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27th Annual SW VA Pediatrics Conference DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: 8/6‐7/2011 DISCLOSURE OF POTENTIAL CONFLICT OF INTEREST: William Dalton, PhD Karen Schetzina, 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 as a real or apparent conflict of interest in the context of this presentation. 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. 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 practice William Dalton, PhD Karen Schetzina, MD, MPH 8/6/2011 Learning Objectives Child Obesity Treatment in Primaryy Care: What’s the PLAN? William T. Dalton III, PhD Karen E. Schetzina, MD, MPH, CLC, FAAP • Describe the latest evidence on effective behavioral treatment approaches for child obesity in primary care • Understand how to overcome common challenges in treating child obesity • Integrate evidence-based behavioral approaches and tools for addressing child obesity into primary care practice Primary Care Research Study In Memoriam: Tiejian Wu, MD, PhD 1962‐2011 Purpose: 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. Questions/Discussion 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] 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 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 Eric Parks, MD 8/6/2011 Disclosure Statement of Unapproved/Investigative Use Sports Injuries in the Pediatric Athlete: Considerations for the Stars of Tomorrow Eric D. Parks, MD Watauga Orthopaedics Kingsport, TN I, Eric D. Parks, MD, DO NOT anticipate discussing the unapproved/investigative d/ use off a commercial product/device during this activity or presentation. 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Disclosure Statement of Financial Interest Outline I, Eric D. Parks, MD DO NOT have a financial interest/arrangement or affiliation i / ffili i with ih one or more organizations that could be perceived as a real or apparent conflict of interest in the context of the subject of this presentation. 27th Annual SW VA Pediatrics Conference • Why Exercise? • Epidemiology • Pressures/Risk factors for injury • Ove Overuse use Injuries ju es • Acute Injuries – Pediatric Fractures • Summary – Osteochondroses • • • • • Knee Pelvis Elbow Shoulder Foot – Spondylolysis – Stress Fractures 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Why Exercise? • Regular exercise increases self-esteem, and reduces stress/anxiety – Farmer ME. Am J Epidemiol. 1998 • Athletes are less likely to be heavy smokers and use drugs – Kino-Quebec, 2000. Physical Activity: a determinant of health in youth – Escobedo E b d LG LG. JAMA JAMA. 2003 • Athletes are more likely to stay in school – Zill N. Adolescent Time Use, Risky Behavior and Outcomes. 1995 • Learn teamwork, self-discipline, sportsmanship, leadership, and socialization – Cahill BR. Intensive Participation in Children’s Sports. 1993 • Builds self-esteem, confidence, fitness, agility 27th Annual SW VA Pediatrics Conference Some Active Kids on Our Hands • ~45 million children/adolescents 6-18 yo participate in organized sports on a yearly basis – 1997- 32 million – 2008- 44 million • 7 million adolescents participate in organized highschool sports on a yearly basis – 4.1 million males – 2.9 million females • National Federation of State High School Associations. 2005 27th Annual SW VA Pediatrics Conference Childhood Obesity Exercise • Current public health guidelines 60min of exercise/day – Strong WB. J Pediatr. 2005 recommend What fits into your busy schedule better, exercising 1 hour a day or being dead 24 hours a day? • Physical activity declines significantly during adolescence – Brodersen NH. Br J Sport Med. 2006 • Overweight children perceive themselves to be just as active as their non-overweight contemporaries – Gillis LJ. Clin J Sport Med. 2006 • The energy expended playing active Wii Sports games was not intense enough to contribute to daily recommendations – Graves L. Br J Sports Med. 2008 27th Annual SW VA Pediatrics Conference Sports Injuries Epidemiology • 30-40% of all accidents in children occur during sports • ~2.5 million sports injuries treated annually in ER for patients ≤18 yrs old • Sports/over-exertion leading cause for all injury related visits to PCP • Rate of sports injuries was 22.44 per 1000 exposures • 10-14 year olds at greatest risk • 22% of adolescents experience some sports-related injury – 62% occurred during organized sports – 20% during physical education classes – 18% during non-organized sports 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Sports Injuries Sports Injuries Epidemiology Financial Burden • 25-30% occur during organized sports • 40% occur during non-organized sports – Hergenroeder AC. Pediatrics. 1998 • males >> females • males 10-19 y/o • $588 million in direct expenses • $6.6 billion indirect costs – US Consumers Product Safety Commission. Jan 2006 • Sports are the leading cause of injury and hospital emergency room visits in adolescents – football, basketball & bicycle injuries MC • females 10-19 y/o – basketball, bicycle & gymnastics injuries MC – Emery CA. Clin J Sport Med. 2003;13:256-268 • CDC estimates that ½ of all sports injuries in children are preventable • Backx FJG. Am J Sports Med. 1991 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Sports Injuries Epidemiology • 30-50% of adolescent sports-related injuries are overuse – Watkins J. J Sports Med Phys Fitness. 1996;36(1):43-48. • 15% off allll adolescent d l t injuries i j i are to t the th physes ph and apophyses – Pill SG. J Musculoskeletal Med. 2003;20:434-442 Definitions • Physis – Primary ossification center located at the ends of long bones – Responsible for longitudinal growth • Apophysis – Secondary ossification center located where major tendons attach to bone – Provide P id shape h andd contour t to t growing i bone b but b t add dd no length l th • Osteochondroses – disorders affecting bone and cartilage together • Osteochondrosis – disease of the ossification centers in children • Apophysitis – irritation of the musculotendinous attachment 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 The Physis General Anatomy • Cartilage is less resistant to tensile forces than bones, ligaments, and muscle-tendon units • Bones grow faster than muscle-tendon units j y leadingg to a muscle strain in an adult mayy • Same injury result in growth center injuries in adolescents • The “Weak Link” 27th Annual SW VA Pediatrics Conference Physeal Anatomy • Zone of Growth – Longitudinal growth – Area of greatest concern 27th Annual SW VA Pediatrics Conference Impact of Growth on Injury Risk • Injuries tend to be most common during peak growth velocity • Zone of Maturation – C Calcification l ifi i – Replaced by osteoblasts – MC area for fracture • Zone of Transformation – Complete remodeling – Metaphyseal vessel penetration 27th Annual SW VA Pediatrics Conference • Peak P k height h i h velocity l i precedes d peakk flexibility fl ibili gains i • Decreased BMD in the 2-3 yrs preceding peak height velocity 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Pathophysiology • Repetitive tensile forces • Stress to the physis • Microtrauma leads to: – – – – – Pain Inflammation Widening Avulsion Microfracturing Overuse • “When microtrauma occurs to bone, muscle, or tendonious units as a result of repetitive stress with insufficient time to heal.” • Long term complications exist for physeal injuries 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Risk Factors for Overuse Risk Factors for Injury • Intrinsic – ↑ vulnerability to stress in growing skeleton – Inability to detect injury – Skeletal variants ariants • Pes planus, overpronation, patella alta, external tibial torsion 27th Annual SW VA Pediatrics Conference Extrinsic • • • • • • • Pressure Training errors Sports camps Year round training Single vs Multi-sport Early specialization Improper technique • • • • • • Weekend tournaments Motivation sources Personal coaches Team vs club sport 10 yr / 10,000 hr rule Evaluation programs 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 The Gradual Progression • Multi-sport athlete • Recent increase in activity • Pain with activity, not with rest, still normal performance f • Pain with activity, rest, and decline in performance Key Points During Evaluation • 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/ muscletendon unit • Pain with firing muscle-tendon unit against resistance • Radiographs? – Help to rule out other pathology 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Treatment Patellofemoral Friction Syndrome General Principles • • • • • • • • 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 • • • • Most common cause of anterior knee pain Estimated prevalance of 20% Mean age 14 years “The Great Imitator” of symptoms – Location and quality of pain • Walking stairs, incline/decline • “Theatre sign” 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 PFS Osgood-Schlatter’s Disease (OSD) Tibial Tubercle Apophysitis Risk Factors and Treatment • • • • Muscle imbalances Flexibility issues Over-pronation, pes planus Specific sports • Treat from the hip to the waist • Orthotics, bracing, taping? • 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 27th Annual SW VA Pediatrics Conference Osgood-Schlatter’s Disease (OSD) Osgood-Schlatter’s Disease Tibial Tubercle Apophysitis Sequelae • Point tender +/- swelling at tibial tubercle • Pain with quadriceps stretch or contraction, poor quad flexibility • Widened Wid d physis h i or ffragmented d tibial ibi l tubercle b l on radiographs • Tight quadriceps or hip flexors – Postive Thomas test 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Osgood-Schlatter’s Disease (OSD) Osgood-Schlatter’s Disease (OSD) Radiographs Pathology • • • • • Chronic traction/stress at apophysis Cartilage swelling Cortical bone fragmentation Patellar tendon thickening Infrapatellar bursitis • Long term- prominent tibial tubercle, intratendon ossicles, ? ↑ risk of rupture • • • • • 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference 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 27th Annual SW VA Pediatrics Conference • • • • • • Relative rest Quadriceps and hip flexor stretching Ice NSAIDs Cho-Pat strap Knee pads 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Sinding-Larsen-Johansson Syndrome (SLR) • Apophysitis at the inferior the patella • 10-12 years old • Most common in running jumping athletes – Basketball, soccer, gymnastics pole of & El salto del Colacho- “the devil’s jump” • “Adolescent Jumper’s Knee” Sinding-Larsen-Johansson Syndrome (SLR) • Tenderness at the inferior pole of the patella • Pain worsened with explosive activity • Tight Ti h quadriceps di • Radiographs may reveal fragmentation of the inferior pole and/or calcification at the proximal patella tendon 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Sinding-Larsen-Johansson Syndrome (SLR) Patella Sleeve Fracture 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Sinding-Larsen-Johansson Syndrome (SLR) Treatment • • • • • Relative rest Quadriceps stretching Ice NSAIDs Cho-Pat strap Osteochondritis Dessicans • Avascular necrosis of cartilage bed • May be result of direct trauma vs iatrogenic • MC location- lateral portion of medial femoral condyle d l • 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 Osteochondritis Dessicans Radiographs Treatment • 4 views- AP, lateral, sunrise, and tunnel • MRI for stability • Treatment will depend on the stability of the lesion • Protected/NWB for 6 weeks • Bracing B i • Follow up imaging • Unstable- surgical 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Sever’s Disease Sever’s Disease Calcaneal Apophysitis Calcaneal Apophysitis • Affects boys and girls equally • Ages 8-13 years • Most common in soccer, basketball, & gymnastics i – Repetitive heel impact & traction stress from the achilles tendon • Bilateral in 60% of cases 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 27th Annual SW VA Pediatrics Conference Sever’s Disease Sever’s Disease Risk Factors Treatment • Repetitive explosive activities • Repetitive trauma – Jumping, landing, cleats, etc. • • • • • • • • • Recentt increase R i in i activities ti iti Tight heel cord Before/during rapid periods of growth Beginning of new season 27th Annual SW VA Pediatrics Conference • • • • • Relative rest Heel cord stretching Heel cups Ice NSAIDs 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Sever’s Disease Calcaneal Apophysitis Pelvic Apophysitis • 10-14 years old • Insidious onset of hip pain or sharp pain sudden – 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 27th Annual SW VA Pediatrics Conference Pelvic Apophysitis Pelvic Apophysitis • Ischial tuberosity 38% – Hamstrings & Adductor • ASIS 