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Esophogeal and diaphramatic diseases

  1. 1. Esophagus and Diaphragmatic diseases Surgery Dr. Musab Idris
  2. 2. ESOPHAGUS Key points  Anatomy & histology  Physiology  Esophageal symptoms assessment  Esophageal testing
  3. 3. Introduction  The oesophagus is a muscular tube connecting the pharynx to the stomach and measuring 25–30 cm in the adult.  Its primary function is as a conduit for the passage of swallowed food and fluid, which it propels by antegrade peristaltic contraction.  It also serves to prevent the reflux of gastric contents whilst allowing regurgitation, vomiting and belching to take place
  4. 4. Anatomy of oesophagus  The oesophagus is a muscular tube protected at its ends by the upper and lower esophageal sphincters.  Oesophagus begins at the level of the sixth cervical vertebra and it enters into the superior mediastinum through the upper thoracic outlet then it descends into the posterior mediastinum and exits the thorax through oesophageal hiatus of the diaphragm and enters the abdominal cavity
  5. 5. Anatomy of oesophagus  The esophagus is divided into three parts:-  The cervical portion extends from the cricopharyngeus to the suprasternal notch  The thoracic portion extends from the suprasternal notch to the diaphragm  The abdominal portion extends from the diaphragm to the cardiac portion of the stomach.
  6. 6. Upper End : C6 (the inferior pharyngeal constrictor merges with the cricopharyngeus) __ Upper esophageal sphincter (UES) Lower End: T11 (thickened circular smooth muscle) __ Lower esophageal sphincter (LES)
  7. 7. RELATIONS OF CERVICAL PART:-  Posterior: Cervical vertebral.  Laterally: lower lobes of thyroid gland, carotid sheath.  Anteriorly: Trachea,& Recurrent laryngeal nerves
  8. 8. RELATIONS OF THORACIC PART:-  ANTERIOR RELATIONS:- Trachea. 1. Trachia 2. Left recurrent laryngeal nerve. 3. Left principal bronchus. 4. Pericardium. 5. Left atrium  POSTERIOR RELATIONS:- 1. Bodies of the thoracic vertebrae. 2. Thoracic duct. 3. Azygos vein. 4. Right posterior intercostal arteries. 5. Descending thoracic aorta (at the lower end).
  9. 9.  LATERAL RELATIONS  On the Right side: 1. Right mediastinal pleura. 2. Terminal part of the azygos vein.  On the Left side: 1. Left mediastinal pleura. 2. Left subclavian artery. 3. Aortic arch. 4. Thoracic duct
  10. 10.  The esophagus has 3 areas of narrowing:  Superiorly: level of cricoid cartilage, juncture with pharynx  Middle: crossed by aorta and left main bronchus  Inferiorly: diaphragmatic sphincter  They have a considerable clinical importance: 1. They may cause difficulties in passing an esophagoscope or gastroscope. 2. In case of swallowing of caustic liquids this is where the burning is the worst and strictures develop. 3. The esophageal strictures are a common site of esophageal carcinoma.
  11. 11. Histology  Mucosa.  Stratified squamous epithelium  Lamina propria,  Muscularis mucosa.  Submucosa.  Muscularis propria.  Skeletal muscle. Upper 1/3  Smooth muscle. Lower 2/3  Adventitia.  No serosa, ( unique )
  12. 12. Anatomy- innervation  The innervation of the oesophagus comprises:-  An extrinsic Parasympathetic and sympathetic supply and the intrinsic intramural plexuses.  Parasympathetic Supply provides the predominant motor and sensory innervation of the oesophagus.
  13. 13. Anatomy-blood supply  Segmental orientation.  Blood supply to other viscera.
  14. 14. LYMPH DRAINAGE  The upper third is drained in the deep cervical nodes.  The middle third is drained into the superior and inferior mediastinal nodes.  The lower third is drained in the celiac lymph nodes in the abdomen.
  15. 15. Esophageal physiology  1. Fasting State:- the oesophageal body is relaxed and the upper and lower oesophageal sphincters are tonically contracted to prevent gastro-oesophageal reflux and aspiration.  2. Swallowing state:-  The oropharyngeal phase : Swallowing begins when a food bolus is propelled into the pharynx from the mouth. It is voluntary.
  16. 16.  The esophageal phase. It is involuntary.  It takes approximately 8 to 10 seconds from initiation of the swallow to entry into the stomach .  In rapid sequence and with precise coordination, the larynx is elevated and the epiglottis seals the airway.
  17. 17.  Primary Peristalsis:  Food bolus, contracts proximally to distally  Secondary Peristalsis:  Esophageal distention(residual food bolus)and reflux  Tertiary Contractions:  Nonperistaltic propel bolus in a retrograde direction to proximal esophagus
  18. 18. Esophageal Symptom Assessment  Heartburn.  Dysphagia:sensation of food being delayed in its normal passage from mouth to stomach. Patients often complain of a sensation of food “sticking.”  Odynophagia.  Regurgitation.  Aspiration.
