24791_Protien Energy Malnutrition Nov2008

8/12/2019 24791_Protien Energy Malnutrition Nov2008

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Soad Jaber 2009

PROTEIN ENERGY

MALNUTRITIONSevere childhood undernutrition

SCU


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Why more common in children?

High nutrient requirement/unit weight. Dependence on adults for food

Water - Higher body water> older childrenFat - Rapid increase in the 1st 6 monthsGrowth - Rapid from birth till six months

Growth rate increase at puberty.

More for boys than girls.


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Developmental Milestones:Neonates Good swallowing + sucking.12 weeks Can-swallows food placed on anterior

tongue.20 weeks Can drink from held cup with biting

movements.28 weeks Teeth begin to erupt.

Feeds self biscuits., chewing movements.7 months Shuts mouth. Shakes head to refuse foods.9 months Fingers feeding10 months Drinks from cup.12 months Holds spoon unable to get food to mouth.

15 months Control spoon + cups.18 months Plays with food.


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How to assess nutritional

status????? - Clinically

- Anthropometrically - Bio-chemically - Clinical "Signs" Muscular, skeletal Tone. ,muscle wasting

,delayed walking

Abdomen- Hepatomegally.. spleenomegally,ascites.. CVS --Cardiomegally ,oedema CNS--- Apathy, confusion, psychosis, depression.


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Anthropometrictechniques

The trend overtime serial reading, NOT single

Weight for age reflect the combined effect of both recentand longer term level of nutrition.

Height for age long term problem,comulative effect ofundernutrition during the life of the child.

Weight for height and age ,recent nutritional experiences.Less


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Weight < 90%

expected

Weight> 80%

expected

WastedNormalHeight > 90%

StuntedShortHeight < 90%

INTERPRETATION OF

WEIGHT AND HEIGHT FOR AGE


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PROTEIN ENERGY

MALNUTRITION Definition :( WHO) * Marasmus Weight less than 60% of expected weight - no

oedema.

Kwashiorkor Weight between 60-80% of expected weight +oedema

No oedema Oedema

Kwashiorkor 80%80%Underweightfor age

60%Marasmic-Kwashiorkor

Marasmus60%

Wellcome Classification


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Gomez Classification for

Malnutrition1ry PEM is a spectrum ranging from:

* mild form

Decrease weight for length.

*severe formDecrease length and weight for age.


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Aetiology of (PEM) Leading cause of death (less than 5 years of age)

1ry:. Protein + energy intakes below requirement for normalgrowth

2ry:the need for growth is greater than can be supplied. : decreased nutrient absorption : increase nutrient losses

Linear growth ceases

Static weight

Weight loss

Wasting

Malnutrition and its signs


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Kwashiorkor:

Ga language of West Africa = Supplanted one - Childwho recently have been weaned (Pregnant mother) and emotional deprivationHistory:1933 Cecily * Ghanaian children

* Weaned recently* Oedema and hair changes* Fatty liver

1967 Mc-Cane * Anaemia

* Cardiac* Skin changes1971 Frood-Paskitt * Biochemical


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Pathogenesis:Kwashiorkor: Normal energy intake, Lack of protein Edema:1970.decrease oncotic pressure,

Recent> Increase Renin activity,N a and fluidretention.

Amino aciduria due to proximal tubulardysfunction

Failure of adaptation .Hepatomegaly due to fatty infiltration from

lipogenesis of excess CHO - Biochemical and haematological changes


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Pathogenesis:

Marasmus: - Lack of all nutrients stimulate cortisone

secretion which result in muscle wasting, thereleased a. a will synthesize albumin to prevent

edema. - Growth and energy expenditure limited, in

response to dietary stress - Adaptation to reduce protein + energy - Biochemical and haematological tests within

normal -Abdomin,flat due to ms wasting, OR distended

due to 2ry lactose intolerance.


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Causes:

Social.ecomomic.poverity.ignorance.maternalmalnutrtion.enviromental.

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.


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Marasmus:

Inadequate caloric intake due to insufficient diet .

Improper feeding habits . Emotional deprivation.

Metabolic abnormalities

Congenital malformation

Severe impairment of any body system


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Management:

- Accurate historyof social and economic factors.poverety,ignorance. environmental factors.

diet history: maternal malnutrition, breast milk and other feedinghabits .food allergies ,food taboos.chronic illness ,burns .HIV. cystic fibrosis .malignancies .inbornerror of metabolism ,

- Evaluation of growth parameters: weight, height, headcircumference

- Evaluation of the degree of illness and dehydration:skin fold thickness - Biochemical evaluation* mild * moderate * severe


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1) Mild - moderate with no complication

- Home management

food increase calories + energy Multivitamin 1st week

Iron replacement 2nd week.

antibiotics for infection

2) Severe marasmic or severe kwashiorkor


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2) Severe marasmic or severe kwashiorkorComplicated cases or marasmic kwashiorkorHospital management

INITIAL PHASE

1st day:History --- clinical exam -- rehydrationPrevent heat lossNGT feeding ORS, IVF (glucose and electrolytes)Treatment of infection,bacterial and parasitic.

2nd-7th day:a) Continue rehydration by NGT,

b) start diet by NGT .calories 80-100/kg/day ,Protein 3-4g/kg/d. small volumes2hourly then 4hourly to6 hourly. and increase calories gradually, c) multivitamin. Vit A, folic acid. Without IRON for the 1stweek.

d) Correct anaemia ( packed RBC carefully)

If diarrhea starts or fails to resolve may be lactose intolerance lactose free milk or cow milkprotein intolerance start soy protein hydrolysate formula.


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Follow-up:1st sign of improvement:

-Awareness in the child-Appetite (kw)-Weight loss (kw)

Weight gainrapid Marasmus

Slow (10th

day) Kwashiorkor


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Failure of improvement:

1) Combined marasmic -kwashiorkor

2) Infection TB ,,,parasite

3) drowsiness -Severe hypokalemia-Hepatic failure-Protein intolerance

4) Rapid gain of weight - Cardiac failure- Grossly disturbed metabolism- Unable to tolerate the rate of re feeding (oedema)

5) Profuse diarrhea- GIT infection- Food intolerance (discharidase)- Other nutrients deficiency


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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


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Complications (cotn)

2) Hypoglycaemia apnoea

3) Hypothermia bradycardia

4) Heart failure death

5) Vit deficiencies Vit A blindness6) Permanent growth stunting

7) Prolonged illness developmental delay

cognitive functionslow intellectualachievement

P ti


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Prevention:Improve nutritional status Improve water supplyWithout change in food supply Proper sanitation

Health educationSocial worker visits,

Reduce infection rate ImmunizationSupervision of feeding

Good weaning practice

Long term communityhealth measures

Effective for

one generation


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24791_Protien Energy Malnutrition Nov2008

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