The sinusitis cycle JAMES S. REILLY, MD, Birmingham, Alabama
Recent dllcoverlel make It necenary to reevaluate many of the traditional assumptlonl concerning Iinulltil. Within the palt 10 years, Inveltlgatorl have detailed the pathophYllology of Iinulltil. Occlullon of theilnul ostia Inltlatel thellnulltll cycle; untreated, thll leadl to chronic Iinulltil. Anatomic abnormalltlel allo predllpole the patient to chronic Iinulltli because of oltlal blockage. Inveltlgators have Identified and detailed the prevalence of both aerobIc and anaerobic envlronmentl within the Iinulel, demonstratingthat ostial blockage creates an Ideal culture medium within the sinul. KeepIng the ostial panageways open Is essential to allow reversal of the Iinusltis cycle, elpeclally In the prelence of predllposlng factors. (OTOlARYNGOL HEAD NECK SURG 1990;103:856.)
Only within the past 10 years has sinus disease been studied in a truly scientific fashion. Before the application of radiologic examination by computed tomography (CT), minimal information was available to the clinician, and this severely limited understanding of sinus disease as well as sinus anatomy. Often, clinicians recognized only advanced disease, manifested either by complications spread outside the sinuses or by changes sufficient to substantiate alterations on plain radiographs. So, while clinicians were practicing cost containment by ordering plain x-ray films only when indicated by persistence of symptoms, researchers were showing that this traditional radiographic method of imaging the paranasal sinuses lacked the precision needed to document sinusitis reliably, both in children and adults. 1,2 As a result, clinicians have tended to underdiagnose sinusitis. Perhaps this is the reason medical myths have developed about recurrent acute and chronic sinusitis. The most common myths about sinusitis are: • Chronic sinusitis is always allergic in origin. • Chronic and recurrent acute sinusitis are incurable. With technologic advance, investigators are challenging these and many other suppositions concerning sinusitis. Anatomlo Development CT imaging provides today's clinicians with highquality, three-dimensional images of the structures of the ethmoid sinus, the most common source of sinus disease. This technique shows clearly that predisposing
23/0/24793
anatomic factors work in concert with microflora in the development of sinusitis. Furthermore, the technique has provided information about anatomic development between infancy and adolescence that can singularly affect the diagnosis, as well as the treatment, of sinusitis in both children and adults. Only the ethmoid and maxillary sinuses are present at birth (Fig. 1). During infancy, tremendous growth of midface and skull dramatically increases the size of the paranasal sinuses. The ethmoid sinuses are fully developed-adult size-by approximately age 14 years (Fig. 2); the maxillary sinuses grow slowly and reach full size with the appearance of all of the maxillary teeth, sometime during adolescence (Fig. 3),304 The ethmoid sinuses, the most important in terms of chronic sinus disease. consist of 3 to 18 small. air-filled cavities divided by a thin, bony lamina. and drain through the ostia into the middle and superior meatus. Ostia within the maxillary sinus open into the hiatus semilunaris, high on the sinus cavity's medial wall. As a result, drainage from the maxillary sinus is difficult• and stasis and infection of secretions are common. The maxillary and ethmoid sinuses are the more common sites of clinical infection during childhood. The sphenoid sinus develops sometime after age 2 years. and the frontal sinuses begin to develop from the ethmoid air cells into the frontal bone by around age 6 years. Both the frontal and the sphenoid sinuses may frequently become infected in pansinusitis. Infections specific to these two sinuses become clinically important between 8 and 18 years of age.
Pathophysiology of Sinusitis Normal ciliary function. intact mucous membranes. and normal mucous production are integral to sinus
I"
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Fig. 1. RUdimentary ethmoid and maxillary sinusesin an infant. (Illustrator. Figs. 1-3: Paul Singh-Roy.) FIg. 2. Ten-year-old child wlth developed and clinically im portant sinuses.
clearance. Occlusion of the sinus ostia seems to initiate acute sinusitis which, if untreated or inadequately tt:eated, can singularly produce chronic sinusitis. PosSIble causes of sinus ostial obstruction include local ~Ucosal swelling, local insult, and mechanical obstruction. In a study of 23 patients with acute rhinitis by Drettner and Lindholrn," two thirds exhibited unmistakable obstruction of the ostia. This blockage of the ostia initiates a cycle of events leading to sinusitis (Fig . 4). To break this cycle, it is essential to reopen and drain the ostia and the ostiomeatal complex. Functional obstruction of the ostia reduces oxygen tension within the maxillary sinus and also appears to be associated with the size and the patency of the maxillary sinus ostia ." The resultant hypoxic environment in the maxillary sinus, or the ethmoid or frontal sinuses, can lead to a change from a predominantly aerobic flora Or bacteria to an anaerobic flora, partly as a result of the development of an acid pool of secretions that affects metabolic activity and bacterial multiplication . Sable et al. 7 studied 16 children with acute frontal sinusitis and associated complications and found that II children had either anaerobes or aerobes, or both, in the sinus secretions. In addition, the local protective function of the cilia , the sinus mucosa, and the bactericidal function of the
granulocytes become impaired. Resolution of acute sinus infection is greatly hindered by mucosal damage, which further constricts and occludes the ostia . This vicious cycle correlates well with radiographic evidence of chronic sinusitis. Su et al. K have shown that anaerobic bacterial counts increase in the sinus secretions and, furthermore, in the sinus mucosa with chronic sinusitis, and that even bacteria directly invade the sinus wall. Recent studies demonstrate clearly that chronic sinusiti s is generally associated with an anatomic derangement, particularly of the ostiomeatal complex, the focal point for both ethmoid and maxillary sinus disease . The size of the infundibulum and the position of both the ostia and the overlying middle turbinate specifically inhibit or stop the outflow of mucus. Predisposing factors identified by CT scan include deformed uncinate processes, the concha bullosa , agger nasi cells, Haller's cells , and reverse scroll concha." These derangements are of primary importance in chronic sinusitis and may be factors in recurrent or lingering acute sinusitis. Adenoid hypertrophy and adenoiditis probably play an important adjunctive role in chronic sinusitis in children. 10
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OlolaryngologVHead and Neck Surgery
REILLY
Fig. 3. Flfteen-yeer-old adolescent has poranasol sinuses thot are 90% adult size.
