severe malnutrition case report

8/10/2019 Severe Malnutrition Case Report

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CASE REPORT

SEVERE MALNUTRITION

MARASMUS-KHWARSIORKOR TYPE

Compiled By:

ANDIKA PRADANA !"!"

IRA NOLA LIN##A !""$

DEPARTEMENT O% PEDIATRICS

H& ADAM MALIK #ENERAL HOSPITAL

%ACULTY O% MEDICINE

SUMATERA UTARA UNIVERSITY

MEDAN

'""

TABLE O% CONTENTS

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T*,le o) Co.e./ &&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&

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C0*p.e( ": I.(od1+.io

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

1.2. Objective .............................................................................. 2

C0*p.e( ': Li.e(*.1(e Re2ie3 &&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&

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2.1. Defnition .............................................................................. 3

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

2.3. Classifcation and Clinical indings ..........................................

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2.!. "at#op#ysiology .................................................................. $2.%. Diagnosis and &ork 'p ...................................................... 12

2.(. )anagement .............................................................................. 1$

2.$. Complication .............................................................................. 2*

2.+. ollo, 'p and "rognosis ...................................................... 3-

C0*p.e( 4: C*/e Repo(.

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C0*p.e( 5: Di/+1//io *d S1mm*(y

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!.1. Discussion .............................................................................. !3

!.2. ummary .............................................................................. !(

Re)e(e+e/

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CHAPTER I

INTRODUCTION

1.1. Background

Malnutrition is globally the most important risk factor for illness and death,

contributing to more than half of deaths in children worldwide; child malnutrition was

associated with 54% of deaths in children in developing countries in 200! "rotein#energy

malnutrition $"M&, first described in the '20s, is observed most fre(uently in

developing countries but has been described with increasing fre(uency in hospitali)ed

and chronically ill children in the *nited +tates!1he -orld .ealth /rgani)ation estimates that by the year 205, the prevalence of

malnutrition will have decreased to !1% globally, with !4 million children younger

than 5 years affected as measured by low weight for age! he overwhelming ma3ority of

these children, 2! million, will live in developing countries with 0% of these children

in sia, particularly the southcentral region, and 21% in frica! n additional 15 million

$2'!0%& children will have stunted length6height secondary to poor nutrition!

Malnutrition itself is a very essential aspects determining the health status of a child!

7ot only because it is pretty much correlated with the calorie and energy spent for each

day, but malnutrition itself also brings a lot of systemic manifestations! 8ow protein

intake will disturb the balance of energy homeostatic in body causing a decline in fat

strorage and brings lipolysis! he state of low protein intake also results in declining

amount of albumin and immunoglobulin, both of which are the essential factor that

determines the immunological status of a child! .ence a malnutrition child will much

easily suffer from a lot of infections, whether bacterial, viral, parasites or fungal! 8ow

protein levels in body will also abrupt the growth and development of children associated

with mielini)ation and neurotrasmitter production of neural tissue in the brain!

he effects of changing environmental conditions in increasing malnutrition is

multifactorial! "oor environmental conditions may increase insect and proto)oal

infections and also contribute to environmental deficiencies in micronutrients!

/verpopulation, more commonly seen in developing countries, can reduce food

production, leading to inade(uate food intake or intake of foods of poor nutritional

(uality! 9onversely, the effects of malnutrition on individuals can create and maintainpoverty, which can further hamper economic and social development!

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:n addition to protein energy malnutrition, children may be affected by micronutrient

deficiencies, which also have a detrimental effect on growth and development! he most

common and clinically significant micronutrient deficiencies in children and childbearing

women throughout the world include deficiencies of iron, iodine, )inc, and vitamin and

are estimated to affect as many as two billion people! Micronutrient deficiencies and

protein and calorie deficiencies must be addressed for optimal growth and development to

be attained in these individuals!

9onsidering all these imperative effects brought on malnutrition in every aspects of

daily life, this paper is composed to furtherly eplore several more theoritical and clinical

aspects about malnutrition, particularly the diagnosis and management of severe

malnutrition in the field!

1.2. Objectie

he aim of this study is to eplore more about the theoritical aspects on malnutrition,

and to integrate the theory and application of malnutrition case in daily life

CHAPTER II

!ITERATURE RE"IE#

2.1. $a%nutrition

2.1.1. De&inition

he -orld .ealth /rgani)ation $-./& defines malnutrition as


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$"M& applies to a group of related disorders that include marasmus, kwashiorkor, and

intermediate states of marasmus#kwashiorkor!2

he term marasmus is derived from the >reek word marasmos, which means

withering or wasting! Marasmus involves inade(uate intake of protein and calories and is

characteri)ed by emaciation! he term kwashiorkor is taken from the >a language of >hana

and means


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:n general, marasmus is an insufficient energy intake to match the body=s re(uirements!

s a result, the body draws on its own stores, resulting in emaciation!

:n nonedematous "M $marasmus& initially there is failure to gain weight and irritability,

followed by weight loss and listlessness until emaciation results! he skin loses turgor

and becomes wrinkled and loose as subcutaneous fat disappears! 8oss of fat from the

sucking pads of the cheeks may occur late, and the infant=s face may retain a relatively

normal appearance, compared with the rest of the body, eventually becoming shrunken

and wi)ened! he abdomen may be distended or flat with the intestinal pattern readily

visible! here is muscle atrophy and resultant hypotonia! he temperature is usually

subnormal and the pulse slow! :nfants are usually constipated but may develop a

starvation diarrhea with fre(uent small stools containing mucus!2

Aoth of the above pictures depict the characteristic of severly malnourished children

diagnosed with marasmus due to deficiency of calory intake!

b! Bhwarsiorkor

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:n kwashiorkor, ade(uate carbohydrate consumption and decreased protein intake lead to

decreased synthesis of visceral proteins! he resulting hypoalbuminemia contributes to

etravascular fluid accumulation! :mpaired synthesis of A#lipoprotein produces a fatty

liver!2,4

Edematous PEM $kwashiorkor& may initially present as vague manifestations that

include lethargy, apathy, or irritability! -hen well advanced, there is inade(uate growth,

lack of stamina, loss of muscle tissue, increased susceptibility to infections, vomiting,

diarrhea, anoreia, flabby subcutaneous tissues, and edema! he edema usually develops

early and may mask the failure to gain weight, but the liver may enlarge early or late!

he edema is often present in internal organs before it is recogni)ed in the face and

limbs! ?ermatitis is common, with darkening of the skin in irritated areas but not in areas

eposed to sunlight, in contrast to pellagra! ?epigmentation may occur after

des(uamation in these areas, or it may be generali)ed! he hair is sparse and thin and, in

dark#haired children, may become streaky red or gray! he teture is coarse in chronic

disease! 2

he following are the usual appearences of children diagnosed with khwarsiorkorC

$


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c! Marasmus D Bhwarsiorkor

his type is actually a combination of both, khwarsiorkor and marasmus as well! :n this

case, signs and symptomps and marasmus could be found coincidently with

khwarsiorkor! he child look very thin with bones and ribs could be inspected very

prominently, with mild edema found minimally, particularly in the lower etremities!

+

he clinical appearence hightlights

the presence of pitting edema

associated with low albumin levels

in blood!

9ra)y pavement dermatosis is also

present in this case which occur as

depigmentation lesion particularly in

etremities resulting from En

deficiency!

his picture represents hepatomegaly

and ascites which occur to this

patient due to low protein levels in

blood!


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:n addition to "M, children may be affected by micronutrient deficiencies, which also have

a detrimental effect on growth and development! he most common and clinically significant

micronutrient deficiencies in children and childbearing women throughout the world include

deficiencies of iron, iodine, )inc, and vitamin and are estimated to affect as many as two

billion people!4 Micronutrient deficiencies and protein and calorie deficiencies must be

addressed for optimal growth and development to be attained in these individuals!

2.1.-. Pato')+io%og)

"rotein nergy Malnutrition $"M& is a result of a chronic and cumulative failure to

meet physiology energy and nutrient re(urements! ?ietary protein is needed to provide amino

acids for synthesis of body proteins and other compounds that have various functional roles!

nergy is essential for all biochemical and physiologic functions in the body! Furthermore,

micronutrients are essential in many metabolic functions in the body as components and

cofactors in en)ymatic processes! "rotein nergy Malnutrition affects virtually every organ

system! he manifestation of this process depend on different factorsC age, concomitant

infection, prior nutrition state, and the nature of the dietary restriction! 4

:n the absent of infection, fasting result in a initial depletion of fat an then glycogen

stores mediated by metabolic and endocrine changes that have the common goal of

preserving vital function, allowing human to survive until dietary energy can be restore!

