ENT and Allergy Magazine Volume I, Issue VIII - ENT & Allergy ...

4 

W e l c o m e t o ENT & Al l e r g y As s o c i a t e s 

“Me d i c i n e f o r t h e 21s t Ce n t u r y ”...2012 Ed i t i o n 

In the pages that follow, we hope to once again provide you with clinically useful information that you 

can use in your practice now…and perhaps entertain you a little bit along the way. 

We recognize that as primary caregivers, your skill, training and insight are the keys to better 

outcomes for your patients. And we, at ENT and Allergy Associates LLP, are gratified that you have 

chosen to send so many of them to us for specialized care. You have our commitment that we will always 

strive to deliver the highest quality medical care to each and every one of those patients…with compassion, 

expertise and respect. 

e n t a n d a l l e r g y . c o m 

Wayne B. Eisman, M.D., F.A.C.S. 

In most cases, we are the same ENT and Allergy physicians that have practiced with you in the same 

neighborhoods for years. And as we have come together to realize the many benefits of sharing space, resources, expertise and 

collaborating clinically, we have also attracted to our Practice, from all over the nation, some of the finest young physicians 

coming out of residency programs today. These talented young men and women are bringing new ideas and the latest techniques 

into our environment. They make us at ENT and Allergy, and you-the bedrock physicians who daily care for our friends and 

neighbors-better as we all combine to offer a more robust level of clinical expertise to our mutual patients. 

We have sought to provide our physicians with state-of-the-art facilities and technology. We have created an integrated 

healthcare model with subspecialists in the communities and tertiary hospital interconnections that we believe represents a 

cutting edge model for superior healthcare delivery in the 21st century. This is good for you. This is good for us. And, most 

importantly, it is good for our patients. 

In our offices, as always, your patients will experience a warm, caring environment. In fact, at ENT and Allergy they are visiting 

a physician who lives in the community like you. A person who sends their kids to the same schools as you, and has the 

same personal stake in the well being of the community. This is our commitment to you, our fellow physicians. To move forward 

together to provide the best medical care for your patients in this rapidly changing healthcare environment. 

Please take the time to flip through the following pages. We hope that you will gain some useful clinical insight and maybe 

enjoy one of the lighter moments inside. 

As always, we would like to thank our many sponsors, whose participation has made it possible for us to provide you with 

this educational publication. 

And most importantly, we want to once again thank all of you, our valued colleagues, for your continued partnership as we strive 

to serve our mutual patients with the finest medical care possible. Please feel free to e-mail me at weisman@entandallergy.com 

with any comments, questions or suggestions you might have about the magazine or our services. 

Best, 

Wayne B. Eisman, M.D. 

President, ENT & Allergy Associates, LLP 

Medical 

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Windsor: 103 Executive Boulevard, 3rd 

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8 

HPV — Or a l Ca n c e r , An Em e r g i n g Pa r a d i g m Sh i f t 

Kevin Braat, M.D. 

Otolaryngology & Head and Neck Surgery 

ENT and Allergy Associates, LLP 


Cancer of the oral cavity 

and oropharynx accounts 

for approximately 85% of 

all head & neck cancers. 

This is a cancer group that arises in 

the mucosal surfaces of the upper 

aerodigestive tract and is almost 

exclusively squamous cell carcinoma. 

The overall incidence of this form of 

cancer has not changed in decades 

and recent statistics are about 37,000 

new cases annually. 

Historically, oral cancer has been 

associated with tobacco and alcohol 

exposure and poor oral hygiene. 

Men were 6 times more likely to have 

this type of cancer and blacks twice 

as likely as whites. There has always 

been a high incidence of local and 

regional recurrence with an overall 

5 year disease-free survival of only 

about 50%. 

Since the 1980’s, there has been about 

a 50% decline in the incidence of tobacco and alcohol related 

oral cancers, but the overall incidence of the disease has not 

declined due to the growing number of Human Papilloma Virus 

(HPV) related oral cancers. In fact, the incidence of HPV + oral 

cancer has risen by 270% in the past 20 years. The overall male 

to female ratio has dropped to 2:1 and females now out-number 

males in the less than 35 year age group. 

HPV is one of the most common virus groups in the world today 

with over 130 different types identified. These viruses can infect 

any cutaneous or mucosal surface. Most are harmless, producing 

no disease or harmless skin lesions. Transmission can be from 

solid surfaces such as a shower floor or gym mat, skin to skin, 

saliva or other body fluids. 

HPV is now considered a sexually transmitted disease (STD) 

and certain strains of this virus group are directly linked to 

causing cancer. This viral-cancer link was first established 

with cervical cancer and is now well established with oral 

and rectal cancers. The risk of infection increases with the 

number of lifetime sex partners and the risk of oral cancer is 

directly proportional with the number of oral sex partners. 

One to five oral sex partners doubles the risk of developing an 

HPV + oral cancer and there is a 5-fold increased risk with 6 or 

more partners. 

The strains of this virus family which are most commonly 

sexually transmitted includes HPV strains 6 and 11, which 

are the viruses responsible for condyloma (genital warts), and 

strains 16,18, 31 and 45 which are considered the most oncogenic 

strains and responsible for the majority of cervical, genital, rectal 

and oral cancers. 

Interestingly, contact with the virus does not mean that one will 

become infected and most people will clear the virus without 

infection. It appears that repeated exposure increases the risk 

of infection and once infected, the virus gets incorporated 

into the host DNA and human cells begin producing the virus. 

It is possible for an infected host’s immune system to clear the 

virus, but the how’s and why’s of this are not understood. It 

is believed the less than 1% of those who come into contact 

with an oncogenic strain of this virus and/or become infected 

will ultimately go on to form a cancer. It has been hypothesized 

that a genetic immune system defect may be responsible for 

certain individuals’ inability to clear the virus. There has been 

no link with age or any identified synergism with tobacco and/or 

alcohol and HPV + cancers. 

Cervical cancer was the second most common cause of cancer 

deaths in women in the 1950’s. Pap smear technology, which 

identifies women with an increased risk of developing cervical 

cancer, reduced this cancer type to the 7th most common

9 

There is a >90% 5 year survival with early stage diagnosis of oral 

cancer, but most are late stage diagnoses which reduces the 5 year 

survival to about 50%. 

cause of cancer death by the 1960’s. Subsequent identification 

of the human papilloma virus as the etiologic agent for cervical 

cancer was the ground breaker for subsequent investigation 

into the cancer-causing potential of this virus family. We 

now know that all cervical cancer is HPV+, with types 16 and 18 

being most common. 

HPV 16 is the most common virus identified in oral cancer. 

Primary lesions are small, hard to see and are usually 

asymptomatic. Most common locations are the tonsils, base of 

tongue, oropharynx and nasopharynx. Due to these difficultto-see 

locations and lack of symptoms, most patients present 

with stage IV disease. Studies have shown that patients 

presented with large malignant cervical lymph nodes can have 

very small (1-2 mm) primary lesions. In the past, these were 

considered “unknown primary” head & neck cancers, but with 

advanced imaging technology and heightened awareness of 

common HPV primary sites, the origin of the cancers are 

becoming less of a mystery. 

Oral cancer screening should be a part of every annual medical 

and dental examination. There is a >90% 5 year survival with 

early stage diagnosis of oral cancer, but most are late stage 

diagnoses which reduces the 5 year survival to about 50%. The 

history should be directed to elicit any warning signs such as 

a sore or lesion that does not heal within 2 weeks, lumps or 

thickening, white or red patches, persistent soreness or fullness 

in throat, pain or difficulty chewing or swallowing and chronic 

hoarseness. The most common abnormal physical finding will 

be a painless neck mass obviating the need for a careful and 

thorough soft tissue neck examination. 

Some ancillary tests have been marketed to medical and dental 

professions to facilitate the early detection of HPV and oral 

cancer. There are saliva tests to detect HPV, but the implications 

of a positive test in the absence of any visible lesion is not 

fully understood since statistically, >99% of people who come 

in contact with the virus will not go on to form any cancer 

and results may increase anxiety and additional unnecessary 

testing and healthcare expenses. There are colored light devices, 

or “scopes”, that are designed to detect abnormal mucosal 

changes, but these are not specific for cancer and have very 

high false positive and negative results, so these devices are 

not considered valuable screening tools by most oral cancer 

experts. Older methods of scraping the oral mucosal surface for 

cytologic evaluation, a technique which mimics the Pap smear, 

never proved as successful in the mouth due to the keratinizing 

nature of oral cancer and the inability of this technique to yield 

sections of the basement membrane necessary to make a cancer 

diagnosis. The new oral brush cytology techniques are proving 

to be much more effective and reliable since they do sample 

basement layer tissue where these cancers originate and is a 

technology which is growing in popularity and availability. 

Any persistent mucosal abnormality should be referred for 

surgical evaluation. A common abnormal finding is the benign 

oral papilloma, which is an HPV related disease. These lesions 

are excised and HPV screening is routinely done; they are rarely 

caused by one of the oncogenic strains of HPV. Recurrence 

after excision is uncommon, but monitoring is indicated for 

higher risk HPV strains. Suspicious lesions can be brush biopsied, 

which is a simple and painless office procedure and provides 

adequate information to determine if additional diagnostic 

procedures are indicated. 

