Malnutrition and obesity - PowerPoint Presentation

Slide1

Malnutrition and obesity

CONF.DR.INGRITH MIRON

DR. MOCANU ADRIANA

Slide2

What is malnutrition?

World Health Organization definition:

The term is used to refer to a number of diseases, each with a

specific cause related to one or more nutrients (for example, protein, iodine or iron)

and each characterized by cellular imbalance between the

supply of nutrients and energy on the one hand, and the body's demand for them to ensure growth

, maintenance, and specific functions, on the other.

Slide3

HUMAN NUTRITION

Obesity & under-nutrition are the 2 ends of the spectrum of malnutrition.

A healthy diet provides a balanced nutrients that satisfy the metabolic needs of the body without excess or shortage.

Dietary requirements of children vary according to age, sex & development.

Slide4

Macro and

micro nutrients

Macro-nutrients

Protein (amino acids)

Energy (carbohydrates)

Fat (fatty acids)

Micro-nutrients

Water soluble vitamins

(assist in energy-release of carbohydrates and red blood cell formation)

Fat soluble vitamins

(development & metabolism)

Minerals

Slide5

Malnutrition: definition

Malnutrition

:

chronic state of nutrition due to insufficient food intake (caloric and / or protein) specific for infants and small child.

Along with major deficits of nutrients occur also deficiencies in vitamins and minerals (

d

eficiency anemia, rickets,

avitaminoses

).

Depression of cellular immunity caused by malnutrition favors increased susceptibility to infection, which worsens the initial deficit, the infection is often the one that causes death.

Half of the states of malnutrition : first 6 months of life, overlapping maximum period of CNS development (neuronal proliferation - to a maximum of 18 months).

Slide6

Types of malnutrition

Severe Protein-Energy Malnutrition (>3 S.D.)

Kwashiorkor (low protein)

Marasmus (low calories)

Mild/moderate undernutrition (>2 S.D.)

Stunting

Underweight

Wasting

Micro-nutrient deficiency

Iodine

Iron

Vitamin A

Vitamin D

Slide7

OVERVIEW OF MALNUTRITION

The majority of world’s children live in developing countries

Lack of food & clean water, poor sanitation, infection & social unrest lead to LBW & PEM

Malnutrition is implicated in >50% of deaths

of children <5years (

5 million/yr

).

Slide8

OVERVIEW OF MALNUTRITION

WHO estimated that 32% of

children

in developing countries are underweight (182 million).

78% of these children live in South-east Asia & 15% in Sub-

Sahar

i

an Africa.

The reciprocal interaction between PEM & infection is the major cause of death & morbidity in young children.

Slide9

EPIDEMIOLOGY

The term protein energy malnutrition has been adopted by WHO in 1976.

Highly prevalent in developing countries

among

children <

5 years;

severe forms 1-10

%

& underweight 20-40%

.

All children with PEM have micronutrient deficiency.

Slide10

Classification/Terminololgy

T

he

term malnutrition (

Anglo-Saxon School)

or dystrophy (

French School)

define the states of malnutrition through food intake deficiency- qualitatively and/or quantitatively.

•

P

rotein energy malnutrition (PEM);

•

Protein

malnutrition (PM).

Slide11

Classification/Terminololgy

WHO proposes

2

terms (referring to states of severe malnutrition)

•

M

arasmus

- severe PEM;

• Kwashiorkor - severe PM.

These terms are unsatisfactory for practice - do not include light and intermediate states of

malnutrition

→

new terminology.

WHO - classification of malnutrition

•

Primary malnutrition

• Secondary

malnutrition.

Slide12

Primary Malnutrition :ETIOLOGY

Primary malnutrition

correct

food intake;

n

egativ

prognosis due to disturbed growth that can not be influenced therapeutically (frequent association with mental deficiency);

commonly associated with: fetal malnutrition, low birth weight and small height sometimes.

The causes of primary malnutrition:

organics (severe malformations: renal, digestive, cardiac)

genetically conditioned diseases (chromosomal, metabolic)

fetal infections (toxoplasmosis, syphilis, cytomegalovirus).

Slide13

Etiology of Primary Malnutrition

Failure of

lactation

.

