Upper Gastrointestinal Surgery - part 3 doc

or clinemetry. Sensory testing can also be done with electrically induced potentials and motor neurone integrity can be assessed using electromagnetic resonance stimulation. All these investigations are useful in a difficult case, where the standard investigations and therapies have been unsuccessful. Hiatus Hernia The presence or absence of a hiatus hernia is not important in the distinction of the diagnosis of GORD, but is important in the decision about potential treatment strategies. Hiatus hernia may be present as a sliding or rolling hernia (Figure 6.4). Sliding hernias (type 1) are very common, and may contribute to the symptoms of dysphagia. The remaining symptoms in sliding hiatus hernia are usually due to the presence of acid reflux rather than the presence of the hernia itself. In contrast, a rolling (type 2) hiatus hernia will present definitive symptoms of vomiting, regurgitation, chest pain of a char- acter different to heartburn, pressure symptoms within the chest, which if related to a large hernia may cause dyspnoea. A combination of both sliding and rolling or para-oesophageal hiatus hernia (type 2b) can also occur, but this is rare. Complications of GORD The complications of reflux include oesophagitis, with varying degrees of ulceration (see Figure 6.1, LA grading), stricture formation in the oesophagus, and Barrett’s oesophagus with a growth of intestinal metaplasia in the lower oesophagus. Barrett’s columnar lined lower oesophagus occurs in 10% of patients with GORD. In contrast to reflux itself, which does seem to have a genetic familial tendency, the development of Barrett’s oesophagus does not, 6 · UPPER GASTROINTESTINAL SURGERY 72 1111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 3011 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 311 72 Figure 6.3. Graph of refluxing pH trace. and seems to occur sporadically. The degree of reflux in Barrett’s oesophagus is usually severe when measured. Paradoxically, some patients with Barrett’s oesophagus have little in the way of reflux symptoms despite severe acid exposure. The presence of Barrett’s oesophagus appears to reduce the sensitivity of the oesophagus to acid reflux. For a detailed review of the malignant potential of Barrett’s oesophagus refer to Chapter 26. In both symptomatic reflux disease and Barrett’s oesophagus, there is a significant increase in the risk of adenocarcinoma of the oesophagus. In symptomatic refluxers this risk has been defined in a Swedish epidemiological study. Lagergren and co-workers [2] identified that a patient who refluxes daily for more than 20 years is 43 times more likely to develop adenocarcinoma than someone who has had no reflux. Complications also include aspiration pneumonitis and chronic laryngitis, and in children there can be significant malnutrition and failure to thrive. The Role of Antireflux Surgery The only continuous therapy for GORD is the repair of the valve mechanism of the gastro- oesophageal junction [3,4]. Currently, this is done by a formal surgical operation at the gastro-oesophageal junction, usually by a laparoscopic approach [5]. It should be remem- bered that antireflux surgery provides continuous protection to the lower oesophagus from the noxious effects of reflux [3]. Antireflux surgery has no effects on normal digestion, it allows normal acid protection against ingested bacte- ria, and it has no carcinogenic side effects. When it is successful, it can provide continuous complete symptom control, and allows the patient the psychological benefit of being restored to normal. It has no long-term potential systemic effects [4,6,7]. There is the possi- bility that it provides cost-effective care, although this depends on the true costs of long- term or even lifelong medication and the subsequent development of complications [8,9]. Indications for Antireflux Surgery Patient Desire Antireflux surgery is indicated for patients who have a justifiable desire to be free of reflux, and who are fit to undergo a surgical procedure. What is meant by a justifiable desire? Patients, who despite regular proton pump inhibitors, at full and maintenance dose, have further troublesome symptoms such as volume reflux, BENIGN DISEASE OF THE OESOPHAGUS 73 111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 3011 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 311 73 Figure 6.4. Diagram illustrating differing types of hiatus hernia. night-time aspiration symptoms with coughing or choking. Sometimes, asthma can be exacer- bated by GORD and, if this is well documented, it may be an indication for surgery. Recurring heartburn or chest pain, despite being on optimum regular therapy, is relatively rare, but does occur. It also occurs in the situation of delay, interruption or dose reduction of proton pump inhibitors, which may occur because the patient forgets to take or obtain their medication. Patients with long-term side effects of proton pump inhibitors, such as diarrheoa, headache