Lesson 20, Volume 16—Adult Chronic Sinusitis and Its Complications

By G. Douglas Campbell Jr., MD, FCCP


Objectives

  1. Review the pathophysiology of chronic rhinosinusitis.
  2. Learn appropriate diagnostic strategies.
  3. Become familiar with current management practices.
  4. Understand when surgery should be considered.

Key words

chronic rhinosinusitis; cystic fibrosis; fungal rhinosinusitis; sinusitis

Abbreviations

AFS = allergic fungal rhinosinusitis


Sinusitis represents a common health problem frequently encountered by primary health-care providers, allergists, and otolaryngologists, but its importance to physicians treating lung diseases is that sinusitis may act as a trigger for diseases in the lower respiratory tract. In 1996, the American Academy of Otolaryngology–Head and Neck Surgery proposed replacing the term sinusitis with rhinosinusitis, because the mucous membranes of the nose and sinuses are embryologically related and contiguous, disease management is similar, and isolated sinusitis infection without rhinitis is rare (Table 1).1 They also classified rhinosinusitis based upon its temporal course and the presence of certain clinical findings (Table 2). Although clinical findings are important in identifying patients with rhinosinusitis, the diagnosis is usually confirmed by radiographic or endoscopic studies.


Table 1—Factors Associated with Chronic Rhinosinusitis*

Major Factors

Minor Factors

Facial pain or pressure†

Headaches

Facial congestion or fullness

Fever (all nonacute)

Nasal obstruction or blockage

Halitosis

Nasal discharge/purulence/
discolored postnasal drainage

Fatigue

Hyposmia or anosmia

Dental pain

Purulence in nasal cavity on examination

Cough

Fever‡

Ear pain, pressure, or fullness

*The presence of two or more major factors or one major and two or more
minor factors with symptoms lasting > 12 weeks is strongly suggestive of
chronic rhinosinusitis. Reprinted with permission from Lanza and Kennedy.14
†Facial pain/pressure alone does not constitute a suggestive history for
rhinosinusitis in the absence of another major nasal symptom or sign.
‡Acute rhinosinusitis only.


Table 2—Classification of Adult Rhinosinusitis*

Classification

Duration

Strong History

Include in Differential

Special Notes

Acute rhinosinusitis

< 4 wk

> 2 major factors, 1 major factor and 2 minor factors, or nasal purulence on examination

1 major factor or > 2 minor factors

Fever or facial pain does not constitute a suggestive history in the absence of other nasal signs or symptoms

Subacute rhinosinusitis

4-12 wk

Same as chronic

Same as chronic

Consider acute bacterial rhinosinusitis if symptoms worsen after 5 d, if symptoms persist for > 10 d, or in presence of symptoms out of proportion to those typically associated with viral infection

Recurrent acute rhinosinusitis

> 4 episodes/yr with each episode lasting > 7-10 d and absence of signs or symptoms between episodes

Same as acute

   

Chronic rhinosinusitis

> 12 wk

> 2 major factors, 1 major factor and 2 minor factors, or nasal purulence on examination

1 major factor or > 2 minor factors

Facial pain does not constitute a suggestive history in the absence of other nasal signs or symptoms

Acute exacerbation of chronic rhinosinusitis

Sudden worsening of chronic rhinosinusitis with return to baseline after treatment

     

*Reprinted with permission from Lanza and Kennedy.14


It is estimated that annually 35 million Americans have rhinosinusitis, resulting in 25 million office visits and 73 million days of restricted activity each year, and accounting for approximately 20% of all office visits to allergy and immunology specialists and 200,000 sinus surgeries.2,3 Health-care expenditures for rhinosinusitis for 1996 were reported to be $5.8 billion, of which $3.5 billion was for the treatment of chronic rhinosinusitis.4 Twelve percent of adults < 45 years of age report symptoms of chronic rhinosinusitis.5 More worrisome is the fact that the reported prevalence of rhinosinusitis doubled between 1990 and 1995, and in 1995, 13 million antibiotic prescriptions were written for the treatment of rhinosinusitis.6,7 Fortunately, rhinosinusitis is an uncommon cause of both hospitalization, accounting in 1993 for only 35,000 discharges (19,000 discharges for chronic rhinosinusitis), and death.8

