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28 Frontal Sinusitis
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allergens are dened, immunotherapy is com­menced early. As the frontal sinus is secondarily involved, a simple Draf IIa surgical opening will sufce for most. Access for topical therapies is less of an important concept, and inhalant aller­gen immunotherapy is pursued [28].
Primary Diuse Type 2 Dominant: Allergic Fungal Rhinosinusitis (AFRS)
As previously described, the nature of this hyper­sensitivity disorder is mucosal dysfunction, oedema and expansile changes in the sinus cavity which often results in the involvement of the adjacent functional unit. Thus, AFRS may be considered diffuse in nature. Management goals include the complete removal of fungal elements and to establish mucus clearance either by restor­ing mucociliary clearance or by allowing clear­ance by nasal irrigation. A Draf III frontal sinus opening is almost always required unless the frontal recess has been very widely expanded by the disease already. Removal of fungal debris and delivery of topical corticosteroid therapies require a very large opening.
Primary Diuse Non-type 2 Dominant: Non-eosinophilic Chronic Rhinosinusitis (Non-eCRS)
The nature of this condition is inammatory but non-type 2. Non-eCRS patients tend to be older and do not respond well to corticosteroids [29,
30]. The presence or lack of polyps in this dened
group does not separate these patients from those of the eCRS group, which is the basis for endotype- based classication and why the subse­quent management strategy is important.
The goal of management is to reduce inam­mation. Medical management relies on treating the bacterial colonisation and the anti­inammatory effects of a macrolide (anti IL8) rather than heavy use of corticosteroids [30]. Clinically, non-eCRS is not hypersecretory with thick mucin. Although crusting forms, mucus plugs are uncommon. The principals of surgery are to provide access for nasal irrigations to overcome the secondary mucostasis, provide access to topical antibacterial agents and relieve obstruction. Thus, surgery in the form of a Draf
IIa is usually all that is required for ventilation, drainage and the application of topical irrigation.
Frontal Sinus intheSetting ofSecondary CRS
Here the sinonasal disease is secondary to another disease process. Anatomical distribution is again characterised into localised and diffuse groups.
Secondary CRS: Localised
When the frontal sinus is secondarily involved because of another localised inammatory pro­cess, the management is usually limited to the management of the inammatory process.
Fungal Ball
Fungal ball is a good example of a localised for­eign body reaction in the form of fungal debris which accumulates in the sinus and causes an inammatory reaction. Management requires the removal of the entire fungal ball and refashioning of the involved sinus whose function will often return. Accordingly, surgical intervention is lim­ited to either simply treating the maxillary dis­ease and/or a Draf type 1 and OMC procedure. An excellent outline of fungal ball management may be found in EPOS2020 [1].
Odontogenic Sinusitis
Dental infections/periapical abscess of tooth may result in purulent secretions within the sinus cav­ity causing odontogenic sinusitis. Whilst this is commonly within the maxillary sinus, changes may extend to the frontal sinus. This often resolves following endodontic work/tooth extrac­tion, but surgical intervention is limited to either simply treating the maxillary disease and/or a Draf type 1 and OMC procedure.
Tumours
When tumours are present within the sinonasal cavity, there is often a signicant amount of oedema and sinus dysfunction as a secondary component. This dysfunction often self-resolves following tumour removal. Typically, if the tumour is in the ethmoid and maxilla but poste-
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rior to the anterior ethmoid artery, the frontal sinus and its pathway are spared, and a Draf I procedure is all that is required.
If the tumour is in the anterior ethmoid or anterior to the anterior ethmoid artery, then a Draf IIa, b or c is the minimum required to ensure that the frontal sinus and drainage pathways are patent and functioning. If the tumour is in the frontal sinus, then a Draf III is almost always required with or without an external approach. Frontal sinus tumours however are no longer within the secondary CRS category, and this is well addressed elsewhere in this book.