or neurological symptoms, often desire a surgical alternative [1,4]. Recently, because of the acknowledged link between gastro-oesophageal symptoms and the subsequent development of adenocarcinoma of the oesophagus, patients who are reminded of their symptoms due to symptom breakthrough, or who are anxious about the long-term effects of partially treated reflux, may wish to stop their reflux in the belief that it might influence the subsequent malignant potential. This is currently a common desire but there is no scientific data to support the particular argument that surgery might prevent cancer [6]. Patient Fitness Patients should only be considered for antireflux surgery if they are truly fit. This is usually a balance of issues, which includes a physio- logical age of less than 70 years in most com- munities. There needs to be a lack of morbid obesity, no symptomatic cardiac problems, good respiratory function (unless there is controlled reversible airways disease), good mobility and an independent lifestyle. Particu- lar problems do occur in patients who are mentally retarded and in cerebral palsy, where there are combinations of additional risks, dif- ficulties in assessing the patients’ own desires, their symptoms and their understanding of consent. There is also limited outcome data in this group, and advising their carers on the true risks is difficult to base on published material. Patients with rheumatic diseases lim- iting mobility vary in their outcome. People with scleroderma do benefit from antireflux surgery when carefully chosen, but those with rheumatoid arthritis often have too many other co-morbidity problems to be able to benefit from the operation without complications [10]. Reflux Complications In the presence of some complications, antireflux surgery is sometimes desirable. In particular, strictures that require frequent dilatation may do better when their reflux is controlled surgically rather than with proton pump inhibitors. When Barrett’s oesophagus is present, there may be additional problems with symptoms, bleeding or failure to heal ulceration and, in this circumstance, surgery may be considered a better method of control- ing of reflux injury. It is important again to emphasise that there is no data to support any attempts at cancer risk reduction in Barrett’s oesophagus by antireflux surgery. Long-term Medication vs Surgery For the majority of patients who are well controlled on proton pump inhibitors, there is no clear benefit in changing the strategy to antireflux surgery. Lundell et al, in 1998, [11] identified in a prospective randomised study with 5 years of follow-up that if patients were well controlled on proton pump inhibitors at the beginning of the study, randomising them to medical treatment or surgery resulted in the same quality of life, as long as they were allowed to adjust the dose of their proton pump inhibitors to deal with any recurrent symptoms when medically treated. Thus, if patients are very satisfied with their medical therapy, there is little to be gained with an operation. In stark contrast, when patients have a particular desire, and when there are clear indications for them to consider surgery, there is often a dramatic improvement in their quality of life [7]. The surgeon should consider specifically the patient’s own risks and potential benefits, and also the surgical unit’s own experience and outcome figures. Contraindications Contraindications to antireflux surgery may include patients who do not have reflux. Patients who fail to show acid reflux on pH monitoring are unlikely to benefit. Patients who have a primary motility disturbance, such as achalasia or nutcracker oesophagus on manometry, will not benefit from antireflux surgery unless it is an adjunct to a myotomy [10]. Patients with significant irritable bowel 6 · UPPER GASTROINTESTINAL SURGERY 74 1111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 3011 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 311 74 syndrome, gas bloat preoperatively, fibromyal- gia and arthritis are relatively contraindicated. Clearly patients who have no desire for surgery should remain on medical therapy. Fundoplication and Hiatas Hernia Repair Antireflux surgery usually requires correction of any hiatus hernia by reduction of the oesoph- agogastric junction into the abdominal cavity [3], identification of the diaphragmatic crura, and separation of the oesophagus from these. A window is usually created behind the oesophagus if a fundoplication is to be performed. Repair of the diaphragmatic crura is undertaken with non-absorbable sutures, approximating the left and right diaphragmatic crural pillars, and leaving sufficient space for the oesophagus to expand during the swallowing of a bolus of food. Some operators place a 50 or 60 French bougie at this stage of the operation, in order to gauge the size of their hiatal repair. The second part of the operation is fundoplication, taking part of the fundus of the stomach around the lower