malnutrisi pada anak

Case Report

Infection Unit

Severe Nutrition Type Marasmus And Persistent Diarrhea

Presentator: Prakash Kanayasan

Navin Kanvinder Singh

Day, Date : Wednesday, 19 October 2011

Supervisor : dr. Hj Tiangsa Br Sembiring, Sp.A (K)

Introduction

Malnutrition is a broad term which refers to both undernutrition (subnutrition) and

overnutrition. Individuals are malnourished, or suffer from undernutrition if their diet does not

provide them with adequate calories and protein for maintenance and growth, or they cannot

fully utilize the food they eat due to illness. People are also malnourished, or suffer from

overnutrition if they consume too many calories. Malnutrition can also be defined as the

insufficient, excessive or imbalanced consumption of nutrients. Several different nutrition

disorders may develop, depending on which nutrients are lacking or consumed in excess.

According to the World Health Organization (WHO), malnutrition is the gravest single threat to

global public health.1

The World Health Organization (WHO)2 defines malnutrition as "the cellular imbalance

between the supply of nutrients and energy and the body's demand for them to ensure growth,

maintenance, and specific functions." The term protein-energy malnutrition (PEM) applies to a

group of related disorders that include marasmus, kwashiorkor, and intermediate states of

marasmus-kwashiorkor. The term marasmus is derived from the Greek word marasmos, which

means withering or wasting. Marasmus involves inadequate intake of protein and calories and is

characterized by emaciation. The term kwashiorkor is taken from the ‘Ga’ language of Ghana

and means "the sickness of the weaning." Williams first used the term in 1933, and it refers to an

inadequate protein intake with reasonable caloric (energy) intake. Edema is characteristic of

kwashiorkor but is absent in marasmus.

http://www.medicalnewstoday.com/articles/160774.php

http://emedicine.medscape.com/article/984496-overview

Studies suggest that marasmus represents an adaptive response to starvation, whereas

kwashiorkor represents a maladaptive response to starvation. Children may present with a mixed

picture of marasmus and kwashiorkor, and children may present with milder forms of

malnutrition. For this reason, Jelliffe suggested the term protein-calorie (energy) malnutrition to

include both entities. Although protein-energy malnutrition affects virtually every organ system,

this article primarily focuses on its cutaneous manifestations.2

In general, marasmus is an insufficient energy intake to match the body's requirements.

As a result, the body draws on its own stores, resulting in emaciation. In kwashiorkor, adequate

carbohydrate consumption and decreased protein intake lead to decreased synthesis of visceral

proteins. The resulting hypoalbuminemia contributes to extravascular fluid accumulation.

Impaired synthesis of B-lipoprotein produces a fatty liver. 4

In 2000, the WHO4 estimated that malnourished children numbered 181.9 million

(32%) in developing countries. In addition, an estimated 149.6 million children younger than 5

years are malnourished when measured in terms of weight for age. In south central Asia and

eastern Africa, about half the children have growth retardation due to protein-energy

malnutrition. This figure is 5 times the prevalence in the western world.4

Approximately 50% of the 10 million deaths each year in developing countries

occur because of malnutrition in children younger than 5 years. In kwashiorkor, mortality tends

to decrease as the age of onset increases. Dermatologic findings appear more significant and

occur more frequently among darker-skinned peoples. This finding is likely explained by the

greater prevalence and the increased severity of protein-energy malnutrition in developing

countries and not to a difference in racial susceptibility4.

Marasmus most commonly occurs in children younger than 5 years. This period

is characterized by increased energy requirements and increased susceptibility to viral and

bacterial infections. Low intake of calories or an inability to absorb calories is the key factor in

the development of kwashiorkor. A variety of syndromes can be associated with kwashiorkor. 4

Patients with protein-energy malnutrition present with poor weight gain or

weight loss, slowing of linear growth; and behavioral changes, such as irritability, apathy,

decreased social responsiveness, anxiety, and attention deficit nonhealing wounds. Signs include

diarrhea and psychomotor changes. This may signify a catabolic process that requires nutritional

intervention. 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. 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. 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. 4

Immune impairment and infections are usually associated with marasmus.

Thymus atrophy is a characteristic manifestation of marasmus, but all T lymphocyte–producing

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. 4

Management of moderate marasmus can be performed on an outpatient basis, but severe

marasmus or marasmus complicated by a life-threatening condition generally requires inpatient

treatment. In these cases, management is divided into an initial intensive phase followed by a

consolidation phase (rehabilitation), preparing for outpatient follow-up management. The WHO

has developed guidelines to help improve the quality of hospital care for malnourished children

and has prioritized the widespread implementation of these guidelines.4

The guidelines highlight 10 steps for routine management of children with malnutrition, as

follows:4

Prevent and treat the following:

o Hypoglycemia

o Hypothermia

o Dehydration

o Electrolyte imbalance

o Infection

o Micronutrient deficiencies

Provide special feeds for the following:

o Initial stabilization

o Catch-up growth

o Provide loving care and stimulation

o Prepare for follow-up after discharge

Nutritional management of the acute phase of severe marasmus in week 1 coresponds to

maintenance of vital functions and tissue renewal . During this period, the electrolyte imbalance,

infections, hypoglycemia, and hypothermia are treated, and then feeding is started. Oral

renutrition of a child with marasmus should be started as early as possible, as soon as the child is

stable and the hydroelectrolyte imbalances are corrected. The term gut rest has no physiological

basis. Enteral feeds decrease diarrhea and prevent bacteremia from bacterial translocation.In

cases of shock, intravenous (IV) rehydration is recommended using a Ringer-lactate solution

with 5% dextrose or a mixture of 0.9% sodium chloride with 5% dextrose. Enteral hydration

using ReSoMal should be started as early as possible, preferably at the same time as the IV

solution.4

The first step is often simply rehydration. Dehydration in children with marasmus is

difficult to evaluate, is overdiagnosed, or is misinterpreted as septic shock. Rehydration should

be enteral except in case of coma or shock, when intravenous therapy is required. Rehydration

solution should be adapted to marasmic children with a low sodium content and a high potassium

content. This can be prepared using standard WHO solution as a base or by directly

administering a modified oral rehydration (ReSoMal) solution if available. The overall goal of

nutrition rehabilitation is to overcome the anorexia often associated with marasmus, as well as to

avoid the causes that lead to anorexia.4

The next step is transitional state that is to avoid cardiac failure while providing enough

energy to avoid catabolism. The goal usually is to provide 80-100 kcal/kg/d in 12 meals per day

or continuously by NG tube to avoid hypoglycemia. This amount of calories should be reached

progressively in a few days to avoid life-threatening problems such as cardiac failure or

hypokalemia. The WHO had recommended the use of the liquid products, such as the F75

solution, which provides 75 kcal/100 mL, mainly as carbohydrates. This solution provides a

limited amount of fat, which is often malabsorbed because of the associated pancreatic

insufficiency, and a limited amount of proteins, which can precipitate renal failure during initial

refeeding of children with marasmus. F75 is available as a ready-to-use formula or can be

