2. COMPLICATIONS
OF
SUPPURATIVE OTITIS MEDIA
By:
SIDRA NAWAZ

3. INTRODUCTION:
• A complication of otitis media is defined as
a spread of infection beyond the
pneumatized area of the temporal bone
and the associated mucosa.
• Though there is a general decline in the
incidence of complications, they are still
frequently seen in our country.

4. FACTORS INFLUENCING DEVELOPMENT
OF COMPLICATION
1. Age:
 First decade of life.
 Elderly when patient’s
resistance is low.
1. Poor Socio-economic Group:
 Over crowding.
 Poor health education.
 Poor personal hygiene.
 Limited access to health
care.

5. 3. Virulence Of Organisms:
 Streptococcus pneumoniae
type III.
 Haemophilus influenzae.
 Pseudomonas aeruginosa.
 Staphylococcus aureus.
3. Immune-Compromised Host:
 AIDS.
 Uncontrolled diabetes.
 Transplant ptients receiving
immunosuppressive drugs.
 Cancer patients receiving
chemotherapy.

6. 5. Preformed Pathways:
 Dehiscence of bony
facial canal.
 Previous ear surgery.
 Fracture of temporal
bone.
 Stapedectomy.
 Perilymph fistula.
 Congenitally enlarged
aqueduct of vestibule.
 Dehiscence in the
floor of middle ear.

7. 6. Cholesteatoma:
 Osteitis or granulation tissue in chronic otitis media
destroy the bone and help infection penetrate deeper.

8. PATHWAYS OF SPREAD OF INFECTION
1. Direct Bone Erosion:
 In acute infections;
 Process of hyperaemic
decalcification.
 In chronic infection;
 Osteitis.
 Erosion by cholesteatoma.
 Erosion by granulation
tissue.

9. 2. Venous Thrombophlebitis:
 Infection from the mastoid
bone can cause;
 Thrombophlebitis of
venous sinuses.
 Cortical vein thrombosis

10. 3. Preformed Pathways:
 Congenital dehiscences.
 e.g. in boby facial canal floor of middle ear over
the jugular bulb.
 Patent sutures.
 e.g. petrosquamous sutures.
 Previous skull fractures. The fracture sites heal only
by fibrous scar which permits infection.
 Surgical defects.
 e.g. stapedectomy, fenestration and
mastoidectomy with exposure of dura.
 Oval and round windows.
 Infection from labryinth can travel along internal
acoustic meatus, aqueducts of the vastibule and that
of the cochlea to the meninges.

11. CLASSIFICATION

13. INTRATEMPORAL
COMPLICATIONS
OF
OTITIS MEDIA

14. MASTOIDITIS
 The term Mastoiditis is used when infection spreads
from the mucosa, lining the mastoid air cells, to involve
bony walls of the mastoid air cell system.
Types Of Mastoiditis:
 Acute Mastoiditis
 Masked (Latent) Mastoiditis

15. ACUTE MASTOIDITIS
 Inflammation of mucosal lining of antrum and mastoid air
cell system.

16. Aetiology:
 Acute suppurative otitis media.
 High virulence of organisms.
 Lowered resistance of patient.
 Due to;
• Measles.
• Exanthematous Fevers.
• Poor nutrition.
• Diabetes.
Causative Organisms:
 Beta-Haemolytic Streptococcus
(most common).

17. PATHOLOGY:
 Two main pathological processes are responsible:
 Production of pus under tension.
• Extension of inflammatory process to mucoperiosteal lining of
air cell system increases the amount of pus produced due to
large surface area involve.
 Hyperaemic decalcification and osteoclastic
resorption of bony walls.
• Hyperaemia and engorgement of mucosa causes dissolution of
calcium from the bony walls of the mastoid air cells
(hyperaemic decalcification).
 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).

