approach to an adolescent with obesity by: camille-marie a. go

APPROACH TO AN ADOLESCENT WITH OBESITY

By: Camille-Marie A. Go

ObjectivesObjectives

To present a case of a child with obesity

To discuss the burden of disease, pathophysiology, management and possible complications of obesity

Our Patient

P.N. 14 year old Male Filipino Roman Catholic San Mateo, Rizal

Chief complaint

Rapid weight gain

and hyperglyce

mia

General: (-) weight loss, (+) voracious appetite Cutaneous: (-) rashes, (-) discoloration, (-) jaundice HEENT: (-) blurring of vision, (-) nasoaural discharge,

(-) epistaxis, (-) gum bleeding Cardiovascular: (-) cyanosis, (-) chest pain, (-) orthopnea, (-) easy fatigability (-) palpitation Respiratory: (-) cough, (-) colds, (-) difficulty of breathing,

(-) sneezing Gastrointestinal: (-) vomiting (-) abdominal pain, (-)

diarrhea, (-) constipation, bowel movement once a day

Review of Systems

GUT: yellow urine, (-) edema of the hands and feet, (-) frothy urine

Metabolic: (-) polydipsia, (-) polyuria Extremities: (-) swelling, (-) joint swelling, (-)

limitation in movement Nervous/Behavioural: (-) headache, (-) dizziness, (-)

nausea, (-) tremors, (-) convulsions , (-) change in sensorium (-) behavioral change

Hematopoietic: (-) pallor, (-) easy bruisability (-) prolonged bleeding

Review of Systems

Family History

(+) DM – both parents; maternal GM

(+) HPN - maternal GM

(+) obesity - father (-) PTB (-) Heart disease (-) Thyroid disorders (-) Blood dyscrasia (-) Mental retardation, (-) Seizure

BCG 3 doses of Hepatitis B DPT x 3 OPV x 3 Measles MMR Boosters: of BCG and MMR No untoward reactions

Immunization History

Born to a 30 year old G2P1 (1001) nonsmoker nonalcoholic mother

Prenatal check up since 1 month AOG; (+) MVS, Feso4 (+) GDM at 6 months AOG, advised diet

modification; repeat exam after 1 month normal Delivered Full term via NSD assisted by OB; (+) good

cry and activity (+) small for gestational age Newborn Screening and Hearing Screening not done;

Birth and Maternal History

Breastfed until two months old Milk formula thereafter Complementary feeding at 6 months High carbohydrate and high fat diet prepared by

the mother Fastfood 2x – 3x weekly Fond of junk foods and chocolates

Nutritional History

Food Food CHO (g) CHON (g) Fats (g) KcalBreakfast 3 pcs

hotdog4 cups of riceWater

 184g

24g16g

18g 258 kcal800 kcal

Snacks 6 pcs BiscuitsOrange juice

23g10g

2g   100kcal40 kcal

Lunch 2 cups Pork Sinigangvegetables3 cups of rice

 6g138g

32g2g12g

24g 344kcal32 kcal600 kcal

Snacks 6 pcs BiscuitsOrange juice

23g10g

2g   100kcal40 kcal

Dinner 3 cups Chicken Adobo4 cups of ricewater

 184g 

32 g16g

24 g 344 kcal800 kcal

Total ACIRENI

% intake

3,458 kcal2,800 kcal 123.5%

Home: Concrete house with 6 household members Nuclear patriarchal clan

Education: Second year high school at school in San Mateo, Rizal Favorite subject: Math Average grade - 89%. Aspires to be a successful accountant when he grows

up

Psychosocial History

Activity: Fond of computer games Spends 4 to 6 hours per day Most of activities are sedentary

Drugs: No intake of alcoholic beverage or cigarette use Does not know anyone using prohibited drugs

Sexual: Has female crushes among his schoolmates No girlfriend. He has not courted any girl.

Psychosocial History

Suicide: No personal history of attempted suicide Sees himself as overweight, not happy or proud of it

Safety: Walks on the sidewalk to school Does not ride in cars with drivers who are intoxicated

Spirituality: Hears mass every Sunday together with his whole

family Actively participates in church activities

Psychosocial History

No previous history of hospitalization, or transfusions, or allergies

No history of communicable diseases (measles, varicella)

Underwent Circumcision at 10 years of age

Past Medical History

Conscious, coherent, oriented to 3 spheres, not in cardiorespiratory distress, ambulatory, over-nourished, well-hydrated, well-looking

Wt: 75kg (z> 3) ; Ht: 163cm (z<0); BMI: 28.2 (z>3) CR 110 beats/min; RR 30 breaths/min; T 36.5 C; BP