>rowth is slowed, reducing the energy need to maintain this, and changes occur in the body

composition! Metabolic rate epressed in relation to height or lean body mass decrease! Arain

and visceral are relative preserved resulting in total body water, which is mainly etracelullar

but may also in intracelullar!,2

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hese metabolic ad3ustement to starvation are mediated, at least in part, by hormones!

9ortisol consentrate rises but remains responsive to stress! :nsulin secretion falls, and there in

a reduction in plasma insulin levels, a reduce respons to glucose and peripheral insulin

resistance! >rowth hormone is generally high and the normal supression by glucose load is

lost, although eception occures in marasmus! here is low activity in :nsulin >rowth Factor

$:>F#&, the metabolic effector of growth promoting affect of growth hormone! he last

effect of these hormonal changes are mobili)ation of fat, degradation of muscle protein and

reduction in basal rate! :ncrease aldosterone contribute to potassium loss already

compromised by the effect of energy restriction and reduced adenosine triphosphate synthesis

on the sodium pump!,2, 4,5

?uring protein deprivation, skeletal muscle is lost as structural protein is recycle to

conserve essential en)yme and provide energy for metabolic process! here is both fall in

muscle protein synthesis and an increase in breakdown which provide essential amino acid tothe liver for energy resource on production of acute phase proteins in liver and are opposite ot

those seen in starvation! his production of acute phase protein of infection are mediated by

protein cytokines, lipid derived factors such as prostaglandin, leukotrien, and platelet

activating factor! ndocrine change also play a role, the concentration of catabolic hormon

such as glucocorticoid, glucagon, and epinephrine increase! he cytokine increase

interleukin, norepinefrin, cortisol, and glucagon is the main stimulus for the mobili)ation of

acute protein phase in the liver! 9ytokine also enhance the effect of stress related hormone onthe production of acute phase proteins! Aecause of the interaction between food restriction

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and infection in phatogenesis of malnutrition, any integrated approach to eplaining the

pathophysiology has to take both in to account! he diference between kwarshiorkor and

marasmus may be partitially eplain by n increased shift toward the metabolic conse(uences

of infection in children with kwarshiorkor! :n addition, preceding nutritional status may

modify the metabolic effect of infection! n eample is the increase rate breakdown and

synthesis of protein in response to infection in children with marasmus but not those with

kwarshiorkor and slower recovery from infectious diarhea! !/%

+ome changes in organs system in nergy "rotein MalnutritionC

a& :mune +ystem

:mmune response changes occur early in the course of significant malnutrition in a

child! hese immune response changes correlate with poor outcomes and mimic the changes

observed in children with ac(uired immune deficiency syndrome $:?+&! (

9ell mediated immunity is altered in severe malnutrition! he thymus, necessary

reduce in si)e and production of thymic hormone is reduced! 8oss of delayed

hypersensitivity, fewer lymphocytes, impaired lymphocyte response, impaired phagocytosis

secondary to decreased complement and certain cytokines, and decreased secretory

immunoglobulin $:g& are some changes that may occur! he seems to be related to protein

metabolism! +ome studies report particularly low concentration of 9 in kwarshiorkor! (

hese immune changes predispose children to severe and chronic infections, most

commonly, infectious diarrhea, which further compromises nutrition causing anoreia,

decreased nutrient absorption, increased metabolic needs, and direct nutrient losses! (

b& ndocrine system

ndocrine changes mediate the metabolic adaptation to starvation and have been

mentioned! hese changes have important conse(uences on the clinical management of

severely malnourished child! "ancreatic atrrophy is the common findings in marasmus, and

the consistent findings in severe malnutrition of a reduction in serum insulin levels! hese

hormonal effects rapidly reverse on refeeding, with weight gain! (

yroid gland function is altered in malnutrition! ?uring nutrition deprivation, at first

thyroine increases, but as malnutrition becomes more severe, and especially if kwarshiorkor

develops, total thyroine decreases! here is also a decrease in thyroid binding protein, but

this does not account for all of the reduction in thyroine and suggest the primary effects on

synthesis! :ncreased thyroid stimulating hormone secretions heralds recovery! here is also a

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reduction in deiodenation in thyroine to triiodothyronine, resulting in reduced

triiodothyronine!1

9ortisol consentration rise, especially in kwarshiorkor, and the circardian rhytm is

abolished, but the response to adrenocorticotropic hormon is preserve! 9ortisol levels also

rise with infection; 0% children with kwarshiorkor showed a rise in cortisol in response to

infection compare with only 50% of those with marasmus! his reduce response in marasmus

may eplain why these children are so susceptible to hypoglycemia! 1

combination of malnutrition and anlterd all the endocrine consentration causes

hypothalamic hypogonadism! he hypothalamic#pituitary#gonadal ais shuts down as the

body struggles to survive, directing finite energy resources to support more vital functions!

Aoth males and females eperience decreased libido and interruption of pubertal

development, depending on the timing of the illness!

c& 9ardiac +ystem

9ardiac output is reduce in children with acute "M compares with cardiac output on

recovery! 9ardiac muscle, however, shows only nonspecific changes and muscle contractility

is normal! 9oncomitant deficiencies such as hypokalemia, anemia, and vitamin deficiencie

may effect the heart!(

d& @espiratory +ystem

he reduction in muscle mass that occures in severe malnutrition affect respiratory

muscle, including the diaphragm, this is lead to reduce muscular functin, which influence

vital capacity and maimal inspiration and inspiratory pressure! his weakness may be

eacerbated by electrolite abnormalities such as low phosphate and hypokalemia! he

ventilator response to hipoksia is blunted, but not the response to hypercapnia! ?espite these

alterations, tachypnea and subcostal retraction remain useful signs in dignosing pneumonia in

malnutrition!(

e& >astrointestinal ract

?iarrhea and malnutrition often occure together! +evere malnutrition affect the

intestinal tract with reduce gastric acid production, thinning of the small intestinal mucosa

and flattening of disappearance of the villi with relative sparing cripts! 8ost of the villi

architecture of small intestine for any reason reduce disaccharide activity because the

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disaccharide, especially lactase, are found at the villous tips! hus, lactose malabsorption is a

common finding in "M!(

Fat malabsorption is also seen in both persistent diarrhea and "M! s well as the

mucosal changes, bacterial overgrowth in the upper small intestine has been described in

"M and may lead to bile salt decon3ugation, further imparing fat absorbtion! (

f& .ematology

nemia is common in severe malnutrition may be attributed ether to iron deficiency

and or reduced red cell production in adaptation to a smaller lean body mass! ?espite the fact

the most children have been consuming a diet deficient in bioavailable iron in kwarshiorkor,

there is elevate hepatic iron and bone marrow iron show stainable iron in half of children! (

g& +kin, .air, and eeth

:n marasmus, the dry wrinkled loose skin is a result of almost total loss subcutaneous

fat! his lead to a relative increase in surface area, reduce protection from ambient

temperature, and therefore increased susceptibility to hypotermia! .air is thin, grow slowly,

and falls out readily!%/ (

ven a single episode of prolonged malnutrition in the first year of life delays primary

dentition and is associated with higher prevalence of primary dentition caries and possibly

also permanent dentition caries!%/ (

h& Arain Function and ?evelopment

arly studies of malnourished children showed changes in the developing brain,

including, a slowed rate of growth of the brain, lower brain weight, thinner cerebral corte,

decreased number of neurons, insufficient myelini)ation, and changes in the dendritic spines!

