Chapter 15. Acute & Chronic Sinusitis

• The vast majority of cases of acute rhinosinusitis are self-limiting viral events.
• Chronic rhinosinusitis is an inflammatory disease whose causes are often multifactorial.
• In chronic rhinosinusitis, nasal endoscopy and/or CT scan may be necessary to make the diagnosis if symptoms do not correlate well with findings.

Rhinosinusitis is one of the most commonly diagnosed medical conditions in the United States, affecting an estimated 16% of the adult population annually. Direct health care costs are significant, estimated to be over $5.8 billion per year. According to the recent 2007 data from the National Health Interview Survey, rhinosinusitis continues to be one of the top 10 leading diagnoses of office visits in the United States. Of all antibiotics prescribed in 2002, 9% of pediatric prescriptions and 18% of adult prescriptions were written for a diagnosis of acute sinusitis.

Rhinosinusitis is broadly defined as symptomatic inflammation of the paranasal sinuses and nasal cavity. The term rhinosinusitis is used because sinusitis is almost always accompanied by inflammation of the contiguous nasal mucosa. There have been a number of iterations of the actual definition that are described in this section. The Rhinosinusitis Task Force in 1997 classified rhinosinusitis based on both symptom duration and by history. A history suggestive of rhinosinusitis includes two or more major factors, or one major and two minor factors (Table 15–1). In 2003, another task force that included the American Academy of Otolaryngology – Head and Neck Surgery (AAO-HNS) proposed revised guidelines that required physical exam findings for the diagnosis of chronic rhinosinusitis (CRS). Findings on nasal endoscopy or anterior rhinoscopy should include one or more of the following: purulent drainage, polyps, polypoid changes in the mucosa, and edema or erythema of the middle meatus. These guidelines also suggest that CT scans can be a helpful to confirm the diagnosis of symptomatic patients with equivocal physical exam findings. In 2004, a multidisciplinary panel further classified CRS as CRS with nasal polyps, CRS without nasal polyps, and allergic fungal rhinosinusitis (AFS) to better guide clinical research and patient care.

• Acute rhinosinusitis: ≤4 weeks
• Subacute rhinosinusitis: Duration of 4–12 weeks
• CRS: ≥12 weeks
• Recurrent acute rhinosinusitis: Greater than four or more episodes of acute rhinosinusitis per year, with each episode lasting ≥7–10 days, with symptom resolution between episodes
• Acute exacerbations of CRS are a sudden worsening of CRS with a return to baseline after treatment.

Most recently in 2007, new clinical practice guidelines were developed to improve and update the diagnosis of rhinosinusitis. CRS is now defined as 12 weeks or longer of two or more of the following symptoms:

• Mucopurulent drainage (anterior, posterior, or both)
• Nasal obstruction (congestion)
• Facial pain-pressure-fullness
• Decreased sense of smell.

And inflammation as seen by one or more of the following:

• Purulent mucus or edema in the middle meatus or ethmoid region
• Polyps in the nasal cavity or the middle meatus
• Radiographic imaging showing inflammation of the paranasal sinuses.

The nasal cavity serves to warm and humidify inhaled air. There are a variety of theories on the function of the paranasal sinuses. Proposed functions include (1) acting as resonating chambers for the voice, (2) providing protection to the brain and orbit from trauma, (3) moisturizing and humidifying ambient air, and (4) lightening the weight of the facial skeleton.

The sinonasal mucosa is lined by pseudostratified columnar ciliated epithelium. This respiratory epithelium is made up of a variable number of ciliated cells (∼75%), mucus-secreting goblet cells (∼20%) and basal cells (∼5%). There are approximately 50–200 cilia on the apical surface of epithelial cells that beat in a coordinated fashion. Under normal conditions, the entire mucus blanket of the nose or sinus is cleared in 10 minutes. Ciliary beat frequency can vary in response to chemical, thermal, mechanical, and hormonal stimuli. Additionally, changes in pH have a profound impact on ciliary beat frequency. Impairment of mucociliary clearance may result in mucus stasis, which under the proper conditions can support bacterial growth and infection.

