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Presentation and Management of common esophageal diseases

Presentation and Management of common esophageal diseases. Dr. Waseem HAJJAR MD, FRCS,Assistant Professor

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Presentation and Management of common esophageal diseases

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    2. Presentation and Management of common esophageal diseases Dr. Waseem HAJJAR MD, FRCS, Assistant Professor & Consultant thoracic surgeon

    3. Topics Anatomy of the esophagus. Definitions. Causes of Dysphagia. Gastro-Esophageal Reflux Disease (GERD). Achalasia. Hiatus Hernia. Esophageal tumours.

    4. Anatomy of the esophagus It is an epithelial lined muscular tube, 25cm long, and extends from the level of C6 to T11. Has 3 portions: Cervical Thoracic. Abdominal. It’s muscular coat has 2 layers: Outer longitudinal. Inner circular. The upper 1/3 is composed of striated muscle, while the lower 2/3 is composed of smooth m. Lack of a serosal layer contribute to increase in anastomatic leak.

    5. Cont. It is lined by keratinised squamous epithelium which changes to columnar epithelium 2cm above the gastro-oesophageal junction. It has 2 sphincters: The upper esophageal sphincter. The lower esophageal sphincter (LES). Anatomical areas of narrowing are: At the level of cricoid cartilage. In the mid-thorax, from compression by the aortic arch and left main stem bronchus. At the level of the oesophageal hiatus of the diaphragm.

    8. Blood supply : segmental from superior and inferior thyroid, aortic branches, inferior phrenic and left gastric. Nerve supply : by vagus with nerve endings in myentric plexus.

    9. 2 sphincters : the upper: cricopahryngeal 3cm w, a closing pressure of 40-100 mmHg The lower: (LES) no defined thickened band but a physiological one is present of a pressure 15-35 mmHg

    10. LES Mechanical factors which keep it closed Acute angle of entry of esophagus into the stomach Valve like action of mucosal folds Antireflux mechanism: Resting pressure 15-30 mmhg Intra-abdominal length which is exposed to positive pressure

    11. LES Is under hormonal and neural factors. Between swallows vagal stimulation maintains the sphincter closed. Gastrin realsed from the stomach contracts the LES During swallowing efferent vagal impulses are inhibited causing the muscles relax via nitric oxide and probably vasointestinal peptide (VIP). Secretin and CCK released from the intestine oppose gastrin therefore relax the sphincter. Secondary esophageal peristalsis acts a second line defense which helps clear refluxed material back into the stomach

    12. Definitions Dysphagia: Difficulty in swallowing. Odynophagia: Painful swallowing.

    14. Gastro-Esophageal Reflux Disease (GERD)

    15. Background Gastro-esophageal reflux is a normal phenomenon experienced intermittently by most people. GERD occurs when the amount of gastric juice exceeds the normal limit with or without esophageal mucosal injury (esophagitis).

    16. pathophysiology Factors that prevent gastric juice reflux into the esophagus: LES (normal length and pressure). Gastro-esophageal junction must lie intra-abdominally. The angle at which the esophagus joins the stomach (angle of His). Esophageal clearance must be able to neutralize the acid refluxed from the stomach. The stomach must empty properly. Contraction of the crural muscle of the diaphragm (pinchcock-like action).

    17. Cont. GERD develops due to one or more of the fallowing: Functional (frequent transient LES relaxation) or mechanical (hypotensive LES) problem of the LES, (most common). Certain foods (eg, coffee, alcohol), medications (eg, calcium channel blockers, nitrates, beta-blockers), or hormones (eg, progesterone) can decrease the pressure of the LES. Reduced esophageal clearance of acid because of poor esophageal peristalsis. Obesity and pregnancy (increased intra-abdominal pressure). Hiatus hernia (impairment of the pinchcock-like action of the diaphragm). Delayed gastric emptying.

    18. Epidemiology 7% of the general population have heartburn, and 20-30% of them have GERD. No gender preference. Affects all age groups.

    19. Clinical features Heartburn is the major feature, retrosternal, burning pain, radiating to the epigastrium, aggravated by bending and lying down, and relieved by antacids. Regurgitation of food and acid into the mouth. Waterbrash (salivation). Dysphagia (stricture, or non-specific motility disorder). Respiratory symptoms: cough , nocturnal asthma, pneumonia. Clinical examination is usually normal.

    20. DDx MI. Peptic ulcer disease. Cholecystitis. Esophageal cancer.

    21. Investigation GERD is a clinical Dx. Patients under 45y without alarm symptoms should be treated initially without investigations. Investigations include: Barium swallow (Erosions, ulceration, stricture, hiatus hernia) Esophagogastroduodenoscopy (EGD) Identifies the presence and severity of esophagitis. Excludes other diseases as peptic ulcer disease. Esophageal monometry (function of LES and esoph. Body) Ambulatory 24hr pH monitoring (gold standard).