Once an oral cancer diagnosis is made, a staging work-up is 

necessary and, if fortunate enough to have an early stage oral 

cancer, surgical excision is frequently possible. Radiation is 

considered for early stage disease only if clear surgical margins 

can not be obtained. As stated previously, the vast majority of 

these cancers are a late stage diagnosis and most treatment 

protocols employ both chemotherapy and radiation therapy, 

reserving surgery for treatment failures. 

e n t a n d a l l e r g y . c o m

10 

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Can this cancer be prevented HPV prevention through 

vaccination has been in the media forefront for the past few 

years. In 2006, the FDA approved Gardasil, a vaccine which 

protects against HPV strains 6, 11, 16 and 18. The initial 

approval was for females age 9-25 and the subsequent CDC 

recommendation was to immunize females up to age 26. In 

October 2011, the CDC updated their recommendation to 

include male vaccination, preferably before becoming sexually 

active. There have been subsequent studies showing reduced 

cervical cancer rates in women who are immunized up to 

45 years of age. The field of cancer vaccines has been energized 

by the clinical success and public acceptance of this technology 

which will undoubtedly lead to a lot more on this topic in the 

not too distant future. 

In summary, our generation is facing a relatively new malignant 

lesion which is sexually transmitted, has a predilection for 

a younger and more affluent patient population and carries 

a significant morbidity and mortality. That’s the bad news, 

but there may be a “silver lining” in all of this. Anti-smoking 

campaigns have been effective in reducing the incidence 

of all forms of smoking related cancer, especially cancers of 

the upper aerodigestive tract. Screening for many different 

types of cancers has reduced cancer deaths in properly selected 

patient populations. Although HPV + oral cancers are on 

the rise, specific risk factors have been identified and these 

cancers are significantly more responsive to therapy and 

have a longer disease-free survival compared to same stage 

HPV negative cancer, so with time and optimization of 

treatment protocols, outcomes are anticipated to improve. 

HPV is potentially curable, aggressive immunization programs 

and education has the potential to impact transmission. 

Heightened awareness in oral and primary care medical 

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12 

M e a t Al l e r g i e s — A No v e l Fo r m o f Fo o d Al l e r g y 

T r i g g e r e d By Ti c k Bi t e s 

Erin McGintee, M.D. 

Allergy, Asthma and Immunology 



Tick-borne illnesses are ever on the 

rise in endemic areas of Eastern 

Long Island. From Lyme disease 

to Rocky Mountain Spotted 

Fever, from erlichiosis to babesiosis, just 

about every resident of the Hamptons 

can share a story about an ailment they 

have experienced as the result of a tick 

bite. Well now there is another adverse 

reaction to tick bites that can be added to 

the list: meat allergy. 

In February 2009, researchers at the 

University of Virginia identified a novel 

allergy to mammalian meat. Patients with 

this allergy develop allergic reactions 

3-6 hours after ingestion of mammalian 

meat, such as beef, pork, or lamb. 

Poultry, fish, and shellfish do not trigger 

allergic reactions in these patients. The 

responsible allergen for this reaction 

has been identified as galactose-α-1,3- 

galactose (nicknamed α-gal), which is a 

blood group carbohydrate (sugar) present 

in all non-primate mammals. Patients 

with this allergy develop IgE antibody 

that recognizes and binds to the α-gal 

sugar, subsequently triggering an allergic 

reaction. This allergy differs from most other food allergies in 

several important ways. First, the allergy develops in response 

to a carbohydrate allergen, whereas in the vast majority of other 

food allergies, the causative allergen is a protein. Second, the 

reaction is delayed by 3-6 hours. Most IgE-mediated food 

allergies occur within minutes of food ingestion, and almost 

universally will occur within 2 hours. Third, patients who 

develop this allergy have previously been able to tolerate meat 

without issue, while most other food allergies present early in 

life. This unexpected finding raised a question for researchers: 

What is the inciting trigger for the development of this allergy 

As more and more patients were identified with α-gal allergy, 

it became clear that there was a regional distribution of cases, 

centralized in the Southeastern United States. Researchers 

looked at the possibility that a regional inhalant or fungal 

allergen could have been the inciting factor, but the results 

of these studies were negative. Similarly, they were unable 

to demonstrate an association between exposure to regional 

parasites and the development of the allergy. They did note 

that the distribution of α-gal cases was similar to the areas 

with high prevalence of tick-borne illnesses such as Rocky 

Mountain Spotted Fever and erlichiosis infections. Additionally, 

a number of patients reported that they seemed to develop 

the allergy after experiencing multiple tick bites. Subsequent 

research looking at the relationship between tick bites and 

development of α-gal allergy was able to demonstrate a strong 

correlation between a history of tick bites and level of IgE 

antibodies specific for α-gal. Additionally, researchers were 

able to show that patients with high levels of IgE antibodies to 

α-gal also had IgE antibodies that recognized proteins derived 

from the Lonestar Tick. Perhaps the most compelling evidence 

of all was the prospective study of three patients who did not 

have any measurable IgE antibody to α-gal, then gave a history 

of adult or larval tick bites, and subsequently had increases in 

α-gal IgE antibody in their blood that were 20-fold or more. 

Patients with α-gal allergy can present with symptoms ranging 

from generalized hives, swelling, and itching, to anaphylaxis, 

which is a multi-system allergic reaction that, in severe cases, 

can lead to death. Due to the fact that reactions to α-gal occur 

3-6 hours after meat ingestion, the classic patient with α-gal 

allergy gives a history of awakening in the middle of the

13 

Any patient with a history of possible tick exposure, who is 

now experiencing unexplained allergic reactions, should seek 

out consultation... 

night with severe itching, redness, and hives over their entire 

body. Patients with more severe episodes may also describe 

abdominal cramping, vomiting, diarrhea, wheezing, shortness of 

breath, or even loss of consciousness. 

The patients invariably give a history of ingesting mammalian 

meat several hours prior to the reaction. Reactions do not 

necessarily occur each time a patient ingests meat. Reactions 

are more likely to occur when a large quantity of meat is 

consumed. Meats that are higher in fat are more likely to 

trigger a reaction than leaner cuts. Dairy products do contain 

a small amount of α-gal, and patients with this allergy will often 

demonstrate IgE antibody for milk, but this is rarely of any 

clinical significance. Gelatin, which is usually derived from 

beef or pork, does contain α-gal, and there have been cases of 

patients experiencing clinical symptoms after gelatin ingestion. 

It is not yet known what predisposes some patients to develop 

this allergy. The Lonestar Tick is an aggressive species, and 

in indigenous areas, tick and chigger bites are a frequent 

occurrence. It is clear that α-gal allergy is more likely to develop 

in patients who have sustained multiple bites. In my experience, 

α-gal allergy is more commonly seen in patients with jobs 

or hobbies that increase their risk of tick exposure. Patients 

with the allergy often spend time hiking or mountain biking, 

hunting, landscaping, or gardening. 

Additionally, patients who develop the allergy tend to experience 

local reactions to tick or chigger bites that persist for weeks or 

even longer. Due to the fact that α-gal is a mammalian blood 

group carbohydrate, there is some suspicion that certain blood 

types predispose a patient to develop the allergy, but thus far 

this research has not shown any correlation between a specific 

blood type and development of the allergy. In my own case 

series, I have identified two sets of first cousins with the allergy, 

and a father and daughter who both have allergy to α-gal. This 

suggests that there could be some sort of genetic predisposition 

for development of the allergy. 

Due to the fact that there is a 3-6 hour delay in the onset of 

symptoms, as well as the fact that meat has historically never 

been considered a common allergen, patients often do not 

make the connection between meat ingestion and development 

of symptoms. Similarly, due to the regional distribution of the 

Lonestar Tick, physicians who are not familiar with this allergy 

may not consider this diagnosis in patients presenting with acute 

attacks of hives or anaphylaxis. 

Prick skin testing, the test of choice for diagnosing most IgEmediated 

food allergies, is of little use in identifying patients 

with allergy to α-gal. If the diagnosis is suspected, there are 

both commercial and research labs that are capable of testing a 

blood specimen for α-gal-specific IgE. Patients will also typically 

have measurable IgE antibodies to mammalian meats, cat, dog, 

and milk. As with most food allergy tests, false positive tests 

for α-gal allergy do occasionally occur. A positive test is more 

likely to correlate with true allergy to α-gal if the amount of IgE 

that is specific for α-gal makes up 30% or more of the patient’s 

total serum IgE. 

Most of the α-gal cases reported in the medical literature came 

from southeastern states, with the majority of cases occurring 

in Virginia, Arkansas, Tennessee, North Carolina, Missouri, and 

Oklahoma. However, the Lonestar Tick has become ubiquitous 

on the east end of Long Island, and so it serves to follow that 

cases of α-gal allergy are on the rise. To date, I have identified 27 

patients with this food allergy. 

As I have previously discussed, allergy to α-gal tends to be 

prevalent only in areas that are heavily populated by the Lonestar 

Tick. However, the Hamptons are unique in that, while they 

are clearly becoming a hotspot for α-gal allergy, they are also 

a hotspot for tourists and visitors from all over the New York 

Tri-State area. For this reason, I would expect to see an increase 

in the incidence of α-gal allergy throughout the entire region 

served by our offices. Any patient with a history of possible tick 

exposure, who is now experiencing unexplained allergic reactions, 

should seek out consultation with one of our experienced 

allergists at ENT and Allergy Associates. 

