PROTEIN ENERGY MALNUTRITION

Mentor :

dr. Pulung M. Silalahi, Sp. A

Written by :

Arlha Aporia Debinta 07120100068

Faculty of Medicine Universitas Pelita Harapan

Pediatric Department

Rumah Sakit Bhayangkara tk.I R.S. Sukanto-Jakarta

Periode: 3 November 2014 – 11 January 2015

FOREWORD

Thank you to my Lord Jesus Christ for His eternal blessing and perpetual

kindness throughout this writing process right from the start until the completion

process. It is only by His grace that I can finish this academic writing on time.

This academc writing entitled “Protein Energy Malnutrition” is given as a

part of clinical practice duty as a Co-Ass in RS Bhayangkara Tingkat 1 Raden

Said Sukanto, in the Pediatrics department.

The sources that I use for the writing contain information from textbooks,

journals and online references.

The author would like to give special mention to mentor, dr Pulung M.

Silalahi, Sp. A, for guiding author throughout the entire writing process.

I hope that this writing can be a positive use to the readers, be it as an

additional information or future references. I realize that the writing is still lacking

in many areas but I hope the readers can give critical remarks so that further

improvement can be made in the future.

Jakarta, November 2014

author

i

Table of Contents

FOREWORD.................................................................................................................................. I

CHAPTER I INTRODUCTION..................................................................................................1

1.1 Background................................................................................................................................. 1

1.2 Purpose of Writing................................................................................................................... 1

1.3 Problems....................................................................................................................................... 1

1.4 Benefits of the article.............................................................................................................. 2

CHAPTER II LITERATURE REVIEW.....................................................................................3

2.1 Definition.......................................................................................................................................... 3

2.2 Epidemiology.................................................................................................................................. 3

2.3 Etiology............................................................................................................................................. 3

2.4 Growth Status................................................................................................................................. 5

2.5 Classification................................................................................................................................ 10

2.6 Pathophysiology......................................................................................................................... 12

2.7 Clinical Manifestations............................................................................................................. 13

2.8 Diagnosis........................................................................................................................................ 16

2.9 Treatment...................................................................................................................................... 17

2.10 Complication.............................................................................................................................. 35

2.11 Prognosis..................................................................................................................................... 36

CHAPTER III CONCLUSION.................................................................................................. 37

3.1 Conclusion..................................................................................................................................... 37

3.2 Prevention..................................................................................................................................... 37

ACKNOWLEDGEMENTS ....................................................................................................... 38

ii

CHAPTER I

INTRODUCTION

1.1 Background

Globally, Protein Energy Malnutrition (PEM) continues to be a major health

burden in developing countries and the most important risk factor for illnesses and

death especially among young children. The World Health Organization estimates

that about 60% of all deaths, occurring among children aged less than five years

in developing countries could be attributed to malnutrition. The improvement of

nutrition therefore, is the main prerequisite for the reduction of high infant and

under five mortality rates, the assurance of physical growth, social and mental

development of children as well as academic achievement1. In severe cases for

children under five, malnutrition may lead to various diseases such as infection,

liver diseases, impaired brain growth or organ dysfunctions. In addition, children

with PEM may also have slower motor development, lower cognitive function and

even high risk of death. Protein itself is a macronutrient required to synthesize

new proteins such as thyroid hormones, neurotransmitter and heme in the body. If

it is diminished, the body in starvation mode will start to use protein as a source of

energy, causing muscle breakdown to occur and many other diseases will be

implemented as a series of cascade in result. As a general practitioner, it is

important to know the pathophysiology, classification, clinical manifestations, and

most importantly treatment of PEM right from the start in order to eradicate

malnutrition and health problems in children as much as possible.

1.2 Purpose of Writing

Provide further and detailed understanding of protein energy malnutrition starting

from definition, classification, etiology, pathophysiology, clinical manifestation,

treatment and complication in a thorough review.

1.3 Problems

Definition, epidemiology, and risk factor of protein energy malnutrition

1

Etiology, pathogenesis, and clinical manifestations of protein energy

malnutrition

Diagnosis, differential diagnosis, treatment, and prevention of protein

energy malnutrition

1.4 Benefits of the article

In order to present a detailed information and knowledge for other for

readers targeted as fellow health workers

To provide an adequate information to be used for subsequent academic

writing purposes

2

CHAPTER II

LITERATURE REVIEW

2.1 Definition

The World Health Organization (WHO) defines malnutrition as "the cellular

imbalance between the supply of nutrients and energy and the body's demand for

them to ensure growth, maintenance, and specific functions." Protein Energy

Malnutrition (PEM) is usually used to describe a group of related disorders that

include marasmus, kwashiorkor, and intermediate states of marasmus-

kwashiorkor. The term marasmus is derived from the Greek word marasmos,

which means withering or wasting. Marasmus involves inadequate intake of

protein and calories and is characterized by emaciation. The term kwashiorkor is

taken from the Ga language of Ghana and means "the sickness of the weaning."

Williams first used the term in 1933, and it refers to an inadequate protein intake

with reasonable caloric (energy) intake. Edema is characteristic of kwashiorkor

but is absent in marasmus3.

2.2 Epidemiology

Protein-energy malnutrition (PEM) is currently the most widespread and serious

health problem of children in the world. At any time approximately 100 million

children suffer from the moderate or severe forms of PEM3. Protein energy

malnutrition is one of the major nutritional problems in Indonesia. According to

Riset Kesehatan Dasar (Riskesdas) in 2007, Indonesia’s child nutrition problem has

slightly showed an improvement, from 5,4% in 2007 to 4,9% in 2010. It is stated the

province that suffered the most number of cases is Nusa Tenggara Barat with 24,8%

of its children suffering from various cases of malnutrition, be it mild or moderate.

2.3 Etiology

There are many factors that directly and indirectly contribute to the cause of PEM

such as:

Socio-economic factor

Social and economic factor both provides the biggest contribution to PEM.

Low family income is one the main reason to why children are suffering

from Protein Energy Malnutrition. Financial restrain causing families not

3

to be able to buy proper food containing nutrients required for children’s

growth. It is proven by the geographical distribution of the disease,

showing that under nutrition and malnutrition are highly found in poor

countries such as Haiti.

