Cases That Test Your Skills

The patient who ‘spilled salt’

Current Psychiatry. 2008 June;7(6):91-97

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

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References

Reference

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HISTORY: ‘They’re out to get me’

Mrs. V, age 64, tells her primary care physician she has felt “bad” for 2 weeks. She complains of depressed mood, middle insomnia, diminished appetite, poor concentration, and poor energy. She denies suicidal thoughts but reports feeling alone, overwhelmed, and unable to manage her daily life.

Mrs. V is very concerned about losing her job because she cannot function at work. She believes her coworkers may be plotting to get her fired. The primary care physician refers Mrs. V to us to evaluate her mood.

According to her daughter, Mrs. V has had multiple psychiatric hospitalizations; the most recent occurred 2 years ago when she was admitted for paranoia and disorganized behavior. The daughter also mentions that her mother has a remote history of daily alcohol use, drinking until she was intoxicated. Mrs. V says she occasionally drinks beer and she scores 2 out of 4 on the CAGE questionnaire, which may indicate alcohol dependence.

During mental status examination, Mrs. V is alert and oriented to person, place, and date. She is pleasant and cooperative but shows apparent thought blocking and some tangentiality. She has substantial difficulty answering questions and articulating symptoms. Speech is slow in rate and rhythm. Mrs. V’s mood is severely depressed and her affect constricted.

She denies suicidal or homicidal ideations or visual or auditory hallucinations. Cognitive testing reveals mild deficits in recall memory and poor concentration. Her insight is limited and her judgment fair.

Her medical history includes hypertension, hyperlipidemia, coronary artery disease, cardiac catheterization, and hyponatremia. Her medication regimen consists of aripiprazole, 15 mg/d; diltiazem, 180 mg/d; atenolol, 25 mg/d; aspirin, 325 mg/d; atorvastatin, 10 mg/d; sertraline, 50 mg/d; and ibuprofen, 600 mg as needed for hip pain. She also reports taking diuretics in the past.

Vital signs include blood pressure, 125/95 mm Hg; respirations, 16/min; temperature, 98.2° F; and pulse rate, 72/min. Serum investigations reveal sodium, 119 mEq/L (normal range: 135 to 145 mEq/L) and random blood sugar, 160 mg/dL (normal range: 60 to 114 mg/dL).

The authors’ observations

The combination of major depression with psychosis and hyponatremia makes Mrs. V’s case challenging. Hyponatremia in psychiatric inpatients can prompt medical consultation, thus possibly halting or delaying psychiatric treatment.

Hyponatremia has been associated with the use of:

diuretics
selective serotonin reuptake inhibitors (SSRIs)
serotonin-norepinephrine reuptake inhibitors (SNRIs)
tricyclic antidepressants
calcium antagonists.

Elevated creatinine levels, chronic obstructive pulmonary disease, hypertension, systolic blood pressure, and diabetes also can lead to hyponatremia.

Among psychiatric inpatients, the risk of hyponatremia is doubled in women.¹ It is unclear, however, if female gender is an independent risk factor for hyponatremia. Sharabi et al² reported that patients of both sexes age >65 have a 9-fold greater risk of developing hyponatremia than younger counterparts.

In addition, hyponatremia risk during any antidepressant treatment is highest:

in the summer
during the first weeks of treatment
with concomitant drug use, especially with diuretics.³

The authors’ observations

Clinical Point

SSRI use in elderly persons has been associated with hyponatremia

To identify the cause of Mrs. V’s hyponatremia, we determine her volume status and measure serum osmolality.⁴ Next, we mea-sure urinary sodium and osmolality and assess her extracellular fluid status. We also evaluate her renal and adrenal function, which were within normal limits. Although Mrs. V reports fatigue and weakness, there is no evidence of dehydration.

Based on Mrs. V’s initial lab results (Table 1), we classify her hyponatremia as euvolemic, with high urine osmolarity (≥100 mOsm/L). That helps narrow our differential diagnosis to glucocorticoid deficiency, hypothyroidism, and SIADH (Table 2).⁵ We exclude psychogenic polydipsia, “tea and toast” syndrome, or beer potomania because they usually present as euvolemic hyponatremia with low urinary osmolality.

SSRI use in elderly persons has been associated with hyponatremia, which in some cases may be consistent with SIADH. Unfortunately, few psychiatrists are aware of this potentially fatal side effect.

SIADH occurs in association with reduced serum osmolality. It is characterized by:

hypotonic hyponatremia (serum sodium
inappropriately elevated urine osmolarity (>200 mOsm/L) relative to plasma osmolarity
elevated urine sodium (typically >20 mEq/L).⁴

We diagnose Mrs. V with SIADH because she has these lab findings in the absence of diuretic therapy; in the presence of euvolemia without edema; and in the setting of otherwise normal cardiac, renal, adrenal, hepatic, and thyroid function.

The key to the pathophysiology, signs, symptoms, and treatment of SIADH is understanding that the hyponatremia is a result of excess water and not a sodium deficiency. Hyponatremia’s signs and symptoms primarily are related to CNS dysfunction and correlate with how rapidly and severely the condition develops.

The patient who ‘spilled salt’

References

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