Sinonasal Olfactory Disorders
Summary
Sinonasal olfactory dysfunction has a high prevalence in the general population. Within the otorhino laryngological patient population, sinonasal diseases are responsible for about threequarters of olfactory dysfunction. The underlying causes are most frequently inflammatory diseases of the nose or the paranasal sinuses (75%), which are defined and characterized in this section. It is assumed that most sinonasal diseases affect the olfactory epithelium secondarily. Current information about the pathophysiology and treatment strategies of sinonasal diseases is included in this chapter because improvement in olfactory dysfunction is usually achieved by improvement of the underlying disease.
Introduction and Epidemiolgy
Rhinitis and rhinosinusitis are broad terms that refer to conditions characterized by inflammation of mucosa of the nose and paranasal sinuses, typically subdivided on the basis of a temporal profile into acute, recurrent acute, or chronic rhinosinusitis.1–3 It is now widely accepted that in cases of rhinitis, the paranasal sinuses are commonly affected as well.4 However, separate definitions for the different entities exist. Rhinitis is defined according to the consensus report of the International Rhinitis Management Working Group5 as an inflammation of the lining of the nose, and is characterized by nasal symptoms including anterior or posterior rhinorrhea, sneezing, nasal blockage, or itching of the nose. These symptoms occur on two or more consecutive days for more than 1 hour on most days.5 Considering the etiology, we can distinguish between infectious and noninfectious, and between inflammatory and noninflammatory, subtypes of rhinitis ( Table 7.1 ).6 Allergies and acute viral infections of the upper respiratory tract are the most common causes of rhinitis. Viral rhinitis is the most prevalent disease affecting humans.7 Allergic rhinitis (AR) is the most common form of noninfectious rhinitis, the lifetime prevalence of AR being above 20%.8 Several other noninfectious conditions can cause similar symptoms: hormonal imbalance, physical agents, anatomical anomalies, and the use of certain drugs.6 Olfactory impairment in rhinitis is usually reversible, but on many occasions the loss of olfaction persists.9 Persistent postviral or postinfectious olfactory dysfunction has been attributed in particular to influenza-like infections.10 If it follows one isolated acute infection of the upper respiratory tract, it should be classed as postviral (postinfectious) olfactory dysfunction rather than rhinitis (see Chapter 8). Other differential diagnoses of rhinitis are condensed in Table 7.2 .
Acute rhinosinusitis (ARS) is described as the presence of drainage accompanied by nasal obstruction or facial pain/pressure. ARS is most commonly preceded by a viral upper respiratory tract infection (URTI); the US adult population suffers from an average of 2.18 URTIs per person per year, of which an estimated 0.5 to 2% develop into acute bacterial rhinosinusitis.11,12
The criteria for an ARS episode should include a total duration of greater than 10 days, so it cannot to be confused with a viral respiratory infection, and less than 4 weeks to distinguish it from chronic rhinosinusitis (CRS). Recurrent acute rhinosinusitis (RARS) is defined by four or more episodes of bacterial ARS per year with complete resolution of symptoms between episodes—although the literature has diagnostic ranges from two to four per year. CRS is defined as more than 12 weeks of symptoms without an intervening symptom-free period,13 and is estimated to affect 13% of the US population, or 32 million adults.14 This temporal classification system says very little about the etiology of CRS, which remains idiopathic in the overwhelming majority of cases. A very small fraction, however, are associated with systemic diseases such as Wegener granulomatosis, sarcoidosis, or cystic fibrosis, and these are beyond the scope of this chapter.
Rhinosinusitis is defined according to the Rhino sinusitis Task Force (RTF)15 and the European Position Paper on Rhinosinusitis and Nasal Polyps (EPOS) guideline documents.13 In terms of symptoms, diagnosis requires at least two symptoms of nasal obstruction/blockage/congestion, purulent nasal discharge (anterior or posterior), facial pain/pressure, and hyposmia. The EPOS guidelines ( Table 7.3 ) go one step further and stipulate that at least one symptom must be obstruction/blockage/congestion or nasal discharge. The guidelines for the diagnosis of CRS include both subjective and objective criteria. Although the sensitivity of symptoms is high, the specificity is low. Positive computed tomography (CT) scans with Lund–Mackay scores ( Table 7.4 ) of 4 or more are found in only 20 to 36% of patients meeting symptom criteria for CRS.16–18 Therefore, the diagnosis of CRS should be accompanied by objective evidence in the form of endoscopic or radiographic correlation. Specifically, endoscopic evidence of CRS may take the form of middle meatal edema, polyps, or purulence. CT evidence of CRS is characterized by air–fluid levels, thickened mucosa, or polyps, within the sinuses. These objective CT or endoscopic findings are important as they typically divide CRS into two broad subtypes: chronic rhinosinusitis without nasal polyps (CRSsNP) and chronic rhinosinusitis with nasal polyps (CRSwNP), which will be discussed in more detail below.