In addition to the direct impact of rhinosinusitis on the general population, there are known associations with rhinosinusitis and other disease states, especially in older individuals.9 The association between asthma and rhinosinusitis is well known.3,10 Up to 78% of asthma patients complain of rhinosinusitis, while 38% of patients with chronic rhinosinusitis have asthma, and untreated rhinosinusitis can worsen asthma and make it more resistant to therapy.11 The association of rhinosinusitis and chronic bronchitis, termed sinobronchial syndrome, has been appreciated and studied for decades.12 Today, it is commonly recognized in specific diseases such as cystic fibrosis, primary ciliary dyskinesia, allergic bronchopulmonary aspergillosis, hypogammaglobulinemia, and diffuse panbronchiolitis. Recognition of this association and aggressive treatment of chronic rhinosinusitis results in improvement in both illnesses. Chronic rhinosinusitis is also associated with nasal polyposis. Approximately 20% of patients with chronic rhinosinusitis have nasal polyps, with a subset due to aspirin-sensitivity syndrome (Samter syndrome). Rhinosinusitis is also associated with resistant otitis media infections.

The similarities in anatomy and function between the upper and lower respiratory tracts and the association of disease activity between these two areas have led to the concept of "one-airway disease."13

A partial list of the most common etiologies is presented in Table 3. Chronic rhinosinusitis is most likely multifactorial in origin and it is frequently impossible to identify a specific cause.14 Treatment often requires prolonged use of multiple different types of therapeutic agents.


Table 3—Some Predisposing Factors for Rhinosinusitis

Infectious agents (especially upper respiratory viral agents)
Exposure to external irritants

Air pollution
Smoking
Cocaine abuse

Anatomical abnormalities

Septal deviation
Turbinate hypertrophy
Nasal polyposis
Prolonged use of nasogastric tube

History of hyperactivity

Allergic rhinitis
Asthma

Deficiencies in immune response

IgG or IgA subclass deficiencies
Common variable immunodeficiency
AIDS

Certain comorbid conditions

Pregnancy
Poorly controlled diabetes mellitus
Cystic fibrosis
Ciliary dyskinesia


This paper will review the anatomy of the sinuses and the pathophysiology of chronic rhinosinusitis, discuss appropriate strategies for the recognition and medical management of rhinosinusitis, and briefly review situations in which surgical intervention should be considered.

Anatomy

While there is some uncertainty as to the function of the paranasal sinuses, their presence appears to be beneficial by reducing the bony weight of the skull, warming and humidifying inspired air, and adding resonance to vocalization.

The paranasal sinuses consist of four independently draining cavities located on either side of the nasal septum. These paired cavities are the frontal, maxillary, ethmoid, and sphenoid sinuses (Fig 1). The frontal, maxillary, and anterior ethmoid sinuses drain into the nasal area through the middle turbinate via the osteomeatal complex, and the posterior ethmoid and sphenoid sinuses drain into the superior turbinate through the sphenoethmoidal recess. The sinuses, like the bronchi, are lined with ciliated pseudostratified columnar cells, and the presence of numerous goblet cells ensures the constant production of mucus to trap particulate matter and desquamative material that the cilia then propel into the nasopharynx. In each sinus, there is a complete change of the mucous blanket every 20 to 30 min!15 For the sinuses to function properly, flow from the sinuses through the ostia (which are approximately 1 to 3 mm in diameter) into the nasopharynx must be unimpeded.


Figure 1. Contiguous CT of normal sinuses and the structures of the sinuses: inferior turbinates (A), middle turbinates (B), ethmoid sinus (C), frontal sinus (D), maxillary sinus (E), and osteomeatal complex (F).


Pathophysiology of Rhinosinusitis

Sinusitis refers to inflammation of the mucous membranes lining the paranasal sinuses. The sinuses, like other parts of the respiratory tract, are susceptible to a number of infectious and noninfectious insults (Table 3). The location and anatomical structure, especially the narrow ostia, affects clinical response. With chronic rhinosinusitis, there is ongoing inflammation characterized by eosinophilia that results in damage to the mucosa and ciliary components of the sinus and changes in the vasoelastic properties of mucus. The reader is referred to other sources for a more complete discussion of the role of inflammation in chronic rhinosinusitis.16

