• 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.