Pr•••nc. of Bact.rla In Slnu••• For many years . medical tradit ion held that normal. healthy paranasal sinuses of both adults and children were sterile . Onl y with in the past two decades has this assumption been proved false . II In 1975. Evans et al . " established the bacteriology of maxillary sinusitis in adults. and in 1981. Brook l l showed that all sinuses contain some anaerobic organism s and that more than a third of the sinuses harbor a mixed environment of ana erobic and aerobic organism s . Similarly. Su et al. " found a mixture of aerobes and anaerobes growing in diseased sinuses . suggesting that normal bacterial flora can proliferate as a result of osti al occlusion without inoculation by external pathogenic bacteria. Th e relative prevalence of aerobic ver sus anaerobic
organi sms in sinusitis has been a subject of some controversy. Early studies stress the predominance of aerobes in chronic sinusitis . J 4 ,1 ~ As late as 1975. Evans et al ." found that only 12% of organisms cultured from sinus secretions were anaerobes. However. the majority of Evans et al. 's subjects had acute or subacute sinus disease. Indeed, only four patients had chronic sinus disease in that study. In contrast, Frederick and Braude" earlier found that anaerobic organisms were present in 52% of the chronic sinus infections studied. This finding has been greatly reinforced by a recent study of 66 chronic sinu sitis cases in which 88 % were colonized by anaerobic organisms. 17 Aerobes present in both normal and d isea se states include the gram-positive streptococci (a, 13. and Streptococcus pneumoniaei and Staphylococcus aureus, and
Downloaded from oto.sagepub.com at University of Sussex Library on June 4, 2016
VOlume103 Number 5 Part 2 November 1990
Sinusitis cycle 819
?
Secretions thicken; pH changes. ~ Mucosal gas metabolism changes.
Secretions stagnate.
I
\
Cilia and epithelium are damaged.
Mucosal congestion or anatomic obstruction blocks air flow and drainage.
\
Change in host milieu creates culture medium for bacterial g,owth covity
7_0
Ostium Isclosed.
Mucosal thickening creates further blockage. ~
. "
Bacterial Infection develops In the sinus cavity,
Retained secretions cause tlssJe Inflammation.
Fig. 4. The sinusitis cycle (otter Draf").
gram-negative Moraxella (formerly Branhamella) catarrhalis. Haemophilus irfiuenzae, and Escherichia Coli. Anaerobic organisms include the gram-positive peptococci and Propionibacterium species. The Bacteroides species and Fusobacterium species also playa significant role in chronic sinusitis. Wald et a1. 1X•19 discovered the most common aerobic organisms in children to be S. pneumoniae. H. influenzae (nontypable), and M. catarrhalis. In a study of 30 children with acute and subacute sinusitis, Wald er al. IX found only aerobic organisms, with a predominance of S. pneumoniae and H. infiuenzae. In cases of chronic maxillary sinusitis, however, Brook!' showed that anaerobes were more common than aerobes. The anaerobes found include Streptococcus. Bacteroides, and Veil/onella species. In another study of the complications of sinusitis in children, Brook et al. 20 demonstrated the occurrence of anaerobic organisms in all eight children studied, with only one aerobic organism cultured. Brook'? also reported that 44% of the Bacteroides species from within the paranasal sinus were producers of f3-lactamase enzyme, which has implications for
the treatment of sinusitis (as well as the treatment of other infections of the head and neck, including adenoiditis, tonsillitis, and otitis media). High 13lactamase producers include Bacteroides species, especially B. fragilis. But other f3-lactamase producers include Fusobacterium, H. inftuenzae, and M. catarrhalis. Both Wald et al, 1M and Brook" found that f3-lactamase-producing bacteria were present in 25% of the aspirates in children with subacute maxillary sinusitis. Predllpollng Factors With bacteria already clearly present in the sinuses, ciliary dysfunction and retention of secretions set the stage for sinus infection. Obstructive sinus ostia isolate bacterial pathogens in a gas- and fluid-filled milieu that favors their rapid growth, and acute sinusitis naturally results. Any of a wide variety of factors may initiate the process. Systemic factors. The systemic diseases and syndromes that predispose adult patients to acute sinusitis include cystic fibrosis, immune deficiency, bronchiectasis, and immotile cilia syndrome. 22.23
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Head and Neck Surgery
In cystic fibrosis, sinusitis is considered a corollary of the disease. Thick and tenacious nasal mucus tends to clog the sinus ostia, setting the stage for bacterial infection in the closed cavities. Immunodeficiency is well documented as a predisposing factor to sinus infection. 24.2~ Because of the high incidence of sinusitis in patients with hypogammaglobulinemia, it can be inferred that normal levels of immunoglobulins protect against sinusitis. The immotile cilia syndrome-of which Kartagener's syndrome is a variation-involves hereditary ciliary dysfunction that obviously predisposes to closed ostia and sinusitis." Patients with Down syndrome are also considered prone to sinus disease, as are those with the clinical triad of nasal polyposis, aspirin intolerance, and asthma. 