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2 Vol. 64, No. 4 2013

Northeast Florida Medicine

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VOLUME 64, NUMBER 4 Sleep Health, Winter 2013

Winter 2013

EDITOR IN CHIEF Raed Assar, MD (Chair)


MANAGING EDITOR Laura Townsend ASSOCIATE EDITORS Laura Armas-Kolostroubis, MD Abubakr Bajwa, MD, FCCP Kim Barbel-Johnson, MD Ruple J. Galani, MD

Winter CME

Kathy Harris (Alliance) Sunil Joshi, MD (Vice Chair) James J. Joyce, MD Daniel Kantor, MD Neel G. Karnani, MD Mobeen Rathore, MD James St. George, MD

EXECUTIVE DIRECTOR Bryan Campbell DCMS FOUNDATION BOARD OF DIRECTORS Eli N. Lerner, MD, President Mobeen Rathore, MD, President-Elect Daniel Kantor, MD, Vice President Raed Assar, MD, Secretary Sunil Joshi, MD, Treasurer Ashley Booth Norse, MD, Im. Past President Cynthia Anderson, MD Elizabeth Burns, MD Paul Chappano, MD Rui Fernandes, MD Ruple J. Galani, MD E. Rawson Griffin, MD Robert G. Harmon, MD Mark L. Hudak, MD TraChella Johnson Foy, MD James J. Joyce, MD Neel G. Karnani, MD Harry M. Koslowski, MD Stephen E. Mandia, MD Jesse P. McRae, MD Jason D. Meier, MD Nathan P. Newman, MD Alexander Pogrebniak, MD James St. George, MD

Obstructive Sleep Apnea


Vandana Seeram, MD; Tracy Ashby, DO; Jesse Onyenekwe, MD; Adil Shujaat, MD; Abubakr A. Bajwa, MD, FCCP; Lisa Jones, MD and James D. Cury, MD

Obstructive sleep apnea (OSA) is a chronic condition which is common in the primary care setting. With an estimated prevalence of two to four percent and many associated comorbidities, it is important to identify and treat patients early. Obesity, snoring and daytime sleepiness are classic signs of OSA. However, all patients do not present this typically, so providers must be vigilant in screening and treating patients.



From the Editor’s Desk



Patient Page

Residents’ Corner

57 Trends in Public Health 58 From the President’s Desk Northeast Florida Medicine is published by the DCMS Foundation, Jacksonville, Florida, on behalf of the County Medical Societies of Duval, Clay, Nassau, Putnam, and St. Johns. Except for official announcements from the County Medical Societies, no material or advertisements published in NEFM are to be seen as representing the policy or views of the DCMS Foundation or its colleague Medical Societies. All advertising is subject to acceptance by the Editor in Chief. Address correspondence and advertising to: 1301 Riverplace Blvd. Suite 1638, Jacksonville, FL 32207 (904-355-6561), or email:

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Obstructive Sleep Apnea: One Diagnosis With Many Implications Abubakr A. Bajwa, MD, FCCP Guest Editor

Out of Sleep Lab Testing for Obstructive Sleep Apnea


Vichaya Arunthari, MD and Kamonpun Ussavarangsi, MD

CPAP Adherence: A Review


Furqan S. Siddiqi, MD; Adil Shujaat, MD; James D. Cury, MD and Abubakr A. Bajwa, MD, FCCP

Surgery for Obstructive Sleep Apnea Iman Naseri, MD, FACS


A Review of Pulmonary Hypertension in Obstructive Sleep Apnea


Adil Shujaat, MD; Abubakr A. Bajwa, MD, FCCP; Vandana Seeram, MD; Lisa Jones, MD and James D. Cury, MD

Cardiovascular Effects of Sleep Apnea


Vandana Seeram, MD; Adil Shujaat, MD; Abubakr A. Bajwa, MD, FCCP; Lisa Jones, MD and James D. Cury, MD

Overlap Syndrome: A Review of Current Literature


Kavita Pal, MD; Amit Babbar, MD; Amita Singh, MD and Ankur Girdhar, MD

Pediatric Obstructive Sleep Apnea Rahul K. Kakkar, MD, FCCP, FAASM


Northeast Florida Medicine Vol. 64, No. 4 2013 3

Patient Page

Symptoms & Risk Factors of Sleep Apnea The symptom most commonly associated with sleep apnea is snoring, but not everyone who snores has sleep apnea. Symptoms of sleep apnea include: • Loud or frequent snoring • Choking or gasping while you sleep • Pauses in breathing • Morning headaches • Excessive daytime sleepiness • Insomnia due to difficulty staying asleep • Waking up with dry mouth or a sore throat • Frequent need to urinate during the night • Trouble concentrating • Memory or learning problems • Moodiness, irritability or depression

A common misconception is that sleep apnea only affects older, overweight men. This widely-held assumption is wrong: anyone can have sleep apnea, regardless of gender, age or body type. Risk Factors of sleep apnea include: • Excess weight – An adult with a BMI of 25 or higher is considered to be overweight. Your risk of sleep apnea increases with the amount of excess body weight. • Large neck size (>17 inches for men, > 16 inches for women) – A large neck will have more fatty tissue that can block your airway. • Older age (40+ for men, 50+ for women) – Sleep apnea occurs more often in older adults, especially people older than 60. • Being male – Men have twice the risk having sleep apnea compared to women • Smoker – Smokers have a higher risk of sleep apnea • Hypertensive – High blood pressure is very common in people with sleep apnea • Family history – Sleep apnea can appear more often among family members. This may be a result of either inherited traits or common lifestyles.

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From the Editor’s Desk

Times of Change This Northeast Florida Medicine Journal edition will be issued from the new headquarters of the Duval County Medical Society (DCMS). The old location carried a certain sentimental value and the decision to move was painful for many of our members. However, the decision was necessary to protect the long term financial viability of DCMS. Change is a constant. This editorial will highlight some of the great medical discoveries which occurred during the past 160 years since the founding of DCMS. It is hoped that this review will highlight the case for change as DCMS moves forward in serving its community. While physicians in North Florida have not changed their tradition of caring for their patients, the science and practice of Raed Assar, MD, MBA medicine have significantEditor-in-Chief ly changed for the better.

(EKG) in 1913. Edward Mellanby discovered that rickets was due to lack of vitamin D in the diet in 1921. Insulin was used to treat diabetes in 1922.

In the same year of the founding of DCMS (1853), Charles Pravaz and Alexander Wood developed the syringe. It is hard to imagine medicine without the syringe. In 1857, Louis Pasteur discovered the fermentation process. In 1867, Joseph Lister described the use of antiseptic surgical methods. This allowed physicians to reduce the risk of surgical infections and again was a major advancement for medicine. In 1870, both Robert Koch and Louis Pasteur formulated the germ theory of disease. The development of the anthrax and rabies vaccines by Louis Pasteur came in 1881 and 1882. The anthrax vaccine had a tremendous economic impact on the world by saving livestock from the devastating effect of this disease. In 1882, Koch discovered the TB bacillus.

In 1963, Thomas Fogarty invented the balloon embolectomy catheter. The measles and mumps vaccines were developed in 1964 and 1967 respectively. Dr. Christiaan Barnard performed the first human heart transplant in 1967.

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Wilhelm Conrad Roentgen discovered X-rays in 1895. This changed the practice of medicine and surgery forever. In 1896 and 1897, typhoid fever and bubonic plague vaccines were produced. Felix Hoffman produced aspirin in 1899. Karl Landsteiner described the classification of blood types into A, B, AB, and O groups in 1901. Paul White used the electrocardiograph

Then, the discovery of penicillin by Alexander Fleming happened in 1928. Yellow fever vaccine was introduced in 1935. In that same year, Percy Julian produced physostigmine for glaucoma and cortisone for rheumatoid arthritis. In 1937, Bernard Fantus established the first blood bank in Chicago. Karl Dussik presented the medical ultrasound in 1942. Selman Waksman discovered streptomycin in 1943. The first influenza vaccine was introduced in 1945. In 1950, John Hopps invented the first cardiac pacemaker and then Paul Zoll applied electric charges externally to the chest to resuscitate two patients in 1952. In the same year, Jonas Salk developed the first polio vaccine. Rosalind Franklin used X-ray diffraction to study the structure of the DNA followed by James Watson’s and Francis Crick’s early description of the structure of the DNA. In 1954, Gertrude Elion developed the first effective drug to treat leukemia, 6-mercaptopurine, which was a major stepping stone in the fight against cancer. In the same year, Joseph Murray performed the first kidney transplant.

The world of medicine was in for another game changer in 1975 when Robert Ledley invented the CT scan. It changed medicine, surgery, and emergency medicine greatly. The first test-tube baby was born in 1978. Smallpox was eradicated in 1980. The hepatitis B vaccine was developed in 1981. The HIV virus was identified in 1983. Alec Jeffreys developed a genetic fingerprinting method in 1984. Many of these changes also occurred during periods of significant turmoil, war, or change in the world. Regardless, medicine was moving forward and contributing positively by saving lives. As DCMS moves its headquarters and undergoes changes, it will continue to fulfill its mission of “helping physicians care for the health of our community.” Please continue to support this medical society through your membership and participation. Thank you.

Dr. Assar is Aetna’s Medical Director for North Florida. Articles or opinions provided by Dr. Assar do not necessarily reflect the views of Aetna. DCMS online . org

Northeast Florida Medicine Vol. 64, No. 4 2013 5

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6 Vol. 64, No. 4 2013

Northeast Florida Medicine

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BECOME A PARTNER IN MEDICINE The Duval County Medical Society’s Partners in Medicine program offers several different options for getting involved with the DCMS and its members including: advertising in our quarterly journal (Northeast Florida Medicine), advertising in the Take a look at who is already a Partner in Medicine: PIM LEVELS INCLUDE:

DCMS Membership Directory, exhibiting at our annual meeting and/or supporting an educational or general membership meeting!

PHYSICIAN LEVEL ................................................ $10,000

FELLOWSHIP LEVEL ............................................. $5,000

Duval County Medical Society

RESIDENT LEVEL ....................................................$2,500

PARTNER LEVEL...................................................... $1,000

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To learn more about becoming a Partner in Medicine, contact Bryan Campbell, DCMS Executive Director, at or by calling 904.355.6561. Northeast Florida Medicine Vol. 64, No. 4 2013 7

Residents’ Corner: Mayo Clinic Graduate School of Education

Editor’s Note: In an effort to connect more Duval County Medical Society members with residents, in each 2013 issue there will be a “Residents’ Corner” with information about a residency program in the area, details about research being done and/or a list of achievements/accomplishments of the program’s residents. This “Residents’ Corner” features the Mayo Clinic Graduate School of Education.

By William Palmer, M.D. Overview of Residency Program Mayo Clinic School of Graduate Medical Education was one of the first medical specialty teaching programs in the world, with more than 24,000 graduates of residencies and fellowship programs across all medical and surgical specialties. In 1986, Mayo Clinic in Jacksonville, Fla. became Mayo’s first campus outside of Rochester, Minn.. Mayo Clinic hospital, which recently completed the initial phase of a $100 million expansion to 304 beds, has 22 operating rooms and offers care in 20 medical and 15 surgical specialties, and also includes a full service Emergency Department. An additional $16.7 million has been used to construct a new outpatient primary care clinic on Gate Parkway in Jacksonville that houses 24 physicians and supporting staff. Currently at Mayo Clinic in Florida, there are more than 160 residents and fellows in training, and 300+ students total when including pharmacy and medical students. Residents and fellows are allotted further clinic opportunities at nearby institutions including Nemours Children’s Clinic, Wolfson Children’s Hospital, University of North Florida, UF Health Jacksonville, and the Jacksonville Naval Hospital. Resident Research A cornerstone of Mayo Clinic, medical research is highly encouraged and supported by the institution and staff physicians. Trainees are deeply involved in research that not only advances medical knowledge leading to new therapies, but also quality improvement projects that enhance the efficiency of delivery of patient care. Below are a few examples of ongoing research: • Gastroenterology Fellow Victoria Gomez, M.D. was awarded the 2012 National Community Outreach Video of the Year by the American Society of Gastrointestinal Endoscopy for her educational film about screening colonoscopy. (

• Hematology/Oncology Fellow Jennifer Crozier, M.D. was highlighted in multiple national news outlets including the Wall Street Journal and interviewed on National Public Radio regarding her recent publication in Cancer on HER2+ breast malignancy. • Internal Medicine Resident David Cangemi, M.D. recently published a retrospective analysis of small bowel tumor diagnosis with double balloon enteroscopy in Clinical Gastroenterology and Hepatology. Resident Community Outreach Through the Mayo Fellows Association training organization, Mayo Clinic residents and fellows are extremely active in the local community, providing their time and clinical expertise to those in need. Here are several examples of their activities: • A yearly can-food drive for Second Harvest Food bank • A yearly holiday clothing drive for Mission House of Jacksonville • Annual golf tournament for The Cystic Fibrosis Foundation of America • Campus-wide blood drive for The Blood Alliance • Benefit events for the WeCare organization of Jacksonville Mayo History and Focus From its humble beginnings as a family venture between a father and his two sons, Mayo Clinic eventually became America’s first integrated group practice; a model that is now the standard in the United States. Mayo Clinic’s three-shield logo represents the practice’s three primary focuses; first and primary to the organization is the patient care practice, represented by the central shield and primary statement of the organization that “the needs of the patient always come first.” The other two shields represent the areas of education and research.

• Internal Medicine resident David Snipelisky, M.D. recently published on the value of the troponin post-operatively following orthotopic liver transplantation in Journal of Transplantation.

William Palmer, M.D. is a PGY-4 Fellow in the Department of Gastroenterology and Hepatology at Mayo Clinic in Florida. He is currently completing a hybrid program in Gastroenterology and Transplant Hepatology, with plans to continue further clinical and research work in the area of liver transplantation.

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Guest Editorial

Obstructive sleep apnea: One diagnosis with many implications In this issue of Northeast Florida Medicine, we discuss a very important subject. Obstructive sleep apnea remains very prevalent and remains under diagnosed. The implications of untreated obstructive sleep apnea go beyond the short term effects such as fatigue, tiredness and sleepiness. Untreated obstructive sleep apnea leads to a number of health related issues including increased cardiovascular morbidity and mortality. There have significant advances in diagnostic and therapeutic approaches to manage sleep apnea. In addition the incidence of sleep apnea in pediatric population also seems to on the rise. Continuous Positive Airway Pressure (CPAP) therapy Abubakr A. Bajwa, MD, FCCP remains the gold standard, Guest Editor however a number of patient either don’t tolerate it or are no adherent to it. Recognizing and managing patients who do not tolerate CPAP therapy is a dilemma that every sleep medicine practitioner deals with on d a daily basis. In this issue, Dr. Vandana Seeram and colleagues write a general overview of sleep apnea for a general practitioner. Advances in diagnostic technique have led to home sleep testing by a variety of methods. With an increasing number of insurance companies mandating home sleep studies, familiarization with this form of testing is necessary for any practitioner. Dr. Vichaya Arunthari provides insight into the out of lab sleep testing and the benefits and pitfalls related to it. Not only it is important to diagnose sleep apnea but even more is to monitor patients with sleep apnea to ensure compliance. Compliance with CPAP for sleep apnea remain notoriously low due to a number of factors and Dr. Furqan Siddiqi and I address the issues related to compliance and steps that can be taken to improve compliance and adherence to therapy for sleep apnea. When CPAP therapy fails or not tolerated sometimes surgical options are explored and Dr. Iman Naseri discusses those options in his article exploring surgical management of obstructive sleep apnea.

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The issue also addresses some important cardiovascular consequences of sleep apnea with Dr. Adil Shujaat discussing pulmonary hypertension in sleep apnea. Pulmonary hypertension is being increasingly recognized primarily because of advances in echocardiographic techniques and increased awareness. With an array of therapies available for treating pulmonary hypertension it is important to diagnose and treat this devastating disease early. Clearly diagnosing and treating sleep apnea reduces long term fatal and non-fatal cardiovascular events in this population. Dr. Vandana Seeram reviews this in detail in her second article for this issue. Dr. Ankur Girdhar discusses overlap Syndrome. Finally, Dr. Rahul Kakkar’s detailed review of sleep apnea in pediatric population sheds light on evaluation, diagnosis and management in children. We hope you find this issue informative and insightful. My sincere thanks to everyone who has participated in shedding light on this important topic. Abubakr A Bajwa MD FCCP

Renew your CMS membership for 2014 by visiting

Northeast Florida Medicine Vol. 64, No. 4 2013 9

Northeast Florida Medicine 2014 Advertising Prospectus

Northeast Florida Medicine is published quarterly by the DCMS Foundation on behalf of the Medical Societies of Duval, Clay, Nassau, Putnam and St. John’s Counties, with print distribution to more than 2,000 Northeast Florida physicians and affiliated healthcare professionals, journal content is posted on our website, (, and is serviced by Google and Yahoo search engines. Rates below are effective 1st Quarter 2014 issue of Northeast Florida Medicine and throughout 2014.

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Display Format: High resolution PDF (300+ dpi). Send your PDF ad via email to Color ads should be CMYK format. Plan for ¼” bleed space on all sides of ad. 2014 Production Schedule: Spring (Cardiology) - Ad due December 1, 2013 Summer (Rheumatology) - Ad due April 1, 2014 Autumn (Dermatology) - Ad due July 1, 2014 Winter (Urology) - Ad due September 19, 2014

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Advertising Policy: Northeast Florida Medicine is not responsible for statements and opinions of authors or the clai made by advertisers. The appearance of advertising does not guarantee or endorse the claims of advertisers, & acceptance of advertising is subject to approval. Delinquent invoice may result in removal of advertising. Ads cancelled after closing date are subject to a 50% cancellation fee. Invoices are sent prior to print.

10 Vol. 64, No. 4 2013

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Sleep Health Section

Obstructive Sleep Apnea: A General review for the Primary Care Physician Background:

The Duval County Medical Society (DCMS) is proud to provide its members with free continuing medical education (CME) opportunities in subject areas mandated and suggested by the State of Florida Board of Medicine to obtain and retain medical licensure. The DCMS would like to thank the St. Vincent’s Healthcare Committee on CME for reviewing and accrediting this activity in compliance with the Accreditation Council on Continuing Medical Education (ACCME). This issue of Northeast Florida Medicine includes an article, “Obstructive Sleep Apnea: A General review for the Primary Care Physician” authored by Vandana Seeram, MD, which has been approved for 1 AMA PRA Category 1 credit.TM For a full description of CME requirements for Florida physicians, please visit Faculty/Credentials: Vandana Seeram, MD is Assistant Professor, Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine at the University of Florida, College of Medicine Jacksonville.

Objectives: 1. 2. 3.

Identify the common risk factors and conditions associated with obstructive sleep apnea (OSA). Evaluate via screening tools, patients who are at risk for having OSA, and those who should be referred for further testing. Evaluate the patient’s compliance to their treatment regimen as well as possible causes for non-compliance

Date of release: Dec. 1, 2013

Date Credit Expires: Dec. 1, 2015

Estimated Completion Time: 1 hour

How to Earn this CME Credit: 1.

Read the “Obstructive Sleep Apnea: A General review for the Primary Care Physician” article, complete post-test following the article and email your test to Patti Ruscito at or 904.353.5848.


Go to to read the article and take the CME test online.


All non-members must submit payment for their CME before their test can be graded.

CME Credit Eligibility:

A minimum passing grade of 70% must be achieved. Only one re-take opportunity will be granted. A certificate of credit/completion will be emailed within four to six weeks of submission. If you have any questions, please contact Patti Ruscito at 904.355.6561 or

Faculty Disclosure:

Vandana Seeram, MD reports no significant relations to disclose, financial or otherwise with any commercial supporter or product manufacturer associated with this activity.

Disclosure of Conflicts of Interest:

St. Vincent’s Healthcare (SVHC) requires speakers, faculty, CME Committee and other individuals who are in a position to control the content of this educations activity to disclose any real or apparent conflict of interest they may have as related to the content of this activity. All identified conflicts of interest are thoroughly evaluated by SVHC for fair balance, scientific objectivity of studies mentioned in the presentation and educational materials used as basis for content, and appropriateness of patient care recommendations.

Joint Sponsorship Accreditation Statement

This activity has been planned and implemented in accordance with the Essential Areas and policies od the Accreditation Council for Continuing Medical Education through the joint sponsorship of St. Vincent’s Healthcare and the Duval County Medical Society. St. Vincent’s Healthcare designates this educational activity for a maximum of 1 AMA PRA Category 1 credit. TM Physicians should only claim credit commensurate with the extent of their participation in the activity.

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Northeast Florida Medicine Vol. 64, No. 4 2013 11

Sleep Health Section

Obstructive Sleep Apnea: A General review for the Primary Care Physician Vandana Seeram, MD; Adil Shujaat, MD; Abubakr A. Bajwa, MD, FCCP; Lisa Jones, MD and James D. Cury, MD Division of Pulmonary, Critical Care and Sleep Medicine, University of Florida College of Medicine, Jacksonville, FL Tracy Ashby, DO and Jesse Onyenekwe, MD

Division of Internal Medicine, University of Florida College of Medicine, Jacksonville, FL

Abstract: Obstructive sleep apnea (OSA) is a disease characterized by intermittent and repetitive narrowing of the airway during sleep. Risk stratification can be accomplished by identifying key history and physical examination findings which warrant further evaluation. The diagnosis of sleep apnea must be made before the initiation of treatment to correctly identify patients who should benefit from treatment, and monitor the risks associated with morbidity and mortality of OSA. Available treatments include behavioral, medical and surgical options. Primary care physicians can have a major impact on the morbidity and mortality associated with OSA through identification of high risk patients, timely diagnosis, and routine assessment of treatment and compliance.


AHI = 0–5 Normal range AHI = 5–15 Mild sleep apnea

Obstructive sleep apnea (OSA) is a chronic condition which is common in the primary care setting. With an estimated prevalence of two to four percent and many associated comorbidities, it is important to identify and treat patients early.1 Obesity, snoring and daytime sleepiness are classic signs of OSA. However, all patients do not present this typically, so providers must be vigilant in screening and treating patients. Untreated sleep apnea has been shown to cause substantial cognitive and cardiovascular morbidity and mortality.2 It is an independent risk factor for stroke, hypertension, cardiac ischemia, arrhythmias, pulmonary hypertension, insulin resistance, epilepsy and perioperative complications. Studies have also revealed the risk of motor vehicle accidents in OSA was increased two-fold.3 Recognition of risk factors, utilization of screening techniques, timely diagnosis and treatment, and monitoring of compliance are essential aspects of managing this chronic disorder. Here we attempt to give a general overview of OSA as it applies to the primary care physician (PCP).

Address correspondence: Vandana Seeram, MD, University of Florida Health, 655 West 8th ST, Suite 7-088, Jacksonville, FL 32209. Phone: (904) 244-4075 / Fax: (904) 244-5047 E-mail: 12 Vol. 64, No. 4 2013

OSA is caused by repeated collapse of the upper airway during sleep, which leads to sleep disturbance, hypoxemia and hypercapnia. The apnea-hypopnea index (AHI) is used to diagnose obstructive sleep apnea. Apnea is defined as absence of airflow for 10 seconds or more, whereas hypopnea is defined as reduced airflow by 30 to 50 percent with arousal or decreased oxygen saturation by three to four percent. The summation of apnea and hypopnea events per hour determines the apnea-hypopnea index (AHI). OSA is defined as an AHI of greater than five. Severity of OSA can further be categorized into:4

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AHI = 15–30 Moderate sleep apnea AHI > 30 Severe sleep apnea Overnight polysomnography (PSG) is the best test for calculating the apnea hypopnea index and remains the gold standard for diagnosis. It uses multiple modalities to evaluate physiologic variables during sleep. More recently testing with portable monitors and split night study has become more popular. With portable monitors, airflow, respiratory effort, and oxygen saturation are collected to calculate the respiratory disturbance index (RDI) per hour rather than an AHI. This is because portable monitors do not permit identification of actual sleep time.3 Prior to referral for diagnostic testing, practitioners should perform a comprehensive evaluation which allows them to risk stratify the patients likelihood of OSA and determine severity of symptoms.