oesophagus just above the oesophagogas- tric junction. There are a number of different ways of doing this, and these include a Nissen fundoplication [12] (a 360° wrap, requiring mobilisation of the short gastric arteries) and the Nissen Rosetti modification, in which the anterior wall of the gastric fundus is brought behind the oesophagus and sutured to the greater curvature of the stomach brought across the front without mobilisation of the short gastric vessels. Other variations of fundoplication include the Toupet [13,14], which is a 240° posterior wrap, leaving the anterior part of the oesophagus uncovered (Figure 6.7). The wrap is fixed both to the lateral walls of the oesophagus, and to both diaphragmatic crura. A claimed advantage of the Toupet operation is that it is less constricting, and therefore suffers less early postoperative dysphagia [14]. Other variations include the Watson anterior fundoplication, the Lind fundoplication, and the Hill gastropexy [15–17]. BENIGN DISEASE OF THE OESOPHAGUS 75 111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 3011 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 311 75 Figure 6.5. Diagram of laparoscopic hiatal repair. Figure 6.6. Diagram of laparoscopic fundal wrap. Outcomes and Complications With good case selection, 90% of patients who undergo antireflux surgery have a good or excel- lent outcome, with relief of their symptoms of regurgitation, dysphagia and potentially other less typical manifestations of gastro- oesophageal reflux disease. For patients who have atypical symptoms, such as asthma, laryngitis, cough, and variations of chest and abdominal pain, the outcomes are less predictable. In most studies dysphagia is common in the early postoperative period, but resolves in all except approximately 5%, by 3 months postopera- tively. A graded introduction of solid diet is required during this period. In the 10% of patients in whom there is a less satisfactory outcome the problems include disruption of the wrap (3–5%), persistent dysphagia (3–5%), and persistent symptoms of bloating that are a disturbance to quality of life. There are occasionally more serious complications such as para-oesophageal herniation, splenic injury at the time of surgery requiring splenectomy, oesophageal or gastric perforation, and possibly other more unusual problems. Reoperation rates in large reported series vary between 3 and 10% [5–7,14,18]. For the 90% who do well there is often a significant quality of life improvement including improvement of sleep disturbance, allowance of physical activities and exercises previously restricted, restoration of normal social eating habits and the feeling of being free of a previ- ous label of disease [7]. The outcome in relation to oesophagitis shows almost universal healing of ulceration. Barrett’s oesophagus, however, does not regress completely, and usually per- sists although it remains asymptomatic. It is not known what the effect on cancer risk is in relation to reflux protection either by medication or by antireflux surgery. [6] Non-reflux Oesophagitis Inflammation of the mucosa of the oesophagus, although most commonly caused by reflux of gastric contents, can be associated with several other pathologies. Caustic Injury Injury by ingestion of caustic substances can be significant, and have long-term consequences. The degree of damage is dependent on two main factors: firstly, the caustic potential of the substance involved, for example pH, and secondly, the transit time of the relevant substance. The commonest substances involved are household cleaners, such as bleach, and other acid or alkaline solutions. In liquid form the transit time in the oesophagus is often short. The rapid action of these caustic substances means that attempts to dilute the solution, and therefore reduce injury, are usually unsuccessful. Gastric injury and perforation may also occur. Caustic crystals may also be ingested and cause localised burns. These rarely enter the oesophagus, as the caustic action usually occurs in the pharynx, causing burns proximal to the oesophagus. The alkaline anode of disc batteries can cause very localised but significant burns to any area of the gastrointestinal (GI) tract should they become lodged at any time. Tablets, such as potassium chloride, can have a similar effect, and the resulting burns are often deep and may cause perforation. After ingestion, prevention of significant caustic injury is difficult. Treatment is primar- 6 · UPPER GASTROINTESTINAL SURGERY 76 1111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 3011 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 311 76 Figure 6.7. Diagram of Toupet fundoplication. ily supportive with a primary role of preventing stricture formation, reducing inflammation, and reducing the risk of perforation. Steroids can be used in mild to moderate burns to reduce the inflammatory response, but are contraindicated in severe injury. Repeat dilatation is often required should a stricture develop, and