Up to 30% of the adult population is allergic by skin testing to at least one common aeroallergen, and the percentage is probably much greater among patients presenting with a history of chronic sinusitis₁₁. Allergic rhinitis is probably the second most common predisposing condition to chronic sinusitis in children (after viral upper respiratory infection) and perhaps the most common predisposing factor in adults₁₁. A combination of allergic history and positive skin prick testing is key in the management of chronic sinusitis in a patient with allergic rhinitis. This condition causes mucosal inflammation and hypertrophy predisposing to blockage of the ostiomeatal complex. This is the reasoning behind innovating research directed at treating the anti-inflammatory response as a route of medical management in chronic rhinosinusitis₁₂,₁₃.

Sign and symptoms of chronic rhinosinusitis occur in response to irritant exposure. There is increasing evidence to support the theory that exposure to air pollution can impair mucociliary protection and potentates sensitivities to common aeroallergens by stagnation of this agents. Avoidance and protection against smoke, pollution, and occupational irritants usually is advised to counteract these predisposing factors₁₃.

Use of intranasal saline has been shown to decrease nasal symptoms and improve quality of life in allergic rhinitis and chronic rhinosinusitis. Saline spray increases mucociliary flow rates counter acting the effects of irritants and other numerous factors that affect mucociliary clearance. It also has a brief vasoconstrictive effect that leads to some short term symptomatic relief. Nasal saline irrigation also mechanically rinses away predisposing agents such as aeroallergens like pollen, mold, dust, and particulate of air pollution. Although it has some symptomatic relief, patients with chronic rhinosinusitis are told to use saline at least twice daily as a preventative measure rather than starting when clinical symptoms manifest.

An acidic milieu is thought to cause the “gel” state (more viscous) of mucus to predominate, where as an alkaline milieu is thought to cause the “sol” state to predominate. This is the rationale for adding baking soda to saline irrigation solutions₁₄.

Characteristically, chronic sinusitis forms thick viscid secretions. Any assistance in reducing viscosity of the secretion is helpful aiding sinus drainage and patient comfort.

Guaifenesin is the most commonly used mucolytic agent₁₄. High doses of this medication are required to obtain an effect on mucous. At these amounts, patients often experience emesis and abdominal pain. Other agents used previously are saturated solution of potassium iodide, acetyl cysteine and carbocysteine.

Systemic corticosteroid: It is sometimes contradictory to use an anti-inflammatory agent that can lead to immunosuppression like corticosteroids in the treatment of sinusitis which is consider having a significant association with microbial infection. Nonetheless, a short course of steroids can induce a significant anti-inflammatory and beneficial effect in the management of severe nasal mucosal congestion in allergic rhinitis patients. This brief period induce symptomatic relief and reduction of nasal and sinus mucosal inflammation promoting a better scenario for the management with topical agents, improving compliance and rate of benefit. Corticosteroids have multiple immunomodulator mechanisms including stabilization of mast cells against mediator release, block formation of inflammatory mediators, and inhibit chemotaxis of inflammatory cells₁₃,₁₄. It is important to keep in mind the adverse effect of systemic steroid use and the contraindications that include diabetes, peptic ulcer disease, glaucoma, severe hypertension, and advanced osteoporosis. Even a short course of steroids can significantly increase the blood pressure and glucose levels in patients with predisposition to hypertension and diabetes. Close monitoring and immediate withdrawal for side effects is warranted.

Topical corticosteroid: Topical nasal corticosteroids are a very effective form of treatment for allergic rhinitis and chronic rhinosinusitis. Their anti-inflammatory effect is localized and their systemic absorption has been shown to be negligible. The local reduction of inflammation prevents blockage and improve patency of the ostiomeatal complex. After use by at least 7 days, nasal corticosteroids have been shown to inhibit both immediate and late-phase reactions to antigenic stimulation in patients with allergic rhinitis. An estimated 90% of patients with allergic rhinitis will experience improvement in nasal allergy symptoms including chronic nasal congestion with topical nasal steroid preparations accounting for a marked increase in popularity of these medications over the last decade.