References: 

Commins SP, Satinover SM, Hosen J, et al. Delayed anaphylaxis, 

angioedema, or urticaria after consumption of red meat in 

patients with IgE antibodies specific for galactose-α-1,3- 

galactose. J Allergy Clin Immunol. 2009;123:426–33. 

Commins SP, James HR, Kelly LA, et al. The relevance of tick 

bites to the production of IgE antibodies to the mammalian 

oligosaccharide galactose-α-1,3-galactose. J Allergy Clin Immunol. 

2011; 127(5): 1286-93. 


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ENT & ALLERGY Ph y s i c i a n Pr o f i l e s 

15 

Stephen Abrams, M.D., F.A.C.S. 


Wayne 

Patrick M. Ambrosio, D.O. 


Woodbridge and Old Bridge 

Ricardo Arayata, M.D., F.A.C.A.A.I. 


New Rochelle and Purchase 

Anna Aronzon, M.D. 


Wall Street 

Jonathan Aviv, M.D., F.A.C.S. 


East Side and Sleepy Hollow 

Andrew Azer, M.D.* 


Old Bridge and Woodbridge 

Carol G. Baum, M.D., 

M.B.A., F.A.C.P., F.A.A.A.A.I. 


Bronx and West Side 

Paul A. Bell, M.D. 


Garden City 

Robin M. Brody, M.D. 


Englewood and Hackensack 

Michael Bergstein, M.D., F.A.C.S. 


Yorktown and Sleepy Hollow 

Dennis Burachinsky, D.O.* 


Somerville 

Andrew L. Blank, M.D., F.A.C.S. 


Bayside 

Mark E. Carney, M.D. 



Bradley Block, M.D. 


Garden City 

John Cece, M.D., F.A.C.S. 


Wayne 

Ryan Borress, M.D. 


Poughkeepsie 

Dorothy Chau, M.D. 



I. David Bough, Jr, M.D., F.A.C.S. 


Oradell and West Nyack 

Won-Taek Choe, M.D. 


East Side and Englewood 

Kevin Braat, M.D. 


East Hampton, Riverhead and 

Southampton 

Farhad Chowdhury, D.O. 




Shawn C. Ciecko, M.D. 



Jason P. Cohen, M.D. 


Fishkill and Poughkeepsie 

Tahl Colen, M.D. 


Bay Ridge, Fifth Avenue and 

Somerville 

John County, M.D., F.A.A.A.A.I. 


Yorktown and Sleepy Hollow 

Jeffrey N. Cousin, M.D. 


Yonkers and Tuckahoe 

Robert Cusumano, M.D., F.A.C.S. 


Oradell 

Michael A. D’Anton, M.D. 


Wayne 

Paul Davey, M.D. 



Southampton 

Richard DeMaio, M.D. 


Fishkill and Newburgh 

Jay N. Dolitsky, M.D., F.A.A.P. 


Fifth Avenue and Garden City 

Lee D. Eisenberg, M.D., F.A.C.S. 



Wayne Eisman, M.D., F.A.C.S. 


White Plains 

Moshe Ephrat, M.D., F.A.C.S. 


Lake Success 

Gary S. Fishman, M.D., F.A.C.S. 


Carmel 

* Indicates New Doctors to the Practice

16 


Mark L. Fox, M.D., F.A.C.S. 


Tuckahoe 

Debora Geller, M.D. 



Aylon Y. Glaser, M.D. 


Hoboken 

Harrison J. Glassman, M.D., F.A.C.S. 


Bronx 

David A. Godin, M.D., F.A.C.S. 


Fifth Avenue 

Daniel R. Gold, M.D. 


White Plains 

Steven M. Gold, M.D. 


Englewood 


John J. Huang, M.D., F.A.C.S. 



Jennifer Lee, M.D. 


Bay Ridge 

Michael Hugh, M.D. 


Carmel, Poughkeepsie and 

Yorktown 

Jonathan A. Lesserson, M.D. 


Hackensack and Oradell 

Jeffrey H. Jablon, M.D., F.A.C.S. 


Purchase and New Rochelle 

Douglas Leventhal, M.D.* 


Oradell 

Cynthia Jerome, M.D., 

F.A.A.A.A.I., F.A.C.A.A.I. 


White Plains 

Marc J. Levine, M.D., F.A.C.S. 


West Nyack 

Nagalingam Jeyalingam, M.D. 


Newburgh 

Guy Lin, M.D. 


East Side 

Steven B. Kase, M.D. 


White Plains 

Pei Lin, M.D.* 


Woodbridge 

Matthew J. Kates, M.D., F.A.C.S. 


New Rochelle 

Peter LoGalbo, M.D., 

F.A.C.C.P., F.A.A.A.A.I. 



Scott R. Messenger, M.D., F.A.C.S. 


Yorktown 

Ron Mitzner, M.D. 


Lake Success 

Dan Moskowitz, M.D., F.A.C.S. 

Eric Munzer, D.O. 

Otolaryngology & Head and Neck Surgery Otolaryngology & Head and Neck Surgery 

White Plains 


Krzysztof Nowak, M.D. 


Yonkers and Tuckahoe 

Sheldon Palgon, M.D. 


Wall Street, Bay Ridge 

and Park Slope 

Smruti Parikh, M.D. 


Parsippany and Somerville 

Debra S. Reich, M.D. 


Yorktown 

Edward Rhee, M.D., F.A.C.S. 


West Nyack 

Hector P. Rodriguez, M.D., F.A.C.S.* 


West Side 

Eric Roffman, M.D. 


West Nyack and Oradell 

Richard A. Rosenberg, M.D., F.A.C.S. 


White Plains 

Hyman Ryback, M.D. 

F.R.C.S., F.A.C.S. 


White Plains 

Steven H. Sacks, M.D, F.A.C.S. 


East Side 


17 

Steven I. Goldstein, M.D., F.A.C.S. Michael A. Gordon, M.D., F.A.C.S. 


Bronx and Tuckahoe 

Garden City 

Lynelle C. Granady, M.D. 


East Side 

Robert P. Green, M.D., F.A.C.S. 


East Side 

Daniel Grinberg, M.D., F.A.C.S. 


West Nyack 

Ramez Habib, M.D., F.A.C.S. 


Bay Ridge West and Park Slope 

Adrianna M. Hekiert, M.D. 


Somerville 

Natasha Keenan, M.D. 


West Side 

Robert J. Marchlewski, M.D., 

F.A.A.P., F.A.C.A.A.I. 


Garden City 

Paul E. Kelly, M.D. 



Southampton 

Scott B. Markowitz, M.D. 


East Side 

Mitchell T. Kolker, M.D. 


Newburgh and Fishkill 

Stephen Mattel, M.D., F.A.C.S. 


Wayne 

Kenneth N. Kunzman, M.D. 


Somerville 

Erin McGintee, M.D. 



Southampton 

David B. Lawrence, M.D., F.A.C.S. 


Purchase 

Vishvesh Mehta, M.D. 



Amy D. Lazar, M.D. 


Somerville 

Michael G. Mendelsohn, M.D., 

F.A.C.S., F.A.A.P. 


Garden City 

Brian L. Lebovitz, M.D., F.A.C.S. 


Parsippany 

Art Menken, M.D.* 


Poughkeepsie 


John T. Parrinello, M.D., 

F.A.A.A.A.I., F.A.C.A.A.I. 


Newburgh 

Rami Payman, M.D. 

George Pazos, M.D. 


Poughkeepsie 

Carmel and Yorktown 

Prashant Ponda, M.D. 


Newburgh and Fishkill 

Joel Portnoy, M.D.* 


Lake Success and Riverhead 

Maria T. Quilop, M.D. 


Bronx 

Jay Rechtweg, M.D.* 


Garden City 

John Sadowski, M.D. 


West Nyack 

Brian Safier, M.D. 


Bayside and Lake Success 

Zarina Sayeed, M.D. 


Parsippany 

Eric Scarbrough, M.D. 


Riverhead 

B. Todd Schaeffer, M.D., F.A.C.S. 


Lake Success 

John J. Scheibelhoffer, M.D., F.A.C.S. 


Wayne 

Daniel A. Scher, M.D. 


Wayne 


18 


Charles M. Schultz, M.D. 


Parsippany 

Frank G. Shechtman, M.D., F.A.C.S. 


White Plains 

Michael Shohet, M.D., F.A.C.S. Abraham I. Sinnreich, M.D., F.A.C.S. 


West Side 


Justin M. Skripak, M.D. 


Hoboken and Oradell 

Jonathan C. Smith, M.D., F.A.C.S. 


Bronx 

Theresa Sohn, M.D. 


Wayne 


Christopher Song, M.D., F.A.C.S. 



Milo Vassallo, M.D., Ph.D. 



Derek Soohoo, M.D., F.A.C.S. 


New Rochelle and Yonkers 

Tamekia Wakefield, M.D. 


Bayside 

Gangadhar Sreepada, M.D. 


Wayne 

Jared M. Wasserman, M.D. 



Gerald D. Suh, M.D. 