Not all cases of chronic rhinosinusitis are caused by bacterial infections. Because cultures are generally obtained by sampling via an invasive procedure and sampling is often performed only after one or more failed courses of antibiotic treatment, few studies investigating the etiology of bronchitis have been reported. A review of studies from adults with chronic rhinosinusitis shows that the most common pathogens cultured in chronic rhinosinusitis include coagulase-negative Staphylococcus spp (51% of isolates), Staphylococcus aureus (20%), anaerobes (3%), and Streptococcus pneumoniae (4%). In addition, organisms frequently encountered in acute rhinosinusitis (eg, Haemophilus influenzae and, in children, Moraxella catarrhalis) may also be recovered in chronic rhinosinusitis. The clinical significance of coagulase-negative staphylococci and anaerobes is debatable.17,18 In one newer study, the incidence of enteric Gram-negative bacilli was reported to be 27%; these pathogens were recovered more often from patients who had prior sinus surgery or were using irrigation.19 Pseudomonas aeruginosa is seen with prolonged use of oral steroids and in patients with cystic fibrosis. It is appreciated that a number of factors affect the spectrum of pathogens recovered, including recent antimicrobial therapy, the prior presence or development of antimicrobial resistance, duration of rhinosinusitis, prior sinus surgery, and the type of culturing and processing methods used.

Diagnosis of Chronic Rhinosinusitis

Clinical Criteria

The clinical signs and symptoms of rhinosinusitis are variable. The presence of nasal symptoms is common in the general population; on any given day, up to 40% of individuals without evidence of rhinosinusitis have nasal symptoms.20,21 Among patients presenting with chronic rhinosinusitis, even when symptoms are present, they are frequently lower grade than in an acute setting except in the setting of acute exacerbations. Recently, criteria were developed to help identify the patients most likely to have rhinosinusitis (Table 1).22 The presence of chronic rhinosinusitis was suggested by the duration of symptoms of for > 12 weeks and the presence of either (1) two or more major factors (as listed in Table 1) or (2) one major and two minor factors or the presence of nasal purulence.14 Acute exacerbation of chronic rhinosinusitis was defined as a sudden worsening of chronic rhinosinusitis.

Chronic rhinosinusitis also should be considered among patients who present with difficult-to-control asthma or who have risk factors for sinusitis (mechanical obstruction, polyps, immune deficiencies).

The physician should obtain a thorough history and perform a thorough physical examination. The history should be directed not only at eliciting factors listed in Table 3, but also at identifying allergic triggers, the presence of other underlying disease (eg, immotile cilia syndrome, HIV disease), and factors that may worsen rhinosinusitis (eg, smoking). A general head and neck examination may be helpful. The presence of swelling, edema, or erythema in the orbital or cheekbone areas, cervical adenopathy, postnasal drainage, or pharyngitis may point to sinus involvement. Tenderness to palpation may be noted occasionally. Percussion of the forehead and cheeks and transillumination in a completely dark room can occasionally show abnormalities, but findings may be falsely positive as a result of anomalies in normal sinus development. Diminished visual acuity or frank loss of vision are ominous signs of extrasinus disease suggesting the need for prompt surgical intervention.

Examination via anterior rhinoscopy or nasal endoscopy is often helpful and may reveal hyperemia, edema, crusting, purulence, polyps, or nasal deviation/obstruction. Nasal endoscopy can allow culturing, with 80% of the accuracy of the more painful sinus puncture and lavage.

Radiologic Examination

Historically, the physician relied upon plain radiographic examination of the sinuses (Waters occipitomental view, Caldwell occipitofrontal view, and a lateral view to visualize the sphenoid sinuses) to determine if the patient had chronic rhinosinusitis. Plain radiologic examination for chronic rhinosinusitis is sometimes helpful, especially if an air fluid level is seen (which is unusual), but because of interobserver error, the presence of normal anatomical anomalies, and poor correlation between the extent of sinus abnormality and symptom severity, other radiographic tests are used.23

Presently, contiguous coronal CT scanning of the sinuses is considered the gold standard. Coronal CT scanning is better able to identify anatomic abnormalities, identify mucosal thickening, and quantitate severity of illness; it can also be used to detect nasal polyps that originate in the paranasal sinuses (Fig 1, Fig 2).24,25 A limiting factor in using coronal CT scanning is cost. While coronal CT scanning is necessary if surgical intervention is being considered, in the routine medical treatment of chronic rhinosinusitis, at least one author suggests that CT scanning be reserved for cases in which symptoms persist after maximal medical management, there are complications of therapy, or the clinician suspects cancer.26,27


Figure 2. Contiguous CT scans comparing normal (A) and abnormal (B) sphenoid sinuses. Note the total opacification of the sphenoid sinus with marked sclerosis of the sphenoid wall and intersphenoidal sinus septum. This patient had significant polyposis that is not well visualized on CT scan but can be best identified with MRI scanning.


