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Asian Journal of

Ear, Nose Throat


An IJCP Group Publication Dr Sanjiv Chopra Prof. of Medicine & Faculty Dean Harvard Medical School Group Consultant Editor

from the desk of EdItor

Dr Deepak Chopra Chief Editorial Advisor

Dr KK Aggarwal CMD, Publisher and Group Editor-in-Chief Dr Veena Aggarwal Joint MD & Group Executive Editor Anand Gopal Bhatnagar Editorial Anchor Editor Dr VP Sood Editorial Board Dr Dinesh Mehta (USA) Dr A Mahadevaiah (Bangalore) Dr Aru Handa (New Delhi) Dr BS Gendeh (Kuala Lumpur) Dr PP Singh (New Delhi) Dr AK Gupta (Udaipur) Dr M Allaudin (Dhaka) Dr Jasveer Singh (New Delhi) Dr Piyush Verma (New Delhi) Dr Rakesh Parsad Srivastava (Kathmandu) Dr (Mrs.) Nishi Gupta (New Delhi) Dr Amar Singh (Muscat)

July-September 2010

Noise Exposure and Its Control VP Sood

from the desk of group editor-in-chief Cold Urticaria


KK Aggarwal

Clinical Practice Endoscopic Cartilage Tympanoplasty in Medinat Zayed Hospital, UAE

Drug Therapy

Dr Alka Kriplani Asian Journal of Obs & Gynae Practice

Dr Praveen Chandra Asian Journal of Clinical Cardiology Dr Swati Y Bhave Asian Journal of Paediatric Practice Dr Vijay Viswanathan The Asian Journal of Diabetology Dr M Paul Anand, Dr SK Parashar Cardiology Dr CR Anand Moses, Dr Sidharth Das Dr A Ramachandran, Dr Samith A Shetty Diabetology Dr Ajay Kumar Gastroenterology Dr Koushik Lahiri Dermatology Dr Georgi Abraham Nephrology Dr Sidharth Kumar Das Rheumatology Dr V Nagarajan Neurology Dr Kamala Selvaraj, Dr Thankam Verma Obs and Gyne

Advisory Body Heart Care Foundation of India

Non-Resident Indians Chamber of Commerce & Industry World Fellowship of Religions

Dr VP Sood Editor


Ahmed Qureshi

IJCP Editorial Board

Dr VP Sood Asian Journal of Ear, Nose and Throat


Montelukast with Levocetirizine for Asthma and Allergic Rhinitis


Aru Handa

Review Article Headache – A Review


Uma Garg, MK Garg

Case Report Tympanomastoid Carcinoma


Jasveer Singh, Ipsit Panda

Isolated Malignant Lymphoma of the Parotid Gland


A Ravikumar, Senthil Kannan, John Samuel, Shalini Balakrishnan

Dr KK Aggarwal Group Editor-in-Chief

Asian Journal of

Ear, Nose Throat


Published, Printed and Edited by Dr KK Aggarwal, on behalf of IJCP Publications Ltd. and Published at Daryacha, 39, Hauz Khas Village New Delhi - 110 016 E-mail: Printed at IG Printers Pvt. Ltd., New Delhi E-mail: Š Copyright 2010 IJCP Publications Ltd. All rights reserved The copyright for all the editorial material contained in this journal, in the form of layout, content including images and design, is held by IJCP Publications Ltd. No part of this publication may be published in any form whatsoever without the prior written permission of the publisher.

July-September 2010

Case Report Pleomorphic Adenoma of the Hard Palate


Vaishali Sangole, Kalpana Rajiv Kumar, Suman Rao, Rachana Nautiyal, Sujata Gawai

emedinews section From eMedinewS


Editorial Policies The purpose of IJCP Academy of CME is to serve the medical profession and provide print continuing medical education as a part of their social commitment. The information and opinions presented in IJCP group publications reflect the views of the authors, not those of the journal, unless so stated. Advertising is accepted only if judged to be in harmony with the purpose of the journal; however, IJCP group reserves the right to reject any advertising at its sole discretion. Neither acceptance nor rejection constitutes an endorsement by IJCP group of a particular policy, product or procedure. We believe that readers need to be aware of any affiliation or financial relationship (employment, consultancies, stock ownership, honoraria, etc.) between an author and any organization or entity that has a direct financial interest in the subject matter or materials the author is writing about. We inform the reader of any pertinent relationships disclosed. A disclosure statement, where appropriate, is published at the end of the relevant article.


Asian Journal of Ear, Nose and Throat does not guarantee, directly or indirectly, the quality or efficacy of any product or service described in the advertisements or other material which is commercial in nature in this issue.

Photo Quiz Swelling of the Right Ear


Lighter Reading Lighter Side of the Medicine


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From the desk of editor

Noise Exposure and Its Control

Dr VP Sood Editor, Asian Journal of Ear, Nose and Throat Secretary-cum-Managing Trustee Dr Sood Nasal Research Foundation Past President Association of Otorhinolaryngologists of India Founder Patron and Past President All India Rhinology Society


oise is often defined as “unwanted sound”, but this definition is subjective because of the fact that one man’s music or sound is another man’s noise. Perhaps a better definition of noise is “wrong sound, in the wrong place, at the wrong time”. Man is living in an increasingly noisy environments, due to rapid increasing automobiles, industries, disco, crackers noise, etc. Loudness of intensity-of noise depends upon the amplitude of the vibrations which initiates the noise. The loudness of noise is measured in decibels (dB). When we say that a sound is 60 dB, it means that it is 60 dB more intense than the smallest distinguishable or audible noise. Normal conversation produces a sound of 60-65 dB; whispering, 20-30 dB; heavy street traffic, 60-80 dB and boilers sound, riveting, hammering, etc. in the factories 100-120 dB. The basic instrument used to measure the noise is the “Sound Level Meter” which measures the intensity of sound in dB. Audiometer measures the hearing ability of the person in different frequencies. Noise-inducted hearing loss shows a characteristic dip in the curve at the 4000 Hz frequency. Hearing loss can be either temporary or permanent. Noise-induced temporary threshold shift (TTS) is a temporary loss of hearing acuity experienced after a relatively short exposure to excessive noise. During short exposure to loud sound, hearing is recovered fairly rapidly after cessation of the noise. Noise-induced permanent threshold shift (PTS) is an irreversible (sensorineural) loss of hearing that is caused by prolonged loud noise exposure. In this, the inner ear damage may vary from minor changes in the hair cell endings to destruction of the organs of Corti. When this occurs as a result of occupation in industries, it is called ‘occupational hearing loss’. Asian Journal of Ear, Nose & Throat, July-September 2010

From the desk of editor The effects of noise exposure are auditory fatigue resulting on whistling and buzzing in the ears and deafness. The hearing loss may be temporary or permanent. Control of Noise

Noise cannot be totally eliminated, but it can be definitely reduced to provide some protection from noise exposure. Noise control areas are:  Control of noise at source: This may be achieved by segregating the noisy machines, application of mufflers or other noise reducers, to machines. Reduction in noise can be obtained by increasing the distance between people and the noise source. 

Control of transmission: This may be achieved by building enclosures and covering the room walls with sound basing materials. Protection of exposed persons: Hearing protection is recommended for all workers who are consistently exposed to noise louder than 85 decibels. Workers must be regularly rotated from noisy areas to comparatively quiet posts in factories. Periodical audiogram check-ups is mandatory. If it is absolutely impossible to reduce noise to a harmless level then some form of ear protection, i.e. ear-plugs, ear-muffs, and /or helmets, should be used. Education: No abatement program can succeed without participation of public. Therefore, their education through all available media is needed to high-light the importance of loud noise as a community hazards. Legislation: Many states have adopted legislation providing for noise controls which are applicable to a wide variety of sources. Workers have the right to claim compensation if they have suffered a hearing loss in loud noisy work environments. n



Address for correspondence Dr VP Sood Ear, Nose & Throat Center 212, Aditya Arcade, 30, Community Center Preet Vihar, Vikas Marg, Delhi - 92 Ph. No.: 011-22440011, 42420429 E-mail: Website:

Asian Journal of Ear, Nose & Throat, July-September 2010

from the Desk of group editor-in-chief

Cold Urticaria

Dr KK Aggarwal Padma Shri and Dr BC Roy National Awardee Sr Physician and Cardiologist, Moolchand Medcity President, Heart Care Foundation of India Group Editor-in-Chief, IJCP Group Chief Editor, eMedinewS Chairman Ethical Committee, Delhi Medical Council Director, IMA AKN Sinha Institute (08-09) Hony. Finance Secretary, IMA (07-08) Chairman, IMA AMS (06-07) President, Delhi Medical Association (05-06) Krishan Kumar Aggarwal (Facebook)


old urticaria is a type of urticaria characterized by itchy wheals and/or angioedema due to skin mast cell activation and the release of proinflammatory mediators after cold exposure. More than 90% of cold urticaria is idiopathic. The rest are mostly secondary to cryoglobulinemia.1 Cold urticaria is rare in children. Its occurrence portends danger. Recent evidence shows that children with cold urticaria have an increased risk of anaphylaxis.2 The underlying factors are unknown. The symptoms are usually limited to cold-exposed skin areas and develop within minutes of cold exposure. Extensive cold contact may result in systemic reactions including anaphylactic reactions. A cold stimulation test (CST) confirms the diagnosis in most and avoidance of cold exposure is the best prophylaxis. However, complete avoidance is often difficult. A CST is considered positive when the patient develops urticarial skin lesions at the site of the cold challenge. CSTs are performed using ice cubes, cold packs, cold water baths: ď Ź The ice cube test has a sensitivity of 83-90% and a specificity of 100%.3,4 The ice cube should be melting and contained in a thin plastic bag to avoid cold damage of the skin.5 Cold stimulation time thresholds can also be noted.6 This method is readily performed in most clinics. The ice cube test should be performed for 3-5 minutes to diagnose cold urticaria in children. The time should be increased to 10 or 20 minutes if the test shows negative results at 3-5 minutes after antihistamine therapy.7 ď Ź Cold provocation test using cold packs or cold water baths is not recommended as first-line screening tests, as it may induce systemic reactions.6 The test however may be helpful in confirming the diagnosis of cold urticaria in patients who have a negative ice cube test. Asian Journal of Ear, Nose & Throat, July-September 2010

from the Desk of group editor-in-chief Cold stimulation tests are performed for five minutes and test responses are assessed 10 minutes after the end of provocation testing. The test is considered positive if the test site shows a palpable and clearly visible wheal-andflare skin reaction. This reaction is itchy and/or associated with a burning sensation in most cases. The test is considered negative if there is no reaction, or erythema or pruritus/burning only. Suspected patients who show a negative test should be re-evaluated. Further testing is performed using larger areas for provocation (e.g. cold pack or cold water bath) or using triggers that induced urticarial reactions in the past (e.g. cold wind, cold water). Atypical cold urticarias should be considered if the additional stimulation tests are also negative. Treatment involves the use of non-sedating H1 antihistamines for those who are unable to sufficiently avoid cold exposure and have frequent symptoms. Start with second-generation H1 antihistamine, starting at the standard dose and increasing upto four times the standard dose as needed to control symptoms. Treat cold-induced anaphylaxis with epinephrine. References 1. Alangari AA, Twarog FJ, Shih MC, et al. Clinical features and anaphylaxis in children with cold urticaria. Pediatrics 2004;113:e313-7. 2. Anaphylaxis common in children with cold urticaria. Respiratory Rev 2004;9(6). 3. Neittaanmaki H. Cold urticaria. Clinical findings in 220 patients. J Am Acad Dermatol 1985;13:636. 4. Mathelier-Fusade P, Aissaoui M, Bakhos D, et al. Clinical predictive factors of severity in cold urticaria. Arch Dermatol 1998;134:106. 5. Siebenhaar F, Staubach P, Metz M, et al. Peltier effect-based temperature challenge: an improved method for diagnosing cold urticaria. J Allergy Clin Immunol 2004;114:1224. 6. Wanderer AA, Grandel KE, Wasserman SI, et al. Clinical characteristics of cold-induced systemic reactions in acquired cold urticaria syndromes: recommendations for prevention of this complication and a proposal for a diagnostic classification of cold urticaria. J Allergy Clin Immunol 1986;78:417. 7. Visitsuntorn N, Tuchinda M, Arunyanark N, et al. Ice cube test in children with cold urticaria. Asian Pac J Allergy Immunol 1992;10(2):111-5.




