Role of eosinophils in Nasal polyposis

Introduction:

Nasal polyposis is a difficult problem to manage because of its high recurrence rate, incomplete understanding of the various pathophysiological factors involved. No specific etiological factor has been attributed to the development of nasal polypi. Hence the current understanding is that it could be caused by multiple different diseases with varying degrees of severity. That is the reason why categorization of unique presentations of nasal polypi will help in better understanding of etiopathogenesis of nasal polypi.

Studies pertaining to different categories of nasal polypi have identified three disease categories of nasal polypi which show prominent tissue eosinophil infiltration. These include:

1. Chronic hyperplastic eosinophilic sinusitis
2. Allergic fungal sinusitis
3. Aspirin induced hypersensitivity

A brief account of development of eosinophils:

Eosinophils develop from the pleuripotent stem cells of bone marrow. These pleuripotent stem cells differentiates into eosinophil / basophil progenitors.

Transcription factors responsible for stimulating the stem cells to produce cells of eosinphil lineage:

1. GATA-1
2. PU.1
3. C/EPB

Among these three transcription factors GATA-1 is the primary transcription factor responsible for eosinophil differentiation of stem cells.

Cytokines responsible for development of eosinophil lineage:

1. IL-3
2. IL-5
3. Granulocyte macrophage colony stimulating factor

Among these cytokines IL-5 is responsible for selective terminal differentiation of eosinophils. It also stimulates the release of eosinophils from the bone marrow into the peripheral circulation. Studies have shown that anti IL-5 drugs when administered have reduced significantly the number of circulating eosinophils. Blocking the tissue effects of these cytokines may significantly lower the number of circulating / tissue eosinophils.

Factors responsible in attracting eosinophils into tissues:

The process of chemotactic migration of eosinophils to the tissues is known as recuritment. This process of recruitment is facilitated by:

1. Cytokines
2. Chemokines
3. Inflammatory mediators

Platelet activation factor is the most potent inflammatory mediator which induces migration of eosinophils (selective) to the tissues. This is usually secreted by mast cells, endothelial cells, macrophages, neutrophils and eosinophils. Eosinophils migrate preferentially to tissues exposed to environment i.e. (nose, gut and lungs). Human tissuee eosinophils is 100 times more in number than eosinophils circulating the the blood.

Many cytokines play a vital role in eosinophil mediated inflammtion by prolonging its life. The classic example of such substance is Tumor Necoris Factor alpha.

Activation of eosinophils causes release of various biological products, the most prominent of them is the granule protein which is cationic and toxic to numerous helminths thus playing a vital role in the body's defence against helminthic infections.

Substances produced by activated eosinophils:

1. Major basic protein
2. Eosinophil cationic protein
3. Eosinophil derived neurotoxin
4. Chemokines

Management of eosinophilic sinusitis:

Accumulation of eosinophils in the nasal mucosa is seen in:

1. Chronic hyperplastic eosinophilic sinusitis
2. Allergic fungal sinusitis
3. Aspirin induced hypersensitivity

These conditions can be pharmacologically manaaged by:

Leukotrienes modifiers – Drugs belonging to this group reduces eosinophil recruitment and activation. Zafirleukast and Monteleukast are classic examples of drugs belonging to this group.

IL-5 blocking – Mepolizumab. This is humanized anti IL-5 drug.

Etiopathogenesis of antrochoanal polyp various theories

Etiopathogenesis: This disease is commonly seen only in non atopic persons.  Its etiology is still unknown.  Infact this disorder is not associated with nasal allergy.  
Proetz theory:  Proetz suggested that this disease could be due to faulty development of the maxillary sinus ostium, since it was always been found to be large in these patients.  Hypertrophic mucosa of maxillary antrum sprouts out through this enlarged maxillary sinus ostium to get into the nasal cavity.  The growth of the polyp is due to impediment to the venous return from the polyp.  This impediment occur at the level of the maxillary sinus ostium.  This venous stasis increases the oedema of the polypoid mucosa thereby increasing its size.





Bernoulli's phenomenon: Pressure drop next to a constriction causes a  suction effect pulling the sinus mucosa into the nose.


Mucopolysaccharide changes: Jakson postulated that changes in mucopolysaccharides of the ground substance could cause nasal polyp.


