REFERAT ILMU KESEHATAN ANAK

PROTEIN ENERGY MALNUTRITION

Preceptor:
dr. Pulung M. Silalahi, Sp.A

Compiled by:
Naina Karamina Sakina (07120100102)

KEPANITERAAN KLINIK ILMU KESEHATAN ANAK

RUMAH SAKIT BHAYANGKARA TK. I RADEN SAID
SUKANTO
FAKULTAS KEDOKTERAN UNIVERSITAS PELITA HARAPAN
PERIODE 9 JUNI 2014 16 AGUSTUS 2014

FOREWORD
Praise to Almighty God for the gift of grace so that I can finish the task referat given
by the supervisor. Referat is made for the settlement of their clinical duties for Co-Ass the
Faculty of Medicine, University of Pelita Harapan granted by SMF Section of Child Health
Level I Police Hospitals Raden Said Sukanto.
Referat discussed thoroughly on Protein Energy Malnutrition. Materials for referat
taken from books and journals and articles that are available online. The authors hope that
this made referat be useful for the readers. Hope the authors that the presence of this referat
can help understand more thoroughly the topics being discussed.
Thank you to all those who have assisted in the completion of this referat
manufacture. Especially the counselors at the child, especially dr. Pulung M. Silalahi, Sp. A
writer in the making as mentors this referat and all parties that provide direction and support
in the process of resolving this referat.
The author realizes that this referat still far from perfect and has many flaws.
Therefore, the authors are happy to accept all criticisms and feedback given that this referat
be more perfect. Finally, I hope this referat be useful for writers and readers. May God bless
us all. Amen.
Jakarta, June 2014
author

TABLE OF CONTENTS

FOREWORD............................................................................................................. 2
TABLE OF CONTENTS.............................................................................................. 3
CHAPTER I........................................................... Error: Reference source not found
INTRODUCTION................................................... Error: Reference source not found
CHAPTER II.......................................................... Error: Reference source not found
LITERATURE REVIEW........................................... Error: Reference source not found
2.1. Definition...................................................... Error: Reference source not found
2.2. Epidemiology................................................. Error: Reference source not found
2.3. Etiologi........................................................ Error: Reference source not found
2.4. Klasifikasi histopatologi.................................... Error: Reference source not found
2.5. Patofisiologi.............................................. Error: Reference source not found
2.6. Gejala Klinis.................................................. Error: Reference source not found
2.7. Diagnosis.................................................. Error: Reference source not found
2.8. Penatalaksanaan...................................... Error: Reference source not found
2.9. Komplikasi.................................................... Error: Reference source not found
2.10. Prognosis................................................ Error: Reference source not found
CHAPTER III......................................................... Error: Reference source not found

CONCLUSION Error: Reference source

not found
BIBLIOGRAPHY.................................................... Error: Reference source not found

CHAPTER I

INTRODUCTION
1.1

Background
Protein Energy Malnutrition (PEM) is one of the major nutritional problems in
Indonesia. This situation affects many groups of infants who are the future generation.
PEM may cause a disturbance in growth and mental development disorders. Infants
and children with severe PEM level will show clinical signs of kwashiorkor or
marasmus.
In the advanced phase of children under five with PEM will be susceptible to disease
infection, swelling of the liver, the organ and its function abnormalities, skin
inflammation and impaired brain growth. In addition, the impact of PEM in children
under five can lower the immune system so that children are often sick. According to
Schroeder (2001), children under five with PEM are at risk of decline in motor
development, lower cognitive function as well as the capacity and performance of
PEM ultimately have a negative effect on the high risk of death. In addition, children
who had suffered from malnutrition will be difficult to pursue growth according to
age.
PEM in children in certain levels can cause brain weight, cell number, cell size, and
other biochemical substances is lower than in normal children. The younger children
who suffer from the more severe PEM also consequences thereof. This situation will
become even greater when malnutrition starts in the womb. Mental retardation caused
by malnutrition state of mild or moderate tend to be restored by increasing the good
state of nutrition and the environment the child is raised.

1.2

Purpose of writing
Understanding more about the protein energy malnutrition

1.3

Problems
1.3.1

Definition, epidemiology, and risk factor of protein energy malnutrition

1.3.2

Etiology, pathogenesis, and clinical manifestations of protein energy

malnutrition
1.3.3

Diagnosis, differential diagnosis, treatment, and prevention of protein energy

malnutrition

1.4

Benefits of writing
1.4.1 Provide an understanding of protein energy malnutrition diagnosis and
management so that the right can be granted
1.4.2

As a source of knowledge for other academics to be the development of

subsequent papers

CHAPTER II

LITERATURE REVIEW
2.1

Definition
Malnutrition is a cellular imbalance between the supply of nutrients and energy and

the body's demand for them to ensure growth, maintenance, and specific functions. The term
malnutrition encompasses both ends of the nutrition spectrum, from undernutrition
(underweight, stunting, wasting, and micronutrient deficiencies) to overnutrition (overweight,
obesity). Nutritional status is often assessed in terms of anthropometry. International
references have been established that allow normalization of anthropometric measures in
terms of z scores defined as the childs height (weight) minus the median height (weight) for
the age and sex of the child divided by the relevant standard deviation (Table 43-3).

