The Power of Change: A Case of a Adolescent with Multiple Medical Condition A Clinical Case Presentation Alejandro E. Legarda III MD First Year Resident DFCM
Objectives • To present an adolescent with hypertension and obesity and its correlation to Metabolic syndrome and PCOS • To discuss the differential diagnosis for high BP in the young • To discuss the approach to management of adolescent with hypertension, obesity and the diagnose syndromes • To present short-term and long-term wellness plan appropriate for the patients condition
Patient ProfileEJ13 years oldSingleRoman CatholicIncoming 3rd year high school studentChief ComplaintELEVATED BLOOD PRESSURE
Clinical History • The patient was then eight years old and sought a consult due to her re- occurring erythematous vesicular lesions. • Upon consultation, she was diagnosed Five years with Post-streptococcal prior to glomerulonephritis. The patients was admitted in the hospital for a week due consult to this condition. • Patient was documented to suffer from (2007) hypertension. Nifedipine was prescribed to control and manage her hypertension.After hospitalization, patient felt well again. No follow-up consult wasrecommended to the patient.
Clinical History • The patient started gaining weight as food intake severely increased. • Patient’s BP was taken annually Three years in school and showed elevated blood pressure. prior to • The increased blood pressure consult readings was simply ignored by the patient and her parents, (2009) thus resulting in progressive, uncontrolled weight gain.
Clinical History • Patient sought consultation at the UP-PGH Dermatological Department for her vesicular lesions. • Patient featured an incidental finding of 160-90 blood pressure reading. • Assessment reveals: Acne vulgaris with etiology related to PCOSTwo weeks prior to Hypertension secondary to (1) PCOS (2) Cushing’s Syndrome (3) Insect bite hyper consult sensitivity reaction Patient was given: • Amlodipine (5mg./tab) OD • Benzoyl Peroxide gel OD • Tretinoin cream for the face • Cloxacilin (500mg./tab) for 7 days • Mupirocin Bethamethasone ointment ITD • Sunscreen • mild soap Patient was referred to Pedia adolescent, hence the consult.
Clinical History At Consult (March 26, 2012) Patient was seen at the Pedia Adolescent Clinic
Past Medical History(-) Asthma(-) Allergy(-) Pulmonary Tuberculosis(-) Bronchial asthmaNo Accident and injuryHospitalizations:Admitted for (+) PSGN (2007) and Dengue Fever (2009)Surgeries:There was no previous surgeryMedications:Co-amoxiclav for her recurrent skin infections
OB/GYNE HistoryMenarche: January 2011Irregular flow occurring only 3x since her menarcheLasting 4-5 days, Pads 2-4 a dayNo dysmenorrheaNo sexual contact
Birth and Maternal HistoryPatient was born full-term via spontaneousvaginal delivery at a local hospital delivered byan obstetrician with no known feto-maternalcomplications.
NUTRITIONAL HISTORYPatient was breastfed for 3 months and then shiftedto bottle feeding of Bona milk every 3 to 4 hoursstarting at 4 months old up to 12 months old.Complementary feeding was started at 6 monthsold.Patient would skip breakfast but would have 2snacks before a heavy lunch. She would have 2 heavymeriendas, e.g.,2 hamburgers/hotdogs or cups of icecream .Most of the food she eats are either fried orsalty and plenty of desserts. She loves to drink cola.
Immunization HistoryChildhood VaccinationsBacillus Calmette-Guerin (BCG), one doseHepatitis B vaccine, three dosesDiptheria Pertussis Tetatnus (DPT), three dosesOral Polio Vaccine, thress dosesMeasles, one dose
FAMILY GENOGRAM Jorgo Family March 26, 2012I 76 80 68 75II 32 56 54 50 46 Hypertension Accident 52 48 Overweight DiabetesIII EJ 19 18 15 13 Elaisa MJ JJ
Personal and Social HistoryHome:- lives with parents and four siblings in Imus, Cavite-good relationship with parents and siblingsEducation:-Incoming third-year high school student-With above-average grades- has close set of friends in schoolActivities:-Favorite past time– eating-Loves eating street foods and junk foods-Spends most of her free time in front of the TV orcomputer-Not involved in any outdoor activities such as sports
Personal and Social HistoryDrugs:-No history of cigarette or alcohol use-Denies use or history of use of illicit drugsSexual:-Does not showcase any consciousness with body weight andshape-Patient has not attempted to change her appearance-Currently no relationship with the opposite sexSuicidal Tendencies:-Patient exhibits no signs or episodes of depression or suicidalideationSafety:-Patient together with her family lives in a peaceful and orderlycommunity with minimum crime rate- uses public transportation to commute-Not a member of a gang or sorority
Physical ExaminationGeneral Survey:Awake, alert, coherent, in pain, not in cardio-respiratory distress(-) muscle wasting(-) moon face(-) proximal muscle weakness(-) buffalo humpVital Signs:Blood Pressure: 150/90(>99th percentile)Heart Rate: 75 beats/minuteRespiratory Rate: 18 breaths/minuteTemperature: 36.8 C
Physical ExaminationAnthropometrics:Height: 157 cmWeight: 96.5 kgBody Mass Index: 40.7 kg/m2 (Z score: 2.58)Abdominal Circumference 102cm
Physical ExaminationHead and Neck:Anicteric sclerae, pink conjunctivae,pupils 2-3mm OU reactive to light,(+) Short leg length(+) Acanthosis nigricans,(-) masses, (-) cervical lymphadenopathy,(-) anterior neck mass(-) tonsillopharyngealcongestion,(-) neck vein engorgement, (-)ear discharge
