1. Childhood Nutritional disorder
Dr. Aziza Aljohany

2. Introduction
Malnutrition means more than feeling hungry or not having enough food to eat. It is a condition that develops when the body does not get the proper amount of protein, calories, vitamins and other nutrients it needs to maintain healthy tissues and organ function. It occurs in children who are either undernourished or over nourished. Children who are over nourished may become over weight or obese and those who are under nourished are more likely to have severe long term consequences.

3. Malnutrition includes: under nutrition and over nutrition.
Definition
Malnutrition includes: under nutrition and over nutrition.
- Under nutrition: is a consequence of consuming little energy and other essential nutrients or using or excreting them more.
Malnutrition: is a term referring to poor or inadequate nutrition.
Separation from parents, peers, siblings and trusted adults
Fear of harm ,injury , discomfort and pain
Loss of control
Unknown and unfamiliar events and environment
Limited number of coping mechanisms to resolve the stressful events in children
Unclear limits and exceptions
Dealing with new care takers.

4. Prevalence of malnutrition
Malnutrition remains of the worlds highest priority health issues not only because its effects are so widespread and long lasting, but also because it can be eradicated. More than 35% of all preschool age children in developing countries are under weight. The unicef report found that 146 million children under five years in the developing world are suffering from insufficient food intake, repeated infections diseases, muscle wasting and vitamin deficiencies.

5. Etiology 1- Dietary errors
2 – Infection :Acute or chronic as T.B, otitis media pyelo nephritis
3- Gastroenteritis: (acute or chronic )
4- parasitic inf estuations as: Ascaris, ankylostoma ,giardia
5-Congenital anomalies as: Cardiac (P.D.A,V.S.D,F4) ,Renal (renal agenesis, obstructive uropathy) ,G.I.T (pyloric stenosis , cleftlip or palat
6-Metabolic diseases.: Galactosemia, Fructose intolerance, Idiopathic hypocalcaemia
7- Prematurety
8- Some cases of mental retardation
9- Low socio economic status
10-Endocrine causes ( DM.hyperthyroidism )

7. Childhood
Iron Deficiency
Anemia

8. in Africa, Asia, Latin America and the Caribbean
Anemia is a severe public health problem
in Africa, Asia, Latin America
and the Caribbean
ANEMIA –
A PUBLIC HEALTH PROBLEM

9. one of ten most serious risk in countries
Iron deficiency identified as
one of ten most serious risk in countries
with high infant and adult mortalities
ANEMIA –
A PUBLIC HEALTH PROBLEM

10. A decrease in the concentration of circulating red blood cells or
Definition
Anemia is defined as:
A decrease in the concentration
of circulating red blood cells or
in the hemoglobin concentration
and a concomitant impaired
capacity to transport oxygen.

11. WHO Diagnosis Hemoglobin below 11gm/dl in pre school children.

12. Is an abnormal value for at least two of three laboratory indicators of iron status: 1. Serum ferritin 2. Transferrin saturation 3. Free erythrocyte protoporphyrin
Iron deficiency

13. IRON DEFICENCY STAGES reduction in iron stores without reduced serum
Prelatent
reduction in iron stores
without reduced serum
iron levels
Latent
iron stores are exhausted,
but the blood hemoglobin
level remains normal
Iron deficiency anemia
blood hemoglobin
concentration falls below
the lower limit of normal
IRON DEFICENCY STAGES

14. Functions of Iron Formulation of hemoglobin Binding O2 to RBC
and transport
cytochrome myoglobin
Regulation of Body
temperature

15. Functions of Iron Muscle activity Catecholamine metabolism
Immune system
Brain Development
& function
Thyroid function
Cont.

16. Iron deficiency anemia occurs when iron deficiency is severe enough to reduce hemoglobin levels below normal.
ANEMIA

17. Normal values AGE Hgb Mean/ (-2SD) HCT% MCV Newborn 16.5 (13.5)
51 (42)
108 (96)
1 Month
13.9 (10.7)
44 (33)
101 (91)
2 Months
11.2 (9.4)
35 (28)
95 (84)
6 Months
12.6 (11.0)
36 (31)
76 (68)
> 6 Months
12.5 (11.0)
36 (33)
81 (70+ age per yr)

18. Iron cycle

19. Iron deficiency anemia
Mechanism
of development of
Anemia
Normal
Iron deficiency anemia

20. Factors
Contribute
To the
Development Of
Anemia

21. Iron deficiency Anemia
Dietary iron deficiency is the
usual cause
Iron def. is common in children
9mo-3yr
Infants less than 6 months generally
do not develop iron def.
Iron def. anemia in a child over 3yr
should prompt consideration of
occult blood loss
Iron deficiency Anemia

