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Surgery of the Esophagus – I For undergraduate Staff Members of Cardio-thoracic Surgery Departments Egypt DYSPHAGIA Dysphagia is difficulty in swallowing (functional or organic). Odynophagia is painful dysphagia. Psychogenic dysphagia • Globus hystericus → sensation of a lump in the throat. • Phagophobia → fear of swallowing. Esophageal peristaltic waves: Primary peristaltic waves: from the upper to lower esophagus. Secondary peristaltic waves: from the site of a solid bolus in a segment of the esophagus downward. Tertiary peristaltic waves: pathological, nonpropulsive and non-peristaltic. Etiology: • Oropharyngeal dysphagia: Functional & Organic • Esophageal dysphagia: Functional Motility disorders Organic 1. In the lumine: FB 2. In the wall (Mural): A-Congenital: Stenosis, atresia, short esophagus, duplication cysts and congenital webs + dysphagia lusoria (vascular ring). B-Acquired: Strictures (peptic, corrosive, anastomotic), tumours (B or M) or diverticulae. 3. Pressure from outside: Etiology: I-Oropharyngeal dysphagia: Disorders in the mouth, tongue and pharynx. A- Functional: • Loss of tongue function (myasthenia gravis). • Pharyngeal dysfunction (myasthenia gravis, vascular brainstem disease (pseudo-bulbar syndrome), hyperthyroidism, poliomyelitis, scleroderma, amyloidosis). B- Organic: • Mechanical obstruction (Zenker’s diverticulum, tumours as oral carcinoma, inflammatory stricture, postcricoid carcinoma, retropharyngeal abscess). II-Esophageal dysphagia: Functional (esophageal motility disorders) • Achalasia. • Scleroderma. • Diffuse esophageal spasm. • Nutcracker esophagus • Diabetic neuropathy. • Amyloidosis. • Parasitic infection (Chagas’ disease). • Emotional (globus hystericus). • Plummer-Vinson's syndrome. • Contractile lower esophageal ring (Schatzki ring). • Lower esophageal sphincter spasm (hypertensive sphincter). Organic: A. Congenital • Atresia with or without tracheooesphageal fistula • Stenosis • Short esophagus • Dysphagia lusoria (vascular ring) • Foregut duplication. Organic: B. Acquired Intraluminal obstruction: • Foreign body. Lesions in the wall: • Esophageal webs. • Esophageal tumors. • Inflammatory stricture (peptic stricture). • Anastomotic stricture, post-injection sclerotherapy, postSangestaken tube, post traumatic strictures. • Caustic stricture. • Esophageal diverticulae. Extraluminal obstruction. • Compression by tumors, enlarged lymph nodes, retrosternal goiter. • Vascular abnormalities (aortic aneurysm) and enlarged left atrium. • Spurs from anterior cervical spine. • Rolling hiatal hernia, tight hiatal hernia repair, perioesphagitis after vagotomy. Clinical presentation • Grades: • • • • • • Grade I: dysphagia for solids Grade II: dysphagia for semisolids Grade III: dysphagia for liquids Grade IV: dysphagia for own saliva Site: The patient can point to the site of obstruction. Duration: Long: Benign (stricture, achalasia) Short: Cancer Sudden: foreign body Since birth: Congenital Timing: Within 15 minutes from swallowing Nature: Organic: First to solids then to fluids Achalasia: First to fluids then to solids Course: Intermittent (benign), progressive (malignant) Associated: Heart burn → GER (gastroesophageal reflux) Skin changes → Scleroderma Cervical lymph nodes → Neoplasm, T.B Iron deficiency → Plummer-Vinson’s syndrome Emotional → Globus hystericus. Investigations: 1. Esophagogram. 2. Esophagoscopy. 