A less costly alternative is noncontiguous coronal CT images. The cost of this approach is reported to be comparable to that of plain films. With this procedure, four noncontiguous coronal CT images are obtained, one from each of the following: (1) the frontal sinuses, (2) the anterior ethmoid and maxillary sinuses, (3) the posterior ethmoid and maxillary sinuses, and (4) the sphenoid sinuses. When these four noncontiguous cuts were retrospectively compared with the standard 2- to 5-mm contiguous coronal CT examination, the overall sensitivity was 93.3% and specificity was 89.3%; however, the findings are of limited value if surgery is being considered.28 Limited CT examination using axial cuts can also be performed and can be helpful because the entire ethmoid complex can be displayed. Use of both axial and coronal CT examination can allow the physician to obtain the most anatomical information. Once rhinosinusitis has been identified, CT scanning does not have to be performed each time the patient presents with similar symptoms.

Medical Management of Chronic Rhinosinusitis

The goal of medical management is to reduce the swelling and inflammation, especially of the ostia, and promote drainage and a more normal nasal environment. Most treatment regimens for chronic sinusitis include topical steroids, decongestants, empiric antimicrobial agents, and certain nonpharmacologic measures with other agents used in certain settings. Unfortunately, there are few controlled trials comparing different treatments.

Steroids

Steroids, especially topical steroids, are a mainstay of rhinosinusitis treatment. They work by reducing inflammation, decreasing the sensitivity of cholinergic receptors (thereby reducing secretory response), decreasing nasal epithelial basophilia and mucosal eosinophilia, and inhibiting late-phase reaction to allergens.29 When steroids are used in conjunction with antibiotics, patients exhibit symptom improvement, decreases in inflammatory cells, and regression in radiographic abnormalities.30 Newer topical steroids are long-acting and appear to have minimal systemic effects, and they can be used for prolonged periods of time, especially when polyps are present. Oral steroids are beneficial, especially early in the treatment of chronic rhinosinusitis, when disease is resistant, or before surgery in patients with extensive polyps. However, side effects usually limit oral steroid use to short periods, usually < 2 weeks.

Decongestants

Decongestants, either systemic or topical, promote shrinkage of edematous mucosa by stimulating alpha-adrenergic receptors. They aid in thinning the mucus and have minimal drying side effects, but long-term use (> 5 days) is associated with rebound effects, and decongestants should be used with caution in patients who have certain medical conditions (ie, hypertension, ischemic heart disease, hyperthyroidism, diabetes) or are taking monoamine oxidase inhibitors. For this reason, short courses of topical decongestants, especially oxymetazoline hydrochloride, are frequently recommended.

Antimicrobial Therapy

Antimicrobial therapy is indicated in acute exacerbations of chronic rhinosinusitis, and the antimicrobial agents generally recommended are the same agents approved for acute rhinosinusitis (Table 4). There is controversy as to whether antimicrobial agents are effective in all cases of chronic rhinosinusitis, in part because few studies have been performed in this setting.31 Chronic rhinosinusitis is a multifactorial process that in some cases is not caused by bacterial infection. Ideally, therapy should be directed by results of sinus cultures, but this requires a sinus tap, which can be painful and costly; therefore, most initial therapy is empiric. The presence of purulent secretions, facial pain, and radiographic evidence of an air-fluid level are all considered indications for antimicrobial therapy.25 Most of the published literature suggests using the same agents that are effective in acute rhinosinusitis, and the choice is quite large. Selection is based on local resistance patterns, severity of disease, and prior recent antimicrobial use.29,31-34 In choosing antimicrobial therapy in chronic rhinosinusitis, the oral agents listed in Table 4 have been recommended by several authors. Additionally, they have recommended that treatment be of prolonged duration, at least 3 weeks; some recommend therapy for 4 to 6 weeks. With at least one fluoroquinolone, ciprofloxacin, a success rate of 85% was achieved in patients with chronic sinusitis after only 10 days of therapy.29,35,36 Therefore, it is not unreasonable to suggest that therapy with the newer fluoroquinolones for the respiratory tract would be equally effective. If there is inadequate response at 10 days, then a longer duration of therapy should be considered. When using any antimicrobial agent, if response is slow, consideration should be given to adding an agent with anaerobe coverage (eg, clindamycin). Because of the increased incidence of beta-lactam resistance, ampicillin alone is probably of limited usefulness in this disease.