18. CLINICAL FEATURES:
Symptoms:
 Pain behind the ear.
 Fever.
 Ear discharge
( profuse and
increase in
purulence).

19. Signs:
 Mastoid tenderness.
 Ear discharge (Mucopurulent or purulent discharge) .
 Sagging of posterosuperior meatal wall.
 Perforation of tympanic membrane.
 Swelling over the mastoid.
 Hearing loss.
 General findings;
 Patient appears ill.
 Low grade fever.
 In children, high fever with a rise in pulse rate.

20. INVESTIGATIONS:
 Blood counts:
 Shows polymorphonuclear
leucocytosis.
 ESR:
 Usually raised.
 X-Ray mastoid:
 Clouding of air cells due to
collection of exudate in
them.
 Ear swab:
 For culture and sensitivity.

21. DIFFERENTIAL DIAGNOSIS:
 Suppuration of mastoid lymph nodes.
 Furunculosis of meatus.
 It is differentiated from acute mastoiditis by;
• Absence of preceding acute otitis media.
• Painful movements of pinna.
• Swelling of meatus is confined to cartilaginous part only.
• Discharge is never mucoid or mucopurulent.
• Enlargement of pre or postauricular lymphnodes.
• Mild conductive hearing loss.
• Normal looking tympanic membrane.
• X-Ray mastoid with clear air-cell system.
 Infected sebaceous cyst.

22. TREATMENT:
 MEDICAL:
 Hospitalization of
the patient.
 Antibiotics.
 Amoxicillin or
Ampicillin.
 Chloramphenicol
or Metronidazole.

23.  SURGICAL:
 Myringotomy.
 Cortical mastoidectomy.
 It is indicated when there is;
• Subperiosteal abscess.
• Sagging of
posterosuperior meatal
wall.
• Positive reservoir sign.
• No change or worsen
condition of patient .
• Complication of
mastoiditis.

24. COMPLICATIONS OF ACUTE
MASTOIDITIS
 Subperiosteal abscess.
 Labyrinthitis.
 Facial paralysis.
 Petrositis.
 Extradural abscess.
 Meningitis.
 Brain abcess.
 Lateral sinus
thrombophlebitis.
 Otitic hydrocephalous.

25. ABSCESS IN RELATION TO MASTOID
INFECTION
 Postauricular Abscess:
 Commonest abscess.
 Forms over mastoid.
 Pinna is displaced
forwards, outwards and
downwards.
 In infants and children;
forms over the
MacEwen’s triangle.

26.  Zygomatic Abscess:
 Occurs due to infection of zygomatic
air cells.
 Swelling appears infront and above
the pinna.
 Associated oedema of upper eyelid
also present.
 Pus collects either superficial or deep
to the temporalis muscle.
 Meatal Abscess(Luc’s Abcess):
 Pus breaks through the bony wall
between the antrum and external
oseous meatus.
 Swelling is seen in deep part of bony
meatus.
 Abscess may burst into the meatus.

27.  Behind The Mastoid(Citelli’s
Abscess):
 Abscess is formed behind
the mastoid more towards
the occipital bone.
 Parapharyngeal or
retropharyngeal abscess:
 This results from infection
of the peritubal cells due to
acute coalescent
mastoiditis.

28.  Bezold Abscess:
 Occur following acute
coalescent mastoiditis .
 Pus breaks through the thin
medial side of the tip of the
mastoid and presents as a
swelling in the upper part of
neck.

29. MASKED (LATENT) MASTOIDITIS
 It is a condition of slow destruction of mastoid air cells
but without the acute signs and symptoms often seen in
acute mastoiditis.
Aetiology:
 Inadequate antibiotic therapy.
 Use of oral penicillin;
 given in cases of acute otitis media
when acute sypmtoms subsides but
smouldering infection continues in the
mastoid.

30. CLINICAL FEATURES:
 Mild pain behind the ear.
 Persistent hearing loss.
 Tympanic membrane appear thick
with loss of translucency.
INVESTIGATIONS:
 Audiometry:
 Shows conductive hearing loss.
 X-ray mastoid:
 Reveal clouding of air cells with
loss of cell outline.
TREATMENT:
 Surgical:
 Cortical mastoidectomy.

