Chronic Sinusitis

Michael J. Simmons, M.D. Jefferson City Medical Group Department Chair ENT and Sinus Surgery Division

Rhinosinusitis is one of the most commonly diagnosed conditions in the United States. Early in this century, it was estimated that of all antibiotics prescribed in the United States, 18% for adults and 9% for children were prescribed for the diagnosis of sinusitis. 1 Rhinosinusitis in the broadest terms is defined as inflammation of the paranasal sinus cavities and/or the nasal cavity itself. This diagnosis is made with a history of two major factors or one major and two minor factors which include: 2

Major Factors

1. Facial pain and/or pressure

2. Nasal obstruction

3. Purulent/discolored nasal or postnasal drainage

4. Anosmia or hyposmia

5. Fever

Minor Factors

1. Headache

2. Halitosis

3. Fatigue

4. Dental pain

5. Cough

6. Ear pain and/or pressure

On examination, physical findings include purulent drainage, mucosal or turbinate edema or polyps and may be supported by x-rays which show opacification or air/fluid levels in the air spaces of the paranasal sinuses. The vast majority of acute rhinosinusitis episodes are viral events and are expected to be self-limiting without antibiotic requirement. Even acute bacterial sinusitis begins in most cases as a viral upper respiratory infection or an acute exacerbation of inhalant allergic disease which at onset do not require antibiotic treatment. If signs or symptoms last beyond ten days, bacterial infection may be present and antibiotics are indicated if the clinical situation warrants. The general pathogenesis of acute and chronic rhinosinusitis includes inflammation that causes obstruction of the sinus ostium. This triggers a cascade of impaired mucociliary clearance, mucus stasis, and subsequent bacterial overgrowth.

Chronic rhinosinusitis (CRS) is defined by both duration and clinical criteria. Chronic rhinosinusitis is defined as 12 weeks or longer of two major symptoms listed above. An alternative to CRS is recurrent acute rhinosinusitis in which four or greater episodes of bacterial sinusitis requiring antibiotic therapy occur within a year. The patient has symptom resolution between episodes. Chronic rhinosinusitis is further defined by the absence (CRSsNP) or presence of intranasal polyps (CRSwNP).

The pathophysiology of CRS is incompletely understood and is likely multifactorial, resulting from interactions of anatomy, genetics and environmental influences. Unlike acute rhinosinusitis, which is usually caused by an infectious viral agent, CRS may be caused by immunoglobulin E (IgE) mediated allergic disease, bacterial biofilms, osteitis, fungi, and host immune system deficiencies.

Allergic disease mediated by IgE reactions is very common in the United States. Up to 25% of the population has allergic rhinitis. There is an increased prevalence of allergy among those with CRS. The exact mechanism is unknown; but importantly, mucosal edema caused by antigen reactivity may lead to reduced mucociliary clearance.

Bacterial biofilms are often diagnosed in culture positive exacerbations of CRS, frequently post-surgical, and are typically caused by Peudomonas aeruginosa, Staphylococcus aureus and Hemophilus influenza. Only the latter is also common in acute bacterial rhinosinusitis. How frequently these might be a cause rather than an effect of CRS is unknown.

Osteitis is appreciated radiographically as bone remodeling or thickening and histologically may show inflammatory infiltrates and bony sclerosis. This is likely due to an increased concentration of local inflammatory mediators. It is not clearly understood whether this is a consequence of CRS or a causative factor.

Fungi rarely cause infection or invasion in the immunocompetent host but select fungi such as Alternaria and Candida have been shown to upregulate interleukin-5 and IL-13 in some individuals. These chemokines are involved in the eosinophilic response leading to edema and possibly polyp formation. Allergic fungal rhinosinusitis is a subtype of CRS, usually associated with polyps and allergic mucin and generally more isolated disease than CRSwNP.

Immunodeficiencies can increase the potential for patients to develop CRS. Systemic conditions including autoimmune/ granulomatous diseases such as Wegener’s granulomatosis, aspirin sensitivity triad, cystic fibrosis and primary ciliary dyskinesia all lead to high rates of CRS with and without polyposis.

