Oesophagus

The oesophagus extends from the cricoid cartilage (at the level of vertebra C6) to the gastric cardia and is 25 cm long. It has cervical, thoracic and abdominal portions. The oesophagus passes through the diaphragm at the level of the 10th thoracic vertebra and the final 2–4 cm lie within the peritoneal cavity. The relationships are shown in Figure 13.1.

Fig. 13.1 Anatomical relationships of the oesophagus.

The oesophagus has an upper sphincter, the cricopharyngeus, and a lower sphincter that cannot be defined anatomically but is a 3–5 cm high-pressure area located in the region of the oesophageal hiatus of the diaphragm. The oesophagus is held loosely in the hiatus by a thickening of fascia, the phreno-oesophageal ligament. The healthy oesophagus is lined by squamous epithelium and its wall can be divided into two principle layers, muscular and mucosal. The muscular layer has two components with longitudinal fibres outside and circular fibres inside; the upper third of the oesophagus is striated muscle and the remainder is smooth muscle. Between the muscle and the mucosa is the submucosa where numerous mucous glands and lymphatics are found.

The oesophagus receives its blood supply from the inferior thyroid artery in the cervical region, the bronchial arteries and branches from the thoracic aorta in the thorax, and the inferior phrenic and left gastric arteries in the abdomen.

Venous drainage is to the inferior thyroid veins in the neck, the hemi-azygous and azygous veins (systemic circulation) in the thorax, and the left gastric (portal circulation) in the abdomen. The connection between these veins is important in the development of varices in patients with portal hypertension.

Sympathetic nerve supply is derived from pre-ganglionic fibres from spinal cord segments T5 and T6, and post-ganglionic fibres from the cervical vertebral and coeliac ganglia. Parasympathetic supply comes from the glossopharyngeal, recurrent laryngeal and vagus nerves.

The lymphatics run in the submucosa and drain to the regional lymph nodes, and subsequently to the posterior mediastinal, supraclavicular and coeliac lymph nodes.

Stomach and duodenum

The stomach is an easily distensible viscus partly covered by the left costal margin. The diaphragm and left lobe of the liver lie on its anterior surface. Posteriorly, the stomach bed is formed by the diaphragm, spleen, left adrenal, upper part of the left kidney, splenic artery and pancreas. The greater and lesser curvatures correspond to the long and short borders of the stomach respectively, and the organ can be further divided anatomically into four distinct areas based on the microscopic mucosal appearance: namely, the cardia, fundus, body and antrum. The stomach is limited at its proximal end by the oesophagogastric junction situated just below the lower oesophageal sphincter, a physiological sphincter that prevents stomach contents from regurgitating into the oesophagus. Distally, the stomach is limited by the pylorus, a true anatomical sphincter. It is composed of greatly thickened inner circular muscle that helps to regulate the emptying of stomach contents into the duodenum.

The duodenum is divided into four parts, which are closely applied to the head of the pancreas. The first part is approximately 5 cm in length; its importance lies in the fact that it is the most common site for peptic ulceration to occur. The second part has on its medial wall the ampulla of Vater, where the conjoined pancreatic duct and common bile duct deliver their contents to the gastrointestinal tract. The third and fourth parts pass behind the transverse mesocolon into the infracolic compartment.

The stomach has an extensive blood supply (Fig. 13.2) derived from the coeliac axis. When the stomach is used as a conduit in the chest, as in an oesophagectomy, the left gastric, left gastroepiploic and short gastric vessels are divided, and the stomach then relies on the right gastric and right gastroepiploic vessels for viability. Ischaemia does not usually result because of the free communication between the vessels supplying the stomach. The blood supply to the duodenum is derived from both the coeliac axis (via the gastroduodenal artery) and branches from the superior mesenteric artery. The veins from the stomach and the duodenum accompany the arteries and drain into the portal venous system.

Fig. 13.2 Blood supply and anatomical relationships of the stomach and duodenum.

The lymphatics from the stomach accompany the arteries and drainage is to nodes around these vessels. Thereafter, drainage is to other groups around the aorta, liver, splenic hilum and pancreas, and then to the coeliac nodes. The lymphatics of the duodenum drain into the nodes located at the coeliac axis and superior mesenteric vessels.

The parasympathetic nerve supply to the stomach is derived from the anterior and posterior vagal trunks. These pass through the diaphragm with the oesophagus. The anterior trunk gives off branches to the liver and gallbladder and descends along the lesser curvature. The posterior trunk gives off a coeliac branch and descends along the lesser curvature of the stomach, going on to supply the pancreas, small intestine and large intestine as far as the distal transverse colon. The parasympathetic system supplies motor fibres to the stomach wall, inhibitory fibres to the pyloric sphincter (thus effecting relaxation of the sphincter), and secretomotor fibres to the glands of the stomach. Sympathetic fibres accompany the gastric arteries to reach the stomach from the coeliac ganglion. These provide motor fibres to the pyloric sphincter. The duodenum receives a sympathetic and parasympathetic supply from the coeliac and superior mesenteric plexuses

Oesophagus

Oesophageal peristalsis is initiated by swallowing (primary) or luminal distension (secondary) and progresses distally at around 2–4 cm/s requiring the coordinated contraction and relaxation of oesophageal muscle. The lower sphincter relaxes momentarily 2–3 seconds before the peristaltic wave arrives and pressures of about 80 mmHg are usually generated in the oesophageal body. Disruption of any part of this process can result in difficulties with swallowing and/or pain.

Between the outer longitudinal muscle layer and the inner circular layer is a nerve plexus (Auerbach’s or myenteric plexus) receiving parasympathetic motor innervation to smooth muscle cells from vagal nuclei in the dorsal motor nucleus of the brain stem. Between the inner muscular layer and the submucosa is another nerve plexus (Meissner’s or submucosal plexus), which relays signals from the numerous free nerve endings in the mucosa and submucosa to vagal afferent fibres. This sensory information is sent back to the brain via the vagus nerve trunks. Sympathetic innervation arrives via pre-ganglionic sympathetic fibres from the spinal cord that synapse with post-ganglionic nerve cells in sympathetic ganglia before passing with the blood vessels to the oesophagus. Together, the myenteric and submucosal plexuses constitute part of the enteric nervous system of the gut and can be influenced by both neural and hormonal stimuli.