3. Esophageal function studies. Investigations • • • • • • • • • • • Laboratory Increase tumor markers for mediastinal tumours. Iron deficiency anemia in Plummer-Vinson’s syndrome. Radiological Barium swallow, oesophagogram (most important), Fluoroscopy (for motility disturbances), Barium meal in Trendelenburg position (for hiatal hernia and GER), Chest X-ray (plain), CT scan (for masses), MRI, Angiography (dysphagia lusoria). Instrumental & Biopsy Esophagoscopy and biopsy Esophageal function studies. Manometric study (for motility disturbances) 24-hours pH recording (GER). Esophagoscopy Types: • Rigid: done under general anesthesia (Fig.67) • Flexible, fiberoptic: done under conscious sedation Indications: Diagnostic – – – – Cancer eosophagus: locate site, taking biopsy (bite , brush biopsy) Hiatal hernia: to access degree of reflux Achalasia: Identify cause of dysphagia and hematemesis Therapeutic – – – – – Removal of foreign body Insertion of Stent in cancer esophagus Sclerotherapy in haematemesis Dilatation of esophageal stricture Laser therapy Rigid Esophagoscopy Esophageal function studies: Esophageal manometry. is used to evaluate motility of esophageal body, UES and LES. Examples: • Achalasia • Diffuse esophageal spasm Ambulatory 24-hour pH monitoring . Indications: • To detect and quantitate exposure of lower esophagus to gastric acid. • To test the relationship between symptoms and esophageal exposure to acid refluxate. Ambulatory 24-hour bile reflux monitoring. The reflux of bile &/or acid predisposes to esophageal injury (esophagitis) and Barrett’s esophagus and malignancy. Provocative test: Acid perfusion (Berstein test). Determines whether symptoms are reproduced by the infusion of acid into the esophagus. A positive test reproduces the patient’s symptoms only during acid perfusion. Treatment: 1. Medical: • Neuromuscular: Calcium channel blockers. • Emotional: Assurance, Sedatives. • GER: Antacids, H2 blockers, Proton Pump Inhibitors. • Radio-chemotherapy for inoperable tumours. 2. Instrumental: • Esophageal dilatation (Guidewire directed bougies, Balloon). • Esophagoscopic F.B extraction. • Intubation in inoperable carcinoma (pulsion or traction; simple or expandable prosthesis). • Endoscopic laser for benign or malignant strictures. • Hydrostatic dilatation of achalasia 3- Surgical: I-Removal of extrinsic compression: (thyroidectomy, diverticulectomy, hiatal hernia repair, removal of mediastinal masses…) II-Esophageal resection and substitution using: • Stomach: Esphagogastrectomy with esophagogastrostomy. • Colon interposition. • Jejunal conduit (loop, pedicle, free) • Skin flaps in pharyngeal and upper oesophageal neoplasms. III-Esophagocardiomyotomy for achalasia (Heller’ operation). Motility disorders • • • • Achalasia. Diffuse esophageal spasm. Scleroderma: Skin disease and dysphagia. Nutcracker esophagus; contractions in a normal sequence but at an excessive amplitude or duration. Chest pain mimics angina + Dysphagia. • Diabetic neuropathy. • Amyloidosis. • Parasitic infection (Chagas’ disease). Diffuse esophageal spasm (DES) is a condition in which uncoordinated contractions of the esophagus occur. Ba Swallow →Corkscrew appearance of the esophagus (or "rosary bead esophagus" ) ACHALASIA Definition: Failure of relaxation of the lower esophageal sphincter in response to swallowing. Achalasia is a motility disorder of the esophagus. Etiology: It represents a degenerative nerve process with loss of ganglion cells in the myenteric plexus and a reduction in vagal nerve fibers within the wall of the esophagus. There is hypertrophy of the circular muscle layer of the esophagus, while the longitudinal layer retains its normal thickness. • The combination of achalasia, adrenal insufficiency, and alacrima (lack of tear production) in children is known as the triple A (Allgrove) syndrome. • In most cases the cause is unknown (idiopathic). • In some regions of the world, achalasia can also be caused by Chagas disease due to infection by Trypanosoma cruzi. Clinical Picture : • Progressive dysphagia to liquids and solids over several years (first for fluids). • Regurgitation of undigested food especially in recumbent position. • Weight loss. • Coughing or wheezing secondary to aspiration. Investigations: Radiology: CXR is normal, or shows widened mediastinum with an air-fluid level within the dilated esophagus. Absence of gastric air bubble. Pulmonary infiltrates of aspiration . Barium swallow demonstrates smooth tapering of the distal esophagus (bird’s beak, or pencil end) and a dilated or sigmoid esophagus and absence of gastric