PROTEIN ENERGY MALNURITION

MANOJIT SARKAR Final prof

MALDA MEDICAL COLLEGE

INTRODUCTION

UNDERNUTRITION is a condition in which there is inadequate consumption, poor absorption or excessive loss of nutrients.

OVERNUTRITION is caused by overindulgence or excessive intake of specific nutrients.

. The term malnutrition refers to both undernurition as well as overnutrotion.

. However, sometimes the terms malnutrition and protein energy malnutition (PEM) are used interchangeably with undernutrition.

. The term protein energy malnutrition has been adopted by WHO in 1976.

.Highly prevalent in developing countries among < 5 children.

DEFINITION : The term, protein – energy malnutrition, refers to a class of clinical conditions that may result from varying degree of protein lack and energy (calorie ) inadequacy .

The World Health Organization (WHO) defines –

PEM as range of pathological conditions arising from coincidental lack in varying proportions of proteins and calories, occurring most frequently in infants and young children and commonly associated with infection.

The extent of weight loss and growth rate varies with severity of PEM –

In early stages, there is failure to maintain weight or growth rate.

As it becomes progressive, there is loss of weight associated with loss of subcutaneous fat and muscle mass with dysfunction of many vital organs, which leads to a variety of clinical features.

With increasing severity, there is increasing failure in the homeostatic mechanisms of the body and damage to the immune defenses which may result in infections, shock and death.

FAILURE TO THRIVE(FTT) : FTT refers to a condition when the physical growth of a child is less than expected , usually below the third or fifth percentile, or when a child has significant loss of weight in a short time . FTT is divided into 3 categories :

.Organic – with a known medical condition

. Non-organic / psychosocial – without any known medical condition

. Mixed. The clinical features of FTT are growth retardation , developmental delay , mental changes, behavioral problems and soft neurological signs.

FTT and PEM are closely related . FFT is a medical problem or a label for investigation, whereas PEM is a diagnosis .

.Nutritional dwarfing (Stunting): A child is said to stunted if he does not have the height expected for his present age.

.Wasting: A child is said to be wasted if he does not have the weight expected for his present height.

EPILDEMIOLOGY

. Malnutrition is the gravest single threat to the world’s public health.

. Though poverty is the main contributing cause, it is greatly aggravated by lack of proper dietary knowledge

. Protein energy malnutrition (PEM) is one of the most widely spread health and nutritional problems of the developing countries

. Annually, undernutrition kills or disables millions of children

. It often causes disease and disability in the survivors and prevents millions from reaching their full potential

. Childhood undernutrition is an underlying cause in an estimated 35% of all deaths among children < 5yr and 21% of total global disability adjusted life years (DALYs) lost among < 5yr children

. WHO estimates that malnutrition is the biggest contributor to the child mortality in < 5 children, accounting for 55% of child deaths globally, translating to an unnecessary loss of about 3 million young lives every years.

. Of the 146 million underweight children ( <5yr old) from the developing world, 73% or 106 million live in just 10 countries

. INDIA is home to 57 million of this

. In 2013 as per the global estimates of < 5 children, one in four of the world’s children was chronically malnourished, 161 million were stunted and 51 were wasted with 17 million severely wasted.

. Approximately, half of these stunted and two- thirds of all wasted children lived in Asia and almost one – third of both stunted and wasted lived in Africa.

. The prevalence of malnutrition in India varies statewise with highest in Madhya Pradesh. Jharkhand and Bihar and lowest in Kerala, Mizoram, Sikkim, Manipur and Goa.

. The PEM has higher incidence in nutritionally vulnerable groups, young children between 6months to 2years and women during pregnancy and lactation and elderly age group as the nutritional requirements are larger relative to their body size than in older children and adults.

. The damage caused by malnutrition in the intrauterine life or in the first 2 years of life may be due to impairment in the developing brain.

ACUTE VERSUS CHRONIC DEFICIENCY

. Weight and arm circumference are affected within a short duration of inadequate nutrient intake and ill- health, while height and head circumference do not change so rapidly

. A slowing in the rate of growth indicated by poor gain in height would take at least 6 months to manifest itself

. While a slowing of weight gain or loss can be demonstrated within a month.

ETIOLOGY OF MALNUTRITION

Etiology of malnutrition is complex. It is customary to consider it as:

Primary: due primarily to dietary deficiency.

Secondary: due to diseases such as tuberculosis, measles, HIV or malabsorption.

The following factors are responsible:

. Poor Economy, social insecurity . Inadequate breast feeding . Ignorance, Faulty Food Habits and Feeding . Medical reasons . Large families . Closely- spaced family . Working mother . Bad start . Secondary malnutrition

Positive conceptual framework Negative conceptual framework

Child survival ,Development and

protection

Malnutrition and death

Immediate causes

Adequate dietary intake ,Psychosocial healthcare

Inadequate dietary intake,Psychosocial stress,Trauma, diseases

Underlying causes

Adequate maternal and child care,Household food security, Sufficient services and Healthy environment, Education and information

Inadequate maternal and child care,Poor household food security, Insufficient services and Unhealthy environment,Lack of education and information

The United Nations Children’s Fund conceptual framework

Resources and controls: Human, Economic and organizational

Resources and controls: human,Economic and organizational

Political and ideological superstructure

Political and ideological superstructure

Economic structure Economic structure

Existing and potential resources Existing and potential resources

Basic causes

PATHOPHYSIOLOGY OF PROTEIN ENERGY MALNUTRITION

. Many of the manifestations of PEM represent adaptive response to inadequate energy and/ or protein intakes, resulting in decreased activity and energy expenditure

. To meet the energy requirement, initially fat stores are mobilized followed by protein catabolism for maintaining basal metabolism

. Furthermore, micronutrients are essential in many metabolic functions as component, cofactors in enzymatic processes and immune response

. In the etiopathogenesis of PEM, why and what is that among children destined to become malnourished; some develop kwashiorkor while others develop marasmus.