prepared using widely available foods listed in Table 3 below. Recipes and cooking guidelines,

including possible alternative foods, are available through the WHO. The ready-to-use formulas,

as well as the micronutrient mixtures, are commercially available. 4

The third step is rehabilitation. In the rehabilitation phase of treatment, nutritional intake

can reach 200 kcal/kg/d. The goal is to reach a continuous catch-up growth in weight and height

in order to restore a healthy body weight. Only children who have been weaned from their NG

tube can be considered as being in the rehabilitation phase. Therefore, specific goals of this

phase are to encourage the child to eat as much as possible, to restart breastfeeding as soon as

possible, to stimulate the emotional and physical development, to actively prepare the child and

mother to return to home and prevent recurrence of malnutrition.4

During the rehabilitation phase, the F100 formula, with a higher protein content With the

child's increased appetite during this phase, use of the F75 formula only leads to a fat increase,

without an appropriate gain in fat-free mass. The main risk of this phase of the rehabilitation is

that the nutrients provided are not sufficient to sustain the weight gain, which can reach as much

as 15 g/kg/d.Powdered skim milk is used to prepare the F75 or F100 formula. In that form, the

lactose concentration is low, about 10 times less than in breast milk, which is also well tolerated

by children with marasmus. Only in cases of persistent diarrhea or established lactose

intolerance, which is rare, should lactose be excluded. High-fat foods are well tolerated at this

point because they slow gastric emptying and may decrease lactose production. 4

Mortality of hospitalized children with marasmus is high, especially during the first few

days of rehabilitation. Death is usually caused by infections or other causes. If the child has no

clinical sign of infection, the WHO recommends 5 days of oral cotrimoxazole therapy. If the

child presents with clinical signs of infection, hypoglycemia, or hypothermia he or she must be

considered as seriously infected and treated with parenteral ampicillin and gentamicin. Practice

guidelines for acute diarrhea have been established. Persistent and profuse diarrhea has 2 main

causes. Infectious etiology (especially lambliasis): This can be promptly treated with

metronidazole if possible, after stool examination. In osmotic diarrheas sugar of the F75 solution

should be replaced by cereal flour for 1-2 weeks. 4

http://guideline.gov/summary/summary.aspx?doc_id=12679


Case report:

ANS, a 9months and 20days baby boy came to RS HAM emergency department with the main

complain of diarrhea. Patient is origin from Desa Nagori Sinasih Kec Silau.

- Patient has been experiencing diarrhea since 1 month ago with the frequency of more than 3

times a day (watery diarrhea). Volume of diarrhea 100cc per time.

- Vomit is also experienced by patient with the frequency of more than two times a day contains

of what that is eaten with the volume of about 50cc per time.

- Fever(-) cough(-)

- Birth history : spontaneous with the help of midwife. Patient cried spontaneous with no

asphyxia .

- Birth weight: 3700grm. Birth length 33cm. Patient is the 3rd child.

- Patient was breast fed till the age of 4months, given formula milk from age 4month till 6

months old.

- Growth history : at this point, patient can only carry his head and turn around

- History of illness: patient is consulted from RS Perdagangan by a general practitioner with the

diagnosis of persistent diarrhea .

- History of medications : ivfd ringer lactate

- History of defecation : diarrhea

- History of mictuation : normal

- History of Immunization : BCG: 1x

` Hepatitis B 3x

Polio 4x

- History of Previous Drug : Not clear.

- History of Previous Disease : -

Physical examination

Presence Status:

Sensorium: Alert; temperature: 37 oC; BW: 5,1 kg; BL: 65 cm; BW/BL: 57%, BW/A : %,

BL/A : %., Anemic (-), Dyspnea (-), Icteric (-), Cyanosis (-), Oedem (-)

Localized Status:

Head : Old man face (+) Eye: Sunken eyes (+), light reflexes (+/+), isochoric pupil, pale

conjunctiva palpebra inferior (-/-)

Ear and Nose: within normal limit;

Neck : Lymph node enlargement (-), jugular vein pressure: R-2 cmH2O

Chest : Symetric fusiform, HR : 120 bpm, regular, murmur (-)

RR : 48 tpm, regular, rales (-/-)

Abdomen : Soepel, Ascites (-), undulation (-), shifting dullness (-), smilling umbillicus (-)

Hepar/Lien: non palpable, turgor (-), peristaltic ( +)

Extremities: Baggy pants (+), oedem (-), cyanosis, Pols: 120 bpm, regular, adequate

pressure/volume, CFT<3”, (-) BP : 110/90 mmHg

Genitalia : Male, within normal range

Working Diagnosis : Severe nutrition type marasmus with persistent diarrhea

Plan:

- Full blood count

- Feces routine

- Electrolite

- Consul to nutrition and dietary disease

Therapy:

- Cotrimoxazole syrp 2x ½ ctg

- Zinc tablet 1x20mg

- Vitamin A 1x100.000iu

- Multivitamin without ferum 1x cFs I

- Resomal 50cc/2hrs

- F 75 diet 55cc/2hrs/oral

laboratory Result 2st August 2011:

Complete Blood Count Results Normal Value

Hemoglobin (Hb) 7,70 g % 11,3 – 14,1g %

Erytrocyte (RBC) 2,67 x 106/mm3 4,40 – 4,48 x106/mm3

Leukocyte (WBC) 8,22 x 103/mm3 4,5 – 13,5 x103/mm3

Hematocrite 22,80 % 37 – 41 %

Trombocyte (PLT) 69 x 103/mm3 217 – 497 x103/mm3

MCV 80,70 fL 93 – 115 fL

MCH 23,90 pg 29 – 35 pg

MCHC 29.60 g % 28 – 34 g %

RDW 15,70 14,9 – 18,7 %

Neutrofil 26,92 % 37 – 80 %

Limfosit 64,80 % 20 – 40 %

Monosit 6,60 % 2 – 8 %

Eosinophil 1,80 % 1 – 6 %

Basophil 0,100 % 0 – 1 %

Neutrophil absolute 2,15x 103/µL 1,9 – 5,4 x103/µL

Limfosit absolute 5,20 x 103/µL 3,7 – 10,7 x103/µL

Monosit absolute 0,53 x 103/µL 0,3 – 0,8 x103/µL

Eosinophil absolute 0,13 x 103/µL 0,2 – 0,5 x103/µL

Basophil absolute 0,01 x 103/µL 0 – 0,1 x103/µL

GLUCOSE Ad Random

Blood glucose 139 mg/dl <200 mg/dl

Follow Up 15 – 16th September 2011

S : Watery diarrhea (2x), blood (-), mucous (-), vomit (-)

O :

Presence status :

Sensorium : Alert, Body temperature : 36,7 – 36,8 ºC, BW : 5,1 kg, BL : 65 cm,

BW/BL = 57%

Anemic (-), Dyspnea (-) , Icteric (-), Cyanosis (-), Oedema (-)

Localized status :

Head : Old man face (+) Eye : Sunken eyes (+), light reflexes (+/+),

isochoric pupil, pale conjunctiva palpebra inferior (-/-),palpebra

superior oedem (-/-), Mouth cyanosis (-), tears (+), wet lip mucous

Ear / Nose: within normal limit

Neck : Lymph node enlargement (-), jugular vein pressure : R-2 cmH2O.

