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Understanding the pathogenesis of rhinosinusitis depends on defining the specific types of rhinosinusitis.
Acute bacterial rhinosinusitis (ABRS), chronic rhinosinusitis (CRS), and acute exacerbation of chronic rhinosinusitis (AECRS) are three distinct entities.
A number of environmental and host factors predispose to the development of rhinosinusitis; these include allergy, infection, and environmental exposures.
Acute rhinosinusitis is usually the result of a viral infection, whereas ABRS occurs primarily with Streptococcus pneumoniae , Haemophilus influenzae , Moraxella catarrhalis, and Staphylococcus aureus .
The treatment of acute rhinosinusitis has changed with the emergence of resistance to the common pathogens and the routine use of S. pneumoniae and H. influenzae immunizations.
After thorough reviews of the literature, multiple guidelines have been proposed that now suggest amoxicillin with clavulanic acid as a first-line treatment; this is due to the growing emergence of beta-lactamase–producing organisms, particularly H. influenzae . High-dose amoxicillin-clavulanate is recommended in individuals or environments where levels of S. pneumoniae resistance are high. In adult patients with uncomplicated ABRS, a trial of watchful waiting is considered an appropriate alternative to immediate antibiotic therapy.
AECRS is a sudden worsening of symptoms in a patient with CRS. It is often associated with an increase in the bacteria prominent in the exacerbation. Although an increase is seen in the organisms typically associated with ABRS— S. pneumoniae , H. influenzae , M. catarrhalis, and Staphylococcus aureus —a high percentage of anaerobic organisms are also identified.
In order to understand the pathogenesis and pathophysiology of rhinosinusitis, it is important to realize that different types of rhinosinusitis have been defined, and the inciting mechanism may vary dramatically among the different subtypes. Although sinusitis is the term commonly used for any inflammation or infection of sinuses, this term has largely been replaced by rhinosinusitis , because the nose is almost always involved with the infection or inflammation at the same time as the sinuses. Because many potential factors can contribute to rhinosinusitis, some debate has ensued concerning the exact definition. In general terms, rhinosinusitis is defined as “a group of disorders characterized by inflammation of the mucosa of the paranasal sinuses.” In 1997, the Rhinosinusitis Task Force of the American Academy of Otolaryngology–Head and Neck Surgery developed a now well-accepted classification of rhinosinusitis, and this was reported by Lanza and Kennedy. This classification relies on the identification of symptoms to make a diagnosis. The symptoms are broken into major symptoms—purulent nasal drainage, nasal congestion, facial pressure or pain, decreased smell, and posterior purulent drainage—and various minor symptoms. When a patient describes two major criteria or one major and two minor criteria, rhinosinusitis can be diagnosed ( Table 40.1 ). The classification of rhinosinusitis types was based primarily on time frames from the onset of symptoms. More recently, a stricter division for chronic rhinosinusitis (CRS) has been described based on endoscopic findings. These include CRS with nasal polyps (CRSwNP) and without nasal polyps (CRSsNP). The 2012 European position paper on rhinosinusitis and nasal polyps (EPOS 2012) further defines the disease process for both the adult and pediatric populations ( Box 40.1 ).
Major | Minor |
---|---|
Facial pain/pressure | Headache |
Facial congestion/fullness | Fever (nonacute) |
Nasal obstruction/blockage | Halitosis |
Nasal discharge/purulence, discolored posterior drainage | Fatigue |
Dental pain | |
Hyposmia/anosmia | Cough |
Purulence on nasal exam | Ear pain, pressure, and/or fullness |
Fever (acute rhinosinusitis only) |
Inflammation of the nose and the paranasal sinuses characterized by two or more symptoms:
Either nasal blockage/obstruction/congestion or anterior/posterior nasal discharge:
± Facial pain/pressure
± Reduction or loss of smell (± cough in children)
And either:
Endoscopic signs of:
Nasal polyps, and/or
Mucopurulent discharge primarily from middle meatus and/or
Edema/mucosal obstruction primarily in the middle meatus
And/or:
CT changes that include:
Mucosal changes within the ostiomeatal complex and/or the sinuses
CT , Computed tomography.
An inflammatory response is an expected sequela of an infectious process. Sinonasal inflammation can result from a variety of elements that result in sinus ostia obstruction and predisposes patients to infection. Many factors have been described that play a role in the development of acute bacterial rhinosinusitis (ABRS). These include factors related to the host: genetic factors such as immotile cilia syndrome or cystic fibrosis; certain systemic diseases or medical treatments that predispose individuals to infections; neoplasms; and allergic or immune disorders. Although anatomic abnormalities such as large septal spurs and large paradoxic turbinates have been suggested to be associated with rhinosinusitis, it is not currently clear whether a relation exists. Rhinosinusitis may also develop in relationship to environmental factors that include bacterial, viral, or fungal infections or inflammation that occurs secondary to fungal or bacterial colonization ; trauma; primary or secondary tobacco smoke exposure; chronic or acute irritants or noxious chemicals; or iatrogenic factors such as surgery, medications, nasal packing, or nasogastric tube placement. Evidence shows that individuals with allergic rhinitis have a higher incidence of developing both acute and CRS, and an association of ABRS with asthma has also been suggested, although this may also relate to the presence of allergic rhinitis.
The distinctions between acute rhinosinusitis (ARS), recurrent acute rhinosinusitis (RARS), subacute rhinosinusitis (SARS), and CRS and acute exacerbation of CRS (AECRS) are based on the temporal differences in the presentation and in some cases on the clinical presentation. Each of these subcategories may be associated with different pathophysiologic processes, and the predisposition to their development may vary from patient to patient. Given these differing etiologies, the pathogenesis will be described based on this classification.
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