REFERAT ILMU KESEHATAN ANAK

PROTEIN ENERGY MALNUTRITION

Preceptor: dr. Pulung M. Silalahi, Sp.A

Compiled by:

Naina Karamina Sakina (07120100102)KEPANITERAAN KLINIK ILMU KESEHATAN ANAKRUMAH SAKIT BHAYANGKARA TK. I RADEN SAID SUKANTO

FAKULTAS KEDOKTERAN UNIVERSITAS PELITA HARAPAN

PERIODE 9 JUNI 2014 16 AGUSTUS 2014

FOREWORD

Praise to Almighty God for the gift of grace so that I can finish the task referat given by the supervisor. Referat is made for the settlement of their clinical duties for Co-Ass the Faculty of Medicine, University of Pelita Harapan granted by SMF Section of Child Health Level I Police Hospitals Raden Said Sukanto.

Referat discussed thoroughly on Protein Energy Malnutrition. Materials for referat taken from books and journals and articles that are available online. The authors hope that this made referat be useful for the readers. Hope the authors that the presence of this referat can help understand more thoroughly the topics being discussed.

Thank you to all those who have assisted in the completion of this referat manufacture. Especially the counselors at the child, especially dr. Pulung M. Silalahi, Sp. A writer in the making as mentors this referat and all parties that provide direction and support in the process of resolving this referat.

The author realizes that this referat still far from perfect and has many flaws. Therefore, the authors are happy to accept all criticisms and feedback given that this referat be more perfect. Finally, I hope this referat be useful for writers and readers. May God bless us all. Amen.

Jakarta, June 2014

authorTABLE OF CONTENTS2FOREWORD

TABLE OF CONTENTS3

Error! Bookmark not defined.CHAPTER I

Error! Bookmark not defined.INTRODUCTION

Error! Bookmark not defined.CHAPTER II

Error! Bookmark not defined.LITERATURE REVIEW

Error! Bookmark not defined.2.1. Definition

Error! Bookmark not defined.2.2. Epidemiology

Error! Bookmark not defined.2.3. Etiologi

Error! Bookmark not defined.2.4. Klasifikasi histopatologi

Error! Bookmark not defined.2.5. Patofisiologi

Error! Bookmark not defined.2.6. Gejala Klinis

Error! Bookmark not defined.2.7. Diagnosis

Error! Bookmark not defined.2.8. Penatalaksanaan

Error! Bookmark not defined.2.9. Komplikasi

Error! Bookmark not defined.2.10. Prognosis

Error! Bookmark not defined.CHAPTER III

Error! Bookmark not defined.CONCLUSION

Error! Bookmark not defined.BIBLIOGRAPHY

CHAPTER I

INTRODUCTION

1.1 Background

Protein Energy Malnutrition (PEM) is one of the major nutritional problems in Indonesia. This situation affects many groups of infants who are the future generation. PEM may cause a disturbance in growth and mental development disorders. Infants and children with severe PEM level will show clinical signs of kwashiorkor or marasmus.

In the advanced phase of children under five with PEM will be susceptible to disease infection, swelling of the liver, the organ and its function abnormalities, skin inflammation and impaired brain growth. In addition, the impact of PEM in children under five can lower the immune system so that children are often sick. According to Schroeder (2001), children under five with PEM are at risk of decline in motor development, lower cognitive function as well as the capacity and performance of PEM ultimately have a negative effect on the high risk of death. In addition, children who had suffered from malnutrition will be difficult to pursue growth according to age.

PEM in children in certain levels can cause brain weight, cell number, cell size, and other biochemical substances is lower than in normal children. The younger children who suffer from the more severe PEM also consequences thereof. This situation will become even greater when malnutrition starts in the womb. Mental retardation caused by malnutrition state of mild or moderate tend to be restored by increasing the good state of nutrition and the environment the child is raised.

