summary of complications of mastoiditis. presented in academic meeting at ELHC, SA

1. Complications of mastoiditis
Sarita pandey

2. introduction
• Mastoid process is an inferior extension of the petrous temporal bone
• Provides a structural function as an anchor point for large muscles of
the neck
• Contains multiple air cells that develop from single main cavity
(antrum)
• In X section is has a honey comb appearance

3. Mastoid process • Sternocleidomastoid
• Splenius capitus
• Posterior belly of digastric
• Longissimus capitus muscle

4. introduction
• Tympanic cavity of middle ear is in communication with the mastoid
antrum via aditus
• Mastoid air cells are related superiorly to middle cranial fossa and
posteriorly to posterior cranial fossa
• Acute mastoiditis is serious complication of acute OM
• Mastoiditis occurs when supperative infection extends from middle
ear affected by OM to mastoid air cells
• Once mastoiditis sets in it in it self has more complications.

5. Classification of mastoiditis
• Classic or acute Mastoiditis – complication of AOM
• Chronic, latent or masked mastoiditis presents in chronic or
subclinical fashion
• Associated with CSOM or Cholesteatoma

6. Epidemiology
• Acute mastoiditis prior to advent of antibiotics was common
• Developed in 5 – 10% of children with AOM
• Mortality rate 2/100000 children
• Currently 0.12/1000 child per year
• Mortality rate < 0.01/100000
• Estimated that In every 50000 child with AOM 1 child develops
mastoiditis

7. Acute mastoiditis
• Much more common in young children with peak incidence at 6 – 13
months
• Immunocompromised patients more prone to mastoiditis
• Children/adults with intellectual impairment or communication
difficulties thought to be susceptible to mastoiditis
• Pre-existence of cholesteatoma is a known risk factor

8. Infecting organisms
• Streptococcus pneumonia 25% prevalence
• H Influenza
• S. pyognes
• Staphyloccus spp
• Pseudomonas aeruginosa (becoming more common as widespread use of
Abs increases)
• Moraxella Catarrahalis
• Gm neg bact
• Mycobacteria
• Aspergillus & other fungi (immunocompromised patients)

9. Presentation - acute mastoiditis
• History of acute or recurrent episodes of OM
• Otalgia or pain behind ear
• Fever
• Swelling, redness or boggy, tender mass post auricular region
• Irritable infant, with feeding difficulties
• Forward protrusion of external ear, may have fluctuance in the mass
• Ear discharge/ middle ear effusion
•

10. Presentation – chronic mastoiditis
• Presents in a subtle or subclinical fashion after an
episode of AOM
• Recurrent bouts of otalgia and retro- aural pain
• Recurrent headaches
• Febrile episodes
• TM may appear infected or postero-superior retraction/
perforation with pus
• May be no external evidence of peri mastoid
inflammation

11. Investigations:
• FBC – leucocytosis
• Elevated ESR
• Blood cultures
• Pus swab of any pus/ fluid in middle ear
• CT gold standard
• IF intracranial spread suspected LP
• Audiogram once pain under control.

12. Management
• Manage as an IN patient
• To prevent likelihood of complications
• High dose broad spectrum iv antibiotics for at least 48 hours
• Oral antibiotics may be used after 48 hours if clinically improving
• Anti pyretic
• Myringotomy plus grommet as therapeutic and diagnostic procedure

13. Surgical management
• Mastoidectomy
• Mastoid osteitis
• Co –existing cholesteatoma
• Limited improvement after ivi meds

14. Complications of mastoiditis
• Rare due to prompt antibiotic treatment, however with emergence of
resistant organisms – may be higher in future
• Clinically divided into:
• Intratemporal
• Intracranial
• Systemic
• cervical

15. Extension of infection…
• Direct extension through the de-mineralized bone seen in
cholesteatoma
• Haematogenous spread via the veins, through bone and dura to the
venous sinuses.
• Through round or oval window into the auditory meatus on the
vestibular aqueducts
• Dehiscence of bony covering over the jugular bulb or the tegmen
tympani
• Neoplastic or accidental bony erosion
• Through surgical defects in post stapedectomy surgery.

16. Intra - temporal
• Coalescent Mastoiditis
• When mastoid region inflammation cannot be arrested
• Suppuration under pressure causes local acidosis and osseous decalcification,
ischaemia and osteoclastic dissolution of the pneumatic cell walls
• These cells can coalesce into larger cavities filled with purulent exudates and
granulations
• Resulting in empyema & coalescent mastoiditis
• Antonelli et al – concluded that erosion of the cortical plate overlying
the sigmoid sinus was the most sensitive and specific CT scan finding
for distinguishing coalescent vs incipient acute mastoiditis

17. Coalescent mastoiditis
• Spread of the inflammatory debris anteriorly to middle ear via aditus
ad antrum can result in spontaneous resolution if the TM is
perforated
• Infection may spread laterally and produce sub periosteal abscess
• May spread medially to petrous air cells, causing petrositis
• Coalescent mastoiditis is diagnosed when CT demonstrates erosion of
mastoid septa or mastoid walls

