Manejo de infecciones nasosinusales

Manejo de infecciones nasosinusalesJos Ramn Reta Vela R2Dr. Martnez MBDefinicin EPOS (European position paper on rhinosinistis and nasal polyps)Inflamacin de la nariz y de SPN caracterizada por dos o ms sntomas:uno de los cuales debe ser obstruccin/congestin nasal o descarga nasal (anterior o posterior) dolor facial / presin facial hiposmia / anosmia

Signos objetivos de enfermedad nasal (endoscopia o TC)

Definicin. Clnica

Definicin EPOS (European position paper on rhinosinistis and nasal polyps)Signos objetivos de enfermedad nasal (endoscopia o TC)Signos endoscpicos de plipos y/o descarga mucopurulenta del meato medio; y/o edema de la mucosa que obstruya el meato medio

Definicin. Clnica

Definicin EPOS (European position paper on rhinosinistis and nasal polyps)Signos objetivos de enfermedad nasal (endoscopia o TC)Evidencia tomogrfica de cambios en la mucosa, senos o complejo ostiomeatal

Definicin. Clnica

Definicin. Criterios

ClasificacinSegn evolucin temporalPresentacin clnicaDiferente fisiopatologaRinosinusitis aguda 4 semanas

Rinosinusitis aguda recurrente 4 cuadros en 1 ao

Rinosinusitis subaguda 4-12 semanas

Rinosinusitis crnica 12 semanas

An inflammatory response is an expected sequela of an infectious process. Inflammation in the nose and sinuses from a variety of causes can result in sinus ostia obstruction and can predispose to the development of an infection. Many factors have been described as playing a role in the development of acute bacterial rhinosinusitis (ABRS).[1,4,5] These include the following factors related to the host: genetic factors such as immotile cilia syndrome and cystic fibrosis; anatomic variants such as a concha bullosa, septal spur, and paradoxical turbinate; certain systemic diseases or medical treatments that predispose individuals to infections; neoplasms; and allergic or immune disorders. Rhinosinusitis may also develop in relationship to environmental factors, as follows: bacterial, viral, or fungal infections, or inflammation that occurs secondary to fungal or bacterial colonization[2,6]; trauma; primary or secondary tobacco smoke exposure[7] and chronic or acute irritants or noxious chemicals; and iatrogenic factors, including surgery, medications, nasal packing, and nasogastric tube placement.[8] There is growing evidence that individuals with allergies have a higher incidence of both acute and chronic rhinosinusitis, and an association of acute bacterial rhinosinusitis with asthma has also been suggested, although this may also relate to the presence of allergic rhinitis.[9-11]The distinctions between acute rhinosinusitis (ARS), recurrent acute rhinosinusitis (RARS), subacute rhinosinusitis (SARS), chronic rhinosinusitis (CRS), and acute exacerbation of chronic rhinosinusitis (AECRS) are based on the temporal differences in the presentation and, in some cases, on the clinical presentation. Each of these subcategories may be associated with different pathophysiologic processes, and the predisposition to their development may vary from patient to patient. Given these differing etiologies, the pathogenesis is described here on the basis of this classification.

6Manejo medico. Factores

The treatment of CRS is based on a number of factors including the type of rhinosinusi tis (acute,. chronic, or fungal), concurrent medical comorbidities, symptom severity,and response to previous medical treatments (10). 7Manejo medico. Objetivos generales

In general, the treatment of CRS is intended to reduce symptoms, improve quality of life,. and prevent disease progressionor recurrence. More specifically, treatments are aimed at reducing mucosal inflammation, controlling infection, and restoring mucodliary clearance. Medical treatmentshould be considered the cornerstone of disease treatment for CRS, with sinus surgery reserved for medical failures or for patients with complications.

8Manejo medico. Objetivos especficosIn general, the treatment of CRS is intended to reduce symptoms, improve quality of life,. and prevent disease progressionor recurrence. More specifically, treatments are aimed at reducing mucosal inflammation, controlling infection, and restoring mucodliary clearance. Medical treatmentshould be considered the cornerstone of disease treatment for CRS, with sinus surgery reserved for medical failures or for patients with complications.

9Manejo medicoPilar del tratamientoManejo QUIRURGICOFallas en tratamientoPresencia de complicacionesManejo medicoAnti infecciosoAntiinflamatorio

