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C. Hopkins and J.-L. McKenzie
29. Schlosser RJ, Smith TL, Mace J, Soler ZM.Asthma
quality of life and control after sinus surgery
in patients with chronic rhinosinusitis. Allergy.
2017;72(3):483–91.
30. Masterson L, Tanweer F, Bueser T, Leong P.Extensive
endoscopic sinus surgery: does this reduce the revision
rate for nasal polyposis? Eur Arch Otorhinolaryngol.
2010;267(10):1557–61.
31. Morrissey DK, Bassiouni A, Psaltis AJ, Naidoo Y,
Wormald PJ. Outcomes of modied endoscopic
Lothrop in aspirin-exacerbated respiratory disease
with nasal polyposis. Int Forum Allergy Rhinol.
2016;6(8):820–5.
Further Reading
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.
Primary Atrophic Rhinitis
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IsmaZ.Iqbal
26
Introduction
Atrophic rhinitis (AR) was rst described by
Fraenkel in 1876 [1, 2]. The condition is also
known as atrophic rhinosinusitis, rhinitis sicca,
rhinitis fetida and ozaena [1]. It is commonly
found in tropical climates, Mediterranean areas,
Latin and South America and Eastern Europe [3].
The incidence is between 0.3 and 1% in countries
with higher prevalence [4]. There is a predominance in young and middle-aged adults. The condition is commoner in females with a ratio of
5.6:1 [5]. There is also an association with pov-
erty and low social economic status. It is a chronic
condition characterised by thick nasal discharge,
dried crusts with a foul odour and paradoxical
nasal blockage.
Aetiology
AR can be subdivided into primary and
secondary:
Primary atrophic rhinitis (PAR): The aetiology is poorly understood. The commonest theory
for development of PAR is chronic bacterial rhinosinusitis caused by Klebsiella ozaenae.
I. Z. Iqbal (*)
The Newcastle Hospitals NHS Foundation Trust,
Freeman Hospital, Newcastle upon Tyne, UK
e-mail: isma.iqbal1@nhs.net
Secondary atrophic rhinitis (AR) is due to
granulomatous conditions, radiotherapy to the
head and neck, Sjogren’s and previous surgery
(empty nose syndrome).
The symptoms are secondary to progressive
destruction of the ciliary mucosal epithelium due
to atrophy of the exocrine sero-mucous glands
and loss of underlying bone structures [1].
The factors blamed for its genesis are specic
infections, autoimmunity, chronic sinus infection, hormonal imbalance, poor nutritional status,
heredity and iron deciency anaemia [6].
Primary atrophic rhinitis (PAR) has been
reported in families where females are affected
with a positive family history in about 15–30% of
the cases [4]. Some studies have revealed either
an autosomal dominant (67%) or autosomal
recessive penetrance (33%) [7].
Iron and vitamin A deciency have also been
implicated. Oestrogen deciency has also been
suggested which may be consistent with the
female preponderance.
Progressive metaplasia and atrophy of all
mucosal components (epithelium, vessels, and
glands) takes place because of increased osteoclastic activity, resulting in a volumetric decrease
of sinonasal structures [8]. The histopathological
picture consists of patches of squamotransformation of the normal respiratory epithelium which
is pathognomonic for atrophic rhinitis seen in
more than 80% of cases [9].
© 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_26
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I. Z. Iqbal
Whilst most cases have been attributed to
Klebsiella ozaenae, other bacterial agents
involved in the etiopathogenesis of atrophic rhinitis are Pseudomonas aeruginosa, Coccobacillus
foetidus-ozaenae, Diphtheroids bacillus,
Haemophilus inuenzae, Bacillus mucosus or
pertussis, and Proteus species [6].
Diagnosis
Symptoms
Patients typically present with progressively
worsening nasal dryness and congestion, crusting
and reduction in sense of smell with foul smelling nasal crusting. Less common symptoms
include anosmia, headache and epistaxis. The
anosmia is due to the atrophic process involving
the olfactory epithelium as well as insufcient air
reaching the olfactory areas due to crusting.
Nasal obstruction is a combination of loss of
pressure receptors in the nasal epithelium as well
as large crusts blocking the air blast to the olfactory area in the roof of the nose. Epistaxis may
occur as the crusts dislodge.