    24. Ulcerations, linear erosions and esophagitisUlcerations, linear erosions and esophagitis

    28. Cont. Lifestyle modifications includes: Losing weight (if overweight). Avoiding alcohol, chocolate, citrus juice. Avoiding large meals. Waiting after a meal before lying down. Elevation of the head of the bed.

    29. Cont. Medical treatment with: Antacids. H2 receptor blockers. Proton pump inhibitors. Prokinetic agents.

    30. Cont. Surgical treatment: Fundoplication (most commonly Nissen fundoplication). Indications: If symptoms cannot be controlled by medical therapy. The presence of Barrett’s esophagus. The presence of extra-esophageal manifestation of GERD (respiratory, ENT, dental).

    31. Cont. It is performed under GA and the fundus of the stomach is wrapped around the esophagus to create a new valve at the level of the gastro-esophageal junction.

    33. Complications Esophagitis: 50%,, M:F is 2-3:1. Barrett’s esophagus: It is columnar metaplasia of the lower esophagus which extends at least 3cm above the GE junction. M:F is 10:1. Most serious and may progress into cancer. Respiratory complications: Include pneumonia, asthma, and lung fibrosis.

    35. BARRETT’S ESOPHAGUS Biopsy confirmed intestinal metaplasia of the esophagus Chronic esophagitis heals in a metaplastic process—abnormal columnar cells replace squamous cells GERD for more than 1 yr equals 3x risk for barretts, 10yrs ? 6.4 Can progress to dyplasia and ultimately to carcinoma 3-9 % (x 30-125 times the N

    36. ACG recommendationsACG recommendations

    37. Achalasia

    38. Definition Is a primary oesophageal motility disorder characterised by failure of LES to relax and the absence of peristalsis .

    39. pathophysiology

    40. incidence:1/100,000 per year in US No gender difference Typically 25-60 years Cause:unkown but one theory suggest degenerative changes in the vagal nerve

    41. C/F Dysphagia (gradual) Regurgitation Chest pain Weight loss

    42. diagnosis Barium swallow: the esop. Appears dilated and contrast pass slowly into the stomach. the distal esoph. Is narrowed resembling bird beak. Manometry: High LES pressure Absent peristalsis Failure of LES to relax Endoscopy: Dilated esop. With food residue

    43. Diagnosis x-ray study (contrast swallow, fluroscopy)

    45. treatment Drug therapy: Smooth muscle relaxant (nitrate ,calcium channel blocker,,anticholinergic)) 10% of pts. Benefit from this treatment (elderly) Pneumatic dilation: A balloon is insuflatted at the level of the G.O junction to rupture the muscle fibre Success rate 70_80% 50% will require more than 1 dilation.

    46. Cont. Surgery: Used when the dilation fails Heller’s Myotomy(open or laparoscopic) Done by making division of the muscle fibre of the lower esoph. And proximal stomach followed by partial fundiplication to prevent reflux(10%) Relieve symptoms in 85 _95% of pts. If surgery fails ?dilation?2nd operation ---?esophagectomy

    47. Hiatus Hernia

    48. Def: it is an abnormal protrusion of the stomach through esoph. Diphramatic hiatus into the thorax. Caused by weakness mucsles around the hiatus. More common in females ,obes ,middle aged and elderly.

    49. types Type I: sliding hiatus hernia(90%) Type II: paraesophageal hiatus hernia(10%) Type III: combination of both (rare)

    51. Sliding hiatus hernia Occurs when the stomach slides through the diaphragmatic hiatus and the G .O . Junction lies within the chest.

    52. C/F Asymptomatic Heart burn and regurgitation: the most common, due to incompetent LES, aggrivated by bending or lying down and relieved by antacid Dysphagia Large herniation may cause cough, palpitation or hiccups by mechanical effect

    53. investigation Upper GI endoscope Barium swallow

    55. Complication: Reflux?esophagitis?barret’s esophagus-?ca Treatment: Same as GERD

    56. Paraesophageal hiatus hernia Here the G.O. junction lies in its position but the fundus of the stomach has herniated through diaphragmatic hiatus.