Tratamiento medicoTx medico. EsteroidesCorticosteroids constitute first-line therapy in the medical management of CRS. Glucocorticoids have wide-rangingeffects on the nasal mucosa. Studies of glucocorticoids show that they can suppress many phases of the inflammatoryprocess by inhibiting the release of vasoactive mediators, reducing vasodilation, fluid extravasation, edema, andlocal deposition of mediators (12). Glucocorticoid-treated NP have demonstrated a down-regulation of proinflammatorycytokines and adhesion molecules that attract and activate eosinophils (13,13a). Studies of asthma and allergic rhinitis (AR) show that glucocorticoids decrease a wide variety of proinflammatory cytokines, chemokines, adhesion molecules, and mediator-synthesizing enzymessuch as inducible nitric oxide synthase,. cyclooxygenase-2, 588 Section II: Rhinology and Allergy and phospholipase-A2 (13,13a,14). Both topical and oral corticosteroids are used frequently for CRS and are discussed in the following two sections.13Tx medico. EsteroidesCorticosteroids constitute first-line therapy in the medical management of CRS. Glucocorticoids have wide-rangingeffects on the nasal mucosa. Studies of glucocorticoids show that they can suppress many phases of the inflammatoryprocess by inhibiting the release of vasoactive mediators, reducing vasodilation, fluid extravasation, edema, andlocal deposition of mediators (12). Glucocorticoid-treated NP have demonstrated a down-regulation of proinflammatorycytokines and adhesion molecules that attract and activate eosinophils (13,13a). Studies of asthma and allergic rhinitis (AR) show that glucocorticoids decrease a wide variety of proinflammatory cytokines, chemokines, adhesion molecules, and mediator-synthesizing enzymessuch as inducible nitric oxide synthase,. cyclooxygenase-2, 588 Section II: Rhinology and Allergy and phospholipase-A2 (13,13a,14). Both topical and oral corticosteroids are used frequently for CRS and are discussed in the following two sections.14Tx medico. Esteroides tpicosA number of studies have demonstrated the efficacy of intranasal steroids in the management of CRS with NP. These sprays are used most commonly in the management of symptoms associated with seasonal and perennial AR (15). Nasal corticosteroids have been shown to inhibit both immediate- and late-phase reactions to antigenic stimulation in patients with AR ( 16 ). In generaL nasal steroids with low systemic bioavailability (such as mometasone furoate, fluticasone propionate, or furoate) have not been associated with bone growth or adrenal suppression, which was first noted with more systemically bioavailable agents such as bedomethasone dipropionate (17). There is also no dearevidence that the use of nasal corticosteroids correlates with systemic changes in bone mineral biology, cataracts, or glaucoma. Adverse effects such as nasal irritation, epistaxis, and crusting with nasal steroids are rare, occurring in less than 10% of patients (18). Rarely, septal perforations have been reported with nasal steroid spray usage. Therefore, to minimize epistaxis and possible perforation, patients are frequendy instmcted to direct the nasal spray toward the internal lateral aspect of the nasal cavity and not toward the nasal septum. Topical steroids are routinely used to treat CRS with eosinophilic inflammation or NP. Guidelines from the 2007 European Position Paper on Rhinosinusitis and Nasal Polyps (19) recommends topical steroids as the firstline medication based on the results of several randomized controlled trials with fluticasone propionate, bedomethasone dipropionate, budesonide or mometasone furoate. Studies have demonstrated that topical corticosteroids are beneficial in the treatment of small to medium-sized polyps, nasal symptoms, and that this effect can be maintained with continued use (20-24). Corticosteroid nasal sprays have also been shown to delay the recurrence of polyps after surgery (24,25). There has also been some recent literature describing the use ofbudesonide respules (Pulmicort; AstraZeneca, Wilmington, DE) as an adjuvant method of treating eosinophilic or polypoid CRS when the respules are directly applied as a nasal drop or as an additive to nasal irrigation (26,27). In theory. a much higher concentration of corticosteroids can be applied to the sinus mucosa with budesonide respules compared to conventional nasal steroid sprays.Despite proven efficacy of intranasal steroids for CRS with NP. benefit for nonpolypoid CRS has been harder to demonstrate (28-31). A randomized, double-blind, placebo-controlled study on patients with CRS without NP found no significant improvement on endoscopy andsymptoms scores with fluticasone propionate for 16 weeks (32). More research is required to support the use of intranasal steroids for CRS without NP. 15Tx medico. Esteroides tpicosA number of studies have demonstrated the efficacy of intranasal steroids in the management of CRS with NP. These sprays are used most commonly in the management of symptoms associated with seasonal and perennial AR (15). Nasal corticosteroids have been shown to inhibit both immediate- and late-phase reactions to antigenic stimulation in patients with AR ( 16 ). In generaL nasal steroids with low systemic bioavailability (such as mometasone furoate, fluticasone propionate, or furoate) have not been associated with bone growth or adrenal suppression, which was first noted with more systemically bioavailable agents such as bedomethasone dipropionate (17). There is also no dearevidence that the use of nasal corticosteroids correlates with systemic changes in bone mineral biology, cataracts, or glaucoma. Adverse effects such as nasal irritation, epistaxis, and crusting with nasal steroids are rare, occurring in less than 10% of patients (18). Rarely, septal perforations have been reported with nasal steroid spray usage. Therefore, to minimize epistaxis and possible perforation, patients are frequendy instmcted to direct the nasal spray toward the internal lateral aspect of the nasal cavity and not toward the nasal septum. Topical steroids are routinely used to treat CRS with eosinophilic inflammation or NP. Guidelines from the 2007 European Position Paper on Rhinosinusitis and Nasal Polyps (19) recommends topical steroids as the firstline medication based on the results of several randomized controlled trials with fluticasone propionate, bedomethasone dipropionate, budesonide or mometasone furoate. Studies have demonstrated that topical corticosteroids are beneficial in the treatment of small to medium-sized polyps, nasal symptoms, and that this effect can be maintained with continued use (20-24). Corticosteroid nasal sprays have also been shown to delay the recurrence of polyps after surgery (24,25). There has also been some recent literature describing the use ofbudesonide respules (Pulmicort; AstraZeneca, Wilmington, DE) as an adjuvant method of treating eosinophilic or polypoid CRS when the respules are directly applied as a nasal drop or as an additive to nasal irrigation (26,27). In theory. a much higher concentration of corticosteroids can be applied to the sinus mucosa with budesonide respules compared to conventional nasal steroid sprays.Despite proven efficacy of intranasal steroids for CRS with NP. benefit for nonpolypoid CRS has been harder to demonstrate (28-31). A randomized, double-blind, placebo-controlled study on patients with CRS without NP found no significant improvement on endoscopy andsymptoms scores with fluticasone propionate for 16 weeks (32). More research is required to support the use of intranasal steroids for CRS without NP. 16Tx medico. Esteroides sistmicosOral corticosteroids are commonly used in the treatment of CRS with and without NP for recalcitrant cases or when a rapid, short-term improvement is needed (33,34). However, despite widespread use among both general otolaryngologists and rhinologists, there is a lackof strong evidence with respect to indication, dose and duration (35,36). In 2007, a Cochrane review found only one randomized, controlled trial (3 7) on oral steroid therapy for CRS with NP (33). The results of this study and others have shown that oral steroids can dramaticallyreduce polyp size in patients with CRS, reduce nasal obstruction, improve quality of life scores, and decrease inflammatory chemokines and cytokines (37-40). But without other adjuvant treatments, these benefits are usually short-lived (40). Recent evidence suggests thatcombination therapy with oral and intranasal corticosteroids can provide long-term reduction in polyp size and improvements in quality of life without significant adverse effects (41). The most common side effects of oral steroid use include glucose intolerance, hypertension, gastrointestinal bleeding, and altered mood. Adverse effects associated with long-term use of oral steroids include weight gain, glaucoma, cataracts, gastrointestinal complications, adrenal suppression, growth suppression, diabetes mellitus, osteoporosis, and avascular necrosis (most commonly of the hip) (33). These risks must be carefully considered, and patients must be counseled about these side effects prior to initiating long-term therapy. 17Tx medico. Esteroides sistmicosOral corticosteroids are commonly used in the treatment of CRS with and without NP for recalcitrant cases or when a rapid, short-term improvement is needed (33,34). However, despite widespread use among both general otolaryngologists and rhinologists, there is a lackof strong evidence with respect to indication, dose and duration (35,36). In 2007, a Cochrane review found only one randomized, controlled trial (3 7) on oral steroid therapy for CRS with NP (33). The results of this study and others have shown that oral steroids can dramaticallyreduce polyp size in patients with CRS, reduce nasal obstruction, improve quality of life scores, and decrease inflammatory chemokines and cytokines (37-40). But without other adjuvant treatments, these benefits are usually short-lived (40). Recent evidence suggests thatcombination therapy with oral and intranasal corticosteroids can provide long-term reduction in polyp size and improvements in quality of life without significant adverse effects (41). The most common side effects of oral steroid use include glucose intolerance, hypertension, gastrointestinal bleeding, and altered mood. Adverse effects associated with long-term use of oral steroids include weight gain, glaucoma, cataracts, gastrointestinal complications, adrenal suppression, growth suppression, diabetes mellitus, osteoporosis, and avascular necrosis (most commonly of the hip) (33). These risks must be carefully considered, and patients must be counseled about these side effects prior to initiating long-term therapy. 18Tx medico. AntibioticoterapiaAntibiotics are commonly used in the management of CRS to decrease bacterial load and to treat acute bacterial exacerbations of CRS. There are significant differences in the bacteria present in CRS as compared to acute rhinosinusitis. Antibiotic therapy for CRS has traditionallybeen aimed at a mixed population of aerobic and anaerobic bacteria. However, despite level lA evidence of the efficacy of topical steroids in treating rhinosinusitis, no such evidence of antibiotic efficacy in CRS exists and no antibiotic is U.S. Food and Drug Administration FDA)approved for the indication of treating CRS. Commonly used agents include amoxicillin-clavulanate, clindamycin, trimethoprim-sulfamethoxazole, or a fluoroquinolone. The optimal duration of therapy has not been studied prospectively, but is typically 3 to 4 weeks long, with longer courses for recalcitrant cases. When treating CRS with antibiotics, it is important that other modalities, such as nasal irrigation and topical or oral corticosteroids, also be included. The species ofbacteria and the incidence of antibiotic resistance vary widely depending on a variety of factors including the chronicity of the disease and the extent of prior antibiotic therapy. The microbiology of CRS differs from that of arute rhinosinusitis, with a greater incidence of anaerobic bacteria, Staphylococcus aureus, and Pseudomonas aeruginosa, all which must be considered before recommending antibiotics. In a study by Finegold et al. (42) the most common anaerobic bacteria in chronic maxillary sinusitis were PrevoteUa species, anaerobic streptococci, and Fusobacterium species. The most common aerobic bacteria were Streptococcus species, Haemophilus species, P. aeruginosa, S. aureus, and MoraxeUa catarrhalis. The microbiology of chronic frontal sinusitis is slightly different with 21% S. aureus, 21% coagulase-negative staphylococci, 9% Haemophilus injluenzae, and 26% multiple organisms in one study ( 43). Anaerobes were present in 3% and fungi in 4%, and there was no growth in 38%. The bacteriology of odontogenic infections tends to mirrorthat of oral flora. The microbiology of arute exacerbations of CRS is more similar to the microbiology of arute bacterial sinusitis than CRS (44).When possible, antibiotics for recalcitrant infections should be started after cultures have been obtained and be based on sensitivities. The results of antimicrobial susceptibilities and bacterial presence changed the therapy of almost 50% of patients in a retrospective, conserutive series of patients with CRS or arute exacerbations of CRS ( 44 ). If this is not possible, several factors must be considered prior to selecting empiric antimicrobial therapy. The 2004 Guidelines from the Sinus and Allergy Partnership ( 45) recommend a fluoroquinolone or high-dose amo:xicillin-clavulanate for patients who have received antibiotics within the past 4 to 6 weeks, as recent use of prior antibiotics is a riskfactor the presence of antibiotic-resistant bacteria. In cases of penicillin allergy. one alternative would be clindamycin and Bactrim ( rimethoprim-sulfamethoxazole) as the combination provides strong anaerobic and aerobic coverage. Antimicrobial susceptibility rates vary geographically and by anatomic location. Local hospital antibiograms may be helpful