Protein-energy malnutrition (PEM) is manifested primarily by inadequate dietary

intakes of protein and energy, either because the dietary intakes of these 2 nutrients are less
than required for normal growth or because the needs for growth are greater than can be
supplied by what otherwise would be adequate intakes. PEM is almost always accompanied
by deficiencies of other nutrients. Based on the duration and severity of protein and energy
deficiency, PEM is classified into 2 grades, mild-moderate PEM and severe PEM. Mild-

moderate PEM not yet shown the typical clinical manifestation, found only impairment of
growth and underweight children. In severe PEM, besides the clinical symptoms also found
biochemical abnormalities in accordance with the clinical form. Severe PEM, applies to a
group of related disorders that include marasmus (nonedematous malnutrition with severe
wasting), kwashiorkor (edematous malnutrition), and marasmus-kwashiorkor (wasting and
edema). Nonedematous malnutrition was believed to result primarily from inadequate energy
intake or inadequate intakes of both energy and protein, whereas edematous malnutrition was
believed to result primarily from inadequate protein intake. The 3 conditions have distinct
clinical and metabolic features, but they also have a number of overlapping features. A low
plasma albumin concentration, often believed to be a manifestation of edematous
malnutrition, is common in children with both edematous and nonedematous malnutrition.
The term marasmus is derived from the Greek word marasmos, which means
withering or wasting, which is due to prolonged caloric deprivation or inadequate intake of
protein and calories and is characterized by emaciation. It is characterized by severe wasting
of fat and muscle, which results in an old-person skin-and-bones appearance. This is the most
common form of PEM seen in nutritional emergencies where food shortages are severe. In
contrast to the relative anorexia seen in children with kwashiorkor (who may be getting
enough calories but not enough protein), children with marasmus are hungry. It is also be the
result of chronic or recurring infections with decreased food intake.
The term kwashiorkor is taken from the Ga language of Ghana and means "the sickness of
the weaning." It refers to an inadequate protein intake with reasonable caloric (energy) intake.
Kwashiorkor is a disease brought on due to a severe dietary protein deficiency, and this child,
whose diet fit such a deficiency profile, presented with symptoms including edema of legs
and feet, light-colored, thinning hair, anemia, a pot-belly, and shiny skin. Edema is
characteristic of kwashiorkor but is absent in marasmus.
Studies suggest that marasmus represents an adaptive response to starvation, whereas
kwashiorkor represents a maladaptive response to starvation. Children may present with a
mixed picture of marasmus and kwashiorkor, and children may present with milder forms of
malnutrition. For this reason, Jelliffe suggested the term protein-calorie (energy) malnutrition
to include both entities.

In the USA, severe malnutrition has been reported in families who use unusual and
inadequate foods to feed infants whom the parents believe to be at risk for milk allergies and
also in families who believe in fad diets. Many cases are associated with rice milk diets, a
product that is very low in protein content. In addition, protein-calorie malnutrition has been
noted in chronically ill patients in neonatal or pediatric intensive care units as well as among
patients with burns, HIV, cystic fibrosis, failure to thrive, chronic diarrhea syndromes,
malignancies, bone marrow transplantation, and inborn errors of metabolism.
2.2

Epidemiology
Protein energy malnutrition is one of the major nutritional problems in Indonesia.

According to SUSENAS 2002, 26% of under-5s suffer from malnutrition. Approximately

70.0% of the world's malnourished children live in Asia, resulting in the region having the
highest concentration of childhood malnutrition. About half of the preschool children are
malnourished ranging from 16.0% in the People's Republic of China to 64.0% in Bangladesh.
Prevalence of stunting and underweight are high especially in South Asia where one in
every two preschool children is stunted. In 2004 37% of under-5s were underweight (28%
moderately underweight, and 9% severely underweight) and 38% were too short (source
Susenas 2004 - National Socio-Economic Survey Survei Sosial Ekonomi Nasional).
The prevalent rate of mild and severe Protein Energy Deficiency in children under five
in Indonesia in 2000 are 17,13% and 7,53%, along with 19,3% and 8% in 2002, according to
Susenas 2000.
In 2003, the prevalent of protein energy deficiency in children are 27,5% (5 million
under five child with protein energy malnutrition), 19,2% (3,5 million) mild protein energy
deficiency, and 8,3% (1,5 million) severe protein energy deficiency, whereas in 2005, the
prevalent of protein energy deficiency has rise to 19,2 % for mild malnutrition and 8,8 % for
severe malnutrition according to ministry of health republic of Indonesia (2006).
The prevalent of malnutrition has dropped from 18,4% (13% mild malnutrition, 5,4%
severe malnutrition) in 2007 to 17,9% (13% mild malnutrition, 4,9% severe malnutrition) in
2010 according to Riskesdas 2010 data as shown in table below :