Improper

weaning

p

ractices

Poverty

Food

taboos

2 or more children under 5 years of age in same household

Death of

mother

Incompetent/

ignorant

m

other

.

Lack of

family

p

lanning

Slide14

SECONDARY MALNUTRITION

S

econdary malnutrition (exogenous

):

deficiency due to dietary intake qualitatively or quantitatively,

prognosis is generally good by correcting the cause and food intake

,

usually no mental deficits.

Slide15

SECONDARY MALNUTRITION

Classification of secondary malnutrition

(

WHO):

I. Moderate

m

alnutrition:

-

mild (grade I dystrophy, hypotrophy, "poor child");

-

m

edium (grade II dystrophy);

II. Severe malnutrition (

g

rade III dystrophy):

-

energy-protein

m

alnutrition (

PEM

)

:

marasmus

,

atrepsi

a;

-

p

rotein malnutrition (

P

M

)

acute form

(

k

washiorkor

);

c

hronic form (

marasmic

k

washiorkor ).

Slide16

Etiology of secondary malnutrition

A)Dietary deficiency

quantitatively: native

hipogalactia

; late diversification over 6 months of age; improper dilution of milk, restrictive diets, taboos related to food, family, religious, ethnic;

q

uality: carbohydrate deficiency ( cow’s milk

distrofy

), protein deficiency (edematous dystrophy by excess flour, using vegetable protein low biological value), lipid deficiency ( regimes without lipids)

lead to imbalance by decreasing caloric intake.

Slide17

Etiology of secondary malnutrition

B)

infections:enteric

infection;bronchopneumonia

,

otomastoidite

,

chronic urinary tract infection, bacterial or parasitic diarrhea, syphilis, tuberculosis- poor appetite, digestive losses, increased catabolism.

c) psychosocial

events:maternal

deprivation, neglect of physiological rhythm of alimentation, lack of hygiene, pollution, cold,

hospitalism

;

Slide18

Etiology of secondary malnutrition

D) psychosomatic disorders :

- anorexia ,

organic disease (hypertrophic pyloric

stenosis

, congenital malformations that cause repeated vomiting, cystic fibrosis, celiac disease, congenital intolerance to disaccharides,

labio

-

maxillo

-palatine cleft) ,

infantile cerebral palsy with impaired swallowing, pharyngeal

incoordination

.

Slide19

Etiology of secondary malnutrition

Chronic

illnesses

that

commonly

are

associated

with

nutritional

deficiencies

include

the

following

:

Cystic

fibrosis

Chronic

renal

failure

Childhood

malignancies

Congenital

heart

disease

Neuromuscular

diseases

Chronic

inflammatory

bowel

diseases

Slide20

Etiology of secondary malnutrition

In

addition

,

the

following

conditions

place

children

at

significant

risk

for

the

development

of

nutritional

deficiencies

:

Prematurity

Developmental

delay

In

utero

toxin

exposure

(ie, fetal

alcohol

exposure

)

Children

with

multiple

food

allergies

present

a special

nutritional

challenge

because

of severe

dietary

restrictions

.

Patients

with

active

allergic

symptoms

may

have

increased

calori

c

and

protein

needs

.

Slide21

Protein-energy malnutrition pathogenesis

In severe forms when nutritional deficit exceeds a certain limit, the consequences are severe:

• regression of all metabolic activities (decreased basal metabolism, decreased intracellular water, decreasing opportunities to retain water and salt);

• low digestive tolerance (decreased activity of

disaccharideses

, pancreatic secretion, bile acids);

• loss of defense to infection.

Very low digestive tolerance and dietary intake can not maintenance energy needs lead to

autophagic

processes (the metabolism of starvation).

Slide22

Protein-energy malnutrition pathogenesis

S

evere lack of calorie and protein → hypoglycemia, decreased serum amino acids in pancreatic reaction → →

hipoinsulinism

(main endocrine changes in starvation) → decrease peripheral insulin and the appearance adaptive responses:

• mobilization of fatty acids from adipose tissue (

lipolysis

) to the liver to be an energy source;

• decrease in muscle glucose utilization and incorporation of amino acids that are directed to the liver, where they are used for protein synthesis and

neoglucogeneză

(the exhausted body fat);

• hepatic protein synthesis is achieved by sacrificing muscle proteins.