110/60 mmHg (p 25) Warm and moist skin, dark pigmentation of skin

creases and flexural areas, most prominent along the nape

Pink palpebral conjunctivae, anicteric sclerae

Physical Examination:

No alar flaring, no nasoaural discharge, intact tympanic membrane, AU

Moist buccal mucosa, no dental carries, non-hyperemic posterior pharyngeal walls, tonsils not enlarged

Supple neck, no cervical lymphadenopathies, no thyroid enlargement

No retractions, symmetrical chest expansion, clear breath sounds

Adynamic precordium, PMI at 5th left intercostal space midclavicular line, regular rate and rhythm no heaves, thrills, lifts or murmurs

Physical Examination:

Globularly enlarged abdomen, no striae, normoactive bowel sounds, no organomegaly, no tenderness, no masses

Grossly male, bilaterally descended testes, Tanner St. II

Full and equal peripheral pulses, capillary refill time less than 2 seconds, no cyanosis, no edema

No limitation in range of motion of all joints

Physical Examination:

Cerebrum: conscious, coherent, oriented to 3 spheres Cranial nerves: pupils isocoric, 2-3mm equally reactive

to liht, (+) direct and consensual light reflex, extraocular movements full and intact, can clench teeth, (-) gross facial asymmetry, gross hearing intact, (+) gag reflex, can turn head from side to side against resistance, tongue midline

Cerebellum: (-) no involuntary movements, able to do tandem gait

Neurological Exam:

Reflexes: ++ on all extremities Motor: (-) rigidity, (-) spasticity, (-) flaccidity,

(-) deficits Sensory: (-) deficits Meningeal Signs: (-) nuchal rigidity, (-)

Brudzinski’s, (-) Kernig’s, (-) tonic neck reflex

Neurologic Examination

Obesity Hyperglycemia probably

secondary to Diabetes Mellitus Type II

Middle Adolescent with Psychosocial Issues (Body

Image)

Diagnosis:

Obesity

“Excessive storage of energy as FAT relative to lean body mass”

Energy intake exceeds expenditure

Pediatrics Obese - BMI> 95% for gender and age At risk/overweight - BMI=85-95%

Adults Obese – BMI> 30 Overweight – BMI=25-30

Definition based on BMI

Measurement

Weight Weight:Height BMI

kg÷m2

Skin Thickness Waist:Hip Ratio Growth Charts

Patient

Variable definitions Increasing incidence in developed and

developing nations Similar prevalence to US: Latin America,

Caribbean, Middle East, Northern Africa, Central-Eastern Europe

Asia and Africa: no increase in incidence

Incidence: Worldwide

Worldwide

Gayya et. al (2008) FNRI – DOST digest January 2014

Thailand – 23% Taipei – 28% Vietnam – 14 – 16%

Asian Prevalence

Gayya et. al (2008) FNRI – DOST digest January 2014

0%

5%

10%

15%

20%

1963- 1965 1966- 1970 1971- 1974 1976- 1980 1988- 1994 1999- 2002

2 -5 yrs

6 - 11 yrs

12 - 19 yrs

Trends in children and adolescents

Gayya et. al (2008) FNRI – DOST digest January 2014

Etiology

Heterogeneous and Multifactorial Environmental Psychosocial Genetic

Males – Increased visceral fat Females – Increased hip fat At all ages females have more adipose tissue

than males

Sex Difference

Weights of adopted children correlate better with biological parents

BMIs of identical twins reared apart= together

Monozygotic twins more similar in fat deposition and weight than dizygotic twins

Genetics vs. Environment

Reference

ObesityDifferential Diagnosis

Idiopathic Endocrine:

Hypothyroidism Hypercortisolism Growth hormone

deficiency

Genetic Prader-Willi Turner

CNS conditions: hypothalamic damage Medications

Glucocorticoids Phenothiazines Lithium Amytryptiline Estrogen/progesterone

Differential Diagnosis

Polypeptide Y From L cells of small intestine Reduce food intake

Ghrelin Stimulates food intake Elevated in Prader Willi

Physiology of Regulation Of Energy Expenditure

Pathogenesis

LEPTIN - Adipostatic signal (1994)

produced by adipose tissue

Acts on Hypothalamus Decreases food intake Increases energy

expenditure

Low neuropeptide Y stimulates appetite High MSH inhibits appetite Fasting decreases Leptin Eating increases Leptin

