Pharynx & Oesophagus PDF

PHARYNX  Clinical anatomy The upper aerodigestive section between the choanae and the criccopharyngeal muscles Divided into three parts a) nasopharynx – from the choanae to the lower edge of the soft palate b) oropharynx - from the edge of the soft palate to the level of the tip of...

PHARYNX  Clinical anatomy The upper aerodigestive section between the choanae and the criccopharyngeal muscles Divided into three parts a) nasopharynx – from the choanae to the lower edge of the soft palate b) oropharynx - from the edge of the soft palate to the level of the tip of the epiglottis c) hypopharynx – from the tip of the epiglottis to the entrance of the esophagus  All the three areas above have a continuous carpet of mucous membrane of common epithelial cells The continuous mucous membrane is important in spread of inflammation from one area to another The walls of the pharynx consist of layers of muscles that regulate the passage of feeds and air – swallowing and breathing Specialized nerve supply makes this intricate control of swallowing and breathing possible The pharynx is separated from the oral cavity by the anterior faucet – ant palatoglossal pillar  The pharynx contain a specific arrangement of lymphoid tissues referred to as the Waldeyer’s Ring The ring comprise of - Adenoid – pharyngeal tonsil - palatal tonsils – left + right - lingual tonsil at the base of the tongue The tissues play an important role in monitoring the substances that pass through the pharynx and the development of immunity OESOPHAGUS From criccopharyngeal sphincter to the gastro- esophageal junction The narrowest portion of the GIT Has three even narrower parts in its course Upper sphincter is always closed Lower sphincter is physiological 1st oesophageal sphincter is 15 cm from the incisors 2nd is as it crosses the left main bronchus and is 23 cm from incisors 3rd is at diaphragm level and is 40 cm from incisors  Function of the oesophagus is normaly for swallowing i.e. the relocation of feeds from the oral cavity to the stomach and has three phases 1. oral phase – is voluntary 2. pharyngeal phase during which feeds are channeled into the oesophagus and the other 5 pharyngeal openings are closed and protected - velopharyngeal closure prevents reflux into the nose and eustachian tubes - there is pharyngeal peristalsis - faucal pillars and the tongue blocks the food bolus from reentering the oral cavity - there is pharyngeal peristalsis that conveys feeds towards the gullet - air way is protected by the epiglottis - criccopharyngeal opening allows food bolus into the oesophagus 3. oesophageal phase Stage 1 is the only voluntary one and the rest are involuntary  NORMAL SWALLOWING relocation of feeds from oral cavity to stomach Three intricately controlled phases - oral phase - pharyngeal phase - oesophageal phase Ensures protection of the adjacent openings to the food passage Oral Preparatory Phase Break down food Mix with saliva Prevent premature escape into pharynx Oral Phase Tongue elevates ant to post Tongue forms central groove Labial and buccal seal Begins when tongue moves bolus posteriorly, and ends when bolus passes anterior pillar of fauces Voluntary control - ( XII ) Pharyngeal Phase Begins when bolus passes anterior pillar or faucets Ends when bolus passes through upper oesophageal sphincter into oesophagus Velum elevates and contracts, closing nasal passage, bolus propelled through pharynx, larynx closed and elevated, respiration inhibited, upper oesophageal sphincter relaxes Involuntary control – ( IX, X, XII ) Oesophageal Phase Begins when bolus enters oesophagus Ends when bolus passes through lower oesophageal sphincter into stomach 8-20 seconds later Sequential peristaltic wave propels bolus Relaxation of lower oesophageal sphincter  Dysphagia Esophageal dysphagia Oropharyngeal dysphagia True Dysphagia or feeling of a lump? Dysphagia for what? Regurgitation or Aspiration? Gastro-oesophageal reflux current or past? Change of Diet or weight loss? Odynophagia  Dysphagia must be distinguished from globus sensation Globus is a sensation of a lump in the throat in which food transport is not limited globus is not related to swallowing and, in fact, may improve with swallowing  Dysphagia Esophageal dysphagia Oropharyngeal dysphagia  CONSULTATION True Dysphagia or feeling of a lump? Dysphagia for what? Regurgitation or Aspiration? Gastro-oesophageal reflux current or past? Change of Diet or weight loss? Odynophagia  ACUTE DYSPHAGIA History: FB. Previous problems. Examination: Drooling. Pain. Pyrexia. Odynophagia Treatment: Food bolus: Buscopan, fizzy drink, refer at 1 hour FB: Refer  Oropharyngeal dysphagia Esophageal dysphagia Neuromuscular dysfunction Achalasia Nonachalasia Motility Disorders Cerebrovascular accidents Strictures Amyotrophic Lateral Rings/Webs Sclerosis (AML) GERD Parkinson's disease Extraesophageal GERD Myasthenia gravis Tardive dyskinesia. Neoplasia Esophageal Diverticula Foreign Bodies Pill-Induced Injury Infectious Esophagitis Caustic Injury  Oropharyngeal dysphagia abnormality related to the movement of a food bolus from the hypopharynx to the esophagus arises from disease of the upper esophagus, pharynx, or UES.  