Marasmus Down Syndrome

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MALNUTRITION AND DOWN SYNDROME

Presentators : Nurtilawati Siregar, Rahmah Khairuna Damanik

Day, Date : Monday, September 9th, 2013

Supervisor : dr. Pertin Sianturi, Sp.A(K)

CHAPTER 1

INTRODUCTION

1.1. Background

Malnutrition is still the main problem in public health especially in

developing countries, it contributes more than half death case of children under 5

years. It is one of the main problem of nutrition in Indonesia. Its Prevalence is

high especially in children < 5 years. Based on SUSENAS 2002, 26% of children

< 5 years having malnutrition, and 8% among them are in severe malnutrition, but

in Riskesdas 2007, there prevalence decreases to 13% for moderate-malnutrition

and 5.4% for severe malnutrition. 1,2

Severe malnutrition is both a medical and a social disorder. That is, the

medical problems of the child result, in part, from the social problems of the home

in which the child lives. Malnutrition is the end result of chronic nutritional and,

frequently, emotional deprivation by carers who, because of poor understanding,

poverty or family problems, are unable to provide the child with the nutrition and

care he or she requires. Successful management of the severely malnourished

child requires that both medical and social problems be recognized and corrected.

If the illness is viewed as being only a medical disorder, the child is likely to

relapse when he or she returns home, and other children in the family will remain

at risk of developing the same problem.3



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Down syndrome occurs due to an excess number of chromosomes in

chromosome number 21, which is supposed to be two to three. Chromosomal

abnormalities was not heredity. The disorder can cause sufferers experience

physical abnormalities such as congenital heart defects, weakened muscles

(hypotonia), and mental retardation about development of intelligence and

psikomotor delay. Until now, the cause of abnormalities of chromosome number

that is not yet known. In patients with Down syndrome chromosome number 21 is

not a pair, but 3 pieces so the total number chromosomes to 47.When the baby

was growing up, it is necessary to determine the type of IQ examination exercises

selected schools. Another examination is an examination that may be required in

patients with heart because it often suffer heart defects. There are three types of

Down syndrome is Trisomy 21 regular, translocation and mosaic. 4

1.2. Objective

The aim of this study is to explore more about the theoritical aspects on

severe malnutrition and down syndrome, and to integrate the theory and

application of severe malnutrition, in this case marasmus and down syndrome indaily practices.



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CHAPTER 2

LITERATUR REVIEW

2.1. Severe Malnutrition

2.1.1. Definition

Malnutrition essentially means “bad nourishment”. It concerns not enough

as well as too much food, the wrong types of food, and the body's response to a

wide range of infections that result in malabsorption of nutrients or the inability to

use nutrients properly to maintain health. Clinically, malnutrition is characterized

by inadequate or excess intake of protein, energy, and micronutrients such as

vitamins, and the frequent infections and disorders that result.1,2

2.1.2. Epidemiology

Malnutrition is still the main problem in public health especially in

developing countries, it contributes more than half death case of children under 5

years. It is one of the main problem of nutrition in Indonesia. Its Prevalence is

high especially in children < 5 years. Based on SUSENAS 2002, 26% of children

< 5 years having malnutrition, and 8% among them are in severe malnutrition, but

in Riskesdas 2007, there prevalence decreases to 13% for moderate-malnutrition

and 5.4% for severe malnutrition. 1,2

2.1.3. Aetiology

Primarily, it is caused by low in quantity or quality of the food that is

consumed, and high in need or output as a secondary causes. Malnutrition is the

end result of chronic nutritional and, frequently, emotional deprivation by carers

who, because of poor understanding, poverty or family problems, are unable to

provide the child with the nutrition and care he or she requires. 2,3



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2.1.4. Clinical Manifestation3,5

• Marasmus : extreme wasting, old-man face, irritable, subcutaneous fat

loss, baggy pant.

• Kwashiorkor : oedema, moon face, sparse hair with waek roots, apathy,

irritable, muscle hypotrofi, hepatomegaly, crazy pavement dermatosis

• Marasmus-Kwashiorkor : mixed manifestation of marasmus and

kwashiorkor with minimally oedema.

Figure 1, Marasmus Figure 2, Kwashiorkor

• Others : micronutrient deficiencies (vitamin A deficiency, anemia,

stomatitis, skin manifestation) signs and symptomps of co-morbid

(diarrhoea, parasitic, tuberculosis, malaria, and pneumonia)2.1.5. Assesment of Nutritional Status and Criteria for Hospital Admision

Table 1, Clasiffication of malnutrion

Clasiffication of malnutrition

Mild-moderate Severe

Symmetrical oedema No Yes

Weight for height -3 ≤ SD < 2 < -3 SD (severe wasting)

Height for age -3 ≤ SD < 2 < -3 SD (severe stunting)



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Assesment of severe malnutrition is based on clinical and physical

examination (weight for height or length), the result is plotted to CDC

NHCS/WHO curve to determine the clasiffication of malnutrition. These are

(clinical and physical finding) are summarized in table 1. Children was weight for

height is below -3 SD or less than 70% of the median NHCS/WHO reference

values (termed “severely wasted”), or who have symmetrical oedema involving at

least the feet (termed “oedematous malnutrition”) are severely malnourished.