    57. C/F Usually not associated with reflux Dysphagia Epigastric and lower chest pain Palpitation Hiccups Quick fullness and chest compression after eating

    58. Investigation: Chest x-ray confirmed by barium swallow. Complication: Obstruction Volvulus Strangulation Acute or chronic bleeding perforation

    59. Treatment Surgical: Operative reduction of the stomach, approximation of the diaphragmatic defect around the hiatus Fundoplication frequently added to reduce the hernaition recurrence and to prevent GE reflux

    60. Tumours of the oesophagus

    61. BENIGN TUMOURS - Accounts for less than 1% of oesophageal neoplasms. The commonest is the benign mixed stromal cell tumour 75 % (used to be called leiomyoma). Usually in distal two thirds of the esophagus - Usually asymptomatic, but can cause bleeding. - Treated by local enucleation.

    62. Dignosis : Chest radiograph Barium swallow Endoscopy Endoscopic ultrasound

    65. Malignant Tumors

    66. INCIDENCE: Its the 3rd most common cancer of the digestive tract and the 7th leading cause of cancer-related deaths M to F ratio 3 : 1 Black to White 4 : 1 Peak in 50 – 70 years of age

    67. Causes and Risk Factors It is caused by a malignant change in cells that line of the esophagus. Tumors often invade the submucosa and then the muscular layer of the organ. Age >5O Male Alcohol & Tobacco use Low socioeconomic level Other medical conditions Diet Obesity Age is a risk factor and the disease is more common after the age of 50. Risk for developing cancer of the esophagus is about 3 times higher in men. Age is a risk factor and the disease is more common after the age of 50. Risk for developing cancer of the esophagus is about 3 times higher in men.

    68. Pathology: -70 % SCC. -Growth of the cancer occurs by intra-oesphageal spread direct extension lymphatic blood -Distant metastases are present in 25-30% ( liver, lungs and bones)

    69. 1- SQUAMOUSE CELL CARCINOMA. - Upper and middle thirds. - In the far east and among some black males. - Risk factors include alcohol, smoking, leakoplakia, achalasia, and the consumption of salted fish, pickled vegetables and chewing tobacoo.

    70. 2- ADENOCARCINOMA. - Arise from columnar epithelium, at the lower third associated with areas of gastric mucosa. - Male to female ratio is 3:1. - Predominantly a disease of white males. - Most common risk factors are reflux and obesity. smoking increase the risk of cardia tumours.

    71. SPREAD OCCURS BY: 1. local invasion into surrounding structures, trachea, lung and aorta (massive haemorrhage may be terminal event) 2. Lymphatic to paraoesophageal nodes, supraclavicular and abdominal nodes. 3. The blood stream to liver and lung.

    72. Diagnosis: Clinically: Usually late presentation Dysphagia Retrosternal pain on swallowing, coughing up blood and regurgitation . With metastatic disease ( enlarged cervical L.N, jaundice, hepatomegaly, hoarseness and chest pain) General features of malignancy

    73. INVESTIGATIONS - Blood tests may reveal anaemia, liver disease and malnutrition. - Diagnosis is made initially by barium swallow (shouldered stricture) and confirmed by endoscopy and biopsy.

    74. Investigation: Barium swallow. Endoscopy with biopsy and cytology. Endoscopic ultrasonography ( asses depth of invasion and infiltration ) Bronchoscopy (in proximal tumors) Look for metastases (CXR, abdominal U/S, CT chest and abdomen, laproscopy)

    81. Treatment : Depends on the stage

    82. For staging: local T stage and N spread is best assessed by endoscopic ultrasonography. M stage by CXR, abdominal ultrasound, CT chest and abdomen and laparoscopy. - Sometimes bronchoscopy. - Enlarged lymph nodes are aspirated for cytology.

    84. Surgery 50% of tumors are resctable at presntation Curative in early lesions and as a part of multimodal therapy in advanced cases Contraindications include metastatic disease, tumor invasion of nearby structures and severe cardiovascular or pulmonary disease.

    85. RADIOTHERAPY AND CHEMOTHERAPY: For patients not suitable for surgical resection. Neoadjuvant therapy (preoperative treatment) has produced encouraging results in recent randomized controlled clinical trials. [squamous cell ca. can be radiosensitive].

    86. Radiotherapy it is often combined with chemotherapy to reduce dysphagia in patients with advanced or metastatic disease. It also may be used to shrink the tumor before surgery or after surgery to destroy remaining cancer cells . Contraindications (large tumors >9cm, presence of a tracheal broncho-oesophageal fistula) Chemotherapy It may be used in combination with radiation to relieve symptoms but it is not used as a primary treatment for esophageal cancer

    87. PALLIATION: 1-endoscopic dilatation. 2-stent insertion. 3-laser ablation.

    89. Prognosis Poor. Prognosis depends on the stage and the overall 5-year survival rate is 20-25%. Less than 6 months. if the primary is non-resectable. Prevention Avoiding heavy alcohol consumption and tobacco use may help to prevent squamous cell carcinoma Patients with frequent heartburn should undergo regular endoscopic screening.

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