Blood Investigations
A full blood count may reveal a microcytic hypochromic picture (iron deciency anaemia). A
raised erythrocyte sedimentation rate (ESR) as
well as raised autoimmune markers (ANCA,
angiotensin converting enzyme, rheumatoid factor, anti-Ro, anti-La) are important in ruling out
other diagnoses (granulomatous conditions,
Sjogren’s). The serum protein and plasma vitamin level estimations are necessary to exclude
malnutrition.
Mucociliary Clearance
The mucociliary clearance with saccharin transit
time (STT) demonstrates a prolonged time in
PAR.Bist etal. reported the mean value of nasal
mucociliary clearance in a control group was
9.92 ± 2.25 (mean ± SD) minutes, whereas in
PAR, it was 42.82 ± 11.52 (mean ± SD)
(P<0.0001) [6].
Imaging
Signs
Endoscopic examination reveals a markedly large
and wide nasal cavity, visibly dry mucosa and
reduction in turbinate size [1]. There may be detectable fetor. Greenish yellow and black crusts of various sizes may be noticed lining the nasal cavities
[4]. Palpation of the nasal mucosa may reveal loss
of sensation. Nasal septal perforation and saddle
nose deformity may occur in severe cases [4].
Other rare causes with similar presentation
such as tuberculosis, leprosy, scleroma and syphilis should be excluded. If the disease progresses,
chronic pharyngitis, otitis media with effusion or
nasal deformity can also occur [10].
Because of the high incidence of concurrent
sinusitis, CT is frequently included in the diagnostic evaluation of atrophic rhinitis [6]. The
maxillary sinus is the most affected in PAR.
Pace-Balzan etal. [11] reported the following
CT features in PAR:
1. Mucosal thickening of the paranasal sinuses
2. Loss of denition of the ostiomeatal unit
(OMU) secondary to resorption of the ethmoid bulla and uncinate process
3. Hypoplasia of the maxillary sinuses
4. Enlargement of the nasal cavities with erosion
and bowing of the lateral nasal wall
5. Bony resorption and mucosal atrophy of the
middle and inferior turbinate
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Management
The treatment of atrophic rhinitis aims to reduce
the volume of the nasal cavity, promote normal
mucosa regeneration using a Young’s or modied Young’s operation, lubricate the nasal
mucosa or improve the vascularity of the nasal
cavity.
Treatment is aimed at reducing the impact of
the condition and preventing further deterioration
rather than an intent to cure as this is unlikely to
be possible.
Medical
Topical treatment is aimed at improving nasal
dryness, crusting and overall symptom control.
Several topical treatments have been advocated
which are summarised in Table26.1.
Local or systemic antimicrobial treatment
should be commenced following nasal culture for
bacteria or fungi [12]. Ciprooxacin as well as
rifampicin have been used to good effect.
Frequently, these patients have colonisation of
Klebsiella ozaenae. Commonly rifampicin
600mg daily for 12weeks or ciprooxacin 500–
750mg for 8weeks is utilised [12]. A randomised
controlled trial comparing nasal submucosal
injection of placentrex (human placenta) with
oral rifampicin showed objective, subjective and
histopathological improvement with maximum
disease-free interval on regular follow-up with
rifampicin [13]. Awad etal. [14] found rifampicin
with mitomycin-C in alkaline saline wash has
signicantly better improvement in degree of
crustations, severity of epistaxis and normalization of secretion than rifampicin and saline nasal
rinse alone.
There is one study reporting successful treatment of PAR in a paediatric patient with antibiotic
prophylaxis (trimethoprim–sulfamethoxazole)
and saline irrigations for 6 months with no evidence disease recurrence or new infectious complications at 1year [15].