Asian Journal of Ear, Nose & Throat, July-September 2010

clinical practice

Endoscopic Cartilage Tympanoplasty in Medinat Zayed Hospital, UAE Ahmed Qureshi

Abstract Endoscopic cartilage tympanoplasty is a delicate and minimally invasive procedure with a high rate of ear drum closure. Cartilage tympanoplasty is a reliable technique in reconstruction of TM. Hearing results after cartilage tympanoplasty are comparable to any other graft material used. Key words: Functional endoscopic sinus surgery, tympanoplasty, tragal cartilage


new era ushered in the history of Medinat Zayed Hospital when Endoscopic Ear Surgery started in the ENT Department since last year, though functional endoscopic sinus surgery (FESS) was already being done since past 15 years. Since, Wullstein and Zoeller popularized conventional tympanoplasty in the 1950s, various materials have been used for the procedure, including fascia, skin, vein, dura and cartilage. At present, the most common material used in tympanoplasty is temporalis fascia. With the modern introduction of c-slicer, cartilage has been used with great success to reconstruct the tympanic membrane (TM). Hence, in all my reconstructive tympanoplasties this is the most favored and with excellent results. Tympanoplasty is a microsurgical or endoscopic surgical procedure on the eardrum and ossicular bones, so as to repair TM and restore the middle ear hearing mechanism after eradication of disease if present. Hence, the eardrum must be rebuilt and a new connection must be made between the eardrum and the inner ear to re-establish better hearing. In tympanoplasty surgery, three hearing bones malleus, incus or stapes, eroded by disease may be removed, sculpted, replaced or rearranged to make a new connection between the new eardrum and the inner ear for hearing. Harvesting of Graft A thin slice of tragal cartilage with its perichondrium is harvested using the customized ear cartilage slicer. ENT Consultant, Medinat Zayed Hospital Western Region Medical District, Seha, AbuDhabi, UAE

Asian Journal of Ear, Nose & Throat, July-September 2010

The reconstruction is stabilized later before the end of surgery by gelfoam packing that will hold it still and protect it from infection until new blood vessels grow into the graft and incorporate it into the new eardrum. Why Cartilage? Cartilage with perichondrium is more rigid and resists resorption, has good long-term survival and nourished largely by diffusion. There is no cosmetic deformity or even a external scar as the tiny graft is harvested from the undersurface of the tragus in the external auditory canal!! On the other hand, temporalis fascia and perichondrium undergo atrophy in the long-term and leave a scar over and behind the ear. Why Tragal Cartilage? The use of tragal cartilage for reconstruction of the TM is gaining popularity because it solves the fundamental problem of retraction of the newly reconstructed eardrum in ears with chronic eustachian tube dysfunction (ETD). It is easy to harvest and near to the operating field. This thin cartilage layer acts as a natural plastic which has less tendency to retract in the environment of chronic negative middle ear pressure which is present in almost all patients with chronic ETD. It is not unusual for patients repaired with conventional materials such as temporalis fascia to have excellent initial surgical results only to find their TM has retracted once again several years after surgery, which results in conductive hearing loss, erosion of the hearing bones or even cholesteatoma formation. 

clinical practice Evolution of Endoscope in Otology

Cholesteatoma extends from attic (upper portion of the middle ear) to mastoid. Early cholesteatoma does not involve the mastoid. So early detection and endoscopic removal can save a patient from a mastoidectomy.

Before surgery

Just after surgery

After one month

Figure 2. Surgical Results 35

Cartilage group (n - 11)

Pre-op Post-op


Air-bone gap (dB)

Endoscope, that too, in the best Ear Centers in the West was sometimes used till lately, mostly for documentation and diagnostic purposes. Since, it is expensive, was not and still not used widely. The 4 mm zero degree rigid endoscope has changed the role of our approach to middle ear in chronic ear surgery since 1995.

25 20 15 10 5 0

500 Hz

1k Hz

2k Hz

4k Hz

Figure 3.


Wide Field of View (Endoscope)

Narrow Microscopic View

Figure 1.

Operative Steps

After harvesting of graft, endoscopic transcanal surgery consists of elevation of wide tympanomeatal flap. Cholesteatoma sac, if any, is pursued under direct vision after necessary removal of bone and ossicles. Attic is widened, emptied of the body of incus and the head of malleus if eroded. Reconstruction of ossicles and reconstruction of TM is further done.

Endoscopic cartilage tympanoplasty is a delicate and minimally invasive procedure with a high rate of ear drum closure. Cartilage tympanoplasty is a reliable technique in reconstruction of TM. Hearing results after cartilage tympanoplasty are comparable to any other graft material used. Endoscopic technique allows transcanal, minimally invasive, management of attic cholesteatoma with good results. Endoscopic technique increases the potential for preservation of ossicles. Suggested Reading 1. Tarabichi M. Endoscopic middle ear surgery. Ann Otol Rhinol Laryngol 1999;108(1):39-46. 2. Tarabichi M. Endoscopic management of acquired cholesteatoma. Am J Otol 1997;18(5):544-9.





Asian Journal of Ear, Nose & Throat, July-September 2010

1936 Full Page ASAM Ad v2.indd 1

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drug therapy

Montelukast with Levocetirizine for Asthma and Allergic Rhinitis Aru Handa

Abstract Allergic rhinitis (AR) occurs commonly with asthma and also could be an independent risk factor for the development of asthma. Persistent AR and asthma impair the quality-of-life of patients. Patients who have asthma and AR tend to have more severe disease with higher treatment costs and they require almost life-long therapy. The search for treatments to improve the symptoms of patients afflicted with AR and asthma has targeted the CysLTs by antileukotriene agents. In persistent AR patients, the combination of montelukast with levocetirizine is more effective than monotherapy. The role of montelukast as a combined therapy with levocetirizine for both AR and asthmatic patients is an emerging hope for such patients. Key words: Levocetirizine, montelukast, asthma, allergic rhinitis

Epidemiological Features of Asthma and Allergic Rhinitis Allergic rhinitis (AR), an inflammation of nasal mucosa of allergic origin, is one of the most common chronic disorders in practice, with prevalence ranging from 3% to 19% in various countries.1 AR is a heterogeneous disorder that includes seasonal AR (SAR) symptoms (‘hay fever’) and the more difficult diagnostic category, perennial AR (PAR). Asthma is one of the most prevalent chronic illnesses in the United States, affecting 9 million children (12.7%); also there is an increase in morbidity and mortality related to pediatric asthma.2,3 SAR is also becoming more common, affecting 20-40 million people yearly, with an estimated 40% being children.4 It has been estimated that between 60-78% of people with asthma also suffer from AR.4 AR occurs commonly with asthma and could be an independent risk factor for the development of asthma.2 An emerging theory is that asthma and AR are two conditions along the same continuum of inflammatory processes involving a common airway instead of two distinct diseases of the upper and lower airway.4 In fact, researchers have labeled the two conditions the ‘united airway disease’5 and ‘asthma-rhinitis disorder’.6 Rhinitis

Senior Consultant Dept. of ENT Moolchand Medcity, New Delhi

Asian Journal of Ear, Nose & Throat, July-September 2010

and asthma are often associated and are two disorders which interact at various levels. Rhinitis typically precedes the development of asthma and can contribute to unsatisfactory asthma control. The presence and type of asthma is influenced by sensitization, and the duration and severity of AR. Both asthma and SAR are associated with significant costs and morbidity. Together, these two illnesses have had a great impact on healthcare economics. In the US, approximately $3 billion yearly is spent on asthma-related costs including direct costs, such as medical costs and indirect costs related to caregiver missed work days.7 The costs associated with SAR are similar.1 It is estimated that approximately $2.7 billion in direct and indirect costs are associated with SAR.1,4 Concept of United Airways Disease: Rhinitis and Asthma Link A new concept of united airways disease has recently come up.7 The all types of relationships between the upper and lower airways have been confirmed now, which are now an increasing evidence for the frequent coexistence of these two diseases i.e. AR and asthma. The role of upper airways infections in increasing the asthma attacks is now established.7 Rhinitis has been identified as an independent risk factor for asthma development. The nose-bronchi link has shed the light on the fact that allergy is not a disease of a nose itself, but a disorder of the whole upper and lower respiratory tract with a wide-range of clinical features, all these 13

drug therapy observations have led to a new term united airways diseases.7 There is a major involvement of airway epithelial cells in the pathogenesis of both asthma and AR. Impact of Allergic Rhinitis on Asthma

AR and its impact on asthma in collaboration with the World Health Organization (WHO) initiative reclassified AR, like asthma, by duration and severity. The Xyzal in Persistent Rhinitis Trial is the first large, long-term clinical trial studying patients with persistent rhinitis as defined by AR and its impact on asthma.8 The Xyzal in Persistent Rhinitis trial was a 6-month double-blind, placebo-controlled, multicenter, multinational trial in 551 patients. Adults with persistent rhinitis sensitized to both grass pollen and house dust mite were randomized to receive levocetirizine 5 mg/day or placebo. A total of 421 patients completed the full study. In this study, levocetirizine significantly improved both the rhinoconjunctivitis quality-of-life questionnaire overall score and the total five symptoms score from week 1-6 months (all p < 0.001). Medical Outcomes Survey Short Form 36 (SF-36) summary scores were also improved in the levocetirizine group compared with the placebo group. Treatment cessation because of lack of effect, comorbidities and overall costs of disease, and comorbidities per working patient per month (160.27 vs 108.18) were lower in the levocetirizine group. Levocetirizine was shown to improve quality-of-life and symptoms and to decrease the overall costs of the disease over the 6-month treatment period. Integrated Disease Management of Allergic Rhinitis and Asthma The common comorbidities and shared pathophysiologies of asthma and AR have led to the concept of ‘one airway, one disease’ and the need for a common therapeutic approach. To achieve optimal treatment for patients, it is the recommendation of the AR and its impact on asthma workshop group in collaboration with the WHO that patients with persistent AR should be evaluated for asthma, and that patients with asthma should be evaluated for rhinitis.9 A strategy combining the treatment of both upper and lower airway disease in terms of efficacy and safety appears to be optimal.9 In many ways, leukotriene receptor 14

antagonists represent a rational approach to such ‘one airway’ disease management. Leukotriene receptor antagonists are an established treatment option for asthma, with evidence to support their use in mild, persistent disease, pediatric asthma, exercise-induced bronchoconstriction. Evidences are accumulating in AR to suggest that both alone and in combination with an antihistamine leukotriene receptor antagonists like montelukast can alleviate the signs and symptoms of AR. Montelukast

Montelukast is a cysteinyl leukotriene (CysLT) receptor antagonist, an orally active compound that binds with high affinity and selectivity to the cysteinyl leukotriene type 1 (CysLT1), receptor. It is a selective and orally active leukotriene receptor antagonist that inhibits the CysLT1 receptor without any agonist activity. The CysLT (LTC4, LTD4, LTE4) are potent inflammatory eicosanoids released from various cells including mast cells and eosinophils. These important pro-asthmatic mediators bind to CysLT receptors. The CysLT1 receptor is found in the human airway (including airway smooth muscle cells and airway macrophages) and on other pro-inflammatory cells (including eosinophils and certain myeloid stem cells). Mechanism of Action of Montelukast in Allergic Rhinitis and Asthma

CysLTs are endogenous mediators of inflammation and play an important role in allergic airway disease by stimulating bronchoconstriction, mucus production, mucosal edema and inflammation, airway infiltration by eosinophils and dendritic cell maturation that prepares for future allergic response. Montelukast inhibits all these actions by blocking type 1 CysLT receptors found on immunocytes, smooth muscle and endothelium in the respiratory mucosa. CysLTs have been correlated with the pathophysiology of asthma and AR. In AR, CysLTs are released from the nasal mucosa after allergen exposure during both early- and late-phase reactions and are associated with symptoms of AR. Intranasal challenge with CysLTs has been shown to increase nasal airway resistance and symptoms of nasal obstruction. Asian Journal of Ear, Nose & Throat, July-September 2010

drug therapy Clinical Effects of Montelukast in Allergic Rhinitis and Asthma

Levocetirizine in Persistent Allergic Rhinitis and Asthma

Montelukast was initially developed as a treatment for asthma, now it has more recently found use in the treatment of AR.

Levocetirizine has been shown to be effective in AR. A study evaluated clinical efficacy, antiinflammatory actions of levocetirizine and its effects on quality-of-life with a specific instrument in the asthma-rhinitis comorbidity.11 Fifty adult patients with persistent rhinitis with/without asthma were enrolled. After a 1-week run-in for baseline evaluation, they were randomized to levocetirizine or placebo for eight weeks. Cromolyn and salbutamol were permitted on demand. Rhinoconjunctivitis and asthma symptoms were evaluated by diary cards. Quality-of-life was assessed by the specific rhinasthma questionnaire and the generic SF-36 at different time-points. Nasal scrapings and lavages were also performed for inflammatory cell count and mediator assessment. Symptoms began to decrease in the active group at the second week of treatment when the difference with the placebo group became significant (0.05) and so remained until the end of the trial. Starting from two weeks of therapy, there was a significant decrease versus baseline in all the four components of the rhinasthma questionnaire only in the active group. The intergroup comparison became significant (p < 0.05) at four weeks.