Infections: Recurrent nasal infections have also been postulated as the cause for nasal polyp

Mill's theory:

Mills postulated that antrochonal polyp could be maxillary mucoceles which could be caused due to obstruction of mucinous glands.

Ewing's theory:Ewings suggested that an anomaly which could occur during maxillary sinus development could leave a mucosal fold close to the ostium. This fold could later be aspirated into the sinus cavity due to the effects of inspired air causing the development of antrochonal polyp.





Vasomotor imbalance theory: This theory attributes polyp formation due to autonomic imbalance


Polypoidal tissue from the maxillary antrum exits out through the accessory maxillary sinus ostium according to some workers.  This accessory sinus ostium is placed posteriorly, which could be the reason for the polyp to present posteriorly.  The accessory sinus ostium widens progressively, ultimately at one stage merging with the natural ostium of the maxillary sinus forming one huge opening into the maxillary antrum.

Infection / Inflammation:
This theory suggests that acinous mucous glands within the maxillary sinus cavity gets blocked due to infection / inflammtion involving the mucous lining of the sinus cavity. This leads to the formation of a cystic lesion within the maxillary sinus cavity. This cyst gradually enlarges to occupy the whole of the maxillary sinus cavity. It exits the sinus cavity by enlarging the accessory ostium and enters the nasal cavity. Usually these cysts arise from the antero inferior / medial wall of maxillary antrum.
Possible reasons for migration of antrochoanal polyp in to the post nasal space:


1.  The accessory ostium through which the polyp gets out of the maxillary antrum is present posteriorly.


2.  The inspiratory air current is more powerful than the expiratory air current thereby pushes the polyp posteriorly.


3.  The natural slope of the nasal cavity is directed posteriorly, hence the polyp always slips posteriorly.


4. The cilia of the ciliated columnar epithelial cells lining the nasal cavity always beats anteroposteriorly pushing the polyp behind.

Pathology of nasal polyp

Introduction:

Macroscopically polyp appears to arise like a pedicled tissue from the nasal mucosa. Histopathology of thesee nasal polypi are rather diverse ranging from simple inflammatory polyp to benign / malignant neoplasm. Polyp due to chronic rhinosinusitis can be defined as non granulomatous inflammatory tissue projection arising from the nasal mucosa.

Histology of normal sinonasal mucosa:

For sake of convenience components of normal sinonasal mucosa can be categorized under two heads;

1. Structural components
2. Non structural components
   
   
   
   
   Structural components – Include epithelium, basement membrane and submucosal tissue.
   
   
   Non-structural components – Include resident and Non resident cells of lymphoid and myeloid lineage.
   
   
   Epithelium & Basement membrane:
   
   
   The anterior 2 cms of the nasal cavity is lined by skin comprising of keratinized stratified squamous epithelium. It also contains fibrocollagenous dermis and adnexal glands. The rest of the nasal cavity is lined by respiratory type of epithelium which develops from ectoderm. This mucous membrane is also known as Schneiderian membrane.
   The Schneiderian membrane is composed of four cell types:
   1. Ciliated columnar / cuboidal epithelial cells
   2. Interspaced between these cells are goblet cells
   3. Non ciliated columnar cells with microvilli
   4. Basal cells
   
   
   The ratio of columnar to goblet cells is roughly 5:1.
   The normal nasal epithelium may show metaplastic changes i.e. presence of cuboidal / metaplastic squamous epithelium due to constant drying effects of inspired air. Metaplastic changes are commonly seen at the head of inferior turbinate. The columnar epithelium contains tight junctions and they rest on the basement membrane.
   The basement membrane contains collagen fibres of types (I, III, IV, V, VI and VII). Other constituents of basement membrane are:
   Heparan sulfate proteoglycan
   Laminin
   Nidogen
   
   
   The basement membrane is rather thin and delicate in the whole of the nasal cavity. It is usually thick over the inferior turbinate area.
   
   
   In comparison the lining mucosa of the paranasal sinuses are rather thin and less specialized in nature. This difference could be attributed to their different embryological origin and functional differences.
   
