CASE REPORT SEVERE MALNUTRITION MARASMUS-KHWARSIORKOR MARASMUS-KHWARSIORK OR TYPE
Compiled By:
ANDIKA PRADANA
!"!"
IRA NOLA LIN##A
!""$
DEPARTEMENT DEPARTEMENT O% PEDIATRICS H& ADAM MALIK #ENERAL HOSPITAL %ACULTY O% MEDICINE SUMATERA UTARA UNIVERSITY MEDAN '""
TABLE O% CONTENTS
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1.2. 1.2. Objec Objecti tive ve
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4 2.1. Defnition Defnition
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2.2. Epidemiology .................... ............................... ..................... ..................... ..................... ..................... ................ .....
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2.3. 2.3. Clas Classi sifc fcat atio ion n and and Clin Clinic ical al indi inding ngs s
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! 2.!. 2.!. "at#o at#op# p#ys ysio iolo logy gy
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2.%. 2.%. Diag Diagno nosi sis s and and &ork ork 'p
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2.(. )anagement .................... ............................... ..................... ..................... ..................... ..................... ................ .....
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2.$. Complication ........... ...................... ..................... ..................... ..................... ..................... ...................... .............. ...
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2.+. 2.+. ollo ollo, , 'p and and "rog "rogno nosi sis s
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C0*p.e( 5: Di/+1//io *d S1mm*(y &&&&&& &&&&&&&&& &&&&&& &&&&&& &&&&&& &&&&&& &&&&&& &&&&&& &&&&&& &&&&&& &&&&&& &&&&&& &&&&& &&&& !.1. Discussion Discussion !.2. !.2. umma ummary ry
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C0*p.e( ": I.(od1+.io &&&& &&&&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& &&&& && 1.1. Background Background
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1.2. 1.2. Objec Objecti tive ve
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4 2.1. Defnition Defnition
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2.2. Epidemiology .................... ............................... ..................... ..................... ..................... ..................... ................ .....
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2.3. 2.3. Clas Classi sifc fcat atio ion n and and Clin Clinic ical al indi inding ngs s
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! 2.!. 2.!. "at#o at#op# p#ys ysio iolo logy gy
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2.%. 2.%. Diag Diagno nosi sis s and and &ork ork 'p
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2.(. )anagement .................... ............................... ..................... ..................... ..................... ..................... ................ .....
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2.$. Complication ........... ...................... ..................... ..................... ..................... ..................... ...................... .............. ...
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$ 12
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CHAPTER I INTRODUCTION 1.1.
Background Maln Malnut utri riti tion on is glob global ally ly the the most most impo importa rtant nt risk risk facto factorr for for illn illness ess and and deat death, h,
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 maln malnut utrit ritio ion n $"M $"M&, &, first first descr describ ibed ed in the the '20 '20s, s, is obser observe ved d most most fre(u fre(uen ently tly in developing countries but has been described with increasing fre(uency in hospitali)ed and chronically ill children in the *nited +tates! 1 he -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! Malnutritio Malnutrition n itself is a very essential essential aspects determining determining the health status of a child! 7ot only because it is pretty much correlated corre lated 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 effect effectss of changi changing ng enviro environme nmenta ntall condit condition ionss in increas increasing ing malnu malnutrit trition ion is mult multifa ifacto ctoria rial! l! "oor "oor envi enviro ronm nmen ental tal cond condit itio ions ns may may incr increas easee insec insectt and and prot proto) o)oa oall infe infecti ction onss and and also also cont contri ribu bute te to envi enviro ronm nment ental al defi defici cien encie ciess in micro micronu nutr trien ients ts!! /ver /verpo popu pula lati tion on,, more more comm common only ly seen seen in deve develo lopi ping ng coun countr tries ies,, can can reduc reducee food 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, poverty, which can further hamper economic and social development! 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 aspec aspects ts abou aboutt maln malnut utrit ritio ion, n, part partic icul ularl arly y the the diag diagno nosi siss and and manag managem emen entt of severe 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 .ealth /rgani /rgani)ati )ation on $-./& $-./& defin defines es maln malnut utrit ritio ion n as
!
$"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
$2%& 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 sia and eastern frica, about half the children have growth retardation due to protein#energy malnutrition! his figure is 5 times the prevalence in the western world! 2 pproimately 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!2 ccording 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 $,%& 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 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! lthough 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! 2/! a! Marasmus
%
: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
(
: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
$
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!