Systematic reviews10 have evaluated montelukast in the treatment of SAR and PAR, with and without concomitant asthma. In this primary consideration was given to large, randomized, placebo-controlled, double-blind clinical trials in which AR endpoints were assessed and the use of concurrent treatments for AR was excluded. Eight such studies were found in the literature. The primary endpoint in these was daytime nasal symptom severity represented by a composite score derived from individual self-ratings of nasal congestion, rhinorrhea, nasal pruritus and sneezing. Secondary endpoints have included these individual nasal symptom scores, additional scores for eye, ear and throat symptoms, the impact of rhinitis on quality of sleep, global evaluations of outcome by patients and physicians, and measures of the severity of concomitant asthma. A general outcome was that patients treated with montelukast had significantly greater improvements in their symptoms of SAR and PAR than did patients who were given a placebo. In patients with AR with co-morbid asthma, montelukast treatment has significantly resulted in improvements in both their symptoms, as compared to placebo. Montelukast is well-tolerated and has a favorable safety profile; adverse events have occurred at similar frequencies in patients taking either montelukast or placebo. Montelukast provides an effective and well-tolerated oral treatment for allergic airway inflammation in patients with SAR or PAR without asthma, and in patients in whom AR is co-morbid with asthma. Levocetirizine

It is the R-enantiomer of cetirizine, and potent and selective antagonist of peripheral H1-receptors. Binding studies reveal that levocetirizine has high affinity for human H1-receptors (Ki = 3.2 nmol/l). Levocetirizine has an affinity 2-fold higher than that of cetirizine (Ki = 6.3 nmol/l). Levocetirizine dissociates from H1â&#x20AC;&#x2018;receptors with a half-life of 115 Âą 38 minutes. After single administration, levocetirizine shows receptor occupancy of 90% at four hours and 57% at 24 hours. Asian Journal of Ear, Nose & Throat, July-September 2010

The SF-36 detected only sporadic differences between groups. Eosinophils and neutrophils in nasal scraping were significantly decreased in the levocetirizine group versus baseline at all times. Nasal mediators were under the detection limits and no analysis could be performed. In the active group, only two patients used rescue medications compared with 13 patients in the placebo group. They were of opinion that levocetirizine is clinically effective and capable of improving the rhinitis-asthma-related quality-of-life. Rationale of Use of Montelukast and Levocetirizine Combination AR and asthma are common disorders affecting large percentages of the population of Western countries including India. There are multiple treatment options available for AR and asthma and stepwise approaches to therapy have been recommended. Montelukast is a CysLT receptor antagonist that has been found to be effective both in the treatment of AR and asthma. Montelukast has a dual effect on both the nasal as well as bronchial epithelium, so it can be a very good treatment 15

drug therapy modality for a patient suffering from both bronchial asthma and AR. The dose-dependent beneficial effect of levocetirizine in asthmatic patients with AR is also an added advantage. Combining montelukast with levocetirizine benefits the patients to a great extent. Treatment with concomitant administration of an antileukotriene (montelukast) and an antihistamine (levocetirizine), provides significantly better symptom relief compared with the modest improvement of AR and asthma symptoms with each of the treatments alone. Role of Montelukast and Levocetirizine Combination in Patients of Allergic Rhinitis and Asthma The use of montelukast in combination with antihistamines such as loratadine or cetirizine has generally resulted in greater efficacy than when these agents were used alone, and in some studies has produced results comparable with intranasally applied corticosteroids. The review of the literature4 establishes montelukast as a viable alternative for the treatment of SAR. In a randomized, double-blind, placebo-controlled crossover study12 done to investigate the effects of six weeks of treatment of persistent AR with desloratadine, levocetirizine or montelukast alone or in combination. Patients were assigned to two arms: 20 received montelukast, 10 mg/day, desloratadine, 5 mg/day, or both or placebo and 20 received montelukast, levocetirizine or both, 5 mg/day, or placebo. The treatment periods were separated by 2-week washout periods. Symptom scoring, skin prick tests, spirometry, rhinometry and nasal lavage were performed the day before and the last days of the treatment periods. Eosinophil cationic protein levels were evaluated by means of nasal lavage. The mean ± SD total baseline nasal symptom score was 7.7 ± 0.49 before treatment, 3.74 ± 0.54 after desloratadine use, 3.6 ± 0.48 after montelukast use and 3.04 ± 0.4 after montelukastdesloratadine use. The mean ± SD baseline nasal symptom score was 7.95 ± 0.68 before treatment, 3.02 ± 0.64 after levocetirizine use, 3.44 ± 0.55 after montelukast use and 2.14 ± 0.39 after montelukastlevocetirizine use. The greatest improvement in nasal symptoms occurred after combination treatment. 16

Decreases in the level of eosinophil cationic protein were greater after the combined use of montelukast and antihistamine than after each agent given alone. Combining montelukast with levocetirizine gives additional benefits in comparison to each agent alone and it can be considered for patients whose qualityof-life is impaired by persistent AR and asthma. A study on this area assessed the extent to which treating persistent AR with montelukast, desloratadine and levocetirizine alone or in combination improved quality-of-life.13 It was a 32-week randomized, doubleblind, placebo-controlled, crossover study in two arms: 20 patients received montelukast 10 mg/day and/or desloratadine 5 mg/day or placebo; 20 patients received montelukast 10 mg/day and/or levocetirizine 5 mg/day or placebo. The treatment periods were separated by 2-week washout periods. Quality-of-life was assessed on the day before starting treatment and on the last day of each treatment period using the rhinoconjunctivitis quality-of-life questionnaire. Sleep problems were also assessed. In the desloratadine plus montelukast arm, the mean (SEM) quality-of-life score before treatment was 3.1 (0.41). After placebo, this score was 2.16 (0.43), after desloratadine it was 1.79 (0.38), after montelukast it was 1.48 (0.37) and after montelukast plus desloratadine it was 1.59 (0.37). In the montelukast plus levocetirizine arm, the mean quality-of-life score before treatment was 2.58 (0.49). After placebo it was 1.78 (0.46), after levocetirizine it was 1.38 (0.42), after montelukast it was 1.36 (0.37) and after montelukast plus levocetirizine it was 1.26 (0.39). Placebo, montelukast, desloratadine and levocetirizine significantly improved quality-of-life. Conclusion AR is a very common entity in patients with asthma, with prevalence upto 100%, in those with allergic asthma. The temporal relation of AR and asthma diagnosis is variable; the diagnosis of AR often precedes that of asthma. Rhinitis is an independent risk factor for the subsequent development of asthma in both atopic and nonatopic individuals. There are conflicting results regarding the benefits for asthma symptoms of treating co-morbid AR with intranasal corticosteroids. Asian Journal of Ear, Nose & Throat, July-September 2010

drug therapy Montelukast reduces the symptoms of AR, and is comparable with antihistamines and oral decongestants; it is also effective in both SAR and PAR, and improves lung functioning in asthma. Effectiveness increases with greater levels of allergen exposure, and efficacy is also increased when asthma symptoms are more severe. As a result, montelukast is a suggested treatment for both conditions. So, antileukotriene agents such as the leukotriene receptor antagonists (montelukast) offer benefits for treating both AR and asthma and this effect can be amplified if it is combined with antihistamines like levocetirizine. References 1. Skoner DP. Allergic rhinitis: definition, epidemiology, pathophysiology, detection, and diagnosis. J Allergy Clin Immunol 2001;108(1 Suppl):S2-8. 2. Shah A, Pawankar R. Allergic rhinitis and co-morbid asthma: perspective from India - ARIA Asia-Pacific Workshop Report. Asian Pac J Allergy Immunol 2009;27: 71-7. 3. CDC 2003. Asthma in US as assessed from internet. 4. Gonyeau MJ, Partisano AM. A clinical review of montelukast in the treatment of seasonal allergic rhinitis. Formulary 2003;38(6):368-78. 5. Passalacqua G, Ciprandi G, Canonica GW. The nose-lung interaction in allergic rhinitis and asthma: united airways disease. Curr Opin Allergy Clin Immunol 2001;1(1):7‑13.

6. Passalacqua G, Ciprandi G, Pasquali M, Guerra L, Canonica GW. An update on the asthma-rhinitis link. Curr Opin Allergy Clin Immunol 2004;4(3):177-83. 7. Compalcti E, Ridolo E, Passalacqua G, Braido F, Villa E, Canonica GW. The link between allergic rhinitis and asthma: the united airways disease. Expert Rev Clin Immunol 2010;6(3):413-23. 8. Bachert C, Bousquet J, Canonica GW, Durham SR, Klimek L, Mullol J, et al. Levocetirizine improves qualityof-life and reduces costs in long-term management of persistent allergic rhinitis. J Allergy Clin Immunol 2004;114(4):838-44. 9. WHO Report ARIA as assessed from internet 2001 www. cks. 10. Nayak A, Langdon RB. Montelukast in the treatment of allergic rhinitis: an evidence-based review. Drugs 2007;67(6):887-901. 11. Pasquali M, Baiardini I, Rogkakou A, Riccio AM, Gamalero C, Desculzi D, et al. Levocetirizine in persistent allergic rhinitis and asthma: effects on symptoms, quality-of-life and inflammatory parameters. Clin Exp Allergy 2006;36(9):1161-7. 12. Ciebiada M, Górska-Ciebiada M, DuBuske LM, Górski P. Montelukast with desloratadine or levocetirizine for the treatment of persistent allergic rhinitis. Ann Allergy Asthma Immunol 2006;97(5):664-71. 13. Ciebiada M, Ciebiada MG, Kmiecik T, DuBuske LM, Gorski P. Quality-of-life in patients with persistent allergic rhinitis treated with montelukast alone or in combination with levocetirizine or desloratadine. J Investig Allergol Clin Immunol 2008;18(5):343-9.


Asian Journal of Ear, Nose & Throat, July-September 2010




Review Article

Headache â&#x20AC;&#x201C; A Review Uma Garg*, MK Garg**

Abstract According to IHS (International Headache Society) headache may be divided into two types - Primary or Benign headache and Secondary or Organic headache. Truly speaking most of the headaches are primary and very rarely we encounter secondary headaches. Key words: Benign headache, organic headache, migraine, sinus headache


eadache is a very common presenting symptom in all the clinics whether general or specialty. It is a fundamental component of human biology. Most of us if not all have physiologic potential for headache. The over all life time incidence of headache is 90-100% (in young females - 100%). Headache accounts for 20% of absence at work place as a result of this sickness affecting quality-of-life. Migraine is the commonest cause of headache evaluated so far, much more common than we think of. Migraine effects 10-12% of general adult population. M:F is (1:3). Peak prevalence age is during 25-55 years. Other less common causes of headache are hypertension, headache of drug abuse and rarely brain tumors or intra cranial pathologies. Severity of headache does not point towards any diagnosis. The duration and pattern of occurrence and associated symptoms are more important diagnostic indicators. Generation of headache is undoubtedly at higher, central or brain level and whenever it perceives a threat of any kind as a part of protective physiology it reflects as headache. A wide range of triggering factors which may be central or peripheral may initiate the process. According to IHS (International Headache Society) headache may be divided into two types - Primary or

*Associate Professor and Head Dept. of ENT **Associate Professor and Head Dept. of Surgery Muzaffarnagar Medical College and Hospital, Muzaffarnagar Address for correspondence Dr Uma Garg Associate Professor and Head, Dept. of ENT Muzaffarnagar Medical College and Hospital, Muzaffarnagar E-mail:


benign headache and secondary or organic headache. Truly speaking most of the headaches are primary and very rarely we encounter secondary headaches1 (1 in 250,000 i.e. 0004%). Migraine and associated migrainous headaches including sinus problems constitute a major percentage of these primary headaches. The aim of this paper is to give an insight into the pathophysiology of headache thus pointing towards the important life-threatening sinister causes of headache and their management. Sinus headache, a poorly understood cousin of migraine needs to be differentiated clearly thereby indicating surgical treatment. Different descriptions of headache are seen in clinical practice e.g., a knife is continuously being pushed deep into my head or it seems like a ton of weight is lying on my head or whole of my L/R head is pounding. Pathophysiology Pathophysiology of headache is basically supported by hypothesis of neurovascular dysfunction of trigeminal nervous system. Head is supplied by all three branches of trigeminal nerve and upper cervical nerves i.e. greater and lesser occipital nerves. The latter supply posterior aspect of head, neck and upper shoulders. Sensory afferents from these areas have their first central synapse in trigeminal caudate nucleus (TCN).1 From here, second order neurons supply parasympathetic tracts. This in turn leads to activation of the of Trigemino vascular system releasing neuropeptides e.g., CGRP, substance - P and neurokinin - A from trigeminalafferents innervating vascular and other structures within the trigeminal distribution. With this, the Asian Journal of Ear, Nose & Throat, July-September 2010

Review Article parasympathetic tracts innervating the sinus cavities are also stimulated producing rhinorrhea, lacrimation, nasal congestion and facial pain or heaviness. Any offending agent/irritation of nasal mucosa i.e. cold, hot, dust, allergens, chemicals, regional immunologic, infectious anatomic factors may activate the trigemino neurovascular system via TCN and initiate the release of vasodilators leading to headache. This is how headache is also explained in rhinosinusitis. Anything disrupting, irritating the path ways between TCN and upper neck and shoulders can trigger the mechanism. Etiology may be different but ultimate what we get is headache. This is known as convergence hypothesis.2 It is important to note here that many a times there is no recognizable triggering factor. A possible correlation has also been hypothesized between migraine and retinal microvasculature. Retinal and cerebral microcirculation share similar anatomical, embryological, physiological and neurovascular mechanisms. Therefore, a definite association exists between migraine and increased prevalence of retinopathies in middle aged individuals. Retinal microvasculature abnormalities and migraine both have been consistently linked with clinical and subclinical stroke.3 Ultra structural studies show ↓↓sed cerebral magnesium levels, mitochondrial abnormalities leading to ↓O2,↑sed No. levels and P/Q-associated calcium channelopathies. These all are causes of hyperexcitability of the brain eventually leading to migraine.4 Causes  Primary  Secondary - Various metabolic, traumatic, inflammatory, neoplastic, endocrinal, immunologic and vascular causes are described. Some of them are migrainous, ergotamine dependent headache,5 chronic paroxysmal hemicrania, cerebral tumor,5 benign intracranial hypertension, cerebral aneurysm,5 temporal arteritis, meningitis, cough headache, TMJ dysfunction, cervical headache, sinus headache, headache of herpes, headache of depression and many others.

