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Introduction
Protein-energy malnutrition (PEM) is a major public health problem
affecting a high proportion of infants and older children world-wide and accounts
for a high childhood morbidity and mortality. Today the world faces a double
burden of malnutrition that includes both undernutrition and overweight,
especially in developing countries. Malnutrition, in every form, presents
significant threats to human health. According to the World Health Organization
(WHO), 49% of the 10.4 million deaths occurring in children younger than 5
years in developing countries are associated with PEM. Approximately 70% of the
world's malnourished children live in Asia. (Oshikoya and Senbanjo, 2009)
Child with malnutrition is susceptible to infection. Every episode infection
makes the malnutrition worse and adversely affects the malnutrition worse and
adversely affects the immune system further. A wide spectrum of infections such
as measles, malaria, acute respiratory tract infection, intestinal parasitosis,
tuberculosis and HIV/AIDS may complicate PEM with two or more infections coexisting. Although a higher proportion of severely malnourished children do not
survive a significant intercurrent illness, as much as 80% of the overall,
unacceptably high, mortality rate may be contributed by mild-to-moderately
malnourished children.
Clinically, PEM is a disease spectrum that can present as underweight,
marasmus, marasmic-kwashiorkor or kwashiorkor; the severe forms being
marasmus, kwashiorkor, and marasmic-kwashiorkor in which the main detectable
manifestation is growth retardation. (Oshikoya and Senbanjo, 2009) Kwashiorkor
presents with failure to thrive, oedema that appears first on the dorsum of the feet
and ankles and spreads upwards to involve the rest of the body, apathy, anorexia,
diarrhoea and discoloration of the skin and hair. Failure in growth is marked and
weight is reduced in spite of the presence of oedema. Marasmus appearance is
short and light for their age, shrunken and wizened due to lack of subcutaneous
fat. Marasmic-kwashiorkor displays the symptoms of both marasmus and
kwashiorkor. (Simkiss, D., et al.)

PEM occur when there is gap between intake and requirements of nutrition
needed. Condition that can predispose a child to having PEM include poverty,
lack of access to quality food, cultural and religious food customs, poor maternal
education, inadequate breast feeding, and lack of quality healthcare. In addition to
macronutrient deficiency, there is clinical and/or subclinical deficiency of
micronutrients. (Oshikoya and Senbanjo, 2009)
The main features to diagnose severe acute malnutrition
are:

weight-for-length/height < -3SD (wasted) or

mid-upper arm circumference < 115 mm or

oedema

of

both

feet

(kwashiorkor

or

marasmic

kwashiorkor)
Children with severe acute malnutrition should first be assessed with full
clinical examination to confirm whether they have any general danger sign,
medical complications and an appetite. The physical examination must be very
thorough because even small abnormalities can be clinically significant. Clinical
signs of serious complication can be very subtle in children with marasmus.
(WHO, 2013)
After history and physical examination, diagnosing the type and severity
of the malnutrition, as well as diagnosing associated infections and complications
affecting organs or systems, such as the GI, neurological, or cardiovascular
system, are critical. This set of diagnoses results in optimal planning of the
complementary evaluation and therapeutic strategy. Checklist of points for
conducting the physical examination are:

Body temperature (measured with a thermometer) - Allowing


measurement of low temperatures to detect hypothermia as well as
fever

Anemia - Pale mucosa


Edema
Dehydration Letarghy, irritability, thirst, shrunken eyes, dry mouth,

skin turgor
Hypovolemic shock - Weak radial pulse, cold extremities, decreased

consciousness
Tachypnea - Pneumonia, heart failure
Abdominal manifestations - Distension, decreased or metallic bowel

sounds, large or small liver, blood or mucus in the stools


Ocular manifestations - Corneal lesions associated with vitamin A

deficiency
Dermal manifestations - Evidence of infection, purpura
Ear, nose, and throat (ENT) findings - Otitis, rhinitis (Rabinowitz,
2014)

