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Pathogenesis Classification Complications

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1 Pathogenesis Classification Complications
CSOM Pathogenesis Classification Complications Vishav Yadav

2 Introduction Keratin-producing squamous epithelium in the middle ear, mastoid or petrous apex Johannes Müller (1838):German Physiologist coined cholesteatoma i.e. layered paerly tumpour of fat Schuknecht : keratoma

3 DEFINITION Abramson 3D epithelial and connective tissue structure usually in form of sac , mostly confined to middle ear spaces , with tendency of independent growth on cost of underlying bone , with tendency of recurrence despite complete removal .

4 Histologically made up of :
Cystic content – anucleate keratin squames Matrix – keratinizing squamous epithelium Perimatrix – granulation tissue in contact with bone (produces proteolytic enzymes)

5 Classification Congenital Acquired
Primary acquired (retraction pocket) Secondary acquired Tertiary acquired

6 Pathogenesis

7 Congenital cholesteatoma
The incidence of CC - 1% to 5% of all cholesteatomas Congenital cholesteatoma of the middle ear was first described by Howard House Location (AS,PS , petrous pyramid, mastoid and middle ear cleft , CP Angle)

8 Congenital cholesteatoma
Levenson criteria (Modified Derlacki & Clemis) White mass medial to normal TM Normal pars flaccida and tensa No history of otorrhea or perforations No prior otologic procedures Prior bouts of otitis media not grounds for exclusion

9 Congenital cholesteatoma :theories
The accepted cause of CC remains controversial Teed’s epithelial cell rest theory Friedberg’s implantation theory Ruedi’s invagination theory Aimi’s epithelial migration theory Michael’s epidermoid formation theory

10 Epithelial rest Most commonly accepted and quoted theory Teed
An epidermal structure : these rests as ectodermal implants in the fusion plates between the first and second branchial arches that appear around 10 weeks It aided in middle ear and tympanic membrane development. Initially dormant, it undergoes rapid proliferation before resorption around 33 weeks’ gestation CC is thought to form if resorption is incomplete

11 Implantation theory Friedberg observed viable squamous cells in the amniotic fluid present in the middle ear of neonates. Could they be a cause for congenital cholesteatoma?

12 INVASION Ruedi Inflammatory injury to an intact tympanic membrane
Microperforations in the basal layer that lead to invasion of the squamous epithelium by proliferating epithelial cones through a macroscopically intact but microscopically injured tympanic membrane. Epithelial cones fuse and expand forming a middle ear cholesteatoma

13 Epithelial migration theory
First proposed by Aimi He suggested that ectoderm of external canal managed to grow / migrate in to the middle ear cavity somehow overcoming the restraining influence of the annulus.

14 Epidermoid formation theory
First proposed by Michael He observed nests of squamous epithelium in the lateral wall of tympanic cavity below the level of pars flaccida These nests normally involute Failure of this involution process can possibly cause cholesteatoma

15 Acquired inclusion theory

16 Staging (1) aid the clinician in preoperative planning of treatment
(2) Indicate prognosis (3) facilitate exchange of information between different clinicians (4) evaluate the results of treatment.

17 Derlacki and Clemis STAGING
Petrous Pyramid Mastoid Tympanic

18 Potsic STAGING Stage 1: Single quadrant with no ossicular or mastoid involvement Stage 2: Multiple quadrants with no ossicular or mastoid involvement Stage 3: Ossicular involvement but no mastoid involvement Stage 4: Mastoid extension

19 Nelson STAGING Type 1: Mesotympanum with no incus or stapes erosion
Type 2: Mesotympanum or attic with ossicular erosion but no mastoid extension Type 3: Mesotympanum with mastoid extension Clinical Stage Recurrence Rates TYPE 1 15 TYPE 2 59 34 TYPE 3 26 55

20 Acquired cholestaetoma

21 Primary acquired Pathogenesis
Invagination theory of Wittmaack Eustachian tube dysfunction Poor aeration of the epitympanic space Retraction of the pars flaccida Normal migratory pattern altered Accumulation of keratin, enlargement of sac

22 Primary acquired Pathogenesis
Basal cell hyperplasia (Ruedi theory) Inflammatory injury to an intact tympanic membrane Microperforations in the basal layer that lead to invasion of the squamous epithelium by proliferating epithelial cones through a macroscopically intact but microscopically injured tympanic membrane. Epithelial cones fuse and expand forming a middle ear cholesteatoma