antibi- otics should be used in the acute phase as a prophulactic measure. Complete destruction of the oesophagus may require feeding by gas- trostomy, or jejunostomy if a gastrectomy is required. Secondary reconstruction with colon or small bowel interposition is a task for specialised centres. Infective Oesophagitis All forms of infective oesophagitis are uncommon in an otherwise well person. Immunocom- promised patients and those with malignancy, however, do have an increased incidence. Patients present with a variety of symptoms, often non-specific, and they may present with symptoms or signs of an underlying malignant disease or other cause for immunocompromise. Common symptoms at presentation include dysphagia, odynophagia, heartburn, non- specific chest pain, and the patient may complain that they are aware of the passage of food on swallowing. In these cases, diagnosis can only be made by upper GI endoscopy and microscopy and culture of biopsies taken (Table 6.2). Candida is a comensal microbe in the upper GI tract and pharynx. This can become an opportunistic pathogen if systemic antibiotic therapy is given, allowing overgrowth due to removal of regional flora. Herpes simplex (HSV) is primarily a reactivation of a latent virus from the regional gan- glion. It may, however, spread directly from the oropharynx. The patient presents with severe odynophagia often with associated retrosternal burning and/or dysphagia, or they can occasionally present with a severe upper GI bleed. Treatment is primarily with antiviral agents. Cytomegalovirus (CMV) is more common with infection with HIV. Again, it is reactivation of a latent virus, and presents in a similar way to HSV, but dysphagia seems to be a more promi- nent symptom. Eosinophilic Oesophagitis Eosinophilic oesophagitis is an uncommon condition first described as a distinct clinical entity in 1993 [19]. It is characterised by an intense eosinophilic infiltration of the oesophageal mucosa and symptoms of dysphagia, which are often intermittent, progressive and associated with odynophagia. Previously, eosinophilia in the oesophagus was regarded as an inciden- tal component of GORD or a variant of eosinophilic gastroenteritis. However, the clinical syndrome of eosinophilic oesophagitis is not usually seen with either of these. Most recent literature refers to eosinophilic oesophagitis in children, but the adult phenomenon may escape diagnosis due to lack of awareness of this sepa- rate pathology. The hallmark of this condition is intermittent and often painful dysphagia, which may become constant as the disease progresses. Thorough investigations often show essentially normal or mildly abnormal oesophageal endoscopy, pH and manometry studies. Mechanical obstruction is usually absent, and unless a biopsy is taken, these patients are found to be a diagnostic enigma and management dilemma. Presentation The presentation of these patients is quite variable, with some attending accident and emergency departments with acute bolus obstruction. The majority tend to be young, 20–40 years of age. Diagnosis is only confirmed by biopsy of an often normal looking oesophagus, although rings, mucosal reticulation and furrows may be seen (Figures 6.8, 6.9 and 6.10). Histology shows dense eosinophilic infiltration within the oesophageal mucosa. Management Management of these patients has been made difficult by diagnostic problems, and a poor understanding of the disease pathogenesis. Acid suppression has no effect. Antihistamine medication has been used in the past with little BENIGN DISEASE OF THE OESOPHAGUS 77 111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 3011 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 311 77 Table 6.2. Agents in infective esophagitis Usual pathogens Rare pathogens Candida CMV, TB, HIV, HPV, Trypanosoma herpes simplex cruzi (Chagas’ disease) reported success. Oesophageal dilatation has also been undertaken for symptomatic relief but, unfortunately, this can be very uncomfort- able and only provides short-term relief. Corticosteroid therapy has shown some success in the literature. Symptoms soon relapse, however, once treatment is ceased, and the significant side effect profile of long-term steroid therapy in young patients greatly limits their value in this setting. There is some early evidence to show that eosinophil stabilisa- tion, using montelukast (Singulair, MSD), a leukotriene D4 antagonist used in severe asthma, may allow significant symptom relief. Inflammatory Bowel Disease Crohn’s disease may manifest with oesophageal involvement, although this is uncommon. In the typical fashion, skip lesions can be present and fistulation has been reported. Treatment is unchanged from that of intestinal Crohn’s disease, with steroid therapy, stricture dilatation and resection all being described. Irritable Bowel Syndrome (IBS) and Functional Foregut Disorders (FFD) A spectrum of GI symptoms is perceived by patients to relate to the upper GI tract. In relation to the lower