Case Report

Marasmus and Pulmonary Tuberculosis

Presentator: Thivyashwini Komaran
Mungunthanii Krishnamoorthy
Supervisor: dr. Pertin Sianturi Sp. A K!
"ntroduction
Protein is an essential part o# living cells and carbohydrate$ an important constituent o# the
body. The main #unction o# carbohydrate is to supply energy thus it is the ma%or source o# #uel.
Protein on the other hand$ is used as the cell #unctions in order to grow and maintain itsel#&
protein is necessary #or 'ey body #unctions including provision o# essential amino acids$
development and maintenance o# muscles. There are two basic types o# malnutrition. The #irst
and most important is protein(energy malnutrition also called Protein(calorie malnutrition and
Protein(energy under nutrition! is the lac' o# enough protein #rom meat and other sources! and
#ood that provides energy measured in calories! which all o# the basic #ood groups provide. The
second type o# malnutrition which is also very important is micronutrient vitamin and mineral!
de#iciency. Protein(energy malnutrition P)M! is the most lethal #orm o# malnutrition or hunger.
"t is basically a lac' o# calories and protein.
Marasmus can be de#ined as severe and chronic malnutrition producing a gradual wasting
o# tissues owing mainly to insu##icient or unassimilated energy(giving #ood and at times
combined with the lac' o# protein$ occurring especially in in#ants *amabo and +nwu'we$ ,-.-!.
"t can also be described as an insu##icient energy inta'e to match the body/s re0uirements. As a
result$ the body draws on its own stores$ resulting in emaciation Schein#eld$ Mo'ashi and 1in$
,-.-!. Marasmus presents with the #ollowing signs and symptoms: wasting o# the muscles
emaciation!$ bones and %oints are more prominent$ the head appears disproportionally larger
than the body while the s'in is o#ten dry$ patchy with pigmentation. Marasmus is mainly seen in
in#ants between the ages 2(3 months and is not con#ined to any geographical location.
According to Schein#eld$ Mo'ashi and 1in ,-.-!$ marasmus most commonly occurs in children
younger than 4 years. This period is characteri5ed by increased energy re0uirements and
increased susceptibility to viral and bacterial in#ections.6eaning the deprivation o# breast mil'
and the commencement o# nourishment with other #ood! occurs during this high(ris' period.
6eaning is o#ten complicated by geography$ economy$ hygiene$ public health$ culture$ and
dietetics.
Pulmonary tuberculosis is an in#ectious disease caused by Mycobacterium tuberculosis. "n
many cases$ M tuberculosis becomes dormant be#ore it progresses to active T7. "t most
commonly involves the lungs and is communicable in this #orm$ but may a##ect almost any organ
system including the lymph nodes$ C8S$ liver$ bones$ genitourinary tract$ and gastrointestinal
tract 9orne$ ,-.:!.
Transmission o# M. tuberculosis is person to person$ usually by airborne mucus droplet
nuclei$ particles .(4 ; m in diameter that contain M. tuberculosis. Transmission rarely occurs by
direct contact with an in#ected discharge or a contaminated #omite. The chance o# transmission
increases when the patient has a positive acid(#ast smear o# sputum$ an e<tensive upper lobe
in#iltrate or cavity$ copious production o# thin sputum$ and severe and #orce#ul cough.
)nvironmental #actors such as poor air circulation enhance transmission. Most adults no longer
transmit the organism within several days to , wee's a#ter beginning ade0uate chemotherapy$
but some patients remain in#ectious #or many wee's. =oung children with tuberculosis rarely
in#ect other children or adults. Tubercle bacilli are sparse in the endobronchial secretions o#
children with pulmonary tuberculosis$ and cough is o#ten absent or lac's the tussive #orce
re0uired to suspend in#ectious particles o# the correct si5e Kliegman and 8elson$ ,-..!.
Tuberculosis remains one o# the ma%or diseases a##licting children throughout the world.
Although the e<act number o# annual cases o# childhood tuberculosis is un'nown$ the 6orld
9ealth +rgani5ation 69+! has estimated appro<imately . million new cases and >--$---
deaths per year in children due to tuberculosis Star'e$ ,-->!.


C9APT)R ,
1"T)RAT?R) R)@")6
,.. Marasmus
Ae#inition
Marasmus is one o# the : #orms o# serious protein(energy malnutrition P)M!. The other , #orms
are 'washior'or K6! and marasmic K6. These #orms o# serious P)M represent a group o#
pathologic conditions associated with a nutritional and energy de#icit occurring mainly in young
children #rom developing countries at the time o# weaning. Marasmus is a condition primarily
caused by a de#iciency in calories and energy$ whereas 'washior'or indicates an associated
protein de#iciency$ resulting in an edematous appearance. Marasmic 'washior'or indicates that$
in practice$ separating these entities conclusively is di##icult& this term indicates a condition that
has #eatures o# both Rabinowit5 et al$ ,-.>!.
)tiology
P)M$ unli'e the other important nutritional de#iciency diseases$ is a macronutrient de#iciency$
not a micronutrient de#iciency. Although termed P)M$ it is now generally accepted to stem in
most cases #rom energy de#iciency$ o#ten caused by insu##icient #ood inta'e. )nergy de#iciency is
more important and more common than protein de#iciency. "t is very o#ten associated with
in#ections and with micronutrient de#iciencies. "nade0uate care$ #or e<ample in#re0uent #eeding$
may play a part 1atham$ .BBC!.
According to 1atham .BBC!$ the cause o# P)M and o# some other de#iciency diseases prevalent
in developing countries! should not$ however$ be viewed simply in terms o# inade0uate inta'e o#
nutrients. Dor satis#actory nutrition$ #oods and the nutrients they contain must be available to the
#amily in ade0uate 0uantity& the correct balance o# #oods and nutrients must be #ed at the right
intervals& the individual must have an appetite to consume the #ood& there must be proper
digestion and absorption o# the nutrients in the #ood& the metabolism o# the person must be
reasonably normal& and there should be no conditions that prevent body cells #rom utili5ing the
nutrients or that result in abnormal losses o# nutrients. Dactors that adversely in#luence any o#
these re0uisites can be causes o# malnutrition$ particularly P)M. The aetiology$ there#ore$ can be
comple<. Certain #actors that contribute to P)M$ particularly in the young child$ are related to
the host$ the agent the diet! and the environment. The underlying causes could also be
categori5ed as those related to the child/s #ood security$ health including protection #rom
in#ections and appropriate treatment o# illness! and care$ including maternal and #amily practices
such as those related to #re0uency o# #eeding$ breast#eeding and weaning.
Some e<amples o# #actors involved in the aetiology o# P)M are:
the young child/s high needs #or both energy and protein per 'ilogram relative to those
o# older #amily members&
inappropriate weaning practices&
inappropriate use o# in#ant #ormula in place o# breast#eeding #or very young in#ants in
poor #amilies&
staple diets that are o#ten o# low energy density not in#re0uently bul'y and
unappeti5ing!$ low in protein and #at content and not #ed #re0uently enough to children&
inade0uate or inappropriate child care because o#$ #or e<ample$ time constraints #or the
mother or lac' o# 'nowledge regarding the importance o# e<clusive breast#eeding&
inade0uate availability o# #ood #or the #amily because o# poverty$ ine0uity or lac' o#
su##icient arable land$ and problems related to intra(#amily #ood distribution&
in#ections viral$ bacterial and parasitic! which may cause anore<ia$ reduce #ood inta'e$
hinder nutrient absorption and utili5ation or result in nutrient losses&
#amine resulting #rom droughts$ natural disasters$ wars$ civil disturbances$ etc.
)pidemiology
According to Rabinowit5 et al$ ,-.>!$ nearly :-E o# humans currently e<perience one or more
o# the multiple #orms o# malnutrition. Close to 4- million children younger than 4 years have
P)M$ and hal# o# the children who die younger than 4 years are undernourished. Appro<imately
3-E o# these malnourished children live in Asia$ .4E in A#rica$ and 4E in 1atin America.
Marasmus is more #re0uent in children younger than 4 years because this period is characteri5ed
by increased energy needs and increased susceptibility to viral and bacterial in#ections. 6eaning$
which occurs during this period$ is o#ten complicated by #actors such as geography eg$ drought$
poor soil productivity!$ economy eg$ illiteracy$ unemployment!$ hygiene eg$ access to 0uality
water!$ public health eg$ number o# nurses is more than number o# physicians!$ and culture and
dietetics eg$ intra#amily distribution o# high(nutrition #oods!.
