SEVERE CHRONIC HYPONATREMIA: A Pathophysiological Rumination (Part 2)

PART 2: THE PEE IS THE KEY

I mentioned in the previous post that severe hyponatremia is multifactorial and that the contributing etiological factors in any given case may be transient and reversible.  In this post I would like to stress the importance of closely monitoring the urine output of the patient in addition to frequent monitoring of the plasma sodium.  Urine output is an extremely important clinical parameter that needs to be monitored closely but is not really mentioned in textbooks and handbooks.

Overcorrection by more than 12 mEq/L in 24 hours is not easy to achieve if the patient has a stable state of antidiuresis.  In an anuric patient with total body water of 32 L and a starting serum sodium of 108 mEq/L would require an infusion of more than 750 mL of 3% saline: a prescription not many of us would order.  In fact, during our review of cases of severe hyponatremia we found that the very popular Adrogue-Madias equation grossly underestimated the sodium correction in the majority of patients.  Most of the patients' sodium corrected far in excess of what the equation predicted.

The reason for that is that these equations treat the patients as if they were beakers that we can add sodium to and watch the plasma sodium rise as predicted.  However, unless the patient is on dialysis or in oliguric renal failure, they also lose free water in the urine, a fact that the equation does not take into consideration.  In fact, in our case series every patient that had an overcorrection of sodium beyond the desire goals, and had adequate documentation of ins and outs, had a documented large volume dilute diuresis.  Invariably, such large-volume water diuresis emerged suddenly as if an ADH switch was turned off, suggesting resolution of a transient source of ADH secretion.

While small, sudden increases in serum sodium are certainly possible with the addition of too much sodium to the system, very large and dangerous increases require simultaneous loss of free water.  A very illustrative case is one of a 26-year-old female I managed a couple of years ago.  She presented with a serum sodium of 108 mEq/L and received the inescapable 2 L of normal saline bolus in the ER and about 5 hours later her serum sodium was 131 mEq/L. With an estimated total body water of 32 L (and using the Edelman equation, see figure), if we considered her oliguric and try to account for the rise in serum sodium slowly on the basis of addition of sodium chloride to the system, we would require about 1.9 L of 3% saline to be infused in a 5 hour period!  However it is perfectly explained by the almost 7 L of water diuresis that emerged with the 2 L saline bolus.  More on this case in a later post.

In conclusion, very close monitoring of urine output should be an important and integral part of the early management of severe hyponatremia.  The sudden emergence of water diuresis is often the earliest sign of a rising serum sodium and should prompt a stat plasma sodium check. I have often relied upon a well documented q2hr urine output in ICU setting more so than the q2-4hr sodium levels which are fraught with the issue of delayed venipuncture and delays in reporting.

Posted by Hashim Mohmand