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INTRODUCTION
(3)
CHAPTER II
LITERATURE REVIEW
2.1 Marasmus www.unicef.org type of undernutrition
A rapid deterioration in nutritional status in a short time can lead to
marasmus, one form of acute malnutrition. Marasmus is the most common form of acute
malnutrition in nutritional emergencies and, in its severe form, can very quickly lead to
death if untreated.
It is characterised by severe wasting of fat and muscle which the body breaks down to
make energy. Wasting can affect both children and adults.
The body of a wasted child tries to conserve energy as much as possible by
reducing physical activity and growth, reducing internal body processes and shutting
down the bodys response to infection. This reduced activity results in limited function of
the liver, kidney, heart and gut putting the child at risk for:
Infection
the price of materials food, and family expenditures for other needs besides food, c)
beliefs about food and health of the mother, d) the presence or absence of health care,
including cleanliness (Levinson, 1979 in Lismartina, 2000).
2.3 Pathophysiology
Protein-energy malnutrition will occur when the body's need for calories,
protein, or both are not fulfilled by diet. (Arisman, 2004: 92). In a state of lack of
food, the body is always trying to preserve life by meeting basic needs or energy.
The ability of the body to use carbohydrates, proteins and fats is very essential to
maintain life, carbohydrates (glucose) can be used by all body tissues as fuel,
unfortunately the body's ability to store carbohydrates very little, so that after 25
hours was possible shortage. As a result, protein catabolism occurs after a few
hours to produce amino acids are immediately converted into carbohydrates in the
liver and kidneys. Diving fasting fat tissue are broken down into fatty acids,
glycerol and ketone bodies. Muscles can use fatty acids and ketone bodies as an
energy source that is running a chronic food shortage. The body will defend itself
not to break down proteins again after losing roughly half of the body.
2.4 Clinical Signs of Marasmus www.fao.org.human nutrition in a developing
world
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)
F. Diagnosis
In malnourished patients, the most common complain is no increase of body
weight, poor feeding, frequently ill, or bilateral ankle edema, and the whole body.
In patients with kwashiorkor, children look letargis, apatis, and or irritable. The
apparently manifestation of kwashiorkor are swelling of the abdominal wall,
making the body weight undecreased in thr first time of kwashiorkor.
Anthropometry
Clinical Presentation
Severe malnutrition
(BW/BL)
Mild-moderate malnutrition
Looked thin
- 3 SD < - 2 SD
Health
Looked health
- 2 SD 2 SD
Obesity
Looked fat
> 2 SD
**) BW/BL can be > -3 SD if there is severe edema (the whole body).
Malnutrition is categorized to severe malnutrition with complications,
severe malnutrition without complications and mild-moderate malnutrition.
Physical Examination, BW/BL, AC
Severe malnutrition Severe malnutrition without
Mild-moderate
with complications
malnutrition
complications
Children with
Children with
AC>11.5cm<12.5cm
or more signs:
one or more
one or more
(children 6-59
signs:
signs:
months) (BW/BL<-2
-Looked very
body
thin
very thin -
- BW/BL<-3SD
-Minimal
BW/BL<-3SD
And
-AC<11,5cm
edema, bilateral
Goodly feeding
(children 6-59
palm/ankle
-Looked
to -3 SD)
No edema
AC<11,5cm
No clinical
(children 6-59
abnormality
more medical
- BW/BL<-3SD
months)
complications
-AC<11,5cm
signs:
(children 6-59
-goodly feeding
-Anorexia
months)
-without any
-Severe pneumonia
and
-Severe anemia
-goodly feeding
-Severe
-without any
dehydration
medical
complications
And
medical
complications
-level of
consciousness
Some laboratories examination we should do for patients with kwashiorkor
are blood glucose, peripheral blood smear, urinalysis, stool examination,
electrolyte, protein, and ferittin. Maantoux test, chest x-ray, and ECG to exclude
differential diagnosis should be consider.
