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27th Annual SW Virginia Pediatrics Conference Saturday August 6 and Sunday August 7, 2011 M Martha Washington Inn Abingdon, Virginia Saturday, August 6, 2011 7:00 Registration and Breakfast 7:25 Welcome and Announcements 7:30 Child Obesity Treatment in Primary Care: What‟s the PLAN? Karen Schetzina, MD, William Dalton, PhD 8:15 Sports Injuries in the Pediatric Athlete: Considerations for the Stars of Tomorrow Eric Parks, MD 9:00 KEYNOTE ADDRESS Seizures: Diagnosis and Management in Primary Care Tracy Glauser, MD 10:00 Break, Exhibits and Poster Displays 10:30 Anti-epileptics: The Old, the New, and Future Directions Jim Thigpen, PharmD, BCPS 11:15 Life After Cancer: Cases from the Clinic Sharon Castellino, MD 12:10 Adolescent Medicine-Jeopardy! David Chastain, MD Optional Workshop 2-3:30 Putting a PLAN into Practice for Child Obesity Management in Primary Care Karen Schetzina, MPH, MD and Will Dalton, PhD 27th Annual SW Virginia Pediatrics Conference Saturday August 6 and Sunday August 7, 2011 M Martha Washington Inn Abingdon, Virginia Sunday, August 7, 2011 7:30 Updates in Dermatology: Let‟s Get Sun Safe Robert Clemmons, MD 8:30 Update on Craniosynostosis and Deformational Plagiocephaly James Thompson, MD 9:30 Direct Ophthalmoscopy: How to Use One of the Most Powerful Instruments in Your Office Jeffery Carlsen, MD 9:55 Break and Poster Session 10:15 Guidelines for Diagnosis and Management of URTI, Rhinitis and PSI Mark Howell, MD, FACS 11:15 “I‟m Not Listening”! : Assessment & Treatment of Oppositional/Disruptive Behavior in Primary Care Jennifer Correll, MA, PhD (2011) 12:00 What's Up With Spit Up? Darshan Shah, MD 12:45 Adjourn until August 5 - 6, 2012 The 27th Annual SW Virginia Pediatrics Conference is sponsored by the Department of Pediatrics, Quillen College of Medicine, ETSU, in association with Conference Activity Directors and Planning Committee Activity Directors: David Kalwinsky, MD, Chair, Department of Pediatrics, Quillen College of Medicine, East Tennessee State University, Johnson City, TN, & Des Bharti, MD, Professor, Department of Pediatrics, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN Planning Committee: Gayatri Jaishankar, MD, Assistant Professor, Department of Pediatrics, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN Demetrio Macariola, MD, Assistant Professor, Department of Pediatrics, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN Marcella Popescu, MD, Assistant Professor, Department of Pediatrics, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN Dawn Tuell, MD, Assistant Professor, Department of Pediatrics, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN Joy Wachs, PhD, RN, PHCNS-BC, Professor and Coordinator, Continuing Nursing Education Honors-in-Discipline Programs, College of Nursing, ETSU Christine Newell Kwasigroch, MEd, PhD, Program Planner, Office of Continuing Medical Education, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN Presenters : Jeffrey Carlsen, MD Johnson City Eye Clinic & Johnson City Eye Surgery Center, Johnson City, TN Sharon Castellino, MD, FAAP Wake Forrest Baptist Medical Center Winston Salem, NC David Chastain, MD Department of Pediatrics Quillen College of Medicine, Johnson City, TN Robert Clemons, MD, FAAD TriCities Skin and Cancer, Johnson City, TN Jennifer Correll, MA, PhD (2011) Department of Clinical Psychology Behavioral Health and Wellness Clinic East Tennessee State University, Johnson City, TN William Dalton, PhD Assistant Professor Department of Psychology, ETSU Johnson City, TN Tracy Glauser, MD Professor of Pediatrics and Neurology Director, Comprehensive Epilepsy Center Co-Director, Genetic Pharmacology Service Children's Hospital Medical Center Cincinnati, Ohio Mark Howell, MD, FACS Ear, Nose and Throat Associates, Johnson City, TN Eric Parks, MD Primary Care Sports Medicine Watauga Orthopedics, Kingsport, TN Karen Schetzina, MD, MPH Assistant Professor, and Director, Division of Community Pediatrics Research, Department of Pediatrics, Quillen College of Medicine; Adjunct Professor, Department of Epidemiology and Biostatistics ETSU College of Public Health, Johnson City, TN Darshan Shah, MD Assistant Professor, Quillen College of Medicine, Department of Pediatrics, Johnson City, TN Jim Thigpen, PharmD, BCPS Assistant Professor, Department of Pharmacy Practice Bill Gatton College of Pharmacy, ETSU, Johnson City, TN James Thompson, MD, FACS Assistant Professor, Department of Plastic and Reconstructive Surgery Wake Forest School of Medicine Winston-Salem, NC CME Credit: Quillen College of Medicine, East Tennessee State University is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education ofr physicians. The Quillen College of Medicine, East Tennessee State University designates this live activity for a maximum of 10.0 AMA PRA Category 1 Credits™. The Optional PLAN Workshop is designated for 1.5 AMA PRA Category 1 Credits™. AAFP Credit: This Live activity, 27th Annual SW Virginia Pediatrics Conference, with a beginning date of August 6, 2011, has been reviewed and is acceptable for up to 11.50 Prescribed credit(s) by the American Academy of Family Physicians. Physicians should claim only the credit commensurate with the extent of their participation in the activity. Application #: 52610 TN CNE Credit: 9.75 continuing nursing education contact hours for the conference and an additional 1.5 contact hours for the optional workshop. East Tennessee State University College of Nursing is an approved provider of continuing nursing education by the Tennessee Nurses Association, an accredited approver by the American Nurses Credentialing Center's Commission on Accreditation. This event is presented by the Quillen College of Medicine Office of Continuing Medical Education and the College of Nursing Office of Continuing Nursing Education at East Tennessee State University. Nursing Credit: As an Accreditation Council on Continuing Medical Education (ACCME)approved provider, the CME credit offered during this educational activity is accepted by the ANCC, AACN and the NCCPA for recertification. CME Certificates: By submitting the „Request for Credit Form‟ (which is part of your Conference Handouts,) and by signing the sign in sheets each day, credits will be added to your online TRANSCRIPT, which is maintained in the ETSU Office of CME. You may print your transcript online from our website, http://www.etsu.edu/cme. Go to „For Learners‟ „Transcript of Your Earned Credits‟. Please allow 2 weeks from the conference date before requesting your transcript. Check with the Registration Desk for information on how to access and print your transcript, or call our office, 423-439-8027, with questions. Instructions are also printed on our monthly calendar. Disclosure Information: Quillen College of Medicine, East Tennessee State University‟s Office of Continuing Medical Education (OCME) holds the standard that its continuing medical education programs should be free of commercial bias and conflict of interest. It is the policy of the OCME that each presenter and planning committee member of any CME activity must disclose any significant financial interest/arrangement or affiliation with corporate organizations whose products or services are being discussed in a presentation. Each of the following speakers and conference planners* have completed a disclosure form indicating that they or members of their immediate family have NO financial interest/arrangement or affiliation that could be perceived as a real or apparent conflict of interest related to: (a) the content of this activity or (b) the supporters involved with this activity: *Des Bharti Jeffrey Carlsen Sharon Castellino David Chastain Robert Clemons Jennifer Correll William Dalton Tracy Glauser Mark Howell *Gayatri Jaishankar *David Kalwinsky *Chris Newell Kwasigroch *Demetrio R. Macariola Eric Parks *Marcella Popescu Karen Schetzina Darshan Shah James Thigpen James Thompson *Dawn Tuell *Joy Wachs Commercial Support Disclosure: It is the policy of the Office of Continuing Medical Education at Quillen College of Medicine, East Tennessee State University to disclose all Commercial Supporters of this educational activity from which educational grants were received. Unrestricted Educational Grant Support was received from the following: Lundquist Pharmaceuticals The Mission of the Office of Continuing Medical Education at the James H. Quillen College of Medicine is to provide quality educational programs to physicians and other health professionals in Northeast Tennessee, Southwest Virginia and contiguous areas. The office develops and sponsors educational activities that enhance the knowledge, skills, professional performance and relationships required by health professionals to serve patients, the public and their professions. The Syllabus with Full Color Complete Presentations--if permitted by the speaker-- is available as a pdf document on the conference website: http://www.etsu.edu/com/cme/Southwestvapeds.aspx Please note that all presenters may not have provided handouts prior to the conference and may bring material with them for distribution at the time of their presentation. CME Senior Conference Planner: Christine Newell Kwasigroch, MEd-MFT, Ph.D. 423-439-8074 [email protected] If you have questions, concerns, or comments about this activity, please contact: Barbara J. Sucher, M.B.A., Associate Dean for Continuing Medical Education [email protected] or 423-439-8081 We gratefully acknowledge the participation and generous support of the following sponsors: This conference is supported in association with Unrestricted Educational Grants from: Lundbeck, Inc Exhibitors BABE—Breastfeeding Advocacy Benefits Everyone ETSU Pediatric Cardiology Niswonger Children’s Hospital SW Virginia Care Connection for Children Learning Resources available though: Quillen College Medicine Medical Library website: http://com.etsu.edu/medlib/ Mark Your Calendar for these upcoming events: Quillen College of Medicine Office of Continuing Medical Education (CME) offers educational programs for Physicians, Nurse Practitioners and Physician Assistants, as well as for other health care providers in NE Tennessee, SE Kentucky, SW Virginia, and Western North Carolina. Educational Forums on Prescription Drug Abuse There are no fees for these sessions--However, advance registration is required. To register go to http://www.etsu.edu/com/cme • Dates and Locations: • Saturday, September 17, 2011 – Richlands, VA • Sunday, September 18, 2011 – Big Stone Gap, VA • Target Audience: Practicing/Licensed M.D.s/D.O.s, Dentists, APNs, PAs, Pharmacists, Pharmacy Technicians and Interns, and Medical Students in the Commonwealth. • Learning Objectives: As a result of participating in this activity, the attendee should be able to: • Explain and demonstrate the legal and regulatory requirements for using controlled substances to treat chronic pain in Virginia. • Illustrate how health care providers can work with law enforcement to curb prescription drug abuse in our region. • Compare options available for treatment of opiate dependence (i.e., methadone maintenance therapy and buprenorphine) with a focus on safety, efficacy, and appropriate prescribing precautions. • Describe the universal precautions for prescribing controlled substances. • Demonstrate how to use the PMP as a resource in patient-centered care. Women’s Health Across the Lifespan: A Comprehensive Approach Website: http://www.etsu.edu/com/cme/womenshealth2011.aspx When: October 7, 2011 Where: The Millennium Center, Johnson City, TN Target Audience: Primary care and specialist physicians, nurses, nurse practitioners, physician assistants, pharmacists, as well as any practitioner working in teams to provide inter-professional care for their female patients Learning Objectives • Explain the latest evidence for the origins of fibromyalgia Differentiate fibromyalgia from other similar clinical presentations Identify new pharmacological and non-pharmacological treatment strategies for patients with fibromyalgia Assess women with chest pain and determine the appropriate sequence of testing and referral for care and cardiac rehabilitation Develop a plan to screen women for heart disease • • • • Explain the current recommendations regarding hormone replacement therapy and its risks and benefits Differentiate among the various pharmacologic and bio-identical agents with estrogenic activity and determine when each may or may not be indicated Compare the risks, benefits and drug interactions of herbal/alternative medicines and dietary supplements currently in use and be able to explain this to patients Identify and distinguish overlapping and confounding symptoms Psychiatry in the Mountains: Autism & Anxiety Disorder Spectrums • When: October 21, 2011 • Where: The Millennium Centre, Johnson City, TN • Target Audience : Physicians, nurses, psychiatrists and other healthcare professionals on the diagnosis and treatment of autism and anxiety disorders in adults and children • Topics Include: • • • • • • Asperger’s Syndrome Family & School Issues Update on Autism Evaluation, Treatment & Research Treatment of Anxiety: Including Children with Tics, Trichotillomania & Tourette’s Psychotherapeutic Treatment of Appalachian Combat Veterans with PTSD Psychopharmacology of Anxiety Disorders FOR MORE INFORMATION on these or other upcoming CME programs, or to register for any activity, please contact our office at 423-439-8027 or visit our website at http://www.etsu.edu/cme Check our website for a video recording of this and other CME events 27th Annual SW VA Pediatrics Conference 8/6‐7/2011 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: William Dalton, PhD does not anticipate discussing the unapproved /investigative use of a commercial product/device during this lecture. He reports that he DOES NOT have a financial interest/arrangement or affiliation with one or more organizations that could be perceived as a real or apparent conflict of interest in the context of this presentation. DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: Karen Schetzina, MD does not anticipate discussing the unapproved /investigative use of a commercial product/device during this lecture. She reports that she DOES NOT have a financial interest/arrangement or affiliation with one or more organizations that could be perceived as a real or apparent conflict of interest in the context of this presentation. 27th Annual SW VA Pediatrics Conference Child Obesity Treatment in Primary Care: What's the PLAN? • Describe the latest evidence on effective behavioral treatment approaches for child obesity in primary care • Overcome common challenges in treating child obesity • Integrate evidence‐based behavioral approaches and tools for addressing child obesity into primary care tools for addressing child obesity into primary care practice 8/6‐7/2011 Notes: Child Obesity Treatment in Primary Care: What's the PLAN? William Dalton, PhD Karen Schetzina, MPH, MD William Dalton, PhD Karen Schetzina, MD, MPH 8/6/2011 Primary Care Research Study In Memoriam: Tiejian Wu, MD, PhD h 1962‐2011 Purpose: Evaluate a parent‐mediated approach utilizing Evaluate a parent mediated approach utilizing brief motivational interviewing and group visits to treat child (ages 5‐11 years) overweight and obesity in the primary care setting 15-Minute Obesity Prevention Protocol Steps Sample Language STEP 1. ASSESSMENT Weight and height, convert to BMI. Provide BMI information. We checked your child’s body mass index (BMI), which is a way of looking at weight and taking into consideration how tall someone is. Your child’s BMI is in the range where we start to be concerned about extra weight causing health problems. Elicit parent’s concern. —What concerns, if any, do you have about your child’s weight? — He did jump two sizes this year. Do you think he might get diabetes someday? Reflect/probe. So you’ve noticed a big change in his size and you are concerned about diabetes down the road. What makes you concerned about diabetes in particular? Etc. Sweetened beverages, fruits and vegetables, TV viewing and other sedentary behavior, frequency of fast-food or restaurant eating, consumption of breakfast, and others (Use verbal questions or brief questionnaires to assess key behaviors.) Example: About how many times a day does your child drink soda, sports drinks, or powdered drinks like Kool-Aid? Provide positive feedback for behavior(s) in optimal range. Elicit response. You are doing well with sugared drinks. I know it’s not healthy. He used to drink a lot of soda, but now I try to give him water whenever possible. I think we are down to just a few soda’s a week. So you have been able to make a change without too much stress. Reflect/probe. Provide neutral feedback for behavior(s) NOT in optimal range. Elicit response. Your child watches 4 hours of TV on school days. What do you think about that? I know it’s a lot, but he gets bored otherwise and starts picking an argument with his little sister. So watching TV keeps the household calm. Reflect/probe STEP 2. AGENDA SETTING Query which, if any, of the target behaviors parent/child/adolescent may be interested in changing or might be easiest to change. We’ve talked about eating too often at fast-food restaurants, and how TV viewing is more hours than you’d like. Which of these, if either of them, do you think you and your child could change? Well, I think fast food is somewhere we could do better. I don’t know what he would do if he couldn’t watch TV. Maybe we could cut back on fast food to once a week. Agree on possible target behavior. That sounds like a good plan. STEP 3. ASSESS MOTIVATION AND CONFIDENCE 3a: Willingness/Importance On a scale of 0 to 10, with 10 being very important, how important is it for you to reduce the amount of fast food he eats? 0 Not at all 1 2 3 4 5 6 Somewhat 7 8 9 10 Very continued 15-Minute Obesity Prevention Protocol 15-Minute Obesity Prevention Protocol 15-Minute Obesity Prevention Protocol, continued STEP 3. ASSESS MOTIVATION AND CONFIDENCE, continued 3b: Confidence On a scale of 0 to 10, with 10 being very confident, assuming you decided to change the amount of fast food he eats, how confident are you that you could succeed? 0 1 2 3 4 Not at all 5 6 Somewhat 3c: Explore IMPORTANCE and CONFIDENCE ratings with the following probes: Benefits Barriers Solutions 7 8 9 10 Very You chose 6. Why did you not choose a lower number? I know all that grease is bad for him. You chose 6. Why did you not choose a higher number? It’s quick, cheap, and he loves it…especially the toys and fries. REFLECTION: So there are benefits for both you and him. What would it take you to move to an 8? Well, I really want him to avoid diabetes. My mother died of diabetes, and it wasn’t pretty…maybe if he started showing signs of it…maybe if I could get into cooking a bit. STEP 4. SUMMARIZE AND PROBE POSSIBLE CHANGES Query possible next steps. So where does that leave you? OR From what you mentioned it sounds like eating less fast food may be a good first step. OR How are you feeling about making a change? Probe plan of attack. What might be a good first step for you and your child? Or What might you do in the next week or even day to help move things along? Or What ideas do you have for making this happen? If patient does not have any ideas… If it’s OK with you, I’d like to suggest a few things that have worked for some of my patients. Summarize change plan, provide positive feedback. Involving child in cooking or meal preparation Ordering healthier at fast-food restaurants Trying some new recipes at home STEP 5. SCHEDULE FOLLOW-UP Agree to follow up within X weeks/months. Let’s schedule a visit in the next few weeks/months to see how things went. If no plan is made Sounds like you aren’t quite ready to commit to making any changes now. How about we follow up with this at your child’s next visit? OR Although you don’t sound ready to make any changes, between now and our next visit you might want to think about your child’s weight gain and lowering his diabetes risk. We Can! Try Tips To Eat Well and Move More Choose to take small steps today! Try these tips to eat well and move more and see how easy taking small steps toward a healthier life can be. Eating Well (ENERGY IN) • Drink water before a meal. • Eat half your dessert, or choose fruit as dessert. • Avoid food portions larger than your fist. • Drink diet soda instead of regular soda. • Eat off smaller plates. • Don't eat late at night. • Skip buffets. • Grill, steam, or bake instead of frying. • Share an entree with a friend. • Eat before grocery shopping. • Choose a checkout line without a candy display. • Make a grocery list before you shop. • Drink water or low-fat milk over soda and other sugary drinks. • Flavor foods with herbs, spices, and other low-fat seasonings. • Keep to a regular eating schedule. • Eat before you get too hungry. • Don't skip breakfast. • Stop eating when you are full. • Snack on fruits and vegetables. • Top your favorite cereal with apples or bananas. • Include several servings of whole-grain foods daily. • If main dishes are too big, choose an appetizer or a side dish instead. • Ask for salad dressing “on the side.” • Don't take seconds. • Try a green salad instead of fries. • Eat sweet foods in small amounts. • Cut back on added fats or oils in cooking or spreads. • Cut high-calorie foods like cheese and chocolate into small pieces and only eat a few pieces. • Use fat-free or low-fat sour cream, mayo, sauces, dressings, and other condiments. • Replace sugar-sweetened beverages with water and add a twist of lemon or lime. • Every time you eat a meal, sit down, chew slowly, and pay attention to flavors and textures. • Try a new fruit or vegetable (ever had jicama, plantain, bok choy, star fruit, or papaya?) • Instead of eating out, bring a healthy, low-calorie lunch to work. • Ask your sweetie to bring you fruit or flowers instead of chocolate. Moving More (ENERGY OUT) • Walk your children to school. • Take a family walk after dinner. • Join an exercise group and enroll your children in community sports teams or lessons. • Replace a Sunday drive with a Sunday walk. • Do yard work. Get your