More recently, neuroimaging studies have found severe alterations in the dendritic spine

apparatus of cortical neurons in infants with severe protein#calorie malnutrition! hese

changes are similar to those described in patients with mental retardationof different causes!

here have not been definite studies to show that these changes are causal rather than

coincidental!(

i& Aones

9hildren with severe malnutrition often remain stunted after recovery! Aone

demenerali)ation has also been reported and may be attributed to phosphate deficiency! Aone

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change typical of cooper deficiency may also be present as well as scurvy caused by vitamiun

9 deficiency! Gitamin ? deficiency which causes rickets and osteomalacia deserves special

mention! %/ (

2.1./. Diagno+i+ and #ork U'

a& .istory taking

8ow intake of calories or an inability to absorb calories is the key factor in the

development of malnutrition! nutritional history is directed toward identifying underlying

mechanisms that put patients at risk for nutritional depletion or ecess! hese mechanisms

include inade(uate intake, impaired absorption, decreased utili)ation, increased losses, and

increased re(uirements of nutrients! :ndividuals with the characteristics listed below are at

particular risk for nutritional deficiencies!1/2/+

*nderweight

"oor intakeC anoreia, food avoidance $e!g!, psychiatric condition&, or 7"/ status for

more than about 5 days

"rotracted nutrient lossesC malabsorption, enteric fistulae, draining abscesses or

wounds, renal dialysis

.ypermetabolic statesC sepsis, protracted fever, etensive trauma or burns

lcohol abuse or use of drugs with antinutrient or catabolic propertiesC steroids,

antimetabolites $e!g!, methotreate&, immunosuppressants, and antitumor agents

:n children, the findings of poor weight gain or weight loss; slowing of linear growth;

and behavioral changes, such as irritability, apathy, decreased social responsiveness, aniety,

and attention deficit may indicate protein#energy malnutrition! :n particular, the child is

apathetic when undisturbed but irritable when picked up! Bwashiorkor characteristically

affects children who are being weaned! +igns include diarrhea and psychomotor changes! 1/+

dults generally lose weight, although, in some cases, edema can mask weight loss! "atients

may describe listlessness, easy fatigue, and a sensation of coldness! >lobal impairment of

system function is present! +

"atients with protein#energy malnutrition can also present with nonhealing wounds!

his may signify a catabolic process that re(uires nutritional intervention! #year#old child

with coeisting celiac and .artnup disease that resulted in kwashiorkor, anemia, hepatitis,

hypoalbuminia, angular cheilitis, glossitis, con3unctivitis and diffuse alopecia, erythematousskin, des(uamation, erosions, and diffuse hyperpigmentation was reported!,2

1!


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b& 9linical Features

:n marasmus, the child appears emaciated with marked loss of subcutaneous fat and

muscle wasting! he skin is erotic, wrinkled, and loose! Monkey facies secondary to a lossof buccal fat pads is characteristic of this disorder! Marasmus may have no clinical

dermatosis! .owever, inconsistent cutaneous findings include fine, brittle hair; alopecia;

impaired growth; and fissuring of the nails! :n protein#energy malnutrition, more hairs are in

the telogen $resting& phase than in the anagen $active& phase, a reverse of normal!

/ccasionally, as in anoreia nervosa, marked growth of lanugo hair is noted! ,1,

Bwashiorkor typically presents with a failure to thrive, edema, moon facies, a swollen

abdomen $potbelly&, and a fatty liver! -hen present, skin changes are characteristic and

progress over a few days! he skin becomes dark, dry, and then splits open when stretched,

revealing pale areas between the cracks $ie, cra)y pavement dermatosis, enamel paint skin&!

his feature is seen especially over pressure areas! :n contrast to pellagra, these changes

seldom occur on sun#eposed skin!1,

?epigmentation of hair causes it to be reddish yellow to white! 9urly hair becomes

straightened! :f periods of poor nutrition are interspersed with good nutrition, alternating

bands of pale and dark hair, respectively, called the flag sign, may occur! lso, hairs become

dry, lusterless, sparse, and brittle; they can be pulled out easily! emporal recession and hair

loss from the back of the head occur, likely secondary to pressure when the child lies down!

:n some cases, loss of hair can be etreme! .air can also become softer and finer and appear

unruly! he eyelashes can undergo the same change, having a so#called broomstick

appearance!4,

7ail plates are thin and soft and may be fissured or ridged! trophy of the papillae on

the tongue, angular stomatitis, erophthalmia, and cheilosis can occur!

:nflammatory bowel diseases, such as 9rohn disease and ulcerative colitis, may also

produce skin manifestations secondary to malnutrition!

:n elderly persons, an indicative sign of malnutrition is delayed healing and an

increased presence of decubitus ulcers of stage ::: or higher!Gitamin 9 deficiency commonly

manifests as perifollicular hemorrhages, petechiae, gingival bleeding, and splinter

hemorrhages, in addition to hemarthroses and subperiosteal hemorrhages! nemia may result,

and wound healing may be impaired! 7iacin deficiency clinically manifests as pellagra $ie,

dermatitis, dementia, diarrhea& in advanced cases! he dermatitis manifests in sun#eposed

1%


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areas, including the back, neck $9asal necklace&, face, and dorsum of the hands $gauntlet of

pellagra& initially as painful erythema and itching! +ubse(uently, vesicles and bullae may

develop and erupt, creating crusted, scaly lesions! Finally, the skin becomes rough and

covered by dark scales and crusts! +triking demarcation of affected areas from normal skin is

noted!1,

"rotein#energy malnutrition is also associated with an increased likelihood of

calciphylais, a small vessel vasculopathy involving mural calcification with intimal

proliferation, fibrosis, and thrombosis! s a result, ischemia and necrosis of skin occurs!

/ther tissues affected include subcutaneous fat, visceral organs, and skeletal muscle!

9omparison of the clinical features of kwarshiorkor and marasmusC

Feature Bwarshiorkor Marasmus

>rowth failure "resent "resent

-asting "resent "resent, marked

/edema "resent bsent

.air 9hanges 9ommon 8ess common

Mental 9hanges Gery common *ncommon

?ermatosis, flaky#paint 9ommon ?oes not occur

ppetite "oor >ood

nemia +evere $sometimes& "resent, less severe

+ubcutaneous fat @educed but present bsent

Face May be oedematous ?raw in, monkey#like

Fatty infiltration of liver "resent bsent

c& nthropometric

he term anthropometric refers to comparative measurement of the body!

nthropometric measurements are used in nutritional assessments! hose that are used

to assess growth in infant, child, and adolesencts include length, height, weight for

length, and head circumference $length is used in infants and toddlers, rather than

height, because they are unable to stand&! :ndividual measurements are usually

compared to reference standards on a growth chart!

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ntropometric measurements used for adults usually include height, weight, body mass

inde, waist to hip ratio, and precentace of body fat! hese measures are then compared

to referance standards to assess weight status and the risk for various diseases!

nthropometric measurements re(uire precise measuring techni(ues to be valid!

d& 8aboratory Findings

-here facilities permit, the teset given in table below may help to diagnose specific

problems! hey are not needed, however, to guide or monitor treatment! he

interpretation of test result is fre(uently altered by malnutrition! For this reason,

laboratory test may misguide ineperienced workers! he most important guide to

treatment is fre(uent careful assessment of the child!,2

est @esult and significance

Te+t+ tat (a) be u+e&u%

Alood glucose >lucose concentration H54 mg6dl is

indicative of hypoglycaemia

amination of blood smear by

microscopy

"resence of malaria parasites is indicative

of infections

.aemoglobin or packed#cell volume .aemoglobin H40 d6l or packed#cell

volume H2% is indicative of very severe

anemia

amination and culture of urine specimen "resence of bacteria on microscopy is

indicative of infections

amination of faeces by microscopy "resence of blood is indicative of dysentry

9hest I#@ay "neumonia causes less shadowing of the

lungs in malnourished children that inwell#nourished children

Aones may show rickets or fractures of the

ribs

+kin test for tuberculosis /ften negative in children with

tuberculosis or those previously

vaccinated with A9> vaccine

Te+t+ tat are o& %itt%e or no a%ue

+erum proteins 7ot useful in management, but may guide

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prognosis

est for human immunodeficiency virus

$.:G&

+hould not be done routinely; if done,

should be accompanied by counselling of

the childJs parents and result should beconfidential

lectrolytes @arely helpful and may lead to

inappropriate therapy

2.1.0. $anage(ent

he usual approach to treatment of "M includes three phases! he first relatively

brief phase $24D4hr& is a stabili)ation phase! ?uring this phase, dehydration, if present, is

corrected and antibiotic therapy is initiated to control infection! Aecause of the difficulty of

estimating hydration, oral rehydration therapy is preferred! :f intravenous therapy is

necessary, estimates of dehydration should be reconsidered fre(uently, particularly during thefirst 24hr of therapy!'

