Course Clinical Features Laboratory Findings Prognosis

Marasmus-like protein-energy

malnutrition

Chronic illness (e.g., chronic lung

disease, cancer)

Months History of weight loss Normal or mildly

reduced serum proteins

Variable; depends on

underlying disease

Muscle wasting

Absent subcutaneous fat

Kwashiorkor-like protein-energy

malnutrition

Acute, catabolic illness (e.g.,

severe trauma, burns, sepsis)

Weeks Normal fat and muscle Serum albumin <2.8 gm/

dL

Poor

Edema

Easily pluckable hair

Data from Bennett JC, Plum F (eds): Cecil Textbook of Medicine, 20th ed. Philadelphia, WB Saunders, 1996, p. 1156.

weak and bedridden may show physical signs of protein and energy malnutrition: (1) depletion of subcutaneous fat in the arms, chest wall, shoulders, or metacarpal regions; (2) wasting of

the quadriceps femoris and deltoid muscles; and (3) ankle or sacral edema.

Bedridden or hospitalized malnourished patients have an increased risk of infection, sepsis, impaired wound healing, and death after surgery.[68] The biochemical mechanisms responsible

for secondary PEM in patients with cachexia are complex. In contrast to patients with anorexia nervosa, described next, patients with cachexia show loss of fat as well as muscle mass,

which may occur before a decrease in appetite. Cachectic patients show increased expenditure of resting energy; in contrast, in chronic starvation, the basal metabolic rate is decreased.

Cytokines produced by the host during sepsis, for example, or by tumors have been postulated to be involved in cachexia: tumor necrosis factor, interleukin-1, interleukin-6, and interferon-

g. In addition, as discussed in Chapter 7 , lipid- and protein-mobilizing factors have been isolated from animals and people with cancer cachexia.[69]

Morphology.

The central anatomic changes in PEM are (1) growth failure; (2) peripheral edema in kwashiorkor; and (3) loss of body fat and atrophy of muscle, more marked in marasmus.

The liverin kwashiorkor, but not in marasmus, is enlarged and fatty; superimposed cirrhosis is rare.

In kwashiorkor (rarely in marasmus), the small bowelshows a decrease in the mitotic index in the crypts of the glands, associated with mucosal atrophy and loss of villi and microvilli. In

such cases, concurrent loss of small intestinal enzymes occurs, most often manifested as disaccharidase deficiency. Hence, infants with kwashiorkor initially may not respond well to a fullstrength,

milk-based diet. With treatment, the mucosal changes are reversible.

The bone marrowin both kwashiorkor and marasmus may be hypoplastic, mainly because of decreased numbers of red cell precursors. How much of this derangement is due to a

deficiency of protein and folates or to reduced synthesis of transferrin and ceruloplasmin is uncertain. Thus, anemia is usually present, most often hypochromic microcytic anemia, but a

concurrent deficiency of folates may lead to a mixed microcytic-macrocytic anemia.

The brainin infants who are born to malnourished mothers and who suffer PEM during the first 1 or 2 years of life has been reported by some observers to show cerebral atrophy, a

reduced number of neurons, and impaired myelinization of the white matter, but there is no universal agreement on the validity of these findings.

Many other changesmay be present, including (1) thymic and lymphoid atrophy (more marked in kwashiorkor than in marasmus); (2) anatomic alterations induced by intercurrent

infections, particularly with all manner of endemic worms and other parasites; and (3) deficiencies of other required nutrients, such as iodine and vitamins.

Date: 2016-04-22; view: 933