Treatment of PEM divided into 4 phases with 10 steps which are treatment
for

Hypoglycaemia,

Hypothermia,

Dehydration,

Electrolytes,

Infection,

Micronutrients no iron with iron, Initiate feeding, Catch-up feeding, Sensory


stimulation, Prepare for follow-up. (WHO, 2013)
Case Report
Objective:
To report the case of children with kwashiokor and the treatment.
Case:
DT, 2 months 2 days old boy was admitted on December, 14th 2015 at time 09:00
pm with complaint of swelling of his whole body. It has been occured since 3 days
ago. Swelling started from his scrotum and spread to his both lower extremities
and then throughout his whole body.History of inadequate breastfeeding (-) An
ulcer is found at the parietal part of his skull. Blueness of his skin was not found.
Shortness of breath (-),Coughing was not found. Nausea and Vomitting (-). Fever
(+) since 5 days before admission, the temperature was not too high and was
decreased by anti-pyretic drug. Urinating system was normal, with yellow clear in
the color with a lesser amount of urine, defecation was normal with a normal stool
consistensy During the admission the fever was still occured.

History of previous illness:


He had ever been hospitalized in RS Royal Prima at the early of December of
2015 for High fever and was given paracetamol and rehydration solution. After
being discharged, he never got to control and never frequently took the medication
given by the doctor for his illness.
History of birth : born caesarean section, immediately crying upon birth,with no
no blueness found. with the birth weight of 3200gr PBL=50cm
History of nutrition : 2 month of exclusive breast feeding, and additional food
was also given
History of obstetric : the mother was 39 years old when she was having him, no
history of consuming drugs and herbs, no history of having DM and hypertension
during pregnancy
History of immunization: : not clear

Physical Examination
General status
Body weight: 4,4 kg, Body length: 54 cm,
Head cimcurmference: 37cm, Mid-upper arm circumference: 12 cm
Weight-for-age: z-scores
Length-for-age: z-scores
Weight-for-length:z-scores
Presens status
Consciousness: alert
Blood Pressure: 90/40 mmHg
Heart Rate: 124 x/i

Respiratory Rate: 44 x/i


Body Temperature: 37,7 oC.
Anemic (+). Icteric (-). Cyanosis (-). Edema (-). Dyspnea (-)
Local status
Head

: Fontanelle not closed, swelling of the head. Eyes:


Isochoric pupil, pale inferior palpebra conjunctiva +/+,
light reflex on both eyes. Ears/ nose/ mouth: within normal
limit.

Neck

: No lymph node enlargement

Thorax

: Symmetrical fusiformis, intercostal space clearly visible,


protruding spine. HR: 128x/i, regular, murmur (-). RR:
39x/i, regular, ronchi (-). Breath sound: vesicular.
Additional sound (-).

Abdomen

: Soepel, normal peristaltic, liver and spleen unpalpable,


skin pinch returns quickly

Extremities

: swelling (+). Pulse 128x/i, regular, adequate pressure and


volume, warm, CRT < 3, pitting edema (+)

Differential Diagnosis:
-

Suspect Sepsis + Abcess o/t (L) Parietalis + kwashiokor

Working Diagnosis:
-

Suspect Sepsis + Abcess o/t (L) Parietalis + kwashiokor

Management:
-

Diagnostic Planning:
-

Complete Blood Test

Urine and fesces analysis


Ferum Profile
Urine and Fesces Examination
Plain abdominal x-ray
Barium enema
Albumin

Laboratory Finding: October 15th , 2015


Haematology
Haemoglobin
Eritrocyte
Leucocyte
Haematocrite
Thrombocyte

g/dL
6
3
10 /mm
103 /mm3
%
103 /mm3

Result
7.00
2.43

Normal
11.1 14.4
3.71 - 4.25

15.83

6.0 - 17.5

22.0
158

35 - 41
217 497

MCV
fL
90.50
MCH
pg
28.80
MCHC
g%
31.80
RDW
%
21.40
Neutrofil
%
66.30
Limphocyte
%
19.10
Monocyte
%
11.20
Eosinofil
%
3.30
Basofil
%
0.100
From the table above, we found anemia and thrombocytopenia.

