Malnutrition 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 and have severe long term
consequences (Marasmus).

Children who are over nourished may become

over weight or obese (Obesity, Hypervitaminoses).
 Other Perinatal
Deaths associated 25% 23%
with Under-nutrition

4% 55%
HIV/AIDS
5% 18% Acute
Measles Respiratory
10%
Infection
15%

Malaria
Diarrhea

3
 Malnutrition is sometimes referred to as
protein-energy malnutrition (PEM).

Classically, three types of PEM have been

described:
o 1. Marasmus
o 2. Kwashiorkor
o 3. Marasmic kwashiorkor
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 6
months 2 years (Infantile atrophy).
Symptoms:
Failure to thrive, loss of weight (weight < 60% of
expected)
Loss of subcutaneous fat
 1 Dietary errors
2 Infection: Acute or chronic as T.B, otitis media, pyelo nephritis
3 Gastroenteritis: (acute or chronic )
4 Parasitic infestations as: Ascaris, ankylostoma, giardia
5 Congenital anomalies as: Cardiac, Renal (renal agenesis, obstructive
uropathy), G.I.T (pyloric stenosis, cleftlip or palat)
6 Metabolic diseases.: Galactosemia, Fructose intolerance, Idiopathic
hypocalcaemia
7 Prematurity
8 Some cases of mental retardation
9 Low socio-economic status
10 Endocrine causes (Diabetes, hyperthyroidism )
 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, Gastro
enteritis
Liability to infection - Intercurrent infection : Broncho
pneumonia is the cause of death
Weak feeble pulse, sub-normal temp, pulse rate
Unhealthy (sick) face and pale appearance
Hypovolemia (decreased blood volume)
Hypothermia & Hypoglycemia
Hemorrhagic tendency, purpura
 1.Blood analysis : (W.B.C, Electrolytes Sugars,
ketones, plasma proteins, normal or lowered )

2.Urire analysis: culture, sugar, ketones, calcium,

phosphate, aminoacids

3. Stool analysis for parasites

4. X- ray for chest and heart

5. Tuberculin test for T.B

6. ENT examination for otitis media

1 Prevention :-
o Proper diet (balanced nutritional diet)
o Encourage breast feeding up to weaning
o Proper vaccination as measles, T.B. whooping cough
2 Curative treatment:-
Adequate balanced feeding
Gradual increase in the amount and concentration of formula
(total calories is120-200 calories/kg/day)
Vitamins and minerals supplementation
Emergency treatment for complications
Blood transfusion
Treatment of the cause
Definition
It is a clinical syndrome and a form of malnutrition
characterized by slow rate of growth due to deficient
of protein intake, vitamins & minerals deficiency,
high carbohydrate diet (inadequate supply of
calories).
Incidence
Commonly in toddlers between the age 1-3 years,
following or with weaning
Causes
Same as Marasmus
 Clinical features
Growth retardation : Weight is diminished (60-80%)
Edema : Hypoproteinemia, The cheeks become bulky, pale, waxy in
appearance (doll-like-cheeks)
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
Hair changes: The hair is sparse, dys-pigmentation (reddish or greyish),
atrophic, easily pickable.
G.I.T Manifestations: Anorexia, vomiting in severe cases, diarrhea
Hepatomegaly: Liver and Skin changes (dermatitis in areas due to
pigmentation, napkin dermatitis, petechiae over the abdomen, fissures,
ulceration)
Poor resistance and liability to infections
 1. Blood analysis: (Albumin < 2.5 g/ml/d), 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
Definition
Its a combination of caloric deficiency (marasmus) and
protein deficiency.

Clinical picture
The clinical picture of this disease represents
manifestations from both diseases as:
loss of subcutaneous fat as in marasmus
Edema, hair and skin changes as in KWO.
 Micronutrient deficiencies

Zinc Vitamin D Cobalt

Iodine Thiamin Riboflavin
Vitamin B6 Vitamin E Magnesium
Manganese Iron Selenium
Folate Vitamin B12 Niacin
Vitamin A Phosphorus Vitamin K
Vitamin C Cobalamin Chromium

Micronutrient deficiencies are common throughout the world

including in most emergency-affected populations.
 Vitamin A Deficiency (VAD)

Leading cause of preventable blindness among pre-school

children

Also affects school age children and pregnant women

Weakens the immune system and increases clinical

severity and mortality risk from measles and diarrhoea
Supplementation with vitamin A capsules can reduce child
mortality by 23%.

