Sialendoscopy

Introduction:

Common disorders of salivary glands involve obstruction involving their ductal system. Salivary gland calculi comprises the most common cause of enlargement of salivary glands. Obstructions could be caused by the presence of calculi, strictures of the duct etc. Sialoendoscopy is the most preferred mode of treating obstructions involving major salivary glands. Major advantage of this procedure is that it can be performed under local anesthesia as an office procedure.

History:

It was Konigsberger and his colleagues first used sialoendoscopy and lithotripsy to treat salivary gland calculi in 1990. During the year 1991 Gundlach and colleagues published their experience of doing sialoendoscopic procedures. Katz in 1991 used a 0.8 mm flexible endoscope to diagnose sialolithiasis and to remove them from major salivary glands. It was Kongisberger and colleagues who successfully used a flexible mini endoscope and intracorporeal lithotriptor to fragment major salivary gland calculi, thus opening up new vistas.
In 1994 Arzoz and his colleagues first introduced a 2.1 mm rigid endoscope which had a 1mm working channel as sialendoscope. This was indeed a mini urethroscope. They also used a Pneumoballistic lithotriptor along with this endoscope to hit the calculus and break it. This work was followed by Nahlieli who published his three years experience with rigid sialendoscope in the year 2000.


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Pseudocyst of Pinna

This condition involves the Pinna and can frequently recur even after successful treatment. It goes by various names i.e. intercartilagenous cyst, endochondral Pseudocyst and idiopathic cystic chondromalacia. This condition was first described by Engel in 1966.

Clinical features:

1.Presents as painless, spontaneous dome shaped cystic swelling on the anterior surface of auricle.
2.This condition is predominantly seen in adult males
3.It is uncommon before 20 and after 60 years of age.
4.Majority of these cysts are found in the scaphoid and triangular fossae of the pinna
5.Majority of these cysts have been reported in Chinese. Chinese have attributed this problem due to the firm pillow they use to sleep. Studies have not demonstrated any racial differences.
6.Right ear is more commonly affected than the left. This has been attributed to the habit of majority of individuals to sleep on their right side.

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Congenital Epulis

Introduction:
“Epulis” is a Greek term meaning Gums. This term is used to denote a wide variety of lesions involving the gums regardless of their pathology.
This is a rare congenital growth affecting the gingival mucosa of neonates. It is also known as Neumann’s tumor. It is truly a benign condition affecting predominantly female infants. It may even be multiple. This tumor was first described in 1871 by Neumann and hence the name.

These tumors are commonly present at birth arising from the gingival mucosa of maxilla / mandible. These infants may have feeding and breathing difficulties because of the mass effect. Ultrasound studies have shown that this tumor can arise as early as 26th week of gestation.

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Rhinitis medicamentosa

Introduction:

Rhinitis medicamentosa is a condition characterised by nasal congestion without rhinorrohea or sneezing. This condition is caused by the use of topical nasal decongestants for a prolonged period of time. Use of these topical decongestants for more than a week is sufficient to cause this problem. This condition should be differentiated from rhinitis caused by use of drugs like oral contraceptives, antihypertensives and psychotrophic drugs.

History:

The term rhinitis medicamentosa was coined by Lake in 1946.

Synonyms:

Rebound rhinitis / chemical rhinitis

Pathophysiology:

The nasal mucous membrane is rich in resistance blood vessels draining into capacitance venous sinusoids. These resistance blood vessels include small arteries, arterioles and arteriovenous anastomosis. The capacitance vessels (venous sinusoids) are innervated by sympathetic fibers. Sympathetic stimulation causes activation of alpha 1 and alpha 2 receptors present in the walls of the capacitance vessels which leads to decreased blood flow and constriction of venous sinusoids causing nasal decongestion. Parasympathetic stimulation causes release of acetyl choline which increases nasal secretions. Parasympathetic stimulation also causes release of VIP (vasoactive intestinal polypeptides) causing vasodilatation of the resistance blood vessels leading on to dilatation of sinusoids there by causing nasal congestion. In addition to sympathetic and parasympathetic innervation the nasal mucosa is richly endowed with sencory type c fibers. These sensory fibers on stimulation releases neurokinin A, calcitonin gene related peptide and substance P. These substances cause down regulation of sympathetic vasoconstriction causing nasal congestion. The exact pathophysiology of rhinitis medicamentosa is still not clear. Various hypothesis exist. Almost all of them focus on dysregulation of sympathetic / parasympathetic tone by exogenous vasoconstriction molecules.

