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.
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.
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.
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.
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
Wael: If I am ever ordering q3hr BMPs, that to me is a patient who is at risk and requires close monitoring. The first 48hrs are the most critical in severe hyponatremia and I almost always have a foley placed. Most pts with SIADH on fluid restriction (even when on 3% saline) do not make much urine. With the DDAVP protocol (see upcoming posts) I see even less… mostly in the 20-40ml/hr range. I tell the nurses to call me (and also to draw stat serum sodium) if the urine output increases suddenly to more than (say) 300 ml/hr. That's when I know that the ADH levels are falling (or solute induced diuresis has started) and the pt's sodium is going to shoot up. I've found urine out put increase to be an extremely reliable and the first clinical sign of over correction.
Thank you for the very insightful posts. I'm eager to hear more about the 7L urine in response to 2 L fluid case. I assume the presumed ADH in her case was not secondary to dehydration.
I would like you to expand more on the way you would use urine output in your management. If you are not getting the serum Na, don't you need to know the urine Na as well?