or irregularly. It is unilateral, throbbing and moderate to severe in intensity and aggravated by activity, light or sound. To diagnose migraine, the subject must give history of H/O at least 5 attacks of headache of 4-72 hours of duration if untreated. No secondary cause is found. Nausea, vomiting, phonophobia, photophobia and lacrimation may accompany the event. Aura may be there with varying disability. Other Migrainous Headache Include tension headache or cluster headache. These may be bilateral, less disabling and are not usually aggravated by activity. These are no associated features.  Ergotamine dependent headache is seen in those migraine subjects who take ergotamine as soon as they think that migraine is coming as prophylactic treatment. But repeated intake leads to more frequent headache not responding to migraine.  CPH: Rare form of U/L headache. Common in men and responds to indomethacin.  Cerebral tumor: A rare cause of headache, much rare than commonly though of. It needs a cluster of symptoms to diagnose a cerebral tumor.  Benign intracranial hypertension: Rarer, S/S of raised intracranial pressure are present.  Cerebral aneurysm: Is a vascular catastrophe, sudden severe pain radiating to neck exacerbated by head and neck movements. Sometimes a dull unilateral headache may be present for several weeks. CT may be inconclusive at this stage of aneurysmal expansion. DSA may be helpful.  Temporal arteritis: Presents with temporal headache which may not be severe. Steroids can be started early while waiting for arterial biopsy results.  Meningitis: Fever, severe headache, neck stiffness and drowsiness suggest diagnosis. CSF picture distinguishes from other causes.  Cough headache: This is different from headache of raised intracranial pressure aggravated by coughing. This is benign and has got a limited natural history improving slowly on its own.


Management  Investigations  Treatment

It is a common, chronic, incapacitating paroxysmal disorder with attacks of headache recurring regularly

There are three important aspects of evaluation of headache history, history and the history.

Asian Journal of Ear, Nose & Throat, July-September 2010


Review Article 

History: About duration, onset, pattern, change in type, associated features, H/O of smoking/ alcohol. Examination: G/E, CVS, fundus examination, ENT examination (especially for sinusitis). Investigations: a) LAB n Complete hemogram n Blood sugar levels n ECG n LP b) Radiological AP Skull


Water’s view (OM) Last view

Figure 1.

Treatment If Migraine: Therapy of migraine is directed towards control of the:  Acute attacks  Prophylactic - In between the attacks  Behavioral therapy  Surgical Acute Therapy

Aim is to achieve rapid relief from symptoms and reduce disability. A simple plan for acute treatment is: At zero hours: Simple analgesics e.g., PCM (1000 mg), aspirin (600 mg), NSAIDs like ibuprofen (400-800 mg), tolfenamic acid, naproxen sodium, diclofenac suppository (100 mg). Two hours: Combination therapy antiemetics like domperidone (20 mg)



Four hours: Triptans are given e.g., (Sumatriptan, Naratriptan, Rizatriptan). Triptans are not given during aura. Medical therapy for igraine could be started in preheadache period and can be continued in postheadache period for better results. 20

Sumatriptan is a faster acting triptan and can be used with a triptan having long half life in those who have headache recurrence following triptan therapy. Dosage - Sumatriptan 50 mg6; Rizatriptan 5-10 mg. Other triptans include frovatriptan, almotriptan, zolmitriptan and eletriptan. (2) IM Diclofenac (75 mg) with IM metoclopramide. The problem with the opiates is addiction. Prophylactic

Base of skull PNS


Lateral view

Rescue therapy - (1) for those not responding to above medication. It includes subcutaneous sumatriptan (5 mg), butorphenol spray, parenteral phenothiazines, nasal sumatriptan and nasal zolmitriptan.

Needs to be considered in following situations:  Frequent headache >2/week or 3 attacks/month.  Interference with daily routine as attacks are very severe.  Failure of acute therapy or CI or adverse side effects.  Presence of associated or complicating conditions with e.g., n Hemiplegic migraine7 n Basilar migraine7 n Migraine with prolonged aura n Migrainous infarction Medication should atleast be given for three months. Various drugs for Prophylaxis are:  b-blockers: propranolol, timolol, metoprolol, tiagabine, atenolol  Levatiracetam, zonisamide  Anticonvulsant divalproex, topiramide, gabapentin.8 Sodium valproate (400-1,500 mg/day)  TCA- When frequency more and intensity less. Amitryptiline 50-100 daily  5HT antagonists - Pizotifen (Single bed time dose) 1.5-3.0 mg daily  Serotonin antagonists 

Botulinum toxin9





Acute Prophylactic

Asian Journal of Ear, Nose & Throat, July-September 2010

Review Article 


Regular sleep and exercise preferably


Avoid glare, stress, travel


Maintain headache diary





Try three different strategies in succession before embarking on decision to refer the patient to a neurologist. Tension If the patient does not fit into Cluster migraine it may be: Cervicogenic

Among all these flunarizine has been found to be most effective for headache occurring at night sleep. (It is a calcium channel blocker). Behavioral Therapy 

Regular meals

Avoidance of alcohol, fizzy drinks, OC’s



If battery of investigations reveals a surgically treatable cause then surgery is indicated e.g., sinusitis, cerebral tumors. Whether acute/prophylactic, assurance with explanation is best treatment.

Sinus Headache

Evaluate HA pattern

New onset or change In existing HA pattern

Stable HA pattern >6 months

Assess for Underlying disease

Evaluation positive: Evaluate and treat as directed by medical evaluation

Evaluation Normal: Consider presumptive diagnosis of major complaint Primary HA

Episodic pattern <15 days/month

Chronic pattern <15 days/month

Headache is major complaint

HA is a component of other sinus symptoms

Presumptive of migraine

ENT evaluation

Positive Tx underlying pathology

Evaluate for medication overuse (>2 days/week)

If present: Stop rebounding medicines

If absent: Try different acute HA medicine

Negative Tx symptomatically New or different preventive, schedule followup and consider HA consultation

Figure 2. Management algorithm for sinus headache.

Asian Journal of Ear, Nose & Throat, July-September 2010


Review Article Flag Signs  Headache which builds up apoplectically with in a few seconds.  Headache beginning abruptly with strenuous exertion.  Headache associated with neck pain (meningismus).  Headache radiating to back of neck (cerebral aneurysm).  Headache-associated with neurological 12 symptoms (SAH).  Headache associated with ophthalmic symptoms (Pituitary).13  Headache-associated with menstrual 13 disturbances (pituitary).  Headache not confirming to any of the primary headaches.14  Headache similar to a headache long back in past which has been forgotten.  The first worst headache ever experienced before and lands the patient in emergency hospital. Conclusion  Mostly headaches are primary and migrainous even sinus headache.  Prophylactic treatment is better and more result fetching than acute cases.  Exclusion of secondary causes is mandatory keeping in mind the flag signs. Sinus headache is considered a subclass in migrainous headaches because these both share the same pathway, same symptoms, same triggering factors and response to sumatriptan. In sinusitis, headache is more in those subjects who are more prone to migraine. So the headache which seems to be sinus headache can be treated medically. Surgical treatment is reserved for the cases which do not respond to medical treatment.  Fear of stroke i.e. ischemic stroke is ↑sed especially in females who take OC’s or who smoke. PS if patient primarily presents predominantly


with headache and nasal symptoms are in the midst of associated migraine symptoms as nausea and photophobia likely diagnosis is migraine. Patient c/o pain not very severe and nasal symptoms e.g., nasal pain, obstruction/purulence are prominent-sinusitis and migraine can coexist comorbidly.

References 1. Cady RK, Schreiber CP. Sinus headache: a clinical conundrum. OCNA 2004;37:267-88. 2. Which Headache. A guide to the diagnosis and management of headache. Worthing (UK): Professional Postgraduate services Eurpe Ltd., 1991. 3. Retinal Vascular Caliber and Migraine: The Blue Maintain Eye study Grald Liew, Poul Mitchell, Tien Yin Wong, Jie Jin Wang. 4. Welch KM, Ramadan NM. Mitochondria, magnesium and migraine. J Neurol Sci 1995;134:9-14. 5. Zilkha KJ. Headache and facial pain. Scott Brown’s Otolaryngol 1987;4:341-7. 6. Roger, Martin V, Nauskop A, Rogers A. Efficacy of Rizatriptan 10mg administered early in migraine attack. Headache 2006;46:913-4. 7. Motta E, Rosciszewska D, Miller K. Hemiplegic migraine with CSF abnormalities. Headache 1995;35:368-70. 8. Mathew N, Saper J, Magnis - Millen L. Efficacy and safety of gabapentin in migraine prophylaxis (abstracts) In: 17th Annual Meeting of the American Pam Society, San Diego, Ca. 9. Silber stein SD, Mathew N, Saper J, et al. Migraine Clinical Research group. Botulinum toxin type A as a migraine preventive treatment. Headache 2000;40:445‑50. 10. Schoenen J, Jacquy J, Lenarts M. Effectiveness of high dose riboflavin in migraine prophylaxis. Neurology 1998;50:466-70. 11. Sheftell FD, Rapoport AM, Walker B, et al. Leukotriene antagonists in the prophylaxis of migraine. Headache 1999;39:81. 12. Ostergaard JR. Headache as a warning symptom of impending aneurysmal subarachnoid hemorrhage. Cephalgia 1991;11:53-5. 13. Hockaday JM, Peet KMS, Hockaday TDR. Bromocriptine in migraine. Headache 1976;16:109-14. 14. Rapapart A, Sheftell D, Purdy A. Advanced Therapy of Headache 1999;7:293-301.




Asian Journal of Ear, Nose & Throat, July-September 2010

case report

Tympanomastoid Carcinoma Jasveer Singh*, Ipsit Panda**

Abstract Tympanomastoid malignancies constitute only 0.8% of otorhinolaryngological malignancies. Predominance in females has been reported in literature. Histopathologically squamous cell malignancies are more common than other forms. Treatment regime varies from one center to other. The surgical excision sparing the vital structures are followed, but in advanced cases, chemotherapy along with radiation has been preferred depending upon the stage of the diseases, tolerance/expectance to the extensive surgery and postoperative morbidity. Few cases of tympanomastoid malignancies has been reported in our center. The two are being reported here, which have been monitored and followed after the chemotherapy along with radiations. The prognosis have been reported poor, inspite of early detection, proper regimen of chemotherapeutic agents and radiotherapy. Key words: Squamous cell carcinoma, chemotherapy, radiation


quamous cell carcinoma, though the most common variety of malignant tumors of external ear and tympanomastoid region, is still a rare tumor amongst the otolaryngological malignancies. With the local infiltration of this malignancy to surgically inaccessible areas and surrounding areas like the parotid space, temporomandibular joint, glenoid fossa, temporal region and masticator space and also through perineural, lymphatic and hematogenous spread, surgery remains the palliative mode of treatment in the late stages. If diagnosed early, the chief mode of treatment remains surgery followed by radiotherapy. Prognosis depends upon the staging. Promptness in treatment may prolong life. Case Report Case 1

A 49-year-old female patient presented with insidious intermittent pain in right ear that was radiating to right side of the head. It was progressive and gradually changed to continuous type. There was no aggravating factor and pain was relieving with medications. Patient complained of insidious scanty discharge from right ear that was nonfoul smelling, off and on turned purulent and was blood stained on attempted instrumentation to get relief from itching. It was not *Chief Consultant **Resident Dept. of Otorhinolaryngology, NRCH, New Delhi

Asian Journal of Ear, Nose & Throat, July-September 2010

associated with any aggravating factor and relieved with medications. Patient visited a local dispensary for the last 10 months and was taking medications as advised. Two months back she noticed some growth arising from inside of the ear and visible from outside. On local examination, there was a vague swelling over the right cheek adjacent to the pinna measuring 3 × 4 cm, tender, nonmobile with ill defined margins. Right ear examination showed a pink polypoid mass arising from external ear canal extending upto the orifice of the canal. On gentle probing it was firm in consistency. It was associated with mucopurulent discharge from the same ear. A single level II cervical lymph node could be palpated on right side measuring approximately 1.5 × l cm, nontender, hard in consistency. Biopsy was taken from the mass. Histopathology report suggested a well diffentiated squamous cell carcinoma. Contrast enhanced CT of temporal bone showed:  Extensive osseous destruction of right temporal bone in its mastoid and squamous part and the zygomatic process.  The right EAC, middle ear, facial canal filled with tumor mass and right condylar process of mandible showed bony destruction.  Heterogeneously enhancing soft tissue mass (5.5 cm, 5.2 cm, 3.5 cm) seen filling right EAC, middle ear, mastoid antrum and air cells and 23

case report

extending to right parotid space, right TM joint, right masticator space, right parapharyngeal space not separable from right lateral aspect of nasopharynx. Intracranial extension in right temporal region involving the sigmoid sinus. Right internal carotid artery and internal jugular vein encased by tumor mass. Multiple enlarged right parotid lymph nodes (Largest measuring 1.6 - 1.3 cm). Single level-ll cervical node (1.7 - l.l cm).

