Dr. Qasim's Esophagus Lecture 1 PDF

ESOPHAGUS Surgical anatomy Esophagus  Key points  Anatomy & histology  Physiology  Esophageal symptoms assessment  Esophageal testing  Anatomy  The esophagusis a muscular tube connecting the pharynx to the stomach  23-25 cm in lengthcombo of both  Con...

ESOPHAGUS Surgical anatomy Esophagus  Key points  Anatomy & histology  Physiology  Esophageal symptoms assessment  Esophageal testing  Anatomy  The esophagusis a muscular tube connecting the pharynx to the stomach  23-25 cm in lengthcombo of both  Contains two sphincters  Lined by squamous  epithelium  < 3 cm below diaphragm  The structure and function are much more complex.  A thorough understanding of the anatomy and physiology is essential to understanding esophageal disease states. Anatomy Sites of external compression  The Aorta.  Left main stem bronchus.  Diaphragm.  **Clinical application in foreign body impaction.  Histology  Mucosa.  Stratified squamous epithelium  Lamina propria,  Muscularismucosa.  Submucosa.  Muscularispropria.  Skeletal muscle. Upper 1/3  Smooth muscle. Lower 2/3  Adventitia.  No serosa, ( unique ). Anatomy innervation  Vagus nerve Smooth muscle  Myentericplexus. ( peristalsis)  Meissner's plexus.  Neurotransmitters:  ACH ( excitatory) , proximal  NO ( inhibitory ) , distal  Anatomy blood supply  Segmental orientation.  Blood supply to other viscera. Physiology  Primary Peristalsis:  Food bolus, contracts proximally to distally  Secondary Peristalsis:  Esophageal distention (residual food bolus) and reflux  Tertiary Contractions:  Nonperistalticpropel bolus in a retrograde direction to proximal esophagus  Physiology Upper esophageal sphincter Lower esophageal sphincter UES LES  10–40 mm Hg  Composed of the  Below Diaphragm cricopharyngeus muscle  Physiological sphincter (not a  Rest : Tonic contracture true anatomic sphincter)  Pharyngeal phase: Relaxation Esophageal testing  Barium swallow  Endoscopy  Manometry.  24-hours PH monitoring  endoscopy  Evaluation  Mucosa  Structural abnormalities.  Rigid or flexible  Diagnostic and/or therapeutic.  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 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)  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.  Atypical Symptoms Dyspepsia(epigastric burning and fullness) Nausea and Vomiting Hematemesis Globus Coughing Throat clearing Throat pain Hoarseness Wheezing/stridor Dyspnea Apnea Halitosis FOREIGN BODIES IN THE OESOPHAGUS  The most common is a food bolus, which usually signifies underlying disease  It is usually possible to remove foreign bodies by flexible or rigid endoscopy  Beware of button batteries in the esophagus  PERFORATION  Perforation of the oesophagus is usually iatrogenic (at therapeutic endoscopy) or due to ‘barotrauma’ (spontaneous perforation).  Surgical emphysema is virtually pathognomonic  Many instrumental perforations can be managed conservatively, but spontaneous perforation is often a life-threatening condition that regularly requires surgical intervention Barotrauma (spontaneous perforation, Boerhaave syndrome)  This occurs classically when a person vomits against a  Boerhaave syndrome is the closed glottis. The pressure most serious type of in the oesophagus perforation. WHY????. increases rapidly, and the  This causes rapid chemical irritation in the mediastinum oesophagus bursts at its and pleura followed by weakest point in the lower infection if untreated. third, sending a stream of Barotrauma has also been material into the described in relation to other mediastinum and often the pressure events when the patient strains against a closed pleural cavity as well glottis (e.g. defaecation, labour, weight-lifting).  Diagnosis of spontaneous perforation  The clinical history is usually of severe pain in the chest or upper abdomen following a meal or a bout of drinking. Associated shortness of breath is common. Many cases are misdiagnosed as myocardial infarction, perforated peptic ulcer or pancreatitis if the pain is confined to the upper abdomen.  There may be a surprising amount of rigidity on examination of the upper abdomen, even in the absence of any peritoneal contamination. Other types of perforation  Penetrating injury  Perforation by knives and bullets is uncommon, even in war, as the oesophagus is a relatively small target surrounded by other vital organs.  Foreign bodies Pathological perforation  The oesophagus may be perforated during removal of a foreign body but, occasionally, an object that has been  Rare. Erosion into an adjacent left in the oesophagus for several structure with fistula days will erode through the wall. formation is more common.  