Добавил:
kiopkiopkiop18@yandex.ru t.me/Prokururor I Вовсе не секретарь, но почту проверяю Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз: Предмет: Файл:

Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4446_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
30.08.2026
Размер:
49 Мб
Скачать
22 Allergic and Non-allergic Rhinitis
251
41. Auge J, Vent J, Agache I, Airaksinen L, Campo Mozo P, Chaker A, etal. EAACI position paper on the stan­dardization of nasal allergen challenges. Allergy. 2018;73(8):1597–608.
42. Gosepath J, Amedee RG, Mann WJ.Nasal provoca­tion testing as an international standard for evaluation of allergic and nonallergic rhinitis. Laryngoscope. 2005;115(3):512–6.
43. San Nicolo M, Braun T, Eder K, Berghaus A, Groger M. Clinical relevance of IgE to prolin and/or pol­calcin in pollen-sensitized patients. Int Arch Allergy Immunol. 2016;169(2):101–7.
44. Ha EK, Na MS, Lee S, Baek H, Lee SJ, Sheen YH, et al. Prevalence and clinical characteris­tics of local allergic rhinitis in children sensitized to house dust mites. Int Arch Allergy Immunol. 2017;174(3–4):183–9.
45. Al Ahmad M, Arifhodzic N, Nurkic J, Jusufovic E, Hanoun AL, Rodriguez T.Role of nasal challenge and local eosinophilia in indirect exposure to cat in aller­gic rhinitis patients. Eur Ann Allergy Clin Immunol. 2018;50(3):125–31.
46. Al-Ahmad M, Jusufovic E, Arifhodzic N, Nurkic J, Hanoun AL. Sensitization to cat: when is nasal challenge needed? Int Arch Allergy Immunol. 2019;179(2):108–13.
47. Blanca-Lopez N, Campo P, Salas M, Garcia Rodriguez C, Palomares F, Blanca M, etal. Seasonal local allergic rhinitis in areas with high concentrations of grass pollen. J Investig Allergol Clin Immunol. 2016;26(2):83–91.
48. Krajewska-Wojtys A, Jarzab J, Gawlik R, Bozek A. Local allergic rhinitis to pollens is underdi­agnosed in young patients. Am J Rhinol Allergy. 2016;30(6):198–201.
49. Hamizan AW, Rimmer J, Alvarado R, Sewell WA, Kalish L, Sacks R, etal. Positive allergen reaction in allergic and nonallergic rhinitis: a systematic review. Int Forum Allergy Rhinol. 2017;7(9):868–77.
50. Comite P, Minale P, Ferrero F, Mussap M, Ciprandi G. Der p 1 IgE measurement for distinguishing between sensitization and allergy. Immunol Lett. 2015;166(2):145–6.
51. Demoly P, Passalacqua G, Pfaar O, Sastre J, Wahn U. Management of the polyallergic patient with allergy immunotherapy: a practice-based approach. Allergy Asthma Clin Immunol. 2016;12:2.
52. Klimek L, Hammerbacher AS, Hellings PW, Fokkens WJ, Hoffmann HJ, Muraro A, et al. The inuence of European legislation on the use of diagnostic test allergens for nasal allergen provocation in routine care of patients with allergic rhinitis. Rhinology. 2015;53(3):260–9.
53. Matricardi PM, Dramburg S, Potapova E, Skevaki C, Renz H. Molecular diagnosis for aller­gen immunotherapy. J Allergy Clin Immunol. 2019;143(3):831–43.
54. Canonica GW, Ansotegui IJ, Pawankar R, Schmid­Grendelmeier P, van Hage M, Baena-Cagnani CE, et al. A WAO-ARIA-GA(2)LEN consensus docu-
ment on molecular-based allergy diagnostics. World Allergy Organ J. 2013;6(1):17.
55. Matricardi PM, Kleine-Tebbe J, Hoffmann HJ, Valenta R, Hilger C, Hofmaier S, et al. EAACI molecular allergology user’s guide. Pediatr Allergy Immunol. 2016;27(Suppl 23):1–250.
56. Stringari G, Tripodi S, Caffarelli C, Dondi A, Asero R, Di Rienzo Businco A, etal. The effect of component­resolved diagnosis on specic immunotherapy pre­scription in children with hay fever. J Allergy Clin Immunol. 2014;134(1):75–81.