Pathogenesis
@arious e<tensive reviews o# the pathophysiological processes resulting in marasmus are
available. ?nli'e 'washior'or$ the clinical se0uelae o# marasmus can be considered as an
evolving adaptation in a child #acing an insu##icient energy inta'e. Marasmus always results
#rom a negative energy balance. The imbalance can result #rom a decreased energy inta'e$ an
increased loss o# ingested calories eg$ emesis$ diarrhea$ burns!$ an increased energy e<penditure$
or combinations o# these #actors$ such as is observed in acute or chronic diseases. Children adapt
to an energy de#iciency with a decrease in physical activity$ lethargy$ a decrease in basal energy
metabolism$ slowing o# growth$ and$ #inally$ weight loss.
Pathophysiological changes associated with nutritional and energy de#icits can be described as
.! body composition changes$ ,! metabolic changes$ and :! anatomic changes Rabinowit5 et
al$ ,-.>!.
7ody Composition Changes
7ody mass: 7ody mass is signi#icantly decreased in a heterogeneous way.
Dat mass: Dat stores can decrease to as low as 4E o# the total body weight and can be
macroscopically undetectable. The remaining #at is usually stored in the liver$ giving a
parado<ical appearance o# a #atty liver. Although this is o#ten observed in 'washior'or$ it
also occurs to a lesser e<tent in marasmus. A study #rom 8igeria e<amined serum lipids
in malnourished children.These authors #ound that total cholesterol$ low density
lipoprotein cholesterol$ and high density lipoprotein cholesterol levels were signi#icantly
higher in children with 'washior'or than in those with marasmus.
Total body water: The proportion o# water content in the body increases with the
increased seriousness o# P)M marasmus or 'washior'or! and is associated with the loss
o# #at mass$ which is poor in water. The proportion o# e<tracellular water also increases$
o#ten resulting in edema. )dema is signi#icant in 'washior'or but can also be present in
marasmus or in the #re0uently encountered mi<ed #orms o# P)M. The increase in
e<tracellular water is proportional to the increase in the total body water. Auring the #irst
days o# therapy$ part o# the e<tracellular water shi#ts to the intracellular compartment and
part o# it is lost in the urine$ resulting in the observed initial weight loss with treatment.
Protein mass: Mainly represented by muscle and some organs eg$ heart!$ protein mass
can decrease as much as :-E in the most serious #orms. The muscle #ibers are thin with
loss o# striation. Muscle cells are atrophic$ and muscle tissue is in#iltrated with #at and
#ibrous tissue. Total recovery is long but appears to be possible.
+ther organ mass: The brain$ s'eleton$ and 'idney are preserved$ whereas the liver$ heart$
pancreas$ and digestive tract are #irst a##ected.
Pediatric and adult physiologic change: Dinally$ physiologic changes are di##erent in
in#ants and children when compared with adults. Dor e<ample$ in#ants with marasmus
have an increased tendency to hypothermia and hypoglycemia$ re0uiring the #re0uent
administration o# small meals. This can be e<plained by the body composition imbalance
o# children with marasmus in #avor o# high(energyFconsuming organs$ such as the brain
and 'idney$ compared with energy(storage organs$ such as muscle and #at.
Assessment o# #at and muscle mass: As described below$ assessment o# the #at and
muscle mass loss can be clinically per#ormed by measuring arm or s'in#old thic'ness$
such as triceps s'in#old. The diagram illustrates the validity o# this assessment method.
7ecause arm circum#erence is relatively constant in healthy children aged .(4 years$ it
roughly represents a general assessment o# nutritional status.
Metabolic Changes
Potassium: Potassium is the electrolyte most studied in marasmus. Total body potassium
de#icit is associated with decreased muscle mass$ poor inta'e$ and digestive losses. This
potassium de#icit$ which can reach .4 m)0G'g$ contributes to hypotonia$ apathy$ and
impaired cardiac #unction.
+ther electrolytes: Plasma sodium concentration is generally within the re#erence range$
but it can be low$ which is then a sign o# a poor prognosis. 9owever$ intracellular sodium
level is elevated in the brain$ muscle$ and red and white blood cells$ e<plaining the
sodium e<cretion in the #irst days o# recovery.
+ther minerals: A de#icit in calcium$ phosphorus$ and magnesium stores is also observed.
"ron de#iciency anemia is consistently observed in marasmus. 9owever$ in the most
serious #orms$ iron accumulates in the liver$ most li'ely because o# the de#icit in transport
protein. These patients are at higher ris' o# mortality& there#ore$ iron is supplemented
only a#ter the acute recovery phase is completed. Hinc$ selenium$ and magnesium are
more signi#icantly reduced in 'washior'or but are also constantly de#icient in marasmus.
Several studies have shown improved recovery #rom malnutrition and decreased
mortality with supplementation o# these : micronutrients. A Cochrane review concluded
that 5inc supplementation is clearly o# bene#it in children aged 2 months or older with
diarrheal diseases in areas where these conditions are an important cause o# childhood
mortality.
@itamins: 7oth #at(soluble vitamins ie$ A$ A$ )$ K! and water(soluble vitamins eg$ 7(2$
7(.,$ #olic acid! must be systematically administered. @itamin A is essential to retinal
#unction$ has a trophic e##ect on epithelial tissues$ and plays a ma%or role as an
antio<idant agent. @itamin A de#icit a##ects visual #unction eg$ con%unctivitis$ corneal
ulcer$ night blindness$ total blindness! and digestive$ respiratory$ and urinary #unctions.
Durthermore$ vitamin A supplementation programs have resulted in decreased mortality
and morbidity$ in particular$ during diarrheal disease and measles.
@itamin and micronutrient de#iciencies can be di##erentiated in , categories listed below.
Patients with de#iciencies o# type . nutrients present with late and speci#ic clinical signs. "n
contrast$ patients with de#iciencies o# type , nutrients are di##icult to identi#y because blood
levels are unreliable and the clinical signs are nonspeci#ic$ such as the growth retardation with
mild de#iciency and weight loss with signi#icant de#iciency. Durthermore$ type , nutrient
de#iciencies are o#ten combined. There#ore$ these de#iciencies are global and re0uire a global
nutritional rehabilitation$ such as 69+ standardi5ed solution.
Metabolic Changes
The overall metabolic adaptations that occur during marasmus are similar to those in starvation$
which have been more e<tensively investigated. The primary goal is to preserve ade0uate energy
to the brain and other vital organs in the #ace o# a compromised supply. )arly on$ a rise in
gluconeogenesis leads to a perceived increased metabolic rate. As #asting progresses$
gluconeogenesis is suppressed to minimi5e muscle protein brea'down$ and 'etones derived #rom
#at become the main #uel #or the brain.
6ith chronic under#eeding$ the basal metabolic rate decreases. +ne o# the main adaptations to
long(standing energy de#iciency is a decreased rate o# linear growth$ yielding permanent
stunting. The energy saving is partially attenuated by the diversion o# energy #rom muscle to the
more metabolically active organs. Durther adaptations to crisis situations$ such as signi#icant
in#ections$ may have some parallels to those that are observed in a stressed$ malnourished animal
model.

The rise in energy e<penditure and urinary nitrogen e<cretion #ollowing surgery were
signi#icantly less in malnourished rats. This suggests that malnutrition can impair the ability o#
the organism to mobili5e substrates to respond to stress. 9owever$ the healing process in these
animals remained normal$ indicating the ability to prioriti5e this biological activity.
)nergy metabolism
o 6ith reduced energy inta'e$ a decrease in physical activity occurs #ollowed by a
progressively slower rate o# growth. 6eight loss initially occurs due to a decrease
in #at mass$ and a#terwards by a decrease in muscle mass$ as clinically measured
by changes in arm circum#erence
o Muscle mass loss results in a decrease o# energy e<penditure. Reduced energy
metabolism can impair the response o# patients with marasmus to changes in
environmental temperature$ resulting in an increased ris' o# hypothermia.
Durthermore$ during in#ection$ #ever is reduced compared to a well(nourished
patient. "n case o# nutrient de#iciency$ the metabolism is redirected to vital
#unction re0uiring 3-(.-- 'calG'gGd!. Auring recovery$ the energy cost o# catch(
up growth has to be added up to .-- 'calG'gGd!. At this stage$ energy needs can
be massive.
o Protein metabolism: "ntestinal absorption o# amino acids is maintained$ despite
the atrophy o# the intestinal mucosa. Protein turnover is decreased as much as
>-E in severe #orms!$ and protein(sparing mechanisms regulated by comple<
hormonal controls redirect amino acids to vital organs. Amino acids liberated
#rom catabolism o# muscle are recycled by the liver #or the synthesis o# essential
proteins. Total plasma proteins$ including albumin$ are decreased$ whereas
gamma globulins are o#ten increased by the associated in#ections.
o Albumin: An albumin concentration lower than :- gG1 is o#ten considered as the
threshold below which edema develops #rom decreased oncotic pressure.
