Protein Malnutrition and Edema in an Older Adult: Pathophysiology Case Study (Genetics, Symptoms, Physiologic Response and Cells)

Overview: protein malnutrition in an older adult

Protein malnutrition, often described as protein-energy malnutrition, occurs when protein intake or absorption is too low to meet the body’s needs for tissue maintenance, repair, immune function and synthesis of plasma proteins. This patient has two causes acting together:

• Reduced intake: without dentures, chewing protein-rich foods such as meat, fish, eggs and legumes is difficult, so intake falls.
• Reduced absorption: malabsorption syndrome limits the absorption of amino acids and other nutrients from the small intestine, even when food is eaten.

When protein deficiency outweighs energy deficiency, the picture resembles kwashiorkor-type (edematous) malnutrition. Its hallmark is edema caused by low plasma protein levels, particularly low albumin (Rogers, 2023). Malnutrition is common in nursing home residents and is diagnosed using criteria such as the Global Leadership Initiative on Malnutrition (GLIM): unintentional weight loss, low BMI or reduced muscle mass, combined with reduced intake or absorption, or with inflammation (Cederholm et al., 2019).

1. The role of genetics

In this patient, genetics does not appear to play a direct role. The patient’s protein malnutrition is acquired: it results from inadequate intake (lack of dentures) and an existing malabsorption syndrome, compounded by the physiologic changes of aging.

Genetics can, however, contribute to malabsorption in other patients, and it is worth considering when the cause of malabsorption is unknown:

• Celiac disease is strongly associated with the HLA-DQ2 and HLA-DQ8 genotypes. It can be diagnosed for the first time in older adults.
• Cystic fibrosis (CFTR mutations) causes pancreatic insufficiency and fat and protein malabsorption.
• Lactase non-persistence (genetically determined lactose intolerance) can limit dairy intake, an important protein source for older adults.
• Rare inherited disorders of amino acid transport, such as Hartnup disease, impair protein absorption.

If this patient’s malabsorption had a genetic basis, such as undiagnosed celiac disease, treatment of the underlying cause, such as a gluten-free diet, would be essential to correct the malnutrition.

2. Why the patient presents with generalized edema of the extremities and abdomen

The patient’s edema is best explained by hypoalbuminemia, which disrupts the balance of Starling forces across the capillary wall:

• Albumin, made in the liver from dietary amino acids, is the main protein responsible for plasma oncotic (colloid osmotic) pressure, the force that holds fluid inside blood vessels.
• With too little protein, the liver produces less albumin, so plasma oncotic pressure falls.
• Capillary hydrostatic pressure, which pushes fluid out, is now relatively unopposed, so fluid moves from the vessels into the interstitial spaces.
• This produces pitting edema in dependent areas, such as the legs and feet (or the sacrum in bedbound patients), and ascites, fluid in the peritoneal cavity, which explains the swollen abdomen.

Other features often accompany this presentation: muscle wasting that may be hidden by edema, weakness, fatigue, thin and fragile skin, poor wound healing, hair thinning, frequent infections and, in edematous malnutrition, an enlarged fatty liver (Rogers, 2023).

3. The physiologic response and why it occurred

The stimulus is a prolonged deficiency of dietary and absorbed protein. The body responds in several ways to survive with limited amino acids:

1. Protein catabolism and muscle wasting: to supply amino acids for essential functions, such as gluconeogenesis, immune and acute-phase proteins, and enzymes, the body breaks down skeletal muscle protein. This leads to sarcopenia, weakness and reduced mobility, which in turn increases the risk of falls, pressure injuries and dependence.
2. Reduced hepatic protein synthesis: with fewer amino acids available, hepatocytes reduce production of albumin, transferrin and lipoproteins. Low albumin causes edema. Low lipoprotein production impairs export of fat from the liver, which can cause hepatic steatosis (fatty liver).
3. Fluid and sodium retention: as fluid leaks into the tissues, the kidneys sense reduced effective circulating volume. The renin-angiotensin-aldosterone system (RAAS) and antidiuretic hormone (ADH) are activated, causing sodium and water retention. This compensatory response, meant to protect blood pressure, worsens the edema, because low oncotic pressure lets the retained fluid leak out of the vessels.
4. Impaired immune function: protein deficiency reduces lymphocyte production and function, antibody synthesis and the integrity of skin and mucosal barriers, which increases susceptibility to infections such as pneumonia and urinary tract infections.
5. Intestinal atrophy: the intestinal lining has a high protein turnover. In malnutrition, the villi atrophy and enzyme production falls, which worsens malabsorption. A vicious cycle develops: malnutrition causes malabsorption, which deepens malnutrition.
6. Metabolic adaptation: basal metabolic rate falls to conserve energy, contributing to fatigue and low activity.