Placental extracts injections inside the nasal
mucosa may have the effect of narrowing the
nasal fossae and to stimulate vasodilatation, but
Table 26.1 Topical nasal treatment
Treatment Action
Saline douche—alkaline,
hypertonic, isotonic
Glycerine-glucose (25%)
drops
Sodium bicarbonate and
sodium diborate (Equal
combination of the two)
in Sodium chloride
Dexpanthenol (ointment
or spray)
Sesame oil Nasal moisture,
Vitamin A oil
Liquid parafn nose
drops
Oestradiol in arachis oil
(10,000units/mL)
Kemicetine anti-ozaena
solution (90mg of
chloramphenicol,
0.64mg of oestradiol
dipropionate, 900IU of
vitamin D2 and
propylene glycol in each
millilitre)
Topical vitamin E Anti-inammatory,
Removal of crusts,
allergens, inammatory
mediators
Inhibition of bacterial
growth (lactic acid effect
of glucose) stimulates
commensal bacteria
Glycerine antiinammatory, stimulates
cell maturation, stimulates
vasodilation and reduces
crusts
Antiseptic and bactericidal
effect as well as removing
crusts
Reduce transepidermal
water loss, to activate
invivo and invitro
broblast proliferation,
and accelerate the
re-epithelialisation process
improvement in the nasal
ciliary beat frequency
Lubricates nasal mucosa
and removal of crusts.
Long-term use not
recommended due to
reports of parafn
granulomas and
inhalational lipoid
pneumonias
Vasodilator effects of
oestrogen therapy
Antibiotic, vasodilatory
and immunostimulant
antioxidants,
immunostimulants,
stabilizing the cell
membrane and promoting
the skin barrier function
their effects disappear in approximately 8weeks
after the treatment [13].
Dexpanthenol spray, in a saline product, for
patients with atrophic rhinitis was efcient, but
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I. Z. Iqbal
not superior in efcacy compared to placebo
[16]. However, assessment of nasal breathing
resistance and the extent of crust formation did
improve with dexpanthenol.
Topical a-tocopherol acetate (vitamin E) in a
study of 44 patients with PAR showed an
improvement of the nasal dryness sensation and
increased inspiratory nasal ow [17].
Rhinomanometric examination showed increase
of nasal airow at follow-up (P< 0.05); nasal
mucociliary clearance showed a reduction in
mean transit time (P < 0.05); and endoscopic
evaluation showed signicative improvement of
hydration of nasal mucosa and signicative
decreasing nasal crusts and mucous accumulation (P<0.05) [17].
A nasal obturator can reduce nasal dryness
with minimal cosmetic implications. These can
be made from a material called dimethylpolysiloxane or from an acrylic resin [18].
Surgical
Surgery is considered in patients that do not
improve with medical treatment. Decreasing the
nasal cavity size would prevent drying of the
mucosa and crusting. Reducing the size of the
nasal cavity or closure of the nasal cavity also
promotes regeneration of normal tissue by reducing or removing exacerbating factors. Stellate
ganglion injections to block its activity to cause
nasal congestion and secretions have been
reported. However, this technique is not currently
used [4].
Reduction inSize ofNasal Cavity
Young’s procedure as well as implants have been
described. The implants may be autologous
(bone, cartilage, muscle, fat), homologous
(lyophilized bone, fat, human placenta extract)
or synthetic (Teon, acrylics, silicone, silastic).
The major problems of their use are implant
rejection, leakage and chronic infection of the
implant [19].
Young described closure of the nasal cavity
for AR [20]. However, this has an impact on quality of life and the risk of wound breakdown. A
modied Young’s technique was therefore introduced and has demonstrated a complete recovery
in 50% (n=10) patients [21].
In a study of 17 patients with AR whose nostrils
were closed using a septal mucoperichondrial ap,
15 patients were cured of symptoms, but the exact
outcome parameters were not specied [22].
Symptoms resolved in six patients following
implantation of two plastipore plates into the
oor of the nose and septum of both nasal passages in eight patients [19]. One plate extruded,
but symptoms resolved with reimplantation.
Turbinate reconstruction with autologous
costal cartilage implants in patients with PAR
was effective in improving the SNOT-25 score
(108 to 8/125) and CT sinus ndings [8]. SNOT25 is a modication of SNOT-22 and includes
additional empty nose syndrome specic
questions.
