Otitis Media with Effusion

OME is defined as a middle ear space with fluid in the absence of an acute ear infection. OM and OME represent greater than 2.2 million episodes diagnosed per year in the United States. OME is most prevalent in early childhood. Screening surveys have reported a point prevalence of middle ear effusion from infancy to age 5 years to range between 15% and 40%. The peak incidence is in the winter months. Allergy has been believed to play a major role in OME and is detailed in the article by Hurst elsewhere in this issue. On otoscopy, fluid is present without evidence of infection ( Fig. 1 ). Many investigators have established a link between IgE-related diseases and OME.

Serous otitis media. Air fluid levels and “air bubbles” are present.

Acute Otitis Media

AOM is a viral or bacterial infection associated with fever, ear pain, irritability, and may be associated with a concurrent upper respiratory tract infection. AOM is the most common childhood infection for which antibiotics are prescribed in the United States. The diagnosis is most closely associated with otoscopic findings of tympanic membrane bulging or redness. Coker and colleagues determined that otoscopic findings were critical in detecting the disease relative to subjective findings or complaints. The diagnosis of RAOM is made when recurrent ear infections are noted. The exact underlying mechanism is poorly understood and multifactorial. Risk factors associated with developing RAOM include male gender, sibling history of recurrent OM, early occurrence of infection, day-care attendance, parental smoking, absence of breastfeeding, and second-hand smoke. A meta-analysis by Uhari and colleagues found that sibling history, day-care attendance, parental smoking, breastfeeding less than 3 months, and pacifier use are significant risk factors for AOM. COM has also be linked to underlying allergy (see Hurst and Venge ).

Otitis Media with Effusion

OME is defined as a middle ear space with fluid in the absence of an acute ear infection. OM and OME represent greater than 2.2 million episodes diagnosed per year in the United States. OME is most prevalent in early childhood. Screening surveys have reported a point prevalence of middle ear effusion from infancy to age 5 years to range between 15% and 40%. The peak incidence is in the winter months. Allergy has been believed to play a major role in OME and is detailed in the article by Hurst elsewhere in this issue. On otoscopy, fluid is present without evidence of infection ( Fig. 1 ). Many investigators have established a link between IgE-related diseases and OME.

Serous otitis media. Air fluid levels and “air bubbles” are present.

Acute Otitis Media

AOM is a viral or bacterial infection associated with fever, ear pain, irritability, and may be associated with a concurrent upper respiratory tract infection. AOM is the most common childhood infection for which antibiotics are prescribed in the United States. The diagnosis is most closely associated with otoscopic findings of tympanic membrane bulging or redness. Coker and colleagues determined that otoscopic findings were critical in detecting the disease relative to subjective findings or complaints. The diagnosis of RAOM is made when recurrent ear infections are noted. The exact underlying mechanism is poorly understood and multifactorial. Risk factors associated with developing RAOM include male gender, sibling history of recurrent OM, early occurrence of infection, day-care attendance, parental smoking, absence of breastfeeding, and second-hand smoke. A meta-analysis by Uhari and colleagues found that sibling history, day-care attendance, parental smoking, breastfeeding less than 3 months, and pacifier use are significant risk factors for AOM. COM has also be linked to underlying allergy (see Hurst and Venge ).

Mechanisms of Eustachian Tube Dysfunction

Three main theories exist to explain why OM or OME develop. Some researchers believe that local inflammation at the nasal side causes retrograde edematous spread up the tube to cause obstruction. Others believe in a mucociliary dysfunction mechanism that results in physical stasis of secretions, resulting in mechanical blockage of the tube. The last theory proposed describes the direct inflammatory changes within the tube itself that result in edema, vascular engorgement, and hypersecretion of the lining of the tube. A closure of the middle ear space to the atmosphere occurs. Once the middle ear space is closed off, the air diffuses into the bloodstream (nitrogen first, then oxygen). The loss of air causes a negative pressure relative to the surrounding tissues. This negative pressure causes retraction of the tympanic membrane. The negative pressure developed results in a transudate to develop in the middle ear space. Patients may complain of fullness or a pressure sensation in the ear. The tympanogram may be a B or C type, depicting fluid or a negative pressure, respectively ( Fig. 3 ). The clinician must determine a cause for the tubal dysfunction and must carefully evaluate the ear and the nasopharynx for abnormalities.