2.3

Etiology

Social and economic factors

Biological factors

Environmental factors
Amongst the social, economic, biological, and environmental factors the common
causes are :
-

Lack of breast feeding and giving diluted formula

Improper complementary feeding

Over crowding in family

Ignorance

Illiteracy

Lack of health education

Poverty

Infection

Familial disharmony

Role of free radicals and Aflatoxin

Two new theories have been postulated recently to explain the pathogenesis of
kwashiorkor. These include free radical damage and aflatoxin poisoning. These may
damage liver cells giving rise to kwashiorkor.

Age of the host

PEM frequent happens in infants and young children whose rapid growth increases
nutritional requirement. PEM in pregnant and lactating women can affect the growth,
nutritional status, and survival rates of their fetuses, new born, and infants. Elderly
can also suffer from PEM due to alteration of GI system.

Protein Energy Malnutrition can be divided into primary or secondary. Primary PEM is
caused by inadequate nutrient intake. Secondary PEM results from disorders or drugs that
interfere with nutrient use.
Primary PEU: Worldwide, primary PEM occurs mostly in children and the elderly who lack
access to nutrients, although a common cause in the elderly is depression. PEM can also
result from fasting or anorexia nervosa. Child or elder abuse may be a cause.
In children, chronic primary PEM has 2 common forms: marasmus and kwashiorkor. The
form depends on the balance of nonprotein and protein sources of energy. Starvation is an
acute severe form of primary PEU.
Secondary PEU: This type most commonly results from the following:
Disorders that affect GI function: These disorders can interfere with digestion (eg,
pancreatic insufficiency), absorption (eg, enteritis, enteropathy), or lymphatic
transport of nutrients (eg, retroperitoneal fibrosis, Milroy disease).
Wasting disorders: In wasting disorders (eg, AIDS, cancer, COPD) and renal failure,
catabolism causes cytokine excess, resulting in undernutrition via anorexia and
cachexia (wasting of muscle and fat). End-stage heart failure can cause cardiac
cachexia, a severe form of undernutrition; mortality rate is particularly high. Factors
contributing to cardiac cachexia may include passive hepatic congestion (causing
anorexia), edema of the intestinal tract (impairing absorption), and, in advanced
disease, increased O2 requirement due to anaerobic metabolism. Wasting disorders can

decrease appetite or impair metabolism of nutrients.

Conditions that increase metabolic demands: These conditions include infections,
hyperthyroidism, pheochromocytoma, other endocrine disorders, burns, trauma,
surgery, and other critical illnesses.
2.4

Pathophysiology

Why edematous malnutrition develops in some children and nonedematous malnutrition

develops in others is unknown. One factor may be the variability among infants in nutrient
requirements and in body composition at the time the dietary deficit is incurred. It also has
been proposed that giving excess carbohydrate to a child with nonedematous malnutrition
reverses the adaptive responses to low protein intake, resulting in mobilization of body
protein stores. Eventually, albumin synthesis decreases, resulting in hypoalbuminemia with
edema. Fatty liver also develops secondary, perhaps, to lipogenesis from the excess
carbohydrate intake and reduced apolipoprotein synthesis. Other causes of edematous
malnutrition are aflatoxin poisoning as well as diarrhea, impaired renal function and
decreased Na+/K+-ATPase activity. Free radical damage has been proposed as an important
factor in the development of edematous malnutrition. This proposal is supported by low
plasma concentrations of methionine, a dietary precursor of cysteine, which is needed for
synthesis of the major antioxidant factor, glutathione. This possibility also is supported by
lower rates of glutathione synthesis in children with edematous compared with nonedematous
malnutrition.
In general, marasmus is an insufficient energy intake to match the body's requirements. As a
result, the body draws on its own stores, resulting in emaciation. In kwashiorkor, adequate
carbohydrate consumption and decreased protein intake lead to decreased synthesis of
visceral proteins. The resulting hypoalbuminemia contributes to extravascular fluid
accumulation. Impaired synthesis of B-lipoprotein produces a fatty liver.
Protein-energy malnutrition also involves an inadequate intake of many essential nutrients.
Low serum levels of zinc have been implicated as the cause of skin ulceration in many
patients. In a 1979 study of 42 children with marasmus, investigators found that only those
children with low serum levels of zinc developed skin ulceration. Serum levels of zinc
correlated closely with the presence of edema, stunting of growth, and severe wasting. The
classic "mosaic skin" and "flaky paint" dermatosis of kwashiorkor bears considerable
resemblance to the skin changes of acrodermatitis enteropathica, the dermatosis of zinc

