Health Questions and Answers

Rhinosinusitis

Define sinusitis.
Strictly speaking, sinusitis is inflammation of the mucosal lining of the paranasal sinuses secondary to many potential triggers. The term rhinosinusitis has been emphasized recently to highlight the importance of nasal cavity mucosal pathology in the overall disease process.

Describe the pathophysiology of sinusitis.
Mucosal edema of the paranasal sinuses is the basic event leading to both acute and chronic disease. Edema may lead to obstruction of the drainage routes of the sinuses, causing stasis of secretions and an overall physiologic change in the sinus cavity. These local changes lead to impaired mucociliary clearance, alteration in local immune defenses, and ultimately bacterial overgrowth.
Perhaps the two most important potenital triggers underlying sinusitis are upper respiratory viral infection and upper airway allergy. Additional factors include environmental hypersensitivites, mucociliary dysfunction (primary and acquired), anatomic relationships (septal deviation, nasal polyposis), immunodeficiencies, and fungal hypersensitivities.

How do allergies predispose a patient to rhinosinusitis?
Type I atopy leads to the elaboration of multiple early- and late-phase inflammatory mediators. The result will be a multitude of mucosal changes in a sensitive patient. Mucus hypersecretion, edema, and impaired mucociliary function can occur, setting the stage for bacterial infection.

Which sinus is most often involved in rhinosinusitis?
In the majority of cases, the maxillary sinus and anterior ethmoid sinuses are involved. This can be predicted by the anatomy of the middle meatus or infundibulum, the location for drainage of the “anterior sinuses” (maxillary, anterior ethmoid, frontal sinuses)

Describe the signs and symptoms of acute bacterial rhinosinusitis (ABRS).
In can be very difficult to distinguish between ABRS and other causes of acute nasal congestion (viral rhinitis, allergic/nonallergic rhinitis). The 1996 Task Force on Rhinosinusitis developed a list of symptoms and signs to serve as a guideline in making the diagnosis of ABRS. A diagnosis of ABRS may be made in adults or children with a viral upper respiratory infection does not dissipate within 10 days (or worsens after 5-7 days) and is accompanied by some or all of these symptoms.
SIGNS AND SYMPTOMS OF ABRS
Nasal drainage
Nasal congestion
Facial pain/pressure (especially when unilateral and focused in the region of a particular sinus group)
Postnasal drip
Hyposmia/anosmia
Fever
Cough
Fatigue
Maxillary dental pain
Ear fullness/pressure

What are the most common organisms associated with ABRS?
Streptococcus pneumoniae (20-40%), Haemophilus influenzae (20-35%), and Moraxella catarrhalis (2-10%) are the most common pathogens associated with ABRS. Less common pathogens include Staphylococcus aureus (0-9%), anaerobes (0-9%), and streptococcal species (3-9%).
A relatively new issue in the management of ABRS is evolving antibiotic resistance. Essentially all of the most common pathogens in ABRS now demonstrate decreased antibiotic sensitivities to many of the commonly used drugs and related drug classes. This has directly affected antibiotic selection in the treatment of ABRS. The incidence of beta-lactamase production in isolates of H. influenzae is 30-40%, and for isolates of M. catarrhalis it is 92%.

Which organisms are associated with chronic bacterial rhinosinusitis (CRS)?
The same organisms found in acute disease are also prevalent in chronic rhinosinusitis. The following pathogens are more frequently associated with chronic rhinosinusitis: S. aureus, Pseudomonas aeruginosa, Proteus species, Enterobacter species, Klebsiella species, coagulase-negative Staphylococcus species, and possibly anaerobes. Generally speaking, gram-negative rods and staphylococcal species become more important pathogens in patients with CRS.

PREVALENCE OF ANTIMICROBIAL RESISTANCE AMONG ISOLATES OF S. PNEUMONIAE
Penicillin “nonsusceptible” 30%
Trimethoprim/sulfamethoxazole 37%
Macrolides 29%
Doxycycline 21%
Clindamycin 10%
Source: From Jacobs MR, Felmingham D, Appelbaum PC, Gruneberg RN, and the Alexander Project Group: The Alexander Project 1998-2000: Susceptibility of pathogens isolated from community-acquired respiratory tract infections to commonly used antimicrobial agents. J Antimicrob Chemother 52:229-246, 2003.

