(2) marasmus kwashiorkor 12022009

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KWASHIORKOR

Marie Ellaine T. Nielo, M.D., DPPS

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Kwashiorkor

Socially descriptive West African word meaning a disease occurring in a young child displaced from his mother by a subsequent pregnancy

Protein malnutritionNutritional edema syndromeMalignant malnutritionMelnahrschaden (flour malnutrition)Plurideficiency syndrome

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KWASHIORKOR

Protein malnutritionNutritional edema syndromeMalignant malnutritionMelnahrschaden (flour malnutrition)Plurideficiency syndrome

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KWASHIORKOR

West African word: disease occurring in a young child displaced from his mother by a subsequent pregnancy

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KWASHIORKOR

4 months to 5 years of ageMain incidence: 1-3 years of age

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KWASHIORKOR

Principal cause: nutritional imbalance in early childhood due to a diet that is very low in protein, but contains Cal in the form of CHO

Common in places where starchy foods are the main staple, inadeq supplemented by protein rich foods of animal or vegetable protein

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KWASHIORKOR

Weaning diets based on tubers (esp cassava, sweet potatoes), bananas, rice and corn, contain insufficient protein in relation to the calories supplied for the growth of the young child

All staples need supplementation with protein-rich foods

Sweetened condensed milk when used too dilute and together with an excess of rice tends to cause kwashiorkor

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KWASHIORKOR

Freq contributing factors: def of Vit B complex, Vit A, certain minerals and specific a.a.

All factors may operate singly or in combination

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KWASHIORKOR

Possibly never exclusively dietary in etiology

Contributing factors: Respiratory infectionsDiarrheaHookwormMalariatuberculosis

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Diagnostic Signs of Kwashiorkor

EdemaMuscle wastingPsychomotor changes

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Diagnostic Signs of Kwashiorkor

EDEMACardinal signOccurs first above the ankles

detected by pitting after moderate pressure for about 3 seconds over the lower third of the medial surface of the tibia

Becomes generalized

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Diagnostic Signs of Kwashiorkor

EDEMADue to lowering of the albumin

fraction of the serum proteinsChildren with gross edema have

serum levels <1.5 g/dlChildren with mild edema have

serum levels >2.0 g/dl

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Diagnostic Signs of Kwashiorkor

EDEMAMore marked in the SC tss of

dependent partsLegsForearmsPenisScrotumLower backLower part of the face

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Diagnostic Signs of Kwashiorkor

EDEMAAscites: due to secondary

disturbances

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NUTRITIONAL DISORDERS

…continuation

12/02/2009

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Gomez classification

The child's weight is compared to that of a normal child (50th percentile) of the same age.

percent of reference weight for age = ((patient weight) / (weight of normal child of same age)) * 100

It is useful for population screening and public health evaluations

Does not distinguish between the different clinical forms of malnutrition

Provides an approximate grading as to prognosis

Gomez classification

Weight for age(based on 50th percentile of weight for age)

Status

>90% Normal

76-90% First degree malnutrition

61-75% Second degree

<60% Third degree17

Wellcome classification of severe malnutrition

Weight as percentage

(degree of weight loss)

EDEMA NO edema

60-80% Kwashiorkor Undernutrition

<60% Marasmic-kwashiorkor

Marasmus

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Revised Waterlow classification

Adopted by the WHOCan distinguish between deficits in weight

for height (wasting) and deficits in height for age (stunting)

Wasting: acute malnutritionStunting: chronic malnutrition

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Revised Waterlow classification

Chronic malnutrition results in stunting. Malnutrition also affects the child's body

proportions eventually resulting in body wastage.

percent weight for height = ((weight of patient) / (weight of a normal child of the same height)) * 100

percent height for age = ((height of patient) / (height of a normal child of the same age)) * 100

Revised Waterlow classification

Normal Mild Moderate Severe

Height for age (stunting)%

>95

90-95 80-90 <80

Weight for age (wasting)%

>90 80-89 70-79 <70

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Protein – Energy Malnutrition

Mild-Moderate PEM: (latent, hidden or marginal malnutrition) 1st and 2nd levels underweight for age (between 61-90% of standard weight)

Severe PEM: cases of 3rd level underweight for age (which will include Kwashiorkor, nutritional marasmus and marasmic kwashiorkor)

Principal Features of Protein-Cal Def

Marasmus Kwashiorkor

Usual age 0-2 yrs 1-3 yrs

Edema None Lower legs, sometimes face or generalized

Wasting Gross loss of subcutaneous fat “all skin and bone”

