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Marasmus
Author: Simon S Rabinowitz, MD, PhD, FAAP; Chief Editor: Jatinder Bhatia, MBBS more...

Updated: Mar 22, 2012
Background
Marasmus is one of the 3 forms of serious protein-energy malnutrition (PEM). The other 2 forms are kwashiorkor
(KW) and marasmic KW. These forms of serious PEM represent a group of pathologic conditions associated with
a nutritional and energy deficit occurring mainly in young children from developing countries at the time of weaning.
Marasmus is a condition primarily caused by a deficiency in calories and energy, whereas kwashiorkor indicates
an associated protein deficiency, resulting in an edematous appearance. Marasmic kwashiorkor indicates that, in
practice, separating these entities conclusively is difficult; this term indicates a condition that has features of both.
[1, 2]
These conditions are frequently associated with infections, mainly GI. The reasons for a progression of nutritional
deficit into marasmus rather than kwashiorkor are unclear and cannot be solely explained by the composition of
the deficient diet (ie, a diet deficient in energy for marasmus and a diet deficient in protein for kwashiorkor). The
study of these phenomena is considerably limited by the lack of an appropriate animal model. Unfortunately, many
authors combine these entities into one, thus precluding a better understanding of the differences between these
clinical conditions.
Marasmus is a serious worldwide problem that involves more than 50 million children younger than 5 years.
According to the World Health Organization (WHO), 49% of the 10.4 million deaths occurring in children younger
than 5 years in developing countries are associated with PEM.
See the image below.
Malnutrition hotspot map. Image courtesy of the World Health Organization (WHO) and United Nations Children's Fund (UNICEF).
Malnutrition has been a permanent priority of the WHO for decades. Although a higher proportion of severely
malnourished children do not survive a significant intercurrent illness, as much as 80% of the overall, unacceptably
high, mortality rate may be contributed by mild-to-moderately malnourished children because this cohort is so
much higher.
[3]
Accordingly, newer strategies need not be limited to only severely malnourished children.
Although PEM occurs more frequently in low-income countries, numerous children from higher-income countries
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are also affected, including children from large urban areas and of low socioeconomic status, children with chronic
disease, and children who are institutionalized. Recently, studies of hospitalized children from developed countries
have demonstrated an increased risk for PEM. Risk factors include a primary diagnosis of mental retardation,
cystic fibrosis, malignancy, cardiovascular disease, end stage renal disease, oncologic disease, genetic disease,
neurological disease, multiple diagnoses, PICU admission, or prolonged hospitalization.
[4, 5]
In these conditions,
the challenging nutritional management is often overlooked and underestimated, resulting in an impairment of the
chances for recovery and the worsening of an already precarious neurodevelopmental situation.
PEM results in not only high mortality (even for hospitalized children), without any improvement over the last 2
decades, and also results in morbidity, stunted linear growth, and compromised neurological development. The
social and economic implications of PEM and its complications are incalculable.
This article focuses mainly on marasmus that results from an insufficient nutritional intake as observed under
impaired socioeconomic conditions, such as those present in developing countries. Marasmus is most frequently
associated with acute infections (eg, gastroenteritis, respiratory illnesses, measles), chronic illnesses (eg,
tuberculosis, HIV infection) or drastic natural or man made conditions (eg, floods, droughts, civil war).
Pathophysiology
Various extensive reviews of the pathophysiological processes resulting in marasmus are available. Unlike
kwashiorkor, the clinical sequelae of marasmus can be considered as an evolving adaptation in a child facing an
insufficient energy intake. Marasmus always results from a negative energy balance. The imbalance can result
from a decreased energy intake, an increased loss of ingested calories (eg, emesis, diarrhea, burns), an increased
energy expenditure, or combinations of these factors, such as is observed in acute or chronic diseases. Children
adapt to an energy deficiency with a decrease in physical activity, lethargy, a decrease in basal energy
metabolism, slowing of growth, and, finally, weight loss.
Pathophysiological changes associated with nutritional and energy deficits can be described as (1) body
composition changes, (2) metabolic changes, and (3) anatomic changes.
Body Composition
Body mass: Body mass is significantly decreased in a heterogeneous way.
Fat mass: Fat stores can decrease to as low as 5% of the total body weight and can be macroscopically
undetectable. The remaining fat is usually stored in the liver, giving a paradoxical appearance of a fatty liver.
Although this is often observed in kwashiorkor, it also occurs to a lesser extent in marasmus. A study from
Nigeria examined serum lipids in malnourished children.
[6]
These authors found that total cholesterol, low
density lipoprotein cholesterol, and high density lipoprotein cholesterol levels were significantly higher in
children with kwashiorkor than in those with marasmus.
