Child Growth and Development PDF

THE HEALTHY CHILD: NUTRITION WEANING TEETHING PUBERTY DR. ALESSANDRO CATTONI GENERAL AND SPECIALISTIC PÆDIATRICS SCHOOL OF MEDICINE AND SURGERY WHY DO YOU NEED TO STUDY PEDIATRICS? WHY DO YOU NEED TO STUDY PEDIATRICS? Because the child is not the miniature of an...

THE HEALTHY CHILD: NUTRITION WEANING TEETHING PUBERTY DR. ALESSANDRO CATTONI GENERAL AND SPECIALISTIC PÆDIATRICS SCHOOL OF MEDICINE AND SURGERY WHY DO YOU NEED TO STUDY PEDIATRICS? WHY DO YOU NEED TO STUDY PEDIATRICS? Because the child is not the miniature of an adult!  WHY DO YOU NEED TO STUDY PEDIATRICS? Because the child is not the miniature of an adult! Specificities we will come across in our classess: 1. Growth: how does growth occur and how do we check it 2. Biochemical parameters: reference ranges for each age 3. Deciduous teeth as a part of a growing body 4. Skeletal maturation  WHY DO YOU NEED TO STUDY PEDIATRICS? Accordingly:  Different body proportions  Different body composition  Different body surface/weight ratio  Different nutritional needs  Different energetic needs  Specifities related to a growing being  WHY DO YOU NEED TO STUDY PEDIATRICS? Accordingly:  Different body proportions  Different body composition  Different body surface/weight ratio Body surface-based dosage  Different nutritional needs xx mg/m2  Different energetic needs  Specifities related to a growing being DEFINITIONS IN CHILDHOOD Newborn 0-28 days Infants 29 days-12 months Toddler > 12 months LACTATION FEEDING IN CHILDHOOD Birth → 4th-6th months Breastfeeding or Formula feeding 4th-6th month → 12th month Breastfeeding or Formula feeding Weaning 12th month onwards Free balanced diet Milk (cow or vegetal) BREASTFEEDING VERSUS FORMULA During the first year ( finger foods need to be properly prepared  HONEY - Not to be presented before 12° month - Can contain spores of Clostridium botulinum => Consuming may lead to infant botulism (intestinal toxemia) due to a more frequent production of neurotoxins. - Food-borne botulism is caused by ingestion of pre-formed toxin (food contamination)–12-48 hours incubation period HONEY AND BOTULISM Food Botulism: intake of food containing a pre-formed toxin – incubation: 12-48 h; Childhood botulism: spores are introduced in the bowel; the toxin in produced within the bowel itself –incubation: 3-30 days Wound botulism – incubation: 4- 14 days AFTER THE FIRST 12 MONTHS OF LIFE… AFTER THE FIRST 12 MONTHS OF LIFE… Breakfast 15% of daily caloric intake ideally based on: milk or yoghurt (semi-skimmed), integral bread with jam fresh fruit plain cereals Morning break 5% ok daily caloric intake Afternoon break 10% ok daily caloric intake AFTER THE FIRST 12 MONTHS OF LIFE… Main meals Lunch should account for 40% of daily caloric intake Dinner should account for 30% of daily caloric intake All the meals should include a variable intake of carbohydrates, proteins, lipids and fibers Water 1600 mL: 4-6 years 1800 mL: 7-10 years AFTER THE FIRST 12 MONTHS OF LIFE… To be improved To be discouraged Fruit, vegetables Saturaded fats Nuts Red meat Integral cereals Salt Fish Olive oil and other unsaturated fats  VEGETARIAN / VEGAN DIET - Risk for multiple deficiencies: Iron, Zync, Calcium, Vitamin A – B2 – B12 - D, Docosanoic Acid Proteins - Need to supplement pregnant and nursing mothers and infant (B12 0.4mcg-0.5mcg/die) - Soja (and its derivates) and beans can be used as a supplement  VEGETARIAN / VEGAN DIET - Can be a healthy diet but needs strict nutritional supervision and full adherence to professional recommendation - => IF NOT High risk of severe neurological exitus for the child (B12 deficiency) - Oveall, we tend to discourage vegeterian/vegan diet in childhood unless we are sure that a strict supervision occurs Growth… GROWTH: DEFINITION  Whole body of mechanisms which concur to the development of the human being since conception to adulthood  Co-occurrency of different factors: Genetic factors Hormonal: GH, thyroid hormones, insulin, IGF-1, sexual hormones Environmental factors  Biologically dependending on: Cellular growth Cellular differentiation CHILD: A «MINIATURE» ADULT? NO!  