23 Primary acquired Pathogenesis
Squmaous metaplasia (Sade theory) transformation of cuboidal epithelium to squamous epithelium from chronic infection

24 Secondary acquired Pathogenesis
Presence of preexisting perforation in pars tensa Often associated with posterosuperior marginal perforation or large central perforation

25 Secondary acquired Pathogenesis
Immigration & Invasion: Habermann medial migration along permanent perforation of TM Implantation & invasion –foreign body, blast injury Metaplasia – transformation of cuboidal epithelium to squamous epithelium from chronic infection Papillary ingrowth – intact pars flaccida, inflammation in Prussack’s space, break in the basal membrane, cords of epithelium migrate inward

26 Tertiary acquired Pathogenesis
iatrogenic – surgery, foreign body, blast injury Tympanoplasty Ossiculoplasty Stapedotomy Typmpanostomy tubes

27 spread

28 Anatomic Considerations
Epitympanic cholesteatoma patterns of spread from Prussack’s space Posterior epitympanum Posterior mesotympanum Anterior epitympanum

29 Prussak’s space Medially :neck of malleus
laterally :Shrapnell’s membrane Sup : lat malleal fold Anteriorly anterior malleolar fold & anterior ligament

30 Cholesteatoma spread

31 Cholesteatoma spread Posterior epitympanum – through superior incudal space to mastoid antrum

32 Cholesteatoma spread Posterior mesotympanum – inferiorly through posterior pouch of Von Troeltsch to stapes, round window, sinus tympani and facial recess

33 Cholesteatoma spread Anterior epitympanum – anterior to head of malleus, may gain access to supratubal recess To ant mesotympanum via anterior pouch of von Troeltsch

34 Sinus Tympani (Infrapyramidal Reccess)
*Medially – Medial Wall Of Middle Ear with Oval & Round Window Niches *Laterally – Pyramid & Facial Nv *Superiorly– Ponticulus *Inferiorly – Subiculum -can extend as far as 9mm into the mastoid -probably the most inaccessible site in middle ear & mastoid

35 Pathology Molecular models Preneoplastic transformation events
Defective wound-healing process Collision between host inflammatory response, normal middle ear epithelium, and bacterial infection

36 Preneoplastic transformation
Hyperproliferative keratinocytes Increased proliferation Decreased terminal differentiation Expression of epithelial markers in the basal and suprabasal layers (cytokeratins –10,13,16, filaggrin, involucrin); confirm they arise from pars flaccida and overlying EAC skin High expression of epidermal growth factor receptor, transforming growth factor Upregulation of p53

37 Defective wound healing
Chronic inflammatory response around matrix (granulation/perimatrix) Infiltration of activated T-cells and macrophages Production of cytokines (TGF,TNF,IL-1,IL- 2,FGF,PDGF) Causes increased migration and invasion of cholesteatoma epithelium and fibroblasts

38 Host response vs. bacteria
Bacterial related antigens producing host inflammatory response may stimulate the migrating epithelium’s uncoordinated proliferation Granulation induces invasion of keratinocytes Granulation – contains proteases, acid phosphatases, bone resorption proteins, osteoclast-activating factors, prostaglandins

39 complications

40 Intracranial Extradural abscess Subdural abscess (empyema) Sigmoid sinus thrombophlebitis Meningitis Brain abscess Otitic hydrocephalus

41 Extratemporal complications:
Subperiosteal abscess Migrating thrombophlebitis of IJV Intratemporal Facial paralysis Labrynthine infections Labyrinthine fistula Petrositis Mastoiditis Other rare complications: Abscess: Bezold’s abscess Luc’s abscess Citeli’s abscess Distant pyaemic abscess

42 Possible routes of spread:
Extension through bone Infected clot within small veins Normal anatomical pathways Non anatomical bony defects Surgical defects Into brain tissue along periarteriolar spaces of Robin Virchow

43 General principles: The complications are multiple in about 1/3rd of the cases The symptoms of intracranial spread of infection are those of infection and those of brain tissue compression Otalgia is never a symptom of uncomplicated cholesteatoma Investigation and treatment must run concurrently The principles of treatment : Systemic antibiotic therapy Local neurosurgical attention to the complication(s) Treatment of the ear lesion

