Otosclerosis

Vidian neurectomy

Otosclerosis

Radiological anatomy of frontal sinus

Rhinitis

Rhinitis

Ménière's disease

Open Approach Conservative Laryngectomy an Overview

Eosinophlic oesophagitis

Introduction:

Eosionophlic oesophagitis ¹ is a relatively new disease entity. It is characterised by chronic / intermittent dysphagia, reflux like symptoms and intermittent oesophageal food impaction.

This condition was first reported by Landres in 1978 ². In 1993 Attwood and DeMeester reported 12 cases of dysphagia with no evidence of anatomic obstruction. They also reported dense eosinophilic infiltrates in the oesophagus. Attwood hence applied the criteria of presence of more than 20 eosinophils / high power field as histological criteria for diagnosing this condition ³.

Incidence:

True incidence of this disorder is still uncertain ^4. Review of literature puts this figure as high as

1% ⁵. It is more common in men than in women. Male : female ratio is 3:1. Age of presentation may vary between 2^nd – 4^th decades.

Conditions associated with oesophageal eosinophilia:⁶

1. Eosinophlic oesophagitis
2. GERD
3. Collagen vascular disorders
4. Parasitic infections
5. Eosinophlic gastroenteritis

Pathophysiology of eosinophlic oesophagitis:

1. This is a primary disorder involving oesophagus
2. Biopsy of oesophageal mucosa should contain atleast 50 eosinophils / high power field.
3. There should not be associated eosinophlic infiltration of stomach / intestine.
4. Eosinophlic microabscess can be see in the oesophagus extending up to its lumen
5. The caliber of oesophageal lumen is drastically reduced.
6. Asthma / atopia +
7. Peripheral eosinophilia common

Endoscopic features:

Linear furrowing of oesophageal mucosa.

Presence of white plaques / exudates

Presence of concentric rings / strictures of oesophageal mucosa.

Appearance of crepe paper mucosa is diagnostic.

Multiple biopsies should be studied before a categorical diagnosis of this condition could be made. Multiple biopsy specimen increases the accuracy of diagnosis.

Diagnosis of eosinophlic oesophagitis should not be made until GERD has been categorically ruled out by performing ambulatory pH testing or performing repeat biopsy after a 8 week trial course of proton pump inhibitor.

Clinical features:

1. Abdominal pain
2. Chest burns
3. Dysphagia
4. These patients are very slow eaters

Classification of eosinophlic oesophagitis:

Vasilopoulous ⁷ proposed the first classitication of eosinophilic oesophagitis.

Type I : Early small caliber oesophagus

Type II: Advanced small caliber oesophagus

Type III: Ringed oesophagus

Managment:

1. Avoidance of food allergen
2. Topical steroids
3. Oral steroids
4. Leukotriene inhibitors

Oesophageal dilatation is reserve for patients with extreme dysphagia

References:

1. Furuta GT, Liacouras CA, Collins MH, et al. Eosinophilic esophagitis in children and adults: a systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology.

2007;133:1342-1363.

2. Landres RT, Kuster GGR, Strum WB. Eosinophilic esophagitis in a patient with vigorous achalasia. Gastroenterology 1978;74:1298-1301.

3. Attwood SEA, Smyrk TC, DeMeester TR, et al. Esophageal eosinophilia with dysphagia: a distinct clinicopathological syndrome. Dig Dis Sciences 1993;38:109-116.

4. Ronkainen J, Talley NJ, Aro P, et al. Prevalence of oesophagealeosinophils and eosinophilic oesophagitis in adults: the population-based Kalixanda study. Gut. 2007;56:615-620.

5. Arora AS, Yamazaki K. Eosinophilic esophagitis: asthma of the esophagus? Clin Gastroenterol Hepatol 2004;2:523-530.

6. Rodrigo S, Abboud G, Oh D, et al. High intraepithelial Eosinophil counts in esophageal squamous epithelium are not specific for eosinophilic esophagitis in adults Am J Gastroenterol 2008;103:435- 442.

7. Vasilipoulos S, Shaker R. Defiant dysphagia: small-caliber esophagus and refractory benign esophageal strictures. Current Gastroenterology Reports 2001;3:225-230.

