MALNUTRISI

Nurlaili Muzayyanah
Departemen IKA FK UII
 PREVALENSI GIZI KURANG DAN BURUK DI
INDONESIA (SUSENAS 1989-2003)

40 37.5
35.6
35 31.6
29.5
30 26.4 24.7 26.1 27.3 27.5
25
20
15 11.6 10.1
7.2 8.1 7.5 8 8.55
10 6.3 6.3
5
0
1989 1992 1995 1998 1999 2000 2001 2002 2003
What is Malnutrition?

Malnutrition = “lack of nutrients / poor nutrition”

Two principle constituents:

• Protein-energy malnutrition
• Deficiency in micronutrients
Malnutrition
 Kwashiorkor: protein deficiency
 Marasmus: energy deficiency
 Marasmic/ Kwashiorkor: combination of chronic
energy deficiency and chronic or acute protein
deficiency
 MASA “EMAS” DAN KRITIS
Kehamilan & Pertumbuhan Janin Pertumbuhan Bayi & Anak

Pertumbuhan otak
Membangun tinggi Membangun berat Untuk Mencapai Tinggi dan Berat badan
optimal
badan potensial badan potensial
(rapid increase in (rapid increase in
cell number) cell size)

Butuh gizi mikro &

protein Dibutuhkan seluruh zat gizi (makro
Butuh Kalori
dan mikro) secara seimbang

Konsepsi 20 mg LAHIR 2 TAHUN

 PRIORITAS INTERVENSI PADA “EMAS” DAN KRITIS
Investasi terlambat
,
Investasi tepat waktu Mutu SDM rendah

100%

80%

Surat Al Baqarah ayat 233

“Para ibu hendaklah menyusukan anak-
anaknya selama dua tahun penuh, yaitu
ASI & bagi yang ingin menyempurnakan penyusuan”
MP-ASI

lahir 6 bl umur
2 th 5 th
Sumber: FKM-UI, Ascobat Gani
 Causes of malnutrition
Child malnutrition
death and disability

Inadequate Disease
Diet

Poor water/ sanitation Inadequate

Insufficient
inadequate health maternal and
access to food
services child care
CLASSIFICATION OF MALNUTRITION IN CHILDREN

MILD MODERATE SEVERE

MALNUTRITION MALNUTRITION MALNUTRITION
Percent Ideal 80-90 % 70-70 % LESS THAN 70 %
Body weight

Percent Usual 90-95 % 80-85 % LESS THAN 80 %

Body weight

Albumin (g/dL) 2.8-3.4 2.1-2.7 LESS THAN 2.1

Transferrin 150-200 100-149 LESS THAN 100

(mg/dl)

Total Lymphocyte 1200-2000 800-1199 LESS THAN 800

Count (per µL)

15
Pathophysiology
 Cardiac
 Output, heart rate and blood pressure decrease
 Postural hypotension
 Immune system
 T lymphocytes and complement decreased
 Susceptible to bacterial infection
 Cytokines (glycoproteins)
 Poor immune response
 TNF inc leading to anorexia, muscle wasting and lipid changes
Pathophysiology
 Decreased total body potassium
 Not electrolytes, but problem in rehabilitation
 GI function
 Poor absorption of lipids, and sugars
 Decreased enzyme and bile production

 Increase incidence of diarrhea, and bacterial

overgrowth
Marasmus:

Inadequate caloric intake due to insufficient diet .

 Improper feeding habits .

 Emotional deprivation.

 Metabolic abnormalities

 Congenital malformation

 Severe impairment of any body system

21
25
 KWASHIORKOR

Kwashiorkor:
 Insufficient intake of protein of good biological value.
 Impaired absorption of protein e.g. chronic diarrhoea.
 Abnormal losses of protein e.g.
severe nephrosis . Severe or prolonged infection
 Failure of protein synthesis e.g.
chronic liver diseases.
 Kwashiorkor (low protein)
 Decreased muscle mass (failure to gain weight and of linear
growth)
 Swollen belly (edema and lipid build-up around the liver)

 Changes in skin pigment (pellagra); may lose pigment where

the skin has peeled away (desquamated) and the skin may
darken where it has been irritated or traumatized
 Hair lightens and thins, or becomes reddish and brittle.

 Increased infections and increased severity of normally mild

infection, diarrhea
 Apathy, lethargy, irritability

 Death does not occur from actual starvation but from

secondary infection
Kwashiorkor
32
Complications:
1) Infection:
1. Immunological defect
- Cell mediated> humoral
- Measles> fatal disease

2. Subtle infection
- Lack of fever
- Hypothermia
- No increase in WBC
- Inability to localize infection
Complications (cot’n)

2) Hypoglycaemia apnoea
3) Hypothermia bradycardia
4) Heart failure death
5) Vit deficiencies Vit A  blindness
6) Permanent growth stunting
7) Prolonged illness developmental delay
cognitive function
slow intellectual
achievement
Prevention:
Improve nutritional status Improve water supply
Without change in food supply Proper sanitation
Health education
Social worker visits,
Reduce infection rate Immunization
Supervision of feeding
Good weaning practice

Long term community

Effective for health measures
one generation
Kasus Gizi Buruk, Kec. L. Abang, Bekasi
Fitria – Umur 18 bulan (Juli 1999),
BB : 5.1 Kg
Marasmus (+ ISPA)

Intervensi selama 9 bulan:

Perawatan + PMT: Rp 3000/hari
BB menjadi 10.5 kg.
 Major Micronutrient Deficiencies

 Iron Anemia
 Iodine Iodine Deficiency Disorders
(IDD)
 Vitamin A
Xeropthalmia
 Zinc  Multiple disorders
Iron Deficiency
 Iron is critical for body:
 Carries oxygen to tissues from lungs
 Transports electrons within cells