Total body water: The proportion of water content in the body increases with the increased seriousness of
PEM (marasmus or kwashiorkor) and is associated with the loss of fat mass, which is poor in water. The
proportion of extracellular water also increases, often resulting in edema. Edema is significant in
kwashiorkor but can also be present in marasmus or in the frequently encountered mixed forms of PEM.
The increase in extracellular water is proportional to the increase in the total body water. During the first
days of therapy, part of the extracellular water shifts to the intracellular compartment and part of 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 30% in the most serious forms. The muscle fibers are thin with loss of striation. Muscle cells are
atrophic, and muscle tissue is infiltrated with fat and fibrous tissue. Total recovery is long but appears to be
possible.
Other organ mass: The brain, skeleton, and kidney are preserved, whereas the liver, heart, pancreas, and
digestive tract are first affected.
Pediatric and adult physiologic change: Finally, physiologic changes are different in infants and children
when compared with adults. For example, infants with marasmus have an increased tendency to
hypothermia and hypoglycemia, requiring the frequent administration of small meals. This can be explained
by the body composition imbalance of children with marasmus in favor of high-energyconsuming organs,
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such as the brain and kidney, compared with energy-storage organs, such as muscle and fat.
Assessment of fat and muscle mass: As described below, assessment of the fat and muscle mass loss
can be clinically performed by measuring arm circumference (see image below) or skinfold thickness, such
as triceps skinfold. The diagram illustrates the validity of this assessment method. Because arm
circumference is relatively constant in healthy children aged 1-5 years, it roughly represents a general
assessment of nutritional status.
Physiopathological principle of arm circumf erence measurement in children aged 1-5 years and the relationship with severity of
malnutrition.
Minerals and Vitamins
Potassium: Potassium is the electrolyte most studied in marasmus. Total body potassium deficit is
associated with decreased muscle mass, poor intake, and digestive losses. This potassium deficit, which
can reach 15 mEq/kg, contributes to hypotonia, apathy, and impaired cardiac function.
Other electrolytes: Plasma sodium concentration is generally within the reference range, but it can be low,
which is then a sign of a poor prognosis. However, intracellular sodium level is elevated in the brain,
muscle, and red and white blood cells, explaining the sodium excretion in the first days of recovery.
Other minerals: A deficit in calcium, phosphorus, and magnesium stores is also observed. Iron deficiency
anemia is consistently observed in marasmus. However, in the most serious forms, iron accumulates in the
liver, most likely because of the deficit in transport protein. These patients are at higher risk of mortality;
therefore, iron is supplemented only after the acute recovery phase is completed. Zinc, selenium, and
magnesium are more significantly reduced in kwashiorkor but are also constantly deficient in marasmus.
Several studies have shown improved recovery from malnutrition and decreased mortality with
supplementation of these 3 micronutrients. A Cochrane review concluded that zinc supplementation is
clearly of benefit in children aged 6 months or older with diarrheal diseases in areas where these conditions
are an important cause of childhood mortality.
[7]
Vitamins: Both fat-soluble vitamins (ie, A, D, E, K) and water-soluble vitamins (eg, B-6, B-12, folic acid)
must be systematically administered. Vitamin A is essential to retinal function, has a trophic effect on
epithelial tissues, and plays a major role as an antioxidant agent. Vitamin A deficit affects visual function
(eg, conjunctivitis, corneal ulcer, night blindness, total blindness) and digestive, respiratory, and urinary
functions. Furthermore, vitamin A supplementation programs have resulted in decreased mortality and
morbidity, in particular, during diarrheal disease and measles.
Vitamin and micronutrient deficiencies can be differentiated in 2 categories listed below. Patients with deficiencies
of type 1 nutrients present with late and specific clinical signs. In contrast, patients with deficiencies of type 2
nutrients are difficult to identify because blood levels are unreliable and the clinical signs are nonspecific, such as
the growth retardation with mild deficiency and weight loss with significant deficiency. Furthermore, type 2 nutrient
deficiencies are often combined. Therefore, these deficiencies are global and require a global nutritional
rehabilitation, such as WHO standardized solution.
Below are characteristics of type 1 and type 2 deficiencies, according to Golden from a 1991 report.
Type 1 deficiencies
Specific clinical signs
Clinical signs appear after a latency period
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Used in specific metabolic pathways
Are independent of one another
Variable tissue concentration
Type 2 deficiencies
Nonspecific clinical signs
Nutrient status related to daily intake
Used in various organs and metabolic pathways
Nutrient interaction
Constant tissue concentration
Below are lists of nutrient classification according to the clinical response to deficiency in type 1, with reduction of
tissue concentration, and type 2 with growth deficit.
