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SINUSITIS
Annu. Rev. Med. 1991.42:471-489. Downloaded from www.annualreviews.org Access provided by Lancaster University - UK on 02/05/15. For personal use only.
R. A. Friedman, M.D., and J. P. Harris, M.D., Ph.D.
Division of Otolaryngology, Department of Surgery, University of California San Diego Medical Center; and the Research Service of the Veterans Administration Medical Center, San Diego, California 92 103 KEY
WORDS:
paranasal sinus infection
ABSTRACT
Paranasal sinusitis is one of the most common diseases treated in out patient centers across the United States. Improved bacterial culture tech niques have revealed the variety of pathogens involved in acute and chronic sinusitis. The growing numbers of antibiotic-resistant bacterial strains and of immunocompromised patients have changed the clinical face of sinusitis. New diagnostic modalities, including magnetic resonance imaging, are facilitating more rapid and accurate disease detection.
INTRODUCTION Approximately 0.5% of common colds are complicated by the devel opment of paranasal sinusitis. Adults average two to three colds per year and children six to eight, which makes sinusitis one of the most common infectious diseases seen in outpatient centers. Chronic sinusitis is now considered the most common chronic disease seen in the United States. Despite the prevalence of the disease, progress has been slow in the areas of bacteriology, diagnosis, and treatment.
ANATOMY The functional significance of the paranasal sinuses has eluded anatomists and physiologists since the sinuses were first described almost 2000 years ago. Theories purport that the sinuses (a) impart vocal resonance; (b) filter, warm, and humidify inspired air; (c) act as shock absorbers for the 471 0066- 42 19/9 1/0401-0 471 $ 02 .00
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FRIEDMAN & HARRIS
intracranial contents; (d) secrete moisturizing mucus; (e) contribute to facial development, and if) represent vestigial structures. The four paired paranasal sinuses-frontal, maxillary, ethmoid, and sphenoid-bear the names of the facial bones they occupy. During development, however, pneumatization may extend to adjacent bones (1-3). For example, the maxillary sinuses frequently extend into the zygomatic bones, and the ethmoid sinuses can invade the sphenoid, frontal, or maxillary bones. The sinus mucosa, like other respiratory mucosa, consists of pseudo stratified cilated columnar epithelium. Below the epithelium and basement membrane lies the lamina propria, with its lymphoid aggregates and serous and mucinous glands. Interspersed with the epithelial cells are numerous goblet cells. The maxillary sinus, or antrum of Highmore, begins as a bud in the lateral wall of the ethmoid portion of the nasal capsule at approximately the third month of gestation (see Figure I). Within the middle meatus, the developing uncinate process of the ethmoid bone projects medially to form a groove above, the infundibulum. This is the site of the maxillary bud. At birth the size of the sinus is approximately 6 to 8 cm3, and by 4 to 5 months of age the sinus is readily visible radiographically. The maxillary sinus continues to grow rapidly until age 3 years and then progresses more slowly until age 7 years. At this age another rapid growth phase ensues until approximately age 12, when the sinus extends as far laterally as the orbit and inferiorly as the floor of the nasal cavity. Much of the growth after age 12 years comes from pneumatization of the maxillary alveolus after the permanent teeth erupt and place the floor of the sinus 4 to 5 mm below the level of the nasal cavity (see Figure 2). The maxillary sinus volume is approximately 15 cm3• On average, it has an anteroposterior dimension of34 mm, a transverse dimension of25 mm, and a height of33 mm (3). When viewed transversely the sinus is triangular, with the base at the lateral nasal wall and the apex extending into the zygoma. The roof of the sinus, the orbital floor, is twice as wide as the floor, the maxillary alveolus. The anterior wall is the facial surface of the maxilla and the posterior wall is the infratemporal surface. The floor is limited anteriorly by the first premolar and posteriorly to a recess behind the third molar. The ostium of the maxillary sinus is located within the middle meatus in the hiatus semilunaris (see Figure 3). Accessory ostia occur in 25 to 30% of individuals (3). The shape of the ostium depends upon the influence of the ethmoid bulla superiorly and upon the uncinate process inferiorly. The blood to the maxillary sinus is primarily supplied by branches of the maxillary artery. The venous drainage occurs primarily via the anterior facial vein, although the maxillary vein also contributes to some degree.
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Annu. Rev. Med. 1991.42:471-489. Downloaded from www.annualreviews.org Access provided by Lancaster University - UK on 02/05/15. For personal use only.
Adult frontal sinus
Nasal septum---,l-+-�
Late adult
Figure
1
Developmental stages of maxillary and frontal sinuses. (Reproduced with per·
mission from Ref. 29, p. 846.)
The maxillary vein communicates with the pterygoid venous plexus in the infratemporal fossa, which in turn anastamoses with the dural venous sinuses via the foramen ovale. It is these valveless venous connections that permit the intracranial extension of maxillary sinusitis. In the third fetal month, the ethmoids begin as evaginations of the lateral nasal wall in the region of the ethmoid bone. The anterior cells remain in this region, but the posterior group expand upward toward the superior meatus. At birth the anteromiddle group measure 5 mm high, 2 mm long, and 2 mm wide (3). The posterior group are 5 x 4 x 2 mm. The ethmoid and maxillary sinuses are the only sinuses large enough at birth to be clinically implicated in rhinosinusitis. The ethmoid sinuses are typically not apparent radiographically until age one year. By the age of 12 years
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Annu. Rev. Med. 1991.42:471-489. Downloaded from www.annualreviews.org Access provided by Lancaster University - UK on 02/05/15. For personal use only.
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Figure 2
Coronal section of head illustrating maxillary, frontal, and ethmoid sinuses. (Reproduced with permission from Ref. 29, p.
847.)
475
SINUSITIS Frontal sinus Anterior ethmoidal cells (under middle concha)
Posterior ethmoidal
cells (under superior concha)
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Middle ethmoidal cells (under middle concha)
Inferior concha
Figure 3
DcvclopIhcntal stages of ethIhoid
and sphenoid sinuses. (Reproduced with per
Ref. 29, p. 848.)
mission frolll
the ethmoids have attained their adult size. At this time the
ant eri or
group
average 24 mm high, 23 mm l on g and 11 mm wide, and the posterior ,
group average 21
There are
x
21
us uall y
x
12 mm (3).
2 to
8 anterior and middle ethmoid cells and
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8
posterior cells, with the posterior group being larger. The infundibulum is a crescentic depression created by the uncinate process below and the
ethmoid bulla above. The opening of this depression is the hiatus semi lunaris (see
Figure 3). Anatomically, the anterior ethmoid cells are defined
as those whose ostia open into the infundibulum of the middle meatus. The middle cells are those opening in relation to the ethmoid bulla. The posterior cells have their ostia in the superior meatus (see Figure
3).
The
ethmoid air cells are not confined to the ethmoid bone. Frequently their pneumatization extends anteriorly to the nasal and lacrimal bones,
teriorly to the orbital
pos sphenoid bone, inferiorly to the maxilla and superiorl y to plate of the frontal bone. The ethmoid sinuses are py ramidal
the
,
in shape in the anteroposterior dimension. The lateral wall, the thin lamina
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476
FRIEDMAN & HARRIS
paprycea, accounts for the frequency of orbital complications associated with infection in this region (see Figure 2). The blood supply to the ethmoid sinuses is derived from the internal carotid arterial system via the anterior and posterior ethmoid arteries, which are branches of the ophthalmic artery. Additional blood is provided by branches of the maxillary artery. Blood is drained by the nasal veins and the ethmoidal veins. The latter are tributaries of the ophthalmic veins, which communicate freely with the cavernous sinus. The frontal sinus develops as an evagination of the ethmoid bone ante riorly within the nasal capsule in a region known as the frontal recess (see Figure 1). At birth the sinus is indistinguishable from the surrounding ethmoid sinus and continues to develop slowly. At age one year the sinus is hardly perceptible, and it is not until age five to six years that pneu matization extends up onto the vertical portion of the frontal bone. The sinus can be recognized radiographically at approximately age six years. The sinus continues to grow rapidly until the late teens. The average dimensions of the adult frontal sinus are 28 mm high, 24 mm wide, and 20 mm deep (3). The sinus is generally pyramidal in shape. Some individuals display little vertical pneumatization but have extensive development of supraorbital cells. The two frontal sinuses are separated by a bony septum. The frontal sinus typically drains into the infundibulum of the middle meatus via the nasofrontal duct. Blood is supplied to the frontal sinuses via the supraorbital and supratrochlear arteries. The venous drainage is via the superior ophthalmic vein through the superior orbital fissure to the cavernous sinus. The sphenoid sinus can be identified as a small evagination of the sphenoethmoid recess at birth (see Figure 3). Invasion of the sphenoid bone commences at approximately age five years, and within a few years it has extended posteriorly to the sella turcica. The sphenoid sinus is fully
developed by the late teens. The average dimensions of the adult sphenoid sinus are 20 mm high, 23 mm long, and 1 7 mm wide (3). The paired sinuses are separated by a bony septum. Sculpted into the walls of the well-pneumatized sphenoid sinus are structures such as the internal carotid artery and the optic nerve. Their close proximity to the walls of the sinus can present potential hazards during instrumentation of the sphenoid sinus. The sphenoid sinus opens into the sphenoethmoid recess above the superior concha. The ostium is approximately 10 mm above the floor of the sinus. The blood supply to the sphenoid sinus comes from branches of the internal and external carotid arteries. The venous drainage occurs via branches of the maxillary vein and thus communicates with the pterygoid venous plexus (2, 3).