82 - 100
24 - 30
28 - 32
14.9 - 18.7
37 - 80
20 - 40
2-8
1-6
0-1

Haemostasis
Prothrombin Time
Patient
Control
INR
APTT
Patient
Control
Thrombin Time
Patient
Control
Clinical Chemistry
Random Blood Glucose
Ureum
Creatinine

Normal

Result
seconds
seconds

17.2
13.8
1,26

Seconds
seconds

28.2
32.0

Seconds
seconds

15.6
17.5
Result
112.10
15.80
0.11

g/dL
mg/dL
mg/dL

Normal
40-60
<50
0.17-0.42

Haematocrite
Natrium (Na)
Kalium (K)
Chloride (Cl)

%
mEq/L
mEq/L
mEq/L

13.5
130
3.6
101

37 - 41
135-155
3.6 5.5
96-106

Result
Yellow clear
Negative
Negative
Negative
1.000
7.0
Negative
Negative
Negative
Negative
Negative

Normal
Yellow
Negative
Negative
Negative
1.005 1.030
5-8
Negative

0-1
0-1
0-1
Negative
Negative

<3
<6

Laboratory Finding: October 20th, 2015


Urinalisis
Complete Urine
Color
Glucose
Bilirubin
Keton
Spesific gravity
pH
Protein
Urobilinogen
Nitrit
Leucocyte
Blood
Urine Sediment
Erytrocyte
Leucocyte
Epitel
Casts
Cristal
Fesces
Macroscopic
Color
Consistency
Blood
Mucus
Microscopic
Egg worm
Amoeba
Erytrocyte
Leucocyte

LPB
LPB
LPB
LPB
LPB

Brown
Watery
Negative
Negative
LPB
LPB
LPB

Barium Enema: October 16th, 2015

Negative
Negative
0-1
0-1

Negative
Negative

Negative

Negative
Negative
Negative
Negative

Plain Abdominal X-ray : October 19th, 2015

Follow Up
Date

P
Therapy

Diagnostic

16/10/
2015

Lost
appetite,
Bloody
vomit (+)
and bloody
stool (+)

Sens : Alert
- Marasmus
- Gastrointestinal
T : 37,9 C
bleeding
BW : 4,9kg
- Anemia
BH : 64cm
Head: eye reflect +/+,
isocor, pale conj. Palpebra
inferior+/+,
Ear/Nose/Mouth: normal
Neck: JVP R+2 cm H2O
Thorax
:
Symmetris
fusiformis, retraction (-),
HR : 125x/I, reguler,
murmur (-) RR : 30x/i,
reguler, ronchi -/Abdomen : soepel, normal
peristaltic, Hepar: palpeble
2cm BAC Lien: palpeble
SIII
Extremities : pulse 125x/i,
reguler, adequate pressure
and volume, warm, CRT
<3, pretibial edema (-)

- IVFD D5%
NaCl 0,225%
20gtt/I
(micro)
- Folic acid
1x1mg
- Vitamin B
Complex 1x1
tab
- Vitamin C 1x1
tab
- Diet F75
80cc/3 hours
+ 1,6cc
mineral mix - Transfusion
PRC
25cc/24jam
- Inj
ceftriaxone
250mg/
12hours/iv

Consult
gastrohepato
logy division
Consult
hematooncol
ogy division
Consult
nutrition and
metabolic
disease
division
Complete urine
and fesces
analysis
Check Iron
profile
Peripheral
blood smear
Barium Enema

17/10/
2015

19/10/
2015

Lost
appetite,
Bloody
vomit (-),
bloody
stool (-),
fever (+)