in guiding empiric antimicrobial choices.Recent investigations have confirmed the presence of biofilms on the mucosa of patients with CRS ( 46). Bacterial biofilms are highly organized structures composed of communities of bacteria encased within a protective extracellular matrix. Biofilms are notoriously difficult to eradicate,and might explain the high incidence of symptom relapse in some patient with CRS. P. aeruginosa, H. injluenzae, and S. aureus are the most common biofilm-forming bacteria seen in sinus infections. Interestingly, persistent symptoms after functional endoscopic sinus surgery and surgical failures have been recently been attributed to the presence of biofilms (47,48). The most common treatments for biofilm-assodated sinusitis include topical antibiotics, surgery. mechanical debridement, and surfactants (46,49). Antifungal therapy for CRS is still controversial atthis time. Recent double-blind, placebo-controlled trials have not shown substantial improvement of CRS based on objective and subjective criteria after treatment with amphotericin B (50,51). Another placebo-controlled trial by Kennedy et al. (52) found no improvement with theantifungal terbinafine on symptoms or radiographing findings in patients with CRS. The preceding topical antifungal and oral antifungal studies were not restricted to patients with fungus present on culture or histopathologically. Seiberling and Wormald (53) showed in a retrospectivecase series, restricted to patients with refractory allergic or nonallergic sinusitis associated with fungus histopathologically that oral itraconazole improved symptoms and endoscopic examination. Better designed studies targeting patients with evidence of fungus histopathologically arerequired to fully answer the question of the role of antifungals in a subset of patients with CRS associated with fungus. 19Tx medico. AntibioticoterapiaAntibiotics are commonly used in the management of CRS to decrease bacterial load and to treat acute bacterial exacerbations of CRS. There are significant differences in the bacteria present in CRS as compared to acute rhinosinusitis. Antibiotic therapy for CRS has traditionallybeen aimed at a mixed population of aerobic and anaerobic bacteria. However, despite level lA evidence of the efficacy of topical steroids in treating rhinosinusitis, no such evidence of antibiotic efficacy in CRS exists and no antibiotic is U.S. Food and Drug Administration FDA)approved for the indication of treating CRS. Commonly used agents include amoxicillin-clavulanate, clindamycin, trimethoprim-sulfamethoxazole, or a fluoroquinolone. The optimal duration of therapy has not been studied prospectively, but is typically 3 to 4 weeks long, with longer courses for recalcitrant cases. When treating CRS with antibiotics, it is important that other modalities, such as nasal irrigation and topical or oral corticosteroids, also be included. The species ofbacteria and the incidence of antibiotic resistance vary widely depending on a variety of factors including the chronicity of the disease and the extent of prior antibiotic therapy. The microbiology of CRS differs from that of arute rhinosinusitis, with a greater incidence of anaerobic bacteria, Staphylococcus aureus, and Pseudomonas aeruginosa, all which must be considered before recommending antibiotics. In a study by Finegold et al. (42) the most common anaerobic bacteria in chronic maxillary sinusitis were PrevoteUa species, anaerobic streptococci, and Fusobacterium species. The most common aerobic bacteria were Streptococcus species, Haemophilus species, P. aeruginosa, S. aureus, and MoraxeUa catarrhalis. The microbiology of chronic frontal sinusitis is slightly different with 21% S. aureus, 21% coagulase-negative staphylococci, 9% Haemophilus injluenzae, and 26% multiple organisms in one study ( 43). Anaerobes were present in 3% and fungi in 4%, and there was no growth in 38%. The bacteriology of odontogenic infections tends to mirrorthat of oral flora. The microbiology of arute exacerbations of CRS is more similar to the microbiology of arute bacterial sinusitis than CRS (44).When possible, antibiotics for recalcitrant infections should be started after cultures have been obtained and be based on sensitivities. The results of antimicrobial susceptibilities and bacterial presence changed the therapy of almost 50% of patients in a retrospective, conserutive series of patients with CRS or arute exacerbations of CRS ( 44 ). If this is not possible, several factors must be considered prior to selecting empiric antimicrobial therapy. The 2004 Guidelines from the Sinus and Allergy Partnership ( 45) recommend a fluoroquinolone or high-dose amo:xicillin-clavulanate for patients who have received antibiotics within the past 4 to 6 weeks, as recent use of prior antibiotics is a riskfactor the presence of antibiotic-resistant bacteria. In cases of penicillin allergy. one alternative would be clindamycin and Bactrim ( rimethoprim-sulfamethoxazole) as the combination provides strong anaerobic and aerobic coverage. Antimicrobial susceptibility rates vary geographically and by anatomic location. Local hospital antibiograms may be helpful in guiding empiric antimicrobial choices.Recent investigations have confirmed the presence of biofilms on the mucosa of patients with CRS ( 46). Bacterial biofilms are highly organized structures composed of communities of bacteria encased within a protective extracellular matrix. Biofilms are notoriously difficult to eradicate,and might explain the high incidence of symptom relapse in some patient with CRS. P. aeruginosa, H. injluenzae, and S. aureus are the most common biofilm-forming bacteria seen in sinus infections. Interestingly, persistent symptoms after functional endoscopic sinus surgery and surgical failures have been recently been attributed to the presence of biofilms (47,48). The most common treatments for biofilm-assodated sinusitis include topical antibiotics, surgery. mechanical debridement, and surfactants (46,49). Antifungal therapy for CRS is still controversial atthis time. Recent double-blind, placebo-controlled trials have not shown substantial improvement of CRS based on objective and subjective criteria after treatment with amphotericin B (50,51). Another placebo-controlled trial by Kennedy et al. (52) found no improvement with theantifungal terbinafine on symptoms or radiographing findings in patients with CRS. The preceding topical antifungal and oral antifungal studies were not restricted to patients with fungus present on culture or histopathologically. Seiberling and Wormald (53) showed in a retrospectivecase series, restricted to patients with refractory allergic or nonallergic sinusitis associated with fungus histopathologically that oral itraconazole improved symptoms and endoscopic examination. Better designed studies targeting patients with evidence of fungus histopathologically arerequired to fully answer the question of the role of antifungals in a subset of patients with CRS associated with fungus. 20