Esophageal dysphagia ↙ ↘ Solids only Solids & liquids ▼ ▼ Mechanical obstruction Motility disorder ↙ ↘ ↙ ↘ Intermittent progressive Intermittent progressive ▼ ▼ ▼ ▼ Rings/Webs Strictures Esophageal Achalasia Malignancy spasm Scleroderma  Oropharyngeal dysphagia typically present with difficulty initiating a swallow and immediately experience coughing, choking, gagging, or nasal regurgitation when attempting to swallow  most common caused by disruptions in swallowing secondary to neuromuscular dysfunction this setting, the symptoms may be more severe when swallowing liquids The history and physical examination should focus on neurologic signs and symptoms Neuromuscular dysfunction Cerebrovascular accidents Amyotrophic Lateral Sclerosis (AML) Parkinson's dis­ease Myasthenia gravis Tardive dyskinesia.  Rarely, structural abnormalities caused such as ♥ cervical osteophytes ♥ hypopharyngeal diverticulum (Zenker's diverticulum) ♥ tumors ♥ postcricoid webs typically note difficulty with a solid food bolus leaving the mouth  Oropharyngeal swallow is best assessed by videofluoroscopy, also known as the modified barium swallow Videofluoroscopy not only serves to confirm the presence of oropharyngeal dysfunction It can also assess the degree of aspiration Esophageal Disease States Achalasia Nonachalasia Motility Disorders Strictures Rings/Webs Gastroesophageal Reflux Disease Extraesophageal GERD  Neoplasia Esophageal Diverticula Foreign Bodies Pill-Induced Injury Infectious Esophagitis Caustic Injury 1. Achalasia  Achalasia a primary esophageal motility problem of unknown cause characterized by insufficient LES relaxation and loss of esophageal peristalsis hereditary, degenerative, autoimmune, and infectious factors as possible causes  Pathologic changes occur in the myenteric plexus consist of a patchy inflammatory infiltrate of T lymphocytes, eosinophils, and mast cells loss of ganglion cells and myenteric neural fibrosis  selective loss of post-ganglionic inhibitory neurons, nitric oxide and vasoactive intestinal polypeptide The postganglionic cholinergic neurons are spared, leading to unopposed cholinergic stimulation.  This produces high basal LES pressures, and the loss of inhibitory input results in insufficient LES relaxation Aperistalsis along the esophageal body—a process mediated by nitric oxide.  m/c symptoms of achalasia include ♥ dysphagia for solid & liquid ♥ regurgitation ♥ chest pain Patients with achalasia localize their dysphagia to the cervical or xiphoid areas.  Initially, the dysphagia may be for solids only most patients have dysphagia for solids and liquids at time of presentation Regurgitation occurs in 75% of achalasia and becomes a greater problem as the esophagus dilates with progression of disease  Choking and Coughing may awaken the patient from sleep Chest pain 40% Weight loss 60% (minimal loss) barium esophagram with fluoroscopy is the best initial diagnostic study  This test will reveal a loss of primary peristalsis in the distal two thirds of the esophagus In the upright position, there will be poor emptying with retained food and saliva producing a heterogeneous air-fluid level at the top of the barium column. Achalasia  The esophagus may be dilated (Figure 80-18). esophagus is dilated with a "bird's beak" tapering of the distal esophagus Retained secretions form the heteroge- nous air-fluid level seen at the top of the barium column.  chronic disease be massive with sigmoid-like tortuosity sigmoid- like tortuosity with large amount of retained debris. late-stage achalasia  smooth tapering of the lower esophagus leading to closed LES, resembling a bird's beak presence of epiphrenie diverticulum may suggest achalasia Bird’s beak deformity at LES  Esophageal manometry can be used to diagnosis In the body of the esophagus, aperistalsis is always present all swallows are typically with low contraction amplitudes.  Manometry Elevated resting LES pressure (>35 mmHg ) Incomplete LES relaxation Absence of peristalsis Manometry Manometric findings in achalasia The aperistalsis is manifested by isobaric contractions without propagation The LES pressure, which is elevated, shows minimal relaxation with swallowing. Manometry Manometric findings in achalasia The aperistalsis is manifested by isobaric contractions without propagation The LES pressure, which is elevated, shows minimal relaxation with swallowing.  Abnormal LES relaxation in all ach alasia 70% - 80% of patients absent/ inco mplete LES relaxation with swallow s baseline LES pressure is usually el evated but may be normal in up to 45% of patients Esophagus is dilated with retained fiuid and debris.  