| Insufficient consumption of protein and
carbohydrates causes loss of both body mass and adipose tissue, although one or the other loss
may predominate in an individual.
Protein energy malnutrition (PEM) occurs in two circumstances: in developing nations, it
may be present in the endemic form and in famine conditions, it may approach 25%. Causes
The primary disorder occurs when socioeconomic factors limit the quantity and quality
of food; it is a particular problem when vegetable proteins of low biological value are
major components of the diet and when the incidence of infectious diseases is high. The
problem is accentuated when the energy intake is insufficient so that dietary proteins are
oxidised as fuel rather than utilised for synthesis of body protein. In children of
developing nations two syndromes of PEM have been distinguished:
1. Marasmus, manifested
by growth failure, loss of adipose tissue, generalised wasting of protein mass and no
edema is thought to be due to combined effects of protein and energy, malnutrition.
2. Kwashiorkor, manifested by
growth failure, edema, hypoalbuminemia, fatty liver and preservation of subcutaneous fat
is thought to be due to specific protein malnutrition.
Mixed forms are both common in children and adults and the distinction between pure
protein malnutrition and PEM has little clinical significance.
Clinical manifestations
Mild to moderate PEM:
Children fail to gain height and weight; adults generally lose weight though edema may
mask weight loss. Alternatively, if the individual was obese, a residue of fat can hide
loss of protoplasm. Levels of albumin, transferrin and prealbumin in the serum may be low.
Severe PEM:
Severe PEM is characterised by decrease in muscle mass as is evident in body
composition and in laboratory findings. Listlessness, easy fatigability, sensation of
coldness, dry cracked skin, drawn facies, and dyspigmentation of the skin and hair are
common. Skin ulcers occur in advanced stages. The blood pressure is low, the pulse is
decreased and the temperature may be low.
Treatment
In the case of moderate to mild PEM, any precipitating events must be addressed, and
the intake of protein and carbohydrates should be increased sufficiently to allow replenishment
of deficits. It is appropriate to administer multivitamins to all such patients. It is
also essential during repletion that the availability of all minerals and trace elements
is adequate to prevent life threatening hypokalemia, hypomagnesemia and hypophosphatemia
(deficiencies of calcium, magnesium and phosphorus, respectively) from developing.
Provided the patient can eat and swallow, most patients can be treated orally. However, if
anorexia is a major problem or if the individual is without teeth, the diet may have to be
supplemented with liquid formulas. Since the patient will have been without much food for
a long period of time, starting oral feedings, especially if the caloric density is too
high at first, can present problems. Food must be reintroduced slowly, carbohydrates first
to supply energy followed by protein foods. This is important to avoid any metabolic or
electrolyte discrepancies in the body.
Proteins
Carbohydrates
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