children to help rake, weed, plant, etc. • Get off the bus a stop early and walk. • Work around the house. Ask your children for help doing active chores. • Walk the dog to the park. • Go for a half-hour walk instead of watching TV. • Pace the sidelines at kids' athletic games. • Choose an activity that fits into your daily life. Being physically active with your family is a great way to spend time together. • Park farther from the store and walk. • Use an exercise video with your kids if the weather is bad. • Avoid labor-saving devices, such as a remote control or electric mixers. • Play with your kids 30 minutes a day. • Dance to music. Play your favorite dance music for your children and have them play their favorites for you. • Make a Saturday morning walk a family habit. • Walk briskly in the mall. • Choose activities you enjoy—you'll be more likely to stick with them. Ask children what activities they want to do. • Explore new physical activities. • Acknowledge your efforts with non-food related rewards, such as a family day at the park, lake, or zoo. • Take the stairs instead of the escalator. • Swim with your kids. • Turn off the TV and play ball at the park. • Take your dog on longer walks. • When walking, go up the hills instead of around them. • Use a family activity planner to make time each day for activity. • Buy a set of hand weights and play a round of Simon Says with your kids—you do it with the weights, they do it without. Source: Adapted from www.smallstep.gov We Can! Try Tips To Eat Well and Move More Tracking Sheet Pick a tip each week from the list of Everyday tips to help you eat well and move more! Fill in the tips on this tracking chart to encourage you to keep it up. Put the tracking sheet on your refrigerator or other central location for your family to see that you are making steps toward maintaining a healthy weight. Week Week 1 (___/___) Week 2 (___/___) Week 3 (___/___) Week 4 (___/___) Week 5 (___/___) Week 6 (___/___) Eating Well Tip Moving More Tip Notes for Healthy Active Living Name Date Ideas for Living a Healthy Active Life 5 Eat at least 5 fruits and vegetables every day. 2 Limit screen time (for example, TV, video games, computer) to 2 hours or less per day. 1 Get 1 hour or more of physical activity every day. 0 Drink fewer sugar-sweetened drinks. Try water and low-fat milk instead. My Goals (choose one you would like to work on first) n Eat fruits and vegetables each day. n Reduce screen time to minutes per day. n Get minutes of physical activity each day. n Reduce number of sugared drinks to per day. From Your Doctor Patient or Parent/Guardian signature Doctor signature Healthy Active Living An initiative of the American Academy of Pediatrics William Dalton, PhD Karen Schetzina, MD, MPH 8/6/2011 Resources: AAP Obesity Initiative http://www.aap.org/obesity/index.html NIH We Can! http://www.nhlbi.nih.gov/health/public/heart/obesity/wecan/ [email protected] [email protected] 27th Annual SW VA Pediatrics Conference 8/6‐7/2011 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: Eric Parks, MD does not anticipate discussing the unapproved /investigative use of a commercial product/device during this lecture. He reports that he DOES NOT have a financial interest/arrangement or affiliation with one or more organizations that could be perceived h ld b d as a real or apparent conflict of interest in the context of this presentation. Sports Injuries in the Pediatric Athlete: Considerations for the Stars of Tomorrow • Recognize the common overuse injuries sustained by the young athlete • Make recommendations to parents of young athletes regarding risks of overuse during sports Notes: Sports Injuries in the Pediatric Athlete: Considerations for the Stars of Tomorrow Eric Parks, MD Eric Parks, MD 8/6/2011 Sports Injuries The Physis Epidemiology • 30-50% of adolescent sports-related injuries are overuse – Watkins J. J Sports Med Phys Fitness. 1996;36(1):4348. • 15% of all adolescent injuries are to the physes and apophyses – Pill SG. J Musculoskeletal Med. 2003;20:434-442 27th Annual SW VA Pediatrics Conference • Cartilage is less resistant to tensile forces than bones, ligaments, and muscle-tendon units • Bones grow faster than muscle-tendon units • Same injury leading to a muscle strain in an adult may result in growth center injuries in adolescents • The “Weak Link” 27th Annual SW VA Pediatrics Conference Key Points During Evaluation Treatment General Principles • History and physical exam – Recent change in activity or training • Insidious onset of pain that worsens with activity and improves with rest • Point tenderness with or without swelling • Pain with passive stretch of attached ligament/ muscle-tendon unit • Pain with firing muscle-tendon unit against resistance • Radiographs? – Help to rule out other pathology 27th Annual SW VA Pediatrics Conference • • • • • • • • Relative rest Cross training Flexibility Ice Counter-balance bracing ?NSAIDS ORIF with certain avulsions Resection of retained, non-fused ossicles 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 PFS Patellofemoral Friction Syndrome • • • • Most common cause of anterior knee pain Estimated prevalance of 20% Mean age 14 years “The Great Imitator” of symptoms Risk Factors and Treatment • • • • Muscle imbalances Flexibility issues Over-pronation, pes planus Specific sports – Location and quality of pain • Walking stairs, incline/decline • “Theatre sign” • Treat from the hip to the waist • Orthotics, bracing, taping? 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Osgood-Schlatter’s Disease (OSD) Osgood-Schlatter’s Disease (OSD) Tibial Tubercle Apophysitis Tibial Tubercle Apophysitis • Occurs in 20% of young athletes – most common pediatric overuse injury • • • • 20% of OSD is bilateral Girls 8–13yo 8 13yo Boys 10-15yo Aggravated by running, jumping, or other explosive activities • Occasionally aggravated by kneeling or direct trauma 27th Annual SW VA Pediatrics Conference • Point tender +/- swelling at tibial tubercle • Pain with quadriceps stretch or contraction, poor quad flexibility • Widened Wid d physis h i or fragmented f t d tibial tibi l tubercle t b l on radiographs • Tight quadriceps or hip flexors – Positive Thomas test 27th Annual SW VA Pediatrics Conference Eric Parks, MD • • • • • 8/6/2011 Osgood-Schlatter’s Disease (OSD) Osgood-Schlatter’s Disease (OSD) Risk Factors Treatment Repetitive explosive activities Recent increase in activities Tight quadriceps and/or hip flexors External tibial torsion Patella alta • • • • • • Relative rest Quadriceps and hip flexor stretching Ice NSAIDs Cho-Pat strap Knee pads 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Sinding-Larsen-Johansson Syndrome (SLR) Sinding-Larsen-Johansson Syndrome (SLR) • Apophysitis at the inferior pole of the patella • 10-12 years old p g athletes • Most common in runningg & jjumping – Basketball, soccer, gymnastics • “Adolescent Jumper’s Knee” 27th Annual SW VA Pediatrics Conference • • • • Tenderness at the inferior pole of the patella Pain worsened with explosive activity Tight quadriceps Radiographs may reveal fragmentation of the inferior pole and/or calcification at the proximal patella tendon 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Sinding-Larsen-Johansson Syndrome (SLR) Treatment • • • • • Relative rest Quadriceps Q p stretchingg Ice NSAIDs Cho-Pat strap Osteochondritis Dessicans • Avascular necrosis of cartilage bed • May be result of direct trauma vs iatrogenic • MC location- lateral pportion of medial femoral condyle • Age 9-18 years old • Consider in adolescent presenting with painless effusion 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Osteochondritis Dessicans Sever’s Disease Treatment Calcaneal Apophysitis • Treatment will depend on the stability of the lesion • Protected/NWB for 6 weeks • Bracing • Follow up imaging • Unstable- surgical 27th Annual SW VA Pediatrics Conference • Affects boys and girls equally • Ages 8-13 years • Most common in soccer, basketball, & gymnastics – Repetitive heel impact & traction stress from the achilles tendon • Bilateral in 60% of cases 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Sever’s Disease Sever’s Disease Calcaneal Apophysitis Risk Factors • • • • • Heel pain worsened with activity No swelling Point tender at posterior calcaneus Pain with medial-lateral compression Pain with calf stretch or contraction against resistance • Tight heel cord, weak dorsiflexors, subtalar overpronation 27th Annual SW VA Pediatrics Conference Sever’s Disease Treatment • • • • • Relative rest Heel cord stretching Heel cups Ice NSAIDs 27th Annual SW VA Pediatrics Conference • Repetitive explosive activities • Repetitive trauma – Jumping, landing, cleats, etc. • Recent R iincrease in i activities i ii • Tight heel cord • Before/during rapid periods of growth • Beginning of new season 27th Annual SW VA Pediatrics Conference Pelvic Apophysitis • 10-14 years old • Insidious onset of hip pain or sudden sharp pain – Running, jumping, kicking sports • Point tender • Pain with stretch or contraction of involved muscle • Widening of physis or avulsion of apophysis 27th Annual SW VA Pediatrics Conference Eric Parks, MD • • • • • • • 8/6/2011 Pelvic Apophysitis Medial Epicondyle Apophysitis Treatment Little League Elbow Relative rest until pain free (~4-6 weeks) WBAT without limping NSAIDs Ice Stretching & strengthening Progressive return to activities Rare need for surgery 27th Annual SW VA Pediatrics Conference Medial Epicondyle Apophysitis Little League Elbow • X-rays may reveal widening of medial epicondyle apophysis &/or fragmentation of medial epiphysis • 85% of X-rays are normal – Hang DW. Am J Sports Med. 2004 27th Annual SW VA Pediatrics Conference • Most common in 9 to 14 y/o overhead athletes • ~18-29% incidence of elbow pain in youth and HS baseball players • Point P i t tenderness t d over medial di l epicondyle i d l • Classically worsened by repetitive throwing • Hypertrophy of medial epicondyle • Flexion contracture • Pain with valgus stress & milking maneuver 27th Annual SW VA Pediatrics Conference Little League Elbow Treatment • If apophysis not significantly displaced (<5mm) – (Relative) rest 4 - 6 weeks – Isometric strengthening, stretching, resistive strengthening – Throwing Thro ing mechanics evaluation e aluation – Gradual return to throwing after 6 - 12 weeks • Interval Throwing Program – Follow pitch counts & types • If apophysis significantly displaced (>5mm) surgery is warranted 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 USA Baseball Medical & Safety Advisory Committee Pitch Counts 2008 27th Annual SW VA Pediatrics Conference USA Baseball Medical & Safety Advisory Committee Days Off 2008 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Little League Shoulder Proximal Humeral Epiphysiolysis • Fatigue fracture of the proximal humeral physis – Does not fuse until ages 14-20 • Typically high-performance male pitchers • Rotatory torque stresses to the epiphyseal growth plate • 9-14 9 14 years old • Pain • Inability to perform • Decreased ROM • TTP at anterior proximal humerus • Remember– physis is the weak link! Proximal Humeral Epiphysiolysis • Treatment – Relative rest for 4-6 weeks p g – Interval throwingg program – Thrower’s 10 program 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Spondylolysis Spondylolysis Epidemiology • • • • Little League Shoulder Lesion in the pars interarticularis of the neural arch Incidence of 6-8% in general population 6.4% for Caucasian males 1.1% for African-American females – Roche MA, MA Rowe GG. GG Anat Rec. Rec 1951 • Overall incidence of 4.4% by age 6, 5.2% by age 12, and 6% by adulthood – Frederickson BE. J Bone Joint Surg. 1984 • Males>>>Females • 85-95% occur at L5 with the remainder typically at L4 – Amato ME. Radiology. 