Why this response occurred: these are adaptive survival mechanisms. The body prioritizes vital organs by sacrificing skeletal muscle and non-essential protein synthesis. In an 83-year-old with low physiologic reserve and ongoing deficiency from both poor intake and malabsorption, these adaptations become maladaptive, producing visible edema, wasting and vulnerability to complications.

4. The cells involved

5. How another characteristic would change the response

Age

Age is the key characteristic in this case. Older adults are especially vulnerable because of the “anorexia of aging” (reduced appetite, taste and smell), poor dentition, slower gastric emptying, reduced muscle reserve, polypharmacy, cognitive impairment and dependence on others for meals. Their response is more severe and recovery is slower: muscle mass is lost quickly and regained slowly, wounds heal poorly, and the risk of infections, falls and death is higher.

In a child, protein deficiency typically causes classic kwashiorkor: edema, a distended abdomen, skin and hair changes, growth failure and developmental delay, because protein is also needed for growth. In a younger adult with more muscle reserve, edema would usually develop later and recovery would be faster.

Gender

Older women generally have less muscle mass and are more likely to live longer, live alone and have osteoporosis, so protein deficiency may lead more quickly to sarcopenia, frailty and fractures. Older men may have more muscle reserve but also more cardiovascular disease, which can complicate fluid balance and edema.

Genetics and comorbidities

If the malabsorption were caused by a genetic condition such as celiac disease, specific treatment such as a gluten-free diet would be needed. Comorbidities would also change the response:

• Heart failure would worsen fluid retention.
• Liver cirrhosis would further impair albumin synthesis.
• Chronic kidney disease or nephrotic syndrome would add protein loss and complicate protein replacement.

Nursing and treatment implications

• Nutrition: refer to a dietitian for a high-protein, energy-dense diet with modified texture (soft, minced or pureed) and oral nutritional supplements. Treat the underlying malabsorption, which may include pancreatic enzymes or a gluten-free diet.
• Dental: refer for dentures or dental care, and refer to speech-language pathology if swallowing is impaired.
• Refeeding syndrome: severely malnourished patients are at risk when nutrition is restarted. Start slowly and monitor phosphate, potassium, magnesium, glucose and fluid status (da Silva et al., 2020).
• Edema and skin: elevate the legs, reposition regularly, protect fragile skin, monitor daily weight and intake and output, and watch for respiratory compromise from ascites.
• Monitoring: weekly weights, food intake records, nutrition screening (for example, with the Mini Nutritional Assessment) and functional status.
• Facility follow-up: address systemic causes in the nursing facility, such as mealtime assistance, adapted utensils and routine nutrition screening.

Conclusion

This 83-year-old’s generalized edema and ascites result from protein malnutrition caused by poor intake (no dentures) and malabsorption. Inadequate amino acids reduce albumin synthesis by hepatocytes, lowering plasma oncotic pressure and shifting fluid into the tissues and abdomen, while RAAS activation worsens fluid retention. Muscle catabolism, immune suppression and intestinal atrophy are part of the body’s attempt to survive protein deficiency, but in an older adult with limited reserve they become harmful. Genetics is not the main cause here, but age, gender, genetic malabsorption disorders and comorbidities can all change the response. Early recognition, nutrition and dental intervention, and careful refeeding are essential.

References

Cederholm, T., Jensen, G. L., Correia, M. I. T. D., Gonzalez, M. C., Fukushima, R., Higashiguchi, T., Baptista, G., Barazzoni, R., Blaauw, R., Coats, A. J. S., Crivelli, A., Evans, D. C., Fuchs-Tarlovsky, V., Gramlich, L., Keller, H., Llido, L., Malone, A., Mogensen, K. M., Morley, J. E., … Compher, C. (2019). GLIM criteria for the diagnosis of malnutrition: A consensus report from the global clinical nutrition community. Clinical Nutrition, 38(1), 1–9. https://doi.org/10.1016/j.clnu.2018.08.002

da Silva, J. S. V., Seres, D. S., Sabino, K., Adams, S. C., Berdahl, G. J., Citty, S. W., Cober, M. P., Evans, D. C., Greaves, J. R., Gura, K. M., Michalski, A., Plogsted, S., Sacks, G. S., Tucker, A. M., Worthington, P., Walker, R. N., & Ayers, P. (2020). ASPEN consensus recommendations for refeeding syndrome. Nutrition in Clinical Practice, 35(2), 178–195. https://doi.org/10.1002/ncp.10474

Evans, D. C., Corkins, M. R., Malone, A., Miller, S., Mogensen, K. M., Guenter, P., Jensen, G. L., & ASPEN Malnutrition Committee. (2021). The use of visceral proteins as nutrition markers: An ASPEN position paper. Nutrition in Clinical Practice, 36(1), 22–28. https://doi.org/10.1002/ncp.10588

Rogers, J. L. (Ed.). (2023). McCance & Huether’s pathophysiology: The biologic basis for disease in adults and children (9th ed.). Elsevier.