Secondary CRS: Diuse
The nature of secondary diffuse disorders is a failure of the body’s defence mechanisms to ght and control mucosal disease. These are broadly separated into three causative groups: mechani­cal, inammatory (auto immune) and immunity (immunodeciency).
Mechanical Cause
Conditions such as primary ciliary dyskinesia and cystic brosis demonstrate a mechanical dysfunction of mucociliary clearance. Mucostasis and resultant bacterial colonisation ensue. Management aims are based on creating a cavity that allows for mechanical washout; how­ever, a Draf III is often not useful due to the fron­tal hypoplasia which is common in these groups.
Inammatory Cause
Granulomatosis with polyangiitis (GPA) and eosin­ophilic granulomatosis with polyangiitis (EGPA) are the most common examples of secondary dif­fuse inammatory disease. These autoimmune con­ditions result in a destructive change in the sinus cavity, but this is a broader autoimmune condition involving multiple body systems and which should be managed as such. Frontal sinus surgery rarely plays a role in managing these patients.
Immunity/Immunodeciency
These disorders include selective IgA deciency, combined variable immune deciency and poorly controlled diabetes. Careful management of the underlying immunodeciency is integral to the
care of these patients. Persistent frontal disease, despite maximal correction of underlying immu­nodeciency, should be managed as per the guidelines of primary localised CRS.
Perioperative Care inFrontal Sinusitis
Conscientious perioperative care is integral in the success of frontal sinusitis surgery due to the risk of scarring and stenosis.
Draf I procedures are dressed intraoperatively with nger cot dressing or resorbable packing such as hyaluronic acid gel. They are discharged home on the day of surgery and followed up at 3weeks and 3months post-surgery.
As the authors’ approach to any Draf II is via Carolyn’s windows approach, all dressings and follow-up are identical. At the end of the proce­dure, the lateral wall ap is replaced, and any exposed bone is covered by inferior turbinate free grafts. Glove nger spacers and hyaluronic acid gel are placed to secure the aps. Patients are dis­charged the day of surgery and followed up 1week, 3weeks and 3months.
Draf III procedures are completed by replac­ing the lateral nasal wall mucosal grafts, with or without the septal extension and covering any exposed bone with free mucosal grafts [11]. The grafts and surgical opening are covered by a
0.5 mm silastic sheet (Medtronic, Jacksonville, FL) cut accordingly to allow for contouring to the surgical shape [11]. The silastic is supported by absorbable dressing (Nasopore, Polyganics Groningen, the Netherlands). Patients go home the day of surgery and are followed up in 3weeks and 3months post-operatively.
Effective delivery of topical therapy to the frontal sinus is an essential component in the post-surgical management of the frontal sinus. Nasal irrigations allow for lavage of mucus and debris and the delivery of topical pharmacothera­pies to the mucosa. All patients commence irriga­tions the day following the procedure. Draf III frontal sinusotomies allow signicantly greater access and ow rate of topical pharmacotherapy compared to Draf IIb followed by Draf IIa, and
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this difference should be considered when mak­ing surgical decisions [31].
Key Learning Points
• Frontal sinusitis is a broad concept due to its many varied aetiologies of CRS.
• Frontal sinusitis is classied by the EPOS2020 which gives guidance to the underlying dis­ease process.
• Acute frontal sinusitis is most often viral in aetiology, but in unilateral disease, then bacte­rial frontal sinusitis is likely, and antibiotic use should be culture driven.
• In CRS, frontal sinus surgery techniques achieve an anatomical modication, from sur­gery, to aid a management plan.
• Surgical techniques, such as the removal of the ager nasi, front maxilla process (‘Carolyn’s window’) overcome the narrow anteroposte­rior distance and aid in frontal recess surgery.
• Mucosal aps and grafts should be applied where possible to cover exposed bone as heal­ing is greatly improved.
References
1. Fokkens WJ, Lund VJ, Hopkins C, Hellings PW, Kern R, Reitsma S, et al. European position paper on rhinosinusitis and nasal polyps 2020. Rhinology. 2020;58(Suppl S29):1–464.
