Complications of mastoiditis

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 complica tion 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

22. 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

23. 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

24. 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

25. Dural venous phlebothrombosis

26. 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

27. subdural

28. 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

29. 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

30. 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

31. 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

32. 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

33. Diagnosis??