44 Organisms involved: multiple organisms
Intracranial complication: G-ve organisms Staphylococci- beta lactamase producing Obligate anaerobes Bacteroides fragilis Extratemporal and temporal complications: Pseudomonas Proteus

45 When to suspect complications
High grade fever Headache with vomiting Copious ear discharge Gait changes Visual alterations Seizure activity Neck stiffness Unusual persistent pain

46 Extradural abscess Etiology :Bone erosion Sigmoid perisinus abscess

47 Pott’s puffy tumour

48 Clinical features: Diagnosis : Site and size Duration and rate
Incidental finding Headache with malaise Intermittent relief from pain during episodes of aural discharge Diagnosis : Operative findings CT scan

49

50 Management : Surgical exploration
????Don’t remove the granulation tissue attached to the dura Appropriate antibiotics

51 Subdural Abscess(empyema)
Spread of infection Loculated infection Thrombophlebitis Obliteration of subdural space Commonly associated organisms: Strp. milleri H. influenzae

52

53 Clinical features: Severe headache Fever Drowsiness
Focal neurological deficit Seizure Paralysis The course is much more rapid than brain abscess Papilledema is uncommon, as are the cranial nerve palsy Seizures and FND differentiates from meningitis

54 Diagnosis CT scan MRI LP : helpful but risky ↑pressure
Normal sugar content Cultures are sterile Marked pleocytosis

55 Management : Removal of subdural fluid Massive antibiotics
Treatment of ear disease Antiepileptics

56 Lateral sinus thrombophlebitis
Sigmoid sinus Transverse sinus Usually preceded by the development of extradural perisinus abscess Spread of infection Torcula herophili (confluence of sinuses) Superior sagittal sinus Superior and inferior petrosal sinus Cavernous sinus Brain abscess Internal jugular vein Subclavian vein

57

58

59 Commonly associated organisms:
Beta hemolytic streptococci Staphylococus aureus Now a days : mixed flora : Venezio et al in 1982 grew Proteus mirabilis, staphylococci, streptococcus pneumoniae and Bacteroides oralis

60 Clinical features: Classical picture before antibiotics:
Severe pyrexial wasting illness Develop over several weeks Picket fence fever Headache and neck pain Emaciation with anaemia Spread along the IJV: Perivenous inflamation Perivenous edema Suppuration of the lymph node Paralysis of the lower cranial nerves ↑ICP Hydrocephalus Superior extension Superior sagittal sinus Cavernous sinus

61 Septic embolisation (sinus thrombophlebitis)
Lung fields Large joints Subcutaneous tissue Other viscera Pleuroperitoneal cavity Mastoid emissary vein: suboccipital abscess Griesinger’s sign: oedema of the postauricular soft tissues overlying the mastoid process as a result of thrombosis of the mastoid emissary vein

62 Investigations : Hemogram Blood cultures Lumbar puncture :
Low WBC count Normal CSF pressure Queckstedt or Tobey-Ayer test CT scan: An empty triangle at the level of the sigmoid sinus, clot surrounded by a high-intensity rim of contrast-enhanced dura: delta sign Angiography Venography MRI

63 Tobey-Ayer test (for sinus thrombosis)
The jugular vein on the side of the suspected thrombosis is compressed A rise in spinal fluid pressure should occur Its absence indicates presence of thrombosis.

64

65

66 Treatment : ???? Anticoagulants : Administration of antibiotics
Exposure of the sinus: incision and removal of contents Perisinus cells need to be cleared: chances of delayed sinus thrombosis if not cleared ???? Anticoagulants : If in spite of the treatment the infection is progressively involving the cortical veins Role of IJV ligation: if the thrombus is getting dislodged then the need to ligate IJV

67 Meningitis( leptomeningitis )
The commonest intracranial complication Childhood otogenic meningitis is seen most often as a complication of acute middle ear infection In adults, it is now more commonly a complication of chronic disease

68 Organisms responsible for acute infection:
Pathways of spread: Bone erosion Suppurative labrynthitis Rupture of established brain abscess Organisms responsible for acute infection: Hemophilus influenzae type B Streptococcus pneumoniae type III Organisms responsible in chronic infection: G-ve enteric organisms Proteus Pseudomonas Anaerobes such as Bacteroides species