26 Local factora. URI, as well as allergic rhinitis, are the most significant local factors that predispose patients to sinusitis. Additional local factors include overuse of topical decongestants, hypertrophied adenoids, deviated nasal septum, nasal polyps that generally occur in advanced disease, tumors or foreign bodies, barotrauma (from flying, swimming, or diving), cigarette smoke or other forms of pollution, as well as abnormalities from adjacent dental structures or from dental procedures. Viral infections-specifically URIs-commonly precede bacterial sinusitis. The congestion and ciliary dysfunction caused by the viral infection close the ostia, particularly those of the maxillary sinuses, which are not mere openings but tubular channels approximately 6 mm long. Closure of any sinus ostium creates an ideal culture medium, not only for the flora already in the area, but for bacteria that may arrive in the closed sinus cavities from blood and from lymphatic channels. Bacteria may also enter the maxillary sinuses from dental abscesses or from postextraction complications. In these cases, facilitating ciliary movement and drainage plays a key role in the resolution of sinusitis. That allergies predispose to sinus disease is no longer under serious question. Firm data have not yet shown a direct causal relationship between allergy and sinusitis, but several recent studies strongly suggest one. For example, Slavin et al." demonstrated hyperemia and increased metabolic activity in the paranasal sinuses after exposure to ragweed pollen. The association of asthma and sinusitis, though not established by firm data, is now generally accepted by clinical observation. Patients with asthma and sinusitis have demonstrated improvement in their asthmatic symptoms after their sinusitis has been recognized and effectively treated. 28 By the time an allergy-associated condition becomes full-blown sinusitis, purulent secretions and congestion
often outweigh sneezing, itching, and other allergic symptoms. The immediate problem has become infection, which necessitates antibiotics and decongestants and does not indicate antihistamines. The anticholinergic drying action of antihistamines can lead to further mucous inspissation. Pedlatrlo Venus Adult Sinusitis
Sinusitis is a concomitant of upper respiratory and other head and neck infections that account for an estimated 33% to 50% of all patients seen by primary care physicians. Most adults have two to three URis per year and children have six to eight, with 0.5% to 5% demonstrating a distinct clinical presentation of sinusitis." The higher prevalence of URI and associated sinusitis in children may result from their immature immune systems and smaller nasal passages, which predispose to infections. Theoretically, children are more prone to URI and sinusitis because of their close interactions in group settings, such as daycare centers. The common clinical presentation of sinusitis in children includes symptoms of upper respiratory tract infection lasting more than 10 days, low-grade fever, and irritability; nasal drainage and daytime cough may worsen at night. The patient may experience a change in the consistency, taste, or smell of nasal secretions, which can be purulent, mucoid, cloudy, thick, or thin. Some children report facial pressure or pain, particularly if aggravated by changes of position, such as bending the head down. Headache occurs in children only after the age of 5 years, in most cases. WaidJO has also noted dental pain in children, which may result from either dental infection or referred pain from irritation of the nerve to the sinuses. Severe symptoms that occur in both adults and children include high fever, > 39° C (103.2° F), extensive purulent nasal drainage, and periorbital edema. CONCWSION
With improved understanding of the pathophysiology of sinusitis, we have established the following principles to guide clinical management. I. Occlusion of the sinus ostia initiates the sinusitis . cycle, which, if untreated, leads to chronic sinusitis. 2. Ostial blockage creates an ideal culture medium within the sinus. 3. Keeping the ostial passages open is essential to allow resolution of sinusitis. REFERENCES I. Lusk RP, Lazar RH, Muntz HR. The diagnosis and treatment of recurrent and chronic sinusitis in children. Pediatr Clin North Am 1989;36:1411-21.
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Slnusll1s cycle
2. Kennedy OW. Zinreich SJ. Rosenbaum AE, Johns ME. Functional endoscopic sinus surgery. Theory and diagnostic evaluation. Arch Otolaryngol 1985;111:576-82. 3. Lang J. Clinical anatomy of the nose, nasal cavity. and paranasal sinuses. Translated by P.M. Snell. Stuttgart/New York:Thieme, 1989:56-98. 4. Hawkins DB. Advances in sinus disease in pediatrics. Otolaryngol Clin North Am 1989;22:553-68. 5. Drettner B. Lindholm C-E. The borderline between acute rhinitis and sinusitis. Acta Otolaryngol 1967;64:508-13. 6. Aust R. Drettner B. Oxygenation in the human maxillary sinus under normal and pathological conditions. Acta Otolaryngol 1974;78:264-9. 7. Sable NS. Hengerer A. Powell KR. Acute frontal sinusitis with intracranial complications. Pediatr Infect Dis 1984;3:58-61. 8. Su W-Y. Liu C. Hung SoY. Tsai WF. Bacterological study in chronic maxillary sinusitis. Laryngoscope 1983;93:931-4. 9. Starnmberger H. WolfG. Headaches and sinus disease: the endoscopic approach. Ann Otol Rhinol Laryngol 1988;97(suppl 134):1-23. 10. Fujita A. Takahasi H. Honjo I. Etiological role of adenoids upon otitis media with effusion. Acta Otolaryngol 1988;454 (suPpl):210-3. II. Brook I: Aerobic and anaerobic bacterial flora of normal maxillary sinuses. Laryngoscope 1981;91:372-6. 12. Evans FO Jr. Sydnor JB. Moore WECo et al. Sinusitis of the maxillary antrum. N Engl J Med 1975;293:735-9. 13. Brook I. Bacteriologic features of chronic sinusitis in children. JAMA 1981;246:967-9. 14. Catlin Fl. Cluff LE. Reynolds RC. The bacteriology of acute and chronic sinusitis. South Med J 1965;58:1497-1502. 15. Paiva T. Gronroos JA. Paiva A. Bacteriology and pathology of chronic maxillary sinusitis. Acta Otolaryngol 1962;54: 159-75. 16. Frederick J. Braude AI. Anaerobic infection of the paranasal sinuses. N Engl J Med 1974;290:135-7. 