32% – Sartorius • AIIS 18% – Rectus Femoris • Lesser trochanter 9% – Iliopsoas • Iliac crest 3% – ITB/Tensor Fascia Latae – Abdominal muscles 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 ASIS Avulsion Fracture ASIS Avulsion Fracture Sartorius Sartorius 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference AIIS Avulsion Fracture Ischial Tuberosity Avulsion Fx Rectus Femoris Adductors & Hamstrings 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Ischial Tuberosity Avulsion Fx Pelvic Apophysitis Adductors & Hamstrings Treatment • • • • • • • 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 27th Annual SW VA Pediatrics Conference Medial Epicondyle Apophysitis Medial Epicondyle Apophysitis Little League Elbow Little League Elbow • Most common in 9 to 14 y/o overhead athletes • ~18-29% incidence of elbow pain in youth and HS baseball players • Point tenderness over v medial epicondyle p y • Classically worsened by repetitive throwing • Hypertrophy of medial epicondyle • Flexion contracture • Pain with valgus stress & milking maneuver 27th Annual SW VA Pediatrics Conference • X-rays may reveal widening of medial epicondyle apophysis &/or fragmentation of medial epiphysis • 85% of X-rays X rays are normal – Hang DW. Am J Sports Med. 2004 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Medial Epicondyle Apophysitis Baseball Overuse Injuries Little League Elbow Epidemiology • The acceleration phase: • Incidence of baseball overuse injuries is 2-8% annually • Mechanism: • Annual incidence of elbow pain in 9-12 y/o baseball players is 20-40% – Gomez JE. Pediatr Clin North Am. 2002 – Traction injury – Strongg contraction of the flexor-pronator p muscle attachments as the arm is started forward – Valgus stress causes tension on the UCL • Valgus moment with throwing: – – – – Lateral compression at radiocapitellar joint Medial tension at epicondyle and UCL Posterior shear Hyperextension valgus overload syndrome – Walter K. Contem Ped. 2002 • In adolescents, 52% & 86%increased risk of shoulder and elbow pain respectively if throwing curve ball or slider – Lyman. USA Baseball. 2002 • 67% of HS UCL reconstructions began throwing curve ball before age 14 – Petty 2004 • 6 fold increase in elbow surgeries b/t ’94-’99 and ’00-’04 – Fleisig GL. ASMI. 2005 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Medial Epicondyle Apophysitis Medial Epicondyle Avulsions • Classic Little League Elbow is an apophysitis of the medial epicondylar growth plate • Constellation of Findings: – – – – – – Apophysitis p p y of Medial Epicondyle p y Medial Epicondylitis Cubital Tunnel Syndrome UCL Injury rare Capitellar OCD Premature closure of proximal radial physis 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Little League Shoulder Little League Elbow Proximal Humeral Epiphysiolysis Treatment • If apophysis not significantly displaced (<5mm) – (Relative) rest 4 - 6 weeks – Isometric strengthening, stretching, resistive strengthening – Throwing mechanics evaluation – 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 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 99-14 14 years old Pain Inability to perform Decreased ROM TTP at anterior proximal humerus Remember– physis is the weak link! 27th Annual SW VA Pediatrics Conference Little League Shoulder Proximal Humeral Epiphysiolysis • Treatment – Relative rest for 4-6 weeks – Interval throwing program – Thrower Thro er’ss 10 program 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 USA Baseball Medical & Safety Advisory Committee USA Baseball Medical & Safety Advisory Committee Pitch Counts 2008 Days Off 2008 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Spondylolysis • Lesion in the pars interarticularis of the neural arch Low Back Pain Epidemiology • 30.4% in 11-17 year old athletes – Olsen TL. Am J Public Health. Apr 1992;82(4):606-8 • No cases of spondylolysis in non-ambulatory ( =143) (n=143) – Rosenberg NJ. Spine. Jan-Feb 1981 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Spondylolysis Spondylolysis Epidemiology Clinical Presentation • Incidence of 6-8% in general population • 6.4% for Caucasian males • 1.1% for African-American females – Roche MA, Rowe GG. Anat Rec. 1951 • Overall incidence of 44.4% 4% by age 6, 6 5.2% 5 2% by age 12, 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 Spondylolysis Imaging • • • • • • 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 27th Annual SW VA Pediatrics Conference Spondylolysis Imaging Xrays Bone scan SPECT scan Thin-sliced CT scan MRI 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Spondylolysis Treatment • • • • • Relative rest & activity modification Time (>3 months) Flexion-based core strengthening NSAIDs Bracing? Stress Fractures • Mechanism – repeated forceful impact and repetitive loading on immature trabecular bone – repeated microtrauma is greater than ability to repair – If still painful after the above • Surgery 27th Annual SW VA Pediatrics Conference Stress Fractures History • Recent change in activity level, equipment, or playing surface • Insidious onset of pain Worse w with activity v y • W • Improves with rest • Prior stress fractures • Menstrual irregularities, weight changes, eating disorder, nutrition 27th Annual SW VA Pediatrics Conference 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 – Female Athlete Triad 27th Annual SW VA Pediatrics Conference 27th Annual SW VA Pediatrics Conference Eric Parks, MD 8/6/2011 Stress Fractures Stress Fracture Imaging 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 27th Annual SW VA Pediatrics Conference Summary 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 • Be wary of overuse physeal injuries • Know where the common overuse physeal injuries occur • Relative R l i rest iis a good d start with i h 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 Tracy Glauser, MD 8/6/2011 Seizures: Diagnosis and Management in Primary Care Tracy Glauser, M.D. Professor of Pediatrics and Neurology Director, Comprehensive Epilepsy Center Cincinnati Children’s Hospital Medical Center Cincinnati, Ohio Disclosure Statement of Financial Interest Disclosure Statement of Unapproved/Investigative Use I, Tracy Glauser MD, DO anticipate discussing the unapproved/investigative use of a commercial product/device during this activity or presentation. Epilepsy and its Treatments: The Modern Era • I, Tracy Glauser MD, DO 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 the subject of this presentation, they are: Affiliation/Financial Interest: Grant/Research Support: Consultant: Speaker's Bureau: Major Stock/Shareholder : Advisory Board: g ( ) Name of Organization (s): NIH, Oxley foundation Supernus, Sunovion, Eisai, ucb Pharm, Lundbeck, Questcor Supernus, Sunovion, Eisai, ucb Pharm, Lundbeck, Questcor None None TA Glauser 2011 Tracy Glauser, MD 8/6/2011 Epilepsy and its Treatments” The Modern Era Epilepsy and its Treatments: The Modern Era “Who can forget that without putting pen to paper, Locock…turned the tide of hopelessness that…had immersed the epileptic… ” “For doctors, there is this moral: Never miss a scientific meeting on epilepsy, and give close attention to the discussion ” Sir Charles Locock TA Glauser 2011 Definitions Lennox and Lennox, Epilepsy and Related Disorders 1960; p.854 TA Glauser 2011 Magnitude of the Problem “Seizure” - an electrical storm on the surface of the brain. “Epilepsy” – recurrent unprovoked seizures “Epilepsy Syndrome” – a groups of epilepsy related signs and symptoms that travel together 10% of people experience at least one seizure Approximately 1% of people develop epilepsy – 40 million people worldwide – 2.3 million people in the US TA Glauser 2011 Estimated annual cost of epilepsy: $12.5 billion Epilepsy has significant effects on self-image, family and peer relationships Epilepsy Foundation: A Report to the Nation. TA Glauser 2011 Tracy Glauser, MD 8/6/2011 Current Management of Epilepsy Diagnosis the Seizure Current Management of Epilepsy Diagnose seizure and epilepsy Classify seizure type Classify y epilepsy p p y - identifyy syndromes y Set treatment goals, establish bond Start therapy based on seizure type or epilepsy syndrome History is the key Ask about – Premonitions of the event (aura) – Repetitive R titi motor t movements t – Involuntary head or eye movements – Alterations in consciousness – Stereotyped events – Confusion, tiredness after the event TA Glauser 2011 TA Glauser 2011 International Classification of Epileptic Seizure Types Imitators of Seizures Tics Syncope g Breathholding Headaches Night terrors Non-epileptics events Partial Seizures – Simple partial – Complex partial – Secondarily generalized Generalized Seizures Generali ed Sei res – – – – – Prensky A.L. In: Dodson, Pellock, eds. Pediatric Epilepsy. TA Glauser 2011 Absence Myoclonic Atonic Clonic Tonic-clonic Unclassified epileptic seizures ILAE. Epilepsia. 1981;22:489-501. TA Glauser 2011 Tracy Glauser, MD 8/6/2011 Types of Partial Seizures Simple Incidence of Seizure Types Complex Consciousness Not Impaired Simple Partial 14% Complex Partial 36% Consciousness Impaired (With or Without Automatisms) Generalized Tonic-Clonic 23% Secondarily Generalized Partial Unknown 7% Consciousness Impaired and Bilateral Cerebral Involvement ILAE. Epilepsia. 1981;22:489-501. Unclassified 3% TA Glauser 2011 Current Management of Epilepsy Classify Epilepsy, Identify Syndromes Basic question: What is the underlying cause of the patient’s seizures? Answer: One of two categories – Idiopathic – Symptomatic Look for specific epilepsy syndromes Myoclonic 3% Absence 6% Hauser A. Epilepsia. 1992;33 (suppl 4):S6-S14. Other Generalized 8% TA Glauser 2011 Classification of Epilepsy Symptomatic (secondary) Focal or diffuse cerebral injury Neurologic abnormalities Frequent seizures Difficult to control Idiopathic (primary) No identifiable pathology Normal development Relatively R l ti l self-limited lf li it d Medication-responsive Genetic predisposition Dreifuss FE. In: Dodson, Pollock, eds. Pediatric Epilepsy. TA Glauser 2011 TA Glauser 2011 Tracy Glauser, MD 8/6/2011 Epilepsy Syndromes: Features Etiology of Epilepsy Degenerative 3.5% Infection 2.5% Neoplastic 4.1% Specific seizure types Typical EEG patterns Vascular 10.9% Associated clinical features Trauma 5.5% Natural history Congenital 8.0% Idiopathic 65.5% Hauser. Epilepsia. 1992;33 (suppl 4):S6-S14. Response to therapy Precipitating factors / Inheritance patterns TA Glauser 2011 Common Epilepsy Syndromes West Syndrome Lennox Gastaut Syndrome (LGS) Benign Epilepsy with Centrotemporal Spikes (Benign Rolandic Epilepsy, BECTS, BRE) Childhood Absence Epilepsy (CAE) Idiopathic generalized epilepsies with variable phenotypes – Juvenile Absence Epilepsy (JAE) – Juvenile Myoclonic (JME) – Epilepsy with GTCs only West Syndrome Seizure type: Infantile Spasms EEG pattern: Hypsarrhythmia Clinical: Psychomotor retardation / regression Tracy Glauser, MD Infantile Spasms 8/6/2011 Interictal EEG Pattern: (Hypsarrhythmia) Brief contraction of muscles of neck, trunk, extremities Bilateral and symmetrical (usually) Intensityy varies Usually (80%) occur in clusters often after awakening or when sleepy Spasms per cluster vary Intensity of spasms waxes, then wanes West Syndrome West Syndrome - Treatment Natural History: Goal – No spasms (by EEG) and no hypsarrhythmia on EEG Options –ACTH –Vigabatrin –Topiramate –Steroids Best response if treated early –Onset 4-6 months (90% by 1 year) Untreated - spasms and hypsarrhythmia –Untreated resolve by 3 yo but spasms often replaced by other seizure types –Development delayed esp in children with symptomatic causes; those with delayed sz control Tracy Glauser, MD 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 Atonic seizure Sudden loss of postural tone that involves either the body or only the head 8/6/2011 Tonic seizure Brief (seconds) May appear as –flexion of the head and trunk, –adduction dd ti off arms with ith elevation l ti off shoulders –sudden falls Can be –asymmetrical or unilateral –precipitated by stimuli such as noise, contact, movement, or by falling asleep Atypical Absence Seizures Occur in two-thirds of patients with LGS Gradual onset and termination Longer than typical absences Followed by postictal cognitive impairment “Clouding" rather than loss of consciousness Associated manifestations include eyelid or perioral myoclonus, progressive flexion, and localized motor phenomena, such as neck-stiffening or head-nodding Tracy Glauser, MD Lennox-Gastaut Syndrome Natural History: –Onset 2-8 years 8/6/2011 Lennox-Gastaut Syndrome: Treatments Seizures difficult to control Medical options –Poor Poor response to therapy –Lamotrigine Lamotrigine, Felbamate Felbamate, Topiramate Topiramate, Rufinamide –Slow spike-wave / atypical