  19. 19. Esophageal Symptom Assessment Dysphagia
  20. 20. Esophageal testing  Barium swallow  Endoscopy  Manometry  Twenty-four-hour pH and combined pH-impedance recording
  21. 21. Esophageal testing:- endoscopy  Endoscopic Evaluation. The first diagnostic test in patients with suspected esophageal disease is usually upper gastrointestinal endoscopy.  Evaluation:- Mucosa Structural abnormalities.  Rigid or flexible, the flexible fiberoptic esophagoscope is the instrument of choice because of its technical ease, patient acceptance, and the ability to simultaneously assess the stomach and duodenum.  Diagnostic and/or therapeutic
  22. 22. Esophageal testing endoscopy : indications  Weight loss  Upper gastrointestinal bleeding,  Dysphagia, odynophagia and chest pain,  Partial or no response to empiric therapy,  Evaluation for Barrett's esophagus  Foreign body
  23. 23. Complication of reflux disease High Grade dysplasia in Barrett’s mucosa, Early adenocarcinoma arising in Barrett’s mucosa.
  24. 24. Esophageal testing:- radiography  Radiographic Evaluation:- Barium swallow evaluation is undertaken selectively to assess anatomy and motility.  The anatomy of large hiatal hernias are more clearly demonstated by contrast radiology than endoscopy, and the presence of coordinated esophageal peristalsis can be determined by observing several individual swallows of barium traversing the entire length of the organ, with the patient in the horizontal position.
  25. 25.  Esophageal disorders shown clearly by a full-column technique include:-  circumferential carcinomas,  peptic strictures,  large esophageal ulcers,  and hiatal hernias.
  26. 26. Esophageal testing manometry  Measures:-  Intraluminal pressures .  Coordination of the pressure activities of LES, esophageal body, and UES.  Assessment of patients with symptoms suggestive of esophageal motor dysfunction ( achalasia , Scleroderma,DES )
  27. 27. Twenty-four-hour pH and combined pH impedance recording  Prolonged measurement of pH is now accepted as the most accurate method for the diagnosis of gastro- oesophageal reflux.  It is particularly useful in patients with atypical reflux symptoms, those without endoscopic oesophagitis and when patients respond poorly to intensive medical therapy.
  28. 28.  Prolonged monitoring of esophageal pH is performed by placing the pH probe or telemetry capsule 5 cm above the manometrically measured upper border of the distal sphincter for 24 hours.  It measures the actual time the esophageal mucosa is exposed to gastric juice, measures the ability of the esophagus to clear refluxed acid, and correlates esophageal acid exposure with the patient’s symptoms.
  29. 29. Oesophageal Tears
  30. 30. Oesophageal Tears  Oesophageal tears are ruptures to any part of oesophageal wall. Although rare, full ruptures have a mortality of between 50 – 80%, so early recognition and treatment is essential.  There is a wide spectrum in the severity of oesophageal tears, the main two subcategories being superficial mucosal tears (Mallory-Weiss tears) and full thickness ruptures(perforation).
  31. 31. Oesophageal Perforation  Oesophageal perforation is a full thickness rupture of the oesophageal wall; if it is spontaneous (often due to vomiting), it is often called Boerhaave’s syndrome.  Perforation will result in leakage of stomach contents into the mediastinum and pleural cavity, which triggers a severe inflammatory response which will rapidly become overwhelming, resulting in a physiological collapse, multi-organ failure, and death. Rapid identification and management is therefore essential.
  32. 32.  Oesophageal rupture is a surgical emergency and patients deteriorate rapidly, rapid identification and management is therefore essential.  Etiology  The two most common causes are iatrogenic (such as endoscopy) or after severe forceful vomiting.  The most common site of perforation is just above the diaphragm in the left postero-lateral position, although it can occur elsewhere in the oesophagus.  They are rare, with an incidence of 3.1 per million per year and most cases occur in patients with an otherwise normal oesophagus.
  33. 33. Clinical Features  The classic picture* is of a patient who presents with severe sudden-onset  retrosternal chest pain,  respiratory distress,  and subcutaneous emphysema following severe vomiting or retching.
  34. 34. Investigation  Routine bloods, including a group and save, must be taken urgently for all those with suspected perforation.  Initial imaging via a chest radiograph (CXR) may demonstrate evidence of pneumomediastinum or intra-thoracic air-fluid levels (however do not delay definitive imaging while awaiting the CXR)  The investigation of choice is an urgent CT chest abdomen pelvis with IV and oral contrast
  35. 35. Management  These patients are often septic and haemodynamically unstable. Urgent and aggressive resuscitation is therefore essential.  Definitive management varies depending on whether the perforation was spontaneous or iatrogenic and on the age and comorbidity of the patient.
