Disorders of the oesophageal hiatus cause considerable morbidity ranging from that of an intermittent nuisance to serious disabling disease. Diagnosis is often difficult and treatment mostly medical. Surgical treatment must be judicious and carefully selected to be effective.

The oesophagus is a muscular tube connecting the pharynx and the stomach and traversing the posterior mediastinum. The lining is normally squamous epithelium which is surrounded first by circular and then longitudinal smooth muscle. The whole lies in the loose connective tissue of the posterior mediastinum. The vagal plexus is closely attached to the oesophagus and coalesces on the distal third to form the anterior and posterior vagal trunks. The distal 4 to 6 cm of the oesophagus passes into the abdominal cavity through the crura of the left diaphragm just anterior to the aorta and posterior to the left lobe of the liver. Connective tissue to the right becomes the lesser omentum while that to the left forms the gastrophrenic ligament. The blood supply to the oesophagus in the neck is from the thyroid vessels while in the thorax the arterial supply is both directly from the aorta and from the bronchial arteries. Venous drainage is to the azygos system. The left gastric vessels supply the distal oesophagus. Lymphatic drainage is to peri-oesophageal nodes and thence to the thoracic duct which lies between the oesophagus and the vertebra column.

The nerve supply is autonomic via the vagus and the thoracic sympathetic chain. There are, therefore, cholinergic, adrenergic, and also nitrergic nerves, the last being crucial in relaxation of the distal oesophagus.

A bolus of food or fluid is propelled from the pharynx into the oesophagus. The larynx is raised, the epiglottis tilted posteriorly, and the cords are closed to prevent food entering the trachea. The superior oesophageal sphincter at the level of the cricoid cartilage relaxes to receive the bolus which is carried down the oesophagus by a peristaltic wave preceded by a wave of relaxation. Relaxation is mediated through nitrergic nerves while peristalsis is cholinergic (see also Section 14.1 93).

The pressure within the thoracic oesophagus is negative with respect to the abdomen and reduces still further with each breath, yet food generally stays within the stomach once there. This is a function of the distal oesophageal high pressure zone. Manometric studies show a pressure inversion point between the abdomen and the thorax at the crura. The distal 3 cm of oesophagus have an even higher luminal pressure suggesting a functional sphincter even though there is no obvious anatomic structure. It is this high pressure zone in achalasia which is at a particularly high pressure and cannot relax because of loss of nitrergic nerves, possibly as the result of previous Herpes zoster infection. The functional integrity of the high pressure zone is important for continence between the stomach and the oesophagus. Continence is probably also enhanced by the obliquity of the cardia and its position distal to the apex of the gastric fundus creating a type of flutter valve. The fundus, when full and distended, also exerts some pressure upon the abdominal oesophagus. The diaphragmatic crura appear to play no part in gastro-oesophageal continence at rest but are important at moments of sudden rises in intra-abdominal pressure, for example during coughing and straining, when contraction of the diaphragm pinches the oesophagus tightly shut.

Absolute continence of the cardia would be disastrous since it is necessary to vomit and release gas from time to time. Selective incontinence is achieved by contracting the longitudinal muscle to shorten the oesophagus and open the angle at the cardia. Gas is then released by relaxation of the high pressure zone while vomiting is accompanied by vigorous reverse gastric peristalsis against a closed pylorus.

A number of substances affect the high pressure zone either enhancing the pressure or inducing relaxation (Table 1) 286. Some may be important in normal physiological function or the pathophysiology of reflux disease, although some of the effects may be pharmacological.

The most important disease state is caused by disorders of the oesophageal hiatus that produce pathological reflux of gastric contents into the distal oesophagus. Some reflux must be considered normal and therefore pathological reflux is defined as more reflux than the 95 per cent confidence limits for the normal population. Translated into numerical terms; reflux is pathological if the distal oesophageal lumen is at a pH below 4 for more than 4 per cent of a day or there are more than 10 reflux episodes per 24 h (see also Section 14.6 96). An acid reflux episode is defined as a drop in luminal pH below pH 4. The much rarer alkaline reflux of duodenal contents raises the pH above 7.5. Physiological reflux is rapidly cleared from the oesophagus back into the stomach by successive peristaltic waves until the pH is restored to 7. Prolonged exposure of the oesophagus to acid may be caused not only by frequent episodes of reflux but also by large volume reflux and defective oesophageal clearance, or a combination of all three.