Regeneration ofNasal Tissue
An improvement in nasal symptoms, Sino-Nasal
Outcome Test-25 (SNOT-25) scores and endoscopic ndings has been reported following
intranasal injection of platelet-rich plasma (PRP),
but histology remained unchanged [23]. Injection
of PRP in AR led to improvement in Nasal
Obstruction Symptom Evaluation (NOSE), SinoNasal Outcome Test-22 (SNOT-22) scores and
nasal mucociliary function [24] .
Conclusion
PAR is characterised by the formation of thick
dry nasal crusts on a background of paradoxical
nasal obstruction and foetor. It is common in
tropical countries. Treatment is aimed at reducing symptoms and encouraging regeneration of
tissue. Surgical treatment is considered once
medical treatment is unsuccessful. Numerous
surgical procedures have been described to
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325
reduce nasal cavity size, promote regeneration of
normal mucosa and increase lubrication of the
dry nasal mucosa.
Key Learning Points
• Primary atrophic rhinitis (PAR) is a progressive chronic degenerative condition of
unknown aetiology
• PAR is characterized by progressive nasal
mucosal atrophy, wide nasal cavities with paradoxical nasal congestion and formation of
viscid secretions and dried crusts with characteristic foetor
• Treatment of PAR aims to reduce the nasal
cavity size, promote mucosa regeneration
lubricating the nasal mucosa and improve vascularity of the nasal cavity
• Topical treatment to reduce nasal crusting and
nasal drying is rst line of treatment
References
1. Hildenbrand T, Weber RK, Brehmer D.Rhinitis sicca,
dry nose and atrophic rhinitis: a review of the literature. Eur Arch Otorhinolaryngol. 2011;268(1):17–26.
2. Ly TH, deShazo RD, Olivier J, Stringer SP, Daley W,
Stodard CM.Diagnostic criteria for atrophic rhinosinusitis. Am J Med. 2009;122(8):747–53.
3. Lobo C, Hartley C, Farrington W.Closure of the nasal
vestibule in atrophic rhinitis—a new non-surgical
technique. J Laryngol Otol. 1998;112(6):543–6.
4. Dutt SN, Kameswaran M. The aetiology and management of atrophic rhinitis. J Laryngol Otol.
2005;119(11):843–52.
5. Bunnag C, Jareoncharsri P, Tansuriyawong P,
Bhothisuwan W, Chantarakul N. Characteristics of
atrophic rhinitis in Thai patients at the Siriraj hospital.
Rhinology. 1999;37(3):125–30.
6. Bist SS, Bisht M, Purohit JP.Primary atrophic rhinitis: a clinical prole, microbiological and radiological
study. ISRN Otolaryngol. 2012;2012:404075.
7. Amreliwala M, Jain S, Raizada R, Sinha V, Chaturvedi
V. Atrophic rhinitis: an inherited condition. Indian J
Clin Pract. 1993;4:43–6.
8. Park MJ, Jang YJ.Successful management of primary
atrophic rhinitis by turbinate reconstruction using
autologous costal cartilage. Auris Nasus Larynx.
2018;45(3):613–6.
9. Chen H-S. Desquamation and squamotransformation of rhinomucosa as a prodromal sign of atrophic rhinitis. ORL J Otorhinolaryngol Relat Spec.
1984;46(6):327–8.
10. Moore EJ, Kern EB.Atrophic rhinitis: a review of 242
cases. Am J Rhinol. 2001;15(6):355–61.
11. Pace-Balzan A, Shankar L, Hawke M. Computed
tomographic ndings in atrophic rhinitis. J
Otolaryngol. 1991;20(6):428–32.
12. Nielsen B, Olinder-Nielsen A, Malmborg
A.Successful treatment of ozena with ciprooxacin.
Rhinology. 1995;33(2):57–60.
13. Jaswal A, Jana AK, Sikder B, Nandi TK, Sadhukhan
SK, Das A. Novel treatment of atrophic rhinitis: early results. Eur Arch Otorhinolaryngol.
2008;265(10):1211–7.
14. Awad OGA-N, Hasan MM.Topical Mitomycin-C can
help as an adjunct to alkaline nasal wash and rifampicin in primary atrophic rhinitis. Am J Otolaryngol.
2019;40(2):137–42.
15. Magalhães C, Viana M, Alves V, Nakamura R, Duarte
D.Pediatric atrophic rhinosinusitis: what can we do?