absences remit but other seizures continue –Valproate, Zonisamide, Clobazam Ketogenic diet Surgical –Corpus callosotomy –VNS BECTS/BRE: Terminology BECTS/BRE Seizure type: Benign Rolandic Epilepsy (BRE) Benign Partial Epilepsy of Childhood with Centrotemporal Spikes C t t lS ik (BECTS) Benign Focal Epilepsy of Childhood Sylvian Epilepsy –Partial with motor, sensory, and autonomic activity of face, mouth, and throat, hypersalivation common. common Seizures can generalize. generalize –Over 50% only have seizures in sleep. Seizures when awake often occur shortly after awakening. EEG pattern: centrotemporal spikes Clinical: –No significant neurological deficits –Normal neuroimaging Tracy Glauser, MD BECTS/BRE – interictal awake 8/6/2011 BECTS/BRE – interictal asleep BECTS/BRE BECTS/BRE BECTS/BRE – treatment Natural History: –Onset 3-13 years (most 5-10 years) –Remission can be within 3 years of onset (always by age 16 years) –Seizures typically infrequent (80% have < 5 seizures but can have daily seizures) –Associated with behavioral and learning problems –Seizure frequency is not predictable by degree of EEG abnormality None Carbamazepine Gabapentin Many others Tracy Glauser, MD Childhood Absence Epilepsy Seizure types: – Absence EEG pattern: 8/6/2011 Absence Seizures Abrupt onset and end Duration around 5-20 seconds Complete loss of awareness – Generalized 3 to 3.5 Hz spike-wave No post-ictal state – Normal background Automatisms and mild myoclonus may be seen Clinical: – Normal development Absence - ictal Mild myoclonic activity around the eyes may be preset Seizures may be subtle Childhood Absence Epilepsy Natural History: – Onset 4-10 years (peak 5-7 years) – Females 60% – Remission in adolescence Tracy Glauser, MD 8/6/2011 Epilepsy Treatments in the US (1900 – present) CAE- Treatment 1912 Phenobarbital (Luminal) 1993 1935 Mephobarbital (Mebaral) 1993 Gabapentin (Neurontin) 1938 Phenytoin (Dilantin) 1994 Lamotrigine (Lamictal) 1947 Mephenytoin (Mesantoin) 1996 Topiramate (Topamax) 1954 Primidone ((Mysoline) y ) 1997 Tiagabine g (Gabitril) ( ) 1957 Methsuximide (Celontin) 2000 Zonisamide (Zonegran) 1957 Ethotoin (Peganone) 2000 Levetiracetam (Keppra) 1960 Ethosuximide (Zarontin) 2000 Oxcarbazepine (Trileptal) 1968 Diazepam (Valium) 2005 Pregabalin (Lyrica) 1974 Carbamazepine (Tegretol) 2008 Rufinamide (Banzel) 1975 Clonazepam (Klonopin) 2008 Lacosamide (Vimpat) 1978 Valproic acid (Depakene) 2009 Vigabatrin (Sabril) 1981 Clorazepate (Tranxene) 2010 ACTH (Acthar) Summary of Evidence and Recommendations Partial onset seizures Seizure type or epilepsy syndrome Seizure type or epilepsy syndrome Class II Class III GTC: Adults 0 0 23 Level A: None Level B: None Level C: CBZ, LTG, OXC, PB, PHT, TPM, VPA Level A: OXC Level B: None Level C: CBZ, PB, PHT, TPM, VPA GTC: Children 0 0 14 Level A: GBP, LTG Level B: None Level C: CBZ 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 Class II Class III 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 POS: Elderly 1 2 Summary of Evidence and Recommendations Generalized onset seizures Class I Class I 1 Felbamate (Felbatol) Level of efficacy and effectiveness evidence (in alphabetical order) Level of efficacy and effectiveness evidence (in alphabetical order) Tracy Glauser, MD 8/6/2011 Summary of Evidence and Recommendations Epilepsy syndromes Seizure type or epilepsy syndrome BECTS JME Class I Class II Class III Level of efficacy and effectiveness evidence (in alphabetical order) The Place of Guidelines in Clinical Decision Making Evidence Patient/Physician Factors 1.Patient data 0 0 0 0 2 0 Level A: None Level B: None Level C: CBZ, VPA Level A: None Level B: None Level C: None 1. Cultural beliefs Knowledge 2.Basic, clinical, and epidemiologic research 2. Personal values 3 R d i d ttrials 3.Randomized i l Clinical 4.Systematic reviews Decisions Guidelines 3 Experiences 3. E i 4. Education Ethics Constraints 1. Formal policies, laws 2. Community standards 3. Time 4. Reimbursement Figure. Factors that enter into clinical decisions. Solving the problem Mulrow CD, et al. Ann Intern Med. 1997. Solving the problem – Needs for the system • Human aspects - Adaptation to the pace of change - Stronger synchrony of efforts - Culture of shared responsibility - New clinical research paradigm - Notion of clinical data as a public good - Incentives aligned for practice-based evidence - Public engagement - Trusted scientific broker - Leadership • Human + Information Technology - Clinical decision support systems - Universal electronic health records - Tools for database linkage, mining, and use Institute of Medicine (IOM). 2007. page 5 The Learning Healthcare System: Workshop Summary; Washington, D.C. National Academies Press Tracy Glauser, MD Why Clinical decision support systems? 8/6/2011 Future approaches to seizure and epilepsy diagnosis and management Collect from humans to accommodate the reality that although professional judgment will always be vital to shaping care, the amount of information required f any given for i d decision i i iis moving i b beyond d unassisted human capacity I saw your patient John Johnson in the Neurology Clinic at Cincinnati Children's Hospital Medical Center in follow‐up evaluation and management of idiopathic localization‐related vs. generalized epilepsy. The patient's last visit in our clinic was on 01/01/01. Interval Seizure History : Since the last visit , the patient's seizures have remained unchanged in intensity , frequency or duration. Improve the computer’s understanding Institute of Medicine (IOM). 2007. page 5 The Learning Healthcare System: Workshop Summary; Washington, D.C. National Academies Press Teach the computer Use the computer’s help 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 Jim Thigpen, PharmD 8/6/2011 Describe the known mechanisms of antiepileptic drug classes Identify the most common and serious adverse drug reactions for the medications d d f h d discussed Determine the appropriate medication choice(s) for a specific seizure type Discuss the potential implication of pharmacogenetics in epilepsy Jim Thigpen, PharmD, BCPS Assistant Professor East Tennessee State University Bill Gatton College of Pharmacy K+ Bromide (1857) Paraldehyde (1882) Phenobarbital (1912) Primidone (1952) Phenytoin (1953) Ethosuximide (1958) Diazepam (1963) Valproic acid (1978) Carbamazepine (1974) Felbamate (1993) Lamotrigine (1995) Gabapentin (1993) Topiramate (1995) Oxcarbazepine (1990) Vigabatrin Levetiracetam (1999) Zonisamide (2004) Tiagabine Ezogabine (2011) Brivaracetam Eslicarbazepine Perampanel Clobazam Ganaxolone ICA‐105665 BGG492 Carisbamate 2DG NTP‐2014 CPP‐115 Tonabersat YKP‐3089 IV Topiramate Sigma‐1 Agonists Jim Thigpen, PharmD Sodium channel blockers 8/6/2011 Prevent the return of the sodium channel to the Calcium channel blockers L, N, and T channels active state by stabilizing them in the inactive state, preventing the repetitive firing of axons ti th titi fi i f “Pacemakers” of normal rhythmic brain activity By “locking” these channels, the underlying slow depolarizations needed to generate seizures are inhibited Phenytoin, Carbamazepine, Oxcarbazepine, Zonisamide, Lamotrigine Ethosuximide GABA enhancers An influx of chloride increases the “negativity” of the cell so the cell has greater difficulty reaching the action potential GABA agonists ▪ Benzodiazepines, barbiturates GABA uptake inhibitor ▪ Tiagabine GABA transaminase ▪ Vigabatrin Glutamic acid decarboxylase modulation ▪ Gabapentin, Valproate Glutamate blockers Inhibition of the excitatory neurotransmitter ▪ N‐methyl‐D‐aspartate (NMDA) ▪ Alpha‐amino‐3‐hydroxyl‐5‐methylosoxazole‐4‐ propionic acid (AMPA) ▪ Kainate receptors Felbamate, Topiramate Jim Thigpen, PharmD Carbonic anhydrase inhibitor 8/6/2011 ↑ Hydrogen ions, ↓ pH, extracellular shift of K+, Synaptic vesicle protein 2A (SV2A) binding agents increase in seizure threshold SV2A appears to be important for the availability of calcium‐dependent neurotransmitter vesicles f The lack of SV2A results in ↓ action potential‐ dependent neurotransmission Used mainly for refractory seizures with catamenial pattern Acetazolamide Most common and best characterized AEDs Prevent sodium channels from returning to their active state Prevents repetitive firing of the axons Stabilizes the neuronal membranes Blocks and prevents posttetanic potentiation Limits development of maximal seizure activity Reduces the spread of seizures Levetiracetam Phenytoin (Dilantin®) First discovered in 1908, recognized as an anticonvulsant in 1938, FDA approved in 1953 Jim Thigpen, PharmD Phenytoin 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 8/6/2011 Zonisamide (Zonegran®) Zonisamide (Zonegran®) 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 Drug → Phenytoin Fosphenytoin Carbamazepine Oxcarbazepine Lamotrigine Zonisamide Partial and secondarily generalized Partial and secondarily generalized Partial and tonic/clonic Partial and secondarily generalized Partial and secondarily generalized, Lennox/Gastaut Partial and myoclonus GI, CNS, rash, vitamin K, hormonal dysfunction, etc… Infusion‐ related CNS, nausea CNS, nausea CNS (few), GI, somnolence CNS, cognitive effects, weight gain 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 Drug ++++ NO, but effective and economical ++++ Status, peripheral IV Rash Oligohidrosis, Rash, kidney stones Gamma‐aminobutyric acid (GABA) is the most important inhibitory neurotransmitter Benzodiazepines Emergency treatment Limited long‐term use Barbiturates Affect the duration of chloride channel opening ADR profile limits use Jim Thigpen, PharmD Clonazepam (Klonopin®) Used for all types of myoclonus and is useful in patients with concomitant anxiety 8/6/2011 Higher affinity for the GABA‐A receptor site Status epilepticus Caution with withdrawal IV, IM, Rectal Children tolerate sedative effects better than Intranasal ▪ midazolam adults Some children have hypersalivation Phenobarbital The most commonly prescribed AED of the 20th century Potent and broad spectrum CNS effects, especially cognition, behavior Drug interactions (enzyme inducer) Diazepam (Valium®, Diastat®) Lorazepam (Ativan®) Midazolam (Versed®) Primidone Metabolized to phenobarbital Also used for essential tremor at low doses Reuptake of GABA is facilitated by at least four specific transporting compounds Inhibition of these transporters makes increased amounts of GABA available at the d f l bl h synaptic cleft GABA prolongs inhibitory postsynaptic potentials Jim Thigpen, PharmD Tiagabine (Gabitril®) 8/6/2011 GABA is metabolized by transamination of GABA‐transaminase (GABA‐T) Inhibition of GABA‐T leads to an increase in hb f l d the extracelluar concentration of GABA Vigabatrin (Sabril®) Inhibits GABA transporter‐1 (GAT‐1) Used as second‐line or add‐on therapy for partial 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 Vigabatrin (Sabril®) A structural analog of GABA, binding irreversibly Most common side effect is drowsiness to GABA‐T Used for refractory partial seizures Depression (5%), agitation (7%), confusion and ▪ Less effective vs. primarily generalized tonic‐clonic ▪ May worsen myoclonic or generalized absence ▪ Myoclonus or Lennox‐Gastaut do not respond well Infantile spasms ▪ Tuberous sclerosis rarely psychosis Little effect on cognitive function VGB causes visual field changes (nasal constriction followed by concentric constriction, with preservation of central vision) in 50% ▪ Use is restricted Jim Thigpen, PharmD Gabapentin (Neurontin®) 8/6/2011 Developed to have a structure similar to GABA but Gabapentin (Neurontin®) No pharmacokinetic drug interactions the drug has little or no action on the receptor MOA is only speculated Only modest reduction in partial seizures and secondarily generalized seizures Well tolerated, most side effects are minor and occur mainly at high doses ▪ Increased intracellular concentration of GABA ▪ Inhibits branched chain amino acid transferase, which reduces their conversion to glutamate ▪ Somnolence, dizziness, ataxia, nystagmus Binds with the alpha2 subunit of calcium channels in the brain and spinal cord, which may explain its effect on pain Pregabalin (Lyrica®) Valproate (Depakote®) Very similar in all aspects to gabapentin DOC for many primarily generalized epilepsies and Approved for adjunct therapy for partial seizures partial seizures Discovered by accident Disco ered b 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 Used mainly as a pain medication ▪ Increased free fraction of drug (7‐9% to 15%) Jim Thigpen, PharmD Valproate (Depakote®) 8/6/2011 Felbamate (Felbatol®) 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 Blocks NMDA receptors, calcium and sodium Effective against multiple seizure types Nausea, vomiting, tremor, sedation, confusion, Occurrence of