 Integral part of important enzyme reactions

 Anemia is caused most commonly by iron deficiency

(anemia is found in 40-60% of women and children
in developing countries)
Iron Deficiency Consequences
 Iron deficiency results in:
 Decreased work capacity and work productivity
 Permanently impaired development
 Psychomotor development of anemic children will be
reduced by 5-10 IQ points
 Increasedmorbidity and mortality from infections
 Decreased growth
Anemia
 Most common global nutrition problem
 Common causes of anemia
 Iron deficiency anemia (IDA)
 Infections (malaria, hookworm, HIV)
 Other vitamin deficiencies
 Hemoglobinopathies

 Health impact
 Perinatal & maternal mortality
 Delayed child development
 Reduced work capacity
 Anemia- Risk Factors

•Low dietary intakes

• Diet poor in iron-rich foods/animal
foods
• High intake of inhibitors (Tea)

• Infections (malaria, helminthes infection,

schistosomiasis)

• Blood loss
Anemia- Signs & Symptoms

 Tiredness and fatigue

 Headache and
breathlessness
 Pallor: pale
conjunctivae, palms,
tongue, lips and skin
Anemia- Treatment
 Dietary diversification
 Foods that are rich in iron include:
 Meat
 Fortified cereals
 Spinach
 Cashew nuts
 Lentils and beans

 Fortification

 Iron supplements
 Iodine Deficiency Disorders

Source: State of the World’s Children, 1998

Iodine Deficiency Disorders (IDD)

 Significant cause of preventable brain damage in children

 Health effects:
 Increased perinatal mortality

 Mental retardation

 Growth retardation

 Preventable by consumption of adequately iodized salt

 Iodine Deficiency Affects the
Brain

Cretinism

Goiter

Reduced
intellectual
performance

*Goiter manifests only a small portion of IDD

IDD- Risk Factors
 Low iodine level in food
 products grown on iodine-poor soil
 erosion, floods
 mountainous areas
 distance from sea (low fish intake)

 Non-availability of iodized food (salt)

Iodine Deficiency: Severe

 Goiter: most commonly recognized consequence

(enlarged thyroid)
 Occurs when thyroid gland is unable to meet the
metabolic demands of the body through sufficient
hormone production – thyroid compensates by
enlarging (works in short term)
 Cretenism: proximal pyramidal signs, intellectual
impairment, primitive reflexes
 Only occurs with severe fetal iodine deficiency
Iodine Deficiency: Moderate
 Studies comparing 2 Villages
 Consistentresults: meta-analysis showed 13.5 IQ point
difference between groups
 Intervention Studies
 Prenatal supplementation (esp. 1st trimester): clear
impact – prevents cretenism, and affects mental
development in children
 Childhood supplementation: many mediocre studies, but
positive impact
Vitamin A Deficiency

 Vitamin A is important
because it is essential to
vision, fetal development,
immune response

 250 million children of pre-

school age lack sufficient
Vitamin A in their diet.
 350,000 become blind each
year, and half of them die
within a year of becoming
blind….
 Vitamin A Deficiency

• Associated with blindness and increased severity of

infections such as measles and diarrhoeal disease

• WHO estimates that 2.8 million children under 5 years old

have signs of clinical xerophthalmia (childhood blindness)

• WHO estimates that 14 million pre-school children

already have some eye damage from Vitamin A deficiency
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:

 night blindness
 Bitot’s spots
 corneal xerosis and/ or ulcerations
 corneal scars caused by xerophthalmia
 WHO Classification of Xerophthalmia

1N Night blindness
2B Bitot’s spots
X3 Corneal xerosis
2B X3
X4 Corneal
ulcerations -
Keratomalacia
X5 Corneal scars
- permanent X4 X5
blindness
VAD- Risk Factors

• Low availability of vitamin A-rich foods

• Lack of breastfeeding
• High rates of infection (measles, diarrhoea)
• Malnutrition
VAD- Treatment
 Supplementation
 Capsules given during immunization days
 Food Forms
 As pre-formed vitamin A in foods from animals
 Liver, fish
 As pro-vitamin A in some plant foods
 red palm oil, carrots, yellow maize
 Fortified blended foods (CSB or WSB)
High dose oral supplements of vitamin A

 Rapid and targeted

 Highly effective in lowering

mortality in infants and
children in third world
communities

 Highly effective in reducing

complications in measles

 Reduced prevalence of
malaria in children in Papua
New Guinea
Zinc Deficiency

 Zinc essential for the function of many enzymes and

metabolic processes
 Zinc deficiency is common in developing countries with
high mortality
 Zinc commonly the most deficient nutrient in
complementary food mixtures fed to infants during
weaning
 Zinc interventions are among those proposed to help
reduce child deaths globally by 63% (Lancet, 2003)
Zinc Deficiency- Signs & Symptoms

 Hair loss
 Skin lesions
 Diarrhea
 Poor growth
 Acrodermatitis enteropathica
 Death
Zinc Deficiency- Assessment

 No simple, quantitative biochemical test of zinc status

 Serum Zinc
• Can fluctuate as much as 20% in 24-hour period
• Levels decreased during acute infections
• Expensive
 Hair zinc analysis
Zinc Deficiency- Treatment

 Regular zinc supplements can greatly reduce common infant

morbidities in developing countries
• Adjunct treatment of diarrhea
 20mg /day x 10 days
• Pneumonia
• Stunting
 Zinc deficiency commonly coexists with other micronutrient
deficiencies including iron, making single supplements
inappropriate
 Dietary diversification
• Animal protein (oysters, red meat)