The mucus secreted by goblet cells is comprised of primarily of water, gycoproteins, immunoglobulins, leukocytes, salts, and neurotransmitters. The mucus consists of 2 layers: the superficial gel phase and the inner sol phase. Aerosolized pathogens and particles larger than 0.5–1 μm are trapped in the mucus gel layer and eventually transported posteriorly to the nasopharynx and oropharynx to be swallowed. Within the sinuses, the mucus blanket is transported toward the natural sinus ostia, despite the presence of accessory ostia. Mucus also plays a critical role in olfaction. Airborne olfactants must dissolve in the nasal mucosa overlying the olfactory epithelium before the olfactory response is initiated. Surgical antrostomies that do not include the true sinus ommNstium can result in mucus recirculation, which can be a source of persistent postoperative symptoms.

Acute Rhinosinusitis

Acute rhinosinusitis, in contrast to CRS, is most often caused by an infectious agent. Acute rhinosinusitis is defined as up to 4 weeks of purulent nasal drainage accompanied by nasal obstruction, facial pain, facial pressure, or fullness. The clinician must then distinguish between viral rhinosinusitis (VRS) and acute bacterial rhinosinusitis (ABRS). This distinction is made based on illness pattern and duration.

• Viral Rhinosinusitis
  • Symptoms of acute rhinosinusitis are present less than 10 days
  • Symptoms are not worsening.
• Acute Bacterial Rhinosinusitis
  • Signs or symptoms of acute rhinosinusitis are present 10 days or more beyond the onset of upper respiratory symptoms
  • Signs or symptoms of acute rhinosinusitis worsen within 10 days after an initial improvement.

In most cases, bacterial sinusitis is preceded by a viral upper respiratory infection. Other common conditions that can predispose a patient to acute sinusitis are cigarette smoke, anatomical factors such as nasal septum deformities, concha bullosa, and allergies. More than 200 different viruses are known to cause the symptoms of the common cold. The most frequently detected viruses include rhinovirus, respiratory syncytial virus, influenza virus, and parainfluenza virus. Approximately 2% of VRS progresses to bacterial rhinosinusitis in adults.

Three cardinal symptoms have been found to have high sensitivity and specificity for ABRS. These include purulent rhinorrhea, facial pain/pressure, and nasal obstruction. Secondary symptoms that support the diagnosis include anosmia, fever, aural fullness, cough, and headache. Another finding suggestive of ABRS is if patients worsen after an initial improvement in symptoms. The most common organisms responsible for ABRS include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.

Chronic Rhinosinusitis

CRS is defined as an inflammatory condition of the nasal cavity and paranasal sinuses lasting for longer than 12 weeks. The pathophysiology of CRS remains incompletely understood, but it is believed to be multifactorial, resulting from interactions between host anatomy, genetics, and the environment. A simplified way to approach CRS is illustrated in Table 15–2. CRS can be thought of first resulting from mucosal inflammation, causing swelling and obstruction at the sinus ostium. This can lead to mucus stasis, which can then lead to bacterial superinfection. The signs and symptoms of CRS often vary in severity and prevalence. Nasal obstruction (81–95%), is the most common symptom, followed by facial congestion-pressure-fullness (70–85%), discolored nasal discharge (51–83%), and hyposmia (61–69%). High fevers are usually absent, although fatigue and myalgias are common (Table 15–1).

Unlike in acute rhinosinusitis, which is usually caused by an infectious agent, there is no one causative factor that accounts for CRS. There is evidence of numerous factors contributing to CRS including:

• Biofilms
• Osteitis
• Allergy
• Superantigens from Staphylococcus aureus
• Fungi
• General Host Factors
• Infectious

There is growing evidence that bacterial biofilms may play a role in certain cases of recalcitrant chronic sinusitis that do not respond to traditional medical and surgical therapies. Biofilms are three-dimensional aggregates of bacteria encased in a protective extracellular matrix. Biofilms are initiated when free-floating planktonic bacteria anchor to various biological or inert surfaces. The most common biofilm formers in CRS are Pseudomonas aeruginosa, S. aureus, and Haemophilus influenzae. Bacteria in biofilms are more resistant to host defenses such as immune system phagocytosis, and can be up to 1000 times more resistant to antibiotic treatment. Biofilms have been shown to have an adverse effect on postoperative outcomes of CRS patients. Patients with bacterial biofilms show worse postoperative endoscopy scores and increased mucosal inflammation.