2. Gwaltney JM Jr. Acute community-acquired sinusitis. Clin Infect Dis. 1996;23(6):1209–23; quiz 24–5.
3. Hoffmans R, Wagemakers A, van Drunen C, Hellings P, Fokkens W. Acute and chronic rhino­sinusitis and allergic rhinitis in relation to comor­bidity, ethnicity and environment. PLoS One. 2018;13(2):e0192330.
4. Revai K, Dobbs LA, Nair S, Patel JA, Grady JJ, Chonmaitree T. Incidence of acute otitis media and sinusitis complicating upper respiratory tract infection: the effect of age. Pediatrics. 2007;119(6):e1408–12.
5. Grayson JW, Hopkins C, Mori E, Senior B, Harvey RJ. Contemporary classication of chronic rhinosi­nusitis beyond polyps vs no polyps: a review. JAMA Otolaryngol Head Neck Surg. 2020;146(9):831–8.
6. Stevens WW, Peters AT, Tan BK, Klingler AI, Poposki JA, Hulse KE, etal. Associations between inammatory Endotypes and clinical presentations in chronic rhinosinusitis. J Allergy Clin Immunol Pract. 2019;7(8):2812–20.e3.
7. Wormald PJ, Hoseman W, Callejas C, Weber RK, Kennedy DW, Citardi MJ, etal. The international fron­tal sinus anatomy classication (IFAC) and classica­tion of the extent of endoscopic frontal sinus surgery (EFSS). Int Forum Allergy Rhinol. 2016;6(7):677–96.
8. Dalgorf DM, Harvey RJ. Chapter 1: Sinonasal anatomy and function. Am J Rhinol Allergy. 2013;27(Suppl 1):S3–6.
9. Weber R, Draf W, Kratzsch B, Hosemann W, Schaefer SD. Modern concepts of frontal sinus surgery. Laryngoscope. 2001;111(1):137–46.
10. Conger BT Jr, Riley K, Woodworth BA. The Draf III mucosal grafting technique: a prospective study. Otolaryngol Head Neck Surg. 2012;146(4):664–8.
11. Knisely A, Barham HP, Harvey RJ, Sacks R. Outside-in frontal drill-out: how I do it. Am J Rhinol Allergy. 2015;29(5):397–400.
12. Seiberling K, Jardeleza C, Wormald PJ.Minitrephination of the frontal sinus: indications and uses in today’s era of sinus surgery. Am J Rhinol Allergy. 2009;23(2):229–31.
13. Hadley JA, Mösges R, Desrosiers M, Haverstock D, van Veenhuyzen D, Herman-Gnjidic Z.Moxioxacin ve-day therapy versus placebo in acute bacterial rhi­nosinusitis. Laryngoscope. 2010;120(5):1057–62.
14. Anon JB, Jacobs MR, Poole MD, Ambrose PG, Benninger MS, Hadley JA, et al. Antimicrobial treatment guidelines for acute bacterial rhinosi­nusitis. Otolaryngol Head Neck Surg. 2004;130(1 Suppl):1–45.
15. Dubin MG, Ebert CS, Coffey CS, Melroy CT, Sonnenburg RE, Senior BA.Concordance of middle meatal swab and maxillary sinus aspirate in acute and chronic sinusitis: a meta-analysis. Am J Rhinol. 2005;19(5):462–70.
16. DelGaudio JM, Evans SH, Sobol SE, Parikh SL.Intracranial complications of sinusitis: what is the role of endoscopic sinus surgery in the acute setting. Am J Otolaryngol. 2010;31(1):25–8.
17. Bakhshaee M, Fereidouni M, Nourollahian M, Movahed R. The presence of fungal-specic IgE in serum and sinonasal tissue among patients with sinonasal polyposis. Eur Arch Otorhinolaryngol. 2014;271(11):2871–5.