The oncology board was of the opinion to give her neoadjuvant chemotherapy followed by external beam radiotherapy. She was put on neoadjuvant chemotherapy (4 cycles in a weekly interval, each cycle consisting of Ifosfamide 2 g + Carboplatin 150 mg + 5-Flurouracil l g + Interferon 3 million units daily for 3 days). The tumor as well as the parotid lymph node regressed significantly. Then, she received external beam radiotherapy, a cumulative dose of 6,600 Grey in 33 fractions over 6½ week. During the course she suffered no major morbidity arising from radiation except the skin changes, oral and oropharyngeal mucositis. Tumor regressed markedly with local relief of pain leaving behind facial weakness. Six months after the therapy, patient is still doing well. Case 2

An old lady, 70 years of age, presented to the ENT department with a mass protruding from her right external auditory canal since three months. Initially, she complained of irritation and discharge from the right ear which bled with attempted instrumentation. She had not taken any advice from a specialist. Gradually, she noticed occlusion of his right ear canal and then got referred to our institution from the local dispensary. CT scan of the head showed destructive lesion occupying the external auditory canal, the middle ear, TM joint, parotid space and infratemporal fossa in the right side. Histopathology of the mass showed squamous cell carcinoma. The oncology board decided to treat her with radiotherapy and adjuvant chemotherapy.

Case 1


First radiotherapy (Total 6,000 Grey in 35 fractions over 7 weeks) was given following which patient had ipsilateral facial palsies with radionecrosis of skin with exfoliation of mass around the right pinna. Patient had Asian Journal of Ear, Nose & Throat, July-September 2010

case report radionecrosis of conchal cartilage. She was sent back to home after radiotherapy, but she reported after 2 months with mass in the right postural region and external auditory canal. Chemotherapy (3 cycles, each cycle seven days apart, each consisting of Ifosfamide 2 g + Carboplatin 150 m + 5-Flurouracil l g) was given to her, but the mass did not regress. It fungated in the later stage. The tumor was extending intracranially and the space around the mastoid, i.e. infratemporal fossa, parotid space and TM joint. The palliative chemotherapy was planned by oncology board, but patient did not turn up for the treatment and succumbed to her disease within one year of disease detection. Discussion Tumors of external ear canal are uncommon out of which the most common malignant type is squamous cell carcinoma, others being adenocarcinoma, basal cell carcinoma, melanoma, rhabdomyosarcoma and metastatic disease. The age group commonly involved is 40-60 years. The incidence rate is 1/10,00,000 women/year as compared to 0.8/10,00,000 men/year. The etiology is mostly due to chronic irritation and inflammations from CSOM although irradiation for intracranial and nasopharyngeal carcinomas and exposure to ultraviolet rays play a less significant part. The main presenting complaints are otorrhea, otalgia, mass in EAC, hearing loss, periauricular mass, facial palsy, tinnitus and vertigo. It is aggressive locally as well as shows perineural invasion. In 10% cases lymph nodes are involved and the parotid nodes are the first in this case. It also distantly metastasize to lung, bones and liver. Involvement of lymph node and metastasis show a poor prognosis and stage the tumor to a higher grade. Mode of investigation to look for extension is high resolution CT scan and MRI.

Case 2

Asian Journal of Ear, Nose & Throat, July-September 2010

The tumor is staged as per the University of Pittsburg staging system. T1: Limited to external auditory canal. T2: Limited to external auditory canal + Partial thickness bony canal involvement OR soft tissue involvement <0.5 cm. T3: Full thickness bony canal involvement + soft tissue involvement >0.5 cm. OR Involvement of middle ear and mastoid OR Facial nerve involvement. 25

case report

T4: Tumor invading carotid canal, jugular bulb, medial wall of middle ear, cochlea, petrous apex, dura, OR Radiological soft tissue involvement >0.5 cm.

Conclusion Tympanomastoid carcinoma is a rare condition with a poor prognosis. Awareness of this clinical condition is necessary because physician and ENT practitioners may easily miss the diagnosis. Any earache and ear discharge for more than three months and granulations within the canal or bleeding along with mass in the external auditory canal, which; not being relieved by usual conservative treatment of otorrhea, should raise the suspicion of malignancy. A proper clinical evaluation, histopathology and radiology help to reach a proper diagnosis and proper management. Primary radiation is ineffective as curative treatment. When the pathologic margins are clear, early debulking surgery with adjuvant radiotherapy offers the best chance of survival. Involvement of the dura poses a challenge to the clinical benefits of any mode of treatment. Radiation associated tumors have got a higher propensity to recur. Surgeons and the patient should understand the risk and realistic outcome of each of the treatment protocol.

References 1. Arora S, Sharma JK, Pippal S, Sethi Y, Yadav A. Temporal bone carcinoma with intracranial extention. Brazilian J Otorhinolaryngol 2009;75(5). 2. Jin YT, Tsai ST, Li C, Chang KC, Yan JJ, Chao WY, et al. Prevalence of human papilloma virus in middle ear carcinoma associated with chronic otitis media. Am J Pathol 1997;150(4):1327-33. 3. Leonetti JP, Smith PG, Kletzker GR, Izquierdo R. Invasion patterns of advanced temporal bone malignancies. Am J Otol 1996;17(3):438-42. 4. Lim LHY, Goh YH, Chan YM, Chong VF, Low WK. Malignancy of the temporal bone and external auditory canal. Otolaryngol Head Neck Surg 2000;122(6):882â&#x20AC;&#x2018;6. 5. Moffat DA, Wagstaff SA, Hardy DG. The outcome of radical surgery and postoperative radiotherapy for squamous cell carcinoma of the temporal bone. Otolaryngol Head Neck Surg 2005;115(2):341-7. 6. Stankovic M. Carcinoma of temporal bone: Outcome of surgical therapy depending on stage and type of tumor. Archives Oncology 2004;12(suppl:l). 7. William IK, Cliford RH, Samuel HS. Cancer of the external auditory canal and temporal bone. Otolaryngol clinics of northern Am 1996;29(5):827-52.





Asian Journal of Ear, Nose & Throat, July-September 2010

case report

Isolated Malignant Lymphoma of the Parotid Gland A Ravikumar*, Senthil Kannan**, John Samuel†, Shalini Balakrishnan‡

Abstract Reported here is a case of isolated malignant lymphoma of the parotid gland in a 60-year-old female. Routine clinical examination and radiological evaluation pointed to a diagnosis of a benign parotid gland lesion, possibly a Warthin’s tumor. Only histopathological analysis gave the exact diagnosis of a malignant lymphoma of the parotid. This article highlights the importance of definitive diagnosis with the help of a histopathological analysis, as radiological assessment is said to be practically noncontributive to the histological diagnosis. Key words: Lymphoma, parotid gland, MALT


alignant lymphoma of the parotid gland is very rare. Primary lymphomas of the salivary glands account for 4.7% of lymphomas at all sites. The salivary glands are usually involved secondary to primaries elsewhere. Malignant lymphoma originating in the parotid gland is relatively rare and occurs in 1-5% of lymphomas where the parotid gland is the original site of the tumor. Mucosa-associated lymphoid tissue (MALT) neoplasms are extranodal non-Hodgkin’s lymphomas and salivary glands are few of the common sites involved in these cases. Case Report A 60-year-old female presented to the ENT Clinic at Sri Ramachandra Medical Centre with complaints of swelling in front of the right ear of more than one year duration of insidious onset. The swelling gradually increased in size during that period. She had no complaints of pain over the swelling, restriction in mouth opening or difficulty in swallowing. There was no significant history of loss of appetite or weight, fever or malaise. On examination, she had a preauricular *Professor and Head **Associate Professor † Assistant Professor ‡ Postgraduate Dept. of ENT, Head and Neck Surgery Sri Ramachandra Medical College and Research Institute, Chennai Address for correspondence Dr John Samuel Assistant Professor Dept. of ENT, Head and Neck Surgery Sri Ramachandra Medical College and Research Institute Porur, Chennai - 116 E-mail:

Asian Journal of Ear, Nose & Throat, July-September 2010

swelling on the right side, about 3 × 3 cm in size, which was firm to hard in consistency, nontender and nonmobile. The overlying skin was stretched and shiny. The opening of the Stenson’s duct in the oral cavity was unremarkable. There were no palpable lymph nodes in the neck. Examination of the ear, nose and throat was otherwise normal. Examination of the cardiovascular system and respiratory system was normal. Abdomen showed no hepatosplenomegaly or abnormal masses. Routine blood and urine investigations including hemoglobin level, total and differential counts, coagulation profile, liver and renal functions were within normal limits, but the blood glucose levels were found to be elevated. Fine needle aspiration cytology of the swelling showed aggregation of lymphoepithelial tissue. Computerized tomography of the neck and face showed multiple faintly enhancing soft tissue nodules within the superficial lobe of the right parotid gland without adjacent infiltration (Figs. 1a and 1b). With a working diagnosis of right benign parotid tumor, patient underwent right superficial parotidectomy under general anesthesia. Intraoperatively, the superficial lobe was found to be enlarged and firm in consistency. Two enlarged lymph nodes were identified within the parotid gland, one adjacent to the upper buccal branch and the other along the cervical branches of the facial nerve. The superficial lobe and the lymph nodes were removed in toto and sent for histopathological analysis. Postoperatively, patient had a Grade II facial nerve paralysis on the right side. The 27

case report

Figure 1a. Axial section of preoperative CT scan neck showing faintly enhancing nodules in the superficial lobe of the right parotid gland.

Figure 2a. Photomicrograph picture showing presence of sheets of atypical lymphocytes.

Figure 1b. Coronal section of preoperative CT scan neck showing enlarged superficial lobe of right parotid gland.

Figure 2b. Immunohistochemistry picture showing atypical lymphocytes positive for LCA.

surgical wound healed well and the facial nerve paralysis progressed to Grade III as per House-Brackmann classification at the two weeks follow-up.

The patient was subjected to more detailed evaluation for any other extranodal site involvement. A CT scan of the neck and ultrasound examination of the abdomen was normal. The medical oncologistâ&#x20AC;&#x2122;s opinion was to observe the patient for any recurrence of tumor and no immediate chemotherapy requirement. CT scan of the neck taken 12 months postoperatively showed no evidence of recurrent tumor. Presently the right facial nerve function has improved to normal (Figs. 3 and 4).

The histopathological picture showed presence of increased adipose tissue with atypical lymphocytes. By immunohistochemistry, the atypical lymphocytes were diffusely positive for LCA (leukocyte common antigen - CD45) and moderately positive for B-cell marker (CD20). A few scattered T-cell (CD3) were also noted, but were negative for cytokeratin. Kappa and Lambda light chains were also noncontributory. The lymph nodes excised showed loss of architecture with medium sized atypical lymphocytes arranged diffusely. The picture was that of a diffuse small B-cell type non-Hodgkinâ&#x20AC;&#x2122;s lymphoma of the parotid gland (MALT type) (Figs. 2a and 2b). 28

Discussion The parotid gland is covered by the investing layer of the deep cervical fascia of neck. There are 6-8 lymph nodes outside this fascia and 10-12 lymph nodes embedded in the glandular tissue, largely in the superficial lobe. There are very few nodes in the deep lobe. MALT Asian Journal of Ear, Nose & Throat, July-September 2010

case report with this underlying disease. MALT neoplasms are extranodal non-Hodgkin’s lymphomas. The most common site of the MALT lymphoma is the gastrointestinal tract. However, these tumors have been reported to occur in the salivary glands, lung, skin, soft tissues, breast, thyroid gland, thymus and ocular adnexa and orbit.2 In our case, the parotid gland was the only site of tumor, as evidenced by the investigations done.

Figure 3. One year postoperative CT scan neck showing no recurrent tumor.