air bubble. Endoscopy: • Dilated esophageal body containing food residue (despite fasting). • Easy passage of the rigid oesophagoscope through the esophagogastric junction but failure of esophagogastric junction to open spontaneously with repeated air insufflation using the fiberoptic esophagoscope. Esophageal function studies: Esophageal manometry demonstrates incomplete relaxation of the LES with swallowing and ineffective peristalsis of the body of the esophagus. Esophagogram in achalasia: smooth central narrowing, Bird’s peak- Parrot’s peak – Pencil end, dilated esophagus, narrowing present below cupola of diaphragm & absence of gastric air babble. Complications • Mucosal ulcerations by irritation of retained food. • Aspiration which leads to pneumonitis. • Malignancy in 2-3% (squamous cell carcinoma usually at dilated site). Management Medical treatment: • Oral medications as nitrates, calcium channel blockers and sildenafil (taken 20 min before meal). Pneumonetic dilatation: Balloon pneumatic dilatation produces a forceful disruption of the lower esophageal sphincter. Botulinum toxin: It is endoscopically injected into the lower sphincter to weaken it. Pneumatic dilatation of the lower esophagus Surgical Treatment: – Esophagocardiomyotomy (modified Heller): Surgical longitudinal section of the outer longitudinal and inner circular smooth muscle without damaging the submucosa and mucosa. Myotomy achieved using an abdominal or thoracic approach. Incision extends for about 7-10 cm including lower end of the esophagus and oesophago-gastric junction. – Laparoscopic or thoracoscopic myotomy (VATS). – Esophageal resection and reconstruction is considered in patients who have failed esophageal myotomy (or re-myotomy), or who have an endstage megaesophagus. Modified Heller’s myotomy VATS CORROSIVE ESOPHAGEAL INJURY From accidental (children) or suicidal (adults) ingestion of strong alkali or acid. Liquefaction necrosis from alkali, coagulation necrosis from acid. In Egypt → commercial caustic potash. This is a mixture of potassium hydroxide, potassium carbonate and sodium carbonate. It is used primarily for washing clothes, cleaning floors and in some homes for making soap. Classification of corrosive esophageal burns • First degree (superficial) burn: Superficial mucosal hyperemia, mucosal edema with or without superficial sloughing. • Second degree (medium, transmucosal) burn: The submucosal and muscular layers are involved, being left exposed after desquamation of the mucosa. • Third degree (deep, full-thickness burn): Necrosis through the entire wall of the esophagus, causing periesophagitis and possibly perforation with mediastinitis, pericarditis or broncho-esophageal fistula. Clinical Picture: I. Acute Phase: – – – – – Pain and inability to swallow. Excessive salivation. Respiratory distress. Dehydration. In severe cases, there might be laryngitis and stridor. II. Chronic Phase: This started 4-6 weeks from the incidence of potash ingestion • Dysphagia • Dehydration • Weight loss PPOS Barium Swallow Treatment: I- Initial management of acute corrosive esophagitis: • • • • • Antibiotics. Parenteral or oral fluids. Corticosteroids. Tracheostomy with stridor. Neither instrumentation (Gastric lavage) nor dilatation should be performed at this stage to avoid esophageal perforation. • Esophagoscopy and radiography: Done at any time after corrosive ingestion provided the condition of the patient allows. • If no burn is found in the esophagus, antibiotics are discontinued. Oral feedings are started as soon as the patient comes out of anesthesia following esophagoscopy. • In the presence of first degree burn, antibiotics are continued for ten days. Oral feedings are started progressing from clear liquid diet to a full diet over a period of three days. • In the presence of second and/or third degree burn, a siliconized catheter splint is applied through transcervical pharyngostomy or oesophagostomy. If the patient refuses splinting, he is followed and managed as in the