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1.1. Background .............................................................................. 1
1.2. Objective .............................................................................. 2
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2.1. Defnition .............................................................................. 3
2.2. Epidemiology .............................................................................. 3
2.3. Classifcation and Clinical indings ..........................................
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 .............................................................................. !(
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!

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!

,he -orld .ealth /rgani)ation estimates that by the year 205, the prevalence of
malnutrition will have decreased to 0!1% globally, with 2!4 million children younger
than 5 years affected as measured by low weight for age! ,he overwhelming ma3ority of
these children, 2!4 million, will live in developing countries with 00% of these children
in 5sia, particularly the southcentral region, and 21% in 5frica! 5n 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 maintain
poverty, which can further hamper economic and social development!
: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 5 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 e;plore 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 e;plore more about the theoritical aspects on malnutrition,
and to integrate the theory and application of malnutrition case in daily life
2.1. $a%nutrition
2.1.1. De&inition
,he -orld .ealth /rgani)ation $-./&

defines malnutrition as <the cellular
imbalance between the supply of nutrients and energy and the body=s demand for them to
ensure growth, maintenance, and specific functions!< ,he term protein#energy malnutrition
$"%M& applies to a group of related disorders that include marasmus, kwashiorkor, and
intermediate states of marasmus#kwashiorkor!
,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 <the sickness of the weaning!< -illiams first used the term in '22, and it refers to
an inade(uate protein intake with reasonable caloric $energy& intake! %dema is characteristic
of kwashiorkor but is absent in marasmus!
2.1.2. E'ide(io%og)
:n 2000, the -./

estimated that malnourished children numbered 4!' million
$22%& in developing countries! :n addition, an estimated 4'!1 million children younger than
5 years are malnourished when measured in terms of weight for age! :n south central 5sia and
eastern 5frica, about half the children have growth retardation due to protein#energy
malnutrition! ,his figure is 5 times the prevalence in the western world!
5ppro;imately 50% of the 0 million deaths each year in developing countries occur
because of malnutrition in children younger than 5 years! :n kwashiorkor, mortality tends to
decrease as the age of onset increases!

5ccording to the statistical survey carried by ?epartment of .ealth, @epublic
:ndonesia on 2005, of 24 million :ndonesian population, 1 percents or about 4,5 million
people were diagnosed as severe malnutrition, and most of them were children below 5 yers
old! /n 2002, it was documented that several area in :ndonesia which got a high prevalence
of severe malnutrition included Makassar $,4%& and 8ombok $',%&! :n @+! "irngadi
Medan, it was recorded that of all kinds of malnutrition, 42% of all the malnutrition cases
were marasmus type!