57. Moreno C, Justicia JL, Quiralte J, Moreno-Ancillo A, Iglesias-Cadarso A, Torrecillas M, et al. Olive, grass or both? Molecular diagnosis for the allergen immunotherapy selection in polysensitized pollinic patients. Allergy. 2014;69(10):1357–63.
58. Hatzler L, Panetta V, Lau S, Wagner P, Bergmann RL, Illi S, etal. Molecular spreading and predictive value of preclinical IgE response to Phleum pratense in children with hay fever. J Allergy Clin Immunol. 2012;130(4):894–901.
59. Posa D, Perna S, Resch Y, Lupinek C, Panetta V, Hofmaier S, etal. Evolution and predictive value of IgE responses toward a comprehensive panel of house dust mite allergens during the rst 2 decades of life. J Allergy Clin Immunol. 2017;139(2):541–9.
60. Knol EF.Requirements for effective IgE cross- linking on mast cells and basophils. Mol Nutr Food Res. 2006;50(7):620–4.
61. Gomez E, Campo P, Rondon C, Barrionuevo E, Blanca-Lopez N, Torres MJ, et al. Role of the baso­phil activation test in the diagnosis of local allergic rhinitis. J Allergy Clin Immunol. 2013;132(4):975–6. e1–5.
62. WHO position paper. Allergen immunotherapy: therapeutic vaccines for allergic diseases. Arerugi. 1998;47(7):698–704.
63. Bousquet J, Pfaar O, Togias A, Schunemann HJ, Ansotegui I, Papadopoulos NG, et al. ARIA Care pathways for allergen immunotherapy. Allergy. 2019;74(11):2087–102.
64. Calderon MA, Cox L, Casale TB, Moingeon P, Demoly P. Multiple-allergen and single-allergen immunotherapy strategies in polysensitized patients: looking at the published evidence. J Allergy Clin Immunol. 2012;129(4):929–34.
65. Bachert C, van Cauwenberge P, Olbrecht J, van Schoor J.Prevalence, classication and perception of allergic and non-allergic rhinitis in Belgium. Allergy. 2006;61(6):693–8.
66. Corriveau MN, Claus B. Allergic and nonaller­gic rhinitis. In: Kennedy DW, Hwang PH, editors. Rhinology: diseases of nose, sinuses, and skull base. New York: Thieme Medical Publishers, Inc.; 2012. p.82–91.
67. Fokkens W, Saleh H, Georgalas C.Nonallergic rhi­nitis: denition, classication, and management. In: Georgalas C, Fokkens W, editors. Rhinology and skull base surgery. NewYork: Thieme Medical Publishers, Inc.; 2013. p.229–45.
252
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
M. Al-Ahmad et al.
68. Fokkens WJ. Thoughts on the pathophysiology of non-allergic rhinitis. Curr Allergy Asthma Rep. 2002;2(3):203–9.
69. Van Rijswijk JB, Blom HM, Fokkens WJ. Idiopathic rhinitis, the ongoing quest. Allergy. 2005;60(12):1471–81.
70. Blom HM, Godthelp T, Fokkens WJ, KleinJan A, Mulder PG, Rijntjes E. The effect of nasal steroid aqueous spray on nasal complaint scores and cellular inltrates in the nasal mucosa of patients with non­allergic, noninfectious perennial rhinitis. J Allergy Clin Immunol. 1997;100(6 Pt 1):739–47.
71. Dolovich J, Kennedy L, Vickerson F, Kazim F.Control of the hypersecretion of vasomotor rhinitis by topi­cal ipratropium bromide. J Allergy Clin Immunol. 1987;80(3 Pt 1):274–8.
72. Van Rijswijk JB, Boeke EL, Keizer JM, Mulder PG, Blom HM, Fokkens WJ.Intranasal capsaicin reduces nasal hyperreactivity in idiopathic rhinitis: a double­blind randomized application regimen study. Allergy. 2003;58(8):754–61.
73. Graf P. Rhinitis medicamentosa: a review of causes and treatment. Treat Respir Med. 2005;4(1):21–9.
74. Slavin RG. Occupational rhinitis. Ann Allergy Asthma Immunol. 1999;83(6 Pt 2):597–601.
75. Ellegård EK, Karlsson NG, Ellegård LH.Rhinitis in the menstrual cycle, pregnancy, and some endocrine disorders. Clin Allergy Immunol. 2007;19:305–21.
