DNP 604 Module 1 Hypernatremia Case Study Example

Sodium 162 After a Week of Fever: A Hypernatremia Case Study in Cellular Water Balance

Student Name

Edson College of Nursing and Health Innovation, Arizona State University

DNP 604: Advanced Human Pathophysiology Across Lifespan

Instructor Name

Month Day, Year

Sodium 162 After a Week of Fever: A Hypernatremia Case Study in Cellular Water Balance

The Case

Mrs. R, 86, lives in a nursing home and has moderate dementia. For a week she has had a urinary tract infection with fever and has eaten and drunk little. Staff noticed increasing drowsiness. In the emergency department she is lethargic, with dry mucous membranes, a heart rate of 108 and blood pressure of 98/60. Serum sodium is 162 mmol/L, BUN 48 mg/dL, creatinine 1.6 mg/dL (baseline 0.9) and glucose 130 mg/dL. Urine is concentrated.

Question 1: What is the pathophysiology of her hypernatremia?

Hypernatremia is almost always a problem of too little water relative to sodium rather than too much sodium. Mrs. R lost free water through fever and insensible losses and did not replace it. Normally, rising plasma osmolality triggers thirst and release of antidiuretic hormone, which concentrates urine. In older adults, thirst sensation is blunted, and dementia limits the ability to ask for or reach water. Her concentrated urine shows that her kidneys are trying to conserve water, so the problem lies with intake and losses, not with diabetes insipidus.

Question 2: What happens at the cellular level?

Sodium is the main determinant of extracellular osmolality. As extracellular sodium rises, water moves out of cells by osmosis toward the higher solute concentration, and cells shrink. Brain cells are most affected because the skull limits room for change and brain function depends on cell volume. Shrinkage can stretch and tear bridging veins, causing hemorrhage in severe cases.

Within hours, brain cells begin to adapt by taking up electrolytes, and over about two days they accumulate organic osmolytes such as myo-inositol and glutamine, which draw water back in and restore volume. This adaptation is why chronic hypernatremia, present for more than 48 hours, carries a theoretical risk if corrected too quickly: as plasma becomes less concentrated, water could move into brain cells that still hold extra osmolytes, causing cerebral edema.

Question 3: How do her findings fit?

Her lethargy reflects brain cell dehydration. Tachycardia, low blood pressure and dry membranes show extracellular volume depletion, since she has lost both water and some sodium. The rising BUN and creatinine, with a BUN-to-creatinine ratio above 20, suggest reduced kidney perfusion from volume loss.

Question 4: How should she be treated, and how fast?

Treatment begins with restoring circulation with isotonic fluid if she is hypotensive, then replacing the free water deficit with hypotonic fluid such as 5% dextrose in water or by mouth or tube if possible, while treating the infection. The free water deficit can be estimated as total body water multiplied by (serum sodium divided by 140, minus 1). For an older woman weighing 55 kg, total body water is about 0.45 times weight, or 24.8 L, giving a deficit of about 3.7 L, plus ongoing losses.

Customary teaching limits the fall in sodium to roughly 0.5 mmol/L each hour, or 10 to 12 mmol/L per day, in chronic hypernatremia. Recent evidence has challenged this. In a cohort of 4,265 adults with severe hypernatremia, those corrected faster than 0.5 mmol/L per hour had lower 30-day mortality than those corrected slowly, with no signs of neurologic complications (Feigin et al., 2023). A pediatric cohort likewise found no association between rapid correction and cerebral edema, seizures or death, while slow correction was linked to longer stays (Didsbury et al., 2023). These are observational studies and cannot prove that faster correction saves lives, but they suggest that undertreatment carries risks too. A 2024 systematic review likewise concluded that current recommendations on correction rates do not rest on high-quality research (Pokhriyal et al., 2024). A reasonable plan is steady correction with sodium checked every four to six hours and close neurologic monitoring.

Question 5: What nursing and advanced practice implications follow?

Prevention matters most: scheduled fluid offering for residents with dementia, monitoring intake during illness and early laboratory checks when residents become drowsy or febrile.

References

Didsbury, M., See, E. J., Cheng, D. R., Kausman, J., & Quinlan, C. (2023). Correcting hypernatremia in children. Clinical Journal of the American Society of Nephrology, 18(3), 306-314. https://doi.org/10.2215/CJN.0000000000000077

Feigin, E., Feigin, L., Ingbir, M., Ben-Bassat, O. K., & Shepshelovich, D. (2023). Rate of correction and all-cause mortality in patients with severe hypernatremia. JAMA Network Open, 6(9), e2335415. https://doi.org/10.1001/jamanetworkopen.2023.35415

Pokhriyal, S. C., Joshi, P., Gupta, U., Roy, P., Parkash, S., Kunwar, K., Al-Ghuraibawi, M. M. H., Nagpal, S., Yadav, R., & Panigrahi, K. (2024). Hypernatremia and its rate of correction: The evidence so far. Cureus, 16(2), e54699. https://doi.org/10.7759/cureus.54699