Parental lack of nutritional information

Parents, especially mothers, provides a vital role in the family to access

nutritional status of the children and to provide daily nutritional needs

served in food. However due to low economic status in poor countries that

usually followed by low education, many mothers do not know or even

able (financially) to how to provide enough nutrients to their children.

Inadequate health resources

Lack of medical services and public health services in developing

countries results to many prevention, promotional acts to stop malnutrition

fail to happen. Nutritional education to parents, cheap and accessible

medical services, and food aid have to be sufficiently provided in order to

abolish malnutrition.

Diagram showing various factors leading to malnutrition

4

2.4 Growth Status

It is important to know a growth status of a child before making a diagnosis of

malnutrition or even PEM. One simple way to access this growth progress is

through anthropometry data. It is important to know:

Height

Reduced growth as a consequence of adaptation to lack of food also affects

height. Weight can swing up and down, but obviously this is not the case with

height. All that happens is that growth in height slows down and the

individual will end up short. Those children whose heights are less than the

mean heights of children in their age group are called 'stunted'.

Weight

When food is inadequate, the organism adapts first of all by reducing growth

and the clinical signs are those of such adaptation. Thus, weight gain slows

down, and so weight for age has been commonly used to assess the degree of

mild to moderate malnutrition. Those children who weigh less than the mean

weights of children in their age group are thus called "wasted'

In defining the stages of malnutrition, two processes have to be taken into account.

These are; the period over which malnutrition occurs, so as to decide whether it is

acute or chronic, or acute on chronic. Acute forms chiefly affect body weight more

than height, whereas in the chronic form both height and weight are affected4.

5

The variable of body weight and height presented in the form of three

anthropometric indicators, which is : weight for age (W/A), height for age (H/A),

and weight for height (W/H). This data is acquired by plotting an international

growth standard statistical distribution distributed by the World Health

Organization (WHO). The WHO standards were constructed using longitudinal

length and weight data measured at frequent intervals.

Several classification method is used to describe certain nutritional status of the

children such as4:

Gomez

classification (weight for age standard)

The Gomez classification does not take height into consideration therefore

it is oftenly criticized for being inaccurate.

Waterlow classification (type and chronicity)

Instead of using just weight for age measurements, the classification

established by Waterlow combines weight-for-height (indicating acute

episodes of malnutrition) with height-for-age to show the stunting that

results from chronic malnutrition. One advantage of the Waterlow

6

classification over the Gomez classification is that weight for height can be

examined even if ages are not known.

WHO Classification

The World Health Organization (WHO) defines severe acute malnutrition

as a mid upper arm circumference (MUAC) < 11.5 cm, a weight-for-

height z-score (WHZ) below −3, or the presence of bilateral pedal oedema

in children with kwashiorkor.

To measure the nutritional status of children, the rate of weight and height

of every child is converted into standardized values (Z-score) by using

WHO 2005 anthropometric standard. Furthermore, based on a Z-score of

each indicator of nutritional status of children is determined by the

following restrictions:

Growth chart representing girls from age 0-2 years

a. Classification of Nutritional Status based on weight/age (WFA) indicator:

Malnutrition : Z score <-3

Less Nutrition : 0 Zscore> = -3.0 s / d Zscore <-2

Good Nutrition : 0 Zscore> = -2.0 s / d Zscore <= 2

More Nutrition : 0 Zscore> 2.0

b. Classification of Nutritional Status based on height/age (HFA) indicators:

Very Short : Zscore <-3.0

Short : Zscore> = - 3.0 s / d Zscore <-2.0

Normal : Zscore> = -2.0

7

c. Classification of Nutritional Status based on weight / height indicator:

Very Skinny : Zscore <-3

Skinny : 0 Zscore> = -3.0 s / d Zscore <-2

Normal : 0 Zscore> = -2.0 s / d Zscore <= 2

Chubby : 0 Zscore> 2.0

d. Classification of Nutritional Status based on combined height/age (HFA)

and weight/height (WFH) indicators:

Short-Skinny : Zscore TB / U <-2.0 and ZScore weight / height <-

2.0

Short-Normal : Zscore TB / U <-2.0 and Zscore weight / height

between -2.0 s / d 2.0

 Short-Fat : Zscore TB / U <-2.0 and Zscore BB / TB> 2.0

Normal-Thin TB : TB Zscore / U> = -2.0 and Zscore weight / height

<-2.0

Normal-Normal TB : TB Zscore / U> = -2.0 and Zscore weight / height

between -2.0 s / d 2.0 TB

Normal-Fat : Zscore TB / U> = -2.0 and Zscore BB / TB> 2.0

According to WHO, malnutrition is classified as moderate and severe,

as shown in table 3 :

8

Protein energy malnutrition also can be differentiate using Wellcome Trust

Working Party system, as shown in the table below : 4

1. Kwashiorkor : Body weight > 60% from normal + edema

2. Marasmus : Body weight < 60% from normal without edema

3. Marasmic–Kwashiorkor : Body weight > 60% from normal + edema

NUTRITIONAL STATUS Weight

(Harvard)

Edema WFH

Normal > 80% (-) N

Mild –

moderate

PEM

Underweight

= Undernourished

60 – 80 % (-)

PEM Kwashiorkor

Marasmus-

kwashiorkor

Marasmus

Nutritional

Dwarfism

60 – 80 %

< 60 %

< 60 %

< 60%

(+)

(+)

(-)

(-)

N

McLarens Scoring System For Protein Energy Malnutrition

Clinical Manifestations / Laboratory Score

Edema

Dermatosis

Edema + dermatosis

Hair changes

Hepatomegaly

Albumin Serum Protein Total Serum

< 1,00 < 3,25

1,00 – 1,49 3,25 – 3,99

1,50 – 1,99 4,00 – 4,74

2,00 – 2,49 4,75 – 5,49

2,50 – 2,99 5,50 – 6,24

3

2

6

1

1

7

6

5

4

3

9

3,00 – 3,49 6,25 – 6,99

3,50 – 3,99 7,00 – 7,74

> 4,00 > 7,75

2

1

0

Score : 0 – 3 = Marasmus

4 – 8 = Marasmus - Kwashiorkor

9 – 15 = Kwashiorkor

2.5 Classification

Firstly malnutrition can be divided into:

Primary malnutrition which means malnutrition resulting from inadequate

food intake

Secondary malnutrition which means there is increased nutritional need or

decreased nutrient absorption or increased nutrient losses5.

