IHP 310 Module 8 Final Case Analysis example

One Antibiotic Too Many: A Final Case Analysis of Trimethoprim-Sulfamethoxazole Hyperkalemia in a 76-Year-Old Man With Heart Failure and Kidney Disease

[Student Name]

Southern New Hampshire University

IHP 310: Pathophysiology and Pharmacology Concepts

Module Eight Final Project

[Instructor Name]

[Date]

The organization, setting and figures below are a composite written as a model document. No real employer, client, colleague or patient is described.

One Antibiotic Too Many: A Final Case Analysis of Trimethoprim-Sulfamethoxazole Hyperkalemia in a 76-Year-Old Man With Heart Failure and Kidney Disease

The Patient Record

Mr. Haddad is a composite 76-year-old retired baker with heart failure with reduced ejection fraction, stage 3 kidney disease (his most recent eGFR was 38), and hypertension. His medications are lisinopril 20 mg daily, spironolactone 25 mg daily, metoprolol succinate 100 mg daily and furosemide 40 mg daily. His last potassium, two months ago, was 5.0 mmol/L. At an urgent care visit for a red, warm, swollen lower leg without pus, he was prescribed trimethoprim-sulfamethoxazole double strength twice daily. Five days later he came to the emergency department with weakness and lightheadedness. His heart rate was 44, his potassium 6.8 mmol/L and his creatinine had risen from 1.7 to 2.3 mg/dL. His electrocardiogram showed peaked T waves and a widened QRS complex.

The Background Conditions

When the ejection fraction is reduced, each beat moves too little blood forward. The body responds by activating the renin-angiotensin-aldosterone system and the sympathetic nervous system, which retain salt and water and constrict vessels. These responses help in the short term but damage the heart over time, which is why guideline therapy blocks them with ACE inhibitors, beta-blockers and mineralocorticoid receptor antagonists such as spironolactone (Heidenreich et al., 2022). Chronic kidney disease means fewer working nephrons, so the kidneys have less capacity to excrete potassium, a problem made worse whenever kidney perfusion falls.

How the Body Handles Potassium

Most of the body's potassium is inside cells, and blood levels are kept in a narrow range. The kidney excretes potassium mainly in the collecting duct, where aldosterone stimulates sodium reabsorption through epithelial sodium channels. Moving sodium into the cells creates an electrical gradient that pulls potassium out into the urine. Anything that lowers aldosterone, blocks its receptor, blocks the sodium channel or reduces the number of working nephrons will raise blood potassium.

How Each Drug Pushed Potassium Up

Mr. Haddad had four potassium-raising influences at once. Lisinopril lowers angiotensin II and therefore aldosterone. Spironolactone blocks the aldosterone receptor directly. His kidney disease reduces excretion capacity. Trimethoprim, one component of the antibiotic, blocks the epithelial sodium channel in the collecting duct, acting like the diuretic amiloride and shutting down the last pathway still working. Each drug had a reason on its own; together they closed every route by which his kidneys could get rid of potassium. The rise in creatinine suggests reduced kidney perfusion as well, possibly from the infection and reduced intake, which worsened the problem further.

Medication Review

The table summarizes every medication in the record.

Table 1

Medication Review for Mr. Haddad

Treating the Emergency

Treatment of severe hyperkalemia follows its mechanism. Intravenous calcium gluconate is given first, because calcium stabilizes the heart cell membrane against the effects of high potassium within minutes, although it does not lower potassium. Insulin with glucose, and inhaled albuterol, move potassium from the blood into cells, buying time. Removing potassium from the body requires the kidneys, a loop diuretic, a gut potassium binder or, if these fail, dialysis. All potassium-raising drugs are held, and the heart is monitored continuously until the rhythm and potassium normalize.

What the Evidence Shows About This Combination

The danger is documented at the population level. Among older adults taking spironolactone, a prescription for trimethoprim-sulfamethoxazole was associated with more than twice the risk of sudden death within 14 days compared with amoxicillin (Antoniou et al., 2015). In older adults taking ACE inhibitors or angiotensin receptor blockers, the same antibiotic was associated with a higher risk of sudden death than amoxicillin, corresponding to roughly three sudden deaths within 14 days per 1,000 prescriptions (Fralick et al., 2014). These studies are observational and cannot prove cause, but they are consistent with the known mechanism and with Mr. Haddad's course.

Why the Antibiotic Was Chosen and What Should Have Been Chosen

The urgent care prescriber likely chose trimethoprim-sulfamethoxazole because it covers methicillin-resistant Staphylococcus aureus, a common concern in skin infections. But Mr. Haddad's cellulitis had no pus, abscess or drainage. Nonpurulent cellulitis is usually caused by streptococci, which a beta-lactam such as cephalexin treats well, and trimethoprim-sulfamethoxazole is not a reliable choice against streptococci on its own. The decision therefore added risk without adding benefit. A quick look at his medication list, three drugs known to raise potassium, and his kidney function should have ruled the drug out. This is the kind of whole-record reasoning the course has practiced: matching the drug to the likely organism, and then checking the drug against the patient's other conditions and medicines before it is prescribed.

Recommendations

For Mr. Haddad, the antibiotic should be changed to a beta-lactam such as cephalexin, which covers the streptococci that cause most nonpurulent cellulitis. Once potassium and kidney function recover, lisinopril and metoprolol should be restarted and spironolactone reconsidered at a lower dose with potassium and creatinine checked within a week, because these drugs reduce his heart failure risk. He and his family should be given a written list of antibiotics and pain relievers to avoid, including trimethoprim-sulfamethoxazole and NSAIDs.

For the health system, the urgent care prescriber did not have an alert for the interaction, and no potassium check was scheduled. An electronic prescribing alert for trimethoprim-sulfamethoxazole in patients on spironolactone, ACE inhibitors or angiotensin receptor blockers with reduced kidney function, paired with an automatic order for a potassium check within three to five days when the combination is unavoidable, would target exactly this failure.

Conclusion

Mr. Haddad's life-threatening hyperkalemia resulted from an antibiotic added to a regimen and a kidney already limited in its ability to excrete potassium. Tracing each condition and drug to its effect on potassium handling explains the emergency, guides its mechanism-based treatment and points to a safer antibiotic. The case gathers the course's themes, pathophysiology across systems, drug mechanisms and appropriateness judged in context, into one record.

References

Antoniou, T., Hollands, S., Macdonald, E. M., Gomes, T., Mamdani, M. M., & Juurlink, D. N. (2015). Trimethoprim-sulfamethoxazole and risk of sudden death among patients taking spironolactone. Canadian Medical Association Journal, 187(4), E138-E143. https://doi.org/10.1503/cmaj.140816

Fralick, M., Macdonald, E. M., Gomes, T., Antoniou, T., Hollands, S., Mamdani, M. M., & Juurlink, D. N. (2014). Co-trimoxazole and sudden death in patients receiving inhibitors of renin-angiotensin system: Population based study. BMJ, 349, Article g6196. https://doi.org/10.1136/bmj.g6196

Heidenreich, P. A., Bozkurt, B., Aguilar, D., Allen, L. A., Byun, J. J., Colvin, M. M., Deswal, A., Drazner, M. H., Dunlay, S. M., Evers, L. R., Fang, J. C., Fedson, S. E., Fonarow, G. C., Hayek, S. S., Hernandez, A. F., Khazanie, P., Kittleson, M. M., Lee, C. S., Link, M. S., . . . Yancy, C. W. (2022). 2022 AHA/ACC/HFSA guideline for the management of heart failure: A report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation, 145(18), e895-e1032. https://doi.org/10.1161/CIR.0000000000001063