1. MALNUTRITION
INTRODUCTION
According to the World Health Organization (WHO), malnutrition is the gravest
single threat to global public health. Malnutrition is a broad term which refers to
both undernutrition and overnutrition. Individuals are malnourished, or suffer from
undernutrition if their diet does not provide them with adequate calories and protein
for maintenance and growth, or they cannot fully utilize the food they eat due to
illness. People are also malnourished, or suffer from overnutrition if they consume too
many calories.
Definition
Malnutrition can be defined as the insufficient, excessive or imbalanced
consumption of nutrients. Several different nutrition disorders may develop,
depending on which nutrients are lacking or consumed in excess.
Epidemiology
The World Bank estimates that India is ranked 2nd in the world of the number
of children suffering from malnutrition, after Bangladesh (in 1998), where 47% of the
children exhibit a degree of malnutrition. The UN estimates that 2.1 million Indian
children die before reaching the age of 5 every year – four every minute – mostly from
preventable illnesses such as diarrhoea, typhoid, malaria, measles and pneumonia.
Every day, 1,000 Indian children die because of diarrhoea alone.The 2011 Global
Hunger Index Report ranked India 15th, amongst leading countries
with hunger situation. At the same time as a large number of population suffers
from malnutrition, more than 100 million people (11% of Indian population) in India
are overnourished.

2. Etiology
Lack of knowledge-People do not understand the nutritional nature of their
Child‘s health problem
Poverty- lack of means to obtain and provide food to their child (as in the case
of war)
Famine and vulnerability-destitution, being orphan (Example HIV taking away
parents Lives)
Infections- there is a reciprocal relationship between malnutrition and infection.
During infection, the requirement for nutrients increases, there will be
increased loss of nutrients due to diarrhea genesis of fever and other acute phase
reactants is atthe expense of nutrients.
Emotional deprivation- In orphan children and in children whose parents are
negligent in giving careto their children, due to different reasons, children will
lose appetite for feeding and hence end upin state of malnutrition
Cultural factors- Different biases as to who should take the lion‘s share of the
family ‗s food (Example, age bias—older children are given more food than the
smaller ones,
Sex bias—male children are more favored in getting nutritious food than female
children in some families, etc.)
Mal-distribution of foodstuffs- within the family, it occurs between the different
ages and sexes dueto biases, food prejudices and taboos. It also occurs between
the different regions of a country because of inappropriate
Food and nutrition policy, poor marketing and distribution system due to
different reasons like embargo,country under-siege
PEM
Protein Energy Malnutrition (PEM) is a malnutrition resulting from the
deficiency of protein and/or energy in diet. PEM is an important nutritional problem

3. among preschool age children. This leads to various degrees of growth retardation.
When growth retardation is severe, functional deficiencies, like resistance to
infection and poor intellectual development may result. The main cause of PEM is
food inadequacy.
Epidemiology:
PEM characteristically occurs in children less than 5 years of age, whenever the
diet is poor in energy and proteins.
Etiology
PEM was earlier attributed to the concept of ‗protein gap‘ (deficiency of proteins in
diet), which has now given way to the new etiological theory of ‗Food gap‘, wherein it
is not only the deficiency of proteins but inappropriate food (low in energy density,
protein and micronutrients - Vitamin A, Iron, Zinc) which is poor both quantitatively
and qualitatively, is the chief cause of PEM.
Under-nutrition in fetal life, esp. last trimester.
Lactationfailure.
Low energy dense weaning foods.
Incorrectly constituted formula.
Contaminated water and infections.
Classification of PEM :
Even though Marasmus and Kwashiorkor are the two main and polar forms of
PEM, clinically it can be broadly classified into five forms.
Classification of PEM (FAO/WHO)
Type Percent of
standard body
weight
Oedema Deficit in
weight for
height
Kwashiorkor 80-60 + +

