This article defines chronic rhinosinusitis (CRS) and shares contemporary principles for its diagnosis and management, focusing on practical considerations for rhinoplasty surgeons. Nasal obstruction, the most common symptom of CRS, is frequently the chief complaint of patients seeking functional rhinoplasty surgery. Because correcting sites of anatomic obstruction to nasal airflow alone is unlikely to adequately treat CRS, rhinoplasty surgeons must have a firm understanding of the origin, diagnosis, and management of this disease process. With no single cause identified, CRS is likely an umbrella diagnosis or syndrome encompassing numerous causative factors, with the common end point of chronic sinonasal inflammation.
Chronic rhinosinusitis (CRS), a disease characterized by symptomatic chronic inflammation of sinonasal mucosa, is estimated to affect 14% of the adult U.S. population. CRS has been shown to affect a patient’s quality of life similar to debilitating chronic medical conditions, such as congestive heart failure, chronic obstructive pulmonary disease, angina, and back pain. The treatment of CRS accounts for a significant portion of health care use in the United States, with annual health care costs ranging from $4.3 to $5.8 billion and an estimated 257,000 patients undergoing surgery for refractory CRS annually. Nasal obstruction, the most common symptom of CRS, is also frequently the chief complaint of patients seeking functional rhinoplasty surgery. Because correcting sites of anatomic obstruction to nasal airflow alone is unlikely to adequately treat CRS, rhinoplasty surgeons must have a firm understanding of the origin, diagnosis, and management of this disease process. To date, a single underlying cause for this disorder has not been identified. More appropriately, CRS is likely an umbrella diagnosis or syndrome encompassing numerous causative factors, with the common end point of chronic sinonasal inflammation. This article defines chronic rhinosinusitis (CRS) and shares contemporary principles for its diagnosis and management, focusing on considerations of practical relevance for the rhinoplasty surgeon.
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Nasal obstruction, a common complaint of patients seeking functional rhinoplasty, is the most common symptom of chronic rhinosinusitis (CRS).
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CRS is an inflammatory process affecting the nose and paranasal sinuses that lacks a single clear origin.
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Treatment of CRS usually requires a multipronged approach incorporating nasal saline irrigations, topical steroids, management of comorbid conditions, and surgery in refractory cases.
Chronic rhinosinusitis defined
Rhinosinusitis is defined as inflammation of the nose and paranasal sinuses characterized by two or more symptoms, one of which must be nasal blockage/obstruction/congestion or nasal discharge, and another either facial pain/pressure or a reduced sense of smell. For accurate diagnosis, the patient must also show endoscopic evidence of inflammation, including polyps, mucopurulent discharge, or edema, or computed tomographic mucosal changes within the osteomeatal complex or sinuses. Although acute rhinosinusitis is defined by a symptomatic period of up to 4 weeks with an eventual complete resolution of symptoms, the duration of symptoms in CRS is greater than 12 weeks and patients are never entirely symptom-free.
CRS can be further subdivided based on the presence or absence of nasal polyps. On a microscopic level, polyps are edematous structures consisting of loose connective tissue, glands, and inflammatory cells. The most abundant inflammatory cell in polyp tissue is the eosinophil, which is activated and sustained by the cytokine interleukin 5 (IL-5).
No clear evidence explains why polyps develop in some patients and not in others. The prevalence of nasal polyps in the general population is 4%, whereas in patients with asthma the prevalence increases to between 7% and 15%. Despite the similarities between allergic rhinitis and nasal polyposis, including watery rhinorrhea, mucosal swelling, and eosinophilia, nasal polyps are only found in 0.5% to 1.5% of patients with positive skin prick tests for common allergens. An association clearly exists between nasal polyposis and aspirin sensitivity, as evidenced by Samter’s Triad (aspirin sensitivity, nasal polyposis, and asthma), yet not all patients with aspirin sensitivity have nasal polyps and vice versa.
An additional variant of CRS called allergic fungal rhinosinusitis has been described by Bent and Kuhn based on five criteria: (1) nasal polyposis, (2) allergic mucin, (3) CT scan findings consistent with CRS, (4) positive fungal histology or culture, and (5) type I hypersensitivity diagnosed through history, skin test, or serology. Ferguson described a related entity called eosinophilic mucin rhinosinusitis , which shares many of the clinical and pathophysiologic features of allergic fungal sinusitis but lacks the presence of fungus as a key element.