G. Management
Children with malnutrition should be treated with four phases, they are:
stabilization,
transition,
rehabilitation,
and
further
management
Medical
N
Steps
Stabilization
tion
H 1-2
H 3-7
Preventing
1
and
nd
management
th
2 -6
th
th
7 -66
ome
weeks
weeks
importa
treating
nt
---
things
hypoglycemia
we must
Preventing
2
and
attend
treating
hypothermia
are:
---
Preventing
3
and
on't
treating
dehydration
give Fe
---
before
2nd
Treating
4
electrolyte
----
week
imbalance
(Fe
Treating
5
given in
infection
-------------------
stabiliza
Stabilized
6
tion
micronutrient
Without Fe
deficiencies
-------------------------
With Fe
phase).
Don't
-----Feeding
7
for
give
intraven
stabilization and
ous
transition
fluid
Feeding
8
for
drip
unless
growth
the
Stimulating
9
for
patient
development
Preparation
1
for
0
is
further
management at
home
is
in
shock
or
severe
dehydration.
Don't give high protein diet in stabilization phase.
Don't give diuretics to patients with kwashiorkor.
Mild-moderate
Severe dehydration
dehydration
Presentation*
Alert
Irritable
Letargis
Tears
Eyes
Sunken
Very sunken
Lips mucosa
Dry
Very dry
Thirsty*
Want to drink
Thirsty
Cannot drink
Turgor *
Good
<
Poor
No complications
Complications (shock,
hypoglycemia, hypothermia,
plus
dermatosis, URI,UTI, or
Ampicillin iv or im
Followed by
amoxicillin orally
2 days
No improvement of any
Specific antibiotics
Stabilization Phase
Fluid and feeding allowance in stabilization phase to a malnourished patient without
any warning signs (shock, unconscious, and vomiting/diarrhea/dehydration). Give 50ml of
glucose 10% orally rapidly, monitor heart rate, respiratory and alertness every 30 minutes in
the first 2 hours, and every 1 hour in the next 10 hours.
In the first 2 hour, give F-75 every 30 minutes, doses for 2 hours based on body
weight (with or without edema). Monitor heart rate, respiratory, alertness and provision of
F75 every 30 minutes. In the next 10 hours, continue the provision of F75 in children every 2
hours. Monitor heart rate, respiratory and provision of F75. If the child is still breastfeeding,
give ASI between the provisions of F75. If the child can consume almost of F75, change the
time of provision to be every 3 hours or every 4 hours if the child can consume the whole of
F75. You'd better give F75 orally as much as you can. Consider NGT if the child cannot
consume the whole F75.
Reduce to give F75 based on minimal calories requirements in stabilization phase (with
or without edema) if you find any warning signs; heart rate and respiratory rate increased,
jugular vein blocked, or edema increased (e.g.: markedly periorbital edema).
Transition and Rehabilitation Phase (4)
If every doses of F75 given per 4 hours could be finished by children, change F75 to
be F100 as much as the volume of F75 for 2 day. Monitor heart rate, respiratory and
provision of F100 every 4 hours. If the child is stable, continue F100 based on body weight in
the third day. Increase 10 ml every 4 hours until the child couldnt finish the formula, but not
to exceed the maximal doses of F100.
In the fourth day of transition phase, give F100 every 4 hours based on body weight
between minimal and maximal doses. Continue F100 for next 14 days (last day of transition
phase).
In rehabilitation phase, give F100 and solid food based on body weight. If the BW <
7kgs, give F100 plus soft food and fruits extract. If the BW>7kgs, give F100 plus soft food
and fruits. Continue giving the food until BW/BL>-2 SD standard WHO 2005.
Reduce to give F100 if you find any warning signs; heart rate and respiratory rate
increased, jugular vein blocked, or edema increased (e.g.: markedly periorbital edema).
Evaluate for 1 hour.
H. Prognosis (12)
Getting treatment early generally leads to good results. Treating kwashiorkor in its
late stages will improve the child's general health. However, the child may be left with
permanent physical and mental problems. If treatment is not given or comes too late, this
condition is life-threat
CHAPTER III
CASE REPORT
3.1 Objective
The objective of this paper is to report a case of 2 years and 3 months old girl with a diagnosis of
Bronchopneumonia.