Cannon wave (-)

Chest : Symmetric fusiform

HR : 112 - 120 bpm, regular, murmur (-)

RR : 30 - 36 tpm, regular, rales (-/-),skin turgor (N)

Abdomen : Soepel, peristaltik (+) N

Hepar/Lien: non palpable

Extremities : Baggy pants (+), muscle hypertrophy (+), pols: 112 - 120 bpm,

regular, adequate pressure/volume, CFT<3”, warm, pitting oedem

(-). BP : 100/70 mmHg

Anogenital : Male, within normal limit.

A: Severe nutrition type Marasmus with persistent diarrhea

P : - Cotrimoxazole syrp 2x ½ ctg


- Multivitamin without ferum 1x cFs I

- Resomal 50cc/2hrs


Planning: Routine feces examination

Electrolite examination


S : Watery diarrhea (2x), blood (-), mucous (-), vomit (-)

O :

Presence status :

Sensorium : Alert, Body temperature : 36,8 ºC, BW : 5,1 kg, BL : 65 cm, BW/BL

= 57%


Localized status :

Head : Old man face (+) Eye : Sunken eyes (+), light reflexes (+/+),

isochoric pupil, pale conjunctiva palpebra inferior (-/-),palpebra

superior oedem (-/-), Mouth cyanosis (-), tears (+), wet lip mucous



Cannon wave (-)


HR : 128 bpm, regular, murmur (-)

RR : 28 tpm, regular, rales (-/-),skin turgor (N)



Extremities : Baggy pants (+), muscle hypertrophy (+), pols: 120 bpm, regular,

adequate pressure/volume, CFT<3”, warm, oedem (+/+).

BP : 100/70


A: Severe nutrition type Marasmus with Persistent diarrhea



- Multivitamin without ferum 1x cth I


Planning : Feces culture examination

Laboratory Result 17th September 2011: Urine

Urine Results

Colour Yellow

Erytrocyte (RBC) 0-2

Leukocyte (WBC) 2-4

Epitel 0-1

Cristal -

Bacteria -

Glucose -

Bilirubin -

Keton -

pH 8,0

Protein -

Urobilinogen -

Nitrate -

Blood -

Laboratory Result 17th September 2011: Feces

Feces Results

Colour Yellow

Consistency Dilute

Blood -

Mucous -

Worm eggs -

Amoeba +

Erytrocyte 0 -1

Leucocyte 0 – 1


S : Diarrhea (-), vomit (-), complete diet

O :

Presence status :

Sensorium : Alert, Body temperature : 36,7 ºC, BW : 5,5 kg, BBI : 8,1kg BW/BL

= 67%


Localized status :

Head : Old man face (+), hair can’t be plucked out easily, Eye : Sunken

eyes (+), light reflexes (+/+), isochoric pupil, pale conjunctiva

palpebra inferior (-/-), palpebra superior oedem (-/-), Mouth cyanosis

(-), tears (+), wet lip mucous



Cannon wave (-)






Extremities : Baggy pants (+), muscle hyperthrophy (+), pols: 92 bpm, regular,

adequate pressure/volume, CFT<3”, warm, thin subcutan fat (+),

BP : 100/60


A: Severe nutrition type Marasmus

P : - Cotrimoxazole syrp 2x ½ cth



- F 100 diet 55cc/2hrs/oral (120kkal/kgBW/day)

Follow Up 21 – 22nd September 2011


O :

Presence status :

Sensorium : Alert, Body temperature : 37 ºC, BW : 5,5 kg, BBI : 8,1kg BW/BL =

67%


Localized status :

Head : Old man face (+), hair can’t be plucked out easily, Eye : Sunken


palpebra inferior (-/-), palpebra superior oedem (-/-), Mouth cyanosis




Cannon wave (-)






Extremities : Baggy pants (+), muscle hyperthrophy(+), pols: 106 bpm, regular,

adequate pressure/volume, CFT<3”, warm, thin subcutan fat (+).

BP : 100/70


A: Severe malnutrition type Marasmus





- Lacto B 2x1



O :

Presence status :

Sensorium : Alert, Body temperature : 36,8 ºC, BW : 5,5 kg, BBI : 8,1kg,

Bl=65cm BW/BL = 67%


Localized status :

Head : Old man face (+), hair can’t be plucked out easily Eye : Sunken


palpebra inferior (-/-),palpebra superior oedem (-/-), Mouth cyanosis




Cannon wave (-)








BP : 110/60


A: Severe malnutrition type Marasmus





- Lacto B 2x1

Planning : Echocardiography

Consult to Haemato oncology

Lab : Hb : 7.00

Ht : 22,8

L : 8,02

T : 69.00



O :

Presence status :


Bl=65cm BW/BL = 67%


Localized status :







Cannon wave (-)









A: Severe malnutrition type marasmus





Advice Haemato oncology :

Anemia ec DD/ 1. Non deficiency anemia

+ Severe malnutrition type marasmus

2. Chronic disease

Lab results : 26th September 2011

Hematology Result Referance

Reticulocyte 11.61% 0.2 – 2.5

Ret. He 29.4 pg 28.8 – 32.9

Hemostasis Result Referance

Ferritin 100.00 ng/mL Adult : 15 – 300

Child : 15 – 240

Ferum 67 mg/dL 61 – 157

TIBC 242 µg/dL 112 – 346

Imunoserology Result Referance

CD 4 % 47 31 – 60

CD 4 absolute 2577 Cell/uL 410 – 1590

Follow Up 27 - 28th September 2011


O :

Presence status :


Bl=65cm BW/BL = 68%


Localized status :







Cannon wave (-)








BP : 100/70



P : - Folic acid 1x 1 mg

- Basefort 1x 1 cth

- Cotrimoxazole syrp 1x ½ cth

- Semi solid diet 3 x 500 calories with11 gr protein plus F 100 120cc/6hrs/oral

Follow Up 29th - 30th September 2011


O :

Presence status :


Bl=65cm BW/BL = 68%


Localized status :



palpebra inferior (-/-) ,palpebra superior oedem (-/-), Mouth cyanosis




Cannon wave (-)








BP : 100/60 mmHg



P : - Folic acid 1x1 mg

- Multivitamin with Fe 1x1

- Semi solid diet 3 x 500 calories with 11 gr protein plus F100 120 cc/6hrs/oral

Planning : Mantoux test

Patient is allowed to go home with scheduled control to the pediatric

department

DISCUSSION AND SUMMARY

According to Medilexicon's medical dictionary: 1

Malnutrition is "Faulty nutrition resulting from malabsorption, poor diet, or overeating."

http://www.medilexicon.com/medicaldictionary.php

Undernutrition is "A form of malnutrition resulting from a reduced supply of food or from

inability to digest, assimilate, and use the necessary nutrients."