. Amongst various theories postulated was Gopalan’s theory on adaptation and dysadaptation

. Antidiuretic effect of ferritin, loss of edema without change in serum albumin, noxious insults producing reactive oxidative free radicals, decreased Na, K, ATPase activity, depressed cellular protein synthesis

. Latest theory on Golden suggests deficiency of type-I (functional nutrients), like zinc and type-II nutrients like phosphorus, Mg, Mn, Cu, vit- D and C in the diets of malnourished children due to decrease in appetite

. No amount of additional energy as lipids or carbohydrates would enhance convalescence of PEM, unless specific nutrients are supplied in the balanced form.

HUMAN NUTRITION

. NUTRIENTS are substances that are essential for human life, growth and wellbeing

. MACRONUTRIENTS ( carbohydrate, protein and lipid) are essential for energy, cell multiplication and repair

. MICRONUTRIENTS are trace elements and vitamin which are essential for metabolic processes

. A healthy diet provides a balanced nutrients that satisfy the metabolic needs of the body without excess or shortage

. Dietary requirements of children vary according to the age, sex and development.

OVERVIEW OF PEM

. The majority of world’s children live in developing countries . Lack of food and clean water, poor sanitation, infection and social unrest lead to LBW and PEM . Malnutrition is implicated in > 50% of death in < 5 children

CHILD MORTALITY

The major contributing factors :

Diarrhea 19%

ARI 19%

Perinatal causes 18%

Malaria 5%

Measles 7%

55% of the total have malnutrition.

ASSESSMENT OF NUTRITIONAL STATUS

Nutrition forms the most predominant influence on the development of the growing child. Human survival has always depended upon food and hence, nutrition has determined his place of living and his way of living. Assessment of nutritional status can be done by evaluating:

. Dietary factors

. Clinical features of malnutrition

. Anthropometric measurements

. Biochemical parameters

. Morphological parameters

. Radiological parameters, and

. Epidemiological data regarding morbidity and mortality

DIETARY ASSESSMENT

. Breast feeding & weaning practices . 24-hr dietary recall . Home visit . Calculation of protein & calorie in children food . Feeding technique & food habits. Nutritional status is related to the nutrient intake especially among pre-school children. Accurate diet assessment is difficult and time consuming. A good rappot with the mother is essential for correct replies to the questions. Clinicians can have an overall assessment regarding breast feeding and weaning practices and food intake prior to the illness by a 24-hr recall method. Average of a three days recall during the mid- week is recommended. A food frequency table to record the frequency of intake of each food items is also desirable. The calculated intake should be finally compared with the Recommended Dietary Allowances (RDA) for age. A rough idea about the adequacy of vitamins and minerals in the diet should also be obtained.

BREAST FEEDING AND WEANING PRACTICES

Breast feeding and weaning practices are the important dietary habits that determine child health as well as morbidity and mortality. Breast feeding forms the integral part of the well known child survival package. The components of which are growth monitoring, oral rehydration therapy, breast feeding, immunization, food supplementation, female education and family planning (GOBIFFF).

DIET DURING ILLNESS: Maternal beliefs regarding diet common childhood illness are often wrong and unscientific. It is not uncommon to starve the child during diarrhea, measles, respiratory infections etc. Mother must be taught to continue feeding during illness and to select easily digestible food items during illness

CLINICAL ASSESSMENT: In clinical assessment, features indicating wasting, stunting, edema, vitamin deficiencies and those specific for various diseases should be looked for. Absence of such clinical signs denotes normal nutritional status.

CLINICAL ASSESSMENT

. Useful in severe forms of PEM

. Based on through physical examination for features of PEM and vitamin deficiencies

. Focuses on skin, eye, hair, mouth and bones

. Chronic illness to be excluded

ADVANTAGES –

. First and easy to perform

. Inexpensive

. Non-invasive

LIMITATIONS –

. Did not detect early cases

. Trained staff needed.

ANTHROPOMETRIC ASSESSMENT

Anthropometry is a simple valuable tool and the gold standard for evaluating the nutritional status. Age- dependent indices-

. Weight for Age- by far the simplest, most widely used and most reliable index.

. Height for Age- its value lies in chronic malnutrition and stunting.

Age- independent indices-

. Weight for Height- it is only partially age- independent, is calculated as follows: Percentage of weight for height = Actual weight X 100/ Expected weight for actual height

. Mid- arm circumference(MAC)- is measured midway between the point of the acromian and olecranon process. Between second and fifth years, it is said to remain constant between 16.25 and 16.75 cm. This is because of replacement of the baby fat with muscle tissue.

Any child in this age group with a circumference < 12.5 cm of the reference international standard is to be considered suffering from severe malnutrition and between 12.5 cm and 13.5cm mild- to- moderate malnutrition

Shakir tape method : is a simple and age- idependent tool for assessing malnutrition by mid-arm circumference with a special tape has colored zones- < 12.5cm (wasted) = Red 12. to 13.5cm (borderline) = Yellow >13.5 cm (normal) = green.

QUAC-stick method : is a simple, easy, inexpensive and yet reliable method of detecting early malnutrition of cute onset with a stick graduated with figures for mid- arm circumference in relation to height.

From the graduations in the stick, nutritional status in terms of 50, 60, 70 or 80% of the standard can be easily read.