Around one litre of alkaline saliva is produced each day by the salivary glands which helps lubricate the food bolus and neutralizes refluxed gastric acid.

Stomach

Food is passed from the oesophagus into the stomach, where it is stored, ground and partially digested. As food enters the stomach, the muscles in the stomach walls relax and intragastric pressure rises only slightly. This effect is known as receptive relaxation, and is mediated by the vagus nerve. It is followed by muscular contractions that increase in amplitude and frequency, starting in the fundus and moving down towards the body and antrum. In the antrum, the main role is the grinding of food and propulsion of small amounts (now called chyme) into the duodenum when the pyloric sphincter relaxes.

Gastric emptying is controlled by two mechanisms: hormonal feedback and a neural reflex called the enterogastric reflex. In the former, fat in the chyme is the main stimulus for the production of a number of hormones, the most powerful being cholecystokinin, which exerts a negative feedback effect on the stomach, decreasing its motility. The enterogastric reflex is initiated in the duodenal wall, and this further slows stomach emptying and secretion.

Gastric secretions

Classically, gastric secretion has been divided into three phases:

Mucus is produced by all regions of the stomach. It is composed mainly of glycoproteins, water and electrolytes, and serves two important functions. It acts as a lubricant, and it protects the surface of the stomach against the powerful digestive properties of acid and pepsin. Bicarbonate ions are secreted into the mucus gel layer and this creates a protective buffer zone against the effects of the low pH secretions. Alkaline mucus is produced in the duodenum and small intestine, where it has a similar function of mucosal protection.

The parietal cells in the stomach are responsible for the production of acid. Acid secretion by these cells is stimulated by two main factors: acetylcholine, released by the vagus nerve, and gastrin from the antrum. Acetylcholine and gastrin act on neuroendocrine cells located close to the parietal cells. On stimulation, these cells release histamine, which has a paracrine action on the parietal cell, stimulating acid production and secretion. Parietal cells secrete acid via an active transport mechanism, the proton pump. Somatostatin, gastric inhibitory peptide and vasoactive intestinal peptide inhibit acid secretion.

Pepsin is a proteolytic enzyme produced in its precursor form, pepsinogen, by the peptic cells found in the body and fundus of the stomach. Pepsinogen production is stimulated by acetylcholine from the vagus nerve. The precursor is then converted to its active form, pepsin, by the acid contents of the stomach.

Intrinsic factor is also produced by the parietal cells. It is a glycoprotein that binds to vitamin B₁₂ present in the diet and carries it to the terminal ileum. Here specific receptors for intrinsic factor exist and the complex is taken up by the mucosa. Intrinsic factor is broken down and vitamin B₁₂ is then absorbed into the bloodstream.

Dysphagia

Dysphagia is defined as difficulty in swallowing. It is a serious symptom and requires proper investigation regardless of clinical diagnosis. Certain points in the history, however, are often helpful in making a differential diagnosis:

Table 13.1 Causes of dysphagia

Odynophagia

This symptom is defined as pain on swallowing. It may occur in patients with oesophagitis or due to oesophageal spasm. The latter may be due to a mechanical obstruction (benign or malignant) or due to intrinsic dysmotility of the oesophageal musculature.

Heartburn

Retrosternal pain is a very common symptom and most people will have experienced it at some time. It is usually associated with gastro-oesophageal reflux and may be brought on by eating a heavy meal, alcohol or bending over. General practitioners will see many patients in their clinical practice who complain of heartburn and will treat them effectively with acid suppressing medication such as proton pump inhibitors.

Dyspepsia

Dyspepsia is something of a ‘catch all’ term used to describe the symptoms of indigestion. Patients may have some or all of the following; epigastric pain, belching, heartburn, nausea, early satiety or reduced appetite. These symptoms are very common in the general population. Current guidance from the National Institute for Clinical Excellence (NICE) in the UK, recommends lifestyle advice, medication review and empirical treatment for the majority of patients with dyspepsia but without so-called alarm symptoms (weight loss, progressive dysphagia, iron deficiency anaemia, epigastric mass and persistent vomiting) (EBM 13.1). Unfortunately, the symptoms of early upper GI malignancy are very similar to dyspepsia and only advanced malignancies tend to cause alarm symptoms. Patients with advanced upper GI malignancy have a poor prognosis despite aggressive therapy, which creates a dilemma; which patients with dyspepsia should be referred for endoscopy? NICE guidance on dyspepsia should be applied with caution and doctors should have a low threshold for endoscopy in any patient who does not improve quickly with simple treatment. It is also imperative that a careful history is taken and anaemia excluded.

Regurgitation and Vomiting

Regurgitation is an effortless process whereby food is regurgitated into the mouth and is associated with achalasia, hiatus hernia and pharyngeal pouches. In severe cases regurgitation can lead to aspiration with coughing/choking, asthma and aspiration pneumonia. Vomiting is an active process whereby the stomach contents are forcefully expelled by powerful contractions of the abdominal musculature at the same time as relaxation of the lower oesophageal sphincter. Potential causes of vomiting are multiple and include infection, inflammation, endocrine disorders, drugs and medication, gastrointestinal obstruction, and physiological such as morning sickness in pregnancy.

Abdominal pain

Epigastric pain is a common upper gastrointestinal symptom. Pain relieved by eating traditionally suggests a duodenal ulcer whereas gastric ulcer pain is aggravated by food. However, the differential diagnosis for epigastric pain is extensive and includes conditions such as liver metastasis, pancreatic pathology, abdominal aortic aneurysm, gall stones, irritable bowel and even myocardial infarction.

Endoscopy

Flexible oesophagogastroduodenoscopy (OGD) is now the first-line investigation for almost all upper GI symptoms. Flexible OGD is carried out either under light intravenous sedation or a local anaesthetic throat spray. The patient should be fasted for 4 hours before the procedure. It is important to monitor pulse and oxygen saturation throughout the procedure to identify and rectify any possible respiratory depression that might follow sedation. Therapeutic procedures can also be done at the time of OGD including dilatation of strictures, insertion of stents, thermal ablation of tumours, removal of foreign bodies and control of bleeding.

Computed tomography (CT)

CT is used most commonly to investigate and stage malignancy but may also be helpful when investigating patients with benign conditions such as large hiatus hernias, a suspected gastric volvulus or upper GI perforation. Staging upper GI CT scans are often done after the patient has drunk water to distend the oesophagus and stomach. Emergency scans looking for evidence of gut perforation will use oral water soluble contrast.

