Medical Treatment for Acute Sinusitis

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Background

Many classifications, both clinical and radiological, have been proposed in the literature to define acute sinusitis.[1] Although no consensus on the precise definition currently exists, acute sinusitis may be defined as a bacterial or viral infection of the sinuses of fewer than 4 weeks' duration that resolves completely with appropriate treatment. Subacute sinusitis represents a temporal progression of symptoms for 4-12 weeks. Recurrent acute sinusitis[2] is diagnosed when 2-4 episodes of infection occur per year with at least 8 weeks between episodes, and, as in acute sinusitis, the sinus mucosa completely normalizes between attacks. Chronic sinusitis is the persistence of insidious symptomatology beyond 12 weeks, with or without acute exacerbations, and is discussed in Sinusitis, Chronic, Medical Treatment.



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Air-fluid level (arrow) in the maxillary sinus suggests sinusitis.

Embryology

To properly diagnose and treat infectious disorders of the paranasal sinuses, the clinician should have knowledge of the developmental milestones. The development of the paranasal sinuses begins in the third week of gestation and continues until early adulthood.

During the third week of embryonic development, proliferation and medial migration of ectodermal cells form the notochord. After the heart tube and pericardium have rotated from the cranial position to lie anteriorly, the notochord, which is initially in the caudal region of the embryonic disc, rotates to lie posterior to the primitive foregut. The paraxial layer of mesenchyme, which lies adjacent to the notochord, differentiates into the somite ridges, intermediate cell mass, and lateral plate mesoderm. From these mesodermal structures the branchial arches develop, the first of which gives rise to internal nasal structures.

The paranasal sinuses develop in conjunction with the palate from changes in the lateral wall of the nasal cavity. At 40 weeks' gestation, 2 horizontal grooves develop in the mesenchyme of the lateral wall of the nasal cavity. Proliferation of maxilloturbinate mesenchyme between these grooves results in an outpouching of tissue medially into the nasal lumen. This outpouching is the precursor of the middle and inferior meatus as well as the inferior turbinate. Ethmoidoturbinate folds develop superiorly to give rise to the middle and superior turbinates. Once the turbinate structures are established, sinus development begins and continues until early adult life.

Anatomy

The paranasal sinuses are air-filled bony cavities that extend from the skull base to the alveolar process and laterally from the nasal cavity to the inferomedial aspect of the orbit and the zygoma. They are lined with pseudostratified columnar epithelium that is contiguous, via ostia, with the lining of the nasal cavity. This epithelium contains a number of mucous-producing goblet cells. The arterial supply of the paranasal sinuses is from branches of the internal and external carotid arteries, while the venous and lymphatic drainage path is through the sinus ostia into the nasal cavity plexus. In addition, venous drainage occurs through valveless vessels corresponding to the arterial supply. The focal point of sinus drainage is the ostiomeatal complex, which is located in the middle meatus and is composed of the maxillary, frontal, and anterior ethmoid ostia. The posterior ethmoids empty into the superior meatus, and the sphenoids empty into the sphenoethmoidal recess.

The exact function of the paranasal sinuses is not well understood. The possible roles of the sinuses may include reducing the weight of the skull; dampening pressure; humidifying and warming inspired air; absorbing heat and insulating the brain; aiding in sound resonance; providing mechanical rigidity; and increasing the olfactory surface area.

The sinus mucosa has less secretory and vasomotor function than the nasal cavity does. Cilia are concentrated near and beat toward the natural sinus ostia. Blockage of the ostium results in stasis of mucous flow, which can lead to development of disease.

Pathophysiology

The sinuses are normally sterile under physiologic conditions. Purulent sinusitis can occur when ciliary clearance of sinus secretions decreases or when the sinus ostium becomes obstructed, which leads to retention of secretions, negative sinus pressure, and reduction of oxygen partial pressure. This environment is then suitable for growth of pathogenic organisms. Factors that predispose the sinuses to obstruction and decreased ciliary function are allergic, nonallergic, or viral insults, which produce inflammation of the nasal and sinus mucosa and result in ciliary dysmotility and sinus obstruction. Approximately 90% of patients who have viral upper respiratory tract infections (URTIs) have sinus involvement, but only 5-10% of these patients have bacterial superinfection requiring antimicrobial treatment.

Anatomical variations that narrow the ostiomeatal complex, including septal deviation, paradoxical middle turbinates, and Haller cells, make this area more sensitive to obstruction from mucosal inflammation. Mechanical obstruction of the ostiomeatal complex from foreign bodies, polyps, or tumors can also result in acute sinus disease. Systemic diseases that result in decreased mucociliary clearance, including cystic fibrosis and Kartagener syndrome, can be predisposing factors for acute sinusitis in rare cases. Patients with immunodeficiencies (eg, agammaglobulinemia, combined variable immunodeficiency, and immunodeficiency with reduced immunoglobulin G [IgG]– and immunoglobulin A [IgA]–bearing cells) are also at increased risk of developing acute sinusitis.