Even though the clinical pictures of rhinitis and rhinosinusitis are merging, the diseases will be discussed separately within this chapter to cover different time courses, etiologies, and therapy of the olfactory disorder.
Acute Viral Rhinitis—Acute Bacterial Rhinosinusitis
Clincal Course
Acute viral rhinitis (common cold) is defined as a as sudden onset, acute inflammation of the upper airway lasting less than 10 days.6 Common initial symptoms/signs are burning sensations located in the nose or nasopharynx, consistent with an underlying viral infection. The cardinal symptoms of acute viral rhinitis are nasal obstruction/blockage, nasal discharge (anterior/postnasal drip), hyposmia or anosmia, and, depending on the clinical course, general symptoms. The nasal symptom–sign complex for rhinovirus and influenza occurs within 3 days after exposure; that for respiratory syncytial viruses (RSV) is delayed by as much as 7 days.7 The systemic symptoms of fever, headache, malaise, myalgia, and anorexia are related to the effects of cytokines released from immune cells, and these responses develop rapidly in the first days of infection when the virus is detected by the immune system. The local symptoms of nasal congestion and rhinorrhea are dependent on the generation of inflammatory mediators such as prostaglandins and bradykinin.19 Headache and purulent secretion indicate bacterial rhinosinusitis.
Pathophysiology
Acute viral rhinitis/rhinosinusitis is an inflammatory process of the nose and the paranasal sinuses, caused mostly by infection with rhinoviruses, RSV, adenoviruses, influenza viruses, parainfluenza viruses, coronaviruses, and others.7,20 The viral infection frequently begins in the nasal/nasopharygeal mucosa and, upon detection by the host, invokes two interactive and temporally overlapping defense systems: A generalized, innate immune response and a virus-specific, adaptive immune response. Both systems include inflammatory pathways that facilitate and actively recruit antiviral proteins and effector cells to the site of infection.7 Rhinoviruses account for 30 to 50% of all colds, and coronaviruses are the second most common agent, accounting for 10 to 15% of colds.19 These infections do not usually cause a substantial destruction of olfactory epithelium. Nasal obstruction due to mucosal swelling with hypersecretion is partly responsible for the typical temporary olfactory disorder that accompanies these viral URTIs. Nasal congestion in viral rhinitis is caused by the dilation of large veins in the nasal epithelium (venous sinuses) in response to the generation of vasodilator mediators of inflammation such as bradykinin, and swelling of mucous membranes that block odor transport toward the olfactory mucosa. The nasal discharge associated with viral rhinitis is a complex mix of elements derived from glands, goblet cells, plasma cells, and plasma exudates from capillaries, with the relative contributions from these different sources varying with the time course of the infection and the severity of the inflammatory response.19 Moreover, numerous proinflammatory cytokines/chemokines and other mediators (e.g., histamine, leukotrienes, prostaglandins) have been reported to be involved in the inflammatory regulation of viral rhinitis and might contribute to the olfactory disorder. However, appropriate studies supporting this hypothesis are lacking.
If the clinical course is prolonged (more than 7 to 10 days) or complicated (e.g., purulent nasal secretion), bacterial superinfection should be assumed. Some of the main pathogens are Streptococcus pneumoniae or pyogenes, Haemophilus influenzae, Staphylococcus aureus, or Moraxella catarrhalis.21 Overall, however, only ~1% of viral respiratory infections lead to acute bacterial rhinosinusitis.13 Pathologically, swelling of the nasal mucosa promotes blockade of the osteomeatal complex in the middle meatus, followed by subsequent impairment of ventilation and drainage of the sinuses, and bacterial superinfection. Other nonswellinginduced mechanisms, such as enhanced bacterial adhesion during the viral replication phase, also promote superinfection (e.g., between influenza A virus infections and streptococci).