SINUSITIS
477
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SYMPTOMS AND SIGNS Patients with infection of the paranasal sinuses may complain of headache, nasal congestion, rhinorrhea, postnasal drip, productive cough, and phar yngitis. The sinus headache is generally located in the area of the involved sinus. Symptoms are localized to the forehead, around or behind the eyes, the maxillary teeth, and the vertex, temporal, or parietal areas of the skull. Frontal sinusitis can often be referred to the scalp along branches of the supraorbital nerve. In a review of 30 cases of sphenoid sinusitis, Lew et al (4) found the most common presenting symptoms to be severe frontal, temporal, or retro-orbital headache that radiated to the occipital regions, or pain in the trigeminal (VI to V3) distribution, or both. The pain may be intermittent or constant and is exacerbated by placing the head in a dependent position. Patients with acute sinusitis typically describe pain or pressure that is most severe during the day. Chronic sinusitis is less fre quently associated with pain or prcssurc. Other causes of headache includ ing migraine, muscle tension, or intracranial lesions must be considered in the differential diagnosis. Pertinent historical features include recent upper respiratory tract infection, trauma, allergy, swimming, flying, or dental repair. Additionally, patients may rcport previous surgery or recent work in a poorly ventilated area with volatile or noxious material. Patients with acute or chronic sinusitis commonly display purulent rhinorrhea that is yellow or green and malodorous. Postnasal drip has similar characteristics and may be associated with a foul taste, halitosis, or chronic pharyngeal discomfort. Physical examination may yield signs of recent upper respiratory tract infection or chronic nasal allergy. Rhinoscopy either with nasal speculum and headlight or with nasal en doscopy is essential. The presence of yellow or green discharge in the middle or superior meatus with edematous and erythematous mucosa is diagnostic. Nasal polyps, large "blue" inferior turbinates, and clear mucus bridging the nasal septum and turbinates anteriorly suggest allergic rhinitis. Nasopharyngoscopy using a mirror and headlight or a fiberoptic naso pharyngoscope may reveal a string of mucus draining down along the posterior aspect of the inferior turbinate indicative of maxillary sinus disease. Additionally, an enlarged inferior turbinate posteriorly is indica tive of allergic rhinitis. Palpation and percussion of the acutely involved sinuses may reveal tenderness, while patients with chronic sinusitis rarely describe such tenderness. Percussion of the maxillary teeth commonly elicits tenderness of the involved maxillary sinus. Gwaltney et al (5) found transillumination of the sinuses to be clinically useful in the hands of experienced examiners.
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FRIEDMAN & HARRIS
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Ophthalmalogic examination is essential in patients with sinus disease. Visual acuity and field testing as well as ocular motility should be assessed. Proptosis, chemosis, periorbital edema, erythema, or fiuctuance are indi cators of a suppurative orbital or intracranial complication. Ophthal moplegia, anesthesia in the distribution of the ophthalmic division of the trigeminal nerve, ptosis, and mydriasis are indicative of a superior orbital fissure syndrome. With associated visual changes the process has likely involved the orbital apex.
PATHOGENESIS The mucociliary system of the nose and paranasal sinuses provides mueh of the local defense against infection (see Table 1). Secretory IgA also protects against viral and bacterial pathogens (6). Microbes, pollutants, and other irritants are trapped in the mucous of the nose and sinuses and propelled toward the nasopharynx. The mucus blanket travels at a rate of approximately 1 em per minute and the nose and sinuses produce mucus at a rate of a liter per day. When this protective system breaks down, colonizing pathogenic bacteria proliferate and infection ensues. Bacteria
typically infect the sinuses by traversing the ostia from the nasal cavity. The maxillary sinus may become seeded by an odontogenic infection. Retention of secretions is the fundamental event in infection of the sinuses and several factors contribute: (a) mucosal swelling leading to diminished patency of the ostia; (b) abnormalities of the cilia leading to impaired transport secondary to a quantitative reduction, a structural abnormality, or incoordination of movement; and (c) overproduction of secretions. The patency of the ostia is a major factor in the development of sinusitis. Recent upper respiratory tract infection or exacerbation of allergic rhinitis leads to mucosal edema and diminished ostial patency. Aust et al (7), studying normal subjects, found an inverse relationship between diameter of the maxillary sinus ostium and the time required for emptying the sinus Table 1
Factors predisposing to sinusitis
Upper respiratory tract infection
Tumors
Allergic rhinitis
Foreign bodies
Overuse of topical decongestants
Swimming/diving
Hypertrophied adenoids
Cigarette smoke
Deviated nasal septum
Barotrauma
Nasal polyps
Dental extraction/injections
Immune deficiency
Bronchiectasis
Cystic fibrosis
Immotile cilia syndrome
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of contrast material. Johansson et al (8) found that experimentally induced ostial dysfunction in the prcsencc of pathogenic bacteria resulted in puru lent sinusitis in all subjects. Neither occlusion alone nor innoculation with pathogenic bacteria alone induced significant disease. The diameter of the maxillary sinus ostium is also a major factor in gas exchange between the sinus and the nasal cavity. During normal nasal breathing, 90% of sinus air is exchanged in five minutes. With diminution of ostial size the partial pressure of oxygen begins to decline. Oxygen tension drops further when ostial closure is accompanied by infection. Carenfelt et al (9) examined infected maxillary sinus aspirates and showed them to have oxygen tensions near zero, elevated carbon dioxide tensions, and lowered pH. Low oxygen tension not only favors increased bacterial growth, but, also may impair local defenses. Ciliary movement is essential to propel the mucus blanket. The cilia beat as a group in a spiral fashion toward the sinus ostium. Mucociliary trans port may be compromised by low oxygen tension within the sinus. In addi
tion to local factors, structural abnormalities such as the absence of dynein arms in Kartagener's syndrome lead to ciliary dysfunction. Finally, viral in fection may lead to destruction of ciliated epithelial celIs (ciliocytophoria). The ostia of the maxillary and sphenoid sinuses are superiorly located. For drainage to occur in the upright position the mucus must be propelled against the force of gravity. This combined with mucus overproduction, ostial edema, or ciliary dysfunction places these sinuses at an additional risk for infection. Gwaltney et al (5) and Su et al (10) demonstrated conclusively that cultures obtained from the nose and nasopharynx correlate poorly with those obtained directly from the sinus by aspiration or open antrostomy. Karma et al (11) studied 61 chronically inflamed maxillary sinuses. Bac teriologic findings from nasal mucus, sinus mucus, and sinus mucosa frequently differed. Mucosal samples more than doubled the bacteriologic yield of the samples taken from sinus secretions. Because normal sinus mu cosa is known to be sterile, it was concluded that samples taken directly from sinus mucosa more reliably reflect the bacteriology of chronic sinusitis. Gwaltney et al (5) reported Streptococcus pneumoniae and non-typable Haemophilus irif/uenzae as the primary pathogens in more than half the cases of acute bacterial sinusitis. Other prominent pathogens include Bran hamella catarrhalis and viruses. Staphylococcus aureus and S. epidermis have also been implicated as pathogens in acute and chronic sinusitis. The majority of the data suggest both species more commonly colonize the nasal mucus in acute sinusitis. Evans et al (19), Gwaltney et al (5), and Su et al (10) found Staphylococcus aureus, S. epidermis, and diptheroids frequently isolated from the nasal secretions of normal subjects. None
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except S. aureus were isolated in significant concentrations from the mucosa of patients with chronic maxillary sinusitis. Despite the environment in the acutely infected sinus, Gwaltney et al (5) isolated anaerobic organisms in fewer than 10% of patients. In contrast, anaerobic organisms play a significant role in chronic sinusitis. Brook (12) isolated anaerobic bacteria from 88% of aspirates of 72 chronically inflamed maxillary sinuses. They were the sole isolates in 56% of subjects. Anaerobic isolates in descending order included anaerobic cocci, Bac teroides melanogenicus, B. jragilis, Propionibacterium acnes, and Fuso bacterium species. Many aerobic and facultative isolates were identified including Staphylococcus aureus and Streptococcus pyogenes. As many as 44% of anaerobic isolates have been shown to produce beta-lactamase, including 25-50% of Bacteroides melanogenicus.
NONBACTERIAL INFECTION Fungal infections of the nose and paranasal sinuses are uncommon. Asper gillosis, mucormycosis, candidiasis, histopl asmosis and coccidiomycosis can occur. Aspergillus jumigatus is the most common fungal pathogen encountered, and the maxillary sinus is the most commonly involved site. Immunosuppressed patients are at highest risk. Diagnosis frequently necessitates antrostomy with tissue biopsy. ,
Aspergillosis
Paranasal sinusitis secondary to Aspergillis infection is increasing. The number of cases tripled in the past three decades. This entity was first described in healthy patients but is increasingly recognized in immuno compromised patients, such as those with diabetes mellitis (3, 13). Aspergillis is a saprophyte of soil, dust, and decaying organic material. Seven species have been identified that are pathogenic in humans. Asper gillis colonies grow in a wide range of temperatures. The organism grows well in damp, decaying vegetation heated by bacterial fermentation. Asper gillis is endemic in the Sudan, where it has been cultured from bedding, straw roofs, and the soil of Sudanese dwellings. A.jlavus is the sole species implicated in disease in the Sudan. A. jumigatus is the most commonly encountered species in the United States. The usual portal of entry is the respiratory tract. Aspergillis is commonly cultured from the external auditory canals of patients with mycotic otitis externa. It is not contagious and sources of infection are endogenous. Aspergillis appears as a greenish-black, tarry or rubbery mass within the sinus cavity. The organism characteristically has septate hyphae and
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SINUSITIS
48 1
dichotomous branching (Figure 4). Aspergillis can be distinguished from the Phycomycetes not only by their septate hyphae, but by the 45° angle of their branching compared to the random branching of hyphae seen in the latter. Microscopic identification is best made with silver stains (Gridley, PAS, and methenamine silver). A direct culture should be per formed on Sabouraud's agar with an antibiotic to inhibit bacterial growth. Aspergillis is frequently a colonizer of the paranasal sinuses and becomes pathologic when the ostia are obstructed. This fungus grows best in an anaerobic environment; the presence of ostial occlusion, elevated intra sinus pressures, and anaerobic bacteria contribute to its pathogenicity. Three clinical types of paranasal aspergillosis exist (14). Infections can be noninvasive, invasive, and fulminant. The noninvasive type is similar to chronic rhinosinusitis presenting with rhinorrhea and nasal obstruction. Radiographs may show clouding or opacification of the sinuses. The maxillary sinus is the most commonly involved. Intranasal examination reveals nonspecific signs of mucosal inflammation. Antral lavage is neither
curative nor diagnostic. Left untreated, aspergillis infection will become invasive. Invasive asper gillosis typically presents with orbital or maxillary extension. Radiography reveals a paranasal sinus mass with orbital displacement and bony erosion. Invasive aspergillosis behaves much like a malignant neoplasm and occasionally presents with intracranial involvement. Like the Phyco-
Figure 4
Dichotomous branching at 45° angles in
A.fumigalus.