1984. 27th Annual SW VA Pediatrics Conference Clinical Presentation • Insidious back pain exacerbated by strenuous activity • Occasional radiation to the buttocks • Rising to an upright posture against resistance elicits pain • Pain exacerbated by hyperextension & rotation bilateral, unilateral • Hamstring tightness in 80% of patients • Tenderness in lumbar spine to palpation • Hyperlordosis 27 Annual SW VA th Pediatrics Conference Eric Parks, MD • • • • • 8/6/2011 Spondylolysis Stress Fractures Treatment History Relative rest & activity modification Time (>3 months) Flexion-based core strengthening NSAIDs Bracing? – If still painful after the above • Surgery • Recent change in activity level, equipment, or playing surface • Insidious onset of pain • Worse with activityy • Improves with rest • Prior stress fractures • Menstrual irregularities, weight changes, eating disorder, nutrition – Female Athlete Triad 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Stress Fractures Stress Fractures Clinical Examination • Focal tenderness may be elicited with compression or percussion • Fulcrum test, Hop test, & Tuning fork • Plain xx-rays rays often normal early in disease course – New bone formation after 2-3 weeks • Further imaging may be needed – Bone scan or MRI 27th Annual SW VA Pediatrics Conference Treatment • Relative rest – Cross-training – Limit impact activities • Immobilization • Gradual return to play • May take 6-8 weeks • Be aware of tenuous stress fractures – Anterior tibial cortex, tension-sided femoral neck, Jones, etc. 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Summary • • • • 60 minutes of exercise is recommended daily Video gaming is not intense enough Adolescents are not little adults Overuse injuries occur frequently in adolescents 27th Annual SW VA Pediatrics Conference Summary • Be wary of overuse physeal injuries • Know where the common overuse physeal injuries occur • Relative rest is a good start with most overuse physeal injuries • Know common adolescent fractures, including physeal fractures 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference 8/6‐7/2011 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: Tracy Glauser, M.D. does not anticipate discussing the unapproved /investigative use of a commercial product/device during this lecture. He reports that he DOES NOT have a financial interest/arrangement or affiliation with one or more organizations that could be perceived h ld b d as a real or apparent conflict of interest in the context of this presentation. Seizures: Diagnosis and Management in Primary Care • Recognize the signs and symptoms of 3 important i h i d f3i epilepsy syndromes • Classify a patient's seizure as either partial onset or generalized onset py p • Select first line therapy for partial onset seizures in children Notes: Seizures: Diagnosis an dManagement in Primary Care Tracy Glauser, MD Tracy Glauser, MD 8/6/2011 Definitions • “Seizure” ‐ an electrical storm on the surface of the brain. • “Epilepsy” – recurrent unprovoked seizures • “E “Epilepsy Syndrome” – il S d ” a groups of epilepsy f il related signs and symptoms that travel together Current Management of Epilepsy • • • • • Diagnose seizure and epilepsy Diagnose seizure and epilepsy Classify seizure type Classify epilepsy ‐ identify syndromes Set treatment goals, establish bond g , Start therapy based on seizure type or epilepsy syndrome Tracy Glauser, MD 8/6/2011 Current Management of Epilepsy Diagnosis the Seizure • History is the key • Ask about – Premonitions of the event (aura) – Repetitive motor movements – Involuntary head or eye movements – Alterations in consciousness – Stereotyped events – Confusion, tiredness after the event Imitators of Seizures • • • • • • Tics Syncope Breathholding Headaches Night terrors Night terrors Non‐epileptics events Prensky A.L. In: Dodson, Pellock, eds. Pediatric Epilepsy. Tracy Glauser, MD 8/6/2011 International Classification of Epileptic Seizure Types • Partial Seizures – Simple partial – Complex partial Complex partial – Secondarily generalized • Generalized Seizures – Absence – Myoclonic – Atonic At i – Clonic – Tonic‐clonic • Unclassified epileptic seizures ILAE. Epilepsia. 1981;22:489-501. Classification of Epilepsy Symptomatic (secondary) • Focal or diffuse cerebral injury • Neurologic abnormalities • Frequent seizures Frequent seizures • Difficult to control Idiopathic (primary) • No identifiable pathology • Normal development • Relatively self‐limited • Medication‐responsive • Genetic predisposition Tracy Glauser, MD 8/6/2011 West Syndrome • Seizure type: Infantile Spasms • EEG pattern: Hypsarrhythmia • Clinical: Psychomotor retardation / regression Lennox‐Gastaut Syndrome • Seizure types: – Tonic; atonic atypical absence; generalized tonic clonic, – Myoclonic seizures, CPS less common • EEG pattern: – Generalized slow spike‐wave (1.5‐2.5 Hz) – Background slowing • Clinical: – Psychomotor retardation / regression Tracy Glauser, MD 8/6/2011 BECTS/BRE • Seizure type: – Partial with motor, sensory, and autonomic activity of face, mouth, and throat, hypersalivation common. Seizures can generalize. – Over 50% only have seizures in sleep. Seizures when awake often occur shortly after awakening. • EEG pattern: centrotemporal EEG pattern: centrotemporal spikes • Clinical: – No significant neurological deficits – Normal neuroimaging Childhood Absence Epilepsy • Seizure types: –Absence Absence • EEG pattern: –Generalized 3 to 3.5 Hz spike‐wave –Normal background • Clinical: –Normal development Tracy Glauser, MD 8/6/2011 Summary of Evidence and Recommendations Partial onset seizures Seizure type or epilepsy syndrome Class I Class II Class III Level of efficacy and effectiveness evidence (in alphabetical order) POS: Adults 3 1 30 Level A: CBZ, LEV, PHT Level B: VPA Level C: GBP, LTG, OXC, PB, TPM, VGB POS: Children 1 0 17 Level A: OXC Level B: None Level C: CBZ, PB, PHT, TPM, VPA POS: Elderly 1 1 2 Level A: GBP, LTG Level B: None Level C: CBZ Summary of Evidence and Recommendations Generalized onset seizures Seizure type or epilepsy il syndrome Class I Class II Class III Level of efficacy and effectiveness evidence (in alphabetical order) GTC: Adults 0 0 23 Level A: None Level B: None Level C: CBZ, LTG, OXC, PB, PHT, TPM, VPA GTC: Children 0 0 14 Level A: None Level B: None Level C: CBZ, PB, PHT, TPM, VPA Absence seizures 1 0 6 Level A: ESM, VPA Level B: None Level C: LTG Tracy Glauser, MD 8/6/2011 Summary of Evidence and Recommendations Epilepsy syndromes Seizure type or epilepsy il syndrome Class I Class II Class III Level of efficacy and effectiveness evidence (in alphabetical order) BECTS 0 0 2 Level A: None Level B: None Level C: CBZ, VPA JME 0 0 0 Level A: None Level B: None Level C: None The Place of Guidelines in Clinical Decision Making Evidence Patient/Physician Factors 1.Patient data 1. Cultural beliefs Knowledge 2.Basic, clinical, and epidemiologic research 2. Personal values 3.Randomized trials Clinical 4.Systematic reviews Decisions Guidelines 3. Experiences 4. Education Ethics Constraints 1. Formal policies, laws 2. Community standards 3. Time 4. Reimbursement Figure. Factors that enter into clinical decisions. Mulrow CD, et al. Ann Intern Med. 1997. 27th Annual SW VA Pediatrics Conference 8/6‐7/2011 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: Jim Thigpen, PharmD does not anticipate discussing the unapproved or investigative use of a commercial product/device during this lecture. He p reports that he DOES NOT have a financial interest/arrangement or affiliation with one or more organizations that could be perceived as a real or apparent conflict of interest in the context of this presentation. Anti‐epileptics: The Old, the New and Future Directions • Describe Describe the known mechanisms of antiepileptic drug the known mechanisms of antiepileptic drug classes • Identify the most common and serious adverse drug reactions for the medications discussed • Determine the appropriate medication choices for a specific sei re t pe specific seizure type • Discuss the potential implication of pharmacogenetics in epilepsy Notes: Anti-epileptics: The Old, the New and Future Directions Jim Thigpen, PharmD, BCPS Jim Thigpen, PharmD Phenytoin (Dilantin®) 8/6/2011 Partial and secondary generalized seizures Phenytoin Antiepileptic effect on calmodulin Drug interactions ▪ Highly protein bound, CYP450 inducer Adverse drug effect profile ▪ GI, rash, blood dyscrasias, headache, vitamin K and folate deficiencies, hormonal dysfunction, bone marrow effects, teratogenic effects Serum monitoring ▪ In the presence of low serum albumin or other highly protein bound drugs, “free” (unbound) drug levels should be obtained Fosphenytoin (Cerebyx®) Prodrug for parenteral administration ▪ Far better tolerated than phenytoin through peripheral IV ▪ If central line is used, “regular” phenytion is fine Can be infused 3X faster, can be given IM May achieve target levels of phenytoin faster Far more expensive than phenytoin Carbamazepine (Tegretol®) Partial and tonic clonic seizures Trigeminal neuralgia and bipolar disorder Induces its own metabolism (autoinduction) ▪ Usually seen in the first three weeks Active metabolite (10,11‐epoxide) ▪ Must be considered when CNS side effects are seen Jim Thigpen, PharmD Carbamazepine (Tegretol®) 8/6/2011 Oxcarbazepine (Trileptal®) CNS side effects are dose‐related ▪ Think 10,11‐epoxide Partial and secondary generalized seizures Aplastic anemia, agranulocytosis, No epoxide metabolite May aggravate myoclonic or absence thrombocytopenia, rash, and SJS are idiosyncratic Hyponatremia CNS effects are dose‐related Hyponatremia and rash is similar to that seen with ▪ Altered sensitivity to serum osmolality by hypothalamic osmoreceptors or ↑ sensitivity of kidneys to ADH carbamazepine Inducer of CYP3A4 Van Amelsvoort T, et al. Epilepsia 1994 35(1):181‐8. Lamotrigine (Lamictal®) Chemically unrelated to any other AED Blocks sodium channel conductance and also inhibits release of glutamate Partial onset and secondarily generalized tonic‐ clonic seizures and Lennox‐Gastaut Can cause worsening of myoclonic seizures Lamotrigine (Lamictal®) Few CNS side effects ▪ Headache, ataxia, diplopia, psychosis, somnolence Rash is the main concern, SJS in 0.1% ▪ Seen more commonly with taken with valproate ▪ Slow titration Low incidence of congenital malformations Jim Thigpen, PharmD Zonisamide (Zonegran®) 8/6/2011 Also affects on T‐type calcium channels and