chronic stage. II- Patients who present in the chronic stage of corrosive esophagitis are examined by esophagoscopy and esophagography and managed as follow: • Esophageal dilatation: If there is short smooth segment (less than twovertebrae), patients are dilated antegradely, using Savary dilators. If there is Long segment or irregular strictures (more than two-vertebrae); patients are dilated retrogradely, using Tucker’s dilators. Gastrostomy feeding is required. Esophageal perforation following dilatation is treated conservatively: Stop oral intake, give massive antibiotics, drain any collection (mediastinal abscess, empyema), and institute gastrostomy feeding. II- Patients who present in the chronic stage of corrosive (Cont.): • Retrosternal colon interposition is indicated if dilatation failed. A segment of transverse colon interposed between the proximal esophagus and the stomach. ESOPHAGEAL CANCER Premalignant lesions: • Achalasia, • Barrett’s esophagus, • Reflux stricture, • Post-corrosive stricture, • Plummer-Vinson syndrome. Clinical Picture: • Primary tumour: Dysphagia, regurgitation, vomiting, odynophagia, pain (epigastric, back, neck) arising from local tumour infiltration, esophagitis, and metastasis to intraabdominal lymph nodes or bone, respiratory symptoms (cough after swallowing) suggesting aspiration or an esophagotracheal or bronchial fistula. General symptoms of weight loss and cachexia are present in 50% of patients. Clinical Picture: Cont. • Distant metastases: lung, liver, bone, adrenal, kidney, abdominal lymph nodes, …. • Physical examination: Enlarged cervical or supraclavicular lymph nodes, signs of aspiration (rales, rhonchi, consolidation), upper abdominal mass, hepatomegaly, generalized wasting. Investigations: • Laboratory: Anemia, hypoproteinemia, abnormal liver function tests, hypercalcemia. • CXR: Pulmonary metastases, infiltrates or pneumonia, soft-tissue mass or air-fluid level in the mediastinum. • Barium esophagogram: Defines level and extent of oesophageal obstruction → fixed irregular filling defect, rate tail appearance and shouldering. • Esophagogastroscopy: flexible or rigid esophagoscope. It defines the site and extent of the tumor. Multiple biopsies are taken to obtain a histologic diagnosis. Obstructing tumors may be dilated or stented during esophagoscopy. Investigations: Cont. • CT: to assess extent of local disease and enlarged nodes. Scanning of the brain, lung, and liver for the possibility of metastases. • Endoscopic ultrasound: To assess the depth of tumor penetration and peri-esophageal lymph node metastasis. • Bronchoscopy: if a malignant fistula is suspected. • MRI: Has little advantage over CT. Barium swallow in cancer esophagus: Filling defect, rat tail appearance, shouldering, irregular eccentric stricture. Esophagogram: Upper, middle and lower 1/3 Endoscopic image of patient with esophageal cancer TNM subsets T descriptor • Tis Carcinoma in situ. • T1 Tumor invades lamina propria, muscularis mucosa or submucosa. • T2: Tumor invades muscularis propria. • T3 Tumor extends into periesophageal tissue. • T4 Tumor invades adjacent structures. N descriptor • N0 No regional lymph node metastasis. • N1 Regional lymph node metastasis . M descriptor • M0 No distant metastases • M1 Distant metastases. Stage 0 • Tis N0 M0 I • T1 N0 M0 IIA • • T2 N0 M0 T3 N0 M0 IIB • • T1 N1 M0 T2 N1 M0 III • • T3 N1 M0 T4 Any N M0 IV • Any T Any N M1 Pathology of esophageal cancer Squamous cell carcinoma : • 80% of all primary esophageal cancers. • Mid-third (50%), lower-third (25%), upper-third (15%). • Macroscopic types: Fungating, ulcerating, infiltrating, polypoid. • Histologically: Well-differentiated or poorlydifferentiated. • Submucosal proximal tumor spread is frequent. • Metastasis to regional lymph nodes > 50%. • Metastasis to lung 50% and liver 50%. Pathology of esophageal cancer Cont. Adenocarcinoma : • 20 - 40% of primary esophageal cancer. • Should be distinguished from adenocarcinoma of gastric origin. Criteria in favor of