22. Iron deficiency Anemia
Dietary deficiency
Increased demand (growth)
Impaired absorption
Blood loss (e.g.)
- gut problems
- lung
- nose
- kidney
- menstrual problems
- trauma
Iron deficiency Anemia
(cont.)
Causes

23. Iron deficiency Anemia Clinical Manifestation
Pallor is the most important sign
Mild to Moderate iron deficiency
( hemoglobin levels of g/dL)
few symptoms of anemia;
irritable, Pagophagia
Severe iron deficiency
Irritability , Anorexia, Tachycardia,
Cardiac dilation, Systolic murmurs
Iron deficiency Anemia
(cont.)
Clinical Manifestation

24. Iron deficiency Anemia Clinical Manifestation (Cont.)
Iron deficiency may have effects on neurologic and intellectual functions
Iron – deficiency anemia and even iron deficiency with out anemia affect :
*Attention span
*Alertness
*Learning
Iron deficiency Anemia
(cont.)
Clinical Manifestation (Cont.)

25. Iron deficiency Anemia
Decreased cognitive performance often accompanies iron deficiency and iron deficiency anemia
Iron deficiency Anemia
(cont.)
Clinical Manifestation (Cont.)

26. Iron deficiency Anemia
Koilonychia: "spoon nails” Iron deficiency anemia
Iron deficiency Anemia
(cont.)
Clinical Manifestation (Cont.)

27. Iron deficiency Anemia
Smooth, bald, burning tongue; Iron deficiency anemia
Iron deficiency Anemia
(cont.)
Clinical Manifestation (Cont.)

28. Iron deficiency Anemia
Angular Cheilosis or Stomatitis
Iron deficiency Anemia
(cont.)
Clinical Manifestation (Cont.)

29. Laboratory Findings Prelatent
Hgb (N), MCV (N), iron absorption (), transferrin saturation (N), serum ferritin (), marrow iron ()
Latent
Hgb (N), MCV (N), TIBC (), serum ferritin (), transferrin saturation (), marrow iron (absent)
Iron deficiency anemia
Hgb (), MCV (), TIBC (), serum ferritin (), transferrin saturation (), marrow iron (absent)

30. Laboratory Findings (Cont.)
With increasing deficiency ,RBCs become deformed
and misshapen and present characteristic :
- Microcytosis
- Hypochromia
- Poikilocytosis
- Increased RBC distribution width (RDW)
Reticulocyte percentage
may be normal or moderately elevated
Nucleated RBCs occasionally seen
Thrombocytosis (some time)
Normal white blood cells

31. Additional diagnostic tests - Free erythrocyte protoporphyrin
Laboratory Findings (Cont.)
Additional diagnostic tests
- Free erythrocyte protoporphyrin
(elevated)
- Serum ferritin (decreased)
- Serum iron (decreased)
- Iron binding capacity (increased)
- Iron saturation (decreased)

32. 1.Use oral iron PRINCIPLES OF TREATMENT 2.Replace iron deficit
in total
3.Establish
and treat
the cause

33. PRINCIPLES OF TREATMENT
4.The therapeutic
dose should be
calculated in
terms of
elemental
iron
PRINCIPLES OF
TREATMENT
(Cont.)
5. A daily total
of 4 -6 mg/kg of
elemental iron in three divided doses provides
an optimal
amount of iron
6.A parenteral iron preparation (iron dextran) is an effective form of iron

34. response of iron-deficiency anemia
The regular
response of iron-deficiency anemia
to adequate amounts of iron is an important diagnostic and therapeutic features.
PRINCIPLES OF
TREATMENT
(Cont.)

35. PRINCIPLES OF TREATMENT
(Cont.)
PRINCIPLES OF
TREATMENT
Oral administration
of simple ferrous salts ( sulfate, gluconate, fumartate) provides inexpensive and satisfactory therapy

36. Blood transfusion Is indicated only when 1.Anemia is very severe
2.Superimposed infection may interfere with the response
In severely anemic children with hemoglobin values less than 4 g/dL
should be given only
2 -3 mL/kg of packed cells at any one time
Packed
or sedimented
RBCs
should be
administered
slowly

37. Responses to iron therapy in iron- deficiency anemia
Time after Iron Administration
Response hr
Subjective improvement; decreased irritability,
increased appetite hr
Initial bone marrow response hr
Reticulocytosis, peak at 5 -7 days
4 -30 days
Increase in hemoglobin level
1 -3 mo
Repletion of stores