At the initial inflammatory phase there is overexpression of interleukin-6 (IL-6), IL-8, and intercellular adhesion molecule (ICAM). A possible source of these cytokines and ICAM is airway epithelial cells. The CXC-chemokine IL-8 has potent chemotactic properties for neutrophils, which are capable of releasing proteases and cytokines (e.g., IL-8, tumor necrosis factor α) as effector cells in ARS.13 These proinflammatory mediators also activate T-helper (Th) cells, and mediate the migration of macrophages into the inflamed tissue. IL-1β, IL-12, and other proinflammatory cytokines are upregulated to initiate and maintain cellular defense. As these inflammatory processes involve the olfactory epithelium, olfactory disorders associated with ARS may also be a result of infiltration of the olfactory epithelium with inflammatory cells, of interaction with the involved inflammatory mediators, or of a direct infection-related functional impairment (e.g., virulence factors or immunomodulatory bacterial products).
Olfactory Dysfunction
Olfactory dysfunction is temporary and mild or moderate in most patients with acute viral rhinitis or acute bacterial rhinosinusitis (ABRS), and typically olfactory function mirrors the clinical course of the respiratory disease. Akerlund et al9 studied olfactory thresholds and nasal mucosal changes in patients with experimentally induced common colds. They found that individuals with an induced coronavirus 229E rhinitis had impaired olfaction and that the change in smelling ability correlated to the nasal congestion but not to the nasal discharge. Hummel et al22 found the following effects on olfaction after the onset of viral rhinitis: a transient increase in olfactory threshold; a decrease of odor intensity rating; and a decrease in the N1 peak of chemosensory event-related potential (CSERP) amplitude to olfactory and trige minal stimuli. They also studied the effect of nasal decongestion with oxymetazoline during the cold and reported that N1 CSERP amplitudes to olfactory stimuli—but not olfactory thresholds or trigeminal CSERP—exhibited a significant increase. Hummel et al22 concluded from this observation that viral rhinitis has a small effect on olfactory function that may be independent of nasal congestion. To summarize, it appears that the temporary olfactory dysfunction associated with viral rhinitis results mainly from conductive causes owing to nasal blockage, but an inflammatory interaction with the olfactory epithelium or central olfactory structures also appears possible. The endonasal regions that have been shown to influence the olfactory performance are depicted in Fig. 7.1 .
Treatment
Temporary hyposmia or anosmia, occurring during acute viral infection of the upper respiratory tract, is thought not to require specific therapy. Usually, viral rhinitis is treated symptomatically with drugs such as topical antihistamines, topical anticholinergic drops, decongestants, and antiphlogistic drugs. However, their effects on olfactory function remain unclear.
ABRS resolves without antibiotic treatment in most cases. Antibiotic or anti-inflammatory therapy should be considered in patients suffering from repeated severe episodes of ABRS with significant prolonged olfactory dysfunction. Antibiotic therapy should target the main pathogens. First-line therapy at most centers is usually amoxicillin, or a macrolide antibiotic in patients allergic to penicillin, because of the low cost, ease of administration, and low toxicity of these agents. If patients fail to respond to the initial course of treatment, an alternative antibacterial agent should be considered. Ideally, a nasal swab test should be conducted before initiating an alternative regimen.
Decongestants, mucolytic agents, and nasal or oral steroids are in widespread use is adjuvant therapies. While the evidence for treatment with decongestants and mucolytics mainly results from clinical experience, several studies have documented positive effects of flunisolide, budesonide, and mometasone on ABRS symptoms. If local decongestants are used, they should be placed on cotton as so-called high inlay in the middle meatus.13 The efficacy of antibiotics or adjuvant drugs on olfactory disorders in ABRS has not been systematically evaluated.
Related posts:
The Human Vomeronasal System
Clinical Disorders of the Trigeminal System
Assessment of Olfaction and Gustation
Functional Anatomy of the Olfactory System II: Central Relays, Pathways, and their Function
Miscellaneous Causes of Olfactory Dysfunction
Functional Anatomy of the Olfactory System I: From the Nasal Cavity to the Olfactory Bulb
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