Describe the categories of fungal sinusitis.
Acute fulminant invasive fungal sinusitis is less than 4 weeks in duration and nearly universally involves patients who have some form of immunosuppression. The fungus is angioinvasive and destroys bone and tissue. It has a relatively high mortality and requires extensive surgical debridement of all nonviable tissue as well as systemic intravenous antifungal medication such as amphotericin B.
Chronic invasive fungal sinusitis is most commonly found in patients with diabetes mellitus, and Aspergillus fumigatus is the most common pathogen.
Granulomatous invasive fungal sinusitis has also been called indolent fungal sinusitis. It predominates in immunocompetent individuals, but it is invasive. The invasion is limited to the superficial mucosa. Granulomas surround the invasive fungal elements and limit deeper penetration. Fungus balls, or mycetomas, usually present as a unilateral opacification of either the maxillary or sphenoid sinus. Patients are classically immunocompetent without evidence of atopy.
Allergic fungal sinusitis is believed to be a type I, IgE-mediated hypersensitivity to fungal antigens present in the paranasal sinuses. Diagnostic criteria include fungal atopy, nasal polyposis, computed tomographic (CT) scan with evidence of hyperdense sinus infiltrate, allergic mucin with eosinophils, and fungal identification by culture or histopathology.
Eosinophilic fungal rhinosinusitis: Recent work at the Mayo Clinic has suggested a new or competing hypothesis for the etiology of chronic sinusitis, and in particular, the role of fungi. Though still controversial, their research proposes a T cell-mediated response to fungal antigens as the basic mechanism behind the chronic inflammatory state seen in many forms of chronic sinus disease.

What is Samter’s triad?

Samter’s triad is a syndrome with the following clinical features: (1) aspirin sensitivity (intolerance), (2) nasal polyposis, and (3) bronchospasm/asthma. When exposed to aspirin or nonsteroidal anti-inflammatory drugs, these patients will experience bronchospasm, worsening upper and lower airway inflammation, and often exacerbation of their sinus symptoms. Although not clearly understood, the pathophysiology appears to be at least in part due to dysfunction in the arachidonic acid metabolism pathway. These patients will typically have increased levels of the leukotrienes B4, C4, and D4 both in the serum and in the involved respiratory tissues. Approximately 10% of patients with nasal polyposis have aspirin intolerance.
KEY POINTS: PATHOPHYSIOLOGY, ETIOLOGY, AND CLASSIFICATION
The most common pathogens in both adult and pediatric ABRS are S. pneumoniae, H. influenzae, and M. catarrhalis.
The following antibiotic resistance patterns are important in ABRS: penicillin-resistant S. pneumoniae (25-40%), beta-lactamase-producing H. influenzae (30-40%), and beta-lactamase-producing M. catarrhalis (92%).
Eosinophilic infiltration is the hallmark of most forms of chronic hyperplastic rhinosinusitis; 50% of patients have asthma.
Samter’s triad includes aspirin sensitivity, asthma, and nasal polyposis.

What are the potential complications of sinusitis? Which complication is most common and why?
Complications include disease extension into the orbit or intracranial structures, facial cellulites, cavernous sinus thrombosis, osteomyelitis, visual changes, and mucocele formation. Orbital complications (preseptal or orbital cellulitis) are most common, owing to easy extension of infection along the thin sinus bone surrounding the orbit on three sides. Meningitis is usually regarded as the most common intracranial complication of sinusitis and can arise from the sphenoid or ethmoid sinuses. Although now rare owing to early treatment, epidural and subdural abscesses are associated with frontal sinusitis most commonly. A brain abscess may also occur in the setting of sinusitis (approximately 15% of cases) and carries a high mortality rate (20-30%). It is most often associated with frontal or ethmoid disease.

What are the treatment goals for ABRS?
The primary goals of this treatment are as follows: (1) to return the sinuses to a healthy state; (2) to decrease the duration of the patient’s symptoms; (3) to prevent complications associated with acute sinusitis; and (4) to prevent the development of chronic disease.

