Acute Sinusitis Medication
- Author: Itzhak Brook, MD, MSc; Chief Editor: Michael Stuart Bronze, MD more...
Viral rhinosinusitis does not require antimicrobial treatment. Standard nonantimicrobial treatment options include topical steroids, topical and/or oral decongestants, mucolytics, and intranasal saline spray.
Antimicrobial therapy is the mainstay of medical treatment in sinusitis. The choice of antibiotics depends on whether the sinusitis is acute, chronic, or recurrent.
Antibiotic efficacy rates are as follows :
Levofloxacin, moxifloxacin, and amoxicillin/clavulanate - Greater than 90%
High-dose amoxicillin, cefpodoxime proxetil, cefixime, cefuroxime axetil, and trimethoprim-sulfamethoxazole - 80-90%
Clindamycin, doxycycline, cefprozil, azithromycin, clarithromycin, and erythromycin - 70-80%
Cefaclor - 50-60%
On the basis of the 2000 Sinus and Allergy Health Partnership treatment guidelines for acute bacterial rhinosinusitis, patients are divided into 3 groups, as follows:
Adults with mild disease who have not received antibiotics: Amoxicillin/clavulanate, amoxicillin (1.5-3.5 g/day), cefpodoxime proxetil, or cefuroxime is recommended as initial therapy.
Adults with mild disease who have had antibiotics in the previous 4-6 weeks and adults with moderate disease: Amoxicillin/clavulanate, amoxicillin (3-3.5 g), cefpodoxime proxetil, or cefixime is recommended.
Adults with moderate disease who have received antibiotics in the previous 4-6 weeks: Amoxicillin/clavulanate, levofloxacin, moxifloxacin, or doxycycline is recommended.
Patients who remain symptomatic despite appropriate antibiotic therapy may be evaluated with sinus endoscopy, CT scanning, or sinus aspiration/culture.
The penicillins are bactericidal antibiotics that work against sensitive organisms at adequate concentrations and inhibit the biosynthesis of cell wall mucopeptide. The penicillins are also available in combination with agents that inactivate beta-lactamase enzymes, extending their antibiotic spectrum.
The piperacillin-tazobactam combination includes an antipseudomonal penicillin plus beta-lactamase inhibitor. It inhibits biosynthesis of cell wall mucopeptide and is effective during the stage of active multiplication.
The ticarcillin-clavulanate combination inhibits the biosynthesis of cell wall mucopeptide and is effective during the stage of active growth. It has antipseudomonal penicillin plus a beta-lactamase inhibitor that provides coverage against most gram-positive, gram-negative, and anaerobic organisms.
Penicillin V potassium is a first-line antibiotic choice. It inhibits biosynthesis of cell wall mucopeptide. It is bactericidal against sensitive organisms when adequate concentrations are reached and most effective during the stage of active multiplication. Inadequate concentrations may produce only bacteriostatic effects.
Amoxicillin-clavulanate is a second-line agent; this drug combination treats bacteria resistant to beta-lactam antibiotics.
Amoxicillin is a first-line antibiotic choice. It interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.
Piperacillin inhibits the biosynthesis of cell wall mucopeptides and the stage of active multiplication; it has antipseudomonal activity.
Cephalosporins are structurally and pharmacologically related to penicillins. They inhibit bacterial cell wall synthesis, resulting in bactericidal activity. Cephalosporins are divided into first, second, third and fourth generation. First-generation cephalosporins have greater activity against gram-positive bacteria, and succeeding generations have increased activity against gram-negative bacteria and decreased activity against gram-positive bacteria.
Cefprozil is a second-line agent. It binds to one or more of the penicillin-binding proteins, which, in turn, inhibits cell wall synthesis and results in bactericidal activity.
Cefuroxime is a second-line agent. It is a second-generation cephalosporin that maintains the gram-positive activity of first-generation cephalosporins, adding activity against Proteus mirabilis, H influenzae, Escherichia coli, Klebsiella pneumoniae, and M catarrhalis.
