1) Facial nerve palsy is a potential complication of both acute and chronic suppurative otitis media (CSOM). The facial nerve can become inflamed or damaged, causing weakness or paralysis of the muscles on the affected side of the face. 2) Labyrinthitis refers to inflammation of the inner ear structures and can occur when infection spreads from CSOM to the inner ear through defects in the otic capsule bone. This can cause symptoms like vertigo, hearing loss, and nystagmus. 3) Acute mastoiditis is inflammation of the air cells in the mastoid bone behind the ear. It develops when infection from the middle ear spreads to the mast

1. EXTRACRANIAL /INTRATEMPORAL
COMPLICATIONS OF CSOM
Dr Harjitpal Singh
Assistant Professor(ENT),
Dr RKGMC, Hamirpur

2. EXTRACRANIAL (INTRATEMPORAL)
i. Acute mastoiditis
ii. Subperiosteal abscesses.
iii. Petrositis and Gradenigo’s syndrome
iv. Labyrinthitis
v. Facial nerve palsy
vi. Osteomyelitis of temporal bone
vii. Septicemia or pyemia
viii. Otogenic tetanus.

3. EXTRACRANIAL COMPLICATIONS

4. FACTORS LEADING TO COMPLICATIONS
• Inadequate antibiotics.
• High virulence of bacteria.
• Poor resistance.
• Presence of diabetes, tuberculosis, leukemias.
• Antibiotic resistance of organisms.
• Preformed pathways.
• Immunocompromised patients

5. SPREAD OF INFECTION
• Direct spread – demineralization / resorption
of bone
• Thromboplebitis of veins - bone & dura
• Normal pathway
oval /round window
cochlear/ vestibular aqueduct
dehiscence of tegmen tympani / bone
over jugular bulb
dehiscence of suture line

6. SPREAD OF INFECTION(cont.)
• Non anatomical bone defect:
Trauma
Accidental
Surgical
Neoplastic Erosion
• Surgical defects – stapedctomy Sx
• Spread along Periarteriolar Space of Virchow

7. SPREAD OF INFECTION(cont.)

8. SUSPICION OF INTRACRANIAL
COMPLICATIONS
Otalgia
Headache
Drowsiness

9. ACUTE MASTOIDITIS
• Acute inflamation of mucoperiosteum of
mastoid folllowed by bone destruction.

10. ACUTE MASTOIDITIS(cont.)
Acute
Mastoiditis
Masked
Mastoiditis

11. ACUTE MASTOIDITIS(cont.)
• Acute mastoiditis occurs when the infection from mucosa of
middle ear cleft spreads to bony walls of mastoid antrum.
• The determining factors being high virulence of organisms or
lowered resistance of the patient
• Usually, it occurs in a well-pneumatized mastoid bone.
• Beta-hemolytic streptococci are the usual organisms.
• Clinical Features:
Severe pain
Otorrhoea
Tenderness in mastoid antrum
Oedema and sagging of external auditory canal

12. ACUTE MASTOIDITIS(cont.)
PATHOLOGY: Two main pathological processes are
responsible:
1. Production of pus under tension.
2. Hyperaemic decalcification and
osteoclastic resorption of bony walls.
Both these processes combine to cause destruction and
coalescence of mastoid air cells, converting them
into a single irregular cavity filled with pus
(empyema of mastoid).
Pus may break through mastoid cortex leading to
subperiosteal abscess which may even burst on
surface leading to a discharging fistula

13. ACUTE MASTOIDITIS(cont.)
SIGNS:
• Mastoid tenderness: Tenderness should always be
compared with that of the healthy side
• Ear discharge. Mucopurulent or purulent discharge,
often pulsatile (LIGHT-HOUSE EFFECT).
• Sagging of posterosuperior meatal wall. It is due to
periostitis of bony party wall between the antrum and
deeper posterosuperior part of bony canal.
• Perforation of tympanic membrane. Perforation may
sometimes appear as a nipple-like protrusion.
Sometimes, tympanic membrane is intact but dull and
opaque especially in those who have received
inadequate antibiotics.

14. ACUTE MASTOIDITIS(cont.)
SIGNS:
• Swelling over the mastoid. Initially, there is oedema of
periosteum, imparting a smooth “ironed out” feel over
the mastoid. Later retroauricular sulcus becomes
obliterated and pinna is pushed forwards and
downwards. Pus may burst through bony cortex, a
subperiosteal fluctuant abscess is formed which may
further burst on skin or form a fistula.
• Hearing loss. Conductive type of hearing loss is always
present.
• General findings. Patient appears ill and toxic with
lowgrade fever. In children, fever is high with a rise in
pulse rate.

