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Severe Hyponatremia with High Urine Sodium and Osmolality

¹ Department of Internal Medicine, Erasmus MC Rotterdam, the Netherlands; ² Department of Internal Medicine; Albert Schweitzer Hospital, Dordrecht, the Netherlands.

^aAddress correspondence to this author at: Erasmus Medical Center, Department of Internal Medicine, P.O. Box 2040, 3000 CA Rotterdam, the Netherlands. Fax +31-10-7031146; e-mail j.vanderhoek@erasmusmc.nl.

The first 300 words of the full text of this article appear below.

CASE

A 49-year-old woman (previous history of childhood asthma, no medication) presented to the emergency department with nausea and vomiting that had occurred for 5 days and slurred speech for 1 day prior to presentation. The patient denied use of alcohol and illicit drugs. Physical examination revealed her blood pressure to be 125/70 mmHg; she had no postural drop and had a regular pulse of 72 beats/min. She had no fever and no signs of contracted extracellular fluid volume. Results of further physical and neurological examination were unremarkable and revealed no goiter, pigmentation, or vitiligo. Her laboratory results are shown in Table 1 . Additional diagnostic tests included chest x-ray, abdominal ultrasound, and brain computed tomography, none of which revealed abnormalities. The syndrome of inappropriate antidiuretic hormone secretion (SIADH)¹ was suspected. However, fluid restriction (500 mL/day) did not lead to increased serum sodium.

QUESTIONS TO CONSIDER

• What is the differential diagnosis in a patient with severe hyponatremia and a high urine sodium and osmolality?
  
• Name three hormones that, when disturbed, can all independently result in hyponatremia with a high urine sodium and osmolality?
  
• What should be excluded before the diagnosis?
  

DISCUSSION

Because of the lack of response to therapy for SIADH, the diagnosis was reconsidered and hypothyroidism and/or adrenal insufficiency were suspected, especially because serum glucose was also low. Serum thyroid-stimulating hormone was 63 mU/L (reference interval 0.4–4.0 mU/L) with free thyroxine of 5 pmol/L (reference interval 9–24 pmol/L; to convert pmol/L of free thyroxine to ng/dL, divide by 13). Random cortisol was 151 nmol/L (reference interval 150–700 nmol/L; to convert nmol/L of cortisol to µg/L, divide by 0.0157), and a stimulation test with the 1–24 fragment of adrenocorticotropic hormone (ACTH) showed a baseline cortisol of 56 nmol/L, which increased only to 57 nmol/L (normal response >500 nmol/L). Plasma ACTH was 1124 ng/L . . . [Full Text of this Article]

approach to a patient with severe hyponatremia
atypical presentation of primary adrenal insufficiency

POINTS TO REMEMBER