Malnutrition is caused mainly by not consuming what the National Health Service (NHS), UK,

calls "the right balance of nutrients from major food groups". These include: 1

Carbohydrates

Fruit and vegetables

Protein

Dairy - vegans are able to find abundant nutrients from non-animal sources

Fats

Subnutrition occurs when an individual does not consume enough food. It may exist if the

person has a poor diet that gives them the wrong balance of basic food groups. According to the

Food and Agriculture Organization (FAO), the number of people globally who were

malnourished stood at 923 million in 2007, an increase of over 80 million since the 1990-92 base

period.1

The World Health Organization (WHO) says that malnutrition is by far the largest contributor to

child mortality globally, currently present in half of all cases. Underweight births and inter-

uterine growth restrictions are responsible for about 2.2 million child deaths annually in the

world. Deficiencies in vitamin A or zinc cause 1 million deaths each year.

WHO adds that malnutrition during childhood usually results in worse health and lower

educational achievements during adulthood. Malnourished children tend to become adults who

have smaller babies. While malnutrition used to be seen as something which complicated such

diseases as measles, pneumonia and diarrhea, it often works the other way round - malnutrition

can cause diseases to occur. 1

In 2000, the WHO2 estimated that malnourished children numbered 181.9 million (32%) in

developing countries. In addition, an estimated 149.6 million children younger than 5 years are

malnourished when measured in terms of weight for age. In south central Asia and eastern

Africa, about half the children have growth retardation due to protein-energy malnutrition. This




figure is 5 times the prevalence in the western world. The World Health Organization (WHO)

estimates that every year ten million children under the age of five died and 50 percent of them

died with protein-energy malnutrition (PEM). Marasmus most commonly occurs in children

younger than 5 years. This period is characterized by increased energy requirements and

increased susceptibility to viral and bacterial infections.

In this case the patient is only 9 months old and his weight for age suggest malnutrition.

His BW/BL is 57%.

Globally, as well as in developed, industrialized countries, the following groups of people are

at highest risk of malnutrition (subnutrition):1

Elderly people, especially those who are hospitalized or in long-term institutional care

Individuals who are socially isolated

People on low incomes (poor people)

People with chronic eating disorders, such as bulimia or anorexia nervosa

People convalescing after a serious illness or condition

Signs and symptoms of malnutrition (subnutrition) include:

Loss of fat (adipose tissue)

Breathing difficulties, a higher risk of respiratory failure

Depression

Higher risk of complications after surgery

Higher risk of hypothermia - abnormally low body temperature

The total number of some types of white blood cells falls; consequently, the immune

system is weakened, increasing the risk of infections.

Higher susceptibility to feeling cold

Longer healing times for wounds

Longer recover times from infections

Longer recovery from illnesses

Lower sex drive

Problems with fertility

Reduced muscle mass

Reduced tissue mass





Tiredness , fatigue, or apathy

Irritability

In more severe cases of malnutrition:

Skin may become thin, dry, inelastic, pale, and cold

Eventually, as fat in the face is lost, the cheeks look hollow and the eyes sunken

Hair becomes dry and sparse, falling out easily

Sometimes, severe malnutrition may lead to unresponsiveness (stupor)

If calorie deficiency continues for long enough, there may be heart, liver and respiratory

failure

Total starvation is said to be fatal within 8 to 12 weeks (no calorie consumption at all)

In our case, our patient experienced loss of fat, the cheeks looked hollow and the eyes sunken.

Children who are severely malnourished typically experience slow behavioral development, even

mental retardation may occur. Even when treated, undernutrition may have long-term effects in

children, with impairments in mental function and digestive problems persisting; in some cases

for the rest of their lives.

Malnutrition, the result of a lack of essential nutrients, resulting in poorer health, may be caused

by a number of conditions or circumstances. In many developing countries long-term (chronic)

malnutrition is widespread - simply because people do not have enough food to eat.

In more wealthy industrialized nations malnutrition is usually caused by1:

Poor diet - if a person does not eat enough food, or if what they eat does not provide

them with the nutrients they require for good health, they suffer from malnutrition. Poor

diet may be caused by one of several different factors. If the patient develops dysphagia

(swallowing difficulties) because of an illness, or when recovering from an illness, they

may not be able to consume enough of the right nutrients.

Mental health problems - some patients with mental health conditions, such as

depression, may develop eating habits which lead to malnutrition. Patients with anorexia

nervosa or bulimia may develop malnutrition because they are ingesting too little food.



http://www.medicalnewstoday.com/releases/8877.php

http://www.medicalnewstoday.com/releases/8877.php

Mobility problems - people with mobility problems may suffer from malnutrition,

simply because they either cannot get out enough to buy foods, or find preparing them

too arduous.

Digestive disorders and stomach conditions - some people may eat properly, but their

bodies cannot absorb the nutrients they need for good health. Examples include patients

with Crohn's disease or ulcerative colitis. Such patients may need to have part of the

small intestine removed (ileostomy). Individuals who suffer from Celiac disease have a

genetic disorder that makes them intolerant to gluten. Patients with Celiac disease have a

higher risk of damage to the lining of their intestines, resulting in poorer food absorption.

Patients who experience serious bouts of diarrhea and/or vomiting may lose vital

nutrients and are at higher risk of suffering from malnutrition.

Alcoholism - an alcoholic is a person who suffers from alcoholism - the body is

dependent on alcohol. Alcoholism is a chronic (long-term) disease. Individuals who

suffer from alcoholism can develop gastritis, or pancreas damage. These problems also

seriously undermine the body's ability to digest food, absorb certain vitamins, and

produce hormones which regulate metabolism. Alcohol contains calories, reducing the

patient's feeling of hunger, so he/she consequently may not eat enough proper food to

supply the body with essential nutrients.

In poorer, developing nations malnutrition is commonly caused by1:

Food shortages - in poorer developing nations food shortages are mainly caused by a

lack of technology needed for higher yields found in modern agriculture, such as nitrogen

fertilizers, pesticides and irrigation. Food shortages are a significant cause of malnutrition

in many parts of the world.

Food prices and food distribution - it is ironic that approximately 80% of malnourished

children live in developing nations that actually produce food surpluses (Food and

Agriculture Organization). Some leading economists say that famine is closely linked to

high food prices and problems with food distribution.

Lack of breastfeeding - experts say that lack of breastfeeding, especially in the

developing world, leads to malnutrition in infants and children. In some parts of the

world mothers still believe that bottle feeding is better for the child. Another reason for

lack of breastfeeding, mainly in the developing world, is that mothers abandon it because



they do not know how to get their baby to latch on properly, or suffer pain and

discomfort.

In this patients originates from a place called Desa Nagosih. It is considered to be a rural area

where food shortage normally occurs. Besides, from the clucking that we got from out patient’s

mother, we found that our patient has been breastfed in a minimal amount not reaching the

recommended six months. The mother could not produce enough milk due to lack of nutritional

food. Thus this contributes to the present malnourished condition of this patient

Echocardiography was performed on this patient. This is because, imaging and

radiographic scans may be ordered to help evaluate the health of internal organs and the normal

growth and development of muscles and bones.normally in long term malnutrition patients, a

disturbance or failure of organ growth is a complication.