Representative tympanograms: Type A, “normal pressure” in a normal patient; Type B, commonly referred to as “flat” in a patient with serous otitis media; Type C, “negative pressure” seen in patients with eustachian tube dysfunction.

( Courtesy of Dr Brad Stach, Detroit, MI.)

Contact Dermatitis or Dermatophytid of the Ear

Contact dermatitis (A Gel and Combs type 4 hypersensitivity reaction, T-cell medicated) can occur as a result of using certain shampoos, perfumes, creams, or lotions. The metal in an ear ring (chromium or nickel) may cause a localized reaction (scaling, edema, erythema of the ear lobe). Ear drops or ear molds (made from plastic) from hearing aids may cause similar reactions in the canal or concha of the ear. In addition to contact hypersensitivities, the external ear is a common site of a dermatophytid or ID reaction, characterized by preauricular or postauricular fissures and skin eruptions around the ear. This condition is a result of hematogenous spread of fungi or their allergic products (antigens) from the primary site of the fungal infection, usually the feet, to an alternative site on the body. Classic sites of the primary fungal infection are toe or fingernails, the skin, or vagina. Tricophyton, Oidiomycetes (Candida), and Epidermophyton are collectively referred to as TOE fungi, and are the most common fungi responsible for this reaction. On identification of a possible ID reaction, the otolaryngic allergist should investigate fungal infections in other areas of the body so to not overlook these abnormalities.

Ménière’s Disease and its Mimics

There has been growing evidence that Ménière’s disease is partly related to allergic disease; this is comprehensively reviewed in the article elsewhere in this issue on Ménière’s disease. Ménière’s disease is characterized by aural fullness, fluctuating hearing loss, tinnitus, and vertigo. Patients with Ménière’s disease may be disproportionately afflicted by benign positional vertigo (BPV). Aural fullness can be simulated by eustachian tube dysfunction and Ménière’s disease. Tinnitus is frequently associated with sensorineural hearing loss; however, when this hearing loss is in the low frequencies, the likelihood that Ménière’s disease is the cause is greater than for the more common high-frequency hearing loss associated with presbycusis and loud noise exposure.

Nasal Masses

Nasal masses or enlarged adenoids cause nasal obstruction. Enlarged adenoids may need to be removed if they are obstructing the posterior nasopharynx. A differential diagnosis for tumors in the nasal cavity includes chordoma, chemodectoma, neurofibroma, angiofibroma, inverting papilloma, squamous cell carcinoma, sarcoma, encephalocele, or meningocele.

Nasal Irritants

There are several substances that may cause nasal irritation resulting in mucosal edema and erythema. Chemical exposures may result in type 1 (immediate) or type 4 (delayed) Gel and Coombs reactions. Repeated exposures are usually necessary to develop allergic reactions to various chemicals. There are more than 3800 different chemical compounds in cigarette smoke that cause increased sensitivity of the airways to allergens. Passive smoking in children has been shown to lead to higher rates of childhood infections, higher middle ear effusion rates, decreases in pulmonary function tests, increased childhood asthma rates, and sudden infant death syndrome.

“Sensory irritation” is acute and reversible eye, nose, and throat irritation that occurs after exposure to coarse particulate matter or water-soluble gases or vapors. Nonallergic, noninfectious building-related illness or “sick building syndrome” is predominantly related to sensory irritation. Indoor irritations include extremes of temperature or humidity, combustion products (poorly functioning combustion appliances, cigarette smoke, improper exhaust ventilation), volatile organic compounds (from furnishings) or reactive chemicals, such as cleaning products (ammonia, chlorine). Environmental control with subsequent reduction of exposure to the noxious substance is recommended, if possible, to reduce nasal exposure.

