This document discusses cholesteatoma and chronic suppurative otitis media (CSOM). Cholesteatoma is defined as the presence of keratinizing squamous epithelium in the middle ear or mastoid. There are various theories for its origin, including invagination of the tympanic membrane or basal cell hyperplasia. CSOM is a long-standing middle ear infection characterized by ear discharge and permanent perforation. It is classified as tubotympanic or atticoantral, with atticoantral being more dangerous due to higher risk of bone-eroding complications like cholesteatoma. Treatment involves surgical resection for atticoantral CSOM and conservative
Chronic Suppurative Otitis Media: Tubotympanic Type (CSOM TT)Dr Krishna Koirala
Chronic Suppurative Otitis Media: Tubotympanic Type (CSOM TT) is an important topic for MBBS and MS ENt students. Dr Krishna Koirala will be explaining this topic in a simplified way.
Chronic Suppurative Otitis Media: Tubotympanic Type (CSOM TT)Dr Krishna Koirala
Chronic Suppurative Otitis Media: Tubotympanic Type (CSOM TT) is an important topic for MBBS and MS ENt students. Dr Krishna Koirala will be explaining this topic in a simplified way.
Chronic suppurative otitis media is a long standing infection of a part or whole of the middle ear cleft characterized by continuous or intermittent discharge through a persistent tympanic membrane perforation.
Incidence is higher in developing countries b/c of
Poor Socioeconomic standards, poor Nutrition, lack of health education
Affects both sexes
Affects all age groups
It is divided into two types
TUBOTYMPANIC : also called the safe or benign type; it involve anteroinferior part of middle ear cleft; i.e eustachian tube and mesotympanum and is associated with central perforation.
ATTICOANTRAL: also called unsafe or dangerous type; it involves posterosuperior part of the middle ear cleft; i.e. attic, antrum and mastoid. And is associated with an attic or marginal perforation and this type of CSOM is often associated with bone-eroding process such as cholesteatoma, granulation or osteitis
Chronic Otitis Media - Squamosal type ( UG)AlkaKapil
Chronic Otitis Media - Squamosal / atticoantral/ unsafe Type
Theories of cholesteatoma
cholesteatoma
levenson's criteria
congenital cholesteatoma
classification of cholesteatoma
sade's classification of retraction of pars tensa
Toss classification of pars flaccida retraction
cholesterol granuloma
clinical features of Squamosal CSOM
Complications of COM/CSOM
Investigations - HRCT Temporal bone
Mastoid exploration
cortical mastoidectomy
modified radical mastoidectomy
Radical mastoidectomy
Chronic Suppurative Otitis Media Attico - antral disease.pptDrKrishnaKoiralaENT
CSOM AA is defined as Chronic pyogenic infection of the middle ear cleft lasting for >3 months with cholesteatoma & granulation tissue in attic or postero-superior quadrant of pars tensa
Unsafe/ Dangerous : Higher chances of complication due to bone erosion
Hallmark of Disease : Cholesteatoma/granulations
Cholesteatoma is defined as a three-dimensional sac lined by matrix of keratinizing stratified squamous epithelium that rests on a thin layer of fibrous tissue and contains desquamated keratin debris which grows at the expense of surrounding bone
It is not a tumor and has no cholesterol
Better term : Epidermosis
Cases of bone destruction in cholesteatoma:
Hyperemic decalcification
Osteoclastic bone resorption
Acid phosphatase ,collagenase, acid proteases proteolytic enzymes, leukotrienes, cytokines
Bacterial toxins
Pressure necrosis
Pathological Changes in cholesteatoma
1. T.M. retraction pocket (attic or P.S.Q.)
2. T.M. perforation (marginal or attic)
3. Cholesteatoma formation
4. Osteitis & granulation tissue formation
5. Ossicles: destruction
6. Middle ear mucosa: edematous, red, polypoid
7. Aural polyp: red, fleshy
8. Mastoid bone: erosion, sclerosis
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
2. CONTENTS
Cholesteatoma
Origin
Classification
Expansion of
cholesteatoma &
destructive of bone
Chronic suppurative
otitis media(CSOM)
Epidemiology
Types
Clinical features
Investigations
Treatments
3.