Esthesioneuroblastoma

Introduction:

This tumor arises from the olfactory nerve. These are rare malignant tumors arising from the olfactory epithelium situated at the roof of the nasal cavity, cribriform plate, upper portion of supeior turbinate and corresponding upper portion of nasal septum. These tumors typically involve the upper portion of nasal cavity and the cribriform plate area. These tumors classically arise from the basal cells of olfactory neuroepithelium. No clearl cut genetic / other causes have been attributed for this tumor. This tumor represents about 3% of all malignant tumors involving the nasal cavity.

This tumor was first reported by Berger etal in 1924. Since then only less than 1000 cases have been reported in literature.

Incidence:

Affects both male and female patients with equal frequency.

Age incidence shows a bimodal peak (peaking at the second and the sixth decades of life).

Etiopathogenesis (theories):

1. Belongs to peripheral neuroectodermal family. (Not supported by immunohistochemistry)
2. Presence of Trisomy 8 has been documented in these tumor cells

None of these theories convincingly explain etiopathogenesis of this tumor.

Clinical features:

This tumor classically involves the nasal cavity with extension into the ethmoid sinus, anterior skull base and orbit. Since these tumors are very aggressive ones they tend to metastasize extensively. Spread to cervical nodes are common. Retropharyngeal nodes are the first echelon node. Rarely these tumors may be active in an endocrine sense. These tumors have known to cause ectopic secretion of ACTH causing Cushing's syndrome.

Common presenting symptoms were usually associated with the nasal cavity:

1. Nasal block
2. Epistaxis
3. Anosmia

Staging system:

Staging a tumor helps in deciding the optimal management modality and also in determining the prognosis of the disease.

Kadish staging system:

This system stages Esthesioneuroblastoma into three stages:

Stage A: Tumor limited to nasal cavity

Stage B: Tumor extending to paranasal sinuses

Stage C: Tumor extending beyond paranasal sinuses

Major inadequacy of this staging system is too broad a staging at the level of Stage C.

Modified TNM staging system:

Tumor

T1 – tumor involving nasal cavity and / or paranasal sinuses (excluding sphenoid) sparing most of the superior ethmoidal cells

T2- tumor involving nasal cavity and / or paranasal sinuses including sphenoid with extension to the cribriform plate

T3 – tumor extending to orbit with involvement of extradural anterior cranial fossa

T4 – tumor involving brain

Node

N0 – No nodal metastasis

N1 – any form of nodal metastasis

Metastasis

M0 – No metastasis

M1 – Metastasis present

Hyam came out with a histopathological grading system which turned out to be more accurate than the preceding two staging systems.

Hyam's Histopathological grading system

Grade	LA preservation	Mitotic index	Nuclear polymorphism	Fibrillary matrix	Rosettes	Necrosis
I	+	Zero	None	Prominent	HW	None
II	+	Low	Low	Present	HW	None
III	+/-	Moderate	Moderate	Low	FW	Rare
IV	+/-	High	High	Absent	None	Frequent

Fw – Flexner-wintersteiner

HW – Homer – Wright

Management:

This tumor is managed with wide surgical resection with adequate tumor margins. Radiotherapy is indieated as primary treatment modality in unresectable tumors and as a follow up to surgical debulking.

Maxillectomy a review

Maxillectomy a Review

Pathophysiology of allergic fungal sinusitis

Introduction:

Allergic fungal sinusitis is known to cause extensive sinonasal polyposis. This article discusses the pathophysiologic mechanisms involved. Studies have revealed that this is a form of non invasive fungal sinusitis causing sinonasal polyposis. Hypersenstivity to fungus has been implicated as the probable cause. Hypersensitivity to Aspergillus / dematiaceous fungi (this group of fungi secrete melanin in their cell walls) have been commonly implicated to the cause.

Role of hypersensitivity:

Eventhough hypersensitivity to fungus has been implicated as the cause for allergic fungal sinusitis the precise nature of this hypersensitivity is still not clear. Studies reveal that patients with allergic fungal sinusitis show elevated levels of IgE and IgG to fungal proteins. Hence a combination of Coomb's Type I and Type III hypersensitivity to these fungal allergens could play a role.