15. ACUTE MASTOIDITIS(cont.)
DIFFERENTIAL DIAGNOSIS:
1. Suppuration of Mastoid Lymph Nodes: No history
of preceding otitis media, usually superficial.
2. Furunculosis of Meatus: Absence of preceding
otitis media. Painful movements of pinna. Swelling
of meatus is confined to the cartilaginous part
only. Discharge is never mucoid or mucopurulent.
An absolutely normal looking tympanic
membrane. X-ray mastoid with clear air-cell system
3. Infected Sebaceous Cyst

16. MASKED MASTOIDITIS
• Slow destruction of mastoid air cells
• Acute sign and symptoms of acute mastoiditis are
absent
• In this condition, cells of mastoid coalesce into larger
cavities filled with pus under pressure. Septa of cells
demineralize and disappear leading to large pockets of
pus in mastoid antrum. Condition is treated as any
other mastoiditis.
• Aetiology: The condition often results from inadequate
antibiotic therapy in terms of dose, frequency and
duration of administration.

17. MASKED MASTOIDITIS(cont.)
Clinical Features:
Patient is often a child, not entirely feeling well, with
mild pain behind the ear.
Tympanic membrane appears thick with loss of
translucency.
Slight tenderness may be elicited over the mastoid.
Audiometry shows conductive hearing loss.
X-ray of mastoid will reveal clouding of air cells with
loss of cell outline.

18. MANAGEMENT OF MASTOIDITIS
• Hospitalization of the Patient
• Antibiotics: Specific antimicrobial is started
• Myringotomy. When pus is under tension it is relieved
by wide myringotomy.
• Cortical Mastoidectomy. It is indicated when there is:
(a) Subperiosteal abscess.
(b) Sagging of postero superior meatal wall.
(c) Positive reservoir sign,
(d) No change in condition of patient or it worsens in
spite of adequate medical treatment for 48 h.
(e) Mastoiditis, leading to complications, e.g. labyrinthitis,
facial paralysis, intracranial complications, etc.

19. ABSCESS IN RELATION TO MASTOID
• POSTAURICULAR ABSCESS
• ZYGOMATIC ABSCESS
• BEZOLD ABSCESS
• CITELLI’S ABSCESS
• MEATAL ABSCESS / LUC’S ABSCESS
• PARAPHARYNGEAL / RETROPHARYNGEAL ABSCESS

20. ABSCESS IN RELATION TO MASTOID
(A) Abscesses in relation to mastoid: (1) Postauricular,
(2) Zygomatic and (3) Bezold abscess.
(B) Citelli, Postauricular and Bezold abscesses seen
from behind.

21. POSTAURICULAR ABSCESS
• Commonest abscess that forms over the mastoid.
• Pinna is displaced forwards, outwards and
downwards.
• In infants and children, abscess forms over the
MacEwen’s triangle; pus in these cases travels
along the vascular channels of lamina cribrosa.

22. ZYGOMATIC ABSCESS
• It occurs due to infection of zygomatic air cells
situated at the posterior root of zygoma.
• Swelling appears in front of and above the pinna.
• There is associated
oedema of the upper eyelid.
• In these cases, pus collects either
superficial or deep to the
temporalis muscle.

23. BEZOLD ABSCESS
• Pus bursts through the medial side of the tip of
mastoid and collects under the sternomastoid or
digastric triangle.

24. BEZOLD ABSCESS (cont.)
• It can occur following acute coalescent mastoiditis.
• The abscess may lie deep to
(i)sternocleidomastoid, pushing the muscle
outwards,
(ii) follow the posterior belly of digastric and
present as a swelling between the tip of
mastoid and angle of jaw,
(iii) be present in upper part of posterior
triangle,
(iv) reach the parapharyngeal space or
(v) track down along the carotid vessels

25. BEZOLD ABSCESS (cont.)
CLINICAL FEATURES: Onset is sudden.
There is pain, fever,
Tender swelling in the neck
Torticollis.
History of purulent otorrhoea
DIFFERENTIAL DIAGNOSIS:
(a) Acute upper jugular lymphadenitis.
(b) Abscess/mass in the lower part of the
parotid gland.
(c) An infected branchial cyst.
(d) Parapharyngeal abscess.
(e) Jugular vein thrombosis.

26. MEATAL ABSCESS ( LUC’S ABSCESS)
• In 1913 Henri Luc first described the subperiosteal
temporal abscess as a complication of AOM.
• It develops after spread of infection directly along
a subperiosteal route from the middle ear along
the external meatus to reach the temporal region.
• Swelling is seen in deep part of bony meatus.
• Abscess may burst into the meatus.

