Oesophagus & Stomach
Benign Surgical Diseases of the Gastro-oesophageal junction
Anatomy of the Oesophagus Upper oesophageal sphincter (Cricopharyngeal constriction)
Ian J Beckingham Keith Graetz
Aortic constriction Oesophageal body
Abstract This article focuses on Gastro-oesophageal reflux disease (GORD) and Achalasia, their symptoms, diagnosis, and surgery.
Right crus
Keywords Anatomy; Dor wrap; gastro-oesophageal reflux; GORD; laparo
Lower oesophageal sphincter
scopic fundoplication; Nissens fundoplication; oesophagus
The oesophagus acts as a conduit through the thorax for the passage of solid and liquid matter (Figure 1). It is approximately 25 cm long and is made up of both striated and smooth muscle extending from the pharynx to the gastro-oesophageal junction (GOJ). The proportion of smooth muscle fibres increases to 100% at the lower end of the oesophagus with fibres arranged in inner circular and outer longitudinal layers. Propulsion of a food bolus in a peristaltic wave is controlled by the myenteric nerve plexus in the muscular layer of the oesophagus. The lower oesophageal sphincter (LOS) is 2–3 cm long and is found at the point at which the oesophagus passes through the crus of the diaphragm and enters the stomach. The muscle layers may be a little thickened, particularly the circular layer, but will there is no visible external marking of the muscle outer surface. The LOS complex is the primary site of the two most important benign diseases of the oesophagus that will present to the surgeon – gastro-oesophageal reflux disease (GORD) and achalasia.
Stomach
Figure 1
flat or bending forward (postural reflux) but in many patients is non-postural. The majority of patients cope with adjustments to their lifestyle (e.g. cessation of smoking, reduction in alcohol, sleeping with extra pillows, avoiding tight fitting clothing, not eating late at night, avoidance of spicy and irritant foods) together with self-medication with antacids. An increasing number of patients take Proton Pump Inhibitors (PPI’s) which even though they have become cheaper with the availability of generic and non-prescription PPI’s and H2 receptor antagonists still represent an annual budget of £300 million to the NHS. There remain a significant number of patients whose symptoms are either not fully controlled with medication, who experience side-effects from medication or have volume (alkaline) reflux which does not respond to standard anti-reflux medications. This latter group typically complain of regurgitation (often described as vomiting by patients but is usually effortless and often postural) as their dominant symptom. These patients, together with those who prefer a more permanent treatment option are candidates for surgery.
Gastro-oesophageal reflux disease (GORD) Gastro-oesophageal reflux is the involuntary passage of gastric contents from the stomach back into the oesophagus. It is a normal physiological process which occurs to some extent in all individuals but when associated with pain is referred to as Gastro-Oesophageal Reflux Disease (GORD). It has been estimated that up to 25% of the population experience symptoms suggestive of GORD on a regular basis (Table 1).1,2 Pain, classically described as retrosternal burning, typically occurs after eating, and in some individuals is related to body position such as lying
Symptoms of GORD • Heartburn • Epigastric or chest pain (masquerading as cardiac pain) • Dysphagia • Odynophagia (painful swallowing) • Otalgia • Chronic nausea • Regurgitation of food (“vomiting”) • Poor dentition and dental caries • Halitosis • Cough/wheeze/aspiration
Ian J Beckingham BMBS FRCS MD is a Consultant Laparoscopic UGI Surgeon at the Queens Medical Centre, Nottingham University Hospitals NHS Trust, Nottingham, UK. Conflicts of interest: none declared. Keith Graetz MA BChir FRCS DM is a Locum Consultant General Surgeon at the Queens Medical Centre, Nottingham University Hospitals NHS Trust, Nottingham, UK. Conflicts of interest: none declared.
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Table 1
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from the number of episodes of reflux and the duration of reflux episodes and is considered abnormal if >18. Correlation of measured acid reflux episodes with patient symptoms should be >50%. Patients with an appropriate history of GORD, a high DeMeester score (>18), good symptom and acid reflux correlation are most likely to benefit from surgical management of their disease.
With more widely available pH and impedance testing there is an increasing recognition of atypical reflux symptoms including nocturnal aspiration and lung damage, nausea, otalgia, sore throats and dental caries which may respond to medical and/or surgical intervention.