Type I hypersensitivity reaction is rather immediate and is caused by IgE and IgG4 immunoglobins.

Type III hypersensitivity reaction is known to be causeed by immune complex formation and is caused by IgG and complements.

Current hypothesis suggests that allergic fungal sinusitis develops in susceptible persons due to a combination of local anatomic as well as environmental factors. Fungi enter the nose and trigger immune response causing inflammatory changes. This inflammation induces polyp formation and accumulation of allergic mucin. Fungi which are trapped within the mucosa of nasal cavity causes continuing stimulation of immune reaction causing a vicious cycle leading on to extensive nasal polyp formation.

Diagnostic criteria of Allergic fungal sinusitis

Introduction:

Diagnosis of allergic fungal sinusitis is made from a combination of clinical, radiological, microbiologic and histopathologica information. Hence the diagnosis of allergic fungal sinusitis cannot be made with certainty till surgery is over.

Diagnostic criteria include:

1. Presence of allergic mucin: Allergic mucin is thick tenacious and dark colored. It is very difficult to remove this secretion with a suction. When suction is applied it resembles an elastic strand of tissue. In rare cases this allergic mucin may assume the shape of fungal ball. Microscopically allergic mucin contains onion skin laminations of necrotic and degranulating eosinophils on mucin background. Occasionally charcot layden crystals can also be seen. Fungal hyphae may be present but are scarce. Fungal stains are necessary to demonstrate these hyphae. These hyphae don't invade tissue. If evidence of tissue invasion is present then diagnosis of allergic fungal sinusitis should not be entertained.
2. Presence of nasal polypi with evidence of eosinophilic inflammatory infiltrate.
3. Evidence of Type I hypersensitivity
4. Imaging: CT scan paranasal sinuses reveal multiple opacified sinuses with central hyperattenuation, mucocele formation, erosion of lamina papyracea / skull base, pushing borders. Bone erosion in patients with nasal polyposis should raise suspicion of allergic fungal sinusitis

Role of MRI in the diagnosis of AFRS:

This is indicated when there are intracranial and orbital complications due to allergic fungal sinusitis. MRI reveals central low signal on T1 and T2 weighted images. These areas correspond to allergic mucin associated with peripheral high signal intensity due to the presence of oedematous mucosa.

Drainage system of paranasal sinuses a review

Introduction:

Study of drainage system of paranasal sinuses is important in the present day context of Functinal endoscopic surgery and Baloon dilatation techniques in managing sinus infections and ostial obstruction. These minimally invasilve tools have thrown further light into the drainage pattern of various paranasal sinuses.

The following are the documented various racial variations:

1. The volume of maxillary sinus varies between races and sexes
2. White population has a higher incidence of concha bullosa of middle turbinate and paradoxical bending of middle turbinate when compared to that of other races
3. Infra orbital / suprabullar cells are commonly seen in white races
4. Sphenoethmoidal cells are commonly seen in chinese
5. Bent uncinate process and complete absence of sinuses are common in chinese

Studies have revealed extensive intercommunication between various paranasal sinuses. It can be safely construed that all paranasal sinuses in addition to their major drainage channel also contains openings connecting one with the other.

Development of nose and paranasal sinuses:

Study of embryology of nose and paranasal sinuses will go a long way in enhancing our understanding of the drainage patterns of various paranasal sinuses. The whole nasal cavity and adjoining paranasal sinuses develop from a cartilagenous anlage called the nasal capsule. This nasal capsule appears between the 7^th and 8^th weeks of embryonal life. The first area where this cartilage begins to develop is in the nasal septal area. The lateral nasal wall develops much later. The following are the chronology of development of lateral nasal wall:

1. The cartilage of inferior turbinate develops during the 8^th week of gestation
2. Middle turbinate begins its development during the 9^th week of gestation
3. Superior turbinate begins to develop during the 12^th week of gestation.
4. Uncinate begins to develop during the 9^th week
5. Ethmoidal bulla begins its development during 12^th week
6. Anterior ethmoidal cells starts their develoment during 22^nd week
7. Posterior ethmoid cells begin their development during 40^th week

The nasal capsule has tight connections to its surroundings, especially to the cartilagenous anlage of body and minor ala of sphenoid bone. This factor helps in the normal development of sphenoid bone thus ensuring normal develpment of sphenoid sinus.