   
   The superior turbinate, superior portion of nasal septum, roof of the nasal cavity, and superior and medial portions of the middle turbinate are lined by olfactory epithelium. The olfactory epithelium is also pseudostratified ciliated columnar epithelium containing bipolar olfactory cells, microvillar cells and supporting sustentacular cells. Due to increasing age / infections the olfactory epithelium may be replaced in patches by normal nasal mucous membrane.
   
   
   Submucosa:
   This lies under the basement membrane overlying the cartilage / bony frame work of the nasal cavity. It is composed of loose fibrovascular connective tissue, numerous seromucinous and minor salivary glands. It also contains blood vessels, nerves, myeloid and lymphoid cells. The blood vessels include extensive arterial and venous anastomosis. These blood vessels communicate with venous erectile tissue. This erectile tissue is more prominent over the turbinates.
   
   
   Non structural components:
   Lymphoid tissue in the nasal mucosa comprises of:
   1. single lymphocytes scattered among the epithelial cells and lamina propria
   2. NALT – Nasal associated lymphoid tissue resembling payer's patches of the gut. These are not encapsulated.
   NALT is not well formed like Payer's patches of the gut. They become enlarged and pronounced during nasal infections.
   The lymphoid cells include:
   
   
   1. T cells
   2. B cells
   3. Plasma cells
   4. Natural killer cells
   
   
   Conditions causing nasal polypi include:
   
   
   1. Chronic rhinosinusitis
   2. Samter's triad – This include bronchial asthma, aspirin sensitivity and nasal polyposis
   3. Eosinophilic mucous chronic rhinosinusitis (including AFRS)
   4. Cystic fibrosis
   5. Young's syndrome
   6. Churg – Strauss disease
   
   
   Macroscopic features of nasal polypi:
   1. Pale smooth shining and oedematous
   2. Soft in consistency when compared to surrounding nasal mucosa
   3. Long standing nasal polypi can be firm and white due to metaplasia of lining mucosa and presence of extensive fibrosis
   
   
   Polypi due to chronic rhinosinusitis does not show surface mucosal ulceration. Presence of surface ulceration macroscopically in polyp tissue should arise suspicion of other pathologies. Presence of thick dark tenaceous secretions along with nasal polypi is caused due to Eosinophilicc mucous chronic rhinosinusitis / AFRS etc.
   
   
   Microscopic changes:
   
   
   Microscopic changes seen in polypoid tissue are:
   
   
   1. Structural changes involving lining epithelium, submucosa and rarely underlying bone
   2. Presence of inflammatory exudate
   
   
   Typical nasal polyp is lined by ciliated columnar epithelium. Their basement membrane is of varying thickness. The stroma contains lymphocytes.
   
   
   Histological classification of nasal polypi:
   
   
   1. Oedematous / allergic nasal polypi
   2. Chronic inflammatory nasal polypi
   3. Seromucinous / glandular polypi
   
   
   Oedematous / allergic nasal polypi: Is the commonest variety. This type is seen in patients with allergy. The association between nasal allergy and polyposis still remains controversial. These polypi are lined by ciliated columnar epithelium with ulceration, mucositis, epithelial hyperplasia, squamous metaplasia. The basement membrane is thickened and the submucosa is oedematous. Mucous retention cysts may also be seen. Inflammatory cell infiltrate include eosinophils, plasma cells and lymphocytes. Polypi in patients with cystic fibrosis have thin basement membrane with less stromal eosinophilia and predominantly neutrophilic infiltrations. Hence cystic fibrosis polypi are termed as neutrophilic polyp. Mucous secretions in patients with cystic fibrosis are thick and densly eosinophilic in nature.
   
   
   Chronic inflammatory polyp: This is also known as fibroinflammatory polyp. This type of polypi are less common. This type of polypi may be caused when oedematous polypi are traumatized. Thee stroma may undergo secondary inflammatory change causing myofibroblastic proliferation. These polypi may mimic soft tissue neoplasm. The surface epithelium shows squamous metaplasia which is a manifestion of chronicity of the disease. The submucosa characteristically show fibrosis. This is a classic feature of this type of polyp.
   
   
   Seomucinous polypi: Hyperplasia of seromucinous glands are rare. These are considered to be true neoplasm.
   
   
   Underlying bone shows remodelling. This is all the more true in long standing disorders.
   