Figure 4. One year postoperative picture showing normal facial nerve function on right side.

is a specialized component of the immune system that protects the free surface of a variety of organsespecially in the gastrointestinal tract, which is directly exposed to external agents. The salivary glands do not normally contain MALT but may acquire it as a result of an autoimmune inflammatory disorder, usually Sjögren’s syndrome.1 Despite the increased incidence of lymphoma in Sjögren’s syndrome, most of the major salivary gland lymphomas arise without association Asian Journal of Ear, Nose & Throat, July-September 2010

It has been reported that 80-85% of parotid gland tumors are benign and 15-20% are malignant.3 Primary lymphomas of the salivary glands account for 4.7% of lymphomas at all sites.1 The salivary glands are usually involved secondary to primaries elsewhere in the head and neck region. Malignant lymphoma originating in the parotid gland is relatively rare and occurs in 1-5% of tumors where the parotid gland is the original site of the tumor.4 It is common knowledge that tumors originating in the parotid gland are without characteristic features in their various imaging presentations and that differentiation between benign and malignant tumors is difficult. However, some workers have reported that these tumors can be differentiated by tumor margins, tumor homogeneity, infiltration into the adjacent tissue and signal intensity on MRI. There are also some correlations between the malignancy seen in histopathological examinations and the findings from imaging studies.5-9 It is commonly believed that the differentiation of malignant lymphoma originating in the parotid gland from other tumors, including benign tumors, is difficult; however, some authors have reported that malignant lymphomas showed tumor homogeneity surrounded by well-defined margins and were rarely associated with necrosis.10,11 It is necessary to consider the possibility of malignant lymphoma when the lesion rapidly increases in size and exhibits necrosis or an infiltrative tendency in the imaging presentations, strongly suggesting epithelial tumors. Punctuate calcification, both intracystic and parenchymal, may be present and may result from end-stage inflammatory lesions. Microscopically, normal salivary tissue is replaced by a dense lymphocytic infiltrate. This infiltrate appears heterogeneous with a mixture of small lymphocytes, centrocyte-like monocytoid cells and rare isolated blastic cells. All these cells are shown 29

case report immunohistochemically of B-cell origin Our case showed a positive test for CD20, CD5 and CD79a, with a positive Bcl-2, which was diagnostic of B-cell lymphoma. The neoplastic infiltrate is seen to be located in the marginal zone around reactive B-follicles and lymphoepithelial lesions, which are the hallmarks of extra-nodal marginal zone B-cell lymphoma of MALT, are characteristic.12 Irregular calcifications are seen at the center of some salivary ducts. Our patient had no clinical evidence of Sjögren’s syndrome. In general, malignant lymphoma originating in the parotid gland is histologically described as low-grade non-Hodgkin’s lymphoma, frequently belonging to the B-cell type and rarely relapses into other sites.9,13,14 However, there have been cases reported suggesting a correlation with a histologically intermediate or high grade of non-Hodgkin’s lymphoma. In a study by Suchy and Wolf15 of patients with localized MALT lymphoma, the treatment of choice was field radiotherapy if the disease extended to local lymph nodes or, surgery if the diseasewas extranodal only. Patients with disseminated lymphoma were usually treated with chemotherapy. Malignant lymphoma is known to be associated with a high rate of response to local treatment or chemotherapy, which results in an extended disease-free interval and long-term survival. Our patient had isolated surgical treatment of the tumor and no local or regional recurrence was seen after a one year follow-up. References 1. Balm AJ, Delaere P, Hilgers FJ, Somers R, Van Heerde‑P. Primary lymphoma of mucosa-associated lymphoid tissue (MALT) in the parotid gland. Clin Otolaryngol Allied Sci 1993;18(6):528-32. 2. Corr P, Vaithilingum M, Thejpal R, Jeena P. Parotid MALT lymphoma in HIV infected children. J Ultrasound Med 1997;16(9):615-7. 3. Batsakis JG. Tumor of the Head and Neck. 2nd edition, Williams and Wilkins Baltimore 1979:2-75.

4. Nagata M, Kumazawa H, Iwai H, Momotani A, Shiraishi S, Yamashita T. Study of malignant lymphoma in the parotid gland region 1996;99(6):918-25. 5. Freling NJ, Molenaar WM, Vermey A, Mooyaart EL, Panders AK, Annyas AA, et al. Malignant parotid tumors: clinical use of MR imaging and histologic correlation. Radiology 1992;185(3):691-6. 6. Swartz JD, Rothman MI, Marlowe FI, Berger AS. MRI of parotid mass lesions: attempts at histopathologic differentiation. J Comput Assist Tomogr 1989;13(5):789‑96. 7. Vogl TJ, Dresel SH, Späth M, Grevers G, Willimzig C, Schedel HK, et al. Parotid space: plain and gadoliniumenhanced MR imaging. Radiology 1990;177(3):667‑74. 8. Som PM, Biller HF. High grade malignancies of the parotid space: identification with MRI. Radiology 1989;173:82-6. 9. Tabor EK, Curtin HD. MR of the salivary glands. Radiol Clin North Am 1989;27(2):379-92. 10. Hashida I, Tamaki Y, Sakurai H, Takahashi T, Maebayashi K, Hayakawa K, et al. Malignant lymphoma of the parotid gland: a study of six cases. Gann no Rynsho 1995;41:863-7. 11. Hyman GA, Wolff M. Malignant lymphomas of the salivary glands. Review of the literature and report of 33 new cases, including four cases associated with the lymphoepithelial lesion. Am J Clin Pathol 1976;65(4):421-38. 12. Isaacson PG, Spencer J. Malignant lymphoma of mucosa-associated lymphoid tissue. Histopathology 1987;11(5):445-62. 13. Jacobs C, Hoppe RT. Non-Hodgkin’s lymphomas of head and neck extranodal sites. Int J Radiat Oncol Biol Phys 1985;11(2):357-64. 14. Furukawa M, Okabe Y, Umeda R. Malignant lymphoma of the parotid gland. Auris Nasus Larynx 1982;9(3):165‑71. 15. Suchy BH, Wolf SR. Bilateral mucosa-associated lymphoid tissue lymphoma of the parotid gland. Arch Otolaryngol Head Neck Surg 2000;126(2):224-6.





Asian Journal of Ear, Nose & Throat, July-September 2010

case report

Pleomorphic Adenoma of the Hard Palate Vaishali Sangole*, Kalpana Rajiv Kumar**, Suman Rao†, Rachana Nautiyal‡, Sujata Gawai‡

Abstract Pleomorphic adenoma is the most common benign tumor of the salivary glands, predominantly encountered in the parotid gland. It may arise from minor salivary glands and present as an intraoral mass over the palate. We report the case of a 25-year-old female with pleomorphic adenoma over the hard palate. Key words: Minor salivary glands, pleomorphic adenoma, hard palate


alivary gland tumors are most commonly located in the parotid gland. Seventy-five percent the remaining arise in submandibular gland (8%). Tumors arising in the minor salivary glands account for 22% of all salivary gland neoplasms. The majority are malignant; only 18% are benign. Most reports indicate a female preponderance varying from 1.2:1 to 1.8:1 for various histologic types.2,3 The palate is the most common site for pleomorphic adenomas arising from the minor salivary glands and occurring on the hard and soft palate with about equal frequency.4 Grossly the tumor is rounded to bosselated and is surrounded by a fibrous capsule of varying thickness. Microscopically they are characterized by variable, diverse, structural histologic patterns in patterns of sheets, strands or islands of spindle and stellate cells, with a myxoid or a chondroid configuration. Even in the absence of a capsule, the tumor is clearly demarcated from the surrounding tissues. A clinical differential diagnosis of condylomata acuminata, squamous cell carcinoma, oral papilloma, minor salivary gland tumor, Kaposi’s sarcoma, syphilitic gumma and intraoral molluscum contagiosum were considered.

Lecturer Associate Professor † Professor and Head ‡ Resident Dept. of ENT, Mahatma Gandhi Mission Medical College and Hospital, Kamothe, Navi Mumbai Address for correspondence Dr Vaishali Sangole Kesar Garden, IRIS-1203 Kharghar, Sector-20 Navi Mumbai - 410 210 E-mail: *


Asian Journal of Ear, Nose & Throat, July-September 2010

We report a patient suffering from a giant pleomorphic adenoma of the hard palate resected using a transoral approach. Case Report A 25-year-old female came to us with a history of swelling in the hard palate of one and a half year duration. Swelling was slow growing and painless. There was no preceding history of trauma and her past history was unremarkable. On examination, the swelling was 5 × 4 cm sized, on the right side of hard palate just crossing the midline, firm, labulated, nonpulsatile, nontender, adherent to the underlying structures with erythematous mucosa. There was no regional lymphadenopathy. A clinical differential diagnosis of oral papilloma, squamous cell carcinoma, minor salivary gland tumor, syphilitic gumma, Kaposi’s sarcoma, intraoral molluscum contagiosum, condylomata acuminate were considered. Fine needle aspiration cytology (FNAC) of the swelling was done which was reported as pleomorphic adenoma salivary gland. The hematological and serological examination for syphilis was negative. Radiograph of maxilla did not show any bony invasion. Under GA the swelling was explored. Incision was made in the midline of the swelling right down to the periosteum. The capsule of the swelling was not welldefined. However, the tumor was demarcated clearly from the surrounding tissue. The swelling was removed with a wide margin along with the surrounding periosteum. No satellite nodules were present. The bleeding was easily controlled. The incision was closed in layers. 31

case report Histopathology revealed tumor composed of epithelium and stroma. Stroma was chondromyxoid in nature admixed with well-differentiated ducts at places. Occasional foci of squamous metaplasia were also seen. There was no evidence of mitotic figures. Hence, the histopathological appearance from this area was considered to be pleomorphic adenoma of the minor salivary gland. There has been no recurrence in the last one year. Discussion Tumors of the minor salivary glands are responsible for 2-4% of the head and neck, 10% of tumors of oral cavity and 15-23% of the salivary glands.5 Pleomorphic adenoma, also known as benign mixed tumor is the most common tumor of salivary glands.

Figure 1. Photograph showing swelling 5 Ă&#x2014; 4 cm sized, on the right side of hard palate just crossing the midline which was firm, lobulated, nonpulsatile, nontender, adherent to the underlying structures with erythematous mucosa.

Figure 2. Histopathology revealing tumor composed of epithelium and stroma. Stroma was chondromyxoid in nature admixed with well- differentiated ducts at places. Occasional foci of squamous metaplasia were also seen. There was no evidence of mitotic figures. Hence, the histopathological appearance from this area was considered to be pleomorphic adenoma of the minor salivary gland.


Figure 3. Clinical photograph of a five-year-old male child showing, a swelling approximately 2 Ă&#x2014;1 cm, firm, nontender, nonfluctuant with no discharge on pressing and a visualized hair at the center. Fibrosed area of scar tissue from the previous procedure is also seen.

It mostly arises in the parotid or the submandibular salivary glands.l It may also arise in the minor salivary glands that are distributed throughout the oral cavity. The most frequent site of pleomorphic adenoma of the minor salivary glands is the hard and soft palate, followed by the upper lip, oral mucosa, floor of mouth, tonsil, pharynx, retromolar area and nasal cavity.3 Pleomorphic adenomas do not usually present a sexual predisposition and they can appear at any age with the same clinical behavior.5 The term pleomorphic describes the embryogenic basis of origin of these tumors, which contains both epithelial and mesenchymal tissues. lt has been postulated that these tumors arise from intercalated and myoepithelial cells.l Intraoral pleomorphic adenoma appear as slowly growing, painless mass, with firm consistency, usually in the fourth or fifth decade.9 Pain, tenderness and ulceration are unusual. Microscopically, pleomorphic adenomas of the minor salivary glands consist of epithelial cells and mesenchymal elements that tend to be more cellular, with less myxoid or chondroid component, and located within submucosa, in contrast with tumors of the major salivary glands. Variation may include squamous metaplasia, calcification, cartilagelike tissue, oxyphillic cells and rarely malignant transformation.1,9 Although it is a benign tumor, it has a high recurrence rate and in small number of cases, a benign pleomorphic adenoma may degenerate into a malignant tumor.l,9 Pleomorphic adenomas of the oral cavity lack a welldefined fibrous capsule, a feature associated with a high recurrence rate.9 Asian Journal of Ear, Nose & Throat, July-September 2010

case report The diagnosis of pleomorphic adenoma is established on the basis of history, physical examination, cytology and histopathology. Computed tomography (CT) and magnetic resonance imaging diagnosis is necessary to evaluate the location, size and extension to the surrounding superficial and deep structures. The treatment of pleomorphic adenoma of the hard palate is surgical excision with a surrounding cuff of normal tissue.1,9 The excision should include periosteum or bone if these are included.9 In earlier decades the technique of choice for removal was enucleation.10 However, incisional biopsies are never indicated as the tumor are so easily disseminated. We preferred transoral route to excise the tumor. Despite the drawbacks of this approach (limited access, poor maneuverability and need for nasal intubation), sufficient access can be obtained using a Davis Boyle mouth gag after previously verifying the functionality of both temporomandibular joints (TMJ) and adequate cervical mobility. Due to the initial benignity of the process, the most conservative possible surgical technique is preferable whenever resection is possible.7 The prognosis is excellent if resection is adequate. Irradiation is reserved for recurrences and inoperable cases.8 Malignant transformation has been reported 2-9%, generally to adenocarcinoma or undifferentiated carcinoma. The risk of malignancy increases with the duration of the tumor and mean age of the patient.9 Regular follow-up is required to detect local recurrence and malignization. Most recurrences can be attributable to inadequate surgical techniques such as simple enucleation leaving behind microscopic pseudopod-like extensions.9