Int J Pediatr Otorhinolaryngol. 2015;79(5):763–5.
16. Kehrl W, Sonnemann U. Dexpanthenol nasal spray
as an effective therapeutic principle for treatment
of rhinitis sicca anterior. Laryngorhinootologie.
1998;77(9):506–12.
17. Testa D, Marcuccio G, Lombardo N, Cocuzza SG,
Guerra G, Motta G.Role of α-tocopherol acetate on
nasal respiratory functions: mucociliary clearance and
rhinomanometric evaluations in primary atrophic rhinitis. Ear Nose Throat J. 2021;100(6):NP290–5.
18. Sajjad A.A new technique for nasal stent fabrication
for atrophic rhinitis: a clinical report. J Prosthodont.
2011;20(4):326–8.
19. Goldenberg D, Danino J, Netzer A, Joachims
HZ. Plastipore implants in the surgical treatment of
atrophic rhinitis: technique and results. Otol Head
Neck Surg. 2000;122(6):794–7.
20. Young A.Closure of the nostrils in atrophic rhinitis. J
Laryngol Otol. 1971;85(7):715–8.
21. Poddar SK, Jagade M. Modication of modied
young’s operation in the management of primary atrophic rhinitis. Indian J Otolaryngol Head Neck Surg.
2001;53(3):252–4.
22. El Kholy A, Habib O, Abdel-Monem M.Septal mucoperichondrial ap for closure of nostril in atrophic rhinitis. Rhinology. 1998;36(4):202–3.
23. Mostafa HS, Ayad EE.Platelet-rich plasma (PRP) a
biogenic stimulator in treatment of primary atrophic
rhinitis. Egypt J Otolaryngol. 2020;36(1):1–7.
24. Lee MH, Lee J, Song EA, Kim SW, Kim SW.Plateletrich plasma injection in patients with atrophic
rhinitis. ORL J Otorhinolaryngol Relat Spec.
2021;83(2):104–11.
Fungal Sinus Disease
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Christopherde Souza, AishanPatil, AnishPatil,
andRosemariede Souza
27
Introduction
Fungi are made up of several thousand species of
eukaryotic spore-bearing organisms. More than
60,000 species of fungi are known. Fungi reproduce by both sexual and asexual means. Fungi are
eukaryotic and are usually lamentous; they have
no chlorophyll; cell walls are made of chitin. Two
major groups of organisms make up fungi.
(a) Unicellular fungi are called yeasts.
(b) Filamentous fungi are called moulds
Yeast is unicellular and reproduces by budding; moulds coalesce as colonies of intertwined
hyphae referred to as mycelia.
C. de Souza (*)
Lilavati Hospital, Holy Family Hospital,
Mumbai, India
Department of Otorhinolaryngology, SUNY
Brooklyn, New York, NY, USA
Department of Otorhinolaryngology, LSUHSC,
Shreveport, LA, USA
Mumbai, India
A. Patil
Specialist Registrar, Vascular Surgery, Dundee, UK
A. Patil
Royal Wolverhampton NHS Trust, Wolverhampton,
UK
R. de Souza
BYL Nair Hospital, Mumbai, India
Of the 60,000 fungal species, only about 300
have been documented as playing a denitive
role in causing disease in humans. These fungal
pathogens largely belong to three major groups.
They are (1) Zygomycetes, (2) Aspergillus species and (3) various Dematiaceous genera.
Fungi are ubiquitous organisms and reside primarily in the entire respiratory tract. Microscopic
colonisation by fungi of the nose and paranasal
sinuses can be found in both the normal and in
the diseased states.
Diagnosing Fungal (Mycotic)
Infections
Conrmation and identication of mycotic infection may require a combination of diagnostic
studies (Table 27.1). Fungi are difcult to culture, and growth is often negative. However, PCR
(polymerase chain reaction) of the sinus mucus is
much more likely to detect and identify a pathogenic fungus [1, 2].