Non-relaxation of LES Asynchronous contraction and Non-peristaltic Fibrotic and atrophic Retention and stagnation of chronic food Retention esophagitis  All should undergo upper GIT endoseopy to exclude Pseudoaehalasia arising from a tumor at the GEJ Pseudoaehalasia may mimic with classic achalasia both clinically and manometrically suspected in older age with short duration of symptoms and more significant weight loss  Therapy 1.Medical therapy 2.Pneumatic dilation of the LES 3.Surgical myotomy 4.Botulinum toxin injection  The two most effective treatments - graded pneumatic dilation - surgical myotomy  1.Medical therapy – Nitrates, calcium channel block ers (nifedipine) – Cause smooth muscle relaxatio n but with limited success  2.Pneumatic dilation of the LES -good short-term results -2% to 5% risk of perforation - performed endoscopy uses air pressure to dilate and disrupt the circular muscle fibers of the LES  Balloon dilators,: three diameters (3, 3.5, and 4 cm) are positioned ov er a guidewire After pneumatic dilation  gastrograffin study by barium swallow to exclude esophageal perforation relief of symptoms in 50% to 93% Pneumatic dilation of the LES  3.Surgical myotomy -fail repeated pneumatic dilations -an anterior myotomy across the LE S (Heller's myotomy) usually associa ted with an antire-flux procedure -laparoscopy  good-to-excellent response rate of 8 0% to 94% A potential compli cation of myotomy is GERD, which o ccurs in 10% to 2 0%  4.Botulinum toxin injection -Inhibits release of excitatory acetylcholine from nerve endings (thus causing lower LES pressures) -Good short-term results, but long term efficacy unknow -Effective in about; 85% of patients  However, symptoms recur in more than 50% of patients after 6 months do not improve LES relaxation or i mprove peristalsis do not provide complete symptom r elief The clinical response is short acting efficacy decreases with time. 2.Non-achalasia M otility Disorders Non-achalasia Motility Diso rders Other described primary motility dis orders of the esophagus Defined based on the presence of s pecific manomctrie criteria  Most often noted on manometry in patients with chest pain or dysphagia 2.1 Diffuse esophageal spasm (DES) 2.2 Scleroderma or progressive systemic sclerosis (PSS) 2.3 Other systemic conditions  Diffuse Esophageal Spasm Repetitive, high amplitude contractions of smooth muscle portion of the esophagus The striated portion and LES relaxation normally. Histopathology : muscular hypertrophy with lymphocytic infiltration of Auerbach’plexus  S&S: dysphagia and chest pain (substernal) or esophageal colic which may occur with or without swallowing. Triggered by emotional stress, hot or cold liquids and GE reflux  DES may present with: a) chest pain if the contraction amplitudes are high b) dysphagia if the contraction amplitudes are low.  Investigations: CXR, cardiac evaluation, barium study and manometry LES relaxation is also normal in DES The classic finding on esophagogram is the "corkscrew" esophagus  Radiographic – Classic “corkscrew” – Beak-like taper – Increase in esophageal wall thickness  Manometrie :simultaneous and repetitive contractions in the esophageal body but in contrast to achalasia, some normal peristalsis is maintained  Typical : corkscrew pattern Manometry : prolong, high amplitude nonperistalsis Both UES and LES normal, but elevate LES pressure may be found.  "Nutcracker" esophagus is another common manometrie diagnosis in n oncardiac chest pain defined by high-amplitude peristalsi s  distal esophageal contraction ampli tude less than 30 mmHg in 30% or more of wet swallows a food bolus may not be effectively transported, resulting in dysphagia  Treatment 1.Reassuring the disease is not heart disease. 2.Medication : nitroglycerine, calcium blocker, anticholinergic, PPI (Rx for GERD) (not completely effective)  3.Surgery : – 3.1 Dilation: help only in LES dysfunction, improve dysphagia temporarily – 3.2 Surgical myotomy  Scleroderma progressive systemic sclerosis (PSS ) Secondary motility disorders are co mmonly a result of systemic conditio ns The most common condition affectin g esophageal motility  Esophageal motor disturbances occur in several of the collagen vascular diseases – Dermatomyositis – Polymyositis – Lupus erythematosus – Scleroderma (extremely common)  Characterized by : Smooth muscle atrophy and collagen deposition in the submucosa Decrease peristalsis and LES resting pressure Refulx esophagitis, ulceration, bleeding  Radiography Dilate esophagus with decreased motility (unlike achalasia, persistent patent GE junction and no air fluid level) Scleroderma  Endoscopy: Reflux esophagitis  Other systemic conditions results in esophageal hypomotility – hypothyroidism – diabetes mellitus – amy-loidosis  Investigation Esophageal manometry and intraesophageal pH readings are the most sensitive means of detection Diminished contractions in LES and distal two thirds of the esophagus  Treatment Standard antireflux medicine In patients with intractable symptoms gastroesophageal reflux surgery should be considered  3.Strictures.  