aplastic anemia and hepatic failure channels irritability and weight gain are dose‐related Hepatoxicity is most serious idiosyncratic effect Metabolic effects include hypocarnitinemia, hyperglycemia and hyperammonemia led to withdrawal from the U.S. market Available only for a very limited use ▪ Severe partial epilepsy or Lennox‐Gastaut Meador, et al. NEJM 2009;360(16);1597‐605 Topiramate (Topamax®) Topiramate (Topamax®) Derived from D‐fructose, initially developed as an Adjunct therapy for drug‐resistant generalized 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% 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 Jim Thigpen, PharmD Topiramate (Topamax®) 8/6/2011 Start slow and titrate to minimize/prevent Approved in June, 2011, for adjunct therapy in 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®) Ezogabine (Potiga®) 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 Levetiracetam (Keppra®) Thought to inhibit synaptic vesicle protein 2A No significant drug interactions (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 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%) Jim Thigpen, PharmD Lacosamide (Vimpat®) 8/6/2011 Enhances the slow inactivation of voltage‐gated Rufinamide (Banzel®) Prolongation of the inactive state of the sodium 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% ↓ 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 Eslicarbazepine (Stedesa®, Zebinix) Investigated for partial‐onset seizures with or without secondary generalization Still at the FDA Similar side effects to oxcarbazepine Brivaracetam Eslicarbazepine Perampanel Clobazam Ganaxolone ICA‐105665 BGG492 Carisbamate 2DG NTP‐2014 CPP‐115 Tonabersat YKP‐3089 IV Topiramate Sigma‐1 Agonists Jim Thigpen, PharmD Pharmacogenetics encompasses the principle of testing for how genetic variation among individuals affects variation in response to medicine d Provides the ability to identify potential adverse drug reactions or lack of effectiveness of a drug before administration 8/6/2011 The application in epilepsy High prevalence Wide variety of individual responses to drugs Readily qualified outcomes of seizure control Validated scales to classify both seizures and adverse effects Szoeke, CE, et al. neurology.thelancet.com Vol 5 February 2006 “Pharmacoresistance” is the inability to achieve complete seizure control despite trials of at least three appropriate AEDs, taken at appropriate doses, excluding k d l d seizures due to drug non‐adherence or extraordinary provoking events Same Seizure Disorder Same Seizure Disorder Same Medication and Dose Same Medication and Dose Seizure Free Continued Seizure Episodes Common in patients treated in epilepsy clinics Jim Thigpen, PharmD 8/6/2011 Genetic polymorphisms on metabolism CYP4502D6 ▪ Poor vs normal metabolizers Neural tube defects and VPA Product Function CYP3A4 Cytochrome P450 enzyme Associated with hydroxylation MRP Multidrug resistance‐ associated protein Transmembrane transport PRNP Cellular prion protein Associated with neuron protection P‐glycoprotein ▪ Phenytoin ▪ Lamotrigine ▪ Valproate V l t Rats bred with resistance to phenytoin Potential Candidate Drug transporters Drug Metabolism CYP450 enzymes ▪ Valproate ▪ Tiagabine ▪ Topiramate Glucuronidation ▪ Lamotrigine Genetic variation and response to AEDs Pharmacokinetics and application of pharmacogenomics Drug transport genes End‐organ drug targets Metabolism End‐organ targets Sodium channels ▪ SCN1A Immunogenetic I i background b k d HLA‐B*1502 ▪ Carbamazepine Jim Thigpen, PharmD Future directions Clinical trial complexities Individual genotypes Potential savings Application in practice ▪ Felbamate 8/6/2011 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 Sharon Castellino, MD 8/6/2011 Objectives Life after cancer Cases from the clinic Sharon M Castellino, MD, MSc, FAAP Pediatric Hematology/Oncology S W S. W. Virginia Pediatric Conference, Conference Abingdon VA , Aug 2011 • To describe childhood cancer survivors at risk for chronic health conditions • To describe the leading morbidities in childhood cancer survivors • To review recommendations for health surveillance following childhood cancer therapy Epidemiology 1 in 350 children in U.S. with cancer by 20 yrs. age ~ 14 new cases for every y 100,000 , children under age 15 yrs. Consistent increase in the incidence of cancer in children Survival: Now a reality 100 Leukemia-85% CNS Tumors-67% 80 60 Lymphoma-84% Neuroblastoma-66% Rhabdo-65% 40 20 Wilms Tumor-91% Bone Tumors-65% Retinoblastoma-94% 0 Overall-80% Sharon Castellino, MD Case 1: 10 yr old female with weight loss Treated for Neuroblastoma 5 years previously HPI: Recent asthma flare, with persistent cough. Appetite is fair- picky eater- no consistent calcium source in diet. She fatigues easily with moderate activity at school, and has question of shortness of breath at times. times 8/6/2011 Case 1: 10 yr old female with weight loss Chemotherapy Doxorubicin 295 mg/m2 Cyclophosphamide 13150 mg/m2 Melphalan M l h l 216 mg/m2 / 2 Neck/axillary fields ROS: pain on bottom of feet; constipation Etoposide 2206 mg/m2 PMH: Hearing loss- wears hearing aids Cisplatin 383 mg/m2 Current Meds: Singulair; Pulmocort Carboplatin 332 mg/m2 Retinoic Acid Case 1: 10 yr old female with weight loss Workup Physical: Slight child with well healed scar on abdomen. Scattered nevi on trunk and back- small/homogeneous in color and shape; Neck: No thyroid asymmetry/ no nodules palpable; Lungs: CTA; CV: 2+ pulses; nl S1, S2. Abdomen: soft; no HSM; Tanner 1; No scoliosis; No edema d Lab: CBC and CMP wnl (Albumin 3.5) Echo: FS 34%; normal function; CXR and Sinus CT clear Radiation Therapy Left abdomen Case 1 Parasympathetic Autologous HSCT Sharon Castellino, MD 8/6/2011 Case 1: Differential diagnosis Question: The most likely cause of weight loss and fatigue is: Case 1: 10 yr old female with weight loss Bone Age: 7 yrs and 10 months (compared to chronologic age 10y 6m) TSH 5.6 uIU/ml; free T4 0.8 mg/dl A. Pulmonary dysfunction after radiation to chest fields B. Relapsed neuroblastoma PFTs: FVC 85%; FEV1 87%; FEF 25-75 88%; DLCO 61% C. Thyroid dysfunction D. Cardiac dysfunction due to anthracycline and radiation exposure in childhood Case 2: 30 yr old male Treated for T cell Non-Hodgkin Lymphoma 22 yrs. ago HPI: Overall well. Came to clinic after phone discussion with oncology nurse talked to him. His main concern is that his wife and he have been trying to conceive for 3 yrs. without success. Case 2: Chemotherapy Doxorubicin 377 mg/m2 Cyclophosphamide 4231 mg/m2 ROS Tobacco ROS: T b 1ppd 1 d VM 26 2619 mg/m2 / 2 PMH: Presented at age 8 yrs. (1988) with mediastinal mass, hepato-splenomegaly, naso-pharyngeal mass; No marrow disease; Disease in spinal fluid. Prednisone Varicocele repair in L testes at age 28. 6 mercaptopurine Current Meds: none Cytoside arabinoside L-asparaginase Radiation Therapy Cranio-spinal 30 Gy Sharon Castellino, MD Case 2: Workup Physical: Well app young adult male with male pattern baldness. Skin: multiple nevi < 6 mm on back- scar at prior bx site in lumbo sacral spine area; HEENT: Normocephalic, OP clear; good dentitia; no corrective lenses ; No cataracts; Neck: no thyroid nodules palp.; N carotid No tid b bruit; it L Lymph: h N No adenopathy; d th L Lungs: CTA bilat; no wheezes; nl resp effort; CV: Nl S1 S2 - no murmur, rubs or gallop, 2+ pulses throughout; GU: Tanner V male Endocrine problems after cancer Seen after radiation of hormone-producing glands: Pituitary (brain radiation) Thyroid Th id ((neck k radiation) di ti ) Ovaries (abdomen/pelvis) Testes (pelvis or testes)) 8/6/2011 Case 1: 10 yr old female with weight loss Labs: Hepatitis C Ab: non reactive; Total Cholesterol 257 mg/dL; LDL 194 mg/dl; free T4/ TSH wnl; Testosterone 143 ng/dl ( low); FSH/LH within normal limits ECHO: C O Mild concentric hypertrophy Not screened: GH deficiency 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 • Brain tumors • Hodgkin’s disease • Head/Neck irradiation Sharon Castellino, MD Thyroid Dysfunction 8/6/2011 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/ chest field Endocrine Disorders • Hyperthyroidism • Usually with higher doses of radiation >35 Gy • Survivors 8 times more at risk • Thyroid nodules • Wide variation in incidence depending on screening method ((US vs. p palpation) p ) • Survivors 27 times more at risk • Higher doses of radiation >25 Gy and females highest risk 20% of females will have thyroid nodule at 20 yrs • 7.5% of nodules were malignant, 18.3 times general population Thyroid cancer was also reported in pts without nodules Endocrine and Growth Disorders • Growth Disorders • Multi-factorial (eg, hormone deficiency, growth plate radiation, precocious puberty, nutritional) • 13% of brain tumor survivors 2 or more standard deviations below normal • Most os a affected ec ed c cranial a a o or ccraniospinal a osp a RT esp esp. less ess than a 10 0 years old • Other studies showed spinal RT to be associated with shorter stature • Survivors of leukemia - similar results • Dose dependent >20 Gy 8 times risk of shorter stature while 4 times for <20 Gy • Obesity Risk increases w short stature Sharon Castellino, MD Growth Hormone deficiency • Diminished spontaneous ( physiological) GH secretion in presence of preserved peak responses to provocative testing • GH deficiency: first manifestation of neuroendocrine injury j y following g cranial irradiation • Severity and time to onset is dose dependent • Incidence of GH deficiency increases with timeelapsed • Dx and treatment by endocrinologist • Current data do not suggest an increased risk of tumor recurrence with GH replacement initiated 2 yrs after end of therapy Case 3: 14 yo male- asymptomatic 8/6/2011 Fertility • Risks for Infertility: • Higher dose of alkylating agents • Radiation: head; pelvis • ? Peripubertal age at treatment • PMD role due to uncertainty • Follow Tanner stage and monitor for normal pubertal milestones • Sperm /oocyte production can start months or years after treatment Advocate good sexual health in all patients regardless of treatment risks to fertility ( protection; Gardasil vaccine) Case 3: 14 yo male- asymptomatic Treated for Neuroblastoma 10 years previously Treated for Neuroblastoma 10 years previously HPI: Patient comes to clinic for regularly scheduled screening visit. Mother’s main concern is of shuffling gait due to out toeing. Echocardiogram: Compared to prior echo 3 years previously ROS: A lot of loose stools daily; no incontinence; wears hearing g aids PMH: Current Meds: Sharon Castellino, MD 8/6/2011 Case 3: Screening Echocardiogram Case 3: Annual Screening Physical: Well appearing teen, who appears smaller than stated age ( Wt and Ht: 5%ile). OP: enamel dysplasia; agenesis of posterior roots; Neck: no thyroid asymmetry; CV: Nl S1, S2; no murmur; Back: R thoracic rib hump on bend test Lab: CBC, thyroid function, UA, Metabolic panel wnl Hill, Castellino, Williams, Ped Cardiology 2009 Case 3: Work up CCSS Cumulative Incidence of Second cancer in Hodgkin’s Cohort An NCI-funded Resource Question: The most likely cause of the intra-cardiac mass is B Endocarditis B. E d diti in i an immunosuppressed i d child hild C. Second Malignant Neoplasm Probability of S SMN A. Recurrent neuroblastoma 25.3% (95% CI: 21.2, 29.4) 0.4 Females 0.3 10.9% (95% CI:8.1, 13.8) 0.2 Females, non-breast Males 0.1 10.6% (95% CI: 7.3,13.8) 0.0 5 10 15 20 25 Years Since Diagnosis 30 35 Castellino, Blood 2011 Sharon Castellino, MD CCSS An NCI-funded Resource 8/6/2011 Childhood Cancer Survivor Study (CA 55727) Mortality Patterns in 5 yr survivors Case 1 18 year old female treated at 12 years of age: Hodgkin lymphoma Treatment: modified mantle radiation; anthracycline chemotherapy You are ready to transition her to adult care and she is reluctant l t t to t return t to t her h oncologist, l i t since i she h is i 6 years in remission Mertens, J Natl Cancer Inst 2008 Case 3 Objectives 22 year old female treated at 10 years of age: Synovial Sarcoma Treatment: • To describe the prevalence of late sequelae in childhood cancer survivors • To describe the survivor population at risk for chronic health care needs Sharon Castellino, MD CCSS An NCI-funded Resource 8/6/2011 Childhood Cancer Survivor Study (CA 55727) Study Population • Retrospective Cohort • < 21 yrs. at Diagnosis • Diagnosis 1970-1986 g • 5-Year Survival • Leukemia, Lymphomas: 20,720 Eligible Lost (n=3017) 17 703 Contacted 17,703 Refusal (n=3189) 14,372 Participants HL, NHL, CNS, Bone, Wilms, NBL, Soft-tissue sarcoma Oeffinger, 2006 Early treatment era (1962-70) Recent treatment era (1971-83) Diller, J Clin Oncol 2009 Hudson, JCO 1997 Sharon Castellino, MD CCSS An NCI-funded Resource 8/6/2011 Childhood Cancer Survivor Study (CA 55727) Mortality Risks