A 62-year-old woman is brought to the hospital with sudden onset headache followed by nausea and vomiting. Upon arrival to the emergency room, she is lethargic with a Glasgow Coma Scale of 5. Significant vital signs include a blood pressure of 220/130 mm Hg. She is emergently intubated. CT scan of the head reveals subarachnoid hemorrhage in the basilar cisterns. She undergoes placement of a right frontal extraventricular device and coiling with improvement of her neurological examination. Over the following days, she is weaned off propofol. However, on the seventh day, her urine output increases to 4 L/d and she becomes hypotensive with blood pressure of 89/60 mm Hg and pulse rate of 118 beats/min. Laboratory data show:
What is the MOST likely cause for the patient’s acute changes?
A. CSW syndromeCorrect Answer: A
The pathophysiology of CSW syndrome remains poorly understood. There are two proposed mechanisms that lead to CSW. One of the mechanisms involves the disruption of the sympathetic neural input which normally promotes the reabsorption of sodium. The other mechanism is natriuresis induced by natriuretic peptides that are released in patients with brain injury. Both of these mechanisms lead to decreased activation of the renin-angiotensin-aldosterone system, leading to decreased sodium absorption at the proximal tubules.
CSW syndrome and SIADH both have similar laboratory values, including low serum osmolality, high urine osmolality, and high urine sodium levels. The most important distinguishing feature is the extracellular fluid volume status. Patients with CSW will have low extracellular fluid, reflected by their hypotension, whereas SIADH patients are generally euvolemic.
Evaluation of 24 hour uric acid excretion may also aid in the diagnosis as patients with SIADH. Uric acid is normally resorbed in the proximal tubule along with sodium. Both SIADH and CSW results in loss of uric acid via urine. However, an important differentiating feature is that in patients with SIADH, serum uric acid level and fractional excretion of uric acid normalize after correction of the serum sodium level, whereas the uric acid level remains low and uric acid excretion remains elevated in patients with CSW, despite correction of hyponatremia.
Common causes for CSW include subarachnoid hemorrhage, intracranial tumors and infections. Overall, the prevalence of CSW is less common than SIADH, but it is important to exclude as the treatment for CSW and SIADH vary vastly. The treatment for CSW includes administration of fluids and mineralocorticoids. In contrast, SIADH is treated with water restriction.
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