Table 4—Antimicrobial Choices for Treating Rhinosinusitis

Amoxicillin-clavulanate
Cefprozil
Cefuroxime axetil
Cefdinir
Azithromycin
Clarithromycin
Trimethoprim/sulfamethoxazole
Doxycycline
Levofloxacin
Ciprofloxacin
Gatifloxacin
Moxifloxacin


Nonpharmacologic Measures

Hydration (eight glasses of water per day) and avoidance of caffeine, alcohol, and tobacco are also suggested when treating cases of rhinosinusitis.37 Nasal humidification should be provided, using a saline solution nasal spray (over-the-counter sterile physiologic saline solution) or nasal douche (either using a commercial preparation or simply mixing 8 oz of warm tap water and 1/2 teaspoon of salt) applied by ear bulb syringe. Oral hydration requires 6 to 8 glasses of water per day. Use of mucolytic agents (eg, guaifenesin) at a dose of 2,400 mg/d has been advocated to reduce mucus viscosity and promote clearance.38

Antihistamines

Antihistamines have been advocated for management of chronic rhinosinusitis, especially when there was reason to believe that there was an allergic trigger. Unfortunately, to date no studies have shown that their use in this setting is beneficial.39 They do have a beneficial role in preventing or treating acute allergic flares in patients with chronic rhinosinusitis.

Ipratropium Bromide

Ipratropium bromide acts as a topical anticholinergic and is helpful in reducing sneezing and decreasing the symptoms of nasal drainage. There have been no studies evaluating its role in chronic rhinosinusitis.

Prophylaxis

Prophylaxis is also important. Some have suggested that all patients with a history of chronic sinus problems should receive influenza vaccine each year, and pneumococcal vaccine with a booster every 5 years; those aged > 65 years should also receive a conjugated H influenzae type B vaccine.33

Medical Management in Special Situations

HIV

Among HIV-positive individuals, rhinosinusitis is common (estimates range from 7 to 60%), frequently severe, and often recurrent. Reasons postulated for this include obstruction of natural sinus ostia by nasopharyngeal benign lymphoid hyperplasia, lymphoma, or Kaposi's sarcoma, and decreased mucociliary clearance. In addition, immunologic defects in cell-mediated and macrophage function, an increase in the levels of IgE (purported to be the cause of the increased incidence of allergic symptoms among HIV-positive patients), and decreases in IgG levels may also play a role.40 Despite the increased incidence of rhinosinusitis, only limited microbiologic studies have been reported. The cumulative findings to date suggest that among HIV-positive patients with early disease (CD4 count of > 200/mm3), the microbiology is similar to that in the non-HIV population and the treatment should be similar.40 P aeruginosa has been recovered in HIV-positive patients, but only among those with a CD4 count of < 200/mm3. Cytomegalovirus and fungi have recently been reported as causes of rhinosinusitis. Increasing use of antibiotic prophylaxis may increase the risk of multiresistant virulent pathogens and fungal superinfections. In all HIV-positive patients with a CD4 count > 200/mm3 in whom conventional therapy has failed and in all patients with a CD4 count < 200/mm3, the physician should consider sinus lavage cultures for bacteria, fungi, and respiratory viruses (including cytomegalovirus); aggressive medical management, including prolonged antimicrobial therapy for P aeruginosa; and sinus surgery.40

Fungal Sinusitis

The reported incidence of fungal sinusitis has increased in the past decade. Whether this is the result of improved diagnostic techniques, better awareness, increasing prevalence of immunosuppression, or all of the above is presently unknown. Because fungi can be recovered in nasal secretions of otherwise healthy individuals, deShazo41 states that fungal sinusitis can be accurately diagnosed only by histologic examination of material or tissue removed from the sinuses. The possibility of fungal sinusitis should be entertained in any patient with chronic sinusitis, particularly if the condition is resistant to medical management. The presence on CT scan of focal or diffuse areas of radiodensity and decreased T1- and T2-weighted signal intensity on MRI scanning is also suggestive of fungal sinusitis.41