Acute sinusitis in the intensive care population is a distinct entity, occurring in 18-32% of patients with prolonged periods of intubation, and is usually diagnosed during the evaluation of unexplained fever. Cases in which the cause is obstruction are usually evident and can include the presence of prolonged nasogastric or nasotracheal intubation. Moreover, patients in an intensive care setting are generally debilitated, predisposing them to septic complications, including sinusitis.

Ciliary function is also reduced in the presence of low pH, anoxia, bacterial toxins, smoking, dehydration, foreign bodies, and drugs (eg, atropine, antihistamines, phenylephedrine). Approximately 10% of cases of acute sinusitis result from direct inoculation of the sinus with a large amount of bacteria. Dental abscesses or procedures that result in communication between the oral cavity and sinus can produce sinusitis by this mechanism. Facial trauma or large inoculations from swimming can produce sinusitis as well.

A study by Santee et al suggested that acute sinusitis in children causes changes in the nasopharyngeal microbiota, with these changes being linked to increased frequency of upper respiratory tract infections. Changes found included a reduction in the relative abundance of certain taxa, such as Faecalibacterium prausnitzii and Akkermansia spp, as well as enrichment of Moraxella nonliquefaciens.[3]

Epidemiology

Frequency

United States

Sinusitis affects 1 out of every 7 adults in the United States, with over 30 million individuals diagnosed each year. Acute bacterial sinusitis is the fifth most common diagnosis prompting antibiotic administration and accounts for 0.4% of ambulatory diagnoses.[4] The economic burden of acute sinusitis in children is $1.77 billion per year.[5]

History

Acute sinusitis is a clinical diagnosis; thus, an understanding of its presentation is of paramount importance in differentiating this entity from allergic or vasomotor rhinitis and common URTIs. No specific clinical symptom or sign is sensitive or specific for acute sinusitis, so the overall clinical impression should be used to guide management. A history of purulent secretions and facial or dental pain are specific symptoms that may point to a bacterial etiology. In a patient in intensive care, acute sinusitis should be suspected in the presence of sepsis of unknown origin.

 

Physical

Anterior rhinoscopic examination, with or without a topical decongestant, is important to assess the status of the nasal mucosa and the presence and color of nasal discharge. Predisposing anatomical variations can also be noted during anterior rhinoscopy. Sinus transillumination and palpation are of little predictive value. A basic evaluation of ocular and neurological function is also necessary in order to rule out potential complications.

Endoscopic examination may reveal the origin of the purulent discharge from the middle meatus and may provide information about the nature of ostiomeatal obstruction. The use of endoscopy may also aid in the etiologic diagnosis of acute sinusitis by allowing the careful attainment of purulent secretions from the sinus ostia for culture.

Causes

The bacteria most commonly involved in acute sinusitis are part of the normal nasal flora. These bacteria can become sinus pathogens when they are deposited into the sinuses by sneezing, coughing, or direct invasion under conditions that optimize their growth. The most common bacterial pathogens in acute sinusitis are Streptococcus pneumoniae (30-40%), Haemophilus influenzae (20-30%), and Moraxella catarrhalis (12-20%). Staphylococcus aureus and Streptococcus pyogenes are isolated in rare cases. Sixty-six percent of patients with acute sinusitis grow at least 1 pathogenic bacterial species on sinus aspirates, while 26-30% percent of patients have multiple predominant bacterial species.

Anaerobic organisms have been found in fewer than 10% of patients with acute bacterial sinusitis, despite the ample environment available for their growth. The exceptions are in sinusitis resulting from a dental source and in patients with chronic sinus disease, in whom anaerobic organisms are usually isolated.

Gram-negative organisms, including Pseudomonas aeruginosa (15.9%), Escherichia coli (7.6%), Proteus mirabilis (7.2%), Klebsiella pneumoniae, and Enterobacter species, predominate in nosocomial sinusitis, accounting for 60% of cases. Polymicrobial invasion is seen in 25-100% of cultures. The other pathogenic organisms found in nosocomial patients are gram-positive organisms (31%) and fungi (8.5%). Viruses are the most common trigger of acute sinusitis. Rhinovirus, influenza, and parainfluenza viruses are the primary pathogens in 3-15% of patients with acute sinusitis.