Nonallergic Rhinitis

Nonallergic rhinitis (NAR) is defined as any nonimmune-related rhinitis, and consists of a cluster of syndromes that cause rhinitis. In 1998 Dykewicz and colleagues noted, in a guideline of the Joint Task Force on Practice Parameters in Allergy, Asthma, and Immunology, that 50% of the patients who presented for allergic rhinitis actually had some other form of rhinitis. NAR may be triggered by endogenous or exogenous stimuli. The nose responds similarly in inflammation and irritation: sneezing, congestion, rhinorrhea, and itching. This response leads to similar presentation for allergy and NAR. NAR is considered a “diagnosis of exclusion” by many allergists. After allergy testing is negative, it is the clinician’s responsibility to determine which diagnostic category best describes the patient’s complaints.

Settipane and Lieberman divided nonallergic rhinitis into 12 categories ( Box 1 ). The different types are described briefly here. A complete description by Wilson and colleagues is available elsewhere in this issue and is beyond the scope of this article.

Vasomotor Rhinitis (Idiopathic Rhinitis)

In the article by Settipane and Klein, vasomotor rhinitis (VMR) was the most common diagnosis in 61%, nonallergic rhinitis with eosinophilia syndrome (NARES) in 33%, sinusitis in 16%, BENARS (blood eosinophilia nonallergic rhinitis syndrome) in 4%, elevated IgE in 12%, and hypothyroid state in 2% of patients. VMR implies idiopathic, perennial, nonallergic rhinitis with a negative skin test, normal IgE levels, and with no inflammatory changes on nasal cytology. VMR symptoms are more obstructive/congested as compared with sneezing, rhinorrhea, and itching. Itching, sneezing, and eye irritation are more commonly seen in allergic rhinitis. At present, this disorder is thought to be related to excessive parasympathetic activity or reduced sympathetic activity of the nasal mucosa. There are other theories that have been proposed but lack definitive evidence.

NARES

This disorder was first described by Mullarkey and colleagues in 1980. Patients with NARES typically have more intense nasal symptoms of watery rhinorrhea, pruritus, sneezing paroxysms, hypoanosmia, and have negative skin or in vitro tests for allergy. Nasal smears are characterized by diffuse eosinophilia. Fifteen percent to 33% of the adults with NAR are found to have this condition. NARES may be associated with Samter’s triad (asthma [non-IgE mediated], aspirin sensitivity, and nasal polyposis) or may be a variant of this disease. BENARS is felt to be a subset of NARES, and is defined by elevated numbers of eosinophils in the peripheral blood.

Basophilic/Metachromatic Nasal Disease

Basophilic/metachromatic nasal disease, also known as nasal mastocytosis, is very similar to NARES, as both require histologic diagnoses. The hallmark of this disease is mast cell infiltration of the tissue (>2000 per mm ³ ) with eosinophilia. Patients typically complain of nasal blockage, congestion, and rhinorrhea in comparison with the sneezing and pruritus seen in NARES. Pale boggy and bluish turbinates may be seen on examination. In contrast to NARES, nasal basophilic/metachromatic disease is not associated with nasal polyps, aspirin sensitivity, or asthma. Its etiology is currently unknown.

Conditions Associated with Sinusitis and Nasal Polyps

Chronic rhinitis does have a propensity to be associated with sinusitis, and is very common in our patient population. These conditions are covered in other articles in this issue.

Vasculitities/Autoimmune and Granulomatous Diseases

There are several systemic diseases that may cause rhinitis. Churg-Strauss vasculitis, systemic lupus erythematosus, relapsing polychondritis, and Sjögren syndrome are autoimmume-related diseases associated with nasal complaints. Granulomatous diseases, such as sarcoidosis and Wegener granulomatosis, have been noted to cause common nasal symptoms and should be considered in the differential of systemic diseases that may cause rhinitis.