Two distinct clinical syndromes have been described, kwashiorkor and marasmus,

and represent the severe forms of PEM. They occupy the two ends of a spectrum

with a mixture of the clinical features of both in between.

Severe childhood undernutrition (SCU), whether primary or secondary, is a

spectrum ranging from mild undernutrition resulting in some decrease in length-

for-age and/or weight-for-age through severe forms of undernutrition resulting in

more marked deficits in weight-for-age and length-for-age as well as wasting (a

low weight-for-length measure).

Historically, the most severe forms of SCU6:

Marasmus (non-edematous SCU with severe wasting)

Non-edematous SCU was believed to result primarily from inadequate

energy intake or inadequate intakes of both energy and protein. Marasmus

can affect people of any age of vulnerable groups. Main groups are elderly

people and slimmers, as well as people suffering from cancer, aids and eating disorders.

Symptoms of Marasmus include impaired absorption, immune response, diarrhea, and

extreme emaciation (loss of vital body fat reserves, muscles and organ proteins). In

children, usually occurs a t those who shows failure to thrive.

10

Kwashiorkor (edematous SCU)

Edematous SCU was believed to result primarily from inadequate protein

intake. Kwashiorkor is likely caused by the body being not able to cope with

added oxidative stress of infection due to general food and antioxidant deficiency.

Symptoms of Kwashiorkor include severe oedema (swelling of organs due to increased

tissue fluid), liver enlargement, dermatitis (inflammation of skin) and changes in

hair colour and texture. Failure in growth is marked and weight is reduced

in spite of the presence of oedema.

Physiological functions of the various systems are markedly disturbed,

with diarrhoea, electrolyte disturbance, circulatory insufficiency,

metabolic imbalance and poor renal function. Hence the child with

11

kwashiorkor should be thought of as an emergency in need of intensive

medical and nursing care, and not just simply malnourished

Marasmic - Kwashiorkor, has features of both disorders (wasting and

edema).

Marasmic - Kwashiorkor is a mixture of both conditions. Sometimes a child can

switch from one to the other.

2.6 Pathophysiology

Protein is found between 10-15% of total energy in diet. It is believed that the

infant requires a higher proportion of essential amino acids than the adult. These

include the amino acids recognized as essential (or indispensable) for the adult

(leucine, isoleucine, valine, threonine, methionine, phenylalanine, tryptophan,

lysine, histidine) as well as cysteine, tyrosine, and perhaps arginine. The estimated

average requirement of protein for children: 1.2 g/kg/24 hr for the 7–12 mo old,

1.05 g/kg/24 hr for the 1–3 yr old, and 0.95 g/kg/24 hr for the 4–8 yr old.

Body in starvation mode will start to use protein as a source of energy, causing

muscle breakdown to occur, leading to various consequences. As the fat stores of

the body are consumed and muscle tissue depleted total body water increases as a

percentage of body weight. A direct relationship can be demonstrated between

12

weight deficit and total body water. A proportionate increase occurs in the extra

cellular fluid. On recovery, some of the excess extra cellular fluid is taken up by

the re-generating cells and some is lost by diuresis. As the tissue cells break down,

potassium and nitrogen are lost in equal proportions initially. Later there is

increased loss of potassium in diarrhoeal stools causing a cellular deficit of

potassium. The body will start to experience fatigue or lack of energy due to

hypokalemia.

The diagram illustrates below shows how malnutrition leads to a cascade of

consequences,

2.7 Clinical Manifestations

Clinical features of Marasmus7:

“Old man face”: Simian (Monkey like) appearance of face since the child

appearance only comprise of skin and bones.

Failure to thrive: Children will have below normal standards of weight.

There will be prominent ribs and loss of subcutaneous fat.

Wasting: Muscle wasting is prominent, skin hanging is especially seen

around buttocks and thighs, namely “baggy pants” appearance.

Less iritable : Compared to kwashiorkor, marasmic children have deep

sunken eyes and rather less irritable.

13

Hair changes in texture more than color.

Clinical feature of Kwashiorkor:

Edema due to hypoproteinemia leading to fluid retention. The edema is

pitting and may vary from mild pitting to anasarca.

Mental changes: the child might be apathetic and lethargic.

Skin changes : shows crazy pavement appearance showing

hyperpigmented and desquamated skin, sometimes with mosaic form.

Hepatomegaly due to fatty infiltration of the liver.

Other features occuring in both Marasmus and Kwashiorkor:

Vomiting and diarrhoea leading to dehydration.

Anemia due to reduced dietary intake of hematopoietic factors like

preotein and folic acid. Most common type of anemia is iron deficiency

anemia.

Infection such as respiratory infection

Other nutritional deficiency such as:

o Xerophtalmia (lack of Vitamin A)

Usually shows Bitot sign, keratomalasia and Corneal ulcer

14

o Vitamin B complex deficiency

Differentiating Marasmus and Kwashiorkor:

15

2.8 Diagnosis

Used often to diagnose malnutrition in Indonesia is a guideline provided by WHO

that states:

Weight for height < -3SD or <70% from 50th percentile

Edema on dorsal part of the feet to all parts of the body or

o Kwashiorkor weight for height > -3 SD

o Marasmic-Kwashiorkor < -3 SD

If anthropometric data cannot be used, clinical features must be reviewed by

looking at visible severe wasting and lack of subcutaneous fat especially on

shoulder, arms, backside and thigh region. Alsa, prominent ribs are seen.

It should be noted that children with BB/U < 60% are not necessarily

malnourished but it is because the child is short-statured, therefore not requiring

hospitalization.