Fungal causes of sinusitis are discussed in Allergic Fungal Sinusitis and Sinusitis, Fungal.

A study by Khalid et al indicated that the likelihood of developing acute rhinosinusitis is 33% greater in individuals with a 25-hydroxyvitamin D level below 20 ng/mL. Information was derived from the National Health and Nutrition Examination Survey 2001-2006.[6]

Laboratory Studies

Some authors have reported on the use of laboratory tests including sedimentation rate, white blood cell counts, and C-reactive protein levels to help diagnose acute sinusitis.[7] These tests appear to add little to the predictive value of clinical findings in the diagnosis.

Cultures are not routinely obtained in the evaluation of acute sinusitis but should be obtained in a patient in intensive care or with immunocompromise, in children not responding to appropriate medical management, and in patients with complications of sinusitis. Because the nose is colonized with multiple nonpathogenic species of bacteria, care must be taken when evaluating culture results. A specific organism is considered pathogenic when more than 104 colony-forming units of the species are grown on culture or when polymorph counts are greater than 5000 cells/mL.

Imaging Studies

Imaging studies are not necessary when the probability of sinusitis is either high or low but may be useful when the diagnosis is in doubt, based upon a thorough history and physical examination. Plain sinus radiographs may demonstrate mucosal thickening, air-fluid levels, and sinus opacification. Limitations of plain films include interobserver variability, inability to distinguish infection from a polyp or tumor disease, and poor depiction of the ethmoid and sphenoid sinuses.

CT scanning has poor specificity for the diagnosis of acute sinusitis, demonstrating sinus air-fluid levels in 87% of individuals with simple URTIs and 40% of asymptomatic individuals. CT scanning is the modality of choice, however, in specific circumstances such as in the evaluation of a patient in intensive care, when complications are suspected, or in the preoperative evaluation of surgical candidates. CT scanning can give valuable information regarding the anatomical and mechanical contributions in the development of acute sinusitis. Coronal views with bone windows are the preferred sinus study for evaluating each of the sinuses as well as the ostiomeatal complex.

Magnetic resonance imaging (MRI) is excellent for evaluating soft tissue disease within the sinuses, but it is of little value in the diagnostic workup for acute sinusitis.

Medical Care

The primary goals of management of acute sinusitis are to eradicate the infection, decrease the severity and duration of symptoms, and prevent complications. Most patients with acute sinusitis are treated in the primary care setting. Further evaluation by an otolaryngologist is recommended when (1) continued deterioration occurs with appropriate antibiotic therapy, (2) episodes of sinusitis recur, (3) symptoms persist after 2 courses of antibiotic therapy, or (4) comorbid immunodeficiency, nosocomial infection, or complications of sinusitis are present. The goals of management of acute sinusitis are the provision of adequate drainage and appropriate systemic treatment of the likely bacterial pathogens.

Drainage of the involved sinus can be achieved both medically and surgically (see the Medication and Surgical Care sections). Aggressively treat patients in intensive care who develop acute sinusitis in order to avoid septic complications. Consider removal of nasotracheal and nasogastric tubes and promote drainage either medically or surgically.

In retrospective and prospective studies of pediatric patients with acute respiratory tract infection, including 4234 and 667 with acute sinusitis in the retrospective and prospective studies, respectively, Gerber et al found clinical outcomes with broad-spectrum antibiotics to be no better than those with narrow-spectrum antibiotics. In the retrospective patient cohort, for example, broad-spectrum antibiotics were associated with a 3.4% treatment failure rate, versus a 3.1% rate for the narrow-spectrum drugs. Moreover, in the prospective study, the risk of adverse events, as documented by clinicians, was higher for broad-spectrum antibiotics (3.7%) than for the narrow-spectrum treatments (2.7%).[8]

A retrospective cohort study by Pynnonen et al, conducted at a single academic institution, suggested that antibiotics are being overused in the treatment of patients with mild acute sinusitis of short duration. The investigators found that 66% of such patients were being given antibiotics, with antibiotic use varying according to the individual provider, the provider’s specialty (with emergency medicine providers tending to use more antibiotics), and whether a medical trainee was present.[9]

A study by Bergmark and Sedaghat indicated that in the United States, the antibiotic prescription rate for cases of acute rhinosinusitis is over 50% by primary care providers (PCPs) and emergency departments (EDs), reporting that PCPs prescribed antibiotics to 57.0% of adults presenting with acute rhinosinusitis and that EDs prescribed antibiotics to 59.1% of such patients. Among pediatric patients, the rates for PCPs and EDs were 52.9% and 51.4%, respectively. The investigators did find, however, that PCPs in the Northeast United States were more likely to prescribe antibiotics for acute rhinosinusitis than were those in other parts of the country.[10]