The disease is divided into noninvasive (allergic fungal rhinosinusitis, mycetoma) and invasive fungal disease (acute invasive, chronic invasive, or granulomatous invasive fungal sinusitis). Management in almost all cases requires surgical intervention. In recent years, a better appreciation of the spectrum of sinus fungal involvement has developed, and the reader is referred to several review articles that discuss this disease in more complete detail.41-44

In noninvasive disease, allergic fungal rhinosinusitis (AFS) can be thought of as the nasal equivalent of allergic bronchopulmonary aspergillosis. It normally presents in young, otherwise healthy patients as chronic rhinosinusitis, is frequently associated with polyposis, and involves multiple sinuses. It is estimated to account for 2 to 7% of all cases of chronic rhinosinisutis, and frequently the patient experiences asthma and has undergone several sinus surgeries. The sinus contents are described as looking like peanut butter or cottage cheese, but foul-smelling. AFS is frequently refractory to aggressive medical and surgical therapies. In one prospective study, the criteria proposed for optimizing the diagnosis of AFS included the presence of thick, viscous, often green mucus containing eosinophils; maxillary sinusitis; and the presence of specific IgE to Aspergillus fumigatis in the setting of chronic rhinosinusitis. Other immunoallergic tests, clinical findings, and radiographic findings were found to be of little help.45 Sinus mycetomas are also noted to occur, mainly in immunocompetent individuals; they may involve any sinus but are frequently unilateral.41 The clinical presentation includes chronic rhinosinusitis, episodes of expelling gravel-like material nasally, headaches, facial pain, or seizures. These can be detected using coronal CT scanning. Eosinophilic mucin is not present unless the patient has concomitant AFS.

Acute (fulminant) invasive fungal sinusitis is seen primarily in immunosuppressed patients. It has been reported at autopsy in 22 to 28% of leukemic patients.27 Aspergillus spp are most commonly reported, but other species include Candida, Rhizopus, and Mucor. Rhinosinusitis caused by Mucor spp has occasionally been noted in diabetic patients. Therapy is aggressive, with antifungal agents (especially amphotericin B) and antibiotics, treatment of underlying illness, and surgery with wide débridement. Chronic invasive fungal rhinosinusitis has only recently been reported, and to date this disease has mainly been seen in diabetic patients. Treatment has been similar to that for the acute form. Granulomatous invasive fungal sinusitis has largely been seen in immunocompetent North Americans. The most common fungus is Aspergillus flavus and treatment includes débridement and itraconazole.

Cystic Fibrosis

Sinus involvement in patients with cystic fibrosis is common (up to 10% of patients) and may cause exacerbations in the lower respiratory tract. Chronic purulent drainage and nasal congestion are frequent complaints, and most patients present with polyposis, often bilateral and occasionally significant in size. The spectrum of pathogens recovered from the sinuses is similar to those recovered from the lower respiratory tract. As the disease progresses, more virulent organisms are recovered from both the lower and upper respiratory tract, including P aeruginosa and S aureus (including methicillin-resistant S aureus), and these pathogens frequently are resistant to common antimicrobial agents.

Although presently there are no guidelines for management of chronic rhinosinusitis in cystic fibrosis patients, many physicians start with aggressive medical management, including decongestants and prolonged use of topical steroids, antihistamines, and antimicrobial agents. Because chronic rhinosinusitis disease and lower respiratory tract exacerbations frequently occur in tandem, antimicrobial choices are often based upon results of a sputum culture. Therapy is of prolonged duration (often 3 weeks or more), usually with two or more agents, when resistant and virulent pathogens are recovered. Early surgical intervention, proposed by the authors of one preliminary study, may reduce morbidity, improve exercise tolerance, and delay progressive respiratory failure.46 Considerations for surgical management include a significant decrease in pulmonary function as a result of rhinosinusitis, chronic symptoms unrelieved by medical management, or the presence of a mucocele. Sinus surgery should be entertained in all such patients prior to undergoing lung transplantation.

Surgical Management of Chronic Rhinosinusitis

Chronic rhinosinusitis may not respond to aggressive medical therapy, although this appears to be less common than it was in the past.47 Absolute indications for surgery in the setting of chronic rhinosinusitis have been established (Table 5),48 but relative indications have been harder to determine. Certainly one relative indication for surgery is failure of adequate medical management.