4. Marasmic-
Kwashiorkor
<60 + ++
Marasmus <60 0 ++
Dwarfing <60 0 Minimal
Underweight 80-60 0 +
Assessment of Nutritional Status
Nutritional Status Assessment
Anthropometry
Biochemical & lab methods
Clinical assessment
Diet survey
Ecological studies
Functional assessment
Vital statistics
Classification of Nutritional Status Based on Anthropometric
Parameters Weight for age : There are standard weights laid down for a
particular age. Thus a given child‘s weight (for his particular age), is compared to the
‗standard‘ weight of a ‗normal‘ child.
Gomez classification:
The Gomez classification is one of the commonest classifications used to
classify malnourishment into various grades

5. Weight of 'normal child' of sameage
X100Weight for age (%)= Weight of child
The Indian Academy of Paediatrics (IAP) classification on the other hand puts the
degree of malnutrition into four grades .This classification is used by the ICDS in
India.
Weight for height : The weight for height classification doesn‘t take age into
consideration. Weight is also related to height. Many a times age is not known.
Wasting and Stunting : In the Waterlow classification weight for height and height
for age are used to classify children as normal, wasted, stunted and wasted and
Gomez Classification
Malnutrition
grade
Weight/Age (%) of normal
Normal >90%
Grade I (Mild) 75 – 89 %
Grade II
(Moderate)
60 – 74 %
Grade III
(Severe)
< 60 %
Indian Academy of Paediatrics (IAP)
Classification Malnutrition grade Weight/Age (%) of
normal
Normal > 80%
I Grade 70-80%
II Grade 60-70%
III Grade 50-60%
IV Grade <50

6. stunted. Children with low weight for height are considered as wasted and those with
low height are ‗stunted‘.
Wasting and Stunting - Waterlow classification
Weight for height Height for age Nutritional status Interpretation
Normal Normal Normal Normal
Low Normal Wasted Acute malnutrition
Normal Low Stunted Nutritional dwarf
Low Low Wasted and stunted Acute or Chronic
malnutrition
Marasmus
Marasmus is a form of severe malnutrition characterized by energy deficiency.
A child with marasmus looks emaciated. Body weight may be reduced to less than
80% of the average weight that corresponds to the height.
Clinical features of Marasmus
Diarrhoea is frequent with acid stools. Many infants are hungry but some are
anorexic.
There is often dehydration. Weight is much below standard for age.
Temperature may be subnormal
The abdomen may be shrunken or distended with gas
Peristalsis may be easily visible because of thinness of abdominal wall
The muscles are weak and atrophic.
There is loss of subcutaneous fat.
The skin and mucus membranes are dry and atrophic
Psychological disturbances resulting from a lack of mother‘s care, can depress
the appetite.
Growth retardation
‗Wisened old man‘s look.

7. Hair changes like easily pluckable hair
Infection
Vitamin deficiency
Kwashiorkor
The term Kwashiorkor was introduced by Cicely Williams into modern
medicine. It comes from language of ‗Ga‘ tribe of Ghana, meaning ―Sickness the older
child gets when the next baby is born‖.while marasmus is seen in an early and
abruptly weaned baby in an urban setting, the other ‗pole‘ of PEM, Kwashiorkor is
typical in an older child who is breast fed for a rather prolonged period and weaned
late in a rural setting. Poverty, insufficient food and land, poor agricultural practice.
Clinical features of Kwashiorkor
(i) There are oedema, anorexia, diarrhoea and apathy
(ii) Failure of growth is an early sign. Oedema is more marked in the lower limbs.
(iii) The characteristic dermatosis consist of areas of both hypo-and
hyperpigmentation the first becomes thickened as if varnished lie then peels and
appears like "flaky paint" leaving cracks or denuded areas of shallow ulceration In
modera te cases the derrnatosis resembles crazy paling; when severe, the
desquamated part looks as if there has been a burn. The lower limbs, buttocks and
perenium are usually most affected but ulcers can occur over pressure points and
deep cracks in skin folds.
(iv) The hair is sparse. There maybe changes in pigmentation with diffuse patches
or streaks which maybe red or grey in colour. ;
(v)Some degree of anemia is always present and may be severeapathy is a
characteristic feature and child appears constantly unhappy.Many patients show a
mixture of some of as of both marasmus kwashiorkor and die and are said to have
marasmic kwashiorkor

