Hyponatremia in a 46-Year-Old Man After Head Trauma

Federico J. Teran, MD; Eric E. Simon, MD; Vecihi Batuman, MD

Disclosures

July 19, 2017

Discussion

The patient's hyponatremia with low plasma osmolality and high urine osmolality suggests syndrome of inappropriate antidiuretic hormone (SIADH) secretion.[1] When the plasma osmolality is low, the appropriate kidney response is to dilute the urine below the osmolality of the plasma, usually to maximally dilute levels of 50-60 mOsm/kg. This patient's measured plasma osmolality is low and close to the calculated osmolality (2 x [sodium] + [glucose]/18 + [BUN/2.8]), which rules out pseudohyponatremia. Pseudohyponatremia may be seen in patients with high levels of lipids or proteins, which displace serum water, resulting in an erroneous measurement of serum sodium.

Cerebral salt-wasting syndrome is more difficult to distinguish from SIADH. Some investigators consider it a variant of SIADH. The high urine sodium level and marked hypouricemia with renal urate wasting are consistent with cerebral salt wasting. Although cerebral disease is not a prerequisite of this syndrome, the patient does have a history of head trauma. Maesaka and colleagues[2,3,4] have argued that the term cerebral salt wasting should be replaced by renal salt wasting, as indeed the kidney is the organ responsible for the salt wasting. The proposed pathophysiology is relentless salt wasting in the kidney, possibly due to a salt-wasting factor or hormone, resulting in hypovolemia and triggering release of antidiuretic hormone. This syndrome, similar to SIADH, is also associated with hypouricemia and hyperuricosuria; however, unlike SIADH, both the hypouricemia and hyperuricosuria remain irreversible (fixed), which could be the distinguishing feature.[4] In this patient, repeat urine uric acid measurements were not performed; therefore, a salt-wasting syndrome cannot be definitively ruled out. However, such patients are often clinically hypovolemic and occasionally have orthostatic hypotension, which were absent in this patient, again favoring the diagnosis of SIADH.

SIADH is a disorder of water balance characterized by hypotonic hyponatremia and impaired water excretion in euvolemic individuals.[5,6] It is a common cause of hyponatremia and can be seen in diverse settings, including lung cancer (small cell), drug use (carbamazepine, certain selective serotonin reuptake inhibitors [SSRIs]), neurologic diseases (strokes, encephalitis, trauma), pulmonary diseases (pneumonia, tuberculosis), endocrine disorders (eg, hypothyroidism, pituitary disorders), and pain.[6]

Diagnosis is based on the exclusion of other hyponatremic conditions, the presence of hypo-osmolality with inappropriately high urine osmolality (less than maximally dilute) that is often hyperosmolar to serum (typically ≥400-500 mOsm/kg), and a urine sodium concentration usually above 30 mEq/L. Low serum urea levels and low serum uric acid levels with increased fractional excretion of uric acid (>9%-10%) are commonly associated with SIADH and may be helpful in confirming the diagnosis.[5,6]

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