Possible mechanisms of rhinitis medicamentosa include:

1. Secondary decrease in the production of endogenous norepinephrine through a negative feed back mechanism
2. Sympathomimetic amines used as topical decongestants have effects on both alpha and beta receptors. Their alpha effects predominate over beta effects causing nasal decongestion. This beneficial alpha effect is short lived while beta effect is more prolonged. After cessation of alpha stimulation the sympathomimetic amines still keep stimulating beta receptors causing rebound nasal congestion.
3. Rebound increase in parasympathetic activity causing increased nasal secretion and nasal mucosal congestion
   
   
   
   
   
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Primary itching of external auditory canal and its management

Introduction:

Patients with itchy ear are said to be suffering from “itchy ear syndrome”. Sometimes the itching in the external auditory canal may be so severe that it may even disrupt sleep.

Classification of itchy ear:

Itchy ears has been classified into primary and secondary types.

Secondary itching: of the external auditory canal may be caused by:

1.Dermatitis – contact / seborrhoeic
/ dermatomycosis
2.Systemic disorders causing itching include – jaundice, diabetes, and renal pathology


Primary itching:

In patients with primary itching there is no evidence of dermatitis or systemic disorders which have been attributed to be the causative factors of secondary itching. These patients may at the most have pathogenic colonization of the external auditory canal.
These patients are commonly middle aged or elderly women.

Predisposing features of primary itching include:

1.Excess moisture in the external auditory canal
2.Changes in pH of cerumen
3.Obstruction to external auditory canal due to presence of wax


Management:

These patients can be managed by

1.Topical application of 2% acetic acid
2.Appication of soothing agents like coconut oil
3.Application of topical steroids like triamcinalone
4.Application of silver nitrate gel
5.Oral antihistamines

Long term application of topical steroids is frought with a lot of complications. This includes thinning of epidermis, decreased microvasculature and a reduction in the number of keratinocytes.

Current therapy:

Pimecrolimus
a new topical immunosuppressive agent has shown immense promise in the management of this disorder. This is an immunomodulating agent which has been successfully used in the management of atopic dermatitis. This drug is a macrolactum derivative and is known to inhibit calcineurin which is known to cause itching in these patients.

Role of sphenoplatine ganglion block in managing cluster headaches

Introduction:
Cluster head ache (suicide headache) is one of the most painful of all headache syndromes. It is characterized by very severe orbital / temporal pain occuring usually on the same side lasting between 15-150 minutes if not treated. Cluster headache attacks are usually associated with rhinorrohea, lacrimation, conjunctival injection, perspiration and psychomotor agitation. These clusters usually occurs during “cluster periods” which range between 6-12 weeks with painless intervel inbetween.

Pathophysiology:

Current views suggest that cluster headaches are caused by central mechanisms which are triggered by reflex arc involving the sphenopalatine ganglion. Hypothalamus has been suspected to play an important role in the pathophysiology of cluster headaches. That is the reason for using deep brain stimulation of the posterior nucleus of hypothalamus in managing drug resistant cases of cluster headaches.

Role of sphenopalatine ganglion block:

Recent studies have shown promising results when sphenopalatine ganglion is blocked. This can be carried out transnasally with minimal intervention under endoscopic vision. This can easily be achieved by a mixture of local anesthetics and steroids. These drugs should be delivered as close to sphenopalatine ganglion as possible. After decongesting and anesthetizing the nasal cavity a solution of triamcinolone acetonide (40 mg), 1% bupivacaine (4 mL), and 2% mepivacaine with 1/100,000 adrenaline (2 mL) in an average of three (range 2– 4) weekly sessions Injection is usually administered with a 20 gauge needle close to the tail of the middle turbinate (this is the approximate location of sphenopalatine ganglion). Care is taken not to damage the sphenopalatine artery. Two to three injections may be adminstered in a space of 4 – 6 weeks.

Carotid blow out syndrome

This is an extremely high risk condition associated with significant degrees of morbidity and mortality. This condition commonly results from invasion and destruction of cervical carotid vasculature from head and neck squamous cell carcinomas. Prompt diagnosis of this condition and active intervention will help in saving lives of these patients.


Causes of carotid blow out syndrome:


1.Aneurysms
2.Infections – cause vasovasorum thrombosis leading on to necrosis of carotid walls.
3.Secondary carcinomatous deposits in cervical lymph nodes
4 Following irradiation for secondary carcinomatous deposits in the neck – Free radicals caused during irradiation causes thrombosis of vasovasorum leading on to breakdown of carotid artery wall. Patients develop fibrosis and thinning of the cartotid arterial wall leading on to blow out.