Initial history taking should include information regarding8:

Asking whether there is sudden deep sunken eyes

Diarrhea and vomitting information

Urination

Whether extremities feel cold

Further information regarding this information should also be obtained:

Dietary habit before sickness

Breastfeeding information

Feeding intake

16

Whether or not there is a decline in appetite

Contact with patient diagnosed with tuberculosis

Whether within the last three months, patient suffer from measles

Chronic cough

Information regarding (death of) siblings

Birth weight

Child developmental milestones

Immunization history

Whether there is monthly documentation of weight increment

Environmental information (including family and social background)

HIV status of patient and/or parents

Physical examination should include:

Whether edema is present

Assess nutritional status

Sign of dehydration (thirst, sunken eyes, poor skin turgor)

Presence of shock signs (cold extremities, poor capilarry refill time)

Fever

Respiratory rate

Pallor

Assess hepatosplenomegaly

Distended abdomen (look for bowel sound)

2.9 Treatment

Upon hospitalization, it is important to differentiate children with PEM with

infectious patients as malnourished childrena re susceptible to infection. Secondly

it is required to place children in warm condition (25-300C). It is also important to

do close monitoring from time to time. Lastly, patients’ should not be bathed too

many times, and please be reminded to do rapid drying of patients’ body after

bathing.

In the hospital, doctors should be working alongside with nutritionist. An accurate

weighing scale will alse be needed to provide correct data taking. Its also

important to provide precise feeding. Patients’ weight should be recorded

17

frequently in order to assess progress of the treatment. Its is also important to

include parents in treatment process as a part of educational experience.

Generally, WHO has provided 10 initial steps as a guideline to manage PEM

cases.

It is described as a time frame that should be closely adhered to

The usual approach to the treatment of the child with severe malnutrition is

divided into three phases (Table 43-5). These are:

• Initial treatment (days 1-7): life-threatening problems are identified and

treated in a hospital or a residential care facility, specific deficiencies are

corrected, metabolic abnormali- ties are reversed and feeding is begun.

• Rehabilitation (weeks 2-6): intensive feeding is given to recover most of the

lost weight, emotional and physical stimulation are increased, the mother or

carer is trained to con tinue care at home, and preparations are made for

discharge of the child.

• Follow-up (weeks 7-26): after discharge, the child and the child’s family are

followed to prevent relapse and assure the continued physical, mental and

emotional development of the child.

In addition, the guidelines for the treatment of severe malnutrition are divided in

five sections:

A. General principles for routine care (the’10 steps’)

18

This 10 Steps should be done withing two steps (initial steps in Day 1-

2) and longer rehabilitation phase (week 2-6)

Things to be corrected are:

1.Treat/prevent hypoglycaemia

All severely malnourished children are at risk of hypoglycaemia and,

immediately on admission, should be given a feed or 10% glucose or

sucrose. Frequent 2 h feeding is important. If there is any suspicion of

hypoglycaemia and when blood glucose can be measured quickly (e.g.

with Dextrostix®), this should be done immediately. Hypoglycaemia

is present when the blood glucose is < 3 mmol/litre (< 54 mg/dl). If

blood glucose cannot be measured, it should be assumed that all

children with severe acute malnutrition are hypoglycaemic and given

treatment.

Treatment:

Give 50 ml of 10% glucose or sucrose solution (one rounded

teaspoon of sugar in three tablespoons of water) orally or by

nasogastric tube, followed by the first feed as soon as possible.

Give the first feed of F-75 therapeutic milk, if it is quickly

available, and then continue with feeds every 2 h for 24 h; then

continue feeds every 2 or 3 h, day and night.

If the child is unconscious, treat with IV 10% glucose at 5

ml/kg or, if IV

access cannot be quickly established, then give 10% glucose or

sucrose solution by nasogastric tube (see p. 345). If IV glucose

is not available, give one teaspoon of sugar moistened with one

or two drops of water sublingually, and repeat every 20 min to

prevent relapse. Children should be monitored for early

swallowing, which leads to delayed absorption; in this case

another dose of sugar should be given. Continue with 2 h oral

or nasogastric feeds to prevent recurrence.

Start on appropriate IV or IM antibiotics

Monitoring

19

If the initial blood glucose was low, repeat the measurement

(using finger or heel prick blood and measure with the

Dextrostix®, when available) after 30 min.

If blood glucose falls to < 3 mmol/litre (< 54 mg/dl), repeat the

10% glucose or oral sugar solution.

If the rectal temperature falls to < 35.5 °C, or if the level of

consciousness deteriorates, repeat the Dextrostix®

measurement and treat accordingly.

Prevention

Feed every 2 h, starting immediately (see initial refeeding, p.

209) or, whendehydrated, rehydrate first. Continue feeding

throughout the night.

Encourage mothers to watch for any deterioration, help feed

and keep the child warm.

Check on abdominal distension.

2. Treat/prevent hypothermia

Treatment:

If the axillary temperature is <35.0oC, take the rectal temperature using

a low reading thermometer.

If the rectal temperature is <35.5oC (<95.9oF):

feed straightaway (or start rehydration if needed)

rewarm the child: either clothe the child (including head), cover

with a warmed blanket and place a heater or lamp nearby (do

not use a hot water bottle), or put the child on the mother’s bare

chest (skin to skin) and cover them give antibiotics (see step 5)

Monitor:

• body temperature: during rewarming take rectal temperature

two- hourly until it rises to >36.5oC (take half-hourly if

heater is used)

• ensure the child is covered at all times, especially at night

• feel for warmth

20

• blood glucose level: check for hypoglycaemia whenever

hypothermia is found

Prevention:

•feed two-hourly, start straightaway (see step 7)

•always give feeds throughout the day and night

•keep covered and away from draughts

•keep the child dry, change wet nappies, clothes and bedding

•avoid exposure (e.g. bathing, prolonged medical examinations)

•let child sleep with mother/carer at night for warmth

Note: If a low reading thermometer is unavailable and the child’s

temperature is too low to register on an ordinary thermometer, assume

the child has hypothermia.

3. Treat/prevent dehydration

Note: Low blood volume can coexist with oedema. Do not use the IV

route for rehydration except in cases of shock and then do so with care,

infusing slowly to avoid flooding the circulation and overloading the

heart.

Treatment:

The standard oral rehydration salts solution (90 mmol sodium/l)

contains too much sodium and too little potassium for severely

malnourished children. Instead give special Rehydration Solution for

Malnutrition (ReSoMal).