The modified QUAC- stick : this utilizes a rod that is colored with green , yellow and red and the upper zone is red.

Red= severe PEM

Yellow = borderline

Green= normal nutritional status.

Triceps skin fold thickness : is measured by a standard caliper (Lange, Herpenden or Best) in 1to 6 years children. > 10 mm- normal 6to 10 mm- mild to moderate malnutrition < 6mm- severe malnutrition.

Mid- arm muscle circumference(MAMC) - is calculated by following formula: MAMC = MAC- (3.14 X Triceps skin fold thickness).

Bangle method : is useful in pre- school children, consists in slipping a bangle with a diameter of 4 cm up to forearm. This method though simple and easy, is not quite reliable. In case, it can slip over the elbow- mal nutrition is present.

Chest/ Occipto- Frotal circumference(OFC) ratio :

< 1 after 1-2 years, points to PEM.

Quetlet index :

Weight (kg)X 100/ Height (cm) 2

0. 14- 0.16 = normal <0.14 = gross malnutrition.

Dugadale index :

Weight (kg) X 1.6/ Height (cm) 0. 88 to 0.97 - normal <0.79 - malnutrition.

Rao and Singh weight/ height2 ratio :

Weight (kg) X 100/ Height (cm)2

> 0.15 - normal 0.13- 0.15 - moderate PEM <0.13 - severe PEM.

Kanawati and McLaren’s index : Mid- arm circumference divided by occipito- frontal circumference >0.31 – normal 0.31- 0.28- mild PEM 0.28- 0.25 – moderate PEM < 0.25 – Severe PEM.

Ponderal index : measurement of IUGR. Weight (gm) X100/ Length (cm) 3

> 2.5 – term baby > 2 – Symmetric IUGR < 2 - Asymmetric IUGR.

BIOCHEMICAL INDICATORS OF PEM The striking biochemical changes include lowering of serum albumin, esterase, amylase, lipase, alkaline phosphatase, transferrin, ceruloplasmin, essential amino acids, calcium, phosphorus, sodium, potassium, iron, magnesium etc. Urinary creatinine gives an indirect evidence of muscle mass. The alpha- 1 globulin is foud to be raised. Reduction in carrier proteins is an early indicator of PEM.

MORPHOLOGICAL INDICATORS OF PEM

The changes that occur in the mucosa and hair shaft. In the buccal smear, nearly 70% of cells may be seen mutilated as against <10% in normal children. Difference in texure of hair is an early sign.

RADIOLOGICAL INDICATORS OF PEM

Retardation of bone age, osteoporosis and rarely evidence of rickets and scurvy. Transverse lines that represent periods of arrested growth at the growing end of long bones may be noted prior to the onset of frank PEM. The bone age usually corresponds to the height age rather than chronological age.

EPIDEMIOLOGICAL ASSESSMENT

Vital statistics like infant mortality, neonatal mortality, perinatal mortality, still birth and under five mortality are useful indicators to evaluate nutritional status in the community.

EVOLUTION OF PEM Dietary Hypothesis

According to widely accepted dietetic hypothesis - Kwashiorkor is predominantly a protein deficiency and Marasmus an energy deficiency. Of course, both proteins and energy lack- exist in both the syndromes.

Adaptation Hypothesis

The noted nutritionist, Gopalan, the so- called adaptation hypothesis- Marasmus is an extreme degree of adaptation to prolonged inadequacy of proteins and energy in the diet. Kwashiorkor is a stage of adaptation failure or dysadaptation which may follow two situations: First : continued prolongation of the stress of malnutrition. Second : sudden precipitation or aggravation by a fulminant infection such as measles, pertusis, pneumonia or acute diarrheal episode. Relatively mild effect of adaptation may be responsible for nutritional dwarfing.

Aflatoxin Contamination Hypothesis

More recently, it has been postulated that aflatoxin contamination of food may well be an important factor in the causation of kwashiorkor.

Golden’s Hypothesis of Free Radicals

According to Golden’s hypothesis –

Kwashiorkor results from overproduction of free radicals (because of infection, toxins, iron etc) and breakdown of protective mechanism (provided by vitamin A & E, carotene, zinc copper, selenium, manganese etc).

Jellife’s Hypothesis of Interaction and Sequelae

According to Jelliffe-

Kwashiorkor results from mixture of interactions and sequelae of dietary imbalances and/ or deficiency, infection, parasitosis, emotional trauma from maternal deprivation due to abrupt weaning from breast, toxins like aflatoxin or ochratoxin.

CLASSIFICATION OF PEM

Syndromal Classification

. Kwashiorkor

. Nutritional marasmus

. Marasmic kwashiorkor

. Prekwashiorkor

. Nutritional dwarfing (Stunting)

. Underweight

. Invisible PEM

NUTRITIONAL DWARFING (STUNTING) :

Prolonged PEM starting fairly early in life and going on over numbers of years without developing kwashiorkor or marasmus results in nutritional dwarfing.

PREKWASHIORKOR : Affected children have poor nutritional status and certain features of kwashiorkor like hair changes, moon face and hepatomegaly but do not have edema.

MARASMIC KWASHIORKOR : When marasmic children develop edema, it is termed as marasmic kwashiorkor.

UNDERWEIGHT :

The child is undernourished, but does not have any features of marasmus or kwashiorkor. The weight for age is 60 – 80% of the expected.

INVISIBLE PEM :

The is not very evident. Toddlers who show addiction to breast milk and improper start of weaning foods must be suspected to have invisible PEM. It has been reported that the average moderately undernourished child in the 6 – 24 months age range looks entirely normal, but is too small for age, has lowered resistance to infection and therefore easily succumbs to illness.