deficiency.
Marasmus and kwashiorkor can both be associated with impaired glucose clearance that
relates to dysfunction of pancreatic beta-cells.[3] In utero, plastic mechanisms appear to
operate, adjusting metabolic physiology and adapting postnatal undernutrition and
malnutrition to define whether marasmus and kwashiorkor will develop.[4]

2.5

Clinical Manifestations

Nonedematous malnutrition (marasmus) is characterized by failure to gain weight and

irritability, followed by weight loss and listlessness until emaciation results. The skin loses
turgor and becomes wrinkled and loose as subcutaneous fat disappears. Loss of fat from the
sucking pads of the cheeks often occurs late in the course of the disease; thus, the infants
face may retain a relatively normal appearance compared with the rest of the body, but this,
too, eventually becomes shrunken and wizened. Infants are often constipated, but they can
have starvation diarrhea, with frequent small stools containing mucus. The abdomen may be
distended or flat, with the intestinal pattern readily visible. There is muscle atrophy and
resultant hypotonia. As the condition progresses, the temperature usually becomes subnormal
and the pulse slows.
Clinical features of marasmus
Poor growth. In all cases the child fails to grow properly. If the age is known, the weight will
be found to be extremely low by normal standards (below 60 percent or -3 SD of the
standard). In severe cases the loss of flesh is obvious: the ribs are prominent; the belly, in
contrast to the rest of the body, may be protuberant; the face has a characteristic simian
(monkey-like) appearance; and the limbs are very emaciated. The child appears to be skin and
bones. An advanced case of the disease is unmistakable, and once seen is never forgotten.
Wasting. The muscles are always extremely wasted. There is little if any subcutaneous fat
left. The skin hangs in wrinkles, especially around the buttocks and thighs. When the skin is
taken between forefinger and thumb, the usual layer of adipose tissue is found to be absent.
Alertness. Children with marasmus are quite often not disinterested like those with
kwashiorkor. Instead the deep sunken eyes have a rather wide-awake appearance. Similarly,

the child may be less miserable and less irritable.

Appetite. The child often has a good appetite. In fact, like any starving being, the child may
be ravenous. Children with marasmus often violently suck their hands or clothing or anything
else available. Sometimes they make sucking noises.
Anorexia. Some children are anorexic.
Diarrhoea. Stools may be loose, but this is not a constant feature of the disease. Diarrhoea of
an infective nature, as mentioned above, may commonly have been a precipitating factor.
Anaemia. Anaemia is usually present.
Skin sores. There may be pressure sores, but these are usually over bony prominences, not in
areas of friction. In contrast to kwashiorkor, there is no oedema and no flaky-paint dermatosis
in marasmus.
Hair changes. Changes similar to those in kwashiorkor can occur. There is more frequently a
change of texture than of colour.
Dehydration. Although not a feature of the disease itself, dehydration is a frequent
accompaniment of the disease; it results from severe diarrhoea (and sometimes vomiting).

Edematous malnutrition (kwashiorkor) can occur initially as vague manifestations that

include lethargy, apathy, and/or irritability. When kwashiorkor is advanced, there is lack of
growth, lack of stamina, loss of muscle tissue, increased susceptibility to infections,
vomiting, diarrhea, anorexia, flabby subcutaneous tissues, and edema. The edema usually
develops early and can mask the failure to gain weight. It is often present in internal organs
before it is recognized in the face and limbs. Liver enlargement can occur early or late in the
course of disease. Dermatitis is common, with darkening of the skin in irritated areas, but in
contrast to pellagra not in areas exposed to sunlight. Depigmentation can occur after
desquamation in these areas, or it may be generalized. The hair is sparse and thin, and in
dark-haired children, it can become streaky red or gray. Eventually, there is stupor, coma, and
death.