Assessing Risk for Late Effects Disease factors • 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 10.0-14.7), 12.9-17.7), 9-17 7) Ewing Sarcoma (SMR 13.3) Treatment factors Host factors • Compared to: Hodgkin Lymphoma (SMR 7.8); Kidney tumor (SMR 4.6) Treatment factors Chemotherapy dose mechanism of action metabolism of drug Radiation total vs fractional dose dose rate treatment time treatment volume machine energy Surgery Abdominal Intracranial Amputation 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 • Ifosfamide: Fanconi syndrome • Steroids: osteoporosis Sharon Castellino, MD 8/6/2011 Psychosocial Late Effects • Academic and occupational achievement Case 5 18 year old female treated at 12 years of age: • Family and interpersonal relationships Hodgkin lymphoma Treatment: modified mantle radiation; anthracycline chemotherapy • Adaptation to chronic illness or disability • Insurance discrimination and access to healthcare Case 5: Question: What are the long term risks/if any ? A. Recurrent Hodgkin Lymphoma B. Thyroid disease C. Breast cancer D Melanoma D. M l E. Stroke F. Coronary Artery disease/other CV risks G. None of the above H. (A, B, C, E, F) Mantle Field Sharon Castellino, MD 8/6/2011 Dental Abnormalities • Enamel dysplasia • Incomplete calcification • Disorders of tooth development • Foreshortening of roots • Premature P t close l off apices i • Tooth agenesis, microdontia • Arrested tooth development Anthracycline Cardio Vascular (CV) toxicity • Myocyte death myofibrillar loss and vacuolar degeneration subsequent hypertrophy of surviving myocytes --> reduced wall thickness interstitial i t titi l fib fibrosis i • Severity correlates with Cum anthracycline dose Age at exposure Chest radiation fields Sharon Castellino, MD 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 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 Neurocognitive Sequelae • Risks: • Age at cranial radiation • Radiation dose • Female sex • • • • MTX - intra-thecal and high systemic dose Cognitive deficits Leukoencephalopathy Seizures and other overt CNS symptoms 8/6/2011 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 Sharon Castellino, MD 8/6/2011 Objectives • To describe the prevalence of late sequelae in childhood cancer survivors • To describe the survivor population at risk for chronic health care needs • To review recommendations for health surveillance following childhood cancer therapy Comprehensive follow-up of cancer survivors Bhatia, S. Hematology 2005;2005:507-515 Copyright ©2005 American Society of Hematology. Copyright restrictions may apply. COG Long-Term Follow-Up Guidelines for Childhood Cancer Survivors • Goal: Increase quality of life and decrease health care costs • Promote healthy life-styles • Provide on-going monitoring of health status • Identify late effects at an early stage • Timely Intervention against late effects Sharon Castellino, MD Screening and management Based on treatment exposure • Summary of cancer treatment • Diagnosis, age • Chemotherapy agents used with doses and cumulative doses • Radiation doses and fields • Transplant - HSCT(ie BMT) Did patient have GVHD • Surgery history • Other treatment/exposure: transfusion 8/6/2011 Screening and Management All Survivors • Annual screening: • Educational and vocational progress • Mental health: Depression/ Anxiety/PTSD/Social withdraw • Healthcare insurance and access • If patient received chemotherapy: Oral and dental exam every 6 months • Full review of symptoms for subtle issues • Based on exposures (chemotherapy, radiation, surgery) Case: HL survivor Annual exam: listen for carotid bruits; teach self breast exam; skin- attention to RT field; thyroid; mental health screening; sexual health CBC ; Free T4, TSH; Lipids Breast MRI and mammography - age 25 or 8 years after RT Echo – and EKG : per guidelines; based on anthracycline and chest RT ; pregnancy counseling - No isometric exercise -CV health Childhood cancer survivorship--future directions Bhatia, S. Hematology 2005;2005:507-515 Copyright ©2005 American Society of Hematology. Copyright restrictions may apply. Sharon Castellino, MD 8/6/2011 Cure • Derived from cura = care • Definitions: • successful medical treatment; recovery or relief f from a disease di “The pediatric cancer survivor is a vivid and important illustration of the power of medicine to conquer cancer” Patenaude and Kupst (J Pediatric Psychology) Psychology), 2005 • state where the expectation of life of a group of patients free of disease is similar to that of the general population of the same sex and age • to restore to health, soundness, or normality Conclusions- PCP • The general pediatrician’s role in monitoring growth and other toxicities is increasingly important • 75% will develop a chronic disease by 40 years age, and 40% a serious health problem • Many effects do not become apparent for many years following treatment Facilitating transition to young adult health 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 Sharon Castellino, MD Neuroendocrine Dysfunction Growth Impairment • GH deficiency • common following > 18-20 Gy to hypothalamic/pituitary region 8/6/2011 Late effects • Frequency and pathogenesis are difficult to assess: • clinically apparent > 2 yrs following radiotherapy • patient must be a long term survivor to manifest effect • 60-80% of irradiated brain tumor patients will have impaired serum GH response to provocative stimulation • numbers of affected and unaffected patients must be known in order to assign a probability risk • dramatic effects are noted, but subtle/subclinical damage goes unrecognized 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 Rob Clemons, MD 8/6/2011 Legal Stuff Updates in Dermatology: Lets Get Sun Safe | I have no financial interest in any products discussed in this presentation but I do work cheap if your interested. Robert J. Clemons, MD, FAAD TriCities Skin and Cancer True or False | 1. You can not acutely sunburn through the car windshield | 2. 2 Sunscreens and blocks cause skin cancer | 3. You can only maintain Vitamin D levels with sun exposure | 4. Indoor tanning can increase Vitamin D synthesis Ultraviolet Light Rob Clemons, MD Ultraviolet Spectrum 8/6/2011 The Basics of Ultraviolet Light | Ultraviolet spectrum | UVC (200-290nm)- predominately absorbed by water and ozone in atmosphere. Highly carcinogenic. | UVB (291-320nm)- Burning wavelength. Blocked by i d hi ld St l associated i t d with ith non-melanoma l ki windshields. Strongly skin cancers in animal models. | UVA II (321-340nm)- Delayed tanning wavelength of 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 Effects of Solar Radiation | Ultraviolet radiation in the UVC, UVB, and short wavelength UVA spectrum are associated with y dimer formation of DNA Pyrimidine | P53 mutations | Immunosuppressive effects by | Reducing Langerhans cell populations in the epidermis | Decreasing peripheral T cell populations in the circulation Rob Clemons, MD 8/6/2011 Effects of UV Radiation | Acute effects: Sunburn Sunburn Freckles Photodermatosis | Chronic effects: Rhytids Lentigos Actinic Keratosis Non-Melanoma Skin Cancer Melanoma Poikiloderma of Civatte Get The Facts | It is estimated that a person receives approximately 80% of their accumulative solar radiation before they reach 18 years of age. | Skin Cancer Foundation has a different view of lifetime UV exposure based on a 78 year life span | Ages 1-18 22.73% | Ages 19-40 46.53% | Ages 41-59 73.70% | Ages 60-78 100.0% Skincancer.org Rob Clemons, MD 8/6/2011 Statistics From The American Academy of Dermatology Actinic Keratosis | More than 3.5 million skin cancers in more than 2 million people are diagnosed each year | 1 out of 5 Americans will be diagnosed with skin cancer in their lifetime | Melanoma incidents have increased for the past 30 years | 3% per year increase in young white females 15-39 y/o | 4% per year in white adults > 65 y/o since 1985 | In 2004, the total cost of treating non-melanoma skin cancer was $1.5 billion o www.aad.org Basal Cell Carcinoma Melanoma Rob Clemons, MD 8/6/2011 Be Sun Smart | Wear Broad-spectrum UVA/UVB water resistant sunscreen | Seek Shade | Know the high UV hours of the day 10-4 | When your shadow is shorter than you are tall e t a cautious ca tio s near nea water, ate snow, sno | Be extra and sand | Sun Protective Clothing Be Sun Smart | Tight cotton weave clothing | Universal Protection Factor clothing (UPF) | Wide brimmed hat | Avoid Tanning Beds- Think about self tanner | Supplement Diet with Vitamin D Why Do Sunscreens Fail??? | Bad product | Did not apply frequently enough Sunscreens and Sunblock | Did not apply enough at each application Rob Clemons, MD 8/6/2011 Sunscreens and Sunblock Where Did All the White Noses Go? | Sunblock (physical agents) | Scatter and physically block UV light | 4 main types | Zinc oxide | Titanium dioxide | Talc | Red Veterinary petroleum | Sunscreens (chemical agents) | Non-opaque and absorb UV radiation of various wavelengths Sunblock Chemical Sunscreens | UVB Sunscreens | PABA and PABA Esters (260-315nm) | PABA (Para Aminobenzoic Acid) | Padimate A | Standard Physical Blocks | Padimate O | Micronized Zinc Oxide (290-380nm) | Micronized Titanium Dioxide (290-320nm) | Glycerol aminobenzoate | Cinnamates (270-320nm) | Octyl methoxycinnamate (280-310nm) | Cinoxate (270-328nm) o www.skincancer.org | Salicylates (290-320nm) | Homosalicylate | Octyl salicylate | Triethanolamine salicylate | Octocrylene (280-320nm) o www.skincancer.org Rob Clemons, MD 8/6/2011 Chemical Sunscreens UVA Sunscreens: The rest of the story | UVA Sunscreens | Etrocrylene (296-380nm) | Benzophenones | UV light to breakdown many g appears pp y chemical sunscreens that protect against UVA | Oxybenzone y ((270-350nm)) | Dioxybenzone (206-380nm) | Sulisobenzone (250-380nm) | Avobenzone/ Parsol 1789 (310-400nm) | Helioplex (Neutrogena) | Ecamsule/Mexoryl SX (La Roche-Posay) | Methylanthranilate (200-380nm) o www.skincancer.org Sun Protection Factor | 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 Sun Protection Factor What does it really mean? | 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 Rob Clemons, MD Do Sunscreens Cause Skin Cancer??? 8/6/2011 FDA New Requirements | Proposed to eliminate confusion in the public and mislabeling | What defines “Broad Spectrum” | Must be an SPF>15 | Must demonstrate UVA protection proportional to its UVB protection according to its SPF | Defines what products can claim they reduce risks of skin cancer and photo aging | There may be more to the question | Eliminate Eli i the h terms sunblock, bl k waterproof, f and d sweat prooff | Strong UVB protection allows people to stay outside longer without burning but continue to get UVA damage | Eliminate the term “instant protection” | New requirements for water resistance claims | UVA protection low and does not last | Must label protective for either 40 or 80 minutes while swimming or sweating | “waterproof” claims may fall short | 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 o www.fda.org Seek the Shade!!! Shade Suggestions | Umbrella or other shade structure | If your shadow is shorter then you are tall | Be cautious from 10am to 4pm | Remember reflective sun off water, snow, and sand Rob Clemons, MD 8/6/2011 Shade Structure Grants | Sponsored by the American Academy of Dermatology | $8,000 grants awarded each year toward the purchase of permanent shade structures designed to provide UV protection to outdoor areas | AAD provides a permanent sign that stresses the importance of sun safety | Applicants must | Be a nonprofit organization or a public school that serves children under the age of 18 years. | Demonstrate an ongoing commitment to sun safety by instituting a sun safety and skin cancer awareness program at least one year prior to the application Sun Protective Clothing | Be sponsored by an AAD member o www.aad.org 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 1,700 700 | 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 Don’t Forget the Wide Brimmed Hat Rob Clemons, MD 8/6/2011 Facts About Indoor Tanning Avoid Indoor Tanning | More than 1 million people use tanning beds every day in the United States | 70% of patrons are Caucasian females between 16 and 29 years of age | 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, 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 o www.aad.org Self Tanners: Tan in a Can Facts About Indoor Tanning | Dihydroxyacetone (DHA) | Derived from sugar beets and sugar cane | Color change based on the percentage of product | 1-15% | OTC usually 3-5% | Takes effect in 2-4 2 4 hours and continues to darken for up to 24 hours | Gives minimal SPF protection by itself (SPF 2-3) | Some products adding sunscreens to the tanner | Limited effect and need to reapply sunscreen 2 hours after tanner | Last for 2-4 weeks as the stratum corneum sheds | Less effect if frequently in water | Last longer if exfoliate heavily before application | Only one report of contact dermatitis in hairless Mexican dogs. | Federal government instituted a 10% tax to indoor tanning | Effective lobbying deflected the proposed “botax” in favor of an indoor tanning tax | Two bills entered into the House and Senate are aimed at repealing the tax Rob Clemons, MD 8/6/2011 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 Supplement Diet with Vitamin D Di t | 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 Sun Protection for Newborns Sunburns: How To Treat | Sun Avoidance | Sunscreens have not been tested safe under g six months of age | Recognize quickly and get out of sun | UPF clothing | Moisturize | Shade structures | Hydration | If necessary, find a pure physical block with zinc oxide and titanium dioxide | NSAIDS early Rob Clemons, MD 8/6/2011 Photodermatosis Case #1 Case #1 | 12 year old boy from West Virginia | Just returned from a spring break trip to Myrtle Beach | 1. Photoallergic contact dermatitis | Red itchy papules coalescing into plaques on the ears 2 | 2. Subacute Cutaneous Lupus Erythematosus | Had the same problem two years ago during spring break but last year they went in August and he was fine | 3. Polymorphic Light Eruption | 4. Porphyria | Labs were normal to include an antinuclear antibody, CBC, and urine studies Polymorphic Light Eruption 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 | Di i i h iin mid Diminishes id tto llate t summer | Topical corticosteroids | In adults | Hydroxychloroquine | | Forearms | V of the neck In children | Face | Ears | 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 | Treatment | Antihistamines | Broad spectrum sunblock with physical barrier protection | 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 James Thompson, MD Update on Plagiocephaly and Craniosynostosis 8/7/2011 Definitions Craniosynostosis (craniostenosis) – refers to the fusion of the cranial sutures Plagiocephaly – Greek “slanting head” is a descriptive term regarding head shape. James T. Thompson, M.D. F.A.C.S. Assistant Professor Department of Plastic and Reconstructive Surgery Wake Forest University School of Medicine Winston-Salem, NC Brachycephaly – a descriptive term referring to a shortened head shape cranial sutures leads to the shape abnormality à Overall incidence ~ 1:2500 à Causes Fetal constraint Abnormal brain development genetic syndromes Maternal smoking Amine containing drugs Synostotic or Deformational Synostotic Scaphocephaly Craniosynostosis à Fusion of one or more Synostotic – related to fused cranial sutures. sutures Deformational – caused by external forces with no suture fusion. Sagittal synostosis Most common type ~ 1:1800 births à about 60% of all nonsyndromic cases Almost all are nonsyndromic 2% hereditary Male : Female = 4 : 1 Classic features: à Frontal bossing à Elongated skull à Pointed occiput James Thompson, MD 8/7/2011 Synostotic Plagiocephaly Synostotic Trigoncephaly Metopic synostosis Incidence ~ 1:5000 births Male : Female = 3:1 ~ 90% nonsyndromic ~ 6% hereditary Classic features Unicoronal synostosis Incidence ~ 1:5000 Usually nonsyndromic Classic features: à Ipsilateral frontal flattening à Ipsilateral anterior ear displacement à Contralateral frontal bossing à Forehead ridging à Triangular shaped forehead à Hypotelorism Synostotic Plagiocephaly Synostotic Brachiocephaly Bicoronal synostosis Incidence ~ 1:20,000 births Almost always syndromic y à Eg. Crouzons, Aperts, Pfeiffers Classic features: à Shortened head à Tall forehead à Recessed supraorbital rim 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 James Thompson, MD 8/7/2011 Synostotic Plagiocephaly Frontosphenoidal synostosis Synostotic Plagiocephaly Treatment Unknown incidence Classic features: à Ipsilateral frontal flattening à Ipsilateral anterior ear displacement à Contralateral frontal bossing Rationale for treatment: à Neurodevelopmental outcomes with craniosynostosis Gault DT, Renier D, Marchac D, et al Intracranial pressure and intracranial volume in children with craniosynostosis. Plast Reconstr Surg 1992: 90:377-381. KA, Figueroa A, A Jocher CA, CA et al. al Longitudinal Kapp-Simon KA assessment of mental development in infants with nonsyndromic craniosynostosis with and without cranial release and reconstruction. Plast Reconstr Surg 1993; 92:831-839. Low grade increased ICP Cognitive and behavioral dysfunction Ophthalmologic pathology Impaired psychosocial function à Correction of deformity to avoid stigmatization 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 Synostotic Plagiocephaly Treatment à Bicoronal incision à Surgically corrected deformity à Blood loss à ICU à Restore cranial volume à Correct deformity Traditional surgery Less invasive surgery à Springs à Endoscopic + Helmets James Thompson, MD Deformational plagiocephaly à Associated factors Intrauterine restriction / Multiple gestation Torticollis Premature birth / ICU stay Supine positioning à Incidence unknown but probably 15-30% of all infants 8/7/2011 Clinical exam Ipsilateral occipital flattening Contralateral occipital bossing Ipsilateral forehead bossing Ipsilateral p anterior ear displacement “Parallelogram shape” à Male > Female (3:2) à R>L Other findings Anterior displacement of the skull base Anterior displacement of the TMJ Crossbite James Thompson, MD 8/7/2011 Cephalic index = head width/length Normal = 0.75 >0.80 brachycephaly >0 80 = b h h l <0.70 = dolichocephaly (scaphocephaly) Is this purely a cosmetic deformity? Neurodevelopment Ear problems (infections) TMJ problems Eye problems Classification I (6a) (6 ) II (6b) III (6c) Miller et al. Peds 105(2): 2000. Telephone survey of 63 families who had been previously seen for plagiocephaly At least 9 years old Children with plagiocephaly more likely to have used speech, occupational, or physical therapy Siblings used as controls Not statistically significant for females. James Thompson, MD 8/7/2011 Motor skills delayed Fowler et al. J Child Neurol. 23:742, 2008 à Case/Control format with 49 infants Kordestani et al. PRS. 117(1):207-218, 2006. à Bayley Scales of Infant Development-II à 110 patients (control = normative data) à Found more patients fell into the delayed category than expected. à 23 patient who had no confounding factors tested normal. Motor skills delayed à Hammersmith Infant Neurologic Assessment Low birthweight à Motor tone abnormally high and low in infants with plagiocephaly à Weakness: controls not matched well, only studied infants seeking treatment ICU admission Male gender Family history Other Congenital defects Motor skills delayed Speltz et al. Pediatrics. 125:e537-e542, 2010 à Case/control format 235 infants à Bayley Scales of Infant Development III (BSID-III) à Infants with plagiocephaly scored lower à Controls well matched (socioeconomic, ethnicity) and were screened for plagio à Weaknesses: Only studied infants seeking treatment, case group scored higher than expected. expected Collett et al. Arch Pediatr Adolesc Med. 2011;165(7):653-658. à Bayley Scales of Infant Development III (BSID-III) à Case/control format 225 with DP 230 without à Looked at age 18 months à Scores still lower than control group across the board à Helmet therapy had no effect on scores à But both groups scored in the normal range James Thompson, MD Motor skills delayed 8/7/2011 Association Causation à Does motor delay cause iincreased d plagio l i or vice i versa? à Theory of gyri flattening Anecdotal observation y Increased ear infections but not statistically significant. Abnormal tympanograms suggesting abnormal eustachian tube function. About 26% had a posterior crossbite No attempt to address the significance of this or discuss symptoms Denis et al. Child Nerv Syst 12: 1996 No comment on functional problems or symptoms One study showing some dental malocclusion in 5 year olds Lee et al CPCJ 45(3), 2008 Increased ear infections Purzycki et al. J Craniofac Surg. 20(5):1407-11: 2009 One study showing TMJ displacement in infants St. John et al. J Oral Maxillofac Surg 60:873-877, 2002 Strabismus and Astigmatism associated with plagiocephaly Due to formation of binary vision before 6 months Miller et al. Peds 105(2): 2000 Survey of 68 families No increased incidence of visual disturbances James Thompson, MD Positioning Physical therapy Hutchison Pediatrics 2004;114;970-980 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 Torticollis 8/7/2011 Helmets à Usually resolves 200 infants followed from birth to 24 months old Showed improvement with positioning alone Active à Dynamic helmets that have to be custom made and adjusted weekly to mold the head into shape Surgery à $$$$$ à Rarely needed Passive à Passive helmets rely on rapid infant head growth as the dynamic factor à Can be prefabricated and custom fit à $ James Thompson, MD Active D.O.C. 8/7/2011 Passive Danmar à Cranial technologies à Level 4 Research presented at the ASPS 2006 154 patients completed the study protocol à 91% achieve normal cranial shape and symmetry à Successful for plagiocephaly and brachycephaly Success correlated significantly with severity Success correlated significantly with compliance Success correlated with age at treatment - Patients are followed with a laser scanner that produces 3D images of the head James Thompson, MD Before 8/7/2011 After Before After Before After Before After James Thompson, MD Outcomes Lee et al CPCJ 45(3), 2008 à 5 year follow up à 28 Infants treated with the D.O.C. helmet improvement after treatment à Some regression in cranial base asymmetry and cranial vault asymmetry à Orbito-tragal asymmetry continued to improve Xia et al. Arch Pediatr Adolesc Med. Aug;162(8):719-27. 2008 8/7/2011 à Meta analysis Must differentiate between synostotic and non synostotic plagiocephaly Milder cases of plagiocephaly will resolve with p positioning g More severe cases will have lasting effects If helmet therapy is desired it is best to refer before 6 months of age à No randomized controlled trials à 5 of 7 cohort studies show helmets better than positioning Deformational plagiocephaly is associated with delayed or abnormal motor development 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. Randomized trials of helmet therapy Long term analysis of children with plagiocephaly p Neurodevelopment Other facial development problems 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 Jeffrey Carlsen, MD 8/7/2011 Jeff Carlsen, MD I have no financial interest in any products that may be discussed during the course of this presentation 110 Medtech Parkwayy Johnson City, TN 37604 Phone# 423-929-2111 Fax# 423-929-0497 Direct Ophthalmoscopy How to use one of the most powerful instruments in your office Jeffrey Carlsen, MD 8/7/2011 Direct ophthalmoscopy ophthalmoscope Introduced in 1850 ago by Helmoltz Examination of the internal structures of the eye through the pupil to diagnose eye pathology and systemic pathology via ophthalmic manifestations Ophthalmoscope controls On/off brightness Focus wheel. Clockwise increases power .. Focal point nearer observer p and vice versa Light aperature Direct ophthalmoscope exam Prepare the ophthalmoscope position the patient- fixation target RED REFLEX External eye fundus Jeffrey Carlsen, MD Mydriatics “dilation” Light Reflex to assess eye alignment Mydriacil…tropicamide Phenylep phenylephrine Cyclogyl DON’T BE AFRAID TO USE THESE STRABISMUS 8/7/2011 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 (leading ( g cause of visual loss in children) Strabismus has a profound social and developmental impact on a child Self esteem Social interaction Red Reflex Reflection of the ophthalmoscope light off the choroidal vessels Jeffrey Carlsen, MD 8/7/2011 Abnormal red reflex cornea Abnormal Red Reflex Abnormal red reflex lens Cataract Types… with systemic diseases Corneal opacity, dystrophy….. Keratoconus Dystrophy scar Direct ophthalmoscope Fundus Exam Fixation target Optic nerve is about 15 degrees nasal Have ve patient p e look oo at your yo ear Turn lens wheel clockwise as you get closer and vice versa Jeffrey Carlsen, MD 8/7/2011 Fundus exam Optic nerve Orient yourself. Find a vessel and then follow to the nerve Optic nerve Every Hero has his weakness Monocular instrument. 