I

KWASHIORKOR

.The earliest description of kwashiorkor in the English medical literature was made in 1933 by Cicely Williams, a noted British Physician

. Later, in 1935, she introduced the “KWASHIORKOR”, the local name for the disease in Ghana

. It was said to mean the “ RED BOY”, because of the characteristic pigmentary changes.

. Kwashiorkor mainly can occur infancy but its maximum incidence is in the 1 to 4yr of life.

. Kwashiorkor is not only dietary in origin infection, psycho- social and cultural factors are also responsible

. Kwashiorkor is an example of lack of physiological adaptation to unbalanced deficiency where the body utilized protein and conserve subcutaneous fat

. One theory suggested that kwashiorkor is a result of liver insult with hypoproteinemia and edema. Food toxin like aflatoxins have been suggested as precipitating factors.

CLINICAL PRESENTATION A classical case of kwashiorkor is dull, apathetic and miserable, evincing hardly any interest in the surroundings.

Essential features (Minimal Diagnostic Criteria) :

. Growth retardation – as evidenced by low weight and low height

. Muscle wasting with retention of some subcutaneous fat

. Psychomotor changes- as evidenced by mental apathy in the form of silent ,listless, inertness, lack of interest in the surroundings

. Hypoalbuminemic pitting edema, at least over the pretibial region.

Nonessential features : . Hair changes – . Light colored hair, areas of alopecia, changes in texture (coarseness, silkiness) and easy pluckability . Alternate bands of light and dark color have earned the name” flag sign “ which signifies period of inadequate nutrition over a prolonged period.

. Skin changes – . Light colored skin (Depigmentation)

. Flaky- paint dermatosis – Most classical dermatosis consists of areas of hyperpigmentation intervened by areas of raw red skin caused by shedding of the superficial skin flakes . Crazy- pavement dermatosis

. Reticular pigmentation, mosaic dermatosis, pellagra- like lesions

. Superadded skin infections like pyodermas and scabies.

. Gastrointestinal manifestations- . Diarrhea, vomiting, anorexia.

. Mineral and vitamin deficiencies – . Iron deficiency anemia, keratomalacia and irreversible blindness.

. Superadded infections – . Tuberculosis, bronchopneumonia, enteritis, measles , pyodermas etc.

. Clubbing – As a result of the accompanying steatorrhea

. Renal- GFR and renal plasma flow are diminished, aminoaciduria and inefficient excretion of acid load.

. Cardiovascular- cold, pale extremities due to poor circulatory insufficiency, bradycardia and hypotension.

GRADING OF KWASHIORKOR :

Grades

1 2

3

4

Characteristics

Pedal edema

+ Puffiness of face

+ Edema of chest wall and back

+ Ascites

MARASMUS

. The term marasmus is derived from the Greek marasmos which means wasting

. Marasmus involved inadequate intake of calories and protein and is chracterized by emaciation

. Marasmus represents the end result of starvation where both calories and protein are deficient

. Marasmus represents an adaptive response to starvation

. In marasmus the body utilizes all the fat stores before using the muscles

. Seen most commonly in the first year of life due to lack of breast feeding and the use of diluted animal milk

. Poverty or femine and diarrhea are the usual precipitating factors

. Ignorance and poor maternal nutrition are also contributory.

CLINICAL PRESENTATION–

. Remarkable wasting of both muscles and subcutaneous fat . The face is wizened and shrivelled - just as in case of monkey

. In the early stages – . The child is irritable, hungry and crave for food. . In the later stage – . Miserable and apathetic, refusing to take anything. . Anemia.

Essential features (Minimal diagnostic criteria) :

. Growth retardation

. Gross muscle and subcutaneous fat wasting

. Absence of edema.

Nonessential Features :

. Hair changes are usually not present

. Skin changes

. GI manifestations – . Diarrhea, marasmic child is , however, hungry rather than anorexic, in advanced stage may anorexic.

. Mineral and vitamin deficiencies – . Anemia

. Shrunken liver

. Superadded infections and infestations

. Psychomotor changes – . In the form irritability rather than listlessness

. Clubbing.

GRADING OF NUTRITIONAL MARASMUS :

Grades

1

2

3

4

Characteristics

Loss of fat from axilla and groin

Loss of fat from thigh and buttock

Loss of fat from chest and abdomen

Loss of buccal pad of fat

SEVERE ACUTE MALNUTRITION

Severe acute malnutrition ( SAM) among children 6- 59 months of age is defined by WHO and UNICEF as any of the following :

(i) weight- for-height bellow -3 standard deviation of the median of WHO growth reference

(ii) visible severe wasting

(iii) presence of bipedal edema

(iv) mid- arm circumference <11.5 cm.

This classification is used to identify children at high- risk of death. Children with SAM require urgent attention and management in the hospital.

Three immediate causes of malnutrition: . Low dietary intake . Low birth weight . Infection.

CLINICAL MANIFESTATION OF MALNUTRITION

Organ

Hair

Face

Eyes

Hematological

Signs

. Lack of lustre . Thinness and sparseness . Straightness . Dyspigmentation . Flag sign . Easy pluckability

.Diffuse depigmentation . Moon face. Old man or monkey face

. Pale conjunctiva

. Bitot’s spot

. Conjuctival xerosis

. Corneal xerosis

. Keratomalacia

. Anemia

Oral cavity

Endocrinal

Skin & subcutaneous tissue

GIT

. Angular stomatitis . Cheilosis . Atrophic papillae . Mottled enamel . Spongy, bleeding gums.

. Thyroid and parotid enlargement, hypogonadism.