2.1.*. C%a++i&ication and C%inica% ,inding+
,here are simply 2 different types of malnutrition known worldwide, include
khwarsiorkor, marasmus, and the mi; type between khwarsiorkor and marasmus type! ,he
distinction between the first two types of malnutrition is based on the presence of edema
$kwashiorkor& or absence of edema $marasmus&! Marasmus involves inade(uate intake of
protein and calories, whereas a child with kwashiorkor has fair#to#normal calorie intake with
inade(uate protein intake! 5lthough significant clinical differences between kwashiorkor and
marasmus are noted, some studies suggest that marasmus represents an adaptation to
starvation whereas kwashiorkor represents a dysadaptation to starvation!
a! Marasmus
:n general, marasmus is an insufficient energy intake to match the body=s re(uirements!
5s 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!
Aoth of the above pictures depict the characteristic of severly malnourished children
diagnosed with marasmus due to deficiency of calory intake!
b! Bhwarsiorkor
:n kwashiorkor, ade(uate carbohydrate consumption and decreased protein intake lead to
decreased synthesis of visceral proteins! ,he resulting hypoalbuminemia contributes to
e;travascular fluid accumulation! :mpaired synthesis of A#lipoprotein produces a fatty
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, anore;ia, 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
e;posed 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 te;ture is coarse in chronic
,he following are the usual appearences of children diagnosed with khwarsiorkorC
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 e;tremities!
,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
e;tremities resulting from En
,his picture represents hepatomegaly
and ascites which occur to this
patient due to low protein levels in
: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 5 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!
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!
: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 e;pressed in relation to height or lean body mass decrease! Arain
and visceral are relative preserved resulting in total body water, which is mainly e;tracelullar
but may also in intracelullar!
,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 e;ception 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 to
the 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 on
the production of acute phase proteins! Aecause of the interaction between food restriction
and infection in phatogenesis of malnutrition, any integrated approach to e;plaining the
pathophysiology has to take both in to account! ,he diference between kwarshiorkor and
marasmus may be partitially e;plain 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! 5n e;ample 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 $5:?+&!
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 5 $:g5& are some changes that may occur! ,he seems to be related to protein
metabolism! +ome studies report particularly low concentration of 92 in kwarshiorkor!
,hese immune changes predispose children to severe and chronic infections, most
commonly, infectious diarrhea, which further compromises nutrition causing anore;ia,
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
thyro;ine increases, but as malnutrition becomes more severe, and especially if kwarshiorkor
develops, total thyro;ine decreases! ,here is also a decrease in thyroid binding protein, but
this does not account for all of the reduction in thyro;ine and suggest the primary effects on
synthesis! :ncreased thyroid stimulating hormone secretions heralds recovery! ,here is also a
reduction in deiodenation in thyro;ine to triiodothyronine, resulting in reduced
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; 40% 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 e;plain why these children are so susceptible to hypoglycemia!
5 combination of malnutrition and anlterd all the endocrine consentration causes
hypothalamic hypogonadism! ,he hypothalamic#pituitary#gonadal a;is shuts down as the
body struggles to survive, directing finite energy resources to support more vital functions!
Aoth males and females e;perience 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 ma;imal inspiration and inspiratory pressure! ,his weakness may be
e;acerbated 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
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
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! 5s 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
5nemia 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 retardation of different causes!
,here have not been definite studies to show that these changes are causal rather than
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
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
%/ (
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! 5 nutritional history is directed toward identifying underlying
mechanisms that put patients at risk for nutritional depletion or e;cess! ,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!
"oor intakeC anore;ia, 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, e;tensive trauma or burns
5lcohol abuse or use of drugs with antinutrient or catabolic propertiesC steroids,
antimetabolites $e!g!, methotre;ate&, 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, an;iety,
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!
5dults 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! 5 2#year#old child
with coe;isting celiac and .artnup disease that resulted in kwashiorkor, anemia, hepatitis,
hypoalbuminia, angular cheilitis, glossitis, con3unctivitis and diffuse alopecia, erythematous
skin, des(uamation, erosions, and diffuse hyperpigmentation was reported!
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 loss
of 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 anore;ia nervosa, marked growth of lanugo hair is noted!
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#e;posed skin!
?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! 5lso, 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 e;treme! .air can also become softer and finer and appear
unruly! ,he eyelashes can undergo the same change, having a so#called broomstick
7ail plates are thin and soft and may be fissured or ridged! 5trophy 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! 5nemia 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#e;posed
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
"rotein#energy malnutrition is also associated with an increased likelihood of
calciphyla;is, a small vessel vasculopathy involving mural calcification with intimal
proliferation, fibrosis, and thrombosis! 5s 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 5bsent
.air 9hanges 9ommon 8ess common
Mental 9hanges Gery common *ncommon
?ermatosis, flaky#paint 9ommon ?oes not occur
5ppetite "oor >ood
5nemia +evere $sometimes& "resent, less severe
+ubcutaneous fat @educed but present 5bsent
Face May be oedematous ?raw in, monkey#like
Fatty infiltration of liver "resent 5bsent
c& 5nthropometric
,he term anthropometric refers to comparative measurement of the body!
5nthropometric 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!
5ntropometric 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!
5nthropometric 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 ine;perienced workers! ,he most important guide to
treatment is fre(uent careful assessment of the child!
,est @esult and significance
Te+t+ t.at (a) be u+e&u%
Alood glucose >lucose concentration H54 mg6dl is
indicative of hypoglycaemia
%;amination of blood smear by
"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
%;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 in
well#nourished children
Aones may show rickets or fractures of the
+kin test for tuberculosis /ften negative in children with
tuberculosis or those previously
vaccinated with A9> vaccine
Te+t+ t.at are o& %itt%e or no a%ue
+erum proteins 7ot useful in management, but may guide
,est for human immunodeficiency virus
+hould not be done routinely; if done,
should be accompanied by counselling of
the childJs parents and result should be
%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 $24D44hr& 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 the
first 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!
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! 5fter 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!
5ccording 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
2! Failure of treatments
4! "atients dicharge before end of treatment
5! %mergency situation
5ll these aspects should be well understood in order to manage severe malnutrition in
1. Ten Princi'a% 1te'+
,he ten principal steps in managing severe malnutrition should be conducted step by step
based on the treatment phase!
5ll the steps could be e;plained by the following tableC
No Treat(ent
1tabi%i2ation Tran+ition Re.abi%itation ,o%%o3 U'
#eek 2
2 .ypothermia
2 ?ehydration
4 %lectrolyte 9orrection
5 ,reatment of :nfection
1 Micronutrition
?efficiency 9orrection
0 :nitial @efeeding
4 9orrectional @efeeding
$9atch *p >rowth&
' +timulation
0 "repare for ?ischarge

