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8.1.5 Recent Advances
Following novel therapies have been introduced
for improving SNOT 22 scores
(a) aPDT (Antimicrobial Photodynamic ther-
apy)—Non-invasive non-antibiotic broadspectrum antimicrobial treatment. It has been
shown to be effective against biolm- forming
microorganisms [15]. This works on a simple
principle, it introduces a non-toxic molecule
that turns bactericidal on exposure to visible
light, by forming free radicals.
(b) Steroid saline irrigations—Can be started
immediately post-operatively for cavity
cleaning purpose and to prevent recurrence
of polyps. E.g., Budesonide preparation can
be done as follows:
2.5 mg/2 ml ampules are used; they are
dissolved in 240 ml of water. Then nasal
douching is done on either side thrice a day.
It can be reduced to twice a day after the rst
week and once a day after the rst month.
(c) Steroid stents—These stents are inserted in
nasal cavities to keep the sinus openings patent. They gradually release a steroid that
reduces local inammation in post- operative
period. However, their role in decreasing the
symptoms and SNOT 22 scores in patients of
CRS remains doubtful [16].
(d) Biologicals—omalizumab, dupilumab,
mepolizumab. They are experimental expensive therapies. They have been successful in
about 40% of recalcitrant cases.
(e) Personalized therapies using cytokines.
(f) Immunotherapy—Allergen immunotherapy
has been shown to decrease post-operative
exacerbations, decreases the need for revision surgery and lead to decreased dependence on steroids [17].
8.1.6 Other Therapies
The following therapies are described for AFRS
patients that fail high concentration budesonide
and budesonide irrigations. Tab Montelukast
10mg OD—causes the signicant improvement
in some patients. It is symbiotic with budesonide
irrigations. Betadine rinses, Itraconazole, aPDT
are the other therapies. Short course of systemic
steroids is good option for refractory cases.
Biologicals and cytokine therapy are in experimental stage.
Oral itraconazole is proven to be benecial in
selected cases of AFRS. They are started at
200mg BD and the responders are subsequently
tapered to the lowest effective dose within
2 months. Non-responders are given a trial of
2 months after which the drug is stopped.
Itraconazole therapy requires regular monitoring
of liver function tests and cardiac function. The
EPOS 2012 paper does not recommend routine
use of systemic or topical antifungals like
amphotericin B for routine management of
AFRS, as there is insufcient evidence supporting its use [3].
8.2 Part B: Antifungal Therapy
8.2.1 Introduction
Surgical debridement is the preferred treatment
modality for fungal sinusitis. Antifungals with
surgical debridement are the treatment strategy
for invasive fungal sinusitis. The incidence of
invasive fungal infection increases because of
widespread use of antibiotics, steroids and immunosuppressant drugs. With the advancement in
knowledge and technology, the graph of organ
transplantation and intervention is raised.
Antifungals are used by some clinicians in extensive AFRS in pre-operative period or in follow up period, when the surgeon is not sure for
disease clearance or in patients with persistent
symptoms after surgery, to reduce the recurrence
rate. Fungal sinusitis occurs in different forms
and due to various pathogens, each requiring a
specic treatment regime aimed at the causative
pathogen. Antifungal agents have varying toxicity and the benet versus toxicity ratio needs to
be weighed before starting treatment. The newer
antifungal agents that are less toxic are very
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expensive. The management protocol for invasive fungal sinusitis is antifungal treatment and
debridement of the involved part.
