Portal Vein Pulsatility Index to Differentiate Hypervolemic and Hypovolemic Hyponatremia

The Pre-brief

Hypotonic hyponatremia is a common electrolyte disorder defined by a blood serum sodium value of less than 136 meq/L. Hyponatremia usually occurs in the state of a pathologic reduction in free water clearance. Reductions in free water clearance can occur in situations with either inappropriate antidiuretic hormone (ADH) excess or neurohormonal activation in a low-effective circulating volume state. Hypotonic hyponatremia can be further broken down by extracellular volume such as hypovolemic, euvolemic, and hypervolemic states (Figure 1). Precision in the diagnosis of volume status is notoriously low when dependent on the traditional examination findings of pitting edema and diagnostic studies such as chest x-ray, leading to inappropriate interventions. Urine electrolytes can be helpful, but analogous neurohormonal activation in hypovolemic and hypervolemic hyponatremia will exhibit similar urine sodium values, hence the diagnostic conundrum. Euvolemic hyponatremia will display high urine electrolyte values. Now, the terms hypovolemic and hypervolemic may be reductionist and not entirely accurate, but we will use these terms for the sake of discussion. Hypervolemic pathologic states include congestive heart failure, nephrotic syndrome, and cirrhosis. In contrast, hypovolemic pathologic conditions include prolonged dehydration in the context of severe malnutrition (aka “tea and toast” diet), excessive diuretic use… The focus of this post will be venous congestion related to congestive heart failure. How can we differentiate hypervolemic and hypovolemic hyponatremia; I propose the use of portal vein pulsatility.

Physiology

As Figure 3 describes, it is commonly understood that hyponatremia can progress to acute kidney injury in the setting of low effective circulating volume (includes hyper and hypovolemia). As the Renin-Angiotensin-Aldosterone System (RAAS) activates to preserve systemic perfusion, elevated levels of Angiotensin II force the proximal tubules to retain sodium (and therefore free water). Since RASS only reacts to the “effective” circulating volume, the resulting hyponatremia (and subsequently low sodium levels in the urine) can occur in either volume up or down states. What’s needed is a tie-breaker that helps us discern venous congestion; contrast with euvolemic hyponatremia which exhibits elevated urine electrolytes. Several studies have shown the predictive association between pulse-wave doppler pulsatility in the portal vein (PV) and AKI in critically ill post-surgical patients (1,2). Under normal circumstances, flow is relatively uniform through the PV. In congested/ hypervolemic states, pulsatility increases as estimated via the pulsatility index (Figure 2), with >50% being highly suggestive of venous congestion and hypervolemia (1, 2). Furthermore, a small case series have demonstrated portal vein pulsatility to predict better characterize hyponatremia(5).