ESD, though more technically demanding, provides en bloc resection of the index lesion with better margins for histological diagnosis. EMR is easier and large areas can be resected in a piecemeal manner. If histological examination of the resected tissue demonstrates the absence of invasive cancer, or T1a tumour, only the ‘biopsies’ can be regarded as curative. When T1b lesions are found on histology, or when the resection margins (lateral or deep) are involved, additional therapy including oesophagectomy should be considered. Regardless of treatment performed, the patient should enter a surveillance programme to detect recurrent or persistent Barrett’s oesophagus or neoplasia.
Radiofrequency ablation (RFA) of Barrett’s oesophagus.
(a) A 90° probe
used to ablate small patches of Barrett’s oesophagus.
Radiofrequency ablation (RFA) of Barrett’s oesophagus.
(b) Short segment of Barrett’s mucosa on white light endoscopy.
Radiofrequency ablation (RFA) of Barrett’s oesophagus.
(d) Ablation using the RFA probe; the mucosa appears white.
Radiofrequency ablation (RFA) of Barrett’s oesophagus.
(e) The ablated mucosa has been scraped away using the probe, revealing a raw area.
Radiofrequency ablation (RFA) of Barrett’s oesophagus.
(f) Barrett’s ablation by a circumferential RFA catheter. Top panels show inflation of the RFA balloon
so that the electrodes are in opposition to the oesophageal mucosa. Bottom panels
show that the mucosa has been ablated (appears white in colour); it is then scraped off
using a hood mounted on the end of the endoscope. The right bottom panel shows the
final raw area after the mucosa has been ablated and scraped off.
Motility Disorders and Diverticula
Pathology and aetiology
The term achalasia originated from the Greek word ‘khalasis’, meaning ‘failure to relax’. It is uncommon, with a prevalence of 1.8–12.6 per 100 000 persons per year. The aetiology remains uncertain but is postulated to be due to loss of the inhibitory ganglion cells in the myenteric (Auerbach’s) plexus, possibly related to a virus-induced autoimmune effect. Histology of muscle specimens generally shows a reduction in the number of ganglion cells with a variable degree of chronic inflammation. During a normal swallow, the food bolus will trigger primary peristalsis in the oesophagus by sequential activation of excitatory lower motor neurones. At the same time, relaxation of the LOS allows oesophageal emptying. The mismatch in excitatory and inhibitory activity results in the failure of LOS relaxation and absent peristalsis. With time, the oesophagus dilates and contractions disappear, so that the oesophagus empties mainly by the hydrostatic pressure of its contents. This is nearly always incomplete, leaving residual food and fluid. The air-fluid level in the stomach evidenced on radiography taken in the erect position in normal individuals is frequently absent, as no bolus with its accompanying air passes through the LOS. The oesophagus becomes progressively more tortuous and dilated (megaoesophagus); persistent retention oesophagitis due to fermentation of food residues may predispose to the increased incidence of carcinoma of the oesophagus. In South America, chronic infection with the parasite Trypanosoma cruzi causes Chagas’ disease and the destruction of the myenteric plexus has marked clinical similarities to achalasia. A rare genetic syndrome (Allgrove syndrome) is associated with familial adrenal insufficiency, alacrimia and achalasia.
The disease is most commonly diagnosed between 30 and 60 years of age. It typically presents with dysphagia (to both solid and liquid), regurgitation and heartburn (often mistaken for GORD), although chest pain/odynophagia is also common in the early stages. Patients often present late and, having had relatively mild symptoms, remain untreated for many years. Patients may or may not have experienced weight loss. Frequently, patients will adjust their diet according to symptoms and can maintain their body weight after an initial drop. An ‘Eckardt score’ was developed to assess the severity of symptoms and monitor treatment outcome (Table 66.1). Aspiration-related respiratory symptoms and pneumonia can also occur when there is significant stasis of food residue in the dilated oesophagus. The retained food substance can cause fermentation and therefore halitosis. Patients may report regurgitating food that they have ingested before.