Physical ExaminationChest and Lungs:Equal chest expansion, no deformities,no lesions, clear breath sounds,(-) crackles/rales/wheezesHeart:Adynamic precordium, distinct heart sounds,apex beat at 5th intercostal space left midclavicular line,regular rate and rhythm, no murmurs
Physical ExaminationAbdomen:flabby(+) Striae lower abodomenno deformitiesno lesionsSoft normoactive bowel sounds(-)masses or tendernessliver span 8 cm right midclavicular lineintact Traube’s spaceno costo-vertebral angle tenderness
Physical ExaminationExtremitiespink nailbedsfull and equal pulsesno cyanosis/clubbing/ edemano crepitationsno limitation of passive and active motionon both upper extremities(-) shooting pain on straight leg raise ofboth lower extremities(-) limitation of motion due to painno crepitations on hips, knees or anklesno joint swelling or deformities(-) Pain on active leg raise of bothlower extremities
Physical ExaminationNeuro ExamCranial Nerve (CN) ExaminationCN I –intact gross olfactionCN II –pupils 2-3 mm OU briskly reactive to lightCN III,IV,VI –full range of extraocular muscle movementCN V –brisk corneals, good masseter tone,CN VII –no facial asymmetry, no altered tasteCN VIII –intact gross hearing, no lateralization on Weber TestCN IX –no altered taste, can swallowCN X –can swallowCN XI –good symmetrical shrugCN XII –can protrude tongue, no deviation
Physical ExaminationSensoryPain: Intact on all dermatomesLight Touch: Intact on all dermatomesVibratory: Intact on all dermatomesMotorNormal GaitGood muscle tone, no atrophy, no limb size discrepancyFull motor strength on both upper extremitiesTanner Stage 3External genitalia with dark, coarsecurly hair spreads over mons pubisElevation of Breast contour; areolae enlarged
Salient Features of the CaseSALIENT FEATURES OF THE CASEA 13-year old femaleChief complaint of elevated blood pressureHistory of hypertension ,DM and ObesityPrevious history of renal disease (+) poluyuria, (+)polyphaga.AmenorrheaObesityAnthropometrics: Height: 157 cm, Weight: 96.5 kg, BodyMass Index: 40.7 kg/m2 (Z score: 2.58),(+) Short neck length(+) Acanthosis nigricans nape area,Flabby abdomen with (+) Striae
Initial ImpressionHypertension, Stage II-- etiology to bedeterminedAcne Vulgaris probably secondary to PCOSDM suspectObese, Type 2Amenorrhea secondary to PCOS
ManagementDiagnostics:Complete Blood Count (CBC)Plasma sodium, potassium and calciumBUN, CreatinineFasting plasma glucoseLipid profileUrinalysisWhole AB ultrasoundChest X--rayECGTSH, FT4
TherapeuticsContinue the following medications:Cloxacillin 500 for 7 daysTretnoin Cream for the faceMupirocine Betamethasone ointment, TIDSun screen useMild soap useStart Amlodipine 5mg once a day
Approach to Hypertension
European Society of HypertensionThe study mentioned childhood BP has been shown totrack into adulthoodUnlike adults, the diagnostic criteria for elevated BP inchildren are based on the concept that BP in childrenincreases with age and body size, making it impossible toutilize a single BP level to define hypertension.
Specific recommendations for office BPmeasurement in children and adolescentsThe recommended method is auscultatory.Use K1 for systolic BP and K5 for diastolic B.If the oscillometric method is used, the monitor needs to be validatedand if hypertension is detected by the oscillometric method, it needs tobe confirmed using the auscultatory method.The Use the appropriate cuff size according to arm width (40% of thearm circumference) and length (4_8 cm, 6_12 cm, 9_18 cm, 10_24 cm,to cover 80–100% of the individual’s arm circumference).
Blood Pressure for Girls by Age and Height Percentiles
Systolic and diastolic ambulatory blood pressure (systolic/diastolic) values for clinical use
Task Force for Blood Pressure in Children, the Fourth Report on the Diagnosis, Evaluation, and Treatment of High Blood Pressure in Children and AdolescentsThe normal BP in children is defined as SBP and DBP less than90th percentile for age, sex and height.Hypertension is defined as SBP and/or DBP persistently 95thpercentile or more, measured on at least three separate occasionswith the auscultatory method.Rule out White-coat (or isolated office) and masked (orisolated ambulatory) hypertensions
Definition and Classification of Hypertension in Children and Adolescents
Diagnostic Algorithm of Hypertension
Clinical Data To NoteFAMILY HISTORYHypertensionCardiovascular and cerebrovascular diseaseDiabetes mellitusDyslipidemiaObesityHereditary renal disease (Policystic kidney disease)Hereditary endocrine disease (pheochromocytomaglucocorticoid-remediable aldosteronism, multiple endocrine neoplasia type 2, von Hippel–Lindau)Syndromes associated with hypertension (neurofibromatosis)
Clinical Data To NotePERINATAL HISTORYBirth weight, gestational age, oligohydramnios,anoxia, umbilical artery catheterizationPREVIOUS HISTORYHypertensionUrinary tract infection, renal or urological diseaseCardiac, endocrine (including diabetes) or neurologicaldiseaseGrowth retardationSymptoms suggestive of secondary hypertensionDysuria, thirst/polyuria, nocturia, hematuriaEdema, weight loss, failure to thrivePalpitations, sweating, fever, pallor, flushingCold extremities, intermittent claudicationVirilization, primary amenorrhea and male pseudohermaphroditismSymptoms suggestive of target organ damageHeadache, epistaxis, vertigo, visual impairmentFacial palsy, fits, strokesDyspnea