38. Failure of iron therapy
occur when:
A child does not receive the
prescribed medication
2. Iron is given in a form that is
poorly absorbed
3. There is continuing unrecognized blood loss such as :
* intestinal or pulmonary loss
* loss with menstrual periods
4. An incorrect original diagnosis

39. 1st May 2010
Iron obtained from animal products is much more easily absorbed by the body than iron from plant sources,
Khorfakkan Scientific Anemia Day

40. Home Message Anemia is a sign, not a disease.
Anemias are a dynamic process.
Its never normal to be anemic.
The diagnosis of iron deficiency anemia mandates further work-up

42. Rickets

43. Background
9/19/2018
Rickets
is a disease of growing bone that is unique to children and adolescents.
It is caused by a failure of osteoid to calcify in a growing person.
Failure of osteoid to calcify in adults is called Osteomalacia.

44. Vitamin D deficiency rickets occurs when the metabolites of vitamin D are deficient.
Less commonly, a dietary deficiency of calcium or phosphorus may also produce rickets

45. Vitamin D-3 (cholecalciferol)
is formed in the skin from a derivative of cholesterol under the stimulus of ultraviolet-B light.
9/19/2018
Natural nutritional sources of
vitamin D are limited primarily
to fatty, ocean-going fish.

46. Source of vitamin D
Ultraviolet light
Cod liver oil
Ergosterol (vitamin D-2)
Dairy milk is fortified with vitamin D
(400 IU/L)
Human milk contains little vitamin D(less than IU/L)

47. Pathophysiology

48. Cholecalciferol (i.e., vitamin D-3) is formed in the skin from 5-dihydrotachysterol.
which circulates in the plasma as the most abundant of the vitamin D metabolites and is thought to be a good indicator of overall vitamin D status

49. This steroid undergoes hydroxylation in 2 steps.
The first hydroxylation
Occurs at position 25 in the liver, producing calcidiol (25- hydroxycholecalciferol)
*Calcidiol circulates in the plasma as the most abundant of the vitamin D metabolites and is thought to be a good indicator of overall vitamin D status

50. The second hydroxylation
Occurs in the kidney at the 1 position, where it undergoes hydroxylation to the active metabolite calcitriol
(1,25-dihydroxycholecalciferol )
This cholecalciferol, which circulates in the bloodstream in minute amounts, is not technically a vitamin but a hormone.

51. Calcitriol
Acts at 3 known sites to tightly regulate calcium metabolism:
it promotes absorption of calcium and phosphorus from the intestine
(2) it increases reabsorption of phosphate in the kidney
(3) it acts on bone to release
calcium and phosphate.

52. Epidemiology The frequency increasing internationally
1.Children to wear sunscreen while outdoors
2.Children spend more time indoors watching television or playing electronic games, instead of playing outdoors

53. Clinical Presentation

54. Knock knee deformity (genu valgum)
which circulates in the plasma as the most abundant of the vitamin D metabolites and is thought to be a good indicator of overall vitamin D status
Bowleg deformity (genu varum)

55. Wrist enlargement
Rib beading (rachitic rosary)

56. Frontal bossing
Tibial bowing

57. Scoliosis
Harrison's sulcus and pot belly

58. Approach Considerations
Serum measurements in the workup for rickets may include the following:
1.Calcium.2.Phosphorus.3.Alkaline phosphatase4.Parathyroidhormone 5.25-hydroxy vitamin D
6.1,25-dihydroxyvitamin D
Radiography is indicated in patients
with rickets
Infants who are breastfed are at risk for rickets, especially those who:
a. receive no oral supplementation
b. have darkly pigmented skin

59. Serum Chemistry
Calcium (ionized fraction) is low
Calcidiol (25-hydroxy vitamin D) is low
Parathyroid hormone is elevated
Phosphorus level is invariably low for age
Alkaline phosphatase levels
are uniformly elevated.

60. Radiography
Cupping of the metaphysis
Fraying of the edge
Widening of the osteoid tissue
Hypominiralization of bones

61. Anteroposterior and lateral radiographs of the wrist of an 8-year-old boy with rickets demonstrates cupping and fraying of the metaphyseal region.
Infants who are breastfed are at risk for rickets, especially those who:
a. receive no oral supplementation
b. have darkly pigmented skin

62. Radiograph in a 4-year-old girl with rickets depicts bowing of the legs caused by loading.

63. Treatment & Management
Treatment for rickets may be administered gradually over several months or in a single-day dose

64. If the gradual method is chosen, 125-250 mcg (5000-10,000 U) is given daily for 2-3 months until:
Healing is well established
Alkaline phosphatase concentration is approaching the reference range