Asian Journal of Ear, Nose & Throat, July-September 2010

References l. Suen JY, Synderman NL, Benign neoplasms of the salivary glands. In: Otolaryngology-Head and Neck Surgery. Mosby Year Book, 2nd edition, Vol.2, Cummings CW, Fredrickson JM, Harker LA, et al. (Eds.), 1993:1029-42. 2. Eveson JW, Cawson RA. SaIivary gland tumors: a review of 2410 cases with particular reference to histological types, site, age, and sex distribution. J Pathol 1985;146(1):51-8. 3. Spiro RH. Salivary neoplasms: overview of 35-year experience with 2,807 patients. Head Neck Surg 1986;8(3):177-84. 4. Waldron CA, el-Mofty SK, Gnepp DR. Tumors of the intraoral minor salivary glands: a demographic and histologic study of 426 cases. OraI Surg Oral Med Oral Pathol 1988;66(3):323-33. 5. Sànchez Legaza E, y cols. Adenoma pleomorfo del paladar duro. ORL-DIPS 2005;32:154-8. 6. GiI-Carcedo LM. E1 acceso quirurgico a los tumores de cavidad oral. Tumores de lengua movil. Tumores de orofaringe. En: El Abordaje en el. Tratamiento Quirurgico de los Tumores de Cabeza Cuello. Ponencia Oficial para 1992 de la SEORL y PCF 1992;43-56. 7. Moraitis D, Papakostas K, Karkanevatos A, Coast GJ, Jackson SR. Pleomorphic adenoma causing acute airway obstruction. J Laryngol Otol 2000;114(8):634-6. 8. Perez CA, y cols. Treatment of pleomorphic adenoma. In: Principles of Practise of Radiation Oncology. JB Lippincott Company. Philadelphia 1987:521. 9. Feinmersser R, Gay I. Pleomorphic adenoma of the hard palate: an invasive tumor? J Laryngol Otol 1983;97(12):1169‑71. 10. Thakray AC, Lucas RB. Tumors of the major salivary glands. In: Atlas of Tumor Pathology, Ser.2, Fascicle‑10, Washington DC, 1974. Armed Forces Institute of Pathology.





emedinews section

From eMedinewS Most Papillary Thyroid Cancer Patients Survive Regardless of Treatment

eMedinewS Try This it Works: Removing Nasal Foreign Bodies

A study published in the May issue of Archives of Otolaryngology-Head and Neck Surgery reports that in patients with papillary thyroid cancer that has not metastasized, the outcomes appear to be favorable despite treatment within the first year after diagnosis. The 20-year survival rate from cancer was estimated to be 97% for those who did not receive treatment and 99% for those who did.

First administer 4 or 5 drops of adult-strength xylometazoline hydrochloride to the affected nostril and allow 5 minutes for vasoconstriction of the inferior turbinate and nasal mucosa. Then ask the child to take a deep breath through the mouth and exhale through the affected nostril while you occlude the contralateral nostril. This removes the foreign body about 30% of the time and at least moves it more anteriorly-for easier removal with bayonet forceps-in about half of cases.

Medilaw Avoiding malpractice risks in the patient handoff

Handoff is the transition when patients are transferred from one doctor to another, or from an outpatient setting to a hospital or nursing home. This has been often described as “Achilles’ heel” and “time bomb”. Problems with handoff communication are one of the root causes in up to 70% of adverse sentinel events compiled by the Joint Commission. The probability of something going wrong viz. needed follow–up care that slips through the cracks or critical information that is not communicated in a timely manner can have life or death impact for the patients. It is also an important reason of malpractice lawsuits against health professionals. It is the responsibility of the treating physician to ensure that the covering physician is up to the mark regarding the patients’ needs, each time he or she falls ill or is going on a vacation. Every referral to a specialist also carries similar responsibility. The Joint Commission in 2006 added a requirement that hospitals seeking accreditation standardize their approaches to handoff communication as part of its patient safety goals. Several studies have often shown all sides to fail to relay timely crucial information to colleagues. Medical schools rarely teach about what constitutes an effective handoff. A 2005 study in Academic Medicine reported that only 8% of schools talk about handoffs in a formal didactic session. Reference 1. Mark E, Crane. Avoiding malpractice risks in the patient handoff. Medscape Business of Medicine. Drs Monica and Brahm Vasudeva


News to Use: Do it Know Before Your Mobile is Lost  Each mobile carries a unique IMEI i.e. International Mobile Identity No which can be used to track your mobile anywhere in the world.  Dial *#06# from your mobile.  Your mobile shows a unique 15 digit.  Note down this no. anywhere but except your mobile as this is the number which will help trace your mobile in case of a theft.  Once stolen you just have to mail this 15 digit IMEI no. to  No need to go to police.  Your Mobile will be traced within next 24 hrs via a complex system of GPRS and internet.  You will find where your hand set is being operated even in case your number is being changed. Role of Statins in Sinusitis Release of inflammatory mediators is an active process that involves the release of polyunsaturated fatty acids from phospholipids for enzymatic conversions of biologically active mediators. Hence it has been hypothesized that counter-regulatory lipid synthesis inhibitors, such as statins can block the release of these mediators. An ex–vivo analysis of the inflammatory mediators in 20 patients with symptomatic sinusitis, who underwent sinus surgery, was performed. All patients on statin therapy showed statistically significant Asian Journal of Ear, Nose & Throat, July-September 2010

emedinews section (p < 0.005) decrease in the expression of cytokines and chemokines, vs patients not on any anti-inflammatory agents. This study concluded that statins may induce significant anti-inflammatory effects in sinusitis and suggests that statins may have a role in the treatment of chronic airway inflammation. (Am J Respir Crit Care Med 181;2010:A4219) Question of the Day What is the Treatment of Choice for Treatment Failure in Acute Rhinosinusitis?

Treatment failure is defined as progression of symptoms at any time during treatment or failure to improve after seven days of therapy. Patients who fail firstline therapy require alternative antibiotic selection. Levofloxacin or high-dose amoxicillin-clavulanate (4 g/250 mg/day)‑have been recommended. Suggested Reading 1. Anon JB, Jacobs MR, Poole MD, et al. Antimicrobial treatment guidelines for acute bacterial rhinosinusitis. Otolaryngol Head Neck Surg 2004;130:1. Dr Shiv Aggarwal. Florida

How is ARS Diagnosed? Acute rhinosinusitis (ARS) i.e. inflammation of the nasal cavity and paranasal sinuses lasting less than four weeks, is subdivided into acute viral rhinosinusitis (AVRS) and acute bacterial rhinosinusitis (ABRS). ABRS occurs in 0.5-2% of episodes. The diagnosis of ARS is based on the presence of: Purulent rhinorrhea Nasal congestion and/or facial pain Symptoms do not accurately distinguish viral from bacterial infection. ABRS is suggested by the presence of symptoms for seven or more days, especially if symptoms initially improve and then worsen. Cultures from nasal swabs or secretions are inaccurate. Radiography is generally not indicated in the initial evaluation of ARS. Suggested Reading 1. Meltzer EO, Hamilos DL, Hadley JA, et al. Rhinosinusitis: Establishing definitions for clinical research and patient care. Otolaryngol Head Neck Surg 2004;131:S1. 2. Rosenfeld RM, Andes D, Bhattacharyya N, et al. Clinical practice guideline: adult sinusitis. Otolaryngol Head Neck Surg 2007;137:S1. Dr Shiv Aggarwal. Florida

Asian Journal of Ear, Nose & Throat, July-September 2010

What is Treatment Failure in Otitis Media? With appropriate antimicrobial therapy, the signs of systemic and local illness in otitis media usually resolve within 24-72 hours. Lack of improvement after 48-72 hours in a patient treated with antimicrobial therapy suggests either presence of another disease or inadequate initial therapy.1-3 Inadequate therapy is usually related to infection with an organism resistant to β-lactam antibiotics (nontypeable Haemophilus influenzae and drug-resistant Streptococcus pneumoniae are becoming increasingly important). But, infection with less common organisms, such as Staphylococcus aureus, also must be considered, particularly in children with tympanostomy tubes. Fluid may persist in the middle ear for prolonged periods even though the antimicrobial agents have sterilized the effusion and the acute signs and symptoms are no longer present; persistent middle ear effusion after the resolution of acute symptoms is not an indication of treatment failure. References 1. Al-Shawwa BA, Wegner D. Trimethoprim-sulfamethoxazole plus topical antibiotics as therapy for acute otitis media with otorrhea caused by community-acquired methicillin-resistant Staphylococcus aureus in children. Arch Otolaryngol Head Neck Surg 2005;131:782. 2. Santos F, Mankarious LA, Eavey RD. Methicillinresistant Staphylococcus aureus: pediatric otitis. Arch Otolaryngol Head Neck Surg 2000;126:1383. 3. Pichichero ME, Casey JR. Emergence of a multiresistant serotype 19A pneumococcal strain not included in the 7‑valent conjugate vaccine as an otopathogen in children. JAMA 2007;298:1772. Dr VP Sood

Cancers of Neck, Throat Less Fatal If Caused by HPV Cancers of the neck and throat are much less likely to be fatal if they are caused by the human papilloma virus (HPV), rather than alcohol and smoking, according to a study presented at the American Society of Clinical Oncology annual meeting and published in the New England Journal of Medicine. The research ‘provides another good argument for vaccination of both men and women with the HPV vaccine, which has previously been targeted primarily at women because the virus causes cervical cancer, researchers from the National Institutes of Health and Harvard Medical School wrote in an editorial accompanying the report. Dr Brahm and Monica Vasudeva


photo quiz

Swelling of the Right Ear


22-year-old man presented for evaluation of a painless swelling on his right ear that he first noticed about five months earlier. He denied any history of trauma. The patient was otherwise healthy with no significant medical history. The scaphoid fossa of the right auricle demonstrated a nontender, noninflammatory, almond-shaped nodule approximately 1.5 cm × 1 cm (see accompanying‑ Figure). Question Based on the patient’s history and physical examination, which one of the following is the most likely diagnosis? A. Chondrodermatitis nodularis chronica helicis B. Othematoma C. Pseudocyst of the auricle (benign idiopathic cystic chondromalacia) D. Relapsing polychondritis E. Subperichondral abscess Discussion The answer is C: pseudocyst of the auricle. An auricular pseudocyst, also referred to as benign idiopathic cystic chondromalacia, is an uncommon condition characterized by a painless, cystic swelling of the concha of the pinna.1 It most commonly affects healthy young men2 and rarely is there a history of antecedent trauma. There appears to be no racial predisposition.3 The exact etiology is unknown, but it is thought to be related to degenerative cartilage.4 The diagnosis can usually be made on clinical grounds, and routine histology is rarely necessary. However, when biopsy is performed, a characteristic finding is an intracartilaginous space with no epithelial lining.3 Needle aspiration of the cyst typically reveals a clear or yellow sterile fluid with the consistency of olive oil.5 Source: Adapted From Am Fam Physician 2007;75(9):1379-80.


Treatment goals include permanent removal of the pseudocyst with good aesthetic outcome and preservation of the normal anatomic architecture.3 It should be noted that simple needle aspiration of the pseudocyst, without additional treatment, always results in prompt reaccumulation of fluid, usually in less than three days.3 Definitive treatment by surgical excision with pressure dressing or compression buttoning usually results in a satisfying outcome; surgical excision remains the treatment of choice.6 Other treatment options include high-dose oral corticosteroids, simple aspiration with compression Selected Differential Diagnosis of Auricular Swelling Condition


Chondrodermatitis Exquisitely tender nodule on nodularis chronica helicis the outer helix; often a history of trauma Othematoma

History of trauma; may demonstrate pain and redness

Pseudocyst of the auricle Painless, cystic swelling of the concha of the pinna; usually no history of trauma Relapsing polychondritis

Autoimmune cartilage disease; ear manifestations are a painful, red, swollen superior portion of the pinna, sparing the noncartilaginous earlobe

Subperichondral abscess Pain and surrounding erythema; purulent aspirate

Asian Journal of Ear, Nose & Throat, July-September 2010

photo quiz bolsters, and punch biopsy with pressure dressing.7 Intralesional injection of corticosteroids,8,9 sclerosing agents,10 and minocycline4 also have been attempted with varying degrees of success. Aspiration followed by intralesional triamcinolone acetonide is another option and may be attempted up to three times before moving to surgical treatment.8,9 Chondrodermatitis nodularis chronica helicis, the most common diagnosis to exclude in the work-up, typically presents as an exquisitely tender nodule on the outer helix that may interfere with sleep. There is often a preceding history of trauma. It is most common in men older than 40 years. An othematoma invariably involves a history of notable trauma and may demonstrate clinical signs of inflammation, including pain and redness. Relapsing polychondritis is a rare multisystem autoimmune disease that can affect all cartilage throughout the body, including the ear, eyes, nose, and respiratory system.11 Relapsing polychondritis of the ear is manifested as a painful, red, swollen superior portion of the pinna, sparing the noncartilaginous ear lobe. Subperichondral abscess typically presents with pain and surrounding erythema. Diagnosis can be confirmed by aspiration of purulent fluid. References 1. Kopera D, Soyer HP, Smolle J, Kerl H. “Pseudocyst of the auricle”, othematoma and otoseroma: three faces of the same coin?”. Eur J Dermatol 2000;10:451-4.