Clinical signs of kwashiorkor

All cases of kwashiorkor have oedema to some degree, poor growth, wasting of muscles and
fatty infiltration of the liver. Other signs include mental changes, abnormal hair, a typical
dermatosis, anaemia, diarrhoea and often evidence of other micronutrient deficiencies.
Oedema. The accumulation of fluid in the tissues causes swelling; in kwashiorkor this
condition is always present to some degree. It usually starts with a slight swelling of the feet
and often spreads up the legs. Later, the hands and face may also swell. To diagnose the
presence of oedema the medical attendant presses with a finger or thumb above the ankle. If
oedema is present the pit formed takes a few seconds to return to the level of the surrounding
skin.
Poor growth. Growth failure always occurs. If the child's precise age is known, the child will
be found to be shorter than normal and, except in cases of gross oedema, lighter in weight
than normal (usually 60 to 80 percent of standard or below 2 SD). These signs may be
obscured by oedema or ignorance of the child's age.
Wasting. Wasting of muscles is also typical but may not be evident because of oedema. The
child's arms and legs are thin because of muscle wasting.
Fatty infiltration of the liver. This condition is always found in post-mortem examination of
kwashiorkor cases. It may cause palpable enlargement of the liver (hepatomegaly).
Mental changes. Mental changes are common but not invariably noticed. The child is usually
apathetic about his or her surroundings and irritable when moved or disturbed. The child
prefers to remain in one position and is nearly always miserable and unsmiling. Appetite is
nearly always poor.
Hair changes. The hair of a normal Asian, African or Latin American child is usually dark
black and coarse in texture and has a healthy sheen that reflects light. In kwashiorkor, the hair
becomes silkier and thinner. African hair loses its tight curl. At the same time it lacks lustre, is
dull and lifeless and may change in colour to brown or reddish brown. Sometimes small tufts
can be easily and almost painlessly plucked out. On examination under a microscope,

plucked hair exhibits root changes and a narrower diameter than normal hair. The tensile
strength of the hair is also reduced. In Latin America bands of discoloured hair are reported
as a sign of kwashiorkor. These reddish-brown stripes have been termed the "flag sign" or
"signa bandera".
Skin changes. Dermatosis develops in some but not all cases of kwashiorkor. It tends to
occur first in areas of friction or of pressure such as the groin, behind the knees and at the
elbow. Darkly pigmented patches appear, which may peel off or desquamate. The similarity
of these patches to old sun-baked, blistered paint has given rise to the term "flaky-paint
dermatosis". Underneath the flaking skin are atrophic depigmented areas which may
resemble a healing burn.
Anaemia. Most cases have some degree of anaemia because of lack of the protein required to
synthesize blood cells. Anaemia may be complicated by iron deficiency, malaria, hookworm,
etc.
Diarrhoea. Stools are frequently loose and contain undigested particles of food. ometimes
they have an offensive smell or are watery or tinged with blood.
Moonface. The cheeks may appear to be swollen with either fatty tissue or fluid, giving the
characteristic appearance known as "moonface".
Signs of other deficiencies. In kwashiorkor some subcutaneous fat is usually palpable, and
the amount gives an indication of the degree of energy deficiency. Mouth and lip changes
characteristic of vitamin B deficiency are common. Xerosis or xerophthalmia resulting from
vitamin A deficiency may be seen. Deficiencies of zinc and other micronutrients may occur.

Comparison of the features of kwashiorkor and marasmus

Feature

Kwashiorkor

Marasmus

Growth failure

Present

Present

Wasting

Present

Present, marked

Oedema

Present (sometimes mild)

Absent

Hair changes

Common

Less common

Mental changes

Very common

Uncommon

Dermatosis, flaky-paint

Common

Does not occur

Appetite

Poor

Good

Anaemia

Severe (sometimes)

Present, less severe

Subcutaneous fat

Reduced but present

Absent

Face

May be oedematous

Drawn in, monkey-like

Fatty infiltration of liver

Present

Absent

Marasmic kwashiorkor
Children with features of both nutritional marasmus and kwashiorkor are diagnosed as having
marasmic kwashiorkor. In the Wellcome classification (see above) this diagnosis is given for
a child with severe malnutrition who is found to have both oedema and a weight for age
below 60 percent of that expected for his or her age. Children with marasmic kwashiorkor
have all the features of nutritional marasmus including severe wasting, lack of subcutaneous
fat and poor growth, and in addition to oedema, which is always present, they may also have
any of the features of kwashiorkor described above. There may be skin changes including

flaky-paint dermatosis, hair changes, mental changes and hepatomegaly. Many of these
children have diarrhoea.

MARASMUS

2.6

KWASHIORKOR

Diagnosis

Anamnesis and physical examination

Common complaint that can be found when doing the anamnesis is the lack of growth, thin
child, or underweight. other than that other complaints are children who is difficult or doesnt
want to eat, often suffer from recurrent pain, or the onset of swelling on both legs, sometimes
to the whole body. A checklist for taking the childs medical history and conducting the
physical examination is given in the box below.

Tests
Where facilities permit, the tests given in Table 4 may help to diagnose specific problems.
They are not needed, however, to guide or monitor treatment. The interpretation of test results
is frequently altered by malnutrition. For this reason, laboratory tests may misguide
inexperienced workers. The most important guide to treatment is frequent careful assessment
of the child.