18. Loftus PA, Wise SK. Allergic fungal rhinosinus­itis: the latest in diagnosis and management. Adv Otorhinolaryngol. 2016;79:13–20.
19. Reilly JS.The sinusitis cycle. Otolaryngol Head Neck Surg. 1990;103(5(Pt 2)):856–61; discussion 61–2.
20. Barham HP, Osborn JL, Snidvongs K, Mrad N, Sacks R, Harvey RJ.Remodeling changes of the upper air­way with chronic rhinosinusitis. Int Forum Allergy Rhinol. 2015;5(7):565–72.
21. Grayson JW, Li W, Ho J, Alvarado R, Rimmer J, Sewell WA, etal. Topography of polyp recurrence in eosinophilic chronic rhinosinusitis. Int Forum Allergy Rhinol. 2020;10(5):604–9.
22. Harvey RJ, Snidvongs K, Kalish LH, Oakley GM, Sacks R. Corticosteroid nasal irrigations are more effective than simple sprays in a randomized double-
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blinded placebo-controlled trial for chronic rhinosi­nusitis after sinus surgery. Int Forum Allergy Rhinol. 2018;8(4):461–70.
23. Fokkens WJ, Lund V, Bachert C, Mullol J, Bjermer L, Bousquet J, et al. EUFOREA consensus on bio­logics for CRSwNP with or without asthma. Allergy. 2019;74(12):2312–9.
24. Ho J, Earls P, Harvey RJ. Systemic biomarkers of eosinophilic chronic rhinosinusitis. Curr Opin Allergy Clin Immunol. 2020;20(1):23–9.
25. Ho J, Li W, Grayson JW, Alvarado R, Rimmer J, Sewell WA, etal. Systemic medication requirement in post-surgical patients with eosinophilic chronic rhino­sinusitis. Rhinology. 2021;59(1):59–65.
26. Grayson JW, Cavada M, Harvey RJ. Clinically relevant phenotypes in chronic rhinosinusitis. J Otolaryngol Head Neck Surg. 2019;48(1):23.
27. Scadding GK, Lund VJ.Investigative rhinology. 1st ed. London: Taylor & Francis; 2004.
28. DelGaudio JM, Loftus PA, Hamizan AW, Harvey RJ, Wise SK.Central compartment atopic disease. Am J Rhinol Allergy. 2017;31(4):228–34.
29. Turner JH, Chandra RK, Li P, Bonnet K, Schlundt DG. Identication of clinically relevant chronic rhinosinusitis endotypes using cluster analy­sis of mucus cytokines. J Allergy Clin Immunol. 2018;141(5):1895–7.e7.
30. Oakley GM, Christensen JM, Sacks R, Earls P, Harvey RJ. Characteristics of macrolide responders in persistent post-surgical rhinosinusitis. Rhinology. 2018;56(2):111–7.
31. Barham HP, Hall CA, Hernandez SC, Zylicz HE, Stevenson MM, Zito BA, etal. Impact of Draf III, Draf IIb, and Draf IIa frontal sinus surgery on nasal irrigation distribution. Int Forum Allergy Rhinol. 2020;10(1):49–52.
Complications ofRhinosinusitis
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Introduction
In the era of antibiotics and endoscopic sinus sur­gery, complications of rhinosinusitis—acute or chronic—are relatively rare. Introduction of widely available, cost-effective computed tomog­raphy scanning with intravenous contrast admin­istration has resulted in their earlier diagnosis and management. However, complications do still occur and, in some cases, can prove life­threatening. Hence, the clinician must have a high index of suspicion and be familiar with the appropriate diagnostic algorithm, as well as the principles of their management.