9owever$ in marasmus$ albumin concentration can occasionally be below this
value without edema. Prealbumin concentration is a sensitive inde< o# protein
synthesis. "t decreases with decreased protein inta'e and rapidly increases in a
#ew days with appropriate nutritional rehabilitation. "nsulinli'e growth #actor .
"ID(.! is another sensitive mar'er o# nutritional status.
o Carbohydrate metabolism: This has mainly been studied in order to e<plain the
serious and o#ten #atal hypoglycemia that occurs in the initial renutrition phase o#
children with marasmus. The glucose level is o#ten initially low$ and the glycogen
stores are depleted. Also$ a certain degree o# glucose intolerance o# unclear
etiology is observed$ possibly associated with a peripheral resistance to insulin or
with hypo'alemia. "n the initiation o# renutrition or in association with diarrhea or
in#ection$ a signi#icant ris' o# pro#ound and even #atal hypoglycemia occurs.
Small and #re0uent meals are recommended$ including during the night$ to avoid
death in the early morning. Durthermore$ the digestion o# starch is impaired by the
decreased production o# pancreatic amylase. 1actose malabsorption is #re0uent
but is generally without clinical conse0uences. "n most cases$ renutrition using
mil' is possible.
o Dat metabolism: Aietary #ats are o#ten malabsorbed in the initial phase o#
marasmus renutrition. The mobili5ation o# #at stores #or energy metabolism ta'es
place under hormonal control by adrenaline and growth hormone. 7lood lipid
levels are usually low$ and serious dysregulation o# lipid metabolism can occur$
mainly during 'washior'or and rarely during marasmus.
Anatomic Changes
Aigestive tract
The entire digestive tract #rom mouth to rectum is a##ected. The mucosal sur#ace becomes
smooth and thin$ and secretory #unctions are impaired. A decrease in gastric hydrochloric acid
9Cl! e<cretion and a slowing o# peristalsis is observed$ yielding bacterial overgrowth in the
duodenum. Proportionally$ the digestive tract is the organ system that loses the largest mass
during marasmus. 9owever$ these important alterations o# the digestive tract inter#ere only
moderately with normal nutrient absorption. There#ore$ early enteral renutrition is not
contraindicated but is encouraged because some o# the nutrients necessary #or the recovery o# the
intestinal mucosa are used directly #rom the lumen.
"n addition to the anatomic changes associated with P)M$ the #re0uent intestinal in#ections by
viruses and bacteria and the to<ins they produce also contribute to the changes in the digestive
tract. 1iver volume usually decreases$ as do other organ volumes. An enlarged liver suggests the
possibility o# other diagnoses$ such as 'washior'or or hepatitis. 1iver synthetic #unction is
usually preserved$ although protein synthesis is decreased$ as re#lected by the decreased albumin
and prealbumin levels. Ilycogen synthesis is decreased$ #urther increasing the ris' #or
hypoglycemia. The deto<i#ying #unction o# the liver is impaired with structural changes in the
liver cells. There#ore$ drugs that are metaboli5ed by the liver should be administered with
caution$ and liver #unction should be monitored.
)ndocrine system
Many o# the adaptations seen in marasmus are mediated by thyroid hormones$ insulin$ and
growth hormone. As in any stressed state$ the adrenergic response is activated. This response is
#unctional in marasmus but less so in 'washior'or. Muscle proteins are converted into amino
acids and are used #or the hepatic synthesis o# lipoproteins. These lipoproteins contribute to the
mobili5ation o# triglycerides #rom the liver. "n contrast$ during 'washior'or$ this #unction is
impaired$ resulting in liver steatosis$ which is not usually present in marasmus. 9owever$ any
precipitating #actor$ such as gastroenteritis or inappropriate renutrition$ can disrupt this #ragile
adaptive mechanism.
Durthermore$ in serious marasmus$ a signi#icant degree o# hypothyroidism$ with a decrease in the
si5e o# the thyroid gland and repercussions on the brain #unction and psychomotor development
e<ists. "n less severe #orms$ the impaired thyroid #unction has #ewer clinical conse0uences.
"nsulin levels are low and contribute to a certain degree o# glucose intolerance$ especially during
'washior'or. There#ore$ high(carbohydrate diets are inappropriate. Irowth hormone levels are
initially within the re#erence range$ but they progressively decrease with time$ e<plaining the halt
in linear growth observed with marasmus.
A#ter initiation o# renutrition$ the hormonal milieu is reversed allowing #or substantial anabolism
and a rapid linear growth spurt. 9owever$ i# the marasmic state has gone on too long$ then the
adult height is less than the genetic potential. Recently$ investigators have obtained data that
suggest a role #or additional hormones in P)M. 1evels o# serum gherlinan appetite stimulating
peptide! were increased

and serum levels o# leptin a satiety hormone! and "ID(. were decreased
in children with P)M compared with healthy controls.
J.-K
9ematopoietic system
A moderate normochromic or slightly hypochromic anemia is usually present$ with normal R7C
si5e. "ron and #olate de#iciencies$ intestinal parasites$ malaria$ and other chronic in#ections
e<acerbate the anemia. 9owever$ iron stores are present in the liver. There#ore$ iron
supplementation should not be initially implemented. +ral iron is poorly tolerated by the
digestive tract. The other blood cells eg$ thrombocytes$ 67Cs! are also a##ected$ but with
generally limited clinical conse0uences. 7lood clotting mechanisms are usually preserved$
e<cept in the case o# serious vitamin K de#iciency.
"mmune system
"mmune impairment and in#ections are usually associated with marasmus. Thymus atrophy is a
characteristic mani#estation o# marasmus$ but all T lymphocyteFproducing tissues are a##ected.
9owever$ 7(lymphocyte tissues$ such as Peyer patches$ the spleen$ and the tonsils$ are relatively
preserved. Cellular immunity is most a##ected$ with a characteristic tuberculin anergy. 9owever$
antibody production is maintained. "n marasmus$ a general ac0uired immunode#iciency occurs$
with a decrease in secretory immunoglobulin A "gA! and an impairment o# the nonspeci#ic local
de#ense system$ such as mucosal integrity and lympho'ine production. 7acteriemia$ candidiasis$
andPneumocystis carinii in#ection are #re0uently present. "mmune impairment is less #re0uent
with moderate malnutrition. "mmunological recovery is generally rapid$ e<cept i# measles is
associated.
7rain and nervous system
Cerebral tissue is usually preserved during marasmus. 7rain atrophy with impairment o# cerebral
#unctions is only present in severe #orms o# marasmus. )##ects on the brain are more important i#
malnutrition ta'es place during the #irst year o# li#e or during #etal li#e. "rritability and apathy are
characteristic o# marasmus but improve rapidly with recovery. The permanent developmental
conse0uences o# marasmus are di##icult to evaluate. +ngoing studies are evaluating these long(
term conse0uences$ as well as the bene#it o# nutritional supplementation with various vitamins
and minerals.
Cardiovascular system
Cardiac muscle #iber is thin$ and the contractility o# the myo#ibrils is impaired. Cardiac output$
especially systolic #unction$ is decreased in the same proportion as the weight loss. 7radycardia
and hypotension commonly occur in severe #orms o# malnutrition. )lectrolyte imbalances
present during marasmus modi#y the )CI #indings. 6ith this impaired cardiac #unction$ any
increase o# intravascular volume during rehydration or blood trans#usion can result in a
signi#icant cardiac insu##iciency. 6ith the rapid metabolic$ energy$ and electrolyte changes o# the
initial phase o# renutrition$ this period is also a period o# high ris' #or arrhythmia or cardiac
arrest. There#ore$ close clinical monitoring is critical in children with circulatory compromise.
Aiagnostics
The condition o# P)M is o#ten li'ened to an iceberg$ o# which ,- percent is visible above the
water and about 3- percent submerged. The severe #orms o# P)M ( 'washior'or$ nutritional
marasmus and marasmic 'washior'or ( constitute the top$ e<posed part o# the iceberg: they are
relatively easy #or a doctor or health wor'er to diagnose simply #rom their clinical
mani#estations$ described below. +n the other hand$ children with moderate or mild malnutrition
o#ten do not have clear clinical mani#estations o# malnutrition& rather$ they are shorter andGor
thinner than would be e<pected #or their age$ and they may have de#icits in psychological
development and perhaps other signs not easy to detect. Mild and moderate P)M are diagnosed
mainly on the basis o# anthropometry$ especially using measurements o# weight and height and
sometimes other measurements such as arm circum#erence or s'in#old thic'ness 1atham$ .BBC!.