Strictures defined as any loss of lumen area within the esophagus The normal esophagus measures 2 0 mm in diameter The predominant clinical symptom of strictures is dysphagia, which is usually when the lumenal diameter is less than 15 mm.  Even less severe strictures can cau se intermittent dysphagia to large fo od piece ; meat and bread There are multiple intrinsic and extri nsic causes for esophageal strictur es  Etiology of Esophageal Strictures Intrinsic strictures – Acid (peptic) – Pill-induced – Chemical/lye – Post-nasogastric tube – Infectious esophagitis – Sclerotherapy – Radiation-induced – Esophageal/gastric malignancies – Surgical anastomotic – Congenital – Systemic inflammatory disease – Epidermolysis bullosa  Extrinsic strictures – Pulmonary/mediastinal malignancies – Anomalous vessels and aneurysms – Metastatic submucosal infiltration (bre ast cancer, mesothelioma, adenoeare inoma of gastric eardia)  Intrinsic strictures are most commo n, with acid/ peptic cause accountin g for the majority of cases (60%-70 %) Strictures / Caustic Ingestion  Treatment esophageal dilation. There are several different types: of dilat ors, including: (1) mercury-filled, rubber Maloney dilator s; (2) wire-guided rigid Savary-Gilliard dil ators; (3) balloon dilators that can either be thro ugh-the-scope (TT8) or wire guided  Maloney bougies are used in unco mplicated, short, straight strictures The wire-guided Savary-Gilliard an d TTS balloons are both best suited for long, tight, or tortuous strictures.  Complications of esophageal dilation – perforation (0.5%) – bleeding (0.3%) – bacteremia (20%-50% ) Those with radiation-induced or mali gnant strictures are at higher risk of perforation. To minimize the risk of perforation, t he "rule of. threes" applies.  That is, no more than three sequen­t ial dilators should be performed per session. The goal of esophageal dilation is t o obtain an objective diame­ter of gr eater than 15 mm Approximately 90% of; patients dila ted to 15 mm have no recurrence at ; 24 months  Refractory esophageal strictures are d efined by lack of response to two or m ore dilations. The causes, for refractory strictures ca n include ongoing insults from pills or nonsteroid a] antiinfkunmatory drugs(NSAlDs) uncontrolled acid reflux inadequate lumen diameter with dilations  PPIs are superior to H-2 blockers in preventing the recurrence of acid-re lated strictures The treatment of refractory stricture s includes the elimination of the off ending agents (pills and acid) and g entle dilation to 15 mm.  Intralesional steroids injected before dilation are safe and probably effecti ve for refractory strictures Surgery may be considered in those who fail to respond to aggressive me dical therapy and dilation. 4.Rings/Webs  Rings/Webs common findings on upper endosc opy, many are asymptomatic Symptoms can include intermittent solid food dysphagia, aspira­tion, an d regurgitation.  Rings are circumferential, can consi st of mucosa or muscle, and most c ommonly occur in the distal esopha gus Esophageal webs occupy only part of the esophageal lumen, are alway s mucosal, and are usually located i n the proximal esophagus.  Esophageal webs can be found as 5% of asymptomatic individuals When symptomatic, usually dysphagia iron deficiency was noted by gas- troenterologists Plummer and Vinson in the United States, as well as otolaryngologists Paterson and Kelly in the United Kingdom.  Plummer-Vinson or Paterson-Kclly syndrome to the triad of proximal e sophageal webs, iron deficiency an emia, and dysphagia Barium radiography is the most sen sitive test to diagnose esophageal webs  endoscopic visualization, web will a ppear as a thin, eccentric lesion wit h normal-appuaring mucosa Some webs are located so proximal ly that routine passage of the endos cope through the UES with fracture the web  Treatment of symptomatic esophag eal webs consists of mechanical dis rup­tion This can be accomplished with bou gie or balloon dilators.  Schatzki's ring (B ring) occurs at th e GEJ at the distal margin of the LE S most common cause of intermittent solid food dysphagia and food impa ction The presence of symptoms depend s on the luminal diameter  If the ring diameter is less than 13 mm, the patient will have symptoms If greater than 20 mm the patient will almost never have symptoms Between 13 and 20 mm, which accounts for the majority of Sehatzki's rings, symptoms are variable The pathogenesis of esophageal rings is controversial  Recurrent symptoms requiring repe at dilation is not uncommon, and so me authors recommend maintainin g the patient on acid suppression gi ven the possible association with G ERD  The second type of esophageal ring is the A ring", which is a muscular ring most common ly detected on barium swallow This lower esophageal muscular ring is rarely symptomatic and occurs at the proximal margin of the LES approximately 2 cm proximal to SGM.  "Ringed" esophagus is a rare condi tion that occurs in young men The syndrome consists of endosco pie findings of multiple esophageal rings in patients with dysphagia The cause is unclear GERD. congenital abnormality, and possible allergic conditions have be en implicated Esophageal Webs and Rings  Treatment Treatment consists of dilation with bo ugienage and possibly acid suppressi on Many of these patients require more t han one treatment session to obtain a desired esophageal lumen of 15 mm They are also at higher risk of painful deep mucosal tears  5. Gastroesophageal Reflux Disease  Gastroesophageal Reflux Disease chronic symptoms or mucosal dam age caused by the abnormal reflux of gastric contents into the esophag us. Reflux esophagitis refers to a sub group of GERD that involves histop athologically characteristic change s in the esophageal mucosa  Nonerosive reflux disease (NERD) refers to endoseopy-negative patie nts with typical GERD symptoms NERD accounts for approximately 50% of patients Reflux esophagitis for 30% to 40% Barrett's esophagus in the remainin g 10% to 20% Barrett’s esophagus Barrett’s esophagus with ulceration Barrett’s esophagus  Pathophysiology Transient relaxation of the GE sphincter Esophageal motility disorders Delayed gastric emptying Hiatal hernia Acidic gastric contents Bile acids (more severe eophagitis )  normal antireflux barrier between th e stomach and the esophagus is im paired transient / permanently defects in the esophagogastric barri er such as LES incompetence, TLE SR, and hiatal hernia in the devel opment of GERD  TLESRs are short relaxations of the LES that do not occur in response to swallow TLESRs are the primary mechanism for gastroesophageal reflux in healthy persons and in those with mild GERD  severe GERD and related complications have a permanent structural alteration – low LES pressure – a large hiatal hernia  Symptoms develop when the offens ive factors in the gastroduodenal co ntents overcome several lines of es ophageal defense As more components of esophagea l defense break down, the severity of reflux increases  Classic symptoms of GERD are he artburn defined as a retrosternal burning di scomfort, and acid regurgitation Symptoms often occur after meals  Other in typical reflux are dysphagi a, odynophagia, and belching Atypical GERD symptoms include a sthma, chest pain, cough, laryngitis , and dental erosions.  There is no diagnostic gold.standar d for detecting GERD Classic symptoms of acid regurgitat ion and heartburn are specific but n ot sensitive for the diagnosis of GE RD as determined by abnormal 24-hour pH monitoring.  initial empiric trial of antisecretory t herapy in a patient with classic GE RD symptoms Further diagnostic should be done – if there is a failure to respond to a n empiric course – if alarm signs such as dysphagia, odynophagia, weight loss, chest pain, or choking are present.  Atypical symptoms Atypical chest pain Globus sensation Hoarseness Onset after age 45 Nausea Recurrent laryngitis Cough Recurrent sore Odynophagia throat Asthma Subglottic stenosis Dental enamel loss  Endoscopy is the technique of choice t o evaluate GERD Reflux esophagitis is present when ero sions or ulcerations are present at SC M There are many grading systems to ch aracterize the severity of esophagitis, the most common of which is the Los Angeles classification  Results are normal in 25% of patien ts with erosive esophagitis and 33 % of patients with nonerosive reflux disease  Radiologic Finding Only 1/3 of patients have radiologic findings – Erosions – Ulcerations – Strictures – Hiatal hernia – Thickening of mucosal folds Not the test of choice for diagnosis Esophagogram Extensive linear superficial ulcerations and erosions involving the distal 1/3 of the esophagus.  Endoscopy Useful for diagnosing complications of GERD – Barrett’s – Esophagitis – Strictures Not sensitive for GERD itself Only 50% of patients manifest evidence on endoscopy Gastroesophageal Reflux Disease Esophagoscopy  Ambulatory pH Mornitoring Diagnostic gold standard pH monitor placed in esophagus above sphincter Patient symptom log Correlate symptoms with low pH  TREATMENT Lifestyle modifications Antacids Histamine H2 receptor antagonists Prokinetic Agents Proton Pump inhibitors Anti-reflux surgery Newer endoscopic treatments  LIFESTYLE MODIFICATION Head of bed elevated six inches Decreased fat intake Smoking cessation Weight loss Avoidance of recumbency for 3 hours post- prandially Avoidance of large meals and trigger foods Avoidance of exacerbating medications  The goals of treatment in GERD are to – relieve symptoms – heal esophagitis – prevent recurrence of symtoms – prevent complications A variety of lifestyle modifications are r ecommended in the treatment off GER D.  