Expansion of mucous membrane forms the paranasal sinuses. The first air filled sacs in the ethmoid bone begins from the bulla ethmoidalis area. Bulla ethmoidalis gives rise to anterior and middle ethmoid air cells. Ventral to anterior ethmoidal cells the developing primordial ethmoidal infundibulum extends infero laterally towards the inferiorly placed precursor of maxillary bone. This forms the primordial maxillary sinus. At birth only the ethmoid and rudimental maxillary sinus are present. The frontal and sphenoid sinus develops after birth due to gradual pneumatization of frontal and sphenoid bones respectively.

During the process of pneumatization mucous membranes encounter each other. When this happens the underlying mesenchymal layer may disappear causing intersinus communications to form. Eventhough these channels of communication plays very little role in ventilation and drainage of sinuses infections can spread to other sinuses via these channels.

Drainage pathways of paranasal sinuses:

Frontal sinus: May show three types of drainage patterns.

1. Direct drainage via frontal recess
2. Drainage via ethmoido nasal route
3. Drainage via ethmoido maxillar route

Multiple drainage patterns are commonly seen in frontal sinus. Direct drainage is seen only in a fraction of patients. If the frontal sinus drains directly via frontal recess presence of anterior ethmoidal cells can cause obstruction to drainage of frontal sinus leading on to frontal sinus infection.

Ethmoidal cells:

These cells drain directly via upper / middle meatus.

These cells may share common drainage channel with maxillary sinus

These cells may drain via maxillary sinus

Sphenoid sinus:

Drains directly into the nasal cavity. 

Coronal view showing various drainage patterns

1. Natural ostium / accessory ostium of maxillary sinus
2. Maxilloethmoid nasal route
3. Nasal ostia of ethmoidal sinus

4a. Ethmoideo-nasal route

4b. Ethmoideo-maxillary route

Saggital view showing the drainage patterns of paranasal sinuses

Fs – Frontal sinus

Ms- maxillary sinus

Ss- Sphenoid sinus

The following points should be borne in mind before performing Balloon sinuplasty / FESS procedures for chronic sinus infections:

1. Accessory sinus ostia exist for each paranasal sinuses
2. Many sinuses do not drain directly into the nasal cavity but indirectly drains via adjacent sinuses. For example sphenoid sinus drains both via posterior ethmoidal cells and directly into the nasopharynx.
3. Major drainage pathway of frontal sinus is over the ethmoidal sinus, via the ethmoids into the maxillary sinus and then into the nasal cavity
4. These pathways are not normally accessible during normally performed endonasal surgeries. Inadvertant manipulation can cause fractures of thin septa between these sinuses thereby impairing normal drainage patterns
5. Presence of secondary / accessory ostia is a definite sign of chronic sinus infection
6. Presence of accessory / secondary ostia ensures recirculation of mucous due to mucociliary mechanism which tends to beat towards the natural ostium
7. If accessory ostium is present Balloon sinuplasty invariable ends up dilating the accessory ostium instead of natural one.

It makes real sense if these drainage patterns could somehow be ascertained prior to surgical procedure instead of performing blind dilatation.  

Courtesy drtbalu's otolaryngology online

Online journal of otolaryngology

Introduction:

Publishing an article in an indexed journal is a patience testing process which involves lot of expenditure also. This online journal of otolaryngology makes the whole process of article publishing a little easier and totally expense free procedure.  This journal has been started with the only intention to help out the potential publisher.
This journal will publish articles submitted by you after subjecting them to peer review which is the standard in medical journal publishing.

How to submit article to this journal?

You can go through the entire tutorial of article submission from here:


You can enter the website by clicking the image below:

Velopharyngeal insufficiency and its management

velopharyngeal_insuff

Anatomy of chordatympani nerve

Introduction:

The chorda tympani nerve is a branch of facial nerve. It exits the facial nerve just before it exits via the stylomastoid foramen. It is one of the three cranial nerves that is involved in transmission of taste fibers from the tongue. Chorda tympani nerve conveys taste fibers from the anterior 2/3 of tongue. Mechanism of taste sensation is rather unique in that it involves a complicated feed back loop with each nerve acting to inhibit the signal of other nerves. The chorda tympani exerts stong inhibitory influence on other taste fibers as well as pain fibers from the tongue. When chorda tympani nerve is damaged its inhibitory function is disrupted, causing the other taste fibers to act in an uninhibited manner.