4. presence of keratinizing squamous
epithelium in the middle ear or
mastoid
“skin in the wrong place”
2 parts
Matrix
Central white mass
DEFINITION
6. ORIGIN OF
CHOLESTEATOMA
Wittmaack’s theory
Invagination of TM
from the attic/
posterosuperior part
of pars tensa in the
form of retraction
pockets
Ruedi’s theory
Basal cell
hyperplasia
Proliferate- infection,
lay down
keratinizing
squamous
epithelium (KSE)
7. ORIGIN OF
CHOLESTEATOMA
Habermann’s theory
Epithelial invasion
From the meatus/
outer drum surface
Pre-existing
perforation(marginal
)- part of the annulus
tympanicus-
destroyed
Sade’s theory
Metaplasia
Like respiratory
mucosa elsewhere
d/t repeated
infection
squamous
9. CONGENITAL
CHOLESTEATOMA
Embroyonic epidermal cell rests in the middle
ear cleft/ temporal bone
Middle ear, petrous apex, cerebellopontine
angle
Middle ear: white mass behind an intact
tympanic membrane conductive hearing loss
Discovered: routine exam/myringotomy
May spontaneously rupture- TM discharging
ear
10. PRIMARY ACQUIRED
CHOLESTEATOMA
No h/o previous OM/ pre-existing perforation
Invagination of pars flaccida
Persistent negative pressure in the attic
retraction pocket which accumulates keratin
debris.
Infected expand middle ear
Basal cell hyperplasia
Proliferation of the basal layers of PF induced by
subclinical childhood infection
Squamous metaplasia
Normal pavement epithelium of attic undergoes
metaplasia, keratinizing squamous epithelium
11. SECONDARY ACQUIRED
CHOLESTEATOMA
Already a pre-existing perforation in pars
tensa
Associated with posterosuperior marginal
perforation
Migration of squamous epithelium
KSE of EAC/ outer surface of TM migrates
through the perforation into the middle ear
Metaplasia: repeated infections of middle ear-
pre-existing perforation
12. EXPANSION OF
CHOLESTEATOMA AND
DESTRUCTION OF BONE
Enter the middle ear cleft invades the
surrounding structures
Attic cholesteatoma: extend backwards into
the aditus, antrum, mastoid. Downwards into
the mesotympanum; medially, it may surround
the incus and/or head of malleus.
Destroy bone, ear ossicles, erosion on bony
labyrinth
Enzymes : collagenase, acid phosphatase,
proteolytic enzymes(osteoclast, mononuclear
inflammatory cells)
13. Long standing infection of a part or whole of
the middle ear cleft characterized by ear
discharge and permanent perforation
CHRONIC SUPPURATIVE
OTITIS MEDIA (CSOM)
17. TUBOTYMPANIC-
SAFE/BENIGN
It involves the
anteroinferior part of
middle ear
Often associated with
central perforation
There is no risk of
serious complications
AETILOLOGY
Sequela of AOM-
following
exanthematous fever,
leaving behind a large
central perforation
Ascending infection
via the ET- recurring
otorrhoea
Persistent mucoid
otorrhoea: allergy to
ingestants
18. TUBOTYMPANIC-
SAFE/BENIGN
PATHOLOGY
Perforation of pars
tensa
Middle ear mucosa-
oedematous/velvety
Polyp- pale
Ossicular chain-
intact, mobile,may
show necrosis
Tympanosclerosis
Fibrosis and
adhesions
BACTERIOLOGY
Aerobics:
pseudomonas
aeruginosa, Proteus,
E.coli, Staph aureus
Anaerobes:
Bacteroids fragilis,
anaerobic
Streptococci
19. TUBOTYMPANIC-
SAFE/BENIGN
CLINICAL
FEATURES
Ear discharge
Nonoffensive,mucoid
, mucopurulent
Hearing loss
Conductive
Perforation
Always central
Middle ear mucosa
Perforation is large,
pale pink,moist
INVESTIGATIONS
Examination under
microscope
Audiogram
Culture and
sensitivity of ear
discharge
Mastoid X-ray/CT
scan temporal bone
20. TREATMENT
Aural toilet
remove all discharge
and debris by dry
mopping, suction
clearance or
irrigation
Ear drops
antibiotics ear drops
containing neomycin,
polymyxin,
chloromycetin, or
gentamycin +
steroids
Systemic antibiotics
useful in acute
Precautions
keep water out of
ear, rubber inserts
use
Treatment of
contributory causes-
such as infected
tonsils, adenoids,
maxillary antra and
nasal allergy
Surgical : remove
aural polyps/
granulations
Reconstructive
21. ATTICOANTRAL-
UNSAFE/DANGEROUS
Posterosuperior part
of the cleft
Associated with an
attic/marginal
perforation
Bone-eroding
process:
cholesteatoma,
granulation/osteitis
Risk of
complications is
higher
AETIOLOGY AND
BACTERIOLOGY
Same with
tubotympanic
22. PATHOLOGY
o Cholesteatoma
o Osteitis and granulation tissue
o Osteitis involves outer attic wall, posterosuperior
margin of tympanic ring
o Granulation tissue surrounds it may even fill the attic,
antrum, posterior tympanum, mastoid
o Fleshy red polypus: meatus
23. PATHOLOGY
o Ossicular necrosis
o Destruction may be limited to the long process of
incus, may also involves stapes superstucture, handle
of malleus/ entire ossicular chain
o Greater hearing loss
o Cholesteatoma hearer
o Cholesterol granuloma
o Mass of granulation tissue with foreign body giant cells
surrounding the cholesterol crystals.