   
   
   

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History of nasal polypi

Introduction:

Nasal polypi were first described about 4000 years ago. Egyptians were pioneers in identification and treatment of nasal polyposis. They were more familiar with the anatomy of the nose because they used intranasal route to suck out the brain during mummification procedures. It was Hippocrates who is considered to be the father of Rhinology who coined the term polyp. He used this term because these intranasal polypi resembled sea polypi.

“Nasal polyps are sacs of phlegm that cause nasal obstruction and deranges the sense of smell”

Hippocrates.

“ A Nasal polyp shows itself by bad smell of the nose”

Samuel of Egypt

“Large polyp from the nose can dangle into the throat stangling a person to death”

Celsus

Etiopathology:

During early first century A.D. Celsus documented that nasal polypi enlarged in size during moist weather. He also hypothesized that nasal polypi were local manifestation of a systemic disorder.

Boerhaave during the 17^th century hypothesized that polypi was elongation of nasal mucosa. At about the same time Manne and Heister suggested that polypi are caused by obstruction to nasal mucosal glands. Billroth in 1843 demonstrated that the lining mucosa of nasal polypi resembled normal nasal mucosa and went to the extent of suggesting that nasal polypi could be due to hypertrophy of nasal mucosa.

During 19^th century Virchow taught his students that nasal polypi were primary tumors like myxomas and fibromas. Eggston & Wolff came close to suggesting that nasal polypi could be caused by passive oedema involving the nasal mucosa.

Relationship of nasal polypi with that of allergy: Kern & Shenck in 1933 demonstrated that allergy was common in patients with nasal polypi. It was 25% more common in this group when compared to that of normal individuals. They also suggested that ethmoidal sinus commonly gave rise to these polypi due to their complex anatomy.

Eggston's theory of etiology of nasal polypi:

Eggston suggested that nasal polypi could result due to basic vascular changes involving the submucosal vessels of nasal mucous membrane due to inflammation leading on to periphlebitis which obstructed venous return causing congestion of the nasal mucous membrane. He considered this oedema to be passive in nature.

Acid mucopolysaccharide theory of Burn: According to Burn the stroma of nasal polyp contains acid mucopolysaccharides. He attributed that the presence of mucopolysaccharides in the stroma could play some role in the pathophysiology of nasal polyposis.

Berden opined that the accumulation of reagin and edema in the stroma of nasal polypi could be features suggestive of allergic inflammation.

The association between nasal polypi and cystic fibrosis was demonstrated by Lurie in 1959.

Samter and Beer in 1969 reported the classic “Samter's triad” which comprise of aspirin sensitivity, nasal polypi and bronchial asthma.

History of nasal instruments:

Introduction of nasal speculum facilitated examination of nasal cavity in a big way. Hippocrates introduced a tubular nasal speculum which was designed from a protype speculum used by Hindu surgeons. It was Fabricious Hildanous who designed an aural speculum in 1560 which closely resembled the currently available nasal speculum. This Hildanous speculum has undergone minor modifications to evolve into a nasal speculum.

Morrel Mekenzie utilized mirror to reflect sunlight into the nasal cavity to visualize its contents. Kirstein designed the modern head light used in otolaryngological practice.

Development of X-rays is considered to be a turning point in many ways in the diagnosis of nasal polyp. Various views were evolved to visualize the paranasal sinuses.

Historic medical management of nasal polypi:

Hippocrates used a variety of nasal packs / tampoons dipped in pepper and honey in managing patients with nasal polypi. According to him repeated sneezing induced by exposure to pepper caused some relief.

Celsus treated nasal polypi with application of caustic agents.

Galen used oil / and irritants like turpentine local application used to treat nasal polypi.

Daniel Bovet was the first to use antihistamines in the management of nasal polypi.

Historic surgical management of nasal polypi:

Italian physician Rolando used string with knots to remove polypi. He managed topass this knotted thread into the nasal cavity. Knots were tied to the thread 1 cm apart. When the threat is pulled out it dislodges the polyp and brings it along with it.

Hippocrates described a method of dislodging the polyp from the nasal cavity and delivering it via the post nasal space. He introduced a wire loop into the nasal cavity to snare the polyp lying within the nasal cavity.

 

Figure showing a primitive head light

The Tamilnadu Dr MGR Medical University MBBS Prefinal Otolaryngology August 2007 question paper with solution

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Endoscopic inferior meatal antrostomy has it got any role today?