Type 1 nutrients
Selenium
Iodine
Iron
Copper
Calcium
Manganese
Thiamin
Riboflavin
Ascorbic acid
Retinol
Tocopherol
Calciferol
Folic acid
B-12 vitamin
Pyridoxine
Type 2 nutrients
Sodium
Sulfur
Essential amino acids
Potassium
Sodium
Magnesium
Zinc
Phosphorus
Water
Metabolic Changes
The overall metabolic adaptations that occur during marasmus are similar to those in starvation, which have been
more extensively investigated. The primary goal is to preserve adequate energy to the brain and other vital organs
in the face of a compromised supply. Early on, a rise in gluconeogenesis leads to a perceived increased metabolic
rate. As fasting progresses, gluconeogenesis is suppressed to minimize muscle protein breakdown, and ketones
derived from fat become the main fuel for the brain.
With chronic underfeeding, the basal metabolic rate decreases. One of the main adaptations to long-standing
energy deficiency is a decreased rate of linear growth, yielding permanent stunting. The energy saving is partially
attenuated by the diversion of energy from muscle to the more metabolically active organs. Further adaptations to
crisis situations, such as significant infections, may have some parallels to those that are observed in a stressed,
malnourished animal model.
[8]
The rise in energy expenditure and urinary nitrogen excretion following surgery were
significantly less in malnourished rats. This suggests that malnutrition can impair the ability of the organism to
mobilize substrates to respond to stress. However, the healing process in these animals remained normal,
indicating the ability to prioritize this biological activity.
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Energy metabolism
With reduced energy intake, a decrease in physical activity occurs followed by a progressively
slower rate of growth. Weight loss initially occurs due to a decrease in fat mass, and afterwards by a
decrease in muscle mass, as clinically measured by changes in arm circumference (see image
below).
Physiopathological principle of arm circumf erence measurement in children aged 1-5 years and the relationship with
severity of malnutrition.
Muscle mass loss results in a decrease of energy expenditure. Reduced energy metabolism can
impair the response of patients with marasmus to changes in environmental temperature, resulting in
an increased risk of hypothermia. Furthermore, during infection, fever is reduced compared to a well-
nourished patient. In case of nutrient deficiency, the metabolism is redirected to vital function
(requiring 80-100 kcal/kg/d). During recovery, the energy cost of catch-up growth has to be added
(up to 100 kcal/kg/d). At this stage, energy needs can be massive.
Protein metabolism: Intestinal absorption of amino acids is maintained, despite the atrophy of the intestinal
mucosa. Protein turnover is decreased (as much as 40% in severe forms), and protein-sparing mechanisms
regulated by complex hormonal controls redirect amino acids to vital organs. Amino acids liberated from
catabolism of muscle are recycled by the liver for the synthesis of essential proteins. Total plasma proteins,
including albumin, are decreased, whereas gamma globulins are often increased by the associated
infections.
Albumin: An albumin concentration lower than 30 g/L is often considered as the threshold below which
edema develops from decreased oncotic pressure. However, in marasmus, albumin concentration can
occasionally be below this value without edema. Prealbumin concentration is a sensitive index of protein
synthesis. It decreases with decreased protein intake and rapidly increases in a few days with appropriate
nutritional rehabilitation. Insulinlike growth factor 1 (IGF-1) is another sensitive marker of nutritional status.
Carbohydrate metabolism: This has mainly been studied in order to explain the serious and often fatal
hypoglycemia that occurs in the initial renutrition phase of children with marasmus. The glucose level is
often initially low, and the glycogen stores are depleted. Also, a certain degree of glucose intolerance of
unclear etiology is observed, possibly associated with a peripheral resistance to insulin or with
hypokalemia. In the initiation of renutrition or in association with diarrhea or infection, a significant risk of
profound and even fatal hypoglycemia occurs. Small and frequent meals are recommended, including during
the night, to avoid death in the early morning. Furthermore, the digestion of starch is impaired by the
decreased production of pancreatic amylase. Lactose malabsorption is frequent but is generally without
clinical consequences. In most cases, renutrition using milk is possible.
Fat metabolism: Dietary fats are often malabsorbed in the initial phase of marasmus renutrition. The
mobilization of fat stores for energy metabolism takes place under hormonal control by adrenaline and
growth hormone. Blood lipid levels are usually low, and serious dysregulation of lipid metabolism can occur,
mainly during kwashiorkor and rarely during marasmus.