Table 66.1 Clinical scoring system for achalasia (Eckardt score).
|Weight loss (kg)||Dysphagia||Retrosternal pain||Regurgitation|
|3||>10||Each meal||Each meal||Each meal|
A high index of suspicion is needed in the diagnosis of achalasia as symptoms can be mild and chronic and can be easily misdiagnosed as GORD. Endoscopy typically shows frothy saliva pooling in the oesophagus and the presence of food residue. The oesophagus may be dilated and can be tortuous. The OGJ appears tight and spastic but can usually allow an endoscope to pass with gentle pressure. A normal endoscopy however does not exclude achalasia, as 30–40% of endoscopies are reported as normal before a final diagnosis of achalasia is made. It is an important investigation to exclude ‘pseudo-achalasia’, often referring to cancer of the gastric cardia mimicking achalasia (Figure 66.24).
Barium contrast study typically shows a hold-up of contrast in the distal oesophagus, abnormal contractions in the oesophageal body and a tapering stricture in the distal oesophagus, described as a ‘bird’s beak’ or ‘rat’s tail’ (Figure 66.25). Progressive dilatation leads to a ‘sigmoidal’- shaped oesophagus. A timed barium oesophagogram is used to quantify the height of the retained contrast at a specific time after ingestion to determine the severity of the disease. All these investigations are suggestive of achalasia but definitive diagnosis relies on HRM.
There are three subtypes of achalasia on HRM, all require an abnormal IRP and 100% absent peristalsis. Type I achalasia has an elevated median IRP and 100% failed peristalsis. Type II achalasia is seen with an elevated median IRP, absent contractility and pan-oesophageal pressurisation present in more than 20% of swallows. Type III achalasia is the spastic type, which is defined as an elevated IRP, absent peristalsis and evidence of spasm in 20% or more of the swallows (Figure S66.5). Categorisation into different types has prognostic significance in their responses to treatment. In general, the results are best with type II achalasia.
Figure S66.5 Three types of achalasia categorised by high-resolution manometry. Elevated integrated relaxation pressure (IRP) signifi es failed relaxation of the lower oesophageal sphincter. Type I achalasia (a): failed peristalsis with distal contractile integral (DCI) 0 mmHg/s/cm. Type II achalasia (b): pan-oesophageal pressurisation. Type III achalasia (c): reduced distal latency (DL) <4.5 s (spasm). CDP, contractile deceleration point; NA, not applicable; OGJ, oesophagogastric junction; UOS, upper oesophageal junction.
Pseudo-achalasia in a patient with cancer of the oesophagogastric junction. The patient was referred as having possible achalasia based on a barium contrast study (a). Endoscopy could not get past the obstruction, prompting a computed tomography scan (b), making a diagnosis of cancer. The resected surgical specimen (c).
Barium contrast study showing the typical ‘rat’s tail’ appearance of achalasia.
Oesophageal perforation is associated with high morbidity and mortality rates. It is an emergency and prompt treatment should be instituted because delayed diagnosis and treatment are associated with a marked increase in mortality rate.
In stable patients with a clear history and contained perforation, sometimes conservative expectant treatment can be successful. This usually applies to cervical/pharyngeal perforation when patients are much less septic. Antibiotics should be given; patients are kept nil by mouth and should wait for the perforation to heal by itself. In intrathoracic perforations, patients are usually sicker. They should be resuscitated with intravenous fluid and given antibiotics and oxygen supplement. Electrolyte disturbances are corrected if present. Septic shock is treated appropriately. The objectives of treatment are (i) seal the perforation if possible, (ii) adequate drainage, and (iii) supportive measures, including nutrition (alimentary preferred over parenteral), cardiorespiratory support and sepsis control.