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!
+
: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! ?ietar y 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 *
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 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
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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 retardation of 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 13
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, erythematous skin, des(uamation, erosions, and diffuse hyperpigmentation was reported! ,2
1!
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 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%
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
c&
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
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 $length is used in infants and toddlers, rather than height, because they are unable to stand&! :ndividual measurements are usually compared to reference standards on a growth chart!
1(
ntropometric measurements used for adults usually include height, weight, body mass inde, waist to hip ratio, and precentace of body fat! hese measures are then compared to referance standards to assess weight status and the risk for various diseases! nthropometric measurements re(uire precise measuring techni(ues to be valid! d&
8aboratory Findings -here facilities permit, the teset given in table below may help to diagnose specific problems! hey are not needed, however, to guide or monitor treatment! he interpretation of test result is fre(uently altered by malnutrition! For this reason, laboratory test may misguide ineperienced workers! he most important guide to treatment is fre(uent careful assessment of the child! ,2 est
@esult and significance
Te+t+ tat (a) be u+e&u%
Alood glucose
>lucose
concentration
H54
mg6dl
is
indicative of hypoglycaemia amination
of
blood
smear
by
"resence of malaria parasites is indicative
microscopy
of infections
.aemoglobin or packed#cell volume
.aemoglobin H40 d6l or packed#cell volume H2% is indicative of very severe anemia
amination and culture of urine specimen
"resence of bacteria on microscopy is indicative of infections
amination of faeces by microscopy
"resence of blood is indicative of dysentry
9hest I#@ay
"neumonia causes less shadowing of the lungs in malnourished children that in well#nourished children Aones may show rickets or fractures of the ribs
+kin test for tuberculosis
/ften
negative
tuberculosis
or
in
children
those
with
previously
vaccinated with A9> vaccine Te+t+ tat are o& %itt%e or no a%ue
+erum proteins
7ot useful in management, but may guide
1$
prognosis est for human immunodeficiency virus +hould not be done routinely; if done, $.:G&
should be accompanied by counselling of the childJs parents and result should be confidential
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 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! */1Ay 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+
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 tabi%iation
No
Treat(ent
.ypoglycemia
2
.ypothermia
?ehydration
4
lectrolyte 9orrection
5
reatment of :nfection
1
Micronutrition ?efficiency 9orrection
:nitial @efeeding
Da) 142
Da) *45
Tran+ition
Reabi%itation
,o%%o3 U'
#eek 2
#eek *40
#eek 5420
Without Iron Supplementation
Formula 75 Formula 75 to 9orrectional @efeeding 100 $9atch *p >rowth&
'
+timulation
0
"repare for ?ischarge
With Iron Supplementation
Formula
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*
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('+
lert $not lethargic& 8oss of consciousness $lethargic&
Treat(ent
>ive 50 ml of ?etrose 0% per oral or via 7> >ive ?etrose 0% intravenous as much as 5 ml per each kilogram body weight, followed by 50 ml of ?etrose 0% orlaly >ive ?etrose 0% intravenous as much as 5 ml per
+hock
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 1,5 o9! .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-
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
-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 $@e+oMal& solution if available! ',0 he following table highlights the composition of standard /@+, the new reduced# osmolarity /@+, and @e+oMal!
Co('o+ition
>lucose +odium "otassium 9hloride 9itrate Magnesium Einc 9opper /smolarity
',0
Reo$a%
tandard OR
Reduced
7((o%8!9 25 45 40 0 0! 0!045 00
7((o%8!9 '0 20 0 0 !!! !!! !!!
o+(o%arit) OR 5 5 20 15 0 !!! !!! !!! 245
$m/sm68& 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
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, add 9hloramphenicol 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 clinical trials! &. 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
#
+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! */1here 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! */1he nutritional re(uirements according to treatment phase should be ad3usted to the amount listed belowC */1Nutrient+
nergy "rotein Fluid intake
tabi%iation 00 kcal6kg6day D ,5 g6kg6day 0 ml6kg6day or 00 ml6kg6day if
Treat(ent Pa+e Tran+itiona% Reabi%itation 50 kcal6kg6day 50#200 kcal6kg6day 2# g6kg6day 4#1 g6kg6day 50 ml6kg6day 50 D 200 ml6kg6day
2!