Sens : Alert
- Marasmus
- Gastrointestinal
T : 37,7 C
bleeding
BW : 4,9kg
- Anemia
BH : 64cm
Head: eye reflect +/+,
isocor, pale conj. Palpebra
inferior-/-,
Ear/Nose/Mouth: normal
Neck: JVP R+2 cm H2O
Thorax
:
Symmetris
fusiformis, retraction (-),
HR : 100x/I, reguler,
murmur (-) RR : 24x/i,
reguler, ronchi -/Abdomen : soepel, normal
peristaltic, Hepar: palpeble
2cm BAC Lien: palpeble
SIII
Extremities : pulse 100x/i,
reguler, adequate pressure
and volume, warm, CRT

- IVFD D5%
- Scheduled for
NaCl 0,225%
Abdominal
20gtt/I
X-ray
- Expecting
(micro)
- Folic acid
Barium
1x1mg
Enema result
- Vitamin B
Complex 1x1
tab
- Vitamin C
1x50mg
- Diet F75
80cc/3 hours
+ 1,6cc
mineral mix
- Transfusion
PRC
25cc/24jam
- Inj
ceftriaxone
250mg/12ho
urs/iv

10

<3, pretibial edema (-)

20/10/
2015

Lost
appetite,
Bloody
stool (-),
fever (-)

21/10/
15

Bloody
stool (-),
fever (-)

Resultfrom Gastrointestinal
divison: recommend to do
Abdominal x-ray 2 position
Routine urine analysis, LFT
Sens : Alert
T : 37,5 C
BW : 4,9kg
BH : 64cm
Head: eye reflect +/+,
isocor, pale conj. Palpebra
inferior-/-,
Ear/Nose/Mouth: normal
Neck: JVP R+2 cm H2O
Thorax
:
Symmetris
fusiformis, retraction (-),
HR : 100x/I, reguler,
murmur (-) RR : 24x/i,
reguler, ronchi -/Abdomen : soepel, normal
peristaltic, Hepar: palpeble
2cm BAC Lien: palpeble
SIII
Extremities : pulse 100x/i,
reguler, adequate pressure
and volume, warm, CRT
<3, pretibial edema (-)
Sens : Alert
T : 36,8 C
BW : 4,9kg
BH : 64cm
Head: eye reflect +/+,
isocor, pale conj. Palpebra
inferior
+/+,
Ear/Nose/Mouth: normal
Neck: JVP R+2 cm H2O
Thorax
:
Symmetris
fusiformis, retraction (-),
HR : 92x/I, reguler,
murmur (-) RR : 24x/i,
reguler, ronchi -/Abdomen : soepel, normal
peristaltic, Hepar: palpeble

Marasmus
- IVFD D5%
- Abdominal XGastrointestinal
NaCl 0,225%
ray
bleeding
20gtt/I
Anemia
(micro)
- Inj. Ranitidine
5mg/12
hours/ IV
- Folate acid
1x5mg
- Vitamin B
Complex 1x1
tab
- Vitamin C
1x50mg
- Diet F75
80cc/3 hours
+ 1,6cc
mineral mix
- Inj
ceftriaxone
250mg/12ho
urs/iv
Marasmus
- IVFD D5%
Gastrointestinal
NaCl 0,225%
bleeding
20gtt/I
Anemia
(micro)
- Inj. Ranitidine
5mg/12
hours/ IV
- Folic acid
1x1mg
- Vitamin B
Complex 1x1
tab
- Vitamin C
1x50mg
- Diet F75
80cc/3 hours
+ 1,6cc

11

2cm BAC Lien: palpeble


SIII
Extremities : pulse 92x/i,
reguler, adequate pressure
and volume, warm, CRT
<3, pretibial edema (-)
Laboratorium result :
- Reticulocyte 3,17%
- Combs test (-)
- CRP 2,8
Procalcitonin 1,22

mineral mix
- Cotrimoxazole
syr 2xcth1/2

Result from Nutrition and


metabolic disease division:
Food recall 24 hours:
Morning:
porridge1/2
portion + carrot piece
Afternoon: porridge
portion + potato piece
Night: porridge portion +
carrot piece
Breast feeding on demand.
Therapy : - diet F75 80cc/3
hours + 1,6cc mineral mix
Vit. A 100.000 unit
(1x)
- Vit.B comp 1x1 tab
- Vit.c 1x50mg
- Cotrimoxazole 2x
tspn
22/10/
2015