Although CRS encompasses a broad spectrum of distinct entities with unique clinical and pathologic phenotypes, they have a basic underlying commonality: symptomatic long-standing inflammation in the nose and paranasal sinuses. These distinct subtypes should be identified early in the workup of patients with sinonasal complaints, because they may each require distinct treatment algorithms and respond differently to medical and surgical management.
Origin of chronic rhinosinusitis
Rhinosinusitis is often erroneously considered astrictly infectious process. Instead, it should be considered a multifactorial inflammatory process affecting the contiguous mucous membranes of the nose and paranasal sinuses. Although infection may be present and worsen CRS, additional factors also play important roles in initiating and sustaining chronic inflammation in the nose and paranasal sinuses.
Allergy
A history of atopy may predispose a patient to developing CRS. Researchers have theorized that the swelling of nasal mucous membranes that accompanies allergic rhinitis may result in sinus ostial narrowing or obstruction, which can compromise ventilation and lead to mucous retention and infection. Furthermore, just as the upper and lower airways are believed to represent a unified system, the nose and paranasal sinuses are also believed to be a physiologic continuum, responding in concert to their environment rather than in isolation.
Allergic markers seem to be more prevalent in patients with CRS. Benninger reported that 54% of patients with CRS had atopy based on positive skin prick tests. Multiple studies have shown that 50% to 84% of patients undergoing sinus surgery have a high incidence of positive skin prick tests.
Although only 0.5% to 4.5% of patients with allergic rhinitis have nasal polyps, the presence of allergy in patients with nasal polyps ranges from 10% to as high as 64%. Levels of total and specific IgE have been associated with eosinophilic infiltration in nasal polyps. Multiple studies have implicated food allergy as having a role in nasal polyposis.
Not all studies support the role of allergy in the pathogenesis of CRS. In one study, no increase was seen in the incidence of rhinosinusitis during the pollen season in pollen-sensitized patients. However, despite the lack of clear causal evidence for the role of allergy in CRS, failure to address allergy in patients with CRS reduces the probability of surgical success. Furthermore, in patients undergoing immunotherapy, those who experienced the most subjective benefit for immunotherapy were those with a history of rhinosinusitis.
Asthma
Although asthma is not a true cause of CRS, rhinoplasty surgeons should be aware of the strong association between the two disease processes. The unified airway theory holds that allergic inflammation coexists in the upper and lower airways. Although rhinosinusitis and asthma frequently occur in the same patients, their interrelationship is not well understood. Studies in children have shown improvements in asthma symptoms and asthma medication use after surgery for CRS in pediatric patients with both conditions.
The sinuses of asthmatic patients have shown radiographic evidence of abnormal mucosa. In one study, all patients with steroid-dependent asthma had abnormal mucosal changes on CT compared with 88% of patients with mild to moderate asthma.
Wheezing is reported in 31% of patients with nasal polyps, and asthma is reported by 26% of patients with nasal polyps compared with 6% of controls. Late-onset asthma is associated with the development of nasal polyps in 10% to 15% of patients. Although nasal polyps are twice as prevalent in men as in women, the coexistence of nasal polyps and asthma is twice as common in women than in men.
Anatomic Factors
Several variations in sinonasal anatomy have been proposed to have a role in CRS, including concha bullosa, nasal septal deviation, and variations in the uncinate process. Despite a solid mechanistic foundation for this theory, investigators in two separate studies found no correlation between CRS and bony anatomic variations in the nose. Several studies show that the prevalence of anatomic variations is no more common in patients with CRS than in the general population. However, in a systematic review of the literature on the role of septal deviation in CRS, multiple studies showed that increasing angles of septal deviation were associated with increasing prevalence of rhinosinusitis. Although the association of septal deviation and rhinosinusitis was statistically significant, the overall clinical effect was modest, with an odds ration of 1.47. In all studies that examined the laterality of rhinosinusitis associated with septal deviation, inflammation was present bilaterally. Based on these studies, the presence of variant anatomic structures may alter sinus ventilation and contribute to ostial obstruction, but alone is not sufficient for the development of CRS.