8. (vi)Some children adapt to prolonged insuffi cient food by a marked retardation of
growth they resemble children a year or more youngermuscles are always wasted
so as children may no longer be able to walk or stand.
Biochemical and metabolic disorders
(i) High body water content, loss of the fat and loss of protein from the wasted
muscles
(ii) Plasma concentrations of essential aminoaciids especially branched chain
amino acids andwith protein, the concentration of amino acids in the plasma rise.
(iii) The plasma concentrations of some enzymes such as cholinesterase, alkaline
phosphatase, amyease, and lipase are lowered.
(iv)The blood urea is usually low and may fall to 6g/100 ml
(v)The plasma albumin level is low owing to a failure of synthesis in the liver In
severe cases, it is Dually below 20 and sometimes below 10 g/I. ply a IgG is often
raised if infections are present but over immunoglobulins are usually normal baa
transferrin is lowered, especially in severe cases, and may be a better guide to
prognosis than Plasma albumins
(vi) I here is fatty liver And the excess of fat in the liver is triglyceride. Plasma
triglyceride and cholesterol are low due to it decreased ability of the liver cells to
mobilize lipid ,~ the form of lipoproteins
(vii) Blood glucose is usually normal. Hypoglycemia may occur and is a
complicated matter to be kept in mind.
(viii) Plasma potassium level is below normal due to diarrhoea. Plasma magnesium
level is also low due to increased losses in the stools
(ix) Plasma [H+] may be either raised or lowered
(x) The total body water may increase from 60 per cent to 80 per cent. The severity
of clinical oedema is not closely associated with the size of the increase in total
body water or with the level of plasma albumin. The cause and nature of the oedema
still reforms in part a mystery.

9. (xi) Malnourished children are likely to have infections and may have complications
requiring drug treatment Some antibiotics and antimalarials act by interfering with
nutrition more in the microorganism than in the human host, and they need to be
used with care in Protein Energy Malnutrition (PEM). The antibiotics streptomycin,
chloramphenicol and the tetracyclines inhibit protein synthesis by interfering with
the action of messenger or transfer RNA.
All drugs should be used with caution.
Changes in organ system.
There is atrophy of cells of pancreas and intestinal mucosa.
Plasma concentration of Gh may be raised. Plasma concentration of cortisol is
normal, and plasma thyroxine is often low.
Lymphoid tissues atrophy.
There is atrophy of heart.
There is enlarged fatty liver.
Case Management
Management of a case of PEM focuses on the correction of specific nutrient
deficiencies (dietary management), treatment of complications and supper imposed
infections. The treatment approach is classified into two phases—The acute
stabilization phase in which the main focus is treatment of infection and other
complications like dehydration, hypoglycemia, hypothermia and other electrolyte
imbalances. The rehabilitation phase focuses on the restoration of the lost tissue and
promotion of catch up growth.
Dietary Management
1. Acute Phase
Children are most at risk of dying during the acute phase. Dehydration, infection and
severe anemia are the main dangers. In PEM, cardiac and renal functions are impaired
and in particular malnourished children havea reduced capacity to excrete excess

10. water and a marked inabilityto excrete Sodium. The amount of fluid given and the
Sodium load must be carefully controlled to avoid cardiac failure. A cautious approach
is required aiming at administration of about 100kcal/kg/day and 1-1.15g of
protein/kg/day. Small frequent feeds (as much as 12 times in 24 hours for the first two
days and gradually tapering the number of feeds to be 6 in 24 hours after a week) are
ideal as they reduce the risks of diarrhea, vomiting, hypoglycemia and hypothermia.
Schedule for Oral Feeding in the First Week
Day Number of
Feeds/per day
Volume per
feed (Ml/Kg)
Energy
Kcal/kg/day
Protein
Gram/kg/Day
1-2 12 11
3-5 8 16 100 1.0
6-7 6 22
The maintenance formula can be made as follows:
25 gram of Dried skimmed milk (DSM)
100 gram of Sugar
30 gram of Oil per 1000ml
Gives
75 Kcal and 0.9 gram of protein per each 100 ml
It is important to give additional Potassium 4mmol/kg/d, Magnesium 2mmol/kg/d,
Zinc 2mg/kg/d), Copper 0.2mg/kg/d and a multivitamin preparation and folic acid. Do
NOT give ironearly before infection is controlled. High dose vitamin A should be
given even if there are no eye signs of deficiency.
Rehabilitation Phase
The aim of this phase is to restore wasted tissues and promote a rapid rate ofcatch-up
growth through administration of high energy and protein. A vigorousapproach is
required. In this phase there is no danger of recovery syndrome.