Gastric emptying studies

These nuclear medicine scans require the patient to swallow radio-labelled liquid and solids (a two-phase study). The speed that the stomach empties can then be monitored using a gamma ray detector. Patients whose major complaint is nausea and vomiting but appear to have no structural abnormality of their upper GI tract should undergo a two-phase gastric emptying study to look for gastroparesis, a common condition in diabetics secondary to autonomic neuropathy.

Endoluminal ultrasound

Endoscopic ultrasonography (EUS) uses a variety of endoscopes containing high frequency ultrasound probes at their tips to investigate patients with upper GI disorders. By placing the probe within the GI lumen great detail of the underlying structures can be obtained. EUS is mostly used for staging the ‘T’ and ‘N’ component of TNM staging for oesophagogastric cancer (Fig. 13.8). In addition, EUS is increasingly being used to allow fine needle biopsy of suspicious lymph nodes, especially when the status (positive or negative for cancer) will have profound implications for the intention of a patient’s treatment (curative or palliative). EUS is also useful for investigating submucosal lesions of the stomach such as gastrointestinal stromal tumours (GISTs) (Fig. 13.9) (see p. 176).

Fig. 13.8 Endoscopic ultrasound (EUS).

A The normal layers of the oesophagus and a small T1 cancer confined to the mucosa marked with an arrow.B A full-thickness T3 tumour of the oesophagus. Note the complete destruction of the normal oesophageal layers.

Fig. 13.9 A Endoscopic view of a 2-cm diameter polypoid submucosal gastric lesion.B EUS confirms the lesion is arising from the muscularis propria and likely to be a GIST.

Manometry and pH studies

Measurements of lower oesophageal pH can be made over a 24-hour period using an intraluminal electrode placed 5 cm proximal to the lower oesophageal sphincter attached to a catheter passed through the nose and pharynx. Alternatively, oesophageal pH can be measured over three days using a Bravo capsule® which is clipped to the oesophageal mucosa and is wireless (Fig. 13.10). Patients can indicate symptom events during the recording and these can be correlated with the pH trace. A composite scoring system (the DeMeester score) is then used to diagnose pathological GORD. Oesophageal pressure and peristalsis can also be analysed during a series of swallows (station manometry) or over a longer period (ambulatory manometry) (Fig. 13.11). To diagnose gastro-oesophageal bile reflux in patients with duodenogastric reflux a Bilitec probe® is used.

Fig. 13.10 Endoscopic view of a wireless Bravo capsule clipped to the oesophageal mucosa 5cm proximal to the gastro-oesophageal junction.

These record for up to 72 hours before falling off and passing harmlessly through the gut.

Fig. 13.11 Recording of the intraluminal pressure of the oesophagus.

Gastro-oesophageal reflux disease (GORD) and Barrett’s oesophagus

Patients typically complain of heartburn, regurgitation of acid into the back of their throat, nausea, waterbrash (hypersalivation), epigastric pain and occasionally vomiting. Reflux symptoms are very common affecting up to 30% of the population. The lower oesophageal sphincter usually prevents reflux by the following mechanisms:

Anti-reflux surgery

Although surgical treatment of patients with severe anti-reflux disease has always been associated with good long-term outcomes, it has taken the introduction and refinements of laparoscopic techniques to bring the surgical option to more patients. The indications for surgery include those whose symptoms cannot be controlled by medical therapy, those with recurrent strictures despite treatment, and young patients who do not wish to continue taking acid suppression therapy for several decades. Symptoms that fail to be brought under control with acid suppression therapy are usually due to high-volume alkaline reflux, and surgery is an extremely effective cure (EBM 13.3). The presence of Barrett’s metaplasia alone is not considered a suitable indication for anti-reflux surgery.

13.3 Surgery for gastro-oesophageal reflux disease

‘It has been shown that, following anti-reflux surgery, quality of life is improved and costs are reduced significantly compared with medical treatment. Anti-reflux surgery should be offered to patients with proven symptomatic reflux that cannot be controlled symptomatically with medical therapy.’

For further information: www.acg.gi.org/physicians/guidelines/GERDTreatment.pdf.

Surgery involves reduction of the hiatus hernia if present, approximation of the crura around the lower oesophagus, and some form of fundoplication. This takes the form of mobilizing the fundus of the stomach from its attachments to the undersurface of the left hemidiaphragm and the left crus, and then wrapping it around the oesophagus, either anteriorly or posteriorly. The most common procedure currently performed is the Nissen fundoplication, in which the fundus is taken posteriorly around the lower oesophagus and sutured to the left anterior surface of the left side of the proximal stomach as a 360° wrap (Fig. 13.12). Other procedures involving a partial (incomplete) fundoplication include the Toupet (posterior 270° wrap) and the Watson (anterior 180° wrap) repairs. Current data do not demonstrate much difference between the various approaches although early postoperative dysphagia is commoner with 360° wraps compared to the partial wraps. All procedures have a success rate in curing the symptoms of reflux of around 90% at a year and 70–80% at 10 years. Unwanted complications after surgery include gas bloat (inability to belch), dysphagia, early satiety and increased flatus. These operations are now carried out laparoscopically, with excellent results in skilled hands.

Fig. 13.12 Fundoplication for GORD.

A Gastric fundus wrapped around the lower oesophagus.B Fundal wrap sutured in position.

Summary Box 13.1 Gastro-oesophageal reflux disease

• Reflux type symptoms are very common

• ‘Life style’ advice to patients is important (i.e. smoking, dieting etc)

• Proton pump inhibitors are generally effective treatment

• GORD for > 10 years (especially men) is a risk factor for Barrett’s oesophagus

• Screening and surveillance for Barrett’s patients increasingly relevant

• Laparoscopic anti-reflux surgery is clinically effective and cost efficient.

Hiatus hernia

A hiatus hernia is an abnormal protrusion of the stomach through the oesophageal diaphragmatic hiatus into the thorax. There are two types, sliding (90%) and rolling (10%) (Fig. 13.13). A sliding hernia occurs when the stomach slides through the diaphragmatic hiatus, so that the gastro-oesophageal junction lies within the chest cavity. It is covered anteriorly by peritoneum, and posteriorly is extraperitoneal. A rolling or para-oesophageal hernia is formed when the stomach rolls up anteriorly through the hiatus; the cardia remains in its normal position and therefore the cardio-oesophageal sphincter remains intact.

