Fig. 8.1
Gastroesophageal reflux
Reflux occurs due to increased relaxation of lower esophageal sphincter allowing a spontaneous reflux or increased abdominal pressure (stress reflux). Whereas some reflux is normal, several factors may predispose patients to pathological reflux, including hiatus hernia [4], lower esophageal sphincter hypotension, loss of esophageal peristaltic function [5], increased compliance of gastric hypersecretory states, delayed gastric emptying, and overeating [6]. GERD can often be due to the presence of multiple factors.
A consistent paradox in gastroesophageal reflux disease is the imperfect correspondence between symptoms attributed to the condition and endoscopic features of the disease. In a population-based endoscopy study in which 1,000 Northern Europeans were randomly sampled, the prevalence of Barrett’s esophagus was 1.6 % and that of esophagitis was 15.5 % [7]. Although gastroesophageal reflux is the most common cause of heartburn, other disorders, e.g., achalasia and eosinophilic gastritis, may also contribute to the condition [8].
GERD with esophageal changes seen on endoscopy is known as endoscopy-positive GERD, while a disease with no demonstrable esophageal changes is known as endoscopy-negative or nonerosive reflux disease.
Contributory or Predisposing Factors for GERD
1.
Obesity: there is a direct correlation between high body mass index and frequency and severity of GERD.
2.
Pregnancy: during pregnancy the lower esophageal sphincter pressure reduces, and with increasing abdominal pressure, the risk of GERD increases.
3.
Hiatal hernia: is an important risk factor for severe acid reflux.
4.
Connective tissue disorders like scleroderma, mixed connective tissue disease, and Sjögren’s and sicca syndrome can also give rise to GERD.
Clinical Presentation of GERD
Heartburn
Acid regurgitation
Indigestion/dyspepsia
Dysphagia
Epigrams trick pain
Abdominal bloating
Belching
Halitosis
Gastrointestinal bleeding
Wheezing/asthma
Nocturnal cough
Choking or aspiration of gastroesophageal contents
Atypical chest pain
Diagnostic Tests
When symptoms of gastroesophageal reflux disease are typical and the patient responds to therapy, no diagnostic tests are necessary to verify the diagnosis [9]. Diagnostic tests help to avert misdiagnosis; to identify any complications like a stricture, Barrett’s metaplasia, or adenocarcinoma; and to evaluate treatment failures.
Important alternative diagnoses to consider include coronary artery disease, gallbladder disease, gastric or esophageal cancer, peptic ulcer disease, esophageal motility disorders, and eosinophilic esophagitis.
1.
Complete blood count to look for iron deficiency.
2.
ECG for patients older than 45–50 years.
3.
Upper gastrointestinal endoscopy is a standard test to look for esophagitis and peptic ulcer disease. If Barrett’s esophagus or esophagitis (eosinophilic or H. pylori gastritis) is suspected, then endoscopic biopsies can be taken.
4.
Esophageal manometry and 24 h ambulatory pH monitoring are indicated for persistent and refractory symptoms.
5.
Gastric emptying scintigraphy – a nuclear medicine test can help in identifying patients who have gastroparesis causing a refractory GERD or those who are candidates for fundoplication.
6.
Acid suppression test can be done by giving a trial of proton pump inhibitors.
7.
Combined impedance-pH monitoring where quantifying exposure to esophageal acid and identifying reflux events regardless of acidic content are determined to establish GERD [10].
Treatment of GERD
1.
Lifestyle modification: losing weight, avoiding foods that aggravate GERD, large meals, and alcohol should also be avoided.
2.
H2-receptor antagonists for symptomatic relief.
3.
Proton pump inhibitors – help by reducing gastric acid secretion and are more effective than H2 blockers. They provide symptomatic relief and prevent recurrence. In a large meta-analysis of 136 randomized controlled trials involving more than 35,000 patients with esophagitis, the rate of healing among patients treated with proton pump inhibitors (83 %) was greater than that with H2 antagonists (52 %), and both rates were higher than a placebo [11]. In all trials, there were no major differences in efficacy noted among various proton pump inhibitors when used in standard doses.
4.
Some patients with nighttime reflux benefit with a H2 antagonist at night and a PPI in the morning.
5.