Slide23

Protein-energy malnutrition pathogenesis

Infection -

is

the vicious circle in severe malnutrition, worsening starvation and being the main cause of death by:

• loss of appetite;

• digestive losses (diarrhea);

• increased catabolism (febrile illness);

• disorders of intermediary metabolism by reducing metabolic efficiency of nutrients;

• increased urinary nitrogen loss, K, Mg, Zn, P, vitamin A, C, B2.

Slide24

Pathogenesis

of protein malnutrition

The acute form

(

typical Kwashiorkor

)

• occurs after 6-8 months;

• diversification normal calorie but devoid of protein;

• deposits of fat are consumed, stature is normal and causes severe loss of protein

(proteins from the

liver, muscle,

pancreatic proteins, serum albumins deficiency) and loss of

intracellular K (preservation mitosis), hepatic fatty infiltration if infection occurs - marked reduction albumin (hepatic synthesis deficient) → fluid retention (decrease in colloid osmotic pressure capillary) → edema.

Slide25

Pathogenesis

of protein malnutrition

Chronic

form (

Marasmic

Kwashiorkor) -

secondary

selective protein intake deficiency is characterized by:

- sufficient caloric intake;

- normal secretion of insulin:

favors

lipogenesis

(fatty acids are not available in place of amino acid oxidation - fatty tissue is preserved);

reduced level of plasma amino acids by three mechanisms:

• reduce the release of amino acids from muscle;

• stimulates the passage of serum amino acids in muscle;

• favors the

the

incorporation of amino acids into the muscle.

Slide26

MARASMUS

/KWASHIORKOR

Marasmus represents an adaptive response to starvation, whereas kwashiorkor represents a maladaptive response to starvation

I

n Marasmus

t

he body utilizes all fat stores before using muscles.

Slide27

Assessment of Nutrition

Status

Clinical

Anthropometric

Dietary

Laboratory

Slide28

Investigations for PEM

Full blood counts, inflammatory

markers;

Blood glucose profile,

lipidic

profile

Iron

, vitamin

levels;

Microbiology: septic

screening,stool

& urine for parasites &

germs;

Electrolytes, Ca, Ph &

Mg;

S

erum

proteins, protein electrophoresis;

immunological status: cellular immunity - decreased T cell, interferon, IDR lack of response to tuberculin;

humoral

immunity - low

IgA

(

secretory

IgA

),

IgM

- high, low

IgG

.

Decrease complement

C3

;

Exclude HIV &

malabsorption

.

Slide29

Investigations for PEM

In essence:

• decrease

serum albumins

→ edema;

• decrease

apoproteins

(lipoproteins carrier);

• storage of fat in the liver (fatty infiltration);

Clinical

outcomes:

oedema

,

hepatomegaly

(fatty liver), changes in hair growth and skin (areas of hypo-or

hyperpigmentation

, fissures), diarrhea (villous atrophy), predisposition to infection (

humoral

and cellular immunity disturbed).

Slide30

Anthropometric assessment of malnutrition

anthropometric criteria :

percentiles method (normal 10-90).

standard derivations method (normal + / - 2 SD).

ponderal

index (PI)

PI = actual weight of the child / ideal weight (W of child of the same age located on the 50th percentile of the growth curve).

After the PI values

​​

: 3

degrees of PEM(Gomez)

degree I

(PI

= 0.89 to

0.76);

degree II

(PI

= 0.75 to

0.60);

degree III

(

PI =

0.60).

PI = 0.90- underweight or child at risk of malnutrition.

Slide31

Anthropometric assessment of malnutrition

The protein malnutrition are two degrees:

degree I PI = 0.8-0.6 -

KWASHIORKOR;

degree II PI= 0.6 –

MARASMIC KWASHIORKOR

Nutritional

index

(NI)

- index diets.

NI

= actual weight / weight appropriate waist.

After this indicator there are 3 degrees of malnutrition:

grade I

(NI=

0.89 to

0.81);

grade II

(NI=

0.80 to

0.71);

grade

III (NI= 0.70).

H

ead circumference (HC)

- highlights the true growth in the first two years.

Midarm

circumference

(measured at the ½ distance between the

acromion

and

olecranon

)

pathological - under 13 cm - available in children over 2 years.