Avoid with a history of kidney stones provides neuroprotective effects through free radical scavenging di l i Partial seizures and myoclonus Dizziness, anorexia, headache, ataxia, tremor, weight gain Confusion, speech abnormalities, mental slowing Oligohidrosis due to effect on carbonic anhydrase Skin reactions (SJS and TEN) have been reported ▪ Do not use in sulfa‐allergic Some drug interactions with other AEDs (PHT, CBZ, PB, VPA) leading to reduced ZNS levels Good alternative in adherence due to long t1/2 ▪ Gradual titration Gamma‐aminobutyric acid (GABA) is the most important inhibitory neurotransmitter Benzodiazepines Zonisamide (Zonegran®) Clonazepam (Klonopin®) Used for all types of myoclonus and is useful in patients with concomitant anxiety Emergency treatment Higher affinity for the GABA‐A receptor site Limited long‐term use Caution with withdrawal Barbiturates Children tolerate sedative effects better than Affect the duration of chloride channel opening adults Some children have hypersalivation ADR profile limits use Jim Thigpen, PharmD Diazepam (Valium®, Diastat®) Lorazepam (Ativan®) Midazolam (Versed®) 8/6/2011 Phenobarbital The most commonly prescribed AED of the 20th century Status epilepticus Potent and broad spectrum IV, IM, Rectal CNS effects, especially cognition, behavior Intranasal ▪ midazolam Drug interactions (enzyme inducer) Primidone Metabolized to phenobarbital Also used for essential tremor at low doses Tiagabine (Gabitril®) Vigabatrin (Sabril®) Inhibits GABA transporter‐1 (GAT‐1) Used as second‐line or add‐on therapy for partial A structural analog of GABA, binding irreversibly or secondarily generalized seizures No significant idiosyncratic adverse reactions CNS effects most common (dizziness, asthenia, nervousness, tremor, depressed mood and emotional lability) but also some GI and rash Can worsen absence epilepsy or in partial epilepsy with generalized spike wave Used for refractory partial seizures ▪ Less effective vs. primarily generalized tonic‐clonic ▪ May worsen myoclonic or generalized absence ▪ Myoclonus or Lennox‐Gastaut do not respond well to GABA‐T Infantile spasms ▪ Tuberous sclerosis Jim Thigpen, PharmD Vigabatrin (Sabril®) 8/6/2011 Gabapentin (Neurontin®) Developed to have a structure similar to GABA but Most common side effect is drowsiness the drug has little or no action on the receptor Depression (5%), agitation (7%), confusion and MOA is only speculated ▪ Increased intracellular concentration of GABA ▪ Inhibits branched chain amino acid transferase, which reduces their conversion to glutamate Binds with the alpha2 subunit of calcium channels rarely psychosis Little effect on cognitive function VGB causes visual field changes (nasal in the brain and spinal cord, which may explain its effect on pain constriction followed by concentric constriction, with preservation of central vision) in 50% ▪ Use is restricted Gabapentin (Neurontin®) No pharmacokinetic drug interactions Pregabalin (Lyrica®) Very similar in all aspects to gabapentin Only modest reduction in partial seizures and Approved for adjunct therapy for partial seizures secondarily generalized seizures Well tolerated, most side effects are minor and occur mainly at high doses Used mainly as a pain medication ▪ Somnolence, dizziness, ataxia, nystagmus Jim Thigpen, PharmD Valproate (Depakote®) 8/6/2011 DOC for many primarily generalized epilepsies and Valproate (Depakote®) In utero exposure has been linked to lower IQ ▪ VPA should not be used as a first‐line agent for women of childbearing potential f hildb i t ti l partial seizures Discovered by accident Enhances GABA function, may stimulate GAD, also produces selective modulation of sodium channels Highly bound to plasma proteins, but decreases at higher levels, kidney or liver disease and during pregnancy Nausea, vomiting, tremor, sedation, confusion, irritability and weight gain are dose‐related Hepatoxicity is most serious idiosyncratic effect Metabolic effects include hypocarnitinemia, hyperglycemia and hyperammonemia ▪ Increased free fraction of drug (7‐9% to 15%) Meador, et al. NEJM 2009;360(16);1597‐605 Felbamate (Felbatol®) Blocks NMDA receptors, calcium and sodium channels Effective against multiple seizure types Occurrence of aplastic anemia and hepatic failure led to withdrawal from the U.S. market Available only for a very limited use ▪ Severe partial epilepsy or Lennox‐Gastaut Topiramate (Topamax®) Derived from D‐fructose, initially developed as an antidiabetic drug Inhibits sodium conductance, enhances GABA, inhibits the AMPA subtype glutamate receptor, and is a weak carbonic anhydrase inhibitor Levels are reduced by 50% when given with phenytion or carbamazepine Can reduce ethyl estradiol levels by 30% Jim Thigpen, PharmD Topiramate (Topamax®) 8/6/2011 Adjunct therapy for drug‐resistant generalized Start slow and titrate to minimize/prevent epilepsies, including juvenile myoclonic epilepsy, absence and generalized tonic‐clonic seizures, b d li d t i l i i and Lennox‐Gastaut syndrome FDA approved for partial onset and secondarily generalized tonic‐clonic seizures, primary generalized tonic‐clonic, and Lennox‐Gastaut Ezogabine (Potiga®) Topiramate (Topamax®) adverse effects Ataxia, impairment of concentration, confusion, dizziness, fatigue, paresthesia, somnolence, disturbance of memory, depression, agitation and slowness of speech are common Cognitive effects occur more commonly at higher doses and with rapid titration rate Levetiracetam (Keppra®) Approved in June, 2011, for adjunct therapy in Thought to inhibit synaptic vesicle protein 2A uncontrolled partial‐onset seizures CNS side effects include dizziness, fatigue, confusion ,tremor, problems with coordination, double vision, attention, memory and weakness Should be available by years end (SV2A) , which appears to be important for the availability of calcium‐dependent il bilit f l i d d t neurotransmitter vesicles ready to release their content The lack of SV2A results in decreased action potential‐dependent neurotransmission Jim Thigpen, PharmD Levetiracetam (Keppra®) 8/6/2011 No significant drug interactions Lacosamide (Vimpat®) Enhances the slow inactivation of voltage‐gated Used for monotherapy for tonic‐clonic, partial‐ onset, myoclonic seizures in children Adverse effects include headache (25%), infection (23%), asthenia (22%), somnolence (22%), dizziness (18%), pain (15%), pharyngitis (11%) and flu‐like syndrome (10%) Rufinamide (Banzel®) Prolongation of the inactive state of the sodium channel, suppressing neuronal hyperexcitability and stabilizing cell membranes d t bili i ll b FDA approved for Lennox‐Gastaut and may be used to treat partial seizures Shown to shorten the QT interval Headache, dizziness, fatigue, somnolence and nausea most common Wisniewski CS. Ann Pharmacother 2010;44:658‐67 sodium channels and binding collapsing response mediator protein 2 di t t i Low potential for drug interactions Dizziness, headache, diplopia, N & V Small increases in P‐R interval Refractory partial‐onset seizures saw 37% ↓ Secondarily generalized T‐C sz saw 60‐90% ↓ Eslicarbazepine (Stedesa®, Zebinix) Investigated for partial‐onset seizures with or without secondary generalization Still at the FDA Similar side effects to oxcarbazepine D Drug → Phenytoin Fosphenytoin Carbamazepine Oxcarbazepine Lamotrigine Partial and secondarily generalized GI, CNS, rash, vitamin K, hormonal dysfunction, etc etc… Zonisamide Partial and secondarily generalized Partial and tonic/clonic Partial and secondarily generalized Partial and secondarily generalized, Lennox/Gastaut Partial and myoclonus Infusion‐ related CNS, nausea CNS, nausea CNS (few), GI, somnolence CNS, cognitive effects, weight gain g g Not likely Marrow toxicity, SJS, ↓ Na+ Marrow toxicity, SJS, ↓ Na+ +++ ++ + ++ +/‐ YES YES YES Details ↓ Seizure type Common ADRs Rare/severe Blood dyscrasias ADRs Drug Interactions Preferred P f d Drug ++++ NO, but NO effective and economical ++++ Status, Status peripheral IV Rash Oligohidrosis, Rash, kidney stones 27th Annual SW VA Pediatrics Conference 8/6‐7/2011 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: Sharon Castellino, MD do not anticipate discussing the unapproved /investigative use of a commercial product/device during this lecture. She reports that she DOES NOT have a financial interest/arrangement or affiliation with one or more organizations that could be perceived h ld b d as a real or apparent conflict of interest in the context of this presentation. Life After Cancer: Cases from the Clinic • Describe the survivor population at risk for chronic health conditions • Describe the leading morbidities in childhood cancer survivors • Review recommendations for health surveillance Review recommendations for health surveillance following childhood cancer therapy Notes: Life After Cancer: Cases from the Clinic Sharon Castellino, MD Sharon Castellino, MD 8/6/2011 Endocrine problems after cancer • Most common late effect after cancer • Affects 20-50% of survivors followed into adulthood • Most common in survivors of: • Stem cell/bone marrow transplant Endocrine problems after cancer Seen after radiation of hormone-producing glands: • Pituitary (brain radiation) • Thyroid (neck radiation) • Ovaries (abdomen/pelvis) • Testes (pelvis or testes) • Brain tumors • Hodgkin’s disease • Head and Neck irradiation Wake Forest School of Medicine 1 Thyroid Dysfunction • Clinically significant dysfunction with elevated TSH can be seen after thyroid exposure of >10Gy • Peak incidence of hypothyroidism: 2-4 years following irradiation • Risk of benign and malignant thyroid neoplasms following therapeutic radiation to head and neck • Serial thyroid function tests and annual thyroid palpation in all survivors who received radiation in head/neck field Wake Forest School of Medicine 2 CCSS An NCI-funded Resource Childhood Cancer Survivor Study (CA 55727) Mortality Risks • Mortality highest in • Patients diagnosed at 0-4 yrs age (SMR 9.1) • Those with initial diagnosis: Leukemia (SMR 10.0-14.7), CNS tumor (SMR 12.9-17.7), Ewing Sarcoma (SMR 13.3) • Compared to: Hodgkin Lymphoma (SMR 7.8); Kidney tumor (SMR 4.6) Wake Forest School of Medicine Sharon Castellino, MD Chemotherapy associated morbidity • Alkylators/ VP16: secondary leukemia; MDS; gonadal toxicity • Platinum: ototoxicity; renal dysfunction (impaired GFR and tubular function) • Vinca alkaloids: peripheral neuropathy; ? CV • Methotrexate: leukoencephalopathy; hepatic dysfunction • Anthracyclines: CV dysfunction 8/6/2011 Medical Late Effects • Cardiovascular • Endocrine • Musculoskeletal abnormalities • Growth • Neurocognitive • Chronic graft vs host disease • Opthalmalogic • Transfusion acquired diseases (Hep B, C) • Renal • Pulmonary • Second Malignancies • Ifosfamide: Fanconi syndrome • Steroids: osteoporosis Wake Forest School of Medicine Psychosocial Late Effects Dental Abnormalities • Academic and occupational achievement • Enamel dysplasia • Incomplete calcification • Family and interpersonal relationships • Disorders of tooth development • Foreshortening of roots • Adaptation to chronic illness or disability • Premature close