Currently, there are many products available, with no evidence to indicate that one is better than others. Initially, the spray is usually administered at the highest dose recommended and continued for at least 1 month. Often, a prolong treatment course of 3 to 6 months will be prescribed to help prevent recurrence. In patient with hyperplastic sinusitis or severe accompanying allergies, an indefinite course of nasal steroid therapy is prescribed₁₃,₁₄.

Some common adverse effects of topical nasal steroid use include nasal irritation, mucosal bleeding, and crusting. Septal perforation is a rare complication and the risk can be increased for patients living in very dry climates. The ingredient propylene glycol contained in the preparations is responsible for this complains. This can be alleviated by switching to an aqueous delivery system. The addition of nasal saline wash in conjunction with topical steroids can lessen or eliminate these common adverse effects.

A recent report has suggested that topical steroids may lead to open angle glaucoma₁₅. However, this was convincingly demonstrated only with prolonged use of pulmonary aerosols, which generally result in greatly increased blood level of active drug. A second study of nasal topical steroids only failed to show any increased in risk for ocular complications₁₆.

Decongestants are α-adrenergic agonists that induce a sympathetic response leading to vasoconstriction of dilated mucosal blood vessels. Decongestants are best used for short (3–5 days) courses at the beginning of treatment for sinusitis or allergic rhinitis.

Systemic decongestant: The most common oral decongestants are pseudoephedrine and phenylpropanolamine. This systemic agents achieve symptomatic relief, but lead to several adverse effects that are related to its sympathetic stimulation including insomnia, heart palpitations, and elevated blood pressure. Oral decongestants are indicated principally for symptomatic relief of nasal congestion and have not been shown to have therapeutic efficacy for the treatment of sinusitis₁₃,₁₄.

Topical decongestant: Topical agents include phenylephrine and oxymetazoline. This agents lead to a local excitation of alpha adrenergic receptors leading to a localize vasoconstriction and decrease of mucosal edema. All topical agents exhibit rebound vasodilation, which can be demonstrated by rhinometric analysis of nasal resistance as early as 3 days after beginning therapy. Clinical rebound congestion or rhinitis medicamentosa usually requires at least 10 days to 2 weeks of topical decongestant use to become apparent. This is the reasoning of using decongestants for short (3–5 days) courses at the beginning of treatment for sinusitis or allergic rhinitis₁₃,₁₄.

The use of antibiotics in chronic sinusitis is a topic of high controversy. It's efficacy, duration of therapy and agents to be use have been extensively debated. Some consensus is apparent on the idea that antibiotic therapy for chronic sinusitis should be based on culture results. This is based on the increase in antibiotic resistance that has been increasing consistently throughout the decades.

The culture can be obtained by direct visualization under endoscopy of purulent secretions from the middle meatus. Although the maxillary tap is the gold standard for culture diagnosis, this method is highly uncomfortable to the awake patient. Although there is not a definite large randomize control trial comparing both techniques, the endoscopic technique correlates well with the maxillary tap and is less traumatic to the alert patient. Nevertheless, the maxillary taps still a very effective tool especially on the ICU setting₁₇.

For initial empiric therapy, the antibiotic must cover the bacteria known to occur in this condition, specifically, staphylococcus, anaerobes, and gram negative bacilli. For this reason, amoxicillin/clavulanic acid is the preferred choice. Alternatives include clindamycin, cefuroxime and clarithromycin.Second line therapy would include ciprofloxacin, cefprozil or levofloxacin.

Bacterias have developed multiple mechanisms of resistance. Alteration of the penicillin binding proteins is the most common reason for penicillin resistance in Streptococcus pneumoniae infections. This mechanism of resistance is overcome by increasing the penicillin component to a much higher dose. This is the rational behind dosing children with 60 to 90 mg/kg per day instead of 40 mg/kg for amoxicillin. Haemophilus influenzae also utilize this type of resistance, but to a lesser degree.