he second phase includes continued antibiotic therapy with appropriate changes if the initial

combination was not effective and introduction of a diet providing maintenace re(uirements

of energy and protein along with ade(uate electrolytes, trace minerals, and vitamins! his

phase usually lasts for an additional week to 0 days! :f the infant is unable to take the

feedings from a cup or bottle, administration of feedings by nasogastric tube rather than by

the parenteral route is preferred!*/1-

Ay the end of the second phase, any edema that was present has usually been

mobili)ed, infections are under control, the child is becoming more interested in his or her

surroundings, and his or her appetite is returning! he child is then ready for the final phase

of treatment, which consists primarily of feeding! .e or she should be switched gradually to a

recovery diet providing up to 50 kcal6kg624 hr and 4 g6kg624 hr of protein! fter ad3ustment

to this diet, the child can be fed ad libitum! /nce ad libitum feedings are allowed, intakes of

both energy and protein can be substantial!*/1-

1+


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ccording to the ?epartment of .ealth @epublic of :ndonesia, there are 5 aspects to

be considered in managing children diagnosed with severe malnutrition, and those areC'

! en principal steps

2! reatment of comorbidities

! Failure of treatments

4! "atients dicharge before end of treatment

5! mergency situation

ll these aspects should be well understood in order to manage severe malnutrition in

children!

1. Ten Princi'a% te'+

he ten principal steps in managing severe malnutrition should be conducted step by step

based on the treatment phase!

ll the steps could be eplained by the following tableC

No Treat(ent

tabi%iation Tran+ition Reabi%itation ,o%%o3 U'

Da)

142

Da)

*45#eek 2

#eek

*40

#eek

5420

.ypoglycemia

2 .ypothermia

?ehydration

4 lectrolyte 9orrection

5 reatment of :nfection

1 Micronutrition

?efficiency 9orrection

:nitial @efeeding

9orrectional @efeeding

$9atch *p >rowth&

' +timulation

0 "repare for ?ischarge

a. te' 16 H)'og%)ce(ia correction

9hildren diagnosed with severe malnutrition are highly at risk to get hypoglycemia!

his state is diagnosed when the level of blood glucose is below 54 mg6dl! +igns and

symptomps of children developing hypoglycemia could be very not spesific! hey can

include gradually loss of consciousness, lethargic and weak arterial pulse! +ymptomps

1*

Without Iron

SupplementationWith Iron

Supplementation

Formula 75

Formula

Formula

75 to

100


20/46

such sweating and palpitation could occasionaly be identified, and the patient could

pass away with the only symptomps is gradually loss of consciousness! '

:t is essential to understand that in every health care facilities where it is pretty hard to

detect blood glucose level, all children diagnosed with severe malnutrition should be

assumed as hypoglymic children, hence hypoglycemia correction should be done

immediately! ',0

he management of hypoglycemic children is based on consciousness state, 3ust like

belowC ',0

ign+ and )('to('+ Treat(ent

lert $not lethargic& >ive 50 ml of ?etrose 0% per oral or via 7>

8oss of consciousness

$lethargic&

>ive ?etrose 0% intravenous as much as 5 ml per

each kilogram body weight, followed by 50 ml of

?etrose 0% orlaly

+hock

>ive ?etrose 0% intravenous as much as 5 ml per

each kilogram body weight, followed by @inger

8actat K ?etrose 0% $C& for 5 ml each kilogram

body weight, sould be given in hour

?etrose 0% solution can be prepared at home by dilute 5 grams of sugar into 50 ml

of water for early correction at home! fter glucose correction, the blood glucose test

should be repeated in the net 0 minutes, and if the blood glucose level is still below

the borderline value, the treatment should be repeated for the second time! ',0

b. te' 26 H)'oter(ia correction

.ypothermia is a condition potentially causing death to a severe malnourished child!

his condition is diagnosed while aillar temperature is below 1,5o9! .ypothermia

fre(uently occurs along with hypoglycemia and serious infection causing a large

number of death among children! ',0

he simplest thing that can be done to a hypothermic child is called LBangoroo

techni(ueJ, in which the baby or child should be hugged tightly by mother and

covered with blanket until the head! his will enable skin to skin contact between child

and mother! ',0

2-


21/46

nother thing to do is to place the child 50 cm below source of light and the body

temperature should monitored once every 0 minutes! nd the warming effort should

be stopped while the temperature reaches o9!',0

c. te' *6 De)dration correction:t is sometimes difficut to identify dehydration signs on a severely malnourished child!

+everal things to identify includeC',0

# 8ethargic! he children look apatis, not fully alert and unaware of circumstances!

t the final stage, the children can get loss of consciousness!

# +unken eye! :t is important to take a detailed history to the parents aboout the

appearence of eye, since several child do have a sunken eye even in a not

dehydrated state! ear production is fre(uently absent!

# hirsty! ?ehydrated patient is fre(uently very thristy and drinks very eagerly and

this can be a very important and easily identified symptomps of dehydration in

children! 8ip mucose seems very dry!

# +kin pinch returns slowly more than 2 seconds! Aut it can occur in a very

malnourished child even not in a dehydrated state!

he treatment of a dehydrated and malnourished child include consumption of

@ehydration +olution for Malnutrition $@e+oMal&, with amount of fluid descriptionsC

# 5 ml6kg bodyweight every 0 minutes for the first 2 hours

# Followed by another @esomal for as much as 5#0 ml6kg body weight6hour, given

alternately with Formula 5 as the early diet! hey are give every hour for 0

hours!

# :f rehydration state has been reached, Formula 5 should be given every 2 hours!

he composition of @ehydration +olution for Malnutrition according to -./

guideline isC

Co('o+ition A(ount

-./ /@+ $/ralit& sachet $200 ml&

+ugar 0 grams

Mineral mi solution, includeC

# B9l ',5 grams

# ripotassium citrate 2,4 grams

# Mg9l2!1.2/ 0,5 grams

# En setat , grams

# 9u+/4 0,51 grams

-ith 000ml of waters

ml

21


22/46

-ater added until the volume get into 400 ml!

d. te' -6 E%ectro%)te i(ba%ance correction

lectrolyte imbalance like a state of hypokalemia and hypomagnesemia is fre(urntly

occur to a patient with dehydration along with severe malnutrition! he potassium

deficit will adversely affect cardiac function and gastric emptying ability, while

magnesium is essential for potassium to enter cells and be retained! :t is important to

be reali)ed that the mineral mi solution does not contain iron as this is withhels

during the stabili)ation phase! ',0

he treatment includes admission of @ehydration solution for Malnutrition as well!

his will fi both, the dehydration and electrolyte imbalance state!

he /@+ can be used for watery diarrhea, at the recommended volume of 5#5

m86kg6h, with a total of 0 m86kg for the first 2 hours! Aecause the risk of cardiac

failure is increased in children with marasmus, compliance with the rehydration

regimen is even more critical than in children who are well nourished! herefore,

closely monitor the rehydration phase and promptly address signs of cardiac failure,

such as tachypnea, tachycardia, edema, or hepatomegaly! ',0

@ehydration solution should be adapted to marasmic children with a low sodium

content and a high potassium content! his can be prepared using standard -./

solution as a base or by directly administering a modified oral rehydration $@e+oMal&solution if available!',0

he following table highlights the composition of standard /@+, the new reduced#

osmolarity /@+, and @e+oMal! ',0

Co('o+itionReo$a%

7((o%8!9

tandard OR

7((o%8!9

Reduced

o+(o%arit) OR

>lucose 25 5

+odium 45 '0 5

"otassium 40 20 209hloride 0 0 15

9itrate 0 0

Magnesium !!! !!!

Einc 0! !!! !!!

9opper 0!045 !!! !!!