Anatomic Changes
Digestive tract
The entire digestive tract from mouth to rectum is affected. The mucosal surface becomes smooth and thin, and
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secretory functions are impaired. A decrease in gastric hydrochloric acid (HCl) excretion and a slowing of
peristalsis is observed, yielding bacterial overgrowth in the duodenum. Proportionally, the digestive tract is the
organ system that loses the largest mass during marasmus. However, these important alterations of the digestive
tract interfere only moderately with normal nutrient absorption. Therefore, early enteral renutrition is not
contraindicated but is encouraged because some of the nutrients necessary for the recovery of the intestinal
mucosa are used directly from the lumen.
In addition to the anatomic changes associated with PEM, the frequent intestinal infections by viruses and
bacteria and the toxins they produce also contribute to the changes in the digestive tract. Liver volume usually
decreases, as do other organ volumes. An enlarged liver suggests the possibility of other diagnoses, such as
kwashiorkor or hepatitis. Liver synthetic function is usually preserved, although protein synthesis is decreased, as
reflected by the decreased albumin and prealbumin levels. Glycogen synthesis is decreased, further increasing the
risk for hypoglycemia. The detoxifying function of the liver is impaired with structural changes in the liver cells.
Therefore, drugs that are metabolized by the liver should be administered with caution, and liver function should be
monitored.
Endocrine system
Many of the adaptations seen in marasmus are mediated by thyroid hormones, insulin, and growth hormone. As in
any stressed state, the adrenergic response is activated (see image below).
Hormonal adaptation to the stress of malnutrition. The evolution of marasmus.
This response is functional in marasmus but less so in kwashiorkor. Muscle proteins are converted into amino
acids and are used for the hepatic synthesis of lipoproteins. These lipoproteins contribute to the mobilization of
triglycerides from the liver. In contrast, during kwashiorkor, this function is impaired, resulting in liver steatosis,
which is not usually present in marasmus. However, any precipitating factor, such as gastroenteritis or
inappropriate renutrition, can disrupt this fragile adaptive mechanism.
Furthermore, in serious marasmus, a significant degree of hypothyroidism, with a decrease in the size of the
thyroid gland and repercussions on the brain function and psychomotor development exists. In less severe forms,
the impaired thyroid function has fewer clinical consequences. Insulin levels are low and contribute to a certain
degree of glucose intolerance, especially during kwashiorkor. Therefore, high-carbohydrate diets are inappropriate.
Growth hormone levels are initially within the reference range, but they progressively decrease with time,
explaining the halt in linear growth observed with marasmus.
After initiation of renutrition, the hormonal milieu is reversed allowing for substantial anabolism and a rapid linear
growth spurt. However, if 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 for additional hormones in PEM. Levels of
serum gherlin(an appetite stimulating peptide) were increased
[9]
and serum levels of leptin (a satiety hormone) and
IGF-1 were decreased in children with PEM compared with healthy controls.
[10]
Hematopoietic system
A moderate normochromic or slightly hypochromic anemia is usually present, with normal RBC size. Iron and
folate deficiencies, intestinal parasites, malaria, and other chronic infections exacerbate the anemia. However, iron
stores are present in the liver. Therefore, iron supplementation should not be initially implemented. Oral iron is
poorly tolerated by the digestive tract. The other blood cells (eg, thrombocytes, WBCs) are also affected, but with
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generally limited clinical consequences. Blood clotting mechanisms are usually preserved, except in the case of
serious vitamin K deficiency.
Immune system
Immune impairment and infections are usually associated with marasmus. Thymus atrophy is a characteristic
manifestation of marasmus, but all T lymphocyteproducing tissues are affected. However, B-lymphocyte tissues,
such as Peyer patches, the spleen, and the tonsils, are relatively preserved. Cellular immunity is most affected,
with a characteristic tuberculin anergy. However, antibody production is maintained. In marasmus, a general
acquired immunodeficiency occurs, with a decrease in secretory immunoglobulin A (IgA) and an impairment of the
nonspecific local defense system, such as mucosal integrity and lymphokine production. Bacteriemia,
candidiasis, and Pneumocystis carinii infection are frequently present. Immune impairment is less frequent with
moderate malnutrition. Immunological recovery is generally rapid, except if measles is associated.
Brain and nervous system
Cerebral tissue is usually preserved during marasmus. Brain atrophy with impairment of cerebral functions is only
present in severe forms of marasmus. Effects on the brain are more important if malnutrition takes place during the
first year of life or during fetal life. Irritability and apathy are characteristic of marasmus but improve rapidly with
recovery. The permanent developmental consequences of marasmus are difficult to evaluate. Ongoing studies are
evaluating these long-term consequences, as well as the benefit of nutritional supplementation with various
vitamins and minerals.
