Malnutrition Flashcards
Protein Energy Malnutrition
a. Multi-nutritional deficiency complex, energy deficiency most outstanding
b. ENERGY REQUIREMENTS “TRUMP” ALL
c. If negative energy balance,
i. obligatory negative N balance
PEM – Major Types/Broad “Categories”
- Marasmus:
i. Severe wasting, due to energy deficiency
ii. Slower onset, better adaptation - Kwashiorkor:
i. Edematous PEM, generally w/o wasting
ii. Protein deficiency (+ metabolic stress + micronutrient deficiency/imbalance)
iii. Rapid onset, “mal-adaptation”
Protein Energy Malnutrition
a. Starvation: pure caloric deficiency
i. Host adapts to conserve lean body mass & increase fat metabolism
b. Cachexia: associated w/ inflammatory or neoplastic conditions
i. Not reversed by feeding; anorexia
c. [Sarcopenia: subnormal amount of skeletal muscle, w/o weight loss]
Global Magnitude of PEM
Of the world’s children…
20% underweight
(low weight-for-age)
26 % stunted [“chronic”]
8 % wasted [“acute”]
~ 45% of child deaths are related to malnutrition
Protein energy malnutrition (PEM) is a multi-nutritional deficiency complex in which a deficiency of energy is most commonly the outstanding deficit. However, other nutrient deficiencies/imbalances have major impact on specific manifestations and complications.
The spectrum of manifestations is dependent on the relative severity of the energy or protein deficit, duration of the deficiencies, age of the host, cause of the deficiencies, and association with other nutritional or infectious diseases.
- Marasmus refers to severe wasting of fat and muscle mass, due primarily to energy deficiency; it is most equivalent to “simple” starvation.
- Kwashiorkor refers to edematous PEM, without wasting and classically attributed to “protein deficiency”; now clear related to metabolic stress & inflammation .
- Marasmic kwashiorkor is a combination of chronic energy deficiency and chronic or acute protein deficit, and is manifested clinically with evidence of both wasting and edema.
Pathophysiology of Marasmus (“severe acute malnutrition/SAM”):
a. Reduction in energy expenditure ( physical activity, bradycardia, hypothermia)
b. Decreased activity of sodium pump
c. Shift in fuel utilization to mobilization of body fat ( ketones, gluconeogenesis)
d. Muscle protein catabolism (but w/ overall protein turnover)
e. Decreased inflammatory response & impaired immune function
f. 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.
Pathophysiology of Kwashiorkor:
a. The etiologic mechanisms of kwashiorkor are not completely understood, it is generally considered a failure of the normal adaptive response of protein sparing that is normally seen in a fasting state.
b. As noted above, classically protein deficiency in the face of adequate energy intake was thought to be etiologic, but clearly this is an oversimplification.
c. Contributing factors include infectious stress, cytokine release, relative micronutrient deficiencies and possibly free radical exposure and oxidative damage.
d. Potential role of the enteric microbiome recently highlighted (
e. Fat reserves and muscle mass tend to be unaltered; this may lead to the assumption that nutritional status is adequate.
i. Other characteristic clinical findings include skin lesions (“flaky paint”), hair texture and pigmentation changes (“flag sign”), and generalized edema (“moon facies”).
f. The list below indicates some of the metabolic derangements seen in kwashiorkor, which is associated with a relatively higher mortality than marasmus.
1. Hypoalbuminemia & enlarged fatty liver—> edema
2. Increased permeability of biological cell membranes edema
3. Impaired sodium/potassium homeostasis (sodium excess, potassium deficiency)
4. Hypotransferrinemia (anemia)
5. Impairment of immune system (infection)
Causes of PEM
a. Social & economic factors
-Poverty
– Inadequate breastfeeding
-Ignorance
– Inappropriate weaning/CF
-Monotonous/restricted diets, plant-based
b. Biologic factors: maternal under-nutrition, low birth weight infants – persistence of effects (epigenetic?)
c. Environmental factors: overcrowding, infectious burden, agricultural patterns, etc
Who is at risk for Protein energy malnutrition?
a. Infants (0-12 mo): marasmus/severe wasting most common
b. Older infants (12 - 24 mo): esp kwashiorkor; voluntary restrictive/alternative feeding
c. Acute weight loss: e.g. anorexia nervosa, s/p bariatric surgery, intentional restriction, social deprivation
d. Chronic illnesses: alcoholism, pancreatitis, HIV/AIDS, malabsorption
e. Elderly: wasting/loss of LBM (sarcopenia)
PEM: “Underweight”
Low Weight-for-Age
> 2 SD below median
(50th%)
< 3rd %ile for age
Underweight not = Wasting
PEM: Stunting
“chronic malnutrition”
Length-for-Age
(% of Median)
Normal 95 - 105 %
Stunting:
< - 2 Z-Score Len/age
Severe: < 85 % median
≤ - 3 Z-score Len/age
WASTING:
decreased Wt relative to Length
(≈ BMI)
“Ideal Body Weight”
(50th % Wt/ht)
%IBW Interpretation
90-110 Normal weight 80-89 Mild wasting 75-79 Moderate < 75 Severe wasting (e.g. 7 kg/10 kg (IBW)=70%)
Mild PEM: WASTING
83 % IBW = mild
Other terms:
“Failure to thrive”
Undernutrition
Marasmus:
“Normal” Response to Starvation
Muscle–> increased Utilization of Triglycerides/f.a.