Leptin

Common obesity due to multiple allelic variations in hundreds of genes

Monogenic obesity Leptin deficiency Leptin insensitivity

Leptin and Obesity

Central role of energy intake Lesions cause hyperphagia and obesity

Hypothalamus

Environmental Factors:Increased Energy Input

High caloric-density food

Supersized portions Eating out Working parents Advertising

Environmental Factors:Decreased Energy

Expenditure

TV Computers Transportation Inadequate safe

areas for physical activity

Sedentary Lifestyle

Diabetes (Type 2) Hypertension and Heart Disease Neurologic Complications Respiratory Disease Orthopedic Condition Psychosocial Disorders Hyperlipidemia GI Manifestations Menstrual Disorders

Complications

Clustering of CV risk factors related to insulin resistance

Not well defined in Pediatrics Insulin resistance Dyslipidemia Hypertension Obesity

DOES OUR PATIENT HAVE MS?

Metabolic Syndrome

Course in the Clinics

First consult Laboratories:

Type 2 Diabetes Mellitus with Obesity

Metformin (20 mkday) Referred to Nutrition Clinic

for dietary modification Increase physical activity

Universal Assessment of Obesity Risk: Steps to Prevention and Treatment

American Academy of Pediatrics. Pediatric Obesity Clinical Decision Support Chart. Elk Grove Village, IL: American Academy of Pediatrics; 2008.

Steps to Prevention and Treatment of Pediatric

Obesity

Steps to Prevention and Treatment of Pediatric

Obesity

Prevention Plus BMI >85%Diet Modification

Build on prevention Eating behaviors

Family meals at least 5 to 6 times per week Allow child to self-regulate his or her meals Avoid overly restrictive behaviors—“Parents

provide, child decides.” Structured activity

American Academy of Pediatrics. Pediatric Obesity Clinical Decision Support Chart, 2008

Prevention Plus BMI >85%Diet Modification

Goal: weight maintenance with growth a decreasing BMI as age increases

Monthly follow-up for 3 to 6 months If no improvement go to Stage 2

American Academy of Pediatrics. Pediatric Obesity Clinical Decision Support Chart, 2008

Prevention Plus BMI >85%Physical Activity/Inactivity

60 minutes of moderate physical activity per day or 20 minutes of vigorous activity 3 times a week Community activity programs Family activities Pedometer use

Limit screen time to <2 hours per day No TV/computer in bedroom

American Academy of Pediatrics. Pediatric Obesity Clinical Decision Support Chart, 2008

American Academy of Pediatrics. Pediatric Obesity Clinical Decision Support Chart, 2008

Global IDF/ ISPAD Guideline

Approved for Type 2 diabetes and hyperinsulinemiaDecreases hepatic glucose productionEnhances insulin sensitivityResults in modest weight lossSide effects: nausea, flatulance, bloating, diarrhea, lactic acidosis

Pharmacotherapy: Metformin

Not approved for pediatrics Drug options

Appetite suppressants Serotonin agonists Inhibitors of fat absorption Antihyperglycemic agents

Pharmacotherapy

Second consult Gradual weight loss of 1.8%

75 kilograms to 73.6 kilograms BMI from 28.2 to 27.7 (z > 2) TABLE OF LABS

Course in the Clinics

Steps to Prevention and Treatment of Pediatric

Obesity

Structured Weight Management

Dietary and physical activity behaviors Balanced macronutrient diet with low

amounts of energy-dense foods Increased structured daily meals and

snacks Supervised active play: 60 minutes a day Screen time: 1 hour or less a day

Increased monitoring

Structured Weight Management

Weight maintenance Decreases BMI as age and height increases

Weight loss 1 lb/month: 2–11 years oldor 2 lb/week: older overweight/obese children and

adolescents If no improvement in BMI/weight after 3 to 6

months Stage III

Counseling

Steps to Prevention and Treatment of Pediatric

Obesity

ObesityTreatment: Surgery

Gastric bypass Gastic plication Gastric banding Jejuno-ileal bypass

no longer performed

Not routine for children

Course in the Clinics

Sustained weight loss 73.6 kilograms to 72.7

kilograms BMI

27.7 to 27.3 (z >2)

Course in the Clinics

Regular follow up at the Endocrinology clinic every three months

Continuation of weight loss 70kg, with a BMI of

25.9 (z > 1) Disappearance of the

skin hyperpigmentation around the nape area

OverweightDiabetes Mellitus Type II,

controlledADOLESCENT?

Final Diagnosis:

Childhood ObesityConclusion

Heterogeneous disorder

Multifactorial causes

Global epidemic Genetics Sedentary lifestyle Too much in Too little out