When operative repair is attempted, the video-assisted thoracoscopic approach is less invasive, when the expertise is available. Adequate drainage and decortication are first performed. The site of the perforation is exposed; this is aided by intraoperative endoscopy. Often the mucosal tear is longer than the disrupted muscle layer outside, thus the muscle needs to be split to fully expose the mucosal rent. The oesophagus is then repaired in two layers with fine absorbable sutures: first the mucosa, then the muscle layer. Lavage of the thoracic cavity is then carried out and drains are placed next to the oesophagus along the posterior mediastinum, in addition to the thoracic cavity. The chance of successful repair depends on the condition of the tissue being sutured. Delayed diagnosis increases the chance of failure as the tissue becomes oedematous and friable. Sometimes local tissues may be used to buttress the closure, such as gastric fundus, pericardium or intercostal muscle flaps.
In patients with significant pleural fluid and pneumothorax that result in respiratory compromise, a wide-bore chest tube is inserted to the appropriate side for drainage while waiting for more definitive investigations such as a CT scan. Endoscopy can be both diagnostic and therapeutic. The location and size of the perforation site should be ascertained. Foreign bodies are retrieved. Endoscopic sealing of the perforation site with clips and self-expanding metallic stents may be possible (Figure 66.33). The stent is usually removed around 4–6 weeks later. Healing is expected to have occurred. A nasogastric tube can be placed at the same time for nutritional support.
Surgical intervention is indicated in the presence of significant sepsis when drainage is not affected by other means (such as interventional radiology), and no effective closure of the perforation can be done otherwise. These conditions are usually present when the perforation is large, when the perforation is in the intrathoracic oesophagus, when the pleura is breached, when there is a large septic load and when the presentation is delayed.
When the diagnosis is delayed, closure of the perforation is unlikely to succeed; conversion of the perforation into a controlled fistula is another option. A simple way would be to place a T-tube through the defect and repair around it, in addition to adjacent drains. With modern supportive treatment, oesophageal diversion (cervical oesophagostomy; often an end stoma is required for effective diversion and OGJ ligation) with later staged reconstruction is rarely needed. Oesophagectomy is even more uncommonly indicated, perhaps except for extensive caustic burn with perforation when the oesophagus is necrotic.
Stent for oesophageal perforation. (a) Leakage of oral contrast outside the oesophagus; (b) contrast flowing through the stent, no leakage is seen.
Carcinoma of the Oesophagus
Careful disease staging is essential to guide therapy. Current staging classification according to the American Joint Committee on Cancer (AJCC)/Union for International Cancer Control (UICC) (8th edition) is shown in Table 66.4. The T stage advances as the tumour invades from mucosa deep to muscle, adventitia and beyond the oesophagus. Regional nodes encompass the paratracheal nodes from the neck, through the mediastinum to the upper abdomen, including the coeliac nodes. The segregation of N1 to N3 is by the number of involved lymph nodes. Location is defined by the position of the epicentre of the tumour in the oesophagus (Figure 66.1). Stage groupings differ among squamous and adenocarcinomas. Separate groupings are assigned for clinical (cTNM), pathological (pTNM) and post-neoadjuvant (ypTNM) systems. Because of the complexity, these are not reproduced in this chapter but readers can refer to the staging manual.
Controversy exists as to whether adenocarcinoma of the OGJ should be staged as oesophageal or gastric cancer.
TABLE 66.4 TNM classification of oesophageal cancer.