31. PETROSITIS
 Spread of infection from middle ear and mastoid to the
petrous part of temporal is called Petrositis.

32. PATHOLOGY:
 Petrous bone may be
of three types:
 Pneumatised with air
cells extending to the
petrous apex.
 Diploic containing only
marrow space.
 Sclerotic.

33.  Usually two cell tracts are recognized:
 Posterosuperior tract which starts in the mastoid and
runs behind or above the bony labyrinth to the petrous
apex.
 Anteroinferior tract which starts at the hypotympanum
near the eustachian tube runs around the cochlea to
reach the petrous apex.
CLINICAL FEATURES:
 Gradenigo’s syndrome:
 Consist of a triad;
• External rectus palsy.
• Deep-seated ear or
retro-orbital pain.
• Persistent ear
discharge.

34.  Other symptoms;
 Fever.
 Headache.
 Vomiting.
 Neck rigidity.
INVESTIGATIONS:
 CT Scan of temporal bone:
 Show bony details of petrous
apex and air cells
 MRI
 Differentiate diploic marrow
containing apex from fluid or
pus

35. TREATMENT:
 Suitable intravenous antibacterial
therapy.
 Surgical:
 Cortical, modified radical or
radical mastoidectomy.

36. FACIAL PARALYSIS
 It can occur as a complication of both acute and chronic
otitis media.

37. AS COMPLICATION OF
ACUTE OTITIS MEDIA
 Dehiscent of bony canal spread the inflammation of
middle ear to epi- and peri-neurium, causes facial
paralysis,
 Facial nerve function is fully recovers if acute otitis media
is controlled with systemic antibiotics.
 Myringotomy or cortical mastoidectomy may sometime
required.

38. AS COMPLICATION OF
CHRONIC OTITIS MEDIA
 Facial paralysis results from cholesteatoma or from
penetrating granulation tissue.
 Cholestatoma destroys bony canal and then cause
pressure on nerve.
 Treatment is urgent exploration of the middle ear and
mastoid.

39. LABYRINTHITIS
 Labyrinthitis is an inflammation of the inner ear that is
often a complication of infection of the middle ear (
otitis media ). It is usually caused by the spread of
bacterial or viral infections from the head or respiratory
tract into the inner ear.
TYPES OF LABYRINTHITIS:
 There are three types of labyrinthitis:
 Circumscribed Labyrinthitis.
 Diffuse Serous Labyrinthitis.
 Diffuse Suppurative Labyrinthitis.

40. Circumscribed Labyrinthitis
(Fistula of Labyrinth)
 There is thinning or erosion
of bony capsule of labyrinth,
usually of the horizontal
semicircular canal.
Aetiology:
 Chronic suppurative otitis
media with cholesteatome.
(most common)
 Neoplasms of middle ear
e.g. carcinoma or glomus
tumour.
 Surgical or accidental
trauma to labyrinth.

41. Clinical Features:
 Transient vertigo induced by
pressure.
Diagnosis:
 It is diagnosed by “Fistula test”
which can be performed in two
ways;
 Pressure on tragus.
• Sudden inward pressure applied on
tragus.
• Air pressure increase and stimulate
the labyrinth.
• Patient complain of vertigo.
• Nystagmus may also be induced.

42.  Siegle’s speclum.
• Positive pressure is applied to
ear canal.
• Patient complains of vertigo
usually with nystagmus.
• Quick component of nystagmus
would be toward affected ear
(ampullopetal displacement of
cupula).
Treatment:
 Mastoid exploration is often
required in chronic otitis media
and lasteatoma.
 Systemic antibiotic therapy.

43. Diffuse Serous Labyrinthitis
 It is diffuse intralabyrinthine inflammation without pus
formation and is a reversible condition if treated early.
Aetiology:
 Pre-existing circumscribed labyrinthitis associated
with chronic middle suppuration or cholesteatoma.
 In acute infections of middle ear, cleft inflammation
spreads through annular ligament or the round
window.
 It can follow stapedectomy or fenestration operation.