8.2.2 Classication ofAntifungals [18]
1. Antibiotics:
(a) Polyenes: Amphotericin B, Nystatin,
Hamycin
(b) Heterocyclic benzofuran: Griseofulvin
(c) Echinocandins: Caspofungin, Micafungin,
Anidulafungin
2. Antimetabolite: Flucytosine (5-FC)
3. Azoles:
(a) Imidazoles:
(i) Topical: Clotrimazole, Econazole,
Miconazole, Oxiconazole
(ii) Systemic: Ketoconazole
(b) Triazoles (systemic): Fluconazole,
Itraconazole, Voriconazole, Posaconazole
4. Allylamine: Terbinane
5. Other topical agents: Tolnaftate, Undecylenic
acid, Benzoic acid, Quiniodochlor, Ciclopirox
olamine, Butenane, Sodium thiosulfate
8.2.3 Antifungal Agents Used
forTreatment ofFungal
Sinusitis
1. Amphotericin B
Amphotericin B, is most commonly used
polyene antifungal agent and it remains the
standard drug of choice for managing lifethreatening systemic fungal infections [1]. It
was isolated by Gold et al. in 1955 from
Streptomyces nodosus. It is the standard drug
for all types of invasive fungal infections,
including invasive aspergillosis, zygomycosis
and severe infections of blastomycosis, coccidioidomycosis, sporotrichosis and histoplasmosis. Amphotericin B is also proved to
be effective in the treatment of candidemia
and disseminated candidiasis. Local irrigation
of amphotericin B is reported to be controversial treatment to control of invasive sino-
orbital infections. Retrobulbar injection of
amphotericin B is also used for the treatment
of invasive sino-orbital Aspergillosis.
Amphotericin B binds to sterols, more preferentially to ergosterol, which is a major component of the fungal cell membrane. This
results in an increased permeability of the cell
membrane, leading to leakage of intracellular
components and eventually cell death [19,
20]. Owing to its lipophilic nature, amphoteri-
cin B also binds to cholesterol in the mammalian cell membrane, but to a lesser degree,
which probably accounts for its toxicity. Also,
its interaction with host cells can have a positive effect by activation of macrophages
through an oxidation-dependent process.
Amphotericin B is available in four
formulations:
(a) Amphotericin B Deoxycholate
It is actually a colloidal suspension of
amphotericin B, in which deoxycholate
(bile salt) is used as solubilizing agent.
This formulation has high toxicity. It has
poor CNS penetration. The patient should
be hydrated with 500–1000mL of saline
before starting the amphotericin infusion.
This supplements the sodium required to
maintain the intravascular volume and
inhibits the tubuloglomerular feedback
system, which reduces the risk of nephrotoxicity. Continuous administration versus 5 h administration of the drug is
controversial therapy, continuous infusion
have less toxicity prole whereas 5h infusion have more fungicidal effect. The
usual protocol is to administer test dose
by diluting 10–15 mg of the drug in
50–100 mL of 5% dextrose, and given
slowly intravenously over 20 minutes. If
there is no reaction, then the complete
dose can be administered. The standard
dose ranges from 0.25 to 1 mg/kg/day
given once daily, diluted in 5% dextrose,
to be given slowly intravenously (over
2–6 h) [19, 21]. There are two ways to
administer the drug. The rst is to start
with a low dose and titrate gradually till
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the maximum dose is achieved. This
method is no longer recommended. The
second method which is preferred is to
start with a standard dose as per patients’
body weight and maintain the same till
total cumulative dose is achieved. The
maximum daily dose in adults is 1.2mg/
kg, and in children is 1.5mg/kg but more
than 1 mg/kg body weight increases the
chances of side effect drastically which in
turn increases the treatment duration and
hospital stay. The total cumulative dose
ranges between 2 and 3 g given over
2–3months. The renal function tests and
serum electrolytes should be monitored
twice weekly and complete haemogram
once weekly. As amphotericin B is sensitive to light, the infusion bottle and tubing
should be covered and protected from
sunlight, to maintain drug effectiveness.
The use of concomitant nephrotoxic drugs
must be avoided.
Amphotericin B is highly toxic and has
various side effects. The immediate side
effects are infusion related and usually
begin 1–1.5h after starting the infusion.
They are very common and occur in more
than half of the patients. It is probably due
to the release of cytokines (Interleukins
and tumour necrosis factor α). The
infusion- related side effects commonly
include fever, chills, rigor, headache, nausea, vomiting. Acute anaphylaxis may
rarely occur. These may be managed
symptomatically by premedication with
paracetamol, antihistamines and antiemetics. Hydrocortisone injection 0.6mg/
kg with the infusion may reduce the severity of the reaction. Thrombophlebitis is
also commonly seen with amphotericin
infusion. It can be reduced by slowing
down the rate of infusion of amphotericin
B, adding small amount of heparin to the
infusion (1000 units/L), using a central
line, or by diluting the concentration of
the infused drug. Nephrotoxicity is
another common side effect in patients
receiving amphotericin B, occurring in up
to 80% of patients. The contraindication
of amphotericin is acute renal failure.
