Saturday, February 5, 2011

OMG, that is not pseudohyponatraemia!

One fine day during my rounds (on public holiday, the Chinese New Year), my junior medical doctor asking me whether to correct the patient's Na of 120 or not because one of the nephrology doctors said that the patient is actually having pseudohyponatraemia. I asked him back, a little bit excited " Wow, since when the hospital is able to measure serum osmolality?" In a confused manner he showed me the entered notes:
"Calculated patients's osmolarity is 290 i.e. 2 (120) + glucose (10) and BUN of 40. Therefore this patient has pseudohyponatraemia"
I was taken aback, and said "OMG, that is NOT pseudohyponatraemia!" Later, I attempted to explain to him and my interns about the classification of hyponatraemia, definition of pseudohyponatraemia and the meaning of effective osmolarity. Since he is a very junior doctor and he was bewildered with my explanation, I decided to stop my bedside teaching at that point. Furthermore, that was my first patient (out of twelve) on a public holiday ICUrounds. I reassured him that I will discus this issue later.

The background of my hospital: I am working in one of the public hospitals in Malaysia (general hospital) and don't you believe it our lab has no facility to measure serum and urine osmolality! Very Very Frustrating..
Back to the issue above, there are a couple of questions to be answered:
1. How is hyponatraemia classified?
2. What is the corrected osmolality?
3. Types of hyponatraemia in advanced renal failure?
4. And that will lead to the main question, either to treat the hyponatraemia or not.
Yes, let us back to basics

Calculated osmolarity= 1.86 x ( [Na] + [K] ) + [glucose] + [urea]


Hyponatraemia

Hyponatraemia is defined as serum sodium of less than 135 mmol/l and may be classified as isotonic, hypertonic or hypotonic, depending upon the MEASURED osmolality.
In evaluation of hyponatraemia, the history and physical examination should be directed toward identification of findings that are typical of the particular causes of hyponatraemia and assessment of volume status.
Three lab tests provide important initial information in the differential diagnosis of hyponatraemia:
1. Serum osmolality
2. Urine osmolality
3. Urine sodium concentration

Serum osmolality (Sosm)ranges from 275 to 290 mosmol/kg is reduced in most hyponatraemic patients because it is primarily determined by the serum Na concentration and accompanying anions.
In patients with advanced renal failure, the hyponatraemia is due to an inability to excrete water resulting from the impairment of renal function. Although this will tend to lower the Sosm, this effect is counterbalanced to a variable degree by the associated elevation in blood urea nitrogen (BUN) resulting in Sosm that may be normal or elevated.
However there is a difference between the measured serum osmolality and effective serum osmolality in patients with renal failure. In contrast to sodium and glucose, urea is an ineffective osmole, since it can freely cross cell membranes and therefore does not obligate water movement out of the cells. Thus, patients with hyponatraemia and renal failure have a low effective serum osmolality that becomes apparent if the measured Sosm is corrected for the effect of urea:
Corrected Sosm = Measured Sosm - BUN (mmol/L)
For this reason I prefer the classification according to the tonicity.
Tonicity:
Osmolality is a measure of the number of the osmol/kg of water. The osmolality of the ECF is due largely to sodium salts. Clinical effects of hyperosmolality, due to excess solute, depend upon whether the solute distributes evenly throughout the total body water (e.g. permeant solute of alcohol or urea) or distributes in the ECF only (e.g. impermeant solutes of mannitol or glucose). With impermeant solutes, hyperosmolality is associated with a shift of fluid from the ICF to the ECF compartment. Hyperosmolality due to increased impermeant solutes is known as hypertonicity.

Pseudohyponatraemia
Plasma normally contains 93% water and 7% solids (5.5% proteins, 1% salts and 0.5% lipids). If the solid phase is elevated significantly (e.g. in hyperlipidaemia or hyperproteinaemia), any device which dilutes a specific amount of plasma for analysis will give falsely lower values for all measured compounds. This effect produces "factitious hyponatraemia" or pseudohyponatraemia (since it represents a labarotary artefact) and is associated with a normal measured serum osmolality.
Thus a normal serum Na concentration of 142 mEq/l (measured per litre of plasma) actually represents a concentration in the physiologically important plasma water of 153/L (142 / 0.93 = 153). In patients with marked hyperlipidaemia or hyperproteinaemia, the proportion of the plasma that is water falls to a lower value. As a result, the sodium concentration per liter of plasma will fall, which is an artifact since the physiologically important sodium concentration per liter of plasma water is normal. Supposed that the plasma water constitute 80% of the plasma in a patient with hyperlipidaemia. The Na concentration of 120mEq/l (measured per L of plasma) would be corrected to 150mEq/l.
Many lab analysers measure Na with ion-selective electrodes which utilise indirect potentiometry in which the plasma sample is diluted before measurement. This analysers will report a low Na concentration. Ion selective electrodes will reveal a normal sodium concentration if an instrument employing direct potentiometry is used.
I hope this would explain why I was surprised with the conclusion made by that doctor from that particular (neprology) dept.

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