24. SYMPTOMS
Ear discharge
• Scanty,foul smelling
• Total cessation of discharge- seriously
Hearing loss
• Normal: ossicular chain is intact
• Conductive type
Bleeding
• Granulation/polyps
• Cleaning
25. SIGNS
PERFORATION
• Either attic or posterosuperior marginal type
• can be missed due to crust
RETRACTION
POCKET
• Invagination of TM is seen in the attic/
posterosuperior part of PT
• Early: shallow,self cleansing Later:
deep,acumulation of keratin mass,infected
CHOLESTEATOMA
• Pearly white flakes can be sucked from the
retraction pocket
Grade Description
I Slight retracted TM, not touching incus
II Deep retraction, touching incus, middle ear mucosa not
affected
III Middle ear atelectasis. It lies on the promontory, ossicles
IV Also called Adhesive otitis media where TM becomes
adherent to promontory
26. INVESTIGATIONS
Examination under microscope. May reveal
presence of cholesteatoma, evidence of bone
destruction etc
Tuning fork test & audiogram
X-ray mastoids/CT temporal. Attic and antrum
destruction caused by cholesteatoma best
seen lateral in CT.
Culture and sensitivity of discharge
27. FEATURES INDICATING
COMPLICATIONS IN CSOM
Pain.; extradural, perisinus or brain abscess and
sometimes otitits externa
Vertigo: erosion of lateral semicircular canal
Persistent headache: intracranial involvement
Facial weakness: facial canal
Listless child with refusal of feeding: extradural
abscess
Fever,nausea,vomiting: IC infection
Irritability & neck rigidity: menigitis
Diplopia : (Gradenigo syndrome) petrositis
Ataxia: labyrinthitis/cerebellar abscess
Abscess around the ear: mastoiditis
29. SURGICAL
Primary aim is to
remove disease,
render ear safe
Secondary aim to
preserve or
reconstruct hearing
CWD:
Mastoid cavity open
Diseased area is fully
exteriorized
Atticotomy,modified
radical
mastoidectomy, RM
CWU
Approach by meatus,
mastoid but retained
the posterior bony
meatal wall intact
Dry ears, permits easy
reconstruction of
hearing mechanism
CANAL WALL UP CANAL WALL DOWN
MEATUS Normal appearance Widely open meatus
communicating with mastoid
DEPENDENCE Does not require routine
cleaning
Dependence on DR for
cleaning mastoid cavity
once/twice a year
RECURRENCE/
RESIDUAL SX
High rate- cholesteatoma Low rate
2ND LOOK
SURGERY
Require: after 6months of
surgery/rule out
cholesteatoma
Not required
PATIENTS
LIMITATIONS
No. can swim Swimming infection of
mastoid cavity
AUDITORY
REHABILITATIO
N
Easy to wear a hearing
aid if needed
Problems in fitting d/t large
meatus & infected mastoid
cavity
31. CONSERVATIVE TREATMENT
Cholesteatoma is small, easily accesible to
suction clearance under microscope
Elderly >65 years old
Unfit for GA/ refused
Polyps,granulation tissue: cup forceps/ cauterized
by chemical agents (silver nitrate/ trichloroacetic
acid)
Aural toilet, dry ear precautions
32. CONCLUSION
TUBOTYMPANIC/SAFE ATTICOANTRAL/UNSAFE
DISCHARGE Profuse, mucoid odourless Scanty, purulent, foul smelling
PERFORATION Central Attic/marginal
GRANULATION
S
Uncommon Common
POLYPS Pale Red and fleshy
CHOLESTEATO
MA
Absent Present
COMPLICATIO
NS
Rare Common
AUDIOGRAM Mild to moderate
conductive deafness
Conductive/mixed deafness
33. REFERENCES
Diseases of ear, nose, throat and head & neck
surgery, PL Dhingra 6th edition,page 65-74