Case Report: Chronic Hyponatremia Secondary to SIADH in an Older Adult

Abstract

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) is a well-recognized cause of chronic hyponatremia, particularly in older adults. Management focuses on identifying the underlying etiology and preventing rapid or severe sodium decline. We report a case of long-standing SIADH with fluctuating sodium levels, managed conservatively with increased oral sodium intake and close laboratory monitoring, highlighting the challenges of unexplained sodium variability and patient-centered self-management.

Introduction

SIADH is characterized by inappropriate secretion of antidiuretic hormone resulting in impaired free water excretion and dilutional hyponatremia. Chronic hyponatremia may remain asymptomatic but carries risks of neurological complications when sodium levels decline rapidly or fall below critical thresholds. Individualized management is essential, particularly in older patients.

Case Presentation

A 73-year-old individual with a known diagnosis of SIADH presented with a history of chronic, fluctuating hyponatremia. Sodium levels have ranged from a documented high of 137 mmol/L to a current level of 130 mmol/L. Despite extensive evaluation, no clear precipitating cause for sodium fluctuations has been identified.

The patient reports episodes of frequent urination as a common early sign of sodium decline. Notably, some decreases in sodium occur without warning symptoms, contributing to significant anxiety. During a prior emergency department visit for dehydration, the patient was informed that further sodium decline could have resulted in coma, reinforcing ongoing fear related to sudden hyponatremia.

Management and Self-Monitoring

Management has focused on conservative measures aimed at stabilizing serum sodium levels. The patient follows an unrestricted salt intake, including dietary salt supplementation and salt tablets. Salt tablets are used more aggressively during perceived symptomatic periods or when laboratory values demonstrate decline. There has been no evidence of peripheral edema despite liberal sodium intake.

During episodes of sudden sodium drops without symptoms, the patient increases salt intake through fluids and supplements while consciously avoiding panic responses. This approach has successfully prevented progression to severe hyponatremia over several years.

Laboratory monitoring is performed every three months, including serum sodium and thyroid function tests. Additionally, whenever other laboratory studies are ordered, the patient requests concurrent sodium measurement to allow close trend monitoring.

Environmental factors such as cold exposure were not previously considered but may represent a contributing variable to recent sodium decline and warrant further observation.

Psychological impact is also notable, as fear of rapid deterioration remains a persistent concern despite years of successful self-management.

Associated Conditions and Illnesses Linked to Hyponatremia

Hyponatremia may occur secondary to a wide range of medical conditions beyond SIADH.
Known illnesses and clinical states associated with low sodium levels include:

Endocrine disorders

Hypothyroidism

Adrenal insufficiency (including Addison’s disease)

Renal conditions

Chronic kidney disease

Acute kidney injury with impaired water excretion

Cardiopulmonary diseases

Congestive heart failure

Chronic lung diseases (including pneumonia and malignancy-related pulmonary disorders)

Neurologic conditions

Stroke

Head trauma

Central nervous system infections

Brain tumors

Malignancies

Small cell lung carcinoma (a well-known cause of SIADH)

Other solid tumors capable of ectopic ADH secretion

Infectious and inflammatory states

Severe infections or sepsis

Postoperative stress responses

Medication-related causes

Diuretics

Antidepressants (SSRIs, TCAs)

Antiepileptic drugs

Antipsychotics

Chemotherapy agents

Volume-related states

Dehydration

Excess free water intake

Gastrointestinal losses (vomiting, diarrhea)

In older adults, hyponatremia is often multifactorial, with overlapping contributions from medications, comorbid illnesses, and altered renal water handling. Even mild reductions in sodium may increase the risk of falls, cognitive impairment, and hospitalization.