Changes in bone have been appreciated clinically and radiographically in CRS. The presence of inflammation and remodeling within the bone of the paranasal sinuses has been demonstrated in both animal and human studies. Histologically, there is bony remodeling, an inflammatory infiltrate, and bony sclerosis, likely due to an increase in local inflammatory mediators. Studies suggest that the inflammation associated with CRS may spread through the Haversian system within the bone to involve other sinuses. Despite aggressive treatment of the overlying sinus mucosa, chronic inflammation can persist in the underlying bone, which may contribute to some cases of recalcitrant CRS.

There is some epidemiologic data supporting a link between allergy and CRS. Approximately 20% of the population of the United States has allergy. Allergic rhinitis is an IgE-mediated disease in which exposure to an inhaled antigen elicits inflammatory changes in the nasal mucosa. Allergy is thought to cause a proportion of CRS and all cases of allergic fungal sinusitis (by definition). There is an increased prevalence of allergy among patients who have CRS, and when present, it can increase the severity of CRS. In these patients, treatment of allergies can improve the course of the disease, hastens symptom recovery, and improve mucosal appearance. Still, the precise mechanism that allergic rhinitis may predispose people to CRS remains unclear.

Recent evidence has suggested that exotoxins secreted by colonizing S. aureus play a role in the pathophysiology of a subset of patients with CRS with nasal polyposis. Superantigens have the ability to activate up to 30% of the T-cell population by bypassing normal antigen processing within antigen-presenting cells. In this theory, the superantigens result in immune activation, cytokine release, and inflammation. This theory suggests that superantigens can play an important role in polyp formation or maintenance of patients with CRS with nasal polyps.

Over the last 10 years, there has been a significant amount of interest in the role of fungi in CRS, and the potential use of antifungal medications to treat CRS. Work from the Mayo clinic has demonstrated fungal hyphae in 96% of patients with CRS. Select fungi such as Alternaria and Candida have been shown to up-regulate IL-5 and IL-13 in some individuals, which are important chemokines involved in the eosinophilic response. This theory suggests that, in a susceptible host, an immunologic response is mounted that includes the proliferation or recruitment of eosinophils, which results in the clinical expression of CRS. However, others have disputed the role of fungus in CRS. A recent European multicenter randomized controlled study demonstrated that topical amphotericin B had no significant beneficial effect for patients with CRS with and without nasal polyps. Another study found that nasal amphotericin B spray was is ineffective in treating objective markers of sinus inflammation, and actually worsened patient symptoms. Further studies are needed to clarify the exact role of fungi in CRS pathogenesis.

Genetic factors and immune deficiency can significantly increase the potential for patients to develop CRS. These general host factors can lead to diffuse inflammation of the sinonasal mucosa. This inflammation can cause obstruction at the sinus ostium that can trigger a cascade of impaired mucociliary clearance, mucus stasis, and subsequent bacterial overgrowth. Systemic diseases include autoimmune/granulomatous diseases such as Wegener's granulomatosis, aspirin sensitivity triad (Samter's Triad), cystic fibrosis, immunodeficiency, and primary ciliary dyskinesia. Patients with these conditions are at a high risk for failing conventional medical and surgical management for CRS.

Bacterial, viral, and fungal infections can all be sources of sinonasal inflammation in CRS. Bacteria may play both direct and indirect roles in the pathophysiology of CRS, as seen with the biofilm and superantigen theories. The most common organisms isolated in CRS patients include S. aureus, coagulase-negative staphylococci, anaerobes, Pseudomonas aeruginosa.

Fungal Rhinosinusitis

Many different genera of fungus have been documented to cause sinus disease including Aspergillus, Bipolaris, Rhizopus, and Alternaria. Fungal sinusitis can vary from a relatively benign process to an acute life-threatening disease depending on the host and a variety of factors including diabetes, immunosupression, and allergy.

