Have you ever wondered why there are so many different (medical) terms for acid reflux?  There are so many terms because different  medical specialist groups use different terms that they invented to describe their viewpoints.  The table below shows the most common ones.

Most Common Medical Terms for Acid Reflux
Gastroesophageal reflux disease (GERD)
Laryngopharyngeal reflux (LPR)
Gastro-oesophageal reflux disease
Extraesophageal reflux disease
Supraesophageal reflux disease
Esophago-pharyngeal reflux
Gastropharyngeal reflux
Atypical reflux disease
Esophageal erosions
Barrett’s esophagus
Reflux esophagitis
Reflux laryngitis
Silent reflux
Esophageal reflux
Airway reflux

Reflux is like the elephant in the famous tale of the three blind men and the elephant: The first blind man, feeling the leg of the elephant, exclaims, “I can see it clearly; the elephant is like a tree.” The second blind man holds the trunk and says, “No, the elephant is like a very large snake.” The third blind man grasps an ear. “Aha, you are both wrong,” he says. “The elephant is rather like a giant leaf.” Each of the blind men embraces a part of the truth, but none understands its entirety.

In the case of reflux, the three blind men are represented by three medical specialties, each one focusing on a different part of the aerodigestive tract: (1) The otolaryngologist (ENT physician) specializes in the ears, nose, and throat; (2) the gastroenterologist (GI physician) specializes in the esophagus (the swallowing tube that connects the throat with the stomach); and (3) the pulmonologist (PUL physician) specializes in the lungs. Many other medical specialties encounter patients with reflux as well, including internists, family practitioners, pediatricians, and critical care specialists.

GIs are unfamiliar with the signs and symptoms of airway reflux, but they insist on using diagnostic tests designed for esophageal reflux to evaluate airway reflux, because that’s what they know and understand.

Many gastroenterologists make their livings performing sedated endoscopies, mainly  esophagoscopy (aka EGD, esophagogastroduodenoscopy) and colonoscopy. This involves intravenous sedation, recovery, and it is sometimes associated with serious (even life-threatening) complications.

Sedated EGD is overkill for screening the esophagus for pathology such as Barrett’s in patients with acid reflux. We recommend transnasal esophagoscopy instead. Transnasal esophagoscopy (TNE) can be done in the doctor’s office without sedation, with comfort, and without complications.  Is TNE new? Not really. At the Voice Institute of New York, we have been performing TNE routinely for more than a decade. Gastroenterologists, however, have been reluctant, or at least slow, to embrace this technology. Why?

Last year, there were 10,000,000 sedated endoscopies done in the United States by approximately 10,000 gastroenterologists (GIs). If every GI did endoscopy (which they don’t), then each would have performed 1,000 last year,  that is, 20 per week or 4 per day.

The “facility fees” alone for sedated endoscopy were $10,000,000,000, that’s right, $10 billion!  The average facility fee for endoscopy last year was $1,000. And that’s just the fee that the endoscopy facility received; this does not include the doctors’ professional fees. Do the math; if the GI doctor owned her/his endoscopy facility, and many are owned by groups of GIs, the take “facility fee” take-home would be $1,000,000, that is $1,000 per X 1,000 procedures). GI doctors appear to have a significant conflict of interest in favor of sedated EGD procedures.

When GIs perform sedated EGDs, usually they do not examine the throat. Indeed, the endoscope is usually passed blindly, that is, without viewing the path into the esophagus. This is one of the reasons that GIs do not recognize airway reflux. By the way, it is time to stop using all those different terms for acid reflux. It now makes sense just to use two: ESOPHAGEAL REFLUX and AIRWAY REFLUX.

Patients with Airway Reflux DO NOT Usually Have Esophageal Reflux

We have published articles examining how ineffective GI diagnostics were in patients with airway reflux. We found that 80% of patients with airway reflux did not have esophageal findings of reflux. This is because the airway is 500 times more susceptible to damage from reflux than the esophagus. The latter organ is robust by comparison so that the acid/etc. can pass through the esophagus quickly and then do damage to structures in the airway. In addition, we found that the positive predictive value of esophageal (only) reflux (pH) monitoring in patients with airway reflux was 49%.  Would you get a test that got it right less than half of the time?  And impedance testing isn’t much better.

GIs also do not understand the importance and impact of diet in people with airway reflux. A month ago, I had a patient come see me from Oregon. She had airway reflux, and I started her on the Reflux Induction Diet and antireflux medication. A few days ago she returned dramatically improved. “Your reflux diet makes all the difference in the world,” she reported; then she added, “I went back to my GI and told him what happened, and you know what he said?  ‘I have reflux too, but I don’t want to change my diet; I love burgers and fries and all … so I take pills and they help’.”  After that interaction the patient confided that she wouldn’t be seeing that GI doctor ever again.

Almost One in Five Americans Have Airway Reflux

In the Time Square Study, we found that 22% of Americans had esophageal reflux and 18% had airway reflux. Not surprisingly, many of the people with airway reflux had “silent reflux,” meaning that they suffered acid reflux without heartburn or indigestion. These numbers are a wake-up call. It is time to recognize that airway reflux is common, important, and still under-diagnosed and under-treated. What are the symptoms?

Symptoms of Airway Reflux
Hoarseness
Chronic cough
Choking episodes
Difficulty swallowing
Lump-in-the-throat sensation
Food and/or pills getting stuck
Too much throat mucus
Chronic throat clearing
Shortness of breath
Post-nasal drip
Sore throat
Sinusitis
Asthma

“Asthma” is a very interesting presenting symptom in my clinic. True asthma is characterized by wheezing, trouble getting air out. About 8% of people with airway reflux have reactive airway disease, including laryngospasm, paradoxical vocal fold movement, and pseudo-asthma. With reflux, patients have difficulty getting air in (not out), and they almost always know the difference.

“When you have an ‘asthma’ attack, do you have more trouble getting the air in or out,” I ask, and 90% my patients respond “IN” without hesitation. Most people with adult-onset asthma actually have reflux-related reactive airways disease, and  when the reflux is effectively treated, the “asthma” usually disappears. The same is true of chronic cough symptoms; most are due to reflux.

At present, ENT (ear, nose, and throat) doctors are the ones to see for people with airway reflux, not gastroenterologists. Here is a slight but important paradox: Endoscopy (esophagoscopy, TNE) is not how you diagnose airway reflux. That takes a throat examinations and sometimes special (pH) testing. If one has reflux, however, a screening endoscopy should be performed to rule-out significant esophageal disease. We now know that people with airway and esophageal reflux have a similar incidence of esophageal cancer and pre-cancer. Silent reflux causes just as much cancer and the non-silent type.

Meanwhile, what is missing? What is needed?  In a way, the biggest problem with airway reflux is that most physicians, even those who recognize its symptoms, don’t have a way to confirm the diagnosis. At the Voice Institute of New York, we do special airway reflux testing, and we are now working on two new diagnostics for airway reflux; see www.KoufmanReflux.com. The first is a spit-in-a-cup screening test (similar to a pregnancy test) that detects pepsin, the principle enzyme of the stomach. Pepsin is only made in the stomach so that if a person has detectable pepsin in their spit, they have acid reflux (either airway or esophageal reflux). In preliminary testing, the spit test for pepsin is approximately 90% accurate.  This is terrific for a screening test. We hope that we can have the test, known as Koufman Reflux Test Strips (YouTube video) on the market by the summer of 2012. It will help physicians and their patients by making the right diagnosis.

Also under development by Koufman Diagnostics, is a definitive,  turn-key, airway reflux pH testing system that may be employed by any physician regardless of medical specialty (e.g., pulmonology, gastroenterology, otolaryngology, family practice) to make a definitive diagnosis of airway (and/or esophageal) reflux. The system uses ambulatory pH-monitoring technology with foolproof probe-placement and a software that makes interpretation foolproof.  This test is also coming this year.

If you think you have airway reflux, see an ENT doctor, or come see me here at The Voice Institute of New York.  Also, the book,  Dropping Acid: The Reflux Diet Cookbook & Cure, may help.

]]> http://www.jamiekoufman.com/2012/02/02/why-most-gastroenterologists-just-don%e2%80%99t-understand-airway-reflux-at-all/feed/ 0 http://www.jamiekoufman.com/2011/11/30/the-silent-reflux-epidemic/ http://www.jamiekoufman.com/2011/11/30/the-silent-reflux-epidemic/#comments Thu, 01 Dec 2011 04:02:34 +0000 Jamie A. Koufman, M.D., F.A.C.S. http://www.jamiekoufman.com/?p=529

Pepsin in Barrett's Esophagus (Discussed at bottom)

It’s pernicious!

And you probably have it, because 125 million people do. Half don’t even know they have it, and their doctors don’t know it either. Millions of Americans have undiagnosed and untreated acid reflux, sometimes for years or even life-long. How could this be? Because too-specialized medical specialists can’t see the reflux forest for the trees; because many millions have “silent reflux”; and because the role of one particular food additive, ACID. Indeed, acid in food has been overlooked as a cause of massively widespread and uncontrolled airway reflux. The latter, airway reflux, is a term for stomach juice backflow into the breathing passages, including the ears, nose, throat, and lungs.