Comprehensive Evaluation By collecting a brief sleep history for all patients, identifying at risk patients, and obtaining more detailed information for patients with symptoms of OSA, practitioners will have a comprehensive approach to screening for OSA. Knowledge of common risk factors and associated conditions is paramount to this evaluation. Well established risk factors include obesity, advanced age, male gender, anatomic airway abnormalities, alcohol consumption, and tobacco use. Alcohol contributes to apnea by DCMS online . org

Sleep Health Section

Figure 1 relaxing the upper airway dilator muscles, while smoking leads Stepwise approach to evaluation and diagnosis of to inflammation in the upper airway affecting its structure and to evaluation and diagnosis of patients with suspected OSA function.5 Associated conditions include congestive heartFigure failure1. Stepwise approachpatients with suspected OSA (CHF), atrial fibrillation, hypertension, diabetes mellitus, ischemic heart disease, epilepsy, and stroke.1,3-6 Practitioners should keep these risk factors and conditions in mind when collecting Positive signs and symptoms of a brief sleep history on all patients. sleep apnea Risk stratification can be accomplished by identifying key history and physical examination findings which warrant further evaluation. The main symptoms of OSA are loud snoring, fatigue and daytime sleepiness. Some people, however, have no symptoms, have never been observed to be snoring, or having witnessed apneas. As such, a person may be slow to recognize that there is an underlying problem. Other common signs and symptoms include restless sleep, awakening with choking, gasping or a feeling of being smothered, morning headaches, dry mouth or sore throat on awakening, nocturia, awakening feeling unrested or groggy with difficulty concentrating and low energy levels during the day. 1,4,5 Some key physical exam findings include obesity (BMI >30), increased neck circumference (>17 inches for male or >16 inches for female), and structural abnormalities.1,4 Craniofacial abnormalities include retrognathia, tonsilar hypertrophy, high arched palate, nasal polyps, turbinate hypertrophy, Mallampati score of three or four, and upper airway narrowing.1 After a PCP has an index of suspicion, risk assessment followed by objective testing are used to diagnose obstructive sleep apnea.

Diagnosis Many clinical prediction models have been developed based on key findings from history and physical exam to aid in the diagnosis of OSA and improve the diagnostic accuracy of objective testing.7-11 These screening tools utilize highly associated variables such as BMI, neck circumference, snoring, choking during sleep, etc. The more popular and most studied include the Berlin questionnaire, Wisconsin sleep questionnaire, STOP questionnaire, and STOP-BANG questionnaire.12 Of these, the STOP-BANG questionnaire has been validated for its ease of use and high sensitivity for moderate to severe OSA (Table 1, page 14).13 These clinical prediction models have been found to have reasonably high sensitivities (76 to 96 percent), but relatively low specificities (13 to 54 percent).14 Therefore, they can help guide a primary care physician in identifying potential patient that might benefit from further testing, but should not replace clinical assessment. Once high risk patients have been identified, physicians should proceed with objective testing in a timely manner. The diagnosis of sleep apnea must be made before the initiation of treatment to correctly identify patients that should benefit from treatment, and monitor the risks associated with morbidity and mortality of OSA. Also, initiation of treatment before diagnosis would not identify the severity of the disease which is needed to make appropriate treatment decisions. The gold standard for

DCMS online . org

Screening questionnaire

High risk assessment

Low risk assessment

Objective testing

High Index supsciion

Comorbid medical conditions



Polysomnograph y

Portable Monitoring



Polysomnograph y

Investigate for other causes and follow patient clincially

the diagnosis of OSA is polysomnography. Polysomnography is a comprehensive recording of the physiological changes that occur during sleep. During a full night’s sleep, it provides information on eye movement (EOG), brain function (EEG), muscle tone and contraction (EMG), heart rate and rhythm (ECG) and respiratory and gas exchange abnormalities (pulse oximetry). In-home portable monitoring is an acceptable alternative for some patients who are suspected of having moderate to high pre-test probability of OSA.15 Portable monitoring should NOT be used if another sleep disorder is suspected or the patient has comorbid medical conditions that predispose to non-OSA sleep related breathing disorders. The diagnosis of OSA is confirmed if the number of obstructive events (apneas and hypopneas + respiratory-related arousals) on PSG is greater than 15 events per hour or greater than five events per hour in a patient who reports any of the following: unintentional sleep episodes during wakefulness, daytime sleepiness, un-refreshing sleep, fatigue, insomnia, waking up breath

Northeast Florida Medicine Vol. 64, No. 4 2013 13

Sleep Health Section Table 1 STOP-bang questionnaire Snoring

Snoring loudly


Daytime sleepiness

Observed apnea

Have you or household members noticed you stopped breathing during sleep

Pressure (hypertension)

Treated with medication for hypertension


BMI >35 kg/m2


Age over 50

Neck circumference

Neck circumference greater than 40 cm


Male gender

* High risk of OSA if > 3 or more risk factors present.

holding, gasping, or choking, or the bed partner describing loud snoring, breathing interruptions, or both during the patient’s sleep.1 Once the criteria for the diagnosis of OSA are met, the severity of the disease is then classified into mild, moderate or severe as mentioned earlier. This is on the basis of symptoms and the apnea hypopnea index (AHI). PCP’s should be aware that Medicare and Medicaid services (CMS) only approve positive airway pressure for mild to severe OSA as defined by the AHI on the patient’s overnight polysomnography and in some instances the patients referring provider must have a face to face evaluation and document their suspicion for OSA.

Treatment Once the diagnosis is made and the severity assigned, treatment should be initiated as soon as possible. Patient education is the first step in initiating therapy. Patients should be informed of the results of testing and given a general overview of OSA and its consequences. Next, modifiable risk factors and potential treatment modalities should be discussed. If there is a modifiable risk factor, behavior modification is indicated even if initiated concomitantly with specific therapies for OSA.1 Available treatments include behavioral, medical and surgical options. The American Academy of Sleep Medicine (AASM) recommends offering positive airway pressure therapy to all patients who have OSA on the basis of expert consensus.16 Behavioral treatment: The supine position tends to worsen OSA during sleep. Positional therapy, consisting of a method that keeps the patient in a non-supine position and more in the lateral recumbent may correct or improve OSA in such patients.1 This therapy could be used as a primary or adjunct therapy. If used as primary therapy baseline OSA severity should be recorded before initialing therapy to monitor efficacy. PCPs should express education of sleep positions and positional devices like pillows, backpacks or posture alarms to patients who qualify. Another recommendation is attaching tennis balls to the back of the patient’s night clothes

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to cause position changes when they roll on their back.17 CNS depressants range from medication to alcohol with alcohol being the most modifiable risk factor. PCPs should emphasize alcohol avoidance since it can exacerbate OSA.18 Medication lists should be reviewed, and CNS depressants could be avoided or switched to reasonable alternatives. Weight loss should be recommended for all overweight patients. Referrals to bariatric surgical programs should also be considered. Success should be monitored and after a substantial weight loss. A repeat PSG should be performed if the patient is on PAP to see if such therapy is still indicated.1 Medical treatment Positive airway pressure (PAP) is considered the standard, first line therapy for moderate to severe OSA and an optional therapy for mild OSA.19 It can be delivered through different modes of positive airway pressures such as continuous (CPAP), bi-level (BiPAP) or auto titrating (APAP). It has been shown that positive airway pressure therapy reduces the frequency of respiratory events during sleep, decreases daytime sleepiness, and improves quality of life.20 A PSG is usually preformed in the laboratory to determine titration and optimal PAP levels. Regardless of the mode used, close follow up should be used to assess adequacy of treatment with subjective findings like daytime sleepiness, snoring, choking during sleep as well as objective data through repeat PSG.

Oral/Nasal Appliances The rationale behind treatment with oral and nasal appliances is to decrease obstruction of the airway during sleep or increase the size of the upper airway. The most common devices include mandibular repositioning and advancement appliances and tongue retaining devices. Dental evaluation is required prior to their use and they are typically only appropriate for patients with mild OSA.1 More recently, a nasal device which creates expiratory positive airway pressure has been utilized. The apparatus is

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Sleep Health Section a one way valve placed over each nostril creating resistance upon expiration. To date, studies have shown only modest improvement in OSA with this device.21 If therapy with these appliances is initiated, sleep study with the device is necessary to ensure effectiveness of treatment.

The benefits are only achieved through consistency with treatment modalities, especially compliance with PAP. Compliance seems to be highest in patients who achieved symptomatic relief after initiation of therapy. Other factors affecting compliance include disease awareness and comfort of device. Patients who elect to be treated with positive airway pressure should be evaluated frequently, especially during the first few weeks of therapy, because this is usually the time that people tend to stop therapy if it becomes too difficult. These evaluations may include frequent telephone calls and as-needed opportunities to meet face to face with a clinician. The purpose of frequent evaluations is to quickly identify and manage any side effects that develop, since this may affect long-term adherence with the therapy. Once any side effect is identified attempts should be made to alleviate or resolve them. Interventions may be as simple as changing or re-fitting the mask that is being used, adding or increasing the humidification or treatment of nasal sinusitis to better allow tolerance of this non-invasive positive pressure.

Surgical treatment Numerous surgical procedures have been developed to augment apneas in patients with OSA, including nasal, oral, pharyngeal, and laryngeal interventions. Uvuloplasty and maxillomandibular advancement are among the most common upper airway surgeries performed for OSA. While PAP remains the recommended therapy of choice, surgery has been shown to be efficacious in some carefully selected patients with surgically correctable obstructions. However, the data is limited and mostly based on case reports and smaller studies.22 As with other therapies, follow up polysomnography is needed to assess effectiveness of treatment following the intervention. Some patients may still require PAP therapy despite surgery, however, the pressures needed for overcoming their obstruction is usually markedly reduced.

Conclusion As the prevalence is increasing, primary care physicians are becoming the main gateway for patients diagnosed with OSA. Reassessment is generally conducted by a sleep specialist who is also the mainstay of long term follow-up, however this is not always feasible. One retrospective study comparing treatment of OSA by primary physicians versus sleep specialists found that there was no difference between treatment compliance with CPAP in either treatment group. This suggests that treatment through the

Compliance and ongoing health care needs for patients with OSA Obstructive sleep apnea is a chronic disorder that requires regular assessment and long-term management. It is well established that treatment of OSA with CPAP improves quality of life, driving performance, blood pressure and sleepiness for many patients.

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Sleep Health Section primary care provider may be just as effective and likely more timely than through specialist.23 Moving forward, primary care physicians can have a major impact on the morbidity and mortality associated with OSA through identification of high risk patients, timely diagnosis, and routine assessment of treatment and compliance. v


12. Abrishami A, Khajehdehi A, Chung F.A systematic review of screening questionnaires for obstructive sleep apnea. Can J Anaesth. 2010 May;57(5):423-38. 13. Silva GE, Vana KD, Goodwin JL, Sherrill DL, Quan SF. Identification of patients with sleep disordered breathing: comparing the four-variable screening tool, STOP, STOP-Bang, and Epworth Sleepiness Scales. J Clin Sleep Med. 2011 Oct 15;7(5):467-72.

1. Epstein LJ, Kristo D, Strollo PJ Jr, Friedman N, Malhotra A, Patil SP, Ramar K, Rogers R, Schwab RJ, Weaver EM, Weinstein MD; Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med. 2009 Jun 15;5(3):263-76.

14. Rowley JA, Aboussouan LS, Badr MS. The use of clinical prediction formulas in the evaluation of obstructive sleep apnea. Sleep 2000;23:929–938.

2. Pataka A, Riha R. Continuous Positive Airway Pressure and Cardiovascular Events in Patients with Obstructive Sleep Apnea. Curr Cardiol Rep (2013) 15:385

16. Giles TL, Lasserson TJ, Smith BJ, et Al. Continuous positive airways pressure for obstructive sleep apnea in adults. Cochrane Database Syst Rev. 2006 Jan 25;(1):CD001106.

3. Park JG, Ramar K, Olson EJ. Updates on definition, consequences, and management of obstructive sleep apnea. Mayo Clin Proc. 2011 Jun;86(6):549-54;

17. Heinzer RC, Pellaton C, Rey V, et Al. Positional therapy for obstructive sleep apnea: an objective measurement of patients’ usage and efficacy at home. Sleep Med. 2012 Apr;13(4):425-8.

4. The Report of an American Academy of Sleep Medicine Task Force. Sleep-related breathing disorders in adults: Recommendations for syndrome definition and measurement techniques in clinical research. Sleep 1999; 21: 667-89. 5. Lam JC, Sharma SK, Lam B. Obstructive sleep apnoea: definitions, epidemiology & natural history. Indian J Med Res. 2010 Feb; 131:165-70. 6. Parati G, Lombardi C, Narkiewicz K. Sleep apnea: epidemiology, pathophysiology, and relation to cardiovascular risk. Am J Physiol Regul Integr Comp Physiol. 2007 Oct;293(4):R1671-83. 7. Deegan PC, McNicholas WT. Predictive value of clinical features for the obstructive sleep apnoea syndrome. Eur Respir J 1996;9:117–124. 8. Viner S, Szalai JP, Hoffstein V. Are history and physical examination a good screening test for sleep apnea? Ann Intern Med 1991;115:356–359. 9. Flemons WW, Whitelaw WA, Brant R, Remmers J. Likelihood ratios for a sleep apnea clinical prediction rule. Am J Respir Crit Care Med 1994;150: 1279–1285. 10. Crocker BD, Olson LG, Saunders NA, Hensley MJ, McKeon JL, Allen KM, Gyulay SG. Estimation of the probability of disturbed breathing during sleep before a sleep study. Am Rev Respir Dis 1990; 142:14–18.

15. Collop NA, Anderson WM, Boehlecke B, Claman D, Goldberg R, Gottlieb DJ, Hudgel D, Sateia M, Schwab R, Portable Monitoring Task Force of the American Academy of Sleep Medicine.J Clin Sleep Med. 2007;3(7):737.

18. Issa FG, Sullivan CE, Alcohol, snoring and sleep apnea. J Neurol Neurosurg Psychiatry. 1982;45(4):353. 19. Kushida CA, Littner MR, Hirshkowitz M, et al. Practice parameters for the use of continuous and bilevel positive airway pressure devices to treat adult patients with sleep-related breathing disorders. Sleep. 2006;29:375–80. 20. Giles TL, Lasserson TJ, Smith BJ, White J, Wright J, Cates CJ. Continuous positive airways pressure for obstructive sleep apnoea in adults. Cochrane Database Syst Rev. 2006. 21. Simon S, Collop N. Latest advances in sleep medicine: obstructive sleep apnea. Chest. 2012 Dec;142(6):1645-51. 22. Caples SM, Rowley JA, Prinsell JR, Pallanch JF, Elamin MB, Katz SG, Harwick JD. Surgical modifications of the upper airway for obstructive sleep apnea in adults: a systematic review and meta-analysis. Sleep. 2010 Oct;33(10):1396-407. 23. Scharf SM, DeMore J, Landau T, Smale P. Comparison of primary-care practitioners and sleep specialists in the treatment of obstructive sleep apnea. Sleep Breath. 2004 Sep; 8(3): 111-24.

11. Rauscher H, Popp W, Zwick H. Model for investigating snorers with suspected sleep apnea. Thorax 1993; 48:275–279.

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“Obstructive Sleep Apnea: A General review for the Primary Care Physician” CME Questions & Answers (circle one answer)/Free to DCMS Members/$50.00 charge non-members* (Return by October 1, 2015 by FAX: 904-353-5848, by mail: 555 Bishopgate Lane, Jacksonville, FL 32204 OR online:

1. Which of the following risk factors are associated with increased risk of obstructive sleep apnea (OSA) a. Increasing age b. Female gender c. Neck circumference greater than 17 inches for male or 16 inches for female d. a & c e. All of the above 2. There are no validated screening tools to help identify patients that are at higher risk of having OSA a. True b. False 3. On overnight polysomnography, an apnea-hypopnea index (AHI) of less than 5 indicates the absence of clinically significant OSA a. True b. False 4. Medical treatment of OSA with non-invasive positive airway pressures (PAP) has been shown to: a. Be a first line therapy for moderate to severe OSA b. Be an optional therapy for mild OSA. c. Reduces the frequency of respiratory events during sleep, decreases daytime sleepiness, and improves quality of life. d. All of the above 5. Compliance with PAP therapy is highest in which of the following groups of patients? a. Patients who achieved symptomatic relief after initiation of therapy b. Patients with a higher AHI c. Patients with a better awareness of the disease and the importance of therapy d. Patients who are comfortable while using the device e. a, b & c f. a, c & d g. All of the above

Evaluation questions & CME Credit Information (Please evaluate this article. Circle one number using this scale: 1= Strongly Agree to 5= Strongly Disagree) The article met the stated objectives: 1 2 3 4 5 The article was appropriate to my practice: 1 2 3 4 5 The topic was current and well presented: 1 2 3 4 5 Comments:   Name (Print) Email  Address/City/State/Zip  Phone Fax

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Sleep Health Section

Out of Sleep Lab Testing for Obstructive Sleep Apnea Vichaya Arunthari, MD and Kamonpun Ussavarangsi, MD. Division of Pulmonary, Critical Care and Sleep Medicine, Mayo Clinic Florida

Abstract: Obstructive sleep apnea is an under diagnosed condition

with an impact towards quality of life and significant cardiovascular consequences. With increased awareness and benefits associated with treatment there has been an increase in number of sleep centers to aid in the diagnosis and initiation of treatment over the decade. Despite this growth there are still limited resources to reach the demand. While the traditional approach or diagnostic method being an in-laboratory polysomnography, portable monitoring has emerged as an alternative tool. There has been increasing data to support the use of portable monitors in a selected group of patients with a high probability for moderate to severe obstructive sleep apnea without significant comorbidities. As practitioners who evaluate patients suspected to have sleep disordered breathing, we need to familiarize ourselves with this technology and incorporate this into our practice.

Introduction Obstructive sleep apnea (OSA) is a chronic condition with repetitive complete or partial cessation of airflow during sleep accompanied by preservation of respiratory drive manifested as persistent respiratory muscle effort.1,2 The pathophysiology of OSA involves abnormal pharyngeal narrowing and closure during sleep which develops as a result of the summation of a variety of predisposing anatomic and physiological aberrations in the maintenance of upper airway patency during sleep. Upper airway patency depends on the balance of forces acting on the walls (transmural pressure) and the resistance of the walls to collapse (wall elastance). OSA patients appear to have varying degrees of anatomic narrowing combined with reduced neuromuscular dilatory compensatory mechanisms during sleep. The prevalence of OSA depends on how it is defined. The Wisconsin Sleep Cohort Study defines OSA as the presence of at least five obstructive events (apneas and hypopneas) per hour with associated daytime somnolence. Based on this definition, four percent of men and two percent of women have

Please address correspondence to: Vichaya Arunthari, MD, Mayo Clinic Florida, 4500 San Pablo Rd. Jacksonville, Fl 32224

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OSA.3 However, when a cut off apnea hypopnea index (AHI) score of five or more alone is used in the general population of middle-aged adults it is thought to affect approximately 24 percent of men and nine percent of women.4 In an Australian study the prevalence was similar at 26 percent in men.5 The way in which patients present with OSA depends on several factors including age, gender, race and comorbidities. The main presenting symptom by the patient is excessive daytime sleepiness6 which impairs the ability to sustain attention to tasks, in working memory, and in quality of life.7 Different scales are used to assess the degree of daytime sleepiness such as the Profile of Mood States, Stanford Sleepiness Scale, and the more widely used Epworth Sleepiness Scale.8 The latter is useful to evaluate the response to therapy in patients with OSA.9 The most common symptom or observation made by the bed partner is snoring.10 However snoring may not be a good predictor for sleep apnea because it is also common in the general population. In one report 40 percent of women and 60 percent of men are habitual snorers.9 Other presenting symptoms for OSA include witnessed apneas, nocturnal choking or snorting, non-restorative sleep, morning headaches, insomnia, dry mouth and fatigue.11 The strongest risk factor for sleep apnea is obesity. The prevalence of OSA progressively increases as the body mass index increase. Other risk factors include craniofacial and upper airway soft tissue abnormalities. Craniofacial features that augment the risk for OSA may include high and narrow hard palate, elongated soft palate, small chin, an abnormal overjet, a wide craniofacial base tonsillar hypertrophy, and adenoid hypertrophy. Furthermore, there is a genetic predisposition as a positive family history increases the risk of sleep disordered breathing by twofold to fourfold. OSA may also be aggravated by alcohol ingestion, sedatives, sleep deprivation, and supine posture. The main health risks associated with untreated sleep apnea are cardiovascular12, metabolic, and risk due to excessive sleepiness. Hypertension, myocardial infarction, congestive heart failure, and stroke are examples of cardiovascular disorders that have been growing in association with OSA.13,14,15,16 There is also evidence supporting a connection between OSA and increased risk for a variety of these metabolic states; including insulin resistance, the metabolic syndrome, and type2 diabetes

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mellitus. Furthermore, there is considerable evidence linking untreated OSA to increased risk of automobile accidents due to excessive sleepiness.

Portable monitoring (PM) or home sleep study has been suggested as an alternative instrument for the diagnosis of OSA.20,21

Home Sleep Testing/Portable monitoring

There has been growing evidence since 2005 to support that PM is not inferior to in-laboratory PSG for the diagnosis and treatment of OSA, as well as clinical outcomes in a selected population with a high suspicion for moderate to severe OSA. In 2005, a study by Whitelaw and colleagues22 randomized 288 patients with a suspicion of symptomatic OSA to an in-laboratory PSG versus home monitoring. After a diagnosis of OSA all patients were treated for four weeks with an auto-adjusting continuous positive airway pressure (CPAP). Measured outcomes included the Sleep Quality of Life Index (SAQLI), Epworth Sleepiness Scale (ESS), compliance and the respiratory disturbance index (RDI) between the two groups was not statistically different. They also concluded that the ability of physicians to predict the outcome of CPAP treatment was not significantly better with PSG.

In general, there are four types of sleep study monitoring devices. Type I devices refers to an in-laboratory, technician attended overnight polysomnography (PSG). A type II device is a device that can record same variables as a type I device, however, this is unattended by a sleep technologist. Type III devices monitor at least four parameters including two respiratory variables (respiratory movement and airflow), one cardiac variable, oxyhemoglobin saturation via pulse oximetry. Other parameters that may be recorded include snoring, body positioning determination, and sleep stages. A sleep technologist is not present during the recording. Type IV devices monitor only one to three parameters which provides limited information such as oxyhemoglobin saturation, airflow and heart rate. Portable monitors (PM) utilized in the literature mainly refers to type III devices. A nocturnal, laboratory based PSG in an attended setting is often considered the gold standard or the most common tool used to diagnose OSA.17 A PSG not only is used to diagnose OSA, but also to assess the severity and identification of other sleep disorders that can accompany OSA. The PSG allows direct monitoring and quantification of respiratory events and physiologic consequences such as hypoxemia, arousals, and awakenings that are believe to cause daytime symptoms. Various sensors are applied to the patient such as oral nasal airflow, thoracic and abdominal excursion, oximetry, body position sensor and EEG channels which are used to identify sleep stages and documented arousals.18 Apneas and hypopneas during sleep are recorded to provide an apnea hypopnea index (AHI) which is used to grade severity. Due to increased awareness of the association with daytime symptoms and cardiovascular consequences, there is a substantial growing demand to access diagnostic studies and treatment. With the limited number of available sleep laboratories and sleep specialist, there may be a substantial waiting time. Waiting time across the country varies between sleep centers ranging from a few weeks to few months. In other countries the waiting time may be even longer.19 In the United Kingdom the average time to obtain a PSG after a sleep consultation is around four months, giving an average overall wait from referral to CPAP approximately 14 months. The total wait time for completion of a PSG in some parts of Canada may be from eight to 30 months. Moreover, in-lab PSG is labor intense, complex, expensive, and burdensome.