65. In nutritional rickets: 1.Phosphorus level rises in 96 hrs
If the vitamin D dose is administered in a single day, it is usually divided into 4 or 6 oral doses. An intramuscular injection is also available
In nutritional rickets:
1.Phosphorus level rises in 96 hrs
2. Radiographic healing is visible in 6-7 days
Infants who are breastfed are at risk for rickets, especially those who:
a. receive no oral supplementation
b. have darkly pigmented skin

66. Rickets Medications
Vitamin D is a fat-soluble vitamin used to prevent or treat vitamin D deficiency

68. FOOD PYRAMID Fats, oils and sweets Use sparingly
Milk , yogurt and cheese group
2-3 servings
Meat, poultry,fish,dry beans eggs and nuts group
2-3 servings
Vegetable group
3-5 servings
Fruit group
2-4 servings
Bread,cereal,rice and pasta group
6-11 servings

69. Vitamin

70. VITAMINS
REQUIREMENT
SOURCES
FUNCTIONS
DEFICIENCY
Vitamin A
600 µg/day
Liver, Egg, Butter, Cheese, Fish, meat, Green leafy vegetables, papaya, mango.
Production of retinal pigments.
Support skeletal growth
Anti infective
Protect from cancers
Maintain integrity and function of granular and epithelial tissue
Night blindness
Conjunctival xerosis
Corneal ulceration
Keratomalacia
Vitamin D
2.5µg/day
Liver, Egg yolk, butter, cheese.
Promotes absorption and reabsorption of Ca and P.
Stimulates mineralization of bone
Enhances bone resorption
Permits normal growth
Rickets
Osteomalacia
Vitamin E
0.8mg/g of essential fatty acids
Vegetable oils, butter, egg yolk.
Antioxidant
Sterility
Hemolytic and hypo plastic anemia
Degenerative changes in muscles and heart.

71. VITAMINS
REQUIREMENTS
SOURCES
FUNCTIONS
DEFICIENCY
Vitamin K
0.03mg/kg/day
Fresh green leafy vegetables, cow’s milk, intestinal bacteria(K2)
Stimulate the production of coagulation factors.
Blood clotting time prolonged.
Bleeding
Prothrombin content of blood decreases.
Thiamine (Vit B1)
1.5mg/day
Whole grain cereals, wheat, gram, yeast, pulses, oil seeds, nuts, meat, fish egg.
Involved in direct oxidation pathway for glucose
Essential for utilization of carbohydrates.
Beriberi
Wernicke’s -encephalopathy opthalmoplegia polyneuritis, ataxia
Riboflavin (Vit B2)
0.6mg/1000kcal of energy
Milk, egg, liver, kidney, green leafy vegetables
Cellular oxidation
Co-factor
Angular stomatitis
Cheilosis
Glossitis

72. VITAMINS
REQUIREMENTS
SOURCES
FUNCTIONS
DEFICIENCY
Niacin
18mg/day
Liver, kidney, meat, fish, legumes, ground nut
Metabolism of carbohydrate, fat and proteins.
Normal functioning of skin, intestine, nervous system
Pellagra
Glossitis
Stomatitis
Pyridoxine (Vit B6)
2mg/day
Milk, liver, meat, egg yolk, fish, legumes, vegetables
Metabolism of amino acids fat, carbohydrates
Peripheral neuritis
Pantothenic acid
10mg/day
All foods
Biosynthesis of corticosteroids
Folate (Folacin and folic acid)
100µg/day
Liver, meat, dairy products, egg, milk, fruits , cereals
Synthesis of the nucleic acids
Normal development of blood cells in the marrow
Found during pregnancy and lactation- Megaloblastic anemia, Glossitis, Cheilosis, diarrhoea

73. VITAMINS
REQUIREMENTS
SOURCES
FUNCTIONS
DEFICIENCY
Vitamin B12
1µg/day
Liver, kidney, meat, fish, egg, milk, cheese
Synthesized by bacteria in the colon
Synthesis of fatty acids myelin
Synthesis of DNA along with Folate
Megaloblastic anemia (Pernicious anemia)
Demyelinating neurological lesions in the spinal cord
infertility
Vitamin C
60mg/day
Fresh fruits, green leafy vegetables, germinating pulses
Formation of collagen
Tissue oxidation
Formation of hemoglobin
Absorption of iron from the intestinal wall.
Scurvy- Swollen bleeding gums, subcutaneous bruising into the skin and joints, anemia and weakness

75. Protein – energy malnutrition
1- Marasmus
Definition:
It is a clinical syndrome and a form of under nutrition characterized by failure to gain weight due to inadequate caloric intake.
Incidence:
commonly in infants between the age of 6mo. - 2years (Infantile atrophy).