A study by Fleming-Dutra et al found that, based on the 2010-2011 National Ambulatory Medical Care Survey and National Hospital Ambulatory Medical Care Survey, sinusitis was responsible for 56 ambulatory antibiotic prescriptions per 1000 population in the United States, the highest rate of such prescriptions for a single diagnosis.[11]

Surgical Care

Sinus puncture and irrigation techniques allow for a surgical means of removal of thick purulent sinus secretions. The purpose of surgical drainage is to enhance mucociliary flow and provide material for culture and sensitivity. A surgical means of sinus drainage should be used when appropriate medical therapy has failed to control the infection and prolonged or slowly resolving symptoms result or when complications of sinusitis occur. Another indication for sinus puncture is to obtain culture material to guide antibiotic selection if empiric therapy has failed or antibiotic choice is limited. This is particularly important in patients who are immunocompromised or in intensive care. Sinusitis can be a prominent source of sepsis in these patients. In adults, sinus puncture can usually be achieved using local anesthesia; however, in children, a general anesthetic is usually necessary.

In today's era of minimally invasive surgical techniques, sinus endoscopy is commonly used to achieve sinus drainage. It offers the advantages of (1) being able to open multiple sinuses or to decompress the orbit in cases of complications and (2) allowing the surgeon to open the natural ostia of the involved sinuses.

The techniques and complications of open and endoscopic sinus surgical approaches are discussed in articles dealing with their individual surgical management.

A study by Patel et al suggested that after complicated acute pediatric sinusitis resolves following initial medical or surgical intervention, few patients require subsequent surgical treatment. The investigators reviewed the records of 86 children and adolescents, aged 2 months to 18 years, with either orbital (80 patients) or intracranial (6 patients) complications of acute sinusitis; the children were treated either surgically (27 patients) or medically (59 patients) during the acute phase of the disease. The study determined that four of the patients treated surgically and five of those treated medically needed surgery following the initial resolution of their sinusitis; eight of the nine patients required it because medical therapy failed for persistent rhinosinusitis, and one needed it after a second complication developed.[12]

Consultations

Ophthalmological or neurosurgical consultation should be obtained when either orbital or intracranial complications develop.

Guidelines Summary

Guidelines for the management of acute sinusitis in adults have been released by the following organizations:

Diagnosis

The 2014 AAAAI/ACAAI practice parameter provides the following classification for rhinosinusitis[13] :

Acute rhinosinusitis (ARS)

Some or all of the following symptoms must exist for less than 12 weeks:

Recurrent acute rhinosinusitis ​ (RARS)

The patient must have had at least 3 episodes of ARS in 12 months.

Chronic rhinosinusitis (CRS)

The patient must have ARS symptoms of varying severity that have lasted longer than 12 weeks.

AAO-HNSF guidelines

In its 2015 updated clinical practice guidelines for management of adult sinusitis, the AAO-HNSF made a strong recommendations that clinicians should distinguish between acute rhinosinusitis caused by bacterial sources and those episodes caused by viral upper respiratory infections and noninfectious conditions. Symptoms or signs of acute bacterial rhinosinusitis (ABRS) include one of both of the following[14] :

A clinician should diagnose ABRS when symptoms or signs of ARS either:

In addition, the AAO-HNSF guidelines recommend against radiographic imaging for patients who meet diagnostic criteria for ARS unless a complication or alternative diagnosis is suspected.[14]

IDSA guidelines

In the 2012 IDSA guidelines, a diagnosis of ABRS is made in the presence of any of the following clinical presentations[15] :

University of Michigan Health System guidelines

The 2011 University of Michigan Health System guidelines recommend that a sinus computed tomography (CT) scan be performed while the patient is symptomatic. If symptoms of rhinosinusitis persist for more than 3 weeks despite antibiotics or recur more than three times per year. Because CT scans provide much better definition, plain sinus radiography series are not recommended.[16]

Treatment

AAO-HNSF guidelines

AAO-HNSF recommendations for treatment include the following[14] :

IDSA guidelines

In contrast to the AAO-HNSF guideline, the IDSA guidelines recommend initiation of antimicrobial therapy with amoxicillin-clavulanate rather than amoxicillin alone, as soon as the clinical diagnosis of ABRS is established. Either doxycycline or a respiratory fluoroquinolone (levofloxacin or moxifloxacin) is recommended as an alternative agent for empiric antimicrobial therapy in adults who are allergic to penicillin.[15] However, in 2016 the US Food and Drug Administration (FDA) issued an advisory that the serious side effects associated with fluoroquinolone antibacterial drugs generally outweigh the benefits for patients with sinusitis and that fluoroquinolones should be reserved for patients who do not have alternative treatment options.[17]  Patients who clinically worsen after 3 days of empiric antimicrobial therapy with a first-line agent or who do not improve after 3-5 days of such treatment should be evaluated for the possibility of resistant pathogens, a noninfectious etiology, a structural abnormality, or other causes for treatment failure.[15]