Sometimes hidden, sometimes fat, blubbery

Muscle wasting Obvious Sometimes hidden

Growth retardation Obvious Sometimes hidden

Mental changes Usually apathetic, quiet

Usually irritable, moaning, sometimes apathetic

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Variable Features of Protein-Cal DefMarasmus Kwashiorkor

Appetite Usually good Usually poor

Diarrhea Often (past or present)

Often (past or present)

Skin changes Seldom Often – diffuse depigmentationOccasional – flaky paint or enamel dermatosis

Hair changes Seldom Often – sparse, straight, silky, dyspigmentation, grayish or reddish

Moonface Seldom Often

Hepatic enlargement Seldom Always 24

Biochem/ Pathology of Protein-Cal Def

Marasmus Kwashiorkor

Serum albumin Usually normal (or low)

Low

Urinary urea/g creatinine Usually normal (or low)

Low

Urinary hydroxyproline/g creatinine

Low Low

Serum essential a.a. index Normal Low

Anemia Uncommon Common: sometimes megaloblastic, sometimes Fe def

Liver biopsy Normal or atrophic Fatty change

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Marasmus

From Greek word for “withering” Used for the severely wasted, underweight

child Infantile atrophy Inanition Athrepsia Cachexia Decomposition

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Marasmus

“Balanced” starvation (low in both protein and calories)

Common in the first year of life or earlier Can occur at all ages

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Marasmus

Common causes of inadequate lactationPsychological factorsMaternal illnessMaternal malnutritionMaternal stressNecessity to work

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Unsuccessful breastfeeding or insufficient breast milk supply with little or no other food given

BOTTLEFED:

BREASTFED:

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CLINICAL MANIFESTATIONS

failure to gain weightweight loss until emaciationwrinkled skin: due to loss of SC tssOld man facies: shrunken and wizened

faceAbdomen: distended or thin with visible

intestinal pattern

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CLINICAL MANIFESTATIONS

Muscle wasting best seen and felt in the buttocks, thighs, scapular region, upper arms

Loose skin folds in the buttocksPotbelly and “winged scapulae”Apathetic and quiet infant

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CLINICAL MANIFESTATIONS

Subnormal tempSlow pulse rateBasal metabolic rate reducedConstipationStarvation type of diarrhea: frequent small

stools containing mucus

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CLINICAL MANIFESTATIONS

Growth retardation: body wt 60% of expected weight

Wasting of muscle and SC fat are observed

Light brown and sparse hair may be found

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CLINICAL MANIFESTATIONS

ASSOCIATED VIT deficiency Keratomalacia Angular stomatitis

ASSOCIATED CONDITIONS: Dehydration resulting from infectious diarrhea Intestinal parasitism Oral moniliasis tuberculosis

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Diagnostic Signs of Kwashiorkor

MUSCLE WASTINGRetention of some SC tss Marked reduction in the circumference of

the upper armTested by the infant’s ability to hold his

head when gently pulled from a lying to a sitting position

Smythe, 1958

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Diagnostic Signs of Kwashiorkor

PSYCHOMOTOR CHANGES Looks miserable, doesn’t smileRetarded motor developmentPsychological trauma due to maternal

withdrawal associated with weaning from the breast

Possible biochemical change affecting the brain suggested by abN in EEG

Nelson and Dean, 1959

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Common Signs of Kwashiorkor

Hair changesDiffuse depigmentationMoonfaceAnemia

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Common Signs of Kwashiorkor

HAIR CHANGESLoss of hairBrittle dry hairDyschromotrichiaLong, scanty pale hairFlag sign

May serve to indicate the duration of the deficiency state

Indicates alternating periods of protein adequacy and deprivation

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Common Signs of Kwashiorkor

DIFFUSE DEPIGMENTATION OF THE SKINOccurs all over the body esp where the skin

has peeledGeneral lightening of the pigment of the skin

of the faceCaused by interference with melanogenesisNot essential for the diagnosis of

kwashiorkor

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Common Signs of Kwashiorkor

MOONFACE edema may be so light as to be

undetectable by pittingPuffiness of the face may be noted

(particularly of the lax SC tss of the face)There is rounded prominence of the

cheeks, which protrudes beyond the level of the nasolabial folds

Relatively frequent early sign

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Common Signs of Kwashiorkor

ANEMIAUsually due to iron and folic acid

deficienciesMay be aggravated by hookworm infection in

some cases

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Occasional Signs of Kwashiorkor

Flaky paint rash or Enamel DermatosesHepatomegalyAssociated Vitamin DefAssociated Conditioning Infections