Drug-Induced Rhinitis

There are several drugs that cause nasal side effects ( Box 2 ). Aspirin and nonsteroidal anti-inflammatory medications are associated with upper airway reactions including nasal polyposis and asthma. Psychotropic agents (ie, thioridazine, amitriptyline, perphenazine) and antihypertensive medications (ie, α-blockers, β-blockers, angiotensin-converting enzyme [ACE] inhibitors, vasodilators) may cause nasal congestion or other nasal symptoms. Oral contraceptives and/or hormonal replacement are well-known causes of rhinitis. With the increased use of phosphodiesterase type 5 inhibitors in men with erectile dysfunction, rhinitic complaints should trigger a discussion on medication use. Cocaine and topical decongestants/vasoconstrictors (ie, oxymetazoline, xylometazoline, phenylephrine, ephedrine) have been associated with rhinitis medicamentosa, and cause rebound nasal congestion and rhinitis. Decongestant use should be addressed when these types of complaints are mentioned during a patient encounter.

Structurally Related Rhinitis

Anatomic defects account for 5% to 10% of the complaints in nonallergic rhinitis. The structural abnormalities that may cause rhinitis include nasal septal deviation, turbinate hypertrophy, adenoid hypertrophy, nasal valve collapse, or masses. These conditions are described in detail in previous sections of this article.

Atrophic Rhinitis

Atrophic rhinitis is typically encountered in too aggressive turbinate reduction, granulomatous diseases, trauma, radiation damage, and chronic cocaine use. In undeveloped countries, bacterial infestation secondary to Klebsiella pneumoniae subspecies ozaenae causes nasal cavity crusting, bleeding, fetor, and mucosal atrophy, also leading to atrophic rhinitis. The nasal mucosa changes from a functional ciliated columnar respiratory epithelium to a nonciliated squamous metaplasia type that is nonfunctional. Mucociliary clearance and neurologic regulation no longer occur. The patient complains of nasal congestion and obstruction due to the loss of the normal laminar flow of the nasal cavity. These patients’ nasal cavities are usually widely patent on examination despite subjective obstruction.

Physical/Irritant Rhinitis

This category includes physical changes in the environment including temperature, barometric pressure, inhaled substances, and ingested foods. Cold temperature changes have been reported to result in profuse rhinorrhea. Facial pressure, headaches, and rhinorrhea are common nasal complaints in patients who are exposed to extreme changes in barometric pressures (ie, aviation workers and mountain climbers). Mast cell degranulation and stimulation of irritated nerve endings are felt to be the offending mechanism’s pathophysiology. Gustatory rhinitis occurs when a patient ingests a certain food, usually hot or spicy: mucoid or watery rhinorrhea ensues. This reaction occurs acutely and lasts as long as the person is ingesting the inciting substance. Raphael and colleagues have theorized that the afferent sensory nerves are stimulated. This stimulation activates the parasympathetic nerves that supply the nasal mucosal glands, which causes the rhinorrhea and associated sweating and epiphora that may accompany the symptom complex. However, skin testing with abstracts of the suspected foods is commonly negative.

Air pollution can occur indoors or outdoors. Known substances to cause nasal irritation include dust, sulfur dioxide, formaldehyde, wood smoke, cigarette smoke, ozone, and volatile chemicals. Patients complain of dryness, sneezing, congestion, and rhinorrhea. The exact mechanism is unknown but has been theorized in the section on nasal irritants in this article. Ozone and volatile chemicals have been shown to induce a neutrophilic influx in the mucosa.

Occupational Rhinitis

The incidence of occupational rhinitis is estimated to be 5% to 15%. A complete medical and workplace history is important because these patients have multiple complaints, including sensory abnormalities with altered sensations of smell. Patients may also have nosebleeds, crusting, impaired mucociliary transport, and nasal hyperactivity. Immunologic hyperreactivity is discussed in previous sections. Allergens may include animal proteins, wheat, latex, pyrethrum in insecticides or other garden products, acid anhydrides in adhesives, and toluene in body spray paints. Annoyance reactions occur in patients with heightened olfactory awareness. These patients complain about perfumes, exhaust fumes, room deodorizer, cleaning agents, floral fragrances, and cosmetics. Irritant reactions occur when a specific respiratory irritant is inhaled beyond a threshold level. Air pollution and ozone are examples of irritants in large cities that are discussed regularly in the news. Tobacco smoke, toluene, paint fumes, nitrogen oxide, and formaldehyde are other examples of nasal irritant. Chronic exposure to formaldehyde, wood, leather, dust, nickel, or chlorophenol is associated with hypertrophic mucosa, metaplasia, and carcinoma in some cases. A corrosive reaction results after exposure to high concentrations of soluble chemical gases causing inflammation to nose, mouth, ocular mucosa, and skin. Mucosal and skin burns as well as ulcerations may occur. Chemicals known to cause corrosive reactions include ammonium chloride, vinyl chloride, hydrochloric acid, organophosphates, and acrylamide. Irritants cause neurogenic inflammation, which is believed to be the predominant pathway model for chemical sensitivity. Irritant receptors on sensory nerves (ie, C fibers) induce neuropeptide release. Vasodilation and edema ensue, which results in a nonimmune-mediated inflammation.