© 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_27
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Table 27.1 Diagnostic methods for detecting and identifying fungi
Investigation Comments
Microscopy of
fresh clinical
specimens
Histopathology Tissue samples retrieved from
Culture Fungal cultures take a
Serology
Polymerase chain
reaction tests
Radiological
imaging
Potassium hydroxide (KOH)
preparations or Calcouor
white stains help identify the
presence of fungi
the affected area
Frozen section should be
considered for necrotic material
and tissue biopsies
Evidence of fungal invasion
conrms the presence of
‘invasive fungal rhinosinusitis’
considerable period of time
A positive culture may be
present when invasive fungal
infection is absent
Cultures will identify a specic
fungus and guide antifungal
medication
Mycotic Infection
of progressing to invasive disease, but this is no
longer true. In 2020, signicant numbers of
immunocompetent COVID-19 patients developed serious fungal infection, often caused by
mucormycosis, especially following the use of
high-dose corticosteroids.
How Do Fungi Cause Disease?
To cause an infection, the fungus has to rst
gain access via a portal of entry, attach to cells
and grow within the host. They must be able to
replicate at 37 °C, obtain nutrients and evade
natural defence mechanisms [4]. For dimorphic
fungi, this also means transformation of an initial morphologic conversion to a tissue form of
growth.
The outcome of inhaling fungal spores
depends upon several factors:
• The number and size of inhaled spores
• The integrity of the nonspecic and specic
host defences
• The virulence/pathobiological potential of the
particular fungus
Fungal infections can pose major medical challenges [3]. The incidence of mycotic infection
and the number and diversity of pathogenic fungi
have all increased exponentially in recent times.
Five categories of fungal entities are recognised:
• Saprophytic colonisation
• Fungal balls (mycetomas)
• Allergic fungal rhinosinusitis
• Chronic invasive (granulomatous and nongranulomatous disease)
• Acute invasive
True fungal infection is subdivided into nonin-
vasive and invasive, and manifestations may
overlap or progress from noninvasive to an invasive form. The latter is a particular risk with a
decline in host immunity, and the latter should
always be considered and assessed. Compromise
of the immune system greatly increases the risk
of fungal infection. Immune competent individuals were previously considered as having no risk
Pathogenesis ofInammation from
Fungal Disease
1. Some fungi are capable of colonising epithelial tissues surfaces without causing invasive
manifestations. Fungal rhinosinusitis is often
characterised by colonisation rather than invasion. Colonisation induces profound inammatory and immune responses resulting in
severe damage to the host.
2. Occasionally, fungi cause serious human disease by producing potent toxins and mutagens.
3. Less potent fungal irritants and enzymes also
attack host cells leading to inammation or
immunopathology.
4. Fungal cell wall antigens can also stimulate
an allergic response in the host [5].
The status of the host immunity will ultimately determine whether the individual at risk
will develop non-invasive or invasive fungal rhinosinusitis, and conditions like diabetic ketoacidosis serve to promote the latter.
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Prevention andProphylaxis ofFungal
Infection
Prevention of fungal sinusitis in the immunocompromised patient includes:
• Minimising exposure to the fungi most likely
to cause rhinosinusitis
• Using prophylactic antifungal agents to diminish the risk of tissue invasion
Risk Factors
Patients with haematologic disease are at risk
during the neutropenic phase. The duration of
neutropenia is the most important risk factor in
leukaemic patients, but this risk increases with
corticosteroids, broad-spectrum antibiotics and
the choice of chemotherapeutic agents.
Bone marrow transplant recipients are at
greatest risk in the immediate post-transplant
period before engraftment and in graft-versushost disease (GVHD). Chronic GVHD is associated with increased risk of invasive aspergillosis,
especially with corticosteroid use [6, 37].
be directed at this pathogen [8]. Patients most at
risk are those with haematologic malignancies
and prolonged neutropenia and those who
undergo bone marrow transplantation. The use of
uconazole to prevent invasive candidiasis in
bone marrow transplant recipients has been a
hugely successful advance.
Patients undergoing intense chemotherapy or
bone marrow transplantation who have suffered a
previous attack of aspergillosis are particularly at
risk of infection, and whilst secondary prophylaxis is recommended, a third will develop a
relapse of aspergillosis [9].