25/10/
2015

Bloody
stool (-),
fever (-)

Sens : Alert
- Marasmus
- Gastrointestinal
T : 37 C
bleeding
BW : 4,9kg
Post
BH : 64cm
Hemorrhagic
Head: eye reflect +/+,
Anemia
isocor, pale conj. Palpebra
inferior
+/+,
Ear/Nose/Mouth: normal
Neck: JVP R+2 cm H2O
Thorax
:
Symmetris
fusiformis, retraction (-),
HR : 98x/I, reguler,
murmur (-) RR : 24x/i,
reguler, ronchi -/-

- IVFD D5%
NaCl 0,225%
20gtt/I
(micro)
- Inj. Ranitidine
5mg/12
hours/ IV
- Folic acid
1x1mg
- Vitamin B
Complex 1x1
tab
- Vitamin C
1x50mg

12

26/10/
2015

Bloody
stool (-),
fever (-)

Abdomen : soepel, normal


peristaltic, Hepar: palpeble
2cm BAC Lien: palpeble
SIII
Extremities : pulse 98x/i,
reguler, adequate pressure
and volume, warm, CRT
<3, pretibial edema (-)
Sens : Alert
- Marasmus
Gastrointestinal
T : 37 C
bleeding
BW : 4,9kg
Post
hemorrhagic
BH : 64cm
anemia
Head: eye reflect +/+,
isocor, pale conj. Palpebra
inferior
+/+,
Ear/Nose/Mouth: normal
Neck: JVP R+2 cm H2O
Thorax
:
Symmetris
fusiformis, retraction (-),
HR : 98x/I, reguler,
murmur (-) RR : 24x/i,
reguler, ronchi -/Abdomen : soepel, normal
peristaltic, Hepar: palpeble
2cm BAC Lien: palpeble
SIII
Extremities : pulse 98x/i,
reguler, adequate pressure
and volume, warm, CRT
<3, pretibial edema (-)

Diet F100
80cc/3 hours
+ 1,6cc
mineral mix
Cotrimoxazole
syr 2xcth1/2

IVFD D5%
NaCl 0,225%
20gtt/I
(micro)
Inj. Ranitidine
5mg/12
hours/ IV
Folic acid
1x1mg
Vitamin B
Complex 1x1
tab
Vitamin C
1x50mg
Diet F100
80cc/3 hours
+ 1,6cc
mineral mix
Cotrimoxazole
syr 2xcth1/2

PBJ

Discussion
Marasmus is one of the 3 forms of severe protein-energy malnutrition
(PEM) that represent pathologic conditions associated with a nutritional and
energy deficit occurring mainly in young children from developing countries at
the time of weaning. Marasmus is a condition primarily caused by a deficiency in
calories and energy. (Rabinowitz, 2014)
Marasmus is more frequent in children younger than 5 years because this
period is characterized by increased energy needs and increased susceptibility to

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viral and bacterial infections. Weaning, which occurs during this period, is often
complicated by factors such as geography (eg, drought, poor soil productivity),
economy (eg, illiteracy, unemployment), hygiene (eg, access to quality water),
public health (eg, number of nurses is more than number of physicians), and
culture and dietetics (eg, intrafamily distribution of high-nutrition foods). No
racial predilection in the prevalence of malnutrition is evident, but a strong
association with the geographic distribution of poverty is observed. No sexual
predilection is observed, although, in some parts of the world, cultural practices
place girls at a disadvantage for PEM. (Rabinowitz, 2014)
Marasmus always results from a negative energy balance. The imbalance
can result from a decreased energy intake, an increased loss of ingested calories
(eg, emesis, diarrhea, burns), an increased energy expenditure, or combinations of
these factors, such as is observed in acute or chronic diseases. Children adapt to
an energy deficiency with a decrease in physical activity, lethargy, a decrease in
basal energy metabolism, slowing of growth, and, finally, weight loss. The
pathophysiological processes cause body composition, metabolic and anatomic
changes. (Rabinowitz, 2014)
In this case, we found an 9 months old boy came with complaint of lost
appetite and weight loss. Since he was 7 months old, his weight was not
increasing. This condition began when he suffered gastrointestinal bleeding 2
months ago which happen again at the moment. He has never finished the meal
served which cause decreased energy intake. The slowing growth appears on the
not increasing weight these last 2 months.
Body fluid compartments are altered by many factors such as nutritional
status and disease. Children with marasmus have a high total body water but
contrarily, there is a significant reduction in adipose mass as well as lean body
mass. (Oshikoya and Senbanjo, 2009) Protein mass can decrease as much as 30%
in the most serious forms, mainly represented by muscle and some organs (eg,
heart). Muscle cells are atrophic, and muscle tissue is infiltrated with fat and
fibrous tissue. Assessment of the fat and muscle mass loss can be clinically