Symptoms are a result of electrolyte wasting (potassium and magnesium) due to
impaired urine concentrating ability [19,
21, 22]. It is also associated with renal
tubular acidosis. Nephrotoxicity can be
minimized by 500–1000 mL of normal
saline infusion before and after amphotericin B infusion. If serum creatinine
rises above 3mg/dL, it should be temporarily discontinued or substituted with a
lipid-based amphotericin formulation.
Patients receiving a total dose greater
than 4–5g of amphotericin B deoxycholate may have permanent renal dysfunction. Amphotericin B has also been
reported to directly suppress erythropoietin production leading to normochromic
normocytic anaemia. Infrequently, neutropenia and thrombocytopenia may also
be seen [19, 21].
(b) Lipid-Based Formulations of Ampho-
tericin B
Recently, lipid-based formulations of
amphotericin B have been made available,
using various lipid carriers. These lipidbased formulations of the drug have fewer
side effects as compared to amphotericin
B deoxycholate. They are selectively
delivered into the reticuloendothelial system, such as the liver and spleen, and to a
lesser extent, the lungs. There are three
lipid preparations: amphotericin B colloid
dispersion (ABCD), amphotericin B lipid
complex (ABLC) and liposomal amphotericin B (LAMB). Their standard doses
are ABCD: 3–5 mg/kg, ABLC: 5mg/kg
and LAMB: 1–5 mg/kg. The standard
cumulative dose is 5–7 g but it can
exceed further which is depends on clinical condition and patient tolerance. The
dose-related efcacy of lipid- based for-
mulations is lower than conventional
amphotericin B but, as higher doses can
be used, it makes them more efcacious.
Lipid-based formulations of ampho-
tericin B are particularly used for the
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treatment of invasive fungal infections in
patients intolerant of or refractory to
Amphotericin B deoxycholate. LAMB is
used as empiric therapy for fungal infections in febrile neutropenic patients. It is
also used in the treatment of patients with
Aspergillus, Candida, Cryptococcus sp.
infections refractory to or intolerant of
Amphotericin B deoxycholate. It is the
drug of choice for rhinocerebral mucormycosis, which requires administration of
high dose of polyenes after debridement
[23]. Liposomal Amphotericin B also has
better CNS penetration than Amphotericin
B deoxycholate or ABLC.
It has multiple advantages over amphotericin B
deoxycholate and is well tolerated by the
patient. It produces a milder reaction on infusion, causes minimal anaemia and nephrotoxicity. The only disadvantage of this drug is
that it is expensive. Colloidal suspension creates more side effects than liposomal preparation by upregulation of the inammatory
gene.
2. Azoles
Lately, azoles are gaining importance in
the treatment of fungal rhinosinusitis as they
are active against multiple fungal pathogens
without the serious side effects of amphotericin B deoxycholate. They have also shown
effectiveness in treatment of systemic mycoses. Azoles inhibit cytochrome P450 enzyme
and thus impair ergosterol synthesis, which is
an essential component of the fungal cell
membrane [21, 24]. This leads to damage of
cell membrane of fungus by increasing its permeability and causing cell death.
These drugs include imidazoles (clotrima-
zole, miconazole, ketoconazole) and triazoles
(itraconazole, uconazole). Ketoconazole,
given orally, has been used successfully for
the treatment of invasive mycosis. However,
its use has been mostly replaced by triazoles
owing to their superior efcacy, pharmacokinetics and safety prole. Fluconazole is available in both oral and intravenous preparations.