Reflux is increasing so rapidly that one wonders if we all will have it soon. Since the 1970’s, prevalence of reflux has increased an average of 4% per year. Reflux is now epidemic, affecting 40% of the American population. Twenty-two percent have GERD (gastroesophageal reflux disease) with heartburn and indigestion, and another 18% have silent reflux, also called LPR or laryngopharyngeal reflux.

A frightening implication of this increase is that millions of Americans may be at risk for the development of reflux-related cancer. That’s right—reflux causes cancer! During this same period of time, the prevalence of esophageal cancer has increased 850% and now is the fastest growing cancer in the U.S. In addition, as many as 10% of people with reflux symptoms have Barrett’s esophagus, a reflux-caused, pre-cancerous condition.

So why do we have a reflux epidemic? ACID! It now seems likely that the primary cause of this reflux/cancer epidemic can be traced to acidification of foods/beverages, which until now has been virtually ignored as a problem. In 1973, following an outbreak of food poisoning, Congress enacted Title 21 and charged the FDA (Food and Drug Administration) with providing “Good Manufacturing Practices” to insure that bottled and canned foods and beverages crossing state lines would not be contaminated by bacteria. Thus, for two generations, almost everything bottled and canned has had acid added to discourage bacterial growth and prolong shelf-life. After all this time, it appears that the most dangerous food additive of all may have been simply overlooked.

Recognizing and understanding “silent reflux” is crucial. The symptoms of reflux are not just digestive—like indigestion and heartburn (chest pain after eating)—they also include hoarseness, chronic cough, post-nasal drip, a lump-in-the-throat sensation, difficulty swallowing, choking episodes, shortness of breath, sinusitis, and asthma. If you have any of those symptoms, you probably have silent reflux. The term “silent” is derived from the observation that the reflux (backflow from the stomach) can easily be overlooked if it occurs at night while people are asleep or during the day in small amounts with no heartburn. It just may go unnoticed.

Remember, if you have unexplained or mysterious throat, breathing, airway, or digestive symptoms, think of silent reflux. The dots are now connected: The reflux and esophageal cancer epidemics are related to too much acid in our foods and beverages. BTW, the average 12-29-year-old in the United States consumed 160 gallons of soft drinks last year; that’s almost a half-gallon a day! We must have a national dialog about not only reflux and unhealthy eating but about food additives, especially ACID, and also about how we preserve food.

If you have reflux, you personally must become active, because this must be a grass roots movement. It is the role of government to protect its people; and we the people have gotten reflux and cancer from the unintended consequences of acid in our food. I believe that the end game is clear. If we insist on having FDA-mandated acidity (pH) on all food and beverage labels, the American people will solve the reflux/cancer problem for themselves.

Nov. 8, 2011 New York Times Articles by Tara Parker-Pope: Tired of the Burn? Low-Acid Diet May Help and A Heartburn-Free Thanksgiving

The figure at the top of this post is a biopsy of Barrett’s esophagus, the reflux-related, precancer. This specimen is stained in a special way, using IHC (immunohistochemistry) for human pepsin. This photo shows that pepsin is produced in Barrett’s. The implications of this have a bearing on the potential importance of long-term low-acid diet in people with Barrett’s.  In other words, dietary acid can activate the pepsin. Indeed, although only anecdotal at this point, the author has seen the regression of Barrett’s in some of her patients on a long-term low-acid diet. This is an exciting new conceptual breakthrough!

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FIX HEALTHCARE & HEAL THE NATION (see Dr. Koufman’s CV)

Click the title above to view the slide show (which may be viewed full screen by clicking the expand icon on the bottom-right of the slide).  There are 40 slides in the show. The synopsis is below and the accompanying manuscript is in preparation.

Synopsis

Most Americans clearly favor free-market systems, but in healthcare we don’t have a free market. “Capitalism” can not fix the healthcare crisis because for-profit medicine is intrinsically unethical. Indeed since the 1970s, market forces have evolved a dangerous, powerful, and self-perpetuating corporate behemoth. The transformation of healthcare has been driven by market power over prices—due to price inelasticity of demand—and perverted (hegemonic) investment strategies.

The American “medical-industrial complex” can itself be likened to a cancer that will soon outgrow its own blood supply and die. The two choices appear to be national healthcare or national bankruptcy. Creation of an actual National Health Service would bolster economic development, reboot rational markets (creating competitive cost containment), and would form the cornerstone first tier of a rational (likely three-tier) healthcare delivery system.

Jamie A. Koufman, M.D., F.A.C.S., Director of The Voice Institute of New York was awarded the 2011 James E. Newcomb Award at the American Laryngological Association (ALA) during the recent 132^nd Annual ALA Meeting April 27th in Chicago, Illinois. This award, established in 1939, is given annually to a member of the Association in recognition of  outstanding contributions to research and the medical literature in the field of laryngology.

The list of distinguished past winners includes Dr. Chevalier Jackson, Dr. Joseph Ogura, Dr. John Kirchner, Dr. John Conley, Dr. Stuart Strong, and Dr. Gerald Healy.  The Newcomb Award has been likened to a “Lifetime Achievement Award” for research and publications in laryngology.

Presidential Address of Jamie A. Koufman, M.D., F.A.C.S.
American Broncho-Esophagological Association (President 2008-09)
Presented at the Annual Meeting of the Society, Scottsdale, AZ, April 29, 2009

Dear members and guests of the American Broncho-Esophagological Association, it has been my honor and pleasure to be president of this society. During this past year, among other things I have examined the advantages, disadvantages, and influences of medical specialization on healthcare in America with a particular focus on how this impacts our patients with aerodigestive tract symptom. The title of my talk is “Specialization: When Being the Best Isn’t Good Enough,” because I believe that medical over-specialization is a problem. Many complex patients have a committee of non-communicating doctors with no one doctor actually taking responsibility for the patient’s care. Here is a multiple choice question for your consideration that makes the point:

A 55-year-old school teacher has chronic cough and vocal fatigue since onset of symptoms with an upper respiratory infection in 1997. Which is the best doctor to diagnose and treat her problems?

A.  Pulmonologist
B.  Otolaryngologist
C.  Gastroenterologist
D.  Allergist
E.  None of the above.

With a normal chest x-ray, the patient’s primary care doctor sends the chronic cough patient to a pulmonologist for evaluation.  The lung doctor does a PPD, spirometry, bronchoscopy, and finds nothing. Thinking that the patient might have “atypical reflux disease” (laryngopharyngeal reflux, LPR), the pulmononlogist sends the patient to an otolaryngologist who examines the patient and concurs that the diagnosis may be LPR. So, the otolaryngologist refers the patient to a gastroenterologist who performs upper endoscopy, and finding a normal esophagus, declares the patient does not have reflux disease. The GI doctor speculates that the likely cause of the patient’s cough is allergy, and therefore, the patient is sent to an allergist-immunologist. The latter physician, finding no allergies, sends the patient back to the primary care physician. So, the correct answer to the question above is “E. None of the above.”

You may not know this, but chronic cough is one of the most common symptoms for which a patient seeks medical attention in the United States. Chronic cough patients, most often referred to me by gastroenterologists and pulmonologists, account for 20% of my practice. Indeed, in my experience, these patients are often passed from doctor to doctor; and even though they are referred to me for evaluation for LPR, not all of them have reflux, but the majority do. There are many patients who have reflux as the only cause of cough and those patients, even on proton pump inhibitors and other medications, may continue to have cough for as long as they reflux, even neutral-pH reflux. Such patients often will tell you that reflux is the cause of their cough. They may report, for example, that they have regurgitation when they bend over, that they cough after meals, and that they sometimes awake in the night from a sound sleep coughing violently and gasping for air.

In addition to LPR-related coughers, there is a significant group of patients who have “neurogenic cough,” which is a kind of “sick nerve syndrome” usually related to a post-viral vagal neuropathy (PVVN). People with PVVN and neurogenic cough usually have a history of having had an upper respiratory infection weeks, months, or years prior, around the time of the onset of symptoms.

The typical pattern of neurogenic cough is daytime (all day long), but not at night. Specific things like change in temperature (e.g., going from warm to cold), and certain odors (e.g., perfume, diesel fuel or gasoline smell) may precipitate cough. In addition, such patients often describe having a “hair trigger” cough, and that speaking or chuckling may precipitate coughing. When patients have cough associated with voice use, it is almost always a neurogenic cause. It is important to note that neurogenic and reflux-related cough patients form a very large population of patients, and that these patients are essentially without a doctor/specialist.

Specialization is a very America idea, in spite of the fact that it results in fragmentation of medicine; after all, everyone wants to see the “best.” So, you do actually get things like this inane example: “Yes, I’m the very best doctor in the country for doing a stapedectomy on the right ear for otosclerosis. And no matter; if you have similar trouble in your left ear, my partner who happens to be left-handed, is the best surgeon in the country for fixing otosclerosis of the left ear. Between us, we are the best if you have otosclerosis in either ear.”