These include – avoidance of precipitating foods(f atty foods, alcohol, caffeine) – avoidance of recumbency for 3 h ours postprandially – elevation of the head of the bed – smoking cessation – weight loss  Histamine receptor antagonists (H2RAs) in standard doses achieve complete symptom relief in 60% of patients and heal esophagitis in bout 50%  PPIs are superior to H2RAs in both healing rosive esophagitis and symptoms relief, with healing 90% GERD is a chronic relapsing disease with almost universal recurence of symptoms after treatment withdrawal requires maintenance therapy in many patients  longterm therapy with PPIs is again superior to H2RAs, with remission maintained in 80% and 50% of patients, respectively  "step-down" therapy is recommend ed Antireflux surgery, now laparoscopic approach, remains an option for carefully selected patient s with well documented GERD  Surgical Treatment Nissen fundoplication – Total or partial Their aim is to: – Restore normal anatomy (intra- abdominal segment of esophagus) – Re-creating an appropriate high- pressure sound at the esophagogastric junction – Maintaining this repair in the normal anatomic position 6.Extraesophageal GERD  Extraesophageal GERD Patients with GERD may present wi th symptoms other heartburn and r egurgitation This includes asthma, chest pain, c hronic cough, laryngitis, and dental erosions  lack of the classic heartburn and re gurgitation symptoms Esophagitis/Barrett's esophagus is usually not present an empiric trial of bid PPIs is indicat ed as initial treatment because ther e is no definitive diagnostic gold sta ndard for GERD.  If treatment fails – full investigation – ambulatory pH testing Confirm diagnosis of GERD when – symptoms relieve by specific antireflu x therapy Extraesophageal GERD Laryngitis Asthma Chest pain Chronic cough Dental erosions 7.Neoplasia  Neoplasia uncommon when present is typically malignant. The two main culprits are – esophageal squamous cell carcin oma – esophageal adenocarcinoma. Benign Esophageal Tumors and Cysts Benign tumors are rare (< 1 %) Classified in two groups – Mucosal – Extramucosal (intramural)  More useful classification: – 60% of benign neoplasms are leiomyomas – 20% are cysts – 5% are polyps – Others (< 2 percent)  Leiomyomas Most common benign tumor of the esophagus Intramural Occur between 20-50 years of age with no gender preponderance  80% occur in the middle and lower third of the esophagus, rare in the cervical region Obstruction and regurgitation may occur in large lesions Bleeding is a more common symptom of the malignant form of the tumor: leiomyosarcoma Cancer Malignant Tumors of the Esophagus Usually are in advanced stages at the time of diagnosis (involving the muscular wall and extending into adjacent tissues) Alcohol consumption and cigarette smoking seem to be the most consistent risk factors  Esophageal squamous cell carcinoma – Esophageal squamous cell carcinoma (95% of all esophageal cancers) is a disease of men (5: 1) – most often in the upper and midthoracic segments – least frequently in the cervical esophagus  Adenocarcinoma – approximate 8% of primary esophageal cancers – Most often occur in the distal third of the esophagus in the 6th decade of life. – Male to female ratio is 3:1 – Patients with Barretts metaplasia are 40 times more likely to develop adenocarcinoma  Clinical Presentation Dysphagia is the presenting complaint in 80-90% of patients with esophageal carcinoma Early symptoms are sometimes nonspecific retrosternal discomfort or indigestion  As the tumor enlarges, dysphagia becomes more progressive. Later symptoms include weight loss, odynophagia, chest pain and hematemesis  Diagnosis Barium swallow Esophagoscopy Esophageal biopsy Brushings for cytologic evaluation Barium Barium Cancer: apple core appearance Current AJCC 2002 staging  Treatment Surgical resection is the standard treatment for early esophageal cancer in Stages I, II and most cases of III  During the past decade, outcomes with surgery have improved resulting in a better 5 year survival due to: – Better staging techniques – Increased rate of curative resection – A decreased rate of postoperative death – Palliative endoscopic measures  Palliative endoscopic measures includ e – repeated dilation, – laser/photo dynamic therapy ablatio n – esophageal stent placement – percutaneous gastrostomy tube plac ement  Neoadjuvant /adjuvant therapy Neo-adjuvant Chemotherapy Neo-adjuvant Radiation Neo-adjuvant Chemo-Radiation Adjuvant Chemotherapy Adjuvant Radiation Adjuvant chemoradiation 8.Esophageal Dive rticula  Esophageal Diverticula is a sac that protrudes from the esoph ageal wall As in the rest of the Gl tract a true diverticulum is one that contain s all layers of the wall.  Esophageal diverticula are most pr actically classified, based on anato my, into four categories: – Zenker's diverticula – midesophageal diverticula – epiphrenic diverticula – intramural pseudodiverticulosis.  Zenker's divertieulum referred to as an esophageal diverticulum its location is proximal to the esophagus, above the UES, and it should be considered a hypopharyngeal diverticulum.  