76. Jacobs RL, Freedman PM, Boswell RN.Non-allergic rhinitis with eosinophilia (NARES syndrome): clini­cal and immunologic presentation. J Allergy Clin Immunol. 1981;67(4):253–62.
77. Rondon C, Fernandez J, Canto G, Blanca M. Local allergic rhinitis: concept, clinical manifestations, and diagnostic approach. J Investig Allergol Clin Immunol. 2010;20(5):364–71.
78. Moneret-Vautrin DA, Hsieh V, Wayoff M, Guyot JL, Mouton C, Maria Y.Nonallergic rhinitis with eosino­philia syndrome a precursor of the triad: nasal polypo­sis, intrinsic asthma, and intolerance to aspirin. Ann Allergy. 1990;64(6):513–8.
79. Malmberg H, Grahne B, Holopainen E, Binder E.Ipratropium (Atrovent) in the treatment of vasomo­tor rhinitis of elderly patients. Clin Otolaryngol Allied Sci. 1983;8(4):273–6.
80. Sapci T, Yazici S, Evcimik MF, et al. Investigation of the effects of intranasal botulinum toxin type A and ipratropium bromidenasal spray on nasal hyper­secretion in idiopathic rhinitis without eosinophilia. Rhinology. 2008;46(1):45–51.
81. Robinson SR, Wormald PJ. Endoscopic vidian neu­rectomy. Am J Rhinol. 2006;20(2):197–202.
82. Georgalas C, Jovancevic L. Gustory rhinitis. Curr Opin Otolaryngol Head Neck Surg. 2012;20(1):9–14.
AL GRAWANY
Acute Sinusitis andIts Complications
MatthewKim, AaronPearlman, AshutoshKacker, andMichaelG.Stewart
23
Key Points
• AVRS accounts for most cases of ARS.
• AVRS and AR can predispose for devel­opment of ABRS.
• Diagnosis of ARS (including AVRS and ABRS) is primarily clinical.
• Initial management of ARS consists of supportive therapy.
• Antibiotics should be considered after 7 days of symptoms or double-worsening.
• Further evaluation, including imaging, should be considered in patients with treatment failure or suspected complications.
• Management of orbital complications usually entails parenteral antibiotics and multidisciplinary evaluation, with sur­gery typically reserved for Chandler grades III-V.
• Management of intracranial complica­tions entails parenteral antibiotics, sur­gery, and multidisciplinary evaluation.
M. Kim · A. Pearlman · A. Kacker · M. G. Stewart (*) Department of Otolaryngology—Head and Neck Surgery, Weill Cornell Medical College and NewYork-Presbyterian Hospital, New York, NY, USA e-mail: mk3183@cumc.columbia.edu;
anp2022@med.cornell.edu; ask9001@med.cornell.edu; mgs2002@med.cornell.edu
• Episodes of RARS are managed simi­larly to ABRS, with surgery reserved for patients with frequent infections.
• Immunologic testing and imaging (to evaluate for anatomic factors and rule out CRS) may be helpful in RARS.
23.1 Introduction
Rhinosinusitis is one of the most commonly diagnosed and treated disease entities within oto­rhinolaryngology. Contemporary understanding of rhinosinusitis as more than simply an anatomic or infectious pathologic process has led to a more sophisticated nosology in the realm of rhinosi­nusitis, including distinctions based on chronic­ity and etiology, with even more specic classications based on pathophysiologic mecha­nisms now coming to fruition. While this para­digm shift is best evidenced by current concepts surrounding the diagnosis and management of chronic rhinosinusitis, there has been a similar evolution in philosophy with regard to diagnosis of acute rhinosinusitis and the role and timing of antibiotic therapy. This chapter reviews the eval­uation and treatment of acute viral rhinosinusitis, acute bacterial rhinosinusitis, and recurrent acute rhinosinusitis. Orbital and intracranial compli­cates of acute bacterial rhinosinusitis and their management are also reviewed.