Surgery to correct reflux is reserved for patients with severe symptoms that are refractory to treatment or if it is a complicated GERD, e.g. Barrett’s esophagus, esophageal bleeding, or aspiration.
Fundoplication, in which the proximal stomach is wrapped around the distal esophagus to create an antireflux barrier, is an alternative approach to chronic gastroesophageal reflux disease. Follow-up of patients who have received medical therapy as compared with surgery have shown no significant differences in the prevalence of Barrett’s esophagus or in the prevalence of an adenocarcinoma [12].
Infectious Causes of Dysphagia
Infectious esophagitis is most commonly seen in immunocompromised patients. Fungal and viral diseases are the most common agents in this population. There are some rare instances where infectious esophagitis is seen in immunocompetent patients. Approximately 30 % of HIV patients have viral or fungal esophagitis during the course of their illness. Patients on chemotherapy, posttransplant patients on immunosuppressants, malignancies, head and neck radiation, and antibiotic exposure inhaled steroids are the other risk factors for infectious esophagitis.
Etiology
1.
Fungal Esophagitis:
Candidiasis (Fig. 8.2) is the most common infectious disease of the esophagus in patients with HIV accounting for 70 % of the cases. Candida albicans is most common species but other species have also been implicated.
Fig. 8.2
Endoscopic image of esophageal candidiasis in a patient on chemotherapy
2.
Viral Esophagitis:
Cytomegalovirus is the most common cause of viral esophagitis (Fig. 8.3) in HIV patients and is seen if the CD4 count is less than 100.
Fig. 8.3
Endoscopy picture of CMV-associated esophagitis before ganciclovir treatment (Journal of Clinical Microbio 2009)
Varicella zoster can cause severe esophagitis in immunocompromised hosts. It can be seen in children with chickenpox or adults with herpes zoster infection.
Herpes simplex virus is an uncommon cause of esophagitis (Fig. 8.4) in both immunocompetent and immunocompromised patients. It can be either a primary infection or more commonly reactivation of a latent virus in the distribution of the superior cervical, vagus, or laryngeal nerves [13].
Fig. 8.4
Focal ulcerations (arrow) are typical of herpes simplex virus esophagitis (Picture courtesy MERCK Manual)
3.
Bacterial causes for esophagitis is rare even in HIV patients.
Causative organisms could be Mycobacterium avium-intracellulare, Mycobacterium tuberculosis, and Nocardia
Clinical Presentation
Clinical presentation will depend upon the etiology of infectious esophagitis. In case of candidiasis, dysphagia is the most common symptom. Patients may also have oral thrush. Odynophagia, fever, and vomiting are less common. In case of Cytomegalovirus, odynophagia and chest pain are more commonly associated with low-grade fever and vomiting. Herpes simplex virus presents with both dysphagia and odynophagia as well as pain and fever. Esophagogastroduodenoscopy can differentiate between different types of infections either grossly or on histopathologic appearance of the lesions [14].
Treatment for Infective Esophagitis
Treatment focuses on eradicating the causal organism.
1.
Esophageal Candidiasis: Fluconazole – 200 mg loading dose followed by 100 mg OD for 5–10 days. In azole-resistant Candida, oral dose of fluconazole can be increased or echinocandins can be initiated.
2.
Cytomegalovirus Esophagitis: Intravenous ganciclovir is the drug of choice. Alternate therapy is intravenous foscarnet. Treatment can continue for at least a month. Relapses are common.
3.
HSV Esophagitis: Acyclovir 5 mg/kg IV, three times a day for 7–14 days, is the drug of choice.
Drug-Induced Esophageal Injury Leading to Swallowing Disorders
Medication-induced esophageal injury can occur at any age with a variety of commonly used medications. Most of the medications are over-the-counter medicines. These can be divided into those that cause direct injury to esophageal mucosa [15] and those that may contribute to the toxicity due to the contact time of the pill. Cellulose fiber and guar gum pills may swell and lodge in the esophagus causing complete obstruction.
Medication-induced esophagitis may be due to an underlying anatomic or motility disorder of the esophagus, allowing for a prolonged exposure of the drug to esophageal mucosa. Patients with esophageal stricture, left atrial enlargement, esophageal dysmotility, and esophageal diverticuli have a greater risk of drug-induced esophagitis.
