The patient who ‘spilled salt’

Current Psychiatry. 2008 June;07(06):91-97

June 1, 2008|Current Psychiatry

Mrs. V has psychotic depression and hyponatremia. Is beer drinking or diuretic use causing her low serum sodium? Or could it be something else?

We monitor Mrs. V for anorexia, nausea, and malaise because they would be the earliest findings, followed by headache, irritability, confusion, muscle cramps, weakness, obtundation, seizures, and coma. These occur as osmotic fluid shifts and results in cerebral edema and increased intracranial pressure. When sodium concentration drops below 105 mEq/L, life-threatening complications are likely.

Table 1

Mrs. V’s laboratory results

		Mrs. V’s results
	Normal range	Before Tx	After Tx
Serum sodium (mEq/L)	135 to 145	119	127
Serum potassium (mEq/L)	3.5 to 5.0	3.6	3.8
Creatinine (mg/dL)	0.5 to 1.7	0.74	0.84
Glucose (mg/dL)	60 to 114	160	150
Osmolarity
Serum (measured; mOsm/L)	275 to 300	258	242
Urine (mOsm/L)		257	180
Urine sodium (mEq/L)	20 to 40	48	42

Table 2

Mrs. V’s laboratory results

Hypovolemic hyponatremia	Euvolemic hyponatremia	Hypervolemic hyponatremia
Vomiting Diarrhea Laxative abuse Renal disease Nasogastric suction Salt-wasting nephropathy Addison’s disease	Normal urinary sodium Glucocorticoid deficiency Hypothyroidism Certain drugs SIADH	Congestive heart failure Nephrotic syndrome Cirrhosis
	Low urinary osmolality Psychogenic polydipsia ‘Tea and toast’ syndrome Beer potomania
SIADH: syndrome of inappropriate antidiuretic hormone
Source: Reference 5

SSRIs and SIADH

Bouman et al⁶ estimated that the incidence of SSRI-induced SIADH in elderly patients is 12%. Liu et al⁷ described 706 cases of hyponatremia associated with SSRI use in unpublished reports. Fluoxetine was most commonly the cause (75.3% cases), followed by paroxetine (12.4%), sertraline (11.7%), and fluvoxamine (1.5%). Resuming the same drug resulted in hyponatremia in 16 of 24 of these cases (66.7%).

Kirby et al,⁸ however, found no clear advantages in different SSRIs’ propensity to cause hyponatremia. Seventy-one percent of patients treated with the SNRI venlafaxine developed hyponatremia, compared with 32% taking paroxetine and 29% receiving sertraline. It is unclear whether a specific SSRI or venlafaxine has a stronger association with hyponatremia than any other antidepressant.

Hyponatremia’s nonspecific symptoms and wide range of time to detection (1 to 253 days) suggest clinicians usually detect the condition by chance rather than specifically assessing for it.⁹

TREATMENT: Medication change?

Coordinating Mrs. V’s depression and hyponatremia treatment is critical. We propose discontinuing sertraline and treating Mrs. V’s symptoms with electroconvulsive therapy (ECT). She refuses ECT, stating “I don’t feel that bad. My father was treated with ECT and I am scared of it.”

Clinical Point

To treat SSRI-induced hyponatremia, consider switching the patient to an antidepressant from a different class and restrict fluid intake

We decide to switch to mirtazapine, a tetracyclic antidepressant. In a case report mirtazapine was successfully used in a similar patient.¹⁰ We continue to monitor Mrs. V’s serum sodium concentrations and emphasize the importance of complying with fluid restrictions, instructing her to limit her fluid intake to 250 to 500 mL (1 to 2 glasses) per day.

The authors’ observations

SSRI-induced hyponatremia can be transient or persistent and recurrent. The usual approach is to discontinue the SSRI and try a different antidepressant. Because hyponatremia has been associated with all SSRIs and SNRIs, it would be prudent to choose an alternate antidepressant agent outside these classes. If patients must continue taking an antidepressant that causes hyponatremia, avoid concurrent use of drugs that cause hyponatremia, restrict fluid intake, and consider adding a medication that prevents hyponatremia, such as demeclocycline or fludrocortisone.

SSRI-induced hyponatremia may resolve:

with SSRI discontinuation alone¹¹
with fluid restriction and without discontinuation of the SSRI¹¹
with drug discontinuation, fluid restriction, and sodium chloride and potassium supplementation.¹²

FOLLOW-UP: Analysis error?

Despite modifications to Mrs. V’s diet, her fasting serum glucose level remains >100. She is diagnosed with diabetes mellitus type 2 and treated with metformin. We continue mirtazapine, which has successfully controlled Mrs. V’s depressive symptoms. Her serum sodium levels start normalizing.

The authors’ observations

Clinical Point

In patients with serum hyperglycemia, low serum sodium levels do not reflect a true hypo-osmotic state

In patients with serum hyperglycemia— such as Mrs. V—correct laboratory analysis yields low serum sodium levels, but these levels do not reflect a true hypo-osmotic state. Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space. For each 100 mg/dL increase above normal serum glucose concentration, serum sodium concentration is diluted by a factor of 1.6 mEq/L. Systemic osmolarity is normal or increased, but not decreased as would be the case in true (hypo-osmotic) hyponatremia.

Related resources

Siegel AJ. Hyponatremia in psychiatric patients: update on evaluation and management. Harv Rev Psychiatry 2008;16(1):13-24.
Atalay A, Turhan N, Aki OE. A challenging case of syndrome of inappropriate secretion of antidiuretic hormone in an elderly patient secondary to quetiapine. South Med J 2007;100(8):832-3.

Drug brand name

Aripiprazole • Abilify
Atenolol • Tenormin
Atorvastatin • Lipitor
Demeclocycline • Declomycin, Declostatin, others
Diltiazem • Cardizem, Dilacor, others
Fludrocortisone • Florinef
Fluvoxamine • Luvox
Ibuprofen • Advil, Motrin, others
Metformin • Glucophage, Diabex, others
Mirtazapine • Remeron
Paroxetine • Paxil
Sertraline • Zoloft
Venlafaxine • Effexor

References

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