Fungus
The presence of fungi in the human sinonasal cavity has been established. The influence of fungi can range from benign colonization, to noninvasive fungus balls, to fulminant invasive disease in immunocompromised patients. Over the past decade, considerable debate has surrounded the role of fungi in CRS. In 1999, investigators proposed that eosinophilic infiltration and fungi were present in the sinuses of most patients with CRS. These findings were based on positive fungal cultures using a new culture technique. However, using the same culture technique, normal controls were found to have a similar percentage of positive fungal cultures, casting doubt on the causative role of fungi in CRS. Although a wide variety of fungi have been identified in the sinuses of patients with CRS, the presence of fungi does not confirm an etiologic role in the disease process. Studies have not shown systemic or topical antifungals to be of benefit to patients with CRS.
Osteitis
Patients with CRS characteristically display areas of increased bone density and irregular thickening on CT, a finding that may be a marker of chronic inflammation. Researchers have proposed that bony thickening may be a sign of inflammation of the bone, which may serve to perpetuate inflammation of the overlying mucosa. Studies in rabbits showed that inflammation spread through the Haversian canals, resulting in chronic osteomyelitis at sites distant from the primarily involved sinus. The concept of osteitis may explain why a nidus of inflammation in one sinus can result in pansinusitis, and may also account for why CRS can be refractory to even the most aggressive forms of treatment.
Biofilms
A biofilm is a layer of adherent microorganisms attached to a surface and encased in a self-produced polysaccharide matrix. Bacteria growing in biofilms can be unusually fastidious, resistant to fluctuations in moisture, pH, and temperature, and refractory to antibiotic therapy. Biofilms have been identified as playing a potential role in otitis media, chronic tonsillitis, and adenoiditis in children with CRS, and they have also been seen on the mucosal surface of patients with CRS and on frontal recess stents. The presence of bacterial biofilms could account for the chronicity of sinus inflammation in certain patients and could explain why patients experience improvement while on antibiotic therapy but relapse after finishing the medication.
The presence of biofilms in patients with CRS does not explain the role these entities play in the disease process. In a recent study of patients with CRS with nasal polyps undergoing sinus surgery, biofilms were seen in both the treatment and control groups, suggesting that these entities are likely not sufficient to cause CRS without other cofactors. Further studies are needed to clarify whether biofilms are innocent bystanders, initiators of mucosal inflammation, or perpetuators of a disease process already set in motion by other factors.
Superantigens
Superantigens are microbe-produced toxins that bypass the specificity of the immune response and therefore activate up to 30% of lymphocytes. They have been proposed to play a role in CRS, particularly in patients with nasal polyposis. In one study, 55% of patients with CRS with nasal polyps had toxin-producing Staphylococcus aureus in the nasal mucus adjacent to the polyps. Three different enterotoxins were isolated and the corresponding variable β region of the T-cell receptor was upregulated in the polyp lymphocytes. The investigators proposed that the upregulation of lymphocytes by superantigens may result in the production of several cytokines that are responsible for the massive upregulation of eosinophils, lymphocytes, and macrophages, the three most common inflammatory cells in nasal polyps.
Mucociliary Impairment
Normal mucociliary clearance plays an important role in preventing chronic inflammation through transporting particles and bacteria trapped in the mucous blanket toward the sinus ostia, into the nasal cavity, and ultimately into the esophagus. As mucociliary clearance fails, bacterial export ceases and sinus mucosa is left vulnerable to noxious bacterial byproducts. Patients with Kartagener syndrome and primary ciliary dyskinesia frequently experience CRS, as do patients with cystic fibrosis whose viscous mucous cannot be adequately cleared through normal ciliary activity. Secondary ciliary dyskinesia develops in patients with CRS and, although likely reversible, restoration of normal ciliary function can take considerable time.
Other Factors
Although cigarette smoking was found to be associated with a higher prevalence of CRS in Canada, a Korean study did not support these findings. Like many chronic medical conditions, low income has been associated with a higher prevalence of CRS. Helicobacter pylori DNA has been identified in 11% to 33% of sinus samples of patients with CRS but not in controls, although a causal relationship has not been proven. Direct nasopharyngeal reflux of gastric acid has been implicated in patients with CRS refractory to endoscopic sinus surgery. Finally, iatrogenic factors, including creation of a surgical antrostomy separate from the natural maxillary sinus ostium, can lead to mucous recirculation and persistent symptoms of CRS.