© Springer Nature Switzerland AG 2021 A. Al-Qahtani et al. (eds.), Textbook of Clinical Otolaryngology,
https://doi.org/10.1007/978-3-030-54088-3_23
253
254
M. Kim et al.
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
23.1.1 Classication
• Acute rhinosinusitis (ARS) refers to inam­mation of the nasal cavity and paranasal sinuses lasting up to 4weeks. The term “rhi­nosinusitis” is preferred over sinusitis because there is almost always a component of rhinitis with sinusitis
– 4–12weeks: subacute rhinosinusitis – >12weeks: chronic rhinosinusitis (CRS)
• Acute bacterial rhinosinusitis (ABRS) refers to secondary bacterial infection of the parana­sal sinuses
• Acute invasive fungal sinusitis refers to a life­threatening, fulminant fungal infection seen in immunocompromised individuals (see chapter on fungal sinusitis)
23.1.2 Epidemiology
• One of the most common health complaints prompting medical evaluation and antibiotic prescription
– Global prevalence 6–15%
• Associated with signicant healthcare expen­ditures and decreased productivity
• Majority of cases occur in association with viral upper respiratory tract infection
– Allergic rhinitis is also common predispos-
ing factor.
• Other risk factors include:
– Age (<15 or >45years) – Smoking history – Anatomic variants (deviated nasal septum,
concha bullosa, nasal polyposis)
– Nasal foreign bodies (including nasal can-
nula, nasogastric tube)
23.1.3 Pathophysiology
• Most frequently caused by viral infection
– Symptom onset within 24h of infection – Most common pathogens: rhinovirus >
inuenza>parainuenza >adenovirus
Table 23.1 Causes of ARS (descending frequency)
Acute rhinosinusitis Viral Rhinovirus Inuenza Parainuenza Adenovirus Bacterial Streptococcus pneumoniae Haemophilus inuenzae Moraxella catarrhalis Staphylococcus aureus Fungal Aspergillus spp. Zygomycetes (Rhizopus, Rhizomucor, Mucor,
Absidia)
• Progression to ABRS in 0.5–2% – Mucosal edema mucociliary clear-
ance  mucus stasis  bacterial superinfection
– Most common pathogens: Streptococcus
pneumoniae > Haemophilus inuenzae > Moraxella catarrhalis > Staphylococ- cus aureus (Table23.1)
23.1.4 Clinical Presentation
• Acute viral rhinosinusitis (AVRS) and ABRS
present with similar symptoms
• Nasal symptoms – Congestion/obstruction – Purulent rhinorrhea/postnasal drip – Facial pain/pressure – Decreased olfaction
• Extranasal symptoms – Fever – Fatigue – Cough – Ear pressure/fullness – Throat pain – Dental pain – Halitosis – Headache
• Features suggestive of ABRS – Lack of improvement after 7–10days – “Double sickening or worsening” (worsen-
ing after a period of improvement)
AL GRAWANY
23 Acute Sinusitis andIts Complications
255
23.1.5 Diagnostic Evaluation
• Exam ndings – Facial exam: edema/erythema, tenderness – Anterior rhinoscopy: mucosal edema, tur-
binate hypertrophy, copious clear or puru­lent rhinorrhea
– Oral exam: postnasal drainage, pharyngeal
erythema
• Nasal endoscopy helpful in certain cases – Severe symptoms – Unilateral disease – Failure to respond to treatment – Suspected mass – Recent surgery – Immunocompromised patient – Suspected complicated infection
• Diagnosis based primarily on history and
exam
– Routine imaging NOT indicated – Imaging indicated under special
circumstances
Suspected orbital or intracranial complication Suspected recurrent acute rhinosinusitis
– Comparison of imaging modalities
Ultrasonography: not recommended Plain lm radiography (X-ray): histori­cally used, not recommended Computed tomography (CT): excellent bony resolution, radiation exposure Magnetic resonance imaging (MRI): excellent soft tissue resolution, no radia­tion exposure, sensitive for intracranial and orbital infection
• Cultures – Not required for diagnosis, but can have
treatment implications
– Middle meatal cultures correlate well with
maxillary sinus aspiration
– Nasal or nasopharyngeal swab cultures not
clinically useful
23.1.6 Treatment
• Symptomatic relief – Indicated for both AVRS and ABRS
– Systemic agents: analgesics/antipyretics,
decongestants, mucolytics
– Topical agents (sprays): steroids, saline,
decongestants (limit use to 3–5days)
• Antimicrobial therapy for ABRS – Watchful waiting appropriate up to 7days
after diagnosis
– Antibiotics typically started for clinical
worsening or persistent symptoms after 7days
– First-line antibiotic choice is amoxicillin or
amoxicillin/clavulanate
Alternatives in Penicillin-allergic patients: third-generation cephalospo­rin ± clindamycin, doxycycline, uoroquinolone
• Macrolides and trimethoprim­sulfamethoxazole no longer recom­mended for initial therapy due to increasing prevalence of resistance
– Duration of treatment 5–10days – Risk of antibiotic therapy
Allergic reactions GI upset Development of bacterial resistance
• Treatment failure: worsening or failure to improve after 7days of initial treatment
– Consider alternate diagnoses
Facial pain and headache syndromes Rhinitis Nasal airway obstruction
– Evaluate for possible complications of
ABRS (see below) – Middle meatal cultures – Change antibiotic
High-dose amoxicillin/clavulanate Respiratory uoroquinolone
– Failure of multiple antibiotic courses
Imaging to evaluate for anatomic abnor­mality or complicated ABRS
Middle meatal culture – Relapse after treatment
Mild  longer course of same antibiotic Moderate to severe consider change in antibiotic and/or imaging
