#17 Hyponatremia w/ Dr Joel Topf
Sit back and grab some salty treats as you enjoy the mindful musings of master nephrologist Dr. Joel Topf (Twitter: @Kidney_Boy) who joins Nick & Cyrus to chat about hyponatremia in critical illness - a very common but potentially very serious condition. Here we discuss diagnosis and management of hyponatremia with special attention to those in the intensive care unit. Of course, no discussion is complete without plenty of time dedicated to osmotic demyelination syndrome (aka: central pontine myelinolysis) which gets plenty of face-time during this episode. Give it a listen and leave feeling confident in your ability to diagnose and manage a very prevalent condition in our patient population!
Quick Take Home Points:
Hyponatremia is common but can be serious if mismanaged. Osmotic Demyelination Syndrome (ODS) is rare but catastrophic. For people with severe hyponatremia (serum sodium less than 125 mEq/L), the recommended rate of correction is 6-8 mEq/L/day to reduce the risk ODS.
Check serial sodium using either point of care or laboratory, but don’t mix and match.
3% normal saline can be safely given peripherally.
Treatment of hypokalemia will increase serum sodium. Be cautious in patients with both mild hypokalemia and severe hyponatremia.
Use the ddAVP clamp technique to avoid overcorrection.
Show Notes:
Context about hyponatremia in the critically ill
Hyponatremia is a challenging and often humbling problem! Unlike hypokalemia or hyperkalemia, for example, we don’t have classic EKG findings we can point to in order to clearly determine the clinical relevance of a patient’s low sodium. It is important to view the patient’s sodium in the context of their illness and presentation, and approach with humility!
Get help if you need it!! Dr. Topf recommends getting assistance from your friendly neighborhood nephrologist if there is cause for question or concern, rather than following an algorithm and potentially getting burned in tricky cases. Sometimes the labs tell the story and sometimes they don’t. Sometimes the history can be very misleading!
For example, Dr. Topf describes a patient with a serum sodium of 116 mEq/L with nausea and vomiting…
They could have hyponatremia due to volume depletion
They may have nausea & vomiting → SIADH → hyponatremia
Or event their acute hyponatremia → increased ICP → nausea and vomiting
All of this is possible, but it would be easy to anchor on volume depletion → hyponatremia and treating it as such, erroneously!
Definitions:
Hyponatremia is defined as a serum sodium level of < 134 mEq/L, with severe hyponatremia defined as < 125 mEq/L.
Osmolarity: total concentration of solutes in a liter of solvent
Tonicity: specifically refers to the concentration of solutes that do not easily cross cell membranes, thereby affecting water movement. This cannot be readily measured, and thus, we measure osmolarity (more of a “catch all”) instead.
Approach to hyponatremia
Start off by checking a serum osmolarity. We cannot check for tonicity, so this is the next best thing we can do to confirm “true” hyponatremia. The best time to do this is right at presentation, however, it should still be done if the patient has received treatment (such as NS)! Other labs like glucose, total protein and lipids can be checked to rule out hyponatremia secondary to the effects of hyperglycemia or the relatively rare pseudohyponatremia whereby the sodium is reported as low as a function of the lab assay in the setting high protein or lipid content within the blood, however, the sodium content of the “water portion” the blood is normal from a concentration standpoint.
Other labs you will want to check include urine osmolarity and the urine sodium in order to establish the neurohormonal state.
The urine osmolarity is going to be the “ADH dipstick” as Dr. Topf calls it!
Urine osmolarity should be relatively low if serum ADH levels are low (low anti-diuresis is pro-diuretic, therefore high free-water content in the urine, resulting in a low urine osmolarity) - and typically UOP will be high.
This in conjunction with hyponatremia suggests primary polydipsia or low solute intake (tea & toast diet or “beer potomania).
Conversely, if ADH levels in the serum are high - i.e. an anti-diuretic state - whatever urine is produced should be concentrated, and thus the urine osmolarity will be high.
Checking the serum sodium
Obviously, treating hyponatremia requires checking the serum sodium!
How often? Q4-Q2 hours in patients with near-severe or severe hyponatremia, favoring Q2 in those receiving active management.
Q2 labs likely means and ICU admission (practically speaking).
Also, consider that point of care testing versus the testing run in your chemistry lab are different assays, and therefore will often not correlate. Pick a modality and stick with it! We would suggest using the electrolytes from your blood gas analyzer because it is a faster test and non-dilutional - so you will not be tricked by pseudohyponatremia.