Origin of chronic rhinosinusitis
Rhinosinusitis is often erroneously considered astrictly infectious process. Instead, it should be considered a multifactorial inflammatory process affecting the contiguous mucous membranes of the nose and paranasal sinuses. Although infection may be present and worsen CRS, additional factors also play important roles in initiating and sustaining chronic inflammation in the nose and paranasal sinuses.
Allergy
A history of atopy may predispose a patient to developing CRS. Researchers have theorized that the swelling of nasal mucous membranes that accompanies allergic rhinitis may result in sinus ostial narrowing or obstruction, which can compromise ventilation and lead to mucous retention and infection. Furthermore, just as the upper and lower airways are believed to represent a unified system, the nose and paranasal sinuses are also believed to be a physiologic continuum, responding in concert to their environment rather than in isolation.
Allergic markers seem to be more prevalent in patients with CRS. Benninger reported that 54% of patients with CRS had atopy based on positive skin prick tests. Multiple studies have shown that 50% to 84% of patients undergoing sinus surgery have a high incidence of positive skin prick tests.
Although only 0.5% to 4.5% of patients with allergic rhinitis have nasal polyps, the presence of allergy in patients with nasal polyps ranges from 10% to as high as 64%. Levels of total and specific IgE have been associated with eosinophilic infiltration in nasal polyps. Multiple studies have implicated food allergy as having a role in nasal polyposis.
Not all studies support the role of allergy in the pathogenesis of CRS. In one study, no increase was seen in the incidence of rhinosinusitis during the pollen season in pollen-sensitized patients. However, despite the lack of clear causal evidence for the role of allergy in CRS, failure to address allergy in patients with CRS reduces the probability of surgical success. Furthermore, in patients undergoing immunotherapy, those who experienced the most subjective benefit for immunotherapy were those with a history of rhinosinusitis.
Asthma
Although asthma is not a true cause of CRS, rhinoplasty surgeons should be aware of the strong association between the two disease processes. The unified airway theory holds that allergic inflammation coexists in the upper and lower airways. Although rhinosinusitis and asthma frequently occur in the same patients, their interrelationship is not well understood. Studies in children have shown improvements in asthma symptoms and asthma medication use after surgery for CRS in pediatric patients with both conditions.
The sinuses of asthmatic patients have shown radiographic evidence of abnormal mucosa. In one study, all patients with steroid-dependent asthma had abnormal mucosal changes on CT compared with 88% of patients with mild to moderate asthma.
Wheezing is reported in 31% of patients with nasal polyps, and asthma is reported by 26% of patients with nasal polyps compared with 6% of controls. Late-onset asthma is associated with the development of nasal polyps in 10% to 15% of patients. Although nasal polyps are twice as prevalent in men as in women, the coexistence of nasal polyps and asthma is twice as common in women than in men.
Anatomic Factors
Several variations in sinonasal anatomy have been proposed to have a role in CRS, including concha bullosa, nasal septal deviation, and variations in the uncinate process. Despite a solid mechanistic foundation for this theory, investigators in two separate studies found no correlation between CRS and bony anatomic variations in the nose. Several studies show that the prevalence of anatomic variations is no more common in patients with CRS than in the general population. However, in a systematic review of the literature on the role of septal deviation in CRS, multiple studies showed that increasing angles of septal deviation were associated with increasing prevalence of rhinosinusitis. Although the association of septal deviation and rhinosinusitis was statistically significant, the overall clinical effect was modest, with an odds ration of 1.47. In all studies that examined the laterality of rhinosinusitis associated with septal deviation, inflammation was present bilaterally. Based on these studies, the presence of variant anatomic structures may alter sinus ventilation and contribute to ostial obstruction, but alone is not sufficient for the development of CRS.