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Mulgrew and colleagues from Vancouver, British Columbia23 performed a randomized, controlled, open-label trial comparing PSG with ambulatory CPAP titration in patients at high risk for moderate to severe OSA based on clinical parameters and home monitoring. After three months there was no difference between the groups in the AHI on CPAP, ESS score and SAQLI. Interestingly, this study also demonstrated that CPAP therapy adherence was better in the ambulatory group than in the PSG group for reasons not entirely known. In a Veterans hospital based study, Berry and colleagues24 performed a randomized trial of 106 patients. Patients were selected based on having a high likelihood of sleep apnea to undergo a PSG pathway with CPAP titration or PM pathway followed by an unattended auto-titrating positive airway pressure to select an effective CPAP pressure. After six weeks of CPAP therapy the investigators found that CPAP usage and clinical outcomes were comparable. In another study25 from Canada, all patients underwent both home testing and in-laboratory PSG and the authors concluded that after four weeks of CPAP therapy there was no significant difference in CPAP adherence and clinical outcomes such as ESS, sleep quality and quality of life. Another Veterans Affairs based hospital trial in 2011 by Kuna et al.26 296 patients with suspected OSA were randomized to PM versus in-laboratory PSG approach. Again, this demonstrated that after three months functional outcomes and CPAP adherence was identical in both groups, and a non-significant trend towards better CPAP usage in the PM group. Finally, more recently, Rosen et al.27 reported the largest study to date (HomePAP study) reviewing the home-based method compared to a sleep laboratory evaluation and treatment approach. This was a randomized, open label, parallel

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group, multicenter trial comparing PM followed by an auto-titrating CPAP with a PSG followed by a CPAP titration performed in a sleep lab. Patients enrolled were based on a high probability of moderate to severe OSA, who were excessively sleepy with an ESS score of 12 or higher and with an adjusted neck circumference of at least 43 cm. These patients were followed for three months. Acceptance of CPAP therapy, titration pressures, effective titrations, time to treatment, and functional outcomes were not significantly different between the two groups. Another important finding in this study is that CPAP usage was nearly an hour more in the PM arm compared to the PSG arm. (4.7 ± 2.1 hours and 3.7 ± 2.4 hours respectively) Furthermore, the percentage of nights used more than or equal to four hours was 12.6 percent higher in the home based testing group.

Conclusion Based on growing evidence to support PM, The American Academy of Sleep Medicine (AASM) has set forward recommendations or clinical guidelines for the use of PM in the diagnosis of OSA published in 2007.28 It is recommended that PM should be performed in conjunction with a sleep evaluation in patients with a high pre-test probability of moderate to severe OSA without co-morbid conditions. Benefits of utilizing PM include increased access to diagnosis and treatment, potential to decrease healthcare expenditures, less technically complex, being more comfortable for the patient and can be performed in a flexible setting. However, PM is not without its limitations. One of particular interest is the failure rates of the device that varies which may be due to data loss, poor quality signal, and inadequate study. PM records monitoring time and not sleep time which may underestimate true AHI. Some devices may not be able to record sleep stage or position. Moreover, there are significant differences among PM within the same class that needs to be considered such as cost, reliability, durability, and reporting of the data. Long term data regarding adherence, impact towards cardiovascular comorbidities, improvements in daytime symptoms, and patient preference are likely to follow. For the time being there is quite robust short term data demonstrating essential equivalency of a home based testing approach and an in-laboratory approach in diagnosing and applying initial treatment. PM appears to be very appealing to many practitioners and to incorporate this into their practice needs thorough evaluation and forming an algorithm that best suits their patients’ needs. Technology is rapidly changing with more devices to come. We need to be updated with information and familiarize ourselves of these devices to make an appropriate selection that fits your practice and to be used in the right patient population. v

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References: 1. Olson EJ, Moore WR, Morgenthaler TI et al. Obstructive sleep Apnea-hypopnea syndrome. Mayo Clin Proc 2003; 78:1545-1552. 2. Heatley EM, Harris M, Battersby M, et al. Obstructive sleep apnoea in adults: a common chronic condition in need of a comprehensive chronic condition management approach. Sleep Medicine Reviews 2013; 17(5): 349-355. 3. Young T, Palta M, Dempsey J, et al. The occurrence of sleep disordered breathing among middle-aged adults. N Engl J Med 1993; 328:163:608-13. 4. Young T. Ratinale, design, and findings from the Wisconsin Sleep Cohort Study: toward understanding the total societal, burden of sllep disordered breathing. Sleep Med Clin 2009; 4(1):37-46. 5. Bearpark H, Elliot L, Grunstein R, et al. Snoring and sleep apnea: a population study in Australian men. Am J Respir Crit Care Med 1995; 151:1459-65. 6. Kryger MH. Diagnosis and management of sleep apnea syndrome. Clini Cornerstine 2000; 2(5): 39-47. 7. Basner RC. Continuous positive airway pressure for obstructive sleep apnea. N Engl J Med 2007; 356: 1751-8. 8. Johns MW. Daytime sleepiness, snoring, and obstructive sleep apnea. The Epworth Sleepiness Scale. Chest 1993; 103(1): 30-36. 9. Gharibeh T, Mehra R. Obstructive sleep apnea syndrome: natural history, diagnosis, and emerging treatment options. Nat Sci Sleep 2010; 2: 233-255. 10. Skomro RP, Kryger MH. Clinical presentations of obstructive sleep apnea syndrome. Progress in Cardiovascular Diseases 1999; 41: 331-340. 11. Chervin RD. Sleepiness, fatigue, tiredness, and lack of energy in obstructive sleep anea. Chest 2000; 118(2):372379. 12. Parish JM, Somers VK. Obstructive sleep apnea and cardiovascular disease. Mayo Clin Proc 2004; 79(8): 1036-1046. 13. Jennum P, Kjellberg J. Health, social and economical consequences of sleep-disordered breathing: a constolled national study. Thorax 2011; 66(7): 560-566. 14. Huang QR, Qin Z, Zhang S, Chow CM. Clinical patterns of obstructive sleep apnea and its comorbid conditions: a data mining approach. J Clin Sleep Med 2008; 4(6): 543-550.

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Sleep Health Section 15. Young T, Skatrud J, Peppard PE, Risk factors for obstructive sleep apnea in adults. J Am Med Assoc 2004; 291(16); 2013-2016.

23. Mulgrew AT, Fox N, Ayas NT, Ryan CF. Diagnosis and initial management of obstructive sleep apnea without polysomnography. Ann Intern Med 2007; 146:157-166.

16. Wolf J, Lewicka J, Narkiewicz, K. Obstructive sleep apnea: An update on mechanism and cardiovascular consequences. Nutr Metab Cardiovasc Dis 2007; 17(3):233-240.

24. Berry RB, Hill G, Thompson L, McLaurin V. Portable monitoring and autotitration versus polysomnography for the diagnosis and treatment of sleep apnea. SLEEP 2008; 31(10):1423-1431.

17. Kryger MH, Roth T, Dement WC, editors. Principles and practice of sleep medicine. 5th edition. Elsevier Sauders 2001. 18. Avidan AY, Barkoukis. Review of sleep medicine. 3rd edition. Elsevier Saunders 2012. 19. Flemons WW, Douglas NJ, Kuna ST, et al. Access to diagnosis and treatment of patients with suspected sleep apnea. Am J Respir Crit Care Med 2004; 169: 668-672. 20. Flemons WW, Littner MR, Rowley JA, Gay P, et al. Home diagnosis of sleep apnea: a systematic review of the literature: an evidence based review. Chest 2003; 124: 1543-1579. 21. Chesson AL Jr, Berry RB, Pack A. Practice parameters for use of a portable monitoring devices in the investigation of suspected obstructive sleep apnea in adults. Sleep 2003; 26: 907-913. 22. Whitelaw WA, Brant RF, Flemons WW. Clinical usefulness of home oximetry compared with polysomnography for assessment of sleep apnea. Am J Respir Crit Care Med 2005; 171: 188-193.

25. Skomro RP, Gjevre J, Reid J et al. Outcomes of homebased diagnosis and treatment of obstructive sleep apnea. Chest 2010; 138(2):257-263. 26. Kuna ST, Gugubhagavatula I, Maislin G et al. Noninferiority of functional outcome in ambulatory management of obstructive sleep apnea. Am J Respir Crit Care Med 2011; 183: 1238-1244. 27. Rosen CL, Auckley D, Benca R et al. A multisite randomized trial of portable sleep studies and positive airway pressure autotitration versus laboratory-based polysomnography for the diagnosis and treatment of obstructive sleep apnea: the HomePAP study. SLEEP 2012; 35(6):757-767. 28. Collop N et al. Clinical guidelines for the use of unattended portable monitors and the diagnosis of obstructive sleep apnea in adult patients: Portable Monitoring Task Force of the American Academy of Sleep Medicine. J Clin Sleep Med 2007; 3:737-747.

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CPAP Adherence: A review Furqan S. Siddiqi, MD, Adil Shujaat, James D. Cury and Abubakr A. Bajwa, MD

Abstract: There are several factors that can affect adherence to CPAP. These include, but are not limited to, patient related factors, device related factors and pressure related issues. Adherence to CPAP use is necessary to achieve maximum benefit from CPAP therapy. A number of strategies can be tried to improve compliance and adherence to CPAP therapy which include patient education, device parameter changes and sleep aids.

Background Although continuous positive airway pressure (CPAP) is first line therapy for obstructive sleep apnea, adherence and compliance to its use has been problematic.1-3 From studies published in the early 1990s, optimal adherence to CPAP therapy is defined as at least 4 hours per night for 5 nights a week.1-3 Newer studies suggest that more use is better, and that there is a treatment dose effect on subjective daytime sleepiness after three months.4,5 Based on this data, most of the insurance companies have now adopted the policy to continue to provide coverage for therapy only if patients are compliant with an average use of four hours or more on 70 percent of the days. Advances in technology have also made it easier to monitor CPAP use in sleep apnea patients. Not only information about daily usage can be downloaded, but the newer machines are also capable of detecting apnea hypopnea episodes. There are a number of factors that impact adherence and compliance and there are a number of strategies that can be adopted to improve adherence.

Factors influencing CPAP adherence Several factors make compliance with CPAP very challenging. Compliance is not as hard to measure in modern day as it was initially, since it was mostly self-reported. Now with hour meter reading, compliance can be accurately measured.1, 6, 7 There are several factors that affect compliance. It’s important to understand these factors since they play a very important role in education, diagnosis and management of these patients. 1. Disease and patient related factors: There is data to suggest that patterns of adherence establish as early as after three days of use after initiating therapy for sleep apnea.8 Since the pattern of use noticed in the initial days after initiation is typically what the longer term pattern will

Please send correspondence to: Dr Furqan Shoaib Siddiqi or call 316-655-7363

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turn out to be, it is important to educate the patient about the importance of this therapy and develop expectations before CPAP is initiated. At one time disease characteristics like severity of sleep apnea and subjective daytime sleepiness were initially thought to be related to adherence, these relationships are weak and not entirely proven.1,3,9-11 Although there is no difference in compliance based age or gender, there are several studies that suggests that African Americans are more likely to be non-adherent than Caucasians.8,12,13 The reason for this difference is not entirely clear, but socioeconomics and belief systems may be a factor. Individual’s nasal anatomy, patency and airway resistance effect delivery of air using CPAP. Several studies have looked at nasal dimensions and cross sectional area, and have shown that patients with smaller nasal dimensions have significantly lower CPAP use.14-17 Although nasal surgery in individuals with narrow nasal cross sectional areas may improve compliance, solid data to prove this approach is lacking. 2. Psychological and social factors Several studies have looked at psychological condition as a potential factor to affect compliance. Type D personality and depression have shown to be related to higher reports of side effects from CPAP and hence lower adherence.18,19 Anxiety, PTSD may also have links with poor adherence.20,21 It is possible that treating these individuals cognitive behavioral therapy may improve adherence however solid evidence is lacking to date. Some of the factors are more difficult to tackle and involve social support system or socioeconomic status of individuals. Studies have shown that lack of social support and lower socioeconomic status play a significant adverse role on CPAP adherence compliance.13 These studies have shown the importance of individualizing therapy, education and follow up for a diverse ethnic and social population. 3. Device related factors Due to positive pressure application during sleep, there is a tendency towards dryness of the mouth, and as a result some discomfort may occur, especially in individuals requiring higher pressure settings. Studies have shown mixed outcomes regarding humidification and its impact on adherence. In the study by Massie et al compliance was higher in patients who received heated humidity compared to no humidity, but no difference was noticed when compared to cold pass-over humidity. Another randomized trial did not show any significant difference between heated humidity and no humidity on CPAP adherence and sleepiness.22-24 Heated humidity is a universal Northeast Florida Medicine Vol. 64, No. 4 2013 23

Sleep Health Section option on CPAP machines, and can easily be turned on or off based on individual needs. A number of masks and interfaces are available to be used with CPAP. The choice of mask really depends on patient and their comfort level with the mask. No study to-date has showed that changing masks improves adherence. Other studies are fairly small and haven’t individually examined the specific aspects of mask interface and possible association with compliance.25-27 Flexible pressure reduces airway pressure during exhalation and returns to baseline during inhalation. An initial study showed increased use among individuals who were placed on CPAP with flexible pressure compared to those placed on conventional CPAP but subsequent larger randomized studies have not shown any benefit of using flexible pressure on adherence.29,30 4. Treatment titration procedures Positive airway pressure devices with auto titration have gained popularity and are now common in clinical practice. Two randomized trials have shown that certain sleep apnea patients benefit with auto titrating PAP and improve adherence. Another study showed improved compliance with auto titration in only younger patients. A randomized trial comparing CPAP and auto titrating PAP showed no difference in adherence but did show less side effects in patients with auto titration PAP.31,32 Auto titrating devices remain a useful tool since it has the ability to titrate the pressure down when the machine is not detecting significant apnea hypopnea events for example in individuals who may have less events in lateral position. Table 1 summarizes the factors explored and their impact on adherence. In summary, a number of factors play a role in affecting adherence and compliance to CPAP. Some of these factors can be anticipated in advance while others only emerge as the therapy is initiated. Nonetheless, these factors can be manipulated to achieve optimal compliance.

Improving compliance: 1. Patient education Education about disease state, treatment options and importance of adherence is standard practice and likely influences some behavior in terms of understanding and accepting the treatment options. To date there is no clear evidence that a more intensive educational effort results in higher rates of adherence. The largest study to date compared four strategies: reinforced education by prescriber and home care provider; reinforced education by prescriber and standard care by home care provider; standard education by prescriber and reinforced education by home care provider and finally standard education by both prescriber and home care provider. The average adherence rates were similar in all groups at six and 12 months. After application of variety of educational resources including video demonstration and group discussion, adherence with CPAP went up from 4.4 to 5.1 hours per night in one study, but was not significant.33,34 2. Medications Studies have shown that those who have worse sleep effi-

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ciency on CPAP titration night are less adherent to CPAP use. Retrospective studies suggested use of hypnotics with initial CPAP usage may improve adherence. A two week course of eszopiclone on CPAP adherence showed that there was a significantly higher use of three hours and 57 minutes per night in patients who used the drug compared to two hours and 42 minutes in the groups that did not use eszopiclone.35 Although promising, the results cannot be generalized across the board and additional research is needed in assessing the impact of pharmacologic agents on CPAP adherence. 3. Cognitive behavioral therapy (CBT) Addressing psychological and perceptual constructs that may impact adherence by CBT seems to have a positive effect in terms of duration of CPAP use and discontinuation of therapy. At least two studies addressed symptoms, cognitive testing performance, treatment relevance, goal development, changes in symptoms with CPAP, troubleshooting advice, treatment expectations, and treatment goal refinement. These studies showed that in middle aged sleep apnea patients that patients undergoing such therapy used CPAP for about 3.2 hours more at 12 weeks and lower discontinuation rates at 13 weeks.36-38 In summary, a combination of education, cognitive behavioral therapy and medications before CPAP initiation and in some cases after initiation can be helpful in improving compliance. In the end, an individualized approach to assess the root cause of non-adherence may lead to relatively simple solution. Despite all the research done the adherence to CPAP continues to be a problem. In patients who have significant sleep apnea and are non-compliant to CPAP alternative approaches to managing sleep apnea such as oral devices or surgery should be considered. v

References: 1. Kribbs, N.B., et al., Objective measurement of patterns of nasal CPAP use by patients with obstructive sleep apnea. Am Rev Respir Dis, 1993. 147(4): p. 887-95. 2. Engleman, H.M., S.E. Martin, and N.J. Douglas, Compliance with CPAP therapy in patients with the sleep apnoea/hypopnoea syndrome. Thorax, 1994. 49(3): p. 263-6. 3. Reeves-Hoche, M.K., R. Meck, and C.W. Zwillich, Nasal CPAP: an objective evaluation of patient compliance. Am J Respir Crit Care Med, 1994. 149(1): p. 149-54. 4. Stradling, J.R. and R.J. Davies, Is more NCPAP better? Sleep, 2000. 23 Suppl 4: p. S150-3. 5. Antic, N.A., et al., The effect of CPAP in normalizing daytime sleepiness, quality of life, and neurocognitive function in patients with moderate to severe OSA. Sleep, 2011. 34(1): p. 111-9. 6. Rauscher, H., et al., Self-reported vs measured compliance with nasal CPAP for obstructive sleep apnea. Chest, 1993. 103(6): p. 1675-80. 7. Engleman, H.M., et al., Self-reported use of CPAP and benefits of CPAP therapy: a patient survey. Chest, 1996. 109(6): p. 1470-6. 8. Budhiraja, R., et al., Early CPAP use identifies subsequent adherence to CPAP therapy. Sleep, 2007. 30(3): p. 320-4.

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Sleep Health Section Table 1 Factors impacting adherence

Factors Explored

Impact on Adherence

Disease and patient related factors Age

No impact


No impact


Blacks more non adherent

Nasal anatomy

Smaller nasal dimensions linked to lower CPAP use

Disease severity

Weak link, more severe sleep apnea linked to more CPAP use


Weak link, more sleepiness linked to more use

Psychological and Social factors Neighborhood

Area of residence and possibly socioeconomic status impacts use

Higher reported side effects and lower adherence

Type D personality


Weak links

Device related factors

Heated humidity

Mixed outcomes, improved adherence in one study and no difference in the randomized trial

Type of mask

No impact shown to date

Flexible pressure (EPR, C-flex)*

No impact on adherence

Treatment titration procedures

Auto titrating PAP

Improved adherence in some studies and less reported side effects

*EPR: expiratory pressure release

9. Engleman, H.M., et al., Effect of continuous positive airway pressure treatment on daytime function in sleep apnoea/hypopnoea syndrome. Lancet, 1994. 343(8897): p. 572-5.

16. Morris, L.G., et al., Acoustic rhinometry predicts tolerance of nasal continuous positive airway pressure: a pilot study. Am J Rhinol, 2006. 20(2): p. 133-7.

10. Sin, D.D., et al., Long-term compliance rates to continuous positive airway pressure in obstructive sleep apnea: a population-based study. Chest, 2002. 121(2): p. 430-5.

17. Nakata, S., et al., Nasal resistance for determinant factor of nasal surgery in CPAP failure patients with obstructive sleep apnea syndrome. Rhinology, 2005. 43(4): p. 296-9.

11. Krieger, J., Long-term compliance with nasal continuous positive airway pressure (CPAP) in obstructive sleep apnea patients and nonapneic snorers. Sleep, 1992. 15(6 Suppl): p. S42-6.

18. Lewis KE, Seale L, Bartle IE, Watkins AJ, Ebden P. Early predictors of CPAP use for the treatment of obstructive sleep apnea. Sleep. 2004 Feb 1; 27(1):134–8.

12. Scharf, S.M., et al., Racial differences in clinical presentation of patients with sleep-disordered breathing. Sleep Breath, 2004. 8(4): p. 173-83.

19. Stepnowsky C, Bardwell WA, Moore PJ, Ancoli-Israel S, Dimsdale JE. Psychologic correlates of compliance with continuous positive airway pressure. Sleep. 2002; 25:758–62.

13. Platt, A.B., et al., Neighborhood of residence is associated with daily adherence to CPAP therapy. Sleep, 2009. 32(6): p. 799-806.

20. Wells, R.D., et al., Adherence, reports of benefits, and depression among patients treated with continuous positive airway pressure. Psychosom Med, 2007. 69(5): p. 449-54.

14. Li, H.Y., et al., Acoustic reflection for nasal airway measurement in patients with obstructive sleep apnea-hypopnea syndrome. Sleep, 2005. 28(12): p. 1554-9. 15. Sugiura, T., et al., Influence of nasal resistance on initial acceptance of continuous positive airway pressure in treatment for obstructive sleep apnea syndrome. Respiration, 2007. 74(1): p. 56-60.

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21. Brostrom, A., et al., Association of Type D personality to perceived side effects and adherence in CPAP-treated patients with OSAS. J Sleep Res, 2007. 16(4): p. 439-47. 22. Massie, C.A., et al., Effects of humidification on nasal symptoms and compliance in sleep apnea patients using continuous positive airway pressure. Chest, 1999. 116(2): p. 403-8.

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Sleep Health Section 23. Neill, A.M., et al., Humidified nasal continuous positive airway pressure in obstructive sleep apnoea. Eur Respir J, 2003. 22(2): p. 258-62.

31. Hukins, C., Comparative study of autotitrating and fixed-pressure CPAP in the home: a randomized, single-blind crossover trial. Sleep, 2004. 27(8): p. 1512-7.

24. Mador, M.J., et al., Effect of heated humidification on compliance and quality of life in patients with sleep apnea using nasal continuous positive airway pressure. Chest, 2005. 128(4): p. 2151-8.

32. Massie, C.A., et al., Comparison between automatic and fixed positive airway pressure therapy in the home. Am J Respir Crit Care Med, 2003. 167(1): p. 20-3.

25. Anderson, F.E., et al., A randomized crossover efficacy trial of oral CPAP (Oracle) compared with nasal CPAP in the management of obstructive sleep apnea. Sleep, 2003. 26(6): p. 721-6. 26. Khanna, R. and L.R. Kline, A prospective 8 week trial of nasal interfaces vs. a novel oral interface (Oracle) for treatment of obstructive sleep apnea hypopnea syndrome. Sleep Med, 2003. 4(4): p. 333-8. 27. Massie, C.A. and R.W. Hart, Clinical outcomes related to interface type in patients with obstructive sleep apnea/hypopnea syndrome who are using continuous positive airway pressure. Chest, 2003. 123(4): p. 1112-8. 28. Mortimore, I.L., A.T. Whittle, and N.J. Douglas, Comparison of nose and face mask CPAP therapy for sleep apnoea. Thorax, 1998. 53(4): p. 290-2. 29. Pepin, J.L., et al., Pressure reduction during exhalation in sleep apnea patients treated by continuous positive airway pressure. Chest, 2009. 136(2): p. 490-7. 30. Dolan, D.C., et al., Longitudinal comparison study of pressure relief (C-Flex) vs. CPAP in OSA patients. Sleep Breath, 2009. 13(1): p. 73-7.