27. CITELLI’S ABSCESS
• Formed due to draining of pus from mastoid tip
to the Diagastric Triangle.
• Formed behind the
mastoid in the occipital
region

28. PARAPHARYNGEAL/RETROPHARYNGEAL
ABSCESS
• This results from infection of the peritubal cells
due to acute coalescent mastoiditis.

29. MANAGEMENT OF ABSCRSSES
• CT a computed tomography scan of the
mastoid and neck swelling may establish the
diagnosis
• Cortical mastoidectomy for coalescent
mastoiditis
• Drainage of neck abscess
• Administeration of intravenous antibiotics

30. PETROSITIS/GRADENIGO'S SYNDROME
In 1904 the syndrome was introduced by Giuseppe Gradenigo
It is also called Gradenigo-Lannois syndrome.
It is due to petrous apicitis which is a complication of otitis media and
mastoiditis involving the apex of the petrous temporal bone.
SYMPTOMS: Triad of symptoms consisting of
1) Periorbital unilateral pain related to Trigeminal nerve involvement,
2) Diplopia due to inflammation of the Abducens nerve in Dorello’s
canal
3) Persistent otorrhea, associated with bacterial otitis media with apex
involvement of the petrous part of the temporal bone
(petrositis).
 Other symptoms can include photophobia, excessive lacrimation, fever, vomiting and
reduced corneal sensitivity.

31. GRADENIGO'S SYNDROME(cont)
 The retroorbital or periauricular pain is due to inflammation/irritation
of the first (ophthalmic) division of the trigeminal nerve
 Lateral rectus palsy due to Abducens nerve palsy leads to horizontal
diplopia
 Sometimes there can be transient weakness of ipsilateral Facial Nerve.
 The classical syndrome related to otitis media has become very rare
after the antibiotic era.
MANAGEMENT:
• High resonance computed tomography
• I/V antibiotics
• Mastoid exploration: Cortical, radical or modified radical mastoidectomy.
• Exeneration of the cell tracts leading to petrous apex

33. LABYRINTHITIS
• Inflammation of the labyrinth is called
labyrinthitis.
• In chronic suppurative otitis media, cholesteatoma
may cause erosion of the otic capsule/semicircular
canals, usually of the lateral semicircular canal or
the stapes footplate and promontory, by the
action of enzymes associated with it. Thus
exposing the labyrinth to the infective process
which leads to Inflammation of the labyrinth.

34. LABYRINTHITIS(cont.)
• It may result from the following:
 Acute suppurative otitis media
 After stapedectomy, removal of polypi or
granulations arising from the promontory
Through preformed pathways
Fracture lines
• There are two types of labyrinthitis:
1. Localized or circumscribed.
2. Diffuse type: • Serous labyrinthitis
• Suppurative labyrinthitis.

35. LABYRINTHITIS(cont.)
LOCALIZED LABYRINTHITIS:
• It is a type of fistula of the labyrinth.
• There is localized erosion of bony labyrinth exposing the
membranous labyrinth.
CAUSES:
• Cholesteatoma causing erosion of lateral semicircular canal
(SCC) or foot plate of stapes.
• Middle ear neoplasms: carcinoma or glomus tumors.
• Accidental or surgical injuries.
• Syphilis, tuberculosis, osteomyelitis.
• Auto immune–Cogan’s disease.

36. LOCALIZED LABYRINTHITIS(cont.)
CLINICAL FEATURES:
• Vertigo- Patient complains of transient vertigo often
induced by pressure on tragus, cleaning the ear
or while performing Valsalva manoeuvre.
• Fistula test becomes positive due to exposure of
membranous labyrinth. It can be elicited by
Pressure on tragus/Siegel’s speculum
• The quick component of nystagmus would be
towards the affected ear(ampullopetal
displacement of cupula).
• Features of CSOM are present

37. LOCALIZED LABYRINTHITIS(cont.)
TREATMENT:
• Systemic antibiotic therapy
• Antivertiginous drugs such as cinnarizine 25 mg or
betahistine (vertin) 16 mg three times a day
• Mastoid exploration is done to eliminate the cause.
• After control of acute phase vestibular head exercises are
given.

38. LABYRINTHITIS(cont.)
SEROUS LABYRINTHITIS:
It is a diffuse inflammation of the labyrinth without pus
formation and is a reversible condition.
CAUSES:
• May follow localized labyrinthitis, associated with chronic
middle ear suppuration or cholesteatoma
• After acute inflammation of middle ear.
• May be seen after stapedectomy orfenestration operation.