They should be admitted to hospital where they can be observed, treated and fed

day and night. Another criteria for hospital admission is if there are other signs

such as: anorexia, severe pneumonia, anemia, high fever, severe dehydration,

lethargy, hypothermia, hypoglicemia.3

2.1.6. Diagnosis1,2,3

a. History : usual diet before current episode of illness, Breastfeeding history,

Food and fluids taken in past few days, Recent sinking of eyes, Duration and

frequency of vomiting or diarrhoea, Appearance of vomit or diarrhoeal stools,

Time when urine was last passed, Contact with people with measles or

tuberculosis, Any deaths of siblings, Birth weight, Milestones reached (sitting up,

standing, etc., Immunizations.

b. Physical Examiination : weight and length or height, Oedema, Enlargement or

tenderness of liver, jaundice, Abdominal distension, bowel sounds, “abdominal

splash” (a splashing sound in the abdomen), Severe pallor, Signs of circulatory

collapse: cold hands and feet, weak radial pulse, diminished consciousness,

Temperature: hypotermia or fever, Thirst, Eyes: corneal lessions indicative of

vitamin A deficiency, Ears, mouth, throat : evidence of infection, Skin : evidence

of infection or purpura, Respiratory rate and type of respiration: sign of

pneumonia or heart failure, Appearance of faeces.

c. Other Investigations:

• Blood Glucose : < 54 mg/dl = hypoglicemia



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• Blood Smear : malaria

• Hb or Ht : < 4 g/dl or < 12% = severe anemia

• Urynalysis/culture : bacteria + or > 10 WBC/ big view = infection

• Faeces : blood (+) = dysentri, Giardia (+)/ other parasites = infection

• CXR : Pneumonia, heart failure, fracture

• Tuberculin Skin Test : often negative

2.1.7. Treatment

There are five key-points in management of severe malnutrition, they are :

ten main steps, treatment of co-morbid, failure to respond to treatment, education

before discharge, and management of emergency condition (such as shock and

severe anemia). 2

a. Ten main steps, consists of 3 phase : initial, rehabilitation, and follow-up

phase. The time-frame for management of severe malnutrition is shown

in table 2.2

Initial Treatment : this phase begins with admission to hospital and lasts

until the child’s condition is stable (during 1 week). This is divided into

stabilitation (day 1-2) and transition (day 3-7). It focuses on life-

threatening condition, spesific deficiencies, and feeding is begun.

Rehabilitation (weeks 2-6) : intesive feeding, emotional and physical

stimulation, and preperation for discharge.

Follow Up (weeks 7-26) : preventing relapse and assure continued

physical, mental, and emotional development of the child.



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Table 2, Time Frame for management of severe malnutrition

1) Treat and prevent Hypoglicemia

Patients with severe malnutrition are at risk of developing hypoglicemia, it’s

important cause of death during the first 2 days of treatment. Diagnose based on

blood glucose level below 54 mg/dl. Signs of hypoglicemia include hypothermia,

lethargy, and loss of conscioussness, and often manifests only drowsiness before

death. Unlike in common setting, hypoglycemia in severly malnourished children

doesn’t usually manifest as sweating and pallor. If hypoglicemia is suspected,

treatment shoud be given immediately without laboratory confirmation (in setting

without laboratory facilities,every severly malnourished children must be

suspected and treated as hypoglicemia).3,6

Table 3, signs and treatment of hypoglicemia

Signs Treatment

Conscious, able to drink Give 50 ml D10%, or sugar 10% solution (by

dilute 5 grams of sugar with 50 ml of water)

Lethargy Give D10% 5 ml/BW (iv), then give 50 ml D10%,



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or sugar 10% solution (bolus) via oral or NG route

Shock Give D10% 5 ml/BW (iv), then drip RL and D10%(1:1) 15 ml/BW in 1 hour

2) Treat and prevent Hypothermia

Hypothermia is defined as axillary temperature < 36,5 °C (measure in 5

minutes) or rectal temperature < 35,5 °C. Severly malnourished children are at

greater risk of hypothermia than other children and need to be kept warm, and

they are probably hypoglicemic also. If those are present, they may have serious

systemic infection. All hypotermic children should be treated for hypoglicemia

and infection as well. 3,5

Severly malnourished children have difficulty in controlling temperature

because of low calories, warming these patients can conserves their energy

Following measures are important for all severly malnourished children3,6,7 :

• Cover the child, including his head.

• Stop draughts in the room. Move the child away from windows.

• Maintain room temperature of 25 − 30°C (77 − 86°F) if possible.

• Keep the child covered at night.

• Warm your hands before touching the child.

• Avoid leaving the child uncovered while being examined, weighed, etc.

• Promptly change wet clothes or bedding.

• Dry the child thoroughly after bathing.

