Saturday 29 October 2011

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.

Friday 28 October 2011

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


Thursday 27 October 2011

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:








Monday 24 October 2011

Velopharyngeal insufficiency and its management

velopharyngeal_insuff

Saturday 22 October 2011

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



Friday 21 October 2011

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.

Thursday 20 October 2011

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

Monday 17 October 2011

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.



Sunday 16 October 2011

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

Tuesday 11 October 2011

Susac syndrome

Introduction: Susac syndrome was first described by Susac etal in 1979. This syndrome is characterised by rapidly progressing encephalopathy, blindness and hearing loss. Pathophysiology: This is actually an endotheliopathy affecting precapillary arterioles. This endotheliopathy could probably be immune mediated. This causes rapid tissue infarction which leads to these problems. Women are commonly affected than men. Typical vulnerable age group is between 20 – 40. Clinical features: 1. Severe head ache 2. Rapid dementia 3. Micro infarcts seen in corpus callosum demonstrable in MRI scans 4. Photopsia and black spots due to retinal artery occlusion 5. Scintillating scotoma 6. Rapidly progressive sensori neural hearing loss on both sides 7. Vertigo 8. Nystagmus Management: High dose steroid therapy is the main treatment modality. Intravenous administration of immunoglobulin. Cyclophosphamide administration. Rituximab is the currently used drug in the management. This is a monclonal antibody against CD20 protein. This receptor protein is found on the surface of B lymphocytes.