Nutritional status of under 5 children measured according to age, body weight, and height.
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). 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:
a. Classification of Nutritional Status based on weight/age (WFA) indicator:
Malnutrition

: Zscore <-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

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

The World Health Organization (WHO) defines severe acute malnutrition as a midupper 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.
According to WHO, malnutrition is classified as moderate and severe, as shown
in table 3 :

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

KEADAAN GIZI
Gizi

BB

Edema

BB /

(Harvard)
> 80%

TB
(-)

60 80 %

(-)

normal
PEM
ringan
sedang)

Underweight
=
Undernourished

PEM

Kwashiorkor
Marasmuskwashiorkor
Marasmus

60 80 %

(+)

< 60 %

(+)

< 60 %

(-)

< 60%

(-)

Nutritional

Dwarfism

2.7

Treatment

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 childs family are followed
to prevent relapse and assure the continued physical, mental and emotional
development of the child.

The guidelines for the treatment of severe malnutrition are divided in five sections:
A.

General principles for routine care (the10 steps)

B.

Emergency treatment of shock and severe anaemia

C.

Treatment of associated conditions

D.

Failure to respond to treatment

E.

Discharge before recovery is complete

A. GENERAL PRINCIPLES FOR ROUTINE CARE

There are ten essential steps:
1.Treat/prevent hypoglycaemia
2. Treat/prevent hypothermia
3. Treat/prevent dehydration
4. Correct electrolyte imbalance
5. Treat/prevent infection
6. Correct micronutrient deficiencies
7. Start cautious feeding
8.Achieve catch-up growth

9.Provide sensory stimulation and emotional support

10. Prepare for follow-up after recovery
These steps are accomplished in two phases: an initial stabilisation phase where the acute
medical conditions are managed; and a longer rehabilitation phase. Note that treatment
procedures are similar for marasmus and kwashiorkor.
Step 1. Treat/prevent hypoglycaemia
Hypoglycaemia and hypothermia usually occur together and are signs of infection. Check for
hypoglycaemia whenever hypothermia (axillary<35.0oC; rectal<35.5oC) is found. Frequent
feeding is important in preventing both conditions.
Treatment:
If the child is conscious and dextrostix shows <3mmol/l or 54mg/dl give:

50 ml bolus of 10% glucose or 10% sucrose solution (1 rounded teaspoon of sugar in

3.5 tablespoons water), orally or by nasogastric (NG) tube. Then feed starter F-75 (see
step 7) every 30 min. for two hours (giving one quarter of the two-hourly feed each
time)

antibiotics (see step 5)

two-hourly feeds, day and night (see step 7)

If the child is unconscious, lethargic or convulsing give:

IV sterile 10% glucose (5ml/kg), followed by 50ml of 10% glucose

or sucrose by Ng tube. Then give starter F-75 as above

antibiotics

two-hourly feeds, day and night

Monitor:

blood glucose: if this was low, repeat dextrostix taking blood from finger or heel, after
two hours. Once treated, most children stabilise within 30 min. If blood glucose falls to
<3 mmol/l give a further 50ml bolus of 10% glucose or sucrose solution, and continue
feeding every 30 min. until stable

rectal temperature: if this falls to <35.5oC, repeat dextrostix

level of consciousness:

if this deteriorates, repeat dextrostix

Prevention:

feed two-hourly, start straightaway (see step 7) or if necessary, rehydrate first

always give feeds throughout the night

Note: If you are unable to test the blood glucose level, assume all severely malnourished
children are hypoglycaemic and treat accordingly.
Step 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 mothers 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

blood glucose level: check for hypoglycaemia whenever hypothermia is found

(Appendix 2 provides an example of a chart for recording temperature, pulse and
respiratory rates).

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 childs temperature is too low to
register on an ordinary thermometer, assume the child has hypothermia.
Step 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

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

Step 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.

Step 5. Treat/prevent infection

In severe malnutrition the usual signs of infection, such as fever, are often absent, and
infections are often hidden. Therefore give routinely on admission:

broad-spectrum antibiotic(s) AND

measles vaccine if child is > 6m and not

immunised
(delay if the child is in shock)
Note: Some experts routinely give, in addition to broad-spectrum antibiotics, metronidazole

(7.5 mg/kg 8-hourly for 7 days) to hasten repair of the intestinal mucosa and reduce the risk
of oxidative damage and systemic infection arising from the overgrowth of anaerobic bacteria
in the small intestine.
Choice of broad-spectrum antibiotics:
if the child appears to have no complications give:

Co-trimoxazole 5 ml paediatric suspension orally twice daily for 5 days (2.5 ml if

weight <6 kg). (5 ml is equivalent to 40 mg TMP+200mg SMX).