Bayside and Yonkers 

Karen Wirtshafter, M.D., F.A.C.S. 


Parsippany 

Jason Surow, M.D., F.A.C.S. 


Oradell 

Stanley Yankelowitz, M.D., F.R.C.S. 


Bronx 

Raj Tandon, M.D. 


Hoboken 

Francisca Yao, M.D. 



Michael B. Tom, M.D., F.A.C.S. 


Yonkers 

Hale Yarmohammadi, M.D., MPH 


Fifth Avenue and Wall Street 

Irene Yu, M.D. 


New Rochelle and Purchase 

Richard T. Yung, M.D., F.A.C.S. Jill F. Zeitlin, M.D. 


White Plains 

Sleepy Hollow 

Warren H. Zelman, M.D., 

F.A.C.S., F.A.A.P. 


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ENT & ALLERGY Au d i o l o g i s t s Pr o f i l e s 

Phyllis Schaffer-Cohen, Au.D. 

Director of Audiology 

Renee E. Angelo, Au.D. 

Yorktown 

Sara Beckerman, Au.D. 

Fifth Avenue 

Susan Bloom, M.S. 

West Nyack 

Karen Bromberg, Au.D. 

Wall Street and Bay Ridge 

Diane Butfilowski, M.S. 

West Nyack 

Carmelina Cerrone, M.A. 

Fishkill 


Jenna Elias, Au.D. 

Lake Success and Fifth Avenue 

Kelle Harrison, M.S. 

Poughkeepsie 

Laura McElhennon, M.A. 

West Nyack 

Kimberly Emanuele, Au.D. 

Poughkeepsie 

Marian Henniges, Au.D. 

New Rochelle 

Brian McGovern, Sc.D. 

Wayne 

Emily Esca, Au.D. 

Bronx 

Julia Jantas, Au.D. 

Hoboken and Old Bridge 

Mala Rushabh Mehta, M.A. 

Hoboken and Wayne 

Theresa Faughnan, M.A. 

Tuckahoe 

Kelly Kamp, Au.D. 

Fifth Avenue 

Aisling Meier, Au.D. 

Yonkers 

Arielle Feiman, Au.D. 

Carmel and West Nyack 

Michael Kaufer, Au.D. 

Bayside 

Maggie Miller, Au.D. 

Newburgh and Poughkeepsie 

Nicole Ferguson, Au.D. 

Bay Ridge West 

Michelle Kraskin, Au.D. 

Bayside 

Elizabeth Nemec, Au.D. 

Englewood 

April Ferise, Au.D. 

Parsippany 

Bonnie Kupchik, M.A. 

Bronx 

Kerri O’Connor, Au.D. 

Garden City 

Robert Rosengarten, M.S. 

Old Bridge 

Nicole Rubin, M.A. 

Garden City 

Ilene Shapiro, M.A. 

White Plains 

Soyfa Shlafman, Au.D. 

Park Slope and Bay Ridge 

Katelyn Stoehr, Au.D. 

Riverhead 

Barbara Rooney Tartaglia, Au.D. 

Yonkers 

Marisa Thylstrup, Au.D. 

Tuckahoe, White Plains and 

Yorktown 

CariAnne Degennaro-Zimny, M.A. 

White Plains 

Tammy Zirke, Au.D. 

Parsippany 

Phyllis H. Zlotnick, M.A. 

Hackensack and Wayne

21 

Jessica Comparetto, M.A. 

Sleep Hollow and White Plains 

Maureen Connington, Ph.D. 

West Side 

Beata Contri, Au.D. 


Vincent D’Auria, Au.D. 

Yorktown 

Nicole Deweese, Au.D. 

Woodbridge and Somerville 

Francesca DiNatale-Lepsis, Au.D. 

Garden City 

Dorothy Ditoro, Au.D. 

Bronx 

Renee Freund, M.A. 

Oradell 

Dana Leggieri, Au.D. 

Wayne 

Mary O’Sullivan, M.A. 

Yonkers 

Harriet Friedman-Wilson, Au.D. 


Linda Liebowitz, M.S. 

Hackensack 

Lorianne K. Owen, M.A. 

Somerville 

James Gahn, M.A. 


Jennifer Lohr-Seitz, M.S. 

Riverhead and Southampton 

Rochelle Levine Port, M.A. 

Carmel 

Anna Gershteyn, Au.D 

Lake Success 

Anthony Macera, M.A. 

White Plains 

Barbara M. Posen, M.S. 

White Plains 

Kaley Gray, Au.D. 

Englewood and Oradell 

Margaret Hartner Mass, Au.D. 

Newburgh 

Patricia Reciniello, M.A. 

Garden City 

Gregg A. Goldhagen, M.S. 

East Side 

Patricia Mazzullo, Au.D. 

Bay Ridge and Bay Ridge West 

Angela M. Riemma, Au.D. 

Purchase and Yorktown 

Catherine Hadeshian, M.A. 

Purchase and Bronx 

Laura McCrone, Au.D. 

Oradell 

Alison Rooney, Au.D. 

East Side 


Evmorfia Tzanis, M.A. 

Sleepy Hollow 

Emily Ward, Au.D. 

East Hampton, Southampton, 

Riverhead 

Sue A. Weinstein, M.S. 

White Plains 

Carol Wesemann, Au.D. 

Lake Success 

Richard Winter, Au.D. 

Bronx 

Yevgenia Yubliler, Au.D. 

Englewood and Oradell 

Lisa Zeitoun, Au.D. 

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W h a t We Ca n Le a r n f r o m Li s t e n i n g t o Ou r Pa t i e n t s 

23 

Jared Wasserman, M.D. 



The human larynx can become subject to a 

wide variety of pathologies. Many of these 

disorders may result in a change to vocal 

function that can be readily appreciated. 

Consequently, to the trained ear, most laryngeal 

diagnoses can be made simply by listening. This is 

especially true of neurological disorders affecting 

the voice. The difficulty lies in the fact that these 

disorders are not well understood and therefore, not 

known about in the general population. Spasmodic 

Dysphonia (SD) is one of the more common 

neurological voice disorders treated by ENT voice 

specialists, laryngologists. It is a fairly stubborn problem. 

Because the cause is unknown, management is 

based on the philosophy of treatment with temporary 

relief of the symptoms. 

SD was first described in 1871, as a form of nervous 

hoarseness. However, we know today that it is a form 

of chronic dysphonia characterized by inappropriate 

laryngeal muscle contractions. It is, in fact, a focal, 

task specific dystonia, limited to the muscles of the 

larynx. There are two major forms of the disorder. 

Adductor Spasmodic Dysphonia, which accounts for 

nearly 85% of all cases. It is characterized by excessive 

glottal closure during speaking in an irregular, strained, 

tremulous pattern. Patients will sometimes complain 

that they feel strangled and cannot “get the words 

out.” The less common form, Abductor Spasmodic 

Dysphonia, is associated with irregular spasms of 

breathy voice breaks. 


SD has generally been considered a rare disorder, but 

more than likely many cases have gone undiagnosed, 

simply because it may be mistaken for other common 

forms of hoarseness, like essential vocal tremor. It 

commonly affects females more than males and 

typically initially presents in the 3rd to 4th decade of 

life. It can be linked to an emotionally stressful event; however 

the trigger is frequently unknown. No genetic link has been 

clearly established, yet there appears to be an association with a 

family history of dystonias. 

Spasmodic Dysphonia is a type of focal dystonia; an abnormal 

activity of only one muscle group, the vocal cords in this case. 

Despite there being no other significant neurological symptoms, 

the cause of SD is thought to be found centrally in the brain 

and not peripherally in the vocal cord muscles or the nerves 

innervating them. In the Adductor type of SD, patients present 

with speech that is characterized by a strangulated quality. 

The strained voice is noted with an irregular pattern of voice 

breaks. Symptoms are typically worse during stressful events 

and often improve with drinking alcohol or singing. During 

laryngoscopy and examination of the vocal cords, the quick 

spasms and squeezing closed of the vocal cords are typically 

seen. The less common form, Abductor SD is characterized 

with voice breaks and spasms of breathiness. Laryngoscopy may 

show the vocal cords with quick movements of opening. 

The diagnosis of Spasmodic Dysphonia relies heavily on 

listening to the patient. Because so much is unknown regarding

24 


this ailment, there are no laboratory studies to confirm its 

diagnosis. Radiographic studies are used only to evaluate other 

causes of dystonia not indicative of Spasmodic Dysphonia. On 

physical examination, it is important to rule out other dystonias, 

tremors, or neurological signs. However, perceptual analysis 

of the voice is generally considered the most specific method 

of diagnosis. Because SD is a task specific dystonia, certain 

sentences have been found helpful in eliciting the specific voice 

breaks. These include: 

“We mow our lawn all year.” 

“The dog dug a new bone.” 

“How high is Harry’s hat” 

Other evaluations include aerodynamic and acoustic measurements 

performed by a Speech Language Pathologist. 

Although not diagnostic, some of the findings such as airflow 

and subglottic pressure are characteristic of each subtype of SD. 