Table 5—Absolute Indications for Surgical Intervention in Chronic Rhinosinusitis*

Indications

Specific Findings

Extrasinus involvement

Brain abscess
Meningitis
Subperiosteal/orbital abscess
Cavernous sinus thrombosis
Contiguous infection
Impending complication (eg, Pott's tumor)

Sinus mucocele or pyocele

 

Nasal polyps

Massive polyps causing near or complete obstruction of the nasal lumen

Neoplasm

 

Invasive or allergic fungal rhinosinusistis

 

Cerebrospinal fluid rhinorrhea

 

*Data adapted from Anand et al.48


References

  1. Report of the Rhinosinusitis Task Force Committee Meeting: Alexandria, Virginia, August 17, 1996. Otolaryngol Head Neck Surg 1997; 117(3 pt 2):S1–S68
  2. Collins JG. Prevalence of selected chronic conditions: United States, 1986-88. National Center of Health Statistics. Vital Health Stat 10 1993; (182):1–87
  3. Kaliner MA, Osguthorpe JD, Fireman P, et al. Sinusitis: bench to bedside; current findings, future directions. J Allergy Clin Immunol 1997; 99:S829–S848
  4. Lund VJ. Rhinosinusitis. Br J Hosp Med 1997; 57:308–312
  5. Adams PF, Marano MA. The National Health Interview Survey. 1994; Vital Health Stat 1995; 10:83–83
  6. Diagnosis and treatment of acute bacterial rhinosinusitis. Evidence Report/Technology Assessment: No. 9. Rockville, MD: Agency for Health Care Policy and Research; March 1999
  7. McCaig LF, Hughes JM. Trends in antimicrobial drug prescribing among office-based physicians in the United States. JAMA 1995; 273:214–219
  8. National Ambulatory Medical Care Survey. Vital Health Statistics. Rockville, MD: US Department of Health and Human Services; 1994: AHCPR publication 93-00007
  9. McMahan JT. Paranasal sinusitis: geriatric considerations. Otolaryngol Clin North Am 1990; 23:1169–1177
  10. Bresciani M, Paradis L, Des Roches A, et al. Rhinosinusitis in severe asthma. J Allergy Clin Immunol 2001; 107:73–80
  11. Settipane RJ, Hagy GW, Settipane GA. Long-term risk factors for developing asthma and allergic rhinitis: a 23-year follow-up study of college students. Allergy Asthma Proc 1994; 15:21–25
  12. Greenberg SD, Ainsworth JZ. Comparative morphology of chronic bronchitis and chronic sinusitis, with discussion of "Sinobronchial" syndrome. South Med J 1966; 59:64–74
  13. Muller BA. Sinusitis and its relationship to asthma: can treating one airway disease ameliorate another? Postgrad Med 2000; 108:55–61
  14. Lanza DC, Kennedy KW. Adult rhinosinusitis defined. Otolaryngol Head Neck Surg 1997; 117(suppl):S1–S7
  15. Maran AG, Lund VJ. Nasal physiology. In: Maran AG, Lund VJ, eds. Clinical rhinology. New York, NY: Thieme Medical Publishers, 1990; 37
  16. Hamilos DL. Chronic sinusitis. J Allergy Clin Immunol 2000; 106:213–227
  17. Gwaltney JM Jr. Acute community-acquired sinusitis. Clin Infect Dis 1996; 23:1209–1223
  18. Osguthorpe JD, Hadley JA. Rhinosinusitis: current concepts in evaluation and management. Med Clin North Am 1999; 83:27–41
  19. Nadel DM, Lanza DC, Kennedy DW. Endoscopically guided cultures in chronic sinusitis. Am J Rhinol 1998; 12:233–241
  20. Rachelefsky GS. National guidelines needed to manage rhinitis and prevent complications. Ann Allergy Asthma Immunol 1999; 82:296–305
  21. Sibbald B. Epidemiology of allergic rhinitis. In: Burr ML, ed. Epidemiology of clinical allergy. Monographs in allergy. Basel, Switzerland: S. Karger, 1993; 61–79
  22. Hadley JA, Schaefer SD. Clinical evaluation of rhinosinusitis: history and physical examination. Otolaryngol Head Neck Surg 1997; 117(suppl):S8–S11
  23. Zinreich SJ. Paranasal sinus imaging. Otolaryngol Head Neck Surg 1990; 103:863–868