OR b) if the child is severely ill (apathetic, lethargic) or has complications (hypoglycaemia;
hypothermia; broken skin; respiratory tract or urinary tract infection) give:

Ampicillin 50 mg/kg IM/IV 6-hourly for 2 days, then oral amoxycillin 15

mg/kg 8-hourly for 5 days, or if amoxycillin is not available, continue with ampicillin
but give orally 50 mg/kg 6-hourly

AND

Gentamicin 7.5 mg/kg IM/IV once daily for 7 days

If the child fails to improve clinically within 48 hours, ADD:

Chloramphenicol 25 mg/kg IM/IV 8-hourly for 5 days

Where specific infections are identified, ADD:

specific antibiotics if appropriate

antimalarial treatment if the child has a positive blood film for malaria
parasites.

If anorexia persists after 5 days of antibiotic treatment, complete a full 10- day course. If
anorexia still persists, reassess the child fully, checking for sites of infection and potentially
resistant organisms, and ensure that vitamin and mineral supplements have been correctly
given.

Step 6. Correct micronutrient deficiencies

All severely malnourished children have vitamin and mineral deficiencies. Although anaemia
is common, do NOT give iron initially but wait until the child has a good appetite and starts
gaining weight (usually by the second week), as giving iron can make infections worse.
Give:

Vitamin A orally on Day 1 (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) unless there is

definite evidence that a dose has been given in the last month
Give daily for at least 2 weeks:

Multivitamin supplement

Folic acid 1 mg/d (give 5 mg on Day 1)

Zinc 2 mg/kg/d

Copper 0.3 mg/kg/d

Iron 3 mg/kg/d but only when gaining weight

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 zinc and copper needed, as well as potassium
and magnesium. This solution can also be added to ReSoMal.
Note: A combined electrolyte/mineral/vitamin mix for severe malnutrition is available
commercially. This can replace the electrolyte/mineral solution and multivitamin and folic
acid supplements mentioned in steps 4 and 6, but still give the large single dose of vitamin A
and folic acid on Day 1, and iron daily after weight gain has started.
Step 7. Start cautious feeding
In the stabilisation phase a cautious approach is required because of the childs fragile
physiological state and reduced homeostatic capacity. Feeding should be started as soon as
possible after admission and should be designed to provide just sufficient energy and protein
to maintain basic physiological processes. The essential features of feeding in the stabilisation
phase are:

small, frequent feeds of low osmolarity and low lactose

oral or nasogastric (NG) feeds (never parenteral preparations)

100 kcal/kg/d

1-1.5 g protein/kg/d

130 ml/kg/d of fluid (100 ml/kg/d if the child has severe oedema)

if the child is breastfed, encourage to continue breastfeeding but give the prescribed
amounts of starter formula to make sure the childs needs are met.

The suggested starter formula and feeding schedules (see below) are designed to meet these
targets.
Milk-based formulas such as starter F-75 containing 75 kcal/100 ml and 0.9 g protein/100 ml
will be satisfactory for most children (see Appendix 5 for recipes). Give from a cup. Very
weak children may be fed by spoon, dropper or syringe.

A recommended schedule in which volume is gradually increased, and feeding frequency

gradually decreased is:

For children with a good appetite and no oedema, this schedule can be completed in 2-3 days
(e.g. 24 hours at each level). Appendix 6 shows the volume/feed already calculated according
to body weight. Appendix 7 gives the feed volumes for children with severe oedema. Use the
Day 1 weight to calculate how much to give, even if the child loses or gains weight in this
phase.
If, after allowing for any vomiting, intake does not reach 80 kcal/kg/d (105 ml starter
formula/kg) despite frequent feeds, coaxing and re-offering, give the remaining feed by NG
tube (see Appendices 6 and 7 (Column 6) for intake volumes below which NG feeding should
be given). Do not exceed 100 kcal/kg/d in this phase.
Monitor and note:

amounts offered and left over

vomiting

frequency of watery stool

daily body weight

During the stabilisation phase, diarrhoea should gradually diminish and oedematous children
should lose weight. If diarrhoea continues unchecked despite cautious refeeding, or worsens
substantially, see section C4 (continuing diarrhoea).
Step 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 (see Appendix 5 for recipes). Modified porridges
or modified family foods can be used provided they have comparable energy and protein
concentrations.
Readiness to enter the rehabilitation phase is signalled 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 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 (Appendix 9 provides example)

each week calculate and record weight gain as g/kg/d3

If weight gain is:

poor (<5 g/kg/d), child requires full reassessment (see Section D)

