Учебники / Rhinosinusitis - A Guide for Diagnosis and Management 2008

Fig. 13.4 Axial CT of right (R) medial periorbital abscess (arrow) and partial opacification of ethmoids bilaterally

joint surgery by otolaryngology to drain the sinus and ophthalmology to drain and monitor the orbit. Cavernous sinus thrombosis caused by sinusitis results in septic thrombosis of the cavernous sinus that can result in blindness, intracranial abscess, or death. In addition to broad-spectrum antibiotics, joint neurosurgical and sinus drainage procedures are needed to drain the infection and control the spread of the disease.

Less common periorbital abscesses have been described that occur in the superior orbit arising from frontal sinusitis, requiring drainage through extended Lynch incisions. It is also possible to have infections/abscesses based laterally in the orbit, but these usually arise from an infected lacrimal gland and are usually caused by S. aureus, and, less often, S. pneumoniae.

In contrast to OC, intracranial complications are more common in adolescents and usually arise (Fig. 13.5) from infections of the frontal sinus or from the sphenoid sinus. The risk of intracranial complications from acute sinusitis is 3% in children, similar to the 3.7% seen in adults [34]. The majority (67%) of patients with intracranial abscesses (and 5% of children with community-acquired bacterial meningitis) have had preceding frontal or sphenoid sinusitis [35]. Subdural abscesses are more common than epidural or intraparenchymal infections.

Children with intracranial complications have more subtle symptoms than those with periorbital complications (POC). They tend to present with complaints of headaches and fever; some also have signs of meningeal irritation. The diagnosis is confirmed by either CT or MRI of the brain and sinus with contrast. Patients with intracranial infections require broad-spectrum antibiotics that cross the blood– brain barrier and cover aerobic bacteria (especially S. pneumoniae and S. aureus) and anaerobic bacteria (especially Streptococcus milleri). Antibiotic choices should include third-generation cephalosporins (Cefotaxime or Ceftriaxone) along with Vancomycin to cover gram-positive organisms and, less often, Impipenem or Flagyl to cover anaerobic bacteria. Neurosurgical and ENT drainage of the sinuses are

Fig. 13.5 (a) Coronal CT image of brain with enhancement: left (L) frontal brain abscess (arrow) and opacified sinuses on left (L). (b) Axial MRI with contrast demonstrating left (L) frontal abscess (arrow)

usually performed at the same time. Except for very small intracranial collections, craniotomy is usually necessary along with endoscopic drainage of the sinuses.

Meningitis is a complication of sinusitis that may be underreported because of unrecognized sinusitis. Children with obvious sinus disease (opacified sinus or airfluid levels on CT or MRI) should have drainage procedures if they fail initial IV antibiotic.

Isolated sphenoid sinusitis can lead to severe headaches with or without fever and, less commonly, result in vision changes. It is most common in adolescent males. Given the proximity of the sinus to the brain and increased risk of intracranial spread, these children require close observation, aggressive antibiotic therapy (usually intravenous), and prompt surgical drainage of the sinus if they fail to improve after 24 to 48 h of therapy.

Summary

1.The diagnosis of bacterial AR in children should be made based on clinical grounds, but CT should be considered if the child is very ill or if extranasal complications are suspected.

2.Duration of symptoms is the most important factor in differentiating viral from bacterial disease.

3.When bacterial RS is suspected, antibiotics should be chosen that address S. pneumoniae and be given in appropriately higher doses to cover penicillinresistant strains. Follow-up evaluation is recommended if the patient fails to improve, because there is a 10% to 20% expected failure rate when less invasive beta-lactamase-producing bacteria such as H. influenzae and M. catarrhalis are responsible for the disease.

4.Children with chronic or recurrent sinusitis who fail to respond to medical therapy should undergo CT (coronal cuts) to locate the location and nature of the persistent disease or to identify anatomic anomalies or tumors.

5.Full evaluation should be done prior to elective surgery to identify coexisting adenoid hypertrophy or allergy, to rule out basic immune abnormalities (especially failure of the child to have been adequately immunized with the S. pneumoniae vaccine), and to determine if the child has the genes for cystic fibrosis (including homozygous and heterozygous states). Treatment of identified abnormalities should be considered before sinus surgery, including adenoidectomy, allergy control, and booster vaccination.