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Avoiding pitfalls in endoscopic skull base surgery

Introduction:

The advantages of endoscopic approach to skull base are many. They include:

1. It is the most direct route to anterior skull base. This approach provides access to the following areas Sella, Cribriform plate, Planum sphenoidale, suprasellar cistern, Clivus, Pterygopalatine fossa and adjacent parasellar areas.
2. In this approach there is decreased retraction of brain and cranial nerves when compared to that of conventional neurosurgical apporaches.
3. Endoscope offers excellent visualization of the tumor and the surrounding neurovascular structures
4. Post operative recovery time is short when compared to that of conventional neurosurgical approaches
   

As with any other procedure this method also has its flip side, which includes a steep learning curve, and need to collaborate with neurosurgeon. A cohesive collaboration with neurosurgeon is a must for successful endoscopic skull base surgical procedures.The complicated anatomy of skull base has managed to bridge these two specialities. In a nut shell an otolaryngologist navigates the pathway to the intracranial lesion while the neurosurgeon removes the tumor.

Dangers of endoscopic skull base surgery:

Since the skull base has many vital structures it should be performed with the highest degree of deligence and skill. The potential complications of any endoscopic skull base surgery include:

1. CSF rhinorrhoea
2. Injury to great vessels (internal carotid artery and its branches inside the skull)
3. Injury to optic nerve
4. Injury to other cranial nerves
   
5. Bleeding from cavernous sinus
6. Meningitis
   
   
   
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Gradenigo's syndrome E module

In continuation with my effort in creating learning modules I have come out with a module titled "Gradenigo's syndrome".

Nasal topical therapeutics

Intranasal drug delivery systems for the management of local and systemic
ailments have caught up recently. Initially this route of drug administration
was attempted for the management of allergic rhinosinusitis. Now inflammatory sinusitis is also managed by intranasally administered drugs. The reasons for interest in this route of drug administration because of its high vascularity, porous endothelial basement membrane and a high total blood flow per volume of tissue. Since first pass metabolism is avoided in this drug delivery method the drug is metabolized slowly thus helping in reducing the dosage of the drug. This also goes a long way in reducing the potential toxicity of the administered drug even if it has a very low therapeutic index. The complex nasal anatomy and the varying dynamics of nasal air flow make this drug delivery modality a little bit unpredictable. This is more so especially in patients with nasal cold which is associated with congestion of nasal mucosa and turbinates.







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Unique e module on chronic tonsillitis by drtbalu

I have given a unique e learning module on chronic tonsillitis.

This will be very useful for exam going students of otolaryngology.

You can expect more such modules in future:

E book of the week : Role of Debriders in Otolaryngology

E book of the week:


"Role of Microdebriders in Otolaryngological surgery"


This freely downloadable e book discusses the current role of
Microdebriders in Otolaryngology.

 

Role of Microdebrider in Otolaryngological surgery

E book of the week "Tuberculosis of tonsil a review of literature"

E book of the week:


"Tuberculosis of tonsil a review of literature"

A rare case of tuberculosis tonsil

Introduction:

Tuberculosis involving the tonsil is very rare. These days it is still rare because of better milk processing techniques like pasteurization which eradicates the bovine strain of tuberculosis. Even though tonsils are situated in an exposed area where infected material like sputum and food stuffs come into contact this lesion is rare because of the following features:

1. Antiseptic and cleansing action of saliva (first and foremost)

2. Presence of saprophytic organisms in the oral cavity which prevents growth of tubercle bacilli

3. The stratified squamous epithelial lining of the tonsil also offers some degree of protection

Tuberculosis of tonsils may be:

Primary - Due to ingestion of infected milk (Bovine strain)

Secondary - Due to pulmonary infection. The coughed out infected sputum finds its way to the throat to involve the tonsils.

Diagnosis of tuberculosis of tonsil is not straight forward. It needs high degree of suspicion.

Pointers for the diagnosis of tuberculosis tonsil:

1. Asymmetric enlargement of tonsil

2. Tonsillar enlargement without exudate

3. Obliteration of crypts

4. Painful deglutition

5. Presence of enlarged mobile jugulodigastric nodes

Clinical photograph of a patient with Tuberculosis tonsil


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Vocal cord paralysis

Definition: Vocal cord paralysis is caused by paralysis of intrinsic muscles of larynx. This is a symptom of an underlying disorder and not a disease by itself. The intrinsic muscles of the vocal cord are supplied by the vagus nerve. The term vagus means "wanderer" which is the apt term to describe this nerve becuase of its long anatomical course.