2. Cohen PR, Grossman ME. Pseudocyst of the auricle. Case report and world literature review. Arch Otolaryngol Head Neck Surg 1990;116:1202-4. 3. Lim CM, Goh YH, Chao SS, Lynne L. Pseudocyst of the auricle. Laryngoscope 2002;112:2033-6. 4. Oyama N, Satoh M, Iwatsuki K, Kaneko F. Treatment of recurrent auricle pseudocyst with intralesional injection of minocycline: a report of two cases. J Am Acad Dermatol 2001;45:554-6. 5. Ophir D, Marshak G. Needle aspiration and pressure sutures for auricular pseudocyst. Plast Reconstr Surg 1991;87:783-4. 6. Choi S, Lam KH, Chan KW, Ghadially FN, Ng AS. Endochondral pseudocyst of the auricle in Chinese. Arch Otolaryngol 1984;110:792-6. 7. Paul AY, Pak HS, Welch ML, Toner CB, Yeager J. Pseudocyst of the auricle: diagnosis and management with a punch biopsy. J Am Acad Dermatol 2001;45: (6 suppl):S230-2. 8. Kunachak S, Prakunhungsit S. A simple treatment for endochondral pseudocyst of the auricle. J Otolaryngol 1992;21:139-41. 9. Miyamoto H, Oida M, Onuma S, Uchiyama M. Steroid injection therapy for pseudocyst of the auricle. Acta Derm Venereol 1994;74:140-2. 10. Zhu LX, Wang XY. New technique for treating pseudocyst of the auricle. J Laryngol Otol 1990;104:31-2. 11. Gergely P Jr, Poor G. Relapsing polychondritis. Best Pract Res Clin Rheumatol 2004;18:723-38.


Asian Journal of Ear, Nose & Throat, July-September 2010




lighter reading

1. Don’t worry. I think it is sharp enough.

Ep o nyms


Lighter Side of the Medicine

2. Nurse, did this patient sign the organs donation card? 3. Damn! Page 84 of the manual is missing! 4. Everybody stand back! I lost a contact lens!

Confucius A man who has committed a mistake and doesn’t correct it, is committing another mistake.

5. Hand me that...uh...that uh.....thingie

M yt h

6. Better save that. We’ll need it for the autopsy. 7. “Accept this sacrifice, O Great Lord of Darkness” 8. Whoa, wait a minute, if this is his spleen, then what’s that?

Feeding a child a lot of candy or food with a lot of sugar in it will make them hyperactive.

9. “Ya know, there’s big money in kidneys. Hell, he’s got two of ’em

A guy walks into work and both his ears are all bandaged up. The boss says, “What happened to your ears?” He says, “Yesterday I was ironing a shirt when the phone rang and I accidentally answered the iron.” The boss says, “Well that explains one ear, but what about the other ear?”

M nemo n i c s

10. What do you mean “You want a divorce?”

He says, “Well, I had to call the doctor!”

I l l u s i o n

Use the mnemonic SITTT as an aid in evaluating the cause of hematuria S = Stone I

= Infection

T = Trauma T = Tumor T = Tuberculosis

Clinical Tips Do it and teach Lifting pressure off the neck nerves 

Sit straight in a chair.

Close one fist and place it beneath the chin.

Push up gently with the fist.

I l l u s i o n 38

Resist with the chin. Maintain the chin in a horizontal position. Push up harder still with the closed fist. But resist it still more with the chin. Relax and repeat.

The exercise maintains strength of the neck muscles and is good for cervicals too.

Asian Journal of Ear, Nose & Throat, July-September 2010


Announcements, Conferences and Courses Information for Asian Journal of Ear, Nose and Throat (July-September 2010) 28th International Congress of the International Association of Logopedics and Phoniatrics (IALP) August 22-26, 2010 Venue: Athens, Greece Contact: Congress Secretariat E-mail: Website: Glasgow University Temporal Bone Rhinology Head and Neck Intensive Dissection Course August 25-27, 2010 Venue: Glasgow, UK Contact: Mr Brian F Oâ&#x20AC;&#x2122; Reilly Tel. No.: +44 (0)141 211 1668 E-mail: brian.oâ&#x20AC;&#x2122; Coblation: Diagnosis and Treatment of Snoring and Mild-to-Moderate Sleep Apnea August 26-28, 2010 Venue: Bergen, Norway Contact: Arthrocare Tel. No.: +46 854 617 200 E-mail: Website: 4th World Voice Congress September 6-9, 2010 Venue: Seoul, Republic of Korea Contact: Secretariat Tel. No.: +82 2 566 6067 Fax No.: +82 2 566 6087 E-mail: Website: 2010 Temporal Bone Surgical Dissection 5-day Courses September 13-17, 2010 Venue: Michigan, USA Contact: Laura Eldred E-mail: Website: Bonelabbrochure.pdf Asian Journal of Ear, Nose & Throat, July-September 2010

18th Annual Conference on Management of the Tinnitus Patient September 16-18, 2010 Venue: Lowa City, USA Tel. No.: +1 800 551 9029 Fax No.: +1 319 335 4039 Website: conferences.htm 114th American Academy of ORL, Head and Neck Surgery Annual Meeting and OTO EXPO September 26-29, 2010 Venue: Boston, USA Contact: Marketing Co-ordinator Fax No.: +1 703 519 1546 E-mail: Website: Courses on Middle Ear and Lateral Skull Base Surgery September 27 to October 1, 2010 Venue: Piecenza, Italy Contact: Secretary Gruppo Otologico Tel. No.: +39 0523 754362 Fax No.: +39 0523 453708 E-mail: Rhinology Update 22nd National Endoscopic Sinus Surgery Course (An Advanced Course) & 33rd All India Rhinoplasty Course (An Advanced Course)

November 11-15, 2010 Venue: New Delhi, India Contact: Dr VP Sood (Course Chairman) Ear, Nose and Throat Center, 212, Aditya Arcade 30, Community Center, Preet Vihar Vikas Marg, Delhi-110092 Tel. No. : 011- 22440011, 42420429 E-mail: Website:



Asian Journal of Ear, Nose & Throat, July-September 2010

Asian Journal of

Ear, Nose Throat

Information for Authors Manuscripts should be prepared in accordance with the ‘Uniform requirements for manuscripts submitted to biomedical journals’ compiled by the International Committee of Medical Journal Editors (Ann. Intern. Med. 1992;96: 766-767). Asian Journal of Ear, Nose and Throat strongly disapproves of the submission of the same articles simultaneously to different journals for consideration as well as duplicate publication and will decline to accept fresh manuscripts submitted by authors who have done so. The boxed checklist will help authors in preparing their manuscript according to our requirements. Improperly prepared manuscripts may be returned to the author without review. The checklist should accompany each manuscript. Authors may provide on the checklist, the names and addresses of experts from Asia and from other parts of the World who, in the authors’ opinion, are best qualified to review the paper. Covering letter –

– –

The covering letter should explain if there is any deviation from the standard IMRAD format (Introduction, Methods, Results and Discussion) and should outline the importance of the paper. Principal/Senior author must sign the covering letter indicating full responsibility for the paper submitted, preferably with signatures of all the authors. Articles must be accompanied by a declaration by all authors stating that the article has not been published in any other Journal/Book. Authors should mentioned complete designation and departments, etc. on the manuscript.

Manuscript Three complete sets of the manuscript should be – submitted and preferably with a CD; typed double spaced throughout (including references, tables and legends to figures). – The manuscript should be arranged as follow: Covering letter, Checklist, Title page, Abstract, Keywords (for indexing, if required), Introduction, Methods, Results, Discussion, References, Tables, Legends to Figures and Figures. – All pages should be numbered consecutively beginning with the title page. Note: Please keep a copy of your manuscript as we are not responsible for its loss in the mail. Manuscripts will not be returned to authors.

Asian Journal of Ear, Nose & Throat, July-September 2010

Title page Should contain the title, short title, names of all the authors (without degrees or diplomas), names and full location of the departments and institutions where the work was performed, name of the corresponding authors, acknowledgment of financial support and abbreviations used. – The title should be of no more than 80 characters and should represent the major theme of the manuscript. A subtitle can be added if necessary. – A short title of not more than 50 characters (including inter-word spaces) for use as a running head should be included. – The name, telephone and fax numbers, e-mail and postal addresses of the author to whom communications are to be sent should be typed in the lower right corner of the title page. – A list of abbreviations used in the paper should be included. In general, the use of abbreviations is discouraged unless they are essential for improving the readability of the text. Summary – The summary of not more than 200 words. It must convey the essential features of the paper. – It should not contain abbreviations, footnotes or references. Introduction – The introduction should state why the study was carried out and what were its specific aims/objectives. Methods – These should be described in sufficient detail to permit evaluation and duplication of the work by others. – Ethical guidelines followed by the investigations should be described. Statistics The following information should be given: – The statistical universe i.e., the population from which the sample for the study is selected. – Method of selecting the sample (cases, subjects, etc. from the statistical universe). – Method of allocating the subjects into different groups. – Statistical methods used for presentation and analysis of data i.e., in terms of mean and standard deviation values or percentages and statistical tests such as Student’s ‘t’ test, Chi-square test and analysis of variance or non-parametric tests and multivariate techniques. – Confidence intervals for the measurements should be provided wherever appropriate.


Review Article Results – These should be concise and include only the tables and figures necessary to enhance the understanding of the text. Discussion – This should consist of a review of the literature and relate the major findings of the article to other publications on the subject. The particular relevance of the results to healthcare in India should be stressed, e.g., practicality and cost. References These should conform to the Vancouver style. References should be numbered in the order in which they appear in the texts and these numbers should be inserted above the lines on each occasion the author is cited (Sinha12 confirmed other reports13,14...). References cited only in tables or in legends to figures should be numbered in the text of the particular table or illustration. Include among the references papers accepted but not yet published; designate the journal and add ‘in press’ (in parentheses). Information from manuscripts submitted but not yet accepted should be cited in the text as ‘unpublished observations’ (in parentheses). At the end of the article the full list of references should include the names of all authors if there are fewer than seven or if there are more, the first six followed by et al., the full title of the journal article or book chapters; the title of journals abbreviated according to the style of the Index Medicus and the first and final page numbers of the article or chapter. The authors should check that the references are accurate. If they are not this may result in the rejection of an otherwise adequate contribution. Examples of common forms of references are: Articles Paintal AS. Impulses in vagal afferent fibres from specific pulmonary deflation receptors. The response of those receptors to phenylguanide, potato S-hydroxytryptamine and their role in respiratory and cardiovascular reflexes. Q. J. Expt. Physiol. 1955;40:89-111. Books Stansfield AG. Lymph Node Biopsy Interpretation Churchill Livingstone, New York 1985. Articles in Books Strong MS. Recurrent respiratory papillomatosis. In: Scott Brown’s Otolaryngology. Paediatric Otolaryngology Evans JNG (Ed.), Butterworths, London 1987;6:466-470. Tables – These should be typed double spaced on separate sheets with the table number (in Roman Arabic numerals) and title above the table and explanatory notes below the table. Legends – These should be typed double spaces on a separate sheet and figure numbers (in Arabic numerals)


corresponding with the order in which the figures are presented in the text. – The legend must include enough information to permit interpretation of the figure without reference to the text. Figures – Two complete sets of glossy prints of high quality should be submitted. The labelling must be clear and neat. – All photomicrographs should indicate the magnification of the print. – Special features should be indicated by arrows or letters which contrast with the background. – The back of each illustration should bear the first author’s last name, figure number and an arrow indicating the top. This should be written lightly in pencil only. Please do not use a hard pencil, ball point or felt pen. – Color illustrations will be accepted if they make a contribution to the understanding of the article. – Do not use clips/staples on photographs and artwork. – Illustrations must be drawn neatly by an artist and photographs must be sent on glossy paper. No captions should be written directly on the photographs or illustration. Legends to all photographs and illustrations should be typed on a separate sheet of paper. All illustrations and figures must be referred to in the text and abbreviated as “Fig.”.

Please complete the following checklist and attach to the manuscript: 1. Classification (e.g. original article, review, selected summary, etc.)____________________________ 2. Total number of pages ______________________ 3. Number of tables __________________________ 4. Number of figures _________________________ 5. Special requests __________________________ 6. Suggestions for reviewers (name and postal address) Indian 1.___________ Foreign 1._ ___________ 2.___________ 2._ ___________ 3.___________ 3._ ___________ 4.___________ 4._ ___________ 7. All authors’ signatures______________________ 8. Corresponding author’s name, current postal and e-mail address and telephone and fax numbers _______________________________________

Issue Editor Dr VP Sood

Asian Journal of Ear, Nose and Throat

For Editorial Correspondence: Dr K.K. Aggarwal Group Editor-in-Chief

Asian Journal of Ear, Nose and Throat Daryacha, 39, Hauz Khas Village, New Delhi - 110 016. Tele/Fax: 26965874/75, 26865644 E-mail: Website:

Asian Journal of Ear, Nose & Throat, July-September 2010