Dysphagia

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Onto this week's topic:

Have you ever had to swallow something big and had it stuck in your throat? It’s a really uncomfortable sensation, right? Can you imagine what it would feel like having difficulty swallowing everything you eat all the time? Today’s topic—dysphagia—literally means difficulty swallowing. It can be due to a range of conditions/diseases, so let’s start with a broad overview:

Esophageal diverticula are defined as outpouchings of one or more layers of the esophageal tract. They are commonly associated with motility disorders, and clinical features include dysphagia, regurgitation, retrosternal pain, and intermittent vomiting; however, they can also be asymptomatic in some people.

Esophageal diverticula are classified according to their location:

·      Pharyngoesophageal (Zenker’s) diverticulum

o   Most frequent form of esophageal diverticulum

o   Posterior pharyngeal outpouching found most often on the left side, above cricopharyngeal muscle and below the inferior pharyngeal constrictor muscle

o   Symptoms: dysphagia, regurgitation of undigested food, halitosis

o   Treatment: endoscopic or surgical myotomy of cricopharyngeal muscle +/- surgical excision of sac

·      Mid-esophageal diverticulum

o   Secondary to mediastinal inflammation (“traction” diverticula) or motor disorders

o   Usually asymptomatic and no treatment is required

·      Diverticulum just proximal to lower esophageal sphincter (pulsatile type)

o   Usually associated with motor disorders

o   Usually asymptomatic and no treatment required

Peptic strictures caused by esophagitis usually presents as dysphagia with a long history of reflux symptoms, but reflux symptoms may disappear as stricture develops. The diagnosis is made through endoscopy or barium study (if endoscopy contraindicated or unavailable). Treatment includes endoscopic dilatation and indefinite PPI therapy; if these two are unsuccessful, consider anti-reflux surgery.

Sometimes esophagitis does not have to cause strictures to cause dysphagia. Infectious esophagitis—severe mucosal inflammation and ulceration can result from viral or fungal infections. Risk factors include diabetes, chemotherapy, and immune-compromised states. Patients characteristically present with odynophagia, less often with dysphagia. The diagnosis is made via endoscopic visualization (whitish-yellow plaques—Candida (most common); focal ulcers—Herpes (second most common) or CMV) and biopsy. Treatment is based on investigation findings. For candida, Nystatin swish and swallow, ketoconazole, and fluconazole are prescribed. Herpes is often self-limiting and is treated with anti-viral agents like acyclovir, valacyclovir, or famcyclovir. CMV is treated with IV anti-viral agents gancyclovir or famcyclovir.

Esophageal webs refer to partial occlusions of the upper esophagus. Esophageal rings refer to circumferential narrowing of the lower esophagus. These can be asymptomatic with the lumen diameter is >12mm, provided peristalsis is normal. Dysphagia occurs with large food boluses. A special case is the occurrence of a Schatzki’s ring, which is a mucosal ring at the squamous-columnar junction above a hiatus hernia; it causes intermittent dysphagia with solids. Treatment involves disrupting ring with endoscopic bougie.

The significance of esophageal webs comes with exam questions about Plummer-Vinson Syndrome Triad!

·      Iron deficiency anemia

·      Dysphagia

·      Esophageal webs

This is a very rare condition (prevalence < 1/1,000,000) but the prognosis is good when treated with iron supplementation and esophageal dilatation.

Esophageal motor disorder falls under neuromuscular category. Patients present with dysphagia of both solids and liquids; some may also present with chest pain. It may be idiopathic or due to achalasia (no pain), scleroderma (no pain), diabetes mellitus, and diffuse esophageal spasm (DES—may have chest pain; rare and hard to diagnose due to intermittent presentation). Tests such as esophageal manometry (motility study) will help confirm diagnosis; barium swallow can sometimes be helpful too.

Gastro-esophageal Reflux Disease (GERD) and Barrett's Esophagus

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Onto today's topic:

Who hasn’t had the experience of heartburn or reflux? It is an extremely common condition, and TV ads promoting various brands of antacids can be seen all the time. I myself always pack some antacids with me on holiday—feasting and lounging occasionally give way to reflux. But what is reflux? What causes it, and how is it treated?

The definition of gastroesophageal reflux disease is: a condition in which the stomach contents (solid or liquid) moves backwards from the stomach into the esophagus. This is due to inappropriate relaxations of lower esophageal sphincter; most common contributing factors include: delayed esophageal clearance, delayed gastric emptying, obesity, pregnancy, acid hypersecretion from Zollinger-Ellison syndrome (very rare). A hiatus hernia can worsen reflux but does not cause it.

The most common clinical feature of GERD is “heartburn” and acid regurgitation (together are 80% sensitive and specific for reflux). Sour regurgitation—also known as water brash—can also be present, as well as the sensation of a lump in the throat (bolus sensation) and frequent belching. Non-esophageal symptoms such as cough, chest pain, and hoarseness are increasingly recognized of being poor prognosis indicator of reflux.