17. Brook I. Bacteriology of chronic maxillary sinusitis in adults. Ann Otol Rhinol Larvngol 1989;98:426-8. 18. Wald ER. Byers C. Guerra N, Casselbrant M. Beste D. Subacute sinusitis in children. J Pediatr 1989;115:28-32. 19. WaldER. Milmoe Gl, Bowen A'D. Ledesma-Medina J. Salamon N. Bluestone CD. Acute maxillary sinusitis in children. N Engl J Med 1981;304:749-54. 20. Brook I. Friedman EM. Rodriguez WJ. Controni G. Complications of sinusitis in children. Pediatrics 1980;66:568-72. 21. Brook I. Beta-Iactamase-producing bacteria in head and neck infection. Laryngoscope 1988;98:428-31. 22. Slavin RG. Sinusitis in adults. J Allergy Clin Immunol 1988;81:1028-32. 23. Slavin RG. Medical therapy of sinusitis and nasal polyps. Presented at the American Academy of Allergy and Immunology (Postgraduate Course), Baltimore. Md., March 28. 1990. 24. Stiehm ER. Immunodeficiency disorders: General considerations. In: Stiehm ER. Gulginiti VA. eds. Immunologic disorders in infants and children. Philadelphia: WB Saunders, 1980:183219. 25. Oxelius V, Laurell A. Lindquist B, et al. 19O subclasses in selective IgA deficiency. N Engl J Med 1981;304:1476-7. 26. Minor MW. Lockey RF. Sinusitis and asthma. South Med J 1987;80:1141-7. 27. Slavin RG, Zilliox AP. Samuels LD. Is there such an entity as allergic sinusitis? [Abstract]. J Allergy Clin Immunol 1988; 81:284. 28. Rachelefsky GS. Katz RM. Siegel SC. Chronic sinus disease
161
with associated reactive airway disease in children. Pediatrics 1984;73:526-9. 29. Wald ER. Epidemiology. pathophysiology and etiology of sinusitis. Pediatr Infect Dis 1985;4:S51-4. 30. Wald ER. Diagnostic considerations. The diagnosis and management of sinusitis in children: proceedings of a closed conference. Pediatr Infect Dis 1985;4:S61-4. 31. Draf W. Endoscopy of the paranasal sinuses. New York: Springer-Verlag. Inc. 1983.
DISCUSSION
Dr. Kennedy: In your experience, Dr. Reilly, is sore throat a common presenting complaint of children with sinusitis? Dr. Reilly: No. Although adults as well as children may perceive that bad-tasting purulent secretions from the sinuses originate in the throat, description of this symptom as "sore throat" is not common. Dr. Kennedy: Might not the adenotonsillar hypertrophy and chronic inflammation often seen in the throat be secondary to mucopurulent discharge from the sinuses? . Dr. Reilly: That is a strong possibility, but it has not been proved. There is a high incidence of sinusitis in children who undergo adenotonsillectomy for recurrent infection of the tonsils and adenoids. Adults may have recurrent localized symptoms of tonsillitis, generally without manifestations of acute disease, but there has been little investigation for concomitant sinus disease in these patients. Dr. Kennedy: We now have photographic documentation of purulent secretions from the ostiomeatal complex, which emanate from the infundibulum and pass posteriorly around the eustachian tube and down into the oropharynx. Perhaps we have been underestimating the involvement of sinus disease in adenotonsillar problems because of our previous reliance on plain radiographs, which could only reveal disease in the maxillary and frontal sinuses clearly. Now we are returning to a more careful clinical evaluation of the ostiomeatal complex as the underlying source. Dr. Druce: Do abnormalities of the ostiomeatal complex specifically relate to sinusitis, or is it likely that many people without symptoms or suspicion of sinusitis would show such abnormalitites on endoscopic or CT examination? Dr. Kennedy: In the United States it is estimated that 30% of the asymptomatic population have evidence of mucosal thickening somewhere in the sinuses. I However, unless the thickening is severe enough to obstruct a sinus os, this may not lead to symptoms. Nevertheless. a very minor degree of obstruction, particularly of an internal os of the frontal sinus, can cause excruciating pain. A jet pilot with sinus barotrauma. for example,
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162 REILLY
will tell you his headache is the worst he has ever had. As for other sinus abnormalities, it appears that concha bullosa occurs in about 15% of the normal population and in 30% of our patients with chronic sinusitis who undergo CT evaluation. Dr. Zlnrelch: In 230 patients with known chronic inflammatory sinus disease, we found anatomic variations or abnormalities in 143 (62%). In another group of patients with no symptoms or history of chronic inflammation, we found anatomic variations or abnormalities in only 11%. Dr. Kennedy: In patients referred to us for chronic sinusitis, we see many who have a septal reconstruction as a first procedure for relieving a complaint of nasal obstruction. Often the initial straightening of the crooked septum was of no benefit, and the procedure was repeated. Only subsequently does the ethmoid sinusitis become more evident, as does the realization that the patient's complaint of nasal obstruction was
related not so much to air flow through the nose as to sinus congestion. Dr. Druce, does this square with your experience? Dr. Druce: Yes. Many patients who come to us follow that scenario. The important questions for the physician who evaluates septal deflection are: Is the septal deflection predisposing the patient to ostial blockage? Is allergic mucosal disease present, and if so, are the patient's symptoms related more to allergy than to septal deflection? I know of no useful guidelines for answering these questions; every situation is different, requiring careful clinical evaluation for sinus involvement and/or allergic reaction. REFERENCE I. Havas TE. Motbey IA. Gullane Pl. Prevalence of incidental at: normalities on computed tomographic scans of the paranasal SInuses. Arch Otolaryngol 1988;114:856-9.