Specific Medications Associated with Esophagitis (Table 8.1)
Table 8.1
Some of the esophagitis-inducing orally administered medications
Doxycycline |
Tetracycline |
Alendronate |
Aspirin |
Naproxen |
Potassium chloride |
Ascorbic acid |
Iron sulfate |
Quinidine |
1.
Antibiotics: Clindamycin, doxycycline, penicillin, rifampin, and tetracycline are some of the antibiotics associated with esophagitis.
3.
Other medications like ascorbic acid, ferrous sulfate, lansoprazole, potassium chloride, and quinidine.
4.
5.
Biphosphonates: This class of drugs is one of the commonest causes of medication-induced esophagitis. The injury has mainly been reported with alendronate, pamidronate, and etidronate. Risedronate has low potential for causing esophageal injury because of the rapid esophageal transit and therefore minimal contact with esophageal mucosa [19–21].
Overall the incidence of injury is small but it can be serious and even fatal. Unfortunately reflux-type symptoms are common and can be difficult to differentiate from medication-induced mucosal injury [22].
Diagnosis can be made endoscopically with marked exudates, inflammation, stricture formation, hemorrhage, and esophageal perforation being seen.
6.
Chemotherapy-Induced Esophagitis
Dactinomycin, bleomycin, cytarabine, daunorubicin, 5-flurorouracil, methotrexate, and vincristine are some of the agents that can cause severe odynophagia, as a result of oropharyngeal mucositis. These drugs can also involve the esophagus but esophageal damage is uncommon in the absence of oral changes [23]. Treatment is aimed at symptom control, prevention of superimposed injury from acid reflux, maintenance of adequate hydration, and removal of offending medication. For symptom control, topical local anesthetics like viscous lidocaine solution can be given. Prevention of superimposed reflux is best treated by giving twice daily proton pump inhibitor. For patients with severe odynophagia, prohibiting oral intake and giving intravenous hydration may be necessary for a few days.
Also proper administration of potentially injurious medications will help avoid occurrence of esophageal injury. On the basis of sometimes normally slow transit of medications through the esophagus particularly for gelatin capsules and larger tablets, it is recommended that medications should be ingested with 8 oz of water, patients should remain upright for half an hour, and patients with underlying potential risk for esophageal injury should look for alternative, safer medicines [24].
Achalasia (Fig. 8.5)
Fig. 8.5
Achalasia cardia
Achalasia is characterized by impaired lower esophageal sphincter relaxation with swallowing and aperistalsis in the smooth muscle esophagus. The resting lower esophageal pressure is elevated in about 60 % of the cases [25].
These physiologic alterations result from damage to innervation of smooth muscle segment of the esophagus.
The neuroanatomic changes responsible for achalasia include loss of ganglion cells within the myenteric plexus and degeneration of vagus nerve and its dorsal motor nucleus. Of all these three possibilities, loss of ganglion cells is well substantiated [26]. The cause of ganglion cell degeneration in achalasia is pointing towards an autoimmune process caused by a latent HSV-1 infection in genetically susceptible individuals [27, 28].
Immunohistochemical analyses of the myenteric plexus infiltrate in these patients reveal that the majority of inflammatory cells are either resting or activated cytotoxic T cells [29]. Achalasia may also be associated with degenerative neurological disorders such as Parkinson’s disease. These patients were noted to have Lewy bodies in the degenerating ganglion cells of the myenteric plexus [30].
Clinical Features
Dysphagia is the main symptom of esophageal motility disorders.
The associated symptoms of heartburn, chest pain, odynophagia, regurgitation, hiccups, halitosis, and weight loss are suggestive of esophageal dysphagia. Patients generally experience dysphagia to solid foods and some do experience variable dysphagia to liquids.
With long-standing disease, there is progressive esophageal dilatation, and regurgitation becomes more frequent. Some of these patients also have bronchopulmonary complications [31].
Investigations
1.
Upper endoscopy should be the first investigation for evaluating new-onset dysphagia as one can detect most structural causes of dysphagia and also obtain biopsies. It has its limitations in assessing extraluminal structures, abnormal esophageal motility, and subtle obstructing lesions.
2.
Contrast imaging of the esophagus and oropharynx is useful for a functional evaluation of the oropharyngeal phase of swallowing.
3.
Barium esophagogram can provide information on upper esophageal sphincter function, peristalsis, and bolus clearance through esophagogastric junction.
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