  36. 36.  The principles of definitive management (both operative and non-operative) following initial resuscitation involves  Control of the oesophageal leak  Eradication of mediastinal and pleural contamination  Decompress the oesophagus (typically via a trans- gastric drain or endoscopically-placed NG tube)  Nutritional support
  37. 37. Surgical Management  The majority of patients with a spontaneous perforation will need immediate surgery to control the leak and wash out of the chest. This is almost always via a thoracotomy.  Patients also need an on-table endoscopy to determine the site of perforation and therefore the site of the incision.  Leakage is common and the patients should have a CT scan with contrast at 10-14 days before starting oral intake. They may therefore warrant a feeding jejunostomy to be inserted at the time of surgery for nutrition
  38. 38. Non-Operative Management  Patients with iatrogenic perforations are often more stable than those with spontaneous perforations* and may be suitable for non-operative management.  Other patients potentially suitable for non-operative management include those with minimal contamination, a contained perforation, no symptoms or signs of mediastinitis, or no solid food in pleura or mediastinum
  39. 39.  Non-operative treatment involves:  Initial suitable resuscitation and transfer to Intensive Care / High Dependency Unit  Appropriate antibiotic and anti-fungal cover  Nil by mouth for 1-2 weeks, with endoscopic insertion of an NG tube on drainage  Large-bore chest drain insertion  Total Parenteral Nutrition (TPN) or feeding jejunostomy insertion
  40. 40. Prognosis  Morbidity and mortality is high (between 50–80%) and therefore early identification and treatment will most influence outcomes.
  41. 41. Mallory-Weiss Tears  Mallory-Weiss tears are lacerations in the oesophageal mucosa, usually at the gastro- oesophageal junction.  They tends to occur after a period of profuse vomiting, and in turn results in a short period of haematemesis. They account for approximately 5% of all cases of haematemesis.  They are generally small and self-limiting, in the absence of clotting abnormalities or anti-coagulation drugs. Presentation with haemorrhagic shock is possible but rare.
  42. 42. Investigation and Management  The investigation and management of Mallory-Weiss tears is the same as for any other upper GI bleed.  Most cases can be managed conservatively, rarely warranting interventional or surgical management.
  43. 43. GASTROESOPHAGEAL REFLUX DISEASE
  44. 44. GASTRO-OESOPHAGEAL REFLUX DISEASE  Gastro-oesophageal reflux disease (GORD) is a condition whereby gastric acid from the stomach leaks up into the oesophagus.  It is a very common problem, affecting around a quarter of the population in Western countries and represents approximately 4% of primary care appointments. It is twice as common in men compared to women.
  45. 45. pathophysiology  The lower oesophageal sphincter controls the passage of contents from the oesophagus to the stomach.  As part of its normal function, episodic sphincter relaxation is expected, yet in GORD these episodes become more frequent and allow the reflux of gastric contents into the oesophagus.  The refluxed acidic gastric contents (or rarely alkaline bile) result in pain and mucosal damage in the oesophagus
  46. 46. Risk Factors  The risk factors for gastro-oesophageal reflux disease include :-  age  obesity  male gender  alcohol  smoking  caffeinated drinks, and fatty or spicy foods.
  47. 47. Clinical features  The classic triad of symptoms is retrosternal burning pain (heartburn), epigastric pain (sometimes radiating through to the back) and regurgitation.  Most patients do not experience all three.  Symptoms are often provoked by food, particularly those that delay gastric emptying (e.g. fats, spicy foods).  As the condition becomes more severe, gastric juice may reflux to the mouth and produce an unpleasant taste, often described as ‘acid’ or ‘bitter’.
  48. 48. The Los Angeles Classification of Reflux  The Los Angeles classification can be used to grade reflux oesophagitis based on severity from the endoscopic findings of mucosal breaks in the distal oesophagus:  Grade A – breaks ≤5mm  Grade B – breaks >5mm  Grade C – breaks extending between the tops of ≥2 mucosal folds, but<75% of circumference  Grade D – circumferential breaks (≥75%)
  49. 49. Relationship Between Hiatal Hernia and Gastroesophageal Reflux Disease.  A hiatal hernia can occur from long-lasting GERD or GERD could be a symptom of a hiatal hernia.  When GERD progresses, it can cause the lower esophageal sphincter to lose its function, which may cause a hiatal hernia.  A hiatal hernia could also worsen GERD symptoms.
  50. 50.  A hiatal hernia occurs when the hole in the diaphragm (hiatus) through which food and liquids pass from the esophagus into the stomach enlarges. This facilitates acid reflux and can cause the stomach to slide upward into the chest.  This condition in severe cases can lead to more serious complications such as obstruction or strangulation of the stomach.
  51. 51. Investigations  GERD is a clinical diagnosis & many patients can be treated without investigations:-  Endoscopy. to confirm the presence of esophagitis.  24 hour intra luminal pH monitoring of the esophagus.  Esophageal manometry.  Barium study: It may show a hiatus hernia.
  52. 52. Differential Diagnosis  Important gastrointestinal differentials to consider include:  Malignancy (oesophageal or gastric)  Peptic ulceration  Oesophageal motility disorders  Oesophagitis
  53. 53. Management  All patients with gastro-oesophageal reflux disease should be advised to take conservative steps in its management, including avoiding known precipitants (alcohol, coffee, fatty foods), weight loss, and smoking cessation.  Medical Management  Proton pump inhibitors (in addition to lifestyle changes) are the first-line treatment and are very effective for the majority of patients.