/smolarity

$m/sm68&

00 245

e. te' /6 Treat(ent o& In&ection

+everely malnourished children is at a very great risk to develop infection, not only by

community infection, but also the normal flora as well! his condition was brought on

22


23/46

the systemic manifestation of low protein intake of malnourished children! state of

hipo#immunoglobulinemia will predispose them to get opportunistic infection from

normal flora! ',0

:nfection of the lower respiratory tract infections is especially common, and although

signs of infection should be carefully looked for, they are often difficult to detect! his

is because unlike well nourished children who respond to infection with fever and

inflammmation, malnourished children with even serious infection may only become

drowsy or lethargic! .ence, antibiotic admission should be given to these patients, as a

prophylais one and as a therapeutic as well! ',0

# For children without any clear evidence of infection, a broad spectrum antibiotic

such 9otrimoa)ole $trimethoprim 5 mg6kgA- K sulfamethoa)ole 25 mg6kgA-

orally twice daily for 5 days!# 9hildren with complications such septic shock, hypoglycemia, hypothermia,

evidence of skin infections, respiratory tract and genitourinary tract infection or

children who appear lethargic& should be givenC

First 8ine reatments, includeC

mpicillin, 50 mg6kgA- :M or :G for the first 2 days, followed by moicillin 5

mg6kgA- orally every hours for the net 5 days&, along with

>entamycin ,5 mg6kgA- :M or :G once daily for days!

+econd 8ine reatments,

:f the child fails to improve within 4 hours, add9hloramphenicol 25 mg6kgA-

:M or :G every hours $or every 1 hours if meningitis is suspected& for the net 5

days!

+ome institutions routinely give malnourished children metronida)ole ,5

mg6kgA- every hours for days in addition to broad spectrum anti microbials!

.owever, the efficacy of this treatment has not been estabilished yet by clinicaltrials!

&. te' 06 $icronutrion De&&icienc)

+everely malnourished children are at greater risk to develop vitamin and mineral

deficiency, and therefore supplementation of multivitamin should be considered in the

treatment of malnutrition as they serve as coen)yme and cofactor for daily metabolism!

he supplementation includeC',0,

# Folic cid 5 mg on the first day, followed by mg6day for the net several days!

# Einc, 2 mg6kg body weight

# 9u, 0, mg6kg body weight

23


24/46

# +ulfas Ferrosus mg6kg body weight, given after the stabili)ation and transitional

phase are completed

# Gitamin , given orally on the first day, with appropriate dose depending on age as

listed belowC

Age Do+e in Internationa% Unit

Aelow 1 months 50!000 :* $half of the blue pills&

1 to 2 months 00!000 :* $one blue pills&

to 5 yeras 200!000 $one red pills&

:f there are evidences of vitamin deficiency, or the patient was 3ust suffered from

measles in the last months, vitamin supplementation should be given on day , 2

and 5! ',0,

g. te' 56 Initia% Re&eeding

lmost all severely malnourished children have infections, impaired liver and

intestinal function along with problems related to electrolyte imbalance when first

admitted to hospital! Aecause of these problems, they are unable to tolerate the usual

amounts of dietary protein, fat and sodium as well! :t is important, therefore, to begin

feeding these children with a diet that is low in these nutrients, and high in

carbohydrate!*/1-

here are three steps of giving diet to to the patients, ad3usted to the treatment phase!

hose in stabili)ation phase should get the early diet containg 5 kcal each 00 ml,

which is well known as Formula 5 $F 5& -./! -hile the patients who have

already been in the transitional phase should get an alternating diet from F5 to F00!

nd for those who have reached the rehabilitation phase could consume F5 -./

as the correctional diet! */1-

he nutritional re(uirements according to treatment phase should be ad3usted to the

amount listed belowC */1-

Nutrient+Treat(ent Pa+e

tabi%iation Tran+itiona% Reabi%itation

nergy 00 kcal6kg6day 50 kcal6kg6day 50#200 kcal6kg6day

"rotein D ,5 g6kg6day 2# g6kg6day 4#1 g6kg6day

Fluid intake 0 ml6kg6day or

00 ml6kg6day if

50 ml6kg6day 50 D 200 ml6kg6day

2!


25/46

edema presents

he composition of Formula 5 according to the -orld .ealth /rgani)ation should be

as listed belowC

# ?ried skim milk 25 grams

# +ugar 00 grams# Gegetable oil 2 grams

# lectrolyte 20 ml

# -ater to make 000 ml

o prepare the F#5 diet, add the dried skimmed milk, sugar, vegetable oil to some

water and mi! Aoil for about 5# minutes, then allow to cool! dd the electrolyte

solution then mi again! Make up the volume to 000 ml with water, and should be

consumed every 2 hours within 24 hours! lectrolyte fluid can be made from

potassium solution! */1-

:t is essential to reali)e that the patients should always complete each feed and should

be fed from a cup and spoon directly! Feeding bottles should never be used, even for a

very young infants, as they predispose as source of infections! 9hildren who are very

ill may be fed using a dropper or syringe, and the children should be securely held in a

sitting position to avoid aspiration risk! ',0

. te' :6 Correctiona% Re&eeding

9orrectional refeeding should be given alternatingly from F 5 to F 00 in the

transitional phase, and F 5 in the rehabilitation phase! he composition of F 00 and

F 5 are as listed belowC',0

F 00 F 5

# ?ried skim milk 5 grams '0 grams

# +ugar 50 grams 15 grams

# Gegetable oil 10 grams 5 grams

# lectrolyte 20 ml 2 ml

# -ater to make 000 ml 000 ml

o avoid overloading the intestine, liver and kidneys, it is essential that food be given

fre(uently and in small amounts! 9hildren who are unwilling to eat should be fed by

7>, while children who can eat should be given diet every 2, or 4 hours, day and

night! Aut is important to remeber, that eating orally is more recommended than 7>

feeding! :f the child could take three (uarters of the dayJs diet orally, then the 7>

should be removed!',0

he calory taken each day should not be over the re(uirements since the patients could

develop metabolic imbalance! :f vomitting occurs, both the amount given at each feed

and the interval between feeds should be reduced! ',0

2%


26/46

:f the childJs appetite improves, treatmen has been successful then! he initial phase of

treatment ends when the children becomes hungry, indicating that the child is now

ready to begin the rehabilitation phase! 7evertheless, the transition should be gradual

to avoid the risk of heart failure which can occur if children suddenly consume large

amounts of feed! @eplace the F5 with F 00 in the transitional phase! ',0

Treatment Evaluation:

Aody weight should be measured daily to evaluate the efficacy of initial and

correctional refeeding! ',0

# :f weight gain is less than 5 gr6kgA-6day, the child should be reassesed

# :f weight gain is between 5 to 0 gr6kgA-6day, an undetected infection should be

suspected

# :f weight gain is more than 0 gr6kgA-6day, then the therapeutic program has

reached its target!

i. te' ;6 ti(u%ation

+everely malnourished children have delayed mental and behavioural development,

which,if not treated, can become the most serious long term result of malnutrition!

motional and physical stimulation through play programmes that start during

rehabilitation phase and continue after discharge can substantially reduce the risk of

permanent mental retardation and emotional impairment! 9are must be taken to avoid

sensory deprivation! ',0

:t is essential that the mother be with her child in hospital and that she be encouraged to

feed, hold, comfort and play with her child as much as possible! he room should be

brightly coloured with decorations that interset children! oys should be safe, washable,

and appropriate for the childJs age and level of development! ',0

Malnourished children need interaction with other children during rehabilitation! fter

the initial phase of treatment, the child should spend prolonged periods with other

children! ctivities should be selected to develop both motor and language skills, and

new activities and materials should be introduced regularly! childJs effort to perform a

task should always be praised and never critici)ed! ',0

"hysical activities promote the development of essential motor skills and may also

enhance growth during rehabilitation! "lay should include such activities as rolling on a

matress, climbing stairs and walking! he duration and intensity of physical activities

should increase as the childJs nutritional status and general condition improve! ',0

2(


27/46

j. te' 1aining weight at normal or increased rate

ll vitamin and mineral deficiencies have been treated

dema, vomitus, hypothermia and diarrhea are no longer present

Mother Bnows how to prepare apropriate foods and feed the child well

.ealth

worker

ble to ensure follow up of the child and support for the mother

2. Treat(ent o& Co(orbiditie+

a! Gitamin deficiency

:f the patient is diagnosed with vitamin deficinecy, vitamin supplementation

should be given according to patientJs age on day , 2 and 4! ',0,

b! *lceration of the eye

ny kind of eye problems should be evaluated to get the appropriate therapy, based on

how severe the problem is, 3ust like what listed belowC ',0

E)e Prob%e(+ Treat(ent

AitotJs +pot only, without any other eye

problem

ntibiotic eyedrops is not indicated

+uppurative and inflamatory process 9hloramphenicol or tetrasiclin eyedrops

should be given

2$


28/46

9orneal ulcer 9hloramphenicol 0,25 D % eyedrops,

gtt61 hours for to 0 days

tropine eyedrops %, gtt6 hours for #

5 days

c! ?ermatosis

En defficiency is a common problem among malnourished children and causing a skin

lesion called dermatosis! his should be treated with En supplementation orally, and

the skin will respond effectively! ',0

dditional treatment such Bmn/4solution % topically 0 minutes a day could be

added as well! ?iaper should be changed fre(uently to avoid diaper dermatitis in

babies!',0

d! "arasitic :nfections

+tool eamination should be done to look for worms egg that could possibly presents!