The chorda tympani nerve carries with it two types of fibres which traverse via lingual nerve to reach their destination. These fibers include:

1. Special sensory fibers providing taste sensation from anterior 2/3 of tongue.
2. Presynaptic parasympathetic fibers to submandibular ganglion providing secretomotor fibers to submandibular and sublingual salivary glands
3. Presynaptic parasympathetic fibers is also supplies the blood vessels of the tongue. When stimulated the chorda tympani nerve causes dilatation of blood vessels of the tongue.

Central connections:

Chorda tympani nerve contains fibers from two brain stem nuclei. They are:

Superior salivatory nucleus: This nucleus houses cell bodies of secretomotor preganglionic parasympathetic neurons

Nucleus of tractus solitarius: The superior portion contributes to chorda tympami fibers. It receives central processes of taste neurons which have their cell bodies in the ganglia of the three cranial nerves conveying taste sensation. After synapsing in this nucleus secondary axons ascend in the lateral lemniscus to relay in the thalamus. This pathway then passes through the posterior limb of internal capsule to reach the primary gustatory cortex.

Connections seen within the facial canal:

Sensory branch of facial nerve Nervus intermedius of Wrisberg joins the facial nerve here. It conveys special sensory fibers from taste buds present in the anterior 2/3 of tongue and soft palate. It also contains secretomotor fibers to salivary glands present below the oral cavity. Nerves intermedius exits the brain stem adherent to the vestibuo cochlear nerve. At the level of internal auditory meatus it leaves this nerve to merge with that of facial nerve.

Chorda tympani nerve exits from the facial nerve before the facial nerve exits via the stylomastoid foramen. It is the largest branch of facial nerve in its intrapetrous compartment. It arises below the nerve to stapedius. It traverses antero superiorly via the posterior canaliculus usually accompanied by posterior tympanic branch of stylomastoid artery. This canaliculus opens into the middle ear cavity through an aperture situated at the junction of posterior and lateral walls of tympanic cavity. This opening lies just medial to the fibrocartilagenous annulus. The posterior canaliculus is roughly 0.5 mm in diameter. Chorda tympani nerve shows a large number of variations. In some patients the chorda tympani nerve may arise from more proximal portion of facial nerve, even close to the geniculate ganglion. The length of the posterior canaliculus is also highly variable ranging from 3 – 14 mm. In 10% of individuals there may not be a posterior canaliculus at all but could be replaced by a groove.

If the chorda tympani nerve originates outside the temporal bone then the posterior canaliculus will be separate from that of the facial nerve canal. In fetus and young infants the chorda tympani nerve leaves the facial nerve outside the skull, but the postnatal growth of mastoid process causes it to migrate to a more proximal position. Since the facial canal grows more than the mastoid segment of facial nerve the chorda tympani nerve typically diverges from the facial nerve in an infant of 1 yr of age.

Course of chorda tympani in the tympanum:

The chorda tympani arches across pars flaccida medial to the upper part of the handle of malleus and traverses above the insertion of tensor tympani. In patients with congenital anamolies of malleus chorda is also displaced laterally.

Chorda tympani nerve exits the middle ear via a separate bony canal, the anterior canaliculus also known as the canal of Hugier. This canal runs in the medial portion of petrotympanic fissure. Anterior tympanic branch of maxillary artery accompanies this nerve along this canal. Chorda exits the skull through a small foramen behind the base of spine of the sphenoid. At its exit it is closely related to the medial surface of temporomandibular joint.

Course of Chorda in the infratemporal fossa:

In the infratemporal fossa the chorda tympani nerve descends medial to the spine of sphenoid and angles forward to join the lingual nerve about 2 cms below the skull base. This junction lies close to the lower border of lateral pterygoid muscle.