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Occasional Signs of Kwashiorkor

Flaky paint rash or Enamel DermatosesPathognomonic, if presentPatches of skin turn reddish, then purple, with

macules and vesiclesLater dark brown patches form which become

dry and peel off, sometimes leaving raw weeping areas like burns

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Occasional Signs of Kwashiorkor

Flaky paint rash or Enamel DermatosesMostly seen in the hidden parts of the body

(buttocks, groin, and trunk)Grave prognosisMoist groin rashNoma or cancrum oris (effect of malnutrition

and infection)

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Occasional Signs of Kwashiorkor

HEPATOMEGALYFirm smooth surface and edgeBiopsy: fatty infiltrationNecorsis or fibrosis may occurCirrhosis is rare

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Occasional Signs of Kwashiorkor

ASSOCIATED VITAMIN DEFPhotphobiaKeratomalaciaAngular stomatitis

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Occasional Signs of Kwashiorkor

ASSOCIATED CONDITIONING INFECTIONS

Passage of 3 semisolid stools/dayReflects the alteration of the intestinal

enzymes and functions that occur in PEMRespiratory infections

Bronchopneumonia

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INTERMEDIATE SEVERE SYNDROMES

Changing circumstances may result in a transition from one clinical picture to another

An infant with marasmus due to an inadequate breastfeeding may develop kwashiorkor during the 2nd yr of life when CHO foods are given

A child with early kwashiorkor can be forced into marasmus by severe diarrhea and ill-advised prolonged “therapeutic” starvation

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OVERNUTRITION

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OVERNUTRITION

A generalized excessive accumulation of fatty SC tss

OVERWEIGHT10% above the desirable weight standard

OBESE20% above the desirable weight standard

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OVERNUTRITION

EtiologyDue to overeating or excessive intake of

food compared with utilizationGenetic constitutionPsychic disturbances Insufficient exercise/ lack of activity

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OVERNUTRITION

Etiology: rareEndocrine and metabolic disturbances

ThyroidAdrenalsPituitarygonads

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OVERNUTRITION

CLINICAL MANIFESTATIONS facial features appear disproportionately fine on a

heavy looking child Nose and mouth small with a double chin

Adiposity is present in the mammary regions Abdomen is pendulous with white or purple striae In boys, external genitalia appear

disproportionately small In girls, menarche is not delayed

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OVERNUTRITION

CLINICAL MANIFESTATIONSObesity of the ext: usually greater in the

upper arms and thighsHands are relatively small and fingers

taperingSkinfold measurement with calipers placed

over the triceps muscle at the midpoint of the back of the right upper arm flexed at 90deg has been found useful in assessing fatness of children

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OVERNUTRITION

TREATMENT 2 principles:

1. Decrease energy intake Done by someone familiar with growth and

development needs of the child Avoid a restrictive diet

2. Increase energy output Initial exam: rule out pathological causes of

obesity

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OVERNUTRITION

TREATMENT 3-day food recall is done to itemize the

child’s diet so that a picture of the child’s eating habits is obtained

Particular likes and dislikes are to be noted Remember: a restrictive diet will most likely

fail

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OVERNUTRITION

TREATMENT: Simple steps

1. Avoid all sweets, cakes, biscuits, sweetened drinks, ice cream and chips.

2. Avoid or reduce intake of all fried foods and added fats (butter, margarine)

3. Limit milk intake to no more than 2 glasses per day

Skimmed/ low fat milk should be done under supervision for children <5 yo

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OVERNUTRITION

TREATMENT: Obtain activity history Increase physical activity such as walking,

or taking part in school sports Involve children in hobbies to prevent

boredom

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VITAMIN DEFICIENCIES

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VITAMIN A DEFICIENCY

IN MOST DEVELOPING COUNTRIES:Carotenoids in the diet provide 60% of

the total vitamin A activity ingested

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VITAMIN A DEFICIENCY

Utilization of the carotenoids depends upon:

1. Absorption (reduced with steatorrhea or inadeq fat in the diet)

2. Conversion to Vitamin A in the intestinal mucosa ( carotene has highest potency as proVit A which is absorbed in the small bowel and stored in the liver prior to release)

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VITAMIN A DEFICIENCY

Utilization of the carotenoids depends upon:

1. Absorption (reduced with steatorrhea or inadeq fat in the diet)

2. Conversion to Vitamin A in the intestinal mucosa ( carotene has highest potency as proVit A which is absorbed in the small bowel and stored in the liver prior to release)