11. The synthesis of new tissue requires protein and other nutrients. Synthesis alsorequires
a considerable amountof energy.
Normal rate of growth of children is such that they gain a weight of 1gram/kg/day by
taking 105 kcal/kg/d and
0.78gram of protein /kg/d. Toincrease this rate of growth by 20 times the normal, the
energy and protein intakes need to be increased to 200kcal/kg/day and 5kcal/kg/day,
respectively.
Modification of differentmilks to provide 1 literof high-energy formula
Milk (g) Sugar (g)Vegetable oil (g)
Dried skimmed milk 80 50 60
Whole dried milk 110 50 30
Liquid cow's milk900 50 30
The formulas above provide 100kcal and 3g protein/100ml.
Health promotion
(a) Good ante-natal care
(b) Education on food, hygiene and family planning
(c) Education on the importance of colostrum, diet duringlactation
(d) Various measures under the ICDS initiative, like goodnutrition, immunization,
education, hygiene and sanitation
(e) Promotion of breast feeding
(f) Good weaning practices, correct time of weaning,importance of low cost weaning
foods
(g) Prevention and control of infections during weaning
(h) Improve family diet
(j) Correct knowledge on balanced diet
(k) Utilization of family planning practices

12. (l) Hygiene & sanitation
Specific protection
Diet : Protein and energy rich food should be consumed bychildren. Special attention
must be paid to diet during weaning.Adequate quantities of fruits and vegetables must
be includedin the diet.
Immunization : The child must be immunized as per thenational schedule.
Growth monitoring : Vulnerable children must beidentified. Children must be
monitored through growth charts.Early diagnosis of growth failure must be done and
treated as appropriate
Early diagnosis and treatment : Early diagnosis and treatment of infections is also
vital. To achieve this, healthworker must be alert and mothers should be aware of the
signs and symptoms of common infections. Preparation and use ofORS should be
known to all mothers. The services availablethrough the IMNCI initiative must be
fully utilized.
Medical advice : In extreme and serious cases early medicaladvice and treatment
facilities must be available. Hospitalizationof the case remains the only choice in
complicated cases.
Residential Units : Mothers are admitted with their sick children. The mother gets
hands on experience in the practical learning of preparation and administration of a
therapeutic diet for her child with an expert. This demonstration and involvement of
the mother in her child‘s recovery goes a long way in understanding the problem and
mitigating it.
Day Care Centre : The mother attends the day care centre along with the child where
cooking and feeding is taught to the mother. While the child attends every day,
involvement of the mother is partial.
Domicilliary Rehabilitation : The expert comes home and assesses the situation as a
whole. The mother is then rendered suitable advice with regards not only to feeding
but also about improving various domestic contributory factors to PEM.