1.2Purpose of writing

Understanding more about the protein energy malnutrition

1.3 Problems

1.3.1Definition, epidemiology, and risk factor of protein energy malnutrition

1.3.2Etiology, pathogenesis, and clinical manifestations of protein energy malnutrition

1.3.3Diagnosis, differential diagnosis, treatment, and prevention of protein energy malnutrition

1.4Benefits of writing

1.4.1 Provide an understanding of protein energy malnutrition diagnosis and management so that the right can be granted

1.4.2 As a source of knowledge for other academics to be the development of subsequent papersCHAPTER II

LITERATURE REVIEW

2.1Definition

Malnutrition is a 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 malnutrition encompasses both ends of the nutrition spectrum, from undernutrition (underweight, stunting, wasting, and micronutrient deficiencies) to overnutrition (overweight, obesity). Nutritional status is often assessed in terms of anthropometry. International references have been established that allow normalization of anthropometric measures in terms of z scores defined as the childs height (weight) minus the median height (weight) for the age and sex of the child divided by the relevant standard deviation (Table 43-3).

Protein-energy malnutrition (PEM) is manifested primarily by inadequate dietary intakes of protein and energy, either because the dietary intakes of these 2 nutrients are less than required for normal growth or because the needs for growth are greater than can be supplied by what otherwise would be adequate intakes. PEM is almost always accompanied by deficiencies of other nutrients. Based on the duration and severity of protein and energy deficiency, PEM is classified into 2 grades, mild-moderate PEM and severe PEM. Mild-moderate PEM not yet shown the typical clinical manifestation, found only impairment of growth and underweight children. In severe PEM, besides the clinical symptoms also found biochemical abnormalities in accordance with the clinical form. Severe PEM, applies to a group of related disorders that include marasmus (nonedematous malnutrition with severe wasting), kwashiorkor (edematous malnutrition), and marasmus-kwashiorkor (wasting and edema). Nonedematous malnutrition was believed to result primarily from inadequate energy intake or inadequate intakes of both energy and protein, whereas edematous malnutrition was believed to result primarily from inadequate protein intake. The 3 conditions have distinct clinical and metabolic features, but they also have a number of overlapping features. A low plasma albumin concentration, often believed to be a manifestation of edematous malnutrition, is common in children with both edematous and nonedematous malnutrition.

The term marasmus is derived from the Greek word marasmos, which means withering or wasting, which is due to prolonged caloric deprivation or inadequate intake of protein and calories and is characterized by emaciation. It is characterized by severe wasting of fat and muscle, which results in an old-person skin-and-bones appearance. This is the most common form of PEM seen in nutritional emergencies where food shortages are severe. In contrast to the relative anorexia seen in children with kwashiorkor (who may be getting enough calories but not enough protein), children with marasmus are hungry. It is also be the result of chronic or recurring infections with decreased food intake.

The term kwashiorkor is taken from the Ga language of Ghana and means "the sickness of the weaning." It refers to an inadequate protein intake with reasonable caloric (energy) intake. Kwashiorkor is a disease brought on due to a severe dietary protein deficiency, and this child, whose diet fit such a deficiency profile, presented with symptoms including edema of legs and feet, light-colored, thinning hair, anemia, a pot-belly, and shiny skin. Edema is characteristic of kwashiorkor but is absent in marasmus. 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.

In the USA, severe malnutrition has been reported in families who use unusual and inadequate foods to feed infants whom the parents believe to be at risk for milk allergies and also in families who believe in fad diets. Many cases are associated with rice milk diets, a product that is very low in protein content. In addition, protein-calorie malnutrition has been noted in chronically ill patients in neonatal or pediatric intensive care units as well as among patients with burns, HIV, cystic fibrosis, failure to thrive, chronic diarrhea syndromes, malignancies, bone marrow transplantation, and inborn errors of metabolism.2.2Epidemiology

Protein energy malnutrition is one of the major nutritional problems in Indonesia. According to SUSENAS 2002, 26% of under-5s suffer from malnutrition. Approximately 70.0% of the world's malnourished children live in Asia, resulting in the region having the highest concentration of childhood malnutrition. About half of the preschool children are malnourished ranging from 16.0% in the People's Republic of China to 64.0% in Bangladesh.

Prevalence of stunting and underweight are high especially in South Asia where one in every two preschool children is stunted. In 2004 37% of under-5s were underweight (28% moderately underweight, and 9% severely underweight) and 38% were too short (source Susenas 2004 - National Socio-Economic Survey Survei Sosial Ekonomi Nasional).