Unilateral vocal fold paralysis occurs due to dysfunction of recurrent laryngeal or vagus nerve causes a breathy voice. The breathiness of voice is caused by glottic chink which allows air to escape when the patient attempts to speak. Normal voice production is dependent on proper glottal closure resulting from bilateral adduction of the vocal cords. This adduction of vocal folds combined with subglottic air pressure causes the vocal folds to vibrate causing phonation.

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Surgical management of puberphonia recent concepts

Introduction:


Mutational falsetto is also commonly known as Puberphonia. This condition is caused due to the failure of the voice to drop in its pitch from the higher levels after puberty. These patients hence suffer from lack of resonance in voice, breathiness of voice and lack of pitch variations. These patients have easy fatigability of voice and are unable to raise their voice in noisy environments.

This condition is caused due psychological problems in the patient which prevents lowering of the pitch of the voice of an adolesecent to that of a adult range. Puberphonia is more common in adolescent males and may also occur rarely in females.


The following are the probable psychological factors that could lead to the developement of puberphonia:


1. Over identification of the affected boy with his mother
2. Failure of the boy to accept his adult male role
3. Social immaturity
4. Anxiety to maintain a Soprano voice
5. Incordination of muscles of vocalization

Surgical management of Puberphonia:


When all the above conservative methods fail then surgery will have to be resorted to. Isshiki type III relaxation thyroplasty has shown promise in managing these patients. This surgical procedure lowered the pitch of voice in these patients by shortening the length of the vocal folds. In the classic Isshiki type III thyroplasty 2 – 3 mm of vertical strips of cartilage were excised on each side of midline of thyroid cartilage. This procedure caused retrusion of the middle portion of the thyroid cartilage causing a reduction in the length of the vocal folds.

Various modifications of Type III Ishikki thyroplasty have been proposed.


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Anatomical changes that occur in ethmoid sinuses following FESS

Introduction:


The bony walls of paranasal sinuses demonstrate excellent degree of plasticity. This feature allows alterations in the size and dimensions of paranasal sinuses during growth phase. The process of pneumatization of paranasal sinuses begins in utero and continues through teenage years.

Causes of pathological expansile alterations of paranasal sinuses include:


1. Allergic fungal sinusitis
2. Extensive sinonasal polyposis
3. Mucocele formation
4 Benign tumors


While performing endoscopic sinus surgery it should be borne in mind that it is being performed in a setting of bony changes, with an intention to halt the expansile / contractile changes that are likely to take place.


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Dysontogenic cysts of floor of mouth

Introduction:

Dysontogenic cysts are otherwise known as dermoid cysts. These cysts develop due to defective embryonic development. This cyst includes any cyst which are filled with sebum like material with evidence of presence of specialized skin derivatives.

Meyer's classification of Dysontogenic cysts of floor of mouth:

Meyer classified dysontogenic cysts of floor of mouth into 3 types, namely

Epidermoid

Dermoid

Teratoid

Epidermoid cyst: is usually lined with stratified squamous epithelium without adnexal structures.

Dermoid cyst: is lined with stratified squamous epithelium with the presence of adnexal structures. These adnexal structures include sebaceous cysts, hair follicles and sweat glands.

Teratoid cyst: Features of teratoid cysts include the presence of lining squamous epithelium, respiratory epithelium, dermal appendages and distinct mesodermal components.

Eventhough dysontogenic cysts can occur anywhere in the body, about 10% of them occur in the floor of the oral cavity. Congenital cysts occuring in the infancy have also been reported.

Clinical features:

These include:

1. Dysphagia
2. Dysphonia
3. Stridor

Pathophysiology:

These cysts can be congenital / acquired in nature.

Congenital cysts are derived from ectodermal differentiation of multipotential cells that could have been pinched off during the closure of the anterior neuropore. Commonly accepted theory explaining congenital cysts is that it is caused due to entrapment of midline ectodermal tissue during fusion of first and second branchial arches during the third week of gestation. Lateral dysontogenic cysts are said to arise from the first pharyngeal pouch or first branchial cleft.

Acquired dysontogenic cysts can be explaine by Baker's theory. According to Baker trauma is the commonest cause of acquired dysontogenic cysts. Trauma causes implantation of epithelial cells into deep tissues. These implanted tissues results in formation of cystic cavities filled with keratin.

Differential diagnosis:

These cysts should be differentiated from:

1. Ranula
2. Obstructed wharton's duct
3. Thyroglossal tract cyst
4. Branchial cleft cyst
5. Lymphatic malformation
6. Pleomorphic adenoma
7. Enlarged submental glands
8. Prominent submental fat mass

Investigations:

Ultrasound examination will help in differentiating cystic from solid lesions. It ofcourse has the advantage of being easily available, cost effective and rapidly performed investigation.