33. Meurice, J.C., et al., A multicentre trial of education strategies at CPAP induction in the treatment of severe sleep apnoea-hypopnoea syndrome. Sleep Med, 2007. 8(1): p. 37-42. 34. Golay, A., et al., A new educational program for patients suffering from sleep apnea syndrome. Patient Educ Couns, 2006. 60(2): p. 220-7. 35. Lettieri, C.J., et al., Effects of a short course of eszopiclone on continuous positive airway pressure adherence: a randomized trial. Ann Intern Med, 2009. 151(10): p. 696-702. 36. Aloia, M.S., et al., Brief behavioral therapies reduce early positive airway pressure discontinuation rates in sleep apnea syndrome: preliminary findings. Behav Sleep Med, 2007. 5(2): p. 89-104. 37. Richards, D., et al., Increased adherence to CPAP with a group cognitive behavioral treatment intervention: a randomized trial. Sleep, 2007. 30(5): p. 635-40. 38. Aloia, M.S., et al., Improving compliance with nasal CPAP and vigilance in older adults with OAHS. Sleep Breath, 2001. 5(1): p. 13-21.

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Sleep Health Section

Surgery for Obstructive Sleep Apnea Iman Naseri, MD, FACS

Abstract: Obstructive sleep apnea accounts for one of more than 80 varieties of sleep disordered breathing. It is the only type which elicits physiologic obstruction of the upper airway, and happens to be the most common type found in the United States (US). It is estimated that almost half of the U.S. population 25 years of age and older have obstructive sleep apnea (158.4 million adults). Unfortunately, more than 25 million Americans will have undiagnosed obstructive sleep apnea (OSA). Among this group, only one percent is estimated to be receiving treatment. Awareness and adequate understanding of this condition is important. More importantly, healthcare providers must also be committed to recognizing this condition with a high index of suspicion. Because of the variety of anatomic sites that may cause the obstruction(s) in OSA, there are multiple choices for surgery that may be available to address each specific site. Therefore, each patient’s unique anatomy requires a uniquely tailored surgical plan which may target multiple sites in the upper airway.

In many adults, OSA results from a disproportionate anatomy of the upper airway and its supporting structures.3 Therefore, great variability exists in the site(s) of obstruction that are often distinct in every patient. The obstruction in adults is often site-specific and highly variable. The level and site of obstruction can be divided according to region or function (Table I, page 28).2,4,5 They often involve obstruction of the airflow within the nasal cavity, nasopharynx, oropharynx, base of tongue and hypopharynx.


Because of the variety of anatomic sites that may cause the obstruction(s) in OSA, there are multiple choices for surgery that may be available to address each specific site. Therefore, each patient’s unique anatomy requires a uniquely tailored surgical plan which may target multiple sites in the upper airway. This is unlike other definitive surgical options such as an appendectomy or a cholecystectomy, as the numerous available surgical options for OSA also poses a challenge in selection that may result in unpredictable outcomes. There is no one definitive surgical treatment for OSA. Surgical options are varied based on a patient’s individual antomomy and examaintion findings. The past decade has been a renaissance in terms of our understanding of sleep and upper airway dynamics, allowing us to offer more effective surgery for OSA. Now that we have the variety in the types of surgeries for OSA, the main challenge that limits surgical success lies in the methods used to match the surgery with the patient’s examination findings.

Obesity is undoubtedly one of the main reasons that there is such a high prevalence of OSA in the US. More than onethird of US adults (35.7 percent) are obese.1 Specifically, the state of Florida has an obesity average of 26.6 percent (Georgia=28.0 percent, Alabama=32.0 percent). Although it is a major contributing factor in the pathophysiology of OSA, obesity is one of many variables in the dynamics that create physiologic obstruction of the upper airway. In order to understand the treatment of OSA, a brief review of OSA physiology is needed, First, in the most pragmatic sense, OSA essentially represents the obstruction of the airflow that is taken in from the mouth and nose during its course to the trachea. Nonetheless, there is an evolving expansion in our understanding of the complex mechanisms involved in maintaining the stability of the upper airway. Aside from anatomy, there is the addition of vascular and neuromuscular tone and reflexes, central ventilatory control, sleep and arousal effects, surface tension forces, lung volume effects and expiratory collapse, all intricately involved in the dynamics of upper airway homeostasis.2

Please send correspondence to: Iman Naseri, MD, FACS Assistant Professor, Otolaryngology - Head & Neck Surgery at University of Florida College of Medicine Jacksonville, 653 West 8th St, 2nd Floor Faculty Clinic, Jacksonville, FL 32209. O: 904-244-3498 / F: 904-244-7730 Email: DCMS online . org

In children, the leading cause for OSA is adeno-tonsillar hypertrophy. Additional factors that have a major role in creating upper airway obstruction in children include skeletal and craniofacial variability and aberrations that alter airway size and resistance.6,7

Evaluation for OSA surgery In evaluating a patient for OSA surgery, there are several key factors to consider. A comprehensive overnight sleep study is necessary to ensure that each patient’s sleep apnea is correctly evaluated and, in respect to OSA, it is accurately quantified and treated. The sleep study evaluation should be preferably done within one year of the visit. It is also common that such patients have often been unsuccessful in their initial treatment by CPAP or BIPAP, in addition to other conservative and non-surgical treatment modalities such as behavior modification, oral appliances, avoidance of alcohol, and sedative medications.

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Sleep Health Section When evaluating patients that have “failed a CPAP trial,” it is important to know why they failed. Some patients often note their noncompliance from their inability to use a full-face mask versus a nasal mask. Other causes of patient failure is the inability to tolerate their machine at high pressures, which often leads to a feeling of claustrophobia. In latter subset of this population, the primary goal of surgery may be to achieve improved tolerance by a reduction in pressure setting requirements or better fit and tolerance to a nasal mask or pillow instead of a full face mask. These goals are more commonly set with patients with severe OSA who cannot tolerate the longer and more invasive surgical recommendations that may be required to achieve significant reductions in their AHI (apnea hypopnea index) scores. The focus of OSA surgery is to relieve the site(s) of obstruction in the upper airway. For this, the most common objective measure is the comparison of the preoperative sleep study to a

Table 1 Surgical Procedures Grouped by Location of Obstruction Nasal cavity and/or nasopharyngeal Septoplasty Turbinate reduction Internal/external nasal valve repair Adenoidectomy Maxillary advancement (Lefort I)

Retropalatal and/or oropharynx Tonsillectomy Uvulopalatopharyngoplasty (UPPP) Midline glossectomy* Genial tubercle advancement Genioglossus advancement Mandibular advancement

Hypopharyngeal Supraglottoplasty/epiglottopexy Hyoid myotomy/release and/or hyoid suspension Radiofrequency ablation of soft palate/tongue base Tracheostomy** * Currently may be performed via robotic technique, Trans-Oral Robotic Surgery (TORS) **Tracheostomy is not categorized as it may satisfy one or more of the location groups listed above.

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postoperative study. Generally, a greater decrease in the AHI is equivalent to a greater reduction in the severity of OSA. The specific surgical procedures for OSA are listed in Table 1, grouped by their target anatomic region. In general, there are two categories of OSA surgery that are distinguished based on their cumulative complexity, operative time and postoperative recovery requirements. They can be considered as primary and secondary surgery. The secondary surgery may be composed of multiple multi-level procedures such as a hyoid suspension with midline glossecotmy and maxillomandibular advancement. Mild to moderate OSA is often treated with the more conservative primary procedures such as a septoplasty, uvulopalatopharyngoplasty (UPPP), palatine or lingual tonsillectomy among others. Patients who do not achieve adequate reduction in their OSA severity from primary surgery, or patients who have severe to profound OSA (AHI>80), may then undergo the more extensive secondary types of surgery. Overall, the best outcomes are available to patients with mild to moderate OSA. The goal of the surgeon is to elucidate the sites of obstruction. There is ongoing controversy in the accuracy of various methods used to assess the possible sites of obstruction and there is a variety of methods that are used in this evaluation. This includes cephalometric analysis, in-office fiberoptic nasopharyngoscopy and Mallampati classification.8 However, these assessments have inherent issues with reliability and various biases such as inter-observer differences. There are significant soft tissue changes that dynamically alter the upper airway with changes in position and sleep-awake states that alter muscle tone. Therefore, it is believed that the best evaluation of the upper airway is in supine position. This thought has led to the use of the Muller maneuver, sleep endoscopy and others.9-11 The goal of ridding the need for CPAP is not always achievable when considering surgery. Therefore, it is crucial that a surgical consultation details specific goals and endpoints. If patients are able to tolerate their CPAP machine after the surgery, and this was a treatment goal established prior to surgery, then surgery was successful. If surgery failed to provide a previously established goal of total relief in mild OSA, then the patient will continue to live with OSA, albeit mild, which may go untreated. This group of patients may have been noncompliant with CPAP therapy, but may show improved compliance if they undergo a new CPAP trial. The successful surgical treatment of OSA is highly dependent on the availability of a multi-disciplinary approach to ensure congruency throughout the path of each patient’s journey from evaluation to treatment end-point, being surgical or non-surgical modalities. This interdisciplinary team approach maximizes treatment efficiency and outcomes by capitalizing on the unique expertise of each subspecialty member. These members may include a board-certified sleep specialist, an otolaryngologist and an oral & maxillofacial surgeon. In patients who have a chief complaint of snoring without

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Sleep Health Section the presence of OSA, there are multiple nonsurgical options available. These include Pillar procedure, injection somnoplasty, radiofrequency ablation of the inferior turbinates, soft palate or base of tongue reduction. These procedures have also been shown to improve mild to moderate OSA.12

Conclusion As the use of current surgical options become more focused on their selection and application, the outcomes will gradually improve for OSA patients undergoing surgery. However, future conservative and surgical therapies in the horizon may well serve to supplement the success of the current options. These future therapies will likely involve less invasive modalities with the use of robotics, hypoglossal nerve stimulation, and the use of nasal expiratory positive airway pressure (EPAP) as an alternative to CPAP therapy.13-19 The treatment of OSA is an evolving specialty practice, which is best performed via a multidisciplinary approach. Surgical therapy requires an understanding of the intricate dynamics of the upper airway and the variety of available surgical options and techniques. Multi-level surgery is often required to tailor a distinct surgery plan for each OSA patient. Future options for OSA treatment will span medical and surgical management options including the use of robotic technology to improve access and postoperative recovery. v

References: 1. Ogden CL. Prevalence of Obesity in the United States, 2009-2010. 2012. 2. Woodson BT, Franco R. Physiology of sleep disordered breathing. Otolaryngol Clin North Am. Aug 2007;40(4):691-711. 3. Rojewski TE, Schuller DE, Clark RW, Schmidt HS, Potts RE. Videoendoscopic determination of the mechanism of obstruction in obstructive sleep apnea. Otolaryngol Head Neck Surg. Apr 1984;92(2):127-131. 4. Sher AE, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep. Feb 1996;19(2):156-177. 5. Fujita S, Woodson BT, Clark JL, Wittig R. Laser midline glossectomy as a treatment for obstructive sleep apnea. Laryngoscope. Aug 1991;101(8):805-809. 6. Arens R, McDonough JM, Costarino AT, et al. Magnetic resonance imaging of the upper airway structure of children with obstructive sleep apnea syndrome. Am J Respir Crit Care Med. Aug 15 2001;164(4):698-703.

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7. Zucconi M, Caprioglio A, Calori G, et al. Craniofacial modifications in children with habitual snoring and obstructive sleep apnoea: a case-control study. Eur Respir J. Feb 1999;13(2):411-417. 8. Mallampati SR, Gatt SP, Gugino LD, et al. A clinical sign to predict difficult tracheal intubation: a prospective study. Can Anaesth Soc J. Jul 1985;32(4):429-434. 9. Launois SH, Feroah TR, Campbell WN, et al. Site of pharyngeal narrowing predicts outcome of surgery for obstructive sleep apnea. Am Rev Respir Dis. Jan 1993;147(1):182-189. 10. Shepard JW, Jr., Gefter WB, Guilleminault C, et al. Evaluation of the upper airway in patients with obstructive sleep apnea. Sleep. Aug 1991;14(4):361-371. 11. Borowiecki BD, Sassin JF. Surgical treatment of sleep apnea. Arch Otolaryngol. Aug 1983;109(8):508-512. 12. Choi JH, Kim SN, Cho JH. Efficacy of the Pillar implant in the treatment of snoring and mild-to-moderate obstructive sleep apnea: a meta-analysis. Laryngoscope. Jan 2013;123(1):269-276. 13. Eastwood PR, Barnes M, Walsh JH, et al. Treating obstructive sleep apnea with hypoglossal nerve stimulation. Sleep. Nov 2011;34(11):1479-1486. 14. Oliven A. Treating obstructive sleep apnea with hypoglossal nerve stimulation. Curr Opin Pulm Med. Nov 2011;17(6):419-424. 15. Schwartz AR, Smith PL, Oliven A. Electrical stimulation of the hypoglossal nerve: a potential therapy. J Appl Physiol. Jun 27 2013. 16. Van de Heyning PH, Badr MS, Baskin JZ, et al. Implanted upper airway stimulation device for obstructive sleep apnea. Laryngoscope. Jul 2012;122(7):1626-1633. 17. Berry RB, Kryger MH, Massie CA. A novel nasal expiratory positive airway pressure (EPAP) device for the treatment of obstructive sleep apnea: a randomized controlled trial. Sleep. Apr 2011;34(4):479-485. 18. Kryger MH, Berry RB, Massie CA. Long-term use of a nasal expiratory positive airway pressure (EPAP) device as a treatment for obstructive sleep apnea (OSA). J Clin Sleep Med. Oct 15 2011;7(5):449-453B. 19. Walsh JK, Griffin KS, Forst EH, et al. A convenient expiratory positive airway pressure nasal device for the treatment of sleep apnea in patients non-adherent with continuous positive airway pressure. Sleep Med. Feb 2011;12(2):147-152.

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Sleep Health Section

A Review of Pulmonary Hypertension in Obstructive Sleep Apnea Adil Shujaat, MD; Abubakr A. Bajwa, MD, FCCP; Vandana Seeram, MD; Lisa Jones, MD and James D. Cury, MD Division of Pulmonary, Critical Care and Sleep Medicine, University of Florida College of Medicine, Jacksonville, FL

Abstract: Pulmonary hypertension (PH) is common in patients with obstructive sleep apnea (OSA) and it is usually multifactorial. The discovery of PH in a patient with OSA warrants evaluation for another underlying cause (e.g. obesity hypoventilation syndrome, left heart failure, and chronic obstructive pulmonary disease) and treatment of that cause. The development of PH in patients with OSA adversely affects exercise capacity and survival. Pulmonary hypertension secondary to OSA alone is also common, usually mild and results from chronic intermittent hypoxia and exaggerated inspiratory thoracic pressure swings during sleep. It responds to nocturnal positive airway pressure (nPAP) therapy. Pulmonary arterial hypertension specific therapy and surgery are treatment options that may need to be considered in patients in whom PH persists despite nPAP therapy or in those who are unable to tolerate nPAP therapy.

Introduction Pulmonary hypertension (PH) in patients with obstructive sleep apnea (OSA) may be secondary to OSA alone or more commonly secondary to OSA in combination with obesity hypoventilation syndrome (OHS), left heart failure (LHF), chronic obstructive pulmonary disease (COPD), and/or chronic thromboembolic disease. PH secondary to OSA belongs to group 3 of the WHO classification of PH, that is, PH associated with lung diseases and/or hypoxemia (Table 1).1

Prevalence The prevalence of PH in OSA varies depending on the definition of PH, the method of measuring the pulmonary artery pressure (echocardiography versus right heart catheterization), and the presence or absence of another cause of PH that may be seen in patients with OSA (e.g., OHS, LHF or COPD). The prevalence of PH in patients with OSA in studies excluding other cardiopulmonary diseases ranges from 19 percent to 59 percent.2-8 Most studies have reported no association between severity of OSA as measured by apnea-hypopnea index (AHI) and the presence or severity of PH.9-14

Please send correspondence to: Adil Shujaat, MD University of Florida Health, 655 West 8th ST, Suite 7-088, Jacksonville, FL 32209. Phone: (904) 244-4075 Fax: (904) 244-5047. E-mail:

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Significance The development of PH in patients with OSA adversely affects exercise capacity and survival.9 In a series of 83 patients with OSA who underwent right heart catheterization within six months of being diagnosed, patients with PH, defined as mean pulmonary artery pressure (mPAP) > 25 mm Hg, (n = 58, 70%) had a lower six-minute walk distance (6MWD) compared to those without PH (285.5 ± 122 m vs 343 ± 213 meters, p = 0.4).9 The difference did not reach statistical significance probably because of the small sample size; however, it was clinically significant. The survival rate at one, four, and eight years for patients with PH was 93 percent, 75 percent, and 43 percent compared to 100 percent, 90 percent, and 76 percent for patients without PH, respectively.9 Patients with severe PH, defined as mPAP > 40 mm Hg, (n = 27; 33 percent) had more nocturnal desaturation (p = 0.045), worse pulmonary hemodynamics, and greater mortality (37 percent) than the groups with mild or moderate PH (16 percent) or no PH (16 percent).9

Pathophysiology In hemodynamic terms mPAP depends upon cardiac output (CO), pulmonary vascular resistance (PVR), and pulmonary artery wedge pressure (PAWP) (Figure 1). PH secondary to OSA results mainly from an elevated PVR and partly from the high CO state characteristic of obesity. The elevated PVR in turn results from pulmonary vasoconstriction, vascular remodeling, and polycythemia—all of which in turn result from chronic intermittent nocturnal hypoxemia associated with the episodes of apnea and hypopnea. Lastly, pulmonary arterial transmural pressure also rises directly as a result of exaggerated inspiratory swings in intrathoracic pressure and the consequent increase in venous return associated with the episodes of apnea.15, 16 Such chronic intermittent swings may lead to right ventricular (RV) hypertrophy and enlargement without the development of resting awake PH or left ventricular (LV) hypertrophy.17, 18 Moreover, recent studies have shown that long-standing hypoxia in OSA results in endothelial dysfunction and an imbalance of vasoconstriction and vasodilatation. Nocturnal DCMS online . org

Sleep Health Section Figure 1

Table 1 Updated World Health Organization (WHO) classification of pulmonary hypertension (Dana Point, 2008)[1]


Pathophysiology of pulmonary hypertension in obstructive sleep apnea mPAP = mean pulmonary artery pressure, PAWP = pulmonary artery wedge pressure, CO = cardiac output, PVR = pulmonary vascular resistance, LV = left ventricular.

positive airway pressure (nPAP) therapy for OSA results in enhanced release of nitric oxide by the pulmonary vasculature19 which suggests a deficiency of this potent vasodilator exists in patients with OSA. On the other hand, intermittent hypoxia induces increased responsiveness to the potent vasoconstrictor endothelin-1 (ET-1) in the pulmonary arteries.20 Nocturnal positive airway pressure therapy for OSA can reduce nocturnal hypoxia but does not affect ET-1 plasma levels.21

1’. Pulmonary veno-occlusive disease (PVOD) and/ or pulmonary capillary hemangiomatosis (PCH) 2.

Pulmonary hypertension owing to left heart disease 2.1 Systolic dysfunction 2.2 Diastolic dysfunction 2.3 Valvular disease


Pulmonary hypertension owing to lung disease and/or hypoxia 3.1 Chronic obstructive pulmonary disease (COPD) 3.2 Interstitial lung disease 3.3 Other pulmonary diseases with mixed restrictive and obstructive pattern 3.4 Sleep-disordered breathing 3.5 Alveolar hypoventilation disorders 3.6 Chronic exposure to high altitude 3.7 Developmental abnormalities


Chronic thromboembolic pulmonary hypertension (CTEPH)


Pulmonary hypertension with unclear multifactorial mechanisms 5.1 Hematologic disorders: myeloproliferative disorders, splenectomy 5.2 Systemic disorders: sarcoidosis, pulmonary Langerhan’s cell histiocytosis, lymphangioleiomyomatosis, neurofibromatosis, vasculitis 5.3 Metabolic disorders: glycogen storage disease, Gaucher disease, thyroid disorders 5.4 Others: tumoral obstruction, fibrosing mediastinitis, chronic renal failure on dialysis

Severity of PH and RV function PH secondary to OSA is usually mild to moderate (mPAP 20–35 mm Hg) and not associated with right heart failure (RHF). Severe PH (mPAP > 35–40 mm Hg) and RHF in patients with OSA suggest an additional cause of PH (e.g., OHS, left heart failure or COPD).22-25 Most studies have reported no association between severity of OSA as measured by AHI and the presence or severity of PH.9-14 On the other hand, echocardiographic studies in OSA patients without significant pulmonary comorbidities have found elevated awake arterial partial pressure of carbon dioxide (PaCO2), AHI > 40,26 and obesity to be important risk factors for reduced RV ejection fraction.27

Diagnosis PH should be suspected in patients with progressive exertional dyspnea, pretibial edema, exertional desaturation, and disproportionately reduced diffusing capacity.

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Pulmonary arterial hypertension (PAH) 1.1 Idiopathic PAH 1.2 Heritable 1.2.1 BMPR2 1.2.2 ALK1, endoglin (with or without hereditary hemorrhagic telangiectasia) 1.2.3 Unknown 1.3 Drug- and toxin-induced 1.4 Associated with 1.4.1 Connective tissue diseases 1.4.2 HIV infection 1.4.3 Portal hypertension 1.4.4 Congenital heart disease 1.4.5 Schistosomiasis 1.4.6 Chronic hemolytic anemia 1.5 Persistent pulmonary hypertension of the newborn

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Clinical Features: Most patients with OSA are obese, and obesity reduces the yield of cardiac auscultation for the classic signs of PH and right heart failure, that is, loud P2, S3 gallop, and systolic murmur of tricuspid regurgitation. Obesity also makes it difficult to evaluate the jugular veins. The presence of peripheral edema, however, is a highly specific sign of PH in morbidly obese patients with OSA.25 Non-invasive diagnostic studies: Obesity also reduces the yield of ECG, chest X-ray and transthoracic echocardiography (TTE) for the detection of PH and RV hypertrophy and enlargement. Moreover, use of Doppler echocardiography (DE) for detection of PH is especially prone to error9, 28, 29 and although DE estimates of right ventricular systolic pressure correlate strongly with systolic pulmonary artery pressure measured by RHC, there is large variation among individual patients.9 Lastly, use of TTE for determination of RV ejection fraction is difficult because of the complex geometric shape of the right ventricle. CT pulmonary angiography and cardiac MRI may overcome such limitations. The combination of TTE and CTPA has been found to exclude PH with a negative predictive value of 100 percent in a series of patients belonging to various groups of the WHO classification of PH.30 Cardiac MRI has become the gold standard for noninvasive assessment of cardiac dimensions, volumes, and ejection fraction because of its higher spatial resolution and lower intraobserver and interobserver variabilities.31 Even if TTE shows PH or enlargement of the right heart chambers or inferior vena cava, RHC is required to confirm PH unless TTE also shows evidence of left heart disease, for example, low LV ejection fraction (< 50%), high LV filling pressure (E:E’ > 15), LVH, left atrial enlargement, valvular incompetence. Right Heart Catheterization (RHC): RHC remains the “gold standard” for making a diagnosis of PH, accurately determining its severity, and ruling out left heart disease, especially occult LV diastolic dysfunction. An elevated PAWP is not uncommon in patients with OSA and does not necessarily imply LV dysfunction as it may be secondary to obesity. Exercise during RHC can help distinguish the cause of an elevated PAWP in such patients. Moreover, RHC also measures CO and allows calculation of PVR. However, the invasive nature of the procedure precludes its more widespread use. Since PH in patients with OSA is more often than not multifactorial, its diagnosis should prompt a search for other causes of PH, particularly OHS, LHF, COPD or PE before attributing the PH to OSA.