• Oral steroids not recommended for routine use – Not helpful as monotherapy
256
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
<10d
Nasal obstruction Purulent rhinorrhea Facial pain/pressure
Exam findings
10d
M. Kim et al.
Immune workup
Imaging
Other medical workup
“Double worsening”
AVRS
“Watchful waiting”
NSAIDs/analgesics
Topical decongestant
Saline irrigation
Oral decongestants
(up to 7d)
Lack of resolution
Shared
decision-
making
5-10d course of ABX
Topical steroids
Treatment failure
Middle meatal culture
Change ABX
imaging
Fig. 23.1 ARS treatment algorithm
– May shorten time to symptom resolution
when used in conjunction with antibiotics
Risk of adverse effects
• Oral antihistamines not recommended for ABRS
– May be helpful in allergic patients for
AVRS – Can lead to nasal dryness – Can cause drowsiness and xerostomia
(Fig.23.1)
23.1.7 Complications
• Suspect in patients with atypical signs and symptoms:
– Persistent high fever – Periorbital edema/erythema, proptosis,
diplopia/extraocular motility impairment, vision changes
– Cranial nerve palsy
ABRS
RARS
Return to baseline
Recurrent infection
Suspected complication
Imaging
Admision and IV ABX
Multidisciplinary consultation
– Headache, meningeal signs – Altered mental signs
• Predisposing factors – Winter months (increased incidence of
AVRS)
– Age
Infant: highest risk of meningitis 3–6 years: highest rate of hospitaliza­tion for complication of ABRS 10–29 years: highest risk of intracranial complication
• Teenage males likely to have simul­taneous orbital and intracranial complications
• Orbital complications – Most common complication of acute
rhinosinusitis
Due to two-way communication between ethmoid and ophthalmic venous plexuses
AL GRAWANY
23 Acute Sinusitis andIts Complications
257
• Valveless ophthalmic veins commu­nicate anteriorly with facial veins and posteriorly with cavernous sinus
Periorbita is the only soft tissue barrier between orbit and sinonasal cavity
• Fuses anteriorly with tarsal plates to form orbital septum
Usually polymicrobial
• Viridans streptococci and staphy­locci are most common organisms
– Chandler classication system of orbital
complications
I: Preseptal orbital cellulitis
• Periorbital edema/erythema
• No chemosis or ocular symptoms
• Can occur in absence of sinusitis
– Infection of eyelid and orbital
adnexa – Trauma – Foreign body
II: Postseptal orbital cellulitis
• Proptosis, chemosis, ophthalmoplegia
• Can have decreased visual acuity later in disease course
III: Orbital subperiosteal abscess
• Symptoms similar to group II
• Usually normal vision unless abscess very large
IV: Orbital abscess
• Symptoms similar to group III
• Usually complete ophthalmoplegia and decrease in vision
V: Cavernous sinus thrombosis
• Symptoms similar to group IV
• Additional involvement of V1 and V2
• Bilateral eye symptoms
• Can have associated meningismus, frank meningitis, or sepsis
– Orbital apex syndrome
• Frontal bone osteomyelitis with subperiosteal Presents similar to cavernous sinus thrombosis with frank optic nerve involvement Trigeminal involvement would be lim­ited to V1 branches
– Superior orbital ssure (Rochon–
Duvigneaud) syndrome
Similar to orbital apex syndrome but spares optic nerve
– Evaluation
Comprehensive ophthalmologic exam Imaging
• CT is the gold standard – IV contrast useful if concern for
abscess or cavernous sinus thrombosis
• MRI is better for cavernous sinus
thrombosis
– Management
Medical therapy—oral agents—is usu­ally sufcient (Chandler I–II) Intravenous antibiotics (Chandler II–V)
• High-dose penicillin/beta-lacta-
mase inhibitor (e.g., ampicillin/sul­bactam) or third-generation cephalosporin
• Adjunct medications: systemic/topi-
cal steroids and decongestants, saline irrigations, mucolytics
Surgery (Chandler IV–V)
• Subperiosteal abscess (III): size
>2cm and age >9 years more likely to require surgical intervention
• Lack of improvement over 48–72h
on medical therapy alone also indica­tion for surgery
• Lateral and superior abscesses likely
require external orbitotomy Anticoagulation for cavernous sinus thrombosis is controversial
• Thought to stop progression of
thrombosis, decrease clot propaga-
tion, and allow better antibiotic
penetration
• Risk includes systemic or intracra-
nial hemorrhage and septic
embolization
abscess (“Pott’s puffy tumor”)
