Tonicity, osmolality, effective and ineffective Osmoles

Consider these questions that may arise in the assessment of patients with hyponatremia:

In patients with hyperglycemia, is correction of the serum sodium necessary?  Is the corrected serum sodium a valid indication of the risk for neurologic complications, or should one use the uncorrected sodium?

High blood alcohol levels may be associated with an elevated osmolality even in the presence of hyponatremia. Does this impact how we should interpret the serum sodium level? 

How does one interpret serum sodium in the face of extreme hypertriglyceridemia?

The answers to these types of questions depend on an understanding of the concepts of tonicity, osmolality, effective osmoles, and ineffective osmoles. These advanced concepts are covered in the JAMA Internal Medicine review linked here: 

Hyponatremia, Hyposmolality, and Hypotonicity:  Tables and Fables


Below is table 2 from the article which summarizes the key concepts.

What is beer potomania and what is the associated mechanism of hyponatremia?

 
This topic was reviewed in an article linked here: 

Beer Potomania—An Unusual Cause of Hyponatremia


General considerations

Beer potomania is an unusual syndrome of hyponatremia in patients with heavy alcohol consumption (usually beer) and very little solute intake. 

Mechanism of hyponatremia

Beer itself has sufficient caloric content for patients to subsist, with little additional food source, for an extended time. All of the solute in beer (ethanol) is metabolized, leaving only free water. Even when the vasopressin axis and renal tubular function are normal (leading, in the context of hyponatremia, to maximal urinary dilution, less than or equal to 100 mOsm per liter) these patients cannot normally excrete a free water load or maintain water balance. This is because, given the limits on the capacity of the kidneys to dilute the urine, free water clearance is dependent on the amount of solute delivered to the distal nephron.   For example, a person consuming a normal diet might be able to deliver 1,000 mOsm per day to the nephron. Assuming maximum urinary diluting capacity (50 mOsm/L) such a person would be capable of a daily excretion of 20 L free water per day. Put another way, that person could drink 20 L in a day's time, maintain neutral water balance, and not become hyponatremic., On the other hand, in beer potomania, solute intake, if any, is very low. Let's say for example a person has a daily solute intake of 150 mOsm.  Assuming normal diluting capacity such an individual would be limited to 3 L daily free water excretion. Considering that a six pack of beer contains just over 2 L, that person would have difficulty maintaining water balance.

Additional points to consider

Tea and toast syndrome can be considered the physiological equivalent of beer potomania. A review of tea and toast syndrome is linked here: 

Tea and Toast Syndrome: A Case Report

Beer potomania is a relatively uncommon cause of hyponatremia in alcoholism. In patients hospitalized with alcoholism volume depletion is probably the most common cause followed by acute anti-diuresis due to stress related vasopressin secretion.

Beer potomania may not always present in pure form. There may be concomitant other disturbances in water balance. 

Among hyponatremic patients, those with beer potomania are at particularly high risk for osmotic demyelination syndrome. This complication has been reported in as many as 18% of patients with beer potomania. In such patients who are hospitalized, the mere provision of solute, whether via IV fluids or diet, is likely to restore some degree of free water clearance capacity and result in a brisk water diuresis.