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MD Consult: Books: Goldman: Cecil Medicine: Chapter 234 – PROTEIN-ENERGY MALNUTRITION

Goldman: Cecil Medicine, 23rd ed.

Copyright © 2007 Saunders, An Imprint of Elsevier


Samuel Klein


Normal nutritional status represents a healthy relationship between nutrient intake and nutrient requirements. An imbalance between intake and requirements over time can lead to malnutrition, manifested by alterations in intermediary metabolism, organ function, and body composition. The term protein-energy malnutrition has been used to describe macronutrient deficiency syndromes, which include kwashiorkor, marasmus, and nutritional dwarfism in children and wasting associated with illness or injury in children and adults.


Primary protein-energy malnutrition is caused by lack of access to adequate nutrient intake and usually affects children and elderly persons. The functional and structural abnormalities associated with primary protein-energy malnutrition are often reversible with nutritional therapy. However, prolonged primary protein-energy malnutrition can cause irreversible changes in organ function and growth.

Secondary protein-energy malnutrition is caused by illnesses that alter appetite, digestion, absorption, or nutrient metabolism and can be divided into three general, but often overlapping, categories: (1) diseases that affect gastrointestinal tract function, (2) wasting disorders, and (3) critical illness. Gastrointestinal disease can cause protein-energy malnutrition by premucosal (maldigestion), mucosal (malabsorption), or postmucosal (lymphatic obstruction) defects ( Table 234-1 ). The nutritional status of patients with protein-energy malnutrition caused by gastrointestinal tract dysfunction can often be restored to normal if adequate nutritional support can be provided by dietary manipulations, enteral tube feeding, or parenteral nutrition. Wasting disorders, such as cancer, acquired immunodeficiency syndrome, and rheumatologic diseases, are characterized by involuntary loss of body weight and muscle mass in the setting of a chronic illness. These patients often experience wasting because of (1) inadequate nutrient intake related to anorexia and possibly gastrointestinal tract dysfunction and (2) metabolic abnormalities caused by alterations in regulatory hormones and cytokines. The alterations in metabolism are responsible for the greater loss of muscle tissue observed in these patients than in those with pure starvation or semistarvation. Restoration of muscle mass is unlikely with nutritional support unless the underlying inflammatory disease is corrected. Weight gain that occurs after nutritional support is initiated is usually caused by increases in fat mass and body water, without significant increases in lean tissue. Patients with critical illness exhibit marked metabolic alterations, manifested by increased energy expenditure, altered endogenous glucose production and lipolytic rates, and protein breakdown. Therefore, protein and energy requirements are increased in critically ill patients. However, providing aggressive nutritional support may ameliorate but does not prevent net lean tissue losses without correction of the underlying illness or injury.

TABLE 234-1   — 

Primary Abnormality Pathophysiology Representative Disorders
Premucosal defect Pancreatic insufficiency Chronic pancreatitis
    Cystic fibrosis
  Pancreatic duct obstruction
Bacterial overgrowth Motility diseases
  Blind loop syndromes
  Small intestine diverticula
Rapid gastric emptying and intestinal transit Post–gastric surgery syndrome
Mucosal defect Inadequate bowel syndrome Intestinal resection
    Gluten-sensitive enteropathy
Immunoproliferative small bowel disease
Radiation enteritis
Intestinal ischemia
AIDS enteropathy
Postmucosal defect Lymphatic obstruction Congenital intestinal lymphangiectasia
    Milroy’s disease
Secondary intestinal lymphangiectasia
Retroperitoneal carcinoma
Retroperitoneal fibrosis
Chronic pancreatitis
Crohn’s disease
Whipple’s disease
Constrictive pericarditis
Chronic congestive heart failure

AIDS = acquired immunodeficiency syndrome.

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