MRI: Provides excellent soft tissue detail. It helps in differentiating mass from surrounding soft tissues. T2 weighted images of dysontogenic cysts shows hyperintense areas due to high proteinaceous content.

Treatment:

Complete excision of the mass is the ideal treatment modality. Almost all dysontogenic cysts of floor of the mouth can be approached through intraoral approach. All submental cysts should be approached through the neck. A cyst that has breached the floor of mouth musculature should ideally be approached through the neck.

Inverted papilloma of nose and its management

Introduction: Inverted papilloma is a benign lesion occuring in the nasal cavity and paranasal sinuses. Eventhough these tumors are classified as benign they are known to cause local destruction, known to recur and also can under go malignant transformation to squamous cell carcinoma.

History: Ward in 1854 described the macroscopic features of papilloma of nose. He used the term papillomatous neoplasm to describe this lesion. Billroth in 1855 used the term villous carcinoma to describe inverted papilloma because of its propensity to destroy local tissues and recurrence after surgery. Hopmann in 1883 used the terms hard and soft papilloma to ascertain the stoma : epithelium ratio. This classification ofcourse was not useful because the number of epithelial layers varied within the various areas of the same specimen.
Ringertz in 1938 coined the term inverted papilloma after recognizing the characteristic endophytic growth pattern demonstrated by this type of papilloma. Kramer and Som in 1935 used the term genuine papilloma of the nasal cavity. Berendes in 1966 after taking congnizance of the destructive properties of this lesion used the term Malignant papilloma to indicate this mass. Hyams in 1971 classified nasal papillomas as inverted papilloma (to indicate papillomas with endophytic growth) and fungiform papilloma. He also included a third group cylinderical papilloma to accomodate the variantions seen in these papillomas. Batsakis in 1987 used the term inverted Schneiderian papilloma indicating its origin from the Schneiderian membrane (nasal mucosa). Michaels in 1996 regarded the three types of nasal papilloma as three completely distinct entities whereas Eggers in 2005 considered these three types of nasal papillomas as hybrid lesions.

Synonyms: As indicated above various synonyms have been used to indicate inverted papilloma of nose. They include:

1.Schneiderian papilloma
2.Inverted papilloma
3.Benign papilloma of nose
4.Cylindroma
5.Malignant papilloma of nose




Definition: The mucosal lining of nose and paranasal sinuses is known as Schneiderian membrane in memory of Victor conrod Schnider who described its histology. Papillomas arising from this membrane is very unique in that they are found to be growing inwards and hence the term inverted papilloma. These papillomas are unique in their history, biology and location. Papillomas involving the vestibule is not included in this group because histologically, biologically and behavior wise it is different.



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Inverted papilloma nose

Rhinosporidiosis still an enigma

Introduction:

Rhinosporidiosis has been defined as a chronic granulomatous disease characterized by production of polyps and other manifestations of hyperplasia of nasal mucosa. The etiological agent is Rhinosporidium seeberi.

Theories of mode of spread:

1. Demellow's theory of direct transmission
2. Autoinoculation theory of Karunarathnae (responsible for satellite lesions)
3. Haematogenous spread - to distant sites
4. Lymphatic spread - causing lymphadenitis (rarity)
   
   
   
   
   
   
   Reasons for endemicity of Rhinosporidiosis:
   It has to be explained why this disease is endemic in certain parts of South India and in the dry zone of Srilanka. If stagnant water could be the reason then the chemical and physical characteristics of the water needs to be defined. In addition other aquatic organisms may also be playing an important synergistic reaction. This aspect need to be elucidated. Text book of microbilogy is repleate with examples of such synergism i.e. lactobacillus with trichomonas, and Wolbachia with filarial nematodes.
   
   
   
   
   
   These studies prompted Prof Ahluwallia et al to conclude that:
   
   
   
   1. Chronic inflammation almost always precedes rhinosporidiosis
   2. During this period if the patient consumes dry / fried tapioca and is malnourished it invariably leads to granulomatous polyp in the nose.
   3. Dirty pond water in which the patient takes bath causes inflammation of the nasal mucosa
      
      
      
      The following are the reasons making the study of this disease rather difficult:
      
      
      1. Till date no pure extract containing rhinosporidial trophozoite / spores / sporangium is available
      2. Attempts made to culture these organsim have not been successful
      3. The role of electron dense bodies in disease propagation is yet to be studied. Studies have shown that these electron dense bodies stain positively to Feulgen staining indicating that it contains nucleic acids
      4. The absence of good animal model for studying this disease is one major drawback.
         
         
         
         
         
         Rhinosporidiosis still an enigma