14

performed by measuring arm circumference or skinfold thickness, such as triceps


skinfold. (Rabinowitz, 2014)
Children with marasmus shows clinical manifestastion, such as:

Children looked very thin and have old-man face


Mental status change, irritability
Dry, flagging and wrinkled skin
Loss of subcutaneous fat
Muscle atrophy, rib and backbone clearly visible
Bradychardia and lower blood pressure than normal healthy children
In the case we found a very thin baby with appearance of old-man face. He

is very irritable and easily crying. There is muscle atrophy and loss of
subcutaneous fat. The ribs are clearly visible called piano sign. On the bottom
it has appearance of baggy-pants.
The overall metabolic adaptations that occur during marasmus are similar
to those in starvation. A rise in gluconeogenesis leads to a perceived increased
metabolic rate. As the chronic underfeeding progresses, the basal metabolic rate
decreases. Reduced energy metabolism can impair the response of patients with
marasmus to changes in environmental temperature, resulting in an increased risk
of hypothermia. One of the main adaptations to long-standing energy deficiency
is a decreased rate of linear growth, yielding permanent stunting. (Rabinowitz,
2014)
Decreased oral absorption in digestive tract was attributed to the with
villous atrophy of the jejunal mucosa. (Oshikoya and Senbanjo, 2009) The
mucosal surface becomes smooth and thin, and secretory functions are impaired.
A decrease in gastric hydrochloric acid (HCl) excretion and a slowing of
peristalsis is observed, yielding bacterial overgrowth in the duodenum.
(Rabinowitz, 2014)

15

As in any stressed state of malnutrition, the adrenergic response from the


endocrine system is activated. Serum insulin levels are depressed and growth
hormone (GH) are elevated. The adrenal glands are atrophic at autopsy but plasma
cortisol concentrations were elevated. Cortisol binds to serum proteins; therefore,
hypoalbuminaemia would cause increase free plasma level of cortisol which may
contribute to the abnormal glucose tolerance. (Oshikoya and Senbanjo, 2009)
Children with severe malnutrition have a smaller and
thinner cardiac muscle and a lower stroke volume. Cardiac
output, especially systolic function, is decreased in the same
proportion as the weight loss. Bradycardia and hypotension
commonly occur in severe forms of malnutrition. Electrolyte
imbalances present during marasmus modify the ECG findings.
Other anatomic changes that occur in children with marasmus
are hematopoietic system that cause anemia, brain and nervous
system that reflected by irritability and apathy, and immune
system impairment. (Rabinowitz, 2014)
No differential diagnosis for marasmus are noted. However, when edema
is present, it can reflect a kwashiorkor component of the malnutrition or an
underlying cardiac or renal insufficiency. In these circumstances, additional

16

laboratory tests or radiographic tests may be needed. Laboratory tests adapted


from the WHO include the following:

Blood glucose: Hypoglycemia is present if the level is lower than 3

mmol/L.
Examination of blood smears by microscopy or direct detection test:
Presence of parasites is indicative of infection. Direct test is suitable but

expensive.
Hemoglobin: A level lower than 40 g/L is indicative of severe anemia.
Urine examination and culture, Multistix: More than 10 leukocytes per
high-power field is indicative of infection. Nitrites and leukocytes are

tested on Multistix also.