|T: Primary tumour|
|Tx||Tumour cannot be assessed|
|T0||No evidence of primary tumour|
|Tis||High-grade dysplasia, defined as malignant cells confined to the epithelium by the basement membrane|
|T1||Tumour invades the lamina propria, muscularis mucosae or submucosa|
|T1a: Tumour invades the lamina propria or muscularis mucosae|
|T1b: Tumour invades submucosa|
|T2||Tumour invades the muscularis propria|
|T3||Tumour invades adventitia|
|T4||Tumour invades the adjacent structures|
|T4a: Tumour invades the pleura, pericardium, azygos vein, diaphragm or peritoneum|
|T4b: Tumour invades other adjacent structures, such as the aorta, vertebral body or airway|
|N: Regional lymph nodesa|
|Nx||Regional nodal status cannot be assessed|
|N0||No regional lymph node metastasis|
|N1||Metastasis in one or two regional lymph nodes|
|N2||Metastasis in three to six regional lymph nodes|
|N3||Metastasis in seven or more regional lymph nodes|
|M: Distant metastases|
|M0||No distant metastasis|
Regional nodes extend from the paratracheal/oesophageal nodes in the neck to the coeliac nodes.
Anatomy of the oesophagus, divisions of the oesophagus and measurements endoscopically from the incisors. The three relatively ‘narrow’ parts of the oesophagus are at the level of the cricopharyngeus muscle (upper oesophageal sphincter), where the left main bronchus and aorta cross the oesophagus and the oesophagogastric junction (lower oesophageal sphincter).
According to the latest staging definitions, a tumour involving the OGJ with its epicentre no more than 2 cm into the gastric cardia is staged as adenocarcinoma of the oesophagus, while those with a centre located at more than 2 cm distal to the anatomical OGJ are staged as gastric cancer.
Siewert’s classification, referring to adenocarcinomas that involve the OGJ (Figure S66.6) assigns tumours whose epicentres are located within an area 5 cm proximal and 5 cm distal to the junction into types I–III (oesophageal, cardiac and subcardiac). The three types of cancers differ in terms of the patient’s demographics, possible aetiology, histopathological features and prognosis. Although the Siewert type is often referred to for guiding treatment, such as the type of surgery that should be performed, one has to be aware that it is the proximal and distal extent of cancer that is more relevant in decision-making, rather than the Siewert type, since the latter only refers to the epicentre of the tumour regardless of length. The accuracy of pretreatment assignment to a Siewert type is also suboptimal.
Siewert’s classification of adenocarcinoma around the oesophagogastric junction. Type I cancer refers to tumours with their epicentre located at 1–5 cm proximal to the oesophagogastric junction; type II cancers have their epicentre located at 1 cm proximal and 2 cm distal to the junction; type III cancers have their epicentre located 2–5 cm distal to the junction. Note that, by current definition, a type III cancer is staged as a gastric cancer. Any cancer with its epicentre below the oesophagogastric junction but not touching the actual junction is also staged as gastric cancer.
Choice of surgical approach
The choice of the appropriate technique depends mainly on: (i) the location of the tumour, (ii) the intended extent of lymphadenectomy, and (iii) the reconstructive technique. The surgeon should be well versed in the methods adopted to different clinical situations. For ease of description, the following sections discuss the surgical approach by tumour location.
Cervical oesophageal cancer
Surgery involves removing the pharynx, larynx and oesophagus (pharyngo-laryngo-oesophagectomy); a gastric pull-up is used to anastomose with the neo-pharynx. In cases where involvement of the cervical oesophagus is limited, pharyngo-laryngo-cervical oesophagectomy can be carried out without the need for total oesophageal resection. The resultant gap can be bridged using either a free jejunal graft, or various musculocutaneous flaps. Definitive chemoradiotherapy has become the preferred alternative treatment to preserve the larynx. Surgery is therefore mostly reserved for salvage, when there is an incomplete response or for recurrent disease.
Intrathoracic oesophageal cancer
The surgical procedures usually performed are:
- Left thoracoabdominal incision. Via a large incision traversing the chest and upper abdomen, the whole left upper quadrant of the abdomen and left thoracic cavity are accessed at the same time for oesophagectomy, gastroplasty and anastomosis (Figure 66.52a).
- Lewis–Tanner (or Ivor Lewis) procedure. This is a two-phase oesophagectomy consisting of laparotomy for gastric mobilisation and tubularisation, followed by a right thoracotomy for oesophageal resection. The gastroplasty is delivered into the right thoracic cavity for an oesophagogastrostomy near the apex of the chest (Figure 66.52b).