A shrun'en wasted appearance is the classic presentation o# marasmus. Anthropometric
measurements are critical to rapidly assess the type and severity o# the malnutrition. The
6ellcome Classi#ication o# Malnutrition in Children was generally used$ but the 69+ has
revised this classi#ication see the table below!. This simple classi#ication allows a clear
presentation o# the clinical cases and allows comparisons between countries. Stunted children are
usually considered to have a milder chronic #orm o# malnutrition$ but their condition can rapidly
worsen with the onset o# complications such as diarrhea$ respiratory in#ection$ or measles.
The most perceptible and #re0uent clinical #eature in marasmus is the loss o# muscle mass and
subcutaneous #at mass. Some muscle groups$ such as buttoc's and upper limb muscles$ are more
#re0uently a##ected than others. Dacial muscles are usually spared longer. Dacial #at mass is the
last to be lost$ resulting$ in severe cases$ in the characteristic elderly appearance o# children with
marasmus. Anore<ia is #re0uent and inter#eres with renutrition. An irritable and whining child
who cannot be com#orted or separated #rom the mother demonstrates behaviours o#ten observed
with marasmus. Apathy is a sign o# serious #orms o# marasmus: children are increasingly
motionless and seem to Llet themselves die.L "n contrast$ during rehabilitation$ even the slightest
smile is a positive sign o# recovery. Children/s behaviour is probably one o# the best clinical
signs o# the severity and evolution o# marasmus.
Several clinical signs must be assessed in order to detect complications$ with special attention to
in#ectious complications see chec'list below!. The physical e<amination must be very thorough
because even small abnormalities can be clinically signi#icant. Clinical signs o# serious
complication can be very subtle in children with marasmus. A body temperature o# :C.4MC can
correspond to a #ever o# :B(>-MC in a child without marasmus$ and a small cough can be the only
sign o# a serious pneumonia. A#ter history and physical e<amination$ diagnosing the type and
severity o# the malnutrition$ as well as diagnosing associated in#ections and complications
a##ecting organs or systems$ such as the I"$ neurological$ or cardiovascular system$ are critical.
This set o# diagnoses results in optimal planning o# the complementary evaluation and
therapeutic strategy.
Chec'list o# points #or conducting the physical e<amination
o Body temperature (measured with a thermometer) ( Allowing measurement o# low
temperatures to detect hypothermia as well as #ever
o Anemia ( Pale mucosa
o Edema
o Dehydration ( Thirst$ shrun'en eyes
o Hypovolemic shock ( 6ea' radial pulse$ cold e<tremities$ decreased consciousness
o Tachypnea ( Pneumonia$ heart #ailure
o Abdominal manifestations ( Aistension$ decreased or metallic bowel sounds$ large or
small liver$ blood or mucus in the stools
o Ocular manifestations ( Corneal lesions associated with vitamin A de#iciency
o Dermal manifestations ( )vidence o# in#ection$ purpura
o Ear nose and throat (E!T) findin"s ( +titis$ rhinitis
Ienerally$ #or diagnosis and treatment o# marasmus$ no #urther evaluation is necessary other than
the clinical evaluation. Most laboratory results are within the re#erence range despite signi#icant
changes in body composition and physiology. Durthermore$ in regions where malnutrition is
#re0uent$ health structures are poorly e0uipped$ and laboratory evaluations are either impossible
to obtain or unreliable.
"# they are available$ some laboratory results can be use#ul to monitor treatment or to diagnose
speci#ic complications.
1aboratory tests adapted #rom the 69+ include the #ollowing:
7lood glucose: 9ypoglycemia is present i# the level is lower than : mmolG1.
)<amination o# blood smears by microscopy or direct detection test: Presence o# parasites
is indicative o# in#ection. Airect test is suitable but e<pensive.
9emoglobin: A level lower than >- gG1 is indicative o# severe anemia.
?rine e<amination and culture$ Multisti<: More than .- leu'ocytes per high(power #ield is
indicative o# in#ection. 8itrites and leu'ocytes are tested on Multisti< also.
Stool e<amination by microscopy: Parasites and blood are indicative o# dysentery.
Albumin: Although not use#ul #or diagnosis$ it is a guide to prognosis& i# albumin is lower
than :4 gG1$ protein synthesis is massively impaired.
9"@ test: 9"@ test should not be routinely per#ormed& i# completed$ it should be
accompanied by counseling o# the child/s parents and the result should be con#idential.
)lectrolytes: Measuring electrolytes is rarely help#ul and it may lead to inappropriate
therapy. 9yponatremia is a signi#icant #inding.
Radiological e<aminations are rarely used #or the same reasons as the laboratory e<aminations.
Thoracic radiography can show a pulmonary in#ection despite lac' o# clinical signs$ a primary
tuberculosis lesion$ cardiomegaly$ or signs o# rachitism.
S'in test results #or tuberculosis are o#ten negative in children who are undernourished with
tuberculosis or those previously vaccinated with 7acille Calmette(IuNrin 7CI! vaccine
Rabinowit5 et al$ ,-.>!.
Management
Management o# moderate marasmus can be per#ormed on an outpatient basis$ but severe
marasmus or marasmus complicated by a li#e(threatening condition generally re0uires inpatient
treatment. "n these cases$ management is divided into an initial intensive phase #ollowed by a
consolidation phase rehabilitation!$ preparing #or outpatient #ollow(up management. The 69+
has developed guidelines to help improve the 0uality o# hospital care #or malnourished children
and has prioriti5ed the widespread implementation o# these guidelines.
The guidelines highlight .- steps #or routine management o# children with malnutrition$ as
#ollows:
..TreatGprevent hypoglycaemia
,.TreatGprevent hypothermia
:.TreatGprevent dehydration
>.Correct electrolyte imbalance
4.TreatGprevent in#ection
2.Correct micronutrient de#iciencies
C.Start cautious #eeding
3.Achieve catch(up growth
B.Provide sensory stimulation and emotional support
.-. Prepare #or #ollow(up a#ter recovery
These steps are accomplished in two phases: an initial stabilisation phase where the acute
medical conditions are managed& and a longer rehabilitation phase. 8ote that treatment
procedures are similar #or marasmus and 'washior'or. The appro<imate time(scale is given in
the bo< below Ashworth$ ,--:!:
Prognosis
)<cept #or complications mentioned above$ prognosis o# even severe marasmus is good i#
treatment and #ollow(up care are correctly applied Rabinowit5 et al$ ,-.>!.
,., Tuberculosis
Ae#inition
Tuberculosis$ or T7$ is an in#ectious bacterial disease caused by Mycobacterium tuberculosis$
which most commonly a##ects the lungs. "t is transmitted #rom person to person via droplets #rom
the throat and lungs o# people with the active respiratory disease. 6ho."nt$ ,-.>!
)tiology
According 9erchline and Amorosa ,-.>!$ T7 is caused by M.tuberculosis, a slow(growing
obligate aerobe and a #acultative intracellular parasite. The organism grows in parallel groups
called cords as seen in the image below!. "t retains many stains a#ter decoloration with acid(
alcohol$ which is the basis o# the acid(#ast stains used #or pathologic identi#ication.
Mycobacteria$ such as M.tuberculosis$ are aerobic$ nonFspore(#orming$ non(motile$ #acultative$
curved intracellular rods measuring -.,(-.4 ;m by ,(> ;m. Their cell walls contain mycolic$
acid(rich$ long(chain glycolipids and phospholiglycans mycocides! that protect mycobacteria
#rom cell lysosomal attac' and also retain red basic #uchsin dye a#ter acid rinsing acid(#ast
stain!.
)pidemiology
Morbidity and mortality associated with T7 are greatest in developing nations$ where B4E o# all
cases and B3E o# all deaths associated with T7 occurred in .BB-. The highest prevalence and
estimated annual ris' o# in#ection are #ound in Southeast Asia rate$ ,:C per .--$---! and sub(
Saharan A#rica rate$ .B. per .--$---! . +# the :.: million cases o# T7 noti#ied to the 6orld
9ealth +rgani5ation in .BB4$ C3E were #rom Asia$ sub(Saharan A#rica$ and island regions. 7y
contrast$ during these same time periods$ industriali5ed countries 6estern )urope$ Australia$
Canada$ *apan$ 8ew Healand$ and ?nited States! had an average annual incidence o# ,: per
.--$--- and accounted #or only >E o# total noti#ied cases.
Aistinct di##erences in the epidemiology o# T7 are observed between developing and
industriali5ed nations. "n countries where the standard o# living is low and health resources are
scarce$ the ris' o# recent in#ection is high and 3-E o# cases involve persons in their productive
years .4F4B years o# age!. "n economically developed countries where progressive declines in
the incidence o# T7 have been achieved$ the annual ris' o# in#ection is low. The ma%ority o# T7
cases arise as a result o# endogenous reactivation o# remote in#ection ac0uired when T7 was
more prevalent& this results in disease rates highest in the elderly O24 years o# age!. Active
disease mani#esting in younger patients usually arises in racial and ethnic minorities or in
association with human immunode#iciency virus 9"@! in#ection 1eung$ .BBB!.