Laryngopharyngeal Reflux

Gastroesophageal reflux (GER) is the retrograde movement of stomach contents into the esophagus in the absence of belching or vomiting. Gastroesophageal reflux disease (GERD) occurs when GER is associated with other signs, symptoms, or complications. LPR is retrograde flow of reflux material into the esophagus and larynx.

It is estimated that 30% of Americans suffer from GERD, while 7% to 10% experience daily heartburn and 25% to 30% have weekly symptoms. Between 25 and 75 million Americans are affected by GERD. Thirteen percent of all Americans use antacids 2 or more times a week. The estimate of GERD in patients presenting to the otolaryngology clinic is been estimated to be 4% to 10%. Fifty percent of the patients who were evaluated for speech and voice disorders in the clinics of Koufman and colleagues had LPR.

Laryngeal inflammation is responsible for the signs and symptoms of LPR. These symptoms include a globus sensation, throat clearing, vocal fatigue, voice breaks, sore throat, neck pain, excessive throat mucus, chronic or nighttime cough, dysphagia, odynophagia, postnasal drip, halitosis, ear pain, laryngospasm, asthma exacerbation, diminished singing range, heartburn or regurgitation, and hoarseness. In addition, LPR can occur in a subpopulation of patients who do not have classic GERD. These patients present with laryngeal findings without the classic heartburn and substernal pain seen in GERD patients. Belafsky and colleagues developed a Reflux Symptom Index (RSI), which includes a self-administered survey of 9 questions used to assess patients with LPR. The instrument has proved to be reproducible and valid. Each question has a rating from 0 (no problem) to 5 (severe problem). A score of 10 or greater is associated with a high likelihood of a positive dual-channel pH probe. In another study, these investigators demonstrated that improvements in the RSI were noted before changes in physical findings occurred.

Diagnosis is made using direct visualization of the vocal folds with a mirror examination, an endoscope, or a videostrobe. Physical findings seen in patients with reflux include laryngeal edema, loss of clear epithelial markings, hypervascularity of the posterior commissure and arytenoids, hyperkeratosis of the posterior commissure (pachydermia), increased mucous production, laryngeal ulceration, granuloma formation, subglottic stenosis, and pseudosulcus formation. This thickening of the undersurface of the vocal fold extends from the anterior portion of the vocal fold to the posterior commissure ( Figs. 6 and 7 ). By contrast, true sulcus vocalis involves the free edge of the vocal fold and extends to the vocal process. The presence of pseudosulcus is sensitive and specific for reflux 70% and 77% of the time, respectively. Other studies found the positive predictive value of pseudosulcus in detecting LPR to be 90%.

Severe laryngeal pachydermia in a patient with laryngopharyngeal reflux.

( Courtesy of Dr Glendon Gardner, Detroit, MI.)

Posterior glottic edema and erythema in a patient with laryngopharyngeal reflux.

A Reflux Finding Score has also been developed by Belafsky and colleagues. This scale evaluates 8 findings associated with reflux. Seven of these findings involve edematous changes to the larynx and associated structures. Only one finding is associated with redness or erythema of these structures. Scores may range from 0 to 26. A score of 7 or higher is associated with a positive pH probe with a 95% certainty. Overall, this suggests that among all the aforementioned reflux findings, the clinical hallmark of extraesophageal reflux (EER) is edema as a result of reflux-induced trauma to the larynx. EER is synonymous with the term LPR for the purposes of this article.