Slide32

Assessment of malnutrition- functional criteria

Appreciation

of the

digestive tolerance

:

paradoxical

reaction to hunger (disproportionate weight loss);

food

paradoxical reaction (weight loss to increased food intake, sometimes diarrhea);

s

ensitivity

to

fasts

- by spacing

meals:

hypoglycaemia

, especially nocturnal → apnea, sudden death.

i

mmunological

reactivity

:

-

i

ncreased

responsiveness to infection;

-

r

eactivity

collapsed (serious infection without fever,

leukocytosis

, sometimes opportunistic).

Slide33

Assessment of malnutrition

Neuropsychological

development:

Archaic reflexes;

Muscle

tone;

Posture

;

Mobility

;

Development

of language;

Affection

.

They are affected differently depending on the severity of malnutrition

.

Slide34

Clinical features in

m

arasmus

Marked muscle wasting and loss of subcutaneous

fat;

Monkey

facies

;

Skin becomes loose and hangs in

folds;

Abdomen protuberant due to hypotonic

muscles;

Temperature is usually

sub-normal;

Child is

alert.

Slide35

Clinical features of kwashiorkor

Generalized edema more marked in lower

e

xtremeties

, muscle

wasting;

Growth

retardation;

Psychomotor

changes;

Apathy and

irritability;

Fine

and

discoloured

hair;

Anemia;

Usually flaky

p

aint

dermatitis;

Enlarged liver due to fatty

changes.

Slide36

Complications of

PEM

Hypoglycemia

Hypothermia

Hypokalemia

Hyponatremia

Heart failure

Dehydration & shock

Infections (bacterial, viral & thrush)

Slide37

TREATMENT: Prevention of

Malnutrition

Primary Prevention

Health Education to mothers about good nutrition and food hygiene

Immunization of children.

Growth monitoring on Growth Charts specially of all children under 3 years of age

Secondary Prevention

Mass Screening of high risk populations, using simple tools like Weight for age

.

Tertiary Prevention

Good Nutritional Care, supplementary feedings and rehabilitation,

counselling

of mothers.

Slide38

TREATMENT: Prevention of Malnutrition

Natural nutrition - first 4-6 months;

Artificial

nutrition - milk type, dilution, enrichment rice mucilage;

- Compliance with immunization schedule, the correct treatment of infections;

-

Inadequate conditions and social environment.

Slide39

TREATMENT

OBJECTIVES

:

• accurate assessment of the

form and degree of malnutrition;

• pointing out the

main deficiencies

(protein, fat, carbohydrates, fluid and electrolyte minerals and vitamins),

immune status

and the possibility of

co-infection

;

• finding the

cause

which produced malnutrition;

•

recovery

plan

individualized for the nutritional deficiency as quickly as possible.

Slide40

TREATMENT

General principles:

The recovery of

PEM (II

and III

degree)

:

I. The initial phase

•

Correction of water & electrolyte imbalance

;

•

Treatment

of infectious complications

.

II. Repair phase

•

Dietary therapy

;

•

Correction

of deficiencies

(anemia, rickets,

hypovitaminosis

, etc).

III.

C

onvalescence phase

•

Restoration

of body composition;

•

Enhancing healing

.

Optimal objective is to resume growth after 2-3 weeks of starting the diet and clinical recovery in 6-8 weeks.

Slide41

TREATMENT

I)

Parenteral

nutrition for 2-3 days

→

enteral

nutrition with flow probe using

hyperproteic

and

hypercaloric

solutions ;

II

) Early initiation of oral nutrition : hypoallergenic preparations rich in proteins and calories, low

osmolarity

:

Alfare

,

PeptiJunior

,

Pregestimil

,

Nutramigen

,

Pregomin

or amino acid formulas, such as

Neocate

.

Keep in parallel

parenteral

intake of carbohydrates, amino acids, lipids.

Simultaneously treating infections,

hypoproteinemia

, anemia, multivitamins deficiencies .

This variant is also little used because it requires specials dietetics and carefully

monitorization

of nutritional therapy .