Downloaded from oto.sagepub.com at University of Sussex Library on June 4, 2016
Recent dllcoverlel make It necenary to reevaluate many of the traditional assumptlonl concerning Iinulltil. Within the palt 10 years, Inveltlgatorl have detailed the pathophYllology of Iinulltil. Occlullon of theilnul ostia Inltlatel thellnulltll cycle; untreated, thll leadl to chronic Iinulltil. Anatomic abnormalltlel allo predllpole the patient to chronic Iinulltli because of oltlal blockage. Inveltlgators have Identified and detailed the prevalence of both aerobIc and anaerobic envlronmentl within the Iinulel, demonstratingthat ostial blockage creates an Ideal culture medium within the sinul. KeepIng the ostial panageways open Is essential to allow reversal of the Iinusltis cycle, elpeclally In the prelence of predllposlng factors. (OTOlARYNGOL HEAD NECK SURG 1990;103:856.)
Only within the past 10 years has sinus disease been studied in a truly scientific fashion. Before the application of radiologic examination by computed tomography (CT), minimal information was available to the clinician, and this severely limited understanding of sinus disease as well as sinus anatomy. Often, clinicians recognized only advanced disease, manifested either by complications spread outside the sinuses or by changes sufficient to substantiate alterations on plain radiographs. So, while clinicians were practicing cost containment by ordering plain x-ray films only when indicated by persistence of symptoms, researchers were showing that this traditional radiographic method of imaging the paranasal sinuses lacked the precision needed to document sinusitis reliably, both in children and adults. 1,2 As a result, clinicians have tended to underdiagnose sinusitis. Perhaps this is the reason medical myths have developed about recurrent acute and chronic sinusitis. The most common myths about sinusitis are: • Chronic sinusitis is always allergic in origin. • Chronic and recurrent acute sinusitis are incurable. With technologic advance, investigators are challenging these and many other suppositions concerning sinusitis. Anatomlo Development CT imaging provides today's clinicians with highquality, three-dimensional images of the structures of the ethmoid sinus, the most common source of sinus disease. This technique shows clearly that predisposing
23/0/24793
anatomic factors work in concert with microflora in the development of sinusitis. Furthermore, the technique has provided information about anatomic development between infancy and adolescence that can singularly affect the diagnosis, as well as the treatment, of sinusitis in both children and adults. Only the ethmoid and maxillary sinuses are present at birth (Fig. 1). During infancy, tremendous growth of midface and skull dramatically increases the size of the paranasal sinuses. The ethmoid sinuses are fully developed-adult size-by approximately age 14 years (Fig. 2); the maxillary sinuses grow slowly and reach full size with the appearance of all of the maxillary teeth, sometime during adolescence (Fig. 3),304 The ethmoid sinuses, the most important in terms of chronic sinus disease. consist of 3 to 18 small. air-filled cavities divided by a thin, bony lamina. and drain through the ostia into the middle and superior meatus. Ostia within the maxillary sinus open into the hiatus semilunaris, high on the sinus cavity's medial wall. As a result, drainage from the maxillary sinus is difficult• and stasis and infection of secretions are common. The maxillary and ethmoid sinuses are the more common sites of clinical infection during childhood. The sphenoid sinus develops sometime after age 2 years. and the frontal sinuses begin to develop from the ethmoid air cells into the frontal bone by around age 6 years. Both the frontal and the sphenoid sinuses may frequently become infected in pansinusitis. Infections specific to these two sinuses become clinically important between 8 and 18 years of age.
Pathophysiology of Sinusitis Normal ciliary function. intact mucous membranes. and normal mucous production are integral to sinus
I"
Downloaded from oto.sagepub.com at University of Sussex Library on June 4, 2016
~~~e 103
Number 5 Part 2 '""""mber199Q
Sinusitis cycle
IS7
Fig. 1. RUdimentary ethmoid and maxillary sinusesin an infant. (Illustrator. Figs. 1-3: Paul Singh-Roy.) FIg. 2. Ten-year-old child wlth developed and clinically im portant sinuses.
clearance. Occlusion of the sinus ostia seems to initiate acute sinusitis which, if untreated or inadequately tt:eated, can singularly produce chronic sinusitis. PosSIble causes of sinus ostial obstruction include local ~Ucosal swelling, local insult, and mechanical obstruction. In a study of 23 patients with acute rhinitis by Drettner and Lindholrn," two thirds exhibited unmistakable obstruction of the ostia. This blockage of the ostia initiates a cycle of events leading to sinusitis (Fig . 4). To break this cycle, it is essential to reopen and drain the ostia and the ostiomeatal complex. Functional obstruction of the ostia reduces oxygen tension within the maxillary sinus and also appears to be associated with the size and the patency of the maxillary sinus ostia ." The resultant hypoxic environment in the maxillary sinus, or the ethmoid or frontal sinuses, can lead to a change from a predominantly aerobic flora Or bacteria to an anaerobic flora, partly as a result of the development of an acid pool of secretions that affects metabolic activity and bacterial multiplication . Sable et al. 7 studied 16 children with acute frontal sinusitis and associated complications and found that II children had either anaerobes or aerobes, or both, in the sinus secretions. In addition, the local protective function of the cilia , the sinus mucosa, and the bactericidal function of the
granulocytes become impaired. Resolution of acute sinus infection is greatly hindered by mucosal damage, which further constricts and occludes the ostia . This vicious cycle correlates well with radiographic evidence of chronic sinusitis. Su et al. K have shown that anaerobic bacterial counts increase in the sinus secretions and, furthermore, in the sinus mucosa with chronic sinusitis, and that even bacteria directly invade the sinus wall. Recent studies demonstrate clearly that chronic sinusiti s is generally associated with an anatomic derangement, particularly of the ostiomeatal complex, the focal point for both ethmoid and maxillary sinus disease . The size of the infundibulum and the position of both the ostia and the overlying middle turbinate specifically inhibit or stop the outflow of mucus. Predisposing factors identified by CT scan include deformed uncinate processes, the concha bullosa , agger nasi cells, Haller's cells , and reverse scroll concha." These derangements are of primary importance in chronic sinusitis and may be factors in recurrent or lingering acute sinusitis. Adenoid hypertrophy and adenoiditis probably play an important adjunctive role in chronic sinusitis in children. 10
Downloaded from oto.sagepub.com at University of Sussex Library on June 4, 2016
"I
OlolaryngologVHead and Neck Surgery
REILLY
Fig. 3. Flfteen-yeer-old adolescent has poranasol sinuses thot are 90% adult size.