It is difficult to estimate dehydration status in a severely malnourished

child using clinical signs alone. So assume all children with watery

diarrhoea may have dehydration and give:

• ReSoMal 5 ml/kg every 30 min. for two hours, orally or by

nasogastric tube, then

• 5-10 ml/kg/h for next 4-10 hours: the exact amount to be given

should be determined by how much the child wants, and stool

loss and vomiting. Replace the ReSoMal doses at 4, 6, 8 and 10

hours with F-75 if rehydration is continuing at these times, then

21

• continue feeding starter F-75

During treatment, rapid respiration and pulse rates should slow down

and the child should begin to pass urine.

Monitor progress of rehydration: Observe half-hourly for two hours,

then hourly for the next 6-12 hours, recording:

• pulse rate

• respiratory rate

• urine frequency

• stool/vomit frequency

Return of tears, moist mouth, eyes and fontanelle appearing less

sunken, and improved skin turgor, are also signs that rehydration is

proceeding. It should be noted that many severely malnourished

children will not show these changes even when fully rehydrated.

Continuing rapid breathing and pulse during rehydration suggest

coexisting infection or overhydration. Signs of excess fluid

(overhydration) are increasing respiratory rate and pulse rate,

increasing oedema and puffy eyelids. If these signs occur, stop fluids

immediately and reassess after one hour.

Prevention:

To prevent dehydration when a child has continuing watery diarrhoea:

• keep feeding with starter F-75

• replace approximate volume of stool losses with ReSoMal. As a

guide give 50-100 ml after each watery stool. (Note: it is

common for malnourished children to pass many small unformed

stools: these should not be confused with profuse watery stools

and do not require fluid replacement)

• if the child is breastfed, encourage to continue

22

4. Correct electrolyte imbalance

All severely malnourished children have excess body sodium even

though plasma sodium may be low (giving high sodium loads will

kill). Deficiencies of potassium and magnesium are also present and

may take at least two weeks to correct. Oedema is partly due to these

imbalances. Do NOT treat oedema with a diuretic.

Give:

• extra potassium 3-4 mmol/kg/d

• extra magnesium 0.4-0.6 mmol/kg/d

• when rehydrating, give low sodium rehydration fluid

(e.g. ReSoMal)

• prepare food without salt

The extra potassium and magnesium can be prepared in a liquid form

and added directly to feeds during preparation. Appendix 3 provides a

recipe for a combined electrolyte/mineral solution. Adding 20 ml of

this solution to 1 litre of feed will supply the extra potassium and

magnesium required. The solution can also be added to ReSoMal.

5. Treat/prevent infection

In severe acute malnutrition, the usual signs of bacterial infection, such

as fever, are often absent, yet multiple infections are common.

Therefore, assume that all children with severe acute malnutrition have

an infection on their arrival in hospital, and treat with antibiotics

23

immediately. Hypoglycaemia and hypothermia are often signs of

severe infection.

Treatment

Give all severely malnourished children:

broad-spectrum antibiotic

measles vaccine if the child is ≥ 6 months and not vaccinated or

was vaccinated before 9 months age. Delay vaccination if the child

is in shock.

Choice of broad-spectrum antibiotics

If the child has uncomplicated severe acute malnutrition, give oral

amoxicillin for 5 days. If there are complications (hypoglycaemia,

hypothermia or the child look lethargic or sickly) or any other medical

complication, give parenteral antibiotics:

benzylpenicillin (50 000 U/kg IM or IV every 6 h) or ampicillin

(50 mg/kg IM or IV every 6 h) for 2 days, then oral amoxicillin

(25–40 mg/kg every 8 h for 5 days) plus

gentamicin (7.5 mg/kg IM or IV) once a day for 7 days.

These regimens should be adapted to local resistance patterns.

Note: Metronidazole 7.5 mg/kg every 8 h for 7 days may be given

in addition to broad-spectrum antibiotics; however, the effi cacy of

this treatment has not been established in clinical trials.

Treat other infections as appropriate:

If meningitis is suspected, do a lumbar puncture for confi rmation,

where possible, and treat with the antibiotic regime.

If you identify other specifi c infections (such as pneumonia,

dysentery, skin or soft-tissue infections), give antibiotics as

appropriate. Add antimalarial treatment if the child has a positive

blood fi lm for malaria parasites or a positive malaria rapid

diagnostic test.

Only give TB treatments for those strongly suspected.

6. Correct micronutrient deficiencies

24

All severely malnourished children have vitamin and mineral defi

ciencies. Although anaemia is common, do not give iron initially, but

wait until the child has a good appetite and starts gaining weight

(usually in the second week), because iron can make infections worse.

Multivitamins including vitamin A and folic acid, zinc and copper are

already present in F-75, F-100 and ready-to-use therapeutic food

packets. When premixed packets are used, there is no need for

additional doses.In addition, if there are no eye signs or history of

measles, then do not give a high dose of vitamin A because the

amounts already present in therapeutic foods are enough.

Treatment

Give vitamin A on day 1 and repeat on days 2 and 14 only if child

has any signs of vitamin A deficiency like corneal uleration or

history of measles. Dosage is 50.000 IU for <6 months, 200.000

IU for 6-12 months and 200.000 for >12 months.

Start iron at 3 mg/kg/day for 2 days on F-100 catch up formula. Do

not give iron in stabilization phase and do note give iron if the

child is receiveing ready to use therapeutic food. If the child os not

on pre-mixed therapeutic food, give the following micronutrients

daily for at least 2 weeks:

o Folic acid 5mg on day 1 and 1mg daily

o Multivitamin syrup at 5 ml

o Zinc at 2mg/kg per day

o Copper at 0,3mg/kg/day

7. Start cautious feeding

The essential features of initial feeding are:

• frequent (every 2–3 h) oral small feeds of low osmolality and low

lactose

• nasogastric feeding if the child is eating ≤ 80% of the amount offered

at two consecutive feeds

• calories at 100 kcal/kg per day

25

• protein at 1–1.5 g/kg per day

• liquid at 130 ml/kg per day or 100 ml/kg per day if the child has

severe oedema

• in addition, if the child is breastfed, encourage continued

breastfeeding, but make sure the prescribed amounts of starter formula

are given:

8.Achieve catch-up growth

In the rehabilitation phase a vigorous approach to feeding is required

to achieve very high intakes and rapid weight gain of >10 g gain/kg/d.