You have diagnosed the patient with ABRS. What is your management?
Studies in both adult and pediatric populations have confirmed that patients with ABRS treated with antibiotics will experience more rapid resolution of symptoms when compared with placebo. Although the spontaneous resolution rate for ABRS may approach 50%, the literature supports the use of antimicrobials in properly diagnosed patients.
In addition to antibiotics, the medical management of ABRS should include adjunctive treatments directed at reducing mucosal inflammation. These commonly include nasal steroids, topical decongestants (e.g., oxymetazoline, phenylephrine [Neo-Synephrine]), oral decongestants (e.g., pseudoephedrine), mucolytics (e.g., guaifenesin), and nasal saline irrigation.
The addition of topical corticosteroids to antibiotic therapy has recently been shown to improve patient symptoms within the first 7 days of treatment. Topical decongestants such as oxymetazoline or phenylephrine may be recommended for short-term use (2-5 days) as an adjunct to these therapies. These agents reduce mucosal and turbinate edema, allowing more effective drainage of the paranasal sinuses. In general, antihistamines are to be avoided in ABRS because anticholinergic adverse effects will thicken and dry secretions.

What are the antibiotics of choice in the treatment of pediatric ABRS?
A 10- to 14-day course is also recommended for children. Similar to the adult guidelines, the pediatric protocols are based on the current increased antibiotic resistance patterns encountered in clinical practice.
Agents for children with moderate disease or recent antibiotic use are amoxicillin/clavulanate and ceftriaxone. As in adults, failure of this group to elicit improvement should prompt reevaluation.

Discuss the role of anti-inflammatory agents in the treatment of CRS.
Whereas the importance of bacterial infection in CRS still remains debated, the importance of chronic inflammatory mucosal disease cannot be overemphasized. In many cases, attempts to control the inflammatory component of the disease are the cornerstone of therapeutic intervention. Important treatment options include prolonged intranasal steroids, the use of systemic steroids (oral, intramuscular), leukotriene receptor antagonists (e.g., montelukast, zafirlukast), and immunotherapy for allergic disease in select patients. The length and type of therapy will depend on clinical symptoms, stage of disease, and suspected underlying triggers. Patients with hyperplastic CRS will also have asthma in 50% of cases. These patients have been shown to have increased respiratory tissue eosinophilia with difficult-to-control mucosal inflammation.

Describe the role of antimicrobial treatment in CRS.
As outlined previously, the incidence of S. aureus, Staphylococcus epidermidis, P. aeruginosa, and other gram-negative organisms appear to be higher in CRS than in ABRS. This presents a problem in many cases due to reduced antibiotic sensitivities for these organisms. The end result may be a limited number of oral antibiotic options, potentially increasing the need for alternative delivery options (e.g., intravenous, topical). In cases where bacterial infection is suspected to be a major factor, the typical approach will be culture-directed antibiotic therapy for a minimum of 4 weeks. Duration of therapy will be dependent on patient symptoms, repeat culture data, nasal endoscopy, and CT findings.
KEY POINTS: MEDICAL MANAGEMENT OF ABRS

  • The medical therapy for ABRS includes topical decongestants, topical corticosteroids, nasal saline irrigation, and antibiotics defined by specific guidelines.
  • Medical management of ABRS involves agents that target the inflammatory process in addition to antibiotics.
  • Complications of ABRS include facial cellulitis, orbital cellulitis, meningitis, cavernous sinus thrombosis, and intracranial abscess formation.

What role does fungus play in CRS?
The issue of fungal rhinosinusitis still remains controversial, although data suggest it is an important factor in some patients with CRS. If fungal CRS is suspected and confirmed, several options for treatment are available. Although oral antifungal protocols have been recommended (e.g., itraconazole daily for 3-6 months), their efficacy has not been established. Antifungal sinus irrigations have been used in some form for decades. Recently, the Mayo Clinic group began using amphotericin B (100 µg/mL) 20 mL per nostril per day as a topical treatment method. Preliminary data have been encouraging, but prospective controlled data are pending.