:f there are evidence of parasitic infections, pirantel pamoat 0 mg6kg body weight

could be given orally! ',0

:f amebiasis or giardiasis is proven to be etiologies of diarrhea in children,

administration of metronidaole ,5 mg6kg body weight 6 hours is indicated for

days! ',0

e! uberculosis9hildren who got history of contact with tuberculosis patients should undergo

evaluation and assesment to detect A infection! A scoring system should be assesed

in those kind of children, and A regimen should be started if the patients is diagnosed

with A! ',0

*. ,ai%ure o& Treat(ent

Failure of treatment can be categori)ed into 2 kinds of conditions, they areC ',0

a! ?eath

?eath in the first 24 to 2 hours is common among children diagnosed with

hypoglycemia, hypothermia, dehydrated or sepsis! hus, those conditions should be

priorities in treating severely malnourished children!

b! :nade(uacy of -eight >ain

s much as 0 gr6kg body weight6 day or more is epected as a minimum weighy gain

to reach the goal of treatments! -eight gain below that standard should raise suspicion

of systemic infection that is still not detected!

-. Patient di+carge+ be&ore end o& treat(ent

2+


29/46

For patient who ask to dischargebefore end of treatment, an education and counselling

should be given about how to serve the food ade(uately, in a small protion but more

fre(uently and how to overcome and give initial treatment to comorbidities!

:t is also important to eplain about the importance of immuni)ation to these kind of

children! ',0

/. E(ergenc) ca+e

wo conditions that should obtain serious care include shock and severe anemia! "atients

presenting with shock should be ressucitated with initial crystalloid @8 5 ml6kg body

weight for the first one hour, followed by @ehydration +olution for Malnutrition

$@e+oMal& for the net several hours. ',0

"atients presenting with severe anemia $those with .b levels below 4 gr6l& should get a

whole blood transfusion 0 ml6kg body weights! -hile those with .b levels between 4 to1 gr6l should receive transfusion of packed red cells as much as 0 ml6kg body weight if

respiratory distress evidences are found! ',0

2.1.5. Co('%ication

+everal complications that can occur to a severly malnourished children include the

folowingsC ,2,4

"oor response to the nutritional rehabilitationC :f the above recommendations are

applied, children with marasmus should improve rapidly, gain weight regularly, and

return to age#appropriate developmental status! *sually, poor response to treatment is

due to insufficient intake or an underlying infection, especially .:G or tuberculosis!

.owever, poor response to therapy re(uires a complete reassessment of the situation,

rather than simply adding a medication or a micronutrient, which is usually ineffective!

"sychosocial problemsC /ften during this period of the rehabilitation, underlying

causes of the child=s marasmus are understood, such as the previously described

psychosocial factors! 9hanges in these underlying factors are often difficult because they

are associated with the general socioeconomic conditions! .owever, changes should be

attempted! he underlying factors should be taken into consideration when planning the

child=s return to home and further follow#up care!

8ong#term se(uelae, with particular attention to developmental issues, must be

mentioned! :f growth and development have been etensively impaired and if early

massive iron deficiency anemia is present, mental and physical retardation may be

permanent! pparently, the younger the infant at the time of deprivation, the moredevastating are the long#term effects! 1/2/!

2*


30/46

2.1.:. ,o%%o3 U' and Progno+i+

ny patient at risk for nutritional deficiency should be referred to a registered

dietitian or other nutritional professional for a complete nutritional assessment and dietarycounseling! ,2,4

/ther subspecialty referrals should be considered if findings from the initial

evaluation indicate that the underlying cause is not poor nutritional intake! :f signs indicate

malabsorption, a gastroenterologist should be consulted! Further, in pediatric cases, a

pediatrician, preferably one with eperience in the management of protein#energy

malnutrition $"M&, should oversee care of the patient! ny patient with significant

laboratory abnormalities, as discussed above, may benefit from consultation with the

appropriate subspecialty $eg, endocrinology, hematology&! ,2,4

9hildren with poor nutrition secondary to inade(uate intake and6or neglect should be

referred to the appropriate social agencies to assist the family in obtaining resources and

providing ongoing care for the child! ,2,4

Follow up to severely malnourished children includeC1/2/!

@elapseC Aecause risk of relapse is greatest soon after discharge, the child should be

seen after week, 2 weeks, and month! t each visit, the health worker must be sure

that all the points mentioned above are assessed! he child must be measured, weighed,

and the results recorded! :mmuni)ation should be performed according to national

guidelines!

7eurodevelopmental assessmentC ?uring the first 2 years of life, the nervous system

is growing and particularly at risk if nutritional deficiencies are present; therefore,

regular assessment of neurodevelopment is important, including head growth

measurement, neurodevelopmental item assessment, and intelligence (uotient $:O&

evaluation at each visit! 1/2/!

cept for complications mentioned above, prognosis of even severe marasmus is

good if treatment and follow#up care are correctly applied! 1/2/!

3-


31/46


32/46

.istory of sei)ure happen five days ago! :t happens two times with duration

aprroimately five minutes! .and#foot rigid and blink eyes! fter sei)ure he limp and become

unconscious but this time no sei)ure!

.istory of reduction body weight since three months ago! hat time heJs 2 kg but

now kg!

Alacky red skin rash happen about one month ago and white rash in mouth happen

since two months ago!

.e was born by caesarean section in 9ibubur .ospital Pakarta, with birth body weight

was 2100 grams and body length unknown and ">@ score was not recorded! here was

tight pelvis pregnancy complication! .istory of immuni)ation was incomplete!

Feeding historyC

From birth to yearC breast milk only

From 2 until 1 monthsC breast milk with porridge

From 1 until 2 monthsC breast milk with formula milk

.istory of growth and developmentC

+tandingC months

-alkingC year

+aying wordsC ,5 years

.istory of previous illness C .e has been diagnosed 8ung A in Pakarta in

?ecember 202 and consumed / for one month, but he went back to +iantar and stop

/ because his condition got worse!

.istory of previous medications C cyklovir, / $"yra)inamid, @ifampicin&!

.istory of parents C Father .:G $K& and Mother has died three years ago!

P)+ica% E=a(ination

Generalized status

Aody weightC kg, Aody lengthC 0 cm,

*pper arm circumferenceC cm, .ead circumferenceC cm

Aody weight in 50th percentile according to ageC 2 kg

Aody length in 50th percentile according to ageC 5 cm

32


33/46

Aody weight in 50th percentile according to body lengthC 1 kg

A-6A8C 61 00% Q 1'% $severe malnutrition&

A-6ageC 62 00% Q 52% $severe malnutrition&

A86age C 065 s 00% Q % $normal&

Present status

9onsciousnessC 9ompos Mentis

A"C 00610 mm.g

.@C 06min

@@C 226min

Aody temperatureC ,o9

>eneral stateC mild

7utrition stateC severe

Aody -eightC kg

Aody 8engthC 0 cm

Localized status

Head C

Alacky red rash $K&! 9orneal refle $K6K&, isochore pupil, pale con3unctiva palpebral inferior!

NeckC

8ymph node enlargement $#&! Alacky red rash $K&!

ThoraxC

+ymmetrical fusiformis! 9hest retraction $#&! .yperpigmentation papul $K&! 9rust $K&! .@C

0 bpm, reguler, murmur $#&! @@C 226i, reguler, ronchi $#6#&!

AbdomenC

+oepel, peristaltic $K& 7! .yperpigmentation papul $K&! 9rust $K&!

ExtremitiesC

"ulse 006i, regular, ade(uate pressure and volume, warm, 9@ H R! .yperpigmentation

papul $K&! 9rust $K&!