Fungal Ball

A fungal ball is the development of a noninvasive conglomeration of fungal hyphae into a mass. This condition arises due to the implantation of fungus into an otherwise normal sinus. Patients are usually immunocompetent with no other risk factors. The maxillary sinus is most commonly involved, followed by the sphenoid and ethmoid sinuses. Treatment is simple surgical removal of the fungal ball with aeration of the affected sinus. Antifungal therapy is usually unnecessary after surgery.

Allergic Fungal Rhinosinusitis (AFS)

Allergic fungal sinusitis is a subtype of CRS characterized by the presence of allergic mucin, which is thick inspissated mucus with eosinophils and fungal hyphae. The widely accepted diagnostic criteria for AFS were described by Bent and Kuhn in 1994. The five criteria are type I hypersensitivity to fungi, nasal polyps, characteristic CT scan findings (Figure 15–1), eosinophilic mucin without fungal invasion into sinus tissue, and positive fungal stains. Typically, polypoid tissue is seen anterior to a mass consisting of mucin, fungal elements, Charcot-Leyden crystals, and eosinophils. Sinus expansion and bony remodeling are hallmark features of this process. Typical CT scan findings include heterogeneous areas of signal intensity within the affected sinuses. The areas of increased signal intensity are thought to be due to the accumulation of heavy metals such as iron, manganese, and calcium within the inspissated allergic mucin. Magnetic resonance imaging (MRI) scans can also assist in the diagnosis. Treatment is primarily surgical with postoperative topical and systemic steroids. Immunotherapy, systemic steroids, and postoperative management by an allergist may be necessary to reduce recurrence.

Invasive Fungal Sinusitis

Invasive fungal sinusitis is a disease seen almost exclusively in immunocompromised individuals. This condition is characterized by the rapid development of progressive invasive fungal infection. The typical fungal pathogens are Aspergillus, Mucor, and Rhizopus. Gillespie and O'Malley reviewed 25 patients with invasive fungal sinusitis, and looked at their presentation. Nearly two-thirds presented with either fever or facial periorbital pain, and up to half presented with nasal congestion and headache. In this study, 88% presented with two or more of these findings, and just over a quarter had visual complaints or ophthalmoplegia. Rapid diagnosis and treatment is essential to limit the disease progression. In one small study, biopsy of the middle turbinate at had a 75% sensitivity and 100% specificity in diagnosing invasive fungal sinusitis. Pathologic examination of the black necrotic intranasal or palatal debris demonstrates arterial and venous thrombosis due to direct fungal invasion. The treatment consists of (1) debriding all involved structures, (2) aggressive intravenous antifungal therapy, and (3) normalizing the underlying immunocompromised state (usually neutropenia or uncontrolled diabetes).

Staging Systems

Many staging systems have been used to stratify patients with CRS according to objective levels of disease. Two commonly used staging systems found in the literature will be described briefly in this section.

Lund–Mackay Staging

The Lund–Mackay staging system is widely used in radiologic assessment of CRS. The scoring system is based on CT scan findings that are obtained after an adequate trial of medical treatment. Each sinus group is then assigned a numeric grade: 0 = no abnormality, 1 = partial opacification, and 2 = total opacification. The sinus groups include the maxillary, frontal, sphenoidal, anterior ethmoidal, and posterior ethmoidal sinuses. The ostiomeatal complex is scored only as 0 (not obstructed) or 2 (obstructed). Thus, a total score of 0–24 is possible, and each side can be considered separately (0–12).

Lund–Kennedy Endoscopic Scores

In this staging system, the endoscopic appearances of the nose are also quantified for the presence of polyps (0 = none, 1 = confined to middle meatus, 2 = beyond middle meatus), discharge (0 = none, 1 = clear and thin, 2 = thick and purulent), and edema, scarring or adhesions, and crusting (for each: 0 = absent, 1 = mild, 2 = severe).