The problem with patients who have symptoms like chronic cough or other reactive airway diseases is that the patients often don’t fit any of the specialists’ boxes. Just think about it for a moment: globus, dysphagia and many otolaryngologic symptoms cross both anatomic and medical specialty lines. And the concept that diseases fit within the boundaries of our medical specialties – nose/sinuses, throat, lung, esophagus – is preposterous. It would seem that the creation of certain medical specialties was predominantly for the convenience of physicians.

Reactive Airways Disease

Asthma
Allergic rhinitis
Vasomotor rhinitis
Paroxysmal laryngospasm
Paradoxical vocal fold movement
Vocal cord dysfunction (“VCD”)
Neurogenic (“neuropathic”) cough
Gastroesophageal reflux disease
Laryngopharyngeal reflux (“silent reflux”)

It is likely that allergic rhinitis, post-nasal drip, vasomotor rhinitis, paroxysmal laryngospasm, paradoxical vocal fold movement, asthma, and neurogenic cough are all manifestations of reactive airway disease and that reflux is a common feature in many patients. It is amazing to me how many patients have sinus disease and asthma related to LPR.

As I was flying out here for this meeting, I opened my New Yorker Magazine (dated June 1, 2009), and found an article, “The Cost Conundrum” by Atul Gawande. This was an amazing article and coincidence, and a real eye-opener. The bottom line: Overutilization of specialists was one of the main reasons for the high cost of healthcare in the United States. Here is essence of the story. In 2006, the median income for McAllen, Texas was $12,000; however, Medicare spent over $15,000 per enrollee in McAllen. In nearby El Paso County, which has similar demographics, only $7,000 per year was spent on each Medicare enrollee.

But by all contemporary metrics, McAllen’s health care was not as good as El Paso’s. Healthcare services in McAllen were found to be grossly overutilized. In McAllen, for example, if you had chest pain having eaten 16 tacos, instead of getting an antacid in the emergency room you might be admitted and end up having a cardiac workup including cardiac catheterization. If you had numbness of your fingers, you would probably end up having nerve conduction studies. As a matter of fact, overutilization also resulted in high rates of unnecessary surgery.

In McAllen, there was this complex medical network in which most patients went from doctor to doctor to doctor, having “all of the most advanced tests and treatments.” It was profoundly wasteful. Dr. Gawande concluded, “Someone has to be responsible for the totality of care; otherwise, you get a system that has no brakes.”

Integrated Aerodigestive Medicine

It is my belief that reactive airways disease is really just one complex syndrome and we as otolaryngologists need to be responsible for managing patients who have diseases of the nose, sinuses, and aerodigestive tract including the esophagus and lower airway. For us to defer to gastroenterologists and pulmonologists makes no sense whatsoever as many of our patients are not going to get effective treatment at the hands of those specialists.

We need to create a new “specialty” perhaps called “Integrated Aerodigestive Medicine.” This is not a new concept, the idea of a holistic approach to the management of patients with confounding symptoms. Its time has come. I urge you, my colleagues, to learn more about things like neurogenic pain, chronic cough, swallowing disorders, “asthma,” and reflux. These conditions are all within our domain.

It is also time for otolaryngologists to begin routinely assessing the aerodigestive tract using modern technology. When Chevalier Jackson invented modern endoscopy, over a hundred years ago, he did not accept limits based upon arbitrary anatomic subdivisions. He examined the esophagus and the lungs, larynx, and sinuses as though they were all part of the same system. They are. With the availability of distal chip technology, modern endoscopes allow complete evaluation of the aerodigestive tract, including biopsies, in the comfortably awake patient … in the office.  Manometry and reflux testing are also essential. These are all part of our specialty.

At present, esophageal cancer and precancer are epidemic, and it is our responsibility to screen our patients for potentially life-threatening neoplasia. As a matter of fact, attention to the lifestyle/dietary issues and needs of our patients also now needs to fall within our domain. It is time for otolaryngologists to become “integrated aerodigestive tract physicians” – otherwise we will continue to fragment our own patients’ medical care.

Recommended Reading

Gawande, Atul. The Cost Conundrum. New Yorker Magazine (June 1, 2009)

Koufman JA, Stern J Bauer M, “Science You Can Digest,” from Dropping Acid: The Reflux Diet Cookbook & Cure, pages 159-185, Brio Press, Minneapolis, 2010. ( Available on Amazon)

www.refluxcookbookblog.com (“The Missing Link”)

www.chronic-cough.net

A technological revolution has occurred in laryngology rendering many time-honored surgical procedures obsolete. Significant advances in flexible endoscopes, laser delivery systems, and topical anesthesia have made it possible to perform surgery and many other office-based laryngeal procedures safely, with excellent results, patient acceptance, and cost savings. Unfortunately, reimbursement issues still create financial disincentives to the widespread proliferation of remarkable clinical advancements.

Perspective on New Technology in Laryngology

Since introduction of the rigid, distal-lighted esophagoscope by Chevalier Jackson over 100 years ago, the evolution of endoscopic surgery has generally paralleled advances in illumination, optics, and instrumentation. Until the 1960s, most otolaryngologic endoscopy (e.g., laryngoscopy, bronchoscopy, esophagoscopy) was performed with the patient awake using rigid instruments and the techniques described by Jackson.

In the 1960s, use of the operating microscope for laryngeal surgery spawned a new generation of endoscopic instrumentation, including wide-bore laryngoscopes, microlaryngeal instruments, optical telescopes, and the carbon-dioxide (CO₂) laser with micro-manipulator. In addition, general anesthesia that allowed sharing of the airway (e.g., jet ventilation) became safer and more accepted.  Most operative (rigid) laryngoscopy and bronchoscopy, as well as esophagoscopy for foreign body removal, were done in the operating room under general anesthesia.

When flexible fiberscopes became available in the 1970s, otolaryngologists began to examine the aerodigestive tract (especially the larynx) of awake, unsedated patients in the office. Diagnostic transnasal flexible laryngoscopy (TFL) was routinely performed with only topical nasal anesthesia. Until relatively recently, however, because the optics of TFL were not as good as those provided by the optical telescopic view, the per oral examination method remained popular despite the fact that laryngeal biomechanics could not be assessed.¹

Introduced in 1999, the distal-chip camera for aerodigestive endoscopy created a new paradigm, and an instrument for transnasal esophagoscopy (TNE) was the first major advance.^2,3 The TNE endoscope offered brilliant illumination and unsurpassed, high-resolution imaging with a working channel.⁴ The 2.0mm channel permitted air-insufflation, suction, and the introduction of small, flexible forceps, and laser fibers. Advances in techniques of anesthesia and laser technology (that allowed laser energy to be delivered through a flexible fiber) quickly followed. Since the external diameter of that endoscope was 5.1mm, most patients could easily tolerate having it passed transnasally. Soon after introduction of the TNE endoscope, a smaller, 4.1 mm external diameter, endoscope without a working channel became available for TFL.

In the last decade, the focus has been on the growth and development of “minimally invasive” (less invasive) methods for both diagnosis and treatment, particularly targeting expensive, high-prevalence diseases. In many cases, it has been the combination of technologies that has resulted in new applications.^5-20 For the author, more than half of her laryngeal surgery is unsedated, office-based, laryngeal laser surgery (UOLS) using several different wavelength lasers alone or in combination.²⁰ The advantages of UOLS are shown in Table 1 below. In addition to being cost-saving,²¹ UOLS is generally preferred by most patients to traditional surgery.²²

It cannot be overemphasized that the emergence of UOLS as a viable technology was made possible by the confluence of three developments: (1) distal-chip quality imaging, (2) efficient anesthesia techniques for UOLS, and (3) development of several different wavelength lasers and fiber delivery systems.

Technique of Anesthesia for UOLS

Having a quick and effective anesthesia technique is one of the keys to successful UOLS. When we started out, we really didn’t know what to do. We were uncertain as to the minimum, let alone the optimum anesthesia that patients needed to comfortably tolerate such procedures. At first, we used the old techniques of Jackson that involved spraying the pharynx with a topical anesthetic, then insertion of xylocaine-soaked cotton balls on curved instruments into the piriform sinuses, followed by direct spraying of the endolarynx using TFL-guidance. This made the anesthesia procedure more difficult and time consuming than the surgery for both the doctor and the patient.

We also had patients breathe nebulized 4% xylocaine for 10-20 minutes, sometimes in combination with oral diazepam and/or topical throat spray. The nebulization method seemed to give variable levels of anesthesia; it worked well for some patients but not for others. The next alternative that we tried was performing bilateral superior laryngeal nerve blocks. When this worked really well, the patients coughed excessively because they tended to aspirate their own secretions; and when one or both injections didn’t find their mark, the patient complained of discomfort.  Again, this technique seemed too complex and unpredictable for everyday application. Indeed, we tried many combinations of methods before settling on what has become for us the simplest and most predictably effective method. The author mentions all of the above suboptimal methods in the hope of helping new UOLS surgeons avoid our trial-and-error learning curve. What is the technique we now recommend?