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mycetes, aspergillis has a tendency to invade arteries, which may lead to thrombosis or hemorrhage-most importantly within the internal carotid artery. The patient's general health and immunocompetence may influence the progression to invasive disease; however, both invasive and non invasive types have been reported in healthy patients. The fulminant form of the disease occurs in immunocompromised pati ents. Children with acute leukemia undergoing radiation and chemo therapy are most susceptible. The earliest nasal lesion is crusting of the anterior aspect of the inferior tubinate or septum. The tissue beneath the crust is insensitive. The infection spreads to the lateral nasal wall within days. Proptosis, chemosis, and ophthalmoplegia indicate orbital involve ment. The disease rapidly progresses to the lungs, liver, and spleen. Patho logically, the hyphae invade dura, blood vessels, and bone. The treatment of the noninvasive and invasive varieties of aspergillosis is primarily surgical. Most cases are cured by excision and aeration of the sinuses. If the fungus spreads into the orbit or the cranium, amphotcricin B should be administered. Fulminant disease is treated by systemic ampho tericin B and debridement of all gross disease. Mucormycosis
Mucormycosis is an infection caused by fungi in the class Phycomycetes. They are distinguished by the random branching of their nonseptated hyphae. The organisms important in humans include species of the genera Mucor, Rhizopus, and Absidia, all of which are within the order Mucorales. These fungi, commonly recognized as bread mold, are found in soil, vegetable debris, and manure. Mucormycosis can be classificd into six different categories: (a) rhinocerebral mucormycosis, which is commonly seen in patients with diabetes or hematologic diseases; (b) pulmonary and disseminated mucormycosis, also seen in debilitated patients; (c) gastro intestinal mucormycosis present in severely malnourished or uremic patients and patients suffering from amebiasis; (d) mucormycosis of burn wounds; (e) central nervous system mucormycosis; and (f) endocarditis, usually following cardiac surgery. Severe localized infections of the head and neck occur in patients with impaired immunologic function. McNulty (15) and Pillsbury (16) impli cated diabetic ketoacidosis, burns, neutropenia, leukemia, lymphoma, uremia, sepsis, severe dehydration, long-term immunosuppressive therapy (including steroids), and broad spectrum antibiotics as etiologic factors in the development of mucormycosis. Survival statistics for patients with no underlying disease and with diabetes mellitus are 75% and 60% respec tively. McNulty (15) noted a survival rate of only 10% in patients with more significant diseases.
SINUSITIS
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Of patients with rhinocerebral mucormycosis, 70% are in diabetic ketoacidosis. This association is likely explained by the fact that Rhizopus species have an active ketone-reductase system and proliferate in a low pH and glucose-rich environment. The abnormal polymorphonuclear chemotaxis and phagocytic activity existing in severe hyperglycemia con tribute to the pathogenicity. Fungus can invade the nose, paranasal sinuses, lungs, and gas trointestinal tract. Once inside, the fungus moves into blood vessels, which leads to hemorrhagic ischemia and thrombosis. The resulting vascular insufficiency causes dry gangrene. The initial signs of infection include nonspecific turbinate engorgement and nasal obstruction. The diagnosis should be suspected in the presence of persistent rhinitis in an immu nocompromised or debilitated host. Progression of the disease leads to ischemic necrosis of the turbinates and the development of bloody rhi norrhea. The nasal turbinates, septum, or palate appear black on exam ination. Disease ultimately extends to the orbital apex via the ethmoid arteries and into the cavernous sinus. Signs of orbital extension include proptosis, chemosis, ptosis, ophthalmoplegia, and loss of vision. Once within the cavernous sinus, fungal invasion of the internal carotid artery may ensue, leading to thrombosis. Pillsbury (16) found the time course of this deeply invasive disease may be as little as three days. Transnasal biopsy is the only reliable method of diagnosis. Special fungal stains (PAS, methenamine silver) should be performed, although invasion of the nonseptated hyphae can frequently be recognized on frozen section. The first goal of therapy is control of the underlying disease. Pillsbury (16) found reversal of dehydration and acidosis improve survival, even in nondiabetic patients. Immediate debridement of all infected and devi talized tissue is performed. This may include orbital exenteration if vision is lost. High doses of amphotericin B are then administered. An alternate day regimen of 1 mg per kg up to a total of 2 g is necessary. Renal function must be closely monitored because amphotericin B is nephrotoxic. The addition of low doses of heparin to the intravenous infusion diminishes the associated thrombophlebitis.
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SINUSITIS IN THE NASOTRACHEALLY INTUBATED PATIENT Maxillary sinusitis secondary to nasotracheal intubation is a well-known entity. The reported incidence of sinusitis in these patients is 2- 5%. Infec tion, as in most paranasal sinus infections, likely results from the presence
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FRIEDMAN & HARRIS
of the large-bore tube as well as from local edema, which leads to ostial dysfunction and secondary obstruction. Deutschman et al (17) contend that the high incidence of bilateral involvement and pansinusitis suggests an obstructive role for nasogastric tubes as well. Linden et al (18) reviewed 19 cases of maxillary sinusitis in naso traeheally intubated patients. The admission diagnosis in 14 of the 19 patients was multiple trauma. Seventeen of the 19 patients had roent genographic evidence of sinusitis. Twenty-seven antral taps were perfor med, and 21 positive cultures were obtained; 42% of the cultures were polymicrobial. The most commonly cultured organism was Staphylococcus aureus (16%), followed by Enterobacter species (12.9%), Pseudomonas aeruginosa (12.9%), and Bacteroides fragilis and B. melaninogenicus (12.9%). Sinusitis secondary to nasotracheal intubation should be suspected in the presence of unexplained fever, leukocytosis, negative nitrogen balance despite adequate nutritional support, and increased carbon dioxide pro duction or increased oxygen consumption. Deutschman et al found a high incidence of pulmonary seeding and bacteremia, as well as one case of septic shock. Controversy exists regarding the best method of diagnosing suspected sinusitis in these patients. Routine sinus radiographs are successful in most cases. Sinus computerized tomography (CT) is helpful in assessing involvement of the ethmoid or sphenoid sinuses. Many patients are receiv ing broad spectrum antibiotics at the time of diagnosis. The use of antral aspiration is essential for adequate culture and antibiotic sensitivity testing. Additionally, antral irrigation can be performed at the time of sampling. Sinusitis should be considered in nasotracheally intubated patients with unexplained sources of fever or sepsis. Treatment must be aggressive and include removal of the tube, diagnostic and therapeutic antral lavage, topical and systemic decongestants, and appropriate antibiotics guided by culture and sensitivity testing.
DIAGNOSIS AND TREATMENT History and physical examination are essential to the management of paranasal sinus disease but can often be misleading. Gwaltney et al and Evans et al found the clinical features to be of little help in making the diagnosis of acute sinusitis. They also found that the history of purulent rhinorrhea and facial pain correlated poorly with subsequent sinus as piration. Additional studies are frequently necessary in the complete evaluation.
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A complete blood count with white ceIl differential may reveal a leu kocytosis with a leftward shift in acute sinusitis. Blood studies are fre quently normal in chronic disease. Quantitative evaluation of serum immu noglobulin levels for evidence of IgA or IgG subclass 2 and 4 deficiencies, as well as sweat chloride tests for cystic fibrosis, are helpful in the diagnosis of chronic sinusitis (6). Additionally, allergic testing and ciliary motility studies may be helpful. Transillumination of the sinuses is of value in the hands of some experi enced physicians. Gwaltney et al (5) found that normal light transmission and complete absence of light transmission of the maxillary sinus cor related well with the presence and absence of disease, respectively, based upon sinus aspiration. Evans et al (19) noted that dullness on trans illumination was not predictive of disease. McNeill et al (20) found that transillumination correlated with clinical disease in only 68% of patients. Transillumination is less helpful in patients with chronic sinus disease because of persistent mucosal abnormalities.
The initial radiologic evaluation of the paranasal sinuses is by plain x ray. Most paranasal sinus pathology can be demonstrated by this tech nique, but there is much controversy as to whether X-ray examination of the sinuses is reliable. Many factors other than infection can lead to opacification of the sinuses. A thick antral wall may lead to opacification of the maxillary sinuses. Overlying soft tissue swelling can cloud the sinuses. McNeill et al (20) and Vuorinen et al (21) found approximately 82% correlation between evidence of maxillary sinusitis from X-ray and that from antral aspiration. Thcse studies found less correlation in sinuses that show mucosal thickening (63%). A mucosal thickness of 5 mm or greater in the maxillary sinus, as determined by using a Water's view, better discriminates between those with and without evidence of disease or aspir ation. Follow-up radiographs are essential for detection of asymptomatic treatment failures. For patients with complicated presentations or chronic complaints in whom plain radiographs are unhelpful, more sophisticated testing is recommended. Conventional CT scanning is helpful in evaluating the anatomy and extent of disease in patients with chronic sinusitis and in patients requiring surgical intervention. CT reveals excellent soft tissue and bony detail. High-field magnetic resonance imaging of paranasal sinus disease is also excellent for evaluation of soft tissue (22, 23). This modality is especiaIly useful in cases of suspected malignancy of the nose and paranasal sinuses. There is a paucity of information regarding the use of maxillary sinus puncture for aspiration and irrigation. Many clinicians sample nasal secretions in cases of acute and chronic sinusitis. Axelsson & Brorson (24) found only a 64% correlation between bacteria cultured from the nasal
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versus sinus secretions in patients with acute maxillary sinusitis. Addition ally, Axellson & Brorson (24) and Karma et al (11) found staphylococcal species and diptheroids to be present primarily in cultures of nasal secretions and rarely in sinus secretions, which indicates their likely role as contaminants. Current indications for antral aspiration and lavage are (a) sinusitis in an immunocompromised or chronically debilitated host; (b) failure of resolution of symptoms after 24 to 48 hours of empiric antibiotic therapy; (c) progression of symptoms while on antibiotics; (d) an orbital or intracranial complication of maxillary sinusitis; (e) maxillary sinusitis in a newborn; and (f) severe pain. The frontal sinus can be aspirated and irrigated through a trephine. The ethmoid sinuses require surgical drainage, either externally or intranasally. Treatment of acute sinusitis should initially he aimed at drainage of retained secretions. This can be facilitated by the use of topical and sys temic decongestants. Topical decongestants should be used for no longer than seven days to avoid developing rhinitis medicamentosa. Gwaltney et al (5) found equal success rates with the use of ampicillin, amoxacillin, trimethaprim-sulfamethoxazole, and cefaclor. The emergence of pen icillinase-producing bacteria may require the use of amoxicillin and cla vulanic acid in resistant infections. Further treatment should be guided by bacterial culture and antibiotic sensitivity testing. Treatment of chronic sinusitis requires anaerobic coverage as well as control of predisposing factors such as allergy. Patients with complicated acute sinusitis and those with refractory chronic sinusitis require surgical intervention.