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Table 2 Treatment options for pulmonary hypertension secondary to obstructive sleep apnea with or without obesity hypoventilation syndrome Medical treatment Nocturnal positive airway pressure therapy Continuous positive airway pressure (CPAP) BiPAP Oxygen PAH specific therapy Surgical treatment Tracheostomy Bariatric surgery PAH = pulmonary arterial hypertension

Treatment (Table 2) Medical treatment: Nocturnal Positive Airway Pressure (nPAP) therapy: Nocturnal positive airway pressure therapy in the form of continuous positive airway pressure (CPAP) or BiPAP is the standard treatment of OSA. The few studies of the effects of nPAP therapy on pulmonary hemodynamics in patients with OSA have shown an improvement in PH.8, 32, 33 Only one study excluded patients with other cardiopulmonary disease.8 This prospective, quasi-controlled study showed a significant improvement in echo estimated mPAP from 25.6 ± 4 to 19.5 ± 1.6 mm Hg (p < 0.001) after six months of nocturnal CPAP therapy in six patients with PH secondary to OSA. The AHI was 63 ± 18 events per hour and BMI 41 ± 7 kg/m2 in those patients.8 RV ejection fraction has also been shown to improve significantly after long-term CPAP treatment in both pediatric and adult populations.34-36 However, nPAP therapy may not be effective in patients with severe PH. Moreover, a considerable number of patients may not tolerate such therapy.37 Oxygen: Long-term oxygen therapy improves exercise capacity and survival in stable COPD patients with hypoxemia and is associated with a mild improvement in pulmonary hemodynamics.38, 39 Nocturnal oxygen therapy may be indicated in patients with PH secondary to OSA who cannot tolerate nocturnal PAP therapy. However, benefits are unknown. Moreover, oxygen therapy without nPAP in patients with OSA and hypercapnia may result in worsening hypoventilation by

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Sleep Health Section Table 3 Pulmonary Arterial Hypertension Specific Therapy Class of Drug


Phosphodiesterase 5 inhibitor

Sildenafil (Revatio®, Viagra®)


Three times a day

Tadalafil (Adcirca®, Cialis®)


Once a day

Endothelin receptor antagonist

Bosentan (Tracleer®)


Twice a day

Ambrisentan (Letairis®)


Once a day


Iloprost (Ventavis®)


Six times a day

Trepostinil (Tyvaso®)


Four times a day

Trepostinil (Remodulin®)

Subcutaneous or Intravenous

Continuous infusion

Epoprostenol (Flolan®)


Continuous infusion

inhibiting the hypoxic drive to breath. PAH specific therapy for PH secondary to OSA: Drugs from three pharmacologic classes (phospodiesterase-5 inhibitors, endothelin receptor antagonists, and prostaglandins) delivered by oral, inhaled, continuous subcutaneous, and continuous intravenous routes are approved by the FDA for treatment of WHO group I PH: pulmonary arterial hypertension (PAH) (Table 3).40 All of these drugs have been shown to improve symptoms and functional capacity, and IV epoprostenol has also been shown to improve survival in PAH.41 Since the lung parenchyma is otherwise normal in OSA and OHS, PH secondary to OSA with or without OHS is similar to WHO group I PH. Such PH may, therefore, respond to PAH specific therapy with a favorable effect on exercise capacity. Moreover, the recent discovery of the role of endothelial dysfunction in the pathophysiology of such PH also provides a rationale for the use of such therapy. PAH specific therapy may be indicated in patients with PH secondary to OSA in whom PH persists despite nPAP therapy or in those who are unable to tolerate nPAP therapy. In our experience, the use of such therapy for similar indications results in significant improvement in both exercise capacity and pulmonary hemodynamics. The use of PAH specific therapy may also prove to be lifesaving in patients with OSA who are in right heart failure. Lastly, PAH specific therapy may be used to improve the cardiopulmonary status of morbidly obese patients with OSA who wish to undergo bariatric surgery, but are considered high risk because of severe PH. However, the use of PAH specific therapy in patients with OSA needs to be studied before such therapy may be recommended for such indications. Such therapy is extremely expensive and may not be covered by patient’s health insurance. Moreover, it may be potentially harmful as it may result in pulmonary edema and possibly death if LV diastolic

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dysfunction, which is common in such patients, is overlooked. It is worthwhile to perform a vasodilator challenge or exercise during RHC to exclude occult LV diastolic dysfunction prior to considering such therapy. Surgical Treatment: Surgery for OSA: Tracheostomy: Hemodynamic studies of patients with OSA have demonstrated increases in pulmonary arterial transmural pressure during obstructive breathing events that resolve with tracheostomy.42–44 However, these studies were done prior to the widespread availability of CPAP. Nevertheless, tracheostomy may be considered as a last resort therapy, particularly in those who are unable to tolerate nPAP therapy for OSA. Surgery for weight loss: Nocturnal PAP therapy alone may not result in significant improvement in the severe degree of PH that is seen in patients with OSA combined with OHS. The persistence of PH despite compliance with nPAP therapy in such patients may warrant consideration of bariatric surgery. One study of the effects of bariatric surgery and weight loss on pulmonary hemodynamics in 18 patients with OHS showed a significant improvement in mPAP from 36 ± 14 to 23 ± 7 mm Hg (p < 0.0001) after three to nine months and decrease in percent ideal body weight from 224 ± 59 to 167 ± 57 (p < 0.0001), a 42 ± 19% loss of their excess weight.45 PH was present in all but one patient, and it was severe in seven (41 percent). PH was out of proportion to left heart disease, as defined by pulmonary artery end-diastolic pressure to wedge pressure gradient greater than five mm Hg, in thirteen (76.5 percent) of the 17 patients with PH. PH persisted in ten patients but it was not severe in any of them.45

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Sleep Health Section Conclusion Pulmonary hypertension in patients with OSA is common. It is more often than not multifactorial and adversely affects exercise capacity and survival. Pulmonary hypertension secondary to OSA responds to nPAP therapy. Pulmonary arterial hypertension specific therapy and surgery are treatment options that may need to be considered in patients in whom PH persists despite nPAP therapy or in those who are unable to tolerate nPAP therapy. However, pulmonary arterial hypertension specific therapy is extremely expensive, may be potentially harmful and needs to be studied before it may be recommended as additional or alternative treatment for PH in such patients. On the other hand, surgery is invasive and may not result in reversal of PH. The discovery of PH in a patient with OSA should lead to a search for other underlying causes of PH as diagnosis and treatment of such causes is as important as treatment of OSA itself and in most cases may obviate the need to resort to extreme forms of treatment like PAH specific therapy or surgery. v

References 1. Simonneau G, Robbins IM, Beghetti M, et al. Updated clinical classification of pulmonary hypertension. J Am Coll Cardiol. 2009; 54(1) S43â&#x20AC;&#x201C;S54 2. Schroeder JS, Motta J, Guilleminault C. Haemodynamic studies in sleep apnea. In: Guilleminault C, Dement WC, eds. Sleep Apnea Syndromes. New York: Alan R. Liss; 1978:177 3. Krieger J, Sforza E, Apprill M, et al. Pulmonary hypertension, hypoxemia, and hypercapnia in obstructive sleep apnea patients. Chest. 1989;96(4):729-737 4. Apprill M, Weitzenblum E, Krieger J, et al. Frequency and mechanism of daytime pulmonary hypertension in patients with obstructive sleep apnoea syndrome. Cor Vasa. 1991;33(1):42-49 5. Sanner BM, Doberauer C, Konermann M, et al. Pulmonary hypertension in patients with obstructive sleep apnea syndrome. Arch Intern Med. 1997;157(21):2483-2487 6. Sforza E, Laks L, Grunstein RR, et al. Time course of pulmonary artery pressure during sleep in sleep apnoea syndrome: role of recurrent apnoeas. Eur Respir J. 1998;11(2):440-446 7. Bady E, Achkar A, Pascal S, et al. Pulmonary arterial hypertension in patients with sleep apnoea syndrome. Thorax. 2000;55(11):934-939 8. Alchanatis M, Tourkohoriti G, Kakouros S, et al. Daytime pulmonary hypertension in patients with obstructive sleep apnea: the effect of continuous positive airway pressure on pulmonary hemodynamics. Respiration. 2001;68(6):566-572 DCMS online . org

9. Minai OA, Ricaurte B, Kaw R, et al. Frequency and impact of pulmonary hypertension in patients with obstructive sleep apnea syndrome. Am J Cardiol. 2009;104(9):1300-130 10. Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med. 2002;165 (9):1217-1239 11. Guidry UC, Mendes LA, Evans JC, et al. Echocardiographic features of the right heart in sleep-disordered breathing: The Framingham heart study Am J Respir Crit Care Med. 2001;164(6):933-938. 12. Morera J, Hoadley SD, Roland JM, et al. Estimation of the ratio of pulmonary to systemic pressures by pulsed-wave Doppler echocardiography for assessment of pulmonary arterial pressures. Am J Cardiol. 1989;63(12):862-866 13. Catterall JR, Douglas NJ, Calverley PM, et al. Transient hypoxemia during sleep in chronic obstructive pulmonary disease is not a sleep apnea syndrome. Am Rev Respir Dis. 1983;128(1):24-29 14. Veerman DP, Imholz BP, Wieling W, et al. Circadian profile of systemic hemodynamics. Hypertension. 1995;26(1):55-59 15. Podszus T, Peter JH, Guilleminault C, et al. Chest 1990 Pulmonary artery pressure during sleep apnea. Chest. 1990 Mar;97(3 Suppl):81S. 16. Schäfer H, Hasper E, Ewig S, et al. Pulmonary haemodynamics in obstructive sleep apnoea: time course and associated factors. Eur Respir J. 1998 Sep;12(3):679-684 17. Salejee I, Tarasiuk A, Reder I, et al. Chronic upper airway obstruction produces right but not left ventricular hypertrophy in rats. Am Rev Respir Dis. 1993 Nov;148(5):1346-1350 18. Shiomi T, Guilleminault C, Stoohs R, et al. Leftward shift of the interventricular septum and pulsus paradoxus in obstructive sleep apnea syndrome. Chest. 1991 Oct;100(4):894-902 19. Lattimore JD, Wilcox I, Adams MR, et al. Treatment of obstructive sleep apnoea leads to enhanced pulmonary vascular nitric oxide release. Int J Cardiol. 2008;126(2):229-233 20. Wang Z, Li AY, Guo QH, et al. Effects of cyclic intermittent hypoxia on ET-1 responsiveness and endothelial dysfunction of pulmonary arteries in rats. PLoS ONE. 2013;8(3):e58078 21. Karkoulias K, Lykouras D, Sampsonas F, et al. The role of endothelin-1 in obstructive sleep apnea syndrome and pulmonary arterial hypertension: pathogenesis and endothelin-1 antagonists. Curr Med Chem. 2010;17(11):1059-1166

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Sleep Health Section 22. Chaouat A, Weitzenblum E, Krieger J, et al. Pulmonary hemodynamics in the obstructive sleep apnea syndrome. Results in 220 consecutive patients. Chest. 1996;109(2):380-386 23. Bradley TD, Rutherford R, Grossman RF, et al. Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome. Am Rev Respir Dis. 1985;131(6):835-839 24. Hawrylkiewicz I, Palasiewicz G, Plywaczewski R, et al. Comparison of pulmonary hemodynamics in patients with COPD and patients with overlap syndrome with similar severity of airway obstruction and gas exchange. Pol Arch Med Wewn. 1999;102(5):961-966 25. O’Hearn DJ, Gold AR, Gold MS, et al. Lower extremity edema and pulmonary hypertension in morbidly obese patients with obstructive sleep apnea. Sleep Breath 2009; 13:25–34 26. Nahmias J, Lao R, Karetzky M. Right ventricular dysfunction in obstructive sleep apnoea: reversal with nasal continuous positive airway pressure. Eur Respir J. 1996;9(5):945-951 27. Sforza E, Krieger J, Weitzenblum E, et al. Long-term effects of treatment with nasal continuous positive airway pressure on daytime lung function and pulmonary hemodynamics in patients with obstructive sleep apnea. Am Rev Respir Dis. 1990;141(4 Pt 1):866-870 28. Atwood CW Jr, McCrory D, Garcia JG, et al. American College of Chest Physicians. Pulmonary artery hypertension and sleep-disordered breathing: ACCP evidence-based clinical practice guidelines. Chest. 2004;126(1 Suppl):72S-77S 29. McGoon M, Gutterman D, Steen V, et al. Screening, early detection, and diagnosis of pulmonary arterial hypertension: ACCP evidence-based clinical practice guidelines. Chest. 2004;126(1 Suppl):14S-34S 30. Shujaat A, Bajwa AA, Bellardini J, et al. Diagnostic accuracy of echocardiography combined with chest CT in pulmonary hypertension (Abstract accepted for poster presentation at the annual meeting of ACCP that will be held in Chicago in October 2013. Control ID 1704792) 31. Grothues F, Moon JC, Bellenger NG, et al. Interstudy reproducibility of right ventricular volumes, function, and mass with cardiovascular magnetic resonance. Am Heart J. 2004;1472:218-223 32. Sajkov D, Wang T, Saunders NA, et al. Continuous positive airway pressure treatment improves pulmonary hemodynamics in patients with obstructive sleep apnea. Am J Respir Crit Care Med. 2002;165(2):152-15

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33. Arias MA, Garcia-Rio F, Alonso-Fernandez A,et al. Pulmonary hypertension in obstructive sleep apnoea: effects of continuous positive airway pressure: a randomized, controlled cross-over study. Eur Heart J. 2006;27(9):1106-1113 34. Fletcher EC, Schaaf JW, Miller J, et al. Long-term cardiopulmonary sequelae in patients with sleep apnea and chronic lung disease. Am Rev Respir Dis. 1987;135(3):525-533 35. Nahmias J, Lao R, Karetzky M. Right ventricular dysfunction in obstructive sleep apnoea: reversal with nasal continuous positive airway pressure. Eur Respir J. 1996;9(5):945-951 36. Tal A, Leiberman A, Margulis G, et al. Ventricular dysfuntion in children with obstructive sleep apnea: radionuclide assessment. Pediatr Pulmonol. 1988;4(3):139-143 37. Weaver TE, Kribbs NB, Pack AI, et al. Night-to-night variability in CPAP use over the first three months of treatment. Sleep. 1997; 20:278–283 38. Stuart-Harris C, Bishop JM, Clark TJH, et al. Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Lancet. 1981;1(8222):681–686 39. Kvale PA, Conway WA, Coates EO Jr, et al. Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease. A clinical trial. Ann Intern Med. 1980;93(3):391–398 40. Barst RJ, Gibbs JS, Ghofrani HA, et al. Updated evidence-based treatment algorithm in pulmonary arterial hy- pertension,” J Am Coll of Cardiol. 2009; 54(1) S78–S84. 41. Barst RJ, Rubin LJ, Long WA, et al. A comparison of continuous intravenous epoprostenol (prostacyclin) with conventional therapy for primary pulmonary hypertension. N Engl J Med. 1996;334(5):296–302 42. Motta J, Guilleminault C, Schroeder JS, et al. Tracheostomy and hemodynamic changes in sleep-inducing apnea. Ann Intern Med. 1978;89(4):454–458 43. Tilkian AG, Guilleminault C, Schroeder JS, et al. Hemodynamics in sleep-induced apnea. Studies during wakefulness and sleep. Ann Intern Med. 1976;85(6):714–719 44. Marrone O, Bellia V Ferrara G, et al. Transmural pressure measurements. Importance in the assessment of pulmonary hypertension in obstructive sleep apneas. Chest 1989; 95(2):338–342 45. Sugerman HJ, Baron PL, Fairman RP, et al. Hemodynamic dysfunction in obesity hypoventilation syndrome and the effects of treatment with surgically induced weight loss. Annals of Surgery. 1988;207(5):604-613

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Cardiovascular Effects of Sleep Apnea Vandana Seeram, MD; Adil Shujaat, MD; Abubakr A. Bajwa, MD; FCCP; Lisa Jones, MD and James D. Cury, MD Division of Pulmonary, Critical Care and Sleep Medicine, University of Florida College of Medicine, Jacksonville, FL

Abstract: Obstructive sleep apnea (OSA) is a common disorder associated with both the development and worsening of cardiovascular disease. It is considered to be an independent risk factor for hypertension and is implicated in the pathogenesis of multiple other cardiovascular diseases as well as to worsening of the symptoms and increased morbidity. The current standard treatment for OSA is continuous positive airway pressure (CPAP). This aims to eliminate the episodes of apnea and the consequential hemodynamic changes during sleep. Treatment using positive airways pressure therapy (PAP) has been shown in randomized, controlled trials in selected populations to reduce some, but not all of these cardiovascular and cerebrovascular risks. The quality of the evidence as well as morbidity and mortality data with this entity is limited and we will try to focus on the potential role of OSA in the pathogenesis as well as progression of cardiovascular disease including hypertension, atherosclerosis and the metabolic syndrome, acute coronary syndromes, arrhythmia and congestive heart failure. Additionally, the relationship between treatment with PAP therapy and outcomes will be explored.

Introduction Obstructive sleep apnea (OSA) is the most common form of sleep disordered breathing worldwide. OSA is characterized by the repetitive, partial or complete collapse of the upper airway during sleep because of the loss of muscle tone that occurs during sleep which causes impaired ventilation and sleep disturbance.1 Recurrent episodes of nocturnal asphyxia and recurrent arousals from sleep induce a series of secondary physiological responses including arterial oxygen desaturation, surges in sympathetic activity, and acute hypertension. In patients with moderate-to-severe OSA, these cycles may occur

Please address correspondence to: Vandana Seeram, MD University of Florida Health, 655 West 8th ST, Suite 7-088, Jacksonville, FL 32209. Phone: (904) 244-4075 Fax: (904) 244-5047 / E-mail:

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hundreds of times a night and therefore it is not surprising that there is increasing evidence that OSA is an independent risk factor for adverse cardiovascular events.2 An observational study from 1985 with 3,847 men and 3,664 women 40 to 69 years of age first reported a highly significant link between hypertension and snoring with a relative risk (RR) being 1路94 in men and 3路19 in women. This association was also found when adjusting for body-mass index. A significant association between angina pectoris and habitual snoring was observed in men (RR = 2路22).3 Snoring, the most common disorder of sleep, heralds the presence of an unstable upper airway and alerts perceptive clinicians to the possibility of OSA. In that study snoring was used as a surrogate to OSA, and subsequent studies focused on the link between OSA and cardiovascular disease. This review will focus on the potential role of OSA in the pathogenesis of cardiovascular disease as well as the relationship between successful management and improved outcomes.

Hypertension An association between OSA and hypertension was suggested by a series of population, cohort and observational studies in patients attending hypertension clinics, and sleep clinics. OSA figures from sleep clinics may underestimate hypertension as the focus is on the diagnosis and management of sleep disturbances. Additionally, patients in hypertension clinics may not be properly evaluated or tested for OSA. Worsnop and colleagues from Australia recruited random patients from public settings who subsequently underwent blood pressure assessment as well as polysomnography.4 They were assessed for confounding variables and a logistic regression model was used to account for these differences. They showed that treated or untreated hypertensives are more likely to have an apnea-hypopnea index (AHI)>5 than are normotensive individuals. BMI was a major confounding variable in this association,

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but age and sex also contributed. The association between OSA and hypertension persisted when allowance was made for the confounding variables. They estimated that 30 to 40 percent of individuals with systemic hypertension had some evidence of OSA. Moreover, there are reports that about 40 percent of subjects with resistant systemic hypertension have undiagnosed OSA. Data on 2,677 adults referred to a sleep clinic with suspected sleep apnea showed that the number of apneic events, in addition to age, body mass index, and neck circumference, was profoundly related to hypertension. They reported a linear relationship between hypertension and severity of OSA, with each extra apneic episode per hour increasing the odds of hypertension by one percent.5 Increased variability of blood pressure and loss of the nocturnal blood pressure dip have also been reported.6 Obstructive sleep apnea and hypertension share a significant number of risk factors. In 2003 the American College of Chest Physicians asked an expert panel to review the association between systemic hypertension and sleep disordered breathing (SDB). They concluded that any causal association between systemic hypertension and SDB was inconsistent and weak.7 There were other significant cofactors that may exist in patients with SDB can account for the presence of systemic hypertension such as body mass, alcohol consumption or family history of hypertension.7 In the past few years there have been many studies published which take into consideration some extent of these flaws. Not all of them report that OSA is an independent risk factor for hypertension but generally, the more severe the OSA, the more prevalent and severe the hypertension.8-12 A group from Spain looked at the general population in a two phase cross sectional study and they found that the prevalence of OSA (AHI ≥ 5) increased with age in both sexes with an odds ratio (OR) of 2.2 for each 10-year increase. AHI was associated with hypertension after adjusting for age, sex, body mass index, neck circumference, alcohol use and smoking habit.8 This study added evidence for a link between OSA and hypertension. OSA clearly causes night time rises in arterial blood pressure, however, there is some uncertainty to the daytime effect of OSA on systemic hypertension. One of the most quoted population-based cross-sectional studies was the Wisconsin Sleep Cohort Study10 which reported moderate, statistically significant associations between sleep-disordered breathing and hypertension. The Wisconsin Sleep Cohort Study data (sleep disordered breathing, blood pressure, habitus, and health history) on 709 subjects was analyzed at baseline and after four years of follow-up (and after eight years of follow-up in the case of 184 of these participants). Hypertension was about four times more common in the group with the highest AHI than in those with the lowest

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AHI. In the Sleep Heart Health Study,11 6,132 middle-age subjects had unattended (no technician was present) home, full polysomnographic studies; adjusting for confounders resulted in an odds ratio (OR) of 1.37 (95 percent confidence interval [CI] 1.03 to 1.83) for hypertension, between the highest and lowest categories of AHI. Treatment of OSA with nasal continuous positive airway pressure (CPAP) has led to falls in office and ambulatory blood pressure in small, nonrandomized studies.13,14 Pepperell et al conducted a United Kingdom (UK) based study to determine if adequately treated sleep apnea with nasal CPAP caused reductions in BP.15 Therapeutic nasal CPAP reduced mean arterial ambulatory blood pressure by 2·5 mm Hg, whereas sub therapeutic nasal CPAP increased blood pressure by 0·8 mm Hg (difference −3·3 [95 percent CI −5·3 to −1·3]; p=0·0013, unpaired T test). This benefit was seen in both systolic and diastolic blood pressure, and during both sleep and wake. The benefit was larger in patients with more severe sleep apnea than those who had less severe apnea, but was independent of the baseline blood pressure. The benefit was especially large in patients taking drug treatment for blood pressure. 15

Atherosclerosis and the metabolic syndrome Patients with OSA have many features in common with the “metabolic syndrome.” Metabolic syndrome includes systemic hypertension, central obesity16 and insulin resistance.17 The link of OSA to metabolic syndrome might be due to the common link of obesity. AHI remains an independent predictor of insulin resistance and this association between OSA and insulin resistance was seen in both obese and non-obese subjects as indicated by higher levels of fasting serum insulin.18 In another cross sectional analysis from the Sleep Heart Health Study, the respiratory disturbance index, a surrogate of the AHI, correlated with BMI, waist-to-hip ratio, hypertension and diabetes. For patients younger than 65 years of age, the Sleep Heart Study showed a trend for lower high-density lipoprotein and elevated triglycerides.19 In a small controlled study of patients with type II diabetes and OSA treated with nasal CPAP,20 there was improved insulin sensitivity with insulin responsiveness in terms of glucose disposal measured by hyperinsulinemic euglycemic clamps, while weight and drug treatment remained stable. At the macrovascular level, cross-sectional studies have reported impaired brachial artery flow-mediated dilation (FMD) and pulse wave analysis, increased carotid intima-media thickness (IMT) and arterial stiffness with blunted endothelium-dependent dilatation, increased carotid IMT and

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aortic stiffness in patients with OSA compared with matched control subjects.21,22 Small randomized controlled trials have found improvements in FMD and with CPAP-withdrawal demonstrating deterioration.23 The effect was therefore dependent on ongoing use.