The accepted treatment for Spasmodic Dysphonia today is 

Botulinum toxin therapy (Botox). Because there is no cure for 

Spasmodic Dysphonia, Botox injections into the vocal cord offer 

an excellent treatment option. The therapy involves injecting 

small doses of the toxin into the vocal cord muscles causing a 

chemical denervation by blocking the release of acetylcholine 

at the neuromuscular junction. The procedure is performed in 

the office under EMG guidance to confirm accurate placement 

of the toxin into the desired muscle. Most patients will see 

the desired effect of the treatment begin at 48 - 72 hours after 

the injection, with the therapeutic benefit lasting on average, 

3 months. For the Adductor type of SD, the thyroarytenoid 

muscles are injected bilaterally. In essence, the vocal cords are 

partially and temporarily “paralyzed” in the open position. 

This may yield a breathy voice for up to 1-2 weeks, with the 

voice ultimately smoothing out. As the Botox effect wears off, 

the typical SD symptoms will return. Patients are advised to be 

careful with swallowing, especially when breathy, to decrease the 

chance of aspiration. 

Spasmodic Dysphonia is a cryptic neurologic voice disorder. 

It is uncommon, but not as rare as once thought. More than 

likely, nearly any physician can diagnose this, once their trained 

ear knows what to listen for. Unfortunately, there is no cure 

for this SD. However, EMG guided Botox injections provide 

an excellent source of symptom relief which is temporary, but 

comfortably repeatable. 

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27 

E u s t a c h i a n Tu b e Dy s f u n c t i o n 

Richard A. Rosenberg, M.D. F.A.C.S. 



Eustachian tube dysfunction is a relatively common 

problem. Tympanostomy remains the gold standard for 

the treatment of chronic Eustachian Tube dysfunction. 

The American Academy of Pediatrics, the American 

Academy of Family Physicians and the American Academy of 

Otolaryngology-Head and Neck Surgery all state that in children 

with OME who are candidates for surgery, tympanostomy 

tube placement is the preferred initial choice. Approximately 

1 million children have tympanostomy tubes placed per 

year in North America. 7% of children in the United States 

have tympanostomy tubes by age 3. Many of these children 

will go on to require multiple tubes and have chronic middle 

ear abnormalities. 

Recently, Eustachian Tube Tuboplasty has been developed and 

used in a limited basis on patients with ET dysfunction who 

have had multiple tympanostomies with minimal benefit. Both 

microdebridement and laser techniques have been used. The 

results have been promising. In a surgical trial (Otol Neurotol 

2004;25:1-8) Dr. Dennis Poe evaluated the effect of laser 

tuboplasty on 56 patients (108 eustachian tubes). The patients 

had laser vaporization of mucosa and cartilage from the luminal 

posterior wall along with a laser myringotomy. About 65% of 

ears had normal middle ear pressures after 3 years. There were 

no intraoperative complications. 8% had peritubal synechia. 

A promising new, and technically simpler approach is now 

being developed. This is balloon dilation of the Eustachian tube. 

Balloon dilation of an occluded lumin is not a new medical 

technique. It has been used in multiple fields including: urology, 

gastroenterology, neurology, vascular medicine and cardiology. 

Since 2005, it has been used for the dilation of sinus ostia with 

excellent results and few complications. 

An approximately 10mm segment in the cartilaginous eustachian 

tube is closed at rest (the valve area). This valve opens by 

the actions of the levator veli palatini and tensor veli palatini 

muscles. Tubal dysfunction is most commonly due to inflammatory 

processes occurring within this area. This is the area of 

concern with balloon dilation. 

The procedure is carried out transnasally under general anesthesia. 

A catheter is inserted into the affected eustachian tube and a 

balloon is inflated for 2 minutes at 10 atmospheres of pressure. 

There is no osteal fracturing. Dilation causes submucosal and 

cartilage tears. The tears cause changes to the structure of the 

eustachian tube which lead to permanent dilation. 

Drs. Edward McCoul and Vijay Anand (International Forum 

of Allergy and Rhinology, Vol 00, No. 0 2011) performed 

balloon dilation on 22 patients (35 dilations). Strict criteria 

were set. All patients had failed to improve on 2 months of 

medical therapy. All were adults (18 years and older), had an 

abnormal tympanogram and abnormal otoscopic exam, and the 

presence of unilateral or bilateral symptoms of eustachian tube 

dysfunction. Significant improvement was seen in tympanometry 

and otoscopy at 3 weeks, 6 weeks, 12 weeks and 6 months. They 

concluded that balloon eustachian tube dilation was an effective 

surgical intervention for the treatment of eustachian tube 

dysfunction in adults. They found advantages of the technique 

to include: ease of use, employment of existing endoscopic 

instrumentation, and compatibility with endonasal procedures. 

Balloon dilation of the eustachian tube appears to be a 

promising alternative therapy for those patients who have 

failed both medical treatment and have had unsuccessful 

use of tympanotomy tubes. It provides the practicing otolaryngologist 

a new and safe method of treating a difficult and often 

frustrating problem. 


28 

A s p i r i n Ex a c e r b a t e d Re s p i r a t o r y Di s e a s e – 

N o t Al l As t h m a i s t h e Sa m e 

Krzysztof Nowak, M.D. 

Allergy, Asthma, and Immunology 



In the past, aspirin exacerbated respiratory disease 

(AERD), more commonly known as the aspirin triad 

or Samter’s triad after the researcher who formally 

described that syndrome first in 1968. The syndrome 

consists of 3 features: asthma, chronic rhinosinusitis with 

nasal polyps, loss of sense of smell and severe reactions to 

aspirin and other cyclooxygenase-1 (COX-1) inhibiting 

non-steroidal anti-inflammatory drugs (NSAIDs). The 

affected people who ingest these drugs develop symptoms 

within 30 minutes to 3 hours. They typically start having 

worsening nasal congestion followed by bronchospasm 

that may last for many hours and is difficult to 

treat – such patients may require sometimes 2 or 3 days 

of hospitalization. 

The interesting feature of AERD is that reactions to 

NSAIDs are not allergic in nature at all – they are not 

immunologically mediated. The condition is caused by 

complex metabolic derangements of the arachidonic 

acid metabolism, which result in overproduction of 

leukotrienes. In spite of decades of research, some elements 

of the pathophysiology of AERD are still not completely 

understood. It is assumed that the 5-lipoxygenase pathway 

of the arachidonic acid metabolism is not sufficiently 

inhibited by prostaglandin PGE2, whose levels are 

decreased in patients with AERD. NSAIDs - which block 

production of PGE2 – further acutely exacerbate this 

metabolic abnormality, leading to severe respiratory 

symptoms. As a result of chronic over-production of 

leukotrienes and some other pro-inflammatory agents, 

chronic and uncontrolled airway inflammation ensues, 

which leads to development of severe rhinosinusitis with 

nasal polyps and often intractable asthma. It is also crucial 

to note that after ingestion of COX-1 inhibitors (NSAIDs), a 

refractory period develops for a few days when patients do 

not respond to any additional doses of these medications. This 

phenomenon is used for treatment. 

AERD typically begins in the third decade of life with 

persistent rhinitis, followed by asthma, aspirin sensitivity, and 

development of nasal polyps. In women, the age of onset is 

usually earlier than in men and the disease tends to be more 

severe. The condition affects less than 5 percent of the general 

asthmatic population, but among glucocorticoid-dependent 

asthmatics and asthmatics with chronic rhinosinusitis and 

nasal polyps, NSAID sensitivity may affect up to 20 to 40 

percent. Unfortunately, an AERD diagnosis is often missed 

and some patients even go misdiagnosed for many years. 

The most recent patient with AERD in this author’s practice is 

a 34 year old woman who developed her symptoms in her late 

teens. For the past decade, she has been hospitalized multiple 

times, and has had countless ER visits and has been taking 

high-dose steroids resulting in mild Cushingoid symptoms. 

Her case might be considered typical. Most likely focus 

solely on only asthma or rhinitis symptoms and failure to 

recognize NSAIDs sensitivity is the cause of the much delayed 

proper diagnosis. 

Treatment of AERD involves asthma management according 

to the published guidelines. Many patients require chronic use 

of oral corticosteroids. Leukotriene inhibitors, such as zileuton 

(5-LO inhibitor), and leukotriene receptor antagonists, such as 

montelukast, are strongly recommended. Nasal polyps require 

nasal endoscopic surgery and have a high rate of recurrence. 

Following sinus surgery, treatment with topical corticosteroids 

is very important.

29 

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30 

S k i n Ca n c e r Re c o n s t r u c t i o n – 

W e Ha v e Co m e a Lo n g Wa y ! 

Paul Kelly, M.D. 




Introduction 

Skin cancer, while not a reportable 

disease, is estimated to affect 3.5 

million people this year alone. While 

the non-melanoma cancer (basal cell 

and squamous cell) makes up the greatest 

majority of this number, the melanoma 

tumors account for the most deaths 

from skin malignancy. The largest organ 

in the body is the skin cover and with 

life expectancy increasing to the mid to 

late 70s, the likelihood of a cutaneous 

malignancy is high. Our diagnostic ability 

and our push towards education of the 

public sector has perhaps heightened 

the incidence, but it will clearly show 

to decrease mortality. At ENTA and 

within the division of Advanced Facial 

Plastic Surgery, our diagnostic and 

reconstructive abilities have also evolved 

and can identify patients at risk and 

post reconstruction can return these 

patients to a very acceptable and similar 

façade as pre-skin cancer. Many who 

find themselves with a skin blemish that 

may be a malignancy will subconsciously 

delay treatment for fear of the potential 

skin removal defect and ultimately the 

cosmetic outcome. The good news is 

that we now have such good new 

diagnostic acumen and reconstructive 

options that patient education can now 

focus on treatment and ultimately a return 

of our patients to their normal lives. 