  24. Newman LJ, Platts-Mills TA, Plhillips CD, et al. Chronic sinusitis: relationship of computed tomographic findings to allergy, asthma, and eosinophilia. JAMA 1994; 271:363–367
  25. Wagner W. Changing diagnostic and treatment strategies for chronic sinusitis. Cleve Clin J Med 1996; 63:396–405
  26. Zinreich SJ. Rhinosinusitis: radiologic diagnosis. Otolaryngol Head Neck Surg 1997; 117(suppl):S27–S34
  27. Evans KL. Recogntion and management of sinusitis. Drugs 1998; 56:59–71
  28. Goodman GM, Martin DS, Klein J, et al. Comparison of a screening coronal CT versus a contiguous coronal CT for the evaluation of patients with presumptive sinusitis. Ann Allergy Asthma Immunol 1995; 74:178–182
  29. Benninger MS, Anon J, Marbry RL. The medical management of rhinosinusitis. Otolaryngol Head Neck Surg 1997; 117(suppl):S41–S49
  30. Meltzer EO, Orgel HA, Backhaus JW, et al. Intranasal flunisolide spray as an adjunct to oral antibiotic therapy for sinusitis. J Allergy Clin Immunol 1993; 92:812–823
  31. Kaliner M. Medical management of sinusitis. Am J Med Sci 1998; 316:21–28
  32. Casiano RR. Sinusitis: a complex and challenging disease. Mediguide to Infectious Diseases 2001; 21(1):1–8
  33. Pankey GA. Bacterial sinusitis: treatment options. International Reports on Community-Acquired Infections. 2000; 1(1):1–8
  34. Brook I, Thompson DH, Frazier EH. Microbiology and management of chronic maxillary sinusitis. Arch Otolaryngol Head Neck Surg 1994; 120:1317–1320
  35. Johnson PA, Rodriguez HP, Wazen JJ, et al. Ciprofloxacin versus cefuroxime axetil in the treatment of acute bacterial sinusitis. J Otolaryngol 1999; 28:3–12
  36. Legent F, Bordure P, Beauvillain C, et al. A double-blind comparison of ciprofloxacin and amoxycillin/clavulanic acid in the treaatment of chronic sinusitis. Chemotherapy 1994; 40(suppl)8–15
  37. Pankey GA, Gross CW, Mendelsohn MG. Contemporary diagnosis and management of sinusitis. 3rd ed. Newton, PA: Handbooks in Health Care, 2000
  38. Wawrose SF, Tami TA, Amoils CP. The role of guaifenesin in the treatment of sinonasal disease in patients infected with the human immunodeficiency virus (HIV). Laryngoscope 1992; 102:1225–1228
  39. Zeiger RS. Prospects for ancillary treatment of sinusitis in the 1990's. J Allergy Clin Immunol 1992; 90:478–495
  40. Belafsky P, Kissinger P, Davidowitz SB, et al. HIV sinusitis: rationale for a treatment algorithm. J La State Med Soc 1999; 151:11–18
  41. deShazo RD. Fungal sinusitis. Am J Med Sci 1998; 316:39–45
  42. deShazo RD, Swain RE. Diagnostic criteria for allergic fungal sinusitis. J Allergy Clin Immunol 1995; 96:24–35
  43. deShazo RD, O'Brien M, Chapin K, et al. A new classification and diagnostic criteria for invasive fungal sinusitis. Arch Otolaryngol Head Neck Surg 1997; 123:1181–1188
  44. deShazo RD, O'Brien M, Chapin K, et al. Criteria for the diagnosis of sinus mycetoma. J Allergy Clin Immunol 1997; 99:475–485
  45. Serrano E, Percodani J, Uro-Coste E, et al. Value of investigation in the diagnosis of allergic fngal rhinosinusitis: results of a prospective study. J Laryngol Otology 2001; 115:184–189
  46. Halvorson DJ, Dupree JR, Porubsky ES. Management of chronic sinusitis in the adult cystic fibrosis patient. Ann Otol Rhinol Laryngol 1998; 107:946–952
  47. Gaynor EB. Current concepts in the treatment of sinusitis. Arch Otolaryngol Head Neck Surg 1995; 121:702
  48. Anand VK, Osguthorpe JD, Rice D. Surgical management of adult rhinosinusitis. Otolaryngol Head Neck Surg 1997; 117(3 pt 2):S50–S52

Copyright ©2003 American College of Chest Physicians