Investigation of GORD
Oesophageal impedance There is increasing recognition of a group of patients with volume or alkaline reflux where pH studies are within normal limits but typical symptoms of GORD often with regurgitation, are present. Electrical impedance monitoring is a similar technique to pH studies but relies on the generation of a current within the probe sensors rather than assessment of hydrogen ion concentration and can specifically detect “volume” reflux in addition to patients with conventional GORD. Correlation with patient symptoms is still necessary to determine those patients who are likely to have disease that will be improved with surgery. Most patients with GORD are already taking PPIs which need to be stopped prior to performing pH studies resulting in symptom recurrence, poor compliance and sometimes leading to erroneous results. The benefit of electrical impedance studies is that antacid therapy does not need to be stopped prior to performing the test. Impedance monitoring is likely to replace pH studies as the gold standard investigation of GORD as it becomes more widely available.
The investigation of GORD prior to surgical intervention involves the exclusion of other diagnoses which may have a degree of symptom overlap (Table 2). Oesophago-gastro-duodenoscopy (OGD) Around 30% of patients with GORD referred for OGD will show evidence of inflammation, however, this proportion is significantly less if patients have been on PPIs. Evidence of complications of GORD may be seen (eg strictures or ulceration) and anatomical features such as hiatus hernia noted, and other disease processes such as peptic ulcer disease and cancer excluded. pH studies and manometry Confirmation of the diagnosis of GORD and the correlation of symptoms with reflux episodes is usual before proceeding to surgery. pH studies and manometry have been the “gold standard” test for confirming the diagnosis and also excluding less common conditions including achalasia and scleroderma which can masquerade as reflux. The test involves the placement of a fine nasogastric probe to a point just distal to the gastro-oesophageal junction. Accurate placement of the pH/impedance catheter is guided by initial manometric testing to identify the position and length of the lower oesophageal sphincter (LOS). Pressure-measuring electrodes are located at 5 cm intervals along the probe. Recordings of the pressures generated at different levels within the oesophagus are then measured during dry and wet swallows to measure peristalsis and LOS function. The manometry probe is then replaced with a pH probe which typically measures acidity in the oesophagus and stomach. Patients are requested to document when they experience symptoms of GORD and eat meals. Recording is carried out over a 24 hour period with the patient performing their normal daily activities. Typical findings on manometry include a short or low pressure LOS. Motility may be normal or impaired (secondary to reflux damage). Impaired motility often improves following anti-reflux surgery.3 The pH studies in GORD should demonstrate regular and/or prolonged reflux episodes of acid (pH <4) into the oesophagus with an overall pH <4 for >4% of the measured period. The DeMeester score is a calculated figure derived
Barium swallow Barium studies provide a good assessment of anatomy and peristaltic function of the oesophagus but correlate poorly with the diagnosis GORD as they are reliant on the patient having an episode of reflux during the investigation. They are of most use in the investigation of patients with complications or recurrent symptoms following surgery.