Additionally, the IDSA recommends intranasal saline irrigation and intranasal corticosteroids as adjunct treatments.[15]

AAAAI/ACAAI guidelines

The 2014 AAAAI/ACAAI practice parameter recommends the use of intranasal corticosteroid as monotherapy or with an antibiotic, for treatment of ABRS.[13]

University of Michigan Heath System

The University of Michigan Heath System ABRS treatment recommendations include[16] :

Pediatric management

In 2013, the American Academy of Pediatrics (AAP) released clinical practice guidelines for the diagnosis and management of acute bacterial sinusitis in children. According to the guidelines, a diagnosis of acute bacterial sinusitis should be made when a child with an acute upper respiratory tract infection (URI) presents with persistent illness (ie, nasal discharge and/or daytime cough) lasting more than 10 days without improvement; a worsening course or new onset of nasal discharge, daytime cough, or fever after initial improvement; or severe onset (ie, fever and purulent nasal discharge) for at least 3 consecutive days.[18]

Other key action statements include the following[18] :

The 2014 AAAAI/ACAAI practice parameter recommends that clinician's look for the presence of otitis media when evaluating a patient with rhinosinusitis. The AAAAI/ACAAI also notes there is no evidence to support the use of nasal irrigations, antihistamines, decongestants, or mucolytics as ancillary therapy in the treatment of ABRS in children.[13]

International guidelines

In 2017, the Korea Centers for Disease Control and Prevention released guidelines for antibiotic use in adults aged 19 years or above with acute upper respiratory infections, including the following for cases of acute sinusitis[19] :

Medication Summary

Medical drainage is achieved with topical and systemic vasoconstrictors. Oral alpha-adrenergic vasoconstrictors, including pseudoephedrine and phenylephrine, can be used for 10-14 days to allow for restoration of normal mucociliary function and drainage. Because oral alpha-adrenergic vasoconstrictors may cause hypertension and tachycardia, they may be contraindicated in patients with cardiovascular disease. Oral alpha-adrenergic vasoconstrictors may also be contraindicated in competitive athletes because of rules of competition. Topical vasoconstrictors (eg, oxymetazoline hydrochloride) provide good drainage, but they should be used only for a maximum of 3-5 days, given the increased risk of rebound congestion, vasodilatation, and rhinitis medicamentosa when used for longer periods.

Mucolytic agents (eg, guaifenesin, saline lavage) have the theoretical benefit of thinning mucous secretions and improving drainage. They are not, however, commonly used in clinical practice in the treatment of acute sinusitis. Intranasal steroids have not been conclusively shown to be of benefit in cases of acute sinusitis.

Antihistamines are beneficial for reducing ostiomeatal obstruction in patients with allergies and acute sinusitis; however, they are not recommended for routine use for patients with acute sinusitis. Antihistamines may complicate drainage by thickening and pooling sinonasal secretions.

In cases of suspected or documented bacterial sinusitis, the second principle of treatment is to provide adequate systemic treatment of the likely bacterial pathogens (ie, S pneumoniae, H influenzae, M catarrhalis). The physician should be aware of the probability of bacterial resistance within their community. Approximately 44 % of H influenzae and almost all of M catarrhalis strains have beta-lactamase–mediated resistance to penicillin-based antimicrobials in children. As many as 64% of S pneumoniae strains are penicillin resistant because of altered penicillin-binding proteins. Multiple drug–resistant S pneumoniae strains are also found in substantial numbers of children in daycare settings.[20]

Initial selection of the appropriate antibiotic therapy should be based on the likely causative organisms given the clinical scenario and the probability of resistant strains within a community. The course of treatment is usually 14 days. First-line therapy at most centers is usually amoxicillin or a macrolide antibiotic in patients allergic to penicillin because of the low cost, ease of administration, and low toxicity of these agents. Amoxicillin should be given at double the usual dose (80-90 mg/kg/d), especially in areas with known S pneumoniae resistance.