COMPLICATIONS Serious complications of paranasal sinusitis are rarely seen since the intro duction of antimicrobial therapy. Few physicians today have seen the orbital and intracranial complications of uncontrolled infection. With the increase in antibiotic-resistant bacteria and immunocompromised hosts, the clinician should be aware of the possible complications of extensive infection. Mucoceles
The mucocele is a chronic, cystic lesion of the paranasal sinuses. These cysts are lined with pseudostratified columnar epithelium and occasional goblet cells. Mucoceles are slowly expansile lesions, frequently existing many years before becoming symptomatic (3). Their expansion within the sinus of origin leads to bony sclerosis and eventual erosion and subsequent extrasinus extension. The symptoms depend upon the sinus of origin and the extent of erosion. Mucoceles may arise from obstruction of the sinus
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ostium secondary to trauma, chronic inflammation, neoplasia, or prior surgery. They may also arise from obstruction of a minor salivary gland duct within a sinus. Approximately 10% of all mucoceles occur in the maxillary sinuses. The maxillary mucocele is commonly observed as an incidental finding on sinus radiographs. Symptoms are unusual and these lesions typically regress spontaneously, requiring no further intervention. When the diagnosis is unclear, mucoccles can be aspirated through the canine fossa or the inferior meatus. The most common clinically significant lesions arise in the frontal sinus, followed by those in the anterior ethmoids. Frontal headache, proptosis, and diplopia secondary to downward and outward displacement of the globe are the most common initial complaints (25). Radiographically, there is clouding of the involved sinuses, loss of the normal scalloped appearance of the frontal sinuses, and sclerosis of the sinus walls. Mucoceles of the sphenoid and posterior ethmoid sinuses are rare. Close et al (26) describe a series of three patients with intracranial extension. Symptoms were related to the site of extension and frequently included cranial neuropathies involving nerves two through six. Occipital and vertex headache associated with diplopia or visual field disturbances were the most common complaints. Clinical suspicion followed by CT scanning led to diagnosis. These lesions require surgical intervention. Orbital Complications
The spread of infection to the orbits is the most common complication of paranasal sinusitis. Direct extension can occur through neurovascular foramina, through congenital or acquired dehiscenses, or through thin bone such as the lamina papyracea. Additionally, the valveless ethmoid, angular, nasofrontal, and ophthalmic venous systems allow spread via septic thrombophlebitis. Chandler et al (27) provided the following classi fication scheme correlating physical findings with orbital disease: Inflammatory edema-lid edema; no limitation of extraocular movement, and normal visual acuity. 2 . Orbital cellulitis-diffuse edema of orbital contents and infiltration of the adipose tissue with inflammatory cells and bacteria without discrete abscess; may be some impairment of visual acuity. 3. Subperiostial abscess-collection of pus beneath the periostium of the lamina papyracea; globe displaced downward and laterally. 4. Orbital abscess-a discrete collection of pus within the orbital tissues; exophthalmos and chemosis; complete ophthalmoplegia and severe impairment of vision. I.
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5. Cavernous sinus thrombosis-bilateral eye findings; edema over the mastoid emissary vein; prostration and meningismus. Extension of infection to the orbit from the frontal sinus may occur through its thin floor. When the infection spreads to involve the squama of the frontal bone, osteomyelitis and subperiostial abscess ensue. The resulting soft tissue swelling is called Pott's puffy tumor (2 8). Orbital complications can frequently be managed by intravenous anti biotic therapy and a drainage procedure. Patients should be hospitalized and observed closcly for evidence of orbital abscess or cavernous sinus thrombosis. Surgical intervention is required if (a) orbital cellulitis pro gresses despite appropriate antibiotics; (b) fever, erythema, and edema fail to regress or worsen after 2 4 to 48 hours of antibiotic therapy; (c ) orbital or subperiostial abscess are found by ultrasound or CT scan; and (d) visual acuity is lost. Intracranial Complications
The intracranial complications secondary to sinusitis include the following: meningitis, epidural abscess, subdural empyema, venous sinus thrombosis, and cerebral abscess (28). These complications can result from direct extension, septic thrombophlebitis, and hematogenous spread. Meningitis is the most common intracranial complication of paranasal sinusitis. Nuchal rigidity, diminished mentation, and coma should alert the phy sician to the possibility of an intracranial complication. After CT scan and lumbar puncture, intravenous antibiotics should be started on an empiric basis. Signs of increasing intracranial pressure (including diplopia, vomit ing, severe headache, and altered mental status) are considered emergent. Treatment should be undertaken in cooperation with a neurosurgeon and otolaryngologist. Literature Cited
l. Rice. D., Schaefer, S. D. 1988. Endo scopic Paranasal Sinus Surgery. New York: Raven 2. Hollinshead, W. H. 1982. Anatomy for Surgeons, Vol. l. New York: Harper & Row . 3rd ed. 3. Cummings, C. W. 1986. Otolaryn gology-Head and Neck Surgery, Vol. I. St. Louis: Mosby 4. Lew, D. et al. 1983. Sphenoid sinusitis. N. Engl. J. Med. 309(19): 1149-54 5. Gwaltney, J. M. et al. 1981. Etiology and antimicrobial treatment of acute sinu sitis. Ann. 0101. 90: 68 6. Slavin, R. G. 1988. Sinusitis in adults. 1. Allergy c/in. Immunol. 81(5): 1028-31
7. Aust, R., Drettner, B., Hemmingsson, A. 1976. Elimination of contrast medium from the maxillary sinus. Acla Ololaryngol. 81: 468-74 8. Johansson, P. et a\. 1988. Experimental acute sinusitis in rabbits. Acla 010laryngol. lOS: 357-66 9. Carenfelt, C., Lundberg, C. 1977. Puru lent and non-purulent maxillary sinus secretions. Acta Otolaryngol. 84: 138-44 10. Su, W. Y. et a\. 1983. Bacteriological study in chronic maxillary sinusitis. Laryngoscope 93: 931-34 II. Karma, P. et a\. 1979. Bacteria in chronic maxillary sinusitis. Arch. 0101. 105: 36890
Annu. Rev. Med. 1991.42:471-489. Downloaded from www.annualreviews.org Access provided by Lancaster University - UK on 02/05/15. For personal use only.
SINUSITIS 12. Brook, I. 1989. Bacteriology of chronic maxillary sinusitis in adults. Ann. Otol. Rhinol. Laryngol. 98: 426-28 13. Jahrsdoerfer, R., Ejercito, V. , Johns, M., Cantrell, R., Sydnor, B. 1979. Asper gillosis of the nose and paranasal sinuses. Laryngoscope 92: 6-13 14. Romett, J., Newman, R. 1982. Asper gillosis of the nose and paranasal sinuses. Laryngoscope 92: 764-66 15. McNulty, J. 1982. Rhinocerebral mu cormycosis: predisposing factors. Laryn goscope 92: 1140-43 16. Pillsbury, H. 1977. Rhinocerebral mucormycosis. Arch. Otolaryngol. 103: 600-4 17. Deutschman, C. et al. 1986. Paranasal sinusitis associated with nasotracheal intubation: a frequently unrecognized and treatable source of sepsis. Crit. Care Med. 14: 111-14 18. Linden, B., Aguilar, E., Allen, S. 1988. Sinusitis in the nasotracheally intubated patient. Arch. Otolaryngol. Head Neck Surg. 114: 860-61 19. Ev�ms, F. et al. 1975. Sinusitis of the maxillary antrum. N. Engl. J. Med. 293: 735-39 20. McNeill, R. A. et al. 1963. Comparison of the findings on transillumination, x ray and lavage of the maxillary sinus. J. Laryngol. 77: 1009-13 21. Vuorinen, P. et al. 1962. Comparison
22.
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24.
25.
26.
27.
28.
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of results of roentgen examination and puncture and irrigation of the maxillary sinuses. .J. Laryngol. Otol. 76: 259-64 Lloyd, G. 1989. Diagnostic imaging of the nose and paranasal sinuses. J. Laryn gol. 0101. 103: 453-60 Potchen, M. et al. 1986. High-field mag netic resonance imaging of paranasal sinus inflamm atory disease. Laryngo scope 96: 267-71 Axelsson, A., Brorson, J. 1980. The cor relation between bacteriological findings in the nose and maxillary sinus in acute maxillary sinusitis. Laryngoscope 90: 635 Gardiner, L. 1986. Complicated frontal sinusitis: evaluation and management. Otolaryngol. Head Neck Surg. 95: 33342 Close, L. G., O'Conner, W. E. 1983. Sphenoethmoidal mucoceles with intra cranial extension. Otolaryngol. Head Neck Surg. 91: 350-57 Chandler, J. et al. 1970. The patho genesis of orbital complications in acute sinusitis. Laryngoscope 80: 141427 Rood, S. R. et al. 1982. Complications of Acute and Chronic Sinus Disease. Self instructional packet. Am. Acad. Oto laryngol. Head Neck Surg. Found. Graney, M. J. 1986. Anatomy. In Oto laryngology-Head and Neck Surgery. St. Louis: Mosby. 958 pp.