Fig. 13.13 Types of hiatus hernia.

A Sliding hernia.B Rolling hernia (para-oesophageal).C Mixed hernia.

Rolling and sliding hernias are caused by weakness of the muscles around the hiatus. They tend to occur in middle-aged and elderly patients. Women are affected more frequently than men and there is a higher incidence in the obese.

Achalasia

This disorder affects the whole oesophagus. The main feature is failure of relaxation of the lower oesophageal sphincter; as the disease progresses, the obstructed lower oesophagus dilates and peristalsis becomes uncoordinated.

Achalasia is thought to be due to a partial or complete degeneration of the myenteric plexus of Auerbach, and in the later stages of the disease loss of the dorsal vagal nuclei within the brain stem can be demonstrated. Infestation with the protozoon, Trypanosoma cruzi, which occurs in South America (Chagas’ disease), also causes degeneration of the myenteric plexus, leading to a motor disorder of the oesophagus that is indistinguishable from achalasia.

Diffuse oesophageal spasm

This disorder tends to occur in middle-aged to elderly patients. Complaints are of intermittent dysphagia and retrosternal pain, which can mimic angina. The symptoms are caused by repetitive irregular peristalsis of the oesophageal body and oesophageal manometry is required to make the diagnosis. Diffuse oesophageal spasm can be precipitated by GORD and this should be excluded by 24-hour pH studies.

Nutcracker oesophagus

In this uncommon disorder, the symptoms are caused by repetitive forceful peristalsis. Manometry demonstrates normal peristalsis but with excessive amplitudes and pressures exceeding 150 mmHg. Medical treatment is similar to that of diffuse oesophageal spasm, but the results are disappointing. Dilatation and surgical myotomy also have poor results.

Plummer–Vinson syndrome

This syndrome, first described by Paterson and Brown Kelly, is characterized by a post-cricoid web that results in dysphagia. The web is related to iron deficiency anaemia, but may be congenital or traumatic in origin. The squamous epithelium becomes hyperplastic and there is hyperkeratosis and desquamation, which leads to web formation.

Pouches

Pouches are protrusions of mucosa through a weak area in the muscle wall. The best-known type of pouch lies in the pharynx and is associated with raised cricopharyngeal pressure, with the pouch developing through Killian’s dehiscence, between the thyropharyngeus and cricopharyngeus muscles. Incoordination of swallowing and failure of relaxation of the cricopharyngeus muscle cause the herniation. The pharyngeal pouch usually develops posteriorly and is then forced by the vertebral column to deviate to the side, usually the left. Oesophageal pouches can occur around the tracheobronchial tree in relation to pressure from adjacent lymph nodes, if enlarged, and also just above the gastro-oesophageal junction in patients with raised lower oesophageal sphincter pressure.

Perforation

Investigations

The most important factor in diagnosing oesophageal perforation early on is the examining doctor including it in his or her differential diagnosis of any patient who collapses with chest pain, shortness of breath or vomiting.

Erect chest X-ray

In addition to excluding a perforated duodenal ulcer (air under the diaphragm), an erect chest X-ray may show surgical emphysema with gas in the soft tissues of the mediastinum, often extending up to the neck. The mediastinum may also be widened, and if the pleural cavity has also been ruptured, there will be a hydropneumothorax.

CT scan and contrast swallow

The diagnosis is confirmed by a chest CT scan or water-soluble contrast swallow, which will also demonstrate whether the perforation is localized to the mediastinum or open to the pleural or peritoneal cavities (Fig. 13.14). If oesophageal perforation cannot be excluded after radiological imaging and clinical suspicion remains high an experienced endoscopist should perform an OGD. One potential catch is spontaneous pneumomediastinum which can occur in young adults and teenagers after violent vomiting or coughing and is thought to be due to the rupture of a pulmonary bullous. There is no oesophageal injury and the treatment is conservative.

Fig. 13.14 Coronal CT image showing iatrogenic pharyngeal perforation with massive surgical emphysema.

Benign tumours

These account for less than 1% of oesophageal neoplasms. The most common is the benign leiomyoma which is often asymptomatic but may cause bleeding or dysphagia. It is best treated by local enucleation, with good results.

Carcinoma of the oesophagus

The incidence of carcinoma of the oesophagus has risen in populations of developed countries over the last two decades to a figure of around 15/100 000 in parts of the UK, due primarily to an increase in adenocarcinoma. The male to female ratio is 3:1 and adenocarcinoma is predominantly a disease of Western white males. In the Far East and other parts of the world, particularly among some black males, there is a greater incidence of squamous cell carcinoma.

The most important risk factors for adenocarcinoma of the oesophagus are reflux and obesity, with a slightly increased risk of cardia tumours with smoking. Risk factors for squamous cell carcinoma include alcohol, smoking, leucoplakia, achalasia, the consumption of salted fish or pickled vegetables, and chewing tobacco and betel nuts.

Surgical resection

Patients with disease confined to the oesophagus and who are fit for surgery should be considered for resection in a high volume cancer centre. Oesophagectomy with palliative intent is no longer appropriate as few patients recover enough to gain any benefit before they die of their disease.

There are several methods currently used to resect the oesophagus:

• Ivor Lewis two-phase oesophagectomy. This involves a laparotomy during which the stomach is fully mobilized on its vascular pedicles, along with the lower oesophagus. A right thoracotomy is then carried out to resect the oesophagus, and the mobilized stomach is brought up into the chest and anastomosed to the proximal oesophagus. This is the preferred choice for middle and lower-third tumours (Fig. 13.15)

• Left thoracolaparotomy. This is a good approach for tumours around the oesophagogastric junction, particularly when the tumour extends down into the proximal stomach and a more extensive gastric resection is required

• Transhiatal oesophagectomy. This approach involves mobilization of the stomach via an abdominal incision, the oesophagus (some of it by blunt dissection) through the hiatus, and the cervical oesophagus via a left sided neck incision. Once the oesophagus is removed, the stomach is brought up into the neck and anastomosed to the cervical oesophagus. This technique is best suited for very early tumours not requiring a radical lymphadenectomy but is rapidly being replaced by minimally invasive surgery

• Minimally invasive oesophagectomy. Increasingly surgeons are using laparoscopic and thoracoscopic techniques to mobilize the oesophagus. The commonest technique is to mobilize the stomach laparoscopically and then perform a thoracotomy to resect the oesophagus and perform an anastomosis, a so called ‘hybrid technique’. Alternatively both the abdominal and chest phase of the surgery can be done using minimally invasive techniques.