Diagnosis 

The diagnosis of non-melanoma skin 

cancer is relatively clear, with our ability 

to recognize the early melanoma 

both clinically and histologically (under 

the microscope) gaining by leaps 

and bounds. 

The basal cell carcinoma is the most 

common skin malignancy without 

metastatic potential. Its pathology, or 

problem, comes from its ability to destroy 

tissue in the area of origination. The 

typical basal cell presents as a flat but 

occasionally heaped edged lesion which 

frequently in the early phases comes and 

goes. The lesion will flake or exfoliate 

much like normal skin, but it will do so at 

an accelerated rate leading to the typical 

dry flakey and frequent red patch. The 

lesion will eventually stay present and 

will become inflamed and irritated. This 

lesion may bleed easily when abraded 

even gently. Key for diagnosis is the 

fluctuating nature and the persistent spot’s 

redness. Fig 1 

Fig 1 

The squamous cell carcinoma is the 

second most common non-melanoma 

malignancy with the ability to metastasize 

to other areas and to lymph nodes. This 

tumor or skin cancer growth is much 

more aggressive in its ability to destroy 

the surrounding tissue and its ability to 

spread to distant sites – such as from the 

lip to the lymph nodes of the neck. The 

squamous cell has a tendency to be more 

of a raised lesion with bleeding more 

common. Like the basal cell, it is not a 

painful process until the inflammation 

out runs the lesion. This skin cancer is 

more common on the lower parts of 

the face – such as the lower lip and ears 

and on the scalp. The Key is to look for 

the red irritated site that fails to resolve 

on its own and is marked by occasional 

bleeding. Fig 2 

The melanoma is the most deadly form 

of skin cancer, responsible for about 

7,000 deaths a year. This lesion is more 

notable for this reason and for the 

primary characteristic of dark coloring. 

Fig 2 

The melanoma can spread to distant 

sites and does so readily and quickly. 

This lesion will show irregular borders, 

a combination of dark and light brown 

colors and then, of course, bleeding. The 

research in melanoma is continuing to 

provide amazing new treatment options. 

A most recent project shows promise for 

the use of immunotherapy and radiation 

– even distant metastsis in this limited 

case study showed resolution with 

immune system manipulation and the 

use of radiation to the primary melanoma 

site. Fig 3 

Fig 3 

Treatment 

Skin cancer treatment begins with 

prevention and much effort is spent by 

primary doctors and doctors who treat 

or reconstruct skin cancer and skin 

cancer defects in educating patients 

on “Safe Sun”. Advice offered from the 

most appropriate sun screens – ones with 

more physical blocks and containing agents

31 

Fig 4 

Fig 5 

Skin lesion – Squamous Cell Carcinoma 

Pre-effudex 

like Titanium Dioxide and Zinc Oxide – 

to protective clothing, and suggestions for 

“sun breaks” during the most damaging 

sun shine hours. Should the damage be 

done and the skin rebel with the formation 

of skin lesions, then prompt diagnosis 

and either topical treatment initiated, in 

example for treatment, of superficial basal 

cell carcinoma or surgical resection via 

MOH’s surgery are best. 

Topical preparations for superficial 

basal cell cancers or pre-cancerous 

skin lesions include 5-FU (flurouracil) 

and Imiquimod. The former is 

a chemotherapeutic agent which, when 

used topically, can stop cancer cells in this 

manner. The latter makes use of the new 

research in the use of immunmodlators 

and their effects on cancer cell 

growth patterns and spread. Topical 

preparations are not to be considered 

for any invasive lesions and should be 

abandoned if the response is poor or 

the lesion should recurr after use. Fig 4 

MOH’s Surgery is a complex 3-dimensional 

resection procedure performed 

usually by a dermatologist trained in 

both dermatology and pathology for 

99% definitive tumor resection. The 

procedure is one that preserves normal 

healthy skin and follows via a mapping 

procedure even the smallest cells of 

skin cancer change. The benefit of this 

procedure is seen in the preservation of 

tissue, especially on the face, and the surety 

of complete removal. The down side is 

that the defect created with the MOH’s 

During treatment 

After treatment 

procedure is sometimes quite large and 

patients need to be prepared for a reconstructive 

effort. The MOH’s surgeon 

will often times be able to anticipate the 

need for a Facial Plastic Surgeon and 

have you meet with him/her prior to the 

MOH’s procedure for discussion and 

outline of potential surgical repair techniques. 

Fig 5 

Reconstruction 

As Facial Plastic Surgeons, we acutely 

understand not only the anatomy of the 

face but we respect the aesthetic units of 

the face. These two simple facts allow for 

an advanced approach to reconstruction 

of facial defects. Gone are the days when 

our efforts at reconstruction focused 

soley on simple closure if the defect 

was amenable and not too large or the 

placement of a skin graft as the work 

horse of our reconstructive repetoire. 

Today we have the ability to offer local 

reconstructive flaps which take natural 

localized tissue and via a strategic 

rearrangement of that tissue, we return the 

face to as close to pre-MOH’s appearance 

as possible. This is not to say that the 

simple closure is not in our bank of 

repair options, nor to discount the full 

thickness skin graft, but it is to say that 

large defects are not the scarlet letter of 

deformity. Knowing that reconstruction 

can be quite good and understanding 

the effort is multi-faceted often alleviates 

the patient’s fear of the procedure and 

even encourages some to address skin 

areas that they inherently know may be 

a malignancy. 

Post-MOH’s resection with negative 

margin for cancer 

Fig 6 

Pre-MOH’s 

Post-MOH’s 


32 

During an office consultation for MOH’s 

reconstruction, options of repair are 

routinely presented to patients ranging 

from the most simple to the more complex. 

As is evident in the preceding photos 

and the one marked Fig 6, the defect 

that may result after the skin cancer 

is definitively removed can vary from a 

little defect to one of significant loss of 

tissue. Fig 6 

Before repair 

After repair – 3 stages 


Photos are always taken pre-MOH’s 

and during the reconstructive process. 

I will routinely suggest to patients the 

reconstructive effort which will provide 

the best cosmetic and functional outcome. 

At times, this suggestion is based on 

life style, stage of life and other medical 

factors such as medical problems and 

medicine taken routinely. The majority 

of all facial reconstructive efforts can 

safely and easily be performed in the 

office under local anesthesia with oral 

sedation medicine. It is common for these 

efforts to take place in 2-3 stages – fine 

tuning the ultimate outcomes. 

Results 

The following reconstructive efforts 

have returned the patients to a normal 

lifestyle and cosmetically are very sound 

in their presentation. One of our goals 

in the division of Facial Plastic and 

Reconstructive surgery is to create a 

better awareness of the options available 

and we pride ourselves on the effort of 

our repair. 

Before repair 

Before repair 


After repair – 1 stage 

Medicine has evolved over the last 

decade and with people living longer, 

the possibility of having skin cancer has 

increased significantly. Early recognition 

by our patients and primary doctors will 

ensure that appropriate care is received 

and long term outcomes are as good as 

possible. Our commitment to offering 

functional and aesthetic outcomes from 

a reconstructive perspective pervades 

our day to day operations and care plans. 

Our specific training in facial plastic 

and reconstructive surgery makes us 

uniquely qualified to offer excellent 

care to our patients. We are committed 

to being the security blanket post- 

Before repair 

Before repair 

MOH’s and will work to return the area 

of concern to as close to pre-MOH’s as 

possible. Protect yourself from the sun 

each and everyday regardless of the season 


After repair – 1 stage 

or weather, preach sun protection to your 

children (especially those 18 years of age 

and younger) and know that we are here 

to help with this very common problem.

“Wh a t c h a Sa y ” – 

H e a r i n g Lo s s Ma y Ha v e a Hi g h e r Co s t 

33 

Daniel Gold, M.D. 



The manifestations of hearing loss, especially in older 

adults, may be subtle. It usually begins insidiously and 

is often characterized by an inability to understand 

speech, rather than an inability to hear. The refrain 

of “I can hear you, but I can’t understand you” and “My hearing 

is fine; everyone just mumbles”, is all too common. 

Approximately 36 million American adults over the age 50 

report some degree of hearing loss in a 2010 survey by the 

National Institute on Deafness and Other Communication 

Disorders. The vast majority of these do not seek or believe they 

need treatment. This “disability”, however, may be more than 

just a social inconvenience. 

Recent epidemiologic studies have found age related hearing 

loss (ARHL) to be independently associated with poorer 

cognitive function and incident dementia. Compared with 

individuals with normal hearing, those with mild, moderate 

and severe hearing loss have a 2-, 3-, and 5- fold increased risk 

of developing dementia, respectively. The specific mechanisms 

are still unclear, but are likely related to the effects of hearing 

loss on cortical processing, increased cognitive load and social 

isolation. The effects of treating the hearing loss on cognitive 

function, however, still remain to be studied. To date, only a 

moderately sized trial on a cohort of US veterans demonstrated 

the positive effects of hearing aids on cognition and other 

functional domains at 4 months post–treatment. Further 

study is necessary involving a multidisciplinary collaboration 

between primary care, gerontologists, otolaryngologists and 

audiologists to better qualify whether treating hearing loss 

could affect outcomes critical to public health such as delaying 

cognitive decline and dementia. 