Introduction:

Since the introduction of Functional endoscopic surgery inferior meatal antrostomy as a procedure has taken a back seat due to the apprehension that it could tamper with the normal mucociliary clearance mechanism. Infact studies performed in 1980's reported that if inferior meatal antrostomy is created the mucous bridges across the antrostomy and travels towards the natural ostium of the maxillary sinus. This can utmost be considered to be only partially true. Current studies have demonstrated that drainage of mucous does occur via the opening created in the inferior meatus.

Current indications for inferior meatal antrostomy:

1. Patients with chronic sinusitis not responding to FESS
2. Patients in whom mucociliary clearance is already affected due to cystic fibrosis / Young's syndrome. These patients usually benefit from inferior meatal antrostomy
3. Mycetoma present in the maxillary sinus cavity
4. To visualize the difficult to see areas inside maxillary sinus cavity
5. When regular post op surveillance is needed

Endoscopic inferior meatal antrostomy:

Nasal endoscope is a very useful tool for otolaryngologist. By using this tool the whole procedure can be performed under direct visualization. This procedure can be performed under both LA / GA.

Nasal decongestion:

Nasal mucosa is decongested by using pledgets soaked in 4% xylocaine mixed with 1 in 10,000 adrenaline. The pledget should be squeezed dry before insertion. This is done to avoid xylocaine overdosage. Pledgets should be placed in inferior meatus, floor of the nasal cavity, and middle meatus. If general anesthesia is used throat pack should be given to prevent aspiration.

Infiltration:

2% xylocaine with `1 in 100,000 units adrenaline is used to infiltrate the inferior turbinate and the corresponding portion of nasal septum. 0 degree nasal endoscope is used for purposes of visualization. A Freer's elevator is inserted into the inferior meatus and the inferior turbinate is up fractured so that it lies perpendicular to the floor of the nasal cavity. This procedure is a must for adequate visualization of the inferior meatal area. The location of Hasner's valve (lower end of nasolacrimal duct) is identified at the junction of anterior third and middle third of the lateral nasal wall. A 90 degree angled J curette is ideal to perform antrostomy. The lateral nasal wall is perforated with J curette about 1 cm posterior to Hasner's valve. The opening is then enlarged with the help of back biting forceps. Now insertion of a 30 degree nasal endoscope will help in better visualization of the interior of maxillary sinus cavity.

Manipulation of simple fractured nose using mallet and champagne cork

Introduction:

Fractures involving nasal bones are common.   Manipulating simple fractures involving nasal bones using mallet and champagne cork was reported in a private communication by M ROLLIN, N DE ZOYSA, G MOCHLOULIS of UK.

Procedure:

As for any other nasal surgical procedure the patient is evaluated.  This procedure can be performed either under local anesthesia / general anesthesia.  The champagne cork is enclosed in a sterile glove finger and tied.  

The patient is placed in supine position and the head is stabilized.  The champagne cork is placed over the skin overlying the deviated nasal pyramid.  Disimpaction of fractured nasal bones is achieved by a firm tap of the cork with a mallet.  The rounded end of the cork is used for disimpaction and the flatter end for realignment.

This technique can be used safely to treat simple fractures involving nasal bones with minimal risk of skin trauma.  This technique is more suitable in managing late presenting fractures.

Coblation tonsillectomy

Introduction:

Tonsillectomy is a commonly performed surgical procedure these days. With the advent of latest surgical equipments and innovations the risks involved in the surgical procedure has been considerably reduced. One such emerging technological innovation is the introduction of coablation technology which is currently being used to perform tonsillectomy.

Emerging technology – Current expectations:

Technological innovations in any surgical procedure should focus on the following parameters:

1. Bloodless surgical field
2. Reduction in the surgical time
3. Reduced post operative pain
4. Improved healing rates
5. Affordability
6. Safety

Coablation:

This is also known as “Controlled ablation” / “Cold ablation”. This technology uses bipolar high frequency electrical energy to exite the electrolytes in a conductive medium. This excitation creates a plasma field which is higly focussed. The ions present in the plasma field are highly energized and this energy is sufficient to break organic molecular bonds found in the living tissue. This energy dissolves soft tissue at relatively low temperatures, while preserving the integrity of surrounding tissue. Sodium chloride solution is commonly used as a conducting medium in coablation surgical procedures.