44. Clinical Features:
 Vertigo.
 Nausea.
 Vomiting.
 Spontaneous
nystagmus.
 Sensorineural hearing
loss.
 Suppurative
labyrinthitis.
 Loss of vestibular and
cochlear function.

45. Treatment:
 Medical:
 Bed rest.
 Antibacterial therapy.
 Labyrinthine sedatives.
• Prochloperazine (stemetil).
• Dimenhydrinate
(Dramamine).
 Myringotomy
 Surgical:
 Cortical mastoidectomy.

46. Diffuse Suppurative Labyrinthitis
 This is diffuse pyogenic infection of the labyrinth with
permanent loss of vestibular and cochlear function.
Aetiology:
 Serous labyrinthitis.
 Pyogenic organism invading through surgical or pathalogical fistula .
Clinical Features:
 Severe vertigo.
 Nausea and vomiting
 Spontaneous nystagmus.
 Total loss of hearing.
Treatment:
 Same as for serous labyrinthitis.

47. INTRACRANIAL
COMPLICATIONS
OF
OTITIS MEDIA

48. EXTRADURAL ABSCESS
 It is a collection of pus between bone and dura.
 It may occur both in acute and chronic infection of middle
ear.

49. PATHOLOGY:
 In acute otitis media, bone over the dura is destroyed by
hyperaemic decalcification.
 In chronic otitis media it is destroyed by cholesteatoma.
 In such cases, the pus come in direct contact of dura.
 Infection can be spread by venous thrombophlebitis. In
this case bone over dura remain intact.
 Affected dura may be covered with granulations or
appear unhealthy and discoloured.

50. CLINICAL FEATURES:
 Persistent headache.
 Severe pain in the ear.
 General malaise with low
grade fever.
 Pulsatile purulent ear
disscharge.
 Disappearance of headache
with free flow of pus from
the ear (Spontaneous
abscess drainage).

51. DIAGNOSIS:
 CT Scan.
 MRI.

52. TREATMENT:
 Cortical or modified radical or radical mastoidectomy.
 An antibiotic cover.

53. SUBDURAL ABSCESS
 This is collection of pus between dura and archnoid.

54. PATHOLOGY:
 Infection spreads from the ear by erosion of bone and
dura or by thrombophlebitic process in which case
intervening bone remains intact.
 Pus rapidly spreads in subdural space and comes to lie
against the convex surface of cerebral hemisphere
causing pressure symptoms.

55. CLINICAL FEATURES:
 Meningeal irritation.
 Headache.
 Fever(102 F or more)
 Malaise.
 Increasing drowsiness.
 Neck rigidity.
 Positive Kernig’s sign.
 Cortical venous thrombophlebitis.
 Veins over the cerebral hemisphere undergo thrombophlebitis leading
to aphasia, hemiplegia, hemianopia.
 Raised intracranial tension.
 Papilloedema.
 Ptosis.
 Dilated pupil.

56. DIAGNOSIS:
 CT Scan.
 MRI.

57. TREATMENT:
 Craniotomy.
 To drain subdural
empyema.
 Intravenous antibiotics.
 To control the
infection.

58. MENINGITIS
 It is inflammation of leptomeninges (pia and archnoid)
usually with bacterial invasion of CSF in subarachnoid
space.

59. MODE OF INFECTION:
 In infants and children;
 Blood borne infection.
 In adults;
 Follows chronic ear
disease.
 Spreads by bone erosion
or retrograde
thrombophlebitis.
 It may associated later
with; extradural abscess
or granulation tissue.

60. CLINICAL FEATURES:
 Fever (102-104F) often with
rigors and chills.
 Headache
 Neck rigidity
 Photophobia.
 Mental irritiablity.
 Nausea.
 Vomiting (Projectile).
 Drowsiness may progress to
delirium or coma.
 Cranial nerve palsies and
hemiplegia.

61. ON EXAMINATION:
 Neck rigidity.
 Positive Kerning’s Sign.
 Positive Brudzinki’s sign.
 Tendon reflexes.
 Exaggerated initially.
 Later become sluggish.
 Papilloedema( seen in late
stages).