Slide42

TREATMENT

III)

after fluid replacement and electrolyte -

digestive tolerance

:

with carrot soup or rice mucilage (in various concentrations ) in a dose of 150-200 ml / kg ( not exceeding 1000 ml / day)

carbohydrates were obtained from glucose 5%, 7 %, 10 % and chicken mixed proteins (

h

ypoallergenic,

100g , 17g protein).

a

fter normalization of the stools ( 7 days) :oil gradually (3-4 ml / day ) and after 10 days from the beginning of

enteral

diet

→

hypoallergenic

preparation can be inserted

(

!

preparations lactose free-

can induce cow's milk protein intolerance ) .

week 4

:sugar (restoring lactose tolerance is difficult , 3-4 months);

f

lour

products containing gluten will not enter until full

recovery;

increases in protein - calorie intake by

parenteral

administration of carbohydrates , amino acids and

proteins;

treat the infection , iron or vitamin deficiencies

.

Slide43

TREATMENT

Malnutrition has its weight age.

• correct food intake : 8-10% protein, 54-50% fat, 50-60% carbohydrates:

1 g

lipid

- 9 kcal;

1 g

protein

- 4.1 kcal;

1 g carbohydrate - 4.1 kcal.

• complete metabolism of 1 g of protein are required 35-40 kcal.

• a protein intake

˃

5 g / kg / day is dangerous, resulting

hyperammonemia

, increased blood urea nitrogen

;

• Increasing K intake to 4-5

mEq

/ l

.

Slide44

TREATMENT

R

ecovery of PEM degree II(

advenced

) and III (

Suskie

) contains:

calorie - 175 kcal / kg / day;

protein - 4 g / kg / day;

lipid - 9.59 g / kg / day;

carbohydrate - 18.3 g / kg / day.

• Research and treating infection with antibiotics (ideally etiologic) is mandatory.

• In severe malnutrition ↓

IgG

: iv administration of gamma globulin

• protein malnutrition (low

albuminand

proteinemia

): human albumin administered iv (1 g / kg / day).

• basal energy needs - 70 kcal / kg / day.

Slide45

TREATMENT

Mild forms of MPC

• Treat at home by correcting the diet (food ration for age - increasing protein intake to 0.5-1 g / kg / day

→

20 to 30 kcal / kg / day).

• correction of the causes: maternal

hipogalactia

,

hypocaloriec

diet

with incorrect

mixed or artificial

nutrition,

extending over six months natural nutrition with delayed/incorrect diversification

.

• Quick recovery in 1-2 weeks.

Slide46

TREATMENT

PEM (severe forms degree II-III , III)

• Treat only in hospital.

• The first 24 hours

- fluid replacement and electrolyte

and acid-base fluid resuscitation.

• The following 48-72 hours (sometimes more) partial or total

parenteral

nutrition, reaching 80-90 kcal / kg / day.

Slide47

TREATMENT

the rate of protein :4-5 g / kg / day (

i

ncreasing protein is progressively 1-1.5 g / kg / day, reaching in 4-5 days at this rate)

180-160 kcal / kg to 180-200 kcal / kg / day

f

rom day 3-4 start exploratory digestive maintaining iv administration sugars, amino acids ;

Diet exploratory :rice mucilage 3%, 5%, 8%; carrot soup 300 ‰ or 500 ‰,

sweetener - glucose 5%, 7%, 10% (even 15%).

7-8 lunches, from 30-50 ml ground in 2-3 days, if tolerance is good - 140-150 kcal / kg.

Slide48

TREATMENT

Criteria

to follow:

• normalization of the stools ;

• growth rate - slow resume after 2-3 weeks to restore digestive tolerance and achieve optimum value caloric and protein intake (early treatment can decrease the growth rate - restore electrolyte balance, after the disappearance of edema).

• avoid prolonged fasts - risk of

hypoglycaemia

.

• immune recovery 25-30 days after initiation of dietary therapy.

•

histochemical

normalization of intestinal mucosa after 3-4 months.

Slide49

OBESITY

Obesity

-

chronic

disorder

of

the

nutrition

in

infants

,

children

and

adolescents

characterized

by

the

accumulation

of

fat

in

adipose

tissue

and

other

tissues

and

organs

as a

result

of

energy

imbalance

.

The

prevalence

of

the

disease

is

on

the

rise

:

according

to

WHO 22

million

children

under

5

years

are

obese

,

the

prevalence

becoming

triple in

the

past

30

years

and

overcoming

the

prevalence

of

malnutrition

.