Big-Picture Difference: SIADH vs. Cerebral Salt Wasting (CSW)

Feature	SIADH	Cerebral Salt Wasting (CSW)
Core problem	Inappropriate excess ADH secretion leading to water retention	Renal loss of sodium due to impaired sodium reabsorption
Primary mechanism	Water retention dilutes serum sodium	True sodium loss with secondary volume depletion
Volume status	Euvolemic or mildly hypervolemic	Hypovolemic
Sodium abnormality	Dilutional hyponatremia	Absolute sodium depletion
Urine sodium	Inappropriately elevated	Elevated
Urine osmolality	Inappropriately concentrated	Concentrated
Serum uric acid	Low (normalizes with correction)	Low (persists despite correction)
Clinical context	Malignancy, pulmonary disease, medications, idiopathic	CNS injury, subarachnoid hemorrhage, neurosurgery
Treatment approach	Fluid restriction; salt supplementation in select cases	Volume repletion with isotonic or hypertonic saline
Response to fluids	Worsens hyponatremia	Improves sodium and volume status

Clinical Pearl

Misdiagnosing CSW as SIADH can be dangerous: fluid restriction in CSW worsens hypovolemia, while liberal sodium and fluid intake in SIADH may aggravate hyponatremia. Careful assessment of volume status and clinical context is essential.

Diagnostic Criteria Used to Differentiate SIADH and Cerebral Salt Wasting (CSW)

Differentiating SIADH from CSW is clinically critical, as management strategies are fundamentally opposite. Diagnosis relies on a combination of volume status assessment, laboratory findings, and clinical context, as no single test is definitive.

Key Diagnostic Features

Criterion	SIADH	Cerebral Salt Wasting (CSW)
Volume status	Euvolemic or mildly hypervolemic	Hypovolemic (signs of volume depletion)
Serum sodium	Low	Low
Serum osmolality	Low (<275 mOsm/kg)	Low
Urine sodium	Elevated (>40 mmol/L)	Elevated (>40 mmol/L)
Urine osmolality	Inappropriately high (>100 mOsm/kg)	High
Serum uric acid	Low; normalizes after sodium correction	Low; remains low despite correction
Fractional excretion of uric acid (FEUA)	Elevated during hyponatremia, normalizes with treatment	Persistently elevated
Response to isotonic saline	Minimal or worsening hyponatremia	Improvement in sodium and volume status
Edema	Absent	Absent
Blood pressure / orthostasis	Normal	Often low or orthostatic
Clinical setting	Malignancy, pulmonary disease, medications, idiopathic	Acute CNS disease or injury

Practical Bedside Differentiators

Volume assessment is the most important distinguishing feature but may be challenging in older adults.

Persistent hypouricemia after sodium correction strongly favors CSW.

Clinical response to saline is often the most revealing diagnostic clue:

Worsening hyponatremia suggests SIADH

Improvement supports CSW

Relevance to the Present Case

The absence of hypovolemia, lack of edema despite liberal sodium intake, chronic course, and stability with oral sodium supplementation favor a diagnosis of SIADH rather than CSW. No acute central nervous system pathology has been identified to suggest CSW.

Key Clinical Takeaway

Correct differentiation between SIADH and CSW is essential, as fluid restriction in CSW can worsen outcomes, while volume expansion in SIADH may exacerbate hyponatremia. A systematic approach integrating laboratory trends and clinical response remains the gold standard.

Conclusion

Chronic SIADH with unexplained sodium variability requires a patient-centered approach emphasizing education, symptom recognition, flexible sodium supplementation, and regular laboratory monitoring. This case underscores the importance of individualized management strategies and acknowledges the emotional burden associated with living with potentially life-threatening electrolyte disturbances.

References:

Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations
https://pubmed.ncbi.nlm.nih.gov/24074529/

The Syndrome of Inappropriate Antidiuresis
https://www.nejm.org/doi/10.1056/NEJMcp066837

Syndrome of Inappropriate Antidiuretic Hormone Secretion
https://www.ncbi.nlm.nih.gov/books/NBK507777/?utm_source=chatgpt.com

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH)
https://pubmed.ncbi.nlm.nih.gov/19523572/

Diagnosis and Treatment of Hyponatremia: Compilation of the Guidelines
https://pmc.ncbi.nlm.nih.gov/articles/PMC5407738/?utm_source=chatgpt.com

SIADH versus adrenal insufficiency: a life-threatening misdiagnosis
https://pubmed.ncbi.nlm.nih.gov/30728045/

Addison’s Disease: A Rare but Life-Threatening Endocrine Emergency
https://swaresearch.blogspot.com/2026/01/key-clinical-signs-of-addisons-disease.html

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