Fig. 13.15 Reconstruction after Ivor–Lewis oesophagectomy.

Palliation

The majority of patients who present with oesophageal cancer (about 70%) will have palliative rather than curative treatment. It is therefore essential that a full range of palliative treatments are easily available and that an experienced hospital clinician with good specialist nurse support co-ordinates the care, working closely with community services.

Best supportive care: Some patients are too frail for any interventional treatment and require a holistic approach to their symptoms involving medication to counter nausea, vomiting and pain. Emotional and dietary support are also important.

Endoscopic stent: Patients with significant dysphagia who are not candidates for radical therapy should be considered for a palliative stent as this is a safe and effective method of relieving the distress of not being able to swallow (Fig. 13.16). They are inserted under intravenous sedation endoscopically but can also be screened into position by interventional radiologists. Chest pain for the first few days after insertion is common and patients should be started on a proton pump inhibitor to reduce reflux symptoms. Complications include perforation during insertion, migration of the stent, blockage and tumour ingrowth. The latter can be rectified by laser ablation or placement of a second stent. Stents cannot be used for very proximal tumours involving the cervical oesophagus.

Fig. 13.16 Self-expanding metal stent inserted to relieve dysphagia from an incurable oesophageal tumour.

Palliative chemotherapy: This has been shown in a number of randomized clinical trials to improve patients’ symptoms (i.e. dysphagia) and double life expectancy for those with advanced oesophagogastric cancer.

Palliative radiotherapy and brachytherapy: Intraluminal radiotherapy (brachytherapy) has been shown to provide a better quality of life for patients with incurable oesophageal cancer than a stent. However, availability of this treatment in the UK is still limited. External beam radiotherapy can provide good palliative care for squamous oesophageal carcinoma but requires more visits by the patient to hospital.

Summary Box 13.2 Oesophageal cancer

• Always investigate dysphagia

• GORD, Barrett’s and oesophageal adenocarcinoma are linked

• Early diagnosis can allow curative endoscopic or surgical therapy

• Late diagnosis (the norm) results in poor prognosis

• Curative treatment now usually multimodal

• Surgical outcomes better in high volume centres.

Peptic ulceration

Peptic ulceration affects areas of mucosa exposed to acidic gastric contents. The main pathology is an imbalance between the acid-pepsin system and the mucosal ability to resist digestion. Duodenal ulcers occur four times more commonly than gastric ulcers.

Pathology

Duodenal ulcers usually occur in the first part of the duodenum and 50% occur on the anterior wall. The majority of gastric ulcers develop on the lesser curvature in the distal half of the stomach. They may co-exist with duodenal ulcers in 10% of patients. Duodenal ulcers may be acute (Fig. 13.17) or chronic. Ulcers with a history of less than 3 months’ duration and with no evidence of fibrosis are considered to be acute. Gastric ulcers generally run a chronic course.

Fig. 13.17 Endoscopic view of an acute duodenal ulcer.

Gastric ulcers may be benign or malignant. Malignancy was once thought to be a complicating factor of benign gastric ulceration. It is now realized that malignant change in a benign ulcer is rare, and that such ulcers are in fact probably malignant from the outset. Duodenal ulcers are very rarely malignant.

Clinical features

Recurrent well-localized epigastric pain is typical of peptic ulcer disease. Classically, the pain of a gastric ulcer occurs during eating and is relieved by vomiting. Patients with duodenal ulceration characteristically describe pain when they are hungry. This pain is relieved by food, antacids, milk and vomiting. Often, however, these well-defined features are not present, and it is usually impossible to differentiate between the pain of gastric ulceration and that of duodenal ulceration. Other symptoms associated with peptic ulcer disease include heartburn, anorexia, waterbrash (a sudden flow of saliva into the mouth) and intolerance of certain foods. Intermittent vomiting may occur. Where persistent vomiting is troublesome, the possibility of gastric outlet obstruction should be considered. Such vomiting tends to be projectile and may contain recognizable food eaten many hours previously.

Special forms of ulceration

Stress ulceration refers to erosions or ulceration of the stomach or duodenum occurring in certain circumstances. These include severe illness, trauma, prolonged mechanical ventilation, multiple organ failure, sepsis and major surgery. The aetiology is not fully defined, although acid and mucosal ischaemia appear to be key elements. Medical prophylaxis using proton pump inhibitors may be useful in such circumstances.

Cushing’s and Curling’s ulcers are special forms of stress ulceration that occur following central nervous injury and burns, respectively. Hypersecretion of acid is not always essential for stress ulceration to occur, but does appear to be important in both of these conditions. In neurosurgical injury, raised intracranial pressure may be responsible for an increase in vagal activity and hence the increase in gastric secretion. The ulcers resulting from hypersecretion are usually single and, in common with other forms of peptic ulceration, may be complicated by perforation and bleeding.

Medical management

General measures helpful in the management of peptic ulcers include the avoidance of NSAIDs, smoking and excessive alcohol. If NSAIDs cannot be avoided in patients with a history of peptic ulceration PPIs should be prescribed (e.g. omeprazole or lansoprazole). These agents act by irreversibly inhibiting H⁺/K⁺ ATPase and thus are powerful inhibitors of acid secretion.

Surgical management

Duodenal ulceration

Surgery for uncomplicated duodenal ulceration is now extremely rare. Operations such as a truncal vagotomy, highly selective vagotomy, or gastric resectional surgery have had little role since the introduction of eradication therapy.

Gastric ulceration

Failure of conservative therapy to heal a gastric ulcer is an indication for surgical intervention. Where malignancy cannot be excluded or is suspected, resection of the ulcer is the treatment of choice. The extent and type of resection will be determined by the position of the ulcer within the stomach and its suspected malignant potential. Benign distal ulcers may be treated by a Billroth I gastrectomy, whereby the distal part of the stomach is removed and the proximal stump anastomosed to the duodenum. More proximal ulcers usually necessitate a Polya-type reconstruction involving anastomosis of the gastric remnant to the jejunum (Fig. 13.18).

Fig. 13.18 Gastrectomy for peptic ulceration.