Brain–> increased Utilization ketones (decreased glucose)
Liver—> decreased Gluconeogenesis
Muscle—> decreased Protein degradation (↑↑ recycling a.a., but continues, esp skel mus)
Liver/Kidney—> decreased Urea production & excretion
(Result: Utilization of fat stores, minimize muscle wasting–> decreased Basal Metabolic Rate)
“Normal” Responses to Starvation
a. Decreased Physical activity/ ↑ resting
b. Decreased Basal Metabolic Rate:
i. Hypothermia, hypotension, bradycardia
c. Decreased Endocrine changes:
decreased insulin, decreased thyroid, ↑ epinephrine & corticosteroid
d. GI tract: mucosal atrophy, decreased secretions, decreased motility
e. Myocardial atrophy, decreased cardiac output;
Loss of functional reserve & physiologic responsiveness to stress
Kwashiorkor:
“Abnormal” Adaptive Response
a. Classic etiologic description:
i. protein deficiency (qualitative &/or quantitative) w/ adequate energy
b. Current: + Infectious stress, cytokine release, + micro-nutrient deficiency, oxidative damage, (“dysbiosis”?)
c. ** Hypoalbuminemia & edema **
d. Increased insulin, decreased lipolysis (esp. w/ continued CHO )
e. Increased hepatic fatty acid syn (increased CHO & decreased lipolysis, decreased protein)—> fatty, enlarged liver
Clinical & Metabolic Effects of PEM
Marasmus Kwashiorkor Weight loss ++++ ++ Loss of muscle ++++ + Loss of fat ++++ + Edema — ++++ Psych ’s ++ ++++ Anorexia +/ — ++++ Hepatomegaly — ++
Clinical & Metabolic Effects of PEM
Other stats
Marasmus Kwashiorkor Infections ++ ++++ Diarrhea +++ +++ Skin lesions — ++ Hair changes +/- ++
Principles of Management Severe PEM:
(esp Kwashiorkor – higher mortality)
a. GO SLOWLY!!
b. Resolve life-threatening conditions (e.g. infections)
c. Restore nutritional status w/o abruptly disrupting homeostasis / “adapted state”
d. Ensure nutritional rehabilitation (Macronutrients & micronutrients)
Refeeding Syndrome
a. Broad range of metabolic consequences occurring due to rapid reinstitution of nutrients (& energy/substrate) in pt w/ PEM; can result in sudden death
b. Catabolic state—> anabolic state:
i. Fluid shifts—> heart failure
ii. Requires E, nutrients, enzymes
c. Common derangements: K+, P+, Mg,++ Thiamine
Refeeding Syndrome
K+, P+, Mg,++ Thiamine
a. Potassium: Increased insulin secretion (in response to feeding)—> intracellular glucose & K+—>
Decreased serum K+ —> altered nerve/muscle function
b. Phosphorus: Increased insulin secretion–> intracellular P;
i. Increased intracellular phosphorylated intermediates (including glucose); P “trapped” intracelluar;
i. Decreased serum P–> altered nerve/muscle function
c. Magnesium: increased requirement w/ increased metabolic rate; (= co-factor for ATPase)
d. Thiamine: rapid depletion (co-factor glycolysis) w/ CHO—> cardiomyopathy +-encephalopathy
Refeeding Syndrome: Management
a. Refeed slowly (start w/ 50-75% of basal needs)
b. Avoid fluid overload (enteral vs IV)
c. Monitor levels – supplement as necessary (K, P, Mg); provide micronutrients
d. Monitor vital signs
e. Monitor physical exam (e.g. edema, rash)
f. Resolution of edema before full feeding (wt loss first w/ edematous PEM)
Difference Between Kwashiorkor and Marasmus
Kwashiorkor
1. This disease is caused by the deficiency of protein in the diet of child.
- Kwashiorkor occurs in children in the age group 1-5 years.
- The disease is more common in villages where there is small gap period between successive pregnancies.
- In this disease, swelling of body is observed due to retention of fluids.
- Wasting of muscles is not evident.
- Skin changes color and become broken and scaly.
Marasmus
1. This disease is caused by deficiency of protein as well as energy nutrients (that is carbohydrates and fats) in the diet.
- Marasmus occurs in children below the age of 1 year.
- This disease is more common in towns and cities where breast-feeding in discontinued quite early.
- No swelling of body takes place in Marasmus.
- In Marasmus, wasting of muscles is quite evident. The child is reduced to skin and bones.
- Skin does not change color and does not break.
