Understanding the clinical correlation

Walter Jackson*, a 71-year-old patient with a medical history of hypertension and hyperlipidemia, recently diagnosed with small-cell lung cancer (SCLC), arrives in your medical-surgical unit from the postanesthesia care unit after undergoing a robotic lobectomy to resect his SCLC. Upon admission to your unit, he exhibits stable vital signs with a blood pressure of 118/74 mmHg, heart rate of 80 beats per minute, respiratory rate of 16 breaths per minute, and temperature of 98.1° F (36.7° C).

You review Mr. Jackson’s normal lab results from the morning before surgery (sodium 135 mEq/L, potassium 4.5 mmol/L, BUN 10 mg/dL, creatinine 0.8 mg/dL, glucose 97 mg/dL, calcium 8.7 mg/dL, chloride 100 mEq/L, and bicarbonate 24 mEq/L). During your physical exam, you note that Mr. Jackson is awake and oriented with no acute focal deficits and that he has normal heart, lung, and abdominal exams. You find no air leak or crepitus at the entry point of his chest tube.

Mr. Jackson rates his pain as 5/10 and receives scheduled oxycodone 5 mg orally. When you reassess him 1 hour later, you find him resting comfortably. You check on Mr. Jackson before ending your shift. He has no significant pain, and his vital signs are stable; however, you note that he doesn’t remember earlier events, which you note in his electronic health record.

Reassessment

When you assess Mr. Jackson the next day, you find him lethargic and difficult to waken. He opens his eyes when you say his name. Also, he’s confused and withdraws his extremities in response to pain. He undergoes evaluation by use of the Glasgow Coma Scale (GCS), a neurological assessment tool that evaluates a patient’s level of consciousness after a brain injury based on three criteria—eye response, verbal response, and motor response. Mr. Jackson scores 11 on the GCS (eye response, 3; verbal response, 4; motor response, 4), which indicates moderate impairment. You notify the nurse practitioner (NP) of the patient’s status change and suggest ordering labs.

When reviewing the new lab results, you note a sodium level of 120 mEq/L, potassium 3.8 mmol/L, serum osmolality <200 mOsm/kg, and urine osmolality >120 mOSm/kg. Given his lung cancer history, you believe that hyponatremia may have caused his altered state. You call the rapid response team.

On the scene

When the rapid response team arrives, Mr. Jackson’s blood pressure is 90/59 mmHg, heart rate 112 beats per minute, and respiratory rate 20 breaths per minute; his temperature is normal. The team evaluates the patient and reviews the morning lab work. Given the recent sodium level, coupled with the patient’s history and change in mental status, the acute care NP suspects syndrome of inappropriate antidiuretic hormone secretion (SIADH). She orders a 100 mL bolus of 3% normal saline to run over 1 hour and places the patient on a 1-L fluid restriction. The NP also orders hourly vital signs, serum sodium every 6 hours, and serum osmolality, urine sodium, and urine osmolality every 12 hours. The patient is transferred to the intensive care unit for monitoring.

Outcome

Over the next 2 days, Mr. Jackson’s mental status improves, and his serum sodium levels return to normal. The surgical oncologist and nephrologist determine that the recent SCLC caused the SIADH.

As the patient is discharged home, you instruct him to follow up in 2 days with his medical oncologist for repeat blood work. You also advise him to call the provider if he experiences signs of SIADH, including headache; difficulty concentrating; muscle weakness or cramps; excessive thirst, nausea or vomiting; or increased lethargy. Mr. Jackson’s medical team will closely monitor him with weekly blood work throughout SCLC treatment.

About SIADH

SIADH occurs in the presence of excess antidiuretic hormone (ADH), which leads to impaired water excretion and retention. Common laboratory values associated with SIADH include hyponatremia, increased urine serum sodium, increased urine osmolality, and hypokalemia. SCLC produces ectopic production of ADH, making it a cause of SIADH in this patient population; 80% of patients with SCLC and 10% of those with non-SCLC develop SIADH.

Treatment

Clinical severity drives SIADH treatment. For mild hyponatremia (Na <135), fluid restriction to less than 800 mL/day is recommended. Given the difficulty of adhering to this limit, some organizations watch the patient’s sodium levels while others may prescribe salt tablets. For moderate hyponatremia (Na <130), fluid restriction and salt tablets are recommended. The administration of loop diuretics combined with salt tablets can decrease the urine concentration while increasing excess water excretion. For patients with severe hyponatremia (Na <120) accompanied by neurological deterioration, hypertonic saline or 3% normal saline can help increase serum sodium by 4 to 6 mEq (no more than 10 mEq) within the first 24 hours. (See SIADH symptoms.)