62. DIAGNOSIS:
 CT Scan.
 MRI
 Lumbar puncture.
 CSF Examination.
 CSF is turbid.
 Cell count is raised.

63. TREATMENT:
 Medical:
 Antimicrobial therapy.
 Surgical:
 Myringotomy.
 Cortical mastoidectomy.

64. OTOGENIC BRAIN ABSCESS
 In adults;
 75 % of brain abscesses.
 Follows chronic
suppurative otitis media
with cholesteatoma.
 In children;
 25% of brain abscesses.
 Follows acute otitis
media.

65. ROUTE OF INFECTION:
 Direct extension of middle ear infection through tegmen
or by retrograde thrombophlebitis.
 Direct extension through the Trautmann’s triangle or by
retrograde thrombophlebitis.
 Often associated with;
 Extradural abscess.
 Perisinus abscess.
 Sigmoid sinus thrombophlebitis or labyrinthitis.

66. BACTERIOLOGY:
 Aerobic includes,
 Streptococcus pnemoniae.
 Streptococcus
haemolyticus.
 Proteus mirabilis.
 Esch coli.
 Ps. Aeruginosa.
 Anaerobic includes,
 Peptostreptococcus.
 Bacteroides fragilis.
 H.influenzae.

67. PATHOLOGY:
 Brain abscess develops
through four stages;
 Stage of invasion(initial
encephalitis).
 Stage of localisation(latent
abscess).
 Stage of
enlargement(manifest
abscess).
 Stage of termination
(rupture of abscess).

68.  Stage of invasion (initial encephalitis)
 Patient may have
headache.
 Low-grade fever
 Malaise.
 Drowsiness.

69.  Stage of localization (latent abscess)
 No symptoms.
 Stage may last for
several weeks.

70.  Stage of enlargement (manifest abscess)
 Abscess begins to enlarge.
 A zone of oedema appears
around the abscess.
 Clinical features at this stage
are due to:
• Raised intracranial tension.
• Disturbance of function in
the cerebrum or
cerebellum, causing focal
symptoms and signs.

71.  Stage of termination(rupture of abscess)
• Expanding abscess
ruptures into the
ventricle or
subarachnoid space
resulting in fatal
meningitis.

72. CLINICAL FEATURES:
 Clinical features can be
devided into :
 Those due to raised
intracranial tenssion.
 Those due to area of
brain affected
(localising features).

73. Symptoms and signs of raised
intracranial tension:
 Headache.
 Often severe and generalised.
 Nausea.
 Vomiting.
 Projectile in nature.
 Level of consciousness.
 Lethargy Drowsiness Confusion Stupor
Coma.
 Papilloedema.(Appears Late).
 Slow pulse.
 Subnormal temperature.

74. Localising features:
 Temporal lobe abscess.
 Nominal aphasia.
 Homonymous hemianopia.
 Contralateral motor paralysis.
 Epileptic fits.
 Pupillary changes and oculomotor
palsy.
 Cerebellar abscess
 Headache
 Spontaneous nystagmus
 Ipsilateral hypotonia and
weakness.
 Ipsilateral ataxia.
 Past pointing and intention tremor.
 Dysdiadokokinesia.

75. INVESTIGATIONS:
 Skull X-rays.
 Midline shift.
 If pineal gland is calcified.
 Reveals gas in the abscess cavity.
 CT Scan.
 Site and size of an abscess.
 Reveals associated complications.
 X-Ray mastoids or CT scan of
temporal bone.
 Evaluate associated ear disease.
 Lumbar puncture.
 Rise in pressure of CSF.
 Increase protein content .
 Normal glucose level.
 CSF contains polymorphs or lymphocytes.

76. TREATMENT:
 Medical.
 Chloramphenicol.
 Cephalosporins third generation.
 Aminoglycoside antibiotic.
 Dexamethasone/ Mannitol (to
lower the intracranial tension).
 Neurosurgical.
 Repeated aspiration through a
burr hole.
 Excision of abscess.
 Open incision of the abscess and
evacuation of puss.
 Otologic.
 Treatment of associated ear
disease.