Cardiovascular system
Cardiac muscle fiber is thin, and the contractility of the myofibrils is impaired. Cardiac output, especially systolic
function, is decreased in the same proportion as the weight loss. Bradycardia and hypotension commonly occur in
severe forms of malnutrition. Electrolyte imbalances present during marasmus modify the ECG findings. With this
impaired cardiac function, any increase of intravascular volume during rehydration or blood transfusion can result in
a significant cardiac insufficiency. With the rapid metabolic, energy, and electrolyte changes of the initial phase of
renutrition, this period is also a period of high risk for arrhythmia or cardiac arrest. Therefore, close clinical
monitoring is critical in children with circulatory compromise.
Epidemiology
Frequency
United States
Marasmus is rarely reported in American children. In 1995, 228 deaths were attributed to marasmus in the United
States. Most of these deaths were in elderly adults, and only 3 occurred in children. However, these data do not
include deaths associated with marasmus complicating anorexia nervosa.
Incidence of nonfatal marasmus is unclear in the United States because most patients have an underlying
condition, and marasmus is not reported as an admission or discharge diagnosis. However, a report from a tertiary
care center in Massachusetts reported prevalence rates of severe (1.3%), moderate (5.8%), and mild (17.4%)
acute PEM in hospitalized children, based on the Waterlow criteria.
[11]
In the same cohort, chronic PEM (deficits
in height for age) was found to be severe (5.1%), moderate (7.7%), and mild (14.5%).
Acute (33%) and chronic (64%) malnutrition, based on comparing weight and height with controls, was found
among a cohort of 160 children hospitalized with congenital heart disease in a regional pediatric cardiothoracic
center at the University of Michigan.
[12]
Malnutrition was inversely correlated with age and was present in 80% of
the hospitalized infants. These studies, as well as reports from Western Europe, suggest that marasmus is
underappreciated amongst chronically ill children in the United States.
[3, 4]
International
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Nearly 30% of humans currently experience one or more of the multiple forms of malnutrition. Close to 50 million
children younger than 5 years have PEM, and half of the children who die younger than 5 years are undernourished
(see image below). Approximately 80% of these malnourished children live in Asia, 15% in Africa, and 5% in Latin
America.
[13]
Distribution of 10.4 million deaths among children younger than 5 years in all developing countries. World health Organization (WHO),
1995.
Because as many as 20-30% of severely malnourished children die during treatment by the health services,
[14]
interest in reporting the prevalence of malnutrition in hospitalized children in different countries has been renewed.
A recent review article estimated the prevalence of acute malnutrition over the last 10 years in hospitalized children
in Germany, France, the United Kingdom, and the United States to be 6.1-14%; the prevalence is as much as
32% in Turkey.
[4]
However, a recent German study determined that the prevalence of malnutrition was even higher
(24% with 1.7% severe, 4.4% moderate, and 17.7% mild) in a cohort of unselected children admitted to a large
tertiary care children's hospital in 2003-2004.
[5]
Furthermore, a worsening of nutritional status in hospitalized
children in Brazil,
[15]
France,
[16]
and Turkey.
[17]
Paradoxically, a massive global epidemic of obesity, especially in countries in rapid economic transition, is
simultaneously emerging in children and adolescents.
Mortality/Morbidity
Five million children younger than 5 years die every year of malnutrition. Approximately 70 million present with
wasting, and 230 million present with some stunting. Fifty percent of the children in Asia are malnourished, 30%
are malnourished in Africa, and 20% are malnourished in Latin America.
Race
No racial predilection in the prevalence of malnutrition is evident, but a strong association with the geographic
distribution of poverty is observed.
Sex
No sexual predilection is observed, although, in some parts of the world, cultural practices place girls at a
disadvantage for PEM.
Age
Marasmus is more frequent in children younger than 5 years because this period is characterized by increased
energy needs and increased susceptibility to viral and bacterial infections. Weaning, which occurs during this
period, is often complicated by factors such as geography (eg, drought, poor soil productivity), economy (eg,
illiteracy, unemployment), hygiene (eg, access to quality water), public health (eg, number of nurses is more than
number of physicians), and culture and dietetics (eg, intrafamily distribution of high-nutrition foods).

Contributor Information and Disclosures
Author
Simon S Rabinowitz, MD, PhD, FAAP Professor of Clinical Pediatrics, Vice Chairman, Clinical Practice
Development, Pediatric Gastroenterology, Hepatology, and Nutrition, State University of New York Downstate
College of Medicine, The Children's Hospital at Downstate
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Simon S Rabinowitz, MD, PhD, FAAP is a member of the following medical societies: American Academy of
Pediatrics, American Association for the Advancement of Science, American College of Gastroenterology,
American Gastroenterological Association, American Medical Association, New York Academy of Sciences,
North American Society for Pediatric Gastroenterology and Nutrition, Phi Beta Kappa, and Sigma Xi
Disclosure: Abbott nutrition Honoraria Speaking and teaching
Coauthor(s)
Mario Gehri, MD Consulting Staff, Department of Pediatrics, Hpital De L'Enfance, Centre Hospitalier
Universitaire Vaudois, Switzerland
Disclosure: Nothing to disclose.