The prevalent rate of mild and severe Protein Energy Deficiency in children under five in Indonesia in 2000 are 17,13% and 7,53%, along with 19,3% and 8% in 2002, according to Susenas 2000.

In 2003, the prevalent of protein energy deficiency in children are 27,5% (5 million under five child with protein energy malnutrition), 19,2% (3,5 million) mild protein energy deficiency, and 8,3% (1,5 million) severe protein energy deficiency, whereas in 2005, the prevalent of protein energy deficiency has rise to 19,2 % for mild malnutrition and 8,8 % for severe malnutrition according to ministry of health republic of Indonesia (2006).

The prevalent of malnutrition has dropped from 18,4% (13% mild malnutrition, 5,4% severe malnutrition) in 2007 to 17,9% (13% mild malnutrition, 4,9% severe malnutrition) in 2010 according to Riskesdas 2010 data as shown in table below :

2.3Etiology

Social and economic factors

Biological factors

Environmental factors

Amongst the social, economic, biological, and environmental factors the common causes are :

Lack of breast feeding and giving diluted formula

Improper complementary feeding

Over crowding in family

Ignorance

Illiteracy

Lack of health education

Poverty

Infection

Familial disharmony

Role of free radicals and Aflatoxin

Two new theories have been postulated recently to explain the pathogenesis of kwashiorkor. These include free radical damage and aflatoxin poisoning. These may damage liver cells giving rise to kwashiorkor.

Age of the host

PEM frequent happens in infants and young children whose rapid growth increases nutritional requirement. PEM in pregnant and lactating women can affect the growth, nutritional status, and survival rates of their fetuses, new born, and infants. Elderly can also suffer from PEM due to alteration of GI system.

Protein Energy Malnutrition can be divided into primary or secondary. Primary PEM is caused by inadequate nutrient intake. Secondary PEM results from disorders or drugs that interfere with nutrient use.

Primary PEU: Worldwide, primary PEM occurs mostly in children and the elderly who lack access to nutrients, although a common cause in the elderly is depression. PEM can also result from fasting or anorexia nervosa. Child or elder abuse may be a cause.

In children, chronic primary PEM has 2common forms: marasmus and kwashiorkor. The form depends on the balance of nonprotein and protein sources of energy. Starvation is an acute severe form of primary PEU.

Secondary PEU: This type most commonly results from the following: Disorders that affect GI function: These disorders can interfere with digestion (eg, pancreatic insufficiency), absorption (eg, enteritis, enteropathy), or lymphatic transport of nutrients (eg, retroperitoneal fibrosis, Milroy disease). Wasting disorders: In wasting disorders (eg, AIDS, cancer, COPD) and renal failure, catabolism causes cytokine excess, resulting in undernutrition via anorexia and cachexia (wasting of muscle and fat). End-stage heart failure can cause cardiac cachexia, a severe form of undernutrition; mortality rate is particularly high. Factors contributing to cardiac cachexia may include passive hepatic congestion (causing anorexia), edema of the intestinal tract (impairing absorption), and, in advanced disease, increased O2 requirement due to anaerobic metabolism. Wasting disorders can decrease appetite or impair metabolism of nutrients. Conditions that increase metabolic demands: These conditions include infections, hyperthyroidism, pheochromocytoma, other endocrine disorders, burns, trauma, surgery, and other critical illnesses.

2.4 PathophysiologyWhy edematous malnutrition develops in some children and nonedematous malnutrition develops in others is unknown. One factor may be the variability among infants in nutrient requirements and in body composition at the time the dietary deficit is incurred. It also has been proposed that giving excess carbohydrate to a child with nonedematous malnutrition reverses the adaptive responses to low protein intake, resulting in mobilization of body protein stores. Eventually, albumin synthesis decreases, resulting in hypoalbuminemia with edema. Fatty liver also develops secondary, perhaps, to lipogenesis from the excess carbohydrate intake and reduced apolipoprotein synthesis. Other causes of edematous malnutrition are aflatoxin poisoning as well as diarrhea, impaired renal function and decreased Na+/K+-ATPase activity. Free radical damage has been proposed as an important factor in the development of edematous malnutrition. This proposal is supported by low plasma concentrations of methionine, a dietary precursor of cysteine, which is needed for synthesis of the major antioxidant factor, glutathione. This possibility also is supported by lower rates of glutathione synthesis in children with edematous compared with nonedematous malnutrition.