Advantages of coablation:

1. It operates at relatively cool temperatures (40 – 70 degrees centigrade)
2. Its cutting effect is very precise with very minimal effect on the surrounding tissue
3. The plasma field which is generated by this equipment is about 100 – 150 microns thick. This is the reason for its precision

Plasma field:

This is the technology involved in coablation surgical procedures. Plasma field is defined as a collection of charged particles (equal amounts of positive and negative ions). Plasma field resembles gas physically in some respects, but show significant differences as well. Plasma field is a good conductor of electricity and is affected by the presence of magnetic field, where as it is not so with gases.

Crudely put plasma is a state of matter in which many electrons are free and unbound and move independently. Coablation technology utilizes this phenomenon by generating an electrical field between two small electrodes. This electrical field when made to pass through a medium like normal saline which conducts it rather well, the sodium and chloride molecules become energized and separate from the solution. These sodium and chloride ions are responsible for the formation of plama field.

The wand used in coablation surgical procedures has channels for suction and irrigation. Normal saline should flow through irrigation channel and central suction should be connected to the suction channel.

Below you will be seeing the video of coablation tonsillectomy:

 

Anatomy of vidian nerve

Introduction:

The vidian nerve is formed by post synaptic parasympathetic fibers and presynaptic sympathetic fibers. This is also known as the “Nerve of pterygoid canal”.

Nerves that gets involved in the formation of vidian nerve:

1. Greater petrosal nerve (preganglionic parasympathetic fibers)
2. Deep petrosal nerve (post ganglionic sympathetic fibers)
3. Ascending sphenoidal branch from otic ganglion

Vidian nerve is formed at the junction of greater petrosal and deep petrosal nerves. This area is located in the cartilagenous substance which fills the foramen lacerum. From this area it passes forward through the pterygoid canal accompanied by artery of pterygoid canal. It is here the ascending branch from the otic ganglion joins this nerve.

The vidian nerve exits its bony canal in the pterygopalatine fossa where it joins the pterygopalatine ganglion.

Vidian canal:

It is through this canal the vidian nerve passes. This is a short bony tunnel seen close to the floor of sphenoid sinus. This canal transmits the vidian nerve and vidian vessels from the foramen lacerum to the pterygopalatine fossa.

According to CT scan findings the vidian canal is classified into:

Type I: The vidian canal lies completely within the floor of sphenoid sinus

Type II: In this type the vidian canal partially protrudes into the floor of sphenoid sinus

Type III: Here the vidian canal is competely embedded in the body of sphenoid bone

 

Study of these anatomical differences of vidian canal in relation to the floor of sphenoid sinus helps in deciding the surgical approach to the nerve.

CT images showing the anatomical types of vidian canal and their relationship to the floor of sphenoid sinus

 

The Tamilnadu Dr MGR Medical University Prefinal MBBS otolaryngology March 2008 question paper with solution

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Oral Candidiasis

Introduction:

Oral candidiasis is a very common fungal infection involving the oral cavity mucosa. These infections are caused by saprophytic fungi belonging to the genus candida. Common organisms involved in oral candidiasis include:

Candida albicans

Candida glabrata

Candida tropicalis

Among these organism candida albicans has been implicated as the common causative organism in oral candidiasis. Candida albicans is dimorphic in nature, capable of existing in two forms i.e yeast and hyphal forms. The hyphal form is associated with oral candidiasis. Studies have shown that candida albicans can exist in the oral cavity as normal commensal.

Predisposing factors causing oral candidiasis:

1. Poorly controlled diabetes mellitus
2. In HIV positive patients with CD 4 count less than 200/microlitre
3. Patients with xerostomia – Use of medications in the elderly are the common cause of xerostomia. Medications known to cause xerostomia include: antidepressants, diuretics and drugs with anticholinergic effects.
4. Use of broad spectrum antibiotics that could alter the normal gut flora.
5. Use of systemic steroids

Clincially oral candidiasis can present as both erythematous / white forms. White forms are otherwise known as pseudomembranous type / hyperplastic candidiasis.
  You can view the full article here.http://www.drtbalu.co.in/oral_candidiasis.html

Burning Mouth syndrome

Introduction:

Burning mouth syndrome is defined as an idiopathic condition involving the mucosal lining of oral cavity causing excess deep burning pain in the absence of identifiable cause lasting atleast for a period of 6 months. This condition was first described by Fox in 1935.