Clinical Data To NoteSleep history:Snoringapnea,daytime somnolenceRisk factor history:Physical exercise, dietary habitsSmoking, alcoholDrug intake:Anti-hypertensivesSteroids, cyclosporinetacrolimus or otherTri-cyclic anti-depressantsatypical antipsychoticsdecongestantsOral contraceptivesillegal drugsPregnancy
Physical Examination To Note Data to record:HeightWeightBody mass indexExternal features of syndromes/conditions associated withhypertensionNeuroﬁbromatosisKlippel–Trenaunay–WeberFeuerstein–MimsVon Hippel–LindauMultiple endocrine neoplasiaPseudoxanthoma elasticumTurner,WilliamMarfanCushingHyperthyroidism,LupusVasculitisCongenital adrenal hyperplasia
Physical ExaminationData to RecordCardiovascular examinationPulse and BP measurement in both arms and legsBruits/murmurs – heart, abdomen, ﬂanks, back,neck, headSigns of left ventricular hypertrophy or cardiac failureAbdomenMasses – Wilms, neuroblastoma, pheochromocytoma, autosomaldominant and recessive polycystic kidney disease, multicystic kidneydisplasia, obstructive uropathyHepatosplenomegaly – autosomal recessive polycystic kidney diseaseNeurological examinationFundoscopy for hypertensive changes and retinalamartoma (von Hippel–Lindau)Evidence of VIII nerve palsyOther neurological defects including stroke
Patient PE PresentationSignificant Anthropometrics:Height: 157 cmWeight: 96.5 kg,Body Mass Index: 40.7 kg/m2 (Z score: 2.58)(+) Short neck length(+) Acanthosis nigricans nape areaFlabby abdomen with (+) Striae(+) AcneOther details were none pertinent
Target Organ Damage To NoteHeartBlood VesselsKidneyNeuroFundoscopy
HeartLeft Ventricular Hyperthrophy (LVH) remains to date the mostthoroughly documented form of end-organ damage caused byhypertension in children and adolescents.
Blood VesselsMorphological changes of the arterial wall, thickening of the intima-mediacomplex.Children with familial hypercholesterolemia have higher IMTOverweight and obesity are associated with increased IMT in children with orwithout essential hypertension.
KidneyHypertension-related renal damage is basedon a reduced renal function or an elevatedUAE. Proteinuria is a marker of glomerulardamage in primary and secondaryglomerulopathies. An indication for BP-lowering interventions.Microalbuminuria (20–300mg/g creatinine,2–30 mg/mmol creatinine, 30–300 mg/day,20–200mg/min) has been shown to predict thedevelopment of diabetic nephropathy .Overt proteinuria (>300 mg/day) indicatesthe existence of established renal parenchymaldamage.
Neuro and FundoscopyCerebral seizures, stroke, visualimpairment and retinal vascular changes arecomplications associated with severehypertension.Fundoscopy was also done in because ina study of 97 children and adolescents withessential hypertension, found that 51%displayed retinal abnormalities, as detectedfrom direct ophthalmoscopy.
Obesity and HypertensionUsing the 2000 CDC growth charts, at risk of overweightfor ages 2 to 20 years overweight is defined as a BodyMass Index (BMI)-for-age between the 85th and the 95thpercentiles.Overweight in children is defined as a BMI-for-age at orabove the 95th percentile on the charts.BMI is weight in kilograms divided by height in meterssquared (kg/m2).BMI is used differently to define overweight in childrenand adolescents than it is in adults. In children andadolescents, BMI changes with age and gender.
Obesity and HypertensionOverweight children and adolescents are atincreased risk for various chronic diseasesin later life.The psychosocial consequences ofoverweight are significant. Overweight inchildren has been linked to socialdiscrimination, a negative self-image inadolescence that often persists intoadulthood, parental neglect, and behavioraland learning problems.
Obesity and HypertensionBeing overweight is probably the mostimportant of the conditions associated withelevated BP in childhood and accounts formore than half the risk for developinghypertension.Adiposity is the most powerful risk factorfor higher BP.Waist circumference (abdominal obesity)has been shown to play a role.Dietary habits like high salt intake, havebeen implicated as factors favoring higher BPvalues.
Obesity and HypertensionThe CDC mentions the Common MedicalConsequences of Overweight (Dietz,1998)hyperlipidemiaglucose intolerancehepatic steatosischolelithiasissleep apneaObesityhypoventilation syndromehypertensiona variety of orthopedic complications
Laboratory Investigations Routine tests that have to be performed in all hypertensive childrenFull blood count and proteinuriaPlasma sodium, potassium and Renal ultrasoundcalcium, urea, creatinine Chest Xray, ECG and 2-DFasting plasma glucose echocardiographySerum lipids (cholesterol, LDLcholesterol, HDLcholesterol)Fasting serum triglyceridesUrinalysis plus quantitativemeasurement ofmicroalbuminuria
Recommended additional screening tests Plasma renin activity, plasma aldosterone concentration Urine and plasma catecholamines or metanephrines Tc99 dimercaptosuccı´nic acid scan Urinary free cortisol More sophisticated tests that should await results of above screening Color Doppler ultrasonography Captopril primed isotope studies Renal vein renin measurements Renal angiography I123 metaiodobenzylguanidine scanning Computed tomography/ Magnetic resonance imaging Urine steroid analyses and more complex endocrine investigations Molecular genetic studies (Apparent mineralocorticoid excess, Liddle’s syndrome, etc)
SECONDARY HYPERTENSIONSustained hypertension can beclassified as secondary when aspecific cause can be found, thenit can be corrected with specificintervention.There should be work-up shouldbe done if hypertension .