Tx medico. AntibioticoterapiaAntibiotics are commonly used in the management of CRS to decrease bacterial load and to treat acute bacterial exacerbations of CRS. There are significant differences in the bacteria present in CRS as compared to acute rhinosinusitis. Antibiotic therapy for CRS has traditionallybeen aimed at a mixed population of aerobic and anaerobic bacteria. However, despite level lA evidence of the efficacy of topical steroids in treating rhinosinusitis, no such evidence of antibiotic efficacy in CRS exists and no antibiotic is U.S. Food and Drug Administration FDA)approved for the indication of treating CRS. Commonly used agents include amoxicillin-clavulanate, clindamycin, trimethoprim-sulfamethoxazole, or a fluoroquinolone. The optimal duration of therapy has not been studied prospectively, but is typically 3 to 4 weeks long, with longer courses for recalcitrant cases. When treating CRS with antibiotics, it is important that other modalities, such as nasal irrigation and topical or oral corticosteroids, also be included. The species ofbacteria and the incidence of antibiotic resistance vary widely depending on a variety of factors including the chronicity of the disease and the extent of prior antibiotic therapy. The microbiology of CRS differs from that of arute rhinosinusitis, with a greater incidence of anaerobic bacteria, Staphylococcus aureus, and Pseudomonas aeruginosa, all which must be considered before recommending antibiotics. In a study by Finegold et al. (42) the most common anaerobic bacteria in chronic maxillary sinusitis were PrevoteUa species, anaerobic streptococci, and Fusobacterium species. The most common aerobic bacteria were Streptococcus species, Haemophilus species, P. aeruginosa, S. aureus, and MoraxeUa catarrhalis. The microbiology of chronic frontal sinusitis is slightly different with 21% S. aureus, 21% coagulase-negative staphylococci, 9% Haemophilus injluenzae, and 26% multiple organisms in one study ( 43). Anaerobes were present in 3% and fungi in 4%, and there was no growth in 38%. The bacteriology of odontogenic infections tends to mirrorthat of oral flora. The microbiology of arute exacerbations of CRS is more similar to the microbiology of arute bacterial sinusitis than CRS (44).When possible, antibiotics for recalcitrant infections should be started after cultures have been obtained and be based on sensitivities. The results of antimicrobial susceptibilities and bacterial presence changed the therapy of almost 50% of patients in a retrospective, conserutive series of patients with CRS or arute exacerbations of CRS ( 44 ). If this is not possible, several factors must be considered prior to selecting empiric antimicrobial therapy. The 2004 Guidelines from the Sinus and Allergy Partnership ( 45) recommend a fluoroquinolone or high-dose amo:xicillin-clavulanate for patients who have received antibiotics within the past 4 to 6 weeks, as recent use of prior antibiotics is a riskfactor the presence of antibiotic-resistant bacteria. In cases of penicillin allergy. one alternative would be clindamycin and Bactrim ( rimethoprim-sulfamethoxazole) as the combination provides strong anaerobic and aerobic coverage. Antimicrobial susceptibility rates vary geographically and by anatomic location. Local hospital antibiograms may be helpful in guiding empiric antimicrobial choices.Recent investigations have confirmed the presence of biofilms on the mucosa of patients with CRS ( 46). Bacterial biofilms are highly organized structures composed of communities of bacteria encased within a protective extracellular matrix. Biofilms are notoriously difficult to eradicate,and might explain the high incidence of symptom relapse in some patient with CRS. P. aeruginosa, H. injluenzae, and S. aureus are the most common biofilm-forming bacteria seen in sinus infections. Interestingly, persistent symptoms after functional endoscopic sinus surgery and surgical failures have been recently been attributed to the presence of biofilms (47,48). The most common treatments for biofilm-assodated sinusitis include topical antibiotics, surgery. mechanical debridement, and surfactants (46,49). Antifungal therapy for CRS is still controversial atthis time. Recent double-blind, placebo-controlled trials have not shown substantial improvement of CRS based on objective and subjective criteria after treatment with amphotericin B (50,51). Another placebo-controlled trial by Kennedy et al. (52) found no improvement with theantifungal terbinafine on symptoms or radiographing findings in patients with CRS. The preceding topical antifungal and oral antifungal studies were not restricted to patients with fungus present on culture or histopathologically. Seiberling and Wormald (53) showed in a retrospectivecase series, restricted to patients with refractory allergic or nonallergic sinusitis associated with fungus histopathologically that oral itraconazole improved symptoms and endoscopic examination. Better designed studies targeting patients with evidence of fungus histopathologically arerequired to fully answer the question of the role of antifungals in a subset of patients with CRS associated with fungus. 