Synonyms:

Glossodynia, Glossopyrosis, Oral dysesthesia, Stomatodynia & Sore tongue. Among these terms Glossodynia is favoured by ICD (International Classification of Diseases).

Sex prediliction:

It affects females 7 times more commonly than males. Studies have shown about 90% of sufferers are perimenopausal women.

Common sites involved:

1. Tongue
2. Hard palate
3. Lips
4. Buccal / Labial mucosa
5. Soft palate
6. Floor of mouth

Associated symptoms:

a. Dryness of mouth – This is purely a subjective sensation not backed by real time reduction in the amount of saliva secreted. Hence this sensation could mean altered sensation to be the cause rather than hyposalivation.

b. Altered taste

Read the full article from here.http://www.drtbalu.co.in/bms.html

The Tamilnadu Dr MGR Medical University MS ENT Basic sciences March 2010 question paper with solution

My effort to solve previous years question papers of the Tamilnadu Dr MGR Medical University continues,  I have uploaded the MS ENT March 2010 Basic sciences question paper with solutions.  You can get it from 
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Meniere's disease Second edition

History:

In late 19th century Prosper Meniere described a condition characterized by ear block, tinnitus, and vertigo. He even correctly identified the site of lesion to be labyrinth. It wont be a understatement to say that precious little has been added to the knowledge and understanding of the disorder since then. Prosper Meniere infact lived far ahead of his time. He was born in 1799 in France. In 1848 he began to translate the text book on hearing loss authored by Kramer. The book was written in German. This kindled his interest in otology.

In his classical seminal reports he goes on to describe a series of patients who presented with neural deafness, with hearing loss greater for low frequencies. Deafness was commonly unilateral in these patients. These patients usually  present with tinnitus, vertigo, nausea and vomiting. He reported that these patients had a normal ear drum. He also reported that these symptoms were completely reversible.

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Open conservative partial laryngectomy

Introduction:
Organ preservation is becoming common these days. This applies
to larynx also. Laryngeal malignancies if identified early can be
effectively managed by conservative resection procedures of
larynx.
Advantages of organ preservation:
1. The patient need not live with the stigma of permanent
tracheostomy
2. Speech is preserved to the maximum extent
3. There is effective separation of air and food channels
4. Post operative recovery is very fast
5. Option of salvage total laryngectomy is still an option if the
conservative procedure fails

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Vertical partial laryngectomy

Introduction:




Vertical partial Laryngectomy is a conservative laryngeal surgical procedure which involves removal of one half of the larynx while the other half is preserved. The dead space created after removal of one half of the larynx is closed using various flaps. This surgery was first proposed by Solis – Colen in 1869 to manage early malignant lesions involving vocal folds.


Indications:


1. Malignant tumors involving a single vocal cord early T1, T2 and select T3 lesions


2. Anterior commissure of the vocal cord should be free of the lesion






This surgery is not suitable for patients with growth vocal cord involving the anterior commissure and the opposite cord.


Advantages:


1. This is a conservative procedure where in patient is able to speak without the aid of prosthesis


2. Patient need not have a permanent tracheostome


3. Patient does not have any swallowing problems


You can view the video clipping of the surgery below:
 

Tumor Biology pertaining to laryngeal malignancy

Introduction:




Recent advances in tumor biology and genetics have increased our understanding of the basic mechanisms involved in the development of laryngeal malignancy and in predicting its clinical course. The following genes / enzymes may be of use in diagnosis & in predicting the prognosis of various malignant lesions involving the larynx.