- McKeown or three-stage oesophagectomy. This consists of the mobilisation of the thoracic oesophagus and lymphadenectomy via a thoracotomy (usually right side), followed by abdominal and neck incisions for preparation of the oesophageal substitute (usually the stomach) and its delivery to the neck for a cervical anastomosis.
- Left thoracic resection (Sweet oesophagectomy). Via a single posterolateral incision on the left chest wall (usually fifth to sixth intercostal space), the oesophagus is mobilised. The diaphragm is opened and the gastroplasty prepared from this opening. The stomach is delivered to the left thoracic cavity for anastomosis.
- Transhiatal oesophagectomy. Through a cervical and abdominal approach, the oesophagus is mobilised via both directions, being stripped out bluntly from its mediastinal bed. The gastric conduit is delivered to the neck for cervical anastomosis (Figure 66.53).
- Minimally invasive surgical approaches. Traditional open procedures (described above) are increasingly replaced by minimally invasive methods, by a combination of video-assisted thoracoscopy (VATS) and laparoscopy or robotic techniques (Figure 66.54). Both thoracic and abdominal phases can be performed via minimally invasive techniques, or one phase can be minimally invasive and the other by open surgery (hybrid procedures). The anastomosis can be constructed in the chest or the neck.
The common open approaches for surgery of the oesophagus: (a) left thoracoabdominal; (b) two-stage Lewis–Tanner (Ivor Lewis) approach. In the McKeown approach a third incision in the neck is made to allow anastomosis to the cervical oesophagus.
Transhiatal oesophagectomy whereby the oesophagus is mobilised blindly using fingers from the neck and hand inserted from the abdomen.
Oesophagogastric junction cancer
The options detailed above for intrathoracic cancers also apply to cancers of the OGJ. Suitability depends in part on the extent of oesophageal and gastric involvement by cancer and the intended extent of resection and lymphadenectomy. In addition, an extended total radical gastrectomy can be performed. The whole stomach and the lower oesophagus (accessed via the oesophageal hiatus from the abdomen) are resected and intestinal continuity is restored with a jejunal Roux loop (Roux-en-y reconstruction). In selected patients with early disease, a proximal gastrectomy can be performed as nodal spread to the distal stomach is rare.
To lessen the chance of acid reflux from a direct oesophagogastrostomy, double-tract reconstruction, double-flap (antireflux) anastomosis or jejunal interposition are options (Figure S66.7).
Figure S66.7 Various ways of reconstruction after proximal gastrectomy for cancer of the gastric cardia. (a) Jejunal interposition.
Figure S66.7 Various ways of reconstruction after proximal gastrectomy for cancer of the gastric cardia. (b) Left panel: double tract reconstruction; right panel: direct oesophagogastric anastomosis.
Extent of Lymphadenectomy
Lymphadenectomy ensures adequate nodal sampling for staging, improves local disease control and increasingly there is evidence to show the prognostic impact of extended lymphadenectomy. The most appropriate extent of lymph- adenectomy remains somewhat controversial. Transhiatal oesophagectomy does not allow adequate mediastinal nodal dissection (for the mid-and upper thoracic part oesophageal mobilisation is mostly a ‘blind’ procedure) and thus is often chosen by surgeons who perform only a limited lower mediastinal dissection for OGJ adenocarcinoma. Squamous cell cancers are mostly more proximally located and the transhiatal approach may be dangerous except in early cancers.
The extent of lymphadenectomy can be defined as ‘fields’. Two-field dissection refers to lymphadenectomy of the mediastinum and upper abdomen around the coeliac trifurcation. The mediastinal ‘field’ is further classified as (i) standard: lymphadenectomy below the tracheal bifurcation, (ii) extended: standard lymphadenectomy plus right paratracheal nodal dissection including those around the right recurrent laryngeal nerve, and (iii) total: extended lymphadenectomy plus nodal dissection along the left recurrent laryngeal nerve chain (Figure 66.55). The third field refers to bilateral cervical lymphadenectomy, including those in the paratracheal as well as supraclavicular fossae.