Loss of hearing may also hit individuals square in the 

pocketbook. New data shows that hearing loss may have an 

economic impact by affecting an individual’s earning power. 

As baby boomers remain in the workforce longer, the effect 

of hearing loss in the workplace will continue to magnify. The 

Better Hearing Institute estimates that untreated hearing loss 

can decrease an individual’s income by as much as $30,000 per 

year. This may come from an inability to follow instructions 

and/or communicate with customers, which puts them at 

a disadvantage compared with normal hearing coworkers. 

Mistakes made because of misunderstanding verbal instructions 

not only impairs employment, but is likely associated with 

increased job stress as the impaired individual struggles to 

compensate for the hearing loss and avoid making mistakes. 

This problem may be mitigated, at least partly, through 

amplification. If hearing aids are worn, there maybe a reduction 

in the risk of loss of income of 90 to 100% for patients with 

mild hearing loss, and 65 to 77% for those with moderate to 

severe hearing loss. NIDCD data, however, shows that still only 

20% of patients who will benefit from hearing aids wear them. 

More concerning, only half of all individuals with untreated 

hearing loss have even undergone a professional hearing test. 

The magnitude of the societal cost of hearing loss should inspire 

us to develop, promulgate and follow clinical guidelines to 

identify and treat hearing loss in all age groups. 

All too often a mail order, or strip mall approach, is taken to 

treating hearing loss. The current approach toward treating 

hearing loss remains shaped by a medical model of disability in 

which hearing impairment is simply addressed by dispensing 

a medical device, i.e. a hearing aid. In reality, adult hearing 

loss is similar to any other physical impairment and requires 

concerted counseling, rehabilitate training, environmental 

accommodation, and patience. A device alone will rarely provide 

satisfactory results without appreciation of the distinctive 

circumstances and needs of the individual treated. This may 

require the integration of expert knowledge by the primary 

physician, ENT specialist and a qualified hearing professional 

to best understand the needs of the patient. A qualified and 

highly trained audiologist is invaluable to guiding patients 

through the myriad of assistive devices and helping them 

choose what is right for them. The goal of treatment is not 

only the device, but to ensure that older adults are able to 

integrate and apply the variety of available hearing technologies 

in their daily lives. 

As a society with a rapidly aging population, implementing 

innovative strategies to promote successful treatment of 

hearing disability in older adults is a public health, economic, 

and moral imperative. Concerted and interdisciplinary public 

health and research initiatives joining primary physicians, 

otolaryngologists, and community advocates to study and treat 

hearing loss in older adults could potentially have substantial 

implications for society and the health of older adults – a message 

to which everyone needs to listen. 

National Institute on Deafness and Other Communicative Disorders. Statistics 

about hearing, balance, ear infections and deafness: Quick statistics. www.nidcd. 

nih.gov/health/statistics/pages/quick.aspx. Accessed May 20, 2012. 

Lin FR, Ferrucci L, et al. Hearing loss and cognition in the Baltimore 

Longitudinal Study of Aging. Neuropsychology. 2011; 25(6):763-770. 

Lin FR, Metter EJ, et al. Hearing loss and incident dementia. Arch Neurol. 

2011;68(2):214-220. 

Murlow CD, Aguilar C, Endicott JE, et al. Quality of life changes and hearing 

impairment: a randomized trial. Ann Intern Med. 1990;113(3):188-194. 

Kochkin, S. The efficacy of hearing aids in achieving compensation equity in the 

workplace. Hearing Journal. 2010;63(10):19-26. 


34 

R h i n o p l a s t y — Yo u r Qu e s t i o n s Ab o u t Co s m e t i c 

N a s a l Su r g e r y An s w e r e d 

Michael Bergstein, M.D., F.A.C.S. 




Michael J Bergstein, MD, FACS is a board certified Facial Plastic and 

Reconstructive surgeon. Dr. Bergstein is an Assistant Clinical Professor 

of Otolaryngology/Head and Neck Surgery at the Mount Sinai School 

of Medicine. He has been in practice in the Westchester area for 

twenty years specializing in all aspects of nasal reconstructive and sinus surgeries. 

Dr. Bergstein is the Chief of Otolaryngology at Phelps Memorial Hospital. He is 

a Senior Attending Physician at Northern Westchester Hospital and Hudson Valley 

Hospital Center as well as the Mount Sinai Medical Center in New York City. 

What is the most common reason for 

Rhinoplasty (plastic surgery of the nose) 

Most patients have nasal cosmetic 

surgery performed to enhance their 

appearance. When a patient looks in 

the mirror all they see is an unattractive 

nose. Sometimes it’s a negative comment 

from someone else that pushes the patient 

to undergo surgery. 

The primary and perhaps only medical 

reason for the operation is difficulty 

breathing through the nose, usually due 

to a “deviated nasal septum.” The septum 

is the partition that separates the right 

nostril from the left inside the nose. If the 

septum is crooked or bent on the inside of 

the nose it will obstruct nasal breathing. 

The reason for a septum becoming 

crooked is usually from trauma which 

doesn’t necessarily mean a broken nose. 

Just getting hit in the nose with a basketball 

can be enough to move the septum over. 

Such patients don’t always recall being 

injured. Many undergo nasal surgery 

without repairing their nose cosmetically. 

Can you tell us about the psychological 

component of this surgery 

I spend a significant amount of time 

counseling my patients to make sure 

they have given the operation the proper 

amount of thought and consideration. 

I want to be sure that it’s not a spur of the 

moment serendipitous idea. Twenty five 

years of performing nasal constructive 

surgery has given me a sense of patients 

who have realistic expectations and those 

who don’t. Patients should be emotionally, 

psychologically and physically ready to 

undergo nasal constructive surgery. 

How do you design the new nose 

I’m looking for the nose to be in proportion 

to and balance with the other aspects of 

the patients’ facial features. The goal is to 

create a nose that enhances all the other 

features of the patients’ face such as their 

eyes, hair, cheekbones and lips. 

Often patients come in with a picture of 

what they want their nose to look like. I 

tell them that while that is an attractive 

nose on that face, it may not be the nose 

that matches their particular appearance. 

The nose has to harmonize with the rest 

of the face. 

Above all, the nose needs to be functional, 

that is, the patient must be able to breathe 

properly and well after the procedure. 

Does the Rhinoplasty make patients happier 

Absolutely! I’ve seen personality changes 

in patients as a result of having their 

cosmetic nasal surgery. Patients who 

might have been shy and insecure have 

become more outgoing and confident. 

Why does the nose often change in 

appearance a year after the surgery 

The nose will look better immediately 

after the surgery, but it takes a whole year 

for the skin to adhere completely to this 

change of the nasal structure. Patients 

can be happy knowing the appearance is 

only going to get better. 

Are some patients disappointed after the 

surgery 

The most common reason for disappointment 

is when surgeons are too aggressive 

in removing tissue either on the tip of 

the nose or on the bump. This can result 

in an imbalance in their appearance and 

unnatural “surgical” look. 

What risks are involved 

Rhinoplasty is the most common 

operation that I perform. The risks are 

generally minimal. 

One risk is post-operative bleeding, so we 

make sure before the surgery with blood 

tests that the patient can adequately clot 

and does not have a bleeding disorder. 

There is also a minimal risk with any use 

of anesthesia. 

Each patient is unique in terms of the 

risk involved, however, we do a thorough 

preoperative history and physical examination 

to determine if there are any 

unusual risk factors. 

What is the approximate cost of a 

Rhinoplasty 

This varies greatly depending on which 

doctor the patient chooses. If the procedure 

is being done for medical reasons, 

(e.g., deviated nasal septum) to help with 

the patient’s breathing, insurance may 

cover part of the cost. In my practice, the 

cost usually ranges from $4000-6000. 

How has cosmetic surgery changed over 

the years 

In recent years, patients are interested 

in a more natural look. Years ago, plastic 

surgeons would give everyone the same 

nose. Patients now want their nose to blend 

naturally into the face. I strive to give my 

patients the most natural appearing and 

most cosmetically enhancing nose that 

they will be happy with for a lifetime.

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36 

A Ru n n y No s e : 

W h e n Is It a Si g n o f a Mo r e Da n g e r o u s Co n d i t i o n 

B. Todd Schaeffer, M.D., F.A.C.S. 




CSF Rhinorrhea 

Cerebrospinal Fluid (CSF) is a clear fluid produced by 

the choroid plexus in the ventricles of the brain. It acts as 

a shock absorber and cushions the brain and spine. The 

CSF circulates around them in the sub-arachnoid space. 

A communication with this space through the arachnoid 

(thin layer), dura (thick fibrous layer) and a bony defect 

at the skull base, into the paranasal sinuses, leads to a 

leakage of clear fluid from one side of the nose. 