The normal clinical sign of marasmus are firstly the patient looks very thin, until the

bones wrapped in skin, face like a parent, patient is normally whiny and fussy. The child

normally has wrinkled skin, subcutaneous fatty tissue is very little to none and on the buttock

area looks like wearing baggy pants. Anaemia is usually present. Some kids also present with

sunken abdomen. Mostly patients present with infections and diarrhea. Stools may be loose, but

this is not a constant feature of the disease. Diarrhoea of an infective nature, as mentioned above,

may commonly have been a precipitating factor. 1

Other clinical manifestation are wasting and stunting that are defined below.

I. wasting: acute current, short-duration malnutrition, where weight for age and weight for

height are low but height for age is normal;

II. stunting: past chronic malnutrition, where weight for age and height for age are low but

weight for height is normal;

III. wasting and stunting: acute and chronic or current long-duration malnutrition, where

weight for age, height for age and weight for height are all low.3

It is difficult to differentiate kwashiorkor and marasmus. Understanding the clinical signs can

help make a better diagnosis3.

Comparison of the features of kwashiorkor and marasmus

Feature Kwashiorkor Marasmus

Growth failure Present Present

Wasting Present Present, marked

Oedema Present (sometimes mild) Absent

Hair changes Common Less common

Mental changes Very common Uncommon

Dermatosis, flaky-paint Common Does not occur

Appetite Poor Good

Anaemia Severe (sometimes) Present, less severe

Subcutaneous fat Reduced but present Absent

Face May be oedematous Drawn in, monkey-like

Fatty infiltration of liver Present Absent

For instance, in this case it is clearly visible that he has baggy pants sign, wasting, no mental

changes, oedema is absent, dermatosis is not found anemia is suspected and old man face is

present. His chief complaint is persistent diarrhea. This patient has no signs of fussiness or

irritability. Based on his symptom it is more likely to diagnose him marasmic instead of

kwashiorkor.

In patients with marasmus metabolic changes occur to cope with the energy deficiency of

the body. 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. 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. 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.4

In general patients with marasmus experience fat stores depletion. Fat storage 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. 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.4

There are several classification used around the world for classifying PEM . Wellcome classification of severe forms of protein-energy malnutrition4

Percentage of standard weight for age Oedema present Oedema absent

60-80 Kwashiorkor Undernourishment

<60 Marasmic kwashiorkor Nutritional marasmus

The Gomez classification of malnutrition based on weight-for-age standards4

Classification Percentage of standard weight for age

Normal >90

Grade I (mild malnutrition) 75-89.9

Grade II (moderate malnutrition) 60-74.9

Grade IIIa (severe malnutrition) <<60

Management of moderate marasmus can be performed on an outpatient basis, but severe

marasmus complicated by a life-threatening condition generally requires inpatient treatment. In

these cases, management is divided into an initial intensive phase followed by a consolidation

phase (rehabilitation), preparing for outpatient follow-up management. The WHO has developed

guidelines to help improve the quality of hospital care for malnourished children and has

prioritized the widespread implementation of these guidelines.4

Severe malnutrition is defined in these guidelines as the presence of severe wasting (<70% weight-for-height or <-3SD) and/or oedema.5

The guidelines are divided in five sections

A. General principles for routine care (the’10 steps’)

B. Emergency treatment of shock and severe anaemia

C. Treatment of associated conditions

D. Failure to respond to treatment

E. Discharge before recovery is complete

There are ten essential steps in treating malnutrition5:

1.Treat/prevent hypoglycaemia

2.Treat/prevent hypothermia

3.Treat/prevent dehydration

4.Correct electrolyte imbalance

5.Treat/prevent infection

6.Correct micronutrient deficiencies

7.Start cautious feeding

8.Achieve catch-up growth

9.Provide sensory stimulation and emotional support

10. Prepare for follow-up after recovery

These steps are accomplished in two phases that are an initial stabilisation phase where the acute

medical conditions are managed and a longer rehabilitation phase.5

Step 1

Hypoglycaemia and hypothermia usually occur together and are signs of infection. Check for

hypoglycaemia whenever hypothermia (axillary<35.0oC; rectal<35.5oC) is found. Frequent

feeding is important in

preventing both conditions.

Treatment:

If the child is conscious and dextrostix shows <3mmol/l or 54mg/dl give:

• 50 ml bolus of 10% glucose or 10% sucrose solution (1 rounded

teaspoon of sugar in 3.5 tablespoons water), orally or by nasogastric (NG) tube. Then feed starter

F-75 every 30 min. for two hours (giving one quarter of the two-hourly feed each time)

• antibiotics

• two-hourly feeds, day and night

If the child is unconscious, lethargic or convulsing give:

• IV sterile 10% glucose (5ml/kg), followed by 50ml of 10% glucose or sucrose by Ng tube.

Then give starter F-75 as above

• antibiotics

• two-hourly feeds, day and night

Monitor:

• blood glucose: if this was low, repeat dextrostix taking blood from finger or heel, after two

hours. Once treated, most children stabilize within 30 min. If blood glucose falls to <3 mmol/l

give a further 50ml

bolus of 10% glucose or sucrose solution, and continue feeding every 30 minutes until stable

• rectal temperature: if this falls to <35.5oC, repeat dextrostix

• level of consciousness: if this deteriorates, repeat dextrostix

Prevention:

• feed two-hourly, start straightaway (see step 7) or if necessary,rehydrate first5

Step 2.

Treatment:

If the axillary temperature is <35.0oC, take the rectal temperature using a low reading

thermometer.

If the rectal temperature is <35.5oC (<95.9oF):

• feed straightaway (or start rehydration if needed)

• rewarm the child: either clothe the child (including head), cover with a warmed blanket and

place a heater or lamp nearby (do not use a hot water bottle), or put the child on the mother’s

bare chest (skin to skin) and cover them

• give antibiotics

Monitor:

• body temperature: during rewarming take rectal temperature two hourly until it rises to

>36.5oC (take half-hourly if heater is used)

• ensure the child is covered at all times, especially at night

• feel for warmth

• blood glucose level: check for hypoglycaemia whenever hypothermia is found

Prevention:

• feed two-hourly, start straightaway (see step 7)

• always give feeds throughout the day and night

• keep covered and away from draughts

• keep the child dry, change wet nappies, clothes and bedding

• avoid exposure (e.g. bathing, prolonged medical examinations)

• let child sleep with mother/carer at night for warmth5

Step 3. Treat/prevent dehydration

Note: Low blood volume can coexist with oedema. Do not use the IV route for rehydration

except in cases of shock and then do so with care, infusing slowly to avoid flooding the

circulation and overloading the heart.

Treatment:

The standard oral rehydration salts solution (90 mmol sodium/l) contains too much sodium and

too little potassium for severely malnourished children. Instead give special Rehydration

Solution for Malnutrition (ReSoMal).