a. 1te' 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
Without Iron
With Iron
Formula 75
75 to
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
,he management of hypoglycemic children is based on consciousness state, 3ust like
1ign+ and 1)('to('+ Treat(ent
5lert $not lethargic& >ive 50 ml of ?e;trose 0% per oral or via 7>,
8oss of consciousness
>ive ?e;trose 0% intravenous as much as 5 ml per
each kilogram body weight, followed by 50 ml of
?e;trose 0% orlaly
>ive ?e;trose 0% intravenous as much as 5 ml per
each kilogram body weight, followed by @inger
8actat K ?e;trose 0% $C& for 5 ml each kilogram
body weight, sould be given in hour
?e;trose 0% solution can be prepared at home by dilute 5 grams of sugar into 50 ml
of water for early correction at home! 5fter glucose correction, the blood glucose test
should be repeated in the ne;t 20 minutes, and if the blood glucose level is still below
the borderline value, the treatment should be repeated for the second time!
b. 1te' 26 H)'ot.er(ia correction
.ypothermia is a condition potentially causing death to a severe malnourished child!
,his condition is diagnosed while a;illar temperature is below 21,5
9! .ypothermia
fre(uently occurs along with hypoglycemia and serious infection causing a large
number of death among children!
,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!
5nother thing to do is to place the child 50 cm below source of light and the body
temperature should monitored once every 20 minutes! 5nd the warming effort should
be stopped while the temperature reaches 20

c. 1te' *6 De.)dration correction
:t is sometimes difficut to identify dehydration signs on a severely malnourished child!
+everal things to identify includeC
# 8ethargic! ,he children look apatis, not fully alert and unaware of circumstances!
5t 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 20 minutes for the first 2 hours
# Followed by another @esomal for as much as 5#0 ml6kg body weight6hour, given
alternately with Formula 05 as the early diet! ,hey are give every hour for 0
# :f rehydration state has been reached, Formula 05 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 4',5 grams
# ,ripotassium citrate 22,4 grams
# Mg9l2!1.2/ 20,5 grams
# En 5setat 2,2 grams
# 9u+/4 0,51 grams
-ith 000ml of waters
4 ml
-ater added until the volume get into 400 ml!
d. 1te' -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!
,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 00 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!
@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!
,he following table highlights the composition of standard /@+, the new reduced#
osmolarity /@+, and @e+oMal!
1tandard OR1
o+(o%arit) OR1
>lucose 25 05
+odium 45 '0 05
"otassium 40 20 20
9hloride 00 40 15
9itrate 0 0 0
Magnesium 2 !!! !!!
Einc 0!2 !!! !!!
9opper 0!045 !!! !!!
200 2 245
e. 1te' /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
the systemic manifestation of low protein intake of malnourished children! 5 state of
hipo#immunoglobulinemia will predispose them to get opportunistic infection from
normal flora!
: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
prophyla;is one and as a therapeutic as well!
# For children without any clear evidence of infection, a broad spectrum antibiotic
such 9otrimo;a)ole $trimethoprim 5 mg6kgA- K sulfametho;a)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
5mpicillin, 50 mg6kgA- :M or :G for the first 2 days, followed by 5mo;icillin 5
mg6kgA- orally every 4 hours for the ne;t 5 days&, along with
>entamycin 0,5 mg6kgA- :M or :G once daily for 0 days!
+econd 8ine ,reatments,
:f the child fails to improve within 44 hours, add 9hloramphenicol 25 mg6kgA-
:M or :G every 4 hours $or every 1 hours if meningitis is suspected& for the ne;t 5
+ome institutions routinely give malnourished children metronida)ole 0,5
mg6kgA- every 4 hours for 0 days in addition to broad spectrum anti microbials!
.owever, the efficacy of this treatment has not been estabilished yet by clinical
&. 1te' 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
# Folic 5cid 5 mg on the first day, followed by mg6day for the ne;t several days!
# Einc, 2 mg6kg body weight
# 9u, 0,2 mg6kg body weight
# +ulfas Ferrosus 2 mg6kg body weight, given after the stabili)ation and transitional
phase are completed
# Gitamin 5, 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 5 deficiency, or the patient was 3ust suffered from
measles in the last 2 months, vitamin 5 supplementation should be given on day , 2
and 5!
g. 1te' 56 Initia% Re&eeding
5lmost 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

