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Macronutrient deficiencies
(Protein Energy Malnutrition)
Dr. IKG Suandi, SpA
Objectives
To understand the sign & symptom of patient with protein energy malnutrition (PEM) To built diagnosis of patient with protein energy malnutrition (PEM) To understand the treatment and prevention of the patient with protein energy malnutrition (PEM)
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Introduction
Protein Energy Malnutrition (PEM) is a leading cause of death among children < 5 yrs of age
Primary PEM caused by social or economic factors that result of lack of food (protein & calorie deficiencies).
Secondary PEM occurs in children with various conditions associated with increased caloric requirements1 (infection, trauma, & cancer), increased caloric loss2 (malabsorption, & cystic fibrosis), reduced caloric intake3 (anorexia, cancer, oral intake restriction, & social factors), or combination4 of these three variables
I. Marasmus
Marasmus is the most common form of primary PEM, is caused by severe caloric depletion (inappropriate weaning practice)
Secondary forms of marasmic PEM are associated with such diseases as cystic fibrosis, tbc, cancer, celiac disease, or acquired immunodeficiency syndrome (AIDS), chronic diarrhea
Clinical manifestation: Body weight for age below 60%, or below 70% of the ideal weight for height Depleted body-fat stores; growth stunting; loss of muscle mass and subcutaneous fat stores Skin is dry and thin, the hair may be thin, sparse, and easily pulled out Generally apathetic and weak; bradycardia and hypothermia Atrophy of the filiform papillae of the tongue and monilial stomatitis is frequent
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II. Kwashiorkor
Presenting with pitting edema that starts in the lower extremities and ascends with increasing severity
Is caused by inadequate protein intake in the presence of fair to good caloric intake
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Pressure
pitting edema
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Kwashiorkor may be a complication of critical illness (when inadequate amounts of protein are provided for a prolonged time):
burns / cancer acute and chronic infection multi-organ system failure inflammatory bowel disease anorexia nervosa and postoperative surgery
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Clinical manifestation:
Kwashiorkor.
the body weight: 60-80% of the expected weight for age revealed a relative maintenance of subcutaneous adipose tissue a marked atrophy of muscle mass a minor pitting edema the hair is sparse, easily pluckable, and appears dull brown, red, or yellow-white
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generalized edema with involvement of the eyelids, abdomen, scrotum and lower extremities
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Flag sign: the hair may be thin, sparse, and easily pulled out appears dull brown, red, or yellow-white
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Flag sign: the hair may be thin, sparse, and easily pulled out appears dull brown, red, or yellow-white
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Kwashiorkor.
Skin changes: from hyperpigmented hyperkeratosis to an erythematous macular rash, a superficial desquamation
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A large, soft liver with indefinite edge, lymphatic tissue is atrophic Chest examination may revealed basilar rales, abdomen distended, bowel sounds tend to be hypoactive
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Complication of malnutrition
Infection1, sepsis, pneumonia, gastroenteritis Hypoglycemia2 Hypothermia3, bradycardia4 Vitamin A deficiencies5 altered immune response and increased morbidity (infection and blindness) and mortality (from measles)
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abdomen distended
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Treatment of malnutrition
Nutrient provided increasing metabolic rate stimulating anabolism & thus increasing nutrient requirements GI tract may not tolerate a rapid increase in intake nutritional rehabilitation should be initiated advanced slowly to minimize these complications Fluid and solute load must be monitored to avoid stressing the compromised myocardial function
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Calories can be safely started at 20% above the childs recent intake (50-75% of the normal energy requirement is safe) can be increased 10-20%/day may require 150% or more of the recommended calories Monitoring: electrolyte imbalances, poor cardiac function, edema, or feeding intolerance
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Summary of selected hormonal changes and their main metabolic effects usually seen in severe Protein Energy Malnutrition
Hormonal activity in Influenced in PEM by Hormone Insulin Low food intake: glucose & amino acids (aa) Low P intake: aa reduced IGF-I synthesis Energy (E) deficit Decrease Protein (P) deficit Decrease muscle protein synthesis / lipogenesis / growth Metabolic effects of changes in PEM
Growth hormone
Increased
visceral synthesis & lipolysis urea synthesis muscle & cartilage P, collagen synth, lipolysis, growth; prod. of GH lipolysis; glycogeno-lysis inhibit insulin secretion muscle P catabolism, visceral P turn over, lipolysis, gluconeogenesis Na & water retention to appearance of edema glucose oxidation & BEE; reverse T3 Delayed menarche
Decreased
Stress of food def., infections ( glucose) Stress of hunger Fever ( glucose) blood volume & serum Na? extra -cellular K? ? Low protein & energy intake?
Normal but can increase Normal or moderately increased Increased ; T4 usually T3 decreased Decreased
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