Dispo, dispo, dispo!
There is no magic sodium level that must, under all circumstances, dictate disposition.
Patients who are going to get the DDAVP clamp (see below) should be on, at least, a step down unit so that their labs can be more closely followed.
Patients who are thought to be at higher risk for osmotic demyelination syndrome (ODS) or other concerning findings, should be in an ICU.
Liver disease/cirrhosis, alcohol use disorder, altered mental status, hypokalemia, malnutrition.
3% saline administration - which is safe to be given via peripheral IV - may necessitate ICU admission in certain institutions.
Patients who are anticipated to get DDAVP & repeated doses of 3% saline who will need recurrent timely lab draws are likely best served in the ICU.
Institutional policy will often dictate disposition - these are some of our thoughts based on discussion with Dr. Topf.
Osmotic Demyelination Syndrome (ODS) - The elephant in the room
There is a ton of literature on this terrifying condition, however, Joel casts some valuable light on this:
Based on most recent data, the incidence of this condition resulting in severe disability is much lower than historically thought / classically taught.
Data suggests that osmotic demyelination as a finding is fairly common, but often it does not result in long-lasting symptoms in many cases.
Risk factors: Liver disease/cirrhosis, alcohol use disorder, altered mental status, hypokalemia, malnutrition.
Rate of correction:
Original report of ODS (NEJM 1986) showed correction >12 mEq/L/day was associated with ODS
Thus the previous guidance was to correct by 8-10 mEq/L/day
More recent guidance suggests a more cautious goal: 6-8 mEq/L/day
Unfortunately, recent data suggests a worrisome reality:
Many patients were overtreated and did completely fine… which seems reassuring…
… However, of the 12 cases of ODS identified, >50% occurred in patients who corrected SLOWER than 8 mEq/L/day!
Our take away: There is much more involved in the manifestation of ODS than simply the rate of correction of sodium. We would recommend assessing the patient and their risk factors for ODS, trying to achieve a correction rate between 6-8 mEq/L/day - because that’s something we have control over.
Hypokalemia and Hyponatremia - two birds of a feather
Dr. Topf reminds us that every mL of potassium chloride is functionally equivalent to about two mL of 3% saline.
In a patient with hypokalemia that is aggressively repleted, cell membrane Na/K activity will cause exchange of potassium for sodium, resulting in an increase in serum sodium as a function of cellular efflux into the serum.
That efflux - coupled with sodium infusion - could result in a significant and perhaps unexpected rise in serum sodium that results in rapid overcorrection!
Our take away: If the patient has severe, life-threatening hypokalemia - it must be treated. However, there is no need to gild the lily and replete a potassium of 3.2 to 3.6 (assuming no EKG changes) in the setting of severe hyponatremia which takes precedence. Treat the sodium first, carefully, Then address the potassium.
3% sodium and severe hyponatremia with seizures
Dr. Topf follows the European Endocrinology Society guidelines for this and gives the severely hyponatremic seizing patient 150 mL of 3% saline, checks a serum sodium, and then gives another 150 mL of 3% prior to the results. This is generally enough to get a patient out of the danger zone.
You could alternatively follow the American guidelines and give 100 mL of 3% q20 minutes up to a total of 300 mL.
This can be done in conjunction with antiepileptic treatment for the seizure.
Either approach should be adequate to correct the sodium enough to remove that as a causative factor for seizure, allowing you to treat the patient “normally” based on their likely underlying disease (water restriction vs solute administration, etc.).
Around a 5-point (or so) increase in serum sodium is usually sufficient.
Dosed as 2 micrograms Q8 hours until the serum sodium is around 125 mEq/L.
Why? This “sets” the patient’s ADH levels such that they don’t experience an acute rise in serum osmolarity and a subsequent drop in ADH that results in the production of large-volumes of dilute urine that can contribute to over correction.
Can give “reactively” if a patient being treated develops acute large-volume urine output, although, we recommend the proactive strategy.
Note: While “on the clamp” 3% sodium will need to be used to raise the sodium to the desired goal.
Who to treat? Your high risk patients as mentioned above, as well as those who are thought to have profound volume depletion who are likely to over-correct once volume is restored.
Otherwise healthy, robust patients without the aforementioned risk factors, with hyponatremia of unknown chronicity may not need the clamp - but it could be used if a marked increase in dilute UOP is identified.