For

children

who

have

an

overweight

or

obese

parent

,

the

risk

of

becoming

obese

adults

is

higher

than

in normal

weight

children

.

If

both

parents

are

obese

, a

child's

risk

of

becoming

obese

is

80%. 80% of

obese

adolescents

become

obese

adults

.

Slide50

OBESITY

Obesity

is

a plurifactorial

disease

,

favorable

factors

being

:

prenatal

factors

: maternal caloric

intake

, maternal

diabetes

,

dismaturity

,

small

size

and

small

head

circumference

at

birth

;

perinatal

factors

:

cold

climate at

birth

.

post-natal

factors

:

the

intensity

of

the

increase

in body

fat

by

the

age

of 1

year

, artificial

feeding

from

birth

,

adolescence

weight

.

Slide51

OBESITY - pathophysiological

mechanisms and clinical features

The

major disturbances encountered in obesity are insulin and glucose homeostasis,

dyslipidemia

and

hypercortisolemia

.

clinical

picture

a) Characteristic anthropometric data of obesity are:

-excessive weight according to height, excessive weight in relation to the ideal weight for age;

-

normal-sized or even increased height compared to the average age;

-increased upper-arm circumference comparing to age values​​;

-subcutaneous fat thickness increased compared to normal age;

-sexual maturation and somatic maturation(bone age) normal or accelerated.

b

) somatic appearance: generalized symmetrically increased fat deposits, breast enlargement and distension of the abdomen.

Slide52

OBESITY : Symptoms

-psychological problems: bad image of oneself, feelings of inferiority and rejection from the same aged children community, depression, frustration, tendency to antisocial behavior, difficult family relationships and social immaturity, increased dependence to the family.

-

mechanical overload-related symptoms represented by the excess weight: cardio-circulatory inadequacy, fatigue,

polipnea

and

dyspnea

on moderate effort, lower limb orthostatic edema, joint pain.

-skin changes:

intertrigo

, skin folds irritation, itching,

abcesses

, acne.

-nonspecific disorders: headache, vertigo, dizziness, fatigue, flatulence, constipation, difficult digestion, menstrual disorders in adolescents.

Slide53

OBESITY: LABORATORY DATA

• carbohydrate metabolism: over 50% of obese children have impaired glucose tolerance.

• lipid metabolism: hypercholesterolemia,

hypertriglyceridemia

, elevated levels of LDL and

apolipoprotein

B, decreased HDL and

apolipoprotein

AI.

• protein metabolism: moderate increase in serum protein, the α2-and β-globulins.

• hormonal profile:

elevated

levels of insulin and

cortisol

; thyroid

function is generally normal.

• fluid and electrolyte balance

:

sodium retention and potassium excretion are

elevated;aldosterone

excretion is significantly increased.

Slide54

OBESITY: Positive diagnosis

- clinical appearance ;

-

anthropometric data :

body mass index(BMI), size of skin fold.

WHO recommendations

:

-

overweight

:

BMI

˃

1 SD

or

between 95-99

percentile;

-

obesity

:

BMI

˃

2

SD

or

above the 99th percentile

;

- by

the age of 2

years ,

overweight

: reporting

the actual weight to ideal weight for height , age and sex.

The

correct definition of obesity in children is given by the content of body fat mass measured by

bioelectric impedance

.

Up

to age 16

years

:obesity

→

fat

mass

˃

20 % reference values for age and sex

;

O

ver

16 years

:

obesity

→

fat mass

˃

25 %

of body weight in

boys

and

˃

32 %

for

girls.

Slide55

OBESITY: DIFFERENTIAL DIAGNOSIS

            In case of suspected genetic or endocrine obesity, differential diagnosis should be done with

:

Laurence-Moon-

Bardet-Biedl

syndrome

,

Prader-Willi

syndrome

,

Albright (

pseudohypoparathyroidism

),

Cushing's

syndrome,

Stein-

Leventhal

syndrome

(or

Policystic

ovarian syndrome)

Frolich

syndrome

( or

Adiposogenital

Distrophy

)

Mauriac syndrome

(complication of

diabet

mellitus type I)

Von

Gierke

glycogenosis

(storage disease).

