This document discusses fungal sinusitis, describing the different types including invasive, noninvasive, allergic, and chronic. Invasive fungal sinusitis is the most lethal form with mortality rates of 50-80% and usually affects immunocompromised patients. Clinical presentation varies depending on type but may include fever, facial pain, nasal congestion, and proptosis. Diagnosis involves imaging like CT and MRI to identify fungal invasion of sinus tissues and bones. Treatment requires aggressive surgical debridement and antifungal therapy along with managing any underlying immunosuppression. Prognosis depends on extent of invasion, with intracranial spread having the highest mortality.

3. By
Lt Col Saeed Ullah MBBS, FCPS
Classified ENT specialist
CMH Quetta

5.  Inflammation of the sinuses due to a fungus.
 Direct effect of the fungus or indirect.

6.  400,000 known fungal species or which 400
are human pathogens and 50 of which cause
systemic or CNS infection
 Clinical presentation, imaging features, and
treatment differ based on type of fungal
sinusitis
 Broadly categorized into invasive and
noninvasive

7.  Invasive
◦ Presence of fungal hyphae within the mucosa,
submucosa, bone, or blood vessels of the paranasal
sinuses
 Noninvasive
◦ Absence of fungal hyphae within the mucosa and
other structures of the paranasal sinuses

9.  Most lethal form of fungal sinusitis –
mortality 50-80%
 Rare in immunocompetent patients
 Two clinical populations
◦ Poorly controlled Diabetics
◦ Immunocompromised with severe neutropenia
(chemotheraphy patients, BMT, organ transplants,
AIDS)

10. Absidia Spp.
Rizomucor Spp.
Rizopus Spp.
Cunninghamella Spp.

11.  Fever
 Facial pain
 Nasal congestion
 Epistaxis
 Proptosis
 Visual disturbance
 Headache
 Mental status changes, seizures as spread
occurs

12.  Necrotic nasal septum ulcer (eschar)
 Nasal discharge due to Sinusitis
 Hypertelorism due to rapid orbital spread
 Meningitis due to intracranial spread
 Angioinvasion and hematogenous
dissemination common
 73% of patients with intracranial spread die

16.  General
 Specific

17.  Severe nasal cavity soft tissue thickening
 Hypoattenuating mucosal thickening
within lumen of paranasal sinus
 Rapid aggressive bone destruction of
sinus walls
 Fungi can also spread along vessels with
spread beyond the sinus with intact bony
walls
 Intracranial extension
 cavernous sinus thrombosis
 carotid artery invasion or occlusion

18.  Unilateral ethmoid involvement with bone
destruction, intraorbital spread and proptosis

19.  Better for evaluating intracranial and
intraorbital extension
◦ Evaluate for inflammatory change in orbital fat and
extraocular muscles
◦ Obliteration of periantral fat is a subtle sign of
extension
◦ Leptomeningeal enhancement progressing to
cerebritis and abscess

20. Aspergillus involving the sphenoid sinus with invasion of the left cavernous
sinus, thrombosis, extension to the left sylvian fissure and infratemporal
fossa with cerebral infarctions.

21. Aspergillus in left maxillary sinus with extension anterior and posterior to
the retroantral space. There is diffuse involvement of the muscles of
mastication.

22.  Aggressive surgical debridement and
systemic antifungal therapy
 Reversal of underlying cause of
immunosuppression if possible
 Recovery from neutropenia is most predictive
of survival
 Intracranial spread is most predictive of
mortality

23.  Inhaled fungal organisms deposited in nasal
passageways and paranasal sinuses
 Progression over months to years with fungal
organisms invading mucosa, submucosa,
blood vessels, and bony walls
 Organisms – Mucor, Rhizopus, Aspergillus,
Bipolaris, and Candida

24.  Usually immunocompetent
 History of chronic rhinosinusitis
 Usually persistent and recurrent disease
 Maxillofacial soft tissue swelling
◦ Orbital invasion with proptosis,
◦ Cranial neuropathies
◦ Decreased vision
◦ Invade cribiform plate causing headaches,
seizures, decreased mental status

25.  Noncontrast CT – soft tissue mass within
one or more of paranasal sinuses, bone
involvement often gives mottled appearance
with or without sclerosis
◦ May mimic malignancy with masslike appearance
and extension beyond sinus confines
 MRI – decreased signal on T1, markedly
decreased signal on T2 weighted images

27.  Surgical exenteneratin of affected tissues and
systemic antifungal
 Needs aggressive treatment

28.  Most common form of fungal sinusitis
 Common in warm, humid climates
 Hypersensitivity reaction to inhaled
fungal organisms
 IgE type I immediate hypersensitivity and
type III hypersensitivity are involved

29.  Common organisms implicated – Bipolaris,
Curvularia, Alternaria, Aspergillus, and
Fusarium
 “Allergic mucin” within affected sinus which is
inspissated mucous the consistency of peanut
butter with eosinophils on histology

30.  Younger individuals, third decade,
immunocompetent
 Often associated history of atopy with allergic
rhinitis or asthma
 Chronic headaches, nasal congestion, and
chronic sinusitis for years

31.  Bilateral with multiple sinuses involved.
 Often has a nasal component
 Noncontrast CT – high attenuation allergic
mucin within lumen of sinuses – can mimic
a mucocele
 MRI