The daily dose varies between 200 and
800 mg, depending on the severity of infection. It is highly water soluble and its absorption is not affected by the presence of food or
gastric pH6. It has excellent activity against
most Candida species and is widely used for
various fungal infections by Candida albi-
cans. Fluconazole has better CNS penetration
than itraconazole. Itraconazole is very effective against Aspergillus and black moulds,
that typically cause fungal sinusitis. It is the
drug of choice in these cases, unless there is
extensive bone invasion where initial therapy
is amphotericin B [23]. There have also been
reports of the efcacy of itraconazole for the
treatment of allergic fungal rhinosinusitis and
fungal ball. Both oral and intravenous preparations are available. The daily dose is 100–
400mg/day depending on the indication. Its
oral absorption and availability is highly variable and unpredictable. It is better absorbed
when administered with food or acidic beverages. The side effects of azoles are gastritis,
rash, headache, the elevation of liver enzymes,
and aldosterone-like effects in high doses
(itraconazole). Hepatotoxicity, peripheral
neuropathy, pancreatitis and androgen related
side effects (alopecia, gynecomastia, loss of
libido, etc.) are side effect of long-term use
[25].
3. Newer Drugs
(a) Voriconazole: It is a synthetic derivative of
uconazole, a second-generation triazole.
It is useful for the treatment of acute and
chronic invasive aspergillosis. It is preferred over amphotericin B where the
cause of fungal infection is not known.
Both oral and intravenous preparations are
available and it is good alternative to
amphotericin B in invasive aspergillosis. It
is given as loading dose of 6mg/kg iv BD
for 2 doses, followed by 3mg/kg iv BD for
30days. On signs of improvement, it can
be changed to 200mg BD orally to complete 24 weeks [26]. The side effects
include mild elevation of liver enzymes
and transient visual disturbances. The limiting factor is that the drug is expensive.
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(b) Posaconazole: It is an azole, active against
yeasts and moulds including zygomycetes, aspergillosis, candida and cryptococcal infection. It is used as salvage therapy
in invasive fungal sinusitis after failure or
intolerance to other antifungals [27]. It is
available in oral preparations and the
doses are 200mg thrice daily as preventive management for invasive fungal
infection. The therapeutic doses are
800mg daily in divided doses for invasive
fungal infection.
(c) Echinocandins: This class of antifungal
agents acts by inhibiting 1, 3 β-glucan
synthesis a critical component for maintenance of fungal cell wall integrity [21]. It
is approved for treatment of invasive
aspergillosis resistant to conventional
antifungal and empirical management of
neutropenic patients suspected of having
fungal sinusitis. Drugs belonging to this
class are caspofungin, micafungin,
anidulafungin.
8.2.4 Antifungal Drug Resistance
inducing drug resistance. Studies have shown that
an increase in resistance to azole antifungal drugs
may allow some cross-resistance to amphotericin
B. The possible mechanism is azoles cause an
alteration in ergosterol synthesis which consequently decreases the number of potential binding
sites on the fungal cell membrane for amphotericin B or multiple drug resistance (MDR) pumps.
In invasive mycoses, when the site of infection is
necrotic with poor vascularity, debulking surgery
is essential to overcome antifungal resistance and
tissue samples should be evaluated for the sensitivity of drug against particular organism. A suboptimal length of treatment, prolong drug
exposure, repeated and prophylactic treatment
may also lead to drug resistance. Lastly, the
underlying disease must be controlled or prevent
fungal infections in high- risk patients. In vitro
assessment of drug susceptibility, newer drugs are
the alternatives in patients resistant to or not
responding to conventional treatment. Failure to
treatment is dened as no improvement or worsening of clinical or radiological features in
7–14 days after starting standard antifungal
treatment.
Drug resistence is the major cause of treatment
failure. This can occur in circumstances such as
wrong diagnosis, multiple pathogens or immune
reconstitution inammatory syndrome, seen in
patients receiving immune-modulating therapies,
which may be confused with failure to control the
fungal infection [27]. Also, in patients with severe
immunosuppression, the antifungal cannot overcome the severe immunodeciencies until the
host immunity is improved. Recent studies have
shown that early treatment of fungal infection
with a lower burden of organisms reduces treatment failure [28, 29]. Some fungal strains possess
more virulent characteristics than others and
infection with such strains may have a poorer
prognosis. Toxicity from polyenes (nephrotoxicity) and azoles (hepatitis) can be a cause of treatment failure [30, 31]. Drug-drug interaction,
drug-target interaction, upregulation of drug
transporters, biolms and reduced cellular concentration can lead to morbidity and mortality by
8.2.5 Duration ofMedical Therapy
forFungal Sinusitis
Treatment end point should be tailor made and
multiple factors can be considered in each patient.