Ermindo R Di Paolo, PhD Pharmacist, Department of Pharmacy, University Hospital CHUV, Lausanne,
Switzerland
Disclosure: Nothing to disclose.
Natalia M Wetterer, MD Resident Physician, Department of Pediatrics, New York Medical College
Disclosure: Nothing to disclose.
Esther N Prince, MD Pediatric Gastroenterology Fellow, State University of New York Downstate Medical
Center
Disclosure: Nothing to disclose.
Specialty Editor Board
Maria Rebello Mascarenhas, MBBS Associate Professor of Pediatrics, University of Pennsylvania School of
Medicine; Section Chief of Nutrition, Division of Gastroenterology and Nutrition, Director, Nutrition Support
Service, Children's Hospital of Philadelphia
Maria Rebello Mascarenhas, MBBS is a member of the following medical societies: American
Gastroenterological Association, American Society for Parenteral and Enteral Nutrition, and North American
Society for Pediatric Gastroenterology and Nutrition
Disclosure: The 5-minute pediatric consult Royalty editor
Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of
Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Nothing to disclose.
Jatinder Bhatia, MBBS Professor of Pediatrics, Chief, Section of Neonatology, Department of Pediatrics,
Medical College of Georgia
Jatinder Bhatia, MBBS is a member of the following medical societies: American Academy of Pediatrics,
American Association for the Advancement of Science, American Dietetic Association, American Pediatric
Society, American Society for Clinical Nutrition, American Society for Parenteral and Enteral Nutrition, Society
for Pediatric Research, and Southern Society for Pediatric Research
Disclosure: Nothing to disclose.
Merrily P M Poth, MD Professor, Department of Pediatrics and Neuroscience, Uniformed Services University
of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics,
Endocrine Society, and Pediatric Endocrine Society
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Disclosure: Nothing to disclose.
Chief Editor
Jatinder Bhatia, MBBS Professor of Pediatrics, Chief, Section of Neonatology, Department of Pediatrics,
Medical College of Georgia
Jatinder Bhatia, MBBS is a member of the following medical societies: American Academy of Pediatrics,
American Association for the Advancement of Science, American Dietetic Association, American Pediatric
Society, American Society for Clinical Nutrition, American Society for Parenteral and Enteral Nutrition, Society
for Pediatric Research, and Southern Society for Pediatric Research
Disclosure: Nothing to disclose.
Additional Contributors
The authors and editors of Medscape Reference gratefully acknowledge the use of images and information from
the United Nations Children's Fund (UNICEF).
References
1. Scrimshaw NS, Viteri FE. INCAP studies of kwashiorkor and marasmus. Food Nutr Bull. Mar
2010;31(1):34-41. [Medline].
2. Spoelstra MN, Mari A, Mendel M, Senga E, van Rheenen P, van Dijk TH, et al. Kwashiorkor and
marasmus are both associated with impaired glucose clearance related to pancreatic -cell dysfunction.
Metabolism. Mar 2 2012;[Medline].
3. Pelletier DL, Frongillo EA Jr, Schroeder DG, Habicht JP. The effects of malnutrition on child mortality in
developing countries. Bull World Health Org. 1995;73 (4):443-8. [Medline].
4. Joosten KF, Hulst JM. Prevalence of malnutrition in pediatric hospital patients. Curr Opin Pediatr. Oct
2008;20(5):590-6. [Medline].
5. Pawellek I, Dokoupil K, Koletzko B. Prevalence of malnutrition in paediatric hospital patients. Clin Nutr.
Feb 2008;27(1):72-6. [Medline].
6. Akuyam SA, Isah HS, Ogala WN. Serum lipid profile in malnourished nigerian children in zaria. Niger
Postgrad Med J. September 2008;15 (3):192-6.
7. Emery PW. Metabolic changes in malnutrition. Eye. October 2005;19 (10):1029-32. [Medline].
8. [Best Evidence] Lazzerini M, Ronfani L. Oral zinc for treating diarrhoea in children. Cochrane Database
Syst Rev. 2008;(3):CD005436. [Medline].
9. Altinkaynak S, Selimoglu MA, Ertekin V, Kilicarslan B. Serum ghrelin levels in children with primary
protein-energy malnutrition. Pediatr Int. Aug 2008;50(4):429-31. [Medline].