,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 05 kcal each 00 ml,
which is well known as Formula 05 $F 05& -./! -hile the patients who have
already been in the transitional phase should get an alternating diet from F05 to F00!
5nd for those who have reached the rehabilitation phase could consume F25 -./
as the correctional diet!
,he nutritional re(uirements according to treatment phase should be ad3usted to the
amount listed belowC
Treat(ent P.a+e
1tabi%i2ation Tran+itiona% Re.abi%itation
%nergy 00 kcal6kg6day 50 kcal6kg6day 50#200 kcal6kg6day
"rotein D ,5 g6kg6day 2#2 g6kg6day 4#1 g6kg6day
Fluid intake 20 ml6kg6day or
00 ml6kg6day if
50 ml6kg6day 50 D 200 ml6kg6day
edema presents
,he composition of Formula 05 according to the -orld .ealth /rgani)ation should be
as listed belowC
# ?ried skim milk 25 grams
# +ugar 00 grams
# Gegetable oil 20 grams
# %lectrolyte 20 ml
# -ater to make 000 ml
,o prepare the F#05 diet, add the dried skimmed milk, sugar, vegetable oil to some
water and mi;! Aoil for about 5#0 minutes, then allow to cool! 5dd 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!
: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!
.. 1te' :6 Correctiona% Re&eeding
9orrectional refeeding should be given alternatingly from F 05 to F 00 in the
transitional phase, and F 25 in the rehabilitation phase! ,he composition of F 00 and
F 25 are as listed belowC
F 00 F 25
# ?ried skim milk 45 grams '0 grams
# +ugar 50 grams 15 grams
# Gegetable oil 10 grams 05 grams
# %lectrolyte 20 ml 20 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, 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!
,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!
: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 F05 with F 00 in the transitional phase!
Treatment Evaluation:
Aody weight should be measured daily to evaluate the efficacy of initial and
correctional refeeding!
# :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
# :f weight gain is more than 0 gr6kgA-6day, then the therapeutic program has
reached its target!

i. 1te' ;6 1ti(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!
: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!
Malnourished children need interaction with other children during rehabilitation! 5fter
the initial phase of treatment, the child should spend prolonged periods with other
children! 5ctivities should be selected to develop both motor and language skills, and
new activities and materials should be introduced regularly! 5 childJs effort to perform a
task should always be praised and never critici)ed!
"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!
j. 1te' 1<6 Pre'are &or Di+c.arge
?uring rehabilitation, preparation should be made to ensure that the child is fully
reintegrated into the family and community after discharge!
9riteria for dischargeC
5 child may be considered to have recovered and be ready for discharge when the
childJs weight for height has no longer been in the severe malnutrition $A-6!A8 N
,o achieve this goal, it is essential that the child receives as many meals as possible
per day! :n some instancies, a child may be discharged before he or she has reached
the target weight for height for discharge, however, since the child is not yet
recovered, he or she will need continuing care as an outpatient!
9hild -eight for height has no longer been in the severe malnutrition
$A-6!A8 N 00%&
%ating in ade(uate amount of a nutritious diet that mother can prepare at
>aining weight at normal or increased rate
5ll 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
5ble to ensure follow up of the child and support for the mother
2. Treat(ent o& Co(orbiditie+
a! Gitamin 5 deficiency
:f the patient is diagnosed with vitamin 5 deficinecy, vitamin 5 supplementation
should be given according to patientJs age on day , 2 and 4!
b! *lceration of the eye
5ny kind of eye problems should be evaluated to get the appropriate therapy, based on
how severe the problem is, 3ust like what listed belowC
E)e Prob%e(+ Treat(ent
AitotJs +pot only, without any other eye
5ntibiotic eyedrops is not indicated
+uppurative and inflamatory process 9hloramphenicol or tetrasiclin eyedrops
should be given
9orneal ulcer 9hloramphenicol 0,25 D % eyedrops,
gtt61 hours for 0 to 0 days
5tropine eyedrops %, gtt64 hours for 2#
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!
5dditional treatment such Bmn/
solution % topically 0 minutes a day could be
added as well! ?iaper should be changed fre(uently to avoid diaper dermatitis in
d! "arasitic :nfections
+tool e;amination 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!
:f amebiasis or giardiasis is proven to be etiologies of diarrhea in children,
administration of metronida;ole 0,5 mg6kg body weight 64 hours is indicated for 0
e! ,uberculosis
9hildren 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!
*. ,ai%ure o& Treat(ent
Failure of treatment can be categori)ed into 2 kinds of conditions, they areC
a! ?eath
?eath in the first 24 to 02 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
5s much as 0 gr6kg body weight6 day or more is e;pected 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+c.arge+ be&ore end o& treat(ent
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 e;plain about the importance of immuni)ation to these kind of
/. 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 ne;t several hours.
"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 to
1 gr6l should receive transfusion of packed red cells as much as 0 ml6kg body weight if
respiratory distress evidences are found!
2.1.5. Co('%ication
+everal complications that can occur to a severly malnourished children include the