Pathogenesis
M. tuberculosis$ the in#ectious agent o# T7$ is a thin$ slightly curved bacillus that is an obligate
aerobe. "n comparison to other bacteria$ M tuberculosis has a cell wall with a very high lipid
content that resists staining by the usual Iram method. 9owever$ it accepts basic #uchsin dyes
and is not easily decolori5ed even with acid(alcohol& this resistance to decolori5ation by acid(
alcohol is termed acid(#ast. As this property is shared only by members o# the mycobacterial
#amily and a #ew other organisms Nocardia$ Rhodococcus$ and Corynebacterium species!$ it
#orms the basis #or the simple$ rapid$ and relatively speci#ic traditional techni0ue o# identi#ication
by means o# an acid(#ast smear.
M. tuberculosis is transmitted via airborne droplet nuclei that are produced when persons with
pulmonary or laryngeal T7 cough$ snee5e$ spea'$ or sing. The particles$ which measure .F4 ;m
in si5e$ can be 'ept airborne by normal air currents #or prolonged periods o# time$ resulting in
dispersion throughout a room or building. The presence o# acid(#ast bacilli in the sputum smear
is the main indicator o# potential #or transmission& other source patient characteristics that
increase the probability o# transmission include positive sputum culture #or M tuberculosis$
presence o# cavitation on the chest radiograph$ presence o# T7 laryngitis$ and high(volume and
watery respiratory secretions.
"n#ection occurs when a susceptible person inhales droplet nuclei that contain tubercle bacilli. As
the distribution o# inhaled droplet nuclei is determined by the ventilatory pattern and volumes o#
the various lung lobes$ the site o# implantation pre#erentially occurs in the middle and lower lung
5ones$ although any lobe may be a##ected. +nce lodged in the alveolus$ M tuberculosis is
ingested by alveolar macrophages. Resistance to establishment o# tuberculous in#ection is 'nown
to be under genetic control$ and the course o# in#ection depends on the interaction between the
inherent microbicidal power o# the alveolar macrophage and the virulence o# the ingested
bacillus. "# the alveolar macrophage cannot destroy or inhibit M.tuberculosis$ the bacilli multiply
within its intracellular environment$ causing the host macrophage or its progeny to burst. The
cycle continues as released bacilli are ingested by other alveolar macrophages and monocytes are
recruited #rom the blood. Auring this period o# rapid growth$ tubercle bacilli are spread through
lymphatic channels to regional hilar and mediastinal lymph nodes and through the bloodstream
to more distant sites in the body. The logarithmic phase o# bacillary growth is arrested with the
development o# cell(mediated immunity and delayed(type hypersensitivity at ,F.- wee's a#ter
the initial in#ection
Aevelopment o# speci#ic immunity is usually ade0uate to limit #urther multiplication o# the
bacilli& the host remains asymptomatic& and the lesions heal. Some o# the bacilli remain dormant
and viable #or many years$ and this conditionPre#erred to as latent T7 in#ectionPmay be
detectable only by means o# a positive puri#ied protein derivative tuberculin s'in test or
radiologically identi#iable calci#ication at the site o# the primary lung in#ection or in regional
lymph nodes. "n appro<imately 4E o# in#ected individuals$ immunity is inade0uate and clinically
active disease develops within . year o# in#ection& in another 4E o# the in#ected population$
endogenous reactivation o# latent in#ection occurs remote #rom time o# initial in#ection 1eung$
.BBB!.
Aiagnostics
According to the 6orld 9ealth +rgani5ation ,-.:!$ the ris' #or T7 is increased when there is an
active case in#ectious$ smear(positive pulmonary T7! in the same house or when the child is
malnourished$ has 9"@GA"AS or had measles in the past #ew months. Consider T7 in any child
with:
A history o#:
une<plained weight loss or #ailure to grow normally
une<plained #ever$ especially when it continues #or longer than , wee's
chronic cough i.e. cough #or Q .> days$ with or without a whee5e!
e<posure to an adult with probable or de#inite in#ectious pulmonary T7.
+n e<amination:
#luid on one side o# the chest reduced air entry$ stony dullness to percussion!
enlarged non(tender lymph nodes or a lymph node abscess$ especially in the nec'
signs o# meningitis$ especially when these develop over several days and the spinal #luid
contains mostly lymphocytes and elevated protein
abdominal swelling$ with or without palpable lumps
progressive swelling or de#ormity in the bone or a %oint$ including the spine
"nvestigations
Try to obtain specimens #or microscopic e<amination o# acid(#ast bacilli Hiehl(8eelsen
stain! and #or culture o# tubercle bacilli. Possible specimens include three consecutive
early(morning$ #asting gastric aspirates$ CSD i# clinically indicated! and pleural #luid
and ascites #luid i# present!. As the detection rates with these methods are low$ a
positive result con#irms T7$ but a negative result does not e<clude the disease.
8ew rapid diagnostic tests are more accurate and may be more widely available in
#uture.
+btain a chest R(ray. A diagnosis o# T7 is supported when a chest R(ray shows a
miliary pattern o# in#iltrates or a persistent area o# in#iltrate or consolidation$ o#ten with
pleural e##usion$ or a primary comple<.
Per#orm a puri#ied protein derivative s'in test PPD or mantoux test!. The test is usually
positive in children with pulmonary T7 reactions o# Q .- mm suggest T7& S .- mm in a
child previously vaccinated with 7CI is e0uivocal!. The puri#ied protein derivative test
may be negative in children with T7 who have 9"@GA"AS$ miliary disease$ severe
malnutrition or recent measles.
Rpert MT7GR"D should be used as the initial diagnostic test in children suspected o#
having multidrug(resistant T7 MAR(T7! or 9"@(associated T7.
Routine 9"@ testing should be o##ered to all children suspected o# T7.
Management
Iive a #ull course o# treatment to all con#irmed or strongly suspected cases.
6hen in doubt$ e.g. in a child with strongly suspected T7 or who #ails to respond to
treatment #or other probable diagnoses$ give treatment #or T7.
Treatment #ailures #or other diagnoses include antibiotic treatment #or apparent bacterial
pneumonia when the child has pulmonary symptoms!$ #or possible meningitis when the child
has neurological symptoms! or #or intestinal worms or giardiasis when the child #ails to thrive or
has diarrhoea or abdominal symptoms!.
Suspected or con#irmed childhood T7 should be treated with a combination o# anti(T7
drugs$ depending on the severity o# disease$ 9"@ status and level o# isonia5id resistance.
Dollow the national T7 programme guidelines #or recommended treatment.
To reduce the ris' #or drug(induced hepatoto<icity in children$ #ollow the recommended
dosages:
F "sonia5id 9!: .- mgG'g range$ .-F.4 mgG'g!& ma<imum dose$ :-- mgGday
F Ri#ampicin R!: .4 mgG'g range$ .-F,- mgG'g!& ma<imum dose$ 2-- mgG 'g per day
F Pyra5inamide H!: :4 mgG'g range$ :-F>- mgG'g!
F )thambutol )!: ,- mgG'g range$ .4F,4 mgG'g!.
"# national recommendations are not available$ #ollow the 69+ guidelines according to the
regimens given below:
Four-drug regimen: 9RH) #or , months$ #ollowed by a two(drug 9R! regimen #or >
months #or all children with suspected or con#irmed pulmonary T7 or peripheral
lymphadenitis living in an area o# high 9"@ prevalence or where resistance to 9 is high
or children with e<tensive pulmonary disease living in areas o# low 9"@ prevalence or
low 9 resistance&
Three-drug regimen: 9RH #or , months$ #ollowed by a two(drug 9R! regimen #or >
months #or children with suspected or con#irmed pulmonary T7 or tuberculous
peripheral lymphadenitis living in areas o# low 9"@ prevalence or low 9 resistance or
9"@(negative&
"n cases o# suspected or con#irmed tuberculous meningitis$ spinal T7 with neurological
signs or osteo(articular T7$ treat #or ., months with a #our drug regimen 9RH)! #or ,
months$ #ollowed by a two(drug 9R! regimen #or .- months&
"n in#ants aged -F: months! with suspected or con#irmed pulmonary T7 or tuberculous
peripheral lymphadenitis$ treat promptly with the standard regimens described above$
with ad%ustment o# doses to reconcile the e##ect o# age and possible to<icity in young
in#ants.
ntermittent regimens: "n areas with well(established directly observed therapy$ thrice(wee'ly
regimens can be considered #or children 'nown to be 9"@(negative. They should not be used in
areas with a high 9"@ prevalence$ because there is a high ris' o# treatment #ailure and
development o# multidrug(resistant T7.