. Xerosis

. Follicular hyperkeratosis

. Petechiae, purpura

. Pellagrous dermatosis

. Flaky- paint dermatosis

. Scrotal and vulval dermatosis

. Crazy- pavement dermatosis

. Pyoderma

. Oedema

. Amount of subcutaneous fat reduced.

. Hepatomegaly, splenomegaly

. Shrunken liver.

Cardiovascular

Musculoskeletal system

Nervous system

. Cardiomegaly, microcardia . Tachycardia, bradycardia.

. Muscle wasting

. Craniotabes

. Frontal & parietal bossing

. Epiphyseal enlargement

. Beading of ribs

. Wide open anterior fontanelle

. Knock- knees or bow legs

. Diffuse or local skeletal deformities

. Deformities of thorax

. Musculo- skeletal haemorrhages.

. Psychomotor change

. Mental confusion

. Sensory loss

. Motor weakness

. Loss of position sense

. Loss of ankle and knee jerks

. Calf tenderness.

Serious Complications of Advanced PEMCOMPLICATIONS

Superadded infections

Dehydration & dyslectrolytemia

Hypothermia

Hypoglycemia

Anemia

REMARKS

. Both overt & hidden: Septicemia, pneumonia, pyoderma, scabies, UTI, tuberculosis.

. Usually accompanying diarrhea, often with lactose intolerance.

. Rectal temperature < 35⁰ C may prove fatal & causing sudden death.

. It contributes to poor response to nutritional therapy and carries a poor prognosis.

. Moderate to severe anemia may result from malnutrition as such or superadded infections contributing to development of anemia.

Congestive cardiac failure

Convulsion & tremor

Vitamin & mineral deficiencies

Bleeding

Sudden infant death syndrome

It is usually precipitated by excessive intake of sodium and fluid or severe anemia. Since cardiac size is invariably small in PEM.

. Probably due to hypoglycemia, dyslectrolytemia and septicemia.

. Low nutritional intake and infection may contribute.

. DIC may complicate the clinical picture.

. Sudden death 4- 7 days after admission. Usually, the cause remains unclear.

Pathological changes in PEM

ITEM

Proteins

Carbohydrate

Lipids

Electrolytes

Water

Minerals

REMARKS

. Reversal of albumin/ globulin ratio

. Increased NE/ E amino acid ratio; > 3.5 in kwashiorkor

. Low glycogen, hypoglycemia- often asymptomatic

. Increased NE/ E fatty acid ratio ; > 3 in kwashiorkor

. Normal/ high sodium, low potassium

. Increased TBW; high ECF/ ICF ratio

. Low Ca, P, Mg, Iron, Copper, Chromium, Zinc.

NE- Non- essential, E- Essential, TBW- Total body water, ECF- Extra cellular fluid, ICF- Intra cellular fluid.

Hormonal Changes in PEM

HORMONE

GH

Glucocorticoids

Insulin & IGF

Somatomedins

Glucagon

Thyroxin

MARASMUS

. N/ H

. VH

. N/L

. L

. H

N/ L

KWASHIORKOR

. VH

. H

. L

. VL

. VH

. N/ H

GH- Growth hormone, H- High, VH- Very high, N- Normal, L- Low.

Energy expenditure in a normal child

ITEM

BMR

Activity

Growth

Fecal loss

Specific dynamic action (SDA)

ENERGY EXPENDITURE (%)

50

25

12

8

5

Energy (Calorie) requirement is as follows : According to Holiday and Seger formula –

. Up to 10 kg = 100kcal/kg

. 11 to 20 kg = 1000 + 50 kcal/ kg for each kg above 10 kg

. > 20kg = 1500 + 20 kcal / kg for each kg above 20 kg.

Energy (Calorie) requirement varies from age to age. On an average- . Carbohydrate – 50%

. Fat - 30%

. Protein - 20%

Daily requirement for proteins

Age ( Years)

< 1

1- 3

4- 6

7 – 9

10- 12

13- 15

16- 19

Adult

Protein ( gm / kg)

3.5 to 2.6

2.5 to 2

3

2.8

2

1.7

1.5

1

Daily requirement for calories

Age ( Years)

< 1

1- 3

4- 6

7- 9

10- 12

13- 15

16- 19

Adult

Calories / kg

110

100

90

80

70

60

50

40

Bedside calculation of calories

Age (Years)

123456789101112

Adolescent boy

Adolescent girl

Energy (kcal)

100011001200130014001500160017001800190020002100

2400

2100

Gomez’s classification according to weight for age

Nutritional status

. Normal

. First degree PEM

. Second degree PEM

. Third degree PEM

Wt. for age (Harvard) (% of expected)

>90

75 – 90

60 – 75

<60

Welcome Trust or International Classification

Wt. for age(Boston)(% of expected)

60 – 80

60 – 80

<60

<60

Oedema

+

_

_

+

Clinical type of PEM

Kwashiorkor

Undernutrition

Nutritional marasmus

Marasmic Kwashiorkor

The IAP classification of malnutrition

Nutritional status

. Normal

. Grade – I PEM

. Grade – II PEM

. Grade – III PEM

. Grade – IV PEM

Wt. for age (% of expected)

>80

71 – 80 (mild)

61 – 70 (moderate)

51 – 60 (severe)

< 50 (very severe)

Jelliffe’s classification according to weight for age

Nutritional Status

Normal

First degree PEM

Second degree PEM

Third degree PEM

Fourth degree PEM

Weight for age (Harvard) ( % of expected)

>90

80- 90

70- 80

60- 70

< 60

WHO Classification of PEM

Criteria

Symmetrical edema

Weight for height( Index of wasting)

Height for age( Index of Stunting)

Moderate PEM( % of expected)

No

70- 79( Wasting)

85- 90( Stunting)

Severe PEM( % of expected)

Yes

<70( Severe wasting)

<85( Severe stunting)

. Wt for Ht= Weight of the child divided by ideal weight of a normal child of same height x 100.