Surgical Management

What is the role of surgical intervention in rhinosinusitis?
Surgery is a key component in the comprehensive management of rhinosinusitis. For complicated acute sinusitis, such as subperiosteal or epidural abscesses, the role of surgery is acute decompression of the affected sinuses as well as the area of abscess. For chronic or recurrent sinusitis, the role of surgery is to facilitate the natural drainage of the sinuses, when possible, through correction of identifiable anatomic aberrations. Generally speaking, surgery is not a cure for CRS but an adjunctive treatment option for select patients. Medical management remains the primary option for rhinosinusitis and is effective in the majority of patients.

What surgical procedures are commonly performed for nasal obstruction?
Septoplasty is the correction of a deviation in the nasal septum responsible for obstruction of the nasal airway. This deviation may involve the cartilaginous or bony segments of the nasal septum and commonly involves both. This procedure may also be necessary during endoscopic sinus surgery to provide access to the middle meatus.
Inferior turbinate hypertrophy also frequently contributes to nasal obstruction. Reduction of the inferior turbinates may be performed by many methods, including excision, electrocautery, radiofrequency ablation, and submucous resection/reduction. The function of the inferior turbinates is complex and invaluable; thus radical resection or surgical maneuvers that potentially disrupt function should be avoided.

What is functional endoscopic sinus surgery (FESS)?
Endoscopic sinus surgery has become the preferred technique for the surgical management of most forms of rhinosinusitis. FESS describes a series of techniques that use nasal endoscopes for access to the paranasal sinuses rather than external approaches. The concept of functional surgery implies using techniques that facilitate the natural drainage patterns of the sinuses through the osteomeatal complex, rather than creating alternative drainage pathways that are contrary to physiologic mucociliary flow. The key concept is atraumatic surgical technique, mucosal preservation, and restoration of normal sinus physiology.

Describe the preoperative evaluation of patients undergoing FESS.
An accurate history including previous medical therapy is vital to identify candidates likely to benefit from surgery. Complete head and neck physical examination including nasal endoscopy will allow the nasal anatomy and mucosa to be evaluated. Coronal sinus CT scans are an important component of this evaluation. These are vital for evaluating the sinus anatomy and for identifying the presence of mucosal disease. Several CT staging systems exist for grading the extent of rhinosinusitis. Overall, FESS may be considered an option in patients with persistent symptoms of rhinosinusitis combined with objective evidence of disease on endoscopy and/or CT despite maximal medical therapy.


What are the basic principles of FESS surgery?

As emphasized previously, the goal of FESS is to minimize mucosal trauma to the paranasal sinuses while providing drainage for the sinuses. Thus, resection of diseased mucosa and anatomic structures must be minimized to optimize functional outcome. Osteomeatal complex obstruction or infundibular disease may first be addressed by the performance of a maxillary antrostomy. The maxillary sinus ostium is exposed by removing the uncinate process. If indicated, the maxillary ostium may be enlarged using a variety of instruments. Then, as indicated, an anterior ethmoidectomy may be performed by first opening the ethmoid bulla. Dissection proceeds posteriorly along the inferomedial aspect of the ethmoid labyrinth until the basal lamella of the middle turbinate is encountered, marking the demarcation between the anterior and posterior ethmoid cells. The dissection then proceeds superiorly along the lamella to the skull base. Remaining ethmoid cells are dissected with the skull base superiorly and lamina papyracea laterally serving as limits of dissection. Superiorly, the frontal recess is identified. If frontal disease is present, the outflow tract may be cleared of cells and mucosal disease allowing for ventilation of the frontal sinus. As indicated, the posterior ethmoids may be dissected by continuing the anterior dissection posteriorly through the basal lamella. If necessary, a sphenoidotomy can be performed by first identifying the natural ostium of the sphenoid sinus followed by enlarging the os (natural sphenoid opening) inferiorly and medially. The sphenoid os is located medially to the superior turbinate 80% of the time. The sphenoid os may be approached via a transnasal or transethmoidal route.
KEY POINTS: SURGICAL MANAGEMENT OF ABRS

  1. FESS has replaced external approaches as the standard surgical management of rhinosinusitis.
  2. The key concepts of FESS involve atraumatic surgical technique, mucosal preservation, and restoration of normal sinus physiology.
  3. Coronal sinus CT scans are essential studies to obtain before FESS to define pathology and minimize surgical complications (e.g., presence of low-lying cribriform plate).
  4. The major complications of FESS include orbital injury, intracranial injury, and cerebrospinal fluid leak. Prompt recognition and resolution of these conditions are imperative.