The most appropriate extent of lymphadenectomy remains a contentious issue. For patients with squamous cell cancers, most surgeons would perform at least a total two-field lymphadenectomy since lymph node mapping data in Japan showed significant nodal metastases, especially around the bilateral recurrent laryngeal nerves. In selected patients and in particular those with upper thoracic cancers, additional third-field nodal dissection is performed (three-field lymphadenectomy). For oesophageal adenocarcinoma, most surgeons perform an infracarinal two-field lymphadenectomy. For OGJ tumours (in particular those with limited oesophageal extent and centre on the OGJ), surgeons are divided among those who prefer oesophagectomy and those who perform extended total gastrectomy with limited lower oesophageal resection and lymphadenectomy. The issue is unsettled. The extent of resection (and lymphadenectomy) has to be balanced against associated morbidities and physiological reserve of the individual patient.
Restoration of intestinal continuity after oesophageal extirpation is mostly done using a gastric conduit. The right gastro-epiploic vessels are its main blood supply. A pyloric drainage procedure is optional, with some surgeons advocating its use to facilitate gastric emptying, after the inevitable vagotomy. In the case of a previous gastrectomy, or if concomitant pathology (such as gastric cancer) requires its removal, the colon (right ileocolon, left or transverse colon) can be used. The surgery is more extensive and three anastomoses are required.
The lymph node station nomenclature according to the Japanese classification. Extent of mediastinal lymphadenectomy. (a) Standard mediastinal lymphadenectomy includes stations below the tracheal bifurcation. (b) Extended mediastinal lymphadenectomy includes standard lymphadenectomy + right paratracheal nodal dissection including those around the right recurrent laryngeal nerve. (c) Total mediastinal lymphadenectomy includes extended lymphadenectomy + left paratracheal area and nodes along the left recurrent laryngeal nerve. Two-field lymphadenectomy includes mediastinal dissection plus nodal dissection around the coeliac axis and three-field dissection includes cervical lymphadenectomy.
The conduit can be placed in the right thoracic cavity (as in after a Lewis–Tanner oesophagectomy) or the neck for cervical oesophagogastrostomy. In the case of a neck anastomosis, three choices of routes of reconstruction exist: posterior mediastinal, retrosternal or subcutaneous.
A jejunal limb is commonly used for reconstruction after extended total gastrectomy for OGJ tumours. A long jejunal limb is also possible, usually reaching the tracheal bifurcation. For longer loops, microvascular augmentation techniques may be needed (Figure S66.8).
Colonic interposition. (a) Vascular anatomy for a right ileocolonic interposition. The ileocolic artery is divided. The ileocolon is based on the middle colic and right colic arteries (the right colic artery may be sacrificed to gain more length if the ileocolonic segment is not long enough and it is the limiting vessel). (b) Vascular anatomy for a left colonic interposition. The blood supply is based on the ascending branch of the left colic artery; the middle colic artery is divided. The proximal transverse colon is brought up to the neck as an isoperistaltic conduit. (c) Anatomy after a right ileocolonic interposition. The terminal ileum is divided. The caecal end of the ileum is brought up to the neck for oesophagoileal anastomosis. The proximal end of the divided transverse colon (note preservation of the marginal artery by dissection close to the colonic wall) is anastomosed to a loop of jejunum (note the previous total gastrectomy in this patient). An ileocolonic anastomosis completes the bowel continuity. AB, ascending branch of left colic artery; ICA, ileocolic artery; IMA, inferior mesenteric artery; LCA, left colic artery; MA, marginal artery; MCA, middle colic artery; RCA, right colic artery; SMA, superior mesenteric artery.