Overcorrection or rapid correction can cause osmotic demyelination syndrome (ODS), a medical emergency in which the myelin sheath is destroyed and results in devastating neurological injury. ODS symptoms include dysphagia, behavioral or movement disturbances, seizures, obtundation, and coma.

Vasopressin receptor antagonists also can help raise serum sodium levels. These medications, particularly vasopressin 2 (V2) receptor agonists, mediate the antidiuretic response and produce aquaresis (diluted urine) without causing a reduction in serum sodium. The loss of free water will raise the serum sodium levels and improve mental status.

V2 receptor agonists, such as tolvaptan, can be given orally or intravenously (the preferred route for severe hyponatremia). Studies indicate that low-dose, short-term tolvaptan is more effective at treating hyponatremia than fluid restriction and salt tablets. Patients with SIADH require ICU monitoring to ensure frequent assessment of sodium levels.

Nursing implications

Nursing care for patients with symptomatic hyponatremia includes monitoring vital signs and lab results and administering prescribed treatments. It also entails ensuring patients adhere to fluid restriction, providing education to patients and families about the signs and symptoms of hyponatremia, and helping to prevent falls. In addition, nurses monitor strict intake and output as well as changes in the patient’s mental status. Collaboration with the medical team helps to prevent patient decompensation.

Early detection and prevention

Diagnosis and management of SCLC, including surgery, chemotherapy, immunotherapy, and radiation, impact both patients and families. The addition of SIADH can further complicate management and treatment adherence. Many patients with cancer struggle to maintain adequate fluid and dietary intake. As nurses, we must understand the difficulty of adhering to restricted fluids.

Older patients face the risk of developing symptomatic hyponatremia not just related to a cancer diagnosis but to factors such as diuretic (thiazide) and antidepressant medications, hypothyroidism, and poor dietary intake. Prolonged hyponatremia can contribute to falls, gait disturbances, and confusion. Clinicians must maintain caution when prescribing medications to older patients, especially those at risk of developing hyponatremia. Early detection and intervention can prevent patient decline and improve neurological outcomes.

*Name is fictitious.

Bernadette Sosnowski-Funk is a nurse practitioner in cardiothoracic surgery at NYU Langone Health in New York City, New York, and an assistant professor of nursing at Hofstra Northwell School of Nursing and Physician Assistant Studies in Hempstead, New York. Stefanie Keating is a nurse practitioner in oncology at Northwell Health and an assistant professor of nursing at Hofstra Northwell School of Nursing and Physician Assistant Studies.

American Nurse Journal. 2025; 20(6). Doi: 10.51256/ANJ062518

References

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Fratangelo, L., Nguyen, S., & D’Amelio, P. (2023). Hyponatremia and aging- related diseases: Key player or innocent bystander? A systematic review. Systematic Reviews, 12 (84). https://doi.org/10.1186/s13643-023-02246-w

Krisnapan P, Tangpanithandee S, Thongprayoon C, et al. Safety and efficacy of vaptans in the treatment of hyponatremia from syndrome of inappropriate antidiuretic hormone secretion (SIADH): A systematic review and meta-analysis. J Clin Med. 2023;12(17):5483. doi:10.3390/jcm12175483

Mentrasti G, Scortichini L, Torniai M, et al. Syndrome of inappropriate antidiuretic hormone secretion (SIADH): Optimal management. Ther Clin Risk Manag. 2020; 16:663-72. doi: 0.2147/TCRM.S206066

Sterns RH, Emmett M, Forman JP. Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH).
UpToDate. May 17, 2024. uptodate.com/contents/pathophysiology-and-etiology-of-the-syndrome-of-inappropriate-antidiuretic-hormone-secretion-siadh

Wu R, Li C, Wang Z, Fan H, Song Y, Liu H. A narrative review of progress in diagnosis and treatment of small cell lung cancer patients with hyponatremia. Transl Lung Cancer Res. 2020;9(6):2469-78. doi:10.21037/tlcr-20-1147

Key words: syndrome of inappropriate antidiuretic hormone secretion, SIADH, hyponatremia, small cell lung cancer