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Further
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SINUSITIS
Annu. Rev. Med. 1991.42:471-489. Downloaded from www.annualreviews.org Access provided by Lancaster University - UK on 02/05/15. For personal use only.
R. A. Friedman, M.D., and J. P. Harris, M.D., Ph.D.
Division of Otolaryngology, Department of Surgery, University of California San Diego Medical Center; and the Research Service of the Veterans Administration Medical Center, San Diego, California 92 103 KEY
WORDS:
paranasal sinus infection
ABSTRACT
Paranasal sinusitis is one of the most common diseases treated in out patient centers across the United States. Improved bacterial culture tech niques have revealed the variety of pathogens involved in acute and chronic sinusitis. The growing numbers of antibiotic-resistant bacterial strains and of immunocompromised patients have changed the clinical face of sinusitis. New diagnostic modalities, including magnetic resonance imaging, are facilitating more rapid and accurate disease detection.
INTRODUCTION Approximately 0.5% of common colds are complicated by the devel opment of paranasal sinusitis. Adults average two to three colds per year and children six to eight, which makes sinusitis one of the most common infectious diseases seen in outpatient centers. Chronic sinusitis is now considered the most common chronic disease seen in the United States. Despite the prevalence of the disease, progress has been slow in the areas of bacteriology, diagnosis, and treatment.
ANATOMY The functional significance of the paranasal sinuses has eluded anatomists and physiologists since the sinuses were first described almost 2000 years ago. Theories purport that the sinuses (a) impart vocal resonance; (b) filter, warm, and humidify inspired air; (c) act as shock absorbers for the 471 0066- 42 19/9 1/0401-0 471 $ 02 .00
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intracranial contents; (d) secrete moisturizing mucus; (e) contribute to facial development, and if) represent vestigial structures. The four paired paranasal sinuses-frontal, maxillary, ethmoid, and sphenoid-bear the names of the facial bones they occupy. During development, however, pneumatization may extend to adjacent bones (1-3). For example, the maxillary sinuses frequently extend into the zygomatic bones, and the ethmoid sinuses can invade the sphenoid, frontal, or maxillary bones. The sinus mucosa, like other respiratory mucosa, consists of pseudo stratified cilated columnar epithelium. Below the epithelium and basement membrane lies the lamina propria, with its lymphoid aggregates and serous and mucinous glands. Interspersed with the epithelial cells are numerous goblet cells. The maxillary sinus, or antrum of Highmore, begins as a bud in the lateral wall of the ethmoid portion of the nasal capsule at approximately the third month of gestation (see Figure I). Within the middle meatus, the developing uncinate process of the ethmoid bone projects medially to form a groove above, the infundibulum. This is the site of the maxillary bud. At birth the size of the sinus is approximately 6 to 8 cm3, and by 4 to 5 months of age the sinus is readily visible radiographically. The maxillary sinus continues to grow rapidly until age 3 years and then progresses more slowly until age 7 years. At this age another rapid growth phase ensues until approximately age 12, when the sinus extends as far laterally as the orbit and inferiorly as the floor of the nasal cavity. Much of the growth after age 12 years comes from pneumatization of the maxillary alveolus after the permanent teeth erupt and place the floor of the sinus 4 to 5 mm below the level of the nasal cavity (see Figure 2). The maxillary sinus volume is approximately 15 cm3• On average, it has an anteroposterior dimension of34 mm, a transverse dimension of25 mm, and a height of33 mm (3). When viewed transversely the sinus is triangular, with the base at the lateral nasal wall and the apex extending into the zygoma. The roof of the sinus, the orbital floor, is twice as wide as the floor, the maxillary alveolus. The anterior wall is the facial surface of the maxilla and the posterior wall is the infratemporal surface. The floor is limited anteriorly by the first premolar and posteriorly to a recess behind the third molar. The ostium of the maxillary sinus is located within the middle meatus in the hiatus semilunaris (see Figure 3). Accessory ostia occur in 25 to 30% of individuals (3). The shape of the ostium depends upon the influence of the ethmoid bulla superiorly and upon the uncinate process inferiorly. The blood to the maxillary sinus is primarily supplied by branches of the maxillary artery. The venous drainage occurs primarily via the anterior facial vein, although the maxillary vein also contributes to some degree.
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Figure
1
Developmental stages of maxillary and frontal sinuses. (Reproduced with per·
mission from Ref. 29, p. 846.)
The maxillary vein communicates with the pterygoid venous plexus in the infratemporal fossa, which in turn anastamoses with the dural venous sinuses via the foramen ovale. It is these valveless venous connections that permit the intracranial extension of maxillary sinusitis. In the third fetal month, the ethmoids begin as evaginations of the lateral nasal wall in the region of the ethmoid bone. The anterior cells remain in this region, but the posterior group expand upward toward the superior meatus. At birth the anteromiddle group measure 5 mm high, 2 mm long, and 2 mm wide (3). The posterior group are 5 x 4 x 2 mm. The ethmoid and maxillary sinuses are the only sinuses large enough at birth to be clinically implicated in rhinosinusitis. The ethmoid sinuses are typically not apparent radiographically until age one year. By the age of 12 years
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SINUSITIS Frontal sinus Anterior ethmoidal cells (under middle concha)
Posterior ethmoidal
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Middle ethmoidal cells (under middle concha)
Inferior concha
Figure 3
DcvclopIhcntal stages of ethIhoid
and sphenoid sinuses. (Reproduced with per
Ref. 29, p. 848.)
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the ethmoids have attained their adult size. At this time the
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posterior cells, with the posterior group being larger. The infundibulum is a crescentic depression created by the uncinate process below and the
ethmoid bulla above. The opening of this depression is the hiatus semi lunaris (see
Figure 3). Anatomically, the anterior ethmoid cells are defined
as those whose ostia open into the infundibulum of the middle meatus. The middle cells are those opening in relation to the ethmoid bulla. The posterior cells have their ostia in the superior meatus (see Figure
3).
The
ethmoid air cells are not confined to the ethmoid bone. Frequently their pneumatization extends anteriorly to the nasal and lacrimal bones,
teriorly to the orbital
pos sphenoid bone, inferiorly to the maxilla and superiorl y to plate of the frontal bone. The ethmoid sinuses are py ramidal
the
,
in shape in the anteroposterior dimension. The lateral wall, the thin lamina
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FRIEDMAN & HARRIS
paprycea, accounts for the frequency of orbital complications associated with infection in this region (see Figure 2). The blood supply to the ethmoid sinuses is derived from the internal carotid arterial system via the anterior and posterior ethmoid arteries, which are branches of the ophthalmic artery. Additional blood is provided by branches of the maxillary artery. Blood is drained by the nasal veins and the ethmoidal veins. The latter are tributaries of the ophthalmic veins, which communicate freely with the cavernous sinus. The frontal sinus develops as an evagination of the ethmoid bone ante riorly within the nasal capsule in a region known as the frontal recess (see Figure 1). At birth the sinus is indistinguishable from the surrounding ethmoid sinus and continues to develop slowly. At age one year the sinus is hardly perceptible, and it is not until age five to six years that pneu matization extends up onto the vertical portion of the frontal bone. The sinus can be recognized radiographically at approximately age six years. The sinus continues to grow rapidly until the late teens. The average dimensions of the adult frontal sinus are 28 mm high, 24 mm wide, and 20 mm deep (3). The sinus is generally pyramidal in shape. Some individuals display little vertical pneumatization but have extensive development of supraorbital cells. The two frontal sinuses are separated by a bony septum. The frontal sinus typically drains into the infundibulum of the middle meatus via the nasofrontal duct. Blood is supplied to the frontal sinuses via the supraorbital and supratrochlear arteries. The venous drainage is via the superior ophthalmic vein through the superior orbital fissure to the cavernous sinus. The sphenoid sinus can be identified as a small evagination of the sphenoethmoid recess at birth (see Figure 3). Invasion of the sphenoid bone commences at approximately age five years, and within a few years it has extended posteriorly to the sella turcica. The sphenoid sinus is fully
developed by the late teens. The average dimensions of the adult sphenoid sinus are 20 mm high, 23 mm long, and 1 7 mm wide (3). The paired sinuses are separated by a bony septum. Sculpted into the walls of the well-pneumatized sphenoid sinus are structures such as the internal carotid artery and the optic nerve. Their close proximity to the walls of the sinus can present potential hazards during instrumentation of the sphenoid sinus. The sphenoid sinus opens into the sphenoethmoid recess above the superior concha. The ostium is approximately 10 mm above the floor of the sinus. The blood supply to the sphenoid sinus comes from branches of the internal and external carotid arteries. The venous drainage occurs via branches of the maxillary vein and thus communicates with the pterygoid venous plexus (2, 3).