Precautions: Streptomycin should not be used as part o# #irst(line treatment regimens #or children
with pulmonary T7 or tuberculous peripheral lymphadenitis. "t should be reserved #or the
treatment o# multidrug(resistant T7 in children with 'nown susceptibility to this medicine
6orld 9ealth +rgani5ation$ ,-.:!.
Prognosis
Dull resolution is generally e<pected with #ew complications in cases o# non(MAR( and non(
RAR(T7$ when the drug regimen is completed. Among published studies involving A+T
treatment o# T7$ the rate o# recurrence ranges #rom -(.>E.

"n countries with low T7 rates$
recurrences usually occur within ., months o# treatment completion and are due to relapse.

"n
countries with higher T7 rates$ most recurrences a#ter appropriate treatment are probably due to
rein#ection rather than relapse.
Poor prognostic mar'ers include e<trapulmonary involvement$ an immunocompromised state$
older age$ and a history o# previous treatment. "n a prospective study o# .BB patients with T7 in
Malawi$ ., 2E! died. Ris' #actors #or dying were reduced baseline T8D(T response to
stimulation with heat('illed M tuberculosis!$ low body mass inde<$ and elevated respiratory rate
at T7 diagnosis 9erchline and Amorosa$ ,-.>!.
C9APT)R :
CAS) R)P+RT
#ase
R6 is a : years and 3 months old boy. 9e was brought to Adam Mali' Ieneral 9ospital on
the .4th o# March ,-.> with the main complain o# decreased body weight. 9e has been
e<periencing this condition #or the past 4 months be#ore being admitted. 9is current weight and
height is B'g and 3Bcm respectively& his ma<imum body weight was ..$4'g. "n the past 4
months$ his appetite also decreased. The patient consumed a small amount o# #ood during this
period. 7e#ore becoming ill$ R6 could consume 2 spoons o# rice$ a small #ist#ul o# sardines or
either one chic'en #oot or head i# the side dish is chic'en. 9e currently has no #ever or diarrhea
and no history o# #ever and diarrhea. 9e did vomit twice in the past day volume : .-mlG< $
yellow$ li0uid!. The patient is currently having cough. The cough is productive and he has had it
#or the past : wee's. There is no history o# the patient being in contact with an adult su##ering
#rom chronic cough. Currently when the patient cries$ there are tears. 9e is pale and has been #or
the past : wee's. The patient has had C pints o# blood trans#used.
$mmuni%ation history : Complete
&rowth history : 7e#ore he became ill$ the patient was able to wal'. Currently he is unable to
wal'. 9e is able to tal' normally.
'eedin" history : - F ,$4 years : 7reast mil'
2 F 3 months : Strained porridge
3 F B months : Porridge$ breast mil'
,$4 years Fnow : 8ormal #ood
History of previous illnesses( Mantou< test results - mm
History of previous medication: 8ot clear
)hysical E*amination :
Consciousness: Compos mentis 7ody temperature : :C.-UC
Anemic (! "cteric (! Cyanosis (! Ayspnea (! )dema (!
76GAge: 42.,4E
76G79: 2B.,:E
79GAge: 3B.--E
.. 9ead: +ld man #ace V!$ )ye: 1ight Re#le< VGV!$ "sochoric pupil$ Pale in#erior palpebral
con%unctiva (!$ )G8: normal$ Mouth: +ral thrush
,. 8ec': 1ymph node enlargement (!
:. Thora<: Symmetrical #usi#ormis$ retraction (!$ )asily seen ribs V!
9R: .,- bpm$ regular$ murmur (!
RR: ,, <Gminute$ regular$ ronchi (G(!$ stridor V!
>. Abdomen: Soepel$ Peristaltic V! normal$ 1iverGSpleen: 8ot palpable
4. )<tremities: Pulse .,- bpm$ regular$ ade0uate vascular pressure and volume$ warm
e<tremities$ CRTS :W
+orkin" Dia"nosis : Marasmus V 7ronchopneumonia
Differential Dia"nosis : Marasmus V 7ronchopneumonia
Treatment
Three way
Dolic ac. .< 4 mg$ continuation .< .mg
Multivitamin without iron .< . cth
@itamin A .< ,--.-- "? ta'en once!
"n%. Ampicilin ,,4 mgG2 hrsG "@
Aiet DC4 BCccG, hrsG 8ITV Mineral mi< ..Bcc
,aboratory 'indin"s
-
'ollow up . /0
th
1arch 23/4
S: 6eight loss
+: Sense: CM T: :CUC
Anemia (!$ icteric (!$ cyanosis (!$ dyspnea (! edema (!
9ead: +ld man #aceV!$ )yes 1R VGV!$ isochoric pupil$ Pale in#erior palpebral con%unctiva (!$
)G8: 8ormal M: oral thrush
8ec': 18 enlargement (!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: .,-<Gi$ reg$ murmur (!
RR: ,><Gi$ reg$ rhonchi (!$ stridor V!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable$ ascites$ umbilicus smile V!
)<tremities: Pulse .,-<Gi$ regular$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ baggy pants V!
A: Marasmus V bronchopneumonia
P: Three way
Dolic ac. .< 4 mg$ continuation .< .mg
Multivit. wGo iron .< . cth
@it. A .< ,--.-- "? ta'en once!
"n%. Ampicilin ,,4 mgG2 hrsG "@
Aiet DC4 BCccG, hrsG 8ITV Mineral mi< ..Bcc
'ollow up- /5
th
1arch 23/4
S: Cough V!$ Dever (!
+: Sense: CM$ T: :CUC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8: 8ormal
M: oral thrush
8ec': 18 enlargement (!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: ..-<Gi$ reg$ murmur (!
RR: ,2<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable$ ascites$ umbilicus smile V!
)<tremities: Pulse ..-<Gi$ regular$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!
A: Marasmus V bronchopneumonia
P: Dolic ac. .< . mg
Multivit. wGo iron .< . cth
"n%. Ampicillin ,,4 mgG2 hrsG "@
Aiet DC4 BCccG, hrsG 8ITV Mineral mi< ..Bcc
'ollow up- /6
th
1arch 23/4
S: Cough V!$ Dever (!
+: Sense: CM T: :C.,UC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8: 8
M: +ral thrush
8ec': 18 enlargement (!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: ..2<Gi$ reg$ murmur (!
RR: ,><Gi$ reg$ rhonchi (!$ stridor V!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse ..2<Gi$ regular$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!
A: Marasmus V bronchopneumonia
P: Three way
Dolic ac. .< .mg
Multivit. wGo iron .< . cth
"n%. Ampicilin ,,4 mgG2 hrsG "@
Aiet DC4 .>- ccG: hrsG 8ITV Mineral mi< ..Bcc
'ollow up- /7
th
1arch 23/4
S: Cough V!$ Dever (!
+: Sense: CM T: :C.,UC
9ead: +ld man #ace V!$ )yes 1R VGV!$ pale in#erior palpebral con%unctiva (!$ isochoric
pupil )G8G: 8ormal$ M: +ral thrush
8ec': 18 enlargement (!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: .-><Gi$ reg$ murmur (!
RR: ,3<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse .-><Gi$ regular$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ baggy pants V!
A: Marasmus V bronchopneumonia
P: Three way
Dolic ac. .< . mg
Multivit. wGo iron .< . cth
"n%. Ampicillin ,,4 mgG2 hrsG "@
Aiet DC4 .>-ccG: hrsG 8ITV Mineral mi< ..Bcc
'ollow up- /8
th
1arch 23/4
S: Cough (!$ Dever (!
+: Sense: CM T: :CUC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8$
8ec': 18 enlargement (!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: .-><Gi$ reg$ murmur (!
RR: ,B<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse .,-<Gi$ regular$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!
A: Marasmus V bronchopneumonia
P: Three way
Dolic ac. .< . mg
Multivit. wGo iron .< . cth
"n%. Ampicillin ,,4 mgG2 hrsG "@
Aiet DC4 .>-ccG: hrsG 8ITV Mineral mi< ..Bcc
'ollow up- 23
th
1arch 23/4
S: Cough V!$ Dever (!
+: Sense: CM T: :CUC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8$
8ec': 18 enlargement (!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: .--<Gi$ reg$ murmur (!
RR: ,2<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse .--<Gi$ regular$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!
A: Marasmus V bronchopneumonia
P: Three way
Dolic ac. .< . mg
Multivit. wGo iron .< . cth
"n%. Ampicilin ,,4 mgG2 hrsG "@
Aiet DC4 .>-ccG: hrsG 8ITV Mineral mi< ..Bcc
'ollow up- 2/
st
1arch 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :CUC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8
8ec': 18 enlargement V!$ sinistra :cm < 4cm$ pain upon palpating (!$ hyperemia (!$
immobile
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: .--<Gi$ reg$ murmur (!