Pr•••nc. of Bact.rla In Slnu••• For many years . medical tradit ion held that normal. healthy paranasal sinuses of both adults and children were sterile . Onl y with in the past two decades has this assumption been proved false . II In 1975. Evans et al . " established the bacteriology of maxillary sinusitis in adults. and in 1981. Brook l l showed that all sinuses contain some anaerobic organism s and that more than a third of the sinuses harbor a mixed environment of ana erobic and aerobic organism s . Similarly. Su et al. " found a mixture of aerobes and anaerobes growing in diseased sinuses . suggesting that normal bacterial flora can proliferate as a result of osti al occlusion without inoculation by external pathogenic bacteria. Th e relative prevalence of aerobic ver sus anaerobic
organi sms in sinusitis has been a subject of some controversy. Early studies stress the predominance of aerobes in chronic sinusitis . J 4 ,1 ~ As late as 1975. Evans et al ." found that only 12% of organisms cultured from sinus secretions were anaerobes. However. the majority of Evans et al. 's subjects had acute or subacute sinus disease. Indeed, only four patients had chronic sinus disease in that study. In contrast, Frederick and Braude" earlier found that anaerobic organisms were present in 52% of the chronic sinus infections studied. This finding has been greatly reinforced by a recent study of 66 chronic sinu sitis cases in which 88 % were colonized by anaerobic organisms. 17 Aerobes present in both normal and d isea se states include the gram-positive streptococci (a, 13. and Streptococcus pneumoniaei and Staphylococcus aureus, and
Downloaded from oto.sagepub.com at University of Sussex Library on June 4, 2016
VOlume103 Number 5 Part 2 November 1990
Sinusitis cycle 819
?
Secretions thicken; pH changes. ~ Mucosal gas metabolism changes.
Secretions stagnate.
I
\
Cilia and epithelium are damaged.
Mucosal congestion or anatomic obstruction blocks air flow and drainage.
\
Change in host milieu creates culture medium for bacterial g,owth covity
7_0
Ostium Isclosed.
Mucosal thickening creates further blockage. ~
. "
Bacterial Infection develops In the sinus cavity,
Retained secretions cause tlssJe Inflammation.
Fig. 4. The sinusitis cycle (otter Draf").
gram-negative Moraxella (formerly Branhamella) catarrhalis. Haemophilus irfiuenzae, and Escherichia Coli. Anaerobic organisms include the gram-positive peptococci and Propionibacterium species. The Bacteroides species and Fusobacterium species also playa significant role in chronic sinusitis. Wald et a1. 1X•19 discovered the most common aerobic organisms in children to be S. pneumoniae. H. influenzae (nontypable), and M. catarrhalis. In a study of 30 children with acute and subacute sinusitis, Wald er al. IX found only aerobic organisms, with a predominance of S. pneumoniae and H. infiuenzae. In cases of chronic maxillary sinusitis, however, Brook!' showed that anaerobes were more common than aerobes. The anaerobes found include Streptococcus. Bacteroides, and Veil/onella species. In another study of the complications of sinusitis in children, Brook et al. 20 demonstrated the occurrence of anaerobic organisms in all eight children studied, with only one aerobic organism cultured. Brook'? also reported that 44% of the Bacteroides species from within the paranasal sinus were producers of f3-lactamase enzyme, which has implications for
the treatment of sinusitis (as well as the treatment of other infections of the head and neck, including adenoiditis, tonsillitis, and otitis media). High 13lactamase producers include Bacteroides species, especially B. fragilis. But other f3-lactamase producers include Fusobacterium, H. inftuenzae, and M. catarrhalis. Both Wald et al, 1M and Brook" found that f3-lactamase-producing bacteria were present in 25% of the aspirates in children with subacute maxillary sinusitis. Predllpollng Factors With bacteria already clearly present in the sinuses, ciliary dysfunction and retention of secretions set the stage for sinus infection. Obstructive sinus ostia isolate bacterial pathogens in a gas- and fluid-filled milieu that favors their rapid growth, and acute sinusitis naturally results. Any of a wide variety of factors may initiate the process. Systemic factors. The systemic diseases and syndromes that predispose adult patients to acute sinusitis include cystic fibrosis, immune deficiency, bronchiectasis, and immotile cilia syndrome. 22.23
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In cystic fibrosis, sinusitis is considered a corollary of the disease. Thick and tenacious nasal mucus tends to clog the sinus ostia, setting the stage for bacterial infection in the closed cavities. Immunodeficiency is well documented as a predisposing factor to sinus infection. 24.2~ Because of the high incidence of sinusitis in patients with hypogammaglobulinemia, it can be inferred that normal levels of immunoglobulins protect against sinusitis. The immotile cilia syndrome-of which Kartagener's syndrome is a variation-involves hereditary ciliary dysfunction that obviously predisposes to closed ostia and sinusitis." Patients with Down syndrome are also considered prone to sinus disease, as are those with the clinical triad of nasal polyposis, aspirin intolerance, and asthma. 