Different body parts proportions  Different body composition  Different ratio in body surface/weight  Different caloric need (40 Kcal/Kg adult, 100 Kcal/Kg infant)  Clinical peculiarities due to growth processes % of adult GROWTH MONITORING Growth can be monitored by examining the following parameters:  Length (< 2 y.o.) and Height (> 2 y.o.)  Weight  Head circumference HEIGHT PERCENTILES Example: Age: 11.0 y.o. Weight: 50 Kg  Percentile: 75-90° 81° percentile 19 on 100 peers are heavier 80 on 100 peers are less heavy STATURAL GROWTH  0-4 y.o.: Length at birth 51-52 cm Rapid growth in the first 4 years Height doubled (102 cm) at 4 y.o.  4 y.o. - puberty Regular growth /in slight progressive decrease  Puberty Puberal spurt around 12 y.o. in girls / 14 y.o. in boys Following progressive decrease up to adult age STATURAL GROWTH  Birth: 51-52 cm  1 y.o. : 75 cm  2 y.o. : 85 cm  4 y.o. : 102 cm  4 y.o. to puberty: 4-6 cm/year  Puberal spurt: 30 cm in boys 20 cm in girls STATURAL GROWTH  Genetic factors Parents’ height Ethnicity  Environmental factors Diet  Hormonal factors Growth hormones Gonadal hormones Thyroid hormones Insulin SHORT STATURE  Armonic  Disarmonic POTENTIALLY PATHOLOGIC CONDITIONS: 1) Low height: < 3° percentile 2) Growth curve decrease SHORT STATURE - CAUSES  Physiological: Familiar short stature Costitutional growth and developmental delay  Non-endocrinological: Intra-uterine growth delay Systemic diseases Malabsorption causes (celiac disease, chronic IBDs, etc…) Genetic syndromes (achondroplasy etc…) Congenital metabolic defects Psychosocial deprivation SHORT STATURE - CAUSES  Endocrinological: GH deficiency Hypothyroidism Untreated premature puberty Untreated congenital adrenogenital syndromes Insulin dependent diabetes (not properly treated)  Idiopathic PONDERAL GROWTH:  Weight represents, overall in infancy, the main general wealth index  Ponderal growth: Birth: 3.5 Kg (m), 3.3 Kg (f) 5-6 months: doubled 12 months: tripled 2 y.o.: quadrupled Since 2 y.o. to puberty: + 2.5 Kg/y  Extimation of weight of a child from 4 y.o. to puberty: 2 x age + 8 POOR WEIGHT GAIN - CAUSES  Infant Insufficient caloric intake Milk→weaning SGA (small for gestational age) Gastro-esofageal reflux Vaccine milk protein intolerance Celiac disease (after weaning) Genetic syndromes Congenital metabolic defects Cystic fybrosis Food adversion POOR WEIGHT GAIN - CAUSES  Child and adolescent Celiac disease IBDs Cystic fibrosys Other malabsorption causes (pancreatic diseases, hepatopathy) Hyperthyroidism Sistemic inflammatory disorders (es. connective tissue diseases) Chronic infective disorders Chronic hemopathies (es. thalassemia) Eating disorders (es. anorexia nervosa) HEAD CIRCUMFERENCE  Direct index of the CNS status of the baby  Indicative of content: brain, liquor, skull  Anterior fontanel evaluation is always useful  Growth rythm: Birth: 35 cm 12 months: + 12 cm/year 24 months: +2-3 cm/year 36 months: + 1cm/year MACROCEPHALY CAUSES  Hydrocephalus (obstructive and not)  Genetic syndromes (achondroplasia, osteogenesis imperfecta)  Perinatal infections exitus (toxoplasmosis, rubella, meningitis)  Fetal alcohol syndrome  Familiarity MICROCEPHALY CAUSES  Antenatal infections (CMV, Rubella, Zika virus)  