Diagnostic Modalities

Physical Examination

A complete head and neck exam with anterior rhinoscopy is essential in all patients suspected of having rhinosinusitis. Findings of mucopurulence, edema, septal deflection, and polyps should be noted. The middle meatus is often well visualized after appropriate decongestion.

Endoscopic Evaluation

Rigid endoscopy or flexible fiberoptic endoscopy are useful to better evaluate the nasal cavity, sinuses, and nasopharynx. Findings that should be noted in the examination are septal deviations, edema of the turbinates, and the presence of mucus, pus, polyps, or erythema. Two critical areas to examine are the osteomeatal complex lateral to the middle turbinate and the sphenoethmoidal recess. Endoscopically guided cultures should be taken of any purulence in the nasal cavity or sinuses and sent for aerobic, anaerobic, fungal, and acid-fast bacilli cultures.

Imaging Studies

Computed tomography (CT) scanning is currently the method of choice for sinus imaging. Because a viral upper respiratory infection may cause abnormalities on CT that are indistinguishable from rhinosinusitis, imaging in ABRS has limited usefulness except when complications are suspected. On the other hand, symptoms of CRS do not correlate well with findings. Therefore, CT and/or nasal endoscopy is necessary to make the diagnosis. In addition to providing excellent visualization of mucosal thickening, air fluid levels, and bony structures, coronal scans give optimal visualization of the osteomeatal complex and are conveniently oriented for the surgeon in terms of surgical planning. Sagittal views can help delineate frontal sinus anatomy and confirm the presence of Onodi cells (Figure 15–2).

When compared to CT scans, MRI of the sinuses provides better soft tissue contrast resolution and tissue characterization. MRI offers better differentiation of benign obstructed secretions from tumor, and can be a helpful modality with suspected orbital or intracranial extension. For these reasons, MRI scanning should be the imaging method of choice in the evaluation of soft tissue masses, complicated sinus inflammatory diseases, and intracranial or intraorbital extension of sinus pathology.

Historically, standard radiographs were used to evaluate the sinuses. The conventional paranasal sinus evaluation included the following views: Caldwell (to visualize the frontal and ethmoid sinuses), Waters (for the maxillary sinuses), lateral (for the anterior and superior walls of the frontal, maxillary, and sphenoid sinuses), and submental vertex views (for the ethmoid and sphenoid sinuses).

Laboratory Tests

Laboratory tests and immunologic studies may be helpful for patients who fail to improve with conventional medical and surgical treatments. A variety of conditions such as Wegener granulomatosis, Churg–Strauss syndrome, and sarcoidosis can be causes of recurrent sinusitis. Nasal crusting can occur secondary to dryness of the mucosa in Sjogren syndrome. Some common laboratory tests for these conditions include cytoplasmic-antineutrophil cytoplasmic antibody, perinuclear-antineutrophil cytoplasmic antibody, IgE, erythrocyte sedimentation rate, c-reactive protein, rheumatoid factor, and antinuclear antibody. Testing for HIV and IgG levels should be also considered in refractory patients.

Differential Diagnosis

The differential diagnoses of acute and chronic sinusitis are many and include the following: the common cold, temporomandibular joint (TMJ) pain, headache (including migraine), trigeminal pain, and sinus neoplasms. Allergic and odontogenic causes of symptoms should also be excluded. The symptoms of facial pressure and pain, purulent nasal discharge, nasal congestion, hyposmia, tooth pain, and a poor response to nasal decongestants can help differentiate these entities.

Sinus neoplasms are relatively uncommon, but are critical to exclude. A history of unilateral nasal obstruction and epistaxis warrants further workup, including CT scan and nasal endoscopy. Changes in vision and cranial nerve deficits, particularly in the distribution of the infraorbital nerve, should also cause suspicion. Palatal numbness or dry eyes can also be due to lesions in the pterygopalatine fossa (see Chapter 17, Paranasal Sinus Neoplasms).