Table 1. Dosage, Route, and Spectrum of Activity of Commonly Used First-Line Antibiotics*



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See Table

*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism

Patients who live in communities with a high incidence of resistant organisms, those who fail to respond within 48-72 hours of commencement of therapy, and those with persistence of symptoms beyond 10-14 days should be considered for second-line antibiotic therapy. The most commonly used second-line therapies include amoxicillin clavulanate, second- or third-generation cephalosporins (eg, cefuroxime, cefpodoxime, cefdinir), macrolides (ie, clarithromycin), fluoroquinolones (eg, ciprofloxacin, levofloxacin, moxifloxacin), and clindamycin.

In patients with dental causes of sinusitis or those with foul-smelling discharge, anaerobic coverage using clindamycin or amoxicillin with metronidazole is necessary.

Table 2. Dosage, Route, and Spectrum of Activity of Commonly Used Second-Line Antibiotics*



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See Table

*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism; -, no activity against microorganism

Patients with nosocomial acute sinusitis require adequate intravenous coverage of gram-negative organisms. Aminoglycoside antibiotics are usually the drugs of choice for the treatment of such patients because of their excellent gram-negative coverage and sinus penetration. Selection of an antibiotic is usually based on the culture results of attained maxillary secretion.

In addition to surgical management, complications of acute sinusitis should be managed with a course of intravenous antibiotics. Third-generation cephalosporins (eg, cefotaxime, ceftriaxone) in combination with vancomycin provide adequate intracranial penetration, making them a good first-line choice.

Table 3. Dosage, Route, and Spectrum of Activity of Commonly Used Intravenous Antibiotics*



View Table

See Table

*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism; -, no activity against microorganism

Described below are recommended antibiotic regimens.

Amoxicillin (Trimox, Amoxil, Biomox)

Clinical Context:  First-line antibiotic. Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Cefdinir (Omnicef)

Clinical Context:  Classified as a third-generation cephalosporin and inhibits mucopeptide synthesis in the bacterial cell wall. Typically bactericidal, depending on organism susceptibility, dose, and serum or tissue concentrations.

Clarithromycin (Biaxin)

Clinical Context:  First-line antibiotic. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Cefuroxime (Ceftin, Kefurox, Zinacef)

Clinical Context:  Second-line PO and first-line IV antibiotic. Maintains gram-positive activity that first-generation cephalosporins have; adds activity against P mirabilis, H influenzae, E coli, K pneumoniae, and M catarrhalis.

Condition of patient, severity of infection, and susceptibility of microorganism determine proper dose and route of administration.

Ceftriaxone (Rocephin)

Clinical Context:  Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin binding proteins. Has good penetration.

Vancomycin (Vancocin, Lyphocin, Vancoled)

Clinical Context:  Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or who have infections with resistant staphylococci. For abdominal penetrating injuries, it is combined with an agent active against enteric flora and/or anaerobes.

To avoid toxicity, current recommendation is to assay vancomycin trough levels after third dose drawn 0.5 h prior to next dosing. Use CrCl to adjust dose in patients diagnosed with renal impairment.

Used in conjunction with gentamicin for prophylaxis in penicillin-allergic patients undergoing gastrointestinal or genitourinary procedures. Effective for resistant S pneumoniae.

Amoxicillin/Clavulanate (Augmentin)

Clinical Context:  Drug combination treats bacteria resistant to beta-lactam antibiotics.

Class Summary

Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.

Complications

Local complications

Mucoceles are chronic epithelial cysts that develop in sinuses in the presence of either an obstructed sinus ostium or minor salivary gland duct. They have the potential for progressive concentric expansion that can lead to bony erosion and extension beyond the sinus.

Maxillary sinus mucoceles are usually found incidentally on sinus radiographs and are of little significance in the absence of symptomatology or infection. Surgical treatment is not usually necessary, and these lesions often regress spontaneously over time.

Frontoethmoidal and sphenoethmoidal mucoceles, on the other hand, tend to be symptomatic and have a high potential for bony erosion. Frontoethmoidal mucoceles should be completely removed and the sinus obliterated. Sphenoethmoid mucoceles should be widely opened into the nasal cavity.

Osteomyelitis is a potential local complication most commonly occurring with frontal sinusitis. Osteomyelitis of the frontal bone is called a Pott puffy tumor and represents a subperiosteal abscess with local edema anterior to the frontal sinus. This can advance to form a fistula to the upper lid with sequestration of necrotic bone. This rare complication should be managed with a combination of systemic antibiotics, surgical drainage of affected sinuses, and debridement of necrotic bone.