  54. 54. Surgical Therapy for Gastroesophageal Reflux Disease  Indications for an antireflux operation include the following :  Failure of medical management  Complications of GERD (eg, Barrett esophagitis or peptic stricture)  Patient preference (eg, desire to discontinue medical therapy because of quality-of-life concerns, financial concerns, or inability to tolerate medication)
  55. 55.  Extraesophageal manifestations (asthma, hoarseness, cough, chest pain, aspiration)  Mixed and paraesophageal hernia  Recurrent reflux or complications after previous antireflux surgical therapy
  56. 56. Nissen Fundoplication  The Most common surgical procedure is the NissenFundoplication.  NIssen fundoplication is the definitive surgical treatment for GERD.  During the Nissen fundoplication, the upper part of the stomach is wrapped around the LES to strengthen the sphincter, prevent acid reflux, and repair a hiatal hernia.
  57. 57. Complications of GORD  Stricture  Reflux-induced strictures occur mainly in late middle- aged and elderly people, but they may present in children.  Esophageal stricture are generally smooth , scarred ,circumferential narrowing usually in the distal esophagus, These can cause food to become “stuck” or can cause pain when swallowing (Odynophagia, Dysphagia) and treated with per-endoscopic dilatation.
  58. 58. Barrett’s oesophagus (columnarlined lower oesophagus)  Barrett’s oesophagus is a metaplastic change in the lining mucosa of the oesophagus in response to chronic gastro-oesophageal reflux.  The hallmark of ‘specialised’ Barrett’s epithelium is the presence of mucus-secreting goblet cells (intestinal metaplasia).  It may be difficult to distinguish a Barrett’s oesophagus from a tubular, sliding hiatus hernia during endoscopy, as the two often coexist
  59. 59. GIANT DIAPHRAGMATIC (HIATAL) HERNIAS
  60. 60. GIANT DIAPHRAGMATIC (HIATAL) HERNIAS  A hernia is defined as the protrusion of a whole or part of an organ through the wall of the cavity that contains it into an abnormal position.  A hiatus hernia describes the protrusion of an organ from the abdominal cavity into the thorax through the oesophageal hiatus. This is typically the stomach herniating although rarely small bowel, colon, or mesentery can also herniate through*.
  61. 61.  Hiatus hernia are extremely common, however the exact prevalence in the general population is difficult to accurately state, simply because the majority are completely asymptomatic.  However it is estimated that around a third of individuals over the age of 50 have a hiatus hernia.
  62. 62. Classification Hiatus herniae can be classified into two subtypes:-  Sliding hiatus hernia (80%)– the gastro-oesophageal junction (GOJ), the abdominal part of the oesophagus, and frequently the cardia of the stomach move or ‘slides’ upwards through the diaphragmatic hiatus into the thorax.
  63. 63.  Rolling or Para-Oesophageal hernia (20%) – an upward movement of the gastric fundus occurs to lie alongside a normally positioned GOJ, which creates a ‘bubble’ of stomach in the thorax. This is a true hernia with a peritoneal sac.  The proportion of the stomach that herniates is variable and may increase with time, eventually may evolve to have almost the entire stomach sitting in the thorax.  A mixed type hiatus can also occur, which has both a rolling and sliding component.
  64. 64. Types of Hiatus Hernia
  65. 65. Incidence and Etiology  Structural deterioration of the phrenoesophageal membrane over time may explain the higher incidence of hiatal hernias in the older age group.  These changes involve thinning of the upper fascial layer of the phrenoesophageal membrane (i.e., the supradiaphragmatic continuation of the endothoracic fascia) and loss of elasticity in the lower fascial layer (i.e., the infradiaphragmatic continuation of the transversalis fascia).
  66. 66. Risk Factors  Age is the biggest risk factor for developing a hiatus hernia, due to a combination of age-related loss of diaphragmatic tone, increasing intrabdominal pressures (e.g. repetitive coughing), and an increased size of diaphragmatic hiatus.  Pregnancy, obesity, and ascites are also risk factors, due to increased intra-abdominal pressure and superior displacement of the viscera.
  67. 67. Clinical Features  The vast majority of hiatus herniae are completely asymptomatic.  Patients may experience gastroesophageal reflux symptoms, such as burning epigastric pain, which is made worse by lying flat and are often more severe and treatment-resistant.  Other signs and symptoms that can occur include vomiting and weight loss(a rare but serious presentation)
  68. 68.  bleeding and / or anaemia (secondary to oesophageal ulceration).  hiccups or palpitations (if the hiatus hernia is of sufficient size, it may cause irritation to either the diaphragm or the pericardial sac),  swallowing difficulties (either oesophageal stricture formation or rarely incarceration of the hernia).  The clinical examination is typically normal. In patients with a sufficiently large hiatus hernia, bowel sounds may be auscultated within the chest.