Acute Coronary Syndromes

prevent one event per10 years was 3.5. Even after adjustment for age, gender, cardiovascular risk factors, and comorbidities at baseline, OSA treatment was an independent predictor for events.28 CPAP treatment has been associated with a lower frequency of ST-segment depression and relief of nocturnal angina in patients with CAD and OSA.29


As mentioned, OSA has been implicated in the development of systemic hypertension and the development of atherosclerosis. A third mechanism involved in the pathogenesis of coronary artery disease has been implicated in patients with OSA. They present with endothelial dysfunction related to systemic inflammation. A small observational study found attenuated endothelium-dependent vasodilation of resistance vessels in patients with OSA compared with matched normal subjects. This risk is independent of other risk factors for atherosclerosis such as age, body mass index, percent body fat, plasma lipids or plasma glucose.24

Heart rhythm disorders temporally associated with obstructive apneic events have been highlighted for decades. OSA is implicated as a cause of both bradyarrhythmias and tachyarrhythmias, with the risk of arrhythmia being related to the severity of the OSA. Sleep is normally a time when the parasympathetic modulation of the heart predominates and myocardial electrical stability is enhanced. OSA disturbs this, creating an autonomic profile in which both profound vagal activities leading to bradycardia and sympathetic over activity favoring ventricular ectopy are commonly observed.30

There is selective and dose-dependent activation of inflammatory pathways by intermittent hypoxia and reoxygenation, and support a specific role for this event in the pathophysiology of cardiovascular complications in OSA.25 There are the downstream consequences of production of inflammatory genes such TNF-q and adhesion molecules are promoted by lipid peroxidation and endothelial dysfunction, resulting in an environment of systemic inflammation. This facilitates the recruitment and accumulation of macrophages and fat cells that further activates lipid peroxidation and promotes endothelial cell damage and atherosclerosis. Higher CRP levels have been reported in patients with OSA, but it is difficult to determine if this is an independent contribution or as a result of obesity in these patients.

Obstructive apneas and hypopneas are associated with repeated inspiratory efforts against the collapsed upper airways producing considerable negative intrathoracic pressure, which may be as low as -80 mmHg and can cause severe intrathoracic pressure swings. This mechanism repeated during each episode, may stretch the cardiac wall and intrathoracic vessels, possibly leading to mechanical remodeling of both atria and the left ventricle; thereby increasing the risk for the onset of atrial and ventricular dysrhythmias.31 Analysis of electrocardiographic recordings in 458 patients having sleep studies showed that patients with sleep apnea have higher prevalence of cardiac arrhythmias than non-apneic patients. Furthermore, snoring alone, without concomitant sleep apnea, is not associated with increased frequency of cardiac arrhythmias.32

The diurnal variation in the onset of MI in OSA patients is strikingly different from the diurnal variation in patients without OSA. MI occurred between midnight and 6 a.m. in 32 percent of OSA patients and seven percent of patients without it. These findings suggest that OSA may be a trigger for MI.26 Patients who have both OSA and known coronary artery disease have higher rates of major adverse cardiac events (cardiac death, reinfarction, and target vessel revascularization) than those without OSA.27 The quantitative coronary angiography at six month follow-up depicted significantly greater late loss, and a higher restenosis rate indicating that OSA appears to be an independent predictor for angiographic outcomes after PCI.27

Treatment of OSA with CPAP significantly reduced arrhythmia recurrence in AF.33 After an average follow-up period of 32 months, 32 percent of the patients without CPAP therapy experienced atrial fibrillation recurrence while only 21 percent of patients with effective CPAP therapy did.34 OSA was an independent predictor for pulmonary vein antrum isolation (PVAI) failure. Treatment with CPAP improved PVAI success rates. Patients not treated with CPAP in addition to having higher prevalence of non-PV triggers were eight times more likely to fail the procedure.34 In patients who had been treated with catheter ablation therapy for atrial fibrillation, the risk of ablation failure was shown to be independently associated with the severity of OSA35 with the probability of relapse significantly increased among patients with severe OSA.35

Patients with mild-moderate OSA (n = 288), events were more frequent in untreated patients with an absolute risk reduction of 28.5 percent. The number needed to treat to

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Due to the very limited data available, it is currently not known whether there is a causal relationship between OSA and ventricular arrhythmias. To date, there is also no evidence proving that CPAP is an effective therapy to re-establish a normal heart rhythm in OSA patients with ventricular arrhythmias. As such, patients with OSA and arrhythmia, additional arrhythmia specific treatment should be considered in these patients. The findings of observational studies also support the hypothesis that OSA may be a causal factor for sudden cardiac death, which may result from malignant cardiac arrhythmias or acute ischemic heart disease.36

Heart Failure Obstructive sleep apnea is common in patients with heart failure. In a prospective study of 81 patients with heart failure, it was noted that 51 percent of male patients with stable heart failure suffer from sleep-related breathing disorders, 40 percent from central, and 11 percent from obstructive sleep apnea.37 Unlike OSA, patients with central sleep apnea (CSA) have a periodic cessation of breathing with no respiratory effort, followed by hyperventilation. The key mechanisms of periodic breathing in heart failure patients is enhanced sensitivity to carbon dioxide that may predispose some patients with heart failure to the development of central sleep apnea.38 The AHI is a powerful independent predictor of poor prognosis in clinically stable patients with CHF. An AHI > 30/h provides prognostic information over and above New York Heart Association functional class and left ventricular ejection fraction.39 There is repetitive intrathoracic pressure changes that accompany obstructive apneas. Negative intrathoracic pressure increases left ventricular afterload, as well as impairs left ventricular relaxation. Echocardiographic studies have shown both systolic and diastolic dysfunction with increasing AHI. One hundred sixty-nine consecutive patients with OSA diagnosed by polysomnography were hospitalized for the administration of nasal continuous positive airway pressure. LV systolic dysfunction was observed in 7.7 percent (13 of 169 patients). In seven patients with LV dysfunction, LVEF was measured following treatment of OSA and reached normal values. OSA may be a direct cause of daytime LV systolic dysfunction that can resolve following reversal of nocturnal apneas.40 Sixty-eight consecutive patients with OSA confirmed by polysomnography underwent echocardiography. Diastolic function of the left ventricle was determined by transmittal valve pulse-wave Doppler echocardiography. Diastolic dysfunction with an abnormal relaxation pattern was common in patients with OSA. More severe sleep apnea was associated

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with a higher degree of left ventricular diastolic dysfunction.41 Treatment of OSA with CPAP improves quality of life, but no published study has been adequately powered to show a mortality benefit.

Conclusion The majority of individuals with OSA and vascular disease remain undiagnosed, largely due to limited physician awareness of this association. Patients with hypertension, obesity or heart failure should be asked routinely about OSA and referred for a sleep study if they are symptomatic. Recently, there has been increased interest in the role of CPAP to prevent cardiovascular disease and aid in controlling hypertension. The role of CPAP in patients with decompensated heart failure is unquestioned. It improves the hypoxic respiratory failure that results from cardiogenic pulmonary edema, however, its role in chronic heart failure has not yet been clearly established. Preliminary evidence from interventional studies suggests that treatment of OSA may reduce cardiac arrhythmias. However, there is very little data from randomized controlled trials on this topic and future research in patients with OSA should address this important issue. It will take a series of carefully conducted pathophysiological and clinical studies to bridge these gaps in our knowledge with respect to OSA and cardiovascular disease and the effects of treatment on this group of disorders. v

References 1. Bradley TD, Phillipson EA. Pathogenesis and pathophysiology of the obstructive sleep apnea syndrome. Med Clin North Am. 1985 Nov;69(6):1169-85. 2. Loke YK, Brown JW, Kwok CS, Niruban A, Myint PK. Association of obstructive sleep apnea with risk of serious cardiovascular events: a systematic review and meta-analysis. Circ Cardiovasc Qual Outcome 2012;5:720e8. 3. Koskenvuo M, Kaprio J, Partinen M, Langinvainio H, Sarna S, Heikkila K. Snoring as a risk factor for hypertension and angina pectoris. Lancet 1985;1:893–6 4. Worsnop C, Naughton M, Barter C, Morgan T, Anderson A, Pierce R. The prevalence of obstructive sleep apnea in hypertensives. Am J Respir Crit Care Med 1998; 157:111—5. 5. Lavie P, Herer P, Hoffstein V. Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study. BMJ 2000;320:479–82.

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6. Wilcox I, Grunstein RR, Collins FL, Doyle JM, Kelly DT, Sullivan CE. Circadian rhythm of blood pressure in patients with obstructive sleep apnea. Blood Press 1992;1:219–22.

17. Elmasry A, Lindberg E, Berne C, et al. Sleep-disordered breathing and glucose metabolism in hypertensive men: a population-based study. J Intern Med 2001;249:153–61.

7. Dart R, Gregoire J, Gutterman D, Woolf S. The association of hypertension and secondary cardiovascular disease with sleep-disordered breathing. Chest 2003;123:244—60

18. Ip MS, Lam B, Ng MM, Lam WK, Tsang KW, Lam KS. Obstructive sleep apnea is independently associated with insulin resistance. Am J Respir Crit Care Med 2002;165:670–6.

8. Duran J, Esnaola S, Rubio R, Iztueta A. Obstructive sleep apnea-hypopnea and related clinical features in a population-based sample of subjects aged 30 to 70 yr. Am J Respir Crit Care Med 2001;163:685—9

19. Newman AB, Nieto FJ, Guidry U, et al. Relation of sleep-disordered breathing to cardiovascular disease risk factors: the Sleep Heart Health Study. Am J Epidemiol 2001;154:50–9.

9. Davies C, Crosby J, Mullins R, Barbour C, Davies R, Stradling J. Case-control study of 24 h ambulatory blood pressure in patients with obstructive sleep apnoea and normal matched control subjects. Thorax 2000;55:736—40.

20. Brooks B, Cistulli PA, Borkman M, et al. Obstructive sleep apnea in obese non–insulin-dependent diabetic patients: effect of continuous positive airway pressure treatment on insulin responsiveness. J Clin Endocrinol Metab 1994;79:1681–5.

10. Peppard P, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000;342:1378—84. 11. Nieto F, Young T, Lind B, Shahar E, Samet J, Redline S, et al. Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA 2000;283:1829—36. 12. Ohayon M, Guilleminault C, Priest R, Zulley J, Smirne S. Is sleep-disordered breathing an independent risk factor for hypertension in the general population (13,057 subjects)? J Psychosom Res 2000;48:593—601. 13. Mayer J, Becker H, Brandenburg U, Penzel T, Peter JH, von Wichert P. Blood pressure and sleep apnea: results of long-term nasal continuous positive airway pressure therapy. Cardiology 1991;79:84–92. 14. Wilcox I, Grunstein RR, Hedner JA, et al. Effect of nasal continuous positive airway pressure during sleep on 24-hour blood pressure in obstructive sleep apnea. Sleep 1993;16:539–44. 15. Pepperell JCT, Ramdassingh-Dow S, Crosthawaite N, et al. Ambulatory blood pressure after therapeutic and subtherapeutic nasal positive airway pressure for obstructive sleep apnea: a randomized parallel trial. Lancet 2002;359:204–10 16. Grunstein R, Wilcox I, Yang TS, Gould Y, Hedner J. Snoring and sleep apnea in men: association with central obesity and hypertension. Int J Obes Relat Metab Disord 1993;17:533–40.

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21. Kohler M, Craig S, Nicoll D, Leeson P, Davies RJ, Stradling JR. Endothelial function and arterial stiffness in minimally symptomatic obstructive sleep apnea. Am J Respir Crit Care Med 2008; 178: 984-8. 22. Tanriverdi H, Evrengul H, Kara CO, Kuru O, Tanriverdi S, Ozkurt S, et al. Aortic stiffness, flow-mediated dilatation and carotid intima-media thickness in obstructive sleep apnea: non-invasive indicators of atherosclerosis. Respiration 2006; 73: 741-50. 23. Ip MS, Tse HF, Lam B, Tsang KW, Lam WK. Endothelial function in obstructive sleep apnea and response to treatment. Am J Respir Crit Care Med 2004; 169: 348-53. 24. M. Kato, P. Roberts-Thomson, B. G. Phillips et al., “Impairment of endothelium-dependent vasodilation of resistance vessels in patients with obstructive sleep apnea,” Circulation, vol. 102, no. 21, pp. 2607–2610, 2000. 25. S. Ryan, C. T. Taylor, and W. T. McNicholas, “Selective activation of inflammatory pathways by intermittent hypoxia in obstructive sleep apnea syndrome,” Circulation, vol. 112, no. 17, pp. 2660–2667, 2005. 26. Kuniyoshi FH, Garcia-Touchard A, Gami AS, Romero-Corral A, van der Walt C, Pusalavidyasagar S, et al. Day-night variation of acute myocardial infarction in obstructive sleep apnea. J Am Coll Cardiol. 2008; 52: 343–6 27. Yumino D, Tsurumi Y, Takagi A, Suzuki K, Kasanuki H. Impact of obstructive sleep apnea on clinical and angiographic outcomes following percutaneous coronary intervention in patients with acute coronary syndrome. Am J Cardiol. 2007; 99:26–30

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28. Buchner NJ, Sanner BM, Borgel J, Rump LC. Continuous positive airway pressure treatment of mild to moderate obstructive sleep apnea reduces cardiovascular risk. Am J Respir Crit Care Med. 2007; 176:1274. 29. Franklin KA, Nilsson JB, Sahlin C, Naslund U. Sleep apnea and nocturnal angina. Lancet. 1995;345:1085–7 30. Roche F, Xuong AN, Court-Fortune I, et al. Relationship among the severity of sleep apnea syndrome, cardiac arrhythmias, and autonomic imbalance. Pacing Clin Electrophysiol 2003; 26: 669–677 31. Dimitri H, Ng M, Brooks AG, et al. Atrial remodeling in obstructive sleep apnea: implications for atrial fibrillation. Heart Rhythm 2012; 9: 321–327. 32. Hoffstein V, Mateika S. Cardiac arrhythmias, snoring, and sleep apnea. Chest 1994;106:466–71. 33. Kanagala R, Murali NS, Friedman PA, Ammash NM, Gersh BJ, Ballman KV, et al. Obstructive sleep apnea and the recurrence of atrial fibrillation. Circulation. 2003;107:2589–94. 34. Patel D, Mohanty P, Di Biase L, et al. Safety and efficacy of pulmonary vein antral isolation in patients with obstructive sleep apnea: the impact of continuous positive airway pressure. Circ Arrhythm Electrophysiol 2010; 3: 445–451.

35. Matiello M, Nadal M, Tamborero D, et al. Low efficacy of atrial fibrillation ablation in severe obstructive sleep apnoea patients. Europace 2010; 12: 1084–1089 36. Tobaldini E, Brugada J, Benito B, et al, Cardiac autonomic control in Brugada syndrome patients during sleep: The effects of sleep disordered breathing, Int J Cardiol 2013; 168: 3267–3272 37. Javaheri S, Parker TJ, Liming JD, et al. Sleep apnea in 81 ambulatory male patients with stable heart failure: types and their prevalences, consequences, and presentations. Circulation 1998; 97:2154–9. 38. Javaheri S. A mechanism of central sleep apnea in patients with heart failure. N Engl J Med 1999; 341:949–54. 39. Lanfranchi PA, Braghiroli A, Bosimini E, et al. Prognostic value of nocturnal Cheyne-Stokes respiration in chronic heart failure. Circulation 1999;99:1435–40. 40. Laaban JP, Pascal-Sebaoun S, Bloch E, Orvoen-Frija E, Oppert JM, Huchon G. Left ventricular systolic dysfunction in patients with obstructive sleep apnea syndrome. Chest 2002; 122:1133–8. 41. Fung JW, Li TS, Choy DK, et al. Severe obstructive sleep apnea is associated with left ventricular diastolic dysfunction. Chest 2002; 121: 422–9.

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Sleep Health Section

Overlap Syndrome: A review of current literature Kavita Pal, MD and Amit Babbar, MD Department of Internal Medicine, UF College of Medicine

Amita Singh, MD and Ankur Girdhar, MD Department of Pulmonary and Critical Care, UF College of Medicine

Introduction Amongst the most common respiratory disorders there are chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA). Both diseases are highly prevalent all over the world, and by chance alone there will be an occurrence of both these diseases in a single patient. The presence of COPD and OSA leads to a condition labeled by Flenley as Overlap Syndrome (OS).1 The coexistence of these two diseases is clinically significant as they complicate the natural course of each other.2,3 Overlap patients have both more pronounced nocturnal oxygen desaturation as well as day time hypercapnia than patients with COPD or OSA alone. This increases the risk of development of pulmonary hypertension and cardiovascular disease in patients with Overlap Syndrome (OS).4 In this review, an emphasis is made that OS is a common and clinically important disease with unique characteristics other than its individual components. Although disease diagnosis, prognosis and optimal treatment still remains unclear.

Epidemiology and Prevalence It is difficult to accurately estimate the prevalence of OS. This is in part due to the varying definitions for describing COPD and OSA used in previous studies. Also, there are multiple confounders which affect the development of OS. These include obesity, cigarette smoking and age. COPD and OSA are widely prevalent diseases. COPD affects approximately 20 million people in the United States.5 According

Please address correspondence to: Ankur Girdhar, MD Department of Pulmonary and Critical Care UF College of Medicine, Jacksonville, FL 32209 E-mail: Phone: 904-244-4075, Fax: 904-244-5047

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to the CDC data, the overall prevalence among US adults of COPD is 6.3 percent. This appears to be increasing with age, with a higher than 11.6 percent prevalence seen in adults aged 65 years or older compared with a prevalence rate of 3.2 percent in those aged 18 to 44 years.6 On the other hand, OSA is increasingly prevalent, in adults and children, in modern society especially secondary to the obesity epidemic. The estimated prevalence has been two percent for women and four percent for men.7,8 However, these rates continue to rise. Data from the Wisconsin Cohort Study indicate that the prevalence of OSA in people aged 30-60 years is nine to 24 percent for men and four to nine percent for women. Aging is an important consideration of risk for OSA. OSA prevalence increases two to three times in people older than 65 years of age, compared with individuals aged 30 to 64 years of age.9,10 Recent studies have postulated that OSA is as much prevalent in COPD patients as in general population.2,3,11 One study reported that OS occurs in 10 to 20 percent of patients with OSA.12 Based on these findings a recent review article estimated that both COPD and OSA can occur together in one percent of adult population.2 If the multiple confounders are factored in the prevalence of OS in its subclinical underdiagnosed form might be much higher.

Clinical significance and pathophysiology of OS (Figure 1, page 44) OS assumes an important clinical role when we observe that patients with both COPD and OSA have a greater degree of hypoxemia and hypercapnia than COPD patients matched for the GOLD criteria, which establishes the stages of severity of COPD. Patients with OS also suffer from more severe pulmonary hypertension and right heart failure leading to increased morbidity and mortality.3,4 There are many proposed mechanism by which these two individual diseases complicate each other. Studies have shown that there is a rostral shift of peripheral edema in patients with COPD in supine position leading to increase in apneas

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Figure 1


OSA • AHI > 5

• FEV1/FVC < 70

• AHI or RDI severity

• GOLD stage • Sleep disturbances • Nocturnal hypoxia

• Sleep disordered breathing • Nocturnal intermittent hypoxia

Overlap Syndrome • FEV1/FVC < 70 and AHI > 5 • Severe nocturnal hypoxia • Daytime hypercapnia

and hypopneas at nighttime.13 Patients with COPD alone can have subjective and objective changes during sleep with complaints of both initiating and maintaining sleep, as well as excessive daytime sleepiness.14 There is a correlation between the presence of cough, wheezing or sputum production and difficulty falling or staying asleep. Sleep quality is therefore generally poor in all stages of COPD.14 Conversely, one could imagine ways in which OSA might exacerbate COPD. In an animal model, repetitive upper-airway collapse increased lower airway resistance.15 There is also a speculation that patients with OSA might smoke more heavily or frequently than those without OSA, in order to lose or maintain weight, or to counteract excessive daytime sleepiness. OSA is characterized by frequent arousal during sleep, secondary to obstruction of the upper airway leading to nocturnal desaturation. The individual with OSA will rarely recognize the symptoms or the pauses in breathing, which will usually be recognized by witnesses. During REM sleep, muscles relax, including the muscles around the airway at the throat and neck.16 The relaxation allows the tongue and soft palate to also relax. In OSA, caused by obesity, age, craniofacial abnormalities, weak muscles, and several other

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risk factors, the relaxation further impedes the flow of air thus resulting in airway obstruction and nocturnal hypoxemia.

Systemic consequences of OS Nocturnal hypoxia: Given the features of sleep disturbances and nocturnal hypoxemia in patient with COPD and OSA, patients with OS essentially have two reasons for nocturnal oxygen desaturation, and are at risk for prolonged periods of hypoxemia at night.17 Chaouat and coworkers found that nocturnal hypoxemia was higher in patients with overlap (50 ± 6%) than in patients with sleep apnea hypopnea syndrome (SAHS) alone (63.8 ± 6.6%) (P < 0.05).4 The sleep heart health study also had similar results.17 This alone appears to increase morbidity and mortality considerably compared to nocturnal hypoxemia from OSA alone.11 The same study by Chaouat and colleagues also showed that patients with overlap had a lower PaO2 and more hypercapnic than patients with SAHS alone.4 It would therefore be feasible to say that patients with higher rates and prolonged hypoxemia from nocturnal desaturation will have poorer quality of sleep and increased daytime sleepiness.

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Sleep Health Section Cardiovascular diseases: There is a higher risk of development of cardiovascular diseases in both COPD and OSA. This is as a result of the systemic effects of both these diseases. The additional systemic effects in COPD, as well as in OSA, have been ascribed to presence of systemic inflammation and oxidative stress.18,19 Both cause inflammation via various mediators like tumor necrosis factor alpha, interleukin-6, and interleukin-8.20 In COPD, hypoxia is the main cause for development of systemic inflammation and oxidative stress.21,22 Systemic inflammation and reactive oxygen species further lead to endothelial dysfunction and arterial stiffening.23 Similarly, in OSA due to the sleep disordered breathing there is occurrence of intermittent hypoxia in the night. In addition, presence of sleep fragmentation results in sympathetic nervous system activation, systemic vasoconstriction and increased afterload to the heart.24 There is increased insulin resistance and dyslipidemia in patients with OSA due to additive effects of obesity and nocturnal hypoxia.24,25 These mechanisms combine to promote the development of cardiovascular disease. Hawrylkiewicz and colleagues observed that 16 percent of those with OSA had pulmonary hypertension, compared with 86 percent of those with OS.26 COPD in itself, independent of smoking, age and gender, increases the risk of cardiovascular morbidity and mortality.27 There have been no designated studies for the morbidity and mortality of OS, but an interesting study by Lavie and colleagues demonstrated a sevenfold increase in mortality in patient with OSA with the co-morbidity of COPD.28 Patients with the OS also have shown to have a significantly worse quality of life (measured with the St Georgeâ&#x20AC;&#x2122;s Respiratory Questionnaire), when compared to COPD-only controls.29

sleepiness, loud snoring, witnessed breathing interruptions, or awakenings due to gasping or choking. Patients with the following symptoms are at high risk for OSA and should be evaluated: obesity (BMI > 35), congestive heart failure, atrial fibrillation, treatment of refractory hypertension, type2 diabetes, nocturnal dysrhythmias, stroke, pulmonary hypertension, high-risk driving populations, or preoperative for bariatric surgery. A thorough evaluation for suspected OSA should include the following: witnessed apneas, snoring, gasping/choking at night, excessive sleepiness not explained by other factors, non-refreshing sleep, total sleep amount, sleep fragmentation/maintenance insomnia, nocturia, morning headaches, decreased concentration, memory loss, decreased libido, and irritability.32 In a patient in whom OSA is suspected, objective sleep studies (Polysomnography or home testing with portable monitors) are required for the diagnosis of OSA.33 The diagnosis of OSA is confirmed if the number of obstructive events (apneas, hypopneas plus respiratory event related arousals) on PSG is greater than 15 events per hour or greater than five per hour in a patient who reports any one of the following symptoms: unintentional sleep episodes during wakefulness; daytime sleepiness; un-refreshing sleep; fatigue; insomnia; waking up breath holding, gasping, or choking; or the bed partner describing loud snoring, breathing interruptions, or both during the patientâ&#x20AC;&#x2122;s sleep.34 Thus when a patient is diagnosed with either OSA or COPD, clinicians should always consider the presence of both disease states, and should proceed with the appropriate objective diagnostic studies.