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.

Protein-energy malnutrition also involves an inadequate intake of many essential nutrients. Low serum levels of zinc have been implicated as the cause of skin ulceration in many patients. In a 1979 study of 42 children with marasmus, investigators found that only those children with low serum levels of zinc developed skin ulceration. Serum levels of zinc correlated closely with the presence of edema, stunting of growth, and severe wasting. The classic "mosaic skin" and "flaky paint" dermatosis of kwashiorkor bears considerable resemblance to the skin changes of acrodermatitis enteropathica, the dermatosis of zinc deficiency.

Marasmus and kwashiorkor can both be associated with impaired glucose clearance that relates to dysfunction of pancreatic beta-cells.[3] In utero, plastic mechanisms appear to operate, adjusting metabolic physiology and adapting postnatal undernutrition and malnutrition to define whether marasmus and kwashiorkor will develop.[4]2.5Clinical Manifestations

Nonedematous malnutrition (marasmus) is characterized by failure to gain weight and irritability, followed by weight loss and listlessness until emaciation results. The skin loses turgor and becomes wrinkled and loose as subcutaneous fat disappears. Loss of fat from the sucking pads of the cheeks often occurs late in the course of the disease; thus, the infants face may retain a relatively normal appearance compared with the rest of the body, but this, too, eventually becomes shrunken and wizened. Infants are often constipated, but they can have starvation diarrhea, with frequent small stools containing mucus. The abdomen may be distended or flat, with the intestinal pattern readily visible. There is muscle atrophy and resultant hypotonia. As the condition progresses, the temperature usually becomes subnormal and the pulse slows. Clinical features of marasmusPoor growth. In all cases the child fails to grow properly. If the age is known, the weight will be found to be extremely low by normal standards (below 60 percent or -3 SD of the standard). In severe cases the loss of flesh is obvious: the ribs are prominent; the belly, in contrast to the rest of the body, may be protuberant; the face has a characteristic simian (monkey-like) appearance; and the limbs are very emaciated. The child appears to be skin and bones. An advanced case of the disease is unmistakable, and once seen is never forgotten.

Wasting. The muscles are always extremely wasted. There is little if any subcutaneous fat left. The skin hangs in wrinkles, especially around the buttocks and thighs. When the skin is taken between forefinger and thumb, the usual layer of adipose tissue is found to be absent.

Alertness. Children with marasmus are quite often not disinterested like those with kwashiorkor. Instead the deep sunken eyes have a rather wide-awake appearance. Similarly, the child may be less miserable and less irritable.

Appetite. The child often has a good appetite. In fact, like any starving being, the child may be ravenous. Children with marasmus often violently suck their hands or clothing or anything else available. Sometimes they make sucking noises.

Anorexia. Some children are anorexic.

Diarrhoea. 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.

Anaemia. Anaemia is usually present.

Skin sores. There may be pressure sores, but these are usually over bony prominences, not in areas of friction. In contrast to kwashiorkor, there is no oedema and no flaky-paint dermatosis in marasmus.

Hair changes. Changes similar to those in kwashiorkor can occur. There is more frequently a change of texture than of colour.

Dehydration. Although not a feature of the disease itself, dehydration is a frequent accompaniment of the disease; it results from severe diarrhoea (and sometimes vomiting).

Edematous malnutrition (kwashiorkor) can occur initially as vague manifestations that include lethargy, apathy, and/or irritability. When kwashiorkor is advanced, there is lack of growth, lack of stamina, loss of muscle tissue, increased susceptibility to infections, vomiting, diarrhea, anorexia, flabby subcutaneous tissues, and edema. The edema usually develops early and can mask the failure to gain weight. It is often present in internal organs before it is recognized in the face and limbs. Liver enlargement can occur early or late in the course of disease. Dermatitis is common, with darkening of the skin in irritated areas, but in contrast to pellagra not in areas exposed to sunlight. Depigmentation can occur after desquamation in these areas, or it may be generalized. The hair is sparse and thin, and in dark-haired children, it can become streaky red or gray. Eventually, there is stupor, coma, and death.