Figure #1 Left Sphenoid 

Bony defect in left lateral sinus with encephalocele 

Having a “runny nose“ is very common and is 

frequently associated with a cold, virus, allergy or 

sinus infection. Thirty-seven million Americans 

suffer with chronic sinusitis and fifty million have 

some form of respiratory allergies. Recently, Cathy, a fortythree 

year old over weight diabetic woman, called her primary 

care doctor (PCP) with a new problem. Her nose started 

to “run” without sustaining any trauma. She asked 

what should she do She denied any symptoms of facial 

pressure, headache, fever, postnasal drip or congestion. Her 

PCP thought it sounded like allergies and told her to 

start the over the counter antihistamine 

Loratidine. Cathy had some health issues which were 

controlled but had no history of sinusitis, asthma or allergies. 

She did note some increased blurring of vision but attributed 

this to requiring stronger glasses. After a few days, the nasal 

discharge worsened, especially when she leaned forward 

(Figure #2). She kept a tissue up by her nose for most of the 

day. She visited her ENT doctor who determined she had onesided 

(unilateral) clear rhinorrhea consistent with a cerebrospinal 

fluid leak (CSF). She was sent to the Emergency room at 

Long Island Jewish Hospital and came under the care of Dr. B. 

Todd Schaeffer, an endoscopic sinus and skull base surgeon and 

Dr. Steven Schneider, an endoscopic neurosurgeon. A CT scan 

showed a very large pneumatized lateral sphenoid sinus with 

a skull base defect (Figure #1). Inflammatory tissue was in the 

most lateral recess on the left side. 

Figure #2: Clear rhinorhea 


Traumatic vs Spontaneous 

Elevated Intracranial Pressure 

Motor Vehicle Accidents 

Pseudotumor Cerebri 

Gun Shot Wounds 

Surgery i.e. tumor removal, 

sinus surgery 


A lumbar drain was placed and an eye exam confirmed papilledema 

consistent with benign intracranial hypertension most 

likely due to pseudotumor cerebri. Cerebrospinal Fluid (CSF) 

is a clear fluid produced by the chorid plexus located in the 

ventricles of the brain. It acts as a shock absorber and cushions 

the brain and spine. The CSF circulates in the subarachnoid 

space. A communication with this space through the arachnoid 

(thin layer), dura (thick fibrous layer) and a bony defect at the 

skull base, (in the paranasal sinuses), causes the unilateral clear 

fluid “runny nose.” Cross contamination of nasal contents with 

CSF is a set-up for meningitis and intracranial infection and 

therefore, sealing the leak is paramount.

37 

A CT cisternogram confirmed the sphenoid sinus as the site 

of leakage. An endoscopic transnasal trans-sphenoidal repair 

with naso septal flap was performed. This was extremely 

difficult since the lateral recess where the leak was found 

was lateral and posterior to the pterygopalatine fossa in the 

infratemporal fossa. This was especially challenging since the 

repair was lateral and inferior to foramen rotundum and ovale. 

The instruments were just barely able to reach with visualization 

supplied with angled scopes transnasally. Pseudotumor Cerebri 

is benign intracranial hypertension found in obese females 

with complaints of headache, nausea, vomiting, tinnitus, double 

vision that can cause papilledema and eventually visual loss. 

CSF leak is a complication due to chronically high intracranial 

pressure leading to bony defects and spontaneous leaks. 

Figure #3: Second patient with spontaneous cribriform CSF 

leak. Skull base defect with meningocele. This was repaired 

endoscopically transnasally with local mucosal flap. Repaired with 

Dr. Mark Eisenberg (Endoscopic Skull Base Neurosurgeon). 

Diagnostic Testing for CSF Leak 

CSF rhinorrhea can easily be misdiagnosed because it is often 

left off the differential diagnosis of rhinorrhea. While a “runny 

nose” is commonly thought to be from an allergy, cold, virus 

or sinus infection, a careful history of unilateral crystal clear 

watery rhinorrhea may help elucidate the correct diagnosis. If 

the diagnosis is in doubt, a nuclear medicine pledget test can 

confirm there is a leak. After a lumbar puncture, a radioactive 

tagged isotope is placed back into the CSF. If a cotton pledget 

placed in the nose is positive for the isotope, this confirms an 

active leak and the side. A CT Cisternogram helps confirm 

the site of a leak. After a lumbar puncture, contrast material is 

injected into the subarachnoid space where the CSF circulates. 

Figure #4: Third patient with CSF leak at Left Supraorbital 

ethmoid. This was an encephalocele repaired through a transnasal 

endoscopic approach 

The patient is tilted upside down followed by a CT scan with 

the head down leaning forward. The contrast material seen in 

the nasal cavity elucidates the area of leak Beta-2 transferrin 

is found almost exclusively in CSF and not in blood, mucous 

or tears. When clear nasal fluid collected is positive for 

this marker, it confirms a CSF leak on that side. The specific 

site is determined by CT, CT cisternogram or endoscopy. 

Intraoperative localization using fluorescein produces greenish/ 

yellow CSF fluid. An off-label use of fluorescein is used when 

this is injected preoperatively into the CSF in diluted amounts. 

Etiology of CSF Leaks 

Trauma 

Tumors 

Iatrogenic 

Spontaneous/Unknown 

Key Points to CSF Repair 

Transnasal endoscopic repair with navigation. 

Lumbar drain as needed 

Materials used for multilayer closure 

Bone 

Fat 

Fascia 

Duragen/Dural repair 

Tisseel (glue) 

DuraSeal ( non-toxic hydrogel) 

Nasoseptal Flap 

B. Todd Schaeffer, M.D., F.A.C.S 

Endoscopic Sinus and Skull Base Surgeon 

Dr. Schaeffer has been performing advanced 

endoscopic sinus surgery for twenty years. 

He has performed more endoscopic 

skull base surgery than any other 

sinus surgeon on Long Island. 

He commonly works with skull 

base neurosurgeon Dr. Mark 

Eisenberg. As a team, they have 

successfully treated pituitary tumor 

removal, closure of CSF leaks, removal of encephaloceles, 

chordomas, clival tumors, meningiomas, craniopharyngiomas, 

odontoidectomy, spinal cord decompression, biopsies at the 

skull base, removal of malignant sinus/nasal tumors and skull 

base reconstruction. The key to their success is collaboration 

together and the support staff of North Shore University 

Hospital and Long Island Jewish Medical Center. Experience 

and team collaboration counts. Visit NOSEMD at You Tube or 

Google NOSEMD. 

www.PituitaryMD.com www.SchaefferMD.com 


38 

A Va c c i n e f o r Al l e r g y Su f f e r e r s 

Prashant Ponda, M.D. 




The plight of the allergy sufferer is a life of fear 

of season’s change and the plying of medications 

to treat their multiple symptoms. Each year, 

hundreds of millions of individuals worldwide 

mask their allergy symptoms with a variety of over-thecounter 

and prescription medications. There is, however, 

a lasting treatment available for certain types of allergies. 

Allergen immunotherapy (allergy shots) has been used 

for over one hundred years in the treatment of allergic 

disease. It is indicated for the treatment of allergic 

rhinitis (hay fever), allergic asthma, and stinging insect 

allergy (i.e. bee sting allergy). There is no medication in 

the injections, but rather the exact allergens to which a 

patient is sensitized as detected through skin testing. 

Rather than inhaling the allergen (or being stung), it is 

given as a subcutaneous injection(s). Its mechanism of 

action in generating immunity is therefore similar to any 

other vaccines that patients receive, such as the flu shot or 

tetanus shot. 

Since patients are allergic to the contents of the injections, the 

dose is built-up weekly over a period of several months until a 

maintenance dose is achieved. This maintenance dose is then 

administered once per month over a period of approximately 

3-5 years. Most patients see a significant reduction in symptoms 

and medication use within the first year of receiving allergy 

shots. Ultimately, the goal is to shift a person’s immune system 

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from allergy toward tolerance, so exposure to the allergen does 

not result in a clinical reaction. 

This is in stark contrast to being continuously dependent on 

medications over the long-term to try to control the symptoms 

of allergic disease. By using the power of one’s own immune 

system, coupled with the natural allergen delivered as a 

vaccine, one can greatly reduce, and commonly eliminate, his or 

her symptoms and medication use. 

Communications Solutions 

for Health Care Providers 

Jared M. Wasserman, M.D. 

Dr. Jared Wasserman received his medical 

degree from the Mount Sinai School of Medicine 

where he was elected to Alpha Omega Alpha 

Medical Honor Society. He completed an 

internship in General Surgery and a residency in 

Otolaryngology-Head and Neck Surgery a the 

SUNY Downstate Medical Center/Long Island 

Co lege Hospital. He then served as a clinical 

fe low and completed advanced training in 

laryngology a the Ma sachuse ts Eye and Ear 

Infirmary of Harvard Medical School. 

Dr. Wa serman is Board Certified by the American 

Board of Otolaryngology-Head and Neck Surgery. 

He is a member of the American Academy of 

Otolaryngology Head and Neck Surgery, The 

Triological Society and the Medical Society of the 

State of New York. 

In addition to treating pediatric and adult diseases 

of the ear, nose and throat, Dr. Wa serman also 

specializes in diseases of the head and neck, care 

of the profe sional and performing voice, voice 

restoration surgery and complex laryngeal and 

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