believed to form as a result of an area of weakness Killian's triangle, which exists between the cricopharyngeal sphincter and the inferior pharyngeal constrictor muscle Zenker’s diverticulum Occurs in Killian’s area. Associated with failure of cricopharyngeal dilatation. Symptoms: regurgitation, dysphagia, weight loss.  Symptoms include – oropharyngeal dysphagia – regurgitation – halitosis – cough – aspiration pneumonia  Barium swallow is an excellent test Many small diverticula are asympto matic patients with large diverticula shoul d be offered treatment  The classic treatment – open surgical resection of the divertic ulum with division of the cricopharyng cus muscles Another option for extremely large diverticula – diverticulopexy – suspension of the diverticulum in a cr anial direction.  Midesophageal diverticula are most c ommonly asymptomatic, occur in the midesophagus Traction diverticuli form as a result of external pulling of the esophageal wal l from neighboring inflammatory or fibrotic tissue, such as adjacent tuber culous mediastinitis  Traction diverticuli are located in th e middle third of the esophagus. Midesophageal traction diverticula are the only true diverticula in the e sophagus  Epiphrenic diverticula, located near the diaphragmatic hiatus, occur in t he distal esophagus near the LES These diverticula are often the resu lt of a motility disorder such as ach alasia or DES  manometric studies in patients with epiphrenic diverticulum to rule out a n associated motility disorder Most diverticula are asymptomatic, but occasionally chest pain or regur gitation can be prominent symptom s Midesophageal Diverticula Epiphrenic Diverticula  Treatment Treatment consists of managing the underlying motilit y disorder diverticulotomy with/without my otomy for symptomatic diverticu la 9.Foreign Bodies Foreign Bodies  Foreign Bodies The esophagus is one of the locations where intervention is often required Underlying alterations in the lumen of the esophagus play an important role in the risk of a swallowed object beco ming lodged  The esophagus has several areas of physiologic narrowing – the upper esophageal sphincter – the level of the aortic arch – the diaphragmatic hiatus/LES wh ere a foreign body can become i mpacted.  The key to the management of forei gn bodies is understanding that diff erent foreign bodies require differe nt interventions It is important to distinguish a true f oreign body from a food impaction.  A trial of pharmacologic therapy with.1 to 2 mg of glucagon given intravenously, which relaxes the LES, can be given but is rarely successful in relieving a food' impaction. 10.Pill-Induced Injur y  Pill-Induced Injury Pill-induced injury to the esophagus is an underappreciated entity. over 70 drugs are capable of produ cing injury to the esophagus Drugs commonly associated with pi ll-induced injury include potassium chloride tablets, doxycycline, quuud ine, NSAIDs. iron, and alendronate  Pills can damage the esophagus by various mechanisms such as acidit y, size, and contact time with esoph ageal mucosa There is a wide spectrum of injury from acute self-limited esophagitis t o refractory strictures  The typical sites of pill-induced injur y are at the level of the aortic arch and the distal esophagus, where th ere is anatomic narrowing. 11.Infectious Esop hagitis  Infectious Esophagitis Infectious esophagitis is common, e specially in immunosuppressed hos ts such as patients with human imm unodeficiency virus (HIV), transplan t patients, and chemotherapy patie nts.  The cardinal symptom of infectious esophagitis is – odynophagia – pain – swallowing immunodeficient patients can prese nt with a variety of symptoms includ ing heartburn, nausea, fever, or ble eding.  The three most common causes of infectious esophagitis are – Candida albicans – cytomegalo virus (CMV) – herpes simplex virus (HSV)  Treatment consists of antifungal the rapy, most commonly with fluconaz ole100 to 200 mg/day for10 to 14 d ays In patients with only mild immunolo gic deficiencies, the topical antifung al agents clotrimazole and nystatm are reasonable alternatives 12.Caustic Injury  Caustic Ingestion Esophagus, pharynx, larynx Bases ( most severe injuries ) – Drain cleaners – Electric dishwasher soap – Hair relaxant Acids Bleaches  Mechanism of injury Alkalis – pH > 7 – Liquefaction necrosis Acids – pH < 7 – Coagulation necrosis Bleaches – pH = 7 – Irritants  Severity of burn Type Amount Concentration Time of contact Stricture formation  Signs and symptoms Pharyngeal or Esophageal laryngeal – Dysphagia – Odynophagia – Odynophagia – Mucosal – Chest or back erythema, pain ulceration Gastric – Drooling – Epigastric pain or – Tongue edema tenderness – Stridor – Vomiting – Hoarseness – Hematemesis  Radiography Radiologic exam – Chest & neck radiographs Barium swallow – Will not reveal 1st and 2nd degree injuries  Esophagoscopy Esophagoscopy in virtually all patients at 24-48 hours post-ingestion < 24 hours – underestimation of injury > 48-72 hours with risk of iatrogenic perforation – barium swallow Rigid vs. flexible debatable Endoscopy to upper limit of severe burn  Management 1. Stable airway dexamethasone (adult 20 to 30 mg intravenous bolus, pediatric 0.5 to 1 mg/kg) can help prevent further deterioration  2. Acute airway obstruction Blind nasotracheal intubation should be avoided If direct visualization of the larynx for intubation is not possible because of edema and exudate, emergent cricothyrotomy or tracheotomy is a safer choice  Therapy Choice of therapy depends on the degree of injury. 