18. Coalescent mastoiditis
• Latent mastoiditis (subclinical and often “masked”)
• Indolent temporal bone infection with few clinical symptoms
• Often owing to previous usage of broad spectrum antibiotic to treat Middle
ear disease
• TM is intact and middle ear shows no abnormalities at otoscopy
• Disease progresses silently until an intracranial complication such as venous
Dural thrombosis occurs
• CT diagnostic, demonstrates the temporal bone disease and the intracranial
complication

19. Sub periosteal abscess
• Decalcification of the outer mastoid cortical bone results in abscess
that can extend towards
• Ext auditory canal
• Spread along the zygomatic bone
• Post auricular region

20. Perisinus abscess
• When osteolysis occurs in the
internal mastoid cortex
• Direct apposition of the
inflammatory debris to dura
over the sigmoid sinus
• Resulting in formation of
perisinus and epidural abscess

21. Petrositis
• Petrositis or petrous apicitis – rare complication that theoretically
occurs only in individuals with pneumatized petrous apex
• Patient present with CN VI palsy, deep facial pain and ipsilateral
otorrhoea ( Gradenigo syndrome)
• Facial pain due to focal meningitis over the petrous apex with
irritation of the gasserian ganglion in the Meckel cave
• Abducens nerve involvement occurs at its course through the Dorello
canal
• CT demonstrates erosive changes of the petrous apex with abn
enhancement of adjacent meningitis

23. Other intratemporal complications
• Labyrinthitis
• CN VII palsy
• SNHL
• More common in chronic otitis media with cholesteatoma
• Infection can spread into the labyrinth via the round or oval window
or by direct invasion of the bony labyrinth
• May result in suppurative labyrinthitis
• Suspect when patient with infected ear develops sudden vertigo,
nystagmus and hearing loss

24. Intracranial complications
• Epidural abscess
• Most common intracranial complication
• Results from spread by contiguity following bone destruction in coalescent
mastoiditis
• Can occur in middle cranial fossa
• Posterior cranial fossa is more common
• Due to osseous destruction in the Trautmann triangle over the
sigmoid sinus plate or in the posterior cortex of petrous pyramid
• CT is mandatory for Diagnosis

25. Dural venous thrombophlebitis
• As an result form extradural abscess
• Sigmoid sinus thrombosis as a protective mechanism in attempt to localise
infection
• Thrombus may cause propagation to jugular vein, to other sinuses
• Through emissary veins to subcutaneous tissue
• Diagnosis may be difficult to make on basis of clinical picture alone
• May be completely asymptomatic
• Present as sign of toxaemia, intracranial hpt or hydrocephalus
• Mastoidectomy with surgical exposure of the dura and removal of the
granulation tissue
• Use of anticoagulation and ligation of IJV are controversial

26. Dural venous phlebothrombosis

27. Subdural empyema
• Several veins and veinules in middle normally communicate through
intact bone and dura with vessels in subarachnoid space and brain
parenchyma
• Spread of infection and microorganisms through these veins reach
subdural and subarachnoid space
• Develops in interhemispheric fissure and along the tentorium
cerebelli
• CT = widening of the extra cerebral space with compression of
adjacent sulci
• Loculations within collection common

28. subdural

29. Other intracranial complications
• Meningitis
• Hydrocephalus
• Encephalitis
• Parenchymal cerebral or cerebellar abscesses
• Occurrence in young children by haematogenous dissemination
• Invasive organisms such as H. influenza type B more common
• Neurologic sequalae of MR or SNHL

30. Carotid artery involvement
• Exceptional in the AB era
• Potential life threatening complication
• Internal carotid more likely to be involved
• Due to large no of lymph nodes adherent to ICA
• Spread of infxn from adjacent IJV most likely to be mechanism of
infection

31. • Protracted clinical course
• Recurrent haemorrhage from Throat, nose or ear
• Horner syndrome
• Diagnosis often made at an advanced stage, when patient develops
haemorrhage, pseudo aneurysm or hemiplegia
• MR angiography most helpful and can show features of carotid artery
spasm
• Worst scenario – carotid occlusion /rupture

32. Other Head &Neck complications
• Bezold abscess
• along the medial aspect of mastoid tip up to sheath of SCN
• Citelli’s abscess
• along posterior belly of digastric
• Luc’s abscess
• along the posterior wall of the external auditory canal
• Para pharyngeal and retropharyngeal abscess
• Case in literature due to spread of the infection along the EU tube and
spreading into the Retropharyngeal and Para pharyngeal spaces

33. Bezold Abscess
• Occurs as a result of osteolysis at the mastoid tip
• The pus/debris may extend inferiorly into the soft tissue of the neck
and form an abscess
• Aeration of mastoid bone with resulting thinning of osseous walls is
believed to be predisposing factor for bezold abscess
• Incomplete mastoid pneumatisation in infancy and early childhood is
responsible for rare appearance in children
• Very few cases reported in children under 5 years of age

34. Diagnosis??