Many patients who had surgery for ulcer disease in the 1960s and 70s are still alive today and suffer long-term side effects similar to those experienced by patients having a gastrectomy for cancer.

Perforation

Management

The initial management, as for other causes of peritonitis, consists of resuscitation, oxygen therapy, intravenous fluids and broad spectrum antibiotics, and the passage of a nasogastric tube. Intravenous opiate analgesia and PPIs should be given as necessary. A urinary catheter enables close monitoring of urine output.

Operative management is usually indicated although patients who do not have generalized peritoneal signs or systemic sepsis may be successfully managed conservatively so long as frequent reassessment shows no deterioration in their condition. Surgeons are increasingly using a laparoscopic approach to treatment but open surgery should not be considered inferior.

Duodenal ulcers

Surgery usually involves simple closure, whereby the ulcer is under-run with sutures or plugged using an omental patch (Fig. 13.19), coupled with a thorough peritoneal lavage. All patients should receive 72 hours of intravenous PPI therapy and then H. pylori eradication therapy and a healing course of oral PPIs.

Fig. 13.19 Closure of perforated duodenal ulcer.

Gastric ulcers

Approximately 15% of perforated gastric ulcers prove ultimately to be malignant. However, current practice suggests biopsy of the ulcer wall, followed by simple closure or local excision of the ulcer, is best. If the ulcer turns out to be malignant, a minority will progress to gastric resection following tumour staging (see below).

Summary Box 13.3 Peptic ulcer disease

• Helicobacter pylori is the most important cause – eradicate it

• NSAID medication next commonest cause

• Surgery now only for complications (bleeding and perforation)

• Always biopsy a gastric ulcer – some will be malignant

• If an ulcer fails to heal with medical therapy look for rare causes (i.e. ZE).

Acute haemorrhage

The differential diagnosis of upper gastrointestinal bleeding is summarized in Table 13.2. Upper gastrointestinal bleeding presents with haematemesis (vomiting blood) and/or melaena (the passage of black tarry stool that has a very characteristic smell). Melaena results from the digestion of blood by enzymes and bacteria. Less commonly, melaena may be the result of a bleed from the right colon. Very rarely, if bleeding is very brisk, upper gastrointestinal bleeding may present as fresh rectal bleeding, in which case signs of cardiovascular instability are present. Slow chronic blood loss may be asymptomatic and detected on rectal examination by a positive faecal occult blood test.

Table 13.2 Causes of upper gastrointestinal bleeding.

Diagnosis

Management

Detection and endoscopic treatment

The aims of management of bleeding peptic ulcers are to identify the bleeding point, arrest the bleeding (bleeding ceases spontaneously in 90% of patients) and prevent recurrence. Once resuscitation has occurred, endoscopy is used to detect the site of bleeding (Fig. 13.20), doing so in 80–90% of cases. The endoscopist should also have the necessary experience and training to attempt control of the bleeding using techniques such as adrenaline (epinephrine) 1:10 000 injection and application of heater probes and clips. Bleeding from the ulcer base, the presence of a visible vessel and adherent clot overlying the ulcer are features associated with a significantly increased risk of further bleeding.

Fig. 13.20 Endoscopic view of bleeding duodenal ulcer.

In patients in whom endoscopy does not identify the bleeding point, angiography may be used, but the limitation of this investigation is that it can only detect active bleeding of greater than 1 ml/min. In these patients, selective embolization can be used to stop the bleeding and thus avoid the need for surgery.

Surgical management

Emergency surgery may be indicated if endoscopy reveals bleeding from a major artery and where attempted injection sclerotherapy is unable to control the bleeding directly; 50% of patients with active arterial bleeding and 30% with a visible vessel at the ulcer base are ultimately likely to require surgery. When bleeding recurs after therapeutic endoscopy, a further endoscopy may be able to control the bleeding. Recurrent bleeding is associated with significant morbidity and mortality, particularly in the elderly. Continuing bleeding is particularly common in those with a chronic ulcer and is more common in gastric ulceration. The type of operation used depends on the site of the bleeding ulcer and the co-morbidity of the patient:

Benign gastric neoplasms

Benign tumours of the stomach may arise from epithelial or mesenchymal tissue. Adenomatous polyps may be single or multiple and are the most common benign epithelial neoplasm. Gastrointestinal stromal tumours (GISTs) arise from the pacemaker cells in the gastric wall and have a variable natural history. Diagnosis is usually by endoscopy and EUS; biopsies are rarely helpful as the lesions are submucosal. Small asymptomatic GISTs (up to 2 cm diameter) can safely be left alone but larger ones should be either kept under surveillance (2–5 cm) or resected (> 5 cm). Symptomatic gastric GISTs (bleeding, pain, obstruction) should usually be resected (Fig. 13.21) and laparoscopic techniques are often possible.

Fig. 13.21 ALarge dumb-bell shaped gastric GIST lesion in situ.BLesion resected showing intact gastric mucosa over its luminal aspect.

Malignant gastric neoplasms

Advanced gastric cancer

The vast majority of malignant gastric tumours found in Western countries are locally advanced gastric adenocarcinomas. These tumours have invaded into the muscularis propria and sometimes through to the serosa. The risk of peritoneal metastases and lympho-vascular invasion is much higher than for early tumours. Advanced gastric tumours often invade the adjacent gastric wall via submucosal lymphatics creating a diffusely thickened and rigid stomach (linitis plastica) (Fig. 13.22). Invasion into adjacent structures such as the pancreas can also occur (Fig. 13.23).

Fig. 13.22 Barium meal showing extensive gastric carcinoma with narrowing of the lumen (arrowed).

Fig. 13.23 Resection specimen showing invasion of a gastric cancer into the tail of the pancreas. The spleen has been removed en bloc with the stomach and distal pancreas.

Factors affecting survival in advanced gastric cancer

The survival of patients with advanced gastric cancer depends upon the stage of the tumour at presentation and on the general fitness of the patient. Treatment with curative intent implies surgical resection, increasingly combined with perioperative chemotherapy. For surgery to be curative, excision of the primary tumour must be adequate, with margins clear of the tumour and with satisfactory en bloc resection of all possible involved lymph nodes (EBM 13.8).

13.8 D1 versus D2 (radical) lymph node dissection in gastric cancer

‘Subgroup analysis suggests a survival benefit for T₃ and T₄ tumours with more radical surgery. Learning curves of surgeons and centres performing low-volume cancer surgery may confound any benefit of more radical surgery.’