3.2 Case
K, a 2 years and 3 months girl, with 7 kg of BW and 79 cm of BH, is a new patient of infection
unit in Pediatric Department in Central Public Hospital Haji Adam Malik Medan on September
2nd 2015 at 14.55. Her chief complaint was dyspnea.
History of disease:
K ,a girl, 2 years and 3 months old, came to Haji Adam Malik Hospital at September 2 nd 2015
with dyspnea as the chief complaint. The patient have been experienced this since morning.
Patient looks weak since a day before. Dyspnea (+) since 2 days ago. Dyspnea doesnt caused by
activity or weather. Cough (+) been experienced for 2 weeks. At first was dry, but then became
productive. History of recur cough since this past 2 months. Her grandmother also had productive
cough for a month. History of fever was 2 months ago, lasted for this two weeks, up and down.
Diarrhea was experienced for a day, without losing weight. Vomitting was denied. No history of
family having the same condition.
History of previous illness: The patient is a new patient
History of medication:History of family: No family history of DM and other diseases
History of parents medication: unclear
History of pregnancy: Patients mother was 27 years old during pregnancy. The gestation age
was 36 weeks. No history of complication neonate and maternal problem.
History of birth: Birth assisted by GP. The baby was born paravaginal and she cried
spontaneously. Bluish was not found. Body weight 2700 gram, body length 46 cm, and head
circumference was not measured.
History of feeding: 6 months of exclusive breast feeding, additional food since 7 months old and
family food was given from 19th week onward.
History of immunization: BCG, Polio 4 times, Hepatitis B 3 times, DPT 3 times, and Measles.
History of growth and development: Face down: 4 months old, Sit down: 6 months old, Crawl:
8 months old, Stand up: 10 months old, Walk: 13 months old, Talk: 12 months old.
Physical Examination:
Present status: Level of consciousness: Conscious, Body temperature: 38C, HR: 100 bpm,
RR: 48 bpm, BW: 7 kg, BH: 79 cm, BW/A: -3 < SD BL/A: -3 < SD < -2, BW/BL: -3 < SD ,
anemic (-), icteric (-), dyspnea (+), cyanosis (-), edema (-).
Localized status:
Face edema (-), Eyes: superior and inferior palpebral edema (-), Light reflex +/+,
isochoric pupil, pale wasnt found in inferior conjunctiva palpebral.
Ears: within normal range
Nose: within normal range
Mouth: within normal range
-)
Symmetrical fusiform, suprasternal, intercostal and substrenal retraction (+), Cor
S1,S2 (+), HR: 100 bpm, regular, murmur (-), RR: 48 bpm, regular, rhonchi (+/+) wheezing (-/-),
rales (-/-)
Symmetric, supple, normal peristaltic, liver and spleen: unpalpable.
00 bpm regular, p/v adequate, warm acral, CRT < 3, clubbing finger(-),
pretibial oedema (-).
Laboratory finding
Complete blood analysis (September 2nd , 2015)
Test
Hemoglobin
Erythrocyte
Leucocyte
Thrombocyte
Hematocrite
Eosinophil
Basophil
Neutrophil
Lymphocyte
Monocyte
Neutrophil absolute
Lymphocyte absolute
Monocyte absolute
Eosinophyl absolute
Basophyl absolute
MCV
MCH
MCHC
RDW
Result
10.40
3.77
18.13
332
32.30
1.00
0.900
62.90
27.50
7.70
11.41
4.99
1.39
0.18
0.16
85.70
27.60
32.20
12.60
Unit
g%
106/mm3
103/mm3
103/mm3
%
%
%
%
%
%
103/L
103/L
103/L
103/L
103/L
fL
Pg
g%
%
Referral
12.0-14.4
4.40-4.48
4.5-13.5
150-450
37-41
1-6
0-1
37-80
20-40
2-8
2.4-7.3
1.7-5.1
0.2-0.6
0.10-0.30
0-0.1
81-95
25-29
29-31
11.6-14.8
Referral
< 200
135-155
3.6-5.5
96-106
7.35-7.45
38-42
85-100
22-26
19-25
(-2) (+4)
95-100