SINUSITIS
477
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SYMPTOMS AND SIGNS Patients with infection of the paranasal sinuses may complain of headache, nasal congestion, rhinorrhea, postnasal drip, productive cough, and phar yngitis. The sinus headache is generally located in the area of the involved sinus. Symptoms are localized to the forehead, around or behind the eyes, the maxillary teeth, and the vertex, temporal, or parietal areas of the skull. Frontal sinusitis can often be referred to the scalp along branches of the supraorbital nerve. In a review of 30 cases of sphenoid sinusitis, Lew et al (4) found the most common presenting symptoms to be severe frontal, temporal, or retro-orbital headache that radiated to the occipital regions, or pain in the trigeminal (VI to V3) distribution, or both. The pain may be intermittent or constant and is exacerbated by placing the head in a dependent position. Patients with acute sinusitis typically describe pain or pressure that is most severe during the day. Chronic sinusitis is less fre quently associated with pain or prcssurc. Other causes of headache includ ing migraine, muscle tension, or intracranial lesions must be considered in the differential diagnosis. Pertinent historical features include recent upper respiratory tract infection, trauma, allergy, swimming, flying, or dental repair. Additionally, patients may rcport previous surgery or recent work in a poorly ventilated area with volatile or noxious material. Patients with acute or chronic sinusitis commonly display purulent rhinorrhea that is yellow or green and malodorous. Postnasal drip has similar characteristics and may be associated with a foul taste, halitosis, or chronic pharyngeal discomfort. Physical examination may yield signs of recent upper respiratory tract infection or chronic nasal allergy. Rhinoscopy either with nasal speculum and headlight or with nasal en doscopy is essential. The presence of yellow or green discharge in the middle or superior meatus with edematous and erythematous mucosa is diagnostic. Nasal polyps, large "blue" inferior turbinates, and clear mucus bridging the nasal septum and turbinates anteriorly suggest allergic rhinitis. Nasopharyngoscopy using a mirror and headlight or a fiberoptic naso pharyngoscope may reveal a string of mucus draining down along the posterior aspect of the inferior turbinate indicative of maxillary sinus disease. Additionally, an enlarged inferior turbinate posteriorly is indica tive of allergic rhinitis. Palpation and percussion of the acutely involved sinuses may reveal tenderness, while patients with chronic sinusitis rarely describe such tenderness. Percussion of the maxillary teeth commonly elicits tenderness of the involved maxillary sinus. Gwaltney et al (5) found transillumination of the sinuses to be clinically useful in the hands of experienced examiners.
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Ophthalmalogic examination is essential in patients with sinus disease. Visual acuity and field testing as well as ocular motility should be assessed. Proptosis, chemosis, periorbital edema, erythema, or fiuctuance are indi cators of a suppurative orbital or intracranial complication. Ophthal moplegia, anesthesia in the distribution of the ophthalmic division of the trigeminal nerve, ptosis, and mydriasis are indicative of a superior orbital fissure syndrome. With associated visual changes the process has likely involved the orbital apex.
PATHOGENESIS The mucociliary system of the nose and paranasal sinuses provides mueh of the local defense against infection (see Table 1). Secretory IgA also protects against viral and bacterial pathogens (6). Microbes, pollutants, and other irritants are trapped in the mucous of the nose and sinuses and propelled toward the nasopharynx. The mucus blanket travels at a rate of approximately 1 em per minute and the nose and sinuses produce mucus at a rate of a liter per day. When this protective system breaks down, colonizing pathogenic bacteria proliferate and infection ensues. Bacteria
typically infect the sinuses by traversing the ostia from the nasal cavity. The maxillary sinus may become seeded by an odontogenic infection. Retention of secretions is the fundamental event in infection of the sinuses and several factors contribute: (a) mucosal swelling leading to diminished patency of the ostia; (b) abnormalities of the cilia leading to impaired transport secondary to a quantitative reduction, a structural abnormality, or incoordination of movement; and (c) overproduction of secretions. The patency of the ostia is a major factor in the development of sinusitis. Recent upper respiratory tract infection or exacerbation of allergic rhinitis leads to mucosal edema and diminished ostial patency. Aust et al (7), studying normal subjects, found an inverse relationship between diameter of the maxillary sinus ostium and the time required for emptying the sinus Table 1
Factors predisposing to sinusitis
Upper respiratory tract infection
Tumors
Allergic rhinitis
Foreign bodies
Overuse of topical decongestants
Swimming/diving
Hypertrophied adenoids
Cigarette smoke
Deviated nasal septum
Barotrauma
Nasal polyps
Dental extraction/injections
Immune deficiency
Bronchiectasis
Cystic fibrosis
Immotile cilia syndrome
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of contrast material. Johansson et al (8) found that experimentally induced ostial dysfunction in the prcsencc of pathogenic bacteria resulted in puru lent sinusitis in all subjects. Neither occlusion alone nor innoculation with pathogenic bacteria alone induced significant disease. The diameter of the maxillary sinus ostium is also a major factor in gas exchange between the sinus and the nasal cavity. During normal nasal breathing, 90% of sinus air is exchanged in five minutes. With diminution of ostial size the partial pressure of oxygen begins to decline. Oxygen tension drops further when ostial closure is accompanied by infection. Carenfelt et al (9) examined infected maxillary sinus aspirates and showed them to have oxygen tensions near zero, elevated carbon dioxide tensions, and lowered pH. Low oxygen tension not only favors increased bacterial growth, but, also may impair local defenses. Ciliary movement is essential to propel the mucus blanket. The cilia beat as a group in a spiral fashion toward the sinus ostium. Mucociliary trans port may be compromised by low oxygen tension within the sinus. In addi
tion to local factors, structural abnormalities such as the absence of dynein arms in Kartagener's syndrome lead to ciliary dysfunction. Finally, viral in fection may lead to destruction of ciliated epithelial celIs (ciliocytophoria). The ostia of the maxillary and sphenoid sinuses are superiorly located. For drainage to occur in the upright position the mucus must be propelled against the force of gravity. This combined with mucus overproduction, ostial edema, or ciliary dysfunction places these sinuses at an additional risk for infection. Gwaltney et al (5) and Su et al (10) demonstrated conclusively that cultures obtained from the nose and nasopharynx correlate poorly with those obtained directly from the sinus by aspiration or open antrostomy. Karma et al (11) studied 61 chronically inflamed maxillary sinuses. Bac teriologic findings from nasal mucus, sinus mucus, and sinus mucosa frequently differed. Mucosal samples more than doubled the bacteriologic yield of the samples taken from sinus secretions. Because normal sinus mu cosa is known to be sterile, it was concluded that samples taken directly from sinus mucosa more reliably reflect the bacteriology of chronic sinusitis. Gwaltney et al (5) reported Streptococcus pneumoniae and non-typable Haemophilus irif/uenzae as the primary pathogens in more than half the cases of acute bacterial sinusitis. Other prominent pathogens include Bran hamella catarrhalis and viruses. Staphylococcus aureus and S. epidermis have also been implicated as pathogens in acute and chronic sinusitis. The majority of the data suggest both species more commonly colonize the nasal mucus in acute sinusitis. Evans et al (19), Gwaltney et al (5), and Su et al (10) found Staphylococcus aureus, S. epidermis, and diptheroids frequently isolated from the nasal secretions of normal subjects. None
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except S. aureus were isolated in significant concentrations from the mucosa of patients with chronic maxillary sinusitis. Despite the environment in the acutely infected sinus, Gwaltney et al (5) isolated anaerobic organisms in fewer than 10% of patients. In contrast, anaerobic organisms play a significant role in chronic sinusitis. Brook (12) isolated anaerobic bacteria from 88% of aspirates of 72 chronically inflamed maxillary sinuses. They were the sole isolates in 56% of subjects. Anaerobic isolates in descending order included anaerobic cocci, Bac teroides melanogenicus, B. jragilis, Propionibacterium acnes, and Fuso bacterium species. Many aerobic and facultative isolates were identified including Staphylococcus aureus and Streptococcus pyogenes. As many as 44% of anaerobic isolates have been shown to produce beta-lactamase, including 25-50% of Bacteroides melanogenicus.
NONBACTERIAL INFECTION Fungal infections of the nose and paranasal sinuses are uncommon. Asper gillosis, mucormycosis, candidiasis, histopl asmosis and coccidiomycosis can occur. Aspergillus jumigatus is the most common fungal pathogen encountered, and the maxillary sinus is the most commonly involved site. Immunosuppressed patients are at highest risk. Diagnosis frequently necessitates antrostomy with tissue biopsy. ,
Aspergillosis
Paranasal sinusitis secondary to Aspergillis infection is increasing. The number of cases tripled in the past three decades. This entity was first described in healthy patients but is increasingly recognized in immuno compromised patients, such as those with diabetes mellitis (3, 13). Aspergillis is a saprophyte of soil, dust, and decaying organic material. Seven species have been identified that are pathogenic in humans. Asper gillis colonies grow in a wide range of temperatures. The organism grows well in damp, decaying vegetation heated by bacterial fermentation. Asper gillis is endemic in the Sudan, where it has been cultured from bedding, straw roofs, and the soil of Sudanese dwellings. A.jlavus is the sole species implicated in disease in the Sudan. A. jumigatus is the most commonly encountered species in the United States. The usual portal of entry is the respiratory tract. Aspergillis is commonly cultured from the external auditory canals of patients with mycotic otitis externa. It is not contagious and sources of infection are endogenous. Aspergillis appears as a greenish-black, tarry or rubbery mass within the sinus cavity. The organism characteristically has septate hyphae and
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dichotomous branching (Figure 4). Aspergillis can be distinguished from the Phycomycetes not only by their septate hyphae, but by the 45° angle of their branching compared to the random branching of hyphae seen in the latter. Microscopic identification is best made with silver stains (Gridley, PAS, and methenamine silver). A direct culture should be per formed on Sabouraud's agar with an antibiotic to inhibit bacterial growth. Aspergillis is frequently a colonizer of the paranasal sinuses and becomes pathologic when the ostia are obstructed. This fungus grows best in an anaerobic environment; the presence of ostial occlusion, elevated intra sinus pressures, and anaerobic bacteria contribute to its pathogenicity. Three clinical types of paranasal aspergillosis exist (14). Infections can be noninvasive, invasive, and fulminant. The noninvasive type is similar to chronic rhinosinusitis presenting with rhinorrhea and nasal obstruction. Radiographs may show clouding or opacification of the sinuses. The maxillary sinus is the most commonly involved. Intranasal examination reveals nonspecific signs of mucosal inflammation. Antral lavage is neither
curative nor diagnostic. Left untreated, aspergillis infection will become invasive. Invasive asper gillosis typically presents with orbital or maxillary extension. Radiography reveals a paranasal sinus mass with orbital displacement and bony erosion. Invasive aspergillosis behaves much like a malignant neoplasm and occasionally presents with intracranial involvement. Like the Phyco-
Figure 4
Dichotomous branching at 45° angles in
A.fumigalus.