In addition to keep the child warm, we can use one of the following : have the

mother hold the child with his skin next to her skin when possible (kangaroo

technique), and cover both of them. Keep the child’s head covered.3,6,7

3) Treat and prevent Dehydration



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Table 4, Assesment of Dehydration

Signs of Dehydration Assesment

Lethargic Not awake & alert, drowsy, doesn’t show

interest in what is happening around him

Restless, irritable Happens all the time, especially when he is

touched or handled

Absence of tears Observe when he cries whether the child has

tears or not

Sunken Eyes Severly malnourished children may always

shows sunken eyes, regardless of the

hydration status, so ask the mother if the

child’s eyes appear unusual

Dry mouth and tongue Feel the tounge and inside of the mouth with

a clean, dry finger to determine if they are

dry

Thirsty See if the child reaches out for the cup when

we offer the ReSoMal. When it’s taken

away see if the child wants more

Skin pinch goes back slowly Use the thumb or first finger to pinch skin

on the child’s abdomen halfway between

umbilicus and the side of abdomen. Pinch

the skin for one second and then release, ifthe skin stays folded for brief time, the skin

goes back slowly.

Many of these signs of dehydration are unreliable in a child with severe

malnutrition, making it difficult to detect and determine the severity of

dehydration. Following signs are reliable in a child with severe malnutrition :

history of diarrhoea, thirsty, hypothermia, sunken eyes, weak and rapid radial

pulse, cold hands and feet, urine flow.3,5



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Treatment of dehydration in severly malnourished children is different, these

children have abnormally hi-sodium and lo-potasium. WHO recomends modified

oralit which is called ReSoMal (rehydration solution for malnutrition) that is

contained less sodium and more potasium (it is intended for severly malnourished

children with diarrhoea). ReSoMal can be made by diluting one-packet standard

WHO-ORS, 8 ml mineral mix (one packet dilute in 20 ml water) and 10 gram

sugar in 400 ml water. NG tube should be used in all weak or exhausted children.

And in those who vomit, have fast breathing, or painful stomatitis.3,6,7

If the severely malnourished child has watery diarrhoea or vomitting, assume

dehydration (also ask about dysentry as will affect choice of antibiotics) and give

ReSomal as follows : 5 ml/BW every 30 minutes for the first 2 hours (orally or

NG tube), then 5-10 ml/BW/hour in alternate hours for up to 10 hours, F-75 is

given in alternate hours during this period until the child is rehydrated. These rates

are slower than for children who are not severly malnourished. Reassess the child

at least every hour. The exact amount of ReSoMal to give should be determined

by the eager of drink, amount of going losses (vomit, stool), and also the signs ofoverhydration especially signs of heart failure. Rehydration is completed when the

signs above (table) have disappeared. After rehydration, give 50-100 ml of

ReSoMal after each loose stool (< 2 years), and 100-200 ml for > 2 years. This

treatment is continued until diarrehoea stops.3,6,7

Be aware the signs of shock during diarrhoea, such as lethargy,

unconciousness, cold hands and feet, delayed capillary refill time, diminished

urine flow.7

4) Correction of electrolyte imbalances

Severe malnutrion patients are at risk having electrolyte imbalance and need to

be corrected. ReSoMal consists of glucose, sodium, potasium, chloride, citrate,

magnesium, zinc, copper (table 5). Beside ReSoMal when diarrhoea, correction



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of electrolyte imbalance also got from feeding WHO-formula according to the

phase (see next step).3,6,7

Table 5, component of ReSoMal

Component Consentration (mmol/L)

Glucose 125

Sodium 45

Potassium 40

Chloride 70

Citrate 7

Magnesium 3

Zinc 0.3

Copper 0.045

Osmolarity 300

5) Treat infections3,6,7

Give all severly malnourished children antibiotics for presumed infection. Give

the first dose while other initial treatments are going on, as soon as possible.

Selection of antibiotics depends on the presence or absence of complications (like

septic shock, hypoglicemia, hypothermia, dermatosis, resp/urinary tract infection,

or lethargic/sickly appereance.

• If no complication : oral cotrimoxazole (25 mg Sulfamethoxazole + 5 mg

trimethroprim/kg) every 12 hours for 5 days

• If there is complications : gentamicin 7.5 mg/kg IM/IV once daily for 7 days +

ampicilin 50 mg/kg IM/IV every 6 hours followed by amoxicilin 15 mg/kg every

8 hours for 5 days.



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• If the child fails to improve within 48 hours, add chloramphenicol 25 mg/kg

IM/IV every 8 hours for 5 days. And give additional antibiotics if spesificinfection are detected.

6) Correction of miconutrient deficiencies

Severly malnourished children are at risk having micronutrient deficiencies and its

consequences. So give supplemental every day as the following rule : multivitamin

supplemental (without iron in the stabilisation & transition phase, with iron in the

rehabilitation phase), folic acid 5 mg in the first day then give 1 mg/BW, vitamin A

based on age 50.000 IU for < 6 months, 100.000 IU for 6-12 months, and 200.000 IU

for > 1 years. Iron should never be given during initial phase because it can lead to

free iron in the body and cause : promoting bacterial growth and increasing the risk of

infection, formation of free radicals, and increasing the need of calories to be used for

converting free iron to ferritin.3,6,7

7) Begin Feeding

Feeding is obviously a critical part of managing severe malnutrition, however,

feeding must be started cautiously, in frequent, small amounts. If feeding begins too

aggressively, or if feeds contain too much protein or sodium, the child’s systems may

be overwhelmed, and the child may die. To prevent death, feeding should begin as

soon as possible with F-75, the “starter” formula used until the child is stabilized