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

3 Calculating weight gain : The example is for weight gain over 7 days, but the same
procedure can be applied to any interval:
* substract from todays weight (in g) the childs weight 7 days earlier ;
* divide by 7 to determine the average daily weight gain (g/day) ;
* divide by the childs average weight in kg to calculate the weight gain as g/kg/day.
Step 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

structured play therapy 15-30 min/d (Appendix 10 provides examples)

physical activity as soon as the child is well enough

maternal involvement when possible (e.g. comforting, feeding, bathing,

play)

Step 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 childs 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 Ringers lactate with 5%

dextrose; or half-normal saline with 5% dextrose; or half-strength Darrows solution
with 5% dextrose; or if these are unavailable, Ringers lactate

measure and record pulse and respiration rates every 10 minutes

give antibiotics (see step 5)

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 childs 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
itchy rash
dark red urine
confusion
shock

Also monitor the respiratory rate and pulse rate every 15 minutes. If either of
themrises,transfusemoreslowly. Followingthetransfusion,iftheHbremains 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

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):

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, 510% 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 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 Lugols 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 HIVrelated chronic diarrhoea. Treatment should be the same as for HIV negative children.
e)

Psychological problems

Check for:

abnormal behaviour such as stereotyped movements (rocking), rumination (selfstimulation 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 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:

give appropriate meals at least 5 times daily

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

assist and encour age the child to complete each meal

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)

breastfeed as often as the child wants

2.8

Complication

There are many complications that can caused by protein energy malnutrition, those are
infection, congenital malformation of the gastrointestinal tract or heart, malabsorbsion,
metabolic disorders, chronic kidney disease, disorders of the central nervous, disorders intake
of vitamins and minerals, nutritional anemia, and many more.

2.9

Prevention

Promotion of breast feeding

Development of low cost weaning

Nutrition education and promotion of correct feeding practices

Family planning and spacing of births

Immunization

Food fortification

Early diagnosis and treatment

2.10

Prognosis

The extent of growth failure and the severity of hypoproteinemia, hypoalbuminemia, and
electrolyte imbalances are predictors of a poorer prognosis. Additionally, underlying HIV
infection is associated with a poor prognosis.

CHAPTER III
CONCLUSION

BIBLIOGRAPHY

1. World Health Organization. Management of Severe Malnutrition : A Manual for

Physicians and Other Senior Health Workers. Geneva; 1999.
2. Prevalensi Kurang Energi Protein Anak Balita, Susenas 1995, Biro Pusat
Statistik, 1997.
3. Departemen Kesehatan RI Direktorat Jenderal Bina KesehatanMasyarakat
Direktorat Bina Gizi Masyarakat. Pedoman Respon Cepat Penanggulangan Gizi
Buruk , 2008.
4. Badan Penelitian dan Pengembangan Kesehatan Kementerian Kesehatan RI. Riset
Kesehatan Dasar, Riskesdas 2007; 2007; 34-40
5. Badan Penelitian dan Pengembangan Kesehatan Kementerian Kesehatan RI. Riset
Kesehatan Dasar, Riskesdas 2010; 2010; 17-22
6. Nelson
7. Pedoman Pelayanan Gizi Buruk.
8. Harrison
9. Pedoman Pelayanan Medis IDAI
10. UKK Nutrisi dan Penyakit Metabolik 2011
11. Ann Ashworth, Sultana Khanum, Alan Jackson, Claire Schofield. Guidelines for
the Inpatient Treatment of Severely Malnourished Children. World Health
Organization ; 2003
12.
13. Feigin J, Cherry J, Harrison N, Kaplan M. Feigin & Cherrys textbook of pediatric
infectious diseases. 6th edition. Philadelphia Elsevier Saunders; 2009.
14. Kliegman RM, Stanton BF, Schir NF, Behrman RE. Nelson Textbook of
Pediatrics. 19th edition. Philadelphia: Elsevier Saunders; 2011.
15. Fisher DJ, Steele RW. Pediatric urinary tract infection. Emedicine medscape
[Internet}. 2013; Available from: http://emedicine.medscape.com/article/969643overview
16. Miesien, Tambunan T, Munasir Z. Profil klinis infeksi saluran kemih pada anak di
rumah sakit cipto mangunkusumo. Sari Pediatri. 2006 Maret; 7(4):200-6
17. Alatas H, Tambunan T, Trihono PP, Pardede S. Buku Ajar Nefrologi Anak. Edisi
2. Jakarta: Balai Penerbit FKUI; 2010
18. Roberts KB, Downs KB, Finnell SM, Hellerstein S. Urinary tract infection:
clinical practice guideline for the diagnosis and management of the initial UTI in

febrile infants dan children 2 to 24 months. Pediatrics. 2011 September;

128(3):594-610
19. Welsh A. Urinary tract infection in children: diagnosis, treatment, and long-term
management. National Institute for Health and Clinical Excellence. London:
RCOG Press; 2007