Treatment of Chronic Rhinosinusitis

Medical management of CRS can be simplified into three groups: antimicrobial, anti-inflammatory, and mechanical. It is helpful to break down treatments from each group, and combine them when appropriate into a comprehensive treatment plan. Also, it is important at this time to consider the side effects of each therapy, and weigh them with the patient's symptom severity and other medical conditions. In general, medical management of CRS should include 3–4 weeks of culture directed (or broad spectrum) antibiotics, a nasal steroid spray, and nasal saline irrigation. Strong consideration should be given to a tapered course of oral steroids unless contraindicated.

Antibiotics

Antimicrobial medications are best given for patients with CRS after cultures have been performed. After the correct antibiotic is chosen, there are multiple ways to deliver it, including oral, intravenous, or topical. Oral antibiotics are the mainstay of treatment in the management of CRS to clear infection and to treat exacerbations of CRS. In contrast to antibiotic therapy for acute sinusitis, antibiotics should be used for at least 3–4 weeks. Ideally, antibiotic therapy should be culture-directed, particularly after failure of prior antibiotic use.

Topical antibiotics have the theoretical advantage of high local levels of drug with minimal systemic absorption, lower costs, and decreased morbidity when compared to IV antibiotics. A study by Vaughn and Carvalho showed that after a 3-week course of culture directed nebulized antibiotics, patients demonstrated improvements in posterior nasal discharge, and facial pain/pressure. These patients also had a longer infection-free period, and improved endoscopic exams. There were no major side effects to treatment, and minor side effects were usually benign and self-limiting.

Antifungal therapy for CRS is still controversial at this time. Recent double-blind, placebo controlled trials have not shown substantial improvement in CRS based on objective and subjective criteria after treatment with amphotericin B. Nonetheless, some patients with CRS treated with oral antifungals do benefit.

Steroid Nasal Sprays and Oral Steroids

Mucosal inflammation and polyposis, which can lead to the obstruction of sinus ostia, are critical in the pathogenesis of most cases of CRS. Nasal steroid sprays directly address this problem by reducing mucosal inflammation and the site of polyps, thereby limiting postoperative recurrence. Common adverse effects with nasal steroids include nasal irritation, mucosal bleeding, and crusting. Systemic side effects are uncommon, and therefore nasal steroids are often prescribed for maintenance therapy in those with CRS. For better frontal sinus penetration, an eyedropper can be used to instill standard nasal steroid spray solution. Placement of drops at home can be done by the patient kneeling and then placing the forehead on the floor (Moffit's position) or with the head hanging off the bed (Mygind's position).

Systemic steroids are highly effective at reducing mucosal inflammation and nasal polyp bulk in CRS. Oral steroids decrease white blood cell migration, production of inflammatory mediators, antibody production, histamine release, and swelling through a variety of mechanisms. However, a thorough discussion with patients regarding the risks of systemic steroid administration is mandatory. A tapered regimen may be given during severe CRS flare-ups and in the postoperative period, but their use should be limited and carefully monitored.

Nasal Irrigation and Other Mechanical Treatments

Nasal saline irrigation is an important component in the treatment of CRS. Frequent rinsing prevents the accumulation of nasal crusts and promotes mucociliary clearance. Hypertonic saline may increase the rate of clearance in certain cases. Nasal irrigation is well tolerated by patients, without any evidence of significant harmful side effects. Work by the senior author has demonstrated the efficacy of 1% baby shampoo nasal irrigations for patients with CRS recalcitrant to surgery and isotonic saline irrigations. Patients with CRS were treated with twice-a-day sinus irrigation with 1% baby shampoo, which led to improvement in SNOT-22 scores for nearly 50% of patients who remained symptomatic despite surgical and conventional medical management. Greatest improvements were in reducing thickened nasal secretions and postnasal drainage. Baby shampoo nasal irrigation has promise as an inexpensive, well-tolerated adjuvant therapy to conventional medical therapies for symptomatic patients after FESS.

Decongestants, and Leukotriene Antagonists, and Other Therapies

Systemic decongestants and mucolytic agents such as guaifenesin may provide some symptomatic relief. Given the favorable side effects of these agents, they are often added to the therapeutic regimen. Leukotriene receptor antagonists (montelukast, zafirlukast) and macrolide antibiotics, which have anti-inflammatory effects, may also prove to be useful therapeutics.