22Tx medico. Irrigaciones nasalesSaline nasal irrigation has been recommended in the most recent clinical guidelines published in 2007 for CRS and a Cochrane review (6,65). Saline irrigation mechanically removes mucus, crusts, debris, and allergens from the sinonasal cavity, and potentially has the additional benefit of improving mucociliary clearance. ciliary beat frequency, and protecting the sinonasal mucosa (65). Large volume. low-pressure nasal irrigation is more effective than saline sprays or nebulizers in penetrating the sinus ostia (66,67) . In eight randomized trials, nasal saline irrigation for CRSimproved symptoms, quality of life. endoscopic findings, and was well tolerated and without significant harmful side effects (65).Saline irrigation may prevent rhinosinusitis. In a randomized trial, daily hypertonic saline nasal irrigation improved disease-specific quality of life after 6 months (68). With 87% adherence to therapy, side effects in this study were minimal and included: nasal irritation. epistaxis,nasal burning, tearing, and headaches. In a follow- up study, a subset of patients reported reduced sinus symptoms and sinusitis-related medication use for an additional 12 months (69). Other recent data suggest that Dead Sea Salt hypertonic saline irrigation may be morebeneficial than standard hypertonic saline irrigation for CRS symptoms (70). Studies on the effects of hypertonic saline irrigation on cilia and mucociliary clearance are conflicting. In vivo data suggest that hypertonic solutions may improve mucociliary clearance more than isotonic saline (71 ), however, there are some in vitro data suggesting that hypertonic may cause a temporary decrease in ciliary beat frequency (72, 73).Clinicians should work with patients to develop strategies that facilitate incorporating saline nasal irrigations as part of routine sinus care. It is also important to emphasize that rinse bottles be cleaned at least once a week, as there is evidence that irrigation may increase the frequency of gram-negative organisms on culture (74} .23Tx medico. Irrigaciones nasalesSaline nasal irrigation has been recommended in the most recent clinical guidelines published in 2007 for CRS and a Cochrane review (6,65). Saline irrigation mechanically removes mucus, crusts, debris, and allergens from the sinonasal cavity, and potentially has the additional benefit of improving mucociliary clearance. ciliary beat frequency, and protecting the sinonasal mucosa (65). Large volume. low-pressure nasal irrigation is more effective than saline sprays or nebulizers in penetrating the sinus ostia (66,67) . In eight randomized trials, nasal saline irrigation for CRSimproved symptoms, quality of life. endoscopic findings, and was well tolerated and without significant harmful side effects (65).Saline irrigation may prevent rhinosinusitis. In a randomized trial, daily hypertonic saline nasal irrigation improved disease-specific quality of life after 6 months (68). With 87% adherence to therapy, side effects in this study were minimal and included: nasal irritation. epistaxis,nasal burning, tearing, and headaches. In a follow- up study, a subset of patients reported reduced sinus symptoms and sinusitis-related medication use for an additional 12 months (69). Other recent data suggest that Dead Sea Salt hypertonic saline irrigation may be morebeneficial than standard hypertonic saline irrigation for CRS symptoms (70). Studies on the effects of hypertonic saline irrigation on cilia and mucociliary clearance are conflicting. In vivo data suggest that hypertonic solutions may improve mucociliary clearance more than isotonic saline (71 ), however, there are some in vitro data suggesting that hypertonic may cause a temporary decrease in ciliary beat frequency (72, 73).Clinicians should work with patients to develop strategies that facilitate incorporating saline nasal irrigations as part of routine sinus care. It is also important to emphasize that rinse bottles be cleaned at least once a week, as there is evidence that irrigation may increase the frequency of gram-negative organisms on culture (74} .24Tx medico. AntihistamnicosAntihistamines are commonly prescribed medications for patients with AR There is a lack of evidence that antihistaminesare effective in the treatment of CRS, but these drugs have been used for patients with concurrent allergies. Firstgeneration antihistamines, including diphenhydramine, can cause sedation, dry mouth, urinary retention, and potentially drying of nasal and sinus secretions. These side effects are far less common or absent in newer second generation antihistamines. Some common antihistamines are listed in Table 39.3. Unlike oral antihistamines, nasal antihistamines are not only effective for rhinorrhea, sneezing, and itchy nose, butare also effective for nasal congestion. Combination of an antihistamine nasal spray with a nasal steroid spray may significantly increase symptom control in AR. compared to either spray used alone (75).25Tx medico. AntihistamnicosAntihistamines are commonly prescribed medications for patients with AR There is a lack of evidence that antihistaminesare effective in the treatment of CRS, but these drugs have been used for patients with concurrent allergies. Firstgeneration antihistamines, including diphenhydramine, can cause sedation, dry mouth, urinary retention, and potentially drying of nasal and sinus secretions. These side effects are far less common or absent in newer second generation antihistamines. Some common antihistamines are listed in Table 39.3. Unlike oral antihistamines, nasal antihistamines are