"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 e;tensively impaired and if early
massive iron deficiency anemia is present, mental and physical retardation may be
permanent! 5pparently, the younger the infant at the time of deprivation, the more
devastating are the long#term effects!

2.1.:. ,o%%o3 U' and Progno+i+
5ny patient at risk for nutritional deficiency should be referred to a registered
dietitian or other nutritional professional for a complete nutritional assessment and dietary
/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 e;perience in the management of protein#energy
malnutrition $"%M&, should oversee care of the patient! 5ny patient with significant
laboratory abnormalities, as discussed above, may benefit from consultation with the
appropriate subspecialty $eg, endocrinology, hematology&!
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!
Follow up to severely malnourished children includeC

@elapseC Aecause risk of relapse is greatest soon after discharge, the child should be
seen after week, 2 weeks, and month! 5t 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

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!
%;cept for complications mentioned above, prognosis of even severe marasmus is
good if treatment and follow#up care are correctly applied!
7ame C M 9 +
5ge C 1 years
+e; C Male
?ate of 5dmission C March, 2th 202

C.ie& Co('%aint C ?iarrhea
.istory C
,his problem has already been occuring to this patient since he three years old! ,he
diarrhea was intermitten, volume half glass6day, e(ual amount between water and dregs, with
slime but no blood, and the fre(uency three to five times a day!
.istory of fever since three years ago! :t was intermitten with temperature not too
high, down with febrifuge, no shiver, but a few days later it happen again!
.istory of sei)ure happen five days ago! :t happens two times with duration
aprro;imately five minutes! .and#foot rigid and blink eyes! 5fter 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 5">5@ 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 4 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 /5, for one month, but he went back to +iantar and stop
/5, because his condition got worse!
.istory of previous medications C 5cyklovir, /5, $"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
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 44% $normal&
Present status
9onsciousnessC 9ompos Mentis
A"C 00610 mm.g
.@C 0;6min
@@C 22;6min
Aody temperatureC 20,
>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!
Neck C
8ymph node enlargement $#&! Alacky red rash $K&!
+ymmetrical fusiformis! 9hest retraction $#&! .yperpigmentation papul $K&! 9rust $K&! .@C
0 bpm, reguler, murmur $#&! @@C 22;6i, reguler, ronchi $#6#&!
+oepel, peristaltic $K& 7! .yperpigmentation papul $K&! 9rust $K&!
"ulse 00;6i, regular, ade(uate pressure and volume, warm, 9@, H 2R! .yperpigmentation
papul $K&! 9rust $K&!
Male, within normal limit
!aborator) ,inding+6
Para(eter+ "a%ue Nor(a% "a%ue
om!lete "lood ount
.emoglobin 4,01 gr% 2,0 D 4,4 gr%
.ematocrite 4,' % 24 D 44%
%rithrocyte ,42 ; 0
4,2 D 4,40 ; 0
8eucocyte 2520 6mm
4500 D 000 6mm
"latelet 221!000 6mm
50000 D 450000 6mm
M9G 42 fl 45 D '5 fl
M9. 21,2 pg 24 D 22 pg
M9.9 22 gr% 22 D 25 gr%
@?- 1,1 % ,1 D 4,4 %
?iftel 0 6 0 6 04 6 ' 6 2
Di&&erentia% Diagno+i+6
+uspect ,umor 5bdomen e!c dd6 # -ilms ,umor
# 7euroblastoma
#orking Diagno+i+6
+uspect ,umor 5bdomen e!c dd6 # -ilms ,umor