WHO (2002) estimates that 21% of all children suffer from

VAD, mostly in Africa and Asia
 VAD - Signs & Symptoms

Clinical deficiency is defined by:

o Night blindness
o Bitots spots
o Corneal xerosis and/ or ulcerations
o Corneal scars caused by xerophthalmia

Risk Factors:

Low availability of vitamin A-rich foods

Lack of breast feeding
High rates of infection (measles, diarrhoea)
 Supplementation
o Capsules given during immunization days
o High dose oral supplements of vitamin A (To reduce
measles, malaria, and death)

Food Forms
o As pre-formed vitamin A in foods from animals
Liver, fish
o As pro-vitamin A in some plant foods
Red palm oil, carrots, yellow maize
Fortified blended foods
Definition: Its is a systemic metabolic disease due to
deficiency of vitamin D, results in inadequate deposition of
calcium in developing cartilage and bone leading to bone
deformities, hypotonia and some times affecting CNS.
Vitamin D: Reabsorption of ca and phosphours by kidneys

Two types:-
D2 called as Calciferol and D3 called as Chole calciferol
Biologically, D2 and D3 which are present (in-active) form
and transformed to active form in the liver as (Calcitriol)
 Dietary deficiency of vitamin D and Calcium
Lack of exposure to sun rays
Malabsorption of Vit. D as in obstructive jaundice
Taking of anti-convulsive drugs
Poor utilization of Vit. D by the tissues as in :-
hyper parathyroidism, renal disorders
hypo phosphatemia
recurrent attacks of diarrhea
High proportion of phosphorous in some cows milk
leads to impaired absorption of calcium.
1. Age --- common in infants (6 months - 2years)
2. Preterm babies and twins
3. Season --- more in winter than in summer
4. Diet --- Inadequate intake of vitamin D and calcium and
vitamin C in diet.
5. The disease is more common in artificial feed babies than
breast feed infants
6. Heredity factor
7. Atmospheric condition --- More common in big cities and
heavy crowded areas
8. Race ---- more common in dark races
1. Delayed motor development specially walking
2. Delayed dentition
3. Deformities of the bones
4. Bone fractures, limbs deformities
5. Tetany due to hypocalcaemia
6. Anemia
7. G.I.T disturbances as: Gastro Entities, Constipation.
8. Respiratory complications as pneumonia, broncho
pneumonia
9. Low resistance, liability to infection as urinary tract
infections
 A - Early manifestations:

Softening or thinning of the skull

in infant 3-8 months.

Enlargement of lower radio ulner

epiphysis.

Sweating at fore head, irritability

B - Late manifestations:
1- Head
Enlargement of the head box-like shape of skull
Delayed closure of anterior fontanel
Delayed eruption of teeth
2-Thorax
Rickety rosary beads
Transverse and longitudinal groove at lower part of the chest
Pigeon chest
B - Late manifestations:
3- Spine : Rounded upper back
4- Pelvis : Contracted pelvis
5- Extremities : Deformities, green stick,
fractures
6- Muscles : Weakness of muscles
7- Constipation and enlarged spleen
1- Prevention Of rickets:-

Exposure of all infants to ultra violet rays.

Daily intake of diet rich with Vit. D and
supplementation of Vit. D (400-800 IU / d).
The infant need 400IU/d. Premature baby receives
800-1200 IU / d - 2nd - 4th month
Pregnant and lactating mothers need Vit. D
supplementation.
2- Active treatment :-
Oral calcium with Vit. D intake should be increased.
Vit. D (1500-5000)IU/ d for 2months or shock
therapy by Vit. D (600-6000) IU/d by IM injection
deeply one dose every 2 weeks (3 doses)
After healing, give Vit. D (400-800) IU and repeat
blood analysis for calcium.
Surgical correction of deformities
Treatment of any complications
Thiamine, Riboflavin, Niacin, Pyridoxine
Cofactors to enzymes in energy metabolism, hence, deficiencies show
up in quickly growing tissues such as epithelial cells

Typical symptoms for the Nerve cells use lots of

group include: energy, so symptoms
also show up in the
nervous tissue:
Dermatitis
Glossitis Peripheral neuropathy
Cheilitis Depression
Diarrhea Mental confusion
Lack of motor
coordination
Malaise
Pathology: Accumulation of pyruvic and lactic acid in
body fluids
1. Cardiac dysfunction
2. Peripheral neuropathy
3. Brain hemorrhages
4. Movement disorders
5. Mental disturbance
Three forms:
1. Wet beriberi
2. Dry beriberi
3. Infantile beriberi
Prevention:
1. Richest sources are pork, whole grain, enriched cereal grains and
legumes
2. Improved milling of rice conserve thiamine
3. Proper cooking method - Excessive cooking of vegetables or
polishing of cereals destroy
4. In breast-fed infants, prevention achieved by maternal diet