Budesonide is used for the maintenance treatment of asthma and as prophylactic therapy in children aged 12 months to 8 years. While not FDA approved for use in CRS, use of budesonide respules (Pulmicort Respules; AstraZeneca LP, Wilmington, Delaware) for patients with nasal polyps or significant mucosal edema has been gaining popularity in the United States. A recent study for patients with chronic sinusitis found that use of budesonide 0.25 mg once a day for 30 days improved SNOT-20 scores without suppression of the hypothalamic–pituitary–adrenal axis. Budesonide can be used both in nasal irrigation or can be applied directly from respules.

Oxymetazoline hydrochloride and other topical nasal decongestant sprays cause intense vasoconstriction of the nasal mucosa. Rebound swelling (rhinitis medicomentosa) may incite a vicious cycle, leading to complete nasal obstruction and subsequent sinus disease. Oxymetazoline spray may be used for very short periods of time (less than 3 days) for symptomatic relief usually in ABRS or acute exacerbations of CRS.

Allergy Management

For patients with documented allergic disease, ongoing allergy management is beneficial. Environmental avoidance, topical nasal steroids, and immunotherapy may prevent exacerbations of allergic rhinitis. Immunotherapy is most effective for pollen, dust, molds, and pet dander allergies. Traditionally, treatments are via a subcutaneous route, but more recently sublingual immunotherapy has been gaining popularity especially in Europe. There is also a potentially beneficial role in aspirin desensitization for those patients with aspirin-exacerbated respiratory disease and Samter's triad.

Sinus Surgery

Maximal medical therapy for CRS is typically defined as 4–6 weeks of broad spectrum or culture-directed antibiotics, nasal steroids, nasal irrigation, allergy management, and a short course of oral steroids. Surgical therapy may be necessary if the patient remains symptomatic, and there is evidence of persistent mucosal disease or sinus obstruction on CT scan or endoscopic evaluation. Patients with clear anatomic abnormalities, large sinonasal polyps, or allergic fungal sinusitis may be better candidates for primary surgical therapy.

Patients should be strongly encouraged to stop smoking prior to considering sinus surgery. Current tobacco use is associated with worse outcomes after endoscopic sinus surgery when compared to nonsmokers. Work by Senior et al. demonstrated active smokers have higher rates of disease relapse after sinus surgery, requiring more revision surgeries than nonsmokers. In this study, 100% of patients with severe disease required a revision operation for persistent symptoms.

Functional Endoscopic Sinus Surgery (FESS)

Indications

Kennedy coined the term “functional endoscopic sinus surgery” to emphasize that surgery should aim at restoring normal sinus function and ventilation without excessive removal of potentially reversibly diseased tissue. Functional endoscopic sinus surgery is based on several key observations: (1) widely patent antrostomies in nonanatomic positions may fail to drain sinuses due to the directionality of mucociliary flow; (2) the ostiomeatal unit is anatomically constricted; and (3) the stripping of sinus mucosa leads to delayed healing and the loss of normal ciliary function. Thus, a conservative endoscopic technique has been developed. The keys to the technique are the use of “through-cutting” instruments that preserve sinonasal mucosa and the excellent visualization made possible with modern telescopes. Mucosal polyps can be carefully débrided, the natural ostia enlarged, and the ethmoid sinuses unroofed, which opens them to the nasal cavity. The improvement in symptoms with FESS may be expected in more than 90% of patients.

Relationship with Other Treatments

Sinus surgery should be considered as only a part of the treatment plan. Any underlying medical conditions, such as diabetes mellitus, immunodeficiency, tobacco use, and atopic disease, must also be addressed if ultimate success in treatment is to be obtained. Patients will require meticulous postoperative care including debridements, and, finally, long-term medical maintenance therapy.