Diagram showing relationship of chorda to middle ear structures

Functions of chorda tympani nerve:

1. It carries taste sensation from the anterior 2/3 of tongue
2. Supplies secretomotor fibers to the salivary glands in the floor of the mouth
3. Conveys general sensation from the anterior 2/3 of tongue which includes pain and temperture
4. Supplies secretomotor fibers to the parotid gland
5. Supplies efferent vasodilator fibers to the tongue

BIPP Pack

Introduction:

Bismuth iodine paraffin paste is routinely used to pack nasal cavities. This was first used by James Morrison Rutherford Professor of surgery Durham to dress first world war soldier's wounds.

BIPP Pack:

This is a sterile gauze (ribbon) impregnated with a paste containing:

1. one part bismuth subnitrate
2. Two parts iodoform
3. One part sterile liquid paraffin by weight

Role of Bismuth subnitrate:

It is a topical astringent and antiseptic. It is soluble in weak acid but insoluble in water and alcohol. It contributes to the antibacterial properties of BIPP pack by releasing dilute nitric acid on hydrolysis.

Bismuth is not completely safe from complications. It is considered to be less toxic than antimony and polonium. It has a half life of 5 days in the body but is known to remain in kidney for a long time. Bismuth can cause neurotoxicity because it is known to interfere with oxidative metabolism of brain. This complication is very rare when BIPP pack is used to pack the nasal cavity.

Symptoms of Bismuth toxicity:

1. Head ache
2. Nausea
3. Stomatitis
4. Bismuth line in the gingiva (Bismuth line)

Absorption of bismuth is more when packing is made on tissues that has already been injured. Hence considerable amount of caution should be exercised before repeated nasal packing due to epistaxis.

Iodoform:

Its chemical name is triiodomethane.

This is another component of BIPP pack. It has a dinstinctive color and smell. It is insoluble in water and is highly soluble in chloroform / ether. Iodoform decomposes to release iodine which is an antiseptic. Iodine toxicity is common when BIPP packing is used to pack large wounds.

Paraffin:

Serves to lubricate the area packed. It minimizes trauma which could occur during packing.

Uses of BIPP Packs:

1. Used to pack ears following surgery
2. Used to pack nasal cavities after nasal surgeries

Bismuth is radio opaque. BIPP packs also contain a radio opaque marker strip which makes its identification easier when it is lost inside the cavities. Plain radiograph of the area is sufficient to identify the pack.

Chronic otitis externa

Introduction:

Chronic otitis externa is a chronic inflammation involving the skin lining of the external auditory canal of unknown etiology. Diverse mechanisms from allergy to autoimmune reaction has been implicated. Things which are pretty clear about this condition are that:

1. It is not acute & painful as acute otitis externa
2. It is not an invasive condition involving the skull base (like malignant otitis externa)

Characterstic features:

1. It waxes and wanes showing intervening periods of remissions and exacerbations affecting the quality of life
2. It is bilateral in more than half of these patients
3. Pruritis is common
4. Clear / seromucinous discahrge is seen during periods of exacerbations
5. Aural fullness is also common

Two types of chronic otitis externa have been encountered.

Chronic otitis externa with seborrhoea:

This condition is characterised by lack of cerumen. These patients may have clear ear discharge, sometimes this discharge could be seen admixed with white flakes. The skin lining the external canal may be erythematous and shiny in appearance.

Chronic exematous otitis externa:

This condition is characterised by weepy, moist, erythematous and tender skin in the external auditory canal. It can also spread to involve the pinna causing perichondritis.

Causes of chronic otitis externa:

1. Allergy
2. Contact dermatitis
3. Wegner's granulomatosis
4. Reduced cerumen production
5. Cerumen produced ineffective against pathogens ?

Studies also reveal that the relative humidity is higher and pH is also higher in these ears. If pH could be lowered it would make the environment inhospitable for pathogens.

Role of Dermatophytid reaction in chronic otitis externa:

Low grade fungal infections elsewhere in the body can set up inflammatory allergic reaction in the skin lining the external auditory canal. Hence it is worthwhile making a meticulous search for the presence of fungal infections elsewhere in the body and treating it aggressively. Yeast elimination from diet is strongly advocated. If serum IgE is elevated then immunotherapy could be considered.