69 Clinical features: Headache and neck stiffness Malaise
Pyrexia mental hyperactivity Exaggerated Tendon reflexes Photophobia Vomiting

70 Diagnisis : Lumbar puncture
Rise in fluid pressure above the normal mm Hg Gross appearance of fluid: cloudy and then turbid On histological inspection PMN cells ranging from x109 /l Biochemical tests: Protein content may rise from normal of mg/l to a raised level of 2-3g/l Chloride content may fall from the normal 120mmol/l to 80mmol/l Fall in glucose level from the normal value of mmol/l to zero Bacteriological examination : gram staining and then culture D/d : Rupture of brain abscess Rupture of subdural abscess CT scan MRI PCR

71 Treatment : Medical : Surgical :
Repeated LP to lower the raised pressure Large doses of systemic antibiotics Systemic antibiotics must continue for 10 days after apparent clinical recovery Dexamethasone?? Surgical : Certainly deterioration or failure of response over 48hrs implies loculated infection in the mastoid, needing surgical drainage

72

73 Failure of an adequate response to antimicrobial therapy may be a result of :
Organism resistant to chosen antibiotics Persistent leakage of infected material into the CSF Persistence of a previously unidentified other complication/Leakage into the CSF from an unrecognized brain abscess.

74 Brain abscess It is a focal suppurative process within the brain parenchyma serrounded by a region of encephalitis. Bimodal age of distribution with peaks in the paediatric age group and in the 4th decade of life. Almost always develop in the temporal lobe or the cerebellum Temporal lobe abscess is twice as common as cerebellum

75 Various routes of spread:
Through an osteitic tegmen tympani , with middle fossa extradural abscess Local pachymeningitis followed by thrombophlebitis Extension of infection along periarteriolar Virchow-Robin spaces Cerebellar abscess are frequently preceded by lateral sinus thrombophlebitis

76

77 Bacteriology :polymicrobial (also extradural)
Anaerobes Streptococcus & staphylococcus G- organism: Escherichia coli Proteus Klebsiella Pseudomonas

78 Clinical presentation:
Very toxic and drowsy Brain abscess is associated with the triad of: Headache High grade fever Focal neurological deficits Cerebellar abscess: Dizziness Ataxia Nystagmus Vomiting Temporal lobe lesion: Seizure Visual field defects Nominal aphasia

79

80 Diagnosis : Imaging : Computed tomography
Hypodense area by an area of edema, ring sign MRI: superior to CT scan except for delineation of temporal bone is poor.

81

82

83 Other d/d: Meningitis Subdural abscess Lateral sinus thrombophlebitis
Otitic hydrocephalus Other masses such as brain tumour.

84 Management : High-dose antimicrobial medication
Patient should be first stabilized neurologically: ? Aspiration with high dose of antibiotics ?Total excision ?parenteral antibiotics

85 Otitic hydrocephalus Syndrome (pseudotumour cerebrii) associated with otitis media with Increased intracranial pressure Normal CSF findings Spontaneous recovery No abscess No associated ventricular dilation: benign raised intracranial tension.

86 Pathophysiology: Symonds: decreased absorption of CSF secondary to blockage of arachnoid villi Sahs and Joynt: secondary to brain edema Weed and Flexner: disruption in venous circulation as a cause .

87

88 Clinical presentation
Symptoms : Headache Drowsiness Vomiting Blurring of vision Diplopia Signs: Papilledema 6th cranial nerve palsy Optic disc atrophy

89 Diagnosis : Management: ↑CSF pressure Normal CSF biochemistry
MRI is the modality of choice Management: Lowering of the elevated intracranial pressure Medical therapy: Corticosteroids Mannitol Diuretics Acetazolamide Eradication of ear disease

90 Facial nerve paralysis
In CSOM ostietis and subsequent bone erosion likely expose the nerve to infection This results in inflammation and ultimately facial nerve compression The tympanic segment is the most common area of involvement HRCT of the temporal bone Management : Intravenous antibiotics Prompt surgical intervention: Any attached granulation to the nerve should not be removed Healthy bone should be removed from the nerve on either side of the diseased segment. Concomitant corticosteroids

91 Labyrithitis It has two clinically distinguishable subtypes:
Localised, circumscribed, or serous labyrinthitis without total or permanent loss of function Diffuse, purulent or suppurative labyrinthitis with permanent total destruction of the sensory elements within the labyrinth

92 Serous labrynthitis As the result of osteitis of the labyrinth capsule or of extension along preformed pathways Potential pathway include: oval window Round window membrane Cholesteatomatous fistula

93 Clinical features: Symptoms Signs:
Vestibular symptoms precede cochlear symptoms by hours to days when the site of invasion is semicircular canal Symptoms Profound vertigo Nausea Vomiting Signs: Spontaneous nystagmus towards the unaffected ear. Some degree of ataxia with pastpointing High frequency sensorineural hearing loss Distortion of hearing.