Surgery for GORD The aim of surgery for GORD is to control symptoms and remove the need for long term antacid therapy. As discussed above, only a small percentage of patients with GORD need surgery for their disease. Laparoscopic fundoplication has become the gold standard surgical procedure for GORD and is performed using a 4 or 5 port technique under general anaesthesia (Figure 2). The higher short and long term morbidity of open abdominal and transthoracic surgery, together with the now widespread availability and good results from the laparoscopic procedure have resulted in these open procedures being seldom used except for revision/redo fundoplication. More recent endoscopic therapies, including endoscopic plication and radiofrequency have proved disappointing in both the degree of and the longevity of symptom control and certainly offer no advantages over surgery at the present time. The most popular procedure currently performed in the UK is the 360° Nissen fundoplication. After port placement the liver is retracted anteriorly to allow access to the gastro-oesophageal junction (GOJ). The first step involves opening the pars flaccida of the lesser omentum and identifying the right crus. The
Differential diagnosis of GORD • Carcinoma of the oesophagus • Peptic ulcer disease • Benign stricture of oesophagus • Scleroderma • Achalasia Table 2
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Complications of GORD surgery As with any form of surgery the complications can be divided into either early or late, conversion to an open procedure should occur infrequently (<5%). Bleeding from the major gastric vessels or from liver trauma may occur intraoperatively. Post-operatively all patients will experience a degree of dyspahgia. Most surgeons will advise patients to take a liquid/semisolid diet for the first few weeks following the operation until oesophageal function returns to normal. As long as liquids are tolerated reassurance is all that is necessary at this stage. Persistent dysphagia occurs in less than 5% of patients at 3 months post-surgery. Assessment should be with barium swallow to look for excessive hiatal tightness or fibrosis, or malposition or slippage of the wrap. Sometimes peristalsis is seen to be poor and oesophageal manometry may be required. If symptoms are debilitating and persist, revisional correction with conversion to a partial wrap or undoing of the wrap altogether may be necessary. Popularisation of the partial fundoplication has seen a marked reduction in these problems without a significant failure to control reflux.4,5 Failure to control reflux symptoms or recurrence of symptoms after a period of previously good control may be associated with wrap disruption. There may be a history of vomiting or retching prior to the return of symptoms. In some cases this represents a loosening of the wrap and settles down after a few weeks, in other cases there may be permanent wrap disruption requiring revisional surgery. The first line of investigation is a barium swallow and if this is normal repeat pH/impedance studies may be required. In some series up to 10% of patients were found to be taking PPIs after surgery but when appropriately investigated the majority did not demonstrate reflux. There is a tendency in any patient who has any form of problem following anti-reflux surgery to be put back onto PPIs on the assumption that it is a recurrence of symptoms although it rarely is the case. Some patients have a “sensitive oesophagus” and experience any transient hold up of food at the wrap as pain. A liquid soothing anti-acid preparation is more appropriate in this small group. “Gas bloat” or “post-fundoplication” syndrome is the trapping of intra-luminal gas within the fundus of the stomach. It usually presents with epigastric pain and an inability to release gas from the upper gastrointestinal tract via the mouth. Abdominal bloating and increased rectal flatus are also common. Patients should be warned of these symptoms pre-operatively particularly if symptoms of irritable bowel syndrome are present as these may be exacerbated. Occasionally (2–3%) patients experience diarrhoea. Fortunately for most patients these symptoms are an irritation rather than a problem but occasionally symptoms are severe enough to require undoing the wrap.
Port placement for laparoscopic fundoplication surgery
5mm 5mm
5mm 5mm 10mm
Figure 2
phreno-oesophageal ligament (the peritoneal layer that binds the anterior surface of the oesophagus and stomach to the diaphragm) is divided up to the hiatus, down the left crus and across the cardia of the stomach onto the diaphragm and upper pole of the spleen. A window is made behind the oesophagus and stomach and anterior to the crura. The GOJ is now mobile and any hiatus hernia present will be evident and can be reduced by freeing up any attachments within the thoracic cavity. The crural hiatus is closed loosely around the oesophagus using non-absorbable sutures. The fundus is then brought through the posterior window behind the oesophagus and sutured to itself to provide a loose, floppy wrap (Figure 3). A number of studies have demonstrated conclusively that routine freeing of the short gastric vessels is unnecessary. The wrap is then fixed to the oesophagus with further non-absorbable sutures to prevent slippage. A 50–56 fr bougie is often inserted into the oesophagus via the mouth to allow accurate tightening of the wrap. It should be noted that there are many variations and modifications of the approach described here but the general principles remain the same. More recently many surgeons have taken to performing partial wraps to reduce the side effect profile of fundoplication. The anterior (Dor) and posterior (Toupet) 180° wraps have become most popular and several large trials have confirmed symptom control equivalent to the full fundoplication with faster recovery of swallowing.4,5
Completed Nissen’s and Dor wraps
Achalasia
a Nissen 360˚ wrap fundoplication
As discussed above, GORD is a consequence of a “relative” laxity of the gastro-oesophageal sphincter complex with involuntary passage of gastric contents back into the oesophagus. Achalasia represents the other extreme with high LOS pressures and a failure of relaxation of the muscle. The oesophageal body (the main part of the oesophageal muscle above the LOS) is aperistaltic.
