eMedicine Specialties > Infectious Diseases > HEENT Infections

Sinusitis, Acute

Author: Brian E Benson, MD, Staff Physician, Department of Otolaryngology, St Luke's-Roosevelt Hospital Center; Clinical Instructor, Department of Otolaryngology, Hackensack University Medical Center
Coauthor(s): Linas Riauba, MD, Assistant Professor of Clinical Medicine, Department of Medicine, Section of Infectious Disease, University Hospital, University of Medicine and Dentistry of New Jersey; Tracey Quail Davidoff, MD, Senior Clinical Instructor, Department of Emergency Medicine, Rochester General Hospital
Contributor Information and Disclosures

Updated: Feb 10, 2009

Introduction

Background

Sinusitis is characterized by inflammation of the lining of the paranasal sinuses. Because the nasal mucosa is simultaneously involved and because sinusitis rarely occurs without concurrent rhinitis, rhinosinusitis is now the preferred term for this condition.1 By definition, symptoms of acute rhinosinusitis last less than 3 weeks, symptoms of subacute rhinosinusitis last 21-60 days, and symptoms of chronic rhinosinusitis last more than 60 days. The Agency for Healthcare Research and Quality accepted this terminology in 1999.

Rhinosinusitis may be further classified according to the anatomic site (maxillary, ethmoidal, frontal, sphenoidal), pathogenic organism (viral, bacterial, fungal), presence of complication (orbital, intracranial), and associated factors (nasal polyposis, immunosuppression, anatomic variants).

Pathophysiology

The vast majority of rhinosinusitis episodes are caused by viral infection. Most viral upper respiratory tract infections are caused by rhinovirus, but coronavirus, influenza A and B, parainfluenza, respiratory syncytial virus, adenovirus, and enterovirus are also causative agents.

Almost 90% of patients with upper respiratory tract infections have radiographic evidence of paranasal sinus involvement. However, only 0.5-2% of viral rhinosinusitis cases are complicated by bacterial infection.2

The pathophysiology of rhinosinusitis is related to 3 factors: obstruction of sinus drainage pathways (sinus ostia), ciliary impairment, and mucus quantity and quality.

  • Obstruction of the natural sinus ostia prevents normal mucus drainage. Edema, inflammation, polyps, tumors, trauma, scarring, anatomic variants (eg, concha bullosa [pneumatized middle turbinate], septal deviation), and nasal instrumentation (nasogastric tubes or packing) can result in decreased patency of sinus ostia. Hypoxia within the obstructed sinus is thought to cause ciliary dysfunction and alterations in mucus production, further impairing the normal mechanism for mucus clearance.
  • Contrary to earlier models of sinus physiology, the drainage patterns of the paranasal sinuses depend not on gravity but on the mucociliary transport mechanism. The metachronous coordination of the ciliated columnar epithelial cells propels the sinus contents toward the natural sinus ostia. Any disruption of the ciliary function results in fluid accumulation within the sinus. Poor ciliary function can result from the loss of ciliated epithelial cells; cold air; high airflow; viral, bacterial, or environmental ciliotoxins; inflammatory mediators; contact between two mucosal surfaces; scars; and primary ciliary dyskinesia (Kartagener syndrome).
  • Sinonasal secretions play an important role in the pathophysiology of rhinosinusitis. The mucus that lines the paranasal sinuses is composed of a thin periciliary layer, which enables ciliary mobility, and a thick gel layer, which anchors the tips of the cilia. This mucous blanket contains mucoglycoproteins, immunoglobulins, and inflammatory cells. Alterations in the water content of the mucous blanket can impair ciliary mobility. Overproduction of mucus can overwhelm the mucociliary clearance system, resulting in retained secretions within the sinuses.
  • Acute bacterial rhinosinusitis is very frequently associated with viral upper respiratory tract infection, although allergy, trauma, neoplasms, granulomatous and inflammatory diseases, midline destructive disease, environmental factors, dental infection, and anatomic variation, which may impair normal mucociliary clearance, may also predispose to bacterial infection.

Frequency

United States

Rhinosinusitis affects 35 million people per year in the United States and accounts for close to 16 million office visits per year.3 According to the National Ambulatory Medical Care Survey (NAMCS), approximately 14% of adults report having an episode of rhinosinusitis each year, and it is the fifth most common diagnosis for which antibiotics are prescribed. In 1996, Americans spent approximately $3.39 billion treating rhinosinusitis.4

Approximately 0.5-2% of cases of viral rhinosinusitis are complicated by bacterial superinfection.

Sinusitis is more common from early fall to early spring.

Mortality/Morbidity

Forty percent of acute rhinosinusitis cases resolve spontaneously. Untreated or inadequately treated rhinosinusitis may lead to complications such as meningitis, cavernous sinus thrombophlebitis, orbital cellulitis or abscess, and brain abscess.