(stabilisation phase). F-75 is specially made to meet the child’s needs without

overwhelming the body’s systems at this early stage of treatment. F-75 contains 75

kcal and 0.9 g protein per 100 ml. F-75 is low in protein and sodium and high in

carbohydrate, which is more easily handled by the child and provides much-needed

glucose.3,8,9

The goals to be achieved in this phase are : energy : 80-100 kal/kgBW/day,

protein 1-1,5 gr/kg, volume 130 ml/kgBW/day (100 ml if oedema) and the children

should also continue to be breastfed between feeding. Appendix A shows the amount

of diet at each feed to achieve the goals (dose of F-75 based on BW). For the first 2



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hours give a quarter of the dose F-75/2 hours every 30 minutes, then for next 10 hours

continue F-75/2 hours. If well-tolerated, continue F-75 every 3 and 4 hours. After

finishing F-75/4 hours and the children are well-tolerated, continue the feeding in the

next phase (transition and rehabilitation).2,3,8

In transition phase the children are given with F-100 but using the F-75 dose

(Appendix A) every 4 hours for 2 days, in the third days children are given with F-100

dose (Appendix B) every 4 hours, the dose is up-titrated 10 ml until the children

cannot tolerate but not exceed the maximum dose in table. In the fourth day give F-

100 every 4 hours until the end of transition phase (7-14 days) according to children

condition. It is important to note that it is the child’s appetite and general condition

that determine the phase of treatment and not the length of time since admission.3,8

8) Increase feeding to recover lost weight (Catch-up formula)

When the child is stabilized (usually after 2 − 7 days) and after the appetite has

returned, the “catch-up” formula F-100 is used to rebuild wasted tissues. F-100

contains more calories and protein: 100 kcal and 2.9 g protein per 100 ml. In this

phase : energy : 150-220 kal/kgBW/day, protein 4-6 gr/kg. The child should remain in

hospital for the first part of rehabilitation phase. The patient can be transferred to

nutrition rehabilitation center if all folowing criterias have been met : eating well,

mental state has improved (smiles, responds to stimuli, interested in surroundings),

sits, crawls, stands or walks (depending on age), normal temperature, no vomitting or

diarrhoea, no oedema, gaining weight > 5 g/kgBW per day for 3 successive days.3,8,9,10

9) Stimulate emotional and sensorial development

Severly malnourished children have delayed mental and behavioural development,

which if not treated can become serious long-term result of malnutrition, emotional

and physical stimulation through play programmes that starts during rehabilitation and

continue after discharge can substianlly reduce risk of of permanent mental retardation

and emotional impairement. Take a look for : the environment, activities (play &

physical).2,3



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10) Prepare for discharge

During rehabilitation, preparations should be made to ensure that the child is fully

reintegrated into the family and community after discharge. As the child’s home is the

environment in which severe malnutrition developed, the family must be carefully

prepared to prevent its recurrence. Give sugestion to come back to the hospital for

evaluation regulary one a week in the first month, one in two weeks in the second

month, and one a month in the next three-four months.2,3

The patients are determined as recover from the severe malnutrition if weight-

lenght > -2 SD and no clinical manifestation. And criteria for discharge as following2,3:

• No oedema, awake and active

• Weigth for lenght > - 3 SD

• No complications

• Increase BW 50 g/kgBW/week for 2 weeks

• Mother given the knowledge about nutrition for her child.

• Good appetite

b. Treatment of Co-Morbid2,3

• Vitamin A Deficiency

• Dermatosis

• Parasitic infestation

• Persisten Diarrhoea

• Tuberculosis

c. Failure to respond to treatment2,3



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There are two kinds of failure in this treatment. First when the patient die, for

the first 24 hours after admision can be caused by hypoglicemia, hypothermia,

dehydration, and sepsis. And for the next 24-72 hours is caused by aggresive feeding

(exceed in volume and calories). The next is related to the improvement of body

weight, the inadequency of increasing BW may be caused by infection, dietary, and

also physicological. So it is important to evaluate the body weight (good if > 10

g/kgBW/day, fair 5-10 f/kgBW/day, and poor < 5 g/kgBW/day) and investigate the

cause of the failure of the treatment.

d. Discharge before the end of rehabilitation phase2,3

Give education to the parents about dietary (hi-calory and hi-protein,

frequency 5 times a day, full portion, multivitamin supplementation, breastfeeding is

continued), back to the hospital for evaluation, and vaccination.