It is difficult to estimate dehydration status in a severely malnourished child using clinical signs

alone. So assume all children with watery diarrhea may have dehydration and give:

• ReSoMal 5 ml/kg every 30 min. for two hours, orally or by nasogastric tube, then

• 5-10 ml/kg/h for next 4-10 hours: the exact amount to be given should be determined by how

much the child wants, and stool loss and vomiting. Replace the ReSoMal doses at 4, 6, 8 and 10

hours with F-75 if rehydration is continuing at these times, then

• continue feeding starter F-75 (see step 7)

During treatment, rapid respiration and pulse rates should slow down and the child should begin

to pass urine.

Monitor progress of rehydration:

Observe half-hourly for two hours, then hourly for the next 6-12 hours, recording:

• pulse rate

• respiratory rate

• urine frequency

• stool/vomit frequency

Return of tears, moist mouth, eyes and fontanelle appearing less sunken, and improved skin

turgor, are also signs that rehydration is proceeding. Itshould be noted that many severely

malnourished children will not show these changes even when fully rehydrated. Continuing rapid

breathing and pulse during rehydration suggest coexisting infection or overhydration. Signs of

excess fluid (overhydration) are increasing respiratory rate and pulse rate, increasing oedema and

puffy eyelids. If these signs occur, stop fluids immediately and reassess after one hour.

To prevent dehydration when a child has continuing watery diarrhoea:

• keep feeding with starter F-75 (see step 7)

• replace approximate volume of stool losses with ReSoMal. As a guide give 50-100 ml after

each watery stool. (Note: it is common for malnourished children to pass many small unformed

stools: these should not be confused with profuse watery stools and do not require fluid

replacement)

• if the child is breastfed, encourage to continue5

Step 4. Correct electrolyte imbalance

All severely malnourished children have excess body sodium even though plasma sodium may

be low (giving high sodium loads will kill). Deficiencies of potassium and magnesium are also

present and may take at least two weeks to correct. Oedema is partly due to these imbalances.

Give:

• extra potassium 3-4 mmol/kg/d

• extra magnesium 0.4-0.6 mmol/kg/d

• when rehydrating, give low sodium rehydration fluid (e.g. ReSoMal)

• prepare food without salt

The extra potassium and magnesium can be prepared in a liquid form and added directly to feeds

during preparation. Appendix 3 provides a recipe for a combined electrolyte/mineral solution.

Adding 20 ml of this solution to 1 litre of feed will supply the extra potassium and magnesium

required. The solution can also be added to ReSoMal.5

Step 5: Treat/prevent infection

In severe malnutrition the usual signs of infection, such as fever, are often absent, and infections

are often hidden.

Therefore give routinely on admission:

• broad-spectrum antibiotic(s) and

• measles vaccine if child is > 6m and not immunized (delay if the child is in shock)5

Step 6. Correct micronutrient deficiencies

All severely malnourished children have vitamin and mineral deficiencies. Although anaemia is

common, do not give iron initially but wait until the child has a good appetite and starts gaining

weight (usually by the second week), as giving iron can make infections worse.

Give:

• Vitamin A orally on Day 1 (for age >12 months, give 200,000 IU; for age 6-12 months, give

100,000 IU; for age 0-5 months, give 50,000 IU) unless there is definite evidence that a dose has

been given in the last month

Give daily for at least 2 weeks:

• Multivitamin supplement

• Folic acid 1 mg/d (give 5 mg on Day 1)

• Zinc 2 mg/kg/d

• Copper 0.3 mg/kg/d

• Iron 3 mg/kg/d but only when gaining weight

Appendix 3 provides a recipe for a combined electrolyte/mineral solution. Adding 20 ml of this

solution to 1 litre of feed will supply the zinc and copper needed, as well as potassium and

magnesium. This solution can also be added to ReSoMal.5

Step 7. Start cautious feeding

In the stabilisation phase a cautious approach is required because of the child’s fragile

physiological state and reduced homeostatic capacity. Feeding should be started as soon as

possible after admission and should be designed to provide just sufficient energy and protein to

maintain basic physiological processes. The essential features of feeding in the stabilisation

phase are:

• small, frequent feeds of low osmolarity and low lactose

• oral or nasogastric (NG) feeds (never parenteral preparations)

• 100 kcal/kg/d

• 1-1.5 g protein/kg/d

• 130 ml/kg/d of fluid (100 ml/kg/d if the child has severe oedema)

• if the child is breastfed, encourage to continue breastfeeding but give the prescribed amounts of

starter formula to make sure the child’s needs are met. The suggested starter formula and feeding

schedules (see below) are designed to meet these targets. Milk-based formulas such as starter F-

75 containing 75 kcal/100 ml and 0.9 g protein/100 ml will be satisfactory for most children (see

Appendix 5 for recipes). Give from a cup. Very weak children may be fed by spoon, dropper

or syringe. A recommended schedule in which volume is gradually increased, and feeding

frequency gradually decreased is:

Days Frequency Vol/kg/feed Vol/kg/d

1-2 2-hourly 11 ml 130 ml

3-5 3-hourly 16 ml 130 ml

6-7+ 4-hourly 22 ml 130 ml

For children with a good appetite and no oedema, this schedule can be completed in 2-3 days

(e.g. 24 hours at each level). Appendix 6 shows the volume/feed already calculated according to

body weight. Appendix 7 gives the feed volumes for children with severe oedema. Use the Day 1

weight to calculate how much to give, even if the child loses or gains weight in this phase.5

If, after allowing for any vomiting, intake does not reach 80 kcal/kg/d (105 ml starter

formula/kg) despite frequent feeds, coaxing and re-offering, give the remaining feed by NG tube

Do not exceed 100 kcal/kg/d in this phase.

Monitor and note:

• amounts offered and left over

• vomiting

• frequency of watery stool

• daily body weight

During the stabilisation phase, diarrhoea should gradually diminish and oedematous children

should lose weight. If diarrhoea continues unchecked despite cautious refeeding, or worsens

substantially, see section C4 (continuing diarrhoea).5

Step 8. Achieve catch-up growth

In the rehabilitation phase a vigorous approach to feeding is required to achieve very high

intakes and rapid weight gain of >10 g gain/kg/d. The recommended milk-based F-100 contains

100 kcal and 2.9 g protein/100 ml (see Appendix 5 for recipes). Modified porridges or modified

family foods can be used provided they have comparable energy and protein concentrations.

Readiness to enter the rehabilitation phase is signalled by a return of appetite, usually about one

week after admission. A gradual transition is recommended to avoid the risk of heart failure

which can occur if children suddenly consume huge amounts.To change from starter to catch-up

formula replace starter F-75 with the same amount of catch-up formula F-100 for 48 hours then,

increase each successive feed by 10 ml until some feed remains uneaten. The point when some

remains unconsumed is likely to occur when intakes reach about 30 ml/kg/feed (200 ml/kg/d).5

Monitor during the transition for signs of heart failure:

• respiratory rate

• pulse rate

If respirations increase by 5 or more breaths/min and pulse by 25 or more beats/min for two

successive 4-hourly readings, reduce the volume per feed (give 4-hourly F-100 at 16 ml/kg/feed

for 24 hours, then 19 ml/kg/feed for 24 hours, then 22 ml/kg/feed for 48 hours, then increase

each feed by 10 ml as above).