Race

Acute rhinosinusitis has no racial predilection.

Sex

Acute rhinosinusitis has no sexual predilection.

Age

Sinusitis occurs in all age groups.

Clinical

History

A history of occupational or allergic rhinitis, vasomotor rhinitis, nasal polyps, rhinitis medicamentosa, or immunodeficiency should be sought in an evaluation for rhinosinusitis. Rhinosinusitis is more common in individuals with congenital defects that affect humoral immunity and ciliary motility, in those with cystic fibrosis, and in persons with AIDS. Obtain a history of diabetes or organ transplant if invasive fungal sinusitis is being considered.

Acute bacterial rhinosinusitis is commonly overdiagnosed. In fact, acute bacterial rhinosinusitis is the correct diagnosis in only 40-50% of cases in which a primary care physician initially classifies a patient as likely having the condition.5

The natural history of rhinovirus infection, as described by Gwaltney et al, lasts from 1-33 days. One fourth of patients have symptoms that last longer than 14 days.6

  • Patients with uncomplicated upper respiratory tract infections usually report some of the following symptoms: sneezing, rhinorrhea, nasal congestion, hyposmia/anosmia, facial pressure, postnasal drip, sore throat, cough, ear fullness, fever, and myalgia.
  • Although diagnostic criteria for acute rhinosinusitis have been proposed,1 no single sign or symptom has strong diagnostic value for bacterial rhinosinusitis.7 However, acute bacterial rhinosinusitis should be suspected in patients who exhibit symptoms of viral upper respiratory tract infection that do not improve after 10 days or that worsen after 5-7 days.
  • Symptoms of acute bacterial rhinosinusitis include the following:
    • Facial pain or pressure (especially unilateral)
    • Hyposmia/anosmia
    • Nasal congestion
    • Nasal drainage
    • Postnasal drip
    • Fever
    • Cough
    • Fatigue
    • Maxillary dental pain
    • Ear fullness/pressure
  • A change in the color or characteristic of the nasal discharge is not a specific sign of bacterial rhinosinusitis.
  • A previous diagnosis of rhinosinusitis is not a predictor of acute bacterial rhinosinusitis.7

Physical

  • Purulent nasal secretions
  • Purulent posterior pharyngeal secretions
  • Mucosal erythema
  • Periorbital edema
  • Tenderness overlying sinuses
  • Air-fluid levels on transillumination of the sinuses (60% reproducibility rate for assessing maxillary sinus disease)
  • Facial erythema

Causes

The most common pathogens isolated from maxillary sinus cultures in patients with acute bacterial rhinosinusitis include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Streptococcus pyogenes, Staphylococcus aureus, and anaerobes are less commonly associated with acute bacterial rhinosinusitis.

  • S pneumoniae are gram-positive, catalase-negative, facultatively anaerobic cocci that account for 20-43% of acute bacterial rhinosinusitis cases in adults. The rise of antimicrobial resistance in S pneumoniae is a major concern. A 1998 surveillance study of respiratory tract isolates estimated that 12.3% of S pneumoniae isolates obtained from the paranasal sinuses had intermediate resistance to penicillin; 37.4% were penicillin-resistant. The paranasal sinuses represented the anatomic location with the highest resistance rate.8 Resistance to macrolide, clindamycin, trimethoprim-sulfamethoxazole (TMP-SMX), and doxycycline was more common in isolates with intermediate penicillin resistance and those that were penicillin-resistant.
  • H influenzae are gram-negative, facultatively anaerobic bacilli. H influenza type B was a leading cause of meningitis until the widespread use of the vaccine. Nontypeable strains of H influenza are responsible for 22-35% of acute bacterial rhinosinusitis cases in adults. M catarrhalis are gram-negative, oxidase-positive, aerobic diplococci. M catarrhalis is the responsible pathogen in 2-10% of acute bacterial rhinosinusitis cases in adults. Beta-lactamase production is the mechanism of antimicrobial resistance for both M catarrhalis and H influenza. Of isolates from the paranasal sinus, 32.7% and 98% were found to be beta-lactamase–positive for H influenza and M catarrhalis, respectively.
  • Although accounting for 10% of episodes of acute bacterial rhinosinusitis, S aureus is now recognized as an increasingly common pathogen in acute bacterial rhinosinusitis.9 While methicillin-resistant S aureus (MRSA) still represents a minority of episodes of S aureus rhinosinusitis, increasing trends of drug-resistant S aureus may alter future treatment recommendations.10
  • Rarely, sinusitis is caused by fungi, including genera in the order Mucorales and Aspergillus or Candida species. Fungal infections are more common in people with diabetes and those who are immunocompromised. Clinicians should maintain a high index of suspicion for acute invasive fungal sinusitis in immunocompromised patients with orbital or CNS complications of rhinosinusitis.