Usually a clinical diagnosis is made based on the history, and a trial of pharmacotherapy using PPI (symptom relief 80% sensitive for reflux) usually takes place. When the patient has a history of reflux accompanied by red flags (e.g. anorexia, dysphagia, bleeding, weight loss etc.), persistent reflux symptoms or previous severe erosive esophagitis after therapeutic trial of PPI for 4~8 weeks, history of esophageal stricture with persistent dysphagia, or is at high risk for Barrett’s esophagus (male, age > 50, obese, white, tobacco use, and long history of symptoms), then endoscopy is indicated. Endoscopy usually will reveal two kinds of findings: Non-erosive reflux disease (NERD) where the esophagus is normal—the treatment will consist of symptom relief with PPI PRN—and esophagitis, where treatment will aim to heal the inflammation—either through indefinite PPI therapy or surgical fundoplication. Repeat endoscopy after 6~8 weeks of PPI therapy is indicated if the patient has severe esophagitis (because it may mask underlying Barrett’s esophagus), if the patient has known Barrett’s esophagus, or if there is recurrence of symptoms. Esophageal manometry is a study of esophageal motility and can be done to diagnose abnormal peristalsis and/or decreased LES tone—but it cannot detect the presence of reflux. Esophageal manometry is usually done before surgical fundoplication (wrapping the gastric fundus around the lower end of esophagus; procedure of choice for GERD when all medical management has failed) to ensure that the esophagus is functional. 24-hour pH monitory is a very accurate test but rarely required or performed.

So to recap, the most effective therapy for GERD is PPI; it usually needs to be continued as maintenance therapy, with adjuvant antacids or H2-blocks as needed. Dietary changes such as avoidance of alcohol, coffee, spices etc. will help the symptoms but will not alter disease progression. The only true beneficial lifestyle changes are weight loss (from obesity) and elevating the head of bed for improvement of nocturnal symptoms.

Possible complications of GERD include:

·      Esophageal stricture disease—scarring can lead to dysphagia (mostly solids)

·      Ulceration

·      Bleeding

·      Barrett’s esophagus and esophageal adenocarcinoma

What is Barrett’s esophagus? It is defined as a metaplasia of normal squamous esophageal epithelium to abnormal columnar epithelium containing intestinal metaplasia. The etiology of Barrett’s esophagus is thought to be acquired via long-standing GERD and subsequent damage to the squamous epithelium; however, it has been found that increased gastric acid secretion is also associated with Barrett’s esophagus as opposed to reflux alone. Risk factors include being male, age > 50, Caucasian, smoking, obesity, hiatus hernia, and long history of reflux. In North America and Western Europe, 0.5~2% of adults are thought to have Barrett’s esophagus; up to 10% of GERD patients will have already developed Barrett’s esophagus by the time they seek medical attention. The diagnosis of Barrett’s esophagus relies on biopsy through endoscopy, and often endoscopy will show erythematous epithelium in the distal esophagus. Barrett’s esophagus is a predisposition to pre-malignant changes (i.e. the change before the change before actual cancer). The abnormal columnar epithelium will undergo dysplasia (low or high-grade) before progressing to adenocarcinoma; the rate of malignant transformation starts off at approximately 0.12% per year for patients with Barrett’s esophagus and rises with the degree of dysplasia.

Management includes acid suppressive therapy with high-dose PPI indefinitely or surgical fundoplication. Patients should have an endoscopy every 3 years if there is no dysplasia. For patients with low-grade dysplasia, regular surveillance is warranted, and endoscopic ablation/resection can be considered. For patients with high-grade dysplasia, regular and frequent surveillance must be done. In these patients, intensive biopsy, endoscopic ablation/resection, or esophagectomy produce similar outcomes; however, evidence increasingly favor endoscopic ablation with mucosal resection.

Bonus: Eosinophilic Esophagitis

Eosinophilic esophagitis is an inflammatory condition with prominence of eosinophils on esophageal biopsy. It is most commonly found in children but is increasingly recognized in adults. The etiology is unknown and may be an “allergic” disorder in children. Clinical features include odynophagia or dysphagia (mostly of solids), with the history often dating back to childhood. The first presentation may be to the ER with food bolus impaction.

The main investigation is endoscopy, which may reveal multiple rings or “crepe-paper” appearance. Biopsy showing increased eosinophils is necessary to confirm the diagnosis.

Management includes corticosteroid spray (e.g. fluticasone), which is swallowed, not inhaled (as in asthma) and leukotriene B4 inhibitors (e.g. Montelukast). Elimination diets that cut out food allergies have been an effective therapy in children.

The main complication of Eosinophilic esophagitis is increased risk of perforation with endoscopic dilatation procedures.