77. LATERAL SINUS THROMBOPHLEBITIS
(Syn. Sigmoid Sinus Thrombosis)
 It is an inflammation of inner wall of lateral venous sinus
with formation of a thrombus.

78. AETIOLOGY:
 Complication of acute
coalescent mastoiditis.
 Complication of masked
mastoiditis.
 Complication of chronic
suppuration of middle ear.
 Cholesteatoma.

79. PATHOLOGY:
 The pathological process can be divided into the
following stages.
 Formation of perisinus abscess.
 Endophlebitis and mural thrombus formation.
 Obliteration of sinus lumen and intrasinus abscess.
 Extension of thrombus.

80. BACTERIOLOGY:
 In acute infection;
 Hemolytic streptococcus.
 Pneumococcus.
 Staphylococcus.
 In chronic infection with cholesteatomas;
 B. proteus.
 Ps.pyocyaneus.
 Esch. Coli.
 Staphylococci.

81. CLINICAL FEATURE:
 Hectic Picket-fence type of
fever with rigors.
 Headache.
 Progressive anaemia and
emaciation.
 Tobey-Ayer test.
 To record CSF pressure by
manometer.
 To see the effect of manual
compression of one or both
jugular vein
.

82.  Papilloedema.
 Griesinger’s sign.
 due to thrombosis of
mastoid emissary vein.
 Oedema appears over the
posterior part of mastoid.
 Crowe Beck test.
 Pressure on jugular vein of
healthy side produces
engorgement of retinal
veins and supraorbital
veins.
 Engorgement of veins
subside on release of
pressure.
 Tenderness along jugular
vein.

83. INVESTIGATIONS:
 Blood smear.
 To rule out malaria.
 Blood culture.
 To find causative organism.
 CSF examination.
 CSF is normal except of rise in
pressure.
 To exclude meningitis.
 X-ray mastoids.
 Clouding of air cells (acute
mastoiditis.
 Destruction of bone
(Cholesteatoma).
 Culture and sensitivity of ear
swab.

84.  Imaging studies.
 CT Scan
• Show sinus thrombosis by
typical delta sign.
 MRI
• Better delineates
thrombus.
 MR venography.
• To assess progression or
resolution of thrombus.

85. TREATMENT:
 Intravenous antibacterial
therapy.
 Mastoidectomy and
exposure of sinus.
 Ligation of internal jugular
vein.
 Rarely required.
 Indicated when failure of
treatment to control embolic
phenomenon and rigors or
tenderness and swelling along
jugular vein is spreading.

86.  Anticoagulant therapy.
 Rarely required.
 Used when thrombosis is
extending to cavernous sinus.
 Supportive treatment.
 Repeated blood transfusion.

87. OTITIC HYDROCEPHALUS
 It is characterised by raised intracranial pressure with
normal CSF finding. It is seen in children and adolscents
with acute or chronic middle ear infection.

88. MECHANISM:
 Lateral sinus thrombosis accompanying middle ear
infection causes obstruction to venous return.
 If thrombosis extends to superior sagittal sinus, it will
also impede the function of arachnoid villi to absorb CSF.
 Both these factors result in raised intracranial tension.

89. CLINICAL FEATURES
 Symptoms:
 Severe headache.
 Nausea.
 Vomiting.
 Diplopia due to paralysis of Vith
cranial nerve.
 Blurring of vision due to
papilloedema or optic atrophy.
 Signs:
 Papilloedema may be 5-6 diopters.
 Nystagmus due to raised intracranial tension.
 Lumber puncture. CSF pressure exceeds 300mm of water
(normal70-120mm H2O)

90. TREATMENT:
 Medical:
 Acetazolamide.
 Corticosteroids.
 Repeated lumber
puncture.
 Placement of a lumbar
drain.
 Middle ear infection
may require antibiotic.