More on Sinusitis, Acute

Overview: Sinusitis, Acute
Differential Diagnoses & Workup: Sinusitis, Acute
Treatment & Medication: Sinusitis, Acute
Follow-up: Sinusitis, Acute
References

References

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  2. Gwaltney JM Jr. Acute community-acquired sinusitis. Clin Infect Dis. Dec 1996;23(6):1209-23; quiz 1224-5. [Medline].

  3. Lucas JW, Schiller JS, Benson V. Summary health statistics for U.S. adults: National Health Interview Survey, 2001. Vital Health Stat 10. Jan 2004;(218):1-134. [Medline].

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  5. Hansen JG, Schmidt H, Rosborg J, Lund E. Predicting acute maxillary sinusitis in a general practice population. BMJ. Jul 22 1995;311(6999):233-6. [Medline].

  6. Gwaltney JM, Hendley JO, Simon G. Rhinovirus infections in an industrial population. II. Characteristics of illness and antibody response. JAMA. Nov 6 1967;202(6):494-500. [Medline].

  7. Hickner JM, Bartlett JG, Besser RE. Principles of appropriate antibiotic use for acute rhinosinusitis in adults: background. Ann Intern Med. Mar 20 2001;134(6):498-505. [Medline].

  8. Jacobs MR, Bajaksouzian S, Windau A, Good CE, Lin G, Pankuch GA. Susceptibility of Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis to 17 oral antimicrobial agents based on pharmacodynamic parameters: 1998-2001 U S Surveillance Study. Clin Lab Med. Jun 2004;24(2):503-30. [Medline].

  9. Payne SC, Benninger MS. Staphylococcus aureus is a major pathogen in acute bacterial rhinosinusitis: a meta-analysis. Clin Infect Dis. Nov 15 2007;45(10):e121-7. [Medline].

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  11. [Best Evidence] Zalmanovici A, Yaphe J. Steroids for acute sinusitis. Cochrane Database Syst Rev. Apr 18 2007;CD005149. [Medline].

  12. [Best Evidence] Williamson IG, Rumsby K, Benge S, Moore M, Smith PW, Cross M, et al. Antibiotics and topical nasal steroid for treatment of acute maxillary sinusitis: a randomized controlled trial. JAMA. Dec 5 2007;298(21):2487-96. [Medline].

  13. [Best Evidence] Ahovuo-Saloranta A, Borisenko OV, Kovanen N, Varonen H, Rautakorpi UM, Williams JW Jr, et al. Antibiotics for acute maxillary sinusitis. Cochrane Database Syst Rev. Apr 16 2008;CD000243. [Medline].

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  15. Cunha BA. Antibiotic Essentials. 7th ed. Boston, MA: Jones and Bartlett Publishers; 2008.

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Further Reading

Keywords

acute sinusitis, rhinosinusitis, acute rhinosinusitis, common cold, seasonal allergy, bacterial infection, flu, Streptococcus pneumoniae, S pneumoniae, Haemophilus influenzae, H influenzae, acute ethmomaxillary sinusitis, rhinitis, subacute sinusitis, subacute rhinosinusitis, maxillary sinusitis, ethmoidal sinusitis, frontal sinusitis, sphenoidal viral sinusitis, bacterial sinusitis, fungal orbital sinusitis, intracranial sinusitis, maxillary rhinosinusitis, ethmoidal rhinosinusitis, frontal rhinosinusitis, sphenoidal viral rhinosinusitis, bacterial rhinosinusitis, fungal orbital rhinosinusitis, intracranial rhinosinusitis, acute viral rhinosinusitis, acute bacterial rhinosinusitis, acute viral sinusitis, acute bacterial sinusitis

Contributor Information and Disclosures

Author

Brian E Benson, MD, Staff Physician, Department of Otolaryngology, St Luke's-Roosevelt Hospital Center; Clinical Instructor, Department of Otolaryngology, Hackensack University Medical Center
Brian E Benson, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Otolaryngic Allergy, American Academy of Otolaryngology-Head and Neck Surgery, and Sigma Xi
Disclosure: Nothing to disclose.

Coauthor(s)

Linas Riauba, MD, Assistant Professor of Clinical Medicine, Department of Medicine, Section of Infectious Disease, University Hospital, University of Medicine and Dentistry of New Jersey
Linas Riauba, MD is a member of the following medical societies: American Medical Association and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Tracey Quail Davidoff, MD, Senior Clinical Instructor, Department of Emergency Medicine, Rochester General Hospital
Tracey Quail Davidoff, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Forensic Examiners, American College of Physicians, and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Thomas Herchline, MD, Professor of Medicine, Wright State University Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio
Thomas Herchline, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Gordon L Woods, MD, Consulting Staff, Department of Internal Medicine, University Medical Center
Gordon L Woods, MD is a member of the following medical societies: Society of General Internal Medicine
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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