b Dor 180˚ anterior fundoplication
Figure 3
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It occurs with an incidence of 1-2 per million and may affect any age group from infants to the elderly with an equal male to female ratio. It bears a strong similarity to Chagas’ disease, a disease common to South America caused by Trypanosoma cruzi, a flagellate protozoan. Classically it presents with dysphagia and regurgitation of undigested food (Table 3). Clinical examination often reveals little other than weight loss and halitosis. OGD is the first line investigation of any patient with new onset dysphagia. The clinical findings in achalasia are of a dilated tortuous oesophagus often containing food debris but these features are only seen in later stages and early appearances may be normal. The lower oesophageal sphincter may appear tight but rarely occludes passage of the gastroscope. A barium swallow will show dilatation of the oesophagus with a hold up at the LOS with a classic bird’s beak appearance and aperistalsis of the main oesophageal body with tertiary contractions. Oesophageal manometry provides the definitive diagnosis. Pneumatic balloon dilatation has in the past been the mainstay of treatment. The results are very operator dependent and recurrence rates are high, with occasional oesophageal disruption and development of reflux in a number of patients. Botulinum toxin injection of the lower oesophageal sphincter has been used to paralyse the LOS with good initial results in some patients but recurrence of symptoms within 3–6 months in most. Surgical management offers the potential for good disease control and excellent symptom relief and again with the development of the laparoscopic approach has become the standard treatment in most units.6 Heller’s cardiomyotomy is the classic operation described for achalasia. The GOJ is identified and an 8 cm myotomy performed in the midline avoiding the anterior vagus nerve. The myotomy is taken down to the mucosa with great care to avoid perforation. It is extended into the thorax and down onto the stomach
wall to ensure complete division of the LOS (which is 2.5–3.5 cm long and has no external markings). Some surgeons choose to perform a fundoplication to prevent/reduce reflux and a partial 180° anterior or posterior wrap is usual. Mucosal tears can be repaired and “patched” with an anterior wrap. Results of surgery are good and patients should be alleviated of their regurgitation with improvement in their swallowing. The oesophageal body however never recovers its function and remains aperistaltic. Swallowing is therefore dependent on forward propulsion from the pharyngeal muscles and gravity to carry the food bolus across he redundant LOS and patients should be forwarned that their swallowing is unlikely to be perfect following surgery. ◆
References 1 Dent J, Brun J, Fendrick AM, et al. An evidence-based appraisal of reflux disease management: the Genval Workshop Report. Gut 1999; 44(suppl. 2): S1–6. 2 Klauser AG, Schindlbeck NE, Muller-Lissner SA. Symptoms in gastrooesophageal reflux disease. Lancet, Elsevier, London, UK 1990; 335: 205–8. 3 Beckingham IJ, Cariem AK, Callanan MD, Louw JA, Bornman PC. Oesophageal dysmotility is not associated with poor outcome after laparoscopic Nissen fundoplication. Br J Surg 1998; 85: 1290–3. 4 Strate U, Emmermann A, Fibbe C, et al. Laparoscopic fundoplication: Nissen versus Toupet two-year outcome of a prospective randomized study of 200 patients regarding preoperative esophageal motility. Surg Endosc 2008 Jan; 22(1): 21–30. 5 Wijnhoven BP, Watson DI, Devitt PG, et al. Laparoscopic Nissen fundoplication with anterior versus posterior hiatal repair: long-term results of a randomized trial. Am J Surg 2008 Jan; 195(1): 61–5. 6 Beckingham IJ, Griffin M. Achalasia of the cardia; dilatation or division? Is pneumatic balloon dilatation justifiable anymore? Ann R Coll Surg Eng 2006; 88: 11–2.
Symptoms of achalasia • Dysphagia • Regurgitation of food • Halitosis • Chest pain • Dyspepsia • Chronic cough/nocturnal aspiration • Weight loss
Further reading Beckingham IJ, Callanan MD. PC Bornman Laparoscopic cardiomyotomy for achalasia after failed balloon dilatation. Surg Endosc 1999; 5: 493–6. Mahon D, Rhodes M, Decadt B, et al. Randomized clinical trial of laparoscopic Nissen fundoplication compared with proton-pump inhibitors for treatment of chronic gastro-oesophageal reflux. Br J Surg 2005 Jun; 92(6): 695–9.
Table 3
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