Diagnostic Testing for LPR

Diagnostic tests used to assess for reflux include an esophagogram, sensory testing with endoscopy, pH testing, monometry, impedance testing, and direct biopsy using transnasal endoscopy. A barium esophagogram may be useful to assess the esophagus for any type of structural or functional abnormality. An esophagogram is usually ordered together with a dynamic swallowing study to evaluate the whole swallowing mechanism at one time. The dynamic swallow is often performed with a speech and language pathologist. Findings that may be seen with this test include strictures, rings, webs, hiatal hernia, erosive esophagitis, candida esophagitis, cricopharyngeal bars, extrinsic compression, motility disturbances, aspiration, residuals in the pharynx, diverticula, and underlying neoplastic processes. Unfortunately, the sensitivity of the esophagogram in detecting EER is low (20%–60%) and its specificity is 64% to 90%, with an accuracy of 69%.

Laryngeal Sensory Testing

Laryngeal sensory testing has been shown to be helpful in identifying EER. The posterior laryngeal edema that results from reflux may be quantified with sensory testing. A pressure-generated pulse of air is delivered to the vocal fold, and the laryngeal adductory reflex is initiated to contract the vocal fold. As the edema progresses on the vocal fold, the puff of air required to elicit a response becomes much greater (5 mm or more). This test was found to be as sensitive and specific for reflux as the pH probe (50% and 83%, respectively). As patients improved with treatment, the pulse of air required to elicit a response decreased as the “neuropathy due to edema” improved. Unfortunately, this method functions most as a research tool, as many otolaryngologists do not use a sensory testing device.

pH Probe Testing

The dual pH probe is considered the gold-standard test to assess for reflux. There is considerable controversy regarding the technique and what is considered a “normative” value. In addition, patient tolerance for the procedure is often poor. Merati and colleagues performed a meta-analysis on 16 studies in the literature and found that laryngeal probe acid exposure time was reliable in differentiating patients with LPR from normal subjects. Some of the patients in this study who were considered to have LPR actually would have normal pH probes by gastroenterology criteria. These patients may have been suffering from other conditions such as nonacid reflux, sinusitis, allergies, and postnasal drip. Dual pH probes are the accepted devices to identify EER. Postma demonstrated that 59% of the patients he studied would have been inappropriately diagnosed as having a negative pH probe based on only one esophageal probe. The pharyngeal sensor was needed to make the diagnosis. Fourteen percent of Koufman’s patients had a positive upper probe result despite a normal esophageal pH acid exposure time. Although the pH probe is the gold standard, the test is invasive, has a sensitivity of only 75% to 80%, and the false-negative rate may approach 50%. Poor calibration and small variation of probe placement may affect the results. Close monitoring of patient activities during the test is essential. Patient positioning, diet, reflux symptoms, and smoking habits should be carefully monitored.

While there is general agreement for normative values from the distal esophageal probe in determining whether reflux is present, controversy exists regarding the normative values of the proximal pH probe. Most researchers have agreed that a pH drop to 4 or less is considered pathognomonic for EER. Others have documented that a small percentage of their normal subjects had proximal pH probe drops to 4 or less. Still others such as Hanson and colleagues, Contencin and Narcy, and Koufman believe these criteria to be too rigorous and note that pepsin, the main cause of tissue inflammation and damage, is active at pH levels of 5 or greater. In addition, reflux-related damage has been noted for days after the inciting event. In the larynx, defenses against reflux are virtually nonexistent on a mucosal level. Therefore, negative probe results need to be interpreted carefully. There are also vagally mediated reflux reflexes eloquently described by Shaker, such as the glottic closure reflex and the cricopharyngeal/upper esophageal sphincter contraction reflexes, which may cause globus and laryngospasm in the face of distal esophageal exposure to acid.

Wireless pH probe technology has been explored as an alternative to traditional pH probes. These probes consist of a transnasally or transpharyngeally placed capsule that may be attached to the mucosa of the esophagus; the sensor then detaches from the wall in about 3 days. A remote monitor on the waist records the data. These devices are capable of a longer recording time, providing more data for analysis. Their major limitation is that the proximal probe often cannot be placed close to the upper esophageal sphincter because of sensation at this area.