Slide56

OBESITY: TREATMENT

Treatment protocol includes:

- dietary

treatment,

- physical

activity program

,

-

behavioral therapy,

- drug

therapy,

-surgery

,

- treatment

of complications

,

-

family nutrition education.

Dietary treatment remains a therapeutic basis.

Slide57

OBESITY: TREATMENT

a)Dietary treatment

during growth and development needs to ensure their normal ongoing, so that can not be overcome certain minimum amounts of caloric intake and dietary protein:

-110 c

alories

/ kg / day in infants <

6

months;

-

90 calories / kg / day in infants 6-12 months;

- 60 calories

/ kg / day of ideal weight

under 12 years;

- 850

Calories / day in teenager during the

weightloss

period,1000 calories / day after the initial period of minimum one month.

Slide58

OBESITY: TREATMENT

In

most obese children good results are obtained by decreasing initial caloric intake with 30%.

Nutritional content of the diet

:

20

% proteins

,

40% carbohydrates,

40

%

fats,

5-6

meals / day, with the following distribution of calories: 20% at breakfast, 30% at lunch, 20% at dinner and two snacks by 15% in 5 meals / day version and by 10% in snacks in the 6 meals / day version.

Diet

is suitable for inducing a weight loss of 0.5-2 kg / week.

In

obese infants, the treatment goal is not to reduce weight, but slowing down the rate of weight gain in relation to increasing waistline.

Slide59

OBESITY: TREATMENT

b

) physical activity:

important role in weight loss programs (

discrepancy

between caloric intake and physical energy

expenditure).

Activitaty

will be chosen according to the personality, preferences and abilities of the child

.

c) behavioral therapy:

to correct the habits that caused weight excess and promote a healthy lifestyle.

       

d

) drug treatment:

minor role.

      

e) surgery: surgical techniques recommended for adult are not appropriate for child.

Slide60

OBESITY:EVOLUTION AND PROGNOSIS

           Prophylaxis should start from prenatal period by identifying parents with increased familial risk for obesity.

           Factors that may influence the evolution and prognosis of obesity are:

-etiology of obesity: endocrine obesity is refractory to dietary therapy versus exogenous obesity;

-

severity: more severe degrees respond poorly to therapy and have higher risk of complications;

-during evolution: as the disease is aging, eating habits are harder to be influenced by therapeutic measures;

-age: critical periods in the development of obesity are infancy, preschool and adolescent;

-the response to dietary

treatment.

Slide61

OBESITY: EVOLUTION AND PROGNOSIS

Slimming regime favorable results are

:

acquiring

a feeling of well being,

lowering

blood pressure

,

improving heart function

,

reducing the number of apneas / hour, increase blood oxygen saturation and lung capacity,

decreased

basal hyperglycemia and

hyperinsulinemia

and reduced postprandial insulin resistance, relieving joints symptoms.

Slide62

OBESITY: COMPLICATIONS

Complications

of obesity:

orthopedic

complications

:

genu

valgum

, flat feet, Blount disease,

coxa

vara

,

epiphysitis

of femoral head, aseptic necrosis of the femoral head,

hyperlordosis

, leg pain after prolonged

standing.

metabolic

complications

:

dyslipidemia

,

hyperinsulinemia

, insulin resistance, type II diabetes,

hyperuricemia

(rare).

Slide63

OBESITY: COMPLICATIONS

hormonal complications

:

hiperandrogenemy

, menstrual cycle disorders,

hypercortisolism

reagent.

respiratory

complications

: hypoventilation syndrome, obstructive apnea during sleep, asthma. The extreme manifestation of alveolar hypoventilation is Pickwick

syndrome.

cardiovascular complications:

hypertension, right ventricular hypertrophy, coronary atherosclerosis or generalized atherosclerosis.

Slide64

OBESITY: COMPLICATIONS

digestive

complications

: hepatic

steatosis

,

cholelithiasis

,

cholecystitis

.

psychological

complications

:

neuro

-cognitive deficits, feelings of inferiority, family conflict, social isolation, school problems, truancy, emotional and mental immaturity.

endocrine

complications

: polycystic ovary disease.

skin

complications

: fungal and bacterial skin infections,

trophic

disorders of the lower limbs, nail dysplasia.