Anatomic changes at the oesophageal hiatus such as a sliding hiatus hernia or resection of the distal oesophagus make incompetence of the continence mechanism more likely (Fig. 1) 890. Obesity is a frequent concomitant of sliding hiatus hernias and may be aetiological by inducing a chronic rise in intra-abdominal pressure displacing the stomach in a cephalad direction into the thorax. Age is also important for reflux is commoner at either extremes of age. The gastro-oesophageal mechanism is not fully mature in infancy and becomes incompetent again in senescence. Furthermore, oesophageal peristalsis, and therefore clearance, is less efficient. In old age these defects are commonly accompanied by a hiatus hernia making pathological reflux even more likely. A hiatus hernia per se does not always induce reflux. Gastric emptying may also be slower than normal and therefore contribute to reflux.

Reflux is both painful and damaging to the oesophagus. Gastric contents are corrosive and ‘burn’ the oesophageal squamous epithelium. Gastric and duodenal juices together are more destructive than either alone indicating that the damage is not purely pH dependent. The refluxate causes inflammation and loss of the squamous epithelium which, in severe cases, may produce deep chronic ulceration and/or peptic strictures. In some patients the oesophageal squamous epithelium is replaced by columnar metaplasia, the so-called Barrett's oesophagus, which has either gastric or intestinal characteristics. The oesophagitis is graded macroscopically from normal (grade 0) to grade 4 which is severe confluent oesophagitis with ulceration, stricture formation, or columnar metaplasia (Table 2) 287. There is surprisingly poor correlation between the severity of inflammation and the symptoms although the severity of the oesophagitis is a combination of the corrosive content of the refluxate and the length of time of the exposure. Grade 4 oesophagitis therefore represents the most severe reflux, although it is not clear why some patients produce strictures and others a columnar-lined Barrett's oesophagus. The latter may represent a local change in epithelial cell differentiation induced by reflux but whether this is an idiosyncratic response, or one to a particular pattern of reflux, is not clear. Barrett's oesophagitis tends to occur in younger patients with severe daytime reflux while strictures usually form silently in elderly patients who tend to have nocturnal reflux and diminished oesophageal clearing. Such patients present with dysphagia and seldom complain of reflux or heartburn.

An important complication of Barrett's oesophagitis is the propensity for developing adenocarcinoma within the columnar epithelium. The risk is about 1 per 100 patient years but the risk is greater in those patients with intestinal metaplasia. It is, therefore, sometimes suggested that the risk is sufficiently great to warrant endoscopic surveillance annually but the cost for each life saved is high.

Retrosternal burning pain (heartburn) is the most common symptom of reflux. Mild symptoms are frequent, and almost normal, after meals, particularly if people stoop a lot soon after a heavy meal. Symptoms may however be severe, persistent, and unrelated to posture and may also be accompanied by acid brash (an acid taste in the mouth). Nocturnal reflux may be sufficiently painful to wake a patient from sleep and occasionally food may be regurgitated into the mouth. Such patients often complain of a foul taste in the mouth on waking. Nocturnal reflux may present in the elderly as recurrent respiratory tract infections as a result of frequent aspiration, and in rare cases reflux may be responsible for attacks of asthma in younger patients. Whether the asthma is caused by inhalation of acid gastric juice or is a reflex bronchospasm induced by acid in the distal oesophagus is uncertain. Odynophagia (painful swallowing) may also be a manifestation of oesophagitis and occasionally reflux may cause diffuse oesophageal spasm which produces severe crushing chest pain mimicking angina or a myocardial infarct.

Peptic strictures usually present in older patients with gradually progressive dysphagia, first for solids then liquids, but with surprisingly little weight loss and often no heartburn. In contrast, patients with carcinoma of the oesophagus usually present with rapidly progressive dysphagia and marked weight loss despite the brevity of the history.

The history is the most important indication for the diagnosis which is confirmed by endoscopy (Table 3) 288. This demonstrates the oesophagitis or the columnar transformation of the distal oesophageal mucosa (Figs. 2 and 3) 891,892. A sliding hiatus hernia is often visible with the squamocolumnar junction of the oesophagus and the stomach at a variable distance above the crura of the diaphragm. When oesophagitis is absent but the history is strongly suggestive of reflux, 24-h oesophageal pH measurement may demonstrate pathological reflux and a temporal correlation between reflux episodes and the symptoms (Fig. 4) 893. If the symptoms are atypical then an acid infusion test (Bernstein test) may help correlate the retrosternal pain with acid in the oesophagus. The test is positive when the patient consistently complains of pain when 0.1M hydrochloric acid is infused into the oesophagus and the pain reliably goes when the infusate is changed to saline.

Rarely oesophageal manometry is helpful in the diagnosis of diffuse oesophageal spasm, produced by acid reflux, as a cause of non-cardiac chest pain and in the presence of a normal electrocardiogram and exercise test.