Treatment should be continued till there is complete resolution of all symptoms of fungal sinusitis for at least 2weeks, resolution of endoscopic
ndings, resolution of radiological ndings, negative fungal culture and biopsy the suspected
area. Serum biomarkers such as galactomannan,
β-D-glycan and Aspergillus specic PCR can be
considered as end point for treatment as they
have high negative predication value. Sometime
patient tolerance and co-morbidities are the
major limiting factor for complete treatment [32].
8.2.5.1 Combination ofAntifungal
Simultaneous administration of two or more antifungal drugs is a controversial topic in view of
signicant side effects, patient tolerance but it
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has shown advantages against certain organism
and drug resistance. Flucytosine with amphotericin B combination demonstrated survival benet
in cases of Cryptococcal meningitis. Calcium—
calcineurin signalling pathway plays a dominant
role in immunity. Synergistic action of calcineurin inhibitors such as cyclosporine A, tacrolimus
(FK 506) and pimecrolimus with azoles is helpful to kill resistant fungi. Glucocorticoid (dexamethasone, budesonide, hydrocortisone),
antimetabolic agents (mycophenolic acid,
mizoribine), the target of rapamycin and few traditional Chinese medications (tetrandrine, artemisinin, matrine) showed addictive effect with
antifungal. These drugs are more studied with
candida species. Hydrocortisone with amphotericin in human and rapamycin with azoles in rat
showed some synergistic effectiveness against
Aspergillus infection [33].
8.2.5.2 Recent Advances
Urea derivative of amphotericin B is showed
more potent outcome with less adverse effects in
the animal model. Isavuconazole is potent orally
and intravenously available azole and it is
approved by the US FDA for the invasive form of
aspergillosis and mucor infections. Fungal sphingolipid, calcineurin, Hsp 90, etc. are the newer
target sites for drugs. VT 1129, VT 1161 and VT
1598 are the newer tetrazoles and they claimed to
be more specic for fungal cytochrome 51 and
less for mammalian 450 cytochrome.
Aminocandin (IP960 or HMR3270), CD 101,
enfumafungin, etc. are the newer echinocandins
against Aspergillus and candida species [34, 35].
relationship to the orbit, anterior cranial fossa
and vascular structures, sinus surgery has many
potential complications. Thorough knowledge of
anatomy, detailed assessment of pre-operative
imaging and advanced technology such as endoscopes, microdebrider and Image guidance with
hypotensive anaesthesia can reduce the chance of
complications drastically. Revision surgery,
extensive nasal polyposis, dehiscence of sinuses
lining wall, distorted anatomy are the common
reason behind complications. Normal anatomical
various such as hypoplastic or extensive pneumatized sinuses, long and high cribriform plate,
asymmetrical low lying ethmoidal roof are the
other factors. Dehiscent bony canal over optic
nerve, internal carotid artery and anterior ethmoid artery can induce catastrophic
complication.
Posterior choana, middle turbinate/ remnant
of it, sphenoid sinus, skull base, septum and
maxillary sinus roof are the stable intranasal
landmarks to be considered especially in revision
surgery. The factors with poorer outcomes
include previous surgery, extensive disease, poor
knowledge of anatomy and radiology. Outdated
technology and the presence of risk factors such
as smoking, asthma, aspirin sensitivity, allergies
and in immune deciency, etc. are the other factors for poor outcome. The list of complications
is illustrated in Table 8.5. Nasal complications
are the most common complications followed by
orbital and intracranial complications.