abdomen and a variable bowel habit the irritable bowel syndrome is a commonly diagnosed condition, where no specific pathology is identified. It is often associated with symptoms of upper GI dysfunction, and the term functional foregut disorder has been coined. The range of symptoms includes reflux- like sensations, central chest pain and even dysphagia, when no abnormality can be found 6 · UPPER GASTROINTESTINAL SURGERY 78 1111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 3011 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 311 78 Figure 6.8. Endoscopic appearance of eosinophilic oesophagitis rings. Figure 6.9. Endoscopic appearance of eosinophilic oesophagitis furrows. Figure 6.10. Endoscopic appearance of eosinophilic oesophagitis cobblestone. on endoscopy, biopsy, manometry or 24-hour pH monitoring. Functional testing with imped- ance plethysmography and sensory tests may show levels of mucosal hypersensitivity. Our understanding of the brain–gut axis is now growing and while there are clear relationships between the brain and the mucosal and mural sensitivity of the oesophagus [20], there are no clear therapeutic strategies yet defined. The use of tricyclic antidepressants may modulate central responses, and identification of the neu- rotransmitters of hypersensitivity may, in the future, allow specific strategies of management. Motility Disorders Achalasia This is a failure of oesophageal motility and coordination that results in chronic dysphagia. The condition presents in a bimodal age distri- bution with peaks in the age ranges 20–40 years and 70–90 years, and is relatively rare (1/100 000 of population) Aetiology and Presentation In Western societies achalasia is a sporadic, idiopathic condition. In South America it is related to the infective agent Trypanosoma cruzi, and is called Chagas’ disease. It is familial in 1% of cases and can be related to other neurodegenerative diseases such as Parkinson’s. The usual presenting complaint is dysphagia to solids, which most patients say has been gradu- ally progressive over several years. Misdiagnosis is common, and a label of GORD, chest pain or dyspepsia is often given. Postural regurgitation is typical of achalasia. The description by the patient is often characteristic and clearly points towards the pathology. They complain of non- acidic, undigested and non-bilious food regurgitation, which can be foul tasting or smelling due to extended fermentation in the dilated non-motile oesophagus. This occurs especially at night when the patient is lying flat; they awake coughing and choking. This classical patient may also have considerable weight loss, and complain of fear of eating due to social embar- rassment from regurgitation. They will also tend to drink copious amounts of fluid with meals in an attempt to wash the food bolus down. Pathophysiology Oesophageal manometry is the definitive investigation in achalasia (Figure 6.11). The dis- tinguishing feature is failure of the lower oesophageal sphincter to relax on swallowing. The lower oesophageal pressure tends to be greater than normal (approximately × 1.5–2), BENIGN DISEASE OF THE OESOPHAGUS 79 111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 3011 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 311 79 Oesophageal body 15 cm above sphincter Oesophageal body 10 cm above sphincter Oesophageal body 5 cm above sphincter Lower oesophageal sphincter Figure 6.11. Manometry trace of achalasia. although the pressure does not necessarily relate to the severity of symptoms. There is often a progressive weakening and discoordi- nation of oesophageal peristalsis. In a small number of patients painful, strong, simultaneous contractions occur; this is sometimes called vigorous achalasia. Barium/contrast studies show a dilated lower oesophagus with a classical sigmoid shape (Figure 6.12). There is a gradual smooth tapering of the distal oesophagus. Where there is an air/fluid level in the oesophagus, it is usually dilated and in this situation the gastric air/fluid level is absent. Treatment Treatment of achalasia is by dilatation or surgical myotomy. The increasingly popular Botulinum toxin (Botox) injection has yet to provide superior control of symptoms than the two standard therapies. Dilatation of achalasia requires the complete disruption of the lower oesophageal sphincter necessitating a balloon dilator 30–40 mm in diameter (Figure 6.13). These are usually passed over a guide wire under radiological control and may require sedation or a general anaesthetic. Success with dilatation seems to depend upon a strict proto- col, and many specialised units achieve 60–80% satisfaction with long-term relief of dysphagia. Because dilatation may fail, the surgical option of Heller’s myotomy is an important alternative. It is reasonable to try balloon dilatation, but repeated attempts may increase the risk of perforation and increase the difficulty of any subsequent myotomy. In most specialist centres the access for myotomy is by laparoscopic