  69. 69. Differential Diagnosis  The important differentials that must be thought of and excluded are:  Cardiac chest pain  Gastric or pancreatic cancer*  Particularly if there is evidence of gastric outlet obstruction, early satiety, or weight loss.  Gastro-oesophageal reflux disease
  70. 70. Investigations  Oesophagogastroduodenoscopy (OGD) is the gold standard investigation, (showing upward displacement of the Gastro-Oesophageal Junction (GOJ, also termed the ‘Z-line’).  They can also be diagnosed incidentally, either on a CT or MRI scan*. A contrast swallow may also be used to diagnose a hiatus hernia, although are less commonly used
  71. 71. Figure – An OGD of a Hiatus Hernia, showing upward displacement of the Z-line
  72. 72. Management  Conservative  The first line pharmacological management for a symptomatic hiatus hernia is a Proton Pump Inhibitor (PPIs).  Any patient should be advised of lifestyle modification, including weight loss, alteration of diet (low fat, earlier meals, smaller portions).  Smoking cessation and reduction in alcohol intake should be advised,
  73. 73. Surgical Management  Surgical management is indicated when:  Remaining symptomatic, despite maximal medical therapy  Increased risk of strangulation/volvulus* (rolling type or mixed type hernia, or containing other abdominal viscera)  Nutritional failure (due to gastric outlet obstruction)
  74. 74. There are two aspects of hiatus hernia surgery:  Cruroplasty – The hernia is reduced from the thorax into the abdomen and the hiatus reapproximated to the appropriate size. Any large defects usually require mesh to strengthen the repair.  Fundoplication – The gastric fundus is wrapped around the lower oesophagus and stitched in place (Fig. 4)  Aims to strengthen the LOS thus helping to prevent reflux and keep the GOJ in place below the diaphragm – the wrap may be full or partial (usually dependent on surgeon preference)
  75. 75. Complications of Surgery  Despite complications, the success rate of repair is excellent with some centres reporting that >90% of patients have a good long term outcome. The specific complications relating to hiatus hernia surgery may include:  Recurrence of the hernia  Abdominal bloating  Dysphagia  Fundal necrosis
  76. 76. Complications  Hiatus hernias, especially the rolling type, are prone to incarceration and strangulation, like any other type of hernia.  A gastric volvulus can also occur whereby the stomach twists on itself by 180 degrees, leading to obstruction of the gastric passage and tissue necrosis, and requires prompt surgical intervention.  Clinically, this can present with Borchardt’s triad:  Severe epigastric pain  Retching without vomiting  Inability to pass an NG tube
  77. 77. ESOPHAGEAL DIVERTICULA  An esophageal diverticulumi s an outpouching of mucosa through the muscular layer of the esophagus  It can be asymptomatic or cause dysphagia and regurgitation.  Diagnosis is made by barium swallow; surgery is rarely required.  There are several types of esophageal diverticula, each of different origin.
  78. 78.  Diverticula of the esophagusmay be characterized by their location in the esophagus(proximal, mid-, or distal esophagus), or by the nature of concomitant pathology.  Diverticula associated with motor disorders are termed Pulsion diverticula and those associated with inflammatory conditions are termed Traction Diverticula.
  79. 79. Classification  1.According to the origin:  a)congenital;  b)acquired.  2. According to the histological structure:  a)true (have all layers of esophageal wall);  b)false (absent muscular layer of esophageal wall).
  80. 80.  3. According to the localization:  a)pharyngoesophageal(Zenker's);  b)bifurcational;  c)epiphrenic.  4. According to the clinical course:  a)complicated;  b)uncomplicated.
  81. 81. Zenker's(pharyngeal) diverticula  Zenker's(pharyngeal) diverticula are posterior outpouchings of mucosa and submucosa through the cricopharyngeal muscle, probably resulting from an incoordination between pharyngeal propulsion and cricopharyngeal relaxation.  The most common esophageal diverticulum  Occurs between the ages of 30-50 (believed to be acquired)
  82. 82.  KEY POINTS: FOUR SYMPTOMS OF ZENKER'S DIVERTICULUM  Regurgitation of undigested food  Bad breath (Halitosis)  Lump on side of neck  Dysphagia in lower neck  “gurgling” sound when drinking  Complications:  Malnutrition : results from patient being unable to eat well  Aspiration pneumonia
  83. 83. Midesophageal(Traction) Diverticula  Are typically associated with mediastinalgranulomatousdisease (TB, histoplasmosis) or secondarily, by motility disorders.  They are usually small with a blunt tapered tip that points upward  These are usually an incidental finding on barium swallow
  84. 84. Epiphrenic(Supradiaphragmatic) Diverticula  Generally occur within the distal 10cm of the thoracic esophagus  These are pulsiondiverticulathat arise due to esophageal motor dysfunction or mechanical distal obstruction (hiatalhernia, DES, achalasia, reflux esophagitisand carcinoma)
  85. 85. Diffuse intramural esophageal diverticulosis  Diffuse intramural esophageal diverticulosisis due to dilation of the deep esophageal glands and may lead to chronic candidiasis or to the development of a stricture that is usually high up in the esophagus.  These patients may present with dysphagia.