Clinical signs of kwashiorkorAll cases of kwashiorkor have oedema to some degree, poor growth, wasting of muscles and fatty infiltration of the liver. Other signs include mental changes, abnormal hair, a typical dermatosis, anaemia, diarrhoea and often evidence of other micronutrient deficiencies.

Oedema. The accumulation of fluid in the tissues causes swelling; in kwashiorkor this condition is always present to some degree. It usually starts with a slight swelling of the feet and often spreads up the legs. Later, the hands and face may also swell. To diagnose the presence of oedema the medical attendant presses with a finger or thumb above the ankle. If oedema is present the pit formed takes a few seconds to return to the level of the surrounding skin.

Poor growth. Growth failure always occurs. If the child's precise age is known, the child will be found to be shorter than normal and, except in cases of gross oedema, lighter in weight than normal (usually 60 to 80 percent of standard or below 2 SD). These signs may be obscured by oedema or ignorance of the child's age.

Wasting. Wasting of muscles is also typical but may not be evident because of oedema. The child's arms and legs are thin because of muscle wasting.

Fatty infiltration of the liver. This condition is always found in post-mortem examination of kwashiorkor cases. It may cause palpable enlargement of the liver (hepatomegaly).

Mental changes. Mental changes are common but not invariably noticed. The child is usually apathetic about his or her surroundings and irritable when moved or disturbed. The child prefers to remain in one position and is nearly always miserable and unsmiling. Appetite is nearly always poor.

Hair changes. The hair of a normal Asian, African or Latin American child is usually dark black and coarse in texture and has a healthy sheen that reflects light. In kwashiorkor, the hair becomes silkier and thinner. African hair loses its tight curl. At the same time it lacks lustre, is dull and lifeless and may change in colour to brown or reddish brown. Sometimes small tufts can be easily and almost painlessly plucked out. On examination under a microscope, plucked hair exhibits root changes and a narrower diameter than normal hair. The tensile strength of the hair is also reduced. In Latin America bands of discoloured hair are reported as a sign of kwashiorkor. These reddish-brown stripes have been termed the "flag sign" or "signa bandera".Skin changes. Dermatosis develops in some but not all cases of kwashiorkor. It tends to occur first in areas of friction or of pressure such as the groin, behind the knees and at the elbow. Darkly pigmented patches appear, which may peel off or desquamate. The similarity of these patches to old sun-baked, blistered paint has given rise to the term "flaky-paint dermatosis". Underneath the flaking skin are atrophic depigmented areas which may resemble a healing burn.

Anaemia. Most cases have some degree of anaemia because of lack of the protein required to synthesize blood cells. Anaemia may be complicated by iron deficiency, malaria, hookworm, etc.

Diarrhoea. Stools are frequently loose and contain undigested particles of food. ometimes they have an offensive smell or are watery or tinged with blood.

Moonface. The cheeks may appear to be swollen with either fatty tissue or fluid, giving the characteristic appearance known as "moonface".

Signs of other deficiencies. In kwashiorkor some subcutaneous fat is usually palpable, and the amount gives an indication of the degree of energy deficiency. Mouth and lip changes characteristic of vitamin B deficiency are common. Xerosis or xerophthalmia resulting from vitamin A deficiency may be seen. Deficiencies of zinc and other micronutrients may occur.

Comparison of the features of kwashiorkor and marasmusFeatureKwashiorkorMarasmus

Growth failurePresentPresent

WastingPresentPresent, marked

OedemaPresent (sometimes mild)Absent

Hair changesCommonLess common

Mental changesVery commonUncommon

Dermatosis, flaky-paintCommonDoes not occur

AppetitePoorGood

AnaemiaSevere (sometimes)Present, less severe

Subcutaneous fatReduced but presentAbsent

FaceMay be oedematousDrawn in, monkey-like

Fatty infiltration of liverPresentAbsent

Marasmic kwashiorkorChildren with features of both nutritional marasmus and kwashiorkor are diagnosed as having marasmic kwashiorkor. In the Wellcome classification (see above) this diagnosis is given for a child with severe malnutrition who is found to have both oedema and a weight for age below 60 percent of that expected for his or her age. Children with marasmic kwashiorkor have all the features of nutritional marasmus including severe wasting, lack of subcutaneous fat and poor growth, and in addition to oedema, which is always present, they may also have any of the features of kwashiorkor described above. There may be skin changes including flaky-paint dermatosis, hair changes, mental changes and hepatomegaly. Many of these children have diarrhoea.