Cefpodoxime is a second-line agent. It binds to one or more penicillin-binding proteins, which, in turn, inhibits cell wall synthesis and results in bactericidal activity.
Cefixime is a second-line agent. By binding to one or more penicillin-binding proteins, it arrests bacterial cell wall synthesis and inhibits bacterial growth.
Ceftriaxone is a third-generation cephalosporin with broad-spectrum, gram-negative activity; it has lower efficacy against gram-positive organisms and higher efficacy against resistant organisms. It arrests bacterial growth by binding to one or more penicillin binding proteins. It has good penetration.
Classified as a third-generation cephalosporin, cefdinir inhibits mucopeptide synthesis in the bacterial cell wall. It is typically bactericidal, depending on organism susceptibility, dose, and serum or tissue concentrations.
Cefaclor is used for treatment of infections caused by susceptible organisms including H influenzae and for treatment of otitis media, sinusitis, and infections involving the respiratory tract. It may not be appropriate in acute sinusitis, owing to less activity and the potential for severe allergic reactions.
Cefotaxime is a third-generation cephalosporin with broad gram-negative spectrum, lower efficacy against gram-positive organisms, and higher efficacy against resistant organisms. It arrests bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins, which, in turn, inhibits bacterial growth.
Ceftazidime is a third-generation cephalosporin with broad-spectrum, gram-negative activity, including pseudomonas; lower efficacy against gram-positive organisms; and higher efficacy against resistant organisms. It arrests bacterial growth by binding to one or more penicillin-binding proteins, which, in turn, inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell wall synthesis, thus inhibiting cell wall biosynthesis.
Macrolide antibiotics have bacteriostatic activity and exert their antibacterial action by binding to the 50S ribosomal subunit of susceptible organisms, resulting in inhibition of protein synthesis. Macrolide antibiotics are often used in patients allergic to penicillins.
Erythromycin is a first-line treatment in patients allergic to penicillin. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Clarithromycin is a second-line agent. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Azithromycin, an advanced-generation macrolide, works similarly to clarithromycin but with shorter dosage time.
This agent is used for treatment of susceptible bacterial infections of upper and lower respiratory tract: in children, it is used for otitis media caused by susceptible strains of H influenzae; it is used for many other infections in patients allergic to penicillin.
Fluoroquinolones have broad-spectrum activity against gram-positive and gram-negative aerobic organisms. They inhibit DNA synthesis and growth by inhibiting DNA gyrase and topoisomerase, which is required for replication, transcription, and translation of genetic material.
Levofloxacin is used to treat acute maxillary sinusitis caused by S pneumoniae, H influenzae, or M catarrhalis. Fluoroquinolones should be used empirically in patients likely to develop exacerbation due to resistant organisms to other antibiotics. This is the L stereoisomer of the D/L parent compound ofloxacin, the D form being inactive. It provides good monotherapy with extended coverage against Pseudomonas species, as well as excellent activity against pneumococcus. The agent acts by inhibition of DNA gyrase activity. The oral form has bioavailability that is reportedly 99%.
Ciprofloxacin is a broad spectrum antibiotic with activity against gram-positive and gram-negative aerobic organisms. It inhibits bacterial DNA synthesis and, consequently, growth, by inhibiting DNA gyrase and topoisomerase, which are required for replication, transcription, and translation of genetic material.
Moxifloxacin inhibits the A subunits of DNA gyrase, resulting in inhibition of bacterial DNA replication and transcription.
Anti-infectives such as vancomycin, clindamycin, metronidazole, and sulfamethoxazole-trimethoprim are effective against some types of bacteria that have become resistant to other antibiotics.
Trimethoprim-sulfamethoxazole is a first-line agent with more convenient dosing. It inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.