Epidemiology, Microbiology andPathophysiology
Epidemiology: In almost all large epidemiologi­cal studies, orbital complications appear twice as often as intracranial ones and males are signi­cantly more frequently affected than females [1]. ARS was more often the precipitating factor in children, whereas CRS with or without nasal pol­yposis was more important in adults [2]. There is a clear seasonal pattern in their incidence, mirroring URTIs [3]. The recent restrictions associated with measures to deal with the COVID-19 pandemic have resulted in reduced incidence of URTIs—
V. Chatzinakis Endoscopic Skull Base Center, Hygeia Hospital, Athens, Greece
C. Georgalas (*) Endoscopic Skull Base Center, Hygeia Hospital, Athens, Greece
Medical School, Nicosia University, Nicosia, Cyprus
Athens, Greece
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. C. Swift et al. (eds.), Contemporary Rhinology: Science and Practice,
https://doi.org/10.1007/978-3-031-28690-2_29
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however, there are no studies showing a corre­sponding decrease in acute sinusitis cases or their complications [4]. Although orbital complications tend to occur primarily in young children, intracra­nial complications can occur at any age, albeit with a predilection for the second and third decade of life.
Microbiology: Pathogens involved seem to differ between children and adults. Predominant pathogens in children are Streptococcus pneu-
moniae, Haemophilus inuenza, Moraxella catarrhalis and Staphylococcus aureus [5]. In adults, anaerobic, odontogenic and polymicro-
bial infections predominate and have a more severe presentation. Pathogens most commonly involved in the pathogenesis of adult intracranial complications are Streptococcus and Staphylococcus species and anaerobes.
Pathophysiology: Two main mechanisms are involved: direct extension and haematogenous or lymphatic spread. This is more of theoretical rather than practical value, since there is no clini­cal way of distinguishing between the two mech­anisms, and it does not affect management.
Orbital complications are usually the result of direct extension, from the ethmoids to the orbit. The lamina papyracea is the thinnest bone in the body and “cribriform” in structure: multiple minor veins and arteries enter the orbit via lam­ina papyracea. Cavernous sinus thrombosis, nowadays classied as an endocranial rather than orbital complication [6], is considered a result of retrograde thrombophlebitis via the diploic veins.
Other authors suggest a classication based in etiology: suppurative versus systematic or “unusual.” For this chapter, we chose a more descriptive classication that takes into consider­ation both the underlying cause and the anatomi­cal area affected.
Complications ofAcute Rhinosinusitis
Orbital Complications
The most widely used classication of orbital complications/infections was created by Chandler and included ve domains: preseptal cellulitis, orbital cellulitis, subperiosteal abscess, orbital abscess and cavernous sinus thrombosis. Today, “preseptal cellulitis” is considered more of an eyelid than an orbital infection, as the brous orbital septum is the anterior limit of the orbital contents [8].
Most orbital complications typically present with chemosis, proptosis, tenderness and restric­tion of eye movements (Fig.29.1). However, a subperiosteal abscess (located outside of the extraocular muscles) may cause ophthalmoplegia and impaired visual acuity. An intraconal abscess is likely to form as a result of diagnostic delay. Cavernous sinus thrombosis is a “standalone”
Classication Systems
Several different ways of classifying complica­tions of rhinosinusitis have been proposed. The most widely accepted classication is an anatom­ical one, dividing them into orbital (60–75%), intracranial (15–20%) and osseous (5–10%) [7].
Fig. 29.1 A child with chemosis and proptosis due to orbital abscess of the right eye. Tenderness and eye move­ment restriction were also present
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a
Fig. 29.2 Computed tomography of a subperiosteal abscess of the left eye (a). Patient with severe proptosis and oedema (b)
b
intracranial complication, rather than the end stage of orbital infection [9].
CT has been found to have slightly higher predictive accuracy than clinical assessment and is an important diagnostic tool (Fig.29.2) [10]. In small children with subperiosteal abscesses, there have been a number of studies showing good outcomes with intravenous anti­biotics alone, but surgical treatment should never be postponed if vision is affected or response to iv antibiotics is poor after 24 h [11, 12].