Discuss the surgical approaches to the frontal sinus.
Advanced endoscopic techniques have allowed for better visualization and improved management of frontal sinus disease. Although often requiring special instrumentation and extensive experience, endoscopic frontal sinusotomy has become the preferred approach in many cases. Angled forceps, curved suction devices, and the 45-degree endoscope are just a few of the technologic advances that have made endoscopic frontal sinus surgery possible. Computer-aided sinus surgery or image-guided sinus surgery has also added to our ability to safely and effectively approach the frontal sinus endoscopically. The frontal sinus may also be approached externally via a Lynch incision superior to the medial canthus and inferior to the medial aspect of the eyebrow. Additional external approaches include a bicoronal flap for direct access to the anterior table of the frontal sinus, with an osteoplastic flap developed to enter the sinus. This approach is most commonly used for frontal sinus cranialization, for frontal sinus obliteration procedures, or for access to anterior skull base lesions.

What are the complications of FESS?
The major complications of FESS involve orbital and intracranial injury. Orbital injury ranges from periorbital ecchymosis and emphysema to orbital hematoma and blindness. Prompt recognition of developing orbital complications is paramount to preventing further and permanent damage to the eye. Anisocoria, ophthalmoplegia, and proptosis are ominous signs demanding prompt action. Measures to relieve orbital pressure include the administration of steroids or mannitol or the performance of orbital decompression via lateral canthotomy, external ethmoidectomy, or endoscopic orbital decompression.
Intracranial complications of FESS include CSF leak, meningitis, direct brain injury, carotid artery injury, and tension pneumocephalus. The most likely sites of skull base breach include the cribriform plate and roof of the ethmoid sinus. If identified intraoperatively, successful endoscopic repair is likely (> 90% success).
Other complications of FESS include lacrimal injury, anosmia, major hemorrhage from the ethmoid or sphenopalatine arteries, synechiae, and mucociliary dysfunction secondary to overresection of anatomic structures.

Last Updated: 03/10/2010

References:

  1. Benninger MS, Ferguson BJ, Hadley JA, et al: Adult chronic rhinosinusitis: Definitions, diagnosis, epidemiology, and pathophysiology. Otol Head Neck Surg 129:S1-S32, 2003.
  2. Jacobs MR, Felmingham D, Appelbaum PC, et al: The Alexander Project 1998-2000: Susceptibility of pathogens isolated from community-acquired respiratory tract infections to commonly used antimicrobial agents. J Antimicrob Chemother 52:229-246, 2003.
  3. Kennedy DW, Bolger WE, Zinreich SJ: Diseases of the Sinuses: Diagnosis and Management. Hamilton, Ontario, B.C. Decker Inc., 2001.
  4. Lanza DC, Kennedy DW: Adult rhinosinusitis defined. Otolaryngol Head Neck Surg 117:S1-S7, 1997.
  5. Lund VJ, Kennedy DW: Staging for rhinosinusitis. Otolaryngol Head Neck Surg 117:S35-S40, 1997.
  6. Senior BA, Kennedy DW, Tanabodee J, et al: Long-term results of functional endoscopic sinus surgery. Laryngoscope 108:151-157, 1998.
  7. Sinus and Allergy Health Partnership: Antimicrobial treatment guidelines for acute bacterial rhinosinusitis. Otolaryngol Head Neck Surg 130(Suppl 1): 1-45, 2004.
  8. Stankiewicz JA: Complications of endoscopic sinus surgery. Otolaryngol Clin North Am 22:749-758. 1989.
  9. Williams JW Jr, Aguilar C, Cornell J, Chiquette ED, et al: Antibiotics for acute maxillary sinusitis [update of Cochrane Database Syst Rev 2000;(2):CD000243; PMID: 10796515]. Cochrane Database of Systematic Reviews. (2):CD000243, 2003.

5 Responses to “Rhinosinusitis”

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