Complications

The complications of surgical therapy are related to the close anatomic proximity of the paranasal sinuses to the brain and orbits. An intimate knowledge of the patient's individual anatomy is critical to reduce complications. Serious morbidity is rare, and includes cerebrospinal fluid leak (CSF) leaks, orbital injury, and intracranial hemorrhage. Injury to the medial wall of the orbit may cause the prolapse of orbital fat into the nasal cavity. A violation of the orbital wall, with subsequent hemorrhage and orbital hematoma, may lead to compression of the optic nerve and blindness. Damage to the cribriform plate region may lead to CSF leak, herniation of cranial contents, meningitis, or intracranial bleeding. In one large meta-analysis of patients who underwent FESS, the authors found the major complication rate was 0.85%, with CSF leak being the most common complication. Minor complications occurred in 6.9% of patients, with orbital penetration and middle turbinate adhesions being the most common.

Complications of Rhinosinusitis

Orbital Infection

Chandler divided the progression of sinonasal orbital infections into five stages (Table 15–3). The first stage is periorbital edema, which presents with cellulitis of the eyelids without visual loss or ophthalmoplegia. The second stage describes infection extending through the orbital septum and is classified as orbital cellulitis. These patients present with pain, proptosis, and chemosis. With orbital cellulitis, there may be some degree of ophthalmoplegia related to edema of the extraocular muscles, and a mild decrease in visual acuity related to corneal edema. The third stage involves formation of a subperiosteal abscess. The fourth stage is the formation of an orbital abscess. Severe proptosis, chemosis, ophthalmoplegia, and visual loss are usually present. The fifth stage results from retrograde thrombophlebitis of the valveless ophthalmic veins that can lead to cavernous sinus thrombosis.

Periorbital edema can usually be treated in an outpatient setting with oral antibiotics and close follow-up in the absence of medical comorbidities such as uncontrolled diabetes. Orbital cellulitis usually responds to intravenous antibiotics, whereas subperiosteal and orbital abscesses require operative drainage of the abscess with concurrent sinus surgery. Cavernous sinus thrombosis can truly be life-threatening. Even in the post-antibiotic era, the mortality rate of cavernous sinus thrombosis is 30%. Intravenous antibiotic treatment should be instituted immediately, and, if indicated, the involved sinuses should be surgically drained. The role of anticoagulation to prevent further thrombus formation and systemic steroid therapy is controversial. The incidence of all orbital complications is higher in the pediatric population than in adults.

Intracranial Complications

In the antibiotic era, intracranial complications of sinusitis have become less commonplace, but nevertheless continue to occur and be associated with significant morbidity and mortality. Meningitis usually occurs by extension of infection from the ethmoid or sphenoid sinuses. On examination, patients with this complication may have a diminished sensorium or may be obtunded. The typical signs of meningitis, such as Kernig and Brudzinski signs, may be present. If meningitis secondary to sinus infection is suspected, a high-resolution CT scan of the brain with contrast and a sinus CT scan should be obtained. A CT scan of the brain is critical both to rule out mass effect and to delineate any other intracranial complications. Lumbar puncture is diagnostic and provides material for culture. The treatment for meningitis involves intravenous antibiotics and surgical drainage of the sinuses. Anaerobic organisms are reported to be the most common pathogens in suppurative intracranial complications of sinusitis, but aerobic and mixed infections are also common.

An epidural abscess is a collection of purulent material between the bone of the skull and the dura, typically in relation to frontal sinusitis. The further spread of infection, either by direct extension or by hematogenous seeding, may lead to subdural empyema and eventually to brain abscess (Figure 15–3). Draining both the abscess and the offending sinuses is mandatory, and long-term antibiotics are often necessary. Regardless of the treatment, morbidity is high, particularly with subdural involvement, and can result in long-term neurologic sequela.

Pott Puffy Tumor

Pott puffy tumor is an osteomyelitis of the frontal bone with the development of a subperiosteal abscess manifesting as a puffy swelling on the forehead or scalp. It usually occurs as a complication of frontal sinusitis. Treatment is prompt surgical drainage and initiation of broad-spectrum antibiotics.

We would like to acknowledge Ashish R. Shah, MD, Frank N. Salamone, MD, and Thomas A. Tami, MD for their contribution to this chapter in the previous editions of CDT.