First, we spray the nose with an ephedrine and pontocaine solution and then put a cotton or new-gauze pack in one side of the nose. The author being right handed, with the viewing monitor to her right, routinely uses the right side of the patient’s nose unless it is obstructed. The nasal packing is left in for 10-20 minutes; and sometimes the patient will note that his or her incisors feel numb. Adequate nasal anesthesia is important. Actually, when patients occasionally do complain about discomfort during UOLS, it is usually due to nasal pain.  By the way, for TNE the above nasal anesthesia is all that is used for the vast majority of patients.

Second, the clinician should explain that the numbing process is quick and painless but that it is none-the-less unpleasant. We tell them that it is unnatural to have any liquid squirted into the larynx, because it will make them cough and sputter. This is assured as the right response, that is, the coughing and such disperses the anesthetic. Generally, three or four sprays of 4% xylocaine are needed. The standard TNE scope is 60 cm. long and the volume of the working channel is about 3.3 ml. That means if 5.0 ml of anesthetic is squirted through the TNE scope into the endolarynx approximately 1.7 ml of anesthetic will be delivered; the rest will be suctioned up.

The first squirt is delivered from above the palate; the second is aimed at the epiglottis and valleculae, and the third (and fourth) are squirted into the endolarynx. The author recommends having the patient phonate a sustained vowel and squirt at the end of the breath. That’s it, next the clinician can insert a laser fiber and go to work. It is worth noting that the posterior larynx is more difficult to anesthetize and that the patient will complain of discomfort about half of the time when having a vocal process granuloma removed.

Clinical Applications and Selection of Wavelength Laser for UOLS

For decades, the carbon-dioxide (CO₂) laser was the workhorse in laryngology. It was used mostly in the operating room with a small spot size for excision of lesions such as papillomas, granulomas, polyps, and carcinomas. In recent years, the CO₂ laser has been used sparingly for benign disease on the vocal fold striking zones due to potential scarring. Nevertheless, as a water-absorbing laser, it remains the gold standard for removal of most lesions not involving the free edge.

UOLS had its real origins with the pulsed-dye laser (PDL).^5,9 At 585nm, it is primarily absorbed by hemoglobin. UOLS it has been shown to be safe and effective, especially for RRP (recurrent respiratory papillomas).^12,18-20 A summary of the author’s approach to the laryngeal RRP patient is shown in Table 2. One of the chief advantages of the PDL wavelength is that both sides may be treated at the anterior commissure without significant risk of web formation. In addition, for certain lesions such as polypoid degeneration, it may be the wavelength laser of choice.²⁰

A hollow-core CO₂ laser fiber was introduced in 2004 and it has great potential application in the vaporization and/or excision of bulky lesions.²⁰ The first UOLS case done was that of a woman with extensive and obstructing laryngotracheal papillomas that filled the airway to the carina.²⁰ In that case, the PDL was insufficient to maintain the airway, and the CO₂ laser delivered by UOLS was life saving.  Later on, the CO₂ laser was used first to remove bulk of the disease, and then the PDL was used after to treat residual epithelial disease.

This is the laser team and the patient (Joyce Douglas); she had obstructing tracheal papillomas.

Different wavelength lasers have different properties based upon their absorption. The Thulium:YAG laser is actually intermediate between the CO₂ and the PDL in many ways. We have found it especially useful for the treatment of laryngotracheal amyloid.²⁰ The KTP and the PDL lasers are quite similar in their tissue absorptive characteristics.

Contained within this issue of Current Opinion, there are reported the experiences and opinions of several authors using different wavelengths. These emerging technologies are all part of an evolutionary process; and as of this writing, there is no one best laser. The author’s current wavelength selections/applications are shown in Table 3.

Table modified from: Koufman JA, Rees CJ, Frazier WD, Kilpatrick LA, Wright SC, Halum SL, Postma GN. Unsedated office-based laryngeal laser surgery: Review of 443 cases using three wavelengths. Otolaryngol Head Neck Surg 2007;137.

Current Limitations and Future Proliferation of UOLS

TNE and UOLS provide bone fide advances that simultaneously decrease morbidity and cost.^4,20-22 In spite of the rather obvious advantages over traditional surgery for some, not all, applications, these technologies have not proliferated as rapidly as might have been expected. There appear to be two reasons for this. First, there has been some resistance from providers and payers who may have economic interests in maintaining status quo technology, networks and/or referral patterns. And in some cases the issue is lack of training.

Second, the principal barrier to proliferation is inadequate reimbursement. While marginal profitability can justify making a capital investment, sure economic loss is an overwhelming deterrent. In the face of such economic disincentives, advanced technology like TNE and UOLS will stagnate. Hopefully, those issues will be resolved soon as the potential cost savings to society are tremendous, measured in millions, perhaps billions of dollars.

Conclusions

The spectrum of laryngological office-based procedures has expanded dramatically in the last decade since the advent of the distal-chip camera and new laser technology. These procedures are well-tolerated by patients and at the same time minimize morbidity and are cost saving. In the next generation, each of the advances shown in Table 4 will continue to proliferate.

References

1. Koufman JA, Radomski TA, Joharji GM, Russell GB, Pillsbury DC. Laryngeal biomechanics of the singing voice. Otolaryngol Head Neck Surg 1996;115:527-37.

2. Aviv JE, Takoudes TG, Ma G, Close LG.  Office-based esophagoscopy: a preliminary report.  Otolaryngol Head Neck Surg 2001: 125: 170-75.

3. Belafsky PC, Postma GN, Daniel E, Koufman JA.  Transnasal esophagoscopy.  Otolaryngol Head Neck Surg 2001: 125: 588-89.

4. Postma GN, Cohen JT, Belafsky PC, Halum SL, Gupta SK, Bach KK, Koufman JA. Transnasal esophagoscopy revisited (over 700 consecutive cases). Laryngoscope 2005;115:321-3. * Largest reported series by several pioneers in the field

5. Franco RA Jr, Zeitels SM, Farinelli WA, Faquin W, Anderson RR.  585-nm pulsed dye laser treatment of glottal dysplasia.  Ann Otol Rhinol Laryngol 2003: 112: 751-58. * Landmark report by leaders in the field

6. Hsiung MW, Kang BH, Su WF, Pai L, Wang HW.  Clearing microvascular lesions of the true vocal fold with the KTP/532 laser.  Ann Otol Rhinol Laryngol 2003: 112: 534-39.

7. Kanagalingam J, Hurley R, Gran HR, Patel A.  A new technique for the management of inaccessible anterior glottic lesions.  J Laryngol Otol 2003: 117: 302-6.

8. Peretti G, Piazza C, Bolzoni A, Mensi MC, Rossini M, Parrinello G, Shapshay SM, Antonelli AR.  Analysis of recurrences in 322 Tis, T1, or T2 glottic carcinomas treated by carbon dioxide laser.  Ann Otol Rhinol Laryngol 2004: 113: 853-58.

9. Zeitels SM, Franco RA Jr, Dailey SH, Burns JA, Hillman RE, Anderson RR.  Office-based treatment of glottal dysplasia and papillomatosis with the 585-nm pulsed dye laser and local anesthesia.  Ann Otol Rhinol Laryngol 2004: 113: 265-76.

10. Halum SL, Butler SG, Koufman JA, Postma GN.  Treatment of globus by upper esophageal sphincter injection with botulinum A toxin. ENT Journal 2005;84:74.

11. Clyne SB, Halum SL, Koufman, JA, Postma GN.   Pulsed-Dye laser (PDL) treatment of laryngeal granulomas.  Ann Otol Rhinol Laryngol 2005;114:198-201.

12. Zeitels SM, Akst LM, Burns JA, Hillman RE, Broadhurst MS, Anderson RR.  Office-based 532-nm pulsed KTP laser treatment of glottal papillomatosis and dysplasia.  Ann Otol Rhinol Laryngol 2006: 115: 679-85.

13. Zeitels SM, Akst LM, Burns JA, Hillman RE, Broadhurst MS, Anderson RR.  Pulsed angiolytic laser treatment of ectasias and varices in singers.  Ann Otol Rhinol Laryngol 2006: 115: 571-80.

14. Basterra J, Zapater E, Moreno R, Hernandez R.  Electrosurgical endoscopic cordectomy with microdissection electrodes: a comparative study with CO2 laser.  J Laryngol Otol 2006: 120: 661-64.

15. Hirano S, Yamashita M, Kitamura M, Takagita S.  Photocoagulation of microvascular and hemorrhagic lesions of the vocal fold with the KTP laser.  Ann Otol Rhinol Laryngol 2006: 115: 253-59.

16. Zeitels SM, Burns JA, Akst LM, Hillman RE, Broadhurst MS, Anderson RR.  Office-based and microlaryngeal applications of a fiber-based thulium laser. Ann Otol Rhinol Laryngol 2006: 115: 891-96.