e. Management of emergency condition

2.2 Down Syndrome

2.2.1 Definition

Down syndrome is a genetic disorder known as Trisomy, because individuals

who get a Down syndrome have excess chromosome. They have three chromosome

21 where the normal only has two. This will change the excess chromosome genetic

balance of the body and result in changes in the characteristics physical and

intellectual abilities, as well as disturbances in physiological function body.4

2.2.2 Epidemiology

Abnormality is found throughout the world, in all ethnic groups. Estimated

incidence of 1.5: 1000 births, and there were 10% among patients with mental

retardation. Found statistically more born to mothers over the age of 30 years,

although not infrequently also found that babies born to young mothers. In this last

group, in the form of a translocation chromosome abnormalities.11



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2.2.3 Aetiology11

Down syndrome are born to mothers aged older (high risk), women over 35

should be aware of this possibility. The incidence of Down syndrome increases

evident in women who gave birth after age 35 years and over. Female egg cell has

been established at the time the woman was still in the womb to be cured one by one

each month. By the time a woman becomes older, the condition of the egg cells

sometimes become less well and at the time the egg is fertilized by the male germ

cells undergoing division are less than perfect. The cause of the excess of

chromosome 21 could also be due to congenital birth of mother or father who has two

pieces of chromosome 21, but it is not in its rightful place, as one of the chromosome

21 attached to another chromosome during cell division so that chromosome 21 does

not divide perfectly. Factors that play a role in the occurrence of chromosomal

abnormalities are:

1. Maternal age : usually the mother over the age of 30 years, probably due to a

hormonal imbalance.

2. Disorders of pregnancy.

3. Endocrine disorders in women : old age can occur relative infertility, thyroid

disorders or ovarian.

2.2.4 Clinical Manifestation11,12

Children with this syndrome are very similar to each other. Mental

retardation in addition there is also a very prominent physical retardation. Thinking

skills can be classified as an idiot and will not be able to exceed a 7-year-old child.

Usually very interested in music. Child's face is very typical. Head rather small and

brakisefalik with flat occipital region. Wide face, high cheekbones, flat nose, squinty

eyes far apart and tilted upwards and the side (like the Mongols). Ear a bit strange,

thick lips and large tongue, rough and fissured-gap. The growth of the teeth are very

disturbed.

Smooth and loose skin, but the color is normal. In the folds of the neck are

excessive. On the pinkie finger looks short and bent inward. Distance between fingers



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I and II, both on the hands and feet are rather large. Genitals are usually small.

Hypotonic muscles and joints from excessive movement. Congenital heart defects

such as ventricular septal defect is often found, growth in infancy is sometimes good,

but then it became slow.

2.2.5 Diagnosis11

Diagnosis based on:

1. Clinical symptoms

2. Additional examination

a. Dermatoglifik

b. Chromosome examination

3. Anatomic pathology

Brains of children with disorder are usually smaller than normal and bigger

children, the growth of the brain growing up.

2.2.6 Treatment

No special treatment

CHAPTER III

CASE REPORT

Name : REA

Age : 1 year 3 months

Sex : Male

Date of Admission : August, 17 th 2013

Main Complaint : vomiting



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History : It is experienced by patients is approximately 2 days, the frequency of

vomiting was not counted. Content of what they eat and drink

- Diarrhoea (+) 2 days, 2x/day frequency, consistensi water more than pulp (+),

lenders (+), blood (-)

- Now this patient's fever, history of recurrent fever (+), fever is up and down,

down with fever-reducing medicine.

- The body weight decreased since the age of 6 months.

- urination (+) normal.

• History feeding

0.1 years old: ASI

0-6 months: exclusive breastfeeding

6-9 months: cereal + milk

9-12 months: breast + formula (SGM) + cereal

• History of birth

Patient is the second son of the two brothers, was born normal, helped midwife,

BW = 2600gr BH = 48cm, immediately cried

• History of growth and development

Now this patient can only prone itself, babbling, imitating the words,smilling, and

looking at his hands.

Physical Examination

BW/Age: < -3SD

BH/Age: < -3SD

BW/BH: < -3SD

Presens status

Sens. Compos Mentis, Body temperature: 37,0oC, Pulse: 140 bpm, Respiratory

Rate: 40 bpm.

Localized status



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• Head : old man face (+),dismortik Face (+)

Eye : concave,light reflexes (+/+), isochore pupil, pale conjunctivapalpebra inferior (-/-),icteric sclera (-/-) , Ear : Normal ,Mouth : Normal ,

Nose: nasal canul O2 attached

1. Neck : Lymph node enlargement (-)

2. Thorax: Symmetrical fusiform, easily seen ribs(+), retraction (-)

HR: 140x/i, reguler, sigh (-). RR: 40 x/i, regular, crackles (-/-)

3. Abdomen : Soepel,Peristaltic(+)normal.Liver/Spleen/Renal: undeterminate

4. Extremities: pulse : 140 x/i, regular, adequate pressure and volume, warm

acral, CRT <3”, baggy pants (+), muscle hypertrophy (+),

TD=90/60mmhg.

