Protein-Energy Malnutrition

Protein-energy malnutrition (PEM) is classically described as 1 of 2 syndromes, marasmus and kwashiorkor, depending on the presence or absence of edema. Each type may be classified as acute or chronic. Additionally, marasmus can precede kwashiorkor. Many patients exhibit symptoms of both disease states.

Marasmus, or PEM without edema, is defined as inadequate intake of all nutrients, but especially energy. Its extreme form is characterized by muscle wasting and depletion of body fat stores. Other findings may include hypothermia, bradycardia, hypotension, decreased metabolic rate, loss of skin turgor, and constipation.

Kwashiorkor, or PEM with edema, is characterized by muscle atrophy, maintenance or gain of body fat, and peripheral edema. Other characteristics include anasarca (generalized edema), hepatomegaly, dry and peeling skin, anorexia, hypothermia, and apathy.

The exact pathogenesis of kwashiorkor is unknown. Derived from an African term meaning “the disease that occurs when the next baby is born,” kwashiorkor was initially thought to result from a diet high in calories (mainly carbohydrates, such as maize) yet deficient in protein. However, recent evidence points away from dietary protein deficiency as the primary cause. While many of these patients exhibit hypoalbuminemia, this is thought to be a consequence of the disease and not a trigger. Aflatoxin poisoning, oxidative stress, immune system dysfunction, and the gut microbiota may play causative roles.[1],[2],[3],[4]

Mixed marasmus-kwashiorkor (edematous malnutrition) can occur in those who have inadequate dietary intake of all nutrients. This condition is typically triggered by an infection or inflammatory state.

PEM affects multiple organ systems and therefore places affected individuals at increased risk of severe illness and death by increasing the likelihood of micronutrient deficiencies, dehydration, infection, and sepsis.

PEM is primarily a problem in resource-limited countries. Worldwide, PEM is the leading cause of death in children under the age of 5. The highest prevalence is in Africa and south-central Asia.[5] PEM is also found in developed countries under various circumstances, including anorexia nervosa, cancer, hemodialysis, dementia, and severe chronic disease states. The condition has also been found in infants placed on severely restricted diets and in 5% of a population of patients who underwent Roux-en-Y gastric bypass surgery to control obesity.[6],[7],[8]

Diagnosis

Diagnosis of PEM is based on a variety of factors. While it was once thought that serum albumin levels were indicative of nutrition status, new guidelines indicate this measure does not take into account the complexity of hepatic protein synthesis. Altered serum albumin and pre-albumin levels can be accounted for by a number of factors, including the acute-phase response, hydration status, disease state, clinical condition, albumin leakage from intra- to extra-vascular spaces, and severe zinc deficiency.[9]

In lieu of albumin levels, the Academy of Nutrition and Dietetics and the American Society of Parenteral and Enteral Nutrition have established new standards to diagnose malnutrition in adults. Rather than a single parameter, the recommendations are based on a set of measurable characteristics indicative of nutrition status. To be diagnosed with PEM, patients must meet at least 2 out of the following 6 characteristics: insufficient energy intake, significant weight loss, loss of muscle, loss of subcutaneous fat, fluid accumulation unrelated to hypervolemia, and reduced hand-grip strength.[9]

Treatment

Treatment for PEM varies based on the severity and etiology of the problem. Patients suffering from eating disorders will need an appropriate dietary intervention in conjunction with mental health support. Malnutrition due to social/environmental reasons or food insecurity may require a case-management consultation to help the patient connect with resources. For hospitalized patients, a team approach that includes the doctor, nurse, dietitian, and other clinicians is recommended to implement an appropriate nutrition care plan. Patients with malnutrition may benefit from oral nutrition supplements and, in some cases, parenteral or enteral nutrition to help improve nutrition status. Lastly, regardless of etiology, nutrition education is essential for long-term health of a patient with malnutrition.[10]

Some individuals treated for PEM are at risk for refeeding syndrome, in which hypophosphatemia, hypokalemia, and hypomagnesemia may lead to disturbances in the cardiac, neurologic, gastrointestinal, respiratory, hematologic, skeletal, and endocrine systems. The World Health Organization has developed guidelines to help prevent these complications and to establish a transition to normalcy. Treatment consists of 3 phases: stabilization, rehabilitation, and follow-up.[11]

The initial (stabilization) phase proceeds from days 1-7. It consists of treatment and prevention of hypoglycemia, hypothermia, dehydration, and infection; correction of electrolyte imbalance and micronutrient deficiencies; and a cautious feeding regimen.

A rehabilitation phase proceeds from weeks 2-6. It consists of achievement of catch-up growth, provision of sensory stimulation, and emotional support.

Follow-up is necessary, as some patients relapse. Provision of nutritional supplements is recommended for those of all ages affected by PEM to prevent malnutrition from recurring. Furthermore, education on the benefits of breastfeeding and hygiene have also been found to be helpful interventions in the pediatric population.[5]

References

  1. Fuhrman MP, Charney P, Mueller CM. Hepatic proteins and nutrition assessment. J Am Diet Assoc. 2004;104(8):1258-64.  [PMID:15281044]
  2. Briend A. Kwashiorkor: Still an Enigma – The Search Must Go On. Emergency Nutrition Network (ENN). https://www.ennonline.net/attachments/2314/Kwashiorkor-still-an-enigma-CMA.... Accessed October 16, 2020.
  3. Hendrickse RG. Of sick turkeys, kwashiorkor, malaria, perinatal mortality, heroin addicts and food poisoning: research on the influence of aflatoxins on child health in the tropics. Ann Trop Med Parasitol. 1997;91(7):787-93.  [PMID:9625935]
  4. Sive AA, Dempster WS, Malan H, et al. Plasma free iron: a possible cause of oedema in kwashiorkor. Arch Dis Child. 1997;76(1):54-6.  [PMID:9059163]
  5. Felípez L, Sentongo TA. Drug-induced nutrient deficiencies. Pediatr Clin North Am. 2009;56(5):1211-24.  [PMID:19931072]
  6. Kuhl J, Davis MD, Kalaaji AN, et al. Skin signs as the presenting manifestation of severe nutritional deficiency: report of 2 cases. Arch Dermatol. 2004;140(5):521-4.  [PMID:15148094]
  7. Carvalho NF, Kenney RD, Carrington PH, et al. Severe nutritional deficiencies in toddlers resulting from health food milk alternatives. Pediatrics. 2001;107(4):E46.  [PMID:11335767]
  8. Faintuch J, Matsuda M, Cruz ME, et al. Severe protein-calorie malnutrition after bariatric procedures. Obes Surg. 2004;14(2):175-81.  [PMID:15018745]
  9. Marcason W. Should Albumin and Prealbumin Be Used as Indicators for Malnutrition? J Acad Nutr Diet. 2017;117(7):1144.  [PMID:28648265]
  10. Tappenden KA, Quatrara B, Parkhurst ML, et al. Critical role of nutrition in improving quality of care: an interdisciplinary call to action to address adult hospital malnutrition. J Acad Nutr Diet. 2013;113(9):1219-37.  [PMID:23871528]
  11. World Health Organization. Management of Severe Malnutrition: A Manual for Physicians and Other Senior Health Workers. World Health Organization. http://www.who.int/nutrition/publications/severemalnutrition/9241545119/en/. Accessed July 6, 2020.
Last updated: December 11, 2020