Diagnosis of Secondary Causes of Hypertension
MY MANAGEMENTDiagnostic ExaminationsLaboratory Plan:Complete blood countPlasma sodium, potassium and calcium,BUN, CreaFasting plasma glucoseLipid ProfileUrinalysisWhole AB ultrasoundChest Xray, ECGTSH, FT4
APPROACH TO MANAGEMENTNon pharmacologic Strategy Recommendations:GOALS:BMI<85th percentile: Maintain BMI to prevent becomingoverweightBMI 85–95th percentile: Weight maintenance (younger children)or gradual weight loss in adolescents To reduce BMI to <85th percentileBMI>95th percentile: Gradual weight loss (1–2 kg/ month) to achieve value <85th percentile
GENERAL RECOMMENDATIONSModerate to vigorous physical aerobic activity--40 min, 3–5 days/week and avoid more than 2 hours daily of sedentary activitiesAvoid intake of excess sugar, excess soft drinks, saturated fat and salt and recommend fruits, vegetables and grain productsImplement the behavioural changes (physical activity and diet) tailored to individual and family characteristicsInvolve the parents/family as partners in the behavioural change processProvide educational support and materialsEstablish realistic goalsDevelop a health-promoting reward systemCompetitive sports participation should be limitedonly in the presence of uncontrolled stage 2 hypertension
For my patient…A. Counseling and Implement Behavioural Change1.CEA(Catharsis Education Action): Patient2.Motivational Interviewing- Pre Contemplation stage3. CEA(Catharsis Education Action): : Parents
Counseling and ImplementBehavior Change: CEA PatientPatient was not so much concerned of herweight.She doesn’t know the risk and the healthissues regarding hypertension.She was not aware why she came to PGH forconsult and really wanted to go home.She was also not aware her that beingoverweight has some health risks as well.
Use of Motivational Intervierwing Transtheoretical Model, "process involving progress through a series of stages:" Precontemplation (Not Ready)-"People are not intending to take action in the foreseeable future, and can be unaware that their behaviour is problematic.‖ Contemplation (Getting Ready)-"People are beginning to recognize that their behaviour is problematic, and start to look at the pros and cons of their continued actions.― Preparation (Ready)-"People are intending to take action in the immediate future, and may begin taking small steps toward behaviour change.― Action – "People have made specific overt modifications in modifying their problem behaviour or in acquiring new healthy behaviours.― Maintenance – "People have been able to sustain action for awhile and are working to prevent relapse."
Use of Motivational IntervierwingMotivational Interviewing- Pre Contemplation stagePatient was on pre -contemplation stage at that time and Iwas hoping to make her aware and give her insight to bringher to the stage where she can contemplate.When I asked about her hypertension, she said she knewhad it for years but no one told her about the dangers.
B. Counseling and Implement Behavior Change3. CEA: ParentsThe parents are also unaware of the risk of hypertension andthe eating habits and lifestyle that increase her obesity.They couldn’t believe that this would happen at her age.The whole family is at risk since everyone except the wife isobese.
My Management Plan for the Patient…Non-pharmacologic strategiesA. Counseling and Behavior Change- DoneB. I advised the patient to have Regular BP monitoring at homeC. Physical Activity: I mentioned to the patient to start to lessensedentary activities and start to walk more around the subdivision andplay with pets. A Exercise program was not done yet as I want for thepatient to reach the preparation/actionD. Eating Habits: Change of eating was advised. The Patient love toskip breakfast and lessen snack intake.E. A Diet Program: I was planning to put the patient into a lowEnergy Diet of 2000kcal C350 P75 F 35 from a 3022kcal diet on thenext follow up
Approach to Medical Management on HypertensionPharmacologic/Therapeutic StrategiesAside from the non-pharamacologic strategies, I had a dilemmaon how will I use therapeutic strategies for my patientEVIDENCE FOR THERAPEUTICMANAGEMENTReduce mortality and sequelea in life-threateningconditionsReduce left ventricular hypertrophyReduce urinary albumin excretionReduce rate of progression to end-stage renal disease
Approach to Medical Management on HypertensionTherapeutic management of hypertensionIndications for Antihypertensive Drug Therapy in Children Symptomatic HypertensionSecondary hypertensionHypertensive target-organ damageDiabetes (types 1 and 2)Persistent hypertension despite non-pharmacologic measures>99 percentile BMI
Approach to Medical Management on HypertensionTherapeutic ManagementTreating Hypertension with drugs are most indicated in end organdamage of the Heart and Kidney/RenalEffect to Organ Damage:In the Heart, Regression of LVH was reported in three children withessential hypertension receiving enalapril, in 19 children with primaryand secondary hypertension treated with ramipril for 6 months, and in65 children with chronic kidney disease (CKD) stage 2–4 receivingramipril for up to 2 years.In Renal:the Effect of Strict Blood Pressure Control and ACE Inhibition onProgression of Chronic Renal Failure in Pediatric Patients (ESCAPE) trial,which has shown efficient BP and proteinuria reduction for the ACEinhibitor ramipril in 352 children with CKD
Approach to Medical Management on HypertensionMonotherapyChoice of anti-hypertensive agents ACEIsAngiotensin receptor antagonists (ARBs)Calcium antagonistsBeta-blockersDiureticsCombination therapyIn children with renal disease, monotherapy is often not sufficient toachieve adequate BP control. Therefore, early combination therapy isrequired. The best choices of antihypertensive drug combinations arethose recommended in the ESH/ESC 2007 Guidelines .