RR: ,2<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse .--<Gi$ regular$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ enlargement o# a<illary 18 V! :cm < :cm
A: Marasmus V bronchopneumonia
P: Three way
Dolic ac. .< .mg
Multivit. wGo iron .< . cth
"n%. Ampicillin ,,4 mgG32 hrsG "@
Aiet DC4 .>-ccG: hrsG 8ITV Mineral mi< ..Bcc
,aboratory 9esult- 2/
st
1arch 23/4
$11:!ODE'$#$E!#; )9O'$,E
Anti H$< (= 1ethode) 8on(reactive 8on(reactive
Anti H$< (9apid /) 8on(reactive 8on(reactive
Anti H$< (9apid 2) 8on(reactive 8on(reactive
Anti H$< (9apid =) 8on(reactive 8on(reactive
'ollow up- 22
nd
1arch 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :2.CUC
9ead: )yes 1R VGV!$ isochoric pupil$ con%.palp.in# pale (!$ )G8GM: 8$
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: .,-<Gi$ reg$ murmur (!
RR: :-<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse .,-<Gi$ regular$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ subcutaneous #at thinning V!
A: Marasmus V bronchopneumonia
P: Three way
Dolic ac. .< . mg
Multivit. wGo iron .< . cth
"n%. Ampicilin ,,4 mgG2 hrsG "@
Aiet D.-- .2-ccG: hrsG 8ITV Mineral mi< :., cc
'ollow up- 2=
rd
1arch 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :2.4UC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8$
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: B2<Gi$ reg$ murmur (!
RR: ,2<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse B2<Gi$ regular$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!
A: Marasmus V bronchopneumonia
P: Three way
Dolic ac. .< . tab
Multivit. wGo iron .< . cth
"n%. Ampicilin ,,4 mgG2 hrsG "@
Aiet D.-- .2-ccG: hrsG 8ITV Mineral mi< :.,cc
'ollow up- 24
th
1arch 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :C.,UC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: B2<Gi$ reg$ murmur (!
RR: ,,<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse B2<Gi$ regular$ ade0uate pGv$ warm e<tremities$ CRT S:W
A: Marasmus V bronchopneumonia
P: Three way
Dolic ac. .< . tab
Multivit. wGo iron .< . cth
"n%. Ampicillin ,,4 mgG2 hrsG "@
Aiet D.-- .2-ccG, hrsG 8ITV Mineral mi< :., cc
'ollow up- 20
th
1arch 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :CUC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: .,-<Gi$ reg$ murmur (!
RR: :-<Gi$ reg$ rhonchi (!$ stridor V!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse .,-<Gi$ regular$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ subcutaneous #at thinning V!$ baggy pants V!
9asil D8A7 : Suatu proses radang 'roni' spesi#i' yang la5im pada tuber'ulosa
A: Marasmus V bronchopneumonia
P: Three way
Dolic ac. .< .tab
Multivit. wGo iron .< . cth
"n%. Ampicillin ,,4 mgG2 hrsG "@
Aiet D.-- .3-ccG: hrsG 8ITV Mineral mi< :.2cc
'ollow up- 25
th
1arch 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :C.,UC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: ..-<Gi$ reg$ murmur (!
RR: ,2<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse ..-<Gi$ regular$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ subcutaneous #at thinning V!$ baggy pants V!
A: Marasmus V bronchopneumonia
P: Three way
Multivit. wGo iron .< . cth
"n%. Ampicillin ,,4 mgG2 hrsG "@
Aiet D.-- .--ccG: hrsG 8ITV Mineral mi< :.2cc
'ollow up- 26
th
1arch 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :CUC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: B-<Gi$ reg$ w (!
RR: ,2<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse B-<Gi$ reg$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ subcutaneous #at thinning V!$ baggy pants V!
A: Marasmus V bronchopneumonia
P: Three way g
Multivit. wGo iron .< . cth
"n%. Ampicillin ,,4 mgG2 hrsG "@
Aiet M7 3--'cal V D.-- ,--ccG 3 hours
Rimcure Paed . < , tab
'ollow up- 27
th
1arch 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :CUC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: .,2<Gi$ reg$ murmur (!
RR: :-<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse .,2<Gi$ regular$ ade0uate pGv$ warm e<tremities$ CRT S: muscle
hypotrophy V!$ subcutaneous #at thinning V!$ baggy pants V!
A: Marasmus V Pulmonary tuberculosis
P: Three way
Multivit. wGo iron .< . cth
Aiet M7 3-- ''al V D.-- ,--ccG3 hrs
Rimcure Paed . < , tab
'ollow up- 28
th
1arch 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :CUC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: .,2<Gi$ reg$ murmur (!
RR: :-<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse .,2<Gi$ reg$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ subcutaneous #at thinning V!$ baggy pants V!
A: Marasmus V Pulmonary tuberculosis
P: Three way
Multivit. wGo iron .< . cth
Aiet M7 .--- ''al V D.-- ,--ccG3 hrs
Rimcure Paed . < , tab
'ollow up- =3
th
1arch 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :C.,UC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: .,><Gi$ reg$ murmur (!
RR: :,<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse .,><Gi$ reg$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ subcutaneous #at thinning V!$ baggy pants V!
A: Marasmus V Pulmonary tuberculosis
P: Three way
Multivit. wGo iron .< . cth
Aiet M7 .--- ''al V D.-- ,--ccG3 hrs
Rimcure Paed . < , tab
'ollow up- =/
st
1arch 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :CUC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: ..3<Gi$ reg$ murmur (!
RR: :-<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse .,-<Gi$ reg$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ subcutaneous #at thinning V!$ baggy pants V!
A: Marasmus V Pulmonary tuberculosis
P: Three way
Rimcure Paed .< .tab
Multivit. wGo iron .< . cth
Aiet M7 .--- ''al V D.-- ,--ccG3 hrs
'ollow up- /
st
April 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :C.,UC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: B,<Gi$ reg$ murmur (!
RR: :-<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse B,<Gi$ reg$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ subcutaneous #at thinning V!$ baggy pants V!
A: Marasmus V Pulmonary tuberculosis
P: Three way
Multivit. wGo iron .< . cth
Aiet M7 .--- ''al V D.-- ,--ccG3 hrs
Rimcure Paed . < , tab
'ollow up- 2
nd
April 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :CUC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: .--<Gi$ reg$ murmur (!
RR: ,3<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse .--<Gi$ reg$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ subcutaneous #at thinning V!$ baggy pants V!
A: Marasmus V Pulmonary tuberculosis
P: Three way
Rimcure Paed .< , tab
Multivit. wGo iron .< . cth
Aiet M7 .--- ''al V D.-- ,--ccG3 hrs V Mineral Mi< >.-cc
'ollow up- =
rd
April 23/4
S: Dever (!$ "tchiness (!
+: Sense: CM T: :CUC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: B,<Gi$ reg$ murmur (!
RR: ,2<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse B,<Gi$ reg$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ subcutaneous #at thinning V!$ baggy pants V!
A: Marasmus V Pulmonary tuberculosis
P: Three way
Rimcure Paed .< , tab
Cetiri5in syr .< . cth
Aiet M7 .--''al V D.-- ,,-ccG3 hrs V Mineral mi< >.> cc
,aboratory 9esults- =
rd
April 23/4
#O1),ETE B,OOD #O:!T
Hemo"lobin (H&B) gE .-.B- ...:(-.>..
Eritrosit (9B#) .-
2
Gmm
:
:.B: >.>-( >.>3
,eukosit (+B#) .-
:
Gmm
:
,.33 >.4( .:.4
Hematokrit E :,.4- :C( >.
Trombosit (),T) .-
:
Gmm
:
.>, ,.C( >BC
1#< #1 3,.C- 3.( B4
1#H Pg ,C.C- ,4( ,B
1#H# gE ::.4- ,B( :.
9D+ E .3.>- ...2( .>.3
1)< #1 3.B- C.,( .-.-
)#T E -..:
H$T:!& >E!$?(
!eutrofil E 44.2- :C( 3-
,imfosit E ,2.C- ,-( >-
1onosit E .4.:- ,( 3
Eosinofil E ..C- .( 2
Basofil E -.C-- -( .
!eutrofil Absolut .-
:
GX1 ..2- ,.>( C.:
,imfosit Absolut .-
:
GX1 -.CC ..C( 4..
1onosit Absolut .-
:
GX1 -.>> -.,( -.2
Eosinofil Absolut .-
:
GX1 -.-4 -..-( -.:-
Basofil Absolut .-
:
GX1 -.-, -( -..