Vancomycin is a potent antibiotic directed against gram-positive organisms and active against Enterococcus species (useful in septicemia and skin structure infections; Enterococcus is very rare in sinusitis). Vancomycin is indicated for patients who cannot receive or have failed to respond to penicillins and cephalosporins or who have infections with resistant staphylococci.
Metronidazole is an imidazole ring-based antibiotic that is active against various anaerobic bacteria and protozoa. It is used in combination with other antimicrobial agents (except C difficile enterocolitis).
Clindamycin is a semisynthetic antibiotic produced by 7(S)-chloro-substitution of 7(R)-hydroxyl group of parent compound lincomycin. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Clindamycin widely distributes in the body without penetration of the CNS. It is protein bound and is excreted by the liver and kidneys.
Carbapenems are structurally related to penicillins and have broad-spectrum bactericidal activity. The carbapenems exert their effect by inhibiting cell wall synthesis, which leads to cell death. They are active against gram-negative, gram-positive, and anaerobic organisms.
The imipenem-cilastin combination is used for the treatment of multiple-organism infections in which other agents do not have wide-spectrum coverage or are contraindicated because of the potential for toxicity.
A bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis, meropenem is effective against most gram-positive and gram-negative bacteria. Compared with imipenem, meropenem has slightly increased activity against gram-negative organisms and slightly decreased activity against staphylococci and streptococci.
Aminoglycosides are bactericidal antibiotics used to primarily treat gram-negative infections. They interfere with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits.
Gentamicin is an aminoglycoside antibiotic effective against Pseudomonas aeruginosa; E coli; and Proteus, Klebsiella, and Staphylococcus species. Gentamicin is also variably effective against some strains of certain gram-positive organisms, including S aureus, enterococci, and L monocytogenes. Dosing regimens are numerous; adjust the dose based on creatinine clearance and changes in volume of distribution.
Tobramycin is used in skin, bone, and skin structure infections caused by S aureus, P aeruginosa, Proteus species, E coli, Klebsiella species, and Enterobacter species. It is indicated in the treatment of staphylococcal infections when penicillin or potentially less-toxic drugs are contraindicated and when bacterial susceptibility and clinical judgment justify its use. Like other aminoglycosides, tobramycin is associated with nephrotoxicity and ototoxicity.
Tetracyclines inhibit protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. They may block dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Doxycycline has broad-spectrum activity and is a synthetically derived bacteriostatic antibiotic in the tetracycline class. Doxycycline inhibits protein synthesis, and thus bacterial growth, by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.
These agents cause vasoconstriction, which reduces nasal congestion. Topical agents are locally active vasoconstrictor agents such as phenylephrine and oxymetazoline, which provide immediate symptomatic relief by shrinking the inflamed and swollen nasal mucosa. Oral decongestants such as pseudoephedrine can be used for 10-14 days to allow for restoration of normal mucociliary function and drainage.
Phenylephrine produces vasoconstriction. It is possibly helpful and is not harmful.
Oxymetazoline is applied directly to mucous membranes. It stimulates alpha-adrenergic receptors and causes vasoconstriction. Decongestion occurs without drastic changes in blood pressure, vascular redistribution, or cardiac stimulation.
The alpha-adrenergic effects of tetrahydrozoline on nasal mucosa produce vasoconstriction.
Phenylephrine produces vasoconstriction. It is possibly helpful and is not harmful.
Nasal saline spray and steam inhalation help by moistening dry secretions, reducing mucosal edema, and reducing mucus viscosity. The symptomatic relief gained in some patients can be substantial; moreover, these are benign modalities of therapy.
Saline nasal sprays loosen mucus secretions to help remove mucus from the nose and sinuses.
Mucolytic agents such as guaifenesin have the theoretical benefit of thinning mucous secretions and improving drainage.
Guaifenesin increases respiratory tract fluid secretions and helps to loosen phlegm and bronchial secretions. It is indicated for patients with bronchiectasis complicated by tenacious mucous and/or mucous plugs.