not only effective for rhinorrhea, sneezing, and itchy nose, butare also effective for nasal congestion. Combination of an antihistamine nasal spray with a nasal steroid spray may significantly increase symptom control in AR. compared to either spray used alone (75).26Tx medico. DescongestionantesOral and nasal decongestants are used for rhinorrhea and nasal congestion_ but side effects prohibit prolonged use(76). Pseudoephedrine is available behind the counter. Phenylephrine is only a weak decongestant, while phenylpropanolaminewas removed from the market because of an association with stroke in young women. Common side effects can include anxiety, insomnia, irritability, headache. palpitations, hypertension, and decreased urinary flow. Contraindications include patients with cardiacdisease such as coronary artery disease. and concurrent use of monoamine oxidase inhibitors (MAO)-inhibitors. Prolonged and repeated use of nasal decongestant sprays often results in rhinitis medicamentosa, or severe rebound congestion. after drug withdrawal27Tx medico. DescongestionantesOral and nasal decongestants are used for rhinorrhea and nasal congestion_ but side effects prohibit prolonged use(76). Pseudoephedrine is available behind the counter. Phenylephrine is only a weak decongestant, while phenylpropanolaminewas removed from the market because of an association with stroke in young women. Common side effects can include anxiety, insomnia, irritability, headache. palpitations, hypertension, and decreased urinary flow. Contraindications include patients with cardiacdisease such as coronary artery disease. and concurrent use of monoamine oxidase inhibitors (MAO)-inhibitors. Prolonged and repeated use of nasal decongestant sprays often results in rhinitis medicamentosa, or severe rebound congestion. after drug withdrawal28Tx medico. anticolinrgicosIpratropium bromide (Atrovent) nasal spray is generally used two to four times per day to treat rhinorrhea due to allergic and vasomotor rhinitis (77, 78). It is an anticholinergic (parasympatholytic) agent that acts by inhibiting vagally mediated reflexes by antagonizing the action of acetylcholine, thus decreasing secretions from the serous and seromucous glands lining the nasal mucosa. To increase theeffectiveness in treating rhinorrhea. anticholinergic sprays can be combined with an intranasal steroid spray (77).29Tx medico. Inhibidores de leucotrienosInhibitors or antagonists of leukotrienes are approved by the U. S. Food and Drug Administration for the treatment of allergy and asthma. Leukotrienes are inflammatory mediators that are produced by a number of cell types including mast cells, eosinophils, basophils, macrophages, and monocytes (79). Activation of specific receptors leads to a variety of biologic effects including contraction of human airway smooth muscle, chemotaxis, and increased vascular permeability. Leukotrienes as well as other arachidonic add metabolites have been found in high levels in patients with asthma as well as from patients with NP. Studies have demonstrated that leukotriene inhibitors can reduce sinonasal symptomsand NP, especially in patients with Aspirin-exacerbated respiratory disease (79,80). There is also some evidence that leukotriene-receptor antagonists might be useful after ESS in patients with NP to limit polyp regrowth and improve nasal and pulmonary symptoms (81). At this time, more research is required to determine which subset of patients with CRS with NPs will benefit most from leukotriene inhibitors. 30Tx medico. inmunoterapiaThe association of AR and CRS is unclear, but because many of the symptoms of AR mimic symptoms of CRS, AR should be thoroughly evaluated and treated in patients with CRS. Rhinitis is common, affecting up to 40% of children and between 10% and 30% of adults (77). Allergen avoidance is the mainstay of management for patients with AR, with antihistamines and topical nasal steroids for symptomaticrelief (82). AR causes symptoms similar to those seen in CRS, such as nasal congestion and nasal drainage. Allergy may cause sinusitis by inducing mucus hypersecretion and obstruction of the ostiomeatal complex by mucosal edema. Subcutaneous immunotherapy (SCIT) is effective for perennial and seasonal AR. SCIT improves symptoms, reduces medication required, and prevents developmentof new allergies and asthma in children. These effects can persist for at least 3 years after discontinuation of treatment The mechanism of SCIT is not completely understood but is associated with the generation of allergen-specific T regulatory cells, which are known to be capable of suppressing allergen-induced proliferation and cytokine response. In addition, antibody class switching of B cells from allergen-specific IgE to allergen-specific IgG4 occurs and these allergen-specific IgG4 antibodies may inhibit binding between allergen and IgE on mast cells and basophils (83). A Cochrane review concluded that SCIT is a safe and valid treatment for AR ( 84). Sublingual immunotherapy (Sur) has emerged as a promising alternative to injection immunotherapy (85,86). Although highly effective, SCIT commonly causes pain andswelling at the injection site with a rare risk of severe systemic and life-threatening reactions. A recent review found support for SLIT in children and for use in AR due to seasonal allergens and dust mites (85). However, more study is necessary to optimize allergen dosages, treatment duration, and improve criteria for patient selection. 