Nephrologists are often consulted for hyponatremia. Although the causes are many, the basic framework is straightforward: start with the history for clues, then check serum osmolality. Serum sodium is a surrogate for extracellular tonicity; thus, a low sodium should correspond to low osmolality. If osmolality is high, consider other effective osmoles such as glucose (hyperglycemia) or exogenous agents such as mannitol. If osmolality is normal when hypotonicity is expected, consider pseudohyponatremia from severe hypertriglyceridemia or hyperproteinemia (uncommon with modern direct ion-selective electrodes).

Next, look at urine osmolality. If it is high (arbitrary cutoff >100 mOsm/kg), that indicates ADH (anti-diuretic hormone) activity in the kidney. Remember, hyponatremia is almost always due to water excess (thereby diluting the sodium level), not sodium deficit. That means, kidneys should excrete more water (dilute urine) to improve hyponatremia. If urine osmolality is low (<100 mOsm/kg), the kidney is excreting maximally dilute urine yet still cannot correct the low serum sodium concentration—this typically occurs when the patient is ingesting excessive water coupled with low solute. Urine osmolality provides insight into ADH activity; beyond this, it has limited utility in distinguishing among the various causes.

Then look at urine sodium. It will be low (arbitrary cutoff of 20–30 mmol/L) when the kidney perceives a need to conserve sodium as in true hypovolemia or hypervolemia with sluggish circulation (e.g., congestive heart failure) or decreased effective circulating volume (e.g., cirrhosis). Sometimes the kidney wants to conserve sodium but cannot (e.g., diuretic use, adrenal insufficiency), in which case urine sodium will be high despite the patient being hypovolemic. Conversely, urine sodium will be high when there is no need to conserve sodium; in euvolemia, the kidney excretes whatever sodium is ingested. Also note that urine sodium can be influenced by fluids the patient received prior to consultation. In real life, by the time nephrology is consulted, multiple empiric therapies have often been attempted, and it’s common to encounter ambiguous or borderline laboratory values. Below is the simplified hyponatremia algorithm.

These lab values are helpful, but they often group together very different conditions such as hypo and hypervolemia. This is where physical exam (= POCUS) makes a difference by objectively assessing hemodynamic status to narrow the differential. Essentially, the management hinges on hemodynamic status, yet traditional clues like weight, BNP, auscultation, pedal edema, or the clinician’s feelings (“I feel the patient is dry”) are not so reliable. POCUS provides a real-time, bedside way to clarify volume status and guide therapy.

Isolated lung or IVC POCUS is popular with beginners, but it’s only one element of the hemodynamic picture as shown below. VExUS helps, but it still doesn’t inform the forward-flow aspect.

It is a common misconception that a small collapsing IVC is equal to hypovolemia. No, it is NOT.

So, how can we measure stroke volume at the bedside and use it to guide management? Below are some key infographics.
Remember, POCUS is all about interpreting sonographic findings in the right clinical context, so it works best when integrated with the rest of the clinical and laboratory data. Multi-organ POCUS often drives management changes or at least removes a lot of the guesswork, for example:

• Confidently give fluids to a hypovolemic patient (preferably with a DDAVP clamp).
• Use diuretics or urea in euvolemic hyponatremia with confidence, or pay attention to addressing pain/nausea – often overlooked non-osmotic/non-hemodynamic ADH triggers.
• Give diuretics to hypervolemic patients and monitor progress with changes in VExUS waveforms alongside labs.

By contrast, empirically giving normal saline to a euvolemic patient mislabeled as hypovolemic (based on isolated IVC findings) can worsen hyponatremia if their urine osmolality is higher than that of NS and even precipitate unnecessary ICU admission. Conversely, when urine osmolality is lower than saline, a rise in serum sodium with fluids may falsely suggest hypovolemia, even though the patient is actually euvolemic, delaying recognition of the true cause (for example, lymphoma).
In cirrhosis with a high-output state, hyponatremia may respond to vasopressors such as norepinephrine or terlipressin to raise mean arterial pressure by 10–15 mmHg.

Is there any evidence supporting POCUS use in hyponatremia? Yes, below is a table summarizing pertinent case reports published till date (May 2022). Click on the first author for the link. Is there any evidence, especially a randomized controlled trial demonstrating mortality benefit of using POCUS to evaluate hyponatremia? No, POCUS is only a diagnostic tool. Putting the probe on the body does not improve mortality, neither do auscultation nor touching the patient.

A recent prospective study evaluated the role of IVC in classification of hyponatremia. However, isolated IVC is subject to pitfalls as mentioned. Here is my letter explaining why.