approach. Thora- coscopy is also feasible. A Heller’s myotomy requires a longitudinal incision in the lower oesophageal musculature, at least 5 cm long and including the gastro-oesophageal junction. The 6 · UPPER GASTROINTESTINAL SURGERY 80 1111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 3011 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 311 80 Figure 6.12. Achalasia on contrast radiograph. Figure 6.13. Celestin and balloon oesophageal dilators. (Reproduced with kind permission of Salford Royal Hospitals NHS Trust.) operation requires a careful technique to ensure complete sphincter disruption and avoid perforation. Some surgeons recommend the use of a fundoplication anteriorly (Dor fundoplication) to hold open the edge of the myotomy and provide some protection against reflux. The complications of surgery include perforation, sepsis, reflux and occasionally symptom recurrence. Untreated achalasia can lead to severe malnutrition. Aspiration of oesophageal contents can occur, resulting in chest infections, and in the long term squamous carcinoma has an increased incidence. This is thought to be secondary to a chronic irritation by stagnating and fermenting oesophageal contents. Diffuse Oesophageal Spasm This is characterised by diffuse powerful simultaneous contractions in the oesophagus (Figure 6.14), and is a cause of oesophageal pain sometimes found in patients labeled as non-cardiac chest pain. Lower oesophageal sphincter pressure is usually not affected and relaxes completely. The oesophageal wall may be thickened as a result, and may create dysphagic symptoms. The disease is not usually progressive and may resolve spontaneously. The presentation is frequently confused with cardiac disease, as like angina pectoris, it may even be relieved by nitrates. Gastro-oesophageal reflux disease may sometimes precipitate diffuse oesophageal spasm. There is a very variable disease profile with patients complaining of a wide spectrum of frequency, severity, duration and onset of pain. There may be occasional food bolus impaction. Manometry shows uncoordinated motility with simultaneous contractions greater than 20% of normal. Treatment is usually medical, using calcium channel blockers, such as nifedipine, along with reassurance. Balloon dilatation is occasionally used, and in exceptional cases long oesophageal myotomy is indicated. Nutcracker Oesophagus This has a very similar presentation to angina pectoris and is often confused with it. It is BENIGN DISEASE OF THE OESOPHAGUS 81 111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 3011 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 311 81 Figure 6.14. Manometry trace of diffuse oesophageal spasm. [...]... esophageal adenocarcinoma N Engl J Med 1999 ;34 0(11):825 31 1111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 30 11 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 31 1 89 BENIGN DISEASE OF THE OESOPHAGUS 111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 30 11 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 31 1 3 Jamieson GG Anti-reflux operations: how do they work? Br J... 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 30 11 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 31 1 1 03 BENIGN DISEASE OF THE SMALL BOWEL 111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 30 11 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 31 1 Figure 8.2 Small bowel enema showing linear fissures extending through the bowel wall any intra-abdominal or extra-abdominal... 6.15 Manometry trace of poor oesophageal motility 82 1111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 30 11 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 31 1 83 BENIGN DISEASE OF THE OESOPHAGUS 111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 30 11 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 31 1 of gastro-oesophageal reflux but, at present, there is no effective... can be performed by Bougie, laser or balloon dilatation 1111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 30 11 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 31 1 85 BENIGN DISEASE OF THE OESOPHAGUS 111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 30 11 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 31 1 Rings Oesophageal rings tend to arise in the distal oesophagus... Recurrence rate (%) 1 40 8–10 . not, 6 · UPPER GASTROINTESTINAL SURGERY 72 1111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 30 11 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 31 1 72 Figure 6 .3. Graph of. Treatment is primar- 6 · UPPER GASTROINTESTINAL SURGERY 76 1111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 30 11 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 31 1 76 Figure 6.7. Diagram. can be found 6 · UPPER GASTROINTESTINAL SURGERY 78 1111 2 3 4 5 6 7 8 9 1011 1 2 3 4 5 6 7 8 9 2011 1 2 3 4 5 6 7 8 9 30 11 1 2 3 4 5 6 7 8 9 4011 1 2 3 4 5 6 7 8 9 5011 1 2 31 1 78 Figure 6.8. Endoscopic

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