of apices • Tooth agenesis, microdontia • Insurance discrimination and access to healthcare Wake Forest School of Medicine • Arrested tooth development Wake Forest School of Medicine Sharon Castellino, MD Anthracycline Cardio Vascular (CV) toxicity • Myocyte death • myofibrillar loss and vacuolar degeneration • subsequent hypertrophy of surviving myocytes --> > reduced wall thickness • interstitial fibrosis • Severity correlates with • Cum anthracycline dose • Age at exposure • Chest radiation fields Wake Forest School of Medicine Gonadal dysfunction - male • Effect of radiation and alkylator therapy on spermatogenesis is a frequent cause of infertility • oligospermia is dose related • recovery of spermatogenesis can occur later • Testosterone production is less often affected • Workup : semen sample, bone age, FSH/LH, testosterone Wake Forest School of Medicine 8/6/2011 Gonadal Dysfunction -female • Oocytes are very radiation sensitive • Alkylating agents cause destruction of resting oocytes and absent primordial follicles • prepubertal gonad is more resistant to d damage • Follow-up: Tanner stage progression; evidence of primary or secondary amenorrhea • Risk for perinatal mortality and low birthweight infant in women treated with abdominal RT Wake Forest School of Medicine Neuroendocrine Dysfunction Growth Impairment • GH deficiency • common following > 18-20 Gy to hypothalamic/pituitary region • clinically apparent > 2 yrs following radiotherapy • 60-80% of irradiated brain tumor patients will have impaired serum GH response to provocative stimulation Wake Forest School of Medicine Sharon Castellino, MD Neurocognitive Sequelae • Risks: • Age at cranial radiation 8/6/2011 COG Long-Term Follow-Up Guidelines for Childhood Cancer Survivors • Goal: Increase quality of life and decrease health care costs • Radiation dose • Promote healthy life-styles • Female sex • Provide on-going monitoring of health status • MTX - intra-thecal and high systemic dose • Identify late effects at an early stage • Cognitive deficits • Timely Intervention against late effects • Leukoencephalopathy • Seizures and other overt CNS symptoms Wake Forest School of Medicine Wake Forest School of Medicine Screening and management Based on treatment exposure Screening and Management All Survivors • Summary of cancer treatment • Annual screening: • Diagnosis, age • Educational and vocational progress • Chemotherapy agents used with doses and cumulative doses • Mental health: Depression/ Anxiety/PTSD/Social withdraw • Radiation doses and fields • Healthcare insurance and access • Transplant - HSCT(ie BMT) • Did patient have GVHD • Surgery history • Other treatment/exposure: transfusion Wake Forest School of Medicine • If patient received chemotherapy: • Oral and dental exam every 6 months • Full review of symptoms for subtle issues • Based on exposures (chemotherapy, radiation, surgery) Wake Forest School of Medicine Sharon Castellino, MD 8/6/2011 Conclusions- PCP • The general pediatrician’s role in monitoring growth th and d other th ttoxicities i iti iis iincreasingly i l important • 75% will develop a chronic disease by 40 years age, and 40% a serious health problem •M Many effects ff t do d nott become b apparentt for f many years following treatment • Facilitating transition to young adult health Wake Forest School of Medicine References • Diller et. al. Chronic Disease in the Childhood Cancer Survivor Study Cohort: A Review of Published Findings. 2009. J Clin Oncol 27: 2339-2355 • http://www.survivorshipguidelines.org Wake Forest School of Medicine 27th Annual SW VA Pediatrics Conference 8/6‐7/2011 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: David Chastain, MD does not anticipate discussing the unapproved /investigative use of a commercial product/device during this lecture. He reports that he DOES NOT have a financial interest/arrangement or affiliation with one or more organizations that could be perceived h ld b d as a real or apparent conflict of interest in the context of this presentation. Adolescent Medicine Jeopardy! • Cite the predominant mortalities of adolescence • Make a visual diagnosis of common adolescent clinical presentations Notes: Adolescent Medicine Jeopardy! David Chastain, MD 27th Annual SW VA Pediatrics Conference 8/6‐7/2011 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: Rob Clemons, MD does not anticipate discussing the unapproved /investigative use of a commercial product/device during this lecture. He reports that he does not have a financial interest/arrangement or affiliation with one or more organizations that could be perceived h ld b d as a real or apparent conflict of interest in the context of this presentation. Updates in Dermatology: Let's Get Sun Safe • Identify sunscreen ingredients to make better recommendations for your patients • Assess new FDA guidelines for sunscreen manufacturers Notes: Updates in Dermatology: Let’s Get Sunsafe! Rob Clemons, MD Robert Clemons, MD 8/7/2011 The Basics of Ultraviolet Light | Ultraviolet spectrum | UVC (200-290nm)- predominately absorbed by water and ozone in atmosphere. Highly carcinogenic. Be Sun Smart | Wear Broad-spectrum UVA/UVB water resistant sunscreen | Seek Shade | UVB (291-320nm)- Burning wavelength. Blocked by windshields. Strongly associated with non-melanoma skin cancers in animal models. | UVA II (321-340nm)(321 340 ) Delayed D l d tanning i wavelength l h off light. Moderately associated with non-melanoma skin cancers in animal models. | UVA I (341-400nm)- Long wavelength deeper penetrating wavelength of light but less associated with non-melanoma skin cancers. Associated with several solar dermatosis | Know the high UV hours of the day 10-4 | When your shadow is shorter than you are tall | Be extra cautious near water, snow, and sand | Sun Protective Clothing | Tight cotton weave clothing | Universal Protection Factor clothing (UPF) | Wide brimmed hat | Avoid Tanning Beds- Think about self tanner | Supplement Diet with Vitamin D | Sunblock (physical agents) Scatter and physically block UV light | 4 main types | Zinc oxide Titanium dioxide | Talc | Red Veterinary petroleum Sunblock | Standard Physical Blocks | | | |Micronized Zinc Oxide (290-380nm) |Micronized Titanium Dioxide (290-320nm) o www.skincancer.org Sunscreens (chemical agents) | Non-opaque and absorb UV radiation of various wavelengths Why Do Sunscreens Fail??? | Bad product | Did not apply frequently enough | Did not apply enough at each application | UV light appears to breakdown many chemical sunscreens that protect against UVA | Helioplex (Neutrogena) | Ecamsule/Mexoryl SX (La Roche-Posay) Robert Clemons, MD Chemical Sunscreens 8/7/2011 www.skincancer.org | UVB Sunscreens |PABA and PABA Esters (260-315nm) |PABA (Para Aminobenzoic Acid) |Padimate A |Padimate O |Glycerol aminobenzoate |Cinnamates (270-320nm) |Octyl methoxycinnamate (280-310nm) |Cinoxate (270-328nm) |Salicylates (290-320nm) |Homosalicylate |Octyl salicylate |Triethanolamine salicylate Chemical Sunscreens | UVA Sunscreens |Etrocrylene (296-380nm) |Benzophenones |Oxybenzone (270-350nm) |Dioxybenzone (206-380nm) |Sulisobenzone (250-380nm) |Avobenzone/ Parsol 1789 (310-400nm) |Methylanthranilate (200-380nm) owww.skincancer.org |Octocrylene (280-320nm) Sun Protection Factor--SPF | Sun Protection Factor denotes how long it will take for UVB rays to redden the skin compared to without the product | Historically it was felt that sunburn=radiation damage and if you didn’t burn then you didn’t damage | Only relates to UVB and not UVA | An SPF 15 product protects the person from 93% of the UVB rays | An SPF 30 product protects the person from 97% of the UVB rays | An SPF 50 product protects the person from 98% of the UVB rays FDA New Requirements www.fda.org |Proposed to eliminate confusion in the public and mislabeling |What defines “Broad Spectrum” |Must be an SPF>15 protection p proportional p |Must demonstrate UVA p to its UVB protection according to its SPF |Defines what products can claim they reduce risks of skin cancer and photo aging |Eliminate the terms sunblock, waterproof, and sweat proof |Eliminate the term “instant protection” Robert Clemons, MD 8/7/2011 FDA New Requirements, cont... |New requirements for water resistance claims |Must label protective for either 40 or 80 minutes while swimming or sweating |Products that do not meet these standards must include directions to use a water resistant sunscreen if swimming or sweating |SPF labeling can only go to SPF 50+ since there is no evidence that higher SPF values denote better protection |Rules will take effect by Summer of 2012 Facts About Indoor Tanning www.aad.org | 28 million people in the United States tan annually and 2.3 million are teenagers | World Health Organization finally has labeled indoor tanning devices as a carcinogen in the same category as cigarettes | The American Academy of Pediatrics joined the AAD, the Skin Cancer Foundation Foundation, and the WHO in demanding a ban on indoor tanning for young people. | Studies have shown a 75% increased risk of melanoma in people who use indoor tanning | Indoor tanning devices use predominately UVA wavelengths with some UVB | UVA wavelengths do not efficiently stimulate Vitamin D synthesis Sun Protective Clothing | The SPF/UPF of clothing differs with many factors including tightness of the weave, color, dry or wet, wear and tear/stretching | Standard cotton T shirt provides an SPF of 7 | Same T shirt when wet becomes an SPF of 3 | Dark blue denim shirt is an SPF or 1,700 | Universal Protection Factor (UPF) | Colorless dyes and sunblock applied during manufacturing that provide sun protection analogous to SPF rating for UVB | Ratings start at UPF 15 and go up to 50+. Most advertise at 50+ | Tinosorb- a laundry additive that adds UPF to standard clothing and lasts for up to 20 washes Vitamin D: The Great Debate | Vitamin D can be obtain from 3 sources | UVB radiation |5 minutes of noon day sun in the summer maximizes the extent of Vitamin D synthesis |UVB is a carcinogen | Diet |Oily Fish, Cod Liver |Fortified orange juice and dairy products and yogurts |cereals | Oral supplementation |400 IU of Vitamin D for infants up to 12 months |600 IU of Vitamin D for children and adults |800 IU of Vitamin D for patients over 65 years of age Robert Clemons, MD Sun Protection for Newborns |Sun Avoidance |Sunscreens have not been tested safe under six months of age |UPF clothing |Shade structures |If necessary, find a pure physical block with zinc oxide and titanium dioxide Polymorphic Light Eruption, cont... | In adults |Forearms |V of the neck | In children 8/7/2011 Polymorphic Light Eruption |Most common photosensitivity disorder in children |Nonscarring papules and vesicles |Pruritic |Sun exposed sites usually within hours to days of new exposure to sunlight in spring and summer |Lasts for 1-6 days |Diminishes in mid to late summer Polymorphic Light Eruption |Treatment |Antihistamines |Topical corticosteroids |Face |Hydroxychloroquine |Ears |Broad spectrum sunblock with physical barrier protection | Likely a variant of juvenile spring eruption occurring on the ears of