76. Assessment of Marasmic Child/Infant
failure a to thrive ,loss of weight (weight < 60%of expected)
loss of subcutaneous fat : measured at many parts of the body according to the degress:-
1 st degree : s.c fat in the abd. wall
2 nd degree : s.c fat in the abd. wall and limbs
3 rd degree : s.c fat in the abd. wall and limbs and face

77. Assessment of Marasmic Child/Infant (Cont.)
Muscle wasting ( thin muscles and prominence of bony surfaces )
G.I.T disturbances as anorexia in advanced cases, hungry, constipation or diarrhea or starvation diarrhea
liability to infection
Hypovolemia
Weak feeble pulse, subnormal temp, pulse rate
Senile face and pallor

78. Complications of Marasmus
Intercurrent infection : Broncho pneumonia . is the cause of death
Gastro enteritis
Hemorrhagic tendency, purpura
Hypothermia
Hypoglycemia
Edema(marasmic kwashiorkor )

79. Investigations for Marasmic Infant
1.Blood analysis : (W.B.C ,Electrolytes Sugars, ketones,Plasma proteins , normal or lowered )
2. Urire analysis: culture, sugar, ketones, ca, phosphate, aminoacids
3.Stool analysis for parasites
4. X- ray for chest and heart
5. Tuberculin test for T.B
6. E.N.T examination for otitis media

80. Treatment 1- Prevention :- proper diet ( balanced nutritional diet )
encourage breast feeding up to weaning
proper weaning
proper vaccination as measles , T.B. whooping cough
Education regarding the cheap sources of balanced diet, family planning.
Proper follow up of the growth rate
Early treatment of defects or associated diseases

81. Treatment (Cont.) 2 – Curative treatment:-
A- Proper dietary management:-
Adequate balanced feeding. teaching about nutritional needs.preparation of diet, technique of administration of food
If there is vomiting or anorexia, give IV fluids or naso gastric tube feeding.
Gradual increase the amount and concentration of formula (total calories is cal kg d)
B – Treatment of the cause
C- Emergency treatment for complications
D – Blood transfusion
E – Vitamins and minerals supplementation

82. Kwashiorkor
Definition It is a clinical syndrome and a form of malnutrition characterized by slow rate of growth due to deficient of protein intake, high CHO diet and vitamins & minerals deficiency (adequate supply of calories). Incidence Commonly in toddlers between the age 1- 3years, following or with weaning

83. Etiology Un balanced diet (of protein, CHO.)
improper weaning (during and post weaning period )
faulty management of marasmic baby
Ignorance poverty due to lack of basic health education
precipitating factors as(acute infection with measles, diarrhea and malaria, parasitic infestations)

84. Assessment Edema : Growth retardation :-
1- Essential features (cardinal manifestation):
Growth retardation :-
Weight is diminished (60-80%) of expected
Edema :
It is due to hypo proteinemia. It is starts in the feet and lower parts of the legs) then becomes generalized edema . The cheeks become bulky, pale, waxy in appearance (doll-like- cheeks)

85. 1- Essential features - Diminished muscle fat ratio:
Generalized (muscle wasting) with subcutaneous fat
- Fatty liver :
It is detected by liver biopsy
- Mental changes :
The infant has apathy never smile, looks sad his cry is weak

86. 2-Early features (usual manifestation)
Hair changes : The hair is sparse , dys pigmentation( reddish or greyish),atrophic ,easily pickable.
G.I.T Manifestations: Anorexia ,vomiting in severe cases, diarrhea due to k

87. 3-Occasional or variable features
- Vitamins and minerals defection and vit.D , A,C minerals as iron, zinc, Mg,
Hepatomegaly.
Skin changes (dermatitis in areas due to pigmentation ,napkin dermatitis, petechiae over the abdomen, fissures,ulceration
Poor resistance and liability to infections

88. Complication of kwashiorkor
Secondary infection ,fungal and bacterial infection
Hemorrhagic tendency, purpura
Gastroenteritis
Hypoglycemia
Hypothermia
Heart failure due to anemia and infection.

89. Investigations for kwashiorkor
9/19/2018
1. Blood analysis: (Albumin < 2.5gmld) , total protein, amino acids, Enzymes (amylase ,lipase, alkaline phosphate, , Glucose (hypoglycemia) , k ( hypokalemia )
2. Low pancreatic and intestinal enzymes
3. Urine analysis, culture for infection
4. Stool analysis for parasites
5. Chest x-ray
6. Tuberculin test

90. Thank you