  86. 86. Symptoms and Signs  Traction and epiphrenicdiverticulaare rarely symptomatic, although their underlying cause may be.  Diagnosis and Treatment  All diverticulaare diagnosed by videotaped barium swallow. Specific treatment is usually not required, although resection is occasionally necessary for large or symptomatic diverticula(removed by surgically – cricopharyngeal myotomy).  Diverticula associated with motility disorders require treatment of the primary disorder (distal myotomy).
  87. 87. MOTILITY DISORDERS AND DIVERTICULA
  88. 88. Oesophageal motility disorders  The esophagus functions solely to deliver food from the mouth to the stomach where the process of digestion can begin.  Efficient transport by the esophagus requires a coordinated, sequential motility pattern that propels food from above and clears acid and bile reflux from below.  Disruption of this highly integrated muscular motion limits delivery of food and fluid, as well as causes a bothersome sense of dysphagia and chest pain.
  89. 89.  Primary esophageal causes of dysmotility include  Achalasia  Diffuse esophageal spasm  Eosinophilic esophagitis  Systemic disorders causing esophageal dysmotility include  Systemic sclerosis  Chagas disease
  90. 90. Achalasia  Achalasia is a neurogenic esophageal motility disorder characterized by impaired esophageal peristalsis and a lack of lower esophageal sphincter relaxation during swallowing.  Achalasia is thought to be caused by a loss of ganglion cells in the myenteric plexus of the esophagus, resulting in denervation of esophageal muscle.
  91. 91.  Etiology of the denervation is unknown, but viral and autoimmune causes are suspected, and certain tumors may cause achalasia either by direct obstruction or as a paraneoplastic process.  Chagas disease which causes destruction of autonomic ganglia, may result in achalasia.  Increased pressure at the lower esophageal sphincter (LES) causes obstruction with secondary dilation of the esophagus.  Esophageal retention of undigested food and liquid is common.
  92. 92.  clinical presentations:  solid dysphagia 90-100% (75% also with dysphagia to liquids)  post-prandial regurgitation 60-90%  chest pain 33-50%  pyrosis 25-45%  weight loss  nocturnal cough and recurrent aspiration
  93. 93. Investigations  1. Chest x ray showing: Absence of gases in the fundus of the stomach.  2. Barium swallow: Dilated esophagus, the lower end gradually narrows (bird's beak deformity).  3. Upper endoscopy: For diagnosis & to exclude cancer esophagus, in achalasia the endoscope can pass easily through the narrowing without resistance.  4. Manometry: It shows aperistalsis with failure of the lower esophageal sphincter to relax
  94. 94. Figure -The characteristic feature of achalasia on barium swallow; a bird’s beak appearance caused by failure of relaxation of the lower oesophageal sphincter
  95. 95. Treatment  Balloon dilation or surgical myotomy of the LES  Peroral endoscopic myotomy  Sometimes botulinum toxin injection  No therapy restores peristalsis; treatment of achalasia is aimed at reducing the pressure at the LES.
  96. 96. Pneumatic Dilation  Pneumatic dilation is an endoscopic therapy for achalasia.  An air-filled cylinder-shaped balloon disrupts the muscle fibers of the lower esophageal sphincter, which is too tight in patients with achalasia.
  97. 97. How is Pneumatic Dilation Performed?  During an outpatient upper endoscopy, the endoscopist passes a catheter with a deflated balloon through the mouth and into the stomach.  The balloon is centered over the lower esophageal sphincter and inflated with air.  The pneumatic dilating balloon used to treat achalasia is 30 to 40 mm (about 1.2 to 1.6 inches) in diameter.  If symptoms do not improve adequately with the first dilation, a second or third procedure may be performed at a later date with a larger dilator.
  98. 98.  Pneumatic dilation is often performed with X-ray guidance.  Perforation is the major complication, The risk of perforation increases with bigger balloons, and they should be used cautiously for progressive dilatation over a period of weeks.  Forceful dilatation is curative in 75–85% of cases.
  99. 99. Laparoscopic HELLER’S MYOTOMY  Laparoscopic Heller myotomy has now become the method most commonly used to treat achalasia.  The goal of treatment is to relieve the functional outflow obstruction secondary to the loss of relaxation.  At the time of laparoscopy, the muscle fibers of the esophagus are teased apart to reduce the LES pressure.  Advantages of this method are the shorter length of stay (1 day), minimal postoperative discomfort, and excellent response rate of 90%
  100. 100.  The major complication is gastro- oesophageal reflux, and most surgeons therefore add a partial anterior fundoplication (Heller–Dor operation).