Clinical conditions for which specific antihypertensive drug classes are recommended or contraindicated
My Therapeutic ManagementFor our patient, she was given a monotherapy of Amlopidine, 5mg./tab once daily.
Initial Management summary Non-pharmacologic strategies Counseling and Behavior Change- Done B. I advised the patient to have Regular BP monitoring at home C. Physical Activity: I mentioned to the patient to start to lessen sedentary activities and start to walk more around the subdivision and play with pets. A Exercise program was not done yet as I want for the patient to reach the preparation/action D. Eating Habits: Change of eating was advised. The Patient love to skip breakfast and lessen snack intake. E. A Diet Program: I was planning to put the patient into a low Energy Diet of 2000kcal C350 P75 F 35 from a 3022kcal diet on the next follow up
Initial Management summaryMedical Theraphy For our patient, she was given a monotherapy of Amlopidine, 5mg./tab once daily.
1st Follow-up April 2012Maintained BP 150/90…no decrease in BP despite of Amlodipine 5mg tablet.Started to jog for several minutes around the house and roam around the area with her dog.Lessened her calorie intake thanks to the parents modifying the food menu at home. Parents started to prepare healthier food with less salt content.Parents have been very supportive.Siblings stopped eating with the patient for snacks and joined the patient in jogging as well.One of her sibling, who still was a bad influence to her was transferred to their grandmother’s house.
1st Follow-up April 2012 1st Follow-up April 2012 Glucose 6.4, BUN 3.30, Crea 45.5, Chole 5.0, Trigly 5.01 HDL 0.98, LDL 1.74, AST 38,Results ALT 46, Albumin 42 Calcium 2.44, Na- 138, K 4.8 Hgb:139, Hct 0.432, Plt 356 WBC 8.7 ECG- Sinus Rhythm, Within Normal Limits Urinalysis : Dark yellow, 1.030, RBC 0-2, WBC 3-4 EC Whole Ab Ultrasound: normal 3+ Sugar (-) Albumin (-) With the current labs results, I CXR: Normal Chest Findings was able to rule out many etiology of hypertension Thyriod FT4- 20.6, Free T3- including the secondary ones 5.5, TSH IRM 6.1 however there was elevation in Triglyceride and there was Impaired Fasting Glucose
1st Follow-up April 2012 Previous Salient Features… New Finding from theSALIENT FEATURES OF THE DiagnosticsCASE13-year old female Impaired FastingChief complaint of elevated Glucoseblood pressureHistory of hypertension ,DM andObesity Elevated TriglyceridePrevious history of renal disease(+) poluyuria, (+) polyphaga. Ruled outAmenorrhea Cardiovascular, RenalObesity and some secondary etiology(+) Short neck length(+) Acanthosis nigricans napearea,(+) Striae
1st Follow-up April 2012 Hypertension stage II secondary to 1) Obesity 2) Metabolic Syndrome T/c PCOS sedondary to Metabolic Syndrome Hyperlipidemia Impaired Fasting Glucose
METABOLIC SYNDROME Group of characteristics: Most expert groups define metabolic syndrome as the presence of three or more of the following characteristics in a person: Obesity, especially in the abdominal area (defined by some groups as a waist size greater than 94 to 102 cm (38 to 41 in) in men or greater than 80 cm (32 in) in women) Impaired fasting glucose (fasting blood sugar of 100 to 125 mg/dL or 5.6 to 7 mmol/L) Increased blood pressure (130/85 or higher) or if you take medicine for high blood pressure Increased fasting levels of triglycerides (greater than 150 to 180 mg/dL or 1.7 mmol/L) or decreased fasting HDL cholesterol (less than 40 mg/dL or 1 mmol/L for men or 50 mg/dL or 1.3 mmol/L for women)
METABOLIC SYNDROME IN CHILDREN AND ADOLESCENTS Definition Metabolic syndrome also occurs in children and adolescents but there is no consensus on the definition The International Diabetes Federation (IDF) definition of metabolic syndrome in children 10 to 16 years old is similar to that used by the IDF for adults, except that the definition for adolescents uses ethnic-specific waist circumference percentiles and one cutoff level for HDL rather than a sex-specific cutoff. For children 16 years and older, the adult criteria can be used. For children younger than 10 years of age, metabolic syndrome cannot be diagnosed, but vigilance is recommended if the waist circumference is ≥90 percentile.
METABOLIC SYNDROME IN CHILDREN AND ADOLESCENTS Risk factors Among obese children, the prevalence of the metabolic syndrome is high and increases with worsening obesity. The prevalence of metabolic syndrome is high among obese children and adolescents and increases with the severity of the obesity, and with central adiposity in particular.
Clinical Implications of Metabolic SyndromeThe definition of metabolicsyndrome may be clinicallyuseful for risk stratification andtherapeutic intervention inpediatrics. However, lifestylemodification that emphasizesreduction of established riskfactors, such as promotion ofexercise, weight loss, andsmoking cessation, is the maintherapeutic goal in obesechildren and adolescents,regardless of a metabolicsyndrome diagnosis.