The recommended milk-based F-100 contains 100 kcal and 2.9 g

protein/100 ml. Modified porridges or modified family foods can be

used provided they have comparable energy and protein

concentrations. Readiness to enter the rehabilitation phase is signaled

by a return of appetite, usually about one week after admission. A

gradual transition is recommended to avoid the risk of heart failure,

which can occur if children suddenly consume huge amounts.

To change from starter to catch-up formula:

• replace starter F-75 with the same amount of catch-up formula

F- 100 for 48 hours then,

• increase each successive feed by 10 ml until some feed remains

uneaten. The point when some remains unconsumed is likely to

occur when intakes reach about 30 ml/kg/feed (200 ml/kg/d).

Monitor during the transition for signs of heart failure:

• respiratory rate

• pulse rate

If respirations increase by 5 or more breaths/min and pulse by 25

or more beats/min for two successive 4-hourly readings, reduce the

volume per feed (give 4-hourly F-100 at 16 ml/kg/feed for 24 hours,

then 19 ml/kg/feed for 24 hours, then 22 ml/kg/feed for 48 hours, then

26

increase each feed by 10 ml as above).

After the transition give:

• frequent feeds (at least 4-hourly) of unlimited amounts of a

catch- up formula

• 150-220 kcal/kg/d

• 4-6 g protein/kg/d

• if the child is breastfed, encourage to continue (Note: breast milk

does not have sufficient energy and protein to support rapid

catch-up growth). See Appendix 8 for range of volumes for free

feeding with F-100.

Monitor progress after the transition by assessing the rate of

weight gain:

• weigh child each morning before feeding. Plot weight each week

calculate and record weight gain as g/kg/d3

If weight gain is:

• poor (<5 g/kg/d), child requires full reassessment

• moderate (5-10 g/kg/d), check whether intake targets are being

met, or if infection has been overlooked

• good (>10 g/kg/d), continue to praise staff and mothers

Calculating weight gain : The example is for weight gain over 7 days,

but the same procedure can be applied to any interval:

* substract from today’s weight (in g) the child’s weight 7 days earlier

* divide by 7 to determine the average daily weight gain (g/day) ;

* divide by the child’s average weight in kg to calculate the weight

gain as g/kg/day.

9.Provide sensory stimulation and emotional support

In severe malnutrition there is delayed mental and behavioural

development.

Provide:

• tender loving care

• a cheerful, stimulating environment

27

• structured play therapy 15-30 min/d

• physical activity as soon as the child is well enough

• maternal involvement when possible

(e.g. comforting, feeding, bathing, play)

10. Prepare for follow-up after recovery

A child who is 90% weight-for-length (equivalent to -1SD) can be

considered to have recovered. The child is still likely to have a low

weight-for-age because of stunting. Good feeding practices and

sensory stimulation should be continued at home. Show parent or carer

how to:

• feed frequently with energy- and nutrient-dense foods

• give structured play therapy

Advise parent or carer to:

• bring child back for regular follow-up checks

• ensure booster immunizations are given

• ensure vitamin A is given every six months

B. Emergency treatment of shock and severe anaemia

1. Shock in severely malnourished children

Shock from dehydration and sepsis are likely to coexist in severely

malnourished children. They are difficult to differentiate on clinical signs

alone. Children with dehydration will respond to IV fluids. Those with

septic shock and no dehydration will not respond. The amount of fluid

given is determined by the child’s response. Overhydration must be

avoided.

To start treatment:

• give oxygen

• give sterile 10% glucose (5 ml/kg) by IV

• give IV fluid at 15 ml/kg over 1 hour. Use Ringer’s lactate with 5%

dextrose; or half-normal saline with 5% dextrose; or half-strength

Darrow’s solution with 5% dextrose; or if these are unavailable,

28

Ringer’s lactate

• measure and record pulse and respiration rates every 10 minutes

• give antibiotics

If there are signs of improvement (pulse and respiration rates fall)

• repeat IV 15 ml/kg over 1 hour; then

• switch to oral or nasogastric rehydration with ReSoMal, 10 ml/kg/h

for up to 10 hours. (Leave IV in place in case required again); Give

ReSoMal in alternate hours with starter F-75, then

• continue feeding with starter F-75

If the child fails to improve after the first hour of treatment

(15 ml/kg), assume that the child has septic shock. In this case:

• give maintenance IV fluids (4 ml/kg/h) while waiting for blood,

• when blood is available transfuse fresh whole blood at 10 ml/kg

slowly over 3 hours; then

• begin feeding with starter F-75 (step 7)

If the child gets worse during treatment (breathing increases by 5 breaths or

more/min and pulse increases by 25 or more beats/min):

stop the infusion to prevent the child’s condition worsening

2. Severe anaemia in malnourished children

A blood transfusion is required if:

Hb is less than 4 g/dl

or if there is respiratory distress and Hb is between 4 and 6 g/dl

Give:

whole blood 10 ml/kg body weight slowly over 3 hours

furosemide 1 mg/kg IV at the start of the transfusion

It is particularly important that the volume of 10 ml/kg is not exceeded in

severely malnourished children. If the severely anaemic child has signs of

cardiac failure, transfuse packed cells (5-7 ml/kg) rather than whole blood.

Monitor for signs of transfusion reactions. If any of the following signs

develop during the transfusion, stop the transfusion:

• fever

29

• itchy rash

• dark red urine

• confusion

• shock

Also monitor the respiratory rate and pulse rate every 15 minutes. If either

of themrises, transfuse more slowly.

Following the transfusion,ift Hb remains less than 4 g/dl or between 4 and 6

g/dl in a child with continuing respiratory distress, DO NOT repeat the

transfusion within 4 days. In mild or moderate anaemia, oral iron should be

given for two months to replenish iron stores BUT this should not be started

until the child has begun to gain weight.