  101. 101. Peroral Endoscopic Myotomy (POEM)  Peroral endoscopic myotomy (POEM) is an endoscopic therapy for achalasia.  It uses upper endoscopy rather than conventional surgery, which involves an incision in the skin. In patients with achalasia, the lower esophageal sphincter is too tight.  The goal of all treatment of achalasia is to weaken the lower esophageal sphincter
  102. 102. How Is POEM Performed?  While the patient is under general anesthesia, the endoscopist passes the flexible endoscope through the mouth into the esophagus.  A small incision is made in the innermost layer of the esophagus (the mucosa). The endoscope is then tunneled down the remaining length of the esophagus in the layer called the submucosa.  In the lower esophagus, the endoscopist cuts the muscle fibers of the lower esophageal sphincter.  The endoscope is removed and the first incision made in the mucosa is closed to complete the procedure.
  103. 103. Diffuse Oesophageal Spasm  Diffuse oesophageal spasm (DOS) is a disease characterised by multi-focal high amplitude contractions of the oesophagus.  It is thought to be caused by the dysfunction of oesophageal inhibitory nerves. In some individuals, DOS can progress to achalasia.
  104. 104. Clinical Features  Patients with diffuse oesophageal spasm will typically present with severe dysphagia to both solids and liquids. Central chest pain is a common finding, usually exacerbated by food.  Interestingly, the pain from DOS can respond to nitrates, making it difficult to distinguish from angina pectoris (yet this pain is rarely exertional). Examination is often normal.
  105. 105. Investigations  Diffuse oesophageal spasm is investigated in the same manner as other motility disorders, with the definitive diagnosis made via manometry.  Endoscopy is usually normal.  Manometry characteristically shows a pattern of repetitive, simultaneous, and ineffective contractions of the oesophagus. There may also be dysfunction of the lower oesophageal sphincter.
  106. 106. Figure 4 – Barium swallow showing a corkscrew appearance, as seen in cases of diffuse oesophageal spasm
  107. 107. Management  The initial management is through agents which act to relax the oesophageal smooth muscle, typically nitrates or calcium channel blockers (CCBs) as first line. These limit the strongest of the contractions, and so provide a symptomatic improvement, although their long-term efficacy is uncertain.  Patients with diffuse oesophageal spasm and documented hypertension of the lower oesophageal sphincter may benefit from pneumatic dilatation.  Myotomy is reserved for the most severe cases and must be used with caution
  108. 108. Other Causes of Oesophageal Dysmotility  A number of autoimmune and connective tissue disorders are associated with oesophageal dysmotility. These include systemic sclerosis (most common), polymyositis, and dermatomyositis.  In these cases treatment is directed at the underlying cause (e.g. immunosupression in autoimmune- mediated disease), with nutritional modification and proton pump inhibitors as required.
  109. 109. CARCINOMA OF THE ESOPHAGUS
  110. 110. CARCINOMA OF THE ESOPHAGUS  More than 8,500 new cases of oesophageal cancer are diagnosed each year, with the incidence of cancers of the lower oesophagus / gastro-oesophageal junction rinsing faster than any other solid organ tumour. They are 3 times more common in men.  There are two main types of oesophageal cancer:  Squamous cell carcinoma (more common in the developing world) typically occurring in the middle and upper thirds of the oesophagus  Strongly associated with smoking and excessive alcohol consumption, as well as chronic achalasia, low vitamin A levels and, rarely, iron deficiency
  111. 111.  Adenocarcinoma (more common in the developed world) typically occurring in the lower third of the oesophagus  Arises as a consequence of metaplastic epithelium (termed Barrett’s oesophagus) which progresses to dysplasia, to eventually become malignant  Risk factors for this subtype are long-standing GORD, obesity, and high dietary fat intake  Other rare subtypes of esophageal malignancy include leiomyosarcoma, rhabdomyosarcoma, or lymphoma.
  112. 112. Clinical Features  Early stage oesophageal cancer often lacks well- defined symptoms, which may account for the majority of patients presenting in the later course of the disease.  However, as the condition progresses, the symptoms that can present include:  Dysphagia – characteristically progressive, initially being to solids (especially meats or breads) then liquids  Any patient with dysphagia should be assumed to have oesophageal cancer until proven otherwise.
  113. 113.  Significant weight loss – due to both dysphagia and cancer-related anorexia (this is a marker of late-stage disease)  Other less common symptoms include odonyphagia or hoarseness
  114. 114.  NICE guidance states the red-flag symptoms for a suspected oesophageal malignancy requiring urgent endoscopy are:  Patients with dysphagia  Any patient >55yrs with weight loss and upper abdominal pain, dyspepsia, or reflux  On clinical examination, patients may have evidence of recent weight loss or cachexia, signs of dehydration, supraclavicular lymphadenopathy, or any signs of metastatic disease (e.g. jaundice, hepatomegaly, or ascites)
  115. 115. Differential Diagnosis  Importantly, the dysphagia should be classified as either a mechanical or neuromuscular disorder, as this can significantly affect future investigations.  However, any patient presenting with dysphagia should be assumed to have oesophageal cancer until proven otherwise.