The treatment of OS consists of the management of its component disease states, the goals of which are to maintain appropriate oxygenation at all times. Treatment of the underlying COPD is thought to benefit patients of OS. Martin and colleagues found that in 36 patients with moderate to severe COPD, inhaled Ipratropium four times daily significantly improved nocturnal oxygen saturation after only four weeks. The patients in this study also had improved subjective sleep quality with significant increase in REM sleep time of approximately 66.5 minutes with Ipratropium vs. 48.6 minutes after placebo.35 Furthermore, Lacedonia et al reported that the severity of nocturnal hypoxia influences the degree of daytime hypoxemia in OS. In their study, they found that CPAP therapy has been shown to improve daytime PaO2 values in OS patients.36 Oxygen therapy alone (without CPAP) was evaluated in a study by Alford et al.37 They observed that in patients with OS who were given 4 L of supplemental O2 showed improvement of nocturnal oxygenation, however the duration of obstructive events increased from 25.7 seconds to 31.3 seconds. This resulted in an end-apneic PCO2 increase from 52.8 mm Hg to 62.3 mm Hg with corresponding decreases in pH. A recent study compared two groups of OS patients treated with LTOT: one with CPAP and one without. The five year survival rate was 71 percent and 26 percent in the

COPD should be considered in a patient who presents symptoms of cough, sputum production, dyspnea or history of exposure to risk factors for the disease (exposure to cigarettes, etc). Once suspected in a patient, the diagnosis of COPD requires spirometry. The post-bronchodilator forced expiratory volume in one second/forced vital capacity <0.7 confirms the presence of airflow limitation that is not fully reversible.30 Patients with COPD often have sleep derangements, which varies with the severity of COPD. In patients with severe COPD, sleep symptoms are often present. However, even in patients with mild obstructive airway disease, minimally altered sleep quality is present.31 According to The American Thoracic Society and European Respiratory Society (ATS/ERS) guidelines, sleep studies are indicated in a COPD patient in special circumstances that include clinical suspicion of co-existing sleep apnea or the presence of complications (e.g. polycythemia or cor pulmonale that cannot be explained by the awake PaO2).30 However, given the high mortality of untreated OS and the benefits of early intervention (see treatment section below), patients with mild COPD should be screened with sleep studies even in the absence of subjective sleep abnormalities. OSA should be considered in patients who exhibit daytime DCMS online . org


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Sleep Health Section CPAP-treated and non CPAP-treated group, respectively.38 Additional evidence of CPAP therapy was provided by a study on early treatment of OS patients with nasal CPAP. In this study arterial blood gases, mean pulmonary artery pressure, Epworth Sleepiness Score, and percentage of total recording time spent with oxygen saturation less than 90 percent, all improved and stabilized after three months of CPAP therapy. In addition, these results were all stable at 12 months follow up.39 In a study by Marin et al. that OS patients had an increased risk of death from any cause compared to the patients with COPD only. Their study found that effective treatment with CPAP was associated with improved survival and decreased hospitalizations.40 However, not all treatment modalities for the component disease states have been proven to improve the syndrome. An example of this is weight loss. While there is an established benefit of weight loss for those with OSA, currently there has been no benefit found for weight loss in COPD or OS.41 Thus it may warrant further studies for the benefits of weight loss early on in OS patients. Patients with COPD should be screened early for OSA. Further randomized trials are needed to assess other treatment modalities for OS, including the utilization of Bipap (noninvasive ventilation) and early weight loss.

Conclusion The understanding about the syndrome of co-existence of COPD and OSA is gradually increasing. The most important aspect to consider about this syndrome is that patients with overlap have a more important sleep-related O2 desaturation than patients with COPD with the same degree of bronchial obstruction. They have an elevated risk of developing both hypercapnic respiratory insufficiency and pulmonary hypertension when compared with patients with OSA alone. A high index of suspicion, while evaluating a patient with either OSA or COPD, is imperative to diagnose the overlap syndrome. Daytime hypercapnia and pulmonary hypertension in patients known to have only one disease (either OSA or COPD), mild in severity, should prompt assessment for the other disorder. Timely diagnosis and treatment of coexistent OSA may reduce cardiovascular morbidity and mortality in patients with COPD and vice versa. The interaction between these two diseases is unclear, however. Longitudinal studies currently underway would help determine the prevalence and complex pathophysiology of OS. v

References 1. Flenley DC. Sleep in chronic obstructive lung disease. Clin ChestMed 1985; 6(4):651-661.

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2. McNicholas WT. Chronic obstructive pulmonary disease and obstructive sleep apnea: overlaps in pathophysiology, systemic inflammation, and cardiovascular disease. Am J Respir Crit Care Med 2009; 180:692–700. 3. Shteinberg M, Weiler-Ravel D, Adir Y. The OS: obstructive sleep apnea and chronic obstructive pulmonary disease. Harefuah 2009; 148:333–336. 4. Chaouat A, Weitzenbum E, Krieger J, et al. Association of chronic obstructive pulmonary disease and sleep apnea syndrome. Am J Respir Crit Care Med 1995; 151:82–86. 5. Mannino DM, Buist AS. Global burden of COPD: risk factors, prevalence, and future trends. Lancet.2007;370(9589):765–773. 6. CDC. Methodologic changes in the Behavioral Risk Factor Surveillance System in 2011 and potential effects on prevalence estimates. MMWR 2012; 61:410–413. 7. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. Apr 29 1993;328(17):1230-1235. 8. Centers for Medicare and Medicaid Services. Decision Memo for Continuous Positive Airway Pressure (CPAP) Therapy for Obstructive Sleep Apnea (OSA) (CAG00093R2). 9. Bixler EO, Vgontzas AN, Ten Have T, Tyson K, Kales A. Effects of age on sleep apnea in men: I. Prevalence and severity. Am J Respir Crit Care Med. Jan 1998;157(1):144-148. 10. Young T, Shahar E, Nieto FJ, Redline S, Newman AB, Gottlieb DJ, et al. Predictors of sleep-disordered breathing in community-dwelling adults: the Sleep Heart Health Study. Arch Intern Med. Apr 22 2002;162(8):893-900. ). 11. Sanders MH, Newman AB, Haggerty CL, et al. Sleep and sleep-disordered breathing in adults with predominantly mild obstructive airway disease. Am J Respir Crit Care Med 2003; 167:7–14. 12. Lo´ pez-Acevedo M, Torres-Palacios A, Elena Ocasio-Tasco´n M, et al. OS: an indication for sleep studies? Sleep Breath 2009; 13:409–413. 13. Redolfi S, Yumino D, Ruttanaumpawan P, et al. Relationship between overnight rostral fluid shift and obstructive sleep apnea in nonobese men. Am J Respir Crit Care Med 2009; 179:241–246. 14. Klink ME, Dodge R, Quan SF. The relation of sleep complaints to respiratory symptoms in a general population. Chest. 1994;105(1):151–154. 15. Nadel JA, Widdicombe JG. Reflex effects of upper airway irritation on total lung resistance and blood pressure. J Appl Physiol 1962; 17:861-865.

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Sleep Health Section 16. Remmers JE, deGroot WJ, Sauerland EK, Anch AM. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol. 1978 Jun;44(6):931–938. 17. Sanders MH, Newman AB, Haggerty CL, Redline S, Lebowitz M, Samet J, O’Connor GT, Punjabi NM, Shahar E, Sleep Heart Health Study Am J Respir Crit Care Med. 2003 Jan 1; 167(1):7-14. 18. Wouters E. Local and systemic inflammation in chronic obstructive pulmonary disease. Proc Am Thorac Soc 2005; 2:26–33. 19. 16 Ryan S, Taylor CT, McNicholas WT. Systemic inflammation: a key factor in the pathogenesis of cardiovascular complications in obstructive sleep apnoea syndrome? Thorax 2009; 64:631–636. 20. Eid A, Ionescu A, Nixon L, et al. Inflammatory response and body composition in chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2001; 164:1414–1418. 21. Wouters E. Local and systemic inflammation in chronic obstructive pulmonary disease. Proc Am Thorac Soc 2005; 2:26–33. 22. Agustı´ A, Noguera A, Sauleda J, et al. Systemic effects of chronic obstructive pulmonary disease. Eur Respir J 2003; 21:347–360. 23. MacNee W, Maclay J, McAllister D. Cardiovascular injury and repair in chronic obstructive pulmonary disease. Proc Am Thorac Soc 2008; 5:824–833. 24. McNicholas WT, Bonsignore MR. Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities. Eur Respir J 2007; 29:156–178. 25. Lavie L. Obstructive sleep apnoea syndrome: an oxidative stress disorder. Sleep Med Rev 2003; 7:35–51. 26. Hawrylkiewicz I, Sliwinski P, Gorecka D, Plywaczewski R, Zielinski J. Pulmonary haemodynamics in patients with OSAS or an OS. Monaldi Arch Chest Dis.2004;61(3):148–152. 27. Sin DD, Man SF. Chronic obstructive pulmonary disease: a novel risk factor for cardiovascular disease. Can J Physiol Pharmacol. 2005;83(1):8–13. 28. Lavie P, Herer P, Lavie L. Mortality risk factors in sleep apnoea: a matched case-control study. J Sleep Res. 2007;16(1):128–134. 29. Mermigkis C, Kopanakis A, Foldvary-Schaefer N, Golish J, Polychronopoulos V, Schiza S, et al. Health-related quality of life in patients with obstructive sleep apnoea and chronic obstructive pulmonary disease (OS) Int J Clin Pract. 2007;61(2):207–211.

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30. American Thoracic Society / European Respiratory Society Task Force. Standards for the Diagnosis and Management of Patients with COPD [Internet]. Version 1.2. New York: American Thoracic Society; 2004 [updated 2005 September 8] 31. Sanders MH, Newman AB, Haggerty CL et al. Sleep and sleep-disordered breathing in adults with predominantly mild obstructive airway disease. Am J Respir Crit Care Med 2003;167:7-14 32. Epstein LJ; Kristo D; Strollo PJ; Friedman N; Malhotra A; Patil SP; Ramar K; Rogers R; Schwab RJ; Weaver EM; Weinstein MD. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med 2009;5(3):263–276. 33. Kushida CA, Morgenthaler TI, Littner MR, et al. Practice parameters for the treatment of snoring and Obstructive Sleep Apnea with oral appliances: an update for 2005. Sleep 2006;29:240-3. 34. American Academy of Sleep Medicine. International classification of sleep disorders, 2nd Edition: Diagnostis and coding manual. Westchester, IL: American Academy of Sleep Medicine; 2005. 35. Martin RJ, Bartelson BL, Smith P, Hudgel DW, Lewis D, Pohl G, et al. Effect of ipratropium bromide treatment on oxygen saturation and sleep quality in COPD. Chest 1999;115(5):1338-1345. 36. Lacedonia D, Carpagnano GE, Aliani M et al. Daytime PaO2 in OSAS, COPD and the combination of the two (OS). Respiratory Medicine;2013 (107): 310-316 37. Alford NJ, Fletcher EC, Nickeson D. Acute oxygen in patients with sleep apnea and COPD. Chest 1986;89(1):30-38. 38. Machado MCL, Vollmer WM, Togeiro SM, et al. CPAP and survival in moderate-to-severe obstructive sleep apnoea syndrome and hypoxaemic COPD. Eur Respir J 2010; 35:132–137. 39. Toraldo D, De Nuccio F, Nicolardi G. Fixed-pressure nCPAP in patients with obstructive sleep apnea (OSA) syndrome and chronic obstructive pulmonary disease (COPD): a 24-month follow-up study. Sleep Breath 2010; 14:115–123. 40. Marin JM, Soriano JB, Carrizo SJ, et al. Outcomes in patients with chronic obstructive pulmonary disease and obstructive sleep apnea: the OS. Am J Respir Crit Care Med 2010; 182:325–331. 41. Poulain M, Doucet M, Major GC, Drapeau V, Se´rie`s F, Boulet LP, et al. The effect of obesity on chronic respi ratory disesases: pathophysiology and therapeutic strategies. CMAJ 2006;174(9):1293-1299.

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Pediatric Obstructive Sleep Apnea Rahul K. Kakkar, MD, FCCP, FAASM

Introduction Obstructive Sleep Apnea (OSA) is a common, but under-recognized health problem in children, characterized by repeated events of partial and/or complete obstruction of upper airway occurring during sleep and causing sleep fragmentation, intrathoracic pressure swings, intermittent hypoxemia, impaired ventilation and culminating in a systemic inflammatory response. In 1963 abnormal carbohydrate metabolism was described in a child with Pickwickian syndrome.1 In 1975 Guilleminault described a series of 35 patients in which 30 individuals, including three children, were non-obese.2 A few years later, adenotonsillar hypertrophy was described as a cause of pediatric OSA.3 Four children showed improvement in symptoms with adenotonsillectomy (AT). The use of continuous positive airway pressure (CPAP) therapy in the management of pediatric OSA was first described by Schmidt-Nowara.4 The last three decades have seen the shift towards early diagnosis and treatment of pediatric OSA and its differentiation from adult OSA. Two important studies published in 1992 emphasized the different criteria for scoring pediatric OSA than those used for adults.5,6

Epidemiology Early epidemiological studies reported a prevalence of OSA in one to three percent of children.7,8 These and many other subsequent studies were fraught with inaccuracies due to small sample size, use of adult criteria, and lack of polysomnography evidence. In a review, Lumeng and Chervin9 put the reasonable estimates of prevalence of OSA in children by various criteria as follows: parent-reported ‘‘always’’ snoring, 1.5 to six percent; parent-reported apneic events, 0.2 to four percent; varying constellations of parent-reported, four to 11 percent; and OSA diagnosed by varying criteria on diagnostic studies, one to four percent.

Address Correspondence to: Rahul K. Kakkar, MD Phone: 904-296-1300 / Fax: 904-239-3066 E-mail:

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Adenotonsillar hypertrophy and obesity confer a higher risk of OSA in children. However, there is considerable residual OSA following AT in children (>40 percent).10 Moreover, the prevalence of OSA across different age groups in children remains same despite the highest incidence of adenotonsillar hypertrophy in preschool children. As far as obesity and OSA are concerned, the definition and measurements of height and weight have been inconsistent. The prevalence of OSA in obese children is about 30 percent, and there is a dose response relationship between weight and prevalence, as well as severity of OSA.11,12 Obesity causes or worsens OSA by deposition of fat in lateral pharyngeal wall. OSA is more prevalent among African American children.12 The prevalence in boys is about one and a half to two times higher than in girls, even in prepubertal age groups.9 Some pediatric populations have a significantly high risk of OSA such as Down’s syndrome (57-100 percent),13 Prader Willie syndrome (93 percent),14 neuromuscular disorders (50 percent),15 Chiari Malformation and meningomyelocele (60 percent),16 congenital malformation of face, neck, tongue, mouth and/or chest as in Achondroplasia, Pierre Robin Sequence, Treacher- Collins syndrome, craniofacial dysostoses and mucopolysaccharidoses. Emerging evidence suggests high prevalence of OSA in children with sickle cell disease, asthma and congenital heart disease. Key Point: OSA is common in children and is associated with adenotonsillar hypertrophy, obesity, neuromuscular disease, craniofacial abnormalities, sickle cell disease, asthma and in African Americans.

Symptoms and Signs A myriad of clinical symptoms and signs are described in children with OSA, however, history, physical examination, audio-video recordings, overnight pulse oximetry and standardized questionnaires are insufficient to diagnose OSA in children.18 Snoring is the most common symptom of OSA. The prevalence of snoring in general pediatric population is about eight to 10 percent, however, it is reported to occur in about 50 percent of obese children.19 Habitual snoring is defined as a report of “frequent or always” on parent reported questionnaires. Snoring occurring about three to four times a week is considered as “frequent,” and snoring occurring DCMS online . org

Sleep Health Section more than four times a week is considered to be “always.”20 All children should be screened for snoring, and all children with habitual snoring should undergo assessment for OSA. Variants of snoring have been described as snorting, loud breathing, and difficulty breathing at night. Other nocturnal symptoms include witnessed pauses in breathing, struggling to breathe at night, mouth breathing, restless sleep, night sweats, sleeping in abnormal position (Figure 1) and drooling of saliva. Bedwetting is a frequent problem and is reported in about 40 percent of children with OSA.21 Frequent visits to physicians for respiratory symptoms are also commonly reported. Daytime symptoms include excessive sleepiness, hyperactivity, inability to focus, behavioral problems, morning headaches, poor school performance, fatigue, daytime napping and difficulty waking up in the morning. Depression and other psychiatric diagnosis like attention deficit hyperactivity disorder (ADHD) are common. The physical examination in children with OSA may be completely normal or reveal adenotonsillar hypertrophy (Figure 2), “long face syndrome” (Figure 3) with high arched palate, gummy smile, increased vertical height, steep mandibular plane and disuse atrophy of nose. Mid-face hypoplasia and retrognathia are associated with compromised upper airway space. Children with Down’s syndrome and neuromuscular disease exhibit hypotonia. The ability to achieve adequate neuromuscular activation to maintain airway patency during sleep and stability of ventilatory control and alterations in arousal threshold are important contributors in the pathogenesis of OSA.22 Key Point: OSA in children can masquerade a variety of neuropsychiatric and physical illnesses like depression, ADHD and poor school performance.

Diagnosis Many validated questionnaires have been developed to evaluate OSA in children. They are more useful in research than in the clinical care. In a review of sleep questionnaires, only two instruments met the desirable criteria for evaluating sleep disorders.23, 24 We use SRBD (sleep related breathing disorders) scale of Pediatric Sleep Questionnaire developed by the University of Michigan.25 This instrument has a sensitivity and specificity of 0.85 and 0.87 respectively for an apnea hypopnea index (AHI) of > 5 per hour. Polysomnography (PSG) remains the best method to diagnose OSA in children. Less expensive home sleep testing (HST) or overnight oximetry are neither sensitive nor specific enough to assess OSA in children. Pediatric PSG are more complicated than adult PSG, and require end-tidal and transcutaneous CO2 (EtCO2 and TcCO2) and, for younger children, one technician per child per study. High quality video monitoring is imperative in performing pediatric PSG. The studies are scored according to the criteria established by the AASM (American Academy of Sleep Medicine). An obstructive apnea (OA) is defined as > 90 percent drop in the peak signal excursion measured by an oronasal thermistor, positive airway

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Figure 1 Characteristic sleeping position of a child with sleep apnea. Capua et al. J Can Dent Assoc; 2009; 75:285-9 Reprinted with permission of the Canadian Dental Association

Figure 2 Enlarged tonsils in a child with OSA. Verma SK et al. Natl J Maxillofac Surg. 2010 Jan-Jun; 1(1): 35–40

Figure 3 Long Face in DiGeorge Syndrome. Note vertically long face, flattened malar region and retrognathia Courtesy: Wu et al. (2013) PLoS ONE 8(1): 54404

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Sleep Health Section Table 1 Common features of type I and type II OSA39 Habitual snoring (at least 3 nights/wk) Agitated sleep with frequent awakenings Diaphoresis Night terrors and nightmares Bedwetting Breathing pauses reported by parents Nasal speech pattern and stuffy nose Mouth breathing and limited nasal airflow

Figure 4 Mechanisms underlying cardiovascular complications of OSA Courtsey: Dumitrascu et al. 2013 Oxidative Medicine and Cellular Longevity Volume 2013, Article ID 234631

pressure (PAP) device or alternative signals for two or more breaths, with preservation of respiratory effort throughout the period of apnea. If a portion of apnea showed absence of respiratory effort, it is classified as mixed apnea.26 A hypopnea is defined as a drop in peak signal excursion of > 30 percent of pre-event baseline using nasal pressure, PAP device or alternative signals for two or more breaths and associated with > 3 percent oxygen desaturation or an arousal.26 Sleep related hypoventilation is defined by an elevation of arterial CO2 (measured by EtCO2 or TcCO2) above 50 mmHg for more than 25 percent of total sleep time.26 Apnea Hypopnea index (AHI) is defined as number of apneas and hypopnea per hour of sleep. In children an AHI> 1 is considered abnormal. An AHI of one to five is considered mild, an AHI of five to 15 as moderate and an AHI > 15 to be severe OSA. Cost constraints of modern healthcare and lack of ready availability of pediatric sleep specialists begs the question which children should undergo PSG? In recent years, three societies have proposed different, but overlapping guidelines for performing PSG in children.26 -28 In general, PSG is indicated for diagnosis of obstructive sleep apnea, to assess the efficacy of treatment following surgery or oral appliance therapy, for positive airway pressure (PAP) titration or for evaluation of residual symptoms following surgical treatment of OSA. Key Point: Attended polysomnography is the only reliable way of diagnosing OSA in children. Clinical symptoms or absence thereof, is insufficient to diagnose or exclude the diagnosis of OSA in children. 50 Vol. 64, No. 4 2013

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Frequent visits to primary care physician for respiratory-related symptoms Retrognathia Reprinted with permission of the American Thoracic Society. Copyright Š 2013 American Thoracic Society.

Consequences of untreated OSA in children Untreated OSA in children can lead to neurobehavioral, cardiovascular and metabolic consequences. The OSA causes a systemic inflammatory response from a combination of intermittent hypoxia, sleep fragmentation, alveolar hypoventilation and increased respiratory effort. They are mediated by inflammatory cytokines, changes in the levels of leptin, cortisol and adrenaline and surges in blood pressure and heart rate (Figure 4). The latter are caused by exaggerated chemoreflex and blunted baroreflex responses of the carotid body. There is emerging evidence that OSA due to tonsillar hypertrophy (Type I) and due to obesity (type II OSA) have different effect on children.30 While children with type I OSA often have hyperactivity, attention deficit and recurrent otitis media, children with type II OSA demonstrate excessive sleepiness, cardiovascular complications, depression, low social esteem, social withdrawal, systemic hypertension, insulin resistance and elevated lipids levels (Tables 1 & 2). Type III OSA is due to craniofacial abnormalities and neuromuscular disease but their unique long term consequences and symptoms have not been clearly outlined. Neurobehavioral complications strongly associated with OSA include deficits in behavior and emotion regulation, scholastic performance, sustained attention, selective attention,

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Sleep Health Section Table 2 Differences between type I and type II OSA39 Symptom / Finding Excessive daytime sleepiness

OSA Type I*

OSA Type II*





– or +

Attention problems



Truncal/visceral obesity

– or +


Enlarged neck circumference

– or +


Enlarged tonsils/adenoids



Recurrent otitis media/tympanostomy tube placement





Weight gain Hyperactive behavior

Depression and low self-esteem Shyness and social withdrawal



Left ventricular hypertrophy



Systemic hypertension/altered blood pressure regulation



Insulin resistance


Serum lipid abnormalities



Elevated C-reactive protein




Elevated liver enzymes

* – : absent + to ++++ : infrequent to very frequent

Reprinted with permission of the American Thoracic Society. Copyright © 2013 American Thoracic Society.

and alertness.31 Excessive sleepiness in adolescents is associated with increased risk of motor vehicle accidents. Threshold for developing neurocognitive complications seems to be much lower than the threshold for cardiovascular morbidity (see below). Chronic snoring remains the best predictor of the neurobehavioral morbidity. Cardiovascular complications of OSA in children include elevated blood pressure, arrhythmias, left ventricular dysfunction, endothelial dysfunction, abnormal heart rate variability and pulmonary hypertension. The evidence is strongest for the occurrence of systemic hypertension with a combined odds ratio (OR) of 3.15 (95 percent CI 2.01- 4.93)32 (Figure 5, page 52). The association with other cardiovascular morbidities is weak based upon the current literature. The threshold for development of cardiovascular disease in children with OSA has also been studied. The signs of cardiac strain may develop in children with OSA with an AHI level ranging from five to 10. An AHI >10 should be considered as consistent with cardiac strain. There is a dose response relationship between worsening AHI and risk and severity of hypertension and other cardiovascular abnormalities like left ventricular hypertrophy. In children, OSA is associated with worse insulin resistance, lower adiponectin levels and increased excretion of urinary catecholamines.33 Whether these abnormalities are due to OSA or due to increased BMI itself remains controversial. Many other markers of innate immunity and inflammation are reported to

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be abnormal in small studies but warrant further studies. Key Point: OSA in children appears to have at least two distinct phenotypes with different clinical presentation and long-term consequences.