6.CT and/or MRI with contrast imaging of the sinuses and orbit and brain should be obtained in ill children who have severe disease, and the child should be promptly referred to appropriate specialists if orbital or neurological signs of complication are present.

References

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Chapter 14

Spectrum of Fungal Sinusitis

Kevin C. Welch and James N. Palmer

Fungi are diverse and ubiquitous organisms. Their spores are frequently respired and can be found throughout the nose and sinuses. Generally, the human immune system is naturally equipped to eliminate these airborne invaders; however, in approximately 10% of patients, fungal spores and elements become manifest as disease. The manifestation of disease within the nose and paranasal sinuses varies widely from the benign to the utterly malignant and fatal.

Fungal infections of the paranasal sinuses can be broadly divided into two categories based on the histopathological diagnosis of tissue invasion. For the purposes of this chapter, fungal disease is either noninvasive or invasive [1,2]. The primary manifestations of noninvasive disease are the development of fungal balls or allergic fungal sinusitis (AFS). Invasive fungal sinusitis occurs either as an acute, rapidly progressive sinusitis or in a chronic fashion.

This chapter outlines the diagnosis and treatment of the various forms of fungal sinusitis. A summary of forms of fungal sinusitis can be found in Table 14.1.

Noninvasive Fungal Sinusitis

Characteristics of Fungus

The fungal species typically responsible for noninvasive human infections are divided into two categories based upon their morphological appearance: yeasts and molds. Yeasts are typically round, budding, and reproduce asexually by fission. Molds amalgamate into colonies typified by interwoven hyphae; they produce spores, which can be sexual or asexual. These fungi responsible for noninvasive disease are usually dematiaceous (dark colored) or hyaline (lightly colored) species, are ubiquitous in nature, and typically demonstrate septate hyphal forms. Dematiaceous species responsible for noninvasive disease include members of the

J.N. Palmer

Department of Otorhinolaryngology – Head and Neck Surgery, University of Pennsylvania Health System, Philadelphia, PA, USA

e-mail: james.palmer@uphs.upenn.edu

following genera: Bipolaris, Curvularia, Pseudallescheria, Penicillium, Fusarium, and Alternaria. Hyaline molds seen in noninvasive disease are typically members of Aspergillus.

Fungal Balls

Fungal balls present in the setting of an immunocompetent host with chronic rhinosinusitis (CRS) or the patient with recurrent acute rhinosinusitis of one sinus, typically the maxillary sinus [2]. Symptoms related to fungal balls are nonspecific, or may not even be present. Physical examination with rigid endoscopy reveals a spectrum of disease that ranges from mild edema to frank polyposis with mucopurulence in the patient with concomitant CRS or AFS. Intraoperatively, fungus balls appear as focal lesions that are gritty, dirt like, and vary in color depending upon the fungal elements.

Diagnosis

Imaging of the paranasal sinuses will show unilateral or single sinus disease that, with the exception of a differential density, is often nonspecific. As previously mentioned, the intraoperative findings (Fig. 14.1) confirm the diagnosis when characteristic isolated sinus lesions are identified that often must be scraped or flushed from the sinus. Although the offending agents are typical dematiaceous or hyaline species, often cultures are unrevealing [2,3]. On microscopic examination, densely packed septated fungal hyphae are typically identified. Underlying sinonasal mucosa may demonstrate an influx of leukocytes with evidence of chronic inflammation.

Treatment

Therapy for fungal balls is aimed at elimination of disease and restoration of sinus ventilation and outflow, performed through endoscopic techniques. Extirpation of the fungal ball typically results in a cure, and recurrence rates are minimal [3]. Systemic or topical antifungal medications are not indicated.

