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.