pem & vitamin a deficiency

PEM & Vitamin A deficiency

Dr.Praseeda.BK

PEM

The cellular imbalance between

To ensure growth, maintenance, and specific functions

supply of nutrients & energy

and the body's demand for them

Malnutrition

Reasons..

• Inadequate intake of food (Quality & Quantity)

• Infections

Malnutrition infection cycle

Factors related to Malnutrition

Social & EconomicBiological factors

Poverty Ignorance Female genderRural areaLow birth weightIlliterate mother Scheduled caste/

scheduled tribe Cultural & social practices

Maternal malnutrition, prematurityBirth spacing < 47 monthsAge of mother: 18 – 23 yrsBirth order > 3Underweight status of mothers

Infectious diseaseDiarrhea, TB, measles, Malaria, AIDS

Environmental Unsanitary living, Droughts, floods, wars, forced migrations

Nutritional intakes

Nutrition needs

Nutritionalintakes

Nutritional status

The result is Under- Nutrition

UNDERNUTRITION

ACUTE UNDERNUTRITION

CHRONIC UNDERNUTRITION

• Marasmus• kwashiorkor• Marasmic- kwashiorkor• Wasting

• Stunting• Underweight

Features Marasmus Kwashiorkor

Clinical Always Present

Muscle Wasting Obvious Sometimes hidden by edema & fat

Fat wasting Severe Loss of subcutaneous fat

Often retained but not firm

Oedema None In lower legs ,face, forearms.

Weight for height Very low Low but masked by edema

Mental changes Quiet & Apathetic Irritable , moaning , apathetic

Features Marasmus Kwashiorkor

Clinical Sometimes Present

Appetite Usually good Poor

Diarrheoa Often Often

Skin changes None Flaky paint dermatosis

Hair changes Seldom Sparse , silky ,easly pulled out

Hepatic enlargement

None Sometimes due to fat accumulation

Features Marasmus Kwashiorkor

Biochemical Sometimes Present

Serum albumin Normal or slightly decreased

Low

Urinary Urea per g Creatinine

Normal or slightly decreased

Low

Hydroxyproline creatinine ratio

Low Low

Plasma aminoacid ratio

Normal Elevated

Physical examination• History- including detailed dietary history.

-Anthropometric measurements.» Weight »Length/height »Mid upper arm circumference MUAC)»Chest circumference»Head circumference»Anthropometric Measurements of

Nutritional Status

WEIGHTAt 5-6 month double of birth weight

At 3 years weight 5 time double of birth weight

At 6 years weight 6 times double of birth weight.

HEIGHT

• 1 yr 72-75 cm• 2 yrs 88-90 cm • 4 yrs 100 cm.

>13.5

13.513.5

Prevention

1. Health Promotion

1. Measures directed to pregnant & lactating women

2. Promotion of breast feeding3. Development of low cost weaning food4. Measures to improve family diet 5. Nutrition education 6. Home economics 7. Family planning & spacing of births 8. Family environment

2. Specific Protection

1. Child’s diet must contain protein & energy rich foods

2. Immunization

3. Food fortification

3. Early diagnosis & Treatment1. Periodic Surveillance 2. Early diagnosis of any lag in growth 3. Early diagnosis & treatment of infections and

diarrhoea4. Development of programmes for early

rehydration of children with diarrhoea 5. Development of supplementary nutrition

programmes during epidemics 6. Deworming of heavily infested children

Rehabilitation

• Nutritional rehabilitation services

• Hospital treatment

• Follow up care

Vitamin A deficiency

Sources 1. Animal foods – Retinol(preformed vit A) Liver, Eggs,Cheese,Fish, Meat

2.Plant foods – Carotene(provitamines) GLV ,mango, papya, carrots, yellow pumkin,

red palm oil.

3.Fortified foods – vanaspati, margarine, milk

xerophthalmia

• The term xerophthalmia was given by a joint WHO and USAID committee in 1976 to cover all ocular manifestations of Vitamin A deficiency in human.