RDA:
Infants 0.4 mg, Older children 0.6-1.2 mg, Nursing mothers 1.5 mg,
Adults 1-1.3mg

Treatment:
1. Children: 10 mg daily for several weeks
2. Adults 50 mg
Functions:
1. Important in amino acid, fatty acid, carbohydrate metabolism
& cellular respiration
2. Needed also by retinal eye pigments for light adaptation

Clinical Manifestations:
1. Characteristic lesions of the lips, stomatitis and cheilosis
2. Localized dermatitis of the face
3. Ocular photophobia, blurred vision, itching of the eyes,
lacrimation & corneal vascularization

Diagnosis:
1. Urinary riboflavin determination
2. RBC riboflavin load test
RDA: Infants & children <10yrs 0.6-1.4mg
Children >10yrs 1.4-2mg depending on food intake
Adults 0.025mg/gm dietary protein

Prevention:
1. Best sources: eggs, liver, meat, fish, milk, whole or enriched
ground cereals, legumes, green leafy vegetables
2. Also present in beer
3. Impaired absorption in achlorhydria (less HCl in stomach),
diarrhea & vomiting

Treatment:
1. Riboflavin 2-5mg daily and increase B complex
2. Parenteral administration if relief not obtained
Causes:
1. Diets low in niacin &/or tryptophan
2. Amino acid imbalance or as a result of malabsorption
3. Excessive corn consumption

Clinical Manifestations:
1. Weakness, irritability, numbness & dizziness
2. Classical dermatitis, diarrhea & dementia
3. Erythema, drying, scaling & pigmentation, vesicles
4. Predilection for back of hands, wrists, forearms (pellagrous
glove), neck (Casals necklace) & lower legs (pellagrous boot)
5. GIT - diarrhea, stomatitis or glossitis; feces pale, foul milky,
soapy
6. Mental changes include depression, irritability, disorientation,
insomnia & delirium
Diagnosis:
1. History & manifestations of diet poor in niacin or tryptophan
2. In niacin deficiency, urinary levels of N-methyl-nicotinamide low or
absent

RDA: Infants & children <10 yrs 6-10mg

Older individuals 10-20 mg

Prevention:
1. Rich sources include meat, peanuts and legumes, whole grain and
enriched breads and cereals
2. Avoid too large proportion of corn

Treatment:
1. Niacin 50-300mg daily which may be taken for a long time
2. Skin lesions may be covered with soothing lotions
Functions:
1. Vitamin B6 is involved in the synthesis of amino
acids, neurotransmitters and niacin
2. Plays important role in clinical conditions such as
anemia, cardiac decompensation, radiation effects,
skin grafting, dermatitis

Causes:
1. Losses from refining, processing, cooking & storing
2. Malabsorptive diseases such as celiac disease
(difficult in digestion)
Clinical Manifestations:

Three different types

a. Neuropathic, due to insufficient neurotransmitter
synthesis, such as irritability, depression &
somnolence, seizures
b. Pellagrous, due to low endogenous niacin
synthesis, such as dermatitis, stomatitis & glossitis
c. Anemic, due to low iron synthesis
Diagnosis: Large amount of xanthurenic acid in urine

Prevention:
1. Firm requirement not established but usually recommended:
Infant 0.1-0.5mg, Child 0.5-1.5mg & Adult 1.5-2mg
2. Rich sources include yeast, whole wheat, corn, egg yolk, liver
and lean meat

Treatment:
1. Pyridoxine 100mg IM injection for seizures due to deficiency
2. Children should be given 2-10mg IM injection or 10-100mg
oral vitamin B6
Functions:

1. Needed for RBC & DNA formation, cell multiplication

especially in GI cells

2. Newly discovered functions:

a. Prevents neural tube (nerve) defects

b. Prevents heart disease
c. Prevents colon cancer
Causes:
Deficient dietary intake: goats milk deficient & powdered milk
poor source
Deficient absorption celiac disease, achlorhydria, anticonvulsant
drugs, zinc deficiency & bacterial overgrowth
Impaired metabolism ascorbic acid deficiency, hypothyroidism,
drugs like trimethoprim & alcoholism
Increased requirement during rapid growth & infection
Increased excretion/loss may occur subsequent to vitamin B12
deficiency & chronic alcoholism
Increased destruction possible in cigarette smoking
Clinical Manifestations:
1. Megaloblastic anemia, irritability, failure to gain weight &
chronic diarrhea
2. Thrombocytopenic hemorrhage (bleeding) in advanced cases

Laboratory Findings: Blood tests for Anemia, Serum folic acid,

RBC folate levels, Serum iron & vitamin B12

RDA: 20-50 mcg/24 h

Treatment:
1. Injection or infusion: Folic acid 2-5mg/24 hrs, for 3-4 wks
2. Satisfactory response - lower the dose to 50 mcg/24 hrs
Causes:
Congenital Pernicious Anemia: Lack of secretion of intrinsic
factor by stomach
Breast-fed infants whose mothers had deficient diets or
pernicious anemia
Vitamin B12 malabsorption from disease of intestine

Clinical Manifestations:
1. Megaloblastic anemia that becomes severe
2. Neurological includes ataxia, paresthesias, clonus & coma
3. Tongue smooth, red & painful
RDA: Infants 0.5 mcg/day
Older children & adults 3 mcg/day

Laboratory Findings:
Blood - Anemia, Serum vitamin B12 <100 pg/ml
Urinary - Excess of methylmalonic acid

Treatment:
1. Injection vitamin B-12 1-5mcg/24hrs
2. If there is neurological involvement 1mg IM daily for at
least 2wks
3. Pernicious Anemia: Monthly vitamin B12 1mg IM necessary
throughout patients life
Functions:
1. Collagen, steroids and epinephrine synthesis process
2. Ascorbic acid also aids iron absorption

Clinical Manifestations:
1. Weakened collagen fibrils
2. Severe deficiency results in decreased wound healing,
osteoporosis, hemorrhaging, bleeding into the skin and friable
bleeding gums with loosened teeth
4. Presenting feature in infant with painful, immobile legs
(pseudoparalysis)
5. Low grade fever & anemia usually present
6. Impairment of growth & development
Diagnosis:
Bleeding, swollen gums: Chronic gingivitis & pyorrhea with pus
X-ray findings of the bones (Knee atrophy, pencil-point thinness)
Tenderness of limbs: age >2 yrs (Arthritis & osteomyelitis)
Prevention :
1. A minimum daily intake of 30 mg is recommended by WHO for
all age levels.
2. Every infant should receive supplement starting 2 nd week of life.
3. Lactating mothers should have at least 50mg vitamin C daily.
4. Guava & papaya richer in vitamin C than citrus fruits, also in most
green leafy vegetables, tomatoes & fresh tubers
Treatment:
Ascorbic acid 200-500 mg daily or 100-150 ml of fruit juice.
 Most common global nutrition problem
Common causes of anemia
o Iron deficiency anemia (IDA)
o Infections (malaria, hookworm, HIV)
o Other vitamin deficiencies
o High intake of inhibitors (Tea)
o Hemoglobinopathies
o Blood loss
Health impact
o Perinatal & maternal mortality
o Delayed child development
o Reduced work capacity
Signs and Symptoms
Tiredness and fatigue
Headache and breathlessness
Pallor: pale eye, palms, tongue, lips and skin
Diagnosis:
Blood test for anaemia (Hemoglogin / Hematocrit)
Defined by WHO as:
o Hb <11.0 g/dL children
o Hb <12.0 g/dL Adults
Prevention:
Meat, Spinach, Fortified cereals, Cashew nuts,
Lentils and beans
Treatment: Iron supplement
 Thyroid hormone imbalance
Significant cause of preventable brain damage in children
Health effects:
o Increased perinatal mortality
o Mental retardation
o Growth retardation
Preventable by consumption of adequately iodized salt
Iodine Deficiency Affects the Brain

Cretinism

Goitre

Reduced
intellectual
performance
Causes:
Low iodine level in food
o products grown on iodine-poor soil (Erosion, floods,
draught, mountainous areas)
o distance from sea (low fish intake)
Non-availability of iodized food (salt)
Diagnosis:
Measure urinary iodine excretion (UIE)
Measure levels of thyroid hormones in blood
Measure degree of goitre
Grade 0 No Goitre
Grade 1 Palpable Goitre
Grade 2 Visible Goitre