Hyponatremia Best Describes This Patient's Condition
The patient's agitation and irritability are most likely explained by hyponatremia (serum sodium 121 mmol/L), which represents a severe electrolyte disturbance requiring immediate attention. While multiple laboratory abnormalities are present, hyponatremia is the only value that directly causes the presenting neuropsychiatric symptoms in this clinical scenario 1.
Understanding the Clinical Picture
This 80-year-old patient presents with a constellation of electrolyte abnormalities, but we must prioritize based on which abnormality explains the acute symptoms:
- Sodium 121 mmol/L (severe hyponatremia, normal 135-145 mmol/L)
- Potassium 5.9 mmol/L (hyperkalemia, normal 3.5-5.0 mmol/L)
- Calcium 2.8 mmol/L (hypercalcemia if this represents ionized calcium, though context suggests total calcium which would be high-normal)
- Albumin 1.8 g/dL (hypoalbuminemia, normal 3.5-5.5 g/dL)
Why Hyponatremia Is the Primary Problem
Neuropsychiatric manifestations are the hallmark of hyponatremia. Sodium levels below 125 mmol/L commonly produce confusion, agitation, irritability, and altered mental status 1. The brain is exquisitely sensitive to changes in serum osmolality, and hyponatremia causes cerebral edema leading to these symptoms 1.
The medication regimen directly explains the hyponatremia. This patient is on both lisinopril (ACE inhibitor) and a thiazide diuretic—a combination that frequently causes hyponatremia in elderly patients 1. Thiazide diuretics impair free water excretion and are the most common medication cause of hyponatremia in the elderly 1. ACE inhibitors can potentiate this effect 1.
Why the Other Abnormalities Don't Explain the Symptoms
Hyperkalemia (K+ 5.9 mmol/L): While elevated and requiring attention, potassium at this level typically does not cause agitation or irritability 2. Hyperkalemia's primary manifestations are cardiac (ECG changes, arrhythmias) and neuromuscular (weakness, paralysis), not neuropsychiatric symptoms 2. The combination of lisinopril and thiazide can cause hyperkalemia, but this is not producing the patient's presenting symptoms 1, 2.
Hypercalcemia: The calcium value of 2.8 mmol/L (approximately 11.2 mg/dL if converted) could represent mild hypercalcemia, but this level rarely causes acute neuropsychiatric symptoms 1. Moreover, the low albumin (1.8 g/dL) means the corrected calcium is likely lower than the measured total calcium, making clinically significant hypercalcemia unlikely 1.
Hypoalbuminemia (albumin 1.8 g/dL): While this indicates significant protein depletion or loss, hypoalbuminemia itself does not cause acute neuropsychiatric symptoms 1. It may reflect chronic illness, malnutrition, or renal protein loss, but it does not explain the acute presentation of agitation and irritability 1.
Immediate Management Priorities
Stop the thiazide diuretic immediately as it is the most likely culprit for the severe hyponatremia 1. The thiazide should not be restarted until sodium normalizes and alternative antihypertensive strategies are implemented 1.
Assess volume status carefully to determine if this is hypovolemic, euvolemic, or hypervolemic hyponatremia, as this guides fluid management 1. In elderly patients on thiazides, this is often hypovolemic hyponatremia 1.
Correct sodium slowly at a rate not exceeding 8-10 mmol/L in 24 hours to avoid osmotic demyelination syndrome, which can cause permanent neurological damage 1. For symptomatic patients, initial correction can be slightly faster (1-2 mmol/L per hour for the first 3-4 hours), but total correction must remain within safe limits 1.
Address the hyperkalemia concurrently by holding the lisinopril temporarily and rechecking potassium within 2-3 days 2, 3. The hyperkalemia is likely multifactorial from the ACE inhibitor, possible renal impairment, and the patient's age 2, 3.
Common Pitfalls to Avoid
Do not correct sodium too rapidly. Overly aggressive correction (>10-12 mmol/L in 24 hours) can cause osmotic demyelination syndrome, leading to permanent neurological sequelae including quadriplegia, pseudobulbar palsy, and death 1.
Do not restart the thiazide diuretic. If blood pressure control is needed after sodium normalizes, switch to a calcium channel blocker (such as amlodipine) or continue the ACE inhibitor alone if hyperkalemia resolves 1, 4. The combination of thiazide plus ACE inhibitor in an elderly patient has already proven problematic 1, 4.
Do not assume all abnormalities require simultaneous aggressive correction. While multiple electrolyte disturbances are present, the hyponatremia is causing the acute symptoms and takes priority 1. The hyperkalemia requires monitoring and medication adjustment but is not immediately life-threatening at 5.9 mmol/L without ECG changes 2, 3.
Do not overlook medication compliance as a red flag. The family reports good compliance, which means these electrolyte disturbances occurred despite appropriate medication use—this is a medication-induced problem, not a compliance issue 1. This should prompt immediate medication review and adjustment 1.
Answer: A - Hyponatremia
Hyponatremia (serum sodium 121 mmol/L) is the laboratory abnormality that best describes and explains this patient's acute presentation of agitation and irritability. The other abnormalities are present but do not account for the neuropsychiatric symptoms 1.