Beyond the clinical signs and symptoms and allowing for the diagnostic criteria for CRS, staging the condition includes several modalities. The physical examination should reflect infection and edema and document the presence or absence of a nasal septal deviation or polyps. Specialty examination would include nasal endoscopy in the decongested state. Imaging is best performed by non-contrast enhanced CT scan of the sinuses in coronal and axial planes. If non-obstructed mucosal disease is seen on CT, IgE antigen screening may be appropriate. If compromised immune system conditions are suspected, laboratory evaluations such as cytoplasmic-antineutrophil cytoplasmic antibody (C-ANCA), P-ANCA, erythrocyte sedimentation rate (ESR), c-reactive protein, immunoreactive trypsinogin (IRT) or sweat test may be warranted. 3

Medical treatment for CRS can be stratified into three groups: anti-inflammatory, antimicrobial and mechanical.

Anti-inflammatory medications include topical and systemic steroids. Nasal steroid sprays are a mainstay of CRS therapy. They directly address the mucosal inflammation and polyps which are the basis for sinus ostial obstruction. They are useful in allergic and non-allergic mediated cases of CRS. They may be delivered in pump or aerosol devices or may be mixed within saline solution for larger volume application. Within the broader scope of anti-inflammatory treatment, if allergy is clinically suspected, IgE inhalant allergen testing followed by directed immunotherapy is indicated for long-term reduction of CRS exacerbations and reduced primary allergic symptomatology.

To that end, antihistamines and leukotriene antagonists are beneficial in the treatment of allergic disease.

Antimicrobial treatments for CRS are best directed toward sensitivities of positive bacterial cultures. Frequently treated exacerbations often lead to identifying antimicrobial resistant bacteria on cultures. Those bacteria which form biofilms are often implicated. In post-surgical exacerbations, topical antibiotic preparations may be delivered directly through powered atomized concentrations or in high volume saline/ antibiotic irrigations. This allows for topical delivery of medication that otherwise might require intravenous delivery. Macrolide antibiotics have also been shown to exert an antiinflammatory effect beyond their antimicrobial action and may be a good empiric choice.

Mechanical treatments are used to promote mucociliary clearance. Nasal saline irrigation is the most important type. It must be stressed as an important daily necessity to reduce exacerbations of CRS. Additional benefits for mucociliary clearance can be derived from systemic mucolytic agents such as guaifenesin and brief uses of topical decongestants such as oxymetazoline hydrochloride.

Surgical treatment for CRS is primarily endoscopic sinus surgery (ESS). The indications for surgery are based on the proper clinical diagnosis of CRS, lack of benefit from sufficient medical management and endoscopic and radiographic staging which supports ostial manipulation and/or removal of paranasal sinus tissue. This procedure has various iterations to include officebased balloon ostial dilation of the maxillary sinuses to complete operative spheno-ethmoidectomy with or without frontal sinus drill out. Endoscopic sinus surgery is useful for both CRSsNP and CRSwNP. The latter diagnosis has a higher rate of recurrent disease, often resulting in additional procedures and greater need for long-term medical management. Placement of mometasone furoate drug eluting stents within the operative ethmoid cavities has been shown to reduce recurrence of CRSwNP. 4

Additionally, newer therapies for CRSwNP involve the uses of monoclonal antibodies targeted toward IgE and interleukin mediated disease. Omalizumab (Xolair R) inhibits the binding of IgE to the high-affinity IgE receptor, thus down-regulating mast cells and basophils, reducing IL-4, IL-5 and IL-13, all potent mediators allergic respiratory disease found in asthma and CRSwNP. 5 Dupilumab (Dupixent R) is a fully human IgG4 monoclonal antibody against IL-4 receptor alpha subunit. By blocking this subunit, dupilumab inhibits IL-4 and IL-13 which drive type 2 inflammatory disease (asthma, atopic dermatitis and CRSwNP). 6

In summary, rhinosinusitis is a common diagnosis and frequently diagnosed by the family physician. If CRS is diagnosed in spite of appropriate management, then indications for imaging and referral for more advanced care may be warranted.

References found on page 31.