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28 Frontal Sinusitis
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allergens are dened, immunotherapy is commenced early. As the frontal sinus is secondarily
involved, a simple Draf IIa surgical opening will
sufce for most. Access for topical therapies is
less of an important concept, and inhalant allergen immunotherapy is pursued [28].
Primary Diuse 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 Diuse Non-type 2 Dominant:
Non-eosinophilic Chronic Rhinosinusitis
(Non-eCRS)
The nature of this condition is inammatory 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 dened
group does not separate these patients from those
of the eCRS group, which is the basis for
endotype- based classication and why the subsequent management strategy is important.
The goal of management is to reduce inammation. Medical management relies on treating
the bacterial colonisation and the antiinammatory 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 intheSetting
ofSecondary 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 inammatory process, the management is usually limited to the
management of the inammatory 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
inammatory 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 signicant 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: Diuse
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, inammatory (auto immune) and immunity
(immunodeciency).
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.
Inammatory Cause
Granulomatosis with polyangiitis (GPA) and eosinophilic granulomatosis with polyangiitis (EGPA)
are the most common examples of secondary diffuse inammatory 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/Immunodeciency
These disorders include selective IgA deciency,
combined variable immune deciency and poorly
controlled diabetes. Careful management of the
underlying immunodeciency is integral to the
care of these patients. Persistent frontal disease,
despite maximal correction of underlying immunodeciency, should be managed as per the
guidelines of primary localised CRS.
Perioperative Care inFrontal
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
3weeks and 3months 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
1week, 3weeks and 3months.
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 3weeks
and 3months 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 signicantly 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 classied 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 modication, 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
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the effect of age. Pediatrics. 2007;119(6):e1408–12.
5. Grayson JW, Hopkins C, Mori E, Senior B, Harvey
RJ. Contemporary classication of chronic rhinosinusitis beyond polyps vs no polyps: a review. JAMA
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6. Stevens WW, Peters AT, Tan BK, Klingler AI,
Poposki JA, Hulse KE, etal. Associations between
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7. Wormald PJ, Hoseman W, Callejas C, Weber RK,
Kennedy DW, Citardi MJ, etal. The international frontal sinus anatomy classication (IFAC) and classication 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.
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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.Moxioxacin
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-specic 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, etal. 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
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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, etal. 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
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Otolaryngol Head Neck Surg. 2019;48(1):23.
27. Scadding GK, Lund VJ.Investigative rhinology. 1st
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28. DelGaudio JM, Loftus PA, Hamizan AW, Harvey RJ,
Wise SK.Central compartment atopic disease. Am J
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29. Turner JH, Chandra RK, Li P, Bonnet K, Schlundt
DG. Identication of clinically relevant chronic
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2018;141(5):1895–7.e7.
30. Oakley GM, Christensen JM, Sacks R, Earls P,
Harvey RJ. Characteristics of macrolide responders
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31. Barham HP, Hall CA, Hernandez SC, Zylicz HE,
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2020;10(1):49–52.

Complications ofRhinosinusitis
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VasileiosChatzinakis andChristosGeorgalas
29
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
andPathophysiology
Epidemiology: In almost all large epidemiological studies, orbital complications appear twice as
often as intracranial ones and males are signicantly 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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V. Chatzinakis and C. Georgalas
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 inuenza, 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 classied as an endocranial rather
than orbital complication [6], is considered a
result of retrograde thrombophlebitis via the
diploic veins.
Other authors suggest a classication based in
etiology: suppurative versus systematic or
“unusual.” For this chapter, we chose a more
descriptive classication that takes into consideration both the underlying cause and the anatomical area affected.
Complications ofAcute
Rhinosinusitis
Orbital Complications
The most widely used classication 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”
Classication Systems
Several different ways of classifying complications of rhinosinusitis have been proposed. The
most widely accepted classication 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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357
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 conrmed 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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V. Chatzinakis and C. Georgalas
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 ofChronic
Rhinosinusitis
Complications ofChronic
Rhinosinusitis withNasal 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
359
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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V. Chatzinakis and C. Georgalas
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. Outow
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 ofChronic
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 inammatory 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.
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