Barium contrast studies may demonstrate a hiatus hernia but are little value in the diagnosis of reflux. A barium swallow is, however, an important, non-invasive first investigation of dysphagia for three reasons: (a) to diagnose a pharyngeal pouch which is a hazard for the endoscopist; (b) to give an anatomical reference point should surgery be necessary; and (c) so that endoscopy can be arranged for a suitable occasion when dilatation or laser therapy is available. Cineradiography is, however, valuable in the diagnosis of dysphagia caused by neurological or pharyngeal muscular disorders, some of which may be secondary to pathological reflux.

Initial management of reflux calls for the adaption of a number of important general corrective measures such as weight reduction; avoiding heavy meals just before retiring to bed or doing heavy work; stopping smoking; avoiding anticholinergic drugs and excess alcohol, and taking antacid alginates for relief of symptoms. Antacid alginates are better at providing relief than antacids alone because the alginate lines the oesophageal epithelium and provides added protection from contact with acid. These measures alone are sufficient for most patients with mild symptoms and an important adjunct for all patients with pathological reflux (Table 4) 289.

More severe symptoms and oesophagitis require more specific therapy such as acid suppression, initially with H&sub2; antagonists or if that is insufficient then a proton pump inhibitor, such as omeprazole or lansoprazole, which provides more complete acid suppression. Symptomatic volume reflux may persist even after adequate acid suppression and may require regular medication with a prokinetic drug such as metoclopramide, domperidone, or cisapride to enhance gastric emptying and oesophageal clearing.

Surgery is reserved for the few patients who remain severely symptomatic with proven reflux resistant to medical therapy or younger patients who require continuous long-term specific medication to control symptoms. For the latter patients there is some unease about prescribing drugs for a lifetime.

The essence of surgical management is to increase distal oesophageal pressure and prevent excess reflux while allowing physiological reflux. The majority of operations are performed through the abdomen and are based on the fundal wrap originally described by Nissen (Fig. 5) 894. This operation is usually performed through a supraumbilical midline incision but laparoscopic techniques are now being developed and applied successfully. The oesophagus is mobilized from the hiatus and the stomach reduced into the abdomen if there is a hiatus hernia and the oesophagus is sufficiently long. The hiatus is narrowed by suturing the crura together to restore a normal anatomic size. The greater curve of the stomach is then mobilized by dividing the short gastric vessels and the fundus wrapped around the distal oesophagus. The stomach is sutured to itself around the oesophagus with about four stitches above the hepatic branches of the vagus nerve. The wrap is loosely fashioned over a 48 FG oesophageal bougie passed down the oesophagus and is only 2 cm long. Too tight a wrap produces marked and lasting dysphagia and too long a wrap induces gastric bloat by making the gastro-oesophageal junction too competent, so preventing belching or vomiting.

The Nissen fundoplication is a 360° fundal wrap. Numerous modifications have been expounded by surgeons, mainly varying the amount of wrap to as little as 180° around the distal oesophagus. In general the efficacy in preventing reflux increases with the circumference of the wrap as do the risks of gas bloat and dysphagia. If the oesophagus is substantially shortened a transthoracic approach is appropriate and either a Nissen fundoplication is fashioned within the chest or a Belsey operation performed (Fig. 6) 895. Belsey's procedure invaginates the oesophagus into the fundus of the stomach, like an old-fashioned inkwell, and includes the diaphragm. In effect this operation produces a 270° wrap which is effective but is associated with the greater trauma of a thoracic incision.

A simple and novel operation to increase lower oesophageal pressure was devised by Angelchik in the United States. A silicone ring prosthesis, somewhat like a small doughnut, is tied around the abdominal oesophagus. The operation is quick easy and readily repeatable and although it is as effective in restoring the high pressure zone and controlling reflux as a well performed fundoplication, the greater long-term morbidity from migration of the prosthesis is unacceptable.

The great majority of patients with peptic oesophageal strictures can be managed successfully by endoscopic dilatation under sedation followed by continuous treatment with a proton pump inhibitor. It appears that omeprazole therapy will reduce the need for and frequency of redilatation which is required, on average, every 15 to 18 months with simple antacid or H&sub2; antagonist therapy. Between one-third and one-half of the patients with strictures need only one dilatation but a small number, who have transmural fibrosis, restricture rapidly and require frequent dilatation or need to self dilate regularly using a mercury weighted bougie. Men with strictures respond significantly less well than women and relapse quicker and more frequently.

Some younger or fitter patients should have antireflux surgery after dilatation to prevent relapse or the need for continuous medical therapy. Rarely the strictures are so fibrotic and unyielding, and restenosis so rapid, that resection of the stricture is necessary.