Treatment Childhood OSA can be treated with surgical and non-surgical methods. Surgical methods include AT and other surgeries. Non-surgical treatment methods include positive airway pressure therapy, oral appliance therapy, nasal steroids, weight loss, positional therapy and avoidance of CNS depressants.

Surgical treatment of childhood OSA Adenotonsillar hypertrophy is the major cause of OSA in children two to 10 years of age. Many studies have shown that AHI is proportional to the size of tonsils, while others have shown that the size of tonsils does not predict the AHI accurately. AT remains the cornerstone of treatment of OSA in children. A recent meta-analysis concluded that the overall success with AT is about 60 percent.10 Similar analysis performed by other researchers has also revealed the overall

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Figure 5 Meta-analysis of AHI and hypertension using fixed effect model: forest plot


Kow Ka-Li Ann Acad Med Singapore 2008;37:715-21

Study Reference

Amin 2004 Guiteminault Leung Amin 2002 Reade Li











Odds Ratio

success rate of AT is to be less than 60 percent.34 In the analysis by Bhattacharjee, only 27 percent of children treated with AT achieved a complete remission, despite a significant reduction in the AHI in most children (Figure 6). Therefore, it is imperative to retest the children, especially those younger than 3 years of age, children with moderate to severe OSA at baseline, residual symptoms, obesity, craniofacial abnormalities and other comorbidities like Downâ&#x20AC;&#x2122;s syndrome, about eight to 12 weeks following AT to evaluate for residual OSA. Lack of snoring is not equal to lack of sleep apnea following AT. AT results in significant improvement in both neurocognitive and cardiovascular indices.35 Various other surgeries are described, like inferior turbinectomy, uvulopalatopharyngoplasty (UPPP), modified UPPP, tongue base reduction surgery, supraglottoplasty, repose tongue, genioglossus advancement and maxillary distraction. Tracheotomy is rarely performed and is generally reserved for children with severe congenital caraniofacial abnormalities. Key Point: AT is very effective in children with OSA but significant residual OSA remains after AT and warrants follow-up sleep studies. Absence of snoring is not absence of sleep apnea.

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Non-surgical treatment of childhood OSA Positive airway pressure (PAP) therapy delivered by a continuous PAP (CPAP) or bi-level PAP (bi-PAP) device is the mainstay of treatment in adults with OSA. The therapy is extremely effective even in children but acceptance and adherence to treatment remain significant challenges. While a variety of interfaces are available for treatment in the financially lucrative adult OSA market, the variety of masks available for children is limited. A successful pediatric CPAP adherence program requires a multidisciplinary team approach from respiratory therapists, pulmonologists and behavior specialists. PAP therapy is associated with significant improvement in neurobehavioral measures inchildren.36 However, there are in sufficient clinical studies on the cardiovascular benefits of CPAP therapy in children. Due to generally poor adherence in children, it is reserved for residual OSA after AT or for non-surgical patients. PAP therapy requires follow-up studies as pressure requirements and mask fittings change with the childâ&#x20AC;&#x2122;s growth. Alternatives to PAP include oral appliances, nasal steroids, leukotriene inhibitors, and weight loss. Oral appliance therapy

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Obese Non-Obese

Percentage of Total


Figure 6 Response of OSA to adenotonsillectomy50


Reprinted with permission of the American Thoracic Society. Copyright Š 2013 American Thoracic Society.




0 AHI<1



Adenotonsillectomy Response

Figure 7 Verma SK et al. Natl J Maxillofac Surg. 2010 Jan-Jun; 1(1): 35â&#x20AC;&#x201C;40

includes rapid maxillary expander (RME)37 (Figure 7) and mandibular advancement devices (MAD),38 which appear to be promising in small studies but need large prospective randomized trials. Montelukast alone or in combination with nasal budesonide has shown to be effective in treating mild to moderate OSA in children.39 Weight loss in obese teenagers has been shown to impact OSA favorably.40 In summary, there is lack of randomized control trials on long term and even short-term outcomes with non-surgical therapy in children with OSA. It appears that a multidisciplinary approach with the early involvement of pediatric otolaryngologist, behavioral therapist, orthodontics and nutritional counseling may afford the best prospect for children who either fail surgical treatment or are not candidates for surgery. Key Point: Many treatments other than AT are available for treating OSA in children, which appear promising but lack large scale studies.

Conclusion Pediatric OSA remains a commonly prevalent and pervasively under-recognized illness in general pediatric population. Children with OSA present with a myriad of clinical symptoms, which in the absence of awareness of OSA, can lead to

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misleading conclusions, often with serious but preventable and reversible consequences. Every child should be screened for snoring and every child with habitual snoring or otherwise at high risk of OSA should undergo attended polysomnography with end-tidal and transcutaneous CO2 monitoring. Treatment with AT remains the cornerstone despite inadequate response in a significant number of children. Children should be re-evaluated for residual or recurrent OSA after the surgery and considered for alternative therapies. CPAP therapy remains challenging in children and a multidisciplinary approach to treating children with OSA should be implemented in any community. v

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21. Smith PE, Calverley PM, Edwards RH , et al. Hypoxemia during sleep in Duchenne muscular dystrophy. Am Rev Resp Dis. 1988;137:884–8. 22. Suresh S, Wales P, Dakin C, Harris MA, Cooper DG , authors. Sleep-related breathing disorder in Duchenne muscular dystrophy: disease spectrum in the paediatric population. J Paediatr Child Health. 2005;41:500–3.

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23. Kirk VG, Morielli A, Gozal D, et al. , authors. Treatment of sleep-disordered breathing in children with myelomeningocele. Pediatr Pulmonol. 2000;30:445–52. 24. Murray C, Seton C, Prelog K, Fitzgerald DA , authors. Arnold Chiari type 1 malformation presenting with sleep disordered breathing in well children. Arch Dis Child. 2006;91:342–3. 25. Mogayzel PJ Jr., Carroll JL, Loughlin GM, Hurko O, Francomano CA, Marcus CL , authors. Sleep-disordered breathing in children with achondroplasia. J Pediatr. 1998;132:667–71 26. Buchenau W, Urschitz MS, Sautermeister J, et al. , authors. A randomized clinical trial of a new orthodontic appliance to improve upper airway obstruction in infants with Pierre Robin sequence. J Pediatr. 2007;151:145–9. 27. Leighton SE, Papsin B, Vellodi A, Dinwiddie R, Lane R. Disordered breathing during sleep in patients with mucopolysaccharidoses. Int J Pediatr Otorhinolaryngol. 2001;58(2):127-138 28. Aurora RN; Zak RS; Karippot A; et al. Practice parameters for the respiratory indications for polysomnography in children. Sleep 2011;34:379-388. 29. Silvestri JM, Weese-Mayer DE, Bass MT, Kenny AS, Hauptman SA, Pearsall SM. Polysomnography in obese children with a history of sleep-associated breathing disorders. Pediatr Pulmonol. 1993;16:124–9. 30. Montgomery-Downs HE; O’Brien LM; Holbrook CR; Gozal D. Snoring and sleep-disordered breathing in young children: subjective and objective correlates. Sleep 2004;27:87-94. 31. Brooks LJ, Topol HI. Enuresis in children with sleep apnea. J Pediatr. 2003 ;142:515-8. 32. Katz ES, D’Ambrosio CM. Pathophysiology of Pediatric Obstructive Sleep Apnea. Proc Am Thorac Soc 2008:5: 253–262. 33. Bruni O, Ottaviano S, Guidetti V, et al. The sleep disturbance scale for children (SDSC) construction and validation of an instrument to evaluate sleep disturbances in childhood and adolescence. J Sleep Res 1996;5(4):251-61 34. Luginbuehl M, Bradley-Klug KL, Ferron J, Anderson WM, Benbadis SR. Pediatric sleep disorders: validation of the sleep disorders inventory for students. Sch Psych Rev 2008;37(3):409-31

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35. Chervin RD, Hedger K, Dillon JE, Pituch KJ. Pediatric sleep questionnaire (PSQ): validity and reliability of scales for sleep-disordered breathing, snoring, sleepiness, and behavioral problems. Sleep Med 2000;1:21-32. 36. Berry RB, Budhiraja R, Gottlieb RJ, et al. Rules for scoring respiratory events in sleep: update of 2007 AASM Manual for the Scoring of Sleep and Associated Events. J Clin Sleep Med 2012; 8:597-619. 37. Aurora RN, Zack RS, Karipott S, et al. Practice parameters for respiratory indication of polysomnography in children. Sleep 2011;34:379-88. 38. Marcus CL, Brooks LJ, Draper KA, et al. Diagnosis and management of childhood sleep apnea syndrome. Pediatrics 2012;130:576-84. 39. Roland PS, Rosenfeld RM, Brooks LJ, et al. Clinical practice guideline: Polysomnography for sleep-disordered breathing prior to tonsillectomy in children. Otolaryngol Head Neck Surg. 2011; 145:S1-S15. 40. Capdevila OS, Kheirandish-Gozal L, Dayyat E, Gozal D. Pediatric obstructive sleep apnea- complications, management and long term outcomes. Proc Am Thorac Soc 2008;5:274-82 Official journal of the American Thoracic Society. 41. Beebe DW. Neurobehavioral morbidity associated with disordered breathing during sleep in children: a comprehensive review. Sleep 2006;29:1115-­1134 42. Horne RS, Yang JS, Walter LM, et al. Elevated blood pressure during sleep and wake in children with sleep-disordered breathing. Pediatrics. 2011 l;128(1):85-92 43. Khositseth A, Chokechuleekorn J, Kuptanon T, Leejakpai A. Rhythm disturbances in childhood obstructive sleep apnea during apnea-hypopnea episodes. Ann Pediatr Cardiol. 2013;6 :39-42. 44. Amin RS, Kimball TR, Bean JA, et al. Left ventricular hypertrophy and abnormal ventricular geometry in children and adolescents with obstructive sleep apnea. Am J Respir Crit Care Med. 2002;165:1395-9 45. Amin RS, Caroll JL, Jeffries JL, et al. Twenty-four–hour Ambulatory Blood Pressure in Children with Sleep-disordered Breathing. Am J Respir Crit Care Med 2004;169: 950–956 46. Kheirandish-Gozal L, Khalyfa A, Gozal D, et al. Endothelial Dysfunction in Children With Obstructive Sleep Apnea Is Associated With Epigenetic Changes in the eNOS Gene. Chest 2013; 143:971–977

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47. Aljadeff G, Gozal D, Schechtman VL, et al. Heart rate variability in children with obstructive sleep apnea. Sleep. 1997;20:151-7.

59. Goldbart AD, Greenberg-Dotan S, Tal A. Montelukast for children with obstructive sleep apnea: a double-blind, placebo-controlled study. Pediatrics 2012;130:575-80.

48. Kwok KL, Ng DK, Chan CH. Cardiovascular changes in children with snoring and obstructive sleep apnoea. Ann Acad Med Singapore. 2008 ;37:715-21

60. Kheirandish L, Goldbart AD, Gozal D Intranasal steroids and oral leukotriene modifier therapy in residual sleep-disordered breathing after tonsillectomy and adenoidectomy in children. Pediatrics. 2006;117:61-6

49. Kelly A; Dougherty S; Cucchiara A; et al. Catecholamines, adiponectin, and insulin resistance as measured by HOMA in children with obstructive sleep apnea. Sleep 2010; 33:1185-119. 50. Li AM, Ng C, Ng SK, et al. Adipokines in Children With Obstructive Sleep Apnea and the Effects of Treatment. Chest 2010; 137:529–535

61. Verhulst SL, Franckx H, Van Gaal L, et al. The effect of weight loss on sleep-disordered breathing in obese teenagers. Obesity. 2009;17:1178-83. 62. Verhulst S. Toward a multidisciplinary approach to the treatment of obstructive sleep apnea in the obese child. Otolaryngol Head Neck Surg. 2009;141:549.

51. Bhattacharjee R, Kheirandish-Gozal L, Spryut K, et al. Adenotonsillectomy outcomes in treatment of obstructive sleep apnea in children. AJRCCM 2010; 182:676-83 Official journal of the American Thoracic Society. 52. Teo DT, Mitchell RB. Systematic review of effects of adenotonsillectomy on cardiovascular parameters in children with obstructive sleep apnea. Otolaryngol Head Neck Surg. 2013 ;148(1):21-8. 53. Giordani B, Hodges EK, Guire KE, et al. Changes in neuropsychological and behavioral functioning in children with and without obstructive sleep apnea following Tonsillectomy. J Int Neuropsychol Soc. 2012;18(2):212-22. 54. Marcus CL, Radcliffe J, Konstantinopoulou J, et al. Effects of positive airway pressure on neurobehavioral outcomes in children with obstructive sleep apnea. Am J Respir Crit Care Med. 2012;185: 998–1003 55. Downey R, Perkin RM, MacQuarrie J. Nasal continuous positive airway pressure use in children with obstructive sleep apnea younger than 2 years of age. Chest. 2000;117:1608-12. 56. Pirelli P, Saponara M, Guilleminault C. Rapid maxillary expansion in children with obstructive sleep apnea syndrome. Sleep. 2004; 27: 761-6. 57. Schessl J, Rose E, Korinthenberg R, Henschen M. Severe obstructive sleep apnea alleviated by oral appliance in a three-year-old boy. Respiration 2008; 76:112–6. 58. Cozza P, Gatto R, Ballanti F, Prete L. Management of obstructive sleep apnoea in children with modified monobloc appliances. Eur J Paediatr Dent 2004; 5(1):24–9.

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Trends in Public Health

Of Weights and Measures: Bearing Up Under the Obesity Epidemic in Duval County Ikechi Konkwo, MD, MPH; Kelli Wells, MD; Katryne Lukens-Bull, MPH and Radley Remo, MPH

The current burden of obesity in the U.S. and its implications for an aging population is a source of extreme concern. The association of overweight and obesity with other disease syndromes adds a disturbing dimension to the discourse. We present the trends in Duval County and discuss the findings in the light of current state and national initiatives. Obesity is defined in terms of the body mass index (BMI) which is a standardized measure of weight relative to the height of an individual with the formula: weight (lb.) ÷ [height (in)]2 x 703 or weight (kg) ÷ [height (m)]2. A BMI of 30 and above is classified as obese, 25-29.9 as overweight, 18.5-24.9 as normal, and less than 18.5 as underweight. Of the estimated 661,000 adults living in Duval County, 34.2% are considered obese. Only about 34% are estimated to be at healthy weight. One in four adults reported a weight gain of five pounds or more in the past year. For our adolescents the data is also not encouraging, in 2011 Duval County Youth Risk Behavior Survey found that 1 out of 3 high school students were overweight or obese. Obesity is an issue in prenatal care. In 2012 in Duval County, 55.7% of babies were born to overweight/obese mothers (based on pre-pregnancy BMI). Normal pre-pregnancy weight was more common among White mothers (50.3%) than Black mothers (37.4%). Older mothers (45+) were more likely to be overweight/obese (68.2%) while teenmoms were less likely to be overweight/obese (18.7%) prior to pregnancy. Half of all births in Duval County in 2012 were paid for by Medicaid. Mothers whose births were paid for by Medicaid were significantly more likely to be overweight/ obese (58.9%) compared to mothers with private insurance (41.1%) (p<.000). Outcomes varied significantly according to pre-pregnancy BMI status, with consistently more adverse outcomes in the obese population. There was three times the incidence of hypertension in pregnancy, twice the incidence of gestational diabetes and one and half times the incidence of C-sections in obese mothers. Based on 2012 hospitalization data (n=127,824), 12.2% of hospitalized patients had a diagnosis of obesity/overweight (ICD9-CM 278.00 – 278.02) as either a primary or co-morbid diagnosis, which amounted to 15,548 visits for 9,518

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residents in Duval County. The total charges for these visits was $8.5 million. Thirty eight percent (38.8%) were repeat hospital admissions within the same year. Circulatory disorders accounted for 19.4% of all visits for residents with a diagnosis of overweight/obese, costing a total of $2 million (24% of the total charges). Heart disease accounted for most (68%) of these hospitalizations. Costs for patients diagnosed with a circulatory disorder were higher when a co-morbid diagnosis of obesity/overweight was present (p<.000). Medicare was the largest payer by insurance status for patients with an overweight/obesity diagnosis. In 2012 in Duval County, 24 residents had overweight and obesity (ICD10 E66) listed as a primary cause of death. For an additional 62 residents, overweight and obesity was listed as a secondary contributing cause of death. These deaths accounted for 1.2% of all deaths in the county. Of these 86 deaths, most (58.1%) were 45-64 years of age. The most common cause of death was heart disease (27.9%). In Duval County residents who died of chronic conditions (heart disease, stroke, hypertension, diabetes and COPD) and in whom overweight/obese was listed as a contributing cause, 54.3% died before age 55. Health Zone 1 accounted for more deaths (24.4%) than any other health zone, with a higher proportion of patients hospitalized with obese/overweight diagnosis (15%) and fewer mothers with pre-pregnancy healthy weight BMI (34.8%). Conversely, Health Zone 6 (the beaches) had the fewest deaths (8.1%), fewest hospitalizations with obese/overweight diagnosis (7.8%) and the highest number of pre-pregnancy healthy weight BMI (55.1%) Clearly, Health Zone 1, with the most socio-economically challenged individuals, is disproportionately affected by obesity. The recent ‘Healthiest Weight Florida’ initiative from Florida’s State Surgeon General and Secretary of Health, Dr. John Armstrong, is poised to address the health risks of obesity. The effort is a comprehensive approach that seeks to improve built environment, increase breast-feeding initiation rates and duration and encourage children and adults to live healthier, active lifestyles. In Duval County we hope to demonstrate the efficacy of this collaborative community effort. v

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From the President’s Desk

How the moment flies! It seems just a few days ago that we started our DCMS journey together and yet, almost a year has gone by. We have made great strides, you and I. I pledged to try to make this the best year in our history and with your help, to reinfuse some of the zest of years gone by. Let’s look at some of the highlights of the past twelve months and see how we did. As we entered the year we faced a very flat budget, almost working at a deficit. Our home was falling apart and cost us as much in repairs as it would to rent an office in a downtown building. We seemed to be out of synch with the interests of our membership who in turn seemed to be avoiding DCMS activity. We began immediately to turn around the budget by increasing activities and events with help from our sponsors and members. Our theory was that no activity was out of bounds if it was of value to the membership. With the help of Bryan Campbell and his very able staff, all avenues of membership participation Eli Lerner, MD and benefits were explored. 2013 DCMS President We began an ongoing program of going out to areas of the community for small meetings of special interest to members. These meetings range from financial advice to young physicians just coming in to practice to those on the verge of retirement as well as practice management programs for all members. They have been an immediate success and continue to be an important part of our services. We have participated in community programs, such as high school athletic screening exams and school physicals for children living in underprivileged areas, as well as participating in free clinics throughout the county and supporting We Care and other like-minded organizations. We partnered with outside organizations to help them present topics of medical ethics and garnered CME’s for those programs. We began development of a new program with University of Florida Health. We will be presenting an ongoing program of how to deal with the business and ethical issues of private practice presented to the Residents at UFH and Mayo Clinic. The program is currently being vetted now and has the support of Dean Wilson and Dr. Linda Edwards, who look forward to this program to help educate the residents in areas that are not covered in their official training program. I am most proud of bringing the program forward and will do everything that I can to assure its success.

this noble effort has been a work of love. Many of us attended and participated in the programs presented which act to unify the entire Northeast Florida medical community and give us all the ability to express and codify our thoughts on community health, ethics, and economics. Our annual visit from the President-Elect, Dr. Ardis Hoven, was wonderfully done and she has become one of our greatest fans as a result of the experience. She helped us bring the diversity of our medical community together and set the path for us to forge an alliance with our Navy colleagues which has become stronger than ever before. The fruit of those labors was bourn out at the Annual DCMS-Navy dinner, which was well attended, and the most collegial event of the year. Social events were a joy this year, beginning with a Night at the Ballpark with well over one hundred people showing up for the game and hamburgers and hot dogs. The event was sweetened by a home team win. Our tour of the locker room at Everbank Stadium was also a strong event. It is a seven million dollar testimony to the desire of Shahid Khan to make a big difference in our city and the explanation of the future scoreboards and stadium swimming pools were very interesting. Opening Night at the Jacksonville Symphony was awesome, presenting very youthful piano soloist-director Teddy Abrams. Many of our personal friends from DCMS were in attendance and we all had a wonderful time. The biggest event of the year, however, was the sale of our building. As you know, the building became an anchor over the past few years, drowning us in expenses and repairs that were devastating. We sold the building and moved out in October to our new offices in the Wells Fargo Building on South Bank at less annualized cost than our current costs were. Another milestone accomplished which make us a leaner organization with more funds to go to DCMS activities while operating out of one of the finest buildings in our city. Personally, this has been my busiest year in Organized Medicine and I have enjoyed it immensely. Being your President has been difficult at times but never boring. It, for me, has been a work of joy and pleasure, especially helping to implement new programs and watching them grow. I shall never forget this year, helping return health to our organization nor will I ever be able to give you back as much as you gave me. My greatest satisfaction now is leaving you under the leadership of our new President and my personal friend, Dr. Mobeen Rathore. I know that he will be a great leader and President. He is highly regarded in his field of Pediatrics and Infectious Disease and I know that he will be a strong, outstanding President. Thank you for allowing me to serve as your President. Eli Lerner, M.D.; F.A.C.S

We once again participated in Dr. Yank Coble’s Caring Community Conferences at UNF. Helping to assure the success of

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Your Compassionate Guide leads to quality time.


Your patients have a guide to walk with, listen to and help them find quality time through all stages of advanced illness—Community Hospice of Northeast Florida. Ask us how we can help your patients find that quality time. Call Community Hospice today.

904.407.6500 • 866.253.6681 toll free • Community Focused • Community Supported counties since 1979 DCMS online . orgServing Baker, Clay, Duval, Nassau and St. Johns Northeast Florida Medicine Vol. 64, No. 4

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Duval County Medical Society Foundation 555 Bishopgate 1301 RiverplaceLane Blvd. Suite 1638 Jacksonville, FL Jacksonville, FL 32204 32207


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The Doctors Company is devoted to helping doctors avoid potential lawsuits. For us, this starts with patient safety. In fact, we have the largest Department of Patient Safety of any medical malpractice insurer. And, local physician advisory boards across the country. Why do we go this far? Because sometimes the best way to look out for the doctor is to start with the patient. To learn more about our medical malpractice insurance program, call our Jacksonville office at (800) 741-3742 or visit

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Northeast Florida Medicine - Winter 2013 - Sleep Health  

Our Winter 2013 issue on Sleep Health is guest edited by DCMS member Dr. Abubakr Bajwa. It offers CME credit on Ibstructive Sleep Apnea. CME...

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