edema presents he composition of Formula 5 according to the -orld .ealth /rgani)ation should be as listed belowC # ?ried skim milk # +ugar # Gegetable oil # lectrolyte # -ater to make
25 grams 00 grams 2 grams 20 ml 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 +ugar Gegetable oil lectrolyte
5 grams 50 grams 10 grams 20 ml
'0 grams 15 grams 5 grams 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%
: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(
j.
te' 1<6 Pre'are &or Di+carge ?uring rehabilitation, preparation should be made to ensure that the child is fully
reintegrated into the family and community after discharge! 9riteria for dischargeC ',0 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 0%& 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
Criteria -eight for height has no longer been in the severe malnutrition
$A-6!A8 N 0%& ating in ade(uate amount of a nutritious diet that mother can prepare at
Mother .ealth
home >aining weight at normal or increased rate ll vitamin and mineral deficiencies have been treated dema, vomitus, hypothermia and diarrhea are no longer present Bnows how to prepare apropriate foods and feed the child well ble to ensure follow up of the child and support for the mother
worker
2. Treat(ent o& Co(orbiditie+ a! Gitamin deficiency :f the patient is diagnosed with vitamin deficinecy, vitamin supplementation
should be given according to patientJs age on day , 2 and 4!
',0,
b! *lceration of the eye ny kind of eye problems should be evaluated to get the appropriate therapy, based on how severe the problem is, 3ust like what listed belowC ',0 E)e Prob%e(+
AitotJs +pot only, without any other eye
Treat(ent
ntibiotic eyedrops is not indicated
problem +uppurative and inflamatory process
9hloramphenicol or tetrasiclin eyedrops should be given
2$
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/ 4 solution % 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! 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! ',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+
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 to 1 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 more devastating are the long#term effects! 1/2/!
2*
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 dietary counseling! ,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 includeC 1/2/! •
@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-
CHAPTER * CAE REPORT
7ame
CM9+
ge
C 1 years
+e
C Male
?ate of dmission
C March, th 20
Cie& 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!
31
.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
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! Neck C 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
Urogenital C Male, within normal limit
!aborator) ,inding+6 Para(eter+ om!lete "lood ount .emoglobin .ematocrite rithrocyte 8eucocyte "latelet M9G M9. M9.9 @??iftel
"a%ue
Nor(a% "a%ue
4,1 gr% 4,' % ,2 0 1 6mm 50 6mm 221!000 6mm 2 fl 21,2 pg 2 gr% 1,1 % 0 6 0 6 6 ' 6
2,0 D 4,4 gr% D 44% 4,2 D 4, 0 1 6mm 4500 D 000 6mm 50000 D 450000 6mm 5 D '5 fl 2 D 2 pg D 5 gr% ,1 D 4, %
Di&&erentia% Diagno+i+6
+uspect umor bdomen e!c dd6 # -ilms umor # 7euroblastoma
K
+evere Malnutrition Marasmic # Bhwarsiorkor ype
#orking Diagno+i+6
+uspect umor bdomen e!c dd6 # -ilms umor # 7euroblastoma
K
+evere Malnutrition Marasmic # Bhwarsiorkor ype
$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!
# # # # #
+erum lectrolytes, +erum lbumin Alood >lucose ad random bdominal 9 +can *rinalysis Fluid Aalance per 1 hours
,O!!O# UP
>une /t ? 5t@ 2<11 Aulging of the lower abdomen $K&! "allor $K&! bdominal pain $#&!
3%
O
he patient ate the whole diet provided! +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
7eck hora
$K&6$K&! :sochoric pupil! +unken eye $#&! Pugular vein pressure @#2 cm.2/! 8ymph node enlargement $#&! +imetris fusiformis! @etraction $#&! .@C 0 D '2 bpm, reguler! Murmur $#&! @@C 2 D 25 6i, regular! Areath soundC vesicular! dditional soundC $#&! Aulging $K& in regio hypogastrium, ' cm in si)e, immobile, soft and
bdomen
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 $K& pretibia! Female, within normal limit
>enital
#aborator$ %indings: +>/C *68
7aC m(68
+>"C *68
BC ,' m(68
lbuminC 2, gr6dl
9l C m(68
*reumC 14,50 mg6dl BreatininC 2,2 mg6dl
?ipstick urineC 8eu 6 7it 6 *ro 6 "rotein 6 p. 6 Alood 6 +> 6 Bet 6 Ail 6 >lu K2 6 K 6 #
A
6
K
6 1,5 6 K
6 ,06 # 6 # 6 #
+uspect umor bdomen e!c dd6 # -ilms umor # 7euroblastoma
P
K
+evere Malnutrition Marasmic # Bhwarsiorkor ype
$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 :: 9otrimoa)ole tab 2 40 mg ransfusion "@9 5 cc 6 2 hours
3(
Diagno+tic P%anning6
# # #
9omplete blood count post transfusion bdominal 9 +can *rinalysis
>une : 4 11t@ 2<11 Aulging of the lower abdomen $#&! "allor $#&! bdominal pain $#&!
