This is a "dilutional" hyponatremia. Essentially, it is the result of water moving into the extracellular fluid to dilute whatever extraneous osmotically active agent is present there.

Historically, such hyponatremia has not yet appeared in the CICM fellowship exam. However, HONK makes numerous appearances, and on occasion the candidates have been asked to calculate the corrected sodium (eg. in Question 19 from the second paper of 2010).

hyperosomolar hypernatremia

The resulting expansion of the extracellular compartment produces a dilution of the remaining electrolytes.

Observe. Let us take a cylinder model of human fluid physiology, and give it a massive dose of undiluted intravenous glucose syrup. And lets prevent the body from disposing of it properly by killing the kidneys and impairing the cellular uptake of glucose. Lets cook up a HONK.

infusion of undiluted 100g glucose.

Changes to the initial conditions

Let us say that we have given 100g of glucose, which is about 556mmol. Without functioning GLUT transporters, this syrup will distribute into the extracellular fluid alone.

Voila. Hyponatremia. Without getting rid of any sodium, we have produced a low serum sodium, and the serum osmolarity is significantly higher than it should be, owing to the presence of 36mmol/L of glucose.

result of the infusion of undiluted 100g glucose

Calculation of the Corrected Sodium

There is a famous equation which describes the "correction" of sodium.

hyperglycaemic hyponatremia

Does it fit our model? According to the above equation, the sodium should drop by 10.2mmol/L. The model predicts a drop of 11.6mmol/L. So the model is not wildly incorrect.

The "corrected" sodium is what one will be left with after one gets rid of all the glucose. It is useful to be able to predict this, because without fluid deficit correction a severe hypernatremia may result during the management of a HONK state. However, one should not be fooled by the use of the term "corrected sodium" to assume that the sodium from the lab results is somehow "incorrect". The sodium concentration reported by the lab is the accurate concentration of sodium in the body fluids. And all the other ions in the body fluids are diluted to the same extent. Thus, one should use the "uncorrected" sodium to calculate the anion gap (this issue is discussed with greater detail in the chapter on anion gap calculation)

What are the causes of hyperosmolar hyponatremia?

Just about any extracellular osmolar load.

The common ones are:

  • Glucose as above
  • Mannitol - following a mannitol infusion... although this turns into hypernatremia very quickly, as mannitol is a free-water-sucking osmotic diuretic
  • Glycine causes a high osmolar gap hyponatremia, usually without hyperosmolarity because it is absorbed together with large amounts of water
  • Alcohol intoxication can cause hyperosmolarity, and thus hyponatremia, but the more common causes of a hyponatremic drinker woud probably be beer potomania and hypertriglyceridaemia. Typically, the inhibition of ADH by alcohol actually leads to massive diuresis and dehydration after a long night on the piss, and thus hyperosmolar hyponatremia is only a concern within the first few hours of drinking.

References

Yun JJ, Cheong I. Mannitol-induced hyperosmolal hyponatraemia. Intern Med J. 2008 Jan;38(1):73.

Rothenberg, David M., Arnold S. Berns, and Anthony D. Ivankovich. "Isotonic hyponatremia following transurethral prostate resection." Journal of clinical anesthesia 2.1 (1990): 48-53.

Liamis, George L., et al. "Mechanisms of hyponatraemia in alcohol patients."Alcohol and Alcoholism 35.6 (2000): 612-616.

Taivainen, Hanna, et al. "Role of plasma vasopressin in changes of water balance accompanying acute alcohol intoxication." Alcoholism: Clinical and Experimental Research 19.3 (1995): 759-762.