39. SEROUS LABYRINTHITIS(cont.)
CLINICAL FEATURES:
• Mild cases complain of vertigo and nausea
• in severe cases, vertigo is worse with marked nausea,
vomiting and even spontaneous nystagmus. Quick
component of nystagmus is towards the affected ear.
• Some degree of sensorineural hearing loss (SNHL) may be
present as cochlea is also affected.
• If not treated, may pass onto suppurative labyrinthitis
with total loss of vestibular and cochlear function.

40. SEROUS LABYRINTHITIS(cont.)
TREATMENT:
• Medical treatment:
 Complete bed rest with affected ear upwards
 Antibacterial therapy is given to control infection.
 Labyrinthine sedatives-stemetil/cinnarizine/betahistine.
• Surgical treatment:
 Myringotomy if it follows ASOM
 Cortical mastoidectomy if after ASOM
 Modified radical mastoidectomy if with cholesteatoma

41. LABYRINTHITIS(cont.)
SUPPURATIVE LABYRINTHITIS:
This is diffuse pyogenic infection of the labyrinth with
permanent loss of vestibular and cochlear functions
CAUSES:
• May be seen after serous labyrinthitis
• Infection through pathological/surgically created windows.
BACTERIOLOGY: B. hemolytic-streptococci
Pneumococci
Haemophillus
Proteus
Pseudomonas & Staphylococci.

42. SUPPURATIVE LABYRINTHITIS(cont.)
CLINICAL FEATURES:
• Severe vertigo with nausea and vomiting due to acute
vestibular failure.
• Spontaneous nystagmus to the healthy side
• There is total loss of hearing.
• Patient is markedly toxic & lies curled up in bed on
healthy side.
• Headache, fever or pain does not occur from a labyrinth
filled with pus because pus is scanty and its
absorption in systemic circulation is not possible due
to intact labyrinth capsule.

43. SUPPURATIVE LABYRINTHITIS(cont.)
TREATMENT:
• It is same as for serous labyrinthitis.
• Rarely, drainage of the labyrinth is required. It is done if
intralabyrinthine suppuration is acting as a source of
intracranial complications, e.g. meningitis or brain
abscess.
• Labyrinthectomy is rarely done when there is total loss of
labyrinth function
• Labyrinth (SCC) is drained by entering above the horizontal
part of facial nerve.
• Cochlea and saccule are drained by entering below the
facial canal.

44. FACIAL NERVE PARALYSIS
• It can occur as a complication of both acute and
chronic otitis media.
• In ASOM, if bony canal wall of facial nerve is
dehiscent and nerve lies under mucosa,
inflammation may spread to epi- and perineurium
causing facial nerve palsy.
• In CSOM, palsy occurs due to cholesteatoma or
granulation tissue, causing destruction of bony wall
and pressure on the nerve with inflammation
leading to slowly progressive palsy.

45. FACIAL NERVE PARALYSIS(cont.)

46. FACIAL NERVE PARALYSIS(cont.)
CLINICAL FEATURES:
• Features will be of acute or chronic SOM with
facial nerve palsy such as
Inability to close the eye
Inability to blow
Loss of wrinkles on the face and forehead
• Facial nerve function fully recovers if acute otitis
media is controlled with systemic antibiotics.
• In CSOM, facial paralysis is insidious but slowly
progressive.

47. FACIAL NERVE PARALYSIS(cont.)
TREATMENT:
• In ASOM cases antibiotics and anti-inflammatory drugs.
Patient may require myringotomy or cortical
mastoidectomy operation.
• In CSOM leading to VII nerve palsy, exploration of mastoid
for removal of cholesteatoma and decompression of
nerve in the facial canal.
• Granulation tissue surrounding the nerve is removed but if
it actually invades the nerve sheath, it is left in place.
• If a segment of the nerve has been destroyed by the
granulation tissue, resection of nerve and grafting are
better left to a second stage when infection has been
controlled and fibrosis has matured.

48. OSTEOMYELITIS OF TEMPORAL BONE
It is not very common
complication and occurs when infection spreads
to the marrow spaces of temporal bone.

49. SEPTICEMIA OR PYEMIA
It may occur as a complication of
acute or chronic SOM, if treatment is not taken
for a long time and the virulence of organism is
high or patient has a poor resistance.

50. OTOGENIC TETANUS
• Very rare
• It follows unhygienic cleaning of the ear or
bathing in infected water and in cases where
there has been no immunization.
• The treatment is same as for tetanus by injection
of antitetanic serum and antibiotics besides
general measures