Mechanisms of Acidic and Nonacidic Refluxate Damage to the Mucosa

Recent work by Johnston colleagues has shown that pepsin exists in the laryngeal epithelium in reflux patients. When pepsin is incorporated into the cell via endocytosis, cellular cytotoxic events can occur. Pepsin does not require the presence of acid to remain active. Some investigators have suggested that pepsin may cause the depleted levels of carbonic anhydrase noted in the esophageal mucosa of LPR patients. Carbonic anhydrase (CA) and its related isoenzymes CA-I through CA-IV are present in esophageal mucosa where they can convert carbon dioxide into bicarbonate, which can move into the extracellular space and neutralize the acid. Decreased levels of the isoenzyme CA-III were found in the vocal fold epithelium of LPR patients.

Bile salts and acids in nonacidic refluxate may also cause damage to the laryngeal mucosa. Sasaki and colleagues demonstrated that the bile salts taurocholic acid and chenodeoxycholic acid in an acidic and basic pH, respectively, produced laryngeal inflammation comparable to hydrochloric acid at a pH of 1.2. Localized inflammation clearly is the hallmark of this disease process, and needs to be reversed in order for healing to take place.

Monometry

Monometry is useful to assess for esophageal dysmotility and for weakness of the upper and lower esophageal sphincter contraction. Dysmotility is common in EER and can include ineffective motility, hypertensive lower esophageal sphincter, nutcracker esophagus (esophageal spasm), and achalasia. Monometry has not been considered a useful a tool for diagnosing EER because of the short duration of testing, which may not accurately assess the transient relaxations of the lower esophagus that are thought to be important in the pathogenesis of EER.

Impedance Testing

The multichannel intraluminal impedance device uses a pH sensor to detect nonacidic gastroesophageal reflux. Using electrical conductivity of the bolus in the esophagus, the device is able to distinguish between solid or liquid as well as direction of flow, antegrade or retrograde. Using the pH sensor, acid events are delineated from nonacid events. Because persistent symptoms even after adequate acid-suppressive therapy have been attributed to nonacidic reflux events, impedance testing is likely to play a larger role in the diagnosis of this disease process in the future.

Transnasal Esophagoscopy

Further diagnostic testing may include transnasal esophagoscopy (TNE) with biopsy, which may show inflammatory changes to the esophageal mucosa. A diagnosis is made from looking at the amount of eosinophils per high-power field (HPF) that are present (in 5 or more fields). These histologic changes are felt to represent pathologic changes in the lining of the esophagus, even when the esophagus appears “normal.” TNE has been found to be more than adequate to evaluate the esophagus. Dickman and colleagues have demonstrated that the esophageal assessment is sufficient to diagnose reflux-related disease in patients with traditional esophageal reflux symptoms such as heartburn, regurgitation, and dysphagia, but who do not have gastric or duodenal symptoms such as abdominal pain, nausea, or a history of gastric or duodenal ulcer. Complete assessment of the stomach and duodenum is not necessary. TNE can be used to evaluate the esophagus in patients with suspected reflux disease to rule out Barrett esophagitis as well as adenocarcinoma. The presence of acid-induced reflux causes changes in the stratified squamous epithelium converting it to columnar epithelium normally present in the stomach mucosa. This condition is called Barrett esophagitis. Barrett esophagitis has been linked to adenocarcinoma. Because the incidence of adenocarcinoma has risen significantly in the United States and western Europe (in some studies: 175%), early diagnosis of Barrett esophagitis may prevent patients from progressing on to adenocarcinoma. Similarly, early adenocarcinoma lesions may be identified before they are far advanced and cause dysphagia. Five-year survival rates of early esophageal cancer are 80% to 90%; but 5-year survival for symptomatic esophageal cancer is less than 10%. Because cough and hoarseness are better predictors for esophageal adenocarcinoma than heartburn or regurgitation, patients with persistent laryngopharyngeal symptoms despite antireflux treatment should have an esophageal endoscopy. TNE is safer than a traditional endoscopy, and avoids the cardiac and pulmonary complications associated with this procedure.