Orbital complications

Orbital complications are the most common complications encountered with acute bacterial sinusitis. Infection can spread directly through the thin bone separating the ethmoid or frontal sinuses from the orbit or by thrombophlebitis of the ethmoid veins. Diagnosis should be based on an accurate physical examination including ophthalmological evaluation and appropriate radiological studies. CT scanning is the most sensitive means of diagnosing an orbital abscess, although ultrasound has been found to be 90% effective for diagnosing anterior abscesses.[21] The classification by Chandler, which is based on physical examination findings, provides a reasonable framework to guide management. This classification consists of 5 groups of orbital inflammation[22] :

Medical management, including sinus drainage and intravenous antibiotics, is advocated for any degree of orbital complication. The use of decongestant and antibiotic therapy is discussed in the Medical Care and Medication sections.

Among the classifications by Chandler, surgical drainage of both the infected sinuses and the orbit are advocated for groups 3-5 if inadequate improvement or progression of orbital cellulitis occurs despite medical therapy or if the patient has loss of visual acuity. Surgical procedures are discussed in Surgical Care.

Intracranial complications

Intracranial complications may occur as a result of direct extension through the posterior frontal sinus wall or through retrograde thrombophlebitis of the ophthalmic veins. Subdural abscess is the most common intracranial complication, although cerebral abscesses and infarction that result in seizures, focal neurological deficits, and coma may occur. Intracranial complications of sinusitis should be managed surgically with drainage of both the affected sinus and the cranial abscess.

Subdural empyema is a life-threatening infection that may complicate acute sinusitis. Boto et al (2011) reported the case of a previously healthy 10-year-old girl who developed subdural empyema due to Gemella morbillorum infection after an untreated maxillary, ethmoidal, and sphenoidal sinusitis.[23] Despite immediate drainage of the empyema and treatment with broad-spectrum antibiotics, she developed frontal cerebritis and refractory intracranial hypertension, needing urgent decompressive craniectomy. She recovered gradually with slight right-sided hemiparesis and aphasia.

Systemic complications

Sinusitis can result in sepsis and multisystem organ failure caused by seeding of the blood and various organ systems. Reports of bacteremia, thoracic empyema, and nosocomial pneumonia have been documented in the intensive-care population with acute sinusitis, and the mortality rate in this group can be as high as 11%. Fukushima et al (2012) reported on a case of a 39-year-old man admitted for the onset of acute purulent meningitis.[24] A cerebrospinal fluid culture grew Streptococcus sanguis. Sinusitis was found to be the cause of the meningitis. Treatment with intravenous antibiotics was successful.

Patient Education

For excellent patient education resources, see eMedicineHealth's patient education article Sinus Infection.

What is the definition of acute sinusitis?What is the embryology of the paranasal sinuses involved in acute sinusitis?What is the anatomy of the paranasal sinuses involved in acute sinusitis?What is the function of the paranasal sinuses involved in acute sinusitis?What is the pathophysiology of acute sinusitis?What are the factors that contribute to the development of acute sinusitis?What is the pathophysiology of acute sinusitis in the intensive care population and in children?How common is acute sinusitis in the US?How is acute sinusitis differentiated from other conditions with similar symptoms?What is the role of the physical exam in the diagnosis of acute sinusitis?What causes acute sinusitis?Which vitamin deficiency is associated with acute sinusitis?What are the differential diagnoses for Medical Treatment for Acute Sinusitis?What is the role of lab testing in the workup of acute sinusitis?What is the role of imaging studies in the workup of acute sinusitis?What are the treatment goals of acute sinusitis?What are the different methods of drainage in acute sinusitis?Are broad-spectrum or narrow-spectrum antibiotics preferred in the treatment of acute sinusitis?Are antibiotics overused in the treatment of acute sinusitis?How effective are surgical procedures in the treatment of acute sinusitis?When is surgery indicated for acute sinusitis?Which specialist consultations are indicated for complications of acute sinusitis?What are the AAAAI/ACAAI guidelines on treatment for acute sinusitis?Which organizations have released treatment guidelines for acute sinusitis?What are the AAAAI/ACAAI guideline criteria for a diagnosis of acute rhinosinusitis (ARS)?What are the guideline criteria for a diagnosis of recurrent acute rhinosinusitis (RARS)?What are the guideline criteria for a diagnosis of chronic rhinosinusitis (CRS)?What are the AAO-HNSF guidelines for a diagnosis of acute bacterial sinusitis (ABRS)?What are the diagnostic criteria for acute bacterial rhinosinusitis (ABRS)?When is sinus CT scanning indicated for rhinosinusitis according to the University of Michigan Health System guidelines?What are the AAO-HNSF guidelines on treatment for acute sinusitis?What are the IDSA guidelines on treatment for acute sinusitis?What are the University of Michigan Health System guidelines on treatment for acute sinusitis?What are the AAP guidelines for the diagnosis and management of acute sinusitis in children?What are the Korea CDC guidelines on antibiotic use for the treatment of acute sinusitis?Which medications are used for drainage in the treatment of acute sinusitis?How are mucolytic agents used in the treatment of acute sinusitis?What is the role of antihistamines in the treatment of acute sinusitis?What are the considerations for the use of antibiotics in the treatment of acute sinusitis?What are the first-line antibiotics for the treatment of acute sinusitis?When are second-line antibiotics indicated in the treatment of acute sinusitis?How are IV antibiotics used in the treatment of nosocomial acute sinusitis?Which medications in the drug class Antibiotics are used in the treatment of Medical Treatment for Acute Sinusitis?What are the local complications of acute sinusitis?What are the orbital complications of acute sinusitis?How are orbital complications of acute sinusitis treated?What are the intracranial complications of acute sinusitis?What are the systemic complications of acute sinusitis?What patient education is available on acute sinusitis?