‘Bile’ diversion by antrectomy and Roux-en-Y has been shown to be useful in some patients with intractable reflux and is advisable after resection of a stricture because a vagotomy is performed of necessity. Vagotomy produces gastric outlet obstruction which in turn needs gastric drainage, but a pyloroplasty would potentiate ‘bile’ reflux and therefore the Roux-en-Y is the best drainage procedure (Fig. 7) 896. It is important to make the duodenojejunal anastomosis at least 45 cm distal to the gastrojejunostomy, or bile will reflux into the stomach and thence into the oesophagus.

Para-oesophageal or rolling hiatus hernias are less common than the sliding variety but are potentially more serious. The anatomic difference from the sliding hernias is that the distal oesophagus and cardia remain in their normal intra-abdominal position while the fundus and body of the stomach roll through the widened hiatus to lie in the posterior mediastinum, beside the oesophagus. In extreme cases the entire stomach and pylorus may lie within the chest (Fig. 8) 897,898. The condition is fairly common in the old and very elderly and is often totally asymptomatic. Occasionally there is a combination of a rolling hernia with a sliding hernia.

1.Patients may suffer intermittent respiratory and cardiac embarrassment, particularly postprandially, because of pressure from a distended intrathoracic stomach.

2.Patients may get acute gastric dilatation or gastric volvulus and become acutely and seriously ill.

3.Gastric ulceration is relatively common in rolling hernias and the ulcer may penetrate mediastinal structures such as the aorta or pericardium.

While most para-oesophageal hernias are usually asymptomatic and are diagnosed from chest radiographs taken for other reasons, some patients present with intermittent epigastric or chest pain, particularly after meals, accompanied by quite marked shortness of breath. Sometimes intermittent dysphagia or vomiting are the presenting symptoms. Sudden severe upper abdominal and chest pain with cyanosis and progressive cardiovascular collapse herald gastric volvulus or acute gastric dilatation. Because of the rotation and angulation of the stomach in these cases, vomiting is usually impossible and the stomach becomes progressively distended and ischaemic. The stomach may perforate as a consequence of the ischaemia but death may supervene earlier unless the patient is resuscitated rapidly and the stomach decompressed by passing a nasogastric tube or endoscope. Urgent surgical correction is also essential.

Rarely a patient may present with dyspepsia, or the complication of haematemesis and melaena, because of a gastric ulcer. If the ulcer erodes the aorta or left atrium the haemorrhage is catastrophic and rapidly fatal.

Diagnosis is usually by a plain anteroposterior chest radiograph which shows a large gastric bubble and fluid level behind the heart. Barium contrast studies may occasionally provide useful additional information (Fig. 9) 899. Endoscopy is difficult because the stomach is full and rotated, and it is often impossible to get out of the stomach and into the duodenum. The endoscopic diagnosis is, therefore, usually gastric outflow obstruction rather than intrathoracic gastric volvulus because the endoscopist is seldom aware that everything is in the thorax. The endoscopist must also be careful to decompress the stomach at the end of the procedure lest the gas distension precipitates an acute gastric dilatation. Computed tomography is also diagnostic but has no advantages over a chest radiograph or a barium meal.

Medical treatment is of no value. Surgical correction is necessary if the patient is disabled by symptoms or is acutely ill. Rapid fluid replacement, gastric decompression, oxygen therapy, and intravenous antibiotics are important preoperative measures for the acutely ill patient with gastric volvulus.

An elective operation in an old patient is usually best performed through an upper midline abdominal incision. The stomach can usually be reduced easily through the hiatus into the abdomen. The hernial sac is excised and the crura approximated, with non-absorbable sutures, to close the hiatus around the oesophagus. An anterior gastropexy, fixing the lesser curve of the stomach to the anterior abdominal wall with three or four sutures, prevents any possible recurrence. A posterior stapled gastroenterostomy provides alternative or additional fixation for the stomach and ensures adequate gastric drainage. A gastroenterostomy alone, which can be performed quickly and easily through a very small incision, may be quite sufficient for some frail patients.

It is dangerous to attempt to deliver the stomach from the thorax through an abdominal incision in acute cases or those with a penetrating peptic ulcer because of the risk of gastric rupture. For these cases a left thoracotomy through the 7th or 8th rib is the best approach and provides good access to decompress and mobilize the stomach. Peptic ulcers may be excised or a partial gastrectomy performed. The hiatus is then repaired after excising the hernial sac and returning the stomach into the abdomen. This operation is however much more traumatic for elderly or frail patients and carries a greater risk of complications.

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