2 dimensional therefore cannot assess depth/height High magnification 15x/ small field of view 15 degress Must build a collage and piece together the whole picture Jeffrey Carlsen, MD 8/7/2011 Subconjunctival Hemorrhage Can be subtle or quite dramatic Minor trauma, valsalva, eye rubbingg Tx.: r/o bad actors, reassurance Spontaneous resolution If recurrent, then consider blood dyscrasia Chalazion/ Hordeolum Nodule near lid margin secondary to inspissated secratory gland. Meibomian, zeiss, of moll May or may not have an infectious component. Treatment includes: Lid hygiene: heat and lid scrubs. May consider antiobiotic. Surgery to drain if necessary. Trauma High index of suspicion Usually but not always: pain and decreased vision Think of in unilateral presentation, exposure to power tools or compressed air If suspicious, refer Chalazion Tearing Hypersecretion Dry eye Allergies Misdirected lashes Conjunctivitis Blink abnormality Foreign body/trauma Hypoexcretion NLD stenosis NLD obstruction Jeffrey Carlsen, MD 8/7/2011 Tearing in infants Abnormal or overflow tearing is common in infants; approximately 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 ll 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. R f earlier Refer li if ffrequent iinfections, f i as this hi may cause fibrosis of the NLD 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. 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 Jeffrey Carlsen, MD 8/7/2011 NLD If less then 2yrs old, then simple probing has a very high success rate If older then 2y/o or previous failed probing, then NLD stent or dilatation If failed stent or older then 5-10y/o, then may need dacrocystorhinostomy 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 Bl k S, S Hedrick H d i k J, J Tyler T l R, R ett al.l Increasing I i bacterial b t i l resistance it Block in pediatric conjunctivitis (1997-1998). Antimicrob Agents 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 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 Mark Howell, MD 8/7/2011 Mark A. Howell M.D., F.A.C.S. Ear Nose and Throat Associates, Ear, Associates P P.C. C Johnson City, Tennessee Currentt Philosophy C Phil h and d Accurate Diagnosis of Pediatric Rhinitis, URTI and Paranasal Sinus Infection Goals • 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 intervention WHY? • Increasing resistance patterns of respiratory tract pathogens to antibiotics • Lack of objective clinically useful dx modalities for URTI’s • Increasing burden to accurately dx URT symptoms to differentiate allergic,viral and bacterial etiologies for appropriate therapy Mark Howell, MD 8/7/2011 Anatomy Physiology • External Bone and Cartilage • Internal Bone and Cartilage • Turbinates T bi Diagnostic Difficulty • • • • • Respiration Olfaction H idifi ti Humidification Filtration Heat Exchange Sinus Anatomy • Nose difficult examination • Unable to visualize sinus as the middle ear 7 • • • • • Four paired sinus groups Frontal Ethmoid Maxillary Sphenoid Mark Howell, MD Sinus Anatomy • Air filled cavities in facial bones • Lined pseudostratified ciliated columnar epithelium with goblet cells • Continuity with nose via ostia for ventilation and drainage Purpose Paranasal Sinuses • Reservoir air, warming and humidification • Voice resonance • Light weight mechanism to add volume to cranial-facial structures 8/7/2011 Nasal-sinus transition space • Ostiomeatal complex(OMC) • Drains anterior ethmoid,frontal and maxillary sinuses • Sphenoid and posterior ethmoid drain posteriorly Paranasal Sinus Development • Maxillary and ethmoid sinuses present at birth • Sphenoid development at 2y/o and pneumatized at 5y/o ;completed 12y/o • Frontal starts 6-8y/o;completed 20y/o • 12y/o nasal cavity and sinuses reach adult proportions Mark Howell, MD Sinus Health Maintenance • • • • • • Anatomy(mechanical obstuction) Ostial patency Mucociliary clearance I Immune competence t Ciliary function Biphasic mucus blanket Local Immune Function • Secretory IgA • Lysozymes • Interferon 8/7/2011 Sinus Physiology • Pseudostratified columnar epithelium • Goblet cells • Biphasic mucus layer(deepsol;superficial gel) sol;superficial-gel) • Cilia-1000hz cycle • Sinuses cleared every 10-15 minutes Goal of Health Maintenance • Prevent mucosal adherence of bacteria and viruses • Facilitate opsonization and destruction of bacteria by immune cells Mark Howell, MD 8/7/2011 Scope of Problem • Children at least 3-8 URTI/yr • 5-13% evolve ARS in children • .5-2% in adults Nasal Symptoms • • • • • • Nasal congestion/obstruction Nasal discharge Nasal pressure/pain It hi Itching Post nasal discharge Cough/Pharyngitis/voice changes 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 Mark Howell, MD Differential Diagnosis and Associations • Anatomic abnormality(nose/sinuses) • Odontogenic Anatomic Associations • Turbinate hypertrophy(allergic/nonallergic rhinitis) • Adenoid hypertrophy(reservoir bacteria;obstructing airflow/mucociliary flow) • Nasal foreign body • Nasal polyposis(Cystic fibrosis/antral choanal polyp) • Tumor 8/7/2011 Other Related Factors • • • • • • • Cystic fibrosis Ciliary dyskinesia Immune deficiency(HIV) Diabetes Cranial facial abnormalities Trauma GERD 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) • Agger nasi cell(frontal sinus) • Cranialfacial anomaly(Down syndrome,Crouzon’s ,Aperts syndrome,cleft palate) • Deviated nasal septum(10-13%) Mark Howell, MD 8/7/2011 Nose and Paranasal Sinuses are anatomically a a o ca y p physiologically ys o og ca y related e a ed as single organ system Rhinitis Hyperfunction of nose due to various stimuli, producing rhinorrhea and nasal obstruction Rhinitis and Rhinosinusitis • Sinusitis is usually preceded by rhinitis and rarely occurs without concurrent rhinitis • Rhinosinusitis therefore is current term • Acute • Subacute • Recurrent acute • Chronic Mark Howell, MD Rhinosinusitis • Acute (up to 4 weeks and total resolution) • Subacute(4-12 weeks) • Recurrent Acute(4 or more episodes year with resolution between attacks) • Chronic(12 weeks or more of signs and symptoms) • Acute exacerbations of chronic rhinosinusitis 8/7/2011 Viral vs. Bacterial ? • • • • Children 3-8 acute respiratory illness/yr Adults 3-4 AURTI,s/yr 90% will have CT sinus findings Only 0 0.5% 5%-2% 2% positive bacterial cultures adults • 6-13% in children evolve to bacterial • 1 billion VURTI expected yearly • 20 million ABRS expected Characteristics Viral Infections • Viral Infection – Spread person-person contact – Secretions -nose,mouth,eyes – Inhalation-viral-laden droplets – Contact-hands,objects(virus remains hours,daycare) Viral agents • • • • • • • • • 200 viral species Rhinovirus(50% common colds) Echo Coronavirus Influenza A and B Parainfluenza RSV Adenovirus Enterovirus Mark Howell, MD 8/7/2011 Relationship VURTI,s to ABRS Signs and Sx of VURTI • Rhino and Corona virus no epith.damage • Influenza and Adeno virus damage UR tract • Incites histamine,bradykinin,cytokines(ITL) , y , y ( ) • Suppress neutrophil, macrophage and lymphocyte function • Animal model RSV enhanced H.influenza infection in URT in cotton rat • Activation parasympathic and inflammatory pathways initiate Sx • Fever,myalgia,pharyngitis • Nasal congestion,rhinorhea,sneezing,PND Cough sore throat • Cough,sore • Facial pressure and pain,ear fullness • Hyposmia/anosmia • Mucopurulent nasal secretions not specific sign of bacterial infection(neutriphil influx) Similarity Sx VURI’s and ABRS create significant difficulty distinguishing transition of viral to bacterial infection Mark Howell, MD 8/7/2011 Xray Dx ABRS? • Acute URI 87% evidence CT scan abnormality(Gwaltney 1994) • Resolution/improvement after 14 days in 79% of subjects without antibiotic Tx y or more sinus aspirates p • URI Sx >10 days demonstrate bacterial growth 60% samples Guide Dx ABRS 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 judgement • • • • 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 Mark Howell, MD Pediatric URI Concensus Team • Prolonged nonspecific upper respiratory signs and symptoms(rhinosinusitis and cough w/o improvement p 10-14 days) y ) • Severe URTI worsening signs /symptoms(fever >39 degrees C; facial swelling/facial pain) 8/7/2011 Viral to Bacterial • Persistent symptoms with no improvement • Severe symptoms(clinical judgement) • Worsening symptoms(biphasic illness) Diagnostic Modalities • Unlike OM the sinus cannot readily be examined as the TM • Maxillary sinus aspirates accurate/not practical • Nasal endoscopy allows visualization of middle meatus t and d cultures lt with ith endoscopic d i control t l may correlate with aspirate but are not complete • Some studies show 60-85%concordance(small #) Mark Howell, MD 8/7/2011 Diagnostic Modalities Imaging • Anterior rhinoscopy supportive but not conclusive • Percussion(tap tenderness) • Tranillumination(significant ( g variability y in interpretation) • Nasal endoscopy(helpful,expertise,equipment ,pt. cooperation often limited in children) • Plain Xray can evaluate maxillary and frontal sinuses • Concordance with sinus aspirate in 70% • Poor evaluation ethmoid sinus • Findings A/F level,opacification more specific • Mucosal thickening increases senstivity but decreases specificity Imaging • Gold standard for inflammation CT • 87% viral URI’s exhibit mucosal thickening • 30% asymtomatic y pt. p exhibit abnormal findings • Negative plain xray more value than negative exam • Findings CT/MRI persist after microbial resolution up to 8 weeks Mark Howell, MD 8/7/2011 Imaging Suggestions Goals Antibiotic Tx • Not needed in acute uncomplicated sinusitis • Diagnostic uncertainty and/or not responding as expected to appropiate medical therapy • Complicated rhinosinusitis with facial cellulitis,orbital and/or suspected intracranial complications should have contrasted CT scans sinuses ,orbits and head • Quicker resolution rate • Return sinuses to health • Prevent complications(meningitis,brain abscess) • Decrease chronic disease 49 49 Selection Antibiotic Therapy Microbiology ABRS(adult) • • • • • • • • • • • • • • • Limited data bacteriologic studies Pathogen distribution PK/PD principals Mechanisms of antimicrobial resistance Data in vitro studies Symptom severity Incidence spontaneous resolution Probability of resistant organism S.pneumoniae 20-40% H.influenzae 22-35% M,catarrhalis 2-10% S Srep spp.3-9% 3 9% Anaerobes 0-9% S.aureus 0-8% Other 4% Mark Howell, MD 8/7/2011 Microbiology ABRS (children) Nasopharyngeal Flora • • • • • • • Exchange between lateral wall nose and NP • Isolates 79% pt. Adenoids and 47% LW nose • Molecular typing respiratory pathogens revealed 89% pt. identical strains both sites S.pneumoniae 25-30% H.influenza 15-20% M.catarrhalis 15-20% S S.pyogenes 2-5% 2 5% Anaerobes 2-5% Sterile 20-35% Nasopharyngeal Flora Mechanisms Resistance S.pneumoniae • Antibiotic Tx increases resistant strains of respiratory pathogens(Dagan;PID,’98) • Adults also;duration shorter(CID,’97) • Respiratory p yp pathogens g isolated NP of 75% of adults • M.catarrhalis resistance with cephalosporins • Erythromycin use S.pneumo Finland • Alteration PBP at 6 know sites • Macrolide resistance with alterations ribosomal binding sites;efflux mechanisms;mutation genes ribosomal proteins(cross resistance clindamycin) • Fluroqinolone changes DNA gyrase and topoisomerase IV;efflux mechanism • Sulphonamides change binding sites Mark Howell, MD Mechanisms of Resistance H. influenza • B-lactamase production hydrolyzes amide bond of B-lactam ring ,inactivating the antibiotic • Alteration PBP(BLNAR;PBP3a,3b) • Efflux pumps(macorlides,azalides ) M.catarrhalis isolates 92% Bl t lactamase producers d 8/7/2011 Prevalence Resistance H.influenza • • • • 30-40% B-lactamase producers BLNAR strains rare U.S.