Working Diagnosis

-Marasmus type Malnutrition (II condition) + susp.Down syndrome

P: Management

- O2 2L / i nasal canul

- Inj. ceftriaxone 150 mg / 2 hours / IV

-Resomal 50cc alternatif with diet F75 40cc /2hours with mineral

mix 0,8cc

- When diarrhea (+): Resomal / x diarrhea

- Multivitamins without Fe 1 x 1 cth

- Folic acid 1x1mg

- Vitamin A 1x200.000 IV

Planning



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- Complete Blood Count

- Blood Glucose

- Electrolite

FOLLOW UP

August, 17th 2013 (First day)

S: Vomiting (+), Diarrhea (+), shortness of breath(-)

O: Sens: GCS 12 (E4V2M6) , Temp: 37o

C, Body weight: 3,4 kg PB = 65cmHead : Old man face (+), dismorfic face (+)

eye : concave, light reflexes (+/+), icteric Sclera (-/-), isochoric pupil, pale

conjunctiva palpebra inferior (-/-), Ear : Normal, Nose: nasal canul O2

attached (+),NGT(+), Mouth: normal

Neck

Thorax

: Lymph node enlargement (-)

: Symmetrical fusiform, easily seen ribs(+),retraction (-)

HR: 120x/1’, reguler, sigh (-).

RR: 32 x/1’, regular, crackles (-/-)

Abdomen : Soepel, Peristaltic (+) normal. Liver/spleen/renal :undeterminateExtremities : Pulse 140 x/i, regular, adequate pressure and volume, warm acral, CRT

< 3”, baggy pants (+), muscle hypertrophy (+), TD=90/60 mmgh

A: Marasmus type Malnutrition (II condition) + susp.Down syndrome

P: Management

- O2 2L / i nasal canul

- Inj. ceftriaxone 150 mg / 2 hours / IV

- Resomal 50cc alternative with diet F75 40cc/2hours with mineral mix 0,8cc

- Multivitamins without Fe 1 x 1 cth

- Folic acid 1x1mg

- Vitamin A 1x200.000 IV



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Plan :

- Complete Blood Count -Electrolite

- Blood Glucose

Laboratory Result:

1. August, 17th 2013

Complete Blood Count

Hemoglobin (HGB) g% 13.20 11.3 – 14.1

Eritrosit (RBC) 106/ mm3 4.87 4.40 – 4.48

Leukosit (WBC) 103/ mm3 45.00 6.0- 17.5

Hematokrit % 37.70 37 – 41

Trombosit (PLT) 103/ mm3 736 217 – 497MCV fL 77.40 81 – 95

MCH Pg 27.10 25 – 29

MCHC g% 35.00 29 – 31

RDW % 15.10 11.6 – 14.8

MPV fL 9.90 7.2 - 10.0

PCT % 0.73

PDW fL 10.7

Diftel

Neutrofil % 83.20 37 – 80

Limfosit % 7.40 20 – 40Monosit % 9.10 2 – 8

Eosinofil % 0.10 1 – 6

Basofil % 0.200 0 – 1

Neutrofil Absolut 103/µL 37.41 1.9 - 5.4

Limfosit Absolut 103/µL 3.33 3.7 - 10.7

Monosit Absolut 103/µL 4.11 0.3 - 0.8

Eosinofil Absolut 103/µL 0.04 0.20 - 0.50

Basofil Absolut 103/µL 0.11 0 - 0.1



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Laboratory Result:


Clinical Chemistry

Blood gas analysis

SATUAN HASIL RUJUKAN

Ph 7.490 7.35-7.45

pCO2 mmHg 42.8 38-42Bicarbonate (HC08) mmHg 153.8 85-100

Total CO2 mmol/L 31.9 22-26

Base excess (BE) mmol/L 33.2 19-25

O2 saturation % 7.8 (-2)-(+2)

CARBOHYDRATE METABOLISM

Blood glucose (As) mg/dL 331.00/ <200

ELEKTROLIT

Natrium (Na) mEq/L 123 135-155

Kalium (K) mEq/L 3.3 3.6-5.5

Klorida (Cl) mEq/L 87 96-106

Laboratory Result:


Clinical Chemistry SATUAN HASIL RUJUKAN

CARBOHYDRATE METABOLISM

Blood glucose (As) Mg/dL 129.00 <200

IMUNOSEROLOGI

TIROID

T3 Total µg/mL 0.67 0.8-2

T4 Total µg/dL 7.09 5-14TSH µU/mL 1.460 0.27-4.2





24

August, 19th 2013 (third day)

S: vomiting (-), Diarrhea (+), shortness of breath (-)

O: Sens: GCS 12 (E4V2M6), Temp: 37oC, Body weight : 3,4 kg, PB: 65cm LLA = 8cm

Head Old man face(+),Dismorfic face (+)

Eye :light reflexes (+/+),Isochoric pupil, pale conjunctiva palpebra inferior

(-),Ear = Normal, Nose= nasal canula O2 (+), NGT (+), Mouth = Normal

Neck

Thorax

Abdomen

Extremities

Lymph node enlargement(-)

Symmetrical fusiformis, easily seen ribs(+),retraction (-).

