Introduction: Hyponatremia is one of the most common electrolyte abnormalities encountered in hospitalized patients, and SIADH is a frequent yet often underrecognized cause of it. SIADH is particularly relevant in small-cell lung cancer (SCLC), where it can be either paraneoplastic or drug-induced. Platinum-based chemotherapy, including carboplatin, has been associated with SIADH, though this is not widely documented in the literature.
We present a case of recurrent, treatment-resistant hyponatremia due to SIADH in a patient receiving carboplatin and etoposide for SCLC, to highlight this underrecognized complication and discuss management considerations.
Description: A 67-year-old male with stage IV SCLC presented with asymptomatic hyponatremia (Na⁺ 113 mmol/L) one week after his most recent carboplatin-etoposide infusion. Labs were consistent with SIADH with low serum osmolality (239 mOsm/kg), high urine sodium (83 mEq/L), and high urine osmolality (389 mOsm/kg), in the setting of clinical euvolemia. He had a history of multiple prior admissions for hyponatremia and was on a tailored tolvaptan regimen.
Initial management included stopping tolvaptan, initiating fluid restriction, and starting 2% hypertonic saline. His sodium overcorrected to 125 mmol/L within 24 hours, requiring D5W boluses to reverse the overcorrection. However, sodium levels began to decline again, necessitating escalation to 3% hypertonic saline and reintroduction of tolvaptan, ultimately stabilizing at 129 mmol/L.
Discussion: Both paraneoplastic secretion of ADH and platinum-based chemotherapy can lead to SIADH in SCLC. While cisplatin is better known for causing electrolyte disturbances, recent findings suggest that carboplatin, particularly when combined with etoposide, may pose an even higher risk. Escitalopram, another potential contributor to SIADH, may have compounded the effect. Given the recurrent nature of this patient’s admissions and the severity of his hyponatremia, cisplatin may actually be a better-tolerated alternative despite its traditionally higher toxicity profile. Managing SIADH in this setting is complex and requires a careful balance of fluid restriction, pharmacologic therapy, and chemotherapy planning.