McCulloch P, et al. Cochrane Database of Systemic Reviews 2004; CD001964.

Poor survival has been correlated with depth of tumour invasion through the stomach wall, involvement of tumour resection margins and the presence of lymph node metastases. Transgression of the tumour through the stomach wall is associated with poor survival, as the tumour is able to spread transperitoneally and therefore seed the peritoneum with malignant cells, making complete surgical excision impossible.

A comprehensive pathological classification of tumours has enabled the prognosis of a particular stage of cancer to be estimated. Such staging is usually classified according to the tumour size (T), the node status (N), and the presence or absence of distant metastases (M) (Table 13.3).

Table 13.3 TNM classification of gastric carcinoma*

T (Tumour)
T1	Tumour invades lamina propria or submucosa
T2	Tumour invades muscularis propria or subserosa
T3	Tumour invades serosa
T4	Tumour invades adjacent structures
N (Node)
N0	No lymph node involvement
N1	Fewer than 7 lymph nodes involved by tumour
N2	7–15 lymph nodes involved by tumour
N3	More than 15 lymph nodes involved by tumour
M (Metastases)
M0	No metastases
M1	Metastases present

* Greene FL, Page DL, Fleming ID, et al, eds. AJCC cancer staging manual. 6th edn. Springer-Verlag: New York; 2002.

Staging of gastric carcinoma

• CT: Any patient with a histological diagnosis of gastric cancer should undergo a CT scan of their chest, abdomen and pelvis unless they are very frail. This should provide information about the M-stage (liver, lung, peritoneum and distant nodes) and can help exclude T4 involvement of adjacent structures such as the pancreas.

• EUS: EUS is excellent at determining T-stage. High frequency probes (10 MHz or more) can accurately differentiate between T1–4 disease and add information of local nodal status (N-Stage).

• Staging laparoscopy: This procedure is essential in patients with locally advanced tumours to detect small volume peritoneal and liver metastases that cannot be detected by CT (Fig. 13.24). Peritoneal washings are also helpful as patients with positive peritoneal cytology for malignancy have a very poor prognosis and rarely benefit from surgery.

• PET-CT: Gastric adenocarcinomas are not always PET-avid. This limits PET’s application as a routine staging procedure looking for metastatic disease.

Fig. 13.24 Staging laparoscopy showing omental metastases and ascities secondary to advanced gastric cancer.

Treatment with curative intent

All patients should have their case discussed by a multidisciplinary Upper GI team. Those with potentially curable disease who are deemed fit enough for radical therapy have the following options:

• Surgery alone: Patient with early gastric cancer should undergo a distal (subtotal) or total D₂ gastrectomy (depending upon the site of the tumour) done by an experienced surgeon working in a high volume cancer centre. The ‘D₂’ description refers to the excision of both the first tier of perigastric lymph nodes and the second tier of nodes along the gastric arteries (Fig. 13.25). Reconstruction of the gastrointestinal tract is usually by Roux en-Y to prevent bile reflux (Fig. 13.26). When oncologically safe to do so, a distal gastrectomy is preferable to a total gastrectomy as it gives a better quality of life

• Combined therapy: Randomized clinical trials in the UK have shown improved survival for patients who have perioperative chemotherapy and surgery compared to those who have surgery alone. The effect seems most pronounced for advanced tumours; the neo-adjuvant or preoperative component of the chemotherapy seems to have the biggest impact on survival (EBM 13.9). Further trials continue to discover if newer agents such as Bevacizamab can improve survival further. The surgery is the same regardless of whether chemotherapy is given or not.

Fig. 13.25 Operative view of the coeliac axis after D2 nodal dissection and removal of all lymph nodes.

Fig. 13.26 Total gastrectomy with curative intent.

13.9 Combination surgery and chemotherapy in gastric cancer

‘In patients with operable gastric or lower esophageal adenocarcinomas, a perioperative regimen of ECF decreased tumor size and stage and significantly improved progression-free and overall survival.’

Cunningham D, Allum WH, Stenning SP, Thompson JN, Van de Velde CJ, Nicolson M, et al. Perioperative chemotherapy versus surgery alone for resectable gastroesophageal cancer. N Engl J Med 2006; 355(1):11-20.

Palliation

• Best supportive care: Some patients are too frail for any anticancer therapy and all focus should be on relieving their symptoms and supporting them and their families through their terminal illness. Nausea and vomiting is treated with antiemetics such as cyclizine or ondansetron. Poor appetite may respond to steroids such as dexamethasone. Pain often requires opiate analgesia. Eating can be particularly difficult for patients with advanced gastric cancer and dietetic support is essential. Towards the end of a patient’s life they may need medication via a subcutaneous infusion from a portable syringe driver.

• Palliative chemotherapy: For patients who are fit enough, valuable improvements in quality of life can be achieved with palliative chemotherapy using combinations of drugs such as epirubicin, cisplatin and 5-fluorouracil. In addition, life expectancy can be extended if the tumour is chemosensitive (EBM 13.10).

• Palliative radiotherapy: Bleeding from advanced gastric tumours can be troublesome and can be greatly reduced by a short course of external beam radiation.

• Stenting: Patients with gastric outlet obstruction who have persistent vomiting may benefit from the endoscopic placement of a self-expanding metallic stent although the results are unpredictable.

• Palliative surgery: Options include a gastric bypass (often done laparoscopically) for distal tumours, or a palliative resection. The latter is a big undertaking for patients with incurable disease and should only be considered in those with distal tumours who have not benefitted from lesser interventions and who are fit (Fig. 13.27).

13.10 The role of palliative chemotherapy in gastric cancer

‘Systematic reviews show a modest survival benefit for palliative chemotherapy in gastric cancer, with ECF (epirubicin, cisplatin and 5-fluorouracil) regimens currently amongst the more effective. Newer combinations with irinotecan- or taxane-based regimens show promising results.’

Wohrer SS, et al. Ann Oncol 2004; 15:1585–1595.

Fig. 13.27 Palliative bypass procedure (gastrojejunostomy) for obstructing distal gastric cancer.