13. Responsibilities of Public Health Nurse in
Managing PEM
The nursing management of PEM consists of providing nutrition rich in the essential
nutrients to correct the dietary insufficiency and to promote normal growth and
development. The digestivecapacity of malnourished child is initially poor. As a result
oral feedings are given in small frequent amounts, limited in proteins and
carbohydrates especially fats that are hard to digest.
In addition, the nurse is responsible for:
1. Maintaining the child‘s body temperature within a normal range.
2. Providing periods of rest and appropriate activity.
3. Providing stimulation.
4. Recording intake, output and daily weight.
5. Turning position in bed frequently.
6. Preventing bedsore and infection by keeping the skin clean and dry.
7. Providing appropriate treatment of bedsore and oral thrush if any.
8. Administering iron and folic acid to correct the accompanying anemia.
9. Diluting liquid iron preparations and giving through a straw to prevent staining of
tooth enamel.
Signs and symptoms
Initially the infant is usually of normal appearance with varying degrees of
constipation,occasional vomiting, crying and restlessness. The disease usually
presents with generalized oedema,dyspnoea, cardiac disturbance, gastrointestinal
derangements, and oliguria.
Types
Pure cardiologic or pernicious form
The infant shows signs of cyanosis and an acute cardiac attack can follow with
the infant usually dying within 2 to 4 hours. The common age for this form of the
deficiency disease is one month up through the third month. It has been reported that
this type of deficiency responds very dramatically to thiamine.

14. Aphonic form
A milder form of infantile beriberi which causes a typical loss of voice due to
paresis or even paralysis of the vocal cords due to neuritis is more frequent in the age
group 4 to 6 months..
Pseudo meningitic form
Older infants (7 to 9 months), in particular, may manifest symptoms that can be
mistaken for bacterial meningitis eg. stiffness of neck and other apparent signs of
meningeal irritation accompanied by vomiting, convulsions and sweating.
Treatment
Infantile thiamine deficiency:
If severe heart failure, convulsions or coma occur, 25–50 mg of thiamine should be
given veryslowly intravenously, followed by a daily intramuscular dose of 10 mg for
about a week. Thisshould then be followed by 3-5 mg of thiamine per day orally for at
least 6 weeks.
Sources
Asparagus is an excellent source of vitamin B1. Very good sources of vitamin
B1 include mushrooms, spinach, flaxseeds, tuna, green peas, and Brussels sprouts.
RIBOFLAVIN
Riboflavin deficiency is rare.Diagnosis of riboflavin deficiency is made
clinically and dramatic improvement is seen on supplementation with Vitamin B2.
Deficiency
Deficiency of riboflavin leads s glossitis ,cheliosis and ulcers over the cornea
with watering of eyes photophobia and blurring of vision. If the pregnant woman is
riboflavin deficient, growth and development of the baby is affected.
Niacin
It is also known as anti pellagra vitamin.

15. Deficiency
Deficiency of niacin is more prevalent in maize eating population. Pellagra is
characterized by diarrhea, skin rash and mental deterioration with muscle weakness
and loss of memory. Skin rash occurs predominantly in sun-exposed areas such as
neck and back of hands leading to pigmented, scaly and cracked skin.
Treatment
Provision of a high-protein diet and B-complex vitamins is needed for complete
restoration of health.
Pyridoxine
Dietary deficiency of pyridoxine is rare.
Deficiency
Deficiency of pyridoxine usually occurs due to genetically inherited absence of
an enzyme or secondary to some drugs such as prolonged use of Isoniazid Cycloserine
Hydralazine D-penicillamine pyrazinamide
Symptoms
Deficiency of pyridoxine leads to irritability, anemia , Hyperacusia, nausea, vomiting,
seizures and wasting or loss of weight. Older children may develop neuritis.
Pyridoxine deficiency can lead to persistent convulsions in an infant
Treatment
Infants respond to intravenous pyridoxine dramatically.
Vitamin B12
Vitamin B12 is essential for the formation of red blood cells and deficiency of
Vitamin B12 anemia.
Deficiency
Vitamin B12 deficiency can also lead to anemia, paralysis and weakness of the
limbs due to involvement of the nerves in the spinal cord. Dietary deficiency of
Vitamin B12 is rare and is usually seen in children on exclusive vegetarian diet with