Intracranial Complications
Sinus disease is the underlying cause of almost 10% of all intracranial suppuration. Complications include epidural or subdural abscesses, brain abscess, meningitis, cerebritis and superior sagittal and cavernous sinus throm­bosis, either alone or in combination (Fig. 29.3). Most patients present with high fever, severe headache, nausea and vomiting, neck stiffness and altered mental state. Subtle behavioural changes often occur.
Fig. 29.3 Contrast-enhanced axial CT of a young child suffering from cavernous sinus thrombosis. Note the bilat­eral at non-fat density lling defect at the cavernous sinuses
Patients with cavernous sinus thrombosis may also display bilateral ptosis, exophthalmos, retro­orbital headache and papilloedema. The diagno­sis is conrmed by a “ow void” that is typically demonstrated by a magnetic resonance venogram (MRV). However, an MRI with contrast may demonstrate an enhanced organized thrombus at
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an early stage in the disease. Contrast enhanced CT-although not the best option-may also be sug­gestive of the condition.
Osseous Complications
Osteomyelitis of (mainly) the frontal bone may present clinically with forehead oedema, giving the impression of a soft tissue mass (Pott’s puffy
Fig. 29.4 Pott’s puffy tumor, secondary to frontal sinus­itis. Note the mild oedema over the left frontal sinus and the underlying area of osteomyelitis (asterisk). Endoscopic drainage was carried out
tumor) (Fig. 29.4). The infection may dissemi­nate via direct extension or haematogenous spread to cause meningitis or epidural or brain abscess. Drainage of pus by trephination or endo­scopic drainage should not be postponed.
Complications ofChronic Rhinosinusitis
Complications ofChronic Rhinosinusitis withNasal Polyps
CRSwNP can cause complications in two ways: either via direct erosion of the orbital wall and skull base or via sinus obstruction and subse­quent mucocele formation. They can also be categorized in anatomic terms: orbital and intra­cranial complications.
Erosion of the lamina papyracea and anterior skull base can occur with longstanding extensive polypoid disease where CT of the sinuses shows a complete white-out of the sinuses and nasal cavities (Fig.29.5). Subsequent infections of the lacrimal apparatus have been documented, as well as erosion of the medial orbital wall leading to orbital cellulitis. Involvement of the skull base and lamina papyracea has been described in up to 50% of cases with allergic fungal rhinosinusitis
a
Fig. 29.5 Nasal polyps and multiple mucoceles eroding/remodeling the lamina papyracea of the left orbit. After com­plete removal of the pathology, the bone appears almost fully restored. (a) Pre-op, (b) post-op
b
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Fig. 29.6 Compressive optic neuropathy due to sphenoiditis
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a
Fig. 29.7 (a) Mucocele of the frontal sinus, eroding the roof of the right orbit. (b) Note mild exophthalmos preopera- tively and upper eyelid oedema. (c) Post-op. (d) Result of Draf III procedure
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b
c
Fig. 29.7 (continued)
d
[13]. Compressive noninfective optic neuropathy with visual loss can also occur (Fig.29.6). Nasal polyps usually expand insidiously, remodeling the lamina papyracea or the skull base, without invading the periorbita or the dura. Outow obstruction, leading to mucocele formation (Fig.29.7), can also be considered a CRSwNP­associated complication (up to 0.6%). The fron­toethmoid region was the most commonly affected area in a series of 82 patients, and patients with aspirin-exacerbated respiratory dis­ease (AERD) were at higher risk [14]. Previous surgery and aspirin sensitivity seem to be risk factors.
Complications ofChronic Rhinosinusitis Without Nasal Polyps
Most complications secondary to CRSsNP are often associated with worsening infection— similar to the complications of ARS—and can involve the eye, brain and lungs. What differs however is the microbiology of these complications.
Chronic inammatory changes near the orbit can lead to enophthalmos via silent sinus syn­drome, epiphora due to obstruction of nasolacri­mal duct, proptosis and optic neuropathy as a result of involvement of the orbit and optic nerve accordingly (Fig.29.8). Fungal or bacterial inva­sion along the skull base can lead to intracranial complications.