(Japan) 22% resistant TMP/SMX PK/PD breakpoints < 3% susceptability to macrolides;azlides Mark Howell, MD 8/7/2011 ABRS-mild to 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) ABRS-moderate (daycare and/or antibiotic therapy within 90 days) • Amoxicillin-clavulanate(80-90mg/kg day two doses • Cefdinir(14mg/kg day 1-2 doses) • Cefuroxime(30mg/kg day) • Cefpodoxime(10mg/kg day 1x) • Switch therapy for pt. not responding to Amoxicillin ABRS-Beta-lactam sensitivity • • • • Non type 1 hypersensitivity Cefdinir,Cefuroxime,Cefpodoxime Type 1 hypersensitivity Clarithromycin(15mg/kg two divided doses) • Azithromycin(10mg/kg day1 and 5mg/kg single dose for four days) • TMP/SMX • Clindamycin(30-40mg/kg day 3-4 divided doses) Mark Howell, MD 8/7/2011 ABRS-nonresponsive to oral therapy Possible Referral Indications • Imaging • Aspiration of sinus • Ceftriaxone(100mg/kg per day divided q 12hr • Cefotaxime(100-200mg/kg day divided q6hr) • • • • Intracranial or orbital complications Possible need sinus aspiration Unusual pathogen Di Diagnosed d or suspected t d immunodeficiency • Recurrent ABRS especially exacerbation associated pulmonary conditions 65 65 Adjunctive Therapy Rhinosinusitis • Decongestants-systemic(improves nasal breathing;insomnia may diminish with use)limited use children • Topical decongestants(,oxymetazolin children>6y/) • Antihistamine-2nd generation avoid anticholinergic drying effects(possible worsening secretion viscosity with limited or any benefit) • Steroids systemic or topical Mark Howell, MD 8/7/2011 Saline Irrigation Complications of Acute Rhinosinusitis • Beneficial as natural approach; young children with discharge and mucostasis • Wash with bulb syringe/nasal aspirator • OTC sinus rinse • Clears secretions • Reduces mucosal edema • Orbital-usually acute ethmoid sinusitis • Preseptal cellulitis-involves eyelid;globe normal • Post-septal p cellulitis with or without abcess; involves orbital contents;eyelid edema;chemosis;proptosis;EOM impairment;visual changes • Urgent CT and hospitalization Intracranial Complications Management Pearls • 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 • 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 mucormycosis • Recurrent rhinosinsitis in children consider cystic fibrosis ciliary dysfunction;adenoids • CT and MRI may resolve these dilemmas Mark Howell, MD 8/7/2011 Absolute Indications for Surgery Relative Indications Sinus Surgery • Rhinosinusitis causing brain abscess,menigitis;subperiosteal orbital abscess;cavernous sinus thrombosis;facial cellulitis • Sinus mucocele or pyocele • Fungal sinusitis • Neoplasm or suspected neoplasm • 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 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 • Antimicrobial therapy should cover key 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 Jennifer Correll, PhD 8/7/2011 Prevalence “I’m Not Listening!”: Assessment & Treatment of Oppositional/Disruptive Behavior in Primary Care A Jennifer A A. Correll Correll, M M.A. Department of Psychology East Tennessee State University What % of visits to pediatric primary care involve a behavioral health concern? 3-5% 8 10% 8-10% 12-15% 18-25% A. B B. C. D. Prevalence Prevalence y National estimates show up to 25% of children seen by y The Top 5 pediatricians present with significant psychosocial concerns (Jellinek et al., 1999) y Recent pilot data from ETSU Pediatrics suggests higher rates of behavior disorders in residency training clinic (Gouge, Polaha, & Powers, in preparation) y Psychosocial concerns in very early childhood, without proper guidance or intervention, strongly predict behavior problems throughout childhood that persists into adolescence (Frick & Lonely, 1999; Hofstra, Ende, & Verhulst, 2002) ADHD Toileting 3. Sleep 4 Oppositional/Defiant Behavior 4. 5. Developmental Delays 1. 2. Jennifer Correll, PhD 8/7/2011 Prevalence Prevalence y Majority of parents feel the most comfortable discussing How much time extra time does it take when a behavioral concern is raised in an acute care visit? behavior problems with their pediatrician. y About 63% y When referred to specialty mental health few follow through with the appointment. appointment y Approximately 30% A. B B. C. D. 3 minutes 7 minutes i 10 minutes 15 minutes Assessment: Informal Assessment: Informal y Look for Red Flags. 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? Jennifer Correll, PhD Assessment: Formal y Formal screening y DSM criteria y Behavior checklist 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 or resentful ¾ Often spiteful or vindictive y Not psychosis y Not Conduct Disorder y Causes Impairment Assessment y Behavior Checklist y Pediatric Symptom Checklist (PSC) y Eyberg Child Behavior Checklist (ECBI) Jennifer Correll, PhD 8/7/2011 Treatment y Behavioral parent training found to be effective intervention for ODD (Hamilton & Armondo, 2008) Parent-Child Interaction Therapy (Eyberg, Boggs, & Algina, 1995) y Over 100 published studies y Short and long term improvement y Internalizing and externalizing disorders y Foster children, abused children y Depressed/”maltreating” mothers y Variety of cultural/ethnic samples y Brief versions Treatment Treatment y Parent-Child Interaction Therapy Child Directed Interaction (CDI) The Child’s Game: 1. Use interactive toys, no rules “rules” 2. Observe 3. Describe 4. Praise 5. Use touch 1. 2. 3. 4. 5. 6. 7. Pre-treatment assessment/feedback (1) Teaching behavioral play therapy skills (1) Coaching behavioral play therapy skills (2-4) Teaching discipline skills (1) Coaching discipline skills (4-6) Post-treatment assessment (1-2) Boosters (as needed) Parent-Directed Interaction (PDI) 1. 2 2. 3. 4. 5. Arrange toys I Instruction i Praise or Warning Praise or Time-out Instruction Jennifer Correll, PhD 8/7/2011 Treatment in Primary Care Treatment in Primary Care y Conceptualizing the problem for parents y Balance between reward and discipline y Skills deficit y Need to be able to 1. Following instructions 2. Coping with anger 3. Persisting on a task 4. Self-quieting 5. Independent transition to sleep y Time in vs. Time out y Creating high contrast Treatment in Primary Care Treatment in Primary Care y Time In y Time In y Attending to average behavior y “Sprinkles of attention” y Overboard verbal reinforcement for completing a desired task Jennifer Correll, PhD 8/7/2011 Treatment in Primary Care Treatment in Primary Care y Time Out y Time-Out y What is it really? Brief, unpleasant consequence during which there is no access to attention or anything fun Treatment in Primary Care y 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 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 Treatment in Primary Care y Time out y Success hinges on 1. Immediacy 2. Saliency 3. Consistency Jennifer Correll, PhD 8/7/2011 Treatment in Primary Care Treatment in Primary Care y Time Out y Building skills y What happens when you start to ignore behavior during time y Compliance Training out? y Patience y Extinction Burst! y Impulse control and choice for older kids Treatment in Primary Care References available upon request y Points to Remember [email protected] 1. 2. 3 3. 4. 5. 6. Conceptualize “problem” as skill deficit and stress twopart/balanced approach Discuss two components to time-in Di Discuss effective ff i time-out i use Warn about extinction burst Set a follow-up meeting to review progress 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 Darshan Shah, MD 8/7/2011 What’s up with Spit up in Newborn? Assistant Professor of Pediatrics Quillen College of Medicine Why this topic? 1) 2) 3) 4) 5) What’s up with Spit up in Newborn? y Crying and spit up y What’s normal? One of the most common Important reason for visit Misconception regarding formula allergy/intolerance GER(D) diagnosis Management controversy Spit up/Vomiting y Normal spit up vs. abnormal Everyone agrees ‘some spit up is normal’ Darshan Shah, MD 8/7/2011 Spit up/Vomiting Spit up/vomiting y What’s important? y Quantity? y How to determine? y Quantity? y 10% y 20% y Quality? y 30% y 40% y Consistency? y 50% Spit up/vomiting Spit up/vomiting y Depends on feeding interval. y Consistency? y More than 5 times in 8 feeding for q3 hr feeding y More than 4 times in 6 feeding for q4 hr feeding y 20% or more for q 3 hr % f h y What’s science behind numbers? y 30% or more for q 4 hr Darshan Shah, MD 8/7/2011 Spit up/vomiting Spit up/vomiting y Quality Common causes of spit up in newborn Physiological(GER) GERD Milk allergy Over feeding Pyloric stenosis y Color: Any color other than milk is a red flag y Projectile nature: Always include in your spit up history; potential red flag Spit up/vomiting Spit up/vomiting Gastro esophageal reflux in newborn y Most common cause of vomiting in new born is overfeeding, overfeeding, overfeeding and overfeeding f di f di f di d f di 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. Darshan Shah, MD 8/7/2011 Spit up/vomiting Spit up/vomiting y Role of Lower Esophageal Sphincter (LES) in vomiting/spit up Swallow Related LES; SLESR ¾ Smooth muscle thickening at JN C l V C i b REFLEX l i ¾ Control : Vagus; Contraction but REFLEX relaxation ¾ External Ring by Diaphragm ligament Pharyngeal Swallowing initiates LESR and primary peristaltic esophageal contraction ¾ This two mechanism creates LESP: It could be saliva, milk or even secretion from respitory tract Spit up/vomiting Spit up/vomiting Transient LES Relaxation; TLESR y TLESR y Independent of Pharyngeal Swallow Important for forventing gas from the stomach to prevent GI bloating GI bl i y Longer in duration; more than 10 seconds y Relax more completely as stretch from Cardia affects external Sphincter y Dependent on body position Lt vs. Rt That’s why there is “Spit up” Importance of burping lies in feeding Darshan Shah, MD 8/7/2011 Spit up/vomiting Spit up/vomiting y SLESR y GER could be acid or non acid event depending on time of feeding y Dependent on Pharyngeal Swallow y Usually lasts 3‐6 seconds y No effect on external sphincter y Independent body position Spit up/vomiting Spit up/vomiting y So, GER /Spit up/Vomiting is very common immediately after feeding (with in one hour) y Acid reflux is more common before feeding. y What’s indication to start treatment in GER? Darshan Shah, MD 8/7/2011 Spit up/vomiting Spit up/vomiting y GER is not reason to start infant on medication y Only Gastro Esophageal Reflux Disease; GERD is the l i di i di i only indication to start on medication Medications for GERD y H2 Receptor antagonist y PPI; not cleared by FDA for less than 1year y Prokinetics GERD: Esophagatis Apnea Growth failure y Always use for short duration of 4‐8 weeks rather than 4‐6 months as GER underlying physiology gets better with time! Spit up/vomiting Spit up/vomiting y Side effects Common causes of spit up in newborn Physiological(GER) GER(D) Milk allergy Over feeding Pyloric stenosis ¾ Increased chances of CAP ¾ Gastroenteritis ¾ Decreased absorption of calcium Darshan Shah, MD 8/7/2011 Spit up/vomiting Spit up/vomiting Milk Allergy CMA or CMPA or CMI y Prevalence Immunologically mediated adverse reaction to cow milk protein Proteins implicated; alpha lactalbumin, beta lactoglobulin and casein Spit up/vomiting y CMA/CMPA/CMI y Two types of clinical syndromes d 9 IgE mediated with in 1‐2 hrs of ingestion 9 Non IgE mediated after 2 hrs 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 Spit up/vomiting IgE mediated CMA y Anaphylaxis y Angioedema y Urticaria y Oral itching and l h d abdominal pain y Nausea/Vomiting/Diarrhe a y RhinoConuctivitis y Wheezing/Exacerbation of RAD y Laryngeal edema Darshan Shah, MD Spit up/vomiting Non IgE mediated Protein losing enteropathy GER© Proctocolitis/proctitis/ente rocolitis Colic © Constipation© Pulmonary hemosiderosis (Heiner syndrome) 8/7/2011 Spit up/vomiting y Mixed type Atopic dermatitis Eosinophilic Esophagatis Eosinophilic gastroenteritis Spit up/vomiting Spit up/vomiting y History of Atopy is strong predictor for CMA 20% chance when one parent has history 32% chance when 1 atopic sibling 43% chance both parents have 72% when both parents have identical atopy y So what to do with newborn presenting with recurrent vomiting/spit up? y Diagnosis : clinical + history Di i li i l hi Or y Clinical+history+ lab eval for allergy Darshan Shah, MD 8/7/2011 Spit up/vomiting Spit up/vomiting y Lab eval for CMA y Allergy test are highly sensitive but low specificity y Also CMA could be manifestation of non IgE type. Skin test Atopy patch test Total IgE Specific IgE(RAST) Spit up/vomiting Spit up/vomiting y Treatment/diagnosis for CMA y Elimination diet is diagnostic and therapeutics for CMA/CMPA/CMI y Which formula to use? Soy based(Prosobee) Extensively Hydrolyzed (Alimentum) Amino acid based (Neocate) Darshan Shah, MD 8/7/2011 Spit up/vomiting Spit up/vomiting y Soy based formula not ideal for CMA as 10% cross reactivity of IgE and 60% for non IgE reaction. y Hydrolyzed formula: S i i l h ll i i I y Soy protein is also not hypoallergenic protein. It can worsen enterocolitis y First choice for non anaphylactic CMA, atopic eczema, gastrointestinal symptoms and food protein induced procto/enterocolitis procto/enterocolitis. Spit up/vomiting Spit up/vomiting y Amino acid formula: y Breast milk allergy: y First choice in anaphylaxis, eosinophilic Esophagatis, CMA i h h f d ll i CMA with other food allergies, growth impairment h i i with CMA. y Rare y Incidence <1% y Maternal avoidance of CMP Darshan Shah, MD Spit up/vomiting y Duration of elimination diet: y Minimum of two weeks for improvement in symptoms. If 8/7/2011 Spit up/vomiting y Reemergence of symptom on introduction after elimination reconfirms CMA. 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 Look out for allergy to peanuts and egg in patient with definite CMA. Spit up/vomiting Spit up/vomiting Common causes of spit up in newborn Physiological(GER) GER(D) Milk AllergyMilk Allergy Over feeding Pyloric stenosis y Pyloric stenosis y y y y y Incidence: 0.02‐0.06% More common in Most important: Vomiting is PROJECTILE Palpation is positive in epigastric area 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