33


34/46

UrogenitalC

Male, within normal limit

!aborator) ,inding+6

Para(eter+ "a%ue Nor(a% "a%ue

om!lete "lood ount

.emoglobin 4,1 gr% 2,0 D 4,4 gr%

.ematocrite 4,' % D 44%

rithrocyte ,2 016mm 4,2 D 4, 016mm

8eucocyte 50 6mm 4500 D 000 6mm

"latelet 221!000 6mm 50000 D 450000 6mm

M9G 2 fl 5 D '5 fl

M9. 21,2 pg 2 D 2 pg

M9.9 2 gr% D 5 gr%

@?- 1,1 % ,1 D 4, %

?iftel 0 6 0 6 6 ' 6

Di&&erentia% Diagno+i+6

+uspect umor bdomen e!c dd6 # -ilms umor

# 7euroblastoma

#orking Diagno+i+6

+uspect umor bdomen e!c dd6 # -ilms umor

# 7euroblastoma

$anage(ent6

# Aedrest, threeway and urinary catheter inserted

# :GF? ?5% 7a9l 0,45% 20 gtt6i micro# ?iet Formula 5 10 cc 6 2 hours $stabili)ation phase&

# Multivitamin without Fe cth ::

# Folic acid tab 5 mg

# 9otrimoa)ole tab 2 40 mg

# Gitamin 200!000 :*

# "acked red cell transfusion 5 cc 6 2 hours

7eededC 4 $ #4,1 & 25 kg Q 124 cc

ransfusion abilityC cc 25 kg Q 5 cc

Diagno+tic P%anning6

# 9omplete blood count post transfusion

# 8iver Function est and @enal Function est

3!

+evere Malnutrition Marasmic #

Bhwarsiorkor ypeK


Bhwarsiorkor ypeK


35/46

# +erum lectrolytes, +erum lbumin

# Alood >lucose ad random

# bdominal 9 +can

# *rinalysis

# Fluid Aalance per 1 hours

,O!!O# UP

>une /t ? 5t@ 2


36/46

he patient ate the whole diet provided!

O +ensC 9M, empC 1, D 1,'o9! nemic $K&! :cteric $#&! dema $K&! 9yanosis $#&!

Aody weightC 25 kg, Aody lengthC 44 cm! *rine output ,4 D 1, cc6kg6hour

*rine colour C yelowish to brown

.ead /ld man face $K&! 9on3unctiva palpebra inferior anemic $K&!8ight refle

$K&6$K&! :sochoric pupil! +unken eye $#&!

7eck Pugular vein pressure @#2 cm.2/! 8ymph node enlargement $#&!

hora +imetris fusiformis! @etraction $#&! .@C 0 D '2 bpm, reguler!

Murmur $#&! @@C 2 D 25 6i, regular! Areath soundC vesicular! dditional

soundC $#&!

bdomen Aulging $K& in regio hypogastrium, ' cm in si)e, immobile, soft and

well marginated! "ain on palpation $#&! 8iver and spleen were not

palpable!+kin pinch returns (uickly! +hifting dullness $#&!tremities "ulse 0#'2 6i, regular, ade(uate p6v, warm, 9@ H R! A"C 00#2060#

0 mm.g $normalC #2 6 1#2&!

Aaggy pants $#&, thinning of subcutaneous fat $K&, muscle hypotrophy $K&!

9ra)y pavement dermatosis $K&! "itting edema $K& pretibia!

>enital Female, within normal limit

#aborator$ %indings:

+>/C *68 7aC m(68 *reumC 14,50 mg6dl

+>"C *68 BC ,' m(68 BreatininC 2,2 mg6dl

lbuminC 2, gr6dl 9l C m(68

?ipstick urineC

8eu 6 7it 6 *ro 6 "rotein 6 p. 6 Alood 6 +> 6 Bet 6 Ail 6 >lu

K2 6 K 6 # 6 K 6 1,5 6 K 6 ,06 # 6 # 6 #

A +uspect umor bdomen e!c dd6 # -ilms umor

# 7euroblastoma

P $anage(ent6


# :GF? ?5% 7a9l 0,45% 20 gtt6i micro

# ?iet Formula 5 10 cc 6 2 hours $stabili)ation phase&


# 9otrimoa)ole tab 2 40 mg# ransfusion "@9 5 cc 6 2 hours

3(


Bhwarsiorkor ypeK


37/46


# 9omplete blood count post transfusion

# bdominal 9 +can

# *rinalysis

>une : 4 11t@ 2


38/46

bdomen Aulging was not found after urinary catheter insertion!! "ain on palpation

$#&! 8iver and spleen were not palpable! +kin pinch returns (uickly!

+hifting dullness $#&!

tremities "ulse # 6i, regular, ade(uate p6v, warm, 9@ H R! A"C 00#065#

0 mm.g $normalC #2 6 1#2&!

Aaggy pants $#&, thinning of subcutaneous fat $K&, muscle hypotrophy $K&!

9ra)y pavement dermatosis $K&! "itting edema $#& pretibia!


#aborator$ %indings:

.emoglobinC ,5 gr% M9G C 1,1 fl

.ematocritC ',5 % M9. C 21,2 pg

rythrocyte C 5,1 016 mm M9.9 C 4,2 gr%

8eucocyte C 040 6 mm @?- C ',1 %

"latelet C 21000 6 mm 8? C 4 mm6hours

?ipstick urineC


K 6 # 6 0,2 6 S 6 5 6 K 6 ,06 # 6 # 6 #

A .ydronephrosis bilateral e!c $T& K severe malnutrition marasmic khwarsiorkor type K

suspect urinary tract infection

P $anage(ent6


# :GF? ?5% 7a9l 0,45% 20 gtt6i micro

# ?iet Formula 5 20 cc 6 2 hours $stabili)ation phase&


# Folic acid mg# :n3ection 9eftriaone gr 6 2 hours

# 9otrimoa)ole tab 2 40 mg


bdominal 9 +can

*rinalysis and urine culture K sensitivity test

3+


39/46

>une 1241: t@ 2


40/46

9ra)y pavement dermatosis $K&! "itting edema $K& pretibia!


T &can 'e!orts:

7o mass in the abdomen could be identified

here is a hyperthrophy of the urinary bladder wall

Muscle hypertrophy due to urinary retention should be suspected!

+uggestionC 9ystoscopy

Urine ulture:

"seudomonas aeruginosa was found, with concentration more than 059F*6ml

+ensitive to Meropenem only

(i!stick urine


K 6 # 6 # 6 K 6 5 6 K 6 ,06 # 6 # 6 #

A .ydronephrosis bilateral e!c! @etensio *rine K +evere Malnutrition Marasmic D

Bhwarsiorkor type K *rinary ract :nfection

P $anage(ent6


# :GF? ?5% 7a9l 0,45% 20 gtt6i micro

# ?iet Formula 00 40 cc 6 hours $transition phase&

# :n3ection Meropenam 250 mg 6 3am


P%anning6

*rinalysis

!-


41/46

CHAPTER -

DICUION AND U$$AR

-.1. Di+cu++ion

4#year#old female was admitted to @+*" .M diagnosed with severe malnutrition

marasmic#khwarsiorkor type! his diagnosis was made based on clinical findings found in

the patient such old man face, thinning of subcutaneous tissue, cra)y pavement dermatosis,

and edema in the lower etremities! he antropometry measurement of this patient reveals

that body weight according to age was below 10% and thus this patient could be diagnosed

as severe malnutrition!

he treatment conducted to this patient had already been in line with the guideline of

malnutrition management from ?epartment of .ealth @epublic of :ndonesia! his patient

was firstly treated in the stabili)ation phase in which hypoglycemia, hypothermia and

dehydration were assesed and treated subse(uently! nalysis of serum electrolyte was

conducted as well to identify whether electrolyte imbalance had been present or not! +ince

the serum 7a was m(6l and the patient did not show any symptomps of hyponatremia,

then this patient was given maintenance fluid with ?etrose 5% 7a9l 0,45% solution!he

re(uirement of the fluid was ad3usted to the stabili)ation phase re(uirements!

"rophylais of infection was given to this patient, applying the use of 9otrimoa)ole

$rimetophrim 5 mg with +ulfamethoa)ole 20 mg& and thus the patient was given 2 40

mg! 9itrimoa)ole was given for as long as 5 days, since the patient came without any

evidence of infection first!