31Tx medico. inmunoterapiaThe association of AR and CRS is unclear, but because many of the symptoms of AR mimic symptoms of CRS, AR should be thoroughly evaluated and treated in patients with CRS. Rhinitis is common, affecting up to 40% of children and between 10% and 30% of adults (77). Allergen avoidance is the mainstay of management for patients with AR, with antihistamines and topical nasal steroids for symptomaticrelief (82). AR causes symptoms similar to those seen in CRS, such as nasal congestion and nasal drainage. Allergy may cause sinusitis by inducing mucus hypersecretion and obstruction of the ostiomeatal complex by mucosal edema. Subcutaneous immunotherapy (SCIT) is effective for perennial and seasonal AR. SCIT improves symptoms, reduces medication required, and prevents developmentof new allergies and asthma in children. These effects can persist for at least 3 years after discontinuation of treatment The mechanism of SCIT is not completely understood but is associated with the generation of allergen-specific T regulatory cells, which are known to be capable of suppressing allergen-induced proliferation and cytokine response. In addition, antibody class switching of B cells from allergen-specific IgE to allergen-specific IgG4 occurs and these allergen-specific IgG4 antibodies may inhibit binding between allergen and IgE on mast cells and basophils (83). A Cochrane review concluded that SCIT is a safe and valid treatment for AR ( 84). Sublingual immunotherapy (Sur) has emerged as a promising alternative to injection immunotherapy (85,86). Although highly effective, SCIT commonly causes pain andswelling at the injection site with a rare risk of severe systemic and life-threatening reactions. A recent review found support for SLIT in children and for use in AR due to seasonal allergens and dust mites (85). However, more study is necessary to optimize allergen dosages, treatment duration, and improve criteria for patient selection. 32Tx medico. MacrolidosThe only antibiotic to show efficacy in a blinded placebocontrolled trial in CRS was long-term macrolide therapy (86). In Japan, a reduced mortality rate from diffuse panbronchiolitis with long-term, low-dose macrolide therapy. prompted investigation of macrolides for a variety ofchronic inflammatory diseases, including cystic fibrosis and CRS, with promising results (87,88). The effectiveness of this therapy is attributed to the drug's anti-inflammatory and immunomodulatory effects, rather than direct antibacterial effects, although macrolides do decrease biofilm formation in certain bacterial species, such as pseudomonas (89,90). Macrolides inhibit inflammatory mediators such as interleukin (IL)-1B, Ilr8, and intercellular adhesion molecule- 1 (90). Other effects include protecting bioactive phospholipids, accelerating apoptosis of neutrophils, andincreasing mucociliary transport (91). Macrolides decrease airway murus secretion, and even have a reparative effect on inflamed airway mucosa (92). Wallwork et al. (93) noted statistically significant improvements in the Sinonasal Outcome Test (SNOT)-20 scores, nasal endoscopy exams,saccharine transit times, and Ilr8 levels in lavage fluid in patients on long-term macrolide therapy compared to placebo. After 3 months of erythromycin or darithromydn in patients with CRS with NPNP, ILB levels in nasal lavage decreased significantly, corresponding with a decrease in the nasal polyp size (94). Low-dose macrolide therapy is worthy of further study in patients with CRS and low or normal IgE levels refractory to other therapies (92). 33Tx medico. MucoliticosGuaifenesin is a mucolytic used to loosen respiratory secretions. Despite widespread use, there is a paucity of evidence for mucolytic use in the treatment of CRS (34). Rosen and Calhoun (95) found no change in mucociliary transport time in human immunodeficiency virus (HIV)+ patientstreated with guaifenesin, but did show improvements in rhinosinusitis symptoms. In a double-blind study involving HN+ patients, Wawrose et al. (96) reported less nasal congestion and thinner postnasal drainage at doses of 2,400 mgf day at 3 weeks. Nausea was the major reportedside effect in doses greater than 1,200 mgf day.34Tx medico. surfactantesA small prospective uncontrolled, unblinded study of 1 8 patients treated with twice daily sinus irrigations with 1% baby shampoo in saline for 4 weeks, resulted in subjective improvement in SNOT 22 scores in slightly less than half of these heavily pretreated symptomatic and refractoryCRS patients (97). Baby shampoo is thought to act as a surfactant with the ability to thin mucus, disrupt microbial cell membranes, and potentially break up biofilms. The same group recently demonstrated that irrigation with the surfactant solution in buffered saline resulted in atransient increase in ciliary beat frequency in vitro, with no evidence of toxicity to the cilia (98). Prospective, blinded, and controlled studies are required to fully evaluate the role of baby shampoo or other surfactants in the treatmentofCRS. 35

bibliografaBailey, Byron J.; Johnson, Jonas T.; Newlands, Shawn D. Head & Neck Surgery Otolaryngology. 5ta edicin. Volumen 1. Captulo 39. Pag 586-594.Brodie H.Cummings otolaryngology Head and Neck Surgery,6ta edicin, volumen 1, captulo 44 pginas 702-713.