8.3.1 Nasal Complications
8.3 Part C: Fess Complications
Functional Endoscopic sinus surgery is highly
sophisticated type of surgery that aims at maintaining the physiological function and anatomical
structure. Powered instrumentations and stereotactic image-guided surgery have improved efcacy and safety of this procedure and have
revolutionized endoscopic sinus surgery and
extended its applications. Because of the highly
variable individual anatomy and the intimate
8.3.1.1 Adhesion (Synechiae)
This is the most common complication of FESS
and it is seen in 4–35% of cases [36]. Synechiae
develop when two opposing raw mucosal surfaces remain in contact after the surgery. Gross
septal deviation, revision surgery, and middle turbinate instability is the major causes of synechiae
formation. The spacer should be placed under the
vision to prevent instability of middle turbinate.
Initially, micro brinous bands develop and
forms a scar tissue. Synechiae at maxillary ostia
and ethmoid cavity have worse effect as it affects
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Table 8.5 Complications of Endoscopic Sinus Surgery
Nasal complications Intracranial complications Orbital complications
• Synechiae (adhesion)
• Haemorrhage
• Stenosis of ostium
• Mucocele/Pyocele
• Olfactory impairment
• Injury to NLD
• CSF Rhinorrhea
• Meningitis
• Encephalocele
• Orbital subcutaneous emphysema
• Fat prolapse
• Extraocular muscle injury
• Orbital hematoma
• Optic nerve injury
Fig. 8.2 NCCT PNS orbit is showing synechiae in between inferior turbinate and septum
the drainage of maxillary, ethmoid sinuses. It also
interferes in post-operative cavity cleaning. To
prevent this, surgery should be performed with
by spacer placement. Regular follow-up with
operative surgeon and proper cavity care can pre-
vent synechiae formation.
care. Any kind of injury to healthy mucosa should
be avoided. Loose hanging mucosa and bony
chips should be removed during surgery and in
post-operative care. Irrigation of the cavity is
required to minimizing the effect of heat injury.
Absorbable and non-absorbable spacer is placed
in between two raw surfaces to prevent approximation and adhesion. Meta-
analysis, review articles showed advantage of spacer placement
against synechiae formation [37–39].
Bolgerization and suture medialization of middle
turbinate are helpful in preventing synechiae formation when middle turbinate is destabilized
8.3.1.2 Haemorrhage
Nasal bleeding can be divided into bothersome
mucosal ooze, bleeding from a named vessel and
life-threatening haemorrhage from maxillary and
internal carotid artery. Surgeon’s scale is proposed to qualify amount of blood in eld [41].
The scale is ranged from 0 to 5 where score 2
means mild ooze and it requires minimal suctioning. In score 3, the eld is improved with suctioning and in score 4, continue suctioning is required
to see the surgical eld. In score 5, the surgical
eld is not improved with continue suctioning.
(Fig. 8.2) [40]. Soft adhesion can be removed
easily but hard adhesion requires sharp instruments to break it and raw surfaces are seperated
1. Mucosal Ooze—It may limit the view of sur-
gical eld which leads to increase operative
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time. It also increases the risk of complications and may lead to termination of procedure. Mucosal ooze can be reduced by
avoidance of NSAIDS, platelet inhibitors.
Pre-operative antibiotics and oral steroid
reduces intraoperative bleeding by reducing
edema, exudates and blood vessels trauma by
reducing the load of inammatory mediators
[42]. Oral steroids also enhance the effect of
vasoconstrictors by increasing the spasticity
of smooth muscles. The doses were varied
from 30–60mg per day with 7days duration
with or without tapering [43]. Pre-operative
steroid can generate serious side effects so it
should be used cautiously [43, 44]. Preoperative administration of tranexamic acid
reduces periorbital edema and intraoperative
bleeding [45, 46]. Hypotensive anaesthesia,
reverse Trendelenburg position, intraoperative
local inltration in pterygopalatine fossa via
greater palatine or sphenopalatine foramen
and application of cotton pledgets with vasoconstrictor reduces mucosal ooze to some
extent [47].
