Rhinitis, Sinusitis, Including Orbital and Cranial Complications, Invasive Fungal Rhinosinusitis



Rhinitis, Sinusitis, Including Orbital and Cranial Complications, Invasive Fungal Rhinosinusitis


Ashton Lehman

Di Coneybeare



INTRODUCTION

Rhinitis, rhinosinusitis, and their suppurative complications present commonly in the emergency department (ED). Rhinitis alone afflicts 10% to 40% of the general population globally and more than 60 million Americans annually, whereas rhinosinusitis afflicts about one in six Americans annually.1,2,3

The sinonasal region—including the nasal cavity and bilateral paranasal sinuses—serves as a conduit for air movement while heating and humidifying inspired air; a filter for airborne particulate matter; a detection system for odorants, irritants, and temperature changes; and a defense system capable of triggering innate and adaptive immune system responses.4 This region is susceptible to a heterogeneous group of infectious and inflammatory conditions, many of which result in overlapping symptomatology in children and adults.5

When rhinosinusitis inflammation or infection extends beyond the paranasal sinuses and nasal cavity to involve neurologic, ophthalmologic, osseous, or soft tissue regions, it is considered complicated. Although rare, such complications (eg, orbital cellulitis, orbital abscesses, meningitis, and brain abscesses) can lead to significant morbidity and mortality.6 Given this potential risk, accurate and expeditious diagnosis and prompt management of sinonasal conditions are critical in ED and urgent care settings.


THE CLINICAL CHALLENGE

Because the sinus and nasal structures abut each other sharing continuous mucosa, many consider diseases of the sinonasal region along a pathologic spectrum.1,2 However, treatment options may differ dramatically depending on the underlying pathophysiology, location, and the severity of disease. Allergic and nonallergic rhinitis often share similar symptoms.3 Likewise, viral rhinitis and rhinosinusitis have significant symptomatologic overlap with acute bacterial rhinosinusitis.2 Differentiating between viral and bacterial rhinosinusitis is challenging to emergency providers. Physical exam findings are often subtle, and many serious suppurative complications of bacterial rhinosinusitis may present without the overt neurologic deficits that traditionally signify their presence.6 Imaging from computed tomography (CT) will result in similar findings in patients with a common cold as well as
in patients with bacterial rhinosinusitis.5 Furthermore, nasal microbiologic results may be misleading; even patients with viral illness may be colonized by common nasopharyngeal flora. For example, Staphylococcus aureus can be present in up to 30% of healthy adults, and fungi are almost ubiquitous.5,6

Uncertainty in diagnosis may lead to inappropriate antibiotics, therapeutics, and costly imaging.6 When to start antibiotics vexes providers the most. Viral infections most commonly afflict patients presenting with rhinosinusitis, and even in the case of bacterial rhinosinusitis, about two-thirds of patients will improve without any pharmaceutical intervention.5 However, if left untreated, serious bacterial rhinosinusitis may progress to life-threatening intracranial and extracranial suppurative complications.




PATHOPHYSIOLOGY

Rhinitis is defined by allergic or nonallergic inflammation of the nasal mucosa. The epithelial layer of the nasal mucosa overlies submucosal layers and filters the external world for the body’s immune system.2 Submucosal layers secrete mucous that protects the nasal airway as a physical barrier and through production of various glycoproteins with antimicrobial and antioxidant properties.2 Epithelial cilia brush mucous posteriorly that has trapped environmental foreign particles.2 In allergic rhinitis, an IgE-mediated process, patients respond to allergens by activating epithelial cells, instigating downstream inflammatory reactions. Excessive mucous production and increased vascular permeability result in congestion and nasal drainage. By contrast, inflammation from nonallergic rhinitis is, by definition, not IgE-mediated. Common causes of nonallergic rhinitis that can directly activate inflammatory reactions include infection (viral or bacterial), food- or drug-triggered, and idiopathic (formally known as vasomotor rhinitis).2,5

The mucosa that lines the nasal cavity extends throughout the four paranasal sinuses on each side (Figure 11.1): frontal, maxillary, sphenoid, and ethmoid.1 Sinus secretions drain via a complex and connected system of ostia that is contiguous through all the paranasal sinuses.6 Pathology of the sinuses is thus caused by inflammation of its mucosa, obstruction of its ostia, structural abnormalities, direct extension of pathology from adjacent structures, and/or ciliary dysfunction.6 Because the nasal and sinus mucosa are contiguous, pathology in either region almost always affects the other, and hence inflammation is often referred to as “rhinosinusitis.”3

Bacterial infections of the sinuses are often caused by stasis of sinonasal mucous, which fosters a breeding ground for bacteria. Infections are mostly polymicrobial, often representative of nasal and oropharyngeal flora. Common pathogens include Streptococcus pneumoniae, Haemophilus influenzae B, Moraxella catarrhalis, S aureus, anaerobes, and fungi.

Intracranial complications of sinusitis can be caused by seeding via septic emboli from diploic veins originating at the base of the skull penetrating the dura or via direct extension through ostia of the skull or from rhinosinusitis-related osteomyelitis.6 Orbital and other extracranial complications of rhinosinusitis occur primarily via direct extension associated with infections of the ethmoid and maxillary sinuses.6

Fungi thrive in the setting of hyperglycemia and acidosis, and this explains why acute invasive fungal infections of the sinonasal region occur almost exclusively in patients with poorly controlled diabetes or those otherwise immunocompromised.1,7 Aspergillus, Mucor, and Rhizopus are implicated in most patients with acute invasive fungal rhinosinusitis.


APPROACH/THE FOCUSED EXAM

During history-taking, noteworthy elements include the presence, character, and time course of symptoms as well as history of neurosurgery or sinonasal surgery. Specific relevant historical features and important comorbid conditions can be found in Table 11.1.

Examination of the sinonasal region includes an external evaluation of the nose, internal evaluation with anterior rhinoscopy and rigid nasal endoscopy, evaluation of facial soft tissues, orbits, oral cavity, and relevant neurologic function. Note edema, erythema, warmth, fluctuance, drainage, or changes in sensation of the facial soft tissues overlying the nasal, maxillary, and frontal regions. Orbital findings such as epiphora (ie, excessive tearing), lid abnormalities, proptosis, extraocular movements, visual acuity, light perception/sensitivity, pupil reactivity, and red desaturation should be assessed. The status of dentition and the presence of fistulae or palatal changes should be noted.

The workup of sinonasal pathology may include imaging in cases with a suspected complication or alternative diagnosis (eg, nonsinonasal causes of facial pain, potential malignant processes
signified by concomitant neurologic deficits).2 If an orbital or intracranial complication is suspected, suggested by severe headache, facial swelling, cranial nerve palsies, proptosis, impaired extraocular movements, or impaired visual acuity, contrast-enhanced CT is the initial imaging modality of choice.5,6 Depending on the presentation and the findings on initial CT imaging, magnetic resonance imaging (MRI) may be pursued. MRI often offers superior resolution of soft tissues, intracranial complications, and orbital complications/pathology.4,6