1. First-degree burns of the esophageal mucosa require no further therapy  2. Second- and localized third- degree injuries without transmural necrosis: pharmacologic reduction or prevention of stricture formation and to maintain a conduit from the hypopharynx to the stomach by esophageal dilation, stenting, or reconstruction  3. Fourth-degree and even selected extensive third-degree esophageal burns: thoracotomy for direct examination of the esophageal wall esophagectomy Foreign bodies  Strictures and narrowing Malignant/benign Cricopharyngeal bar C-spine osteophytes Kyphosis Post cricoid web Cricopharyngeal bar Osteophytes  Neurogenic CVA Motor neurone disease Multiple Sclerosis Parkinson’s disease Myaesthena gravis  GLOBUS PHARYGEUS Previously Globus Hystericus Worse when NOT eating or drinking Actually improves on swallowing No true dysphagia solids/liquids No odynophagia No regurgitation/aspiration Variable history? exclude reflux…..  Laryngopharyngeal Reflux (LPR) Reflux of gastric acid to larynx/pharynx May be “silent” Symptoms include feeling of a lump, odynophagia/chronic sore throat, chronic cough (especially nightime), hoarse voice and “mucous in throat”.  LPR Investigations Nasopharyngoscopy, red post cricoid region. ? Barium swallow? Oesophageal pH manometry  LPR treatment 6 weeks PPI + Gaviscon initially At review further 6 weeks treatment if improving General laryngeal hygiene measures If no better, rigid pharyngo- oesophagoscopy pH manometry ?fundoplication  Pharyngeal pouches HISTORY Long Hx dysphagia Regurgitation esp at night “gurgling” swallow Aspiration (recurrent pneumonia) Weight loss and change in Diet.  Pharyngeal Pouches EXAMINATION Nasopharyngoscopy might show pooling Unlikely to feel anything in neck Barium swallow  Pharyngeal pouches TREATMENT Surgical if fit for GA (External approach) Endoscopic stapling, low morbidity and high success rate.  Pouches BARIUM SWALLOW.jpg Pouches BARIUM SWALLOW.jpg  Summary :Fast track patients Young male patient Short history Odynophagia Smoking and Alcohol Weight loss Aspiration and reguritation  Summary: Globus patients Variable history No true dysphagia Young female No weight loss Associated anxiety  Summary: Pouch patients Older male/female REGURGITATION Gurgling swallow Recurrent chest infections Weight loss Diseases of the pharynx May be a generalized disease of the whole pharyngeal structure May affect the specific pharyngeal structures A. Acute pharyngitis - due to allergic reaction - effect of toxic fumes - bacterial infection e.g. Streptococcal spp Symptoms - odynophagia, fever, lymph adenopathy Mgt. – systemic ABC B. Chronic pharyngitis is a long standing or protracted pharyngeal infection Has low grade complaints Symptoms are also milder than those of the acute form Mgt. is usually by ABC and/or removal of the causative organisms  Other specific infections of the pharynx include fungal infection, diphtheria, TB, retropharyngeal and parapharyngeal abscesses Diseases of the specific structures of the pharynx include - structures of the Waldeyer’s ring a) Adenoiditis nasal obstruction, d/c, mouth breathing, otitis media, CSOM, OME Diagnosis is from history and clin exam Mgt. adenoidectomy b) Tonsillitis - may be bacterial or viral - may exhibit odynophagia, pus exudates, crypt debris, cervical gland enlargement, fever, otalgia, TMJ pain syndrome - may give a complication of peritonsillar abscess (Quincy) - ABC - symptomatic for viral infections - tonsillectomy for recurrent bact infections – done 4 – 6 weeks post healing c) chronic tonsillitis - result from repeated acute attacks or from incomplete resolution d) peritonsillar abscess - infection passes into peritonsillar tissues causing cellulitis - symptoms include odynophagia, drooling, otalgia, trismus, soft palate swelling, jugulodigastric lymph node swellings - Mgt I & D then 4 – 6 weeks later, tonsillectomy Obstructive Sleep Apnea Syndrome Symptoms of snoring, mouth breathing, behavioral changes, poor growth, hypersomnolence -due to physical hypertrophy of adenoid and tonsils -due to congenital malformations such as Down Syndrome Mgt. in case of adenotonsillar hypertrophy is adenotonsillectomy Indications for tonsillectomy - Recurrent infection - Peritonsillar abscess - Sleep apnea - Unilateral hypertrophy - Rheumatoid disease Complications of tonsillectomy - Reactionary bleeding within 24 hrs - Secondary bleeding due to sloughing