17. Kutter J, Lang F, Monnier P, Pasche P.  Transoral laser surgery for pharyngeal and pharyngolaryngeal carcinomas.  Arch Otolaryngol Head Neck Surg 2007: 133: 139-44.

18. Hartnick CJ, Boseley ME, Franco RA Jr, Cunningham MJ, Pransky S.  Efficacy of treating children with anterior commissure and true vocal fold respiratory papilloma with the 585–nm pulsed-dye laser.  Arch Otolaryngol Head Neck Surg 2007: 133: 127-30.

19. Mouadeb DA, Belafsky PC.  In-office laryngeal surgery with the 585-nm pulsed dye laser (PDL).  Otolaryngol Head Neck Surg 2007: 137: 477-81.

20. Koufman JA, Rees CJ, Frazier WD, Kilpatrick LA, Wright SC, Halum SL, Postma GN. Unsedated office-based laryngeal laser surgery: Review of 443 cases using three wavelengths. Otolaryngol Head Neck Surg 2007;137. * Huge series with minor complication rate of 0.9% and a discussion of applications of different wavelength lasers

21. Rees CJ, Postma GN, Koufman JA. Cost savings of unsedated office-based laser surgery for laryngeal papillomas. Ann Otol Rhinol Laryngol 2007;116:45-48. ** First paper that attempts to quantify the potential cost savings of this type of office-based surgery

22. Rees C, Halum SL, Wijewickrama RC, Koufman JA, Postma GN.  Patient tolerance of in-office pulsed dye laser treatments to the upper aerodigestive tract.  Otolaryngol Head Neck Surg 2006: 134: 1023-7.

]]> http://www.jamiekoufman.com/2011/02/13/minimally-invasive-office-based-surgery-in-laryngology/feed/ 1 http://www.jamiekoufman.com/2011/02/12/dr-koufman-to-be-keynote-speaker-at-laryngology-disorders-update-course/ http://www.jamiekoufman.com/2011/02/12/dr-koufman-to-be-keynote-speaker-at-laryngology-disorders-update-course/#comments Sat, 12 Feb 2011 22:03:04 +0000 Jamie A. Koufman, M.D., F.A.C.S. http://www.jamiekoufman.com/?p=433 Dr. Jamie Koufman to be Keynote and Featured speaker at the LARYNGOLOGY DISORDERS UPDATE COURSE. Sponsored by Harvard Medical School Department of Otolaryngology, Massachusetts Eye & Ear Infirmary, Boston, Massachusetts, (May 19-20, 2011), Course Directors: Ramon Franco, Jr., M.D. & Phillip C. Song, M.D.

Lectures of Jamie Koufman, M.D., F.A.C.S., Director, Voice Institute of New York, 200 West 57^th Street, Suite 1203, New York, NY 10019, Tel: (212) 463-8014, Professor of Clinical Otolaryngology, Medical College of New York, jamie@voiceinstituteny.com; www.voiceinstituteofnewyork.com  (Note: PDFs provided for references with asterisks)

WILLIAM MONTGOMERY LECTURE: IN-OFFICE LARYNGOLOGIC SURGERY

Although the concept of office-based laryngeal surgery is old, its emergence as an essential component of contemporary laryngology has been recent. Indeed, within the last decade, the synergistic confluence of three technologies — (1) high-resolution distal-chip endoscopes with operating side-channels, (2) fiber-delivered angiolytic lasers, and (3) safe, efficient, and effective topical anesthesia — have made unsedated endoscopy the state of the art for the diagnosis and treatment of many laryngeal and aerodigestive tract conditions.

Unsedated, office-based laryngeal [laser] surgery (UOLS) is the preferred method for managing papillomas, hemorrhagic polyps, Reinke’s edema, most vascular lesions, leukoplakia, dysplasia, and epithelial malignancy. The morbidity, cost, and complication rates of UOLS are less, and the results are often superior to traditional surgical methods.

From a practical perspective, transnasal esophagoscopy (TNE), while not strictly a laryngeal procedure, also falls under the UOLS umbrella because of all the new office-based endoscopic procedures, TNE is the most often performed. TNE is indicated for patients with globus, dysphagia, laryngopharyngeal reflux, and GERD. The TNE scope is the endoscope most often used to perform other (laryngeal) office-based procedures in our specialty of otolaryngology.

This talk will also highlight some key elements in the evolution of aerodigestive tract endoscopy and surgery, the advantages and disadvantages of different wavelength lasers in laryngology, vocal fold injection augmentation, tracheobronchial procedures, the limitations of current technology, and some of the potential future applications of future technologies.

References

Koufman JA, Rees CJ, Frazier WD, Kilpatrick LA, Wright SC, Halum SL, Postma GN. Unsedated office-based laryngeal laser surgery: Review of 443 cases using three wavelengths. Otolaryngol Head Neck Surg 137:146-51, 2007.

Koufman JA. Introduction to office-based surgery in laryngology. Curr Opin Otolaryngol Head Neck Surg. 15:383-6, 2007.

Franco RA. In-office laryngeal surgery with the 585-nm pulsed dye laser. Curr Opin Otolaryngol Head Neck Surg 15:387-93, 2007.

Rees CJ, Halum SL, Wijewickrama RC, Koufman JA, Postma GN. Patient tolerance of in-office pulsed dye laser treatments to the upper aerodigestive tract. Otolaryngol Head Neck Surg. 134:1023-7, 2006.

Rees CJ, Postma GN, Koufman JA. Cost savings of unsedated office-based laser surgery for laryngeal papillomas. Ann Otol Rhinol Laryngol 116:45-48, 2007.

Amin MR, Postma GN, Setzen M, Koufman JA. Transnasal esophagoscopy: A position statement from the American Bronchoesophagological Association (ABEA). Otolaryngol Head Neck Surg 138:411-13, 2008.

Jobe BA, Hunter JG, Chang EY, et al. Office-based unsedated small-caliber endoscopy is equivalent to conventional sedated endoscopy in screening and surveillance for Barrett’s esophagus: a randomized and blinded comparison. Am J Gastroenterol 101:2693-703, 2006.

LARYNGOPHARYNGEAL REFLUX (LPR): WHAT YOU DON’T YET KNOW

The symptoms of gastroesophageal reflux disease (GERD) are heartburn and indigestion, but most people with laryngopharyngeal reflux LPR) have hoarseness, sore throat, globus, dysphagia, chronic cough, and post-nasal drip, but no heartburn. Because people with LPR often don’t have typical digestive GI symptoms, LPR is sometimes referred to as “silent reflux.”

Reflux (LPR/GERD) is epidemic! Since the 1970s reflux has increased an average of 4% per year. Today, 40% Americans (125 million people) have it, 22% with GERD and another 18% with LPR. Reflux also is affecting younger and younger patients. In a recent study, we reported that 37% of the 20-30-year-old age group had reflux.

Also since the 1970s, the prevalence of reflux-related esophageal adenocarcinoma has skyrocketed an alarming 850%. And during this same time period despite greater emphasis on esophageal surveillance by endoscopy, the mortality of esophageal cancer has increased seven-fold. Similarly, esophageal precancer (Barrett’s esophagus) rates now approach 10% of patients who undergo screening esophageal examination for LPR as well as for GERD.

Why such high rates of reflux disease, Barrett’s, and esophageal cancer? Amazing as it may seem, the answer is the high acidity of the contemporary American diet. Indeed, since mandated by the FDA in 1973, ascorbic, acetic, and citric acids have been used as the primary additives (“preservatives”) in all bottled and canned foods and beverages to discourage bacterial growth and prolong shelf life. By law, the pH of canned and bottled foods and beverages must be pH <4.

Topics also included in this presentation are the cell biology of LPR, including the stability and activity of human pepsin and its role is the pathogenesis of disease (including laryngeal cancer); analysis of the systemic failure of medical specialists (otolaryngology, gastroenterology, and pulmonology) to accurately diagnose and effectively treat LPR; and finally, advances in the diagnosis and treatment of LPR.

References

Koufman JA. The otolaryngologic manifestations of gastroesophageal reflux disease (GERD): A clinical investigation of 225 patients using ambulatory 24-hour pH monitoring and an   experimental investigation of the role of acid and pepsin in the development of laryngeal injury.Laryngoscope 101 (Suppl. 53):1-78, 1991

Koufman JA. Low-Acid Diet for Recalcitrant Laryngopharyngeal Reflux: Therapeutic Benefits and Their Implications. Ann Otol Rhinol Laryngol 120:281-287, 2011.

Koufman JA, Belafsky PC, Daniel E, Bach KK, Postma GN. Prevalence of esophagitis in patients with pH-documented laryngopharyngeal reflux. Laryngoscope 112:1606-1609, 2002.

Johnston N, Dettmar PW, Bishwokarma B, Lively MO, Koufman JA. Activity/stability of human pepsin: Implications for reflux attributed laryngeal disease. Laryngoscope. 117:1036-9, 2007.

Reavis KM, Morris CD, Gopal DV, et al. Laryngopharyngeal reflux symptoms better predict the presence of esophageal adenocarcinoma than typical gastroesophageal reflux symptoms. Ann Surg 239:849-56, 004.