O
he patient ate the whole diet provided! Gomitus $#&! ?iarrhea $#& +ensC 9M, empC ,0 D ,1 o9! nemic $#&! :cteric $#&! dema $#&! 9yanosis $#&! Aody weightC 25 kg, Aody lengthC 44 cm! *rine outputC ,4 D 5,5 cc6kg6hour *rine colour C yelowish to brown .ead
/ld man face $K&! 9on3unctiva palpebra inferior anemic $#&!8ight refle
7eck hora
$K&6$K&! :sochoric pupil! +unken eye $#&! Pugular vein pressure @#2 cm.2/! 8ymph node enlargement $#&! +imetris fusiformis! @etraction $#&! .@C D bpm, reguler! Murmur $#&! @@C D 22 6i, regular! Areath soundC vesicular! dditional soundC $#&!
3$
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 $#& pretibia! Female, within normal limit
>enital
#aborator$ %indings: .emoglobinC ,5 gr%
M9G C 1,1 fl
.ematocritC ',5 %
M9. C 21,2 pg
rythrocyte C 5,1 0 1 6 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 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 K
6 ,06 # 6 # 6 #
A
.ydronephrosis bilateral e!c $T& K severe malnutrition marasmic khwarsiorkor type K
P
suspect urinary tract infection $anage(ent6 # # # # # # #
Aedrest, threeway and urinary catheter inserted :GF? ?5% 7a9l 0,45% 20 gtt6i micro ?iet Formula 5 20 cc 6 2 hours $stabili)ation phase& Multivitamin without Fe cth :: Folic acid mg :n3ection 9eftriaone gr 6 2 hours 9otrimoa)ole tab 2 40 mg
Diagno+tic P%anning6
bdominal 9 +can *rinalysis and urine culture K sensitivity test
3+
>une 1241: t@ 2<11 Aulging of the lower abdomen $#&! "allor $#&! bdominal pain $#&! Fever $K&!
O
he patient ate the whole diet provided! Gomitus $#&! ?iarrhea $#& +ensC 9M, empC , D , o9! nemic $#&! :cteric $#&! dema $#&! 9yanosis $#&! Aody weightC 21 kg, Aody lengthC 44 cm! AA6* Q 50,'% $severe malnutrition& *rine outputC 2 D , cc6kg6hour *rine colourC transparent yellowish .ead
/ld man face $K&! 9on3unctiva palpebra inferior anemic $#&!8ight refle
7eck hora
$K&6$K&! :sochoric pupil! +unken eye $#&! Pugular vein pressure @#2 cm.2/! 8ymph node enlargement $#&! +imetris fusiformis! @etraction $#&! .@C 1 # '0! bpm, reguler! Murmur $#&! @@C 20 # 2 6i, regular! Areath soundC vesicular! dditional
bdomen
soundC $#&! 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#20 6 0 # 0 mm.g $normalC #2 6 1#2&! Aaggy pants $#&, thinning of subcutaneous fat $K&, muscle hypotrophy $K&!
3*
9ra)y pavement dermatosis $K&! "itting edema $K& pretibia! Female, within normal limit
>enital
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 5 9F*6ml +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 K
6 ,06 # 6 # 6 #
A
.ydronephrosis bilateral e!c! @etensio *rine K +evere Malnutrition Marasmic D
P
Bhwarsiorkor type K *rinary ract :nfection $anage(ent6 # # # # #
Aedrest, threeway and urinary catheter inserted :GF? ?5% 7a9l 0,45% 20 gtt6i micro ?iet Formula 00 40 cc 6 hours $transition phase& :n3ection Meropenam 250 mg 6 3am Multivitamin without Fe cth ::
P%anning6
*rinalysis
!-
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
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
?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 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! 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 <3uvenile pause< that occurs after infancy and ends before the endocrine activity of puberty resumes! +e steroids, mainly testosterone, estrogen, and !3
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
!!
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#show all! 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#show all! 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
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