26 Local factora. URI, as well as allergic rhinitis, are the most significant local factors that predispose patients to sinusitis. Additional local factors include overuse of topical decongestants, hypertrophied adenoids, deviated nasal septum, nasal polyps that generally occur in advanced disease, tumors or foreign bodies, barotrauma (from flying, swimming, or diving), cigarette smoke or other forms of pollution, as well as abnormalities from adjacent dental structures or from dental procedures. Viral infections-specifically URIs-commonly precede bacterial sinusitis. The congestion and ciliary dysfunction caused by the viral infection close the ostia, particularly those of the maxillary sinuses, which are not mere openings but tubular channels approximately 6 mm long. Closure of any sinus ostium creates an ideal culture medium, not only for the flora already in the area, but for bacteria that may arrive in the closed sinus cavities from blood and from lymphatic channels. Bacteria may also enter the maxillary sinuses from dental abscesses or from postextraction complications. In these cases, facilitating ciliary movement and drainage plays a key role in the resolution of sinusitis. That allergies predispose to sinus disease is no longer under serious question. Firm data have not yet shown a direct causal relationship between allergy and sinusitis, but several recent studies strongly suggest one. For example, Slavin et al." demonstrated hyperemia and increased metabolic activity in the paranasal sinuses after exposure to ragweed pollen. The association of asthma and sinusitis, though not established by firm data, is now generally accepted by clinical observation. Patients with asthma and sinusitis have demonstrated improvement in their asthmatic symptoms after their sinusitis has been recognized and effectively treated. 28 By the time an allergy-associated condition becomes full-blown sinusitis, purulent secretions and congestion
often outweigh sneezing, itching, and other allergic symptoms. The immediate problem has become infection, which necessitates antibiotics and decongestants and does not indicate antihistamines. The anticholinergic drying action of antihistamines can lead to further mucous inspissation. Pedlatrlo Venus Adult Sinusitis
Sinusitis is a concomitant of upper respiratory and other head and neck infections that account for an estimated 33% to 50% of all patients seen by primary care physicians. Most adults have two to three URis per year and children have six to eight, with 0.5% to 5% demonstrating a distinct clinical presentation of sinusitis." The higher prevalence of URI and associated sinusitis in children may result from their immature immune systems and smaller nasal passages, which predispose to infections. Theoretically, children are more prone to URI and sinusitis because of their close interactions in group settings, such as daycare centers. The common clinical presentation of sinusitis in children includes symptoms of upper respiratory tract infection lasting more than 10 days, low-grade fever, and irritability; nasal drainage and daytime cough may worsen at night. The patient may experience a change in the consistency, taste, or smell of nasal secretions, which can be purulent, mucoid, cloudy, thick, or thin. Some children report facial pressure or pain, particularly if aggravated by changes of position, such as bending the head down. Headache occurs in children only after the age of 5 years, in most cases. WaidJO has also noted dental pain in children, which may result from either dental infection or referred pain from irritation of the nerve to the sinuses. Severe symptoms that occur in both adults and children include high fever, > 39° C (103.2° F), extensive purulent nasal drainage, and periorbital edema. CONCWSION
With improved understanding of the pathophysiology of sinusitis, we have established the following principles to guide clinical management. I. Occlusion of the sinus ostia initiates the sinusitis . cycle, which, if untreated, leads to chronic sinusitis. 2. Ostial blockage creates an ideal culture medium within the sinus. 3. Keeping the ostial passages open is essential to allow resolution of sinusitis. REFERENCES I. Lusk RP, Lazar RH, Muntz HR. The diagnosis and treatment of recurrent and chronic sinusitis in children. Pediatr Clin North Am 1989;36:1411-21.
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2. Kennedy OW. Zinreich SJ. Rosenbaum AE, Johns ME. Functional endoscopic sinus surgery. Theory and diagnostic evaluation. Arch Otolaryngol 1985;111:576-82. 3. Lang J. Clinical anatomy of the nose, nasal cavity. and paranasal sinuses. Translated by P.M. Snell. Stuttgart/New York:Thieme, 1989:56-98. 4. Hawkins DB. Advances in sinus disease in pediatrics. Otolaryngol Clin North Am 1989;22:553-68. 5. Drettner B. Lindholm C-E. The borderline between acute rhinitis and sinusitis. Acta Otolaryngol 1967;64:508-13. 6. Aust R. Drettner B. Oxygenation in the human maxillary sinus under normal and pathological conditions. Acta Otolaryngol 1974;78:264-9. 7. Sable NS. Hengerer A. Powell KR. Acute frontal sinusitis with intracranial complications. Pediatr Infect Dis 1984;3:58-61. 8. Su W-Y. Liu C. Hung SoY. Tsai WF. Bacterological study in chronic maxillary sinusitis. Laryngoscope 1983;93:931-4. 9. Starnmberger H. WolfG. Headaches and sinus disease: the endoscopic approach. Ann Otol Rhinol Laryngol 1988;97(suppl 134):1-23. 10. Fujita A. Takahasi H. Honjo I. Etiological role of adenoids upon otitis media with effusion. Acta Otolaryngol 1988;454 (suPpl):210-3. II. Brook I: Aerobic and anaerobic bacterial flora of normal maxillary sinuses. Laryngoscope 1981;91:372-6. 12. Evans FO Jr. Sydnor JB. Moore WECo et al. Sinusitis of the maxillary antrum. N Engl J Med 1975;293:735-9. 13. Brook I. Bacteriologic features of chronic sinusitis in children. JAMA 1981;246:967-9. 14. Catlin Fl. Cluff LE. Reynolds RC. The bacteriology of acute and chronic sinusitis. South Med J 1965;58:1497-1502. 15. Paiva T. Gronroos JA. Paiva A. Bacteriology and pathology of chronic maxillary sinusitis. Acta Otolaryngol 1962;54: 159-75. 16. Frederick J. Braude AI. Anaerobic infection of the paranasal sinuses. N Engl J Med 1974;290:135-7. 17. Brook I. Bacteriology of chronic maxillary sinusitis in adults. Ann Otol Rhinol Larvngol 1989;98:426-8. 