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mycetes, aspergillis has a tendency to invade arteries, which may lead to thrombosis or hemorrhage-most importantly within the internal carotid artery. The patient's general health and immunocompetence may influence the progression to invasive disease; however, both invasive and non invasive types have been reported in healthy patients. The fulminant form of the disease occurs in immunocompromised pati ents. Children with acute leukemia undergoing radiation and chemo therapy are most susceptible. The earliest nasal lesion is crusting of the anterior aspect of the inferior tubinate or septum. The tissue beneath the crust is insensitive. The infection spreads to the lateral nasal wall within days. Proptosis, chemosis, and ophthalmoplegia indicate orbital involve ment. The disease rapidly progresses to the lungs, liver, and spleen. Patho logically, the hyphae invade dura, blood vessels, and bone. The treatment of the noninvasive and invasive varieties of aspergillosis is primarily surgical. Most cases are cured by excision and aeration of the sinuses. If the fungus spreads into the orbit or the cranium, amphotcricin B should be administered. Fulminant disease is treated by systemic ampho tericin B and debridement of all gross disease. Mucormycosis
Mucormycosis is an infection caused by fungi in the class Phycomycetes. They are distinguished by the random branching of their nonseptated hyphae. The organisms important in humans include species of the genera Mucor, Rhizopus, and Absidia, all of which are within the order Mucorales. These fungi, commonly recognized as bread mold, are found in soil, vegetable debris, and manure. Mucormycosis can be classificd into six different categories: (a) rhinocerebral mucormycosis, which is commonly seen in patients with diabetes or hematologic diseases; (b) pulmonary and disseminated mucormycosis, also seen in debilitated patients; (c) gastro intestinal mucormycosis present in severely malnourished or uremic patients and patients suffering from amebiasis; (d) mucormycosis of burn wounds; (e) central nervous system mucormycosis; and (f) endocarditis, usually following cardiac surgery. Severe localized infections of the head and neck occur in patients with impaired immunologic function. McNulty (15) and Pillsbury (16) impli cated diabetic ketoacidosis, burns, neutropenia, leukemia, lymphoma, uremia, sepsis, severe dehydration, long-term immunosuppressive therapy (including steroids), and broad spectrum antibiotics as etiologic factors in the development of mucormycosis. Survival statistics for patients with no underlying disease and with diabetes mellitus are 75% and 60% respec tively. McNulty (15) noted a survival rate of only 10% in patients with more significant diseases.
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Of patients with rhinocerebral mucormycosis, 70% are in diabetic ketoacidosis. This association is likely explained by the fact that Rhizopus species have an active ketone-reductase system and proliferate in a low pH and glucose-rich environment. The abnormal polymorphonuclear chemotaxis and phagocytic activity existing in severe hyperglycemia con tribute to the pathogenicity. Fungus can invade the nose, paranasal sinuses, lungs, and gas trointestinal tract. Once inside, the fungus moves into blood vessels, which leads to hemorrhagic ischemia and thrombosis. The resulting vascular insufficiency causes dry gangrene. The initial signs of infection include nonspecific turbinate engorgement and nasal obstruction. The diagnosis should be suspected in the presence of persistent rhinitis in an immu nocompromised or debilitated host. Progression of the disease leads to ischemic necrosis of the turbinates and the development of bloody rhi norrhea. The nasal turbinates, septum, or palate appear black on exam ination. Disease ultimately extends to the orbital apex via the ethmoid arteries and into the cavernous sinus. Signs of orbital extension include proptosis, chemosis, ptosis, ophthalmoplegia, and loss of vision. Once within the cavernous sinus, fungal invasion of the internal carotid artery may ensue, leading to thrombosis. Pillsbury (16) found the time course of this deeply invasive disease may be as little as three days. Transnasal biopsy is the only reliable method of diagnosis. Special fungal stains (PAS, methenamine silver) should be performed, although invasion of the nonseptated hyphae can frequently be recognized on frozen section. The first goal of therapy is control of the underlying disease. Pillsbury (16) found reversal of dehydration and acidosis improve survival, even in nondiabetic patients. Immediate debridement of all infected and devi talized tissue is performed. This may include orbital exenteration if vision is lost. High doses of amphotericin B are then administered. An alternate day regimen of 1 mg per kg up to a total of 2 g is necessary. Renal function must be closely monitored because amphotericin B is nephrotoxic. The addition of low doses of heparin to the intravenous infusion diminishes the associated thrombophlebitis.
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SINUSITIS IN THE NASOTRACHEALLY INTUBATED PATIENT Maxillary sinusitis secondary to nasotracheal intubation is a well-known entity. The reported incidence of sinusitis in these patients is 2- 5%. Infec tion, as in most paranasal sinus infections, likely results from the presence
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of the large-bore tube as well as from local edema, which leads to ostial dysfunction and secondary obstruction. Deutschman et al (17) contend that the high incidence of bilateral involvement and pansinusitis suggests an obstructive role for nasogastric tubes as well. Linden et al (18) reviewed 19 cases of maxillary sinusitis in naso traeheally intubated patients. The admission diagnosis in 14 of the 19 patients was multiple trauma. Seventeen of the 19 patients had roent genographic evidence of sinusitis. Twenty-seven antral taps were perfor med, and 21 positive cultures were obtained; 42% of the cultures were polymicrobial. The most commonly cultured organism was Staphylococcus aureus (16%), followed by Enterobacter species (12.9%), Pseudomonas aeruginosa (12.9%), and Bacteroides fragilis and B. melaninogenicus (12.9%). Sinusitis secondary to nasotracheal intubation should be suspected in the presence of unexplained fever, leukocytosis, negative nitrogen balance despite adequate nutritional support, and increased carbon dioxide pro duction or increased oxygen consumption. Deutschman et al found a high incidence of pulmonary seeding and bacteremia, as well as one case of septic shock. Controversy exists regarding the best method of diagnosing suspected sinusitis in these patients. Routine sinus radiographs are successful in most cases. Sinus computerized tomography (CT) is helpful in assessing involvement of the ethmoid or sphenoid sinuses. Many patients are receiv ing broad spectrum antibiotics at the time of diagnosis. The use of antral aspiration is essential for adequate culture and antibiotic sensitivity testing. Additionally, antral irrigation can be performed at the time of sampling. Sinusitis should be considered in nasotracheally intubated patients with unexplained sources of fever or sepsis. Treatment must be aggressive and include removal of the tube, diagnostic and therapeutic antral lavage, topical and systemic decongestants, and appropriate antibiotics guided by culture and sensitivity testing.
DIAGNOSIS AND TREATMENT History and physical examination are essential to the management of paranasal sinus disease but can often be misleading. Gwaltney et al and Evans et al found the clinical features to be of little help in making the diagnosis of acute sinusitis. They also found that the history of purulent rhinorrhea and facial pain correlated poorly with subsequent sinus as piration. Additional studies are frequently necessary in the complete evaluation.
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A complete blood count with white ceIl differential may reveal a leu kocytosis with a leftward shift in acute sinusitis. Blood studies are fre quently normal in chronic disease. Quantitative evaluation of serum immu noglobulin levels for evidence of IgA or IgG subclass 2 and 4 deficiencies, as well as sweat chloride tests for cystic fibrosis, are helpful in the diagnosis of chronic sinusitis (6). Additionally, allergic testing and ciliary motility studies may be helpful. Transillumination of the sinuses is of value in the hands of some experi enced physicians. Gwaltney et al (5) found that normal light transmission and complete absence of light transmission of the maxillary sinus cor related well with the presence and absence of disease, respectively, based upon sinus aspiration. Evans et al (19) noted that dullness on trans illumination was not predictive of disease. McNeill et al (20) found that transillumination correlated with clinical disease in only 68% of patients. Transillumination is less helpful in patients with chronic sinus disease because of persistent mucosal abnormalities.
The initial radiologic evaluation of the paranasal sinuses is by plain x ray. Most paranasal sinus pathology can be demonstrated by this tech nique, but there is much controversy as to whether X-ray examination of the sinuses is reliable. Many factors other than infection can lead to opacification of the sinuses. A thick antral wall may lead to opacification of the maxillary sinuses. Overlying soft tissue swelling can cloud the sinuses. McNeill et al (20) and Vuorinen et al (21) found approximately 82% correlation between evidence of maxillary sinusitis from X-ray and that from antral aspiration. Thcse studies found less correlation in sinuses that show mucosal thickening (63%). A mucosal thickness of 5 mm or greater in the maxillary sinus, as determined by using a Water's view, better discriminates between those with and without evidence of disease or aspir ation. Follow-up radiographs are essential for detection of asymptomatic treatment failures. For patients with complicated presentations or chronic complaints in whom plain radiographs are unhelpful, more sophisticated testing is recommended. Conventional CT scanning is helpful in evaluating the anatomy and extent of disease in patients with chronic sinusitis and in patients requiring surgical intervention. CT reveals excellent soft tissue and bony detail. High-field magnetic resonance imaging of paranasal sinus disease is also excellent for evaluation of soft tissue (22, 23). This modality is especiaIly useful in cases of suspected malignancy of the nose and paranasal sinuses. There is a paucity of information regarding the use of maxillary sinus puncture for aspiration and irrigation. Many clinicians sample nasal secretions in cases of acute and chronic sinusitis. Axelsson & Brorson (24) found only a 64% correlation between bacteria cultured from the nasal
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versus sinus secretions in patients with acute maxillary sinusitis. Addition ally, Axellson & Brorson (24) and Karma et al (11) found staphylococcal species and diptheroids to be present primarily in cultures of nasal secretions and rarely in sinus secretions, which indicates their likely role as contaminants. Current indications for antral aspiration and lavage are (a) sinusitis in an immunocompromised or chronically debilitated host; (b) failure of resolution of symptoms after 24 to 48 hours of empiric antibiotic therapy; (c) progression of symptoms while on antibiotics; (d) an orbital or intracranial complication of maxillary sinusitis; (e) maxillary sinusitis in a newborn; and (f) severe pain. The frontal sinus can be aspirated and irrigated through a trephine. The ethmoid sinuses require surgical drainage, either externally or intranasally. Treatment of acute sinusitis should initially he aimed at drainage of retained secretions. This can be facilitated by the use of topical and sys temic decongestants. Topical decongestants should be used for no longer than seven days to avoid developing rhinitis medicamentosa. Gwaltney et al (5) found equal success rates with the use of ampicillin, amoxacillin, trimethaprim-sulfamethoxazole, and cefaclor. The emergence of pen icillinase-producing bacteria may require the use of amoxicillin and cla vulanic acid in resistant infections. Further treatment should be guided by bacterial culture and antibiotic sensitivity testing. Treatment of chronic sinusitis requires anaerobic coverage as well as control of predisposing factors such as allergy. Patients with complicated acute sinusitis and those with refractory chronic sinusitis require surgical intervention.