- Most common in children aged 1-3 years often related to weaning.

- Marker – serum Retinol level- Normal – 7 micromol / litre(200 micro g/ litre)

• Risk factors– IgnoranceFaulty feeding practicesInfections – measles, diarrhoea, RTILack of education

Current status of VAD in India

• Clinical VAD has declined drastically during the last 40 years.

• There has been virtual disappearance of keratomalacia, and a sharp decline in the prevalence of Bitot spots .

• Prevalence of Bitot spots of 0.5 per cent and more is limited to population groups which are socio-economically backward, poverty stricken and have poor health infrastructure.

XEROPHTHALMIA CLASSIFICATION(modified)

• XN Night blindness• X1A Conjunctival xerosis• X1B Bitot’s spots• X2 Corneal xerosis• X3A Corneal ulceration /keratomalacia affecting less than 1/3rd

corneal surface• X3B Corneal ulceration /keratomalacia affecting more than 1/3rd

corneal surface• XS Corneal scar due to xerophthalmia.• XF Xerophthalmic fundus.

Ocular changes.

1. Night Blindness

• First symptom• Due to impairment in dark adaptaion• Defective rhodopsin function.• May get worse when there is diarrhoea or

other infection

2. Conjunctival xerosis

First clinical signOne or more patches of dry,

lustreless,nonwettable conjunctiva.Interpalpebral conjunctiva(commonly temporal

quadrants)Severe cases involves the entire bulbar

conjunctiva.Desribed as ‘emerging like sand banks at

receding tide’when child ceases to cry

3. Bitot’s spots

- Triangular, pearly white, yellowish foamy spots in the bulbar conjunctiva

- Usually bilateral

- Characterised by metaplasia of conjunctival epithelium and tangles of keratin admixed with gas forming bacteria(corynebacterium xerosis)

- Vitamin A is essential for cell differentiation

4. Corneal xerosis

- Serious stage - Cornea become dull, dry, non-wettable- Severe cases- ulceration leading to scars.• Bilateral punctate corneal epithelial erosions • Can progress to epithelial defects • Reversible on treatment

5. Keratomalacia

Liquefaction of cornea. Medical emergency.Rapid process.Stromal defects occur in late stages due to

colliquative necrosis leading to corneal ulceration ,softening (melting) and destruction of cornea(keratomalacia)

Assessment of Vit A deficiency• Prevalence criteria for determining

xerophthalmiaCriteria Prevalence in population

at riskNightblindness >1%

Bitot’s spots >0.5%

Corneal xerosis/corneal ulceration/keratomalacia

>0.01%

Corneal ulcer >0.05%

Serum Retinol(<10 mcg/dl) >5%

Treatment - Should be treated urgently- early stages reversed by massive doses (2L IU) orally on 2 successive days.

Prevention

Short term actions

Administration of large amount of Vit A orally to vulnerable groups in a periodic basis

Most effective strategy

Medium – term action

Fortification of foods –

dalda,sugar,salt,tea,margarineCereal based foods

Long term action

Elimination of Factors contributing to ocular diseases

Persuading people to consume dark GLVS and other Vit A rich foods.

Promotion of breast feedingImprovement of environmental healthDietary diversification

Dietary diversification

• Cultivation of variety of staple food with a high viatmin and mineral content.

• It holds the ability to concurrently cover multiple micronutrient deficiencies.

• If supported with a nutrition education programme, may be more effective in the developing countries.

Sanitation & hygiene

Safe water supplyEnvironmental sanitationProper hygieneFood safetyRegular dewormingImmunization against DPT, cholera

National programme for prevention of nutritional blindness 1970

• The programme is sponsored by the Ministry of Health and Family Welfare, Government of India

- Beneficiaries children below 5 years.- ObjectivesPromoting consumption of Vit A rich foods

Administration of massive dose of Vit a upto 5 yearsFirst dose of 1 L IU with measles at 9 monthsSubsequent dose of 2 L IU every 6 months upto 5 years

of age9 mega doses

Thank You