18. Wald ER. Byers C. Guerra N, Casselbrant M. Beste D. Subacute sinusitis in children. J Pediatr 1989;115:28-32. 19. WaldER. Milmoe Gl, Bowen A'D. Ledesma-Medina J. Salamon N. Bluestone CD. Acute maxillary sinusitis in children. N Engl J Med 1981;304:749-54. 20. Brook I. Friedman EM. Rodriguez WJ. Controni G. Complications of sinusitis in children. Pediatrics 1980;66:568-72. 21. Brook I. Beta-Iactamase-producing bacteria in head and neck infection. Laryngoscope 1988;98:428-31. 22. Slavin RG. Sinusitis in adults. J Allergy Clin Immunol 1988;81:1028-32. 23. Slavin RG. Medical therapy of sinusitis and nasal polyps. Presented at the American Academy of Allergy and Immunology (Postgraduate Course), Baltimore. Md., March 28. 1990. 24. Stiehm ER. Immunodeficiency disorders: General considerations. In: Stiehm ER. Gulginiti VA. eds. Immunologic disorders in infants and children. Philadelphia: WB Saunders, 1980:183219. 25. Oxelius V, Laurell A. Lindquist B, et al. 19O subclasses in selective IgA deficiency. N Engl J Med 1981;304:1476-7. 26. Minor MW. Lockey RF. Sinusitis and asthma. South Med J 1987;80:1141-7. 27. Slavin RG, Zilliox AP. Samuels LD. Is there such an entity as allergic sinusitis? [Abstract]. J Allergy Clin Immunol 1988; 81:284. 28. Rachelefsky GS. Katz RM. Siegel SC. Chronic sinus disease
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with associated reactive airway disease in children. Pediatrics 1984;73:526-9. 29. Wald ER. Epidemiology. pathophysiology and etiology of sinusitis. Pediatr Infect Dis 1985;4:S51-4. 30. Wald ER. Diagnostic considerations. The diagnosis and management of sinusitis in children: proceedings of a closed conference. Pediatr Infect Dis 1985;4:S61-4. 31. Draf W. Endoscopy of the paranasal sinuses. New York: Springer-Verlag. Inc. 1983.
DISCUSSION
Dr. Kennedy: In your experience, Dr. Reilly, is sore throat a common presenting complaint of children with sinusitis? Dr. Reilly: No. Although adults as well as children may perceive that bad-tasting purulent secretions from the sinuses originate in the throat, description of this symptom as "sore throat" is not common. Dr. Kennedy: Might not the adenotonsillar hypertrophy and chronic inflammation often seen in the throat be secondary to mucopurulent discharge from the sinuses? . Dr. Reilly: That is a strong possibility, but it has not been proved. There is a high incidence of sinusitis in children who undergo adenotonsillectomy for recurrent infection of the tonsils and adenoids. Adults may have recurrent localized symptoms of tonsillitis, generally without manifestations of acute disease, but there has been little investigation for concomitant sinus disease in these patients. Dr. Kennedy: We now have photographic documentation of purulent secretions from the ostiomeatal complex, which emanate from the infundibulum and pass posteriorly around the eustachian tube and down into the oropharynx. Perhaps we have been underestimating the involvement of sinus disease in adenotonsillar problems because of our previous reliance on plain radiographs, which could only reveal disease in the maxillary and frontal sinuses clearly. Now we are returning to a more careful clinical evaluation of the ostiomeatal complex as the underlying source. Dr. Druce: Do abnormalities of the ostiomeatal complex specifically relate to sinusitis, or is it likely that many people without symptoms or suspicion of sinusitis would show such abnormalitites on endoscopic or CT examination? Dr. Kennedy: In the United States it is estimated that 30% of the asymptomatic population have evidence of mucosal thickening somewhere in the sinuses. I However, unless the thickening is severe enough to obstruct a sinus os, this may not lead to symptoms. Nevertheless. a very minor degree of obstruction, particularly of an internal os of the frontal sinus, can cause excruciating pain. A jet pilot with sinus barotrauma. for example,
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will tell you his headache is the worst he has ever had. As for other sinus abnormalities, it appears that concha bullosa occurs in about 15% of the normal population and in 30% of our patients with chronic sinusitis who undergo CT evaluation. Dr. Zlnrelch: In 230 patients with known chronic inflammatory sinus disease, we found anatomic variations or abnormalities in 143 (62%). In another group of patients with no symptoms or history of chronic inflammation, we found anatomic variations or abnormalities in only 11%. Dr. Kennedy: In patients referred to us for chronic sinusitis, we see many who have a septal reconstruction as a first procedure for relieving a complaint of nasal obstruction. Often the initial straightening of the crooked septum was of no benefit, and the procedure was repeated. Only subsequently does the ethmoid sinusitis become more evident, as does the realization that the patient's complaint of nasal obstruction was
related not so much to air flow through the nose as to sinus congestion. Dr. Druce, does this square with your experience? Dr. Druce: Yes. Many patients who come to us follow that scenario. The important questions for the physician who evaluates septal deflection are: Is the septal deflection predisposing the patient to ostial blockage? Is allergic mucosal disease present, and if so, are the patient's symptoms related more to allergy than to septal deflection? I know of no useful guidelines for answering these questions; every situation is different, requiring careful clinical evaluation for sinus involvement and/or allergic reaction. REFERENCE I. Havas TE. Motbey IA. Gullane Pl. Prevalence of incidental at: normalities on computed tomographic scans of the paranasal SInuses. Arch Otolaryngol 1988;114:856-9.
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