Allergic Fungal Sinusitis

Allergic fungal sinusitis is a form of CRS that was initially recognized in 1976 by Safirstein and colleagues, [4] who described a condition of CRS, nasal polyposis, and aspergillus in a patient with allergic bronchopulmonary aspergillosis (ABPA). Later, in 1981, Millar and coworkers [5] reported on a series of patients with CRS and cultures demonstrating Aspergillus and their similarities to patients with ABPA, a pulmonary manifestation of hypersensitivity to Aspergillus species associated with asthma, peripheral eosinophilia, and elevated IgE. Progressively, an entity of CRS associated with allergies to Aspergillus species was described. These patients were

Fig. 14.1 A patient presented with vertex headaches and a unrevealing nasal endoscopy. After computed tomography (CT) and magnetic resonance imaging (MRI) scans were obtained, the patient was brought to the operating room for a sphenoid biopsy. A fungal ball was identified intraoperatively

known to be refractory to conventional medical and surgical therapy; however, they were also known for their high recidivism.

Diagnosis

Clinically, patients with AFS were characterized by nasal polyposis; asthma; peripheral eosinophilia; eosinophilic mucus demonstrating Charcot–Leyden crystals; type I hypersensitivity or atopic disease; and characteristic computed tomographic (CT) findings that included evidence of CRS, calcifications or differential density within the sinus, and often erosion of bone. The proposed mechanism for AFS involves the abnormal immune response to fungal antigens through an IgE-mediated response and through the influx of eosinophils via inflammatory pathways. The resulting inflammation and edema lead to ostial obstruction and stasis of secretions. This clinical scenario was recognized by Bent and Kuhn, [6] who proposed five major criteria for the diagnosis of AFS based on a series of 15 patients with overlapping clinical features: (1) nasal polyposis, (2) evidence of atopic disease or type I hypersensitivity to common fungal agents, (3) eosinophilic mucus without fungal invasion, (4) characteristic CT findings (opacified sinuses, unilateral disease, bony

Fig. 14.2 Features of allergic fungal sinusitis on computed tomography. Note the erosion of normal landmarks and bony features of the paranasal sinuses and the differential density noted in the lesion. These are characteristics of allergic fungal sinusitis

abnormalities, and differential density; Fig. 14.2), and (5) a positive fungal smear. Associated factors included other common, but not always identifiable, conditions such as asthma, peripheral eosinophilia, fungal culture, and bone erosion on CT examination.

Key factors in the diagnosis rested in identification of high levels of IgE in peripheral blood samples, positive skin end-titration, prick testing, or radioallergosorbent test to fungal antigens, and the demonstration of fungi on Grocott’s methenamine silver (GMS) staining in a background of eosinophilic mucus.

Despite criteria for the diagnosis of AFS, much controversy exists in the literature about how many of the major criteria established by Bent and Kuhn [6]. are required to meet the diagnosis. Rather, do patients present with “typical” and “atypical” forms of AFS? This question arises when patients present with the clinical features of AFS but do not demonstrate evidence of fungal growth on culture or on smears, or who fail to demonstrate IgE-mediated fungal allergy. This question has led investigators [7–10] to propose that AFS exists on a spectrum of disease that is central to the eosinophil. Ferguson [7] performed a detailed analysis of the literature regarding AFS and has noted differences in the clinical presentation of certain patients with features of AFS yet who lack fungal growth or IgE-mediated fungal allergy. Although all patients presented with CRS, eosinophilia, and characteristic findings on CT, patients with eosinophilic mucin rhinosinusitis presented more frequently with bilateral disease, aspirin-sensitive asthma, and IgG deficiencies, in contrast to patients with AFS. The role of IgE in AFS was thought to be fundamental to its diagnosis; however, a demonstrable role for IgE, both local and peripheral, in eosinophilic mucin rhinosinusitis and nonallergic eosinophilic fungal sinusitis is less clear. Collins et al. [11] demonstrated local production of IgE in sinonasal mucosa in patients with AFS and highlighted its importance in disease pathogenesis. Carney and colleagues [8]. looked at sinonasal mucosa in patients with AFS, nonallergic eosinophilic fungal sinusitis, and CRS. Peripheral IgE counts were raised in AFS, but they were unelevated in nonallergic eosinophilic fungal sinusitis. However, IgE cell counts within sinonasal mucosa were elevated in all