Telomerase:


A brief introduction to this enzyme is a must. A telomere is a repeating DNA sequence at the end of the chromosome. They can reach a length of 15,000 base pairs. These telomeres function by preventing the chromosome from losing base pair sequence at their ends. They also prevent chromosomes from fusing with each other. Each time a cell undergoes division some amount of telomere is lost. When the telomere becomes too short the chromosome reaches a critical length and can no longer multiply. The cell which contains this critical length chromosome is considered to be too old and undergoes cell death (apoptosis). The length of the telomere is controlled by two mechanisms:


Erosion – Occurs each time a cell divides


Addition – This is determined by the activity of telomerase


Telomerase is an enzyme made of protein and RNA subunits. It elongates the chromosomes by adding TTAGGG sequences to the end of the existing chromosomes. This enzyme is found in abundance in fetal cells, germ cells and tumor cells. If this enzyme telomerase is activated in a cell it continues to grow and divide and is known as the “Immortal cell”.






This enzyme has been linked to carcinogenesis of larynx. The presence of this enzyme in the laryngeal cancer specimen serves as a marker in diagnosing persistent malignancy after irradiation. It is very helpful in picking up radio resistant cases / recurrent cases following irradiation.


PH-20:


This is a hyaluronidase usually expressed by malignant tissues. It is usually found to be elevated in metastatic lesions and hence can be used as a valuable tumor marker in identifying early nodal metastasis.


Herpes simplex virus DNA:


Polymerase chain reaction can be used to identify Herpes simplex virus DNA. This is found to be positive in nearly 75% of patients with laryngeal malignancies. This is due to the fact that this virus protein is a proved carcinogen.


Mutations involving gene p53:


Mutations involving gene p53 correlates with the clinical outcome of patients with laryngeal cancer.


Retinoblastoma protein:


Negative expression of this protein has been associated with higher likelihood of lymph node metastasis with significantly lower 5 years survival rates.






Cyclin D1:


This has been identified by immuohistochemical staining of paraffin embedded specimen. Low levels of cyclin D1 have been associated with radio resistance.

Haller cell

Synonyms: These are also known as Infra orbital recess cells.

Introduction:

These are pneumatized ethmoid air cells that project along the medial roof of the maxillary sinus and the most inferior portion of the lamina papyracea.

This air cell lies below the ethmoid bulla and lateral to the uncinate process.

Commonly these cells arise from anterior ethmoid air cells and are closely related to the infundibulum. Rarely these cells can arise from posterior

ethmoidal cells in which case it does not compromise the infundibulum.

Infections involving these cells can compromise and narrow the infundibulum causing obstruction to the drainage of maxillary sinus ostium.  It has been suggested that infections involving these cells could be a factor in recurrent maxillary sinusitis.

The Tamilnadu Dr MGR Medical University MS(ENT) Basic sciences September 2009 question paper with solution

The Tamilnadu Dr MGR Medical University MS(ENT) Basic sciences September 2009 question paper with solution

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CSF rhinorrhoea repair using bicoronal approach

Clinical details:

30 years old male patient came with c/o watery discharge from left nasal cavity - 3 years duration
H/O Road traffic accident 3 years back following which watery discharge started.
H/O meningitis 2 years back for which he was treated.
H/O Head ache on and off ++.

On examination:

Watery discharge was seen flowing out of left nasal cavity. It was more pronounced when the patient bent down.

Imaging:

CT paranasal sinus showed fracture involving the posterior table of frontal sinus with evidence of pneumatocele in the left
frontal lobe.

Management:

Since the fracture was present laterally in the posterior table of frontal sinus external approach was preferred.

Bicoronal approach was used to expose the anterior table of frontal sinus.

The incision begins in the preauricular crease at the level of tragus and traverses the scalp 3-4 cms behind the hair line.
The incision is carried down through the galea to the loose alveolar plane above the calvarial periosteum and the deep temporal
fascia and the flap is elevated anteriorly until approximately 2cms above the supra orbital rims. At this point the periosteum is
incised and the dissection is continued in the subperiosteal plane. The supraorbital neurovascular bundles are protected.
Laterally the dissection continues in the subgaleal plane up to 1-2 cms above the zygomatic arch. The deep temporal fascia
is incised at this point and the dissection continues deep to the temporal pad of fat over the temporalis muscle and the investing
fascia. The deep temporal artery perforators should be protected if not this could lead to a hallowing in the temoporal area due
to wasting of temporalis muscle.

The anterior table of frontal sinus is exposed. A window is created over the anterior table of frontal sinus using a fissure burr.
The interior of frontal sinus was visualized and the leak was identified over the posterior table of left frontal sinus which was
sealed using tissue glue and abdominal fat.