94 Treatment : Parenteral antibiotics

95 Suppurative labrynthitis
Usually following the serous labyrinthitis Involvement of labyrinth secondary to generalized meningitis Symptoms: same as serous labyrinthitis including the lack of fever Key differences: Symptoms are more rapid and intense The onset of severe vestibular symptoms is accompanied by a complete loss of cochleovestibular response A caloric response is conspicuously absent from the disease ear. d/d: cerebellar abscess

96 Treatment: Close and continuous monitoring for symptoms of intracranial extension Bed rest with minimal head movements Antiemetics Antibiotics If meningeal signs are noted: LP Any signs of intracranial spread: labyrinthectomy Premature surgical trauma can promote dissemination of infection: mastoid exploration to be deferred until acute symptoms subside.

97 Labyrinthine fistula Bone erosion by cholesteatoma
Most common site: dome of the lateral semicircular canal. Symptoms : Episodic vertigo Signs: Fistula test Negative test does not rule out fistula Tullio’s phenomenon Site of fistula: The dome of the LSCC: deviation of eyes towards normal ear. LSCC fistula anterior to the ampulla: deviation towards the affected ear. Erosion of the vestibule: rotatory horizontal deviation towards the diseased ear. SSCC: rotatory movements towards the normal ear PSCC: vertical deviation of the eyes.

98 Investigations: Treatment: HRCT temporal bone Surgery :
Managed according to the site, size and status of hearing The rate of total hearing loss is 8% to 56%

99 Acute petrositis It is the infected petrosal cells with inadequate drainage causing bone changes of coalescence in the cell walls and resulting in symptoms referable to the petrosa. Symptoms: Gradneigo’s syndrome: 1.Deep-boring pain: depending upon the site of involvement: Posterior group of cells: occipital, parietal, or temporal Discharge is from the mastoid Anterior petrositis: Frontal or behind the eye Drainage is from the tympanum 2.Aural drainage 3,Diplopia : 6th cranial nerve palsy occurs when the apex is involved

100 Investigations: HRCT temporal bone Gallium 67 scan Technetium 99m scan Management : Parenteral antibiotics Surgical drainage

101 Chronic Mastoiditis Can occur with:
Long standing perforation Cholesteatoma Once any type of mastoiditis causes continuous purulent drainage for 8 or more weeks, the likelihood of complete resolution with antibiotics significantly decreases. Hallmark triad: Otalgia Postauricular pain Fever Signs: Postauricular tenderness Protrusion of pinna Postauricular erythema Induration over the mastoid: impending subperiosteal abscess.

102 Investigaton : Treatment : Parenteral antibiotics Mastoidectomy:
HRCT temporal bone Treatment : Parenteral antibiotics Mastoidectomy: Significant bony destruction Poor response to up to 2 weeks of conservative management.

103 Subperiosteal abscess
Direct destruction of cortical bone / hematogenous spread through small vascular channels. Well pneumatized mastoids are more susceptible The most common site of cortex breakdown is through the thin trabecular bone Macewen’s triangle Signs and symptoms: Auricle is displaced forward and outward Fluctuant mass can be palpated behind the ear Bezold’s abscess Luc’s abscess

104 Investigations: HRCT temporal bone Management:
Simple mastoidectomy Antibiotics

105 Benzold abscess: Breach in the bony plate forming the inner surface of mastoid tip. Erosion of inner or outer cortex of the mastoid if periphlebitis or phlebitis propagate the infection. Pus track below the sternocleidomastoid or even the layer of cervical fascia. d/d : inflamed lymph nodes Investigation : CT scan Treatment : Complete excision of mastoid pathology Drainage of the abscess Removal of associated granulation tissue.

106 thanks


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