HR: 124x/1’, reguler, sigh(-),RR: 38 x/1’, regular, crackles (-/-)

Soepel,Peristaltic (+) normal. Liver/Spleen/Renal : undeterminate

Pulse 124 x/1’, regular, adequate pressure and volume, warm acral, CRT

< 3”, hypotropy muscle (+), baggy pants (+)

A: Marasmus type malnutrition (II condition) + susp.Down syndrome

P: management

- Resomal 50 cc / x diarrhea

- Folat acid 1 x 1 mg

- Multivitamin without Fe 1 x1 cth

- Diet F75 40cc / 2 hrs with mineral mix 0.8 cc

Plan : - Blood Glucose

- Tiroid

August, 20th 2013 (Fourth day)

S: Vomiting (-), Diarrhea (+), shortness of breath (-)



25

O: Sens: GCS 12 (E4V2M6), Temp: 36,8oC, Body weight : 3,4 kg, PB: 65cm LLA = 8cm

Head Old man face(+),Dismortic face (+)



Neck

Thorax


Symmetrical fusiformis, easily seen ribs(+),retraction (-)

HR: 124x/1’, reguler, sigh (-),RR: 38 x/1’, regular, crackles (-/-)Abdomen Soepel. Peristaltic (+) normal. Liver/Spleen/Renal : undeterminate

Extremities Pulse 124 x/1’, regular, adequate pressure and volume, warm acral, CRT



P: management



- Multivitamin without Fe 1 x1 cth

- Diet F75 40cc / 2 hrs /NGT with mineral mix 0.8 cc

Plan :-

August, 21st 2013 (fifth day)

S: Vomiting (-), Diarrhea (+), shortness of breath (-)



26

O: Sens: GCS 12 (E4V2M6),T: 37.5oC, Body weight : 3,4kg, PB = 65cm, LLA = 8cm

Head

Neck

Old man face(+),Dismorfic face (+)




Thorax Symmetrical fusiformis, easily seen ribs(+),retraction (-)

HR: 112x/1’, reguler, sigh (-).RR: 38 x/1’, regular, crackles (-/-)Abdomen Soepel. Peristaltic (+) normal. Liver/Spleen/Renal : undeterminate




P: management


- Multivitamin without Fe 1 x cth 1


- Contrimoxazole syr 1x 1cth

- Diet F75 40cc / 2 hrs/NGT with mineral mix 0,8 cc

Plan : -

August, 22nd 2013 (sixth day)

S: Vomiting (-), Diarrhea (-), shortness of breath (-)



27

O: Sens: compos mentis, Temp: 37oC, Body weight : 5,2 kg




Neck

Thorax

Lymph node enlargement (-)


HR: 102x/1’, reguler, sigh (-). RR: 32 x/1’, regular, crackles (-/-)Abdomen Soepel,Peristaltic (+) normal. Liver/Spleen/Renal : undeterminate


< 3”, hypotropy muscle (+), baggy pants (+).

A: Marasmus type malnutrition + susp.Down syndrome

P: management


- Multivitamin without Fe 1 x 1cth

- Cotrimoxazole syr 1x1cth

- Diet F100 65cc / 2 hrs/NGT with mineral mix 1,3 cc


Plan:-

August, 23rd 2013 (seventh day)

S : Vomiting (-), Diarrhea (-)



28

O : Sens: Compos Mentis, Temp: 37oC, Body weight : 5,2 kg




Neck

Thorax

Lymph node enlargement (-)


HR: 100x/1’, reguler, sigh (-). RR: 30 x/1’, regular, crackles (-/-)Abdomen Soepel,Peristaltic (+) normal. Liver/Spleen/Renal : undeterminate



A : Marasmus type malnutrition + susp.Down syndrome

P: Management


- Multivitamin without Fe 1 x 1cth

- Cotrimoxazole syr 1x1 cth

- Diet F100 65cc/3 hours/ NGT with mineral mix 1,3cc

Plan: -Blood culture

-Thorax photo

August, 24th 2013 (eighth day)




29





Thorax Symmetrical fusiformis, easily seen ribs(+),retraction(-)

HR: 102x/1’, reguler, sigh (-). RR: 24 x/1’, regular, crackles (-/-)

Abdomen Soepel, Peristaltic (+) normal.Liver/Spleen/Renal: undeterminateExtremities Pulse 102 x/1’, regular, adequate pressure and volume, warm acral,

CRT < 3”, hypotropy muscle (+), baggy pants (+)


P: Management



- Multivitamin without Fe 1x1 cth


- Diet F100 65cc /3hrs/ NGT with mineral mix 1,3 cc

Plan :-

August, 25th 2013 (ninth day)




30

O : Sens: CM, Temp: 37oC, Body weight : 5,3 kg




Thorax Symmetrical fusiform, , easily seen ribs(+) ,retraction (-)

HR : 104 x/1’, reguler, sigh (-),RR : 24 x/1’, regular,Crackles (-/-)

Abdomen Soepel,Peristaltic (+) normal. Liver/Spleen/Renal: undeterminateExtremities Pulse 104 x1’, regular, adequate pressure and volume, warm acral,



P:management


- Folat acid 1x1mg


- Diet F100 100cc /3hrs/ NGT with mineral mix 2 cc

Plan:-

August, 26th 2013 (tenth day)




31




(-),Ear = Normal, Nose= NGT (+), Mouth = Normal

Thorax Symmetrical fusiform, easily seen ribs(+),retraction (-)

HR : 102 x/1’,reguler,sigh (-),RR : 24 x/1’, reguler. Crackles (-/-)