Stool examination by microscopy: Parasites and blood are indicative of

dysentery.
Albumin: Although not useful for diagnosis, it is a guide to prognosis; if

albumin is lower than 35 g/L, protein synthesis is massively impaired.


HIV test: HIV test should not be routinely performed; if completed, it
should be accompanied by counseling of the child's parents and the

result should be confidential.


Electrolytes: Measuring electrolytes is rarely helpful and it may lead to
inappropriate therapy. Hyponatremia is a significant finding.

Treatment for severe malnutrition has 4 phases: initial stabilization,


transition, rehabilitation and follow-up. (Kemenkes, 2011) It involve treatment
for

Hypoglycaemia,

Hypothermia,

Dehydration,

Electrolytes,

Infection,

Micronutrients no iron with iron, Initiate feeding, Catch-up feeding, Sensory


stimulation, Prepare for follow-up. (WHO, 2013)

17

In the initial phase, re-feeding should be gradual. The essential features of


initial feeding are: (WHO, 2013)

frequent (every 23 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
protein at 11.5 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:

The suggested starter formula and feeding schedules given below are
designed to meet these targets. Milk-based formulas, such as starter F-75 (with 75

18

kcal and 0.9 g protein/100 ml), will be satisfactory for most children. As cerealbased F-75 partially replaces sugar with cereal flour, it has the advantage of lower
osmolarity, which may benefit some children with persistent diarrhoea, but it has
to be cooked. (WHO, 2013)
Make a gradual transition from starter F-75 to catch-up formula F-100 or
ready-to-use therapeutic food over 23 days, as tolerated.

Replace starter F-75 with an equal amount of catch-up F-100 for 2 days.
Give a milk-based formula, such as catch-up F-100 containing 100

kcal/100ml and 2.9 g of protein per 100 ml


On the third day if on F-100, increase each successive feed by 10 ml
until some feed remains uneaten. The point at which some feed remains
unconsumed is likely to be when intake reaches about 200 ml/kg per

day.
After a gradual transition, give:
o frequent feeds, unlimited amounts
o 150220 kcal/kg per day
o 46 g of protein/kg per day
If on ready-to-use therapeutic food, start with small but regular meals
of RUTF and encourage the child to eat often (first 8 meals per day, and
later 56 meals per day). (WHO, 2013)

In the case reported, the patient get 80cc F-75 every 3 hours and 1,6cc
mineral mix for the stabilization and transition phase which in finished in 7 days.
On the 8th day start rehabilitation phase, patient was given catch-up feeding F-100
80cc every 3 hours and 1,6cc mineral mix.
All malnourished children should be given a broad-spectrum antibiotic that
suitable to local resistance pattern. In this case, the patient get Ceftriaxone
injection 250 mg every 12 hours.
After the transition, monitor progress by the rate of weight gain. Weigh the
child every morning before feeding, and plot the weight. Calculate and record the
weight gain every 3 days as g/kg per day. If the weight gain is:

Poor (< 5 g/kg per day), the child requires a full re-assessment
Moderate (510 g/kg per day), check whether the intake targets are
being met or if infection has been overlooked

19

Good (> 10 g/kg per day)

REFERENCES
Elsa, 2009. Protein-energy malnutrition. Toulouse Purpan medical school.
Kementrian Kesehatan Republik Indonesia. 2011. Bagan Tatalaksana Anak Gizi
Buruk Buku I.
Oshikoya, K. and Senbanjo, I. 2009. Pathophysiological changes that affect drug
dispotition in protein-energy malnourished children. Nutrition &
Metabolism 6:50.
Rabinowitz,

S.

Marasmus.

Available

from:

http://emedicine.medscape.com/article/984496 [Accessed November 5th,


2015]
World Health Organization. 2013. Pocket book of hospital care for children:
guidelines for the management of common childhood illnesses. Second
Edition. Geneva: World Health Organization.