METABOLIC SYNDROME TREATMENT Reduce or eliminate underlying problems (eg, obesity, lack of activity) by losing weight and becoming more active. Treat cardiovascular risk factors, such as high blood pressure and cholesterol, if these problems persist despite losing weight and exercising. Weight loss The Mediterranean diet is high in fruits, vegetables, nuts, whole grains, and olive oil The DASH (Dietary Approaches to Stop Hypertension) The DASH diet requires you to eat no more than 2400 mg of sodium per day, four to five servings of fruit, four to five servings of vegetables, two to three servings of low-fat dairy products, and all foods must contain less than 25 percent total fat per serving. Lifestyle modification — Prevention or reduction of obesity, particularly abdominal obesity, is the main therapeutic goal in patients with the metabolic syndrome Exercise — . The standard exercise recommendation is a daily minimum of 30 minutes of moderate-intensity (such as brisk walking) physical activity. Increasing the level of physical activity appears to further enhance the beneficial effect
METABOLIC SYNDROME and Polycystic Ovary Syndrome (PCOS) PCOS and Metabolic Sydnrome originally was described by Stein and Leventhal as the association of amenorrhea with polycystic ovaries, and variably, hirsutism and obesity It is now recognized that PCOS represents a spectrum of disease characterized primarily by the following features: Cutaneous hyperandrogenism (eg, hirsutism, treatment- resistant acne, and/or pattern balding [androgenetic alopecia] Menstrual irregularity (eg, oligo- or amenorrhea, or irregular bleeding) Polycystic ovary Obesity and insulin resistance
Clinical Manifestations of TheInsulin Resistance Syndrome in Children
Polycystic ovary syndrome (PCOS) Three sets of diagnostic criteria have been proposed for the diagnosis of PCOS in adults. In adolescents, using the NIH diagnostic criteria in most cases. PCOS risk criterion proposed by the Androgen Excess and PCOS Society (AES), alternatively defined as hyperandrogenism and a polycystic ovary, be considered as indicative of risk for PCOS rather than as diagnostic.
PCOS PrevalenceThe prevalence of PCOS in the adolescent population is unknown.
PCOS DIFFERENTIAL DIAGNOSIS Congenital adrenal hypertension, easy hyperplasia Nonclassic bruising, striae, and Classic CAH due to 21- proximal muscle hydroxylase deficiency weakness. Classic CAH, and to a Hyperprolactinemia lesser extent nonclassic Acromegaly CAH, Virilizing tumors Ovarian steroidogenic Thyroid dysfunction blocks Drugs Other adrenal disorders Disorders of sex Cushings syndrome development include central obesity, Idiopathic dorsal fat pad,
DIAGNOSTIC CRITERIA Cutaneous signs of hyperandrogenism (eg, hirsutism, persistent acne, and/or pattern alopecia) Menstrual irregularity (eg, oligo- or amenorrhea, or irregular bleeding) Polycystic ovary syndrome Obesity and insulin resistance
DIAGNOSTIC APPROACH. Evidence of hyperandrogenism — The criterion of clinical hyperandrogenism is satisfied by hirsutism or other cutaneous signs of hyperandrogenism. Evidence of ovarian dysfunction Exclusion of non-PCOS causes of hyperandrogenemia Additional evaluation after the diagnosis of PCOS
Manifestations of Polycystic Ovary Syndrome in Approximate Proportion to their Relative Incidence and Coincidence ANOVULATORY SYMPTOMS HIRSUTISM,ACNE, ALOPECIA OBESITY
Pathogenesis Intraovarian androgen excess appears to be responsible for both anovulation and the formation of multiple ovarian "cysts" because of stimulated excessive growth of small follicles and hindrance of the maturation of the dominant follicle. There is vigorous debate about whether this pathologic process is primarily a disorder of pituitary gonadotropin secretion or a disorder of ovarian and/or adrenal steroidogenesis. PCOS may result from a metabolic disorder that includes insulin resistance. Abnormal pituitary function Abnormal steroidogenesis Extrinsic factors contributing to dysregulated steroidogenesis
Abnormal Pituitary Function Increased LH relative to FSH was the first laboratory abnormality identified in classic PCOS. Elevated LH levels occur in about half of PCOS patients. Elevated LH is thought to play a role in the pathogenesis of PCOS by increasing androgen production and secretion by ovarian theca cells. Patients with PCOS have an increased LH pulse frequency and amplitude. Obesity seems to attenuate the increase in LH pulse amplitude, in part because the pituitary gonadotropes of obese women with PCOS produce LH isoforms that are rapidly metabolized.
Abnormal Steroidogenesis Alternative hypothesis that PCOS is due to intrinsic ovarian dysfunction. This hypothesis considers that primary functional ovarian hyperandrogenism (FOH) is the essence of PCOS. The intraovarian level of androgens in FOH is higher than in most adrenal causes of androgen excess and results in excessive growth of small ovarian follicles while inhibiting follicular maturation and development of the dominant follicle. These result in the polycystic appearance of the ovary and the anovulatory symptoms.
Extrinsic factors Contributing to Dysregulated Steroidogenesis The insulin/insulin-like growth factors (IGF) system is capable of acting in synergy with trophic hormones, contributing to ovarian or adrenal excess androgen production. In the ovary, insulin acts in conjunction with LH to enhance androgen production and reverse the LH- induced down-regulation of LH binding sites. Insulin and IGFs increase the activities of multiple steroidogenic enzymes in both the ovaries and adrenal glands. This suggests that the hyperandrogenemia and obesity of PCOS are mechanistically linked.
Treatment for PCOS in adolescents is directed at the following clinical manifestations: Menstrual irregularity Cutaneous hyperandrogenism, primarily hirsutism and acne Obesity and insulin resistance
TREATMENT FOR PCOSMenstrual irregularity shouldbe treated in adolescents withPCOS because chronicanovulation increases the riskof developing endometrialhyperplasia, which isassociated with endometrialcarcinoma. In addition,anemia can result fromdysfunctional uterine bleedingor menorrhagia.