Craniostenosis/craniosynostosis  Congenital Hypothyroidism  Genetic/cromosomic abnormalities (eg. Down Syndrome)  Fetal alcohol syndrome  Cerebral malformations  MICROCEPHALY MACROCEPHALY CLINICAL CASE: MARCO, 13 MONTH – REFERRED FOR POOR GROWTH  Regular growth: 50th percentile until the 6th month;  From 6th month onwards, progressive decrease in weight curve  Now on 10° percentile  FAMILY HISTORY  Parents related  Genetic disorders  Chronic diseases  Siblings with a similar history of poor growth  Age of pubertal development in both mother and father/relatives Menarche at 13  PERINATAL HISTORY  Spontaneous pregnancy versus MAP MAP  Birth weight and lenght 3100 g, 52 cm  Hypoglycemia at birth? Jaundice?  Breastfed/Bottle fed/Weaning ongoing? BF + weaning  Stools: steathorrea? Diarrhoea? Vomiting? Stipsis  PREVIOUS MEDICAL HISTORY  Delay in meconium ejection? Probably slight delay  Frequent infections? Severe infections? Frequent wheezing  Severe eczema?  Chronic diseases? Chronic medications (i.e. steroids?)  PHYSICAL EXAMINATION  Hydration status  Skin – eczema?  Organomegaly?  Syndromic features  Cardiac murmurs? Wheezing?  Head circumference and anterior fontanel  BLOOD TESTS  Transglutaminase + IgA  TSH-reflex  FBC, U&Es, creatinin, liver function tests  Calcium , phosphate, vitamin D  Urine test  (IGF-I) CLINICAL CASE: MARCO, 13 MONTH – REFERRED FOR POOR GROWTH  Close monitoring: additional decrese in lenght and weight centile!!! CLINICAL CASE: MARCO, 13 MONTH – REFERRED FOR POOR GROWTH  ADDITIONAL TESTS  Abdomen US  Brain MRI  Heart US  Sweating test CYSTIC FIBROSIS CONFIRMED BY GENETICS  CASE 2 - 6 YEAR OLD GIRL Always healthy Abdominal pain, peri-umbelical, for 2 months Night awakening for pain Height: from 50th pc to 25th “Sticky fecis” What could it be? Hb 9.8g/dL, MCV 78fL, ferritin 2ng/ml, %TRF 10% AST, ALT 20/25 U/L, TSH ok Anti-TTG-A 250U/L (nv 10x normal -EMA positive Puberty PUBERTY  Developmental pathway which leads to appearance and progression of sexual features (primary and secondary sexual features)  High individual variability in terms of age at onset and overall duration  The sequence of tends to be shared by most people  Adolescence: transformations associated with puberal changes plus the psychological and relational changes thypical of this phase  Physiological times of onset: Boy: 9-14 y.o. Girl: 8-13 y.o.  Clinical signs of puberal activation: Testicular volume ≥4 mL in boys Development of breast budding in girls Pubertà: fisiologia GnRH secreting neuron Kisspeptin secreting neuron Pubertà: fisiologia Neurone GnRH secernente secreting GnRH neuron Kisspeptin secreting neuron Pubertà: fisiologia Inhibitory neuron (Dynorfin) Neurone GnRH secernente secreting GnRH neuron Kisspeptin secreting neuron Pubertà: fisiologia Neurone GnRH secernente secreting GnRH neuron Kisspeptin secreting neuron Pubertà: fisiologia Neurone GnRH secernente secreting GnRH neuron Kisspeptin secreting neuron Pubertà: fisiologia Neurone GnRH secernente secreting GnRH neuron TANNER STAGE TANNER STAGE  Intermediate puberty: 8-10 mL Initial puberty: 5-6 mL Advanced puberty: 12-15 mL Adult: Prepubertal: 1-3 mL 20-25 mL PUBERTY: PATHOLOGICAL ONSET  Precocious Puberty: < 8 y.o. in girsl (M2) < 9 y.o. in boys (Testicular volume ≥4 mL)  Delayed Puberty: Absence of pubertal signs > 13 y.o. in girls Absence of pubertal signs > 14 y.o. in boys  Pubertal arrest! Dentition DECIDUOUS DENTITION (20 ELEMENTS) PERMANENT DENTITION (32 ELEMENTS) TEETHING DELAY: POSSIBLE CAUSES DIET AND CARIES - Sugar is the main risk factor for the develompent of caries - Sucrose is the most cariogenic sugas as it is converted into glucans which promote baterial adesion to teeth - Sweetened foods and beverages are not to be offered to children - Avoid offering baby bottle at sleep times - Limit the access to cariogenic foods to meals - Teach since infancy to keep a correct oral hygiene BABY BOTTLE TOOTH DECAY  Progressive and extremely precocious onset of deciduous teeth caries  Cause: prolonged exposure to sugary beverages (e.g.: fruit juice, chamomile) in particular during sleep times, when salivary secretions decrease  Pacifiers dipped in honey or other sweeteners to comfort the baby / Baby bottle with sweetened beverages  Bacterial proliferation favored by sugary environment → cariogenic damage  Decay of deciduous teeth can cause: Difficulties in chewing Difficulties in language articulation Alterations in permanent teeth BABY BOTTLE TOOTH DECAY: PREVENTION  Do not dip pacifiers in honey / juices  Baby bottles only to be provided with water or milk (maternal or formula)  Lower sugar intake with diet  Brushing teeths without toothpaste, since eruption of the first teeth  Fluorine  Planning ad odontoiatric evaluation after the first year of age TEETHING DELAY: DIAGNOSTIC APPROACH - ANAMNESIS Social anamnesis Diet anamensis Familiar anamnesis: infective risk factors (son of HIV+ mother), familiarity for celiac disease Past medical history: previous genetic disease, known hypopituritarism, epilepsy (pharmacological treatments) - BLOOD CHEMISTRY Calcium-phosphorus metabolic panel: calcium, phosphate, alkaline phosphatase, urine calcium e urine creatine on urine spot Celiac disease sierology: tTG-reflex Thyroid funcion: TSH, FT4 If anamnestic doubts: HIV CLINICAL CASE  Mohammed’s mum is concerned because her son has not developed any decidous tooth yet. Mohammed is 19 months old.Your answer is: a. It’s totally normal b. Wait and see approach c. You believe it is potentially a pathological condition and you prescribe additional investigations POTENTIAL CONDITIONS  Growth delay  Hypopituitarism  Hypothyroidism  HypoPTH  Celiac disease  Systemic chronic disorders  Rikets DIAGNOSIS  FAMILY HISTORY  NUTRITIONAL HISTORY  PREVIOUS MEDICAL HISTORY  MEDICATIONS  PHYSICAL EXAMINATION DIAGNOSIS  FAMILY HISTORY  NUTRITIONAL HISTORY  PREVIOUS MEDICAL HISTORY  MEDICATIONS  PHYSICAL EXAMINATION  BLOOD TESTS CALCIUM 7.8 mg/dL (9.3-10.5) PHOSPHATE 3.1 mg/dL (4.3-5) VITAMIN D 5 ng/L (target > 30) PTH 678 pg/mL (15-65) Alkalyne phosphatase 1171 (100-300) RICKETS  Definition: bone mimeralization defect, with particular involvement of bone growth cartilages.  Pathophysiology Inadequate chondrocyte apoptosis in hypertrophic area increase in size with typical enlarged appearance of the epiphyses Less calcified matrix due to lack of sufficient substrates RICKETS  Aetiology: Deficiency Vitamin D deficiency More frequent Calcium deficiency Non-deficiency Genetic forms Very rare Acquired forms  90% 10% inactivation VIT D Tessuto adiposo 25OHD CYP24, CYP3A4 catabolismo 1,25(OH)2D CYP24, CYP3A4  ANd9GcSgAP515EvL41siqdThJeqKnQGIJE-QMf8dk6XBSkSe0R_zbWAwpv2ARQ PTH ASSORBIMENTO Ca 1,25OH2D ESCREZIONE P RIASSORBIMENTO ANd9GcTYb4ly4gXKzBmGVfkZe9aLxZwPE6XpIkOuXKBVLP0x5AzBJ55KuwFNpcs CALCEMIA ASSORBIMENTO Ca eP RICKETS Clinic: Teething delay and /early caries Wide anterior fontanelle Craniotabe Harrison’s signs bracelet Deformation (varism-valgus) lower limbs RACHITISMO Clinica: RACHITISMO Clinica: RACHITISMO Clinica: RICKETS Risk factors for vitamin D deficiency: Low exposure to sunlight Cultural issues Prolonged exclusive breastfeeding beyond 6 months, in the absence of vitamin D supplementation in the infant In breastfed children: vitamin D deficiency in the pregnant mother Malanic hyperpigmentation (ethnicity) RACHITISMO Trattamento [email protected]