C. Treatment of associated conditions

Treatment of conditions commonly associated with severe malnutrition:

1. Vitamin A deficiency

If the child shows any eye signs of deficiency, give orally:

• vitamin A on days 1, 2 and 14 (for age >12 months, give 200,000 IU; for

age 6-12 months, give 100,000 IU; for age 0-5 months, give 50,000 IU). If

first dose has been given in the referring centre, treat on days 1 and 14 only

If there is corneal clouding or ulceration, give additional eye care to prevent

extrusion of the lens:

• instil chloramphenicol or tetracycline eye drops (1%) 2-3 hourly as required

for 7-10 days in the affected eye

• instil atropine eye drops (1%), 1 drop three times daily for 3-5 days

• cover with eye pads soaked in saline solution and bandage

Note: children with vitamin A deficiency are likely to be photophobic and have

closed eyes. It is important to examine the eyes very gently to prevent rupture.

2. Dermatosis

Signs:

• hypo-or hyperpigmentation

• desquamation

• ulceration (spreading over limbs, thighs, genitalia, groin, and behind

30

the ears)

• exudative lesions (resembling severe burns) often with secondary

infection, including Candida

Zinc deficiency is usual in affected children and the skin quickly improves with

zinc supplementation (see step 6). In addition:

• apply barrier cream (zinc and castor oil ointment, or petroleum jelly or

paraffin gauze) to raw areas

• omit nappies so that the perineum can dry

3. Parasitic worms

• give mebendazole 100 mg orally, twice daily for 3 days

4. Continuing diarrhoea

Diarrhoea is a common feature of malnutrition but it should subside during

the first week of treatment with cautious feeding. In the rehabilitation phase,

loose, poorly formed stools are no cause for concern provided weight gain is

satisfactory.

Mucosal damage and giardiasis are common causes of continuing

diarrhoea. Where possible examine the stools by microscopy. Give:

• metronidazole (7.5 mg/kg 8-hourly for 7 days) if not already given

Lactose intolerance. Only rarely is diarrhoea due to lactose intolerance.

Treat only if continuing diarrhoea is preventing general improvement. Starter F-

75 is a low-lactose feed. In exceptional cases:

• substitute milk feeds with yoghurt or a lactose-free infant formula

• reintroduce milk feeds gradually in the rehabilitation phase

Osmotic diarrhoea may be suspected if diarrhoea worsens substantially

with hyperosmolar starter F-75 and ceases when the sugar content is reduced and

osmolarity is <300 mOsmol/l. In these cases:

• use isotonic F-75 or low osmolar cereal-based F-75 (see Appendix 5 for

recipe)

• introduce F-100 gradually

5. Tuberculosis (TB)

If TB is strongly suspected (contacts with adult TB patient, poor growth

despite good intake, chronic cough, chest infection not responding to antibiotics):

31

• perform Mantoux test (false negatives are frequent)

• chest X-ray if possible

If test is positive or there is a strong suspicion of TB, treat according to

national TB guidelines.

D. Failure to respond to treatment

Failure to respond is indicated by:

1. High mortality

Case fatality rates vary widely: >20% should be considered unacceptable,

11-20% poor, 5-10% moderate, and <5% good.

If mortality is >5%, determine whether the majority of deaths occur:

• within 24 hours: consider untreated or delayed treatment of hypoglycaemia,

hypothermia, septicaemia, severe anaemia or incorrect rehydration fluid or

volume

• within 72 hours: check whether the volume of feed is too high or the wrong

formulation is used

• at night: consider hypothermia from insufficient covers, no night feeds

• when changing to catch-up F-100: consider too rapid a transition

2. Low weight gain during the rehabilitation phase

Poor : <5g/kg/d

Moderate : <5g/kg/d

Good : <5g/kg/d

If weight gain is <5 g/kg/d determine:

• whether this is for all cases (need major management overhaul)

• whether this is for specific cases (reassess child as for a new

admission)

Possible causes of poor weight gain are:

a) Inadequate feeding

Check:

• that night feeds are given

• that target energy and protein intakes are achieved: is actual intake (offered

minus leftovers) correctly recorded? Is the quantity of feed recalculated as

32

the child gains weight? Is the child vomiting or ruminating?

• feeding technique: is the child fed frequently and offered unlimited

amounts?

• quality of care: are staff motivated/gentle/loving/patient?

• all aspects of feed preparation: scales, measurement of ingredients, mixing,

taste, hygienic storage, adequate stirring if the ingredients separate out

• that if giving family foods, they are suitably modified to provide

>100kcal/100g (if not, re-modify). If resources for modification are limited,

or children are not inpatients, compensate by replacing F-100 with catch- up

F-135 containing 135 kcal/100ml (see Appendix 5 for recipe)

b) Specific nutrient deficiencies

Check:

• adequacy of multivitamin composition and shelf-life

• preparation of electrolyte/mineral solution and whether this is correctly

prescribed and administered. If in goitrous region, check potassium iodide

(KI) is added to the electrolyte/mineral solution (12 mg/2500 ml) or give all

children Lugol’s iodine (5-10 drops/day)

• that, if modified family foods are substantially replacing F-100, electrolyte/

mineral solution is added to the family food (20 ml/day)

c) Untreated infection

If feeding is adequate and there is no malabsorption, some hidden infection can be

suspected. Urinary tract infections, otitis media, TB and giardiasis are easily

overlooked, hence

• re-examine carefully

• repeat urinalysis for white blood cells

• examine stools

• if possible, take chest X-ray

Alter the antibiotic schedule (step 5) only if a specific infection is identified.

d) HIV/AIDS

In children with HIV/AIDS, good recovery from malnutrition is possible

though it may take longer and treatment failures may be common. Lactose

intolerance occurs in severe HIV-related chronic diarrhoea. Treatment should be

33

the same as for HIV negative children.

e ) Psychological problems

Check for:

• abnormal behaviour such as stereotyped movements (rocking), rumination

(self-stimulation through regurgitation) and attention seeking

Treat by giving the child extra care, love and attention. For the ruminator,

firmness, but with affection and without intimidation, can assist.