. Ht for Age = Height of the child divided by ideal height of a normal child of age x 100.

WHO- cut- off for assessment of PEM in the community

. The assessment of nutritional status is done according to wt- for-ht(or length), ht (or length)- for – age and presence of edema.

. The WHO recommends the use of Z scores or SD scores for evaluating anthropometric data, so as to accurately classify individuals with indices bellow the extreme percentiles.

. SD score = Observed value – Median reference value/ Standard deviation of reference population.

. The calculation of the SDS gives a numerical score indicating how far away from the 50th percentile for age the child’s falls. A score of -2 or -3SDS indicates moderate malnutrition A score of +2 or +3 SDS indicates overweight A score of < -3 SDS indicates severe malnutrition.

Waterlow classification of stunting

% of ideal heightExpected for the age

>95

90- 95

85- 89

< 85

Grade of stunting

No stunting

I

II

III

Waterlow classification of wasting

Weight for height ( % of expected)

>110

91- 110

81- 90

70- 80

<70

Grade of wasting

Over weight

Normal

I

II

III

Arnold Classification

It is based on mid- arm circumference (MAC) : Mild to moderate PEM MAC between 12.5- 13.5 cm. Severe PEM MAC < 12.5 cm.

Classification Based on Skinfold Thickness

Mild PEM : 80- 90 % of expected for age (8- 10 mm) Moderate PEM : 60- 80 % of expected for age (6 – 8 mm) Severe PEM : < 60 % of expected for age (< 6 mm)

The causes of growth retardation are the following :

. Racial/ genetic

. IUGR

. Nutritional

. Emotional deprivation

. Skeletal disorders

. Metabolic disorders

. Endocrine disorders

. Chromosomal disorders

. Constitutional delay

. Chronic systemic disorders.

MANAGEMENT OF PROTEIN ENERGY MALNUTRITIONInvestigations-

. Blood for Hb, TLC, DLC, peripheral smear for malaria

. Blood for- sugar, urea, creatinine,

. Serum protein, albumin,

. Urine for RE/ ME/ CS

. Stool for RE/ ME/ CS, reducing substances

. Mantoux test, chest X – ray, Gastric aspirate for AFB

. HIV screening

. Liver function test

. Blood culture

. Renal function test, lumber puncture if ever indicated.

Domiciliary (Home) Management

Mild and moderate malnutrition-

. Mild and moderate malnutrition make up the greatest portion of malnourished children and account for > 80% of malnutrition associated deaths. It is, therefore, vital to intervene in children with mild to moderate malnutrition at the community level before they develop complications.

. The mainstay of treatment is provision of adequate amounts of protein and energy.

. At least 150 kcal/kg / day should be given.

. A protein intake of 3gm / kg / day is sufficient, milk and vegetable protein should be given.

. Adequate minerals and vitamins provided for appropriate duration.

. The management at home supervised and monitored by weekly visits of-

. Paramedicals ( an anganwadi worker) . Visit to nearby nutrition rehabilitation centre . OPD at health centre/ hospital.

. A prerequisite to domiciliary treatment is absence of- . Severe infection . Fulminant gastroenteritis . Electrolyte imbalance

. Good weight gain, as judged from the growth chart, is by and large the best yardstick of adequacy of response to nutritional rehabilitation.

Severe Acute Malnutrition (SAM)

. THE WHO has developed guidelines for the management of SAM and these have been adapted by IAP. . At the community level, four criteria listed previously should be used to diagnose SAM.

. WHO recommends exclusive inpatient management of children with SAM.

Assessment of the Severely Malnourished Child

History: . The child with severe malnutrition has a complex backdrop with-

. Dietary . Infective . Socioeconomic factors underlying the malnutrition.

Particular attention should be given to

. The usual diet (Before the current illness) including breast feeding

. Presence of diarrhea

. Information on vomiting, loss of appetite

. Persistent cough, contact with tuberculosis

. Presence of HIV infection.

Examination: . Anthropometry provides the main assessment of the severity of malnutrition

. Physical features should be looked for.

Clinical features of prognostic significance include-

. Signs of dehydration

. Shock (cold hands, slow capillary refill, weak and rapid pulse)

. Severe palmer pallor

. Eye signs of vitamin A deficiency

. Localizing signs of infections

. Skin infection or pneumonia, signs of HIV infection

. Fever or hypothermia.

INDICATIONS FOR HOSPITALIZATION IN SEVERE MALNUTRITION

. Hypothermia, hypoglycemia

. Infection . Fluid and electrolyte imbalance . Convulsions . Unconsciousness . Jaundice, marked hepatomegaly, purpura, bleeding . Severe anemia and congestive cardiac failure . Xerophthalmia . Severe dermatosis . Extreme weight deficit . Persistent vomiting . Severe anorexia . Distended tender abdomen . Age < 1 yr

Management of severe malnutritionThe general treatment involves ten steps in two phases:

. The initial stabilization phase focuses on restoring homeostasis and treating medical complications and usually takes 2-7 days of inpatient treatment.

. The rehabilitation phase focuses on rebuilding wasted tissues may take several weeks.