– Suppurative infection of diploic veins – Causes bone demineralization and
necrosis
– Requires medical and surgical therapy
Prolonged IV antibiotics for osteomyelitis
258
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
M. Kim et al.
• Intracranial complications – More common in males and children >7
years
– CRS thought to increase risk due to chronic
mucosal/bony changes that decrease muco­ciliary clearance and hinder antibiotic penetration
Initial symptoms may not be character­istic of ARS
• Persistent headache and fever are typical presenting complaints
– Mechanism: septic thrombophlebitis or
direct bony extension (neurovascular foramina, congenital dehiscence, traumatic fracture)
– Microbiology
Meningitis mostly due to Streptococcus
pneumoniae
Abscess often polymicrobial, including anaerobes
– May be asymptomatic until late in course
due to involvement of non-eloquent frontal lobe
Seizures, focal neurologic decits are late ndings and portend poor progno­sis Can present synchronously and in con­junction with orbital complications
– MRI with contrast is radiographic study of
choice
CT often also obtained for bony anat­omy and surgical planning
– Epidural abscess
Most common intracranial complication Generally associated with frontal sinusitis
• Headache, fever, orbital pain, frontal pain
Favorable prognosis
– Subdural abscess
Also usually a sequela of frontal sinusitis Usually unilateral Tendency to spread over cerebral cortex and into interhemispheric region Higher morbidity and mortality
• Can have rapid progression
– Headaches, fever, letharg→coma
• Meningismus and focal neurologic decits
– Intracerebral abscess
Less common Typically involves frontal and parietal lobes
• Frontal sinusitis>sphenoid/ethmoid sinusitis
Fever, headache, lethargy, vomiting
• Seizures, focal decits are late ndings
Can also have mood swings and
• behavioral changes
Lumbar puncture contraindicated before imaging obtained
• Risk of brain herniation
– Venous sinus thrombosis
Sagittal sinus thrombosis can occur sec­ondary to frontal sinusitis Meningeal signs and signicant neuro­logic complications Often in conjunction with other intra­cranial complications
– Meningitis
Typically secondary to ethmoiditis or sphenoiditis Headache, neck stiffness, fever Can present with sepsis or cranial neuropathy Often in conjunction with other intra­cranial complications
– Management
Broad-spectrum intravenous antibiotics with good intracranial penetration
• Often 4–8week course of antibiotics
Systemic steroids and anticonvulsants Neurosurgical drainage usually indicated Sinus surgery to address culprit sinuses
• Frontal sinus trephination can be useful adjunct to endoscopic techniques
Repeat imaging critical to monitor treat­ment response and prior to discharge to ensure continued resolution without treatment escalation
AL GRAWANY
23 Acute Sinusitis andIts Complications
23.1.8 Recurrent Acute Rhinosinusitis
• Predisposing factors – Viral ARS – Allergic rhinitis – Immunodeciency – Anatomy (e.g., deviated nasal septum, con-
cha bullosa)
• Conrming true ABRS episodes is important – Endoscopy reveals purulence during acute
episode
– Imaging between episodes can conrm
complete resolution and reveal anatomic anomalies
• Management – Immunologic testing
Immunoglobulin deciencies
• Combined variable immunode­ciency (CVID)
• IgA deciency
• Specic antibody deciency
– Role of antibiotics and topical steroids lim-
ited to use during ARS episodes
– Surgery may be benecial in select patients
Appropriateness criteria
4 episodes per year
• ARS conrmed by endoscopy or imaging
• Shared decision-making
• Failed trial of nasal steroid or loss of productivity
Extent of surgery unclear
• Addressing anatomic variants predis­posing to recurrent infection can be helpful
– Balloon sinuplasty may also be benecial
Less evidence than for ESS, for this indication
259
Take Home Messages
• ARS can be characterized by causative pathogen (virus, bacteria, fungus).