boys | Appears to be caused by broad band exposure to light to include UVA 1-2, UVB, and visible wavelengths over sites in the body not acclimated to light |Prophylaxis using gradually increasing doses of UVA to “harden” the skin early in the spring 27th Annual SW VA Pediatrics Conference 8/6‐7/2011 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: James Thompson, MD does not anticipate discussing the unapproved /investigative use of a commercial product/device during this lecture. He reports that he DOES NOT have a financial interest/arrangement or affiliation with one or more organizations that could be perceived h ld b d as a real or apparent conflict of interest in the context of this presentation. Update on Craniosynostosis and Deformational Plagiocephaly • Differentiate plagiocephaly vs craniosynostosis • Describe treatment options Notes: Update on Craniosynostosis and Deformational Plagiocephaly James Thompson, MD James Thompson, MD Definitions • Craniosynostosis (craniostenosis) – refers to the fusion of the cranial sutures • Plagiocephaly – Greek “slanting head” is a descriptive term regarding head shape. – Synostotic – related to fused cranial sutures. – Deformational – caused by external forces with no suture fusion. • Brachycephaly – a descriptive term referring to a shortened head shape – Synostotic or Deformational Synostotic Scaphocephaly • Sagittal synostosis – Most common type ~ 1:1800 births • about 60% of all nonsyndromic cases – Almost all are nonsyndromic – 2% hereditary 2% hereditary – Male : Female = 4 : 1 – Classic features: • Frontal bossing • Elongated skull • Pointed occiput 8/7/2011 Craniosynostosis • Fusion of one or more cranial sutures leads to the shape abnormality • Overall incidence ~ 1:2500 • Causes –Fetal constraint –Abnormal brain development –genetic syndromes –Maternal smoking –Amine containing drugs James Thompson, MD Synostotic Trigoncephaly • Metopic synostosis – Incidence ~ 1:5000 births – Male : Female = 3:1 – ~ 90% nonsyndromic y – ~ 6% hereditary – Classic features • Forehead ridging • Triangular shaped forehead • Hypotelorism Synostotic Plagiocephaly • Unicoronal synostosis –Incidence ~ 1:5000 –Usually non‐syndromic –Classic features: • Ipsilateral frontal flattening • Ipsilateral anterior ear displacement • Contralateral frontal bossing 8/7/2011 James Thompson, MD Synostotic Brachiocephaly • Bicoronal synostosis – Incidence ~ 1:20,000 births – Almost always syndromic • Eg. Crouzons, Aperts, Pfeiffers Eg Crouzons Aperts Pfeiffers – Classic features: • Shortened head • Tall forehead • Recessed supraorbital rim Synostotic Plagiocephaly • Lambdoid synostosis – Incidence unkown, less than 2% of craniosynostosis • Classic features – Trapezoid shape – Ipsilateral occipital flattening – Ipsilateral mastoid bossing – Ipsilateral posterior ear displacement – Contralateral occipital bossing 8/7/2011 James Thompson, MD 8/7/2011 Synostotic Plagiocephaly • Frontosphenoidal synostosis –Unknown incidence –Classic features: • Ipsilateral frontal flattening • Ipsilateral anterior ear displacement • Contralateral frontal bossing Synostotic Plagiocephaly • Treatment – Craniosynostosis is usually treated with surgery – Timing variable but usually between 3‐9 months – Surgery consists of removing the fused suture and expanding the skull • Restore cranial volume • Correct deformity Synostotic Plagiocephaly • Treatment – Traditional surgery • Bicoronal incision g y y • Surgically corrected deformity • Blood loss • ICU – Less invasive surgery • Springs • Endoscopic + Helmets James Thompson, MD Deformational Plagiocephaly – Deformational plagiocephaly • Associated factors –Intrauterine restriction / Multiple gestation –Torticollis –Premature birth / ICU stay –Supine positioning • Incidence unknown but probably 15‐30% of all infants • Male > Female (3:2) • R > L 8/7/2011 Deformational Plagiocephaly • Clinical exam – Ipsilateral occipital flattening – Contralateral occipital bossing – Ipsilateral forehead bossing – Ipsilateral anterior ear displacement – “Parallelogram shape” • Other findings – Anterior displacement of the skull base – Anterior displacement of the TMJ – Crossbite Deformational Plagiocephaly James Thompson, MD Deformational Brachycephaly • Cephalic index = head width/length – Normal = 0.75 – >0.80 = brachycephaly >0 80 = brachycephaly – <0.70 = dolichocephaly (scaphocephaly) Treatment • Positioning – Avoid car seats (except in the car) – Avoid reclining “bouncy” seats – Tummy time – Bump up one side – Turn the crib around – “Entertainment” on one side of the crib – Rotate head from side to side each night 8/7/2011 Deformational Brachycephaly Classification I (6a) II (6b) III (6c) Helmets – Active • Dynamic helmets, custom made and adjusted weekly to mold head into shape • $$$$$ – Passive • Rely on rapid infant head growth as the dynamic factor Rely on rapid infant head growth as the dynamic factor • Can be prefabricated and custom fit • $ – Success correlated significantly with severity, compliance, age at treatment James Thompson, MD 8/7/2011 Conclusions • Must differentiate between synostotic and non synostotic plagiocephaly t ti l i h l • Milder cases of plagiocephaly will resolve with positioning • More severe cases will have lasting effects • If helmet therapy is desired it is best to refer If helmet therapy is desired it is best to refer before 6 months of age Conclusions • Deformational plagiocephaly is associated with delayed or abnormal motor development ith d l d b l t d l t in infants. • No conclusive evidence that deformational plagiocephaly causes long term neurological deficits. • Helmet therapy corrects head shape but other benefits are yet to be proven. 27th Annual SW VA Pediatrics Conference 8/6‐7/2011 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: Jeffrey Carlsen, MD does not anticipate discussing the unapproved or investigative use of a commercial product/device during this lecture. He p reports that he DOES NOT have a financial interest/arrangement or affiliation with one or more organizations that could be perceived as a real or apparent conflict of interest in the context of this presentation. Direct Ophthalmoscopy: How to Use One of the Most Powerful Instruments in Your Office • Improve utilization of direct ophthalmoscope • Recognize common eye conditions with direct ophthalmoscope Notes: Direct Ophthalmoscopy: How to Use One of the Most Powerful Instruments in Your Office Jeffrey Carlsen, MD Jeffrey Carlsen, MD 8/7/2011 Abnormal red reflex Cornea STRABISMUS • Latent or manifest misalignment of the visual axis. i.e. “eyes don’t point the same direction” • Strabismus is a significant risk factor for amblyopia y p which is the leading cause of visual g loss in children • Strabismus has a profound social and developmental impact on a child – Self esteem – Social interaction Direct ophthalmoscope Fundus Exam • Fixation target • Optic nerve is about 15 degrees nasal Have patient look at • Have patient look at your ear • Turn lens wheel clockwise as you get closer and vice versa • • • • Corneal opacity, dystrophy….. Keratoconus y p y Dystrophy Scar Lens • Cataract • Types… with systemic diseases Fundus exam • Orient yourself. Find a vessel and then follow to the nerve Jeffrey Carlsen, MD Subconjunctival Hemorrhage • • • • • Can be subtle or quite dramatic Minor trauma, valsalva, eye rubbing / , Tx.: r/o bad actors, reassurance Spontaneous resolution If recurrent, then consider blood dyscrasia NLD obstruction • Until tear duct opens, you may need to: – Apply pressure (or massage) over lacrimal sac area. – Use antibiotic eye drops or ointment for infection. – Gently clean eyelids with warm water. • For persistent tearing, lacrimal surgery may be necessary. 8/7/2011 Tearing in infants • Abnormal or overflow tearing is common in infants; approx 1/3 of newborns have excessive tears/mucus • Occurs when membrane in nose fails to open before birth, blocking part of tear duct. Valve of Hasner or Rosenmueller. • Tears do not drain properly and collect inside tear drainage system; spill over eyelid, causing tearing. • Strongly predisposes infant to chronic infection, conjunctivitis • Blocked tear duct often opens spontaneously 6–12 months after birth. Managing a NLD obstruction • Most NLD obstructions resolve by 9‐12 months of age; therefore, conservative until then • If still tearing at 9‐12 months, refer. If still tearing at 9 12 months refer • Refer earlier if frequent infections, as this may cause fibrosis of the NLD Jeffrey Carlsen, MD 8/7/2011 Bacterial conjunctivitis secondary to NLD obstruction • Standard bacteria. May also be overgrowth of normal flora • Occurs as normal tear flow is obstructed. (Stagnant fluid is like a petri dish) • Tx: topical antibiotics – – – – Polytrim Sulfacetamide Gentamycin Fluoroquinolones • (reserve these for recalcitrant cases) – Set up for microbial resistance. Use sound prescribing practice Bibliography • Weis AH, Brinser JH, Nazar‐Stewart V. Acute conjunctivitis in childhood. J Pediatr. 1993; 122(1): 10‐14. • Martin M, Turco JH, Zegans ME, et al. An outbreak of conjunctivitis due to atypical Streptococcus pneumoniae. N Engl J Med. 2003; 348(12): 112‐1121 • Block S, Hedrick J, Tyler R, et al. Increasing bacterial resistance in pediatric conjunctivitis (1997‐1998). Antimicrob p j ( ) Agents g Chemother. 2000; 44(6): 1650‐1654 • Pediatric Ophthalmology and Strabismus. American Academy of Ophthalmology Basic and Clinical Science Course, section 6. copyright 2000. • Ophthalmology. Yanoff M, Duker JS. 1998. Mosby publishing • Pediatric Ophthalmology and Strabismus. Kenneth Wright, Peter Spiegel. 