Childhood Nutritional disorder Dr. Aziza Aljohany

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.

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.

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.

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 )

Childhood Iron Deficiency Anemia

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

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

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.

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

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

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

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

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

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

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)

Iron cycle

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

Factors Contribute To the Development Of Anemia

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

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

Iron deficiency Anemia Clinical Manifestation Pallor is the most important sign Mild to Moderate iron deficiency ( hemoglobin levels of 6 -10 g/dL) few symptoms of anemia; irritable, Pagophagia Severe iron deficiency Irritability , Anorexia, Tachycardia, Cardiac dilation, Systolic murmurs Iron deficiency Anemia (cont.) Clinical Manifestation

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.)

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

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

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

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

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)

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

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)

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

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

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.)

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

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

Responses to iron therapy in iron- deficiency anemia Time after Iron Administration Response 12 -24 hr Subjective improvement; decreased irritability, increased appetite 36 -48 hr Initial bone marrow response 48 -72 hr Reticulocytosis, peak at 5 -7 days 4 -30 days Increase in hemoglobin level 1 -3 mo Repletion of stores

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

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

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

Rickets

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.

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

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.

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 20-40 IU/L)

Pathophysiology

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

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

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.

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.

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

Clinical Presentation

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)

Wrist enlargement Rib beading (rachitic rosary)

Frontal bossing Tibial bowing

Scoliosis Harrison's sulcus and pot belly

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

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.

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

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

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

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

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

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

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

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

Vitamin

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.

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

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

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

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).

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

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

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

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

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

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 is120-200cal kg d) B – Treatment of the cause C- Emergency treatment for complications D – Blood transfusion E – Vitamins and minerals supplementation

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

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)

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)

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

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

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

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

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

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