With regard to rhinosinusitis and immunotherapy, it is important to identify, diagnose and treat
any sinus pathology before commencing immunosuppressant treatment. Sinus disease should be
excluded or identied by radiological imaging
scans. Rhinosinusitis following immunosuppressive therapy is more likely to occur with longterm antibiotic use, indwelling catheters, nasal
intubation, systemic steroids and metabolic
abnormalities [10].
Prevention
The Environment
Fungi are ubiquitous, but exposure levels may
increase in certain situations such as building
work on old properties.
Hospital outbreaks are associated with direct
contamination of the ventilation system, as may
occur with demolition or constructive projects in
or near to the hospital [7].
Hospital ventilation systems ducts should be
cleaned regularly to prevent transmission of lamentous fungi, especially in units caring for
immunosuppressed patients. High-efciency particulate air (HEPA) ltration is recommended,
but laminar airow is not.
Prophylactic Antifungal Medications
Prophylaxis should be limited to patients likely to
develop infection and should be given only during period of maximum risk.
The prophylactic drug should target the most
likely fungal organism. As Aspergillosis species
is the most common pathogen, medication should
Fungal Balls (Mycetomas)
Fungal balls, previously known as aspergillomas,
are composed of matted fungal hyphae, typically
within a single sinus.
Pathogenesis
A fungal ball is a non-invasive extra-mucosal
condition that is typically unilateral and most
often found in the maxillary sinus, followed by
the sphenoid sinus. They are more common in
older women but not described in children [11].
The histology characteristically shows a nongranulomatous inammatory mucosal reaction
with a tangled mat of fungal hyphae within the
debris, most often caused by an overgrowth of
Aspergillus spp.
This fungal overgrowth begins with persistent
germinating fungal spores within the nasal cavity
and paranasal sinuses. Aetiological factors
include dental paste, amalgam and the presence
of ferritin and zinc within the sinus lumen.
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Fungal balls can form a community with
bacteria to form bacterial or mixed balls; double balls describe a combination of a fungal ball
and a bacterial ball coexisting within the same
sinus [12]. Mixed balls are more likely in
chronic rhinosinusitis and immunocompromised patients. Persistence of a fungal ball,
despite adequate surgery, can occur secondary
to a biolm [13].
Patients are generally immune competent, but
should they become immunocompromised, the
condition can become invasive [14].
C. de Souza et al.
Clinical Features
Symptoms normally include nasal obstruction,
purulent nasal discharge, dysosmia and facial
pain, similar to bacterial rhinosinusitis. Bilateral
fungal balls have been described but present
with symptoms such as foul odour and severe
mucopurulent anterior and post-nasal discharge.
Inammatory polyps arise from the ipsilateral
affected side of the nose in 10% of patients. A
fungal ball may be associated with a mucocele,
foreign body or an antrochoanal polyp.
Fungal balls within the sphenoid sinus can
induce local inammatory effects that cause nonspecic headaches and occasionally ipsilateral
visual symptoms.
Radiological Imaging
A CT sinus scan typically shows a heterogenous
opacity: radiological features include central
radiodense areas, sclerosis of the lateral sinus
wall, bone erosion of the inner sinus wall and an
irregular surface (Figs. 27.1 and 27.2) [15].
A sinus mycetoma (‘fungus ball’) may
appear on CT as a mass within the sinus, with
accompanying features such as erosion and calcication of the sinus [1]. On MRI, hypointense
signal may be obtained from the fungus ball on
T1- and T2-weighted scans. This is due to the
relatively low free water content of the
mycetoma.
Fig. 27.1 Coronal view of a CT scan showing the typical
appearance of a fungal ball in the right maxillary sinus as
a hyperintense mass
Fig. 27.2 Axial section of a CT scan showing a fungal
mass in the maxillary sinus
In invasive disease, specic radiological signs
may be seen. In the acute phase, it may be difcult to appreciate signs on CT scanning. If seen,
non-contrast CT changes may include hypoattenuation of the mucosa and fat stranding beyond
the sinuses. These features are not diagnostically
specic, and CT changes should be correlated
with the clinical picture. CT scanning is useful
for assessing bony involvement. If localised bone
destruction has occurred, we may see evidence of
intracranial and intraorbital spread.
However, evidence of disease spread beyond
the mucosa may be more easily appreciated on
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