After the transition give frequent feeds (at least 4-hourly) of unlimited amounts of a catch up

formula

• 150-220 kcal/kg/d

• 4-6 g protein/kg/d

if the child is breastfed, encourage to continue. Breast milk does not have sufficient energy and

protein to support rapid catch-up growth.

Monitor progress after the transition by assessing the rate of weight gain:

• weigh child each morning before feeding.

• each week calculate and record weight gain as g/kg/d3

If weight gain is:

• poor (<5 g/kg/d), child requires full reassessment

• moderate (5-10 g/kg/d), check whether intake targets are being met,or if infection has been

overlooked.

• good (>10 g/kg/d), continue to praise staff and mothers5

Step 9. Provide sensory stimulation and emotional support

In severe malnutrition there is delayed mental and behavioural development.

Provide:

• tender loving care

• a cheerful, stimulating environment

• structured play therapy 15-30 min/d (Appendix 10 provides examples)

• physical activity as soon as the child is well enough

• maternal involvement when possible (e.g. comforting, feeding, bathing, play)5

Step 10. Prepare for follow-up after recovery

A child who is 90% weight-for-length (equivalent to -1SD) can be considered to have recovered.

The child is still likely to have a low weight-for-age because of stunting. Good feeding practices

and sensory stimulation should be continued at home. Show parent or carer how to:

• feed frequently with energy- and nutrient-dense foods

• give structured play therapy5

Advise parent or carer to:

• bring child back for regular follow-up checks

• ensure booster immunizations are given

• ensure vitamin A is given every six months5

Diarrhoea is a common feature of malnutrition but it should subside during the first week of

treatment with cautious feeding. In the rehabilitation phase, loose, poorly formed stools are no

cause for concern provided weight gain is satisfactory.Mucosal damage and giardiasis are

common causes of continuing diarrhoea. Where possible examine the stools by microscopy.

Give:

• metronidazole (7.5 mg/kg 8-hourly for 7 days) if not already given .Lactose intoleranceis only

rarely is diarrhoea due to lactose intolerance. Treat only if continuing diarrhoea is preventing

general improvement. Starter F-75 is a low-lactose feed. In exceptional cases substitute milk

feeds with yoghurt or a lactose-free infant formula and reintroduce milk feeds gradually in the

rehabilitation phase. Osmotic diarrhoea may be suspected if diarrhoea worsens substantially with

hyperosmolar starter F-75 and ceases when the sugar content is reduced and osmolarity is <300

mOsmol/l. In these cases use isotonic F-75 or low osmolar cereal-based F-75 and introduce F-

100 gradually.5

If TB is strongly suspected (contacts with adult TB patient, poor growth despite good

intake, chronic cough, chest infection not responding to antibiotics) perform Mantoux test (false

negatives are frequent) chest X-ray if possible. If test is positive or there is a strong suspicion of

TB, treat according to national TB guidelines.5

FAILURE TO RESPOND TO TREATMENT

Failure to respond is indicated by:5

• within 24 hours: consider untreated or delayed treatment of hypoglycaemia, hypothermia,

septicaemia, severe anaemia or incorrect rehydration fluid or volume.

• within 72 hours: check whether the volume of feed is too high or the wrong formulation is used

• at night: consider hypothermia from insufficient covers, no night feeds

• when changing to catch-up F-100: consider too rapid a transition

2. Low weight gain during the rehabilitation phase

Poor: <5g/kg/d

Moderate: 5-10g/kg/d

Good: >10 g/kg/d

If weight gain is <5 g/kg/d determine:

• whether this is for all cases (need major management overhaul)

• Whether this is for specific cases (reassess child as for a new admission)

Possible causes of poor weight gain are:

a) Inadequate feeding

Check:

• That night feeds are given

• That target energy and protein intakes are achieved: is actual intake (offered minus leftovers)

correctly recorded? Is the quantity of feed recalculated as the child gains weight? Is the child

vomiting or ruminating?

Feeding technique: is the child fed frequently and offered unlimited amounts?

• Quality of care: are staff motivated/gentle/loving/patient?

• All aspects of feed preparation: scales, measurement of ingredients, mixing, taste, hygienic

storage, adequate stirring if the ingredients separate out

• That if giving family foods, they are suitably modified to provide >100 kcal/100g (if not, re-

modify). If resources for modification are limited, or children are not inpatients, compensate by

replacing F-100 with catchup F-135 containing 135 kcal/100ml.

b) Specific nutrient deficiencies

Check:

• adequacy of multivitamin composition and shelf-life

• preparation of electrolyte/mineral solution and whether this is correctly prescribed and

administered. If in goitrous region, check potassium iodide (KI) is added to the

electrolyte/mineral solution (12 mg/2500 ml) or give all children Lugol’s iodine (5-10 drops/day)

• that, if modified family foods are substantially replacing F-100, electrolyte/ mineral solution is

added to the family food (20 ml/day)

c) Untreated infection

If feeding is adequate and there is no malabsorption, some hidden infection can be suspected.

Urinary tract infections, otitis media, TB and giardiasis are easily overlooked, hence re-examine

carefully, repeat urinalysis for white blood cells, examine stools and if possible, take chest X-

ray. Later alter the antibiotic schedule only if a specific infection is identified.

d) HIV/AIDS

In children with HIV/AIDS, good recovery from malnutrition is possible though it may take

longer and treatment failures may be common. Lactose intolerance occurs in severe HIV-related

chronic diarrhoea. Treatment should be the same as for HIV negative children.5

Our patient is administered F75 diet 55cc orally every two hours and was later increased

to F100 diet 55cc orally every two hours. For the first few days the patient was give resomal

until the diarrhea stops. Cotrimoxazole syrup was given as a prophylaxis antibiotics. Later on as

patient showed less improvement in weight gain, the F100 diet was increased .

Mortality of hospitalized children with marasmus is high, especially during the first few

days of rehabilitation. Death is usually caused by infections or other causes. If the child has no

clinical sign of infection, the WHO recommends 5 days of oral cotrimoxazole therapy. If the

child presents with clinical signs of infection, hypoglycemia, or hypothermia he or she must be

considered as seriously infected and treated with parenteral ampicillin and gentamicin. Practice

guidelines for acute diarrhea have been established. Persistent and profuse diarrhea has 2 main

causes. Infectious etiology (especially lambliasis). This can be promptly treated with

metronidazole if possible, after stool examination. In osmotic diarrheas sugar of the F75 solution

should be replaced by cereal flour for 1-2 weeks. 2

Malnutrition places stressed patients at a greatly increased risk for morbidity and

mortality. Numerous reports have documented the association between malnutrition and clinical

outcome in a variety of clinical settings.

Some complications are considerably more common in malnourished patients and those with

inadequate nutrient intake than in well-nourished individuals.

These complications include: 3

A longer recovery period.

Impaired host defenses and sepsis.



Impaired wound healing.

Anemia.

Impaired GI tract function.

Muscle atrophy.

Impaired cardiac function.

Impaired respiratory function.