COMPLICATIONS Serious complications of paranasal sinusitis are rarely seen since the intro duction of antimicrobial therapy. Few physicians today have seen the orbital and intracranial complications of uncontrolled infection. With the increase in antibiotic-resistant bacteria and immunocompromised hosts, the clinician should be aware of the possible complications of extensive infection. Mucoceles
The mucocele is a chronic, cystic lesion of the paranasal sinuses. These cysts are lined with pseudostratified columnar epithelium and occasional goblet cells. Mucoceles are slowly expansile lesions, frequently existing many years before becoming symptomatic (3). Their expansion within the sinus of origin leads to bony sclerosis and eventual erosion and subsequent extrasinus extension. The symptoms depend upon the sinus of origin and the extent of erosion. Mucoceles may arise from obstruction of the sinus
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ostium secondary to trauma, chronic inflammation, neoplasia, or prior surgery. They may also arise from obstruction of a minor salivary gland duct within a sinus. Approximately 10% of all mucoceles occur in the maxillary sinuses. The maxillary mucocele is commonly observed as an incidental finding on sinus radiographs. Symptoms are unusual and these lesions typically regress spontaneously, requiring no further intervention. When the diagnosis is unclear, mucoccles can be aspirated through the canine fossa or the inferior meatus. The most common clinically significant lesions arise in the frontal sinus, followed by those in the anterior ethmoids. Frontal headache, proptosis, and diplopia secondary to downward and outward displacement of the globe are the most common initial complaints (25). Radiographically, there is clouding of the involved sinuses, loss of the normal scalloped appearance of the frontal sinuses, and sclerosis of the sinus walls. Mucoceles of the sphenoid and posterior ethmoid sinuses are rare. Close et al (26) describe a series of three patients with intracranial extension. Symptoms were related to the site of extension and frequently included cranial neuropathies involving nerves two through six. Occipital and vertex headache associated with diplopia or visual field disturbances were the most common complaints. Clinical suspicion followed by CT scanning led to diagnosis. These lesions require surgical intervention. Orbital Complications
The spread of infection to the orbits is the most common complication of paranasal sinusitis. Direct extension can occur through neurovascular foramina, through congenital or acquired dehiscenses, or through thin bone such as the lamina papyracea. Additionally, the valveless ethmoid, angular, nasofrontal, and ophthalmic venous systems allow spread via septic thrombophlebitis. Chandler et al (27) provided the following classi fication scheme correlating physical findings with orbital disease: Inflammatory edema-lid edema; no limitation of extraocular movement, and normal visual acuity. 2 . Orbital cellulitis-diffuse edema of orbital contents and infiltration of the adipose tissue with inflammatory cells and bacteria without discrete abscess; may be some impairment of visual acuity. 3. Subperiostial abscess-collection of pus beneath the periostium of the lamina papyracea; globe displaced downward and laterally. 4. Orbital abscess-a discrete collection of pus within the orbital tissues; exophthalmos and chemosis; complete ophthalmoplegia and severe impairment of vision. I.
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5. Cavernous sinus thrombosis-bilateral eye findings; edema over the mastoid emissary vein; prostration and meningismus. Extension of infection to the orbit from the frontal sinus may occur through its thin floor. When the infection spreads to involve the squama of the frontal bone, osteomyelitis and subperiostial abscess ensue. The resulting soft tissue swelling is called Pott's puffy tumor (2 8). Orbital complications can frequently be managed by intravenous anti biotic therapy and a drainage procedure. Patients should be hospitalized and observed closcly for evidence of orbital abscess or cavernous sinus thrombosis. Surgical intervention is required if (a) orbital cellulitis pro gresses despite appropriate antibiotics; (b) fever, erythema, and edema fail to regress or worsen after 2 4 to 48 hours of antibiotic therapy; (c ) orbital or subperiostial abscess are found by ultrasound or CT scan; and (d) visual acuity is lost. Intracranial Complications
The intracranial complications secondary to sinusitis include the following: meningitis, epidural abscess, subdural empyema, venous sinus thrombosis, and cerebral abscess (28). These complications can result from direct extension, septic thrombophlebitis, and hematogenous spread. Meningitis is the most common intracranial complication of paranasal sinusitis. Nuchal rigidity, diminished mentation, and coma should alert the phy sician to the possibility of an intracranial complication. After CT scan and lumbar puncture, intravenous antibiotics should be started on an empiric basis. Signs of increasing intracranial pressure (including diplopia, vomit ing, severe headache, and altered mental status) are considered emergent. Treatment should be undertaken in cooperation with a neurosurgeon and otolaryngologist. Literature Cited
l. Rice. D., Schaefer, S. D. 1988. Endo scopic Paranasal Sinus Surgery. New York: Raven 2. Hollinshead, W. H. 1982. Anatomy for Surgeons, Vol. l. New York: Harper & Row . 3rd ed. 3. Cummings, C. W. 1986. Otolaryn gology-Head and Neck Surgery, Vol. I. St. Louis: Mosby 4. Lew, D. et al. 1983. Sphenoid sinusitis. N. Engl. J. Med. 309(19): 1149-54 5. Gwaltney, J. M. et al. 1981. Etiology and antimicrobial treatment of acute sinu sitis. Ann. 0101. 90: 68 6. Slavin, R. G. 1988. Sinusitis in adults. 1. Allergy c/in. Immunol. 81(5): 1028-31
7. Aust, R., Drettner, B., Hemmingsson, A. 1976. Elimination of contrast medium from the maxillary sinus. Acla Ololaryngol. 81: 468-74 8. Johansson, P. et a\. 1988. Experimental acute sinusitis in rabbits. Acla 010laryngol. lOS: 357-66 9. Carenfelt, C., Lundberg, C. 1977. Puru lent and non-purulent maxillary sinus secretions. Acta Otolaryngol. 84: 138-44 10. Su, W. Y. et a\. 1983. Bacteriological study in chronic maxillary sinusitis. Laryngoscope 93: 931-34 II. Karma, P. et a\. 1979. Bacteria in chronic maxillary sinusitis. Arch. 0101. 105: 36890
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SINUSITIS 12. Brook, I. 1989. Bacteriology of chronic maxillary sinusitis in adults. Ann. Otol. Rhinol. Laryngol. 98: 426-28 13. Jahrsdoerfer, R., Ejercito, V. , Johns, M., Cantrell, R., Sydnor, B. 1979. Asper gillosis of the nose and paranasal sinuses. Laryngoscope 92: 6-13 14. Romett, J., Newman, R. 1982. Asper gillosis of the nose and paranasal sinuses. Laryngoscope 92: 764-66 15. McNulty, J. 1982. Rhinocerebral mu cormycosis: predisposing factors. Laryn goscope 92: 1140-43 16. Pillsbury, H. 1977. Rhinocerebral mucormycosis. Arch. Otolaryngol. 103: 600-4 17. Deutschman, C. et al. 1986. Paranasal sinusitis associated with nasotracheal intubation: a frequently unrecognized and treatable source of sepsis. Crit. Care Med. 14: 111-14 18. Linden, B., Aguilar, E., Allen, S. 1988. Sinusitis in the nasotracheally intubated patient. Arch. Otolaryngol. Head Neck Surg. 114: 860-61 19. Ev�ms, F. et al. 1975. Sinusitis of the maxillary antrum. N. Engl. J. Med. 293: 735-39 20. McNeill, R. A. et al. 1963. Comparison of the findings on transillumination, x ray and lavage of the maxillary sinus. J. Laryngol. 77: 1009-13 21. Vuorinen, P. et al. 1962. Comparison
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of results of roentgen examination and puncture and irrigation of the maxillary sinuses. .J. Laryngol. Otol. 76: 259-64 Lloyd, G. 1989. Diagnostic imaging of the nose and paranasal sinuses. J. Laryn gol. 0101. 103: 453-60 Potchen, M. et al. 1986. High-field mag netic resonance imaging of paranasal sinus inflamm atory disease. Laryngo scope 96: 267-71 Axelsson, A., Brorson, J. 1980. The cor relation between bacteriological findings in the nose and maxillary sinus in acute maxillary sinusitis. Laryngoscope 90: 635 Gardiner, L. 1986. Complicated frontal sinusitis: evaluation and management. Otolaryngol. Head Neck Surg. 95: 33342 Close, L. G., O'Conner, W. E. 1983. Sphenoethmoidal mucoceles with intra cranial extension. Otolaryngol. Head Neck Surg. 91: 350-57 Chandler, J. et al. 1970. The patho genesis of orbital complications in acute sinusitis. Laryngoscope 80: 141427 Rood, S. R. et al. 1982. Complications of Acute and Chronic Sinus Disease. Self instructional packet. Am. Acad. Oto laryngol. Head Neck Surg. Found. Graney, M. J. 1986. Anatomy. In Oto laryngology-Head and Neck Surgery. St. Louis: Mosby. 958 pp.