E. Discharge before recovery is complete

A child may be considered to have recovered and be ready for discharge when

she/he reaches 90% weight-for-length. For some children, earlier discharge may

be considered if effective alternative supervision is available. Domiciliary care or

home-based treatment should be considered only if the following criteria are met:

The child

is aged >12 months

has completed antibiotic treatment

has good appetite and good weight gain

has taken potassium/magnesium/mineral/vitamin supplement for 2 weeks (or

continuing supplementation at home is possible)

The mother/carer

is not employed outside the home

is specifically trained to give appropriate feeding (type, amount and

frequency)

has the financial resources to feed the child

lives within easy reach of the hospital for urgent readmission if the child

becomes ill

can be visited weekly

is trained to give structured play therapy

is motivated to follow the advice given

Local health workers

• are trained to support home care

• are specifically trained to examine the child clinically at home, to decide

34

when to refer him/her back to hospital, to weigh the child, and give

appropriate advice are motivated. When children are being rehabilitated at

home, it is essential to give frequent meals with a high energy and protein

content. Aim at achieving at least 150 kcal/kg/d and adequate protein intake

(at least 4 g/kg/d). This means feeding the child at least 5 times per day with

foods that contain approximately 100 kcal and 2-3 g protein per 100 g. A

practical approach would be using simple modifications of the usual home

foods. Vitamin, iron and electrolyte/mineral supplements can be continued

at home. The carer should be shown how to:

o give appropriate meals at least 5 times daily

o give high energy snacks between meals (e.g. milk, banana, bread, biscuits,

peanut butter)

o assist and encour age the child to complete each meal

o give electrolyte and micronutrient supplements. Give 20 ml (4teaspoons) of

the electrolyte/mineral solution daily. Since it tastes unpleasant, it will

probably need to be masked in porridge, or milk (one teaspoon/200 ml

fluid)

o breastfeed as often as the child wants

2.10 Complication

Of malnutrition

Fatty liver may be result as it is often seen in Kwashiorkor. Fat content

may be up as high as 50%, due to increase in fluz of fatty acids from

adipose tissue for production of energy and decreased hepatic synthesis o

P-lipoporetein that normaly transport triglycerides from the liver.

Pancreas shows marked atrophy of acinar cells.

Heart muscles atrophy leads to reduced cardiac output, resulting to

congestive cardiac failure.

Hemopoietic system results in anemia

Muscle shows glycogen depletion and disorganization of the sarcomere

Of refeeding

35

Refeeding syndrome may complicate the acute nutritional rehabilitation

of children who are undernourished from any cause. The hallmark of

refeeding syndrome is the development of severe hypophosphatemia after

the cellular uptake of phosphate during the 1st week of starting to refeed.

Serum phosphate levels of ≤0.5 mmol/L can produce weakness,

rhabdomyolysis, neutrophil dysfunction, cardiorespiratory failure,

arrhythmias, seizures, altered level of consciousness, or sudden death.

Phosphate levels should be monitored during refeeding, and if low,

phosphate should be administered during refeeding to treat severe

hypophosphatemia.

2.11 Prognosis

Some serious consequences may arise due to PEM. Nutrition affects many organs

and system in the body and it is also usually accompanied by other micronutrient

deficiency. In acute state, PEM may cause death due to hypothermia,

hypoglycemia, dehydration and electrolyte imbalance. Short term consequences of

PEM may cause children to be apathetic, speech and growth retardation that leads

to decrease in cognitive function.

36

CHAPTER III

CONCLUSION

3.1 Conclusion

Malnutrition is closely linked to poverty and socio-economic condition of a

country. It is often overlooked nevertheless the harm that it caused is nothing to

be lightly thought of. Organ dysfunction, cognitive function retardation and even

death may even occur. Treatment of malnutrition is long-term and require detail

consideration by both parts of physician tending the patients and patients’s

parents/carer.

3.2 Prevention

It is important to reduce the number of prevalence of PEM as its serious

consequences that it may cause. Hence educating parents and communities is

thought to be the best preventive solution to reduce this occurrence.

Parents are encouraged to follow a few instructions below in order to reduce the

number of occurrence of PEM.

1. Exclusive breastfeeding up to 6 months, afterwards, the should be

introduced to various kinds of food in addition alongside breastmilk

2. Give children a variety of food with enough composition of carbohydrates,

fats, vitamin and mineral.

3. Be proactive to measure and record children’s height and weight

measurements to check their growth rate.

4. Consult accessible medical services should there be any problems or initial

signs of failure to thrive in babies and children.

37

ACKNOWLEDGEMENTS

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countries. CMAJ 2005, 173(3):279-286. Available from:

http://www.cmaj.ca/cgi/content/full/173/3/279, (Accessed March 2,

2011)

2. Onis M de, Monteiro C, Clugston G. The worldwide magnitude of protein

energy malnutrition: an overview from the WHO Global Database on

Child Growth. Bulletin of the World Health Organization. 1993;71(6).

3. Alleyne, G. A. O., Hay, R. W., Picou, D. l., Stanfield, J. P. and Whitehead,

R. G.

Protein-energy Malnutrition. Edward Arnold, London.

4. Maxine A. Papadakis, Stephen J. McPhee, Michael W. Rabow. Current

Medical Diagnosis and Treatment 2014. 53rd edition. United States of

America: McGraw-Hill Education, Lange; 2014

5. Kliegman RM, Stanton BF, Schir NF, Behrman RE. Nelson Textbook of

Pediatrics. 19th edition. Philadelphia: Elsevier Saunders; 2011

6. Kliegman RM, Stanton BF, Schir NF, Behrman RE. Nelson Textbook of

Pediatrics. 19th edition. Philadelphia: Elsevier Saunders; 2011

7. Ann Ashworth, Sultana Khanum, Alan Jackson, Claire Schofield.

Guidelines for the Inpatient Treatment of Severely Malnourished Children.

World Health Organization ; 2003

8. Kementerian Kesehatan Republik Indonesia. Pedoman Pelayanan Anak

Gizi Buruk. Jakarta; 2011.

9. Ann Ashworth, Sultana Khanum, Alan Jackson, Claire Schofield.

Guidelines for the Inpatient Treatment of Severely Malnourished Children.

World Health Organization ; 2003

10. Fechner A et al: Antioxidant status and nitric oxide in the malnutrition

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11. Departemen Kesehatan RI Direktorat Jenderal Bina KesehatanMasyarakat

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