MARASMUS

KWASHIORKOR

2.6Diagnosis

Anamnesis and physical examinationCommon complaint that can be found when doing the anamnesis is the lack of growth, thin child, or underweight. other than that other complaints are children who is difficult or doesnt want to eat, often suffer from recurrent pain, or the onset of swelling on both legs, sometimes to the whole body. A checklist for taking the childs medical history and conducting the physical examination is given in the box below.

Tests

Where facilities permit, the tests given in Table 4 may help to diagnose specific problems. They are not needed, however, to guide or monitor treatment. The interpretation of test results is frequently altered by malnutrition. For this reason, laboratory tests may misguide inexperienced workers. The most important guide to treatment is frequent careful assessment of the child.

Nutritional status of under 5 children measured according to age, body weight, and height. The variable of body weight and height presented in the form of three anthropometric indicators, which is : weight for age (W/A), height for age (H/A), and weight for height (W/H). To measure the nutritional status of children, the rate of weight and height of every child is converted into standardized values (Z-score) by using WHO 2005 anthropometric standard. Furthermore, based on a Z-score of each indicator of nutritional status of children is determined by the following restrictions:

a. Classification of Nutritional Status based on weight/age (WFA) indicator:

Malnutrition: Zscore = -3.0 s / d Zscore = -2.0 s / d Zscore 2.0

b. Classification of Nutritional Status based on height/age (HFA) indicators:

Very Short

: Zscore = - 3.0 s / d Zscore = -2.0

c. Classification of Nutritional Status based on weight / height indicator:

Very Skinny: Zscore = -3.0 s / d Zscore = -2.0 s / d Zscore 2.0

d. Classification of Nutritional Status based on combined height/age (HFA) and weight/height (WFH) indicators:

Short-Skinny

: Zscore TB / U 2.0

The World Health Organization (WHO) defines severe acute malnutrition as a mid-upper arm circumference (MUAC) 60% from normal + edema

2. Marasmus

: Body weight < 60% from normal without edema

3. Marasmic Kwashiorkor : Body weight > 60% from normal + edema

KEADAAN GIZIBB

(Harvard)EdemaBB / TB

Gizi normal> 80%(-)N

PEM ringan + sedang)Underweight

= Undernourished60 80 %(-)(

PEMKwashiorkor

Marasmus-kwashiorkor

Marasmus

Nutritional Dwarfism60 80 %

< 60 %

< 60 %

< 60%(+)

(+)

(-)

(-)(((((N

2.7Treatment

The usual approach to the treatment of the child with severe malnutrition is divided into three phases (Table 43-5). These are:

Initial treatment (days 1-7): life-threatening problems are identified and treated in a hospital or a residential care facility, specific deficiencies are corrected, metabolic abnormali- ties are reversed and feeding is begun.

Rehabilitation (weeks 2-6): intensive feeding is given to recover most of the lost weight, emotional and physical stimulation are increased, the mother or carer is trained to con tinue care at home, and preparations are made for discharge of the child.

Follow-up (weeks 7-26): after discharge, the child and the childs family are followed to prevent relapse and assure the continued physical, mental and emotional development of the child.

The guidelines for the treatment of severe malnutrition are divided in five sections:

A.General principles for routine care (the10 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 completeA. GENERAL PRINCIPLES FOR ROUTINE CARE

There are ten essential steps:

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: an initial stabilisation phase where the acute medical conditions are managed; and a longer rehabilitation phase. Note that treatment procedures are similar for marasmus and kwashiorkor.

Step 1. Treat/prevent hypoglycaemia

Hypoglycaemia and hypothermia usually occur together and are signs of infection. Check for hypoglycaemia whenever hypothermia (axillary