Author

Ted L Tewfik, MD, Professor of Otolaryngology-Head and Neck Surgery, Professor of Pediatric Surgery, McGill University Faculty of Medicine; Senior Staff, Montreal Children's Hospital, Montreal General Hospital, and Royal Victoria Hospital

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Stephen G Batuello, MD, Consulting Staff, Colorado ENT Specialists

Disclosure: Nothing to disclose.

Chief Editor

Arlen D Meyers, MD, MBA, Professor of Otolaryngology, Dentistry, and Engineering, University of Colorado School of Medicine

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cerescan;RxRevu;Cliexa;The Physicians Edge;Sync-n-Scale;mCharts<br/>Received income in an amount equal to or greater than $250 from: The Physicians Edge, Cliexa<br/> Received stock from RxRevu; Received ownership interest from Cerescan for consulting; .

Additional Contributors

Jack A Coleman, MD, Consulting Staff, Franklin Surgical Associates

Disclosure: Received honoraria from Accarent, Inc. for speaking and teaching.

Acknowledgements

Melvin D Schloss, MD, FRCSC, Director of Pediatric Otolaryngology, Professor, Department of Otolaryngology, McGill University Faculty of Medicine, Canada

Disclosure: Nothing to disclose.

Steven E Sobol, MD, FRCSC, MSc, FAAP Assistant Professor, Director of Pediatric Otolaryngology, Department of Otolaryngology Head and Neck Surgery, Emory University School of Medicine; Otolaryngologist-In-Chief, Children's Healthcare of Atlanta at Egleston

Steven E Sobol, MD, FRCSC, MSc, FAAP is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery

Disclosure: Nothing to disclose.

References

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Air-fluid level (arrow) in the maxillary sinus suggests sinusitis.

Air-fluid level (arrow) in the maxillary sinus suggests sinusitis.

Antibiotic Dosage Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalis Anaerobic bacteria
Sensitive Intermediate Resistant
Amoxicillin500 mg PO tid++++++++++
Clarithromycin250-500 mg PO bid+++++++++++
Azithromycin500 mg PO first day, then



250 mg/d PO for 4 days



+++++++++++
Antibiotic Dosage Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalis Anaerobic bacteria
Sensitive Intermediate Resistant
Amoxicillin/clavulanate500 mg PO tid+++++++++++++++
Cefuroxime250-500 mg PO bid+++++++++++++
Cefpodoxime



+



cefixime



200 mg PO bid



400 mg/d PO



-



++



+++



-



++



-



+



+++



+++



+++



+++



-



Ciprofloxacin500-750 mg PO bid++++++++++
Levofloxacin500 mg/d PO++++++++++++++++++
Trovafloxacin200 mg/d PO++++++++++++++++++
Clindamycin300 mg PO tid+++++++++--+++
Metronidazole500 mg PO tid-----+++
Antibiotic Dosage Streptococcus pneumoniae Haemophilus influenzae Moraxella catarrhalis Gram-negative Anaerobic bacteria
Piperacillin3-4 g IV q4-6h++++-++++++
Piperacillin/tazobactam3.375 g IV q6h++++++++++++++
Ticarcillin3 g IV q4h+++--+++++
Ticarcillin/clavulanate3.1 g IV q4h++++++-+++++
Imipenem500 mg IV q6h+++++++++++++++
Meropenem1 g IV q8h++++++++++++++
Cefuroxime1 g IV q8h+++++++++++++
Ceftriaxone2 g IV bid++++++++++++++
Cefotaxime2 g IV q4-6h++++++++++++++
Ceftazidime2 g IV q8h++++++++++++++
Gentamicin1.7 mg/kg IV q8h-++++++++-
Tobramycin1.7 mg/kg IV q8h-++++++++-
Vancomycin1 g IV q6-12h+++---++