TREATMENT FOR PCOS The combination oral contraceptive pill (OCP), which contains estrogen and progestin, usually is the first-line treatment for adolescents with PCOS and menstrual irregularity, especially in patients with cutaneous signs of androgen excess. OCPs induce regular menstrual periods with a higher degree of reliability than other forms of treatment. Progestin inhibits endometrial proliferation, preventing hyperplasia. Estrogen inhibits the activity of the hypothalamic-pituitary-gonadal axis, reducing ovarian androgen production as well as increasing serum sex hormone binding globulin (SHBG) levels. OCP therapy also will normalize androgen levels within 18 to 21 days. After three months, the efficacy of treatment is assessed by evaluating clinical symptoms and androgen levels. If the treatment is effective, as a general rule, OCPs should be continued until the patient is gynecologically mature (five years postmenarcheal).
TREATMENT FOR PCOSLimitations — The role of OCPs in the management of PCOS in adolescents may be limited for several reasons: OCP therapy may make weight loss more difficult to attain because it promotes salt and water retention. The patient may believe the treatment is curative and defer a definitive diagnostic work-up. OCPs do not permit conception if and when it is desired. In perimenarcheal girls with short stature who have open epiphyses, OCPs are contraindicated because OCPs contain growth-inhibitory amounts of estrogen.
TREATMENT FOR PCOS Progestin Glucocorticoid GnRH agonists
OBESITY AND INSULIN RESISTANCE The treatment of obesity improves ovulation, acanthosis nigricans, androgen excess, and cardiovascular risk in patients with PCOS. Weight reduction is indicated in obese patients with PCOS as part of a program to reduce cardiovascular risk factors. Diet and exercise are the first-line treatment for obese adolescents with PCOS as for obese individuals without PCOS.
Insulin Resistance Obesity is of major importance in the insulin resistance of PCOS, although insulin resistance is disproportionate to the degree of adiposity. Insulin resistance is commonly manifested as acanthosis nigricans The biguanides, of which metformin is the only one available in the US are thus a potential adjunct in the treatment of PCOS; thiazolidinediones also are effective in reducing insulin levels, but have raised safety concerns, as discussed below. Although their mechanisms of action differ, both metformin and thiazolidinediones reduce insulin concentrations, promote ovulation, and lower androgen levels Metformin is the only one of these agents that we currently use in adolescents with PCOS because of concerns of weight gain and rare hepatic and possible cardiac toxicity with thiazolidinediones. Randomized, placebo-controlled trials in adolescents and adults have shown that metformin significantly increases the frequency of menses and ovulation (by about 50 percent), and lowers testosterone levels (by about 20 percent).
1st Follow-up April2012 Pharmacologic Management Changed Amlodipine 5mg to Losartan 50mg/tab as there was no change for one month. Prevent target organ damage and decreased fluid retention
MY USE COUNSELING/MOTIVATIONAL INTERVIEW I once again asked the patient how she was doing. How did she feel about the diet change? I asked if she was fully aware and really understood her condition. ―ok lang‖ ―Ginagawa ko rin dahil sa mama ko.‖ I asked her if she still remembers what I told her about the health risks involved with hypertension and obesity. She said ―Opo doc, naala ko naman.‖ I asked her if her overweight condition made her conscious with her appearance, she said NO during the 1st consult, but she did admitted that it started to beome a concern especially when some of her classmates teases her. She also wanted to be noticed by her crush.
BEHAVIOR CHANGE TOOL AND DECISIONAL BALANCE TECHNIQUE I asked her what are her goals in life. She said she wants to work as an engineer and have a family for own. She wants to travel and meet lots of new friends. I asked her what does eating to much and having a sedentary lifestyle has to do with her dream... ―Magkakasakit ako palagi at baka palagi nasa hospital‖.
BEHAVIOR CHANGE TOOL ANDDECISIONAL BALANCETECHNIQUE I used the Decisional Balance technique for my patient….
Decisional Balance "reflects the individuals relative weighing of the pros and cons of changing.― Decision making was conceptualized by Janis and Mann as a "decisional balance sheet" of comparative potential gains and losses.― Decisional balance measures, the pros and the cons, have become critical constructs in the Transtheoretical Model Sound decision making requires the consideration of the potential benefits (pros) and costs (cons) associated with a behaviors consequences.
Decisional Balance Decisional balance is one of the best predictors of future change. TTM research has found the following relationships between the pros, cons, and the stage of change across 48 behaviors and over 100 populations studied. The cons of changing outweigh the pros in the Pre- contemplation stage. The pros surpass the cons in the middle stages. The pros outweigh the cons in the Action stage
Decisional Balance Maintaining Changing Current Use Use Pattern Benefits Costs ―Hindi “Masarap” Magkakasakit‖ ―Gaganda Ako ― ―Mas Okay ang suot‖ Benefits Costs ―Magkakasakit ako‖ ―Hindi na masarap‖ ―Mas lalo tumaba‖
BEHAVIOR CHANGE TOOL AND DECISIONAL BALANCE TECHNIQUEShe then realized that she would have to change.The patient is now willing to change hence I made a treatment plan to target obesity hence decreased incidence of hypertension.
Treat Obesity Improve symptoms and minimize health risks
APPROACH ON TREATMENT TO OBESITY According the AAP’s Recommendations for Treatment of Child and Adolescent Overweight and Obesity— Comprehensive interventions that include behavioral therapy along with changes in nutrition and physical activity are the most closely studied and seem to be the most successful approaches to improving long-term weight and health status.