2. Bleeding from Named Vessel—Sphenopalatine
artery is the major blood supply of the sinonasal region. Anterior ethmoidal artery is the
branch of the ophthalmic artery. Anterior ethmoid artery can be injured while removal of
antero-superior part of the anterior ethmoid
cell. Low lying anterior ethmoid artery is
found in cases with higher Keros, long cribriform plate, wide antero-posterior frontal
recess and presence of supraorbital recess
[48]. Abnormal course can be assessed by
proper pre-operative radiology. Injury to the
lateral part of the vessel can retract intraorbitally and creates complications by rising
intra-orbital pressure. Avoidance is the best
way to prevent complications and if the dealing is required, it should be done in the middle
part of intranasal course of anterior ethmoid
artery so cauterization of injured vessel is possible. Once it retracts in orbit, external
approach is required to control bleeding and
the management of anterior ethmoid artery
bleeding is mentioned in Chap. 9. The poste-
rior branch of sphenopalatine artery is running
just inferior to sphenoid ostium which can be
injured by the inferior widening of ostium.
Vessel injury can be avoided by separating the
mucosa inferiorly before ostium widening.
The management of sphenopalatine bleeding
is mentioned in Chap. 9.
3. Internal Carotid Injury—Sellar type of pneu-
matization of the sphenoid sinus has thinnest
bony wall over carotid or may even have
dehiscent carotid. Sometimes accessory sphenoid septum is attached over the ICA bulge.
Anomalies and aneurysms of the artery also
predispose to the internal carotid artery injury.
This can be avoided by pre-operative radiological assessment and without pulling or
avulsion of septas in the sphenoid sinus. The
management is mentioned in Chap. 9.
8.3.1.3 Sinus Ostium Stenosis
Sinus ostium stenosis is dened as loss of more
than 50–60% of intraoperative size. Neoosteogenesis at the ostium level can lead to
stenosis (Fig.8.3). Complex anatomy and narrow
outow tract of frontal sinus make it as most vulnerable sinus for recurrence of disease secondary
FO
MT
Fig. 8.3 Neo-osteogenesis with stenosis of left side frontal ostium (FO). MT middle turbinate)
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to stenosis. It is found as high as 60% [49]. The
nal size of the frontal ostium is dened around
1year of post-surgery period. The preservation of
normal ostium wall at least at one side, carpeting
of exposed bone by mucosal graft or ap,
Mitomycin C application, steroid releasing sinus
implants and proper cavity care can reduce the
chances of stenosis [50–52].
8.3.1.4 Mucocele/Pyocele
It is a late complication of endoscopic surgery.
Mucocele appears after years of surgery. The
persistent mucosal inammation and intraoperative trauma can lead to narrowing/obstruction
of sinus cells outow. The mucocele formation
is ranged from 0 to 13% after endoscopic surgeries [53]. Frontal sinus is the most affected
sinus because of its narrow drainage pathway.
Ethmoid and sphenoid are the next common
sinuses in sequence. With the expansion in the
list of endoscopic procedures, the chances of
mucocele formation are increasing (Fig. 8.4).
Complete excision of mucosa is difcult in narrow and hidden part of sinuses. Mucoceles may
be incidental nding or it may present with
headache, orbital symptoms and facial disguring, etc. Extensive diseases have higher chances
of mucocele formation because of signicant
damage to normal mucociliary function while
disease clearing. The measurements mentioned
in the mucosal ooze section and proper cavity
care are also applicable to minimize the chances
of mucocele formation. In extended endoscopic
approaches, complete removal of mucosa under
ap and the proper marking of mucosal surface
of the ap is required for prevention of iatrogenic mucocele [54]. The regular follow-up and
interval MRI helps in early diagnosis [55].
Majority are manageable by endoscopic
approach. Complicated mucoceles require
urgent intervention. The detailed management
of mucoceles is mentioned in Chap. 7.
8.3.1.5 Nasolacrimal Duct Injury
Nasolacrimal duct is the continuation of nasolacrimal sac in the lateral nasal wall. The course is
variable in the medial maxillary wall (Fig.8.5).