Koufman JA, Block C. Differential diagnosis of paradoxical vocal fold movement. American Journal of Speech and Hearing. 17:327-34, 2008.

Johnston N, Bulmer D, Gill GA, Panetti M, Ross PE, Pearson JP, Pignatelli M, Axford A, Dettmar PW, Koufman JA. Cell biology of laryngeal epithelial defenses in health and disease: Further studies.Ann Otol Rhinol Laryngol 112:481-491, 2003.

Johnston N, Knight J, Dettmar PW, Lively MO, Koufman JA. Pepsin and carbonic anhydrase isoenzyme III as diagnostic markers for laryngopharyngeal reflux disease. Laryngoscope 114:2129-34, 2004.

Johnston N, Dettmar PW, Lively MO, Koufman JA. Effect of pepsin on laryngeal stress protein (Sep70, Sep53, and Hsp70) response: Role in laryngopharyngeal reflux disease. Ann Otol Rhinol Laryngol 115:47-58, 2006.

Knight J, Lively MO, Johnston N, Dettmar PW, Koufman JA. Sensitive pepsin immunoassay for detection of laryngopharyngeal reflux. Laryngoscope 115:1473-8, 2005.

Halum SL, Postma GN, Johnston C, Belafsky PC, Koufman JA. Patients with isolated laryngopharyngeal reflux are not obese. Laryngoscope 115:1042-5, 2005.

Belafsky PC, Postma GN, Koufman JA. The validity and reliability of the reflux finding score (RFS). Laryngoscope 111:1313-1317, 2001.

Smoak BR, Koufman JA. Effects of gum chewing on pharyngeal and esophageal pH. Ann Otol Rhinol Laryngol 110:1117-1119, 2001.

Westcott CJ, Hopkins MB, Bach KK, et al. Fundoplication for laryngopharyngeal reflux. J American College of Surgeons 199:23-30, 2004.

DIAGNOSIS AND MANAGEMENT OF VOCAL FOLD BOWING

For 25 years, the author has used transnasal flexible laryngosocpy (TFL) as the first and primary laryngeal examination method for patients with laryngeal and voice disorders. With TFL, laryngeal biomechanics can be routinely assessed. Under normal physiological circumstances, the vocal folds close along their lengths, like two hands clapping on a hinge.

Glottal closure problems are ubiquitous and yet they continue to be under-diagnosed and under-treated. Hyperkinetic biomechanics, muscle tension patterns, are seen in the majority of patients, particularly those with striking-zone pathology.

The focus of this presentation is the diagnosis and treatment of vocal fold weakness, bowing, paresis, atrophy, and presbylaryngis. For enhancing glottal closure, injection augmentation and medialization laryngoplasty are the author’s preferred methods. Patient and procedure selection criteria and timing of surgery are discussed as well as specific technical aspects.

References

Koufman JA. Laryngoplasty for vocal cord medialization: An alternative to Teflon. Laryngoscope 96:726-731, 1986.

Koufman JA. Surgical correction of dysphonia due to bowing of the vocal cords. Annals of Otol Rhinol Laryngol 98:41-45, 1989.

Koufman, JA, Postma, GN. Bilateral medialization laryngoplasty. Operative Techniques in Otolaryngology 10:321-324, 1999.

Koufman, JA, Postma, GN, Cummins, MM, Blalock, PD. Vocal fold paresis. Otolaryngol Head Neck Surg 122:537-541, 2000.

Amin MR, Koufman JA. Vagal neuropathy after upper respiratory infection: A viral etiology? Am J Otolaryngol 22:251-256, 2001.

Mikus JL, Koufman JA, Kilpatrick SE. Fate of liposuctioned and purified autologous fat injections in the canine vocal fold. Laryngoscope 105:17-22, 1995.

Duke SG, Salmon J, Blalock PD, Postma GN, et al. Fascia augmentation of the vocal fold: Graft yield in the canine & preliminary clinical experience. Laryngoscope 111:759-764, 2001.

Koufman JA, Belafsky PC. Unilateral or localized Reinke’s edema (pseudocyst) as a manifestation of vocal fold paresis: The paresis podule. Laryngoscope 111:576-580, 2001.

Koufman JA, Postma GN, Whang C, Rees C, Amin M, Belafsky P, Johnson P, Connolly K, Walker F. Diagnostic laryngeal electromyography: The Wake Forest experience 1955-1999. Otolaryngol Head Neck Surg 124:603-606, 2001.

Koufman JA, Little FB, Weeks DB. Proximal large-bore jet ventilation for laryngeal laser surgery. Arch Otolaryngol 113:314-320, 1987.

ENDOSCOPIC LARYNGEAL CANCER SURGERY

For flat and exophytic leukoplakia, erythroplakia, and even obviously cancerous lesions, neither the laryngeal examination that is performed in the office nor any radiographic assessment can accurately predict the extent, location, and histopathology of laryngeal neoplastic disease. Even high-definition videostroboscopy in the hands of an experienced examiner cannot distinguish in situ from microinvasive from deeply invasive carcinoma. This is because of complex laryngeal anatomy and because there is almost always a significant component of inflammation in association with vocal fold neoplasia. Whether or not the patient has a smoking history, severe coexistent inflammation is often the result of laryngopharyngeal reflux (LPR). The diagnosis and treatment of laryngeal cancer may be further confounded when tangential or partial thickness biopsies fail to provide a definitive diagnosis.

Within this perplexing context, the goals of treatment remain simultaneous cancer cure with voice preservation. Towards those ends, the laryngologist must have many resources at her/his disposal as well as a willingness to individualize every case. This discussion will focus on the management of in situ, T₁, and T₂ disease. The author’s management algorithm includes a broad array of diagnostic and therapeutic tools.

More than half of the cases are managed in the office with the pulsed-dye laser and almost all of the others with endoscopic resection in the operating room using the CO₂ laser with frozen section control of margins. Almost none of the author’s cases are subjected to radiation.

References

DeSanto LW. Selection of treatment for in situ and early invasive carcinoma of the glottis. Can J Otolaryngol 3:552-6, 1974.

Koufman JA. The endoscopic management of early squamous carcinoma of the vocal cord with the carbon dioxide surgical laser: Clinical experience and a proposed subclassification. Otolaryngol Head Neck Surg 95:531-537, 1986.

McGuirt WF, Blalock PD, Koufman JA. Comparative voice results after laser resection or irradiation on T1 vocal cord carcinoma. Arch Otolaryngol 120:951-955, 1994.

THE ART OF SURGICAL VOICE REHABILITATION AFTER CANCER TREATENT

After laryngeal cancer treatment, the combination of soft-tissue deficiency and striking-zone scarring can be vocally crippling. Conversely, some patients with unilateral partial vocal fold resections can have normal voices. Thus, the spectrum of voice outcomes after laryngeal cancer treatment extends from aphonia to normal voice depending on the degree of glottal insufficiency and the condition of the striking zone(s).

Surgical voice rehabilitation requires more innovation and creativity than almost any other area of operative laryngology. The author uses an array of surgical techniques including injection augmentation (alloplastc materials and lipoinjection), grafting (adipose tissue and fascia), laryngeal framework surgery, and even hemicricoidectomy. The latter procedure is for one of the most debilitating and difficult situations to repair, after hemilaryngectomy with sacrifice of the ipsilateral arytenoid.

For this lecture topic, the art of laryngeal reconstruction and rehabilitation after cancer treatment, case examples will be used to illustrate key points.

References

Amin MR, Koufman JA. Hemicricoidectomy for voice rehabilitation following hemilaryngectomy. Ann Otol Rhinol Laryngol 110:514-518, 2001.

Mikus JL, Koufman JA, Kilpatrick SE. Fate of liposuctioned and purified autologous fat injections in the canine vocal fold. Laryngoscope 105:17-22, 1995.

Duke SG, Salmon J, Blalock PD, Postma GN, Koufman JA. Fascia augmentation of the vocal fold: Graft yield in the canine and preliminary clinical experience. Laryngoscope 111:759-764, 2001.

Amin MR, Koufman JA. Endoscopic arytenoid repositioning for unilateral arytenoid fixation.

Laryngoscope 111: 44-47, 2001.

New York, NY (April 16, 2011) – It’s not sex in the city but noise in the city that causes problems for many Broadway performers and opera stars. Dr. Jamie Koufman, a medical doctor who specializes in the care of singers and actors, reports that city noise is a common cause of voice damage. “Every year on April 16^th, we celebrate ‘World Voice Day’ to call attention to the human voice and to the seriousness of voice problems—you don’t know how important your voice is until it’s gone,” says Dr. Koufman, Director of the Voice Institute of New York.

Dr. Koufman just completed a study “Determinants of noise level and noise level cycle in Manhattan bars and restaurants.”  She and her research group measured the noise levels in decibels (dBs) in different establishments and environments in New York City. And here’s the thing about the dB (noise) scale—it is logarithmic, which means that 70 dB is ten times as loud as 60 dB, and 80 dB (screaming) is ten times louder than 70 dB. For most people, a sustained noise level of 80-85 dB is the threshold when noise becomes uncomfortable, even unbearable.