# 7euroblastoma
# Aedrest, threeway and urinary catheter inserted
# :GF? ?5% 7a9l 0,45% 20 gtt6i micro
# ?iet Formula 05 10 cc 6 2 hours $stabili)ation phase&
# Multivitamin without Fe ; cth ::
# Folic acid tab ; 5 mg
# 9otrimo;a)ole tab 2 ; 440 mg
# Gitamin 5 ; 200!000 :*
# "acked red cell transfusion 05 cc 6 2 hours
7eededC 4 ; $ #4,01 & ; 25 kg Q 124 cc
,ransfusion abilityC 2cc ; 25 kg Q 05 cc
Diagno+tic P%anning6
# 9omplete blood count post transfusion
# 8iver Function ,est and @enal Function ,est
+evere Malnutrition Marasmic #
Bhwarsiorkor ,ype
+evere Malnutrition Marasmic #
Bhwarsiorkor ,ype
# +erum %lectrolytes, +erum 5lbumin
# Alood >lucose ad random
# 5bdominal 9, +can
# *rinalysis
# Fluid Aalance per 1 hours
,O!!O# UP
>une /t. ? 5t.@ 2<11
1 Aulging of the lower abdomen $K&! "allor $K&! 5bdominal pain $#&!
,he patient ate the whole diet provided!
O +ensC 9M, ,empC 21,0 D 21,'
9! 5nemic $K&! :cteric $#&! %dema $K&! 9yanosis $#&!
Aody weightC 25 kg, Aody lengthC 44 cm! *rine output 2,4 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 40 D '2 bpm, reguler!
Murmur $#&! @@C 2 D 25 ;6i, regular! Areath soundC vesicular! 5dditional
soundC $#&!
5bdomen Aulging $K& in regio hypogastrium, 4 ; ' 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 40#'2 ;6i, regular, ade(uate p6v, warm, 9@, H 2R! A"C 00#20600#
40 mm.g $normalC #24 6 12#42&!
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 2 m%(68 *reumC 14,50 mg6dl
+>",C 2 *68 BC 2,' m%(68 BreatininC 2,22 mg6dl
5lbuminC 2,0 gr6dl 9l C 2 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 K2 6 ,06 # 6 # 6 #
A +uspect ,umor 5bdomen e!c dd6 # -ilms ,umor
# 7euroblastoma
P $anage(ent6
# Aedrest, threeway and urinary catheter inserted
# :GF? ?5% 7a9l 0,45% 20 gtt6i micro
# ?iet Formula 05 10 cc 6 2 hours $stabili)ation phase&
# Multivitamin without Fe ; cth ::
# 9otrimo;a)ole tab 2 ; 440 mg
# ,ransfusion "@9 05 cc 6 2 hours
+evere Malnutrition Marasmic #
Bhwarsiorkor ,ype
Diagno+tic P%anning6
# 9omplete blood count post transfusion
# 5bdominal 9, +can
# *rinalysis
>une : 4 11t.@ 2<11
1 Aulging of the lower abdomen $#&! "allor $#&! 5bdominal pain $#&!
,he patient ate the whole diet provided! Gomitus $#&! ?iarrhea $#&
O +ensC 9M, ,empC 20,0 D 20,1
9! 5nemic $#&! :cteric $#&! %dema $#&! 9yanosis $#&!
Aody weightC 25 kg, Aody lengthC 44 cm! *rine outputC 2,4 D 5,5 cc6kg6hour
*rine colour C yelowish to brown
.ead /ld man face $K&! 9on3unctiva palpebra inferior anemic $#&!8ight refle;
$K&6$K&! :sochoric pupil! +unken eye $#&!
7eck Pugular vein pressure @#2 cm.2/! 8ymph node enlargement $#&!
,hora; +imetris fusiformis! @etraction $#&! .@C 04 D 40 bpm, reguler!
Murmur $#&! @@C 4 D 22 ;6i, regular! Areath soundC vesicular! 5dditional
soundC $#&!
5bdomen 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 04 # 40 ;6i, regular, ade(uate p6v, warm, 9@, H 2R! A"C 00#0605#
40 mm.g $normalC #24 6 12#42&!
Aaggy pants $#&, thinning of subcutaneous fat $K&, muscle hypotrophy $K&!
9ra)y pavement dermatosis $K&! "itting edema $#& pretibia!
>enital Female, within normal limit
#aborator$ %indings:
.emoglobinC 2,5 gr% M9G C 01,1 fl
.ematocritC 2',5 % M9. C 21,2 pg
%rythrocyte C 5,1 ; 0
6 mm
M9.9 C 24,2 gr%
8eucocyte C 0400 6 mm
@?- C ',1 %
"latelet C 212000 6 mm
8%? C 4 mm6hours
?ipstick urineC
8eu 6 7it 6 *ro 6 "rotein 6 p. 6 Alood 6 +> 6 Bet 6 Ail 6 >lu
K 6 # 6 0,2 6 S 6 5 6 K2 6 ,06 # 6 # 6 #
A .ydronephrosis bilateral e!c $T& K severe malnutrition marasmic khwarsiorkor type K
suspect urinary tract infection
P $anage(ent6
# Aedrest, threeway and urinary catheter inserted
# :GF? ?5% 7a9l 0,45% 20 gtt6i micro
# ?iet Formula 05 20 cc 6 2 hours $stabili)ation phase&
# Multivitamin without Fe ; cth ::
# Folic acid ; mg
# :n3ection 9eftria;one gr 6 2 hours
# 9otrimo;a)ole tab 2 ; 440 mg
Diagno+tic P%anning6
