March 23rd, hyponatremia

Hyponatremia – common issue of hospitalized patients.  We have limited amount of evidence for treating hyponatremia, specifically a lack of RCTs. Searching through the literature there are review articles and case reports/series. If you have the time

Clinical practice guideline on diagnosis and treatment of hyponatraemia in the European Journal of Endocrinology. Spasovski et al

 

Like always, we assess for stability, someone who is hyponatremia and seizing we’d consider given them a bolus of 3% normal saline of 150 mL over 20 minutes (as per europena guidelines, uptodate suggest 100 mL of 3% bolus. Knowing that there is an increased risk of osmotic demyelination (which was originally described in severely malnourished alcoholics).

Once they are stable, we consider acute vs chronic hyponatremia, acute changes can generally be changed more quickly because the brain has not had time to adjust its osmolality (a low number).

More often than not we don’t know the acuity, so correcting it slowly is best.

Next  we need an approach – easiest thing is to first rule out pseudohyponatremia, lipids, protein and glucose. Often books will discuss how glucose is a true cause and this is because the excessive glucose will pull water into the intravascular space.  In DKA we add 3 to the sodium for every 10 glucose above 10 because once we lower glucose, water will dissipate and thus THAT will be the left over value.

Multiple myeloma with excessive protein is a classic pseduohyponatremia – extra points on your future rotations if you know that an arterial blood gas can be used to find a TRUE sodium, important because a pseudo and true hyponatremia can be present at the same time. MM may also present with a normal anion gap!

So you check the serum osm and it comes back at 240, so this is true hyponatremia! Next step is usually to look at the volume status.

I start with the overloaded patient – on exam, pitting edema, increased jVP, ascites (S3 heart sound if you believe you can hear it!). It is due to three things: CHF, liver cirrhosis, and nephrotic syndrome – all of these patients will have elevated ADH levels related to the kidney thinking its underperfused… high ADH levels means reabsorption of water and diluting serum sodium.

 Urine sodium in the above situations is usually on the lower side because of decreased effective circulating volume and thus aldosterone levels are high which will reabsorb sodium.

In all of the above, specifically CHF and cirrhosis, the low sodium usually is a poor prognostic sign, refer to MELD sodium and (http://www.ncbi.nlm.nih.gov/pubmed/15719386), however if serum sodium is less than 120, consider another mechanism (sig. increase free water, new medication, etc.)

Hypovolemic is next consideration because its easier. The classic situation is someone with vomiting or diarrhea (getting rid of isotonic fluids) and ingestion  free water to stay hydrated.

On exam: we look for tachycardia, hypotension, orthostatic vital signs (change in HR 30, SBP 20, and DBP 10), dry axilla, dry mucous membranes.

Other causes are burn victims, blood loss (all with increase free water intake). In this situation urine osm should be high and urine sodium should be low – they are concentrating their urine and reabsorption sodium so water can follow

Pearl: adrenal insufficiency causing hypotension/dehydrated state with an increased urine sodium because aldosterone levels are low.

FYI – free water doesn’t mean they stole it, or it was given to them , it refers to water without solute.

Another situation is after marathons, taking lots of water in. The concern with DROPPING sodium so quickly is cerebral edema.

Finally and most commonly seen issue in my practice is the euvolemic hyponatremia, though often it can be difficult to tease out if its euvolemic or mildly hypovolemic. 

If the urine osm is less than 100, it essentially tells they have psychogenic polydipsia with decrease solute intake.

Euvolemic hypotonic hyponatremia
SIADH: (increase urine osm, normal urine sodium, decrease BUN)
- malignancy, lung, brain, GI, lymphoma
- pulmonary - pneumonia, asthma, copd
- intracranial: trauma, stroke, hemorrhage
- drugs: SSRIs probably the most responsible, antipsychotics, anti-epileptics, MDMA
- other: pain, nausea, post op!

Endocrine: increase ADH is seen with decrease glucorcoticoid (adrenal insuff), also hypothyroid
psychogenic polydipsia: usually drinking >12 L/day of water, urine osm <100, often associated with very low uric acid levels

*from pocket medicine
Low solute: "tea and toaste" beer potomania" - decrease daily solute load, increase free water, insufficient solute to excrete water intake (if only 250 mOsm/day, minimum urine Osm = 60 mOsm/L - excrete in ~4 L; if water ingestion exceeds this, we have water retention).

If symptomatic aka seizure acute decrease LOC, 3% NS 150 mL over 20 min is ideal with repeating lights stat immediately after.

If hypovolemic - treat with NS, give slowly ~75 mL/hr frequent checking of lytes (there is a formula to calculate this).
SIADH - free water restrict, can consider salt tabs if chronic and no CHF, fix underlying cause
hypervolemic - mobilize fluid intravascularly, lasix for CHF, consider albumin in cirrhotics, consider

 Fluid restriction, ~1.5 L/day.“vaptans” are a class of medication that exists but in RCTs give a mild benefit over fluid restriction and are very expensive.

Below is one of the many charts that gives a breakdown, never hurts to have a look before diagnosing a cause of hyponatremia in patients.