STEPS

1.Hypoglycemia

2.Hypothermia

3.Dehydration

4.Electrolytes

5.Infection

6.Micronutrients

7.Initiate feeding

8.Catchup growth

9.Sensory stimulation

10.Prepare for follow-up

STABILIZATIONDays 1-2 Days 3-7

REHABILITATIONWeeks 2-6

No iron With iron

Step 1 : Treat/ Prevent Hypoglycemia All severely malnourished are at risk of hypoglycemia (Blood glucose level < 54mg/dl or 3mmol/l), hence blood glucose should be measured immediately at admission. If blood glucose cannot be measured, one must assume hypoglycemia and treat. Hypoglycemia, hypothermia and infection generally occur as a triad.

Asymptomatic hypoglycemia- 50 ml of 10% glucose or sucrose solution should be given orally or by nasogastric tube followed by the first feed. Symptomatic hypoglycemia- 5ml/ kg of 10% dextrose IV followed by 50 ml of 10% dextrose or sucrose solution by nasogastric tube. Estimation of blood glucose level till it becomes normal and stabilizes. Once stable, the 2 hourly feeding regimens should be started. Start appropriate antibiotics.

Feeding should be started with starter F- 75 (Formula- 75) which is a WHO recommended starter diet for SAM containing 75 kcal/ 100ml of feed as early as possible and then continued 2- 3 hourly. Prevention- Feed 2 hourly staring immediately and prevent hypothermia.

Step 2 : Treat/ Prevent Hypothermia All severely malnourished children are at risk of hypothermia due to impairment of thermoregulatory control, lowered metabolic rate and decreased thermal insulation from body fat. Rectal temp. <35.5 ⁰C or axillary temp. < 35 ⁰C. Always measure blood sugar and screen for infections in the presence of hypothermia.

Treatment-

Clothe the child with warm clothes; head also covered with cap Provide heat using overhead warmer, skin contact or heat convertor Avoid rapid re-warming as this may lead to disequilibrium Feed the child immediately Give appropriate antibiotics.

Prevention-

Place the child’s bed in a draught free area Always keep the child well covered; ensure that head is also covered well Place the child skin- to- skin contact with mother Feed the child 2 hourly starting immediately after admission.

Step 3 : Treat / Prevent Dehydration

Dehydration tends to be over diagnosed and its severity over esimated in severely malnourished children. Loss of elasticity of skin may either be due to loss of subcutaneous fat in marasmus or loss of extracellular fluid in dehydration.

Treatment- Severe shock is managed by Ringer lacted followed by 0.45% glucose saline/ Isolyte-P as maintenance fluid. Rehydration by employing WHO recommended solution for malnutrition (ReSoMal) which provides high glucose and low sodium and has a low osmolarity (300mmol/L). Alternatively, IV half- strength Darrow, half- strength Ringer lactate or even half normal saline with 5% dextrose may be use. Be alert signs of overhydration.

Prevention- Give reduce osmolarity ORS at 5- 10 ml / kg after each watery stool, to replace stool losses If breastfed, continue breastfeeding Initiate refeeding with stater F- 75 formula.

Step 4 : Correct Electrolyte Imbalance

Treatment-

Give supplemental potassium at 3- 4 mEq / kg / day for at least 2 weeks On day 1, give 50% magnesium sulphate 4 mEq / ml IM. Thereafter, give extra magnesium .8- 1.2 mEq / kg day Excess body sodium exists even though the plasma sodium may be low; decrease salt in diet.

Step 5 : Treat / Prevent Infection

Infection may not produce the classical signs of fever and tachycardia in severely malnourished children. Severe infection may be associated with hypothermia. Most common sites of infection are the skin, GI tract, respiratory and urinary tract. Majority of infections are septicemia are caused by gram- negative organisms.

Hypoglycemia and hypoglycemia are markers of severe infection.

Treatment- Treat with parenteral ampicillin 50 mg / kg / dose 6 hourly for at least 2 days oral amoxicillin 15 / kg / dose 8 hourly for 5 days and gentamicin 7.5 mg/ kg or amikacin 15- 20 mg/ kg IM or IV once daily for 7 days.

If no improvement within 48 hours, Change to IV cefotaxim (100- 150 mg / kg / day in 3- 4 divided doses) or ceftriaxone ( 50- 75 mg / kg / day in 2 divided doses)

If other specific infections are identified, give appropriate antibiotics.

Prevention-

Follow standard precautions like hand hygiene Give measles vaccine if the child is > 6 months and not immunized or if the child is > 9months and had been vaccinated before age of 9 months.

Step 6 : Correct Micronutrient Deficiencies All severely malnourished children have vitamin and mineral deficiencies. Up to twice the recommended daily allowance of various vitamins and minerals should be given. Although anemia is common, Iron should not be given initially due to danger of promoting free radical generation and bacterial proliferation.

On day 1, give vitamin A orally- Age > 1year- 2 lakh IU 6- 12months – 1 lakh IU 0-5 months- 50,000 IU

Folic acid- 5 mg on day 1 1mg / day Zinc- 2mg / kg / day

Copper- 0.2 – 0.3 mg / kg / day

Iron- 3mg / kg / day, once the child starts gaining weight; after the stabilization phase. Vitamin K 2.5 mg IM single dose at the time of admission Daily multivitamin supplements containing thiamin, riboflvin and nicotinic acid.

For severe anemia- Hb < 4gm % or 4-6 gm% , blood transfusion should be given.

Step 7 : Initiate Re- feeding

Feeding should be started with a diet which has osmolarity < 300 mOsm / L; lactose not > 2-3 gm / kg / day with appropriate renal solute load and initial percentage of calories from protein of 5%.

Start feeding as soon as possible as frequent small feeds

If unable to take orally, initiate nasogastric feeds

Total fluid recommended is 130 ml / kg / day; reduce to 100 ml / kg / day If there is severe edema

Continue breast feeding

Start with f- 75 starter feeds every 2 hourly

If persistent diarrhea, give a cereal based low lactose F- 75 as starter diet

If diarrhea continues on low lactose diets, give F- 75 lactose free diets.