New York Noise Facts in Common Environments, Places, and Situations (Measured in dBs)

Ambient noise in a very quiet apartment (no TV on)                              30-40 dB
Quiet one-on-one conversation (“confidential voice”) 2 people           40-50 dB
Television on, in a home (depending on how loud you like it)             50-65 dB
Quiet, Romantic with table-cloths and rugs-on-floor restaurant          55-65 dB
Moderately noisy, hustle-n-bustle New York bar/restaurant                 65-75 dB
Very Noisy, packed-with young-people in their 20s, bar                        75-90 dB
Busy New York street noise (including busses, trucks, etc.)                60-90 dB
Two noisy trains entering 42^nd Street Station at the same time          90-95 dB

Most of the time, we talk to each other at about 55-75 dB, but when we get in a noisy environment, we can easily crank up our volume to 80-90 dB. However, at that level, voice fatigue and strain can set in, and vocal cord damage can occur. Nowadays, many trendy New York Bars and clubs maintain a steady ambient noise level of 80-85 dB.

What are the factors that make a bar, club, or restaurant noisy? Young people! People under 30-years of age can scream at each other all night long without tiring out. Yes, they are louder than older people and they have more endurance. Then there is background music. Many bartenders keep turning the music volume up and up as more people come in. Thus, the ambient noise escalates all night until everyone is screaming. Finally, there is the “hardness” of the physical environment. Having a stone floor and metal ceiling, like some places downtown in the Meat Packing District, makes for an echo chamber. The longer sound can reverberate, the more the noise level builds. This is why a big group is less noisy outside where there is no roof overhead. Outside the sound doesn’t reverberate.

If your voice is important to you—say you are a young singer or actor just starting out—don’t take a job as a waiter or bartender at the trendiest and noisiest bar/restaurant in your city, as the next morning when you go to your important audition, your voice may be raspy, hoarse, and not its best. By the way, the I-Phone has an App SPL Meter that displays noise in dBs. This App is great to help you pick restaurants and monitor noise. For most restaurant diners over age 40, a noise level of more than 70-75 dB is more than a desirable level. By the way, you can always ask your server or bartender to turn down the music or even move you to a quieter table.

Finally, we have observed an interesting “noise level cycle.” In places packed with people, it gets louder and louder until some people just give up; then the noise level drops, unconsciously people who were yelling, adjust their voice volumes downward so that the room does get quiet(er) for a while. After a short period of less noise, noise starts to escalate again as people complete with nearby neighbors. Thus, even in a noisy establishment, the noise level cycles usually every 2-5 minutes, with a high/low variation of up to 20 dB. This is worth knowing if you have a voice or hearing problem, because you can choose to wait for a lull (low point) before speaking your piece.

VOCAL DECOMPENSATION

I have been practicing laryngology most of my life (www.voiceinstituteny.com), and throughout my career, I have had the luxury of uninhibited intellectual freedom. I have always sought to understand the pathophysiology of laryngeal function and dysfunction. I examined my first larynx in a patient with a mirror almost 40 years ago, and despite advances in the field of laryngology and the voice, I still strongly disagree with many aspects of the prevailing medical paradigm. And among colleagues, I have encountered tremendous resistance to both new ideas and to the principles of precision diagnostic. For example, for more than two decades, I have believed in précis diagnosis and to that end, I have helped develop several diagnostic methods.

Per oral laryngeal examination methods so alter laryngeal biomechanics that they do not permit assessment of glottal closure and laryngeal biomechanics. Only Transnasal flexible laryngoscopy with a high-resolution (distal-chip camera) optical system is adequate for physiologic laryngeal examination.

Laryngeal electromyography (LEMG) is the only diagnostic test that effectively evaluates the neuromuscular status of the larynx. In my opinion, it is an essential diagnostic tool. Nevertheless the vast majority of otolaryngologists and even laryngologists do not know how to perform LEMG, and the test isn’t even available to most clinicians. (I have done LEMG in my office daily since 1987 without a single complication.)

Reflux testing, including esophageal manometry is essential to diagnose many cases of laryngopharyngeal reflux; however state-of-the-art testing is unavailable to 90% of otolaryngologists.

Within a context of having used different diagnostic tools that most of my colleagues; I am offering here in this article my conceptual model of laryngology. It is a model in which most patients have cumulative and multifactorial disease. This is an article about vocal compensation.

Why and How Professional Singers and Actors Lose It

Even though voice problems in singers and actors seem to occur suddenly, in fact, they may start slowly over a prior period of months or years; and often in retrospect, there may have been protracted warning symptoms that were minimized or ignored. The “obvious” causes of voice problems may be bogus. Acute voice strain is infrequently the underlying cause of acute vocal collapse; although having a perennially vocally-demanding occupation is a key risk factor.

Note to the reader: I recognize that phonotrauma from chronic hard-use is a kingpin variable; however, the point of this article is that occult (hidden, undiagnosed) underlying neuromuscular and inflammatory diseases are often central to the process and progression of vocal destabilization,  independent of “vocal technique” and vocal abuse/misuse/overuse issues.

Many singers and actors blame themselves for “over-doing it” when something goes wrong. In taking the medical history of a Broadway performer, I am struck by how often I hear a string of self-deprecating non sequiturs that frequently end with, “and I know that I shouldn’t have done that.” “Thats” may refer to booze, marijuana, other drugs, dietary indiscretions, such as a chocolate binge or a pepperoni pizza, yelling or singing loudly, or singing/acting during a cold.

It is true that screaming can cause acute vocal fold hemorrhage or that a fudge-bomb brownie can exacerbate reflux laryngitis (laryngopharyngeal reflux, LPR); however, in truth most performers take good care of themselves most of the time; although vocal professional are often inappropriately enchanted by the magic of holistic and herbal medicine. Frequently, I have patients ask me about the benefits of vitamins, herbs, enzymes, acupuncture, etc. to treat their voices, especially for LPR, but to my knowledge, none have been shown to be therapeutic.

Help! I Lost My Voice

For performers, any significant voice loss is a medical emergency. But what brings a singer or actor to the office in a panic?  The most common bona fide out-of-the-blue precipitant of acute problems is the upper respiratory infection (URI). The medical term laryngitis — often mistaken as a synonym for hoarseness – generally refers to a viral infection of the larynx (voice box). Viral laryngitis can cause mild, moderate or severe hoarseness; it typically lasts 3-7 days; and it can be nasty enough to cause cancellation of performances by a sick singer. More often, however, the show can go on with some modifications in the program. Doctors sometimes use an injection of anti-inflammatory steroid to reduce vocal fold swelling, which may improve the voice for few days. Laryngitis accounts for few patients seen at the Voice Institute of New York. What are the underlying causes of voice disorders?

Voice Disorders Are Usually Multifactorial

Recently, I reviewed (IRB-approved protocol) the medical records of 80 unselected, consecutive of my patients with voice disorders. There were 31 males and 49 females with a mean age 56 years; and 81% (65/80) were professional voice users.

Eighty-eight percent (70/80) of the population had hyperkinetic biomechanics (muscle tension dysphonic) on transnasal flexible laryngoscopy (TFL). By clinical and/or pH-monitoring criteria 71% (57/80) had laryngopharyngeal reflux (LPR). Of those, it was the primary diagnosis in 40% (23/57) and an incidental, secondary diagnosis in 60% (34/57).

Excluding mild, asymptomatic presbylaryngis (“old age voice”), 55% (44/80) had neuromuscular disease. Of those, 7 patients had spasmodic dysphonia, 6 had vocal fold paralysis, and 26 had vocal fold paresis. It was the primary diagnosis in 52% (23/44) and it was an incidental, secondary diagnosis in 48% (21/44). Fifty percent (40/80) of the patients had histopathologic lesions including nodules, polyps, cysts, pseudocysts, papillomas, granulomas, dysplasia and carcinoma. Some lesions were incidental, e.g., some small granulomas.

The data of Table 1 indicate that the average patient had 2.68 different diagnoses. As mentioned, in some cases, paresis, reflux, or a vocal fold lesion were primary diagnoses, and in others cases, they were secondary or incidental findings (diagnoses).

Table 1: Multifactorial Causes of Voice Disorders (N = 80)

Hyperkinetic biomechanics (e.g., abnormal laryngeal tension)           88%

Inflammatory disease (e.g., reflux and respiratory infections)              75%

Neuromuscular disease (e.g., paralysis, paresis, SD, tremor)            55%

Neoplastic growths (e.g., polyps, nodules, papillomas, cysts)             50%

Total                                                                                                        268%

Interestingly, 28% (22/80) of the patients had onset of glottal closure symptoms that were associated with a self-identified precipitating event: 15 had a history of upper respiratory infection (URI); 7 dated the onset of symptoms to the time of endotracheal intubation (a breathing tube for surgery) or surgery of the head, neck, or thyroid.

