Transcript Malnutrition and obesyti

Malnutrition and obesity
CONF.DR.INGRITH MIRON
DR. MOCANU ADRIANA
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.
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.
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
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 (deficiency 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).
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
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Iodine
Iron
Vitamin A
Vitamin D
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).
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-Saharian Africa.
• The reciprocal interaction between PEM &
infection is the major cause of death &
morbidity in young children.
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.
Classification/Terminololgy
The term malnutrition (Anglo-Saxon
School) or dystrophy (French School) define
the states of malnutrition through food intake
deficiency- qualitatively and/or quantitatively.
• Protein energy malnutrition (PEM);
• Protein malnutrition (PM).
Classification/Terminololgy
WHO proposes 2 terms (referring to states of
severe malnutrition)
• Marasmus - 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.
Primary Malnutrition :ETIOLOGY
Primary malnutrition
• correct food intake;
• negativ 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).
Etiology of Primary Malnutrition
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Failure of lactation.
Improper weaning practices
Poverty
Food taboos
2 or more children under 5 years of age in
same household
• Death of mother
• Incompetent/ ignorant mother.
• Lack of family planning
SECONDARY MALNUTRITION
Secondary 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.
SECONDARY MALNUTRITION
Classification of secondary malnutrition (WHO):
I. Moderate malnutrition:
- mild (grade I dystrophy, hypotrophy, "poor child");
- medium (grade II dystrophy);
II. Severe malnutrition (grade III dystrophy):
- energy-protein malnutrition (PEM) :marasmus, atrepsia;
- protein malnutrition (PM)
• acute form (kwashiorkor);
• chronic form (marasmic kwashiorkor ).
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;
• quality: 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.
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;
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, labiomaxillo-palatine cleft) ,
- infantile cerebral palsy with impaired
swallowing, pharyngeal incoordination.
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
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 caloric and protein needs.
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).
Protein-energy malnutrition
pathogenesis
Severe 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.
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.
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.
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.
MARASMUS/KWASHIORKOR
• Marasmus represents an adaptive response
to starvation, whereas kwashiorkor
represents a maladaptive response to
starvation
• In Marasmus the body utilizes all fat stores
before using muscles.
Assessment of Nutrition Status
– Clinical
– Anthropometric
– Dietary
– Laboratory
Investigations for PEM
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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;
Serum 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.
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).
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.
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).
Head 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.
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);
• sensitivity to fasts - by spacing meals: hypoglycaemia,
especially nocturnal → apnea, sudden death.
• immunological reactivity :
- increased responsiveness to infection;
- reactivity collapsed (serious infection without fever,
leukocytosis, sometimes opportunistic).
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 .
Clinical features in marasmus
• 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.
Clinical features of kwashiorkor
• Generalized edema more marked in lower
extremeties, muscle wasting;
• Growth retardation;
• Psychomotor changes;
• Apathy and irritability;
• Fine and discoloured hair;
• Anemia;
• Usually flaky paint dermatitis;
• Enlarged liver due to fatty changes.
Complications of PEM
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Hypoglycemia
Hypothermia
Hypokalemia
Hyponatremia
Heart failure
Dehydration & shock
Infections (bacterial, viral & thrush)
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.
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.
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.
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. Convalescence 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.
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 .
TREATMENT
III) after fluid replacement and electrolyte - digestive tolerance :
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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 ( hypoallergenic, 100g , 17g protein).
after 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);
flour 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 .
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 3540 kcal.
• a protein intake ˃ 5 g / kg / day is dangerous, resulting
hyperammonemia, increased blood urea nitrogen ;
• Increasing K intake to 4-5 mEq / l .
TREATMENT
Recovery 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.
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.
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.
TREATMENT
 the rate of protein :4-5 g / kg / day (increasing 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
 from 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.
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.
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.
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.
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.
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.
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.
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 ;
Over 16 years : obesity → fat mass ˃ 25 % of body weight in boys
and
˃ 32 % for girls.
OBESITY: DIFFERENTIAL DIAGNOSIS
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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).
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.
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 calories / 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.
OBESITY: TREATMENT
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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.
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.
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.
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.
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).
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.
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.