Step 8 : Achieve Catchup Growth

Once appetite returns, higher intakes should be encouraged. Starter F- 75 feeds should be gradually replaced with high calorie (100 kcal / 100 ml) and high protein (2.5 – 3 gm / 100 ml), these feeds are called F – 100 diet.

Increase volume offered at each feed and decrease the frequency of feeds to 6 feeds / day.

Add complementary foods as soon as possible to prepare the child for home foods at discharge.

Monitoring progress during treatment- If there is a good weight gain of > 10 gm / kg /day – Same treatment should be continued till recovery For moderate weight gain ( 5- 10 gm / kg / day ) – Food should be checked and screened for systemic infection

For poor weight gain ( < 5 gm / kg / day) – Possible causes- Inadequate feeding, untreated infections, psychological factors, coexisting infections like tuberculosis and HIV.

Step 9 : Provide Sensory Stimulation and Emotional Support

Delayed mental and behavioral development often occurs in severe malnutrition. A cheerful, stimulating environment

Age appropriate structured play therapy for at least 15- 30 min / day

Age appropriate physical activity as soon as the child is well enough

Tender loving care.

Step 10 : Prepare for follow up

Primary failure to respond is indicated by :

Failure to regain appetite by day 4

Failure to start losing edema by day 4

Presence of edema on day 10

Failure to gain weight at least 5gm / kg / day on day 10.

Secondary failure to respond is indicated by :

Failure to gain weight at least 5gm / kg / day for 3 consecutive days during rehabilitation phase.

Results of Nutritional Rehabilitation

. Resumption of alertness and activity, manifested as “first smile” followed by return of appetite within first few days are good signs of recovery.

. Weight gain, after edema has disappeared, is 10 – 15 gm / kg / day which is 5 times that of normal child of same height and 10 times that of normal child of same age.

. Some infants and children with marasmus may develop edema following some correction in their nutrition. The so called “ refeeding edema” results from hyperinsulinemia causing decrease in sodium excretion, due to diet that is predominant in calories (energy) with relative inadequacy of proteins.

. Disappearance of hepatomegaly and enteropathy.

. In 1- 3 months period, the patients attains normal wt. for ht. and can be considered as “ clinically recovered”.

Factors contributing to poor response to nutritional rehabilitation

. Feeding inadequacy

. Failure to adequately treat the accompanying infections

. Failure to properly treat accompanying dehydration and dyselectrolytemia

. Failure to attend to accompanying deficiencies

. Poor facilities : Untrained and poorly motivated staff, inadequate environment

. Serious underlying diseases : Malabsorption, immunodeficiency, inborn errors of metabolism, malignancy.

Phenomena encountered during nutritional rehabilitation

Favorable :

. Resumption of alertness as shown by a smile and interaction with mother

. Initiation of weight gain . Disappearance of edema (by 7- 10 post therapy day)

. Disappearance of enteropathy and hepatomegaly

. Elevation of serum protein

. Attainment of normal weight and height in 2- 4 months.

Unfavorable :

. Pseudotumor Cerebri-

overenergetic nutritional correction in malnourished child may accompanied by a transient rise of ICT, it benign self- limiting.

. Nutritional Recovery Syndrome (Gomez Syndrome)-

The term refers to an interesting sequelae of events seen in children who are being treated with very high quality of proteins during the course of rehabilitation from gross malnutrition. The syndrome is characterized by increasing hepatomegaly, abdominal distention, ascites, prominent thoraco- abdominal venous network, hypertrichosis, parotid swelling, gynecomastia and eosinophilia. Its development may well be related to endocrine disturbances specially increase in estrogen and trophic hormones by pituitary.

. Encephalitis- like –syndrome-

It is manifested by drowsiness, progressive unconsciousness, tremor, rigidity and myoclonus, result of far too much protein in the diet.

. Rickets- During nutritional recovery, as a result of rapid growth, vitamin D, calcium and phosphate consumption may fall short of the body needs, causing rickets.

. Anemia / Micronutrient Deficiency

Prognosis In PEM- Bad prognostic signs include- . Severe dehydration . Hypoglycemia . Hypothermia . Congestive cardiac failure . Superimposed infections . Xerophthalmia . Bleeding diathesis . Hepatic dysfunction . Seizures . Significant changes in sensorium . Cachexia

Causes Of mortality In PEM-

. Dehydration

. Dyselectrolytemia

. Hypoglycemia

. Hypothermia

. Fulminant systemic infections

. Congestive cardiac failure

Criteria for Discharge

. Ideally, the child should be discharged from the hospital when he attains normal weight for height

. Discharge may be made when the child has achieved a weight that is 85% of the normal weight for height and it takes about 2- 4 weeks

. When then child is alert and active, eating at least 120-130 kcal / kg / day with a consistent weight gain (at least 5gm / kg / day)

. Receiving adequate micronutrients

. Free from infection and complete immunization appropriate for age

. Hospital stay should be utilized to educate the mother about the value of high protein and high diet of “family type” so that the she knows how to achieve “ consolidation of cure” at home

. Complete recovery usually takes another 2- 4 months after the child is back home.

LONG- TERM SEQUELAE OF PEM

. Growth Retardation

. Mental impairment

. Cirrhosis of liver

PREVENTION OF MALNUTRITION

Prevention at Family Level . Good antenatal care . Exclusive breast feeding . Complementary feeding

Prevention at Community Level

Prevention at National Level

Prevention Globally