5bdominal 9, +can
*rinalysis and urine culture K sensitivity test
>une 1241: t.@ 2<11
1 Aulging of the lower abdomen $#&! "allor $#&! 5bdominal pain $#&! Fever $K&!
,he patient ate the whole diet provided! Gomitus $#&! ?iarrhea $#&
O +ensC 9M, ,empC 20,2 D 24,
9! 5nemic $#&! :cteric $#&! %dema $#&! 9yanosis $#&!
Aody weightC 21 kg, Aody lengthC 44 cm! AA6* Q 50,'% $severe malnutrition&
*rine outputC 2 D 2, cc6kg6hour
*rine colourC transparent yellowish
.ead /ld man face $K&! 9on3unctiva palpebra inferior anemic $#&!8ight refle;
$K&6$K&! :sochoric pupil! +unken eye $#&!
7eck Pugular vein pressure @#2 cm.2/! 8ymph node enlargement $#&!
,hora; +imetris fusiformis! @etraction $#&! .@C 01 # '0! bpm, reguler!
Murmur $#&! @@C 20 # 22 ;6i, regular! Areath soundC vesicular! 5dditional
soundC $#&!
5bdomen 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 2R! A"C 00#20 6 00 # 40
mm.g $normalC #24 6 12#42&!
Aaggy pants $#&, thinning of subcutaneous fat $K&, muscle hypotrophy $K&!
9ra)y pavement dermatosis $K&! "itting edema $K& pretibia!
>enital Female, within normal limit
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 0
+ensitive to Meropenem only
(i!stick urine
8eu 6 7it 6 *ro 6 "rotein 6 p. 6 Alood 6 +> 6 Bet 6 Ail 6 >lu
K 6 # 6 # 6 K 6 5 6 K2 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
# Aedrest, threeway and urinary catheter inserted
# :GF? ?5% 7a9l 0,45% 20 gtt6i micro
# ?iet Formula 00 400 cc 6 2 hours $transition phase&
# :n3ection Meropenam 250 mg 6 4 3am
# Multivitamin without Fe ; cth ::
-.1. Di+cu++ion
5 4#year#old female was admitted to @+*" .5M 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 e;tremities! ,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! 5nalysis of serum electrolyte was
conducted as well to identify whether electrolyte imbalance had been present or not! +ince
the serum 7a was 2 m%(6l and the patient did not show any symptomps of hyponatremia,
then this patient was given maintenance fluid with ?e;trose 5% 7a9l 0,45% solution!,he
re(uirement of the fluid was ad3usted to the stabili)ation phase re(uirements!
"rophyla;is of infection was given to this patient, applying the use of 9otrimo;a)ole
$,rimetophrim 5 mg with +ulfametho;a)ole 20 mg& and thus the patient was given 2 ; 440
mg! 9itrimo;a)ole was given for as long as 5 days, since the patient came without any
evidence of infection first!
Micronutrien deficiency was corrected with admission of folic acid 5 mg along with vitamin
5 200!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 ma;imally 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 05! +ince she
presented with edema in the lower e;tremities, the fluid re(uirements needed in the
stabili)ation phase was 006day! 5s known that F05 contains 05 kcal each 00ml, then the
re(uirements wasC
Fluid re(uirementsC 00 ml ; 25 kg Q 2500 ml
Feeding formula F05 $05 kcal 6 00ml&
F 05 Q 05 ; 25006 00 per 24 hours
F 05 Q 405 ml 6 24 hours
For the stabili)ation phase, F 05 should be given every 2 hours, then the patient neededC
F 05 Q 405 6 2 times
F 05 Q 50 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 20 ml6kg body weight6day! ,he estimated calory needed then was
recounted to be as the followingC
Fluid re(uirementsC 20 ml ; 25 kg Q 2250 ml
Feeding formula F05 $05 kcal 6 00ml&
F 05 Q 05 ; 22506 00 per 24 hours
F 05 Q 2420,5 ml 6 24 hours
For the stabili)ation phase, F 05 should be given every 2 hours, then the patient neededC
F 05 Q 2420,5 6 2 times