In addition, over half of the vocal professionals dated the onset of symptoms to a performance event. However, while voice strain was reported to be “the precipitant” in many patients, those same patients were virtually always also found to other diagnoses (as shown in Table 1).

Vocal Decompensation and the Last Straw Principle

As it turns out, most singers and actors who present with seemingly sudden-onset voice problems actually have had preceding chronic symptoms that may have been minimized. Some of these often-ignored warning signs are summarized in Table 2.

Table 2: Warning Signs That the Voice / Larynx May Need Attention

Effortful or painful speaking
Vocal fatigue at the end of the day
Loss of the high range of the voice
Hoarseness of the speaking voice
Voice breaks in the singing mid-range
Chronic throat-clearing and/or too much throat mucus
Chronic or morning cough, awaking from sleep coughing
Difficulty swallowing and/or a sensation of a lump in the throat

Many vocal professionals wait until they experience acute decompensation before seeking medical attention. As you might expect, most voice problems are best prevented. While I do not wish to over-intellectualize here, Table 3 is my general theory (model) of life and vocal collapse.

Table 3: The Laws of Decompensation

1st Axiom:       Before: The composition of a system is in dynamic balance
1st Corollary:   Conflicting elements are held together by function and purpose

2nd Axiom:      Decompensation is preceded by often ignored warning signs
2nd Corollary:  During early destabilization, imbalance is assessable (measurable)

3rd Axiom:       Last straw principle: When threshold is exceeded, collapse occurs
3rd Corollary:   Recovery requires stabilization and repair of all essential elements

The Laws of Decompensation provide a loose framework for approaching the practice of laryngology, because for practical purposes, excluding congenital abnormalities and rare diseases, voice disorders have just five (interrelated) etiologies:

(1) Hyperkinetic laryngeal behaviors (aka muscle tension dysphonia)
(2) Inflammation
(3) Neuromuscular disease
(4) Neoplasia (including benign, malignant, and traumatic growths)
(5) Trauma, i.e., phonotrauma that  causes striking-zone pathology (nodules, polyps, cysts, and granulomas)

I refer to this as the HINNT model, and I try to evaluate each of those factors in every patient, every visit. As a result, I actively look for that which is still hidden, and I am willing to discuss potential trouble before it manifests, even though that makes some people uncomfortable.

The overarching principle is that vocal decompensation occurs when compensation fails. In other words, decompensation is a threshold event. Not only that, the interactions of (adaptive and maladaptive) behavioral vocal use patterns with vocal fold inflammation and glottal closure problems, are the common pathway to decompensation.

HINNT: Voice Disorders are Complex and Cumulative

Under normal circumstances, the vocal folds come together along their lengths, like two hands clapping on a hinge. Additionally, phonation (voicing) depends upon a steady stream of (subglottic) air pressure provided by the bellows of the lung/diaphragm apparatus.

Voice quality is largely dependant upon the symmetry of vibrating layered structures of vocal folds, and the glottis (the two vocal folds) acts in many ways like a double-reed instrument. The oscillation of the soft-tissue reeds should be symmetrical in both frequency and amplitude. That is the normal physiologic state.

In patients who develop vocal fold pathology, there is a common vicious cycle, a cascade of events: Increased laryngeal muscle tension leads to phonotrauma leads to increased vibratory vocal fold swelling and stiffness, which leads to further increases in laryngeal/neck muscle tension and subglottal driving pressures. This pressure-tension-trauma cycle escalates until further compensatory increases in subglottal pressure and muscle tension are no longer possible.

The term phonotrauma almost defines itself, “trauma of the vocal folds caused by phonation, vibration of the vocal folds to produce voice.” The striking-zones of the vocal folds by design impact each other on average thousands of times during one minute of speaking or singing. Is speaking and singing then intrinsically phonotraumatic?  If the striking-zones of the vocal folds are colliding millions of times a day, why doesn’t everyone have a voice problem?

The elements of the HINNT model are interactive. For example, patients with mild vocal fold paresis can manage for many months or years until they subsequently develop something else, too, like LPR. Table 4 lists common precipitants of vocal decompensation, the “last straw” list.

Table 4: Common Precipitants of Vocal Decompensation

Laryngopharyngeal reflux
Upper respiratory infection
Increasing vocal demands
Change of occupation
Endotracheal intubation
Head and neck surgery
Allergy and/or asthma

One of the greatest risk factors for vocal decompensation for singers (and actors, too) is success. How so? A singer/actor who is just barely surviving vocally doing a few performances per week may have to quadruple (or more) his or her voice demands, and thereby exceed the threshold for decompensation. This happens especially often to singers who go on tour with heavy performance schedules. Furthermore, it is really hard to eat a healthy diet when one is on tour. With travel and late-night eating, LPR frequently worsens, and this may be the “final straw” that precipiates vocal decompensation.

Laryngopharyngeal Reflux (LPR)

The term reflux literally means backflow from the Latin re- (back) and the verb fluere (to flow). LPR is the backflow of stomach (gastric) contents into the throat (the laryngopharynx). LPR is often silent, occurring without digestive symptoms such as heartburn or regurgitation; it does commonly cause hoarseness, difficulty swallowing, a sensation of a lump in the throat, too much throat mucus, and chronic cough. The reflux symptom index, a validated outcomes instrument, is shown in Appendix A. If the sum of your symptoms (the RSI) is <10, you may have LPR and you should consider seeing a doctor.

Most people with voice disorders have laryngopharyngeal reflux (LPR), and it is the commonest cause of hoarseness and other throat symptoms. Approximately half of voice patients have LPR. Usually LPR can be diagnosed by the laryngeal examination, but sometimes special testing is needed. LPR affects as tens of millions of Americans over age 50 years, and it commonly begins when people are in their thirties. Nevertheless, we do see LPR in young people, even in children and teens. (LPR is an important topic in laryngology and it has been the author’s main research interest for 25 years; several of my publications related to LPR may be found on my website.)

Vocal Fold Paresis

Vocal fold paresis refers to “partial paralysis” of the vocal folds. Such paresis may be associated with vocal fold weakness, thinning, atrophy, or bowing. In fact, I sometimes use the terms interchangeably; although strictly speaking there are differences. “Old age,” presbylaryngis, is associated with age-related vocal fold atrophy alone; whereas paresis implies a neuropathic (“sick nerve”) condition as the cause of muscle loss (atrophe). A post-viral vagal neuropathy that may be likened to Bell’s palsy of the larynx, appears to be a common cause of bilateral (both-sided) vocal fold paresis. Another common cause of vocal fold paresis is an idiopathic (unknown) cause.

The laryngeal findings of vocal fold paresis on videostroboscopy are asymmetrical vocal fold bowing, hypomobility (decreased mobility) of one or both arytenoids (the moving parts), and asymmetry of videostroboscopy. Unilateral increased vibratory amplitude, a floppy vocal fold, may be the most common finding of paresis, but the diagnosis of paresis requires laryngeal EMG (electromyography) for confirmation.

Vocal fold paresis is common; about half of my patients seeking medical attention for a voice disorder have it. The consequences of paresis are related its severity, which nerves and muscles are affected, and the degree of impairment of vocal fold closure. Superior laryngeal nerve paresis may be associated with loss of the high range of the voice; and recurrent laryngeal nerve paresis tends to be associated with loss of power and volume and vocal fatigue. Indeed, paresis is associated with other glottal closure symptoms such as odynophonia (painful speaking) as well. The glottal closure index is shown in Appendix B. If the sum of your symptoms is <10, you may have vocal fold paresis and you should consider seeing a doctor.

To reiterate: From a biomechanical point of view, people with paresis have to compensate for incomplete glottal closure by squeezing the vocal folds together using extra-laryngeal muscles. The increased work of compensatory behaviors leads to increased vocal fold tension, trauma, and stiffness; and consequently, subglottal driving pressures must be increased. Thus, a vicious cycle ensues in which increased vocal fold tension and stiffness requires increased driving pressures. At some point, increased sheering-forces in the striking-zone overwhelm tissue pliability and injury occurs. Indeed, most striking-zone pathology is the result of compensatory laryngeal behaviors and not simply the result of vocal misuse.

Conclusions

Professional singers and actors make high biomechanical demands on the larynx, and the development of phonotraumatic pathology appears to be multifactorial. The model of vocal decompensation presented in this article assumes that people generally compensate effectively for paresis and LPR reflux for as long as possible. The combination of effortful closure and tissue inflammation and its sequelae leads to phonotrauma., and the kind of striking-zone pathology that results from the paresis/LPR duo includes vocal nodules, polyps, cysts, and most of all sulcus (scarring).

Like the rest of the body, wear and tear on the vocal folds, is cumulative. In my experience, it is a rare vocalist or actor who has a completely normal laryngeal examination after age 40. The keys to career longevity appear to be good genetics, good scheduling, and all-around good preventive maintenance. The old adage about diet, exercise, and moderation applies here.

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APPENDIX A: THE REFLUX SYMPTOM INDEX (RSI)

APPENDIX B: THE GLOTTAL CLOSURE INDEX (GCI)

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