Instrumental perforation Aerodigestive fistula is most  Instrumentation is by far the most common cause of perforation. common and usually Modern instrumentation is encountered in primary remarkably safe, but perforation malignant disease of the remains a risk that should never be forgotten. oesophagus or bronchus  The risk is considerably higher in patients with malignancy.  Treatment of oesophageal perforations  What factor(s) enhances spread  The decision between operative of gastro-intestinal fluid to and non-operative management mediastinum???? The aim of rests on four factors. These are: treatment is to limit mediastinal contamination and prevent or  1 the site of the perforation deal with infection. (cervical versus thoracoabdominal oesophagus);  2 the event causing the perforation (spontaneous versus instrumental);  3 underlying pathology (benign or malignant);  4 the status of the oesophagus before the perforation (fasted and empty versus obstructed with a stagnant residue).  Lacerations (Mallory-Weiss Syndrome)  Longitudinal tears in the esophagus at the esophagogastric junction.  The presumed pathogenesis is inadequate relaxation of the musculature of the lower esophageal sphincter during vomiting, with stretching and tearing of the esophagogastric junction at the moment of propulsive expulsion of gastric contents. MALLORY–WEISS SYNDROME  Forceful vomiting may produce a mucosal tear at the cardia rather than a full perforation.  vigorous vomiting produces a vertical split in the gastric mucosa, immediately below the squamocolumnar junction at the cardia in 90 per cent of cases.  The condition presents with haematemesis. Usually, the bleeding is not severe, but endoscopic injection therapy may be required for the occasional, severe case. Surgery is rarely required  CORROSIVE INJURY  Corrosives such as sodium hydroxide (lye, caustic soda) or sulphuric acid may be taken in attempted suicide. Accidental ingestion occurs in children and when corrosives are stored in bottles labeled as beverages.  All can cause severe damage to the mouth, pharynx, larynx, esophagus and stomach. The type of agent, its concentration and the volume ingested largely determine the extent of damage. In general, alkalis are relatively odorless and tasteless, making them more likely to be ingested in large volume.  Alkalis cause liquefaction, saponification of fats, dehydration and thrombosis of blood vessels.  Acids cause coagulative necrosis with eschar formation, and this coagulant may limit penetration to deeper layers of the oesophageal wall. Acids also cause more gastric damage than alkalis because of the induction of intense pylorospasm with pooling in the antrum  The key to management is early endoscopy by an experienced endoscopist to inspect the whole of the oesophagus and stomach.  Minor injuries with only oedema of the mucosa resolve rapidly with no late sequelae.  With more severe injuries, a feeding jejunostomy may be appropriate until the patient can swallow saliva satisfactorily.  The widespread use of broadspectrum antibiotics and steroids is controversial  management  Regular endoscopic examinations are the best way to assess stricture development. Significant stricture formation occurs in about 50 per cent of patients with extensive mucosal damage  emergency surgery for bleeding or perforation, elective oesophageal resection should be deferred for at least three months until the fibrotic phase is established. Oesophageal replacement ( colon) is usually required for very long or multiple strictures Gastro esophageal Reflux Disease  American College of Gastroenterology (ACG)  Symptoms OR mucosal damage produced by the abnormal reflux of gastric contents into the esophagus  Often chronic and relapsing  May see complications of GERD in patients who lack typical symptoms  Physiologic vs Pathologic  Physiologic GERD  Pathologic GERD  Postprandial  Symptoms  Short lived  Mucosal injury  Asymptomatic  Nocturnal sx  No nocturnal sx Pathophysiology  Primary barrier to gastroesophageal reflux is the lower esophageal sphincter LES normally works in conjunction with the diaphragm  If barrier disrupted, acid goes from stomach to esophagus  Gastroesophageal Reflux Disease (GERD) 2. Pathophysiology  a. Gastroesophageal reflux results from transient relaxation or incompetence of lower esophageal sphincter, or increased pressure within stomach  b. Factors contributing to Gastroesophageal reflux 1.Increased gastric volume (post meals) 2.Position pushing gastric contents close to Gastroesophageal juncture (such as bending or lying down) 3.Increased gastric pressure (obesity or tight clothing) 4.Hiatal hernia 31 Gastroesophageal Reflux Disease (GERD) Manifestations 1. Heartburn after meals, while bending over, or recumbent 2. Dyspepsia or