  116. 116. Investigations  Initial Investigations  Any patient with a suspected oesophageal malignancy should be offered urgent upper gastrointestinal endoscopy* (also termed an oesophago-gastro-duodenoscopy, OGD), to be performed within 2 weeks.  Any malignancy seen on OGD will be biopsied and sent for histology.  *Patients who are not fit for an OGD can occasionally have a CT scan (neck and thorax) however this is much less sensitive and specific.
  117. 117. Oesophageal cancer, as seen on upper GI endoscopy
  118. 118. Further Investigations  Before undergoing curative treatment, patients often require a variety of the staging investigations including:  CT Chest-Abdomen-Pelvis and PET-CT scan are used together to investigate for distant metastases  Endoscopic Ultrasound to measure the penetration into the oesophageal wall (T stage) and assess and biopsy suspicious mediastinal lymph nodes  Staging laparoscopy (for junctional tumours with an intra-abdominal component) to look for intra-peritoneal metastases
  119. 119.  Any palpable cervical lymph nodes may be investigated via Fine Needle Aspiration (FNA) biopsy and any hoarseness or haemoptysis may warrant investigation via bronchoscopy.
  120. 120. Management  Sadly, the majority of patients present with advanced disease. Approximately 70% of patients are therefore only treated palliatively.  As with all cancers, the management of oesophageal cancer patients should be determined by the multidisciplinary team (MDT), with input from general surgeons, oncologists, specialist nurses, nutritionists, and the palliative care team.
  121. 121. Curative Management  The choice of curative treatment strategy will depend on tumour type, site and the patient’s general fitness and co-morbidities.  For the majority of patients, this comprises surgery with or without neoadjuvant chemotherapy or chemo- radiotherapy (CRT):
  122. 122.  Squamous cell carcinomasSCCs of the upper oesophagus are technically difficult to operate on and definitive CRT is therefore usually the treatment of choice  SCCs of the middle or lower oesophagus will warrant either definitive CRT or neoadjuvant CRT followed then by surgery
  123. 123.  Adenocarcinomas– neoadjuvant chemotherapy or chemo-radiotherapy followed by an oesophageal resectionPatients who are less fit (but still fit enough to undergo surgery) may simply receive surgical treatment alone
  124. 124. Surgical Treatment  Surgical treatment is a major undertaking as both the abdominal and chest cavities need to be opened.  Patients have one lung deflated for about 2 hours during surgery; 30-day mortality rates are around 4% and it takes 6-9 months for patients to recover to their pre-operative quality of life.  The main complications are anastomotic leak* (8%), re-operation, pneumonia (30%), and death (4%)
  125. 125.  Post-operative nutrition is a major problem for these patients as they lose the reservoir function of the stomach. Many centres will routinely insert a feeding tube into the small bowel (a “feeding jejunostomy”) to aid nutrition.  However, most patients will need to eat 5-6 small meals per day and “graze” to meet their nutritional requirements as they physically cannot fit in 3 normal size but intermittent meals.
  126. 126. Surgical Techniques  The main surgical management option for oesophageal cancer is an oesophagectomy, with a variety of approaches possible. They all involve removal of the tumour, top of the stomach, and surrounding lymph nodes. The stomach is then made into a tube (“the conduit”) and brought up into the chest to replace the oesophagus.
  127. 127.  Specific approaches include:  Right thoracotomy with laparotomy (termed an Ivor- Lewis procedure)  Right thoracotomy with abdominal incision and neck incision (termed a McKeown procedure)  Left thoracotomy with or without neck incision  Left thoraco-abdominal incision (one large incision starting above the umbilicus and extending round the back to below the left shoulder blade)
  128. 128.  For a small number of patients with very early cancers or high grade Barrett’s oesophagus, an option is Endoscopic Mucosal Resection (EMR), which is the removal of just the mucosal layer of the oesophagus.  EMR can be combined with radiofrequency ablation (RFA) or photodynamic therapy (PDT) afterwards to destroy any malignant cells that may be left.
  129. 129. Palliative Management  Those patients deemed too unfit or unsuitable for curative therapy can be offered a range of palliative options.  Patients with difficulty in swallowing should have an oesophageal stent placed where possible (Fig. 3). Radiotherapy and/or chemotherapy can be used for palliation to reduce tumour size and bleeding, temporarily improving the patient’s symptoms.  Photodynamic therapy (PDT) is a treatment that uses a photosensitizing agent, that when exposed to a specific wavelength of light produces a form of oxygen that kills nearby cells.
  130. 130.  Nutritional support is essential for this patient group, as progression of the disease can lead to significant dysphagia and cachexia. Thickened fluid and nutritional supplements should be offered (usually via the nutrition team).  If dysphagia becomes too severe to tolerate enteral feeds, a Radiologically-Inserted Gastrostomy (RIG) tube may need to be inserted, to bypass the obstruction.
  131. 131. Prognosis  The prognosis for oesophageal cancer is generally poor due to late presentation. Overall five-year survival is 5-10%.  The outcome of surgically treated patients have survival depending on stage of the disease, with a 5 year survival for stage 1 cancers at around 60%. Palliative treated patients have a median survival of 4 months.
  132. 132. THE END

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