Other gastric tumours

Ménétrier’s disease

This is a condition of gastric mucosal hypertrophy, in which the mucosal rugal folds are grossly enlarged in the fundus and body of the stomach; the antrum is usually spared. Mucosal hypertrophy may lead to abnormally large secretions of mucus or acid. Over-secretion of acid and protein-rich mucus may contribute to symptoms of epigastric pain and hypoproteinaemia.

Ménétrier’s disease is associated with an increased incidence of malignancy in the stomach and once it has been diagnosed total gastrectomy should be considered in an otherwise fit patient.

Gastritis

This common condition is due to inflammation of the gastric mucosal lining. It may be caused by a variety of injurious agents, both chemical and bacteriological. It is frequently associated with over-indulgence in alcohol. Biliary gastritis is seen in the presence of bile in the stomach (frequently seen after Polya-type partial gastrectomy).

Gastritis may arise as a consequence of extreme stress resulting from shock, and this form is therefore more frequently encountered in the intensive care situation. Such gastritis is thought to be a consequence of mucosal hypoperfusion and acidosis secondary to a shock-like state. This combination leads to mucosal ischaemia and resulting stress gastritis, which can cause loss of mucosa resulting in erosions that may on occasion bleed profusely. Gastritis may be lessened or prevented by resuscitation, administering mucosal protective agents, and neutralizing or minimizing gastric acid secretion. Surgery is undertaken rarely to control massive haemorrhage resulting from gastritis.

Dieulafoy’s lesion

A condition of profuse bleeding from an abnormal vessel situated in the gastric mucosa and not associated with ulceration, Dieulafoy’s lesion is usually found in the upper stomach. Such bleeding is treated initially by injection sclerotherapy, but may require open gastrotomy and oversewing of the bleeding point.

Bezoars

Accumulations of hair (trichobezoars) or vegetable matter (phytobezoars) or combinations of the two (trichophyto-bezoars), these may on occasion form a complete cast of the stomach, and the ensuing reduced nutritional intake contributes to malnourishment. The diagnosis is made by barium examination and surgical removal is advisable.

Duodenal obstruction

Common causes of duodenal obstruction are pyloric stenosis and carcinoma of the pancreas. Rarer causes include blockage by mesenteric lymph nodes, duodenal diverticulum, duodenal atresia, annular pancreas and chronic duodenal ileus. If surgical treatment is required, bypass by duodenojejunal or gastrojejunal anastomosis is often appropriate. Symptomatic diverticula may have to be excised. Chronic duodenal ileus is an ill-defined entity that may affect visceroptotic females and rapidly growing, thin children. It has been suggested that the duodenum is obstructed by the superior mesenteric vessels as they cross its third part, but most surgeons are sceptical about this explanation. The condition is usually self-limiting in children, but in adults surgical bypass may have to be considered.

Duodenal diverticula

The duodenum is the second most common site for diverticulum formation in the gastrointestinal tract. The diverticula rarely develop before the age of 40 years, and are often found at the point of entry of the common bile duct. They are frequently discovered incidentally at endoscopy or on barium meal examination, but can cause obstruction, bleeding and inflammation (diverticulitis). Symptomatic diverticula should be excised if it is certain that they are the cause of problems.

Duodenal trauma

Duodenal damage may follow severe crush injury of the upper abdomen. Retroperitoneal air may be seen on abdominal X-ray.

Surgery for obesity

Obesity is an increasing problem world-wide. It is defined as a body mass index (BMI) greater than 32; morbid obesity represents a BMI greater than 38. (Until recently, the cut-offs were 30 and 35 respectively.) The effect of obesity on the respiratory, cardiovascular, locomotor and metabolic systems, as well as on mental health, can be severe. Patients with morbid obesity have a significantly reduced life expectancy; for example, a person with a BMI of 45 at the age of 25 will have a reduction in life expectancy of 11 years.

Prevention is better than cure and indeed there is no current ‘cure’ for obesity. Weight reduction programmes combining reduced calorie intake with increased exercise have variable results. Weight loss is slow and the programme often requires to be followed for many, many months. Furthermore, a change in eating and exercising behaviour is necessary if the weight loss is to be maintained long-term.

Patients who are morbidly obese can benefit from obesity or bariatric surgery. Such patients need to be assessed very carefully, taking account of their mental state, physical fitness, and the presence of medical conditions that lead to obesity but can be corrected by treatment (e.g. hypothyroidism). The careful selection of patients involves a multidisciplinary team approach.

A number of operations have been performed for obesity in the past. Many of the intestinal bypass operations and jaw wiring procedures are relegated to history. Current obesity surgery is designed to be restrictive or malabsorptive:

Operations for obesity

Current options include gastric banding, vertical banded gastroplasty, gastric bypass and duodenal switch. All these operations can be performed laparoscopically. However, the technical difficulty of such surgery increases in the order that these operations are listed above. The more complex operations are more likely to lead to better excess weight loss in the short term. However, there is increasing evidence to show that the percentage of excess weight loss at 3 years is similar for gastric banding and gastric bypass. The procedures can be combined; for example, gastric banding is technically easier to perform in the very obese patient who has a BMI greater than 55. Once excess weight loss has plateaued, removing the band and performing a gastric bypass may allow further excess weight loss.

The gastric band is a ring with an inflatable inner cuff, which is placed laparoscopically a short distance below the oesophagogastric junction, creating a small (approximately 50 ml) gastric pouch (Fig. 13.28A). The cuff can be inflated or deflated via injections into a port site located in the subcutaneous tissues, in order to tighten or relax the cuff around the stomach. The tighter the cuff, the longer foodstuffs entering the gastric pouch will take to exit through the ring into the remainder of the stomach and intestinal tract, prolonging the feeling of satiety.

Fig. 13.28 AGastric banding.BGastric bypass.

Gastric bypass involves stapling the stomach closed a short distance below the oesophagogastric junction (Fig. 13.28B). A Roux limb is then brought up and anastomosed to the small proximal gastric remnant. Depending on the size of the pouch and calibre of the anastomosis, there will be a degree of restrictive activity, as well as a major malabsorptive element, as food will enter the distal jejunum and proximal ileum without exposure to bile or pancreatic and other digestive enzymes.

Vertical banded gastroplasty is now rarely performed. Duodenal switch is a complex operation reserved for a minority of obese patients.

Most patients with restrictive-type surgery find that they can eat more with time as the gastric remnant dilates. Hopefully, however, the target weight loss will have been achieved and improved eating habits established to allow maintenance of a healthier weight.