According to the American Academy of Otolaryngology approximately 40% of Haemophilus. influenzae and greater than 90% of Moraxella catarrhalis produce beta-lactamase. This enzyme breaks down the b-lactam antibiotics. β-Lactamase-mediated resistance to the early second-generation cephalosporins is high among strains of Haemophilus influenzae and Moraxella catarrhalis. Stabilization of penicillin by adding clavulanate overcomes this enzymatic action.

Newer generation macrolides such as clarithromycin and azithromycin achieve excellent mucosal levels but should be considered backup drugs. Azithromycin appears to be more potent against Haemophilus Influenzae, whereas clarithromycin may be slightly better against intermediate resistant Streptococus pneumoniae.Bacteria's have also developed resistance against macrolide and even fluroquinolones.

Most authors recommend treating chronic sinusitis with a broad-spectrum antibiotic for up to 3 weeks. After 3 to 5 days of treatment there should be symptomatic improvement. After 10 to 15 days of treatment, symptoms should resolve. The logic of continuing therapy for another week is to allow for further diminution of mucosal edema and mucociliary function thus gaining resistance against new infection.

Many clinicians will follow the 3-week treatment course of antibiotics with a 3- to 6-week course of once-daily prophylactic antibiotic therapy for patients with a history of rapid recurrence after previous treatment. The goal is to get the patients through their window of vulnerability to new infection while mucosal recovery.

Prolonged use of low-dose macrolides in patients with chronic rhinosinusitis was found to be effective even when the identified bacterial pathogen was not sensitive to this agent. This management has also been found to decrease the size of nasal polyps.

The observation that macrolide antibiotics were steroid-sparing in patients who had steroid-dependent asthma has been present for decades. This was thought to be due to inhibition of steroid metabolism. The concept of using long-term, low-dose macrolides for treatment of chronic rhinosinusitis evolved further, primarily in Japan₁₈.

An interesting aspect of the pharmacokinetics of macrolide antibiotics is their extensive tissue uptake and intracellular accumulation. Macrolides accumulate in inflammatory cells at concentrations up to several hundred-fold higher than concentrations in extracellular fluid. The macrolide antibiotics decrease cytokine production (IL-5, IL-8, GM-CSF, TGF-β, IL-6, IL-8, TNF-α), altered structure and function of biofilm, reduced expression of cell surface leukocyte adhesion molecules, accelerate neutrophil apoptosis, impaired neutrophil oxidative burst, decrease secretion and improve mucociliary clearance, and Inhibited release of elastase, protease, phospholipase C, and eotaxin A by P aeruginosa₁₈. Clarithromycin is the macrolide most studied in CRS. While Azithromycin lack studies in CRS.

There is a new trend of research in the involvement of GERD in upper airway pathologies. Reflux is said to be associated to chronic rhinosinusitis. The mechanism is not cleared and studies are necessary to further enlighten this discussion. However, it is thought that the reflux of acid content reach the nasopharynx and nasal cavities leading to chronic mucosal irritation and sinusitis. Adult patients with chronic sinusitis and a history of heartburn could benefit from antireflux regimen including precautions and medication. In young children the relation is more evident presumably due to the closer proximity between the esophageal inlet and larynx to the soft palate and nasopharynx. Suspicion should rise in children with chronic congestion, rhinorrhea, excessive spitting up in infancy, low weight percentile, failure to thrive, chronic stridor and reactive airway disease.

Viral infections are the most common predisposing factors for sinusitis in children. Day care is an important risk factor for the development of viral infections due to the proximity and relation characteristics of children in this environment. The current management for viral infections is prevention by frequent hand washing and decrease exposure. Children with chronic rhinosinusitis may benefit from changing to a day care with fewer numbers of children to reduce viral exposure. Also an alternative are vacation periods from the daycare to allow for resolution of symptoms and decrease mucosal inflammation and improve mucocialliary clearance as a measure for improving natural resistance to the condition₁₇.

Interferon alpha-2 (IFN α2) can potentially block the penetration of viruses through respiratory mucosa. Intranasal IFN α2, when used as a once-a-day nasal aerosol, has been shown to potentially prevent colds in people exposed to family members with upper respiratory infections. Although medications like Interferon alpha2 has shown some improvement its usage is limited by its cost₁₃, ₁₄.