16. inadequate intake of milk . Also deficiency of Vitamin B12 is seen in patients with
due to absence of a factor called as 'Intrinsic Factor' in the stomach
Treatment
Cobalamin is available in a solution for injection in doses ranging from 100 to
1000 mcg. Most of the injected doses in excess of 50 mcg are rapidly excreted in the
urine. Thus, when therapy is started, repeated doses are recommended in order to
replenish body store.Oral pills in dose of 1000-2000mcg Can be given.
FOLATE(Vit B9)
Helps the body make red blood cells, break down protein, keeps heart healthy.
Makes DNA
Deficiency
Responsible for neural tube defects .anemia, red tongue.
Cerebral folate deficiency presents within 4–6 mo of age with irritability,
microcephaly, developmental delay, cerebellar ataxia, pyramidal tract signs,
choreoathetosis, ballismus, and seizures.
Hereditary folate malabsorption presents within 1–3 mo of age with recurrent or
chronic diarrhea, failure to thrive, oral ulcerations, neurologic deterioration, and
megaloblastic anemia and recurrent infections.
Treatment
Oral folic acid corrects the low CSF folate levels and improves the clinical
manifestations.
Pregnant women must be given folate supplements.
Vitamin C
Deficiency of vitamin c causes scurvy.
Presentation
Infantile scurvy is uncommon before age 7 months. Early clinical
manifestations consist of pallor, irritability, and poor weight gain. In advanced

17. infantile scurvy, the major clinical manifestation is extreme pain and tenderness of the
arms and, particularly, the legs. The baby is miserable and tends to remain in a
characteristic immobilized posture from subperiosteal pain, with semiflexion of the
hips and the knees.
Treatment
Treatment of Vitamin C deficiency consists of high doses of Vitamin C either
through mouth or injection for several weeks. Children should consume a diet rich in
Vitamin C to avoid further deficiency.
FAT SOLUBLE VITAMINS
Vitamin A deficiency
Vitamin A Deficiency (VAD) is the leading cause of preventable blindness in
children. It also increases the risk of disease and death from severe infections
Etiological Factors :
Vitamin A deficiency is most common in the age group of 1 to 3 years, the
preschool children. It resultsfrom a very complex web of causation involving
ignorance,poverty, infections, lack of food, malnutrition, environmental and social
factors.
SYMPTOMS
Night Blindness
Conjunctival Xerosis
Bitot’s spots
Corneal xerosis
Extra - ocular manifestations : Some extra-ocular manifestations of vitamin A
deficiency are also known. Follicular hyperkeratosis, growth retardation and
anorexia are some of them.
Treatment of Xerophthalmia:
An established case of xerophthalmia responds well to treatment with vitamin
A. The following regime can be followed :

18. 2,00,000 IU (110mg) of Retinol palmitate (oil miscible vitamin A) is administered
orally for 2 days. In cases of persistent vomiting/diarrhoea, water miscible vitamin A
1,00.000 IU is administered as IM Injection, followed by 2,00,000 IU, 1 to 4 weeks
later.
For infants less than 1 year old or less than 8 Kg weight, half the dose is used.
Prevention
Dietary modifications should be achieved through promotion of growth,
production and consumption of vitamin A / beta-carotene rich foods
Nutrition education: Educate the community on the importance of vitamin rich
diet, its regular intake and the harmful effects of its deficiency.
Fortificationof ghee, hydrogenated vegetable oil and butter are being done as a
government policy to augment the vitamin A status of the community.
Technology for the fortification of sugar, mono sodium glutamate, bread and
milk also exists.
Periodic massive dosage: Vitamin A administration is now integrated with
immunization program. The first dose of 100,000 IU is given at 9 months of age
along with measles vaccines. Thereafter, the second and subsequent doses of
200,000 IU are given at 6 monthly intervals till 3 years of age. In all, a total
dose of 9,00,000 IU is administered.
Vitamin D
Essential for formation of bones and teeth. Helps the body absorbs and usecalcium.
Symptoms
In infancy and childhood deficiency of Vitamin D causes deformed bones
characteristic of rickets
Treatment
Rickets and osteomalacia are almost always treated with oral supplements of
vitamin D, with the recommendation to acquire daily exposure to direct
sunlight. An alternative to sunlight is the use of an ultraviolet (UV) lamp.