10. Kilic M, Taskin E, Ustundag B, Aygun AD. The evaluation of serum leptin level and other hormonal
parameters in children with severe malnutrition. Clin Biochem. May 2004;37(5):382-7. [Medline].
11. Hendricks KM, Duggan C, Gallagher L, et al. Malnutrition in hospitalized pediatric patients. Current
prevalence. Arch Pediatr Adolesc Med. Oct 1995;149(10):1118-22. [Medline].
12. Cameron JW, Rosenthal A, Olson AD. Malnutrition in hospitalized children with congenital heart disease.
Arch Pediatr Adolesc Med. Oct 1995;149(10):1098-102. [Medline].
13. Fisberg M, Nobrega FJ. Disturbios da nutricao. Revinter. 1998;140-4.
14. Manejo da desnutricao grave: um manual para profissionals de saude de nivel superior (medicos,
enfermeiros, nutricionistas e outros) e suaas equipes auxillares. Organizacao Mundial da Saude, Brasilia.
9/24/13 Marasmus
emedicine.medscape.com/article/984496-overview 11/13
1999.
15. Rocha GA, Rocha EJ, Martins CV. The effects of hospitalization on the nutritional status of children. J
Pediatr (Rio J). Jan-Feb 2006;82(1):70-4. [Medline].
16. Marteletti O, Caldari D, Guimber D, Mention K, Michaud L, Gottrand F. [Malnutrition screening in
hospitalized children: influence of the hospital unit on its management]. Arch Pediatr. Aug
2005;12(8):1226-31. [Medline].
17. Oztrk Y, Buyukgebiz B, Arslan N, Ellidokuz H. Effects of hospital stay on nutritional anthropometric data
in Turkish children. J Trop Pediatr. Jun 2003;49(3):189-90. [Medline].
18. World Health Organization. WHO Global Database on Child Growth and Malnutrition. Geneva: WHO.
1996.
19. Kim Y, Hahn S, Garner P. Reduced osmolarity oral rehydration solution for treating dehydration caused
by acute diarrhoea in children. Cochrane Database Syst Rev. 2001;(2):CD002847. [Medline].
20. UNICEF. New formulation of Oral Rehydration Salts (ORS) with reduced osmolarity. United Nations
Children's Fund. Available at http://www.supply.unicef.dk/catalogue/bulletin9.htm.
21. Plumpy'nut. Available at http://en.wikipedia.org/wiki/Plumpy'nut.
22. Joint Statement by the World Health Organization, the World Food Programme, the United Nations
System Standing Committee on Nutrition and the United Nations Children's Fund. Community-Based
Management of Severe Acute Malnutrition. May, 2007.
23. [Guideline] World Gastroenterology Organisation (WGO). WGO practice guideline: acute diarrhea. Mar
2008;[Full Text].
24. Schwarz SM, Corredor J, Fisher-Medina J, Cohen J, Rabinowitz S. Diagnosis and treatment of feeding
disorders in children with developmental disabilities. Pediatrics. Sep 2001;108(3):671-6. [Medline].
25. Bhutta ZA, Ahmed T, Black RE, Cousens S, Dewey K, Giugliani E. What works? Interventions for
maternal and child undernutrition and survival. Lancet. Feb 2 2008;371(9610):417-40. [Medline].
26. Ashworth A, Jackson A, Khanum S, Schofield C. Ten steps to recovery. Child Health Dialogue. 1996;10-
2. [Medline].
27. Barennes H, Kahiatani F, Pussard E, et al. Intrarectal Quinimax (an association of Cinchona alkaloids) for
the treatment of Plasmodium falciparum malaria in children in Niger: efficacy and pharmacokinetics.
Trans R Soc Trop Med Hyg. Jul-Aug 1995;89(4):418-21. [Medline].
28. Beaufrere B, Bresson JL, Briend A, et al. Protein and energy requirements in children with severe
malnutrition. Application in a hospital environment for the treatment of malnutrition caused by deficient
intake. Arch Pediatr. 1998;5(7):763- 71. [Medline].
29. Berkley J, Mwangi I, Griffiths K, et al. Assessment of severe malnutrition among hospitalized children in
rural Kenya: comparison of weight for height and mid upper arm circumference. JAMA. Aug 3
2005;294(5):591-7. [Medline].
30. Briend A, Wojtyniak B, Rowland MG. Arm circumference and other factors in children at high risk of death
in rural Bangladesh. Lancet. Sep 26 1987;2(8561):725-8. [Medline].
31. Buchanan N. Drug kinetics in protein energy malnutrition. S Afr Med J. Mar 4 1978;53(9):327-30.
[Medline].