Reduced renal function.

Brain dysfunction.

Delayed bone callus formation.

Atrophic skin.

Malnutrition is a common factor seen in HIV/AIDS patients especially kids.

There is usually a combination of reasons why people with AIDS become malnourished.

First of all, there is the impact of HIV itself. The virus can cause changes in the body's

metabolism. Metabolic disturbances may cause the metabolic rate to go up. This results

in the body burning calories more quickly than is normal and thus requiring more calories

than is normal. If the HIV+ patient is not taking in enough calories to make up for this

increased metabolic rate, he/she can quickly become malnourished. Another metabolic

deregulation that we sometimes find with HIV is cachexia. Normally, when someone is

malnourished, their body burns fat and preserves the lean tissue mass. With cachexia,

there is accelerated tissue loss, with an almost immediate depletion of lean tissue mass.

This speeds up the wasting and brings on immediate threats. Diarrhea is a common

symptom of HIV disease and can contribute to malnutrition. Some of the causes of

diarrhea are amoebas, cryptosporidium and microsporidium. With these conditions, the

body is not able to absorb the calories that it is taking in. Besides the absorption

problems, diarrhea can also cause someone to cut down or stop eating. For these reasons,

chronic diarrhea can bring on severe wasting. Many people with AIDS suffer from

nausea. Chemotherapy for lymphoma can bring this on, as well as many of the drugs used

to fight opportunistic infections. When people are nauseous, they simply do not want to

eat. This is very dangerous for PWAs, and can start the weight loss that can become life

http://www.aegis.com/pubs/nmap/509-lymphoma.html

threatening. A host of oral problems can also stop someone from eating. Gum disease,

herpes in the mouth, lesions in the mouth or esophagus, oral candida, and oral ulcers are

all problems that people with HIV may face. All of these conditions make it painful to eat

or swallow; without realizing it, someone with any one of these conditions can begin to

avoid eating and become malnourished. 2

Our patient was done CD4+ count to eradicate the possibility of HIV causing the

malnutrition and the result suggest no HIV present. The patient has diarrhea that may have been

the cause of his poor hygiene practice by family in food presentation or way of living.

The next discussion is about diarrhea that is present in the patient. Diarrhea occurs

commonly in both children and adults. Diarrhea lasting less than seven days is considered acute.

The majority of diarrheal episodes fall into this category. Diarrhea lasting more than 7 days is

defined as persistent, while diarrhea for more than 30 days is chronic. Malabsorption is the

body's inability to use the food that it takes in, often causing diarrhea.5

Diarrhea lasting more than seven days can be caused by a number of different problems,

including6

Chronic gastroenteritis can be caused by infections, including those caused by viruses,

bacteria and parasites. Most children with chronic diarrhea will have a stool test for polys

and blood, a routine bacterial culture, an ova and parasite test, a test for the Giardia

antigen and C. difficile toxin, especially if he has recently been on antibiotics.10

Postinfectious diarrhea sometimes occurs in children with gastroenteritis and may be

from an intolerance to lactose or proteins in cow's milk. Soy milk or formula (for younger

children) may be helpful for children with this condition.8

Toddler's Diarrhea or chronic nonspecific diarrhea usually occurs in children between the

ages of 6 months and 3 years, and causes loose, watery stools in children without other

symptoms. Although they have chronic diarrhea, children with toddler's diarrhea should

have a normal appetite and will be growing and developing normally, and usually drink

too much juice. If your doctor suspects that you child's diarrhea is from this condition,

then it may help to decrease the amount of fluids your child drinks, and especially avoid

juices with a high sorbital or fructose content, like apple and pear juice. Instead, give him

orange and grape juice. It may also help to increase the amount of fat and fiber in his

diet.6

Malabsorption can be caused by many different medical conditions, including cystic

fibrosis, short bowel syndrome, celiac disease or gluten sensitive enteropathy and

infections, especially Giardiasis. Children with malabsorption typically have very large

and foul smelling stools, which may appear greasy, weight loss or poor weight gain and

abdominal distention. An examination for stool fat content or a 72 hour stool collection

for fat analysis, a test for carbohydrate by checking for reducing substances, and testing

the stool pH may be helpful to see if a child has malabsorption. Children with

malabsorption may also have a low serum albumin concentration. Other testing may

include a small bowel biopsy.6

Inflammatory bowel disease , including Ulcerative Colitis and Crohn's disease, with the

most common symptoms being diarrhea, usually with bleeding, cramping abdominal

pain, obstruction (a blockage of the intestine), malabsorption (failure of the intestines to

absorb minerals and nutrients), and weight loss or poor weight gain. Other symptoms can

include fever, anorexia (poor appetite), anemia (low blood counts), skin rashes, especially

erythema nodosum (tender red bumps or nodules on the front of the lower legs) and

pyoderma gangrenosum (painful skin ulcers), oral aphthous ulcers, and hepatitis

(inflammation of the liver). Children with Crohn disease can also have perirectal disease,

with fistulas, abscesses, or fissures around the rectum.6

lactose intolerance causes diarrhea, abdominal pain, bloating, gas and weight loss can

occur in children who don't have enough of the enzyme lactase to digest lactose in the

foods they eat. While some children do have to avoid all products with lactose, others are

able to handle some foods, such as yogurt, and other foods after taking a lactase enzyme

supplement.6

Other causes of chronic diarrhea can include food intolerances, immune disorders,

metabolic abnormalities, hormone secreting tumors, and other conditions that affect the

pancreas, liver or small intestine.6

http://www.keepkidshealthy.com/welcome/conditions/lactose_intolerance.html

http://www.keepkidshealthy.com/welcome/conditions/crohns_disease.html

http://www.keepkidshealthy.com/welcome/conditions/inflammatoryboweldisease.html

http://www.keepkidshealthy.com/welcome/conditions/celiac_disease.html

http://www.keepkidshealthy.com/welcome/conditions/cysticfibrosis.html

http://www.keepkidshealthy.com/welcome/conditions/cysticfibrosis.html

In our case, our patient comes with the complaint of constant diarrhea more than one

month. The content of the feces is water more than waste. Besides that, our patient also vomits

out whatever which is being eaten up.

Referance

1. American Association for Clinical Chemistry 2011. Accesed on 2011-10-03.

2. World Health Organization. WHO Global Database on Child Growth and Malnutrition.

Geneva: WHO. 1997.

3. Rich Klasco, M.D., FACEP. Kwashiorkor symptoms and diagnosis.

http://www.bettermedicine.com/article/kwashiorkor

4. Noah S Scheinfeld, MD, JD, FAAD; Chief Editor: William D James, MD.


5. Crosworth Ann, Guidelines for the inpatient treatment of the severely malnourished

patient. WHO Publication 2003.

6. DuPont HL, Practice Parameters Committee of the American College of

Gastroenterology. Guidelines on acute infectious diarrhea in adults. The American

Journal of Gastroenterology. 1997;92(11):1962–1975.


7. Ramaswamy K, Jacobson K. Infectious diarrhea in children. Gastroenterology Clinics of

North America. 2001;30(3):611–624

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