!1


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Micronutrien deficiency was corrected with admission of folic acid 5 mg along with vitamin

200!000:* in the first day! he patient was also receiving multivitamin without iron in the

stabili)ation phase! :ron supplementation shouldnot be given to a severly malnourished child

because iron deposition will give a chance to bacteria to grow maimally in a child with low

immunity state! hus, iron supplementation could be given only after the patient completed

the stabili)ation and transitional phase, and was assumed to have a much better

immunological state!

he patient was then immediately given initial refeeding using -./ Formula 5! +ince she

presented with edema in the lower etremities, the fluid re(uirements needed in the

stabili)ation phase was 006day! s known that F5 contains 5 kcal each 00ml, then the

re(uirements wasC

Fluid re(uirementsC 00 ml 25 kg Q 2500 ml

Feeding formula F5 $5 kcal 6 00ml&

F 5 Q 5 25006 00 per 24 hours

F 5 Q 5 ml 6 24 hours

For the stabili)ation phase, F 5 should be given every 2 hours, then the patient neededC

F 5 Q 5 6 2 times

F 5 Q 5 cc $rounded to be 10 cc 6 2hours&

/n the 5th day, the edema was no longer present, and thus the daily fluid re(uirement was

then ad3usted to 0 ml6kg body weight6day! he estimated calory needed then was

recounted to be as the followingC

Fluid re(uirementsC 0 ml 25 kg Q 250 ml

Feeding formula F5 $5 kcal 6 00ml&

F 5 Q 5 2506 00 per 24 hours

F 5 Q 24,5 ml 6 24 hours

For the stabili)ation phase, F 5 should be given every 2 hours, then the patient neededC

F 5 Q 24,5 6 2 times

F 5 Q 20,2 cc $rounded to be 20 cc 6 2hours&

his formula was given for as long as days during the stabili)ation phase, then folowed by

Formula 00 -./ which contains more calories then the previous formula!

!2


43/46

?aily evaluation of treatment was conducted to this patient assesing the weight gain

achieved each day! +ince, the weight gain was below the epected value $less than 5 gr6kg

body weight6 day&, she was then classified as poor response! ccording to the guideline

published, patient with poor response should be evaluated for any comorbid or any infection

that could probably present!

more detail anamnesis was conducted to this patient in order to identify the cause of this

poor response! ccording to her mother, the patient ate the whole diet prepared for her

during the treatment! 7either vomitting nor diarrhea occured to this patient! +ince the patient

complained about pain while urinating on admission, then a suspicion of urinary tract

infection was then raised! *rinalysis by daily dipstick was then conducted, then the result

revealed that leukosituria and high levels of nitrites were present, thus another investigation

was conducted! *rine culture was done and the result revealed the growth of Pseudomonas

aeruginosainfection! *rinary tract infection was then raised to be comorbid diagnosis!

For the suitable treatment, sensitivity and resistancy test of antibiotics were done and itJs

been proved that the only sensitive antibiotic was Meropenem! ntibiotic switch was then

done to in3ection of meropenem 250 mg every hours!

nother important problem in this case is the fact that the patient complained about

menstrual irregularity! +ince she had not been getting any menstruation for the last months,

then a suspicion of amenorrhea was raised! his condition is assumed secondary to the

severe malnutrition problem happened earlier!

Malnutrition and stress causes hypothalamic hypogonadism! he hypothalamic#pituitary#

gonadal ais shuts down as the body struggles to survive, directing finite energy resources to

support more vital functions! Aoth males and females eperience decreased libido and

interruption of pubertal development,depending on the timing of the illness!

he hormones that cause pubertal development and reproduction emanate from the

hypothalamus, the pituitary gland, the gonads, and the adrenal glands! .ypothalamic

gonadotropin#releasing hormone $>n@.& is a 0#amino#acid peptide $coded by a gene on

chromosome & secreted from the median eminence into the hypophyseal portal system in a

pulsatile manner to reach the pituitary gland! he >n@. pulse generator is affected by

biogenic amine neurotransmitters, peptidergic neuromodulators, neuroecitatory amino

acids, and neural pathways! minobutyric acid eerts a suppressive effect on >n@.

secretion and can be an important factor in the relative (uiescence of gonadotropin secretion

that characteri)es the


44/46

progesterone, also inhibit >n@. pulse fre(uency in a negative feedback inhibition, whereas

estrogen has the additional ability to eert positive feedback on gonadotropin secretion at

midpuberty!

>onadotropin#releasing hormone acts on the gonadotropes of the pituitary gland to increase

intracellular calcium concentration and cause phosphorylation of protein kinase, which

stimulates secretion of luteini)ing hormone $8.& and follicle#stimulating hormone $F+.&, in

a pulsatile manner owing to the pulsatile nature of >n@. secretion! >onadotropes eposed

to continuous rather than episodic 8. and F+. decrease the number of >n@. receptors,

decrease the action of the occupied receptors, and decrease gonadotropin secretion $down#

regulation&!

:n girls, F+. binds to cell#surface receptors on ovarian follicular cells to stimulate secretion

of estrogen! 8uteini)ing hormone becomes important later in pubertal development in

completing the menstrual cycle of girls when it affects the theca cell after the onset of

ovulation! Aecause there is damage on >n@. secretion in malnutrition, this phase $secretion

of estrogen that stimulates by F+. and >n@.& is not complete yet and cause amenorrea in

this case!

-.2. u((ar)

his paper reports a case of a 4#year#old female diagnosed with severe malnutrition

marasmic#khwarsiorkor type! comprehensive treatment including ten principal steps to

!!


45/46

manage severely malnourished chid has been conducted to this patient! +he has been

stabili)ed during the first week of treatment, and now she has been in the transitional phase!

RE,ERENCE

! +hasidhar, .arohalli @! Aathia, Patinder! Malnutrition! vailable fromC httpC 66

emedicine!medscape! com6 article6'540#show all6! ccesed on Pune 0th, 20

2! +cheinfeld, 7oah +! lston, ?irk M! "rotein#nergy Malnutrition! vailable fromC

httpC66emedicine!medscape!com6article60412#showall! ccesed on Pune 0th, 20! .ouse .ealth +urvey ''5, and 200 updated! 7utritional status of infant and

children in :ndonesia! ?ivision of @esearch and ?evelopment, ?epartment of .ealth

@epublic of :ndonesia, 200!

4! -illiam 9 .!, Food :nsecurity, .unger, and *ndernutrition! :nC @ichard A, @obert

M B, .al A P! 7elson etbooks of "ediatrics, th dition! "hiladelphiaC he curtis

9enter :ndependence +(uare -est "hiladelphia, "ennsylvania; 2004

5! 7eil + 8, Miriam .!, 7utritional ?eficiency +tates! :nC 9olin et al,! @udolphJs

"ediatrics, 2st dition! 9aliforniaC Mc>raw .ill; 2002

1! @abinowit), +imon +! Ahatia, Patinder! Marasmus! vailable from

httpC66emedicine!medscape!com6article6'44'1#showall! ccesed on Pune 0th 20

! ?ennis M +, 8eonna 9!, 7ormal "ubertal ?evelopment! :nC 9olin et al!, @udolphJs

"ediatrics, 2st dition! 9aliforniaC Mc>raw .ill; 2002

! -aterlow, P 9!, 9lasification and ?iagnosis of "rotein#9alorie Malnutrition! vailable

fromC httpC66bm3!wholibdoc!who!int6article60'4#show! ccesed on Pune 0th,

20

'! Auku Aagan atalaksana nak >i)i Auruk :6::! ?irektorat >i)i Masyarakat, ?ir3en

Aina Besehatan Masyarakat! Pakarta, 2005

!%
http://emedicine.medscape.com/article/1104623-showhttp://emedicine.medscape.com/article/984496-showhttp://bmj.wholibdoc.who.int/article/1098334-showhttp://bmj.wholibdoc.who.int/article/1098334-showhttp://emedicine.medscape.com/article/1104623-showhttp://emedicine.medscape.com/article/984496-showhttp://bmj.wholibdoc.who.int/article/1098334-show


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0! -orld .ealth /rgani)ation! Management of +evere MalnutritionC Manual for

"hysicians and /ther +enior .ealth -orker! >eneva, 2002

! Maria @ M!, Gitamin ?eficiencies and cesses! :nC Fredric et al!, >ellis U BaganJs

9urrent "ediatric herapy, th dition! "hiladelphia, 2002

severe malnutrition case report

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