@$1$A @,$!$@
HAT$
Bilirubin Total mgGd1 -.4C S .
Bilirubin Direk mgGd1 -.:B -( -.,
'osfotase Alkali (A,)) ?G1 32 S ,3.
A?TA ?&OT ?G1 C. S :3
A,TA ?&)T ?G1 >B S >.
1ETABO,$?1E @A9BOH$D9AT
&lukosa darah (sewaktu) mgGd1 ..-.,- S ,--
&$!>A,
:reum mgGd1 .4.B- S 4-
@reatinin mgGd1 -.,. -.:.( -.>C
Asam :rat mgGd1 :.3 S C.-
Elektrolit
!atrium (!a) m)0G1 .:2 .:4( .44
@alium (@) m)0G1 :.3 :.2( 4.4
@lorida (#l) m)0G1 .-4 B2( .-2
'ollow up- 4
th
April 23/4
S: Dever (!$ Cough (!
+: Sense: CM T: :CUC
9ead: )yes 1R VGV!$ isochoric pupil$ pale in#erior palpebral con%unctiva (!$ )G8GM: 8
8ec': 18 enlargement V!
Thora<: SD$ retraction (!$ easily seen ribs V!
9R: B,<Gi$ reg$ murmur (!
RR: ,2<Gi$ reg$ rhonchi (!
Abdomen: Soepel$ peristaltic V! 8$ 1GS: not palpable
)<tremities: Pulse B2<Gi$ reg$ ade0uate pGv$ warm e<tremities$ CRT S:W$ muscle
hypotrophy V!$ subcutaneous #at thinning V!$ baggy pants V!
A: Marasmus V Pulmonary tuberculosis
P: Three way
Rimcure Paed .< , tab
Cetiri5in syr .< . cth
Aiet M7 .--- ''alV D.-- :< ,--cc V Mineral mi< >.-cc
#HA)TE9 4
D$?#:??$O! A!D ?:11A9;
Marasmus is a type o# protein energy malnutrition. "t is characteri5ed by old man #ace$ the
thinning o# the subcutaneous #at layer$ baggy pants$ altered mental state$ muscle atrophy and
easily seen rib bones.
Pulmonary tuberculosis is an airborne in#ection caused by the bacteria Mycobacterium
tuberculosis. "t most commonly a##ects the lungs but it can attac' any part o# the body including
the 'idneys$ spine and brain. Some o# the symptoms o# tuberculosis in#ection are cough lasting
more than : wee's$ coughing up blood or sputum$ pain in the chest$ wea'ness or #atigue$ weight
loss$ no appetite$ chills$ #ever and sweating at night.
Patient R6 came to Adam Mali' Ieneral 9ospital with the main complaint o# decreasing body
weight. Patient R6 has e<perienced this condition #or the past 4 months. The patient has no
history o# #ever but has had productive cough #or the past : wee's. This patient had typical
clinical mani#estation o# marasmus$ such as old man #ace$ ribs can easily be seen$ baggy pants
and no edema. The patient was later on diagnosed with pulmonary tuberculosis.
Patient was administered DC4 which is the YstarterZ #ormula used during initial management o#
malnutrition$ beginning as soon as possible and continuing #or , to C days until the child is
stabili5ed. Severely malnourished children cannot tolerate normal amounts o# protein and sodium
or high amounts o# #at. They may die i# given too much protein or sodium. They also need
glucose$ so they must be given a diet that is low on protein and sodium and high in carbohydrate.
DC4 is specially mi<ed to meet the childZs needs without overwhelming the bodyZs system in the
initial stage o# treatment. ?se o# DC4 prevents death. DC4 contains C4'cal and -.B gram protein
per .--m1. As soon as the child is stabili5ed on DC4$ D.-- is used as a Ycatch(upZ #ormula to
rebuild wasted tissues. D.-- contains more calories and protein : .--'cal and ,.Bgram protein
per .--m1.
@itamin A was given to the patient as de#iciency a##ects visual #unction eg. con%unctivitis and
night blindness! and digestive$ respiratory and urinary #unctions. Multivitamin without iron also
was administered because in the most serious #orm o# marasmus$ iron accumulates in the liver$
most li'ely because o# the de#icit in transport protein.
Rimcure Paed is the antibiotic prescribed #or the pulmonary tuberculosis. "ts composition is
Ri#ampicin C4 mg$ "sonicotine hydra5ine 4- mg and Pyra5inamide .4- mg. Rimcure Paed 'ills
or stops the growth o# bacteria that causes tuberculosis.
Ampicillin was administered at #irst to treat bronchopneumonia. Ampicillin belongs to the class
o# antibiotics called penicillin that are used to treat bacterial in#ections. "t stops bacteria #rom
multiplying by preventing bacteria #rom #orming the walls that surround them.
As the patient was diagnosed with miliaria$ he was given cetiri5ine which is a non( sedating
antihistamine that wor's by bloc'ing histamine 9( .! receptors on cells. 9istamine is released
#rom histamine( storing cells mast cells! and then attaches to other cells that have receptors #or
histamine. The attachment o# the histamine causes the cells to be YactivatedW$ releasing other
chemicals that produce the e##ects that we associate with allergy.
Dolic acid was given to treat or prevent #olic acid de#iciency. "t is a 7(comple< vitamin needed
by the body to manu#acture red blood cells. A de#iciency o# this vitamin causes certain types o#
anemia.
R)D)R)8C)S
Ashworth$ A. ,--:!. !uidelines "or the in#atient treatment o" se$erely malnourished children.
.st ed. Ieneva$ Swit5erland: 6orld 9ealth +rgani5ation.
9erchline$ T. and Amorosa$ *. ,-.>!. Tuberculosis. JonlineK )medicine.medscape.com.
Available at: http:GGemedicine.medscape.comGarticleG,:-3-,(overview[showall JAccessed ,,
Apr. ,-.>K.
9orne$ A. ,-.:!. Pulmonary Tuberculosis. JonlineK 7M* 7est Practice. Available at:
http:GGbestpractice.bm%.comGbest(practiceGmonographG.24GbasicsGde#inition.html JAccessed ,,
Apr. ,-.>K.
*amabo$ T. and +nwu'we$ A. ,-.-!. The "ncidence o# Marasmic(Kwashior'or Among Children
in Port 9arcourt$ 8igeria. Nigerian %ournal o" &griculture, Food and 'n$ironment$ JonlineK 2:
\ >!$ pp.B2(.--. Available at: http:GGn%a#e.orgG8%a#e,-.-@ol28o:]>G.C*AMA7+.pd#.
Kliegman$ R. and 8elson$ 6. ,-..!. Nelson textboo( o" #ediatrics. .st ed. Philadelphia$ PA:
)lsevierGSaunders.
1atham$ M. .BBC!. )uman nutrition in the de$elo#ing *orld. .st ed. Rome: Dood and
Agriculture +rgani5ation o# the ?nited 8ations.
1eung$ A. .BBB!. Pulmonary Tuberculosis : The )ssentials. R+N&$ JonlineK ,.-,!$ pp.:-C(:,,.
Available at:
http:GGwww.med.uottawa.caGradiologyGassetsGdocumentsGchest]cardiac]imagingGarticlesGthe
E,-essentialE,-o#E,-T7.pd#.
+rgani5ation$ 6. ,-.:!. Poc(et ,oo( o" )os#ital Care "or Children. .st ed. Ieneva: 6orld
9ealth +rgani5ation.
Rabinowit5$ S.$ Iehri$ M.$ Ai Paolo$ ).$ 6etterer$ 8. and Prince$ ). ,-.>!. Marasmus. JonlineK
)medicine.medscape.com. Available at: http:GGemedicine.medscape.comGarticleGB3>>B2(
overview[showall JAccessed .C Apr. ,-.>K.
Schein#eld$ 8.$ Mo'ashi$ A. and 1in$ A. ,-.,!. Protein-'nergy Malnutrition. JonlineK
)medicine.medscape.com. Available at: http:GGemedicine.medscape.comGarticleG..->2,:(
overview[showall JAccessed ,, Apr. ,-.>K.
Star'e$ *. ,-->!. Tuberculosis in Children. +eminars in Res#iratory and Critical Care Medicine$
JonlineK ,4:!. Available at: http:GGwww.medscape.comGviewarticleG>3>.,:], JAccessed ,, Apr.
,-.>K.
6ho.int$ ,-.>!. -). / Tuberculosis 0T,1. JonlineK Available at:
http:GGwww.who.intGtopicsGtuberculosisGenG JAccessed ,, Apr. ,-.>K.
6orld Dood Programme and the Centers #or Aisease Control and Prevention$ ,--4!. & Manual :
Measuring and nter#reting Malnutrition and Mortality. Rome: ?89CR.