Links To And Excerpts From CoreIM - 5 Pearls On Hyponatremia Diagnostics

Start at 35:00

In this post I link to and excerpt from CoreIM’s Feb 10,2021 show notes and podcast and the transcript of 5 Pearls On Hyponatremia Diagnostics [There is a second episode coming on Hyponatremia Therapeutics].

Here is CoreIM’s link to the excellent and complete article on Hyponatremia from Amboss.

Here are excerpts from the show notes of 5 Pearls On Hyponatremia Diagnostics:

Show Notes

Pearl 1 – General Approach

Hyponatremia is a significant clinical problem:

Most common electrolyte disorder, occurring in up to 30% of hospitalized patients

Mild chronic hyponatremia is associated with more frequent falls – gait and attention impairments have also been observed

H&P – may be helpful, but don’t ignore other objective data that contradicts!

History:

Quickly assess for red flags (confusion, seizures) → immediate intervention, ICU admission

Ask about dietary history, fluid/EtOH intake, new meds, endocrine ROS, relevant comorbidities

Physical Examination:

Volume status is theoretically helpful as diagnostic algorithms hinge on it, but error prone

Our approach focuses on understanding what each diagnostic test adds vs. rote dependence on algorithm

More helpful given that most hyponatremia in the hospital is multifactorial

Ask yourself where your patient with hyponatremia is on “Cartesian space” with:

Anti-diuretic Hormone (ADH) secretion, as indirectly measured by UOsm relative to

Effective arterial blood volume (EABV), as estimated based on clinical examination and measurement of urine sodium

What if we encounter a patient after intervention, and without complete labs or urine studies?

Still obtain appropriate serum and urine studies as you can assess response to interventions (urine output, change in urine concentration and serum sodium) and the patient’s current ADH/EABV state

Pearl 2 – Serum Osmolality (Normal value 280-285 mOsm/kg)

We expect patients with true hyponatremia to have a low osmolality (<280 mOsm/kg)

This makes sense because sodium is the most significant contributor to osmolality

SOsm= 2 [Na+] + [Glu]/18 + [BUN]/2.8

The equation in countries that use the metric system also entails sodium x 2

Serum osmolality can be thought of as a “quality check” to rule out other osmoles that may be contributing to the hyponatremia.

If osmolality is normal assess if the patient has high triglycerides or an extra protein in blood (e.g. Multiple myeloma, recent IVIG administration) Such cases referred to as “pseudohyponatremia” = lab artifact, not of clinical significance.

Computer expects that aqueous component of blood is 93%, with 7% serum particles

High serum lipids or extra protein changes this ratio and impact the sodium calculation

Want to be sure? Whole blood sample of serum osmolality will not be subject to this error

Such cases referred to as “pseudohyponatremia” – laboratory artifact

If osmolality is elevated (usually >280-285 mOsm/kg), or if normal osmolality without elevated proteins/lipids, look for extra osmoles, either measured or unmeasured!

Measured: Severe hyperglycemia, BUN

Unmeasured: ETOH, Toxic alcohols, iodinated contrast, sucrose

Serum osmolality assessment prompts us to consider effective and ineffective osmoles at play:

Effective osmoles (sodium, glucose, potassium) do not cross the plasma membrane, and therefore cause shifts in water movement (impact tonicity)

Most of the clinical complications that arise as a result of hyponatremia (and its correction) are driven by the fact that sodium is an effective osmole – it impacts tonicity, and therefore cell size.

Ineffective osmoles (ethanol, urea, lactate) cross the plasma membrane more readily, and therefore do not cause shifts in water movement (does not change tonicity)

Serum osmolality is not a serially measured lab!

Measure it once unless there is a significant sodium change that is difficult to contextualize.