Fungus
The presence of fungi in the human sinonasal cavity has been established. The influence of fungi can range from benign colonization, to noninvasive fungus balls, to fulminant invasive disease in immunocompromised patients. Over the past decade, considerable debate has surrounded the role of fungi in CRS. In 1999, investigators proposed that eosinophilic infiltration and fungi were present in the sinuses of most patients with CRS. These findings were based on positive fungal cultures using a new culture technique. However, using the same culture technique, normal controls were found to have a similar percentage of positive fungal cultures, casting doubt on the causative role of fungi in CRS. Although a wide variety of fungi have been identified in the sinuses of patients with CRS, the presence of fungi does not confirm an etiologic role in the disease process. Studies have not shown systemic or topical antifungals to be of benefit to patients with CRS.
Osteitis
Patients with CRS characteristically display areas of increased bone density and irregular thickening on CT, a finding that may be a marker of chronic inflammation. Researchers have proposed that bony thickening may be a sign of inflammation of the bone, which may serve to perpetuate inflammation of the overlying mucosa. Studies in rabbits showed that inflammation spread through the Haversian canals, resulting in chronic osteomyelitis at sites distant from the primarily involved sinus. The concept of osteitis may explain why a nidus of inflammation in one sinus can result in pansinusitis, and may also account for why CRS can be refractory to even the most aggressive forms of treatment.
Biofilms
A biofilm is a layer of adherent microorganisms attached to a surface and encased in a self-produced polysaccharide matrix. Bacteria growing in biofilms can be unusually fastidious, resistant to fluctuations in moisture, pH, and temperature, and refractory to antibiotic therapy. Biofilms have been identified as playing a potential role in otitis media, chronic tonsillitis, and adenoiditis in children with CRS, and they have also been seen on the mucosal surface of patients with CRS and on frontal recess stents. The presence of bacterial biofilms could account for the chronicity of sinus inflammation in certain patients and could explain why patients experience improvement while on antibiotic therapy but relapse after finishing the medication.
The presence of biofilms in patients with CRS does not explain the role these entities play in the disease process. In a recent study of patients with CRS with nasal polyps undergoing sinus surgery, biofilms were seen in both the treatment and control groups, suggesting that these entities are likely not sufficient to cause CRS without other cofactors. Further studies are needed to clarify whether biofilms are innocent bystanders, initiators of mucosal inflammation, or perpetuators of a disease process already set in motion by other factors.
Superantigens
Superantigens are microbe-produced toxins that bypass the specificity of the immune response and therefore activate up to 30% of lymphocytes. They have been proposed to play a role in CRS, particularly in patients with nasal polyposis. In one study, 55% of patients with CRS with nasal polyps had toxin-producing Staphylococcus aureus in the nasal mucus adjacent to the polyps. Three different enterotoxins were isolated and the corresponding variable β region of the T-cell receptor was upregulated in the polyp lymphocytes. The investigators proposed that the upregulation of lymphocytes by superantigens may result in the production of several cytokines that are responsible for the massive upregulation of eosinophils, lymphocytes, and macrophages, the three most common inflammatory cells in nasal polyps.
Mucociliary Impairment
Normal mucociliary clearance plays an important role in preventing chronic inflammation through transporting particles and bacteria trapped in the mucous blanket toward the sinus ostia, into the nasal cavity, and ultimately into the esophagus. As mucociliary clearance fails, bacterial export ceases and sinus mucosa is left vulnerable to noxious bacterial byproducts. Patients with Kartagener syndrome and primary ciliary dyskinesia frequently experience CRS, as do patients with cystic fibrosis whose viscous mucous cannot be adequately cleared through normal ciliary activity. Secondary ciliary dyskinesia develops in patients with CRS and, although likely reversible, restoration of normal ciliary function can take considerable time.
Other Factors
Although cigarette smoking was found to be associated with a higher prevalence of CRS in Canada, a Korean study did not support these findings. Like many chronic medical conditions, low income has been associated with a higher prevalence of CRS. Helicobacter pylori DNA has been identified in 11% to 33% of sinus samples of patients with CRS but not in controls, although a causal relationship has not been proven. Direct nasopharyngeal reflux of gastric acid has been implicated in patients with CRS refractory to endoscopic sinus surgery. Finally, iatrogenic factors, including creation of a surgical antrostomy separate from the natural maxillary sinus ostium, can lead to mucous recirculation and persistent symptoms of CRS.
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