Protein Energy Malnutrition

Question 1

Define protein energy malnutrition (PEM)

Answer 1

multi-nutritional deficiency complex in which a deficiency of energy is most commonly the outstanding deficit

Question 2

Describe the environmental and biological causes of malnutrition

Answer 2

Social and economic factors: poverty, ignorance, inadequate breastfeeding and weaning practices

Biologic factors: maternal malnutrition (low birthweight infants), infectious diseases

Environmental factors: overcrowded &/or unsanitary living conditions, agricultural patterns, droughts, floods, wars

There are major ties between infection and malnutrition.

Question 3

Clinical consequences of malnutrition

Answer 3

Weight loss (more with marasmus)
Loss of muscle (more with marasmus)
Loss of fat (more with marasmus)
Edema (Kwashiorkor only)
Psych changes (both but more with Kwashiorkor) 
Anorexia (more with Kwashiorkor) 
Hepatomegaly (Kwashiorkor only)
Infections (both, especially Kwashiorkor)
Diarrhea	(both)
Skin lesions (Kwashiorkor only)
Hair changes (Kwashiorkor more)

Question 4

Kwashiorkor

Answer 4

Edematous PEM, without wasting and classically attributed to “protein deficiency”

Older infants

Relatively higher mortality than marasmus

Now clearly related to metabolic stress & inflammation

Failure of the normal adaptive response of protein sparing that is normally seen in a fasting state.

Contributing factors include infectious stress, cytokine release, relative micronutrient deficiencies and possibly free radical exposure and oxidative damage. Potential role of the enteric microbiome recently highlighted.

Fat reserves and muscle mass tend to be unaltered; this may lead to the assumption that nutritional status is adequate.

Other characteristic clinical findings include skin lesions (“flaky paint”), hair texture and pigmentation changes (“flag sign”), and generalized edema (“moon facies”).

Metabolic derangements seen in kwashiorkor:

Hypoalbuminemia & enlarged fatty liver → edema

Increased permeability of biological cell membranes → edema

Impaired sodium/potassium homeostasis (sodium excess, potassium deficiency)

Hypotransferrinemia (anemia)

Impairment of immune system (infection)

Question 5

Marasmus

Answer 5

Severe wasting of fat and muscle mass, due primarily to energy deficiency. Slower onset. Better adaptation.

Infants

Most equivalent to “simple” starvation.
(“severe acute malnutrition/SAM”)

The “normal” physiologic response to starvation includes:

Reduction in energy expenditure ( decreased physical activity, bradycardia, hypothermia)

Decreased activity of sodium pump

Shift in fuel utilization to mobilization of body fat (increased ketones, decreased gluconeogenesis)

Muscle protein catabolism (but w/ decreased overall protein turnover)

Decreased inflammatory response & impaired immune function

Impaired function of G-I tract (dysmotility, malabsorption)

(Reduced body mass)

While these and other responses result in decreased nutrient demands and achieve a new equilibrium, if the nutritional deprivation persists, the patient is less able to adapt to complications, such as an infectious insult. As reserves are depleted, the individual is susceptible to injury that a normal host could withstand with little repercussion: ie, loss of functional reserve and loss of physiological responsiveness to stress are the hallmarks of the adaptation to severe PEM.

Question 6

Physical exam findings associated with Kwashiorkor

Answer 6

Misery, edema, hepatomegaly
Erythematous, hyperpigmentation, “Flaky Paint”
Dry, brittle, depigmented “Flag Sign”
“Moon Facies”

Question 7

General appropriate treatment approaches to PEM

Answer 7

GO SLOWLY!!!!

1. Resolve life-threatening conditions:

Cautious restoration of circulation – enteral preferred; avoid over-hydration

Potassium supplements ± Mg++; avoid excessive Na+

Treatment of infections (signs/symptoms may be mild/absent)

Avoid hypoglycemia (preferably by small, frequent oral feeds)

2. Restoring nutritional status without abruptly disrupting homeostasis*
Begin slowly (pt is adapted to malnourished state)

Small frequent (≤ q 4 hr) feeds, liquid oral or via nasogastric tube

Initial goal = maintenance protein and energy requirements (ie, not catch-up amounts)

Diet should be high biologic quality protein, high fat

Replete specific micronutrient deficiencies (especially K, Mg, P, Zn, Vitamin A )

3. Ensuring nutritional rehabilitation:

Gradually advance energy intakes to 1.5x normal and 3-4x protein needs;

Usually begins 1-2 wk after initial stabilization – after resolution of edema

Restoration of appetite may be prolonged, especially in kwashiorkor

Introduction of familiar foods

Emotional & physical stimulation, including physical activity to enhance recovery of cardiorespiratory and skeletal function.

Question 8

Re-feeding syndrome

Answer 8

Refeeding a starved person may result in predictable metabolic derangements, esp due to acute shifts from extracellular to intracellular spaces. Most common & potentially dangerous: K+, P, & Mg++

Potassium: increased insulin secretion (in response to feeding) → intracellular glucose & K+ → decreased serum K+ → altered nerve/muscle function

Phosphorus: increased insulin secretion → intracellular P; increased intracellular phosphorylated intermediates; P “trapped” in intracellular space;

Magnesium: increased requirements w/ increased metabolic rate (= co-factor for ATPase)

Question 9

Malnutrition in hospitalized pts

Answer 9

Malnutrition secondary to chronic disease or to the acute effects of surgery, trauma, sepsis, etc. is estimated to occur in up to 50% of hospitalized patients.