The distance between the duct and anterior maxillary sinus wall is found less than 7 mm in
approximately 88% of cases [56] whereas in
nasal endoscopic evaluation in cadavers, it runs
at and anterior to the maxillary line in 95% of
cases [57]. NLD can be injured while aggressive
removal of uncinate bone, anterior enlargement
of the maxillary ostium and in extended endoscopic approaches to pterygomaxillary fossa and
infratemporal fossa. Not all NLD injuries are presented with tearing. Proper pre-operative knowledge of NLD course, anterior and posterior
nasolacrimal duct approach can reduce the injury
chances [
58]. In extended endoscopic approaches,
sharp cut to NLD or DCR is advised.
Dacrocystostomy is the treatment option for
symptomatic cases. The details of the procedure
are mentioned in Chap. 8.
Fig. 8.4 Right iatrogenic frontoethmoidal mucocele.
Hypodense area is the retained bone wax which is blocking the outow tract of frontal sinus. Anterior wall of the
frontal sinus is also breached which presented as uctuation swelling on the frontal sinus (Pott’s puffy tumour)
8.3.1.6 Empty Nose Syndrome
It is a late complication. It occurs after extensive
and usually recurrent sinus surgeries with the
removal of large areas of mucous membranes and
resection of superior and middle turbinates.
Patient will complain of paradox nasal obstruction in presence of objective wider nasal cavities
b
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Fig. 8.5 Course of
nasolacrimal duct canal.
It is very much away
from anterior maxillary
sinus wall in (a) and in
(b), no gap in between
anterior maxillary wall
and NLD canal
a
and irritating crust formation. The etiology and
management of empty nose syndrome is mentioned in last section.
8.3.1.7 Olfactory Impairment
It may occur due to avulsion of olfactory neuroepithelium from olfactory cleft or over resection
of superior turbinate. It can be prevented by
avoiding unnecessary handling in the olfactory
cleft region and if required, sharp cutting instruments should be used to prevent scarring.
crepitating are the clinical ndings on eyelids. It
is generally self-limiting and reabsorbs in short
period. Patient should be advised to avoid activities like nose blowing, etc. Progressive emphysema can create acute compartment syndrome. It
is painful condition that can present with restriction of extraocular movement and impairment of
vision. It requires urgent decompression of
collected air to prevent permanent vision loss
secondary to vascular compression and optic
nerve stretching (Fig.8.6) [59, 60].
8.3.2 Orbital Complications
The orbit comes in close relationship with all
paranasal sinuses. Periorbita is the only soft tissue barrier in between orbit and paranasal sinuses.
Pre-operative radiology is helpful in accessing
bony anatomy, dehiscence’s of periorbital wall,
fat prolapsed, optic nerve course. The incidence
of orbital complications is ranged from 0.5 to
5%. The list of orbital complications is mentioned in Table8.5.
8.3.2.1 Subcutaneous Emphysema
It is characterized by the presence of air in orbital
tissue. This occurs due to natural communications or by accidental or iatrogenic breach of
partly wall. Orbital emphysema occurs due to
forceful nose blowing, sneezing and mask ventilation. It is mostly seen in eyelids with the normal
sclera and extraocular movement. Creaking and
8.3.2.2 Damage toLamina Papyracea,
Periorbita andOrbital Fat
Prolapse
Median orbital wall is formed by frontal process of
maxilla, lacrimal bone and lamina payracea from
anterior to posterior direction. Lamina papyracea
is the thinnest medial orbital bone and its thickness
reduces with age advancement. Predisposing factors for fat prolapsed are dehiscent Lamina papyracea, revision surgery, extensive disease, distorted
anatomy, excessive bleeding and hypoplastic
Maxillary Sinus (Fig. 8.7). The preservation of
median bony wall and periorbita in dehiscent bony
wall is the key to prevent orbital complications.
Fat is prolapsed when sickle knife inserted blindly
while uncinectomy, dacrocystostomy and undue
pulling of lateral attachment of middle turbinate.
Periorbita touching is painful under local anaesthesia. Retrograde uncinectomy is the safer technique [58]. Powered instruments have damaging
effect on orbital tissue than cold instruments by its
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