2002. Springer Publishing NLD • If less then 2 yrs old, then simple probing has a very high success rate • If older then 2 y/o or previous failed probing, then NLD stent or dilatation then NLD stent or dilatation • If failed stent or older then 5‐10 y/o, then may need dacrocystorhinostomy 27th Annual SW VA Pediatrics Conference 8/6‐7/2011 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: Mark Howell, MD does not anticipate discussing the unapproved or investigative use of a commercial product/device during this lecture. He reports that he DOES NOT have a financial interest/arrangement or affiliation ith financial interest/arrangement or affiliation with one or more organizations that could be perceived as a real or apparent conflict of interest in the context of this presentation. Current Philosophy and Accurate Diagnosis of Pediatric Rhinitis, URTI and Paranasal Sinus Infection • Review anatomy and physiology of URT • Review pathophysiology of nasal and paranasal sinus infections • Apply current guidelines for accurate diagnosis of URTI’s Apply concepts of appropriate pharmocologic • Apply concepts of appropriate pharmocologic intervention Notes: Current Philosophy and Accurate Diagnosis of Pediatric Rhinitis, URTI and Paranasal Sinus Infection Mark Howell, MD Mark Howell, MD • • • • • • • • Differential Diagnosis and Associations Viral URTI (Daycare exposure‐ 2‐3x increase) Rhinitis (allergic, nonallergic, cigarette smoke, environmental) Bacterial rhinosinusitis Adenoid (adenoiditis, hypertrophy) ( ) Congenital (choanal atresia/stenosis) Foreign body Anatomic abnormality (nose/sinuses) Odontogenic Anatomic Associations • Concha bullosa (10‐24% pt. chronic sinusitis) • Paradoxical curve middle turbinate (4‐10%) • Hypoplastic maxillary sinus (7‐17%) Haller cell (10%; 50% bilateral) • Haller cell (10%; 50% bilateral) • Agger nasi cell (frontal sinus) • Cranialfacial anomaly (Down syndrome, Crouzon’s, Apert’s syndrome, cleft palate) • Deviated nasal septum (10‐13%) 8/7/2011 Other Related Factors • • • • • • • Cystic fibrosis Ciliary dyskinesia Immune deficiency (HIV) Diabetes Cranial facial abnormalities Trauma GERD Rhinosinusitis • Acute (up to 4 weeks and total resolution) • Subacute (4‐12 weeks) • Recurrent Acute (4 or more episodes year with resolution between attacks) ith l ti b t tt k ) • Chronic (12 weeks or more of signs and symptoms) • Acute exacerbations of chronic rhinosinusitis Mark Howell, MD 8/7/2011 Signs and Sx of VURTI • Activation parasympathic and inflammatory pathways initiate Sx • Fever, myalgia, pharyngitis • Nasal congestion, rhinorhea, sneezing, PND • Cough, sore throat • Facial pressure and pain, ear fullness • Hyposmia/anosmia • Mucopurulent nasal secretions not specific sign of bacterial infection (neutrophil influx) CDC Position Paper • Antibiotic Tx moderate severe sinusitis not improving after 7 days • Severe sinusitis of any duration (purulent nasal discharge with high fever, erythema, swelling, localized pain) • Clinical judgment Guide Dx ABRS • • • • • • • • Viral URI not resolved 10 days or URI worsens after 5‐7 days and exhibiting Nasal congestion, drainage, PND Facial pain/pressure (esp. unilateral or focused; ear pressure/fullness) Fever, fatigue, cough Maxillary dental pain 80% preceded VURTI 20% preceded allergic URTI Pediatric URI Concensus Team • Prolonged nonspecific upper respiratory signs and symptoms (rhinosinusitis and cough w/o improvement 10‐14 days) • Severe URTI worsening signs and symptoms (fever >39 degrees C; facial swelling/facial pain) Mark Howell, MD Viral to Bacterial 8/7/2011 Imaging Suggestions • Persistent symptoms with no improvement • Not needed in acute uncomplicated sinusitis • Severe symptoms (clinical judgment) • Diagnostic uncertainty and/or not responding as expected to appropriate medical therapy • Worsening symptoms (biphasic illness) o se g sy pto s (b p as c ess) • Complicated rhinosinusitis with facial cellulitis, orbital and/or suspected intracranial complications should have contrasted CT scans sinuses, orbits and head Possible Referral Indications • • • • • Intracranial or orbital complications Possible need sinus aspiration Unusual pathogen Diagnosed or suspected immunodeficiency Recurrent ABRS especially exacerbation associated pulmonary conditions Complications of Acute Rhinosinusitis • Orbital‐usually acute ethmoid sinusitis • Preseptal cellulitis‐involves eyelid;globe normal • Post‐septal cellulitis with or without abcess; involves orbital contents;eyelid edema;chemosis;proptosis;EOM impairment;visual changes • Urgent CT and hospitalization Mark Howell, MD Intracranial Complications • Abscess or meningitis • Usually from acute frontal and/or sphenoid sinusitis • More common in adolescents and adults since younger children have no frontal or sphenoid sinuses 8/7/2011 Management Pearls • Unilateral or isolated “sinusitis” may be related maxillary dental infection and/or abscess; nasal foreign body; neoplasm Immune compromised pt. As DM,HIV beware of compromised pt. As DM,HIV beware of • Immune mucomycosis • Recurrent rhinosinusitis in children consider cystic fibrosis cilliary dysfunction; adenoids • CT and MRI may resolve these dilemmas Absolute Indications for Surgery • Rhinosinusitis causing brain abscess,menigitis;subperiosteal orbital abscess;cavernous sinus thrombosis;facial cellulitis • Sinus mucocele or pyocele • Fungal sinusitis • Neoplasm or suspected neoplasm Relative Indications Sinus Surgery • Recurrent acute rhinosinusitis with persistent obstruction of sinus or specific area of recurring disease is identified • Chronic rhinosinusitis failing to clear on appropriate medical Tx ABRS mild to moderate ABRS moderate no daycare or antibiotics for 90 days Amoxicillin (45‐90 mg/kg per day two doses) Amoxicillin‐clavulanate (45‐90 mg/kg per day two doses) Daycare and/or antibiotic therapy Amoxicillin‐clavulanate within 90 days (80‐90mg/kg day two doses Switch therapy for pt. not responding to Amoxicillin Cefdinir (14mg/kg day 1‐2 doses) Cefuroxime (30mg/kg day) Cefpodoxime (10mg/kg day 1x) ABRS Beta‐lactam sensitivity Non‐type 1 hypersensitivity Type 1 hypersensitivity Cefdinir Cefuroxime Cefpodoxime Clarithromycin (15mg/kg two divided doses) Azithromycin (10mg/kg day1 and 5mg/kg single dose for 4 days) TMP/SMX Clindamycin (30‐40mg/kg day 3‐4 divided doses) ABRS nonresponsive to oral Tx Imaging; Aspiration of sinus Ceftriaxone (100mg/kg per day divided q 12hr Cefotaxime (100‐200mg/kg day divided q6hr) Mark Howell, MD 8/7/2011 Conclusions • ABRS may be diagnosed in patients with viral URI of > 10days or worsens after 5‐7 days and is accompanied by signs and symptoms • A Antimicrobial therapy should cover key ti i bi l th h ld k respiratory pathogens • >30% S. pneumoniae decreased sensitivity to penicillin • 30‐40% H.flu produce B‐lactamase 27th Annual SW VA Pediatrics Conference 8/6‐7/2011 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: Jennifer Correll, PhD does not anticipate discussing the unapproved or investigative use of a commercial product/device during this lecture. She reports that she DOES NOT have a financial interest/arrangement or affiliation with one or more organizations that could be perceived h ld b d as a real or apparent conflict of interest in the context of this presentation. I'm Not Listening! Assessment and Treatment of Oppositional/Disruptive Behavior in Primary Care in Primary Care • Identify the prevalence of oppositional behavior in primary care • Identify brief assessment tools to use in primary care • Demonstrate brief behavioral interventions that can be recommended to parents Notes: I'm Not Listening!: Assessment and Treatment of Oppositional/Disruptive Behavior in Primary Care Jennifer Correll, PhD Jennifer Correll, PhD Assessment: Informal y Ask about noncompliance y If you asked him/her to do 10 things during the day how many would s/he do the first time asked? y How many could you eventually get him/her to do if you kept on him/her? Assessment: Formal y DSM criteria y Behavior checklist y Pediatric Symptom Checklist (PSC) 8/7/2011 Treatment in Primary Care y Conceptualizing the problem for parents y Skills deficit y Need to be able to 1. Follow instructions 2. Cope with anger 3. Persist on a task 4. Self-quiet/soothe 5. Independently transition to sleep y Eyberg Child Behavior Checklist (ECBI) Treatment in Primary Care y Balance between reward and discipline y Time in y Attending to average behavior y “Sprinkles of attention” y Overboard verbal reinforcement for completing a desired task y vs. Time out y Brief, unpleasant consequence during which there is no access to attention or anything fun y What happens when you start to ignore behavior during time out? y Extinction Burst! Treatment in Primary Care Time-Out y Procedure y Adult-sized chair y Area easy to covertly monitor y 2-3 minutes y Parent ends the time-out y Child completes task after time-out y Common Parent Misconceptions 1. Child must be quiet 2. Child must sit still 3. Child must be sorry 4. Child must understand Jennifer Correll, PhD 8/7/2011 Oppositional Defiant Disorder: DSM Criteria y Oppositional Defiant Disorder (DSM-IV) y 6-month pattern of negative, hostile, defiant behavior with 4 of the following: ¾ Often loses temper ¾ Often argues with adults ¾ Often actively defies or refuses to comply with adults’ requests or rules ¾ Often deliberately annoys people ¾ Often blames others for his/her mistakes or behavior ¾ Often touchy ¾ or easily annoyed by others ¾ Often angry g y or resentful ¾ Often spiteful or vindictive y Not psychosis y Not Conduct Disorder y Causes Impairment Treatment in Primary Care y Points to Remember 1. Conceptualize “problem” as skill deficit and stress two-part/balanced approach 2. Discuss two components to time-in 3. Discuss effective time-out use 4. Warn about extinction burst 5. Set a follow-up meeting to review progress 6. Refer if no improvement 27th Annual SW VA Pediatrics Conference 8/6‐7/2011 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: Darshan Shah, MD does not anticipate discussing the unapproved or investigative use of a commercial product/device during this lecture. He p DOES NOT have a reports that hhe financial interest/arrangement or affiliation with one or more organizations that could be perceived as a real or apparent conflict of interest in the context of this presentation. What’s Up With Spit Up? • Identify two important causes of spit up in newborns • Discuss Gastroesophageal Reflux and Cow Milk Allergy Notes: What's Up With Spit Up? Darshan Shah, MD Darshan Shah, MD Spit up/vomiting Common causes of spit up in newborn Physiological(GER) GERD Milk allergy Over feeding Pyloric stenosis Most common cause of vomiting in new born is overfeeding, overfeeding, overfeeding and overfeeding y GER is not reason to start infant on medication y Only Gastro Esophageal Reflux Disease; GERD is the only indication to start on medication GERD: Esophagatis Apnea Growth failure 8/7/2011 Gastro esophageal reflux in newborn Frequently seen in newborn Incidence: 1 episode/day in 50% in 0‐3 months increases to 75% at 4 months and decreases to 5% at 10‐12 months. GER /Spit up/Vomiting is very common immediately after feeding (with in one hour) Acid reflux is more common before feeding. Medications for GERD y H2 Receptor antagonist y PPI; not cleared by FDA for less than 1year y Prokinetics y Always use for short duration of 4 Always use for short duration of 4‐8 weeks rather than 8 weeks rather than 4‐6 months as GER underlying physiology gets better with time! Darshan Shah, MD 8/7/2011 Cow Milk Allergy y Prevalence o 2‐8% noted in literature but recent larger cohort 2.2‐ 2.8% (Ped Cli Nor Ame 2011) o Compare to 50‐75% of GER episode in 0‐4 months CMA uncommon CMA y Lab eval for CMA y Breast milk allergy: y Rare y Incidence <1% y Maternal avoidance of CMP Skin test Atopy patch test Total IgE Specific IgE(RAST) y Duration of elimination diet: y Minimum of two weeks for improvement in symptoms. If not improved after 4 weeks unlikely CMA. y Reintroduction of CMP y Depends on history of previous encounter; if anaphylaxis then do RAST/skin test prior to reintroduction 50‐60% patient can tolerate CM by 1‐2 years and 80‐90% by 2‐3 years. y Pyloric stenosis y Incidence: 0.02‐0.06% y Most important: Vomiting is PROJECTILE y Palpation is positive in epigastric area y BMP/NP will help great if Ped radiologist/ped ultrasound tech unavailable. y Growth failure is evident by 3rd week y Ultrasound/UGI will confirm diagnosis y Reemergence of symptoms on introduction after elimination confirms CMA. y Look out for allergy to peanuts and egg in patient with definite CMA.