APPROACH ON TREATMENT TO OBESITY In the study…showed a guideline on how to treat and manage adolescent obesity based on1. Nutritional Treatment2. Macronutrient Therapy3. Food Behaviors4. Dietary Interventions5. Physical Activity and Reducing Sedentary Activities6. Behavioral Approaches7. Other Interventions8. Recommendations of Stages of Treatment
APPROACH ON TREATMENT TO OBESITY Nutritional Treatment In the guideline, it reviewed nutritional treatment for our patient to decrease obesity which included: Fruits and Vegetables Fruit Juice Sweetened Beverage Dairy Food Calcium Dietary fiber Eight studies evaluating the relationship between fruit and/or vegetable intake and body weight were reviewed. All had mixed results but two studies found an inverse association with adiposity.
APPROACH ON TREATMENT TO OBESITYMacronutrient Therapy Carbohydrate Fat Protein
Glycemic index Glycemic index (GI) has been proposed to affect body weight regulation and risk for obesity- associated complications.80 The GI is defined as the area under the glucose dose-response curve after consumption of 50 g of available carbohydrate from a test food, divided by the area under the curve after consumption of 50 g of available carbohydrate from a control food (either white bread or glucose). Short-term feeding studies indicated that hunger and cumulative food intake were greater 3 to 5 hours after a high-GI versus low-GI meal, controlled for macronutrient and energy contents.
FOOD BEHAVIORS In terms of the FOOD BEHAVIORS of our patient Breakfast Skipping Snacking Eating Out
DIETARY INTERVENTIONS Balanced-Macronutrient/Low-Energy Diet Salt reduced-energy diet The traffic light diet The Food Guide Pyramid
PHYSICAL ACTIVITY It used these measurements to calculate physical activity levels, as follows: physical activity level-total energy and expenditure/basal metabolic rate.
Amount of Physical Activity The American Academy of Pediatrics recommends that 30 minutes of this activity occur during the school day. Very obese children may need to start with shorter periods of activity and gradually increase the time spent being active. Reducing Sedentary Activities Television Viewing and Obesity
Weight RecommendationsAccording to Age and BMI Percentile
The AAP guideline provided a systematic approach which to manageobesity patients. The staged-care process is divided into 4 stages,that is:(1) Prevention Plus (healthy lifestyle changes)(2) Structured weight management(3) Comprehensive multidisciplinary intervention(4) tertiary care intervention.
Weight Recommendations According to Age and BMI Percentile
NONPHARMACOLOGIC PLAN A. Use Prevention Plus Stage 1 Intervention Using the algorithm, our patient is at the >99 percentile hence a Prevention Plus Stage 1 interventions should be based on the family’s readiness to change and include the following:1. Consumption of 5 servings of fruits and vegetables per day2. Minimization or elimination of sugar-sweetened beverages3. Limits of 2 hours of screen time per day, no television in the room where the child sleeps, and no television viewing4. 1 hour of physical activity per day Physical activity can be increased gradually for sedentary children. Children may be unable to achieve 1 hour of activity per day initially but can gradually increase activity to reach 1 hour/day.
NONPHARMACOLOGIC PLANB. Stricter implementation on the Diet Low Energy Diet of 2000kcal C350 P75 F 35 from a 3022kcal diet and a strict decrease of salt content.C. Establishing an exercise plan Jogging at their area for 40 min starting from moderate to vigorous aerobic-based physical activity 3–5 days/week.
My plan for Metabolic Syndrome
My Plan for PCOS
2nd follow-up May 2012 S> Weight loss of 8 pounds for 2 monthS. Lessen of BP from 150/90 to 130/80… No OB consult yet.Patient was advised to take OB consult in the near future.Patient still has no menstruation. Management Maintain medicines and continued diet and exercise plan. Stop Losartan I also advised that their family; the parents and her brothers and sisters to seek consult for the obesity problem as well.
3rd Follow-up August 2012 Patient had weight loss of 2 pounds but having trouble to maintain diet and exercise during the school year due to the availability of food and temptations. BP lowered to 120/80. Patient started to play badminton with family and still continue to jog if she has free time. Plan: Advise to have a more structured diet and exercise to adapt to school by having a list of food to eart in day. Patient was advised to have cooked food from home
Long Term Plan
PSYCHOSOCIAL ISSUES - ADOLESCENT ISSUES Self-Image Addiction to TV and Facebook Role of parents in adolescence
WELLNESS PLAN FOR THE PATIENT Lifestyle Continue the Prevention Plus Plan for our patient with a advice increase Physical and outdoor activities. Screening Patient was advised an annual screening to detect organ damage and risk of other disease like Type II Diabetes Immunizations- Influenza vaccine yearly, Varicella vaccine.
GOING BACK TO THE PATIENT The good news is that the patient’s BP is at 120-130/80-90. Patient hasn’t made substantial weight loss, but the good thing is that during the past three months her lifestyle changed dramatically when compared alongside the years that she was excessively eating. She started to gain self-confidence since the change of eating habits. The family changed their eating habits and have modified their lifestyle accordingly too.
Insight Holistic care Interrelationship of Diseases The Importance of Lifestyle for being Healthy Counseling and Motivation Behavior change as part of being a Doctor The power of change Caring for patient is not a shot deal, have to do lots of follow-up and evaluation Importance of education and value formation in children and adults ( School and Government)
Insight Suggestions: Comprehensive Government Plan to Educate and Change the Lifestyle of our Youth Insight (slide) My message to everyone… As doctors, we are privileged to have the power to change lives. Let us go forth and use this opportunity to be an instrument towards positive change.