indigestion 3. May have regurgitation of sour materials in mouth, pain with swallowing 4. Atypical chest pain 5. Extraesophageal manifestations: Asthma, laryngitis, chronic cough , Sore throat with hoarseness 32  Alarms Alarm Signs/Symptoms  Dysphagia  Early satiety  GI bleeding  Odynophagia  Vomiting  Weight loss  Iron deficiency anemia  Complications  Erosive esophagitis  Stricture  Barrett’s esophagus  Complications  Erosive esophagitis  Responsible for 40-60% of GERD symptoms  Severity of symptoms often fail to match severity of erosive esophagitis Complications  Esophageal stricture  Result of healing of erosive esophagitis  May need dilation  Complications  Barrett’s Esophagus  Columnar metaplasia of the esophagus  Associated with the development of adenocarcinoma Complications  Barrett’s Esophagus  Acid damages lining of esophagus and causes chronic esophagitis  Damaged area heals in a metaplastic process and abnormal columnar cells replace squamous cells  This specialized intestinal metaplasia can progress to dysplasia and adenocarcinoma  Gastroesophageal Reflux Disease (GERD) Diagnostic Tests  a. Barium swallow (evaluation of esophagus, stomach, small intestine)  b. Upper endoscopy: direct visualization; biopsies may be done  c. 24-hour ambulatory pH monitoring Husni Rousan 39 management 1)Dietary and Lifestyle Management  a. Elimination of acid foods (tomatoes, spicy, citrus foods, coffee)  b. Avoiding food which relax esophageal sphincter or delay gastric emptying (fatty foods, chocolate, alcohol)  c. Maintain ideal body weight  d. Eat small meals and stay upright 2 hours post eating; no eating 3 hours prior to going to bed  e. Elevate head of bed on 6 – 8 blocks to decrease reflux  f. No smoking  g. Avoiding bending and wear loose fitting clothing 40 2. Medications  a. Antacids for mild to moderate symptoms, e.g. Maalox, Gaviscon  b. H2-receptor blockers: decrease acid production; given BID or more often, e.g. cimetidine, ranitidine, famotidine, nizatidine  c. Proton-pump inhibitors: reduce gastric secretions, promote healing of esophageal erosion and relieve symptoms, e.g. omeprazole ; lansoprazole  d. Promotility agent( prokinetic ): enhances esophageal clearance and gastric emptying e.g domperidone Husni Rousan 41 3. Surgery indicated for persons not improved by diet and life style changes: Failed medical treatment Severe Oesophagitis Young patients with ongoing regurgitation Respiratory symptoms Barretts Oesophagus.  a. Laparoscopic or open procedures to tighten lower esophageal sphincter. E.g Nissen fundoplication 42  Nissen Fundoplication  Most commonly preferred surgery  360 degree fundus wrap  Effective Complications  Inability to vomit  Gas bloat syndrome  Dysphagia Paul Paul  Recent Techniques for GERD 1. Transoral Endoscopic Suturing – to plicate the GE junction 2. Endoscopic Application of Radiofrequency Energy (Stretta Procedure) Two novel endoluminal therapies approved by the Food and Drug Administration FDA, USA. Paul Complications  Barrett’s Esophagus  Manage in same manner as GERD  EGD every 3 years in patient’s without dysplasia  In patients with dysplasia annual to shorter interval surveillance  Complications  Patient’s with GERD who need regular EGD  Alarm symptoms  Poor therapeutic response  Long symptom duration  “Once in a lifetime” EGD for patient’s with chronic GERD becoming accepted practice  Many patients with Barrett’s are asymptomatic Classification of Hiatus of hernia Definition Part of stomach protrudes through the esophageal hiatus of the diaphragm into thoracic cavity. The classification of hiatus hernia is based upon the position of the gastro esophageal junction. Sliding Hernia Type I Rolling Hernia Type II Combined I + II Type III Type IV Stomach + Viscera Paul  Type I (Sliding hernia)  Due to the laxity of the Phrenoesophageal membrane  Cephalad displacement of the GE junction through the hiatus into the mediastinum  the commonest type  Asymptomatic  5% associated with GERD Paul Type IIII(Rolling TYPE hernia) (ROLLING)  Due to a focal defect in the phrenoesophageal membrane  Superior migration of the fundus of the stomach alongside the GE junction and oesophagus into the mediastinum  GE junction in this type remains in its normal intra-abdominal location Paul  Type III (Hiatus TYPE III hernia) It is the Combination of Type I and Type II Paul Type IV (Hiatus hernia) TYPE IV It is the hernia containing other abdominal viscera like transverse colon and omentum Paul  Complications Gastric volvulus Obstruction Infarction Ischemia – Cameron Ulcer GERD – Barretts Oesophagus Paul Treatment Type 1: Like GERD Type II , III , IV : Surgical Treatment Hernia Repair  Reduction of hernia  Resection of sac  Closure of hiatal defect Paul