19. Rickets heals promptly with 4,000 IU of oral vita-min D per day administered
for approximately one month.
Vitamin E deficiency
Definition
Vitamin E deficiency is a very rare problem that results in damage to nerves
Epidemiology
Premature, very low birth infants (birth weight less 1500 gms or 3 pounds 4 ounce) are
risk of vitamin E deficiency
SYMPTOMS
Vitamin E Deficiency Symptoms in Infants include:
Retrolental fibroplasia (an eye disease) in premature infants
Loss of weight and delayed growth
Poor feeding habits
Developmental problems that include physical and mental problems
Vitamin E Deficiency Symptoms in Children:
Chronic cholestatic hepatobiliary disease (liver disease) causing neurological
deficits
Spinocerebellar ataxia (gross lack of coordination of muscle movements) with
loss of deep tendon reflexes
Loss of vibration and position senses
Ophthalmoplegia (paralysis of extra-ocular muscles responsible for eye
movements)
Muscle weakness
Ptosis (drooping upper eyelid)
Dysarthria (motor speech disorder)
Slow growth in children

20. Vitamin E deficiency that occurs with cholestatic liver disease, or other malabsorption
syndromes, can betreated with weekly injections of 100 mg alpha-tocopherol that may
continue for few weeks.
VITAMIN K
Causes
Newborns are especially prone to vitamin K deficiency. A nursing-mother‘s
milk is low in the vitaminbreast milk can supply only about 20% of the
infant‘srequirement. Infants are born with low levels of vitamin K in their body; they
do not have any vitamin K-producing bacteria in their intestines.
SYMPTOMS
As a result, a form of vitamin K deficiency, called hemorrhagic disease of the
newborn, may develop. This disease involves spontaneous bleeding beneath the skin
or muscle hematoma and hematuria , and occurs in about 1% of all infants. In rare
cases, it causes death due bleeding in the brain.
TREATMENT
Vitamin K deficiency in newborn infants is treated and prevented with a single
injection of phylloquinone (5mg).
MINERALS
CALCIUM
Deficiency of calcium causes Rickets and tetany .
Rickets
The characteristic signs of rickets are a protruding abdomen, beaded ribs
(rachitic rosary), bowed legs, knock knees, cranial bossing , pigeon chest and an
enlargement of the epiphyses.

21. Tetany
Muscle tone decreases and become flabby.It affects hand feet and the face.
Sources of calcium
Richest source: Milk and cheese
Good source: Figs asparagus nuts figs beans cauliflower cabbage and asparagus
Daily requirement:
Infants under one year: 360-540mg
Children 1-18yrs: 0.8-1.2 mg
IRON
Iron deficiency is one of the most common vitamin or mineral deficiencies in
the world, affecting 20% or more of women and children especially in developing
countries. Adolescent women who have started menses or who are pregnant are
particularly at risk for developing iron deficiency.
DIAGNOSIS
Anemia ,low hemoglobin or red cell volume may lead to reduced school and
work performance and may affect cognitive function, as well as leadingto
cardiovascular and growth problems. Diagnosis is made most simply by hemoglobin
level or hematocrit and red cell morphology.
ETIOLOGY
A variety of etiologies exist for anemia, including dietary deficiencies of folate
or vitamin B12, infections and inflammatory states , and conditions that result in
insufficient production of red blood cells or excessive destruction of red blood cells.
In INFANTS
The iron content of a newborn infant is approximately 75 mg/kg body weight,
and much of this ironis found in hemoglobin. The body iron of the new-born is
derived from maternal–fetal iron transfer,80% of which occurs during the third
trimester ofpregnancy. Preterm infants, with less opportunity toestablish iron stores,
have a substantially reducedendowment of body iron at birth than term infants.