Intranasal steroids have not been conclusively shown to be of benefit in cases of acute sinusitis. Study results conflict, with some reporting benefit as monotherapy or in combination with antibiotics and others reporting no benefit (combination or monotherapy).
Beclomethasone has potent vasoconstrictive and anti-inflammatory activity. It has a weak hypothalamic-pituitary-adrenocortical (HPA) axis inhibitory potency when applied topically.
Triamcinolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.
Flunisolide inhibits bronchoconstriction mechanisms, producing direct smooth muscle relaxation. It may decrease the number and activity of inflammatory cells, in turn decreasing airway hyperresponsiveness. Flunisolide decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. It does not depress the hypothalamus.
Anticholinergics block interactions between acetylcholine and muscarinic receptors on the smooth muscle preventing increases in cyclic GMP inhibiting bronchoconstriction and mucus secretion.
Topical ipratropium bromide can be used to decrease rhinorrhea. Anticholinergics such as ipratropium have anti-secretory properties, and when applied locally, inhibit secretions from serous, and seromucous glands lining the nasal mucosa.
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|Antibiotic||Dosage||Streptococcus pneumoniae||Haemophilus influenzae||Moraxella catarrhalis||Anaerobic bacteria|
|Amoxicillin||500 mg PO tid||+++||++||+||++||+||+++
(except beta-lactamase producers)
|Clarithromycin||250-500 mg PO bid||++||++||+||++||+++||+|
|Azithromycin||500 mg PO first day, then
250 mg/d PO for 4 days
|*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism|
|Antibiotic||Dosage||Streptococcus pneumoniae||Haemophilus influenzae||Moraxella catarrhalis||Anaerobic bacteria|
|500 mg PO tid||+++||++||+||+++||+++||+++|
|Cefuroxime||250-500 mg PO bid||+++||++||+||+++||++||++|
|200 mg PO bid
400 mg/d PO
|Ciprofloxacin||500-750 mg PO bid||++||+||+||++||+++||+|
|Levofloxacin||500 mg/d PO||+++||+++||+++||+++||+++||++|
|Trovafloxacin||200 mg/d PO||+++||+++||+++||+++||+++||+++|
|Clindamycin||300 mg PO tid||+++||+++||++||-||-||+++|
|Metronidazole||500 mg PO tid||-||-||-||-||-||+++|
|*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism; -, no activity against microorganism|
|Antibiotic||Dosage||Streptococcus pneumoniae †||Haemophilus influenzae||Moraxella catarrhalis||Gram-negative||Anaerobic bacteria|
|Piperacillin||3-4 g IV q4-6h||+++||+||-||+++||+++|
|Piperacillin/tazobactam||3.375 g IV q6h||+++||+++||+++||+++||++|
|Ticarcillin||3 g IV q4h||+++||-||-||+++||++|
|Ticarcillin/clavulanate||3.1 g IV q4h||+++||+++||-||+++||++|
|Imipenem||500 mg IV q6h||+++||+++||+++||+++||+++|
|Meropenem||1 g IV q8h||+++||+++||+++||+++||+++|
|Cefuroxime||1 g IV q8h||+++||+++||+++||++||++|
|Ceftriaxone||2 g IV bid||+++||+++||+++||+++||++|
|Cefotaxime||2 g IV q4-6h||+++||+++||+++||+++||++|
|Ceftazidime||2 g IV q8h||+++||+++||+++||+++||++|
|Gentamicin||1.7 mg/kg IV q8h||-||+++||+++||++||-|
|Tobramycin||1.7 mg/kg IV q8h||-||+++||+++||++||-|
|Vancomycin||1 g IV q6-12h||+++||-||-||-||++|
|*+, low activity against microorganism; ++, moderate activity against microorganism; +++, good activity against microorganism; -, no activity against microorganism †Does not take into account penicillin-resistant types.|