esophageal origin include: Associated Barrett’s epithelium. Greater than 75% of tumor mass involving the body of esophagus. Direct invasion of periesophageal tissues. Minimal gastric involvement. Clinical symptoms of esophageal obstruction. Treatment: • Early stage tumors (Tis, Stage I): Surgical resection. • Locally advanced (T4) & metastatic (M1) tumors : Are excluded from surgery. I - Surgery: Procedure: esophagectomy with gastric pull up and esophagogastric anastomosis. Idea of procedure : Resection of the esophageal tumour with proximal extension of resected esophagus of 10 cm & distal extension of resection at least 5 cm from tumor. Esophageal reconstruction: this achieved by gastric pull up with the stomach positioned in the posterior mediastinum. The healthy proximal portion of the esophagus is then anastomosed to the stomach (esophagogastric anastomosis). A pyloromyotomy or pyloroplasty is done to improve gastric drainage. Approach : • Right thoracotomy & laparotomy • Left thoracotomy or Thoracoabdominal • Transhiatal (non-thoracotomy, Blind esophagectomy) • Video assisted thoracoscopic surgery (VATS) Esophagectomy for Cancer esophagus Circular Stapler - Product nomenclature Detachable head assembly Tying notch Locking spring Adjusting knob Gap setting scale Anvil Shaft Safety Trocar Orange Tying area Staple Housing Firing handle 56 57 II- Radiotherapy: – Preoperative: Improves resection and reduces local recurrence. – Postoperative: Not recommended as a routine after surgical resection. III- Chemotherapy: • Single agent (cisplatin, 5-fluro-uracil, mytomycin, bleomycin). • Combination (cisplatin + 5-fluro-uracil). • Preoperative: Eliminates micro-metastases and improve respectability. • Postoperative: Cannot be recommended for routine clinical use. Palliation: Causes of irresectability (Inoperable Cancer esophagus) • General: Cachectic patients unfit for surgery, deteriorated cardiac, renal, hepatic and pulmonary functions. • Local: – Tumour more than 10 cm. – Spread to tracheobronchial tree, Aorta. – Peritoneal seedlings. – Celiac and hepatic lymph node affection. • Distant metastesis e.g liver, lung. Types of Palliation • Esophageal dilatation. • Esophageal stents: – Covered self-expandable metallic stents, inserted through endoscopy. – Mousseau Barbin intubation, inserted through laparotomy . • • • • Radiochemotherapy. Endoluminal brachytherapy. Laser therapy. Surgery: – Feeding gastrostomy – Retrosternal Colon interposition or esophagogastrectomy. Those 2 aggressive surgeries are rarely used as palliation. Esophageal stenting Diaphragmatic Herniae I- Congenital: Morgagni’s hernia Bochdalek hernia II- Acquired: Hiatal Hernia Traumatic (Accidental, Iatrogenic) Congenital diaphragmatic hernia Morgagni’s hernia Congenital diaphragmatic hernia Bochdalek hernia Barrett’s esophagus Definition: Lining of the lower esophagus with columnar epithelium instead of squamous epithelium (columnar metaplesia). Pathology: Finding of specialized columnar epithelium, characterized by intestinal metaplasia. Endoscopic appearance in Barrett’s esophagus Etiology Barrett’s esophagus results from chronic GERD. Chronic reflux esophagitis lead to loss of esophageal mucosa and replacement of columnar epithelium with squamous epithelium. Clinical importance of Barrett’s esophagus: Barrett’s esophagus predisposes to esophageal cancer i.e. precancerous, particularly adenocarcinoma. Clinical Picture: Symptoms related to GERD. Investigations: • Radiology (Ba Swallow): Reflux-related findings (mucosal ulceration, strictures). • Endoscopy and biopsy: Barrett’s columnar mucosa is deeper pink compared with the pale squamous mucosa and > 3 cm from the EGJ. Multiple biopsies at 2-cm intervals are taken. Endoscopic application of vital stains (Lugol’s iodine, toluidine blue) improves recognition of columnar mucosa. Treatment: • Control of GERD by medical and surgical anti-reflux therapy. • Endoscopic surveillance to detect early stage adenocarcinoma & surgical resection in high-grade dysplasia.