32. Buchanan N. Effect of protein-energy malnutrition on drug metabolism in man. World Rev Nutr Diet.
1984;43:129-39. [Medline].
33. Buchanan N, Eyberg C, Davis MD. Isoniazid pharmacokinetics in Kwashiorkor. S Afric Med J.
1979;56(8):299-300. [Medline].
9/24/13 Marasmus
emedicine.medscape.com/article/984496-overview 12/13
34. Buchanan N, Robinson R, Koornhof HJ, Eyberg C. Penicillin pharmacokinetics in kwashiorkor. Am J Clin
Nutr. Nov 1979;32(11):2233-6. [Medline].
35. El-Sayed HL, Nassar MF, Habib NM, et al. Structural and functional affection of the heart in protein
energy malnutrition patients on admission and after nutritional recovery. Eur J Clin Nutr. Apr
2006;60(4):502-10. [Medline].
36. Finch RG. Adverse reactions to antibiotics. In: Greenwood D, ed. Antimicrobial Chemotherapy. 4
th
ed.
Oxford, England: Oxford University Press; 2000:200-11.
37. Golden M. The effects of malnutrition in the metabolism of children. Trans R Soc Trop Med Hyg.
1988;82(1):3-6. [Medline].
38. Gomez F, Ramos Galvan R, Frenk S, et al. Mortality in second and third degree malnutrition. In: Bull
World Health Organ. 2000;78(10):1275-80. J Trop Ped and Afr Child Health. 1956;2:77. [Medline].
39. Grantham-McGregor S. A review of studies of the effect of severe malnutrition on mental development. J
Nutr. 1995;125:2233-8 S. [Medline].
40. Krishnaswamy K. Drug metabolism and pharmacokinetics in malnourished children. Clin Pharmacokinet.
1989;17 Suppl 1:68-88. [Medline].
41. Listernick R, Christoffel K, Pace J, Chiaramonte J. Severe primary malnutrition in US children. Am J Dis
Child. Nov 1985;139(11):1157-60. [Medline].
42. Long J, World Health Organization. Management of severe malnutrition: a manual for physicians and
senior health workers. 1999.
43. Martorell R, Habicht J-P, Rivera JA. History and design of the INCAP Longitudinal Study (1969-77) and its
Follow-up (1988-89). J Nutr. 1995;125:1027-41 S. [Medline].
44. Mazouni SM, Guignard JP. [Malnutrition in children and the variability of drug effects]. Rev Med Suisse
Romande. Dec 1996;116(12):965-9. [Medline].
45. Mehta S. Drug metabolism in the malnourished child. Nestle nutr workshop ser. 1988;19:329-38.
46. Mehta S, Nain CK, Sharma B, Mathur VS. Disposition of four drugs in malnourished children. Drug Nutr
Interact. 1982;1(3):205-11. [Medline].
47. Mehta S, Nain CK, Yadav D, et al. Disposition of acetaminophen in children with protein calorie
malnutrition. Int J Clin Pharmacol Ther Toxicol. Jun 1985;23(6):311-5. [Medline].
48. Merritt RJ, Suskind RM. Nutritional survey of hospitalized pediatric patients. Am J Clin Nutr. Jun
1979;32(6):1320-5. [Medline].
49. Polasa K, Murthy KJ, Krishnaswamy K. Rifampicin kinetics in undernutrition. Br J Clin Pharmacol. Apr
1984;17(4):481-4. [Medline].
50. Pollitt E. Developmental sequel from early nutritional deficiencies: conclusive and probability judgments. J
Nutr. Feb 2000;130(2S Suppl):350S-353S. [Medline].
51. Rumack BH, Holtzman J, Chase HP. Hepatic drug metabolism and protein malnutrition. J Pharmacol Exp
Ther. Sep 1973;186(3):441-6. [Medline].
52. Seth V, Beotra A, Bagga A, Seth S. Drug therapy in malnutrition. Indian Pediatr. Nov 1992;29(11):1341-6.
[Medline].
53. Taketomo CK, Hodding JH, Kraus DM. Pediatric dosage handbook. 12
th
ed. Hudson, Ohio: Lexi Comp
Inc; 2005.
54. Tolboom JJ. Management of severe malnutrition and diarrhea. J Pediatr Gastroenterol Nutr. Mar
2000;30(3):346-8. [Medline].
9/24/13 Marasmus
emedicine.medscape.com/article/984496-overview 13/13

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55. Waterlow JC. Classification and definition of protein-calorie malnutrition. Br Med J. Sep 2
1972;3(826):566-9. [Medline].
56. Yadav D. Disposition of acetaminophen in children with protein caloric malnutrition. Clin Pharmacol Ther.
1985;23:311-5.