F 05 Q 202,2 cc $rounded to be 20 cc 6 2hours&
,his formula was given for as long as 0 days during the stabili)ation phase, then folowed by
Formula 00 -./ which contains more calories then the previous formula!
?aily evaluation of treatment was conducted to this patient assesing the weight gain
achieved each day! +ince, the weight gain was below the e;pected value $less than 5 gr6kg
body weight6 day&, she was then classified as poor response! 5ccording to the guideline
published, patient with poor response should be evaluated for any comorbid or any infection
that could probably present!
5 more detail anamnesis was conducted to this patient in order to identify the cause of this
poor response! 5ccording 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
aeruginosa infection! *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! 5ntibiotic switch was then
done to in3ection of meropenem 250 mg every 4 hours!
5nother 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 2 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 a;is shuts down as the body struggles to survive, directing finite energy resources to
support more vital functions! Aoth males and females e;perience 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 4& 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, neuroe;citatory amino
acids, and neural pathways! 5minobutyric acid e;erts a suppressive effect on >n@.
secretion and can be an important factor in the relative (uiescence of gonadotropin secretion
that characteri)es the <3uvenile pause< that occurs after infancy and ends before the
endocrine activity of puberty resumes! +e; steroids, mainly testosterone, estrogen, and
progesterone, also inhibit >n@. pulse fre(uency in a negative feedback inhibition, whereas
estrogen has the additional ability to e;ert positive feedback on gonadotropin secretion at
>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 e;posed
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#
: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. 1u((ar)
,his paper reports a case of a 4#year#old female diagnosed with severe malnutrition
marasmic#khwarsiorkor type! 5 comprehensive treatment including ten principal steps to
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!
! +hasidhar, .arohalli @! Aathia, Patinder! Malnutrition! 5vailable fromC httpC 66
emedicine!medscape! com6 article6'4540#show all6! 5ccesed on Pune 0th, 20
2! +cheinfeld, 7oah +! %lston, ?irk M! "rotein#%nergy Malnutrition! 5vailable fromC
httpC66emedicine!medscape!com6article604122#show all! 5ccesed on Pune 0th, 20
2! .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, 2002!
4! -illiam 9 .!, Food :nsecurity, .unger, and *ndernutrition! :nC @ichard % A, @obert
M B, .al A P! 7elson ,e;tbooks of "ediatrics, 0th %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! 5vailable from
httpC66emedicine!medscape!com6article6'444'1#show all! 5ccesed on Pune 0th 20
0! ?ennis M +, 8eonna 9!, 7ormal "ubertal ?evelopment! :nC 9olin et al!, @udolphJs
"ediatrics, 2st %dition! 9aliforniaC Mc>raw .ill; 2002
4! -aterlow, P 9!, 9lasification and ?iagnosis of "rotein#9alorie Malnutrition! 5vailable
fromC httpC66bm3!wholibdoc!who!int6article60'4224#show! 5ccesed on Pune 0th,
'! Auku Aagan ,atalaksana 5nak >i)i Auruk :6::! ?irektorat >i)i Masyarakat, ?ir3en
Aina Besehatan Masyarakat! Pakarta, 2005
0! -orld .ealth /rgani)ation! Management of +evere MalnutritionC 5 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, 0th %dition! "hiladelphia, 2002

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