33.  Surgical removal of allergic mucin with
restoration of normal sinus drainage is goal
 Longterm use of topical nasal steroids helps
suppress the immune response and minimize
recurrence
 Topical or systemic antifungals are not
indicated

34.  Older individuals, female>male
 Immunocompetent
 Asymptomatic or minimal symptoms with
chronic pressure or nasal discharge
 Cacosmia (perception of foul odor when no
such odor exists)

35.  Mass within the lumen of paranasal sinus
 Frontal sinus most common followed by
sphenoid sinus
 Noncontrast CT – hyperattenuating mass
often with punctate calcifications

36.  High density material with thickened walls of
the maxillary sinus due to chronic
inflammation

37.  Surgical Removal with restoration of drainage
of the sinus
 Antifungal medications usually unnecessary
 Recurrence is rare

40.  It is the failed containment of the
cerebrospinal fluid in the subarachnoid
compartment.
 It indicates a communication with the
subarachnoid space & therefore an opening
of the arachnoid, the dura and the bone to
permit exit of the CSF through the nose.

42.  The actual loss of CSF is of no particular
consequence
 The persistent dural fistula represents a
persistent hazard for a potentially fatal
purulent meningitis
 Persistent CSF rhinorrhea is therefore an
absolute indication for a surgical repair of the
leak.

43.  Anterior
 Middle
 Posterior

45.  Normal CSF
pressure is 40 mm
in infants & 140
mm in adults.

46. Traumatic
 Accidental
◦ Acute
◦ Delayed
 Iatrogenic
◦ Acute
◦ Delayed

47. Non traumatic
 High pressure
 Tumours (direct/ indirect effect )
 Hydrocephalus
 Normal pressure
 Congenital anomalies
 Focal atrophy of olfactory/sellar area
 Osteomyelitic erosion
 Idiopathic

48.  80 % secondary to head trauma with
associated skull base fractures
 16% operations on nose, paranasal sinuses
and skull base.
 Mostly occur through anterior cranial fossa.

49. Anterior cranial fossa
 Cribriform plate (commonest )
 Fovea ethmoidalis
 Posterior wall of frontal sinus

50. Middle cranial fossa fractures
 Sphenoid sinus
 Eustachian tube

51. Posterior fossa
 Clivus
 Petrous temporal bone

52.  Uncommon
 Mostly in adults
 4th decade
 ♂ : ♀ ratio is 1:2
 May occur after an episode of coughing,
sneezing or straining.

53.  Arise from the cribriform area in 75 % of
cases
 They act as a safety valve to decrease the
raised ICP
 84% are associated with slow growing intra
cranial tumours (Pituitary neoplasms are the
commonest)
 16 % are related to hydrocephalus

54.  Mostly are from the cribriform area and the
sella turcica but may be from the middle
fossa.
 90 % are due to potential congenital pathways
 10 % are due to direct erosion of skull base

55.  Is the fluid CSF?
 Cause of leakage
 Site of leakage

56. Any persistant rhinorrhea should be
considered CSF until proved otherwise.
Patient with recurrent pneumococcal
meningitis
Bending the head forward will increase the
rate of flow
Headache
Salty taste
Anosmia
Associated Symptoms

57. Reservoir sign:
After being supine for sometime the patient
is brought in an upright position, with the
neck flexed. A sudden rush of clear fluid is
indicative of CSF fistulae.

58.  Hankerchief Test:
◦ Fluid in rhinitis contains mucous which stifins while
CSF doesnot.
 Halo Sign:
◦ When CSF rhinorrhea is blood stained it dries out
with a central blood stain surrounded by a clear
ring.
 Nasal endoscopy
◦ with or without intrathecal floresein for leak
presence or localization

59.  Biochemistry/ Immunochemistry
◦ Estimation of glucose, proteins and electrolytes can
be done.
◦ A concentration of 30mg/dl or 1.6mmol/l of
glucose is considered confirmatory of CSF
 β-2 Transferrin

60.  Radiology plays the key role
 Bone defects, air fluid levels and erosions can
be seen.
 Plain X rays
◦ Pneumocephalus/ air fluid levels
 CT scan in axial/ coronal views
◦ Skull Base fractures, CSF fistulae

62.  Isotope studies
In case of inactive, intermittent, small or
doubtful leak, CT scan with contrast will not
reveal the leak. In such cases radio nuclied
cisternography is more effective. Indium III-
DPTA is generally used.

64. Intrathecal dyes
◦ Intrathecal floreciene with nasal endoscopes are
used for anterior fossa leaks

66.  Management consists of cooperation between
Neurosurgeon
Neuroradiologist
Otolaryngologist
depending upon severity, etiology, extent of
injury & anatomical site of leak.

67.  Treatment can be divided into
Medical &
Surgical

68.  Majority of acute traumatic leaks heal
spontaneously.
 Bed rest in head up position
 Avoiding coughing, sneezing, nose blowing &
straining.
 Drugs to decrease spinal fluid production like
acetazolamide and frusemide.
 Repeated removal of CSF via lumbar taps or
an indwelling lumbar subarachnoid drain.
 Antibiotics

69.  Intracranial approach
 Extra cranial approach
 Endoscopic repair