• Diagnosis is chiey clinical.
• Treatment depends on etiology and symptom duration.
• Complications of ABRS warrant special attention.
Further Reading
Clayman GL, Adams GL, Paugh DR, Koopmann CF
Jr. Intracranial complications of paranasal sinus­itis: a combined institutional review. Laryngoscope. 1991;101(3):234–9.
Fokkens WJ, Lund VJ, Hopkins C, etal. European posi-
tion paper on rhinosinusitis and nasal polyps 2020. Rhinology. 2020;58(Suppl S29):1–464.
Orlandi RR, Kingdom TT, Hwang PH, etal. International
Consensus Statement on Allergy and Rhinology: Rhinosinusitis. Int Forum Allergy Rhinol. 2016;6(Suppl 1):S22–209.
Peña MT, Preciado D, Orestes M, Choi S.Orbital com-
plications of acute sinusitis: changes in the post­pneumococcal vaccine era. JAMA Otolaryngol Head Neck Surg. 2013;139(3):223–7.
Rosenfeld RM, Andes D, Bhattacharyya N, Cheung
D, Eisenberg S, Ganiats TG, Gelzer A, Hamilos D, Haydon RC III, Hudgins PA, Jones S, Krouse HJ, Lee LH, Mahoney MC, Marple BF, Mitchell CJ, Nathan R, Shiffman RN, Smith TL, Witsell DL.Clinical prac­tice guideline: adult sinusitis. Otolaryngol Head Neck Surg. 2007;137(3 Suppl):S1–31.
Rosenfeld RM, Piccirillo JF, Chandrasekhar SS, et al.
Clinical practice guideline (update): adult sinus­itis. Otolaryngol Head Neck Surg. 2015;152(2 Suppl):S1–S39.
Fungal Sinusitis
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
DanielB.Spielman, ZhongZheng, AbtinTabaee, andMichaelG.Stewart
24
Key Points
• Fungal rhinosinusitis represents a group of distinct clinical entities linked by the presence of pathogenic fungi within the paranasal sinuses that are implicated in the pathophysiology. Given the unique features of each disorder, it is more appropriate to think of the different forms of fungal rhinosinusitis as sepa­rate diseases.
• The following represent the different forms of fungal rhinosinusitis: fungus ball (mycetoma), allergic fungal rhino­sinusitis, acute invasive fungal sinusitis, chronic invasive fungal sinusitis, and granulomatous invasive fungal sinusitis.
• Can be categorized based on different variables:
– Chronicity: Acute (acute invasive
fungal sinusitis) vs chronic (chronic invasive fungal, granulomatous, fun­gus ball, allergic fungal sinusitis)
– Role of fungi: Infection (acute and
chronic invasive fungal sinusitis) vs inammatory trigger (allergic fungal sinusitis, granulomatous, fungus ball)
– Host status: Immunocompetent
(allergic fungal sinusitis, fungus ball, granulomatous) vs immunosup­pressed (acute and chronic invasive fungal sinusitis)
– Presence of tissue invasion: Invasive
(acute and chronic invasive fungal sinusitis) vs noninvasive (allergic fungal sinusitis, granulomatous, fun­gus ball)
• Evaluation includes clinical assessment, imaging, tissue culture and histopathology.
• Multimodality treatment is indicated and differs for the different types of fun­gal rhinosinusitis.
24.1 Introduction
D. B. Spielman · Z. Zheng · A. Tabaee M. G. Stewart (*) Department of Otolaryngology—Head and Neck Surgery, Weill Cornell Medical Center and NewYork­Presbyterian Hospital, New York, NY, USA e-mail: dbs9010@nyp.org; atabaee@med.cornell.edu;
mgs2002@med.cornell.edu
© Springer Nature Switzerland AG 2021 A. Al-Qahtani et al. (eds.), Textbook of Clinical Otolaryngology,
https://doi.org/10.1007/978-3-030-54088-3_24
Fungal pathogens have the potential to cause a wide spectrum of sinonasal disease, affecting both immunocompetent and immunosuppressed patients. Fungal rhinosinusitis represents a group of distinct disease entities ranging from benign noninvasive mycetoma formation to acutely ful-
AL GRAWANY
261