Abdomen Soepel Peristaltic (+) normal. Liver/Spleen/Renal: undeterminateExtremities Pulse 102 x/1’, regular, adequate pressure and volume, warm acral,



P:Management



- Diet F100 100cc/3hours/NGT with mineral mix 2cc

Plan:-

August, 27th 2013 (eleventh day)




32

O : Sens: Compos Mentis, Temp: 37oC, Body weight : 5,3kg





HR :100 x/1’, reguler,sigh (-). RR : 24 x/1’, reguler. Crackles (-/-)




P : Management




Plan :-

August, 28th 2013 (twelveth day)




33






HR : 100 x/1’, reguler,sigh (-).RR : 24 x/1’, reguler. Crackles (-/-)




P : Management




Plan :-

August, 29th 2013 (thirteenth day)




34





Thorax Symmetrical fusiform, easily seen ribs(+) , retraction (-).

HR : 102 x/1’, reguler, sigh (-). RR : 24 x/1’, reguler. Crackles (-/-)




P : Management




Plan :-

August, 30th 2013(fourteenth day)


O : Sens: Compos Mentis, Temp: 37oC, Body weight : 5,3kg



35




Thorax Symmetrical fusiform, easily seen ribs(+) , retraction (-)

HR : 102 x/1’, reguler, sigh (-). RR : 24 x/1’, reguler. Crackles (-/-)




P : Management




Plan :-



36

CHAPTER IV

DISCUSSION AND SUMMARY

Malnutrition essentially means “bad nourishment”. It concerns not enough

as well as too much food, the wrong types of food, and the body's response to a

wide range of infections that result in malabsorption of nutrients or the inability to

use nutrients properly to maintain health. The clinical manifestation are extreme

wasting, old-man face, irritable, subcutaneous fat loss, baggy pant.

Down syndrome is a genetic disorder known as Trisomy, because

individuals who get a Down syndrome have excess chromosome. They have three

chromosome 21 where the normal only has two.

REA, male, 1 year 3 month was admitted to RS Haji Adam Malik with

the main complaint of vomiting, diarrhea, and fever. On physical examination the

patient looks old man face in appereance, dismorfik face, easily seen ribs (+) ,

hypotropy muscle (+), subcutan lipid decreasing (+) and baggy pants (+), flat

nose, smooth and loose skin, thick lips, on the pinkie finger looks short and bent

inward, and the growth of the teeth are very disturbed. Laboratory finding shows

hyperglicemia, shows leucosytosis, and hyponatremia. Now this patient can only

prone itself, babbling, imitating the words, smiling, and looking at his hands.He

was diagnosed with marasmus type malnutrition plus suspect down syndrome,

and is managed with Folat acid 1x1 mg, Multivitamin without Fe 1x1cth,

cotrimoxazole syr 1x1 cth, Diet F100 100 cc/3hrs with mineral mix 2cc, Resomal

50 cc/x diarrhea.



37

REFERENCE

1. IDAI. 2009. Panduan Pelayanan Medik IDAI : Malnutrisi Energi dan

Protein. Hal 183-184.

2. Susanto J.C., Mexitalia M., Nasar S.S., Malnutrisi Akut Berat dan Terapi

Nutrisi Berbasis Komunitas dalam Buku Ajar Nutrisi Pediatrik dan

Penyakit Metabolik Jilid I. 2011. Eds Sjarif D.R., Lestari E.D., Mexitalia

M., Nasar S.S. Jakarta: Badan Penerbit IDAI. Hal 128-154.

3. World Health Organization (WHO). 1999. Management of Severe

Malnutrition : manual for physicians and other senior health workers.

Geneva : WHO. ISBN 92 4 154511 9

4. Davis, A. 2008. Children with Down Syndrome : Implications for

Assessment and Intervention in the School. School Psychology Quarterly.

Vol. 23 No. 2 (P) 271-281

5. World Health Organization (WHO). 2002. Training Course on

management of severe malnutrition : 2. Principles of Care. Geneva :

WHO. WHO/NHD/02/.4(P)2


management of severe malnutrition : 3. Initial Mangement. Geneva :

WHO. WHO/NHD/02/.4(P)3


management of severe malnutrition : 4. Feeding. Geneva : WHO.

WHO/NHD/02/.4(P)4

8. Departemen Kesehatan Republik Indonesia. 2011. Petunjuk teknis tata

laksana anak gizi buruk : buku I. Jakarta : Depkes.

9. Departemen Kesehatan Republik Indonesia. 2011. Petunjuk teknis tata

laksana anak gizi buruk : buku II. Jakarta : Depkes.

10. Kementrian Kesehatan Republik Indonesia. 2011. Pedoman Pelayanan

Anak Gizi Buruk. Jakarta : Departemen Kesehatan.



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11. Bagian Ilmu Kesehatan Anak FKUI. 2007. Kelainan Kromosom : Buku I.

Jakarta : FKUI. Hal 217-219

12.RSCM. 2007. Panduan Pelayanan medis RSCM : Sindrom Down. Hal

347-350

Appendix A (F-75)

Appendix B (F-100)



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Documents

Marasmus Down Syndrome