22. Adolescence
Adolescents have very high iron requirements, and the iron demand of
individual children during periods of rapid growth is highly variable and may exceed
mean estimated requirements. Boys going through puberty experience a large increase
in erythrocyte mass and hemoglobin concentration. The addition of menstrual iron loss
to the iron demand for growth leads to particularly high iron requirements for pre and
postmenarchal adolescent girls.
Causes of Anaemia
Inadequate intake of iron
Poor diet
Poverty
Ignorance
Inadequate folate/vitamin C intake
Poor absorption and bioavailability
Absorption Only 5%
Poor absorption-Non haeme iron
Inhibitors: Phosphates, phytates,oxalates,fibre
Tea (tannin), Eggs (Phosphate), Milk (Calcium)
Excessive loss of iron
Normal man (1mg/day)
Menstruation (2mg/day)
IUDs
Intestinal worms
Malaria
Repeated / frequent pregnancies
Increased demand of iron
Pregnancy
Growth

23. Prevention and Control of Anaemia
1. Breastfeeding and appropriate weaning
2. Dietary modification
3. Deworming
4. Control of infection
5. Supplementation
6. Iron Fortification
7. Nutrition education
8. Home gardening
9. Care of pregnant and lactating women
Daily requirements of iron:
Infants 10-15 mg
1-3yrs 15mg
4-10yrs 10mg
11-18yrs 18mg
Management
Premature neonates:
2 to 4 mg elemental iron/kg/day divided every 12 to 24 hours maximum daily dose
= 15 mg
Infants and children less than 12 years:
Prophylaxis: 1 to 2 mg elemental iron/kg/day maximum 15 mg in 1 to 2 divided
doses.
Mild to moderate iron deficiency anemia:
3 mg elemental iron/kg/day in 1 to 2 divided doses.
Severe iron deficiency anemia:
4 to 6 mg elemental iron/kg/day in 3 divided doses.

24. FLUORINE
Fluorine Excess (Fluorosis) : Ingestion of large amounts of fluorine occurs
when the drinking water contains fluorine in excess of 3-5 ppm.
SYMPTOMS
Fluorosis presents as dental or skeletal fluorosis, depending on the water content
of fluorine, duration and level of exposure.
Dental fluorosis
If exposure takes place during calcification of teeth (first 7 years of life), the
teeth are more likely to get affected by fluorosis. The mottling of teeth is common.
The enamel loses its lustre and the texture becomes rough. There could be brown
bands alternating with white chalky patches. Mottling may progress to small pits.
Upper incisors are affected the most, even though all the teeth are vulnerable.
Skeletal Fluorosis and Fluoride Poisoning :
When the concentration of fluorine exceeds 10 ppm, a crippling skeletal fluorosis
may ensue There may be sclerosis of spine, pelvis and limbs. The ligaments of spine
may be calcified, producing a poker back.The tendinous insertion of muscles may be
ossified, producing the characteristic rose thorn shadow in the X-Ray.
Fluorine Deficiency
It causes dental daries
Prevention
Reduction of sugar intake
Dental hygiene
Fluoridation of water
COPPER
Deficiency Causes:
Myelopathy- Sufferers typically present difficulty walking aused by sensory ataxia
Neutropenia-Causing defective immune systems
Skeletal changes Fractures

25. Anemia
Daily requirements:
Infants and children:0.05mg/kg
Sources:
Liver Kidney other meats shellfish nuts and dried legumes
ZINC
Deficiency of zinc causes hypogonadism and dwarfism
There is loss of taste acuity
Hypogeusia
Anorexia
Hepatosplenomegaly
Delayed closure of epiphyses
Anemia
Daily requirement
Breast fed new born: 0.7-5mg
Infants: 3-5mg
Children 10mg
Adolescents 13mg
Sources of Zinc
Rich sources: Oysters and herrings
Good sources: Meat eggs liver and milk
Fair sources :Cereals pulses nuts vegetables and fruits
IODINE
Deficiency of iodine causes cretinism in children.
Abortions, stillbirths and congenital anomalies and mental/physical
underdevelopment. If iodine deficiency occurs during the most critical period of brain

26. development from the fetal stage up to the third month after birth, the resulting thyroid
failure will lead to irreversible alterations in brain function.
Food Rich in Iodine
Marine vegetation,sea foods, fruits grown on the seaboard.
Prevention
1. Use of Iodized salt or oil
2. Iodine monitoring
3. Manpower training
4. Mass communication