(2) marasmus kwashiorkor 12022009
TRANSCRIPT
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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)