Management:

1. Removal of all / potential irritants
2. Topical steroid therapy
3. A course of oral steroid can be administered in refractory cases
4. Topical application of 1% Tacrolimus ( a nonsteroidal immunosuppresant) has been used with reasonable success

Grommet insertion Revised indication guidelines

Introduction:

Myringotomy with grommet insertion was introduced by Poltizer of Vienna in 1868. He used this procedure to manage “Otitis media catarrhalis”. Soon it became the common surgical procedure performed in children.

Indications:

Bluestone and Klein (2004) came out with revised indications for grommet insertion which took into consideration the prevailing antibiotic spectrum.

1. chronic otis media with effusion not responding to antibiotic medication and has persisted for more than 3 months when bilateral or 6 months when unilateral.
2. Recurrent acute otitis media especially when antibiotic prophylaxis fails. The minimum episode frequency should be 3/4 during previous 6 months / 4 or more attacks during previous year.
3. Recurrent episodes of otitis media with effusion in which duration of each episode does not meet the criteria given for chronic otitis media but the cumulative duration is considered to be excessive (6 episodes in the previous year)
4. Suppurative complication is present / suspected. It can be identified if myringotomy is performed.
5. Eustachean tube dysfunction even if the patient doesnt have middle ear effusion. Symptoms are usually fluctuating (dysequilibrium, tinnitus, vertigo, autophony and severe retraction pocket).
6. Otitis barotrauma inorder to prevent recurrent episodes.

Problems with Grommet insertion:

This procedure is not without its attendant problems. Common problems include:

1. Segmental atrophy of tympanic membrane
2. Tympanosclerosis
3. Persistent perforation sydrome (rare)
   Before treating patients with otitis media with effusion the following factors should be borne in mind.

Pneumatic otoscopy should be used to differentiate otitis media with effusion from acute otitis media.

Duration of symptoms should be carefully documented.

Children with risk for learning / speech problems should be carefully identified.

Hearing should be evaluated in all children who have persistent effusion for more than 3 months.

Grommet insertion can be performed under local anesthesia.

Incision is made in the antero inferior quadrant of ear drum. The incision is given along the direction of radial fibers of the middle layer of ear drum. This causes minimal damage to the radial fibers. It also enables these fibers to hug the grommet in position.

Management of vestibular schwannomas current trends

Introduction:

Management of vestibular schwannomas has undergone lots of changes during the past decade.  Review of published literature exemplifies this fact.  Various currently available management modalities to treat this condition are:

1.      Observation

2.      Stereotactic radiosurgery

3.      Microsurgery

Among these three modalities stereotactic radiosurgery is evincing keen interest because of the precision of the procedure and lesser incidence of side effects.  Advances in imaging technology have enabled early diagnosis of these lesions.  About a decade back the sensitivity of imaging techniques used to identify lesions measuring 30 mm.  Recent imaging modalities are accurate enough to identify even lesions measuring less than 10 mm.  A stage has reached when surgeons are managing more intracanalicular lesions than ever before.

The current management modality of these tumors focusses on:

Preservation of hearing

Preservation of facial nerve functions.

Observation / Watchful waiting:  This modality is preferred in managing patients with small asymptomatic / minimally symptomatic intracanalicular tumors.  Since tumor doubling time of these lesions is prolonged (1-2 mm / year) this method warrants a trial.  Advantages of this method are preservation of hearing and facial nerve function in these patients.  Studies have also revealed that growth rates between intracanalicular and extracanalicular tumors are not significantly different.  It is ideal to perform imaging at least twice a year within the first year of diagnosis and once a year from there on.

Positive features that could warrant this management modality include:

1.      Excellent speech discrimination scores

2.      Growth rate of less than 2.5 mm / year

Microscopic surgery:

This is indicated for small intracanalicular lesions with vestibular symptoms.  Amount of tumor growth also is one important factor that could force the hands of a surgeon.  Growth rate of more than 3mm / year is an indication for surgical intervention.  Hearing can be conserved by using retrosigmoid / middle cranial fossa approach.

Stereotactic radiosurgery:

This is indicated in residual lesions after microscopic excision or rapidly enlarging canalicular lesions.  Advantages of radiosurgery include:

1.      Hearing preservation

2.      Conservation of facial nerve function